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PRINCIPLES AND PRACTICE OF

CARDIOPULMONARY

PHYSICAL THERAPY

THIRD EDITION

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PRINCIPLES AND PRACTICE OF

CARDIOPULMONARY

PHYSICAL THERAPY

THIRD EDITION

Edited by:

Donna Frownfelter, MA, PT, CCS, RRT

NovaCare, Inc.

Contract Services

Region 7

Northwestern University

Programs in Physical Therapy

Chicago, IJlinois

Committed to Excellence

Glenview, Illinois

Elizabeth Dean, PhD, PT

Associate Professor

University of British Columbia

School of Rehabilition Sciences

Vancouver, British Columbia

With 22 contributors and 40] illustrations

Mosby

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 T Mosby
Dedicated to Publishing Excellence

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Editor: Martha Sasser
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THIRD EDITION

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 CONTRIBUTORS

Michael Wade Baskin, PT, RRT Anne Mejia Downs, PT, CCS
OwnerlExecutive Director Department of Physical and Occupational Therapy
GT Physical Therapy and Rehabilitation Instructor, Division of Physical Therapy
West Point, Mississippi Department of Medical Allied Health Professions
School of Medicine
Jean K. Berry, PhD, RN University of North Carolina
Senior Research Specialist Chapel Hill, North Carolina
Medical-Surgical Nursing
University of Illinois at Chicago Willy E. Hammon, BSe, PT
Chicago, Illinois Chief of Rehabilitative Services
The University Hospitals
Gary Brooks, MS, PT, CCS Special Instructor in Physical Therapy
Associate Professor College of Health
Health and Rehabilitation Sciences Clinical Instructor, College of Nursing
The Sage Colleges University of Oklahoma Health Sciences Center
Troy, New York Oklahoma City, Oklahoma

Susan M. Butl er, MMSe, PT, CCS Scott M. Hasson, EdD, PT

Division of Physical Therapy Director
Department of Rehabilitation Medicine Advanced Studies
Maine Medical Center School of Physical Therapy
Portland, Maine Texas Woman's University
Houston, Texas
Margaret K. Covey, MS, RN
Senior Research Specialist and Doctoral Candidate Lyn Hobson, PT, RRT
Medical-Surgical Nursing Rush-Presbyterian-St. Luke's Medical Center
University of Illinois at Chicago Chicago, Illinois
Chicago, Illinois
Gail M. Huber, MHPE, PT
L inda D. Cr ane, MMSe, PT, CCS Instructor
Instructor Programs in Physical Therapy
Division of Physical Therapy Northwestern University
University of Miami School of Medicine Chicago, Illinois
Miami, Florida

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vi Preface

Thomas Johnson, MD Claire Peel, PhD, PT

Associate Professor in Radiological Scienccs Department of Physical Therapy
University of Oklahoma Health Sciences Center School of and Allied Health Professions
Oklahoma Citv. Oklahoma Creighton
Omaha, Nebraska

ArthurV. PhD
Associate Professor
of
Susan K. MS, PT Rush Medical
Rehabilitation T herapy Services Illinois
Henry Ford Hospital
Detroit, Michigan Elizabeth J. Protas,PhD, PT, FACSM
Assistant Dean and Professor
Mary lnaSS l" School of Therapy
President, Physical
Texas Woman's University
Illinois
Houston, Texas

in Michael MD,
Northwestern University Assistant Professor of Medicine
Illinois Rush Medical
'-''''vU,,",V, Illinois
Mary Mathews, BS, RN, CCRN,RRT
Neonatal and Pediatrics Chest MA,PT
Coordinator Assistant Professor
Care Services Physical Program
Luke's Medical Center of Colorado Health Sciences Center
Denver, Colorado

Lisa Mendelson, MS, CPAN Alexandra J.

Practitioner-Teacher, College of Education Coordinator
Rush Luke's Medical Center University of Medical Center
Rush Physical Division
UIIC<lIW. Illinois Physical Medicine and Rehabilitation
Ann Arbor, Michigan
Victoria A. Moerchen, MS,PT
Doctoral Candidate in Motor Control Maureen DNSc,R , FAA
of Kinesiology Satellite Site Coordinator
Clinic
Early Intervention
Waisman Center Adjunct Clinical
Pediatric Consultant and Lecturer Rush College of Nursing
. of Wisconsin of Illinois College of
Madison, Wisconsin Chicago, Illinois

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 To our students

Present, and Future-

For T heir Inspiration, Inquiry, and Enthusiasm

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 CONTEMPORARY DEFINITION OF

CARDIOPULMONARY

PHYSICAL THERAPY

culation,

livery of noninvasive interventions in the

assessment, treatment, and follow-up) of patients with primary or secondary car­

diopulmonary dysfunction from acute, chronic, and acute-on-chronic

conditions, and the cardiopulmonary/cardiovascular manifestations of

disease. CPPT interventions include mobilization, body positioning,

control, coughing and airway clearance maneuvers, and manual tech­

niques. Wherever possible and appropriate, CPPT is applied to oxygen
and to or reduce the need for invasive medical
including Patient education and
patient-driven treatment planning are fundamental of CPPT. In addi­
tion, CPPT has an essential role in the promotion of optimal cardiopulmonary and
cardiovascular health and fitness in the population.

ix

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FOREWORD

Donna Frownfelter and Elizabeth Dean have succeeded in creating a unique set of re­
sources for students and clinicians. The importance of the oxygen transport mecha­
nism is woven throughout this text and accompanying case study book, Clinical Case
Study Guide. The disruption of the mechanism can create cardiopulmonary dysfunc­
tion and can result in reduced function, reduced functional work capacity, and death.
A comprehensive understanding of oxygen transport and the factors that determine
and influence it is therefore essential in order to assess the deficits of the mechanism
and determine treatment interventions.
The third edition of Principles and Practice of Cardiopulmonary Physical Therapy
is not simply a new edition of the former, Chest Physical Therapy and Pulmonary Re­
habilitation. It is a totally new textbook, encompassing both the cardiac and pul­
monary systems in health and dysfunction. The two previous editions have been
praised for their clinical relevance. The new books go a long way to support the state
of the art clinical practice with documented scientific literature.
The authors have many years of experience teaching undergraduate students as well
as consulting and teaching in professional postgraduate courses. These books have
been written in response to questions and concerns raised by students and clinicians.
This is the only text in which Mary Massery has published her work on neuropul­
monary rehabilitation. Several chapters emphasize positioning for respiratory success
and ventilatory strategies to improve rehabilitation potential.
The books are very user-friendly. Each chapter of the text has key terms and questions
for discussion to help the reader focus on the important concepts presented in the chapter.
The combination of the text and case study guide will be an asset in teaching cardiopul­
monary physical therapy. However, either book can be effectively used independently of
the other. The case study guide can be of assistance to physical therapists in helping them
focus on patient evaluation, cardiopulmonary dysfunction, and treatment approaches. I
applaud the authors for these new books and would highly recommend them for stu­
dents and clinicians.

SaLLy C. Edelsberg, MS, PT

Director and Associate Professor
Programs in Physical Therapy
Northwestern University Medical School

xi

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PREFACE

The work that has gone into this third edition has resulted in a completely new book!
When we first discussed the possibilities of a new edition, we knew it would be a total
change from Chest Physical Therapy and Pulmonary Rehabilitation. We wanted to
present a new approach, not just a revision. Elizabeth's research and study of oxygen
transport mechanisms in relation to patient treatment highlighted this concept as the
primary thread that would pull the new book together. The cardiopulmonary system
must be viewed as a whole, interacting with other body systems for optimal function.
Therapy interventions must incorporate cardiopulmonary goals as well as neuromus­
cuiar and musculoskeletal goals for patients to reach maximal rehabilitation potential.
We have attempted to pull together physiological as well as clinical data to meet
the changing needs of health care to provide objective documentation for our interven­
tions. Yet we were diligent in maintaining a text aimed at the undergraduate student or
practicing therapist with minimal background in cardiopulmonary physical therapy.
To that end we have tried to keep the material readable and very user-friendly. Our
hope is that virtually any question that may arise about treating a patient with car­
diopulmonary dysfunction would have some answers in this book.
We both teach undergraduate physical therapy students and thank them for their
input, questions, and concerns about patients with cardiopulmonary dysfunction who
have helped us focus this text to meet students' needs. In addition, through our contin­
uing education seminars with postgraduate physical therapists, we have been chal­
lenged to apply the concepts in light of the changing health care scene. How can we be
most effective and scientifically correct in choosing treatment techniques that have
demonstrated improvement in the oxygen transport mechanism and patient function?
We always learn when we teach, and we hope to share that learning with others
through this text.
We are excited about being able to present an accompanying text, Clinical Case
Study Guide. We are attempting to show the physiological principles presented in our
text, by identifying real-life case studies that physical therapists deal with every day in
their practice. Our hope is that this will be used widely in teaching physical therapy
students and will facilitate their understanding of how to effectively integrate car­
diopulmonary concepts in each of their patients, not just in patients with a primary
cardiopulmonary diagnosis.
To our knowledge, this is the first international book written dealing with car­
diopulmonary physical therapy. It is a blend of physiology and international ap­
proaches to the patient with cardiopulmonary dysfunction. We have had the privilege
of teaching and consulting internationally and have tried to make this text applicable
to all therapists regardless of their situation and the degree of sophisticated equipment.

xiii

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xiv Preface

We realize that in some Third-World hands-on therapy and positioning is the

only mode of available. We believe that this is often all that is needed when
with the proper concepts and thought processes.
We are with the way this edition has come together. We have many
new authors who have added and direction for both cardiac and
monary foci.
We are pleased this is finally completed and thank our families, friends, and col-
for us and us the rough times to see this book
Our hope is that this will be a welcome addition to your professional Ii­
and we welcome your comments and suggestions for future work.

Donna Frownfelter
Elizabeth Dean

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ACKNOWLEDGMENTS

There are so many people that I want to thank and acknowledge for their support and
contributions to this book. First, my family, for their understanding and support dur­
ing stressful deadlines and crunch spots. My husband David has been there for me
since I went to physical therapy school and has always encouraged me to do what my
vision led me to do. My three teenagers, Lauren, Daniel, and Kristin, have helped
keep my life on track and grounded in the reality of daily life while taking time to
"smell the roses." You are special gifts to me, and I love you.
To my students, I thank you for your questions, concerns, and wonderings about
what this cardiopulmonary stuff really means to your patients. You wonder if you can
really be a better therapist because you take these things into account in evaluation
and treatment. Please remember the difference between ordinary and extraordinary is
just that little "extra." I believe that is what incorporating cardiopulmonary attention
does; it adds the little extra. Be an extraordinary therapist, no matter what the health
care environment.
To the contributing authors, I thank you for your time and significant effort in
bringing together the literature and clinical aspects of cardiopulmonary physical ther­
apy. Your dedication to this project has made it much more than Elizabeth and I
could have done alone. You know how important it is to convey the message of treat­
ing the whole patient and helping them reach his or her potential.
To my colleague and soul mate Mary Masse!)/, who I have taught with, travelled
with, given seminars with, laughed with, and cried with, I thank you for all you have
taught me and how special it is to have someone you can always count on to discuss
a difficult patient or a personal issue. We have become quite a team, and I value our
professional and personal relationships. Your contributions to the clinical chapters we
have done together this time have been significant. I look forward to many more pro­
jects and fun times together. There is no greater pleasure for a teacher than to see a
former student travel in that teacher's tracks and surpass her. Thanks Spike!
My deepest thanks go to Elizabeth Dean. You have been an incredible colleague
who has given new life to this book. You have, in a gentle way, helped to ensure that
physiologic and scientific evidence be paired with our clinical experience and treat­
ment techniques. You have truly brought about a book that I could never have com­
pleted alone. Words are not enough to thank you for your commitment to this project
and the countless hours you have spent in a major revision of the former textbook. I
am delighted at what you have done and the depth of knowledge you have brought in
your content and organization of this book. I am honored that you chose this text in
which to share your work, and I have enjoyed working with you and learning from
you. We share a common bond in the relationships we have with our students and our

xv

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xvi Acknowledgements

desire to spread the word about the importance of including cardiopulmonary con­
cerns in the patient's evaluation and plan of treatment. We have grown close in the
last 10 years, and I value our friendship as well as our professional work together.
T hank you hardly is enough, but 'Thanks!"
To my friends, family, and fellow workers at NovaCare, Inc. Contract Services, I
thank you for your patience and understanding of the demands on my time and your
encouragement to continue and finish this project. Your support has meant a great deal
and I hope you feel a part of this, for it is because of you this has really happened. I'm
glad to have a work environment that supports personal and professional growth.
To our Mosby staff: Martha Sasser, thanks for your ideas and vision for going with
this new book. You saw the possibilities and were there with other suggestions to
make it even better (even if some of them came when we thought we were donel). To
Kellie W hite, you kept us on track and helped catch up with chapter authors who
needed a nudge and still had time to have Julia Isabelle-quite an accomplishment!
You will now find what we have, that motherhood is often harder than your other
job! Best wishes! To Mamata Reddy and Amy Dubin, you have pushed us through
the editing process with the gentle and firm hand that we needed and with much sup­
port and help. Thank you for your cooperation and critical eye in making this an ex­
cellent outcome.
Finally, and most importantly, I thank God for the vision, strength, and energy to un­
dertake this book and see it through to completion. My involvement in spreading the
word about the need for optimizing the cardiopulmonary system has always felt like a
mission. It has been amazing to me how many therapists don't see the need and how
they can have an "Aha!" experience in a seminar or class, or even just reading this book.
If I can have a small part in that experience, my "mission" has been fulfilled, and for that
I am grateful.

Donna Frownfelter

To Donna, for having made this dream come true. Our working relationship and
friendship began 10 years ago when I first approached Donna to review a manuscript
entitled 'The Pulmonary Effects of Body Positioning," published in Physical Therapy
in 1985. This publication was the stepping stone to a prolonged and ever-growing in­
terest in oxygen transport and how it is affected by cardiopulmonary interventions
such as body positioning and mobilization. T he enthusiasm, interest, and support of
Donna and my former graduate student, Jocelyn Ross, have fueled my energies in the
exciting dynamic area of cardiopulmonary physical therapy. My heartfelt gratitude to
you both.
To Daniel Perlman, for your encouragement and support of my liaison with Donna
at the outset and over the years. You knew a good thing when you saw it.
To Doug Frost, for your support in getting this project into the end zone. Thank
you for your support and for being there as the book continued to evolve.

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 Acknowledgements xvii

To our dedicated contributors, for your expertise, which has contributed to a vol­
ume on the principles and practice of cardiopulmonary physical therapy that is on the
cutting edge with respect to the scientific and physiologic literature. Thank you for
your contributions and team effort.
To my cardiopulmonary physical therapy colleagues and students for your inquisi­
tiveness and enthusiasm. T hank you all for your inspiration.
And not to forget the Mosby crew-Martha Sasser, Kellie White, Mamata Reddy,
and Amy Dubin-I thank each one of you for your commitment to making this book
the best it can be.

Elizabeth Dean

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 CONTENTS

PARTI CARDIOPUL MONARY FUNCTION IN HEALTH AND DISEASE, 1

Chapter 1 Oxygen Transport: The Basis for Cardiopulmonary Physical Elizabeth Dean
Therapy, 3

Chapter 2 Cardiopulmonary Anatomy, 23 Elizabeth Dean

Lyn Hobson

Chapter 3 Cardiopulmonary Physiology, 53 Elizabeth Dean

Lyn Hobson

Chapter 4 Cardiopulmonary Pathophysiology, 71 Willy E. Hammon

Scott M. Hasson

Chapter 5 Cardiopulmonary Manifestations of Systemic Conditions, 99 Elizabeth Dean

PARTII CARDIOPULMONARY ASSESSMENT, 1J5

Chapter 6 Measurement and Documentation, 1J7 Claire Peel

Chapter 7 History, 127 Willy E. Hammon

Chapter 8 Pulmonary Function Tests, 145 Donna Frownfelter

Chapter 9 Arterial Blood Gases, 153 Donna Frownfelter

Chapter 10 Principles of Chest X-Ray Interpretation, 159 Michael Ries

Thomas Johnson

Chapter 11 Electrocardiogram Identification, 169 Gary Brooks

Chapter 12 Multisystem Assessment and Laboratory Investigations, 189 Elizabeth Dean

xix

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XX Contents

Chapter 13 Special Tests, 197 Gail M. Huber

Chapter 14 Clinical Assessment of the Cardiopulmonary System, 209 Susan M. Butler

Chapter 15 Monitoring Systems in the Intensive Care Unit, 229 Elizabeth Dean

PART III CARDIOPULMONARY PHYSICAL T HERAPY INTERVENT IONS, 249

Chapter 16 Optimizing Treatment Prescription: Relating Treatment Elizabeth Dean

to the Underlying Pathophysiology, 251

Chapter 17 Mobilization and Exercise, 265 Elizabeth Dean

Chapter 18 Body Positioning, 299 Elizabeth Dean

Chapter 19 Physiological Basis for Airway Clearance Techniques, 321 Anne Mejia Downs

Chapter 20 Clinical Application of Airway Clearance Techniques, 339 Anne Mejia Downs

Chapter 21 Facilitating Airway Clearance With Coughing Mary Massery

Techniques, 367 Donna Frownfelter

Chapter 22 Facilitating Ventilatory Patterns and Breathing Mary Massery

Strategies, 383 Donna Frownfelter

Chapter 23 Exercise Testing and Training: Primary Cardiopulmonary Susan K. Ludwick

Dysfunction, 417

Chapter 24 Exercise Testing and Training: Secondary Cardiovascular Phyllis G. Krug

Dysfunction, 425

Chapter 25 Respiratory Muscle Weakness and Training, 443 Maureen Shekleton

Jean K. Berry
Margaret K. Covey

Chapter 26 Patient Education, 453 Alexandra J. Sciaky

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 Contents xxi

PART IV GUIDELINES FOR THE DELIVERY OF CARDIOPULMONARY PHYSICAL

THERAPY: ACUTE CARDIOPULMONARY CONDITIONS, 467

Chapter 27 Acute Medical Conditions, 469 Elizabeth Dean

Willy E. Hammon
Lyn Hobson

Chapter 28 Acute Surgical Conditions, 495 Elizabeth Dean

Mary Mathews

PART V GUIDELINES FOR THE DELIVERY OF CARDIOPULMONARY PHYSICAL

THERAPY: CHRONIC CARDIOPULMONARY CONDITIONS, 511

Chapter 29 Chronic Primary Cardiopulmonary Dysfunction, 513 Elizabeth Dean

Donna Frownfelter

Chapter 30 Chronic Secondary Cardiopulmonary Dysfunction, 567 Elizabeth Dean

Donna Frownfelter

PART VI GUIDELINES FOR THE DELIVERY OF CARDIOPULMONARY PHYSICAL

THERAPY: INTENSIVE CARE, 565

Chapter 31 Comprehensive Patient Management in the Intensive Elizabeth Dean

Care Unit, 567

Chapter 32 Intensive Care Unit Management of Primary EI izabeth Dean

Cardiopulmonary Dysfunction, 579

Chapter 33 Intensive Care Unit Management of Secondary Elizabeth Dean

Cardiopulmonary Dysfunction, 599

Chapter 34 Complications, Adult Respiratory Distress Syndrome, Elizabeth Dean

Shock, Sepsis, and Multiorgan System Failure, 617

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xxii Contents

PART VII GUIDELINE S FOR THE DELIVERY OF CARDIOPULMONARY PHYSICAL

THERAPY: SPECIAL CASES, 633

Chapter 35 The Neonatal and Pediatric Patient, 635 Victoria A. Moerchen

Linda D. Crane

Chapter 36 The Aging Patient, 669 Elizabeth J. Protas

Chapter 37 The Patient With Neuromuscular and Musculoskeletal Mary Massery

Dysfunction, 679

Chapter 38 The Transplant Patient , 703 Susan Scherer

Chapter 39 The Patient in the Community, 721 Donna Frownfelter

PART VIII RELATED ASPECTS OF CARDIOPULMONARY PHYSICAL THERAPY, 735

Chapter 40 The Art of Positioning and Moving Patients, 737 Mary Massery
Donna Frownfelter

Chapter 41 Respiratory Care Practice Review, 749 Michael Wade Baskin

Chapter 42 Care of the Patient With an Artificial Airway, 761 Lisa Sigg Mendelson

Chapter 43 Respiratory and Cardiovascular Drug Actions, 775 Arthur V. Prancan

GLOSSARY, Gl

INDEX, 11

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PAR T 1

Cardiopulmonary Function
in Health and Disease

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 CHAPTER 1

Oxygen Transport: The Basis for

Cardiopulmonary Physical Therapy

Elizabeth Dean

KEY TERMS Cellular respiration Gravitational stress

Exercise stress Oxygen transport pathway

INTRODUCTION
ceptual basis for cardiopulmonary physical therapy
Cardiopulmonary physical therapy is an essential non­ practice. Oxygen transport is the basis for life. Impaired
invasive medical intervention that can reverse or miti­ or threatened oxygen transport, hence, cardiopul­
gate insults to oxygen transport. It can avoid, delay, or monary dysfunction, is a physical therapy priority.
reduce the need for medical interventions, such as sup­ In health, the oxygen transport system is normally
plemental oxygen, intubation, mechanical ventilation, perturbed by movement and activity, changes in body
suctioning, bronchoscopy, chest tubes, surgery, and position, and emotional stress. In disease, disruption
medications. A comprehensive understanding of oxy­ of or threat to this system is always a medical priority
gen transpol1 and the factors that detelTnine and influ­ because of the threat to life or impairment of func­
ence it is therefore essential to the comprehensive as­ tional capacity.
sessment of oxygen transport and optimal treatment The fundamental steps in the oxygen transport
prescription to effect these outcomes. pathway, and their function and interdependence are
This chapter details the oxygen transport system, the described first. Special attention is given to cellular
pathway, and the component steps that provide a coo- respiration and the utilization of oxygen during me­

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4 PART I Cardiopulmonary Function in Health and Disease

+VC02
Airways/lungs
+V02
('\ ('\

. 4
c C
a a
g-
::J
g.
::J

FIGURE 1-1
Scheme of components of ventilatory-cardiovascular-metabolic doupling underlying oxygen
transport. (Modified from Wasserman K et al: Principles of exercise tesling and interpretation,
Philadelphia, 1987, Lea & Febiger.)

tabolism at the cellular level in muscle. Second, the 1992a; Goldring, 1984; Johnson, 1973; Ross, and
factors that normally perturb oxygen transport in Dean, 1989; Weber et aI, 1983).
health are described, namely gravitational stress sec­ Oxygen transpolt variables include oxygen delivery
ondary to changes in body position, exercise stress (002), oxygen consumption (V02) and the oxygen en­
secondary to increased oxygen demand of the work­ hancement ratio (OER) or the utilization coefficient.
ing muscles, emotional stress, and arousal. A thor­ Oxygen demand is the amount of oxygen required by
ough understanding of the effects of those factors that the cells for aerobic metabolism. Oxygen demand is
normally perturb oxygen transport is essential to ac­ usually reflected by V02; however, in cases of severe
curately assess and treat deficits in oxygen transport. cardiopulmonary dysfunction and compromise to oxy­
gen transport, V02 can fall short of the demand for oxy­
gen. Oxygen transport variables, including the compo­
OXYGEN TRANSPORT
nents of 002, V02, and the OER, are shown in Figure
Oxygen transport refers to the delivery of fully oxy­ 1-2. 002 is determined by arterial oxygen content and
genated blood to peripheral tissues, the cellular up­ cardiac output, oxygen consumption by the arterial and
take of oxygen, the utilization of oxygen from the venous oxygen content, difference and cardiac output,
blood, and the return of partially desaturated blood to and oxygen extraction by the ratio of 002 to \'02.
the lungs. The oxygen transport pathway consists of Measures and indices of oxygen transport that re­
multiple steps ranging from the ambient air to the flect the function of the component steps of the oxy­
perfusion of peripheral tissues with oxygenated arter­ gen transpolt pathway are shown in the box above.
ial blood (Figure 1-1). Oxygen transport has become
the basis for conceptualizing cardiopulmonary func­
Energy Transfer and Cellular Oxidation
tion, and diagnosing and managing cardiopulmonary
dysfunction (Dantzker, 1983; Dantzker, Boresman, Cellular metabolism and survival depend on the con­
and Gutierrez, 1991; Dean, 1994a; Dean and Ross, tinuous s y nthesis and degradation of adenosine

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Measures and Indices of the Function of the Steps in the Oxygen Transport Pathway

Control of Ventilation Physiologic shunt

Systolic and diastolic pulmonary artery pressures
PO. I (central drive to breathe)
Pulmonary capillary blood tlow
Ventilatory responses or hypoxia and hypercapnia
Pulmonary capillary wedge pressure
Pao} and Sa02 responses to exercise
Pulmonary vascular resistance
Inspired Gas Pulmonary vascular resistance index
Systemic hemodynamic variables
Alveolar oxygen pressure
Heart rate
Alveolar carbon dioxide pressure
Electrocardiogram (ECG)
Alveolar nitrogen pressure
Systemic blood pressure
Hematologic Variables
Mean arterial blood pressure
Hemoglobin
Systemic vascular resistance
Plasma proteins and their concentrations
Systemic vascular resistance index
Red blood cells and count
Central venous pressure
White blood cells and count
Pulmonary artery pressures
Platelets
Wedge pressure
Clotting factors
Blood volume
Clotting times
Cardiac output
Hematocrit
Cardi<lc index
Pao2
Stroke volume
Paco2 (eml tidal CO2)
Stroke index
P(A-a)o2
Shunt fraction
Cao2
Ejection fraction
CV02
Left ventricular work
C(a-v)o2 difference
Right ventricular work
HCo1
Fluid balance
Sa02
Renal output
pH
Creatinine clearance and blood urea nitrogen (BUN)
Paoe/PAo]
Pao2/Flo2 Diffusion
Serum lactate
D (A-a)o2
Pulmonary Variables Diffusing capacity
Diffusing capacity/alveol<lr volume
Minute ventilation
Tidal volume Gas Exchange
Respiratory rate
Oxygen consumption (Vo2)
Dead space volume
Carbon dioxide production (VCCl:)
Alveolar volume
Respiratory exchange ratio (Vco}iV02)
Alveolar ventilation
Ventilation and perfusion matching
Distribution of ventilation
Paol/PAol
Static and dynamic lung compliance
P(A-a)o2
Airway resistance
Functional residual capacity Oxygen Extraction and Utilization
Closing volume
Oxygen extraction ratio (V02/Do2)
Vital capacity
C(a-v)02 difference
Forced expiratory volumes and flows
P(a-v)o2 differenc e
Other pulmonary volumes, capat:ities, and flow rates
SV02
Inspiratory and expiratory pressures
Metabolic enzymes at the cellular level
Work ofhreathing
Oxyhemoglobin dissociation
Respiratory muscle strength and endurance
Adequacy of Tissue Perfusion and Oxygen
Pulmonary Hemodynamic Variables
Transport
Cardiac output
Tissue oxygenation
Total perfusion
Tissue pH
Distribution of perfusion
Anatomic shunt

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6 PART I Cardiopulmonary Function in Health and Disease

Oxygen delivery
D02 Arterial oxygen content x Cardiac output
t
Oxyhemoglobin + Dissolved oxygen
t
Hgb x 1.34 x 5a02
II Pa02 x 0.003 I

Oxygen consumption
V02 = (Arterial oxygen content - Venou s oxygen content) x Cardiac output
t
Oxyhemoglobin + Dissolved oxygen

Hgb x 1.34 x 5v02

II Pa02 x 0.003
I
Oxygen enhancement ratio
Oxygen consumption V02
OER
Oxygen delivery D02

FIGURE 1-2
FOlmulas for determining oxygen delivery (002), oxygen consumption (Vo2), and oxygen
extraction ratio (OER). (Modified from Epstein CD., Henning R.1.: Oxygen transport variables
in the identification and treatment of tissue hypoxia, Heart Lung 22:328-348, 1993.)

triphosphate (A TP); the major source of energy for that oxygen delivery is inadequate, nonaerobic (anaer­
biological work. Work is performed in biological sys­ obic or non-oxygen-requiring) energy-transferring
tems for contraction of skeletal, cardiac, and smooth processes can also supply ATP. However, supplying
muscle (e.g., exercise, digestion, glandular secretion energy anaerobically is more costly metabolically, that
and thermoregulation, and nerve impulse transmission) is, it is not efficient, is limited, and cannot be slistained
(see box below). These processes require a continuous because of the disruptive effects of lactate, a cellular
supply of A TP, which is made available by aerobic byproduct of anaerobic metabolism, on physiological
(oxygen requiring) processes primarily. In the event processes in general. Metabolic acidosis is a conse­
quence of lactate accumulation. In critically ill pa­
tients, the presence of metabolic acidosis secondary to
Biological Work Requiring Continuous
anaerobic metabolism can be life-threatening. Pro­
Oxygen Supply
longed anaerobic metabolism is lethal in two respects.
Contraction of skeletal muscle First, the patient is increasingly dependent on anaero­
Contraction of cardiac muscle bic metabolism because of inadequate oxygen delivery
Contraction of smooth muscle to peripheral tissues, and second, acidosis interferes
Nerve impulse transmission
with normal cellular processes and homeostasis, which
Active cellular metabolic processes
Active pumping mechanisms
require an optimal pH of 7.40.
The ATP molecule consists of an adenine and a ri-

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 1 Oxygen Transport: The Basis for Cardiopulmonary Physical Therapy 7

---------------------
-
Lactose
I

Galactose --+- Galactose- 1 -P

: t
Starch -Maltose Glucose: __ Glucose- 'I-P
: t
Sucrose - Fructose
-------
: Glucose-6-P
--- --
(CARBOHYDRATE FOODS)
- --------------
t
Fructose-6-P

!
Fructose- 1 ,6-diP

1
Glyceraldehyde-3P

"Glycecol
Pyn
I
te= wdale
Pr
L_____
in-: Amino acids F t:_
Acetyl-Co-A -- Fatty acids -- 1 __

o -a
)+
Citrate

CO2 + Energy
": ;
a Ketoglutarate

FIGURE 1-3
Interrelationships among carbohydrate, fat, and protein metabolism and their points of entry
into the Krebs cycle. (Printed with permission from Shepard R.J,: Physiology and biochemistry
of exercise, Phi ladelphia, 1985, Praeger Scientific.)

bose molecule with three phosphates attached. Split­ electron transfer chain and then use this energy for
ting of the terminal phosphate bond or the two terminal biological work (Ganong, 1993; Shephard, 1985).
phosphate bonds generates considerable amounts of Carbohydrates, fats, and proteins, ingested from
energy. This energy is used to power various chemical foodstuffs in the diet, are oxidized to provide the en­
reactions associated with metabolism. These metabolic ergy for phosphorylation of adenosine diphosphate
processes take place in specialized organelles in the (ADP), that is, the formation of ATP by combining
cells called mitochondria. The primary pathways that ADP with phosphate. These substances are broken
are responsible for the formation of ATP are the Krebs down, and they access the Krebs cycle at the pyruvic
cycle and the electron transfer chain. acid or acetyl coenzyme A (CoA) levels (Figure 1-3).
The complex, enzymatically controlled chemical Some amino acids can enter the Krebs cycle directly.
reactions of metabolism are designed to form and The Krebs cycle degrades acetyl CoA to carbon
conserve energy through the Krebs cycle and the dioxide (C02) and hydrogen atoms (H2)' The primary

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8 PART I Cardiopulmonary Function in Health and Disease

3ADP
3ATP

Mitochondrion
Shuttle

Krebs cycle
NADH etc.

FIGURE 1-4
Electron transfer chain and its with the Krebs (Printed with permission from
and Philadelphia, 1985, Scientific.)

purpose of this is to generate hydrogen ions for tivity and energy is primarily by
the electron transfer chain by two principal electron aerobic metabolism. Oxygen for this process is pro­
acceptors, nicotinamide adenine dinucleotide vided by the oxygen transport pathway. Carbon com­
and flavin adenine dinucleotide (FAD). pounds that enter the in the form of
the numerous reactions of the Krebs and oxidative metabolism
Cellular oxidation or respiration refers to the func­ in the form of aerobic glycolysis in the mitochondria
tion of the electron transfer chain to release energy in in the of the cells.
small amounts and to conserve energy in the forma­ The Krebs and the electron transfer chain are
tion of high energy bonds. It is this process that en­ the biochemical in the mitochondria of the
sures a continual energy supply to meet the needs of cell responsible for harnessing the oxygen for aerobic
metabolism 1-4). metabolism and a continuous supply of oxy­
Three major of energy transfer exist to gen for this process (Shephard, 1985).
supply energy all-out exercise over cose is to produce two molecules of
durations Katch, and Karch, I ATP (glycolysis). Glucose is oxidized to
though these systems are discrete they Cellu­ molecules of yielding a net
lar ATP and creatine phosphate (CP) are immediate molecules of ATP per molecule of
energy sources for the first 10 seconds of exercise. pyruvate molecules enter the Krebs where they
From 30 to 60 glycolysis a short­ are oxidized to and water. This process 30
term energy source. The ATP-CP system and the ATP molecules. Hydrogen ions released in the
colytic system are anaerobic processes. As exercise process are transferred to the electron transfer chain
persists for several minutes, the aerobic yielding 4 ATP molecules for cellular metabolism.
system oredominates. Thus for sustained ohvsical ac- Electrons are removed from hydrogen and funnelled

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 1 Oxygen Transport: The Basis for Cardiopulmonary Physical Therapy 9

Sarcoplasmic
Triad reticulum Mitochondrion
j i
Terminal Transverse
A cisterns tubule

Thick myofilament

Z M Z
line line line

H zone

I band A band I band

I ,

Sarcomere

I band A band I band

I
"

!
'--11
" " Mi"
.-!n ,n, ,,/ ' . '
"

,'"

.
'"''
"
'
"
. .. . . _ _

.
B
, , , . .
. ... .... . . ,", ' . , ",,', . " ...

', :> ?::.

,
" .

:
, .
:',', : . : :
' ::: . :
. '. ,' , .

: :: :: :
, : ::�
',

:> ,'7:'>
' ' • • • ••
. , •• '-" ,•• " . 11/ . . .. " _ ._ "

.. .
, " " ' // , > '
,
,'
' ',

.
. , . " " , , / / , " // , .
."-" ,- . . , . . ,,, .
'" . . . , .. .. , ' ... '/ "
.- . '.'

.
. . ' - ." . . . . ' '''
/ "
" , " "
. . . , ... - ... ..
' . , , , ... ... , ...
..

Thin myofilament I /
'
Thick myofilament Cross bridge H z one Z line

FIGURE 1-5
Schematic of the ultrastructure of a muscle fiber. A, View of muscle mem brane structure and
myofibril arrangement. B, A single functional unit (sarcomere) of a myofibril showing the
interdigitation of the actin and myosin filaments. (Printe d with permission from Tortora, G.J.,
A nagnostakos N.P.: Principles of anatomy and physiology, New York, J 990, Harper & Row.)

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10 PART I Cardiopulmonary Function in Health and Disease

Thin

Myosin
(thick)

Thin

FIGURE 1-6
Arrangement of the thick and thin myofilaments. (From Hasson S.: Clinical exercise physiology,
St. Louis, 1994, Mosby.)

down the electron transport chain by specialized elec­ anaerobic metabolism can only serve as a shol1-term
tron carrier molecules, cytochromes 1 to S. It is only energy source.
the last of these cytochromes, cytochrome oxidase,
that can reduce molecular oxygen to water. This
Muscle Contraction and Metabolism
process is driven by a gradient of high-to-Iow poten­
tial energy. The energy transferred as electrons are The basic mechanism for muscle contraction is excita­
passed from H2 to O2, and is trapped and conserved tion contraction coupl ing (Kirchberger, 1991; T0I10ra,
as high energy phosphate bonds. Oxygen is only in­ and Anagnostakos, 1990). Action potentials mediated
volved in these metabolic pathways at the end of the centrally or through the spinal cord depolarize the
electron transfer chain, where oxygen is the final muscle cell membrane, the sarcolemma, and stimulate
electron acceptor and combines with H2 to form H20. the release of calcium from the lateral sacs of the sar­
More than 90% of ATP synthesis takes place through coplasmic reticulum, The sarcoplasmic reticulum is an
the electron transfer chain by oxidative reactions extensive network of invaginations and tubular chan­
combined with phosphorylation, that is, oxidative nels encasing the muscle fibers or myofibrils. The cal­
phosphorylation. An individual's peak aerobic capac­ cium floods over the myofilaments of the myofibrils.
ity is determined by the availability of oxygen at the Myofilaments consist of thin and thick fibers, actin,
end of the electron transport chain. and myosin protein, which interdigitate with each
For each molecule of glucose that is metabolized, other giving the typical striated appearance to skeletal
36 molecules of ATP are produced; four molecules muscle (Figures I-S and 1-6). Actin is a helical mole­
from substrate phosphorylation (anaerobic), and 32 cule with tropomyosin intertwined along its length.
from oxidative phosphorylation (aerobic). The low Tropomyosin normally inhibits the interaction of actin
ATP yield from anaerobic metabolism explains why and myosin. Calcium causes a conformational change

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 Oxygen Transport: The Basis for Cardiopulmonary Physical Therapy 11

Principles of Oxygen Transport

of the tropomyosin molecule that enables troponin,
also distributed along the actin molecule, to combine A continuous supply of oxygen is needed to meet
with calcium. The combining of calcium and troponin moment-to-moment demands for oxygen commensu­
triggers the movement of actin and myosin. Contrac­ rate with changing metabolic demands for energy at
tion involves the attaching and detaching of the the cellular level in addition to basal metabolic de­
myosin heads (cross bridges) to actin in a cyclical mands (Cone, 1987; Dantzker, 1991; Samsel and
manner, which causes the actin and myosin filaments Schumacker, 1991). Oxygen transport occurs either
to slide past each other. In this way, the muscle is by convection or diffusion. Convection of oxygen
shortened without shortening of the myofilaments. refers to the movement of oxygen from the alveoli to
The energy for muscle contraction in the form of the tissue capillaries. Convection is primarily deter­
ATP is generated within the mitochondria of the my­ mined by the hemoglobin concentration, oxygen satu­
ofibrils (Shephard, 1985). Myosin ATPase splits ATP ration, and cardiac output. The diffusion of oxygen
so that the transfer of this energy can be used for refers to the movement of oxygen from the capillaries
muscle contraction. Specifically, the enzyme ATPase to the mitochondria. Diffusion is determined by
is activated when actin and myosin are joined. ATP is metabolic rate, vascular resistance, capillary recruit­
then available to bind with the cross bridge, causing ment, tissue oxygen consumption, and extraction.
it to detach from actin. Relaxation occurs with the Normally, D02 is regulated by tissue metabolism
cessation of electrical excitation and the rapid re­ and the overall demand for oxygen. Typically, DOl is
moval or sequestration of calcium into the lateral sacs 3 to 4 times greater than oxygen demand, and V02 is
of the sarcoplasmic reticulum. not directly dependent on Do2. In health, the increased
The specific metabolic properties of muscle de­ metabolic demands of exercise constitute the greatest
pend on the constituent muscle fiber types (Fox, challenge to the oxygen transport system. The V02 can
Bowers, and Foss, 1993). The three primary muscle increase 20 times. In response to increased muscle
fiber groups are fast twitch fibers, slow twitch metabolism, blood tlow increases to the peripheral
fibers, and intermediate fibers, which have proper­ muscles through vasodilatation and capillary recruit­
ties of both. The fast twitch fibers (fast glycolytic ment, thereby increasing the availability of oxygen to
fibers) are recruited during short-term sprint type the working tissues and its extraction from the arterial
exercise, which relies mainly on anaerobic metabo­ blood. As D02 and V02 increase, venous return, stroke
lism. These fibers are well-adapted for rapid force­ volume, and heart rate also increase, thereby increas­
ful contractions, because they have large amounts ing cardiac output (CO). The CO can increase more
of myosin ATPase, rapid calcium release and up­ than five times in strenuous exercise.
take and high rate of cross bridge cycling. Slow At rest, regional differences in the proportion of
twitch fibers (slow oxidative fibers) are recruited CO normally delivered to the body organs reflects dif­
during prolonged aerobic exercise. These fibers ferences in organ functions and is not necessarily
have large amounts of myoglobin, mitochondria, matched to the metabolic rate (Guyton, 1987). For ex­
and myochondrial enzymes. Compared with the fast ample, the distribution of CO to the kidneys is 20%,
twitch fibers, slow twitch fibers are fatigue-resis­ and to the mesenteric, splenic, and portal tissues is
tant. The intermediate fibers have both anaerobic 20% to 30%. Comparatively, muscle at rest is 10%
and aerobic metabolic enzymes, which make these and the brain and myocardium are less than 5% each.
fibers capable of both types of muscle work. Al­
though the characteristics of the fiber types are dis­
Oxygen Content of the Blood
tinct, activity and exercise recruits both types of
fibers. Depending on the particular activity or exer­ Oxygen is transported in arterial blood to the tissues
cise, one fiber type may be preferentially recruited in combination with hemoglobin (98%) a n d dis­
over the others. solved in plasma (2%) The majority of oxygen is

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12 PART I Cardiopulmonary Function in Health and Disease

carried in the blood by hemoglobin, compared with a

d(/
relatively minimal amount of oxygen that is dis­
solved in the blood. The oxyhemoglobin dissociation
150
curve represents the relationship between the affinity A;
c l o
of hemoglobin for oxygen and arterial oxygen ten­
sion. The affinity of hemoglobin for oxygen depends
on the tissue oxygen demand. In health, exercising :¥100
muscle increases the demand for oxygen. The heat of
the working muscles and the acidic environment re­
E
E
o
N

0....
Gal enp/ An

sult in reduced oxyhemoglobin affinity, and in­ 50

Diffusion
creased oxygen release. This is reflected by a shift to Shunt
Tissues
the right of the oxyhemoglobin dissociation curve
(see Chapter 9). The affinity of hemoglobin and oxy­
o I�------
gen is increased with the cessation of exercise, Atmosphere • Mitochondria
which is reflected by a leftward shift of the curve.
FIGURE 1-7
Scheme of oxygen partiaf pressures from air to tissue. The
Oxygen Delivery to the Tissues
cascade reflects the removal of oxygen by the pulmonary
capillary blood and the tissues. Depressions caused by the
The final steps in oxygen transport involve the disso­
effects of diffusion and shunt are also illustrated. (Used
ciation of oxygen from hemoglobin and the diffusion
with permission from West lB.: Respiratory p/7ysiology­
of oxygen from the capillaries to the cells (Schu­
the essentials, ed 5, Baltimore, 1995, Williams & Wilkins.)
macker, Samsel, 1989). Diffusion depends on the
quantity and rate of blood flow, the difference in cap­
illary and tissue oxygen pressures, the capillary sur­
face area, capillary permeability, and diffusion dis­ mitochondria (Guyton, 1991). This decremental Pao2
t a n ce (West, 1 9 95). Wi t h i ncreased metabo lic profile down the oxygen transport pathway, from the
demand of the tissues, capillary dilatation and recruit­ airways to the tissues, is termed the oxygen cascade
ment increase capillary surface area and reduce vas­ (Figure 1-7).
cular resistance to flow. Diffusion distance is de­
creased, the movement of oxygen into the cell is
Cardiac Output
facilitated, and the tissue oxygen tension is increased.
The two diffusion gradients that determine effec­ In addition to arterial oxygen content, CO is a primary
tive oxygen transpolt are between the pulmonary cap­ determinant of D02 (Dantzker, 1991). The transport of
illaries and the alveoli, and between the peripheral oxyhemoglobin to the tissues is dependent on convec­
capillaries and the tissue cells. Diffusion of oxygen tive blood flow by way of CO. The CO is the volume
occurs as the blood moves from the aorta to the arte­ of blood pumped from the right or left ventricle per
rioles. The mean oxygen tension in the aorta is about minute. The components of CO are stroke volume
95 mm Hg and in the arterioles is 70 to 80 mm Hg. (SV) and heart rate (HR), that is, CO = SV x HR.
The oxygen gradient between the arterioles and the Stroke volume is the amount of blood ejected from the
cells is the most steep. The mean oxygen pressure is left ventricle during each ventricular systole or heart­
less than 50 mm Hg in the capillaries. The oxygen beat and is determined by the preload, myocardial dis­
tension in the capillaries detennines the rate of diffu­ tensibility, myocardial contractility, and afterload. The
sion to the cells. An optimal diffusion gradient main­ DDl is optimized in patients by increasing CO through
tains the oxygen tension in the cell between 1 to 10 the therapeutic manipulation of preload, myocardial
mm Hg; oxygen tension is less than 0.5 mm Hg in the contractility, afterload, and heart rate.

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 1 Oxygen Transport: The Basis for Cardiopulmonary Physical Therapy 13

Preload
to that consumed. The OER is calculated by dividing
Preload is the end diastolic muscle fiber length of the V02 by 002. Normally, the OER is 23%.
ventricle before systolic ejection, and reflects the left
ventricular end diastolic volume (LVEDV). The
Supply-dependent Oxygen Consumption
LVEDV is dependent on venous return, blood vol­
ume, and left atrial contraction. An increase in ven­ Normally, a decrease in 002 does not reduce V02
tricular volume stretches the myocardial fibers and (Phang, Russell, 1993). With a decrement in 002, the
increases the force of myocardial contraction (Star­ tissues extract a proportionate amount of oxygen
ling effect) and stroke volume. This effect is limited from the blood. In critically ill patients, the 002 may
by the physiologic limits of distension of the my- . be significantly limited to the point where basic
2
ocardium. Excessive stretching such as in fluid over­ metabolic needs for oxygen (300 mllminJM ) are not
load of the heart leads to suboptimal overlap of the being met (Fenwick et ai, 1990; Lorente et aI, 1991;
actin and myosin filaments, thus impairing rather Phang, Russell, 1993). The critical level at which V02
than enhancing contractility. falls is associated with tissue anaerobic metabolism
and the development of lactic acidosis and decreased
pH (Figure 1-8) (Mizock, Falk, 1992; Schumaker,
Afterload
Cain, 1987). Serum lactates correspondingly increase
Afterload is the resistance to ejection during ventricu­ and provide a valid index of anaerobic metabolism in
lar systole. Afterload of the left ventricle is primarily patients with multiorgan system failure.
determined by four factors: the distensibility of the
aorta, vascular resistance, patency of the aortic valve,
The Oxygen Transport Pathway
and viscosity of the blood.
Oxygen transport is dependent on several intercon­
necting steps ranging from oxygen-containing air
Myocardial Contractility
being inhaled through the nares to oxygen extraction
Myocardial contractility reflects actin-myosin coupling at the cellular level in response to metabolic demand
during contraction. Myocardial contractility is assessed (see Figure I-I , p. 4). These steps provide the mecha­
by the ejection fraction, rate of circumferential muscle nism for ventilatory, cardiovascular, and metabolic
fiber shortening, pressure volume relationships, and the coupling. In addition, blood is responsible for trans­
rate of change of ventricular pressure over time. porting oxygen within the body, thus its constituents
and consistency directly affect this process.

Oxygen Debt
The Quality and Quantity of Blood
Tissue oxygen debt or recovery oxygen consumption is
the difference between oxygen demand and oxygen Although not considered a discrete step in the oxygen
consumption. In health, oxygen debt can be sustained transpolt pathway, blood is the essential medium for
for short periods during intense exercise. Anaerobic me­ transporting oxygen. To fulfill this function, blood
tabolism is stimulated to produce ATP under these con­ must be delivered in an adequate yet varying amount
ditions. In patients, the degree of oxygen debt signifi­ proportional to metabolic demands, and have the ap­
cantly correlates with survival (Fenwick et aI, 1990). propriate constituents and consistency. Thus consider­
ation of the characteristics of the circulating blood vol­
ume is essential to any discussion of oxygen transport.
Oxygen Extraction Ratio or Utilization Coefficient
Blood volume is compartmentalized within the in­
The oxygen extraction ratio (OER), or utilization co­ travascular compartment such that 70% is contained
efficient, reflects the proportion of oxygen delivered within the venous compartment, 10% in the systemic

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14 PART I Cardiopulmonary Function in Health and Disease

arteries, 15% in the pulmonary circulation, and 5% In Blood is a viscous fluid composed of cells and
the capillalies (Sandler, 1986). The large volume of plasma. Because 99% of the blood is red blood celis,
blood contained within the venous circulation permits the white blood cells play almost no role in determin­
adjustments to be made as cardiac output demand ing the physical characteristics of blood.
changes. The veins constrict, for example, when car­ Hematocrit refers to the proportion of blood that is
diac output needs to be increased. When blood vol­ 38% for women and
celis. The normal hematocrit is
ume is normal and body fluids are appropriately dis­ 42% for men. Blood is several times as viscous as
t r i b u t e d b e t w e e n t h e i n t r a- a n d e x t r ava scular water, which increases the difficulty with which
compartments, fluid balance is considered normal. blood is pumped through the heart and flows through
When these are disrupted, a fluid balance problem vessels; the greater the number of cells, the greater
exists. In addition, fluid imbalance affects the con­ the friction between the layers of blood, which results
centration of electrolytes, and particularly sodium, in increased viscosity. Thus the viscosity of the blood
which is in the highest concentration in the extracel­ increases significantly with increases in hematocrit.
lular fluid. Four primary fluid problems that have im­ An increase in hematocrit such as in polycythemia in­
plications for oxygen transport are water deficit, creases blood viscosity several times over. The con­
water excess, sodium deficit, and sodium excess (see centration and types of protein in the plasma can also
Chapter 15). Other ions that are often affected in affect viscosity but to a lesser extent.
fluid and electrolyte imbalance deficits include potas­ In the adult, red blood cells are produced in the
sium, chloride, calcium, and magnesium (Figure 1-8). marrow of the membranous bones such as the verte­
These electrolyte disturbances also contribute to im­ brae, sternum, ribs, and pelvis. The production of red
paired oxygen transport by affecting the electrical blood cells from these sites diminishes with age. Tis­
and mechanical behavior of the heart and blood ves­ sue oxygenation is the basic regulator of red blood
sels, and hence cardiac output and the distribution of cell production. Hypoxia stimulates red blood cell
oxygenated arterial blood to the periphery. production through erythropoietin production in bone
(Guyton, 1991).
Viscosity of the blood has its greatest effect in the
small vessels. Blood flow is considerably reduced in
small vessels, resulting in aggregates of red blood ceils
c
.Q adhering to the vessel walls. This etlect is not offset by
c... D02 Dependent D02 Independent
E the tendency of the blood to become less viscous in
I
'"
c
I small vessels as a result of the alignment of the blood
o I
u I cells flowing through, which minimizes the frictional
c I
Q)
: Critical D02 forces between layers of flowing blood cells. In addi­

g I
I
I
I
tion, in small capillaries, blood cells can become stuck
particularly where the nuclei of endothelial cells pro­
trude and momentarily block blood flow.
o 100 200 300 400 500 600 700
The major function of the red blood cells is to
Oxygen delivery (ml/min)
transport hemoglobin, which in turn carries oxygen
from the lungs to the tissues. Red blood cells also
FIGURE 1-8
contain a large quantity of carbonic anhydrase, which
Relationship between oxygen consumption (Voz) and
catalyzes the reaction between COz and HzO. The ra­
oxygen delivery (002)' The Dorindependent phase
represents the normal metabolic state. The D02-dependent pidity of this reaction makes it possible for blood to

phase represents the dependency of Voz on 002 when 002 react with large quantities of CO2 to transport it from
Falls below the critical 002. (Modified from Phang, P.T. the tissues to the lungs for elimination.
and Russel, 1.A.: When does V02 depend on D02? Resp Hemoglobin is contained within red blood cells up
Care 38: 618-630, 1993.) to a concentration of 34 gmll 00 ml of cells. Each

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 1 Oxygen Transport: The Basis for Cardiopulmonary Physical Therapy 15

gram of hemoglobin is capable of combining with blood cells. These values vary according to gender,
1.34 ml of oxygen (see Figure 1-2, p. 6). Therefore in weight, and other factors. Normally, changes in blood
healthy women, 19 ml of oxygen and in healthy men, volume reflect deficits and excesses of fluid through
21 ml of oxygen can be carried in the blood, given imbalances created by losses through the skin and
that the whole blood of women contain an average respiratory tract, and through urinary, sweat, and
of 14 gmll 00 ml of blood and 16 gmll 00 ml of blood fecal losses. Exercise and hot weather are major chal­
in men. lenges to fluid balance in health.
Clotting factors of the blood are normally in a pro­ The plasma contains large quantities of sodium
portion that does not promote clotting. Factors that and chloride ions, and small amounts of potassium,
promote coagulation (procoagulants), and factors that calcium, magnesium, phosphate, sulfate, and organic
inhibit coagulation (anticoagulants) circulate in the acid ions. In addition, plasma contains a large amount
blood. In the event of a ruptured blood vessel, pro­ of protein. The large ionic constituents of the plasma
thrombin is converted to thrombin, which catalyzes are responsible for regulating intracellular and extra­
the transformation of fibrinogen to fibrin threads. cellular fluid volumes and the osmotic factors that
This fibrin mesh captures platelets, blood cells, and cause shifts of fluid between the intracellular and ex­
plasma to form a blood clot. tracellular compartments.
The extreme example of abnormal clotting is dis­
seminated intravascular coagulation, where both he­
Oxyhemoglobin Dissociation
mOlThage and coagulation occur simultaneously. The
acute form of this syndrome occurs in critically ill pa­ The demand for oxygen at the cellular level changes
tients with multiorgan system failure. The mechanism from moment to moment. The properties of oxyhemo­
appears to involve tissue factors, factors that damage globin dissociation ensure that there is a continuous
the blood vessel wall, and factors that increase supply of oxygen at the cellular level. Oxygen com­
platelet aggregation (Green and Esparaz, 1990). The bines with the hemoglobin molecules in the pul­
chronic form of the syndrome occurs in chronic con­ monary circulation and then is released in the tissue
ditions such as neoplastic disease. capillaries in response to a reduced arterial oxygen
Plasma is the extracellular fluid of the blood and tension. The S-shaped oxyhemoglobin dissociation
contains 7% proteins, namely albumin, globulin, and curve (see Chapter 9) shifts to the right in response to
fibrinogen. The primary function of the albumin and reduced tissue pH, increased CO2, increased tempera­
to a lesser extent, globulin and fibrinogen, is to create ture and increased diphosphoglycerate (DPG), a con­
osmotic pressure at the capillary membrane and to stituent of normal blood cells.
prevent fluid leaking into the interstitial spaces. The The delivery of blood and its ability to effectively
globulins serve as carriers for transporting substances transport oxygen is central to all steps in the oxygen
in the blood and provide immunity as the antibodies transport pathway and must be considered at each
that fight infection and toxicity. Fibrinogen is funda­ step in clinical problem solving and decision making.
mental to blood clotting. The majority of blood pro­
teins, including hemoglobin, are also excellent acid­
Steps in the Oxygen Transport Pathway
base buffers and are res ponsi b Ie for 70% of a II
buffering power of whole blood.
Blood flow (Q) depends on a pressure gradient (P) Step One: inspired oxygen and quality

and vascular resistance (R), that is, Q PIR. Hence

=
of the ambient air

blood flow equals the pressure gradient divided by re­ In health, the concentration of inspired oxygen is rel­
sistance. The length of a given blood vessel and the vis­ atively constant at 21 % unless the individual is at al­
cosity of the blood are also detelTninants of blood flow. titude. In which case, the fraction of inspired oxygen
The average blood volume is 5,000 ml. Approxi­ is reduced the higher the elevation.
mately 3,000 ml of this is plasma and 2,000 ml is red Atmospheric air consists of 79% nitrogen, 20.97%

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16 PART I Cardiopulmonary Function in Health and Disease

oxygen and 0.03% CO2. Because nitrogen is not ab­ lined with cilia, fine microscopic hair-like projec­
sorbed in the lungs, it has a crucial role in maintain­ tions, which are responsible for wafting debris, cells,
ing the lung tissue patent. The constituents of the air and microorganisms away from the lungs into larger
have become an increasingly important social, envi­ airways to be removed and evacuated. The airways
ronmental, and health issue because of environmental are also lined with mucus, which consists of two lay­
hazards, pollution, and thinning of the ozone layer re­ ers, the upper gel layer and the lower sol layer with
sulting in deterioration of air quality, an increase in which the cilia communicate.
toxic oxygen free radicals and a reduction in atmos­
pheric oxygen pressure.
Step Three: lungs and chest wall
Many factors influence air quality, (e.g., geo­ Air entry to the lungs depends on the integrity of the
graphical area, season, urban vs. rural area, high vs. respiratory muscles, in particular, the diaphragm, the
Jow elevation, home environment, work environment, lung parenchyma, and the chest wall. Contraction and
indoor vs. outdoor, level of ventilation, air condition­ descent of the diaphragm inflates the lungs. The dis­
ing, enclosed buildings, areas with high particu late tribution of ventilation is primarily determined by the
matter, areas with gaseous vapors and toxic-inhaled negative intrapleural pressure gradient down the
materials, and smoke-filled vs. smoke-free environ­ lungs. The negative intrapleural pressure gradient re­
ments). Poor air quality contributes to changes in the sults in uneven ventilation down the lung, and inter­
filtering ability of the upper respiratory tract, airway regional differences (see Chapter 3). However, there
sensitivity, and lung damage, acutely and over time. are other factors, intraregional differences, that con­
Chronic irritation of the lungs from poor air quality tribute to uneven ventilation within regions of the
can lead to allergies, chronic inflammatory reactions, lung. These intraregional differences reflect regional
fibrosis, and alveolar capillary membrane thickening. differences in lung compliance and airway resistance
At the alveolar level, the inspired air is saturated with (Ross, Dean, 1992). In patients with partially ob­
water vapor. In dry environments, however, the upper structed airways, reduced lung compliance, and in­
respiratory tract may become dehydrated, lose its creased airway resistance increase the time for alveo­
protective mucous covering, become eroded, and pro­ lar filling. Gas exchange is compromised if there is
vide a portal of infection even though the air is ade­ inadequate time for alveolar filling or emptying, that
quately humidified by the time it reaches the lower is, increased time constants (West, 1995). Different
airways and alveoli. time constants across lung units contribute to uneven
patterns of ventilation during inspiration. A lung unit
Step Two: airways
with a long time constant is slow to fill and to empty,
The structure of the airways down the respiratory and may continue to fill when sun'ounding units are
tract change according to their function. The main emptying. A second factor is altered diffusion dis­
airway, the trachea, consists of cartilagenous rings, tance. In diseases where diffusion distance is i n­
connective tissue, and small amounts of smooth mus­ creased, ventilation along lung units is uneven.
cle. This structure is essential to provide a firm and The lungs and the parietal pleura are richly sup­
relatively inflexible conduit for air to pass from the plied with thin-walled lymphatic vessels (Guyton,
nares through the head and neck to the lungs, and 1991). Lymphatic vessels have some smooth muscle
avoid airway collapse. As the airways become and thus can actively contract to propel lymph fluid
smaller and branch throughout the lung tissue, they forward. This forward motion is augmented by
consist primarily of smooth muscle. Airway narrow­ valves along the lymphatic channels. The rise and
ing, or, obstruction and increased resistance to air­ fall of the pleural pressure during respiration com­
flow, is caused by multiple factors, including edema, presses lymphatic vessels with each breath, which
mUCllS, foreign objects, calcification, particulate mat­ promotes a continuous flow of lymph. During expi­
ter and space-occupying lesions, as well as hyperre­ ration and increased intrapleural pressure, fluid is
activity of bronchial smooth muscle. The airways are forced into the lymphatic vessels. The visceral pleura

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 Oxygen Transport: The Basis for Cardiopulmonary Physical Therapy 17

continuously drains fluid from the lungs. This cre­

Step Five: perfusion
ates a negative pressure in the pleural space, keeping The distribution of blood perfusing the lungs is pri­
the lungs expanded. This pressure exceeds the elastic marily gravity dependent, thus the dependent lung
recoil pressure of the lung parenchyma, which col­ fields are perfused to a greater extent than the nonde­
lapses the lungs. pendent lung fields. In the upright lung, the bases are
The peritoneal cavity of the abdomen consists of a better perfused than the apices (see Chapter 3). Venti­
visceral peritoneum containing the viscera and a pari­ lation and perfusion matching is optimal in the mid­
etal peritoneum lining the abdominal cavity. Numer­ zones of the upright lungs (West, 1985). In health,
ous lymphatic channels interconnect the peritoneal the ventilation to perfusion ratio is a primary determi­
cavity and the thoracic duct; some arise from the di­ nant of arterial oxygenation. In the upright lung this
aphragm. With cycles of inspiration and expiration, ratio is 0.8 in the mid-zone.
large amounts of lymph are moved from the peri­
toneal cavity to the thoracic duct. High venous pres­
Step Six: myocardial function
sures and vascular resistance through the liver can in­ Optimal myocardial function and cardiac output de­
terfere with normal flu id balance in the peritoneal pends on the synchronized coupling of electrical ex­
cavity. This leads to the transudation of fluid with a citation of the heart and mechanical contraction. The
high protein content into the abdominal cavity. This sinoatrial node located in the right atrium is the nor­
accumulation of fluid is referred to as ascites. Large mal pacemaker for the heart and elicits the normal
volumes of fluid can accumulate in the abdominal sinus rhythm with its component P-QRS-T configura­
cavity and significantly compromise cardiopul­ tion. This wave of electrical excitation spreads
monary function secondary to increased intraabdomi­ throughout the specialized neural conduction system
nal pressure on the underside of the diaphragm. of the atria, interventricular septum, and the ventri­
Optimal diaphragmatic excursion requires a bal­ cles, and is followed by contraction of the atria and
ance between thoracic and intraabdominal pressures. then the ventricles. Contraction of the right and left
Increases in abdominal pressure secondary to factors ventricles ejects blood into the pulmonary and sys­
other than fluid accumulation can impair diaphrag­ temic circulations respectively.
matic descent and chest wall expansion, for example, Cardiac output depends on several factors in ad­
gas entrapment, gastrointestinal (GI) obstruction, dition to the integrity of the conduction system and
space-occupying lesions, and paralytic ileus. the adequacy of myocardial depolarization (dro­
motropic effect). The amount of blood returned to
Step Four: diffusion the heart (preload), determines the amount ejected
Diffusion of oxygen from the alveolar sacs to the pul­ (Starling effect). The distensibility of the ventricles
monary arterial circulation depends on five factors: to accommodate this blood volume needs to be opti­
the area of the alveolar capillary membrane, diffusing mal, neither too restrictive nor compliant. The con­
capacity of the alveolar capillary membrane, pul­ tractility of the myocardial muscle must be suffi­
monary capillary blood volume, and ventilation and cient to eject the blood (inotropic effect). And
perfusion ratio (Ganong, 1993). The transit time of finally, cardiac output is determined by the aortic
blood at the alveolar capillary membrane is also an pressure needed to overcome peripheral vascular re­
impoltant factor determining diffusion. The blood re­ sistance and eject blood into the systemic circula­
mains in the pulmonary capillaries for 0.75 seconds tion (afterload).
at rest. The blood is completely saturated within one The pericardial cavity, like the pleural and peri­
third of this time. This provides a safety margin dur­ toneal cavities, is a potential space containing a thin
ing exercise or other conditions in which cardiac out­ film of fluid. The space normally has a negative
put is increased and the pulmonary capillary transit pressure. During each expiration, pericardial pres­
time is reduced. The blood can normally be fully sure is increased, and fluid is forced out of the space
oxygenated even with reduced transit time. into t h e me diastinal lymphatic channels. This

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18 PART I Cardiopulmonary Function in Health and Disease

process is normally facilitated with increased volumes sels, the greater their sensitivity to both exogenous
of blood in the hemt and each ventricular systole. neural stimulation and endogenous stimulation by cir­
culating humoral neurotransmitters such as cate­
Step Seven: peripheral circulation cholamines and local tissue factors. This sensitivity is
Once oxygenated blood is ejected from the heart, the essential for the moment-to-moment regulation of the
peripheral circulation provides a conduit for supply­ peripheral circulation with respect to tissue perfusion
ing this blood to metabolically active tissue. Blood and oxygenation, commensurate with tissue meta­
vessels throughout the body are arranged both in se­ bolic demands, and control of total peripheral resis­
ries and in parallel. The arteries and capillaries are tance and systemic blood pressure.
designed to advance blood to pelfuse the tissues with
oxygenated blood. The vasculature is architected so
Step fight: tissue extraction

that the proximal large al1eries have a higher propor­

and utilization of oxygen

tion of connective tissue and elastic elements than Perfusion of the tissues with oxygenated blood is the
distal medium and small arteries, which have a pro­ p r i n c i p a l goal of t he oxygen transport system
gressively higher proportion of smooth muscle. This (Dantzker, 1993). Oxygen is continually being used
structure enables the large proximal arteries to with­ by all cells in the body, thus it diffuses out of the cir­
stand high pressure when blood is ejected during ven­ culation and through cell membranes very rapidly to
tricular systole. Considerable potential energy is meet metabolic needs. Diffusion occurs down a gra­
stored within the elastic walls of these blood vessels dient from areas of high to low oxygen pressure. The
as the heart contracts. During diastole, the forward distance between the capillaries and the cells is vari­
propulsion of blood is facilitated with the elastic re­ able, thus a significant safety factor is required to en­
coil of these large vessels. The thin-walled muscular sure adequate arterial oxygen tensions. Intracellular
arterioles serve as the stopcocks of the circulation and P02 ranges from 5 to 60 mm Hg, with an average of
regulate blood flow through regional vascular beds 23 mm Hg (Guyton, 1991). Given that only 3 mm
and maintain peripheral vascular resistance to regu­ Hg of oxygen pressure are needed to support metab­
late systemic blood pressure. Blood flow through olism, 23 mm Hg of oxygen pressure provide an ade­
these regional vascular beds is determined by neural quate safety margin. Thcsc mechanisms ensure an
and humoral stimulation, and by local tissue factors. optimal oxygen supply over a wide range of varying
Blood pressure control is primarily regulated b y oxygen demands in health and in the event of im­
neural stimulation of the peripheral circulation and paired oxygen delivery because of illness. Normally,
these vascular beds. the rate of oxygen extraction by the cells is regulated
The microcirculation consists of the precapillary ar­ by oxygen demand by the cells, that is, the rate at
teriole, the capillary, and the venule. The Starling effect which ADP is formed from A TP and not by the
govems the balance of hydrostatic and oncotic pres­ availability of oxygen.
sures within the capillary and the surrounding tissue. The adequacy of the quality and quantity of the mi­
The balance of these pressures is 0.3 mrn Hg; its net ef­ tochondrial enzymes, required to support the Krebs
fect is a small outward filtration of fluid from the mi­ cycle and electron transfer chain, and the availability
crovasculature into the interstitial space (see Chapter 3). of myoglobin may be limiting factors in the oxygen
Any excess fluid or loss of plasma protein is drained transport pathway secondary to nutritional deficits and
into the sun'ounding lymphatic vessels, which usually muscle enzyme deficiencies. Myoglobin is a compara­
has a small negative pressure as does the interstitium. ble protein to hemoglobin that is localized within
The integlity of the microcirculation is essential to reg­ muscle mitochondria. Myoglobin combines reversibly
ulate the diffusion of oxygen across the tissue capillary with oxygen to provide an immediate source of oxy­
membrane, and to remove CO2 and waste products. gen with increased metabolic demands and facilitate
The greater the muscular component of blood ves­ oxygen transfer within the mitochondria.

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 Oxygen Transport: The Basis for Cardiopulmonary Physical Therapy 19

Normally, the amount of oxygen extracted by the ergy expenditure, and thus increase rate of metabolism.
tissues is 23%, that is, the ratio of oxygen consumed Several factors related to disease can significantly
to oxygen delivered. Thus this ratio ensures that con­ increase oxygen consumption and metabolic rate over
siderably greater amounts of oxygen can be extracted and above BMR. Such factors include fever, the dis­
during periods of increased metabolic demand. ease process itself, the process of healing and recov­
ery from injury or disease, thermoregulatory distur­
Step Nine: return of partially desaturated
bance, reduced arousal, increased arousal resulting
blood and C02 to the lungs
from anxiety and pain, sleep loss, medical and surgi­
Partially desaturated blood and CO2 are removed cal interventions, fluid imbalance, and medications
from the cells via the venous circulation to the right Dean, 1994b). These factors may contribute to a sys­
side of the heart and lungs. C02 diffuses across the temic increase in BMR or may reflect local changes in
alveolar capillary membrane and is eliminated from tissue metabolism. Autoregulation of the regional vas­
the body through the respiratory system, and the de­ cular beds promotes increased regional blood flow in
oxygenated venous blood is reoxygenated. The oxy­ accordance with their local tissue metabolic demand.
gen transport cycle repeats itself and is sensitively Because gravitational stress and exercise stress are
tuned to adjust to changes in the metabolic demand of fundamental to normal cardiopulmonary function and
the various organ systems, such as digestion in the GI oxygen transport, the effects of gravity and exercise are
system, and cardiac and muscle work during exercise. highlighted. It should be emphasized that the effects of
Factors that intelfere with tissue oxygenation and gravity on fluid shifts and the systeIllic effects of exer­
the capacity of the tissue to use oxygen include ab­ cise are physiologically distinct, that is, exposing an in­
normal oxygen demands, reduced hemoglobin and dividual to a gravitational stress does not adapt that in­
myoglobin levels, edema, and poisoning of the cellu­ dividual to an exercise stress and vice versa. These two
lar enzymes (Kariman, Burns, 1985). factors also augment arousal, through stimulation of the
reticular activating system in the brain stem and the au­
tonomic nervous system (ANS), which when de­
FACTORS THAT NORMALLY PERTURB
pressed, significantly compromises oxygen transport in
OXYGEN TRANSPORT
patient populations. The impact of emotional stress on
Basal metabolic rate (BMR) reflects the rate of me­ oxygen transport is discussed briefly. These concepts
tabolism when the individual is in a completely are described fUlther in Chapters 17 and L8.
rested state, that is, no food intake within several
hours, after a good night's sleep, no arousing or dis­
Gravitational Stress
tressing emotional stimulation, and at a comfortable
ambient temperature. Normally, the BMR is constant Humans are designed to function in a I G gravita­
within and between individuals if measured under tional field. Given that 60% of the body weigllt is
standardized conditions. This rate reflects resting en­ fluid contained within the intra- and extravascular
ergy expenditure of the body's cells to maintain rest­ compartments, and that this fluid has considerable
ing function, including the work of breathing; heart, mass, changes in body position result in significant
renal, and brain function; and thermoregulation. fluid shifts instantaneously and threaten hemody­
Normally, over the Course of the day, the human namic stability (Dean, Ross, 1992a; Dean, Ross,
body is exposed to fluctuations in ambient temperature 1992b). To maintain consciousness and normal body
and humidity, ingestion states, activity and exercise function during changes in body position, the heart
levels (exercise stress), body positions and body posi­ and peripheral vasculature are designed to detect
tion changes (gravitational stress), emotional states these fluid shifts and accommodate quickly to avoid
(emotional stress) and states of arousal. These factors deleterious functional consequences (e.g., reduced
significantly influence oxygen consumption and en­ stroke volume, CO, circulating blood volume, and

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20 PART I Cardiopulmonary Function in Health and Disease

cerebral perfusion). The preservation of the f1uid­ The oxygen transport system is designed to deliver
regulating mechanisms is essential to counter the he­ oxygen from the ambient air to every cell in the body
modynamic effects of changing body position. This to support cellular respiration, that is, the metabolic
capacity is quickly lost with recumbency and is the utilization of oxygen at the cellular level. Blood is the
primary cause of bed rest deconditioning in patient essential medium in which cellular and noncellular
and older populations (Chase, Grave, Rowell, 1966; components transport oxygen from the cardiopul­
Winslow, 1985). Restoration of gravitational stress monary unit to the peripheral tissues. The fundamental
with upright positioning is the only means by which steps in the oxygen transport pathway were described.
these fluid-regulating mechanisms can be maintained These steps included the quality of the ambient air, the
and orthostatic intolerance and its short- and long­ airways, lungs, chest wall, pulmonary circulation, lym­
term sequelae averted. phatics, he31t, peripheral circulation, and the peripheral
tissues of the organs of the body.
In health, the most significant factors that perturb
Exercise Stress
oxygen transport are changes in gravitational stress
Exercise constitutes the greatest perturbation to home­ secondary to changes in body position, exercise stress
ostasis and oxygen transport in humans. Cardiac output secondary to increased oxygen demand of working
can increase five times to adjust to the metabolic de­ muscles, arousal, and emotional stress. A thorough
mands of exercise stress. All steps in the oxygen trans­ understanding of the normal effects of gravitational
port pathway are affected by exercise stress. Ventilation and exercise stress and arousal is essential to under­
is increased, and ventilation and perfusion matching is stand deficits in oxygen transport. In disease, numer­
optimized to maximize oxygenation of blood. Heart ous factors impair and threaten oxygen transport, that
rate and stroke volume are increased to effect greater is, underlying pathophysiology, restricted mobility,
cardiac output of oxygenated blood to the tissues. At recumbency, factors related to the patient's care, and
the tissue level, oxygen extraction is enhanced. factors related to the individual (see Chapter 16).
Thus the physical therapist needs a detailed under­
standing of these concepts to diagnose these deficits
Emotional Stress
and prescribe efficacious treatments.
The body responds to emotional stress similar to ex­
ercise stress with the sympathetic stress reaction. Per­
REVIEW QUESTIONS
ceived threat, the basis of emotional stress, triggers
the fight, flight, or fright mechanism and a series of 1. Describe the oxygen transport pathway, its steps
sympathetically mediated physiological responses. and their interdependence.
This reaction that prepares the body for flight in­ 2. Describe the physiological processes of energy
cludes an increase in heart rate, blood pressure, CO, transfer and cellular oxidation.
blood glucose, muscle strength, mental alertness, cel­ 3. Explain oxygen transport with respect to oxygen
lular metabolism, and increased local blood flow to delivery, uptake and utilization and the interrela­
specific muscle groups, as well as inhibition of invol­ tionship among these processes.
untary function. 4. Outline the factors that perturb oxygen transport
in health.

SUMMARY
References
This chapter described the oxygen transport system,
its component steps, and their interdependence. This Chase, G.A., Grave, c., & Rowell, L.B. (1966). Independence of
framework provides a conceptual basis for the prac­ changes in functional and performance capacities attending
prolonged bed rest, Aerospace Medicille 37: 1232-1237.
tice of cardiopulmonary physical therapy.

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 Oxygen Transport: The Basis for Cardiopulmonary Physical Therapy 21

Cone, lB. (1987). Oxyg.cn transport from capillary to cell. In Sny­ Kariman, K., & Burns, S.R. (1985). Regulation of tissue oxygen
der, J.V., Pinsky, M.R. (eds). Oxygen transport in the criticailv extraction in disturbed in adult respiratory distress syndrome,
ill, Chicago: Year Book. A meri can Review Respi ratory Diseases 132: 109-1 14, 1985.
Dantzker, D.R. (1993). Adequacy of tissue oxygellation. Critical Kirchberger, M.A. (1991). Excitation and contraction of skeletal
Care M edicine 21:S40-S43. muscle. In West J.B., editor (1991). Best and Taylor's physiolog­
Dantzker, D.R. (1991). CardiopulmonGl) , Critical Care, ed 2. Philadel­ ical basis of medical practice. Bahimore: Williams & Wilkins.
phia: WE Saunders. Lorente, J.A., et al (J 991). Oxygen delivery-dependent oxygen con­
Dantzker, D.R. (1985). The intluence of cardiovascular function on sumption in acute respiratory failure, Critical Care Medicine
gas exchange. Clinical Chesl Medicine 4: 149-159. 19.'770-775, 1991.
Dantzker, D.R., Boresman, B., & Gutierrez, G. (1991). Oxygen MCArdle, W.D., Katch, F.l., & Katch, V.L. (1994). Essentials (j(
supply and utilization relationships. American Review of Respi­ exercise physiology, Philadelphia: Lea & Febiger.
ratory Disorders 143:675-679. Mizock, B.A., & Falk, J.L. (1992). Lactic acidosis in critical ill­
Dean, E. (1994a). Oxygen transport: a physiologically-based con­ ness, Critical Core Medicine 20:80-93, 1992.
ceptual framework for the practice of cardiopulmonary physio­ Phang, P.T., Russell, J.A. (1993). When does V02 depend on D02
therapy, Physiotherapy 80:347-355. Respiratory Care 38:618-630.
Dean, E. (1994b). Physiotherapy skilis: positioning and mobiliza­ Ross, J., & Dean, E. (1989). Integrating physiological principles
tion of the patient. 1 n Webber, B.A., Pryor, J.A., editors. into the comprehensive management of cardiopulmonary dys­
(1994b). Physiotherapy for respiralry and cardiac problems, function. Physical Therapy 69:255-259, 1989.
Edinburgh: Churchill Livingstone. Ross, J" & Dean, E. (1992). Body positioning. In e.e. Zadai (Ed.).
Dean, E., & Ross, 1. (1992a). Discordance between cardiopulmonary Clinics in physical therapy. Pulmonary managemell1 in physi­
physiology and physical therapy. Chest 101:1694-1698, 1992a cal therapy. New York: Churchill Livingstone.
Dean, E., & Ross, 1. (1992b). Oxygen transport. The basis for con­ Samsel, R.W., & Schumacker, P.T. (1991). Oxygen delivery to tis­
temporary cardiopulmonary physical therapy and its optimiza­ sues, European Respiralry 10urna14: 1258-1267.
tion with body positioning and mobilization, Physical Therapy Sandler, H. (1986). Cardiovascular effects of inactivity, [n Sandler,
Practice 1:34-44. H., Vernikos, 1., (Eds.). Inactivity physiological effects. Orlando,
Epstein, e.D. & Henning, R.J. (1993). Oxygen transport variables Fla: Academic Press.
in the identification and treatment of tissue hypoxia, Heart Schumacker, P.T., & Cain, S.M.: The concept of critical oxygen
Lung, 22:328-348. delivery, Intensive Care Med i cine 13:223-229.
Fenwick, J.e., et al: Increased concentrations of plasma lactate Schumaker, P.T., & Samsel, R.W. (1989). Oxygen delivery and
predict pathologic dependence of oxygen consumption on oxy­ uptake by peripheral tissues: physiology and pathophysiology,
gen delivery in patients with adult respiratory distress syn­ Critical Care Clinics 5:255-269.
drome, lournal of Critical Care 5:81-86, 1990. Shephard, R.J. (1985). Physiology and biochemistry of exercise,
Fox, E., Bowers R., & Foss M. (1993). The physiological basis for ex­ Philadelphia: Praeger Scientific.
ercise and sport, ed 5, Madison: Wis. 1993, Brown & Benchmark. Tortora, G.J., & Anagnostakos N.P. (1990). Principles of anatomy
Ganong, W.F.: Review of medical physiology, ed 16, Los Altos, and physiology, New York: Harper & Row.
Calif: Lange Medical Publications. Wasserman, K., et al (1987). Principles of exercise testing and in­
Goldring, R.M.: Specific defects in cardiopulmonary gas exchange, terpretation, Philadelphia: Lea & Febiger.
American Review Respiratory Disorders 129:S57-S59, 1984. Weber, K.T., et al (1983). The cardiopulmonary unit: The body's
Green, D., & Esparaz, B. (1990). Coagulopathies in the critically-ill gas exchange system, Clinics Chest Medicine 4:101-110.
patient. [n Cane, R.D., Shapiro, B,A., & Davison, R. (Ed.). (1990). West, J. B. (1985). Respiratory physiology-the essentials, ed 5,
Case sludies in critical care medicine, ed 2, Chicago: Year Book. Baltimore: Williams & Wilkins.
Guyton, A.e. (1991). Textbook of medical physiology, ed 8, West, J.B.: Ventilation, blood flow and gas exchange, (ed 4). Ox­
Philadelphia, 1991, WB Saunders. ford: Blackwell Scientific.
Guyton, A.e. (1987). Human physiology and mechanisms of dis­ Winslow, E.H. (1985). Cardiovascular conseq/./ences of bed rest,
ease, ed 4, Philadelphia: WB Saunders. Heart Lung 14:236-246.
Johnson, R.L. (1973). The lung as an organ of oxygen transport,
Bosic RespiralOry Diseases 2: 1-6, 1973.

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 Cardiopulmonary Anatomy

Elizabeth Dean
Lyn Hobson

KEY TERMS Cardiopulmonary unit Peripheral circulation

Heart Pulmonary circulation
Heart-lung interdependence Respiratory muscles
Lymphatic circulation Thoracic cavity
Parenchyma Tracheobronchial tree

INTRODUCTION
This chapter presents the anatomy of the car­
The heart lies in series with the lungs, constituting diopulmonary system, including the skeletal features
the cardiopulmonary unit, the central component of of t h e t horacic cavity; muscles of respiration;
the oxygen transport pathway (Scharf and Cassidy, anatomy of t h e tracheobronchial tree; lung
1989; Weber et ai, 1983). Virtually all the blood re­ parenchyma; basic anatomy of the heart; and periph­
turned to the right side of the heart passes through eral, pulmonary, and lymphatic circulations (Berne
the lungs and is delivered to the left side of the heart and Levy, 1992; Burton and Hodgkin, 1984; Ganong,
for ejection to the systemic, coronary, and bron­ 1993; Guyton, 1991; Katz, 1992; Murray, 1986; Mur­
chopulmonary circulations. Because of this interrela­ ray and Nadel, 1988; Nunn, 1993; West, 1991; West,
tionship, changes in either lung or heart function can 1995; and Williams et ai, 1989).
exert changes in the function of the other organ. A
detailed understanding of the anatomy of the heart
THORAX
and lungs, and how these organs work synergisti­
cally is essential to the practice of cardiopulmonary The bony thorax covers and protects the principal or­
physical therapy. gans of respiration and circulation, as well as the

23

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24 PART I Cardiopulmonary Function in Health and Disease

FIGURE 2-2
The relationship of the lungs to the bony thorax (posterior
view).

FIGURE 2-1
The relationship of the bony thorax and lungs to the
level with the second costal cartilages. The bifurca­
abdominal contents (anterior view).
tion of the trachea into the right and left mainstem
bronchi al s o occurs at t h e sternal ang le. The
liver and the stomach (Figures 2-1 and 2-2). The pos­ manubrium and body are joined by fibrocartilage,
terior surface is formed by the 12 thoracic vertebrae which may ossify in later life.
and the posterior part of the 12 ribs. The anterior sur­ The body of the sternum is twice as long as the
face is formed by the sternum and the costal carti­ manubrium. It is a relatively thin bone and can be
lage. The lateral surfaces are formed by the ribs. At easily pierced by needles for bone marrow aspira­
birth, the thorax is nearly circular, but during child­ tions. The heart is located beneath and to the left of
hood and adolescence, it becomes more elliptical the lower one third of the body of the sternum. Al­
until adulthood. It is wider from side to side than it is though it is attached by cartilage to the ribs, this por­
from front to back. tion of the sternum is flexible and can be depressed
without breaking. This maneuver is used, with care,
in closed cardiac massage to artificially circulate
Sternum
blood to the brain and extremities. The lower margin
The sternum, or breastbone, is a flat bone with three of the body is attached to the xiphoid process by fi­
parts: the manubrium, body, and xiphoid process. brocartilage. This bone is the smallest of the three
The manubrium is the widest and thickest bone of the parts of the sternum and usually fuses with the body
sternum. Its upper border is scalloped by a central of the sternum in later life.
jugular notch, which can be palpated, and two clavic­
ular notches that house the clavicles. Its lower border
Ribs
articulates with the upper border of the body at a
slight angle, the sternal angle or angle of Louis. This A large portion of the bony thoracic cage is formed
angle can be easily palpated, is a landmark located by 12 ribs located on either side of the sternum. The
between thoracic vertebrae T4 and TS, and is on a first seven ribs connect posteriorly with the vertebral

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 2 Cardiopulmonary Anatomy 25

FIGURE 2-3
The movements of the r ibs. A, "Bucket handle," lower rib. B, "Pump handle," first rib.

MOVEMENTS OF THE THORAX

column and anteriorly through costal cartilages with
the sternum. These are known as the true ribs. The re­ The frequency of movement of the bony thorax joints
maining five ribs are known as the false ribs. The is greater than that of almost any other combination
first three have their cartilage attached to the cartilage of joints in the body. Two types of movements have
of the rib above. The last two are free or floating ribs. been described-the pump-handle movement and the
The ribs increase in length from the first to the sev­ bucket-handle movement (Figure 2-3) (Cherniack
enth rib, and then decrease to the twelfth rib. They and Cherniack, 1983). The upper ribs are limited in
also increase in obliquity until the ninth rib and then their ability to move. Each pair swings like a pump
decrease in obliquity to the twelfth rib. handle, with elevation thrusting the sternum forward.
Each rib has a small head and a short neck that ar­ This forward movement increases the anteroposterior
ticulate with two thoracic vertebrae. The shaft of the diameter and the depth of the thorax and is called the
rib curves gently from the neck to a sudden sharp pump-handle movement. In the lower ribs, there is
bend, the angle of the rib. Fractures often occur at little antero-posterior movement. During inspiration,
this site. A costal groove is located on the lower bor­ the ribs swing outward and upward, each pushing
der of the shaft of the ribs. This groove houses the in­ against the rib above during elevation. This bucket­
tercostal nerves and vessels. Chest tubes and needles handle movement increases the transverse diameter
are inserted above the ribs to avoid these vessels and of the thoracic cage. Thus during inspiration, the tho­
nerves. The ribs are separated from each other by the rax increases its volume by increasing its anteropos­
intercostal spaces that contain the intercostal muscles. terior and transverse diameters.

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26 PART I Cardiopulmonary Function in Health and Disease

MUSCLES OF RESPIRATION

Inspiration

Inspiration is an active movement involving the con­

traction of the diaphragm and intercostals. Additional
muscles may come into play during exertion in
health. In disease, the role of these accessory muscles
of inspiration may have an important role even at
rest. The accessory muscles include the sternocleido­
mastoids, scalenes, serratus anterior, pectoralis major
and minor, trapezius, and erector spinae. The degree
to which these accessory muscles are used by the pa­
tient is dependent on the severity of cardiopulmonary
distress (Clemente, 1985; Murray and Nadel, 1988;
and Williams et ai, 1989).

Diaphragm
The diaphragm is the principal muscle of respiration.
During quiet breathing, the diaphragm contributes ap­
proximately two thirds of the tidal volume in the sit­
ting or standing positions, and approximately three
fourths of the tidal volume in the supine position. It is
also estimated that two thirds of the vital capacity in
all positions is contributed by the diaphragm.
The diaphragm is a large, dome-shaped muscle
that separates the thoracic and abdominal cavities. Its FIGURE 2-4
upper surface supports the pericardium (with which it The diaphragm from below.

is partially blended), heart, pleurae, and lungs. Its

lower surface is almost completely covered by the
peritoneum and overlies the liver, kidneys, suprarenal
glands, stomach, and spleen (Figure 2-4). This large lumbar vertebrae and extends upward to the central
muscle can be divided into right and left halves. Each tendon. The central tendon is a thin, strong aponeuro­
half is made up of three parts-sternal, lumbar, and sis situated near the center of the muscle, somewhat
costal. These three parts are inserted into the central closer to the front of the body. It resembles a trefoil
tendon, which lies just below the heart. The sternal leaf with three divisions or leaflets. The right leaflet
part arises from the back of the xiphoid process and is the largest, the middle is the next largest, and the
descends to the central tendon. On each side is a left leaflet is the smallest.
small gap, the sternocostal triangle, which is located Major vessels traverse the diaphragm through one
between the sternal and costal parts. It transmits the of three openings (see Figure 2-4). The vena caval
superior epigastric vessels and is often the site of di­ opening is located to the right of the midline in the
aphragmatic hernias. The costal parts form the right central tendon and contains branches of the right
and left domes. They arise from the inner surfaces of phrenic nerve and the inferior vena cava. The
the lower four ribs and the lower six costal cartilages. esophageal opening is located to the left of the mid­
They interdigitate and transverse the abdomen to in­ line and contains the esophagus, the vagal nerve
sert into the anterolateral part of the central tendon. trunks and branches of the gastric vessels. The aortic
The lumbar part arises from the bodies of the upper opening is located in the midline and contains the

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 2 Cardiopulmonary Anatomy 27

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I t.

\ ff�
'--- -----

FIGURE 2-5
When the patient is lying on side, the dome of the diaphragm on the lower side rises fUI1her in the
thorax than the dome on the upper side.

aorta, thoracic duct, and sometimes the azygos vein. in this POSItIon. On x-ray, the position of the di­
The diaphragm is also pierced by branches of the left aphragm can indicate whether the film was taken dur­
phrenic nerve, small veins, and lymph vessels. ing inspiration or expiration, and may also indicate
The position of the diaphragm and its range of pathology in the lungs, pleurae, or abdomen.
movement vary with posture, the degree of distention Each half of the diaphragm is innervated by a sep­
of the stomach, size of the intestines, size of the liver, arate nerve-the phrenic nerve on that side. Al­
and obesity. The average movement of the diaphragm though the halves contract simultaneously, it is pos­
in quiet respiration is 12.5 mm on the right and 12 sible for half of the muscle to be paralyzed without
mm on the left. This can increase to a maximum of affecting the other half. Generally, the paralyzed half
30 mm on the right and 28 mm on the left during in­ remains at the normal level during rest. However,
creased ventilation. The posture of the individual de­ with deep inspiration, the paralyzed half is pulled up
termines the position of the diaphragm. In the supine by the negative pressure in the thorax. A special x­
position, the resting level of the diaphragm rises. The ray, moving fluoroscopy, is used to determine paral­
greatest respiratory excursions during normal breath­ ysis of the diaphragm.
ing occur in this position. Howevcr, the lung volumes Contraction of the diaphragm increases the tho­
are decreased because of the elevated position of the racic volume vertically and transversely. The central
abdominal organs. fn a sitting or upright position, the tendon is drawn down by the diaphragm as it con­
dome of the diaphragm is pulled down by the abdom­ tracts. As the dome descends, abdominal organs are
inal organs, allowing a larger lung volume. For this pushed forward, as far as the abdominal walls will
reason, individuals who are short of breath are more allow. When the dome can descend no farther, the
comfortable sitting than reclining. fn a side-lying po­ costal fibers of the diaphragm contract to increase the
sition, the dome of the diaphragm on the lower side thoracic diameter of the thorax. This occurs because
rises farther into the thorax than the dome on the the fibers of the costal part of the diaphragm run ver­
upper side (Figure 2-5). The abdominal organs have a tically from their attachment at the costal margin.
tendency to fall forward out of the way, allowing Thus contraction of these fibers elevates and everts
greater excursion of the dome on the lower side. fn the ribs (Figure 2-6). If the diaphragm is in a low po­
contrast, the upper side moves little with respiration sition, it will change the angle of pull of the muscle's

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28 PART I Cardiopulmonary Function in Health and Disease

.-;;/
"W.M

FIGURE 2-6
Contraction of the costal fibers of the diaphragm causes rib eversion and elevation.

costal fibers. Contraction of these fibers creates a muscle forward to the sternum. There are II external
horizontal pull, which causes the lateral diameter to intercostal muscles on each side of the sternum. They
become smaller as the ribs are pulled in toward the are thicker posteriorly than anteriorly, and thicker
central tendon. than the internal intercostal muscles. They are inner­
As the diaphragm descends, it compresses the ab­ vated by the intercostal nerves, and contraction draws
dominal organs, increasing intraabdominal pressure. the lower rib up and out toward the upper rib. This
At the same time, the intrathoracic pressure decreases action increases the volume of the thoracic cavity.
as the lung volume is increased by the descending di­ There are also 11 internal intercostals per side.
aphragm. Inspiratory airflow occurs as a result of this These are considered primarily expiratory in function.
decrease in intrathoracic pressure (see Chapter 3). Studies have shown that the intercartilaginous or
The pressure gradient between the abdominal and parasternal portion of the internal intercostals con­
thoracic cavities also facilitates the return of blood to tracts with the external intercostals during inspiration
the right side of the heart. to help elevate the ribs. Besides their respiratory func­
Movement of the diaphragm can be controlled to tions, the intercostal muscles contract to prevent the
some extent voluntarily. Vocalists spend years learn­ intercostal spaces from being drawn in or bulged out
ing to manipulate their diaphragms to produce the during respiratory activity.
controlled sounds during singing. The diaphragm mo­
mentarily ceases movement when a person holds his
Sternocleidomastoid
or her breath. The diaphragm is invol untarily in­ The sternocleidomastoids (SCMs) are strong neck
volved in parturition, bearing down in bowel move­ muscles arising from two h e a d s , one from the
ments, laughing, crying, and vomiting. Hiccups are manubrium and one from the medial part of the clavi­
spasmodic, sharp contractions of the diaphragm that cle (see Figure 2-7, p. 29). These two heads fuse into
may indicate disease (e.g., a subphrenic abscess) if one muscle mass that is inserted behind the ear into the
they persist. mastoid process. It is innervated by the accessory
nerve and the second cervical nerve. There are two of
Intercostals these muscles, one on each side of the neck. When one
The external intercostals extend from the tubercles SCM contracts, it tilts the head toward the shoulder of
of the ribs, above, down, and forward to the costo­ the same side and rotates the face toward the opposite
chondral junction of the ribs below, where they be­ shoulder. If the two SCM muscles contract together,
come continuous with the anterior intercostal mem­ they pull the head forward into flexion. When the head
brane (Figure 2-7). This membrane extends the is fixed, they assist in elevating the sternum, increasing

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 2 Cardiopulmonary Anatomy 29

Obllquus internus abdomlnis

Transversus abdomlnlS ......

FIGURE 2-7
Respiratory muscles (anterior view).

the anteroposterior (AP) diameter of the thorax. and inferiorly to the upper surface of the first two
The SCMs are the most important accessory mus­ ribs (see Figure 2-7). They are innervated by related
cles of inspiration. Their contractions can be ob­ cervical spinal nerves. These muscles are primarily
served in all patients during forced inspiration and in supportive neck muscles, but they can assist in res­
all patients who are dyspneic. These muscles become piration through reverse action. When their superior
visually predominant in patients who are chronically attachment is fixed, the scalenes act as accessory
dyspneic (sec Chapter 4). respiratory muscles and elevate the first two ribs
during inspiration.
Scalenes
The anterior, medial, a n d posterior scalenes are
Serratus Anterior
three separate muscles that are considered as a func­ The sen-atus anterior arises from the outer surfaces of
tional unit. They are attached superiorly to the trans­ the first eight or nine ribs. It curves backward, forming
verse processes of the lower five cervical vertebrae a sheet of muscle that inserts into the medial border of

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30 PART I Cardiopulmonary Function in Health and Disease

the scapula. It is innervated by the long thoracic nerve

f"
(cervical nerves CS, C6, and C7). There are two of
these muscles, one on each side of the body. Normally,
they assist in forward pushing of the arm (as in boxing
or punching). When the scapulae are fixed, they act as
accessory respiratory muscles and elevate the ribs to
which they are attached.

Pectoralis Major

The pectoralis major is a large muscle arising from

J
the clavicle, the sternum, and the cartilages of all the
true ribs (see Figure 2-7, p. 29). This muscle sweeps
across the anterior chest to insert into the intertuber­
cular sulcus of the humerus. It is innervated by the
lateral and medial pectoral nerves and cervical nerves
CS, C6, C7, C8, and Tl. There are two of these mus­
cles, one on each side of the body. This muscle acts
to rotate the humerus medially and to draw the arm
across the chest. In climbing and pull-ups, it draws
the trunk toward the arms. In forced inspiration when
the arms are fixed, it draws the ribs toward the arms,
thereby increasing thoracic diameter.

Pectoralis Minor

The pectoralis minor is a thin muscle originating from

the outer surfaces of the third, fourth, and fifth ribs
near their cartilages. It inserts into the coracoid process
FIGURE 2-8
of the scapula. It is innervated by the pectoral nerves Respiratory muscles (posterior view).
(cervical nerves C6, C7, and C8). There are two of
these muscles, one on each side of the body. They con­
tract with the serratus anterior to draw the scapulae to­
ward the chest. During deep inspiration, they contract the spine of the scapula. Its lower belly arises from
to elevate the ribs to which they are attached. the supraspinous ligaments and the spines of the
lower thoracic region, and runs upward to be in­
Trapezius
serted into the lower border of the spine of the
The trapezius consists of two muscles that form a scapula. This large muscle is innervated by the ex­
huge diamond-shaped sheet extending from the head ternal or spinal part of the accessory nerve and cer­
down the back and out to both shoulders (Figure 2- vical nerves C3 and C4. Its main function is to ro­
8). Its upper belly originates from the external oc­ tate the scapulae in elevating the arms and to control
cipital protuberance and curves around the side of their gravitational descent. It also braces the scapu­
the neck to insert into the posterior border of the lae and raises them, as in shrugging the shoulders.
clavicle. The middle part of the muscle arises from a Its ability to stabilize the scapulae makes it an im­
thin diamond-shaped tendinous s h e et, the portant accessory muscle in respiration. This stabi­
supraspinous ligaments and the spines o f the upper lization enables the serratus anterior and pectoralis
thoracic region, and runs horizontally to insert into minor to elevate the ribs.

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 2 Cardiopulmonar)' Anatomy 31

Erector Spinae Obliquus Intemus Abdominis

The erector spinae is a large muscle extending from This muscle originates from the lumbar fascia, the an­
the sacrum to the skull (see Figure 2-8, p. 30). It orig­ terior two thirds of the iliac crest, and the lateral two
inates from the sacrum, iliac crest,
and the spines of thirds of the inguinal ligament (see Figure 2-7, p. 29).
the lower thoracic and lumbar vertebrae. It separates Its post eri or fibers run almost vertically upward to in­
into a lateral iliocostalis, an intermediate longissimus, selt into the lower borders of the last three ribs. The
and a medial spinalis column. This muscle mass in­ other fibers join an aponeurosis attached to the costal
serts into various ribs and vertebral processes all the margin above, the linea alba in the midline and the
way up to the skull. It is innervated by the related pubic crest below. It is innervated by the lower six tho­
spinal nerves. These muscles extend, laterally flex, racic nerves and the first lumbar spinal nerves.
and rotate the vertebral column. They are considered
accessory respiratory muscles through their extension Transversus Abdominis
of the vertebral column. In deep inspiration, these The transversus abdominis arises from the inner sur­
muscles extend the vertebral column, allowing fur­ face of the lower six costal caltilages, the lumbar fas­
ther elevation of the ribs. cia, the anterior two thirds of the iliac crest, and the
lateral one third of the inguinal ligament (see Figure

Expiration 2-7, p. 29). It nms across the abdomen horizontally to

insert into the ap one ur osi s extending to the linea
,

Expiration is a passive process,

occurring when the in­ alba. It is innervated by the lower si x thoracic nerves
tercostals and diaphragm relax. Their relaxation al­ and the first lumbar spinal nerves.
lows the ribs to drop to their preinspiratory position
and the diaphragm to rise. These activities compress Action of the Abdominal Muscles
the lungs, raising intrathoracic pressure above atmos­
These four muscles work together to provide a firm but
pheric pressure, and thereby contributing to air flow
flexible wall to keep the abdominal viscera in position.
out of the lungs.
The abdominal muscles exert a compressing force on
the abdomen when the thorax and pelvis are fixed. This
Rectus Abdominis
force can be used in defecation, urination, parturition,
The rectus abdominis rises from the pubic crest and and vomiting. In forced expiration, the abdominal mus­
extends upward to insert into the xiphoid process cles help force the diaphragm back to its resting posi­
and the costal margin of the fifth, sixth, and seventh tion and thus force air from the lungs. If the pelvis and
costal cartilages (see Figure 2-7, p. 29). It is inner­ vertebral column are fixed, the obJiquus externus abdo­
vated by related spinal nerves, and its action is con­ minis aids expiration further by depressing and com­
sidered within the context of the other abdominal pressing the lower part of the thorax. Patients with
muscles. chronic obstructive pulmonary disease (COPD) have
difficulty in exhalation, which causes them to trap air in
Ob/iquus Extemus Abdominis
their lungs. The continued contraction of the abdominal
This muscle arises in an oblique line from the fifth muscles throughout exhalation helps them force this air
costal cartilage to the twelfth rib (see Figure 2-7, from the lungs. The abdominal muscles also play an
p. 29). Its posterior fibers attach in an almost vertical impOltant role in coughing. First, a large volume of air
line with the iliac crest. The other fibers extend down is inhaled, and the glottis is closed. Then the abdominal
and forward to attach to the front of the xiphoid muscles contract, raising intrathoracic pressure. When
process, the linea alba, and below with the pubic the glottis opens, the large difference in intrathoracic
symphysis. It is innervated by the lower six thoracic and atmospheric pressure causes the air to be expelled
spinal nerves. forcefully at tremendous flow rates (tussive blast).

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32 PART I Cardiopulmonary Function in Health and Disease

Patients with weak abdominal muscles (from neuro­ upper ribs move forward and upward (Cherniack and
muscular diseases, paraplegia, quadriplegia or exten­ Cherniack, 1983).
sive abdominal surgery) often have ineffective coughs Quiet expiration is passive and involves no mus­
(see Chapters 28 and 33). cular contraction although some electrical activity
The four abdominal muscles have many other can be detected. The inspiratory muscles relax, caus­
nonrespiratory functions both individually and as a ing intrathoracic pressure to be raised as the ribs and
group; these are not discussed here. diaphragm compress the lungs by returning to their
preinspiratory positions. This increased pressure al­
internaiintercostais lows air flow from the lungs.
There are II internal intercostal muscles on each side In forced inspiration, a large number of accessory
of the thorax. Each muscle arises from the floor of muscles may contract in addition to the normal in­
the costal groove and cartilage, and passes inferiorly spiratory muscles mentioned. The erector spinae
and posteriorly to insert on the upper border of the rib contract to extend the vertebral column. This exten­
below. These internal intercostals extend from the sion permits greater elevation of the ribs during in­
sternum anteriorly, around the thorax to the posterior s piration. Va rious back muscles ( e .g., erector
costal angle. They are generally divided into two spinae, trapezius, and rhomboids) contract to stabi­
parts-the interosseous portion located between the lize the vertebral column, head, neck, and scapulae.
sloping parts of the ribs, and the intercartilaginous This enables accessory respiratory muscles to assist
portions located between costal carti lages. As dis­ inspiration through reverse action. The SCM raises
cussed previously, the intercartilaginous portions are the sternum. The scalenes elevate the first two ribs.
considered inspiratory in function. Contraction of the The serratus anterior, pectoralis major, and pec­
interosseous portions of the intercostals depresses the toralis minor assist in elevating the ribs bilaterally.
ribs and may aid in forceful exhalation. This muscle All these accessory muscles tend to elevate the ribs,
is innervated by the adjacent intercostal nerves. thus increasing the AP diameter but not the trans­
verse diameter of the thorax. (In fact, the transverse
diameter does increase slightly as a result of the in­
SUMMARY OF RESPIRATORY MOVEMENTS
creased strength of the contraction of the normal in­
In quiet inspiration, the diaphragm, external inter­ spiratory muscles.) The marked increase in AP di­
costals, and intercartilaginous portions of the internal ameter in relation to transverse diameter creates an
intercostals are the primary muscles that contract. impression of en bloc breathing in the patient using
The diaphragm contracts first and then descends, en­ accessory muscles.
larging the thoracic cage vertically. When abdominal In forced expiration, the interosseous portion of
contents prevent its further descent, the costal fibers the internal intercostals and the abdominal muscles
of the diaphragm contract, causing the lower ribs to contract to force air out of the lungs. Forced expira­
swing up and out to the side (bucket-handle move­ tion can be slow and prolonged (as in patients with
ment). This lateral rib movement is assisted by the COPD) or rapid and expulsive (as in a cough). If the
external intercostals and the intercartilaginous portion abdominal contractions are strong enough, the trunk
of the internal intercostals. The transverse diameter of flexes during exhalation. This flexion further com­
the thorax is increased by this bucket-handle move­ presses the lungs, forcing more air from them.
ment. Finally, the upper ribs move forward and up­
ward (pump-handle movement) also through contrac­
UPPER AIRWAYS
tion of their external intercostals and the
intercartilaginous portions of the internal intercostals.
Nose
This increases the AP diameter of the thorax. During
quiet inspiration, the epigastric area protrudes, then Noses vary in size and shape with individuals and na­
the ribs swing up and out laterally, and finally the tionalities. Its framework is comprised of bony and

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 2 Cardiopulmonary Anatomy 33

cartilaginous parts. The upper one third IS primarily are covered with a thin, yellow olfactory mucous
bony and contains the nasal bones, the fr ontal membrane that consists of bipolar nerve cells that are
processes of the maxillae and the nasal part of the olfactory in function. Only a portion of inspired air
frontal bone. Its lower two thirds are cartilaginous reaches the olfactory region to provide a sense of
and contain the septal, lateral, and major and minor smell. When people smell something specific, they
alar nasal cartilages. The nasal cavity is divided into sniff This action lifts the inspired air so that more of
right and left halves by the nasal septum. This cavity it comes in contact with the olfactory region.
extends from the nostrils to the posterior apertures of The anterior portion (vestibule) of the nasal cavity
the nose in the nasopharynx. The lateral walls of the (Figure 2-9) is lined with skin and coarse hairs (vibris­
cavity are irregular as a result of projecting superior, sae) that entrap inhaled patticies. The rest of the cavity
middle, and inferior nasal chonchae. There is a mea­ and sinuses (with the exception of the olfactory region)
tus located beneath or lateral to each choncha through are lined with respiratory mucous membrane. This
which the sinuses drain. The chonchae increase the membrane is composed of pseudostratified columnar
sUlface area of the nose for maximum contact w ith ciliated epithelium (Figure 2-10). It contains goblet
inspired air. The superior chonchae and adjacent sep­ cells, as well as mucous and serous glands that produce
tal wall are referred to as the olfactory region. They secrete mucus and serous secretions. These secretions

Vestibule 01 nasal cavity

FIGURE 2-9
Sagittal section of the head and neck.

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34 PART I Cardiopulmonary Function in Health and Disease

FIGURE 2-10
A, Pseudostrmified columnar ciliated B, Normal movements of cilia.

and bacteria. This mucus is then walls are lined

swept to the the cilia at a rate of 5 to 15
where it is swallowed or The and stratified squamous in the oral
mucous membrane is vascular, with arterial blood sup­ parts.
plied by branches of the internal and external carotid The nasopharynx is a continuation of the nasal
arteries. Venous occurs the anterior cavitIes 2-9, p. It lies behind the nose
facial veins. The mucous membrane is thickest over the and above the soft palate. With the exception of the
chonchae. As air is inhaled, it passes around and over soft its walls are immovable, so its is
the chonchae, whose vascular moist surfaces heat, hu­ never as is the oral and laryngeal phar­
midify, and filter the inspired air. The mucous mem­ ynx. The nasopharynx communicates with the nasal
brane may become swollen and irritated in upper cavity the posterior apertures of
infections and may secrete copious amounts of the nose. It communicates with the
mucus. Because this membrane is continuous with si­ pharynx through an opening, the isthmus.
nuses, auditory tubes and lacrimal canaliculi, people This opening is closed by elevations of the soft palate
suffering f r o m colds often complain of sinus
headaches, watery eyes, and other The oral pharynx extends from the soft palate to
Secretions are often so copious that the nasal passages the ep!.r10ttis (see p. 33). It opens into the
become comDletelv blocked. the oropharyngeal isthmus.
walls lie on the bodies of the second and
third cervical vertebrae. Laterally, two masses of
Pharynx
lymphoid tissue-the be seen.
The is an oval fibromuscular sac located These tonsils form part of a circular band of lym­
behind the nasal cavity, mouth, and larynx. It is ap­ phoid tissue surrounding the into the diges­
12 to 14 cm long and extends from the t!ve and tracts.
base of the skull to the esophagus below, at the level The laryngopharynx lies behind the larynx and ex­
of the cricoid the sixth cervical tends from the above to the inlet of the
vertebra. Anteriorly, it opens into the nasal cavity esophagus below Figure p. The fourth
(nasophar ynx), mouth (oral pharynx) and larynx to sixth cervical vertebrae lie behind the laryngeal

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 2 Cardiopulmonary Anatomy 35

a n d the cartilages of the larynx (e.g., thyroid,

cricoid, epiglottic, right and left arytenoids, cornic­
ulates, and cuneiforms). The thyroid cartilage is the
largest. It has a V-shaped notch in its upper one
third, which projects forward, forming the "Adam's
apple." The entire cartilage is pulled up in swal­
lowing, with the upper part of the cartilage passing
beneath the hyoid bone. The cricoid cartilage is
shaped like a signet ring, with the signet part facing
the posterior. The anterior part of the carti lage is
easily palpated just below the thyroid cartilage. It is
thicker and more prominent than the tracheal rings,
FIGURE 2-11 which lie below. It is the only cartilage that com­
Visualization of the larynx via a laryngoscope. pletely circles the airway. The cricoid cartilage is
connected to the thyroid cartilage by the cricothy­
roid membrane. (This membrane is often punctured
pharynx. In front of the laryngopharynx are the to establish an airway in an emergency when the
epiglottis, the inlet of the larynx and the posterior upper airway is obstructed.) The epiglottic cartilage
surfaces of the arytenoid and cricoid cartilages. is the elastic skele ton of the epiglottis. It is a
leaflike structure attached by ligaments to the hyoid
bone anteriorly and the thyroid cartilage below. It is
Larynx
considered a vestigial structure, and its removal
The larynx is a complex structure composed of carti­ causes little effect. Finally, the arytenoid cartilages
lages and cords moved by sensitive muscles (Figure are two small pyramid-shaped cartilages that articu­
2-11), and is located between the trachea and laryn­ late with the posterior part of the cricoid cartilage.
gopharynx, for which it forms an anterior wall. It acts The vocal cords attach from these cartilages to the
as a sphincteric valve with its rapid closure, prevent­ thyroid cartilage.
ing food, liquids, and foreign objects from entering The true vocal cords (or vocal folds) are two
the airway. It controls airflow, and at times closes so pearly white folds of mucous membrane that stretch
that thoracic pressure may be raised and the upper from the arytenoid cartilage to the thyroid cartilage.
airways cleared by a propulsive cough when the lar­ The space between the true vocal cords is called the
ynx opens. Expiratory airflow vibrates as it passes rima glottidis. It changes shape with movement of the
over the contracting vocal chords, producing the cords but is generally triangular when the cords are
sounds used for speech. (The larynx is not essential open. The rima glottidis and the true vocal cords are
for speech. Humans can speak by learning to dilate grouped together under the term glottis. The glottis is
the upper part of the esophagus so that air vibrates as the narrowest part of the adult airway.
it passes over; this is called esophageal speech). Just above the true vocal cords are two shallow
In adult men, the larynx is situated opposite the grooves in the mucous membrane lining of the larynx.
third, fourth and fifth cervical veltebrae; it is situated These grooves (ventricles of the larynx) contain nu­
somewhat higher in women and children. In children, merous glands that secrete the mucus that covers the
the larynx is essentially the same in girls and boys. At larynx. The false vocal cords (vestibular or ventricular
puberty, the male larynx increases in size consider­ folds) lie just above the venuicles of the larynx. They
ably until its AP diameter is almost doubled. All the are two soft, pink masses of mucous membrane raised
cartilages enlarge, with the thyroid cartilage becom­ slightly from the laryngeal wall. They extend from the
ing prominent anteriorly. thyroid cartilage to the arytenoids. The false cords are
The laryngeal skeleton contains the hyoid bone not as well developed as the true cords and do not

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36 PART I Cardiopulmonary Function in Health and Disease

approximate completely during phonation. However, nation to the right from the level of the cricoid carti­
their closure can help protect the airway from aspira­ lage (see Figure 2-11, p. 35, and Figure 2-12). It trav­
tion of foreign material. els behind the sternum into the thorax to the sternal
There are two main groups of muscles that control angle (opposite the fifth thoracic veltebra), where it
the opening and closing of the glottis-the abductors divides to form the right and left main-stem bronchi.
and adductors. The posterior cricoarytenoid muscle is The tracheal wall is strengthened by 16 to 20 horse­
the most important muscle in the larynx, since it is the shoe-shaped cartilaginous rings. The open P3lts of the
only abductor of the vocal folds. It is vital for respira­ tracheal rings are completed by fibrous and elastic tis­
tion. Contraction of this muscle separates the vocal sue and unstriated transverse muscle. This part of the
folds and widens the lumen of the glottis. There are ring faces the posterior and is very flexible. It indents
eight adductors of the vocal folds: (I) aryepiglottic, or curves inward during coughing. which increases
(2) thyroepiglottic, (3) thyroarytenoid, (4) vocalis, the velocity of expelled air. These cartilages lie hori­
(5) cricothyroid, (6) lateral cricoarytenoid, (7) trans­ zontally one above the other, separated by narrow
verse arytenoid and (8) oblique arytenoid muscles. bands of connective tissue. The trachea is lengthened
Contraction of these muscles results in approximation during hyperextension of the head; swallowing, which
of the vocal cords and narrowing of the glottis. The raises the trachea; and inspiration, when the lungs ex­
adductors of the cords are important in protecting the pand and pull the trachea downward. Its cross-sec­
lower airways. Their contraction prevents fluids, food, tional area becomes smaller with contraction of the
and other substances from being aspirated. All the in­ unstriated transverse muscle fibers that complete the
trinsic laryngeal muscles are innervated by the recur­ tracheal rings.
rent laryngeal nerve (a branch of the vagus nerve) The mucous membrane of the trachea also con­
with the exception of the cricothyroid muscle, which tains columnar ciliated epithelium and goblet cells.
is supplied by the external branch of the superior la­ Each ciliated epithelial eel I contains approximately
ryngeal nerve (also a branch of the vagus nerve). 275 cilia. These structures beat rapidly in a coordi­
The mucous membrane of the larynx is continu­ nated and unidirectional manner, propelling a sheet
ous with that of the laryngopharynx above and the of mucus cephalad from the lower respiratory tract to
trachea below. It lines the cavity of the larynx and the pharynx, where it is swallowed or expectorated.
the structures found within. On the anterior surface The cilia beat in this layer of mucus with a strong,
and upper h a l f of the posterior surface of the forceful forward stroke, followed by a slow ineffec­
epiglottis, and the vocal folds, the mucous mem­ tive backward stroke that returns the cilia to their
brane is stratified squamous epithelium. The rest of starting position. This propelling of mucus by the
the laryngeal mucosa is ciliated columnar epithe­ cilia (mucociliary escalator) is essential. When cilia
lium. The mucous membrane of the larynx has are paralyzed by smoke, alcohol, dehydration, anes­
many mucous glands. They are especially numerous thesia, starvation, or hypoxia, mucus begins to accu­
in the epiglottis, in front of the arytenoid cartilages mulate in distal, gravity-dependent airways, causing
and in the ventricles of the larynx. Some taste buds infiltrates and eventually localized areas of collapse
are also located on the epiglottis and irregularly referred to as atelectasis.
throughout the rest of the larynx. The number of mucus-containing goblet cells is
approximately equal to the number of ciliated epithe­
lial cells. Reserve cells lie beneath the ciliated and
LOWER AIRWAYS
goblet cells. These reserve cells can differentiate into
either goblet cclls or ciliated cells. Beneath the re­
Trachea
serve cells lie the gland cells. There are approxi­
The trachea is a semi-rigid, cartilaginous tube approx­ mately 40 times more gland cells than goblet cells.
imately 10 to II cm long and 2.5 cm wide. It lies in Mucus is composed of 95% water, 2% glycoprotein,
front of the esophagus, descending with a slight incli­ I % carbohydrate, trace amounts of lipid, deoxyri­

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 2 Cardiopulmonary Anatomy 37

Apical
Apical

Posterior

Anterior
Anterior
??'fjfjl;ff?- Apical-posterior

Llnguta

Posterior

Anterior
Anterior
Posterior

FIGURE 2-12
Tracheobronchial tree (a three-quarter view, rotated toward the right side).

bonucleic acid (DNA), dead tissue celis, phagocytes, main-stem bronchus. The azygos vein arches over the
leukocytes, erythrocytes, and entrapped foreign parti­ right main-stem bronchus, the right pulmonary artery
cles. Mucus lines the airways from the trachea to the lies beneath. The right main-stem bronchus divides to
alveoli. Two separate layers have been observed-the form the right upper lobe bronchus, the right middle
sol layer, which lies on the mucosal surface and con­ lobe bronchus and the right lower lobe bronchus. The
tains high concentrations of water, and the gel layer, right upp e r l o b e d i v i d e s i n t o th r e e s e gm e n t al
which is more supelficial and more viscous because bronchi-apical, posterior, and anterior. The apical
of its lower concentration of water. bronchus runs almost vertically toward the apex of
The right main-stem bronchus appears to be an ex­ the lung. The posterior bronchus is directed posteri­
tension of the trachea, being wider, shorter, and more orly in a horizontal direction, while the anterior
vertical than the left main-stem bronchus. Its greater bronchus is directed anteriorly in an almost horizon­
width and more vertical course cause a majority of tal direction. The right middle lobe bronchus divides
aspirated foreign material to pass through the right about 10 mm below the right upper lobe bronchus

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38 PART I Cardiopulmonary Function in Health and Disease

and descends downward anterolateraJly. The right cross-sectional area increases because of the increased
lower lobe bronchus divides into five segmental number of divisions of the airways. The mucous
bronchi. The apical or superior bronchus runs almost membrane is essentially the same, with helical carti­
horizontally, posteriorly. The medial or cardiac laginous plates and cilia becoming more sparse. These
bronchus descends downward medially toward the changes continue throughout the eighth to eleventh
heart. The anterior basal bronchus descends anteri­ generations, which are referred to as bronchioles.
orly. The lateral basal bronchus descends laterally The terminal bronchioles extend from the twelfth
and the posterior bronchus descends posteriorly. Note to the sixteenth generation. The diameter of these air­
that each segment describes its position. ways is approximately I mm. Cartilage is no longer
The left main-stem bronchus is narrower and runs present to provide structural rigidity. The airways are
more horizontally than the right main-stem bronchus. embedded directly in the lung parenchyma, and it is
The aortic arch passes over it, while the esophagus, the elastic properties of this parenchyma that keep
descending aorta, and thoracic duct lie behind it. The these lower airways open. Strong helical muscle
left pulmonary artery lies anteriorly and above the bands are present, and their contraction forms longi­
left main-s t e m b r o n c h u s . T h e l e f t m a i n-stem tudinal folds in the mucosa that sharply decrease the
bronchus has two major divisions-the left upper diameter of these airways. The epithelium of the ter­
lobe bronchus and the left lower lobe bronchus. The minal bronchioles is cuboidal and no longer ciliated.
left upper lobe bronchus has three major segmental The cross-sectional area of the airways increases
bronchi. The anterior bronchus ascends at approxi­ sharply at this level, as the diameter of the terminal
mately a 45-degree angle. The apical-posterior bronchioles ceases to decrease as markedly with each
bronchus has two branches; one runs vertically and generation. All the airways to this level (I to 16 gen­
the other posteriorly toward the apex of the left lung. erations) are considered conducting airways, because
The lingular bronchus descends anterolaterally, much their purpose is to transport gas to the respiratory
like the right middle lobe bronchus of the right lung. bronchioles and alveoli, where gas exchange occurs.
The right lower lobe bronchus divides into four seg­ The conducting airways receive their arterial blood
mental bronchi. The superior or apical bronchus runs from the bronchial circulation (branches of the de­
posteriorly in a horizontal direction. The anterior scending aorta). Airways from below this point re­
bronchus descends anteriorly. The lateral bronchus ceive their arterial blood from the pulmonary arteries.
descends laterally, while the posterior bronchus de­ The respiratory bronchioles extend from the sev­
scends posteriorly. Again the segments describe their enteenth to the nineteenth generation. They are con­
anatomical position. sidered a transitional zone between bronchioles and
The bronchi of the airways continue to divide until alveoli. Their walls contain cuboidal epithelium inter­
there are approximately 23 generations (Table 2-1). spersed with some alveoli. The number of alveoli in­
The main, lobar, and segmental bronchi are made up creases with each generation. The walls of the bron­
of the first four generations. The walls contain U­ chioles are also buried in the lung parenchyma. The
shaped cartilage in the main bronchi. This cartilage airways depend on traction of this parenchyma to
becomes less well-defined and more irregularly maintain their lumen. Muscle bands are also present
shaped as the bronchi continue to divide. In the seg­ between alveoli.
mental bronchi the walls are formed by irregularly Alveolar ducts extend from the twentieth to the
shaped helical plates with bands of bronchial muscle. twenty-second generation. Their walls are composed
The mucous membrane of these airways is essentially entirely of alveoli, which are separated from one an­
the same as in the trachea, but the cells become more other by their septae. Septae contain smooth muscle,
cuboidal in the lower divisions. elastic and collagen fibers, nerves, and capillaries.
The subsegmental bronchi extend from the fifth to The twenty-third generation of air passages is
the seventh generation. The diameter of these airways called alveolar sacs. They are essentially the same as
becomes progressively smaller, although the total alveolar ducts, except that they end as blind pouches.

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 TABLE 2·1

Structural Characteristics of the Air Passages

MEAN
GENERATION DIAMETER AREA
(MEAN) NUMBER (MM) SUPPLIED CARTILAGE MUSCLE NUTRITION EMPLACEMENT EPITHELIUM

Trachea 0 18 Both lungs Links open

U-shaped end of
Individual cartilage
Main bronchi 2 13 lungs Within
connective
2 4 7 tissue Columnar
Lobar bronchi 1 1 1 Lobes sheath ciliated
3 8 5 IlTegular Helical From the alongside
shaped bands bronchial arterial
Segmental bronchi 4 16 4 Segments and circulation vessels
5 32 3 Secondary helical
Small bronchi 1 1 1 lobules plates
11 2,000 1
Bronchioles 12 4,000 1 Strong
and terminal 1 1 1 helical
bronchioles 16 65,000 0.5 muscle Embedded Cubiodal
bands directly in
the lung
17 130,000 Muscle parenchyma Cubiodal to
Respiratory 1 1 0.5 Primary Absent band flat
bronchioles 19 500,000 lobes between between
alveolar From the the alveoli
20 1,000,000 Thin bands pulmonary
Alveolar ducts 1 1 ill circulation F01TI1S the Alveolar
22 4,000,000 0.3 Alveoli alveolar lung epithelium
Alveolar sacs 23 8,000,000 0.3 septa parenchyma

From Weibel MorphometlY of the human lung. New York, 1963, Springer. Used with permission.

w
(0

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40 PART I Cardiopulmonary Function in Health and Disease

(Actually, communication occurs between "blind Other cells located in the distal airways that are
pouches" in the form of the pores of Kohn's, which important in the defense of the lung are the lympho­
are channels ill alveolar walls,. and Lambert's canals, cytes a n d p o l y m o r p h o n ucl ear l e ukoc ytes. I m­
which are communications between bronchioles and murioglobulins (IgA, IgG, and IgM) in the blood
alveoli. These communications are thought to be re­ serum appear to enhance the engulfing activity of the
sponsible for the rapid spread of lung infection. They macrophages. There are two types of lymphocytes
also provide collateral ventilation to alveoli, whose found in the lung-the B-Iymphocyte and the T-Iym­
bronchi are obstructed. Although this ventilation does phocyte. The B-lymphocytes produce gamma globu­
little to arterialize blood, it does help prevent collapse lin antibodies to fight lung infections, whereas the T­
of these alveoli.) Each alveolar sac contains approxi­ lymphoc ytes r e l e a s e a s u b s t a n c e that attracts
mately 17 alveoli. There are about 300 million alveoli macrophages to the site of the infection. The poly­
in an adult man, 85% to 95% of which are covered morphonuclear leukocytes are important in engulfing
with pulmonary capillaries. Alveolar epithelium is and killing blood-borne gram-negative organisms.
composed of two cell types. Type I cells, squamous
pneumocytes, have broad thin extensions that cover
LUNGS
about 95'!c of the alveolar surface. Type II cells, the
granular pneumocytes, are more numerous than type Two lungs, each covered with its pleurae-the vis­
I cells but occupy less than 5% of the alveolar sur­ ceral pleura and the parietal pleura-lie within the
face. This is because of their small, cuboidal shape. thoracic cavity. Each lung is attached to the heart and
These cells are responsible for the production of sur­ the trachea by its root and the pulmonary ligament. It
factant, a phospholipid that lines the alveoli. SUlfac­ is otherwise free in the thoracic cavity. The lungs are
tant keeps alveoli expanded by lowering their surface light, soft spongy organs, whose color darkens with
tension. Type II cells have been shown to be the pri­ age as they become impregnated with inhaled dust.
mary cells involved in repair of the alveolar epithe­ They are covered with the visceral pleura, a thin, glis­
lium. (This has been shown in experiments where O2 tening serous membrane that covers all sUlfaces of the
toxicity was induced in monkeys and in numerous lung. The visceral pleura reflects and continues on the
other conditions where type I cells were destroyed.) med iasti num and inner thoracic wall, where it be­
Type III cells, alveolar brush cells, are rare and are comes known as the parietal pleura. The space be­
found only occasionally in humans. tween the two pleurae is minuscule and contains a
An additional type of cell, the alveolar negative pressure at all times, which helps keep the
macrophage, is found within the alveolus. These cells lungs inflated. A small amount of pleural fluid lubri­
are thought to originate from stem cell precursors in cates the two pleurae as they slide over each other
the bone marrow and reach the lung through the during breathing. In disease, fluid, tumor cells. or air
blood stream. They are large, mononuclear, ameboid may invade the pleural space and collapse the under­
cells that roam in the alveoli, alveolar ducts, and lying lung. Each lung ha an apex, base, arid three sur­
alveolar sacs. They contain Iysosomes, which are ca­ faces (costal, medial, and diaphragmatic). There are
pable of killing engulfed bacteria. (Studies show also three borders (anterior, inferior, and posterior).
them to be most effective i n neutralizing inhaled Each lung is divided by fissures into separate lobes. In
gram-positive organisms.) They also engulf foreign the right lung the oblique fissure separates the lower
matter and are either transported to the lymphatic lobe from the middle, whereas the horizontal fissure
system or migrate to the terminal bronchioles where separates the upper lobe from the middle. The right
they attach themselves to the mucus. They are then lung is heavier and wider than the left lung. It is also
'
carried by the mucus to larger airways and eventually shorter because of the location of the right lobe of the
to the pharynx. Since cilia are not present below the Jiver. The left lung is divided into upper and lower
eleventh generation of air passages, clearance of mat­ lobes by the oblique fissure. It is longcr and thinner
ter and bacteria from these areas is largely dependent than the right lung, because the hem1 and pericardium
on the macrophages. are located in the left thorax. Numerous structures

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 2 Cardiopulmonary Anatomy 41

enter the lung at the hilus, or root of the lung, includ­ rior angle of the scapula with the arm at rest. The in­
ing the main-stem bronchus, the pulmonary artery, ferior border joins the posterior medial border of the
pulmonary veins, bronchial artelies and veins, nerves, lung 2 cm lateral to the tenth thoracic vertebra. The
and lymph vessels. The root, or hilus, of the lungs lies posterior medial border runs 2 cm lateral to the verte­
opposite the bodies of the fifth, sixth, and seventh tho­ bral column from the seventh cervical vertebra to the
racic veltebrae. The lungs are connected to the upper tenth thoracic vertebra.
airways by the trachea and main-stem bronchi. The left lung is generally smaller than the right
and accommodates the position of the heart. The me­
dial border on the anterior aspect runs from the ster­
Surface markings
noclavicular joint to the middle of the sternal angle,

Surface markings of the lungs can be outlined over down the midline of the sternum to the fourth costal
the chest with a basic knowledge of bony landmarks cartilage. A lateral indentation of about 1 \/2 in forms

and gross anatomy of each lung (Table 2-2, and Fig­ the cardiac notch at the level of the fifth and sixth

ures 2-13, 2-14, and 2-15). The apices of both lungs costal cartilages. The courses of the inferior and me­

extend 1 in above the clavicles at the medial ends. dial borders on the posterior aspect are similar in the

The anterior medial border of the right lung runs left and right lungs. In the left lung, however, the in­
from the sternoclavicular joint, to the sternal angle ferior border crosses at the level of the tenth thoracic

downward to the xiphisternum. The inferior border vertebra, not the twelfth observed in the right lung.

runs from the xiphisternum laterally to the sixth rib in The position of the fissures of the lungs can be

the midclavicular line, the eighth rib in the midaxil­ outlined over the chest wall. In both lungs, the

lary line, and the tenth rib in the midscapular line. oblique fissure begins between the second to fourth

The midscapular line runs downward from the infe- thoracic vertebrae. This can be roughly estimated by

Apical Apical post.

AnI. basal

BRONCHOPULMONARY
SURFACE MARKINGS SEGMENTS

FIGURE 2-13
Surface markings of the lungs (anterior aspect). The underlying bronchopulmonary segments are
also shown. (Printed with permission from Cherniak RM, Cherniack L: Respiration in health and
disease, ed 3, Philadelphia, 1983, WB Saunders.)

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42 PART I Cardiopulmonary Function in Health and Disease

TABLE 2-2

Anatomical Arrangement of the Bronchopulmonary Se.gments

RIGHT LUNG: LEFT LUNG:

LOBE BRONCHOPULMONARY SEGMENTS LOBE BRONCHOPULMONARY SEGMENTS

Upper Apical-extends above the Upper Apical posterior-extcnds above the

clavicle anteriorly; smaller area clavicle anteriorly; occupies
posteriorly comparablc area as the apical and
posterior segments of the right lung
Anterior---occupies area between the Anterior---occupies area between the
clavicle and horizontal fissure clavicle and theborder of the lingula
(comparable line to the horizontal
fissure of the right lung)
Posterior-remainder of upper lobe
on the posterior aspect down
to the oblique fissure
Middle Lateral-extends medially (Lingula)'" Superior---occupies upper half of the
from junction of the two fissures lingula
at the third intercostal space to Inferior---occupies lower half of the
occupy one third the anterior lingula
SlIrface of the lobe
Medial-occupies the remaining
anterior surface of the lobe
Lower Anterior---occupics basal area Lower Anterior---occupies area inferior to the
(Base) beneath the oblique fissure anteriorly (Base) oblique fissure anteriorly
Supelior---occupies half the area from Superior---occupic.' onc third of the
the oblique fissure downward* basal area posteriorly from the oblique
on the posterior aspect tissure downward
Lateral-extends from the junction Lateral-occupies the lateral half of the
of the middle lobe over the remaining two thirds of the left lower
midaxillary area to occupy one third lobe beneath the superior scgment on
the area inferior to the superior the posterior aspect
segment on the posterior a pect
Posterior---occupies two thirds Posterior---occupies the medial ponion
of the area posteriorly beneath of the remaining two thirds of the left
the superior segment ower lobe beneath the superior
Medial-occupies a space on segment on the posterior aspect
the inner aspect of the righl base+

'This segmenl can be drained preferentially when the patient lies prone. Superiur segmenls abo called apical.

j" Medial basal segent has no direct exposure to the chest wall, therefore, cannot be directly auscultated. This segment preferenlially dr<lins
when the patienl is positioned for the left lateral basal s e gment because of the comparable angle ur its bronchus.

i: Lingula is not an anatomically uislinct area comp<lred with the right middle lobe; rather, it is Hn<llo mical l y pari of the left upper lobe.

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 2 Cardiopulmonary Anatomy 43

..... -- - 4th rib

-Xiphi­
sternal
j u nc t io n

i
Mi d ax llary line
- 8th rib

SURFACE MARKINGS

FIGURE 2·14
SUlface markings of the lungs (lateral aspect). (Printed with permission from Cherniak RM,
Cherniack L: Respiration in health and disease, ed 3, Philadelphia, 1983, WB Saunders.)

ji.'� J/J l' '-.r'

}:o
T2(spine)
v
Apical
u

I
i
l \ .
�- Lat. basal

BRONCHOPULMONARY
SURFACE MARKINGS SEGMENTS

FIGURE 2·15
Surface markings of the lungs (posterior aspect). The underlying bronchopulmonary segments are
also shown. (Printed with permission from Cherniak RM, Cherniack L: Respiration in health and
disease, ed 3, Philadelphia, 1983, WB Saunders.)

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44 PART I Cardiopulmonary Function in Health and Disease

following a line continuous with the medial border heart is rotated to the left in the chest, resulting in the
of the abducted scapula, around the midaxillary line right side of the heart being foremost. Thus joining
at the fifth rib, and terminating at the sixth costal the two uppermost points outlines the level of the
cartilage anteriorly. The horizontal fissure of the atria and joining the two lower points represents the
right lung originates from the oblique fissure at the margin of the right ventricle.
level of about the fourth intercostal space in the mi­ The heart as a whole is freely movable within the
daxillary line, and courses medially and slightly up­ pericardial cavity, changing position during both con­
ward over the fourth rib anteriorly. The left lung has traction and respiration. During contraction, the apex
no horizontal fissure. moves forward, strikes the chest and imparts the chest
and apex beat, which may be felt and seen. Abnormal
position of the apex beat can indicate cardiac enlarge­
Bronchopulmonary Segments
ment or displacement. During breathing, the move­
The bronchopulmonary segments lie within the ments of the diaphragm determine the position of the
three lobes of the right lung and the two lobes of the heart. This is because of the attachment of the central
left lung. There are 10 bronchopulmonary segments tendon of the diaphragm to the pericardium. Changes
on the right and eight on the left. Brief anatomic de­ in position during quiet breathing are hardly notice­
scriptions of the position of each lobe are provided able, but with deep inspirations, the downwal'd excur­
in Table 2-2, p. 42. Figure 2-13, p. 41, illustrates the sion of the diaphragm causes the heart to descend and
surface markings on the anterior view of the lungs rotate to the right. The opposite occurs during expira­
and the position of the various bronchopulmonary tion. Pathology of the lungs can also change the posi­
segments within the major anatomic divisions pro­ tion of the heart. Atelectasis shifts the heart to the
vided by the fissures. Figure 2-14, p. 43, shows same side. In tension pneumothorax, where air enters
some of these features from the lateral views. Figure the chest usually through an opening in the chest wall
2-15, p.43 illustrates the surface markings and bron­ and cannot escape, the positive pressure shifts the
chopulmonary segments of the posterior aspect of heart away from the side of the pathology.
the lungs. The heart is enclosed by the pericardium, whose
two surfaces can be visualized by considering the
heart as a fist that is plunged into a large balloon. The
HEART
outer surface, a tough fibrous membrane, is called the
The herut is a conical, hollow muscular pump enclosed fibrous pericardium. It encases the heart and the or­
in a fibroserous sac, the pericardium. Its size is closely gans and terminations of the great vessels. This mem­
related to body size and corresponds remarkably to the brane is so unyielding that when fluid accumulates
size of an individual's clenched fist. It is positioned in rapidly in the pericardial cavity, it can compress the
the center of the chest behind the lower half of the ster­ heart and impede venous return. When this occurs
num. The largest portion of the heart lies to the left of often, a window is cut in the pericardium, allowing
the midsternal line; the apex is found approximately 9 the fluid to escape. The inner surface, the serous peri­
cm to the left in the fifth intercostal space. cardium, is a serous membrane that lines the fibrous
The surface markings of the heart can be traced by pericardium. Ten to 20 ml of clear pericardial fluid
joining four points over the anterior chest wall. On separates and moistens the two pericardial surfaces.
the right, the heart extends from the third to the sixth The pericardium with its fluid minimizes friction dur­
costal caltilages at a distance of about to to 15 mm ing contraction. It also holds the heart in position and
from the sternum. On the left, the heart extends from prevents dilation. The serous pericardium consists of
the second costal cartilage to the fifth intercostal an outer layer, the parietal layer, and an inner layer­
space 12 to 15 mm, and 9 cm from the left sternal the visceral layer, or epicardium.
border, respectively. Joining the two points on the The heart is divided into right and left halves by an
left side outlines the left atrium and ventricle. The obliquely placed longitudinal septum (Figure 2-16).

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 2 Cardiopulmonary Anatomy 45

Superior vena cava .......

Pulmonary veins
Pulmonary veins

Atrium

Pulmonary valve

t <?t@iW._ Ventricle
..

FIGURE 2-16
Blood flow of the heart.

Each half has two chambers-the atrium, which re­ amount of work they perform. The ventricles do more
ceives blood from veins, and the ventricles, which work than the atria, and their walls are thicker. The
eject blood into the arteries. The sllperior vena cava, pressure in the aorta is higher than that in the pul­
inferior vena cava, and intrinsic veins of the heart de­ monary trunk. This requires greater work from the
posit venous blood into the right atrium. Blood then left ventricle, so its walls are twice as thick as those
passes through the tricllspid valve to the right ventri­ of the right ventricle. The innermost layer, the endo­
cle. The right ventticle projects the blood through the cardium, is the smooth endothelial lining of the inte­
pulmonary valve into the pulmonary arteries, which rior of the heart. *
are the only arteries in the body containing deoxy­
genated blood. Pulmonary veins return the blood to
Heart Valves
the left atrium and from there, it passes through the
mitral valve to the left ventricle. From the left ventri­ The four valves of the heart, although delicate in ap­
cle it is ejected through the aortic valve into the main pearance, are designed to withstand repetitive clo­
artery of the body-the aorta. sures a g a i n st h i g h pressures (se e F i g u r e 2-16)
The heart is divided into three layers-the epi­ (French, Criley, 1983). Normally, they operate for
cardium, myocardium, and endocardium. The outer­ more than 80 years without need of repair or replace­
most layer, the epicardium, is visceral pericardium ment. The tricuspid and mitral valves function differ­
and is often infiltrated with fat. The coronary blood en tly from the other valves of the h e art. Bei n g
vessels that nourish tile heart run in this layer before
entering the myocardium. The myocardium consists
"For additional information o f tbe clinical aspects o f heart
of cardiac muscle fibers. The thickness of the layers anatomy, referAnd reol i et ai, 1991; Goldberger, 1990;
10

of cardiac muscle fibers is directly proportional to the Sokolow, Mcilroy, Cheitlin, 1990; and Gray s Anatomy.
'

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46 PART I Cardiopulmonary Function in Health and Disease

located between the atria and ventricles, they must ef­ free edges of these valves project into the lumen of
fect a precise closure within a contracting cavity. the vessels. At the end of systole, blood in the aorta
During diastole, the two leaflets or cusps of the and pulmonary artery forces the cusps of the valves
mitral valve and the three cusps of the tricuspid valve shut. These valves are attached in such a manner
relax into the cavities of the ventricles, allowing that they cannot be everted into the ventricles by in­
blood to flow between the two chambers. As the ven­ creased pressure in the vessels. During diastole, the
tricular chambers fill with blood, the cusps of the cusps support the column of blood filling the ven­
valves are forced up into a closed position. Fibrous tricles. Contraction of the ventricles during systole
cords, the chordae tendinae, are located on the ven­ increases pressure within the ventricular chambers,
tricular surfaces of these cusps. These cords connect forcing the cusps to open and allow blood flow into
the cusps of the valve with the papillary muscles of the vessels.
the ventricular walls. As pressure builds in the ven­ The arterial supply of the heart muscle is derived
tricular chambers, contraction of these muscles pre­ from the right and left coronary arteries, which
vents the cusps from being forced up into the atria. arise from the aortic sinuses (Figure 2- 17). The left
Dysfunction or rupture of the chordae tendinae or the coronary artery (LCA) divides into the anterior de­
papillary muscles may undermine the SUppOlt of one scending artery a n d the left circumflex artery.
or more valve cusps, producing regurgitation from These arteries supply most of the left ventricle, the
the ventricles to the atria. left atrium, most of the ventricular septum and, in
The pUlmonic and aortic valves are similar in ap­ 45% of people, the sinoatrial (SA) node. The right
pearance but the aortic cusps are slightly thicker coronary artery (RCA) supplies most of the right
than the pulmo ic cusps. Each valve has three fi­ ventricle, the atrioventricular (A V) node and, in
brous cusps, the bases of which are firmly attached 55% of people, the SA node. Infarction of these ar­
to the root of the aorta or the pulmonary artery. The teries or their branches can thus cause interruption

----

Circumflex branch

Interventricular branch (posterior descending) /

FIGURE 2-17
Blood supply of the heart.

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 2 Cardiopulmonary Anatomy 47

or cessation of the conduction system and death of node retains its position as pacer of the heru1 as long as
the myocardial muscle in the area supplied by the it generates impulses at a faster rate than any other pru1
artery. The severity of the infarction is dependent of the myocardium and as long as these impulses are
on the size of the artery and the importance of the rapidly conducted from the atria to the ventricles. Nor­
area it supplies. mal impulse formation may be interrupted by vascular
The heart is drained by a number of veins. Most of lesions (occlusion of the coronary arteries) or by car­
the veins of the heart enter the coronary sinus, which diac disease (pericarditis). The SA node is especiaUy
then empties into the right atrium. A small portion of susceptible to pericarditis and all other surface cardiac
veins, the thebesian veins, empty directly into the diseases because of its superticiaJ position immediately
right and left ventricles. beneath the epicardium.
The muscle fibers of the heart are self-excitatory,
which enables the heart to rhythmically and automati­
Innervation
cally contract. The normal pacemaker of the heart is
Innervation of the heart involves a complex balance be­ the sinoatrial node located in the posterior wall of the
tween its intrinsic automaticity and extrinsic nerves right atrium. The concentric waves of excitation sent
(Figure 2-18). The SA and A V nodes provide the heart out by the SA node must travel through the A V node
with an inherent ability for spontaneous rhythmic initia­ to reach the ventricles. This node is located in the floor
tion of the cardiac impulse. The rate of this impulse for­ of the light atrium, just above the insertion of the tri­
mation is regulated by the autonomic nervous system cuspid valve. Its main function is to cause a 0.04 sec­
(ANS), which also influences other phases of the car­ ond delay in the atrioventricular transmissions. This
diac cycle. It controls the rate of spread of the excitation has two advantages. It postpones ventricular excitation
impulse and the contractility of both atria and ventricles. until the atria have had time to eject their contents into
The ANS extends its influence to the heaIl via the the ventricles. It also limits the number of signals that
vagus nerve (parasympathetic) and upper thoracic
nerves (sympathetic). These nerves mingle together
around the root and arch of the aorta near the tracheal
bifurcation, forming the cardiac plexus. Extensions
from the cardiac plexus richly supply the SA and A V
nodes. They are so well-mingled that scientists are un­
able to determine which nerves supply which parts of
the heart. Stimulation of the sympathetic nervous sys­
tem causes acceleration of the discharge rate in the SA
node, increase in A V nodal conduction, and increase
in the contractile force of both atrial and ventricular
muscles. Stimulation of the vagus nerve causes car­
diac slowing and decreased A V nodal conduction.
Thus the parasympathetic system decelerates heart
rate and the sympathetic system accelerates heart rate.
Intrinsic innervation of the heart centers around the
SA node, which lies near the junction of the superior
vena cava and the right atrium. It is the normal pace­
maker of the heart, sending concentric waves of excita­
tion throughout the atrium. Without neural influence,
impulse formation from this node would be greater than
100 beats/minute. However, vagal influence decreases FIGURE 2-18
the impulse formation to 60-90 beats/minute. The SA Electrical conduction of the heart.

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48 PART I Cardiopulmonary Function in Health and Disease

can be transmitted by the A V node. The A V node also tion, the QRS complex indicates ventricular depolar­
has its own inherent rhythmicity, firing at a much ization and the T-wave indicates ventricular repolar­
slower rate than the SA node (40-60 beats/minute). Its ization. There is no wave indicating atrial repolariza­
main pathology is a result of occlusion of the right tion, since this is embedded in the QRS complex
coronary artery, which supplies the AV node in 90% (Andreoli et aI,
of the cases. From the A V node arises a triangular of the Electtical Excitation of the Heart and ECG In­
group of fibers known as the AV bundle or bundle of terpretation, Chapter II; Dubin, 1989; Marriott,
His. This bundle divides in the ventricular septum into Conover, 1989; and Wagner, 1994.
two branches-the left bundle branch and the right
bundle branch. Each of these bundles continues to di­
SYSTEMIC CIRCULATION
vide into many fine strands that spread across the ven­
tricles. At the end of the bundle's ramifications are The systemic vascular system is a complex series of
Purkinje's fibers, which are continuous with the car­ blood vessels throughout the entire body. It conveys
diac muscle. The waves of excitation pass through the nutrition and oxygen to all tissues of the body and car­
bundle of His, down the bundle branches, and through ries away their waste products. The driving force for
the Purkinje fibers, which permeate the ventricles and this system is the heart. The vascular system can be
cause them to contract. This wave of depolarization considered to have two major components-the periph­
gives rise to the normal P-QRS-T configuration of the eral and pulmonary circulations (Schlant et aI,
electrocardiogram (ECG) tracing (Figure 2- 19) (see Blood vessels are designed to forward oxygenated
Chapter II). The P-wave indicates atrial depolariza­ blood from the heart during systolic ejection of the

1 1
b± =J==1--+-t----t-11r-I
L-1-+-+--l--+++-+--i--t i-ll rQO.2 m

t-t-tTRl--r1!-t1l-r.o.4 l1 1. second
L-t-+ 1
L -++- rt ti T1 w 1
s con

lj 4-1 -titti-r rT- I· J I

ST PR se ment
g I .+- se ment 5 mm '

l-+-+----t- -rl II ' 1

g mm 0.5 mv I

I_
I-.II I1 [ffiI l'
I
I' It , 1
PI
II I
T
1
1
l ..l -J
I t- I i
I

I r- U
.

I - t-
I :
I---+-+-+-t-.iI I
! 111 0 I I, !I
I I I .
-+---r---,-,--: l ]1
L-+- r-� -t-"t-I-
PR interval I I !... I.
-+-+- \41 rr-4
I

J 1 J -J IOR S.1nterva
1
I
I

I I
OTI interval
I
I

1---+-+-+-t -1"-11T1 '1 II 1 l 1 1

' .1
I I
L.i+-t--+-t-t
I I i
FIGURE 2-19
A normal ECG showing characteristic waves, intervals, and segments.

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 2 Cardiopulmonary Anatomy 49

left ventricle, perfuse the vascular beds commensu­ veins. These veins branch and become increasingly
rate with their metabolic needs and remove metabolic larger. Blood flow through the veins is largely depen­
excreta. Anatomically, the proximal vessels have a dent on muscular or visceral action or pressures.
higher proportion of connective tissue and elastin to These pressures are intermittent and, were it not for
withstand high pulse pressures (e.g., the aorta, which double-cusp valves located within the veins, blood
carries blood to the head, viscera, and limbs). In addi­ would flow backward when the pressure ceases. In the
tion, potential energy is stored in the walls of the extremities, muscular contractions move blood into
larger vessels during systole. During diastole, the the trunk. In the pelvic and abdominal region, blood
elastic recoil of these vessels maintains the forward flow is dependent on intraabdominal pressure exceed­
motion of the blood between ventricular systoles. The ing intrathoracic pressure. Blood flows through the
medium-size blood vessels have comparable propor­ trunk in veins that become increasingly larger until
tions of connective tissue and elastin to smooth mus­ they finally enter the supelior and inferior vena cavae.
cle. As the blood vessels become smaller, smooth
muscle predominates. The arterioles are primarily
PULMONARY CIRCULATION
smooth muscle and their diameter can alter signifi­
cantly. They regulate the blood flow to regional tis­ The vena cavae empty directly into the right atrium.
sue beds and are also responsible for regulating total Blood flow from the right side of the heart through
peripheral resistance and systemic blood pressure. the lungs is known as the pulmonary circulation. The
They are called the stopcocks of the circulation. quantity of blood flowing through the pulmonary cir­
Many factors (e.g., nervous impulses, hormonal stim­ culation is approximately equal to that flowing
ulation, drugs, oxygen, and carbon dioxide concentra­ through systemic circulation. Blood flows from the
tions) determine the degree of contraction of vascular right ventricle into the pulmonary artery, which di­
smooth muscle and whether contraction occurs lo­ vides into right and left branches 4 cm from the ven­
cally or throughout the entire body. tricle. These branches then separate, one going to
Arterioles branch to form the smallest vessels, the each lung, where they continue to divide into smaller
capillaries, which consist of a single layer of endothe­ arteries. The pulmonary arteries and arterioles are
lial cells forming lumen just large enough for the red much shorter, have thinner walls and larger diame­
blood cells to roll along. The capillary bed is enormous; ters, and are more distensible than their systemic
its capacity far exceeding 5 L. Its network is finer and counterparts. This gives the pulmonary system a
denser in active tissue like muscle and brain, and less compliance as great as that of the systemic arterial
dense in less active tissue such as tendon. Gas ex­ system, thereby allowing the pulmonary arteries to
change occurs in the capillary bed, where the red blood accommodate the stroke volume output of the right
cells give up their oxygen, and blood plasma t:ransudes ventricle. Pulmonary vascular resistance and arterial
capillary walls, carrying nutrition to tissue. pressure are one sixth that of the systemic system
The microcirculation specifically consists of the (pulmonary arterial pressure is 20110 mm Hg com­
metarterioles, the capillary bed, and the venules. The pared with 120/80 mm Hg systemically).
capillary wall is a semipermeable membrane that is re­ P u l m o n a r y c a p i l l a r i e s are s h o r t a n d a r i s e
sponsible for the transfer of oxygen, nutrients, and abruptly from much larger arterioles. They form a
waste between the circulation and the interstitial fluid dense network over the walls of the alveoli, making
(see Chapters 1 and 3). The capillary pores selectively a minimum distance over which gas exchange oc­
allow different-size molecules to pass through them. curs. The pulmonary veins are also very short but
This is an essential feature that regulates the move­ have distensibility characteristics similar to those of
ment of fluid in and out of the intra- and extravascular the systemic system. Unlike systemic veins, these
compartments. This process is fundamental to main­ veins have no valves. Pulmonary veins act as a ca­
taining and regulating normal hemodynamics. pacitance vessel, or a blood reservoir for the left
Capillaries form venules, which are the smallest atrium. Contraction of smooth muscle in the veins

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50 PART I Cardiopulmonal'Y Function in Health and Disease

makes the reservoir constrict. This increases blood ture of the bony the muscles of respiration as­
volume in relation to the internal volume of the sociated with the chest wall and of the diaphragm.
vessels. The pulmonary veins become larger until The upper and lower
converge into two veins from each which scribed, a s well as the
then carry oxygenated blood to the left atrium. bronchial tree to the The lung
is defined anatomically in terms of dis­
crete bronchopulmonary segments contained within
LYMPHATIC CIRCULATION
three major divisions of each The specific sur­
The lymphatic circulation an additional face defined the lung fissures and the
route for fluid t o be returned from the interstitium landmarks for the bronchopulmonary segments were
to the systemic circulation, and thus has a central emphasized. The basic anatomy of the heart was de­
role in the of interstitial fluid scribed. The structure of the and
the fluid that flows in the monary circulations was also Special ref­
is interstitial fluid with similar composition t o erence was made to the lymphatic circulation and its
tissue fluid. T h e lymphatics remove excess fluid, central role in the regulation of capillary fluid
large ns, and other large molecules away namics. A detailed of cardiopulmonary
from the interstitial spaces. Although lit­ anatomy is fundamental to the base un­
tle protein leaks from the capillaries into the sur­ the assessment and management of car­
rounding tissue. the absence of its immediate re­ diopUlmonary dysfunction and impaired oxygen
moval is by physical therapists.
all areas of the body drain into a network
of channels. From the lower portion of the
REVIEW QUESTIONS
body, and left head and excess tissue fluid and
drain into the thoracic duct, which empties 1. Describe the thorax and its movements.
into the venous circulation at the junction of the left 2. Describe the respiratory muscles and their func­
internal jugular vein and subclavian vein. tion.
from the right side of the head, arm, and 3. the of oxygen from the atmos­
of the thorax drain into the lymph duct, phere to the alveolar capillary membrane.
which into the venous circulation at the junc­ 4. Describe the movement of oxygenated blood
tion of the internal vein and subclavian from the the heart to the pul­
vein. Lymph from the lower of the body drains monary and circulations.
into the inguinal and abdominal lymphatic channels. 5. Describe the movement of deoxygenated blood
The pressure in the lymphatic is from the oerioherv back to the heart.
which helps to the interstitium 6. \Jrnnh"tlr circulation and
"dry." The lymph vessels are thin-walled with some its physiological
smooth muscle and thus can contract to propel their
contents. In addition, vessels have valves to
References
facilitate the forward motion and to minimize retro­
movement of lymph. Andreoli, K.G., Fowkes. Y.K., Zipes, D.P., & Wallace, A G, .

(199!). Comprehensive cardiac c are (7th ed,). Sl. LOllis:

Mosby.
SUMMARY Berne. R.M" & Levy, M.N. (1992). Cardiovascular physiology
(6th ed,). St Louis: CY Mosby,
This chapter reviewed the anatomy of the cardiopul­ Bunon, G.G., & Hodgkin. J.E. (1984). Respiratorv care: A gllide
monary system. The anatomical features of the respi­ 18 Lippincott.
to clinical practice (2nd ed.). Philadelphia:

ratory pump were described with respect to the struc­ Chemiack, R.M., & Cherniack, L (1983), Respiration in Health
and Disease (3rd ed,), Philadelphia: WB Saunders.

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 2 Cardiopulmonary Anatomy 51

Clemente, CD. (Ed,). (1985), Anatomy of Ihe humon body (30th Scharf, S,M & Cassidy. S,S. (Eds,), (1989). Hear/-lung interac­
ed,), Philadelphia: Lea & Febiger. tions in health and disease. New York: Marcel Dekker,
Dubin, D, (1989) Rapid interpretation of EKGs (4th ed,), Tampa, Sokolow, M" McIlroy, M.B" & Cheitlin. M,D, (1990), Clinical
Florida: Cover Publishing, cardiology (5th cd,). Norwalk, Conn.: Appleton & Lange,
French, W,G" & Criley, I.M, (Eds,). (1983), Practical cardiology: Schlant, R,C" Alexander, R,W., O'Rourke, RA" Roberts, R .. &
Ischemic and valvular hearl New York: John Wiley & Sonnenblick, E,H, (Eds.). (1994), Hurst's lhe hearl, orteries
Sons, and veins (8th ed,). New York: McGraw,Hill.
Ganong, W,F, (1993), Review of medical physiology (l6th ed,), Wagoer, G,S, (1994), Marrioll's practical electrocardiography
Los Altos, Calif.: Lange Medical Publications. (9th ed.), Baltimore: Williams & Wilkins,
Goldberger, E, (1990), Essentials of clinical cardiology, Philadel­ Weber, KT, Jaoicki, J.S" Shroff, S,G" & Likoff. MJ. (1983), The
phia: JB Lippincott, cardiopulmonary unit. The body's gas transport system, Clinics
Guyton, A,C, (1991), Textbook of medical physiology (8th cd,), in chest medicille, 4, 101-110,
Philadelphia: WB Saunders, Weibel, E,R. (1963), Morphometry of the human lung, New York:
Katz, A.M. (1992), Physiology of the heart (2nd cd.). New York: Springer-Verlag,
Raven Press, West, lB, (Ed,), (199l), Best and Taylor's physiological basis of

Marriott, H.1.L, & Conover, M,B, (1989), Advanced concepts in medical practice (12th cd,). Baltimore: Williams & Wilkins,

arrhythmias (2nd ed,), St. Louis: Mosby, West, lB. (1995), Respiratory physiology-the essentials (5th ed,),

Murray, J,E (1986), Till? normal lung. Philadelphia: WE Saunders, Baltimore: Williams & Wilkins,
Murray, J.P., & Nadel, I.A, (1988). Textbook of respiratory medi­ Williams, P,L, Warwick, R., Dyson, M., & Bannister, LH,
cine, Philadelphia: WB Saunders, (1989), G r a y a n atomy (37th E d i n b u r gh:
Nunn, lE (1993), Applied respiratory physiology (4th ed.), Lon­ Churchill Livingsione,
don: BUllerworths,

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 Cardiopulmonary Physiology

Elizabeth Dean
Lyn Hobson

KEY TERMS Control of breathing Oxyhemoglobin dissociation

Control of the heart Respiratory mechanics
Diffusion Ventilation and petfusion matching
Electromechanical coupling Ventilation perfusion
Gas exchange

INTROOUCTION CONTROL OF BREATHING

This chapter reviews the basics of cardiopulmonary The act of breathing is a natural process to which
physiology. A thorough understanding of normal most of us give little thought. Unconsciously, it ad­
physiology provides a basis for understanding the justs to various degrees of activity, maintaining opti­
deficits of cardiopulmonary dysfunction and adapta­ mum arterial levels of POl and Peo2, whether we are
tion to it, and conducting a thorough assessment and resting or physically active. Sighing, yawning, hiccup­
prescribing treatment (Bates, 1989; Berne and Levy, ing, laughing, and vo mitin g are all involuntary acts
1992; Clemente, 1985; Goldberger, 1990; Guyton, using respiratory muscles. Br athing is also under our
1991; Katz, 1992; Murray and Nadel, 1988; Nunn, voluntary control. A person can stop it temporarily by
1993, Sch31f and Cassidy, 1989; Schlant, Alexander, holding his or her breath or can increase it by rapidly
O'Rourke, Roberts, and Sonnenblick, 1994; Sokolow, panting until he or she faints (from cerebral vascular
McIlroy, and Cheitlin, 1990; and West, 1995. constriction as a result of a decrease in arterial Peo2).

53

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54 PART I Cardiopulmonary Function in Health and Disease

InhitJl/lon

S/imv/olion

:;::rJ
MEDULLA .
yj
jl pulmonory streICh receptors

ororecePlors

to Insptrotory tnt , t :d ___

emasenSilive
_
g
r
:, Cells

t ::"
', --. iralOry
-" Cells
Expir%ry -..- .-- ______

mo
Ce//s _ ca rotid and aortic cl1emoreceplors

--------===- to exptrotory tntereostols

I"
FIGURE 3-1
Control of breathing.

Exhalation is used in singing, speaking, coughing, and longed inspiratory gasps (apneustic breathing) occur.
blowing, whereas inspiration is used for sniffing and The pneumotaxic center is in the upper one third
sucking. Parturition, defecation, and the Valsalva ma­ of the pons. It maintains the normal pattern of respi­
neuver are all performed while voluntarily holding our ration, balancing inspiration, and expiration by in­
breath. These activities are directed by control centers hibiting either the apneustic center or the inspiratory
located in the brain. The centers integrate a multitude component of the medullary center.
of chemical, reflex, and physical stimuli before trans­
mitting impulses to the respiratory muscles. The cere­
Central Chemoreceptors
bral hemispheres control voluntary respiratory activ­
i t y , whereas i n v oluntary respiratory activity i s These receptors are located on the ventral lateral sur­
controlled b y centers located i n the pons and medulla faces of the upper medulla. They are bathed in the
(Figure 3-1). cerebrospinal fluid (CSF), which is separated from
blood by the blood-brain barrier. Although this bar­
rier is relatively impermeable to hydrogen (H) and bi­
Medullary and Pontine Respiratory Centers
carbonate (HC03) ions. Carbon dioxide (C02) diffuses
The respiratory center in the medulla is in the reticu­ through the barrier easily. Increased stimulation of
lar formation. It contains the minimum number of central chemoreceptors by a rising arterial PC02 re­
neurons necessary for the basic sequence of inspira­ sults in increased rate and depth of ventilation.
tion and expiration. Although this center is capable of
maintaining some degree of respiratory activity, these
Peripheral Chemoreceptors
respirations are not normal in character.
The apneustic center is in the middle and lower These receptors are located in the carotid bodies,
pons. If uncontrolled by the pneumotaxic center, pro­ which lie in the bifurcations of the common carotid

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 3 Cardiopulmonary Physiology 55

artery and in the aortic bodies located above and tory time. Receptors for this reflex are thought to
below the aortic arch. These bodies receive blood lie in the smooth muscle of airways from the tra­
from small branches of the vessels on which they are chea to the bronchioles. In humans, it takes a lung
located. The receptors respond to an increase in arter­ inflation of more than 800 ml above func tional
ial Peo2 by increasing ventilation but are much less residual capacity to activate the reflex and delay the
important in their response to Peo2 than are the cen­ next breath.
tral chemoreceptors.
The main role of the peripheral chemoreceptors is
Cough Reflex
to respond to hypoxemia by increasing ventilation. If
arterial Peo2 is normal, the P02 must drop to 50 mm Mechanical or chemical stimuli to the larynx, trachea,
Hg before ventilation increases. A rising Pe02 causes carina, and lower bronchi result in a reflex cough and
the peripheral chemoreceptors to respond more quickly bronchoconstriction. The high velocity created by the
to a decreasing Po2. In some patients with severe lung cough sweeps mucus and other irritants up toward the
disease, this response to hypoxemia (the hypoxic pharynx (see Chapter 21).
drive) becomes very important. These patients often
have a permanently elevated Peo2 (C02 retention). The
Stretch Reflex
CSF in these patients compensates for a chronically el­
evated arterial Peo2, by returning the pH of the CSF to The intercostal muscles and the diaphragm contain
near normal values. When these patients have lost the sensory muscle spindles that respond to elongation. A
ability to stimulate ventilation in response to an ele­ signal is sent to the spinal cord and anterior horn
vated Peo2, arterial hypoxemia becomes the major motor neurons. These neurons signal more muscle
stimulus to ventilation (hypoxic drive). fibers to contract (recruitment) and thus increase the
strength of the contraction. Theoretically, such a
stretch reflex may be useful when there is an increase
REFLEXES
in airway resistance or a decrease in lung compliance.
Stretching the ribs and the diaphragm may activate the
Hering-Breuer Reflex
stretch reflex and help the patient take a deep breath.
Hering and Breuer noted in 1868 that distention of The fundamental pathways of the stretch reflex are
anesthetized animal lungs caused a decrease in the shown in Figure 3-2. Research is needed, however,
frequency of inspiration and an increase in expira- to establish the therapeutic role of propriocepti ve

SPINDLE AFFERENT

MUSCLE SPINDLE

FIGURE 3-2

Stretch reflex.

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56 PART I Cardiopulmonary Function in Health and Disease

neurofacilitation techniques based on stretch reflex creasing alveolar pressure. The increased alveolar
theory in altering pulmonary funclion. pressure contributes to air flowing from the lungs.
Normally, expiration is a passive process reflecting
elastic recoil of the lung parenchyma.
Joint and Muscle Receptors

Peripheral joints and muscles of the limbs are believed Resistance to Breathing
to have receptors that respond to movement and en­
hance ventilation in preparation for activity. Ventila­ Compliance
tion has also been shown to be stimulated by a similar The inner walls of the thorax, lined with parietal
reflex in humans and anesthetized animals in response pleura, and the parenchyma of the lung, enclosed in
to passive movement of the limbs. The precise path­ visceral pleura, lie in close proximity to one another.
ways for these reflexes have not been well-established. The pleurae are separated by a potential space con­
taining a small amount of pleural fluid. Muscular
contraction of the intercostals and the diaphragm me­
Mechanoreceptors
chanically enlarges the thorax. The lungs are en­
Changes in systemic blood pressure cause correspond­ larged at this time because of their close proximity to
ing changes in pressure receptors in the carotid and the thorax. The healthy lung resists this enlargement
aortic sinuses. Increase in blood pressure causes me­ and tries to pull away from the chest wall. The ease
chanical distortion of the receptors in these sinuses, with which the lungs are inflated during inspiration is
producing reflex hypoventilation. Conversely, a reduc­ known as compliance and is defined as the volume
tion in blood pressure can result in hyperventilation. change per unit of pressure change. The normal lung
is very distensible or compliant. It can become more
rigid and less compliant in diseases that cause alveo­
MECHANICAL FACTORS IN BREATHING
lar, interstitial or pleural fibrosis, and alveolar edema.
The flow of air into the lungs is a result of pressure Compliance increases with age and in emphysema.
differences between the lungs and the atmosphere. In The elastic recoil or compliance of the lung is also
normal breathing, for inspiration to occur, alveolar dependent on a special surface fluid caJled surfactant,
pressure must be less than atmospheric pressure. which lines the alveoli. This fluid increases compli­
Muscular contraction of the respiratory muscles low­ ance by lowering the surface tension of the alveoli,
ers alveolar pressure and enlarges the thorax (Gold­ thereby reducing the muscular effort necessary to
man, j 979). The decreased pressure causes air to ventilate the lungs and keep them expanded. It is a
flow from the atmosphere into the lungs. Patients complex lipoprotein that is thought to be produced in
who are unable to create adequate negative pressure the type II alveolar cells (see Chapter 2). A decrease
may have to be mechanically ventilated. The ventila­ in surfactant causes the alveoli to collapse. Reex­
tors create a positive pressure (greater than atmos­ panding these alveoli requires a tremendous amount
pheric pressure) that forces air into the lungs where of work on the part of the patient. The patient may
there is atmospheric pressure. The iron lung used dur­ become fatigued and need mechanical ventilation.
ing the poliomyelitis epidemic of the 1950s assisted This occurs in respiratory distress syndrome of the
ventilation using cycles of negative pressure to inflate premature infant (previously called hyaline mem­
the lungs. brane disease) and in adult respiratory distress syn­
Ex halation occurs when alveolar pressure is drome. In another disease, alveolar proteinosis, there
greater than atmospheric pressure. At the cessation of is excessive accumulation of protein in the alveolar
inspiration, the respiratory muscles return to their spaces. This may be because of excessive production
resting positions. The diaphragm rises, compressing of surfactant or deficient removal of surfactant by
the lungs and increasing alveolar pressure. As the in­ alveolar macrophages.
tercostals relax, the ribs drop back to their preinspira­ The elastic properties of the lung tend to collapse
tory position, further compressing the lungs and in­ the lung if not counterbalanced by external forces.

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 3 Cardiopulmonary Physiology 57

FIGURE 3-3
Various relationships between the lungs and the thorax. At. The size the lungs would assume if
they were not acted on by the elastic recoil of the thoracic wall. A2, nOlmal size of lungs within the
thorax BI, The size the thorax would assume if it were not acted on by elastic recoil of the lungs.
B2, Normal position of the chest wall when acted on by elastic recoil of the lungs C, The normal
relationship of lung to thorax. 0, The positions assumed by the lung and thorax in a tension
pneumothorax.

The tissues of the thoracic wall also have elastic re­ posed by the usual elastic forces of the lungs, which
coil, which cause it to expand considerably if unop­ have been damaged by disease.
posed. These two forces oppose each other, keeping
the lungs expanded and the thoracic cage in a neutral
Pressure Volume Relationships
position. If these forces are interrupted (as in pneu­
mothorax), the lung collapses and the thoracic wall Pressure volume curves help to define the elastic
expands (Figure 3-3). Similarly, the overinflated, bar­ properties of the chest wall and lungs (Cherniack,
rel-shaped chest of the patient with chronic obstruc­ Ch e r n i a ck, 1983; Co m r o e, Fo r s t e r, Dub o i s ,
tive pulmonary disease (COPD) is explained in part Briscoe, and Carlsen, 1986). The elasticity of the
by the elastic tension of the chest wall being unop­ respiratory system as a whole is the sum of its two

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58 PART I Cardiopulmonary Function in Health and Disease

and therefore functional residual is the rest­

100 ing volume of the system. Active muscu­
90 lar work is required to effect inspiration, is
*
80 a process. The pressure volume
>-
f-
(3 70 curve also shows the range of lung volumes,
;t 60 cally tidal volume, over which the energy

.f . }
<l(
()
50 ture for breathing is most economicaL In other words,
Z
:::> volume result from relatively small

'1
-'
-' in pressure as noted from the sloDe of the
ff 30 ,U,C"ONAC

0 curve over tidal volume,

f- 20 RESIDUAL
RESIDU CAPACITY In lung this balance of forces is disrupted
10 VOLUME --
More work and more energy are re-
-10 0 +10 +20 +30 to sustain the effort. The is
PRESSURE (em, H20) less able to on normal elastic recoil of either the
chest or both.
FIGURE 3-4
put more energy into the to
The relaxation pressure curve. The pressure in the lung at
function. The limits of respiratory excur­
any volume reflects elastic forces of the lung and chest
sion are determined both elastic and muscular
wall.
forces. At total lung the elastic forces of the
are balanced the inspiratory
muscle force. At residual volume, the elastic forces of
components, the and the chest wall. the chest wall are balanced the maximum
The so-called relaxation pressure curve is shown in tory muscle force. This volume excursion from total
3-4. The curve illustrates the static pressure capacity to residual volume reflects vital
of the chest wall, and the combination of the the curves the elastic forces
two measured at given lung volumes, Functional of the lungs and chest wall are they are
residual capacity reflects the balance o f elastic helpful in understanding the effect of lung dysfunction
forces exerted the chest wall and the lungs, This on pulmonary function and on the clinical presenta­
is an point with significant tion of the patient (Burrows, Knudson, and Ket­
for the clinical and management of pa­ 1983). For in the characteristic
tients with cardiopulmonary dysfunction. barrel chest reflects the unopposed elastic forces of
The relaxation pressure curve static the chest wall, 111 the excursion
pressure measurements, This means that the of the chest as a result of reduced elastic recoil of the
muscles are and the volume in the lungs. At the other extreme is the effect of a
at a in the is determined wound to the chest wall, which the in­
by the balance of forces between the chest wall and trapleural pressure that normally keeps the
the lungs, The chest wall and exert elastic and the chest wall contained. The re­
forces that oppose each other. The chest wall at­ sult of such a puncture is to produce a
tempts to pull the lung out and the lungs to where the lung collapses down to the hilum and the
recoil and pull in the chest wall. The curves labeled chest wall sorinQs outward (see FiQure 3-3, p. 57),
and chest wall are theoretical and illustrate the
elastic force exerted each when permitted to act
Airway ReSistance
unopposed by the other. Normally, these two forces The flow of air into the lungs on pressure dif­
are exerted together and the pressure volume re­ ferences and on the resistance to flow by the airways,
laxation curve, It can be seen that at functional resid­ Resistance is defined as the pressure difference re­
ual caoacitv (FRO. these forces are in equilibrium, quired for one unit flow The air passages in

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 3 Cardiopulmonary Physiology 59

LAMINAR other obstructions. In normal lungs, airflow is a combi­

nation of laminar and turbulent flow and is known as

( [) ,) tracheobronchial flow.
The airways are distensible and compressible, and
thus are susceptible to outside pressures. As these pres­
sures compress the airways, they alter the airway resis­
TURBULENT tance. Transmural pressure is the difference between

'-.=C)Jl 2,) the pressures in the airways and the pressures sur­
, ,;:
rounding the airways. In erect humans, there is a
higher transmural pressure at the apices of the lungs
than at the bases. This expands the alveoli at the apices
relative to those at the bases. Although the alveoli in
the apices have a greater volume at end expiration, the
alveoli in the bases are better ventilated. This is be­
cause the alveoli in the bases operate at lower trans­
mural pressures and thus accommodate a greater vol­
ume during inspiration than those at higher pressures.
Airway resistance decreases during inspiration as a
FIGURE 3-5 result of widening of the airways. During expiration,
The different types of airflow seen within the airways narrow, thus increasing resistance. The posi­
tracheobronchial tree.
tive alveolar pressure that occurs during expiration
partially compresses the airways. If these airways have
lost their structural support as a result of disease, they
humans are divided into upper and lower airways (see may collapse and trap air distally (as in emphysema).
Chapter 2). The upper airways are responsible for 45%
of airway resistance. The resistance to airflow by the
VENTILATION
lower airways depends on many factors and is there­
fore difficult to predict. The branching of the lower air­ Ventilation is the process by which air moves into the
ways is irregular, and the diameter of the lumen may lungs. The volume of air inhaled can be measured
vary because of external pressures, and contraction or with a spirometer. The various lung capacities and
relaxation of bronchial or bronchiolar smooth muscle. volumes are defined in chapter 8.
The lumen diameter may also decrease as a re.sult of Regional differences in ventilation exist through­
mucosal congestion, edema, or mucus. Any of these out the lung. Studies using radioactive inert gas have
changes in the airway diameter may cause an increase shown that when the gas is inhaled by an individual
in airway resistance. Flow of air through these airways in the seated position, and measurements are taken
can be either laminar or turbulent (Figure 3-5). Lami­ with a radiation counter over the chest wall, radiation
nar flow is a streamlined flow where resistance occurs counts are greatest in the lower lung fields, interme­
mainly between the sides of the tubes and the air mole­ diate in the midlung fields, and lowest in the upper
cules. It tends to be cone-shaped, with the molecules in lung fields. This effect is position or gravity depen­
contact with the walls of the tubes moving more dent. In the supine position, the apices and bases are
slowly than the molecules in the middle of the tube. ventilated comparably, and the lowermost lung fields
Turbulent flow occurs when there are frequent molec­ are better ventilated than the uppermost lung fields.
ular collisions in addition to the resistance of the sides Similarly, in the lateral or sidelying position, the
of the tubes seen in laminar flow. This type of flow oc­ lower lung fields are preferentially ventilated com­
curs at high flow rates and in airways where there are pared with the upper lung fields (see Chapter 18).
irregularities caused by mucus, exudate, tumor, and The causes of regional differences in ventilation

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60 PART I Cardiopulmonary Function in Health and Disease

can be explained in terms of the anatomy of the lung greater volume change in relation to resting volume
and mechanics of breathing. An intrapleural pressure which effects greater overall ventilation compared
gradient exists down the lung. In the upright position, with the upper lung fields. In summary, ventilation is
the intrapleural pressure tends to be more negative at favored in the lowermost lung fields regardless of the
the top of the lung, and becomes progressively less position of the body.
negative toward the bottom of the lung. This pressure
gradient is thought to reflect the weight of the sus­
DIFFUSION
pended lung. The more negative intrapleural pressure
at the top of the lung results in relatively greater ex­ Once air has reached the alveoli, it must cross the
pansion of that area and a larger resting alveolar vol­ alveolar-capillary (A-C) membrane (Figure 3-6). The
ume. The expanding pressure in the bottom of the gases must cross through the surfactant lining, the
lung, however, is relatively small and hence has a alveolar epithelial membrane and the capillary en­
smaller resting alveolar volume. This distinction be­ dothelial membrane. Oxygen has to travel further
tween the upper and lower lung fields is fundamental through a layer of plasma, the erythrocyte membrane
to understanding differences in regional ventilation. and intracellular fluid in the erythrocyte, until it en­
The regional differences in resting alveolar volume counters a hemoglobin molecule. This distance is ac­
should not be confused with regional differences in tually small in normal lungs, but in disease states, it
ventilation volume. Ventilation refers to volume may increase. The alveolar wall and the capillary
change as a function of resting volume. The relatively membrane often become thickened. Fluid, edema, or
higher resting volume in the upper lung fields renders exudate may separate the two membranes. These
it stiffer or less compliant compared with the low conditions are often first detected when arterial P02
lung volumes and greater compliance in the lower becomes chronically lower than normal. Oxygen dif­
lung fields. The lower lung fields therefore exhibit a fuses slowly through the A-C membrane in compari-

".<
.rlfflllll".

FIGURE 3-6
The components of the alveolar-capillary membrane.

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 3 Cardiopulmonary Physiology 61

son to CO2 diffusion. As a result, patients with diffu­ or poorly oxygenated lung areas. Although hypoxic
sion problems frequently have hypoxemia with a nor­ vasoconstriction may have an important role to im­
mal Pe02. Sarcoidosis, berylliosis, asbestosis, sclero­ prove the efficiency of the lungs as a gas exchanger,
derma, and pulmonary edema are some diseases that this mechanism may be potentially deleterious to a
decrease the diffusing capacity of the gases. The ca­ patient who has reduced arterial oxygen pressure sec­
pacity may also decrease in emphysema because of a ondary to pulmonary pathology.
decrease in surface area for gas exchange. The acid base balance of the blood also affects
pulmonary blood flow. A low blood pH or acidemia,
for example, potentiates pulmonary vasoconstriction.
PERFUSION
Thus impaired ventilatory function can disturb blood
Pelfusion of the lung refers to the blood flow of the gas composition and in turn, acid base balance. This
pulmonary circulation available for gas exchange. effect can be amplified because of the cyclic reaction
The pulmonary circulation operates at relatively low of pH on pulmonary vasoconstriction. Consideration
pressures compared with the systemic circulation. For of these basic physiologic mechanisms are tanta­
this reason, the walls of the blood vessels in the pul­ mount to optimizing physical therapy intervention.
monary circulation are significantly thinner than
comparable vessels in the systemic circulation. Pul­
Ventilation and Perfusion Matching
monary arterial pressure is low, because perfusion of
the top of the lung is the most distal area. Compared It is essential that ventilated areas of the lung are in
with the systemic circulation, there is little require­ contact with peIfused areas of the lung to effect nor­
ment for significant regional differences in perfusion. mal gas exchange. Conditions that alter the ventila­
Hydrostatic pressure has a significant effect on per­ tion or perfusion of part of the lung also affect the gas
fusion of the lowcr lobes. The hydrostatic pressure re­ exchange in that portion of the lung. Uneven ventila­
flects the effect of gravity on the blood, tending to tion occurs where there is uneven compliance or un­
favor peIfusion of the lower lung fields. This fact has even airway resistance in different parts of the lung.
been substantiated using radioactive tracers in the pul­ The lung is more compliant, that is, easier to inflate
monary circulation and measuring radiation counts at low lung volumes. In the upright position, the
over the lung fields. The nonuniformity of peIfusion apices have a higher resting volume because of a
reflects the interaction of alveolar, arterial, and venous more negative intrapleural pressure than the bases,
pressures down the lung. Normally, blood flow is de­ which renders the apices less compliant than the
termined by the arterial venous pressure gradient. In bases with relatively low resting volumes. Ventilation
the lungs, there are regional differences in alveolar as previously described is favored in the lower lung
pressure that can exert an effect on the arterial venous regions rather than the apices. Uneven airway resis­
pressure gradient. For example, in the upper lung tance may result from airway narrowing (bron­
fields, alveolar pressure approximates atmospheric choconstriction in asthma, mucous plugs, edema,
pressure, which overrides the arterial pressure and ef­ tumor,) or collapse from external pressures as with
fectively closes the pulmonary capillaries. In the lower tumors or emphysema). Uneven compliance may also
lung fields, the opposite occurs. The relatively low vol­ result from fibrosis, emphysema, pleural thickening,
ume of air in the alveoli is oveITidden by the greater effusions, or pulmonary edema.
capillary hydrostatic pressure. Thus the capillary pres­ Nonuniform peIfusion or blood flow can be a re­
sure effectively overcomes the alveolar pressure. sult of gravity, regional differences in intrapleural
Pulmonary blood vessels constrict in response to pressure, regional changes in alveolar pressure, and
low arterial pressures of oxygen. This is termed hy­ obstruction or blockage of part of the pulmonary cir­
poxic vasoconstriction. Hypoxic vasoconstriction in culation. Gravity increases blood flow in the depen­
the lung is believed to serve as an adaptive mecha­ dent portions of the lung and decreases it in the non­
nism for diverting blood away from underventilated dependent portions of the lung. Regional differences

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62 PART [ Cardiopulmonary Function in Health and Disease

ZONE I

ZONEm

FIGURE 3-7
The perfusion of the lung is dependent on posture. In the
upright position three areas can be seen. Zone III has
perfusion in excess of ventilation, in Zone II perfusion and
ventilation are fairly equal and in Zone I ventilation occurs
in excess of perfusion.

in intrapleural pressure change the transmural pres­

sure of blood vessels and thereby the amount of
blood flowing through those vessels. Changes i n
a lveolar pressure also affect the amount o f blood
flowing through the vessels. Overexpanded alveoli
can compress blood vessels, while underexpanded
alveoli may allow more blood to flow through those
vessels. Blood clots, fat, parasites, or tumor cells may
constrict or block part of the pulmonary circulation.
As discussed previously, gravity tends to pull
blood into the dependent positions of the lung (Figure
3-7). In erect humans, therefore, there is greater
blood flow at the bases of the lung. In places, the ar­
FIGURE 3-8
terial blood pressure exceeds the alveolar pressure
Relationship between the size of the airways and the
and causes compression or collapse of the airways
amount of perfusion in the area in the upright position.
(Figure 3-8). Blood flow to the apices is decreased
A, Perfusion is decreased in the apices due to gravity. This
because of gravity. Alveoli in this region are more
enables the alveoli to fully expand. This expansion may
fully expanded as a result of high transmural pres­ compress blood ves els and thereby fUl1her decrease blood
sures and may further decrease blood flow by com­ flow. B, Perfusion is increased in the bases of the lungs due
pressing blood vessels. It follows that the areas of op­ to gravity. The enlarged vessels prevent full expansion of
timal gas exchange occur where there is the greatest alveoli and may in fact compress them to a smaller size.

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 3 CardiopuLmonary Physiology 63

FIGURE 3-9
The effect of positioning on perfusion of the lung. Note that gravity-dependent segments have the
greatest amount of perfusion.

FIGURE 3-10
A, Normal alveolus. B, Dead space. C, Shunt.

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64 PART I Cardiopulmonary Function in Healt.h and Disease

amount of perfusion and ventilation. This occurs to­ ues of POl and PC02. Therefore the lungs must be able
ward the base of the lungs in erect humans. Changes to supply four parts ventilation to about five parts
in posture cause changes in perfusion and ventilation. perfusion. When the ratio is not uniform throughout
Generally, greater air exchange occurs toward the the lung, the arterial blood cannot contain normal
gravity-dependent areas. In side lying, there is greater blood gas values. Regions with low ratios (perfusion
gas exchange in the dependent lung (Figure 3-9). in excess of ventilation) act as a shunt, while regions
In normal lungs, there is an optimal ratio or with high ratios (ventilation in excess of perfusion)
matching of gas and blood. This ratio of ventilation act as dead space (Figure 3-10). Hypoxemia results
to perfusion is 0.8 to maintain normal blood gas val- if regions of abnormal V:Q ratio predominate. An

\\tntilation-Perfusion Ratio
o 2 4

Apex v
Q

Blood flow

Base

Distance Down Lung .05 .10 .15

1/min, % Lung Iume

FIGURE 3-11
The effect of gravity on ventilation, perfusion and ventilation-perfusion matching (V/Q ratio).

PO? ,W

pco ALVEOLAR
DEAD SPACE
.L
' _ _ _ _
Apex t=oo
Po, '
A _ _

L
pco
NORMAL

-
*::::1:;
:::'2::
'd----
SHUNT

Base *=0

Distance Down Lung

FIGURE 3-12
Schemata showing the effect of gravity on ventilation and perfusion down the upright lung.

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 3 Cardiopulmonary Physiology 65

COORDINATION OF CARDIAC EVENTS

elevation in arterial Peo2 may also occur unless the
patient increases ventilation. Therapists who are posi­ The mechanical activity of the heart is precisely regu­
tioning patients with cardiopulmonary pathology may lated with the electrical activity of the heart to effect
find that their patients experience greater distress optimal cardiac output to the organs of the body (An­
when placed in certain positions. Such position-de­ dreoli, Fowkes, Zipes, and Wallace, 1991; Dubin,
pendent distress can be explained by ventilation-per­ 1989; Wagner, 1994). The electrical and mechanical
fusion inequalities that cause poor gas exchange in events of the cardiac cycle are summarized in Figure
the dependent lung. 3-13. These events include the spread of the wave of
The relationship of ventilation and perfusion in the electrical excitation throughout the myocardium, the
lung is summarized in the following figures. Figure resulting sequence of contraction of the atria and ven­
3-11 shows increases in ventilation and peifusion down tricles followed by dynamic changes in pressure and
the upright lung. Optimal ventilation and perfusion blood volume in the heart chambers, the heart sounds
matching, V:Q occurs in the mid-lung zones. In the up­
right position, ventilation is in excess of pelfusion in
the apices, and perfusion is in excess of ventilation in
the bases. Figures 3-12 illustrate the effects of shunt TIME (seconds)
and physiologic dead space on V:Q matching in the up­ 0. 4 0.6 0.8
E.
120
right lung, and their effect on alveolar gas. Specifically, c
3-12 shows a schematic representation of re­ 0, .. .
I
Figure I
100

. b .. ....... .
gional differences in ventilation and perfusion in the
E •

.. .. :: .... . .
S 80 .
... .. . .

upper, middle, and lower zones of the upright lung. W

These gradients are reflected in the alveolar P02 and
a: 60 Ventricle
::J
(/)
Peo2 levels associated with alveolar dead space of the (/) 40
W
apices, appropriate ventilation-perfusion matching in a:
c.. 20 d
the mid-lung, and shunt in the bases. Atrium

DIASTOLE
a:
CARDIAC REflEXES ::s E 120
::J
Ow
The heart behaves automatically, thus is termed a a: 80
f-::J
functional syncytium. Three primary reflexes enable z..J
wO
» 40
the heart to increase stroke volume and cardiac out­
put with moment-to-moment changes in myocardial HEART __ __ -fl ________

demand (French and Ct'iley, 1983). SOUNDS 4th R

The first reflex is the Starling effect which refers
to the increased force of contraction that occurs with
ECG
increased venous return (preload). The second reflex, Q
the Anrep effect, refers to the increase in ventricular
contractile force as a result of an increase in aortic
FIGURE 3-13

pressure (afterload). And third, the Bowdich effect

Summary of electrical and mechanical events of the heart.

refers to the corresponding increase in heart rate

A, Atrial systole. B, Isovolumetric contraction. C, Ejection.

when myocardial contractile force increases. The in­

D, Isovolumetric relaxation. E, Rapid inflow, diastasis, and

tegrated function of these three reflexes ensures that active rapid filling. Note relationship of ventricular pressure

cardiac output adjusts as de mands on the heart and volume. (a) closure of the atrioventricular valves;

change, that is in health, primarily in response to ex­ (b) opening of the semilunar valves; (c) closure of the
ercise, body position and emotional stress. semilunar valves; (d) opening of the atrioventricular valves.

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66 PART I Cardiopulmonary Function in Health and Disease

and the of these events. The cardiac takes Myocardial Depolarization

0.8 second in a heart at 75 beats/min. Ventric­

ular systole or ejection takes about one-third of this
time. Its onset and termination are marked respec­ Ventricular Contraction

by closure and of the atrioventricular

valves (mitral and tricuspid). Diastole, or the period
between successive ventricular systoles in whieh the Tricuspid and Mitral Valves Close

ventricles fill with blood, takes two thirds of the 0.8

second of each cardiac
Pressure Increases and
Pulmonary Aortic Pressure

Phases of Systole and Diastole

Ventricular systole normally has three phases: isovol­ Pulmonic and Aortic Valves Open
umctric contraction period, and
a slower
three phases: passive
period. Ventricular diastole also has
diastasis (a
t

is Completed; Pressure Below

slower filling and active phase. Pulmonary and Aortic Pressure

Heart Sounds Pulmonic A ttiC Valves Close

The heart sounds are described as a low-pitched long

duration sound (SI) followed by a t

Ventricular Pressure Falls Below Atrial Pressure

slower duration sound that resembles the phonic
sounds of LUB-dub. S I is associated with closure of
the atrioventricular valves. is associated with c1o­
Tricuspid and Mitral
l
Open
sure of the semilunar valves. In inspiration, the aortic
valve closes several milliseconds before the pulmonic
valve, resulting in a splitting of the second heart t

Diastolic Filling
S2. During inspiration, intrathoracic pressure becomes
more venous return and
increase, hence pulmonary
heart volume
is prolonged in this
l

Myocardial Depolarization
and closure of the pulmonary valve is de-
Other variations in splitting of occur with FIGURE 3-14
pathology. The presence of a third (S3) or fourth The sequence of pressure in the hearl the
cardiac
heart sound is usually considered abnormal. is usu­
associated with the phase, and
with the active rapid-filling phase.
heart are responsible for the and of the
valves. Coordinated valve opening and closure are im­
Volume and Pressure Changes
portant in promoting the forward movement of blood
Changes in the ventricular volume curve and aortic and mechanical of the heart
pressure wave reflect in atrial and ventricular pump resulting from valvular of blood
pressure during and diastole (Ganong, 1993; ventricular contraction. of blood
Guyton, 1991). The sequence of events appears in a in the retrograde direction gives rise to heart murmurs
tlow chart in Figure 3-14. Pressure gradients within the audible on auscultation of the heart (Goldberger. 1990).

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 3 Cardiopulmonary Physiology 67

fluid to be filtered out of the systemic circulation

TABLE 3-1
into the interstitium. Table 3-1 illustrates the mean
Balance of Forces Moving Fluid pressures determining normal fluid dynamics across
In and Out of the Capillary capillary membranes.
mmHg

Mean forces moving fluid out of capillary TRANSPORT OF OXYGEN BY THE BLOOD
Mean capillary pressure 17.0
Once oxygen reaches the blood, it rapidly combines
Negative interstitial pressure 6.3
Oncotic interstitial pressure 5.0 with hemoglobin to form oxyhemoglobin (West,
TOTAL OUTWARD PRESSURE 28.3 1995). A small proportion of oxygen is dissolved in
the plasma. The use of the hemoglobin molecule as
Mean forces moving fluid into capillary
an oxygen carrier allows for greater availability and
Plasma oncotic pressure 28.0
efficiency of oxygen delivery to the tissues in re­
TOTAL INWARD PRESSURE 28.0
sponse to changes in metabolism. Saturation of the
OUTW ARD PRESSURE - INW ARD oxygen-carrying sites on the hemoglobin molecule is
PRESSURE NET OUTW ARD PRESSURE 0.3
curvilinearly related to the partial pressure of oxygen
=

in the tissues. This relationship is called the oxyhe­

moglobin dissociation curve and is a sigmoid or S­
shaped curve (Figure 3-15). The hemoglobin of arter­
ial blood is 98% or almost completely saturated with
Peripheral Circulation
oxygen. Under normal circumstances, arterial blood
The purpose of the peripheral circulation including is mixed with a small proportion of venous blood
the microcirculation at the tissue level is to provide from the coronary and pulmonary circulation, result­
saturated oxygenated blood and remove partially de­ ing in arterial saturation of less than 100%. The graph
saturated blood. The microcirculation within each shows a range of partial pressures of oxygen that may
organ regulated the blood flow both exogenously via exist in the tissues. At relatively high arterial oxygen
the neurological system and endogenously via the hu­ pressures, the oxygen saturation is high. This reflects
moral system commensurate with the metabolic high association or low dissociation between oxygen
needs of that tissue bed (see Chapter 2). The four and hemoglobin. Saturation does not fall significantly
principal factors that determine the movement of until the partial pressure of oxygen falls below 80
fluid in the microcirculation include the following: mm Hg. Even at P02 levels of 40 to 50 mm Hg, al1er­
1. The capillary hydrostatic pressure from the ial saturation is still 75%. This suggests an enormous
blood pressure, which tends to move blood capacity of the oxyhemoglobin dissociation system to
across the capillary membrane out of the circu­ meet the varying needs of different tissues without
lation into the interstitium severely compromising arterial saturation. A P02 of
2. The capillary oncotic pressure from the pro­ less than 50%, for example, has a profound effect on
teins within the blood vessels, which tends to arterial saturation. This demonstrates an adaptive re­
retain fluid in the circulation sponse of hemoglobin dissociation to respond to low
3. The interstitial hydrostatic pressure, which oxygen tissue pressures by greater dissociation of
tends to move fluid back into the circulation oxygen from hemoglobin as the need arises. As the
4. The interstitial oncotic pressure, which tends P02 improves as a result of increased supply of oxy­
to draw fluid out of the circulation into the gen or decreased demand, the affinity between oxy­
interstitium gen and hemoglobin increases, and arterial saturation
The net forces acting on the capillary fluid are increases. Thus oxygen is not released unless there is
nearly in equilibrium with a slight tendency for a need for greater oxygen delivery to the tissues.

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68 PART I Cardiopulmonary Function in Health and Disease

ARTERIAL OXYGENATION

75
C\J
0

Z
0
i=
«
0:::
::J

(f)

20 27 40 60 80 100
PARTIAL PRESSURE 02

FIGURE 3-15

The oxyhemoglobin dissociation curve.

Different conditions can increase or decrease he­ Anemia (reduced red blood cell count and hemo­
moglobin affinity for oxygen and thereby cause a shift globin) and polycythemia (excess red blood cells and
in the oxyhemoglobin dissociation curve (West, 1995) hemoglobin) produce changes in oxygen content of
(Figure 3-15). A shift to the right results in decreased the blood as well as saturation. Anemia shifts the
oxygen affinity and greater dissociation of oxygen and curve to the right and lowers the maximal saturation
hemoglobin. In this instance, for any given partial achievable. Polycythemia has the opposite effect. The
pressure of oxygen, there is a lower saturation than curve is shifted to the left and maximal saturation ap­
normal. This means that there is more oxygen avail­ proaches 100%.
able to the tissues. Shifts in the curve to the right
occur with increasing concentration of hydrogen ions
TRANSPORT OF CARBON DIOXIDE
(i.e., decreasing pH), increasing Peo2, increasing tem­
peratures, and increasing levels of 2,3-DPG (diphos­ CO2 is an acid produced by cells as a result of cell
phoglycerate), a byproduct of red blood cell metabo­ metabolism. It is carried in various forms by venous
l i s m . W e s t ( 19 9 5 ) s u g g e s t s , "A simple way t o blood to the lungs, where it is eliminated. Most of the
remember these shifts i s that an exercising muscle (in­ CO2 added to plasma diffuses into the red blood cells,
creased metabolic demand), is acid, hypercarbic, (hy­ where it is buffered and returned to the plasma to be
percapnic) and hot, and it benefits from increased un­ carried to the lungs. The buffering mechanism is so
.
loading of oxygen from its capillaries." effective that large changes in dissolved CO2 can
A shift of the curve to the left results in increased occur with small changes in blood pH.
oxygen affinity. Thus for any given partial pressure The transport of CO2 has an important role in the
of oxygen, there is a higher saturation than normal. acid-base status of the blood and maintenance of nor­
This means that there is less oxygen available to the mal homeostasis (Comroe, Forster, Dubois, Briscoe,
tissues. This occurs in alkalemia, hypothermia, and and Carlsen, 1986). The lung excretes 10,000 mEg of
decreased 2,3-DPG. carbonic acid per day. (Carbonic acid is broken down

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 3 Cardiopulmonary Physiology 69

into water and CO2. The CO2 is buffered and elimi­ globin dissociation ensures adequate oxygen delivery
nated through the lungs.) The kidney can excrete only to the tissues once oxygen has diffused through the
100 mEq per day of acids. Therefore alterations in alveolar capillary membrane into the circulation.
alveolar ventilation can have profound effects on the Transport of CO2 and its buffering mechanisms are
body's acid-base status. A decrease in the lung's abil­ central to acid base balance and normal homeostasis.
ity to ventilate causes a sharp rise in Peo2 and a drop
in pH. This causes an acute respiratory acidosis. If
REVIEW QUESTIONS
this change occurs gradually, the pH will remain
within normal limits while the Peo2 is elevated. This I. Describe the control of breathing.
is known as a compensated respiratory acidosis. Hy­ 2. Explain respiratory mechanics with respect to
perventilation or excessive ventilation causes rapid airway resistance and lung compliance.
elimination of C02 from the blood. This results in a 3. Describe the distributions of ventilation, perfu­
decreased Peo2 and an increased pH and is known as sion and diffusion.
an acute respiratory alkalosis. Again, if the change 4. Explain the determinants of ventilation and per­
occurs gradually, the pH remains within normal lim­ fusion matching.
its even though the Peol is decreased. This is a com­ S. Describe electromechanical coupling in the heart.
pensated respiratory alkalosis. 6. Describe oxyhemoglobin dissociation and the
oxyhemoglobin dissociation curve.

SUMMARY
REFERENCES
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pling of electrical and mechanical events in the heart phia: JB Lippincott.

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Guyton, A,C, (l99J), Textbook of medical physiology. (8th ed,j, Sokolow, M., McIlroy, M.B" & Cheitlin, M.D. (1990), Clinical
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 Cardiopulmonary Pathophysiology

Willy E. Hammon
Scott Hasson

KEY TERMS Angina Fibrosis

Bronchiectasis Myocardial infarction

Coronary artery disease Obstructive lung disease

Emphysema Restrictive lung disease

INTRODUCTION
formance. The parameters affected by CAD can be the
The first part of this chapter, beginning with obstruc­ volume of blood pumped and the heart rate. The
tive lung disease, describes the pathophysiology of major purposes of this portion of the chapter are to de­
chronic pulmonary disease. Chronic pulmonary dis­ scribe the etiologic factors of clinical syndromes asso­
ease can be categorized broadly into obstructive and ciated with CAD, briefly describe medical treatment,
restrictive disorders. and discuss issues of prognosis.
Obstructive disorders are characterized by a de­
creased rate of airflow during expiration (as a result
OBSTRUCTIVE LUNG DISEASE
of increased airway resistance). Restrictive disorders
are conditions in which the inspiratory capacity of the Several abbreviations can be found in the literature
lungs is restricted to less than the predicted normal. for a pulmonary disorder characterized by increased
Overlap between the two categories does exist. airway resistance, particularly noticeable by a pro­
The second part of this chapter, beginning with longed forced expiration. Some of these are chronic
coronary artery disease (CAD), describes the patho­ obstructive pulmonary disease (COPD), chronic ob­
physiology of cardiovascular disease. Cardiovascular structive airway disease (COAD), chronic airway ob­
disease is also known primarily as CAD, and is mani­ struction (CAO), and chronic obstructive lung disease
fested in various clinical syndromes. CAD is an ather­ (COLD) (Fishman, 1988).
osclerotic process that occurs in the right and left The first part of this chapter describes chronic
coronary aJ1eries, which ultimately affects heart per- bronchitis, emphysema, asthma, and bronchiectasis

71

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72 PART I Cardiopulmonary Function in Health and Disease

individually. With the possible exception of asthma susceptible to rcspiratory infections, and it takes them
and bronchiectasis, however, it is unusual in the clini­ longcr to recovcr from these infections. In addition, the
cal setting to find a patient with only one of these con­ ilTitation of smoke in the tracheobronchial trec causes
ditions. Most patients have some combination of bronchoconstriction. Although smoking is the most
chronic bronchitis, emphysema, and asthma, and in common cause of chronic bronchitis, other agents that
this chapter, these individuals are referred to as having have been implicated are air pollution, bronchial infec­
COPD. These patients have intermittent episodes of tions, and certain occupations.
wheezing, along with a variable degree of chronic These patients are referred to as "blue bloaters,"
bronchitis and emphysema (Hodgkin, 1975). Radio­ because they usually have stocky body build and are
logically, they may have hyperinfiated lungs, flattened "blue" as a result of hypoxemia (Dornhorst, 1955;
diaphragms, and an enlarged right ventricle as a result Filley et ai, 1968; Fishman, 1988; Nash, Briscoe,
of increased pulmonary artery pressure. Other findings and COUl·nand, 1965. Although many of these pa­
vary from patient to patient, depending on the predom­ tients have a high arterial partial pressure of carbon
inant disease process contributing to their COPD. dioxide (Pac02), the pH is normalized by renal re­
COPD is very common. In 1994 the American tention of bicarbonate (HC03). In the patient with
Lung Association (ALA) estimated that 14.2 million chronic bronchitis, bone marrow tries to compensate
Americans have COPD. In the United States alone, for chronic hypoxemia by increased production of
health care costs for COPD exceed $7.6 billion annu­ red blood cells, leading to p olycythemia (Snider,
ally. Deaths from COPD numbered more than 85,000 Faling, and Rennard, 1994). Polycythemia, in turn,
in 1991; it is the fourth leading cause of death in the makes the blood more viscous, forcing the heart to
United States. work even harder to pump it. Long-term hypoxemia
leads to increased pulmonary artery pressure and
right ventricular hypertrophy.
Chronic Bronchitis
Individuals with bronchitis often expectorate mu­
Chronic bronchitis is a disease characterized by a coid brownish-colored sputum. In an exacerbation,
cough producing sputum for at least 3 months and for 2 usually from infection, they have an even greater
consecutive years (American Thoracic Society, 1962). amount of purulent sputum. Ventilation-perfusion ab­
Pathologically, there is an increase in the size of normalities are common, which increase hypoxemia
the tracheobronchial mucous glands (increased Reid and Paco2 retention (Rochester and Brown, 1976).
index) and goblet cell hyperplasia (Mitchell, 1968; The respiratory rate increases, as does the use of ac­
Reid, 1960; Stoller and Wiedemann, 1990). Mucous cessory muscles. The resultant increased work of
cell metaplasia of bronchial epithelium results in a breathing requires greater oxygen consumption by
decreased number of cilia. Ciliary dysfunction and these muscles, with a greater production of carbon
disruption of the continuity of the mucous blanket are dioxide (C02) than the respiratory system can ade­
common. In the peripheral airways, bronchiolitis, quately meet. This contributes to a further drop in the
bronchiolar narrowing, and increased amounts of arterial partial pressure of oxygen (Pao2) and a rise in
mucus are observed (Cosio, 1978; Wright, 1992). Paco2. The hypoxemia and acidemia increase pul­
The cause of chronic bronchitis is believed to be re­ monary vessel constriction, which raises pulmonary
lated to long-term in-itation of the tracheobronchial tree. artery pressure and ultimately leads to right heart fail­
The most common cause of irritation is cigarette smok­ ure (cor pulmonale).
ing (US Surgeon General, 1984). Inhaled cigarette In the following example, a patient is admitted to
smoke stimulates the goblet cells and mucous glands to the hospital with an exacerbation of chronic bronchi­
secrete more mucus. This smoke also inhibits ciliary tis and presents the following picture: he is of stocky
action. The hypersecretion of mucus and impaired cilia body build, his color is dusky, and he breathes with
lead to a cllronic productive cough. The fact that smok­ moderate-to-marked use of the respiratory accessory
ers secrete an abnormal amount of mucus makes them muscles, depending on the degree of respiratory dis­

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 4 Cardiopulmonary Pathophysiology 73

tress. may be audible or noted by ausculta­ and Rennard,

tion. Intercostal (or retractions may be pre­ 1983). Diuretics and
sent, also on the degree of respiratory dis­
tress. Edema in the extremities in the
ankle and neck vein distention reflect decom­
Emphysema
iJ"'''''''''U cor pulmonale. The may report that
this b r e athing difficu w i th i n c r e a s e d There are two main of emphysema-centrilob­
amounts o f secretions a change in normal ular and panlobular 1976; ThurJbeck, I It
color) or decreased amounts of sputum in­ has been that centrilobular
creased retention of Arterial blood gases 20 times more common than panlobular
show the individual with bronchitis to have a lowered both types are often found in the same pair
Pao2, a raised and a lowered
function tests indicate a reduced vital As its name implies, centrilobular emphysema is
forced v o lume in I second characterized destruction of the respiratory bron­
maximum voluntary ventilation and diffus­ chiole, edema, and thickened bronchi­
capacity, as well as an increased functional resid­ olar walls. These changes are more common and
ual and residual volume. more marked in the upper lobes and superior seg­
an exacerbation, these are usually ments of the lower lobes 1963). This
treated with intravenous fluids, antibiotics, bron­ form of emphysema is found more often in men than
chodilator and low-flow oxygen. CO!1iocosteroids may in women, is rare among nonsmokers, and is com­
be administered. Some with increased secre­ mon among with chronic bronchitis.
tions respond to chest physical therapy and bronchial Pan lobular emphysema, on the other hand, is

Alveoli
A ___

FIGURE 4-1
A, Panlobular is characterized by a destructive enlargement of the alveoli, B, A nonnal
respiratory bronchiole and alveoli. Centrilobular emphysema is characterized a selective
and destmction of the bronchiole.

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74 PART I Cardiopulmonary Function in Health and Disease

characterized by destructive enlargement of the alve­ (Figure 4-2) (Reid, 1967; Thurlbeck, 1991; Thurlbeck,
oli, distal to the terminal bronchiole (Figure 4-1). It 1976). It is thought that bullae develop from a coales­
most often involves the lower lobes. This type of em­ cence of adjacent areas of emphysema or an obstruc­
physema is also found in subjects that have alphaJ­ tion of the conducting airways that permits the flow of
antitripsin deficiency. Airway obstruction in these in­ air into the alveoli during inspiration but does not
dividuals is caused by loss of lung elastic recoil or allow air to flow out again during expiration. This
radial traction on the bronchioles. When individuals causes the alveoli to become hyperinflated and even­
with normal lungs inhale, the airways are stretched tually leads to destruction of the alveolar walls with a
open by the enlarging elastic lung, and during exhala­ resultant enlarged air space in the lung parenchyma.
tion the airways are narrowed as a result of the de­ These bullae can be more than 10 cm in diameter, and
creasing stretch of the lung. However, the lungs of by compression, can compromise the function of the
patients with panlobular emphysema have decreased remaining lung tissue (Figure 4-3). If this happens,
elasticity because of disruption and destruction of surgical intervention to remove the bulla is often nec­
surrounding alveolar walls. This in turn leaves the essary. Pneumothorax, a serious complication, can re­
bronchiole unsupported and vulnerable to collapse sult from the rupture of one of these bullae.
during exhalation. The emphysema patient's most common com­
Bullae, emphysematous spaces larger than I cm in plaint is dyspnea. Physically, these patients appear
diameter, may be found in patients with emphysema thin and have an increased anteroposterior chest di-

FIGURE 4-2
A, AP chest film reveals bullous emphysema with multiple, thin, rounded fibrotic lucencies. B, The
spot film bronchogram of the left midlung field shows intact bronchi and distal emphysematous blebs.
(Courtesy of T. H. Johnson, M.D.)

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 4 Cardiopulmonary Pathophysiology 75

ameter. Typically, they breathe using the accessory heart (Figure 4-4). Pulmonary function tests show a
muscles of inspiration. These patients are often seen decreased vital capacity, FEY" maximum voluntary
leaning forward, resting their forearms on their knees ventilation and a greatly reduced diffusing capacity.
or sitting with their arms extended at their sides and The total lung capacity is increased, while the resid­
pushing down against the bed or chair to elevate their ual volume and functional residual capacity are even
shoulders and improve the effectiveness of the acces­ more increased. Arterial blood gases reflect a mildly
sory muscles of inspiration. They may breathe or moderately lowered Pao2, a normal or slightly
through pursed lips during the expiratory phase of raised Pacol and a normal pH. These patients, unlike
breathing. These patients have been referred to as patients with chronic bronchitis, normally will de­
"pink puffers" because of the increased respiratory velop heart failure in the end stage of the disease
work they must do to maintain relatively normal (Figure 4-5).
blood gases (Dornhorst, 1955; Filley et aI, 1968; Treatment of progressive emphysema that requires
Fishman, 1988; Nash, Briscoe, and Cournand, 1965). hospitalization often includes IY fluids, antibiotics,
On auscultation, decreased breath sounds can be and low-flow oxygen (Snider, Faling, and Rennard,
noted throughout most or all of the lung fields. Radi­ 1994). Some of these patients also receive bron­
ologically, the emphysema patient has overinflated chodilators, corticosteroids, diuretics, and digitalis.
lungs, a flattened diaphragm, and a small, elongated Pursed-lip breathing can relieve dyspnea and improve

FIGURE 4-3
A, AP and B, lateral views of the chest of a patient with advanced bullous emphysematous changes.
Note the bullae in the upper lung fields. The lateral film reveals an increased A-P diameter of the thorax,
flattening of the diaphragms and in increased anterior clear space. (Collrtesy of T. H. Johnson, M.D.)

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76 PART I Cardiopulmonary Function in Health and Disease

FIGURE 4-4
A, AP chest film reveals the increased lucency of lung fields and flattening of the diaphragm of
emphysema. The vascular structures are crowded mediaHy. B, Lateral chest film reveals an
increased AP diameter and flattening of the diaphragms. There is an increase in the anterior clear
space. These are all findings of emphysema. (Courtesy of T. H. Johnson, M.D.)

arterial blood gasses (Muller, Petty, and Filley, 1970; these and other factors in producing emphysema is
Petty and Guthrie, 1974). still not well understood.
The cause of emphysema is uncel1ain. It is known
Prognosis of chronic bronchitis and emphysema
that the incidence of emphysema increases with age. It
is most often found in chronic bronchitics, and there is Chronic bronchitis and emphysema are marked by a
no question that emphysema is more prevalent in cig­ progressive loss of lung function. At the end of 5
arette smokers than in nonsmokers (US Surgeon Gen­ years, patients with COPD have a death rate four to
eral, 1984). The risk of developing COPD is 30 times five times greater than the normal expected value.
greater in smokers than nonsmokers (Fielding, 1985). Death rates reported by various studies depend on the
There also seems to be an hereditary factor, evident in method of selection of patients, types of diagnostic
the severe panlobular emphysema that patients with tests and other criteria (Anthonisen, 1989; Bousky et
an alpha,-antitrypsin deficiency develop relatively ai, 1964; Kanner et ai, 1983; Kanner and Renzetti,
early in life, even though they m a y never h ave 1984). One study reported a 3-year overall mortality
smoked (Eriksson, 1965; Tobin, Cook, and Hutchin­ rate of 23%, with patient age and the initial FEY I
son, 1983). Repeated lower respiratory tract infections value being the most accurate predictors of death
may also play a role. However, the interrelationship of (Anthonisen, Wright, and Hodgkin, 1986). In general,

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 4 Cardiopulmonary Pathophysiology 77

gestive heart failure (CHF), which is secondary to cor

pulmonale; respiratory failure; pneumonia; bronchi­
olitis; and pulmonary embolism.

Asthma

Asthma is a disease characterized by an increased re­

sponsiveness of the trachea and bronchi to various
stimuli, and is manifested by widespread narrowing
of the airways that changes in severity either sponta­
neously or as a result of treatment. During an asthma
attack, the lumen of the airways is narrowed or is oc­
cluded by a combination of bronchial smooth muscle
spasm, inflammation of the mucosa, and an overpro­
duction of a viscous, tenacious mucus.
Asthma is certainly a widespread disease in the
world today. Its incidence is about 3% to 7% in
adults (Barnes, 1993; National Asthma Education
Program, 1991). It is found more often in individuals
under age 25, where estimates of prevalence vary
FIGURE 4-5 from 5% to 15% (Williams and McNicol, 1969).
The chest film reveals peripheral emphysematous lucency. About 80% of children with asthma do not have
The hilar areas are tremendously enlarged by the asthma after the age of 10.
pulmonary arteries in a typical cor pulmonale Asthma that begins in patients under the age of 35
configuration. Cardiomegaly is also present. (Courtesy
is usually allergic or extrinsic. These asthma attacks
ofT. H. 10hnson, M.D.)
are precipitated when an individual comes in contact
with a specific substance to which that person is sen­
sitive, such as pollens or household dust (see box 4-1
the death rates 5 years after diagnosis are 20% to below). Often people with asthma are allergic to a
55%. Other investigators reported an overall mortal­ number of substances, not only one or two.
ity of 47 percent at the end of 5 years (Burrows, and If a patient's first asthma attack occurs after the
Earle, 1969). They believed a 5-year survival rate can age of 35, usually there is evidence of chronic airway
be estimated as follows: 80% in patients with an obstruction with intermittent episodes of acute bron­
FEY I close to 1.0 L; and 40% for patients with an chospasm. These individuals, whose attacks are not
FEY I less than 0.75 L. However, if the above flow triggered by specific substances, are referred to as
rates are found in patients with complications of rest­ having nonallergic or intrinsic asthma (see b o x
ing tachycardia, chronic hypercapnia and a severely below). Chronic bronchitis i s commonly found i n this
impaired diffusing capacity, the survival rates should group, and this is the type of individual often seen in
be reduced by 25%. Other factors that have been as­ the hospital setting.
sociated with a poor prognosis are cor pulmonale, The individual with an acute asthma attack usually
weight loss, radiologic evidence of emphysema, a has been awakened at night or early in the morning with
dyspneic onset, polycythemia, and Hoover's sign (an one or more of the following symptoms: cough, dysp­
inward movement of the ribs on inspiration) nea, wheezing, or chest tightness (McFadden, 1988). In
(Mitchell, Webb, and Filley, 1964; Renzetti, 1967). fact, nocturnal awakenings are such a common occur­
The most common cause of death in patients with rence with asthma, that their absence from the history
COPD (in descending order of frequency) are con­ causes even experienced clinicians to doubt the diagno­

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78 PART I Cardiopulmonary Function in Health and Disease

Factors That May Precipitate an Asthma Attack

Allergic or extrinsic asthma

Pollen (especially ragweed)
Animals
Feathers
Molds
Household dust
Food
Nonallergic or intrinsic asthma
Inhaled irritants
Cigarette smoke
Dust
Pollution
Chemicals
Weather
High humidity
Cold air
Respiratory infections
Common cold
Bacterial bronchitis
Drugs
Aspirin
Emotions
FIGURE 4-6
Stress
A patient in respiratory distress during an acute asthma
Exercise
attack. Note the marked use of the stcrnocleidomastoids
and other accessory muscles during inspiration.

sis (Turner-Warwick, (988). The patient has a rapid high PacD2, a low Pao2, and a pH of less than 7.30 (Mc­
rate of breathing and is using the accessory respiratory Fadden and Lyons, 1968).
muscle (Figure 4-6). The expiratory phase of breathing Medical management of acute asthma has three
is prolonged with audible wheezing and rhonchi. How­ (2) mobilization of
goals: ( l ) relief of bronchospasm,
ever, when severe obstruction is present, the chest be­ secretions, and (3) maintenance of alveolar ventila­
comes silent (Gold, 1976). The patient may cough tion. Th e r e f ore m o s t hospitalized patients with
often, though unproductively, and may complain of asthma are treated with IV fluids, bronchodilators,
tightness in his chest. Radiologically, the lungs may ap­ supplemental oxygen, and corticosteroids.
pear hyperinflated or show small atelectatic areas from An asthma attack that persists for hours and is unre­
retained secretions. The degree of tachypnea, hyperin­ sponsive to medical management is referred to as sta­
flation, accessory muscle use, and pulsus paradoxus tus asthmaticus. The patient may appear dehydrated,
(difference in systolic blood pressure during inspiration cyanotic, and near exhaustion from labored breathing.
and expiration) are useful guides for determining the In contrast to the audible whcczing and rhonchi heard
degree of airway obstruction present (Woolcock, 1994). early in the attack, the chest now has greatly dimin­
Early in the attack, arterial blood gases reflect slight hy­ ished or absent breath sounds. Status asthmaticus re­
poxemia and a low Paco2 (from hyperventilation). If the sults in a significant death rate and is regarded as a
attack progresses, the PaD2 continues to fall as the PacD2 medical emergency. Bilateral manual lower chest com­
climbs above the normal range. As obstruction becomes pression assists expiration and has value as an emer­
severe, deterioration of the patient occurs, evident by a gency treatment of asthma (Fisher, Bowery, and Ladd­

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 4 Cardiopulmonary Pathophysiology 79

FIGURE 4-7
Gross specimen of lung showing large mucus plug within the bronchial tree of a patient who died
from status asthmaticus. (Courtesy of J. J. Coalson, Ph.D.)

Hudson, 1989; Watts, 1989). Patients in respiratory bronchial lumen, further contributing to the stasis of
failure may require mechanical ventilation. secretions. Although the alveoli are overinflated, the
Studies that examine the lungs of patients who die permanent destructive changes found in emphysema
from status asthmaticus find lungs that are signifi­ are not present.
cantly hyperinflated and do not deflate even when
Prognosis of asthma
the thorax is opened (Huber and Koessler, 1922;
Dunnill, 1960; Saetta et ai, 1991). Examination of Most studies following children with asthma for a
the airways reveals a mucosa that is edematous and number of years report a death rate of about 1 %
inflamed. Characteristic of asthma, the basement (Ogilvie, 1962). One large study of 1,000 people with
membrane is thickened. The mucous glands are en­ asthma of all ages in England reported a mortality of
larged, and there is an increase in the number of gob­ 7% as a result of asthma or its complications. This
let cells. Evidence of bronchospasm is seen by the study reported that 2% of the patients with intermit­
hypertrophied and thickened smooth muscle. The lu­ tent asthma died, compared with 9% of those with
mens of most bronchioles, down to the terminal continuous asthma. During the 1960s, there was a
bronchioles, are filled with viscous, sticky mucus sharp increase in the number of deaths among people
(Figure 4-7). It is evident that the occluded bronchi­ with asthma reported by countries around the world.
oles have caused death by asphyxiation. Secretions At the peak of this increase, England and Wales re­
in the tracheobronchial tree of the patient with ported that 7% of the deaths in children between 10
asthma are a combination of mucus, secreted by the and 14 years of age were attributable to asthma. This
mucous glands, and an exudate from the dilated cap­ reflected a 700% increase in only 7 years. Some med­
illaries just below the basement membranae. It has ical authorities feel this increase in deaths was related
been shown that cilia do not sweep the mucoserous to widespread use or abuse of certain pressurized
t1uid nearly as effectively as pure mucus. In addition, aerosol nebulizers containing isoproterenol, but this
sheets of ciliated epithelium have been shed into the has been disputed (Gandevia, 1973). In 1987 there

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80 PART I Cardiopulmonary Function in Health and Disease

were more than 4,300 deaths from asthma in the Un­ bronchi to resemble varicose veins (Figure 4-8). Sac­
tied States, 31% more than in 1980 (McFadden and cular (or cystic) bronchiectasis refers to airways that
Gilbert, 1992). have intermittent sphcrical ballooning (Figure 4-9).
Bronchiectasis is usually localized in a few seg­
ments or in an entire lobe of the lung. Most com­
Bronchiectasis
monly, it is unilateral (although 40% to 50% of the
Bronchiectasis is defined as an abnormal dilation of cases are bilateral) and affects the basal segments of
medium-size bronchi and bronchioles (about the the lower lobes. When the left lower lobe is involved,
fourth to ninth generations), generally associated with it is not unusual to find bronchiectasis in the lingula of
a previous, chronic necrotizing infection within these the left upper lobe as well. Interestingly, bronchiecta­
passages. Ordinarily, there is sufficient cartilage sis of the right middle lobe is relatively common in
within the walls of the larger bronchi to protect them older adults and can contribute to both hemoptysis
from dilation. and repeated infections of this lobe. Upper lobe
The airway deformities can be classified into three bronchiectasis generally involves the apical and poste­
types (Reid, 1950; Luce, 1994). Cylindrical (or longi­ rior scgments and is usually caused by tuberculosis or
tudinal) bronchiectasis is the most common type, bronchopulmonary aspergillosis.
with a uniform dilation of the airways. Varicose Pathologically, the mucosa appears edematous and
bronchiectasis refers to a greater dilation than in ulcerated. Destruction of the elastic and muscular
cylindrical bronchiectasis, causing the walls of the structures of the airway walls is evident with resultant

FIGURE 4-8
A, AP chest film of a bronchogram with cylindrical and varicose bronchiectasis in the lower lung
fields. B, Close-up view of cylindrical and varicose bronchiectatic changes in the left lower lobe.
(Courtesy of T. H. Johnson, M.D.)

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 4 Cardiopulmonary Pathophysiology 81

dilation and fibrosis. The walls are lined with hyper­ Obstruction can cause bronchiectasis by collaps­
plastic, nonciliated, mucus-secreting cells that have ing lung tissue (atelectasis) distal to the obstruction
replaced the nOImal ciliated epithelium. This change (Barker and Bardana, 1988). The increased negative
is significant, because it interrupts the mucociliary pressure in the chest (from the collapsed lung) exerts
blanket and causes pooling of infected secretions, a greater traction on the airways, causing them to ex­
which further damage and irritate the bronchial wall pand and to become distorted. Secretions are re­
(Barker and Bardana, 1988; Currie et ai, 1987). tained, and if the obstruction is prolonged, an infec­
The etiology of bronchiectasis is related to ob­ tio.u occurs that begins to destroy the walls of the
struction of the airways and respiratory infections bronchi, as described above. There has been a signifi­
(Luce, 1994; Simpson, 1975). Some 60% of the cases c a n t reduction in the n u m b e r of p a t i e n t s w i t h
of bronchiectasis are preceded by an acute respiratory bronchiectasis since the introduction o f antibiotics to
infection. The infection involves the bronchial walls. treat respiratory infections.
Portions of the mucosa are destroyed and are re­ Twenty-four-hour sputum volume has been used
placed by fibrous tissue. The radial traction of the as an indicator of severity of disease to categorize pa­
lung parenchyma on the damaged bronchi causes the tients with bronchiectasis (Ellis et aI, 1981). Those
involved airways to become permanently dilated and producing less than 10 ml per day have been catego­
distorted (Barker and Bm·dana, 1988). These areas, rized as having mild bronchiectasis, to to I SO ml as
devoid of normal ciliated cells, contain secretions moderate bronchiectasis and greater than I SO ml as
that eventually become chronically infected. having severe bronchiectasis.

FIGURE 4-9
A, AP chest film of a bronchogram shows saccular bronchiectasis. B, Close-up view of
bronchiectatic areas with grapelike saccular bronchiectasis. (Courtesy of T. H. Johnson, M.D.)

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82 PART I Cardiopulmonary Function in Health and Disease

P atients w ith severe, diffuse, long-standing accumulated overnight. Therapists teaching the pa­
bronchiectasis are rare today. Physically, they are ema­ tient postural drainage positions devised to drain the
ciated, and as many as 25% of them may have clubbed involved segments should keep in mind that this dis­
fingers. A chronic cough, with expectoration of un­ ease causes distortion and dilation of the bronchi;
pleasant-tasting, purulent sputum is typical in these pa­ hence the traditional positions found in books may be
tients. When this sputum is collected and allowed to of limited value in determining the precise segment of
stand, it may separate into three distinct layers: the up­ the lung that is the source of the secretions. If the in­
permost layer is frothy, the middle layer is serous or volvement is in the lower lobes, the patient should be
mucopurulent, and the lowest layer is purulent and placed in the Trendelenburg position and should be
may contain small grayish or yellowish plugs (Dit­ gradually rotated from lying on one side, to supine, to
trich's plugs). Changes of body position, while sleep­ lying on the opposite side, and prone, if tolerated,
ing or on arising, often stimulate coughing as the while doing the FET and/or receiving percussion and
pooled secretions again spill onto the mucosa of nor­ vibration 5 to to minutes per segment over all sur­
mal, larger airways. These individuals may have cor faces of the lower lobe being treated. A similar proce­
pulmonale from fibrosis that has extended to involve dure may be followed while sitting if the upper lobes
the pulmonary capillary bed. Patients with widespread require drainage, but these segments rarely require
bronchiectasis appear dyspneic and have increased drainage, since they usually drain during the course of
work of breathing as a result of hypoxemia and hyper­ the day while the individual is in a more or less erect
capnia from ventilation-perfusion mismatching. Anas­ position. Positions that are especially productive
tomosis of the bronchial and pulmonary vascular sys­ should be emphasized and drained longer. The patient
tems causes shunting of the systemic blood from the should be instructed to do the postural drainage even
hypertrophied bronchial arteries. It also may contribute if the treatment seems unproductive. Secretions may
to a decreased capability to take oxygen into the in­ be mobilized during treatment and it can take several
volved segments of the lung (Liebow, Hales, and Lind­ minutes for the remaining cilia to sweep the mucus far
skog, 1949; Luce, 1994). enough up the tracheobronchial tree to be expecto­
Most patients complain of relatively few symp­ rated or swallowed.
toms, except during a respiratory infection when they Pulmonary function tests of patients with localized
have an increased cough and sputum production. The bronchiectasis show few or no abnormalities. How­
amount of sputum expectorated and the severity of ever, in more widespread disease, there is a reduction
the cough vary from patient to patient, according to in the FEV I, maximum midexpiratory flow rate, max­
the amount of involvement. Hemoptysis does occur imal voluntary ventilation (MVV), diffusing capacity,
in about half of the older patients, evidently because and an increase in the residual volume (Luce, 1994).
of erosion of enlarged bronchial arteries that accom­ Hospitalized patients with bronchiectasis may be
pany the dilated bronchi. treated with postural drainage, percussion, vibration,
Effective postural drainage, percussion, vibration, and/or the forced expiratory technique, intravenous
and the forced expiratory technique (FET) are impor­ fluids, antibiotics, supplemental oxygen and other
tant in the management of bronchiectasis (Gallon, medications (Stoller and Wiedemann, 1990; Luce,
1991; van Hengstum et aI, 1988; Sutton, 1983; Ver­ 1994). Long-term medical management may include
boom, Bakker, and Sterk, 1986) (see Chapter 20). ,It a broad-spectrum antibiotic taken orally 10 to 14
should be done as frequently as indicated in patients days per month, low-flow oxygen for hypoxemia,
with a productive cough. Postural drainage should be postural drainage, avoidance of bronchial irritants
done I hour before retiring at night to facilitate the ex­ (e.g., cigarette smoke and air pollution) and other
pectoration of secretions that would interfere with rest measurers. Some patients may have surgical resection
by stimulating violent coughing when the patient if their area of involvement is quite limited or to con­
changes positions. It should also be done on arising in trol hemoptysis. It is most important that these pa­
the morning to clear the lungs of secretions that have tients drink large volumes of water each day (2 to

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 4 Cardiopulmonary Pathophysiology 83

3 L) to keep their secretions thin so they can be ex­ spondylitis can cause lung restriction. Obesity and as­
pectorated more easily (unless fluid intake is limited cites, by limiting diaphragmatic movement, can also
for cardiac reasons). produce a restrictive defect.
Pulmonary function tests generally show a de­
Prognosis of bronchiectasis
creased vital capacity, inspiratory capacity, and total
Before the antibiotic era, the prognosis for individuals lung capacity, whereas the residual volume can be
with bronchiectasis was poor. As might be expected, normal or reduced. If the restriction is pulmonary in
infection was usually the precipitating cause of death. origin, there is a reduction in the lung compliance
However, at the present time, the prognosis of patients and the diffusing capacity.
with proper medical management is much improved Many of these restrictive disorders are discussed
(Sanderson et aI, 1974; Ellis et ai, 1981). Most studies in Chapter 5. Since obstructive lung diseases are en­
show that about 75% of the patients have an improved countered much more often than restrictive disorders,
symptom complex since diagnosis and lead relatively they have been discussed in greater detail. The fol­
normal lives. Cor pulmonale, a complication of dif­ lowing is a brief examination of some of the restric­
fuse, long-standing bronchiectasis, accounts for about tive lung diseases.
50% of the deaths (Konietzki, Carton, and Leroy,
1969). Pneumonia and hemorrhage are less common
Diffuse Interstitial Pulmonary Fibrosis
causes of death. With modern therapy, only a few pa­
tients succumb to respiratory infections or their com­ This disease is known as diffuse interstitial pul­
plications. Few children who develop bronchiectasis monary fibrosis (IPF) in the United States and cryp­
live beyond their 40s. Repeated bronchopulmonary in­ togenic fibrosing alveolitis in Europe (Reynolds, and
fections can contribute to worsening pulmonary func­ Matthay, 1990). IPF represents a common histologic
tion and an earlier death. Before the antimicrobial era, response to a wide variety of insults (Weg, 1982).
most patients with untreated, widespread, severe Initially, some type of injury to the pulmonary
bronchiectasis died within 25 years. Today prognosis parenchyma causes an influx of inflammatory and
for each individual depends on the extent of the dis­ immune cells, resulting in a diffuse inflammatory
ease process at the time of diagnosis and on proper process distal to the terminal bronchiole (alveolitis).
medical management. Patients with moderate, local­ This can progress to subacute interstitial disease with
ized disease, if treated properly, may have a relatively the presence of acute and chronic inflammatory ceUs.
normal life expectancy. Chronic disease is manifest by thickened alveolar
walls and progression to fibrosis.
The etiologic factors of this condition are uncer­
RESTRICTIVE lUNG DISEASE
tain. Similar conditions can be produced by certain
A restrictive disease is characterized by lungs that are drugs or poisons and are found in patients with
prevented from expanding fully. Normally during in­ rheumatoid arthritis and systemic sclerosis. There
spiration, the diaphragm descends, the dimension of appears to be a genetic factor, since twins, siblings,
the chest increases laterally and anteriorly, and the and other members of the same family have been re­
lung tissue expands as it fills with air. Hence an ab­ ported with diffuse interstitial pulmonary fibrosis.
normality in any of these areas can produce a restric­ This condition has also been reported in a few indi­
tive pattern. For example, a decrease in compliance viduals with Raynaud's phenomenon, ulcerative col­
or elasticity of the lung parenchyma, such as intersti­ itis, and other diseases, but their exact relationship
tial fibrosis, sarcoidosis, pneumoconiosis, and sclero­ remains unclear.
derma, can produce this defect. Pleural abnormalities The most common early symptoms are fatigue,
such as pleural effusion (by direct compression) can dyspnea on exertion, and a chronic unproductive
prevent the lungs from expanding fully. Thoracic cough. As the disease progresses, the patient becomes
changes such as kyphoscoliosis and ankylosing steadily more dyspneic and cyanotic. On auscultation,

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84 PART I Cardiopulmonary Function in Health and Disease

one notes sharply crackling rales. Chest expansion is Since a pattern of DIP is commonly seen along with
reduced and clubbing of the digits is often present. usual interstitial fibrosis (UIP) or IPF, some believe
The chest x-ray usually indicates diffuse reticu­ that DIP likely represents an earlier and more re­
lar markings, most prominent in the lower lung versible stage of IPF.
fields. Sometimes, a gallium citrate Ga 67 isotope Cortiocosteroids are the mainstay of treatment for
scan of the lungs is conducted to assess the overall IPF (Reynolds and Matthay, 1990). A trial of im­
inflammation of the lung parenchyma (Line et ai, munosuppressive therapy is almost a l ways pre­
1978; Turner-Warwick and Haslam, 1987). scribed for a period of time. Obj ective measures
Pulmonary function tests show a reduced vital ca­ such as blood counts, erythrocyte sedimentation rate,
pacity and total lung capacity with no impaired flow pulmonary function testing, particularly exercise
rates (Keogh and Crys tal, 1980; Reynolds and tests with measurement of arterial oxygen desatura­
Matthay, 1990). Compliance is markedly reduced to tion and diffusing capacity BAL fluid analysis and
less than half of the predicted value. A reduced diffus­ the patient's symptoms must demonstrate improve­
ing capacity is the earliest and most consistent change. ment or the medication should be discontinued. A
At first, the arterial Pa02 may be normal at rest but composite clinical roentgenographic, physiological
may drop significantly with exercise. The Paco2 is re­ score (CRP score) of eight variables has been devel­
duced as a result of hyperventilation, and the pH is oped that allows quantification of the clinical course
kept normal by renal compensation. Later the Pao2 is and the re sponse to therapy in individual patients
markedly reduced because of the thickened alveolar (Watters et ai, 1986). If effective, medications are
membrane and ventilation-perfusion mismatching. usually continued for a year and then a decision is
Bronchoalveolar lavage (BAL) is often used to as­ made about continuing or tapering the dosage.
sess the amount of inflanunation and the accumulation Individuals who are not responsive to corticos­
of immune effector cells and proteins in the alveoli teroids may be placed on other immunosuppressive
(Crystal, et ai, 1981; Rudd, Halslam, and Turner-War­ drugs such as cyclophosphamide, azathioprine, or
wick, 198]). The technique consists of wedging a penicillamine (Turner-Warwick, 1987; Reynolds and
fiberoptic bronchoscope in a sublobar airway, then in­ Matthay, 1990). Penicillamine is more effective in
fusing 20 to 50 ml aliquots of saline into the periph­ patients with connective tissue diseases and intersti­
eral airway, which are immediately aspirated by sy­ tial fibrosis other than those with IPF.
ringe. A total of 150 to 300 ml is ins tilled and Patients should stop smoking at once. Supplemen­
recovered. The fluid and cells are analyzed (Reynolds, tal oxygen is important with exercise as there is a
1987). High-intensity alveolitis is defined by 10% or characteristic significant fall in arterial oxygen ten­
more polymorphonuclear granulocytes (PMNs) in sion ( Pa02) (Hammon a n d Mc C a f f ree, 1985;
BAL cell differential counts; low-intensity alveolitis Reynolds and Matthay, 1990). Individuals that re­
consists of 10% PMNs or less (Reynolds, 1986). quire more than 4 L flow/min by nasal prongs may
Lung biopsies that demonstrate an abundance of prefer direct administration of oxygen into the tra­
inflammatory cells suggest early disease, whereas a chea. In addition to supplying higher concentrations
prevalence of fibrosis is indicative of advanced dis­ of oxygen to the lungs, many patients prefer the cos­
ease. A distinct category of IPF has been described metic effective of not wearing obvious nasal prongs.
and may be clinically useful (Liebow, Steer, and Patients that have refractory disease limited to the
Billingsley, 1965). Desquamative interstitial pneu­ lungs may be candidates for single or double lung trans­
monitis (DIP) is characterized by an intraalveolar ac­ plantation. There have been significant advances in the
cumulation of mononuclear cells, relatively intact success of lung transplantation in recent years (Toronto
alveolar walls without destruction or fibrinous exu­ Lung Transplant Group, 1988) (see Chapter 38).
dates (numerous inflammatory cells with little or no Individuals with the subacute form described by
fibrosis). This pattern has correlated with a more be­ Hamman and Rich usually die within 6 months
nign course and a better response to corticosteroids. (Hamman, 1944). Patients with the chronic form,

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 4 Cardiopulmonary Pathophysiolog)' 85

treated with steroids, may survive for as long as 15 complex. Over time, it can eventually result in a form
years. Untreated, these patients most often die within of interstitial pu lmonary fibrosis with honeycombed
I to 4 years. Cause of death is usually related to res­ lung changes on chest x-ray and a restrictive pattern
piratory or heart failure, although an unexpected on pulmonary function tests.
number have died from adenocarcinoma and undif­ This disease is more common in women (Seder­
ferentiated or alveolar cell carcinoma of the lung. linic, Sicilian, and Gaensler, 1988). Their symptoms
include an acute respiratory illness with fever, night
sweats, weight loss, and dyspnea. It can be confused
Pulmonary Infiltrates With Eosinophilia
with tuberculosis, but these patients deteriorate when
Eosinophils are commonly present in lung tissue as treated with antituberculosis drugs. This disease must
part of the body's cellular response to a variety of also be differentiated from eosinophilic granuloma
agents and systemic immunologic diseases (Butter­ and the desquamative form of idiopathic interstitial
worth and David, 1981). They are present in the air­ pneumonitis. Dense infiltrates located in the periph­
ways and lung tissue of patients with idiopathic pul­ ery of the lung on chest x-ray provide an important
monary fibrosis. In interstitial lung disease that clue. Often, a lung biopsy is necessary to confirm the
appears to have an allergic component (e.g., hypersen­ diagnosis. Treatment with cortiocosteroids produces
sitivity pneumonitis, drug-induced lung syndromes, a striking improvement in the patient's symptoms and
sarcoidosis) eosinophils are a minor component of tis­ chest x-ray in just a few weeks.
sue reaction. However, in certain primary or systemic
diseases, eosinophils can be the most conspicuous in­
Eosinophilic granuloma
flammatory cell present in the lung. These conditions Eosinophilic granuloma (or histiocytosis X) can ei­
can be grouped t o g ether and referred to a s ther be a unifocal disease effecting only the lungs or
eosinophilic syndromes (Crofton e t aI, 1952). Consid­ a multifocal disease involving the bones of the skull,
erable overlapping exists among these syndromes as mandible, vertebra, pelvis, ribs, and extremities
their etiologic factors and pathogenesis remains (Groopman and Golde, J 981; Marcy and Reynolds,
poorly understood (Reynolds and Matthay, 1990). 1985). Lung involvement is characterized by an inter­
stitial granuloma composed of moderately large, pale
Simple pulmonary eosinophilia histiocytes and eosinophils, and arteriolitis with
This is a self-limiting disease with chest x-ray eosinophils. The histiocytic process with eosinophils
demonstrating migratory, fleeting areas of pulmonary then involves bronchioles, alveolar ducts, and alveo­
infiltrates located in the periphery of the lungs along lar septa, which results in their destruction. The pro­
with minimal respiratory symptoms and blood liferative endarteritis causes necrosis.
eosinophilia (Crofton et aI, 1952). Certain drugs such This disease most commonly effects men in their
as sulfonamides have been implicated as a cause 30s or 40s. They usually have symptoms of fatigue,
(Reynolds and Matthay, 1990). This disease is also malaise, weight loss, a nonproductive cough, dyspnea
referred to as Loeffler's pneumonia and the PIE syr­ on exertion, and chest pain, sometimes related to a
drome (peripheral infiltrates with blood eosinophilia) pneumothorax or rib lesions. The chest radiograph
(Crofton et aI, 1952). If the Jisease is related to an al­ often indicates a diffuse micronodular and interstitial
lergic rcsponse LO microfilaria, human parasites (e.g., infiltrate initially involving the middle and lower
Ascaris lum.briocoides, Strongyloides stercoralis), or lung fields. In more advanced disease, small cystic
cat and dog parasites (ascarids) that produce visceral areas develop in the infiltrate, producing a honey­
larva migrans, it is termed tropical eosinophilia. comb pattern. Spontaneous pneumothorax is a com­
plication in approximately 25% of cases.
Prolonged pulmonary eosinophilia The course of the disease varies (Reynolds and
As implied by the name, this disease is more chronic Matthay, 1990). Spontaneous regression with residual
than the simple form, with a more severe symptom symptoms may occur in 10% to 25% of cases. In

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86 PART I Cardiopulmonary Function in Health and Disease

many patients, the disease stabilizes or "burns out," findings may include fine inspiratory rales, dullness to
leaving them with a moderate pulmonary impairment percussion and, in the later stages, cyanosis and club­
as a result of fibrosis, cystic lung changes and a re­ bing. Pulmonary function studies usually show a de­
strictive defect on pulmonary function tests. Dyspnea creased vital capacity, functional residual capacity arid
on exertion is common. Some patients have persistent diffusing capacity. Arterial blood gases indicate a low
bronchitis. Cortiocosteroids are not particularly effec­ Pao2, especially during exercise, with normal Paco2,
tive. Treatment is mainly symptomatic, with judicious and pH (Rogers et aI, 1978).
use of antibiotics and bronchodilators. Occasionally, The treatment of choice for patients with moderate
progressive pulmonary disease leads to cor pulmonale to severe dyspnea on exertion from alveolar pro­
and respiratory failure. teinosis is bronchial alveolar lavage (Rogers and
Tatum, 1970; Rogers, Graunstein, and Shuman
1972). The patient is taken to the operating room
Pulmonary Alveolar Proteinosis
where, after general anesthesia and placement of a
Pulmonary alveolar proteinosis is a rare disease of double-lumen tube (which isolates each lung), the pa­
unknown origin, characterized by alveoli filled with tient is turned in the lateral decubitus position with
lipid-rich "proteinaceous" material and no abnormal­ the lung to be lavaged downward. The double-lumen
ity of the alveolar wall, interstitial spaces, conducting tube enables the patient to be ventilated by the upper­
airways or pleural surfaces. Most often it is found in most lung while the lower lung is carefully filled with
men between the ages of 30 and SO, although it has saline to the functional residual capacity. Then an ad­
been reported in patients of all ages and both sexes. ditional 300 to 500 ml saline are alternately allowed
The most common symptoms are progressive dysp­
nea and weight loss, with cough, hemoptysis and chest
pain reported less frequently (Claypool, Rogers, and
Matuschak, 1984). Chest x-ray reveals diffuse bilateral
(commonly perihilar) opacities (Figure 4-10). Physical

FIGURE 4-10 FIGURE 4-11

Pulmonary alveolar proteinosis. PA chest film demonstrates A patient with pulmonary alveolar proteinosis in the
an irregular, patchy, poorly defined confluence of acinar operating room undergoing bronchial alveolar lavage of her
shadows which are symmetrical in both lower lung fields. left lung. Percussion is done over the left lung as the saline
The appearance is very similar to pulmonary edema. runs out, increasing the amount of proteinaceous material
(Courtesy of T. H. Johnson, M.D.) removed during this procedure.

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 4 Cardiopulmonary Pathophysiology 87

to mn into and out of the ung by gravitational flow. and Matthay, 1990). If the patient is assessed during
As the saline flows out, percussion is done over the an acute episode of pulmonary hemorrhage, fine rales
lung being lavaged, and this grcatly increases the and dullness to percussion are present on physical ex-
amount of proteinaceous material washed from the amination. An enlarged liver, spleen, and lymph
lung (Figure 4-1 J). The effectiveness of mechanical nodes may be noted on palpation in 20% to 25% of
percussion, manual vibration, and manual percussion cases. The chest x-ray during acute episodes show
in removing the material from involved lungs has 'Dac naI consolidation for 2 to 3 days, then a reticular
been compared and manual percussion has been pattern identical to other interstitial diseases. The
found to be superior (Hammon, 1983; Hammon ,/' chest x-ray usually returns to normal in lO to 12 days.
'-i
Freeman, and McCaffree, 1986; Hammon, McCaf- However, after recurrent episodes with hemosiderin
free, and Cucchiara, 1993). In this procedure, a pa- deposited in the interstitial spaces, there is progres­
tient is usually lavaged with 20 to 30 L saline and is sive interstitial fibrosis .. Pulmonary function tests in-
then taken to the recovery room and later back to his dicate a decreased diffusing capacity, with or without
or her own room. After 2 or 3 days, the procedure is a fall in the patient's resting Pa02.
repeated on the opposite lung. The hemorrhage is ordinarily confined to the pe-
Most patients have significant clinical improve­ ripheral airspaces. Interestingly, massive blood loss
ment following bronchial alveolar lavage, and many into lung tissue can occur without hemoptysis or no-
have an improvement in their chest x-rays (Claypool, ticeable blood in the trachea or major bronchi
Rogers, and Matuschak, 1984). After lavage, for rea­ (Reynolds and Matthay, 1990). Sputum samples of
sons that are unclear, the material may reaccumulate BAL f l uid may c o n t ain hemosi d e r i n-l a d e n
slowly o r not at all. Some patients d o have sponta­ macrophages. After recurrent episodes of hemoptysis,
neous remissions without undergoing lavage. interstitial fibrosis is present in most cases.
Before bronchial alveolar lavage was done on The prognosis of IPH is variable with death occur-
these patients, almost all children with alveolar pro- ring somewhere between 2Y2 to 20 years after the
teinosis died, and 20% to 25% of the adults died onset of symptoms. Permanent remissions may occur
within 5 years, usually because of respiratory failure with or without corticosteroid administration. No
or cor pulmonale. Some 60% to 70% improved treatment has been shown to effectively alter the out-
greatly or recovered. The effect that bronchial alveo­ come of this disease.
lar lavage has on the long-term outcome remains to
be seen, but present results are encouraging (Clay­
Sarcoidosis
pool, Rogers, and Matuschak, 1984).
Sarcoidosis is a granulomatous disorder of unknown
origin that can effect multiple body systems (Mitchell
IdiopathiC Pulmonary Hemosiderosis
and Scadding, 1974). Typically, initial findings can
Idiopathic pulmonary hemosiderosis (IPH) is a dis­ include bilateral hilar adenopathy, pulmonary infiltra­
ease of unknown origin and is characterized by re­ tion and skin or eye lesions (Sharma, 1977). The
peated episodes of pulmonary hemorrhage, iron-defi­ lungs are the organs most often involved and some
ciency anemia, and in long-term patients, pulmonary 20% to 50% of these patients first seek medical atten­
insufficiency (Soergel and Sommers, 1962). IPH is tion because of respiratory symptoms. It affects
most commonly found in children under the age of blacks 10 to 20 times more often than whites and
10. In children, it is found with equal frequency in women twice as often as men. It usually occurs in the
both genders, but in adults, it is twice as common in third or fourth decade of life.
men as it is women. The intrathoracic changes can be classified into
This disease has an insidious onset. The patient four stages (Siltzbach et aI, 1974; Weg, 1982). In the
has symptoms of weakness, anemia, pallor, lethargy, first stage, the patient is asymptomatic, with the chest
and occasionally, a nonproductive cough (Reynolds x-ray showing bilateral hilar adenopathy and right

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88 PART I Cardiopulmonary Function in Health and Disease

FIGURE 4-12
A, Sarcoidosis in its first stage is manifested by bilateral hilar adenopathy. Usually there are no
significant physical symptoms. B, Disseminated sarcoidosis (third stage) reveals widespread
parenchymal changes with scarring. The hilar adenopathy is usually decreased. (Courtesy of
T. H. Johnson, M.D.)

paratracheal adenopathy (Figure 4- J 2, A). In the second the lungs and pleurae. The most common thoracic
stage a diffuse pulmonary infiltration is found along complication of RA is pleurisy, with or without
with the bilateral hilar adenopathy. Interstitial infiltra­ pleural effusions. Although RA occurs twice as often
tion or fibrosis, without hilar adenopathy, characterizes in women, pleuritis has a striking predilection for men
the third stage (Figure 4-12, B). In the fourth stage, em­ (Reynolds and Matthay, 1990). Pleural disease is one
physematous changes, cysts, and bullae are found. manifestation of RA, occasionaJJy causing fibrothorax
I n 60% to 90% of t h e s e p a t i e n t s w i t h h i l a r and restrictive lung disease that requires decortication.
adenopathy, the disease spontaneously regresses over Interstitial lung disease, indicated by abnormal pul­
a period of I to 2 years. About one third of the pa­ monary function tests demonstrating a restrictive venti­
tients with sarcoidosis involving the lungs also have a latory impairment and a reduced ventilatory capacity, is
spontaneous regression, usually leaving some resid­ evident in about 40% of RA patients (Frank et ai,
ual fibrosis. The remaining two thirds that have 1973). It is also more prevalent in men. The chest x-ray
chronic sarcoidosis have progressive pulmonary im­ demonstrates diffuse interstitial infiltrates, especially in
pairment, along with a variable degree of involve­ the lung bases. Pulmonary nodules, which are patho­
ment of the heart, liver, spleen, lymph nodes, mus­ logically identical to the subcutaneous nodules found in
cles, bones, and central nervous system (CNS). RA, may also oceur and cavitate (Weg, 1982).
Most patients with sarcoidosis need no treatment. C o al miners with RA may have chest x - rays
Corticosteroids, although controversial, are the most demonstrating rounded densities that evolve rapidly
effective forms of therapy for patients with sarcoido­ and undergo cavitation (Caplan's syndrome) in con­
sis that requires treatment (DeRemee, 1977; Turner­ trast to the massive fibrosis found in coal miners'
Warwick et ai, 1986). pneumoconiosis (Caplan, 1953).

Rheumatoid Arthritis SystemiC lupus Erythematosus (SlE)

Rheumatoid arthritis (RA) is a systemic disease that Although systemic lupus erythematosus (SLE) is a
principally involves the joints but also often affects systemic collagen vascular disease, some 50% to

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 4 Cardiopulmonary Pathophysiology 89

90% of these patients have pleural or pulmonary in­ group, progression results in death after several years.
volvement (Hunninghake and Fauci, 1979). Pleuritic Women seem to have a poorer prognosis than men.
chest pain often signals polyserositis associated with
SLE. Pleural effusions are a manifestation of poly­ CORONARY ARTERY DISEASE
serositis and are present in 40% to 60% of individuals
with SLE. Most often they are bilateral. Atherosclerosis
Patients with pulmonary involvement present with
dyspnea on exertion and cough productive of mucoid Pathophysiology
sputum (Weg, 1982). Rarely do SLE patients com­ To discuss CAD the process of atherosclerosis must
plain of supine dyspnea, which suggests diaphrag­ first be described. Although the specific pathogenesis
matic paralysis or a diffuse myopathy of the di­ of atherosclerosis is not known, it is hypothesized
aphragm (Gibson, Edmonds, and Hughes, 1977). that the process is initiated by trauma to the intima of
The chest x-ray usually indicates patchy, nonspe­ the arterial wall. The trauma may be related to vari­
cific densities and/or basilar linear or platelike atelec­ ous primary risk factors such as: high blood pressure
tasis. Pleural effusions and pulmonary infiltrates are and cigarette smoking.
common, whereas diffuse interstitial fibrosis is rarely High blood pressure has been indicated as a poten­
seen (Hunninghake and Fauci, 1979). tial trauma inducer, since increased pressure and turbu­
Pulmonary function tests often indicate a restric­ lence may damage the endothelial cells of the intima,
tive pattem with a decreased diffusing capacity and a thus exposing the media to the circulation. The media,
reduced arterial oxygen saturation. which is composed primarily of smooth muscle is
thought to be the origin of the atherosclerotic lesion.
Cigarette smoking has also been indicated as a po­
Progressive SystemiC Sclerosis (Scleroderma)
tential trauma inducer. However, the hypothesized
Progressive systemic sclerosis (scleroderma) is a rare mode of injury is different than that observed with in­
disease that causes thickening and fibrosis of the con­ creased blood pressure. Cigarette smoke is high in
nective tissue of mUltiple parts of the body with re­ carbon monoxide and hydrocarbons that are carried
placement of many elements of the connective tissue by the red blood cells and the plasma. It is thought
by colloidal collagen. The skin is most often in­ that the hydrocarbons or carbon monoxide bind to the
volved, although the lungs, heart, kidney, bones, and endothelial cells, causing damage and possibly death
other parts of the body can also be affected. to these cells.
Approximately one half to two thirds of the pa­ Once the media is sufficiently exposed to the circu­
tients with progressive systemic sclerosis have pul­ lation the process of atherosclerosis is initiated.
monary involvement (Reynolds and Matthay, 1990). Platelets aggregate at the injury site and release sub­
Many of these patients with pulmonary involve­ stances that induce endothelial and smooth muscle
ment are asymptomatic, although symptoms can in­ cell replication. It is at this site that fatty streaks and
clude weight loss, progressive dyspnea, low-grade fibrous plaques are developed. The cause of fatty
fever, and cough (sometimes producing mucoid spu­ streak development is that low-density lipoproteins
tum). Chest x-ray shows a characteristic fibrosis of the (LDLs) deposit fat into the smooth muscle of the
mid and lower lung fields. Auscultation often reveals media. Why this occurs is unknown, but apparently is
bibasilar rales. Pulmonary function tests reveal a re­ related to the smooth muscle cell proliferation and
strictive defect with impaired diffusion. perhaps increased need for energy. The initial fatty
D-penicil lamine is the best treatment for pul­ streaks are generally only slightly raised and do not
monary involvement in patients with progressive sys­ imperil circulation. However, when a fibrous plaque
temic sclerosis (DeClerk et ai, 1987). develops, the characteristic impingement of the vessel
Prognosis of patients with only skin and joint in­ lumen occurs. The plaque is somewhat hard and con­
volvement is much better than for those that have in­ sists of connective "scar-like" tissue, smooth muscle
volvement of the heart, lungs and kidneys. In the latter and fat. Finally, the plaque may undergo calcification

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90 PART I Cardiopulmonary Function in Health and Disease

or lead to hemorrhaging if the vessel wall necroses. angina, the episodes are more frequent and the dura­
The result is decreased blood flow (ischemia) and tion of each event is usually greater than 15 min­
oxygenation (hypoxia), or complete lack of blood utes. In addition the intensity or the pain may be
flow and oxygen (anoxia) to the target organ. more severe. Unstable angina is usually an indicator
of CAD progression. Individuals with unstable
Risk factors angina are at greater risk to have a myocardial in­
As described above high blood pressure, cigarette farction (MI). Unstable angina is less responsive to
smoking and hyperlipidemia are direct or primary treatment using rest and sublingual nitrates. Often
risk factors for causing atherosclerosis. Secondary times, the individual must be hospitalized and
risk factors are age, gender, race, obesity, stress, and treated with IV nitrates.
activity level. Several risk factors are modifiable and
i n c l u d e: (I) h y pertension, (2) h y pe r l i p idemia, Variant angina
(3) smoking, (4) obesity, (5) stress level, and activity Variant angina occurs while the individual is at rest,
level. It is interesting to note that the "big three" pri­ usually during waking and often at the same time pe­
mary risk factors are all modifiable by the individual. riod. Exertion does not influence variant angina.
Reducing risk factors can reduce the probability of However, the angina may benefit from rest and sub­
CAD by five- to ten-fold (Ornish et aI, 1990). lingual nitrates. Like unstable angina the pain is in­
tense and of longer duration and likely to lead to an
MI. In addition, arrhythmias are more likely to occur
CLINICAL SYNDROMES ASSOCIATED WITH CAD with an individual who has variant angina, as com­
pared with exertion related angina (i.e., stable and un­
Angina Pectoris
stable). Stable and unstable angina are believed to be
Angina pectoris is defined as chest pain that is related caused primari Iy by progressive arterial occlusion
to ischemia of the myocardium. However, the pain and ischemia. It is believed that variant angina is
referred from ischemia may be in the left shoulder, caused by a combination of occlusion and coronary
jaw, or between the shoulder blades. Angina can be artery spasm. Therefore variant angina has been suc­
classified as stable, unstable, or variant. cessfully treated with calcium channel blockers.

Stable angina Prognosis of angina

Stable angina generally occurs during physical effort Individuals do not die from angina. The progression
but may be related to stress. The individual is able to of atherosclerosis of coronary arteries is a change
describe what type and intensity of activity causes the from the clinical signs of angina to MI, which is dis­
angina. Stable angina is characterized by substernal, cussed on p. 91. However, even though there is no
usually nonradiating pain that lasts between 5 to 15 risk for mortality from angina, an individual's
minutes after the offending incident. Care would in­ lifestyle can change drastically. People with angina
volve sublingual nitrates and cessation of the activity may be fearful of being active and may deny that
causing the angina. Usually the angina subsides com­ they are having exertion-related chest pain. Denial of
pletely with treatment. However, angina brought CAD, depression and anger are common manifesta­
about by emotional stress is more difficult to treat, tion for individuals with angina, though it has rarely
since the stress cannot be stopped as easily as cessa­ been studied (Beckham et ai, 1994). The result of
tion of exercise. angina (diagnosed or undiagnosed and denied) can be
depression and potentially further decline in physical
Unstable angina activity. Although rest is an important aspect of treat­
Unstable angina also occurs during physical exer­ ment, it is well-documented that even low levels of
tion or psychological stress. The major difference activity can modify several risk factors and arrest the
between stable and unstable angina is the frequency, progression of the disease process (Niebauer et ai,
duration and intensity of the pain. In unstable 1995). Research is sti II underway to determine if

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 4 Cardiopulmonat'y Pathophysiology 91

CAD is reversible when lifestyle adjustments are ini­ crease in cardiac performance at rest and during mini­
tiated (Ornish et ai, 1990; Schuler et ai, 1992). mal to moderate activity (Cahalin, 1994). However
the location and the extent of the MI is also critical.
MIs located in the inferior portion of the heart are the
Myocardial Infarction
least significant, and partial wall thickness is less sig­
MI is defined as necrosis of a portion of the my­ nificant than a transmural MY.
ocardium. The death of the myocardium occurs as a Treatment, The treatment for an uncomplicated MI is
result of ischemia and anoxia. The vessels affected initially like the complicated MI, where the patient is
are the right and left coronary arteries. The right cared for in the coronary care unit. The medical treat­
coronary artery supplies portions of the inferior sec­ ment is designed to decrease myocardial work and
tion of the left ventricle and the posterior section. oxygen demand. Therefore patients are on oxygen
The left coronary artery branches and forms the cir­ and administered vasodilators (nitroglycerin) to in­
cumflex and anterior descending arteries. The cir­ crease myocardial blood flow and analgesics to help
cumflex supplies the lateral portion of the left ventri­ further reduce ischemic pain. In addition, to reduce
cle, while the anterior descending artery supplies the contractility of the myocardium, calcium channel
anterior portion. In addition, the right coronary blockers or beta-blockers are administered. Finally,
artery supplies the right atrium atrial-ventricular antiarrhythmia medication may be prescribed if an
(AV) bundle and the right ventricle. The left coro­ aberrant cardiac rhythm is present or is highly proba­
nary artery supplies the left atrium and the primary ble to occur.
portion of the conduction pathway. Generally, the Since the course is uncomplicated, this means
clinical symptoms are similar to that of angina, with that a patient's stay in the coronary care unit may be
emphasis on extreme pressure as well as tightness only 2 to 3 days, with a total hospital stay of 7 to 10
over the sternum region. In addition, pain can radiate days. Treatment following leU discharge is oriented
to the jaw, upper back, and shoulders (with left more toward increasing physical activity and in educating
frequent than right). the patient and family in risk factor reduction.
MIs can be classified into categories by size, loca­ This process is described as cardiac rehabilitation
tion, and degree of myocardial wall involvement. The Phase 1.
terms small and large are often used to describe MIs.
However, degrees of complication are also used in Complicated myocardial infarction
conjunction with size. MIs can be described as un­ A complicated MI is different from an uncomplicated
complicated and complicated based on size of the MI case since the patient may have one, a combination,
and recovery of the patient. Location indicates the or all four of the following conditions/complications:
portion of the heart involved and also what coronary (I) arrhythmia, (2) heart failure, (3) thrombosis, and
artery or branch that is at fault. As described above, (4) damage to heart structures.

the general regions of the heart are anterior, posterior, Arrhythmias. Arrhythmias occur in 95% of all pa­

lateral, and inferior. Finally, MIs are classified by the tients with MIs. The type and severity of the arrhyth­

extent of the wall damage. A transmural infarct (or mia is dependent on the extent of myocardial damage

full wall) extends from the endocardi um to the epi­ and the location of the damage. As described earlier,

cardium. There is the potential that only a small por­ the uncomplicated MI patient usually has a small area

tion of the ventricle wall is affected, such as just of the myocardium involved; thus the potential ar­

below the epicardium (subepicardial) and just below rhythmias are less dangerous and occurrence is less

the endocardium (subendocardial). common. Arrythmias that are life-threatening include

(I) complete A V heart block, (2) ventricular paced

Uncomplicated myocardial infarction
arrhytlImia, and (3) ventricular tachycardia, including
An uncomplicated MI is described as a small infarc­ ventricular flutter and fibrillation. In these conditions,
tion with no complications during recovery. UsuaUy either the heart rate is too slow and thus cardiac out­
the result is full recovery without a significant de­ put is impaired, or the heart rate is too rapid with

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92 PART I Cardiopulmonary Function in Health and Disease

poor stroke volume and ejection fraction, and again considered a distinct possibility in all surgical, MI,
impaired cardiac output. Treatment of the above con­ and gunshot patients.
ditions is immediate and requires drugs and poten­ Heart wall or mural wall thromhosis can lead to an
tially, electrical shock (for flutter/fibrillation). Usu­ emboli lodging in the brain, intestine, kidney, artery
ally, an artificial pacemaker is implanted once the to the extremities, or any location in the systemic ar­
patient is stabilized. terial circulation. Usually mural thrombosis do not
Heart failure. Another complication following MI is affect the pulmonary system, since even the smallest
heart failure. Heart failure is a condition where the fragments are caught in capillary beds and do not
heart is weakened and is unable to produce a signifi­ enter into the venous system.
cant cardiac output to meet the bodies need for oxy­ Structural damage. The last complication is structural
gen, nutrition, and removal of waste products. When damage to critical myocardial tissue that affects heart
the heart experiences ischemia the myocardium con­ function. If conductant pathway (bundle branch) tis­
tracts with less force, and conduction abnormalities sue located primarily at the septum is damaged, ar­
may alter the mechanics of the contraction. If an area rhythmias result. In addition, papillary muscles that
of the heart is infarcted, the affected myocardium assist in closing valves can be infarcted. The result of
does not contract, thus affecting overall cardiac out­ improper valve function is decreased cardiac output.
put. Another type of heart failure not directly related Besides these two critical tissues, if significant full
to ischemia and infarction is congestive heart failure thickness damage occurs to the myocardial wall car­
(CHF) (see Congestive Heart Failure, p. 000). diac function is compromised. HeaIt waJJ damage can
Immediately post-MI, cardiac output is reduced result in venlricular aneurysms or ventricular wall
significantly. However, the compensatory response is rupture. Ventricular aneurysm or bulging of the weak­
to increase sympathetic innervation, resulting in in­ ened ventricular wall oecurs in transmural (full wall
creased heart rate and myocardial contractility. The thickness) infarcts. Ventricular wal I rupture, which
result of this compensation is a cardiac output that can occur acutely following transmural infarction, but
may approach normal resting values. However, if the more often occurs in the first to second week post-MI
damage has been great, the kidneys compensate by following an aneurysm is usually fatal. Therefore fol­
retaining sodium and water in an attempt to improve lowing a n MI, it is critical to determine i f an
circulatory volume and venous return. Depending on aneurysm has occurred in the myocardium so that ap­
the amount of myocardial tissue death, the individual propriate surgical intervention can be performed.
may survive with resulting chronic congestive heart Treatment. The treatment for a complicated MI is
failure through persistent fluid retention and hypoten­ initiaJly like the uncomplicated MI, where the patient
sion. If grcater than 40% of the left ventricle is in­ is cared for in the coronary care unit. The medical
farcted, the result is usually cardiogenic shock fol­ treatment once again is designed to decrease myocar­
lowed by death of the individual. dial work and oxygen demand. Patients are on oxy­
Thrombosis. Another complication is increased inci­ gen and administered vasodilators (nitroglycerin) to
dence of thrombosis from deep leg veins and from increase myocardial blood flow and analgesics to
the damaged heart itself. Thrombosis from deep leg help further reduce ischemic pain. Myocardium cal­
veins occurs from lower limb inactivity and circula­ cium channel blockers or beta-blockers are adminis­
tory stasis. This is a complication that can be ob­ tered to reduce contractility. Finally, antiarrhythmia
served for all surgical patients. Emboli from deep leg medication are prescribed if an aberrant cardiac
vein thrombus usually result in pulmonary complica­ rhythm is present.
tions. If the emboli are large or numerous the result Individuals with a complicated MI have a much
can be pulmonary tissue infarction and potentially longer stay in the coronary care unit, and their total
death. The incidence of pulmonary emboli has grown hospital stay time is greatly increased when com­
less since early ambulation is now the rule rather than pared with the uncomplicated MI patient (Topol,
the exception. However, a pulmonary embolj must be 1988). The time in coronary care and total hospital

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 4 Cardiopulmonary Pathophysiology 93

stay are dependent on the complications that occur of pressure and resistance the heart must overcome to
following the MI. Individuals with heart failure, eject blood into the systemic circulation (afterload);
thrombolytic events, or structural damage requiring and myocardial contractility, which is the amount of
surgery may be in the coronary care unit for more force the left ventricle can apply to the blood within
than 2 weeks. Total hospital stay time for compli­ the chamber. If any of these three variables are nega­
cated MI patients may exceed 2 to 3 weeks (Topol, tively affected then cardiac output is reduced. The
1988). However, treatment following ICU discharge cause of heart failure is often decreased contractility.
is similar to that of the uncomplicated MI patient
Acute heart failure
with the goal of increasing physical activity and in
educating the patient and family in risk factor reduc­ If an individual has a significant myocardial infarc­
tion. The major difference in Phase I cardiac rehabili­ tion, the contractility and pumping ability of the heart
tation for the complicated versus the uncomplicated is immediately reduced. The initial result is decreased
MI patient is the initial workload intensity, duration, cardiac output and damming of blood in the veins.
and frequency (i.e., much lower workload for compli­ The result is increased systemic venous pressure.
cated MI patient) (Rowe, 1989). Progression is also This acute phase, which may reduce cardiac output to
usually a bit more conservative, since the probability 40% of normal resting values is short-lived lasting
for a recurrent MI event is much greater in the com­ only a few seconds before the sympathetic nervous
plicated MI patient (Rowe, 1989). system is stimulated, and the parasympathetics be­
come reciprocally inhibited. Sympathetic innervation
Prognosis post-myocardial infarction
causes an increase in contractility of viable myocar­
Prognosis following MI is dependent on many fac­ dial tissue, and the increase in cardiac output may be
tors. Usually cardiovascular peliormance is reduced, 100%. In addition, sympathetic innervation also in­
unless the structural damage to the ventricle is minor creases venous return, since the tone of blood vessels
(as in the case of many uncomplicated MI patients). is increased. The result is increased systemic filling
The most important factor is extent of ventricular pressure, and thus increased preload. The sympa­
damage. However, with early detection of transmural thetic reflex following MI becomes maximally opera­
infarction and improvement in surgical intervention tional within 30 seconds; therefore, besides some
and coronary care, acute post-MI deaths have been pain and fainting, an individual with a mild MI may
reduced (Wenger, 1984). Other critical factors in­ not know they just suffered a heart attack! The sym­
clude remaining cardiac capacity and status of CAD. pathetic response can continue with cardiac output
Even though CAD mortality has declined in the maintained at an adequate level for quiet rest. How­
United States, the disease remains the top cause of ever, the individual may still have persistent ischemic
sudden death in adults. pain that should be assessed as quickly as possible.

Chronic heart failure

Cong.estive Heart Failure
Following a MI several physiological responses
CHF is characterized by the inability of the heart to occur besides sympathetic reflex compensation. The
maintain adequate cardiac output. The etiologic fac­ kidney begins to retain fluid almost immediately fol­
tors of heart failure is usually from ischemia and MI lowing an MI. The reasons appear to be related to de­
secondary to CAD. For the heart to maintain an ap­ creased glomerular pressure secondary to decreased
propriate amount of blood flow to the pulmonary and cardiac output. In addition, there is an increase in
systemic circulation, heart rate and stroke volume renin output and therefore an increase in angiotensin
must be adequate. Usually, stroke volume is the criti­ production. Angiotensin promotes reabsorption of
cal factor to maintain adequate cardiac output. Stroke water and salt from the renal tubules. The effect of
volume is a function of the amount of blood in the left moderate fluid retention is an increase in blood vol­
ventricle at the end of diastole (preload); the amount ume and an increase in venous return. This once

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94 PART I Cardiopulmonary Function in Health and Disease

again increases preload and thus cardiac output. result can be deterioration of the myocardium. As the
However, if the MI was severe, the result can be ex­ heart weakens, not only is systemic blood flow com­
cess fluid retention. This results in detrimental effects promised, but so is the coronary system. The area
of edema and overstretching of the heart, since blood most affected is the suhendocardial region. As these
volume and venous return is too great. cells become infarcted, the heart weakens further
In addition to increased kidney retention of fluid, a until other regions of the heart also become ischemic
second process that is activated immediately follow­ and infarcted. The entire process described from the
ing an MI is recovery of the myocardium. New col­ acute to chronic stages is congestive heart failure.
lateral arteries are formed to supply the peripheral
Prognosis
portions of the infarcted region. This revasculariza­
tion can assist cells that were marginally active to be­ The result without pharmaceutical or surgical inter­
come fully functional again. In addition, the unaf­ vention (heart transplantation) is death. Pharmaceuti­
fected myocardial cells hypertrophy. The result in a cal intervention to halt or to delay heart failure is
mild to moderate MI is a great improvement in car­ with diuretics to reduce fluid levels and cardiac gly­
diac function that takes 6 weeks to several months, cosides such as digitalis to improve myocardial con­
depending on extent of injury. tractility. This pharmacological treatment is com­
bined with modification of salt and fluid intake.
Compensated and decompensated heart failure
Finally, in cases when the heart has not compensated
The final state following acute and chronic physio­ well and the myocardium has sufficiently weakened
logical changes is called compensated heart failure. so that cardiac output is minimal, then heart trans­
In this state, the heart is able to pump blood effec­ plant is the only recourse. Since organ donors are not
tively, but at a reduced cardiac output compared with readily available, the number of individuals who need
the pre-MI condition. The individuals cardiac reserve new hearts far outnumber the donor organs. As de­
has been greatly reduced. The cardiac reserve can be scribed previously, once the heart has had enough tis­
defined as the difference between the maximum car­ sue damage to greatly reduce the cardiac reserve, the
diac output attainable minus the resting cardiac out­ prognosIs IS poor.
put. When an individual exercises or is active at a
heavy load, they experience the same symptoms of
SUMMARY
acute heart failure, because the heart is unable to sup­
ply the cardiac output required of the activity. The The first portion of the chapter has described the es­
symptoms include rapid heart rate, pallor, and di­ sential pathophysiological features of obstructive and
aphoresis. Decompensated failure occurs when the restrictive lung diseases. Obstructive disorders are
heart is so severely damaged or weakened that nor­ characterized by a decreased rate of airflow during
mal cardiac output can not be attained. The result is expiration (as a result of increased airway resistance).
that cardiac output is not high enough to allow for Restrictive disorders are conditions in which the in­
normal renal function. Fluid continues to be accumu­ spiratory capacity of the lungs is restricted to less
lated and the heart is stretched more and weakened than the predicted normal.
further so that only moderate-to-Iow quantities of A knowledge of the pathophysiology of pulmonary
blood can be pumped. With unilateral left ventricle dysfunction assists the practitioner in relating the
heart failure the left ventricle fails, while the right pathophysiology to the clinical signs and symptoms,
ventricle continues to pump vigorously. The result and the appropriate treatment goals and interventions.
can be increased blood volume and pulmonary capil­ The second portion of this chapter has described
lary pressure in the lungs. If this occurs, fluid begins the essential pathophysiological features of CAD.
to filter into the interstitial spaces of the alveoli re­ CAD results from atherosclerosis. The clinical syn­
sulting in pulmonary edema and suffocation. Even if dromes associated with CAD are angina, MI, and
the heart does not have a unilateral dysfunction the heart failure.

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 4 Cardiopulmonary Pathophysiology 95

A knowledge of the pathophysiology of CAD en­ Caplan, A. (1953). Certain unusual radiological appearanccs in
chest of coal miners suffering from rheumatoid arthritis. Tho­
ables the clinical practitioner to relate the etiologic
rax 8, 29-37.
factors and pathophysiology to the clinical signs and
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Cosio, M. (1978). The relations between structural changes in
small airways and pulmonary function tests. New England
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DeClerk, c., et al (1987). D-penicillamine therapy and interstitial
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Siltzbach, L., et al (1974). Course and prognosis of sarcoidosis ington, DC: US Department of Health and Human Resources.
around the world. American Journal o/Medicille 57, 847-852. van Hengstum M., et al (1988). Conventional physiotherapy and
Simpson, D. (1975). Bmnchiectasis. Hosp Med II, 94. forced expiratory manoeuvres have similar effects on tracheo­
Snider, G., Faling, c., & Rennard, S. (19 9 4) . Chronic bronchitis bronchial clearance. European Journal ojRespiralory Diseases
and emphysema. In Murray, J., Nadel, 1. (Eds.). Textbook 0/ 1,758-761.
respirarory medicine. Philadelphia: WB Saunders. Verboom J., Bakker, W., & Sterk, P. (1986). The value of the
Soergel, K., & Sommers, S. (1962). Jdiopathic pulmonary hemo­ forced expiratory technique with and without postural drainage
,idemsis and related syndromes.American Journal ojMedicine in adults with cystic fibrosis. European Journal oj Respiralory
32,499-511. Diseases 69, 169-174.
Stoller, 1., & Wiedemann, H. (1990). Chronic obstructive lung dis­ Watters, H. et al ( 1 986) . A Clinical, radiological and physiological
eases: asthma, emphysema, chronic bronchitis, bronchiectasis, scoring system for the longitudinal assessment of patients with
and related disorders. In George, R., et al. (Eels.). Chest medi­ idiopathic pulmonary fibrosis. American Review 0/Respiralory
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ed.). Baltimore: Williams and Wilkins. Watts, 1. (1989). Thoracic compression for asthma. CheSI 86, 505.
Sutton, P., et al (1988) Use of nebulized saline and nebulized Weg, 1. (1982). Chronic noninfectious parenchymal diseases. [n
terbutaline as an adjunct of chest physiotherapy. Thorax 43, Guenter, c., & Welch, M. (Eds.). Pulmonary medicine (2nd
57-60. ed.). Philadelphia: JB. Lippincott.
Sutton, P., et al (1983). Assessment of the forced expiratory tech­ Wenger N: Early ambulation physical activity: Myocardial infarction
nique, postural drainage and directed coughing in chest physio­ and coronary artery bypass surgely. Heart Lung I: 14-17, 1984.
therapy. European Journal ojRespiralory Diseases 64, 62-68. Williams, H., & McNicol, R. (1969). Prevalence, natural history,
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RespiralOry Diseases 3, I.

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 CHAPTER 5

Cardiopulmonary Manifestations
of Systemic Conditions

Elizabeth Dean

KEY TERMS Connective tissue dysfunction Malnutrition

Endocrine dysfunction Musculoskeletal dysfunction
Gastrointestinal dysfunction Neurological dysfunction
Hematologic dysfunction Obesity
Hepatic dysfunction Renal dysfunction
Immunological dysfunction Systemic disease

INTRODUCTION
lowing: musculoskeletal, connective tissue, neurolog­
This chapter describes the cardiopulmonary conse­ ical, gastrointestinal (GJ), hepatic, renal, hematologi­
quences of systemic diseases. Systemic diseases can cal, endocrine, and immunological systems. Finally,
significantly affect oxygen transport either directly or the cardiopulmonary manifestations of nutritional
in combination with primary cardiopulmonary dys­ d i s o r de r s , s pecifically o b e sity a n d s t a r v a t i o n
function. Although these effects can be as cata­ (anorexia nervosa) are presented.
strophic as those resulting from primary cardiopul­ Physical therapists (PTs) need to be able to predict
monary dysfunction, their presentation is often subtle the impact of systemic disease on oxygen transport
and may elude detection until significant impairment for a given patient to maximize the efficacy of their
is apparent. The pulmonary and pleural complications treatment prescriptions. Compl ications of systemic
of cardiac disease and the cardiac complications of disease appear to be increasingly prevalent. This may
pulmonary disease are described first. Then the car­ reflect both the aging of the population and improved
diopulmonary complications of conditions involving survival and prognosis of patients with multisystem
the following systems are described including the fol- disease. Furthermore, PTs are treating an increasing

99

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100 PART 1 Cardiopulmonary Function in Health and Disease

number of patients without refelTal, and thus may not whether treatment should be modified to avert an in­
be alerted by a referring practitioner to the presence cident, or whether treatment is contraindicated all to­
and significance of underlying systemic disease. gether, is essential.
Lastly, physical therapy by definition physiologically Oxygen transport can be significantly affected by
stresses the patient, therefore, the PTs must be able to dysfunction in the major organ systems of the body
identify all factors that compromise or threaten oxy­ (see box below). The pulmonary and pleural compli­
gen transport so that treatment can be prescribed cations of heart disease and the cardiac complications
most effectively with minimal risk. of pulmonary disease are usually predictable and
A comprehensive understanding of all factors that therefore most readily detected clinically. The car­
affect or threaten oxygen transport is essential particu­ diopulmonary complications of conditions affecting
larly in those patients who are not obviously at risk, other organ systems, however, can be more subtle, if
that is, those without overt cardiopulmonary disease. not more devastating.
The PT must be able to "red flag" a patient with an un­
derlying problem for which physical therapy may be
CARDIAC CONDITIONS
contraindicated or an untoward treatment response an­
ticipated. Alternatively, treatment may need to be The pulmonary complications of heart disease and the
modified or treatment responses monitored more often. cardiac complications of pulmonary disease are well
Specific diagnosis of those factors that contribute known (Scharf and Cassidy, 1989). The mechanically
to or threaten cardiopulmonary and cardiovascular inefficient heart disrupts the normal forward propul­
dysfunction is, therefore, tantamount to efficacious sion of deoxygenated and oxygenated blood to and
treatment across all physical therapy specialties. The from the lungs. Because the right and left sides of the
capacity of the oxygen transport system needs to be healt are in series, a problem on one side inevitably
established to ensure that it can adequately respond to has some effect, that can lead to a problem on the
changes in metabolic demand, including those im­ other side, thus the healt and lung should be thought
posed by physical therapy treatment. Even though of as a single functioning unit. Disruption of the car­
cardiopulmonary dysfunction may not be the primary diopulmonary circuit leads to backlogging of blood
problem, identifying whether cardiopulmonary dys­ and an increased volume of blood in the capacitance
function can limit a patient's response to treatment, vessels, or the veins. Right heart failure contributes to
increased central venous pressure (i.e., right atrial
pressure) and if sufficiently severe, leads to peripheral
edema in the dependent body parts. Because blood is
not being forwarded to the lungs adequately, hypox­

Systems and Systemic Conditions That Affect the emia can result. In turn, hypoxic vasoconstriction of

Cardiopulmonary System and Oxygen Transport the pulmonary circulation leads to increased pul­
monary vascular resistance, and hence, illcreased right
Cardiopulmonary system ventricular afterload and work. Left heart failure can
Musculoskeletal system
result in inadequate forward movement of blood
Connective tissue conditions
Collagen vascular conditions through the left heart, resulting in backlogging in the
Neurological system pulmonary circulation nd cardiogenic pulmonary
Gastrointestinal system edema. Pulmonary edema alters lung mechanics and
Hepatic system lymphatic drainage, and in turn, these effects con­
Renal system
tribute to an increased risk of infection secondary to
Hematological system
Endocrine system
impaired macrophage function and bacterial growth.
Immunological system Excess pulmonary fluid arollnd the alveolar capillary
Nutritional disorders membrane creates a diffusion defect. If fluid accumu­
lation is extreme, backlogging may be transmitted to

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 5 Cardiopulmonary Manifestations of Systemic Conditions 101

the right side of the heart and to the periphery. Com­ the circulation, fluid balance in the lung is dependent
parable to excess fluid in the lungs, backup of fluid in on Starling'S forces, that is, hydrostatic and oncotic
the peripheral circulation can impair tissue perfusion. pressures. In health, several liters of fluid are ab­
Other cardiovascular conditions such as systemic hy­ sorbed from the pleural space, thus when the balance
peltension increases systemic afterload, which in turn of these forces is disrupted in disease, considerable
increases the work of the heart thereby reducing its fluid can accumulate in the pleural space. Impaired
mechanical efficiency. alveolar expansion from pleural effusions is of clini­
Pulmonary function can be significantly altered in cal concern. There is some evidence, however, to
cardiac disease (Bates, 1989). Left heart failure, for support that small effusions displace rather than com­
example, is associated with accumulation of fluid in press the lung (Anthonisen and Martin, 1977).
the pulmonary interstitium. This leads to reduced cal­
iber of the airways and early airway closure, air trap­
PULMONARY CONDITIONS
ping and increased residual volume. The fluid can
produce reflex constriction of bronchial smooth mus­ Lung disease can contribute to cardiac dysfunction in
cle leading to the syndrome of cardiac asthma. The several ways. First, lung disease invariably threatens
combination of airway collapse and bronchoconstric­ oxygen transport by its effects on respiratory me­
tion decreases total lung capacity, flow rates and chanics, and ventilation and peliusion matching. To
forced expiratory volumes. Ventilation and peliusion compensate, the heart attempts to increase cardiac
abnormalities are also associated with cardiac dis­ output which produces a corresponding increase in
ease. Ventilation of underperfused lung zones con­ cardiac work. Overall, ventilation and oxygen trans­
tributes to increased ventilatory dead space, and per­ port is less efficient. Hypoxemia secondary to inade­
fusion of underventilated lung zones leads to a right quate ventilation and perfusion matching may predis­
to left shunt. In left heart failure, airway resistance pose the patient to cardiac dysrhythmias.
contributes to inhomogeneous ventilation and perfu­ Pleural complications can arise from either heart
sion. The normal pattern of increased ventilation to or lung disease. Both heart and lung function can be
the bases is reversed in left heart failure, that is, the compromised by altered fluid balance of the pleurae.
apices of the lungs are better ventilated (James, Fluid balance in the pleural space is comparable in
Cooper, White, and Wagner, 1971). terms of its regulation to that in the alveolar space.
With progression of the pulmonary edema, the alve­ Both are determined by Starling forces. Specifically,
oli become flooded resulting in reduced ventilation, and hydrostatic pressure pushes fluid into these space
significant ventilation and perfusion mismatching. The while oncotic pressure counters the effect of the hy­
alveolar-arterial gradient (A-ao2 gradient) is then in­ drostatic forces. The net effect of these filtration and
creased, diffusing capacity decreased, and arterial par­ absorption forces is a minimal net filtration pressure.
tial pressure of oxygen (Pao2) decreased. Lung compli­ When the balance of these forces is disrupted, heart
ance is inversely related to pulmonary artery pressures and lung function can be threatened. Excessive fluid
and interstitial fluid accumulation (Saxton, Rabinowitz, floods the space usually reflecting both excessive hy­
Dexter, and Haynes, 1956). The net effect of these ab­ drostatic pressure and diminished oncotic pressure.
normalities is both obstructive and restrictive patho­ The lymphatic vessels become overwhelmed and are
physiologic patterns of lung dysfunction, that is, re­ unable to keep the pleural space dry. Pleural fluid ac­
duced forced expiratory volumes and vital capacity, cumulates and either displaces lung tissue (smaJ]-to­
and an overall increase in the work of breathing. moderate effusions) or restricts opening of adjacent
Pleural effusions can result from heart disease, in alveolar sacs, causing atelectasis (severe effusions)
particular, congestive heart failure (CHF). Changes in (Brown, Zamel, and Aberman, 1978), and if suffi­
intravascular pressures lead to transudative pleural ef­ ciently severe, may restrict cardiac filling. Pleural
fusions and cardiac injury leads to exudative effu­ fluid accumulation poses a unique threat to oxygen
sions. Comparable to fluid balance in other parts of transport as a result of its direct physical effect on the

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102 PART I Cardiopulmonary Function in Health and Disease

lungs, heart, or both, thus it warrants special atten­

Cardiopulmonary Manifestations of
tion by PTs.
Musculoskeletal Conditions
Pulmonary lymphatics control fluid balance within
the lung parenchyma. Lymphatic vessels arise within
General Manifestations
the pleurae and not within the alveolar capillary Reduced alveolar venti/atio"
space. They drain fluid from the interlobular septae
Altered respiratory mechanics
and subpleural areas, to the hilar vessels and the pri­
Chest wall rigidity
mary tracheobronchial lymph nodes. Problems aris­ Reduced chest wall excursion
ing within the heart or lungs can contribute to imbal­
Impaired IIlucocilary tra"sport
ances in the major lymphatic inflow and outflow
Airflow obstruction
channels. This contributes to fluid accumulation,
Pulmonary restriction
stagnation, and physical compression of the my­ Atelectasis
ocardium and lungs (Guyton, 1991). Inspissated secretions
Both heart and lung disease can produce deleteri­
Increased work of breatllillg
ous hematologic changes to compensate for hypox­
Inefficient breathing pattern
emia. Increases in the number of red blood cells raise
the hematocrit and the viscosity of the blood. This Illcreased work of tile Ileart
phenomenon increases the work of the heart further. Inefticient breatbing pattern
In addition, viscous blood increases the probability of Constrictive pericorditis

thromboemboli. This risk is superimposed on the ex­

Reduced aerobic capacity
isting risk of thromboemboli in hypoeffective hearts.
Manifestations in Specific Conditions
A thorough understanding of the interrelationship
Rheumatoid arthritis
of the heatt and lungs is essential for diagnosis and op­
Pleuritis with or without effusion
timal management. In addition, the cardiopulmonary
Diffuse interstitial pneumonitis and tibrosis
and cardiovascular manifestations of other primary
Pulmonary arteritis
organ systems must be recognized and anticipated par­ Bronchiolitis
ticularly in patients with multisystem disease. Pleural effusions

Ankylosi"g spondylitis

MUSCULOSKELETAL CONDITIONS Upper lobe fibrobullous disease

Chest wall restriction
Musculoskeletal conditions impact on cardiopul­
monary function secondary to their effects on muscle,
in particular, the diaphragm, muscles of the chest wall,
oropharynx, larynx and abdomen, and on bones and
joints (e.g., althritis, ankylosing spondylitis, kyphosco­ 22). The cardiopulmonary manifestation of muscu­
liosis, and the deformity secondary to neuromuscular loskeletal conditions are summarized in the box above.
diseases and chronic lung diseases). Additional effects The cardiopulmonary deficits associated with
are imposed by inactivity, (i.e., muscle wasting and in­ musculoskeletal disorders of the chest wall include
creased joint rigidity). Increased joint rigidity limits reduced lung volumes consistent with pulmonary re­
the amount of physical activity a patient may pelform, striction, reduced flow rates, reduced inspiratory and
which contributes to cardiopulmonary compromise, in expiratory pressures, increased atelectasis, increased
addition to the local effect of increased chest wall dynamic airway compression, ventilation and perfu­
rigidity and compromised bucket-handle and pump­ sion mismatching, inefficient breathing pattern, im­
handle motions. The normal three-dimensional move­ paired cough and gag reflexes, increased risk of aspi­
ment of the chest wall and normal pulmonary circula­ ration, increased risk of obstruction secondary to
tion and lymphatic function is compromised (Chapter impaired mucociliary clearance, restricted mobility,

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 5 Cardiopulmonary Manifestations of Systemic Conditions 103

compression of mediastinal structures and heart, and connective-tissue changes in the skin can lead to
impaired lymphatic drainage which depends on nor­ chest wall restriction. The cardiopulmonary mani­
mal expiratory and inspiratory cycles (Bates, 1989). festations of connective tissue conditions are sum­
marized in the box below.

CONNECTIVE TISSUE CONDITIONS

NEUROLOGICAL CONDITIONS
Connective tissue/virgule collagen vascular disor­
ders (e.g., scleroderma and systemic lupus erythe­ Cardiopulmonary consequences of neurological dis­
matosus [SLE]), invariably affect the cardiopul­ ease reflects the specific pathophysiologic mechanisms
monary system (Bagg and Hughes, 1979). involved (Griggs and Donohoe, 1982). There are three
Inflammation. and tissue injury can affect the air­ basic patterns of pathology: (1) involvement of the
way, lung parenchyma, pulmonary vasculature, central nervous system (CNS), (2) the peripheral ner­
pleurae, respiratory muscles, heart and pericardium. vous system, and (3) the autonomic nervous system.
Shrinking lung syndrome associated with chronic The cardiopulmonary manifestations of neurological
connective tissue changes is a feature of advanced conditions are summarized in the box on p. 104.
disease and is characterized by a significant loss of
alveolar surface area, diffusion capacity, and lung
Involvement of the CNS
volumes. Fibrotic changes increase the elasticity of
the lung parenchyma and reduce lung compliance, The primary centers for breathing control and control
thereby i n c r e a s i n g work of b r e a t h ing. T h e s e of the heart emanate from the midbrain. The genera­
changes are comparable t o those i n idiopathic pul­ tor for breathing control produces a regular respira­
monary fibrosis. Both the electrical conduction sys­ tory rate through modulation of inspiratory and expi­
tem of the heart and its mechanical behavior are ad­ ratory inhibitory and excitatory neurons.
versely affected by systemic connective tissue Activity of the central generator is affected by
changes (Goldman and Kotler, 1985). Furthermore, arousal and the general alerting reaction of the reticu­
lar activating system. In addition, breathing control is
influenced by the hypothalamus, the orbital cortex,
forebrain, and amygdala (Hitchcock and Leece, 1967).
Cardiopulmonary Manifestations of Connective
Insult to the CNS can result in cardiovascular re­
Tissue/Collagen Vascular Conditions
sponses that precipitate neurogenic pulmonary

General Manifestations edema. Such responses include systemic hyperten­

sion, pulmonary hypertension, intracranial hyperten­
Acute injury to the alveolar-capillary unit
Alveolar hemorrhage sion and bradycardia. The medulla is believed to me­
Interstitial pneumonitis diate the cardiovascular responses associated with
Interstitial pulmonary fibrosis neurogenic pulmonary edema. Marked sympathetic
Pulmonary hypertension stimulation, catecholamine release, and vagotonia ap­
Respiratory muscle dysfunction
pear to precipitate neurogenic pulmonary edema and
Pulmonary edema
Pulmonary infection
the resulting leaking of the alveolar capillary mem­
Abnormal diffusing capacity brane and alveolar flooding (Col ice, 1985). However,
Chest wall restriction the possibility of a primary pulmonary endothelial

Manifestations in Scleroderma permeability abnormality has been suggested (Peter­

son, Ross, and Brigham, 1983).
Restrictive ventilatory impairment
Decreased diffusing capacity Cortical disturbances may have a direct effect on
Diaphragmatic dysfunction cardiopulmonary function. Among the most common
Gastroesophageal reflux and aspiration disturbances seen clinically are cortical infarction
and seizures. Hemispheric infarction can lead to

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 Cardiopulmonary Manifestations of Neurological Conditions

General Manifestations
Impaired mucociliary transport

Reduced mobility
Cilia dyskinesia
Incrcased mucus accumulation
Reduced cough and gag reflexes
Impaired airway protection
Increased airway resistance
Increased risk of airway obstmction
Impaired glottic closure
Increased risk of aspiration

Impaired alveolar velltilation

Reduced lung volumes and capacities, as well as now rates

Weakness of pharyngeal and laryngeal structures
Respiratory muscle weakness
Reduced respiratory muscle endurance

Illcreased work of breathing

Reduced aerobic capacity and decollditiollillg

Manifestations in Specific Conditions

M"ltiple sclerosis

Respiratory muscle weakness

Impaired ventilation secondary to spasm
Increased oxygen consumption secondary to spasm
Increased oxygen consumplion secondary to impaired posture and gait
Impaired gag and cough reflexes
Ineffective cough

Cerebral palsy

Increased oxygen consumption secondary to increased muscle tone

Significantly reduced mobility and activity
Impaired movement economy
Impaired swallowing
Impaircd saliva control
Reduced gag and cough reflexes
Impaired coordination of thoracic and abdominal motion dUling respiration
Ineffective cough and airway clearance mechanisms

Stroke

Reduced movement economy

Spasticity and increased oxygen demands
Flaccidity of respiratory muscles
Impaired respiratory muscle strength
Impaired pulmonary function
Asymmetric chest wall
Weak and ineffective cough

Parkillsoll's disease

Increased oxygen consumption secondary to increased muscle tone

Reduced movement economy
Chest wall restriction and impaired pulmonary function
Ineffective cough

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 5 Cardiopulmonary Manifestations of Systemic Conditions 105

contralateral weakness of the diaphragm and other creased muscle tone, which correspondingly increases
respiratory musc les. E pi l e ptic seizures disrupt basal and exercise oxygen consumption, resulting in
breathing, which causes hypoxemia, respiratory aci­ increased oxygen demands. Even though the demands
dosis, and a metabolic acidosis secondary to extreme are increased in this condition, oxygen delivery is
muscle contraction and lactate accumulation. The as­ compromised. For example, thoracic deformity and
sociated increase in sympathetic stimulation can pre­ spasm of the muscles of the chest wall and abdomen
cipitate cardiac dysrhythmias and pulmonary edema. impair breathing pattern and its efficiency (Fullford
Demyelinating diseases such as multiple sclerosis and Brown, 1976). The airways of patients with cere­
result in progressive deterioration of neuromuscular bral palsy are vulnerable because of poor gag, cough,
function. The muscles of respiration become increas­ and swallowing reflexes. In addition, these patients
ingly involved, resulting in respiratory insufficiency often have poor saliva control, which increases the
(Cooper, Trend, and Wiles, 1985). In addition, with risk of aspiration further. Mental retardation (Bates,
increasing debility cardiopulmonary conditioning is 1989) often complicates the presentation of cerebral
reduced. Weakness of the pharyngeal musculature palsy and prevents these patients from responding ad­
contributes to loss of airway protection in addition to equately to their hydration needs or being able to co­
the loss of cough and gag reflexes. Aspiration is prob­ operate with life-preserving treatments. These patients
lematic for these patients as the disease advances. harbor numerous microorganisms, which adds further
Stroke patients may have central involvement that to their general risk of infection.
affects cardiopulmonary regulation and function, in­ Patients with Parkinson's disease also exhibit sig­
cluding reduced electrical activity of the respiratory nificant cardiopulmonary deficits (Mehta, Wright,
muscles, or peripheral involvement such that weak­ and Kirby, 1978). Oxygen demand is increased com­
ness, spasticity, impaired biomechanics, and gait di­ mensurate with increased muscle tone. Comparable
rectly affect respiratory muscle function and chest to the patients described above, patients with Parkin­
waJl excursion (DeTroyer, De Beyl, and Thirion, son's also have reduced cardiopulmonary condition­
1981). Abdominal muscle weakness contributes to ing levels as a result of compromised agility and abil­
impaired cough effectiveness. Pharyngeal weakness ity to be independently mobile in many cases. These
contributes to sleep apnea in these patients. The com­ patients also have a restrictive pattern of lung disease
mon clinical presentation of unilateral involvement with most lung volumes and capacities being re­
leads to a posture listing to the affected side when re­ duced. Chest wall rigidity impairs the normal pump­
cumbent, sitting and during ambulation. This posture handle and bucket-handle movements, thus it reduces
impairs ventilation and chest wall expansion on the breathing efficiency. The energy cost of breathing is
affected side. Abdominal muscle involvement di­ correspondingly increased. Respiratory insufficiency
rectly affects intraabdominal pressure and the effi­ of Parkinson's disease likely reflects an increase in
ciency of diaphragmatic descent during contraction, tone of the respiratory muscles, chest wall rigidity, as
that is, should the abdominal muscles become flaccid well as increased parasympathetic tone and resulting
the efficiency of diaphragmatic contraction is signifi­ airway obstruction.
cantly reduced. Lung volumes and flow rates are re­ Patients with a history of poliomyelitis with or
duced proportionately giving a restrictive pattern of without cardiopulmonary complications at onset, may
lung function. Reduced activity and exercise around exhibit pulmonary limitation several decades later
the time of the stroke contributes to reduced car­ (Dean, Ross, Road, Courtenay, and Madill, 1991;
diopulmonary conditioning and capacity of the oxy­ Steljes, Kryger, Kirk, and Millar, 1990). These indi­
gen transport system. Finally, a high proportion of viduals are at risk for developing respiratory insuffi­
patients with strokes are hypertensive and older, a ciency as a result of respiratory muscle weakness,
population with a higher prevalence of heart disease chest wall deformity, minor infection and periods of
and atherosclerosis (Chimowitz and Mancini, 1991). relative immobility, or secondary to medical inter­
Cerebral palsy is associated with significantly in­ ventions, (e.g., anesthesia, sedation).

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106 PART I Cardiopulmonary Function in Health and Disease

Diseases and lesions involving the brainstem can the larynx, pharynx, and tongue can lead to upper
lead to various abnormal breathing patterns. Some airway obstruction and increased airway resistance,
common breathing aberrations are Cheyne-Stokes res­ and interfere with maintaining a clear airway. Aspi­
piration, central neurogenic hyperventilation, ap­ ration is a common and serious problem associated
neustic breathing, and ataxic breathing. Cerebellar and with impaired motor control of the larynx, pharynx,
basal ganglia lesions may produce respiratory muscle and tongue.
discoordination and dyspnea (Hormia, 1957; Neu,
Connolly, Schwertley, Ladwig, and Brody, 1967).
Involvement of the Autonomic Nervous System
Spinal cord lesions have a variable effect on car­
diopulmonary function depending on the level of the Cardiopulmonary consequences of disorders of the
lesion. Cervical lesions result in a high mortality rate autonomic nervous system have been documented. Of
as a result of cardiopulmonary complications. All those diseases with an autonomic component, auto­
lung volumes are diminished with the exception of nomic neuropathies, diabetes, and alcoholism have
total lung capacity (TLC), which over time returns to been the most studied. MUltiple system atrophy ac­
normal; tidal volume (TV), which is usually pre­ companies autonomic failure affecting multiple sys­
served (10% of TLC); and residual volume (RV), tems. Because of the anatomic proximity of the auto­
which is significantly increased (Estenne and De­ nomic, respiratory and hypnogenic neurons and the
Troyer, 1987; Fugl-Meyer, 1971). Quadriplegic pa­ degeneration of these structures in this condition, dys­
tients tend to have a greater diaphragmatic contribu­ function of the respiratory control mechanisms paral­
tion to tidal ventilation compared with healthy people lels autonomic and somatic dysfunction. The respira­
(Estenne and DeTroyer, 1985). In addition, these pa­ tory dysrhythmias that are seen in multiple system
tients have impaired cough as a result of loss of in­ atrophy include central, upper airway obstruction, ir­
nervation and paresis of the diaphragm in some cases, regular rate, rhythm, and amplitude of respiration with
and abdominal and intercostal muscles. The contribu­ or without oxygen desaturation, transient uncoupling
tion of accessory muscle activity to ventilation varies of the intercostal and diaphragmatic muscle activity,
considerably (McKinley, Auchincloss, Gilbert, and prolonged periods of apnea, Cheyne-Stokes respira­
Nicholas, 1969). In quadriplegia, with only the acces­ tion, inspiratory gasps, and transient sudden respira­
sory muscles and diaphragm spared, platypnea (in­ tory arrest (Bannister, 1989).
creased dyspnea when upright) may occur (Dantzker, Patients with diabetes and autonomic neuropathies
1991). In the upright position, the diaphragm is flat­ exhibit variable effects on cardiopulmonary status.
tened and less efficient when moved downward by Postural hypotension is a complication of diabetic au­
reduced abdominal pressures. tonomic neuropathy and efferent sympathetic vaso­
Thoracic lesions tend to have less effect on pul­ motor denervation. Norepinephrine levels are gener­
monary function (vital capacity and forced expiratory ally reduced in these patients. The splanchnic and
volumes in particular) than cervical lesions, and the peripheral circulations fail to constrict in response to
significance of this effect is reduced as the level of standing, thus cardiac output falls. The postural effect
the lesion is reduced. Lumbar lesions may have mini­ is exacerbated by reduced cardiac acceleration in pa­
mal or no effect on pulmonary function; however, in­ tients with diabetes. Insulin has been associated with
volvement of the abdominal muscles may limit cough cardiovascular effects, including reduced plasma vol­
effectiveness. ume, increased peripheral blood flow secondary to va­
sodilatation, and increased heart rate. In the presence
of autonomic neuropathies, insulin can induce pos­
Involvement of the Peripheral Nervous System
tural hypotension. Diabetic diarrhea secondary to ab­
Disorders of the peripheral nervous system include normal gut motility can contribute to fluid loss and its
those of the motor neuron, peripheral nerve, neuromus­ sequelae. Cardiopulmonary changes associated with
cular junction and muscle. Neuromuscular disorders of autonomic neuropathy secondary to diabetes include

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 5 Cardiopulmonary Manifestations of Systemic Conditions 107

altered ventilatory responses to hypoxia and hyper­ been associated with inflammatory bowel disease;
capnia, altered respiratory pattern and apneic episodes however, their occurrence is not related to the activity
during sleep, altered bronchial reactivity and impaired or therapy. Biopsy specimens have shown basement
cough (Bannister, 1989; Montserrat et aI., 1985). membrane thickening, thickening of the epithelium,
and infiltration of the underlying connective tissue
with inflammatory cells (Higenbottom, et aI., 1980).
GASTROINTESTINAL CONDITIONS
The pulmonary manifestations of pancreatitis are
The cardiopulmonary manifestations of GI dysfunc­ among the most important sequelae of this disease.
tion are summarized in the box below. Inflammatory Of the deaths that occur in the first week of hospital­
bowel disease and pancreatitis are principal exam­ ization, 60% are associated with respiratory failure
ples of GI dysfunction that affects on cardiopul­ (Renner, Savage, Pantoja, and Renner, 1985). Prob­
monary function. Aspiration is a significant cause of lems include elevated hemidiaphragms particularly
morbidity and mortality in patients with GI dysfunc­ on the right side, basal atelectasis, diffuse pulmonary
tion, thus it should be prevented or detected early. infiltrates appearing more often on the right side than
The pathophysiology, management, and outcome de­ the left side, pleural effusions on the left side more
pend on the nature of the aspirate. Several predispos­ than the right side, and pneumonitis. These findings
ing factors produce aspiration pneumonia including a are not specific for pancreatitis and are probably sec­
decreased level of consciousness, disorders of pha­ ondary to localized peritonitis, subphrenic collec­
ryngeal and esophageal motility, altered anatomy, tions, ascitis, pain, and abdominal distension. In
disorders of gastric and intestinal motility, and iatro­ chronic pancreatitis, abdominal symptoms may be re­
genic factors such as surgery, nasogastric (NG) intu­ duced and thoracic symptoms such as dyspnea, chest
bation, and general anesthesia. pain, and cough may predominate. Chronic effusions
Inflammatory bowel disease can lead to the fol­ may result in pleural thickening.
lowing cardiopulmonary pathologies: vasculitis, fi­
brosis, granulomatous disease, and pulmonary throm­
LIVER CONDITIONS
boembolism. Bronchitis and bronchiectasis have also
Both acute and chronic liver conditions can predis­
pose a patient to cardiopulmonary and cardiovascular
complications (see the box, on p. 108, at left). Hepatic
Cardiopulmonary Manifestations failure can lead to hypoxemia secondary to intrapul­
of GI Conditions monary vascular dilatation and noncardiogenic pul­
monary edema. Hepatopulmonary syndrome, hall­
Risk of aspiration marked by intrapulmonary vascular dilatation,
Gastroesophageal reflux produces both diffusion and perfusion defects in the
lungs and is the principal reason for severe hypoxemia
Increased airway resistance
(Sherlock, 1988). The origin of pulmonary edema is
Bronchospasm
secondary to hepatic encephalopathy and cerebral
Reduced lung volumes edema (Trewby, et aI., 1978).
Elevated hemidiaphragms With respect to chronic liver conditions, car­
Compression atelectasis diopulmonary manifestations have been associated

Arterial hypoxemia with cirrhosis of the liver and hepatitis. The most
common pulmonary abnormalities associated with
Alveolar capillary leak and V/Q mismatch
Alveolar hemolThagc and consolidation worsen these conditions are intrapulmonary vascular dilata­

I
shunt tion with and without shunt, pulmonary hypertension,
Increased pulmonary vascular resistance airflow obstruction, chest wall deformity, pleural ef­
fusions, pancinar emphysema, pleuritis, bronchitis,

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108 PART I Cardiopulmonary Function in Health and Disease

Cardiopulmonary Manifestations Cardiopulmonary Manifestations

of Liver COllditions of Rellal Conditions

Intra pulmonary vascular dilatation Alveo lar hemorrhage

Pulmonary hype11ension Airway ohstruction
Expiratory airflow obstruction Reduced lung volumes
Chest wall deformity Reduced diffusing capacity
Pleural effusions
Panacinar emphysema
Pleuritis
Bronchitis of these patients, physical therapy warrants being es­
Bronchiectasis pecially aggressive given the course of the pul­
Impaired hypoxic vasoconstriction
monary-renal syndromes and the potential for re­
Interstitial pneumonitis
lapses and irreversible organ damage.
Pulmonary fibrosis

HEMATOLOGIC CONDITIONS

bronchiectasis, hypoxic vasoconstriction, and intersti­ Hematologic disorders that can manifest cardiopul­
tial pneumonitis, fibrosis. Hypoxemia results from monary symptoms include abnormalities of the fluid
shunting, ventilation and perfusion mismatching and and cellular components of the blood, and coagu­
diffusion abnormalities. lopathies (Bromberg and Ross, 1988). Cardiopul­
Pleural effusions and ascites interfere with di­ monary manifestations of hematologic conditions are
aphragm function and present unique problems in the summarized in (the box on p. 109). The primary un­
patient with Ii ver disease. Rich lymphatic connec­ derlying mechanisms by which these conditions dis­
tions exist between the abdominal and thoracic cavi­ rupt gas exchange include hemorrhage, infection,
ties. Because of the rich lymphatic supply of the edema, anemia, fibrosis, and malignancies.
pleural space, ascitic fluid can flow into the pleural Abnormalities related to red blood cells and their
space. This effect is enhanced during inspiration ability to transport hemoglobin and oxygen may pro­
when the intraabdominal pressure is relatively posi­ duce signs resembling pulmonary pathology, (e.g.,
tive and the intrapleural space is negative (Crofts, tachypnea, dyspnea, and cyanosis). Abnormalities of
1954). the deformability of red blood cells alter blood viscos­
ity and pulmonary blood flow. The interstitium can be
disrupted by such factors as hemorrhage and malig­
RENAL CONDITIONS
nancies. Coagulopathies disrupt the normal hemosta­
Cardiopulmonary complications can result from renal sis and clotting mechanisms of the blood. Pulmonary
disease and the category of disorders referred to as pul­ hemorrhage and hemoptysis are common sequelae.
monary-renal syndromes (see the box above, at right). The most common causes of pulmonary hemolThage
(Rankin and Matthay, 1982; Matthay, Bromberg, and include vitamin-K deficiency, hemophilia, hepatic
Putman, 1980). The pathophysiologic characteristics failure, and disseminated intravascular coagulation.
of these disorders include alveolar hemorrhage, inter­ Pharmacologic agents such as platelet inhibitors and
stitial and alveolar inflammation, and involvement of anticoagulants can also result in pulmonary hemor­
the pulmonary vasculature. Pulmonary function testing rhage. Pulmonary thromboemboli are common events
may detect both obstructive and restrictive abnormali­ with symptoms including pleuritic chest pain, dysp­
ties as a result of bronchial complications, and inflam­ nea, and hemoptysis.
mation and hemorrhage respectively. Of the erythrocyte disorders sickle cell anemia is
In systemic illness, pathology of the lungs and probably the most common. Acute chest infection
kidneys often coexist. Like the medical management and thrombosis leading to pulmonary infarction may

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 5 Cardiopulmonary Manifestations of Systemic Conditions 109

pending on the amount of plasma protein, particularly

Cardiopulmonary Manifestations
albumin, fluid is retained or lost from the circulation.
of Hematologic Conditions
With reduced protein and oncotic pressure within the
vasculature, more fluid is filtered out of the circula­
General Cardiopulmonary Manifestations
tion into the interstitium. In catabolic states in which
Hemorrhage
protein is broken down in the body, more protein
Edema
Polycythemia
leaks through the capillaries taking water with it, thus
Anemia leading to edema.
Infection

AbnonnaJities of the Fluid Portion of the Blood ENDOCRINE CONDITIONS

Abnormal blood volume
Abnormal tluid balance (water excesses and Endocrine and metabolic disorders can be associated
deficits) with cardiopulmonary complications (see the box on
Abnormal electrolytes p. 110). (Civetta, Taylor, and Kirby, 1989; Guyton,
Abnormal plasma proteins 1991). Disorders of the thyroid gland, pancreas (dia­
Abnormal procoagulants and anticoagulants
betes mellitus [DM]) and adrenal glands are such disor­
Abnormal clotting times
ders that are often seen clinically. Thyroid hormone in­
Abnormalities of the Cellular Portion fluences the central drive to breathe and surfactant
of the Blood
synthesis. Hypothyroidism can lead to sleep apnea,
Abnormal red blood cell COllnt
pleural effusions secondary to altered capillary perme­
Abnormal red blood cells
ability, and pericardial effusions. Decreases in vital ca­
Abnormal deformability of the red blood cells
Abnormal hemoglobin
pacity have also been reported secondary to muscle
Abnormal oxyhemoglobin dissociation (e.g., carbon weakness. Hypelthyroidism increases cellular oxidative
monoxide poisoning) metabolism (the metabolic rate) leading to an increase
Abnormal white blood cells and antibodies in oxygen consumption and CO2 production, and an
Blood dyscmsias
overall increase in minute ventilation. Vital capacity,
lung compliance, and diffusion capacity can be reduced.
In addition, maximal inspiratory and expiratory pres­
sures can be reduced secondary to muscle weakness.
Patients with diabetes are prone to aspiration and
occur with clinical symptoms such as fever, pleuritic respiratory infections. Late complications of diabetic
chest pain, cough, and pulmonary infiltrates. The pul­ neuropathy include renal failure, which may be accom­
monary function of patients with sickle cell anemia is panied by pleural effusions and pulmonary edema. Au­
abnormal with reduced TLC, vital capacity, diffusing tonomic neuropathy may affect vagal activity and air­
capacity, arterial oxygen tensions, and reduced exer­ way tone. Ischemic heart disease and cardiomyopathies
cise capacity (Femi-Pearse, Gazioglu, and Yu, 1970). are common in patients with diabetes and may cause
The hematologic malignancy disorders that can af­ CHF and cardiogenic pulmonary edema. Patients with
fect pulmonary function include the leukemias and diabetes have been reported to have reduced sensitivity
Hodgkin's disease. The three primary mechanisms by to inspiratory loading (O'Donnell, Friedman, Russo­
which these disorders can affect pulmonary function manno, and Rose, 1988), which may impair their sub­
include direct infiltration, increased risk of oppor­ jective responses to exercise.
tunistic infection and secondary effects of treatment, Adrenal insuffiCiency can also compromise oxy­
such as interstitial pneumonitis and fibrosis. gen transport (Civetta, Taylor, and Kirby, 1989). Re­
Disorders of plasma proteins can have significant duced aerobic capacity results from symptoms of
effects on the Starling'S forces maintaining normal weakness, fatigue, and associated muscle and joint
fluid balance within the tissue vascular beds. De­ complaints. Orthostatic intolerance primarily reflects

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110 PART I Cardiopulmonary Function in Health and Disease

reduced inotrophic capacity of the heart and reduced

Cardiopulmonary Manifestations of Endocrine
systemic vascular resistance.
Conditions

Thyroid DisOI'ders IMMUNOLOGICAL CONDITIONS

Hypothyroidism

H ypornetabolic Congenital and acquired defects in the immunologi­

Fatigue and excessive sleep cal status of the lung lead to cardiopulmonary dys­
Reduced conditioning function, including infection and inflammation. In
Decreased vital capacity econdary to muscle
addition, patients who are immunodeficient have an
weakness
increased risk of pulmonary malignancies (Shackle­
Slecp apnea
Decreased heart rate ford and McAlister, (975).
Decreased cardiac output Acquired immunodeficiency syndrome (AIDS),
Decreased blood volume an example of a primary disorder of cell-mediated
Pleural effusions
immunity, has reached epidemic proportions over
Pericardial effusions
the past 20 years. This syndrome leads to lympho­
Hyperthyroidism cyte death. The most serious pulmonary infections
Hypermetabolic associated with AIDS is Pneul110cystis carinii pneu­
Decreased vital capacity and diffusing capacity monia (Murray, Felton, and Garay, 1984). The fact
Fluid loss (diarrhea)
that the patient with the human immunodeficiency
Respiratory muscle weakness
virus (HIV) is more likely to have recurrent pneu­
Fatigue and inability to sleep
Reduced conditioning monia suggests that the infecting organisms persist
in the lung despite treatment (Shelhamer, et aI.,
Pancreatic Disorders (Diabetes)
1984). The clinical presentation includes diffuse
Pulmonary endothelial thickening
pulmonary infiltrates, cough, dyspnea, and hemopt­
Reduced TLC
ysis. These patients can also have symptoms of
Reduced vital capacity and forced expiratory
volumes upper airway obstruction.
Reduced airway vagal tone
Increased risk of aspiration
Possible reduced elastic recoil NUTRITIONAL DISORDERS
Impaired hypoxic and hypercapnic responses
Impaired ventilatory response to exercise The two most common nutritional disorders seen 111

Defective neutrophil production Western countries are obesity, and anorexia nervosa,
Colonization with gram-negative hacilli which is akin to starvation. Obesity contributes in sev­
Pleural effusions and pulmonary edema with
eral ways to impaired oxygen transport (Alexander,
diabetic nephropathy
Reduced sensitivity to increases in inspiratory
1985; Bates, (989). These include alveolar hypoventi­
resistive loading lation and impaired Pao2 and gas exchange as a result
Accelerated atherosclerotic vascular and cardiac of the increased weight of adipose tissue over the tho­
changes racic cavity. Systemic and pulmonary blood pressures
Increased ischemic heart disease
are increased. In addition, large abdomens, and abdom­
Cardiomyopathy
inal contents impinge on diaphragmatic motion, and
Increased risk of infection
can restrict diaphragmatic descent. This can lead to
Adrenal Insufficiency
compression of the dependent lung fields. Recumbency
Orthostatic symptoms
can induce respiratory insufficiency, that is positional
Reduced aerobic capacity secondary to anorexia.

respiratory failure. Obese individuals have a higher in­

weakness and fatigue
cidence of snoring and obstructive sleep apnea sec­
Impaired breathing mechanics secondary to GI
symptoms ondary to weakness, and increased compliance of the
Tendency to retain fluid postpharyngeal structures. In addition, these patients
often have weak ineffectual coughs resulting from expi­

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 5 Cardiopulmon ary Manifestations of Systemic Conditions 111

SUMMARY
ratory muscle weakness and mechanical inefficiency of
these muscles. Work of breathing is markedly in­ This chapter described the cardiopulmonary conse­
creased. Furthermore, in chronic cases, reactive pul­ quences of systemic diseases. Oxygen transport, the
monary vasoconstriction in response to chronic hypox­ purpose of the cardiopulmonary system, can be sig­
emia contributes to right ventricular insufficiency and nificantly affected by dysfunction in virtually all
increased work of the heart and cardiomegaly. organ systems of the body. The pathophysiological
The major cardiopulmonary manifestations of consequences of diseases of the following systems on
anorexia nervosa relate to generalized weakness and oxygen transport were presented: cardiac, pulmonary,
reduced endurance of all muscles, including the res­ musculoskeletal, connective tissue/collagen vascular,
piratory muscles. Cough effectively is correspond­ neurological, gastrointestinal, hepatic, renal, hemato­
ingly compromised. Oxygen transport reserve is min­ logic, endocrine, and immunological systems. In ad­
imal. Because of poor nutrition and fluid intake, the dition, the cardiopulmonary manifestations of nutri­
patient is at significant risk of anemia, fluid and elec­ tional disorders, i ncl ud ing obesi ty and anorex i a
trolyte imbalances, and cardiac dysrhythmias (Wil­ nervosa, were described.
son, et ai, 1991). Common manifestations of nutri­ A knowledge of these effects is essential to the
tional disorders are summarized in the box below. practice of physical therapy across all specialties in
that the prevalence of systemic disease appears to
be increasing. The p r esentation of cardiopul­

Cardiopulmonary Manifestations monary consequences of systemic disease is often

of Nutritional Disorders subtle or obscured, and is associated with a poor

prog nosis, thus early detection and appropriate
Obesity management is essential.

Al v eolar hypov entilat io n PTs need to be able to distinguish diagnostically

Obstructive sleep apnea cardiopulmonary manifestations of systemic dis­
Reduced outward recoil of the chest wall eases to appropriately identify indications for physi­
Increased abdominal contents cal therapy, contraindications, side effects, and un­
Increased llIass of the abdominal wall
usual treatment responses. In addition, detailed
Reduced functional re sidua l capacity
Reduced expiratory reserve vol ume assessment of the patient's problems ensures that
Marked reductions lung volumes, arterial oxygen problems amenable to physical therapy are appro­
tension (Pao2) and saturation (Sao2) in recumbency priately treated, and those that are not are referred
Basal airway closure and resul t ing decrease in Pao2 back to a physician.
Marked pulmonary abnormalities during sleep
Reduced ventilatory responses to CO2
Cardiomegaly REVIEW QUESTION
Rotation and horizontal position of the heart
Axis deviation • Describe the cardiopulmonary manifestions of:
Reduced myocardial pumping efficiency 1. Musculoskeletal dysfunction
Reduced aerobic conditioning and oxygen transport
2. Connective tissue dysfunction
reserve capacity
3. Neurological dysfunction
Starvation or Anorexia Nervosa 4. Hepatic dysfunction
Generalized weakness, debility, and l os s of S. Renal dysfunction
cardiopulmonary co nd itioning 6. Hematologic dysfunction
Impaired mucociliary transport
7. Endocrine dysfunction
Ineffective cough
Fluid and elect rolyte dis turbance s
8. Obesity
Cardiac dysrhythmias 9. Malnutrition (e.g. anorexia nervosa)
Respiratory musc le weak ness

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112 PART I Cardiopulmonary Function in Health and Disease

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Chimowitz, M.1., & Mancini, G .B J . (1991). Asymptomatic coro­ cine, 53, 497-523.
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Civetta, J.M., Taylor, RW., & Kirby, R.R. (1989). Crilical Care. McKinley, C.A., Auchincloss, J.H., Gilbert, R., & Nichol a s, J.
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of RespiralOry Diseases, 123, 631-632. (1988). Diminished perception of inspiratory-resistive loads in
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Shackleford, M.D., & McAlister, W.H. (1975). Primary immunodefi­ Sherlock S. (1988). The liver lung interface. Seminars ill Respira­
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Schalf, S.M. & Cassidy, S.S. (1989). Hearl-Lul1. Inreracliol1s ill Sleep in postpolio syndrome. Chesl, 98, 133-140.
Health and Disease. New York: Marcel Dekker, Inc. Trewby, P.N., Warren, R., Contini, S, Crosbie, W.A., Wilkinson,
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tissue of acquired immunodeficiency syndrome patients treated Wilson, J.D., Braunwald, E., Isselbacher, J.K., Petersdorf', R.G.,
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McGraw Hill.

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PART II

Cardiopulmonary
Assessment

Copyrighted Material
 Measurement and Documentation

Claire Peel

KEY TERMS Documentation Reliability

Measurement Subjective assessment
Objective assessment Validity

INTRODUCTION
surements that relate to the cardiovascular and pul­
Measurement and documentation are critical com­ monary systems is essential for quality patient care.
ponents of the process of providing patient care. Documentation of the results of measurements,
Measurements form the basis for deciding treat­ the interpretation of the results and the patient care
ment strategies and therefore influence patients' re­ plan is important not only for reimbursement but
sponses to therapeutic interventions. Measurements also to assure communication among health care
are also used during treatment sessions to deter­ team members. Timely and appropriate sharing of
mine rate of progression and appropriateness of ex­ information on physiological responses to activity is
ercise prescriptions. Typically, therapists make a often critical for optimal medical management. Doc­
series of measurements and in combination with the umentation needs to be written clearly and concisely,
results of measurements made by other health care and to include objective findings that will facilitate
professionals, form an impression of the client. The efficient and continuous care from all members of
impression includes both physical and psychosocial the health care team.
aspects. If parts of the impression are incorrect be­ This chapter provides a discussion of types and
cause of inaccurate measurements, then the course characteristics of measurements that are common to
of treatment may be misdirected. The result could cardiopulmonary physical therapy, followed by a dis­
be treatment that is either not effective or unsafe. cussion of the process of selecting, performing, and
Consequently, knowledgc of the qualities of mea- interpreting measurements. A discussion of the pur­

117

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118 PART II Cardiopulmonary Assessment

poses and types of documentation follows, including function into those with obstructive lung disease, re­
suggestions for providing objective and outcome-ori­ strictive lung disease, or a combination of both types
ented information. of dysfunction. The categories are mutually exclusive,
that is, all patients fit into one and only one category.
The categories of a nominal measurement scale
CHARACTERISTICS OF MEASUREMENTS
are defined Llsing objective indicators that are univer­
The purpose of performing a measurement is to as­ sally understood. For example, the classification of
sess or evaluate a characteristic or attribute of an in­ patients with heart failure could be based on the pri­
dividual. The characteristic to be measured first must mary cause for the development of the condition (see
be defined, and the purpose of performing each mea­ the box below, at left). In each case, the cause could
surement must be clear. Therapists then can select the be determined by diagnostic testing such as angiogra­
most appropriate method of measurement given the phy or echocardiography. Clear descriptions of the
available resources and their clinical skills. criteria for inclusion in each category facilitate clini­
cians' agreement on the assignment of patients to cat­
egories. A high percentage of agreement indicates
levels or Types of Measurements
high interrater reliability.
Measurements can be described according to their
Ordinal
type or level of measurement. There are four levels of
measurements which are nominal, ordinal, interval Ordinal measurements are similar to nominal measure­
and ratio (Rothstein, Echternach, 1993). Recognizing ments with the exception that the categories are or­
the level of measurement aids in the understanding dered or ranked. The categories in an ordinal scale in­
and interpretation of the result. dicate more or less of an attribute. The scale for rating
angina is an example of an ordinal scale (Pollock,
Nominal Willmore, and Fox, 1978) (see the box below, at right).
Objects or people are often placed in categories ac­ Each category is defined and a rating of grade I angina
cording to specific characteristics. If the categories is less than a rating of grade 4. In an ordinal scale, the
have no rank or order, then the measurement is consid­ differences between consecutive ratings are not neces-
ered nominal. An example of a nominal measurement
is the classification of patients with pulmonary dys-

Allgina Scale

Grade I: Light-The discomfort that is

Commoll Causes for the Developmellt cstablished, but j ust established
of Heart Failure Grade 2: Light moderate---Discom forl from
-

which one can be distracted by a

Myoca rd ial infarction (Mf) or ischemia
noncataclysmic evcnt; it can be "pain"
Cardiac arrhythmias
but usually is not
Renal insufficiency
Cardiomyopathy Grade 3: Moderate-sever Discomfort or pain
Heart valve abnormalities that prevents distraction by a beautiful
Pericardial effusion or myocarditis woman. handsome man. television
Pulmonary embolism or pulmonary hypertension show, or other consuming interest;
Spinal cord injury o nl y a tornado, earthq uake or
Congenital abnormalities expl osio n can distract one from a grade
Aging 3 discomfort or pain

Grade 4: Severe---Discomfort that is the most

From Cahalin, L. P. (1994). Cardiac muscle dysfunction. In Hille­ excruciating pain experienced or
gass, E. A., & Sadowsky, H. S. (Eds.). Essentialsof cardiopul­ imaginable
monary pulmonary physicaltiJerapy. Philadelphia: WB Saunders.

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 6 Measurement and Documentation 119

sarily equal. The difference between grade 1 angina sured using either an interval or a ratio scale. The
and grade 2 is not necessarily the same as between Fahrenheit temperature scale assigns the zero point to
grade 3 and grade 4 angina. Consequently, if num­ the temperature at which water freezes, whereas the
bers are assigned to categories, they can be used to Kelvin scale assigns the zero point to an absence of
represent rank, but cannot be subjected to mathemati­ heat. The Fahrenheit scale is an example of an inter­
cal operations. Averaging angina scores is incorrect val level of measurement, and the Kelvin scale is a
because by averaging, it is assumed that there are ratio level of measurement.
equal intervals between categories. Measuring force production using an isokinetic dy­
Categorical measurements are considered ordinal namometer is an example of an interval measurement
if being assigned to a specific category is considered commonly used in physical therapy. Patients may be
"better than" or "worse than" another category. For able to generate muscle tension and move an extrem­
example, patients with angina could be classified as ity, but register a score of zero because they cannot
having either stable or unstable angina. This mea­ move as fast as the dynamometer. Interval measure­
surement would be considered ordinal, because stable ments can have negative values, and can be subjected
angina usually is considered a better condition to to some arithmetic operations. Adding and subtracting
have compared with unstable angina (Hurst, 1990). values is logical. A patient who generates 10 ft-lbs at
one session and 20 ft-Ibs at the following session in­
Ratio
creased their torque production by 10 ft-Ibs. Interval
Ratio measurements have scales with units that are values cannot be subjected to division or multiplica­
equal in size, and have a zero point that indicates ab­ tion. It cannot be stated that the patient generated
sence of the attribute that is being measured. Exam­ twice as much torque on the second session compared
ples of ratio measurements that are used in cardiopul­ with the first session because it cannot be assumed
monary physical therapy include vital capacity, that a reading of zero indicated no torque production.
cardiac output, and oxygen consumption. Ratio mea­
surements are always positive values, and can be sub­
Reliability
jected to all arithmetic operations. For example, an
aerobic capacity of 4 Llmin is twice as great as an Reliability is defined as the consistency or repro­
aerobic capacity of 2 Llmin. ducibility of a measurement. Ideally, if attempting to
When deciding if a measurement is ratio level or. measure a specific attribute, the value of the measure­
not, the attribute that is being measured is defined. ment should change only when the attlibute changes.
If the zero point indicates absence of the attribute, However, all measurements have some element of
then the scale would be considered ratio. For exam­ error that contributes to the variability of the measure­
ple, cardiac output can be defined as the amount of ment. When the error is relatively high, the value of
blood in liters ejected from the left ventricle over a the measurement can change, even though the attribute
I -minute period. A measurement of zero cardiac has not changed. Believing that a change occurred
output would be absence of the characteristic, or no when it did not could result in an inaccurate clinical
blood ejected from the left ventricle. decision related to treatment planning or progression.
Many factors contribute to variability in the results
Interval
of measurements. The characteristic being measured
Measurements that are at interval level have units on may demonstrate a certain degree of variability. Both
a scale with equal distance between consecutive mea­ blood pressure and heart rate vary depending on both
surements. Interval measurements are differentiated mental and physical factors such as body position,
from ratio measurements, because the zero point is hydration level, anxiety and time of day. For these at­
arbitrary rather than absolute. An arbitrary zero point tributes, multiple measurements often are used to
is one that does not mean an absence of the character­ provide the best estimate of the patient's true heart
istic that is being measured. Temperature can be mea­ rate and blood pressure.

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120 PART II Cardiopulmonary Assessment

Another factor that contributes to the variability of a ment must possess a certain degree of validity. Mea­
measurement is changes in the testing instrument. surements can be reliable but not valid. For example,
Testing instruments may vary in their readings because measurements made using bioelectrical impedance
of changes in environmental conditions or malfunction analyses have been shown to be valid for the estima­
of parts of the instrument. Instruments should be cali­ tion of total body water, but uncertainty exists as to the
brated, that is, compared with a known standard, on a validity of estimates of percent body fat made with this
regular basis to assure accuracy of the readings. Some device (Kusher and Schoeller, 1986).
instruments are relatively easy to calibrate. For exam­ There are various types of validity. Of importance
ple, values obtained using aneroid blood pressure de­ in clinical practice are concurTent, predictive, and pre­
vices can easily be compared with values obtained scriptive validity. Concurrent validity is when a mea­
using mercury manometers. Values obtained using ei­ surement accurately reflects measurements made with
ther palpation or a heart rate monitor can be compared an accepted standard. Comparing bioelectrical imped­
with values obtained from BCG recordings. The mer­ ance measurements for estimating percent body fat
cury manometer and the electrocardiograph (BCG) with estimates made from hydrostatic weighing is an
would be considered the standard method of measure­ example of determ.ining conCUITent validity. In this ex­
ment. Other devices, such as cycle ergometers, are ample, hydrostatic weighing would be considered the
more difficult to calibrate, and the usual approach is to "gold" or accepted standard. Measurements with pre­
rely on the manufacturer's specifications as to the ac­ dictive validity can be used to estimate the probability
curacy of the work rate readings. of occurrence of a future event. Screening tests often
A third factor contributing to measurement vari­ involve measurements that are used to predict future
ability is differences in the methods that therapists events. For example, by identifying people with risk
use to make measurements. If a result is consistent factors for coronary artery disease (CAD), a prediction
when one therapist repeats a measurement, then the is made that the likelihood of developing CAD is
measurement is said to have high intrarater reliabil­ higher than normal. Measurements with prescriptive
ity. Measurements that are consistent when multiple validity provide a guide to the direction of treatment.
therapists perform the measurement under the same The categorical measurement of determining a per­
conditions are said to have high interrater reliability. son's risk for a future coronary event is a measurement
Often, measurements have high interrater reliability, that would need to have predictive validity. By classi­
but lower intrarater reliability because therapists vary fying patients into high vs. low risk categories based
in the specific methods of making the measurement. on the results of a diagnostic exercise test, the inten­
For example, a slight variation in the anatomical site sity, and rate of progression of treatment is determined.
used for measuring skinfold thickness can produce The accuracy of various types of exercise tests
relatively large differences in percent fat estimates often is described by reporting sensitivity and speci­
(Ruiz, Colley, and Hamilton, 1971). Interrater relia­ ficity. Sensitivity is the ability of a test to identify in­
bility is important in clinical settings where a patient dividuals who are "positive," or who have the charac­
may be evaluated and treated by more than one thera­ teristic that is being measured. Specificity is the
pist. If the interrater reliability of a measurement is ability of a test to identify individuals who are "nega­
low, then changes in the patient over time may not be tive," or who do not have the characteristic. If a test
accurately reflected. produces a high number of "false positive" results,
then the sensitivity will be low. A false positive result
means that the test result was positive but the charac­
Validity
teristic was absent. Young women often have posi­
Valid measurements are those that provide meaningful tive stress test results but do not have CAD. The con­
information and that accurately reflect the characteris­ sequence of a false positive test result could be
tic for which the measurement is intended. For a mea­ unnecessary treatment. A high number of "false neg­
surement to be useful in a clinical setting, the measure­ ative" results would produce a low specificity. A

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 6 Measurement and Documentation 121

false negative result would be a negative test result, measurement, subjective measurements usually have
even though the disease or characteristic is present. lower interrater reliability compared to objective mea­
The consequence of a false negative test result is not surements (Rothstein and Echtemach, 1993).
receiving treatment when it is indicated. Objective measurements are not affected by the per­
son performing the measurement, that is, these mea­
surements do not involve judgement of the measurer.
Objective and Subjective Measurements
Heart rate measured by a computerized ECG system is
Measurements vary in degree of subjectivity vs. objec­ an example of an objective measurement. Other exam­
tivity. Subjective measurements are those that are af­ ples include measurement of blood pressure using an
fected in some way by the person taking the measure­ intraarterial catheter or oxygen consumption using a
ment, that is, the measurer must make a judgment as to metabolic system. Objective measurements are not nec­
the value assigned. The assessment of a patient's essarily accurate, but usually have high intelTater relia­
breath sounds is influenced by many factors including bility (Rothstein, and Echtemach, 1993).
the therapist's choice of terminology for describing the Most measurements cannot be classified as either
findings, their perception of normal breath sounds, and objective or subjective. The quality of a measurement
their hearing acuity. The grading of functional skills can be placed on a continuum based on the degree of
may be influenced by the therapist's interpretation of reliability, as shown in Figure 6-\. The attribute or
what constitutes minimal vs. moderate assistance. Be­ characteristic that is being measured also can be
cause of the influence of the person performing the viewed as a subjective o r objective phenomena

Quality of the Measurement

Subjective Objective

Phenomena Being
Measured

Objective
o 100
SO 00
Reliability Continuum

Subjective
o 100
SS OS

FIGURE 6-1
Illustration of the relationship between the quality of a measurement as being subjective or
objective, and the phenomenon being measured. The scales indicate that the objectivity of a
measurement, or reliability, lies along a continuum. For example, a subjective phenomenon may be
measured subjectively (subjective sign [SS]) or objectively (objective sign [OS]). (From Rothstein
1M: On defining subjective and objective measurements. Phys Ther 69:577-579, 1989.)

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122 PART II Cardiopulmonary Assessment

(Rothstein, 1989). A subjective attribute such as pain stage post-MI could provide information to formulate
can be measured in either a subjective manner with a an exercise prescription. However, the risks of per­
low degree of reliability, or in an objective manner forming this procedure at this time in the recovery
with a high degree of reliability. period may outweigh the benefits.

SELECTING MEASUREMENTS PERFORMING MEASUREMENTS

At the initial session with a client, how do therapists When performing mcasurements, care must be
decide on the measurements to be performed? And taken to use procedures that can be replicated for
what additional measurements need to be peltormed future comparisons. Time must be taken to ensure
during the course of treatment and at follow-up evalu­ that conditions are optimal and that the patient is
ations? Many factors influence the choice of the thera­ informed of his or her part in the activity. For ex­
pist, including information obtained from the medical ample, measuring blood pressure in a noisy treat­
record and the patient interview, and knowledge of ment area immediately when the patient arrives for
available treatment options. Therapists also must an appointment may not provide an accurate mea­
strive for efficiency and not repeat tests that have been surement of resting or baseline bJood pressure.
performed by other health care professionals. Charac­ Documenting the conditions in which a measure­
teristics or qualities of measurements, such as reliabil­ ment was made also is important. Conditions may
ity and validity also influence the therapist's decision. include, but are not limited to, time of day, room
Medical and personal information about the client temperature, recent activities performed by the pa­
will be a plimary factor guiding the selection of mea­ tient, and type of measuring device.
surements. For example, appropriate measurements Measurements should be made with an objective
differ for a patient with an acute MI vs. a patient who and open mind, that is, without anticipating the result of
is 3 weeks post-MI. Other factors to consider include the measurement. A measurement that is approached
the size of the infarction and associated complications with a preconceived idea of the outcome may be af­
such as an-hythmias, heart failure, or angina. Informa­ fected by the therapist's expectations. Having confi­
tion collected during the patient interview also may dence in the results of one's measurements is impor­
guide the selection. For example, for patients who dis­ tant, and is developed as clinical skills are developed.
play anxiety when walking on a treadmill is discussed, In clinics where more than one therapist is likely
another mode of exercise may be more appropriate. to evaluate or treat a patient, written procedures for
Measurements need to be selected that are appropriate performing measurements are needed. Therapists also
to the specific pathology, the severity of the condition, need to review the written procedures on a regular
and other characteristics unique to the patient. basis and practice performing the measurements as a
Another important factor to consider in selecting group. Practicing together is especially important for
measurements is the application of the information. therapists who are new to the clinic. The interrater re­
Every measurement should contribute to the deci­ liability for commonly used measurements then can
sions made by the therapist on the course and pro­ be determined. If the reliability is low, the written
gression of treatment. Measurements that do not con­ procedures may need to be revised to assure optimal
tribute to the assessment of the patient result in an consistency of measurement.
inefficient use of the therapist's time and add unnec­
essary costs to medical care.
INTERPRETING MEASUREMENTS
Another factor that i nf! uences the selection of
measurements is the risk-benefit ratio. How do risks Interpreting the results of measurements often is a
of conducting a test or measurement relate to the difficult task. Usually patients' problems are under­
value of the information gained? Subjecting a patient stood not by reviewing the results of a single mea­
to a symptom-limited exercise test during the acute surement, but by viewing the relationships between

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 6 Measurement and Documentation 123

the results of several measurements. For example, and viewed in the context of the patient's personal
the finding that blood pressure does not increase goals. Therapists develop a picture of the severity of the
with activity by itself may not be considered abnor­ cardiopulmonary condition, the stage of recovery, and
mal, if the activity level is low and the patient is tak­ the presence of coexisting conditions. A treatment plan
ing a beta receptor antagonist medication. The find­ is developed based on the composite of findings. The
ing of no increase in blood pressure with signs and plan is implemented and is continuously checked for
symptoms of exercise intolerance during moderate appropriate direction by measurements made during
level activity in another patient may be indicative of treatment sessions. Because of the progressive nature of
inadequate cardiac output. many of the conditions that affect the cardiovascular
A knowledge of what is "normal" is important to and pulmonary systems, each treatment session can be
be able to interpret the results of tests. For some mea­ viewed as a reassessment.
surements, normal values are well-defined. Measure­
ments of resting blood pressure, cholesterol, and
PURPOSES OF DOCUMENTATION
blood glucose have defined categories of normal,
borderline, and elevated. For other measurements, To be useful, measurements need to be recorded or
population normative standards are not well-defined. documented in a concise and organized manner.
For example, what is the normal increase in heart rate Measurements that remain in the mind of the evalua­
when walking at 3.5 mph on a level surt'ace? Values tor often are forgotten or not remembered accurately.
for individuals differ, depending on age, medications, Documentation is becoming more important to assist
fitness level, and walking efficiency. Results need to and to maximize reimbursement, as well as to facili­
be interpreted by considering these factors and patho­ tate efficiency of care through communication be­
logical conditions if present. Each individual has tween health care professionals.
their own "normal" or usual response, and variations Documentation includes information about evalua­
from this value could be considered abnormal. tive findings, the assessment of the patient's condi­
Interpreting the results of tests is similar to putting tion, and the plan for future care. Reasons for docu­
the pieces of a puzzle together to create a picture of mentation include the following:
the patient and their limitations. Information is col­ I. To provide information for other therapists, as­
lected from several sources, including the medical sistants, or aides who may evaluate and/or treat
record, patient interview and physical therapy evalua­ the client.
tion. Measurements performed and interpreted by 2. To provide data for comparison for follow-up
other health care professionals can be obtained from visits.
the medical record and include chest x-ray, blood 3. To provide data to determine treatment effec­
analyses, and echocardiography. During an interview, tiveness and efficiency through collection of in­
the patient reports information about his cunent and formation on the results or outcomes of various
past medical problems. It is important to be sensitive types of care.
to the patient's feelings about his condition, noting 4. To assist therapists in organizing findings to fa­
his stage of emotional recovery. Detecting attitudes cilitate logical decisions on the treatment ap­
related to changing lifestyle habits also is important. proach and overall care plan.
After the interview, the therapist should have a sense
of the patient as a person and begin to plan a strategy
TYPES OF DOCUMENTATION
for optimizing his or her physical function.
Measurements made during the physical examina­ Systems for documenting information vary between
tion may include physiological responses to activity, facilities. In acute care hospitals, physical therapy
breathing patterns, ventilatory capacity, and breath notes may be included as a part of the patient's
sounds. The results of these measurements are inte­ comprehensive medical record. In other facilities
grated with results collected during the chart review such as private practice clinics the patient's record

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124 PART II Cardiopulmonary Assessment

may consist of physical therapy notes and medical ambulation," and "abnormal tone." Written definitions
information that is relative to the physical therapy of commonly used terms that include examples of
care plan. Whatever the system, notes can be classi­ characteristics that illustrate the definition can help to
fied according to the timing and purpose of the doc­ decrease confusion.
umentation, using the following categories: Notes also need to clearly demonstrate the need
I. Initial evaluation, assessment, and plan for professional skills if a physical therapist is per­
2. Interim or progress notes forming the evaluation and/or treatment. Activities
3. Discharge notes that can be performed by physical therapists assis­
4. Follow-up or reevaluation notes tants, aides, nursing personnel or family members
The initial note usually is the longest, containing in­ need to be delegated to the appropriate individual. In
formation on the reason for referral, other medical addition, patients can be instructed in those activities
conditions and information that could affect physical in which they can pelform independently.
therapy management, data collected during the pa­ Another time in which documentation is essential
tient interview and physical examination, an assess­ is when an unusual or adverse event occurs. For ex­
ment or interpretation of the findings and the care ample, abnormal responses to activity that may ap­
plan. Interim or progress notes record short-term pear relatively benign are important to record. Abnor­
changes in the patient's status, and typically are writ­ mal responses may include dizziness, anginal or
ten on a daily or weekly basis. The discharge note musculoskeletal pain, or arrhythmias. An unusually
records the specific outcomes of treatment, the plan high or low heart rate or blood pressure response also
for discharge, including home program, and the plan should be noted. Combined with findings noted by
for follow-up. At follow-up visits, a note is written to the patient or other health care professionals, these
assess changes since the time of discharge and plans results may indicate significant changes in the pa­
for additional treatment. tient's cardiopulmonary status.
The organization of documentation varies be­
tween facilities. Many facilities use the SOAP (sub­
GENERAL GUIDELINES FOR CONTENT
jective, objective, assessment, plan) format (Ketten­
AND ORGANIZATION
bach, 1990). Other facilities have modified this
Writing notes in a clear and concise format is impor­ format, with the same information organized in a dif­
tant so that information is conveyed accurately. Exam­ ferent w a y . The following section presents an
ples of unclear notes are ones in which the handwriting overview of relevant subjective and objective infor­
is illegible, or that contain vague statements that could mation, and a description of items to include in the
be interpreted in more than one way. Concise notes are assessment and plan.
more likely to be read by other health care profession­
als. In most clinicians' schedules, time is not available
Subjective Information
to read through extensive information about a patient
that may not be relevant. A concise note only includes Subjective information contains a degree of judge­
essential infOImation in a writing style that is clear and ment or interpretation by the person reporting the in­
does not include unnecessary phrases. Another impor­ formation. The patient and family's perceptions of
tant rule is to use only standard or accepted abbrevia­ their cardiac or pulmonary condition are considered
tions. Facilities have lists of approved abbreviations subjective information. In the initial note, descrip­
for that facility. The list should be available to those tions of pain or discomfort that may be associated
who write, read, and review records. Within a physical with either a cardiac event or a pulmonary complica­
therapy department, common terms need to be clearly tion are important to include. Some of the informa­
defined and used in a consistent manner by all staff. tion reported by the patient may be objective, such as
Terms that often generate confusion and carry multiple blood cholesterol levels, resting blood pressure val­
meanings include "minimally assisted," "functional ues or number of cigarettes smoked per day.

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 6 Measurement and Documentation 125

In the interim note, it is impoltant to record the pa­ The description of the evaluation and treatment
tient's responses to treatment including feelings of results needs to include specific information on the
angina, dyspnea, or fatigue. Whether a prescribed home activity, or exercise stress, and on the physiological
or ward activity program is performed and the patient's responses. Components of the activity description in­
subjective responses to the program also are important clude the following:
to note. Any reported changes in the ability to function I. Mode of activity (corridor or track walking,
either at home or in the community are important to lower extremity cycling)
record. The most impoltant subjective finding to report 2. Work level or rate (mph, percent grade, esti­
in the discharge note is whether the patient believes mated resting metabolic rate level)
personal treatment goals were achieved. 3. Duration of activity at each work level
The description of the activities should be written
clearly so that the workload can be reproduced. The
Objective Information
responses to activity include changes in heart rate and
Measurable or observable information that is col­ rhythm, blood pressure, respiratory rate, oxygen satu­
lected during the interview, evaluation, and treat­ ration levels, and heart and breath sounds as com­
ment is considered objective. Information from the pared with from preactivity to either during or imme­
medical record may be included if it is relevant to diately after activity. Signs of exercise intolerance,
the patient's current condition. To be relevant, the such as changes in skin color, incoordination, and
information should have potential impact on the di­ sweating, also need to be documented. Whether the
rection of the evaluation and treatment of the patient, patient used oxygen during treatment, or required
such as current medications and results of diagnostic physical assistance also should be noted. By objec­
tests. Results uJ" tests and measurements conducted tively recording the activity prescription and the
as a part of the initial evaluation are objective infor­ physiological responses, therapists can estimate the
mation. A description of the treatment that is pro­ patient's activity tolerance.
vided, and the patient's physiological responses to
treatment also are considered objective information.
Assessment
When recording information collected during the
evaluation, the results of various tests can be cate­ The purpose of the assessment part of a note is to list
gorized as impairments or as functional limitations. the client's major problem(s), identify treatment goals
An impairment is an abnormality of physiological or outcomes, and provide an interpretation of the sub­
function or anatomical structure at the tissue, organ jective and objective findings. The problem list is lim­
or body system level (Jette, 1994). Examples of im­ ited to problems that can be addressed by physical
pairments include decreases in muscle strength or therapy. Problems can be listed in order of priority
range of motion, or abnormal heart rate and blood and stated in functional terms. For example, stating
pressure values. A functional limitation is a restric­ "patient unable to c1imb stairs because of abnormal
tion in performance at the level of the whole person ECG responses and dizziness," rather than stating
(Jette, 1994). Functional Ii mi tations can be attrib­ "abnormal ECG response during activity."
uted to physical, social, cognitive, or emotional fac­ Goals are the outcomes to be achieved by paltici­
tors. Examples of functional limitations include the pating in a physical therapy program and are generated
inability to dress, transfer, ambul ate, or climb by the therapist and patient in consultation. Goals are
stairs. Improvements in functional status usually stated in functional terms as to what the patient will be
are of primary interest to patients and families and able to do at discharge. The following is an example:
to those who reimburse for health care. Measure­
ments of impairments arc important, because they Patient will be able to carry one 25-lb. bag a distance of 50
assist therapists in deciphering the causes or rea­ feet with appropriate heart rate and rhythm responses,
sons for limitations in function. within 2 weeks.

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126 PART II Cardiopulmonary Assessment

To be able to detennine if a goal has been met, the ther­ mation from records can be organized into sections
apist must be able to observe or to measure the activity. describing subjective and objective information, as­
Therapists also estimate the time that it will take to sessment or interpretation of the findings, and the
achieve the outcome. In the discharge note, whether care plan. Subjective and objective information is
each goal has been met is stated. If a goal has not been collected during an interview, medical record review,
achieved, then a reason or explanation is provided. and evaluation and/or treatment session. The assess­
The assessment also includes a brief interpretation ment provides an interpretation of the subjective and
of the subjective and objective findings. Therapists objective findings, and states the desired treatment
can use this section to state their "clinical hypothe­ outcomes. A specific plan to achieve the outcomes
sis," or explanation of the primary problem that pro­ then is described. Documentation can be viewed as a
duces the objective and subjective findings. The ini­ way to assist therapists to organize their findings, re­
t i a l n o t e m a y i n c l u d e statemen t s about the flect on the significance of the findings, and generate
individual's potential t o succeed i n a rehabilitation an efficient and comprehensive care plan.
program, or reasons for not performing tests that
would typically be performed with individuals with
REVIEW QUESTIONS
similar diagnoses. Whether the patient needs to be re­
ferred to other health care professionals or to commu­ l. Describe and give examples of nominal, ordinal,
nity services also can be included. ratio and interval measurements.
2. Identify three factors that contribute to the vari­
ability of measurements.
Plan
3. Define sensitivity and specificity of tests.
The plan provides a description of the approach that 4. Differentiate between objective and subjective
will be taken to assist the patient in achieving the measurements.
stated goals. The plan may include a description of S. Identify four purposes for documenting the re­
treatment that can be provided, education for the pa­ sults of evaluation and treatment sessions.
tient and/or family, and referrals to other services.
Descriptions of home or ward programs should be in­
References
cluded in the plan. At discharge from an inpatient
unit, the plan includes where the patient will be resid­ Hurst, J.W. (J 990). The recognition and treatment of four types of
ing and plans for follow-up. At discharge from an angina pectoris and angina equivalents. In Hurst, J.W., Schlant,
R.C., Rackley, C.E., Sonnonblick, E.H., & Wenger, N.K.
outpatient facility, the plan contains recommenda­
(Eds.). The hean Oth ed.). New York: McGraw-HilI.
tions for follow-up care.
Jelle, A . M. (1994). Physical disablement concepts for physical
therapy research and practice. Physical Therapy 74, 380-386.
Keuenbach, G. (J990). Writing S.O.A.P. notes. Philadelphia: FA Davis.
SUMMARY
Kusher, R.F. & Schoeller, D.A. (J986). Estimation of total body
water by bioelecu'ical impedance analysis. American Journal of
Measurement and documentation are important com­
Clinical Nutrition. 44, 417-424.
ponents of the process of providing patient care.
Pollock, M.L., Wilmore, J.H., & Fox, S.M. (1978). Health and it ­
f

Therapists select measurements because they reveal ness through physical activity. New York: John Wiley and Sons.
information about patient characteristics that is Rothstein, 1.M. (J989). On defining subjective and objective mea­
needed to determine appropriate directions for treat­ surements. Physical Therapy 69, 577-579.
Rothstein, J .M .. & Echternach, J. L. (1993). Primer on measure­
ment. Performing measurements in a consistent way
ment: An introductory guide to measuremelll issues. Alexan­
allows comparison of patient characteristics at varied
dria, V A: American Physical Therapy Association.
points in time. The recording, or documentation, of Ruiz, L.,& Colley, J.R.T. & Hamilton, P.J.S. (1971). Measurement of
the results of measurements and other information triceps skin fold thickness: An investigation of sources of variation.

about the patient serves as a legal record. Although British Joul11al of Preventive and Social Medicine 25, 165-167.

documentation formats vary between facilities, infor­

Copyrighted Material
 History

Willy E. Hammon

KEY TERMS Cough History

Dyspnea Pain

INTRODUCTION
words and pace (Hurst, et ai, 1990). If the therapist ap­
The value of the history depends in large part on the pears hurried, distracted, preoccupied, irritated, or un­
skill of the interviewer. When eliciting the history caring; is often interrupted; or fails to be an attentive lis­
from a patient, therapists must be alert to recognize tener, the patient-therapist relationship will likely suffer.
the symptoms that are indicative of cardiac and pul­ The interviewer must be careful not to allow per­
monary disease. This information is then used in the sonal feelings about the patient's grooming, appear­
decision-making process to select the most appropri­ ance, demeanor, and behavior during the interview to
ate intervention for the individual. unduly question the validity of the chief complaints
(Birdwell, 1993). By the time the patient is referred
for physical therapy, he or she may have seen one or
THE INTERVIEW
more physicians, have been subjected to a number of
Obtaining a thorough and accurate patient history is noninvasive or invasive studies, or have been pre­
truly an art. One imponant goal of histOlY taking is to scribed oral or inhaled medications with variable or
establish a good patient-therapist rapport. The patient unsatisfactory alleviation of symptoms. The patient is
must be allowed to explain the history in his or her own likely to manifest a degree of anxiety and frustration.

127

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128 PART n Cardiopulmonary Assessment

Therefore the therapist's approach, history-taking and 2. Whether the treatment order is narrow or
interviewing style is important for gaining the pa­ broad in scope.
tient's confidence and cooperation. 3. The acuteness of the patient's illness, level of
The patient history interview can be divided into consciousness, and his ability to provide ac­
the data-gathering and interpretative sections (Snider, curate information.
1994). The data-gathering segment begins with ask­ This chapter presents a comprehensive approach to
ing why the patient has sought medical attention and history taking. Therapists may find part or all of this
has been referred for physical therapy services. In information applicable, depending on their particular
other words, what is the patient's chief complaint­ circumstances.
the symptom that caused the patient to seek help?
Each chief complaint should be carefully ex­
QUESTIONNAIRES
plored. Supplementary questions should be nonlead­
ing, using words the patient can easily understand. Printed symptom or medical questionnaires can be ben­
This allows the interviewer to determine the signifi­ eficial or detrimental to the patient-therapist relation­
cance of the complaint. An in-depth knowledge of ship, depending on how they are used. Questionnaires
cardiopulmonary pathophysiology allows the thera­ can expedite the data-gathering portion of the initial
pist to almost simultaneously gather data about the visit by allowing the patient to note in advance, all
patient's symptoms and to interpret the likely type of symptoms, medical conditions, surgeries, occupalions,
cardiopulmonary dysfunction that exists. This in turn medications, and other factors that may influence phys­
serves as a basis for the therapist to begin to select ical therapy intervention. They can reduce the amount
the appropriate assessment and treatment modalities of nontreatment time therapists may otherwise spend
for the individual. inquiring about irrelevant symptoms and conditions.
It is important to remember that patient satisfaction Pri nted questionnaires also allow patients sufficient
is greatest if the patient is allowed to fully express time to recall relevant informalion and respond more
major concerns without interrupting. In addition, the accurately than they often do in an interview selting
risk of missing what is really of greatest concern to the (Miller, 1980). Used in this way, a printed question­
patient is reduced if the patient is allowed sufficient naire can be a valuable tool for expediting a compre­
time to describe it in his or her own words. Studies hensive evaluation of cardiopulmonary patients.
have shown this usually only takes from I to 3 minutes. However, if questionnaires are used improperly,
The patient's view of what is the problem and his or they can depersonalize the history-taking portion of
her suggestions for addressing the problem should be in­ the initial visit (Hurst, et ai, 1990). If the therapist al­
cluded in the interview. Patient satisfaction is improved lows the printed form to become a substitute for in­
by his or her involvement in the interview as well as teraction with the patient, patient satisfaction will be
later in the establishment of short- and long-term goals. low and the patient-therapist relationship will suffer.
The depth of the history taken by the physical ther­
apist (PT) can vary according to the following factors:
DYSPNEA
1. Whether the individual is an inpatient or an
out patient. Many inpatients have detailed Dyspnea, breathlessness or shortness of breath, can be
medical records available for the therapist to re­ defined as the sensation of difficullY in breathing
view. This significantly reduces the amount of (George, 1990). It is one of the most common reasons
information the therapist needs to obtain from that patients seek medical attention. Dyspnea is difficult
the patient during an interview. If the informa­ to quantitate, because it is subjective and at times is
tion in the chart is scant, or if the individual is normal (i.e., at high altitudes, and during or following
an outpatient with only a treatment referral and vigorous exercise). Dyspnea is a symptom of cardiac
little or no medical records available, the thera­ and pulmonary diseases, as well as other conditions.
pist should obtain a more detailed history. When a patient complains of shortness of breath or

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 7 History 129

MITOCHONDRIA MUSCULOSKELETAL CARDIOVASCULAR RESPIRATORY AIR

FIGURE 7-1
Schematic illustration of the oxygen transport system, which involves the interaction between the
respiratory, cardiovascular, and musculoskeletal systems. (Reprinted with permission from Mahler
D: Dyspnea: diagnosis and management. Clirz Chest Med 8 [2),215-230,1987.)

breathlessness, it should be noted that this complaint in the work of breathing, and (3) an abnormality in the
is often unrelated to the patient's arterial oxygen ventilatory system itself (George, 1990).
level (Pao2). Many times, it appears that altered me­ An increased awareness of normal breathing is
chanical factors during breathing contribute to the usually related to anxiety (Miller, 1980). The patient
sensation of breathlessness (Mahler, 1987). Numer­ commonly complains of "not getting a deep enough
ous receptors that have a role in sensing dyspnea breath," a feeling of "smothering," or "not getting air
have been identified and include vagal receptors down in the right places" (Szidan and Fishman,
(e.g., irritant, stretch, and J-receptors), chemorecep­ 1988). These sensations have been designated as psy­
tors, proprioceptive receptors (tendon organs, muscle chogenic dyspnea. The patient's breathing pattern is
spindles, joint and/or skin receptors), and upper air­ irregular, with frequent sighs. When severe, it is asso­
way receptors (Snider, 1994). ciated with tingling of the hands and feet, circumoral
Analyzing the oxygen transpOit system (Figure 7-1) numbness, and lightheadedness. Coaching the patient
can help the therapist deterrrune the likely cause of each to hyperventilate and to reproduce the symptoms may
patient's dyspnea and the most appropriate physical help the patient better understand the cause of these
therapy intervention. The delivery of oxygen from am­ symptoms and how to control them (Miller, 1980).
bient air to the mitochondrion within the cell depends The hyperventilation syndrome is properly diagnosed
on the intact interaction of the respiratory, cardiovascu­ only after organic causes have been excluded and
lar, and muscular systems. Also, carbOn dioxide (C02) pulmonary function tests indicate normal respiratory
is eliminated in the opposite direction. Dyspnea can be mechanics and Pao2.
caused by dysfunction in any of the systems. The second cause of dyspnea is an increase in the
Dyspnea commonly occurs when the body's re­ work of breathing. Greater inspiratory pressures must
quirement for breathing (ventilation) exceeds the be generated by the respiratory muscles to move air in
body's capacity to provide (Snider, 1994). In other and out of the lungs when the mechanical properties
words, the symptom varies directly with the body's of the lungs have changed. This may be related to an
demand for ventilation and inversely with ventila­ increase in lung water resulting from cardiac disease
tory capacity. or the high cardiac output of anemia. A loss of com­
There are three basic causes of dyspnea: (I) an in­ pliance (increased lung stiffness) because of diffuse
creased awareness of normal breathing, (2) an increase inflammatory or fibrotic lung disease often causes

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130 PART II Cardiopulmonary Assessment

shortness of breath. Small or large airways obstruction I. Are you short of breath at rest? If the answer
as a result of bronchoconstriction, sputum, inflamma­ is yes, it suggests a severe physiological dys­
tion, and other effects commonly produces dyspnea. function. The patient likely needs prompt eval­
The third cause of dyspnea is an abnormality in uation by a physician if this is of recent onset
the ventilatory apparatus or pump. The ventilatory and has not had a medical workup.
apparatus consists of the thoracic cage, respiratory 2. Do you have chest pain'? If so what part of
muscles, and nerves. Any of these may become dys­ your chest? Unilateral localized chest pain
functional. Thoracic cage abnormalities include raises the possibility of spontaneous pneumoth­
kyphoscoliosis, extreme obesity, and large pleural ef­ orax, pulmonary embolism, or chest trauma.
fusions. Diseases of the respiratory muscles include 3. What were you doing immediately before or
polymyositis and muscular dystrophy. Neurologic ab­ at the time of onset of shortness of breath?
normalities include spinal cord injuries, phrenic nerve Approximately 75% of spontaneous pneumotho­
injuries, brachial plexus neuropathy, ascending races occur during sedentary activity, 20% dur­
polyneuritis (GuiJlain-Barre syndrome), myasthenia ing some strenuous activity, and 5% are related
gravis, amyotrophic lateral sclerosis, poliomyelitis, to coughing or sneezing. A history of immobi­
neurotoxins, and exposure to paralytic agents. lization of a lower extremity, recent surgery, bed
The time course of the appearance and progression rest, travel requiring prolonged sitting, obesity,
of dyspnea should be identified (Sharf, 1989). Acute CHF, venous disease of the lower extremities,
dyspnea is common in pulmonary embolism, pneu­ are all risk factors for pulmonary embolism. If
mothorax, acute asthma, pulmonary congestion related the patient's symptoms are related to chest
to congestive heart failure (CHF), pneumonia, and trauma, the fact that a fall, a blow, or an accident
upper airways obstruction. Most of these conditions re­ occurred can usually be quickly established.
quire immediate physician evaluation of the acute 4. Do you have any major medical or surgical
problem before physical therapy inlervention. Suba­ conditions? Cystic fibrosis, chronic obstructive
cute or chronic progression of dyspnea generally pre­ pulmonary disease (COPD), interstitial lung
sents as increasingly severe dyspnea with exertion over disease, and malignancies are important causes
time. It occurs with emphysema, restrictive lung disor­ of secondary spontaneous pneumothorax.
ders such as pulmonary fibrosis, chest wall deformi­ If the therapist strongly suspects pneumothorax or
ties, respiratory muscle dysfunction, occupational lung pulmonary emboli because of the history and physi­
diseases, chronic CHF, or large pleural effusions. cal assessment, the patient should be referred for im­
Dyspnea may also be related to body position. mediate medical evaluation.
Therefore when evaluating dyspnea, the patient
should be asked if he or she has difficulty breathing
Dyspnea on Exertion
when reclining horizontally. Is it necessary to be
propped up on several pillows to sleep at night (or­ Dyspnea on exertion is a common complaint of pa­
thopnea)? Does she have more difficulty breathing tients with cardiopulmonary dysfunction. Dyspnea
when reclining on one side (trepopnea)? Does he ever during exercise or exertion usually precedes dyspnea
wake up at night short of breath, and need to sit up or at rest (Wasserman, 1982). It most often is a result of
walk around the room to "catch his breath" (paroxys­ chronic pulmonary disease or CHF. Some causes of
mal nocturnal dyspnea)? dyspnea during exertion or exercise are listed in
Table 7-1.
It is important to establish the amount of activity re­
Acute Dyspnea
quired to produce dyspnea. Various scales (Borg, 1982;
The patient that has acute dyspnea requires a rapid and Mahler and Harver, 1990) have been developed to cate­
thorough history and physical assessment. The thera­ gorize the level of dyspnea and impairment present in
pist should ask several important questions to address patients (Figures 7-2, 7-3 and Table 7-2). The patient
the possible causes of acute dyspnea (Mahler, 1987): should be asked about daily activity, and what activities

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 7 History 131

TABLE 7-1

Disorders Limiting Exercise Performance, Pathophysiology, and Discriminating Measurements*

MEASUREMENTS THAT
DISORDERS PATHOPHYSIOLOG Y DEVIATE FROM NORMAL

Pulmonary

Airflow limitation Mechanical limitation to ventilation VE maxlMVV, expiratory flow pattern, VDNT;
mismatching of VA/Q, hypoxic V02 max, VEiVo2 VE response to hyperoxia,
stimulation to breathing (A-a)po2
Restrictive Mismatching V A/Q, hypoxic stimulation
to breathing
Chest wall Mechanical limitation to ventilation VE max/MVV, Paco2 V02 max
Pulmonary circulation Rise in physiological dead space as Vo/VT, work-rate-related hypoxemia V02 max,
fraction of VT, exercise hypoxemia VENo2, (a-ET)pco2, Orpulse

Cardiac

Coronary Coronary insufficiency Electrocardiogram (ECG), V02 max, anaerobic

threshold O2, VENo2 Orpulse, blood
pressure (BP) (systolic, diastolic, pulse)
Valvular Cardiac output limitation (decreased
effective stroke volume)
Myocardial Cardiac output limitation (decreased
ejection fraction and stroke volume)
Anemia Reduced O2 carrying capacity 02-pulse, anaerobic threshold Vo2, V02 max,
VEiVo2
Peripheral circulation Inadequate O2 flow to metabolically Anaerobic threshold V02, V02 max
active muscle
Obesity Increased work to move body; V02-work rate relationship, Pao2, Paco2,
if severe, respiratory restriction and Vo2max
pulmonary insufficiency
Psychogenic Hyperventilation with precisely regular Breathing pattern, PC02
respiratory rate
Malingering Hyperventilation and hypoventilation Breathing pattern, PC02
with irregular respiratory rate
Deconditioning Inactivity or prolonged bedrest; loss of 02-pulse, anaerobic threshold Vo2, V02 max
capability for effective redistribution of
systemic blood flow

*VA-alveolar ventilation; Q---pulmonary blood flow; MVV-max-imum voluntary ventilation; VoIV.-physiologic dead space/tidal
volume ratio; Or- oxygen: V02-02 consumption; (A-a)P02-alveolar-arterial P02 difference; (a-ET)pco2-anerial-end tidal Peo2
difference. (Reprinted with permission from Wasserman K: Dyspnea on exertion: Is it the heart or lungs? lAMA 248: 2039-2043, 1982.
© 1982 American Medical Association.)

produce breathlessness (Constant, 1993). Does the pa­ cent onset of dyspnea is more characteristic of heart
tient become short of breath climbing a flight of stairs failure than chronic lung disease, which has a longer,
or walking uphill? Is the patient able to walk and talk insidious onset. Acute pulmonary problems such as
simultaneously? Does walking slower affect the indi­ pneumothorax, atelectasis, pneumonia, and other
vidual's dyspnea? conditions superimposed on chronic lung disease can
In addition, when the patient began to notice an in­ also explain a recent increase in symptoms.
crease in shortness of breath should be noted. A re­ Is wheezing present with the dyspnea on exertion?

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132 PART II Cardiopulmonary Assessment

TABLE 7-2

American Thoracic Society Dyspnea Scale

GRADE DEGREE

0 None Not troubled with breathlessness except with strenuous exercise

I Slight Troubled by shortness of breath when hurrying on the level or walking up a slight hill
2 Moderate Walks slower than people of the same age on the level because of breathlessness or has to
stop for breath when walking at own pace on the level
3 Severe Stops for breath after walking about 100 yards or after a few minutes on the level
4 Very severe Too breathless to leave the house or breathless when dressing or undressing

Reprinted with permission from Brooks SM (Chairman): Task group on surveillance for respiratory hazards in the occupational setting.
Survei Ilance for respiratory hazards, ATS News 12-16, 1982.

o Nothing at all

0.5 Very, very slight (just noticeable)

GREATEST BREATHLESSNESS Very slight

2 Slight

3 Moderate

4 Somewhat severe

5 Severe

7 Very severe

9 Very, very severe (almost maximal)

NO BREATHLESSNESS 10 Maximal

FIGURE 7-2 FIGURE 7-3

The visual analogue scale is a vertical line of 100 mm in The Borg category scale for rating breathlessness.
length. The patient is asked to make a mark along this line (Reprinted with permission from Borg G: Psychophysical
that represents his level of breathlessness. The distance of bases of perceived exertion, Med Sci Sports Exerc 14,
the patient's mark above zero represents the measurement 377-381,1982.)
of dyspnea. (Reprinted with permission from Mahler D:
Dyspnea: diagnosis and management, Clin Chest Med 8
[2],215-230,1987.)

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 7 History 133

Has there been an associated weight gain? Does the volume, the patient develops a rapid heart rate and a
patient have a positive smoking history and sputum wide arteriovenous O2 difference (decreased capillary
production? If a positive response is received, these P02) at an inappropriately low work rate. Therefore
suggest that COPD is the primary cause of symptoms the exercising muscles (both skeletal and myocardial)
(Constant, 1993). have increased difficulty getting an adequate oxygen
The basic defect that cardiac diseases produce dur­ supply to perform the necessary work, which results
ing exertion is a limited cardiac output, primarily in dyspnea, fatigue or pain. The lactic acidosis that
caused by a reduced stroke volume (Wasserman, results from the low oxygen delivery to the muscles
1982). To compensate for the relatively low stroke can be measured by either invasive or noninvasive

Functional and Therapeutic Classification of Patients with Heart Disease

Functional Classification
Class I

Patients with cardiac disease but without resulting limitations of physical activity; ordinary physical activity does not
l:ause undue fatigue, palpitation, dyspnea, or anginal pain.

Class II

Patients with cardial: disease resulting in slight limitation of physical activity; they are comfortable at res£. Ordinary
physical activity results ill fatigue. palpitation, dyspnea, or anginal pain.

Class III

Patients with cardiac disease resulting in marked limitation of physical activity; they are comfortable at rest. Less
than ordinary physical activity causes fatigue, palpitation, dyspnea. or anginal pain.

Class IV

Patients with cardiac disease resulting in inability to carry on any physical activity without discomfort; symptoms of
cardiac insufticiency or of the anginal syndrome may be present even at rest. If any physical activity is undertaken,
discomfort increases.

Therapeutic Classification
Class A

Patients with cardiac disease whose physical activity need not be restricted in any way.

Class B

Patients with cardiac disease whose ordinary physical activity need not be restricted but who should be advised
against severe or competitive efforts.

Class C

Patients with cardiac disease whose ordinary activities should be moderately restricted and whose more strenuous
efforts should be discontinued.

Class D

Patients with l:ardiac disease whose ordinary activity should be markedly restricted.

Class E

Patients with cardiac disease who should be at complete rest, confined to bed or chair.

Reprinted with permission from the New York Heart Association (1964). Diseases of the heart and blood vessels; Nomenclature alld crite'
ria for diagnosis. (6th ed.). Boston: Little, Brown.

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134 PART II Cardiopulmonary Assessment

gas-exchange methods during exercise testing. The stenosis, it is probably related to an inadequate car­
functional and therapeutic capacity of the patient with diac output during exercise. Patients with tetralogy of
hean disease can be estimated based on the history Fallot and other forms of cyanotic heart disease, ex­
and symptoms (see box on p. 133). perience both dyspnea and fatigue during exercise
Dyspnea in cardiac patients is usually related to when the aJterial oxyhemoglobin saturation has fallen
metabolic acidosis-induced hydrogen ion stimulus. appreciatively below the resting level.
Also, increased pressure in the right side of the heart
and pulmonary circulation during exertion may stim­
Orthopnea
ulate mechanoreceptors that increase ventilation and
induce dyspnea. Orthopnea is dyspnea brought on in the recumbent
Diseases that involve the lungs or thoracic cage position (Hurst, 1990). The patient may state the need
generally prevent external respiration (ventilation) for two or three pillows under the head to rest at
from keeping pace with internal respiration (in the night. This symptom is commonly associated with
cells) (Wasserman, 1982). In other words, patients CHF but may also be associated with severe chronic
outwalk or outrun their lungs during activities or ex­ pulmonary disease.
ertion. The primary symptom that limits exercise in
pulmonary patients is dyspnea because of the diffi­
Paroxysmal Nocturnal Dyspnea
culty they have eliminating CO2 produced by metab­
olism. Some individuals such as those with pul­ Paroxysmal nocturnal dyspnea (PND) is an impor­
monary fibrosis and some with COPD do experience tant type of shortness of breath. This symptom has
a decrease in P02 with exercise. Hence, dyspnea on strong predictive value as a sign of CHF (Hurst, et
exertion in pulmonary patients is usually related to ai, 1990). The patient usually falls asleep in the re­
hypoxic or hypercapnic stimuli. cumbent position, and 1 or 2 hours later, awakens
from sleep with acute shortness of breath. The pa­
tient sits upright on the side of the bed or goes to an
Dyspnea in Cardiac Patients
open window to breathe "fresh air" to get relief from
The cause of dyspnea in cardiac patients depends on shortness of breath.
whether an associated stiffness of the lungs (fall in The mechanism of PND is the transfer of fluid
compliance) is also present (Szidan and Fishman, from extravascular tissues into the bloodstream (or
1988). Dyspnea is the primary symptom of a decom­ intravascularly) during sleep (Constant, 1993). The
pensating left ventricle (Marriott, 1993). As the ven­ intravascular volume of fluid gradually increAses
tricle fails to eject the normal volume of blood, it pro­ until the compromised left ventricle can no longer
duces chronic pulmonary venous hypertension, manage it. The left atrial pressure rises when the rate
congestion, and pulmonary edema, resulting in stiff or of lymphatic drainage from the lungs is unable to
less compliant lungs. This, along with modest hypox­ keep up with the increased volume of tluid. The in­
emia that augments the respiratory drive, increases creased atrial pressure leads to a sufficiently elevated
ventilation and the work of breathing. Tachypnea is pulmonary capillary pressure to produce interstitial
often seen at rest. Exercise exaggerates the pulmonary edema. Patients who are light sleepers awaken early
congestion and edema, promotes arterial and mixed with dyspnea. Deep sleepers may not awaken until
venous hypoxemia, which also increases the amount they develop alveolar edema.
of dyspnea and tachypnea manifested. Fatigue, result­ Classic PND cannot usually be eliminated by only
ing from low cardiac output, also affects the respira­ elevating the trunk without lowering the legs. The pa­
tory muscles, further increasing the sensation of tient must pool blood in the extravascular tissues of
breathlessness. the legs to get adequate relief, which usually takes at
Dyspnea in cardiac patients without stiff lungs is least 30 minutes. This is why the patient must sit up
primarily seen during exertion or exercise (Szidan, or stand up, and ambulate.
and Fishman, 1988). In uncomplicated pulmonic The patient should be asked about the amount of

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 7 History 135

exercise or work performed during the day before an symptom, if first reported in patients over age 40, is
attack on PND. A true left ventricular failure episode often related to heart failure (Hurst, et aI, 1990). When
of PND is more likely to occur after a day of unusual confilmed that the wheezing is because of heart dis­
exertion, which has caused an increased amount of ease, the patient is said to have cardiac asthma.
extravascular fluid to accumulate in the legs. If the Wheezing in cardiac patients is a manifestation of nar­
patient is participating in an exercise or rehabilitation rowed airways and thickened bronchial walls as a re­
program, the level of exercise may need to be re­ sult of pulmonary edema (Szidan, and Fishman,
duced to prevent PND. 1988). However, if patients have a history of episodes
of wheezing and dyspnea since childhood, COPD, or
asthma is the likely cause. Other pulmonary condi­
Platypnea
tions such as eosinophilic pneumonia, bronchopul­
Platypnea is the onset of dyspnea when assuming the monary aspergillosis, allergic granulomatosis, etc.,
sitting position from the supine position (Sharf, can cause wheezing (Miller, 1980). Wheezing must be
1989). This unusual phenomenon is often found in differentiated from stridor, which is commonly caused
patients with basilar pulmonary fibrosis or basilar ar­ by laryngotracheal narrowing due to tracheostomy
teriovenous malformation. It can be related to the re­ scar, trauma of intubation, laryngeal paralysis,
distribution of blood flow to the lung bases in the sit­ epiglottitis, or tumors. Chronic pulmonary patients
ting position with resultant ventilation-perfusion may also develop heart conditions, so it is good to re­
mismatching and hypoxemia. member patients that complain of wheezing may have
both cardiac and pulmonary disease.

Trepopnea
COUGH
Trepopnea refers to dyspnea in one lateral position
but not the other (Snider, 1994). It is often produced Cough is a common symptom of pulmonary disease.
by unilateral respiratory system pathology such as The cough mechanism consists of three phases:
lung disease, pleural effusion, or airway obstruction. (1) an inspiratory phase, (2) a compressive phase, and
It also is commonly seen in patients with mitral (3) an expiratory phase (Irwin, 1977).
stenosis (Constant, 1993). Occasionally it may be the There are numerous cough irritant receptors lo­
result of a fall in blood pressure in the left lateral de­ cated on the mucosa of the larynx, trachea, bronchi,
cubitus position. If the patient has ischemic heart dis­ pleura, and external auditory canal. These receptors
ease, the reduction in coronary perfusion can cause are most sensitive at the glottis and carina, and di­
either angina or dyspnea. minish rapidly beyond the fourth generation bronchi.
A cough follows stimulation of these mucosal recep­
tors by any of a number of factors including inflam­
Functional Dyspnea
mation, sputum, foreign bodies, noxious gases or
Functional dyspnea is defined as shOltness of breath at odors, chemical substances, endobronchial tumors,
rest but not during exertion (Shmf, 1989). It is most and extrabronchial pressure on the trachea or bronchi
commonly seen in young women who complain of the (Sharf, 1989).
need to take a deep breath or to sigh and interpret this A productive cough is beneficial for clearing the
sensation as shortness of breath. The physical exami­ airways of sputum and foreign material, and gener­
nation and pulmonary function tests are negative. Re­ ally should not be inhibited. However, a dry, hacking
assurance is usually all that is necessary. cough is usually of no value and can have a self­
perpetuating irritant effect on the respiratory mucosa.
A dry cough may be the initial symptom of certain
WHEEZING
interstitial lung diseases such as allergic alveoli tis,
Patients that complain of wheezing associated with sarcoidosis, and pulmonary fibrosis. Some causes and
dyspnea may have pulmonary or cardiac disease. This characteristics of coughs are listed in Table 7-3.

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136 PART II Cardiopulmonary Assessment

TABLE 7-3

Some Causes and Chnracteristics of Coughs

CAUSE CHARACTERISTICS

Acute infection of lungs

Tracheobronchitis Cough associated with sore throat, running nose, and eyes
Lobar pneumonia Cough often preceded by symptoms of upper respiratory infection; cough dry,
painful at first; later becomes productive
Bronchopneumonia Usually begins as acute bronchitis; dry or productive cough
Mycoplasma and viral pneumonia Paroxysmal cough, productive of mucoid or blood-stained sputum associated
with influenza-like syndrome
Exacerbation of chronic bronchitis Cough productive of mucoid sputum becomes purulent

Chronic infections of lungs

Bronchitis Cough productive of sputum on most days for more than 3 consecutive months
and for more than 2 successive years; sputum mucoid until acute exacerbation,
when it becomes mucopurulent
Bronchiectasis Cough copious, foul, purulent, often since childhood; forms layer on standing
Tuberculosis or fungus Persistent cough for weeks to months often with blood-tingling of sputum

Parenchymal inflammatory processes

J nterstitial fibrosis and infiltrations Cough nonproductive, persistent, depends on etiologic factors
Smoking Cough usually associated with injected pharynx; persistent, most marked
in morning, usually only slightly productive unless succeeded by chronic
bronchitis

Tumors

Bronchogenic carcinoma Nonproductive to productive cough for weeks to months; recurrent small
hemoptysis common
Alveolar cell carcinoma Cough similar to bronchogenic carcinoma, except in occasional instance when
large quantities of watery, mucoid sputum are produced
Benign tumors in airways Cough nonproductive, occasionally hemoptysis
Mediastinal tumors Cough, often with breathlessness, caused by compression of trachea and bronchi
Aortic aneurysm Brassy cough

Foreign body

Immediate, while still in upper airway Cough associated with progressive evidence of asphyxiation
Later, when lodged in lower airway Nonproductive cough, persistent, associated with localizing wheeze

Cardiovascular

Left venuicular failure Cough intensifies while supine along with aggravation of dyspnea
Pulmonary infarction Cough associated with hemoptysis, usually with pleural effusion

Reprinted with permission from Szidon J, Fishman A: Approach to the pulmonary patient with respiratory signs and symptoms. In Fishman
A, editor: Pulmol1{//y diseases alld disorders. New York, 1988, McGraw-Hill.

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 7 History 137

Cough may be the only presenting symptom of deep breathing suggests asthma or interstitial lung
asthma. In asthmatics, cough is precipitated by inhal­ disease. Allergens or irritant fumes at home or at
ing cold air or exercise, and is dry. Cough can precip­ work may be a cause of cough. Postviral cough may
itate an asthma attack in sensitive patients and is be present for weeks following a viral illness.
known as cough-induced bronchospasm. Some medications can elicit coughing. Beta­
It is important to determine the length of time blockers prescribed to treat hypertension, migraine
cough has been present (Sharf, 1989). The most com­ headaches, cardiovascular disease (CVD), or glau­
mon cause of an acute cough is a viral respiratory in­ coma may precipitate asthma. Many drugs, including
fection, which generally resolves within a few days chemotherapeutic agents, can cause interstitial lung
or 2 to 3 weeks. Exposure to noxious gases also pre­ disease and coughing.
cipitates acute coughing. Cough and wheezing may result from COPD,
A cough that has persisted for more than 3 weeks asthma, or early left heart failure. Early left heart fail­
can be termed chronic (Snider, 1994). The most com­ ure predisposes the patient to respiratory infections
mon cause of chronic cough is chronic bronchitis, and may be responsible for chronic bronchitis.
and is present in up to 30% of cigarette smokers. The
next most common cause is the postnasal discharge
Cough Complications
syndrome. Patients describe a sensation of secretions
dripping from the back of the nose into the throat, One of the more common complications of cough is
prompting throat clearing or coughing. syncope. Tussive or cough-induced syncope, which is
Various cardiac conditions may stimulate receptors more common in men than women, can be recognized
in the bronchi and provoke coughing (Goldberger, through accurate history taking (Miller, 1980). It is
1990). Because the bronchial veins empty into the typically reported by middle-age men who "smoke
pulmonary veins (leading to the left side of the heart), hard, eat hard, drink hard, and cough hard." They ex­
systemic veins, and the superior vena cava (leading to perience fainting or near-fainting following cough
the right side of the heart), venous congestion and paroxysms. The cause is obscure but may be related to
coughing may occur with either right- or left-side vagal-induced cardiac slowing or vasodilatation, or
CHF. It is more common, however, with left-sided high intrathoracic pressures that impair venous return,
CHF. The onset of a cough in a patient with paroxys­ decrease cardiac output, increase intracranial pressure,
mal tachycardia or acute myocardial infarction (MI) is and result in a reduced cerebral blood flow. Cough
often an early symptom of acute left-side heart failure. syncope is often resolved by smoking cessation.
Coughing may be caused by other cardiovascular Complications of cough include headache, back
conditions such as a large left atrium displacing the pain, muscular tears, hematomas, rib fractures (along
left main-stem bronchus upward, aortic aneurysms the posterior axillary line), occasionally vertebral
placing pressure on the bronchi, or a double aortic compression fractures (in osteopenic patients), urinary
arch compressing the trachea. incontinence (UI) (in women), and inguinal hernias
A specific diagnosis can be made in 80% of cases (in men) may occur (Braman and Corrao, 1987).
of chronic cough by an appropriate history alone
(Stulberg, j 985). Determining the precipitating
CHEST PAIN
causes or the time of onset points the clinician to a
probable diagnosis. For example, does the patient Taking an accurate history is crucial to the proper
cough primarily at night? If so, it points to heart fail­ evaluation of chest pain (Snider, j 994). Although the
ure, esophageal problems, bronchiectasis or asthma definitive cause of chest pain cannot be fully estab­
as the potential cause. An early morning cough is lished without diagnostic medical tests, it is usually
more common in bronchitis and individuals with possible to determine whether the pain originates in
postnasal drip. Cough following meals suggests the pleura, chest wall, or thoracic organs by means of
esophageal disease. Cough precipitated by exertion or careful history taking.

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138 PART II Cardiopulmonary Assessment

Chest pain can be divided into two basic types: palpated at the wrist. If a patient opens and
chest wall pain and visceral pain (George, 1990). The closes a fist, pain will gradually appear and es­
first arises from involved thoracic cage structures and calate in the forearm. The causal mechanism of
tends to be superficial and well-localized. The latter this pain is the same as that of myocardial pain:
arises from the heart, pericardium, aorta, medi­ continuing muscular contraction in the absence
astinum, bronchi, or esophagus. It is described as of an adequate oxygen supply. This type of
deep and difficult to localize. pain requires several contractions of the my­
ocardium to reach its maximal intensity. In
other words, there is a characteristic buildup or
Pleuritic
escalation of angina pain.
Pleuritic chest pain originates from the parietal pleura 2. Can you point to the area of pain with one
or endothoracic fascia, but not the visceral pleura, finger? Anginal pain is characteristically
which has no pain receptors. The patient can usually demonstrated by patients using their entire
identify it as being close to the thoracic cage (Szidan, hand or closed fist against the anterior chest
Fishman, 1988). Pleuritic chest pain worsens sharply wall. It is described as a sign of angina, because
with inspiration as the inflamed parietal pleura is it is so typical (Marriott, 1993). By contrast,
stretched with chest wall motion. Deep breathing, any pain that can be localized by pointing with
coughing, or laughing are extremely painful, requir­ a fingertip is unlikely to be angina.
ing the patient to apply pressure over the involved 3. Is the pain deep inside your chest or does it
area to control the pain. seem as though it is close to the surface?
Pleuritic chest pain is ordinarily found in patients Anginal pain is visceral pain that may be re­
that have other signs of respiratory illness, such as ferred superficially but always has a deep inter­
cough, fever, chills, malaise. Inflammation of the di­ nal component to it.
aphragmatic pleura produces ipsilateral shoulder pain Myocardial ischemia may be completely painless
by way of the phrenic nerve (Miller, 1980). (silent ischemia). Angina may in fact not be painful
The onset of pleuritic chest pain varies according but rather described as discomfort, pressure, squeez­
to its cause (Snider, 1994). Sudden severe pleuritic ing, a tight band, heaviness, burning, indigestion. It
chest pain suggest a spontaneous pneumothorax, pul­ usually is located substernally and radiates into one
monary embolism, or infarct. Pulmonary embolism is or both arms, neck, jaw, or back.
usually accompanied by sudden dyspnea, hemoptysis, Angina is not limited only to patients with CAD
tachycardia, cyanosis, hypotension, anxiety, and agi­ (Marriott, 1993). Individuals that have normal coro­
tation (Marriott, 1993). nary arteries but an insufficient oxygen supply for a
given cardiac workload can also experience angina.
These include individuals with anemia, hypertension,
Cardiac
tachycardia, and thyrotoxicosis. Hypertrophic and di­
There are three cardinal features that are characteris­ lated cardiomyopathy can produce typical angina
tic of cardiac chest pain. The patient should be asked pain, although the latter tends to be intermittent, usu­
the following questions (Marriott, 1993): ally occurring with episodes of CHF. Aortic valve
I. Does the pain have maximal intensity from disease can cause angina as a result of impairment of
the onset or does it build up for several sec­ adequate coronary artery blood tlow.
on ds? Ischemic cardiac pain or angina is Angina is usually precipitated by exertion such as
caused by the myocardium contracting in the walking uphill, against the wind, or in cold weather
absence of an adequate oxygen supply. The (Marriott, 1993). It also is more likely to be brought
same type of pain can be produced by placing a on after a meal or by emotional stress. The rapid
blood pressure cuff around the upper arm and resolution of chest pain by rest or sublingual nitro­
inflating it until the brachial pulse is no longer glycerin strongly suggests a cardiac origin. The pain

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 7 History 139

produced by MI is longer, persisting more than 20 suggest an esophageal origin (Snider, 1994). Also,
minutes; occurs at rest; and is accompanied by nau­ diffuse esophageal spasm is often associated with
sea, diaphoresis, hypotension, and dyspnea. pain on swallowing (odynophagia), dysphagia, and
regurgitation of stomach contents. Swallowing hot or
cold liquids, or emotional stress tend to precipitate
Pulmonary Hypertension
this type of chest pain.
Chest pain related to pulmonary hypertension may
mimic angina pectoris. It is usually found in patients
Chest Wall
with mitral stenosis or Eisenmenger's syndrome (pul­
monary hypertension related to an interventricular Chest wall pain is the most common type of chest
septal defect, patent ductus arteriosus, or atrial septal pain. Clues in the patient's history to this type of pain
defect). This type of chest pain is usually absent at include intermittent occurrence, variable intensity,
rest, occurs during exertion, and is invariably associ­ and local tenderness (Miller, 1980). Because it is
ated with dyspnea (Hurst, et ai, 1990). It is believed often located on the anterior chest wall, many pa­
to be because of dilation of the pulmonary artery or tients believe it is heart pain. However, an important
right ventricular ischemia. The pain is not relieved by differentiation from cardiac pain is that it does not
nitrates. Primary pulmonary hypertension may be ac­ occur during but rather following exertion. It may
companied by syncope and Raynaud's phenomenon worsen with inspiration, but its association with trunk
(Sharf, 1989). motions (flexion, extension, rotation) distinguish it
from pleuritic chest pain.
Localized anterior chest pain as a result of costo­
Pericardial
chondritis of the second to fourth costosternal articu­
Pericardial chest pain is also midline, but because of its lations (Tietze's syndrome) is described as tender to
anatomical relationship with the mediastinal pleura, it touch (George, 1990). A complaint of rib tenderness,
has features that suggest pleural involvement (Snider, together with a history of trauma, fall, long-term
1994). Deep breathing, coughing, swallowing, move­ steroid use, coughing, or upper extremity exertion,
ment and lying down may make it worse. If the central suggests rib fracture.
tendon of the diaphragm is involved, the pain may be Degenerative disk disease and arthritis of the cervi­
referred to the left shoulder or scapular area (Marriott, cal or thoracic spine, thoracic outlet syndrome,
1993). The patient may report that each hemibeat af­ spondylitis, fibromyalgia, kyphoscoliosis, and herpes
fects the pain. Sitting up and leaning forward, or lying zoster can all produce chest wall pain (Epstein, Ger­
on the right side often relieves the pain. ber, and Borer, 1979; Miller, 1980; Pellegrino, 1990;
Snider, 1994; Wise, Semble, and Dalton, 1992). Pri­
mary lung cancer that invades the adjoining chest
Esophageal
wall, ribs, or spine produces severe persistent local­
Diffuse esophageal spasm or esophageal colic is a ized pain (Snider, 1994). Pancoast's syndrome (supe­
common cause of chest pain. It is often confused with rior sulcus tumor), in which a primary lung tumor lo­
cardiac pain because it is located substernally, has a cated in the extreme apex of the lung invades the
squeezing or aching quality, and may radiate into one brachial plexus and produces pain in the shoulder,
or both arms (George, 1990). Furthermore, diffuse scapular region, or medial aspect of the arm and hand.
esophageal spasm may be relieved by sublingual ni­ Chest wall pain may rarely be caused by thrombo­
troglycerin as a result of its generalized function as a sis of a superficial vein on the chest wall (Mondor's
smooth muscle relaxant. disease). It is a self-limiting condition of unknown
Pain that radiates through the chest to the back, origin and can last several weeks (Snider, 1994). The
pain that decreases by a change in position from only physical finding is a subcutaneous cord that can
supine to upright, or relief by ingesting antacids, all be palpated along the lateral chest wall.

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140 PART II Cardiopulmonary Assessment

HEMOPTYSIS FATIGUE AND WEAKNESS

is defined as coughing up blood. It can

vary in amount from blood-streaked sputum to con-
virtually all blood. The site may be
anywhere in the upper or lower respiratory tract.
The timing and frequency of as deter­
mined in the history, can offer clues about its cause.
A history of nosebleeds is since blood
may be aspirated duling and expecto­
rated the following morning. Intermittent bouts of he­
is more characteristic of resoiratorv infec­
tions such as bronchiectasis,
or broncholithiasis (Miller,
blood-streaked
basis is highly of hrr;,nf"hAfT"n

The lung receives its blood supply in two ways: the

pulmonary arteries (a low pressure and the
bronchial arteries (a high pressure off of the
aorta (Shalf, 1989). The appearance of may
vary according to which blood is involved. If the
bronchial vessels are the source, there tends to be large
PEDAL EDEMA
or massive amounts of bright red blood. This is often
the site of bleeding in bronchiectasis, since bronchial ar­ CHF is a common cause of bilateral pedal edema
teries undergo enlargement and extensive anastomosis (Marriott, 1993). Ifowever, several pounds of fluid
with the pulmonary artery system. in mitral steno- (10 to 20 Ibs.) generally accumulate in the body be­
where there is increased I-IUJJJJ'-'JJ<ll fore foot and ankle swell is evident. Therefore
tance, hemoptysis arises from weight gain is an even earlier indication of fluid re­
mucosal bronchial veins tention due to CHF. Occasionally, patients may only
Hemoptysis from the complain about an increase in abdominal result­
artery system tends to occur in small amounts and is ing from ascites. When caused CHF. the onset of
of dark or clotted venous blood ascites virtually occurs after
It may arise from the present If the amount of ascites is
as in the case of the vascular tissue that of restrictive CardlOmyopatny or
found in the walls of abscesses. These abscesses constrictive should be a consideration.
may be caused by infections such as It is important to determine whether the
anaerobic bacteria, or chronic irrita­ had dyspnea on exertion before the onset of lower-ex­
tion from a fungus ball in an abscess cavity. If a tremity edema. If the edema is a result of a
blood vessel ruptures in an abscess functioning left mitral or cor pul­
rhage tends to be massive, even monale, it usually follows on exertion.
Cardiovascular conditions such as mitral Patients with CHF and altered renal function
pulmonary infarction, and commonly report edema of the ankle and lower legs
aortic aneurysm are also associated with hemoptysis while upright during the but indicate a de­
(Hurst, et aI, 1990). Pink frothy is often found crease during the night (Hurst, et ai, 1990). This is
with acute pulmonary edema. should care­ a result of local hydrostatic factors related to the
fully evaluate of and be certain upright position.
of its cause before cautiousIv conducting treatment. Edema may be Dresent in nephrosis or starvation

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 7 History 141

when the total blood protein falls below 5 gmllOO ml nations of obstmctive and restrictive lung disease (e.g.,
(hypoproteinemia). Other causes of pedal edema in­ silicosis). Constmction workers, shipyard workers,
clude liver disease, kidney disease, and anemia. pipefitters, and other industJial workers exposed to as­
Edema of one leg is ordinarily because of local fac­ bestos are at increased risk for developing a restrictive
tors such as thrombophlebitis or varicose veins. lung disease such as asbestosis (Varkey, 1983). Benign
pleural plaques may be found on the diaphragmatic
pleura and bilaterally between the sixth and tenth ribs
HOARSENESS
on the anterolateral or posterolateral chest wall. Pro­
Hoarseness, abnormal vocal cord motion during gressive pleural thickening rarely occurs. These indi­
phonation, is a symptom of laryngeal dysfunction viduals have an increased incidence of malignant neo­
(Miller, 1980). It is usually associated with upper res­ plastic diseases such as bronchogenic carcinoma and
piratory tract infections or allergies, and resolves in 1 malignant mesothelioma.
to 2 weeks (Sharf, 1989). Trauma following intuba­ Coal workers are exposed to coal mine dust.
tion, laryngeal polyps, or tumors are other common About 10% have simple pneumoconiosis, whereas a
causes of hoarseness. However, this symptom is also smaller proportion develop the complicated form­
related to cardiopulmonary conditions. Because the progressive massive pulmonary fibrosis (Brandstetter
recurrent laryngeal nerves pass through the upper and Sprince, 1982).
thorax, intrathoracic pathology that involves one of A history of paroxysmal coughing, chest tightness,
these nerves can cause unilateral vocal cord paralysis, or dyspnea that is worse during the week but remits
resulting in hoarseness (Shalf, 1989). These include on weekends strongly suggests occupational asthma
lung or mediastinal tumors, granulomatous disease, (Brandstetter, and Sprince, 1982). This condition is
enlarged mediastinal lymph nodes, and pericardial or difficult to diagnose because symptoms often occur
mediastinal adhesions. several hours after exposure to the provoking agent.
Several cardiovascular conditions can produce Causal agents include grain dusts, wood dusts, forma­
hoarseness, because the left recurrent laryngeal nerve lin, enzyme detergents, ethanolamines (in spray
loops under the arch of the aorta and above the pul­ paints and soldering flux), nickel and hard metals
monary artery as it returns to the neck (Hurst, et ai, (tungsten carbide). Workers exposed to cotton flax
1990). Therefore an aneurysm of the arch of the and hemp dusts may develop byssinosis, an obstmc­
aorta, a dilated pulmonary artery or atrium resulting tive lung disease. In the early stages, it is reversible,
from an atrial septal defect, or mitral stenosis can but long-term exposure over a number of years
cause hoarseness (Goldberger, 1990). causes chronic irreversible obstructive lung disease.
Hence, if patients manifest hoarseness, it is neces­ A history of fever, cough, shortness of breath,
sary to inquire about the length of time it has been and recurrent pneumonias in farmers in the north­
present, the patient's smoking history, and any his­ ern United States suggests farmer's lung (Brand­
tory of cardiac or pulmonary diseases. stetter, and Sprince, 1982). This is the most com­
m o n h y p e r s e n s i t i v e pneumonitis, c a u s e d b y
inhaling fungal agents such a s thermophilic actino­
OCCUPATIONAL HISTORY
mycetes. Long-term exposure can lead to pul­
Taking an occupational history is particularly impor­ monary fibrosis. There are numerous occupations
tant for pulmonary patients who arrive for physical that expose workers to etiologic factors that cause
therapy with little or no accompanying medical infor­ hypersensitive pneumonitis.
mation. The internal surface of the lung measures 50 to
100 m] and is in constant contact with the environment
SMOKING HISTORY
(Miller, 1980). Jobs that involve exposure to silica or
silicates (e.g., miners, sandblasters, foundry workers, The patient should be asked their tobacco-smoking
stone cutters, brick layers, or quarry workers) or other history (Snider, 1994). The number of pack-years of
inorganic substances place workers at risk for combi­ cigarettes smoked may be calculated (average number

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142 PART II Cardiopulmonary Assessment

of packs/day x number of years smoked) as a relative REVIEW QUESTIONS

risk of lung cancer and COPD. Regular smoking of
1. What are the basic causes of dyspnea?
marijuana is more damaging to the lungs than ciga­
2. What questions can be asked of a patient with
rette smoking.
dyspnea to determine the likely cause?
3. What scales have been developed to quantitate
FAMILY HISTORY dyspnea?
4. What are the principal features of chest pain that
The family history is useful in evaluating the possi­
originate from the pleurae? The chest wall? The
bility of hereditary p ulmonary diseases such a s
thoracic organs?
alphaj-antitrypsin deficiency, cystic fibrosis, allergic
5. What are the cardinal features of cardiac chest
asthma, hereditary hemorrhagic telangiectasia, and
pain?
others (Miller, 1980; Szidan, and Fishman, 1988). A
6. What occupations can place workers at rish for
family history of diabetes, hypertension, CAD, or
respiratory disease?
rheumatic fever raises the possibility of these condi­
tions existing in the patient as well (Marriott, 1993).
References

PRIOR TREATMENT Birdwell, B., Herbers, J., & Kroenke, K. (1 993). Eva lua ting chest
pain: the patient's presen tation style alte rs the phy si c ia n
s dia g­
'

It is important to deterrnine what treatment(s) the pa­ n o s ti c a p p r oach . Arch ives of In/ernal Med i c ine, 153,
tient has received for his or her condition. Specifically, 1991-1995.

has the patient ever received physical therapy for this Borg, G. (1982). Psyc ho physic al bases of perce i ve d exertion. Merl­
icine and Science in SPOrlS and t:rercise, 1 4, 377-381.
or any other condition? What type of treatments were
Braman, S., Corrao, W. (1 987) . Cough: differen/ial diagnosis and
done? Were they helpful in improving or resolving the
/realinel1l. Clinical Ches/ Medicine 8(2), 1 77-188.
condition? In this way we determine what treatment Brandsteller, R .. Sp rince, N. (1982). Occ u p at i on al lun g disease.
modalities have been used, which of these the patient Medical Times, June, 56-63.
believes may have merit, and those with which the pa­ Constant, J. (1993). The evolving checklist in history-taking. In

tient finds objectionable or lacks confidence, thus Constant J.

Bedside cardiology. Bo st on : Linle. Brown.
Epstei n S., Gerber, L., & B o re r, J. (1979). Chest wall syndrome: a
avoiding alienating the patient by not repeating what
,

common cause of unexplained cardiac pai n . Journal of /he

he or she believes to be ineffective therapy is avoided. American Medical Associa/ion, 241, 2793-2797.
George, R. (1990). History an d physical examination. In Geo rge ,

R., et al (Eds.), Chest medicine: Essen/ials of pulmonary and

SUMMARY ai/ical care medicine. Baltimore: Wi l l ia ms and Wilkins.
G o l dbe rger, E. (1990). Symptoms referable to the cardiovascular
Obtaining an accurate and thorough history is the
system. In Goldberger, E. Essentials of clinical cardiology.
cornerstone of the physical t herapy e v a luation Phi la delp hi a: JB Lippincott.
process. The probable cause and severity of many Irwin, R., Rosen, M., & Braman, S. (1977). Cough: a comprehen­
cardiopulmonary symptoms can be determined by sive review. Arch h7lem Medicine 137,1186-1191.

careful history taking. This information enables ther­ Hurst, 1., et al. (1990). The h ist ory: past events and symptoms re­
lated to cardiovascular disease. In Hurst, J. (Ed.). The heall.
apists to select the most appropriate evaluation and
N ew York: McGraw-Hili.
treatment techniques. When properly performed, ac­ Mahler, D. (1987). Dyspnea: diagnosis and management. Clin ics ill
curate h istory taking gains the patient's confidence Ches/ Medicine. 8(2), 215-230.
and cooperation, and provides the basis for a good Mahler, D., & Harvel', A. (1990). Clinical measureme nt s of dysp­
nea. In Mah l e r, D. (Ed.). Dysp/1ea. Mount Kisco, NY: Futura.
patient-therapist relationship.
Marriol!, H. (1993). Taking the history. In Marriol!, H. Bedside
cardiac diagnosis. Ph i ladelphia: JB Lippincott.

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 7 History 143

Miller, D. (1980). The medical history. [n Sackner, M. (Ed.). Szidan, P., & Fishman, A. (1988). Approach to the pulmonary pa­
Diagnostic techniques in pulmonary disease. New York: tient with respiratory signs and symptoms. [n Fishman, A.
Marcel Dekker. (Ed.). Pulmonary diseases and disorders. (2nd ed.). New York:
Pellegrino, M. ( 1990). Atypical chest pain as an initial presentation McGraw-HilI.
of primary fibromyalgia. Archives of Physical Medicine and Varkey, B., (1983). Asbestos exposure: An update on pleuropul­
Rehabilitation 71, 526-528. monary hazards. Postgraduate Medicine, 74(4),93-103.
Sharf, S. (1989). History and physical examination. [n Baum, G., Wasserman, K., (1982). Dyspnea on exertion: is it the heart or the
& Wolinski, E. (Eds.). Textbook of pulmonary diseases. (4th lungs? Journal of the American Medical Association, 248,
ed.). Boston: Lillie, Brown. 2039-2043.
Snider, G. (1994). History and physical examination. [n Baum, G., Wise, C., Semble, E., & Dalton, C. (1992). Musculoskeletal
& Wolinski, E. (Eds.), Textbook of pulmonary diseases. (5th chest wall syndromes in patients with noncardiac chest pain:
ed.). Little, Brown. A study of 100 patients. Archives of Physical Medicine and
SlUlberg, M. (1985). Evaluating and treating intractable cough­ R eha bilitation, 73, 147-149.
Medical Staff Conference, University of California, San Fran­
cisco. West 1 Med, 143,223-228.

Copyrighted Material
 Pulmonary Function Tests

Donna Frownfelter

KEY TERMS Dead space Expiratory reserve volume

Lung capacities Inspiratory reserve volume
Functional residual capacity Residual volume
Inspiratory capacity Tidal volume
Total lung capacity Obstructive component
Vital capacity Predicted values
Lung volume Restrictive component

sis of pulmonary disease or dysfunction and improve­

INTRODUCTION
ment with treatment win be evaluated as a result of in­
Pulmonary function tests (PFfs) help in the evaluation terpreting a patient's pulmonary function tests.
of the mechanical function of the lungs. (Cherniak,
Crapo, and Youtsey, (992). They are based on re­
DEAD SPACE
searched norms taking into account sex, height, and
age. For example, there are predicted values for a The most important function of the lungs is to supply
male, age 65 who is 6 feet tall. (Morris, Koski, and the body with oxygen and to remove carbon dioxide
Johnson, (971). When the patient performs the test ac­ (C02) produced as a waste product of metabolism.
tual results (observed) will be compared with the pre­ As this continuous gas exchange takes place suffi­
dicted value expected of a person of gender, height, cient ventilation is needed to move the gases to the
and age to see if he falls within the "nonnal" range, or alveoli. There is a series of conducting airways in the
has a restrictive or obstructive component based on the lungs from the trachea down to the terminal bronchi,
tests. If the patient is not within the nonnal range, a which do not participate in respiration but only move
bronchodilator is given, and the test will be repeated to the gases to the alveoli. This is the volume known as
see if there is significant improvement with medica­ anatomic dead space. Generally, the anatomic dead
tion. Basically, the pulmonary function tests are cate­ space i s app r opria tely equal to the adult body
gorized as volume, flow, or diffusion studies. Diagno- weight. For example, in a ISO-lb. person, there is an

145

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146 PART II Cardiopulmonary Assessment

approximately I SO mL anat(}mic dead space. A nor­ functioning alveoli. This causes increased work of
mal tidal volume (TV), the breath normally taken, breathing and may result in patient fatigue. Neurolog­
needs to be large enough to reach the alveoli well ical and neuromuscular weakness may result in an in­
past the anatomic dead space. In a normal adult, the ability to take a normal TV. Similarly, surgical proce­
TV is generally 450 to 600 mL. The anatomic dead dures or p a i n f r o m fractured r i b s c a n also
space would thus represent about one third TV vol­ compromise a patient's ability to take a breath. As
ume. The rest of the breath would reach the alveoli the TV drops a large percentage of the breath is
and be considered "alveolar ventilation." With many anatomic dead space. This results in increased work
neurologically impaired patients who have a limited of breathing for the patient and may ultimately result
TV, it is important to note that little alveolar ventila­ in respiratory failure if the patient is unable to pro­
tion may be taking place when the patient is breath­ vide alveolar ventilation.
ing in a rapid and shallow pattern. For example, if a
p a t i e nt's TV w a s 200 mL, IS O mL w o u l d be
lUNG VOLUMES
anatomic dead space and only SO mL of each breath
would be alveolar ventilation. The lung has four volumes, TV, inspiratory reserve
There are many diseases or conditions that can alter volume (IRV), expiratory reserve volume (ERV), and
the volume of dead space that needs to be ventilated. In residual volume (RV) (Figure 8-1).
some cases the dead space decreases, such as in a pneu­ •
TV is the normal breath.
monectomy, where it is physically removed, or in •
IRV is the maximal amount of air that can be in­
asthma, where bronchospasm may narrow the airways. haled from the end of a normal inspiration.
In other conditions such as pulmonary embolus, dead •
ERV is the maximal amount of air that can be ex­
space increases when ventilated areas of lung cease to pired after a normal exhalation.
be perfused. The alveoli continue to receive fresh gas, •
RV is the volume of gas that remains in the lungs
but there is no blood available for gas exchange. This at the end of a maximum expiration.
type of dead space is known as physiologic dead space. Changes in RV can help in the diagnosis of certain
When dead space is increased, a larger percentage medical conditions. An increase in RV means that
of the tidal volume is ventilating the dead space, even with maximum effort, the patient cannot exhale
leaving a smaller percentage for alveolar ventilation. excess air from the lungs. This results in hyperin­
The patient must work harder to get enough air to the flated lungs and indicates that certain changes have

---I
\tj
( C,\.'--
'- '--

FIGURE 8-1
A spirogram (pulmonary function testing).

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 8 Pulmonary Function Tests 147

occurred in the pulmonary tissue, which in time may FRC is the volume of air remaining in the lungs at
cause mechanical changes in the chest wall (e.g., in­ the resting expiratory level. It contains the ERV and
creased AP diameter, flattened diaphragms). These the RV.
changes may be reversible in patients with partial The FRC prevents large fluctuations in Pa02 with
bronchial obstruction, such as young asthmatics, or each breath. An increase in FRC represents hyperin­
irreversible, as in patients with advanced emphy­ flation of the lungs. It causes the thorax to be larger
sema. Restrictive lung disease can cause a decrease in than normal, which results in muscular inefficiency
residual volume, as can cancer of the lung, microat­ and some mechanical disadvantage. Patients on me­
electasis, or musculoskeletal impairment. (Smith and chanical ventilators may increase their FRC with pos­
Dickson, 1994). itive pressure and by additional modes such as posi­
tive end expiratory (PEEP), or BiPap. Spontaneously
breathing patients can also be on continuous positive
LUNG CAPACITIES
airway pressure (CPAP), which keeps the lungs at a
A lung capacity is two or more volumes added to­ positive airway pressure to improve oxygenation.
gether (Figure 8-1). The capacities include total lung
capacity (TLC), vital capacity (VC), inspiratory ca­
AIR FLOW MEASUREMENTS
pacity (IC) and functional residual capacity (FRC).
Forced Expiration
TLC is the amount of gas the lung contains at the
end of a maximum inspiration. It is made up of all four When patients peIform a VC maneuver, it can either
lung volumes. An increased TLC is seen with hyperin­ be slow or fast. During exhalation, the amount of air
flation such as emphysema. A decrease in TLC may be exhaled over time can be measured. In a slow VC a
seen in restlictive lung disease such as pulmonary fi­ patient with emphysema can take a great deal of time
brosis, atelectasis, neoplasms, pleural effusions, and to empty his lungs. In a forced VC a normal individ­
hemothorax, as well as in restrictive musculoskeletal ual can exhale 75% of the VC in the first second of
problems such as spinal cord injury, kyphoscoliosis, or exhalation (FEV I). Patients with emphysema often
as secondary to morbid obesity or pregnancy. have greatly decreased VCs, only 40% of which are
VC is the maximum amount of gas that can be ex­ predicted.
pelled from the lungs by forceful effort following a
maximum inspiration. It contains the IRV, TV, ERV.
Flow Volume Curve
A decrease in VC can occur as a result of absolute re­
duction in distensible lung tissue. This is seen in The flow volume curve is helpful in diagnosing lung
pneumonectomy, atelectasis, pneumonia, pulmonary disease, since it is independent of effort. The curve in
congestion, occlusion of a major bronchus by a tumor Figure 8-2 demonstrates that flow rises to a high
or foreign object, or restrictive lung disease. value and then declines over most of expiration
A decrease in VC may also be seen without pri­ (Rahn, et ai, 1946). In restrictive lung disease, the
mary lung disease or airway obstruction. In neuro­ maximum flow rate is reduced, as is the total volume
muscular or musculoskeletal dysfunction, VC can be exhaled. In obstructive lung disease, the flow rate is
compromised (Guillain-Barre, spinal cord injury, low in relation to lung volume, and a scooped-out ap­
drug overdose, motor vehicle accident with fractured pearance is often seen (see Figure 8-2).
ribs, severe scoliosis, and kyphoscoliosis). Restrictive Another diagnostic test that uses forced expiration
contributing factors such as morbid obesity, preg­ is the flow volume loop. It is a graphic analysis of the
nancy, enlarged heart, and pulmonary effusion may flow generated during a forced expiratory volume
involve the limitation of expansion of the lungs. maneuver followed by a forced inspiratory volume
IC is the maximal amount of air that can be in­ maneuver (Figure 8-3). This graph offers a pictorial
spired from the resting expiratory level. It contains representation of data from many individual tests
the IRV and the TV. (e.g., peak inspiratory and expiratory flow rates,

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148 PART II Cardiopulmonary Assessment

FLOW VOLUME CURVES

Z NORMAL
o
wi=

a:- U
a.. Q)
II)
:> X '
:;>o w -.J OBSTRUCTIVE
o
-.J<..9
u...Z
0::
=:J
o

oI r' ,.,.,.,.,.,.,.,\. """'·'·"""'T .... . /

", . . ..' 'j' xx;,i
",.",., ' '

10 9 8 7 6 5 4 3 2 o
LUNG VOLUME (Liters)

FlliURE 8-2
Comparison of tlow volume curves in the normal patient and in the patient with obstructive and
restrictive lung disease.

-r---- /\,.----;;;50%
+5 PFexp
/ \ j EXPIRATION

U
Q)
II)
,

i 01
o
Ie F; \
-.J
u...
INSPIRATION
-5 PF insp

J __ _
OBSTRUCTION

o 2 4 6
VOLUME (Liters)

FIGURE 8-3
Compatison of flow volume loops in the normal patient and in the patient with obstructive
lung disease.

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 8 Pulmonary Function Tests 149

FVC, and FEV). The shape of the graph may also be in N2 concentration. This high N2 concentration re­
helpful in diagnosing disease, again seeing a more flects closure of airways at the base of the lungs and
scooped-out appearance with obstructive disease. expiration of gas from the upper lung zones, because
in the single breath of 100% oxygen, less oxygen was
initially directed to this area.
CLOSING VOLUME AND AIRWAY CLOSURE
Closing volume is the lung volume at which the
The assessment of closing volume is used to help di­ inflection of Phase IV, the marked increase in N2
agnose small airway disease. A test called the single concentration after the plateau, is observed. Closing
breath nitrogen (N2) washout is used for assessing capacity refers to closing volume and RV. The same
closing volume and closing capacity of the small air­ characteristic tracing of the single breath nitrogen
ways. In this test, the patient takes a single VC breath washout test can be obtained with an inhalation of a
of 100% oxygen. During complete exhalation, the N2 bolus of tracer gas (e.g., argon, helium, xenon-133).
concentration can be measured. The characteristic The closing volume is 10% of the vital capacity in
tracing of N2 concentration can be measured. The young, healthy individuals. It increases with age and
characteristic tracing of N2 concentration vs. lung vol­ is 40% of the vital capacity at age 65. Closing vol­
ume reflects sequential emptying of differentially ven­ ume is used as an aid in the diagnosis of small airway
tilated lung units, resulting in different expiratory N2 disease and as a means of evaluating treatment or
concentrations. Four phases can be identified (Figure drug response.
8-4). Phase I contains pure dead space and virtually
none of the potential N2 from the RV. Phase Il is asso­
MAXIMAL VOLUNTARY VENTILATION
ciated with an increasing N2 concentration of a mix­
ture of gas from the dead space and alveoli. The Maximal voluntary ventilation measures the maximal
plateau in N2 concentration observed in Phase III re­ breathing capacity of the patient. It reflects strengths
flects pure alveolar gas emanating from the bases and and endurance of the respiratory muscles. The patient
middle lung zones. Phase IV occurs toward the end of is asked to pant for 15 seconds into the spirometer tub­
expiration and is characterized by an abrupt increase ing. This is often examined preoperatively with the

CLOSING VOLUA1E and CLOSING CAPACITY

I
z
DEPENDENT AIRWAY BEGIN
I
o
(f)- TO CLOSE ------, I
«f­
(9«
0::: I
f-f­
o:::Z
WW
I
ZU
-z
I
o
U I
I
TLC VOLUME (Liters) RV o
Closing
Vol.
HCVl----!

FIGURE 8-4
The single breath nitrogen washout test to assess airway closure.

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150 PART II Cardiopulmonary Assessment

other results to determine a patient's prognosis for suc­ ration). An obstructive component generally relates to
cess after surgery, such as his or her ability to cough, problems in exhalation air flows and characteristic
to take deep breaths, and to enhance airway clearance. patterns of obstruction, such as in the first second of
expiration FEY I measurement). Patients do not often
have only one primary disease process but many times
DIAGNOSIS OF RESTRICTIVE
have overlapping lung conditions (Clausen, 1984). A
AND OBSTRUCTIVE LUNG DISEASE
diagnosis may read: PFTs consistent with moderate
Physicians use the results of pulmonary function tests emphysema with bronchospastic component; good re­
to diagnose lung disease or characteristic components sponse to bronchodilators. A patient with an abnormal
of lung disease, such as bronchospasm. A restrictive PFr is given a bronchodilator and retested. If there is
component describes conditions that limit the amount a 15% to 20% increase in the PFr after bronchodila­
of volume coming into the lungs (restriction to inspi­ tors are administered, they will be a recommended

NORMAL OBSTRUCTIVE RESTRICTIVE

IRV

IC i
i
VC

IRV
TLC
VC
TV IC
C
TV TI C
ERV
ERV

FRC I
RV

l
F

FRC

RV

FIGURE 8-5
Examples of proportional changes of lung volumes and capacities characteristic of
obstructive and restrictive lung diseases.

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 8 Pulmonary Function Tests 151

part of the patients' medications. However, some pa­ a loss of intrapleural negative pressure. In older indi­
tients are given a trial of bronchodilators, even if there viduals, therefore, airway closure occurs at higher lung
is not such a dramatic response on PFfs). volumes. For example, closure has been reported to
A pictorial demonstration of the differences in ob­ occur at the age of 65 in the upright lung during nor­
structive and restrictive lung disease is shown in Fig­ mal breathing. In the supine position, where FRC is re­
ure 8-5. Disease has a marked effect on pulmonary duced, closure occurs at a significantly younger age
function, yet TV usually remains 10% of total lung (about age 44). In addition to the often compounding
capacity until the disease is relatively severe. Physio­ effect of age, the lung volume at which airway closure
logic pulmonary reserves in both disease processes occurs increases with chronic smoking and lung dis­
are limited and generally affect a patient's response ease, and is changed with the alterations in body posi­
to exercise. Exercise will be limited by the ventila­ tion (Ben)" Pai, and Fairshter, 1990; Zadai, 1985).
tory status ratlier than by a cardiac end point. As ob­
structive lung disease progresses, TLC, FRC, and RV
SUMMARY
are markedly increased. In severe COPD, the in­
creased FRC can compromise the Vc. More energy Pulmonary functions change as a patient's condition
is expended to breathe compared with that expended gets better or worse (Emery et ai, 1991; Emerson,
by a normal individual. This effect can be dispropor­ Lukens, Effron, 1994). There are normal declines in
tionally increased with minimal amounts of activity. volumes and flows with aging as well as disease
In restrictive lung disease, restriction of the chest processes. Basic bedside spirometry is often done to as­
wall or lung tissue can produce a decrease in TLC. A sess the patient's breathing mechanical ability. For ex­
VC of 80% or less of predicted values for a patient is ample, in a patient with Guillain Ban'e, as breathing be­
considered a diagnostic feature. A residual decline in comes labored, the VC is monitored to determine
FRC potentiates airway closure. whether a ventilator is needed. On the other hand, a pa­
The phenomenon of closing volume in the lungs is tient with obstructed airways, such as the patient with
particularly significant to physical therapists (PTs) cystic fibrosis, the pulmonary function tests will im­
who prescribe breathing exercises and body position­ prove (Versteegh, et ai, 1986). In patients with spinal
ing, and can thereby alter pulmonary mechanics and cord injury or neuromuscular weakness, as their
gas exchange. These treatment interventions may strength improves, their vital capacity increases. How­
have a pronounced effect on the lung volumes and ever, because of the lack of abdominal muscles, the
airway closure (Dean, 1985). At low lung volumes flows may be reduced.
(e.g., breathing at FRC, Trendelenberg position, and
in lung disease) intrapleural pressures are generally
REVIEW QUESTIONS
less negative and the pressure of dependent lung re­
gions may equal or exceed atmospheric pressure. In­ 1. What effect will an obstructive component have on
trapleural pressure is less negative because the lungs exercise performance? What effect will a restric­
are less expanded and elastic recoil is decreased. As a tive component have on excercise peliormance?
result, airway closure is potentiated. In young indi­ 2. Why is it important to compare the patient's pre­
viduals, closure is evident at RV; however, in older dicted values with the actual observed values in a
individuals, closure is observed at higher lung vol­ pulmonary function test?
umes, such as at FRC. Premature closure of the small 3. What response should you see to determine if
airways results in uneven ventilation and impaired bronchodilators have a positive effect on pul­
gas exchange with a given lung unit. Airway closure monary function?
occurs more readily in chronic smokers and in pa­ 4. How can pulmonary function tests be used to as­
tients with lung disease. sess patient improvement or decline?
Aging has a significant effect on airway closure. 5. How valuable are pulmonary function tests if pa­
With aging, a loss of pulmonary elastic recoil results in tients do not give maximal effort?

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152 PART II Cardiopulmonary Assessment

References
Rahn, H" et aL (1946), The prcS'urc·volume of the thorax
Berry, R., Paj, U. & Fairshter, R, (1990). Effect of age on changes lung, American Journal of Physiology, 146, J 61.
in !low rates and airway conductance after a deep breath, Jour­ Smith, R.M., & Dickson, R,A. (1994), Changes in residual volume
nal of Applied Physiology. 68, 635-{543. relative to vital capacity and total lung capacity after arthrode­
Cherniak, R,M, (! 992J, Evaluation of respiratory function in health sis of spine in patients who have idiopathic scoliosis. BOI1<'
and Dis Man, (7),505-76, and Join! Surgo)' 76 (I), I
Clausen, J.L. (1984). Pulmonary function tcstlng; guidelines and Ven;tcegh, F.G,A., et a!. (1986), Relationship between pulmonary
controversies, London: Grune and Stratton, function, O2 saturation during sleep and exercise with cystic
Crapo, R.O, (1 Pulmonary function testing, New England brosis. Advanced Cmdiology, lSI-ISS, 1986,
Joumal of Medicine, 331 (I), Williams-Russe, p" el aL (1992), Predicting postoperative compli­
Dean, E. (1985). The effect of body position on pulmonary fUlle­ cations, Is it a real problem Archives of /l1Icrnal Medicine,
Physical Therapy 65, 613-{5 J 8, 152 (6), 1209-12l3,
Emerson, CL., Lukens, T.W., Effron, D, (1994), Physician estima­ Youtsey, J.W. (1990). Basic pulmonary function measurement In
tion of FEV I in acute exacerbation of COPD, Chest, 105(6), Scanlon, CL, Spearman, CB., & Sheldan, R.L. (Ed,.). Egan's
1709-1712, fundamentals of respiratory care. (5th ed.). SL Louis: Mosby.
c.E., et a!. (1991). Psychological outcome of a pulmonary Zadai, C (1985) Pulmonary physiology of The role of re­
rehab program. Ches/, 100 (3), 613-{517, habilitation, Topics in CeriO/ric Rehabililation, 1,49-56,
Morris, J" Koski, A" Johnson, L (1971), Prediction nomograms
(BTPS) spirometric values in normal males and females. Am e r­
ican Review of Respiratory Diseases, 163, 57-{57.

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 Arterial Blood Gases

Donna Frownfelter

KEY TERMS Acid/base balance Hypoxemia

Alveolar ventilation Oxygen saturation

Arterial blood gas Partial pressure of gases

INTRODUCTION
metabolites must be kept from accumulating in high
Arterial blood gases are assessment tools to help the amounts, because the body's cardiovascular and ner­
physical therapist (PT) understand the patient's vous systems operate in a relatively narrow free H+
acid/base balance, alveolar ventilation and oxygena­ ion range (narrow pH). Free H+ ion concentration is
tion status (Cherniak, 1992). They are valuable re­ discussed as pH (-log [H+]). Maintenance of body
sources of information, from respiratory monitoring systems requires an appropriate acid/base balance
in the intensive care unit to following outpatients to (Shapiro, 1994).
evaluate the therapy and progress of their diseases. Approximately 98% of normal metabolites are in
The purpose of this chapter is to help the clinician the form of carbon dioxide (C02)' Carbon dioxide re­
evaluate and interpret arterial blood gases more effec­ acts readily with water to form carbonic acid:
tively and to integrate the information into treatment
CO2 + H20 H2C03
planning and progression of the patient.
Carbonic acid can exist either as a liquid or a gas. Be­
cause carbonic acid can change to CO2, much of the
ACID/BASE BALANCE
acid content can be excreted through the lungs during
Normal body metabolism consists of consumption of respiration.
nutrients and excretion of acid metabolites. Acid The Henderson-Hasselbach equation demonstrates

153

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154 PART II Cardiopulmonary Assessment

how the H+ ion concentration results from the disso­ acidemia o r alkalemia. Acidosis i s a n abnormal
ciation of carbonic acid and the interrclationship of acid/base balance where the acids dominate. Alka­
the blood acids, bases, and buffers: lemia is an abnormal acid/base balance where the
bases dominate. When there is a decrease in the
H2 0 + CO2 H2C03 H+ + HC03­
Heo3-, it is seen in a negative base excess and referred
to as a base deficit, which is usually seen as a negative

Renal Buffering Mechanisms number on the blood gas report, that is, -3.
When interpreting a blood gas, it is helpful to de­
The kidneys are the mai n route of excretion for the termine whether the patient's condition is acute or
normal metabolic acids. Hydrogen ions are excreted chronic. Another method is to examine whether the
in the urine and also resorbed by bicarbonate into situation is uncompensated, partially compensated or
the blood. In this manner, the kidneys can respond completely compensated. The pH is the key to mak­
when there is an acid/base imbalance to return to ing this determination. If the pH is not in the normal
normal homeostasis. 7.35 to 7.45 range, then the patient will be in an acute
state. As it progresses back toward normal, it may be
pa11ially compensated. When a normal pH exists, it is
Normal Blood Gas Values
compensated or chronic.
Acid/base is denoted by the pH. The pH values are For example, in a patient who is retaining a CO2 of
normally 7.35 to 7.45. If the pH is below 7.35, the 55 mm Hg, the pH may read 7.25; this would be con­
patient is considered to be in an acidotic state (more sidered acute. As the body retains base, the pH will
acid). If the pH is above 7.45, the patient is consid­ rise back toward the normal numbers. If the pH was
ered to be in an alkalotic state (more basic). 7.32 with a Peo2 of 55 and + 3 base excess, the read­
Alveolar ventilation is reflected in the partial pres­ ing would be partially compensated. When the pH is
sure of carbon dioxide (Peo2). Normal Peo2 values within normal limits with the Peo2 of 55 and a pH of
are 35 mmHg to 45 mmHg. If the PC02 is below 35 7.35, the reading would be compensated or chronic.
mmHg the patient is said to be hyperventilating (in­
creased ventilation, blowing off more C02 than nor­
PARTIAL PRESSURE Of GASES
mal). If the Peo2 is above 45 mmHg the patient is hy­
p o v e nt i l a t i n g , or not h a v i n g e n o u g h a l v e o l a r To better understand blood gases, it is important to
ventilation o r not blowing off enough CO2 t o main­ remember the properties of gases. The earth's surface
tain normal alveolar ventilation. consists of gas molecules that have mass and are at­
Arterial oxygen is measured as Po2, the partial pres­ tracted to the earth's center of gravity. At the surface,
sure of oxygen. Normal values are 80 to 100 mm Hg. If this atmospheric weight exerts a pressure that can
the P02 is below 80 mmHg in someone less than 60 support a column of mercury 760 mm high.
years old, the patient is hypoxemic. A value of 60 to 80 Dalton'S law states that in a mixture of gases, the
mmHg total pressure is equaJ to the sum of the partial pres­
would be considered moderate hypoxemia, and less sures of the separate gases. Oxygen is 20.9% of the at­
than 40 mmHg is severe hypoxemja (Chemiak, 1992). mosphere, so it has a partial pressure of 159 (760 x
20.9% =159). Nitrogen is 79% of the atmosphere, so
it has a partial pressure of 600 (760 x 79% 600).
=

Base Excess/Base Deficit

Other gases make up 0.1% of the atmosphere.
The blood normally has a capacity to buffer acid Diffusion of gases across semipermeable mem­
metabolites. The normal level of base Heo3 in the branes show gradients from higher concentrations to
blood is 22 to 26 milimoles per liter (mmollL). This lower concentrations. Each gas moves independently
buffering capacity diminishes in the presence o f from the others.

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 9 Arterial Blood Gases 155

During respiration, oxygen and CO2 exchange with no circulation, a dead unit is credited. Figure
across the alveolar capillary membrane. Special situa­ 9-1 demonstrates the regional differences seen In
tions may affect the normal progress of respiration respiratory units.
and gas exchange.
Normally, alveolar units ventilate and capillary
Hemoglobin
units bring oxygenated blood to the tissues, excret­
i n g C02 b a c k i nto t h e alveoli to be removed Hemoglobin (Hgb) is the main component of the red
through the lungs. However, some abnormal situa­ blood cell. It is crucial for oxygen transport. The nor­
tions may occur, such as shunts and dead space mal Hgb is 12 to 16 gmllOO mL blood. In patients that
units. In a shunt unit, the alveoli has collapsed, but have lost blood through surgical procedures or dis­
blood flow continues and is unable to pick up oxy­ ease, the decreased hemoglobin can account for their
gen. An example of this is atelectasis, where a lung extreme weakness as a result of decreased oxygen
segment or part of a segment has retai ned secre­ transport capacity. In addition, patients with advanced
tions and lung tissue distal to the mucous plug col­ chronic obstructive pulmonary disease (COPD) can at
lapses. Circulation continues but oxygenation does times desaturate with exercise when their Po2s are
not occur and the POl decreases. On the other hand, low; during exercise, they use increased oxygen.
a dead space unit can have ventilation but not per­ Cyanosis, a bluish color to the skin, mucous mem­
fusion. This occurs with pulmonary embolism, branes, and nail beds, is indicative of an abnormal
where a blood clot obstructs the circulation. The amount of reduced Hgb concentration, usually greater
oxygen is available in the ventilated alveoli, but than 5 gm of reduced Hgb. The presence of cyanosis

FIGURE 9-1
A, Normal alveolus. B, Dead space. C, Shunt.

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156 PART II Cardiopulmonary Assessment

suggests a high probability of hypoxemia; however, it •

For every 20 mm Hg increase in Peo2, the pH de­
can occur without cyanosis. Two examples may be creases by 0.10.
cited, one in which an anemic patient with hypox­ •
For every 10 mm Hg decrease in PC02, the pH in­
emia can have little cyanosis, and the other in which creases by 0.10.
a patient with polycythemia can have cyanosis with There is also a relationship between the Peo2 and
minimal hypoxemia. the plasma bicarbonate:
There is a predictable relationship between the arter­ •
For every increase of 10 mm Hg in the Peo2, there
ial oxygen saturation of the Hgb and the POz. It is repre­ is a decrease of I mmollL plasma bicarbonate
sented in the oxyhemoglobin dissociation curve as fol­ •
For every 10 mm Hg Peo2, there is a decrease in
lows. When oxygen saturation is monitored during plasma bicarbonate of 2 mmollL.
exercise, saturation is kept at or above 90%. As the Knowing these guidelines, it can be determined if
curve denotes at a level of approximately 60 mm Hg, the changes in the arterial blood gases are in line with
the saturation is about 90%. As the P02 drops at the respiratory problems vs. metabolic problems such as
sharp part of the curve, for every mm Hg POz, there is a acidosis from diabetic ketoacidosis, where the base
marked decrease in oxygen saturation (Guyton, 1986). deficit can be very low, the pH can be low (acidemic),
but the Peo2 can be within normal limits (Shapiro,
1994; Shapiro, Peruzzi, and Templin, 1994).
Chemoreceptor Response to Hypoxemia

The peripheral chemoreceptors, the carotid, and the

RESPIRATORY FAILURE
aortic bodies, are located at the bifurcation of the in­
ternal and external carotid arteries and the arch of the Respiratory failure is defined as the failure of the pul­
aorta. These receptors are nervous tissue that have a monary system to meet the metabolic demands of the
high metabolic rate and an abundant oxygen supply. body, that is, ventilation and oxygenation (Shapiro,
When tissue P02 decreases, their response to the brain Peruzzi, and Templin, 1994). The blood gases usually
is to increase ventilation and cardiac output. When have a pH below 7.30 and a Peo2 above 50. Generally
this is not sufficient to effect a normal POz, supple­ the patient is also hypoxemic.
mental oxygen or increased mechanical assistance During the acute phase, the kidneys have not
such as continuous positive airway pressure (CPAP) started to compensate and the base HCO,- is within
is given (Tarpy, 1994). normal limits. Later, a base excess can be noted as
the kidneys try to compensate for the acidotic pH.
Chronic respiratory failure can be noted by an in­
BLOOD GAS INTERPRETATION
creased Peo2 with a pH within normal limits.
The norms for the pH, Peo2, Po2, and base have pre­ In assessing the Po2, the following ranges are
viously been given and should first be considered. Is used: mild hypoxemia less than 80 mm Hg, moderate
the value normal or not? Is the patient acute, that is, hypoxemia 60 to 80 mm Hg, and severe hypoxemia
uncompensated, partially compensated, or fully com­ below 40 mm Hg.
pensated (chronic)? There are also "acceptable" Positional changes can affect the oxygenation sta­
ranges to consider, as in the following: tus. For example, unilateral right lower lobe atelecta­
•
pH 7.30 to 7.50 sis with the patient lying on the right side causes in­
•
Pe02 30 to 50 mm Hg cre a s e d blood fl o w to the right lung, which i s
•
pH 7.45 alkalemia collapsed. This causes increased shunting and a de­
•
pH 7.35 acidemia crease in oxygenation lying on the right side (differ­
•
Pae02 45 respiratory acidosis (hypercapnia) ential shunting). If the patient lies on the left side, the
•
Pae02 35 respiratory alkalosis (hypocapnea) oxygenation will improve. Lying supine, a mixed P02
A relationship between the pH and the PC02 also can be observed.
exists. There is a predictable change caused by varia­ When hypoxemia is noted, treatment consists of
tion in carbonic acid: oxygen therapy and alleviation of the cause of hypox­

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 9 Arterial Blood Gases 157

emia, if possible. This may be airway clearance tech­ duced less O2 is available. This is particularly impor­
niques or medication, in addition to the oxygen ther­ tant if a patient already has a decreased P02 and is
apy. Oxygen therapy treats the hypoxemia, decreases traveling to an area with lower barometric pressure.
the patient's work of breathing, and decreases my­ Patients on oxygen will need an oxygen prescription
ocardial work. based on the area in which they are living.
Barometric pressure increases, such as a hyper­
baric oxygen chamber with higher barometric pres­
FACTORS AFFECTING ARTERIAL BLOOD GASES
sure, can be helpful in delivering increased oxygen
There are many normal causes that have an affect on for many patients. Wound-healing needs and carbon
arterial blood gases, such as extremes of age-neonatal monoxide poisoning are two .such indications.
to geriatrics. The neonate has many changes going on Increased temperatures (febrile state) can increase
in the initial life process; fetal circulation changes metabolism and therefore increase oxygen consump­
dramatically in the first hours and days of life. In the tion. Decreased temperatures can decrease the oxy­
geriatric patient, decreases in cardiac output (CO), gen consumption, as seen in patients involved in cold
residual volume (R V) of the lungs, and maximal water near drowning, where they survived several
breathing capacity gradually decrease P02 over the minutes under the water, and were resuscitated and
life cycle. It is estimated that after 60 years of age, resumed normal lives.
the P decreases by I mm Hg per year of age from It is important to note on the arterial blood gas
60 to 90 years. report the status of the patient when the blood gas
Exercise or any increase in activity from rest may was drawn. Usually patients are at rest when the
result in increased oxygen consumption for patients blood gas is drawn. If the P is low at rest (60 mm
with cardiopulmonary dysfunction. In the normal Hg) it is close to the sharp part of the oxyhemoglo­
population, the human body compensate by increas­ bin dissociation curve and the patient may desatu­
ing oxygen consumption to meet the workload. Usu­ rate with exercise.
ally, a plateau is reached and a constant oxygen con­ If the patient was on supplemental oxygen and the
sumption for that activity is achieved. In patients with P was only 55 mm Hg, the P02 is still inadequate
cardiopulmonary dysfunction, oxygen consumption with additional 02 (Carpenter, 1991). Similarly, if a
continues to increase even at the same workload in patient is on mechanical ventilation, the blood gases
untrained patients. It is important to monitor oxygen should be within or near normal limits.
saturation to prevent desaturation of these patients
(Guyton, 1986). During pregnancy, hormonal and
SUMMARY
mechanical factors have a negative effect on car­
diopulmonary function. During the last trimester, This cha pter discussed the normal arterial blood
women often observe shortness of breath and diffi­ gases and what their values mean to the therapist.
culty taking a deep breath secondary to diaphrag­ Relationships between pH and Pe02, Pe02 and He03-,
matic encroachment. and O2 saturation and POz have been examined. We
During sleep, there is a decrease in minute ventila­ saw predictable changes that are caused by respira­
tion and a decreased responsiveness to CO2 and hy­ tory changes were described. In addition we noted
poxemia. Many patients with spinal cord injury and that metabolic changes can have marked effects on
COPD have been noted to have hypoxemia during blood gases. Oxygen therapy and airway clearance
sleep studies. This should be considered in any tired techniques can improve hypoxemia, and position
or groggy patient. changes can be detrimental, causing differential
Low barometric pressure associated with high alti­ shunting or i m p r o v i ng the P02 by better
tude significantly decreases the amount of oxygen ventilatiOn/perfusion matching.
available to the individual. As noted before, the par­ As PTs, it is necessary to be acutely aware of the
tial pressure 20% of oxygen is dependent on the total respiratory monitors that can assess and progress pa­
atmospheric pressure. When the total pressure is re­ tients safely to their optimal rehabilitation potential.

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158 PART II Cardiopulmonary Assessment

REVIEW QUESTIONS References

1. Which factors affect arterial blood gases? Carpenter, K.D. (199]). Oxygen transport in the blood.
2. How can exercise have a deleterious effect on Care Nurse, !J (9), 20·33,
Chernlak, R.M. (1992). Evaluation r<:'spiratory function in health
blood
and disease. Dis MOrl. (7),505-576.
3. What predictable occur between pH and
Guyton, A. (1986). Textbook of medical physiology (7th ed,),
and oxygen saturation? Philadelphia: WB Saunders.
4. What two theraDeutic t echniques can improve Shapiro, B.A. (1994), Evaluation blood gas monitors: pelfor-
mance criteria, clinical impact, and cosrlbenefit (editorial com·
ment). Crilical Care Medicine, 22 (4), 546-548,
5. What affect can body position have on blood
Shapiro, B,A" Peruai. W., & Templin, R, Clinical applicalion of
gases?
blood gases, (5th St. Louis: Mosby,
Tarpy, S,P"& Farber. H,W, (1994), Chronic lung
prescnbe home oxygen, Ceriatrics, 49 (2), 27-28,3

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 Principles of Chest X-Ray
Interpretation

Michael Ries
Thomas Johnson

KEY TERMS Air bronchogram Hyperlucency

Air fluid levels Mass formations
Atelectasis Pneumonia
Densities Radiograph
Diffuse patterns Silouette sign

There are three general categories of radiographic One of the first things to check before interpreting
studies of the chest-fixed-position studies, sus­ the film is the quality of the film. An optimal PA
pended motion studies, and motion studies. The rou­ chest film is one in which the dim outline of the ver­
tine posteroanterior (PA) and lateral chest film is a tebral bodies is seen through the mediastinum. Films
fixed-position, suspended motion study. The patient may be overpenetrated (of increased density) or un­
is positioned with chest against the x-ray film holder derpenetrated (of decreased density) and still be ade­
and is asked to hold his breath in deep inspiration. quate for interpretation. Suboptimal films may also
The radiograph (x-ray) is named from the source hide pathology and cause misinterpretation.
of the x-rays to the film. Thus a PA chest film is po­ The purpose of a radiograph is to see inside the
sitioned so that the source of the x-rays is 72 in. be­ otherwise opaque body by shifting the spectrum of
hind the patient and the film is in front. An antero­ light to above the high ranges of the visible spectrum,
posterior (AP) chest film is the reverse, with the thus converting the body structures into densities
back of the patient against the film. During interpre­ rather than colors. The densities recorded on the x­
tation, the conventional position of the fi 1m on the ray film range in shades of gray to black depending
view box is as if the physical therapist (PT) were on the amount of x-ray energy the structures of the
facing the patient. body absorb as the x-ray passes through them.

159

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160 PART II Cardiopulmonary Assessment

FIGURE 10-1
Familiar fruits such as an apple, orange, pear and banana (A and C) transform into two-dimensional
objects when x-rayed (B and D). The pictures (A and C) also show a box of cherry tomatoes and a
jar of bird seed (millet seed) and their x-rays. B, is the radiograph of A, and D, is the radiograph of
C. Changes in position of the same objects from A to C illustrate the changes of shape in the
corresponding x-rays. B to D, and emphasize the need for PA and lateral x-rays for evaluating
three-dimensional structures.

There are five basic densities, varying from very third dimension, which is used to interpret the inter­
radiolucent to very radiopaque. The darkest or most nal problems of a patient.
radiolucent density is gas or air. Fat is moderately ra­ The routine examination of the chest should in­
diolucent. An intermediate or water density is seen clude a PA and lateral chest film on maximum inspi­
reflecting the connective tissues, blood, muscle, skin, ration at least for the first examination. Without the
and other structures. Bone and deposited calcium are lateral film, disease processes behind the heart and
moderately radiopaque. Metal is the most opaque posterior in the thorax may be missed. Very ill pa­
(white or clear). The structures of the body absorb tients who cannot be transported to the radiology de­
most of the x-rays as they pass through the body, and partment must often be evaluated at the bedside from
the remainder of the rays expose the film. a single PA or AP view (taken with the portable x-ray
An example of an x-ray is the familiar fruits or unit). The size of the patient introduces mechanical
objects that have been converted into a two-dimen­ limitations to the performance of a lateral chest film.
sional reproduction of densities in Figure 10-1. Portable x-ray units are not as powerful as the sta­
These three-dimensional structures are reduced to tionary departmental machines.
two dimensions and only the edges or structures tan­ Additional radiographic views may be ordered to
gential to the beam of the x-rays are recorded. Thus verify or e l u c i d a t e f i n d i n g s. These i n clud e
two views, taken at 90° from each other (PA and lat­ (I) oblique views, (2) apical lordotic views, (3) de­
eral), are required for a mental reconstruction of the cubitus views, (4) iaminograms, (5) inspiration and

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 10 Principles of Chest X-Ray Interpretation 161

FIGURE 10-2
These A, PA and B, lateral x-rays anatomically localize the basic structures that must be reviewed
during chest x-ray evaluation. Some of the structures are seen in both views and others are seen in
only one view. During evaluation, one should identify and see the foJlowing basic anatomical
structures.
Soft /issues and ex/ralhoracic s/rucltlres: soft tissues (ST), breast shadows (BS), diaphragm (D).
liver(L). and fundus of stomach (F).
Bony /homx: ribs (RI), vertebrae (V), scapulae (5, seen best on PAl, clavicles (CL. seen best on
PAl and sternum (SN. seen best on lateral).
Medias/ina! s/rucll/res: mediastinum (M), trachea (T), carina (CA). aortic knob (AK). heart (H).
anterior clear .'pace (ACS. seen on lateral) and hilus of lungs (HI).
LUlIgjields: hilus of lungs (HI). pulmon;Jry vessels (arise from hilus and branch outward).
costophrcnic angles (CPA) and lung apices (LA. seen best on PAl.
There arc many other structures that must be evaluated in addition to these basic ones, and
pathologics must be identified.

ex.piration films, (6) special studies requinng con­ since other pathologies may be present. All the
trast materials, (7) physiologic mOlion evaluation anatomical structures on the film should be exam­
with the fluoroscopc, (8) computed tomography (CT ined. A body system approach is recommended:
scan), and (9) magnetic resonance imaging (MRI). bones and soft tissues (including the abdomen), the
Film interpretation requires a solid knowledge of mediastinum from larynx to abdomen, the cardiovas­
gross anatomy and gross pathology. The PT is liter­ cular system, the hila, and finally, the lungs (Figure
ally examining the internal structures of the body 10-2).
without an autopsy or surgical intervention. The The tools of radiographic interpretation include
structures of the body are thus converted into the den­ the following:
sities of air, fat, water, calcium, and metal. The PT 1. The principle of bilateral symmetry ( when
should ex.amine the entire film, not just one area, and structures are paired, then in general one should
should not get "tunnel vision." Once an abnormality look like the other).
is found, the PT should continue to evaluate the re­ 2. The presence or absence of air fluid levels
mainder of the film and should not stop at that point, (there are almost no straight lines in the chest).

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162 PART II Cardiopulmonary Assessment

If a line appears to be straight, then it must be Bronchi are not usually seen unless they are sur­
explained. rounded by fluid or have a disease causing thickening
3. The silhouette sign. When densities are next to of the walls. The vascular pattern may be distorted,
each other, they obliterate normal margins and blurred, increased, or decrcased by pulmonary dis­
show no separation (normal silhouette of a ease. Air space or alveolar disease is manifested by
structure is obliterated). When densities or opacification (white appearance) of air-filled struc­
structures are in front or in back of other densi­ tures of the l ung. Thus pneumonia may appear as
ties or structures, then a margin is seen. patchy coalescent areas of acini, or segmental and/or
4. An a i r b r o n c h o g r a m is seen w h e n t h e air lobar consolidation. An air bronchogram is seen
around a bronchus is pathologically filled with when the air-filled lung tissuc about the bronchus is
fluid or other material. filled with fluid or other material and the bronchus is
5. Lobar and s e g mental collapse follows the filled with air (Figure 10-3).
anatomy of the lung. Certain lung diseases cause a decrease (increase in
6. Pleural changes may be manifested by gas in a translucency) , such as emphysema (generalized) or bUl­
pneumothorax, fluid in a pleural effusion, cal­ lae (localized). Interstitial pulmonary disease is mani­
cium or soft tissue from scarring or mesothe­ fested by distoltion or increase in volume of tissues sur­
home. A hydropneumothorax demonstrates an rounding the air spaces. An enormous number of
air fluid level. diseases can produce interstitial roentgenographic
7. The presence or absence of mass formation as changes. Sometimes a diagnosis is strongly suggested
in tumors, nodular changes or miliary changes. by the roentgenographic appearance, but in most, a his­
The conventional terminology depends on the tologic evaluation is required for diagnosis. Enlarge­
size of the abnormality. ment of the bronchi may result in bronchiectasis (Fig­
8. Air-containing spaces such as bullae or cysts. ure 10-4). Bronchiectasis is characterized by tubular

FIGURE 10-3
A, There is total pneumonic consolidation of right upper lobe with complete alveolar and bronchial
filling. B, Approximately 24 to 36 hours later, the consolidation has cleared markedly with patchy
coalescent residual. A few air bronchograms are seen in the perihilar region.

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 10 Principles of Chest X-Ray Interpretation 163

FIGURE 10-4
A, Fibrosis and saccular bronchiectatic changes are present in the left lower lobe. A few cystic
"circular" changes are present in the right upper lobe but are best seen on the bronchogram. B,
The bronchogram demonstrates the dilated abnOImal bronchi of cystic and saccular
bronchiectasis in the left lower I.obe with fibrosis around them. The right upper lobe reveals a
few cystic changes.

FIGURE 10-5
A, The PA chest film demonstrates the water density of a pneumonic consolidation in the right
lower lobe. The diaphragm is blurred. B, The lateral film shows obliteration of the posterior right
diaphragm and the costophrenic angle by the pneumonic consolidation.

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164 PART II Cardiopulmonary Assessment

shadows that are double-line paraliel shadows follow­

ing the bronchovascular distribution. The shadows may
branch similar to the bronchial tree.
P n eu m on ias are u s u ally classified by their
causative agents of anatomical distribution. A lobar
pneumonia is one that involves the entire lobe, and a
segmental pneumonia involves the anatomical seg­
ment of a lobe. Generalized pneumonic processes
occur with aspiration of vascular spread of an infec­
tious agent (Figure 10-5). The roentgenographic find­
ings of bronchopneumonia are varied. The earliest
manifestation may consist only of peribronchial cuff­
ing. The disease, however, spreads rapidly to the
alveoli. More often, however, bronchopneumonia is
manifested by multiple, ill-defined nodular densities
(acinar nodules) that are patchy. As these acinar nod­
ules become confluent, airspace consolidation devel­ FIGURE 10-6
ops. As the disease progresses, segmental and lobar A 5-cm cavitary ahscess is seen on the le ft with an air fluid
pneumonias can be seen. level and a relatively smooth wall. This patient was

Pulmonary abscesses and cavities may occur sec­ probably recumbent and lying slightly on the left side to

ondary to pneumonia. An abscess occurs when there aspirate materials to this area, which was first a pneumonic
process in the superior segment of the left lower lobe and
is a breakdown of the tissues of the lung, with the
progressed to an abscess cavily.
area replaced by infectious materials (of water den­
sity). When the infectious materials empty into the
bronchus and air communicates with the abscess, a
cavity develops in that area of the lung. Lung ab­
scesses often result from aspiration and they are catheters may result in a traumatic pneumothorax.
often found in the area s dependent at the time of the The appearance is fairly characteristic, and there may
aspiration. Thus abscesses occur in the area that is be an associated air fluid level with a hydropneu­
downward by gravity, depending on the upright or mothorax (secondary to minor bleeding from the
reclining position of thc individual (Figure 10-6). If punctured lung). Pleural effwiions, or the accumula­
the pleura is penetrated by the abscess, an empyema tion of fluid between the lung and chest wall, can be
develops; and if a cavity communicates with the seen in increased hydmstatic pressure (congestive
pleura, a pneumothorax de velops with a br on­ heart failure [CHFJ), diseases of the pleurae (malig­
chopleural fistula. nancies) or diseases of the lung (emphysema sec­
A pneumothorax or gas in the pleural space devel­ ondary to pneumonia).
ops when the pleural .'pace communicates air through Ale/ectasis is thc term used for incomplete expan­
ei ther a defect in the chest wall or a defect in the sion of a portion or all of the lung. A loss of air in the
pleural surface of the lung. As the air accumulates be­ alveoli in the atelectatic area occurs. Atelectasis is a
tween the chest wall and the lung, the lung becomes sign of disease, since it ·is always secondary to an­
compressed and moves away from the chest wall other lesion, such as (I) obstruction of a bronchus;
(separated by air) (Figure 10-7). Chronic interstitial (2) loss of ability for pulmonary expansion as a result
disease and emphysema are often complicated by a of pleural disease, diaphragmatic disease, and masses
spontaneous pneumothorax. Traumatic causes such in the thorax; or (3) volume loss from local or gener­
as automobile accidents or inseltion of central venous alized pulmonary fibrosis. Atelectasis is a loss of vol­

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 10 Principles of Chest X-Ray Interpretation 165

ume in the area involved and results in a decrease in

size or a change in position of the surrounding struc­
tures (Figure 10-8).
Congestive heart failure, uremia and pulmonary
edema may be manifested by a "diffuse" pattern on
the chest film (Figure 10-9). In CHF, there is a pro­
gression of roentgenographic changes as the disease
evolves into pulmonary edema. The first manifesta­
tion is an increase in the antigravity vasculature of
the lungs (redistribution of blood flow to the upper
lobe vessels). The next stage is manifested by a loss
of the distinct margins of the vessels. This is fol­
lowed by accumulation of fluid in the interstitial
spaces (around the alveoli). Pulmonary edema is pre­
sent when the fluid seeps from the interstitium and
makes the alveoli opaque. Pulmonary edema is radi­
ographically indistinguishable from diffuse pneumo­
FIGURE 10-7 nia. CHF usually is associated with cardiomegaly
The chest x-ray reveals separation of the visceral from the (enlargement of cardiac silhouette) and may be asso­
parietal pleural line and absence of vessels laterally. A ciated with pleural effusions and/or pericardial effu­
"straight line" is seen at the rIght base, indicating a gas sions (Figure 10-10).
fluid level in a hydropneumothorax. Fibrotic and irregular
Pulmonary malignancies may be both primary and
pulmonary changes in the lungs indicate underlying
metastatic. Mass formation is characteristic, and there
interstitial disease, which was a pneumoconiosis (silicosis).
may be atelectasis when the mass o b s tructs a

FIGURE 10-8
A, The PA film demonstrates loss of the right heart border and the downward shift of the minor
fissure, with atelectasis of the right middle lobe secondary to a radiolucent foreign body in the right
middle lobe bronchus. No air remains in the middle lobe, thus it is dense. B, The arrow on the
lateral view points to the residual tissue density of the right middle lobe, which is atelectatic.

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166 PART II Cardiopulmonary Assessment

FIGURE 10-9 FIGURE 10-10

The central lung fields reveal increased density and there is The chest film reveals cardiomegaly (enlargement of the
sparing of the peripheral areas in "butterfly" pulmonary cardiopericardial silhouette) and bilateral pleural effusions
edema. The patient has had a thoracotomy, and chest tubes are more marked on the right than on the left. Vascular
are in place. structures are blurred with interstitial edema.

FIGURE 10-11
A, A mass is present in the left hilar area obstructing the left upper lobe bronchus. There is
atelectasis of the left upper lobe and lingula secondary to the malignancy. B, The lateral view
reveals an S-shaped curve of tumor mass and atelectasis.

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 10 Principles of Chest X-Ray Interpretation 167

articulating facets in rheumatoid arthritis of the spine.

An obese individual may have severe difficulty with
respiration, not only because of the excess fat and
added weight on the thorax, but also because of the
increased load on the cardiovasculature system. This
increased load and hypoxemia may result in CHF.

REVIEW QUESTIONS

1. What are the three categories of radiographic

studies of the chest?
2. How may the quality of the film impact interpre­
tation?
3. What are the five basic densities seen on a radi­
FIGURE 10-12 ograph?
This chest x-ray of a kyphoscoliotic patient reveals a 4. What principles are used consistently to interpret
markedly abnormal, reverse S-shaped curve of the thoracic radiographs?
spine deforming the mediastinal structures and ribs. This
5. How can lung disease cause a change in translu­
patient is breathing primarily with the diaphragms.
cency of the Xray?
6. How can mediastinal deviation diagnose pneu­
mothorax or atelectasis?
bronchus (Figure 10-11). Secondary findings such as
widening of the mediastinum, rib metastasis, pleural
Bibliography
masses or pleural fluid, and encasement of vascula­
ture with hyperlucency beyond the tumor may be Felson, B. (1973). Fundamentals of chest roentgenology (2nd ed.).
Philadelphia: WB Saunders.
seen. Alveolar cell carcinoma may appear like a
Fraser, R.G. & Pare, J.A. (I 988). Diagnosis of diseases of the chest
pneumonia. Involvement of the phrenic nerve may
(3rd ed.). Philadelphia: WB Saunders.
result in paralysis of the diaphragm with elevation. Freundlich, I.M. & Bragg, D.G. (I 992). A radiographic approach
Thoracic deformities such as kyphoscoliosis may to diseases of the chest Baltimore: Williams and Wilkins.

severely impair the respiration of an individual (Fig­ Meschan, I. (1976). Synopsis of analysis of roentgen signs in gen·
eral radiology Philadelphia: WB Saunders.
ure 10-12). The abnormal shape and direction of the
Murray, J.F. & Jade, J.A. (1994). Textbook of respiratory medicine
spine interfere with the leverage necessary for move­
Philadelphia: WB Saunders.
ment of the ribs with respiration. Severe impairment Paul, L.W. & Julll, J.H. The essentials of roentgen interpretation
of respiration may occur when there is fusion of the (3rd ed.). New York: Paul B Hober, 1972.

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 Electrocardiogram Identification

Gary Brooks

KEY TERMS Arrhythmia Electrocardiogram (ECG)

Artifact Syncytium
Bradycardia Supraventricular
Depolarization Tachycardia

INTRODUCTION
The ECG is an essential tool in the physician's di­
The heart is a vital link in the oxygen transport sys­ agnosis and medical treatment of cardiac disease. In­
tem, pumping blood to the pulmonary and peripheral formation provided by the ECG may also assist the
circulation systems to supply oxygen and other nutri­ physical therapist (PT) in the assessment of a pa­
ents required for metabolism in all tissues. The beat­ tient's readiness for and response to physical activity.
ing heart generates rhythmic, electrical impulses that PTs in many different practice environments have ac­
cause mechanical contraction, or the pumping action, cess to information afforded by the ECG. For exam­
of cardiac muscle. Some of the electrical current pro­ ple, in an acute care or rehabilitation setting, a pa­
duced by these rhythmic impulses is detectable by tient's baseline ECG, with an interpretation, may be
electrodes that may be placed on the surface of the available within the medical record. Documentation
skin. Current flow during the cardiac cycle is then accompanying a referral for outpatient physical ther­
recorded as the characteristic waveforms of the elec­ apy may include a reference to the patient's ECG. In
trocardiogram (ECG). Mechanical events such as con­ other settings such as an intensive care unit or cardiac
traction and relaxation of the myocardium are infelTed rehabilitation program, ongoing monitoring of a pa­
from the waveforms produced by the ECG. tient's ECG may be performed during evaluation and

169

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170 PART II Cardiopulmonary Assessment

treatment procedures. It is therefore crucial that all polarization, during which a stimulus of greater than
PTs have a basic understanding of the uses and limi­ normal intensity is necessary to depolarize the cell
tations of the ECG in their practices. again. The refractory period of atrial cells is signifi­
This chapter briefly reviews the basic anatomy cantly shorter than that of ventricular cells allowing a
and physiology of the myocardial conduction sys­ more rapid intrinsic atrial rhythm than intrinsic ven­
tem as it relates to the ECG. The configuration of tricular rhythm. Therefore atrial rhythms pace the
the normal ECG is presented and discussed along heart, including the ventricles, given intact atrioven­
with several methods of quickly determining heart tricular (AV) conduction.
rate a n d rhythm from an electro c a r d i o g r a p h i c Closure of the slow Ca++ channels at onset of repo­
record or "strip." Some o f the more common dys­ larization is accompanied by opening of K+ channels,
rhythmias are examined, as are some other patho­ causing a rapid outflow of K+, which restores resting
logic features. Throughout the chapter, the uses and negative membrane potential. During the cell's resting
limitations of the ECG in physical therapy practice phase, Na+ and Ca++ are actively pumped out of the
are highlighted. cell, and K+ is pumped into the cell, restoring ionic
gradients needed for repolarization (Shih, 1994; Guy­
ton, 1991; Smith and Kampine, 1990).
PHYSIOLOGY AND ANATOMY
It is the electrical current produced by ionic
OF THE CONDUCTION SYSTEM
flow that is transmitted through the conductive tis­
Generation of the Action Potential
sues surrounding the heart. This current is de­
The action potential, or cardiac impulse, is generated tectable by surface electrodes, enabling the record­
by ionic flow across myocardial cell membranes. In ing of the ECG.
the cell's resting state, a negative membrane potential
exists, based on the relative concentrations of sodium
The Conduction System
(Na+), Calcium (Ca++), and Potassium (K+) in the in­
ternal and external cellular environments. Membrane Because myocardial cells are arranged as a syn­
potential changes rapidly at the onset of depolariza­ cytium, an impulse propagates, or spreads to adjacent
tion, with the opening of Na+ and Ca++ channels, al­ cells, causing them to make contact also. This
lowing these ions to cross the membrane and enter the arrangement alone does not pellllit the heart to func­
cell. Calcium then becomes available for contraction tion as an effective pump. It is the conduction system
of cardiac muscle myofibrils. During depolarization, that initiates and rapidly transmits impulses to other
the membrane's potential becomes positive and the locations within the myocardium, allowing for effec­
cell contracts. As in skeletal muscle, the Na+ channels tive, coordinated myocardial contraction and pump­
are fast-opening and fast-closing mechanisms, allow­ ing. The conduction system is comprised of special­
ing Na+ to rapidly enter the myocardial cell on depo­ ized cardiac muscle that contracts minimally, because
larization. Unlike skeletal muscle, however, cardiac it contains few contractile myofibrils.
muscle has a prolonged depolarization phase as a re­ Any portion of the conduction system is capable
sult of the slower and extended opening of the Ca++ of self-excitation and may act as a pacemaker, gener­
channels. During depolarization, there is also a de­ ating action potentials. However, because of the in­
crease in membrane permeability to K+, for which trinsically more rapid rate of spontaneous depolariza­
there is an outward gradient. A plateau phase of the tion of the sinoatrial (SA) node, it normally acts as
action potential exists, during which outward flow of the heart's pacemaker. The rate of depolarization of
K+ ions is inhibited. This prolongs depolarization and the SA node determines the heart rate. In the absence
delays return to the resting membrane potential. of an impulse from the SA node, the atrioventricular
Each cell has an absolute refractory period during (AV) node depolarizes spontaneously, taking over as
depolarization, meaning that an additional stimulus pacemaker, with the important difference that the rate
will not cause an additional depolarization. A brief, of depolarization is lower than that of the SA node.
but significant, relative refractory period follows de- The pathway of a normal cardiac impulse may be

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 11 Electrocardiogram Identification 171

R-R

o s
I
I
I
I
I
I

FIGURE 11-1
Relationship of ECG complex to conduction pathway. (From Brown, K.R., & Jacobson. (1988).
MCI.I'lering dysrhYlhmias: A problem-soLving guide. Philadelphia: FA Davis.)

followed, highlighting its relationship to the cardiac suiti ng in a dela y i n g of the impulse b ef o r e i t
cycle. Figure I I-I displays the association of the con­ reaches t h e ventricular conduction system. This
duction system and its components with the ECG. pause in impulse propagation allows the atria to
Atrial depolarization is initiated by a spontaneously contract and fill the ventricles with blood_ The P-R
generated impulse that originates in the SA node. The interval of the ECG represents this period between
impulse is then transmitted throughout the atrial mus­ onset of atrial depolarization and the onset of ven­
cle resulting in atrial contraction. This event is tricular depolarization. Normally the P-R interval
recorded as the P-wave of the ECG. The impulse is lasts between 12 and W seconds (Brown and
also transmitted, via rapidly conducting internodal Jacobson, 1988).
pathways, to the A V node. Atrial repolarization is not Following passage through the AV node, the im­
recorded by the ECG, because it occurs during and is pulse continues to the Purkinje's fibers, which trans­
hidden by ventricular depolarization. mit the impulse rapidly to the ventricular endo­
Impulse conduction within the A V node and the cardium. This initiates ventricular depolarization,
AV bundle (bundle of His) slows considerably, re­ which is represented in the ECG by the QRS complex.

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172 PART II Cardiopulmonary Assessment

The depolarization wave propagates relatively slowly U-wave may be seen. The U-wave was considered
throughout the ventricular myocardium. The span of to have little physiologic or pathologic significance
time elapsing during ventricular depolarization is re­ (Smith and Kampine, 1990). However, U-wave in­
flected by the RS interval, which normally ranges version may now be considered to correlate with
between 0.06 and 0.11 secon s n an Jacobson, myocardial ischemia (American College of Sports
1988; Smith and Kampine, 1990). Ventricular depo­ Medicine, 1991). Note that the ventricles remain in
larization originates in the interventricular septum, a state of contraction until slightly after repolariza­
creating the Q-wave, which is normally small or ab­ tion. This period of contraction corresponds to the
sent. The depolarization wave next spreads to the apex Q-T interval on the ECG. Diastole, therefore, begins
and then to the right and left ventricles, causing the R­ subsequent to the end of the T-wave and continues
and S-waves. Depolarization also propagates in an en­ until the next ventricular depolarization. Note also
docardial to epicardial direction within the ventricles that atrial depolarization and contraction occur dur­
(Lilly, J993; Guyton, 1991). ing diastole.
The T-wave of the ECG represents ventricular re­
polarization. It is preceded by the S-T segment, dur­
THE ELECTROCARDIOGRAM
ing which depolarization has been completed and
Recording the Electrocardiogram
repolarization is yet to begin. The configuration of
the S-T segment is an important marker of myocar­ Before examining the timing of the wave forms and
dial ischemia or infarction. Following the T-wave, a the rhythms of the ECG, a basic understanding of the
----
-

I I n-- ilr-fi-r-.VR 1 IT '-l- I Tl vl

ITl-I-H-j 1 I I ' i - 1- · I I'
.
1 = _t-bD7iTI-- J±J ,
rD . V1 '
-1- ' i. T
-
, -'
;-t-.
1 r "r-;

I · I I ! I ' I I ! -r- I I I ' I ! ! I , .

:

, I I I ! I I ' I 1 I I -, I !. .J +! l I I I '! . t-LLLL

-R
'"
U0.--'-.l.-b.L_L_;'.J.0 io., ,L',. LiII.,LLLL
rl- f I+H i ! ;ffft-TmTfFI' r: i}Tiii H {if
,! I, ! ! I 1 . ,· :. . .! . "IA.....
Iffi1
____ _

K+

ttl-mUll I I 111 1 ! i II ! 1I11I1II1I CB-8 i ± j LU i..Ult LI I I ttr

;;.: . l,w,ll- IIII, .,mOOJ.

m.J , " , ." . ",,=g " • •. , t ru!8fffi
t-+TH-�-r-H+-:-:+.Lf+·H+H-+-!--H-:- =-1._!'I-l-l-H-l-

.-

....

FIGURE 11-2
A normal 12-lead ECG tracing.

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 ]1 Electrocardiogram Identification 173
-------

principles of is needed. A stan­ A VR. A VL, and A VF are derived from the electrical
12-lead and sum of the three standard limb leads. The transverse
medical management of cardiac conditions. An ex­ plane leads are referred to as the precordial leads.
ample of a normal 12-1ead ECG is seen in 11­ Imagine that each of the 12 leads "views" the heart
2. Six leads record the electrical in the frontal from a different angle, therefore
plane, and six leads record signals in the transverse different locations of the heart
plane.
The frontal plane leads include three standard limb
II, and III. Three augmented limb leads, (downward) when current travels away from a lead.

V6

V5

I-- V6

I- V5
-'\.
,.i VA
V3
Vl V2

FIGURE 11-3
leads.

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174 PART II Cardiopulmonary Assessment

Other lead configurations may be used for exercise indicates appropriate conduction of impulses from
testing (American College of Sports Medicine, 1991). atria to ventricles.
Single-lead monitoring is commonly used during ex­ •
What is the P-R interval? A P-R interval of greater
ercise training or in acute care settings. than 0.20 seconds indicates delay in conduction
from atria to ventricles.

Evaluating the ECG Strip

•
Is the QRS complex of normal duration and mor­
phology (shape)? A QRS complex greater than
The evaluation of an ECG should be approached in a 0.12 seconds indicates either that an impulse arose
systematic fashion. The following questions are use­ within a ventricle or was conducted abnormally
ful to appreciate the information that is relevant to through the ventricular conduction system.
current clinical practice (Cummins, 1994). By answering each of these questions, the tendency
•
What is the rate and pattern (regularity) of the to "eyeball" the rhythm and make a quick but inaccu­
rhythm? If the R-R interval, that is, the distance rate assessment is avoided.
between successive R-waves, is inconsistent, is the

Determination of Heart Rate

pattern irregular?
•
Does a P-wave precede every QRS complex? This
indicates appropriate atrial activity. Several quick methods estimate heart rate. Most
•
Is there a QRS complex after every P-wave? This printed and displayed ECG recordings indicate a heart

I J I
m =l-
L-J- -+ -- +-+--r-t-i R !-t- lr-r 0.2second -rIlIl_
L- -+-t-t 4s , .oo n +-+- -r1
rt lIlr r1
segment segment I-++-t -nrmmnml 50.5mmmv. -+-
I--H--+--t---t-I' t
PR
ST
I I ' 0.1mv
I

, I , I! I ! I !

,
-.l
I Ll"
,
I-+- -r-rI, !.i
,
S !
j ' I!
"

PRinterval I ITi1',
-'
, '' 1
I
I 1 1 , aRS-.lInterva .:.. interla,
a. T
I
1-' 1
1.--+-++
- - 111 i ll J
' ..l
1 1

FIGURE 11-4
A normal ECG showing characteristic waves, intervals, and segments, and some of the features of
the traci ng paper.

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 11 Electrocardiogram Identification 175

rate. This must be interpreted with caution, however. the rate would be estimated as falling between 100
The presence of artifact (extraneous deflections of the and 75, or close to 80 beats per minute (BPM).
waveform caused by movement or electrical intelfer­ In many clinics, rulers are available that are cali­
ence) may render inaccurate the displayed or printed brated so that heart rate may be estimated quickly by
heart rate. This is a common problem dUling activity aligning markings on the ruler with features of the
or exercise, the circumstances during which many PTs ECG strip. For example, after the arrow on the ruler
monitor patients. It is possible to calculate or to esti­ is placed on an R-wave, count two R-waves to the
mate a heart rate from a printed ECG strip because, by left and read the number at that position on the ruler.
convention, the recording paper is divided into I mm In Figure 11-6, this method approximates the heart
squares and larger 5 mm squares, which are defined rate as 74 BPM.
by heavier lines (Figure 11-4). Also by convention, It is important to note that the preceding two
the standard paper speed for an ECG recording is a methods are useful only if the rhythm of the ECG
rate of 25 mm/second. Each millimeter of length then strip is regular, that is the R-waves are equally
represents 1125th, or 0.04 seconds, and each 5 mm spaced, occurring at consistent intervals. Should the
block represents one fifth, or 0.20 seconds. Some rhythm be irregular, with R-waves appearing at vary­
monitor systems place a mark on the recording paper ing intervals, another method must be employed to
at 25 mm, or I-second intervals. estimate the heart rate.
There are several methods of estimating heart rate Recall that the ECG graph paper is divided into
from a printed ECG strip. On a printed ECG strip, boxes, with the horizontal spacing representing time
find an R-wave located on or near a heavy vertical intervals of 0.04 seconds for each small (I mm) box
line. Proceeding to the left of that R wave, for each and 0.20 seconds for each larger (5 mm) box. It fol­
subsequent heavy vertical line, assign the following lows that I second in time is represented by five
numbers: 300 for the first heavy line encountered, larger boxes. A mark may be placed at 1- or 3-second
150 for the next followed by 100, 75, 60, 50, and 42 intervals, enabling quicker appraisal of heart rate
(Figure 11-5). Stop at the first heavy vertical line fol­ based on a 6-second strip. The procedure is as fol­
lowing the next R wave that is encountered. The lows. Obtain a printed strip of sufficient length, cov­
heart rate may be estimated as falling between the ering more than 6 seconds. If l-second marks are not
two most recently assigned values. In Figure 11-5, present, it may be convenient to place a mark at every

FIGURE 11-5
"Count-off" method of estimating heart rate.

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176 PART II Cardiopulmonary Assessment

, ,J
, ' , f' f'z', I' .. I t t t fj7r'
-F .r
+b
' r.-- 'f' T ' 'r '4rf'
, , . " •
V2
.• . .

-
• , . ' 1.. ....11
. .... ..; . t 't "
II . t'.. ,. ?r t_" 1"
.. ., '""' '/,j
._
" .-- . ..,
.. 1..
, '''lift' '''t-, . 1. ,". .!.•.
1', :;-rt·
I " t
j .. ... - . "
tH- + ,.. • .r...... ;.. -�

IfPL_, t. l
· '
1 -.1 r
;:It" -I ' - '
111111111 nil ] II r 1 1 II I I
Heart rate (two cycles from reference arrow) chart rate (25 mm/ sec)
"

"I
FIGURE 11-6
Using a rate-ruler to confirm heart rate.

FIGURE 11-7
Heart rale estimation in an irregular rhythm (atrial fibrillation).

Evaluation of Rhythms
fifth large block. Next, select a I-second mark or a
heavy vertical line on the left side of the strip, and Electrocardiographic monitoring is an impOitant evalu­
proceed to the right for a length corresponding to 6 ation tool during the treatment of individuals with his­
seconds. If I-second marks are counted, do not count tory of or potential for acute myocardial infarction (MI)
the starting mark or there will be only as-second or myocardial ischemia. Most cardiac deaths are a re­
strip. Count the number of R-waves within the 6-sec­ sult of lethal arrhythmias, for which there is increased
ond recording, and multiply by lO. That is estimated risk in the presence of infarction or ischemia. Rapid
heart rate. Several 6-second strips may be analyzed to recognition of lethal an·hythmias, or arrhythmias that
document a heart rate range of an irregular rhythm may deteriorate into lethal a.rrhythmias, is essential for
(Figure 11-7). The rate of this irregular rhythm is es­ all health professionals involved in the care of individu­
timated at 70 BPM. als with cardiac disease. The arrhythmias described in

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 11 Electrocardiogram Identification 177

FIGURE 11-8
Normal sinus rhythm.

this chapter are those that must be recognized by rhythmia be a precursor to a more serious or perhaps
providers of Advanced Cardiac Life Support as deter­ lethal arrhythmia? Is this an acute occurrence or a
mined by the American Heart Association (Emergency chronic arrhythmia pattern? The clinical response to a
Cardiac Care Committee and Subcommittees, 1992). patient with an arrhythmia depends on the answers to
Normally, a cardiac impulse is generated by the these questions and the treatment setting.
SA node, causing atrial depolarization. This is fol­
lowed by a slight delay in the A V node, after which ARRHYTHMIA IDENTIFICATION
the impulse is conducted to the ventricles causing
Supraventricular Arrhythmias
ventricular depolarization. These events are seen in
their normal spatial and temporal sequence in normal Supraventricular arrhythmias arise from an abnormal­
sinus rhythm (Figure 1 1-8). A P-wave precedes every ity of impulse generation or conduction "above" the
QRS complex and every P-wave is, in turn, suc­ level of the ventricles. The abnormality may occur in
ceeded by a QRS complex. This occurs within an in­ the atria or at the level of the A V junction. Supraven­
terval of 0.20 seconds (one large box), as determined tricular arrhythmias may be categorized as sinus,
by the P-R interval. The QRS complexes occur atrial, or junctional alThythmias.
within a range of 0.04 to 0.11 seconds, indicating that A cardiac rhythm may be a sinus rhythm, but with
ventricular impulse conduction and depolarization is an irregular or abnormally rapid or slow rate. Sinus ar­
occurring in a normal interval. The positively de­ rhythmia is an in'egular sinus rhythm with varying R-R
flected T-wave indicates normal ventricular repolar­ intervals (Figure Il-9). This is a normal variant that is
ization. Because the SA node spontaneously depolar­ associated with the individual's respiratory pattern.
izes at a rate of between 60 and 100 BPM, the rate of Sinus bradycardia is a sinus rhythm occumng at a rate
normal sinus rhythm must fall within these limits. of less than 60 BPM (Figure 11-10). This rhythm may
The identification of arrhythmias affects clinical significantly reduce cardiac output, causing hemody­
decision making, particularly with regards to a pa­ namic compromise, manifested by hypotension or
tient's readiness for and/or response to activity. Clini­ symptoms such as dizziness, lightheadedness, or syn­
cal significance of arrhythmias range from benign to cope. On the other hand, individuals taking beta-block­
lethal. The clinical significance of a given arrhythmia ers, medication that slows the heart, may exhibit this as
is determined by a number of considerations. Some their normal rhythm, as may individuals who achieve a
of these considerations include the following: Is there high level of physical conditioning. Sinus tachycardia
evidence of hemodynamic compromise? Is the ar­ is a sinus rhythm OCCUlTing at a rate of greater than 100
rhythmia a new or unusual finding? Might the ar­ BPM (Figure 11- 1 1). Sinus tachycardia, or any other

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178 PART II Cardiopulmonary Assessment

ft' 'trr.
" '' fr" '

i' "
:
-, +t-; . ,.. , '- : " ,t" " ,., ' ; - . ,. ; .. .
. ' .
t ...:.·1._ t
.• ,. f ' _

_",-,-::C' . .4 t L L· . .
.

• ' 4 ·

FIGURE 11-9
Sinus arrhythmia.

tt·
,
" ,

.... . .. "
: '!.'" L c

FIGURE 11-10
Sinus bradycardia.

f
l , of fl I,
l'"r
I I (}t L,
L
•
1

1
t::-
° L..1-L r
. "
. .J.:... L
1"�1 t _ '· L t L ' .1' I L

FIGURE 11-11
Sinus tachycardia.

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 11 Electrocardiogram Identification 179

FIGURE 11-12
Premature atrial complex.

form of tachycardia, increases myocardial oxygen de­ abruptly and spontaneously reconverting to the previ­
mand, or the workload on the heart. This may initiate ous rhythm within seconds or minutes. The P-wave is
or exacerbate ischemia in the presence of coronary often not visible, making assessment of atrial or junc­
artery disease (CAD). tional origin difficult, but the duration of the QRS
A common form of arrhythmia is a "premature" complexes occurs within an appropriate interval. The
complex, that is, a beat that occurs sooner than ex­ R-R interval, however, is markedly shortened. Figure
pected given the established rhythm. A premature 11-13 demonstrates supraventricular tachycardia at a
atrial complex, or PAC, is an early beat of atrial origin rate of [90 BPM. Other related forms of SVT include
(Figure [1-12). An R-wave appears closer to its pre­ paroxysmal atrial tachycardia (PAT) and multifocal
ceding R-wave than the other R-waves in the estab­ atrial tachycardia (MAT). Clinically, patients with
[ished rhythm. Closer inspection reveals the presence SVT may perceive a "racing" heart rate, which may
of a P-wave associated with the QRS complex, mean­ be quite distressing. At very rapid heart rates, for ex­
ing that the impulse first depolarized the atria before ample, greater than 170 BPM, diastolic ventricular
being conducted to the ventricles. Sometimes the AV filling time is markedly reduced, which may cause
junction may initiate an early beat, causing a premature hemodynamic compromise. Symptoms associated
junctional complex or PJc. When this occurs, the R­ with inadequate cardiac output, such as dizziness,
wave appears earlier; however, there may be no associ­ lightheadedness, and syncope may ensue. Some indi­
ated P-wave, or there may be an unusual P-wave, one viduals with SVT remain asymptomatic; the rhythm
that is inverted or following the QRS complex. An in­ being detected incidentally, for example, during rou­
verted or late P-wave indicates that the impulse was tine pulse or telemetry monitoring.
conducted in retrograde (backward) fashion. Clinically, Atrial fibrillation is the most common, clinically
a premature atrial or junctional complex may be pal­ encountered arrhythmia, seen in more than 5% of pa­
pated as a "skipped" or early beat during pulse taking, tients over age 69. (National Heart, Lung and Blood
or the patient may perceive a palpitation or skipped Institute, Working group on atrial fibrillation, 1993)
beat. Otherwise, these arrhythmias are usually of little Atrial fibrillation is characterized by inconsistent, ir­
clinical significance (Brown and Jacobson, [988). regular R-R intervals with an absence of true P-waves.
A more serious supraventricular arrhythmia is P-waves may be replaced by multiple, fibrillatory F­
supraventricular tachycardia, or SVT. In this arrhyth­ waves of varying configuration. This arrhythmia signi­
mia, the healt rate is rapid, exceeding 150 BPM. The fies that there is no established sinus or atrial pace­
tachycardia may be sustained, lasting hours or even maker, rather that many impulses are simultaneous[y
days, or may be "paroxysmal" (PSVT), appearing generated from multiple locations within the atria. The

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180 PART II Cardiopulmonary Assessment

FIGURE 11-13
Supraventricular tachycardia.

atria, therefore, are not pumping effectively which, in (Figure 11-15), the QRS complex is not preceded by
turn, may impair ventricular contraction. This is be­ a P-wave. The AV node may generate an isolated
cause of the loss of the additional ventricular filling "escape" beat, or it may take over as the heart's pace­
supplied by atrial contraction. Impulses do conduct maker. Sustained nodal or junctional rhythm is usu­
through the AV junction to the ventricles; however, ally between 40 and 60 BPM, corresponding with the
this occurs inconsistently resulting in the irregular R-R inherent rate of spontaneous AV node depolarization.
interval. The ventricular response to atrial fiblillation
is important. A rapid ventricular response, resulting in
Ventricular Arrhythmias
tachycardia, may cause hemodynamic compromise
with associated symptoms or poor activity tolerance. Ventricular arrhythmias result from spontaneous de­
Of additional clinical significance is the association polarization of a region within ventricular my­
between atrial fibrillation and embolic cerebrovascular ocardium; a region outside the normal pathway for
accidents. Figure 11-7 illustrates atlial fibrillation with impulse generation. For this reason, the site of im­
a "controlled," that is, less than 100 BPM, ventricular pulse generation is called an ectopic focus. Ventricu­
response. Pulse monitoring of an individual in atrial lar arrhythmias may be distinguished from supraven­
fibrillation reveals an irregularly irregular pattern. tricular arrhythmias, in that the QRS duration of a
Another arrhythmia that is characterized by abnor­ ventricular arrhythmia is longer than normal 0.12
mal atrial activity is atrial flutter, seen in Figure 11- seconds. The appearance of ventricular arrhythmias
14. In this rhythm, P-waves are replaced by F-waves may be characterized as being "wide and weird." It is
that have a distinctive morphology often referred to important to point out that not all rhythms with a
as a "saw tooth" or "picket fence" appearance. Of QRS duration greater than 0.11 seconds represent ec­
clinical importance is the ratio of atrial to ventricular topic ventricular beats; some widened QRS rhythms
conduction and whether or not the patient is hemody­ result from d isturbances of impulse conduction
namically stable (Brown and Jacobson, 1988). within the ventricles, rather than from impulse gener­
Because the intrinsic rate of spontaneous depolar­ ation within the ventricles.
ization of the AV node is less than that of the SA The reason for the widening of the QRS complex
node, spontaneous AV node depolarization is nor­ resulting from ventricular impulse conduction distur­
mally prevented. However, in the absence of an atrial bance or impulse generation is apparent when one con­
impulse the AV node depolarizes spontaneously and siders the normal conduction of a sinus impulse within
generates an impulse that then is conducted to the the ventricles. An impulse normally is rapidly con­
ventricles. Thus in junctional rhythm or nodal rhythm ducted to ventricular myocardium via the Purkinje's

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 11 Electrocardiogram Identification 181

ff-- TI "fir rtJ l

hi:. f ,1t;f
TT1 _n_1
,_

FIGURE 11-14
Atrial fluller.

FIGURE 11-15
Junctional rhythm.

fibers. This assures that the impulse reaches all regions during an ectopic beat (Figure 11-16). An ECG
of ventricular myocardium in a timely fashion, with rhythm (bottom) is recorded simultaneously with the
subsequent coordinated depolarization and contraction. record of arterial blood pressure monitoring (top).
Within ventricular myocardium itself, however, propa­ The appearance of the "wide and weird" complex re­
gation of the depolarization wave proceeds more sults in significant diminution of the corresponding
slowly, as a result of the syncytial anangement of my­ arterial pressure wave.
ocm'dial cells. The most common form of ventricular arrhythmia
An impulse generated within the ventricles, out­ is a premature ventricular complex, or PVc. In Fig­
side the normal conduction pathways, initially depo­ ure 11-16 the wide and weird QRS complex appears
larizes surrounding local myocardium. The depolar­ early, interrupting the established rhythm. A pause
ization wave then spreads outward from that focus, often follows a PVC, after which the established
but is propagated at a slower velocity. Ventricular rhythm resumes. Clinically, a PVC may be perceived
contraction, in this case, is not coordinated; some re­ by a patient as a "skipped" beat or a palpitation. If
gions contract well b e fo re the depolarization wave pulse monitoring occurs during a PVC, the examiner
reaches regions remote from the ectopic focus. It fol­ will likely sense a "skipped" or irregular beat.
lows that the ventricular ejection of blood is reduced PVCs sometimes happen in patterns, occurring at

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182 PART II Cardiopulmonary Assessment

l.L I

.... ' If
t' SPEEIJ) =
j
25
I.
MM/SECOND
"
f
+ I I t1 t�-r
1"""'j

l
I +- t
L I 1_-,- Uti .J.:. L . . LL .:]
FIGURE 11-16
Diminished arterial pressure wave following a PVc.

FIGURE 11-17
Ventricul ar bigeminy.

regular i n t e rvals. A pye o ccurs in ventricular

m!EulittIOOIOO·, t1 ' IOOlfirkifmlffE[fffil big eminy on every second b e a t, i n ventricular

Tl-tffhtm flffimf!r.::17YrnCTftlTmrT];T1T ·Hfflt trigeminy on every third beat, and in ventricular

quadrigeminy on every fourth beat. Figure 11-17 il­
lustrates ventricular bigeminy. With these rhythms, a
regularly irregular pattern may be noted during pulse
monitoring. pyes may also occur twice in succession
as a ventricular couplet. seen in Figure 11-18.
pyes that originate from more than one ectopic

rnl%'I@I#tllff#tmlL·'.r,· gMtmIff1F atffi lmmm.. focus are termed multifocal pyes. In this circum­
stance, the waveforms will have different morphol­
FIGURE 11-18 ogy according to the locations of the ectopic foci. Re­
Ventricular couplet. member that the positive or negative deflection of the

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 11 Electrocardiogram Identification 183

FIGURE 11-19
Multifocal PVCs.

FIGURE 11-20
Ventricular tachycardia.

waveforms depends on the direction of depolariza­ to most arrhythmias is beyond the scope of this chap­
tion, as viewed by the lead used for monitoring. In ter; however, some arrhythmias demand an immedi­
Figure 11-19 the first pve seen has an initial positive ate response if observed.
deflection, whereas the second pve seen has an ini­ Ventricular tachycardia (V -tach, or VT) (Figure
tial negative deflection. Each of these pves comes 11-20) is defined as three or more consecutive pves
from a different ectopic focus. at a rate greater than 100 BPM (Akhtar, 1990). This
The physical therapists's (PT's) decision-making is a serious and potentially lethal arrhythmia that may
process in response to observation of ventricular ec­ require emergency measures be undertaken. During
topic beats is complex and may not be easily grasped v-tach all complexes are ventricular in origin. V-tach
by the entry-level practitioner. Factors such as pres­ sometimes occurs in "runs" of three or more ectopic
ence or absence of symptoms, the acuity of the pa­ complexes followed by reversion to the baseline
tient, and whether the rhythm is a new finding all in­ rhythm, or it may be sustained. Effective circulation
fluence a clinical response. The presence of a pattern may be preserved, or it may be seriously compro­
such as bigeminy, couplets, or multifocality is also mised or absent in sustained v-tach. A patient may be
considered. Further elucidation of clinical responses asymptomatic, particularly if only a brief run of

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184 PART II Cardiopulmonary Assessment

. : ;,' -r-±l . ::; .

1 _tl_, ,..,t
.
. .
•1 L& 'I . ' .

t-f.,r.-f+-r"*,
-'-! +O-O '--o-rl-.-...-,-
b-4';""'-"-+- :
J /.
•

. ' +- :- ..!r....
n . J
'

. ,. ,. 1 I 1\ , T
r

FIGURE 11-21
Ventricular fibrillation degenerating into asystole.

v-tach was experienced. If VT is sustained, the pa­ ment artifact. Unwary therapists have hastily sum­
tient may be asymptomatic, symptomatic, or uncon­ moned help on observing v-fib or asystole, only to
scious and pulseless. The PT's response depends on feel foolish when a lead is reattached to the patient.
the rhythm, regardless of whether it is sustained, and These arrhythmias are always accompanied by loss of
the patient is symptomatic or conscious. Clinical re­ consciousness and pulse; a clinician should assess the
sponses range from cessation of activity, ongoing pa­ patient before taking action. Similarly, during activity
tient observation and immediate notification of a or exercise, movement artifact may easily be mistaken
physician to a full code. for v-tach. By assessing the patient and asking him or
Ventricular fibrillation (V-fib, VF) is a lethal ar­ her to "hold still," the issue may be quickly resolved.
rhythmia accompanied by immediate loss of con­
sciousness and loss of circulation, that is, cardiac ar­
Conduction Blocks
rest. It is characterized by disorganized, simultaneous
firing of multiple, ectopic ventricular foci; there is no Conduction blocks are another type of ECG abnor­
organized rhythm (Figure 11-21). Effective ventricular mality with which PTs should be familiar. The propa­
contraction ceases and cardiopulmonary resuscitation gation of a cardiac impulse may be inhibited or termi­
is indicated until defibrillation is available. Death fol­ nated along the conduction pathway. Blockage can
lows unless defibrillation successfully restores an ef­ occur at the sinus node, between the atria and ventri­
fective rhythm. Conditions that render the myocardium cles, Or within the ventricular conduction system.
vulnerable to ventricular fibrillation include v-tach, Sinus block occurs if the impulse cannot propagate
myocardial ischemia or infarction, dilatation of the beyond the sinus node. In this case, the AV junction
heart, hyperkalemia, or electric shock (Guyton, 1991). usually takes over as the pacemaker, and a junctional
If not successfully treated, v-fib may further de­ rhythm is seen with the absence of P-waves.
generate into asystole, which indicates complete ab­ More common are the AV blocks. They are ranked
sence of ventricular electrical activity (Figure 11-21). as first-, secondo, or third-degree, depending on the
Asystole may also occur as a primary event. This is extent of delay or obstruction of the cardiac impulse
known colloquially as "flat line" rhythm. Like ven­ between the atria and ventricles. First-degree AV
tricular fibrillation, asystole requires that cardiopul­ block is characterized by a prolongation of the P-R in­
monary resuscitation begin immediately to save the terval beyond its normal 0.2 seconds (Figure I 1-22).
patient's life. Remember that the P-R interval is measured from the
Care must be taken to distinguish an apparent beginning of the P-wave to the beginning of the QRS
lethal arrhythmia from lead disconnection or move­ complex_ Each impulse is delayed between the atria

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 11 Electrocardiogram Identification 185

FIGURE 11-22
First degree A V block.

-,:.1 l fW'
., .j. . ',
: -I--r !t+t'
' -1 ��+*'-'+
,

FIGURE 11-23
Second degree A V block, Mobitz type I.

and ventricles but each eventually reaches the ventric­ P-wave. The conduction ratio in Figure 11-24 is 3: I,
ular conduction system resulting in a normal QRS or three P-waves for each QRS complex. Both first­
complex. Thus for each P wave, there is a QRS com­ and second-degree A V blocks are considered to be
plex; therefore the conduction ratio is 1: 1. incomplete heart blocks.
Second-degree A V block takes two forms, al­ Third degree A V block or complete heart block
though in each form, there are some sinus impulses is also known as A V dissociation. In this rhythm
that are not conducted to the ventricles. In second­ (Figure 11-25), P-waves are present, but there is no
degree block Mobitz type I, also known as Wencke­ relationship between P-waves or QRS complexes.
bach, the P-R interval lengthens progressively uotil a P-waves may be superimposed on QRS complexes,
P-wave fails to conduct to the ventricles (Figure 11- but none of the sinus impulses are conducted to the
23). Notice how the first three P-R intervals lengthen ventricles; the atria and ventricles are contracting
until, after the fourth P-wave, a QRS complex fails independently of each other. In the absence of clini­
to appear. The cycle then repeats itself. Second­ cal intervention such as artificial pacing, ventricular
degree block Mobitz type 2 (Figure 11-24) is charac­ depolarization is initiated by a junctional or ventric­
terized by a fixed P-R interval with a "dropped" ular pacemaker.
QRS f o llowing every seco nd, t h i r d, or f o u r t h Clioically, A V blocks range in severity from benign,

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186 PART II Cardiopulmonary Assessment

" . fi
'j.,�1 l..r-� /

,. i' L1Ji;! i
t t 1L ? rr

M , +.·::;, "ti
'
; : . L
• •: " ...... +-....
. ..

:;
....

" : .:
FIGURE 11-24
Second degree A V block, Mobitz type 2,

. ,;;Y '
t1ft
:
I. t '

-� I
FIGURE 11-25
Third degree A V block with ventricular pacing,

as is usually the case with first degree AV block, to po­ often treat patients with coronary hearl disease, infor­
tentially lethal. Whether hemodynamic compromise oc­ mation regarding MI or myocardial ischemia is also
curs depends on the extent of impairment of cardiac of interest. Although PTs do not medically diagnose
output caused by too slow of a rate of ventricular con­ myocardial ischemia or MI, they should have a work­
traction (Brown and Jacobson, 1988), Slow rates of ing knowledge of its electrocardiographic evidence.
ventricular contraction may cause lightheadedness or During myocardial ischemia, blood flow to a portion
syncope. In most cases of third degree block, treatment of myocardium is compromised, resulting in alter­
now includes implantation of an artificial pacemaker. ation of myocardial metabolism. In MI, a portion of
In Figure 11-25, the needlelike spikes indicate that an myocardium has died, but an adjacent zone of is­
artificial pacemaker is depolarizing the ventricles at a chemic myocardial cells endures. These ischemic
rate of 60 BPM. cells may remain "leaky," and be unable to repolar­
ize. The persistent current flow from the "leaky" re­
gion results in a current of injury, which is seen as a
MYOCARDIAL ISCHEMIA OR INFARCTION
shifting of the S-T segment above or below the iso­
The EeG provides much more information, beyond electric line (Guyton, 1991; Lilly, 1993). S-T seg­
that gleaned from arrhythmia analysis. Since PTs ment shift has significant diagnostic value. For exam­

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 11 Electrocardiogram Identification 187

FIGURE 11-26
S-T segment elevation during myocardial infarction.

pIe, S-T segment elevation (Figure 11-26) is associ­

ated with transmural Ml. whereas S-T segment de­
pression is associated with nOn transmural or suben­
docardial MI. Also, the O n s e t of S-T s e g m e n t
depression during activity i s often considered diag­
nostic of myocardial ischemia. Figure 11-27 is an ex­
ample of exercise-induced S-T segment depression
observed in one lead during exercise.
The following is a brief discussion on other abnor­
malities of the ECG observed in coronary artery disease
(CAD). A prominent, pathological Q-wave is indicative
FIGURE 11-27
of a t.ransmural MI (Lilly, 1993). Indeed, "non-Q" is syn­ S-T segment depression during exercise.
onymous with nontransmural concerning MI. The pres­
ence of a prominent Q-wave (Figure 11-28) does not,
however, distinguish between an old or an acute event.
The T-wave may also undergo changes during
myocardial ischemia or MI. During ischemia, for
example, the T-wave may invert as a result of pro­
longation of repolarization (Guyton, 1991). Simi­
l a r ly, d uring MI, c h a n g e s in the T - w a v e m a y
"evolve" with the infarct, a t first becoming indistin­
guishable within an elevated S-T segment, then in­
verting, then perhaps reverting to original configu­
ration following the passage of time.

CONCLUSION

Understanding the changes in the ECG during is­

chemia or MI may help PTs integrate all available in­ FIGURE 11-28
formation to optimize patienl evaluation. This knowl­ Significant Q wave.
edge, combined with astute arrhythmia recognition

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188 PART II Cardiopulmonary Assessment

and symptom assessment, provide entry-level PTs 7. What is the possible clinical significance of S-T
with important tools for management of patients at segment depression, of S-T segment elevation?
risk for cardiopulmonary dysfunction. What symptoms might be anticipated in the pres­
ence of those conditions?

REVIEW QUESTIONS
References
1. How may the following dysrhythmias be per­
ceived by a clinician without benefit of ECG Akhtar, M. (1990). Clinical spectrum of ventricular tachycardia.

monitoring? How may they be perceived by a Cireula/ioll, 82, 1561-1573.

American College of Sports Medicine. (1991). Guidelinesfor exer­
patient?
cise /es/il1g and prescrip/ion. (4th ed.). Philadelphia: Lea and
• atrial fibrillation
Febiger.
• supraventricular tachycardia Brown, K . R . , & Jacobson. S. (19 88). Mas/ering dysrhy/hmias: A
• premature ventricular contractions problem solving guide. Philadelphia: FA Davis.

• third degree A V block Cummins, R.O. (Ed.). (1994). Tex/book of advanced cardiac I'fe
SUppOrl. Dallas: American Heart Association.
• ventricular fibrillation
Emergency Cardiac Care Committee and Subcommittees. (1992).
2. What determines the clinical significance of an
Guidelines for cardiopulmonary resuscitation and emergency
arrhythmia? cardiac care, Ill: Adult advanced cardiac life support. Journal
3. What propelty of the SA node allows it to pace of/he American Medical Associa/ion, 268, 2199-224 I.

the heart? Under what conditions do other por­ Guyton, A.C. (199 I). Tex/book oj medical physiology. Philadel­
phia: WB Saunders.
tions of the conduction system act as pacemakers?
Lilly, L.S. (1993). POIhophysiology oj hear! disease. Philadelphia:
4. Does an impulse originating within ventricular
Lea and Febiger.
myocardium generate an effective myocardial National Heart Lung and Blood Institute Working group on atrial
contraction? If not, why not? fibrillation. (1993). Atrial fibrillation: Current understandings

5. Why is ECG monitoring indicated following my­ and research imperatiws. Journal of AmericanCollege nfCar·
diologis/s, 22, 1830-1834.
ocardial infarction?
Shih, H.T. (1994). Anatomy of the action potential in the heart.
6. What event is represented by each of the following: Texas J-iear/lns/i/u/e lournal, 21, 30-41.
• P wave Smith, J.1., & Kampine, J.P. (1990). Circula/OI)' physiology-/he
• QRS complex essentials. Baltimore: Williams and Wilkins.

• T wave
• U wave

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 C HAP T E R 1 2

Multisystem Assessment and

Laboratory Investigations

Elizabeth Dean

KEY TERMS Blood Liver

Endocrine function Lungs

Heart Multisystem assessment

Immune function Peripheral vascular circulation

Kidneys

INTRODUCTION
fected by virtually every organ system in the body.
The purpose of this chapter is to describe the ratio­ The signs and symptoms of systemic disease can
nale for multisystem assessment in the patient man­ mimic other conditions, including cardiopulmonary
aged for cardiopulmonary dysfunction and some dysfunction treated by physical therapists. Therefore
common laboratory tests related to multisystem as­ the physical therapist must be able to differentiate
sessment. The bases of tests to assess the function of these presentations to determine what treatment, if
the following organ systems are presented: blood, any, is indicated, and what treatments may be con­
pulmonary, cardiac, peripheral vascular, renal, en­ traindicated. Knowledge of multisystem function
docrine, liver, and immune systems. The information helps confirm a diagnosis, as well as predict a pa­
in this chapter is supplemental to the elements of car­ tient's response to treatment and his or her recovery
diopulmonary and cardiovascular assessment and re­ and prognosis. In addition, this information is crucial
lated laboratory investigations described in Part 2. in refining and modifying treatment prescription.
The cardiopulmonary system affects and is af- These abilities are particularly important in this era of

189

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190 PART II Cardiopulmonary Assessment

professional accountability and with the advent of di­ response, recovery, and prognosis. The CBC includes
rect patient access. the red blood cell count (RBC), a variety of red blood
cell indices, white blood cell count (WBe), hematocrit
(Hct), hemoglobin (Hgb), and platelet count.
RATIONALE FOR MULTISYSTEM ASSESSMENT
Tests of coagulation and hemostasis reflect bleeding
The cardiopulmonary system supports cellular respi­ pathology, which often involves injury of blood vessels
ration and life. Thus every system and every cell in and cells. Damage to the blood vessel wall leads to con­
the body is affected by the adequacy of oxygen trans­ striction, a primary mechanism of hemostasis. Circulat­
port, which is dependent on cardiopulmonary and ing platelets adhere to exposed subendothelial tissues,
cardiovascular function. In addition, these systems which can predispose thrombus formation.
are affected by virtually every other system in the The fluidity of the blood is regulated by the facili­
body. The cardiopulmonary physical therapist (PT) tation and the inhibition of thrombin formation.
therefore needs thorough knowledge of multisystem When these two processes are in balance, the blood
function and the interdependence of the organ sys­ has an optimal consistency; it is neither too thick nor
tems, an ability to assess multisystem function and to too thin. This allows blood to flow optimally through
integrate this information into a comprehensive and the circulation. Blood vessel injury can disrupt this
progressive treatment plan. balance and can promote coagulation.
The lungs and heart are anatomically and physio­ Disseminated intravascular coagulation (DIC) re­
logically interconnected, and function as a unit to sults from an imbalance between the formation and
transport oxygen via the peripheral circulation to per­ deposition of fibrin, which leads to the formation of
fuse and nourish tissues. Tissue homeostasis is de­ thrombi. The continuous production of thrombin
pendent on the adequacy of the anatomy and physiol­ causes depletion of the coagulation factors and bleed­
o g y of t h e b l o o d . T h e a d e q u a c y of p e r i p h e r a l ing results. Tests used to assess bleeding capacity in­
perfusion determines the adequacy o f the function of clude thrombin time and fibrin clotting time (partial
all organ systems in the body. Therefore a knowledge thromboplastin time [PTT]).
of the failure of the various organ systems can reflect Proteins (amino acids) serve as regulators of me­
impaired oxygen transport or may identify a threat to tabolism. Much clinical information is obtained by
oxygen transport. examining and measuring proteins, because proteins
The elements of laboratory evaluation and testing, regulate many impoltant physiologic functions in the
as well as normal values, have been compiled from body. Plasma proteins serve as a source of nutrition
Bauer (1982), Dean (1987), Fishbach (1988), Guyton for the body tissues and function as buffers when
(1991 ), Jacobs et al. (1984), Le Fever Kee (1990), combined with hemoglobin.
Pagan a and Pagana ( I 992), Siest et al. (1985), and Albumin, a protein formed in the liver, maintains
Wallach (1986). normal water distribution in the body (colloid os­
motic pressure). It transports blood constituents such
as ions, pigments, bilirubin, hormones, fatty acids,
ELEMENTS OF MULTISYSTEM ASSESSMENT
enzymes, and certain drugs. Approximately 55% of
Blood
total protein is albumin. The remainder is globulin,
Some common blood tests are summarized in Table which functions in antibody formation, and other
12-1 along with their normal values. plasma proteins (fibrinogen and prothrombin) in­
The average blood volume consists of 5 L of blood: volved with coagulation.
3 L of plasma and 2 L of cells. Plasma is the medium Lactic acid, a product of carbohydrate metabolism, is
which suspends and transpOIts blood cells. The com­ produced when cells receive inadequate oxygen in rela­
plete blood count (CBC) is one of the most commonly tion to oxygen demand (anaerobic metabolism). When
ordered laboratory procedures. This basic screening the production of lactic acid exceeds its removal from the
test helps to establish the patient's diagnosis, treatment blood by the liver, lactic acid accumulates in the blood.

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 12 Multisystem Assessment and Laboratory Im'estigations 191

TABLE 12-1

Common Test'! of Multisystem Function and Their Normal Values: Blood Tests

TEST NORMAL VALUES (SI UNITS)

Red blood cell count (RBC) Men 2.09-2.71 nmolfL

Women 1.86-2.48 nmolfL

Hemoglobin (Hgb) Men 8.7-11.2 nmolfL

Women 7.4-9.9 nmolfL

Hematocrit (Hcr) Men 40% to 54%

Women 37% t047%

Platelet count 150.000-350.000/mm3

Prothrombin time (PT) 10-14 seconds
Partial thromboplastin time (PTT) 60-85 seconds

White blood cell count (WBCC) 5-10 x 103/iJl

(Differential WBCC includes counts of neutrophils,
eosinophils. basophils, lymphocytes. and monocytes)

Erythrocyte sedimentation rate (ESR) Men 0-15111m/hr

Women 0-20 mm/hr

Proteins

Albumin 38-50 gm/L

Globulin 23-35 gm/L
Fibrinogen 2.0-4.0 gm/L

Lactate Venous 0.5-2.2 mmolfL

Arterial 0.5-\.6 mmollL

Electrolytes (blood)

Sodium (Na+) 135-148 mmollL

Potassium (K+) 3.5-5.0 mmol/L
Calcium (Ca++) TOTAL 4.5-5.3 mmolfL
IONIZED 2. 1-2.6 mmolfL
Chloride (Cl-) 98-106 mmolfL

Cholesterol 3.63-6.48 mmollL

Creatine kinase Men 0.42-1.5 I mmol/sfL

Women 0.17-1.18 mmol/sfL

:-;OTI,: Normal values may vary depending on the laboratory performing the measurement. Within subject variation occurs from age, and
variations in the pre-test sLandardization procedures.

Cholesterol is used in the production of steroid hor­ of cholesterol are associated with atherosclerosis and
mones, bile acids, and cell membr::mes. Cholesterol is increased risk of coronary artery disease (CAD).
found in muscles, red blood cells, and cell membranes. Electrolyte assessment is based on the electrolyte
Low-density and high-density lipoproteins (LDLs and constituents of a b lood or urine sample. Although
HDLs) transport cholesterol in the blood. High levels present in minute quantities, electrolytes are essential

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192 PART II Cardiopulmonary Assessment

in mainlaining normal cellular function and home­ inspection of the integrity of the peripheral circulation
oslasis. The electrolytes that are routinely studied are particularly to the eXlremities, palpation to assess pe­
sodium, potassium, chloride, calcium, phosphorus, ripheral pulses, and auscultation, which can be helpful
and magnesium. in detecting bruits or areas of turbulent blood flow as­
sociated with arterial stenoses.
Some common tests of peripheral vascular func­
Pulmonary Function
tion are summarized in Table 12-2 along with their
See Chapters 8 and 14 for a detailed description of the normal values.
assessment of the pulmonary system and its function.

Kidney Function
Cardiac Function
Urine consists of the end products of cellular metabo­
A detailed description of the assessment of the car­ lism and is produced as large volumes of blood (ap­
diac system and its function appears in Chapters 11 proximately 25% of the cardiac output [CO]) flow
and 14. through the kidneys. When the kidneys are compro­
mised, death can ensue within a few days. Although
fluid is lost through several routes, the kidneys are
Peripheral Vascular Function
primarily responsible for processing and regulating
Assessment of the peripheral vascular circulation is fluid balance in the body.
essential to provide information regarding central and Urea, the major nonprotein nitrogenous end product
peripheral hemodynam.ic of protein catabolism, is measured in the blood as blood
tissue perfusion. This assessment is essential to estab­ urea nitrogen (BUN). The urea is then carried to the
lish the integrity of the patient's hemodynamic status kidneys by the blood to be excreted in the urine.
at rest and during physical and exercise stress which is Creatinine is a byproduct in the breakdown of
associated with most physical therapy treatments. muscle creatine phosphate resulting from energy me­
Laboratory tests include segmental blood pressure tabolism. Production of creatinine is constant as long
studies, skin temperature studies, pulse wave analysis, as muscle mass is constant. Kidney dysfunction re­
Doppler venous studies, and arteriography. The physi­ duces excretion of creatinine resulling in increased
cal examination corroborates the results of the labora­ levels of blood creatinine. Analysis of urine for crea­
tory investigations and includes the patient's history, tinine provides an index of kidney function.

TABLE 12-2

Common Tests of Multisystem Function and TABLE 12-3

Their Normal Values: Tests of Peripheral
Vascular Function Common Tests of Multisystem Function and
Their Normal Values: Tests of Renalf'ullctioll
TEST NORMAL VALUES
NORMAL VALUES
Skin temperature Ranges from ambient TEST (SI UNITS)
temperature to 30DC
Ankle systolic pressures 97% of brachial pressure Blood urea nitrogen (BUN) 3.6-7.1 mmollL
Peri phera/ pu Ises Apex heart rate Creatinine 7.6-30.5 IlmollL
Capillary filling Instantaneous filling
following quick pressure NO'll:: Normal values Jllay vary depending on the laboratory
over the nai I bed performing the measureJllent. Within subject variation occurs from
age, and variations in the pretest standardiz.ation procedures.

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 12 Multisystem Assessment and Laboratory Investigations 193

Increased osmolality stimulates the secretion of marized in Table 12-4 along with their normal values.
anti-diuretic hormone (ADH) that acts on renal
Pancreatic function and insulin production
tubules. This results in the reabsorption of water,
more concentrated urine, and less concentrated serum. Insulin, a hormone produced in the pancreas by the beta
Some common tests of renal function are summa­ cells of the islets of Langerhans, regulates the metabo­
rized in Table 12-3 along with their normal values. lism of carbohydrates along with liver, adipose tissue,
muscle, and other target cells and is responsible for
maintaining a constant level of blood glucose. The rate
Endocrine Function
of insulin secretion is determined primarily by the level
Endocrine glands are responsible for producing those of blood glucose perfusing the pancreas and is also af­
substances and neuromediators responsible for main­ fected by hormonal status, the autonomic nervous sys­
taining homeostasis and enabling the body to adapt tem, nutritional status, smoking, restricted mobility,
when physically and psychologically challenged or physical stress such as traumatic insult to the body dur­
perturbed from a resting state. The key endocrine ing illness and injury, and pharmacologic agents.
glands are the pancre as, thyroid gland, and the Amylase is an enzyme produced in the salivary
adrenal glands. Endocrine glands regulate metabo­ glands, pancreas, and liver, and c onverts starch to
lism and are responsible for increasing blood flow sug ar. Inflammation of the pancreas or salivary
and pressure, and reducing vascular resistance when glands results in more of the enzyme entering the
metabolic demands increase. blood. The amylase test is used to diagnose and mon­
Some common tests of endocrine function are sum- itor treatment of acute pancreatitis.

TABLE 12-4

Common Tests of Multisystem Function and Their Normal Values: Tests of Endocrine Function

NORMAL VALUES
TEST (SI UNITS)

Thyroid Function

Total thyroxine (T4) 65-155 nmol/L

Total triiodothyronine (T3) 1.77-2.93 nmollL

Adrenal Function

Epinephrine 0.0-81.9 nmoll24 hr

Norepinephrine 0.0-591 nmol/24 hr
Cortisol Morning 138-635 nmollL
Evening 82-413 nmollL

Pancreatic Function

Glucose tolerance test At I hl' glucose 1.1-2.75 mmollL

At 2 hl' glucose 0.2-0.88 mmol/L
Insulin 12 hr fasting 35-145 pmollL
Amylase Blood level 25-125 UnitslL

N<Y,E: Normal values may vary depending on the laboraLory peli'orming the measurement. Within subject variation occurs from age, and
variations in the pretest standarLiization procedures.

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194 PART II Cardiopulmonary Assessment

Thyroid
TABLE 12-5
The function of the thyroid gland is to take iodine
Common Tests of Multisystem Function and
from the circulating blood, combine it with amino
Their Normal Values: Tests of Liver Function
acid tyrosine, and convert it to the thyroid hormones
NORMAL VALUES
thyroxine (T4), and triiodothyronine (T3). Thyroid
TEST (SI UNITS)
hormones have a profound effect on metabolic rate.
Increased metabolism causes more rapid use of oxy­ Alkaline phosphatase 0.18-0.40 nmol/slL
Bilirubin (total) 5.1-I 7.1 fJmollL
gen than normal and causes greater quantities of
metabolic end products to be released from the tis­
NOTl'.: Normal values may vary depending on the laboratory
sues. These effects cause vasodilatation in most of
performing the measurement. Within subject variation occurs from
the body tissues, thus increasing blood flow. Increase age and variations in the pretest standardization procedures.
in the thyroid hormones increases cardiac output,
heart rate, force of cardiac contraction, blood volume,
arterial blood pressure, oxygen consumption, and car­
bon dioxide (C02) production, hence an increase in
TABLE 12-6

the rate and depth of breathing, increased appetite, Common Tests of Multisystem FUllction
food intake and gastrointestinal motility. The thyroid and Their Normal Values: Tests
gland also stores T3 and T4 until they are released of Immunological Function
into the blood stream under the influence of thyroid
Differential White Blood Cell Count
stimulating hormone (TSH) from the pituitary gland.
ABSOLUTE VALUE RELATIVE VALUE
Adrenal function (No/uL) (by Percent)

Catecholamines, epinephrine and norepinephrine, are Neutrophils 3,000-7,000 60-70

produced by the adrenal medulla of the adrenal Lymphocytes 1,000-4,000 20-40
glands. Urine samples are used to test for these im­ MOllocytes 100-600 2-6
Eosinophils 50-400 J-4
portant vasoactive neurotransmitters in the investiga­
Basophils 25-100 0.5-1
tion of various disorders. In addition to their vasoac­
tive properties, the catecholamines are essential in
stimulating the sympathetic response in the fight or
flight mechanism. with tests of liver enzymes such as amylase and al­
Cortisol is produced by the adrenal cortex of the kaline phosphatase.
adrenal glands and is involved with metabolism of Some common tests of hepatic function are sum­
carbohydrate, protein, and fat. In addition, it inhibits marized in Table 12-5 along with their normal values.
the action of insulin and thus the uptake of glucose
by the cells. The normal secretion of cortisol varies
Immunological Function
diurnally, that is, high in the morning and low in the
evening. Immunological function is dependent on the ade­
quacy of the function of several tissues and organs,
namely bone marrow, the thymus gland, lymph
liver Function
nodes, and vessels of the lymphatic system, spleen,
Liver function is especially important in that dys­ tonsils, and intestinal lymphoid tissue. Immunologi­
function of this organ can be life threatening. The cal function can break down if insufficient protective
liver has a primary role in carbohydrate and protein immune factors are produced, or the system is over­
metabolism, it produces bile, and is responsible for whelmed by an invading organism for which the
detoxification of the blood. Its function is assessed body has inappropriate or insufficient resistance.

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 12 Multisystem Assessment and Laboratory Investigations 195

Some common tests of immunological function are REVIEW QUESTIONS

summarized in Table 12-6 along with their normal
I. Describe common tests of blood composition.
values. Specific detailed accounts of immmunodiag­
2. Describe pulmonary function tests.
nostic studies and tests for autoimmune deficiencies
3. Describe tests of heart function.
are beyond the scope of this chapter but can be re­
4. Describe tests of peripheral vascular function.
viewed in Fischbach (1988) and Le Fever Kee (1990).
5. Desacribe tests of renal function.
6. Describe tests of endocrine function.
SUMMARY 7. Describe tests of liver function.

This chapter described the rationale for multisystem 8. Describe tests of immune function.
assessment in the patient being managed for car­
diopulmonary dysfunction and some common tests of
References
multisystem function. The cardiopulmonary system
affects and is affected by virtually every organ system Bauer, J.D. (1982). Clinic allaboratOlY melhods (9th ed.). St.
Louis: Mosby.
in the body. Thus primary cardiopulmonary dysfunc­
Dean, E. (1987). Assessment of the peripheral circulation: An up­
tion can lead to multiorgan system complications, and
date for practitioners. The Australian Journal of Physiotherapy,
dysfunction of other organ systems can have car­ 33, 164-171.
diopulmonary manifestations. In addition, the signs Fischbach, F. (1988). A manual of laboratory diagnostic tests (3rd
and symptoms of systemic disease can mimic other ed.). Philadelphia: J.B. Lippincott.

conditions treated by physical therapists. Therefore Guyton, A.c. (1991). Textbook of mediad physiology (6th ed.)
Philadelphia: W. B. Saunders.
the PT must be able to differentiate these presenta­
Jacobs, D.S., Kasten, B.L., Demott, W.R., & Wolfson, W.L.
tions to determine whether a pathology will respond (1984). Laboratory test handbook. Stow: Lexi-Comp, Inc.
to physical therapy management, what treatment is Le Fever Kee, J. (1990). Handbook oflaboratOlY and diagnostic
not indicated and what treatments may be contraindi­ tests lVilh nursing implications. Norwalk: Appleton and Lange.

cated. Multisystem monitoring provides fundamental Pagana, K.D., & Pagana, TJ. (1992). Mosby·s diagno.Slic and lab­
ora/Ory leSI reference. St. Louis: Mosby.
information needed to refine and progress the treat­
Siest, G., Henny, J., Schiele, F., & Yonge, D.S. (1985). Inlerpretalion
ment prescription. These abilities are essential in this ofclinical laboratory lests. Foster City: Biomedical Publications.
era of increased professional responsibility and with Wallach, J. (1986). Interpretation of diagnostic tests. A synopsis of
the advent of direct patient access. laboratory medicine. Boston: Little, Brown.

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 Special Tests

Gail M. Huber

KEY TERMS Echocardiography Stunned myocardium

Ejection fraction Thallium-201 scan
Hibernating myocardium Ventilation-perfusion scan
Positron emission scans

INTRODUCTION
lungs, as well as determining cardiac anatomy, and
In assessing the cardiopulmonary patient, the physi­ direct volume and pressure measures, it is without
cian uses many tools. The patient interview, physical equal. Transesophageal echocardiography is another
examination, chest x-ray, and electrocardiogram invasive test. Following the initial assessment of the
(ECG) provide information to make a diagnosis. problem, these same special tests may be lIsed to as­
When more information is needed, a variety of inva­ sist in the determination of appropriate therapy and
sive and noninvasive tests can be pelformed. Nuclear evaluate prognosis and response to treatment. The
medicine offers a variety of tools for evaluation of noninvasive tests are most important in determining
cardiac and pulmonary function. EChocardiography is ongoing surgical, interventional, or medical therapy.
a noninvasive method that offers information about Physical therapists (PTs) need to understand these
the cardiovascular system, including valve function, invasive and noninvasive tests for several reasons. It
ventricular performance, and estimation of filling is useful to understand how the information is used
pressures. It is particularly useful with children. to make a differential diagnosis and determine treat­
At some point in a patient's workup, the physi­ ment. These tests have helped to clarify our under­
cian may need to use an invasive test. Pulmonary standing of the physiology and pathophysiology of
and cardiac angiography is not without risk; how­ the system. Therapists need to understand the patho­
ever, for evaluating blood flow in the heart and physiological basis f o r a p a t i e n t ' s m o v e m e n t

197

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198 PART II Cardiopulmonary Assessment

dysfunctions to select the most appropriate treat­ moved from time to time for patient use (Kim, 1987).
ment strategies. Many special tests can and are A generator system produces short-lived radionu­
being used in research to evaluate treatment inter­ clides (lskandrian, 1987).
ventions. For example, radiolabeled aerosols are These elements are often attached to other sub­
used to evaluate mucociliary clearance, providing a strates for transport in the body to the particular tis­
method to evaluate the effectiveness of pulmonary sue of interest. The elements have differing character­
hygiene techniques (Miller and O'Doherty, 1992). istics such as energy output and half-life. Because of
C linically, PTs need to use information from the their vaIied distribution in the body tissues, they pro­
tests to develop a framework for predicting how the vide different information.
patient may respond to a physical therapy interven­ Detection of the radioactive energy emitted by a
tion. For example, nuclear imaging can provide in­ specific radiopharmaceutical requires a camera.
formation about left ventricular ejection fraction. When certain materials are struck by ionizing radia­
This information helps the PT determine if the pa­ tion, light is emitted. A scintillation detector detects
tient should be stratified into high-risk or low-risk this light. A gamma camera is a scintillation detector
categories. Monitoring of an exercise session may able to detect photons exiting the body. It uses a
depend on the risk level, and interpretation of the large, collimated crystal monitored by an array of
patient's response to treatment may be effected. photomultiplier tubes (Kim, 1987). A collimator is a
device that allows only those photons traveling in an
appropriate direction to reach the crystal. There are
NUCLEAR IMAGING SYSTEMS
several types of collimators: parallel-hole collima­
AN 0 RAD I 0 PHARMACEUTI CALS
tors, pinhole collimators, and converging and diverg­
A general view of how nuclear imaging systems work ing collimators. The photomultiplier tube records the
should help the PT understand some of the differences amount of light from the crystal and converts it into a
between the wide variety of tests used today. This voltage, that is proportional to the intensity of the
area of medicine is experiencing rapid growth and light (Kim, 1987).
change as technology changes the equipment used to The camera system is connected to a computer
perform the test, the radiopharmaceuticals available, that stores the light images. The computer is able to
and the computer's increasing ability to analyze data. derive two dimensional images from the data. The
Radionuclide imaging allows for the noninvasive computer can also quantify the data and perform a
acquisition of images from a variety of body tissues. variety of data analyses (Iskandrian, 1987).
An imaging system requires three basic parts. The
first requirement is a radiopharmaceutical that emits
Planar Imaging
gamma radiation and is taken up by the body tissue
of interest. Next, a radiation detector or camera is A single crystal camera (Anger) produces a two dimen­
needed. FinalIy, computers are required to collect and sional or planar image. Multicrystal cameras (Blau and
analyze the data. Blender) also produce planar images but are able to per­
Radionuclides are elements that are unstable; they form fast dynamic imaging used in first pass and gated
gain stability by emitting particles or photons. This is studies. Planar imaging may be the only option available
called radioactive decay, and gamma radiation is re­ to obese patients who do not "fit" the single photon
leased. Radionuclides are either cyclotron- or genera­ emission computed tomography (SPECT) camera.
tor-produced. The cyclotron accelerates alpha-parti­
cles, deuterons, and protons to energies suitable for
Tomographic Imaging
the production of the required radionuclide (Kim,
1987). A radionuclide generator is a system of parent If a gamma camera is rotated about the patient and
and daughter radionuclides in equilibrium. The sys­ mUltiple projections obtained, a three-dimensional
tem is constructed so that the daughter can be re­ distribution of tracer is acquired. This is the basis for

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 13 Special Tests 199

SPECT (Kim, 1987). The s ame gamma-emitting TESTS OF THE CARDIOVASCULAR SYSTEM
pharmaceuticals are used. Regular gamma cameras or Radionuclide Imaging
specially designed systems can be used (Iskandrian,
Gated/ungated first pass scan
1987). SPECT imaging produces higher spatial reso­
lution (Schwaiger, 1994), and increased sensitivity In an ungated first pass study, data are collected on a

for coronary artery disease (CAD) over planar images radiolabeled bolus of blood as it passes through the car­

(Beller, 1994). However, attenuation artifacts (ab­ diac chambers. This allows for clear identification of

sorption of the radioactive energy by other body tis­ the four cardiac chambers. During gated first pass stud­

sues such that the camera does not detect it) are ies, data are collected at specific periods in the cardiac

greater than with planar images, particularly those cycle. Each R-wave of the EKG triggers the acquisition

images involving the inferior wall of the heart in men of data, thus the average cycle observed is the compila­

and the anterior wall in women, and may produce tion of several cycles. Gated equilibrium studies or

false-positive scans (Schwaiger, 1994). Quality of the multiple uptake gated acquisition (MUGA) scans aver­

images are dependent on the use of stringent quality age several hundred cardiac cycles. The quality of the

control measures and experience of the staff. Image image is best when the patient has a stable sinus

quality is also patient-dependent. Patients must be rhythm. Patients with irregular heart rates, such as atrial

able to lie perfectly still for 15 to 20 minutes, with fibrillation have images of poorer quality.

their hands over their heads, while data are collected.

Exercise stress studies
PTs can identify patients who would have diffi­
culty with arm movements or with remaining still. Many of the tests pert'ormed using radionuclides are

For these patients, other imaging modalities such as coupled with an exercise test. A treadmill exercise

echocardiography may be appropriate. test is pelformed, and at the peak of exercise, a tracer
P o s itron e m i s s i o n t o m o g r a p h y (PET) u s e s is injected. Shortly afterward, depending on the

positron-emitting radionuclides. The images ob­ tracer, images are acquired. Exercise imaging en­
tained by PET can provide information regarding hances the identification of ischemic areas. These

metabolism in lung tissue and cardiac muscle, my­ tests are then often compared with rest studies.
ocardial perfusion, and myocardial receptor density Rest/stress or stress/rest protocols can be used.
(Maddahi, 1994). PET is valuable in delineating my­
Pharmacologic stress studies
ocardial areas with reversible and irreversible injury
and in assessing the feasibility of surgical revascu­ Many patients are unable to exercise to an intensity
larization, coronary angioplasty, or thrombolysis sufficient to produce stress on the cardiovascular sys­
with respect t o potentially s a l v a g e a b le t i s s u e tem. When patients are unable to exercise, pharmaco­
(Niemeyer, 1992). Many o f the radionuclides used in logic agents can be used to dilate the coronary arteries
PET scans require a cyclotron for generation and a or incr e a s e t h e metab olic demand of the heart.
specialized detection system. PET images offer s u­ Dipryridimole (Persantine) and adenosine are often
perior resolution compared with SPECT images used. Pharmacologic stress tests can be coupled with
(Schwaiger, 1994). PET also allows greater correc­ SPECT and PET nuclear imaging techniques or with
tion for attenuation artifact (Schwaiger, 1994). PET echocardiography to determine regions of ischemic
imaging is a newer technology that offers improve­ myocardium suggesting functionally significant block­
ment in sensitivity and specificity when compared age in the coronary artery supplying that territory.
with SPECT (Mullani, 1992).
Nuclear-derived measurements
PET studies use short scanning times. Protocols
can last about I hour. The studies can be done at rest Data derived from radionuclide images provide infor­
or with a pharmacologic stress agent (Schwaiger, mation about perfusion and function. Radionuclides
1994). Cost may prohibit the widespread use of this taken up by the myocardium provide a picture of the
technology. heart that includes wall thickness and an outline of

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200 PART II Cardiopulmonary Assessment

the chamber. In radionuclide angiography, which in­

Tests to Evaluate Myocardial Perfusion
cludes first pass and gated studies, the blood is high­
lighted as it passes through the chambers. Qualitative Perfusion of the myocardium is a vital factor in the via­
and quantitative measurements can be taken. The bility and function of the heart. Information about my­
most important of these measurements, the ejection ocardial perfusion is used for diagnostic decisions,
fraction (right and left ventricle) is a measure of my­ treatment decisions and prognosis. Peliusion of the my­
ocardial function. It is derived from quantitative ocardium under rest and exercise conditions is impor­
counts of the ventricular area during diastole and sys­ tant in the diagnosis of CAD. Efficacy of reperfusion
tole (lskandrian, 1987): strategies, such as angioplasty and thrombolytic therapy
must be evaluated. Identifying tissue that is viable but
(End-diastolic counts - End-systolic counts) x 100
still at risk is one of the newer applications of myocar­
End-diastolic counts
dial peliusion tests. Information gained from combined
Left ventricu lar ejection fraction (L VEF) has been perfusion and metabolic studies has helped to increase
shown in several studies (Cass study and the Multi­ the understanding of ischemic myocardium. Two types
center Postinfarction Research Group Database) to be of contractile dysfunction have been delineated. Hiber­
highly predictive of 1 year survival (Port, 1994; Mad­ nating myocardium is the result of prolonged ischemia.
dahi, 1994). Right ventricu lar ejection fracti o n The contractility of the muscle fiber is effected so that
(RVEF) has been found t o have a wide range o f nor­ there may appear to be regional wall motion abnonnali­
mal values (35% to 75%) (Kinch, J 994) but is not ties. The tissue is alive but not contracting. It is theo­
that predictive of function without data about wall rized that this is a measure to reduce energy expendi­
motion abnormalities. The strongest radionuclide pre­ ture and ensure myocyte survival. The second
dictor of outcome is the exercise LVEF. When pre­ condition, myocardial stunning, occurs under condi­
dicting outcome, multivariate analysis of clinical tions of acute ischemia. In this case, there is contractile
data, catheterization data and radionuclide measure­ dysfunction during the acutc ischemic episode that per­
ments have shown that the radionuclide results (exer­ sists for some time after perfusion has returned to nor­
cise LVEF, resting end-diastolic volume, and change mal. Both conditions are reversible. Patients demon­
in heart rate [HR)) have the same prognostic power strating hibernating myocardium may benefit from
as the catheterization data (Port, 1994). revascularization procedures. Patients with stunned my­
Another important measurement is wall motion. ocardium may only require supportive care until con­
Quantitative and qualitative evaluation of the move­ tractile function returns. (SchelbeI1, 1994).
ment of the myocardium can be made. Wall thick­
Thallium-201
ness, and movement are compared with systole and
diastole. Assessments are made about akinesia, Thallium-20l is the radioactive isotope most often
global or regional hypokinesia, and dyskinesia. u sed in myocardial perfusion studies (Wacker,
Global left ventricular function is a strong predictor 1994). It is a cyclotron-produced isotope that emits
of survival. It can help clinicians differentiate a weak low-energy radiation (69 to 83 kiloelectron volt
heal1 from one that is stiff, allowing the appropriate [keY)). Administered intravenously, its distribution
treatment. Regional wall function when correlated throughout the body depends on blood flow. Thal­
with knowledge of coronary artery anatomy allows lium concentrations in ·the myocardium depend on
for the identification of potential blockages or areas four processes. First, there is a linear relationship
of infarct. Assessing wall thickness can provide in­ between thallium concentration and coronary blood
formation about hypertrophy or aneurysm but is done flow. Second, extraction-transport across the cell
more reliably by echocardiography. membrane depends on active and passive transport
Anatomical measurements can be made of cham­ mechanisms. Thallium is thought to be transported
ber size. From these data, chamber volume can be across the cell membrane through the sodium-potas­
calculated, as well as stroke volume and cardiac out­ sium ATPase pump (Maddahi, 1994). The third
put (Table 13-1). process is washout, also called redistribution. Thal­

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 13 Special Tests 201

TABLE 13-1

Summary of Special Tests of the Cardiopulmonary System

SPECIAL TESTS CLINICAL FINDINGS

Cardiac Scans
Planar, SPEeT, MUGA, First pass

Thallium-20I Evaluates myocrdial perfusion, used in exercise stress studies and to assess
Technitium-99M-sestamibi reversibility of defects. Quantitatively can be used to determine: EF, SV,
Technitium teboroxime CO, regional function, ventricular volumes, intra-cardiac shunt, valvular
regurgitation.

PET Scans

IS-FOG Assesses myocardial viability by evaluating glucose metabolism. Can

identify areas that improve with reperfusiol1.
II C acetate Assesses myocardial viability by evaluating oxidative metabolism. Can
identify areas that will improve with reperfusion.

Illfarct avid scans

Technetium-99M-pyrophosphate Identifies areas of infarction by binding with elements released by the death
Indium I II antimyosin of myocardial tissue.

Pulmonary Scans
Perfusion scan

MAB Identifies regions of decreased pulmonary perfusion, used to identify

pulmonary embolism.

Velltilation scall

99mTc OTPA Identifies regions of decreased ventilation. Used in conjunction with

I33-Xe perfusion scan to identify patients with pulmonary embolism.
Gallium scan Identification of neoplastic or inflammatory pulmonary lesions

Echocardiography

M-mode Evaluates myocardial structure. 2- 0 used in exercise stress studies.

2 ­D Quantitatively measures: chamber size, wall thickness, valve structure
TEE and function, pressure and flow through valve, valve area, EF.
Doppler

Angiography Quantitative measures of pressure, resistance, flow, O2 consumption,

arteriovenous oxygen difference EF, CO

Abbreviations: EF=ejection fracl.ion, CO=cardiac output, SV=stroke volume

lium enters the cell initially and then is redistributed titatively evaluated. Normally perfused myocardium
until an equilibrium is attained based on a net bal­ demonstrates uniform uptake of the tracer. Uniform
ance between Thallium-201 input through recircula­ uptake can occur as long as blockages are less than
tion and intrinsic Thallium washout (Beller, 1994). 50% of the artery. Ischemic but viable myocardium
Finally, concentrations arc decay-related, dictated initially appears as areas of decreased uptake, these
by the half-life of the isotope (Brown, 1994; lskan­ areas fill in over time, a function of redistribution. Be­
drian, 1987). cause blood flow is decreased, clearance of Thallium­
Thallium-201 images can be qualitatively and quan­ 201 from the defect region is slower (Maddahi, 1994).

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202 PART II Cardiopulmonary Assessment

In infarcted areas, these defects remain unchanged in acutc situations. A patient with an acutc myocardial
over time. Qualitative evaluation requires visual in­ infarction (MI) can be injcctcd with tracer, given
spection of the images. Quantitative evaluation is per­ thrombolytics, stabilizcd, and scanned 4 hours later.
formed by computer. The computer analyzes the The scan results show myocardial pert'usion at the time
amount of radioactivity taken up in a palticuJar region of injection when the myocardium was ischemic. Later
of interest. It then quantifies this count so that regions scans demonstrate the new perfusion situation.
can be compared with each other and with normalized
Technetium-99M-teboroxime
data. In this way, unperfused or hypoperfused areas
can be identified. Another newer isotope is Technetium (Tc)-99M ­
Thallium-201 is used to acquire planar and tomo­ teboroxime. I t i s not yet widely accepted because of
graphic images (SPECT) for rest studies, exercise stress its rapid washout and visualization problems related
studies, and pharmacologic stress studies. The tradi­ to hepatic uptake (Berman et aI., 1991; Go, j 992).
tional Thallium-201 stress study calls for injection of The half-life for teboroxime is 5 to 6 minutes (John­
the tracer at the peak of exercise with collection of the son, 1994). It has a myocardial extraction fraction
stress data shortly after. The redistribution study is com­ higher than either sestamibi or thallium (Johnson,
pleted 4 hours later. Newer study protocols include rein­ 1994). Tc-99M-teboroxime uptake parallels myocar­
jection of thallium before the 4-hour redistribution study dial blood flow under both ischemic and nonischemic
(Go, 1992) and use in dual-isotope studies (Berman, conditions (Johnson, 1994) and does not appear to
1994). Reinjection of thallium and repeat imaging 24 rely on active cellular processes.
hours after initial study can help identify severely is­ Because of the short half-life, rapid acquisition
chemic (greater than 90% blockage) areas, which may imaging systems are required so that the images do
take much longer to demonstrate redistribution. not reflect washout. SPECT and first pass studies can
be performed but Tc-99M-teboroxime does not per­
Technetium-99M-sestamibi
mit gated SPECT acquisition (Berman, 1991). Proto­
New isotopes were approved by the FDA for perfusion cols using this isotope are designed to take advantage
imaging in 1990. Technetium (Tc)-99M-sestamibi was of the rapid uptake and washout. When used with
developed because of the number of advantages it has pharmacologic stress studies, a rest-stress study can
over thallium imaging. Sestamibi provides improved be completed within minutes (Johnson, (994). This
SPECT image quality as a result of higher count rates may have future application in studying reperfusion
and higher energy, in the 140 keY range. Tc-99M-ses­ following balloon angioplasty or reperfusion therapy
tamibi is generator-produced. The isotope has a 6-hour with thrombolytic agents (Johnson, 1994). PET trac­
half-life (Berman et aI, 1994). Because of the short ers are also used to evaluate perfusion and will be
half-life, higher doses can be injected, and although the discussed below. They include, 13-N ammonia, 82­
percentage of extraction is lower, sestamibi uptake in Rb rubidium, or 15-0 water.
relation to flow is similar to that of thallium. These fac­
tors result in higher count rates, which thus allow the
Tests to Evaluate Myocardial Viability
use of gated images and first pass acquisition studies.
Higher count rates are preferred when evaluating obese Identification of the size of an infarct has traditionally
patients. One of the greatest limitations of Tc-99M-ses­ been helpful in determining prognosis. Infarct avid trac­
tamibi is that it does not readily redistribute; therefore ers were used. The tracers bind with elements released
reversibility of defects cannot be ascertained as well as by necrotic myocardial tissue.
with thallium. This factor is one reason thallium is With the development of reperfusion strategies,
much more popular. Two-day protocols or dual isotope angioplasty, bypass grafting, and thrombolytic ther­
protocols can be used to overcome this limitation apy it was noted that areas that appeared to be non­
(Berman, 1994). Lack of redistribution has been ex­ functional on perfusion scans regained function once
ploited in evaluating the impact of thrombolytic therapy the area regained adequate blood supply, Tests were

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 13 Special Tests 203

developed that were able to distinguish these areas of revascularization (Scheiber!, 1994).
stunned or hibernating myocardium. These tests of
11-C-Acetate
myocardial viability often look at metabolism.
According to Maddahi, four different PET ap­ Another way to evaluate myocardial viability is to
proaches have been used for assessment of myocar­ use an isotope that is incorporated into the meta­
dial viability: (I) perfusion-FOG metabolism imag­ bolic pathways related to myocardial oxygen con­
ing, (2) determination of oXidative metabolism with sumption. II-C-acetate in its activated form, acetyl­
II-C-acetate, (3) uptake and retention of 82-Rb and CoA, represents the entry point for all metabolic
(4) the water perfusable tissue index (Maddahi, 1994). pathways into the tricarboxylic acid cycle, which is
tightly coupled to oxidated metabolism. It's advan­
1BF-fluoro deoxyglucose
tage over 18-FOG, is that it does not rely on sub­
18F-f1uoro-deoxyglucose (FOG) is a glucose ana­ strate use (i.e., glucose vs. fat metabolism). It accu­
logue that crosses the capillary and sarcolemmal r a t ely r ef l e c t s o x i d a t i v e m e t a b o l i sm a n d c a n
membrane at a rate proportional to that of glucose. It distinguish viable from nonviable myocardium in
becomes trapped in the myocardium, because it is not b o t h a c u t e a n d c h r o ni c i s che m i c c o nd i t i o n s
a useful substrate in metabolic pathways. FOG distri­ (Bergman, 1994.)
bution is relative to uptake of unlabeled glucose
Technetium-99M-pyrophosphate
(Maddahi, 1994).
Identification of areas with normal metabolism, Technetium-99M-pyrophosphate (TcPyp) identifies
altered metabolism or no metabolism is based on the areas of myocardial infarction by forming a complex
use of glucose as an energy substrate. Normally, with calcium, which is released when myocardial
perfused myocardial cells use fatty acids for adeno­ cells die. TcPyp scans have the best results when ob­
sine triphosphate (ATP) production when in a fast­ tained 24 to 48 hours postinfarction. This time frame
ing state and use glucose as the primary energy is obviously after reperfusion strategies would have
sour ce in the postprandial state. Ischemic m y­ been employed. Sensitivity of this scan is high, but
ocardium uses glucose in the fasting state and the specificity is low, since a number of other processes
postprandial state. Infarcted areas show no meta­ can result in a positive scan (e.g., myocardial trauma,
bolic activity. Therefore increased uptake of FOG in ventricular aneurysm, and uptake in skeletal struc­
the postprandial state occurs in both hibernating and tures) (Niemeyer, 1992).
normal myocardium, but in the fasting state, it oc­
Indium-111-antimyosin
curs only in the hibernating myocardium. Clinical
studies in infarct patients showed that area with per­ Indium III antimyosin is a radiolabled monoclonoal
sistent thallium-20 I perfusion defects have evidence antibody that identifies infarcted myocardial tissue. It
of remaining metabolic activity in 47% of regions binds with myocardial myosin, which is released when
when studied with a PET scan, indicating overesti­ the muscle cell dies. It can be used in conjunction with
mation of irreversible injury. Usc of reinjection and thallium-20I to distinguish infarcted tissue from per­
late redistribution imaging has significantly lowered fused viable tissue. It is most reliable when performed
this number (Hendel, 1994). The implication de­ 48 hours after infarction (Niemeyer, 1992).
rived from this finding is that in areas with perfu­
sion defects, if glucose activity remains, the region
Echocardiography
is viable (mismatch pattern); conversely, if such ac­
tivity is absent, the area is likely to be infarcted or Another noninvasive method of evaluating the heart
necrotic (match pattern) (Niemeyer, 1992). Viewed uses the physical properties of sound. Echocardiogra­
in functional terms, mismatch simply implies the phy provides information about blood flow, structure,
potential for improvement; rnatch implies no poten­ and function of the heart. Motion mode (M-mode)
tial for improvement in contractility after successful and two-dimensional (2-0) images are highly reliable

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204 PART II Cardiopulmonary Assessment

methods of evaluation. Recent developments of tech­ with indication of flow direction in real time (Wag­
nique and technology include color flow Doppler goner, 1990). Color is matched based on the direction
echo, transesophageal echo, and intravascular of flow, and shading is indicative of intensity based
echocardiography. These techniques, when used in on the mean velocity flow estimates (Waggoner and
combination can provide much of the information Perez, 1990). It is primarily used to assess the extent
previously available only by cardiac catheterization of regurgitant jets across "leaky valves," as well as to
(Hartnell, 1994). indicate areas of abnormal shunts such as atrial septal
defects. Turbulence created by narrowed valves cre­
Physics of echocardiography
ates wide color shading.
Imaging systems that use ultrasound require a source
Measurements derived from echocardiography
for generation of the sound wave, a transducer, and a
receiver to pick up the reflected sound waves. Sound Echocardiographic results can be viewed qualita­
is absorbed or reflected differentially by specific tis­ tively and quantitatively. An experienced viewer can
sues. Therefore the sound wave reflected from mus­ analyze the anatomical relationships and structure of
cle differs from that reflected from vascular space, the heart, wall motion, valve movement and configu­
or valvular structures. Returning signals are con­ ration, and chamber size.
verted into electrical signals that generate an image. Quanti tati ve measures are calculated from the
This is the basis for M-mode and 2-D echo. In M­ Doppler frequency shifts. Velocity measures can be
mode echocardiography, the transducer transmits a used in other equations to estimate pressure and valve
single sound wave through the chest wall. A thin area. The modified Bernoulli equation is used to cal­
slice of the heart, an "ice pick" view, directly under culate pressure changes around the valve:
the sound wave, reflects the wave back to the trans­
ducer. M-mode, though useful, is rarely used; 2-D is L'1 P (mm Hg) = 4 X VIllax2 (m/second),
the primary diagnostic mode. In 2-D echocardiogra­ where P is the pressure gradient across the valve and
phy, the transducer is able to pick up a wedge sec­ V is the velocity of blood flow through the valve.
tion of the heart. In 2-D the transducer acts as the
transmitter and receiver. A "real time" two-dimen­ These measurements allow calculation of stenotic
sional picture of the heart is recorded on videotape. valve gradients and right-sided filling pressures,
The heart can be viewed in motion, and wall motion valve regurgitation, and ventricular septal defects
can be evaluated. (Waggoner and Perez, 1990). Valve regurgitation and
Doppler echocardiography relies on the Doppler shunt calculations are more complicated than the
effect to determine velocity. W hen a sound wave is Bernoulli equation alone.
aimed at moving objects such as red blood cells, Another important quantitative measure is the
the known transmitted frequency and the reflected estimated area of the valve. The continuity equation
frequency differ, a phenomenon, known as a fre­ is used to estimate valve area. It is based on the
q u e n c y s h i f t . The g r e a t e r the frequency s h i f t principle of conservation of mass; that is, in a nor­
the greater the speed o f the targeted object (Wag­ mal heart, the volume of blood that enters the right
goner and Perez, 1990). The velocity of flow is atrium should be conserved as it passes through the
the terminology used to express Doppler frequency other chambers. Flow. volume at different sites is
shifts. Both continuous wave and pulsed wave related to the flow velocity and the cross sectional
Doppler are used. area of the site. Therefore AI x VI = A2 X V2,
Color flow Doppler echocardiography was intro­ where VI is the velocity of flow at one side of the
duced in the mid-1980s. It is usually superimposed valve and V2 is the flow velocity at the other side
on a two-dimensional image in real time but can be of the valve, and A is the cross-sectional area
used with M-mode. It is a method that displays (W aggoner and Perez, 1990) (Wilson, Va cek,
anatomic and spatial blood flow velocity estimates 1990).

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 13 Special Tests 205

Transesophageal echocardiography (TEE) saturation can be obtained. When selective coronary

Because of consistent technical difficulties with arteriography is performed, radiopaque contrast mate­
transthoracic echocardiography, the technique of trans­ rial is injected into the left main or right coronary
esophageal echo was developed to improve spatial res­ artery. Cine recordings are made after the injection,
olution. The technique can obtain M-mode, 2-D, and and injections are repeated until the entire coronary
color flow Doppler images by using a small probe tree is visualized.
mounted on the tip of a modified gastroscope. The Cardiac ventriculography is when dye is injected
probe is advanced into the esophagus and positioned so into the ventricle and the entire chamber becomes
that multiple views of the heart are available (Kerber, outlined. Several cardiac cycles are recorded on cine.
1988). Initially, the technique was performed intraoper­ It provides valuable information about global and
atively on anesthetized patients and on intubated pa­ segmental wall motion, valve motion, and the pres­
tients in the intensive care unit. It is now used on awake ence of abnormal anatomy (Grossman, 1986).
patients who are mildly sedated (Schneider, 1993). The
semiinvasive nature of this test has slowed its adoption.
TESTS OF THE RESPIRATORY SYSTEM
It is most useful in ruling out thrombus or heart valve
vegetation as a cause of transient ischemic attack (TIA) Unlike the cardiovascular system, special tests of the
or stroke. Especially excellent views of the left atrium respiratory system are less commonly used in the initial
and atrial appendage are seen. The atrial appendages diagnosis and treatment of disease. This is the result of
cannot be visualized by traditional transthoracic echo. It the generally high quality information obtained from
is also a good assessment of prosthetic valve function. standard x-ray examination when combined with the
patient's respiratory symptoms and the results of the
physical examination (Lillington, 1987). When further
Cardiac Angiography
information is needed to refine the diagnosis or treat­
The standard with which many of the noninvasive tests ment decision several tests are available to clinicians.
are compared is that of cardiac catheterization. It is an Radionuclide imaging of the chest is useful in the non­
invasive test, with a small but serious risk to the pa­ invasive evaluation of pulmonary embolism, whereas
tient. Complications include death, stroke, myocardial pulmonary angiography is the invasive but definitive
infarction (MI), bleeding, arterial trauma or thrombus, test. A computed tomography (CT) scan of the chest
renal dysfunction, and aIThythmias (Reagan, Boxt, and also has a variety of applications (Webb, 1994). Al­
Katz, 1994). The test is indicated in patients with a though magnetic resonance imaging (MRI) provides
high risk of atherosclerotic heart disease whose stress improved tissue contrast in comparison to a CT scan,
perfusion scans are positive. Patient's with diagnosed imaging applications in pulmonary disease continue to
CAD with angina, unresponsive to medical therapy, suffer from technical limitations (Mayo, 1994).
may also need catheterization.

Bronchoscopy
Test Procedure
Bronchoscopy is often used as both a diagnostic and
The cardiac catheterization laboratory requires an x­ therapeutic treatment modality (Mars and Ciesla,
ray generator tube and image intensifier/cine camera. 1993). It allows direct visualization of the trachea and
Data are stored using 35mm file (Reagan, Boxt, and its major subdivisions. Fiberoptic bronchoscopy has
Katz, 1994). virtually replaced bronchography (Lillington, 1987).
The procedure for cardiac catheterization of the In fiberoptic bronchoscopy, a flexible tube is inserted
left side of the heart requires the threading of a into the trachea of mildly sedated patients. This tude
catheter, guided by fluoroscopy, through the femoral is able to enter small brochial subdivisions. Secre­
artery or brachial artcry 10 thc aorta. Direct measure­ tions can be removed for evalutation or as a treat­
ments of chamber pressures, blood flow, and oxygen ment. It is also possible to obtain biopsy samples

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206 PART II Cardiopulmonary Assessment

using tiny forcepts or cell brushings. Bronchoscopy is standard against which ventilation/perfusion scans
particularly important in the diagmosis of bron­ are compared (Juni, 1992). Contrast dye is injected
chogenic carcinoma (Price and Wilson, 1986). into the pulmonary circulation through the pulmonary
artery. Additional techniques such as balloon occlu­
sion, segmental injections, or increased magnification
RADIONUCLIDE IMAGING
improve the sensitivity of the test (Lillington, 1987).
Ventilation-Perfusion lung Scan
Interobserver reliability studies pelformed on the in­
The ventilation-perfusion lung scan is a combination of terpretation of pulmonary angiograms are 83% to
two separate imaging procedures. It is primarily used in 86% (Juni, 1992).
the diagnosis of pulmonary embolism, with limited use
for other clinical problems (Lillington, 1987). The per­
Gallium SCintigraphy
fusion portion requires the injection of radioacti ve
tracer. Technetium-99M-macroaggregated albumin is Gallium-67-citrate concentrates in neoplastic and in­
(almost universally accepted as) the perfusion tracer of flammatory lesions of the lung (Lillington, 1987).
choice (Juni and Alavi, 1991). The ventilation scan re­ Gallium is more sensitive than normal chest x-ray in
quires the inhalation of radioactive gas, usually 133-XE identifying infectious and noninfectious inflamma­
gas or Tc-99M-diethylene triamine penta-acetic acid tory processes. This is particularly important in iden­
(DTPA) aerosol. Other isotopes can be used for ventila­ tifying opportunistic infections in the immunocom­
tion scanning (e.g. Kr-8IM, Xenon-I27) but they are promised patient. In patients with acquired immune
more difficult to obtain. deficiency syndrome (AIDS) the sensitivity of gal­
A normal perfusion scan essentially rules out re­ lium scanning for pneumocystis carinii pneumonia
cent pulmonary embolus. If the perfusion scan is ab­ approaches 94% to 96% (Kramer and Divgi, 1991).
normal, it is compared with the ventilation scan for The radioisotope is injected but it takes 48 to 72
match or mismatch of defects. An interpretation hours before imaging can be pelformed (Miller and
scheme is used, such as Biello or Pioped, which clas­ O'Doherty, 1992).
sifies the probability of pulmonary embolism into Gallium is commonly used in the evaluation of pa­
normal, low, intermediate (indeterminate), or high tients with interstitial lung disease; this includes sar­
(Juni, J 991; MiJJer and O'Doherty, 1992). Patients coidosis, amiodarone toxicity, and following cyto­
with high probability scans should begin anticoagula­ toxic therapy with bleiomycin, as well as many other
tion therapy (Juni, 1991). Patients with intennediate entities (Miller and O'Doherty, 1992). In conjunction
(indeterminate) scans may need to have a pulmonary with neoplasms, the scan's use is limited to assessing
angiogram before beginning treatment (Miller and tumor extent (Kramer and Divgi, 1991).
O'Doherty, 1992).
Miller and O'Doherty (1992) note other applica­
Computed Tomography
tions of ventilation/perfusion scanning to include
monitoring of response to radiotherapy and assess­ A computed tomography (CT) scan of the chest pro­
ment of resectability of bullae. The scan is used to vides a series of cross-sectional x-ray images. Com­
predict whether someone can tolerate a pneumonec­ pared with the standard x-ray, it is not commonly
tomy based on percent flow to the opposite lung and used in the initial diagnQsis of pulmonary disease. CT
extent of disease present. scan has been found to be a useful first-line diagnos­
tic tool in the evaluation of mediastinal disease, in­
cluding mediastinal masses, staging of mediastinal
Pulmonary Angiography
cancers, and identification of cysts (Lillington, 1987).
The diagnosis of pulmonary embolism is the primary High-resolution computed tomography (HRCT)
indication for pulmonary angiography. It is the gold has improved the documentation of morphologic

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 13 Special Tests 207

associated with chronic airflow obstruction.

SUMMARY
Webb's ( review of the application of this new
identified the utility of this test in a vari­ Many tests are available t o card
ety of obstructive diseases. HRCT is sensitive in the monary dysfunction. The attending physician deter­
of although used mines which tests are appropriate for the
such as X medical condition. When the tests are
HRCT is a b l e t o results are and an evaluation of
demonstrate cysts less than 10 m m i n diameter, as the results are documented. PTs need to understand
well as waH thickness. the results of the tests and how wiH apply to
In the diagnosis of HRCT demon­ function and response to exercise. This Ull­
strates a high It is the procedure of choice to the selection of exercise and
after plain chest X-rays. HRCT can discriminate be­ work loads the PT for the Until a
tween the three different of abnormal bronchi PT reaches a certain level, as well as a
seen in bronchiectasis (cylindrical, level of understanding and application of the test
but again there is l ittle clinical results to treatment, it is encouraged
(Webb, 1994). It can be used to differentiate that the PT discuss the test and results with the pa­
spread of cancer versus heart failure when un­ tient's physician. These discussions are excellent
clear clinically. HRCT also can be used to evaluate for learning both for the PT and to
of Overall, HRCT has the understand what physical ther­
but the clinical apy has to offer the with

function is less clear.

REVIEW QUESTIONS
Magnetic Resonance Imaging
Why is the mea­
sure of function?
2. What i s the difference between stunned my­
ocardium and
3.
embolism?
4, Which tests can be used to evaluate myocardial
vjability?
5. Why is a good choice for eval­
cardiac defects?

References

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Friedman, J. (1994). Myocardial perfusion imaging tech­
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plicaliolls. New York: Macmillan. Journal of Nuclear Medicine, 35, 693-698.
Kinch, J., & Ryan, T. (1994). Right ventricular infarction. New Wackers, FJ.T. (1994). Radionuclide evaluation of coronary artery
England Journal o/Medicine, 330, 1211-1215. disease in the 1990's. Cardiology Clinics. 12. 385-389.
Kramer, E., & Divgi, c. (1991). Pulmonary applications of nuclear Waggoner, A.D., & Perez, J. (1990). Principles and physics of
medicine. Clinics ill Chesl Medicine 12:1. 55-75. doppler. Cardiology Clinics, 12, 385-389.
Lillington, G. (1987). A diagnos tic approach to chest disease. Bal­ Webb, W.R. (1994). High-resolution computed tomography of ob­
timore: Williams and Wilkins. structive lung disease. Radiologic Clinics of North A merica,
Maddahi, 1., Schelbert, H., Brunken, R., & DiCarli, M. (1994). 32, 745-757.
Role of Thallium-201 and PET imaging in evaluation of my­ Wilson, D., & Vacek, J. (1990). Echocardiography. Postgraduate
ocardial viability and management of patients with coronary Medicine. 87. 191-202.

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 Clinical Assessment of the

Cardiopulmonary System

Susan M. Butler

KEY TERMS Barrel-chest Hyperresonant

Crackles Resonant
Cyanosis Wheeze
Dyspnea Whispered pectoriloquy
Egophany

INTRODUCTION
the inpatient setting, a chart review is the first point
To develop an effective treatment program for the pa­ of contact, whereas in the outpatient population, the
tient with a cardiopulmonary problem, it is essential information may be only what is obtainable from the
that a thorough evaluation be peliormed by the physi­ patient. Time management is an ever-present issue in
cal therapist (PT). This provides "baseline" data for today's era of cost containment and health care re­
comparison with subsequent reassessments that occur form. Thus a medical chart review should be con­
on a daily basis. Any progress or deterioration in sta­ ducted in an organized fashion. Most PTs develop
tus can then be easily identified with appropriate ad­ their own method.
justments made in the treatment plan. One strategy to chart review is the following se­
quence:
1. Read the history and physical and admission
CHART REVIEW/PATIENT INTERVIEW
medical note (i.e., preadmission symptoms).
The first patient contact can be indirect, through the 2. Read the last medical note.
medical chart, or direct, through patient interview. In 3. Scan remainder of chart.

209

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210 PART II Cardiopulmonary Assessment

4. Read any reports from medical specialists, con­ and respiratory systems. These questions could in­
sultants, i.e., pulmonologist, neurologist, oncologist. clude the following: What is the smoking history?
5. Review any pertinent lab tests. EXAMPI.ES: chest Does the patient have a family history of premature
x-ray, arterial blood gases (ABG's), complete blood coronary artery disease (i.e., a parent or sibling who
count (CBC). had a myocardial infarction)? Can the symptoms pre­
6. Review medications, in particular, pulmonary sented also be signs of a cardiovascular or pulmonary
and cardiac drugs. illness? Does the patient have an active versus a
7. Review the psychosocial information (i.e., fam­ sedentary lifestyle? What activities precipitate symp­
ily, architectural barriers). toms? Do these symptoms include breathlessness?
This last step is crucial in this time of shortened hos­ The patient should be seen as a human being with
pital stays. Any detail of the patient's background multiple organ systems. The patient's prob.lem,
that would affect discharge planning is crucial to whether oI1hopedic or cardiopulmonary, should not be
know even on the first day of treatment. Additional viewed in isolation. An example is the outpatient with
information to review that may be helpful and falls a physical therapy diagnosis of low back pain. When
into the cate gory of "as time allows" is the documen­ questioned about limiting symptoms, the patient might
tation of other allied health professionals (i.e., nurs­ describe cramping leg pain more suggestive of periph­
ing, occupational therapy, speech pathology). Finally, eral vascular disease (PYD).
when the initial chart review is finished, a mental pic­
ture of the patient should exist, even before the PT
PHYSICAL EXAMINATION
steps into the patient's hospital room.
Details regarding the patient interview have been The traditional components of a chest assessment are
covered in chapter 7. However, there are questions visual inspection, auscultation, percussion, and
that should be posed to any patient regardless of pal pation. The information provided by each of
whether their primary condition is cardiopulmonary. these techniques, when integrated with the patient's
The patient whose referring problem is musculoskele­ history and chal1 contents, allows the PT to piece to­
tal or neurologic still must have operational cardiac gether the pieces of the puzzle. For instance, to aus­
cultate breath sounds without observing the symme­
try of the chest wall fails to provide the needed clues
Anatomic Structures
to the total patient picture; thereby the development
Suprasternal /lotch-A depression palpable at the of an appropriate plan of care for the patient is maqe
tip of the sternum more difficult.
Sternomanubrial angll'-A bony bump where the
Before each individual component of the assess­
manubrium meets the body of the sternum; about 5
cm distal to suprasternal notch; also known as
ment is discussed, a review of the pertinent anatomical
angle of Louis; palpating hlle.ral to this junction, landmarks and topographical lines is to be discLlssed.
the .l'econd ribs is found and thus a reference point Knowledge of the superficial anatomy arid its relation­
for identifying intercostal spaces and successive ship to the Llnderlying heart and lungs aids the therapist
ribs; also, a superficial marking for where the
in decision making. The topographical lines allow for
underlying trachea divides into right and left
mainstem bronchi.
more accurate description of the physical findings.
Costal angle-The angle formed by the joining of
the costal margins with the sternum; normally, no
greater than 90 degrees.
TOPOGRAPHICAL ANATOMIC LANDMARKS
Vertebra prominens-The spinous process of the
Key anatomical structures include the following:
seventh ccrvical vertebra (C7); allows numbering
of thoracic vertebra • Sternum
• Clavicles

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 14 Clinical Assessment of the Cardiopulmonary System 211
-------

• Suprasternal notch • Anterior axillary line (AAL), mid-axillary line

• Sternomanubrial angle (angle of Louis) (MAL), and posterior axillary (PAL)-Like the
MCLs, these lines are also bilateral.
• Costal angle
The posterior chest has the following three lines:
• Vertebra prominens
• Vertebral or mid-spinal line - runs through the
See the box on p. 210 and Figures 14-1 and 14-2 for
spinous processes of the vertebrae.
specific definitions and anterior and lateral views of
• Mid-scapular lines (MSL)-lie parallel to the
thorax. Imaginary topographical lines are used to
mid-spinal lines; bisect inferior angles of scapulae.
more clearly describe any physical findings (e.g., lo­
cation of surgical incisions, abnormal breath sounds,
VISUAL INSPECTION
etc.) (Figure 14-3).
The anterior view of the thorax has three vertical Inspection is the foremost element of a chest assess­
lines. These are the following: ment. Not only should the features of the patient be
• Mid-sternal line (MSL)-a vertical line bisecting observed, but also the equipment and any aspect of
. the sternum the patient's surroundings that would contribute to
• Mid-clavicular fine (MCL)-lies parallel to the delineating the true picture of that patient. Remem­
MSL, bisects each clavicle; the lower lung borders ber, the PT has speculated a preliminary picture of
cross the sixth rib at the MCL. the patient based on chart review. Now, the ultimate
Laterally there are three vertical lines, originating test: how realistic was this initial impression? What
in their respective axillary folds: are the outward clinical signs that the therapist should

Clavicle

���-----1��n Manubrium

ManubriostemaI junction
(Angle of Louis)

Nipple

Costal angle

FIGURE 14-1
Topographical landmarks of the chest. (Adapted with permission from Seidel HM et al: Mosby's
guide to physical examination, ed 3, Boston, 1995, Mosby.)

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212 PART II Cardiopulmonary Assessment

Suprasternal notch

Clavicle

/
.1 'j,\ \ Manubrium

'_=:,. c/:.Ay".J
, Costal cartilages

Ribs

Xiphoid process

FIGURE 14-2
Anterior view of the thorax. (With permission from Swartz MH: TeXfbook ofphysical diagnoses­
hi story and examination, ed 2, Philadelphia, 1994, WB Saunders.)

look for? It will be broken down into categories for patient's build-stocky, thin or cachectic? Is the pa­
clarity. tient's mobility limited? Can the patient sit unsup­
ported? Should the assessment be performed in stages
such as supine or alternate sidelying? Is there any extra
General Appearance
equipment in the patient's surroundings? Is the patient
Does the patient appear comfortable? Is there any facial wearing supplemental oxygen? Is the oxygen delivered
grimacing? Is the patient awake and alert or disori­ through a nasal cannula or a mask? What is the fraction
ented? Is there any nasal flaring or pursed-lip breath­ of inspired oxygen (Fi02)? Are there any monitoring
ing? These are signs of respiratory distress. Nasal flar­ lines and where are they located. For instance, if an ar­
ing can be defined as the outward movement of the terial line is present, is it placed in the radial or femoral
nares with inspiration (Swartz, 1994). Are the accessory artery? Are there electrocardiogram (ECG) leads? Is it a
muscles of respiration (i.e, sternocleidomastoid, trapez­ "hard line" (directly connected to monitor) vs. teleme­
ius) hypertrophied? How is the patient positioned? Is try (through radio transmitter)? Are there intravenous
the patient resting comfortably or leaning forward over (IV) sites? Are these peripheral (antecubital) or central
the bedside table and struggling for breath? What is the (subclavian or jugular)? Is there a urinary catheter?

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 14 Clinical Assessment of the System 213

L----j��::::- SuprasternaJ notch

t---t----"1- SlernomanubriaJ angle

t---;---/---'r--- Midsternal line

r--+--t-..4f.1\\--::::---\--- Midclavicular lioe

I
1
A

Anterior axillary liM --t----I

/1
6"///
,"--4i
If
-- Spinous process of C7

Midaxillary li ne ----+ ___ +-_1

1--.....,..-+1-+---+----::>--+- Scapula line

pi
Posterior line ---r----t-+--j
dJ
J/I F'
II---+--/!--":--- Midspinalline

FIGURE 14·3
lines. A, Anterior view. 8, Lateral view. Posterior view. (Adapted with
permission from Swartz MH: Textbook and examination, ed 2,
Philadelphia, 1994, WB Saunders.)

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214 PART II Cardiopulmonary Assessment

Skin
desaturation has been noted, but this is not an exclu­
Does the skin have a pink, healthy color versus a pal­ sive phenomenon. Clubbing has been o bserved in
lor? Is cyanosis present? Cyanosis is a bluish tinge non pulmonary diseases such as hepatic fibrosis and
that can be seen centrally or peripherally. Central Crohn's disease. (George, Light, Matthay, and
cyanosis is a result of insufficient gas exchange Matthay, 1990; Seidel, Ball, Dains, and Benedict,
within the lungs and is not usually seen unless oxy­ 1995; and Swartz, 1994).
gen saturation is less than 80%. A bluish tint may be
seen at the mucous membranes (e.g., tongue, lips).
Neck
Peripheral cyanosis, on the other hand, occurs when
oxygen extraction at the periphery is excessive. This Are the accessory muscles of respirations being re­
type is also more associated with low cardiac output cruited for a resting breathing pattern? Do the stern­
states. Areas to observe for peripheral cyanosis might ocleidomastoid or trapezius muscles appear promi­
be fingertips, toes, nose, or nail beds. A differentiat­ nent? This is an early sign of obstructive lung disease
ing feature between central and peripheral cyanosis is (Swam, (994).
that peripheral cyanosis occurs, usually in the cooler
body parts such as nail beds and vanishes, usually
Jugular venous distension
when the part is warmed. In contrast, central cyanosis
does not disappear when the area is warmed. The jugular veins empty into the superior vena cava
Are any scars, bruises or ecchymoses observed? and reflect right-sided heart function. Right atrial
Are there reddened areas suggestive of prolonged pressure (RAP) is evident based on the extent to
pressure anywhere? Do the bony landmarks appear which the jugular venous pulse (JVP) can be visual­
more prominent than usual? Are there any signs of ized. The more superficial external jugular veins may
trauma to the thorax or any other body parts? Does be seen superior to the clavicles; the internal jugular
the skin appear edematous? Does this edema appear veins, though larger, lie deep beneath the sternoclei­
to limit joint motion? Are there any surgical inci­ domastoids and are less visible. Jugular venous dis­
sions, new and old? Do these incisions appear to be tention (JVD) can be best seen when the patient lies
healed or seem reddened and swollen? Is there evi­ with the head and neck at an optimal angle of 45 de­
dence of clubbing of the digits? Clubbing can be de­ grees (Figure 14-5). Symmetry of JVD should be
fined as the loss of angle between the nail bed and the noted. The veins are distended bilaterally if there is a
distal interphalangeal joint (Figure 14-4). The cause cardiac cause such as congestive heart failure (CHF).
of clubbing has a variety of theories, including in­ A unilateral distention is an indication of a localized
creased perfusion. Its association with arterial oxygen problem. (Seidel, Ball, Dains, and Benedict, (995).

CHEST WALL CONFIGURATION

The normal thoracic cage is elliptically shaped when

free of disease. The anteroposterior (AP) to lateral di­
ameter is 1:2 or 5:7. The angle of the ribs is less than
90 degrees. The ribs articulate with the vertebra, pos­
teriorly, at a 45-degree angle. The thorax should be
FIGURE 14-4
observed both anteriorly and p osteriorly. With
A, Clubbing of the fingers is best assessed by detemtining the
ratio of the diameter at the base of the nail B, to the diameter at chronic obstructive pulmonary disease (COPD), the

the distal interphalangeal joint. This ratio is n ormally less than ribs become more horizontal and the A-P diameter
I. (Reprinted with permission from George RB et al: Chest increases, thus the term barrel chest is used. In in­
medicine, ed 2, Baltimore, 1990, Williams and Wilkins.) fants, the chest is round with the anteroposterior and

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 14 Clinical Assessment of the Cardiopulmonary System 215

Carotid mCfY

Internal jugular vein

Horiz nlal line

FIGURE 14-5
Proper positioning to observe jugular venous distention. (Reprinted with permission from Seidel
HM et al: Mosby's guide to physical examination, ed 3, Boston, 1995, Mosby.)

transverse or lateral diameters of about equal dimen­ pathology. Again, any asymmetry should be observed
sions. As the child grows to adulthood, the chest be­ from both anterior and posterior views.
comes more elliptical. Again, with the aging process, Structural defects of the anterior chest may in­
the chest returns to a more rounded appearance. The clude the following: pectus excavatum, or funnel
increased anteroposterior diameter, in this population, chest-a depressed lower sternum that usually causes
is a result of the multiple factors of decreasing lung restriction only when severe; pectus carinatum, or pi­
compliance, decreased strength of the thoracic and di­ geon chest-a prominent upper sternum which does
aphragmatic muscles and skeletal changes of the tho­ not restrict chest wall movement; and flail chest-the
racic spine. The sym metry of the thoracic cage chest wall moves inward with inspiration, such as
should also be noted. Asymmetry can be the result of with multiple rib fractures.
structural defects or an underlying intrathoracic Other structural defects are spinal deformities.

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216 PART H Cardiopulmonary Assessment

J )
(j>";-.

.-
t \
.JPI4/1h v
} -\,.
.
:Jil! I
(";" \,\"'\\
Jilii/
/
-

..:,:.- \ 'I
A " /
./
/' \{
/(�
./
"',r-­
. \

Normal "Barrel chest" Kyphosis Pectus excavatum Pectus carinatum

FIGURE 14-6
Chest walJ configurations. (Reprinted with permission from Swartz MH: Textbook o/physical
diagnoses-his/ol)! and examination, ed 2, Philadelphia, 1994, WB Saunders.)

These are best viewed posteriorly. Kyphoscoliosis is Dyspnea describes the sensation of breathlessness
one example of how a posterior and lateral spinal devi­ or shortness of breath and is seen in cardiopulmonary
ation can limit chest wall and lung expansion. Another disorders. The level of dyspnea worsens as the sever­
example is a patient with COPD, who usually has a ity of the disease increases. An easy method to docu­
forward head and thoracic kyphosis (Figure 14-6). ment the level of dyspnea is to count the numbers of
words that the patient is able to speak per breath. For
instance, six-word dyspnea is not as significant as
BREATHING PATTERN
one-word dyspnea. The type of activities that elicit
Respiratory rate normally ranges between 12 and 20 shortness of breath should also be ascertained. For
breaths per minute (bpm). Eupnea is the term used to example, is breathlessness precipitated by stair climb­
describe a normal breathing cycle. Apnea is a tempo­ ing, taking a shower, etc? The "normal" ratio of in­
rary halt in breathing. Tachypnea is a rapid, shallow spiratory time to expiratory time is j :2. As the respi­
breathing pattern; this is an indicator of respiratory ratory rate increases this ratio decreases to j: I. This
distress. is seen in respiratory distress, as the patient struggles
Bradypnea exists when respiration is slowed, less to breathe in, the expiratory phase is shortened, and a
than 12 bpm. Causes could be neurologic or metabolic. vicious cycle continues. With pursed lip breathing,
Kussmaul's breathing is an increased rate and depth of the idea is to prolong the expiratory phase and slow
respirations and is associated with metabolic acidosis. the breathing pattern.

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 14 Clinical Assessment of the Cardiopulmonary System 217

AUSCULTATION
sists of ear pieces, tubing, and a chestpiece. The bell
Auscultation is the art of listening to sounds pro­ portion of the chestpiece assesses low-pitched
duced by the body. Lung and heart sounds are the sounds, that is, heart sounds. The diaphragm portion
focus of this chapter. Skill in auscultation is depen­ discerns high pitched sounds (Figure 1 4-7). The tub­
dent on the following four factors: ing should not be so long that sound transmission is
I. A functional stethoscope not dampened. Length of tubing should be between
2. Proper technique about 30 cm (12 in) to 55 cm (21 to 22 in). The ear
3. Knowledge of the different categories of lung pieces should fit the PT's ears comfortably and allow
sounds: normal, abnormal, and adventitious tuning out of external sounds. Other considerations
breath sounds and voice sounds would be to position the ear pieces anteriorly or for­
4. Knowledge of the different categories of heart ward toward the ear canals. Finally, an aside gained
sounds and murmurs from the author's clinical experience: warming the
diaphragm with the hands before placing it on the pa­
tient's skin is a first step in developing good patient
Stethoscope
rapport.
A stethoscope need not be fancy to be effective. A
PT, skilled in auscultation, can use any basic stetho­
Technique
scope and be able to identify lung sounds. The stetho­
scope functions more as a filter to the extraneous Environment is another element in the correct pedor­
noises than as an amplifier. A basic stethoscope con- mance of auscultation. The room or cubicle should be
as quiet as possible. Television and radio should be
turned down or off. Any extraneous noises should be
minimized or eliminated. This is especially important
when auscultation is a new technique for the thera­
pist. The patient should be positioned sitting, if possi­
ble, for lung sounds. The anterior, lateral, and poste­
rior aspects of the chest should be auscultated both
craniocaudally (apices to bases) and side to side (Fig­
ure 14-8). The PT places the diaphragm on the pa­
tient's skin so that it lies flat. The patient is instructed
to breath in and out through the mouth. A slightly
deeper breath than tidal breathing is suggested. A
minimum of one breath per bronchopulmonary seg­
ment allows for a comparison of the intensity, pitch,
and quality of the breath sounds. Movement of the di­
aphragm from one side to the other side while, at the
same time, moving it craniocaudally, enables the PT
to compare the right to the left chest. Clothing should
be removed and/or draped so that it does not interfere
Tubing in the assessment of the breath sounds.

FIGURE 14-7
Chest Sounds
Stethoscope. (Replinted with permission from Wilkins RL,
Hodgkin JE, Lopez B: Lung sOllnds, St. Louis, 1988, Mosby.) Chest sounds may be divided into these categories:

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218 PART II Cardiopulmonary Assessment

A
B

FIGURE 14-8
Stethoscope placement for auscultation of breath sounds. A, The chest. B, The back. (From
Buckingham EB: A primer of clinical diagnosis, ed 2, New York, 1979, Harper & Row.)

I. Breath sounds-normal , abnormal, adventi­ piratory phase. A distinguishing feature is the pause
tious that exists between the inspiratory and expiratory
2. Voice sounds - egophany , bronchophany, phases (Figure 14-9). This sound is also described as
whispered pectoriloquy tracheal as its norma/ location is over the trachea.
3. Extrapulmonary sounds-pl eural or friction Brol1chovesicular suunds are similar in that these are
rubs also high-pitched and have an equal inspiratory and
4. Heart sounds expiratory cycles. However, a differentiating feature
is the lack of a pause (Figure 14-9). Brol1chovesicular
sounds are heard best wherever the bronchi or central
Breath Sounds
lung tissue is close to the surface. These include su­
The terminology of breath sounds given in this chap­ perior to the clavicles and suprascapular (apices), and
ter is a compilation of multiple resources and clinical parasternal and interscapular (bronchi). The ATS­
experience. Recognition of normal breath sounds is AACP, in its 1977 recommendations for pulmonary
the key to the identification of abnormal and adventi­ nomenclature, used the term bronchial to include
tious sounds by offering the listener a point of refer­ both bronchial and bronchovesicular sounds. The fi­
ence. Normal breath sounds can be broken down into nite difference is minor (the pause between the inspi­
bronchial, bronchovesicular, and ves icular_ The ratory and expiratory phases). This recommendation
American Thoracic Society (ATS) and the American is meant to provide uniformity to lung sounds tenni­
College of Chest Physicians (ACCP) has attempted to nology. Vesicular brealh suunds are heard over the
provide standardization of the nomenclature and con­ remaining peripheral lung fields. These sounds have
tinues to conduct surveys of health care professionals primarily an inspiratory component with only the ini­
for use of this terminology in clinical practice. tial one third of the expiratory phase audible. Their
Bronchial sounds can be described as high­ intensity is also softer because of the dampening ef­
pitched and are heard both in the inspiratory and ex­ fect of the spongy lung tissue and the cumulative ef­

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 14 Clinical Assessment of the Cardiopulmonary System 219

BRONCHIAL when it becomes airless-either partially or com­

~
loud, high pitched; hollow quality; pletely. In a consolidation type of pneumonia, the
heard over manubrium; louder on lung tissue is Hairless" because of the complete ob­
expiration; distinct pause between
struction of segmental or lobar bronchi by secretions.
inspiration (I) and expiration (E)
Sound from the adjacent bronchi is enhanced and be­
comes more high-pitched and the expiratory compo­
BRONCHOVESICULAR nent louder and more pronounced. Compression of

/\
mixture of bronchial and vesicular; I:
lung tissue from an extrapulmonary source also pro­
E is 1: 1; heard over main-stem bronchi
-- anteriorly: ICS # 1 and 2, posteriorly: duces bronchial sounds. Examples include compres­
between scapulae sion secondary to increased pleural fluid (pleural ef­
fusion) or tumor. Tubular breath sounds is a term
used synonymously to describe abnormal bronchial

VESICULAR breath sounds.

/'
soft, low pitched; heard over peripheral Decreased or absent breath sounds occur when
lung tissue; no pause between I and E; sound transmission is diminished or abolished. De­
ratio is 3: 1
creased breath sounds are when the normal vesicular
sounds are further diminished. Absent sounds are
FIGURE 14-9 when no sounds are audible. Decreased or absent
Normal breath sounds. sounds can be caused by an internal pulmonary
pathology or can be secondary to an initially nonpul­
monary condition. Hyperinflation caused by emphy­
sema causes decreased sound transmission as a resull
of the destruction of the acinar units and increased air
as a result of loss of normal lung structure. The loss
fect of the air entry from numerous terminal bronchi­ of lung compliance resulting from pulmonary fibrosis
oles. The idea that vesicular sounds reflect air entry also may produce decreased or absent breath sounds.
in the alveoli has been disproved. Thus as the thera­ Extrapulmonary causes include tumors, neuromuscu­
pist auscultates from top to bottom, the breath sounds lar weakness (i.e, muscular dystrophy), and muscu­
are quieter at the bases than at the apices. Infants and loskeletal deformities (i.e., kyphoscoliosis). Pain is a
small children have louder, harsher breath sounds. common cause for decreased or absent breath sounds.
This is as result of the thinness of the chest wall and When the patient attempts to take a deep breath, the
the airways being closer to its surface. volume is limited because of the onset of pain. The
etiologic factors of the pain can be varied-from in­
cisional (i.e., midsternotomy) to traumatic (fractured
Abnormal Breath Sounds
ribs). Given that no underlying pathologies are pre­
Abnormal breath sounds can be described as when sent, decreased breath sounds may also be a reflec­
the sound transmission changes as a result of an un­ tion of the depth of respiration and/or the thickness of
derlying pathologic process. Sound is filtered by the the chest wall (e.g., in obesity or with the presence of
lung tissues because these organs are air-filled; thus bandages). The skill of auscultation lies in the differ­
there is dampened sound transmission over the bases entiation b etween normal and abnormal breath
versus the apices. On the other hand, sound transmis­ sounds.
sion is enhanced when a liquid or solid is the
medium. Certain lung pathologies produce abnormal
Adventitious Breath Sounds
lung sounds. Abnormal sounds can be divided into
three types: bronchial, decreased, and absent. Adventitious breath sounds are the extraneous noises
Bronchial sounds occur in peripheral lung tissue produced over the bronchopulmonary tree and are an

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220 PART II Cardiopulmonary Assessment

indication of an abnormal process or condition. These three." Egophany is also described when there is in­
sounds may be more easily identifiable than abnor­ creased transmission of the vocal vibrations. In this
mal sounds. Adventitious sounds are classified as case, the patient is asked to say "eeee." The underly­
c rackles (rales), rhonchi, and wheezes. Crackles ing process distorts the "e" sound so that an "aaa"
(rales) are described as discontinuous, low-pitched sound is heard over the peripheral area by the exam­
sounds. They occur predominantly during inspiration. iner. Egophany co-exists with bronchophany.
The sound of rubbing hair between the fingers or vel­ Whispered voice sounds also produce low-pitched
cro popping simulates crackles. Crackles usually in­ vibrations over the chest that are muftled by normal
dicate a peripheral airway process. Rhonchi are low­ lung parenchyma. Whispered pectoriloquy describes
pitched but continuous sounds. These occur both in when these whispered voice sounds become distinct
inspiration and expiration. Snoring is a term used to and clear; "one, two, three" or "ninety-nine" are used
describe its quality. Rhonchi are attributed to an ob­ to evaluate this sound. Whispered pectoriloquy can
structive process in the larger, more central airways. be present when bronchophany and egophany are ab­
Wheezes are continuous but high-pitched. A hissing sent. This sign is helpful in identifying smaller or
or whistling quality is present. Wheezes predomi­ patchy areas of lung consolidation.
nantly occur during expiration and are an indication Voice sounds are a means of confirmation of the
of bronchospasm (i.e., asthma). However, wheezes abnormal breath sounds. If a patient with significant
can also be caused by the movement of air through atelectasis secondary to compression of lung tissue
secretions, thus inspiratory wheezes can be described. presents with bronchial breath sounds, then egophany
and bronchophany are also audible.

Extrapulmonary Sounds
HEART SOUNDS
An adventitious sound that is nonpulmonary is the
friction rub. It can be described as a rubbing or leath­ As with lung sounds, superficial topographical land­
ery sound and occurs during both inspiration and ex­ marks assist the therapist in auscultation of heart
piration. The sound is produced by the visceral sounds and murmurs. The left ventricular apex is nor­
(inner) pleural lining rubbing against the parietal mally located at the MCL in the fifth intercostal
(outer) pleura and is a sign of a primary pleural space (rCS). The cardiac apex is also known as the
process such as inflammation or neoplasm. Pain is point of maximum impulse (PM/). There are four ref­
usually associated with a friction rub. erence areas for cardiac auscultation; these do not
c o r r e s p o n d directly to the u n derlying cardiac
anatomy. On the other hand, these areas do relate to
Voice Sounds
the events arising at the individual cardiac valves.
Voice sounds are vibrations produced by the speak­ These four areas are defined as the following:
ing voice as it travels down the tracheobronchial tree • aortic: second rcs, at right sternal border
and through the lung parenchyma when heard with a (RSB)
stethoscope. These sounds, over the normal lung, are • pulmonic: second ICS, at left sternal border
low-pitched and have a muftled or mumbled quality. (LSB)
The transmission of these vocal vibrations can be in­ • tricuspid: fourth and fifth lCS, LSB
creased or decreased in the presence of an underlying • mitral: cardiac apex fifth ICS, MCL.
pulmonary pathologic process. Bronchophany de­
scribes the phenomenon of increased vocal transmis­
Technique
sion. Words or letters are louder and clearer. Causes
are conditions where there is an increased lung den­ An environment that is as quiet as possible is recom­
sity as in consolidation from pneumonia. The patient mended. Positions used for cardiac auscultation in­
is usually asked to repeat "blue moon" or "one, two, clude the following: supine-used for all areas; left

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 14 Clinical Assessment of the Cardiopulmonary System 221

lateral decubitus (sidelying)-iistening to cardiac ever, it is usually abnormal in individuals over age
apex or mitral area, bell usually used; and sitting­ 40. An extra effort must be made to auscultate S3; the
used for all the areas. bell of the stethoscope should be used. The ideal po­
sition to hear S3 would be left side1ying; the bell
would be placed over the cardiac apex. Causes of a
Heart Sounds
pathological S3 may include ventricular failure,
The first heart sound (Sl) signifies the closing of the tachycardia, or mitral regurgitation. "Ken-TUCK'-y"
atrioventricular valves. Its duration is O. 10 seconds; it is one sound that has been used to approximate the
is heard the loudest at the cardiac apex. The two com­ sound sequencing of S3 in the cardiac cycle (SJ, S2,
ponents of Sl are tricuspid and mitral. Both the di­ S3).
aphragm and the bell of the stethoscope can be used The fourth heart sound (S4) signifies the rapid ven­
to hear Sl. Its loudness is enhanced by any condition tricular filling that occurs after atrial contraction.
in which the heart is closer to the chest wall (i.e., thin When present, it is heard before Sl. S4 may be heard
chest wall) or in which there is an increased force to in the "normal" trained individual with left ventricu­
the ventricular contraction (e.g., tachycardia resulting lar hypertrophy. Location of S4 is similar to S3' Its
from exercise). sound can be described as dull because of the sudden
The second heart sound (S2) represents the clos­ motion of stiff ventricles in response to increased
ing of the semilunar valves and the end of ventricu­ atrial contraction. Pathologies eliciting an S4 may in­
lar systole. Its components are aortic and pulmonic. clude systemic hypertension, cardiomyopathies, or
During expiration, these two components are not coarctation of the aorta. "TENN'-ess-ee" is a sound
distinct, since the time difference in the closure of that approximates the sound sequencing when S4 is
the valves is less than 30 milliseconds. However, present (S4, Sb Sz).
during inspiration, a splitting of S2 is audible. This
physiological split results from the increased venous
Murmurs
return to the right heart secondary to the decreased
intrathoracic pressure that occurs during inspiration. Cardiac murmurs are the vibrations resulting from
The pulmonic valve closure is delayed as the right turbulent blood flow. These may be described based
ventricular systolic time is lengthened. A split S2 is on position in cardiac cycle (systole, diastole), dura­
heard normally in children and young adults. The tion, and loudness. SYSlolic murmurs occur between
diaphragm of the stethoscope shou ld be used to hear Sl and S2; diastolic murmurs occur between Sz and
the split. The pulmonic component is the softer SJ' A continuous murmur starts in SJ and lasts
sound and is best heard at the LSB, in the second to through S2 for a portion or all of diastole. The loud­
fourth ICS. The two components may be heard best ness of a murmur is a factor of the velocity of blood
in the aortic and pulmonic areas, respectively. When flow and the turbulence created through a specific
the split is heard both phases of respiration. an un­ opening such as a valve. Grades I to VI are described
derlying cardiac abnormality is suspected. Causes as folJows:
may include right bundle branch block and pul­ •
I: faint-requires concentrated effort to hear
monary hypertension. ( S w a r tz, 1994; T i lki a n , •
II: faint-audible immediately
Conover, 1993). •
III: louder than II-intermediate intensity
•
IV: loud-intermediate intensity; associated with
Gallops palpable vibration (thrill)

The third heart sound (S3) is a faint, low frequency

•
V: very loud-thrill present

sound and reflects thc early (diastolic) ventricular •

VI: audible wilhout stethoscope
filling that occurs after the atrioventricular valves Murmurs that are Grade III or greater are usually as­
open. S3 is normal in children and young adults; how­ sociated with cardiovascular pathology.

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222 PART II Cardiopulmonary Assessment

MEDIATE PERCUSSION

Mediate or indirect percussion allows the therapist to

assess the density of the underlying organs. Striking
the chest wall produces vibrations in the underlying
structures which, in turn, gives rise to sound waves or
percussion tones. The quality of that tone depends on
the density of the tissue or organ, that is, it becomes
louder over air-filled structures. These tones are de­
scribed by the following terms:

%
•
resonant: loud or high amplitude, low-pitched,
longer duration, heard over air-filled organs such /.

as the lungs
•
dull: low amplitude, medium to high-pitched,
short duration, heard over solid organs such as the
liver
•
flat: high-pitched, short duration, heard over
FIGURE 14-10
muscle mass such as the thigh
Mediate percussion technique. (Reprinted with permission
•
tympanic: high-pitched, medium duration, heard from Swartz MH: Textbook of physical diagnoses-history
over hollow structures such as the stomach and examinaliol1, ed 2, Philadelphia, 1994, WB Saunders.)
•
hyper-resonant: very low-pitched, prolonged
duration, heard over tissue with decreased density
(increased air: tissue ratio); abnormal in adults;
heard over lungs with emphysema.

to breathe deeply and hold that breath. The lowest

Technique
level of the diaphragm on maximal inspiration co­
The middle finger of the nondominant hand is placed incides with the lowest point where a resonant tone
firmly on the chest wall in an intercostal space and par­ is heard. The patient is then asked to exhale, and
allel to the ribs. The top of the middle finger of the mediate percussion is repeated. The lowest area of
dominant hand strikes the distal phalanx of the station­ resonance now moves higher, as the diaphragm as­
ary hand with a quick, sharp motion. The impetus of cends with relaxation. The distance between these
the blow comes from the wrist versus the elbow and two points is described as the diaphragmatic excur­
has been likened to that of a paddle ball player (SWaItz, sion; normal is three to five cm (Figure 14-11). Di­
1994) (Figure 14-10). As with auscultation, the thera­ aphragmatic movement is decreased in patients
pist must follow the sequence of apices to bases and with COPO.
side to side so that comparisons can be made. This
technique is not usually used in infants, since percus­
PALPATION
sion is too easily transmitted by a small chest.
PTs use palpation in all areas of practice. Touch is an
integral part of physical therapy. As part of the chest
Diaphragmatic Excursion
examination, palpation is used to assess: areas of ten­
Assessment of diaphragmatic movement can b e derness and/or abnormalities; chest wall excursion;
made with mediate percussion. The patient i s asked edema; taclile fremitus; and tracheal deviation.

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 14 Clinical Assessment of the Cardiopulmonary System 223

Inspiration Expiration

FIGURE 14-11
Diaphragmatic excursion. (Reprinted with permission from Swartz MH: Textbook of physical
diagnoses-history and examination, ed 2, Philadelphia, 1994, WB Saunders.)

Tenderness
is a crunchy sound often associated with articular
Specific superficial or deep landmarks are identified structures. However, when bubbles of air occur
through palpation. Determination of gross spinal within subcutaneous tissue, a crackling sensation can
alignment can be performed by tracing the spinous be palpated. An air leak from a chest tube site is one
processes in a cephalocaudal direction. Structures can cause when crepitus is palpated over the chest wall.
be identified, such as the T-4 vertebra or the sternal Crepitus can also be secondary to a pleural or friction
angle, which only augment the PTs evaluation. Areas rub.
of tenderness can be assessed for degree of discom­
fort and reproducibility. Differentiation of chest wall
Edema
discomfort of an organic nature, such as with angina,
from that of a musculoskeletal condition may b e Palpation allows the PT to assess petipheral edema.
made through palpation. I n a patient complaining of Dependency of body parts can cause swelling from
chest pain, angina may be ruled out if the PT can re­ cardiac and noncardiac conditions. Assessment of
produce or increase the discomfort with increased edema is performed by pressing two fingers into the
tactile pressure. However, one must also determine particular areas for 2 to 3 seconds. If an impression is
that corroborating symptoms (e.g., diaphoresis, left once the fingers are removed, then pitting or de­
tachycardia) are not present. Angina or chest pain pendent edema is present. The degree of edema is
secondary to myocardial ischemia usuaJly results based on the length of time that the indentation lasts.
from exertion and may be relieved by rest. Crepitus I + is the least; 4+ is the worst.

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224 PART II Cardiopulmonary Assessment

Chest Wall Excursion of the sternal angle and meet at the midline,
slightly stretching the skin.
Evaluation of thoracic expansion allows the
4. The patient is asked to inhale.
to observe a "baseline" level by which to measure
5, The hands should be relaxed to allow for
progress or decline in a patient's condition. Chest
movement beneath,
wall movement can be restricted unilaterally as a re­
6. The symmetry and extent of movement are
sult of lobar or a surgical incision. A
assessed.
decrease in chest wall motion occurs in
withCOPO.
The hyperinflation associated withCOPO
an increase in the diameter with a pro-
loss of excursion. Normal
chest wall excursion is about 3.25 inches em) in a
young adult between 20 to 30 years of age. One
method is to use a measure at the level of the
xiphoid. However, the most common method involves
direct hand contact. This technique is in all
planes and from top to bottom. Symmetry and extent
of movement are both noted. Procedures for this
method are described in the
or upper lobe motion
I. The PT faces the patient. The area to be
examined is and as needed.
2. The PT's hands are over the anterior
FIGURE 14-13
chest. The heel of the hand is about the level
Evaluation of middle lobe and lingula motion (anterolateral
of the fourth rib and the fingertips reach excursion), (From Cherniak RM, et al: Respiration ill health
toward the upper and disease, ed 2, Philadelphia, 1972, WB Saunders.)
3, The thumbs Jie horizontal at about the level

\ I

J±�
I ' i

A
FIGURE 14-12 FIGURE 14-14
Evaluation of upper lobe motion. (From Cherniak RM, et Evaluation of lower lobe motion (posterior
al: in health and disease. ed 2, (From Cherniak RM, et al: Respiration in health and
1972, WB Saunders,) disease. ed 2, Philadelphia, ]972, WB Saunders.)

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 14 Clinical Assessment of the Cardiopulmonary System 225

• Anterolateral or middle lobe/lingula motion

(Figure 14-13)
I. See above.
2. The PT's hands are placed with the palms
distal to the nipple line with the thumbs
meeting in the midline. The fingers lie in the
posterior auxiliary foi' d.
3. See steps 4 to 6 above.
• Posterior excursion/lower lobe motion (Figure
14-14)
1. The PT stands behind the patient.
2. The area to be examined is exposed with
draping used as appropriate.
3. The PTs hands are placed flat on the
posterior chest wall at the level of the tenth
rib. The thumbs meet at the midline; fingers
reaching toward the anterior axillary fold.
FIGURE 14-15
4. See steps 4 to 6 above.
Evaluation of fremitus, method one.

Tactile Fremitus

Spoken word produces vibration over the chest wall. aspect of the suprasternal notch. This is repeated on
Voice sounds have been previously discussed under the opposite side. An equal distance between the
auscultation. With the PTs hands placed on the chest clavicle and the trachea should exist bilaterally. Tra­
wall, vibrations from spoken words can be felt and cheal deviation may be caused by a pneumothorax,
are described as tactile fremitus. The presence or ab­ atelectasis or a tumor among other conditions.
sence of tactile fremitus provides information on the Whether the deviation will be ipsilateral or contralat­
density of the underlying lungs and thoracic cavity eral depends on the underlying cause. A right pneu­
(Swartz, 1994). mothorax or pleural effusion will deviate the trachea
away (toward the left); a left lower lobe atelectasis,
however, deviates the trachea toward the affected
Technique (Figures 14-15 and 14-16)
side, that is, the left.
Two methods can be used. The first technique is one
in which the therapist uses the palmar surface of one
CASE STUDIES
or both hands. The second method involves the use of
Case Study One
the ulnar border of one hand. With both techniques,
the sequence is, again, cephalocaudal and side to A 30-year-old man with cystic fibrosis shows symp­
side. In either method, the next step is to ask that the toms of a one-week history of increased sputum pro­
patient speak a predetermined phrase. The two most duction, loss of appetite, fatigue, and 3-lb. weight
commonly used are "99" or "one, two, three." A light loss. 'The results of the initial chest examination are
but firm touch is recommended. as follows:
Inspection: Forward head, kyphotic posture,
increased anteroposterior diameter, appears thin
Tracheal Deviation (Figure 14-17)
and fatigued, no dyspnea observed, effective wet
The trachea's midline position can be examined ante­
cough
riorly. The PT places an index finger in the medial

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226 PART II Cardiopulmonary Assessment

:/"1\" , i '
'
f!
"""- "'\
::--...
\ '.
-II . ..:--_
, :
'

'"

1J;
FIGURE 14-17
Technique for determining the position of the trachea.
(With permission from Swartz MH: TextboQk of physical
diagnoses-history and examination. ed 2. Philadelphia,
1994, WB Saunders.)

FIGURE 14-16
Technique for evaluating tactile fremitus, method two.
(With permission from Swartz MH: Textbook of physical
diagnoses-history and examination, ed 2. Philadelphia,
1994, WB Saunders.)

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 14 Clinical Assessment of the Cardiopulmonary System 227

Auscultation: Decreased breath sounds with Mediate percussion: dull over affected area
scattered crackles throughout all lung fields, Palpation: trachea midline, markedly decreased
especially over right middle and lower chest CWE on right side
Palpation: Limited chest wall excursion (CWE),
especially laterally Case Study Three
Mediate percussion: Dull over right middle and A 72-year-old woman shows symptoms of persistent
lower chest, especially laterally fevers, left chest wall discomfort, and history of fall I
week ago. CT scan shows loculated pleural effusion
Case Study Two on the left. Left chest tube is inserted for drainage;
working diagnosis is empyema. Patient is nonsmoker,
An ll-year-old girl is admitted to Pediatrics with a 4-
Inspection: RR 30; l:E ratio I:2; epidural
day history of recurrent fevers, shortness of breath,
==

and lethargy. CXR showed an RML pneumonia. catheter for pain control

Inspection: tachypnea; respiratory rate (RR) of 44; Auscultation: Absent breath sounds halfway up

Ratio of inspiration to expiration (I:E ratio == I: I; left lower lateral chest wall

weak, shallow cough Mediate percussion: flat over left lower lateral

Auscultation: bronchial over right midanterior chest wall

chest, ego ph any also present Palpation: trachea deviated to right, decreased

TABLE 14-1

Differentiation of Common Pulmonary Conditions

Inspection Palpation Percussion Auscultation

Emphysema Increased anteroposterior Decreased tactile Increased resonance; Decreased lung

diameter; use of accessory fremitus decreased excursion sounds; decreased
muscles, thin individual of diaphragm vocal fremitus
Chronic bronchitis Possible cyanosis; short, Often normal Often normal Early crackJes
stocky individual
Pneumonia Possible cyanosis Increased tactile Dull Late crackles;
fremitus; splinting bronchal breath
on affected side sounds
Pulmonary embolism Sudden onset of dyspnea; Usually normal Usually normal Usually normal
chest pain
Pneumothorax Rapid onset Absent fremitus; Hyperresonant Absent breath sounds
trachea may be
shifted to other side;
may have decreased
chest wall excursion
on affected side
Pleural effusion May be no outward Decreased fremitus; Dullnes s Absent breath sounds
clinical sign trachea shifted to
other side; decreased
chest wall excursion
on affected side
Atelectasis Often no outward Decreased fremitus; Dullness Absent breath sounds
clinical sign trachea shifted to
same side; decreased
chest wall excursion
on affected side

Adapted with permission from Swartz, MH: Textbook ofphysical diag/Uises-history and examirulliOI1, ed 2. Philadelphia, 1994, WB Saunders.

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228 PART II Cardiopulmonary Assessment

eWE on left, range of motion of left shoulder joint 7. Which components of the chest physical examina­
limited in flexion and abduction at about 90 tion a physical therapist include in the initial
nP<Y,.p,,>< maximum assessment of a geriatric with a recent left

See Table 14-1 for a differentiation of Ul<11411U:>C;' total hio renlacement aud a history of COPD?

the elements of a chest examination.

References
SUMMARY Chemiak. R.M., & Cherniak, L. ([983). Respirmiorl in heailh and
disease. (3rd ed.). Philadelphia: WB Saunders.
As demonstrated in the case each element of
Fraser, KG., Pare lA., Pare, P.O. Frazer, R. S .. & Genereux, G.P.:
the chest physical examination contributes to the phys­ (1988). Diagnosis of diseases ill the chest. Philadelphia: WB
ical therapist solving the of the individual pa­ Saunders.
tient. It is through "putting all the together that George, R.B., Light, R.W. Matthay, M.A. & Matthay, RA ( l990).

Chesf medicine (2nd ed.). Baltimore: Williams and Wilkins.

au effective treatment program can be developed.

Lehrer, (1993). Understanding lung sound.," (2nd ed.). Philadel-
phia: WB Saunders.
Mikami, et International symposium on sounds, Chesl
REVIEW QUESTIONS
92(2):342-345, 1987.

Describe the sequence for auscultation of lung Seidel, RM., Ball, J.W., Dains, J.E., & Benedict, G.W. (1995).
Mosby's guide 10 physical examinatioll (3rd ed.). Boston: Mosby.
sounds.
Swartz, M.H. (1994). Textbook of physical diagnoses-llIslOry and
2. State the difference between oerioheral and cen­
examination (2nd ed). PhiJadeJphia: WB Saunders.
tral cyanosis. Tilkian, A.G., & Conover, M.D. (1993). Understanding heart
3. How are normal bronchial breath sounds different sounds and murmurs (3rd ed.). Philadelphia: WB Saunders.
from abnomUlI bronchial breath sounds? Wilkins, R.I., Hodgkin, J.E., & Lopez, B. (1988). Lung sounds. Sl.
Louis: Mosby.
4. Name two causes for a oathollOl?:lC
Wilkins, et al: Lung sound nomencla ture survey, C hest
5. Name two causes for decreased breath sounds.
98(4)886-889,1990.
6. Formulate a plan for evaluation of a patient with Willerson, J.T., & Cohn, J.N. ([995). Cardiovascular medicine.
an acute Right Lower Lobe Pneumonia. New York: Churchill Livingstone.

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 Monitoring Systems
in the Intensive Care Unit

Elizabeth Dean

KEY TERMS Acid base balance Intraaortic balloon counter pulsation

ECG monitoring Intracardiac pressures

Fluid and electrolyte status Intracranial pressure monitoring

Hemodynamic status

INTRODUCTION
may differ among intensive care units, the principles
The primary goal of the intensive care unit (ICU) are similar and relate either directly or indirectly to the
team is the achievement of stable cardiopulmonary foremost goal of optimizing oxygen transport.
function and optimal oxygen transport. This chapter Cardiopulmonary status is often jeopardized with
presents an introduction to monitoring systems used the ICU patient by fluid and electrolyte disturbances
in the evaluation of cardiopulmonary status in the and acid-base imbalance. Regulation of these systems
ICU and describes some related elements of car­ and the clinical implications of imbalance are de­
diopulmonary regulation that are relevant to assess­ scribed first with special reference to the JCU patient.
ment and treatment in physical therapy. The principles of monitoring systems used in assess­
ICUs are becoming more specialized. In major hos­ ing cardiopulmonary sufficiency are presented in­
pital centers, units are often exclusively designed and cluding the electrocardiogram (ECG) monitor, moni­
staffed for the management of specific types of condi­ tors related to left- and right-sided heart function
tions e.g., medical, surgical, trauma, bums, and coro­ utilizing arterial and venous lines, and the intracranial
nary and neonatal care. Although monitoring priorities pressure (ICP) monitor. The intraaortic counter pulsa­

229

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230 PART II Cardiopulmonary Assessment

FIGURE 15-1

General view of a typical leU.

FLUIIJ AND ELECTROLYTE BALANCE

tion technique used to augment myocardial efficiency
is also described. When the normal regulation of fluid intake, utilization,
Familiarity with the extensive monitoring facilities and excretion are disrupted, fluid, electrolyte, and acid­
in the lCU allays some of the apprehensions the base imbalances result. Essentially, all medical and
physical therapist (PT) may have working in a critical surgical conditions threaten these life-dependent mech­
care. On introduction to the unit, the PT is immedi­ anisms to some degree. Minor imbalances may be cor­
ately struck by the high technology atmosphere. rected by modification of the patient's nutrition and
Quality care in this setting depends on harnessing the fluid intake. More major imbalances can be life-threat­
potential of the monitoring equipment to optimize as­ ening and can necessitate prompt medical attention.
sessment, treatment selection, and effectiveness, as Imbalances are reflected as excesses, deficits, or as
well as reduce untoward risk for the patient. an abnormal distribution of fluids within the body
For further detail on the monitoring topics pre­ (Folk-Lighty, 1984; Phipps, Long, and Woods, 1991).
sented refer to Barrell and Abbass (1978), Burki and Excesses result from increased intake and decreased
Albert (1983), Copel and Stolarik (1991), Cromwell, loss of fluid and electrolytes. Deficits result from ab­
Weilbell, and Pfeiffer (1980), DeGowin and De­ normal shifts of fluid and electrolytes among the in­
Gowin (19 81), and W e i d e ma n n, M a t t h a y , and travascular and extravascular fluid compartments of
Matthay (1984). the body. Excesses occur with kidney dysfunction pro­
Figure 15-1 illustrates a general view of a typical moting fluid retention and with respiratory dysfunction
lCU. A closer view of the patient at bedside indicates promoting carbon dioxide retention. Deficits are com­
to the PT the parameters that are being monitored, and monly associated with reduced intake of fluids and nu­
the types of lines, catheters, and leads in place (Figure trition. Diaphoresis and wounds can also contIibute to
15-2). A closer view with the patient's gown removed significant fluid loss. Diarrhea and vomiting drain the
demonstrates precisely where the various lines, leads, gastrointestinal tract of fluid stores. Hemorrhage is al­
and catheters are positioned, and identifies where cau­ ways responsible for fluid and electrolyte loss. Deficits
tion must be observed. Treatments are modified ac­ may be secondary to fluid entrapment and localized
cording to the types and positions of the lines and edema within the body, making this source of fluid un­
leads for each individual patient (Figure 15-3). available for regulation of homeostasis.

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 15 Monitoring Systems in the Intensive Care Unit 231

FIGURE 15-2
A and B, Closer bedside views of patients in an ICU. Note that with all the equipment, the patient is
almost lost. C, Note two IV lines with flow monitors. Blood infusion is also being received.
Continued.

Moderate to severe fluid imbalance can be re­ with fluid overload. Normally, the jugular pulse is
flected in the systemic blood pressure and jugular ve­ not visible 2 em above the sternal angle when the in­
nous pressure (CVP). Elevated blood pressure can be dividual sits at a 45-degree angle. If the jugular pulse
indicative of fluid overload, but an intravascular fluid is noted, this can be a sign of fluid overload.
deficit of 15% to 25% must develop before blood Fluid replacement is based on a detailed assess­
pressure drops. The jugular vein becomes distended ment of the patient's needs. Whole blood is preferred

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232 PART II Cardiopulmonary Assessment

FIGURE 15-2-conl'd
D, Bedside oxygen and suction set-up. E, Close-up piped in O2 and suction units, F, Close-up IVs
and drip monitoring flow devices (IMEO). G, Note IABP, ventilator, IVs, organization of unit at
the head of the bed. ECG unit overhead, suctioning and airway care equipment at the right of the
patient and "Ambu" bag at bedside.

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 IS Monitoring Systems in the Intensive Care Unit 233

FIGURE 15·3
A, Patient after open heart surgery. Note insert of Swan Ganz, CV tubing connection taped to left
chest. On ventilator with oral endotracheal tube, oral airway is in place. Note the nasogastric tube,
ECG leads, and dressing covers sternal split incision site. B, Patient after open heart surgery. Note
ECG leads. Patient is now weaned from ventilator and endou·acheal tube; pacemaker wires are held
intact at upper abdomen in syringe area. Patient has a11erial Li ne in right forearm; Swan Ganz, CVP
also removed. Patient is almost ready to leave ICU; he is receiving an aerosol treatment.

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234 PART II Cardiopulmonary Assessment

to replace blood loss. Plasma, albumin, and plasma complaints of headache, thirst, and nausea, as well as
volume expanders such as Dextran can be used to changes in dyspnea, skin turgor, and muscle strength.
substitute for blood loss and to help reestablish blood More objective assessment is based on fluid intake,
volume. Albumin and substances such as Dextran in­ output, and body weight. Fluid balance is so critical
crease plasma volume by increasing the osmotic pres­ to physical well-being and cardiopulmonary suffi­
sure of the blood, hence the reabsorption of fluid ciency that fluid input and output records are rou­
from the interstitial space. Low molecular weight tinely maintained at bedside. These records also in­
Dextran has the added advantage of augmenting cap­ c l u d e f l u i d v o l u m e lost in w o u n d dra inage,
illary blood flow by decreasing blood viscosity, and gastrointestinal output, and fluids aspirated from any
is therefore particularly useful in treating shock. body cavity (e.g., abdomen and pleural space).
A patient's weight may increase by several pounds
before edema is apparent. The dependent areas mani­
Clinical Picture
fest the first signs of fluid excess. Patients on bed rest
Excesses and deficits of fluids and electrolytes can be show sacral swelling; patients who can sit over the
determined on the basis of laboratory determinations bed or in a chair for prolonged periods tend to show
of serum levels of the specific electrolytes. Elec­ swelling of the feet and hands.
trolyte levels and hematocrit are decreased with fluid Decreased skin turgor can indicate fluid deficit.
excess (hemodilution) and increased with fluid loss Tenting of the skin over the anterior chest in response
(hemoconcentration). to pinching may suggest fluid depletion. Wrinkled,
Excess fluid can be managed by controlled fluid toneless skin is more common in younger patients.
intake, normal diuresis, and diuretic medications. Re­ Weight loss may be deceptive in the patient on IV
placement of fluid and electrolyte losses can be fluids, who can be expected to lose a pound a day.
achieved by oral intake, tube feeding, intravenous This sign should therefore not necessarily be inter­
(IV) infusion, and parenteral hyperalimentation. preted as underhydration.
Assessment of fluid and electrolyte balance is The cardiopulmonary assessment can reveal
based on both subjective and objective findings changes in fluid balance. Lung sounds are valuable in
(Table 15-1). At the bedside, the PT must be alert to identifying fluid overload. Vesicular sounds may be-

TABLE 15-1

Assessment of Fluid and Electrolyte Imbalance

FLUID EXCESSfELECTROL YTE FLUID LOSS/ELECTROL YTE

AREA IMBALANCE IMBALANCE

Head and neck Distended neck veins, facial edema Thirst, dlY mucous membranes
Extremities Dependent edema "pitting," discomfort from Muscle weakness, tingling, tetany
weight of bed covers
Skin Warm, moist, taut, cool feeling when edematous Dry, decreased turgor
Respiration Dyspnea, orthopnea, productive cough, moist Changes in rate and depth of breathing
breath sounds
Circulation Hypertension, jugular pulse visible at 45-degree Pulse rate irregularities. dysrhythmia, postural
sitting angle, atrial dysrhythmias hypotension, sinus tachycardia
Abdomen Increased girth, fluid wave Abdominal cramps

Modified from Phipps WJ, Long Be, Woods NF, editors: Medical-surgical nursing: concepts in clinical practice, cd 4, SI. Louis. 1991,
Mosby.

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 15 Monitoring Systems in the Intensive Care Unit 235

come more bronchovesicular in quality. Crackles and collection system is shown in Figure 15-4. The
may increase in coarseness. In the presence of fluid removal of thick fluids such as blood and organized
retention involving the pleurae, breath sounds dimin­ exudates with chest tubes is often indicated to pre­
ish to the bases. Dyspnea and orthopnea may also be vent entrapment and loculation. Chest tubes are com­
symptomatic of fluid excess. monly inserted in the sixth intercostal space in the
An early sign of congestive heart failure (CHF) mid or posterior axillary line. Chest tubes inserted
with underlying fluid overload is an S3 gallop (Ken­ into the pleural space are used to evacuate air or exu­
TUCK'-y) caused by rapid ventricular filling. date. Chest tubes can also be inserted into the medi­
Vigilance by the PT is essential in all areas of astinum after open heart surgery, for example, to
practice and not only the ICU. Fluid imbalance is evacuate blood.
common in older people and in young children, thus Any collection system is designed to seal the
it needs to be watched for on the ward, in the home, drainage site from the atmosphere and offer minimal
and community. resistance to the drainage of fluid and gas. This is ac­
complished by immersing the end of the collection
tube under water (Figure 15-4). This is referred to as
CHEST TUBE DRAINAGE AND FLUID
an underwater seal system. Additional reservoirs are
COLLECTION SYSTEMS
included to decrease the resistance to fluid leaving
Chest tubes are large catheters placed in the pleural the chest. This resistance is greater in a single reser­
cavity to evacuate fluid and air, and to drain into a voir system in which the reservoir serves both as the
graduated collection reservoir at bedside (Phipps, collection receptacle and underwater seal. A third
Long, Woods, 1991). A typical chest tube drainage reservoir can be added to the system that is attached

FIGURE 15·4
A, Chest tube drainage. B, Anterior view, Mediastinal drains.

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236 PART II Cardiopulmonary Assessment

to the suction and serves as a pressure regulator. The

TABLE 15-2
more elaborate drainage systems are used to precisely
measure fluid loss in patients following thoracic and Signs and Symptoms of Common
cardiovascular surgery. Acid Base Disturbances

The amount of exudate collected in the reservoir is RESPIRA TORY ACIDOSIS METABOLIC ACIDOSIS
measured every several hours or more often if the pa­
Hypercapnia Bicarbonate deficit
tient is losing considerable amounts of fluid or less
Hypoventilation Hyperventilation
than the amount predicted. This information is incor­ Headache Headache
porated into the overall fluid balance assessment. In Visual disturbances Mental dullness
addition, changes in the quantity and quality of exu­ Confusion Deep respirations
Drowsiness Stupor
date should be noted by the PT before, during, and
Coma Coma
after changes in position and therapeutic interventions.
Depressed tendon reflexes Hyperkalemia
Hyperkalemia Cardia dysrhythmias
Ventricular fibrillation (secondary to
ACID-BASE BALANCE (secondary to hyperkalemia)
hyperkalemia)
Control of acid-base balance in the body is achieved
by regulation of hydrogen ion concentration in the RESPIRATORY ALKALOSIS METABOLIC ALKALOSIS
body fluids (Guyton, 1991; Shapiro, Peruzzi, and
Hypocapnia Bicarbonate excess
Kozelowski-Templin, 1994). The pH of the body is Lightheadedness Depressed respirations
normally maintained within a range of 7.35 to 7.45, Numbness/tingling of digits Mental confusion
or slightly alkaline. When pH of the blood drops Tetany Dizziness
Convulsions Numhm:ss/tingling of
below 7.35, a state of acidosis exists; above 7.45, a
digits
state of alkalosis exists. Regulation of pH is vital be­
Hypokalemia Muscle twitching
cause even slight deviations from the normal range Cardiac dysrhythmias Tetany
cause marked changes in the rate of cellular chemical (secondary to hypokalemia) Convulsions
reactions. A pH below 6.8 and above 8 are incompat­ Hypokalemia
Cardia dysrhythmias
ible with life.
(secondary to
Acid-base balance is controlled by several regula­
hypokalemia)
tory buffer systems; primarily carbonic acid-bicarbon­
ate, phosphate, and protein buffer systems. These sys­
tems act very quickly to prevent minute-to-minute
changes in pH. In compensation, pH is returned to
normal primarily by altering the component not pri­
marily affected. If the primary cause is respiratory, the ume, potassium excess (hyperkalemia) is associated
compensating mechanism is metabolic. If the primary with both respiratory and metabolic acidosis, and
cause is metabolic, the compensating mechanism is neuromuscular hyperexcitability is associated with
respiratory. The lungs compensate for metabolic prob­ both respiratory and metabolic alkalosis.
lems over hours, whereas the kidneys compensate for
respiratory problems over days (Chapter 9).
BLOOD GASES

Analysis of the composition of arterial and mixed

Clinical Picture
venous blood provides vital information about respi­
A guide to the clinical presentation of acid-base im­ ratory, cardiac, and metabolic function (Ganong,
balances is shown in Table 15-2. Besides the major 1993; Snider, 1973; Thomas, Lefrak, Irwin, Fritts,
distinguishing characteristics of acid-base imbalance and Caldwell, 1974; Marini, 1987; West, 1995) (see
described in this chapter and elsewhere in this vol- Chapter 9). For this reason, blood gases are usually

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 15 Monitoring Systems in the Intensive Care Unit 237

HYPOXEMIA
analyzed daily in the ICU. In cases where the pa­
tient's condition is changing for better or worse over In health, age and body position are factors that re­
a short period of time or a specific treatment re­ duce arterial oxygen tension (Oakes, 1988). Arterial
sponse is of interest, blood gases may be analyzed oxygen levels diminish with age as a result of reduc­
several times daily. With an arterial line in place, tions in alveolar surface area, pulmonary capillary
frequent blood gas analysis ·is feasible and not trau­ blood volume and diffusing capacity. Normal PaOz
matic for the patient. Should the patient be anemic, levels in older people should exceed 110-0.5 age. In a
however, blood loss associated with repeated arter­ young adult, Paoz ranges from 90 to 100 mm Hg in
ial blood sampling can be detrimental. Thus re­ the upright seated position. In supine, this range is re­
quests for arterial blood gas analysis need to be par­ duced to 85 to 95 mm Hg and in sleeping, to 70 to 85
ticularly stringcnt in anemic patients. mm Hg. These values are significant in that in older
Arterial saturation (Sao2) can be readily monitored people, smokers, and people with pathology, these po­
noninvasively with a noninvasive pulse oximeter. sitional effects are accentuated.
The ear lobe or a finger is initially warmed by rub­ Hypoxemia refers to reduced oxygen tension in
bing before attachment of the oximeter. Within a cou­ the blood. Some common signs and symptoms of var­
ple of minutes, the Sao2 can be directly read from the ious degrees of hypoxemia in adults appear in Table
monitor. Pulse oximetry is a useful adjunct for rou­ 15-3. Although the brain is protected by autoregula-
tine evaluation of the effectiveness of mechanical
ventilation, the effect of anesthesia and treatment re­
sponse. Continuous estimation of Saoz is particularly TABLE 15-3
useful before, during, and after mobilization and ex­
Signs and Symptoms of Hypoxemia
ercise, position changes, and other therapeutic inter­
Paoz SIGNS AND SYMPTOMS
ventions. The Sao2 may appear to be reduced in pa­
tients who are anemic, jaundiced, have heavily 80-100 mm Hg Normal

pigmented skin, or have reduced cardiac output. 60-80 mm Hg Moderate tachycardia, possible onset of
respirat ory distress
Mixed venous oxygen saturation (SV02) provides a
50-60 mm Hg Malaise
useful index of oxygen supply and utilization at the tis­
Lightheadedness
sue level (Copel, and Stolarik, 1991). Svoz is highly Nausea
correlated to tissue oxygen extraction, and thus is a Vertigo
good index of the adequacy of oxygen transport. The Impaired judgment
Incoordination
Sv0:2 is particularly useful as a significant warning sign,
Restless
a guide to myocardial function, and has been used as a
Increased minute ventilation
tool to titrate positive end-expiratory pressure supp0l1. 35-50 mm Hg Marked confusion
NOImal values of SVD2 are 75%. SVD2 values less than Cardiac dysrhylhmias

60% or a drop of 10% for several minutes are cause for Labored respiration
25-35 m m Hg Cardiac an-est
concern. Excessive Svo2 values in excess of 80% are
Decreased renal blood flow
also cause for concern. High SV02 values may occur in
Decreased urine output
patients with left to right shunts, hyperoxia, hypother­ Lactic acidosis
mia, cyanide toxicity, sepsis, anesthesia, and drug-in­ Poor oxygenation
duced paralysis. Despite its general clinical usefulness, Lethargy
Maximal minute ventilation
SV02 is a nonspecific indicator of the adequacy of oxy­
Loss of consciousness
gen transport, that is, of the balance between oxygen <25 mm Hg Decreased minute ventilation
supply and demand. Abnormal Svoz values do not indi­ (secondary to depression of
cate precisely where the problem lies; thus other hemo­ respiratory center)
dynamic variables need to be considered.

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238 PART II Cardiopulmonary Assessment

tory mechanisms, an arterial oxygen tension of 60 of nonpulmonary tissues is little altered. In the lung,
mm Hg produces signs of marked depression of the high concentrations of oxygen replace nitrogen in
central nervous system (NS) reflecting the extreme poorly ventilated regions. This results in collapse of
sensitivity of cerebral tissue to hypoxia. areas with reduced ventilation perfusion matching.
H y poxemia is compensated primarily by in­ Lung compliance is diminished.
creased cardiac output, improved perfusion of vital High concentrations of oxygen (inspired oxygen
organs, and polycythemia. Secondary mechanisms of fractions greater than 50%) directly injure bronchial
compensation include improved unloading of oxygen and parenchymal lung tissue. The toxic effect of oxy­
as a result of tissue acidosis and anaerobic metabo­ gen is both time and concentration dependent. Very
lism, that is, rightward shift to the oxyhemoglobin high concentrations of oxygen can be tolerated for up
dissociation curve. to 48 hours. High concentrations of oxygen in combi­
The progressive physiologic deterioration ob­ nation with positive pressure breathing can predis­
served at decreasing arterial oxygen levels will occur pose the patient to oxygen toxicity. At concentrations
at higher oxygen levels if any of the major compen­ of inspired oxygen less than 50%, clinically de­
sating mechanisms for hypoxemia is defective. Even tectable oxygen toxicity is unusual regardless of the
a mild drop in Pao2 for example, is poorly tolerated duration of oxygen therapy.
by the patient with reduced hemoglobin and impaired
cardiac output. Alternatively, the signs and symptoms
HYPOCAPNIA
of hypoxemia may appear at lower arterial oxygen
levels, (e.g., in patients with chronic airflow limita­ Acute reductions in arterial carbon dioxide levels
tion who have adapted to reduced Pao2 levels). (hypocapnia) results in alkalosis and diminished cere­
bral blood flow secondary to cerebral vasoconstric­
tion. The major consequences of abrupt lowering of
HYPEROXIA
Paco2 are altered peripheral and central nerve func­
Mean tissue oxygen tensions rise less than 10 mm Hg tion. Mechanical ventilation may initially cause an
when pure oxygen is administered to a healthy sub­ abrupt decrease in arterial PC02 and lead to a Iife­
ject under normal conditions. Therefore the function threatening situation. In addition to blood gas anaJy-

FIGURE 15-5
BCG oscilloscope, printout for BCG. Note defibrillator paddles and BP cuff on shelf.

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 15 Systems in the Intensive Care Vnit 239

end tidal measurement is useful in that it chest to provide mal information regarding
provides an index of in rhythm and heart rate, and thereby ensure
close patient monitoring. The positive electrode is
positioned at the fourth intercostal space at the right
HYPERCAPNIA
sternal border. The electrode is at
CO2, the principal end product of metabolism, is a the first intercosta l space in the left midclavicular
relative benign gas. has a key role in ventilation line. The electrode used to electrical
and in in cerebral blood pH, interference is often at the first intercostal
and tone. Acute increases in space in the midclavicular line, the
capnia) depress level of consciousness ground electrode may be wherever conve­
the effect of acidosis on the nervous nient. Other electrode placements may be required,
but slowly increases in for in with or in pa­
relatively well-tolerated. A high is tients with chest burns. The electrode wires are usu­
of alveolar which causes a reduction secured to the patient's gown.
in alveolar and arterial Some patients with se­ Problems with the monitor result from
vere chronic airflow obstruction have been rPT,r.rtp(,\ faulty electrical and move­
to be able to lead relatively normal lives with ment artifact. A thickened baseline can be caused
in excess of 90 mm Hg if hypoxemia is countered Ie electrical interference. An erratic
with supplemental oxygen. Acute administration of often results from and movement. The
oxygen to with chronic disease, how­ cause of any must be explained and unto­
ever, may be because it inteli'eres with the ward in electrical activity of the myocardium
hypoxic drive to breathe observed in these ruled out. It is a dangerous practice for the PT to turn
Acute enhances sympathetic stimula­ off the ECG alarm system during treatment.
an increase in cardiac and in pe­ Cardiac can be broadly
vascular resistance. These effects may help into t a c h dy s r h y th m i a s a n d b radydysrhythmias.
to offset the effect of excess ion on the car­ Tachydysrhythmias are subdivided into
diovascular system, allowing better tolerance of flow ular and subjunctional tachycardias. Bradydysrhyth­
than with metabolic acidosis of a similar degree. mias are subdivided into sinus bradycardia, and those
At extreme levels of hypercapnia, muscle related to heart block and conduction abnormalities.
and seizures may be observed. Trends in Paco2 can The subjunctional or ventricular dys­
be monitored end tidal CO2 measurements. rhythmias are Ventricular
dia and ventricular fibrillation are medical emergen­
cies immediate and treatment.
MONITORING
The characteristic features of ECG
A channel ECG monitor with an oscilloscope, are illustrated in Chapter 11. PTs
strip recorder, and digital heart rate display is in ICU management should be thoroughly famil­
cally located above the at bedside in the lCU iar with ECG interpretation and the implications of
\5-5). The ECG can often be observed both the various dysrhythmias for management.
at bedside as well as at a central monitoring console, For further elaboration of ECG application and inter­
where the ECGs of all patients monitored can pretation refer to Andreoli, Fowkes, and Wal­
be observed lace ( 1991), Dubin (1989), and Fisher (1981).
The ECG monitor allows for continuous surveil­
lance of the of Low and
Clinical Picture
heart rates are determined below and above
which the alarm will be For routine moni­ The clinical associated with dysrhythmic ac­
in the coronary care unit, a modified chest lead tivity of the heart on the nature of the dys­
is often used. Three electrodes are positioned on the rhythmia, the age and condition of the patient, and

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240 PART II Cardiopulmonary Assessment

TABLE 15·4

Clinical Picture of Common Dysrhythmias

IN HEALTHY INDIVIDUALS WITH NO IN INDIVIDUALS WITH

UNDERLYING CARDIOVASCULAR UNDERLYING CARDIOVASCULAR
DYSRHYTHMIA DISEASE DISEASE

I. Tachycardias
A. Supraventricular No symptoms May precipitate
tachycardia Abrupt onset palpitations, light-headness congestive heart failure, acute
nausea, fatigue coronary insufficiency, myocardial
infarction, pulmonary edema
1. Sinus tachycardia Awareness of the heart on exertion Secondary to some precipitating
or with anxiety factor, e.g., fever, electrolyte
imbalance, anemia, blood and fluid
loss, infection, persistent hypoxemia
in COPD, acute MI, congestive
heart failure, thyrotoxicosis
2. Paroxysmal atrial Prevalent, sudden onset, precipitated by Common supraventricular
tachycardia (PAT) coffee, smoking, and exhaustion tachycardia
Spontaneous onset of regular
palpitations that can last for several
hours
May be obscured by myocardial
insufficiency and CHF in older
patients
Increased anxiety and report
of fatigue
3. Atrial flutter Rare Rapid regular-irregular rate
May be difficult to distinguish from PAT Suggests block at AV node
May be precipitated by alcohol, smoking, Atrial flutter waves in jugular venous
physical and emotional strain pulse
4. Atrial fibrillation Rare, occasionally with alcohol excess Usually secondary to a variety
in the young of cardiac disorders
5. Paroxysmal atrial Rare Common arrhythmia seen with
tachycardia with block digitalis toxicity
B. Subjunctional Rare Usually related to MI, pulmonary
embolus, severe CHF
Often unconscious, cyanotic,
ineffective pulse, blood pressure
and respiration
I. Ventricular tachycardia Rare Predisposed to ventricular fibrillation
2. Ventricular fibrillation Rare Ineffective cardiac Ol tpUt,
unconscious, dusky, cardiac
arrest threatens

II. Bradycardias
A. Sinus bradycardia Physiologic in very fit young adults In older patients may suggest sinus
node and conduction system
pathology; can produce syncope or
congc:-;tive heart failure
B. Heart block Rare Hypotension, dizziness, Iight­
headedness, syncope
In chronic block with sustained
bradycardia, congestive heart failure
may be more frequent

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 15 Monitoring Systems in the Intensive Care Unit 241

TABLE 15-4

Clinical Picture of Common Dysrhythmias

IN HEAL THY INDIVIDUALS WITH NO IN INDIVIDUALS WITH

UNDERLYING CARDIOVASCULAR UNDERLYING CARDIOVASCULAR
DYSRHYTHMIA DISEASE DISEASE

Most common dysrhythmia

iatrogenically produced with
digitalis excess
Associated with numerous cardiac
conditions; commonly in age­
related degenerative disease in
conducting system, inferior and
occasionally anterior Mis

specifically the absence or presence of underlying be measured directly from this line. A digital moni­
heart disease. Distinguishing clinical features of com­ tor displays systolic and diastolic blood pressures
mon atrial and ventricular dysrhythmias are outlined above the patient at bedside. High and low blood
in Table IS-4. pressure levels are set, above and below which the
The subjunctional or ventlicular dysrhythmias are alarm will sound. Blood gas analysis can be per­
typically associated with an extremely ill individual. formed routinely with an intraarterial line in place
Cyanosis and duskiness of the mucosal linings and pe­ without repeated puncturing of a blood vessel (Fig­
riphery may be apparent. The patient is unresponsive, ure IS-6).
the pulse if ineffective, and spontaneous respirations
are likely absent. Defibrillation is initiated to restore
Pulmonary Artery Balloon Flotation Catheter
an effective, more normal rhythm. The high incidence
(Swan Ganz Catheter)
of myocardial conduction ilTegularities warrants a de­
fibrillator being present at all times in the lCU for The pulmonary artery balloon floatation catheter or
rapid implementation of this commOn cardioversion Swan Ganz catheter is designed to provide an accu­
procedure by the medical personnel. Ventricular dys­ rate and convenient means of hemodynamic assess­
rhythmias may be tolerated better if ventricular rate is ment in the lCU (Buchbinder, and Ganz, 1976; For­
low, thereby improving cardiac output. Even in this rester, Diamond, McHugh, and Swan, 1971; Swan,
circumstance, however, these dysrhythmias still pre­ 1975). The catheter is usually inserted into the inter­
sent an emergency. nal jugular vein, the subclavian vein, or a large pe­
The ECG of a patient with a pacemaker will re­ ripheral arm vein and directed by the flow of blood
flect either an imposed fixed or intermittent rhythm into the right ventricle and pulmonary artery (see
and rate depending on whether a fixed rate or demand Figure IS-3A (arrow), p. 233). The catheter is se­
pacemaker has been inserted. curely taped to the patient's anTI, which is splinted
with an arm board to prevent dislodging. The proce­
dure is generally associated with little risk and dis­
Intra-Arterial Lines
comfort. Some of the complications that have been
An arterial line is established by direct arterial punc­ associated with pulmonary artery catheterization,
ture, usually of the radial artery. Blood pressure can however, include infection, venous thrombosis, my­

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242 PART II Cardiopulmonary Assessment

atrial pressure (LAP) and the pressure in the left

ventricle (LVP). More elaborate catheters have pac­
ing wires, thermistors for cardiac output determina­
tion, and sensors for arterial saturation. Figure 15-7
shows the normal cardiac pressures in each heart
chamber. Abnormal cardiopulmonary function may
vary these readings.
The PAP increases as a result of elevated pul­
monary blood flow, increased pulmonary arteriolar
resistance secondary to primary pulmonary hyperten­
sion or mitral stenosis, and left ventricular failure.
Measurement of PAP and PAWP in particular allows
for more prudent management of heart failure and
cardiogenic shock.
The PAP, PAWP, and end diastolic LVP are di­
rectly related. Impaired left ventricular contractility
that compromises normal emptying, (e.g., left ven­
tricular failure, mitral stenosis, or mitral insuffi­
ciency), result in an elevated end diastolic LVP,
which in turn elevates PAWP and PAP. An end dias­
tolic PAP or PAWP greater than 12 0101 Hg is consid­
ered abnormal.
The PAP and PAWP are low during hypotension
secondary to hypovolemia. Infusion of normal saline,
FIGURE 15-6 whole blood, or low molecular weight Dextran ele­
Intraarterial blood gas line.
vates the blood volume and blood pressure. Restora­
tion of blood volume returns end diastolic PAP and
PAWP to normal.
Elevation of the end diastolic PAP secondary to
ocardial irritation, air embolism, and pulmonary is­ heart failure with pulmonary edema can typically
chemia or infarct to segmental lung tissue (Puri, be reduced with appropriate medication. The effec­
Carlson, Bander, and Weil, 1980). tiveness of a drug and its prescription parameters
Complex catheters are available for monitoring a can be assessed by the observed changes in the end
variety of parameters. In a two-lumen catheter, the diastolic PAP.
first lumen is used to measure pulmonary artery Deterioration of cardiovascular status and wors­
pressure (PAP) and obtain mixed venous blood sam­ ening of the clinical signs and symptoms of heart
ples. The second lumen terminates in a balloon with failure elevate end diastolic PAP and PAWP, de­
a volume of less than 1 011, which is inflated and de­ crease cardiac output, decrease arterial and right
flated to obtain pulmonary artery occlusion or atrial oxygen tension, a!ld increase the oxygen dif­
wedge pressure (PAOP or PA WP). The average ference between arterial and venous blood. As the
range of the systolic PAP is 20 to 30 mOl Hg, and heart pump continues to fail, arterial oxygen ten­
normally reflects right ventricular pressure (RVP). sion decreases suggesting abnormal lung function
The diastolic PAP ranges from 7 to 12 mOl Hg and and probably elevated LAP. Pulmonary dysfunction
reflects left ventricular pressure in the absence of at this stage includes diffusion abnormalities, redis­
pulmonary disease. The average range of PA WP is tribution of pulmonary blood flow into the less
8 to 120101 Hg and gives an estimation of mean left well-ventilated upper lobes, and right to left shunt­

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 15 Monitoring Systems in the Intensive Care Unit 243

Pulmonary Artery

Aorta

Left Ventricle

Right Ventricle

FIGURE 15·7
Normal cardiac pressures in each heart chamber.

MEASUREMENT OF CENTRAL VENOUS PRESSURE

ing. All patients with acute infarction or shock have
reduced arterial oxygen tension. Pulmonary conges­ Central venous pressure (CVP) is monitored by means
tion must be cleared before the patient responds to of a venous line or catheter inserted into the subclavian,
oxygen administration. basilic, jugular or femoral vein (see Figure 15-3A,
Despite the enormous benefits of direct invasive p. 233). The catheter is advanced to the right atrium by
hemodynamic monitoring to patient assessment and way of the inferior or superior vena cava depending on
management, the benefits of basic hemodynamic as­ the site of insertion. Minimal risk of phlebitis or infec­
sessment are a fundamental part of the cardiopul­ tion is associated with this procedure.
monary assessment regardless of whether the patient Central venous pressure is the blood pressure mea­
has an invasive line in or not (Kirby, Taylor, and sured in the vena cavae or right atrium. Normal CVP
Civetta, 1990). Basic hemodynamic monitoring in­ is approximately 0 to 5 cm H20 and 5 to 10 cm H20
cludes heart rate, ECG, blood pressure, and periph­ if measured at the sternal notch and midaxillary line,
eral tissue pelfusion. respectively. Essentially the CVP provides informa­
tion about the adequacy of right-sided heart function,
including effective circulating blood volume, effec­
INTRAVENOUS LINES
tiveness of the heart as a pump, vascular tone, and
IV lines are routinely established in the supelficial venous return. Measurement of CVP is particularly
veins of patients, such as in the hand, usually before useful in assessing fluid volume and fluid replace­
admission to the ICU. These lines provide an imme­ ment. If the patient has chronic airflow limitation,
diate route for fluids, electrolytes, nutrition, and med­ ventricular ischemia, or infarction, the CVP will re­
ications. The specific lines used depend on the pa­ flect changes in pathology rather than fluid volume.
tient's individual needs determined by the history, Specifically, CVP provides an index of RAP. The
laboratory tests, and physical examination. relationship between RAP and end diastolic LVP is

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244 PART II Cardiopulmonary Assessment

unreliable; therefore end diastolic PAP and PA WP into the femoral artery. To maintain proper placement
are used as the principal indicators of cardiopul­ and good circulation, the leg must be extended. The
monary sufficiency in patients in failure and shock. presence of an intraaortic balloon must be taken into
consideration whenever the patient is being treated
and positioned. Inflation and deflation of the balloon
INTRAAORTIC BALLOON
with helium is correlated with the ECG. The intraaor­
COUNTER PULSATION (IABP)
tic balloon is deflated during venlricular systole and
Intraaortic balloon counter pulsation (Figure 15-8) assists the emptying of the aorta. Stroke volume is
provides mechanical circulatory assistance with the potentiated, afterload is reduced (hence, ventricular
use of an intraaortic balloon. The balloon is inserted pressure), and myocardial oxygen delivery enhanced.

FIGURE 15-8
A, Patient near the window is receiving intraaortic balloon pump (lABP) support. B, Close-up of an IABP unit.

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 15 Monitoring Systems in the Intensive Care Unit 245

The balloon is inflated during diastole, thereby neurons; progressive muscle weakness results. A con­
restoring arterial pressure and coronary perfusion. tralateral weakened hand grasp, for example, may
Counterpulsation improves cardiac output, reduces progress to hemiparesis or hemiplegia. The Babinski
evidence of myocardial ischemia, and reduces ST­ sign, hyperreflexia, and rigidity are additional motor
segment elevation. lntraaortic balloon counterpulsa­ signs that provide evidence of decreasing motor func­
tion is commonly used after open heart surgery, for tion as a result of upper motor neuron involvement.
CHF, medically refractive myocardial ischemia, ven­ Herniation can produce incoordinate respirations
tricular septal defects, and left main coronary stenosis that are correlated with the level of brainstern com­
in patients who have shock. The intraaortic balloon pression. Cerebrate rigidity results from tentorial
pump provides protection for the myocardium in herniation of the upper brainstem. This results in
many instances until surgery can be pelformed. Limb blocking of the motor inhibitory fibers and the famil­
ischemia, the most common complication, occurs in iar extended body posture. Seizures may be present.
10% to 15% of patients. These neuromuscular changes may further com­
Left ventricular assist devices are used postopera­ pound existing cardiopulmonary complications in
tively in patients following open heart surgery who the ICU patient.
have developed cardiogenic shock and are unrespon­ Clinically, increased rcp is best detected by altered
sive to conventional management. These devices take consciousness, blood pressure, pulse, pupillary re­
over the pumping action of the left ventricle and de­ sponses, movement, temperature, and respiration
crease myocardial workload and oxygen consump­ (Luce, 1985). The rcp monitor provides direct mea­
tion. These types of assistive devices may have con­ surement of ICP. A hollow screw is positioned through
siderable potential in the management of refractory the skull into the subarachnoid space. The screw is at­
heart failure. tached to a Luer-Lok, which is connected to a trans­
ducer and oscilloscope for continuous monitoring.
The prevention of further increase in rcp and a
MEASUREMENT OF INTRACRANIAL PRESSURE
corresponding reduction in cerebral perfusion pressure
rncreased intracranial pressure (ICP) resu Its from is a treatment priority. High ICP and low cerebral per­
many neurological insults including head injury, hy­ fusion pressure are highly con-elated with brain injury.
poxic brain damage, or cerebral tumor, and may re­ Measures to reduce venous volume are maintained
quire surgery. rn the adult, the cranial vault is rigid until ICP has stabilized within normal range. Prudent
and noncompliant. rncreases in the volume of the cra­ body positioning is used to enhance venous drainage
nial contents result in an elevated ICP and decreased by elevating the bed 15 to 30 degrees and maintaining
cerebral perfusion pressure. the head above heart level. Neck flexion is avoided.
Changes in consciousness are the earliest and most Fluid intake and output are carefully monitored; the
sensitive indicators of increased rcp (Borozny, 1987; patient may need to be fluid restricted. The Valsalva
Luce, 1985). Altered consciousness reflects herniation maneuver is avoided, since intrathoracic pressure and
of the brainstem and compression of the midbrain. rcp may increase correspondingly.
Compression of the oculomotor nerve and the pupillo­ Normal range of ICP is 0 to \0 mm Hg for adults,
constrictor fibers results in abnormal pupillary reac­ and 0 to 5 mm Hg for patients under 6 years of age.
tions associated with brain damage. The ICP may reach 50 mm Hg in the normal brain;
The effect of rcp on blood pressure and pulse is typically, however, this pressure returns to baseline
variable. Blood pressure may be elevated secondary levels instantaneously. In patients with high levels of
to elevated rcp and hypoxia of the vasomotor cen­ rcp and low cerebral compliance, extra care must be
ter. A reflex decrease in pulse occurs as blood pres­ exercised during routine management and therapy.
sure rises. An ICP elicited by turning or suctioning up to 30 mm
Compression of upper motor neuron pathways in­ Hg may be acceptable provided the pressure drops
terrupts the transmission of impulses to lower motor immediately following removal of the pressure­

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246 PART IJ Cardiopulmonary Assessment

potentiating stimulus. Patients may be mechanically bency. The selection of treatment and the assessment
hyperventilated to keep arterial PC02 at low levels, of treatment response must be based upon quantita­
since hypercapnia dilates c e rebral v e s sels and tive evaluation of the parameters affecting oxygen
hypocapnia constricts them. transport and cardiopulmonary function. Meticulous
To establish whether a patient will tolerate a treat­ monitoring contributes substantially to more rational
ment that requires movement or body positioning, an management of the lCU patient (i.e., the optimization
indication of cerebral compliance is needed. This can of physical therapy efficacy, in addition to minimiz­
be obtained by observing changes in ICP during rou­ ing deleterious treatment outcomes).
tine nursing procedures or by titrating small degrees
of movement or position change and observe the rate
REVIEW QUESTIONS
at which the ICP returns to baseline following the
challenge. Rapid return to baseline minimizes the risk 1. Explain the determinants of fluid and electrolyte
of reduced cerebral perfusion pressure secondary to balance, and factors that contribute to fluid ex­
the increased lCP. A slow return to baseline or sus­ cesses and deficits.
tained elevation of rcp is consistent with poor cere­ 2. Describe the basis of acid and base balance.
bral compliance and indicates treatment should be 3. Describe the physiological effects of hypoxia
modified or possibly not performed at all depending and hypercapnia.
on the absolute level of the lCP. 4. Explain the physiologic basis of ECG monitoring
and common supraventricular and ventricular
dysrhythmias.
ELECTROENCEPHALOGRAM MONITOR
5. Explain (a) the physiologic basis of the pul­
An electroencephalogram, or EEG, provides useful monary artery balloon floatation catheter, and (b)
information about gross cerebral functioning and what is represented by altered CYP, RAP (sys­
changes in level of consciousness. A single-channel tolic and diastolic), PAP (systolic and diastolic),
EEG monitor can be readily used in the lCU to reveal and the PAOP.
evidence of posttraumatic epilepsy when the clinical 6. Describe the basis of intra aortic balloon counter
signs may be inhibited by muscle relaxants. An EEG pulsation.
assessment may also be of some benefit to the PT in 7. Describe intracranial pressure monitoring, its
assessing the effects of arousal, treatment and senso­ physiological basis and clinical implications.
rimotor stimulation on cerebral function.

References
SUMMARY
Andreoli. K. G., Fowkes. V. K.. Zipes. D. P .. & Wallace. A. G. (Eds.)

Monitoring cardiopulmonary function and oxygen (1991). Comprehensive cardilu: care (7th ed.). Sl. Louis: Mosby.
Barrdl. S. E. & Abbas. H. M. (1978). Monitoring during physio­
transport is an essential component of the manage­
therapy after open heart surgery. Physiotherapy. 64(9). 272-273.
ment of the patient in the lCU. Regulation of home­
Borozny. M. L. (1987). Intracranial hypertensi()n: Implications for
ostasis is disrupted in disease or following medical the physiotherapist. Physiotherapy Cwwdu. 39. 360-366.
and surgical interventions. PTs working in the unit Buchbinder, N. . & Ganz, W. (1976). Hemodynamic monitoring:

require a thorough understanding of homeostatic reg­ Invasive techniques. Anesthesi% gy. 45(2). \46-\55.
Burkj. N. K.. & Albert. R. K.'(1983). Noninvasive monitoring of
ulation and monitoring of fluid and electrolyte bal­
arterial blood gases. A report of the ACCP section on respira­
ance, acid base balance, and blood gases. Physical
tory pathophysiology. Chest. 83(4).666-670.
therapy has an essential role in res tOling homeostasis Copel L. c.. & Stolarik. A. (1991). Continuous Sv02 monitoring.
in patients requiring intensive care, using conserva­ A research review. Dimensions of Cri/ica/ C a re Nursin!i. lO,
tive, noninvasive approaches, in addition to averting 202-209.
Cromwell, L.. Wei bell. F. l, & Pfeiffer. E A. (1980). Biomedical
the musculoskeletal, neuromuscular, and multisystem
ins/rumentarion and measuremen/s (2nd ed.). Englewood
complications associated with immobility and recum­
Cliffs: Prentice-Hall.

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 15 Monitoring Systems ill the Intensive Care Unit 247

DeGowin, E, L, & DeGowin, R L (1981), Bedside diagnostic ex­ Oakes, D, F. (1988), Clincfal practitioners pocket 10 respira­
aminatioll (4th cd.). New York: Macmillan. lory care. Old Town: Health Educator Publications.
Dubin, D, (1989). Rapid illterprelatiotl of EKGs, (4th ed,), Tampa, Phipps, W. J., Long, B. & Woods, N. F. (Eds,). (1991). Med­
Fl.: Cover. iced-surgical nursing: concepts and clinical practice (4th ed.).
Fisher, J, D, (1981). Role of electrophysiologic testing in the St Louis: Mosby,
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PART III

Cardiopulmonary Physical
Therapy Interventions

Copyrighted Material
 Optimizing Treatment Prescription:
Relating Treatment to the Underlying
Pathophysiology

Elizabeth Dean

KEY TERMS Clinical decision making Pathophysiological factors

Extrinsic factors Problem definition

Intrinsic factors Problem list

Oxygen transport deficits Restricted mobility and recumbency factors

Oxygen transport threats Treatment prescription

INTRODUCTION I. What is the problem?

2. What is the treatment and why?
The purpose of this chapter is to provide a basis for
3. What is the course of treatment?
clinical decision making and treatment prescription in
cardiopulmonary physical therapy (CPPT) for patients This chapter focuses on the elements involved in
ranging from the medically unstable critically ill pa­ addressing these questions when managing a patient
tient to the medically stable patient with cardiopul­ with impaired to threatened oxygen transport. The
monary dysfunction living in the community. Clinical basic principles for relating CPPT treatment to the pa­
decision making and treatment prescription is based on tient's underlying pathophysiologic problems (i.e., the
the answers to three primary clinical questions related pathophysiological mechanisms responsible for im­
to oxygen transport. With respect to a given patient, pairment of oxygen transport and cardiopulmonary
the following must be considered: function) are described. A physiologically based treat­

251

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252 PART III Cardiopulmonary Physical Therapy Interventions

Fundamental Knowledge and Expertise Steps in Critical Problem-Solving De.flCits

to Critically Problem-Solve Deficits in in Oxygen Transport
Oxygen Transport
I. De t ermine what factors are specifically con­
Norm al c a rd i o p u l m o n ary a n d c a r d i o v a s cul ar tributing to impaired oxygen transport and which
anatomy. as well as physiology and how these are steps in the pathway are affected
affected by normal conditions such as aging and 2. Determine those factors that threaten oxygen
lifestyle habits (e . g .. smoking. stress. and the transport and the steps in the pathway that are
physical environment) involved
Physio lo gic adaptation to hypoxia and cardiopul­ 3. Determine the relative magnitude of the effect of
monary impairment each factor either impairing or threatening oxygen
Cardiopulmonary and cardiovascular pathophysiology transport, and prioritize the importance of each
and disease processes, and how these affect nonnal 4. Distinguish those factors that arc amenable and
cardiopulmonary and cardiovascular function those that are not amenable to CPPT in that the
Multisystem and integrative pathophysiology that latter will modify treatment and affect the moni­
can have a secondary effect on cardiopulmonary toring that is needed
function and oxygen transport 5. Giv en the answers to I through 4. select, priori­
Effects of medical. surgical, and nursing procedures tize, and apply specific treatments prescrip­
on oxygen transport and gas exchange tively to address each factor that nmtributes to
cardiopulmonary dysfunction and is amenable
Investigative laboratory procedures and tests and
toCPPT
their effects on cardiopulmonary function

Pharmacological effects on cardiopUlmonary function

ment hierarchy is presented, with the premise that detailed understanding of the relevant anatomy and
physiologic function, including oxygen transport, is physiology, multisystem and integrative pathophysiol­
optimal when humans are upright and moving. Apply­ ogy, the impact of medical, surgical, and nursing pro­
ing a systematic physiologic approach to the analysis cedures, the effect of various laboratory tests and pro­
of the patient's problems, with respect to deficits in the cedures, and the impact of pharmacological agents on
oxygen transport pathway, leads directly to the most cardiopulmonary function (see box above, at left).
efficacious treatments. Such an approach provides a For a given patient, the cardiopulmonary PT pre­
basis for modifying or discontinuing treatment based scribes treatment by extracting the relevant information
on the use of appropriate treatment outcome measures. from the history, laboratory tests and investigative pro­
cedures, and the assessment (see box above. at right).
Problems are prioritized based on the relative magni­
WHAT IS THE PROBLEM?
tude of each one's effect on impairment of oxygen
Oxygen transport is determined by a multitude of fac­ transport. Once the mechanisms for the cardiopul­
tors which affects different steps in the oxygen trans­ monary and cardiovascular dysfunction have been iden­
port pathway (see Figure I-I, p. 4) (Chapter I). For tified, specific treatments are selected and prioritized.
treatment to be directed specifically to the underlying
problems, the physical therapist (PT) needs to consider
The Problem list
several levels of analysis of the deficits contributing to
impaired or threatened oxygen transport. To be profi­
Impaired oxygen transport
cient in such analysis, the PT must have a thorough Two levels of problems need to be identified. namely,
knowledge of the multiple factors that contribute to ab­ functional and physiologic deficits. The functional
normal gas exchange. This knowledge base includes a deficits are those that affect the patient's ability to

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 16 Optimizing Treatment Prescription: Relating Treatment to the Underlying Pathophysiology 253

ExampLes of Deficits in and Threats to Steps in the Oxygen Transport Pathway

Central Control of Breathing

Altered central nervous system (CNS) afferent input and control of breathing
Impaired efferent pathways

Pharmacologic depression
Substance abuse depression

Airways

Aspiration related to lack of gastrointestinal (GI) motility

Aspiration secondary to esophageal retlux
Obstruction secondary to airway edema, bronchospasm, or mucus
Inhaled foreign bodies

Lungs

Altered breathing pattern secondary to decreased lung compliunce

Ineffective breathing pattern related to decreased diaphragmatic function and increased lung volumes, respiratory
muscle weakness, respiratory muscle fatigue, CNS dysfunction, guarding, reflex, fatigue, and re spirato ry inflam­
matory process
Ineffective airway clearance related to restricted mobility, immobility, sedation, and pulmonary dysfunction sec­
ondary to long smoking history, impaired mucociliary transport, absent cilia. or dyskinesia of cilia, retained secre­
tions, ineffective cough and mucociliary mechanisms, infection, inability to cough efficiently, artificial airway/in­
tubation and cndotracheal tube, drug-induced paralysis, and sedation
Large airway ob:,truction secondary to compliant oropharyngeal structures
Chest wall regidity and decreased compliance
Loss of normal chest wall excursion movements (pump and bucket handle motions) and capacity to move appropri­
ately in all three planes of motion
Chest wall and spinal deformity
Impaired lung t1uid balance and acute lung injury

Blood

Bleeding abnormalities, altered body temperature (hypothermia, hyperthermia). fever, inflammation, hypermetabo­
lism secondary to mediator systems
Altered body temperature related to integumentary disruption
Low hematocrit secondary to GI bleed (more prone to hypoxia)
Anemia
Thrombocytopenia
Dissemin ... ted intravascular coagulation
Abnorm... 1 clotting faclOrs (i,e" halance between clotting and not c1olling, sludging of blood)
Thromboelllboli
Bleeding disorders with liver disease; ...bnormal clotting factors

Continued,

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254 PART III Cardiopulmonary Physical Therapy Interventions

Examples of Deficits in and Threats to Steps ill the Oxygen Transport Pathway-cont'd

Gas Exchange

Alveolar collapse, atelectasis, intrapulmonary shunting or pulmonary edema, shallow breathing and tenacious mucus,
body position, consolidation and alveolar collapse, ventilation/perfusion mismatch, airway constriction, t1uid vol­
ume excess, pleural effusions. breathing at low lung volumes. abdominal distension and guarding. ineffective air­
way clearance, pulmonary microvascular thrombi and altered capillary permeability secondary to circulating medi­
ators. closure of small airways secondary to dynamic airway compression. decreased functional residual capacity,
and intrapulmonary shunting, increased lung surface tension

Diffusion defects

Respiratory Muscles

Upper abdominal surgery. weakness, fatigue. neuromuscular discase. ileus related to gastric distension, mechanical
dysfunction

Myocardial Perfusion

Coronary artery occlusion

Tachycardia

Potential for cardiac dysrhythmia related to reperfusion

Cardiac dysrhythmia related to myocardial hypoxia

Compression by edema or space-occupying lesions

Heart

Decreased venous return and cardiac output, secondary to volume deficit, ascites, myocardial ischemia, hemorrhage,
and coagulopathies

Conduction defects

Mechanical defects

Defects in electromechanical coupling

Abnormal distension characteristics

Abnomlal afterload

Blood Pressure

Volume deficit/bleeding

Alteration in peripheral tissue perfusion related to acute myocardial infarction. myocardial depression, maldistribu­
tion of blood volume, and altered cellular metabolism

Volume excess

Tissue Perfusion

Impaired cardiac output

Impaired secondary to disseminated microvascular thrombi

Atherosclerosis and thromboembolic events, decreased circulating blood volume. decreased circulating blood vol­
ume, decreased vascular integrity. and int1ammatory process

Decreased cardiac output related to reduced venous return. impaired right ventricular function, dysrhythmias, in­
creased afterload, and bradycardia

Low oxygen content in the blood

Thromhoembolism. vasoconstriction secondary to toxins. sepsis, etc., blood flow alterations and hypermetabolism
secondary to mediator systems

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 16 Optimizing Treatment Prescription: Relating Treatment to the Underlying Pathophysiology 255

Examples of Deficits in and Threats to Steps in the Oxygen Transport Pathway-cont'd

Fluid Volume Excess

Related to excessive intravenous administration

Related to impaired excretion

Apparent hypervolemia secondary to restricted mobility and recumbency (e.g., resulting from hemodynamic instability)

Renal failure

Water intoxication

Therapeutic volume expansion. acute myocardial infarction (MI) and acute renal failure. related to renal retention of
sodium and water and increased levels of aldosterone, renin, angiotensin II, and catecholamines

Fluid Volume Deficit

Fluid volume deficit related to volume losses during surgery and inadequate oral intake, blood loss, internal injuries
(e.g.. hematoma and third spacing phenomenon: hormonal imbalance; increased intestinal motility; vomiting; diar­
rhea: tluid sequestration in tissues; nasogastric (NG) suction and diarrhea: hypovolemia; sepsis and shock; surface
capillary leak and fluid loss as in burns and excoriated wounds; tluid shifts)

Tissue Oxygenation

MultisysteJll organ failure with allered peripheral tissue perfusion and gas exchange at the cellular level

Indirect Factors That Contribute to Oxygen Transport Deficits

Infection

Pulmonary and nonpulmonaty infection increase the demands on the oxygen transport system

Cognition

Impaired neurological status and ccntral cardiopulmonary control

Alleration in mental status secondary to inadequate cerebral perfusion with hypotension and cardiogenic shock

Sleep pattern disturbance; altered blood gases and fatigue

Anxiety and agitation relatcd to powerlessness and lack of knowledge, breathlessness, pharmacological paralysis, im­
paired verbal community secondary to intubation, paralysis etc.

Psychosocial Factors

Anxiety related to the condition, shllltncss of breath. hospitalization. et\:.

So\:ial isolation second.uy to impaired wl11l11unication

Fear and hopelessness

Pain response

Nutrition

Altered nutritional needs secondlllY to greater need than resting state (i.e.. increased caloric need and nutrients asso­
ciated with illness, inability to ingest food, inability to absorb food)

Restricted ingestion orders of food and water

High caloric needs sen)l1dary to infectious process and protein catabolism

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256 PART III Cardiopulmonary Physical Therapy Interventions

perform activities of daily living (ADLs) (e.g., re­

Factors That Call Impair Oxygell Trallsport
duced activity or exercise tolerance as a result of re­
duced peripheral oxygenation, reduced mobility re­ I. Cardiopulmonary pathophysiology
lated to deconditioning resulting from resting in bed, primary (acute, chronic, acute on chronic)
extremity or internal injury, anticoagulant therapy,
secondary (chronic, acute on chronic)
drug-induced paralysis, impaired physical mobility re­
Noncardiopulmonary pathophysiology that im­
lated to muscle weakness and partial paralysis, paraly­
pacts upon cardiopulmonary function
sis, depressed level of consciousness, and anemia).
2. Immobility-loss of physical exercise stress
Physiological deficits are those deficits in oxygen
Recumbency-loss of vertical gravitational stress
transport, specifically, at the individual steps in the
pathway, and oxygen transpolt overall. Examples of 3. Extrinsic factors (i.e., those related to the pa­
tient's care)
deficits at each step in the pathway appear in the
boxes on pp. 253-255. 4. Intrinsic factors (i.e .. those related to the patient)

Threatened oxygen transport

Although the complications of restricted mobility and
static body positions are well understood, the precise
prescription parameters for mobilization and body (see box above), namely, the underlying cardiopul­
positioning to avoid these complications have not monary pathophysiology, restricted mobility (loss of
been defined in detail. With respect to cardiopul­ physical exercise stress), recumbency (loss of vertical
monary complications, a one- or two- hourly turning gravitational stress), extrinsic factors (i.e., those re­
regi men is commonly accepted. For the flaccid or co­ lated to the patient's care), and intrinsic factors (i.e.,
matose patient, range-of-motion (ROM) exercises those related to the patient). These categories are ex­
every several hours facilitates blood flow through de­ panded and explained in detail in Chapter 17.
pendent areas and enhances alveolar ventilation as
Restricted mobility and recumbency:

well as mobilizes joints and muscles. Antiembolic

special examples of extrinsic factors

stockings and pneumatic compression devices are

routinely used to minimize circulatory stasis in the Although bed rest can be considered an extrinsic
legs and the potential for thrombi formation. factor (i.e., a therapeutic intervention that con­
The PT has a major role in preventing infection of tributes to cardiopulmonary dysfunction, the nega­
all types but particularly cardiopulmonary infections. tive sequelae of this intervention are often not fully
Both cardiopulmonary assessment and treatment in­ appreciated clinically based on the widespread use
volves handling and close physical contact with pa­ of rest in bed. Therefore to draw to the clinician's
tients. Thus the risk of nosocomial infection is high in attention that the effects of this intervention need to
hospitalized patients. Some standard means of prevent­ be considered in each patient, the effects of re­
ing infection include meticulous hand washing before stricted mobility and recumbency are analyzed sepa­
and after every patient, and care of invasive lines and rately (see Chapters 17 and 18).
catheters. The PT moves and repositions patients often,
thus it is essential that lines, leads, and catheters are
Treatment Goals
continuously monitored. The PT must consider when it
is appropriate to gown, mask and glove to protect and Once the deficits and threats to oxygen transport have
be protected from the patient adequately. been determined, the goals of treatment fall into three
categories: short-term, long-term, and preventive.
Factors that contribute to or

Short-term treatment goals include the following.

threaten oxygen transport
1. To correct or reverse acute cardiopulmonary
Those factors that can impair oxygen transport di­ dysfunction
rectly or threaten it fall into four primary categories, 2. To reduce the rate of deterioration

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 16 Optimizing Treatment Prescription: Relating Treatment to the Underlying Pathophysiology 257

3. To avoid worsening the patient's condition.

Common Treatment Goals in the Management of
Long-term treatment goals include:
the Patient With Cardiopulmonary Dysfunction
I. To enhance the efficiency of the steps in the
oxygen transport pathway overall OVERALL GOAL: To optimize or preserve oxy­
2. To enhance the efficiency of those specific gen transport and gas exchange

steps in the oxygen transport pathway that com­ Treatment directed at specific steps involved
pensate for impaired steps that may or may not Object to enhance the efficiency of all steps in the
be reversibly affected pathway
3. To maximize oxygen transport capacity to sus­ Augment medical management
tain maximal functional activity.
Coordinate with nursing management (e.g., in criti­
And preventive treatment goals include: cal care)
I. To prevent cardiopulmonary dysfunction
Goals Directed at Specific Steps in the Oxygen
2. To prevent multisystem organ complications
Transport Pathway
and nonpulmonary infection that will lead to
Maximize air entry and alveolar ventilation (mini­
further restricted movement and recumbency,
mize airflow resistance)
hence the potential for further deterioration
Maximize air distribution (optimize lung compli­
3. To provide supportive palliative care.
ance and chest wall compliance)

Maximize ventilation and perfusion matching

WHAT IS THE TREATMENT AND WHY?
Optimize diffusion
Clinical Decision Making
Optimize oxyhemoglobin saturation

The basis for clinical decision making in the man­ Reduce work of breathing (increased resistance, re­
agement of the cardiopulmonary patient is to pair the duced or excessive compliance)

most efficacious treatments specificall y with im­ Reduce work of the heart (increased preload, con­
paired or threatened steps in the oxygen transport traction. increased afterload)

pathway. In addition, the patient spends considerable Maximize efficiency of heart mechanics
time between treatments, thus optimal therapeutic ef­ Minimize electrocardiogram (ECG) irregularities
fect is dependent on the efficacy of "between treat­ (identify factors that contribute to irregularities;
ment" treatments (i.e., teaching the patient to carry anticipate problems)

out prescriptive treatment whenever possible and Optimize blood flow distribution
eliciting the assistance of the patient's family or Optimize oxygen extraction ratio
nursing staff).
Reduce excessive or unnecessary energy expenditure
When confined to hospital, many patients spend
Optimize carbon dioxide (C02) removal
considerable time recumbent and in restricted body
positions, turn and move less frequently, and are up­ Optimize blood volume

right and moving a smaller proportion of time. De­ Optimize hydration

pending on the oxygen transport deficits, the body

positions the patient assumes can have a positive,
negative or neutral effect on oxygen transport. Thus,
the positions the patient assumes and his or her re­
duced activity levels, must be monitored and any po­
tential ill effects anticipated and countered. goals and specific treatments are prioritized accord­
Some examples of some common treatment goals ing to the relative significance of the impact of each
in managing the patient with cardiopulmonary dys­ on oxygen transport.
function are shown in the box above. Specific treat­ A physiologically based treatment hierarchy is
ments are identified to address these goals and for shown in the box on p. 258 and 259, and the box on
each deficit or threat to oxygen transport. Treatment p. 260, top right. The treatment hierarchy is based on

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258 PART III Cardiopulmonary Physical Therapy Interventions

Physiologic Treatment Hierarchy for Treatment of Impaired Oxygen Transport

PREMISE: Position of optimal physiological function is being upright and moving

I. Mobilization and Exercise

Goal: To elicit an exercise stimulus that addresses one of the three effects on the various steps in the oxygen trans­
port pathway, or some combination

A. Acute effects

B. Long-term effect

C. Preventative effects

II. Body Positioning

Goal: To elicit a gravitational stimulus that simulates being upright and moving as much as possible i.e., adive. ac­
tive assisted or passive

A. Hemodynamic effects related to fluid shifts

B. Cardiopulmonary effects on ventilation anti its distribution, pelfusion. ventilation. and perfusion matching
and gas exchange

III. Breathing Control Maneuvers

Goal: To augment alveolar ventilation, to facilitate mucociliary transport. and to stimulate coughing

A. Coordinated breathing with activity and exercise

B. Spontaneous eucapnic hyperventilation

C. Maximal tidal breaths and movement in three dimensions

D. Sustained maximal inspiration

E. Pursed lip breathing to end tidal expiration

F. Incentive spirometry

IV. Coughing Maneuvers

Goal: To facilitate mucociliary clearance with the least effect on dynamic airway compression and adverse cardio­
vascular effects

A. Active and spontaneous cough with closed glottis

B. Active assist (self-supported or by other)

C. Modified coughing interventions with open glottis (e.g., forced expiratory technique, hulT)

V. Relaxation and Energy Conservation Interventions

Goal: To minimize the work of breathing. of the heart. and oxygen demand overall

A. Relaxation procedures at rest and during activity

B. Energy conservation, (i.e., balance of activity to rest, performing activities in an energy) efficient manner.
improved movement economy during activ:ty)

C. Pain control interventions

VI. ROM Exercises (Cardiopulmonary indications)

Goal: To stimulate alveolar ventilation and alter its distribution

A. Active

B. Assisted active

C. Passive

Continued.

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 16 Optimizing Treatment Prescription: Relating Treatment to the Underlying Pathophysiology 259

Physiologic Treatment Hierarchy for Treatment of Impaired Oxygen Transport-cont'd

VII. Postural Drainage Positioning

Goal: To facilitate airway clearance using gravitational effects

A. Bronchopulmonary segmental drainage positions

VIII. Manual Techniques

Goal: To facilitate airway clearam;e in conj unction with specific body positioning

A. Autogenic drainage

B. Manual percussion

C. Shaking and vibration

D. Deep breathing and coughing

IX. Suctioning

Goal: To fac ili tate the removal of airway secretions collected centrally

A. Open suction system

B. Closed suction system

C. Tracheal tickle

D. Instillation with saline

E. Use of manual intlation bag (bagging)

the premise that physiologic function, including oxy­

Treatment Plan
gen transport, is optimal when the human organism is
upright and moving. Thus the purpose of the hierar­ The treatment plan consists of those interventions
chy is to exploit those treatments that are most physi­ that will most expediently remediate the problems
ologic first (i.e., active mobilization and exercise in that have been identified. These interventions are pri­
the upright position). Therefore the hierarchy ranges oritized according to the greatest effect they are pre­
from the most physiologic interventions, that is, ac­ dicted to have on remediating the oxygen transport
tive mobilization and exercise in the upright position, deficit or minimizing any threat to oxygen transport,
to those interventions that are the least physiologic. and on maximizing the benefit-to-risk ratio. Depend­
The least physiological interventions, (i.e., conven­ ing on the specific treatment goals and the adequacy
tional chest physical therapy techniques such as of balance between oxygen supply and demand, coor­
ROM, postural drainage and percussion) may simu­ dinating physical therapy treatments with other care
late some of the physiologic effects of being upright (e.g., nursing care and certain tests and procedures) is
and moving; however, their effects are more limited often indicated.
and less scientifically well-substantiated, and affect
fewer steps in the oxygen transport pathway. Thus
Treatment Prescription
they do not substitute for more physiologic interven­
tions higher up in the treatment hierarchy. All inter­ Once the specific pathophysiological problems have
ventions featured in the hierarchy have some role in been identified, they are differentiated as: (I) those
the management of cardiopulmonary dysfunction, but that can be addressed by physical therapy (i.e., nonin­
are recruited in descending order to ensure that the vasive physical interventions) and (2) those that are
most physiological and efficacious interventions are not amenable to physical therapy but need to be con­
exploited first. sidered during treatment to determine whether treat­

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260 PART III Cardiopulmonary Physical Therapy Interventions

ment is contraindicated or needs to be modified, and

Use of Modalities and Aids
specific outcome and treatment response measures
are indicated. Goal: To incorporate the use of those modalities
Problems amenable to physical therapy are priori­ and aids that enhance the ahove interventions

tized, the treatment is indicated for each problem, and Modalities

its parameters are defined. The treatment goals are
Treadmill, ergometer, rowing machine
identified, that is, to reverse pathophysiological
Weights
mechanisms contributing to impaired oxygen trans­
Pulleys
port, to compensate for irreversible pathophysiologi­
cal deficits (improve efficiency of other steps in the Nebulizers and aerosols

oxygen transport pathway), to decelerate deteriora­ Flutter valve

tion, to avoid making patient worse palliative BYPAP' and CPApt
care/support/comfort, and for prevention. Based on
Incentive spirometer
the goal of treatment, the parameters for the treatment
prescription are defined. Treatment parameters in the Pharmacologic Agents
management of a cardiopulmonary patient are shown Oxygen
in the box below.
Bronchodilators

Antiintlammatories
WHAT IS THE COURSE OF TREATMENT? Mucolytics

Once a treatment has been prescribed, the prescrip­ Surfactant

tion must be reviewed at each treatment and modified Analgesics

accordingly, that is, change in the prescription para­
meters, as the patient's condition changes. In addi­ "Bilevel positive airway pressure
tion, the parameters may be modified within a treat- "'Continuous positive airway pressure

Parameters of the Treatment Prescription in the Management of the Cardiopulmonary Patient

Define parameters of treatment based on history, laboratory investigations, tests, and assessment

Treatment type

Intensity (if applicable)

Duration

Frequency

Instruct patient in "between treatment" treatment, and if applicable the nurse. a family member. or both

Reassessment every treatment

Modify as necessary within each treatment

Progress between treatments as indicated

Define treatment outcomes

Determine when treatment is to be discontinued

Request for additional supportive information. tests, and investigations as indicated

Predict time course for optimal effects and course of treatment to determine treatment efficacy; modify as necess,u'y

In conjunction with other interventions (e.g., medical, surgical, nursing, respiratory therapy (weaning» oxygen sup-
plementation. sympathomimetic drugs, ADLs, balance with sleep and rest periods. peak of nutrition and feeds. peak
energy times. peak of drug potency and effects (e.g., pain, reduced sedation. reduced neuromuscular blockade)

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 16 Optimizing Treatment Prescription: Relating Treatment to the Underlying Pathophysiology 261

Assessment and Treatment Outcome Measures Used in the Management of Deficits in Oxygen Transport
Pathway

Central Control of 8reathing 8 Iood-cont 'd

Central drive to breathe test Platelets

Arterial blood gases Hemoglobin

Cerebral perfusion Coagulability

Ambient Air Viscosity

Partial pressures of 02. Nl and CO2 Stasis

Air pollution and quality Hydration

Humidity Immunological status

Pulmonary Circulation
Airways
Pelfusion scan
Clinical assessment including auscultation
Pulmonary artery balloon t1oatation catheter to assess
Pullllonary function tests
central venous pressure, pulmonary artery pres­
Arterial blood gases sures, wedge pressure
Chest X-ray
Heart
Histamine challenge exercise tests
Clinical assessment including percussion. palpation.
Lungs and auscultation

Clinical assessment including inspection. percussion. Inspection and clinical observation tests including
palpation and auscultation jugular venous distension test

Pulmonary function tests Heart rate, systolic and diastolic blood pressures, and
rate pressure product
Ventilation and perfusion scans
ECG
Diffusion capacity test
Hemodynamic studies to assess cardiac output, stroke
Arterial blood gases
volume, cardiac distensibility. and ejection fraction
Chest X-my
Ultrasound procedures to examine mechanical integrity
lmmunulogical status
Scans
Respiratory muscle assessment
Coordination of electromechanical behavior of heart
Assessment of the structure and integrity of chest
Coronary artery perfusion studies
wall
Stress test
Lung water studies
Hemodynamic monitoring including central venous
Blood pressure, pulmonary artery pressures and wedge
Circulating blood volume and cardiac output pressure

Arterial oxygen content Angiography

Venous oxygen content Chest X-ray

Plasma volume Peripheral Circulation

Red and white blood cell counts Clinical assessment

Protein constituents Segmental blood pressures of the extremities

Cun/iIlLted.

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262 PART III Cardiopulmonary Physical Therapy Interventions

Assessment and Treatment Outcome Measures Used in the Management of Deficits ill Oxygen Transport
Pathway-colll'd

Peripheral Circulation--cont'd Tissue-colll'd

Ultrasound studies Vascularization of tissue

Arterial and venous lab studies and investigations Adequacy and efficiency of aJterial ,Uld venous tissue

Adequacy and efficiency of lymphatic drainage system Blood now

of the healt and lungs, and pelipheml circulation
Tissue fluid balance; hydrostatic pressure, oncotic
Stress test pressure, and lymphatic pressure

Tissue Blood work including serum lactates and SV02

Enzyme studies Tissue oxygenation and pH

Tissue biopsies Nutritional and hydration status

ment based on the patient's treatment response. The sential that these measures have certain characteris­
PT also bases the decision when to discontinue a tics. For example, measurements must be objective
given treatment as well as what overall cardiopul­ and their procedures standardized to maximize test va­
monary physical therapy to employ, based on treat­ lidity and reliability. Although PTs specialize in non­
ment response and outcome. invasive assessment procedures as well as treatments,
Measures to assess treatment response and out­ noninvasive measures are prone to imprecision, and
come are selected that reflect (J) the status of oxygen hence measurement error and unreliability. It is there­
transport overall, and (2) the integrity of the step or fore essential that assessment measurements are per­
steps in the oxygen transport pathway that were iden­ formed in a systematic manner according to measure­
tified as being the primary problems contributing to m e n t guid elines to maximize their quality and
cardiopulmonary or cardiovascular dysfunction in the usefulness in guiding and directing treatment (Chapter
original assessment (see box on pp. 261-262.) (see 6). Assessment measurements always precede any
Part II of this text). Cardiopulmonary dysfunction is treatment to ensure that treatment is appropriate, that
determined based on the history, assessment and lab­ is, the baseline measurements. Measurements during
oratory investigations, such as, pulmonary function treatment provides information about the patient's re­
testing, breathing pattern, cardiac function testing, sponses, both beneficial and detrimental. This feed­
fluid balance and renal function, anerial blood gases, back determines the parameters of treatment, and
arterial saturation, vital signs, and hemodynamic whether the treatment should be modified in some
variables, including heart rate and ECG, blood pres­ way, or possibly discontinued. The overall treatment
sure, and rate pressure product. Subjective repOits are response is established by further monitoring and as­
also clinically relevant, such as subjective ratings of sessment at the termination of treatment, and often at
perceived exertion, breathlessness, angina, and fa­ peliodic intervals posttreatment so that delayed effects
tigue. These same measures are used to detect im­ can be monitored. Frequent and periodic measure­
proved oxygen transport and gas exchange. ments over time are refelTed to as serial measurements
Considering that clinical decision making is based and provide useful trend data. The pre- and posttreat­
largely on the results of tests and measures, it is es­ ment responses and any noteworthy responses during

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 16 Optimizing Treatment Prescription: Relating Treatment to the Underlying Pathophysiology 263

treatment are charted with sufficient information REVIEWaUESTlONS

about the procedurcs that were used, that is, assess­
I. Describe the use of the oxygen transport pathway
ment as well as treatment procedures.
as a conceptual model of cardiopulmonary prac­
PTs often require the results of invasive tests such
tice and basis for defining problems related to
as blood work or invasive hemodynamic monitoring
cardiopulmonary dysfunction.
to establish treatment response and outcome; thus,
2. Distinguish between short-term goals, long-term
these need to be requested as required.
goals and preventive goals of cardiopulmonary
physical therapy management.
SUMMARY 3. Explain and distinguish the four categories of
factors (i.e., pathophysiology, restricted mobility
This chapter has provided a framework for clinical
and recumbency, extrinsic, and intrinsic) that
problem solving and decision making based on oxygen
contribute to cardiopulmonary dysfunction.
transport. The process includes diagnosis and treatment
4. Describe the factors that need to be considered in
prescription in the management of patients with car­
treatment prescription.
diopulmonary dysfunction ranging from the medically
5. Desclibe the factors that must be considered In
unstable critically ill patient to the medically stable pa­
determining the course of treatment.
tient with cardiopulmonary dysfunction living in the
community. The purpose of a systematic approach to
clinical decision making is to maximize treatment effi­ Bibliography
cacy and cost effectiveness by focusing on physiologi­ Barlow, D.H., Hayes, S.c., & Nelson, R.O. (1984). The scientist
cal and evidence-based practice. The clinical decision practitioner. Research and accounlahiliry in clinical and edu­

making process involves diagnosis, that is, specific cational sellings. New York: Pergamon Press.
Cutler, P. (1985). Problem solving in clinical medicine. (2nd ed.).
analysis of the patient's problems in relation to the
Baltimore: Williams and Wilkins.
physiology and underling pathophysiology, the contri­
Dantzker, D.R. (1991). Cardiopulmonary critical care. (2nd ed.).
bution of restricted mobility and recumbency, and ex­ Philadelphia: WB Saunders.
trinsic and intrinsic factors. Based on this analysis, Dean, E. (1994). Oxygen transport: A physiologically-based con­

treatment interventions and their parameters are pre­ ceptual framework for the practice of cardiopulmonary physio­
therapy. Physiotherapy, 80, 347-355.
sClibed that have the greatest physiological and scien­
Epstein, C.D.,& Henning R.1. (1993). Oxygen transpOlt variables
tific justification. Treatments and their prescription pa­
,

in the identification and treatment of tissue h ypox i a Heart &

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rameters should have a clear, justifiable rationale. L"ng, 22, 328-348.

Specific monitoring of the steps in the oxygen transport Goldring, R.M. (1984). Specific defects in cardiopulmonary gas ex­
pathway that are impaired is essential to establish and change. American Review of Respiratory Diseases, 129, S57-S59.
confu'm the diagnoses, determine the most efficacious Hillegass, E.A., & Sadowsky, H.S. (1994). Essentials of cardiopul­
monary physical therapy. Philadelphia: WB Saunders.
treatment, evaluate the treatment response, refine and
Irwin, S., & Tecklin, J.S. (1995). Cardiopulmonary physical ther­
progress the treatment, and determine when to discon­ apy (3rd ed.). SI. Louis: Mosby.
tinue a given treatment and cardiopulmonary physical Patrick, D.E (1992). Clinical decision making. In Zadai C (Ed.).
therapy overall. The specific components of the treat­ Clinics in physical therapy. P"lmonCllY management in physi­
caltherapy. New York: Churchill Livingstone.
ment prescription include the treatment, its intensity (if
Riegelman, R.K. (1991). Minimizing medical mistakes. Boston:
applicable), duration, and frequency, as well as its
Little, Brown.
course and progression. A problem-solving approach to Schon, D.A. (1983). The rejlective practitioner. New York: Basic
patient care has become essential in all health care pro­ Books.
fessions, given the prohibitive cost of such care and the Wasserman, K., Hansen, J.E., Sue, D.Y., & Whipp, B.1. (1987).
Principles of exercise testing and interpretation. Philadelphia:
need for all health care to be physiological, evidence­
Lea & Fehiger.
based, cost-effective and ethically justifiable.

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 Mobilization and Exercise

Elizabeth Dean

KEY TERMS Exercise Prescription

Metabolic demand Recumbency factors
Mobilization Restricted mobil ity
Oxygen transport

INTRODUCTION
port in a large proportion of patients. The sequelae of
The first purpose of this chapter is to define the terms immobility and recumbency adversely affect all
mobilization and exercise and then to review the basis steps in the oxygen transport pathway. An under­
for prescribing mobilization and exercise as primary standing of the effects of immobility and reduced ex­
physical therapy treatment interventions to optimize ercise stress on normal human physiological function
oxygen transport. The three distinct objectives of mo­ provides the rationale for prescribing exercise for its
bilization and exercise for the purpose of maximizing preventive effects.
oxygen transport are described. These include the ex­
ploitation of their acute, long-term, and preventive ef­
DEFINITIONS
fects. Mobilization or exercise can be prescribed
specifically to elicit whjch of these effects is indicated. Mobilization is defined as the therapeutic and pre­
The second purpose of this chapter is to review scriptive application of low-intensity exercise in the
the negative effects of immobility and reduced exer­ management of cardiopulmonary dysfunction usually
cise stress on multisystem function with special at­ in acutely ill patients. Primarily, the goal of mobiliza­
tention to cardiopulmonary and cardiovascular func­ tion is to exploit the acute effects of exercise to opti­
tion. Immobility and recumbency are major factors mize oxygen transport. Even a relatively low-inten­
contributing to impaired or threatened oxygen trans- sity mobilization stimulus can impose considerable

265

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266 PART III Cardiopulmonary Physical Therapy Interventions

metabolic demand on the patient with cardiopul­ the submaximal exercise test have been less well-de­
monary compromise. In addition, mobilization is per­ fined (Dean and Ross, 1992a; Dean and Ross, 1993;
formed in the upright position, that is the physiologic Shepherd et aI, 1968).
position (Chapter 18), whcnever possible, to optimize The prescription of mobilization and exercise to
the effects of being upright on central and peripheral optimize oxygen transport in the patient with acute
hemodynamics and fluid shifts. Thus mobilization is cardiopulmonary dysfunction has been a relatively
prescribed to elicit both a gravitational stimulus and neglected area of research compared with exercise
an exercise stimulus. prescription in the management of chronic cardiopul­
Exercise is the term used to describe the therapeu­ monary dysfunction. This is surprising given that
tic and prescriptive application of exercise in the "early mobilization" is a key component of car­
management of subacute and chronic cardiopul­ diopulmonary physical therapy in the management of
monary and cardiovascular dysfunction. Primarily, acutely ill patients. Orlava (1959) was the first to re­
the goal of exercise is to exploit the cumulative ef­ port the beneficial application of mobilization in the
fects of and adaptation to long-term exercise and management of acute cardiopulmonary compromise,
thereby optimize the function of all steps in the oxy­ specifically, bronchopulmonary pneumonia. The
gen transport pathway. physiologic literature supports an unequivocal role
In addition, mobilization and exercise can be pre­ for therapeutic mobilization to maximize oxygen
scribed for their preventive effects. In this case, the transport in patients with acute cardiopulmonary dys­
parameters of the prescription focus on exploiting function (Dean and Ross, 1992b). Despite this con­
their multisystemic effects as well as their cardiopul­ clusive body of literature, Orlava's work has not been
monary and cardiovascular effects. extended significantly in the literature since her work
was published more than 35 years ago.
Unlike exercise prescription for the patient with
BASES FOR THE PRESCRIPTION
chronic cardiopulmonary and cardiovascular dys­
OF EXERCISE STRESS
function, the acute patient cannot be exercise tested
The prescription of exercise is fundamental in the in the conventional manner given the risks of an un­
management of primary and secondary cardiopul­ toward exercise response. Given the profound and di­
monary and cardiovascular dysfunction. Exercise sci­ rect effects of mobilization and exercise on car­
ence has advanced exponentially over the past 30 diopulmonary and cardiovascular function, it is
years and is a primary basis for cardiopulmonary essential that the physical therapist be able to identify
physical therapy. Guidelines have been developed for the specific effects of exercise required and define the
prescribing exercise to maximize functional work ca­ optimal therapeutic stimulus, ie, the stimulus that
pacity or aerobic capacity for healthy persons and in­ yields the maximal benefit to oxygen transport with
dividuals with chronic heart and lung disease (Ameri­ the least risk.
can College of Sports Medicine, 1994; Belman and Acute and chronic cardiopulmonary and cardio­
Wasserman, 1981; Blair, Painter, Pate, Smith and vascular pathology have the additional problem of
Taylor, 1988; Froelicher, 1987; Hasson, 1994; Irwin compromising functional capacity in two important
and Tecklin, 1985; Wasserman and Whipp, 1975; ways. First, in acute illness, the patient tends to be re­
Zadai, 1992). Exercise training is based on the find­ cumbent in bed a greater propOition of time, and sec­
ings of a maximum graded exercise test. Submaximal ond, in both acute and chronic illnesses, the physical
exercise testing is often indicated for patients with se­ activity of the patient is reduced. Recumbency and
verely impaired functional work capacity because of immobility have physiologically distinct effects on
the inherent risks associated with maximal testing oxygen transport and are the primary determinants of
(Compton, Eisenman, and Henderson, 1989). Guide­ bed rest deconditioning (Chase, Grave, and Rowell,
lines for submaximal exercise testing, test interpreta­ 1966; Convertino, Hung, Goldwater, and DeBusk,
tion and prescription of exercise, however, based on 1982; Winslow, 1985). Thus dysfunction of oxygen

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 17 Mobilization and Exercise 267

transport is further exacerbated in patients by the ad­ tions to remediate cardiopulmonary dysfunction, and
ditional factors of recumbency and immobility. The their effects exploited first.
impact of these factors is further exacerbated in
smokers, the young, older adults, obese individuals,
OXYGEN TRANSPORT AND METABOUC
and patients who are mechanically ventilated.
DEMAND IN PATIENTS
Even though the prescription of mobilization and
exercise for their acute effects ,is distinct from that for In health, when individuals have optimal physiologi­
its long-term effects, the efficacy of the acute exer­ cal reserve, both the acute and long-term responses to
cise stimuli needs to be considered in terms of opti­ an exercise stimulus can be predicted. Specifically,
mizing long-term benefit to oxygen transport as well minute ventilation (vE) and cardiac output (CO),
as the short-term acute effects. Both acute and long­ hence oxygen delivery (002), increase commensu­
term exercise needs to be prescribed specifically for a rate with work rate and oxygen demand.
given patient given the mechanisms of their underly­ In patients, whose oxygen transport capacity is re­
ing pathology (American College of Sports Medicine, duced or threatened, mobilization and exercise con­
1994). The prescription parameters should include stitute a significant additional metabolic demand that
(I) the type or types of mobilization or exercise, is superimposed on various other factors that con­
I (2) specific intensity, (3) duration, and (4) frequency. tribute to increased metabolic cost (see box on page
These parameters are defined for each type of ex­ 268). Hospitalized patients tend to be hypermeta­
ercise being prescribed. In addition, (5) the course of bolic. In addition to their basal metabolic demands,
the prescription, that is the time over which the pre­ their energy demands are increased secondary to such
scription is designed to produce its maximum benefit, factors as an increased body temperature, healing and
and (6) the means of progression of the prescription repair processes, increased work of breathing and of
are defined. the heart, and in response to routine interventions and
Exercise has been reported to have beneficial ef­ procedures including cardiopulmonary physical ther­
fects in the management of a multitude of conditions. apy. The goal, therefore, in prescribing mobilization
Its benefits range from enhancing all steps in the oxy­ and exercise, is to ensure a safety margin wherein the
gen transport pathway to other peripheral and central patient's demand for oxygen does not exceed the
effects related to virtually every other organ system. available supply or delivery. In most situations, this
The preventive effects of exercise are central to would be indicated clinically by worsening of the pa­
patient care across all conditions and physical therapy tient's oxygen transport objectively and subjectively.
specialties. Exercise is advocated preventively to Of the physical therapy related interventions, mobi­
avoid the deleterious effects of immobility and to lization, exercise, body positioning, arousal, breathing
provide optimal systemic health protection secondary control maneuvers, coughing, postural drainage, man­
to cardiopulmonary conditioning. ual techniques, bagging, suctioning and range-of-mo­
Mobilization and exercise are the physical thera­ tion (ROM) exercises can significantly increase oxy­
pist's (PT's) "drug" with definable indications, con­ gen consumption and overall metabolic demand
traindications, and side effects for each patient. The (Dean, Murphy, Parrent, and Rousseau, 1995; Weiss­
prescriptive parameters are determined by the effects mann, Kemper, Darvask, Askanazi, Hyman, and Kin­
needed to address the patient's underlying problems ney, 1984). Therefore, the capacity of the oxygen
directly, whenever possible. Mobilization and exer­ transport system to meet the patient's metabolic de­
cise constitute the most potent and direct interven­ mands needs to be established in the physical therapy
tions affecting oxygen transport that are available to assessment. Can the oxygen transport system support
the PT in that, unlike other cardiopulmonary physical the patient's metabolic demands? If so, what reserve
therapy interventions, they affect all steps in the oxy­ capacity is available to support a mobilization or exer­
gen transport pathway. Thus they need to be pre­ cise stimulus? The exercise stimulus is designed to ex­
scribed specifically as primary treatment interven­ ploit the potential of the reserve capacity. Establishing

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268 PART III Cardiopulmonary Physical Therapy Interventions

Factors That Contribute to Increased Metabolic Demand and Oxygen Consumption in Patient Populations

Pathophysiological Factors

Fever (e.g., secondary to an infectious agent or inflammation, surgery, multiple trauma, severe illness)

Thermoregulatory challenges (i.e., too hot or too cold, altered ambient temperature and humidity)

Healing and repairing (i.e., secondary to illness, trauma. surgery)

Com hatting infection

Interventions

Response to routine nursing, medical, and physical therapy inrerventions

Feeding: cnterally or parenterally

Physically being handled, e.g., by health care workers

Body positioning

Changing body position, i.e., passive. active assist, or active changes

ROM exercises, i.e., passive, active assist, or active

Mobilization and exercise

Noxious stimulation, e.g., injections, insertion of lines, procedures, neurological checks

Pharmacologic agents

Psychosocial Factors

Social contact, e.g., health care workers, family

Anxiety

Discomf0l1

Pain

Agitation

Miscellaneous

Noises

Disrupted circadian rhythms when ill, hospitalized or away from daylight

the availability of that reserve is essential to optimize cedures need to be applied in the management of pa­
the efficacy of the therapeutic exercise stimulus, that tients with cardiopulmonary and cardiovascular dys­
is, neither subthreshold or suprathreshold. function in situations in which agitation, anxiety and
Metabolic demand and oxygen uptake are deter­ pain contribute significantly to increased oxygen de­
mined by multiple factors. In patients, the effect of mand. This is especially true in intensive care, where
arousal, anxiety, pain, and noxious stimulation, in ad­ oxygen transport is compromised or threatened in
dition to the hypermetabolic demands of recovery, most patients (see Chapters 32 and 33).
contribute significantly to the energy cost and de­
mand on the oxygen transport system. Thus relaxing
CElLULAR ENERGETICS IN RESPONSE
and calming patients is a central component of car­
TO MOBILIZATION AND EXERCISE
diopulmonary physical therapy as these interventions
can minimize oxygen demand. Although relaxation, The cardiopulmonary unit supports oxygen transport
often coupled with analgesia is central to physical and cellular respiration (Weber, Janicko, Shroff, and
therapy management in other settings, relaxation pro­ Likoff, 1983). Oxygen is continually being Llsed by

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 17 Mobilization and Exercise 269

every cell in the body for oxidative phosphorylation layed rather than eliminated. In disease states, anaer­
and the synthesis of adenosine triphosphate (ATP). obic metabolism occurs when a patient's oxygen
The splitting of a phosphate bond from ATP to form transport system cannot meet the metabolic demand
adenosine diphosphate yields a considerable amount required, e.g., patients with sepsis and multisystem
of energy for metabolism. The e nergy for this organ failure. Serum lactate levels are significantly
process comes from the reduction of hydrogen in the elevated in these patients, resulting in metabolic aci­
formation of water and carbon dioxide, which is the dosis, which is extremely unfavorable to the mainte­
end products of the respiratory or electron transfer nance of homeostasis.
chain. These metabolic processes which comprise During exercise, the cellular P02 is lower than the
oxidative phosphorylation, take place in the mito­ surrounding interstitial fluid P02. Oxygen diffuses
chondria of the cells (Chapter I). rapidly through cell membranes. At the onset of
The balance of oxygen consumption to delivery physical exercise, the increased metabolic demand of
is precisely regulated to ensure that there is not the muscle and supporting tissues increases the oxy­
only an adequate supply of oxygen, but also that gen diffusion gradient. Feedback mechanisms are
under normal resting conditions approximately four triggered to increase oxygen delivery, which de­
times as much oxygen is delivered to the tissues as pends primarily on arterial oxygen content and car­
is used. This safety margin permits the immediate diac output. The first line of defense is the response
availability of oxygen when the system is perturbed to an increase in pericellular pH. The concentration
by physical, gravitational, and mental challenges of carbon dioxide is increased which, as a result of
(see Chapter I). the decrease in pH, facilitates the dissociation of
Anaerobic metabolism occurs during all out short oxygen from hemoglobin, that is, it shifts the oxyhe­
sprint type activities, e.g., hockey, soccer and volley moglobin dissociation curve to the right. The cardiac
ball. Although PTs tend to focus on aerobic rather than output (CO = SV x HR) increases commensurate
anaerobic training, in conditions where oxygen deliv­ with overall metabolic demand. The immediate re­
ery is significantly compromised, patients may rely on sponse to oxygen deficit is an increase in CO to in­
anaerobic metabolism to sustain ATP production and crease oxygen delivery. This averts arterial desatura­
break down to provide energy. Although anaerobic ex­ tion which is not normally observed in health even
ercise implies that the exercise is pelformed in the ab­ with extreme exertion.
sence of oxygen, anaerobic metabolism provides a The increase in systemic CO results in increased
short-term means of supporting phosphorylation using venous return and pulmonary CO. To oxygenate a
substrates other than oxygen to generate and split ATP. greater volume of blood in the lungs, an increased
If insufficient oxygen is available, the amount of ATP volume of air must be inspired. To effect an increase
that can be generated anaerobically is limited. Thus in VE, tidal volume (VT) and respiratory rate (RR)
this process can only be sustained for a short period. are increased. At low intensities of exercise, VT in­
Lactic acid accumulates in the blood during anaerobic creases disproportionately to RR, whereas at moderate
metabolism. In healthy, untrained individuals, lactic to high intensities, VT plateaus and further increases
acid increases exponentially at an exercise intensity of in VE are effected by an increase in RR (Jones and
about 55% of maximal aerobic capacity (McArdle, Campbell, 1982). Exercise is associated with a small
Katch, and Katch, 1994). Anaerobic capacity and but significant increase in airway diameter and length
specifically the anaerobic threshold can increase with of pulmonary structures, hence, a reduction is airway
training, however, anaerobic training effects are less resistance. Zone 2, that is, the zone of greatest ventila­
significant compared with the training effects achieved tion to pelfusion (V/Q) matching of the lungs, is in­
with aerobic training. creased as a result o pulmonary capillary dilatation
Anaerobic metabol ism is thought to be triggered and recruitment. Diaphragmatic excursion is enhanced
by tissue hypoxia. The term anaerobic is a misnomer and the distribution of ventilation and perfusion is
in that oxygen is needed to pay the oxygen debt that more uniform throughout the lung, which helps mini­
it creates. Thus in health, the need for oxygen is de­ mize atelectasis and airway closure. Exercise in­

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270 PART III Cardiopulmonary Physical Therapy Interventions

EFFECTS OF MOBILIZATION AND EXERCISE

creases the excursion, hence, inflation of the lungs in
ON OXYGEN TRANSPORT
three planes (i.e., anteroposterior, transverse, and
cephalocaudal, particularly in the upJight positions). In health, optimal function of oxygen transport de­
Rhythmic inflation and deflation of the lungs as­ pends on the integrity of each step in the oxygen trans­
sociated with physical activity has several clinically port pathway and the interdependent function of all the
important physiologic effects. First, this action in­ steps. As a result of cardiopulmonary and cardiovascu­
creases alveolar ventilation by a primary increase in lar dysfunction, one or more steps in the oxygen trans­
tidal volume. Second, exercise-induced lung motion port pathway can be affected. Because of the interde­
facilitates lymphatic flow and drainage. Optimal pendence of the steps in the pathway and the ability of
lymphatic drainage is essential to maintain optimal functional steps to compensate for dysfunctional steps,
lung fluid balance with the increased volume of gross measures of the efficacy of gas exchange and
blood being processed through the pulmonary circu­ oxygenation can be normal. The number of steps af­
lation and lung parenchyma. This action may ex­ fected by disease and the severity of the disease deter­
plain, in part, the beneficial effect of mobilization on mines the degree of impairment of oxygen transport
the distribution and function of pulmonary immune overall and the degree to which this is reflected in
factors (Pyne, 1994). The increased movement of the gross measures of oxygen transport as a whole.
lungs during exercise has a primary effect on mu­ To optimize the capacity of the various steps in the
cociliary transport and mucus clearance (Wolff, oxygen transport pathway, the oxygen transport sys­
Dolovich, Obminski, and Newhouse, 1977). Related tem needs to be exposed to two principal stressors:
to its effects on mucociliary transp0l1, physical activ­ (I) gravitational stress and (2) exercise stress. These
ity may help minimize bacterial colonization in the stressors are tantamount to life in that they enhance
airways, hence, reduce the risk of pulmonary infec­ the biochemical, physical and mechanical efficiency
tion (Skerrett, Niederman, and Fein, 1989). Finally, of the various steps in the oxygen transport pathway,
lung movement stimulates surfactant production and and the patient's ability to respond rapidly to changes
its distribution over parenchymal tissue. Surfactant is in the physical environment.
essential for reducing surface tension in the alveoli, The fact that the absence of gravitational stress
maintaining alveolar stability, maintaining lung com­ and exercise stress are the two primary factors con­
pliance, thereby, minimizing airway closure and tributing to bed rest deconditioning supports the ex­
areas of lung collapse. ploitation of both gravitational and exercise stress in
The heart and peripheral circulation are primed remediating cardiopulmonary dysfunction. Therefore
and respond to the increased demands of acute exer­ mobilization and exercise are the two most physio­
cise. Hemodynamic adjustments occur immediately logic interventions available to the PT for remediat­
with the onset of exercise stress. To maximize the ing cardiopulmonary dysfunction.
CO available, blood moves from the venous capaci­
tance reservoirs such as the venous compartments of
PRESCRIPTION OF MOBILIZATION AND EXERCISE:
the gut and extremities, particularly the legs. At rest,
ACUTE RESPONSES
most of the circulation, 70%, is contained within the
highly compliant venous circulation. The Starling The clinical decision-making process involved in
Law of the heart regulates the forward movement of defining the optimal mobilization and exercise stimu­
blood commensurate with the volume of blood that is lus is multifactorial. Based on the patient's history,
received. The heart chambers are normally distensi­ history of the present illness, assessment, and results
ble and adjust to changing volumes of blood return­ of the lab tests and procedures, the integrity of each
ing to the heart and pump more forcefully to eject it step in the oxygen transport pathway is determined,
through the pulmonary and peripheral circulations. and the integrity of this system overall to preserve ar­
Muscle enzymes that extract oxygen at the cellular terial oxygenation and pH. The box on p. 271 shows
level are also primed and are produced commensurate some common conditions associated with acute car­
with chronic metabolic demand.

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 17 Mobilization and Exercise 271

exploited are directed at each patient's specific

Acute Pathophysiological Conditions
pathophysiological deficits. Once the specific ef­
That Benefit From the Acute Effects
fects of acute mobilization or exercise that are
of Mobilization alld Exercise
needed are identified and matched to the patient's
Atelectasis pathophysiology, then the mobilization or exercise

Pulmonary consolidation stimulus can be prescribed (see box on p. 273).

The increased metabolic demand of acute exer­
Pulmonary intiltrates
cise results in a slight increase in airway diameter,
Bronchopulmonary and lobar pneumonias
increased VE, alveolar ventilation (VA), VT, RR,
Bronchiolitis
air flow rates, CO, SV, HR, blood pressure (BP),
Alveolitis rate pressure product (RPP), that is, product of heart
Pleural effusions rate and systolic blood pressure (RPP is highly cor­

Acute lung injury and pulmonary edema related with myocardial oxygen consumption, and
therefore myocardial work) oxygen consumption
Hemothorax
(V02), and carbon dioxide production (VC02). The
Pneumothorax
area of greatest ventilation to petfusion matching in
Cardiopulmonary insufficiency
the lungs, zone 2, is increased secondary to in­
Cardiopulmonary sequelae of surgery creased dilatation and recruitment of pulmonary
Cardiopulmonary sequelae of immobility capillaries (West, 1995).
The hemodynamic benefits of exercise are maxi­
mized in the upright position compared with recum­
bent positions in that exercise alone fails to counter
the loss of volume regulating mechanisms associated
with recumbency (Sandler, 1986) See Chapter 18 for
diopulmonary dysfunction for which a rational basis the effects of position changes.
can be made for exploiting the acute effects of mobi­ Mobilization and exercise stimulate the endocrine
lization as a primary treatment intervention. system. Catecholamines, released to support the car­
If the patient presents with acute cardiopul­ diovascular system, sustain a given exercise work
monary dysfunction, then primarily the acute ef­ rate. Increased sympathetic activity secondary to mo­
fects of mobilization are indicated. These effects bilization can help reduce the patient's need for sym­
are distinct from those that occur on assuming the pathomimetic pharmacologic agents (Bydgeman and
upright position. The majority of patients benefits Wahren, 1974). Sympathetic nerve stimulation, for
most from a mobilization and exercise stimulus example, is increased and sympathetic neurotransmit­
when they are in the upright position. The effects of ters are processed more efficiently. This is a signifi­
being upright vs. exercise. however, need to be cant effect that can be used as a goal for the prescrip­
considered separately so that the benefits of their tion of mobilization.
individual and combined contributions can be de­ Central nervous system (CNS) responses to mobi­
termined as well as any adverse reactions. The lization include arousal and priming of the various
physiological benefits of acute exercise are shown organ systems involved (Browse, 1965).
in the box on p. 272. The principal effects that re­ The prescription of mobilization and exercise to
mediate acute cardiopulmonary dysfunction are in­ stimulate their acute benefits parallels that of the pre­
creased VE secondary to increased VT, RR, or scription of exercise for its long-term, central and pe­
both; improved air flow rates and mucus transport. ripheral aerobic effects. The exercise parameters to
Cardiac output is increased secondarily to increased achieve long-term adaptations in healthy people have
stroke volume (SV), heart rate (HR) or both, and been well-defined by the American College of Sports
increased tissue perfusion. The particular benefits Medicine (1994) (Table 17-1) and are well-accepted.
of acute mobilization and exercise that need to be The individual engages in aerobic exercise at a heart

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272 PART III Cardiopulmonary Physical Therapy Interventions

Acute Physiological Effects of Mobilization and Exercise

Pulmonary System Lymphatic System----<oll't

i Regional ventilation i Pulmonary lymphatic drainage

i Regional perfusion Hematologic System

i Regional diffusion i Circulatory transit times
i Zone 2 (i.e., area of ventilation perfusion matching) !- Circulatory stasis
i Tidal volume
Neurological System
i or !- Breathing frequency
i Arousal
i Minute ventilation
i Cerebral electrical activity
i Efficiency of respiratory mechanics
i Stimulus to breathe
!- Airtlow resistance
i Sympathetic stimulation
i Flow rates
i Postural reflexes
i Strength and quality of a cough
Neuromuscular System
i Mucociliary transport and airway clearance
i Regional blood flow
i Distribution and function of pulmonary immune
i Oxygen extraction
factors
Endocrine System
Cardiovascular System
Hemodynamic effects i R e l e ase, di s t ribution, and degradation of
catecholamines
i Venous return
Genitourinary System
i Stroke volume
i Glomemlar tiltration
i Heal1 rate
i Urinary output
i Myocardial contractility
Gastrointestinal System
i Stroke volume, heart rate and cardiac output

i Coronary perfusion i Gut motility

!- Constipation
i Circulating blood volume

i Chest tube drainage Integumentary System

i Cutaneous circulation for thermoregulation

Peripheral circulatory effects
Multisystemic Effects
!- Peripheral vascular resistance
i Peripheral blood flow
!- Effects of anesthesia and sedation

!- Deleterious cardiopulmonary effects of surgery

i Peripheral tissue oxygen extraction
!- Risk of loss of gravitational stimulus (when in con­
Lymphatic System
junction with the upright position) and exercise
i Pulmonary lymphatic flow stimulus

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 17 Mobilization and Exercise 273

Clinical Decision Making and Prescription of Acute Mobilization and Exercise

Step 1

Identify ALL factors contributing to deficits in oxygen transp0l1 (Chapter I), that is, those factors contributed to by:

I. The underlying pathophysiology of the disease or condition

2. Imillobility and recumbcncy

3. Extrinsic factors related to the patient's care, and

4. Intrinsic factors related to the individual patient

Step 2

Determine whether mobilization and exercise are indicated, and if so, which form of either will specifically address
the oxygen transport deficits identified in Step I.

Step 3

Match the appropriate mobilization or exercise stimulus to patient's oxygen transport capacity.

EXAMPLES: activities of daily living (ADLs). walking unassisted, standing erect with assist and taking a few steps,
transferring from bed to chair*, seated dangling position over bed side, moving in bedt

Step 4

Set the intensity within therapeutic and safe limits of the patient's oxygen transport capacity.

Step 5

Combine the various body positions especially in the erect position with the following maneuvers:

I. Thoracic mobility exercises. that is, flexion, extension, side tlexion, and rotation

2. Active. active assist, or passive ROM exercises

3. Breathing control exercises especially coordinated with body movements

4. Coughing, spontaneous and voluntary, supported by self or others

Step 6

Set the dUnltion of the mobilization sessions based on the patient's responses (i.e., changes in measures and indices
of oxygen transport) rather than time.

Step 7

Repeat the mobilization session as often as possible based on its beneficial effects and on is being safely tolerated by
the patient.

Step 8

Increase the intensity of the mobilization stimulus. duration of the session, or both comml!l1surate with the patil!nt's
capacity to maintain optimal oxygen transport when confronted with an increased mobilization stressor, and in the
absence of distress; monitored variables to remain within predetermined threshold range.

':'AII sitting positions requ i re upright ereci silting; propped up, semi recumbenl, slouched or slumped posit ions although approximaling the
u pri gh t position are NOT physiologically comparable

i-No amount of movement or activity is too sm.,lIlo derive benefits acutely or over long-Ierm

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274 PART III Cardiopulmonary Physical Therapy Interventions

TABLE 17-1

Exercise Prescription Parameters to Elicit Long-Term Aerobic Benefits In Healthy Persons

SPECIFICATIONS

Parameter

Exercise Type Rhythmic activity, involving the large muscle groups; the legs, arms or both
InLensity 70% to 85% of the age predicted maximum heart rate or observed maximum heart rate
Duration 20 to 40 minutes
Frequency Three to five times a week
Course 6 to 8 weeks

Adapted from the American Col lege of Sports Medicine, (1994). Guidelines for exerc ise testing and prescription. (6th ed.). Philadelphia:
Williams and Wilkins .

rate intensity of 70% to 85% of a maximum heart rate,

Mobilization Stimuli
for 20 to 40 times three to five times a week. Aerobic
Ambulation-independently, with one or more training effects are usually observed within 2 months.
assisting In severely deconditioned individuals and in some
Cycle ergomelly-Iower and upper extremity patient populations, however, such a prescription

ADLs-independently, with one or more assisting would not be realistic, ethical, or indicated. Thus exer­
cise is prescribed that is sufficient to elicit progressive
Standing-independently, with one or more assisting
physiological adaptation within defined limits of cer­
Transferring-independently, with one or more
tain objective and subjective responses, such as per­
assisting
ceived exertion, shortness of breath, angina, discom­
Dangling-independently, with one or more assisting
fort/pain, and general fatigue. Considerable research,
Cycle ergometry in bed (lower extremity)
however, is needed to refine the prescription of mobi­
Turning in bed lization and exercise for their acute effects in patients
Bed exercises with acute cardiopulmonary and cardiovascular dys­
function. Furthermore, the specifications for low level
Supplemental Aids and Devices for Mobilization
exercise needed to affect long-term acrobic adaptation
For the patient:
have not been elucidated in dctail. However, based on
Walking aids, such as crutches, cane, intravenous
physiological understanding of acute exercise re­
(IV) pole, wheelchair, orthoses
sponses and cardiopulmonary pathophysiology, prin­
Weights
ciples for prescribing mobilization for acute car­
Pulleys
diopUlmonary conditioning can be formulated.
Monkey bar

Grab bars
Mobilization Testing
Grab rope
Evaluating a patient's response to a mobilization
For the PT:
stimulus can be assessed in two ways. First, the pa­
Transfer belts
tient can be exposed to a mobilization challenge test.
Mechanical lifts for patients The patient is monitored before, during, and after
mobilization activities (see box at left). Relatively
low-intensity activities such as bed exercises, moving
in bed, changing body position, sitting up, dangling

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 17 Mobilization and Exercise 275

over bed side, transfer to chair, chair exercises, and in the previous couple of hours, be as attentive and
short walks with assistance, constitute a sufficient aroused as possible and be experiencing minimal
stimulus to elicit the acute effects of exercise. The de­ pain or discomfort. Review of a patient's medication
gree of assistance required to perform the activity schedule will ensure treatments are well-timed with
should be noted, since this significantly influences respect to pain medications, and medications that in­
the patient's individual effort. Second, if the patient's terfere with a good treatment response, such as nar­
status is unstable and oxygen transport is severely cotics. The patient's clothing should not be restric­
jeopardized, then monitoring a patient during stan­ tive, and any lines, leads, and catheters should not be
dard care and procedures, such as turning the patient, taut. Any equipment, monitors, and IVs need to be
ADLs, nursing and medical procedures, can provide appropriately positioned to avoid disconnections or
an indication of the patient's physiological responses mishaps. Mobilizing the patient in intensive care re­
to mobilization and the capacity of the oxygen trans­ quires positioning of the mechanical ventilator and
port system to meet the metabolic demands imposed. other supports before moving the patient. The PT
No movement is too small. Any movement that is must prepare personnel before moving a patient par­
sufficient to perturb the oxygen transport system, no ticularly if one or more assists are required. Despite
matter how minimal, is sufficient to elicit short- and the number of persons assisting, the goal is usually
long-term gains. to have the patient perform as much of the mobiliza­
tion activity as possible. Even small degrees of phys­
ical movement can provide sufficient stress to the
Monitoring
cardiopulmonary system to be beneficial.
Patients for whom mobilization is prescribed require The basic components of the mobilization session
monitoring. Because of the stress to the oxygen trans­ are comparable to the components of an exercise ses­
port system that mobilization elicits, the following sion described by the American College of Sports
variables in addition to the oxygen transport vari­ Medicine for long-term training effects (Figure 17-1).
ables, are most useful to monitor: heart rate (HR), Wherever possible, the session should include the
systolic and diastolic BP, RPP, RR, Sa02, arterial following components: warm-up, steady-rate, cool­
blood gases, ECG and subjective responses. down, and recovery. These components are less dis­
tinct when a patient has minimal functional capacity
or is being mobilized to remediate acute cardiopul­
Mobilization Prescription
monary dysfunction. The rhythmic movement of
Prescribing a mobilization stimulus for its acute ef­ large muscle groups is ideal. Prolonged static maneu­
fects parallels the prescription of exercise for its long­ vers are usually avoided particularly if the patient is
term effects with some important differences. In an severely ill, because of their disproportionate hemo­
acute patient, a mobilization or stimulus often results dynamic response. The movements that are usually
in a greater response gain than such a stimulus in considered when mobilizing a patient include: turn­
subacute and chronic patients. In addition, to the ing, sitting up, shifting, transferring, standing and
rapid favorable response an acute patient may have to taking some steps. These can be extremely metaboli­
acute exercise, the patient may exhibit a negative re­ cally demanding for patients with significant acute
sponse just as quickly. Thus judicious monitoring of cardiopulmonary dysfunction. Thus pacing the mobi­
treatment response in these patients is essential. lization session allows the patient to rest between
The scheduling of and preparation for a mobiliza­ stages. The patient is reassured and encouraged to
tion session is crucial to the response that can be ex­ relax and coordinate deep breathing and coughing
pected. The following conditions should be adhered with the activity. Throughout the session, attention is
to as closely as possible; and their details should be given to the patient's biomechanical alignment, and
recorded so that any factor that significantly influ­ postural erectness and stability. Back extension or
ences the response to treatment can be identified. body positioning minimizes slumping of the chest
The patient should be rested, not have eaten heavily wall and compromised ventilation. In this way, chest

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276 PART III Cardiopulmonary Physical Therapy Interventions

L """1J c """1J without arterial desaturation, hemodynamic insta­

200r .Q 1 ?
' 0..
1 1 .Q
L.. 1 E 0
L.. bility, or respiratory distress.
"""1J
1 0
L.. - Over time, exposure to an acute exercise stimulus
1 801- 1 1 g 1
.:.c 1 1 U 1 .:.c of an appropriate intensity, for an appropriate duration
u 1 u
and at an appropriate frequency will stimulate long­
1601- I

I 1 term exercise adaptation to that stimulus, Underpre­

140r Trai in ,
scribing the exercise stimulus results in less potent ef­
I\ 1 fects and overprescribing results in an excessive,

120f- I :\ : deleterious effect. Although the latter may be toler­

ated in the short run, the patient's well-being may be
'01
100' ' 1'>"
\ I jeopardized, such as suboptimal treatment rc"ponse,
ovettraining signs and symptoms, and injuries.
80 The duration of the session and the frequency of
sessions should be response-dependent rather than
60 time-dependent. The optimal mobilization threshold,
that is, physiological variables increased but not in
excess of predetermined acceptable and safe limits,
o 5 Time (minutes) 35 40 45
should be maintained for as long as possible within
Start Stop
exerCise exercise the patient's fatigue and comfort levels, and in the
absence of adverse responses. The mobilization ses­
FIGURE 17-1
sion should be repeated as often as the patient can
Components of the exercise training session (i,e., stretching,
tolerate, that is, exhibits a beneficial response or no
warmup, training zone, cool down, and stretching,
deterioration and adequately restores between treat­
men ts. Treatmen t sessions for acu te cardiopu 1-
monary dysfunction are usually shorter and more
wall expansion is maximized in three dimensions. common than for the patient with chronic cardiopul­
The erect position is efficient and requires the least monary dysfunction. The patient's condition changes
amount of energy to maintain. Less demand is placed rapidly both with respect to improvement as well as
on the accessory muscles of respiration in erect sit­ deterioration. Progression of mobilization for its im­
ting, and this effect is enhanced further with leaning mediate acute effects is usually rapid. Progression of
forward and support of the arms. exercise for its long-term effects may occur every
several weeks whereas progression of mobilization
for its acute effects may range from as frequently as
Mobilization Training
every treatment to every few days. Over time, expo­
With respect to oxygen transport, the purpose of sure to a progressive mobilization stimulus leads to
the mobilization session is to elicit the immediate long-term physiological adaptations throughout the
effects of an exercise stimulus, no matter how min­ oxygen transport pathway,
imal. The optimal therapeutic dose of the stimulus
is based on the patient's presentation and history
Monitoring
and the specific parameters are determined by the
goals of the treatment and the acute effects of exer­ The more acute the patient's condition, the more
cise that are indicated. The intensity of mobiliza­ physiologic variables usually need to be recorded,
tion for many patients, for example, is that intensity More objective measures are available in special care
that elicits optimal tidal volumes and VA, increased and intensive care units (ICUs), Subjective responses
breathing frequency and air flow rates, enhanced are also vital components of determining the ade­
mucocil i a r y transport, and cough stimulation, quacy of the mobilization stimulus; however, se­

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 17 Mobilization and Exercise 277

verely ill patients are often unable to respond effec­ a response-dependent duration and frequency, there is
tively. Compared with the condition of chronic pa­ a cumulative adaptive response to that repeated stimu­
tients, the condition of acute patients tends to vary lation, or a long-term, training response. In decondi­
more within and between sessions and afterward, tioned individuals with low functional work capacity,
which necessitates greater monitoring. or whose oxygen transport system has been compro­
Monitoring needs to be performed continuously mised by disease, the exercise intensity associated
for patients for whom acute mobilization has been with relatively low-intensity mobilizing activities such
prescribed. First, a baseline of the patient's resting as bed exercises, moving in bed, sitting up, dangling
metabolic state needs to be established. Second, the over bed side, transferring to chair, chair exercises,
metabolic responses to stimuli that perturb oxygen and short walks with assistance, constitute a sufficient
transport and the lability of this response needs to be stimulus for long-term adaptation. However, optimal
established. Obtaining such a profile provides some adaptation only occurs if these activities are pre­
indication of the upper limit of the target intensity scribed at a requisite intensity, duration, and fre­
range for mobilization. The target intensity range can quency and the exercise prescription progressed com­
be defined in terms of an upper and lower level of mensurate with the individual's adaptation.
various physiologic variables. The most commonly Mobilization activities prescdbed to enhance oxy­
used are HR, BP, RPP, RR, perceived exertion or gen transport, can be coupled with resistive muscle
breathlessness. Monitoring during nursing procedures work to increase muscle strength and endurance (e.g.,
and other types of routine care provides an indication weights, use of a monkey bar for moving in bed and
of the patient's functional capacity without having to sitting up, manual resistive exercise, the use of wrist
conduct a modified exercise test. or ankle weights, ergometry, and walking). Coordi­
Alternatively, a mobilization or exercise challenge nating postural, thoracic mobility and upper extrem­
can be given. The patient's response is compared ity exercises with inspiratory and expiratory efforts
with resting baseline measures. The quality as well as can be effective in stimulating increased VT, and im­
the immediacy of the response is documented. The proved ventilation and perfusion matching. Chapters
characteristics of the quality of response is also 2l and 22 illustrate how such movement and breath­
recorded. Is the response commensurate with the in­ ing patterns can be coupled to maximize oxygen
tensity of the exercise stimulus? With cessation of transport in neurological patients. Such coordinated
exercise do the responses revert to baseline? If so, exercise, however, can also be used with patients
how fast? Do the variables return to baseline or re­ with acute cardiopulmonary conditions. Isometric
main above baseline? type exercises, postures that require increased muscle
The variables to be measured depend on the pa­ work for stabilization, and activities that elicit the
tient (see Chapters I and 16). Most commonly, HR, Valsalva maneuver produces disproportionate hemo­
ECG, BP, RPP, RR, and subjective symptoms, are dynamic responses, which could be detrimental. The
basic measures and indices of exercise response that capacity of the patient to respond appropriately to
require no invasive procedures. At the other end of these loads needs to be established beforehand.
the spectrum is the critically ill patient who has vari­ In the management of acute cardiopulmonary dys­
ous invasive lines and monitoring equipment, includ­ function, the parameters of mobilization stimuli in­
ing hemodynamic monitoring and intracranial pres­ clude a relatively low intensity (although often per­
sure monitoring. This patient requires more specific ceived as intense by the patient), short duration, and
and frequent measures of oxygen transport. high frequency of sessions. If the patient is severely
compromised (e.g., end-stage heart or lung disease)
interrupted or interval training is indicated. This type
Adaptation to an Acute Mobilization Stimulus
of training is characterized by either on-off exercise,
When an individual is exposed to repeated exercise which allows for rest in between bouts of exercise, or
stress, that is, of a specific threshold intensity, and for high-low intensity of activity. The volume of work

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278 PART III Cardiopulmonary Physical Therapy Interventions

TABLE 17-2

Relationships Among Mobilization and Exercise Prescription Parameters

Activity and Relative Intensity

SESSION DURAnON SESSION FREQUENCY

Mobilization activities 5to 20 min I time per I to 2 hours to 4 to 6 times per day
Interval continuous aerobic exercise 5to 20 min I time per I to 2 hours to 4 to 6 times per day
Continuous aerobic exercise (light) 5to 20 min I time per I to 2 hours to 4 10 6 times per day
Continuous aerobic exercise (moderate) 20 to 40 min 2 to 3 times daily to once daily
Continuous aerobic exercise (heavy) 20 to 40 min Daily to 3 to 5times per week

that can be achieved in an interrupted protocol by a beds with lines and leads is crucial, because it is these
severely compromised patient, is significantly greater patients who benefit significantly from exercise stress
than during continuous activity. With physiological and also succumb most severely to its removal.
adaptation over time, the exercise period can be in­ The goal is to adapt the patient to multiple ShOl1 mo­
creased and the rest period decreased, and possibly bilization sessions per day, as frequently as once per
eliminated. When high- and low-intensity exercise is hour, and progressively increase the intensity of these
alternated the work load can be progressed by either sessions, reduce the duration and conespondingly re­
increasing the respective loads in each phase or by in­ duce the frequency of sessions. Table 17-2 illustrates
creasing the duration of the higher load period. If the the inverse relationsrup between mobilization and exer­
patient has low functional work capacity but suffi­ cise intensity, duration, and frequency of the sessions.
cient physiological reserve, adaptation can be rapid,
necessitating small, frequent progressions. As the pa­
Multisystem Effects of Mobilization
tient's aerobic capacity increases, the response gains
are correspondingly smaller. If the patient has both Acute exercise affects most organ systems in addition
poor functional capacity and poor physiological re­ to the cardiopulmonary and cardiovascular systems.
serve capacity, progress would be correspondingly The neurological system is primed for activity. To
slower and less significant. counter postural perturbations, reflexes and postural
When mobilization activities are being prescribed control adjustments are activated. Blood flow is in­
to remediate acute cardiopulmonary dysfunction, par­ creased to the working muscles commensurate with
ticularly in patients in the leU, extensive and often the intensity and duration, and therefore overall meta­
invasive monitoring is required. This permits detailed bolic demand of the work. The endocrine system also
assessment, and ongoing metabolic assessment of the adjusts to largely stimulate the cardiopulmonary and
patient's treatment responses and recovery. With cardiovascular systems through a complex system of
these supports, mobilization and exercise can be pre­ neurotransmitters to support the oxygen demands re­
scribed effectively in these patients. Judicious moni­ quired of the work rate imposed.
toring minimizes any inherent dangers of either under
or over prescribing the intensity of the exercise stim­
PRESCRIPTION OF MOBILIZATION AND EXERCISE:
ulus (Part II). Special consideration has to be given to
lONG-TERM RESPONSES
the fact that various monitoring leads, lines, and
catheters may restrict certain body positions and ac­ In health, the long-term effects of exercise occur in re­
tivities. Such encumbrances, however, do not pre­ sponse to a specific and sufficient exercise stimulus to
clude most activities including ambulation. Moving which the individual is exposed for a finite period. With
relatively immobile patients who are tied to their respect to aerobic training or adaptation, the essential

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 17 Mobilization and Exercise 279

Long-Term Physiologic Effects of Mobilization and Exercise

Cardiopulmonary System Neuromuscular System

J, Submaximal minute ventilation Enhanced neuromotor control

i Respiratory muscle strength and endurance i Efficiency of postural retlexes associated with type
of exercise
i Collateral ventilation
i Pulmonary vascularization
i Reflex control

i Movement efticiency and economy

Cardiovascular System

i Myocardial muscle mass Musculoskeletal System

i Myocardial efficiency i Muscle vascularization

Exercise-illduced bradycardia
i Myoglobin

J Stroke volume at rest and submuximal work rates i Muscle metabolic enzymes

J, Resting heart rate and blood pressure i Glycogen storage capacity

J.. Submaximal heart rate. blood pressure, and rate i Improved biomechanical efficiency

pressure product i Movement economy

J.. Submaximal perceived exertion and breathlessness

Muscle hypertrophy
i Efliciency of thermoregulation
i Muscle strength and endurance
J.. Orthostatic intolerance when performed in the up-
i Ligament tensile strength
right position
Maintain bone dellSity
Hematologic System

i Circulating blood volume Endocrine System

i Optimize number of red blood cells i Efficiency of hormone production and degradation
to support exercise
i Optimize hematocrit

J.. Cholesterol Immunological System

J.. Blood lipids i Resistance to infection

Central Nervous System Integumentary System

i Sense of well-being i Efficiency of skin as a heat exchanger

i Concentration i Sweating efficiency

training parameters appear in the box above. As adapta­ tion and hemodynamic responses to submaximal exer­
tion to the exercise stimulus occurs, each step in the cise are decreased. The subjective experience of exer­
oxygen transport system becomes more efficient facili­ cise stress is also reduced. These training effects are
tating oxygen delivery, uptake and extraction at the cel­ commensurate with increases in the efficiency of oxy­
lular level. The long-term effects of aerobic exercise gen transport at each step in the pathway.
are summarized in the box above. In addition to an in­ As the body adapts to the exercise training stimu­
crease in maximal oxygen consumption, training results lus, the intensity needs to be increased to elicit fur­
in an exercise-induced bradycardia and increased stroke ther training benefit. This is the basis for the physio­
volume at rest and a reduction in the physiological de­ logical adaptation to an exercise training stimulus.
mands of submaximal work rates. Specifically, ventila- Depending on the goals of the exercise prescription, a

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280 PART III Cardiopulmonary Physical Therapy Interventions

Chro1lic Pathophysiological Conditions That Benefit From the Long-Term Effects of Mobilizatio1l and Exercise

Cardiovascular Conditions Neurological Conditions-<o1l't

Congenital heart disease Multiple sclerosis

Acquired heart disease Poliomyelilis

Postsurgical heart conditions Endocrine Conditions

Angina Thyroid dysfunclion

Hypertension Diabeles mellitus

Hyperlipidemia Neoplastic Conditions

Hypercholesterolemia Conditions Requiring Organ Transplantation

Congesti ve heart failure Pre- and postsurgical siages

Heal1 transplantation Musculoskeletal Conditions

Peripheral vascular disease OSleoarthrilis

Cardiopulmonary Conditions Rheumatoid al1hrilis

Chronic obstructive pulmonary disease Ankylosing spondylitis

Chronic ventilatory failure Osteoporosis

Interstitial lung disease Connective Tissue Conditions

Asthma Systemic lupus erythelllatosis

Cystic fibrosis Nutritional Disorders

Postthoracotomy conditions Obesity

Lung transplantation Anorexia

Neurological Conditions Other Systemic Conditions

Siroke Chronic fatigue syndrome

Parkinson's disease Chronic depression

Quadriplegia Alcoholism

Paraplegia P regnanc y

Cerebral palsy Renal disease

Down syndrome Liver disease

EXERCISE TESTING AND TRAINING

decision is made after several weeks whether the ex­
IN PATIENT POPULATIONS
ercise intensity needs to be increased to further in­
crease aerobic capacity, or whether a maintenance Numerous conditions including nonprimary car­
program is indicated. The training program is pro­ diopulmonary conditions have been shown to bene­
gressed by establishing a new exercise intensity usu­ fi t from the long-term effects of aerobic exercise
ally based on 70% to 85% of the maximal heart rate (see box above). For eacll patient, however, with
achieved in a repeat of the initial exercise test. each of these conditions, the exercise prescription

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 17 Mobilization and Exercise 281

Common Indications for Exercise Relative and Absolute Contraindications

Testing in Patient POpuUltiOIlS to Exercise Testing

Diagnosis Absolute Contraindications

Coronary artery disease and vasospasm Congestive heart failure (CHF)

Hyperreactive airway disease Acute EKG changes of myocardial ischemia

Cardiac vs. pulmonary limitation to exercise Unstable angina

Peripheral vascular disease Ventricular or dissecting aneurysm

Assessment Ventricular tachycardia

Maximal functional work capacity Multifocal ectopic beats

Chest pain Repetitive ventricular ectopic activity

Dyspnca Untreated or refractory tachycardia

Endurance Supraventricular arrhythmia

Ability to work Recent thromboembolic event (pulmonary or other)

Employmelll options Uncontrolled asthma

Cardiopulmonary and cardiovascular conditioning Uncontrolled heart failure

Movement economy Pulmonary edema

Limitations to exercise Uncontrolled hypertension (above 250 mm Hg

systolic, 120 mm Hg diastolic)
Effect of medication
Acute infections
Adequacy of diabetes management
Relative Contraindications
Prescription
R e c e n t m y ocardial inf a rction (M!) (l e s s than
Exercise program
4 weeks ago)
Medications
Aortic valve disease

Severe cardiomegaly

Pulmonal), hypertension

Resting tachycardia
differs. Comparable with prescribing mobilization
Resting electrocardiogram (ECG) abnormalities
in acute conditions, prescribing exercise for long­
term adaptations is based on the patient's presenta­ Poorly controlled diabetes

tion, history, premorbid status and conditioning Severe electrolyte disturbance

level, lab and investigative reports related to physio­ Severe systemic hypertension
logic reserve capacity, the exercise test and the Significant conduction disturbance
goals of the exercise prescription.
Complete atrioventricular block

Fixed rate pacemakers

Exercise Testing Acute cerebrovascular disease (CVD)

Exercise testing no matter how modified can pose a Respiratory failure

potential risk to the patient, therefore exercise testing Left ventricular failure
must have clear indications, and any contraindications Epilepsy
must be ruled out. The indications for exercise testing
are numerous (see box above, at left). They range
Adapted from Jones. N.L. (1988). Clinical Exercise Testing.
from quantifying maximum functional capacity to as- (3rd Ed.). Philadelphia: WB Saunders.

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282 PART III Cardiopulmonary Physical Therapy Interventions

TABLE 17-3

Subjective Scales of Exercise Responses Based on the Borg Scale of Rating of Perceived Exertion

PERCEIVED EXERTION BREATHLESSNESS DlSCOMFORTIPAIN FATIGUE

0 Nothing at all Nothing at all Nothing at all Nothing at all

0.5 Very very weak Very very light Very very weak Very very light
1 Very weak Very light Very weak Very light
2 Weak Light Weak Light
3 Moderate Moderate Moderate Moderate
4 Somewhat strong Somewhat hard Somewhat strong Somewhat hard
5 Strong Hard Strong Hard
6
7 Very strong Very heavy Very strong Very heavy
8
9
10 Very very strong Very very hard Very very strong Very very hard
Maximal Maximal Maximal Maximal

sessing endurance during low level ADLs. Contraindi­ the ratings can be used to compare the patient's sub­
cations are classified as either relative or absolute (see jective exercise responses over repeated tests.
box on p. 281, at right). Absolute contraindications Depending on the functional impairments and ca­
prohibit the safe conduction of an exercise test, pacity of the patient, the exercise test can be one of
whereas the presence of relative contraindications re­ various types depending on the objective of testing
quires that the test, protocol, physiological variables and potential training. If exercise training is an objec­
monitored, or the end point of the test be modified. tive of the exercise test, the activity used in the test
Both the indications for the test and any contraindica­ should be comparable with that to be used in training.
tions must be clearly established before performing an Physiological responses and adaptation to exercise
exercise test. are highly specific to the training stimulus (the speci­
The guidelines used to test and train healthy peo­ ficity of exercise principle). Thus if walking is to be
ple with no disease states are not directly generaliz­ the training activity, the test should be a walking test
able to chronic medically-stable patient populations. rather than cycling.
Because of functional impairments in these patients There are numerous variants of standard exercise
(e.g., secondary to cardiopulmonary, cardiovascular, tests (Table 17-4). These are categorized as continuous
neuromuscular, and musculoskeletal dysfunction) ex­ and interrupted tests. Continuous tests include maxi­
ercise testing and training must be modified. More­ mal and submaximal incremental tests and steady-rate
over, patients who are physically challenged experi­ tests, and interrupted tests include maximal interval
ence more subjective symptoms in response to and submaximal interval tests. Interrupted tests are de­
exercise compared with healthy people, therefore signed for patients with low functional work capacity
monitoring the subjective responses to exercise is es­ who cannot sustain prolonged periods of aerobic exer­
sential. The Borg scale of rating of perceived exertion cise. These patients can perform more work over time
can be modified for clinical use to score breathless­ when the work load is administered in an interrupted
ness, discomfort, pain, and fatigue (Table 17-3) or periodic manner. Specifically, the test alternates
(Borg, 1970; 1982). If the endpoints of the scale are fixed periods of work and rest, or high and low intensi­
well-described and understood by the patient, then ties of exercise. The proportions of work-to-rest or

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 17 Mobilization and Exercise 283

TABLE 17-4

Exercise Tests That Can Be Applied to Patient Populations

TEST TYPE INDICA TlONS

Continuous Tests

Maximal . Generally medically-stable patient

No significant musculoskeletal abnormalities
Test maximal functional capacity
Basis for aerobic exercise program
Incremental Incremental work rates usually 2 to 5 minutes in duration
Steady-rate Endurance test at a given work rate; usually a comfortable walking or cycling speed
Submaximal For patients for whom maximal testing is contraindicated
Incremental Approximate maximal exercise testing
Test of near maximal functional capacity or some significant propOition of maximum
Steady-rate Establish baseline of response to steady-rate exercise usually at 60 to 75% of predicted
maximum heart rate
Establishes an index of endurance, cardiopulmonary conditioning and may give an
index of movement economy

Interrupted Tests
Maximal or Submaximal Establish level of functional capacity in patients with extremely low functional
work capacity
On-off protocol or high-low intensity protocol, such as 5 min on to I min off; alternate
high- and low-intensity exercise in cycles, such as I minute high to 15 seconds low

high-to-low exercise intensity is set according to the treadmill or ergometer, which jeopardizes stringent
patient's level of impairment. One patient, for exam­ test control (Dean and Ross, 1992a).
ple, may be able to tolerate 3 to 5 minutes of relatively Like other diagnostic or testing procedures, the va­
high intensity work to I to 2 rrlinutes of low-intensity lidity and reliability of the exercise test depend on the
work, whereas another patient may be able to tolerate quality of the procedures used. The preexercise test
only 1 minute of low intensity work to 10 to 20 sec­ conditions and the preparation and testing procedures
onds of rest. need to be standardized (see boxes on pp. 284-285).
For maximal standardization and the capacity to The test is terminated as soon as the sign or symptom
perform more comprehensive monitoring, stationary criteria for terminating the test is reached or the crite­
exercise modalities such as the treadmill, ergometer, ria for prematurely terrrlinating the test is reached (see
or step are recommended. However, there may be in­ box on p. 286). Recording the test conditions and pro­
dications to perform an exercise test without a modal­ cedures in detail is essential. An example of an exer­
ity, such as the 12-minute walk test or some variant cise test data sheet that can be modified to any testing
like 6 or 3 minutes (McGavin, Gupta, and McHardy, protocol using an exercise modality is shown in the
1976). Standardization of such tests, however, is box on p. 287, at left. Many patients are unable to be
more difficult. Practice has a significant effect on the exercise tested using a modality. These patients can
results of the 12-minute walk test, thus this test needs walk on a marked circuit. An example of an exercise
to be repeated several times to achieve a valid test. test data sheet is shown in the box on p. 287, at right.
Also, the instructions for this test are less well­ Systematic and detailed record-keeping will maximize
standardized clinically compared with those for the the test validity and its interpretation as well as ensure

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284 PART III Cardiopulmonary Physical Therapy Interventions

Preexercise Test Conditions

Establish the indications for an exercise test.

Determine absolute and relative contraindications to conducting an exercise test.

Ensure patient is free of any acute illnesses including influenza and colds for 48 hours.

Ensure patient understands the purpose of the test and provides signed consent.

Ensure patient has not eaten heavil y . has avoided caffeinated beverages and has refrained frolll smoking for at least 3
hours before testing.

Ensure patient is rested and has not e x ercised, or is not being excessively exerted for at least 24 hou rs before testing .

Ensure patient is app ro priate ly dressed, for exampl e , shorts, n onbindi n g clothes, short-sleeve shil1. socks, running or
walking shoes that have proper SliPPOI1, and secured laces or fastenings.

Orthoses should be worn unless the test is evaluating changes in functional capacity with and without nn orthosis.

Ensure patient understands the subjective rating scales and is able to read them when held at an nppropr i ate distance.

Select the type of exercise test, the pr otoc 01 and the exercise test termination criteria beforehand.

Ensure the patient is familiar with and has practiced performing the test or test activity preferably before the test day
to reduce arollsal, improve movement efficiency . and maximize test validity.

that the same procedures are used in follow up tests exercise capacity and are unable to tolerate being
thereby maximizing the abi Iity to compare test results. tested on an exercise modality. A major disadvan­
It is imperative that retests are conducted comparably tage, therefore is that the patient cannot be as com­
in every respect to the original test with respect to pa­ prehensively monitored. Thus patients need to be se­
tient preparation and the procedures. lected carefully to undergo a 12-minute walk test or
one of its variants.
Knowledge of the patient's functional ability
Exercise Tests and Protocols
based on verbal report can be useful and can serve as
Depending on the functional capacity of the patient, a guideline for determining the exercise test, its para­
the exercise test can be a continuous maximal, sub­ meters, and what tile patient's termination criteria
maximal incremental or steady-rate, or an interrupted should be. Although these verbal reports do not re­
maximal or submaximal test. The protocol for the test place an exercise test, they can be used as an adjunct.
and the end points to be used in terminating the test The oxygen cost diagram is shown in the box on p.
are determined beforehand depending on the indica­ 290, at left. This visual analog scale is constructed of
tions for the test and the objectives. Some commonly a 100 mm line; the high end of the scale represents
used protocols are shown in Figure 17-2 along with a strenuous activity, that is, walking briskly uphill, and
comparison of the energy expenditure of the various the low end of the scale represents no activity, or
work stages in their protocols. sleep. The patient crosses the line at the point where
The 12-minute w a lk test a n d i t s varian ts, 6 breathlessness does not allow continuation when at
minute- and 3 minute-walk tests, were designed to the patient's best. Figure 17-3 shows an incremental
test patients with lung disease (McGavin, Gupta, ladder of workloads associated with step increments
and McHardy, 1976). These tests have been favored in metabolic cost, (hat is, multiples of resting or near
clinically, because they are functional and do not re­ resting metabolic rate (resting metabolic rate = I
quire exercise equipment. However, these tests are MET, or 3.5 ml 02/mink
i g
often used for patients who have extremely impaired of metabolic costs ranges from very light to very

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 17 Mobilization and Exercise 285

PreparaJion and General Procedures for an Exercise Test

Preparation

Patient ch,mges into exercise clothes and shoes (not new); ensure laces are secure.

If the ergometer is used. the seat-to-pedal distance must be established before the test, and the seat should be adjusted
to allow for 15 degrees or knee extension when the foot is lowennost in the pedal in the revolution cycle; the knee
must not extend fully.

Patient sits quietly in a supported chair to establish a resting baseline.

Monitors are allached (e.g., heart rate, ECG, blood pressure cuff, pulse oximeter) and the subjective rating scales are
explained.

Testing procedures are explained and demonstrated; the patient has an opportunity to answer questions.

General Procedures

Unnecessary conversation and interaction with the patient is kept to a minimum throughout all stages of the test, in­
cluding postexercise recovery, to optimize the validity of the measurements and the test results overall.

Resting baseline measures are taken over 5 minutes or ulltil they have plateaued.

Patient stands 011 treadmill or sits erect on cycle ergometer with feet securely strapped into place on the pedals; the
metatarsal heads should be positioned comfortably over the pedals.

Patient uses two fingers for balance on one side if possible when walking on the treadmill rather than a hand grip, or
ir on the ergometer, not the excessively grasp the handle bar.

Additional baseline measures are recorded in this position for 2 to 3 minutes or until the baseline is stable.

The test timer is started.

The warm-up portion of the protocol begins.

The selected protocol is calTied out.

Patient is monitored objectively and subjectively at least every couple of minutes throughout all stages of the test. in­
cluding postexercise recovery.

The test is terminated when the preset exercise test termination criteria or any of the criteria for prematurely terminat­
ing an exercise test are reached.

The cooldown begins.

When the cooldown portion of the protocol is complete, the patient moves to the supported chair for the postexercise
recovery phase with legs slightly elevated and uncrossed.

Postexercise recovery continues until resting baseline measures have been reached or are within 5% to 10%.

Obtain a report from patient about how patient feels.

Disconnect the monitoring equipment.

Continue to observe patient for any untoward postexercise signs or symptoms.

Monitoring
heavy actIVItIes. One limitation of such charts on
metabolic costs of various activities and exercise is Common variables measured during an exercise test in­
that they can only be used as a rough g uide in pa­ clude HR, ECG, systolic and diastolic BP, RPP, RR,
tients with cardiopulmonary compromise, as they do Sa02 and subjective responses such as perceived exer­
not take into consideration the increased work of tion, breathlessness, discomfort, pain, and fatigue. Mea­
breathing and work of the heart observed in patients sures are taken every few minutes after the patient has
with cardiopulmonary dysfunction. been exercising at a given intensity for a few minutes.

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286 PART III Cardiopulmonary Physical Therapy Interventions

Criteria/or Prematurely Terminating an Exercise Test

Miscellaneous

Wish of individual for any reason

Failure of monitoring equipment

General Signs and Symptoms

Fatigue

Lightheadedness, confusion, ataxia, pallor. cyanosis, dyspnea, nausea, or peripheral vascular insufficiency

Onset of angina

ECG Signs

Symptomatic supraventricular tachycardia

ST displacement (3 mm) horizontal or downsloping from rest

Ventricular tachycardia

Exercise-induced left bundle branch block

Onset of second- or third-degree atrioventricular block

R=wave on T=wave premature ventricular contractions (one)

Frequent multifocal premature ventricular contractions (frequent runs of three or more)

Atrial fibrillation when absent at rest

Appearance of a Q wave

Cardiovascular Signs

Any fall in blood pressure below the resting level

Exercise hypotension (> 20 mm Hg drop in systolic blood pressure)

Excessive blood pressure increase (systolic 220 or diastolic 110 111111 Hg)

Inappropriate bradycardia (drop in heart rate greater than 10 beats/minute with increase or no change ill work load)

Adapted from the American College of Sports Medicine, (1994). Guidelines for exercise testing and prescription.
(6th ed.). Philadelphia: Williams and Wilkins.
Adapted from Jones, N.L. (1988). Clinical Exercise Testing. (3rd Ed.). Philadelphia: WE Saunders.

Exercise Training Prescription

tion of the heart rate response, or some other response,
One of the most conunon indications for exercise test­ to a maximum or near maximum work i'ate that was
ing is to establish whether a training program is indi­ safely tolerated during the exercise test. The training in­
cated and, if so, what the training parameters should be. tensity for a patient who is able to tolerate several in­
The components of exercise training for patients is the cremental work stages on a graded exercise test may be
same as for healthy people, specifically, selection of the optimal between 70% to 85% of the peak heart rate
type of exercise. and its intensity, duration, and fre­ achieved in the test. A patient who is unable to tolerate
quency; and the course of training and its progression. a couple of increases in work stage, is more likely to
The selection of the type of exercise for training and benefit from an exercise intensity range of 60% to 75%
that used in the exercise test, is based on the objectives of the peak heart rate achieved. In some patients. heart
of training. The intensity is usually set at some propor­ rate is an invalid indicator of exercise intensity either

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 17 Mobilization and Exercise 287

Exercise Test Data Sheet for Treadmill Exercise Test Data Sheet for a Walk Test
or Ergometer on a Circuit

Patient name: Patient name:

Patient number: Patient number:

Date: Date:

Weight (kg) Weight (kg)

Height (em) Height (cm)
Body mass index Body mass index
Reason for test: FEY\ Reason for test: FEY\
Fye Fye
Type of test: FEY\lFye Type of test: FEY/Fye

Minute Work rate HR BP RPP RR Sa02 RPE Minute Work rate HR BP RPP RR Sao2 RPE
speed/grade speed/grade
(work/rpm) (work/rpm)

o o

2 2

3 3

4 4

5 5

6 6

Review of preexercise checklist Review of preexercise checklist

Level of hand support Level of hand support

Use of orthoses: type and side Use of orthoses: type and side

How often docs the patient experience the level of How often does the patient expelience the level of
exertion reached in the test (e.g., lx/ wee k , exertion r e a c h e d in t h e test (e.g., I x/week,
lx/month, 3x/day. etc.) lx/month. 3x/day. etc.)

Reason for test termination Reason for test termination

NOTE: 'Relevant notes and comments include abnormal ECG NOTE: 'Relevant notes and comments i nclude abnormal ECG
changes, comments by patient, observations about coordination, changes, comments by patient, observations about coordination,
and anxiety. and anxiety.

Copyrighted Material
 I\)
CD
CD

::0
>-l
-
-
Functional Clinical 02 cost Bicycle -
Treadmill protocols
class status ml/kg/minute METS ergometer ETS (j
Balke "slow" .,
Bruce Kattus Ellestad USAFSam McHENRY Stanford Q.
1 Watt = Ware USAFSam o·
"0
60 KPDS 3=minute =
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2::- stages 3"
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42.0 12 1350
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-£ 16 mph %Gr
1-
38.5 11 1200
4 1 14
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:c 35.0 10 13 2 1 25 17.5
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-0 31.5 9
900
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...r:::. 28.0 8 9
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4 3.5 1 1

FIGURE 17-2
Oxygen cost of work stages of some commonly used exercise test protocols. (Reprinted with
permission from Froehlicher YF: Exercise and the heart, ed 2, Chicago, 1987, Year-Book.)

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 17 Mobilization and Exercise 289

10 + METs
FIGURE 17-3
Swimming
Energy cost in METS of activity and exercise. (crawl,55
(From Underhill, SL et at: Cardiac nursing, ed 2, yard/minute
Philadelphia, 1989, JB Lippincott.) Skiing, fast
9 METs downhill
Walking up
hill,5 mph

8 METs
Cycling, 13 MPH
Swimming, 40 + yard/ minute
Level ski touring, 4 MPH
Cross-country running
7 METs Walking on level,5 to 6 mph

6 METs
Shoveling snow
Digging vigorously
Sawing wood
Tennis
5 METs Skiing
Walking on level, 5 mph

4 METs
Gardening (weeding)
Ballroom dancing
Canoeing, golF
Bedmaking
3 METs Woodworking (drilling, sawing)
Self-care Walking on level ground, 4 mph
washing
dressing

2 METs
Light calisthenics
Driving (can be more MET under stressful conditions)
light housework (sweeping, ironing, mopping)
Walking, 2.2 mph
1 MET
Resting
Eating
Writing
Handsewing
Knitting
Very light activity Light activity Moderate to heavy activity Very heavy activity

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290 PART 1II Cardiopulmonary Physical Therapy Interventions

Oxygen Cost Diagram Used to Assess Patient's Check List Before Exercise Testing or
Breathlessness on Exertion Training Session

Brisk walking uphill Feeling well over the past 48 hours

Medium walking uphill No cold or influenza

Brisk walking on the level No temperature

Slow walking uphill No unaccustomed muscle or joint discomf0l1 or pain

Heavy shopping No chest tightness or pain

Medium walking No unaccustomed breathing difficulty or fatigue

Bedlllaking Adequate night's sleep

Light shopping Have not eaten heav i ly within past 3 hours

Washing yourself Best time of day

Slow walking on the level Wearing or using orthoses, walking aids. and devices

Sitting Clothing appropriate for exercise conditions. such as

indoors or outdoors
Standing
Appropriate socks and footwear that is comfonable.
Sleeping
well-fitting and secured laces <double-knotted)
o
Have water within reach

Taken preexercise medications at specified time

From McGavin CR, Anvinli M, Naoe H, and McHardy GJR: Dysp­
nea, disability, and distance walked: Comparison of estimates of ex­ Have nitroglycerine within reach (cardiac patients)
ercise performance in respiratory disease. 8M} 1:822-823, 1978.
Have inhaler within reach (pulmonary patients)

Have sugar supply within reach (diabetics)

because of the pathology or medications (Dean, 1993; ExerCise Training

Dean and Ross, I 992b). Thus other responses such as
blood pressure, arterial saturation, or subjective para­ General procedures
meters such as rating of perceived exertion or breath­ Before an exercise session, the patient needs to review
lessness can be used. The duration and frequency of the a checklist to ensure that exercise is not contraindi­
exercise program are established based on the patient's cated on that day. This is particularly important for
functional capacity, physiological reserve capacity and patients whose conditions change rapidly or whose
exercise responses (see Table 17-2, for general guide­ disease course tends to fluctuate, such as multiple
lines). Patients with low functional capacities but with sclerosis, cystic fibrosis, and chronic fatigue syn­
adequate physiologic reserve capacity respond to a drome. The box above includes guidelines in prepara­
training stimulus quickly (short training course), thus tion for exercise testing and training sessions. Such a
need to be progressed accordingly. Patients with low checklist, however, must be tailored to each patient.
functional capacities, however, with limited physio­
Specific procedures
logic reserve capacity, adapt more slowly (long training
course). The shorter the training course, the sooner a In the supervised setting, the general procedures
retest is indicated to progress and reset the training pa­ used in exercise training are comparable to those
rameters. To ensure that the patient continues to be used for testing. Specifically, the patient prepares
trained safely and optimally, the training parameters for the training session in a standardized manner,
should be progressed based on an exercise retest. and is monitored according to his or her condition.

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 17 Mobilization and Exercise 291

The components of the session are the same with re­

Physiological Consequences of Bed Rest
spect to a warm-up, cool-down, and recovery. The
main part of the exercise program, however, will I. Fluid volume redistribution
usually be steady-rate or interrupted exercise. Vary­ Decreased plasma and blood volume
ing work rates may be indicated for some patients.
Decreased total heart and left ventricular volumes
In the majority of situations, the goal is to transfer
Increased hematocrit and hemoglobin
the responsibility of surveillance and monitoring
Diuresis and natriuresis
from the PT to the patient. Depending on the pa­
tient's pathology and ability to learn how to monitor II. Muscular inactivity
exercise responses accurately, this process may take Insulin resistance
varying amounts of time. Loss of muscle mass

L(lSS of muscle endurance

Monitoring Loss of muscle strength

III. Altered distribution of weight and pressure

For safety reasons and ensuring that the patient is
within the target training range of the variables selected Venous stasis

to set exercise intensity, the patient must be closely Urine stasis, retention. tendency toward calculus
monitored. This is particularly true if the patient has formation

any risk of untoward or adverse reactions to exercise. If Hyperca1ciuria

patients are considered to be at any fisk, then exercise Bone demineralization

training should only take place in a supervised setting.

Local skin changes

Stable patients may begin an exercise program in a su­

IV. Mixed or unknown etiology
pervised setting, but with training and education they
Increased heart rate at rest and at all levels of
usually can be transfelTed to an unsupervised setting.
activity
Education includes self monitoring of exercise re­
Decreased resting and maximum stroke volume
sponses, maintaining exercise intensity within the ap­
propriate limits, and keeping a record of the details of Decreased maximum cardiac output

their exercise sessions. When the patient is safely carry­ Increased venous compliance
ing out the exercise program independently in the com­ Increased risk of venous thrombosis and throm
munity some mechanism is needed to follow-up on the boembolism
patient's progress. If the objective is continued condi­ Decreased orthostatic tolerance
tioning, then the patient needs to be rescheduled for a
Cardiovascular deconditioning
retest. If the patient is on a maintenance program, the
Decreased V02 max
PT is responsible for reminders about exercise and in­
Anorexia
jury precautions, and notifying the PT or physician if
significant adverse effects are observed. Constipation

Increased sensitivity to thermal stimuli; increased

sweating and hyperemia
PRESCRIPTION OF MOBILIZATION AND EXERCISE:
Alteration in clearance of some drugs
PREVENTATIVE EFFECTS
Increased anxiety, hostility, depression
Humans are designed to be upright and moving.
Increased auditory threshold
When they are recumbent and inactive, gravitational
Increase in focal point. decreased near point
stress (the vertical gravitational gradient) and exer­
of visual acuity
cise stress are removed. Bed rest is one of the most
commonly used yet unquestioned therapeutic prac­
tices. Despite its widespread acceptance, the body po­ From Underhill SL. Woods SL. Froehlicher ES, and Halpenny CJ:
sitions it promotes, namely, being supine and immo- Cardiac 1Illl'.I'illg, ed 2. Philadelphia, 1989,18 Lippincotl.

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292 PART III Cardiopulmonary Physical Therapy Interventions

bile, is nonphysiologic (Chapter 18). The harmful se­ 1951). Thus alveolar-arterial oxygen difference and
quelae of this posture have been well-documented arterial oxygen tension are reduced during periods
(Dean and Ross, I 992b) yet the more severely ill the of bed rest (Cardus, 1967; Clauss, Scalabrini, Ray,
patient, the more-confined that individual is to the and Reed, 1968; Ray et aI, 1974). Closing volumes
bed, and the greater the risk of multisystem complica­ are increased precipitating arterial desaturation in
tions (see box on p. 291). recumbent positions.
The immediate effects of immobility that are ob­ Cardiovascular sequelae of prolonged recumbency
served are those associated with recumbency; these include an increase in resting and submaximal heart
are followed within 24 to 48 hours by cardiopul­ rate (Deitrick, Whedon, and Shorr, 1948), a decrease
monary and musculoskeletal changes. Within 24 in maximum oxygen uptake (Saltin et ai, 1968), and a
hours, significant fluid shifts occur and blood vol­ decrease in total blood volume, plasma volume, and
ume is reduced by 10% to 15%. Within days, these hematocrit (Deitrick et aI, 1948; Saltin et aI, 1968;
effects can significantly impair oxygen transport. Friman, 1979). The combination of an increase in
These systemic effects are more profound in pre­ blood viscosity and a decrease in venous blood tlow
mature infants, young and older people, smokers, results in an increased risk of thromboemboli (Lentz,
obese and deconditioned individuals. These effects 1981; Wenger, 1982).
are further compounded when a patient has either Musculoskeletal changes that occur with bed rest
primary or secondary cardiopulmonary and cardio­ deconditioning include loss of muscle mass and
vascular compromise. The less aerobically fit an strength, muscle and ligament shortening, joint contrac­
individual, the less physiological reserve is avail­ tures, skin lesions, and decubitus ulcers (Rubin, 1988).
able in the cardiopulmonary and cardiovascular CNS changes include slowed electrical activity of
systems. In the event of a medical or surgical in­ the brain, emotional and behavioral changes, slowed
sult, such a patient will have an increased risk of reaction times, sleep disturbances, and impaired psy­
morbidity and mortality than a more fit counter­ chomotor performance (Rubin, 1988; Ryback, Lewis,
part. Thus tl1e importance of aerobic fitness cannot and Lessard, 1971; Zubeck and MacNeil, 1966).
be overemphasized. Metabolic changes that occur during periods of
A primary effect of mobilization and exercise on bed rest include reduced insulin sensitivity and glu­
the cardiopulmonary system is enhanced mucocililary cose intolerance (Mikines, 1991), increased calcium
transport and clearance (Wolff, Dolovich, Obminski, excretion from bone loss and increased nitrogen ex­
and Newhouse, 1 977). Frequent body position cretion secondary to protein loss from atrophying
changes are essential to maintain optimal bronchial muscle (Deitrick et ai, 1948; Donaldson, Huliey, and
hygiene and avoidance of pooling and stagnation of McMillan, 1969; Hulley, Vogel, Donaldson, Bayers,
bronchial secretions, hence, airway obstruction and Friedman, and Rosen, 1971).
airt10w resistance (Chapter 18). Bed rest has been associated with a reduction in
The primary effects of bed rest on the cardiopul­ antibody counts, hence an increased risk of infection
monary system result from recumbency. Pulmonary (Ahlinder, Birke, Norberg, and Plantin, 1970).
sequelae of recumbency included reduced lung vol­ Of clinical significance is the fact that car­
umes and capacities, particularly functional residual diopulmonary and cardiovascular deterioration
capacity (FRC), residual volumes (RV) and forced occur at a faster rate than musculoskeletal deterio­
'
expiratory volumes (FEVs) (Blair and Hickman, ration, and that the rate of recovery from the ill ef­
1955; Craig, Wahba, Don, Couture, and Becklake, fects of bed rest is generalJ y slower than the rate of
1971; Hsu and Hickey, 1976; Powers, 1944; Risser, impairment (Kottke, 1966; Sandler, Popp, and Har­
1980; Svanberg, 1957). A reduction in FRC in rison, 1988).
supine position compared with the sitting position The negative effects of bed rest are accentuated in
has been attributed to both a decrease in thoracic older adults (Harper and Lyles, 1988), and are likely
volume and an increase in thoracic blood volume, to further compound the oxygen transport and other
hence pulmonary venous engorgement (Sjostrand, deficits of patients with pathology.

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 17 Mobilization and Exercise 293

HAZARDS OF BED REST tural alignment, stiffness, and soreness. Bed rest allo­
cates various body parts to being weight bearing.
The literature on the negative sequelae of bed rest has
Skin breakdown most commonly occurs over boney
been unequivocal for 50 years (Chobanian, et aI.,
prominences such as the sacrum, trochanters, elbows,
1974; Dean and Ross, 1992b; Dock, 1944; Harrison,
scapulae, and heels. Muscles imbalance may result
1944; Ross and Dean, 1989). Thus the use of bed rest
from poor postural alignment. Patients are at risk of
as a primary medical intervention requires consider­
bone demineralization. Of particular importance in
able justification. The recumbent, immobile positions
older populations, patients with disabilities, post­
associated with bed rest adversely affect every organ
menopausal women, and patients on steroids is cal­
system and palticularly compromise oxygen transport
cium loss secondary to bed rest or sedentary lifestyle.
by its direct negative effects on the cardiopulmonary
Bed rest affects psychological status. Patients may
and cardiovascular systems. This is particularly signifi­
become depressed, sensorily deprived, or develop a
cant in that in conventional patient management there
psychoneurosis with prolonged bed rest.
is a direct relationship between how sick the patient is
The evidence supports the following:
and the amount of time confined to bed. In addition,
I. Evidence supporting the wide spread use of bed
the musculoskeletal and neurological systems are ad­
rest as a therapeutic intervention is lacking.
versely affected.
2. Currently the use of bed rest is excessive and
The cardiovascular sequelae of bed rest primarily
nonspecific.
include the loss of fluid volume regulating mecha­
3. Bed rest has multisystem negative effects and
nisms, diuresis, and loss of plasma volume. In turn,
therefore must be used judiciously and specifically.
the hematocrit is increased, and the risk of develop­
4. Alternative means of managing very ill pa­
ing deep vein thromboses and thromboemboli is in­
tients, such as those in the intensive care, must
creased. This is exacerbated by increases in blood
be developed.
viscosity, platelet count, platelet stickiness, plasma
fibrinogen (Browse, 1965), and stasis of venous
ALTERNATIVES TO THE NONSPECIFIC
blood flow. The work of the heart is increased in the
USE OF BED REST
immobile, recumbent patient as is the work of breath­
ing. The work of the heart is increased as a result of With respect to developing alternative means of man­
the increased filling pressures and heart rate associ­ aging very ill patients rather than in the recumbent
ated with recumbency, and increased blood viscosity. immobile positions, physical therapists need to be­
The work of breathing is increased by the decreased come vocal in designing furniture and devices that
lung volumes secondary to visceral encroachment on are better suited to the patient's normal physiologic
the underside of the diaphragm, increased intratho­ functioning and to the needs of that patient's course
racic blood volume, and restricted chest wall motion. of recovery. Such appliances would include a greater
With bed rest, the blood vessels of the muscles and number of neurologic and cardiac chairs in ICUs,
splanchnic circulation dilate. With prolonged bed rest, which enable easy transfer of patients from bed to
they may lose their ability to constrict. The ability of chair and upright positioning, greater availability of
these vessels to constrict is essential to prevent the patient-lifting devices, and increased number of or­
pooling of blood and maintain circulating blood vol­ derlies to assist with moving patients.
ume in the upright position. Thus following bed rest, a Rotating beds are electromechanical beds that turn
patient may feel lightheaded or dizzy, or may faint. the patient through an arc of about 30 degrees to ei­
With only a few days of bed rest, skeletal muscle ther side from supine over a 3-minute period (Schim­
atrophies leading to weakness, discoordination and mel, Civetta, and Kirby, 1977). These beds are used
balance difficulty (Lentz, 1981; Saltin, et aI., 1968). for heavy care critically ill patients who are unable to
With severe weakness, excessive strain may b e turn themselves or are difficult to turn. Even though
placed o n ligaments and joints. The limited position­ studies have shown these beds can enhance oxygena­
ing alternatives in bed may contribute to poor pos­ tion in severely c o m promised patients such a s

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294 PART III Cardiopulmonary Physical Therapy Interventions

patients with adult respiratory distress syndrome agement of such patients. However, 30 years ago re­
(Summer, Curry, Haponik, Nelson, and Elston, 1989; striction to a chair was reported to be significantly
Yarnel, Helbock, and Schwiter, 1986), they need to more beneficial than restriction to bed in heart dis­
be used selectively to avoid reliance on passive posi­ ease patients (Levine and Lowe, 1954). Despite this
tioning with the bed vs. more active and active as­ finding, many coronary patients continue to recline in
sisted patient positioning. beds rather than chairs. Mobilizing coronary patients
The use of tilt tables to promote mobilization can be and permitting bathroom privileges has also been re­
hazardous in that leg movement is minimal. Passive ported to be less stressful than being confined to bed
standing on a tilt table constitutes a greater physiologi­ and having to use a bedpan (Andreoli et ai, 1994).
cal stress than active standing. Upright sitting postures
with the legs dependent may elicit greater physiologi­
Prescription of an Adequate Stimulus to Elicit
cal benefit than passive standing with less risk.
the Preventative Effects of Exercise

Although much is known about the protective bene­

INDICATIONS FOR BED REST
fits of cardiopulmonary fitness and conditioning and
Despite the uni versal acceptance of bed rest as a about the negative effects of bed rest and immobility,
medical therapeutic intervention, indications for its little has been documented about defining the appro­
therapeutic use have not been documented. FUlther­ priate exercise stimulus to optimize the preventive ef­
more, considerably more is known about the adverse fects of exercise for a given patient. The preventive
and potentially life-threatening hazards of bed rest effects of an exercise stimulus can be defined as that
than about its potential benefits. Bed rest should exercise dose that will maintain the patient's condi­
clearly be used as selectively as other medical inter­ tioning level and prevent deterioration. At present,
ventions to ensure that specific benefits are being de­ the presCliption of preventative mobilization and ex­
rived and the multisystemic negative sequelae are ercise is nonspecific. Research is needed to make ex­
being minimized. Many procedures such as surgery ercise prescription for the preventative effects of ex­
are associated with considerable pain, thus being rel­ ercise more scientifically based. For example, the
atively immobile and recumbent in bed is believed to following questions need to be answered:
minimize postsurgical discomfort. In some cases, •
How do different types of exercise compare with
however, relative immobilization rather than confine­ respect to preventative aspects?
ment to bed may offer the same benefits without the •
Does exercising in some body positions elicit
dire risks. Patients who are severely limited are phys­
better preventive effects than other body
ically supported by a bed and do not have to work
positions?
against the force of gravity. Minimizing the effects of
•
What principles establish which exercise intensity
gravity and the need to weight bear is often indicated
in patients following orthopedic surgery. The bed en­ and duration are best?

ables a patient with multiple wounds and fractures to •

What principles establish how often the patient
be immobilized and supported in a fixed position that should be mobilized or should petform exercise?
is believed to promote healing. Conditions that are The question arises as to what constitutes an ade­
associated with edema require minimizing the effect quate stimulus to maximize the preventive effects of
of gravity on the affected limbs. Whether edema can exercise for a given patient. Although the preventive
be controlled by localized elevation rather than bed effects of exercise are accepted, this important ques­
rest must be established. Some conditions particularly tion has not been adequately researched. Some gen­
in the acute stages to reduce the work of the heart, eral practices, however, have become accepted clini­
such as MI, require some activity restriction, thus the cally. These include turning patients. The turning
use of the bed has been a mainstay of the early man­ frequency that is widely accepted is every 2 hours.

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 17 Mobilization and Exercise 295

There is no literature, however, to support greater individual steps in the oxygen transport pathway
preventive effects turning a patient every 2 hours vs. that are primarily affected, and oxygen transport as
hourly or every 4 hours. Sitting up and ambulation a whole, such as oxygen delivery, oxygen consump­
are two other practices that are also widely used. The tion, and oxygen extraction at the tissue level, are
timing of these interventions, however, is often based fundamental. Of considerable clinical relevance is
on convenience and what else may be happening with the adequacy of tissue oxygenation; however, to
the patient, or on a once or twice daily regimen rather date, there are no clinically expedient means of as­
than on a prescriptive basis. Patients who are sitting sessing tissue oxygenation.
or walking for preventive reasons often assume sub­
optimal and even deleterious slumped or malaligned
SUMMARY
postures. Patients and their caregivers need to be re­
minded about the importance of proper body position This chapter described three distinct goals associated
at all times and be provided with appropriately sup­ with the prescription of mobilization and exercise in
ported chairs, firm bolsters, and adjustable beds that the management of impaired oxygen transport,
maintain optimal body positions. namely, to exploit their acute, long-term, and preven­
Like exercise prescribed for its beneficial acute and tive effects.
long-term effects, exercise to elicit its optimal preven­ The PT needs a comprehensive and detailed un­
tive effects should be prescribed based on the individ­ derstanding of how mobilization and exercise have
ual (e.g., age; premorbid functional work capacity; the potent and direct effects on oxygen transport acutely,
type, distribution, and severity of disease; and within in the long-term, and preventively. The specific mo­
capabilities of patient). Such preventive mobilization bilization or exercise prescription is based on a com­
or exercise must also be prescribed to avoid any dele­ prehensive multisystem assessment and the treatment
terious effects on the patient's overall condition. goals for a given patient. If the acute effects of mobi­
Frequent ambulation constitutes preventive exer­ lization or exercise on oxygen transport are indicated,
cise. Provided the patient does not require undue the prescription specifies the parameters of an appro­
monitoring and has been cleared as a risk, preventive priate mobilization or exercise stimulus, lIsually, of
exercise can be encouraged by all team members. relatively low intensity, shOtt duration and high fre­
This role of exercise is quite distinct and separate quency. The treatment effects are often immediate.
from the therapeutic interventions of mobilization Because treatment responses can be dramatic, the
and exercise for their specific acute and long-term ef­ prescription is progressed relatively quickly based on
fects that are prescribed for the remediation of acute the treatment response measures. Prescribing mobi­
and chronic cardiopulmonary dysfunction. The appli­ lization to remediate acute cardiopulmonary dysfunc­
cation of mobilization and exercise for optimizing tion requires the same precision and specificity as
oxygen transpott is the specific expertise and within prescribing exercise for chronic cardiopulmonary
the unique domain of the PT. dysfunction. If the long-term effects of exercise are
indicated, the exercise stimulus is defined in an ap­
propriate prescription, i.e., generally higher intensity,
ASSESSMENT OF MOBILIZATION

longer duration, and less frequent compared with the

AND EXERCISE RESPONSES

prescription for the acute effects, and designed to be

/ To prescribe mobilization and exercise for optimal followed for several weeks or more before significant
therapeutic effect, resting baseline measures of rele­ physiologic adaptation can be observed and progres­
vant physiologic oxygen transport responses need to sion of the stimulus is indicated. If the preventive ef­
be recorded so that any perturbation of oxygen fects of mobilization or exercise are required, then
transport and homeostasis caused by exercise can be the prescription focuses on maximizing these benefits
identified. Measures that rencct the function of the for a given patient by prescribing exercise, that is of

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296 PART III Cardiopulmonary Physical Therapy Interventions

sufficient intensity, duration, and frequency, to pre­ Borg, G. (1982). Psychophysical basis of perceived exertion. Med­
ical Science in Sports and Exercise, 14, 377-381.
serve adequate aerobic capacity and endurance for a
Borg, G.A.V. (1970). Psychophysiological bases of perceived
given patient. The principles for prescribing mobi­
exertion. Scandinavian Journal of Rehabili/ation Medicine.
lization and exercise for their optimal preventive ef­ 2, 92-98.
fects have not been scientifically elucidated. These Browse, N.L. (1965). The Physioiogy lind Pa/hol08Y of Bed Res/.

three levels of prescription of mobilization and exer­ Springfield,1I1.: Charles C. Thomas. Publisher
cise are physiologically distinct and need to be pre­ Bydgeman, S., & Wahren, J. (1974). Influence of body position on
the anginal thr shold during leg exercise. European Journal of
scribed specifically for each patient.
Clinical lnves/igation, 4. 201-206.
Cardus, D. (1967). 02 alveolar-arterial tension dirferences after 10
days' recumbency in man. Journal (j( Applied Physiology, 23,
REVIEW QUESTIONS
934-937.

I. Distinguish between mobilization and exercise. Chase, G.A., Grave, c., & Rowell, L.B. (1966). Independence of
changes in functional and performance capacities attending
2. Distinguish among the prescription of mobiliza­
prolonged bed rcst. Aerospace Medicine. 17, 1232-1237.
tion/exercise for its acute effects, chronic effects, Chobanian, A.V., Lillc, RD., Tercyak,A., Blevins, P (1974). The
and preventive effects. metabolic and hemodynamic cfT('cts of prolonged bed rest in

3. Describe the differences in the mobilization/ex­ normal subj ects . Circulation, 49. 551-559.

ercise prescription parameters (i.e., type of exer­ Clauss, R.H., Scalabrini, B.Y . , Ray,J.F., & Reed, G.E. (1968) Ef·
fects of changing body positions upon improved ventilation­
cise stimulus, intensity, duration, frequency, and
perfusion relationships. Circula/ion. 37 (SuppI4). 214-217.
course) when prescribing mobilization/exercise Compton, D.M., Eisenman, P.A., and Henderson, H.L. (1989). Ex­
for its (l) acute effects, (2) chronic effects, and ercise and fitness for persons with disabilities. Sports Medicine,

(3) preventive effects. 7,150-162.

Convertino, V.A., Hung, J .. Goldwater, D., and DeBusk, R.F.
4. Explain the effects of mobilization on enhancing
(1982). Cardiovascular responses 10 exercise in middle-aged
the efficiency of oxygen transport.
men after 10 days of bedrest. Circulation, 65. 134-140.
S. Explain the effects of exercise on enhancing the Craig, D.B., Wahba, W.M., Don, H., Couture, J.G., & Becklake,
efficiency of oxygen transport. M.R. (1971). "Closing volume" and its relationship to gas ex­

6. Describe the negative sequelae of restricted change in the seated and supine positions. Journal of Applied
Physiology, 31, 717-721.
mobility.
Dean, E. (1993). Advance.s in rehabilitation for older persons with
cardiopulmonary dysfunction. In: Advances ill Long-Term
Care. Katz, P.R., Kane, R.L., & Mezey, M.D. (eds.). New
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 Body Positioning

Elizabeth Dean

KEY TERMS Cardiopulmonary function Prescriptive body positioning

Gravity Routine body positioning
Oxygen transport

INTRODUCTION
prescriptions, because no specific patient is being con­
The purpose of this chapter is threefold. First, thera­ sidered. Understanding the physiological effects of
peutic body positioning, which is prescribed to opti­ body position on oxygen transport and how patho­
mize cardiopulmonary function and oxygeQ transport physiology disrupts these normal processes is funda­
is differentiated from routine dY'l'ositioning. Sec­ mental to prescribing body positioning. However, an
ond, the physiological effects of different body posi­ optimal body position can only be prescribed based on
tions and changing body positions on cardiopulmonary consideration of all the factors that impact on oxygen
function and oxygen transport, are described. And transport, that is, effects of the patient's pathophysiol­
third, the prescription of therapeutic body positioning ogy and its specific presentation in that individual, the
is described. Body positions that simulate normal effect of immobility, the effect of extrinsic factors re­
physiological effects of gravity and position change on lated to the patient's care and the effect of intrinsic
oxygen transport are the priority, that is, being upright factors related to the patient (Chapter IS). It is only by
and moving. A hierarchy of body positions ranging an integrated analysis of these factors collectively that
from the most to the least physiological is presented. (1) the most beneficial body positions can be pre­
This chapter concentrates on the principles of pre­ dicted, (2) the least beneficial body positions can be
scribing therapeutic body positioning and body posi­ identified and used minimally, and (3) the appropriate
tion changes. The chapter does not provide treatment treatment outcome measures can be selected.

299

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 O
300 PART III Cardiopulmonary Physical Therapy Interventions

GRAVITY AND NORMAL PHYSIOLOGIC FUNCTION:

""- t0
J
- N
IMPLICATIONS FOR CARDIOPULMONARY -fl .> '0 . :;; o
N
u
O
Z
N N :r: N 0
0.... 0.... 0.... o U 0.. 0 U
PHYSICAL THERAPY content in out
The human is an orthograde animal. From moment to (%) (L minute) (mm Hg) (mil (ml/minut
100 ml)
moment, gravity exerts its influence on the human
body and importantly on oxygen transport. The com­
bined effects of gravity on the lungs, hea11, and pe­
/ I\ /r-",
7 .24 .07 3.3 132 28 553 200 42 751 4 8
ripheral circulation is central to their interdependent
function and establishing normal oxygen transport.
I \ \
I
Knowledge of the effects of gravity on cardiopul­
II I .\
monary function in health and the deleterious effects / I' \ \
of pathophysiological states on cardiopulmonary func­ / t
\ \
tion provide a foundation for the clinical application
I \ f\ \
of body positioning as a primary therapeutic interven­ " \ '\
tion to optimize oxygen transport. Because of its po­ \ / \ 1\ \
tent and direct effect 011 oxygen transport, therapeutic
13 .82 1.29 0.63 89 1'42 582 19.21149 739 60 39
/' "'::j J.- \�- .....
V
__

body positioning is a primary noninvasive physical / "-

therapy intervention that can augment arterial oxy­ I "-
genation so that invasive, mechanical, and pharmaco­ I \
logical forms of respiratory support can be postponed,

7
reduced, or avoided the singlemost important objec­ 1'0
tive of cardiopulmonary physical therapy.
A patient is continually exposed to gravity, thus
every position the patient assumes reflects the effect of FIGURE 18-1
Regional physiologic differences down the upright lung.
gravity on oxygen transport, thus, oxygen transport can
VA alveolar ventilation, Q perfusion, V NQ
be improved, maintained or worsened with changes in
= = =

ventilation perfusion ratio. (Reprinted with permission from

body position. Despite being essential to normal car­
West JB: Respiratory physiology-rhe essenrials, ed 5,
diopulmonalY function, gravity is the principal contribu­
Baltimore, 1995, Williams & Wilkins.)
tor to signjficant inhomogeneity of physiological func­
tion down the lungs (West, 1995). Figure 18-] illustrates
the effect of this gradient with respect to alveolar venti­ hydrostatic, gravitational and compression forces act­
lation (V A), perfusion (Q), ventilation and perfusion ing on the heart, blood volume, lymphatic system,
ratio (V A/Q), Pao2, Peo2, PN2, oxygen content, CO2 lungs, and chest waJi, including the diaphragm, wiJi
content, pH, and the flow of oxygen and CO2 in and out eventually compromise oxygen transport, and any ben­
of the lungs. Thus the lungs should not be likened to eficial effect will be offset. Therefore monitoring is es­
balloons either physiologically or anatomically. sential to ensure the patient is turned to another posi­
Based on a thorough analysis of all factors con­ tion before detrimental effects are observed. Frequent
tributing to impaired oxygen transport and gas ex­ changes in body position and avoidance of prolonged
change (Chapter 16), those body positions that will periods in any single position will minimize the risk of
have an optimal effect and those that may be deleteri­ diminishing returns, which are inevitable. The time
ous must be discriminated. In this way, a greater pro­ course differs according to pathology, type, severity,
portion of time can be spent in beneficial positions and and other factors. The duration a patient assumes a
less time spent in deleterious body positions. When body position should be primarily response-dependent
beneficial positions are assumed for too long, however, rather than time-dependent. Knowledge of the dekteri­

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 18 Body Positioning 301

ous effects of prolonged periods in a single position deleterious to oxygen transport. The side-lying positions
supports the prescription of both frequent body posi­ have an effect that is intermediate between upright and
tion changes and extreme consecutive body positions. supine. The prone position which is under utilized clini­
These perturbations simulate the nOimal perturbations cally, has such a significant beneficial effect on oxygen
that the cardiopulmonary and cardiovascular systems transport that a good rationale should be made for not
are exposed to in health during normal mobility and incorporating this position into the treatment prescrip­
body position changes. The ability to weigh the rela­ tion rather than for using this position.
tive beneficial and deleterious effects of each possible The indications for therapeutic body positioning
body position, that is, over 360 degrees in the horizon­ and the indications for frequent body position changes
tal plane and 180 degrees in the vertical plane (ranging to optimize oxygen transp0l1 are shown in the boxes
from 20 degrees head down to 20 degrees lean for­ on pp. 302-303. For each of the indications listed, an
ward) on a given patient's gas exchange, is critical in optimally therapeutic body position can be selected
prescribing body positioning therapeutically. for a given patient. A description of the physiological
effects of several primary body positions follow,
namely, the upright supine, side lying, head down,
PRESCRIPTIVE VS. ROUTINE BODY POSITIONING
and prone positions. This information, howevcr, can­
The literature supports the benefits of frequent body po­ not be applied out of context. The specific positions
sition changes particularly for the patient who is rela­ prescribed for a patient are based on a consideration
tively immobile, severely debilitated, obtunded, breath­ of the multiple factors that impair oxygen transport
ing at low lung volumes, obese, aged, very young or (Chapter 16) in conjunction with a physiological
who has lost the sigh mechanism. The practice of rou­ analysis of the most justifiable positions.
tinely turning patients every 2 hours is widely accepted. Because of the potent and direct effects of body po­
This practice is based on the belief that the deletelious sitioning on various steps in the oxygen transport path­
consequences associated with assuming a static posi­ way in health and in disease, it is unknown whether the
tion for a prolonged period will be prevented. Recent beneficial effects reported with the use of postural
evidence, however, supports that more frequent turning drainage are attributable to enhanced mucociliary
can have greater physiological benefits in criticaJiy ill transport, or to the direct effect of positioning the good
patients (Dean and Suess, 1995) which suggests less se­ lung down on improving the gas exchange of that lung,
verely ill patients may also benefit. The preventive ef­ by increasing alveolar volume of the affected, nonde­
fects of a routine turning regimen are distinct from the pendent lung, or both. Typically, studies evaluating
acute effects of body positioning on oxygen transport conventional chest physical therapy, including postural
which is the primary focus of this chapter. drainage, have failed to control for the direct effect of
body positioning on cardiopulmonary function, or for
the direct effects of increased arousal and mobilization
PHYSIOLOGICAL EFFECTS OF
that occur when changing a patient's body position
DIFFERENT BODY POSITIONS
(Dean, 1994a). This is an extremely serious method­
Body positioning has potent and direct effects on most ological problem that pervades the literature evaluating
steps of the oxygen transport pathway, thus can be pre­ conventional chest physical therapy, and one that
scribed to elicit these effects specifically. Because hu­ needs to be considered when interpreting the results of
mans function optimally when upright and moving, studies on these procedurers. Unless these potent con­
therapeutic interventions that elicit or simulate being founding variables are controlled, the degree to which
upright and moving (i.e., elicit both gravitational and conventional chest physical therapy had a beneficial
exercise stress) are most justified physiologically. The effect over and above the effects of positioning as well
recumbent supine position, a common position assumed as mobilization and increased arousal cannot be deter­
by hospitalized patients, is nonphysiological, therefore mined (Dean, I 994b).

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302 PART III Cardiopulmonary Physical Therapy Interventions

Indications/or Body Positioning To Optimize Oxygen Transport

Cardiopulmonary Facililate viscerodiaphragmatic breathing

i Regional alveolar volume Change the pattern of breathing

i Regional ventilation
Cardiovascular
i Regional perfusion ..l. Preload and afterload
i Regional diffusion
..l. Work of the heal1
Optimize area of optimal ventilation to perfusion
Improve systolic ejection fraction to pulmonary and
matching
systemic circulations
..l. Pulmonary shunting Alter venous return
i Lung volumes and capacities particularly, functional
..l. Gravitational. mechanical a n d compression
residual capacity, vital capacity and tidal volume
forces on the myocardium. great vessels, medi­
..l. Closure of dependent airways astinal structures. and lymphatic system

Alter breathing frequency Optimize t1uid shift from central to dependent areas
(extremities) and vice versa to maintain nuid vol­
Alter minute ventilation
ume regulating mechanisms
Alter position of the hemidiaphragms
Other Systemic Effects
i Respiratory muscle efticiency
Optimize chest tube drainage
..l. Airway resistance
Facilitate urinary drainage
i Lung compliance
Reduce posturally increased muscle tone
i Air now rates
Facilitate patient arousal
Stimulate cough
Promote relaxation
i Biomechanical efficiency of cough, its strength
and productivity Promote comfort

..l. Work of breathing Control pain

Improve arterial blood gases, gas exchange and oxy­ Promote biomechanically optimal body positions
genation
lntraabdominal pressure
i Mucociliary transpOit and mucus clearance Intracranial pressure
..l. Gravitational, mechanical and compression forces
on the lungs, chest wall, diaphragm and the gut

Upright Positions
exercise stimulus. The upright standing position max­
The physiological position for the human organism is imizes lung volumes and capacities with the excep­
the same as the anatomical position-upright. The tion of closing volume, which is decreased (Svan­
upright positions include walking, standing, and sit­ berg, 1957). Functional residual capacity (FRC), the
ting. The upright position coupled with movement volume of air remaining in the lungs at the end of a
(e.g., walking and cycling) optimizes oxygen trans­ normal expiration, is slightly greater in standing com­
port to the greatest degree in that ventilation and per­ pared with sitting and exceeds that in supine by ap­
fusion are more uniform than without the additional proximately 50% (Figure 18-2). Maximizing FRC is

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 18 Body Positioning 303

associated with reduced airway closure and maximal

Indications for Frequent Changing
arterial oxygenation (Hsu and Hickey, 1976; Ray et
of Body Position
ai, 1974). Figure 18-3 illustrates the relationship of
Cardiopulmonary FRC and closing capacity as a function of age. Be­

Alter chest wall configuration cause of age-related changes, closing capacity of the
dependent airways increases with age; this effect is
Shift distribution of alveolar volume
further accentuated with recumbency. Airway closure
Shift distribution of ventilation
is evident in supine in the healthy 45-year-old person,
Shift distribution of perfusion
and in the upright position in the healthy 65-year-old
Shift distribution of diffusion person (Leblanc, Ruff, and Milic-Emili, 1970). These
Shift distribution of ventilation to perfusion matching effects are further accentuated in patient populations,

Shift mechanical physical compression of the heart thus the upright position is favored and the supine po­
on adjacent alveoli sition should be minimized to prevent airway closure

Shift position of the heart thereby alter chamber end and impaired gas exchange.
disastolic filling pressures. preload, afterload, and With respect to pulmonary function testing, the up­
work of the heart right sitting position with legs dependent is the stan­
Shift distribution of mucus transport and accumulation dard reference position (American Thoracic Society,

Stimulate effective and productive cough 1987). When upright, the diameter of the main air­
ways increases slightly. If the airways are obstructed
Facilitate lymphatic drainage
even small degrees of airway narrowing induced by
Perturb pattern of monotonous tidal ventilation
recumbency can result in significant airway resistance
Alter breathing pattern
(Figure 18-4). The vertical gravitational gradient is
Shift gravitational, mechanical and compression forces maximal when upright, the anteroposterior dimension
on the lungs, chest wall. diaphragm, and the gut
of the chest wall is the greatest, and compression of
Simulate normal inflation-deflation sigh cycles the heart and lungs is minimal (Weber, Janicki,
Shift intraabdominal pressure Sllroff, and Likoff, 1983). The shortened position of
the diaphragmatic fibers is countered by an increase in
Cardiovascular
the neural drive to breathe in the upright position
Shift gravitational. mechanical, and compression
(Druz and Sharp, 1982).
forces on the myocardium, great vessels. medi­
astinal structures. and lymphatic system The distribution of ventilation is determined pri­
ll)arily by the effect of gravity, which changes down
Stimulate fluid volume shifts particularly to the de­
pendent limbs the lung due to the anatomical position and suspen­
sion of the lungs within the chest. At FRC in the up­
Other Systemic Effects
right position, the intrapleural pressures at the apex is
Optimize chest tube drainage
-10 cm H20 and at the base -2.5 cm H20 (Figure 18­
Promote urinary drainage 5). The intrapleural pressure is less negative in the
Shift abnormal postural tone patterns base because of the weight of the lung. Because of

Alter arousal state the greater negative intrapleural pressure in the

apices, thus low compliance, these lung units have a
Promote relaxation
larger initial volume, thus smaller volume changes
Promote comfort
occur during respiration. Because the lung units at the
Control of pain
base have a smaller initial volume, thus high compli­
Prevent skin breakdown, risk of infection. and re­ ance, larger volume changes occur during respiration.
sulting positioning limitations
Therefore depending on their relative position with
Limit lying on a preferred side respect to gravity, different regions of the lung are at
different parts of the pressure volume curve.

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304 PART III Cardiopulmonary Physical Therapy Interventions

Mean height 1.S8 m

Cf)
0-
I­
a:I . 300 =-- 30. ,
::i'::.__ ----- SO_:s:.
0

3.5

'u
'"
c.
B 3.0
'"
:l
1:>
'v;

'" 2. 5
c
.9
U
c
:l
u..
2.0
Bars indicate

:!: 1 standard deviation

1.5 'L.. ---1

FIGURE 18-2
Changes in functional residual capacity in various body positions. (Data reprinted with permission
from Nunn JF: Applied respiratory physiology, London, 1987, Butterworths.)

FRC upright
3

FRC supine
'"
..
!; 2
..
E
.2
o
:>
at
c
:l
-'

OJ __ ________ ______ ________ ______ __

30 40 50 60 70

Age yearsl

FIGURE 18-3
Functional residual capacity (FRC) and closing capacity as a function of age. (Data reprinted with
permission from Nunn JF: Applied respiratory physiology. London, 1987, Butterworths.)

Copyrighted Material
 18 Body Positioning 305

-10 em H20
Erect Supine
Intrapleural
pressure

Bronchus

100%

<1l
Mucus
50% §

FIGURE 18-4
Effect of body position on bronchiolar diameter. (Reprinted
with permission from Browse NL: The physiology and
+10 o
pathology of bed rest, Springfield, III. 1965, Charles C.
Thomas.)
Intrapleural pressure (cmH20)

FIGURE 18-5
A common clinical concern is the patient breathing Schematic of the regional differences in ventilation down
at low lung volumes (e.g., the patient in pain, the sur­ the upright lung. (Reprinted with permission from West 18:
gical patient with thoracic or abdominal incisions, Ventilation! bloodflow and gas excfumge, ed 4, Ox ford,
older and younger patients, obese patients, pregnant 1985, Blackwell Scientific.)

patients, patients with gastrointestinal dysfunction

such as paralytic ileus and ascites, organomegaly, in­ -4 em H20
trathoracic and intraabdominal masses, patients who Intrapleural
are malnourished, mechanical ventilated patients and pressure
patients with spinal cord injuries. Breathing at low (RV)
lung volumes reverses the normal intrapleural pres­
sure gradient such that in the upright lung the apices
have a negative intrapleural pressure compared with �-.,100%

the bases, which have a positive intrapleural pressure,

that is, exceeds airway pressure (Figure 18-6). This
results in the apices being more compliant, thus better <1l
E
ventilated than the bases. The bases are prone to air­ 50% .2
way closure in patients breathing at low lung volumes.
An other f a c t o r t h a t r e v e r s e s t h e n o r m a l in­
trapleural pressure gradient is mechanical ventilation.
Despite its necessity in the management of patients in
respiratory failure, mechanical ventilation contributes o -30

to hypoxemia in several ways. First, it reverses the Intrapleural pressure (cmH20)

normal intrapleural pressure gradient so that the up­
FIGURE 18-6
permost lung fields are preferentially ventilated. Be­ Schematic of the regional differences in ventilation at low
cause the dependent lung fields are preferentially per­ lung volumes. (Reprinted with permission from West 18:
fused, ventilation perfusion mismatch is promoted. Ventilation/ bloodflow and gas exchange, ed 4, Oxford,
Positive pressure ventilation has the additional com­ 1985, Blackwell Scientific.)

Copyrighted Material
306 PART III Cardiopulmonary Physical Therapv Interventions

of intrathoracic pressure and re- the recruitment of pulmonary vessels. Arterial pres­
venous return and cardiac output. These fac­ sure exceeds alveolar pressure and blood flow. Zone
tors in addition to the pressure to 3, in the lower area of the reflects the blood
open the valve can increase the work of flow from the distension of pulmonary vessels; arter­
associated with mechanical ventilation ial and venous pressures exceed alveolar pressure.
and 1990; zone 4 in the most
Arcos, and Hiriart, 1984). of the has minimal to no pulmonary
gravity is the primary determinant of in­ blood flow because of interstitial pressure acting on
differences in the distribution of ventila­ the pulmonary blood vessels a compression
tion in the lung, imrareg ional force 1995).
secondary to differences in and resistance Ventilation (V) and (Q) matchl!1g re-
of lung also contribute of the distributons of V and Q
and Abboud, 1992). These effects are eXa)!,)!,CI Both V and Q increase down
populations (989). V increases disproportion­
The distribution of perfusion down the upright ately more than Q 18-8). As a the
lung is also gravity (Figure 18- mal area for VIQ matching is in the mid zone where
The pressures affecting blood flow through the the ratio is about 1.0 (West,
pulmonary capillaries and in the un­ The uoril!ht position is associated with
even distribution of blood flow are alveolar pressure, effects. These effects reflect primarily
and the arterial and venous pressures. Zone 1, at the the central blood volume that is shifted from the tho­
apex, alveolar pressure predominates arterial and ve­ racic compartment to the dependent venous compart­
nous pressures, thus has minimal to no blood flow. ments on the position from
Zone 2, in the reflects the blood flow from (Blomqvist and Stone, Gauer and Thron,

---+

FIGURE 18-7
Schematic of pressures affecting the pulmonary and blood flow. (Reprinted with
permission from West 1B: VentilaliOIl/bloodjlolV and gas exchange, ed 4, Ox ford, 1985,
Blackwell

Copyrighted Material
 18 Body Positioning 307

15
I/minute 3

% Lung volume

Blood flow
10
2

Ventilation

05

Rib number
BaHam Top

FIGURE 18-8
Distributions of ventilation and blood flow down the upright lung and the distribution of ventilation
perfusion matching down the upright lung. (Reprinted with pennission from West JB:
Ventilationlbloodflow and gas exchange, ed 4, Oxford, 1985, Blackwell Scientific.)

/
5° 15° °
4 45

Blood
flow 4
ml/minute/
1 00 m l
3
,
,
2
Calf Ai ,

0'
Foot

FIGURE 18-9
Effect of body position on peripheral blood flow. (Reprinted with permission from Browse NL:
The physiology and pathology of bed rest, Springfield, 111., 1965, Charles C. Thomas.)

Copyrighted Material
308 PART III Cardiopulmonary Physical Therapy Interventions

Erect Supine

Stagnant area

FIGURE 18-10
Effect of body position on drainage from the pelvis of the kidney. (Reprinted with permission from
Browse NL: The physiology and pathology of bed rest, Springfield, III., 1965, Charles C. Thomas.)

Supine Position
Sandler, \986). End diastolic and stroke volumes are
decreased, which results in a compensatory increase The supine position is clearly not a physiological
in heart rate (Thandani and Parker, 1978). Cardiac position for humans unless sleeping, and is physio­
output is correspondingly decreased. The net effect of logically the least justifiable position for ill patients
these physiological changes is a reduction in myocar­ regardless of whether they exhibit cardiopulmonary
dial work (Langou, Wolfson, Olson, and Cohen, dysfunction (Dock, 1944; Moreno and Lyons, 1961;
1977). This finding in corroborated by the observation Powers, 1944; Winslow, 1985). The nonspecific use
that anginal threshold is increased in cardiac patients and overwhelming acceptance of bed rest has devel­
in this position (Prakash, Parmely, Dikshit, Forrester, oped historically over the past 130 years. In the
and Swan, 1973). Peripheral vascular resistance in­ mid-1800s, that internal organs could be rested as a
creases and blood flow decreases, with the assumption therapeutic intervention comparable with immobi­
of the upright position greater than 45 degrees to off­ lizing and resting injuries of the limbs was the pre­
set dependent fluid shifts and potential blood pressure vailing medical philosqphy. The injudicious appli­
drop (Figure 18-9). Another important effect of body cation and overuse of bed rest to cure all medical
position on fluid volume is the promotion of urinary problems was critically challenged by Harrison
drainage from the renal pelvi to the bladder in the up­ (1944) and Browse (1965). Although there has been
right positions as a result of the reduced area for uri­ a significant decrease in use of prolonged periods of
nary stasis in this position compared with supine (Fig­ bed rest based on innumerable studies of the nega­
ure 18-10). Optimal renal function is essential in tive sequelae of bed rest over t h e past several
preserving normal hemodynamic status. decades (Dean and Ross, 1992b), the merits of bed

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 18 Body Positioning 309

rest as a therapeutic modality and the parameters for

its prescription, that is, indications and specifica­ Erect Supine

tions to achieve healing and recovery without deteri­

oration, have not been scientifically established.
This void in our scientific knowledge seems incon­
gruous given the exponential rate of medical re­
search and advances over the years in understanding
obscure diseases and treatments. Because recum­
bency in bed is nonphysiologic and therefore associ­
ated with dire side effects, rest in bed needs to be as
scientifically investigated and judiciously prescribed

o 0
0,
,
as any medication.
The supine position alters the chest wall configu­ :.
:.. .:-
ration, the anteroposterior position of the hemidi­ : "," . .:::.'.
aphragms, the intrathoracic pressure, and the intraab­
dominal pressure secondary to the shifting of the
abdominal viscera in this position (Behrakis, Baydur, FIGURE 18-11
Jaeger, and Milic-Emili, 1983; Craig, Wahba, Don, Effect of body position on the distribution of mucus within
the bronchi. (Reprinted with permission from Browse NL:
Couture, and Becklake, 1971; Don, Craig, Wahba,
The physiology and pathology of bed rest, Springfield, IJI.,
and Couture, 1971; Druz and Sharp, 1981; Klingstedt
1965, Charles C. Thomas.)
et ai, 1990; Roussos, Fukuchi, Macklem, and Engel,
1976; Saaki, Hida, and Takishima, 1977). The normal
anteroposterior configuration becomes more trans­
verse. The hemidiaphragms are displaced cephalad, Several significant cardiovascular changes occur
which significantly reduces FRC in this position (Hsu on assuming the supine position. A central shift of
and Hickey, 1976). Excess secretions tend to pool on blood volume from the extremities to the central cir­
the dependent side of the airway. Thus the upper side culation initiates orthostatism (Sandler, 1986). This
may dry out, exposing the patient to infection and ob­ fluid shift increases both the preload and afterload of
struction (Fig. 18-11). the right side of the heart. This increased volume
An increase in intrathoracic blood volume also tends to distort the interventricular septum, and re­
contributes to a reduction in FRC, lung compliance, duces left ventricular volume and preload. Prefaut
and increased airway resistance in the supine position and Engel (1981) observed that hypoxic vasocon­
(Nunn, 1987; Sjostrand, 1951). Collectively, these ef­ striction secondary to closure of the dependent air­
fects predispose the patient to airway closure and an ways in the supine position contributed to preferential
increase in the work of breathing. Although a healthy perfusion of the nondependent lung zones. The rela­
person can accommodate to these physiological tively increased central blood volume inhibits the re­
changes, a healthy person does not assume this posi­ lease of antidiuretic hormone. Ten to 15 percent of
tion for prolonged periods without shifting. A hospi­ fluid is lost within 24 hours (Sandler, 1986), which
talized patient, however, is less likely to adapt to these can manifest clinically as cardiac underfilling, ortho­
immediate changes and their long-tenn effects. In ad­ static intolerance, and a negative fluid balance (Dean
dition, they may be less responsive to the need to shift and Ross, 1992a).
position or unable to respond to afferent stimuli Because of a reduction in the vertical gravitational
prompting a need to change position. These effects are gradient, and therefore the intrapleural pressure gra­
accentuated in older people whose arterial oxygen ten­ dient of the lung in supine, the distribution of V/Q
sions progressively diminish with age (Ward, Tolas, matching appears more uniform and evenly matched
Benveniste, Hansen, and Bonica, 1966; Nunn, 1987). in the supine position (Bates, 1989). These changes,

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310 PART III Cardiopulmonary Physical Therapy Interventions

Erect Supine

cm
Above 20
iliac
crest

15

FIGURE 18-12
Effect of body position on the level and movements of the diaphragm during respiration.
(Reprinted with permission from Browse NL: The physiology and pathology of bed rest,
Springfield. Ill., 1965, Charles C. Thomas.)

I
I
1.:-
I.::'
/':-:
,..:-::-
L:':

:: r:-::::,:
(: :' :

---.... nnn rtn<..:<

,

Awake spontaneous

:':
r::::'
j
-:
.:- -.,
·:':::i
/ · 7':
>1
.... f
/ : <
nn n\n
nnnqn ___

Paratyzed
Anasthelized spontaneous

FIGURE 18-13
Position of the diaphragm in an awake spontaneously breathing subject, and in an anesthetized
subject with and without paralysis. The broken line is the end-expiratory position of the diaphragm
in the awake state in the supine position. The shaded area shows the excursion of the diaphragm
during inspiration and expiration.
(From Froese AB, Bryan AC: Effects of anesthesia and paralysis on diaphragmatic mechanics in
man. Anesrhesio[ogy 41 :242-255.)

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 18 Body Positioning 311

however, must be considered in conjunction with Functional

other changes associated with supine, namely re­ Maximal residual

inspiration capacity
duced FRC, reduced vital capacity, reduced flow
rates, increased area of dependent lung, and increased
closure of the dependent airways. These deleterious
factors offset any theoretical benefit of the supine po­
sition on VIQ matching (Ross and Dean, 1992).
The position of the diaphragm and its function, is
dependent on body position. Figure 18-12 illustrates
the effect on body position on the level and movement
of the diaphragm. In the supine position, the resting Functional
Maximal
level of the diaphragm is influenced differentially by residual
inspiration
anesthesia and neuromuscular blockade (Froese and
Bryan, 1974). Figure 18-13 illustrates these effects. In
the spontaneously breathing subject, the excursion of
the diaphragm is greater posteriorly because the de­
pendent viscera beneath the posterior portion of the
diaphragm. During anesthesia with or without paraly­
sis, the diaphragm ascends 2 cm into the chest. When
paralysis is induced, the loss of diaphragmatic tone re­
sults in greater excursion of the nondependent rather
than the dependent part of the diaphragm.
FIGURE 18-14
Outlines of the lungs at two lung volumes in a conscious

Side-Lying Positions spontaneously breathing subject in the right side-lying

position. (Reprinted with permission from Nunn JF:
Compared with the supine position, side lying is Applied respiratory physiology, London, 1987,
more physiological, thus a more justifiable position Butterworths.)
in terms of i t s t h e r a p e utic b e n e f i t (Hu rewitz,
Susskind, and Harold, 1 985; Ibanez, R a u r i ch,
Abizanda, Claramonte, Ibanez, and Bergada, 1981; right side lying. Although effective ventilation is en­
Ross and Dean, 1992; Roussos, Martin, and Engel, hanced to the dependent lung, inspiratory lung vol­
1977). The side-lying position accentuates anteropos­ ume and FRC are significantly reduced.
terior expansion at the expense of transverse excur­ There is evidence to suggest that side lying results
sion of the dependent chest wall. In this position, the in increased end diastolic ventricular pressure on the
dependent hemidiaphragm is displaced cephalad be­ dependent side secondary to compression of the vis­
cause of the compression of the viscera beneath it. cera beneath the diaphragm, and reduced lung com­
This results in a greater excursion during respiration, pliance on that side (Lange, Katz, McBride, Moore,
and greater contribution to ventilation of that lung and Hillis, 1988). Although such changes can be
and to gas exchange as a whole. The FRC in side readily accommodated in health, for the patient with
lying falls between that in upright and supine. Simi­ compromised oxygen transport, they may impair gas
larly, compared with supine, compliance is increased, exchange fUl1her.
resistance is reduced, and the work of breathing re­ Optimal V/Q matching occurs in the upper one
duced, whereas these are reversed when comparing third of each lung in the side lying position (Kaneko,
this position with upright. Figure 18-14 illustrates the Milic-Emili, Dolovich, Dawson, and Bates, 1966).
difference in lung volumes between maximal inspira­ The total area therefore for optimal V/Q matching is
tion and FRC in a spontaneously breathing subject in likely greater than that in the upright position, which

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312 PART III Cardiopulmonary Physical Therapy Interventions

contributes to an improved V IQ matching. These ap­ those with respiratory muscle fatigue may have in­
parent improvements, however, are offset by reduced creased respiratory distress in this posi tion due to
lung volumes and air flow rates in this position. the resistive loading of the diaphragm from the
In both healthy people and patients, arterial oxy­ weight of the viscera beneath.
gen tension is greater in side lying compared with
supine (Clauss, Scalabrini, Ray, and Reed, 1968).
Prone Position
This is true both for patients receiving supplemental
oxygen as well as those who are not. Thus sidelying There is considerable physiological justification for
can be used to enhance the efficiency of oxygen the use of the prone position to enhance arterial oxy­
transport and thereby minimize or avoid the use of genation and reduce the work of breathing in patients
supplemental oxygen. Arterial blood gases are im­ with cardiopulmonary dysfunction. Specifically, the
proved in patients with unilateral lung disease (Re­ prone position increases arterial oxygen tension, tidal
molina, Khan, Santiago, and Edleman, 1981; Sonnen­ volume and lung compliance (Albert, Leasa, Sander­
blick, Meltzer, and Rosin, 1983) when positioned son, Robertson, and Hlastala, 1987; Schwartz, Fen­
with the good lung down and worsened with the af­ ner, and W o lfsdorf, 1975; Wagaman, Shutack,
fected lung down. When lung pathology is bilateral, Moomjiam, Schwartz, Shaffer, and Fox, 1979). These
arterial blood gases are improved when patients lie benefits have also been observed in critically ill pa­
on the right side compared with the left. This can be tients (Langer, Mascheroni, Marcolin, and Gattinoni,
explained by the greater size of the right lung and the 1988). In one study (Douglas, Rehder, Beynen,
reduced compression of the heart on the lung in this Sessler, and Marsh, 1977), supplemental oxygen was
position compared with left side lying (Dean, 1985; reduced in four out of five mechanically ventilated
Zach, Pontoppidan, and Kazemi, 1974). patients whose positioning regimen included the
prone abdomen-free position. The two common vari­
ants of the prone position are prone abdomen-re­
Head Down Position
stricted and abdomen-free. Prone abdomen-restricted
The head down position augments oxygen transport refers to lying prone with the abdomen in contact
in some palients by improving pulmonary mechan­ with the bed, whereas in the prone abdomen-free po­
ics. Patients with chronic airflow limitation, for ex­ sition the patient's hips and chest are elevated so that
ample, tend to have hyperinflated chests and flat­ the abdomen is free.
tened diaphragms in which the contraction of the W h i le both prone positions augment gas ex­
diaphragm is inefficient because of the position of change, the prone abdomen-free position, comparable
its muscle fibers on the length tension curve. The with the hands and knees position (Mellins, 1974),
head down position causes the v iscera to be dis­ enhances lung compliance, tidal volume, FRC and di­
placed cephalad beneath the diaphragm. The di­ aphragmatic excursion to a greater degree. Although
aphragm is positioned more normally and rests at a patients in respiratory failure have been shown to
higher and more mechanically efficient position in benefit significantly from the prone position, certain
the chest (Barach and Beck, 1954; De Troyer, precautions must be observed. The patient must be
1983). In this position, patients may experience re­ positioned so that all pressure points particularly on
lief from dyspnea, reduced accessory muscle use, the head and face, and stress on the mechanical venti­
reduced upper chest breathing patterns and reduced lator tubing and circuitry is minimized. The patient
minute ventilation. Patients with pathology to the should be monitored continuously and not be unat­
bases may also benefit from the head down position tended. A semiprone position can provide many of
in that this position favors gas exchange in the more the physiological benefits of a full prone position,
functional upper lung fields and promotes alveolar and minimize some of the risks, particularly in me­
distension of bases, which are uppermost in the head chanically ventilated patients and patients with cervi­
down position. Other patients, however, such as cal spine pathology. In addition, the semiprone posi­

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 18 Body Positioning 313

tion simulates the prone abdomen-free position. The constituent distributions of ventilation, perfusion, and
scmiprone position may be more conservative, safer, ventilation and perfusion matching. Areas of depen­
and comfortable for the patient who is severely ill, dent atelectasis, physiologic dead space and shunting,
potentially hemodynamically unstable, older, or who and mucus distribution are dramatically shifted. The
has a protruding abdomen. "stir-up" correspondingly s t i mulates lymphatic
For patients who are not able to be effectively mo­ drainage, surfactant production and distribution, and
bilized some variant of the 'prone position is even the distribution and function of pulmonary immune
more important. Excessive recumbency, particularly factors (Pyne, 1994). Frequent physical perturbations
in patients who are being positioned through a re­ also inhibit bacterial colonization (Skerrett, Nieder­
stricted arc (e.g., supine and one-quarter turns to ei­ man, and Fein, 1989). F r e q u e n t b o d y position
ther side) needs to be offst by some variant of the changes redistribute compression forces acting on the
prone position and this position needs to be incorpo­ diaphragm, myocardium, and mediastinal structures,
rated often. [nevitably, patients exposed to a re­ and the compression of the lungs by the myocardium
stricted arc of positioning will develop atelectasis in and mediastinal structures.
the dependent lung fields. The only means of pre­ Frequent body position changes have significant
venting and countering compression and hydrostati­ effects on stimulating the patient and increasing
cally induced atelectasis is by placing those depen­ arousal and a more wakeful state (Figure 18-15). The
dent areas uppermost. more upright the patient is positioned the greater the
The time course for the development of such hy­ neurological arousal and greater the stimulus to
drostatic complications is dependent on the patient. breathe; this effect is augmented by encouraging the
Although objective measures of oxygen transport and patient to be self-supporting. Concomitant with an in­
the adequacy of the steps in the oxygen trans[lort path­ crease in arousal, the patient is stimulated to take
way are essential to monitor, functional changcs will deeper breaths, and hence increase alveolar ventila­
likely precede the appearance of objective changes. tion. When body positioning is coupled with mobi­
lization, vasodilatation, and recruitment of the pul­
monary capillaries is stimulated, which in turn
PHYSIOLOGIC EFFECTS OF FREQUENT
improves the even distributions of ventilation and
CHANGES IN BODY POSITION
perfusion, and hence augments VIQ matching.
The box on p. 303 lists some of the significant physi­
ological effects of frequent changes in body position
PRESCRIPTION OF THERAPEUTIC BODY POSITIONS
that are largely mediated through their effects on res­
AND BODY POSITION CHANGES
piratory mechanics, cardiac mechanics, airway clo­
sure, mucociliary transport, lymphatic drainage, and Prescription of body positioning is based on an analy­
altered neural activation of the diaphragm. These ef­ sis of the factors that contribute to impaired oxygen
fects resulting from the changc in position are distinct transport. Specific positions are selected to simulate
from the benefits derived from a particular body PoS!­ as closely as possible the physiologic function of the
tion. The benefits of changing position can be en­ normal healthy upright cardiopulmonary unit, and the
hanced by moving to an extreme position, ie, moving perturbations and "stirring up" that occurs in the car­
from supine to prone compared with supine to side diopulmonary system during normal mobility and
lying. Extreme body position changes simulate, but being upright. A hierarchy of body positioning alter­
do not replace, the physiological "stir-up" and pertur­ natives based on the physiologic justification of the
bations that occur with normal mobility and being various positions, appears in the box on p. 3 14. These
upright. When the "stir-up" regimen was originally positions range from the most to the least physio­
proposed, Dripps and Waters ( 1941) did not appreci­ logic. The hierarchy is based on the premise that oxy­
ate fully its physiological implications. The net effect gen transport is optimal when upright and moving.
of changing body position is a "stirring up" of the Mobilization in the upright position increases tidal

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314 PART III Cardiopulmonary Physical Therapy Interventions

Physiological Hierarchy of Body Positions

Most Physiologic Therapeutic Body Positions

Normally moving upright in a I G gravitational field and exposed to a range of body positions and body position
changes over the course of several hours

Relaxed erect standing (not too prolonged)

Erect sitting (self supported or with assist) with feet moving (e.g., active, active assisted or passive cycling motion)

Erect silting (self-supported or with assist) with feet dependent

Lean forward sitting with arms supported and feet dependent

24S degree sitting with legs dependent

Erect long sitting (legs non dependent)

< 4S degrees sitting (legs non dependenl)

Prone and semiprone/side lying

Supine

Least Physiological Therapeutic Body Positions

Provisos
The upright erect position implies the back, head and neck are vertical and aligned with flexion only at the hips: the
patient is not slumped or recumbent.

The less able the patient is to assist in positioning the greater the need for more extreme positions and greater the
turning frequency.

If the patient is totally unable to move, that is, in coma or paralyzed, extreme body positions arc also indicated if not
contraindicated because of hemodynamic instability or increased intracerebral pressure. The upright position is
used as much as possible provided the patient is physically supported for safety and monitored in terms of treat­
ment response. Passive standing on a tilt table is hemodynamically questionable; preferably patients should be
placed in a high Fowler's position with legs positioned dependently using the knee breaks in the bed.

Regimens of 360-degree horizontal tuming and ISO-degree vertical turning (ranging from 20 degrees head down to
20 degrees lean forward) are used unless contraindicated. Positioning through a maximal arc simulates as closely as
possible three dimensional movement of the chest wall during normal respiration.

volume, respiratory rate, and hence minute volume, right state. Furthermore, even the mobilized patient
flow rates, mucociliary transport, and clearance, and can benefit from therapeutic body positioning be­
enhances the efficiency and effectiveness of airway tween mobilization sessions.
clearance and coughing. Thus incorporating active Body position needs first to be exploited when
movement into the body position change is optimal. coupled with movement followed by the erect sitting
Despite the well-documented benefits of the judi­ positions with legs dependent. Figure 18-16 illus­
cious application of therapeutic body positioning to trates several variants of the sitting position. Each of
enhance oxygen transport, it does not replace the these positions has distinct effects on oxygen trans­
more physiological intervention of mobilization and port, thus the specific upright position has to be pre­
exercise to maximize oxygen transport. Rather, once scribed specifically as the supported and "propped
the effects of mobilization/exercise have been ex­ up" positions in bed do substitute for upright erect
ploited maximally, then body positioning is the next sitting. These variants only have a role when the pa­
best physiological approximation to a mobilized up­ tient will deteriorate by attempting to position in the

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 18 Body Positioning 315

Aroused Asleep

Cortical

activating

impulses

AFFerent impulses from

sense organs, with collateral

tracts to the reticular formation

FIGURE 18-15
Effect of arousal on cerebral activity. (Reprinted with permission from Browse NL: The physiology
and pathology of bed rest, Springfield, III., 1965, Charles C. Thomas.)

upright erect position, or the patient immediately de­ prone or semiprone positions. Patients can be posi­
teriorates once in the position. Sitting with the feet tioned safely, with appropriate supervision and moni­
down is preferable to long sit because of the hemody­ toring, and comfortably in these full positions by ob­
namic benefits associated with this position. Sitting serving the normal precautions of passive positioning.
up in bed fails to position the patient in a perfectly A common practice is to progressively turn pa­
vertical upright position. Fowler's position in bed can tients in one-quarter turns, such as supine to side
be maximized and the use of knee breaks in the bed lying and back to supine and so forth. However, the
provides a gravitational stimulus to the circulating use of extreme positions and extreme position
blood volume. changes may yield greater benefit with respect to the
A major difficulty with positioning patients in bed is degree of perturbation and "stir-up" elicited (Piehl
the tendency to lose the position. Patients lose optimal and Brown, 1977). Extreme position changes result in
positions in bed very quickly and thus need to be moni­ significant alterations in the distributions of V, Q,
tored to ensure the specific positions are maintained. and V and Q matching. Mucociliary transport is stim­
Pillows should not be used to maintain a body position, ulated, and secretion accumulation and stagnation is
since these are easily compressed and shifted. Blankets minimized. In addition, the more extreme the body
and sheets tightly rolled and secured with tape, and spe­ position, the greater degree of arousal stimulated par­
cially made bolsters are considerably more effective in ticularly in the upright positions, which is essential in
maintaining a patient's body position. critically ill patients.
Although there is a role for modified positions, Another impo r t a n t consideration is the time
such as half side lying these positions are often course of changes in ox.ygen
overused at the expense of full turns to each side, or and position changes. There are three plausible out­

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316 PART III Cardiopulmonary Physical Therapy Interventions

patients (Brackett and Condon, 1984; Fink, Helsmoor­

tel, Stein, Lee, and Cohn, 1990; Gentillelo, Thomp­

f=4
son, Tonnesen, 1988; Gonzalez-Arias, Goldberg,
Supine Baumgartner, Hoopes, and Rubin, 1983; Kelley,
Vi b u l srest, Bell, a n d D u n c a n, 1987; Mein ig,
Leininger, and Heckman, 1986; Summer, Curry,
Haponik, Nelson, & Elston, 1989). These beds are in­

HI
dicated for patients who are moderately hemodynami­
Recumbent cally u nstable and on neuromuscular blockers, and
thus tolerate manual turns poorly. Such turning frames
are contraindicated, however, for patients who are less
ill. Even for those patients who require multiple assis­

h
tants and extra caution and time to turn and position
Propped-up effectively, these issues should never deny a patient a
much needed treatment with proven efi'icacy.
The benefit of these beds on oxygen transport in

hi
critically ill patients has implications for the manage­
ment of less critically ill patients. The continuous me­

Sitting chanical rotation of the Rotobed® can be simulated

by increasing the frequency and arc of positions
when manually positioning patients.

FIGURE 18-16
Approximations of the upright position from supine. The PRACTICAL CONSIDERATIONS IN
recumbent and propped-up positons are not comparable POSITIONING PATIENTS
physiologically to the upright sitting position. (Reprinted with
Prescriptive body positioning takes a significant
permission from Browse NL: The physiology and pathology
amount of the PTs time as well as other team mem­
of bed rest, Springfield, 111., 1965, Charles C. Thomas.)
bers' time. Such prescriptive positioning is based on
clear indications and well-defined parameters; it is
not to be confused with 'routine' positioning. For any
hospitalized patient who is recumbent and inactive
comes: a favorable response, no response, an unfa­ compared with being out of hospital, body position­
vorable response. With the passage of time, all three ing is a 24 hour concern, ie, a concern both during
outcomes will deteriorate. The specific time depends treatment and between treatments. Such patients are
on the multitude of factors contributing to impaired at risk of impaired oxygen transport.
oxygen transport. Despite the time and labor involved in turning a pa­
Because of the significant changes that can be ex­ tient to prone, particularly if mechanically ventilated,
pected with positioning and positioning changes, the the benefits of this position outweigh the time and ef­
physical therapist (PT) has a prime therapeutic oppor­ fort required to prone a p tient even for short periods.
tunity to assess and treat the patient before, during, Gi ven the considerable benefits that can be derived
and after position changes. from the prone position, a good case needs to be made
for not turning a patient prone. Frequently, therapeutic
body positioning can be effectively coordinated with
Mechanical Body Positioning
nursing interventions and other procedures.
Mechanical turning beds such as the Rotobed® have Extreme body positions and body position changes
significant benefits On oxygen transport in severely ill are the goal. However, when these are less feasible,

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 18 Body Positioning 317

modified positions may be used. Even though the tient includes subjective and objective evaluation of
greatest benefits will be derived from extreme indices of the adequacy of oxygen transp0l1 (Part II).
changes as these simulate the normal range o f Among the most imp0l1ant are oxygen delivery, oxy­
changes the human body is exposed to in health, gen consumption, oxygen extraction, and gas ex­
small changes can be effective in altering intrapleural change indicators such as the A-a02 difference and
gradients slightly so that previously closed alveoli Pa02/PA02. Subjectively, the patient's facial expres­
will be opened even though· previously opened ones sion, respiratory distress, dyspnea, anxiety, discomfort
may be prone to closure. Although modified posi­ and pain are assessed. Objectively, heart rate, blood
tions and small degrees of position change should not pressure, respiratory rate, Sa02, flow rates, beside
be relied upon their effects should not be minimized spirometry are readily assessed. The appropriate stan­
in patients for whom extreme positions are con­ dardization and procedures need to be used to ensure
traindicated. Before and after every position change that the measures are both valid and reliable (see
are prime opportunities to assess the patient, and to Chapter 6). Because physiological variables are
encourage deep breathing and coughing, or suction changing from moment to moment, serial measures
the patient as indicated. over a period of time should be taken to establish an
Another important consideration is the time course average value rather than using peak or discrete mea­
of change in oxygen transport with positions and po­ sures which may misrepresent a treatment effect.
sition changes. There are three possible outcomes: a In order to interpret and compare various mea­
favorable response, no response, an unfavorable re­ sures, the Fi02 and any change in FI02 must be
sponse. With the passage of time, all these outcomes recorded. The use of the ratio Pa02/Fl02 enables
will deteriorate. The specific time depends on the comparison of gas exchange within and between pa­
multitude of factors that contribute to the patient's tients when patients Fi02s differ or are changed
oxygen transport and the patient's responses. (Dean and Ross, 1992c). Similarly, for mechanically
ventilated patients, any changes in the ventilatory pa­
rameters must also be noted, in addition to other in­
MONITORING THE RESPONSE TO A BODY

terventions that have a direct effect on oxygen trans­

POSITION OR POSITION CHANGES

port. Only in this way will the clinician be able to

The prescriptive parameters of body positioning and conclude within reasonable doubt that the position or
body position changes include the positions selected, position change was instrumental in enhancing car­
the duration spent in each position, the sequence of diopulmonary function.
position changes, the cycle of all positions, and posi­ Measures are recorded before (pretreatment base­
tion changes overall. Because a patient necessarily line), during, and at periodic intervals following the
assumes a body position at all times, positioning pa­ treatment. A valid stable pretreatment baseline is es­
tients between treatments can contribute as much to sential to determine the therapeutic effect of a given
the overall treatment response as the treatment itself position on oxygen transport. Variables monitored
as the patient is likely to spend more time in the be­ during the treatment are focused on ensuring that
tween-treatment positions than in the within-treat­ the treatment is having a beneficial effect, in addi­
ment positions. tion to its not having any deleterious effect on the
The duration and frequency of the positions and patient subjectively or with respect to any parameter
the frequency of body position changes are response­ of oxygen transport. As long as beneficial effects
dependent rather than time-dependent. Monitoring is are being recorded a position can be safely main­
the basis for defining and modifying the body posi­ tained, however, diminishing returns can be ex­
tioning prescription. The physiological variables to be pected as the period becomes prolonged. Patients
monitored depend on the patient's specific presenta­ maintained in static positions for more than one to
tion, cardiopulmonary dysfunction, and its severity two hours need to be monitored closely. A position
and distribution. Monitoring of the noncritically ill pa­ change is physiologically defensible after this dura­

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318 PART III Cardiopulmonary Physical Therapy Interventions

tion rather than the risk of diminishing returns and ations presented. Thus this chapter has presented prin­
potentially worsening the patient's condition. ciples that must be considered in the decision-making
Although sicker than a noncritically ill counter­ process behind the prescription of therapeutic body
part, the critically ill patient has the advantage of positioning, rather than a treatment prescription for a
having more monitoring lines in place. These lines given patient.
give access to several measures and indices of oxy­
gen transport, and certain hemodynamic and pul­
monary variables are available continuously.
REVIEW QUESTIONS
In summary, the prescription of therapeutic body
positions is based on a detailed analysis of each pa­ I. Describe the effects of gravity on cardiopul­

tient's unique presentation and the factors contributing monary function and oxygen transport.

to impairment of oxygen transport or threatening it. 2. Distinguish between prescriptive and routine

Then those positions that are predicted to result in the body positioning.

best therapeutic outcome are selected and applied, and 3. In reference to the seated upright position, describe

those that are predicted to lead to an adverse result are the effects of different body positions (i.e., supine,
used minimally and with appropriate monitoring. side lying, head down, and prone) on cardiopul­
Monitoring is an essential component to body position monary function and oxygen transport in health.
prescription in that it confirms the prediction of benefi­ 4. In reference to the seated upright position, describe

cial and deleterious positions, establishes when a posi­ the effects of different body positions (i.e., supine,

tion change is indicated, and helps the PT anticipate side lying, head down, and prone) on cardiopul­

the point of diminishing returns of any given body po­ monary function and oxygen transport in disease.

sitions. The specific physiological variables monitored 5. Explain how a physiologically ideal body posi­

are those that reflect the steps in the oxygen transport tion with respect to oxygen transport can be dele­

pathway that are most affected in a given patient. terious over time.
6. Distinguish between the prescription of therapeu­
tic body positions and frequency of body posi­
SUMMARY
tion changes.

The purpose of this chapter was to differentiate rou­ 7. Describe the principles of monitoring oxygen
tine and therapeutic body positioning designed to op­ transport variables during body positioning.

timize oxygen transport. The physiological effects of

different body positions and changing body positions
on cardiopulmonary and cardiovascular function and References
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teriovenolls shunting. Archives of Surgery, 10 9, :\37-541. Wagaman, M.J., Shutaack, J.G., Moomjiam, A.S., Schwartz, J.G.,
Remolina, C., Khan, A.V., Santiago, T.V .. & Edelman, N.H. Shaffer, T.H., & Fox, W.W. (1979). Improved oxygenation and
(1981). Positional hypoxemia in unilateral lung disease. New lung compliance with prone positioning of neonates. Journal of
England Joumal of Medicine, 304, 523-526. Pedia/rics, 94, 787-791.
Rivara , D., Artucio, H., Arcos, J., & Hiriart. C. (1984). Positional Ward, R.J., Tolas, A.G., B enveniste, R.J., Hansen, J.M., & Bonica,
hypoxemia during artificial ventilation. Cri/ical Care Medi­ J.J. (1966). Effect of posture on normal arterial blood gas ten­
cine, 12,436-438. sions in the aged. Ceria/rics, 21, 139-143.
Ross, J., & Dean, E. (1989). Integrating physiologic principles into Weber, K.T.. Janicki, J.S., Shroff, S.G.. & Likoff, M.J. (1983). The
the comprehensive management of cardiopulmonary dysfunc­ cardiopulmonary unit: The body's gas exchange system. Clin­
tion. Physical Therapy, 6 9, 255-259. ics in Chest Medicine, 4, 101-110.
Ross, J., & De an. E. (1992). Body po s itio n i ng. In: Zadai, c.c. West, J.B. (1985). VelJliia/ionlBlood Flow and Cas Exchange (4th
(ed.). Clinics in Physical Therapy, Pulmonary Management in ed.). Oxford: Blackwell Scientific Publications.
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drainage positioning on ventilation homogeneity in healthy Winslow, E.H. (1985). Cardiovascular consequences of bed rest.
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Roussos, C.H., Fukuchi, Y., Macklem, P.T., & Engel, L.A. (1976). Zach, M.B., Ponroppidan, H., & Kazemi, H. (1974). The effect of
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in horizontal man. Journal of Applied Physiology, 40, 4 17-424. can Review ofRespira/ory Diseases, 110,49-53.

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 Physiological Basis for Airway
Clearance Techniques

Anne Mejia Downs

KEY TERMS Active cycle of breathing technique (ACBT) Percussion

Airway clearance techniques (ACTs) Positive expiratory pressure (PEP)
Autogenic drainage (AD) Postural drainage (PD)
Flutter™ Shaking
Forced expiratory technique Trendelenburg
High frequency chest compression (HFCC) Vibration
Manual hyperventilation

INTRODUCTION
Research studying the results of airway clearance
Techniques for assisting the mobilization of secre­ are often difficult to evaluate because the components
tions from the airways have long been advocated for of a given treatment have not been standardized.
use in the patient with an impairment in mucociliary Availability of equipment or education about a tech­
clearance or an ineffective cough mechanism. The nique as well as cultural differences in its application
goals of this therapy are to reduce airway obstruction, confound the results. Differences in the outcome
improve mucociliary clearance and ventilation, and measures for a given technique also occur-some
optimize gas exchange. studies use wet or dry (dehydrated) sputum volume
Airway clearance techniques have been referred or radioaerosol clearance, whereas other studies use
to in the literature in a variety of ways, including pulmonary function tests, radiographic evidence or
chest p h y s i o t h e r a p y , c h esl ph y s i c a l t h e r a p y, arterial blood gases to asses the effectiveness of an
bronchial drainage, postural drainage therapy, and airway clearance technique. Although a treatment has
bronchial hygiene. been shown to be effective in one cross section of pa­

321

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322 PART III Cardiopulmonary Physical Therapy Interventions

tients with pulmonary disease, care must be taken not may interfere with this process. Retained secretions
to generalize the effectiveness of the treatment across or mucus plugs in the airways may interfere with the
other groups of patients or differing time frame exchange of oxygen. The secretions need to be mobi­
(acute vs. chronic). The majority of secretion clear­ lized from the peripheral or smaller airways to the
ance research has been focused on patients with cys­ larger, more central airways where they may be re­
tic fibrosis, as the need for ongoing secretion removal moved by coughing or suction.
is apparent in this population. The following conditions are indications for air­
Recently the "gold standard" of airway clearance, way clearance:
namely a combination of postural drainage, percus­ I. Cystic fibrosis-In this multisystem genetic
sion, and vibration with cough, has been challenged disease, copious (often purulent), thick secre­
(Lapin, 1994). The indications for routine airway tions and mucus plugs block the peripheral and
clearance with certain diagnoses have been ques­ central airways. Even infants diagnosed with
tioned and the conditions leading to effective applica­ cystic fibrosis, whether symptomatic or not,
tion have been examined. Postural drainage and per­ show evidence of small airway obstruction in
cussion has been shown to be ineffective in some the form of bronchial mucus casts (Wood,
cases, and in fact, to be detrimental to the pulmonary 1989). Recurrent bacterial infections combined
status of some patients. Caregivers have also been with this mucus hypersecretion in the lungs
shown to suffer from the performance of percus­ leads to destruction of the bronchial walls, or
sion-repetitive motion injuries of the wrists have bronchiectasis. Airway clearance continues to
been documented as a result of regular performance be an important therapy in the treatment of
of percussion (Ford, Godreau, Burns, 1991, MMWR cystic fibrosis. This practice is supported by
Publication 1989). evidence of deteriorating lung function when
Alternate techniques have arisen out of the need to regular treatments of postural drainage and
find effective methods for those patients not respon­ percussion have been stopped (Desmond,
sive or not tolerant of traditional methods. A desire to 1983, Reisman, 1988).
increase compliance with airway clearance (Currie, 2. Bronchiectasis-This condition results in a
1986), especially in those patients approaching ado­ breakdown of the elastic tissue in the bronchial
lescence and adulthood has led to an investigation of walls, causing severe dilation. Inflamed mucosa
more independent techniques. Many of these tech­ and copious, purulent secretions are present in
niques have been practiced for years in European this condition. Airway clearance has been
countries, but are more recently being introduced to shown to benefit patients with bronchiectasis in
practitioners in the United States. the mobilization of sputum (Mazzocco, 1985,
It is important to remember, however, that secre­ Gallon, 1991).
tion clearance is but one step to take toward realizing 3. Atelectasis-This condition is caused by the
effective gas exchange in the complex oxygen trans­ collapse of an alveolar segment, often by re­
port pathway (Dean, 1992). Airway clearance, when tained secretions. It is a documented sequela of
indicated, should be integrated into a total approach patients who have undergone surgery under
to optimize oxygen transport. general anesthesia, especially thoracic or ab­
dominal surgery. Airway clearance techniques
are indicated where atelectasis is suspected to
INDICATIONS FOR AIRWAY CLEARANCE
be caused by mucus plugging (Marini, 1979,
Oxygen transport is the primary purpose of the car­ Hammon, 1981).
diopulmonary system (see Chapter 1). Ventilation of 4. Respiratory muscle weakness-Many patients
the alveoli is an important step in the oxygen trans­ with neurological or metastatic diseases or gen­
port chain that allows optimal delivery of oxygen to eral debilitation, tend to hypoventilate or have an
the tissues. Several medical and surgical conditions increased work of breathing. They are unable to

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 19 Physiological Basis for Airway Clearance Techniques 323

maintain adequate control of respiratory secre­ tance of gravity (Figure 19-1). Positioning the patient
tions and often have a weak, ineffective cough to enable gravity to assist the flow of bronchial secre­
(Massery, 1987). This is especially true in pa­ tions from the airways has been a standard treatment
tients with diminished diaphragm innervation re­ for some time in patients with retained secretions
sulting from spinal cord injuries (Wetzel, 1990). (Zadai,1981).
5. Mechanical ventilation-Patients on ventilatory Knowledge of the anatomy of the tracheobronchial
support for any reason, including obtunded or tree is vital to an effective treatment. Each lobe to be
comatose patients, are at risk for atelectasis and drained must be aligned so that gravity can mobilize
are unable to independently manage their secre­ the secretions from the periphery to the larger, more
tions (Dickman, 1987). central airways. The mechanism of postural drainage
6. Neonatal respiratory distress syndrome-These is considered to be a direct effect of gravity on
infants are born lacking surfactant in the lungs, bronchial secretions, although a study by Lannefors
which results in atelectasis. Airway clearance (1992) observing that gravity influences regional
techniques may be useful in clearing secretions lung ventilation and volume suggested these other
and preventing atelectasis but must be moni­ mechanisms are also involved.
tored carefully in this population (Finer, 1978). Postural drainage (also k n o w n as b r o n c h i a l
7. Asthma-This condition is characterized by the drainage) has been shown t o b e effective i n mobiliz­
presence of hyperreacti ve airways and mucus ing secretions in patients with cystic fibrosis (Wong,
plugging. Airway clearance techniques may be 1977, Lorin, 1971), bronchiectasis (Mazzacco, 1985),
beneficial to assist with the mobilization of and other pulmonary diseases (Bateman, 1981; Zaus­
mucus plugs but are not helpful in treating un­ mer, 1968). Other treatments such as percussion, vi­
complicated acute exacerbations (Eid, 1991). bration, and the active breathing cycle (ACB) tech­
Chest physical therapy techniques appear not to be nique may be used while the patient is in postural
beneficial in the treatment of patients with pneumo­ drainage positions.
nia or chronic bronchitis without large amounts of se­ There are many contraindications to optimal posi­
cretion production. No differences were found with tioning for PO, especially the head down or Trende­
the inclusion of postural drainage and percussion in lenberg positions required for the lower lobes.
these populations (Britton, 1985; Sutton, 1982;
Rochester, 1980; Wollmer, 1985).
Percussion
Viral bronchiolitis is an asthma-like lung disease
occurring in infants less than 2 years of age. These Percussion, sometimes referred to as chest clapping,
patients do not appear to benefit from airway clear­ is a traditional approach to secretion mobilization. A
ance techniques (Webb, 1985). rhythmical force is applied with cupped hands to the
Also of little benefit, and possibly harmful, is the patient's thorax over the involved lung segments with
inclusion of chest physical therapy in the routine care the aim of dislodging or loosening bronchial secre­
of postoperative patients without extensive secretions tions. This technique is performed with the patient in
(Eid, 1991). Even in patients with a history of lung postural drainage positions and requires a caregi ver
disease, the use of airway clearance techniques have to administer. In the United States,percussion in con­
failed to affect the incidence of atelectasis as a post­ junction with postural drainage continues to be a
operative complication (Torrington, 1984). mainstay of treatment of the person with pulmonary
disease, especially in neonates or patients who are
unresponsive.
Postural Drainage
The proposed mechanism of action of percussion
Postural drainage (PO) is a passive technique, in is the transmission of a wave of energy through the
which the patient is placed in positions that allow the chest wall into the l u n g . T h e resulting motion
bronchopulmonary tree to be drained with the assis­ loosens secretions from the bronchial wall and

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324 PART III Cardiopulmonary Physical Therapy Interventions

Normal Phase: 1 2 3

FIGURE 19·1
Phases of autogenic drainage shown on a spirogram of a normal person. Phase 1: unstick phase 2:
collect, phase 3: evacuate. (VT = tidal volume,ERV expiratory reserve volume. RV reserve
= =

volume, FRC = Punctual residual capacity, IRV inspriatory reserve volume; fRV + VT + ERV
= =

vital capacity)

Vibration
moves them proximally where ciliary motion and
cough (or suction) can remove them. The combina­ Vibration is a sustained cocontraction of the upper
tion of postural drainage and percussion has been extremities of a caregiver to produce a vibratory force
shown to be effective in secretion removal (Denton, that is transmitted to the thorax over the involved
1962; May, 1979, Radford, 1982). A study by Ross­ lung segment. Vibration is applied throughout exha­
man et al. (1982) is in disagreement, finding that me­ lation concurrently with mild compression to the
c h a n i c a l p e rcussion did n o t enhance postural chest wall. Vibration is often applied in postural
drainage in secretion removal. drainage positions following percussion to the area.
A handheld mechanical percussor may be used by A mechanical vibrator may be used by the patient or
a caregiver to decrease fatigue or by the patient for a caregiver in place of manual vibration.
self-administration of percussion. The effectiveness Vibration is proposed to enhance mucociliary
of mechanical versus manual percussion has been transport from the periphery of the lung fields to the
studied. Maxwell and Redmond (1979) found me­ larger airways. Since vibration is used in conjunction
chanical percussion equivalent to manual percussion with PD and percussion, many studies do not separate
in affecting removal of secretions. This is supported out the effects of vibration from the other compo­
by Pryor et a1. (1979) in patients using the forced ex­ nents. In fact in multiple studies, the techniques of
piration technique, although there was a significant PD, percussion, and vibration are described as a single
increase in pulmonary function with manual tech­ entity and referred to as chest physical therapy (CPT),
niques (Pryor, Parker, and Webber, 1981). pulmonary therapy, or postural drainage therapy.
There are many contraindications to percussion. If Pavia (1976) demonstrated a higher, though not sta­
the patient's pulmonary status is of greater concern tistically significant, rate of secretion clearance and
than the relative contraindications, it may be decided sputum production with vibration. However, this study
to modify and administer the treatment. was conducted with subjects in an upright position

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 19 Physiological Basis for Airway Clearance Techniques 325

only, not a replication of the use of vibration clinically. applies shaking or vibration at the very beginning of
Mackenzie et al. (1980) used measurement of total exhalation to mobilize secretions. The timing of this
lung/thorax compliance to assess the effect of secre­ sequence is important to achieve the desired effect
tion clearance. Significant improvement in total (Webber, 1988). It has been likened to simulation of a
lung/thorax compliance was demonstrated after treat­ cough----deep inspiration, pause, and forceful exhala­
ment with postural drainage, percussion, and vibra­ tion. Saline may be instilled into the airway at the be­
tion in mechanically ventilated patients. Feldman et ginning of the cycle, with suctioning a component at
al. (1979) demonstrated improved ventilatory func­ the end of treatment of each side. Manual hyperventi­
tion by showing a significant improvement in expira­ lation is peIt'ormed in postural drainage positions and
tory flows at lung volumes in patients receiving pos­ requires two competent caregivers to peIt·orm.
tural drainage, percussion, vibration, and coughing. The inspiration provided by the manual ventilation
bag, which is deeper than the patient could generate,
promotes aeration of the alveoli. The compression of
Shaking
the thorax augments the high expiratory flow rate
Shaking consists of a bouncing maneuver sometimes from the bag, accelerating the movement of the secre­
referred to as "rib splinging" against the thoracic wall tions from the smaller airways to the larger bronchi
in a rhythmic fashion throughout exhalation. A concur­ (Clement, 1968).
rent pressure is given to the chest wall, compressing Clement (1968) reports this method of airway
the thorax. Shaking is similar in application to vibra­ clearance enables patients to be maintained on ventila­
tion, with shaking being on one end of the spectrum in tors for long periods with normal lung function. It has
application of force, and vibration being on the oppo­ been demonstrated that hyperinflation and suction in
site end, supplying a gentler amount of pressure. Many the treatment of atelectasis was enhanced by the addi­
variations exist throughout the spectrum between these tion of positioning and vibrations (Stiller, 1990).
techniques. Shaking may be used in place of percus­
sion or intermittently with percussion and vibration.
Active Cycle of Breathing
Shaking may be used in postural drainage positions
and requires the assistance of a caregiver. Thompson (1973) in New Zealand described clearing
Shaking is proposed to work in the same manner bronchial secretions in patients with asthma by a
as vibration, mobilizing secretions to the central, technique of forced expirations and diaphragmatic
larger airways from the lung periphery. Since the breathing. British physiotherapists have modified the
compressive force to the thorax is greater, producing technique and further described it in the literature,
increased chest wall displacement, the stretch to the first as the forced expiration technique (FET) (Pryor,
respiratory muscles may produce an increased inspi­ 1979) and later as the ACB technique (Webber and
ratory effort and lung volume (Levenson, 1992). Pryor, 1993).
The same relative contraindications for percussion As described by Webber and Pryor (1993), the
should be observed for shaking, since it does involve ACB consists of repeated cycles of three ventilatory
application of force to the thorax. phases: breathing control, thoracic expansion exer­
cises, and the FET. Breathing control is described as
gentle tidal volume breathing with relaxation of the
Manual Hyperinflation
upper chest and shoulders. The thoracic expansion
This technique is used on patients with an endotra­ phase consists of deep inspiration, and may be ac­
cheal or tracheostomy tube that can be attached to a companied by percussion or vibration peIt'ormed by a
manual ventilation bag. One caregiver uses the bag to caregiver or the patient. This phase helps to loosen
hyperinflate the lungs with a slow, deep inspiration secretions. The forced expiration technique involves
and after a short inspiratory pause, provides a quick one or two huffs (forced expirations). Webber and
release to allow rapid exhalation. A second caregiver Pryor (1993) report huffing from a mid-lung volume

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326 PART III Cardiopulmonary Therapy Interventions

(a medium sized breath and continued down to the hV[)OSi�Cn tlOn. This sug­
low-lung volume will move secretions from the pe­ nJY'HmcrPfl retention of
to the upper secre­ little sputum.
tions may be cleared a huff from lung vol­
ume (a breath The ACB may be performed
Autogenic Drainage
in the sitting position, but has been shown to be more
effective in gravity assisted drainage) posi­ (AD) or was in­
tions (Steven, 1992). troduced Chevaillier in Belgium in 1967 for treat­
The period of breathing control is essential be­ ment of asthmatic patients. He observed that during
tween the other phases to bronchospasm sleep, as well as playing and laughing the day,
(Lapin, 1990). The o f thoracic expansion, mucus was mobilized better than PD and cJap-
which increases collateral AD is an antidyspnea technique based on
ventilation, allowing air to behind secretions and in a relaxed state without use of nMtn ,,1

assist in their mobilization I Mead et at (Chevaillier,

(1 described the of "equal aohragmatic breathing to mobilize secre­

pressure point," which is the basis for the FET. The airflow. It consists of three

pressure point is the point in the airways at low-lung volumes to "unstick"

where the pressure is to the pleural pressure. peJ]DJ1eral secretions, (2) breathing at low- to mid­

The forced expiratory maneuver compres­ volume (tidal volume) to collect the mucus in the
sion of the airway peripherally to the EPP. A huff middle and (3) breathing at mid- to
from high lung volume causes compression within volumes to evacuate the mucus from the central air­
the trachea and bronchi to move secretions from ways 1984). The patient is seated in a re­
these airways. A huff continued to low lung laxed position and exhales actively with the mouth and
volume shifts the EPP more oeripherallv to move open and listens for the movement of mucus
while a wheeze. The phases in the AD tech-
a patient delJ'ict<�d in 19-1.
nhU ;AIA"" of AD's three
by pa­ has been ex­
tients independently has been shown to clear more by Shoni (1989). The first
sputum in a shorter amount of time than PD with self- starts with an inspiration, followed by a breath hold to
combined with and shaking by ensure of lung segments by collateral fill-
a physical therapist (PT) Improvement and then a deep exhalation into the re­
in pulmonary function 1986) and sputum serve volume range. By lowering mid-tidal volume
clearance (Sutton, 1983) have been demonstrated in below functional residual capacity secretions
patients with cystic fibrosis who the FET from peripheral lun!:! regions are mobilized
into their postural drainage treatments. alveolar ducts.
Because huffing has been shown to stabilize col­ tidal volume is lowered in the range of normal
lapsible bronchial wails, it increases the expiratory tory reserve volume. The second of AD consists
flow in patients with obstruction without air­ of tidal volume so that is
way (Hietpas, Another benefit of this from reserve volume into the in-
lies in its ability to maintain oxygen satura­ reserve volume range to mobilize secretions
tion. The decrease in oxygen saturation that has been from the of the lungs. The of the
demonstrated with postural and percussion airflow must be adjusted at each level of so
has been prevented with the use of the ACB technique that the maximal expiratory ailflow is reached without
1990). Hassani et al. (1994) has recently shown being high enough to cause collapse of the
that unproductive cough and FET resulted in the Flow volume curves show that higher flows of
movement of secretions proximally from all regions of duration can be achieved with AD (Dab. 1

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 19 Physiological Basis for Airway Clearance Techniques 327

demonstrating that mucus can be moved further and at The application of PEP consists of a mask or
a faster rate. The third phase consists of deeper inspira­ mouthpiece connected to a one-way breathing valve
tion into the inspiratory reserve volume, with huffing to which expiratory resistors are attached. This re­
often used to help in evacuating the mobilized secre­ sults in positive pressure in the airways during exha­
tions. Control of ailflow during this final phase is es­ lation. A manometer in the circuit determines and
sential to avoid uncontrol led, unproductive coughing. monitors the correct pressure generated by the pa­
The Belgian method has been modified by German tient. A patient uses PEP in a cycle of about 10
practioners to use a combination of diaphragmatic and breaths at tidal volume with slightly active expiration
costosternal breathing in a treatment that is not delin­ followed by huffing or coughing to expectorate secre­
eated into phases (David, 1991). The patient varies his tions (Falk and Kelstrup, 1993).
or her mid-tidal volume in a passive exhalation followed High- or low-pressure PEP may be prescribed. In
by an active exhalation through pursed lips or through low-pressure PEP, the resistance is regulated to
the nose. The German method includes other maneuvers achieve 10 to 20 cms of water pressure during expira­
in conjunction with autogenic drainage, including in­ tion. The pressure should be sustainable during only
halation therapy, FET, chest wall exercises, and sports. slightly active expiration. The prescription for high
Autogenic drainage has been compared with posi­ pressure PEP requires the patient to perform forced
tive expiratory pressure and PD with percussion/ vital capacity maneuvers through the range of expira­
vibration. More sputum was produced with AD in pa­ tory resistances with the mask connected to a spirome­
tients with hyperreactive airways (Davidson, 1988). ter. The appropriate resistor is one that produces a flow
In a 2-year crossover trial, AD was found to be as ef­ volume curve demonstrating a maximal forced vital
fective as conventional CPT among patients with cys­ capacity, good plateau, and no curvilinearity (Prasad,
tic fibrosis for improving pulmonary function 1993). In general, the range of pressure generated with
(Davidson, 1992). However, patients exhibited a high pressure PEP is 50 to 120 cms of water pressure.
strong preference for AD, increasing the likelihood of Low-pressure PEP is used more often, as it offers
compliance. Miller (1993) showed greater clearance equal effectiveness at a lower risk of pneumothorax.
of inhaled radioisotope with AD vs. the ACB tech­ It is theorized that PEP allows more air to enter
nique, with no significant differences in sputum through collateral channels, allowing reinflation of
weight, spirometry, or transcutaneous oxygen satura­ collapsed alveoli. Pressure is built up distal to an ob­
tion. Giles (1993) also studied oxygen (02) saturation struction, promoting the movement of secretions to­
in AD and found an increase in O2 saturation with wards the larger airways (Anderson, 1979; Groth,
AD over PD with percussion and greater sputum re­ 1985). Airway stability is maintained with PEP pro­
covery with AD. moting improved ventilation and gas exchange, as
The learning of AD requires tactile and auditory well as airway clearance (Hardy, 1994). Supplemen­
feedback and continued modifications of the patient's tal oxygen can be supplied during treatment with PEP
technique is necessary, at least initially, to achieve a and nebulized medication has been shown to be ef­
good result. AD takes considerable time to learn and fectively delivered with this treatment as well (An­
requires a great deal of cooperation from the patient. derson, 1982).
Therefore it is not suitable for the very young or dis­ PEP has been shown to benefit patients at risk for
tractable patient. postoperative atelectasis but has also gained wide
practice in the area of airway clearance, especially for
patients with cystic fibrosis (MaJhmeister, 1991). Nu­
Positive Expiratory Pressure
merous studies have demonstrated PEP's effective­
The development and utilization of positive expira­ ness. Tyrrell (1986) has shown the PEP mask to be as
tory pressure (PEP) breathing came about in the effective as conventional physiotherapy over a 1
1980s in Denmark and is now widely used in Europe month period with no difference in pulmonary func­
with increasing acceptance in the United States. tion. Falk (i 984, 1993) demonstrated increased spu­

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328 PART III Cardiopulmonary Physical Therapy Interventions

tum production and clearance with the use of PEP Recently approved by the FDA for use by patients
over FET alone. However. Hofmeyer (1986) found with cystic fibrosis, the Flutter'M continues to be the
FET produced a greater quantity of sputum without focus of study in the United States. Konstan et a!.
the addition of PEP. Oberwaldner (1986) evaluated (1994) compared the amount of sputum expectorated
lung function during 10 months of regular treatments with use of the Flutter'" vs. vigorous voluntary cough
with high-pressure PEP and found reduced pul­ vs. PD, percussion and vibration. More than three
monary hyperinflation and airway instability and times the amount of sputum was produced by subjects
higher flow rates with PEP VS. conventional CPT. with cystic fibrosis using the Flutter'" than with the
These improvements in lung function deteriorated other two methods and no adverse effects were re­
only 2 months after a return to conventional CPT. A pOited. Ambrosino (1991) has reported success in the
study by Plfeger et a!. (1992) compared PEP to AD treatment of COPD patients with the device.
and found that PEP produced the highest amount of Reports in the European literature advocate the
sputum and an increase in lung function when added use of the Flutter'" for airway clearance (Althaus,
to both techniques. Finally, decreased duration of 1989). In comparison with AD, the Flutter'" was
hospitalization has been cited as a benefit of PEP for found to be equal in amount of mucus expectoration
airway clearance (Simonova, 1992). (Lindemann, 1992). When compared with the PEP­
Increased independence for the patient and pre­ m ask, the Flutter'" showed a small increase i n
sumably, better compliance have been cited as advan­ spirometry, whereas the PEP-mask did not, but the
tages of this technique. However, frequent assess­ two techniques were otherwise comparable (Schw.
ment of patient technique and appropriate level of Med. Wschr. 1989).
resistance is recommended (Lapin, 1990). A PEP The advantages of the Flutter'" device lie in its
mouthpiece (Resistex) has recently been FDA ap­ pOltability and ease of learning. Young children can
proved, but the PEP mask has not yet been approved be taught to use the device effectively, and because
by the FDA. of its small size, it can easily be used for multiple
A form of PEP in combination with high fre­ treatments throughout the day.
quency oscillation is available in a device developed
in Switzerland. which is quickly gaining popularity in
High Frequency Chest Compression
the United States. The Flutter™ VRP1 (VarioRaw SA,
Aubonne, Switzerland) is a handheld device that in­ EffOits aimed at mucus clearance by creating a differ­
terrupts the expiratory flow and decreases the col­ ential air flow rate, that is, greater expiratory than in­
lapsability of the airways. The pipe-like device con­ spiratory flow rate, led to the development of a high
sists of a steel ball, a plastic cone, a pertorated cover, frequency chest compression (HFCC) systcm.
and a mouthpiece. The patient completes about lO to Hansen and Warwick (1990) designed a large-vol­
15 deep breaths keeping the cheeks flat while the ume variable frequency air-pulse delivery system to
Flutter'M is tilted to achieve the maximum effects of be used by patients with obstructive lung disease to
the vibration in the chest. This is followed by huffing promote mucus clearance.
to eliminate the airway secretions. The ThAIRapy'" Vest (American Biosystems,
Exhalation through the Flutter'M device causes air­ Inc.) system consists of an inflatable fitted vest con­
way vibrations and oscillating endobronchial pres­ nected to an air-pulse. generator by flexible tubing.
sures (Althaus, 1993) to ease the expectoration of This device provides oscillation of the entire thoracic
mucus. The PEP maintained by the Flutter™ (5 to 35 cavity at varying frequencies (5 to 25 Hz) and is used
cms of water pressure) prevents dynamic airway while sitting upright. The lung volume expired tends
compression and improves airflow acceleration. to increase with lower frequencies (less than to to 12
Therefore the improvement in expectoration is based Hz), whereas the flow rates tend to increase with
on the increase in airway diameter, as well as on the higher frequencies (12 to 20 Hz). Three frequencies
improvement in airflow acceleration (Schibler, 1992). are selected for large volume and three for high

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 19 Physiological Basis for Airway Clearance Techniques 329

flows. Each frequency is used for 3 to 5 minutes with Hospitalized patients with acute exacerbation of
conti I1UOUS ul:J"osolized medication or saline to assist their lung disease have been shown to tolerate HFCC
secretion Illohilil.ation (Warwick, 1992). well (Burnett, 1993), and safety and tolerance of this
Two probahlc mechanisms of action have been of­ method has been demonstrated in long-term mechani­
fered to explain the significant increase in sputum mo­ cally ventilated patients (Whitman, 1993).
bilizJlion (Kious, 1(94). The first mechanism pro­ Expense of the apparatus may be a significant de­
poses that oscillatory airflow· leads to changes in the terrent to its use; it is more costly than other mechan­
con.;islency of mucus, which result in increased spu­ ical aids for airway clearance. However, in a study of
tum mobilil.ation. Significant decreases in mucus vis­ HFCC users insured by Blue Cross and Blue Shield,
coelasticity were observed during administration of a 49% reduction in health care costs was shown in
oscillatory aitflow (Tomkicwicz et aI, (994). The sec­ the year following initial use of the vest as compared
ond mechanism proposes that the difference between with the year prior to HFCC use (Ohnsorg, 1994).
the expiratory and inspiratory velocities produces The impact of the llse of the HFCC device in a hospi­
shear forces s lrong enough to move muclls. Chang et tal department was analyzed with a substantial sav­
al. (1988) lkmonstrated that nonsymmetrical airflow ings resulting from therapy self-administration
(peak expiratory flow rates greater than inspiratory (KIous, 1993).
flow ratt:s) could be a significant factor leading to en­
harlCed mllcus clearance during the administration of
Exercise
HFCC. Each chest compression produces a transient
flow pulse similar to that observed during coughing In addition to its many effects on health and well­
and by using those flows with the greatest rates and being, exercise has been shown to assist in secretion
volumes, sufficient force is obtained to move mucus clearance. It has been suggested that exercise can re­
in the airway (Warwick, 1991). place all or pmt of a conventional chest physiotherapy
High frequency chest wall compression has been routine in some patients or at some stages of lung dis­
shown to inc re as e mucus clearance rates in dogs, ease (Zach, 1982; Andreasson, 1987; Cerny, 1989).
with the most pronounced effect in the II to 15Hz Exercise increases mucociliary transport in pa­
frequency range (King, 1983). Radford et al. (1982) tients with chronic bronchitis (Oldenberg, 1979).
used bronchoscopy to demonstrate a marked increase Higher transpulmonary pressure with aerobic exer­
in speed and flow of mucus by oscillations at even cise may open closed bronchi as well as increase col­
higher frequencies not attainable by manual percus­ lateral ventilation to allow mucus to be movcd (An­
sion. Results of short-term use of the ThAIRapy'" dreasson, 1987). It has also been shown that exercise
vest have been mixed, but show HFCC to be at least induced hyperventilation is more effecti ve than eu­
as effective as conventional CPT. Robinson (1992) capnic hyperventilation in mobilizing bronchial se­
showed no significant i m pro vement or deterioration cretions (Wolff, 1977). The contribution of expira­
of lung function with its use. In two different studies, tory ailflow and exercise-induced coughing are other
Kluft (1992) and Faverio (1994) demonst rated in­ factors in more effective secretion removal.
creased wet and dry sputum weights using HFCC vs. Some studies conclude that exercise alone is not
manual CPT, and Arens (1993) showed similar dry sufficient and recommend its use to complement
sputum weight, but an increase in wet sputum weight other forms of airway clearance. Airway clearance
and a significant improvement in pulmonary function using PD and FET was shown to be more effective
with HFCC vs. conventional CPT. One 2-year study than exercise with a cycle ergometer at inducing spu­
showed improved lung function and greater sputum tum expectoration (Sath, et ai, 1989). Results from
production in subjects with cystic fibrosis with the Bilton et al (1992) demonstrated that any modality
use of HFCC vs. manual CPT (Warwick, 1991). No which included the ACB technique in PD positions
adverse effects were ohsL rvcd with long-term use of alone or in combination with exercise is better than
the ThAIRapy'" vest. exercise alone at clearing sputum.

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330 PART III Cardiopulmonary Physical Therapy Interventions

Other studies have suggested that some forms of 1990). However, if the patient develops atelectasis,
exercise may serve as a replacement for chest physio­ the stress of respiratory embarrassment may also in­
therapy, citing a lack of decrease in lung function fol­ crease intracranial pressure. In this instance, the deci­
lowing the cessation of CPT and continuing with an sion may be made to tip the patient to clear the at­
exercise program (Zach, 1984; Andreasson, 1987). In electasis and then subsequently return to a modified
hospitalized patients with cystic fibrosis, no signifi­ conservative regimen (Frownfelter, 1987).
cant change in pulmonary function was reported A fall in arterial O2 saturation has been reported
when exercise was substituted for two treatments of with the use of postural drainage from additional in
PD, percussion and vibration, and the weight of spu­ chest physiotherapy, although the effects of PD were
tum produced was equivalent (Cerny, 1989). not separated techniques (Selsby, 1990; Huseby,
When mucous clearance was studied, no signifi­
cant differences were found between exercise on a
cycle ergometer, postural drainage, and PEP mask
breathing (Lannefors, 1992). Increases in sputum ex­ Contraindications for Postural Drainage
pectoration on exercise vs. nonexercise days have
All Positions Are Contraindicated
been reported (Zach, 1981; Baldwin, 1994). For pa­ for the Following:
tients with cystic fibrosis who demonstrate compli­
Intracranial pressure (ICP) > 20 mm Hg
ance with an exercise program alone or in addition to
Head and neck injury until stabilized
another form of secretion mobilization, there is evi­
dence of positive prognostic value (Nixon, 1992). Active hemorrhage with hemodynamic instability

It is difficult to compare these studies across the Recent spinal surgery (e.g .• laminectomy) or acute

board; however, because the mode and length of ex­ spinal injury

ercise differs, as does the measurement of effective­ Active hemoptysis

ness of airway clearance. Exercise as an airway clear­ Empyema

ance technique is not suitable for the very young (less Bronchopleural fistula
than 4 to 5 years of age), patients with neuromuscular
Pulmonary edema associated with congestive heart
limitations, or patients with severely limited exercise failllJ'e (CHF)
tolerance. Moreover, the potential need for supple­
Large pleural effusions
mental oxygen during exercise should be monitored.
Pulmonary embolism
Nonetheless, evidence suggests that an exercise pro­
Aged, confused, or anxious patients
gram, in addition to clearing secretions, may decrease
morbidity and mortality t J improving exercise ca­ Rib fracture. with or without flail chest

pacity (Lapin, 1993). Surgical wound or healing tissue

Trendelenburg Position is Contraindicated

.
Contraindications/Precautions to Airway Clearance for the Following:

Patients in whom increased ICP is to be avoided

General precautions and contraindications
to postural drainage positioning Uncontrolled hype11ension

It is essential that the therapist and the health care Distended abdomen

team discuss treatment priorities. A decision to use Esophageal surgery

postural drainage might be made despite a contraindi­ Recent gross hemoptysis related to recent l ung
cation, if the benefits were thought to outweigh the carcinoma
risks in a particular case. Uncontrolled airway at risk for aspiration
For example, it is known that use of the Trende­
lenburg (head down) position increases intracranial AARC Clinical Practice Guideline. (1991). Postural drainage ther­
pressure in neurosurgical patients (Humberstone, apy. RespiraIOI)' Care, 36 (12), 1418-1426.

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 19 Physiological Basis ror Airway Clearance Techniques 331

[976). Therefore O2 saturation levels should be mon­ show an intolerance for percussion as part of chest
itored during treatment, most importantly in those pa­ physiotherapy. Campbell et a1. (1975) demonstrated
tients with known [ow Pa02 values. a fall in FEV I associated with percussion that was
Caution must also be used in treating the patient not evident when percussion was omitted. Adminis­
with end-stage lung disease in postural drainage posi­ tration of a bronchodilator before treatment with per­
tions because of the risk of hemoptysis (Hammon, cussion abolished the fall in FEV I. Wheezing has
1979; Stern, [978). also been associated with percussion and vibration in
Decreased cardiac output (Laws, 1969; Barrell, patients with cystic fibrosis and COPD (Tecklin,
[978) has been associated with chest physiother­ 1975; Feldman, 1979).
apy treatment; however, the effects of postural The box below summarizes the precautions and
drainage were not separated from those of percus­ contraindications for external manipulation of the
sion and vibration. thorax associated with percussion, shaking, and high
In the pediatric population, some experts recom­ frequency chest compression. Vibration involves less
mend caution with the position used to treat the ante­ force to the thorax and may be better tolerated than
rior lower lobes because of the risk of gastroe­ the aforementioned techniques. A nebulized bron­
sophageal reflux. The box on p. 330 summarizes the chodilator may be administered during a treatment of
precautions and contraindications for postural high frequency chest compression to avoid the conse­
drainage. quences of hyperreactive airways.

General contraindications and precautions

Other precautions
to external manipulation of the thorax
Manual hyperinflation has been shown to cause sig­
In patients who are very young, who have limited nificant depression of cardiac output in patients who
ability to cooperate, or who are not compliant with
other airway clearance techniques, percussion, shak­
ing, and vibration offer a method to dislodge retained
secretions. Because of the force transmitted to the Contraindications to External
thoracic cage with these techniques, there are many Manipulation of the Thorax
precautions and contraindications to consider. The
In Addition to Contraindications for Postural
therapist should not make this decision alone, but Drainage:
needs direction from the medical team. Chest physio­
Subcutaneous cmphysema
therapy is not a completely benign procedure and
Recent epidural spinal infusion or spinal anesthesia
should not be peliormed in the absence of good indi­
Recent skin grafts, or flaps, on the thorax
cations (McDonnell, 1986).
Percussion has been shown to contribute to a fall Bums. open wounds. and skin infections of the thorax

in Pa02 in acutely ill patients (Connors, 1980), espe­ Recently placed pacemaker
cially in patients with cardiovascular instability (Oor­ Suspected pulmonary tuberculosis
menzano, 1972) and in neonates (Fox, 1978). The
Lung contusion
factor that seems most associated with or predictive
Bronchospasm
of the effect is the baseline or before-therapy Pa02
Osteomyelitis of the ribs
(McDonneJl, 1986).
Cardiac arrhythmias have been associated with Osteoporosis

chest percussion for bronchial drainage (Hammon, Coagulopathy

1981). Huseby (1976) hypothesizes that hypoxemia Complaint of chest-wall pain
may be the underlying mechanism of CPT-caused
cardiac arrhythmias. AARC Clinical Pracli ce Guideli'ne. (1991). Postural drainage ther­
Patients with hyperreactive airways (e.g., asthma) apy. Respil'(l/ory Care,]6 (12),1418-1426.

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332 PART III Cardiopulmonary Physical Therapy Interventions

are unable to compensate hemodynamically with lit­

Factors to Be Considered When Selecting
tle cardiac reserve (Clement, 1968; Laws, 1969). Sig­
an Airway Clearance Technique
nificant and deleterious increases in ICP have also
been demonstrated (Garradd, 1986). Webber (1988) Motivation
offers these additional contraindications to manual Patient's goals
hyperinflation: severe hypoxemia with few bronchial
Physician/caregiver's goals
secretions as in ARDS, acute pulmonary edema, air
Effectiveness (of considered technique)
leak (e.g., pneumothorax), severe bronchospasm as in
Patielll's age
acute asthma, and hemoptysis.
The use of PEP for airway clearance carries an in­ Patient's abiliLY to concentratc

creased risk of pneumothorax (Oberwaldner, 1986). Ease (of learning and of teaching)
Bronchodilator premedication should be considered Skill of therapists/teachers
when applying PEP in patients who show clinical
Fatigue or work required
and/or physiological signs of airway hyperreactivity
Need for assisLants or equipmelll
(Pfleger, 1992).
LimiLations of technique based on disease type and
The increased aitilow produced by the huff cough,
severity
as in the ACB technique, may aggravate bron­
Costs (direct and indirect)
chospasm (Hietpas, 1979). Additionally, Hietpas cau­
tions that spontaneous explosive coughing may be Desirability of combining methods

precipitated by the movement of secretions into the

larger airways by the huff cough. Hardy, K.A. (1994). A review of airway clearance: new techniques,
indications, and recommendations. Re.ljJimlorv Care, 39 (5), 440-452.
Several precautions must be observed when using
exercise as a form of airway clearance. Desaturation
has been shown to occur with exercise in people with
pulmonary disease (Lane, 1987; Henke, 1984), and a prescribed treatment has a negative influence on pa­
therefore it becomes prudent to monitor oxygen satu­ tient adherence. It has been suggested that enhanced
ration, providing supplemental oxygen for the exer­ compliance might be achieved if the treatment were
cise period when indicated. Exercise-induced bron­ specifically tailored to the individual patient's needs
chospasm must also be considered when pulmonary with regard to clinical status, family functioning, and
compromise is seen with exercise, especiall y with family concerns. Negotiation between the patient and
higher intensity exercise (Godfrey, 1975). When indi­ the caregiver to agree on follow-through with the pre­
cated, it is recommended to provide an inhaled bron­ scribed treatment regimen is also effective (Shultz,
chodilator 20 to 30 minutes before exercise to allevi­ 1980). For this reason, it is imperative to consider
ate this symptom (Orenstein, 1985). Andreasson multiple factors in the recommendation of a specific
(1987) reports a risk of pneumothorax in conjunction technique of airway clearance, especially in the pa­
with exercise in those patients with extensive bullae. tient with a chronic disease (see box above).
The age of the patient will affect the usefulness of
a particular technique. Infants and very young chil­
Factors Affecting Selection of
dren are limited to conventional physical therapy
Airway Clearance Techniques
(postural drainage, perc'ussion,
In the pulmonary population, lack of compliance in they are not able to cooperate with other methods of
performing airway clearance on a regular basis has airway clearance. After the age of 3 or 4, a youngster
been well documented (Currie, 1986; Passero, 1981; may be taught huffing and brcathing control, and as­
Muszynski-Kwan, 1988; Litt, 1980). The problem is sisted with the ACB technique. A vest for use with
worse in the adolescent group. Litt (1980) has also HFCC is now available for children as young as 2 or
shown that the complexity and increased duration of 3 years of age. PEP, FlutterT' and exercise also are

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 19 Physiological Basis for Airway Clearance Techniques 333

suitable for this age group, depending on the child's Accessibility of equipment or trained personnel
attention span and cooperation. Children 12 years of limits the use of some airway clearance techniques.
age and older are capable of using any of the airway Many of these techniques are new or not available to
clearance techniques, including AD, which requires many health care centers, especially in the United
more concentration than a younger child is typically States, since they were pioneered in Europe. Proper
able to exhibit. instruction and review of a patient's technique is im­
The lack of an assistant to provide airway clearance perative to achieve optimal results, and in the case of
is a factor that prompts many patients to seek methods PEP, the reassessment of resistance is recommended.
other than postural drainage and percussion. HFCC, In the case of AD, the method is limited by the num­
PEP, Flutter''", ACB, exercise and AD are techniques ber of instructors available to teach the technique to
that provide independence from a caregiver. These patients and requires a great deal of time on the part
methods have been chosen by adults living on their of the health care team member to learn. The patient
own, students away at school, and adolescents eager must possess motivation and the time to learn the
for independence. For optimal results, each tech­ technique and be willing to "fine tune" the technique
nique's effectiveness must be regularly reevaluated by with the therapist periodically.
a health care team member skilled in the area of air­ In this area of cost containment, the financial re­
way clearance after it has been agreed that a patient ex­ quirements of a technique must also be taken into con­
hibits independence in a given technique. sideration, especially in the case of a chronic condi­
The clinical status of the patient during each hos­ tion. The availability of any given method then, could
pital admission must be evaluated to determine the be determined by the insurance coverage or additional
appropriateness of an ACT. For example, airway hy­ financial resources of the patient. If several methods
perreactivity might be worsened by PO and percus­ prove to be equally effective, it would be prudent to
sion, and care must also be taken when using ACB in select the methods requiring the least expense. Al­
this case. HFCC, Flutter''", and exercise should be though the most common form of airway clearance in
preceded with an inhaled bronchodilator in this case, the United States continues to be postural drainage
and PEP can be performed concurrently with bron­ and percussion by a caregiver, this often proves to be
chodilator administration. AD lends itself well to use quite expensive, especially if a family member is not
by patients with airway hyperreactivity. available for ongoing home treatments. The equip­
Gastroesophageal reflux prohibits patients from ment needed for ACTs varies. The generator required
performing airway clearance in conventional PO po­ for HFCC is expensive to purchase or rent on a
sitions. In this instance, AD, Flutter''', PEP, HFCC, monthly basis. Mechanical percussors or vibrators are
and exercise, or ACB in upright positions, are the moderately priced, and PEP and the Flutter™ valve are
preferred treatments. In infants or neurologically im­ the least expensive of those techniques requiring
paired patients where PO and percussion is the treat­ equipment. A patient independently using ACB or AD
ment of choice, modified PO positions are used and consumes the least financial resources.
sufficient time allowed between a feeding and a treat­ Ultimately, the regular use of a particular ACT by
ment with PD. a patient is governed by personal belief in the effec­
The severity of a patient's lung disease will affect tiveness of the method for his or her own disease
the choice of ACT. Specifically, a patient with end­ process, the manner in which the method affects the
stage lung disease or an acute exacerbation might not patient family's life habits, and the patient's willing­
have the required energy level to carry out an active ness to use the technique on a daily basis. Compli­
airway clearance technique such as AD or PEP effec­ ance is ultimately the best measure of any airway
tively. A more passive technique would be appropri­ c1earancc technique's effectiveness.
ate, at least temporarily. Also a marked decrease in Clinical outcome measures to assess the effective­
PFT's limits the airflow control necessary for AD, ness of an airway clearance technique can be fol­
F1utter™, or PEP. lowed during clinical appointments or periods of hos­

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334 PART III Cardiopulmonary Physical Therapy Interventions

pitalization. Radiographic changes, arterial blood gas must consider many factors in recommending an
values, O2 saturation, and pulmonary function tests alternate form of airway clearance. Age of the pa­
may demonstrate adequate airway clearance or the tient is a prime factor in the appropriateness of a
need to reassess the appropriateness of the technique selected technique. For infants, PO, percussion,
or the application of it by the patient. Though it is and vibration remain the mainstay of secretion
difficult to quantify, many patients subjectively rely clearance. In older children, the active cycle of
on amount of sputum production to guide their choice breathing may be initiated, positive expiratory
of secretion clearance method. This measure provides pressure and Flutter'" may be taught, and high fre­
immediate feedback to the patient without visiting the quency chest compression is available for children
hospital or clinic. after about age 3 or 4. Exercise should be included
in treatment as well. Children 12 years of age or
older and adults have the complete range of airway
SUMIVIARY
clearance techniques at their disposal, including
The goals of airway clearance are to decrease airway autogenic drainage.
obstruction, improve secretion clearance, and im­ Treatments aimed at secretion clearance require an
prove ventilation and gas exchange. Routine applica­ individualized approach to tailor the treatment to the
tion of airway clearance techniques in many condi­ patient's condition and lifestyle, to continuously
tions has not been shown to be effective in achieving reevaluate the patient's status, and to monitor the re­
these goals. ACTs are not without side effects or sponse to treatment.
complications; routine use of these methods is not Acceptance of the specific treatment technique by
recommended without clear indications. the patient and family is paramount; compliance is
Indications for ACTs have been divided into the key to achieving effective treatment, especialJy in
those for acute illness and chronic disease states. chronic lung disease.
In acute illness, traditional chest physical therapy, Further research in the area of airway clearance
that is, PO, percussion, and vibration, has been is certainly needed. Studies with consistent applica­
shown to be beneficial in patients with copious se­ tion of techniques, similar outcome measures, and
cretions and in the treatment of atelectasis (Kir­ consistent study design will assist practitioners in
iloff, 1985). For patients with cystic fibrosis, treat­ evaluating and recommending a given technique of
ment with PEP and exercise in conjunction with airway clearance.
PO, percussion, and vibration were also shown to
be effective in an acute exacerbation (Boyd, 1994).
REVIEW QUESTIONS
Acute asthma, bronchitis, and pneumonia without
copious secretions, bronchiolitis, and routine post­ I. What kinds of pulmonary conditions would not
operative conditions were not shown to benefit be likely to benefit from ACTs?
from PO, percussion, and vibration (Sutton, 1982; 2. Which ACTs would be the easiest (for the thera­
Eid,1991). pist and the patient) to incorporate into a routine
In chronic disease states, patients with cystic fi­ of conventional PO and percussion?
brosis and bronchiectasis were found to benefit from 3. What possible factors could be considered a con­
PO, percussion, and vibration (Kiriloff, 1985). Posi­ traindication to chest percussion with PO in a
tive expiratory pressure and exercise were also shown trauma or postoperative patient?
to be effective in the chronic management of patients 4. What factors might make it difficult for a patient
with cystic fibrosis (Boyd, 1994). to accept a new method of airway clearance?
In those patients for whom traditional chest 5. Which ACTs would be most appropriate during
physical therapy is not effective, the caregiver an acute exacerbation of a pulmonary disease?

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 19 Physiological Basis for Airway Clearance Techniques 335

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 Clinical Application of Airway
Clearance Techniques

Anne Mejia Downs

KEY TERMS Active cycle of breathing technique (ACBT) Manual hyperventilation

Airway clearance techniques (ACTs) Percussion
Autogenic drainage (AD) Postive expiratory pressure (PEP)
Dynamic air therapy bed Postural drainage (PD)
Flutter™ Shaking
Forced expiratory technique (FET) Trendelenburg
High frequency chest compression (HFCC) Vibration

INTRODUCTION
The previous chapter addressed the physiological
Oxygen transport from the lungs to body tissues can basis of each technique, the history of its use, and re­
be limited in patients that possess an ineffective search to establish its effectiveness. This chapter pro­
cough or an impairment of normal mechanisms of vides an introduction to the application of these tech­
mucociliary clearance. The caregiver must augment niques to patients and addresses the benefits and
these mechanisms using the array of techniques avail­ liabilities of each technique.
able for airway clearance. Each technique has a phys­ Airway clearance techniques differ with respect to
iological basis for improving the mobilization of equipment needs, the skill level required to perform
secretions. The caregiver must consider the patho­ them, and their usefulness with various clinical prob­
physiology and the symptoms of the disease, the lems. Matching a patient with an appropriate method
availability of the technique to the patient, and the or combination of methods may increase effective­
patient's acceptance of the technique in prescribing ness, reduce complications, and promote adherence
an optimal method of airway clearance. to the long-term treatment.

339

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340 PART III Cardiopulmonary Physic.al Therapy Interventions

UTILIZATION OF AIRWAY CLEARANCE TECHNIQUES

of tube feedings or meals. The inhalation of bron­
This section will deal with the application of airway chodilator mcdications should take place before air­
clearance techniques (ACTs) with specific instruc­ way clearance maneuvers. Inhaled antibiotics are best
tions for patient treatment. Contraindications and pre­ scheduled after airway clearance has taken place for
cautions for each ACT are addressed in Chapter 21. optimal deposition of medication. Adequate pain con­
This section will speak to practical concerns regard­ trol is necessary to receive a patient's best effort and
ing patient care. cooperation with a treatment. It is also impOitant to
Preparation for any secretion removal technique have all necessary equipment and personnel available
should include evaluation of the patient's pulmonary at the start of the treatment.
status (see Chapter 15) so that measures may be com­
pared before and after a treatment is completed. A
POSTURAL DRAINAGE
physical examination, including inspection, palpa­
tion, measurement of vital signs, and chest ausculta­ Postural drainage (PO) is accomplished by position­
tion provides assessment of a treatment's effective­ ing the patient so that the position of the lung seg­
ness. Laboratory tests including chest x-ray, arterial ment to be drained allows gravity to have its greatest
blood gas measurements, and pulmonary function effect (see Figures 20- I through 20-5). Modified po­
studies should be reviewed, since these may be used sitions are used when a precaution or relative con­
as measures of treatment effectiveness. traindication to the ideal position exists. For example,
Scheduling an optimal time for patient treatment if an increase in intracranial pressure is a concern, the
must take into account several factors. At least I half head of the bed should remain flat instead of being
hour to I hour should be allowed for the completion tipped into Trendelenburg (head down) position.

Both Upper Lobes

Apical Segments

Right Upper Lobe

Anterior Segment
- hIps .:Ire in external rotiltJon,
smilH pillow under knee:s for
:support 0' JoInts and comfort.

1
----

KPS. ,;,1>(1,.,

FIGURE 20-1
Upper lobes.

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 20 Clinical Application of Airway Clearance Techniques 341

Right Upper Lobe Left Upper Lobe Lingula

Posterior Segment

Both Lower Lobes Right Middle Lobe

Superior Segments (Apicall

FIGURE 20-2
Upper, middle, and lower lobes.

Both Lower Lobes Right Lower Lobe

Anterior Segments Lateral Segment

Both Lower Lobes Left Lower Lobe

Posterior Segments Lateral Segment,
RLL Cardiac (Mediall

FIGURE 20-3
Lower lobes.

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342 PART III Cardiopulmonary Physical Therapy Interventions

FIGURE 20-4
A, right upper lobe-posterior segment (anterior view-patient positioned three-fourths prone).
B, right upper lobe-posterior segment (posterior view). NOTE: Upper extremities toward prone,
underneath arm pulled free from under patient's body. This position may also be a modified
position for right lower lobe posterior segment.

FIGURE 20-5
Both lower Jobes-posterior segments (shown using teJeJphone books or piJlows for home use). A
beanbag chair is also helpful for home treatments.

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 20 Clinical Application of Airway Clearance Techniques 343

Equipment Required For Postural Drainage

specific lobe. Extended times in a position may
I. For the hospitalized patient, there exists a vari­ be used by coordinating the positioning with
ety of beds that employ manual or electric de­ nursing care for skin pressure relief. If postural
vices to position the patient. Air therapy beds, drainage is used in conjunction with another
most often used in the intensive care unit (lCU), technique, the time in each position may be de­
are valuable aids allowing ease of positioning, creased. For example, if percussion and vibra­
especially in large or unresponsive patients. tion are performed while the patient is in each
2. Make use of pillows or bedrolls to support PO position, 3 to 5 minutes is sufficient.
body parts or relieve pressure areas. 3. A patient who requires close monitoring should
3. For home treatmcnt, aids in positioning might not be left unattended in a Trendelenberg posi­
include pillows, a slant board (or ironing board tion, but this may be appropriate if patients are
if the patient is small), a foam wedge, sofa alert and able to reposition themselves.
cushions, or a bean bag chair. 4. It is not necessary to treat each affected lung
segment during each treatment; this may prove
to be too fatiguigg for the patient. The most af­
Preparation for Postural Drainage
fected lobes should be addressed with the first
l. Nebulized bronchodilators before PO may fa­ treatment of the day, with the other affected
cilitate the mobilization of sputum. areas addressed at a subsequent treatment.
2. An adequate intake of fluids (if allowed) de­ 5. The patient should be encouraged to take deep
creases the viscosity of the secretions, allowing breaths and cough after the treatment and if
easier mobilization. possible after each position. Having the patient
3. Become familiar with the workings of the sit upright or lean forward optimizes this effort
model of bed the patient is occupying, espe­ (Frownfelter, 1 987).
cially the movement of the bed into the Trende­ 6. Secretions may not be mobilized immediately
lenberg position. after the treatment but possibly 1 half hour to
4. In the ICU, it is imperative to be familiar with 1 hour later. The patient should be thus in­
the multiple lines, leads, and tubes attached to formed and requested to clear secretions then.
the patient. Allow enough slack from each de­ The nurse or family member should be in­
vice to position a patient for postural drainage. cluded in this aspect of treatment, especially
5. Make sure there are enough personnel to posi­ with difficult patients who need such encour­
tion the patient with as little stress to both pa­ agement (Frownfelter, 1987).
tient and staff as possible (Frownfelter, 1987).
6. Have suctioning equipment ready to remove se­
Advantages and Disadvantages of PO
cretions from an artificial airway or the pa­
tient's oral or nasal cavity after the treatment. PO is relatively easy to learn; the patient and/or care­
giver must be familiar with the appropriate position­
ing for the affected lung fields. Treatment in the hos­
Treatment with PO
p i t a l m a y be c o o r d i n a t e d w i t h o t h e r p a t i e n t
1 . After determining the lobe of the lung to be activities-po sitioning for s k i n pressu r e relief,
treated, position the patient in the appropriate po­ bathing, or positioning for a test or procedure. Home
sition, using pillows or bed rolls as needed to sup­ treatment may be coordinated with activities such as
port the patient comfortably in the position indi­ reading or watching television.
cated. See figures 20-1 through 20-5, p. 340-342. However, for many patients, optimal PO positions
2. If postural drainage is used exclusively, each will be contraindicated for a variety of reasons (see
position should be maintained for 5 to 1 0 min­ Chapter 21). Compliance with PO may be reduced
utes, if tolerated, or longer when focusing on a because of the length of the treatment, especially in

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344 PART III Cardiopulmonary Physical Therapy Interventions

FIGURE 20-6
A and B, If children are able to role play the treatment, they will better understand what is expected
and be more cooperative with therapy.

the pediatric population, who will require consider­ breathing. Percussion is used in postural drainage po­
able distractions to maintain a desired position. sitions for increased effectiveness (Sutton, 1985;
The cost of the equipment required for PD is mini­ Bateman, 1979) and may also be used dUling the ac­
mal; inexpensive items may be used for home treat­ tive cycle of breathing (ACB) technique.
ment. However, the cost of a caregiver's time to pro­
vide the treatment, especially in the case of a chronic
Equipment Required for Percussion
disease, may be substantial. A family member may
be willing to learn the procedure, which would pro­ 1. The only equipment required for manual per­
vide a benefit in terms of expense, as well as flexibil­ cussion is the caregiver's cupped hands to de­
ity in scheduling (Figure 20-6). liver the force to mobilize secretions.
2. For the adult and older pediatric population,
electric or pneumatic percussors that mechani­
PERCUSSION
cally simulate percussion are available. This
Percussion is performed with the aim of loosening re­ enables a patient to apply self-percussion more
tained secretions from the airways so they may be re­ effectively. Several models have variable fre­
moved by suctioning or expectoration. A rhythmical quencies of percussion, as well as different lev­
force is provided by clapping the caregiver's cupped els of intensity.
hands against the thorax over the affected lung seg­ 3. Several devices may be used to provide percus­
ment, trapping air between the patient's thorax and sion to infants: padded rubber nipples, pediatric
the caregiver's hands (Figure 20-7). It is performed anaesthesia masks, padded medicine cups, or
during both the inspiratory and expiratory phases of the bell end of a stethoscope.

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 20 Clinical Application of Airway Clearance Techniques 345

FIGURE 20-7
Chest percussion.

Preparation for Percussion

thema occurs with percussion, it is usually a re­
1. Placing the patient in appropriate PD positions sult of slapping or not trapping enough air be­
(as the patient's condition allows) enhances the tween the hand and the chest wall (Imle, 1989).
effect of percussion. 3. An even, steady rhythm will best be tolerated
2. Place a thin towel or hospital gown over the pa­ by the patient, and the rate of manual percus­
tient's skin where the percussion is to be ap­ sion is normally between 100 and 480 times per
plied. The force of percllssion over bare skin minute (lmle, 1989).
may be uncomfortable; on the other hand, 4. The force applied to the chest wall from each
padding that is too thick absorbs the percussion hand should be equal. If the nondominant hand
without benefit to the patient. is not able to keep up with the dominant hand,
3. Adjust the level of the bed so that proper body the rate should be slowed to match that of the
mechanics may be used during the treatment. slower hand. It might also be helpful to start
Fatigue or injury of the caregiver may be the with the nondominant hand and let the domi­
result of lengthy or numerous treatments if nant hand match the nondominant (Frownfelter,
proper body mechanics are ignored. 1987). The force does not have to be excessive
to be effective; the amount of force should be
adapted to the patient's comfort.
Treatment With Percussion
5. If the size of an infant does not allow use of a
I. Position the hand in a cup with the fingers and full hand, percussion may be done manually
thumb adducted. It is important to maintain this with four fingers cupped, three fingers with the
cupped position with the hands throughout the middle fi nger "tented," or the thenar and hy­
treatment, while letting the wrists, arms, and pothenar surfaces of the hand (Crane, 1990).
shoulders stay relaxed. 6. Hand position should be such that percussion
2. The sound of percussion should be a hollow does not occur over bony prominences. The
sound as opposed to a slapping sound. If ery­ spinous processes of the vertebrae, the spine of

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346 PART III Cardiopulmonary Physical Therapy Interventions

the scapula, and the clavicle should all be The expense of a mechanical device for percus­
avoided. Percussion over t h e floating ribs sion is minimal compared with the ongoing cost of a
should also be avoided, since these ribs have caregiver to provide percussion and PD in the hospi­
only a single attachment. tal setting or a home care situation. In the case of
7. Percussion should not be performed over breast young children or unresponsive patients, there are
tissue. This would produce discomfort and di­ few choices for airway clearance. For other popula­
minish the effectiveness of the treatment. In the tions, however, a more independent method would
case of very large breasts, it may be necessary also prove to be more cost-effective if adequate com­
to move the breast out" of the way with one pliance was achieved.
hand and percuss with the other hand.
8. A patient may be taught to perform one-handed
VIBRAnON/SHAKING
self-percussion to those areas that can b e
reached comfortably, either manually o r with a The techniques of vibration and shaking are on oppo­
mechanical percussor. This does however, vir­ site ends of a spectrum. Vibration involves a gentle,
tually preclude the treatment of the posterior high frequency force, whereas shaking is more vigor­
lung segments. ous in nature. Vibration and shaking are performed
with the aim of moving secretions from the lung pe­
riphery to the larger airways where they may be suc­
Advantages and Disadvantages of Percussion
tioned or expectorated. Vibration is performed by co­
The addition of percussion to a PD treatment may en­ contracting all the muscles in the caregiver's upper
hance secretion clearance and shorten the treatment. extremities to cause a vibration while applying pres­
Patients often find the rhythm soothing and are re­ sure to the chest wall with the hands. Shaking is a
laxed and sedated by percussion, especially young stronger bouncing maneuver, which also supplies a
children and infants. concurrent, compressive force to the chest wall.
Patients with chronic lung disease, who have used Like percussion, vibration and shaking are lIsed in
PD and percussion for many years and have found it conjunction with PD positioning. Unlike percussion,
effective, are reluctant to try an alternative method of they are performed only during the expiratory phase
airway clearance. Compliance with this method is de­ of breathing, starting with peak inspiration and con­
pendent on the availability of a family member or tinuing until the end of expiration. The compressive
other caregiver to provide the treatment. Mechanical forces follow the movement of the chest wall.
percussors allow the patients more independence or
decrease fatigue of a caregiver, and are especially use­
Equipment Required for Vibration/Shaking
ful in patients requiring ongoing treatment at home.
Percussion is not well-tolerated by many patients I. For manual techniques, the only equipment re­
postoperatively without adequate pain control. The quired is the caregiver's hands.
force of percussion is also a threat to patients with os­ 2. Mechanical vibrators are available to administer
teoporosis or coagulopathy. Other contraindications the treatment and are useful for self-treatment
are listed in Chapter 21. Percussion has been associ­ by a patient or to reduce fatigue in the caregiver.
ated with a fall in oxygen saturation, which can be 3. For infants, a padded electric toothbrush is an
eliminated with concurrent thoracic expansion exer­ alternative (Crane, 1990).
cises and pauses for breathing control (Pryor, 1990).
Delivering percussion for extended periods on an
Preparation for Vibration/Shaking
ongoing basis can result in injury to the caregiver,
whether a family member or a health care provider. I. Place the patient in the appropriate PD posi­
Repetitive motion injuries of the upper extremities tion or modified position as the patient's sta­
may occur in long-term delivery of percussion for tus allows.
airway clearance. 2. Place a thin towel or hospital gown over the

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 20 Clinical Application of Airway Clearance Techniques 347

patient's skin. The material should not be ment of chest deflation.

thick enough to absorb the effect of the vibra­ 4. If the patient is mechanically ventilated, the
tion or shaking. previously described techniques must be timed
3. Proper body position of the caregiver is impor­ with ventilator-controlled exhalation.
tant to deliver an effective treatment and to de­ 5. If the patient has a rapid respiratory rate, either
crease caregiver fatigue. voluntary or ventilator-controlled, it may be
necessary to apply vibration or shaking only
during every other exhalation.
Treatment with Vibration/Shaking
6. The frequency of manual vibration is between
I. Conventional chest physical therapy is often re­ 12 and 20 Hz; shaking is 2 Hz (Gormezano,
ferred to as a combination of postural drainage 1972; Bateman, 1981).
and percussion, vibration, or shaking. 7. A mobile chest wall is necessary to apply a com­
2. For shaking, with the patient in the appropriate pressive force without causing discomfort. If a pa­
PO position, place your hands over the lobe of tient has limited chest wall movement, vibration
the lung to be treated and instruct the patient to will probably be tolerated better than shaking.
take in a deep breath. At the peak of inspiration, 8. Mechanical vibrators may be used by patients
apply a slow (approximately 2 times per sec­ themselves, realizing that limited attention can
ond), rhythmic bouncing pressure to the chest be paid to the posterior portions of the lungs.
wall until the end of expiration. The hands fol­
low the movement of the chest as the air is ex­
Advantages/Disadvantages of Vibration/Shaking
haled.
3. For vibration, the hands may be placed side by The use of vibration or shaking with PO may enhance
side or on top of one another as shown in Fig­ the mobilization of secretions. Shaking or vibration
ures 20-8 and 20-9. As with shaking, the pa­ may be better tolerated than percussion, especially in
tient is instructed to take in a deep breath while the postsurgical patient.
in a proper PO position. A gentle but steady co­ Manual vibration and shaking allows the caregiver
contraction of the upper extremities is per­ to assess the pattern and depth of respiration. The
. formed to vibrate the chest wall, beginning at stretch on the muscles of respiration during expira­
the peak of inspiration and following the move- tion may encourage a deeper inspiration to follow. A

FIGURE 20-8 FIGURE 20-9

Vibration-hands positioned on both sides of the chest. Vibration-hand p)acement one on top of the other.

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348 PART III Cardiopulmonary Physical Therapy Interventions

Equipment Required for Manual Hyperinflation

mechanical vibrator, more commonly used with pedi­
atric patients, may be preferred by a caregiver to de­ I. A manual ventilation bag, such as the Ambu, at­
liver long-term airway clearance. tached to an oxygen source is needed for lung
The patient cannot apply these techniques her­ inflation. A positive-end expiratory pressure
self, except in a limited manner with a mechanical (PEEP) valve may be attached. This is recom­
vibrator, so compliance and regular administration mended when greater than 10 cm PEEP is being
of vibration depends on caregiver availability. used for mechanical ventilation (Webber, 1993).
The same contraindications for percussion apply, 2. A second trained caregiver is necessary to pro­
since compression to the thorax is involved with shak­ vide shaking or vibration in an appropriate se­
ing and vibration. The technique of vibration is less quence with lung inflation.
constrained by these contraindications than is shaking. 3. Normal saline should be available for installa­
tion into the airways to assist with loosening
secretions.
MANUAL HYPERINFLATION

The technique of manual hyperinflation is used in pa­

Preparation for Manual Hyperinflation
tients with an artificial airway, who are mechanically
ventilated or who have a tracheostomy. This method of 1. It may be necessary to premedicate the patient
airway clearance promotes mobilization of secretions with a sedative or analgesic so that airway
and reinflates collapsed areas of lung. Two caregivers clearance may be better tolerated.
are necessary to provide this treatment and the coordina­ 2. The two caregivers providing the treatment
tion between these two people is key to achieving satis­ should be positioned on opposite sides of the
factory results. This technique is shown in Figure 20-10. bed to allow greater freedom of movement and

FIGURE 20-10
Simulated cough using self-inflating bag and chest compression with vibration.

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 20 Clinical Application of Airway Clearance Techniques 349

Advantages/Disadvantages of Manual Hyperinflation

improved observation of the patient's response
to treatment. Manual hyperinflation may be helpful in managing air­
3. Normal saline (2 to 3 mL) may be used before way secretions in those patients requiring long-term me­
hyperinflation to assist with loosening, thick se­ chanical ventilation. In this patient population, the
cretions (Webber, 1993). choice of airway clearance techniques is limited, espe­
4. The positions for treatment will be primarily cially when the patient is unresponsive. Manual hyperin­
side-lying with the head of the bed flat or flation simulates a cough by augmenting the inspiratory
slightly elevated to patient tolerance. effort, momentarily maintaining a maximal inspiratory
hold, and causing an increased expiratory flow.
However, hyperinflation has the potential to cause
Treatment With Manual Hyperinflation
significant barotrauma. There are a number of con­
1. One caregiver squeezes the manual ventilation traindications to this technique including unstable he­
bag slowly to inflate the lungs. A pause i s modynamics, pulmonary edema, air leak, and severe
maintained momentarily at the peak o f inflation bronchospasm (Webber, 1988). In addition, it is not
to allow collateral ventilation to fill underex­ appropriate for infants with increased pulmonary resis­
panded areas of the lung. Release of the bag tance requiring high inflation pressures or in preterm
should be rapid, resulting in a high expiratory infants at risk of pneumothorax (Webber, 1993). Other
flow rate (Clement, 1968). contraindications are discussed in Chapter 21.
2. A second caregiver provides thoracic compres­ Thus manual hyperinflation requires two well-trained
sion with shaking or vibration to assist with the caregivers. This may be its biggest disadvantage.
mobilization of secretions. The compression
phase should begin just before the inflation
ACTIVE CYCLE OF BREATHING TECHNIQUE
pressure has been released and continue until
the end of the expiratory phase. The active cycle of breathing (ACB) technique involves
3. In a patient who is breathing spontaneously, three phases repeated in cycles: breathing control, tho­
"bag squeezing" with the manual ventilation racic expansion, and the forced expiratory technique
bag should be timed to augment the patient's (FET). This method encourages active participation of
inspiratory effort, making vibration more effec­ the patient and has been shown to be as effective when
tive (Imle, 1989). perfonned by the patient alone as with the aid of a care­
4. After about six cycles of inspiration/expiration, giver (Pryor, 1979). Postural drainage positions may be
the patient's airway is suctioned using sterile used in conjunction with ACB technique. This method
technique. The length of treatment is individu­ of airway clearance may be used with some children as
alized and depends on the amount of secretions young as 3 or 4 years of age. The sequence of ACB
present in the airways and the areas of the technique is shown in the box on p. 350.
lungs affected.
5. Manual hyperint1ation may be performed with Equipment Required for ACB Technique
intubated infants or children using an appropri­
ately sized ventilation bag. Care must be taken 1. The only equipment required for this manual
to apply slow inflation, so as to avoid a high technique is the patient's or caregiver's hands
peak inspiratory pressure, which carries the risk to percuss or shake/vibrate the chest wall dur­
of barotrauma (Webber, 1993). ing the thoracic expansion phase.
6. When manual hyperinflation is contraindicated, 2. Mechanical percussors or vibrators may be
shaking or vibration may be timed with the expi­ used during the thoracic expansion phase, ei­
ratory phase of the ventilator without additional ther for self-percussion by the patient or for use
inflation during inspiration (Webber, 1988). by the caregiver.

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350 PART III Cardiopulmonary Physical Therapy Interventions

ACB Technique

• Breathing control

Diaphragmatic breathing at no nnal tidal volume

• 3-4 Thoracic expansi on exercises

Deep inhalation with relaxed exhalation at

vital capacity

with or without chest percussion

• Breathing control

• Three to four thoracic e xp an sion exe rcises

• Breathing control

• Forced exp iratory technique

One to two huffs at mid to low lung volume

Abdominal muscle contracti on to produce

forced exhalation
FIGURE 20-11
Peak flow meter mouthpiece.
• Breathing control

Adapted from Webber, B., J. (1993). Physiotherapy skills:

Pryor,
techniques and adjuncts. In Webber, B. Pryor, J. (eds.). (1993).
Physiotherapy for respiralory and cardiac problems. Churchill
Livings\one: Edinburgh. ducti ve area of the lungs. The entire treatment
may also be done in the sitting position.
3. A minimum of 10 minutes in any productive
position may be necessary to clear a patient
3. If PD positions are used, equipment for posi­ with a moderate amount of secretions. Patients
tioning will be required. after surgery or with minimal secretions may
4. To teach the huffing maneuver (part of the not require as much time, and very ill patients
FET), it may be helpful to use a peak flow may fatigue before optimal treatment is given
meter mouthpiece to keep the mouth and glottis (Webber, 1993).
open (Figure 20-11). Young children may be
taught games of huffing at cotton balls or tissue
Treatment With the Active Cycle
to improve the technique (Webber, 1993). To
of Breathing Technique
help them focus on the expiratory maneuver,
small children may also be taught to flap their I. Breathing control-The patient is instructed to
arms to their lateral chest as they perform the breathe in a relaxed manner using normal tidal
huff, a technique referred to as the "chicken volume. The upper chest and shoulders should
breath" (Mahlmeister, 1991). remain relaxed and the lower chest and ab­
domen should be active. The phase of breathing
control should last as long as the patient re­
Preparation for ACB Technique
quires to relax and to pr epare for the next
I. Treatment of two or three productive areas during phases, usually 5 to J a seconds.
one session may be tolerated by most patients. 2. Thoracic expansion - The emphasis during this
2. The patient is positioned or positions herself in phase is on inspiration. The patient is instructed
a PD position to stimulate drainage of a pro- to take in a deep breath to inspiratory reserve;

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 20 Clinical Application of Airway Clearance Techniques 351

Ineffective Huffing Effective Huffing

• Mouth half or almost closed • Mouth open, O-shaped to keep glottis open

• Expiratillfi always starting from high lung volume • Forced expiration

• Abdominal muscles not used From mid to low lung volume moves periph­
eral secretions
• Sound more like hissing or blowing
from high to mid lung volume moves proxi­
• Mouth shaped ;)s for "E" sound mal secretions

• Incorrect quality of expiration • Muscles of the chest wall and abdomen contract.

• Too vigorous or long. producing paroxysmal • Sound is like a sigh. but forced.
coughing
• Rate of expiratory flow varies with the following:
Too gentle
The individual
•

• Too short The disease

• "Catching" or "grunting" at the back of the throat The degree of airflow obsu'lIction

• Crackles heard if excess secretions are present

From Partridge, et ai, Physiotherapy, March 1989, Vol. 75, No.3

expiration is passive and relaxed. The caregiver

or the patient may place a hand over the area of
the thorax being treated to further encourage in­
creased chest wall movement. breath in will be effective. This huff will be
3. Chest percussion, shaking, or vibration may be longer and quieter. To clear secretions that
performed in combination with thoracic expan­ have reached the larger, proximal airways, a
sion as the patient exhales. For surgical pa­ huff after a deep breath in will be effective.
tients or those with lung collapse, a breath hold This huff will be shorter and louder.
or a sniff at the end of inspiration encourages 6. The patient must pause for breathing control
collateral ventilation to assist with reexpansion after one or two huffs. This will prevent any in­
of the lung. crease in airflow obstruction.
4. FET: This phase consists of huffing inter­ 7. The ACB technique may be adapted to the indi­
spersed with breathing control. A huff is a vidual patient's needs. If secretions are tena­
rapid, forced exhalation but not with maximal cious, two cycles of the thoracic expansion
effort. This maneuver can be compared with phase may be necessary to loosen secretions
fogging a pair of eyeglasses with warm breath before the FET can follow. In a patient with
so they may be cleaned. Unlike a cough in bronchospasm or unstable airways, the period
which the glottis is closed, a huff requires the of breathing control may be as long as 10 to 20
glottis to remain open. In an effective huff, the seconds (Webber, 1993). After surgery, the pa­
muscles of the abdomen should contract to pro­ tient may be shown how to support the incision
vide greater expiratory force. Other characteris­ with their hands during the FET to achieve suf­
tics of effective vs ineffective huffing are ficient expiratory force.
shown in the boxes above. 8. When a huff from a medium-sized inspiration
5. Two different levels of huffing are character­ through complete expiration is nonproductive
ized in the FET. To mobilize secretions from and dry sounding for two cycles in a row, the
peripheral airways, a huff after a medium-sized treatment may be concluded (Pryor, 1991).

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352 PART III Cardiopulmonary Physical Therapy Interventions

Advantages and Disadvantages of ACB Technique quired for the patient in whom percussion or shaking
during the thoracic expansion phase increases the ef­
Incorporation of the ACB technique into a treatment fectiveness of the treatment.
of PO and percussion allows the patient to participate Care must be taken to adapt the ACB technique for
actively in a secretion mobilization treatment and of­ patients with hyperreactive airways or after surgery.
fers the prospect of independently managing airway This individual approach will be helpful with all pa­
clearance. The ACB may be introduced at 3 or 4 tients using the technique to optimize effectiveness.
years of age, with a child becoming independent in
the technique at 8 to 10 years of age.
AUTOGENIC DRAINAGE
The technique may be adapted for patients with
gastroesophageal reflux, bronchospasm, and an acute Autogenic drainage (AD) is a breathing technique
exacerbation of their pulmonary disease. A decrease that uses expiratory airflow to mobilize bronchial se­
in oxygen saturation caused by chest percussion may cretions. It is a self-drainage method that is per­
be avoided by using the ACB technique (Pryor, formed independently by the patient in the sitting po­
[990). When the technique is performed indepen­ s i t i o n . AD c o n s i s t s of three phases: (1) the
dently, the cost of using ACB technique for the long "unsticking" phase. which loosens secretions in the
term is minimal. peripheral airways, (2) the "collecting" phase, which
However, in young children and in extremely ill moves the secretions to the larger, more central air­
adults, a caregiver wi/I be necessary to assist the pa­ ways, and (3) the "evacuating" phase, which results
tient with this technique. An assistant will also be re- in the removal of the secretions. This technique of
airway clearance requires much patience and concen­
tration to learn and is therefore not suitable for young
children. It is ideal, however, for the adolescent or
adult who prefers an independent method.

Equipment Required for AD

1. No equipment is needed for a patient to perform

the technique of AD. The patient must possess
good proprioceptive, tactile, and auditory per­
ception of the mucus moving; this feedback
makes it possible to adjust the technique of AD.
2. To teach this method to a patient, a caregiver
requires keen tactile and auditory senses to
coach a patient to move between the phases by
listening to and feeling the location and the
quality of the secretions.

FIGURE 20-12
Autogenic drainage: German method. Autogenic drainage Preparation for AD
shown on a spirogram of a normal person. The method is
I. The patient should be seated upright in a chair
not divided into separate phases. (Vt=tidal volume,
with a back for support. The surroundings should
ERV=expiratory reserve volume, RV=reserve volume,
be devoid of distractions, allowing the patient to
FRC=functional residual capacity, IRV=inspiratory reserve
volume, IRV + Vt + ERV = vital capacity). (From David, concentrate on the breathing technique.
A. (1991). Autogenic drainage-the German approach. In 2. The upper airways (nose and throat) should be
Pryor, J. (Ed.), Re pir{/{orv Care, Edinburgh: Churchill cleared of secretions by huffing or blowing
Livingstone.) the nose.

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 20 Clinical Application of Airway Clearance Techniques 353

3. The caregiver should be seated to the side and 5. The evacuating phase-In this phase, the pa­
slightly behind the patient, close enough to hear tient increases inspiration into the inspiratory
the patient's breathing. One hand should be reserve volume range. This middle-to-high
placed to feel the work of the abdominal mus­ lung volume breathing continues until the se­
cles and the other hand placed on the upper cretions are in the trachea and are ready to be
chest (see Figure 20-12). expectorated. The collected mucus can be
evacuated by a stronger expiration or a high­
volume huff. Nonproductive coughing should
Treatment With Autogenic Drainage
be avoided, since it may result in collapse of
l. In all phases, inhalation should be done slowly, airways.
though the n o s e if possible, using the di­ 6. Compression of the airways should be avoided.
aphragm or lower chest. A 2- to 3-second If wheezing is heard, the expiratory t10w rate
breath hold should follow, allowing collateral must be decreased. Beginners may have to use
ventilation to get air behind the secretions. p u rs e d l i ps to a v o i d a i r w a y c o m p r e s s i o n
2. Exhalation should occur through the mouth (Chevaillier, 1992). Instructing the patient t o
with the glottis open, causing the secretions to roll the tongue (if possible) may assist i n con­
be heard. The vibrations of the mucus may also trolling the expiratory flow rate.
be felt with the hand placed on the upper chest. 7. A German modification of AD resulted from
The frequency of these vibrations reveals their the observation that many patients had diffi­
location. High frequencies mean that the secre­ culty breathing in the expiratory reserve vol­
tions are located in the small airways; low fre­ ume range. In the simplified procedure, the pa­
quencies mean that the secretions have moved tient begins by varying the mid-tidal volume
to the large airways (Chevaillier, 1992). without excessive effort. After a passive but
3. The umticking phase-This phase mobilizes rapid expiration, an actively performed expira­
mucus from the periphery of the lungs by lower­ tion follows, achieving exhalation to a low ex­
ing the mid-tidal volume below the functional piratory reserve volume (David, 199 1). See
residual capacity level (Schoni, 1989). In prac­ Figure 9- 1, p. 155. for the difference between
tice, inspiration is followed by a deep expiration the two methods of AD.
into the expiratory reserve volume. The patient 8. The duration of each phase of AD depends on
attempts to exhale as far into the expiratory re­ the location of the secretions. The duration of
serve volume as possible, contracting the abdomi­ a session depends on the amount and viscos­
nal muscles to achieve this. This low lung volume ity of the secretions. A patient who is experi­
breathing continues until the mucus is loosened enced in autogenic drainage will clear secre­
and starts to move into the larger airways. t i o n s in a s h o r t e r a m o u n t of t i m e t h a n a
4. The collecting phase: This phase collects the beginner. An average treatment wiiJ be 30 to
mucus in the middle airways by increasing the 45 minutes in length.
lung volume over the unsticking phase. Tidal
volume breathing is then changed gradually
Advantages and Disadvantages of AD
from expiratory reserve volume toward the in­
spiratory reserve volume range (Schoni, 1989) After instruction in the technique of AD has been
so that the lungs are expanded more with each completed, it may be performed independently by pa­
inspiration. The patient increases both inspira­ tients over 12 years of age and requires no additional
tion and expiration to move a greater volume of equipment. Since it does not require the use of pos­
air. This low to middle lung volume breathing tural drainage positions, it is appropriate for patients
continues until the sound of the mucus de­ with gastroesophageal ret1ux. It is also recommended
creases, signaling its movement into the central f o r use in patients with airway hyperreactivity
airways to be evacuated. (Pfleger, 1992).

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354 PART III Cardiopulmonary Physical Therapy Interventions

Although it is widely used in Europe, the use of PEP is performed in the upright position and can
AD in the United States is limited by the lack of be used during acute episodes, as well as chronic pul­
trained caregivers but is growing in popularity. monary conditions. Children over 4 years of age may
To learn this technique, patients must demonstrate be instructed in the technique, and PEP may provide
good self-discipline and possess the ability to concen­ an independent method of airway clearance in older
trate. This method takes more practice than others. A children and adults.
patient must also be available for periodic reevalua­
tion and refinement of the technique.
Equipment Required For Positive
AD is not the treatment of choice for a patient who
Expiratory Pressure
is unmotivated or uncooperative, and the study of
flow volume curves suggests that AD would not be I. A PEP mask is manufactured by Astra Tech in
appropriate for small children even if they are coop­ Denmark, but is not approved by the Federal
erative (Dab, 1979). Department of Agriculture (FDA) and is not
The period of hospitalization for an acute pul­ available in the United States. However, a self­
monary exacerbation is a difficult time for a patient made PEP mask system may be assembled
to learn AD. In fact, patients who are skilled in the using a soft ventilation mask, a T-piece, a one­
technique choose a more passive (less energy-con­ way valve, and resistors of various sizes or an
suming) form of airway clearance at such a time until adjustable resistor valve (Figure 20-13). The
they return to their baseline pulmonary status. mask should fit tightly but comfortably over the
mouth and nose.
2. Another form of PEP delivery consists of a
POSITIVE EXPIRATORY PRESSURE
mou thpiece attached to a one way valve (for
Positive expiratory pressure (PEP) creates a back use with noseclips) with adjustable expiratory
pressure to stent the airways open during exhalation resistance. The Resistex ™ valve (from Mercury
and promotes collateral ventilation, allowing pressure Medical, Clearwater, Fla.) has recently been
to build up distal to the obstruction. This method of FDA-approved.
airway clearance prevents collapse of the airways, 3. A manometer is placed proximal to the resistor
which eases the mobilization of secretions from the in the initial stages of instruction in the use of
periphery toward the central airways. A mask or PEP. First, the manometer helps to determine
mouthpiece apparatus provides a controlled resis­ and monitor the appropriate level of resistance
tance (10 to 20 cm water pressure) to exhalation and needed for the patient to achieve 10 to 20 cm of
requires a slightly active expiration; tidal volume in­ water pressure throughout exhalation. Sec­
spiration is unimpeded. ondly, the visual display of the manometer
A variation of positive expiratory pressure, known serves as feedback to assist the patient in mas­
as high-pressure PEP, uses the same mask apparatus tering the technique (Mahlmeister, 1991).
but at much higher levels of pressure (50 to 120 cm 4. Aerosol medication by nebulizer or metered
water pressure). Inspiration is performed to total lung dose inhaler may be placed inline to be deliv­
capacity; this is followed by a forced expiratory ma­ ered simultaneously with PEP for airway clear­
neuver against the PEP mask. ance. Deposition .of medication improves with
A form of intermittent PEP is provided by a de­ PEP (Andersen, 1982; Frischnecht-Christensen,
vice called the FlutterT". This pipe like device pro­ 1991).
vides (I) positive expiratory pressure, (2) oscillation 5. Supplemental oxygen may also be placed inline
of the airways (at frequencies of 6 to 20 Hz) and for patients who are hypoxic.
(3) accelerated expiratory flow rates to loosen secre­ 6. With high-pressure PEP mask therapy, spirom­
tions and move them centrally. etry is used to determine the appropriate resis­

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 20 Clinical Application of Airway Clearance Techniques 355

FIGURE 20-13
Self-made PEP mask system.

tance for each patient individually. 2. If aerosolized medication is to be used simulta­

7. The Flutter'M VRPI valve (from VarioRaw, neously, the patient should be instructed in how
Switzerl and), recently FDA - a p p roved, is to stop the flow of the aerosol when the mask
marked in the United States (by Scandipharm or mouthpiece is removed during the PEP treat­
Pharmacy, Birmingham, Ala.). It is a pipe-like ment session.
device consisting of a mouthpiece, a plastic 3. To determine the correct level of resistance for
cone, a steel ball, and a petforated plastic cover. low-pressure PEP, the patient inhales using
8. The PEP mask, mouthpiece, and the Flutter™ tidal volume and exhales actively into the
should be cleaned regularly with hot, soapy mask/mouthpiece. Different resistors are tested
water. The one-way valve should be cleaned (or the resistor valve is adjusted) while the
with hot water only; soap may cause it to stick level of PEP is monitored on the manometer.
or become brittle. In the hospital, the equip­ The resistance is gradually decreased until the
ment will need to be sterilized according to in­ PEP level supplying 10 to 20 cm of water pres­
fection control recommendations. sure has been identif i e d (Falk 1993).
Mahlmeister (199 J) reports most patients
achieve this pressure range with flow resistors
Preparation for PEP
of 2.5 to 4.0 mm in diameter. Selection of the
1. For PEP therapy, the patient should be seated proper resistor produces the desired inspiratory
upright with elbows resting on a table. Use of a to expiratory ratio of l:3 to 1:4 (Mahlmeister,
mask may require securing the device with both 1991). The use of too great a resistance will
hands for a tight seal (Figure 20-14). create too Iow a pressure or an increased respi­

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356 PART III Cardiopulmonary Physical Therapy Interventions

FIGURE 20-15
Use of Flutrer (R) valve.

pressure and frequency while movement of the

device downward results in lower pressure and
frequ e n c y (Al t h a us, 1993). The Flutter™
reaches frequencies of between 6 and 20 Hz.

FIGURE 20-14
Treatment With PEP
Preparation for PEP therapy.
1. The patient should be instructed to breathe into
ratory rate, whereas too small of a resistor will the mask or mouthpiece to tidal volume using
create too high a pressure or a slow respiratory the lower chest and abdomen. Exhalation into
rate (McIlwaine, 1993). the mask or mouthpiece should be slightly ac­
4. For high-pressure PEP, appropriate resistance is tive but not forced.
determined by connecting the outlet of the PEP 2. The patient continues breathing into the mask
mask to a spirometer. Forced vital capacity ma­ or mouthpiece for 10 to 15 breaths, using a nor­
neuvers are peliormed through different expira­ mal respiratory rate. Initially, the patient and
tory resistors. The resistor producing the highest caregiver monitor the effort by means of the
forced vital capacity through the PEP mask is manometer, ensuri'ng that a pressure of 10 to 20
selected for continued use (Oberwaldner, 1986). cms of water pressure is achieved throughout
5. To use the Flutter'" valve, the patient should be exhalation. After the technique is mastered with
seated upright (Figure 20-15). The full effects the appropriate resistor, the manometer may be
of the vibration induced by the Flutter™ may be removed from the system. The appropriate re­
received by changing the angle of the device. sistance should be rechecked periodically dur­
Movement of the Flutter'M upward increases the ing clinical visits or periods of hospitalization.

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 20 Clinical Application of Airway Clearance Techniques 357

against the PEP mask. This is repeated until all

Technique for Using FlutterT"
the mucus is mobilized (Mcllwaine, 1993).
• Inhale deeply and hold breath for 2 to ) seconds. 6. The recommended procedure for use of the Flut­
ter'''' is shown in the box at left. The device is
• Place Flutter"" in mouth and, keeping cheeks as
stiff as possible, exhale through Flutter'M adjust­ held horizontally with the lips tightly around the
ing the degree of tilt to maximize vibrations. mouthpiece. After a deep inspiration through the
nose, the breath is held for 2 to 3 seconds before
• Exhalation need not be forced. Patient best deter­
mines "speed" of exhalation. exhaling deeply through the Flutte r'''. The
cheeks must be kept flat and to use the abdomi­
• Perform multiple exhalations through the Flutter'"
nal muscles for effective exhalation. The vibra­
(usually 5 to 15) with breath hold to maximize
mobilization of mucus. tion of the chest may be palpated by the patient
and caregiver to provide feedback as to the opti­
• Ajier pelforminR multipl e " lo o s e ning " breaths,
mal angle of the device. A Flutte,:'''' session con­
increase depth of breath and speed of exhalatioll
'" sists of I 0 to 15 breaths followed by huffing
Ihrough F/uller to Ilrecipilllle coughing and
mucus expectoration, (this may be done into the device), with a ses­
sion lasting about 15 to 20 minutes. To avoid
• Repeat entire sequence until "clear,"
dizziness due to hyperventilation. a patient
should refrain from forced exhalation. It may be
For more information abollt Flutter"". contact' Sandipharl11; 22 In­
verness Center Parkway; Birmingham, AL 35242; (205) 991-8085. necessary to pause every 5 to to exhalations be­
fore resuming the session (Althaus, 1993).

Advantages and Disadvantages of PEP

3. After a series of 10 to 15 breaths, the mask is PEP therapy does not possess some of the limitations
removed from the face and the patient performs of conventional PD and percussion for secretion clear­
a series of huffs (and coughing if necessary) to ance and is therefore applicable to a wider patient pop­
expectorate any mucus that has been mobilized. ulation. It is relatively easy to learn in one or two ses­
4. The series of PEP breaths followed by huffs sions, and may be applied equally to the pediatric and
should be repeated about four to six times. The adult populations. PEP is appropriate for use in hospi­
total treatment lasts about 15 to 20 minutes and talized patients, as well as long-term use at home.
should be repeated twice to three times during The expense of the equipment is minimal and once
the day. The frequency and duration of the the patient is competent in the technique. it provides
treatment must be individualized for each pa­ independence (except for small children). All of the
tient. During periods of pulmonary exacerba­ PEP devices (the Flutter'" in particular) are quite
tion, patients are encouraged to increase the portable, making airway clearance easier to perform
frequency of PEP treatments, rather than ex­ during travel or when away from home during the day.
tending the length of individual s e s s i o n s Although rare, pneumothorax has been reported
(Mahlmeister, 1991). with high-pressure PEP (Oberwaldner, 1986). A deci­
5. The procedure for use of high-pressure PEP sion to use PEP should be carefully evaluated in
differs from that of low-pressure PEP. The ex­ cases of acute sinusitis, ear infection, epistaxis, recent
piratory pressure used in this method usually oral or facial surgery or injury (Mahlmeister, 199/).
ranges between 50 and 120 cms of water pres­ For PEP therapy to be effective, a patient should be
sure. The patient breathes in and out through able to cooperate and actively participate with the
the mask at tidal volume for 6 to LO breaths, treatment. Pfleger (1992) recommends that patients
then inspiration is done to total lung capacity with airway hyperreactivity should take a bron­
and a forced expiratory maneuver is performed chodilator premedication before the use of PEP.

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358 PART III Cardiopulmonary Physical Therapy Interventions

Low-pressure PEP is more commonly used i n

North America, because it is felt t o be a s effective,
easier, and safer to use and monitor than high-pressure
PEP. In those patients in whom PEP is an appropriate
airway clearance technique, a high degree of accep­
tance has been shown (Falk, 1984; Steen, 1991). This
may translate into better adherence in the long term.

HIGH FREQUENCY CHEST COMPRESSION

The ThAIRapy® (from American Biosystems, Inc.,

St. Paul, Minn.) system of high frequency chest com­
pression (HFCC) (also refelTed to as high frequency
chest wall oscillation) consists of a vest linked to an
air-pulse generator. Figure 20-16 shows a patient
using HFCC. Although the sensation of the device is
somewhat akin to mechanical percussion, it differs
significantly in its mechanism of action. HFCC
works by differential airtlow, that is, the expiratory
flow rate is higher than the inspiratory flow rate, al­
lowing the mucus to be transported from the periph­
ery to the central airways for expectoration. HFCC
has also been shown to decrease the viscosity of
mucus, making it easier to mobilize.
FIGURE 20-16
Patient using high frequency chest compression.
Equipment Required for High Frequency
Chest Compression

I. The air-pulse generator, required for a treat­

ment of HFCC, weighs just over 100 Ibs, but should not feel restricted while the vest is de­
can be wheeled from one room to another. flated. A single layer of clothing should be
2. The inflatable vest is constructed to fit over the worn under the vest.
entire thorax and should extend to the top of the 2. The pressure control setting should be adjusted
thigh when the patient is sitting upright. Five to either the high or the low setting according
different sizes are available (from child to large to patient comfort.
adult). For use in a hospital setting, adjustable 3. The foot/hand control may be placed on the
vests are available, which are fitted to subse­ floor to be activated by stepping on it, or placed
quent patients with velcro straps. under the thigh to be activated by leaning onto
3. Simultaneous use of an aerosolized medication it, or pressed with the hand.
or saline is recommended throughout the treat­
ment. This humidifies the air to counteract the
Treatment With HFCC
drying effect of the increased airflow.
I . The treatment should progress through different
frequencies, from low (7 to 10 Hz) to medium
Preparation for HFCC
(10 to IS Hz) and then to high (IS to 25 Hz), to
1. The patient should be seated upright in a chair. achieve both higher flow rates and increased
The vest should fit properly, but breathing lung volume. Warwick (1991) reported that the

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 20 Clinical Application of Airway Clearance Techniques 359

frequencies associated with the highest flow successfully in reclining patients who are unable to
rates were usually greater than 13 Hz, whereas tolerate the upright sitting position.
those associated with the largest volume were Use of HFCC may result in time savings at home
usually less than 10Hz. as well as in a hospital or long-term care facility.
2. The recommended protocol (American Biosys­ Nebulized medications are administered concurrently
tems, Inc., 1994) gives the option of intermit­ with the airway clearance treatment, and all lobes of
tent or continuous us· e . For the intermittent the lungs are treated simultaneously. The amount of
(only on exhalation) method, the patient should time for patient contact required for a hospital care­
inhale deeply and depress the foot/hand control giver is much less with this method than with con­
at peak inspiration. Exhalation should be pas­ ventional PD and percussion.
sive and relaxed while the vest is pulsating. For A disadvantage of this method of airway clearance
the continuous method, the foot/hand control is the cost of the equipment. A monthly rental fee is
should be depressed while breathing normally. reimbursed by most insurance companies. However,
At least once per minute, the patient should in­ a study by Ohnsorg (1994) demonstrated a decline in
hale to total lung capacity. t o ta l h e a l t h care costs for t h e y e a r a f t e r t h e
3. The average length of time spent at each fre­ ThAIRapy® Vest was put into use b y I I patients. A
quency is 3 to 5 minutes, but this will vary ac­ study of the impact of the device in a hospital setting
cording to patient tolerance, amount, and con­ (KIous, 1993) showed a substantial savings as a result
sistency of secretions, and the phase of the of therapy self-administration. A disadvantage of
patient's illness (acute or chronic). HFCC is its lack of portability. Although the device
4. After treatment at each frequency for the pre­ can be readily moved from room to room in the
scribed length of time, the foot/hand control house, i t does not accommodate use away from
should be released and the patient instructed to home.
huff or cough to clear loosened secretions. The In those patients for whom it is appropriate (and
control is adjusted to the next prescribed fre­ reimbursable), HFCC is an effective method of air­
quency, and the procedure is repeated. way clearance. It provides independence for long­
5. HFCC has been used on a smaller scale with term use at home as well as for acute exacerbations in
patients requiring long-term mechanical venti­ the hospital.
lation. Whitman et al. (1993) found use of the
ThAIRapy'M vest to be safe and effective, and
EXERCISE FOR AIRWAY CLEARANCE
resulted in time savings over conventional PD
and percussion. A regular program of exercise has been shown to im­
6. Patients requiring central intravenous (IV) ac­ prove many variables in patients with lung disease.
cess such as a Porta-cath or Hickman are able Peak oxygen consumption, maximal work capacity,
to use the ThAIRapy"''' Vest with sufficient respiratory muscle endurance, and exercise tolerance
padding (such as a foam doughnut pillow) to all improve with an exercise program (Orenstein,
relieve pressure around the access site. 1981, Andreasson, 1987). Secretion clearance is also
improved with exercise (Zach, 1981; Oldenburg,
1979). Based on improvement in pulmonary function,
Advantages and Disadvantages of HFCC
exercise has been recommended as a replacement,
This method of airway clearance allows indepen­ partial or complete, for conventional chest physical
dence and is easy to learn in a short period. The therapy (PD and percussion) (Zach, 1982; Cerny,
ThAIRapy® Vest is now designed to accommodate 1989; Andreasson, 1987).
children as young as 3 years of age, and a vest may Exercise for secretion clearance has focused on
be custom-made for very large or obese adults. aerobic or endurance exercise to increase ventilation.
HFCC is appropriate with those patients in whom PD The many forms of exercise must be adapted to the
positions are contraindicated, and it has been used individual patient's status and abilities.

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360 PART III Cardiopulmonary Physical Therapy Interventions

Equipment Required For Exercise

5. Supplemental oxygcn and oxygen delivery sup­
I. A walking program requires nothing more than plies will be necessary for those patients who
a suitable pair of shoes and a safe location. demonstrate oxygen desaturation during exercise.
2. The following exercise equipment may be suit­
able for a patient who is beginning an exercise Preparation for Exercise
program: treadmill, bicycle ergometer, mini­
trampoline, or arm ergometer. I. Patients with hyperreactive airways should be
3. For more accomplished exercisers or patients premedicated with a prescribed bronchodilator
with a higher exercise tolerance, equipment before exercise.
may include a stair climber, cross-country ski 2. Baseline vital signs should be recorded before
machine, or rowing machine. beginning the exercise. In a home setting, pa­
4. Tools to monitor a patient's response to exer­ tients should be knowledgeable in pulse taking
cise include a blood pressure monitor, heart and estimating their level of perceived exel1ion.
rate monitor, pulse oximeter, and a scale to For those patients who require closer monitor­
measure patient's level of perceived exertion ing, a pulse oximeter may be rented from an
(Figure 20-17). oxygen supply company.

6 Treatment With Exercise

7 Very, very light 1. The principles of an excrcise prescription ad­

dressing intensity, duration, and frequency, as
8 well as principles of warm up and cool down

9 Very light are addressed in Chapter 24 and should be fol­

lowed when using exercise as a form of airway
1 clearance. Individualizing an exercise program

0 Fairly light for each patient is important.

2. Patients in the hospital for an acute exacerba­
1 tion may not be able to perform endurance ex­
ercise for the first couple of days. They should
1 Somewhat hard be started slowly and progressed as tolerated.

1 Monitoring of heart rate, blood pressure, oxy­

gen saturation, respiratory rate, and level of
2 Hard perceived exertion at periods before and during

1 exercise, and during recovery, will allow titra­

tion of the workload and duration for optimal
3 Very hard performance.
3. The patient should be instructed in huffing or
1 coughing (productive, not prolonged) to expec­

4 Very, very hard torate secretions as they are loosened.

4. A regular, consistent program of exercise must
1 be scheduled around the patient's daily activi­

FIGURE 20-17 ties to achieve adherence (e.g., walking the

Perceived exertion scale. (From Borg, G., 1982. dog, sports at school, stopping by the health
Psychophysical basis of perceived exertion, Med Sci Sports club after work).
Exer, 14(5),377.)

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 20 Clinical Application of Airway Clearance Techniques 361

TABLE 20·1

Airway Clearance Techniques Applied to Patients

TYPE INDEPENDENCE EQUIPMENT AGE REFLUX SEVERE REACTIVE

NEEDED <4 >4 >12 PRESENT EXACERBATION AIRWAYS

Traditional No PD board Yes Yes Yes Modified Modified May cause

CPT" percussor bronchospasm
HFCC Yes Vest and No Yes Yes Yes Yes May include
generator bronchodilator
PEP Yes Mask or No Yes Yes Yes Yes May include
mouthpiece bronchodilator
ACB Yes PD board No Yes Yes Modified Modified Needs care
Technique
AD Yes None No No Yes Yes No Good results
Exercise Yes Variety No Yes Yes Yes No Bronchodilator
Premedication

*Includes pOSlural drainage, percussion, shaking, vibralion, and coughing.

Modified from Maggie Mcllwaine, 1993, unpublished.

Advantages and Disadvantages of

Andreasson (1987) observed that regular contact
Exercise For Airway Clearance
with a caregiver seems to be necessary for success­
Exercise has the advantage of being the only airway ful exercise training as does family support, espe­
clearance technique that is peliormed regularly by cially in young children. Compliance will also be
people without lung disease. This factor that makes it affected by a patient's preference for a particular
appealing to those patients who do not want to call activity, scheduling conflicts, and commitment by
attention to their differences from their peers. Exer­ friends and family members.
cise may improve self-esteem, a sense of well-being,
and quality of life. The level of exercise tolerance in
SELECTION OF AIRWAY CLEARANCE TECHNIQUES
patients with cystic fibrosis has been demonstrated to
be of prognostic value (Nixon, 1992). The process of prescribing an appropriate technique
Because the amount or frequency of exercise re­ for secretion mobilization should be ongoing, with pe­
quired to achieve its benefits would not be tolerated riodic reevaluation of the method and its effects on the
by many patients, it is often recommended as an ad­ patient. Because of the low compliance reported with
junct to other forms of airway clearance. This is par­ conventional chest physical therapy (Passero, 1981), it
ticularly true during an acute exacerbation when ac­ is necessary for caregivers to address the many factors
tivity tolerance is limited, or in infants or patients that may alter a patient's adherence to a particular
with neurological or muscular limitations. method. These factors include the availability of both
Care must be taken in prescribing exercise to pa­ the caregiver to teach the technique and the patient to
tients with hyperreactive airways or with a tendency learn it; the effectiveness of the technique (subjective
toward oxygen desaturation. Use of bronchodilator and objective); support for the technique from family,
medication and supplemental oxygen delivery may friends, and health care personnel; and the cost of the
be necessary to achieve exercise tolerance, but these treatment. Table 20-1 summarizes factors that influ­
patients require close monitoring as well. ence the choice of an airway clearance technique.

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362 PART III Cardiopulmonar)' Physical Therapy Interventions

AVAILABILITY A patient's subjective response to the treatment

has implications for adherence to any technique. The
Many techniques of airway clearance are new to health ease of sputum mobilization and the quantity of spu­
care providers in the United States although they have tum are useful feedback for a patient. How much ef­
been used in Europe for some time. Use of a method fort the treatment requires, or more importantly, how
may be limited by the lack of caregivers trained to in­ much energy remai ns after completion of the treat­
struct patients in a particular technique. This is espe­ ment, will affect the patient's willingness to continue.
cially tllle for AD, which takes longer for a caregiver Complications that occur as a result of a technique
to learn to teach than does ·use of the FlutterT" or or precautions to be observed must guide a patient
ThAIRapyTM Vest. The ACB technique is easily incor­ and caregiver to find an alternate technique in many
porated into conventional chest physical therapy by instances. A patient hospitalized with an acute pul­
learning the FET and modifying the use of percussion monary exacerbation may need to be assisted with a
or shaking. Manual hyperinflation, on the other hand, more passive method of secretion clearance until the
because of increased precautions for its use, requires patient's condition allows a return to a more indepen­
more study and observation before implementation. dent technique. A patient with hyperreacti ve airways
Exercise for airway clearance may be out of the realm may find that bronchospasm renders percussion inef­
of a caregiver who is trained in respiratory care but not fective. The presence of gastroesophageal reflux may
exercise therapy. force the decision to use a technique which can be
The patient's availability must also be taken into pelformed in an upright position. Sinus surgery may
consideration. An outpatient clinic visit does not lend make use of a PEP mask intolerable. Placement of a
itself to instruction in AD, but instruction in PEP, chest tube may necessitate a temporary replacement
ACB technique, HFCC, or Flutter"< can be initiated, for HFCC.
with further training during return visits. On the other
hand, if a patient is admitted for exacerbation of a
SUPPORT
pulmonary disease, the patient is a captive audience
for instruction of AD or a home exercise program When airway clearance must take place on a daily
once the acute stage has passed. basis, it becomes necessary to accommodate a pa­
Reevaluation of any airway clearance technique is tient's schedule. A patient may have a preference for
key to its success. The patient and caregiver must be the most effective treatment performed in the shortest
available to demonstrate and review the technique pe­ amount of time. A patient may also be interested in
riodically so that modifications can be made. A performing another activity during the airway clear­
change in a patient's level of independence or motiva­ ance treatment: AD or Flutter'M may be performed
tion, a decline or marked improvement in pulmonary while riding in a car (as a passenger); HFCC can be
status, or a decrease in the effectiveness of a technique conducted while studying for an examination; and
all necessitate reevaluation of the current method. while running on a treadmill or during percussion by
an assistant, a patient can be watching the news.
Many patients adopt a multifaceted approach to
EFFECTIVENESS
secretion clearance, becoming adept at several meth­
The prime consideration in selecting a technique is ods and using them as conditions dictate. Patients
the effectiveness of the technique measured both sub­ who use AD or exercise primarily will need to use an
jectively and objectively. Objective measures in­ alternate form of airway clearance during an acute
clude: pulmonary function studies, chest x-rays, exacerbation of an illness. Use of HFCC at home
blood gas values, changes in mechanical ventilator may necessitate use of a more portable technique
settings, changes in auscultation, and quantity of spu­ when away from home for long periods. Patients who
tum produced. A patient's response to treatment can rely on an assistant to perform percussion may need
be evaluated by changes in heart rate, respiratory rate, to learn a more independent method for occasions
oxygen saturation, and level of fatigue. when the assistant is not available.

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 20 Clinical Application of Airway Clearance Techniques 363

In a home where more than one family member re­ The effectiveness of these newer techniques com­
quires ongoing airway clearance, as can be the case for pared with more established methods are just begin­
parents of children with cystic fibrosis, spending the ning to be studied. Health care providers have anec­
least amount of time for the greatest benefit becomes of dotally reported their effectiveness, but long term,
primary importance. For an infant or young child, per­ well-designed studies are needed.
formance of secretion mobilization must be carried out
by an adult. As the child grows older and the choices of
INTRAPULMONARY PERCUSSIVE VENTILATOR (IPV)
a technique increase, close supervision remains neces­
sary. In the adolescent, even when physical assistance The intrapulmonary percussive ventilator (IPV) (from
is no longer required, emotional support from family Percussionaire Corp., Sandpoint, Idaho) is an airway
and friends is paramount to continued success with a c l e a r a n c e device t h a t s i m u l t a n e o u s l y delivers
technique. Finally, the support received from health aerosolized solution and intrathoracic percussion
care providers is vital to the patient's motivation to con­ (Homnick, 1994). The functional component in the
tinue with a technique, or to learn a new one. IPY is an apparatus known as the phasitron. The pha­
sitron was originally developed by Bird in 1979 for
the volumetric diffusive respiration (VDR) ventilator.
COST
It is used with thermally injured patients in place of
In this age of health reform, especially in long-term conventional mechanical ventilation. The VDR venti­
care or chronic disease, cost of a treatment must be lator functions by accumulation of subtidal volume
considered. The initial cost of equipment, replace­ breaths, which build to an oscillatory equilibrium that
ment costs, and the expense of assistance required, all is followed by passive exhalation (Rodenberg, 1992).
figure into the total cost of treatment. Figure 20-18 shows a YDR ventilator waveform.
The generator for HFCC is the most costly piece In the IPV, the phasitron provides high-frequency
of equipment presented here, but replacement should impulses during inspiration, and positive expiratory
not be necessary. The vest itself should not require pressure maintained throughout passive exhalation.
replacement except for growth of a child. PEP masks The pressure generated is 10 to 30 cms. of water
and mouthpieces, and the FlutterT" are relatively inex­ pressure. Treatment with IPV is titrated for patient
pensive, with replacement of equipment expected to comfort and visible thoracic movement.
occur occasionally during a lifetime of use (more Homnick et a!. (1994) performed a 6-month study
often for a one-way valve in a self-made PEP). AD using the IPV for airway clearance in patients with
and ACB require no equipment. cystic fibrosis. No significant differences were
Payment of a trained assistant for home use of demonstrated in pulmonary function studies, body
postural drainage and percussion when family sup­ weight, use of antibiotics, or hospital days between
port is not available is at great expense. Depending the IPV and conventional chest physical therapy
on the duration and frequency of treatment, this cost group. Three fourths of the patients estimated in­
may outweigh that for other airway clearance tech­ creased sputum production with IPY and satisfaction
niques on a long-term basis. was high for comfort and independence.
Often the choice of an airway clearance technique
is limited by the reimbursement available for equip­
DYNAMIC AIR THERAPY BED
ment or assistance. Nonetheless, the caregiver must
strike a balance between economic and clinical con­ The E FICA CC'" Dynamic Air Therapy® bed (from
siderations in choosing a mode of therapy. HILLROM, Batesville, Indiana) is used in hospital­
ized patients, primarily in an intensive care setting.
The modes available from the bed are continuous lat­
FUTURE TRENDS IN AIRWAY CLEARANCE
eral rotation, percussion, vibration, and the ability to
A recent resurgence of interest in airway clearance position the patient in postural drainage positions.
has led to the introduction of additional techniques. Use of the bed demands less time of the caregivers

Copyrighted Material
364 PART III Cardiopulmonary Physical Therapy Interventions

11111AlII
1 AI IIIIHulI, llIlHIIH till, IAIlAllA
IUUIUU'IUV !nll,I"HUIVUU UU UlnllIHVIIVUI UUM uAflJUVIIIUVIIVVIIUI I
'II I" I" IlIUVIII' I" .JIII" I" II 'I m '" " .11
frI AI AI AI
11 I fI I' I "
\ I I
I, I,
'VY 'VIII 'YV ,yv

FIGURE 20-18
VDR ventilator waveform. (From Rodeberg, D.A., (1992). Decreased pulmonary barotrauma with
the use of volumetric diffusive respiration in pediatric patients with burns: The 1992 Moyer Award,
Journal of Burn Care Rehabilitation 13, 506-511.)

for hands on airway clearance treatment. presented by patients and choose a technique or combi­
A smaJi pilot study by Samuelson et al. (1994) nation of techniques that best suits each patient's needs.
compared the bed to manual percussion and postural An individualized approach to airway clearance re­
drainage in adult patients with cystic fibrosis. Patients quires consideration of the multitude of variables, both
were randomized to receive four treatments a day with physiological, psychological, and practical that affect a
either the Dynamic Air Therapy® bed or manual chest patient's response to treatment. Health care providers
physical therapy for I week and then switched to the are challenged to keep abreast of techniques and their
other modality for an additional week. Outcome mea­ modifications to best provide for the patient's needs.
sures included pulmonary function studies, 6-minute The role of the caregiver involves more than tech­
walk distance, dyspnea score, and a Quality of WeJl nical expertise. The caregiver is uniquely positioned
Being Scale. Both therapies demonstrated a positive to simplify medical language for a patient and en­
effect from baseline, but a significant improvement courage adherence to airway clearance. Support of a
was found only in the 6-minute walk distance of those treatment by a health care provider can increase the
patients treated with the bed therapy first. benefit derived from the treatment.
Studies on more appropriate patient populations, Further study is needed to compare and standardize
especiaJly nonambulatory, critically ill patients, for techniques, follow long-term outcomes, and establish
whom the Dynamic Air Therapy® beds are generally optimal treatment guidelines. This information will
prescribed, are necessary to demonstrate the most ef­ assist both patients and caregivers to maximize treat­
fective use of this expensive equipment. ment with airway clearance techniques.

SUMMARY REVIEW QUESTIONS

Numerous airway clearance techniques have been 1. Which ACTs can be performed without acquir­
shown to reduce obstruction, enhance mucociliary ing additional equipment?
clearance, and improve ventilation, accomplishing the 2. Are there any ACTs that are not suitable for use
goal of improved oxygen transport. Their effectiveness in an intensive care unit?
has been demonstrated in controlled situations and eval­ 3. What are the airway clearance methods most
uated with sophisticated equipment. Caregivers must in­ suited for instructing a patient/family in during a
corporate this information into the real life situations single outpatient clinic visit?

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 20 Clinical Application of Airway Clearance Techniques 365

4. What outcome measures do you have at your dis­ Gormenzano,J .• Branthwaite,M.A. (1972). Pulmonary physiother­
apy with assisted ventilation. Anaeslhesia, 27, 249-257.
posal for evaluating the effectiveness of airway
Homnick, D., SpiJlers, e., White,F. (1994). The intrapulmonary
clearance?
percussive ventilator compared to standard aerosol therapy and
5. How would you encourage adherence of a pre­ chest physiotherapy in the treatment of patients with cystic ti­
scribed method of airway clearance in: brosis. Abstracted in Pedialr Pulmonology, Suppl. 10,266.

• a fiercely independent adolescent with a spinal [mle, P.e., (1989). Percussion and vibration. In Mackenzie, (Ed.).
CheSi Physical Therapy in the Inlensive Care Unil, 2nd Ed.
cord injury?
(pp. 134-152). Baltimore: Williams & Wilkins.
• a 3 year old newly diagnosed with cystic fibrosis?
Kious,D.,et al. (1993). Chest vest and cystic fibrosis: Better care
• an older patient with bronchiectasis? for patients. Advanced RespiralOry Care Management, 3,44-50.
Kious, D.R. (1994) High-jrequency chest wall oscillation: Princi­
ples and appiicalions. Published by American Biosystems,

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ence,Dallas. compliance with cystic fibrosis therapy. Clinical Pedialrics,
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disease. [n Irwin, S,Tecklin, JS, (Eds.),Cardiopulmonary Physi­ Pryor, J.A., et al. (1979). Evaluation of the forced expiration tech­
cal Therapy (pp. 409-410). St. Louis: Mosby. nique as an adjunct to postural drainage in treatment of cystic
Dab,I., Alexander,F. (1979). The mechanism of autogenic drainage tibrosis. Brilish Medical Joumal, 18,417-418.
studied with flow volume curves. Mon Paed, 10,50-53. Pryor,J.A., Webber B.A., Hodson, M.E. (1990). Effect of chest
David, A. (1991). Autogenic drainage-the Gelman approach. In Pryor. physiotherapy on oxygen saturation in patients with cystic fi­
J (Ed.), Respiratory Care. Edinburgh: Churchill Livingstone. brosis,45, 77.
Falk,M.,el al. (1984). Improving the ketchup bottle method with Pryor,1.A. (1991). The forced expiration technique. In Pryor,1.A.
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ClTesl Physical Thempy (lnd Pulmol/Qly Rehabilil{lIion (2 nd with the use of volumetric diffusive respiration in pediatric pa­
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In Bronchial Hypersecretion: Current Chest Physiotherapy in

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 Facilitating Airway Clearance
With Coughing Techniques

Mary Massery
Donna Frownfelter

KEY TERMS Airway clearance deficits Mucous blanket

Assisted cough Reflex cough
Complications with coughing Smokers cough
Cough Swallowing disturbance
Cough pump Throat clearing
Cough stages

INTRODUCTION

Cough truly serves many purposes: a therapeutic technique, of food goes "down the wrong hole" or into the tra­
a diagnostic signpost, and a social necessity. If it didn't al­ chea rather than the esophagus, a cough is not the
ready exist, we would have to invent it.
usual mechanism to clear mucus.
Glen A. Lillington, MD
A nervous cough or throat clearing may also sig­
The cough is an interesting phenomenon. A cough nal that the airways are irritated, mucus is not clear­
can either be a reflex or a voluntary action. Gener­ ing normally, or the person is in an uncomfortable
ally, in healthy individuals a cough is rarely heard situation. This is something to be aware of especialJy
unless the person has a cold or an irritant is inhaled when treating asthmatics, patients with cystic fibro­
and a sneeze or a cough ensues to evacuate the for­ sis, or patients with psychological problems.
eign body. The mucociliary escalator functions to In reality the mucous blanket and the cough
clear secretions and inhaled particulate matter. Unless mechanism are the two ways the lungs have of pro­
the mucus is very thick, such as in individuals with viding airway clearance under normal everyday cir­
dehydration, inhalation of a foreign body, or a bolus cumstances.

367

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368 PART III Cardiopulmonary Physical Therapy Interventions

It is interesting how many people are unaware of Airway clea rance techniques, such as postural
their coughing. For example, when asked if they drainage, autogenic drainage, or active cycles of
cough, smokers with typical morning and ongoing breathing, need to be used to mobilize the secretions
smoker's coughs will deny that they do. Spouses will to the area where the cough will be effective (see
chime in, "He coughs and hacks all the time." An in­ Chapter 20).
dividual might constantly clear his or her throat and
swallow mucus but will claim to be unproductive of
COUGH ASSOCIATED WITH EATING OR DRINKING
mucus and free of coughing. It is important for thera­
pists to be aware of both the reflex and voluntary na­ If a cough is associated with eating or drinking or
ture of their patients' coughs. taking medications, the patient should be evaluated
Frequent coughing or throat clearing may also in­ for a swallowing disturbance. This usually consists of
dicate other problems than airway clearance deficits. a "cookie swallow," a fluoroscopy study where the
For example, a patient may have postnasal drip from patient is given barium or a variety of consistency
a sinus infection or allergy. When the mucus drips liquids and solids to swallow and observed to see if
down into the back of the throat, it can cause a reflex aspiration into the respiratory tract occurs. Patients
cough to clear it. Other causes include bronchogenic may have dysfunction after a cerebrovascular acci­
carcinoma, nervousness, and smoking. In a pediatric dent (CY A) or prolonged intubation or because high
patient, a foreign body or object inserted or inspired placement of a tracheostomy tube inhibits the proper
into the nose or airway should be ruled out. function of the larynx during swaJlowing. Speech
Cigarette smoking paralyzes the cilia so airway language pathologists working with patients with
clearance is altered. It has been noted that for every dysphagia can help patients learn techniques to pre­
cigarette an individual smokes the cilia are paralyzed vent aspiration. They also help the patient and spouse
for approximately 20 minutes. Many individuals are (significant other) to understand cognitively proper
chain smokers and light up one cigarette after the positioning (usually sitting up in semi-Fowler's) and
other. Consequently, coughing is the only means of proper head and neck position (usually chin tuck and
clearing the lungs. This is understandable when a slight neck flexion) during swallowing. If a patient
smoker coughs up a large amount of mucus in the has dysphagia and cannot or will not follow a safe
early morning on arising. After sleeping for hours the swallowing retraining program and continues to
individual's cilia are able to clear secretions; a cough choke and aspirate food and liquid, aspiration pneu­
assists in airway clearance. During the day the monia will occur and can lead to the patient's condi­
smoker who chain smokes must cough regularly to tion deteriorating and even to death. In a situation
clear secretions because the cilia are paralyzed by the such as this, alternative feeding would need to be
smoke. considered.

COUGH PUMP COMPLICATIONS OF COUGHING

One must appreciate the complexity and intricacy of The act of coughing can be hazardous to the patient.
the cough pump. Mucus is transported up against A patient should never be asked to cough repeatedly
gravity by the mucous blanket and propelled cepha­ as a routine part of treatment. The irritation and pos­
lad by the action of the cough. sible narrowing of the airways during the forced ex­
In general the cough is most effective at high expi­ halation may cause bronchospasm. If a patient is
ratory flow rates and at high volumes. The cough is sounding dry and unproductive, do not encourage fre­
of limited value beyond the sixth or seventh genera­ quent coughing. This is especially true in patients
tion of airway branching. Consequently when a pa­ with asthma.
tient has a lower lobe pneumonia or atelectasis, If a patient demonstrates retained secretions on x­
coughing alone will not clear the retained secretions. ray, encourage hydration (drinking water), use airway

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 21 Facilitating Airway Clearance With Coughing Techniques 369

clearance mobilization techniques, and carefully eval­ for a forceful cough. Generally, adequate inspiratory
uate the cough. Instruct the patient in controlled volumes for a cough are noted to be at least 60% of
coughing when mucus is felt in the throat or upper the predicted vital capacity for that individual. The
airways. The patient may try to cough in a controlled second stage involves closing of the glottis (vocal
fashion after a postural drainage session or use the folds) to prepare for the abdominal and intercostal
forced expiratory technique. The forced expiratory muscles to produce positive intrathoracic pressure dis­
technique uses midlong volume ventilation followed tal to the glottis. The third stage is the active contrac­
by one to two huffs, which can include chest com­ tion of these muscles. The fourth and final stage in­
pression with the arms. Forced coughing can also in­ volves opening of the glottis and forcefully expelling
crease blood pressure and Jower cardiac output. Tus­ the air. The patient should be able to cough three to
sive syncopy can occur when a patient goes into a six times per expiratory effort. A minimal threshold of
series of coughs in which the intrathoracic pressure a FEY) (forced expiratory volume in I second) of at
becomes so high that venous return to the heart is im­ least 60% of the patient's actual vital capacity is a
paired. The cardiac output falls and the patient be­ good indicator of adequate muscle strength necessary
comes very dizzy, progressing to unconsciousness. for effective expUlsion (Figure 21-1). During a cough,
Care must be exercised, especially with patients with alveolar, pleural, and subglottal pressures may rise as
primary lung disease; they must learn to control their much as 200 cm H20 (Bach, 1993; Jaeger, 1993; Lin­
coughing to prevent untoward side effects. der, 1993).

Stages of Cough COUGH EVALUATION

There are four stages involved in producing an effec­ How do you assess whether a patient's cough is ef­
tive cough (Linder, 1993). The first stage requires in­ fective? The answer appears to be obvious: ask the
spiring enough air to provide the volume necessary patient to cough. However, the obvious answer often

FIGURE 21-1
Cough mechanics. A, Stage I: adequate inspiration. B, Stage 2: glottal closure; Stage 3: b u i l ding up of intrathoracic and
intraabdominal pressure. C, Stage 4: glottal opening and expUlsion.

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370 PART In Cardiopulmonary Physical Therapy Interventions

does not adequately analyze the functional perfor­ inspiration or expiration cycle? Did the patient sponta­
mance of a cough, especially for a neurologically im­ neously use trunk extension, an upward eye gaze, or
paired patient. The clinician must first take time to the arms to augment the inspiratory effOlt? Did the pa­
set up the patient for successful evaluation of their tient take enough time to fully inspire before cough­
cough. Guidelines for setting up the patient follow: ing? If the patient inspires adequately, he or she should
I. Do not ask the patient to cough in whatever be able to sustain two to six coughs per expiratory ef­
posture you happen to find him or her in. Ask, fort for a cascade effect. Neurologically impaired pa­
"What position do you like to cough in when tients who have inadequate inspiratory effol1s usually
you feel the need to cough?" Then ask the pa­ present with only one or two coughs per breath and
tient to assume that posture, or assist him or her generally produce a quieter cough (Hoffman, 1987).
in assuming a posture as close to the preferred
posture as possible. Listen closely to his or her
Stage 2: Glottal Closure
answers. A patient should s po n t a n e o u s l y
choose a posture that lends itself to trunk flex­ Did the patient hold his or her breath at the peak of
ion, which is necessary for effective expulsion inspiration before the expulsion phase or did the pa­
and airway protection. A red flag or inappropri­ tient go directly from inspiration to expiration? Did
ate choice would be a preference for coughing you hear a cough or a huff? A huff (or a complete ab­
while supine, which involves the opposite: sence of a hold between inspiration and expiration),
trunk extension and poor mechanical alignment when the patient intended to give you a cough, is an
for airway protection. indication of insufficient glottal closure. This can re­
2. Now the patient is ready to demonstrate cough­ sult from a wide variety of situations including glottal
ing. Do not make the mistake of asking a pa­ edema after prolonged intubation, partial or full
tient to "show me a cough" or he or she may paralysis of the vocal folds, hemiparesis of the vocal
simply "show you" a cough. It may not be the folds, or timing or sequencing difficulty secondary to
way the patient coughs to clear secretions. In­ brain injuries to name a few. A complete lack of glot­
stead continue to set the patient up for success tal closure will not produce any cough sound because
by asking him or her to "show me how you the vocal folds are not approximating.
would cough if you had secretions in your chest
and you felt the need to cough them out." With
Stage 3: Building up of Intrathoracic
these instructions you are asking the patient to
and Intraabdominal Pressure
show you something functional not theoretical.
Cough effectiveness can now be accurately as­ Did you see active contraction of the intercostal
sessed. Guidelines for objective evaluation with pul­ and abdominal muscles? D id the patient sponta­
monary function tests have been indicted. This sec­ neously move into trunk flexion during this phase?
tion focuses on analyzing the movement during all Did the cough have a low resonant sound? Inade­
four stages. An effective cough should maximize the quate force is usually heard as a higher pitch cough,
function of each individual stage. Thus the clinician often called a throaty cough. The sound is quieter
should see a deep inspiratory effort paired with trunk overall and does not produce as many coughs per
extension, a momentary hold, and then a series of ex­ expiratory effort. It is sometimes associated with
piratory coughs on a single breath while the patient neck extension rather than flexion as the patient at­
moves into trunk flexion. tempts to clear the upper airway only. The air ap­
pears to leak out rather than being propelled out of
the larynx during the cough. Like inadequate lung
Stage 1: Adequate Inspiration
volumes, inadequate pressure also prevents the pa­
Did the patient spontaneously inspire a deep breath be­ tient from coughing more than once or twice on one
fore coughing or did he or she cough regardless of the expiratory effort.

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 21 Facilitating Airway Clearance With Coughing Techniques 371

Stage 4: Glottal Opening and Expulsion

tient to take a deep breath and cough because this can
Timing of the opening of the glottis and forcefully ex­ cause more air trapping, which does not facilitate ex­
pelling the air is directly tied into the function of the pulsion of secretions. Patients will be more effective
third stage. During expulsion, does the patient appear trying to take controlled small or medium breaths fol­
to gag before successfully allowing the air to be ex­ lowed by huffs or a small series of coughs.The active
pelled? Does the patient seem to get stuck holding his cycles of breathing and forced expiratory pressure
or her breath? Deficiencies in this area are often re­ technique is also a good choice for these patients.
lated to brain injuries and coordination difficulties. The Several ideas are presented because the therapist
opposite can also occur. Some patients will get stuck at needs a bag of tricks. Some techniques work well
the end of expulsion, especially those with severe neu­ for some patients and not for others. Try several
rological impairments or bronchospasms and may with each patient and let him or her determine what
have difficulty initiating the next inspiratory effort. works best.
Another variation that decreases stress on the pa­
tient is to use a series of coughs starting with a small
PATIENT INSTRUCTION
breath and a small cough, then a medium breath and a
When working with patients, especially those with medium cough, then a larger breath and a large
primary pulmonary disease or primary disease super­ cough. This is a good technique to use with postoper­
imposed on secondary disease (i.e., a patient with a ative patients, who get fatigued trying to maximally
CY A and asthma), there are some helpful techniques cough each time.
to make secretion mobilization more effective. For patients with transient or permanent neuromus­
Patients with asthma tend to go into an expiratory cular weakness or paralysis, further instructions may be
wheeze when they force and prolong exhalation.This necessary (Jaeger, 1993; Braun, 1984). These patients
can lead to bronchospasm and respiratory distress. must use every physical trait to maximize the function
The patient can be taught a pump cough, a variation of each stage of the cough (see Figure 21-1, p.369, and
on a huff technique. A huff may be used when pa­ the box on p. 372). Physically assisting these patients
tients have had an endotracheal tube in for an ex­ during the expulsion stage of the cough only addresses
tended time. The vocal folds are swollen and irri­ one aspect (Slack, 1994; Fishburn, 1990). Care must be
tated. Consequently, they will not close and form a taken to look at all four stages to maximize the airway
tight seal to build up pressure and cough. The patient clearance potential of any assistive cough technique.
is instructed to huff rather than cough to mobilize se­ First, the patient must be positioned for success.The
cretions.It is done with more open vocal folds, a low beginning of any cough requires trunk extension or in­
sound, and less effort, yet it is quite effective in mo­ spiratory movement to maximize inhalation, whereas
bilization of secretions. the expulsion stage requires trunk flexion or expiratory
The pump cough extends the huff and is more ef­ movement to maximize exhalation (Massery, 1994).
fective. The patient is instructed to take three short Thus for any given posture, the clinician must assess
huffs and follow it with three short, easy coughs at the following: (1) whether the posture allows for both
lower lung volume, not deep breaths or deep lung trunk movements, (2) whether flexion and extension
volumes. Three or four sequences are done ...huff, are possible, which movement is more important for
huff, huff, cough, cough, cough, huff, huff, huff, that particular patient, and whether that posture facili­
cough, cough, cough, huff, huff, huff, cough, cough, tates this occunence, (3) how gravity is effecting the
cough.Usually if secretions are present a sponta­ patient's muscle strength and function in this posture,
neous cough might occur or the secretions will mobi­ and (4) whether the patient can still protect the airway
lize with the small cough. in this posture. When these questions are answered sat­
Patients with emphysema have overdistel')ded lungs isfactorily, the clinician is ready to instruct the patient
and difficulty with exhalation. Do not instruct the pa­ in the act of coughing.

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372 PART III Cardiopulmonary Physical Therapy Interventions

scribed previously, these subtle motions may signifi­

Positioning and Patiellt Instructioll to Improve
cantly increase the patient's inspiratory effort and pro­
Cough Effectiveness
vide a more active means for the patient to participate
• Position the patient for success, especially in in his or her own coughing program.
regard to trunk alignment.
Stage two involves closing the glottis. For some
• Maximize inspiratory phase through verbal cues,
positioning, and active arm movement.
patients with weakness or timing problems, a sharp
• Improve hold stage through verbal cues and loud command to "hold it" at the peak of inspiration,
positioning. may be sufficient to facilitate closure. Remember to
• Maximize intrathoracic and intraabdominal allow enough time for the patient to take in a deep
pressures with muscle contractions, physical
inspiratory effort before asking them to "hold."
assist, or trunk movement.
• Instruct the patient in appropriate timing and trunk
Some clinicians rush the first phase, by saying in
movements for expulsion. quick succession: "take a deep breath and hold it,"
• Make the procedure physically active on the thus unintentionally limiting the time of the inspira­
patient's part. tory effort. A more appropriate verbal cue would be:
"take a deep breath in . . .
in .. .in. . .in ... , and
now hold it," allowing adequate time for the patient
to inhale.
Stages three and four (building up pressure and ex­
pulsion) are discussed together because their timing is
An example may provide the best illustration of interdependent. The patient now needs to move into
these instructions. A clinician may pick a modified trunk flexion, with or without the clinician's assis­
sitting position for a patient with generalized weak­ tance, to maximize expulsion. For those patients who
ness (e.g., incomplete spinal cord injury, developmen­ can assist, they can be asked to do the opposite of stage
tal delay, or temporary weakness or exhaustion after a one: (I) "look down while you cough." (2) "Pull both
medical or surgical procedure). The patient looks of your arms down to your hips as you cough."
slumped, so the clinician places a lumbar support (3) "Roll your shoulders forward while you cough."
(e.g., a lumbar roll, a towel, or a pillow) behind the (4) "Bend your trunk forward while you cough." like­
lower back to increase trunk extension in that posi­ wise, patients with more limited aim function can be
tion. The patient is asked if he or she is comfortable asked to do the following: (1) "Squeeze your arms to
and if he or she can swallow safely. Next the clinician your chest while coughing." (2) "Roll your shoulders
tries to maximize the first cough stage by asking the and arms inward while coughing." (3) "Turn your
patient to take in a deep breath. Observing that the pa­ hands down while coughing."
tient did not appear to take in as deep a breath as the In this manner the clinician has used every con­
clinician perceived capable, the clinician adds further ceivable resource to maximize a voluntary cough.
instructions such as the following: (1) "look upward Even the weakest cough can be made more effective
while you inhale." (2) "Raise both of your arms up by applying the following simple concepts: (I) posi­
over your head as high as you can while you inhale," tion for success, (2) maximize inhalation first, (3) ask
(3) "Squeeze your shoulders back while you inhale." for a breath hold, (4) encourage maximal intratho­
(4) "Straighten or extend your back while you inhale." racic and intraabdominal pressures, (5) instruct the
For those with more limited arm function, apply ap­ patient in appropriate timing and trunk movements
propriate ventilatory strategies detailed in Chapter 22. for expulsion, and (6) make the procedure as active
Very subtle movements can then be requested, such as as possible for the patient. However, even with excel­
the following: (I) "Bring your arms up and out while lent instructions, many neurological patients require
you inhale." (2) "Rotate your arms outward while you the clinician's physical assistance to inhale deeper or
inhale." (3) "Turn your forearm up while you inhale." to exhale more forcefully because of muscle weak­
Although less dramatic than the larger movements de­ ness or paralysis (Maclean, 1989).

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 21 Facilitating Airway Clearance With Coughing Techniques 373

ACTIVE ASSISTED COUGH TECHNIQUES

pist places his or her hands on the costophrenic an­
If after instruction and modification in the patient's gles of the rib cage (Figure 21-2). At the end of the
cough as described previously, the patient still can not patient's next exhalation, the therapist applies a
produce an effective cough, then one of the following quick manual stretch down and in toward the pa­
assistive cough techniques may be appropliate. How­ tient's navel to facilitate a stronger diaphragmatic
ever, a patient who needs some assistance to improve and intercostal muscle contraction during the suc­
a cough is not excused from ·an active role in cough­ ceeding inhalation. The therapist can also apply a se­
ing. Keep the act of coughing as active as possible for ries of repeated contractions from proprioceptive
each patient. whether that is accomplished by adding a neuromuscular facilitation (PNF approach (Sullivan,
few verbal cues to improve overall timing or posture 1982). throughout inspiration to facilitate maximal
while the patient independently performs the cough, inhalation. The patient may assist the maneuver by
or whether it is accomplished by adding eye gazes for actively using his or her upper extremities, head and
a very weak patient who cannot move the upper ex­ neck, eyes, trunk, or all of the above to maximize the
tremities and breathes with the assistance of a ventila­ inspiratory phase. The patient is then asked to "hold
tor. Encourage the patient to be responsible for his or it." Just a moment before asking the patient to ac­
her own care by teaching the concepts involved in tively cough, the therapist applies strong pressure
producing an effective cough (Estenne, 1990). In that through his or her hands, again down and in toward
manner, you will help the patient develop the problem the navel. In this manner the therapist is assisting
solving skills necessary for modifications later. Mod­ both the build up of intrathoracic pressure and the
ify and develop additional techniques on the princi­ force of expiration. Of course, the patient would also
ples presented thus far. See the box below for tech­ actively participate by using his or her arms, trunk,
niques presented in this chapter. or other body parts throughout the entire procedure
(see Chapter 22).
This technique's obvious use would be for patients
Manually Assisted Techniques
with weak or paralyzed intercostal or abdominal mus­
Costophrenic assist cles. The therapist must remember to evaluate the ef­
fect of gravity and posture in each position for the ap­
The first assistive cough technique, the costophrenic
propriateness of this technique (Massery, 1987). It is
assist, can be used in any posture. After assessing the
most appropriate position for the patient (most often
sitting or sidelying) and giving the patient instruc­
tions to maximize all four coughing stages, the thera­

Assisted Cough Techniques

Manually assisted lechniques

I. Costophrenic assist
2. H ei m li ch-type or abdominal thrust assist
3. Anterior chest compress i on assist
4. Counlerrotation assist
Self-assisted techniques
I. Prone on elbows head flexion sel f-assisted cough
2. Long-silting self-assisted coughs
3. Short-sitting self-assisted coughs
4. Hands-knees rocking self-assisted cough FIGURE 21-2
5. Standing self-assisted coughs Assisted cough techniques in supine position; costophrenic
assist.

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374 PART III Cardiopulmonary Physical Therapy Interventions

helpful for lower airway clearance but does not di­ the heel of his or her hand, as in a Heimlich choking
rectly assist in upper chest clearance unless the pa­ maneuver. The patient is instructed to assist with ap­
tient is able to move his or her upper body indepen­ propriate trunk movements to the best of his or her
dently while the therapist assists the lower chest. This ability. TechnicalJy, this procedure is very effective
technique is easy to learn and teach and can usually at forcefully expelling the air (Braun, 1984), as in a
be used from the acute phase through the patient's re­ cough, but it can be extremely uncomfortable for the
habilitation phase, thus accounting for its popularity. patient because of (1) its concentrated area of contact,
(2) the abrupt nature, which may elicit an undesired
Heimlich-type assist or abdominal thrust assist
high neuromuscular tone response or worse when
The second technique, the Heimlich-type assist or an combined with the sensory input that the therapist's
abdominal thrust, requires the therapist to place the manual contacts supply, (3) the force, which may
heel of his or her hand at about the level of the pa­ cause an abdominal herniation. Because of its limited
tient's navel, taking care to avoid direct placement on usefulness, the Heimlich type of assist or abdominal
the lower ribs (Figure 21-3). After appropriate posi­ thrust should only be used when the patient does not
tioning, the patient is instructed to "take in a deep respond to other techniques and the need to produce
breath and hold it." Unfortunately, manual facilita­ an effective cough is imminent. Patients with low
tion of inhalation is not feasible with this technique. neuromuscular tone or flaccid abdominal muscles
As the patient is instructed to cough, the therapist fare best with this procedure.
quickly pushes up and in, under the diaphgram with

FIGURE 21-3
Hand position for Heimlich-type assist or abdominal thrust.

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 21 Facilitating Airway Clearance With Coughing Techniques 375

The therapist can simultaneously use both of the enhance the first two cough stages. The therapist then
above techniques in sidelying. If the patient is hemi­ applies a quick force through both arms to simulate
plegic or suffered from an unilateral lung or thorax the force necessary during the expulsion phase. The
disease or trauma, emphasizing one side of the thorax directions of the force are (l) down and back on the
over the other may be an appropriate focus during upper chest, and (2) up and back on the lower chest
airway clearance treatments. One upper extremity is or abdominal arm. Performed together the compres­
used to perform the Heimlich"type of assist while the sion force from both arms makes the letter V.
other does an uni lateral costophrenic assist. In this The anterior chest compression technique is more
manner the therapist can compress simultaneously all effective than the costophrenic assist for patients with
three planes of ventilation in the lower chest. The very weak chest wall muscles because of the added
possibilities of combining techniques and positions compression of the upper anterior chest wall. These
are almost endless once the therapist understands the authors have found sidelying or 3/4 supine position to
principles on which they were developed. be the most effective position for this technique.
However, the anterior chest compression technique is
Anterior chest compression assist not appropriate for patients with a cavus condition of
The third assistive cough is called the anterior chest the upper anterior chest because it promotes further
compression assist, since it compresses both the collapsing of the anterior chest wall.
upper and lower anterior chest during the coughing
maneuver. This is the first single technique thus far to
Counterrotation assist
address the compression needs of the upper and The most effective assistive cough for the widest
lower chest in one maneuver. The therapist puts one cross-section of neurological patients, in these au­
arm across the patient's pectoralis region to compress thors' clinical experience, is the fourth and final
the upper chest and the other arm is either placed par­ method described in sidelying, the counterrotation as­
allel on the lower chest or abdomen (Figure 21-4) or sist. The positioning and procedures required for the
placed like in the Heimlich type of maneuver (Figure counterrotation technique are described in detail in
21-5). The commands are the same as in the other chapter 22 and apply for both the patient and the ther­
techniques. Because of the direct manual contact on apist (Figure 21-6). The therapist should recall that
the chest, inspiration can be easily facilitated first, orthopedic precautions of the spine, rib cage, shoul­
followed by a "hold." Thus the therapist can readily der, and pelvis still persist for this technique.

FIGURE 21-4 FIGURE 21-5

Assistive cough techniques in supine position; variation of Assistive cough techniques in supine position; variation of
the anterior chest compression assist. the anterior chest compression assist.

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376 PART III Cardiopulmonary Physical Therapy Interventions

FIGURE 21-6

Counterrotation assist; A, Hand placement during expulsion phase; B, Hand placement during
inspiration phase.

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 21 Facilitating Airway Clearance With Coughing Techniques 377

The therapist begins by following the patient's tion before passively coughing in a comatose
breathing cycle with his or her hands positioned over patient can reduce high tone and frequently re­
the patient's shoulder and pelvis (see Figure 21-6). duce a high respiratory rate. Both of these re­
The therapist then gently assists the patient in inhala­ duce the possibility of the patient keeping his
tion and exhalation to promote better overall ventila­ or her glottis closed during the expulsion phase.
tion. This sequence is generally repeated for three to 2. Counterrotation is an excellent mobilizer for a
five cycles or until the patient appears to have tight chest, which in itself can facilitate sponta­
achieved good ventilation to all lung segments. neous deeper breaths. Tidal volumes (TVs) can
At this point, the patient is ready to begin the therefore be increased for many patients by mo­
coughing phase of the procedure. The patient is bilizing the chest walls.
asked to take in as deep a breath as possible with the 3. Finally, rotation can be a vestibular stimulator
therapist assisting the patient in chest expansion and may assist in arousing the patient cogni­
(see Figure 21-6, 8). The patient is then instructed tively, allowing him or her to take a more ac­
to "hold it" at the end of maximal inspiration. The tive role in the procedure.
patient is then commanded to cough out as hard as The true beauty of the technique is the fact that no
possible while the therapist quickly and forcefully active participation on the part of the patient is re­
compresses the chest with his or her hands in their quired for success. Incoherent or unresponsive pa­
flexion phase positions (see Figure 21-6, A). tients, such as those patients with low functioning
The importance of following a true diagonal plane following a head trauma, CVA, or cerebral palsy, will
of facilitation during both the flexion and extension still demonstrate good secretion clearance with this
phases of this technique cannot be overemphasized. technique. The mechanics of the procedure dictate
Failure to do so will result in shifting of the air within that the air within the lungs be rapidly and forcefully
the chest cavity rather than the desired forcing out. expelled regardless of the patient's level of active
This air shifting can occur to varying degrees, when participation. Obviously, patient participation is de­
the upper and lower chest are not used together, as in sirable to clear secretions even more effectively and
all the other assistive cough techniques. When done for teaching the patient to eventually clear his or her
properly, the counterrotation assist is the only one to own secretions, but it is not critical.
rapidly close off the chest cavity in all three planes of Clinical experience has demonstrated with patients
ventilation in all areas of the chest. Unless the patient who have extremely tenacious secretions, use of vi­
voluntarily closes his or her glottis, it is impossible to bration instead of quick chest compression during the
withhold the air from being forcefully expelled. cough itself may be more effective. This prolongs the
However, a common mistake made by the therapist is cough phase and gives the secretions time to be
pulling the patient back into trunk extension during moved along the bronchi for successful expUlsion.
the expUlsion phase rather than into trunk flexion. A These patients may also require a series of three or
good rule of thumb: if you can see your patient's face four cough cycles before clearing most of their secre­
when you are applying the compression force, you tions. In general, patients from all the diagnostic
have pulled them into extension. The head and neck groups discussed thus far with or without good cogni­
should stay forward and flexed, thus only a facial tive functioning are appropriate for this procedure.
profile should be seen. The majority of them find it to be the most comfort­
Other effects of countcrrotation make this proce­ able and effective assistive means of expectorating
dure particularly beneficial to patients with low levels secretions.
of cognitive functioning.
I. The rotation component is a natural inhibitor of
Self-assisted Techniques
high tone. Thus this is the least likely of all
techniques discussed so far to elicit an increase The coughing techniques d iscussed in this section
in abnormal tone during the coughing phase. In are intended to be used as self-assisted procedures,
fact the opposite usually prevails. Gentle rota­ thus usually taught later in a patient's rehabilitation

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378 PART III Cardiopulmonary Physical Therapy Interventions

process. Five different techniques will be presented capitalize on the functional increase in chest expan­
in detail. Suggestions for variations are included. sion and compression abilities. For the population of
All self-assisted cough techniques can start out as patients who can assume a prone on elbows posture
physically assisted techniques; however, because independently (i.e., some patients with tetraplegia),
they are more active and require greater gross motor this t ec hniquc may be used functionally. Here, they
movement, they lend themselves to self-assisted can assist their own coughs when the need arises,
techniques. rather than wait for someone to assist them in a posi­
tion change.
Prone on elbows head flexion self-assisted cough The head flexion assist requires good use of head
Prone is not frequently used as a posture for coughing and neck musculature, scen in patients sustaining a
because the position itself inhibits fuJI use of the di­ spinal level injury below C4 (e.g., spinal cord injuries
aphragm by preventing lower anterior chest and ab­ (SCIs), spina bifida). It can be used either as a self­
dominal excursion following a neurologic insull. This assisted or therapist-assisted procedure, using the
forces the patient to use an alternate breathing pattern principles of trunk extension to facilitate inspiration
that facilitates greater accessory muscle use. Because and trunk flexion to facilitate expiration. With the pa­
this change in breathing patterns often occurs sponta­ tient prone on elbows, the therapist instructs him or
neously, prone on elbows can be an effective posture her to bring the head and neck up and back as far as
for promoting spontaneous use of the accessory mus­ possible, breathing in maximally (Figure 21-7). The
cles in a more difficult activity (coughing). However, patient is then instructed to cough out as hard as pos­
without the full use of the diaphragm, the resultant sible while throwing the head forward and down
cough will be weaker than in other postures. Prone on (Figure 21-8). This head-and-neck pattern can be ini­
elbows should not be the exclusive posture for assist­ tially assisted by the therapist to establish the desired
ing a cough. After mastering the timing of the proce­ movement pattern, and gradually progressed to a re­
dure, most patients move back to another posture, sisted pattern to promote increased accessory muscle
usually sitting or sidelying, and to other techniques to participation and to strengthen those muscle groups.

FIGURE 21-7
Head flexion assistive cough in prone on elbows; extension and inspiratory phase.

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 21 Facilitating Airway Clearance With Coughing Techniques 379

FIGURE 21-8
Head flexion assistive cough in pTone on elbows; flexion and coughing phase.

FIGURE 21-9 FIGURE 21-10

Tetraplegic-self-assisted cough in long sitting: maximizing Tetraplegic-self-assisted cough in long sitting: maximizing
the inspiration phase. the expiration or coughing phase.

inhalation, whereas the flexion aspect is used to max­

Long-sitting self-assisted cough imize expiration. The self-directed chest compression
For the first procedure, tetraplegic-Iong-sitting self­ occurs mainly on the supetior-inferior plane of venti­
assist, the patient is positioned on a mat in a long-sit­ lation only.
ting posture (legs straight out in front of the patient) The second procedure, the paraplegic-long-sit as­
and with upper extremity support. The therapist in­ sist, uses the same principles as the techniques de­
structs the patient to extend his or her body backward scribed for the tetraplegic-long-sit assist. These pa­
while inhaling maximally (Figure 21-9). The thera­ tients have active spinal extension musculature and
pist then tells the patient to cough as the patient can achieve greater trunk extension and flexion
throws his or her upper body forward into a com­ safely, achieving greater chest expansion before the
pletely flexed posture, using shoulder internal rota­ cough and greater chest compression on a superior­
tion if possible (Figure 21-10). Once again, the exten­ inferior plane during the cough. The patient positions
si0n aspect of the procedure is used to maximize his or her upper extremities in a butterfly position or

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380 PART III Cardiopulmonary Physical Therapy Interventions

self-assist, is typically performed in a wheelchair or

over the edge of a bed. The patient is instructed to
place one hand over the other at the wrist and place
them in his or her lap. As in the previous technique,
the patient is then asked to extend his trunk backward
while inhaling maximally, followed by a strong vol­
untary cough. During the cough, the patient pulls his
or her hands up and under the diaphragm, resembling
the motion of a Heimlich maneuver (Figure 21-13).
The hands mimic the abdominal muscles, which
would ordinarily contract to push the intestinal con­
tents up and under the diaphragm to aid its recoil
ability. This short-sitting technique uses the di­

FIGURE 21-11 aphragm more substantially than the long-sitting pro­

Paraplegic-self-assisted cough in long-sitting: inspiration. cedure and is therefore generally more effective as an
assistive cough. It is an effective self-assisted method
for patients who have weak diaphragms or abdominal
musculature. Most SCI or spina bifida patients, Cs or
b e l ow , c a n s u c cessf u l l y l e a r n t h i s t e c h n i que.
Tetraplegics usually require trunk support from their
wheelchairs to perform it independently and safely,
whereas most paraplegics can perform it from an un­
supported short-sitting position. Patients who lack
good upper-extremity coordination. such as many
Parkinson's and multiple sclerosis (MS) patients,
cannot perform the procedure quickly or forcefully
enough to make it effective and usually require assis­
tance from another person.
Variations on all sitting techniques can be readily
FIGURE 21-12 made. Use the concepts explained in the introduction
Paraplegic-self-assisted cough in long-sitting: expiration. to cough techniques to develop techniques that work
for your patients. For example, in a wheelchair, ask
uses elbow retraction, depending on the level of in­ your patient to lift his or her arms up while inhaling,
jury (Figure 21-11). During the flexion phase, pa­ hold, and then cough while he or she throws the arms
tients throw themselves onto their legs, thereby com­ down toward feet or lap using maximumlrunk flexion.
pressing both the upper and lower chest (Figure (Use a seat belt for safety.) Another idea is to have the
21-12). This can be taught very successfuJly to pa­ patient hook one arm on a push handle of the wheel­
tients with paraplegia, provided they do not have an chair, move the other upper extremity up and back (as
interfering tone problems. If the patient lacks hip in a PNF D2 pattern), watch the patient's moving hand
flexion or is worried about bony contact or skin in­ to maximize trunk rotation, inhale during the move­
jury, place a pillow (or two as needed) on the legs. ment, hold, and again cough as he or she throws trunk
This will limit the hip flexion and minimize trauma and upper extremity down toward opposite knee.
from the quick thrust onto the legs. When devising the most appropriate self-assisted
cough for your patient, remember to look for combina­
Short-sitting self-assisted cough
tion of trunk, upper extremity, head, neck, and eye pat­
The third assistive cough in sitting, the short-sitting terns that will maximize all four phases of the cough.

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 21 Facilitating Airway Clearance With Coughing Techniques 381

FIGURE 21-13
Assisted cough in short sitting. A, Hand
position for patient with good hand function;
B, Hand position for patients with only wrist
function.

Hands-knees rocking self-assisted cough

The last assistive cough to be discussed is performed
most frequently as a multipurpose activity to increase
the patient's balance, strength, coordination, and func­
tional use of breathing patterns (including quiet breath­
ing and coughing) simultaneously. The patient as­
sumes an all-fours position (hands-knees). He or she is
then instructed to rock forward, looking up and breath­
ing in as he or she moves to a fully extended posture
(Figure 21-14). After this, the patient is told to cough
out as he or she quickly rocks backward to the heels
with a flexed head and neck (Figure 21-15). Once
again, the importance of flexion and extension compo­
nents of a cough are noted. The rocking can be done
with or without a therapist's assistance. For patients
with generalized or spotty weakness throughout (e.g.,
some SCI, head traumas, Parkinson's, MS, cerebral
palsy, or spina bifida patients), this method is perfect
for incorporating many functional goals into a single
activity. It can help prepare them for more challenging
respiratory activities that they will undoubtedly meet
after their discharge from a rehabilitation center.
For patients with limited lower-extremity range of
movement or skin concerns associated with a quick
force, a pillow can be placed on the lower legs, thus FIGURE 21-14
restricting knee flexion and preventing direct contact Assisted cough in hands-knees position; extension or
of bony prominences. inspiratory phase.

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382 PART III Cardiopulmonary Physical Therapy Interventions

5. What is a smoker's cough, and why does it

....
occur?
L . .! _ 6. What are the stages of a cough?
-
I. . '
't . 7. What should the therapist interpret when a pa­
tient's cough is associated with eating or drink­
I .
:: ing?
8. What effect does coughing have on the blood
pressure and cardiac output?
9. What special techniques can be taught to asth­
matic patients to mobilize secreations?
10. What manual techniques are most effective in
FIGURE 21-15
spinal cord patients?
Assisted cough in hands-knees position; flexion or
coughing phase.
References
Standing self-assisted cough Bach. J.R. (1993). Comparison of peak expiratory flows wilh man­

Standing uses the same concepts and can be readily ually assisled and unassisled coughing techniques. Chest
104(5): I 553-{i2.
used for self-assisted coughs, provided the patient has
Braun. S.R.. Giovannoni, R., & O'Connor, M. (1984). Improving
adequate standing balance and/or upper extremity
cough in patients with spinal cord injury. American Journal of
support. Use any technique previously described and Physical Medicine 63( I): 1-10.
modify for this higher developmental posture. Com­ Estenne, M .. Detroyer, A. (1990). Cough in letraplegic subjects: an

binations of trunk, head, and extremity movements active process. Annals of Internal Medicine 12(1):22-28.
Fishburn, M.J.. Marino, R.J., & Dittuno, J.F. (1990). Alelectasis
during the cough maneuver is almost endless, thus
and pneumonia in acute spinal cord injulY Archives of Physical
specific techniques are not itemized.
Medicine and Rehabilitation 71: 197-200.
Hoffman, L.A. (1987). Ineffeclive airway clerarance related 10

neuromuscula.r dysfunction. Nursing Clinics of North America

SUMMARY 22(1):151-66.
Jaeger, R.J., Turba, R.M., Yarkony, G.M., & Roth, E.J. (1993).
In all postures and in all techniques, both for assisted
Cough in spinal cord injured patients: comparison of three
and self-assisted coughs, the importance of initial po­ methods to prodoce cough. Archives of Physical Medicine and
sitioning and ventilatory strategies is of utmost im­ Rehabilitation 74: I 358-{i1.
portance to the success of the airway clearance tech­ Linder. S.H. (J 993). Functional electrical slimulation 10 enhance

nique. There is an effective i dea waiting to be

incorporated for all patients to improve their cough,
cough in quadriplegia. Chest 103( I): 166-9.
MacLean, D., Drummond. .
c., & Macpherson, C . et a!. (1989).
Maximum expiratory airflow during chest physiotherapy on
from the tiniest postural change to full body move­
ventilated patients before and after the application of an ab­
ments and physical assists. Be creative in applying dominal binder. Intensive Care Medicine 5:396-399.
the concepts to all patient populations. Massery, M.P. (1987). An innovative approach to assistive cough
techniques. Topics in Acute Care Trauma Rehabilitation
(3):73-85.
REVIEW QUESTIONS Massery, M.P. (1994).. What's positioning got to do with it? Neu­
rology Report 18(3):11- I 4'.
1. What is the purpose of a cough? Slack, R.S., Shuca11. W. (1994). Respiratory dysfunction wilh trau­
2. W h a t a r e t h e two m e c h a n i s m s f o r a i rw a y malic injury to the central nervous system. Clinics in Chest

clearance? Medicine 15(4):739-49.

Sullivan, R.E., Markos, P.D., & Minor. A.D. (1982). An integraled
3. Why would a therapist assist a patient to cough?
approach to therapeutic exercise: Theory and clinical applica·
4. What techniques are most effective to assist
tion. Reston, Va.: Reston Publishing.
coughing?

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 Facilitating Ventilation Patterns
and Breathing Strategies

Mary Massery
Donna Frownfelter

KEY TERMS Controlled breathing Ventilatory strategies

Diaphragmatic breathing pattern Work of breathing

Jacobsen's progressive relaxation

INTRODUCTIOtJ
tient. No single technique is appropriate in all cases.
Attaining optimal ventilatory patterns requires the use Sound clinical judgment and experience must be exer­
of a variety of techniques. Some are passive in nature, cised when applying these ideas with each patient. It
such as passive positioning of the patient or applica­ is the hope of these authors that the techniques identi­
tion of an abdominal binder for better diaphragmatic fied in this chapter will stimulate the clinician's cre­
positioning. Some require very active participation on ative talents, and that they will extrapolate and im­
the part of the therapist and/or patient, such as in as­ prove on the techniques according to specific patient
sisted-cough techniques or in glossopharyngeal population needs. See the box on next page for spe­
breathing instruction. Other techniques are subtly in­ cific areas covered in the chapter.
corporated into the patient's total physical rehabilita­
tion program, requiring little overt attention to the pa­
POSITIONING CONCERNS
tient's respiratory performance, such as when using
ventilatory strategies. All of these diverse aspects of All patients spend some portion of the day in a hori­
treatment play an important role in the total develop­ zontal position for rest or sleep. Using this opportunity
ment of a successful respiratory rehabilitation pro­ to assist the patient in passive drainage of lung secre­
gram for the neuromuscular and musculoskeletal pa­ tions is a natural beginning in the development of a pa­

383

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384 PART III Cardiopulmonary Physical Therapy Interventions

Just as passive positioning of the patient in bed

Categories of Therapeutic Interventions
helps to maintain bronchial hygiene and improve
Presellted in this Chapter to Optimize
ventilation potential, passive positioning of the pa­
Ventilation Patterns
tient's skeletal frame in an upright posture (sitting,
I. Positioning concerns standing) helps to maximize the patient's mechanical

2. Ventilatory and movement strategies advantage of breathing. For example, patients with
spinal cord injuries (SCIs) resulting in tetraplegia
3. Manual facilitation techniques
will be unable to support their intestinal contents
• Fac i l i tating contr olled breathing patterns
properly under the diaphragm to al]ow for maximal
(diaphragmatic)
expansion of the chest in all three planes of ventila­
• Mobilizing the thorax
tion (see Chapter 37). Use of an abdominal support
Facilitating upper chest breathing patterns
from the iliac crest to the base of the xiphoid process
•

(accessory muscles)
provides positive pressure support to restore intesti­
Promoting symmetrical breath ing patterns
nal positioning in an upright position (Figure 22-1).
•

(unilateral dysfunction)
Research has documented well the significant im­
Reducing high respiratory rates
provements in vital capacity, inspiratory capacity,
•

4. Glossopharyngeal breathing and tidal volume in sitting with use of a strong ab­
S. Enhancing phonation skills dominal support. These binders have also been used
in nursing care to provide for better circulation and
in the prevention of hypotension.
The abdominal binder's value in cosmesis may be
underrated. Many of these neurological patients were
tient's long-term respiratory program. Specific pos­ once normal, healthy individuals with high self-es­
tural drainage positions are covered extensively in this teem who took great pride in their appearances. They
book (see Chapter 21). Using a combination of these now present with a protruding belly (the anterior and
positions in your patient's bed position rotation, in the infelior shift of the intestines resulting from flaccid
hospital, or at home can help to achieve multiple goals. abdominal muscles), which may be psychologically
First, they can assist the patients in clearing secretions disturbing to them. Thus the use of a binder may
passively that they may have difficulty performing ac­ greatly aid in the restoration of that person's self-es­
tively. Second, these position changes provide for skin teem, which should be a high-priority goal in any re­
relief and better circulation. Finally, they assist in re­ habilitation program.
tarding the development of joint contractures or other A rigid type of abdominal support can be used
musculoskeletal abnormalities. A four-position rota­ when the vertebral column and the abdominal viscera
tion (i.e., supine, prone, side-to-side) is usually an ef­ need support. These are called body jackets or total
fective and reasonable means of incorporating these contact thoracic lumbar sacral orthosis (TLSOs).
goals into a long-term prophylactic program. (Figure 22-2). A TLSO is a rigid trunk support
Simple adaptations may make ventilation easier in molded individually to the shape of the patient's en­
each of these postures. For example, in supine, plac­ tire trunk from the axilla down to the pubis. It is
ing the arms lip over the patient's head facilitates made up of two separate front and back pieces, with
'
greater anterior upper chest expansion. Likewise, po­ an anterior cutout in the abdomen to allow for normal
sitioning the pelvis in a slight posterior tilt facilitates diaphragmatic displacement of the viscera. Many of
more diaphragmatic excursion. See Chapter 40 for these jackets also use a strong elastic support across
more detailed explanations. Observation of all pre­ the cutout to allow for diaphragmatic motion but to
cautions and contraindications to passive positioning minimize excessive displacement of the abdominal
is still warranted. contents. This is very appropriate for the growing

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 22 Facilitating Ventilation Patterns and Breathing Strategies 385

"

FIGURE 22-1
A, Abdominal binder-Velcro fastener. B, placement of
abdominal binder.

child who needs more spinal stability or the com­ as well as many other areas of rehabilitation, depends
pletely flaccid tetraplegic patient who may also re­ on good alignment of the body against the forces of
quire the same support. Because head and neck posi­ gravity. Symmetry must be strived for through the
tioning are so interdependent on trunk positioning, a use of a body jacket, lateral trunk supports in the
body jacket may be the difference to these patients wheelchair, abdominal binders, or some other means
between being dependent or independent in an up­ (Figure 22-3). This is especiaJly important for pa­
right posture. It may result in significantly better head tients with hemiplegia where habitual asymmetrical
control, eye contact, longer phonation, and possibly posturing leads to musculoskeletal problems later.
better articulation. However, because it limits trunk Symmetrical breathing patterns and uniform aeration
movement, its usefulness for each patient must be as­ of all lung segments are augmented by careful up­
sessed carefuII y. right positioning. Therefore everything from the type
Logically, the next consideration under passive of neck support to the height and width of the arm
respiratory techniques is proper wheelchair position­ rests to the length and type of the foot supports must
ing. Optimal performance in respiratory functioning, be carefully analyzed for each patient.

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386 PART III Cardiopulmonary Physical Therapy Interventions

FIGURE 22-2

A, patient with CS congenital tetraplegia independent long sitting. B, long sitting with body jacket

support. Note changes in head position and eye contact, hip alignment, and shoulder rotation.

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 22 Facilitating Ventilation Patterns and Breathing Strategies 387

VENTILATORY AND MOVEMENT STRATEGIES

ally, these simple concepts take no more than I to 2
FOR IMPROVING FUNCTIONAL OUTCOMES
additional minutes of therapy, with no additional
Once the patient is positioned for success, motor ac­ equipment costs other than a few extra pillows or
tivities should be introduced that improve the pa­ towels. Therefore time or money are not mitigating
tient's ventilatory support, or the therapist should factors. However, these ideas do require the practi­
capitalize on the patient's good ventilatory support to tioner to look carefully at the patient before begin­
improve the motor activity. Using ventilatory strate­ ning any therapy, asking "Have J positioned my pa­
gies to improve motor performance or movement tient for respiratory success?" "Am J simply treating
strategies to improve ventilation performance enables the patient in whatever position J found them in?"
patients to achieve their functional goals sooner than and "Have I carefully chosen my verbal cues to in­
other patients; patients also get sick less often. Gener­ clude a respiratory response and a functional re­
sponse?" The practitioner must actively include res­
piration in every single activity to help the patient
understand that breathing transcends all activities.
See the box below for a summary of the most impor­
tant ventilatory-movement strategies.

Incorporating Simple Therapy Tasks

Inspiration
After the patient has been carefully positioned for
respiratory success, as described previously, begin
the patient's therapy or daily-living activities. From
an anatomical perspective, the pattern of inspiration
is naturally associated with the following: (1) trunk
extension, (2) shoulder flexion, abduction, and exter­
nal rotation movements, and (3) an upward eye gaze.
Expiration is logically associated with the opposite:
(I) trunk flexion, (2) shoulder extension, adduction,
and internal rotation movements, and (3) a downward

Significant Ventilatory-Movement Strategies

J. Pair trunk extension activities with inspirati o n

2. Pair trunk flexion activities with exhalation

3. Pair shoulder flexion, abduction and/or external

rotation activities with inspiration

4. Pair shoulder extension, adduction and/or inter­

nal rotation activities with exhalation

5. Pair upward eye gaze with inspiration

FIGURE 22-3 6. Pair downward eye gaze with exhalation

Wheelchair alignment considerations.

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388 PART III Ca.-diopulmonary Physical Therapy Interventions

eye gaze. Accordingly then, the simple task of pas­ nity to learn from the beginning of his or her rehabili­
sive range of movement (ROM) can easily include tation process that movement and breathing go hand
the active goal of increasing ventilation by asking the in hand. C1inicaJly, incorporating appropriate breath­
patient to breathe in and look up every time his or her ing pattems with movement early in the rehabilitation
arm is raised up into shoulder flexion. This encour­ process discourages the development of Valsalva pat­
ages the patient to breathe in when his or her chest tems or shallow breathing pattems when the motor ac­
wall muscles are being maximally stretched and the tivities become more difficult and complex.
ribs are naturally opening up, causing both activities
to be more successful. It also begins to teach the pa­
Dynamic Activities
tient to use ventilatory strategies to optimize potential
functional movement, such as in reaching up to a Inhalation promotes trunk extension and exhalation
kitchen cabinet. promotes trunk flexion and vice versa. This basic
theme occurs naturally in all motor activities but
Expiration may have ceased to become spontaneous after a
Likewise, active or passive exhalation should be co­ neuromuscular or musculoskeletal insult. Valsalva
ordinated with the reverse upper extremity ROM pat­ maneuvers during transitional movements, such as
tern (i.e., the arm returning from flexion back to the rolling or coming to sitting or standing, are often
patient's side). This can be done using all types of ex­ noted with these patients. By teaching them strate­
halation patterns, including the following: (1) passive gies that incorporate breathing into their motor
quiet exhalation, (2) forceful exhalation as in blow­ plans for all motor activities, Valsalva patterns can
ing, coughing, or pursed-lips exhalation, or (3) vocal­ be eliminated or minimized while simultaneously
ization patterns. Thus the therapist may ask the pa­ promoting beller cardiac function.
tient to slowly count out loud to 10 while the arm is Every activity of daily living cannot be described
being returned to his or her side. Subconsciously, the in this book, however, suggestions for typical gross
patient learns to correlate exhalation with shoulder motor activities using ventilatory strategies as a
extension while simultaneously learning a much means to improve these motor tasks are presented.
more complex idea-that of controlling his or her Extrapolation of these concepts to all other motor ac­
rate and volume of expiration by including deliberate tivities should be carefully analyzed by each therapist
speech during exhalation maneuvers. for each individual patient.
To improve exhalation potential, increase the pa­
tient's relative trunk flexion alignment. While sti II
Rolling
supine and performing upper-extremity ROM, this Ask patients to attempt to roll and assess whether
can be simply accomplished by asking the patient to they tend to move with trunk extension or flexion to
lift his or her head and watch the hand as it returns to begin the roll. If they roll with a trunk extension pat­
his or her side, which increases abdominal and inter­ tern ask them to breathe in while they roll and to look
costal activation, or by increasing knee flexion, up. If they roll with trunk flexion as their primary
which increases posterior pelvic tilting and trunk movement pattern, instruct them to roll while blow­
flexion. Pairing trunk flexion with exhalation com­ ing out and tucking their chin. In doing :\0, patients
pletes the ventilatory-trunk movement strategy. work with, not against natural whole patterns of
Combining positioning with respiratory verbal movements to increase the likelihood of success.
ROM activities, changes passive
cues, as described in
upper-extremity ROM exercises to dynamic upper-ex­
Coming up to sitting
tremity ROM exercises. It encourages increased inspi­ Pushing up to sitting from sidelying should be evalu­
ratory and expiratory capacities, develops early func­ ated in much the same manner. If patients are more
tional motor planning strategies, and facilitates trunk effective in coming upright when using trunk exten­
mobility. In this manner the patient has the opportu­ sion, have them inhale as they push up to sitting.

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 22 Facilitating Ventilation Patterns and Breathing Strategies 389

Asking them to "look up" as they move will reinforce independent one. Returning to sitting should be ac­
the upper chest movements through the use of the companied with slow controlled exhalation, such as in
symmetrical tonic neck reflex (STNR). If they have pursed-lips blowing or counting out loud, to maximize
more success pushing up with trunk flexion, have the body's controlled descent into gravity's influence.
them blow out and tuck the chin while moving.

Dressing FACILITATING A CONTROLLED DIAPHRAGMATIC

BREATHING PATTERN
Dressing activities can benefit from the same con­
cepts. While putting on lower-extremity items such Why woul.d a therapist want to change a patient's
as pants, socks, and shoes in a long sitting position, breathing pattern? The answer is simple-when the
have the patient first take in a deep breath while ex­ pattern being used is ineffective. Patients generally use
tending his or her trunk. Then have the patient blow a pattern of breathing that is the most efficient for them.
out, huff out, or cough while flexing the trunk to A healthy person uses approximately 5% of the
reach his or her toes. This combines the functional total oxygen consumption for the muscular work of
daily task of dressing with improving breath control, breathing and 10% of their vital capacity. Conse­
trunk control, and airway-clearance techniques. quently, breathing at rest is generally perceived as ef­
Upper-extremity dressing and upper-extremity ex­ fortless under normal conditions.
ercising can incorporate the same ideas. All move­ However, in patients that physical therapists evalu­
ments should be coordinated with harmonious chest ate and treat (often after surgery, respiratory disease, or
wall movements to maximize upper-extremity tasks. dysfunction secondary to neurological insult or injury),
Thus every time the arm is moving up above 90 de­ the vital capacity may be significantly decreased and
grees of shoulder flexion, the patient should be asked the oxygen consumption may be greatly increased re­
to breathe in, allowing for the normal shoulderlrib sulting from the use of accessory muscles or the extra
cage rhythm to occur. Full shoulder flexion requires effort needed to breath or cough. In the example of a
opening of the intercostal spacing and the separation patient with tetraplegia the vital capacity may be re­
of the individual ribs. Many neurological patients duced to 1000 to 1500 m!. If the normal tidal volume
have lost the intrinsic mobility of the chest wall and (normal volume of breathing) is 500 ml that would
thus may have lost some functional shoulder ROM as mean that with each breath the patient would use 33%
well. Not pairing inspiration with shoulder flexion is to 50% of his or her vital capacity (maximal inspiration
likely to limit the patient's shoulder ROM to approxi­ followed by maximal exhalation). This would greatly
mately 140 to 150 degrees. It may also encourage increase the oxygen consumption just for normal quiet
Valsalva maneuvers during the activity and may breathing. The patient would have little pulmonary re­
cause more shoulder pain. serve. During exercise or stress, the patient would have
an increased subjective feeling of shortness of breath
Coming up to standing
(dyspnea) and feel an increase in their work of breath­
Coming up to standing requires both trunk move­ ing. There are specific terms to describe breathing pat­
ments, thus the patient should initiate the forward terns, the most common are listed in the box on p. 390
trunk lean with exhalation and initiate the standing at top. Also see the box on p. 390 at bottom for indica­
phase with inhalation and neck extension. Active neck tions for teaching controlled-breathing techniques.
extension during assumption of standing not only fa­ It should be appreciated that breathing comfort­
cilitates greater inhalation but, along with the influ­ ably and in control is associated with wellness and a
ence of the tonic labyrinthine reflex (TLR), facilitates sense of ease. Even in normal individuals who are
more significant contractions of the trunk and hip ex­ under stress and have increased work levels we are
tensors. Clinically, this often results in a more notice­ more cognizant of the increase in work of breathing.
able upright posture and may make the difference be­ For a patient that is struggling with every breath and
tween an assisted standing pivot transfer and an wonders how he or she will get through the day, ven­

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390 PART III Cardiopulmonary Physical Therapy Interventions

Breathillg Pattern Termillology

Eupnea-Normal breathing, repeated rhythmic inspiratory-expiratory cycles

Hyperpnea-Increased breathing. usually refers to increased tidal volume with or without increased frequency

Polypnea, tachypnea-Increased frequency of breathing

Hyperventilation-Increased alveolar ventilation in relation to metabolic rate (an increase in alveolar ventilation
seen is a decrease in the arterial Peo2

Hypoventilation-Decreased alveolar ventilation in relation to metabolic rate (a decrease in alveolar ventilation)

seen as an increase in Peo2

Apnea-Cessation of respiration in the resting expiratory position

Dyspnea-The patient's subjective feeling of shortness of breath

Apneusis-Cessation of respiration in the inspiratory position

Apneustic breathing-Apneusis intelTupted periodically by exhalation

Cheyne-Stokes respiration-Cycles of gradually increasing tidal volume followed by gradually decreasing tidal
volume (usually followed by an apneic period)

Biot's respiration-Sequences of uniformly deep gasps and apnea, followed by deep gasps

Adapted from Comroe. J. H .• Jr. (1974). Physiology 0/ respiration, (2nd ed). SI. Louis: Mosby.

Indications for Teaching Controlled-Breathing Techniques

Patients with any or t.he following:

• Pulmonary dysfunction either pIimary or secondary causes

• Pain from surgery, trauma, or disease

• Apprehension or nervousness

• Bronchospasm or impending bronchospasm in asthma

• A irw ay clearance dysfunction

• Restriction of inspiration resulting from musculoskeletal dysfunction such as scoliosis. kyphoscoliosis, pectus ex­
cavatum, obesity, pregnancy, pulmonary pathology such as fibrosis, scarring from radiation therapy. neurological
weakness such as spinal cord injury. Parkinson's disease, or myasthenia gravis

• Congestive heart failure, pulmonary edema, or pulmonary emboli

• Rib fractures

• Ventilated patients on assist control or intennittent mandatory ventilation (lMV)

• Metabolic disturbances that have a compensatory respiratory response

• Debilitated or bedridden patients that tend to have constant volume ventilation, retain sel:relions. and are prone to
pneumonia and atelectasis from poor airway clearance

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 22 Facilitating Ventilation Patterns and Breathing Strategies 391

them to relax the neck and chest accessory muscles

Goals of Teaching Controlled-Breathing
and use more diaphragmatic breathing to reduce the
Techniques
work of b r eath ing in co mbination with relaxed
• To decretlse the work of breathing pursed-lip breathing on exhalation. Their treatment

• To improve alveolar ventilation programs focus on energy conservation and pacing

activity with breath control.
• To improve airway clearance by improving cough
However, with secondary pulmonary dysfunction
• To increase strength, coordination. and efficiency
patients, such as spinal cord injury, there is a more
of respil'lltory muscles
restrictive component to inspiration. In this case, they
• To teach the patient how to respond to and control
may have accessory muscles intact, but they are not
breathing
using them to faciliate deep breathing or coughing.
• To assist in relaxation
They may have a strong diaphragmatic breath but the
To mobilize and maintain mobility of the thorax
upper chest collapses on inspiration (paradoxical
•

• To enable patients to feel self-control and confi­ breathing, see Chapter 37). In these cases the goal is
dence in managing disease or dysfunction
to teach them to use the accessory muscles to balance
the upper and lower chest. This facilitates an increase
in vital capacity to prevent atelectasis and pneumonia
tilatory strategies and breathing-control techniques by increasing the volume of ventilation and improv­
can be the key to maximizing potential. See the box ing the cough mechanism.
above for a list of goals in teaching controlled-breath­ The choice of appropriate venti latory strategies
ing techniques. depends on the patient's individual problem. The fol­
Breathing control has long been used in yoga to lowing questions should be considered when evaluat­
foclls and promote meditation. This is a key to maxi­ ing patients:
mizing rehabilitation. If you can not breathe you can­
Does the patient have more difficulty in inspira­
not function! It is of primary importance to assess the
tion or exhalation?
patient's breathing at rest and during exercise. We
•
Is there a normal sequence to inspiration (i.e., ab­
often hold our breath with exertion, especially with
dominal wall rises, then mid chest, then upper
new activities. We must assess the cardiopulmonary
chest, with a full inspiration? Or does the chest
and neuromuscular response to each new activity.
sink and the abdomen rise on inspiration?
•
Does the patient appear to be working hard to
CONSIDERATIONS FOR TEACHING BREATHING breathe? Is the patient using the accessory muscles
CONTROL TO PATIENT'S WITH PRIMARY VERSUS to an extreme?
SECONDARY PULMONARY DYSFUNCTION •
Does the patient have trouble coughing or speak­
ing a normal volume and for the normal length of
Patients with primary lung disease, such as emphy­
sentences?
sema, asthma, bronchitis, or cystic fibrosis, present a
•
Is ventilation the limiting factor in accomplishing
much different picture than patients with spinal cord
' an activity (i.e., transfer, gait, or bed mobility)?
injury, Parkinson's disease, myasthenia gravis, or
Guillain-Barre syndrome. Patients with primary pulmonary disease generally
In general, patients with primary lung disease use benefit from ventilatory strategies that relax the ac­
their accessory muscles and greatly increase the work cessory muscles and facilitate relaxed diaphrag­
of breathing secondary to the shortness of breath or matic breathing.
coughing. They often complain that they have more On the other hand, patients with secondary pul­
difficulty "getting air out," which demonstrates the monary dysfunction usually benefit from the balanced
decreased expiratory flow rates noted on pulmonary use of the diaphragm and accessory muscles to in­
function tests. The goal with these patients is to teach crease vital capacity and breath support for activities.

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392 PART III Car·diopulmonary Physical Therapy Interventions

obstructive pulmonary disease (COPD) patients.

Diaphragmatic Facilitation Techniques
Neurologically impaired patients need modifica­
I. R elaxation technique tion with their activity levels and capabilities.

2. Re patterning techniques

• Relaxed pursed-lip breathing POSITIONING CONCERNS

• Exhalation, hold, and inhalation Position of Pelvis
3. Sniffing
The first step in facilitating any breathing pattern is to
4. Diaphragmatic scoop technique position the patient for respiratory success. The de­
5. Lateral costal facilitation technique tails are discussed in this chapter and Chapter 40.

6. Upper chest inhibiting technique Often the patient's posture and pelvic position has a
dramatic effect on breathing. In general, a slight, rela­
7. Normal timing technique
tive posterior tilt of the pelvis facilitates diaphrag­
matic breathing and a relative anterior tilt facilitates
opening of the anterior chest and upper chest breath­
FACILITATING DIAPHRAGMATIC BREATHING
ing. It is helpful to see what difference a slight, rela­
This section is laid out starting with the easiest interven­ tive change in pelvic position will do to the patient's
tion to facilitate diaphragmatic breathing and progress­ ability to ventilate. This is especially true with sec­
ing to specific inhibition and facilitation techniques. ondary pulmonary problems related to neurological
See the box above for a summary of methods to and neuromuscular dysfunction.
facilitate diaphragmatic ventilation patterns.

RELAXATION OF UPPER CHEST AND SHOULDERS

DIAPHRAGMATIC CONTROLLED BREATHING
Jacobsen's progressive relaxation exercises are famil­
Diaphragmatic breathing is the normal mode of respi­ iar to physical therapists. Jacohsen proposed that a
ration. The diaphragm and intercostals are the normal maximal muscle contraction would yield a maximal
muscles of quiet inspiration. When evaluating a pa­ muscle relaxation. This technique can be applied to
tient's breathing pattern, the use of accessory muscles the upper chest and shoulders. The therapist places
during quiet breathing should be noted; the patient his or her hands on the patient's shoulder girdle. The
with primary pulmonary disease should be instructed patient is asked to shrug his or her shoulders up into
in relaxation of the accessory muscles to decrease the the therapist's hands and hold it. "Don't let me push
work of breathing. In a patient with a spinal cord in­ your shoulders down," is the therapist's command.
jury or other neuromuscular disorders, these muscles Then, "Let your shoulders relax, let them go." The
may assist in balancing ventilation and may be useful emphasis is on the relaxation phase. Verbal com­
in increasing vital capacity, and improving the ability mands can be very important with this procedure. A
to cough, improving breath support for speaking, and strong command to, "Raise your shoulders into my
increasing potential for functional activities. hands" is followed by a quiet, more relaxed, "Now
In general, controlled diaphragmatic breathing needs relax and let them go," repeating quietly, "That's it,
to be emphasized in each posture and with all therapeu­ let them go, feel them t:elax." Sometimes the relax­
tic activities. CatTY-over is not necessarily present. If the ation activity is all that it takes to resume a more nat­
patient is only shown the pattern in supine, it may not ural pattern of breathing and you can move on to
carry over to sitting or during a sliding-board transfer other therapeutic activity. If the patient starts to use
when the activity becomes difficult. A helpful sequence accessory muscles again the technique is repeated.
to use might be teaching the breathing pattern in sidely­ The patient learns to feel the difference between ten­
ing, supine, sitting, standing, walking, stairs climbing, sion and relaxation of the shoulders and can self­
and other functional activities, especially with chronic monitor and perform the relaxation independently.

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 22 Facilitating Ventilation Patterns and Breathing Strategies 393

REPATTERNING TECHNIQUE
rotation), and (4) choosing to use a pillow or pillows
If a patient needs more support to gain control of breath­ under the head. (For details on positioning, see Chap­
ing and is experiencing shortness of breath, a simple ter 40.) For each patient, choices will be different (i.e.,
repatterning technique is very beneficial. An example the amount of knee flexiol1 or the number of pillows).
might be an asthmatic patient with a high respiratory Find the right combination of positioning characteris­
rate who is feeling panicky. When the patient is asked tics that best facilitates diaphragmatic movement for
why he or she is breathing so fast the reply will usually that particular patient. In this manner the therapist sets
be, "I am n ot getting enough air, I can't catch my up the patient for respiratory success before beginning
breath." The patient is asked to start with exhalation. the manual or verbal techniques.
"Try to blow out easily with your lips pursed. Don't Now, begin the techn ique. A s k the patient to
force it just let it come out." By doing this, the respira­ place his or her hands on their stomach for increased
tory rate will automatically be decreased. When the pa­ proprioceptive feedback and the relative extension,
tient feels some control of this step, then ask him or her adduction, and internal rotation position of the shoul­
to "hold the breath at the top of inspiration just for a sec­ ders. In a quiet melodic voice, ask the patient to
ond or two." Make sure the patient does not hold his or "sniff in 3 times." Note if the patient demonstrates
her breath and bear down as in a Valsalva maneuver. more abdominal rise and/or lower chest expansion . If
Lastly, ask the patient to take a slow breath in, hold it, so, draw attention to this fact. During exhalation, tell
and let it go through pursed lips. Patients often learn that the patient to "let it out slow," which helps to inad­
when they are short of breath, this technique will help vertently slow the respiratory rate (RR) and often en­
them gain control, making them feel less panicky. courages some relaxation. Progress the training by
asking the patient to "now sniff in twice." Do you
still see greater diaphragmatic excursion and less
Sniffing
upper chest excursion? If so, continue by asking for
If working toward a generalized controlled-breathing "one long slow sniff." If successful, the therapist
pattern does not improve the patient's ventilatory pat­ should follow with: "now do it quieter," then "now
tern adequately, a technique that more specifically do it slower," "even quieter," and so forth. By this
addresses the n eed to initiate breathing from the di­ time, the patient should be demonstrating an easy
aphragm can be attempted. Sniffing is a simple and onset, slow RR, diaphragmatic pattern with relaxed
effective means of teaching increased diaphragmatic shoulders.
breathing. Sniffing is primarily diaphragmatic breath­ Clinical experience has shown this technique is
ing by nature. Use this technique first when attempt­ highly successful with about 80% of patients who
ing more specific diaphragmatic training with all pa­ have primary pulmonary pathologies or neurological
tients who are capable of attempting sniffing because impairments. The key to success seems to stem from
of its simplicity. the relaxed tones and words that the therapist uses,
As with all procedures, the most imp0l1ant step is which decrease anxiety and imply relaxation and not
the first step: position the patient appropriately to in­ "effort." Once the pattern has been established, the
crease the likelihood of increased diaphragmatic patient can easily be instructed to go through the
breathing resulting from musculoskeletal alignmel1t. training as needed indepen dently. The sequence (in
This includes the following: (I) choosing a gravity­ whole or in part) may be appropriate for patients be­
eliminated position, such as sidelying, or a gravity-as­ fore getting out of bed if they become anxious and
sisted position, such as supported semi-Fowler's sit­ demonstrate excessive upper chest breathing during
ting (supported spin e), (2) choosing a relatively this activity. For other patients, it may be appropriate
posteriorly tilted pelvis with flexed knees, (3) choos­ before or during eating or before climbing stairs. Ob­
ing the arms to be down below 90 degrees of flexion viously, the application of this technique will be indi­
(in relative shoulder extension, adduction, and internal vidualized for each patient, depending on the deficits.

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394 PART III Cardiopulmonary Physical Therapy Interventions

PROCEDURE FOR TEACHING CONTROLLED

DIAPHRAGMATIC BREATHING (SCOOP TECHNIQUE) / Y?. "'.

j ""f f !
/

Minimal patient instruction is necessary to facilitate C .. '

I! /, J ))
diaphragmatic breathing using the scoop technique. It )' -::0.. ,,/
, "-

allows the patient to feel the breathing pattern, then it

is brought to the patient's cognitive awareness. The
.
patient then learns to self-cue to incorporate the
breathing pattern.

r 1
The following is a suggested sequence:
1. Position the patient for success, generally in a
s i d e l yi n g p o s i t i o n w i t h t h e b e d in s e m i ­
Fowler's or supine in semi-Fowler's with a
FIGURE 22-4
bend in the knees to achieve a relative posterior
Therapist's hand placement for diaphragmatic breathing.
pelvic tilt and relax the abdominal muscles.
2. Place your hand on the patient's abdomen at
the level of the umbilicus. Tell the patient you perventilate and blow off too much CO2. The fact
want to feel his or her breathing. Follow the pa­ that they are breathing more with their diaphragms is
tient's breathing pattern for a few cycles until the important consideration. Note also the position of
you are in his or her rhythm. Do not invade the the pelvis and trunk.
patient's breathing pattern rather, at first, fol­ When the patient has mastered the breathing pat­
low their movement. tern in sidelying, try supine. Then progress to sitting
3. After the nonnal rate at the end of the patient's (Figure 22-6), standing (Figure 22-7), walking (Fig­
exhalation, give a slow stretch and "scoop" your ure 22-8), and finally stairs (Figure 22-9). Each de­
hand up and under the anterior thorax as shown velopmental position increases the difficulty in per­
in Figure 22-4. The command, "Breathe into my forming diaphragmatic breathing. In sidelying or
hand," is given as the slow scoop stretch is done. supine the patient is fully supported. The sidelying
4. As the "scoop stretch" is performed instruct the position is especially good for initially teaching di­
patient to, "breathe into my hand" during the aphragmatic breathing because the diaphragm is in a
inspiration. Give a scoop at the end of exhala­ gravity-eliminated position. In supine the patient
tion with each breath. The verbal command can must breathe up against gravity. However, as we
be effectively replaced with audible breathing progress to sitting, the patient must now provide
to facili tate the ventilatory pattern if verbal trunk support and maintain stability up against grav­
cues are ineffective or inappropriate. ity, as well as relax the shoulders. In standing the en­
5. After achieving some success, it is helpful to tire body must be supported, and when walking or
call the patient's attention to the awareness of stairs are added, the element of breathing coordina­
the breathing pattern. For example, the thera­ tion really comes into play.
pist can ask, "Can you feel how your abdomen Coordination of breathing for walking involves
rises as you breathe in?" being careful not to allow patients to breath hold. They
6. The patient's hand can be placed on the ab­ need to keep inspiration and exhalation regular at least
domen with the therapist's hand on top. Rein­ at a ratio of 1'1, preferably exhaling a little longer.
force the breathing pattern, then remove your In general the preferred pattern for patients with pri­
hand and allow the patient to independently mary pulmonary dysfunction is as follows: (I) Pause at
feel the ventilatory pattern (Figure 22-5). the base of the stairs to gain controL (2) Have the pa­
A few things should be taken into consideration. Try tient take a breath in and move as he or she exhales up
not to have patients take too many deep breaths; they one stair. (3) The patient then pauses to inspire and ex­
may begin to feel light-headed because they may hy­ hales as he or she walks up one stair. (4) The patient

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 22 Facilitating Ventilation Patterns and Breathing Strategies 395

FIGURE 22-5 FIGURE 2-6

The patient is encouraged to continue practicing The patient advances to the sitting position for breathing

diaphragmatic breathing to become aware of his breathing retraining. Note the relaxed position of the patient's

pattern. this is usually the first position of the shoulders and hands.

diaphragmatic breathing teaching sequence.

FIGURE 22-7 FIGURE 22-8

The third position in the sequence is standing. Full-length Walking is the fourth stage of retraining. The patient is
min'ors are helpful at this point. encouraged to relax, control his breathing, take long steps
and slow down.

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396 PART III Cardiopulmonary Physical Therapy Interventions

C1 0f
-- \y

FIGURE 22-9 FIGURE 22-10

Stairs are important, especially if the patient has them at Bilateral lower lobe expansion (this also facilitates
home. He is instructed to pause slightly as he breathes in diaphragmatic movement).
and to exhale as he climbs one to two stairs.

Upper Chest Inhibition

should be encouraged to use the handrail and pace his
or her movement slowly and with breath controL If all other manual facilitation techniques cease to
In general neuromuscular patients with lower-ex­ produce the desired increase in diaphragmatic breath­
tremity weakness may benefit from inspiration ing, then inhibiting the upper chest during inhalation
while ascending stairs and exhalation during de­ may be effective.
scent. Going downstairs is an eccentric muscle pat­ Again, position the patient appropriately. These
tern and exhalation is a relative eccentric contrac­ authors usually choose sidelying or 3/4 supine.
tion of the diaphragm. Begin by facilitating the diaphragm, usually with the
Refer to the section on ventilation and movement diaphragm scoop. Slowly bring your other arm
strategies on p. 387 of this chapter to determine appro­ across the upper chest at about the level of the ster­
priate incorporation of breathing in functional tasks. nal angle. Leave it there for a couple of respiratory
cycles without applying any pressure to feel the
upper chest's movement.
LATERAL COSTAL BREATHING
After assessing this movement, gently allow your
Lateral costal breathing also facilitates diaphragmatic arm to follow the upper chest back to its resting posi­
excusion. This may be done bilaterally as in Figures tion when the patient exhales. Now on the patient's
22- I 0, 22-11, 22-12, 22-13, and 22-14 or unilaterally next inspiratory effort, do not move your arm's posi­
as in Figures 22-1S, 22-16, and 22-17. Lower chest tion. Thus your arm position will apply pressure or
lateral costal expansion facilitates diaphragmatic and resistance to the expansion of the upper chest. This
intercostal breathing where the mid chest will recruit gentle pressure will cause postural inhibition to the
primarily intercostal activity. anterior and superior movement of the upper chest.

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 22 Facilitating Ventilation Patterns and Breathing Strategies 397

RGURE22 1 RGURE22 2
Bilateral midchest expansion exercise. Self-assisted bilateral chest expansion exercise. Keep the
patient's shoulders relaxed.

l
j 1
----" ,-"I{

FIGURE22-13 FIGURE22-14
Bi lateral posterior chest expansion exercise. Bilateral posterior chest expansion exercise.

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398 PART III Cardiopulmonary Physical Therapy Interventions

FIGURE 22-15
FIGURE 22-16
Unilateral (segmental) breathing, left field. the left lower
shoulder must remain down,
with hands on ulnar border or palm up in his lap.

FIGURE 22-17
The either hand on the side of the
chest to be by his hand up.

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 22 Facilitating Ventilation Patterns and Breathing Strategies 399

After each expiratory cycle, add more pressure until the chest wall to the lower sternum and touches the
the patient subconsciously increases the lower chest patient with the instructions again to "now breathe
breathing out of necessity. here." Finally, the therapist uses the first hand to
When you note more diaphragmatic and/or lower move up to the upper sternum (usually around the
intercostal muscle excursion, verbally note this to the level of the sternal angle) and asks the patient to
patient. Ask the patient to try to reproduce this pat­ "now breathe here." It is impol1ant that the therapist
tern. With your other arm continue to facilitate the smoothly transitions from one hand to the next to as­
desired response, such as with the diaphragm scoop. sist the patient in developing a smooth motor transi­
Slowly, during each of the next series of inhalation, tion from one area of the chest to the other. The man­
release your inhibition as the patient tries to maintain ual cues provide tactile cuing rather than true motor
the improved lower chest breathing pattern. If the pa­ facilitation. Because of this, the normal timing se­
tient is only partially successful, the inhibition can be quence is obviously a more-advanced technique in­
partially reapplied to assist the patient. If the patient tended for use after achieving initial diaphragmatic
becomes anxious because the therapist's inhibition is training success.
preventing upper chest breathing, then decrease the
inhibition to a comfortable level. This technique
MOBILIZING THE THORAX
should never cause an increase in anxiety or it will
only encourage more upper chest breathing rather For some patients, controlled breathing alone may
than less. not alleviate the inefficient ventilatory patterns even
with utilization of good positioning and appropriate
ventilatory strategies. The thorax itself may be inca­
Normal Timing
pable of moving freely enough to allow for adequate
During normal quiet inspiration (controlled breath­ chest wall excursion necessary for that breathing pat­
ing), the diaphragm contracts, which is seen out­ tern. For example, a patient with a spinal cord inj ury
wardly as a gentle rise of the abdomen. The second who is demonstrating an excessive diaphragmatic
movement is seen as lateral costal expansion of the pattern that is unbalanced by the normal neuromuscu­
lower chest and usually to a lesser extent, lower ante­ lar support of the intercostal and abdominal muscles
rior chest expansion. Lastly, the upper chest rises can breathe using minimal chest wall expansion. This
slightly in primarily a superior-anterior plane with is often noted as belly breathing. It may be necessary
less lateral expansion noted. A normal timing tech­ to mobilize individual rib segments to gain the poten­
nique adapted from the physical therapy approach of tial for chest walJ expansion in aIL three planes of
proprioceptive neuromuscular facilitation (PNF) can ventilation before facilitating a specific breathing pat­
help the patient work on this sequence. After the pa­ tern. If the potential for movement is not there, then
tient has learned to initiate inspiration with his or her the breathing pattern cannot change. Likewise, a pa­
diaphragm and lower chest wall muscles more con­ tient with primary pulmonary dysfunction undergoing
sistently, this technique can help to put the whole se­ chest surgery, or a patient suffering from an acute
quence together. The diaphragm continues to be the chest trauma, may also find the rib cage stiff or sore
primary mover, but the other accessory muscles are and thus limited in its potential expansion. All three
encouraged to do what they should do, which is to as­ of these patients may benefit from the inclusion of rib
sist the diaphragm for better overall ventilation. cage mobilization in their therapy programs. The rib
Generally, the patient is positioned symmetrically cage musculoskeletal limitation may be secondary to
in either supine or supported sitting with a neutral muscular atrophy, spasticity, or pain. Thus patients
pelvic position. The therapist waits until the end of an with either primary pulmonary dysfunction or sec­
expiratory cycle and then, using the hand placement ondary pulmonary dysfunction can benefit from the
of the diaphragm scoop, asks the patient to breathe in concept of chest mobilization.
"here." With the other hand, the therapist moves up It is beyond the scope of this textbook to detail all

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400 PART III Cardiopulmonary Physical Therapy Interventions

her head (shoulder flexion), as far as possible while

Techniques to Mobilize the Thorax
watching his or her hands. Using the appropriate ven­
I. Use of towel or pillow rolls to mechanically tilatory strategy, the patient is also instructed to in­
open up the anterior or lateral chest wall hale during this movement. Because fulJ shoulder
2. Use of upper extremity pattern s to facilitate flexion and inspiration both require opening of the in­
opening of individual rib segments dividual rib segments, pairing them in this gravity-as­
3. Counterrotation of the trunk sisted position wiII promote a greater passi ve chest
wall stretch then either technique alone. If straight
4. Use of ventilatory-movement strategies to facili­
tate opening of the entire thorax flexion is not a viable option, use a buttelily position,
raising the arms up in shoulder flexion, abduction,
5. Specific rib mobilization tu free up an individual
segment and external rotation with elbows bent (like butterfly
wings), again pairing this with voluntary maximal in­
6. Myofascial release techniques to frec up restric­
tive connective tissue on and around the thorax spiration and upward eye gaze. Pairing inspiration
and shoulder flexion maximizes the stretch on the
7. Soft tissue release techniques to lengthen indi­
vidual tight Illuscles chest and encourages better ventilatory strategies.
In sidelying, ask the patient to bring his or her arm
up in straight flexion to maximize anterior chest ex­
the numerous techniques involved in musculoskeletal pansion or to move the arm into abduction to maxi­
mobilization of the thorax, however, some simple mize the lateral costal expansion. Pair either move­
techniques and suggestions for further study are pre­ ment with inspiration and upward eye gaze. If upper
sented. See the box above for a summary of mobi­ extremity movement is not possible, the therapist can
lization techniques. passively use countelTotation of the trunk to mobilize
Once again the therapist should note that the initial the chest while in the sidelying over the towel or pil­
step in achieving success begins with positioning low roll. Continue to ask for active eye gazing.
considerations. Starting in supine, anterior chest wall The same concepts can be used in upright postures,
mobility can be improved by placing a vertical towel such as sitting or standing. Use a vertical towel roll
roll down the length of the thoracic spine and allow­ again along the thoracic spine either along the back of
ing gravity to pull the shoulders back to the bed. In a chair (wheelchair) or along the wall. Move the pa­
this position, the anterior chest is opened up, placing tient's arills passively or actively up into the most flex­
the intercostal and pectoralis muscles on stretch for ion or buttert1y ROM possible. The patient will get a
easier facilitation of upper chest expansion. significantly greater stretch to the anterior chest wall
In sidelying, the lateral aspect of the chest can be using the towel roll than without it. Precautions apply
passively mobilized with gravity'S assistance by plac­ for patients with musculoskeletal problems along the
ing a towel roll(s) or pillow(s) under the lower chest spine and for patients with impaired skin-tolerance.
(ribs 8 to 10) on the weight-bearing side. To determine If these general mobilizing techniques do not pro­
an appropriate amount of sidebending, make sure that duce adequate chest wall mobility to allow for freer
the patient's shoulder and pelvis are still in direct con­ breathing patterns to occur, then more specific tech­
tact with the surface even with the towel roll(s) in niques need to be considered including the following:
place. This maximizes the stretch on the chest without (I) specific rib mobilization, (2) myofascial release to
placing the patient in a position that is too advanced tight connective tissues (e.g., scar tissue secondary to
for his or her present chest wall mobility. Patients vary surgical or traumatic areas), and/or (3) soft tissue re­
from tolerating only a single thin towel roll up to toler­ lease of tight muscle groups (neurological patients
ating three pillows under the lower ribs. often present with tightness in the pectoralis, inter­
In both postures, active or passive stretch ing can costal, and quadratus lumborum muscles groups,
be added after positioning for success. In supine, ask whereas orthopedic patients tend to have more tight­
the patient to bring the arms directly up over his or ness in the neck and back muscles). Use the position­

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 22 Facilitating Ventilation Patterns and Breathing Strategies 401

ing and ventilatory strategies previously suggested

Accessory Muscle Facilitation Techniques
(e.g., sidelying over a towel roll) during these spe­
cific interventions to maximize the potential gains in I. Pec to ral i s facilitation
chest wall mobility. It is beyond the scope of this 2. Sternocleidomastoid and scalenes facilitation
textbook to detail all the numerous techniques in­
3. Trapezius facilitation
volved in musculoskeletal mobilization and release of
4. Diaphragm inhibiting technique
the thorax. These three interventions are intended as
Manual inhibition
suggestions for further study in outside texts.
•

• Postural inhibition

5. Lateral costal facilitation

FACILITATING ACCESSORY
6. Serratus push-up
MUSCLES IN VENTILATION

If the patient is still not demonstrating an optimal

breathing pattern after f acilitating a preferred muscle breathing, the patient would be put in an ad­
breathing pattern through appropriate positioning, vantageous posture by slightly anteriorly tilting the
appropriate ventilatory strategies, chest wall mobi­ pelvis. In supine, this could be as simple as decreas­
l ization, and diaphragmatic retraining, then specific ing the amount of knee flexion that is present or
facilatory or inhibitory techniques should be initi­ using a small towel roll under the lumbar spine.
ated to the accessory muscles of ventilation. Spe­
cific techniques are discussed here in detail. See the
Pectoralis Facilitation
box above for a summary.
Because the diaphragm normally supplies the bulk The pectoralis muscle group is a powerful anterior
of the inspired air during quiet breathing, diaphrag­ and lateral expander of the upper chest and can sub­
matic breathing is the preferred pattern of breathing. stitute quite effectively for paralyzed intercostal mus­
However, after some neurological insults, strictly di­ cles in the upper chest when trained to do so. Train­
aphragmatic breathing may not be possible or even ing usually begins in either modified sidelying or
preferred. Unlike pulmonary rehabilitation programs supine. To increase the use of this muscle during in­
for chronic lung or asthmatic patients, where di­ spiration, the therapist should place his or her hand in
aphragmatic breathing is almost always encouraged the same direction as the contracting muscle fibers.
and use of accessory muscles discouraged, restoration Specific proprioceptive input is very important when
of independent, efficient breathing patterns for the facilitating a muscle, thus make sure the hand is diag­
neurologically impaired patient may require the regu­ onally placed on the upper thorax (Figure 22-18).
lar use of accessory muscles. The heel of the therapist's hand should be near the
Positioning continues to be the single most impor­ sternum and the fingers aligned up and out toward the
tant aspect of all ventilatory facilitation techniques. If shoulder. The patient is then asked to breathe into the
your patient is positioned for success, the probability therapist's hands while the therapist applies a quick
of a successful response is much more likely. By as­ manual stretch (as in repeated contractions PNF) to
sessing the patient's head, upper-extremity, trunk, the muscle fibers (down and in toward the sternum).
pelvic, and lower-extremity positioning before every This elicits the quick stretch reflex of the muscle and
activity or technique, the therapist is empowered to simultaneously provides added sensory input, which
use mechanical positioning and gravity to the pa­ facilitates a stronger and more specific muscle con­
tient's advantage rather than to a disadvantage. For traction. To emphasize an increase in lateral expan­
example, a slightly posteriorly tilted pelvis tends to sion, facilitation should gradually be transferred from
facilitate diaphragmatic breathing, whereas a slightly the sternal arca out toward the therapist's finger tips
anteriorly tilted pelvis tends to facilitate upper chest by the patient's shoulder. Unlike in the case of facili­
breathing. Thus when facilitating more accessory tating a more diaphragmatic pattern, verbal cues

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402 PART III Cardiopulmonary Physical Therapy Interventions

FIGURE 22-18
Hand placement for facilitation of the pectoralis muscles for upper chest breathing.

Trapezius Facilitation
should be strong and demanding to elicit a stronger
maximal voluntary effort. The trapezius muscle assists in superior expansion
of the chest. Facilitation can be initiated in supine
or sidelying positions to decrease the resistance
Sternocleidomastoid and Scalene Facilitation
from gravity. It can be progressed to an upright
This same plinciple can be applied to the sternoclei­ posture in which the patient would have to work
domastoid and scalene muscles. In supine, therapists against gravity.
need only change the angle of their hand alignment to Placing the hands over the tops of the patient's
more specifically facilitate the sternocleidomastoid shoulders, the therapist quick stretches the trapezius
and scalene muscles. Turning the hands parallel to in a downward direction to facilitate a stronger eleva­
the trunk so that the fingers are pointing up toward tion response. Repeated contractions e<in be added to
the neck rather than pointing out toward the shoulder, facilitate the contraction throughout the full ROM.
the therapist applies the same quick stretch and uses Obviously, the shoulder shrug motion should be
the same verbal cues. The altered hand position now paired with inhalation and upward eye gaze to maxi­
specifically facilitates the sternocleidomastoid and mize the facilitation response.
scalene muscles and secondarily influences the pec­
toralis muscles. The sternocleidomastoid and scalene
Inhibition of the Diaphragm
muscles primarily expand the chest in a superior and
anterior plane, whereas the pectoralis muscles expand Two techniques are described to inhibit the excessive
the chest in primarily a lateral and anterior plane, use of the diaphragm during inspiration. Ideally, the
thus accounting for the slight difference in the facili­ therapist is venturing to balance the use of accessory
tation positioning. muscles, especially the intercostal, sternocleidomas­

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 22 Facilitating Ventilation Patterns and Breathing Strategies 403

toid, scalenes, and trapezius muscles with the di­ To perform the diaphragm-inhibiting technique,
aphragm's contraction. This is done to prevent para­ the patient is positioned supine, semi-sitting or side­
doxical movements of the chcst, or worse, to prevent lying with the top arm positioned overhead or pulled
adverse musculoskeletal changes in the chest wall, back at the waist to open up the upper chest. If toler­
such as a pectus excuvatum that can result from mus­ ated, remove pillows from under his or her head, an­
cle imbalance. teriorly tilt the pelvis and assess patient's airway
Inhibiting the diaphragm may be necessary during safety by checking if he or she can still swallow
breathing retraining for somc patients with spinal comfortably. The heel of the therapis t's hand is
cord injuries, polio, spina bifida, developmental de­ placed lightly on the patient's abdomen at about the
lays, head traumas, and cerebral palsy. The di­ level of the umbilicus. No instructions are given to
aphragm may be too weak to produce an adequate the patient at this point. As the patient begins to ex­
tidal volume or vital capacity without the assistance hale a normal breath of air, the therapist gently al­
of accessory muscles. In these cases the diaphragm­ lows the heel of his or her hand to move up and in to­
inhibiting technique is used to encourage the use of ward the central tendon of the patient's diaphragm
the accessory muscles to assist in independent volun­ (see Figure 22-4, p. 394). When expiration for that
tary ventilation. Patients learn to use their weakened breath is completed, the therapist strictly maintains
diaphragm muscles in concert with intact accessory the hand position in that shortened expiratory posi­
muscles. Not only does this allow for an increased tion. During the following inspiratory phase, the di­
tidal volume and vital capacity, but it also provides aphragm will experience some gentle resistance to its
better aeration of all lung segments and better mobi­ inferior descent, causing inhibition to its full ROM.
lization of the entire thorax. On the next expiration, the technique is repeated with
In contrast to the first reason that this technique the therapist carefully pushing the heel of his or her
may be used, an unusually strong diaphragm, acting hand further up and in, maintaining greater inhibition
without support from surrounding m u sculature, during each inspiratory phase. After two or three
specifically the intercostals and abdominal muscles, ventilatory cycles, a patient usually begins to subcon­
may also need to be inhibited. For example, a para­ sciously alter his or her breathing pattern to include
plegic or lower level tetraplegic patient with an intact more upper chest expansion to reconcile the di­
diaphragm but absent abdominal and intercostal mus­ aphragm's transient inability to produce enough
cles may demonstrate a paradoxical breathing pattern chest expansion to yield an adequate tidal volume.
(see compensatory breathing patterns, Chapter 37). In The therapist should carefully observe which acces­
this case the accessory muscles must be encouraged sory muscles the patient spontaneously chooses. Are
to keep the diaphragm in check, attempting to avoid they used symmetrically? What is the general quality
the development of a pectus excuvatum. The goal of of the movement? Is the onset harsh or smooth? Does
this breathing retraining method is to stop the para­ the patient appear fatigued or uncoordinated?
doxical movements of the upper chest during inspira­ It is not until this point that the therapist should
tion by balancing the use of the upper and lower verbally acknowledge any alteration of the patient's
chest. In some cases, spastic intercostal muscles, like breathing pattern. Without changing his or her hand
in some spinal cord injury situations, may intercede position, the therapist tells the patient what it is that
to prevent this paradoxical movement by maintaining he or she likes about the new breathing pattern (e.g.,
the upper chest's position during inspiration in spite balance between upper and lower chest expansion or
of the negative pressure within the chest and grav­ less paradoxical motion of the sternum). Then the pa­
ity's influence on top of the chest. Balancing the tient is asked if he or she notices any difference from
chest's movements should produce an increase in before, bringing this breathing pattern to a consciolls
tidal volume and vital capacity potential and mobilize level. Only after some orientation to this pattern, usu­
a greater portion of the chcst, just as the technique ally no morc than 4 to 6 breathing cycles in the full
does in the first case presented. inhibiting pattern, should the therapist begin to grad­

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404 PART III Cardiopulmonary Physical Therapy Interventions

FIGURE 22-1 9
Diaphragm inhibiting in prone on elbows position.

ually release the pressure being applied. already been achieved. Extra care must be taken not to
While slowly releasing pressure with each cycle of initiate any applied pressure quickly because of the
inspiration, the therapist asks the patient to attempt likelihood of eliciting unwanted abdominal contrac­
cognitively to reproduce the desired pattern. It should tions or spasticity or eliciting a stronger diaphragmatic
take the same number of cycles to release the pres­ contraction resulting from the quick stretch reflex. The
sure as it did to apply it. This technique easily allows technique should never be painful. The therapist must
fo r gradations of i n h ibition, from full inhibition, keep his or her hand on the abdomen, not the rib cage,
where the patient is forced to use upper accessory to properly influence the diaphragm. This technique
muscles or risk becoming short of breath, to barely a can be progressed by c hanging postures, which re­
proprioceptive reminder to change his or her breath­ quires greater tl1lnk control. Can the patient still main­
ing pattern. It also allows for gradation of inhibition tain the overall pattern? Can the patient breathe with­
while the patient is learning to assume control over out paradoxical movements against gravity?
the new breathing pattern. If during the releasing The second technique is for the more advanced pa­
phasc of this technique the patient begins to lose con­ tient and simply presents a physical block to diaphrag­
trol over the new pattern, the therapist can gently matic excursion. The patient is positioned in a prone-on­
reapply some pressure during the next expiratory elbows position (Figure 22-19). With most severely
phase to help the patient regain that control. At that neurologically impaired patients, the lower chest will be
point, the therapist can release or reapply pressure as in direct contact with the surface, so lower anterior and
neccssary until the desired pattern is obtained and full inferior expansion is inhibited and lateral costal expan­
release of pressure is completed. sion is limited. The upper chest is positioned in exten­
This technique is particularly effective with patients sion and the upper extremities are fixated, optimizing the
who are having difficulty cognitively altering their length-tension relationsh.ip of the anterior and superior
own breathing pattern, such as with small children, accessory muscles for easy facilitation. In addition, ante­
brain-damaged patients, or slow motor learners, be­ rior excursion of the upper chest is now in a gravity-as­
cause it requires no cognitive effort until success has sisted posture. Through the use of head and neck pat­

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 22 Facilitating Ventilation Patterns and Breathing Strategies 405

FIGURE 22-20
Static-dynamic upper extremity activities in prone on elbows to encourage upper chest accessory
muscle participalion.

terns, such as in PNF diagonals, or static-dynamic activi­ now assisting anterior excursion of the chest and re­
ties, such as in weight shifting to one supp0!1ing limb sisting posterior excursion. To emphasize the serratus
while reaching out with the other extremity, the therapist anterior muscle's role in posterior expansion, the pa­
can readily facilitate greater upper chest breathing (Fig­ tient is instructed to perform an upper body push-up
ure 22-20). These are the same patterns the therapist can (with or without the therapist's assistance). The serra­
use to achieve other goals, such as increased head and tus anterior muscle causes lateral scapular movement
neck control, increased shoulder stability, or increased thereby facilitating maximal posterior excursion of
upper body balance. Therefore, by helping the patients the thorax. The patient is instructed to take a deep
to coordinate movement goals with ventilatory patterns, breath in during the push-up and to exhale the air
it becomes more likely that the patients will incorporate (passively or forcefully) when returning to the start­
these patterns functionally into daily activities. This is ing position. Forceful exhalation in this activity can
the ultimate goal of any ventilatol)' retraining procedure. be used as a forerunner to effective cough retraining.
The manual diaphragm-inhibiting technique is Gentle or controlled exhalation can be used to en­
usually less threatening to the patient than the prone­ courage greater breath support for vocalization or f6r
on-elbows-inhibition technique. Prone on elbows it­ eccentric trunk muscle training.
self can inhibit the diaphragm so completely for neu­ Emphasizing posterior chest expansion during in­
rological patients lacking spinal extensors that they halation is the only occasion where inspiration would
become extremely short of breath. Consequently, do be paired with trunk flexion. In all other inspiratory
not position the patients in this more demanding pos­ situations, inspiration is paired with trunk extension,
ture until success appears likely. and exhalation is paired with trunk flexion.

Serratus Push-up PATIENTS WITH ASYMMETRICAL DYSFUNCTION

Facilitating greater posterior chest expansion can be Patients with asymmetrical weakness need a different
achieved in a prone-on-elbows position. Gravity is approach from the controlled or upper chest breathing

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406 PART III Cardiopulmonary Physical Therapy Interventions

side with his or her arms positioned down below 90

Promoting Symmetrical Ventilatory Function
degrees of shoulder flexion, lateral chest expansion
for Patients With Asymmetrical DefICits
into that side becomes inhibited because of the
I. Use of positioning to achieve more symmetrical physical batTier. This forces the patient to find an­
alignment of the chest and trunk in both reclin­ other way to meet his or her ventilatory needs,
ing and upright postures
which indirectly facilitates chest expansion on the
2. Use of postural inhibition to the stronger or unin­ opposite side (the uppermost side). The therapist
volved side to promote greater chest wall expan­
can then supply sensory and motor input through his
sion on the weaker or involved side
or her hands to the patient's upper, middle, or lower
3. Timing for emp h asis technique to promote active
chest on the involved or weaker side to facilitate in­
symmetrical breathing anywhere in the thorax
creased ventilation on that side. Early in the rehabil­
itation process or soon after thoracic surgery, the
patient may have difficulty performing lateral chest
expansion against gravity in sidelying (gravity-re­
patterns presented previously. These patients need sisted movement). If so, position the patient in a
facilitation to the weaker side to promote symmetri­ 3/4-supine position to lessen the workload imposed
cal chest wall expansion in both the upper and lower by gravity. Gradually, work the patient up to a full
chest. See the box above for a summary of tech­ sidelying posture to achieve the greatest strengthen­
niques. ing benefits.

Symmetrical Positioning Timing for Emphasis

Symmetrical ventilatory patterns may be effortlessly Another technique to promote symmetrical chest wall
achieved by altering the patient's position in each movements is performed in numerous postures, such
posture to maximize the chest wall's potential to as supine, sitting, or standing. The therapist places his
move in a symmetrical pattern. This is especially true or her hand symmetrically on the lower lateral chest
in an upright position in which asymmetry is gener­ wall, on the mid chest, or on the upper anterior chest
ally more pronounced. For example, hemiplegic pa­ wall. At the end of exhalation, the therapist gives a
tients may lean toward their involved side in sitting quick stretch on the muscles being touched to facili­
because of weakness or spasticity. Likewise, after tate a deep inspiratory effort in that area of the chest.
thoracic surgery, a primary pulmonary patient may Immediately after both sides begin to move into an
lean toward the surgical side to avoid pain caused by inspiratory pattern, the therapist manually blocks (or
chest movement around the incision. Both situations inhibits) expansion of the chest on the stronger side
cause asymmetrical breathing patterns and decrease while giving continued quick stretches on the weaker
ventilation on the involved side. Improving chest side. This facilitates greater expansion on the weak
wall alignment may alleviate the ventilatory deficit side by use of an overflow response. This technique,
on the involved side. adapted from the PNFs timing for emphasis tech­
nique, uses the strength of the stronger side to facili­
tate movement on the 'Yeaker side. It can be applied
Postural Inhibition
to any area of the chest where symmetrical move­
For some patients, more aggressive positioning must ments should be the norm.
be used to achieve greater chest wall excursion and
ventilation on the involved side. This can be accom­
REDUCING RESPIRATORY RATES
plished by inhibiting the chest wall movements on
the uninvolved or stronger side. Usually, the best In addition to altering breathing patterns through fa­
posture in which to achieve this inhibition is sidely­ cilitation and inhibition techniques, reducing respira­
ing. When the patient lies on his or her uninvolved tory rates (RR) may also be necessary before arriving

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 22 Facilitating Ventilation Pattems and Breathing Strategies 407

at an efficient breathing pattern for some patients. sisted cough technique. One medical contraindication
See the box below for a summary of techniques. for this technique is bony instability of the spine be­
Many neurological patients with high neuromuscular cause of its rotary nature.
tone increase their RR to compensate for a decrease In bed or on a mat, place the patient in sidelying
in their tidal volumes (TV) or because of brain-stem with knees bent and arms resting comfortably out in
impairments to the respiratory centers. In addition, front of the head or shoulders. In this technique the
many patients who are anxious, such as asthmatic, or­ higher the upper extremities can be placed within a
thopedic, or surgical patients experiencing pain, may comfort zone, the better the result. Relaxed position­
also demonstrate an excessively high RR. Attempting ing of the patient is essential to the success of this
to restore ventilatory efficiency may require increas­ technique, thus position the patient in an open yet
ing TV while concurrently decreasing RR. comfortable position. Normalizing neuromuscular
tone is the first step in attempting to decrease a high
RR. Patient discomfort is likely to elicit increased
Previous Facilitation Techniques
tone and an increased RR.
The techniques previously described in this chapter The therapist's own position is also important be­
promote an increase in TV by improving the overall cause it directs the force that is applied to the pa­
ventilatory patterns and often cause a secondary reduc­ tient's chest. Initially, the therapist needs to stand
tion in RR. See sections on controlled breathing, mobi­ behind the patient, perpendicular to his or her trunk.
lizing the thorax, and upper chest breathing facilitation. If the patient is lying on the left side, the therapist
places his or her left hand on the patient's shoulder
and his or her right hand on the patient's hip. The
Counterrotation
therapist then leaves his or her hands in place and
The technique described next is specifically devel­ simply follows the patient's respiratory cycle. This
oped to promote a lower RR. The counterrotation allows the therapist to assess the patient's subjective
technique reduces high neuromuscular tone and in­ rate and rhythm and the patient's overall neuromus­
creases thoracic mobility, thus often resulting in an cular tone. Only after this assessment should the
increase in TV and simultaneous reduction in RR. clinician begin the active phase of the technique.
These authors have found this technique to be ex­ Using a PNF technique called rhythmic initiation,
tremely effective for the following: (I) patients with the patient is gently log-rolled in a small ROM in
decreased cognitive functioning after a neurological sidelying. The rolling is gradually increased achiev­
insult or after surgery, (2) very young children be­ ing more ROM from sidelying toward prone. This
cause there are no verbal cues, or (3) patients with progression of movement generally reduces high
high neuromuscular tone. As described in Chapter 21, tone, which usually makes the second phase of the
it can also be easily adapted as a very effective as- technique more effective.
During this phase, the therapist needs to audibly
duplicate the patient's RR. As the patient moves into
greater rolling ROM and begins to slow his or her
Techniques to Reduce High Respiratory Rates RR, the therapist needs to use the patient's audible
cuing as a facilitator for establishing a slower RR.
I. Previous techniques that increased tidal volume
Thus the therapist begins by having the patient estab­
2. Countenotation technique
lish the audible RR and then the therapist slowly
3. Butterfly technique in sitting
takes over. Audible cues can be very strong facilita­
• Straight planes tors of ventilatory rhythms.
• Countenotation Phase two requires the therapist to slowly change

4. Relaxed pursed lip breathing with inspiratory his or her position. Transitioning to a diagonal pos­
and expiratory pauses ture, the therapist now stands or half kneels behind
the patient near his or her hips, turning diagonal to

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408 PART III Cardiopulmonary Physical Therapy Interventions

the patient until the patient's head at roughly removed should be the audible cues. As with the di-
at angle, The hand placement to get biting tech the therapist can
more Assume that the patient is side- reestablish control quickly if needed by simply reap­
lying on the left At the of the plying stronger manual input. If the has an ex-
cycle, the left hand fast RR 50 to 60 breaths/min), the facili­
patient's shoulder on the tation can be every 2 to 3 breaths so as not to
care being taken not to unintentionally use the thumb the patient or
or tips, and the hand back It should be apparent that this technique need not
to the patient's right fossa (the hollow of the be used for goals but rather
21-6, A, The can can be total rehabilita­
then compress the rib cage in all three tion program. It is a natural precursor to active rolling
planes of ventilation at the end of exhalation by gen­ or it can be used as a vestibular stimulator.
tly pulling the shoulder back and down, while simul­
pushing the hip up and forward, This
Butterfly Technique
movement promotes more complete exhalation,
When the patient the next inspiration, the If the has greater motor control, an
therapist switches hand to capitalize on the version of this technique may be appropriate. In un­
improved for TV, The therapist's left hand supported stand behind or in front of the pa-
slides back to the patient's and the ther­ depending on his or her balance and ask
hand slides forward just anterior to the to bring his or her arms up into a butter­
right iliac crest Figure 21 B, p, 376). or assist his or her arms up to this pos­
As the patient inhales, the therapist slowly stretches from a comfortable ROM position for
the chest to maximize volumes (TVs). that patient, to audibly breathe with the pa­
The left hand the scapula (or the tient's RR. When the patient raise the arms
thorax if the is unstable) up and away from up into slightly more shoulder flexion. When the pa­
the spine and the hand the back and tient lower the arms slightly.
down to maximize all three planes of re­ to move in greater and greater increments of range,
in greater inspiration. The therapist should use all the while out loud with your
the flat or heel of the hand whenever possible to Through your audible breathing cues, to "ask"
avoid unintentional patient discomfort and to maxi­ your patient to slow down the RR and take deeper
mize the facilitated area. slower breaths. The use of the followi ng
Initially, the begins and ends the deeper inhalations
cycle according to the patient's RR. as and exhalations: ( l ) shoulder flexion and trunk ex­
tone is relaxed and increased TVs are tension with inspiration and (2) shoulder ex­
through the effects of counterrotation, the tension and trunk flexion paired with exhalation.
therapist slows the rate of rotation down, Thus it becomes and for the pa­
the audible breathing cues to also facil­ tient to increase his or her TV and decrease RR.
itate a slower RR. The patient accommo­ As in the previous technique, the therapist
dates to a slower RR as the therapist more con­ by out loud at the pace and transi­
trol over the patient's pattern. With many audibly at a more desirable
the results can be marked. If the patient can pace, The picks up on this subtle cuing and
cognitively follow commands, he or s h e can be subconsciously reduces his or her own RR even if
alerted to this and to assist in vol­ cannot follow verbal commands.
untarily at the slower rate. This technique can be modified to encourage more
The therapist can progress the by de- intercostal and oblique abdominal muscle contrac­
the manual input. The last facilitation to be tions by using a diagonal rather than a straight

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 22 Facilitating Ventilation Patterns and Breathing Strategies 409

A B

FIGURE 22-21

A, butterfly technique facilitating inspiration; B, butterfly technique facilitating exhaltation;

C, butterfly with twnk rotation facilitating inspiration. All threc planes of respiration are stretched

on the patients right side. D, butterfly with twnk rotation facilitating exhaltation. All planes

compressed on the right side.

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410 PART III Cardiopulmonary Physical Therapy Interventions

of movement. Have the look up and over one and proceeds to force the air back and down the
shoulder as he or she breathes in and brings arms up throat with a maneuver of the tongue,
and behind his or her head. Then have the ynx, and larynx.
look down and away toward the opposite knee as he Research has consistently shown that use of this
or she breathes out and brings arms down to the op­ with severely pa­
knee (Fieure 22-21). tients can increase pulmonary functions signifi­
especially for TV and Vc. If GPB is the only
means of ventilation off of a ventilator or
Relaxed Pursed-lip Breathing
nerve stimulator, mastery of this technique is critical
Use of a relaxed to a survival in case of mechanical failure.
ously described under All should be made to successfullv teach
breathing pattern," is also a technique to reduce RR. GPB to this patient population.
By the expiratory through pursed A clinical example may to illustrate its use­
the patient secondarily decreases his or her RR. fulness. A l4-year-old male sustained a C 1 \"VllllJlilA\V

SCI while in front of a train. After he was

medically two phrenic nerve stimulators were
GLOSSOPHARYNGEAL BREATHING
in his chest. The patient had no nonassisted
A small population of neurological requires means of ventilation. the patient
more than just promoting the use of accessory muscles had limited use of one sternocleidomastoid,
or RR to meet basic needs. In the and intrinsic neck muscles. The patient and family
last decade, more SCls (above C4) have sur­ feared that home would
vived the initial trauma because of advances in med­ be inevitable because of their fear of his
ical technology. the rehabilitation nerve stimulator malfunctioning or a wearing
is then faced with the difficult task of quality out, immediate respiratory distress. The fam­
of life. For these patients, as well as many old polio ily believed it could not bear the psychological bur­
mastery of the breathing den placed on them if the went home to live.
technique allows for voluntary ventila­ GPB instruction was and slowly be­
tion, which many state does improve the cause the stated that he learned motor skills
ity of their Jives. This augmented breathing slowly. After a painstaking 2-month the pa­
lows to some control over their Jives tient learned to breathe without the use of his phrenic
and to control over their which was nerve stimulator for 3 to 5 minutes before
lost as a result of high neurological and hypoventilating. Within the next I to 2
GPB is a this same patient learned to breathe for up to 2 hours
polio patients for a way to reduce their de­ off of his using GPB To the staff's
pendence on the iron lung for ventilation. It was he even learned to talk and his sip-
found that using the lips, soft mouth, GPB. The patient
tongue, pharynx, and larynx, a could actually was then successfully to his home. This
inhale air to sustain life without mechanical does not imply that this was the only factor consid­
ventilation. Only intact cranial nerves are ered in his discharge olanning, but it was oerhaos the
This m e t h o d i s s o m e t i m e s referred t o as most significant.
breathing because it uses the principles of Instruction in GPB takes time and concentration. It
tion common to the The is best to statt off in small time blocks of 10 to 15 min­
of pressure utes because it can be very However, it is
cavity by that internal space, to successful of the technique that
causing the outside air to rush in. At that the patient gets preferably daily training.
the patient closes off the entrance lips) Once the patient has mastered the

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 22 Facilitating Ventilation Patterns and Breathing Strategies 411

sessions can be lengthened considerably, and the pa­ demonstrates to the patient what a stroking maneuver
tient can be taught self-monitoring techniques. Specific looks like several times to give an idea of the motion
goals of GPB training must be explained to the patient required. The therapist continues to mimic the pattern
before the beginning of treatment to gain his or her as the patient attempts to duplicate it. This gives the
support and cooperation. In addition to providing the patient an active model to mimic and decreases feel­
ventilator-or stimulator-dependent patient with a TV ings of uneasiness surrounding the necessary but
necessary for gaining independence from mechanical somewhat silly facial grimaces. If the patient is able
assists, GPB has many other b e n e f i t s. F o r the to breathe independently, his or her ability to breath
tetraplegic patient who has a partially intact diaphragm hold and to close off the nasal passageway should be
(C3 to C4) or the loss of essential accessory muscles checked because air leakage is a common cause of
(C5 to C8), GPB can accomplish the following: (1) in­ failure. The patient is then instructed to take in a
crease VC to produce a more effective cough, (2) as­ maximal inspiration before attempting the stroking
sist in a longer and stronger phonation effort, and maneuvers to eliminate the possibility of using other
(3) act as an internal mobilizer of the chest wall. accessory muscles during the technique.
The muscles used in this technique do not have the If possible, position the patient in an upright or at
same internal proprioceptive, sensory, or visual feed­ least a symmetrical position. Specifically, the patients
back mechanisms as the trunk and limb muscles. Thus are instructed to bring their jaws down and then for­
necessary adjustments in the technique are sometimes ward as if reaching their bottom lip up for a carrot
difficult to see or feel. The patient cannot see his or dangling just in front and above the upper lip (Figure
her tongue pushing the air back or truly feel the phar­ 22-22, A). Slight cervical hyperextension is necessary
ynx swallowing the air into the lungs, so the thera­ to allow for maximal temporal mandibular joint
pist's external feedback system is very influential. (TMJ) excursion. (A contraindication for this tech­
Use of a minor can greatly enhance the visual compo­ nique is a TMJ disorder.) The lips should be shaped
nent of feedback. Small changes, like adjustments in as if they were to make the sound "oop." The patient
posture or a suggestion of another sound to imitate, is then told to close the mouth, reaching the bottom
may be all that is needed for the patient to learn tbe lip up to the top lip (see Figure 22-22, B). The tongue
stroking maneuver correctly. Success in GPB can be and jaw are drawn back toward the throat, with the
assessed objectively with a spirometer and a pulse mouth and tongue formation of the word up or the
oximeter. For those patients incapable of breathing in­ sound "ell" (see Figure 22-22, B). The lower jaw is
dependently, any TV reading will indicate successful moving in roughly a rectangular pattern. Most pa­
intake of air. For patients who are not ventilator de­ tients learn the stroking maneuvers by making the
pendent, a VC reading that is greater than 5% over the sounds at first, as they become more proficient, the
baseline indicates successful use of GPB. Lower-level sounds and excessive head and neck motions dimin­
tetraplegics, C5 to C8, have demonstrated increases in ish. Often, the students (patients) outperform the
VC by as much as 70% to 100%. teacher (therapist), because through consistent use,
Therapists can monitor their own successes with they learn all of its finer subtleties.
this technique by taking VC readings with and with­ Although this technique can be broken down into
out GPB or by subjective analyses. Maximal inhala­ several stages as it has been here for the purpose of de­
tion, followed by three or four successful GPB scription, most of the literature cautions the therapist
strokes, will cause a feeling that the chest will burst if against it. (Zumwalt, Adkins, Dail, and Affeldt, 1956).
an attempt is made to inhale more air. Likewise, a Simple, minimal insuuctions seem to accomplish more,
sensation of "needing to cough" is another subjective perhaps because the continuity of movement is so es­
indication of successful GPB. However, a feeling of sential to the success of the inhalation. Specific instruc­
indigestion is usually indicative of swallowed air in tions can be given later if necessary.
the stomach instead of the lungs. Common problems encountered with GPB instruc­
During the initial treatment session, the therapist tion are as follows: (I) an open nasal passage or glot­

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412 PART III Cardiopulmonary Physical Therapy Interventions

A B c o

FIGURE 22-22
Glossopharyngeal breathing; A, mouth opened to draw in air; B, j aw closed to entrap the air; C, air
pushed back with tongue into trachea; D, vocal folds closed to prevent passive air leaks. Entire
maneuver is then repeated.

tis that allows the air to escape, (2) a feeling of indi­ els begin to fall to the mid 90s and then the low 90s,
gestion indicating that the air is being swallowed into you can anticipate when they will reach 90%. At that
the esophagus rather than the trachea, (3) incorrect point, end the GPB training and put the patient back
shape of the mouth as the air is bein g drawn in, usu­ on the previous ventilatory support system. Oximetery
ally not puckered enough, (4) uncoordinated back­ not only allows for accurate monitoring but also pro­
ward movement of the tongue, (5) inadequate jaw vides a means for an objective means for monitoring
mobility, TMJ dysfunction, or decreased cervical progress over time. In addition, a spirometer objec­
ROM, or (6) incorrect sounds while performing the tively measures improvements in VC using GPB. It
technique, such as the word gulp or an "em" sound. gives the patients concrete indications of success or
A voiding any instruction for the tongue seems to pro­ failure with the technique.
duce better results. Concentrate on assisting the pa­
tient in learning the external physical movements.
ENHANCING VOCALIZATION SKILLS
Tolerance to GPB can be increased when mastery
of a single stroke becomes consistent. For patients In contrast to procedures that assist the patient in in­
using it as an assist to their own voluntary ventilation, halation, procedures intended to improve a patient's
3 to 4 strokes on top of a maximal inspiration is usu­ phonation skill must focus on elongating the expira­
ally sufficient. Ventilator- or stimulator-dependent pa­ tion phase. Coughing is a gross-motor skill that relies
tients may need to use as many as 10 to 14 strokes per more on force than fine control of the ventilatory
breath. These figures should be used only as rough muscles for its effectiveness. Conversely, phonation
guidelines. Each patient will use a slightly different requires precise, fine-motor control of these muscles
technique with a different number of strokes, with the and the vocal folds to provide a consistent air flow
only important factor being a method that works for through the larynx. Both are expiration activities and
them. Fatigue with long trials of GPB can be moni­ depend on the preceding inspiration for optimal per­
tored effectively with an oximeter. The oxygen satura­ formance; however, coughing uses concentric con­
tion level should stay above 90% to maintain adequate tractions of the expiratory muscles to force the air
Pa02 levels. For example, if the patient begins the out, and quiet talking uses primarily eccentric con­
GPB session with an oxygen saturation level in the tractions of the inspiratory muscles to slowly release
upper 90s, fatigue can be monitored and anticipated the air during expiration. Because of these differ­
by watching if the oxygen levels decrease. If the lev­ ences, procedures to improve coughing and phona­

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 22 Facilitating Ventilation Patterns and Breathing Strategies 413

an open anterior chest wall will allow for the greatest

Ellhallcillg Vocalizatioll Skills through
potential for chest wall excursion and thus the largest
ill creased Breath Support
Vc. Use the previously described suggestions for po­
I. Position to achieve a neutral chin tuck and opti­ sitioning to determine if your particular patient needs
mal vocal fold alignment positioning to encourage a more diaphragmatic,
2. Manual techniques upper chest, or unilateral breathing pattern.

• Vibration or shaking

• Percussion or tapping Manual Techniques

3. Eccentric resistance
Several simple techniques can be used to improve
Agonistic reversal technique
eccentric control of the diaphragm and intercostal
•

• Functional resistance muscles in preparation for speech. Vibration or shak­

4. Verbal techniques to refine breath support ing to the lower chest during expiration assists in a

• Singing and whistling slower, more controlled recoil of the diaphragm.

Why this occurs is not fully understood. It may be
• Games
that the sensory and proprioceptive stimulation that
• Wind or brass instruments
the vibration or shaking provides augments the pa­
Stopping and starting vocalizations
tient's concentration on those muscles resulting in
•

longer p h onation. The patient is instructed to

phonate an "ah" or "oh" sound for as long as possi­
ble. The therapist simultaneously vibrates the pa­
tion will be different in focus. See the box above for tient's chest with an even and gentle force through­
a summary of techniques. Coughing is covered in de­ out and slightly beyond the full expiration phase,
tail in Chapter 21. placing his or her hands on the lateral costal borders
Because the patient's TV and total inspiratory ca­ of the thorax, the mid chest, or on the pectoral area,
pacity are the power source for phonation, they be­ depending on which area of the chest needs the most
come important concerns in a phonation program. help in controlling exhalation. This is very different
Generally, a normal TV is adequate for con versa­ from the rapid, forceful pressure that is applied to the
tional speech. However, larger volumes of air, thus patient's chest when promoting a deep cough. Be
greater inspiratory capacities, are required for certain that the patients understand this important
singing, loud talking, or professional speaking. difference. The therapist must stress to the patients
Therefore the breathing pattern facilitation techniques that they should not let air escape before vocalization
described previously in this chapter are ideal before and that they should try to keep the voice intensity
instructing the patient in better expiration control. For consistent throughout the procedure. This will pro­
example, facilitating diaphragmatic and/or accessory mote slow eccentric release of the inspiratory mus­
muscle breathing techniques, along with the use of cles during the en tire course of the vocalization.
quick stretches or repeated contractions, can facilitate Progress can be readily monitored by timing the pa­
the desired deeper inhalation. tient's vocalization, before, during, and after this
technique. About 10 to 12 seconds of vocalization,
or 8 to 10 syllables per breath, is generally consid­
Positioning Concerns
ered adequate for functional use in speech.
Consistent with all previous techniques, the first as­ For children, this technique can be modified. The
pect of improving breath support for vocalization is child is asked to say "ah" or "oh" for as long as possi­
to optimize the patient's position. The vocal folds ble while the therapist percusses or taps lightly with his
have an ideal muscle length-tension relationship or her hands on the child's upper or lower chest so as to
when the head is in a neutral chin tuck. In addition, produce a series of staccato sounds. Most children

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414 PART III Cardiopulmonary Physical Therapy Interventions

enjoy the new sound that this makes and will try repeat­ the arm's descent. The activity can be progressed sev­
edly to phonate longer and louder to accentuate the dif­ eral ways. The activity can include lifting something
ferent intensities. heavy off the shelf and controlling it along with the
Therapeutically, this requires them to take a arm and trunk while lowering the object or weight to a
deeper inhalation before vocalizing, followed by an table or to the patient's lap. Or the postural demands
elongated expiratory phase, both of which are neces­ of the activity can be increased. The patient can still
sary for functional speech. As the child becomes lift the heavy object or weight but he or she can now
more adept at it, the therapist can apply more pro­ be required to do this in standing, which increases the
nounced clapping over the chest, accomplishing a demands on the musculoskeletal system.
wider range of voice intensities and doubling as a
means of percussion for postural drainage.
Verbal Techniques

Speech activities that do not require a therapist's

Eccentric Resistance Techniques
physical assistance can be done in a group or individ­
More specific facilitation can be used to increase ual setting. Singing, for instance, promotes strong
breath support. Ideally, the patient is positioned sym­ and prolonged vocalization with maximal inspiration,
metrically in supine or supported sitting, allowing for which is a significant goal in a phonation program.
maximal chest wall expansion. The patient is in­ Similarly, whistling promotes long, even exhalations
structed to visualize his or her chest being pulled up but is nonverbal. Both are easily incorporated into a
toward the ceiling and held there. They are then told group activity on the nursing floor, in therapy or in
to vocalize slowly trying not to let the chest "fall." the community.
Meanwhile, the therapist is applying consistent pres­ Along recreational lines, games that promote con­
sure to the patient's chest to try to force a quicker ex­ trolled blowing further the refinement of motor con­
halation. The patient is told to resist this motion by trol over the respiratory muscles. This can be accom­
trying to control and prolong expiration. Like the an­ plished by blowing bubbles, especially large ones,
tagonistic reversal technique described in PNF, the blowing out candles, especially trick candles, blow­
therapist is resisting the patient's attempt to eccentri­ ing a ping-pong ball through a maze, or by blowing
cally contract and control the trunk muscles. This air hockey discs across the table rather than pushing
strengthens the eccentric phase of exhalation and pro­ them. Patients with musical inclinations should be
motes greater breath control for vocalization. encouraged to learn to play wind or brass instruments
The same concept can be applied to functional where refined breath control is mandatory for suc­
tasks. Moving into gravity, that is, coming down to cess. Obviously, the possibilities for recreational use
sitting from a standing posture, lying down from a sit­ are endless, and simply require imagination on the
ting posture, and bringing an ann down from reaching part of the therapist.
into a higher cabinet, all require eccentric control of Further refinement of breath control for speech
the muscles involved in that activity to slow the can be promoted by interrupting the outgoing air
body's descent into gravity's influence. Because quiet flow. Functional speech is a series of vocal stops and
speech uses a similar muscular contraction, teaching starts. This procedure is geared toward improving
the patient to count out loud or to otherwise vocalize functional communication skills. The therapist tells
when performing an overall eccentric activity usually the patient to take a deep breath and then to count out
improves both activities. For example, the patient can loud to 100. After a few numbers, the patient is told
be instructed to reach up to a high shelf or cabinet to "hold it." He or she is then told to start up where
while inhaling. Then, using gravity to provide the ec­ he or she left off, with the therapist periodically inter­
centric resistance, the patient is asked to bring his or rupting. Because this activity requires the patient to
her arm back down to his or her lap or side while stop and start the inhalation and exhalation phases at
slowly counting out loud and controlling the rate of will in all aspects of the ventilatory cycle, it is more

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 22 Facilitating Ventilation Patterns and Breathing Strategies 415

advanced and should be used only after some control more desirable. Some may benefit even more from
of exhalation has been mastered. techniques to reduce the high RR or to mobilize the
thorax. For a select patient population, instruction
in GPB may be necessary to support breathing off
SUMMARY
of mechanical ventilatory support. Lastly, the ther­
In summary, use of appropriate choices in positioning apist can now choose to use techniques to improve
together with use of an appropriate ventilatory and the patient in developing adequate breath support
movement strategy for any given task will make the for vocalization and communication.
success of that task all the more likely. If these sim­ It is these authors' hope that the therapist now un­
ple, time-efficient methods of facilitation do not pro­ derstands how widespread the influence of effective
duce adequate ventilatory changes by themselves, it ventilation can be on a patient's recovery from dis­
is then appropriate to add on the next layer of facilita­ ease or trauma. Understanding that facilitating effec­
tion-manual facilitation techniques. Specifically, tive ventilation goes far beyond the old diaphrag­
the techniques that are described in this chapter assist matic exercises, therapists can be empowered to
in facilitating the following: (1) greater diaphrag­ incorporate other techniques and strategies to get
matic breathing patterns (or controlled breathing), their patients healthier quicker and to assist them in
(2) increased chest wall mobility, (3) greater acces­ reaching their greatest rehabilitation potential.
sory muscle breathing patterns (or primarily upper
chest breathing), (4) increased symmetrical breathing
patterns (unilateral disorders), (5) reduction in high REVIEW QUESTIONS
respiratory rates, (6) auxillary techniques GBP, and 1. Why would a therapist want to try to change a
(7) improved phonation support. Obviously, not all patient's breathing pattern?
techniques would be appropriate for any single pa­ 2. How can ventilatory strategies be incorporated
tient. It is up to the therapist to determine which tech­ into a treatment session?
niques would best address their patients' deficits. 3. When would a therapist not teach diaphragmatic
In conclusion, positioning has everything to do breathing?
with increasing ventilation potential and functional 4. What is the role of relaxation in breathing control?
skills. From the beginning of the patient's respira­ 5. When would a therapist consider teaching the pa­
tory program, optimizing ventilation and breath tient to use his upper chest more in breathing?
control through passive and active positioning 6. When would a unilateral breathing pattern be
techniques should be used by all medical disci­ taught?
plines, not just physical therapy. As the patients
progress, the clinician can and should, assist them
in developing better and more efficient movement
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 Exercise Testing and Training:

Primary Cardiopulmonary Dysfunction

Susan K. Ludwick

KEY TERMS Arteriovenous-oxygen difference Forced vital capacity (FVC)

(a-v02 difference) Minute ventilation (YE)
Cardiac output (Q) Oxygen consumption ('\102)
Forced expiratory volume in Stroke volume (SV)
I second (FEV) Tidal volume (TV)

INTRODUCTION

Shortness of breath, especially with activity, is very and then be able to devise therapy programs that
common in patients who have cardiopulmonary dis­ would keep these individuals active within the limits
eases. Shortness of breath can be quick in onset or of their disease in order for them to maintain certain
of a chronic nature. One of the results of shortness levels of independence.
of breath, especially when it is of a chronic nature,
is the vicious cycle of deconditioning it causes in
LUNG DISEASE
patients. Eventually, these individuals may become
deconditioned to the point that activities of daily liv­ In individuals without lung disease the cardiovascular
ing usually taken for granted, such as washing up in system normally limits maximal aerobic exercise.
the morning, may be overwhelmingly fatiguing. Typically, maximal oxygen consumption (Vo2) may
Physical therapists need to understand the underly­ be limited by the heart's inability to increase its cari.i­
ing mechanisms of shortness of breath, evaluate diac output (Q) either by an inability to increase heart
their patients appropriately given their limitations, rate (HR) or stroke volume (SV) or by an inability to

417

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418 PART III Cardiopulmonary Physical Therapy Interventions

Impaired Gas Exchange

provide adequate oxygen delivery to exerCISing
skeletal muscle represented by the arteriovenous­ During exercise, there needs to be a balance of venti­
oxygen difference (a-vo2difference). This relation­ lation to perfusion (VIQ) in the lungs for adequate
ship of V02 to Q is represented by the Fick equation: blood oxygenation to occur. In patients with airways
disease, underventilation of the lungs could occur be­
V02 = Q x a - V02 difference
cause of elastic tissue destruction. Underventilation
However, patients with lung disease may be lim­ results in V/Q mismatches (low V/Q ratio). Hypox­
ited in their exercise capacity for several reasons. emia occurs as a result.
They may be limited by altered lung mechanics, im­
paired gas exchange, development of pulmonary hy­
Pulmonary HypertenSion
pertension, or respiratory muscle fatigue. Each of
these factors make traditional cardiovascular evalua­ In normal individuals, there is typically an increase in
tion of exercise capacity inadequate, since these pa­ the diameter and in the number of blood vessels with
tients are limited by their breathing and not by their exercise. However, in patients with lung disease,
cardiovascular systems. there may be a decrease in the number and/or in the
distensibility of blood vessels. This results in the in­
crease of pulmonary vascular resistance. An increase
Altered Lung Mechanics
in the pulmonary vascular resistance contributes to a
One of the characteristics of obstructive lung dis­ decrease in left ventricular filling. If there is a de­
ease is the destruction of elastic tissue in the lung. crease in left ventricular filling, then there will be a
The destruction of elastic tissue prevents normal decrease in cardiac output, which would limit the
recoil of lung tissue on expiration. Therefore it is ability to do work.
difficult for patients to empty their lungs. This
coupled with the tendency for bronchial walls to
Respiratory Muscle Fatigue
collapse contributes to air trapping. This results in
lung hyperinflation. With exercise, our bodies re­ Respiratory muscles in a normal individual con­
quire an increase in oxygen uptake to perform sume little oxygen at rest or with moderately in­
more work. Minute ventilation increases in order creased ventilation during activity. With exercise,
for oxygen u ptake to improve. We know t h a t oxygen consumption increases greatly. However, a
minute ventilation is t h e product o f tidal volume patient with lung disease would have an increase in
and respiratory rate (TV x RR = VE. If respira­ ventilatory muscle oxygen consumption up to 40%
tory rate increases as a natural response to an in­ of the total body oxygen consumption. The respira­
crease in exercise, it may not allow enough time tory muscles may not be able to keep up with the
for lungs to adequately empty and fill again if elas­ total demand and would start to fatigue (see Chap­
tic tissue is destroyed. Therefore tidal volume can­ ter 25). Another contributing factor in respiratory
not adequately increase with increases in exercise muscle fatigue is the musculoskeletal deformity
intensity. The result is that minute ventilation will that many of these individuals develop with the dis­
not increase in proportion to exercise. If minute ease processes. Muscle fibers need to be at an opti­
ventilation does not increase as required, then oxy­ mal length to work efficiently for adequate force
gen consumption and, therefore, amount of work generation to perform work. However, with muscu­
will be effected. loskeletal deformity, these fibers may be placed at
Patients with restricture lung disease will have lengths that make it difficult for efficient work to
stiffer lungs that are resistant to expansion on inspira­ be done. Eventually, they fatigue because of inade­
tion. The patient will have to work harder to maintain quate force generation needed to support the work
pressures for adequate lung expansion and venti la­ of breathing.
tion. Eventually all lung volumes and capacities be­ Clinically, patients with obstructive lung disease
come decreased. show breathing patterns that are slower and deeper at

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 23 Exercise Testing and Training: Primary Cardiopulmonary Dysfunction 419

rest and with exercise. Specifically, longer expiratory consumption during exercise above which a sus­
cycles are observed because of the extra effort these tained lactic acidosis occurs, is useful in measuring
patients make to empty their lungs before inspiration. exercise tolerance in normals. However, it is not par­
Patients with restrictive lung disease have a pattern of ticularly useful with patients, since peak exercise
rapid, shallow breathing in an effort to maintain ade­ levels may be below the anaerobic threshold. Some
quate minute ventilation in the face of decreased lung have looked at the measurements of FEV [ and FVC
capacities. to predict exercise capacity. However, the literature
has shown that there is no correlation between these
measurements of lung mechanics and exercise ca­
HEART DISEASE
pacity. It makes more sense to define exercise capac­
Patients with acute or chronic cardiac failure or ity by evaluating the patient's functional exercise ca­
valvular heart disease have elevated pulmonary ve­ pacity. This can be done by using timed walking
nous pressures. This develops into intersti tial distances. The 12-minute walk as defined by Ken­
edema. Therefore the lungs are said to be "wet," neth Cooper has been adapted by McGavin, Gupta,
their compliance is decreased, and the work of and McHardy (1976) for use with patients that have
breathing is elevated. chronic bronchitis. This test is also useful in deter­
Clinically, these patients have pulmonary rales on mining exercise capacity in other patient populations
auscultation. They adopt rapid, shallow breathing as well. This evaluation is useful because it corre­
patterns to minimize respiratory muscle work. These lates with V02 as measured on the treadmill. How­
patients, as with patients with chronic lung disease, ever, results are reported in terms of distance walked
will have ventilatory responses to exercise, depend­ and not in how much oxygen was consumed. There­
ing on the severity of the disease. fore it gives a more functional picture of exercise
tolerance since it uses a familiar activity. If 12 min­
utes is too long for some patients, 3- and 6-minute
Assessment
walks are just as useful. These walking tests are sim­
Before starting the actual exercise assessment, it is ple to implement and use simple measurement de­
important to get an idea of the patient's activity level vices. Patients can also use them as methods to mon­
and what activities cause shortness of breath. How itor their own progress.
far can the patient walk before becoming short of To assess patients using the 12-minute walk, one
breath? Can the patient tolerate walking outside? Is must simply instruct the patient to walk as far as pos­
he or she only able to walk comfortably to get about sible in 12 minutes. It is not absolutely necessary to
inside a house or apartment? Can the patient walk up walk without stopping. The patient may slow down
stairs? Does dressing, taking a bath or shower, or or even stop to take a short rest if needed. The only
combing hair cause shortness of breath? Can the pa­ required equipment is a stopwatch and a measured
tient do his or her own grocery shopping? Is the pa­ corridor.
tient able to do any heavy housework, such as vacu­
uming or bed making? Is the patient able to make his
UPPER-EXTREMITY VERSUS lOWER-EXTREMITY
or her own meals?
ACTIVITY
If aerobic capacity is limited because of either
cardiac or ventilatory limitations, how can we func­ Up to this point, we have discussed exercise assess­
tionally assess exercise capacity without the use of ments in reference to lower-extremity activity. How­
expensive testing equipment? Traditional methods of ever, shortness of breath may be of even earlier onset
measuring maximal oxygen uptake, including tread­ when perfomling routine activities of daily living in­
mill testing, may have limited usefulness because volving upper extremities (i.e., grooming, lifting, and
oxygen uptake for the pulmonary patient, as ex­ carrying). This in fact may be the most frustrating
plained before, is limited by ventilation. Anaerobic limitation to patients, since these are the types of ac­
threshold, which is defined as the highest oxygen tivities that we normally take for granted in our

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420 PART III Cardiopulmonary Physical Therapy Interventions

everyday Ii ves. When patients begin to have diffi­ ing expiration. There are no compressive forces
culty performing these activities, they feel a loss of working to narrow the airways. However, in patients
control in their lives. It is important to note that the with airflow limitation, the work of breathing is
exercise responses to these activities are different and shifted to the muscles of expiration. Therefore expi­
should be assessed separately from walking. ration becomes a more active process, resulting in the
CeJli, Rassulo, and Make (1986) have reported the generation of more positive pleural pressures com­
appearance of dyssynchronous thoracoabdominal pressing the airways. Closing off of airways creates
movement when comparing arm activity with leg ac­ the feeling of shortness of breath. An impOItant yet
tivity. Early fatigue was observed to occur despite simple technique that can be taught to patients is the
lower heart rates, minute ventilation, and oxygen up­ practice of purse-lipped breathing to control short­
take when compared with leg work. It was hypothe­ ness of breath. By having the patient expire through
sized that exercise limitation during arm activity was pursed lips, a back pressure is created in the airways
probably because of a smaller contribution of acces­ that helps to keep them from collapsing despite the
sory muscles to the work of breathing, since these positive pleural pressures down on them. This is a
muscles must contribute to postural support of the useful technique that can be used at rest and during
upper extremity during activity. Despite these limita­ exercise to slow down respiratory rate, increase tidal
tions in upper-extremity exercise tolerance, improve­ volume, and increase blood oxygenation.
ments have been demonstrated after an exercise train­ When evaluating exercise tolerance with patients,
ing program. it is impOItant to assess the work of breathing. Borg
Upper-extremity assessments may be considered (1982) has developed two scales that can help to
two ways. They can be either supported or unsup­ quantify dyspnea. In our facility, we have used a sim­
ported (Criner and Celli, 1988). Supported assess­ ple scale of I to 4 to describe shortness of breath (see
ments would be those that may involve the use of an boxes below and on p. 421). On our scale, a score of I
upper-extremity ergometer. Unsupported assessments would represent baseline (comfortable) breathing. A
would include those activities involving reaching. score of 4 would represent shortness of breath so se­
Since activities of daily living involve combing hair, vere that one is not able to talk. Since exercise limita­
washing, dressing, and reaching at various heights, tion is more closely related to ventilatory rather than
assessments imitating these things would be most
useful. One such test that could be used would in­
volve repetitive reaching at a height level to the head. The 15 Point RPE Scale
Reaching up with a light object of approximately I
6
pound may imitate reaching up to kitchen cupboards
7 VERY, VERY LIGHT
to put away groceries. Counting the number of repeti­ 8
tions and timing the activity would give a functional 9 VERY LIGHT
picture of upper-body activity tolerance. 10
II FAIRL Y LIGHT
12
BREATHING 13 SOMEWHAT HARD
14
Patients who have pulmonary diseases have limited 15 HARD
ventilatory reserves, which manifests as shortness of 16
17 VERY HARD
breath. The degree of the shortness of breath may de­
18
pend on the severity of the lung disease. Normally,
19 VERY, VERY HARD
during quiet breathing, average pleural pressures sur­ 20
rounding the large airways are typically negative,
whereas intraluminal pressures are more positive. Borg, G. (1982). PsychologicaJ Bases of Perceived Exertion, Medi­
These positive pressures keep the airways open dur­ cine and Science ill Spor/s and Exercise, 14,378.

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 23 Exercise Testing and Training: Primary Cardiopulmonary Dysfunction 421

reaching over the head, marching while sitting, knee

The 10 Point RPE Scale
extension, and stretching hamstrings with the leg
0 NOTHING AT ALL being stretched propped on another chair in front. Ex­
0.5 VERY, VERY WEAK
ercises should be timed with purse-lipped breathing
I VERY WEAK
to pace the exercise comfortably and control short­
2 WEAK
3 MODERATE ness of breath. An example of this would be:
4 SOMEWHAT STRONG
Start with your arms stretched forward at shoulder height.
5 STRONG
Breathe in through your nose while bringing your out­
6
stretched arms out to either side. Blow out through pursed
7 VERY STRONG
lips while bringing your arms back to the front and crossing
8
9 them in a scissoring manner. Repeat 10 times.
10 VERY, VERY STRONG
Adding scapular retraction exercises to stretch out
MAXIMAL
pectorals (i.e., pinching scapulas together) is helpful
since these patients spend many of their days in for­
Borg, G. (1982). Psychological Bases of Perceived Exertion, Medi­
cine a/ld Science ill SPOI'IS ond Exercise. i 4, 380. ward flexion types of postures. These exercises help
with posture and help to increase lung expansion with
inspiration.

cardiovascular limitation, monitoring heart rate is not

Training Phase
an accurate measure of exercise intensity. Asking pa­
tients to quantify their dyspnea is much more reliable. After completing the warm-up exercises, patients
may now start their walks. The patients should prac­
tice their purse-lipped breathing during their walking.
EXERCISE GUIDELINES
Walking for 12 minutes at a comfOltable pace to keep
After evaluating your patient's exercise capacity, the breathing at a level 3 should be the goa\. Rest periods
exercise program can be developed. Structuring the are acceptable during the 12-minute time. Another
program with the warm-up, training and cool-down
, goal could be to minimize rest periods to the points
phases shouId be done. where a patient could walk for 12 minutes nonstop.
Before starting exercise, purse-lipped breathing The upper-body exercise session could consist of
should be taught since this should be used throughout low-resistance, high-repetition exercises combined
the exercise session to control shortness of breath. In­ with purse-lipped breathing to help with shortness of
struction for teaching this technique could be as fol­ breath. These exercises could consist of PNF patterns
lows: patients should be instructed to take a relaxed or of ring shifting, for example, at a level just above
breath in through their noses. The breaths should be the shoulder. Light weights could be added as a pro­
relaxed. They should not be forced. Exhalation gression in addition to adding repetitions.
should be through pursed lips as if to blow out a can­
dle. Again, expiration should not be forced.
Cool Down

Warm-up The cool-down period would consist of repeating the

warm-up exercises at a pace where breathing would
The exercise program should always start with warm­
be brought down to baseline.
up exercises. Chair exercises are desirable, since sit­
ting up to exercise can help conserve energy that the
Frequency
patient will need for the training portion. Mixing
upper and lower body exercises should be done. Ex­ Patients should exercise at least three to four times
amples of these exercises include arm scissoring, per week.

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422 PART III Cardiopulmonary Physical Interventions

Intensity
more commonly used because walking and running
Patients should exercise so that their breathing are more natural activities. A is more likely
how hard are working. We advocate that to reach his or her maximum oxygen consumption
work no higher than a level 3. After the cool-down and heart rate. However, ECG recordings tend to
breathing should be at baseline. have more artifact and blood pressure are
more difficult to obtain at high intensities. If tread­
mill testing is the of choice, there are sev­
Termination of Exercise Testing or Training
eral different protocols that use different
Several or symptoms will alert the therapist that combinations of elevation and belt The
the session should be This chapter focuses type of treadmill test used on the fitness
clinical situations not using electrocardio­ level of the patient and the reason for doing the test.
(ECG) or sophisticated monitoring systems. For example, certain protocols may be used
response must be watched to test initial aerobic fitness levels in
closely, such as facial appearance of in­ individuals and athletes and then for
creased use of accessory in addition, blood fects of their training programs. Another type of
pressure, heart rate, and pulse oximeter are treadmill test may be used to diagnose cardiac
very important. Exercise should be terminated in any disease. The two most used protocols are
of the following situations: the Bruce and Bakke exercise tests. They have nor­
• Patient mative data from which functional aerobic
• Chest pain occurs or increases from patient's ment can be calculated.
normal
• Patient appears pale and skin is diaphoretic
Energy Conservation and Work Simplification
• Blood pressure is elevated or

with exercise
with energy conservation and work
• Patient complains of leg cramping fication techniques is an important component of
• Oxygen saturation drops below 90% cardiopulmonary An of the pa­
• Patient complains of dizziness tient's work for modifica­
• Patient's coordination is affected by increased tion with the goal of achieving increased functional­
muscle weakness and with prolonged ex­ life needs to be stressed. A brief
ercise

rices to patients.
TRADITIDNAl TESTING
Since most individuals have been accustomed to a
For those without shortness of breath from faster oaced life. oacing is a basic conceot worth dis-
lung disease or cardiac failure who could tolerate
there are more traditional it is to
that are useful in assess- slow down when walking or climbing stairs. Patients
exercise The primary modalities used will not be as tired and out of breath when reaching
are bicycle ergometry and treadmill There their destinations. Rest periods should be planned
are and to both. ECG the If wasting time is a concern while
monitoring and blood pressure readings may be more taking a break, reading a book or doing some hand­
easily obtained if a is tested on a work may make this time more worthwhile.
the to this modality is that a cart to carry items is quite helpful.
this is not as familiar an activity to some as activity while items in­
walking. Therefore maximal heart rates may not be creases oxygen consumption when If oxy­
achieved because of leg fatigue. Treadmill testing is gen consumption is increased, require­

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 23 Exercise Testing and Training: Primary Cardiopulmonary Dysfunction 423

ments also will be increased as described previously. 3. Explain the physiological benefits of exercise
Shortness of breath will increase. If a shopping cart is training with COPD and the perceived mecha­
used, leaning on the cart to take a rest will help to nisms of improvement.
keep breathing under control. 4. Name the components of a pulmonary rehabilita­
Sitting down to work is an energy saver because it tion program.
saves the legs the work of standing. Standing in the 5. Name and discuss techniques of energy conser­
bathroom to shave or wash at the sink can be elimi­ vation.
nated by placing a chair in front of the sink or by sit­
ting on the toilet-seat lid. Buying a shower chair
References
helps make washing easier. After coming out of the
shower or bath, wrapping up in a terry-cloth robe and American College of Sports Medicine. (1993). Resource manual

sitting on the toilet-seat lid can help the patient catch for guidelines for exercise testing and prescription (2nd ed.).
Philadelphia: Lea & Febiger.
his or her breath while drying off. An ironing board
Belman, M.1. (1989). Exercise in chronic obstructive pulmonary
can be used as an adjustable table. Setting it at low
disease, in Franklin, B.A., Gordon, S., & Timmis, G.e. (Eds.).
levels can help with meal preparation while sitting. Exercise in modern medicine. Baltimore: Williams a n d
Organizing work areas can help eliminate unnec­ Wilkins.

essary reaching. Items used most often should be kept Borg, G. (1982). Psychological Bases of Perceived Exertion, Medi·
cine and science in sports and exercise, /4,378.
at a level between the shoulders and the hips. Heavy
Casey, L.e., & Weber, K.T. (1986) Chronic lung disease and chest
appliances can be kept out on counter tops or on the
wall deformities. In Weber, K.T., Janicki, J.S. (Eds.). Car­
stove so that bending, stooping, and lifting is elimi­ diopulmonary exercise testing. Philadelphia: WB Saunders.
nated. Before cooking, filling the sink with soapy Casciari, R.1., Fairshter, R.D., Morrison, J.T. & Wilson, A.F.

water and putting dirty dishes and utensils in immedi­ (1981). Effects of breathing retraining in patients with chronic
obstructive pulmonary disease, Chest, 79, 393-398.
ately makes clean up easier. A dustpan with a long
Celli, B.R., Rassulo, J., & Make, B.1. (1986). Dyssynchronous
handle eliminates bending over when sweeping up.
breathing during arm but not leg exercise in patients with
Understanding the development of shortness of chronic airflow obstruction, The New England Journal of Med·
breath in individuals with cardiopulmonary disease icine, 314, 1485-1490.
and then evaluating them appropriately for exercise Criner, G.1., & Celli, B.R. (1988). Effect of unsupported arm exer­
cise of ventilatory muscle recruitment in patients with severe
programs will help these patients improve their func­
chronic airflow obstruction, American Review of Respiratory
tional capacity for activity. Exercise testing and train­
Disease, 138. 856-861.
ing can range from simple, cost-effective in-home McGavin, e.R., Gupta, S.P., & McHardy, G.J.R. (1976). Twelve­
testing to sophisticated use of metabolic carts and minute walking test for assessing disability in chronic bronchi­

equipment for evaluating and training athletes. In ad­ tis, British Medical Journal, I, 822-823.
Reis, A.L., Ellis, B., & Hawkins, R.W. (1988). Upper extremity
dition to improvements in functional capacity, these
exercise training in chronic obstructive pulmonary disease,
patients may also show some desensitization to their
Chest, 93, 688-692.
shortness of breath with an overall improvement in Tangri, S., & Woolf, e.R. (1973). The breathing pattern in chronic
their sense of well-being. obstructive lung disease during the performance of some com­
mon daily activities, Chest, 63, 126-127.
Thoman, R.L Stroker, G.L., & Ross. J.e. (1966f The efficacy of
REVIEW QUESTIONS pursed-lips breathing in patients with chronic obstructive pul­
monary disease, American Review of Respiratory Disease, 93.
1. Name and explain four limiting factors of exer­ 100-106.
cise in the patient with COPD. Weber, K.T., & Szidon, J.P. (J 986) Exertional dyspnea. In Weber,

2. Explain traditional measures of exercise capac­ K.T., Janicki, J.S. (Eds.): Cardiopulmonary exercise testing.
Philadelphia: WB Saunders.
ity. Which ones are useful for measuring exer­
cise capacity in COPD?

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 Exercise Testing and Training:
Secondary Cardiopulmonary
Dysfunction

Phyllis G. Krug

KEY TERMS Exercise blood gases Respiratory muscle endurance

Nocturnal ventilation Respiratory muscle fatigue

Oxygen desaturation Respiratory muscle strength

INTRODUCTION every system in the body can develop a disorder that

When considering the sensation of shortness of can have respiratory consequences. It is most effi­
breath, one typically pictures someone afflicted with cient to discuss the more common disorders that pre­
a lung disease, such as asthma, bronchitis, emphy­ sent themselves clinically. Case studies are presented
sema, or the like. A largely neglected area from the at the end of the chapter to further elucidate and clar­
perspective of physical therapy and rehabilitation is ify the process clinically.
that population that develops rt:spiratory limitations
secondary to other disease processes.
Psychological Factors
Secondary respiratory problems are those restric­
tions arising out of pathology other than primary lung With respect to shortness of breath, studies related to
disease. Patients falling into this category present those with the diagnosis of chronic obstructive lung
with a vast atTay of underlying pathologies. Virtually diseases have shown that people tolerate shorlnt:ss of

425

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426 PART III Cardiopulmonary Physical Therapy Interventions

breath up to 10 years before seeking medical <lttention review presented here, notes arc included to encour­
(Black, 1982). The patient usually attributes the symp­ age critical analysis of diagnostic material.
toms to aging and lack of exercise before considering
Pulmonary function tests
a medical reason. It has even been documented that
patients will curtail activities, social and recreational, Pulmonary functions tests (PFTs) are used to evaluate
before seeking medical advice. By the time medical flow rates and volume capacities of the lung. Detailed
attention is sought, a damaging cycle has been estab­ descriptions of these are presented in Chapter 8. Un­
lished (Figure 24-1). The results of inactivity con­ derlying assumptions in these reports are that a patient
tribute to feelings of inadequacy and poor self image. (1) has cooperated with the testing procedure, (2) has
The inactivity itself fosters and encourages atrophy, understood the procedure and, (3) has normal respira­
not only in the extremities where it is visibly apparent tory muscle strength to accomplish the test. Let's try
but also in the respiratory muscles. This fUlther adds and understand the factors that could blur optimal re­
to the debilitating process, creating secondary weak­ sults when taking a pulmonary function test. If a result
ness and disabilities that are not necessary and are is produced that shows the patient has poor lung ca­
avoidable. These issues are further addressed in the pacity, you could walk away thinking. "Wow, that's a
approach to treatment and in the case studies. really sick person there, most probably there isn't
much I can do to help because he is so restricted in
lung capacity." If you look further and investigate the
EVALUATION
possibilities, you begin to open windows or possibili­
The evaluation begins before the patient arrives. It ties for improvement. If there is weakness of the res­
begins with the information collected from the diag­ piratory muscles, then the results obtained reflect the
nostic data. Great benefits can be gained from under­ patient's breathing capacity based on weak muscles.
standing the information, but it is equally essential to This leaves open the option of improving the respira­
recognize its limitations. tory muscle strength to see how it may affect the ven­
tilatory capacity. Once you begin to think critically,
many windows may become apparent that can provide
Critical Usage of Pulmonary Diagnostic Reports
options for improving the results. For example, if a
The diagnostic criteria for secondary cardiopul­ patient with scoliosis has reduced volume capacity, it
monary dysfunction is similar to diagnosis criteria for is unclear if it is a fixed piece of data or if there is
primary cardiopulmonary dysfunction. In the short room for improvement from the perspective of posture
and strength. The volume and flow measurements of a
patient with a lot of secretions would be reduced be­
cause of the obstructive nature of the mucus. If that
patient was on an aggressive program of postural
THE FOUR Ds

/ Disease
drainage, would those values improve? Address
whether the values obtained in the pulmonary function
tests reflect a fixed, irreversible value. The author's

Progression clinical experience demonstrates that interventions ad­

Dyspnea
dressing posture, strength, endurance, and optimal

\
Depression
J
Deconditioning
clearance of mucus work to improve values otherwise
believed to be unchangeable.

X-ray
FIGURE 24-1
Flow of progression of respiratory disability. This The use of x-ray testing is critical in identifying infil­
demonstrates the chronic cyclic pattern that haastens trates, pneumonias, tumors, and obstructions. Yet it
deterioration and death. too has its limitations and should not be relied on

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 24 Exercise Testing and Training: Secondary Cardiopulmonary Dysfunction 427

solely to assess a patient's capabilities. Mr. K had a stood that patients will be more comfortable and
diagnosis of chronic obstructive lung disease with ex­ probably perform better on equipment that mimic
tensive scarring from old tuberculosis. His x-ray was their present life styles. Although the step test that
opaque. No viable ventilating lung tissue was seen on has the patient going up and down a step at a given
the left side. Ausculation with a stethoscope revealed rate is effective in identifying a change in the blood
no breath sounds. Yet after months of breathing re­ gases, a patient may feel more comfortable and be
training, thoracolumbar mobilization and soft tissue able to last longer on either a bicycle or treadmill.
mobilization, this patient established a most definite Furthermore, during a step test, the patient may fa­
improvement in breath sounds on the left side. No tigue after only a few repetitions. There is more op­
improvement was noted in his x-ray. So, our tools are portunity to evaluate the following: (I) how quickly
helpful to a point, and we should always give our pa­ the gases change, (2) if they improve over time, and
tient the benefit of the doubt and try. (3) the dynam ics of breath ing mechanics when
choosing a modality that the patient may be able to
Auscultation sustain over a longer period of time.
The stethoscope is effective in identifying many ab­
normalities within the lung, such as bronchospasm,
Respiratory muscle strength and endurance
mucous collection, consolidations, and infiltrates. Yet The foundation of the respiratory system's ability to
it is not uncommon to hear perfectly normal breath work is the strength and endurance of the respiratory
sounds, and the patient will still report tightness in the muscles. Strength and endurance form the foundation
chest, wheezing, and even congestion. It is always im­ because breathing is an ongoing activity from which
portant to have the patient cough or breathe deeply to the body cannot take a vacation; it requires the en­
increase the flow of air so as to pick up any of these durance to continue without stopping. There are times
abnormalities. Yet even if this is done and the breath when the respiratory system requires sudden bursts of
sounds seem normal, always defer to the patient. increased strength, as is evidenced by the need to
cough. Factors predisposing to fatigue are related to
Arterial blood gases muscular ability, ventilatory mechanics, reduction of
Arterial blood gases are designed to measure the energy supply by hypoxemia, reduced cardiac output,
level of oxygen, carbon, dioxide, and pH in the arter­ and malnutrition. The measure of respiratory muscle
ial blood (see Chapter 9). It reflects how effectively strength is done via a gauge that measures inspiratory
the respiratory system is working in supplying the muscle strength and expiratory muscle strength (PI
body with the fuel to carry on the task of living. It is max and PE max). A patient unable to generate 60%
quite common to receive an order for physical ther­ to 80% of these values reflects respiratory muscle
apy including exercise with the information that the weakness (Edwards, 1978). A patient who is unable to
blood gases are within normal limits. It is critical to maintain expected respiratory muscle force with con­
identify if the blood gas values were taken at rest or tinued or repeated contraction demonstrates the level
after exercise. If exercise blood gases are not i n­ of respiratory muscle fatigue, which is the precursor
eluded in the report, there is no way of knowing how of respiratory failure (see box below). A thorough
the patient's oxygenation will be affected by activity
(desaturation). It is possible to have normal resting
blood gases that drop precipitously with activity. This Clinical Signs of Respiratory Muscle Fatigue
can be a result of limited ventilatory ability or venti­
Hypoventilation
lation-perfusion mismatch. It is the responsibility of
Rapid shallow breathing
the therapist of a patient with compromised ventila­
tory ability to request exercise blood gases or use an Paradoxical breathing

oximeter to determine if desaturation is occurring. In Increased Paco2

discussing exercise blood gases, it should be under­

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428 PART III Cardiopulmonary Physical Therapy Interventions

background on a patient includes information on the 100

strength and endurance of the respiratory muscles so
that an effective, practical intervention program can
be planned. An aggressive exercise program cannot be
N 75
initiated if a patient is unable to sustain ventilation to o
..0
properly oxygenate the body. If a patient is in a state ::c
of respiratory muscle weakness and is then expected C I
50
to perform aggressively on a bicycle or treadmill, one Qi
0...
can inadvertently push the patient into respiratory fa­
tigue and possibly failure.

History-Critical Listening
o
o 27 40 60 80 100 150
In attaining a history from the patient, it is critical to
work slowly, so that the patient feels comfortable, P02 mm Hg
and to encourage what could be deemed as simple
FIGURE 24-2
chatter. After discussing a patient's personal inter­
Oxyhemoglobin dissociation curve. Demonstrates the point
ests, family, and home life you will have the informa­ at which oxygen saturation drops precipitously to between
tion to recommend an intervention program that will 40 and 60111111 Hg
be beneficial for the patient and that the patient will
actually do. If it is felt that the patient can improve ally open the perspective of hope for improvement.
his or her endurance to be able to walk a mile and the Because it is not just one system that becomes sud­
patient is only interested in walking a few blocks, the denly ineffective, physical therapists have the latitude
goals have to be set accordingly. Some therapeutic to explore the full course of the history and look for
techniques require a quiet passive posture by the pa­ the gaps where an intervention can be directed. Has
tient. A more tense individual who is pressed for time posture changed over time? Has there been progres­
will not tolerate that kind of intervention. It is there­ sive weakness? Have activity levels diminished?
fore crucial to take the time to get the total picture. Were there frequent respiratory infections? Re­
From the perspective of the history of respiratory sponses to each of these questions can greatly influ­
symptomatology, it is common to hear, "I don't know ence factors in a rehabilitation program. If a patient's
what happened, I was doing just great until r got that posture deteriorated over the years, compromising
cold ... then it all fell apart." Pursue the investiga­ respiratory ability, a program of stretching and
tion, because undoubtedly the history is much longer. strengthening of the postural musculature may pro­
The difference is that the patient was able to cope and vide sufficient space in the thoracic wall for im­
the presenting situation became excessive. The oxy­ proved lung capacity and oxygenation. It takes a
hemoglobin dissociation curve in Figure 24-2 demon­ small amount of objective improvement to make a
strates the underlying physiological process (Stoller, big difference in the quality of life for the individual.
1988). Looking at the S curve, one can see that above Regardless of the underlying cause, attaining a Pao2
60 mm Hg the curve is fairly flat, and Joss or deple­ of at least 60 mm Hg is the primary concern.
tion of oxygen above the level can go undetected Because the work of breathing becomes very diffi­
clinically. However, as the curve demonstrates, there cult in primary lung diseases or restrictions secondary
is a critical point around the Pao2 of 60 where the to other disease processes, the symptomatic presenta­
person will "suddenly" experience severe shortness tions can be quite similar. It very closely simulates
of breath. In reality the oxygen level was dropping the posture of the marathon runner at the end of a
progressively over time but was only critically felt at run. The runner assumes a bent forward posture,
the drop of the curve. Understanding the progression leaning on a wall or gaining support by leaning on
of the deterioration with shortness of breath can actu­ the knees (Figure 24-3). This position is optimal for

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 24 Exercise Testing and Tmining: Secondary Cardiopulmonary Dysfunction 429

FIGURE 24-3

The flexed fOlward posture held when experiencing sho rtne ss of breath. Simi lari t ies between the healthy
marathon runner and the person with chronic respiratory difficulty should be considered in reference to
muscular, skeletal and pressure changes. (Courtesy of David Gorman, The Body Moveahle)

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430 PART III Cardiopulmonary Physical Therapy Interventions

enhancing diaphragmatic excursion. After a few mO­ baseline exercise test to identify exercise capability.
ments, the runner will get up and walk away. Unfor­ It would be premature to begin an exercise training
tunately, the patient experiencing shortness of breath program. The first step wou Id be to address improve­
stays in that bent forward position. A patient may ment of strength and posture. The goal is directed to­
stay that way because it is easier to breath or because ward improvement in height, lung capacity, and mus­
he or she does not realize the precipitating event has cle strength. The baseline data on the exercise test
passed. The point of emphasis is that any chronic dis­ would likely improve. An exercise test subsequent to
ease resulting in shortness of breath will have pos­ postural improvement would be a better baseline for
tural effects. Look for limitation in range of motion an endurance training program.
of the hips and poor mobility of the thorax and the For the patient with underlying neuromuscular
pelvis. This can be evident in a gait pattern that has disease, an endurance training program may overfa­
minimal rotation of the thorax on the pelvis. The tigue muscle groups and cause damage. Therefore
stride length will be shortened, with minimal arm the exercise test, again, is to get a baseline of exer­
swing and an overall stiff, nonfluid gait pattern. The cise ability. The therapeutic intervention would be
gait pattern of those suffering with chronic shortness directed toward muscle re-education, postural exer­
of breath and its associated postural changes can be cises, and strengthening to help the patient move
described as walking cinder blocks, implying that the more efficiently and reduce stress on the affected
muscles from the neck to the pelvis are fixed and do m u s culature. The i m p r ovement in posture and
not allow for normal reciprocal movement. strength provides a better baseline to sustain an exer­
cise test and subsequent training.
A timed-walk test for a patient with severe limita­
Exercise Testing
tion would be appropriate. Measure a walkway in 10-
Exercise testing is performed for a variety of reasons. foot increments and then time the distance walked for
It is a means of (1) gaining baseline information of either 6 or 12 minutes. It may be necessary to further
the patient's activity level, (2) assessing functional modify this test into distance walked for 2 minutes.
ability,(3) prescribing graded-exercise programs, and Instruct the patient to walk as far as possible as fast
(4) evaluating cardiovascular ability. The choice of as possible for the timed segment. Record distance
exercise testing should reflect the needs of the pa­ walked. Monitor the blood pressure, heart rate, respi­
tient, the cost-effectiveness of the procedure, and the ratory rate, ventilatory muscle use, and O2 saturation.
consideration for the need of extensive diagnostic in­ A patient at a higher level of function may benefit
formation and its practical application into the pa­ from a more aggressive exercise test that allows for a
tient's life. The patient's addressed in this chapter are more accurate level of cardiovascular response to ex­
by and large severely limited in their physical abili­ ercise as a basel ine for prescription for endurance
ties because of their underlying disease processes and training. A baseline level is first obtained from the
their secondary respiratory effects. Typically the timed-walk test or the patient can walk on the tread­
overall presentation is one of atrophy, decondition­ mill at 1 to 2 mph, 0% grade for 6 minutes.
ing, and poor mobility that greatly limits the distance A patient whose exercise ability is limited by respi­
walked. The severely limited patient would benefit ratory factors before the healt rate or blood pressure is
with a simplified exercise test to identify exercise ca­ even elevated does not rt;quire a full-graded exercise
pacity. When considering the patient with secondary test with full ECG, metabolic gas analysis, heart rate,
cardiopulmonary restriction, treatment should be and blood pressure measures. Interest should be more
aimed at improving the cardiopulmonary status con­ directed toward the following:(I) how far can this per­
current to the underlying primary process. A few ex­ son walk, (2) what happens to his breathing pattern and
amples can better illustrate this point. The scoliosis respiratory rate, and (3) does the oxygen saturation
patient who has progression of the spinal deformity drop. Based on this, recommendations can be made for
and secondary pulmonary compromise requires a use of supplemental oxygen and possibly more efficient

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 24 Exercise Testing and Training: Secondary Cardiopulmonary Dysfunction 431

Exercise Training
breathing patterns to allow the patient to persevere
longer. For example, if a patient has a diffusion prob­ Design of an exercise prescription must be individu­
lem or a ventilation/perfusion mismatch, it would be alized and must be prescribed within both useful and
helpful to evaluate whether a slower pace would allow achievable levels.
the patient to walk longer. Consider enhancing the time Exercise training should not be limited to a mode
allowed for diffusion of the oxygen. It may be found of exercise equipment, duration of time, or fre­
that a slower pace, with attention directed toward deep quency. A person with a chronic condition has
effective breathing, may yield different values in oxy­ chronic manifestations physically and psychologi­
gen saturation and the distance walked. The choice of cally. Therapy directed toward the chronic physical
testing modality should also take place or location into changes, that is, postural and overall movement, can
consideration. It seems inappropriate to demand that a result in improved endurance. This perspective
severely limited patient being seen in the home undergo should be seriously considered before using preciolls
extensive graded-exercise testing before recommending therapeutic time to put a patient on a treadmill three
an exercise program. The choice of exercise testing times per week to measure a heart rate that does not
should reflect the goals of the patient. If the patient is elevate because the patient is too short of breath. The
ready for an aggressive exercise program, then more severely limited patient may benefit from general
extensive testing is appropriate. Testing can then body movement for a duration of 10 to 15 minutes. It
progress to stage II. A treadmill stess test begins with a could include standing and leaning on a chair and
speed that is comfortable for the patient-usually be­ shifting the hips to the rhythm of music. The goal is
tween 2 to 3 mph. Work is increased every 3 minutes initially just to move, create a challenge to the car­
by either increasing the speed or the incline. It is rec­ diorespiratory system, focus on controlled hrcathing,
ommended to increase the speed by 0.5 mph incre­ and show the patient that he or she can sustai n move­
ments, maintain it at a comfortable walking pace, and ment for prolonged periods. The therapeutic ball has
progress the incline by 2.5% increments after a com­ proven to be beneficial. The 65-cm ball is a good
fortable pace has been established. Measurement of size for a patient to sit on (Figure 24-4). It provides
heart rate and blood pressure should be taken at the end support yet allows for movement. Many severely
of each 3-minute stage and Sa02 oxygen saturation limited patients have been able to sit on a ball shift­
should be monitored throughout and recorded at the be­ ing their weight from side to side, working on leg
ginning and end of each stage. strengthening, pelvic and spinal mobility, and chal­
The test is terminated in the following situations: lenging the cardiorespiratory system. Once a capahle
(I) when the patient reaches 65% to 75% of predicted patient becomes interested in a traditional endurance
maximal heart rate, (2) if oxygen saturation drops training program, the graded-exercise test can pro­
below 90%, (3) if the blood pressure drops with in­ vide the necessary information to prescribe one. The
creasing activity, or (4) the patient experiences symp­ prescription should include intensity, duration, fre­
toms of shortness of breath or muscular discomfort. quency, and modality as follows: (I) Intensity is
If a patient is able to reach 65% of predicted based on 65% to 80% of the predicted heart rate or a
maximum heart rate without cardiop u l monary level where the patient becomes symptomatic or the
symptoms, then the patient is capable of exercise oxygen saturation drops to 90O/C . Consider, for exam­
conditioning. Oxygen saturation should be above ple, an exercise test that is terminated after walking
90%. Below this level requires supplemental oxy­ at a speed of 3 mph, at a 5% elevation, 3 minutes
gen. If the carbon dioxide (C02) increases more that into lhat level. If the limiting factor was shortness of
10 torr of resting level, the patient will be limited in breath with a drop in oxygenation, further testing
exercise potential. Individuals who reach their maxi­ should be conducted with the use of supplemental
mum volume ventilation (MVV) with minimum in­ oxygen. If the limiting factor was shortness of breath
tensity exercise may have difficulty with an en­ without a drop in oxygen, 2.5 mph at 0% elevation
durance training program. can be used as a 5-minute warm-lip, followed by

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432 PART III Cardiopulmonary Physical Therapy Interventions

training at 3 mph for up to 15 minutes with I minute Caution is advised in understanding the underly­
intervals at 2.5% elevation followed by a cool down ing pathology that resulted in cardiopulmonary limi­
of 2.5 mph, 0% elevation, for 5 minutes. (2) Dura­ tations. Post polio syndrome is characterized by
tion of exercise is 15 to 30 minutes per session. Ini­ muscles that were weakened during the initial onset
tially this can be broken down into interval training of the disease and more recently report a recurrence
where short 1- to 2-minute rest periods can be used of symptoms. Studies have shown that these patients
progressively, lengthening the intervals until the pa­ benefit from strengthening and endurance exercise,
tient is able to maintain a c o ntinuous session. but extreme caution must be directed toward avoid­
(3) Frequency of e xercise is three to five times a ing overuse (Dean, 1991 a; Owen, (985). The patient
week on alternate days. (4) Modality depends on pa­ will benefit from a carefully considered, judicious
tient comfort. The target heart rate, or the level be­ exercise program.
fore the patient developed symptoms, is used as the
training level. Flexibility exercises or slow walking
SYSTEMATIC APPROACH IN THE
are recommended for warm-up before the endurance
REHABILITATION PROCESS
exercise program.
Nocturnal Ventilation-The Role of Rest
and the Respiratory Muscles

At this point the therapist is equipped with a vast

array of information. The question is how to plan an
effective intervention. Clinical experience has shown
the importance of first directing attention toward the
work of breathing. The literature is filled with discus­
sions about the role of resting the respiratory muscles
(Braun, 1983). It is suggested that one of the factors
leading to respiratory failure is the respiratory mus­
cles' inability to keep up with the demand of breath­
ing. If we consider the patient with severe scoliosis,
the work of breathing is not shared equally by the
respiratory muscles because of distol1ion of the chest
wall. In addition, the curvature will add an additional
load on the energy expenditure of breathing. Like any
muscle in the muscular system, if a load is put on a
muscle, it will train and get stronger. Yet, if this goes
on for an extended period of time the muscle will be
unable to maintain the added work load and the mus­
cle fibers themselves will begin to break down. This
process is well understood in the fields of sports med­
icine and weight training. It is called overuse atrophy.
This process also occurs in the respiratory system. In
advising a patient in an exercise program, it is clitical
to be aware of how much we are asking our patients
to do. We walk a narrow path between (I) doing

FIGURE 24-4 nothing and allowing the patient to accept life with
Therapeutic ball as part of a program of improving mobility the shortness of breath and promote further atrophy
and endurance. and (2) pushing too hard and risking breakdown of

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 24 Exercise Testing aod Training: Secondary Cardiopulmonary Dysfunction 433

the respiratory system. It is the responsibility of the for good clinical judgement. Sometimes the patient
therapist to be aware of the diagnostic and clinical has a bad day and just does not do well, other times
signs of respiratory muscle fatigue. he or she may be in trouble.
Diagnostic criteria for respiratory muscle fatigue
include the following: (I) increasing pulmonary arte­
Managing the patient with clinical

signs of respiratory fatigue

rial carbon dioxide (Paco2). (2) reduction of high­

frequency signals (greatcr than 80 Hz) of muscular If the patient has a prcscription for oxygen, make
activity on electromyography studies (EMG) despite sure he or she is using it. Get the patient comfortable
continued contraction and dominance of the low­ and use your hands to guide the body into shifting the
frequency signals (lcss than 80 Hz), (3) reduction of work of breathing. This is a very critical factor. In
vital capacity with decrcascs in supine ye t o 50% of dealing with acute shortncss of breath or muscle fa­
sitting Ye, and (4) inspiratory muscle prcssure to tigue the patient undoubtedly will be in a state of
below 66% of predicted mean. panic. Panic complicates the situation by increasing
The clinical signs of rcspiratory muscle fatigue in­ the respiratory rate and consequently reducing tidal
clude the following: (I) paradoxical breathing, (2) in­ volume. The gentle placement of the therapist's
creased respiratory rate, and (3) shallow breathing hands on the lower rib cage along with a calm, firm,
(see box below). First and foremost, we arc looking soothing voice can hclp guide the patient into a more
at change from normal. This is where good baseline calm, efficient breathing pattern. Studies have shown
information is critical. Baseline blood gases, the pa­ that tension alone can reduce the expiratory flow rate,
tient's typical breathing patterns, and the baseline for so the therapist's role in calming the patient is di­
dyspnea should be considered. This is a critical area rectly related to improving the breathing pattern
(Kotses, 1981).

Resting the respiratory muscles

There is increasing interest in the role of resting the

Respiratory Muscle Function Assessment respiratory muscles before it reaches the stage of res­
piratory fatigue and failure. This is accomplished
Pulmonary function test
through nocturnal ventilation using positive- or nega­
•

Effort and strength dependent tive-pressure ventilators (Figures 24-5 and 24-6). The
• Respiratory muscle strength focus is to increase muscle energy supplies and

PI max-inspiratory pressure stores. Mechanical ventilation will assume the work

of the respiratory muscles and allow them to rest.
PE max-expiratory pressure
This may allow the time needed to reverse the factors
• Respiratory muscle fatigue
that led to fatigue. It substantially reduces the oxygen
60% to 80% PI max
consumption of the respiratory muscles, allowing for
• Respiratory muscle enduram:e more oxygen to reach the other tissues. Studies have
Maximum volume ventilation shown that after a mean period of approximately 5

Maximum sustainable ventilation months at home on daily 4- to IO-hour ventilatory

support, there are significant increases in vital capac­
80% MVV for 5 minutes or 60% MVV
for 15 minutes ity, PI max, and PE max (Marino, 1982). It also
showed a reduction in Paco2 along with a reduction
Fatigue: when Ve <minute ventilation)
in hospitalizations and the number of days hospital­
ized. The topic of resting the respiratory system adds

NOTE: Inability to reach a predicted value reflects muscle weak­

a different perspective in regard to traditional pul­
ness or fatigue. monary rehabi litation programs promoted. Before

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434 PART III Cardiopulmonary Physical Therapy Interventions

FIGURE 24-5

Positive pressure ventilator used for nocturnal ventilation.

FIGURE 24-6

Negative pressure ventilator used for nocturnal ventilation.

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 24 Exercise Testing and Training: Secondary Cardiopulmonary Dysfunction 435

initiating a progressive exercise program or for that breath hold. Activities can be divided into two cate­
matter, any sort of exercise program, it is important gories. Static activities and rhythmic activities. Static
to assess the level of respiratory fatigue under which activities are those that are done once. For instance,
the patient is living. Symptoms, clinical observations, picking up a shoe. It is done once, until you are ready
or historical findings that are suggestive of further in­ for the second shoe. The first rule of thumb is to take
vestigation into the benefit of nocturnal ventilation a breath in before the activity to supply the body with
include sleep disorder, progressi ve dyspnea, hyper­ the oxygen it needs, then exhale with the activity. It
capnia, and dyscoordinate breathing patterns. It has is simple but it actually helps, and the patient is able
been recommended that a patient be allowed suffi­ to perform an activity with less shortness of breath.
cient time to adjust to nocturnal ventilation before ad­ The second rule of thumb is to maintain a rhythm
vancing into an active exercise program. This deci­ with activity. If the activity is washing dishes, vacu­
sion must be made with medical guidance. It is uming the carpet, or climbing some stairs, the focus
sometimes recommended that a patient rest on this is to maintain a rhythm. That rhythm will change as
system for a few months to allow the body to reach a the activity continues, but the idea is to control it
stable level of metabolic rest. through the purse-lip breathing. For example, climb­
ing stairs may begin with ease and become more dif­
ficult with each step. Breathe in on step one and ex­
BREATHING TRAINING
hale for step two, three, and four. As the activity
Paced Breathing
continues, modify according to the patient's need. It
These techniques are taught regardless of which mus­ may progress to breathing in on one step and doing
cles patient uses to breathe. Because breathing is the fu II exhalation on the second step. The patient
g
something we do all day lon , it is unfair to expect may still experience shortness of breath but will have
patients to alter their breathing continuously. There­ better control and get further.
fore it is helpful to break down breathing into various
components. Foremost is coordinating breathing with
Signs of Improvement
activity. If a patient is short of breath, he or she needs
to know how to get it back. Pursed-lip breathing is an The direction toward improved posture and more effi­
effective means of helping. Pursed-lip breathing cient quality of movement is a slower process and
works as the center for controlling the respiratory rate should be directed in the realm of kinesthetic aware­
and maintains more efficient emptying of the lung. ness. If you are working with a patient and find that in a
Paced breathing and the rule of thumb are handy certain posture you observed a better breathing pattern
tools that help get through daily activities. Breathing or that with a certain relaxation technique the patient
has a rhythm of inhale and exhale. Generally, the ex­ found relief, you want to harness that sensation. Repeat
hale is longer than the inhale. At rest and with vari­ it, use tactile input, have the patient close his or her
ous relaxation techniques, it is possible to greatly ex­ eyes and imagine it. If the patient has just learned to
tend the length of the exhale. For example, if at rest relax the upper thorax and get a good expansion in the
the person inhales for a count of two, the exhalation lower thorax, he or she will not be able to walk out of
might be for a count of four or five. With deeper re­ that session and breathe that way continuously. How is
laxation the length of the exhalation can be extended this new skill incorporated into a new pattern of breath­
to the count of five, six, or even longer. Patients are ing? It is effective to stop 20 to 30 times per day,
encouraged to develop and heighten this sense of (1) pause, (2) relax the shoulders, (3) focus on the area
awareness and begin to coordinate it with activity. to expand, (4) do the breathing technique for a few rep­
The concern is that frequently a person will perform etitions, and (5) concentrate on it and put it away. The
an activity (i.e., bending down to get a shoe, reaching focus of this exercise is not strength training but rather
to open a door, washing hair, or lifting a package) kinesthetic awareness. About 2 weeks of this compul­
and during the activity actually stop breathing or sive stopping, sensing. and being aware is enough time

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436 PART III Cardiopulmonary Physical Therapy Interventions

that it becomes the way the patient breathes, becoming parted slowly, as opposed to thrust or high-velocity
incorporated into the patient's pattern of breathing. This manipulation. The intent is to regain normal active
obviously will not be successful with someone who range of motion, thus improving alignment and
mechanically, muscularly, or neurally is incapable of stress distribution. The improvement in joint func­
this parit cular tion increases a joint's adaptive potential to mechan­
panded using the tools of imagery. Too often a patient ical stress and reduces the possibility of re-injury to
is taught how to brcathc and does so beautifully in the that joint.
therapy session and then resumes the old pattern after
leaving the office. It is a difficult task to incorporate a
Soft Tissue Therapies
movement performed in a static stationary position and
maintain it during the dynamics of daily life. The The purpose of soft tissue therapy is to normalize ac­
power of suggestion and imagery can be used here. tivity of the muscle fibers, restore extensibility, and
This scenario becomes a home exercise program of reduce pain. Soft tissue mobilization includes mas­
gaining control of the breathing system. Even if the pa­ sage, accupressure, and soft tissue stretching. It uses
tient cannot maintain it through the whole process, it is low-intensity pressure and should not cause pain. If
a crucial activity in self-control and minimizes the applied properly, its techniques should result in local
sense of panic that goes along with activities that result and general relaxation, and reduction in tone. Myofa­
in shortness of breath. It is a very beneficial activity cial release is a method to normalize myofacial activ­
that can then be further advanced while working on a ity, regain tissue extensibility, and reduce pain. It is
bicycle or treadmill. The underlying emphasis is opti­ based on neuroreflexive responses that reduce tissue
mizing the patient's efficiency of movement and tension. With the appropriate application of manual
breathing and reducing the work of breathing. contact and the determination of the best point of
entry into the musculoskeletal system, a relaxation of
tissue tension and decrease in myofascial tightness
OVERVIEW OF THERAPEUTIC OPTIONS
can be attained.
A myriad of therapeutic techniques exist that are vi­
able options in trying to maximize breathing oppor­
Neuromuscular Therapy
tunities. It is beyond the scope of this chapter to
elaborate on the technique, rationale, and method of Proprioceptive neuromuscular facilitation is a method
all the options appropriate for the population. Once of promoting the response of the neuromuscular
asked by a colleague the appropriate treatments for mechanisms through stimulation of proprioceptors.
respiratory patients, I replied, "the same as with any The application of a manual stimulus is used to elicit
disease process." Evaluate the total situation and efficient neuromuscular responses. Its primary objec­
plan an intervention that will reduce stress and in­ tive is to develop trunk or proximal stability and con­
crease opportunity. If the patient population has de­ trol, as well as to coordinate mobility patterns. It can
veloped respiratory problems secondary to an under­ be used to help stabilize vertebral motion and im­
lying d i s e a s e, p o s ture, muscle l e n g t h , m u s c l e prove spinal movement control.
strength, and endurance should be considered. The Muscle energy works under the principle that
manual therapies are excellent vehicles in gaining muscular activity can be used to restore physiologi­
access to improvement. cal joint motion. It uses active muscle contraction
at varying intensitics from a precisely controlled
position in a specific direction against a distinct
Mobilization: Thorax, Rib Cage, Pelvis,
counterforce. It is used to mobilize joint restric­
Sacrum, Hip, Shoulders, and Neck
tions, strengthen weak musculature, stretch tight
Joint mobilization is a nonthrust manipulation. Pres­ myofascia, reduce muscle tonus, and improve local
sures may vary from gentle to vigorous but are im­ circulation.

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 24 Exercise Testing and Training: Secondary Cardiopulmonary Dysfunction 437

Positional Release Therapies

through a treatment. Get comfortable hand contact
Strain/counterstrain is the passive placement of the and feel the tissue soften in your hand, then wait.
body in a position of greatest comfort to reduce pain. Watch what happens to the breathing. Hone in on any
Relief, if achieved by the reduction and arrest of con­ changes and help the patient become aware of any
tinuing inappropriate proprioceptive activity, main­ changes in the pattern of breathing. The diaphragm
tains the motion dysfunction. The underlying basis is and thoracic release are also remarkably effective in
that every neuromuscular Clisorder has a palpable encouraging greater thoracic expansion. These tech­
point of tenderness and a position that can be ob­ niques alone can be effective in relieving wheezing,
tained for comfort. It is a gentle, nontraumatic type of improving aeration and even mobilizing secretions.
manipulation that is especially effective when irregu­ Take the time to explore options. In reference to
lar neuromuscular activities have maintained and per­ the cranial bones, restrictions in the movement of the
petuated abnormal mechanical stress to tissue. A re­ temporal bones has been identified in those suffering
turn to normal length is achieved through positional with shortness of breath, regardless of diagnosis. The
release of abnormal neuroreflexive activities. temporal wobble therapy, ear pull, and finger in ear
(craniosacral technique) have also becn effective in
easing the work of breathing. The focus of the thera­
Craniosacral Therapies
peutic intervention must be to find some relief from
Craniosacral therapy is a gentle hands-on method for the work of breathing first and then begin a plan of
evaluating and treating problems affecting the cran­ enhancement of relief followed by strengthening of
iosacral system. The craniosacral system provides the those new found movements. Endurance activitics,
environment in which your brain and spinal cord de­ that is, treadmills, bicycling or walking, are wonder­
velop and function. The palpable parts of the cran­ ful adjuncts after these important elements have been
iosacral system are the bones of the skull, sacrum, addressed.
and coccyx, which attach to the membranes that en­
close the cerebrospinal fluid. Treatment involves the
CASE STUDIES
usage of fascial and soft tissue release techniques to
Poliomyelitis with Secondary Severe Kyphoscoliosis
detect subtle biological movements. A 10-step proto­
col is used for evaluating and treating the entire body. Mr. L is a 65-year-old male with history of po­
liomyelitis onset at the age of 8 years old. He was left
with a total paralysis of his left arm and a severe scol­
Review
iosis secondary to muscle strength imbalance in the
In evaluating the disease process that results in respi­ trunk. (Figure 24-7). After recovery from the po­
ratory compromise, it is crucial to recognize the long­ liomyelitis, his medical history was unremarkable. He
term chronic effects on the total body. It is short lived independently in a fourth-floor walk-up apart­
sighted to limit the focus to the thorax if there is a ment and worked as a postal clerk until he was admit­
respiratory problem. Take a step back and look at the ted in respiratory failure. At that time his oxygen satu­
total picture and look for those windows of improve­ ration was 80%, his arterial carbon dioxide (Paco2)
ment. Some specific techniques have cdnsistently was 61, and his arterial oxygen level (Pao2) was 53.
been helpful in helping ease the work of breathing. His vital capacity was 1.8 liters-40% of predicted­
Both myofacial release techniques and craniosacral and his ECG showed right ventricular strain sec­
therapies focus on the cranium and the sacrum. The ondary to pulmonary hypertension. Additionally the
mobility of the sacrum and motion of the cranial myocardium was situated in his right cavity secondary
bones have been shown clinically to be directly re­ to pressure gradients that shifted it from its normal po­
lated to the ease of breathing. The performance of sition. His medical management required a tra­
traction on the sacrum, a gentle hold, provides a re­ cheostomy and respiratory support with a ventilator
lease on the thorax. The key is patience. Do not rush and oxygen. He stabilized and was sent for an interim

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438 PART III Cal'diopulmonary Physical Therapy Interventions

The physical therapy program was problem­

oriented and was modified throughout as the patient's
needs changed.

Problem 1: Shortness of breath

at rest and with activity

Mr. L was instructed in breathing techniques, includ­

ing paced breathing, pursed-lip breathing, and relax­
ation exercises to help relax the upper respiratory
muscles and encourage deeper, more efficient expan­
sion of the thorax.

Problem 2: Paradoxical breathing pattern

Because of the severity of the curve, the thorax

moved in a rotation pattern to the right with the in­
hale and to the left with the exhale. It was unclear
how much of this pattern was due to structural factors
or secondary weakness that allowed such severe dis­
tortions. A path of exploration was initiated to find
potential areas of movement and to further evaluate if
there was potential to master those movements. Sub­
tle movements were evoked in the cervical area and
initiated a treatment plan of soft tissue mobilization,
craniosacral therapy, and strengthening exercises.
The window found was that cervical traction allowed
FIGURE 24-7
Mr. L to increase his head range of motion and he
Palil:nt with history of poliomyelitis and subsequent
was able to better relax his sternum and allow for
development of severe scoliosis secondary to muscle
imbalances.
breathing from lower down. The terminology of
lower down is used because it is mechanically impos­
sible for Mr. L to fully use his diaphragm. He was
of rehabilitation. At that facility he was accidentally ex­ able to recruit other muscle groups, in addition to
tubated and the tracheal area was Iladly traumatized. diaphragmatic, to allow for sufficient thoracic ex­
The tracheal trauma left the patient comatose for 4 days. pansion relieving the excessive work of his upper­
About 2 weeks before the patient's respiratory respiratory muscles.
failure, he was at a dinner with friends, and one of the Aside from the primary paralysis of the left arm,
group videotaped the evening. The tape had invalu­ the musculature of the left trunk was also weak and
able information in it. Firstly, in terms of posture, Mr. kinesthetically deprived. The term kinesthetically de­
L's head was totally sunk into the thoracic cavity prived refers to the convex part of the curve that was
leaving him functionally without a neck. Around the essentially folded inward in total paradoxical motion.
dinner table his friends were joking and remarking at Mr. L was totally unaware of that part of his body and
how little he was eating. It is even more noteworthy had no sense of movement. On soft issue mobilization
that he even dOI.cd during conversation at the table. and tactile input on the left side, the patient began im­
The labored breathing, the excessive use of the upper mediately to expand on the left side of the thorax. Be­
respiratory muscles, the sleepiness, loss of appetite, cause of the severity of the curve, it would be impos­
and lack of energy to eat his meal were all signs of sible to have normal expansion on the left, but it was
pending respiratory fatigue and fail ure. unclear if enough force and negative pressure could

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 24 Exercise Testing and Training: Secondary Cardiopulmonary Dysfunction 439

be generated on the left to enable the patient to with the patient reporting "Oh, I am getting more air!"
(I) shin the myocardium back into the left thoracic This was easily confirmed; improved aeration was au­
cavity, (2) increase his vital capacity enough to reduce dible with the stethoscope.
his need for oxygen and possibly prevent future respi­
ratory complications. Mr. L began a home program Problem 3: Poor endurance
using Theraband, which he looped around his left
Mr. L had become so deconditioned and anxious at
shoulder and held across his chest with his right hand
the thought of movement that he was unable to walk
(Figure 24-8). This position allowed him to grade re­
even 20 feet. Outdoor ambulation created severe anx­
sistance to scapular adduction, elevation, and depres­
iety for which he was receiving psychological ther­
sion. He also used weights in trunk exercises. Therapy
apy. He began a gradual program with walking in
sessions focused on manual techniques to mobilize the
place at 2-minute intervals. It is important to note that
rib cage, stretch the muscles, and release the connec­
he was extremely motivated and not only followed
tive tissue. The technique of the diaphragm and tho­
his exercise program, but expanded on it (Figure 24-
racic release were remarkably effective in opening the
9). He also used the P-FJex respiratory muscle trainer
breathing. This method alone was frequently effective
attached to his tracheotomy tube beginning on level I
for IS-minute intervals, twice a day.
After I year on the program, Mr. L grew in height
I 114 inches and increased his vital capacity by 700
ml, he no longer required supplementary oxygen, and
his myocardium shifted into the left thoracic cavity
without any signs of right ventricular strain. His ejec­
tion fraction was 45%. He still demonstrated para­
doxical motion with respiration, but there was a sig­
nificant reduction in the amount of sucking in of the
lower rib cage on the left with inhalation. Ausculta­
tion was remarkable with excellent breath sounds on
the left and right and some reduced air movement
near the lingula. Mr. L progressed up to walking in
place for 25 minutes with 2-pound weights in both
hands (he is able to clasp a weight with his paralyzed
hand) and attached to both ankles. He gained enough
motion in his neck to allow for full range of motion.
Because the pull of gravity will continually work
on Mr. L to pull him back into dysfunctional patterns,
it is impOltant to keep Mr. L on a program. He is seen
once every 2 months to modify and update his exer­
cises and work on his trunk to ensure optimal thoracic
capability. Over this extended time other windows
have been found working on his sacrum and pelvis.
Manual traction, mobilization techniques, and soft tis­
sue releases in these areas all provide for improved
thoracic expansion. Hand placement on the sacrum al­
lows for a slow release and relaxation of the upper
FIGURE 24-8 chest. Manual techniques then followed, encouraging
Creative use of theraband in strengthening of the thoracic progressively increasing diaphragmatic excursion. Mr.
musculature. L is able to cue in to changes in his body and work on

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440 PART III Cardiopulmonary Physical Therapy Interventions

Dystonia With Spasmodic Breathing

Ms. B is a 36-year-old psychologist with the diagno­

sis of dystonia. She has a I O-ye ar history of torticollis
that has been treated with Botox. IL is a treatment
aimed at paralyzing selective muscle fibers to allow
for relief of severe spasms. She presented with recent
onset of shortness of breath and inability to get air.
On palpation over the lower rib cage and diaphragm,
it became evident that there was discoordinate move­
ment of the thoracic musculature. It was unclear
whether this was merely discoordinate movement or
a function of the dystonia. The technique of diaphrag­
matic release as demonstrated in craniosacral therapy
provided immediate release of the symptom of short­
ness of breath and reduced the amount of discoordi­
nate movement of the chest wall. Ms. B was taught
how to perform the technique on herself and was suc­
cessful in the exercise. The P-Flcx was used to give
added resistance to her breathing as a means of ex­
trasensory awareness. It gave her an added awareness
of movement of the thoracic wall and a means of
controlling it. The final phase of her therapy was
mild aerobic activity with the focus of coordinating
breathing with movement and increasing overall en­
FIGURE 24-9
durance. She was on a program for 6 months and was
Respiratory muscle training in p a t ien t with tracheotomy.
followed once per week. Although her symptoms
persist sporadicalJy, she is able to catch it in time and
gain control of her brcathing. According to medical
opinion, it is likely that she has the rare progression
gaining sensory awareness of the area and aim toward of respiratory muscle dystonia. It is undear at this
mastery and control of the movement. time how this situation will progress, but in the
meantime, she has the means of controlling discoor­
Summary of problems
dinate movement and breathing with ease.
Mr. L benefitted from a program that focused on im­
proving his total potential. He had the benefit of night
Postpolio Syndrome
ventilation so that his body was rested. His total en­
durance capability was based on finding those win­ Dr. 0 is a dentist teaching in a dental school and
dows of improvement. The improvement in align­ conducting research in a laboratory. He has a his­
ment and strengthening of the trunk and respiratory tory of poliomyelitis with a possible diagnosis of
muscles provided for maximizing his respiratory ca­ postpolio syndrome (PPS). Diagnosis is difficult
pabilities, overall endurance, and quality of life. At because PPS is characterized by progressive weak­
this point Mr. L is totally independent. He walks 3 ness and pain in the musculature that survived the
miles per day and goes out with his wife and friends. original poliovirus. The underlying mechanism is
He has even traveled abroad with a foreign medical still unclear; it is suggested that the progression is
supply company providing for his ventilatory needs. resultant to long-term overuse and deterioration of

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 24 Exercise Testing and Training: Secondary Cardiopulmonary Dysfunction 441

surviving muscle fibers. Studies show that the di­ primary foundation of rehabilitation potential. Im­
rection of therapy is to unload or rest the overused provement in breathing capacity and overall en­
muscles and shift the work of the musculature. It is durance can be accomplished through techniques to
difficult in the therapeutic setting to identify the improve posture overall. Endurance training based on
weakness that may be from PPS or weakness from graded-exercise tests is an important element in the
simple aging and inactivity. Great caution is needed rehabilitation program but should be placed 10 per­
in this situation because studies have shown that if spective to other therapeutic options.
the PPS muscles are overworked, it can result in
permanent irreversible damage. Dr. 0 presented
with the complaint of cervical pain. On evaluation,
REVIEWaUESTIONS
it became evident that the pain was related to the 1. What laboratory data are needed to determine if
cervical lordosis, resulting from the underlying a patient is a candidate for endurance training?
muscle loss aggravated by the stooped posture nec­ 2. What types of treatment can be beneficial, if a
essary for his long hours of work in the laboratory. patient is not a candidate for endurance training?
Dr. 0 primarily relied on his upper respiratory mus­ 3. What types of interventions can best help a patient
cles for breathing because of diaphragmatic paraly­ enter into a more aggressive exercise program?
sis and extensive intercostal muscle loss. Dr. 0 did 4. Is aerobic training limited to treadmi I I and bicy­
not have much time available for home exercise or cle? Think about the limitations of these modali­
for physical therapy sessions. Exercise prescrip­ ties and suggest alternatives.
tions that would isolate the weak muscles and then
focus on repetitive exercises to strengthen them
would be problematic because of the threat of tissue References
damage to muscles affected by PPS. Dr. 0 was
Astrand, P. & Rodahl, K. (1977). Physical Training. Textbook of
given one e x ercise to perform twice per day, work physiology. New York: McGraw Hill.
rolling, to roll from one end of the room to the Austin, J. (1992). Enhanced respiratory muscular function in nor­

other and back. He was guided in maintaining con­ mal adults after lessons in proprioceptive musculoskeletal edu­
cation without exercise. Che,'I, 102,486-490.
trol of the trunk musculature throughout the activ­
Basmajian, J. (1993). Rational manu.al Iherapies. Baltimore:
ity. This activity was performed semi regularly for a
Willian,s & Wilkins.
year with the goal of improving trunk strength and Black, L. (1982), Early diagnosis of chronic obstructive pulmonary
posture. Over the course of the year, endurance ex­ disease, Mayo Clinic Proceeds 57,765-772,

ercises were added using a home stationary bicycle. Braun, N, (1983), When should respiratory muscles be exercised?
Chest, 84,76.
In I year, Dr. 0 grew I 1/4 inches. He continued to
Dean, E. (1991a), Clinical decision making in the management of the
rely on the upper respiratory muscles for breathing,
late sequelae of poliomyelitis. Physical Therapy, 71.' 757-761.
but his overall improved strength and posture left Dean, E. (199Ib). Effect of modified aerobic training on move­
him pain free. ment energetics in polio survivor. Orthopedics, 14,1243-1246,
Edwards, R. (1978). Physiological analysis of skeletal muscle
weakness and fatigue, Clinical Science and Molecular Medi­
SUMMARY cine, 54,463.
Feldman, R. (1985). The use of strengthening exercises in po s t­
A multitude of therapeutic options exist for those suf­
polio seq uelae : methods and results. Orthopedics, 81.889-891.
fering with respiratory limitations. The presentation Gorman, D. The body moveable. Guelph, Ontario, Canada:Amper­
of symptomatology of dyspnea is similar in primary sand Printing Co,

lung disease and in secondary cardiopulmonary Kotses, H, (1981), "Application of biofeedback to the treatment of
asthma: a critical review, Biofeedback an d Self Regulation,
symptoms. It is crucial to understand the underlying
b,573-593.
pathology so that the therapeutic intervention and ex­
Lisboa, C. (1985), Inspiratory muscle function in patients with se­
ercise prescription reflect the potential of the patient. vere kyphoscoliosis, American Review of Respiratory Disease,
Focusing on issues of respiratory muscle fatigue is a 132,48-51.

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442 PART III Cardiopulmonary Physical Therapy Interventions

Marino, W. (1982). Reversal of clinical sequelae of respiratory Stoller. J. (1988). Oxygen therapy techniques-Current respiralol),
muscle fatigue by intermittent mechanical ventilation. Ameri­ care. Toronto: BC Della.
can Review ofRespiratOlY Disease, 125, 85. Upledger, J. (1992). Craniosacral therapy. Washington: Eastland
Owen. R. (1985). Polio residuals clinic: conditioning exercise pro­ Press.
gram. Orthopedics, 8,882-883. Weiss, H. (1991). The effect of an exercise program on vital capac­
Shneerson, J. ( 1 97 8) . The Cardio respiratory response to exercise ity and rib mobility in pa tients with idiopathic scoliosis. Spine.
in thoracic scol.iosis. Thorax, 33, 457-463. 16, 88-93.

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 Respiratory Muscle Weakness
and Training

Maureen Shekleton
Jean K. Berry
Margaret K. Covey

KEY TERMS Inspiratory muscle trainin g Respiratory muscle fatigu e

Muscle endurance Respiratory muscle w eakness
Muscle s tre ngth Wo rk of breathing

INTRODUCTION
to ventilatory failure and death. Causes of respiratory
Roussos and Macklem (1982) support the notion of a pump failure can be grouped into the following two
two-part respiratory system made up of the lungs, major categories: (I) those in which the respiratory
which are the gas exchanging organs, and a pump, drive is decreased or the sensitivity and function of
which ventilates the lungs. The pump is composed of the respiratory center is altered (i.e., those that affect
the chest wall, the respiratory muscles, and the nerves the central nervous system control), and (2) those in
and centers in the nervous system that control the res­ which the ventilatory response is decreased through
piratory muscles. The respiratory muscles are ex­ impairment of the mechanics of respiration (i.e.,
pected to function continuously throughout life to those that affect the chest wall or musculature) (Groer
p rovide the appropriate level of ventilation for meet­ and Shekleton, 1989).
ing the body's metabolic needs. The focus of this chapter is on the latter category,
Citing the analogy of the heart as the circulatory and more specifically, on the role of weakness and fa­
pump and the consequences of heart failure, Mack­ tigue of the respira tory muscles as a pathophysiologi­
lem (1982) maintains that the respiratory pump can cal mechanism seen in many clinical conditions. The
fail, leading to a condition characterized by hypoven­ view of respiratory muscle fatigue as a cause of venti­
tilation and hypercapnia that may ultimately progress latory failure is an idea becoming more widely ac­

443

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444 PART III Cardiopulmonary Physical Therapy Interventions

cepted among pulmonary clinicians (Sharp, 1984). of origin: central fatigue, transmission fatigue, or
Respiratory muscle fatigue is postulated to be the final contractile fatigue. Central fatigue is due to a de­
common pathway to respiratory failure in all condi­ crease in neural drive, which reduces the number of
tions in which the respiratory musculature is affected firing frequency of motor units. The resulting force
(Cohen, Zagelbaum, Gross, Roussos, and Macklem, generated by voluntary effort is less than that which
1982; Grassino, Gross, Macklem, Roussos, and Zagel­ can be achieved by electrical stimulation of the motor
baum, (1979); Derenne, Macklem, and Roussos, nerves. If electrical stimulation can restore contractile
1978; Roussos and Macklem, 1982). force or if stimulation and force decline in parallel,
Although both the inspiratory and expiratory res­ central fatigue is present. Transmission fatigue results
piratory muscles are susceptible to fatigue, clinically, from an impairment in the transmission of impulses
concern centers on the inspiratory muscles. The di­ along the nerves or across the neuromuscular junc­
aphragm is of particular interest. Under normal con­ tions. Contractile fatigue results from impairment in
ditions, the inspiratory muscles including the di­ the contractile response to neural impulses within an
aphragm, the external intercostals in the parasternal overloaded muscle. Both transmission fatigue and
region, and the scalene muscles are responsible for contractile fatigue are classified as peripheral fatigue.
the active process of breathing, and expiration is a Peripheral fatigue is present if force is decreased but
passive process. An analysis of the phenomenon of electrical stimulation is constant. All three types of
inspiratory muscle fatigue is presented initially in this fatigue are reversible (Mador, 1991).
chapter. This is followed by a discussion of the iden­ Peripheral fatigue can be further categorized ac­
tification and management of inspiratory muscle fa­ cording to the selective loss of contractile force that
tigue and its possible prevention through training of occurs at varying stimulation frequencies. High-fre­
the inspiratory muscles. quency fatigue is a selective loss of contractile force
at high-stimulation frequencies; low-frequency fa­
tigue is the selective loss of force at low-stimulation
THE CONCEPT Of INSPIRATORY MUSCLE fATIGUE
frequencies. High-frequency fatigue is thought to be
It is important to differentiate between muscle weak­ the result of impaired neuromuscular transmission
ness and muscle fatigue, although both may lead to and/or propagation of the muscle action potential.
hypoventilation (Bryant, Edwards, Faulkner, Hughes, This type of fatigue is seen in myasthenia gravis, dur­
and Roussos, 1979). Muscle weakness refers to a loss ing ischemic exercise, with muscle cooling, and with
in the capacity of a rested muscle to generate force partial curarization. It is reversible in minutes. The
that is chronic situation. Muscle fatigue refers to a mechanism underlying low-frequency fatigue is
loss in the capacity of a muscle under load to develop thought to be impaired excitation-contraction cou­
force or velocity that is reversible by rest (NHLBI pling. Recovery from this type of fatigue may take
Workshop Summary, 1990). Fatigue is an acute loss hours to days and possibly longer. Intense dynamic
of contractile force wherein, despite constancy of and static muscular activity can lead to low-fre­
stimulation, force declines from the initial value. If quency fatigue (Edwards, 1983; Moxham, 1990).
fatigue is the inability of a muscle to continue to gen­
erate a required force, then in the respiratory system,
Mechanisms and Etiology of fatigue
fatigue will be manifested by the inability of the in­
spiratory muscles to continue to generate the force re­ The major mechanisms thought to be responsible for
quired to maintain the necessary level of alveolar inspiratory muscle fatigue include an imbalance be­
ventilation to meet the body's metabolic needs. Inspi­ tween energy supply and demand and impaired exci­
ratory muscle fatigue occurs when inspiratory effort tation-activation. Edwards (1983) has proposed a
exceeds the capacity of the inspiratory muscles to model that accounts for the interaction of both mech­
sustain that effort (Rochester, 1982). anisms in the development of muscle fatigue. He has
Physiologically, fatigue has been characterized as also proposed the idea that fatigue serves a protective
one of the following three types, depending on its list function in that serious irreparable damage may be

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 25 Respiratory Muscle Weakness and Training 445

Possible
fatigue mechanism
Psyche
Brain

Impaired motivation
i.e. neural motor
drive and motor
unit recruitment

SP'''' Co ,d
) I mpaired reAex
drive

p",p"r ""'" Impaired neuro­

muscular transmission

Muscle sarcolemma

j
Impaired action
potential

Transverse K*, Na*, H20

,"bO', '! 'y"eo" imbalance

Impaired excitation

Ca**

1
Impaired activation
Impaired energy supply

Actin-myosin
interaction

CN" b'''g' r1 "o"' + heat Thermal damage

Sarcomere damage

Force power
OUlput

FIGURE 25-1
Chain of command for muscular contraction and the possible mechanisms underlying fatigue.
(From Edwards, R.A.T. (1983). Biochemical basis of fatigue in exercise petformance: Catasptrophe
theory of muscular fatigue. In Knuttgen, H., Vogel, J., Poortmans, 1. (Eds.). Biochemistry of
exercise. Champaign, Ill. Human Kinetics Publishers.).

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446 PART III Cardiopulmonary Physical Therapy Interventions

prevented if the muscle is unable to continue per­ pattern of fiber distribution is most pronounced in
forming beyond a critical point. The central nervous the premature infant. This condition exists in infants
system may exert a protective mechanism to avoid for up to a year after birth.
these adverse effects. This idea has persisted and the The energy supply to the muscles depends on an
term central wisdom is used to describe the phenome­ intact oxygen transport system, adequate oxygen-car­
non (Moxham, 1990) (Figure 25- I, p. 445). rying capacity of the blood, blood tlow, substrate
The energy demands of the inspiratory muscles stores and availability, and the efficiency of oxygen
are determined by the work of breathing, the strength uptake and uti lization by the muscles. The energy
and endurance of the respiratory muscles, and the ef­ supply to the inspiratory muscles is compromised
ficiency of the muscles. The work of breathing is the when cardiac output is reduced, the hemoglobin con­
total amount of effort required to expand and contract tent of the blood is low, blood flow to the muscles is
the lungs. It is determined by the degree of compli­ decreased, or energy substrates are lacking.
ance of the lung tissue and the chest wall, the resis­ Excitation-activation depends on intact, function­
tance of the airways, the presence of active expira­ ing, neuromuscular pathways. Impaired excitation-ac­
tion (normally a passive process), and use of the tivation is probably the primary mechanism underlying
accessory muscles of respiration. The work of breath­ respiratory muscle weakness and fatigue in the patient
ing is increased by decreased pulmonary compliance, with a neuromuscular disorder (Edwards, 1979). Dis­
increased airway resistance, active expiration, and ruption of excitation-activation can occur at any point
use of the accessory muscles. along this pathway, which Edwards (1983) refers to as
Strength and endurance are the fundamental prop­ a chain of command for muscular contraction. Pre­
erties of muscle. Strength is defined as the maximal sented in Figure 25-1 is a list of the possible mecha­
force that a muscle can develop with maximal stimu­ nisms that may lead to fatigue by disrupting the neuro­
lation. Contractile force is governed by the force­ muscular pathway. Impaired excitation of the muscle
length (length-tension), force-velocity, and force-fre­ membrane is probably interrelated with energy metab­
quency relationships. Contractile force diminishes in olism. For example, if the ATP supply to the Na+ - K+
conditions characterized by increased lung volume pump is compromised, an alteration in the Na+ and K+
(hyperinflation), since the muscles are stretched be­ concentrations in the transverse tubular system may re­
yond the optimal length to generate maximal force. sult in impaired excitation-contraction coupling.
This stretching of the muscle fibers produces a less Although it is difficult to demonstrate the precise
desirable length-tension relationship and causes a mechanisms causing respiratory muscle fatigue in pa­
loss of the zone of apposition, with resulting decrease tients, support is found for the concept that central
in strength generation. Strength is also determined by nervous system output is modified to avoid overt fa­
the number and size of individual fibers in a muscle. tigue. With extremely high loads imposed on respira­
Strength is adversely affected in conditions in which tory muscles, patients adopt a rapid shallow pattern
the size of the fibers is reduced (atrophy) or the num­ of breathing that reduces the work of breathing and
ber of fibers is reduced (e.g., in malnutrition). can be sustained. Eventually, this pattern of rapid
Endurance is defined as the ability to maintain a shallow breathing will lead to hypercapnia and acido­
contraction against a given load and is determined sis (Moxham, 1990).
by muscle fiber type, blood supply, and the force In summary, those patients who are at risk for the
and duration of the contraction. Normally, the inspi­ development of inspiratory muscle fatigue are those
ratory muscles are fatigue resistant. Approximately in whom energy demands are increased, energy sup­
75% of the muscle fibers in the adult diaphragm are plies are compromised, or whose neuromuscular
of the high oxidative, fatigue resistant type (type I chain of command has been disrupted at some point.
and type IIA). In contrast the diaphragm of the Patients at highest risk for the development of inspi­
neonate contains a relative paucity of type I fibers ratory muscle fatigue are those in whom the work of
that have the greatest endurance capacity, and this breathing is increased, thus increasing the demands

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 25 Respiratory Muscle Weakness and Training 447

for energy, and those who are experiencing hypox­ power spectrum, which is indicative of muscle fa­
emia, acidosis, low cardiac output, or any other con­ tigue in normal subjects exercised to fatigue, in pa­
dition in which the blood supply to the muscle is di­ tients experiencing difficulty being weaned from me­
minished, thus reducing oxygen supply. Patients chanical ventilation, and in animals in whom fatigue
whose nutritional status is poor or who are experienc­ was experimentally induced. When fatigue is present,
ing a catabolic state, such as stress or fever, will have the ratio of high-to-low frequency power, which can
reduced energy stores and may experience muscle fa­ be detected by EMG, shifts as low-frequency power
tigue during times of high need. increases and high-frequency power decreases. The
difficulty in obtaining an EMG at the bedside and in
analyzing the results makes its use in most clinical
Assessment of Fatigue
situations unrealistic at this time.
The clinician will most often have to rely on physi­ In summary, rapid shallow breathing is the initial
cal signs exhibited by the patient to recognize inspi­ sign of inspiratory muscle fatigue (Yang and Tobin,
ratory muscle fatigue. Other laboratory methods that 1991). The physical signs previously described are
would yield more objective evidence of inspiratory reliable and can be used in a clinical situation to de­
muscle fatigue include power spectral analysis of the termine whether the patient is experiencing inspira­
electromyelogram (EMG), measurement of the max­ tory muscle fatigue.
imal relaxation rate, and examination of twitch oc­
clusion pressure.
Treatment of Fatigue
The following signs are indicative of inspiratory
muscle fatigue and are listed in their characteristic The goals of treating inspiratory fatigue are as fol­
order of appearance: lows: (I) restore the balance between energy supply
I. Tachypnea and demand, (2) improve diaphragmatic contractility,
2. Decreased tidal volume and (3) increase the strength and endurance of the in­
3. Increased PC02 (which is a late sign) spiratory muscles. The last goal is obviously a more
4. Bradypnea and decreased minute ventilation long-term preventive approach, whereas the first two
Formerly, development of a discoordinated respi­ goals apply in the more acute situation when inspira­
ratory pattern characterized by inward abdominal tory muscle fatigue is present.
movement on inspiration (a sign referred to as ab­ Energy demands in the patient experiencing fa­
dominal paradox) and alternating abdominal and tho­ tigue can be decreased by reducing the work of
racic respiratory patterns (a sign referred to as respi­ breathing through activities intended to promote
ratory alternans) were t h o u gh t to result f r o m compliance, decrease resistance in the lung, chest
respiratory muscle fatigue. Presently, these changes wall and airways, and promote normal lung volumes
in breathing patterns are thought to result from in­ and pressures. Energy supplies can be enhanced by
creases in respiratory load rather than muscle fatigue ensuring maximal oxygen transpOit to the tissues and
(Mador, 1991; Tobin, Perez, Guenther, Lodato, and the availability of adequate amounts of oxygen and
Dantzker, 1987). However, discoordinated respira­ other energy substrates. Oxygen transport is en­
tory patterns are important clinical signs of respira­ hanced by promoting adequate cardiac output, blood
tory distress and, although they are not specific in flow to the tissues, and oxygen-carrying capacity of
their etiology, they are sensitive indicators of impor­ the blood. Various forms of respiratory therapy are
tant declining respiratory function. available to supplement oxygen supplies. Losses of
In animals in whom inspiratory muscle fatigue has organic and inorganic energy in substrates must be
been experimentally induced the fall in respiratory replenished and adequate levels maintained. Nutri­
rate and minute ventilation immediately precedes res­ tional supplementation and administration of elec­
piratory arrest and death. This sequence of events has trolytes and inorganic phosphate may be necessary to
been observed after an initial change in the EMG augment energy supplies. Rest therapy with mechani­

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448 PART III Cardiopulmonary Physical Therapy Interventions

cal ventilation may be required to allow the fatigued plished by training the inspiratory muscles in much
muscle to recover and to bring energy supplies and the same way that athletes train and condition their
demand into balance. muscles. Inspiratory muscle training may represent a
Much current research is being done in the area of useful clinical approach to prevent the development
pharmacological interventions to improve diaphrag­ of inspiratory muscle fatigue in those patients who
matic contractility. Aminophylline w as initially are at risk.
thought to increase the contractile force of the di­
aphragm at any given level of activation, but further
INSPIRATORY MUSCLE TRAINING
research indicates that this drug increases muscle en­
ergy consumption and potentiates fatigue (Janssens, Inspiratory muscle training (lMT) is currently used in
Reid, Jiang, and Decrarner, 1988). Other drugs with pulmonary rehabilitation to increase the strength and
inotropic properties are the beta-agonists. Clinical in­ endurance of the inspiratory muscles. Patients with
vestigation of the potential usefulness and application chronic obstructive lung disease experience func­
of these pharmacological agents in inspiratory muscle tional weakness of the respiratory muscles, which can
fatigue is ongoing. contribute to dyspnea and functional impairment.
The last goal, that of increasing the strength and Theoretically, IMT should reduce dyspnea by im­
endurance of the inspiratory muscles, can be accom­ proving respiratory muscle function and exercise tOI-

RespiralOn' muslle Ir,lillillg

I
i Sirengill ,tlld cndurancc of respiralon' llluscies

I
Delay lhe onsel of
respiralory llluscle faligut'
IllllJrOl'e
I
Prel'em/dcler I hc Ollsel of
I
Illlpn)IT lissuc o"ygemllio)l
1'espi1';lIOl} insuUiciell(Y allcl • cog"niliol1
faliguc pcn:cplion
pS)Tilo-lllOI01' hlllCiioll

ImpnJl' 1m p1'Ol'c
signs anc! "mplOms \\ell-being.

Improl't' IlllprOl'c
tlaih liling life

FIGURE 25-2
Conceptual framework for respiratory muscle training. (From Kim M: Respiratory muscle training:
Implications for patient care . Hearl and Lung. 13(4):333-40).

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 25 Respiratory Muscle Weakness and Training 449

erance. These effects have yet to be demonstrated in developed a model that outlines the relationship be­
large, controlled studies (Smith, Cook, Guyatt, Mad­ tween the effects of a respiratory muscle training and
havan, and Oxman, 1992). potential patient outcomes (Figure 25-2).
General principles of skeletal muscle training that Inspiratory muscle training has been used to suc­
must be considered when designing and evaluating an cessfully increase muscle strength and endurance in
IMT program for respiratory patients include over­ healthy volunteers and in patients with chronic air
load, specificity, and reversibility. To train a muscle flow limitation (Belman and Mittman, 1980; Larson,
to improve its functional ability, the muscle must be Kim, Sharp, and Larson, 1988), cystic fibrosis
subjected to a stress greater than its usual load (over­ (Keens, Krastens, et ai, 1977). Early Duchenne mus­
load), the training must be directed at developing spe­ cular dystrophy (Wanke et aI, 1994), and in those
cific functional attributes (e.g., strength or endurance) who are quadriplegic (Gross, et ai, 1980).
of the muscle (specificity), and the training must be Theoretically IMT in patients experiencing acute
maintained or function will revert back to pretraining respiratory failure should promote improved function
levels (reversibility) (Kim, 1984; Sharp, 1985). of the muscles, and fatigue resistance should facili­
The effects of strength training on the respiratory tate the process of weaning these patients from me­
muscles may include an increase in the size (hypertro­ chanical ventilation. In conditions requiring full ven­
phy) and number of the muscle fibers by an increase tilatory support, the respiratory muscles may contract
in protein synthesis by the muscle fibers and a de­ at minimal levels for a period of time, possibly lead­
crease in degradation. Endurance training of the inspi­ ing to the development of disuse atrophy. As their
ratory muscles is thought to promote an increase in strength and endurance decrease, the inspiratory mus­
the proportion of fatigue-resistant fibers in the di­ cles will be more prone to fatigue because of the in­
aphragm, an increase in the metabolic capability of teraction of disuse, the underlying pathophysiological
the muscle, and a reduction in the susceptibility of state, and catabolic effects of stress. The ultimate ef­
muscle fibers to the deleterious effects of exercise fect of these interacting processes will be difficulty in
(Leith and Bradley, 1976). Newer evidence suggests weaning the patient from the ventilator. An EMG pat­
an improvement in neuromuscular coordination and tern of fatigue has been documented in the ventila­
efficiency resulting from training (McComas, 1994). tory muscles of neonates who experienced difficulty
Strength training to increase the size and number of in weaning (Muller, Gulston, and G ade, 1979).
myofibrils requires a high load and a slow rate of rep­ Grassino et al. (1979) found an EMG fatigue pattern
etition. Endurance training to increase the metabolic in a patient being weaned from mechanical ventila­
capability of the muscle requires exercise of a suffi­ tion. Cohen et al. (1982) found an EMG pattern of fa­
cient load, speed, and duration, such that cellular con­ tigue in 7 of 12 patients who experienced difficulty
centrations of energy producing substrates drop to during discontinuation of mechanical ventilation.
minimal levels (Kim, 1984). Endurance training of Resolution of the fatigue pattern was observed in
skeletal muscle has been found to be most effective those neonates who recovered and in adult patients
when brief periods of fatiguing exercise are alternated who were successfully weaned (Andersen, Kann,
with periods of rest (Aldrich, 1985) and this concept Rasmussen, Howardy, Mitchell, 1978). There is some
may be applied to inspiratory muscle training regimes. evidence that respiratory muscle training may prove
Improvement in the strength and endurance of the to be an important adjunct therapy to facilitate wean­
inspiratory muscles through training has the twofold ing in the patient who requires mechanical ventilation
effect of enhancing the resistance to inspiratory mus­ of acute respiratory failure (Aldrich and Karpel,
cle fatigue and improving ventilatory function. The 1985; Aldrich et ai, 1989; Shekleton, 1991). How­
work of breathing is reduced and respiratory reserves ever, controlled studies have not been conducted in
are increased. Because the clinical signs and symp­ this patient population.
toms are diminished, the ultimate outcome for the pa­ Two techniques have been used for inspiratory
tient is an improved quality of life. Kim (1984) has muscle training: isocapnic hyperventilation (also

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450 PART III Cardiopulmonary Physical Therapy Interventions

called isocapnic hyperpnea) and inspiratory resistive

or resistance breathing. Isocapnic hyperventilation is
dynamic and is used to increase the endurance of the
inspiratory muscles. Expiratory muscles will benefit
as well with this technique. Patients are asked to
breathe at the highest rate they can manage for 15 to
30 minutes. A rebreathing circuit or the addition of
CO2 to the inspired air must be used with this tech­
nique to prevent hypocapnia (Belman, 1981; Belman,
and Mittman, 1980). Because of this requirement, the
usefulness or this technique will be limited until
portable, inexpensive, easy-to-use equipment for
home use is developed.
I nspi r a t o r y r e s i s t i v e b r e a t h i n g a l l o w s b o t h
strength and endurance training, since i t incorporates
both isometric and isotonic exercises. There are two
devices available for this purpose, a nonlinear device
and a threshold JMT device (Figure 25-3). The non­
linear device has been noted to produce unreliable
training loads if the rate of inspiratory flow is not
controlled (Guyatt, Keller, Singer, Halcrow, and
Newhouse, 1992). With a controJI.ed rate of breath­
ing, patients inspire through a narrow tube that offers
a nonlinear airway resistance for one to three daily
FIGURE 25-3
periods of 15 to 30 minutes. The size of the orifice
Handheld resistive breathing training devices. A, Threshold;
through which the patient inspires is adjusted to pro­
resistance level is altered by tightening screw to increase
vide a level of resistance that the patient can tolerate
tension on the spring. B, P-Flcx; resistance level is altered
without becoming immediately exhausted. In addi­ by changing settings on dial.
tion, this device is not well suited for stronger pa­
tients, since they have difficulty achieving a satisfac­
tory tidal volume with the extremely small orifice at Potential outcomes of a training program geared
higher loads. With the tllreshold device, a reliable in­ toward increasing inspiratory muscle strength and
spiratory pressure load is provided regardless of air­ endurance might include any of the following, de­
flow rate. The load is adjusted by a nurse therapist, pending on the individual patient's conditions and
or patient according to a desired percentage of the goals of treatment: (I) prevention of acute deteriora­
patient's maximal inspiratory pressure (PImax). Usu­ tion of respiratory status and ventilatory failure,
ally, the patient begins training at a low load, equal (2) improvement of ventilatory function and de­
to about one third of the PImax and progresses slowly crease in the work of breathing, which may lead to
in small increments adjusting a screw to alter the ten­ an increase in general exercise tolerance and an im­
sion until the training load reaches 60% of the cur­ proved quality of life as tissue oxygenation improves
rent PImax. The threshold device delivers a reliable and signs and symptoms are attenuated (Pardy,
tension because the poppet valve at the end of the de­ Pardy, Rivington, Despas, and Macklem, 1981a;
vice will not open and allow inspiration unless the 1981b), (3) extension of time before onset of respira­
patient generates the designated negative pressure. tory muscle fatigue, and (4) facilitation of the wean­
Both types of devices are hand held and pOltable and ing process in acute respiratory failure patients who
are easily used and maintained by patients. are being mechanically ventilated.

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 25 Respiratory Muscle Weakness and Training 451

SUMMARY
Edwards, RAT (1979). The diaphragm as a muscle: Mechanisms
Inspiratory muscle training and conditioning is a newer underlying fatigue. American Review of Respiratory [iseases.

area of research and treatment for the respiratory pa­ fJ9, (2 pt 2),81-84.
Edwards, RAT (19 83). Biochemislry of Exercise. Champaign, lL,
tient. As such, further validation of its efficacy and tar­
Human Kinetics Publishers.
geting of specific patient populations at greatest risk
Grassino, A., Gross, D., Macklem, P., Roussos, c., & Zagelbaum, C.
for loss of inspiratory muscl strength will define its (1979). Inspiratory muscle fatigue as a factor limiting ex.ercise.
use in pulmonary rehabilitation programs. At this time, Bullelin European de Physiopalhogie Re.lpiraloire, 15, 105-111.

inspiratory muscle training looks promising as a means Groer, M., & Shekleton, M. (1989). Basic palhophysiology: A
holistic approach. (ed. 3). St. Louis, Mosby.
of offering the respiratory patient one possible method
Gross, D., et al. (1 980) . The effect of training on strength and en­
of control over disease processes that are most often
durance of the diaphragm in quadriplegia. American Journal of
very debilitating and unrelenting in their course. Medicine. 68, 27-35.
Guyatt, G., Keller, J., Singer, J., Halcrow, S., Newhouse, M.
(1992). Controlled trial of respiratory muscle t raining in
REVIEW QUESTIONS chronic airtlow limitation. Thorax, 47, 598-602.
Janssens, Reid Jiang, & Decrame r. (1988).
I. What are three types of respiratory muscle fatigue?
Jardim, J., et al. (1982). Inspiratory muscle conditioning training in
2. Name two major mechanisms thought to be re­ chronic obstructive pulmonary disease (COPD) patients. Amer­
sponsible for inspiratory muscle fatigue. ican Review ofRespiralory Diseases, 125. (pt 2 of 2), 132.

3. What factors determine the work of breathing? Keens, T., et al. (1977). Ventilatory muscle endurance training in
normal subjects and patients with cystic fibrosi s . American Re­
4. What is the initial physical sign of inspiratory
view ifRespiralory Diseas'es, 116, 853-860.
muscle fatigue?
Kim, M.J. (1984). Respiratory muscle training: I mplic at io ns for
S. What rehabilitation techniques should be used to patient care. Hearl and Lung, 13, (4),333-340.
increase the strength and endurance of the inspi­ Larson, M., Kim, MJ. (1984). Respiratory muscle training with the

ratory muscles? incentive spirometer resistive breathing device. Hearl (lnd

Lung, 13. (4),341-345.
Leith, D., Bradley, M. (1976). Ventilato ry muscle strength and en­

References traini ng. Journal of Applied Physiology, 41, 508-516.

durance
Macklem, P. & Roussos, C. (1977). Respiratory muscle fatigue: A
Aldrich, T (1985). The application of muscle endurance training cause of respiratory failure1 Clin Sci Mol Med, 53, 419-422.
teChniques to the respiratory muscles in COPD. Lung, 163, 15-22. Macklem, P.T (1982) The diaphragm in health and diseas e. Jour­
Aldrich, T (1984). Inspiratory muscle resistive training in respira­ ncd ojLaborolory and Clinical Medicine. 99. 601-610.
lory failure. CheSl. 86(2), 302. Mador, JJ. (1991). Respiratory muscle fatigue and breathing pat­
Aldrich, TK., Karpel, J.P., Uhrlass, R.M., Sparapani. M.A., Erami, tern. Chesl, 100, 430-435.
D., Fen·anti. R. (1989). Weaning from mechanical ventilation: Martin, L. (1984). Respiratory musc l e function: A clinical study.
Adjunctive use of inspiratory muscle resistive traini.ng. Hearl and Lung. /3,346-348.
Andcrsen, J., Kann, T, Rasmussen. J.P. , Howardy, P. & Mitchell, McComas, A. (1994). Human neuromuscular adaptations that ac­
J. (1978). Respiratory thoracoabdominal coordination and mus­ company changes in activity, Medicine and Science in Sporls
cle faligue in acute respiratory failure. American Review of and Exercise, 26, 1498-1509.
Respimlorv Dis('(I.I'es, 117 (2),89. Muller, N., Gulston, G., Cade, 0., et al. (1979). Diaphragmatic
Belman, M. (1981). Respiratol)' failure treated by ventilatory mus­ muscle fatigue in the newborn. Journal of Applied Physiology,
cle training: A report of two c a se s. European Journal of Respi­ 46, 688-695.
ralorv Di.l'eoses, 62, 391-395. Moxham, J. (1990). Respiratory muscle fatigue: mechanisms, eval­
Bryant, S., Edwards, R., Faulkner, .I., Hughes, R.L., & Roussos, C. uation and therapy. Brilish Journal ofAnaeslhesia, 65, 43-53.
et al. (1986). Respiratory muscle failure: Fatigue or weakness. National Heart Lung Blood Institute Workshop Summary (1990).
Chesl, 89. (1),116-124. Respiratory muscle fatigue: report of the respiratory muscle fa­
Cohen, c., Zagei bau 111, G., Gross, D., et al. (1982). Clinical mani­ tigue workshop group. American Review of Respiralory Dis­
festations or inspiratory muscle fatigue. American Journal of ea se, 142,474-480.
Medicine, 72, 308-316. Pardy, R.L., Rivington, R.N., Oespas, PJ., & Macklem, P.T.
Derenne, J., Macklem, P., Roussos, C. (1978). The respiratory (l981a). The effects of inspiratory muscle training on exercise
muscles: Mechanics, control, and pathophysiology, Part III. performance in chronic airtlow limitation. American Review of
American Review ofResfliralOry Diseases. 118. 581-60 I. Respiralory Diseases, 123. 26-433.

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Copyrighted Material
 Patient Education

Alexandra J. Sciaky

KEY TERMS Education Methods

Effectiveness Needs assessment
Health behaviors Resources
Learning theory

INTRODUCTION
in their care. Unless effective patient education is im­
In cardiopulmonary physical therapy, sound treat­ plemented this opportunity will be lost.
ment is based on the physiological assessment of the The overall objective of this chapter* is to provide
patient. Similarly, effective patient education is based the clinician with an understanding of the principles
on the learning needs assessment of the patient and practice of effective patient education. To meet
(Rankin & Stallings, 1990). Cardiopulmonary patient this objective, patient education is defined and perti­
education poses a significant challenge because the nent learning theories with examples of how they re­
physical therapist's duties can range from teaching a late to cardiopulmonary patient education are pre­
hospitalized cardiac patient to do a self pulse check to sented. The learning needs assessment of the patient
designing a series of community-based exercise is explained, followed by a description of patient edu­
classes for senior citizens with emphysema. Meeting cation methods and materials. Because the effective­
this challenge is important because the benefits of pa­ ness of patient education efforts are important to
tient education include reduced health-care costs, re­ evaluate, ways to determine this are addressed. Fi­
duced patient anxiety, increased patient knowledge,
satisfaction with care, and incrcased quality of life. In
addition, physical therapists share the responsibility
'The author wishes to thank Jennifer L. Wai ters, D. Min. and
with other health-care providers of ensUling that pa­ Patricia Wren, MPH for their expertise in education and assistanc e
tients have the opportunity to make informed choices in preparing this man uscri pt
.

453

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454 PART III Cardiopulmonary Physical Therapy Interventions

nally, interdisciplinary considerations and educa­

Patient Education Objectives
tional resources are discussed.
I. Enhanced patient-clinician rapport

2. I n creased p a t i ent knowledge of he alth

DEFINING PATIENT EDUCATION
disorder/condition
Physical therapists believe that patient education is an 3. Increased adherence to physical therapy treat-
i m p o r t a n t part of t r e a t m e n t (C h a s e , E l k i ns, ment plant
Readinger, and Shepard, 1993). The teaching role of 4. Decreased health-care costs
the physical therapist has been reported as highly val­
5. Increased patient self-efficacy
ued by patients as well (Grannis, 1981). According to
6. Increased ability to make informed health-care
Bartlett (1985), patient education is "a planned learn­
choices
ing experience using a combination of methods such
as teaching, counseling, and behavior modification
techniques which influence a patient's knowledge
and health behavior." patient education program, and finally evaluating its
Several factors make patient education unique effectiveness. Specific examples of patient education
when compared with other types of teaching. The pa­ learning objectives are listed in the box above.
tient may have limited or no access to the teaching Achieving these objectives will lead to the enjoy­
because of financial and/or geographical barriers to ment of a host of documented benefits of patient edu­
health care. The student may lack a sense of well­ cation. These include reduced length of hospital stay
being because of signs and symptoms of an acute ill­ (Devine & Cook, 1983), reduced patient anxiety
ness, making learning more difficult. The relationship (O'Rourke, Lewin, Whitcross, and Pacey, 1990), im­
between the teacher and the learner in patient educa­ proved health-related knowledge (Rowland, Dickin­
tion may be perceived as hierarchical-a medical au­ son, Newman, and Ebrahim, 1994), increased quality
thority figure instructing a lay person. The student's of life (Manzetti, Hoffman, Sereika, Sciurba, and Grif­
emotional status may be fearful or anxious, depend­ fith, 1994), and improved response to and adherence
ing on the medical situation. There may be superim­ with medical treatment (Mazzuca, 1982). Patient edu­
posed time constraints, such as length of hospital stay cation has also been shown to empower patients to
or clinic appointment, which have a direct impact on take more active roles in their health care (Smith,
patient education. All of these factors may pose barri­ 1987). Patients who are educated partners in their care
ers to learning. As in other types of teaching, how­ are able to be smart consumers in the health-care sys­
ever, patient education is information shared in the tem and adapt more readily to changes in their life
hope that it will not only be understood but applied in styles resulting from illness.
ways that produce the desired changes in health­
related behavior.
Learning Theory: Concepts Pertinent to
Cardiopulmonary Patient Education
Objectives
The American Physical Therapy Association's Com­
The overall objective of patient education is to affect mission on Accreditation of Physical Therapy Educa­
'
a durable cognitive improvement that results in a pos­ tion (1990) requires that the graduate physical thera­
itive change in an individual's or group's health be­ pist be able to "... apply concepts of teaching and
havior. In many cases the physical therapist must em­ learning theories in designing, implementing and
bark on a process to meet this objective in the course evaluating learning experiences used in the education
of treatment. This process consists of assessing the of patients." Twentieth century behavioral scientists
learning needs of the patient, identifying measurable, have developed a variety of learning theories and
realistic objectives, planning and implementing the models attempting to explain the complexities of

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 26 Patient Education 455

human behavior. Subsequent models have pm,, r'(7pf1

that address health behavior. Although a

discllssion of these models is
the scope of this a list of references for fur­ receives on energy
ther reading may be found at the end of this conservation techniques from the staff (verbal persua­
The discussion of the three theoretical sion), and notes that oxygen saturation measured 95%
which follows is to the clinician before state).
with a rationale for patient education practice in The health-belief model, in the early
terms of its basis in learning The concepts are 1950s, theorizes that are likely t o take a
theory, the health-belief and health action in the situations: (I) be-
the behavior-modification approach, Iieve are at risk of illness; they believe that
The theory as by Ban­ the disease poses serious threat to their lives should
dura (1986) that human behavior can be ex- they contract it; they desire to avoid illncss and
believe that certain actions will prevent or reduce the
of the and believe that taking
a myocardial infarction the health action is less than the illness it­
value in following the exercise pro­ self (Roenstock, 1974). This model was originally de­
gram This will attempt to exercise veloped in an attempt to understand why num­
if he or she believes his or her current life bers of people failed to accept care or
poses a threat to health. The tests for early disease detection. Subse­
lieves exercise will reduce that threat (outcome ex­ quent studies have used the model to compli­
pectation) and that he or she personally of ance with for asthma, and dia­
the exercise program betes , 1985).
Outcome and re­ The health-belief model conveys that in the con­
late to patients' beliefs about their capabilities and text of health behavior some stimulus or "cue to ac­
the of their behaviors to successful out­ tion" necessary to initiate the
comes, In essence behavior is i nfluenced by process. These cues can be internal a productive
that create expectations for similar out­ cough) or external instructional video tape on
comes over time. pulmonary hygiene Once the behavior
To function competently in a environment commences, it is understood that many UUHV,",''''Ull

a belief in one's ability to attain a certain structural, and social elements are
level of Bandura terms this se(refficacy of the behavior. In
He argues that percei ved sel f­ barriers unpleasant side may limit or
efficacy influences all aspects of behavior including prevent undertaking the recommended behavior.
new skills and inhibiting or current The behavior-modification has its roots
behaviors, has the four pri­ theory and consists of
mary determinants: (I) performance accomplish­ environmental rewards and
ments, the strongest refers to ments in relationship to a specified behavior
the desired behavior and mastery over the man, 1993). The theme of this approach that an in­
in increased dividual's behavior can gradually be
involves learning a set t o Becker (1
others, Iy those with rewarding out- behavior-modification frequently follows a
comes; (3) verbal and (4) one's physiolog- plan: "identify the problem; describe the
ical state as it relates to ability to perform a in behavioral terms; select a behavior
task. For example, a pulmonary rehabilitation that is identify the antecedents and con-
program increases a when he or set behavioral

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456 PART III Cardiopulmonary Physical Therapy Interventions

Health Care Contract

Date: _ _ _ _ _ __ __

Contract Goal: (Specific outcome to be attained)

I. (client's name), agree to (detailed descriptioll of required behaviors, time and frequency limitations)

in retun! for (positive reinforcements contingent upon completion of required behaviors: timing and mode of delivery
of reinforcements)

I. (provider's name), agrees to (detailed description of required behaviors, time and frequency limitations)

(Optional) I, (significant other's name), agree to (detailed description of required behaviors, time and frequency
limitations)

(Optional) Aversive consequences: (Negative reinforcements for failure to meet Illinium contract requirements).

We will review the terms of this agreement, and will make my desired modifications. on (date). We hereby agree to
abide by the terms of the contract describe above.

Signed: (Client) _ _ __ ____ _ __ _ __ _ _ __ _ ___ _ _ _

_
___ __

Signed: (Significant other. if relevant). ____ ________ ______ _______

Signed: (provider) ___________________ ________ _____

Contract effective from (Date) to (Date) _______ _____

(From Janz NK, Becker MH, Harlman PE: Parienr Educ COUllS 5(4): 165-178, 1984).

devise and implemellt a behavior change program; to facilitate the desired behaviors in the patient. Ide­
and evaluate the program." This plan is very similar ally, once the contract expires, the patient feels com­
to the approach the physical therapist takes on being petent and is able to continue the desired behaviors
referred to evaluate and treat a patient. The physical without the external reinforcements.
therapist identifies the patient's deficits, describes
the problem(s) in functional terms, sets short-term
NEEDS-BASED APPROACH TO PATIENT EDUCATION
and long-term functional goals, designs a treatment
plan to meet those goals, implements the treatment The most important aspect of planning for patient ed­
plan and reevaluates the patient. These similarities ucation is assessing the learners (Kopper, 1987). The
may facilitate the use of the behavioral-modification process of patient education requires assessment of
approach by physical therapists. the total patient, including an understanding of the
Health-care contracts can be useful in implement­ psychosocial, socioeconomic, educational, vocational,
ing the behavior-modification approach. An example and cultural qualities of the person (Verstraete and
of such a contract may be seen in the box above. The Meier, 1973). Assessing educational needs of the pa­
contract should be realistic, measurable, and renew­ tient allows the physical therapist to determine what
able (Herje, 1980). Specific goals, time frames, be­ the patient needs to know to meet the desired cogni­
haviors, and contingencies are written in the contract. tive and behavioral teaching objectives. This assess­
The clinician and patient discuss, then sign the con­ ment also increases patient-teacher rapport and pre­
tract. Positive and negative reinforcements are used vents needless repetition of already familiar material.

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 26 Patient Education 457

LEARNING NEEDS ASSESSMENT Learning Needs Assessment Areas

Tools
Perceptual
Learning needs can be assessed in a variety of ways. Ability to receive input (vision, hearing, and touch)
These include patient and family interviews, ques­
Comprehension of symbols (figures, numbers,
tionnaires and surveys, written tests, and observation words, and pictures)
of patient performance (Haggard, 1989). Interviews
Cognitive
allow the physical therapist to ask questions directed
Knowledge and analytical skills
at determining the patient's view of the illness, in­
cluding associated beliefs and attitudes. Question­ Memory

naires and surveys can be used in conjunction with Motor

the interview to document the patient's responses to Fine- and gross-motor skills
specific questions about his or her condition. Open­ Physical adaptations and responses to illness or
ended questions such as "What are the major prob­ stimuli
lems your illness has caused for you and your fam­ Affective
ily?" elicit more information than a multiple-choice
Attitudes
format. Written tests can be helpful in determining
Value-belief system
what patients already know when the tests are given
before any teaching. These tests can also identify Motivation (readiness to learn)

problems with reading and comprehension skills. Ob­ Environmental

serving patients as they perform a skill, such as di­ Personal and societal resources
aphragmatic breathing, reveals whether or not the pa­ Amount of instructor contact and setting
tient can demonstrate the correct technique. The
Cultural influences (language. traditions, roles,
physical therapist can also pose questions to the pa­ religion. and life style)
tient during the demonstration to determine whether
or not the patient knows the rationale for the exercise.

The cognitive area addresses the learner's knowl­

Areas to Assess
edge and problem-solving skills. The instructor needs
The learning needs assessment encompasses the fol­ to know how much the learner already knows and
lowing five major areas: (I) perceptual, (2) cognitive, what needs to be learned. The instructor also needs to
(3) motor, (4) affective, and (5) environmental (see know if the learner has any problems with memory.
the box at right). By addressing these five areas, the Short- or long-term memory deficits may require that
physical therapist will obtain an accurate picture of the instructor integrate a prompting system into the
the patient's learning abilities, knowledge level, per­ education plan.
formance skills, attitudes, and cultural influences. The patient's fine- and gross-motor skills and func­
The perceptual area encompasses the learner's tional mobility are covered in the motor area. The in­
ability to receive information via the senses. If the structor needs to be aware of the physiological
learner's sight, hearing, or sensc of touch is impaired, changes in the patient that affect abilities to perform
the instructor may need to makc modifications so that activities necessary for a given education program.
the information can be received by the learner. The For example, if a support group is being held in a
comprehension of symbols. such as numbers, words, room that is not wheelchair accessible, patients who
or pictures. also needs to be assessed in the percep­ are wheelchair users will not be able to readily attend.
tual area. The instructor nceds to know what meaning The affective area comprises the learner's attitudes,
the learner attributes to the symbols that will be used beliefs. and readiness to learn. Identifying the learner's
in the education program to ensure clarity. value-belief system will assist the instructor in deter­

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458 PART III Cardiopulmonary Physical Therapy Interventions

Learning Needs Assessment Survey

Your physical therapist would like to help you learn what you need to know to function as independently as possible
and manage your illness/disability. Please answer the following questions to identify your own needs.

Part I.

Name:
Your illness and/or disabi Iity is:

J. Do you have any problems seeing or hearing?

2. Do yu have any body areas which are numb (can't feel)?
3. How long have you had this illness/disability?
4. What problems has it caused you?
5. Are you able to care for yourself at home?
6. Are you responsible for the care of any others at home?
7. Do you have someone at home to help you? If so, whom?
8. What questions or concerns do you have?
9. Do you practice a religion? If so, which?
10. The language you understand best is?
I I. How much education/schooling have you had?

Part II. There are many different ways to learn. Please read the list of ways to learn below and circle the ones which
help you learn best.

Reading materials Group discussion

Lectures (listening) By myself

Demonstrations watching) Games

Videos Computer programs

Audiotapes (cassettes) Seminars

Practice/Stimulation (doing) Role playing

Written tests Other

Part III I would like to know more about: (Check all that apply to you.)

How to clear mucus from my lungs What causes heart disease

How to avoid shortness of breath What I should eat

Exercise My medications

Monitoring myself Planning my social life

What to do if I have chest pain Planning for sexual intimacy

What causes lung disease Coping with my feelings

Other things J would like to know:

The three most important things I need to know are:

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 26 Patient Education 459

mining what is important to the learner and facilitate learning activities. By identifying the patient's needs
motivation. What the instructor feels is important to the physical therapist can then make informed
learn may not be what the patient feels is important to choices in the course of planning and implementing
learn. Identifying what the patient values early will each patient education experience.
prevent instructor (and patient) frustration later.
Cultural influences and personal and societal re­
Formulation and Prioritization of Goals
sources are included in the environmental area. Being
aware of the patient's life style, religion, traditions, As physical therapists set treatment goals for their pa­
roles, and primary language are important for the in­ tients, they should also set educational goals. Treat­
structor to assess to individualize the patient's learn­ ment goals usually describe functional outcomes
ing experience. Presence or absence of the patient's (e.g., the patient will perform a stand and pivot trans­
resources may affect consistency in and access to pa­ fer from bed to chair, i ndependently) and they are
tient education. written in behavioral terms. Educational goals should
All five of these areas can be addressed with the also be written in behavioral terms. For example,
use of a learning needs assessment survey. See Figure "Mr. J will safely perform percussion and postural
26-2 for an example. By using a survey in combina­ drainage to Mrs. J's right lower lobe." The stated be­
tion with the physical therapy patient evaluation, the havior needs to be measurable in some way. Motor
therapist can gather all the necessary information to skills can be observed, knowledge skills can be
create an optimal patient education experience. The tested, and safety can be documented.
survey in the box on p. 458 consists of three parts, Prioritizing the patient's educational goals in con­
which can be adapted to any patient-care setting. In junction with treatment goals enhances the therapist's
the pediatric setting, some of the questions could be efficiency. Referring again to the learning needs as­
asked of the parent(s) or rephrased to address elemen­ sessment survey (see the box on p. 458) to determine
tary-school-aged children. Part I primarily assesses what is important knowledge to the patient will guide
the patient's perception of the illness or disability and the therapist in creating the most appropriate prioriti­
its impact on the patient's life. Part II lists a wide va­ zation of goals. Simplicity is usually best. Over­
riety of teaching methods and asks the patient to indi­ whelming patients with a huge list of items to be ac­
cate which methods are most useful personally. Part complished may discourage them before they even
III identifies specific topics about which the patient start. If the patient's learning needs are very great,
would like to know more. This part is also helpful in start by breaking down the list of goals into smaller
alerting the therapist that referrals to other members groups. Choose the most important goals and try to
of the interdisciplinary health-care team may need to accomplish them first. If you run into a series of fail­
be made. For example, if the patient checked off ures, tackle the next group. Build on each success the
"what I should eat," the therapist should make a re­ patient experiences.
ferral to the dietician.

EDUCATIONAL METHODS
Interpretation of Findings . Method Selection

The next important step after gathering information Using the learning needs assessment survey (see the
with the learning needs assessment survey is to inter­ box on p. 458) will allow the clinician to choose edu­
pret the findings. The physical therapist must look at cation methods that will facilitate optimal learning in
the answer to each item on the survey and use that in­ a given patient or group. The patient(s) can self-select
formation in the process of designing the content and the available learning methods that have the greatest
method for teaching that patient. Interpretation of the learning potential. A combination of methods may be
survey findings means applying the patient's current necessary to achieve the educational goals that have
health concerns and knowledge deficits to future been set. If a patient is not sure which methods to in­

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460 PART III Cardiopulmonary Physical Therapy Interventions

dicate, the therapist can base the choice on the other therapist in determining the settings and populations
information provided in the survey (e.g., sensory in which the methods will be most useful. This is not
deficits, level of schooling, or type of information de­ a comprehensive list. In fact, some health-education
sired). Surveys generally require regular updates to challenges require truly innovative approaches.
ensure that all of the offered methods are listed and In 1988, for example, community health-care
the discontinued methods are removed from the list. providers in Boston were faced with a dilemma. The
incidence of acquired immune deficiency syndrome
(AIDS) among women of color was increasing and
Advantages and Disadvantages
Latino, African-American, and Haitian women were
Each education method has its own advantages and not receiving vital information about how to prevent
disadvantages. Table 26-1 shows 13 education meth­ the transmission of the human immunodeficiency
ods listed with their key advantages and disadvan­ virus (HIV). These communities were largely dis­
tages. The table is designed to assist the physical trustful of the health-care establishment and were not

TABLE 26-1

Comparison Chart for Education Methods (Adult'i and children unless otherwise noted)

TYPE ADVANTAGES DISADVANTAGES

Reading Patient can refer back to material. Requires instlUctor follow-up for comprehension.
Low effort for instructor.
Lecture Time-efficient for instructor. Cost-efficient. Low interaction. May pacify rather than engage.
Demonstration Adds sensory data to learning. Allows for Instructor needs proficiency in skill to be
problem solving and modification. demonstrated.
Video Access to restricted areas. Portrays events that are Noninteractive. May pacify rather than
infrequent, costly, and difficult to reproduce. engage. Costly, requiring electronic
Portable. equipment. Difficult to control quality.
Audiotape Portable. Useful for sight-impaired learner. Requires electronic equipment.
Group discussion Effective use of instructor time. Enlarges pool Not as much individual attention given. Group
of real-life experiences. Nonthreatening to may be hard to control (e.g., too talkative,
some learners. Mutual support possible. shy,hostile). Strong facilitator skills needed.
Clubs, camps, Draws on community and individual resources. Same as above. Some risk of perpetuating
and retreats Needs less professional input and time. myths and false information.
Individual Instructor can tailor learning to student's Inefficient use of instructor time. Limited pool
instlUction needs and desires. More one-on-one time. of experience on which to draw.
Games and directed Helpful for children. Reduccs anxiety. Uses Scheduling space. Finding participants.
activities repetition. Fun. Unexpected experiences
can lead to new understandings or insights.
Computer programs Interactive, self-paced. Large information Expensive. Special equipment and space
capacity. Time-cfficient for instructor. needed. May require expert help.
Seminars and Diversity of instructors and formats. Pool Expense, scheduling, and space.
workshops of expel1s and community resources. Can
tailor content broadly or narrowly.
Role-playing Trial runs, problem-solving, simulated Threatening to some. Can be time-consuming.
experiences. Instructor needs to be skilled in techniques and
dealing with effects on participants.
Oral and written Can provide instructor with evidence of what Literacy and supplies required, if written. May
tests learner needs to be taught and what has been be time-consuming.
learned.

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 26 Patient Education 461

mobilized to stop the spread of HIV. How could they

Cardiopulmonary Patient Education Content
be reached? The Boston Women's AIDS Information
Project (BWAIP) trained lay women to educate other Smoking cessation
women in the places where they congregate, such as Risk-factor modification
beauty salons. Informational brochures, condoms,
Benefits and effects of exercise
and posters were distributed in a number of beauty
Resumption of sexual activity
salons in communities where women were at highest
Normal cardiopulmonary anatomy and physiology
risk for contracting HIV. Lay and professional educa­
tors would give presentations, show videos, and an­ Cardiopulmonary disease process

swer questions of the staff and patrons of these estab­ Airway clearance techniques and suctioning
lishments to empower them to disann myths about Energy conservation and pacing techniques
AIDS, encourage other women to make appropriate
Stress management
behavior changes, and to make referrals to neighbor­
Cardiopulmonary resuscitation (CPR)-basic life
hood health centers for testing and evaluation.
support
Teaching young children about their bodies and
Hemt rate, blooo pressure, and dyspnea self-monitoring
health may also require unique approaches. In 1993,
Nutrition
members of the interdisciplinary team caring for chil­
dren with cystic fibrosis (CF) at Texas Children's Hos­ Medications (schedules. actions, and side effects)

pital, Houston, held a CF Education Day for the chil­ Use of oxygen and other respiratory equipment
dren and their parents. The children ranged in age from Medical procedures (e.g., cardiac catheterization or
7 to .1 I years old. To teach them about anatomy, a spe­ bronchoscopy)
cial anatomy apron was fabricated. The apron had life­ Community resources
sized removable "organs" made of stuffed fabric. The
Emergency procedures
children took turns wearing the apron and learned to
identify and locate the organs by removing and replac­
ing the apron's heart, lungs, intestines, and pancreas.
By evaluating the advantages and disadvantages of
available education methods, the physical therapist
can choose the methods that are most effective and education experience. Although the physical thera­
use them to their best advantage. Consideration must pist may not be responsible for teaching on all these
be given for cost, equipment, scheduling, labor, time, topics, she or he should be familiar with them as
site, flexibility, and reusability. For example, video­ they are taught by others on the health-care team.
taped presentations may be easy for the instructor to Educational materials on all of these topics have al­
schedule, present, and reuse but they can be costly to ready been developed by a variety of health-care
purchase and require expensive equipment to view. providers, educators, and organizations and may be
available for physical therapists' use (see "Interdis­
ciplinary Considerations and Resources").
Content

The specific content of patient education materials

DETERMINATION OF EFFECTIVENESS
and programs should be determined by the needs of
the individual or group being taught. However, there Determining the effectiveness of patient education ef­
are topics common to many cardiopulmonary educa­ forts involves evaluating not only what the patient
tion efforts. These topics are listed in the box above. learned but also how the teacher taught. Sometimes
The physical therapist can use the topics listed in patients learn in spite of educational efforts. As phys­
the table as a checklist to explore the content cov­ ical therapists, we need to examine how effective we
ered (or to be covered) in a given cardiopulmonary are at teaching and strive to improve our teaching

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462 PART III Cardiopulmonary Physical Therapy Interventions

skills just as we strive to improve our treatment sition the woman without disturbing the many tubes
skills. Being able to communicate ideas and receive and lines that were present. Later the woman ex­
feedback from patients from diverse racial, ethnic, pressed that she did not want to have two physical
vocational, religious, and generational backgrounds is therapy clinicians working with her at the same time.
crucial for physical therapists. We develop rapport She confided to the nurse that it was because she felt
with our patients by communicating to them that we it was too much like the Jewish ritual washing of the
have an understanding of their illnesses or disabili­ body after death, which is traditionally pelformed by
ties, as they perceive them, and that we plan to inte­ two people. This interpretation of the therapy sur­
grate their goals or priorities into the treatment plans. prised the physical therapy staff members who
treated the woman because they were also Jewish and
the thought never occurred to them. The next time tl1e
Teacher-Learner Relationship
clinicians went to see the woman, they explained why
According to Locke (1986), the primary step to under­ it was necessary for both of them to be present during
standing others, is an awareness of one's self. Ac­ the treatment. They also encouraged the woman to
knowledging one's own personal values, interests, and have other supportive people present and to play her
biases will significantly increase one's sensitivity to­ favorite recorded music during the therapy session.
ward others. The skilled teacher is aware of her or his
own communication style and its limitations and can
Patient Adherence
convey the desire to help despite those limitations.
The teacher-learner relationship that develops be­ The effectiveness of physical therapy treatment, or
tween physical therapist and patient largely is due to of any medical treatment, depends on the patient
communication between the two in the context of following the health-care provider's recommenda­
culture. Communication is a two-way process con­ tions (adherence.) Unfortunately there is often a gap
sisting of verbal and nonverbal messages. The inter­ between what the patient is asked to do and what the
pretation of these messages depends on the cultural patient actually does. This gap, or nonadherence,
cues operating in the educational setting. Fairchild has an incidence rate estimated between 50% to
(1970) defines culture as all social behavior, such as 80% (Meichenbaum and Turk, 1987). Factors af­
customs, techniques, beliefs, organizations, and re­ fecting patient adherence include knowledge of and
gard for material objects, including behaviors trans­ course of the illness, complexity of the recommen­
mitted by way of symbols. "The primary mode of dations, convenience, availability of support system,
transmission of culture is language, which enables and the patient's beliefs.
people to learn, experience, and share their traditions Patient education can improve adherence when the
and customs" (Locke, 1992). In addition, culture can information given includes what behaviors are ex­
be expressed or experienced via economic and politi­ pected, when they should be performed and what to
cal practices, art, and religion. Health care and medi­ do should problems mise. Plans for patient education
cine have their own cultures. To meet the needs of sessions should strive to remove or avoid barriers to
culturally diverse populations and engage in positive, patient adherence. These efforts include simplifying
productive relationships, physical therapists need to and individualizing treatment regimens, fostering col­
operate from a framework of cross-cultural under­ laborative teacher-learner relationships, enlisting
standing. This understanding and knowledge can then family support, making use of interdisciplinary and
be reflected in patient education efforts. community resources, and providing continuity of
For example, in a large, urban, acute-care hospital care (Meichenbaum and Turk, 1987). By using an ap­
two physical therapy staff members were working to­ proach that integrates these efforts, the physical ther­
gether to treat an elderly Jewish woman who was apist can optimize patient adherence to the prescribed
critically ill. The clinicians worked carefully to repo­ physical therapy program.

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 26 Patient Education 463

INTERDISCIPLINARY CONSIDERATIONS
Health-related organizations can also be rich re­
AND RESOURCES
sources for patient education information. The Amer­
The interdisciplinary health-care team has evolved as ican Heart Association and the American Lung Asso­
the complexity and amount of available medical ciation, for example, have many cardiopulmonary
treatments and information has grown. Physical ther­ materials available to health-care providers for little
apists are trained to function as part of an interdisci­ or no cost. State public health and local community
plinary team and are respohsible for learning the service agencies may also be sources for printed or
areas of responsibility and expertise covered by each audiovisual materials. The Health and Human Ser­
member of their team. The team often consists of li­ vices Department of the Federal government has nu­
censed and nonlicensed health-care providers and merous divisions addressing health education. Cata­
may include any or all of the following: logs listing these publications can be obtained from
Physician the Federal Consumer Information Center, Pueblo,
Nurse Colorado 81009.
Physical therapist Community organizations such as YMCA, YWCA,
Occupational therapist and the American Red Cross offer a wealth of health­
Exercise physiologist education materials and classes. Many of these agen­
Dietician cies also have catalogs of their educational offerings,
Laboratory technologist which can be obtained by telephoning their local of­
Pharmacist fices. Local public, medical, and hospital libraries are
• Social worker also useful for seeking out available health-education
• Chaplain or pastoral care associate materials. Many Chambers of Commerce keep lists of
• Clinical psychologist local support groups or clubs, such as Breather's Club
• Speech therapist or Heartbeats. Regional state colleges or universities
• Vocational rehabilitation counselor have departments dedicated to health education and
• Home-care personnel may have cardiopulmonary materials to share.
All of the above providers may not be present on
every team, but their services should be available for
SUMMARY
patients who need them. By understanding what ser­
vices and patient education material are provided by This chapter defined patient education and described
each discipline, the physical therapist can reinforce selected learning theories as they relate to cardiopul­
previously presented concepts and avoid giving con­ monary patient education. The evaluation of the pa­
flicting information. This also allows the physical tient's learning needs was emphasized and the advan­
therapist to make referrals to the appropriate disci­ tages and disadvantages of a variety of educational
pline when other knowledge deficits are identified. methods were discussed. The role of the teacher-learner
Interdisciplinary team members can also provide relationship and patient adherence were explained in
the physical therapist with important patient feedback reference to the determination of patient education and
and information. Teaching methods found to be suc­ treatment effectiveness. Finally, interdisciplinary
cessful with a given patient by the nurse, for exam­ health-care team interactions and resources for patient
ple, could be communicated to the physical therapist. education materials were considered.
The therapist can then use similar methods with that
patient for physical therapy education objectives.
REVIEW QUESTIONS
Communication between team members is enhanced
by regular team meetings or rounds and by having a I. Discuss the benefits of patient education, includ­
central location to document completed patient edu­ ing impact on health care costs and patient's re­
cation experiences (i.e., the medical record). sponse to treatment.

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464 PART III Cardiopulmonary Physical Therapy Interventions

2. Define the overall obj ective of patient education Liedekerken, P.e., Jonkers, R., DcHaes. W.F., Kok, G.1., & Saan,
J. (Eds.) (1990). Effecti veness of healrh education: review alld
and discuss the potential barriers to learning and
analysis. Assen, Netherlands: Van GorcllJn.
ways to minimize them.
Locke, D.e. (1992). Increasing multicultural IJIlderstandillg: a
3. Explain the rationale for patient education using comp rehensive lIIodel. Newberry Park: Sage Publications.
concepts of adult learning theories or models. Locke, D.C. (1986). Cross-cultural counseling issues. In A.J.

4. Describe the most important aspect of planning Palmo & W.J. Weikel et al (Eds.), Foundations of Ille II ta I

for patient education. health counseling. Springfield, IL: Charles e. Thomas.

Manzelli, J.D., Hoffman, L.A., Sereika, S.M., Sciurba, F.e., &
S. Discuss the components of a learning needs as­
Griffith, B.P. (1994). Exercise, education, and quality of life in
sessment survey and ways to modify it for spe­ lung transplant candidates. Journal of Heart and Lung Trans­
cific patient populations. plantation. 13(2),297-305.
Mazzuca, S. (1982). Does patient education in chronic disease have
therapeutic value. Journal of Chronic Disease, 35. 521-529.
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1 ,
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PART IV

Guidelines for the Delivery

of Cardiopulmonary
Physical Therapy: Acute
Cardiopulmonary Conditions

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 Acute Medical Conditions

Elizabeth Dean
Willy E. Hammon
Lyn Hobson

KEY TERMS Acute exacerbations of chronic Cystic fibrosis

airflow limitation Hypertension
Alveolar proteinosis Interstitial pulmonary fibrosis
Alveolitis Pneumonia
Asthma Stable angina
Atelectasis Stable myocardial infarction
Bronchiolitis Tuberculosis
Bronchitis

INTRODUCTION
circulation to effect cardiac output and tissue perfu­
The purpose of this chapter is to review the manage­ sion (Dantzker, 1983; Dantzker, 1988; Scharf and
ment of primary cardiopulmonary dysfunction sec­ Cassidy, 1989; Wasserman and Whipp, 1975). Thus
ondary to other medical conditions. Several types of impairment of one organ inevitably has implications
medical conditions are presented to illustrate the prin­ for the function of the other organ. In addition, threat
ciples and basis for cardiopulmonary physical therapy to or impairment of oxygen transport has implications
in their management. These principles serve as a for all other organ systems, thus a multisystem ap­
guide to problem solving when the practitioner is con­ proach is essential (see Chapters I and 5). The pri­
fronted with pathologies that are not presented. Al­ mary pulmonary conditions that are presented include
though conditions are usually classified as either pri­ atelectasis, pneumonia, bronchitis, bronchiolitis, alve­
mary lung disease or primary cardiovascular disease, olitis, alveolar proteinosis, acute exacerbations of
the heart and lungs work synergistically to effect gas chronic airflow limitation, asthma, cystic fibrosis, in­
exchange and in series with the peripheral vascular terstitial pulmonary fibrosis, and tuberculosis. For fur­

469

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470 PART IV Guidelines for the Delivery or Cardiopulmonary Physical Therapy: Acute Cardiopulmonary Conditions

ther epidemiological and pathophysiological detail on have reduced lung volumes and are prone to breath­
these conditions refer to Bates (1989), the Epidemio­ ing at low lung volumes and microalelectasis, requir­
logical Standardization Project of the American Tho­ ing prophylactic measures to avoid significant effects
racic Society (1989), Luce (1986), Murray and Nadel of atelectasis on oxygen transport and gas exchange.
(I 988a), Murray and Nadel (1988b), and West (1987). When the conditions for normal lung inflation are re­
The primary cardiovascular conditions presented in­ moved, alveolar collapse occurs instantaneously.
clude hypertension, medically stable angina, and un­ Microatelectasis is associated with reduced lung
complicated myocardial infarction. For further details compliance because of reduced lung expansion. Me­
on these condi tions refer to Goldberger (1990), chanically ventilated patients are prone to microat­
Sokolow, McIlroy, and Cheitlin (1990), and Under­ electasis because the normal mechanics of breathing
hill, Woods, Froelicher, and Halpenny (1989). are violated. In part, this may be explained by re­
Treatment principles are presented that are not in­ stricted mobility, recumbency, and reduced arousal,
tended to be a treatment prescription for a particular in addition to reduced functional residual capacity
patient. The treatment priorities are presented based (FRC). Positive end-expiratory pressure (PEEP) is
on the underlying pathology. However, without dis­ routinely added to minimize these effects. High ven­
cussion of a specific patient and knowledge of other tilator system pressure is required to counter reduced
significant factors (i.e., the effects of restricted mobil­ lung compliance, which indicates that atelectatic lung
ity, recumbency, and the effects of extrinsic and in­ tissue it not readily reexpandible.
trinsic factors) (Chapter 16), the specific parameters Microatelectasis is not detected readily with chest
of the treatment prescription cannot be established. x-ray but is on the basis of clinical findings. Nonethe­
Integration of this information is essential for treat­ less, microatelectasis can be anticipated in every ill
ment to be specific and maximally efficacious. For and hospitalized patient whose normal respiratory me­
specific examples of patient treatment prescriptions chanics are disrupted, and particularly, in recumbent,
refer to the companion text Clinical case studies in relatively immobile patients. These effects are further
cardiopulmonary physical therapy. exacerbated in older patients, patients who are over­
weight, have abdominal masses, spinal deformities, or
chest wall asymmetry, smokers, and sedated patients.
Atelectasis
Commensurate with its distribution, atelectasis
Pathophysiology and medical management
presents with reduced chest wall movement and re­
A t e l e c t a s i s refers to p a r tial collapse of lung duced breath sounds over the involved area. A chest
parenchyma. The pathophysiological mechanisms x-ray shows increased density over the involved areas
contributing to atelectasis are multiple (see box on with a shift of the trachea and mediastinum toward
p. 471). These mechanisms include physical compres­ the collapsed lung tissue. The patient may be tachyp­
sion of the lung tissue (e.g., resulting from increased neic and cyanotic because of shunting. Segmental at­
pleural fluid, pus, pneumothorax, or adjacent areas of electasis results from significant progression of mi­
lung collapse) or from an obstructed airway (e.g., se­ croatelectasis and by obstruction of airways with
cretions or tumor) with subsequent reabsorption of resorption of gas in the distal lung units of a bron­
oxygen from the trapped air by the pulmonary capil­ chopulmonary segment or lobe.
laries resulting in a collapse of the lung tissue distal to The ventilator-dependent patient is predisposed to
the obstruction (i.e., reabsorption atelectasis). developing atelectasis because of an unnatural, mo­
There are two primary forms of atelectasis-mi­ notonous breathing pattern, restricted movement, and
croatelectasis and segmental and lobar atelectasis. abnormal and prolonged recumbent body positions.
Microatelectasis is characterized by a diffuse area of These factors contribute to reduced mucociliary trans­
lung units that are perfused but not ventilated, hence, port, abnormal distribution of pulmonary mucus, and
right-to-Ieft shunt. III and hospitalized patients who the accumulation of mucus in the dependent lung
are deprived of being regularly upright and moving fields. Furthermore, production of mucus may be in­

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Pathophysiological Mechanisms Contributing to Atelectasis

Central Mechanisms

Breathing at low lung volumes (e.g., when in pain or after certain medications)

Inability to gcnerate adeljuate inspiratory pressure and volume

Central disruption of breathing centers controlling normal periodic and rhythmic breathing pattern

Extramural Mechanisms

Chest wall deformity

Asymmetry of intrathoracic ,tructures

Respiratory muscle weakness (e.g., neuromuscular disease)

Phrenic nerve inhibition (e.g., secondary to upper abdominal or cardiovascular thoracic surgery)

Compression of lung parenchyma secondary to pleural tluid accumulation, blood, plasma. and pus

Compression of lung parenchyma during surgery

Reduced lung expansion secondary to reduced movement

Compression of lung parenchyma secondary to static body positioning

Compression of lung parenchyma secondary to prolonged static body positioning

Mechanical ventilation

Increased alveolar surface tension

Mural Mechanisms

Airway narrowing seconuary to increased bronchial smooth muscle tone

Calcification or altered anatomical integrity of airways

Edema of the bronchial wall and epithelium

Intramural Mechanisms

Impaired mucocilial'Y transport

Increased pulmonary secretions

Inspissated pulmonary secretions

Altereu distribution of pulmonary secretions

Mucolls plug

Space.Occupying Lesions

Exuuative and transudative tluid in the lung parenchyma

Foreign-bouy aspiration

Intlammation

Other Factors

Increased compliance and dynamic airway compression secondary to age-related changes to the lung

Increaseu timc constants because of increased airway resistance. reduced compliance. or both

Splinting or casting of chest wall restricting normal three-dimensional chest wall movement

Pain anu altered breathing pattern

Medications including narcotics, sedatives, and relaxants

Oxygen

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472 PART IV Guidelines for the Delivery of Cardiopulmonary Physical Therapy: Acute Cardiopulmonary Conditions

creased due to tracheostomy or the presence of an these interventions distributes ventilation more uni­
endotracheal tube. Mucociliary clearance is further formly rather than directing gas to already open alve­
compromised by reduced ciliary activity resulting oli, which will overdistend these units. The distribu­
from high concentrations of oxygen, medication, tion of ventilation is primarily altered by body
and loss of an effective cough because of an artifi­ positioning and not by deep breathing (Roussos, Fix­
cial airway. ley, Geriest, Cosio, Kelly, Martin, and Engely, 1977).
The effect of atelectasis on oxygen transport re­ Sustained maximal inspiratory efforts may augment
flects its type and distribution. Hypoxemia, right to alveolar ventilation, however, the parameters for such
left shunt, reduced lung compliance, and increased efforts to be maximally therapeutic have not been
work of breathing are common clinical manifesta­ studied in detail.
tions. An increased temperature reflects an inflamma­ If impaired mucociliary transport or excessive secre­
tory or infective process and not atelectasis per se. tions are obstl1lcting airways and contributing to atelec­
tasis, mobilization of pulmonary secretions is the goal
Principles of physical therapy management that may be affected by mobilization and a "stir-up reg­
Because it can develop instantaneously when respira­ imen" (Dripps and Waters, 1941; Ross and Dean,
tory mechanics are disrupted, microatelectasis should 1989). In addition, postural drainage coordinated with
be anticipated and prevented. Those factors that con­ breathing control and coughing maneuvers can facili­
tribute to atelectasis for a given patient are countered tate airway clearance. The addition of modified manual
accordingly with aggressive prophylactic manage­ techniques may be indicated in some patients.
ment (see the box on p. 471).
Once developed, however, atelectasis is treated
Pneumonia
aggressively. Treatment is primarily directed at re­
Pathophysiology and medical management
versing the underlying contributing mechanisms
whenever possible (Don, Craig, Wahba, and Couture, Pneumonia is a common cause of morbidity and mor­
1971; Glaister, 1967; Leblanc Ruff, and Milic-Emili, tality in the hospitalized patient, particularly in very
1970; Lewis, 1980; Ray, Yost, Moallem, Sanoudos, young and very old patients (Bartelett and Gorbach,
Villamena, and Paredes, 1974; Remolina, Khan, San­ 1976). Comparable wi th other systemic infections,
tiago, and Edelman, 1981). For example, atelectasis pneumonia results when the normal defense mecha­
resulting from restricted mobility is remediated with nisms of the respiratory system fail to adequately
mobilization. Atelectasis resulting from prolonged protect the lungs from infection.
static positioning and monotonous tidal ventilation is Air inspired through the nasal passages is cleansed
managed with mobilization, manipulating body posi­ of particulate matter by filtration (cilia sweep it to the
tion to increase alveolar volume of the atelectatic nasopharynx); impaction (irregular contour of the
area, manipulating body position to optimize alveolar chamber causes particles to rain out); swelling of hy­
ventilation, or some combination of these interven­ groscopic droplet nuclei, which are either filtered or
tions. Atelectasis arising from reduced arousal is become impacted; and defense factors located in the
managed by reducing the causative factors contribut­ mucous blanket, such as immunoglobulins (IgA),
ing to reduced arousal coupled with frequent sessions Iysozymes, polymorphonuclear leukocytes, and spe­
of mobilization and the upright position to increase cific antibodies. Particles that escape one of these de­
arousal, promote greater tidal volumes and alveolar fense mechanisms in the nasopharynx may be pre­
ventilation, increase zone 2 (area of optimal ventila­ vented from entering the lower airways of the larynx.
tion and perfusion matching), increase FRC, and min­ The mucosa of the larynx is sensitive to chemical irri­
imize closing volume. tation or mechanical deformation and responds to this
Breathing control and coughing maneuvers aug­ stimuli by producing a cough. The high velocities
ment the cardiopulmonary physiological effects of created by the cough are sufficient to clear several
mobilization and body positioning. Coordinating branches of the tracheobronchial tree of particulate

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 27 Acute Medical Conditions 473

matter. The cough reflex is frequently absent or de­ common cold. The ciliated cells of the respiratory
pressed in hosts who are unconscious from drug tract are the most frequent site of infection. They be­
overdose, epilepsy, alcohol ingestion, or head injury. come paralyzed and degenerate with areas of necrosis
Patients with artificial airways are more susceptible and desquamation. The mucociliary blanket becomes
to infection because all the previously mentioned de­ interrupted because destruction of the cilia leaves a
fense mechanisms are bypassed, causing organisms thin layer of nonciliated basal replacement cells. In­
to be deposited directly in the lower airways. In the flammatory responses cause exudation of fluid and
lower airways the cough mechanism is rendered inef­ erythrocytes in both the alveolar septae and airways.
fective by endotracheal tubes, which prevent approxi­ Congestion and edema become predominant with the
mation of the vocal cords, and by tracheostomy formation of intraalveolar hyaline membranes. These
tubes, which cause air to bypass the cords altogether. changes in the normal mucosal structure and cilia
The trachea and the tracheobronchial tree to the make involved areas of the lung susceptible to super­
level of the respiratory bronchioles are protected by imposed bacterial infections. This is the most com­
the cough reflex, filtration (again by cilia which mon complication seen in viral infections and is usu­
transport particles to the pharynx), impaction, and ally responsible for the fatalities that occur.
chemical factors (IgA). Below the level of the respi­ The patient with viral pneumonia presents with
ratory bronchioles, the cough reflex is ineffective, fever, dyspnea, loss of appetite, and a persistent non­
and filtration and transportation of particles by cilia productive cough. On auscultation, normal breath
cannot occur because cilia are absent. The alveolar sounds are heard throughout both lung fields with
macrophages play an important role in protecting scattered inspiratory crackles. X-ray changes range
these airways from particulate matter. Macrophages from minor infiltrates to severe bilateral involvement.
ingest organisms and transport them to the lymphatic Consolidation and pleural effusions occur less fre­
system or higher in the tracheobronchial tree to quently. Secondary bacterial infections occur fre­
where cilia can sweep them to the pharynx. This quently, causing patients to develop productive
process of phagocytosis can be slowed or stopped by coughs.
hypoxia, alcohol ingestion, air pollutants, corticos­ Influenza may lead to viral pneumonia in I % to
teroids, immunosuppressant agents, starvation, ciga­ 5% of cases. Influenza includes acute viral respira­
rette smoke, and oxygen. Particulate matter may also tory tract infection, characterized by a sudden onset
be removed from the airways below the level of the of headache, myalgia, and fever. The route of infec­
respiratory bronchioles by postural drainage. tion is by inhalation of airborne particles from an in­
fected person. The incubation period is 24 to 72
hours.
Routes of Infection
Pulmonary lesions include edema of the respira­
A host who has impaired or ineffective defense tory epithelium with necrosis and hemorrhage. At the
mechanisms of the respiratory tract becomes suscep­ alveolar level, interstitial edema, proliferation of type
tible to a variety of organisms. The major routes of I cells, hemorrhage, and an increased number of
infection include airborne organisms, circulation, macrophages are seen. In patients with pneumonia,
contiguous infection, and aspiration. secondary bacterial infections are frequent and are
the cause of most fatalities.
Medical treatment of viral infections is supportive
CLASSIFICATION OF PNEUMONIA
and preventative. Patients should receive vaccines
Viral Pneumonias
whenever possible to buildup antibodies against spe­
Most respiratory viral infections are contracted by cific viruses. Once the patient has contracted the or­
droplets from the respiratory tracts of infected per­ ganism, treatment becomes supportive, with rest, sali­
sons. These viruses are responsible for interstitial c y lale s , and high f luid intake b e i n g the m a i n
pneumonias, tracheobronchitis, bronchiolitis, and the treatment priorities. Patients w h o become more

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474 PART IV Guidelines for the Delivery of Cardiopulmonary Physical Therapy: Acute Cardiopulmonary Conditions

acutely ill with viral pneumonia should be on a vigor­ illness characterized by fever, tachypnea, dyspnea, hy­
ous preventative program to lessen the possibility of poxemia, tachycardia, and a cough producing bloody
bacterial infection. or purulent sputum. The clinical findings depend on
Recovery also depends on good nutrition, hydra­ the organism involved and the extent of the pneumo­
tion, sleep, rest, and reduced stress. nia in the lungs. The infective process may cease with
the use of chemotherapeutic agents, aerosols, and
Principles of physical therapy management
physical therapy, or it may spread to contiguous areas,
Patients may respond to mobilization coordinated causing pleural effusions and empyemas.
with breathing control exercises and positional rota­ Bacterial pneumonias can occur as either primary
tion for enhancing alveolar ventilation, mucociliary or secondary infections. Primary pneumonias arise in
transport, and gas exchange overall (Orlava, 1959). otherwise healthy individuals and are usually pneumo­
Extreme body positions may enhance alveolar volume coccal in origin. Secondary pneumonias occur when
and ventilation and ventilation and perfusion match­ the patient's defense system becomes ineffective.
ing (Dean, 1985; Douglas, Rehder, Beynen, Sessler, Pneumococcal pneumonia is caused by pneumo­
and Marsh, 1977; Grimby, 1974; Piehl and Brown, coccal bacteria, a gram-positive organism. It occurs
1976). Vigorous treatment should be initiated at the most frequently in the winter months among adults
first sign of a superimposed bacterial infection, which between 15 and 40 years of age with a predilection for
is often accompanied by a productive cough. At this males. Patients present clinically with an abrupt onset
time, the appropriate devices should be prescribed of illness characterized by fever, cough, purulent or
(e.g., ultrasonic or medication nebulizers to loosen se­ rust-colored sputum, and pleuritic chest pain over the
cretions). Postural drainage may be indicated in addi­ affected lung field. Physical examination may reveal
tion to mobilization for airway clearance. Treatments, decreased expansion of the chest over the affected
particularly mobilization, need to be paced to mini­ area and muscle splinting. On auscultation, there may
mize unduly tiring the patient or increasing oxygen be bronchial breath sounds (indicating consolidation),
demand beyond the patient's capacity to adequately decreased or absent breath sounds, and wheezes or
deliver oxygen. Increasing oxygen demands exces­ crackles over the affected lung. Chest x-rays may
sively may compromise the patient's gas exchange. show infiltrates, consolidation, or atelectasis.
Patient education is also fundamental to the treatment There are four stages associated with bacterial in­
that is to be instituted between treatments (i.e., mobi­ fection of lung tissue-engorgement, red hepatiza­
lization and positional rotation coordinated with tion, gray hepatization, and resolution. The engorge­
breathing control and coughing maneuvers). ment stage occurs within the first few days of
The focus of cardiopulmonary physical therapy in infection and is characterized by vascular engorge­
the management of viral pneumonia is to augment ment, serous exudation, and evidence of bacteria col­
alveolar ventilation, increase perfusion, increase dif­ onization. Red hepatization occurs within 2 to 4 days
fusion, and improve ventilation and perfusion match­ as a result of diapedesis of the red blood cells. The
ing, thereby reducing the threat to oxygen transport alveoli are full of polymorphonuclear leukocytes, fib­
and gas exchange. Treatments are prescribed to opti­ rin, and red blood cells. The organism continues to
mize oxygen transport and gas exchange and to mini­ mUltiply within the fluid exudate. Areas of consolida­
mize fatigue and lethargy. tion become evident. Gr<!y hepatization occurs within
4 to 8 days and is characterized by evidence of abun­
dant fibrin, decreased polymorphonuclear leukocytes,
Bacterial Pneumonia
and dead bacteria. Consolidation continues to be a
Bacterial pneumonia causes the largest number of problem in this stage. Resolution occurs after 8 days
deaths per year by an infective agent and is the fifth as areas of consolidation begin to resolve. Many
most common cause of all deaths in North America. macrophages are seen and evidence of enzymatic di­
The patient presents with an abrupt onset of a severe gestion of exudate is present. The affected tissue be­

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 27 Acute Medical Conditions 475

comes softer with large amounts of grayish-red fluid is the same as that for pneumococcal pneumonia.
present within the alveol i. This process continues for Hemo philus inJluenzae pneumonia is caused by a
2 to 3 weeks with the lung gradually assuming a gram-negative organism and occurs primarily in chil­
more normal appearance. dren as bronchiolitis and in adults who have chronic
Pleural involvement occurs frequently, with the bronchitis. The clinical picture is the same as for the
pleural spaces filling with the same type of fluid other bacterial pneumonias, with numerous areas of
seen within the alveoli. Resolution is much slower infiltration evident on x-ray. On auscultation, breath
because there are few surfaces available for phago­ sounds are generally good, with crackles heard at the
cytosis. Complications that may occur in patients end of inspiration. Treatment of this pneumonia in­
with pneumococcal involvement include empyema, cludes chemotherapeutic agents (ampicill in), oxygen,
superinfections (occur when large numbers of new ultrasonic nebulization, and physical therapy.
organisms invade the lung), abscesses, atelectasis, Other gram-negative organisms causing pneumo­
and delayed resolution (defined as taking more than nia include Esch erichia co li and Pseudomo n as
4 weeks to resolve). aeruginosa. They are seen most frequently in patients
Treatment of pneumococcal pneumonia involves with underlying disease, especially pulmonary dis­
the use of chemotherapeutic agents, with penicillin ease, or in those who are debilitated. They are fre­
being the antibiotic of choice. If the patient is allergic q uently the cause of superinfections in individuals
to penicillin, erythromycin or lincomycin is used. who have received massive doses of broad-spectrum
Thoracentesis is performed when pleural fluid is pre­ antibiotics. Clinically these patients present with
sent. The patient should also receive ultrasonic nebu­ cough, fever, and dyspnea. On auscultation, crackles,
lization and physical therapy. Supplemental oxygen bronchial breathing, and diminished or absent breath
therapy may be indicated. sounds can be noted. X-ray changes frequently show
Staphlococcal pneumonia is caused by a gram­ bibasilar infiltrates, with the amount of involvement
positive organism. It rarely occurs in the healthy being widely variable. As for other bacterial pneumo­
adult but is a frequent cause of pneumonia in chil­ nias, treatment includes chemotherapeutic agents, ul­
dren, infants, and patients with chronic lung diseases, trasonic nebulization, and physical therapy.
especially carcinoma, tuberculosis, and cystic fibro­
Principles of physical therapy management
sis. Clinically, the patient presents with the same pic­
ture as the patient with pneumococcal pneumonia. The goals of management of bacterial pneumonia in­
There are some differences in the chest x-ray (e.g., clude reversing alveolar hypoventilation, increasing
patchy areas of infiltrate). Consolidation occurs infre­ perfusion, reducing right-to-Ieft shunt, increasing
quently in this type of pneumonia. Pleural effusions, ventilation and perfusion matching, minimizing the
empyema, abscesses, bronchopleural fistulas, and effects of increased mucous production, and optimiz­
pneumatoceles (subpleural cyst-like structures) occur ing lymphatic drainage. Bacterial pneumonia is fre­
frequently. Treatment includes chemotherapeutic quently associated with increased mucous produc­
agents, rest, increased fluid intake, ultrasonic nebu­ tion. With respect to airway clearance, management
lization or medication nebulizers, and aggressive focuses on augmenting mucociliary clearance overall,
physical therapy. reducing excess mucous accumulation, and reducing
Streptococcal pneumonia is caused by a gram-posi­ mucous stasis. Patients are often mobile and should
tive organism, Streptococcus pyogenes. It occurs most be encouraged to be so to promote mucociliary trans­
frequently in very young, very old, and debilitated pa­ port and enhance lymphatic drainage (Dean and
tients. The clinical picture is very similar to that of Ross, I 992a; Orlava, 1959; Wolff, Dolovich, Obmin­
staphlococcal pneumonia. Again consolidation is rare ski, and Newhouse, 1977). However, the oxygen de­
and chest x-rays usually show one or more areas of mands of mobilization and exercise should be well
patchy infiltrates. Complications are rare but empyema within the patient's capacity to delivery oxygen.
does occasionally occur. Treatment for this organism These interventions should be prescribed to avoid

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476 PART IV Guidelines for the Delivery of Cardiopulmonary Physical Therapy: Acute Cardiopulmonary Conditions

jeopardizing this balance and unduly fatiguing the pa­ term, the bone marrow produces more red blood
tient (Dean and Ross, I992b). Deep breathing and ef­ cells, leading to polycythemia. The work of the heart
fective coughing are singularly important maneuvers is increased due to increased blood viscosity. Long­
for clearing airways with special attention to the avoid­ term hypoxemia leads to increased pulmonary artery
ance of airway closure (Bennett et aI., 1990). Prescrip­ pressure and right ventricular hypertrophy.
tive body positioning can be used to optimize ventila­ Patients with chronic bronchitis have tenacious,
tion and perfusion matching (Clauss, Scalabrini, Ray purulent sputum that is difficult to expectorate. In an
and Reed, 1968; Douglas et aI., 1977; Hietpas, Roth exacerbation, usually because of inflammation, infec­
and Jensen, 1974; Hasani, Pavia, Agnew, and Clarke, tion, or both, they produce even more sputum, which
199 I; Ross and Dean, 1992; Ross, Dean, and Abboud, tends to be retained and stagnate. Retained secretions
I992b; Zack, Pontoppidan, and Kazemi, 1974). obstruct airways and thus air flow, and reduce alveo­
lar volume. The resulting venti lation and perfusion
inequality increases hypoxemia, CO2 retention, ac­
Acute Exacerbation of Chronic Bronchitis
cessory muscle use, melabolic demand, and breathing
Pathophysiology and medical management
rate. Pao2 is further reduced and Paco2 tends to in­
Chronic bronchitis is a disease characterized by a crease. Hypoxemia and acidemia increase pulmonary
cough producing sputum for at least 3 months and for vasoconstriction, which increases pulmonary artery
2 consecutive years. Pathological changes include an pressure and predisposes the patient to right heart
increase in the size of the tracheobronchial mucous failure (cor pulmonale) over time.
glands (increased Reid index) and goblet cell hyper­ A patient having an acute exacerbation of chronic
plasia. Mucous cell metaplasia of bronchial epithe­ bronchitis tends to have the following characteristics:
lium results in a decreased number of cilia. Ciliary (I) The patient is often stocky in build and dusky in
dysfunction and disruption of the continuity of the color. (2) The patient exhibits significant use of acces­
mucous blanket are common. In the peripheral air­ sory muscles of respiration and has audible wheezing
ways, bronchiolitis, bronchiolar narrowing, and in­ or wheezing that is audible on auscultation. (3) Inter­
creased amounts of mucus are observed. costal or sternal retraction of the chest wall may be
Chronic bronchitis results from long-term irrita­ noted. (4) Edema in the extremities, particularly
tion of the tracheobronchial tree. The most common around the ankles, and neck vein distention reflect de­
cause of irritation is cigarette smoking. Inhaled compensated right heart failure. (5) The patient may
smoke stimulates the goblet cells and mucous glands report that breathing difficulty began with increased
to secrete excessive mucus. Smoke also inhibits cil­ amounts of secretions (with a change in their normal
iary action. The hypersecretion of mucus and ciliary color), which is often difficult to expectorate, and in­
damage and dyskinesis lead to impaired mucous creased cough productivity. (6) Pao2 is reduced, Paco2
transport and a chronic productive cough. The fact increased, and pH reduced.
that smokers secrete an abnormal amount of mucus Pulmonary function tests indicate reduced vital
increases the risk of respiratory infections and in­ capacity, FEY!, maximum voluntary ventilation,
creases the length of the recovery time from these in­ and diffusing capacity and increased FRC and resid­
fections. Although smoking is the most common ual volume.
cause of chronic bronchitis, other factors that have
Principles of physical therapy management
been implicated are air pollution, certain occupational
environments, and recurrent bronchial infections. During an exacerbation requiring hospitalization,
Patients with chronic bronchitis have been referred these patients are usually treated with intravenous
to as blue bloaters because of a tendency to have a fluids, antibiotics, bronchodilators, and low-flow
dusky appearance and be stocky in build. Although oxygen. Diuretics and digitalis are often given to treat
many patients have a high Pac02, the pH is normal­ right heart failure. Airway clearance interventions are
ized by renal retention of bicarbonate. Over the long selected (i.e., mobilization, body positioning, and

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 27 Acute Medical Conditions 477

postural drainage). These interventions are coordi­ thickened basement membrane. The obstruction as­
nated with breathing control and coughing maneuvers sociated with bronchiolitis leads to ventilation and
to facilitate secretion removal and optimize coughing perfusion abnormalities and diffusion defect. Clini­
and expectoration, while minimizing dynamic airway cally, the patient presents with a productive cough.
compression and alveolar collapse. During recovery, Obliterative bronchiolitis has been reported to be
exercise with supplemental oxygen may also benefit the most significant long-term complication o f
the patient. It is important for these patients to avoid heart-l u n g t r a n s p l a n t a t i o n (B u r k e , Gla n v i lle,
bronchial irritants (e.g., cigarette smoking, second­ Theodore, and Robin, 1987).
hand smoke, and air pollutants), and to be adequately Medical management is directed at inflammation
hydrated to thin secretions to facilitate mucociliary control with pharmacological agents, fluid manage­
transport and expectoration. ment, and oxygen administration if necessary. Pre­
Patients with chronic bronchitis can benefit from vention of infection is a priority.
a comprehensive rehabilitation program designed
Principles of physical therapy management
specifically for patients with chronic pulmonary
disease (Murray, 1993; Oldenburg, Dolovich, The principal pathophysiological defects include ven­
Montgomery, and Newhouse, 1979). Specific de­ tilation and pelfusion inequality and diffusion defect.
tails of exercise prescription in the management of These defects result from secretions produced by in­
chronic lung disease and of a comprehensive pul­ flammation and increased mucous production and
monary rehabilitation program are described in from atelectasis of adjacent alveoli. Physical therapy
Chapter 23. treatment should promote mucociliary transpol1 and
the removal of secretions and mucus to central air­
ways, promote alveolar expansion and ventilation,
Bronchiolitis
optimize ventilation and pelfusion matching and gas
Pathophysiology and medical management
exchange, and reduce the risk of infection.
Bronchiolitis results from peripheral airway inflam­ Bronchiol i tis is primari Iy, al though not exclu­
mation. In severe cases the exudate in the peripheral sively, a childhood condition. The effects of inflam­
airways becomes organized into a connective tissue mation and obstruction in small children are always
plug extending into the peripheral airway. The in­ serious because the anatomical and physiological
flammatory process resembles that in other tissues components of the cardiopulmonary s ystem are
(i.e., an inflammatory stage followed by a prolifera­ smaller, respiratory muscle tone is less well devel­
tive healing stage). Such inflammation is associated oped, the anatomical configuration of the chest wall
with vascular congestion, increased vascular perme­ is cylindrical, breathing is less efficient until after the
ability, formation of exudate, mucous hypersecre­ age of 2, spontaneous movement and body position­
tion, and shedding of the epithelium. Fluid is exu­ ing are more restricted (infants in particular spend
dated o u t of the circulation onto the alveola r more time in nonupright positions), and children are
surfaces replacing the surfactant. This in turn in­ at greater risk of infection (see Chapter 35).
creases the surface tension and promotes airway clo­
sure. The secretion production associated with air­
Alveolitis
way irritants and inflammation results from the
Pathophysiology and medical management
excess mucous production in combination with the
inflammatory exudate consisting of fluid protein Bronchioalveolitis is another inflammatory disorder
and cells of the exudate. Airway obstruction results of the peripheral airways that is often associated
if these substances are not removed. The airway ep­ with an extrinsic allergic reaction. Comparable with
ithelium has the capacity to repair and reline the bronchiolitis, alveolitis is prevalent in young chil­
lumen. A rapid turnover of cells may contribute to dren. In adults, chronic alveolitis may be a precursor
cell sloughing and further airway obstruction and a to interstitial pulmonary fibrosis. Acute bouts of

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478 PART IV Guidelines for the Delivery of Cardiopulmonary Physical Therapy: Acute Cardiopulmonary Conditions

alveolitis are reversible, however, chronic inflam­ position with the lung to be lavaged downward. The
mation can produce airway narrowing secondary to Carlen's tube enables the patient to be ventilated by
fibrosis in the alveolar wall and complete obstruc­ the uppermost lung while the lower lung is care­
tion of the airway by organization of the exudate. fully filled with saline to FRC. Then an additional
Chronic inflammation can lead to permanent irre­ 300 to 500 ml of saline is alternately allowed to run
versible parenchymal changes and chronic restric­ into and out of the lung by gravitational flow. As
tive lung disease. the saline flows out, manual percussion over the af­
fected lung being lavaged has been reported to in­
Principles of physical therapy management c r e a s e t h e a m o u n t of p r o t e i n a c e o u s m a t e r i a l
The principles of physical therapy management are washed f r o m t h e lung (see Figure 4-11, p . 86).
comparable with that for the management of bronchi­ (Hammon, 1987).
olitis. Principles of the management of cardiopul­
monary dysfunction in children are presented in
Acute Exacerbation of Chronic Airflow limitation
Chapter 35. Because children and infants in particular
are physically immature, the principles of manage­
PathophYSiology and medical management
ment are different from those for adults. Emphysema. There are two principal types of em­
physema-centrilobular and panlobular. BOlh types
may coexist, however, centrilobular emphysema is
Alveolar Proteinosis
20 times more common than panlobular emphy­
Pathophysiology and medical management sema. Centrilobular is characterized by destruction
Alveolar proteinosis is a condition of unknown etiol­ of respiratory bronchioles (see Figure 4-1, p. 73), as
ogy, characterized by alveoli filled with lipid-rich well as edema, inflammation, and thickened bron­
proteinaceous material and no abnormalities in the chiolar walls. These changes are more common and
alveolar wall, interstitial spaces, conducting airways, more marked in the upper portions of the lungs.
or pleural surfaces. Most often it is found in men be­ This form of emphysema is found more often in
tween 30 and 50 years of age, although it has been re­ men than in women, is rare in nonsmokers, and is
ported in both men and women of all ages. common among patients with chronic bronchitis.
The most common symptoms are progressive dys­ Panlobular emphysema is characterized by destruc­
pnea and weight loss, with cough, hemoptysis, and tive enlargement of the alveoli distal to the terminal
chest pain reported less frequently. Chest x-rays re­ bronchioles (see Figure 4-1, p. 73). This type of em­
veal diffuse bilateral (commonly perihilar) opacities physema is also found in patients who have an antit­
(see Figure 4-10, p. 86). Physical findings include rypsin deficiency. Airway obstruction in these indi­
fine inspiratory crackles, dullness to percussion and, viduals is caused by loss of elastic recoil or radial
in the later stages, cyanosis and clubbing. Pulmonary traction on the bronchioles. When individuals with
function studies usually show decreased vital capac­ normal lungs inhale, the airways are stretched open
ity, FRC, and diffusing capacity. Arterial blood gases by the enlarging elastic lung, and during exhalation
indicate a low P02, especially during exercise, with the airways are narrowed due to the decreasing
often nonnal Pe02 and pH. stretch of the lung. However, the lungs of patients
with panlobular emphysema have decreased elastic­
Principles of physical therapy management
ity because of disruption and destruction of sur­
One treatment for patients with moderate-to-severe rounding alveolar walls. This in turn leaves the
dyspnea on exertion from alveolar proteinosis is bronchioles unsupported and vulnerable to collapse
bronchopulmonary lavage. The patient is taken to during exhalation. This form of emphysema can be
the operating room. After general anesthesia and local or diffuse. Lesions are more common in the
placement of a Carlen's tube (which isolates each bases than the apices and tend to be more prevalent
lung), the patient is turned in the lateral decubitus in older people.

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 27 Acute Medical Conditions 479

emphysematous spaces than I cm in prolonged. On expiration, the may sponta­

may be found in patients with neoLlsly a pursed-lip pattern, which is
4-2, p. It is thought that develop believed to augment alveolar and
from an obstruction of the conducting airways that collateral ventilation and gas exchange in the
permits the flow of air into the alveoli inspira­ by positive back pressures Petty,
tion but does not allow air to flow out again and 1970). In addition, the may ac­
expiration. This causes the alveoli to become tively to compensate for the loss of the passive
inflated and eventually leads to destruction of the elastic recoil that normally the lungs at end
alveolar walls with a resultant air space in tidal volume. Overall the work of breathing is in­
the lung parenchyma. These bullae can be more than creased. As the become more chronically
10 em in diameter compression. can compro­ the chest wall becomes bar­
mise the function of the remaining lung tissue (Figure rel-shaped and Loss of the normal of the
4-3, p. 75). If this happens, intervention to chest and bucket and pump handle motions further
remove the buJla is often necessary. Pneumothorax, a efficient mechanics and
serious complication, can result from the of Dempsey, and 1976).
one of these bullae. The emphysema patient's most common com­
Both types of can lead to chronic is dyspnea. these patients appear
chest wall The loss of elastic recoil of the thin and have an increased anteroposterior chest wall
disturbs the balance between the d iameter. on disease , they
norma.! recoil pul the chest wall in and the breathe the accessory muscles of inspiration
natural tendency of the chest wall to spring out. This (Chapter These patients may be observed leaning
balance is essential in maintaining norma.! FRC forward, their forearms on their knees, or sit-
the air in the at the end of normal end tidal ex­ with their arms extended at their sides,
piration). Because the residual volume of the lungs is down against the bed or chair to elevate their shoul­
H"'vU VU, FRC is correspondingly increased. This in­ ders and improve the effectiveness of the accessory
crease is not functional, because it reflects muscles of
increased dead space, These are still prone to have been referred to as pink
dynamic airway and airway closure be- puffers because of the increased respiratory work
cause of the loss of the normal elastic recoil of the they must do to maintain relatively normal blood
lung (i,e., increased This gases. On auscultation, decreased breath sounds can
contributes to uneven distribution of ventilation and be noted throughout most or all of the fields. Ra­
decreased diffusing The pressure volume diologically, the patient has overinflated
curve is shifted and ventilation is less efficient. lungs, flattened hemidiaphragms, and a small, elon­
With loss of elastic recoil and the normal gated heart Figure p. Pulmonary func­
them patent, the chest wall tion tests show a decreased vital capacity, FEY I,
tends to outward, thereby to the maximum voluntary and a
hyperinflated chest associated with the patient with duced diffusing The total is
chronic airflow limitation. The alveolar units are increased and the residual volume and FRC are even
less uniform and the distribution of venti­ more increased. Arterial blood gases reflect a mildly
lation becomes even less homogeneous. or lowered a normal or slightly
and expiratory times of the alveolar units also be­ raised PaC02, and a normal pH. Emphysema pa­
heterogeneous. The alveoli require unlike patients with chronic bronchitis, tend to
filling times long time con- cardiac with of the
For this reason, the with chronic air­ condition, to failure at the end stage of the
flow limitation adopts a characteristic breathing disease (see 4-5, p. 77). At this stage, cardiac
tern in which and expiration tend to be hypertrophy may be evident.

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480 PART IV Guidelines for the Delivery of Cardiopulmonary Physical Therapy: Acute Cardiopulmonary Conditions

Hypoxemia leads to hypoxic pulmonary vasocon­ patients with a FEY1 less than 0.75 L. However, if
striction, which shunts blood from underventilated to these flow rates are found in patients with complica­
better-ventilated areas of the lung. The afterload tions of resting tachycardia, chronic hypercapnia, and a
against which the right heart has to pump is in­ severely impaired diffusing capacity, the survival rates
creased. This elevates the pulmonary artery blood should be reduced by 25%. Other factors that have
pressure (i.e., pulmonary hypertension). Over the been associated with a poor prognosis are cor pul­
long term, the right heart hypertrophies to work monale, weight loss, radiological evidence of emphy­
against this increased resistance and eventually may sema, a dyspneic onset, polycythemia, and Hoover's
fail (cor pulmonale). Heart enlargement secondary to sign (inward movement of the ribs on inspiration).
any cause alters the electrical conduction pattern ef­ The most frequent causes of death in patients with
fecting electromechanical coupling and cardiac out­ airflow limitation are congestive heart failure (sec­
put. The altered size and heart position within the ondary to cor pulmonale), respiratory failure, pneu­
chest wal.l can be detected by ECG changes. monia, bronchiolitis, and pulmonary embolism.
Treatment of emphysema that requires hospitaliza­ As emphysema becomes chronic, the hemidi­
tion often includes intravenous fluids, antibiotics, and aphragms become more horizontally positioned, plac­
low-flow oxygen (Geddes, 1984; Make, 1983). Some ing the muscle fibers at a less efficient position on
patients require bronchodilators, diuretics, and digi­ their length tension curve (Druz and Sharp, 1982).
talis. Patients with chronic airflow limitation adapt to Breathing when the muscle fibers of respiration are
high Paco2 levels, thus becoming dependent on their mechanicall y disadvantaged increases the work of
hypoxic drives to breathe. Therefore, low flow oxy­ breathing and therefore energy demands and oxygen
gen is administered to these patients to avoid abolish­ cost. Respiratory muscle weakness and fatigue are se­
ing their drive to breathe. rious complications of chronic lung disease that pre­
The etiology of emphysema is uncertain. The inci­ dispose the patient to respiratory muscle failure
dence of emphysema increases with age. It is most (Rochester and Arora, 1983) (Chapter 4 and 32).
often found in patients with chronic bronchitis and is The net effect of these pathological changes on
significantly more prevalent in smokers than non­ gas exchange is hypoxemia, hypercapnia, and re­
smokers. There appears to be a hereditary factor. Se­ duced pH consistent with respiratory acidosis. Long­
vere panlobular emphysema can develop in patients term respiratory insufficiency leads to chronically
with an alpha-antitrypsin deficiency relatively early impaired oxygen transport and gas exchange. To
in life even though they never smoked. Repeated compensate for hypercapnia, production of bicarbon­
lower respiratory tract infections may also play a role ate is increased to buffer retained CO2 (i.e., compen­
in the pathology of emphysema. However, the inter­ sated respiratory acidosis). Red blood cell production
relationship of these and other factors in producing (i.e., polycythemia) is increased to increase the oxy­
the condition is still not well understood. gen-carrying capacity of the blood. The negative ef­
Chronic bronchitis and emphysema are marked by a fect of polycythemia, however, is increased viscosity
progressive loss of lung function and corresponding of the blood, leading to increased risk of circulatory
cardiac dysfunction. At the end of 5 years, patients stasis, thromboses, and increased work of the heart.
with chronic airflow limitation have a death rate four
Principles of physical therapy management
to five times greater than the normal expected value.
Death rates reported by various studies depend on the The patient with emphysema is prone to pulmonary
methods of selection of patients, types of diagnostic infections and respiratory insufficiency. The clinical
tests, and other criteria. In general the death rates 5 picture is hallmarked by alveolar collapse and de­
years after diagnosis are 20% to 55%. The 5-year sur­ struction, ventilation and perfusion mismatching, and
vival rates based on FEY I have been reported as fol­ diffusion defect. These defects result in impaired or
lows: 80% in patients with a FEY I greater than 1.2 L, threatened oxygen transport if the physiological com­
60% in patients with a FEY L close to 1 L, and 40% for pensations are unable to maintain adequate blood

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 27 Acute Medical Conditions 481

gases. Shortness of breath is exacerbated and breath­ the chest wall by the viscera falling against the un­
ing is labored. Increased work of breathing reflects derside of the diaphragm in this position (i.e., vis­
airway obstruction and inefficiency of respiratory cerodiaphragmatic breathing) (Barach, 1974). The
mechanics and the respiratory muscles. Because of muscle fibers of the diaphragm are mechanically
long-term airway disease, mucociliary transport is placed in a more favorable position with respect to
disrupted. Therefore, in the presence of a pulmonary their length-tension characteristics. This effect may
infection and increased production of pulmonary se­ further be augmented in the head-down position in
cretions, secretion removal can be a significant prob­ some patients (Barach and Beck, 1954). Other pa­
lem for the patient. tients, however, cannot tolerate recumbent posi­
Specific treatments are prescribed for the patient tions; in fact, respiratory distress may be increased.
based on the specific clinical findings (i.e., the type If optimal treatment outcome has not been achieved
and severity of the cardiopulmonary dysfunction with mobilization and body positioning coordinated
and the presence of infection). Therefore treatments with breathing control and coughing maneuvers,
include mobilization coordinated with breathing conventional physical therapy procedures may offer
control and coughing maneuvers, which are effec­ additional benefit in some patients (e.g., postural
tive in enhancing alveolar ventilation, mobilizing drainage and manual techniques).
secretions, and in ventilation and perfusion match­ Because of the tendency toward dynamic airway
ing. Body positioning can be prescribed to alter the compression resulting from the highly compliant air­
distribution of ventilation, to aid mucociliary trans­ ways of emphysema patients, open-glottis coughing
port, and to remove pulmonary secretions. Although maneuvers are indicated. Specific outcome measures
"pure" emphysema is t y p i c a l l y dry, p o s t u r a l are recorded before, during, and after treatment to as­
drainage positions can facilitate the removal o f pul­ sess short- and long-term treatment effects. In addi­
monary secretions from specific bronchopulmonary tion, between-treatment treatments are central to
segments if indicated. In any given body position, maximizing overall treatment efficacy. Thus convey­
alveolar volume is augmented in the uppermost lung ing information effectively and specifically to the pa­
fields and alveolar ventilation is augmented in the tient, nursing staff, and possibly family members is
lowermost lung fields. The type and extent of crucial to achieve an optimal treatment outcome.
pathology will determine the degree of benefit these Comparable with the chronic bronchitis patient, an
physiological effects will have on oxygen transport. exercise program for these patients should be pre­
In addition, body positioning is essential to optimize scribed to maximize oxygen transport capacity. Such
respiratory mechanics and enhance pulmonary gas conditioning may reduce the frequency and severity
exchange, thereby reducing the work of breathing of subsequent acute exacerbations. In addition, the
and the work of the heart. The assessment will de­ patient may benefit from other components of a com­
fine the parameters of the treatment prescription that prehensive pulmonary rehabilitation program.
will be effective in relieving the work of breathing
and the work of the heart. This information is essen­
Acute Exacerbation of Asthma
tial not only for prescribing beneficial positions but
also for avoiding deleterious positions. A sitting
Pathophysiology and medical management
lean-forward position will assist ventilation sec­ Asthma is a condition characterized by an increased
ondary to the gravitational effects of the upright po­ responsiveness of bronchial smooth muscle to vari­
sition on cardiopulmonary function. If the arms are ous stimuli and is manifested by widespread narrow­
supported, this position stabilizes the upper chest ing of the airways that changes in severity either
wall and rib cage, thereby facilitating inspiration. spontaneously or as a result of treatment (Hogg,
Some patients with horizontal diaphragms and sig­ 1984; Rees, 1984). During an asthma attack, the
nificant respiratory distress benefit from recumbent lumen of the airways is narrowed or occluded by a
positions in which the diaphragm is elevated within combination of bronchial smooth muscle spasm, in­

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482 PART IV Guidelines for the Delivery of Cardiopulmonary Physical Therapy: Acute Cardiopulmonary Conditions

flammation of the mucosa and an overproduction of

Factors That Precipitate Asthmatic Symptoms
viscous, tenacious mucus.
Asthma is a widespread disorder affecting I % of
Allergic or Extrinsic Asthma
the population. It is common in children under 15
Pollen (especially ragweed)
years of age; its prevalence is estimated to be 5% to
Animals
15%. It is estimated that 80% of asthmatic children
do not have symptoms after the age of 10 years. Feathers

Asthma that begins in patients under the age of 35 Molds

is usually allergic or extrinsic. These asthma attacks Household dust
are precipitated when an individual comes into con­
Food
tact with a given substance to which he or she is sen­
sitive, such as pollens or household dust (see the box Nonallergic or Intrinsic Asthma
at right). Often asthmatic patients can be allergic to a
Inhaled irrita1lts
number of substances rather than to one or two.
lf a patient's first asthma attack occurs after the Cigarette smoke

age of 35, often there is evidence of chronic airway Dust

obstruction with intermittent episodes of acute bron­ Pollution
chospasm. These individuals, whose attacks are not
Chemicals
triggered by specific substances, are referred to as
having nonallergic or intrinsic asthma (see box at Weather
right). Chronic bronchitis is commonly found in this High humidity
group, and this is the type of asthma seen in the hos­
Cold air
pital setting.
The asthmatic patient presents wi th the follow­ Respiratory i1lfectiOlls
ing picture during an attack. Lung volumes and ex­ Common cold
piratory flow rates are reduced, and the distribution
Bacterial bronchitis
of ventilation is less homogeneous (Ross et aI.,
1992a). The patient has a rapid rate of breathing Drugs
and uses the accessory respiratory muscles (Figure Aspirin
4-6, p. 78). The expiratory phase of breathing is
prolonged with audible wheezing. The patient may Emotio1ls

cough frequently, although un prod ucti vely, and Stress

may complain of tightness in the chest. Radiologi­ Excitement
cally, the lungs may appear hyperinflated or show
Exercise
small atelectatic areas (reabsorption atelectasis).
Early in the attack, arterial blood gases reflect
slight hypoxemia and a low PaCo2 (from hyperven­
tilation). lf the attack progresses, the P02 continues
to fall as the Peo2 increases above normal. As ob­ tack more effectively, and also provides a means of
struction becomes severe, deterioration of the pa­ helping to reduce subsequent attacks. Airway clear­
tient is evidenced by a high CO2, a low Po2, and a ance procedures may have a role should the cough
pH of less than 7.3. become productive. Patients should avoid bronchial
Hospitalized asthmatic patients are treated with in­ irritants and substances that worsen or induce signifi­
travenous fluids, bronchodilators, supplemental oxy­ cant bronchospasm or an attack.
gen, and corticosteroids. Breathing control in the An asthmatic attack that persists for several hours
acute attack relaxes the patient, helps manage the at- and is unresponsive to medical management is re­

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 27 Acute Medical Conditions 483

ferred to as status asthmaticus. This condition consti­ bronchial lumen, further contributing to the stasis of
tutes a medical emergency, necessitating admission secretions. Thus optimizing the mobilization of secre­
to the intensive care unit (see Chapter 32). tions and their removal is a priority even in tile pres­
ence of scant secretions. Interventions that optimize
Principles of physical therapy management mucociliary transport are selected to minimize exac­
The hallmark of an acute exacerbation of asthma is erbating bronchospasm and further increases in air­
an increased responsiveness of airway smooth muscle way resistance.
to various stimuli (bronchospasm) (i.e., reversible air­ The primary goals in the management of asthma
way obstruction). Although bronchospasm can be a include reducing airway narrowing, improving alveo­
feature of chronic bronchitis and emphysema, the pri­ lar ventilation, reducing the work and energy cost of
mary cause of airway obstruction in these conditions breathing, reducing hypoxemia or minimizing its
results from anatomical and physiological changes threat, and optimizing lung compliance.
that are not usually reversible. Treatment outcome is assessed with indices of
Physical therapy is directed at improving gas ex­ oxygen transport overall and of the function of the in­
change without aggravating bronchospasm and other dividual steps in the pathway (Epstein and Henning,
symptoms and reversing these when possible. Thus 1993). Bedside spirometry, including peak expiratory
promoting more effective and efficient breathing with flow rate, is a sensitive indicator of ensuing compro­
relaxed controlled breathing maneuvers and con­ mise in oxygen transport. Some patients use a peak
trolled unforced coughing maneuvers in optimal body expiratory flow rate meter at home to detect such
positions is a priority. Overall oxygen demand, in­ changes and as an early indicator of the need for
cluding that associated with an increased work of medical attention.
breathing, needs to be reduced during an exacerba­
tion of asthma. This may require reduced activity,
Acute Exacerbation of Cystic Fibrosis
body positioning that improves breathing efficiency,
judicious rest and sleep periods, altered diet or re­
Pathophysiology and medical management
stricted diet, adequate hydration, maintaining a ther­ Cystic fibrosis (CF) is a complex multisystem disor­
moneutral environment, rest, reduced arousal, re­ der transmitted by an autosomal-recessive gene that
duced social interaction and excitement, and reduced affects the exocrine glands (Landau, 1973). CF in­
environmental stimulation. Although general relax­ volves all of the major organ systems in the body
ation does not directly relax bronchial smooth mus­ and is characterized by increased sweat electrolyte
cle, relaxation will assist breathing control, reduce content, chronic airflow limitation, ventilation inho­
arousal and metabolic demands, and promote more mogeneity, and pancreatic insufficiency. Definitive
efficient breath ing. diagnosis of CF includes positive family history,
Airway narrowing and obstruction is a hallmark of clinical symptoms of poor digestion, growth or re­
this condition secondary to increased bronchial current pulmonary infection, and, most importantly,
smooth muscle tone and airway edema. Even small a positive sweat chloride test. Survival has increased
amounts of pulmonary secretions can obstruct the dramatically since 1940 when survival was reported
lumen of narrowed airways, which leads to reabsorp­ to be approximately 2 years of age. In1980, patients
tion atelectasis distal to the site of obstruction, im­ survival was estimated to be 20 years of age and in­
paired gas exchange, and reduced P aoz. Thus mu­ creasing (Hunt and Geddes, 1985). Thus although
cociliary transport is a priority. Mucous clearance can CF is congenital and manifests in childhood, this
be further impclled by the addition of serous fluid to condition has now become an adult disorder. Adult
pulmonary mucus, resulting from airway irritation patients with CF often have an upper lobe infiltrate,
and inflammation. Cilia are less effective at clearing with evidence of atelectasis and bronchiectasis, and
mucoserous fluid compared with mucus alone. In ad­ chronic staphlococcal infections. The beat fre­
dition, sheets of ciliated epithelium are shed into the quency of the cilia is often slowed to approximately

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484 PART IV Guidelines for the Delivery of Cardiopulmonary Physical Thel'apy: Acute Cardiopulmonary Conditions

3 mm/min, compared w i t h 20 m m/min in age­ The clinical deficits related to oxygen transport in­
matched healthy control subjects (Wood, Wanner, clude impaired mucociliary transport, increased mu­
Hirsch, and Farrell, 1975). Patients can be catego­ cous production, increased difficulty clearing mucus,
rized into three general groups-those with no sig­ impaired ventilation and perfusion matching, right­
nificant pulmonary signs, those with pulmonary to-left shunt, a diffusion defect, respiratory muscle
signs and occasional cough and sputum, and those weakness or fatigue, and reduced cardiopulmonary
with pulmonary signs and constant cough and spu­ conditioning (Chatham, Berrow, Beeson, Griffiths,
tum. Those patients in the last group tend to have Brough, and Musa, 1994). The incrcased production
significantly impaired pulmonary function test re­ of mucus and the difficulty removing mucus in­
sults, reduced diffusing capacity, and increased he­ creases the risk of bacterial colonization and chronic
moptysis, particularly in the presence of an abnor­ respiratory infections. These manifestations of CF are
m a l che s t x - r a y a n d h y p e r i n f la ti o n . A i r w a y worsened with recumbency. Significant postural hy­
hyperreactivity appears t o b e variable. poxemia has been reported in CF patients when mov­
The A-a gradient for nitrogen reflects lung regions ing from sitting to a supine position (Stokes, Wohl,
with low ventilation and perfusion ratios. Peripheral Khaw, and Strieder, 1985). Thus the object of treat­
airways are often abnormal either anatomically or ment is to optimize oxygen transport and pulmonary
functionally because of mucous plugging. The lungs gas exchange. Given the pathophysiological deficits
of patients with CF may be excessively stiff at maxi­ in an acute exacerbation of CF, the specific goals are
mal lung capacity, with a loss of elastic recoil at low to enhance mucociliary transport, promote airway
lung volumes (Mansell, Dubrawsky, Levison, Bryan, clearance, optimize alveolar ventilation and therefore
and Crozier, 1974). Regional ventilation is nonuni­ gas exchange, maximize the efficiency of oxygen
form contributing to ventilation and perfusion mis­ transport overall, and prevent and minimize infection.
match and hypoxemia (Cotton, Graham, Mink, and Although the degree to which patients with chronic
Habbick, 1985; Ross et aI., 1992a). lung conditions, and in palticular CF, can respond to
The chronic pulmonary limitation in CF is related aerobic training may be limited, it is essential that
to increased secretion of abnormally viscous mucus, their capacity to transport oxygen overall is optimized
impaired mucociliary transport resulting in airway ob­ to compensate for deficits in specific steps of the oxy­
struction, bronchiectasis, hyperint1ation, infection, and gen transport pathway (Cystic Fibrosis and Physical
impaired regional ventilatory function, leading to im­ Activity, International Journal of Sports Medicine,
paired ventilation and perfusion matching and gas ex­ 1988; Dean and Ross, 1989). Deconditioning severely
change. Radiologically, changes are most pronounced impairs oxygen transport. Improved aerobic capacity
in the upper lobes, especially the right upper lobe. and cardiopulmonary conditioning is central in the
management of CF. Prescriptive aerobic exercise en­
Principles of physical therapy management
hances the efficiency of oxygen transport overall by
Prophylactic cardiopulmonary physical therapy, in­ reducing airway resistance by mobilizing secretions,
cluding facilitation of mucociliary transport and max­ improving the homogeneity of ventilation in the lungs
imizing alveolar ventilation, in conjunction with the and therefore ventilation and perfusion matching, op­
judicious use of antibiotics provides effective mea­ timizing oxygen extraction at the tissue level, and in­
sures for controlling or s l o w i n g the effects of creasing respiratory muscle endurance (Keens,
bronchial and bronchiolar obstruction. Involvement Krastins, Wannamaker, Levison, Crozier, and Bryan,
of the patient and caregivers in chronic care in the 1977; Zach et aI., 1992). If optimal conditioning is
long term is particularly important. Understanding of maintained, oxygen transport is not as compromised
the pathology and course of CF is essential to modify during acute exacerbations given the improved effi­
treatment prescription during exacerbations and re­ ciency of oxygen transport overall. These effects will
missions of the disease. be lost, however, as the patient deconditions with re­

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 27 Acute Medical Conditions 465

stricted mobility and recumbency the acute sure, because of the concomitant increase in intratho­
episode. Thus it is important that is mlnl­ racic pressure and strain on the heart and lungs. Pa­
maJly restricted during an exacerbation (based on the tients with CF have severe paroxysms of
clinical assessment and morbidity) and that exercise This increases intrathoracic pressure,
conditioning is a of between which in turn venous return and cardiac out­
exacerbations. An important additional effect of put. Although coughing is an essential mechanism for
which has importance for CF clearance in these patients, the untoward
1 Shepard, cardiac effects need to be minimized.
and 1991). This may minimize Over the past other interventions aimed at
the risk of infection and perhaps minimize the secretion clearance in the treatment of CF have in­
of an infection once acquired. cluded the use of the positive ex-
In severe exacerbations the patient is pressure mask, and the flutter valve
stressed has a increased 1993; Webber and Pryor, 1
oxygen in part because of the increased is based on the that the equal pres­
work of breathing and for the and is prone to is shifted along the airways altering the
arterial desaturation. Thus minimizing undue oxygen volume at which the patient breathes. The pa­
demand and the selection of treatment tient initially breathes and at low
interventions and their parameters in conjunction volumes, then at mid and high lung volumes,
with monitoring. These patients become at low lung volumes is believed to loosen
j.Jv,,,.-..tu'-" and distressed readily, Treatment interven­ secretions from the walls of the This is fol­
tions are selected based on the assessment and the pa­ lowed at mid volumes, which be­
tient's to tolerate the treatment and derive lieved to help localize and collect the secretions. Fi­
benefit. Gradual, paced low-intensity mobi­ breathing at lung volumes is believed to
lization and body enhance mu­ centralize and facilitate the removal of the secretions
cociliary transport and clearance and maxi­ with Thus may enhance
mize t he efficiency of t h e s t e p s i n t h e o x y gen manipulat­
transport pathway. Postural can offer addi­ ing volumes and flow rates and controlling
tional benefit in these patients if further clearance i s coughing to avoid unproductive and wastc­
The addition o f manual may be ful of energy. The is coached by
indicated, however, monitoring must be car­ the therapist breathe and deliber­
ried out given their potential deleterious effects on at the volumes set the who gauges
gas (Kirilloff, and Maz­ the patient's ventilatory effort and work with the
Murray, 1979; hands around the chest. The patient is not
1982). "'''''An"
'
,,,,..; to breathe below
... .. volume
Forced and expiratory techniques can and is encouraged to suppress coughing until the ex­
contribute to airway whereas and (i.e., the phase which the patient
other forms of modified is breathing at high volumes),
tis minimize may be a useful adjunct for fa­
tive in removing secretions that have accumulated cilitating airway clearance in with CF. It is a
centrally without compromising ventilation and gas procedure that may use independently and can
1974; Nunn, Sa­ be relatively unobtrusively. It
and Laws, 1965). Forceful the patient's efforts and minimizes the poten­
closes, contributes to tial for airway closure in these
airway closure and thus should be avoided, The PEP mask and flutter valve are believed to re­
lady in with elevated pulmonary artery pres­ duce airway closure and thereby alveolar

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486 PART IV Guidelines for the Delivery of Cardiopulmonary Physical Therapy: Acute Cardiopulmonary Conditions

ventilation and enhance mucociliary clearance in pa­ als exposed to plastics being heated at high tempera­
tients with CF. tures are also exposed to gases that are toxic to the
respiratory system. Chronic pathological changes and
impaired gas exchange can result.
Acute Exacerbation of Interstitial Pulmonary Fibrosis
Medical management is directed at reducing in­
Pathophysiology and medical management
flammation, reducing pulmonary hypertension, and
Interstitial lung disease has been associated with var­ increasing arterial oxygenation. Pharmacological
ious occupations and the inhalation of inorganic and management may include corticosteroids for inflam­
organic dusts. Conditions associated with the inhala­ mation, immunosuppressive agents, and oxygen
tion of inorganic dusts include silicosis, asbestosis, therapy. Removing the patient from the work envi­
talc coal dusts, and beryllium. These conditions are ronment contributing to interstitial pulmonary fibro­
most often seen in miners, welders, and construction sis is essential in managing the disease and its long­
workers. Workers exposed to organic material, such term consequences.
as fungal spores and plant fibers, may develop a seri­
ous pulmonary reaction known as extrinsic allergic
PrinCiples of physical therapy management

alveolitis. Generally, interstitial lung disease is char­ The primary clinical manifestations of an acute exac­
acterized by inflammation of the lung parenchyma, erbation of interstitial pulmonary fibrosis reflect an
which may resolve completely or progress to fibro­ acute on chronic problem usually resulting from an
sis. Interstitial pulmonary fibrosis results from the inflammatory episode, pulmonary infection, or both.
deposition of connective tissue after repeated bouts The mechanisms responsible include reduced alveo­
of infection. lar ventilation, an inflammatory process and its mani­
The pathophysiological deficits are commensu­ festations, potential airway obstruction, and increased
rate with morphological changes of interstitial infil­ work of breathing and of the heart in severe cases.
tration and fibrosis, intraalveolar exudate and alveo­ These patients are prone to desaturation during exer­
lar replacement (Chung and Dean, 1989) (see Figure cise and thus need to be monitored closely.
4-12, p. 88). Lung compliance and lung volumes are In mild cases, mobilization increases the homo­
reduced, expiratory flow at mid lung volume is in­ geneity of ventilation, and ventilation and perfusion
creased (stiff, inelastic lungs), diffusing capacity is matching (Jernudd-Wilhelmsson et aI., 1986). Be­
reduced, and hypoxemia can be present in the ab­ tween treatments and in the management of the se­
sence of hypercapnia (Chung and Dean; 1989; Jer­ verely affected patient, body positioning is used to re­
nudd-Wilhelmsson, Hornblad, and Hedenstierna, duce the work of breathing and arousal, maximize
1986). The chest x-ray of a patient with interstitial alveolar ventilation, maximize ventilation and perfu­
pulmonary fibr osis secondary to sarcoidosis is sion matching, and optimize coughing.
shown in Figure 4-12, p. 88. Other changes include Patients with moderate-to-severe interstitial lung
increased resting heart rate, pulmonary hyperten­ disease may desaturate during sleep (Perez-Padilla,
sion, impaired gas exchange, and shortness of breath West, and Lertzman, 1985) and readily desaturate on
during exercise and, in some cases, at rest. Symp­ physical exertion (Arita, Nishida, and Hiramoto,
toms can be reversed by removing the worker from 1981), thus warranting close monitoring during and
the exposure by a change of employment, by modi­ between treatments. Increased pulmonary vascular re­
fying the materials handling process, or by using sistance secondary to hypoxic vasoconstriction con­
protective clothing and masks. Repeated exposure to tributes to increased work of the right heart and po­
these organic dusts may result in irreversible inter­ tential cardiac insufficiency.
stitial fibrosis. General debility and deconditioning warrant a
Reaction to fumes and gases can also lead to modified exercise program that can optimize the
chronic restrictive patterns of lung disease. Individu­ function of all of the steps in the oxygen transport

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 27 Acute Medical Conditions 487

pathway (Arita et aI., 1981; Chung and Dean, 1989). in milder cases. If fibrosis has occurred, lung compli­
ance will be correspondingly reduced. Airflow resis­
tance may be increased from narrowing or distortion
Tuberculosis
of the bronchioles because of fibrosis. Pleural in­
Pathophysiology and medical management
volvement may result in effusions, empyema, pleural
Although the incidence of tuberculosis, a life-long fibrosis, and spontaneous pneumothorax. Unlike
disease, has declined significantly over the past sev­ parenchymal damage, small amounts of pleural re­
eral decades, this disease has been experiencing a striction can produce significant changes in pul­
resurgence in the industrialized world in recent monary function. Clinically, patients with significant
decades. This may reflect declining sanitation and pleural involvement have significant restrictive dis­
health standards in some segments of the population ease and correspondingly low lung volumes. The
and immigration patterns. work and energy cost of breathing are markedly in­
Most infections result from inhalation of airborne creased. Shortness of breath is a common complaint.
tubercle bacilli, which triggers an inflammatory re­ Comparable with an interstitial pulmonary fibrosis
sponse (luce, 1986). This response includes flooding patient, the patient adopts a rapid shallow breathing
of the affected area with fluid leukocytes, and later pattern to reduce the high cost of elastic work of
macrophages. The area becomes consolidated and breathing. Thus the dead space tends to be hyperven­
pathologically the condition is considered a tubercu­ tilated and alveolar hypoventilation results.
lous pneumonia. The infiltrating macrophages be­ In addition to alveolar hypoventilation, lung tissue
come localized and fused, resulting in the characteris­ and pulmonary vascular damage impairs ventilation
tic tubercle. Within 2 to 4 weeks, the central part of and perfUSion matching and diffusing capacity. In se­
the lesion necroses. Tuberculosis is associated pri­ vere cases, hypoxemia and hypercapnia are present.
marily with pulmonary infection that is comparable Chronic adaptation includes polycythemia and hyper­
with other infectious pneumonias. Tuberculosis, how­ volemia. Right heart failure may ensue.
ever, is distinct in that it may affect other parts of the The lungs become shrunken and geometrically
body. Symptoms include fatigue, fever, reduced ap­ distorted because of fibrotic changes in the lungs.
petite, weight loss, night sweats, hemoptysis, and a These changes can lead to kinking and obstruction of
cough with small amounts of nonpurulent sputum the pulmonary blood vessels and maldistribution of
with pulmonary involvement. The course of the dis­ pulmonary blood flow, which further compromises
ease is variable. Some lesions heal promptly, whereas ventilation and perfusion matching.
other patients experience progression and ensui ng Tuberculosis may be associated with an obstruc­
death. Other systems that can be involved include tive component. An increase in airflow resistance
brain and meninges, kidney, reproductive system, and comparable with emphysema can be present. This ob­
bone. In some individuals the disease appears to struction results from chronic infection, mucosal
remit, whereas in others tuberculosis progresses to af­ edema, retained secretions, and bronchospasm.
fect other organ systems or previously dormant foci Antibiotics can be effective in managing the dis­
can be reactivated. ease such that hospitalization is avoided. If detected
The effects of tuberculosis on pulmonary function early, the prognosis is favorable, provided the patient
are variable, depending on the extent and type of le­ adheres to the medication schedule and the bacilli do
sions. lesions may involve the lung parenchyma, the not become resistant to the medications. Surgery may
bronchi, the pleurae, and chest wall. Parenchymal i n­ be indicated to resect lung segments that are chroni­
volvement can reduce lung volumes, leading to hy­ cally involved. The extent and seveJ;ty of the disease
poventilation of pelfused lung units. Significant dis­ determines the course of recovery.
ease leads to impaired artcrial blood gases, whereas The maintenance of good general health is particu­
areas of unaffected lung may adequately compensate larly important in the management, control, and pre­

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488 PART IV Guidelines for the Delivery of Cardiopulmonary Physical Therapy: Acute Cardiopulmonary Conditions

vention of tuberculosis (e.g., sanitation, balanced whether the patient is being treated for osteoarthritis,
diet, sleep, regular exercise, and stress control). stroke, or cardiopulmonary dysfunction, treatment is
modified accordingly. An exercise prescription in­
Principles of physical therapy management cludes generalized aerobic exercise at an intensity
Although the acute presentation of tuberculosis is com­ that is optimally therapeutic and not associated with
parable with acute pneumonia (refer to pneumonia sec­ any excessive or untoward hemodynamic responses
tion), there are some important differences with respect (Blair, Painter, Pate, Smith, and Taylor, 1988).
to physical therapy management. First, tuberculosis is Labile hypertensive patients are the most difficult
particularly infectious, thus special precautions should patients to prescribe an exercise program for because
be taken by the physical therapist to prevent its spread of the irregularity of their blood pressure responses.
during its infectious stage. Second, patients are prone to The intensity is modified at each session to accom­
excessive fatigue; treatments should be selected to pro­ modate these variations. Because beta-blockers and
mote improved oxygen transport without exceeding the other medications blunt heart rate responses to exer­
patient's capacity to deliver oxygen and without con­ cise, the exercise prescription parameters are defined
tributing to excessive fatigue. Stimulation of the oxy­ on the basis of some other objective hemodynamic
gen transport system with exercise is necessary to avoid response or on subjective responses (e.g., the Borg
the deleterious effects of deconditioning and further scale of perceived exertion).
compromise of oxygen transport. The patient therefore The benefits of a modified aerobic exercise pre­
warrants being monitored closely. scription include elimination of medication, reduction
of medication, and improved pbarmacological control
on the same dose of medication. In addition, the pa­
Hypertension
tient derives all the other multisystem health benefits
Pathophysiology and medical management
of exercise. A program of aerobic exercise should be
Essential hypertension is the most common type of carried out in conjunction with other life-style changes
hypeltension (90% of all reported cases) (i.e., of un­ associated with blood pressure control (e.g., nutrition,
known etiology). Generally, hypertension is classified weight control, stress reduction, and smoking cessation
as mild, moderate, or severe. Hypertension is man­ program). Medications should be monitored by the
aged pharmacologically with vasodilators (i.e., after­ physician during the training program. In addition to
load reducers), diuretics (i.e., volume reducers), and exercise having a direct effect on controlling hyperten­
beta-blocking agents (i.e., inotrophic agents). Hyper­ sion, the effect of exercise on overall metabolism may
tension is a significant health-care concern in that this alter the absorption and degradation of the medica­
condition is frequently associated with heart disease tions, which in turn can reduce the prescriptive re­
and stroke. Thus its consequences can be dire. quirements of that medication. Those types of exercise
that are associated with a disproportionate hemody­
Principles of physical therapy management
namic challenge (e.g., static movements and stabilizing
Physical therapists treat patients with hypertension as postures) are not usually indicated. Rather, aerobic ex­
a primary or secondary condition. A prescription of ercise that is rhythmic, involves the large muscles of
regular aerobic exercise may control hypertension the legs and possibly the arms, and is performed fre­
(Froelicher, 1987; Goldberger, 1990). The prescrip­ quently is indicated (Blail: et aI., 1988).
tion is based on a consideration of the patient's coex­
istent problems and general health status. If obesity is
Angina
a concurrent problem, an exercise program is pre­
Pathophysiology and medical management
scribed to address both concerns.
More frequently, physical therapists treat patients Angina refers to pain resulting from ischemia of the
whose hypertension is a secondary condition. Thus, myocardium and often precedes myocardial infarction.

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 27 Acute Medical Conditions 489

Coronary cutery disease is the primary cause of myocar­ propriately? Is the prescription current? Are
dial infcu'ction and is among the leading causes of death there other medications that may influence the
in the Western world. Life-style factors including rugh­ patient's cardiopulmonary status and response to
fat diet, stress, and low activity levels contribute to ath­ treatment? What are they? Does the patient have
erosclerosis and fat deposition within the coronary the antianginaJ medication present at all times?
blood vessels. When these deposits narrow or totally 5. What physiological parameters should be moni­
occlude the vessel lumen, blood flow is restricted or to­ tored before, during, and after treatment?
tally obstl11cted. As the hecut continues to demand oxy­ 6. What is the patient's knowledge about his or
gen and nutrients to work, blood supply needs to be in­ her condition? Can the patient clearly identify
creased. If one or more of the myocardial blood vessels what triggers the angina and what makes it
is stenosed, insufficient blood reaches the working my­ worse and better? What life-style changes have
ocardial fibers, and ischerrua and pain result. Although been made? What should be reinforced and
the classic description of anginal pain is retrosternal what education is needed?
vice-like, gripping pain radiating to the left side and A key consideration in the management of any pa­
down the arm and up into the neck, anginal pain may tient with cardiovascular dysfunction is minimizing
occur bilaterally anywhere above the umbilicus. Fur­ myocardial strain (Sokolow et aI., 1990). Thus mobi­
thermore, patients vary considerably with respect to the lization and exercise prescription needs to incorpo­
degree to which the severity of the pain correlates with rate an appropriate warm-up, steady-rate, cool-down,
the degree of myocardial ischemia and infarction. Thus and recovery phases, and the type of exercise should
even apparently minimal chest pain may be associated be rhythmic and involve the legs (i.e., areas of large
with significant ischemia and should not be rrunirruzed muscle mass) and possibly the arms as well. Initially,
with respect to its clinical significance. low-intensity activity that restricts the heart rate to no
more than 20 beats above resting heart rate may be
Principles of physical therapy management
indicated to minimize the work of the heart without
The management of patients with healt disease who immobilizing the patient completely. Ejection frac­
are hemodynamically unstable and require intensive tion is not necessarily a good indicator of exercise
monitoring to assess and to monitor physical therapy tolerance because these vruiables are not well corre­
treatment is described in Chapter 32. This chapter ad­ lated (Dean, 1993). Upper-extremity work alone is
dresses the management of the cardiac medical patient more hemodynamically demanding than lower ex­
who is stable and uncomplicated. Physical therapists tremity work and thus is prescribed cautiously if at
must be knowledgeable and proficient in the manage­ all, at least in the early stage. Exercise or physical ac­
ment of the cardiac patient because these patients are tivity, involving sustained static postures and isomet­
referred with cardiac disease as a primary or secondary ric muscle contraction, are contraindicated. Breathing
problem. Because physical therapy invariably involves should be coordinated with activity such that breath
physically stressing a patient either with therapeutic holding and straining are avoided.
exercise or with the application of a therapeutic modal­ A patient with a history of angina, regardless of
ity, the physical therapist must address the following whether that individual is taking antianginal medica­
questions when managing a patient with heart disease: tions, must be hemodynamically monitored (i.e.,
I. Does the patient's cardiac status preclude treat­ heart rate, blood pressure, rate pressure product, and
ment? Why? subjective responses).
2. Is additional information on the patient needed Patients prone to angina may exhibit symptoms in
before physical therapy assessment and treat­ certain body positions (L ange, Katz, McBrid e ,
ment? What information? Moore, a n d Hillis, 1988; Langou, Wolfson, Olson,
3. How should treatment be modified? Why? and Cohen, 1977; Prakash, Parmley, Dikshit, For­
4. Is the patient using antianginal medication ap­ rester, and Swan, 1973). Usually, this reflects an in­

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490 PART IV Guidelines for the Delivery of Cardiopulmonary Physical Therapy: Acute Cardiopulmonary Conditions

creased workload and increased work of the heart. agement of the myocardial infarction patient (Harri­
Recumbent positions increase the mechanical work son, 1944). Because these interventions can place sig­
of the heart by increasing central blood volume nificant demands on cardiopulmonary function and
(Kaneko, Milic-Emili, Dolovich, Dawson, and Bates, oxygen transport, they must be prescribed specifi­
1966). These patients are not encouraged to lie flat, cally by physical therapists with considerable knowl­
instead the head of bed is elevated 10 to 15 degrees. edge and expertise in the area.
Sidelying positions, particularly left sidelying, in­
Principles of physical therapy management
crease the work of the heart by compressing the heart
and impeding ventricular filling and ejection. Patients Physical therapy stresses patients hemodynamically
with impaired oxygen transport and without prior car­ (Dean, Murphy, Parrent, and Rousseau, 1995). Thus
diac disease may exhibit myocardial stress and is­ the adequacy of their cardiopulmonary system to ef­
chemia in these body positions. Thus patients with fect oxygen transport during and between treatments
impaired or threatened oxygenation must be moni­ is essential to establish. The optimal treatment pre­
tored closely, particularly during turning and activi­ scription is based on the patient's overall signs and
ties in which oxygen demand is increased and oxygen symptoms of coronary insufficiency and hemody­
delivery needs to increase cOITespondingly. namic instability. The physical therapist must be
knowledgeable in detecting inadequate myocardial
tissue perfusion and in reducing and preventing my­
Uncompliicated Myocardial Infarction
ocardial tissue damage. In addition, acute or chronic
Pathophysiology and medical management
impaired heart pump function leads to reduced car­
Myocardial infarction commonly referred to as a diac output and systemic tissue perfusion. Clinical
heart attack refers to insufficient myocardial pelfu ­ manifestations include reduced mentation, reduced
sion resulting in a macroscopic area of damage and renal function, fatigue, malaise, and moist, cool, and
necrosis of the heart. Infarction results most fre­ cyanotic skin.
quently from narrowing and occlusion of the coro­ Regardless of whether the patient i s being
nary blood vessels secondary to atherosclerosis. treated in hospital, either on the ward or in the de­
Other causes include occlusion secondary to a throm­ partment, or in the private physical therapy clinic,
bus or embolus, reduced blood pressure, or coronary the patient must be hemodynamically monitored.
vasospasm. Angina, or ischemic chest pai n, often Minimall y, heart rate and blood pressure must be
precedes or accompanies a myocardial infarction. In­ taken before, during, and after treatment, along
farctions vary in severity from being silent (i.e., hav­ with a subjective rating of anginal chest pain. ECG
ing no characteristic signs and symptoms) and thus monitoring is usually continuous in the early stages
going undetected to being fatal. Most infarctions of the infarction. The object of treatment is to have
when detected require some hospitalization and mon­ the patient remain below his or her anginal thresh­
itoring to ensure that the infarction is not evolving old so that anginal pain is avoided. Breathlessness
further and that the patient is medically stable and in or rating of perceived exertion may also be used.
no danger. Chapter 32 describes the management of The rate pressure product (RPP) (i.e., the product
patients with myocardial infarctions who are admit­ of heart rate and systolic blood pressure) is highly
ted to a coronary care unit. This section focuses on correlated with myocardial oxygen uptake and
the patient with mild heart disease, the medical car­ work. Previous stress tests will establish the RPP
diac patient who is discharged from hospital, the pa­ at which angina occurs and the intensity of the ex­
tient who has a history of ischemic heart disease, and ercise dose should be set at 65% to 80% of this
the patient who is hospitalized for a condition other threshold. Patients on beta-blockers have a blunted
than heart disease but develops and is being managed hemodynamic response to exercise, particularly
for myocardial ischemia. Judicious movement and heart rate responses. Use of ratings of perceived
body positioning are essential elements in the man­ exertion to define the upper and lower limits of an

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 27 Acute Medical Conditions 491

acceptable mobilization stimulus may be indicated they can undertake. Thus performing physical activ­
in these patients. ity and exercise while monitored and under the su­
In some cases, patients have labile angina (i.e., the pervision of a physical therapist is often reassuring
onset of angina does not occur reliably at a given and gives the patient confidence for performing ac­
RPP). This patient and the patient who reports angina tivity when unsupervised.
at rest are at higher risk and appropriate precautions The quality and quantity of the patient's sleep and
must be taken. First, the patient must be assessed to a profile of sleep-wake periods should be reviewed to
establish that treatment is not precluded (see pertinent ensure he or she is deriving maximal benefit. REM
questions to be answered before treating a patient sleep with bursts of sympathetic activity during the
with angina). Second, monitoring is essential and early hours of the morning may constitute a period of
may include ECG monitoring. Third, treatments are increased risk for the cardiac patient.
prescribed below symptom threshold, which is usu­ Appropriate safety precautions must be taken in
ally consistent with a low exercise intensity in these all settings where physical therapists practice, given
patients. Comparable with any patient experiencing that most physical therapy interventions physically
low functional work capacity, exercise prescribed on stress patients and that coronary symptoms can occur
an interval schedule enables the patient to achieve a regardless of whether the patient has a known under­
greater volume of work. lying heart disease. In addition, because the popula­
Similar to the patient with angina, body positions tion is aging, physical therapists are treating a grow­
are selected for the patient with a myocardial infarc­ ing number of older persons who are known to have a
tion that will minimize the work of breathing and of higher prevalence of cardiovascular disease.
the heart (Sonnenblick, Ross, and Bruanwald, 1968). Good life-style habits are central to maximizing
Significant central fluid shifts are minimized by en­ recovery and improving the long-term prognosis
couraging the upright position as much as possible to (e.g., good nutrition and hydration, good sleep habits,
reduce the work of the heart (Levine and Lown, stress management, and regular physical exercise that
1952) and by maintaining the head of bed up to 10 to is prescribed by the physical therapist) (Underhill et
15 degrees when the patient is recumbent. Patients aI., 1989).
with elevated intracardiac pressures are less suscepti­
ble to orthostatism (Chapter 18).
SUMMARY
Comparable with the management of the patient
who has a history of angina, body positions, static The primary acute cardiopulmonary medical condi­
postures, activities, and respiratory maneuvers associ­ tions that are treated by physical therapists include
ated with increased hemodynamic strain (e.g., breath primary lung dysfunction (i.e., atelectasis, pneumo­
holding) are avoided. nia, bronchitis, bronchiolitis, alveolitis, alveolar pro­
Relaxation is central in the management of the teinosis, and acute exacerbations of chronic airflow
cardiac patient who is prone to being anxious and limitation, asthma, cystic fibrosis, interstitial pul­
apprehensive. Relaxation interventions include auto­ monary fibrosis, and tuberculosis) and primary car­
genic relaxation, progressive relaxation, Benson's diac disease including hypenension, uncomplicated
relaxation response procedures. biofeedback, and angina, and myocardial infarction. This chapter fo­
meditation (Underhill et aI., 1989). Also, the patient cuses on the pathophysiology underlying these disor­
needs to identify and minimize stress triggers and ef­ ders and the mechanisms by which they threaten or
fective individual-specific nonpharmacological re­ impair heart-lung interaction and oxygen transport.
laxants. Relaxation training with or without pharma­ Thus the basis for the principles of cardiopulmonary
cological support can be integrated into treatment physical therapy are described rather than specific
(Underhill et aI., 1989; Webber and Pryor, 1994). treatment prescriptions. Treatment prescription is
Patients with heart disease are often apprehensive based on the effects of restricted mobility, recum­
and anxious about the intensity of physical activity bency, and extrinsic and intrinsic factors in addition

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492 PART IV Guidelines fOl" the Delivery of Cardiopulmonary Physical Therapy: Acute Cardiopulmonary Conditions

to the underlying is directed Bennett, W.o., Foster, W.M., & Chapman, W.E (1990). Cough­
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. . (1977). Effects of exercise and eucapnic hyperventilation on
tions ill health and disease. New York: Marcel-Dekker. bronchial clearance in man. Joumal of Applied Physiology,
Shephard, RJ., Verde, TJ., Thomas, SG , & Shek, P. (1991). 43,46-50.
Physical activity and the immune system. Canadian Journa/ of Wood, R.E" Wallner, A., Hirsch, J., & Farrell, P.M. (1975). Tra­
Sports Scien ce, J6, 163-185. cheal mucociliary transport in patients with cystic fibrosis and
Sokolow, M., Mcilroy, M.B., Cheirlin, M.D. (1990). Clillical its stimulation by tCl'bullaine. American Review of Respiratory
cardiology (5th ed.). Norwalk: Appleton & Lange. Disease, /]],733-738
Sonnenblick, E.H., Ross, J. Jr., & Braunwald, E. (J 968) Oxygen Zach, M" Oberwaldner, B., & Hausler, F. (1982). Cystic fibrosis:
consllmption of the heart. Newer concepts of its multifactorial physical exercise versus chest physiotherapy. A rchives of Dis­
determination. American Journal of Cardiology, 328-336. eases in Children, 57. 587-589.
Stokes, D.C., WohL M.E.B" Khaw, K.T., & Slrieder, OJ. (1985). Zack, M.B" Polltoppidan, H., Kazemi, H. (1974). The effect of
Postural hypoxemia in cystic fibrosis. Chest, 87, 785-789. lateral positions on gas exchange in pulmonary disease.
Sutton, PP , Pavia, D., Bateman, J.R.M., & Clarke, SW. (1982). can Review of Respiratory Disease, J /0, 149-153.
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lOry Disease, 63, 188-201.

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 Acute Surgical Conditions

Elizabeth Dean
Maureen Fogel Perlstein
Mary Mathews

KEY TERMS Anesthesia Sedation

Cardiovascular surgery Surgery

Risk factors Thoracic surgery

INTRODUCTION
The four categories of factors contributing to or
The purpose of this chapter is to review the manage­ threatening oxygen transport are described in Chapter
ment of cardiopulmonary dysfunction secondary to 16. Specifically, these factors include the underlying
acute surgical conditions. The cardiopulmonary ef­ pathology, restricted mobility, and recumbency, ex­
fects of surgery are described. The two types of trinsic factors related to the patient's care and intrin­
surgery that have the greatest impact on cardiopul­ sic factors related to the patient. This chapter exam­
monary function, namely, thoracic and cardiovascular ines in detail the extrinsic factors related to surgery
surgery, are then presented. These surgeries are par­ and anesthesia and the impact of underlying disease,
ticularly invasive and lengthy, require heavy and pro­ restricted mobility, recumbency, and intrinsic factors
longed anesthesia and sedation, and are associated on the effects of surgery and anesthesia.
with increased risk, thus warranting intensive periop­ Treatment principles are presented. These are not
erative physical therapy. intended to be a treatment prescription for a particular

495

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496 PART IV Guidelines for the Delivery of Cardiopulmonary Physical Therapy: Acute Cardiopulmonary Conditions

patient. The effects of surgery and anesthesia need to

Surgical Factors That Contribute to
be considered in addition to the underlying pathology,
Perioperative Cardiopulmonary Dysfunction
the effects of restricted mobility, body position, and
intrinsic and extrinsic factors (see Chapter 28). All of Type of surgery
these factors must be considered and integrated in the Surgical procedures
treatment prescription and in defining the precise pa­
Anesthetics (general, with or without intubation. or
rameters of the prescription. Such integration is es­ regional) and sedation
sential for treatment to be specific and maximally ef­
Muscle-relaxant agents and neuromuscular blockade
ficacious. For specific examples of patient treatment
Supplemental oxygen and humidification
prescriptions refer to the companion text Clinical
Static body position assumed
case studies in cardiopulmonary physical therapy.
Duration of surgery and static body positioning

Incisions
PERIOPERATIVE COURSE
Use of the cardiopulmonary bypass machine (CBM)
Surgery and its Cardiopulmonary Consequences
Use of the extracorporeal membrane exchanger
Many factors contribute to perioperative cardiopul­ (ECMO)
monary dysfunction (see the box at right). Anesthesia
Dressings and binders
and tissue dissection contribute to major changes in
Splints and fixation devices
lung volume, mechanics, and gas exchange. The ex­
Lines and leads
tent and duration of these changes increase with the
magnitude of the operative procedure and degree of Monitoring devices

anesthesia required. Anesthesia results in depression Chest tubes placement and number
of breathing. Thoracic respiratory excursion is signifi­ Catheters
cantly reduced. The tone and pattern of contraction of
Perioperative pain
the respiratory muscles, particularly the diaphragm
Perioperative pain control management
and the intercostal muscles, change, which contributes
Peri operative fluid balance management
to many of the secondary cardiopulmonary effects ob­
served after surgery (Muller, Volgyesi, B e cker, Perioperative blood and plasma transfusions

Bryan, and Bryan, 1979). The loss of end-expiratory

diaphragmatic tone causes the diaphragm to ascend
into the chest by 2 cm during anesthesia with or with­
out paralysis (Froese and Bryan, 1974). Reductions in The consequences of reduced FRC with anesthesia
functional residual capacity (FRC) are correlated with and surgery have significant implications for postop­
this change and with altered chest wall configuration erative complications and the course of recovery. Air­
and increased thoracic blood volume (Hedenstierna et way closure occurs with anesthesia and this likely
aI.,1985; H e d e n s t i e r n a , Tokics, Strandberg, contributes to intrapulmonary shunting. Compression
Lundquist, and Brismar, 1986). One of the most per­ atelectasis of the dependent lung fields occurs during
vasive and predictable clinical effects observed in the surgery. In addition, compression atelectasis occurs
postoperative period is alveolar collapse. Total lung when lung tissue and sur ounding structures are being
capacity, FRC, and residual volume are significantly physically manipulated. Although reduced airway
decreased. The FRC is reduced by approximately I L caliber in areas of low lung volume can be offset by
in supine compared with the erect sitting position the airway-dilating effect of many inhaled anesthet­
(Behrakis, Baydur, Jaeger, and Milic-Emili, 1983; ics, airway resistance is increased by obstruction of
Nunn, 1989) and is further reduced with the induction the breathing circuits, valves, and tracheal tubes. The
of anesthesia. Anesthesia, however, fails to reduce airways may also be obstructed with foreign matter,
FRC in the sitting position (Nunn, 1989). such as blood and secretions, or from bronchospasm

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 28 Acute Surgical Conditions 497

because of irritation of the airways. Because of the fect is indicated. Patient controlled analgesia (PCA)
decrease in FRC, compliance is decreased and the is an effective means of having the patient regulate
work of breathing is increased. Hypoxemia secondary the amount of analgesia he or she is receiving. Intra­
to transpulmonary shunting is usually maximal venous administration prolongs the peak-effect time
within 72 hours after surgery and often is not com­ of analgesics and therefore helps the patient tolerate
pletely resolved for several days. Persistent reduction longer, more intense treatments. Transcutaneous elec­
in FRC after surgery delays .the restoration of the nor­ trical nerve stimulation (TENS) can be a useful ad­
mal alveolar-arterial oxygen gradient (Alexander, junct in the management of postoperative pain in
Spence, Parikh, and Stuart, 1973). some patients. Pain control with TENS may enable
A complication of thoracic and upper abdominal the patient to participate more fully in mobilization,
surgery, (e.g., cholecystectomy) is irritation or com­ deep breathing, coughing, and bed mobility. Research
pression trauma of the phrenic nerve. This complica­ is needed, however, to evaluate this technique in the
tion may be more common than expected. Inhibition management of acute pain and define the prescription
of the phrenic nerve impairs the contraction of the af­ parameters needed to produce an optimal therapeutic
fected hemidiaphragm, causing it to ascend into the effect. A nonpharmacological, noninvasive means of
thorax and contribute to atelectasis on that side. This managing acute pain would be of considerable bene­
inhibition may last for several days (Dureuil, Viires, fit to patients and would enable them to participate
and Cantineau, 1986; Ford and Guenter, 1984). more fully in physical therapy treatments in the ab­
The FIo2 depends on the mode of 100% oxygen sence of untoward side effects often associated with
administration. Low-flow nasal oxygen reduces hy­ drug administration.
poxemia in the absence of hypercapnia and marked Although sedatives or tranquilizers are prescribed
transpulmonary shunting in the postoperative patient. to make the patient more comfortable and to reduce
Low oxygen flows and low FI02S tend to be delivered suffering, sedatives, in particular, reduce the patient's
via nasal cannulae, whereas higher flows can deliver arousal and often the ability to cooperate actively
higher FIo2s via oxygen masks and masks with reser­ with treatment. Thus these medications must be pre­
voir bags. FIo2 and the body position of the patient at scribed judiciously to ensure the patient is able to co­
the time the blood sample was taken must always be operate with physical therapy and other components
considered when interpreting arterial blood gases. The of care. Oversedation must be avoided if the patient
FIo2 is selected to provide adequate oxygenation with is to derive maximal benefit from cardiopulmonary
the lowest oxygen concentration possible. physical therapy treatments.
After surgery the normal pattern of breathing is Special attention in the postoperative period is
disrupted. Shallow, monotonous tidal ventilation given to the prevention or management of cardiopul­
without normal occasional, spontaneous deep breaths monary complications associated with reduced arousal,
causes alveolar collapse within an hour (Nunn, 1989). surgical pain, and restriction of lung capacity and sec­
Unless resolved, atelectasis becomes increasingly re­ ondary to dressings, binders, and diminished ability to
sistant to reinflation within a few hours. This compli­ cooperate, move spontaneously, and hyperventilate the
cation is exacerbated in patients receiving narcotics. lungs periodically. Patients are prone to aspiration in
Tachypnea and tachycardia are commonly ob­ the immediate postoperative period, particularly while
served with gross atelectasis secondary to hypoventi­ the sedation and anesthetic agents are wearing off.
lalion. Breath sounds are decreased at the bases, and This risk is further increased if an airway is required or
the coarse wheezes associated with mucus obstruct­ if an airway and mechanical ventilation is instituted.
ing airflow are heard on auscultation. Large areas of Postextubation atelectasis must be anticipated and
atelectasis are present. Left lower lobe atelectasis is avoided. To minimize this risk, patients are requested
common after cardiac surgery. not to cat or drink fluids the day before surgery.
If narcotics impair the patient's ability to partici­ Endotracheal intubation and mechanical ventila­
pate in treatment, analgesia with a less systemic ef­ tion are indicated if blood gases fail to improve with

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498 PART IV Guidelines for the Delivery of Cardiopulmonary Physical Therapy: Acute Cardiopulmonary Conditions

conservative management. See Chapter 32 for treat­ tively, he or she will be better oriented and capable
ment priorities for a patient during ventilation and the of cooperating when waking from anesthetic.
course of weaning from the mechanical ventilator. The patient's position is changed frequently in the
The importance of a thorough preoperative as­ initial postoperative period. The patient is usually en­
sessment and teaching by the physical therapist can­ couraged to change his or her body position fre­
not be overstated. The components of preoperative quently, transfer, sit in a chair, and ambulate as soon
teaching are summarized in the box below. In cases as possible after surgery. The importance of frequent
of elective surgery, preoperative teaching includes a postural changes and early ambulation in the initial
general description of the surgery to be performed, postoperati ve period are stressed (Dull and Dull,
the effect of anesthesia and surgery on cardiopul­ 1983). Early ambulation is a priority in the manage­
monary function, and the systemic effects of re­ ment of all surgical patients unless contraindicated.
stricted mobility and recumbency. The lines, leads, After surgery, the patient is detained in the recovery
and catheters usually associated with the surgery are room until the vital signs have stabilized, there is no
explained. The patient i s instructed in breathing apparent internal or external bleeding, and the patient
control maneuvers, supported coughing, chest wall is responding to his or her name. Patients recovering
mobility exercises, mobility exercises for the limbs from minor surgery are usually transferred to a ward
(e.g., hip and knee and foot and ankle exercises), once discharged from the recovery room. A patient is
turning in bed, sitting up, transferring, chair sitting, transferred to the ICU after surgery if complications
and walking erect postoperatively. In addition, the arise during surgery, if the patient cannot be readily
patient is taught methods of maximizing comfort stabilized and requires close monitoring, or if the pa­
with body positioning and supporting the surgical tient has had more serious surgery such as cranial, car­
incision. If the bed has controls the patient can ma­ diovascular thoracic, or emergency surgery, such as
nipulate, she or he is taught how to make bed adjust­ that resulting from mUltiple trauma (Chapter 34).
ments as required. The postoperative course is ex­ P a tients considered for elective surgery are
plained in general terms so the patient can anticipate screened regarding their risks for postoperative
this period. If the patient is well informed preopera­ complications. The physical therapist is often con-

Objectives of the Preoperative Physical Therapy Assessment and Teaching

Develop rapport with patient

Assess the patient and estimate degree of surgical risk (e.g .. age, smoking. previous cardiopulmonary dysfullction,
neuromuscular dysfunction. musculoskeletal deformity, obesity. substance abuse, pregnancy. nutritional status,
and hydration status)

Describe the general preoperative, intraoperative, and postoperative course

Review specific surgical procedures relevant to physical therapy (e.g., anesthesia. type of surgery. body position dur­
ing surgery, airway, mechanical ventilation, duration, incisions, infusions. drainage systems, chest tubes. and re­
covery room)

Provide the rationale for, describe, demonstrate, and have the patient practice and provide feedback on the following
breathing control maneuvers: maximal inspiratory hold, supported coughing maneuvers, relaxation, bed mobility
and positioning, transfers, and mobilization

For patients at risk of postoperative cardiopulmonary dysfunction and complications. review the use of the incelltive
spirometer and conventional airway clearance interventions (e.g .• postural drainage and manual techniques if indicated)

Ask for any questions

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 28 Acute Surgical Conditions 499

su lted by the surgeon to help make a poor-risk pa­ ing suboptimal, suprathreshold physiological states.
tient into a relatively better-risk patient. Patients Suprathreshold states are associated with an inappro­
wit h upper-respiratory tract infections before priate balance between oxygen delivery and demand
surgery may have their surgeries postponed, de­ such that the patient becomes compromised (e.g., he­
pending on the type and extent of surgery to be per­ modynamically unstable), cardiopulmonary distress
formed, levcl of anesthesia indicated, and other is precipitated, or botb).
medical conditions, including cardiopulmonary dis­
ease, age, and smoking history. Patients with lower­
Preparation for Surgery
respiratory tract infections preoperatively constitute
a greater operative risk, hence these patients often To minimize risk and reduce perioperative morbidity
have their surgeries postponed until the infection and mortality, patients need to be in the best medical
has resolved. Patients with chronic cardiopulmonary and physical condition before anesthesia and surgery.
diseases require a prolonged period of preoperative In the case of elective surgery, some patients are pre­
physical therapy in preparation for surgery. Elective scribed modified aerobic training, smoking cessation,
surgery is not usually considered during an exacer­ and weight control programs before surgery.
bation of chronic lung disease. Even minor surgery Preoperative teaching is a central component of
may be potentially hazardous for the patient with physical therapy management of the surgical patient.
previous lung disease. The adverse effects of total Such teaching establishes rapport with the physical
anesthesia on these patients is magnified because of therapist who informs the patient about what to ex­
their reduced pulmonary reserve capacity. Smoking pect before and after surgery. In addition to review­
should be discontinued for as long as possible be­ ing the surgical procedures, the physical therapist re­
fore surgery. The patient is placed on an exercise views, and has the patient perform, deep breathing
conditioning program, a regimen of bronchial hy­ and supported coughing maneuvers, relaxation, bed
giene, oxygen if necessary, and prophylactic antibi­ mobility, positioning, transfers, and mobilization.
otics. Even patients with extremely low functional Preoperative teaching reduces the patient's anxiety
work capacity can enhance the efficiency of the and encourages the patient to be as active as possible
steps in the oxygen transport pathway (Chapter 17) in her or his recovery. Preoperative teaching reduces
with a modified aerobic exercise conditioning pro­ postoperative complications and the length of the
gram. This preoperative preparation may take one to hospital stay.
several weeks, depending on the patient and the in­ There are no strict guidelines ahout which patients
dications for surgery. should receive peri operative physical therapy. Al­
Rest during the postoperative period is prescribed though nonthoracic surgeries are generally associated
judiciously as treatment because rest is the time for with fewer cardiopulmonary complications (e.g.,
healing, repair, and restoration. Sleep deprivation im­ surgery of the extremities or lower abdomen), patients
pairs recovery and healing. Sleep at night is biologi­ with preexisting cardiopulmonary, hematological or
cally more restorative than daytime sleep. Thus day­ neuromuscular pathology, or musculoskeletal pathol­
time and nighttime cues are given to restore the ogy of the chest wall are at greater risk even in these
patient's circadian rhythms. Although injudicious and relative low-risk types of surgeries. In addition, pa­
excessive recumbency, bedrest, and prolonged peri­ tients are at additional risk if they are older or
ods in any given body position are deleterious, spe­ younger, smoke, or are overweight or pregnant. Thus
cial attention is given to maximizing the amount of each surgical patient needs to be assessed individually
quality rest and sleep periods and minimizing disrup­ to establish the degree of relative risk during surgery
tion of nighttime sleep. Rest needs to be prescribed and the need for perioperative physical therapy. In this
both within and between treatments. Appropriate rest way, perioperative complications can be anticipated
periods are interspersed witbin eacb treatment ses­ and avoided or reduced, which is preferable to manag­
sion, according to the patient's needs to avoid reacb­ ing complications once they have developed.

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500 PART IV Guidelines for the Delivery of Cat'diopulmonary Physical Thet'apy: Acute Cardiopulmonary Conditions

Factors Determining the Effect of Surgery MAJOR TYPES OF SURGERY

Thoracic Surgery
A p atient's response to surgery and the cardiopul­
monary complications that may develop depend on Thoracic surgery refers to surgery necessitating
many factors (see the box on p. 496). The type of opening of the chest wall. By convention, this gen­
surgery determines the degree of invasiveness, the eral term usually excludes specialized cardiovascular
type or types of anesthetics and sedatives, whether surgery (i.e., surgery of the heart and great vessels).
the patient needs to be intubated, the static body posi­ Thoracic surgery is commonly performed for lung
tion assumed during surgery, the approximate dura­ resections secondary to cancer (e.g., pneumonec­
tion of the surgery and period of anesthesia, the inci­ tomy, lobectomy, segmentectomy, and wedge resec­
sions that are required, the dressings, the lines, leads, tion). In addition, thoracic surgery is performed to
catheters, and monitoring devices needed, the chest remove an irreversibly damaged area of lung tissue
tubes, the type and degree of pain, and the need for secondary to bronchiectasis, benign tumors, fungal
pain control after surgery. infections, and tuberculosis.
The most common incisions are posterolateral tho­
racotomy and median sternotomy. The posterolateral
Pathophysiology
thoracotomy procedure requires the patient to assume
The type and severity of underlying cardiopulmonary the sidelying position with the involved side upper­
dysfunction increases a patient's risk of compromised most for the duration of the surgery. The uppermost
oxygen transport and gas exchange perioperatively. arm is fully flexed anteriorly. The incision is made
through an intercostal space, corresponding to the lo­
cation of the lesion to be excised. The muscles in­
Restricted Mobility and Recumbency
cised include latissimus dorsi, serratus anterior, exter­
Surgery imposes two nonphysiological states on the nal and internal intercostals laterally, and trapezius
patient that impact significantly on oxygen transport. and rhomboid posterioriy.
These conditions include the following: At the conclusion of the surgery, chest tubes are
I. Restricted mobility placed to evacuate air and fluid from the pleural space
2. Recumbency, specifically a prolonged period by means of an underwater chest tube drainage sys­
of static positioning with the patient breathing tem. The chest tube and drainage system resolve the
at monotonous tidal volumes pneumothorax created by reestablishing negative pres­
sure in the pleural space and help to reinflate the re­
maining atelectatic lung tissue. After thoracic surgery,
Extrinsic Factors
two chest tubes are usually inserted, one at the apex of
Surgery including the factors in the box on p. 496 are the lung to evacuate air and one at the base of the lung
the p rimary extrinsic factors contributing to cardiopul­ to drain serosanguinous fluid. The therapist should be­
monary dysfunction in the perioperative period. come familiar with the various drainage systems, how
drainage can be facilitated with mobilization and body
positioning coordinated with breathing control and
Intrinsic Factors
supported coughing malleuvers, and certain precau­
Intrinsic factors that contribute to cardiopulmonary tions that need to be observed to avoid impairing
dysfunction in the surgical patient include a patient's drainage or disconnecting the tubing.
premorbid status (e.g., preexisting cardiopulmonary, Provided the chest tubes are not kinked, there is
renal, endocrine, and hematologic pathology). In ad­ no contraindication to lying on the side of the chest
dition, life-style factors are significant (i.e., preopera­ tubes. Lying on this side, which is usually the side
tive conditioning level, nutrition, hydration, stress of the surgery and incision, is typically avoided by
levels, weight, and smoking history). the patient. Consistent with the adage, "down with

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 28 Acute Surgical Conditions 501

the good lung," a patient prefers to lie on the non­ nary artery bypass grafting, valve replacements, and
surgical side. However, prolonged periods in any aneurysm repairs. Bypass patients, in whom the
position, and particularly, lying on the unaffected saphenous vein is excised for graft material, have the
side, places these lung fields at risk. To minimize added complication of surgery and wound healing in
the risk of positional complications and hypoxemia, one leg. Mobility exercises on that leg are often re­
the patient is encouraged to turn to both sides stricted until there is no risk of bleeding or interfer­
(Leaver, Conway, and Holgate, 1994; Seaton, Lapp, ence with healing. Comparable with the thoracic sur­
and Morgan, 1979; Sutton, Pavia, Bateman, and gical patient, a cardiovascular patient leaves the
Clarke, 1982). The specific positions and the dura­ operating room with various monitoring Jines and
tion of time spent within each, however, is based on leads, intravenous fluid infusions, possible blood or
a comprehensive assessment of the patient's condi­ plasma infusions, a Swan-Ganz catheter (Chapter
tion and the indications and contraindications for 15), a central venous pressure line, an arterial line, a
each body position. Foley catheter, and oxygen cannulae.
Patients may appear to splint themselves, thereby The preoperative preparation and teaching and
restricting chest wall motion, to avoid including pain the postoperative physical therapy management is
when moving and deep breathing. They also may re­ intensive. Because of the invasiveness of cardiovas­
sist maximal inspiratory efforts when coughing. Al­ cular surgery, patients are usually treated postopera­
though pain likely contributes to breathing at low tively in a specialized intensive care unit (Chapter
lung volumes and ineffective coughing, phrenic nerve 31). The preoperati ve and postoperative physical
inhibition in patients with thoracic and upper abdomi­ therapy management of patients in the intensive care
nal surgeries is likely a more important factor re­ unit is a specialized area and is described in Chapter
stricting lung expansion than is fully appreciated in 34. Providing the patient with information about
many patients (Ford and Guenter, 1984). what to expect during the perioperative course re­
Postoperative complaints of pain are both muscu­ lieves fear and anxiety. In addition, relaxation pro­
loskeletal and pleural in origin. The large number of cedures can be useful. Patients need to be reassured
muscles incised, particularly in the posterolateral tho­ that their incisions and suture lines will not be dis­
racotomy incision, combined with the operative posi­ rupted with movement and physical therapy and that
tion, contributes to the patient's complaints of chest supported coughing and supporting themselves
wall pain, shoulder soreness, and restricted move­ when moving will maximize comfort. Until the pa­
ment. Deep breathing and coughing maneuvers may tient has stabilized, the patient's mobility is re­
be associated with considerable discomfort after stricted to low-intensity mobilization to promote its
surgery. Pain is accentuated by apprehension and benefits on gas exchange and reduce metabolic de­
anxiety. Therefore treatments are coordinated with mands and body positioning to optimize alveolar
relaxation, noninvasive pain control modalities, and ventilation coordinated with deep breathing and
pain medication schedules to elicit the full coopera­ supported coughing maneuvers. Conventional air­
tion of the patient. way clearance interve n tio ns (e.g., postural drainage
and manual techniques) may be prescribed in the
presence of excessive secretions, difficulty in mobi­
Cardiovascular Surgery
lizing secretions, and in the event of productive hy­
Cardiovascular surgery is specialized thoracic drostatic pneumonia.
surgery involving the heart and great vessels. Be­ Patients undergoing cardiovascular surgery are
cause the flow of blood through the cardiopulmonary transferred from the cardiovascular intensive care
system is interrupted, the patient is placed on a car­ unit to the ward as quickly as possible. From the
diopulmonary bypass machine or on a machine called ward, these patients should be referred to a physical
an extracorporeal membrane oxygenator. Cardiovas­ therapist and a cardiac rehabilitation program in the
cular surgery is most commonly performed for coro­ community for continuity of care and to maximize

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502 PART IV Guidelines for the Delivery of Cardiopulmonary Physical Therapy: Acute Cardiopulmonary Conditions

the functional gains resulting from the surgery. Exer­

Goals of Postoperative Physical Therapy
cise is prescribed progressively to maximize oxygen
Related to Oxygen Transport
transport at each step of the rehabilitation period (i.e.,
acute, before and immediately after discharge, and Maximize arousal
long term). The conditioning effects of exercise en­ Maximize alveolar volume
able the patient to resume various activities of daily
Optimize alveolar ventilation
living commensurate with an increasing capacity of
Optimize perfusion
the patient's oxygen transport system to meet the de­
Maximize lung volumes and capacities, especially
mands of these activities. Activities involving strain­
functional residual capacity
ing and isometric contractions are avoided. Weight
Minimize closing volume
lifting may be introduced in a long-term rehabilita­
tion program, but the weights are not sufficient to Minimize intrapulmonary shunting

cause strain. Patients with median sternotomy inci­ Optimize lung compliance
sions are usually prohibited from using their anns to Optimize mucociliary transport
support themselves when sitting or driving and dur­
Optimize mucous clearance
ing activities that may strain the incision site for sev­
Optimize ventilation and perfusion matching and
eral weeks or more.
gas exchange

Maximize expiratory flow rates

PREOPERATIVE PHYSICAL THERAPY: Maximize chest tube drainage
PRINCIPLES OF MANAGEMENT
Optimize fluid balance systemically (renal function)

Preoperative management includes assessment and Optimize lung water balance and distribution
preoperative education; the primary components are Promote optimal lymphatic draining
shown in the box on p. 498. During this time the phys­
Minimize third spacing and collection of fluid
ical therapist has an opportunity to develop rapport
Minimize the risk of aspiration
with the patient. The assessment establishes the risk of
Minimize undue work of breathing
cardiopulmonary complications and prolonged hospi­
tal stay and the type and extent of perioperative physi­ Minimize undue work of the heart

cal therapy required. The assessment establishes what Maximize chest wall mobility and movement in
the postoperative priorities will be; however, these are three planes

modified based on the postoperative assessment. The Optimize body and posture alignment when sitting,
surgical procedures are described and the effects of standing. walking, and recumbent

surgery and anesthesia and sedation on gas exchange Optimize circulatory status and tissue perfusion
are reviewed so that the patient understands the im­ Optimize peripheral blood flow and velocity
portance of being actively involved in physical ther­
Optimize muscle pump actioll
apy, both dUling and between treatments after surgery.
Minimize effects of central fluid shifts with recum­
bency

POSTOPERATIVE PHYSICAL THERAPY: Maintain t1uid-volume regulating mechanisms

PRINCIPLES OF MANAGEMENT Minimize pain nonphal1nacologically and coordinate
with the patient's pain medications if indicated
The goals of postoperative physical therapy manage­
Maximize cardiopulmonary endurance
ment related to oxygen transport appear in the box at
right. It is essential that these goals are addressed be­ Optimize relaxation

tween and during treatments. Thus the patient is in­ Provide instruction to patient on "between-treat­
structed in mobilization and body positioning coordi­ ment" treatment

nated with deep breathing and supported coughing

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 28 Acute Surgical Conditions 503

maneuvers between treatment sessions, and these in­ going thoracic or cardiovascular surgery, are usually
terventions should be performed hourly during wak­ extubated before leaving the operating room or re­
ing hours (Bennett, Foster, and Chapman, 1990; covery area. Provided no complications develop,
Blomqvist and Stone, 1983; Bourn and Jenkins, most other patients do not require an airway. Patients
1992; Hasani, Pavia, Agnew, and Clarke, 1991; Hiet­ undergoing major thoracic surgery or cardiovascular
pas, Roth, and Jensen, 1974; Orlava, 1959). Pain surgery remain intubated and mechanically ventilated
medications are coordinated as needed with treat­ from several to 24 hours after surgery to minimize
ments to maximize treatment efficacy. the work of breathing and hence the work of the heart
In addition to goals related to oxygen transport, other to meet the metabolical demands of respiration.
important postoperative goals include the following: These patients are informed that artificial airway and
I. Maximize joint range of motion mechanical ventilation enables them to breathe more
2. Maximize muscle length and ligament integrity efficiently initially. A patient is also informed that he
with range of motion exercises or she will not be able to speak while the airway is in
3. Maximize patient's ability to perform activities place and may have a sore throat after its removal.
of daily living Patients are usually aroused and repositioned be­
4. Maintain or increase general muscle strength fore leaving the operating room, although this is sel­
and endurance dom remembered by patients. Not recalling the im­
5. Maintain normal cognitive function to avoid mediate postoperative course is common. Patients are
disorientation and hospital-related psychoses. likely to be receiving some form of pharmacological
These goals are achieved with the prescription of analgesia (e.g., morphine). If blood was required in­
general mobility exercise, including hip and knee traoperatively, whole blood, packed cells, or plasma
flexion and extension exercises and foot and ankle may still be infused in the immediate postoperative
exercises. These exercises are performed hourly re­ period or longer. Saline or other solutions are also in­
gardless of whether the patient is sitting in the chair fused for regulation of fluid balance until the patient
or resting in bed. is able to drink and eat normally. Once vital signs
Finally, there are important preventative goals have stabilized, wounds are stable and not draining,
(e.g., minimizing the effects of restricted mobility and and the patient reasonably alert, the patient is trans­
recumbency on all organ systems) (Chapters 17 and ferred to the ward. The patient is retained in the re­
l8). Of particular concern in the surgical patient is the covery area should further monitoring be required. If
risk of thromboemboli and pulmonary emboli and the complications develop and oxygen transport and gas
risk of pressure points and skin breakdown. Thus mo­ exchange threatened, the patient may be transferred
bilization and regular activation of the muscle pumps to the intensive care unit.
to minimize circulatory stasis and frequent body-posi­ The physical therapist may be consulted to assess
tion changes are essential to reduce risks, which can and treat the patient as soon as he or she leaves the
have serious consequences for the patient's recovery. operating room or while in the recovery room. Most
Compression stockings are often put on the patient frequently the physical therapist sees the patient once
after surgery. These are not removed other than for he or she has been transferred to the ward and has
cleaning and redistributing pressure until the patient is been settled. The first 24 hours are critical.
consistently up and about. These stockings facilitate The risk of cardiopulmonary complications is
venous return and increase blood flow and velocity, greatest during the perioperative period and dimin­
thereby minimizing the risk of thrombus formation. ishes as the patient becomes increasingly upright and
Should thrombus formation be suspected, an intermit­ mobile. Atelectasis and aspiration after extubation are
tent compression device may need to be attached to significant risks for the patient who has been intu­
the legs to simulate muscle pump action. bated. The goal immediately after extubation is to
Not all patients who have surgery are intubated. promote optimal alveolar ventilation, maximize lung
Those that are, with the exception of patients under­ volumes and capacities (especially FRC), minimize

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504 PART IV Guidelines for the Delivery of Cardiopulmonary Physical Therapy: Acute Cardiopulmonary Conditions

closing volumes, and maximize expiratory flow rates There are several factors that are particulary im­
and hence cough effectiveness. Areas most suscepti­ portant in surgical patients that can affect their sensi­
ble to atelectasis are those that may have been physi­ tivity to narcotic analgesics, such as morphine
cally compressed during surgery (e.g., the left lower (Gilman, Goodman, and Gilman, 1990: Malamed,
lobe of the cardiovascular surgical patient and areas 1989). First, there is considerable intersubject re­
adjacent to a lobectomy or segmentectomy). sponse variability to these agents. Second, older pa­
Surgery constitutes a significant insult to the body. tients can be expected to be more sensitive to nar­
After the trauma of surgery, anesthesia, sedation, cotics. Three, diverse multisystem pathology has a
fluid loss, incisions, and the significant energy re­ significant effect on the degradation, absorption, bio­
quirements for healing and repair, patients can be ex­ transformation, and excretion of morphine. Four, ex­
pected to be lethargic and difficult to arouse. The re­ aggerated effects of morphine have been reported
laxed state induced by anesthesia, sedation, and when administered in conjunction with other agents,
narcotics increases the risk of aspiration. This risk is such as other narcotic analgesics, phenothiazines,
exacerbated further in some patients by nausea and tranquilizers, or sedative-hypnotics; in addition, such
vomiting associated with anesthesia and narcotics. exaggerated effects have been reported in patients
Moving and positioning the patient upright whenever with respiratory depression, hypotension, and seda­
possible and interacting with the patient stimulates tion and in patients who are unconscious. These situ­
the reticular activating system making the patient ations in which exaggerated drug effects have been
more responsi ve and aroused. The increased meta­ reported are commonly encountered in the intensive
bolic demands that this requires, along with increased care setting and can result in unpredictable responses.
catecholamine release, helps overcome the residual Finally, the physical dependence and abuse potential
effects of anesthesia, sedation, and muscle relaxants of these agents cannot be ignored.
and their threat to oxygen transport, provided the de­ The physical therapist must be familiar with the
mands are not beyond the capacity of the oxygen patient's medications and the medication's indica­
transport system to deliver oxygen. tions, side effects, and contraindications. The physi­
Alternatively, some patients are restless and agi­ cal therapist can determine to what extent oxygen
tated after the effects of anesthesia have worn off. transport may be compromised by medication effects,
Hypoxemia can lead to restlessness and agitation. whether some recommendation needs to be made to
Thus it is important that these patients are not inap­ minimize untoward drug effects on arousal or some
propriately sedated. This compounds their need for other factor that negatively affects oxygen transport
treatment while making them less able to cooperate and gas exchange. For example, although narcotics
with treatment simultaneously (Dripps and Waters, are excellent analgesics, they have widespread sys­
1941; Ross and Dean, \989). temic effects including cardiopulmonary depressant
At the outset of any treatment, the patient must be effects, gastrointestinal depressant effects, and mus­
aroused as much as possible to cooperate fully and cle relaxant effects-all of which compromise oxy­
derive the maximal benefit from treatment. The phys­ gen transport. Thus consideration needs to be given
ical therapist interacts continuously with the patient regarding whether other forms of analgesia can be
to arouse the patient fully, maintain arousal, stimulate used. Have nonpharmacological means of analgesia
normal cognitive function and orientation, and elicit been exploited? If pharmacological analgesia is indi­
feedback from the patient to assess the response to cated, can analgesics other than narcotics be used? Or
treatment. Narcotics depress respiratory status and at least, can the dose of narcotic be reduced so that
arousal, and these effects are accentuated in patients satisfactory pain control can be achieved in combina­
whose metabolic states have been disrupted with ill­ tion with nonpharmacological interventions?
ness and in older persons. Thus the physical therapist Mobilization in the upright position coordinated
must be vigilant in detecting untoward residual ef­ with breathing control and supported coughing ma­
fects of narcotics in the surgical patient. neuvers is encouraged immediately after the patient is

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 28 Acute Surgical Conditions 505

first aroused after surgery, unless contraindicated, to cilitate frequent turning. Cycle pedals can be adapted
help reverse and mitigate reduced arousal, atelectasis, to chairs and recumbent exercise in bed if necessary.
FRC, and impaired mucociliary transport associated Patients whose positioning is restricted with fixation
with surgery. Mobilization augments cardiopul­ and traction devices require hand, wrist, or ankle
monary function (see Chapter 1 7) particularly when weights, and possibly pulleys and other devices, to
the patient is upright (Levine and Lown, 1952; maintain muscle strength and power. Movements per­
Lewis, J 980). These beneficial effects are enhanced formed with moderately heavy weights for multiple
by improved three-dimensional chest wall motion, sets (e.g., three sets of 10 repetitions) develop muscle
improved gut motility, and reduced intraabdominal strength. Movements performed with lighter weight
pressure. Extremity movement during ambulation in­ for multiple sets (e.g., 5 to 10 sets of 10 repetitions)
creases alveolar ventilation, enhances ventilation and tend to develop endurance and aerobic capacity. Be­
perfusion matching by increasing zone 2 of the lungs, cause of the restrictions imposed by these devices,
and optimizes diffusing capacity. The upright posi­ maintaining joint range is essential (i.e., of the neck,
tion is essential such that the spine is erect, upper spinal column, and chest wall, as well as the extremi­
body musculature relaxed, and the chest wall sym­ ties). The rotation component of joint movement is
metrical. Slouching and leaning particularly to the af­ readily compromised, thus this needs to be an integral
fected side reduces alveolar ventilation and con­ component of joint range of motion exercises. Propri­
tributes to uneven distribution of ventilation and oceptive neuromuscular facilitation (PNF) move­
areas of atelectasis (Bake, Dempsey, and Grimby, ments of the extremities can be beneficial. PNF
1976; Don, Craig, Wahba, and Couture, 1971; Glais­ movements of the chest wall can be coordinated with
ter, 1967). In addition, if this abnormal posture is breathing control and supported coughing maneuvers.
maintained, mucociliary transport of the area is im­ Upper body and trunk mobility and strengthening are
paired and mucus collects and stagnates, increasing important goals particularly in the patient with chest
the risk of bacterial colonization and infection. Sym­ wall incisions. The prescription is progressed gradu­
metrical posture is monitored at a] I times (i.e., during ally in the patient with a chest wall incision, particu­
ambulation, sitting at bedside, bed mobility exercises, larly in the patient with a median sternotomy who is
sitting up in bed, and lying in bed). Slouching and fa­ usually restricted to unresisted, upper-extremity mo­
voring the affected side will lead to cardiopulmonary bility exercises in the first several weeks.
complications and possibly musculoskeletal compli­ Prescription of body positioning is essential in the
cations in the short and long term. management of the surgical patient for two reasons.
Mobilization and active exercise in upright pos­ First, without direction, the patient will tend to as­
tures whenever possible are prescribed based on the sume a deleterious body position (i.e., maintaining a
need to enhance multiple steps in the oxygen trans­ restricted number of body positions that favor the af­
port pathway (Dean and Ross, 1992; Ray et aI., fected side for prolonged periods of time with mini­
1974). The priority is to perform as much activity as mal movement and "stirring up"). Thus once the ef­
possible out of bed ancl upright (i.e., ambulation, fects of mobilization have been exploited in a given
transferring, sitting upright in a chair, and chair exer­ treatment session, body positions are prescribed for
cises with or without hand weights or exercise "between-treatment" times that continue to enhance
bands). When in bed, similar devices can be used, in­ oxygen transport for a given patient and discourage
cluding a monkey bar to facilitate moving in bed for excessive time in deleterious body positions. When
patients other than cardiovascular thoracic patients not ambulating, patients are encouraged to assume a
(e.g., the orthopedic patient with extremity fractures wide range of body positions (e.g., semi-prone) be­
and traction). In addition, the use of the monkey bar tween treatments, as frequently as possible, (i.e., at
to perform repetitive bouts of exercise to maintain least every I to 2 hours) (Dean, 1985; Douglas, Re­
upper-extremity strength and some general endurance hder, Beynen, Sessler, and Marsh, 1977; Piehl and
capacity, to relieve pressure and stiffness, and to fa­ Brown, 1976; Remolina, Khan, Santiago, and Edel­

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506 PART IV Guidelines for the Delivery of Cardiopulmonary Physical Therapy: Acute Cardiopulmonary Conditions

FIGURE 28-1

Incentive spirometers.

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 28 Acute Surgical Conditions 507

man, 19S I; Ross and Dean, 1992; Zack, Pontoppidan, mizing FRC, reducing closing volume, maximizing
and Kazemi, 1974). expiratory flow rates, promoting mucociliary trans­
Alveoli are likely to remain patent for I hour after port, promoting airway clearance, optimizing lym­
reinflation. Thus to sustain alveolar inflation and nor­ phatic drainage, minimizing the effects of increased
mal FRC, mobilization and body positioning coordi­ thoracic blood volume, maintaining fluid-volume
nated with breathing control and supported coughing regulating mechanisms, and minimizing the work of
must be carried out frequently (i.e., every I to 2 breathing and of the heart. Sustained maximal inspi­
hours) to maintain optimal alveolar volume and dis­ ration is one intervention that promotes alveolar ex­
tribution of ventilation. Maximal inspiratory maneu­ pansion. Each deep breath is performed to maximal
vers are coordinated with mobilization and body po­ inspiration to total lung capacity with a 3- to 5-sec­
sitioning at \east every hour as tolerated. Maximal ond breath hold. This maneuver may reduce pul­
inspiratory maneuvers alone, however, are unlikely to monary complications by promoting alveolar infla­
be effective because the inspiratory pressure may be tion and gas exchange. The patient is encouraged to
insufficient to inflate atelectatic alveoli. Rather patent repeat this maneuver several times hourly, and fre­
alveol i will tend to be overexpanded. Mobilization quently during mobilization, and before, during, and
and body positioning will directly alter the in­ after body-position changes.
trapleural pressure gradient and thereby optimize Incentive spirometry can be useful in patients who
alveolar expansion (Roussos et at. 1977). are resistant or unable to cooperate fully with maxi­
Normal passive expiratory efforts to end tidal mal inspiratory efforts (Figure 2S-I ). Postoperative
volume are encouraged and maximal or forced expi­ hypoxemia may be reduced with this technique,
ratory efforts are usually avoided to prevent airway which uses the principle of sustained inspiration
closure and potential increase of atelectasis (Has ani using a feedback device (either flow or volume feed­
et aI., 1991; Hietpas et aI., 1974; Nunn, Coleman, back) to achieve maximal inflating pressure in the
Sachithanandan, Bergman, and Laws, 1965). Huff­ alveoli and maximal inhaled volume. The incentive
ing (glottis open) rather than coughing (glottis spirometer can be used independently by the patient.
closed) also minimizes airway closure. There is less This technique ensures that each inspiration is physi­
risk of bronchospasm than with coughing in which ologically optimal and is reproduced precisely from
the glottis is closed, transpulmonary pressure is in­ one inspiration to the next. Patients who are surgical
creased, and a compressive phase is involved. If in­ risks can benefit from being taught the use of the in­
dicated, coughing maneuvers are most effective in centive spirometer during preoperative teaching by
the sitting or slightly lean-forward position in which the physical therapist to promote better inflation of
lung volumes and forced expiratory flow are maxi­ the lungs with incentive spirometry postoperatively.
mized and the respiratory muscles are mechanically The patient continues with a regimen of breathing
advantaged with respect to the length-tension char­ control and coughing maneuvers until full mobility
acteristics of the muscle fibers. Airway closure is and activities of daily living are resumed.
position-dependent (Chapter IS); therefore the de­ The application of intermittent positive pressure
gree of expiration encouraged by the physical thera­ breathing (IPPB) appears to be less effective for the
pist should be based on the patient's body position. postoperative patient than previously believed. The
Airway closure is potentiated in patients who are details of this modality are described in Chapter 41.
older, smoke, or are obese and in patients who are in
horizontal as opposed to upright body positions.
SUMMARY
M obilization and body posi tioning coordinated
with breathing control and supported coughing ma­ This chapter reviews the management of cardiopul­
neuvers offer the greatest benefit to oxygen transport monary dysfunction secondary to acute surgical con­
in the postoperative patient. Specific benefits are de­ ditions. Surgery and its physiological effects are de­
scribed in Chapters 17 and IS. They include maxi­ scribed. Special reference is made to two specialized

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508 PART IV Guidelines for the Delivery of Cardiopulmonary Physical Therapy: Acute Cardiopulmonary Conditions

types of surgery that have the greatest impact on car­ Bennett, W.D., Foster, W.M., & Chapman, W.F. (1990). Cough­
enhanced mucus clearance in the normal lung. journal of Ap­
diopulmonary function, namely, thoracic and cardio­
plied Physiology. 69, 1670-1675.
vascular surgery.
Blomqvist, e.G., & Stone, H.L. (1983). Cardiovascular adjust­
The four categories of factors contributing to or ments /0 graviratiollal stress. Handbook ofphysi()lo y (Vol. 2).
threatening oxygen transport are described in Chapter Washington, DC: American Physiological Society.

16. These factors include pathology, restricted mobil­ Bourn, J., & Jenkins, S. (1992). Post-operative respiratory physio­

ity and recumbency, extrinsic factors related to the therapy. Indications for treatment. Physiotherapy, 78, 80-85.
Dean, E. (1985). Effect of body position on pulmonary function.
patient's care, and intrinsic factors related to the pa­
Physical Therapy, 65, 613-618.
tient. This chapter examines in detail those extrinsic Dean, E., & Ross, J. (1989). Integrating current literature in the
factors related to surgery and anesthesia, and the im­ management of cystic fibrosis: a rejoinder. Physiotherapy

pact of underlying disease, restricted mobility, re­ Canad{1, 4/, 46-47.

Dean, E., & Ross, J. (1992). Mobilization and exercise condition­
cumbency and intrinsic factors on the effects of
ing. In e.e. Zadai (Ed.), Puhllo/1ary management in physical
surgery and anesthesia.
therapy. New York: Churchill Livingstone.
In this chapter, treatment principles are pre­ Don. H.F., Craig, D.B., Wahba, W.M" & Couture, J.G. (1971). The
sented rather than treatment prescriptions for partic­ measurement of gas trapped in the lungs at functional residual

ular patients. For specific examples of patient treat­ capacity and the effects of posture. Anesthesiology, 35, 582-590.

ment prescriptions refer to the companion Douglas, W.W., Rehder. K., Beynen, F.M .. Sessler, A., D., &
Marsh, H.M. (1977). Improved oxygenation in patients with
workbook Clinical case studies i n cardiopulmonary
acute respiratory failure: the prone position. American Review
physical therapy. oJ Respiratol), Disease, //5,559-566.
Dripps. RD., & Waters, R.M. (1941). Nursing care of the surgical
patient. I. The "stir-up." American .lournal of Nursing, 4/, 53-34.
REVIEW QUESTIONS Dull,1. L., & Dull, W.L. (1983). Are maximal inspiratory breathing ex­
ercises or incentive spiromeny betler than early mobilization after
1. Describe the physiological effects of surgery in­ cardiopulmonary bypass surgely? Physical Therapy, 63, 655-659.
cluding the specific surgical procedure, the type, Dureuil, B., (Viires, N., & Cantineau, J.P. (1986). Diaphragmatic

depth and duration of anesthesia, sedation, types contractility after upper abdominal surgery. journal oJ Applied

of respiratory support, static body positioned as­ Physiology, 6/, /775-1780.

Ford, G.T., & Guenter. e.A. (1984). Toward prevention of postop­
sumed during surgery, length of surgery, number
erative complications. American Review of Respiratol)' Dis·
and type of invasive periooperative procedures, eases, /30, 4-5.
and incisions. Froese, A.B. , & Bryan, A.e. (1974). ErI'eCls of anesthesia and

2. Describe surgical risk factors. paralysis on diaphragmatic mechanics in man. Anesthesiology,

3. Relate cardiopulmonary physical therapy treat­ 4/,242-255.

Glaister, D.H. (1967). The effect of posture on the distribution of
ment interventions to the underlying pathophysiol­
ventilation and blood flow in the normal lung. Clinical Science,
ogy associated with surgery and those factors 33, 391-398
listed in Question 1 and provide the rationale for Gilman, A.G., Goodman, L.S., & Gilman, A. (1990). Goodman

your choice. and Gilnwn's th e plwrmacological basis of therapeutics (8th

ed.). New York: Macmillan Publishing.
Hasani, A., Pavia, D., Agnew, J.E., & Clarke, S.W. (1991). The ef­

References fect of unproductive coughinglFET on regional mucus move­

ment in the human lungs. Respiratory Medicine, 85, 23-26.
Alexander, J.L., Spence, A.A., Parikh, R.K., & Stuart, B. (1973). Hedenstierna, G., Standberg, A.; Brismar, B., Lundquist, H., Sven­
The role of airway closure in postoperative hypoxaemia. son, L., & Tokics, L. (1985). Functional residual capacity, Iho­
British journal ofAnaeslhesiology, 59, 1070- 1 079. racoabdominal dimensions and central blood volume during
Bake, B., Dempsey, J., & Grimby, G. (1976). Effects of shape general anesthesia with muscle paralysis and mechanical venti­
changes of the chest wall on distribution of inspired gas. Amer­ lation. Anesthesiology, 62, 247-254.
icall Review of Respira/ory Disease, //4, 1113-/120. Hedenstierna, G., Tokics, L., Strandberg, A., Lundquist, H., &
Behrakis, P.K., Baydur, A., Jaeger, M.J., & Milic-Emili, J. (1983). Brismar, B. (1986). Correlation of gas exchange impairment to
Lung mechanics in sitting and horizontal body positions. Ches/, development of atelectasis during anaesthesia and muscle
83, 643-646. paralysis. Acta Anaesthesiologica Scal1dinavica, 30, 183-191.

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 28 Acute Surgical Conditions 509

Hietpas, B,G" Roth, RD, & Jensen. W,M. (1974), Huff coughing Ray, R, F" Yost, L, Moallem, S., Sanoudos, G,M., V illamenn,
and patency, Respiratory Care, 24, P., & Paredes, R.M. (1974), Immobility, hypoxemia, and
Leaver, H" Conway. JR, & Holgate, S,T, ( The incidence pulmonary shunting, Archi ves of Surge ry, 109,
of post-operative hypoxaemia following and pneu­ 537-54 L
monectomy: a pilot study, PhysiOlherapy, 80. 1-527, Remolina, Khan, A.U" Santiago, T.V" & Edelman, N.H,
Levine, RD, (l984), Anesthesiology, A manual for medical slu­ (1981), Positional hypoxemia il) unilateral lung disease, New
dents. Philadelphia: 1.8. Lippincott Co, England Journal of Medicine. 523-525,
Levine, S,A" & Lown, B, (1952), 'Armchair' treatment of acute Ross, 1., & Dean, E, (1989), Integrating physiological principles
coronary thrombosis, Journal of Ihe American Medical As soci ­ into the comprehensive management of cardiopulmonary dys­
arion, 148, 1365-1369, function, Physical Therapy, 69, 255-259,
Lewis, F.R. (1980), Management of atelectasis and pneumonia, Ross, L & Dean, E, (1992), Body positioning, In CC Zadai (Ed,),
Surgical Clinics of North America, 60, 1391-1401, P u lmo ll ary mana gement in physical Iherapy, N e w York:
Malamed, S,F, ([989), Sedation, A g uide 10 palielll manag ement Churchill Livingstone,
(2nd ed,) 51. Louis: Mosby, Roussos, CS" Fixley, M" Geriest, 1., Cosio, M" Kelly, S" Martin,
Muller, N" Volgyesi, G" Becker, L, Bryan. MR, & Bryan, A. C. KR, & Engel. LA. (1977), Voluntary factors influencing the
(979), Diaphragmatic muscle tone. Joum al of Applied Physi­ distribution of inspired gas, American Rev ie w of Respiratory
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Nuon, 1,F. (1989),The influence of anesthesia on the respiratory sys­ Seaton, D" Lapp, N,L, & Morgan, W,K,c' (1979), Effect of
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transport tissue oxygenation, New York: Springer-Verlag, 5l8-522,
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Laws, J,W, (1965), Hypoxaemia and atelectasis produced by Chest physiotherapy-a review, European Journal of Respira­
forced expiration. Bri tish Journal of A naesthes ia, 3-12, tory Disease, 63. 188-20 I,
Orlava, OE (1959), Therapeutic physical culture in the complex Zack, M,B" Pontoppidan, H., & Kazemi, H. (1974), The effect of
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in acute respiratory failure, Crilical Care Medicine, 4, 13-14,

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PAR T V

Guidelines for the Delivery

of Cardiopulmonary
Physical Therapy: Chronic
Cardiopulmonary
Conditions

Copyrighted Material
 Chronic Primary Cardiopulmonary
Dysfunction

Elizabeth Dean
Donna Frownfelter

KEY TERMS Angina Hypertension

Asthma Interstitial pulmonary fibrosis
Bronchiectasis Lung cancer
Chronic airflow limitation Myocardial infarction
Cystic fibrosis Peripheral vascular disease
Diabetes Val vula heart disease

INTRODUCTION
there is no clear line between obstructive and restric­
The purpose of this chapter is to review the pathophys­ tive patterns of lung disease, pathology can be gener­
iology, medical management, and physical therapy ally defined based on the primary underlying patho­
management of chronic, primary, cardiopulmonary physiological problems. Thus the primary conditions
pathology. Because the heart and lungs are interdepen­ that are presented include obstructive lung disease
dent and function as a single unit, primary lung or (i.e., chronic airflow limitation, asthma, bronchiecta­
heart disease must be considered with respect to the sis, and cystic fibrosis) and restrictive lung disease
other organ and in the context of oxygen transport (i.e., interstitial pulmonary fibrosis). Lung cancer,
overall (Dantzker, 1983; Ross and Dean, 1989; Scharf which has the characteristics of both obstructive and
and Cassidy, 1989; Wasserman and Whipp, 1975). restrictive patterns of patho.logy, is also presented.
The long-term cardiopulmonary management of The long-term cardiopulmonary management of
chronic lung diseases is presented first. Although heart disease is then presented with special attention

513

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514 PART V Guidelines for the Delivery of Cardiopulmonary Physical Therapy: Chronic Cardiopulmonary Conditions

to angina, myocardial infarction, and valvular heart breathing re s ponse to vertilatioll-perfusion imbalance
disease. Chronic vascular diseases, including periph­ and hypoxemia, and tissue defenses against elastase.
eral vascular disease, hypertension, and diabetes, are Decline in pulmonary function and rate of devel­
also presented. opment of the syndrome depend on the combination
The principles of management of the various of causative factors and individual responses to them.
chronic primary cardiopulmonary conditions are pre­
sented rather than treatment prescriptions, which can­
Chronic Bronchitis
not be discussed without consideration of a specific
patient. (For specific examples of patient treatment
Pathophysiology and medical management
prescriptions refer to the companion test Clinical case Chronic bronchitis is usually associated with a his­
studies in cardiopulmonGl)1 physical therapy.) In this tory of smoking and is defined as mucous hyper­
context the goals of long-term management of each secretion and cough producing sputum for three
condition are presented, followed by the essential months or more over a two-year period (Murray and
monitoring required, and the primary interventions for Nadel, 1988a). Over the first few years of smoking,
maximizing cardiopulmonary function and oxygen reversible airways changes occur. Over 10 to 15
transport. The selection of interventions for any given years of smoking, mucous hypersecretion and chronic
patient is based on the physiological hierarchy. The bronchitis become apparent. After 25 to 35 years of
most physiological interventions are exploited first smoking, irreversible airway damage and chronic dis­
followed by less physiological interventions and those ability occur. Smoking is the major cause of lung
whose efficacy is less well documented (Chapter 16). cancer. The pathophysiology of chronic bronchitis is
reviewed in detail in Chapter 29.
The patient is prone to infection and repeated peri­
PRIMARY PULMONARY DISEASE
ods of morbidity. Deterioration of aerobic capacity
OBSTRUCTIVE PATTERNS and functional capacity is related to the severity of
the condition. Nutrition and hydration may be im­
Chronic Airflow Limitation
paired particularly in severe cases because of neglect
Chronic airflow limitation is a descriptive term that and the excessive energy cost of activities of daily
refers to those disorders that previously have been living. Sleep may be irregular, thus the patient's
termed chronic obstructive pulmonary disease (e.g., symptoms are worsened (e.g., reduced endurance, fa­
chronic bronchitis, emphysema, bronchiectasis, and tigue, and lethargy) because of lack of normal physi­
cystic fibrosis). Although there may be a reversible ological restoration from sleep.
component, airflow obstruction associated with these The natural history of chronic bronchitis related to
disorders is largely irreversible. The pathophysiology smoking includes mucous hypersecretion, reduction in
of these conditions is reviewed in detail in Chapter 29. forced expiratory volume (FEV), and increased hetero­
Bates (1989) described the syndrome of chroruc air­ geneity of the distributions of ventilation, perfusion,
flow limitation as being caused by four external fac­ ventilation-perfusion matching, and diffusion (West,
tors, mediated by four primary tissue responses, and 1987). General debility and deconditioning ensue.
modified by four physiological responses. The princi­ Smoking contributes to increased mucous produc­
pal external causative factors include inhaled irritants, tion in the small airways, increased mucus in the large
allergens, infectious, and climate. The four principal airways, respiratory bronchiolitis, reduced elastic re­
tissue responses include large airway changes, small coil, increased airway reactivity, and vascular changes
airway changes, airway hyperreactivity, bronchiolar (Bates, 1989). These changes, lead to nonuniformity
damage, and alveolar destruction. The principal physi­ of time constants in the lung, with consequent inho­
ological responses include a reversible increased air­ mogeneous distribution of inspired gas and premature
way reactivity component, pulmonary vascular re­ small airway closure, and to nonuniformity of ventila­
sponse to alveolar hypoventilation, control of tion, perfusion, and diffusion distributions. Although

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 29 Chronic Primary Cardiopulmonary Dysfunction 515

vaJiable among smokers, pulmonary function changes crease the demand on the left heart to maintain cardiac
generaHy corrcspond to the amount smoked and dura­ output. Similar to right-sided failure, the left heart
tion of the smoking history. Over time, the pulmonary may become hypertrophied, and over time, may fail.
function profile becomes increasingly consistent with The significantly increased intrathoracic prcssures
chronic airflow limitation (i.e., reduced FEY, and re­ generated during chronic coughing reduce venous re­
duced FEY,IFYC), however, these are late indicators turn, cardiac output, and coronary perfusion and in­
of pulmonary changes. Signs of uneven distribution of crease blood pressure. These effects exert additional
ventilation and increased closing volumes, indicative myocardial strain, lead to arterial desaturation, and
of small airway involvement, are early pulmonary increase the potential for cardiac dysrhythmias.
function changes in smokers. Exercise diffusing ca­ The complications of chronic bronchitis are exacer­
pacity is reduced which explains in part the reduced bated by cardiopulmonary deconditioning. Despite the
maximal Y02 of smokers. Dynamic compliance with pathology, the efficiency of oxygen transport along the
breathing frequency is also reduced. Residual volume steps in the pathway is suboptimal. This reduced effi­
is increased as a percent of total lung capacity. Tra­ ciency increases the oxygen demands of the patient
cheal mucous velocity is reduced and secretion clear­ overall who is unable to adequately supply oxygen.
ance is impaired. Any patient with a smoking history, Pharmacological support in the tong-term manage­
regardless of a diagnosis, has some degrcc of chronic ment of chronic bronchitis includes bronchodilators
airflow limitation, which must be considered when (e.g., oral, metered-dose inhalant, inhaled powdered, or
these patients are receiving medical or surgical care. aerosol), corticosteroids (e.g., oral or inhaled), expecto­
The cardiac manifestations of chronic bronchitis rants, antibiotics, inotropic agents (e.g., digitalis), beta­
stem from airway obstruction, secretion accumulation blockers, antidysrhythmic agents, and diuretics. Patients
and reduced capacity to effectively expectorate, poly­ with chronic lung disease must be monitored closely
cythemia, low arterial oxygen tensions, and cardiopul­ during exercise given the potential cardiac effects of
monary deconditioning. Increased airway resistance disease and medications (e.g., beta-blocker agents atten­
secondary to obstruction increases oxygen demand uate the normal hemodynamic responses to exercise and
and hence the work of breathing. This increased de­ bronchodilators, such as ventolin, elicit tachycardia).
mand is superimposed on an oxygen transport system
Principles of physical therapy management
that is already compromised. The cardiovascular sys­
tem attempts to compensate for chronically reduced The goals of long-term management for the patient
arterial oxygen tension by increasing cardiac output with chronic bronchitis include the following:
(i.e., stroke volume and heart rate). As blood gases de­ • Maximize the patient's quality of life, general
teriorate, the production of red blood cells increases health, and well-being and hence physiological
(i.e., polycythcmia) to enhance the oxygen-carrying reserve capacity
capacity of the blood. However, polycythemia in­ • Educate about chronic bronchitis, self-manage­
creases the viscosity of the blood, and in turn, the ment, effects of smoking, nutrition, weight con­
work of the heart to pump blood to the pulmonary and trol, smoking reduction or cessation, other life­
systemic circulations. Furthermore, viscous blood is style factors, medications, infection control, and
prone to circulatory stasis and clotting. role of a rehabilitation program
Low arterial oxygen tensions lead to hypoxic pul­ • Facilitate mucociliary transport
monary vasoconstriction and increased pulmonary • Optimize secretion clearance
vascular resistance (i.e., pulmonary hypertension). • Optimize alveolar ventilation
This also increases the work of the right heart in eject­ Optimize lung volumes a n d capacities a n d
ing blood to the lungs. Chronic overwork of the right flow rates
ventricle leads to hypertrophy, insufficiency, and • Optimize ventilation and perfusion matching
eventual failure of the right heart (cor pulmonale). and gas exchange
Chronically reduced arterial oxygen levels can in­ • Reduce the work of breathing

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516 PART V Guidelines for the Delivery of Cardiopulmonary Physical Therapy: Chronic Cardiopulmonary Conditions

• Reduce the work of the heart health practices (e.g., smoking reduction and cessation,
• Maximize aerobic capacity and efficiency of cold and flu prevention, flu shots, aerobic exercise,
oxygen transport strengthening exercises, nutrition, weight control, hy­
• Optimize physical endurance and exercise ca­ dration, pacing of activities, energy conservation, re­
pacity laxation, and stress management). Chronic bronchitis
• Optimize general muscle strength and thereby and emphysema are often associated with sleep distur­
peripheral oxygen extraction bances. Obstructive sleep apnea is increasingly preva­
Patient monitoring includes dyspnea, respiratory lent with disease severity. Thus activity and sleep pat­
distress, breathing pattern (depth and frequency), ar­ tems need to be assessed to ensure sleep is maximally
terial saturation, cyanosis (delayed sign of desatura­ restorative and is not contributing to the patient's
tion), heart rate, blood pressure, and rate pressure symptoms. Integral to an exercise prescription is the
product. Patients with cardiac dysfunction or low time of day. Exercise is prescribed when the patient is
arteral oxygen tensions require ECG monitoring, par­ least fatigued, most energetic, and when performing
ticularly during exercise. If supplemental oxygen is such a program is most convenient.
used, the FIo2 administered is recorded. Subjectively, Aerobic exercise is an essential component of the
breathlessness is assessed using a modified version of long-term management of the patient with chronic
the Borg scale of perceived exertion. bronchitis to optimize the efficiency of oxygen trans­
Medication that is needed to maximize treatment POit overall and mobilize and remove secretions (Old­
response is administered before treatment (e.g., bron­ enburg, Dolovich, Montgomery, and Newhouse, 1979).
chodilators). Knowledge of the type of medication,
its administration route, and time to and duration of
Emphysema
peak efficacy is essential if treatment is to be maxi­
Pathophysiology and medical management
mally efficacious.
The primary interventions for maximizing car­ Emphysema is associated with a prolonged history
diopulmonary function and oxygen transport in pa­ of smoking and chronic bronchitis and indicates sig­
tients with chronic bronchitis include some combina­ nificant irreversible lung damage. A less common
tion of education, aerobic exercise, strengthening type of emphysema not associated with smoking is
exercises, chest wall mobility exercises, range of mo­ alpha-antitrypsin deficiency. Antitrypsin is essential
tion, body positioning, breathing control and coughing in balancing elastin production and degradation and
maneuvers, airway clearance techniques, relaxation, in preserving optimal lung parenchymal compliance.
activity pacing, and energy conservation. An er­ A deficiency of antitrypsin reduces lung elasticity
gonomic assessment of the patient's work and home and contributes to the characteristic increase in lung
environments may be indicated to minimize oxygen compliance that is the hallmark of emphysema. The
demand and energy expenditure in these settings. pathophysiology of emphysema is presented in detail
The use of supplemental oxygen depends on the in Chapter 4. The principal pathophys iological
severity of the disease. Some patients have no need for deficits include irreversible alveolar damage result­
supplemental oxygen, some need it only during exer­ ing from loss of elastic recoil and the normal tether­
cise, and some patients require continuous oxygen with i n g of t h e a l v e o l i, w h i c h renders t h e lung
proportionately more delivered during activity and ex­ parenchyma excessively compliant and floppy. Ex­
ercise compared with rest. Supplemental oxygen is not cessi ve distension and' dil atation of the termi nal
usually required until lung damage becomes extreme bronchioles and destruction of alveoli reduces the
(i.e., the morphological changes are consistent with the surface area for gas exchange. Hence diffusing ca­
irreversible changes associated with emphysema). pacity is correspondingly reduced. The dead space in
Education is a principal focus of the long-term the lungs and total lung capacity increase s ignifi­
management of the patient with chronic bronchitis. Ed­ cantly. Breathing at normal tidal volume, the pa­
ucation includes the reinforcement of preventative tient's airways close beyond that which normally oc­

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 29 Chronic Primary Cardiopulmonary Dysfunction 517

curs with aging, which contributes to ventilation and poxic vasoconstriction in the lungs. Over time, the
perfusion mismatch and hypoxemia. Time constants heart becomes enlarged and pumps even less effi­
are altered such that alveolar units are not being ciently. In the long-term management of the patient
evenly ventilated. In its nonacute, chronic stages the with emphysema, alveolar ventilation, gas exchange,
primary problems include inadequate and inefficient reduced oxygen transport efficiency, and the work of
gas exchange resulting from the structural damage to breathing and of the heart are the primary pathophys­
the lungs and altered respiratory mechanics of the iological problems. Unlike chronic bronchitis, secre­
lungs, chest wall, and their interaction. The lungs are - tion accumulation may be less problematic in emphy­
hyperinflated, the chest wall becomes rigidly fixed in sema patients during nonacute periods. Nonetheless,
a hyperinflated position, the normal bucket handle optimizing mucociliary transport is an ongoing con­
and pump handle motions of the chest wall are im­ cern in that the consequences of mucous retention
paired, the hemidiaphragms are flattened, the medi­ and infection can be devastating.
astinal structures are shifted, and the heart is dis­
Principles of physical therapy management
placed and rotated, making its function inefficient
(Bake, Dempsey, and Grimby, 1974; Geddes, 1984; The goals for long-term management of the patient
Murray and Nadel, 1988a). The normal mucociliary with emphysema include the following:
transport system is ineffective because years of • Maximize the patient's quality of life, general
smoking destroy the cilia, reduce their number, and health, and well-being and hence physiological
alter their configuration and orientation; thus their reserve capacity
function is correspondingly obliterated or impaired. • Educate about emphysema, self-management,
In addition, these patients are unable to generate smoking reduction and cessation, medications,
high transpulmonary pressures and forced expiratory nutrition, weight control, infection control, and
flow rates because of altered respiratory mechanics. the role of a rehabilitation program
Consequently, coughing maneuvers are weak and in­ • Optimize alveolar ventilation
effective. The administration of supplemental oxy­ • Optimize lung volumes and capacities and flow
gen is limited because these patients rely on their hy­ rates
poxic drive to breathe. This life-preserving drive can • Optimize ventilation and perfusion matching
be attenuated with even moderate levels of oxygen. • Reduce the work of breathing
Thus oxygen administration is limited to low flows. • Reduce the work of the heart
The respiratory muscles are often weak, if not fa­ • Maximize aerobic capacity and efficiency of
tigued (Rochester, and Arora, 1983). Overall, pa­ oxygen transport
tients with emphysema, particularly severe emphy­ • Optimize physical endurance and exercise ca­
sema, tend to be inactive and deconditioned, which pacity
further compromises the efficiency of the oxygen • Optimize general muscle strength and thereby
transport system and the capacity of other steps in peripheral oxygen extraction
the pathway to compensate. • Optimize respiratory muscle strength and en­
There are several physiological compensations durance and overall respiratory muscle efficiency
that occur in response to chronic hypoxemia. Stroke Education focuses on teaching the patient about
volume and cardiac output are increased. The red emphysema, self-management of the disease, the effect
blood cell count increases (polycythemia), however, of smoking and smoking cessation. nutrition, weight
the blood becomes more viscous and requires more control, hydration, relaxation, sleep and rest, stress
work to eject and distribute throughout the body. management, activity pacing, energy conservation, and
Thus the stroke work of the heart is further increased. prevention (e.g., cold and flu prevention, flu shots, aer­
This load on the heart is additional to the increased obic exercise, diet, sleep, and stress management).
afterload on the right ventricle because of an increase Comparable with the patient with chronic bronchi­
in pulmonary vascular resistance secondary to hy­ tis, sleep disturbances are common in the emphysema

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518 PART V Guidelines for the Delivery of Cardiopulmonary Physical Therapy: Chronic Cardiopulmonary Conditions

patient. Activity and sleep patterns are assessed to en­ anaerobic capacity, improved ventilatory muscle
sure sleep is maximally restorative. If obstructive strength and endurance, and increased motivation (Bel­
sleep apnea is disturbing the patient's sleep, medical man and Kengregan, 1981; Belman and Wasserman,
intervention is required. 1981; Dean, 1993). Exercise intensity is prescribed
Patient monitoring includes dyspnea, respiratory based on rating of breathlessness (mod ified Borg
distress, breathing pattern (depth and frequency), ar­ scale) (Chapter 17), in conjunction with objective and
terial saturation, lightheadedness, discoordination, other subjective responses from the exercise test.
heart rate, blood pressure, and rate pressure product. Patients with chronic airflow limitation alter their
Patients with cardiac dysfunction or low arterial oxy­ breathing patterns so that they are breathing on the
gen tensions require ECG monitoring particularly most metabolically efficient portion of the pressure
during exercise. Subjectively, breathlessness is as­ relaxation curve (Chapter 4 and 29). These patients
sessed using a modified version of the Borg scale of tend to breathe with prolonged expiratory phases to
perceived exertion. maximize gas transfer and mixing in the lungs to
Medication that is needed to maximize treatment minimize the effects of altered ventilatory time con­
response is administered before treatment (e.g., bron­ stants. To facilitate such a breathing pattern, the pa­
chodilator). Knowledge of the type of medication, its tient tends to breathe through pursed lips, which may
administration route, and time to and duration of peak create back pressure to maintain the patency of the
efficacy is essential if treatment is to be maximally airways (Muller, Petty, and Filley, 1970). The meta­
efficacious. When patients are on multiple medica­ bolical efficiency of the patient's breathing pattern
tions, the interactions and implications on treatment may be improved further by altering breathing me­
response must be identified. chanics rather than imposing a different breathing
The primary interventions for maximizing car­ pattern that may be suboptimal. Altering breathing
diopulmonary function and oxygen transport in pa­ mechanics involves manipulating the patient's body
tients with emphysema include some combination of position to promote alveolar ventilation, perfusion,
education, aerobic exercise, strengthening exercise, and ventilation and perfusion matching.
ventilatory muscle training (strength and endurance) The increased intrathoracic pressures generated
or ventilatory muscle rest, low flow oxygen, mechan­ during chronic coughing limit venous return, cardiac
ical ventilatory support for home use, chest wall mo­ output, and coronary perfusion. Blood pressure is
bility exercises, range of motion exercises, body posi­ also increased. These effects exert additional myocar­
tioning, breathing control and coughing maneuvers, dial strain, lead to arterial desaturation, and increase
airway-clearance techniques, relaxation, activity pac­ the potential for cardiac dysrhythmias. Breathing
ing, and energy conservation. An ergonomic assess­ control and coughing maneuvers coupled with body
ment of work and home environments may be indi­ positioning and exercise are instructed such that the
cated to minimize oxygen demands in these settings. work of breathing is minimized (i.e., alveolar ventila­
The benefits of aerobic and strengthening exercise tion and gas transfer is as efficient as possible), and
in the long-term management of airflow limitation to coughing is also as efficient as possible (i.e., maxi-­
optimize oxygen transport in patients with compro­ mally productive with the least energy expenditure).
mised oxygen delivery is well established (Dean, Physical therapy is one component of a compre­
1 9 9 3 ; Niederman et aI., 1 9 91 ; R i e s , Ellis, and hensive rehabilitation program in the long-term man­
Hawkins, 1988; ZuWallack, Patel, Reardon, Clark, and agement of emphysema. Such a program also needs to
Normandin, 1991). Patients with severe limitations are include information on health promotion and mainte­
often unable to exercise at a sufficient intensity to ef­ nance, ongoing review and log of medications, respi­
fect aerobic adaptations to the exercise stimulus. Bene­ ratory support (e.g., oxygen aerosol therapy, and me­
fits of exercise in these patients may be explained by chanical ventilatory support), occupational therapy,
desensitization of dyspnea, improved movement effi­ sexual rehabilitation, psychosocial rehabilitation, and
ciency and hence movement economy, improved vocational rehabilitation (Dean, 1993; Murray, 1993).

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 29 Chronic Primary Cardiopulmonary Dysfunction 519

Asthma
heart rate, blood pressure, and rate pressure product.
Pathophysiology and medical management
Patients with cardiac dysfunction or low arterial oxy­
Asthma is a common respiratory condition that is gen tensions require ECG monitoring particularly dur­
characterized hypersensitivity of the airways to exercise. breathlessness is assessed
various in reversible ob­ a modified version of the Borg scale of per­
struction (i.e., and bronchial edema ceived exeltion.
1984; M urray a n d Nadel, I Medication that is needed to maximize treatment
(Chapter In mild cases, no treatment response is administered before treatment (e.g., bron­
other than prophylaxis may be needed. In severe chodilators and antiinflammatories). Knowledge of
cases, asthma can be life Once af­ the type of medication, its administration route, and
fected by the the narrow, increas­ time to and duration of efficacy is essential if
treatment is to be maximally efficacious. When pa-
Breathing narrowed con- tients are on multiple their interactions
tributes to wheezing, reduced alveolar ventilation, and the for must be known.
rapid shallow shortness of breath, in­ The primary interventions for maximizing car­
c reased work of brea t h i n g , des a t u r a t i o n , a n d diopulmonary function and oxygen in pa­
cyanosis. Increased inhomogeneity o f the distribu­ tients with asthma include education, aerobic exer­
tion of ventilation is present in some nonacute chest wall
asthmatic patients Dean, and Ab­
boud, I Although some may ing, and stress management.
mucous hypersecretion, even normal amounts of E ducation is c e n t r a l to t of
pulmonary secretions can obstruct narrowed air­ asthma. The is the basic pathophysiol­
ways leading to atelectasis. Asthma that has welI­ ogy of the disease and its Other central top­
defined triggers is easier to manage than cases ics including preventative health practices are also
where the triggers are less specific. taught cold and flu flu med­

t'f1J1CllJrt8S of physical therapy management

control,
The goals of long-term management of the patient reduction and relaxation and stress man­
with asthma include the following: agement, and the benefits of an life-long
• Maximize the quality of rehabilitation program).
and and hence
mention needs to be made regarding the
reserve capacity
use of medications and inhalers. These are frequently
• Educate about asthma, self-management, nutri­ used (i.e., the patient is unfamiliar
tion, control, reduction and ces­ with the basic pharmacokinetics of the medications
sation, medications and their uses, of used and thus are not ef­
asthmatic and infection control In addition, inhalers are often used improperly;
• Reduce the work of breathing therefore the patient does not derive the full benefit
• Maximize aerobic and of of the medication. The instructions provided _ the
oxygen transport supplier of the inhalers should be strictly followed.
physical endurance and exercise ca­ There are numerous types of all with differ­
pacity ent applications. not adhering to the instructions,
muscle pe- the time and effort is wasted the in­
ripheral oxygen extraction haler ineffectively, the does not derive the full
Patient monitoring includes dyspnea, benefit of the medication, an excessive amount of in­
,,,.,,,, ",,'", breathing pattern (depth and frequency), alter­ haler may be used to for ineffective ap­
of desaturation), plication, there may be increased exposure of the pa­

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520 PART V Guidelines for the Delivery of Cardiopulmonary Physical Therapy: Chronic Cardiopulmonary Conditions

tient to the side effects of the and there is The patient with bronchiectasis has

considerable economic waste. impaired respiratory

A of the of increased pattern, reduced

sensitivity enables the to exert control over cretions, reduced aerobic caDacitv. and is
bronchospastic attacks, The patient is taught to record debilitated.
the freauencv of bronchospastic attacks and The increased intrathoracic pressures
and what relieves them. In this way, the bouts of chronic coughing limit venous return,
learns to avoid or minimize their frequency, caridac output, and coronary perfusion, Blood pres­
severity, and duration and minimizes the amount of sure is also increased. These effects exert additional
medication These are benefits. myocardial lead to arterial desaturation, and
The ex ercise prescription parameters are set increase the potential for cardiac dysrhythmias and
below the bronchospasm threshold, which is estab­
lished based on an exercise test 17 and 23).
tests are performed in a pul­
Principles of physical therapy manal,emrenl
monary function laboratory with appropriate med­ The goals of management of the patient
ical support. Exercise training enables the to with bronchiectasis include the
determine the balance between optimal aerobic ca­ • Maximize the patient's
and medication and the optimal physical en­ and well-being and hence

vironment for exercise. Temperature and humidity reserve capacity and function

can have significant effects on work outout in asth­ • Educate about

matic n.,tipntc nutrition, control,
cessation, medications and their use, and infec­
tion control
Bronchiectasis
• Facilitate mucociliary transport

Pathophysiology and medical management secretion clearance

Bronchiectasis is characterized by dilatation and • Optimize alveolar ventilation

anatomical distortion of the airways and obliteration • Optimize lung volumes and and flow
of t h e b r o n c h i a l t r e e (West, 1987). rates

Bronchiectasis is often the of ventilation and

chronic infection. The associated inflammation • Reduce the work of

leads to occlusion of the airways, which results in • Maximize aerobic of
atelactasis of the and dilata­ oxygen
tion of central by increased traction on the • Optimize ohvsical endurance and exercise ca­
peribronchial sheath (Bates, I In addition, pacity
chronic inflammation weakens the walls of the air­ • Optimize general muscle and thereby
ways, to further dilatation. Fibrotic, connec­ oxygen extraction
tive tissue changes in the wall contribute further to Patient monitoring includes dyspnea,
dilatation and distortion. These anatomical breathing (depth and
"'''''''!,'''::> adversely affect normal mechan­ terial saturation, (a delayed
ics and hence pressure volume characteristics of the tion), heart rate, pressure, and rate pressure
lung. The chest wall becomes hyperinflated and as­ product. Patients with cardiac dysfunction or low ar­
sumes the barrel shape associated with chronic air­ terial oxygen tensions ECG monitoring par­
flow limitation. The overall of bronchiectasis ticularly during exercise. breathlessness
on the number of lung segments involved. is assessed using a modified version of the Borg scale
There is often some reversible airflow limitation as­ of exertion.
sociated with bronchiectasis. Medication that is needed to maximize treatment

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 29 Chronic Primary Cardiopulmonary Dysfunction 521

response is administered before treatment. Knowl­ Between exacerbations, the medical priorities are
edge of the type of medication, its administration to reduce the risk of infection and morbidity and pro­
route, and time to and duration of peak efficacy is es­ mote optimal health, growth, and development.
sential if treatment is to be maximally efficacious.
Principles of physical therapy management
The primary interventions for maximizing car­
diopulmonary function and oxygen transport in pa­ The goals of long-term management of the patient
tients with bronchiectasis include some combination with cystic fibrosis include the following:
of education, aerobic exercise, strengthening exer­ • Maximize the patient's quality of life, general
cise, chest wall mobility exercises, range of motion health and well-being, growth and development,
exercises, body positioning, breathing control and and physiological reserve capacity
coughing maneuvers, airway clearance interventions, • Educate the patient and family about cystic fibro­

optimizing rest and sleep, relaxation, pacing, and en­ sis, self-management, nutrition, prevention of acute

ergy conservation. An ergonomic assessment of the exacerbations of the disease, infection control, and

patient's work and home environments may be indi­ medication's uses, modes of adi
m nistration,

cated to maximize function in these settings. macokinetics and times to peak efficacies.

Education is a central component of the patient's • Facilitate mucociliary transport

long-term self-management rehabilitation program. • Optimize secretion clearance
Preventative health practices are taught (e.g., cold and • Optimize alveolar ventilation
flu prevention, flu shots, smoking cessation, sleep, • Optimize lung volumes and capacities and flow
aerobic exercise, nutrition, weight control, and hydra­ rates
tion, relaxation, stress management, and the long-term • Optimize ventilation and perfusion matching
benefits of an integrative, rehabilitation program). • Reduce the work of breathing
• Reduce the work of and strain on the heart
• Maximize aerobic capacity and efficiency of
Cystic Fibrosis
oxygen transp0l1
Pathophysiology and medical management
• Optimize physical endurance and exercise ca­
Cystic fibrosis is a complex exocrine disease that has pacity
significant systemic effects (Landau and Phelan, • Optimize general muscle strength and thereby
1973; Murray and Nadel, 1988b). The diesase is con­ peripheral oxygen extraction
genital and is hallmarked by nutritional deficits con­ Patient monitoring includes dyspnea, respiratory
tributing to impaired growth and development. Pul­ distress, breathing pattern (depth and frequency), ar­
monary function shows progressive decline with terial saturation, cyanosis (a delayed sign of desatura­
commensurate reductions in homogeneity of ventila­ tion), heart rate, blood pressure, and rate pressure
tion and inspiratory pressures (Chatham et aI., 1994; product. Patients with cardiac dysfunction or low ar­
Cotton, Graham, Mink, and Habbick, 1985; Ross et terial oxygen tensions require ECG monitoring, par­
aI., 1989). Cardiopulmonary involvement can be clas­ ticularly during exercise. Subjectively, breathlessness
sified into three groups, namely, no physical signs in is assessed using a modified version of the Borg scale
the chest, occasional cough and sputum, and constant of perceived exertion.
cough, sputum, and other signs. Patients in each clas­ Medication that is needed to maximize treatment
sification can benefit from physical therapy with re­ response is administered before treatment. Knowl­
spect to enhancing oxygen transport. Moderate and edge of the type of medication, its administration
severe disease is characterized by significant airflow route, and time to and duration of peak efficacy is es­
obstruction secondary to copious, tenacious secre­ sential if treatment is to be maximally efficacious.
tions. In addition, pulmonary hypertension and right The primary interventions for maximizing car­
heart insufficiency may be manifested and eventual diopulmonary function and oxygen transport in
failure may ensue. patients with cystic fibrosis include some combina­

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522 PART V Guidelines for the Delivery of Cardiopulmonary Physical Therapy: Chronic Cardiopulmonary Conditions

tion of education, aerobic exercise, strengthening ex­ drainage can be integrated into breathing control.
ercise, ventilatory muscle training (strength and en­ This procedure focuses on eliciting coughing when
durance), ventilatory muscle rest, supplemental oxy­ it will be most productive, thereby minimizing less
gen, mechanical ventilation for home use, chest wall productive, exhaustive coughing. Patients with cys­
mobility exercises, range of motion exercises, body tic fibrosis often cough so violently and uncontrol­
positioning, breathing control and coughing maneu­ lably that it leads to significant arterial desaturation,
vers, airway clearance interventions, relaxation, pac­ vomi ting, and exhaustion and impedes venous re­
ing, and energy conservation. turn and cardiac output.
Education focuses on teaching preventative health Ventilatory devices such as the positive expiratory
practices and infection control (e.g., cold and flu, flu pressure (PEP) mask and the flutter valve have
shots, aerobic exercise, nutrition, hydration, relax­ shown benefit in some patients with CF with respect
ation, stress management, activity pacing, and energy to reducing airway closure, clearing secretions, and
conservation). enhancing gas exchange (Pryor, 1993; Webber and
Physical activity and aerobic exercise need to be Pryor, 1994). Such aids may be useful adjuncts in
integrated early into the life style of the child with some patients, however, they do not replace the mul­
cystic fibrosis (Cystic Fibrosis and Physical Activ­ tiple benefits of physical activity and exercise on op­
ity, International 10urnal of Sports Medicine, 1988; timizing oxygen transport including mobilizing and
Keens, Krastins, Wannamaker, Levison, Crozier, removing secretions.
and Bryan, 1977; Zach, Oberwaldner, and Hausler,
1992). As much as possible, the child is integrated
RESTRICTIVE PATIERNS
into activities of his or her peer group. A prescribed
Interstitial Lung Disease
aerobic exercise program is designed to optimize
Pathophysiology and medical management
the efficiency of oxygen transport at all steps in the
pathway and thereby enhance functional capacity The pathophysiology of restrictive lung disorders
overall. Physical activity and aerobic exercise en­ and interstitial lung disease (ILD) in particular is
hances mucociliary transport and mucociliary clear­ described in Chapter 4. This clasification of lung
ance, maximizes alveolar ventilation and ventila­ disease is associated with various occupations and
tion and perfusion matching, increases ventilatory the i n h a l a t i o n of i n o r g a n i c and organic dust
muscle strength and endurance and airway diame­ (Chung and Dean, 1989). As the disease pro­
ter, and stimulates a productive effective cough. gresses, total lung capacity (TLC) and vital capac­
Furthermore, physical activity and exercise have ity (VC) are reduced. Residual volume often re­
been associated with improved immunity and re­ mains the same. Maximal flow rates tend to be
duced risks of infection (Pyne, 1994; Shephard, increased as compliance is reduced. The drive to
Verde, Thomas, and Shek, 1991). These are signifi­ breathe, breathing frequency, and the ratio of tidal
cant outcomes for patients with cystic fibrosis who volume to total lung capacity are increased. Glan­
have thick copious secretions. dular hyperplasia may be present, leading to mu­
In addition, breathing control and coughing ma­ cous hypersecretion in some patients. Diffusing ca­
neuvers are included as a component of a long-term pacity may be reduced but may only be apparent
self-management rehabilitation program. Postural during exercise (i.e., art.erial desaturation and dys­
drainage and manual techniques have been the pnea). Exercise-induced desaturation and reduction
mainstay of airway clearance in the past. Exercise, in Pa02 may also reflect shunt and ventilation and
however, has a primary role in secretion mobiliza­ perfusion mismatch (Jernudd-Wilhelmsson, Horn­
tion and as an airway clearance intervention (Dean blad, and Hedenstierna, 1986).
and Ross, 1989). Breathing control and coughing Hemodynamic changes may be present (e.g., in­
stategies are coupled with exercise to facilitate se­ creased pulmonary artery pressure). Chronically in­
cretion clearance. The principles of autogenic creased pulmonary artery pressures and hence in­

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 29 Chronic Primary Cardiopllinl10nal Dysfunction 523

vascular lead to in­

hypertrophy, maneuvel'S, relax­
and energy conservation. An er­
exercise H "Hv assessment of work and home environ­
ments may be indicated to maximize f u nction In
these -'.""'MC'

Principles of physical therapy management Education is a central component of a

The of management of the patient sive rehabilitation program for the management of in­
with interstitial disease include the following: terstitiallung disease. Education includes information
quality of life, general on preventative health removal from
and hence physiological the causative
vention shots,

cessation, nutrition,
tion, medications and their uses, prevention, ation, activity
health promotion, and infection control During aerobic with interstitial
• Optimize alveolar ventilation lung disease are prone to arterial desaturation (Arita,
volumes and capacities Nishida, and 198 Patients who desatu­
ventilation and perfusion matching rate during and
1985) require oxygen
The intensity of the exercise is defined by
• Reduce the work of the heart arterial breathlessness, and work of the
and efficiency of heart, in with other responses.

endurance and exercise ca­

lung Cancer

muscle and thereby

Pathophysiology and 1lIt:UI(;,(l1 management

oxygen extraction Lung cancer is a cause of death for men and

includes incidence is for women. Once
(depth and ar­ 80% of cancer is
terial heart rate, blood pressure, and rate correlated with a and exposure to
pressure Patients with cardiac or coal tars, asbestos, and radioactive dusts. The
low arterial oxygen tensions ECG monitoring, ity of primary malignant tumors are bronchogenic
particularly exercise, breathless­ carcinomas. They are located and thus con­
ness is assessed a modified version of the Borg tribute to bronchial and pneu­
scale of exertion, monia. Pathophysiologically, cancer has features
Medication that is needed to maximize treatment of both obstructive and restrictive lung disease. The
response is administered before treatment. Knowl­ patient presents with obstruction, dyspnea,
of the of its administration cough, and hemoptysis (MlIITaY and I
efficacy is es­ Treatment is limited to surgery, if metastasis has been
sential if treatment is to be efficacious, mled out, or conservative management with radiation
The interventions for maximizing car­ and chemotherapy.
diopulmonary function and oxygen transport in pa­ Bronchogenic carcinomas metastasize
tients with interstitial lung disease include some through the circulation and channels to
c o m b i n a t i o n o f e d u c a t i o n, a e r o b i c e x e r c i s e, other organs including
chest wall mobility exer­ and adrenal glands.

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524 PART V Guidelines for the Delivery of Cardiopulmonary Physical Therapy: Chronic Cardiopulmonary Conditions

If detected early, thoracic surgery may be per­ diac dysfunction or low arterial oxygen tensions re­
fonned to excise the cancerous tumor (Chapter 28). If quire ECG monitoring. Subjectively, breathlessness
inoperable, or in the case of metastases, a patient may is assessed using a modified version of the Borg scale
be managed at home or in a hospice. Patients are de­ of perceived exertion.
bilitated, often undernourished, fatigued, short of Medication that is needed to maximize treatment
breath, lethargic, depressed, and in pain (Saunders response is administered before treatment (e.g., anal­
and McCorkle, 1985). Although these patients are gesics or bronchodilators). Knowledge of the type of
often extremely ill, there is a growing trend to man­ medication, its administration route, and time to and
age these patients in the community whenever possi­ duration of peak efficacy is essential if treatment is to
ble. As the disease progresses, maintaining function be maximally efficacious.
and reducing the rate of deterioration become pri­ The primary interventions for maximizing car­
mary goals. diopulmonary function and oxygen transport in pa­
tients with lung cancer include some combination of
Principles of physical therapy management
education, mobilization, strengthening exercises,
The goals of long-term management of the medical chest wall mobility exercises, body positioning, sup­
patient with lung cancer include the following: plemental oxygen, mechanical respiratory support,
breathing control and coughing maneuvers, airway
• Maximize the patient's quality of life, general
clearance interventions, sleep and rest, relaxation, ac­
health, and well-being and hence physiological
tivity pacing, and energy conservation. Treatments
reserve capacity
are timed whenever possible to coincide with the pa­
• Educate the patient and family about the bene­
tients' peak times during the day.
fits of a palliative program
Patients with cancer may benefit frol11 the immuno­
• Promote self-determination
logical effects, as well as oxygen transport effects of
• Provide supportive care
mobilization and physical activity (Calabrese, 1990).
• Optimize pain control
The prescriptive parameters are adjusted each session
• Facilitate mucociliary transport
given the rapid changes in these patients' conditions.
• Optimize scretion clearance
Patients with lung cancer often cough up and ex­
• Optimize alveolar ventilation
pectorate blood in their sputum. The airways need to
• Optimize lung volumes and capacities and flow
be as clear as possible to avoid obstruction, atelecta­
rates
sis, risk of infection, and pneumonia. Although air­
• Optimize ventilation and pelfusion matching
way clearance is an important goal, treatments should
• Reduce the work of breathing
avoid contributing significantly to bleeding and blood
• Maximize aerobic capacity and efficiency of
loss if possible. This blood loss may contribute to
oxygen transpolt
anemia and fatigue.
• Optimize physical endurance and exercise ca­
Manual airway clearance interventions may be in­
pacity
dicated in some patients. Postural drainage may be
• Otimize general muscle strength and thereby pe­
coupled with percussion and manual vibration. The
ripheral oxygen extraction
impact of manual interventions, however, may con­
• Optimize the benefits of sleep and rest
tribute to bleeding; thus the patient requires stringent
• Minimize the effects of restricted mobility and
monitoring. Metastases to the thoracic cavity and the
recumbency
ribs in particular may preclude percussion in favor of
Patient monitoring includes dyspnea, respiratory manual vibration being petformed over nonaffected
distress, breathing pattern (depth and frequency), ar­ areas. Treatment duration may be limited by the pa­
terial saturation, cyanosis (a delayed sign of desatura­ tient's tolerance. Tolerance may be improved by
tion), heart rate, blood pressure, and rate pressure modifying body position or by shortening treatments
product. Patients who can be mobilized but have car- but increasing their frequency.

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 29 Chronic Primary Cardiopulmonary Dysfunction 525

pist should examine the medication before treatment

PRIMARY CARDIOVASCULAR
to ensure that the expiratory date has not and
Angina
to take responsibility for the medication
Pathophysiology and medical management
near the patient for access to it should the patient de­
refers to pain from reduced treatment.
blood flow to the myocardium. Even though management of the patient
elicited during angina may be with include the following:
stress or, in severe cases, may occur at rest. Atheroscle­ • Maximize the patient's
rosis of one or more of the coronary arteries is the prin­ health, and and hence
cipal cause. Coronary vasospasm is a less common serve
cause of The pathophysiology of is de­ Educate about heart disease,
scribed in detail in Chapter 4. A history of
cessitates further examination to establish the medica­
of the coronary occlusion. If severe, the patient is tions and their use, activity, and exercise
scheduled for coronary surgery 28) to • Maximize aerobic capacity and efficiency of oxy­
restore normal coronary blood flow. The acute and gen transport of all steps in the
long-term management of the cardiac is endurance and exercise 'J H1

presented in 28. In less severe cases, is general muscle strength and thereby pe­
managed with medications (e.g., sublin­ oxygen extraction
and physical Patient monitoring includes hemodynamic moni­
has stabilized, a 2TElaea-E�xer­ toring (i.e., heart rate, blood pressure, rate pressure
else tolerance test may be conducted under supervision product, and responses to treat­
in a cardiac stress testing facility where l2-lead ECG ment, particularly exercise, should also be recorded
monitoring can be performed. The exercise (e.g., rating of Signs of
which the exhibits (i.e., the chest dyspnea, dizzi­
and serve as the basis for n e s s, dis orientation, dis c oordination, cyanosis,
activity and exercise. coughing, and chest sound (i.e., a
The body position in which exercise is performed need to be monitored. is not an
is important in patients with heart disease. Positions symptom under any circurmstance. Should it occur,
of increase the volume of fluid shifted treatment is immediately and
to the central circulation. This in­ emergency measures instituted. Treatments will be
creases venous return and the work of the heart. Thus safer and more prescribed with continous
body positions are selected for these patients EeG Without ECG treat­
to minimize cardiac work during exercise and when ments need to be conservative. If there is any doubt at
resting after exercise Wolfson, and any time about the of a
Cohen, Levine and 1952). and her or his ability to tolerate treatment safely, the
should be referred to a general practitioner or
PrinCiples 01 physical therapy management
cardiologist for clearance before being treated.
Patients may be referred to therapy with a Medication that is needed to maximize treatment
history of angina as a or as a prob­ response is administered before treatment. Knowl­
lem. angina is managed with the same of the of medication, its administration
care and given it can be a route, time to as well as duration of efficacy is
condition. A patient for whom antianginal medication essential if treatment is to be maximally efficacious.
is prescribed must have the medication present. The For the long-term of angina, interven­
medication must not have expired and must be within tions include some combination of education, aerobic
visible access during treatment. The thera­ chest wall

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526 PART V Guidelines for the Delivery of Cardiopulmonary Physical Therapy: Chronic Cardiopulmonary Conditions

activity and energy con­ jury and cell death Injured myocar­
servation. Education includes information about heart dial cells either recover or die the healing
disease and risk factors smoking, diet, stress, period. Thus minimizing further damage and maxi-
weight, and being active in the during this 6-week period is crit­
hot environments) and preventative strate­ ical. infarctions can range from
smoking reduction and low-fat silent and unnoticed by the patient to life
reduced alcohol comsumption, exercise, relax­ threatening. can occur in the my­
ation, activity pacing, and stress management). ocardium but occur primarily in the ventricles. The
Patients with are at risk of an in- the greater the risk of ventricu­
and monitor- acute edema, and left
are needed to detect or frank myocardial ventricular failure. Because myocardial ischemia
infarction. These patients are potentially hemody­ and infarction impair the pumping action of the
namically unstable; thus their re­ heart and thus cardiac output, patients tend to be
sponses during, and after treatment, and in need of oxygen. Even after the oxy­
larly aerobic and should be gen has been discontinued and the has
monitored and recorded. Minimally, heart rate, healed, the patient may continue to be vulnerable
blood pressure, and rate pressure product should be hemodynamically. the myocardium will have
taken alonll with the some that will affect both the electrical ex­
citability and the mechanical function of the heart.
In the may continue to have low
normal arterial blood gases. Hypoxemia is lethal in
that it and predisposes tissues
to must be avoided. Post
namic response. activity and aerobic exer­ myocardial infarction are usually dis-
cise are prescribed at a heart rate or per­ home on several medications (e.g., nitro­
ceived exertion ranges that are below the anginal glycerin, calcium antagonists, beta-blockers, and di­
threshold based on a tolerance text uretics). on the of
1 Peak exercise tests in cardiac usually continue to one or more of
,f'V"""""'"

that may elicit angina o r these medications over the long term. The need for
are performed i n a cardiac stress oxygen is usually short term and restricted to the
laboratory under the supervision of a s hospital stay.
The body position in which aerobic exercise is
Principles of physical therapy management
IS Important in with heart disease.
Positions of increase the volume of tluid After from hospital, many post myocardial
shifted from the periphery to the central circulation. infarction patients see a physical therapist either pri­
This increases venous return and the work of the vately or through a cardiac rehabilitation program.
heart. Thus positions are selected for The majority of will remain on
these patients to minimize cardiac work exer­ rehabilitation program an exercise program
cise and during rest after exercise (Lanllou et for 6 to 12 months.
1977; Levine and Lown, 1952). Regardless of the setting, therapy in­
cludes education, support, and a super­
vised for safely and
Myocardial Infarction
confidence physical exertion. In addition, an
Pathophysiology and medical management
exercise program is specifica!Jy prescribed for the pa­
frequently frank myocardial is­ tient to enhance oxygen transport up-
chemia and infarction. Myocardial ischemia is re­ and utilization at the tissue level)
whereas infarction denotes mvoeardial in­ the metabolic demand on the heart.

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 29 Chronic Primary Cardiopulmonary Dysfunction 527

A GXTT is conducted before leaving the hospital Patient monitoring includes hemodynamic moni­
or when the patient is enrolled in an exercise pro­ toring (i.e., healt rate, blood pressure, and rate pres­
gram. The time between the exercise test and the ex­ sure product). Subjective responses to treatment, par­
ercise prescription and implementation of the exer­ ticularly exercise, should also be recorded (e.g.,
cise program should be minimal. Peak (formerly Borg's rating of perceived exeI1ion). Angina is not an
referred to as maximal) exercise tests are conducted acceptable symptom under any circumstance. Should
in the presence of a cardiologist and provide the opti­ it occur, however, treatment is immediately discontin­
mal basis for an exercise prescription. Submaximal ued and emergency measures instituted. Treatments
exercise tests can be conducted by the physical thera­ will be safer and more precisely presclibed with con­
pist. These can provide the basis for an exercise pro­ tinuous ECG monitoring. Without ECG monitoring,
gram, however, the prescription is conservative com­ treatments need to be conservative. If there is any
pared with that based on a peak exercise test. The doubt at any time about the hemodynamic stability of
principles and practice of exercise testing are de­ a patient and her or his ability to tolerate treatment
scribed in Chapter 17, 23 and 24. Such testing is an safely, the patient should be referred to a general prac­
art and an exacting science and should be carried out titioner for clearance before being treated.
in a rigidly standardized manner to ensure the test re­ Medication that is needed to maximize treatment
sults are maximally valid, reliable, and useful. response is administered before treatment (e.g., an­
Comparable with the angina patient and not overt tiarrhythic agents). Knowledge of the type of medica­
infarction, the following caution must be adhered to tion, its administration route, and time to and dura­
with the patient who has a history of myocardial in­ tion of peak efficacy is essential if treatment is to be
farction. A patient jar whom antianginal medication maximally efficacious.
is prescribed must have the medication present. The The primary interventions for maximizing car­
medication must not have expired and must be within diopulmonary function and oxygen transport in pa­
visible access during treatment. The physical thera­ tients with myocardial infarction include some combi­
pist should examine the medication before treatment nation of education, aerobic exercise, strengthening
to ensure that the expiratory date has not passed and exercises, chest wall mobility exercises, body position­
to take responsibility for positioning the medication ing, breathing control and coughing maneuvers, relax­
near the patient for access to it should the patient de­ ation, activity pacing, and energy conservation. An er­
velop angina during treatment. gonomic assessment of b o th work a n d h ome
The goals of long-term management of the patient environments may be indicated to minimize myocar­
with myocardial infarction include the following: dial strain.
• Maximize the patient's quality of life, general Education focuses on the teaching the basic patho­
health, and well-being and hence physiological physiology of heart disease, its risk factors, and pre­
reserve capacity vention. Health promotion practices are advocated
• Educate about myocardial infarction, self-man­ (e.g., smoking reduction and cessation, good nutrition,
agement, nutrition, weight control, smoking re­ weight control, hydration, quality rest, and sleep peri­
duction and cessation, risk factors, disease pre­ ods). In addition, types of physical activity that im­
vention, medications, life style, activities of pose undue myocardial strain, increase intrathoracic
daily living, and avoiding static exercise, strain­ pressure, and restrict venous return and cardiac out­
ing, and the Valsalva maneuver put, such as heaving lifting, straining, or the Val salva
• Maximize aerobic capacity and efficiency of maneuver, are avoided. The patient is taught to moni­
oxygen transpOlt tor and practice vigilance in monitoling his or her own
• Reduce the work of the heart condition (e.g., new signs of infarction). These pa­
• Optimize physical endurance and exercise ca­ tients are potentially hemodynamically unstable and
pacity thus their hemodynamic responses before, dUling, and
• Optimize general muscle strength and thereby after treatments, particularly exercise, should be mon­
peripheral oxygen extraction itored and recorded (i.e., heart rate, blood pressure,

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528 PART V Guidelines for the Delivery of Cardiopulmonary Physical Therapy: Chronic Cardiopulmonary Conditions

and rate pressure product should be taken, along with Prophylactic antibiotics against endocarditis are
their subjective responses to treatment). administered to most patients with significant valvu­
Peak exercise tests in cardiac patients that may lar involvement and in mild disease before proce­
elicit angina or ST -segment changes are performed in dures such as dental work.
a cardiac stress testing laboratory under the supervi­
Principles of physical therapy management
sion of a cardiologist. The parameters of the exercise
prescription are set based on a peak exercise test. In­ The goals of long-term management of the patient
tensity is set within a heart rate, oxygen consumption, with valvular heart disease include the following:
and exertion range (e.g., 70% to 85%, of the anginal • Maximize the patient's quality of life, general
threshold) (Chapter 17). health, and well-being and hence physiological
Aerobic exercise of large muscle groups rather reserve capacity
than small muscle groups (e.g., arm ergometry) is se­ • Educate about cardiac valvular disease, self­
lected to minimize the increased hemodynamic de­ management, nutrition, weight control, smoking
mand and strain and the increased work of the heart reduction and cessation, cardiac risk factors, dis­
associated with this type of work. Hot and humid con­ ease prevention, medications, life style, activities
ditions also place additional stress on the heart, thus of daily living, and avoiding static exercise, strain­
exercising under these conditions should be avoided. ing, and the Valsalva maneuver
The body position in which aerobic exercise is • Maximize aerobic capacity and efficiency of
performed is important in patients with heart disease. oxygen transport
Positions of recumbency increase the volume of tliud • Optimize physical endurance and exercise ca­
shifted from the periphery to the central circulation. pacity
This increases venous return and the work of the • Reduce the work of the heart
heart. Thus upright body positions are selected for • Optimize general muscle strength and thereby
these patients to minimize cardiac work during exer­ peripheral oxygen extraction
cise and during rest after exercise (Langou et aI., Physical therapists are involved with the manage­
1977; Levine and Lown, 1952; Prakash, Parmley, Dik­ ment of patients with valve defects medically, either
shit, Forrester, and Swan, 1 973). as a primary or secondary problem, and surgically.
After surgery, these patients progress well; the princi­
ples of their management are presented in Chapter
Valvular Disease
28. With respect to the medical management of valve
Pathophysiology and medical management
defects, the goal is to optimize oxygen transport in
Valve dysfunction is either congential or acquired and the patient for whom surgery is not indicated either
may require treatment as a primary condition or is pre­ because the defect is not sufficiently severe or be­
sent as a secondary condition. Any of the heart and cause the patient cannot or refuses to undergo
pulmonary valves may be affected. Rheumatic fever surgery. Although the mechanical defect cannot be
was a common cause of rheumatic heatt disease and in improved, oxygen transport may be improved with
particular mitral valve insufficiency (Goldberger, judicious exercise prescription in some patients. The
1990). Interconnecting lymphatic vessels between the parameters of the exercise prescription are usually
tonsils and the heart are thought to be responsible. Cal­ moderate in that inapprop'riate exercise doses can fur­
cification of valves that impairs opening and closing is ther disrupt the inappropriate balance between oxy­
another example of an acquired valve dysfunction. gen demand and supply and thus further exacerbate
Clinically, patients may present with exertional symptoms. In addition, there is the potential for fur­
dyspnea, excessive fatigue, palpitations, fluid reten­ ther valvular dysfunction if the myocardium is me­
tion, and orthopnea (Sokolow, McIlroy, and CheitJin, chanically strained.
1990). These sypmtoms are often relieved when exer­ The goal of the aerobic exercise prescription is to
tion is discontinued. identify the exercise dose that will optimize the effi­

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 29 Chronic Primary Cardiopulmonary Dysfunction 529

ciency of other steps in the oxygen transport pathway pain, lightheadedness, dizziness, disorientation, dis­
such that the available oxygen delivered to the pe­ c o o r d i n a tion, c y a n o s i s , c ou g h i n g , chest s o u n d
ripheral tissues is maximally used without constitut­ changes (i.e., a gallop) need t o b e monitored. Treat­
ing a significant mechanical strain on the heart. Max­ ments will be safer and more precisely prescribed
imizing work output over time is the goal. Thus the with continuous ECG monitoring. Without ECG
severely compromised patient will perform a signifi­ monitoring, treatments need to be conservative. If
cantly greater volume of functional work over time there is any doubt about the hemodynamic stability of
with short, frequent sessions of exercise rather than a patient and her or his ability to tolerate treatment
longer, less-frequent sessions. safely, the patient should be referred to their general
If the valve defect is a secondary problem, the practitioner for clearance before being treated.
physical therapist must assess the severity of the de­ The primary interventions for maximizing car­
fect and its functional consequences. The following diopulmonary function and oxygen transport in pa­
questions must be addressed: tients with cardiac defects include some combination
I. Does the defect preclude treatment? of education, aerobic exercise, strengthening exercises,
2. Does the defect require that treatment be modi­ chest wall mobility exercises, body p ositioning,
fied, if so, how? breathing control, coughing maneuvers, relaxation, ac­
3. What special precautions should be taken? tivity pacing, and energy conservation. An ergonomic
4. What signs and symptoms would indicate the assessment of both work and home environments may
patient is distressed? be indicated to minimize myocardial strain.
5. What parameters should be monitored? Exercise prescription for patients with valvular heat1
6. Is the patient taking medications as prescribed? disease is modified to ensure that the energy demand is
How might these medications alter the patient's commensurate with oxygen supply. Otherwise, exces­
response to treatment? sive oxygen demand will worsen the patient's response
7. Is there any evidence of heart failure? If so, to physical activity, lead to further distress, and possi­
what will the effects of exercise be? bly reduced functional capacity. Aerobic exercise of
8. If there is no evidence of heart failure at rest, large muscle groups rather than small muscle groups
what is the chance that insufficiency will de­ (e.g., arm ergometry) is selected to minimize the in­
velop with exercise? creased hemodynamic demand and strain and the in­
Comparable with the management of the patient with creased work of the heat1 associated with this type of
a history of angina with or without a history of my­ work. As for other types of cardiac conditions, exercis­
ocardial infarction, body positions, activities, and res­ ing in hot and humid conditions shoud be avoided.
piratory maneuvers that are associated with increased The body position in which aerobic exercise is
hemodynamic strain are avoided. performed is important in patients with heart disease.
Medication that is needed to maximize treatment Positions of recumbency increase the volume of fluid
response is administered before treatment. Knowl­ shifted from the periphery to the central circulation.
edge of the type of medication, its administration This increases venous return and the work of the
route, and time to and duration of peak efficacy is es­ heart. Thus upright body positions are selected for
sential if treatment is to be maximally efficacious. these patients to minimize cardiac work during exer­
These patients are potentially hemodynamically cise and during rest after exercise (Langou et aI.,
unstable; thus their hemodynamic responses before, 1977; Levine and Lown, 1952).
during, and after treatments, particularly exercise,
should be monitored and recorded. Monitoring in­
Peripheral Vascular Disease
cludes hemodynamic monitoring (i.e., heart rate,
Patholphysiology and medical management
blood pressure, and rate prcssure product). Subjective
responses to treatment (e.g., rating of perceived exer­ Peripheral vascular disease results primarily from ather­
tion) should also be recorded. Signs of dyspnea, chest osclerosis and occlusion of the peripheral arteries (e.g.,

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530 PART V Guidelines for the Delivery of Cardiopulmonary Physical Therapy: Chronic Cardiopulmonary Conditions

thoracic aorta, femoral artery, and popliteal artery) • Educate about atherosclerosis, self-management,
(Juergens, Spittell, and Fairbairn, 1980). Diabetes mel­ nutrition, weight control, smoking reduction and
litus, which can result in microangiopathy and auto­ cessation, risk factors, disease prevention, medica­
nomic polyneuropathy, is another contributing factor to tions, life style, activities of daily living, and
peripheral vascular disease in the lower extremjties. avoiding static exercise, straining, and the Valsalva
Al1erial occlusion results in reduced blood flow to maneuver
the extremities and hence reduced segmental blood • Maximize arobic capacity and efficiency of oxy­
pressure distal to the occlusion. In mild cases of arter­ gen transport
ial stenosis the patient may be asymptomatic because • Optimize the work of the heart
considerable stenosis has to occur before significant • Optimize physical endurance and exercise ca­
reduction in peripheral blood flow. Furthermore, if pacity
atheroslerosis develops gradually, collateral circula­ • Optimize general muscle strength and thereby
tion may develop sufficiently to offset progressive peripheral oxygen extraction
vessel narrowing. Clinically, the patient presents with The goals of long-term management of the patient
complaints of limb pain on exercise, coldness in the with peripheral vascular disease secondary to dia­
affected leg, and possibly numbness (Dean, 1987). betes mellitus must incorporate both the principles
The characteristic limb pain results from ischemia and for the managment of the patient with peripheral vas­
is referred to as intermittent claudication. Mild to cular disease secondary to atherosclerosis and sec­
moderately severe cases are managed conservatively. ondary to diabetes mellitus.
Pain at rest is suggestive of severe stenosis and signif­ Patient monitoring includes hemodynamic moni­
icant reduction of blood flow to the limb. Signifi­ toring (i.e., heart rate, blood pressure, and rate pres­
cantly reduced blood flow leads to ischemia color sure product). Subjective responses to treatment,
changes, skin breakdown, ulceration, and eventually particularly exercise, should also be recorded (e.g.,
gangrene. Bypass surgery is carried to revascularize a pain scale and Borg's rating of perceived exertion).
threatened limb or in severe cases where gangrene has These patients have an increased risk of angina.
developed, amputation of the limb is indicated. Angina is not an acceptable symptom under any cir­
Intermittent claudication secondary to mild-to­ cumstance. Thus patients should be cleared by their
moderate arterial stenosis can benefit from aerobic physicians or cardiologists before undertaking a
exercise, which may stimulate the development of therapeutic exercise program. Diabetic patients are
collateral blood vessels around the stenosed vessel. potentially hemodynamically unstable; thus their he­
This condition can severely restrict mobility, which modynamic responses before, during, and after
reduces function in addition to aerobic capacity and treatment, particularly exercise, should be moni­
efficient oxygen transport overall. tored and recorded (i.e., heart rate, blood pressure,
Patients with pelipheral vascular disease from dif­ and rate pressure product should be taken) along
fuse systemic atherosclerosis can be expected to have with their subjective responses to exercise (e.g.,
stenosis of the coronary arteries even though they pain and perceived exertion). If there is any doubt at
may be asymptomatic. These patients are monitored any time about the hemodynamic stability of a pa­
as stringently as cardiac patients. tient and her or his ability to tolerate treatment
safely, the patient shou. l d be referred to a general
Principles of physical therapy management practitioner for clearance before being treated or
The goals of long-term management of the patient continuation of treatment.
with peripheral vascular disease secondary to athero­ Medication that is needed to maximize treatment
sclerosis include the following: response is administered before treatment. Knowl­
• Maximize the patient's quality of life, general edge of the type of medication, its administration
health, and well-being and hence physiological route, and time to and duration of peak efficacy is es­
reserve capacity sential if treatment is to be maximally efficacious.

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 29 Chronic Primary Cardiopulmonary Dysfunction 531

The primary interventions for maximizing car­ The body position in which aerobic exercise is per­
diopulmonary function and oxygen transport in patients formed is important in patients with peripheral vascu­
with pe[ipheral vascular di:;ease secondary to athero­ lar disease. Positions of recumbency eliminate the
sclerosis include some combination of education, aero­ vertical gravitational gradient. This gradient increases
bic exercise, strengthenjng exercises, relaxation, activ­ blood pressure significantly to the lower extremeites.
ity pacing, and energy conservation. An ergonomic Therefore the claudication threshold is lowered in re­
assessment of both work and home environments may cumbent positions. Recumbent positions also increase
be indicated to minimize myocardial strain. venous return and the work of the heart. Thus upright
Education focuses on teaching the basic patho­ body positions are selected for these patients to maxi­
physiology of atherosclerosis, its risk factors, and mize blood pressure in the lower extremities and to
prevention. Health promotion practices are advocated minimize cardiac work during exercise and during rest
(e.g., smoking reduction and cessation, nutrition, after exercise (Langou et aI., 1977).
weight control, hydration, quality rest, and sleep peri­
ods). In addition, types of physical activity that im­
Hypertension
pose undue myocardial strain, increase intrathoracic
pressure, and restict venous return and cardiac output,
Pathophysiology and medical management
such as heaving lifting, straining, or the Valsalva ma­ Hypertension or high blood pressure is a serious
neuver, are avoided. The patient is taught to monitor condition. Most patients experience no symptoms;
and practice vigilance in monitoring signs and symp­ thus adherence to medication regimens is often
toms of vascular insufficiency in the affected limb poor. Approximately 90% of hypertension is termed
and intermittent claudication. Any sign of skin red­ essential hypertension (i.e., no known etiology).
ness in the feet should be monitored closely. In the Hypertension predisposes a patient to stroke, my­
diabetic patient, any threat of skin breakdown re­ ocardial infarction, hemorrhage, and infarction of
quires medical attention and discontinuation of exer­ other vital organs (Sokolow, McIlroy, and Cheitlin,
cise until medical clearance has been obtained. Pa­ 1990). Blood pressure tends to increase with age.
tients with peripheral artery disease are taught to take With the aging of the population, the incidence of
care of their feet particularly before and after exer­ hypertension is increasing. Increased blood pressure
cise. The feet and footwear should be kept clean. The results from increased peripheral vascular resis­
inner surfaces of shoes and socks should be smooth. tance; therefore medications are prescribed that re­
During peak exercise tests, patients with periph­ duce myocardial afterload and peripheral vascular
eral vascular disease secondary to atherosclerosis resistance (Goldberger, 1990).
have an increased risk of angina or ST-segment Patients with existing cardiovascular disease (i.e.,
changes. Such tests therefore should be performed in hypertension) are at risk for other manifestations. In
a peripheral vascular laboratory or cardiac stress test­ addition, this population tends to be older and older
ing laboratory under the supervision of a peripheral populations are known to have a higher prevalence of
vascular specialist or cardiologist. The parameters of cardiac dysrhythmias. Thus knowledge of cardiac sta­
the exercise prescription are based on a peak exercise tus, including ECG history, should be obtained.
test. Walking is the activity/exercise of choice be­
cause this activity is most severely limited by inter­
PrinCiples of physical therapy management
mittent claudication, which has significant implica­ Physical therapy contributes to increased metabolical
tions for function. Intensity of the training stimulus is demands and therefore imposes a hemodynamic load
based on pain rating in conjunction wi th hemody­ resulting in increased heart rate and blood pressure.
namic and other subjective responses. The patient The assessment should document the history of hy­
walks at a comfortable, even cadence within her or pertension, its medical management, and the patient's
his pain tolerance (objectively defined on the pain response. Regardless of the condition being treated,
scale) so that limping and gait deviation is avoided. the hypertensive patient's blood pressure must be

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532 PART V Guidelines for the Delivery of Cardiopulmonary Physical Therapy: Chl"Onic Cardiopulmonary Conditions

monitored and treatment modified accordingly. How­ sure product). Subjective responses to treatment, par­
ever, blood pressure medications are known to atten­ ticularly exercise, should also be recorded. Signs of
uate hemodynamic responses to exercise (Chapter dyspnea, headache, lighheadedness, dizziness, disori­
43) ; thus the limitations of blood pressure measure­ entation, discoordi nation, cyanosis, coughing, and
ment must be considered. chest sound changes (i.e., a gallop) need to be moni­
A program of aerobic exercise can effectively re­ tored. Blood pressure responses that fail to increase
duce high blood pressure in some patients (Blair, with increasing work load and power output may be
1988; Sannerstedt,
Painter, Pate, Smith, and Taylor, indicative of congestive healt failure.
1987). The parameters of the exercise prescription Treatments will be safer and more precisely pre­
needed to control hypertension include an aerobic scribed with contiuous ECG monitoring. Without ECG
type of exercise that is rhythmic and involves large monitoring, treatments need to be conservative. If there
muscle groups, an intensity of 60% to 75% of the pa­ is any doubt about the hemodynamic stability of a pa­
tient's age predicted maximal heart rate, 60 to 90 min­ tient and her or his ability to tolerate treatment safely,
utes in duration, performed 5 to 7 times weekly, for 3 the patient should be referred to a general practitioner
months to achieve an optimal effect. The exercise in­ or cardiologist for clearance before being treated.
tensity should be equivalent to a perceived exertion Medication that is needed to maximize treatment
rating of 3 to 5 on the Borg scale (the patient is able to response is administered before treatment (i.e., hyper­
speak while exercising without gasping) provided that tension medications). Knowledge of the type of med­
blood pressure has not increased excessively. Only ication, its administration route, and time to and dura­
modest exercise intensities are prescribed if the pa­ tion of peak efficacy is essential if treatment is to be
tient has extremely high resting blood pressure to en­ maximally efficacious.
sure that the blood pressure does not rise excessively The primary interventions in the long-term man­
and is not maintained at a high pressure for a pro­ agement of hypertension include education, aerobic
longed period. If the patient's hypertension responds exercise, general body strengthening, range of motion,
to the exercise regimen, exercise needs to be included body mechanics, relaxation, stress management, pac­
into the patient's life style in order for the effects to be ing, and energy conservation. The patient is instructed
maintained. In addition to exercise, many patients lose in self-monitoring blood pressure, recording her or his
weight, adopt healthier life-style habits, and learn blood pressure and those factors that associated with
stress management and coping skills concurrently. both high and low pressures, and blood pressure
The goals of long-term management of the patient changes after having had medication. Such monitoring
with hypertension include the following: enables the patient to self-manage his or her hyperten­
•
Maximize the patient's quality of life, general sion and thereby reduces the need for medication, if
health, and well-being and hence physiological re­ not, eliminate it entirely. Patients, however, should
serve capacity only alter their medications with their physicians' ap­
•
Educate about hypertension, self-management, nu­ proval. Physical therapists work closely with both hy­
trition, weight control, smoking reduction and ces­ pertensive patients and physicians.
sation, risk factors, life-style factors, disease pre­ Systemic blood pressure responses to dynamic ex­
vention, medications and their applications and ercise are greater for upper-extremity than for lower­
side effects extremity work (Dean and Ross, 1992). Thus exer­
•
Maximize aerobic capacity and efficiency of oxy­ cise prescription includes aerobic exercise of the
gen transport large muscle groups to avoid small muscle group
•
Optimize physical endurance and exercise capacity work and increasing peripheral vascular resistance
•
Optimize general muscle strength and thereby pe­ and hence hemodynamic work, and the increased ex­
ripheral oxygen extraction ertion, strain, and work of the heart experienced with
Patient monitoring includes hemodynamic moni­ upper-extremity work. Exercise is also performed in
toring (i.e., heart rate, blood pressure, and rate pres­ erect and upright rather than recumbent positions to

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 29 Chronic Primary Cardiopulmonary Dysfunction 533

minimize the increased work of the heart secondary can be tolerated over the short term. However, these
to central fluid shifts when the patient is Lying in re­ factors may result in a critical situation for the dia­
cumbent positions. betic patient.

Principles of physical therapy management

Diabetes Mellitus
Diabetic patients may be referred to a physical thera­
Pathophysiology and medical management pist for several reasons. First, a newly diagnosed dia­
Diabetes mellitus is a condition associated with im­ betic patient may be referred so that the physical ther­
paired insulin metabolism that can result in serious apist can expose the patient to a quantified exercise
long-term multisystem consequences (Guyton, L991). stimulus under supervised conditions and thereby
The disease. is classified as insulin-d ependent help refine the prescription of insulin. Second a pa­
(100M) and non-insuLin-dependent diabetes mellitus tient may be referred for an exercise prescription to
(NIODM). Insulin is the carrier responsible for trans­ help minimize the insulin dose or avoid insulin ad­
porting glucose into the cells to undergo oxidation. ministration entirely, depending the disease type and
Juvenile-onset diabetes is frequently the insulin­ severity and the patient's response. Third but most
dependent type, whereas adult onset diabetes often is frequently, patients are seen by a physical therapist
non-insulin-dependent. The underlying pathophysiol­ for the treatment of some other condition and also re­
ogy of juvenile and adult-onset diabetes, however, is port diabetes in their histories. A history of diabetes
distinct. Juvenile-onset diabetes results from an inad­ must be considered in the treatment of a patient who
equate number of islets of Langerhan in the pancreas, is referred for any reason to either improve or at least
which are responsible for insulin production. Adult­ not contribute to abnormal blood glucose levels and
onset diabetes, on the other hand, results from re­ late complications.
duced insulin sensitivity. In Western industrialized Diabetic patients are treated cautiously. Exercise
countries, adult-onset diabetes is associated with obe­ increases metabolical demand commensurate with
sity, inactivity, diet, and stress. In addition, medica­ intensity and hence cellular demand for glucose
tions can contribute to blood sugar disturbances. The (Amercan College of Sports Medicine, 1995; Blair
sequelae of diabetes mellitus that frequently result et aI., 1988). Usually, insulin administration is in­
from poor regulation and management of the disease creased in preparation for exercise. Many acti ve di­
include angiopathy, peripheral neuropathy, autonomi­ abetic patients are closely attuned to their dietary
caL neuropathy, gastrointestinal paresis, visual distur­ and insulin needs, which permits them to be as
bance, and renal dysfunction (Bannister, L988; Ewing physically active as nondiabetic individuals. How­
and Clarke, L986). ever, the diabetic patients seen by physical thera­
Patients with diabetes mellitus have an accelerated pists are often labile and less well managed. Thus a
rate of atherosclerotic changes in the vasculature readily available sugar source must be nearby for
compared with age- and gender-matched nondiabet­ insulin reguLation when a diabetic patient exercises
ics. These patients are also prone to peripheral vascu­ or when exercising a diabetic patient on a ergome­
lar disease secondary to microangiopathy, macroan­ ter after anterior cruciate ligament repair in a pri­
giopathy, and autonomical neuropathy. Diabetic vate clinic.
patients constitute a significant proportion of patients In addition, diabetic patients may have hemody­
with peripheral vascular disease who require surgical namic disturbances because of a autonomic neuropa­
amputation of affected limbs. thy and may exhibit impaired fluid-volume regulation
Abnormalities of blood sugar metabolism may be during exercise (Bannister, 1988). Patients may expe­
observed also in nondiabetic patients. Diabetogenic rience postural hypotension and become dizzy and
factors, such as restricted mobility and stress, lead to Iightheaded. In addition, diabetic patients may re­
glucose intolerance and insulin oversecretion (Lip­ quire a longer cool-down period to adjust hemody­
man, 1972). In the nondiabetic patient, these effects namically after exercise.

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534 PART V Guidelines for the Delivery of Cardiopulmonary Physical Therapy: Chronic Cardiopulmonary Conditions

Hypoglycemia or low blood sugar is one of the lant in monitoring signs and symptoms of vascular in­
most common complications of diabetes mellitus. sufficiency in the affected limb. Any sign of skin red­
This condition results from excess administration of ness in the feet should be monitored closely. In dia­
insulin or oral hypoglycemic agent, insufficient food betic patients, any threat of skin breakdown requires
in relation to insulin dose, or an abnormal increase in medical attention and discontinuation of exercise until
physical activity or exercise. Hyperglycemia is com­ medical clearance has been obtained. Healing is con­
mon in obese patients with adult-onset diabetes. High siderably delayed in the diabetic foot. Without appro­
insulin levels are associated with a higher risk of priate attention, infection and potential necrosis can
coronary artery disease. Myocardial infarction and ensue. Patients with peripheral neuropathy are taught
stroke are common causes of death. Another compli­ to monitor their footwear and socks diligently, to en­
cation is cardiac hypertrophy secondary to hyperten­ sure the inner surfaces are clean and smooth before
sion and cardiomyopathy, which predisposes the pa­ each exercise session, and to check for areas of red­
tient to congesti ve heart failure. The incidence of ness or abrasion of their feet after exercise.
peripheral vascular disease is also increased in dia­ Medication that is needed to maximize treatment
betic patients. response is administered before treatment (e.g., in­
The goals of the long-term management of dia­ sulin or oral hypoglycemic agents). Knowledge of the
betes mellitus include the following: type of medication, its administration route, and time
• Maximize the patient's quality of life, general to and duration of peak efficacy is essential if treat­
health and well-being, and hence physiological re­ ment is to be maximally efficacious.
serve capacity The primary interventions in the long-term man­
•
Educate about diabetes mellitus, self-management, agement of diabetes mellitus include education,
nutrition, weight control, blood sugar regulation maintainance of a log of diet and insulin regimens,
and its managment (i.e., the balance between nu­ activity and exercise, aerobic exercise, strengthening
trition, diet, exercise, stress and insulin require­ exercises, relaxation, stress management, activity
ments), medications, smoking reduction or cessa­ pacing, and energy conservation.
tion, relaxation, stress management, foot care, Generally, there are no contraindications to patients
hygiene, and infection control with diabetes mellitus being physically active and par­
•
Maximize aerobic capacity and efficiency of oxy­ ticipating in an exercise program. Daily exercise is ad­
gen transport vocated for insulin-dependent and non-insulin-depen­
•
Optimize physical endurance and exercise capacity dent diabetic patients to optimize glucose control. The
•
Optimize general muscle strength and thereby pe­ exercise prescription parameters are set at 40% to 85%
ripheral oxygen extraction of peak functional work capacity (American College
Patient monitoring includes signs and symptoms of of Sports Medicine, 1991). If the patient is exercising
hypoglycemia (e.g., lightheadedness, weakness, fa­ daily, the exercise parameters are set at the lower end
tigue, disorientation, and glucose tolerance test) or hy­ of this range. If the exercise sessions are less frequent
perglycemia (e.g., glucose tolerance test). Hemody­ (e.g., in the case of a non-insulin-dependent diabetic
namic responses (i.e., heart rate, blood pressure, and patient whose blood glucose is well maintained and
rate pressure product) provide an index of the inten­ whose weight is acceptable) the exercise intensity is
sity of an exercise stimulus, however, these responses set at the higher end of this range.
may be attentuated in the diabetic patient because of The risk of hypoglycemia can be reduced by observ­
the autonomic neuropathy; both parasympathetic and ing the following precautions: frequently monitor blood
sympathetic neuropathies. glucose, decrease the insulin dose (in consulting with
Subjective responses to exercise, including the rat­ the physician) or increase carbohydrate intake before
ing of perceived exertion, may be more valid indica­ exercise, avoid injecting insulin into areas that are ac­
tors of exercise intensity than hemodynamic responses tive during exercise, avoid exercise during peak insulin
in the diabetic patient. The patient is taught to be vigi­ activity, consume carbohydrates before, during, and

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 29 Chronic Primary un'l'u"mu",,,, J Dysfunction 535

aerobic 2, Relate physical therapy treat­

and symptoms of ment interventions to the underlying pathophysi­
ican of Sports Medicine, 1991). ology of each of the above chronic conditions
and provide the rationale for your choice.

SUMMARY
References
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Copyrighted Material
 Chronic Secondary Cardiopulmonary
Dysfunction

Elizabeth Dean
Donna Frownfelter

KEY TERMS Ankylosing spondylitis Muscular dystrophy

Cerebral palsy Osteoporosis
Chronic renal insufficiency Parkinson's disease
Hemiplegia Rheumatoid arthritis
Kyphoscoliosis Scleroderma
Late sequelae of poliomyelitis Spinal cord injury
Multiple sclerosis Systemic lupus erythematosus

INTRODUCTION
injury, and the late sequelae of poliomyelitis. The
The purpose of this chapter is to review the patho­ musculoskeletal conditions that are presented include
physiology, medical management, and physical ther­ kyphoscoliosis and osteoporosis. The collagen vascu­
apy management of chronic, secondary cardiopul­ lar/connective tissue conditions that are presented in­
monary pathology. Specif ically, this chapter clude systemic lupus erythematosus, scleroderma,
addresses chronic cardiopulmonary dysfunction sec­ ankylosing spondylitis, and rheumatoid arthritis. Fi­
ondary to neuromuscular, musculoskeletal, collagen nally, management of the patient with chronic renal
vascular/connective tissue, and renal dysfunction. insufficiency is presented. The principle.<> of manage­
The neuromuscular conditions that are presented in­ ment are presented rather than treatment prescrip­
clude muscular dystrophy, hemiplegia, Parkinson's tions, which cannot be given without consideration of
disease, multiple sclerosis, cerebral palsy, spinal cord a specific patient. (For specific examples of patient

537

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538 PART V Guidelines for the Delivery of Cardiopulmonary Physical Therapy: Chronic Cardiopulmonary Conditions

treatment prescriptions refer to the companion text abnormal ventricular wall motion. Fatty and fibrous
Clinical case studies in cardiopulmonary physical tissue infiltrate the myocardium and conduction sys­
therapy.) In this context the goals of long-term man­ tem and electrical conduction is slowed. Thus sub­
agement of each condition are presented, followed by clinical cardiac involvement is prevalent in patients
the essential monitoring required and the primary in­ with muscular dystrophy and may explain sudden
terventions for maximizing cardiopulmonary function death in this patient population.
and oxygen transport. The selection of interventions Chronic respiratory muscle weakness is character­
for any given patient is based on the physiological hi­ istic of muscular dystrophy and other neuromuscular
erarchy. The most physiological interventions are ex­ disorders. Because the cardiopulmonary system is sel­
ploited followed by less physiological interventions dom stressed due to musculoskeletal dysfunction in
and those whose efficacy is less well documented these patients, respiratory muscle weakness is seldom
(Chapter 16). detected. Such weakness is significant, however, in
that it contributes to several other serious problems,
including thoracic mechanical abnormalities, diffuse
NEUROMUSCULAR CONDITIONS
microatelectasis, reduced lung compliance, a weak
Muscular Dystrophy
cough with impaired mucociliary transport and secre­
Pathophysiology and medical management
tion accumulation, ventilation and perfusion imbal­
Degenerative neurological and muscular diseases, in­ ance, and noctural hypoxemia (Smith, Calverley, Ed­
cluding Duchenne's muscular dystrophy, lead to res­ wards, Evans, and Campbell, 1987; Smith, Edwards,
piratory muscle weakness and alveolar hypoventila­ and Calverley, 1989). Progressive respiratory muscle
tion (Black and Hyatt, 1971; Braun, Arora, and weakness increases the risk of respiratory muscle fa­
Rochester, 1983; Inkley, Alderberg, and Vignos, tigue and failure (Macklem and Roussos, 1977).
1974). Vital capacity, forced expiratory volume, air­ The severity of disease is not consistently corre­
flow rates, and maximum inspiratory and expiratory lated with compromised pulmonary function; thus
pressures are reduced. These patients are at risk for cardiopulmonary function must be assessed individu­
the development of atelectasis, impaired mucociliary ally in each patient (Hapke, Meek, and Jacobs, 1972).
transport, and pneumonia. In addition, long-term gen­ Patients with mild-to-moderate involvement of pe­
eralized muscular weakness, particularly of the tho­ ripheral muscles may exhibit disproportionate respi­
racic cavity and abdomen, as well as restricted mobil­ ratory compromise (Kilbull1, Eagan, Sieker, and Hey­
ity and confinement to a wheelchair, predispose the man, 1959). This may be explained by differential
patient to thoracic deformities (e.g., scoliosis and changes in the degree of involvement of the di­
dropping of the ribs, and further muscle disuse). Pa­ aphragm and the abdominal and intercostal muscles
tients with Duchenne' s muscular dystrophy are sus­ (Nakano, Bass, Tyler, and Carmel, 1976). Over time,
ceptible to dysphagia and upper airway obstruction musculoskeletal changes of the chest wall lead to
secondary to gag reflex depression and hypotonia of spinal deformity and stiffness with loss of its elastic
the pharyngeal structures (Murray and Nadel, 1988a). recoil. Chronic alveolar hypoventilation leads to res­
These factors further compromise or threaten car­ piratory insufficiency and the need for ventilatory as­
diopulmonary function and oxygen transport. sistance. With progressive respiratory insufficiency,
Cardiac dysfunction has also been reported in pro­ noctural hypoventilation with hypercapnia and hy­
gressive muscular dystrophy (Moorman et aI., 1985; poxemia develop (Bach, O'Brien, Krotenberg, and
Perioff, de Leon, and O'Doherty, 1966). Although Alba, 1987). Nocturnal respiratory support should be
the majority of patients have no clinical evidence of considered early to postpone the need for intubation
cardiac dysfunction, a high proportion have abnormal and mechanical ventilation, which is associated with
E CGs at rest or during exercise and a b n o r m a l a poor prognostic outcome in patients who have
echocardiography and radionuclide ventriculography chronically reduced vital capacities and weak cough.
showing reduced left ventricular ejection fraction and Clinically, patients with muscular dystrophy pre­

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 30 Chronic Secondary Cardiopulmonary Dysfunction 539

sent with low functional commensurate • Reduce the work of breathing

with the extent of muscle weakness and • Reduce the work of the heart
cardiopulmonary function, including alveolar • Facilitate mucociliary
orthopnea (shortness of on re- • Optimize secretion clearance
impaired transport, difficulty • Maximize aerobic capacity and efficiency of
clearing and increased work of breath- oxygen transport
Abdominal muscle provides an index • Optimize physical endurance and exercise ca­
of pulmonary function in that it is correlated with
vital and expiratory flow rates et general muscle strength and thereby
aI., 1 The progressive functional peripheral oxygen extraction
loss with Duchenne's muscular dystro­ Patient monitoring includes respiratory
phy increases the susceptibility to the se- LI,,,'""''''', breathing (depth and frequency), ar­
of restricted mobility, including terial of desatura-
monary and reduced Lion), heart rate, blood pressure, and rate pressure
oxygen transport, circulatory muscular weak­ product. Patients with cardiac dysfunction need to be
ness, and bone loss. cleared a before a rehabilita­
medical of the complica­ tion program, when it involves a mobi­
tions of myopathies has significantly increased the lization or exercise program, to refine the prescriptive
life expectancy of p atients, such as those with of the program. If supplemental oxygen is
Duchenne's muscular over the 20 administered is recorded.
years. With age, further complications will breathlessness is assessed a modified version of
arise from the scale of
function (Dean, 1994; nighttime and
Thus in the years ahead an needed because rPt'r'lII'"tl,nl

of patients with myopathies will be car­ with n o c turnal h y p o x e m i a in p at i e n t s with

diopulmonary management and prophylaxis. Duchenne's muscular dystrophy,
Medication that is needed to maximize treatment
PrinCiples of physical therapy management
response is administered before treatment. Knowl­
The of long-term management for the patient of the of medication, its administration
with muscular dystrophy include the route, and time to and duration of efficacy is es­
• Maximize the patient's sential if treatment is to be maximally efficacious .
health, and well-being and hence The interventions for car­
reserve --t"--" J diopulmonary function and oxygen in pa­
• Educate about cardiopulmonary manifestations tients with muscular include some combi­
of muscle medica­ nation of education, mobilization, primarily in the
reduc­ form of functional activities,
tion and cessation, protection, infection primarily in the form of functional activities
control, the role of a rehabilitation program, and maintain strength or reduce rate of ventila­
the eventual need for mechanical tory muscle training, postural correction exercises,
support chest wall mobility range of motion exer­
Optimize alveolar ventilation cises, prevention, body positioning, breath-
volumes and control and coughing maneuvers, clear-
rates ance activity and energy
ventilation and perfusion conservation. An assessment of the pa­
tient's work and home environments may be indi­
from aspiration cated to minimize oxygen demand and energy expen­

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540 PART V Guidelines for the Delivery of Cardiopulmonary Physical Therapy: Chronic Cardiopulmonary Conditions

diture in these settings. Such an assessment includes impaired, leading to secretion accumulation, postural
review of aids and devices (e.g., wheelchair type, drainage may need to be instituted, coupled with deep
weight, and size and noninvasive mechanical ventila­ breathing and coughing maneuvers.
tion). Aids and devices are selected to minimize en­ Although the primary factor contributing to respi­
ergy demand such that energy is conserved for other ratory compromise is respiratory muscle weakness,
activities and undue fatigue is reduced. the capacity of the respiratory muscles to respond to
The use of supplemental oxygen depends on the resistive loading is limited. However, ventilatory
severity of the disease. Some patients have no need muscle training may have some role in selected pa­
for supplemental oxygen, some need it only during tients, particularly children (Adams and Chandler,
exercise, and some patients require continuous oxy­ 1974; Pardy and Leith, 1984). Improved respiratory
gen with proportionately more delivered during activ­ muscle endurance and strength may have a general­
ity and exercise compared with rest. ized effect on functional capacity (Reid and Warren,
Education is a principal focus of the long-term 1984). Patients with signs of ventilatory muscle fa­
management of the patient with muscular dystrophy. tigue, as opposed to weakness, benefit from ventila­
Education includes the reinforcement of preventative tory support at night. Rest of the respiratory muscles
health practices (e.g., infection control, cold and flu at night optimizes their function during the daytime.
prevention, flu shots, aerobic exercise, strengthening Methods of facilitating effecti ve coughing in pa­
exercises, nutrition, weight contrOl, hydration, pacing tients with neuromuscular diseases are extremely im­
of activities, and energy conservation). Weight control portant because they constitute life-preserving mea­
is an important goal in patients with chronic neuro­ sures. Supported and unsupported coughing methods
muscular diseases because they have the least capacity are described in detail in Chapters 20 and 21. Patients
to compensate for the cardiopulmonary sequelae of on noninvasive ventilatory support who are unable to
obesity (Alexander, 1985). Obstructive sleep apnea is generate adequate peak cough expiratory flow rates
related to hypotonia of the upper airway musculature can benefit from manual assisted coughing and me­
and obesity. Thus activity and sleep patterns need to chanical insufflation-exsufflation, thereby minimiz­
be assessed to ensure sleep is maximally restorative ing the need for endotracheal suctioning (Bach, 1993;
and not contributing to the patient's symptoms. Barrach, Beck, Bickerman, and Seanor, 1952). Tra­
Mobilization is an essential component of the long­ cheostomy is delayed as long as possible. Signifi­
term management of the patient with muscular dystro­ cantly reduced maximal insufflation capacity, how­
phy to optimize the efficiency of oxygen transport ever, is an indication for tracheostomy.
overall and minimize the sequelae of restricted mobil­ Whenever possible, deep breathing and coughing
ity, including circulatory stasis. Maximizing ventila­ are coupled with chest wall movement to facilitate
tion with mobilization is limited if the patient has se­ maximal inflation of the lungs before coughing by in­
vere generalized muscular weakness and increased creasing pulmonary compliance (Ferris and Pollard,
fatigue. Functional activities provide the basis for the 1960) and maximal exhalation of the lungs during
mobilization prescription. Although heavy resistive coughing. Body positions are varied and changed fre­
strengthening exercise has been advocated for these quently to simulate shifts in alveolar volume and ven­
patients (Vignos and Watkins, 1966), a conservative tilation and perfusion that occur with normal move­
approach, including an exercise program based on ment and body position changes. Glossopharyngeal
functional goals and energy conservation, is more jus­ breathing is a nonmechanical method of assisting
tifiable physiologically. Chest wall mObility exercises ventilation. The patient is taught to use the tongue
include all planes of movement combined with a rota­ and pharyngeal muscles to swallow boluses of air
tional component. Body positioning to optimize lung past the vocal cords and into the trachea (Bach, Alba,
volumes and airflow rates is a priority. Breathing con­ Bodofsky, Curran, and Schultheiss, ) 987). The effi­
trol and coughing maneuvers are coupled with body ciency of training is monitored with spirometry to en­
movement and positioning. If mucociliary transport is sure the patient is able to achieve acceptable vital ca­

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 30 Chronic Secondary Cardiopulmonary Dysfunction 541

pacities. Some patients are able to support their venti­ can affect cardiopulmonary function. Such infarc­
lation, ventilator-free, for several hours in a day. tions, however, are I ikely to be lethal. More com­
One intervention that is prolonging the life of pa­ monly, after a stroke, chest wall movement and elec­
tients with muscular dystrophy, as well as of patients trical activity on the ipsilateral side are reduced
with other progressive neuromuscular diseases, is the (DeTroyer, DeBeyl, and Thirion, 1981; Fluck,
use of mechanical ventilatory support (Bach, 1992; 1966). Facial and pharyngeal weakness contributes
Curran, 1981). Home mechariical ventilation provides to an inability to control oral secretions, swallow ef­
a noninvasive method of providing positive airway fectively, and protect the upper airway. Altered res­
pressure through an oral or nasal mask. This provides piratory mechanics and efficiency reflect impaired
considerable advantage over invasive, full body or chest wall movement, asymmetry, and the degree of
tracheostomy. ventilatory support. Used in conjunc­ muscle paresis and spasm.
tion with an insufftation-exsufflation device, pul­ Patients with hemiplegia have associated problems
monary complications can be minimized and life ex­ that contribute to cardiopulmonary dysfunction.
pectancy increased. Other forms of noninvasive These patients tend to be older, hypertensive, and
mechanical ventilation include intermittent abdomi­ have a high incidence of cardiac dysfunction. Muscle
nal pressure ventilation, rocking bed, negative pres­ disuse and restricted mobility secondary to hemiple­
sure tank ventilator, and chest shell ventilator. The gia lead to reduced cardiopulmonary conditioning
type of ventilation is determined individually based and inefficient oxygen transport. Spasticity increases
on the indications for ventilation and the patient's metabolical and oxygen demand. Hemiparesis results
status. The use of ventilatory aids as a component of in gait deviations, which reduce movement efficiency
a comprehensive rehabilitation program maintains and movement economy. Reduced movement econ­
pulmonary compliance and cough efficacy. Introduc­ omy results in an increased energy cost associated
tion of these devices early will facilitate increased use with ambulation, which may reduce exercise toler­
as the respiratory muscles progressively weaken. ance because of fatigue (Dean and Ross, 1993). In
Patients with generalized neuromuscular weakness addition, ambulating with a walking aid is associated
require prophylactic management given their high with a significantly increased energy cost compared
risk of developing life-threatening respiratory infec­ with normal walking. This increased energy cost re­
tions and complications. Prophylaxis should include duces the patient's exercise tolerance further and in­
flu shots, avoiding polluted, smoky environments, creases fatigue.
smoking reduction and cessation, controlling the
types of food eaten and chewing well to avoid chok­
Principles of physical therapy management
ing, and regular deep breathing, frequent movement, The goals of long-term management for the patient
and change in body positions (even just shifting and with hemiplegia include the following:
taking some deeper breaths while seated in a wheel­ • Maximize the patient's quality of life, general
chair) to promote mucociliary transport. An optimal health, and well-being and hence physiological
time to take deep breaths and to cough is during reserve capacity
transfers, which usually are physically exerting and • Educate about cardiopulmonary manifestations of
stimulate hyperpnea. hemiplegia, self-management, medications, smok­
ing reduction and cessation, nutrition, weight con­
trol, and the role of a rehabilitation program
Hemiplegia
• Optimize alveolar ventilation
Pathophysiology and medical management • Optimize lung volumes and capacities and flow
Hemiplegia or stroke affects cardiopulmonary func­ rates
tion either directly or indirectly (Fugl-Meyer and • Optimize ventilation and perfusion matching
Grimby, 1984; Griggs and Donohoe, 1982). A cere­ and gas exchange
bral infarct involving the vital centers of the brain • Reduce the work of breathing

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542 PART V Guidelines for the Delivery of Cardiopulmonary Physical Therapy: Chronic Cardiopulmonary Conditions

• Reduce the work of the heart sleep apnea). Thus activity and sleep patterns need to
• Protect the airways from aspiration be assessed to ensure sleep is maximally restorative
• Facilitate mucociliary transport and not contributing to the patient's symptoms.
• Optimize secretion clearance Aerobic excrcise is an essential component of the
• Maximize aerobic capacity and efficiency of long-term management of the patient with hemiplegia
oxygen transport to optimize the efficiency of oxygen transport overall.
• Optimize physical endurance and exercise Maximizing ventilation with mobilization is limited if
capacity the patient has severe generalized muscular weakness
• Optimize general muscle strength and thereby and increased fatigue. Although aggressive mobiliza­
peripheral oxygen extraction tion can be supported in these patients (Malouin,
Patient monitoring includes dyspnea, respiratory Potvin, Prevost, Richards, and Wood-Dauphinee,
distress, breathing pattern (depth, symmetry, and fre­ 1992), appropriate selection of patients for such a reg­
quency), arterial saturation, cyanosis (delayed sign of imen, judicious exercise prescription, and monitoring
desaturation), heart rate, blood pressure, and rate pres­ must be instituted to ensure the treatment is optimally
sure product. Patients with cardiac dysfunction require therapeutic and poses no risk to a patient in this high­
clearance from a cardiologist before participating in a risk group. Chest wall exercises include movement in
rehabilitation program and may require ECG monitor­ all planes combined with rotation. Body positioning to
ing, particularly during exercise. Subjectively, per­ optimize lung volumes and aitflow rates is a priority.
ceived exertion is rated using the Borg scale. Breathing control and coughing maneuvers are essen­
Medication that is needed to maximize treatment tial and should be coupled with body movement and
response is administered before treatment (e.g., anti­ positioning. Exercise is conducted in the upright posi­
hypertensive and cardiac medications). Knowledge of tions to minimize the work of the heart and of breath­
the type of medication, its administration route, and ing during physical exertion. Recumbent positions re­
time to and duration of peak efficacy is essential if duce lung volumes and expiratory flow rates, impair
treatment is to be maximally efficacious. respiratory mechanics, increase closing volumes, in­
The primary interventions for maximizing car­ crease thoracic blood volume, and increase compres­
diopulmonary function and oxygen transport in pa­ sive forces on both the lungs and the heart (Dean and
tients with hemiplegia include some combination of Ross, 1992; Ross and Dean, 1992). Thus significant
education, aerobic exercise, strengthening exercises, periods and intensities of aerobic exercise should be
spasticity control, postural correction exercises, gait petformed standing or sitting. Lower-extremity work
reeducation, chest wall mobility exercises, range of is preferable to upper-extremity work in that the latter
motion exercises, body positioning, breathing control is associated with increased hemodynamic stress.
and coughing maneuvers, airway clearance interven­ Rhythmic exercise of large muscle groups is prefer­
tions, activity pacing, and energy conservation. An er­ able to static exercise and exercise of small muscle
gonomic assessment of the patient's work and home groups, such as the arms, in that it produces smaller
environments may be indicated to minimize oxygen hemodynamic effects.
demand and energy expenditure in these settings. Ambulation or wheelchair locomotion should be
Education is a principal focus of the long-term as efficient as possible so that the metabolical de­
management of the patient with hemiplegia. Educa­ mand of these functional activities is reduced. Per­
tion includes the reinforcement of preventative health forming these activities inefficiently on a frequent
practices (e.g., infection control, smoking reduction basis contributes to an excessive oxygen demand.
and cessation, cold and flu prevention, flu shots, aero­ The patient expends considerable energy in perform­
bic exercise, strengthening exercises, gait reeducation, ing these activities uneconomically, which impairs
nutrition, weight control, hydration, pacing of activi­ the patient's tolerance and contributes to excessive
ties, and energy conservation). Hemiplegia is often as­ fatigue. Conserving energy by performing these ac­
sociated with sleep disturbances (e.g., obstructive tivities more economically from an energetic per­

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 30 Chronic Secondary Cardiopulmonary Dysfunction 543

spective will more energy to "PIc-fArm more of which has been associated with the disease. The de­
these or other activities. gree to which these cardiopulmonary manifestations
neuromuscular weakness of the disease are offset with
their used to treat rest tremor and reverse
infec­ been reported.
Prophylaxis should include The upper extremities are rigid and held
polluted, smoky abducted from the chest wall during locomotion. The
smoking reduction and cessation, the rigidity and dyskinesia associated with Parkinson's
types of food eaten and chewing well to avoid chok­ disease leads to restricted movement and body
ing, and deep breathing, movement, tioning. The becomes deconditioned from dis­
and positions (even just and use. The immobile chest, coupled with reduced
breaths while seated in a wheel­ body position contributes to
nrr,rYI.c>'p mucociliary transport. An monary
breaths and to
Principles nmrSIt:,al therapy management
are
The goals of management for the
with Parkinson's disease include the following:
• Maximize the quality of life,
Parkinson's Disease
health, and and hence physiological
Pathophysiology and medical management
reserve
Parkinson's disease i s associated w i t h reduced • Educate about cardiopulmonary manifestations
dopamine in the basal resulting in the loss of of Parkinson's d self-
normal inhibitory and neuronal smoking reduction a n d
input in the execution of smooth coordinated move­ weight
ment et 199 The clinical manifesta­ infection
tions of the disease include stooped posture, stiffness program
and slowed fixed masklike and • Optimize alveolar ventilation
tremor of the limbs. Patients with Parkinson's disease • Optimize volumes and capacities
and inflexible. Movement initi­ • Optimize ventilation and perfusion

once initiated, movement is not and gas

walks with a quick, • Reduce the work of breathing

These factors contribute to an increased energy cost • Reduce the work of the heart
of movement. activity is restricted and func­ • Protect the

tion is contributing to aerobic Facilitate

reduced movement efficiency, and hence re­ • Maximize aerobic and efficiency of
duced movement economy. oxygen
Although chest wall rigidity and respiratory mus­ • Optimize endurance and exercise
cle weakness are associated with a restrictive capacity
of lung disease in the Parkinsonian patient (Mehta, • Optimize general muscle strength and thereby
Wright, and 1978), obstructive type of peripheral oxygen extraction
tory has been reported (e.g., reduced Patient monitoring includes respiratory

mid-tidal flow rates, increase airway resistance, im­ distress, breathing (depth and frequency),

paired distribution of ventilation, and an increase in arterial saturation, heart rate, blood pressure, and

functional residual Patients with cardiac dys ­

and particularly dur­

tive defect may reflect parasympathetic breathlessness is as­

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544 PART V Guidelines for the Delivery of Cardiopulmonary Physical Therapy: Chronic Cardiopulmonary Conditions

Multiple Sclerosis
sessed using a modified version of the Borg scale
Pathophysiology and medical management
of perceived exertion.
Medication that is needed to maximize treatment Multiple sclerosis is a demyelinating disease of the
response is administered before treatment (e.g., L­ central nervous system. The focal or patchy destruc­
dopa). Knowledge of the type of medication, its ad­ tion of myelin sheaths is accompanied by an inflam­
ministration route, and time to and duration of peak matory response (McFarlin and McFarland, 1982).
efficacy is essential if treatment is to be maximally The course of the disease consists of a variable num­
efficacious. In addition, patients with Parkinson's ber of exacerbations and remissions over the years
may be on a beta-blocker to suppress action tremor. from early adulthood. Exacerbations are also vari­
Because such medication reduces the heart rate and able with respect to severity. The neurological
blood pressure, these patients are prone to orthosta­ deficits include visual disturbance, paresis of one or
tic intolerance. In addition, heart rate and blood more limbs, spasticity, discoordination, ataxia,
pressure responses to treatment and exercises will dysarthria, weak, ineffective cough, reduced percep­
be less valid. tion of vibration and position sense, bowel and blad­
The primary interventions for maximizing car­ der dysfunction, and sexual dysfunction (Wilson,
diopulmonary function and oxygen transport in pa­ Braunwald, Isselbacher, Martin, Fauci, and Root,
tients with Parkinson's disease include some combi­ 1991). Breathing disturbances, including diaphrag­
nation of education, aerobic exercise, strengthening matic paresis, may occur (Cooper, Trend, and Wiles,
exercises, postural correction exercises, gait reeduca­ 1985). Autonomic disturbance in the form of im­
tion, chest wall mobility exercises, range of motion paired cardiovascular reflex function at rest and at­
exercises, body positioning, breathing control and tenuated heart rate and blood pressure responses dur­
coughing maneuvers, activity pacing, and energy ing exercise are relatively common in patients with
conservation. An ergonomic assessment of the pa­ mUltiple sclerosis (Neubauer and Gundersen, 1978;
tient's work and home environments may be indi­ Pentland and Ewing, 1987; Senaratne, Carroll, War­
cated to minimize oxygen demand and energy expen­ ren,and Kappagoda, 1984).
diture in these settings.
Principles of physical therapy management
Education is a principal focus of the long-term
management of the patient with Parkinson's disease. The goals of long-term management for the patient
Education includes the reinforcement of preventative with mUltiple sclerosis include the following:
health practices (e.g., infection control, airway pro­ • Maximize the patient's quality of life, general
tection, smoking reduction or cessation, cold and flu health, and well-being and hence physiological
prevention, flu shots, aerobic exercise, strengthening reserve capacity
exercise, nutrition, weight control, hydration, pacing • Educate about cardiopulmonary manifestations
of activities, and energy conservation). of mUltiple sclerosis, self-management, medica­
Aerobic exercise is an essential component of the tions, smoking reduction and cessation, nutri­
long-term management of the patient with Parkinson's tion, weight control, infection control, and the
disease to optimize the efficiency of oxygen transport role of a rehabilitation program
overall, including maximizing alveolar ventilation and • Optimize alveolar ventilation
mobilizing secretions, as weJl as its musculoskeletal • Optimize lung volumes and capacities and flow
benefits. Maximizing ventilation with mobilization is rates
limited by the degree of hypertonicity and rigidity. • Optimize ventilation and perfusion matching
Chest wall exercises include all planes of movement and gas exchange
with a rotational component. Breathing control and • Reduce the work of breathing
coughing maneuvers are essential and should be cou­ • Reduce the work of the heart
pled with body movement and positioning. • Protect the airways from aspiration

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 30 Chronic Secondary Cardiopulmonary Dysfunction 545

• Facilitate mucociliary transport management, modified aerobic exercise, modified

• Optimize secretion clearance strengthening exercises, pacing of activities, and en­
• Maximize aerobic capacity and efficiency of ergy conservation). Multiple sclel'Osis is associated
oxygen transport with significant fatigue. Thus activity and sleep pat­
• Optimize physical endurance and exercise ca­ terns need to be assessed to ensure sleep is maximally
pacity restorative and not contributing to the patient's symp­
• Optimize general muscle strength and thereby toms. By maintaining a log of activity and rest, the
peripheral oxygen extraction patient can observe relationships between these fac­
Patient monitoring includes dyspnea, respiratory tors and identify when is the optimal time to rest.
distress, breathing pattern (depth and frequency), ar­ Aerobic exercise is an essential component of the
terial saturation, cyanosis (delayed sign of desatura­ long-term management of the patient with multiple
tion), heart rate, blood pressure, and rate pressure sclerosis to optimize the efficiency of oxygen trans­
product. Patients with cardiac dysfunction require port overall. In mild-to-moderate cases the goals of
ECG monitoring, particularly during exercise. Sub­ aerobic exercise are to optimize cardiopulmonary
jectively, fatigue can be assessed using a modified conditioning and enhance movement economy. Opti­
version of the Borg scale. Perceived exertion is as­ mizing cadence of walking or cycling is important to
sessed using the Borg scale. minimize discoordination, energy expenditure, and
Medication that is needed to maximize treatment fatigue and maximize safety. In more severe cases the
response is administered before treatment (e.g., anti­ goal is to maximize ventilation and gas exchange in
spasticity medications). Knowledge of the type of the patient who has severe generalized muscular
medication, its administration route, and time to and weakness, spasm, and excessive fatigue. Subjective
duration of peak efficacy is essential if treatment is to parameters (i.e., fatigue and exertion) provide the
be maximally efficacious. In addition, knowledge of basis for the intensity of the exercise program in con­
the cardiopulmonary side effects of other medications junction with objective measures. Parameters, such as
is needed. intensity and duration, may vary from session to ses­
The primary interventions for maximizing car­ sion depending on the patient's general status, which
diopul monary function and oxygen transport in pa­ tends to be variable. Aquatic exercise may be an al­
tients with multiple sclerosis include some combina­ ternative for patients whose discoordination pre­
tion of education, aerobic exercise, strengthening cludes ambulation and cycling or who are troubled by
exercises (to maintain or reduce rate of decline), re­ heat. The use of a fan may also enhance the palient's
duce abnormal muscle tone, postural correction exer­ work output.
cises, gait reeducation, chest wall mobility exercises, Chest wall exercises include all planes of move­
range of motion exercises, body positioning, breath­ ment with a l'Otational component. Body positioning to
ing control and coughing maneuvers, airway clear­ optimize lung volumes and airflow rates is a priority.
ance interventions, fatigue management, activity pac­ Breathing control and coughing maneuvers are cou­
i n g a nd e nergy conservation. An ergonomic pled with body movement and positioning. If mucocil­
assessment of the patient's work and home environ­ iary clearance is impaired leading to secretion reten­
ments may be indicated to minimize oxygen demand tion, postural drainage may need to be instituted
and energy expenditure in these settings. coupled with deep breathing and coughing maneuvers.
Education is a principal focus of the long-term Methods of facilitating effective coughing in pa­
management of the patient with multiple sclerosis. tients with neuromuscular diseases are extremely im­
Education includes the reinforcement of preventative portant because they constitute life-preserving mea­
health practices (e.g., infection control, cold and flu sures. Supported and unsuppolted coughing methods
prevention, flu shots, smoking reduction and cessa­ are described in detail in Chapters 20 and 21. When­
tion, nutrition, weight control, hydration, fatigue ever possible, deep breathing and coughing are coor­

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546 PART V Guidelines for the Delivery of Cardiopulmonary Physical Therapy: Chronic Cardiopulmonary Conditions

dinated with chest wall movement to facilitate maxi­ ipate actively in a long-term rehabilitation pro­
mal inflation of the lungs before coughing and maxi­ gram. Patients with cerebral palsy who are able to
mal exhalation of the lungs during coughing. Body ambulate do so at exceptional energy expenditure
positions are varied and changed frequently to simu­ both with and without walking aids (Campbell and
late as much as possible shifts in alveolar volume and Ball, 1978; Mossberg, Linton, and Friske, 1990).
ventilation and perfusion that occur with normal Central neurological deficits, generalized hyper­
movement and body position changes (Ray et aI., tonicity, and musculoskeletal deformity contribute
1974). In addition, body positioning is used to maxi­ to increased metabolical demand for oxygen and
mize the patient's coughing efforts. oxygen transport.
Patients with generalized neuromuscular weakness
require prophylactic management given their high
Principles of phYSical therapy management
risk of developing life-threatening respiratory infec­ The goals of long-term management for the patient
tions and complications. Prophylaxis should include with cerebral palsy include the following:
flu shots, avoiding polluted, smoky environments, • Maximize the patient's quality of life, general
smoking reduction and cessation, controlling the health, and well-being and hence physiological
types of food eaten and chewing well to avoid chok­ reserve capacity
ing, and regular deep breathing, frequent movement, • Educate patient and/or family about cardiopul­
and change in body positions (even just shifting and monary manifestations of cerebral palsy, self­
taking some deeper breaths while seated in a wheel­ management, medications, nutrition, weight
chair) to promote mucociliary transport. An optimal control, airway protection, infection control, and
time to take deep breaths and to cough is during the role of a rehabilitation program
transfers, which usually are physically exerting and • Optimize alveolar ventilation
stimulate hyperpnea. • Optimize lung volumes and capacities and flow
rates
• Optimize ventilation and perfusion matching
Cerebral Palsy
and gas exchange
Pathophysiology and medical management
• Reduce the work of breathing
Cerebral palsy results from insult to the central ner­ • Reduce the work of the heart
vous system usually before birth (e.g., substance • Protect the airways from aspiration
abuse and underoxygenation perinatally) (Wilson et • Facilitate mucociliary transport
aI., 1991). The clinical presentation includes spas­ • Optimize secretion clearance
ticity and residual deformity from severe muscle • Maximize aerobic capacity and efficiency of
imbalance, hyperreflexia, and mental retardation. oxygen transport
Although there are varying degrees of cerebral • Optimize physical endurance and exercise ca­
palsy severity, patients most frequently seen by pacity
physical therapy have significant functional deficits • Optimize general muscle strength and thereby
and require long-term care. The loss of motor con­ peripheral oxygen extraction
trol and hypertonicity of peripheral muscles often Maximizing aerobic capacity and efficiency of
restrict the mobility of patients such that they are oxygen transport and optimizing general muscle
wheelchair dependent. Loss of motor function lim­ strength pertain to the patient with cerebral palsy that
its p hysical activity and the exercise stimulus is mild in severity. Unfortunately, many patients seen
needed to maintain an aerobic stimulus and optimal by physical therapists have poorly controlled spastic­
aerobic capacity. Often coupled with motor deficits ity and extreme cognitive deficits, which preclude
are cognitive deficits and mental retardation. These full participation in aerobic and strengthening exer­
afflictions limit the degree to which the patient can cise programs. These patients are at risk for the se­
follow instructions, perform treatments, and partic­ quelae of restricted mobility and recumbency.

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 30 Chronic Secondary Cardiopulmonary Dysfunction 547

Patient monitoring includes dyspnea, respiratory patients often have poor swallowing and saliva con­
distress, breathing pattern (depth and frequency), ar­ trol and thus are prone to aspiration and microat­
terial saturation, cyanosis (delayed sign of desatura­ electasis, particularly when recumbent at night. In­
tion), heart rate, blood pressure, and rate pressure ability to reposition themselves at night further
product. Unless mildly affected and not mentally in­ increases the risk of aspiration and its sequelae.
capacitated, patients with cerebral palsy are less able Mobilization is an essential component of the
to provide subjective ratings of treatment response; long-term management of the patient with cerebral
thus the physical therapist relies particularly on clini­ palsy to stimulate aerobic metabolism and optimize
cal judgment in conjunction with the patient's objec­ the efficiency of oxygen transport overall, including
tive responses to treatment. maximizing alveolar ventilation and mobilizing and
Medication that is needed to maximize treatment removing secretions (Wolff, Dolovich, and Obmin­
response is administered before treatment (e.g., anti­ ski, 1977). Maximizing ventilation with mobilization
spasticity medications). Knowledge of the type of is limited if the patient has generalized spasticity.
medication, its administration route, and time to and Furthermore, mobilization stimuli are selected specif­
duration of peak efficacy is essential if treatment is to ically to minimize eliciting further muscle spasm.
be maximally efficacious. Prescriptive hydrotherapy and equinotherapy (horse­
The primary interventions for maximizing car­ back riding) can provide effective stimulation to the
diopulmonary function and oxygen transport in pa­ cardiopulmonary system in the multiply handicapped
tients with cerebral palsy include some combination individual and minimize the effects of spasticity.
of education, mobilization and coordinated activity With training, coordination of ambulatory patients
(aerobic stimulation), strengthening e xercises can be improved and aerobic energy expenditure re­
(strength is often difficult to assess and treat because duced (Dresen, de Groot, and Bouman, 1985). In ad­
of overwhelming spasticity), chest wall mobility ex­ dition, energy is conserved for performing more ac­
ercises, range of motion exercises, body positioning, tivity. Chest wall exercises includes all planes of
breathing control and coughing maneuvers, and air­ movement with rotation. Body positioning to opti­
way clearance interventions. mize lung volumes and airflow rates is a priority.
Education is a principal focus of the long-term Breathing control and coughing maneuvers are essen­
management of the patient with cerebral palsy. tial and should be coupled with body movement and
Whenever possible, education is directed at the pa­ positioning. If mucociliary transport is impaired lead­
tient, but it more likely is directed at the parents and ing to secretion retention, postural drainage and man­
care providers. Education includes the reinforce­ ual techniques may need to be instituted with appro­
ment of preventative health practices (e.g., infection priate monitoring to ensure they do not have a
control, cold and flu prevention, flu shots, mobiliza­ detrimental effect (Kirilloff, Owens, Rogers, and
tion, coordinated activity, strengthening exercise, Mazzacco, 1985).
nutrition, weight control, and hydration). Patients In this patient population, clearing oral secretions
with cerebral palsy can be expected to have abnor­ and coughing maneuvers, require special attention.
mal sleep patterns. First, central cerebral involve­ Methods of facilitating effective coughing in patients
ment may affect the periodicity of breathing. During with neuromuscular diseases are extremely important
sleep, the effects of such dysfunction are accentu­ because they constitute life-preserving measures. Sup­
ated. Loss of normal periodic breathing and inter­ ported and unsupported coughing methods are de­
spersed sighs impairs mucociliary transport. Secre­ scribed in detail in Chapters 20 and 21. Whenever
tions may accumulate and contribute to airway possible, deep breathing and coughing is coupled with
obstruction and areas of atelectasis. Second, patients chest wall movement to facilitate maximal inflation of
with cerebral palsy are unable to reposition them­ the lungs before coughing and maximal exhalation of
selves during the night in response to both car­ the lungs during coughing. Body positions are varied
diopulmonary and musculoskeletal stimuli. Third, and changed frequently to simulate as much as possi­

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548 PART V Guidelines for the Delivery of Cardiopulmonary Physical Chronic Cardiopulmonary Conditions

Principles of physical therapy management

ble shifts in alveolar volume and ventilation and per­
fusion that occur with nomlal movement and po­ The of long-term management for the patient
smon Microaspiratiolls are likely a common with spinal cord injury include the following:
occurrence in this population, at • Maximize the patient's quality of

night. Nighttime oositioning must be prescribed for and well-being and hence

reserve

• Educate about cardiopulmonary manifestations

require of spinal cord injury, medica­
ri sk of rlpvpIon. tions, reduction and cessation, nutri­
tion, weight infection and the
role of a rehabilitation program
alveolar ventilation
• Optimize lung volumes and caoacities and flow
rates
ventilation and

and gas exchange

transport. • Reduce the work of breathing

• Reduce the work of the heart
• Protect the
Spinal Cord Injury
• Facilitate

Pathophysiology and medical management

secretion clearance

The manifestations and complica­ • Maximize aerobic and efficiency of

tions of spinal cord are related to the oxygen transport
level of the lesion (Murray and Car­ • Optimize physical endurance and exercise
diopulmonary impairment results from the loss of
control of the muscles and the • Optimize muscle strength and thereby
heart below the cord lesion. Loss of peripheral oxygen extraction
matic innervation results in Patient includes
Loss of abdominal and intercostal innervation re­ pattern (depth and frequency), ar­
duces the to transport, and terial sign of desatura­
the ability to clear the airways. Denervation of the tion), heart rate, blood pressure, and rate pressure
heart and orthostatism are less in that the product. Patients with high spinal cord injuries are
heart's autonomous function and increased respon­ somewhat more hemodynamically unstable and have
siveness of the heart and blood vessels to circulati more ECO than control in­
cathecholamines The cough dividuals; thus their cardiopulmonary status should
mechanism of quadriplegic patients is ineffective in be monitored during treatment.
the airways and Oorino, 1992). ceived exertion is monitored
are prone to the Medication that is needed to maximize treatment
effects of restricted mobility the extent of their response is administered before treatment (e.g., anti­
functional motor loss and sensory spasticity of the type of medica­
on cardiopulmonary function (Bach, 1991). Mo­ tion, its administration route, and time to and dura­
bilization and are essential for the tion of peak is essential if treatment is to be
cord injured to maintain car­ maximally efficaciolls.
diopulmonary function and oxygen transport effi­ The primary interventions for maximizing car­
ciency and the optimal strength and endurance of the diopulmonary function and oxygen transport in pa­
respiratory muscles. tients with soinet! cord iniurY include some combina­

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 30 Chronic Secondary Cardiopulmonary Dysfunction 549

tion of education, aerobic exercise, strengthening ex­ the strength and endurance of the respiratory muscles
ercises (to maintain or reduce rate of decline), pos­ (Gross, 1980) and may improve the functional capac­
tural correction exercises, chest wall mobility exer­ ity of some patients. A stronger endurance-trained di­
cises, range of motion exercises, body positioning, aphragm wit! not fatigue as readily as an untrained di­
breathing control and coughing maneuvers, airway aphragm. Standardizing the resistance of the training
clearance interventions, activity pacing, and energy stimulus alone, however, is not sufficient to produce a

conservation. An ergonomic assessment of the pa­ training effect. It is essential that flow rate is con­
tient's work and home environments may be indi­ trolled using a gauge.
cated to minimize oxygen demand and energy expen­ Methods of facilitating effective coughing in patients
diture in these settings. with neuromuscular diseases are extremely important
Education is a principal focus of the long-term because they constitute life-preserving measures. Sup­
management of the patient with spinal cord injury. ported and unsupported coughing methods are de­
Education includes the reinforcement of preventative scribed in detail in Chapters 20 and 21. Whenever pos­
health practices (e.g., infection control, cold and flu sible, deep breathing and coughing is coupled with
prevention, flu shots, aerobic exercise, strengthening chest wall movement to facilitate maximal inflation of
exercise, nutrition, weight control, hydration, pacing the lungs before coughing and maximal exhalation of
of activities, and energy conservation). the lungs during coughing. Body positions are v3lied
Aerobic exercise is an essential component of the and changed frequently to simulate as much as possible
long-term management of the patient with spinal cord shifts in alveolar volume and ventilation and perfusion
injury to optimize the efficiency of oxygen transport that occur with normal movement and body position
overall, including maximizing alveolar ventilation changes (Braun, Giovannoni, and O'Connor, 1984).
and mobilizing and removing secretions. With higher A comprehensive program includes stretching of
lesions, exercise is usually confined to upper-extrem­ the chest wall and passive range of motion exercises
ity work in the form of wheelchair ambulation. of the shoulder girdle. Maximal insufflations are en­
Preservation of upper-extremity muscle function and couraged in optimal body positions. Glossopharyn­
minimization of overuse are primary goals from the geal breathing can enable high quadriplegic patients
outset. Patients can maintain adequate cardiopul­ to be freed from mechanical ventilation for hours at a
monary conditioning with wheelchair exercise, how­ time. Assisted or unassisted coughing is coordinated
ever, exercise prescription should be conservative to with deep breathing and rhythmic rocking motion.
maximize the benefit-to-risk ratio of cardiopul­ Manual assisted coughing and mechanical coughing
monary conditioning relying of upper-extremity aids, including functional electrical stimulation and
work. Patients who are able to walk with leg braces insufflation-exsufflation devices, can be useful
and crutches expend considerable energy doing so. A (Bach, 1991; Linder, 1993). The pneumobelt is a de­
decision needs to be made regarding the benefits of vice that can facilitate ventilation without a tra­
walking at high energy demand vs conserving energy cheostomy (Miller, Thomas, and Wilmot, 1988). This
for other activities. Chest wall exercises can be used device counters loss of abdominal tone and helps pre­
and should include all planes of movement with a ro­ serve normal thoracoabdominal interaction during
tational component. Body positioning to optimize respiration, which is lost because of reduced rib cage
lung volumes and airflow rates is a priority. Breath­ compliance and increased abdominal compliance.
ing control and coughing maneuvers are essential and Patients with spinal cord injuries, particularly
should be coupled with body movement and position­ those with high lesions, require prophylactic man­
ing. Coordination of respiration with aerobic activity agement, given their risk of developing life-threat­
and wheeling is taught to maximize work output. ening respiratory infections and complications. Pro­
Ventilatory muscle training has a role in the long­ p h y l a x i s s ho uld i n c l u d e flu s h o t s, a v o i d i n g
term rehabilitation of some patients with high spinal polluted, smoky environments, smoking reduction
cord lesions. Ventilatory muscle training can increase and cessation, controlling the types of food eaten

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550 PART V Guidelines for the Delivery of Cardiopulmonary Physical Therapy: Chronic Cardiopulmonary Conditions

and chewing well to avoid choking, regular deep • Educate about cardiopulmonary manifestations
breathing, airway clearance, and frequent move­ of the late sequelae of poliomyelitis, self-man­
ment and change in body positions (even just shift­ agement, medications, smoking reduction or
ing and taking some deeper breaths while seated in cessation, nutrition, weight control, infection
a wheelchair is beneficial). An optimal time to take control, orthoses, mobility and ADL aids and
deep breaths a n d to c o u g h is during transfers, devices, and the role of a rehabilitation program
which usually are physically exerting and stimulate • Optimize alveolar ventilation
hyperpnea. • Optimize lung volumes and capacities and flow
rates
• Optimize ventilation and perfusion matching
late Sequelae of Poliomyelitis
and gas exchange
Pathophysiology and medical management
• Reduce the work of breathing
The late sequelae of poliomyelitis are reaching epi­ • Reduce the work of the heart
demic proportions as poliomyelitis survivors from the • Protect the airways from aspiration
late epidemic in the 1940s and 1950s reach 35 to 40 • Maximize aerobic capacity and efficiency of
years after onset. Three types of poliomyelitis were oxygen transport
prevalent during the epidemic in the middle of this • Opti mize physical endurance and exercise ca­
century, namely, spinal (the majority of cases), bul­ pacity
bar, and encephalitic. Many survivors are now pre­ • Optimize general muscle strength and thereby
senting with disproportionate fatigue, increased peripheral oxygen extraction
weakness, deformity, pain, reduced endurance, and Patient monitoring includes dyspnea, respiratory
breathing and swallowing problems (Dean, 1991; distress, breathing pattern (depth and frequency), ar­
Howard, Wiles, and Spencer, 1988), and respiratory terial saturation, cyanosis (delayed sign of desatura­
insufficiency (Lane, Hazleman, and Nichols, 1974). tion), heart rate, blood pressure, and rate pressure
Although cardiopulmonary complications were not product. Subjectively, pain, a feature of the late se­
associated with the spinal form of poliomyelitis at quelae of poliomyelitis, can be assessed using an ana­
onset, late-onset breathing and swallowing complica­ log scale, perceived exertion is assessed using the
tions can appear as a late effect of the disease (Dean, Borg scale, and fatigue and breathlessness can also be
Ross, Road, Courtenay, and Madill, 1991). In addi­ assessed using a modified versions of this scale.
tion, these patients may be deconditioned and have Medication that is needed to maximize treatment
poor movement economy (i.e., expend excessive en­ response is administered before treatment (e.g.,
ergy because of postural deformities) (Dean and analgesia). Knowledge of the type of medication, its
Ross, 1993). Thus delayed-onset cardiopulmonary administration route, and time to and duration of
complications, coupled with the effects of overuse peak efficacy is essential if treatment is to be maxi­
and general deconditioning, increases the risk of car­ mally efficacious.
diopulmonary compromise, reduces the ability to re­ The primary interventions for maximizing car­
cover from these, and increases surgical and anes­ diopUlmonary function and oxygen transport in patients
thetic risk. with the late sequelae of poliomyelitis include some
combination of education, aerobic exercise, strengthen­
PrinCiples of physical therapy management
ing exercises, postural correction exercises, chest wall
The goals of long-term management for the patient mobility exercises, range of motion exercises, body po­
with the late sequelae of poliomyelitis include the sitioning, breathing control and coughing maneuvers,
following: activity pacing, and energy conservation. An er­
• Maximize the patient's quality of life, general gonomic assessment of the patient's work and home
health, and well-being and hence physiological environments may be indicated to minimize oxygen de­
reserve capacity mand and energy expenditure in these settings. Aids

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 30 Chronic Secondary Cardiopulmonary Dysfunction 551

and devices are reviewed to optimize energy expendi­ ported and unsupported coughing methods are described
ture (e.g., electric wheelchair or scooter vs manual in detail in Chapters 20 and 21. Whenever possible,
wheelchair) and to reduce cardiopulmonary distress deep breathing and coughing is coupled with chest wall
(e.g., home mechanical ventilation). movement to facilitate maximal inflation of the lungs
Education is a principal focus of the long-term before coughing and maximal exhalation of the lungs
management of the patient with the late sequelae of dUling coughing. Body positions are varied and changed
poliomyelitis. Education includes the reinforcement of frequently to simulate as much as possible shifts in alve­
preventative health practices (e.g., infection control, olar volume and ventilation and perfusion that occur
cold and flu prevention, flu shots, aerobic exercise, with nonnal movement and body position changes.
strengthening exercises, nutIition, weight control, hy­ Progressive loss of pulmonary function in patients
dration, pacing of activities, and energy conservation). with ventilatory compromise at onset can lead to res­
Activity and sleep patterns need to be assessed to en­ piratory insufficiency. Comparable with other neuro­
sure sleep is maximally restorative and not contribut­ muscular conditions, invasive mechanical ventilation
ing to the patient's symptoms. Functional work capac­ is avoided. Promising alternatives are nasal and oral
ity and activity tolerance may be increased b y methods of noninvasive assisted mechanical ventila­
balancing activity t o rest, and maintaining fatigue tion (Bach, Alba, and Shin, 1989). [n addition, airway
below the patient's critical fatigue threshold, i.e., clearance can be fUlther assisted with manual assisted
threshold requiring prolonged recovery time. coughing, glossopharyngeal breathing, mechanical
Aerobic exercise is an essential component of the exsufflation, and mechanical insufflation-exsufflation
10ng-tenTI management of the patient with the late se­ (Bach et aI., 1993).
quelae of poliomyelitis to optimize the efficiency of Poliomyelitis survivors with ventilatory compro­
oxygen transport overall. The two principal goals of ex­ mise are comparable with other patients with general­
ercise are to optimize cardiopulmonary conditioning ized muscle weakness. Of particular concern in this
and movement economy. Maximizing ventilation with population, however, is the need to establish the role
exercise is limited if the patient has severe generalized of mobilization and exercise as a first line of defense
muscular weakness and increased fatigue. Dispropor­ in the management and prevention of cardiopul­
tionate fatigue and other symptoms experienced by pa­ monary dysfunction. However, for those patients
tients with the late sequelae of poliomyelitis have been whose late effects are due to overuse, additional exer­
attributed to overwork of affected and unaffected mus­ cise may be detrimental. Modified mobilization and
cles, terminal axon degeneration, and impaired impulse exercise, however, may be prescribed in an interval
transmission (Dean, 1991). Exercise is therefore pre­ schedule (McArdle, Katch, and Katch, 1991) (Chap­
scribed judiciously to provide an optimal aerobic train­ ter 17). The patient exercises for a period of time and
ing effect without contributing to further otheruse abuse then rests or reduces to a lower intensity of exercise
(i.e., prescriptive parameters based on subjective re­ to aJlow the muscles to rest. In addition to the multi­
sponses using semi-quantitative scales in conjunction tude of benefits of mobilization and exercise on oxy­
with objective responses). Walking is the most func­ gen transport overall, these interventions also opti­
tional type of aerobic exercise, however, aquatic exer­ mize respiratory muscle strength and endurance. If
cise provides a useful medium for patients with lower­ the patient does not recover within a few hours, the
extremity paresis who require crutches to walk or are mobilization or exercise stimuli was excessive and
confined to a wheelchair. Reducing physical activity should be modified. Chest waH mobility exercises to
and exercise is indicated in some patients to optimize facilitate breathing and coughing may have a role.
aerobic and muscle power. The effect of resting affected Patients with generalized neuromuscular weakness
and unaffected muscles enhances functional capacity. require prophylactic management, given their high
Methods of facilitating effective coughing in patients risk of developing life-threatening respiratory infec­
with neuromuscular diseases are extremely important tions and complications. Prophylaxis should include
because they constitute a life-preserving measme. Sup­ flu shots, avoiding polluted, smoky environments,

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552 PART V Guidelines for the Delivery of Larruopuunonal Physical Therapy: Chronic Cardiopulmonary Conditions

controlling the of food eaten and chewing well and hypercapnia. With severe chest de-
to avoid choking, regular deep breathing, airway of pulmonary
and movement and in and right heart failure can result in a
(even just shifting and taking some situation.
breaths while seated in a wheelchair is benefi­
PrinCiples of physical therapy management
cial). An optimal time to take deep breaths and to
cough is during transfers, which usually are The goals of management for the
cally and stimulate hyperpnea. with thoracic rjptt>rrni include the
quality of
and hence physiological
MUSCULOSKElETAL CONDITIONS
Thoracic Deformities
Pathophysiology and medical management
of thoracic
can result from abnonnalities ications, nutrition, weight control, infection con­
to congenital deformity, trol, smoking reduction and cessation, and the
acquired disease, and trauma . and role of a rehabilitation program
1988b ). of the chest wall alveolar ventilation
reduces the mobility of the bony thorax, thereby in- VUUlIlILC lung volumes and caDacities and flow
the work of Shallow, rapid breath­ rates
ing often results. Minute ventilation is increased at the • Optimize ventilation and perfusion
expense of alveolar ventilation. Severe deformity leads and gas
to of the mediastinal stmctures. The heart • Reduce the work of
can be and rotated, impeding its mechanical • Reduce the work of the heart
function. Examples of chronic deformities that im­ • Protect the airways from aspiration
on pulmonary function are kyphoscoliosis sec­ • Faci litate
ondary to poliomyelitis, tuberculous and • Optimize secretion clearance
other causes and Other exam- • Maximize aerobic and of
of deformity include traumatic injury of the verte­ oxygen transport
bral column, ribs, and sternum. Routine cardiopul­ Optimize physical endurance and exercise
monary assessment should include a musculoskeletal
examination of the spinal column and thoracic cavity. • Optimize muscle and thereby
Normal pulmonary function and gas peripheral oxygen extraction
depend on symmetry of cardiopulmonary anatomy Patient includes dyspnea,
and function. Asymmetry of the chest distress, (depth and frequency), ar­
wall interferes with normal lung re­ terial saturation, (delayed of desatura­
gional of ventilation and in the lion), heart rate, blood pressure, and rate pressure
and the distribution of inspired gas (Bake, product. Patients with cardiac
and Grimby, 1976; Sinha and ECG monitoring particularly during exercise. Subjec­
compliance and tively, exertion is assessed the
increase in work the elastic resis­ and breathlessness is assessed usin!l: a modified
tance of the lung are characteristic of kyphoscolio­ version of this scale.
sis. Altered pressure gradients and uneven lung The primary interventions for maximizing car­
movement the may con­ diopulmonary function and oxygen in pa­
tribute to altered lung water balance and impaired tients with thoracic deformity include some combina­
lymphatic The effects of tion of aerobic
dead space and shunt may be postural correction

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 30 Chronic Secondary Cardiopulmonary Dysfunction 553

tion, chest wall mobility exercises, range of motion Patients with chest wall deformities secondary to
exercises, body positioning, breathing control and neuromuscular conditions require prophylactic man­
coughing maneuvers, airway clearance interventions, agement given their high risk of developing life­
activity pacing, and energy conservation. An er­ threatening respiratory infections and complications.
gonomic assessment of the patient's work and home Prophylaxis should include flu shots, avoiding pol­
environments may be indicated to minimize oxygen luted, smoky environments, smoking reduction and
demand and energy expenditure in these settings. cessation, controlling the types of food eaten and
Education is a principal focus of the long-term chewing well to avoid choking, regular deep breath­
management of the patient with thoracic deformity. ing, airway clearance, and frequent movement and
Education includes the reinforcement of preventative change in body positions (even just shifting and tak­
health practices (e.g., infection control, cold and flu ing some deeper breaths while seated in a wheelchair
prevention, flu shots, smoking reduction or cessation, is beneficial). An optimal time to take deep breaths
aerobic exercise, strengthening exercises, nutrition, and to cough is during transfers, which usually are
weight control, and hydration). physically exerting and stimulate hyperpnea.
Aerobic exercise is an csscntial component of the
long-term management of the patient with thoracic de­
Osteoporosis
formity to optimize the efficiency of oxygen transport
overall. Maximizing ventilation with exercise in pa­
Pathophysiology and medical management
tients with severe deformity may be limited. OptimiZ­ Osteoporosis is a condition associated with reduced
ing alignment to minimize the cardiopulmonary limita­ bone mass per unit volume (Smith, Smith, and Gilli­
tions of the deformity during physical acti vity, gan, 1991). Age-related bone loss begins earlier and
exercise, and rest is a priority. Chest wall exercises in­ accelerates f a s t e r in w o m e n , p ar t i c u larly after
clude all planes of movement with a rotational compo­ menopause, than men. Life-style factors, such as diet,
nent. Body positioning to optimize lung volumes and exercise, and smoking, have a significant role in re­
ailtlow rates is a priority. Breathing control and cough­ ducing bone mass. Caffeine has also been implicated
ing maneuvers are essential and should be coupled as a contributing factor to bone loss secondary to in­
with body movement and positioning. If mucociliary creasing urinary calcium loss.
transport is impaired leading to secretion retention, Osteoporosis is classified as idiopathic osteoporosis
postural drainage may need to be instituted, coupled unassociated with other conditions, osteoporosis asso­
with deep breathing and coughing maneuvers. ciated with other conditions (e.g., malabsorption, cal­
Ventilatory muscle training may have a role in the cium deficiency, immobilization, or metabolic bone
management of patients with reduced inspiratory disease), osteoporosis as a feature of an inherited con­
pressures and associated decreases in total lung ca­ dition (e.g., osteogenica imperfecta or Marfan's syn­
pacity and hypoxemia. drome), and osteoporosis associated with other condi­
Methods of facilitating effective coughing in pa­ tions but the pathogenesis is not understood (e.g.,
tients with musculoskeletal deformity are extremely rheumatoid arthritis, alcoholism, diabetes mellitus, or
important because they constitute life-preserving mea­ chronic airflow limitation) (Wilson et aI., 1991).
sures. Supported and unsupported coughing methods The most common clinical features are vertebral
are described in detail in Chapters 20 and 2l. When­ pain and spinal deformity resulting from vertebral
ever possible, deep breathing and coughing is coupled compression and collapse. Vertebral bodies tend to
with chest wall movement to facilitate maximal infla­ collapse anteriorly, contributing to cervical lordosis,
tion of the lungs before and maximal exhalation during thoracic kyphosis, postural slumping, and loss of
coughing. Body positions are varied and changed fre­ height. Acute episodes may be relieved by restricted
quently to simulate as much as possible shifts in alveo­ mobility. Straining and sudden changes in position
lar volume and ventilation and perfusion that occur can exacerbate an acute episode. C ardiopulmonary
with normal movement and body position changes. complications of osteoporosis are secondary to spinal

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554 PART V Guidelines for the Delivery of Cardiopulmonary Physical Therapy: Chronic Cardiopulmonary Conditions

deformity, chest wall rigidity, and cardiopulmonary Patient monitoring includes heart rate, blood pres­
deconditioning resulting from restricted mobility. sure, and rate pressure product. Patients with cardiac
Osteoporosis is a condition associated with aging dysfunction require ECG monitoring particularly dur­
and older age groups. The pain of acute episodes ing exercise. Subjectively, pain and discomfort are as­
leads to periods of restricted mobility and significant sessed with an analog scale or modified Borg scale, and
cardiopulmonary dysfunction in older persons (Dean, perceived exertion is assessed using the Borg scale.
1993). Exercise that is weight bearing and loads the Medication that is needed to maximize treatment
muscles around bone maintains bone density and de­ response is administered before treatment (e.g.,
celerates bone loss thus has a central role in preserv­ analgesics). Knowledge of the type of medication,
ing bone health. Generally, the growth and remodel­ its administration route, and time to and duration of
lin g of b o n e d e p e n d s h i ghly on t h e e x e r c i s e peak efficacy is essential if treatment is to be maxi­
prescription parameters (e.g., type o f exercise, inten­ mally efficacious.
sity, duration, and frequency). Bone mineral content The primary interventions for maximizing car­
is more closely related to cardiopulmonary condition­ diopulmonary function and oxygen transport in patients
ing than physical activity level. Furthermore, any with osteoporosis include some combination of educa­
detrimental effect of exercise on osteoporosis appears tion, aerobic weight-bearing exercise, strengthening ex­
to relate more to malalignment and injury rather than ercises, chest wall mobility exercises, range of motion
activity itself. exercises, activity pacing, and energy conservation. An
ergonomic assessment of the patient's work and home
Principles of physical therapy management environments may be indicated to minimize oxygen de­
The etiology of osteoporosis is diverse; thus manage­ mand and energy expenditure in these settings.
ment needs to consider the underlying pathophysiol­ Education is a principal focus of the long-term man­
ogy and that several factors may be contributing to agement of the patient with osteoporosis. Education in­
the presentation of osteoporosis in the same patient. cludes the reinforcement of preventative health prac­
The goals of long-term management for the pa­ tices (e.g., infection control, cold and flu prevention, flu
tient with osteoporosis include the following: shots, smoking reduction and cessation, weight-bearing
• Maximize the patient's quality of life, general aerobic exercise, strengthening exercises, range of mo­
health, and well-being and hence physiological tion exercises, nutrition, weight control, hydration, pac­
reserve capacity ing of activities, and energy conservation).
• Educate about cardiopulmonary manifestations Aerobic exercise is an essential component of the
of osteoporosis, self-management, medications, long-term management of the patient with osteoporo­
nutrition, weight control, smoking reduction and sis to optimize the efficiency of oxygen transport
cessation, infection control, and the role of a re­ overall. Upright, weight-bearing aerobic exercise is
habilitation program essential to maintain bone density or reduce the rate
• Optimize alveolar ventilation of bone loss. Maximizing ventilation with exercise is
• Optimize lung volumes and capacities and flow limited if the patient has severe generalized muscular
rates weakness and increased fatigue. Chest wall exercises
/" Optimize ventilation and perfusion matching can be used and should include all planes of move­
and gas exchange ment with a rotational component. Breathing control
• Facilitate mucociliary transport and coughing maneuvers are essential and should be
• Maximize aerobic capacity and efficiency of coupled with body movement and positioning. Strain­
oxygen transport ing, Valsalva maneuvers, and jarring activity and ex­
• Opt imize physical endurance and exercise ercise are contraindicated.
capacity Methods of facilitating effective coughing in pa­
• Optimize general muscle strength and thereby tients with osteoporosis are extremely important be­
peripheral oxygen extraction cause they constitute life-preserving measures. Some

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 30 Chronic Secondary Cardiopulmonary Dysfunction 555

patients fracture ribs and vertebrae during coughing. of SLE, self-management, nutrition, weight con­
Patients at risk should rely on huffing maneuvers that trol, smoking reduction and cessation, medica­
do not require closing the glottis and do not generate tions, infection control, and the role of a rehabil­
high intrathoracic pressures (Hietpas, Roth, and itation program
Jensen, 1979). • Optimize alveolar ventilation
• Optimize lung volumes and capacities and flow
rates
COLLAGEN VASCULAR/CONNECTIVE
Optimize ventilation and perfusion matching
TISSUE DISEASES
•

and gas exchange

Systemic Lupus Erythematosus
• Reduce the work of breathing
Pathophysiology and medical management
• Reduce the work of the hem1
Systemic lupus erythemat osus (SLE) is a disease • Protect the airways from aspiration
characterized by the presence of multiple antibodies • Facilitate mucociliary transport
that contribute to immunologically mediated tissue • Optimize secretion clearance
inflammation and damage (Segal, Calabrese, Ahmad, • Maximize aerobic capacity and efficiency of
Tubbs, and White, 1985). The disease affects the oxygen transport
major organ systems, including the central nervous, • Optimize physical endurance and exercise
musculoskeletal, pulmonary, vascular, and renal sys­ capacity
tems. Symptoms include arthralgic and myalgic stiff­ • Optimize general muscle strength and thereby
ness, pain, and fatigue. peripheral oxygen extraction
The cardiopulmonary manifestations of SLE in­ Patient monitoring includes dyspnea, respiratory
clude atelectasis, resulting from inflammation of the distress, breathing pattern (depth and frequency), ar­
alveolar walls, and perivascular and peribronchial terial saturation, cyanosis (delayed sign of desatura­
connective tissue, effusions secondary to lung infarc­ tion), heart rate, blood pressure, and rate pressure
tion, reduced surface tension, and splinting secondary product. Patients with cardiac dysfunction should be
to pleuritic pain. Other manifestations include pleuri­ cleared by a cardiologist before being prescribed an
tis with or without effusion, pneumonitis, interstitial exercise program. Subjectively, discomfort, pain, fa­
fibrosis, pulmonary hypertension, diaphragmatic dys­ tigue, and breathlessness are assessed using analog
function, pulmonary hemorrhage, systemic hyperten­ scales or modified versions of the Borg scale, and
sion, myocarditis, constrictive pericarditis, dysrhyth­ perceived exertion is assessed using the Borg scale.
mias, tamponade, pericardial pain, arteritis, and Medication. that is needed to maximize treatment re­
defects of the mitral and aortic valves (Dickey and sponse is administered before treatment (e.g., analgesic
Myers, 1988). Other manifestations that affect car­ and antiinflammatory agents). Knowledge of the type
diopulmonary function include anemia, leukopenia, of medication, its administration route, and time to and
thrombocytopenia, thrombosis, splenomegaly, ascitis, duration of peak efficacy is essential if treatment is to
gastrointestinal bleeding, nephritis, and renal insuffi­ be maximally efficacious.
ciency (Wilson et aI., 1991). The primary interventions for maximizing car­
diopulmonary function and oxygen transport in pa­
Principles of physical therapy management
tients with SLE include some combination of educa­
The goals of long-term management for the patient tion, aerob ic exerc i se, strengthen i ng exerc i scs,
with systemic lupus erythematosus (SLE) include the postural correction exercises, chest wall mobility ex­
following: ercises, range of motion exercises, body positioning,
• Maximize the patient's quality of life, general breathing control and coughing maneuvers, airway
health, and well-being and hence physiological clearance interventions, activity pacing, and energy
reserve capacity conservation. An ergonomic assessment of the pa­
• Educate about cardiopulmonary manifestations tient's work and home environments may be indi­

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556 PART V Guidelines for the Delivery of Cardiopulmonary Physical Therapy: Chronic Cardiopulmonary Conditions

cated to minimize oxygen demand and energy expen­ deficit. Pulmonary hypertension may be a complicat­
diture in these settings. ing factor. Broncoal veolar lavage is consistent with
Education is a principal focus of the long-term an acute inflammatory process. Cardiomyopathy is
management of the patient with SLE. Education in­ associated with ischemia, areas of infarction, and my­
cludes the reinforcement of preventative health prac­ ocardial fibrosis (Gray, 1989). Fibrosis of the con­
tices (e.g., infection control, cold and flu prevention, duction system predisposes the patient to conduction
flu shots, smoking reduction or cessation, aerobic ex­ defects and dysrhythmias. Other cardiopulmonary
ercise, strengthening exercises, nutrition, weight con­ manifestations include pericarditis with or without ef­
trol, hydration, pacing of activities, and energy con­ fusion and pulmonary and systemic hypertension
servation). An ergonomic assessment of the patient's from renal involvement. Half of patients with sclero­
work and home environments may be indicated to derma have renal involvement including intimal hy­
minimize oxygen demand and energy expenditure in perphasia, fibrinous necrosis of the afferent arterioles,
these settings. and thickening of the glomerular basement mem­
Aerobic exercise is an essential component of the brane. Fibrotic changes and stenoses occur in the
long-term management of the patient with SLE to op­ small arteries and arterioles systemically. Similar
timize the efficiency of oxygen transport overall, in­ changes in the lymphatic vessels may obliterate
cluding maximizing alveolar ventilation and mobiliz­ lymph flow.
ing and removing secretions. Parameters of the Esophageal involvement contributes to regurgita­
exercise prescription are based on subjective re­ tion of gastric contents. which is exacerbated when
sponses, (e.g., discomfort, pain, breathlessness, and the patient is recumbent or bends over. Bloating and
perceived exertion in conjunction with objective re­ abdominal discomfort may reflect paralytic ileus and
sponses). Optimal types of aerobic exercise include intestinal obstruction. Ascites and fluid accumulation
walking and cycling. Aquatic exercise may be prefer­ in the gut increases abdominal pressure and en­
able for patients with musculoskeletal involvement croaches on diaphragmatic motion.
that precludes walking and cycling. Chest wall exer­
cises can be used and should include all planes of
Principles of physical therapy management
movement with a rotational component. Body posi­ The goals of long-term management for the patient
tioning to optimize lung volumes and airflow rates is with scleroderma include the following:
a priority. Breathing control and coughing maneuvers • Maximize the patient's quality of life, general
are essential and should be coupled with body move­ health, and well-being and hence physiological
ment and positioning. If mucociliary transport is im­ reserve capacity
paired, leading to secretion r e te ntion, p o s tural • Educate about cardiopulmonary manifestations
drainage may need to be instituted, coupled with deep of scleroderma, self-management, nutrition,
breathing and coughing maneuvers. weight control, smoking reduction or cessation,
medications, infection control, and the role of a
rehabilitation program
Scleroderma
• Optimize alveolar ventilation
Pathophysiology and medical management • Optimize lung volumes and capacities and flow
Scleroderma is characterized by the overproduction rates
of collagen and progressive fibrosis of cutaneous and • Optimize ventilation and perfusion matching
subcutaneous tissues (Gray, 1989). The cardiopul­ and gas exchange
monary manifestations of this condition result in in­ • Reduce the work of breathing
terstitial pulmonary fibrosis with significantly re­ • Reduce the work of the heart
duced vital capacity, diffusing capacity, and arterial • Protect the airways from aspiration
oxygen tension (Bates, 1989; Wilson et aI., 1991). • Facilitate mucociliary transport
Reduced static compliance is the primary mechanical • Optimize secretion clearance

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 30 Chronic Secondary Cardiopulmonary 557

• Maximize aerobic and of cold and influenza

oxygen transport
• Optimize physical endurance and exercise
nutrition,
• Optimize muscle strength and thereby hydration, of activities, and energy conserva­
oxygen extraction tion). An ergonomic assessment of the patient's
includes dyspnea, work and home environments may be indicated to
distress, pattern and frequency), ar­ minimize oxygen demand and energy in
terial saturation, cyanosis (delayed of desatura­ these
heart rate, blood pressure, and rate pressure Aerobic exercise is an essential component of the
Patients with cardiac require of the patient with scleroderma
ECG monitoring, during exercise. If sup- to of oxygen overall.
oxygen is used, the FIo2 administered is Chest wall exercises can be used and should include all
recorded. Subjectively, breathlessness is assessed planes of movement with a rotational
using a modified version of the scale of per­ Body to volumes and air­
ceived exertion and exertion is assessed flow rates is a Breathing control and
the Borg scale. maneuvers are essential and should be coupled with
Medication that i s needed to maximize treat­ movement and positioning. If mucociliary trans­
ment response i s administered before treatment port is impaired leading to secretion postural
(e.g., immunosuppressive agents and may need to be instituted coupled with
therapy). of the type of medication, its breathing and coughing maneuvers,
administration route, and time to and duration of
efficacy is essential if treatment is to be max­
Ankylosing Spondylitis
efficacious.
Pathophysiology and medical management
The primary interventions for car­
diopulmonary function and oxygen transport in pa­ Ankylosing spondylitis results in reduced total lung
tients with scleroderma include some combination of capacity, vital capacity, and inspiratory muscle func­
tion (Lisboa, Moreno, Fava, and I
Muhm, and
Ventilatory capacity is preserved that the respi­
maneuvers, ratory muscles are not involved. The disease results
clearance and energy in spinal and chest wall , thus there
conservation, An ergonomic assessment of the pa­
tient's work and home environments may be indi­
cated to minimize oxygen demand and energy expen­ The pa­
diture in these spondylitis has an increased de­
function and therefore is
at risk if administered respiratory depressant medica­
patients have antacids between tions or if he or she thoracic or upper ab­
meals, and do not lie down for a few hours after eat­ dominal surgery (Grim by, FugJ-Meyer, and Blom­
When recumbent, these patients have the head of strand, I
bed elevated to minimize the risk of of gas­ During patients with ankylosing spondyli­
tric contents. tis show minimal chest wall compared with
Education is a principal focus of the persons (Elliott et aI., 1985). Although
management of the patient with scleroderma. Educa­ workload reduced, rather than
tion includes the reinforcement of preventive health capacity, ventilation-perfusion

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558 PART V Guidelines for the Delivery of Cardiopulmonary Physical Therapy: Chronic Cardiopulmonary Conditions

or abnormal blood gases is more to be the limit­ (e.g., reduction or ces­

ing factor. infection cold and flu prevention, flu
reduction and aerobic exer­
Principles of physical therapy management
strengthening nutrition, weight con-
The goals of management for the and hydration),
with spondylitis include the Aerobic exercise is an e sential component of the
• Maximize the patient' of life, long-term management of the patient with
and hence physiological spondylitis to ize the of oxygen
reserve transport overall. Maximizing ventilation with mobi­
• Educate about lization is limited if the has extreme
of ankylosing spondylitIS, selt-management, nu- Chest wall exercises can be used and should
weight control, infection smok­ include all planes of movement with
reduction and and the role of re­ component. Body to vol­
habilitation program
umes and airflow rates is a priority. control
alveolar ventilation
and coughing maneuvers are essential and should be
• Optimize lung volumes and and flow with body movement and Venti­
rates latory muscle training in conjunction with exercise
ventilation and perfusion may have some additional benefit in maximizing aer­
and gas obic
• Facilitate
• Maximize aerobic capacity and efficiency of
Rheumatoid Arthritis
oxygen transport
Pathophysiology and medical management
• Optimize physical endurance and exercise
Rheumatoid arthritis (RA) is disease
• Optimize muscle strength and that is associated with weI I-documented cardiopul­
monary and cardiovascular including
Patient with or without interstitial fibrosis, pul­
breathing pattern monary vasculitis, an increased incidence of bronchi­
arterial saturation, tis and pneumonia endo­
mation), heart rate, blood pressure, and rate pres­ c a r d i t is, dysrhythmias, n e ur i t i s a n d v a s c ul itis
b l o m a n d Nor de mar, 1987; S co t t, Wise,
_ interventions for maxlmlzll1g car­ I
diopulmonary function and oxygen transport in pa­ Functional is limited pain and stiffness
tients with ankylosing include some com­ in the affected muscles and joints, the num­
b i n at i o n of e d u cation, e x e r c is e. s t r e nl!th e n i n g ber of affected, and whether the patient
is having an acute episode. Self-limited ac­
tivity and exercise contributes to cardiopulmonary de-
exercises, range o f motion Movement such as is often in­
tioning, control and cougnmg maneuvers, efficient because of
and energy conservation. An ergonomic as­ limited by musculoskeletal thus submaxi­
sessment of the work and home environ­ mal tests are more functional in this popUlation, Tests
ments may indicated to minimize oxygen demand of cardiovascular status must be
and energy in these to enable the
Education is a focus of the without pain.
management of the patient with ankylosing Graded low -intensity aerobic exercise for pa­
tis. Education includes the reinforcement of preventa­ tients with RA from IS to 35 lllinutes three times a

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 30 Chronic Secondary CardioPIJllJlonary Dysfunction 559

week can be sufficient to enhance aerobic Patient monitoring includes

(Harkcom, Banwell, and distress, pattern (depth and ar­
aerobic capacity, such an terial saturation, (delayed sign of desatura­
exercise prescription results in increased exercise heart rate, blood pressure, and rate pressure
reduced affected joint count, improved activi­ Subjectively, exertion is assessed
ties of reduced joint and general the Borg scale.
fatigue. Should a tlare-up occur while the pa­ Medication that is needed to maximize treatment
tient is on an exercise program, a few days or response i s administered before treatment
weeks of restricted mobility and abstinence from steroids, nonsteroidal antiinflammatory
exercise frequently ameliorate the symptoms. Gen­ analgesics). of the type of its
tl.e mobilization (preferably cou­ administration route, and time to and duration of
pled with range of motion exercises this pe­ is essential if treatment is to be maximally
riod, will minimize the negative effects of reduced efficacious. Gentle rhythmic, exercise is
activity. prescribed, particularly for patients at risk of loss of
Prolonged use of steroids contributes to bone bone mass to long-term steroid use.
Thus physical and exercise The primary interventions for car­
lions are modified accordingly. diopUlmonary function and oxygen transport in pa­
tients with RA include some combination of educa­
Principles of physicallherapy management tion, aerobic exercise, exercises,
postural correction exercises, chest wall mobility ex-
range of motion body
breathing control and coughing maneuvers, airway
• Maximize the quality of life, clearance activity pacing, and energy
health, and well-being and hence physiological conservation. An assessment of the pa­
reserve 'J H.7 tient's work and home environments may be indi­
• Educate about cardiopulmonary manifestations cated to minimize oxygen demand and energy expen­
of rheumatoid diture in these A review of mobility aids and
tion, weight devices is carried out to maximize the func­
medications, infection control, and the tion and exercise tolerance.
role of a rehabilitation program Education is a focus of the
alveolar ventilation management of the patient with RA. Education in­
volumes and and flow cludes the reinforcement of health prac­
rates infection control, cold and flu prevention,
• Optimize ventilation and perfusion reduction or aerobic ex-
and gas exchange strengthening
Reduce the work of nutrition,
• Reduce the work of the heart and energy
• Protect the from aspiration Aerobic exercise is an essential component of the
• Facilitate transport long-term management of the patient with RA to op­
• Optimize secretion clearance timize the of oxygen overall
• Maximize aerobic and of both with to cardiopulmonary conditioning
oxygen transport and improving movement economy. Mild-to-moder­
physical endurance and exercise ate exercise during subacute periods can be benefi­
capacity cial. efficiency of RA l..Iall"'"l

• Optimize muscle and

with persons. The
peripheral oxygen extraction
however, is less in RA patients because of limping

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560 PART V Guidelines ror the Delivery of Cardiopulmonary Physical Therapy: Chronic Cardiopulmonary Conditions

Principles of physical therapy management

and associated deformity and pain. Non-weight­
bearing exercise is beneficial in patients with severe The goals of long-term management for the patient
deformity and pain (e.g., aquatic exercise or water with chronic renal insufficiency include the following:
walking). Given the fluctuations in the patient's con­ • Maximize the patient's quality of life, general
dition from day to day, exercise prescription is modi­ health, and well-being and hence physiological
fied frequently to consider the patient's changing reserve capacity
condition. Chest wall exercises include all planes of • Educate about cardiopulmonary manifestations
movement with a rotational component. Body posi­ of renal insufficiency, self-management, med­
tioning to optimize lung volumes and airflow rates is ications, nutrition, weight control, infection con­
a priority. Breathing control and coughing maneu­ trol, and the role of a rehabilitation program
vers are essential and should be coupled with body • Optimize alveolar ventilation
movement and positioning. • Optimize lung volumes, capacities, and flow
rates
• Optimize ventilation and perfusion matching
Chronic Renal Insufficiency
and gas exchange
Pathophysiology and medical management
• Reduce the work of breathing
Patients with chronic renal disease have significant • Reduce the work of the heart
systemic complications. Cardiopulmonary manifes­ • Protect the airways from aspiration
tations include left ventricular hypertrophy and • Facilitate mucociliary transport
congestive heart failure secondary to chronic vol­ • Optimize secretion clearance
ume and pressure overload (American College of • Maximize aerobic capacity and efficiency of
Sports Medicine, 1991). Patients have a high inci­ oxygen transport
dence of atherosclerosis, coronary artery disease, • Optimize physical endurance and exercise ca­
glucose intolerance, and diabetes. Also, generalized pacity
muscle weakness and fatigue compromises func­ • Optimize general muscle strength and thereby
tional work capacity. peripheral oxygen extraction
Chronically increased fluid volume, although reg­ Patient monitoring includes dyspnea, respiratory
ulated with dialysis, contributes to increased stroke distress, breathing pattern (depth and frequency), ar­
work of the heart and cardiomegaly and hyperten­ terial saturation, cyanosis (delayed sign of desatura­
sion. With respect to pulmonary function, increased tion), heart rate, blood pressure, and rate pressure
fluid volume increases peribronchial fluid and airway product. Subjectively, perceived exertion is assessed
closure. After dialysis, the reduction in body weight using the Borg scale.
is related to a reduction in closing volume, increased Medication that is needed to maximize treatment
vital capacity, and forced expiratory flow rates. response is administered before treatment. Knowl­
The pulmonary-renal syndromes reflect the close edge of the type of medication, its administration
relationship between the lungs and kidneys. These route, and time to and duration of peak efficacy is es­
syndromes are characterized by altered immunologi­ sential if treatment is to be maximally efficacious.
cal status, alveolar hemorrhage, interstitial and alveo­ The primary interventions for maximizing car­
lar inflammation, and pulmonary vascular involve­ diopulmonary function and oxygen transport in pa­
ment (Matthay, Bromberg, and Putman, 1980). tients with chronic renal insufficiency include some
The kidneys have a primary role in the production combination of education, aerobic exercise, strength­
and regulation of certain humoral regulators of me­ ening exercise, chest wall mobility exercises, range of
tabolism, hemodynamics, fluid balance, and oxygen motion exercise, body positioning, breathing control
transport (Rankin and Matthay, 1982) Thus pathol­ and coughing maneuvers, airway clearance interven­
ogy of the kidneys significantly affects those life-sus­ tions, activity pacing, and energy conservation. An er­
taining processes. gonomic assessment of the patient's work and home

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 30 Chronic Secondary Cardiopulmonary Dysfunction 561

environments may be indicated to minimize oxygen ditions presented include muscular dystrophy, hemi­
demand and energy expenditure in these settings. plegia, Parkinson's disease, multiple sclerosis, cere­
Education is a principal foclls of the long-term bral palsy, spinal cord injury, and the late sequelae
management of the patient with chronic renal insuffi­ of poliomyelitis. The musculoskeletal conditions
ciency. Education includes the reinforcement of pre­ presented included kyphoscoliosis and osteoporosis.
ventative health practices (e.g., infection control, cold The collagen vascular/connective tissue conditions
and flu prevention, flu shots, aerobic exercise, presented include systemic lupus erythematosus,
strengthening exercises, range of motion exercises, scleroderma, ankylosing spondylitis, and rheuma­
nutrition, weight control, hydration, pacing of activi­ toid arthritis. Finally, management of the patient
ties, and energy conservation. with chronic renal insufficiency is presented. The
Aerobic exercise is an essential component of the principles of management are presented rather than
long-term management of the patient with chronic treatment prescriptions, which cannot be given with­
renal insufficiency to optimize the efficiency of oxy­ out consideration of a specific patient. In this con­
gen transport overall. Maximizing ventilation with text the goals of long-term management of each
exercise is limited if the patient has severe general­ condition were presented, followed by the essential
ized muscular weakness and increased fatigue. Maxi­ monitoring required, and the primary interventions
mal oxygen uptake increases in hemodialysis patients for maximizing cardiopulmonary function and oxy­
along with improvement in other indices of car­ gen transport. The selection of interventions for any
diopulmonary conditioning (Painter et aI., 1986). Pa­ given patient is based on the physiological hierar­
tients may decrease or eliminate the need for antihy­ chy. The most physiological interventions are ex­
pertension medications. Exercise carried out during ploited followed by less physiological interventions
hemodialysis treatment sessions is feasible and safe and those whose efficacy is less well documented.
for appropriate patients. Because hemodialysis treat­
ments require sessions of several hours multiple
REVIEW QUESTIONS
times weekly, aerobic training (e.g., cycle ergometry)
can be effectively incorporated into treatment time I. Describe the chronic cardiopulmonary patho­
(Shallom, Blumenthal, Williams, Murray, and Den­ physiology secondary to muscular dystrophy,
nis, 1984; Zabetakis et aI., 1982). The exercise pre­ hemiplegia, parkinson's disease, multiple sclero­
scription of patients with blood glucose abnormalities sis, cerebral palsy, spinal cord injury, late seque­
and coronary artery disease is modified accordingly. lae of poliomyelitis, kyphoscoliosis, osteoporo­
Chest wall exercises can be used and should in­ sis, systemic lupus erythematosus, scleroderma,
clude all planes of movement with a rotational com­ ankylosing spondylitis, rheumatoid arthritis, and
ponent. Body positioning to optimize lung volumes chronic renal insufficiency.
and ailflow rates is a priority. Breathing control and 2. Relate cardiopulmonary physical therapy treat­
coughing maneuvers are essential and should be cou­ ment interventions to the underlying pathophysi­
pled with body movement and positioning. ology of each of the above chronic conditions
and provide the rationale for your choice.

SUMMARY
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PART VI

Guidelines for the Delivery

of Cardiopulmonary
Physical Therapy:
Intensive Care

Copyrighted Material
 Comprehensive Patient Management
in the Intensive Care Unit

Elizabeth Dean

KEY TERMS Evidence-based practice Quality care

Function optimization Scientific evidence
Physiological evidence Treatment goals
Prevention Treatment selection and prioritization

INTRODUCTION
(Bar low, Hayes, and Nelson, 1984; Dean, 1985;
Because cardiopulmonary physical therapy in the in­ Dean, 1994a; Hislop, 1975; Ross and Dean, 1989;
tensive care unit (lCU) is a specialty in itself, this Schon, 1983; Worthingham, 1960; Zadai, 1986). A
chapter presents some general aspects of clinical and superior knowledge of cardiopulmonary physiology,
nonclinical management in this setting. An overview pathophysiology, pharmacology, and mu ltisystem
of the general goals of treatment and the rationale for disease and its medical management is essential.
prioritizing treatments according to a physiological Clinical decision making in the lCU and ration­
hierarchy is described. Both clinical and nonclinical al management of patients is based on a t r i pod
aspects of patient management are presented. Finally, approach: (1) a knowledge of the underlying patho­
issues related to the management of the dying patient physiology and basis for general care, (2) the physio­
are addressed. logical and scientific evidence for treatment interven­
The thrust toward evidence-based p ractice in tions, and (3) clinical e xp e rie n ce (Figur e 31-1).
health care and the development of conceptual bases Quality care is a function of these three areas of
for practice have had major implications for car­ knowledge and expertise. Evidence-based practice
diopulmonary physical therapy practice in the ICU and excellent problem solving ability will maximize

567

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568 PART VI Guidelines for the Delivery of Cardiopulmonary Physical Therapy: Intensive Care

Knowledge of underlying therapist must work within narrow windows of opportu­

pathophysiology nity to effect an optimal treatment response. Trc<ltments
are v31iable with respect to their intensity, duration, and
frequency. Usually treatments are short and frequent;
thus the maximally beneficial outcome with the least
risk to the patient is the objective of every treatment.

GOALS AND GENERAL BASIS OF MANAGEMENT

Clinical experience Physiologic and scientific The ultimate goals of cardiopulmonary physical ther­
evidence for treatment apy treatment in the lCU include the following:
interventions 1. To have the patient alert and oriented to person,
time, and place
FIGURE 31-1
2. To have the patient return to premorbid func­
Tripod approach to patient management.
tional level to the greatest extent possible
3. To reduce morbidity. mortality, and length of
the benefit-to-risk ratio of cardiopulmonary physical hospital stay.
therapy interventions (Riegelman, 1991). As a precursor to achieving these three overriding
goals, the immediate goals initially relate to the attain­
ment of optimal oxygen transport and hence car­
SPECIALIZED EXPERTISE OF THE
diopulmonary function and secondly relate to the at­
leu PHYSICAL THERAPIST
tainment of optimal musculoskeletal and neurological
Effective clinical decision making and practice in the function. In the lCU the physical therapist must recog­
ICU demands specialized expertise and skill including nize the implications of cardiopulmonary insuffi­
advanced, current knowledge in cardiopulmonary and ciency on neuromuscular status and that apparent im­
multisystem physiology and pathophysiology, and in pairment of neuromuscular status in not necessarily
medical, surgical, nursing, and pharmacological man­ indicative of neurological dysfunction. Rather, re­
agement (see the box on p. 569). Physical therapists in duced cardiac output and blood pressure, hypoxemia,
the lCU need to be first-rate diagnosticians. Given the hypercapnia, and increased intracranial pressure (lCP)
multitude of factors that contribute to impaired oxygen may be indirectly responsible for these changes.
transport (Dean, 1983; Dean, I 994b; Dean, 1994c), the
physical therapist must be able to analyze these to de­
Restricted Mobility and Recumbency
fine the patient's specific oxygen transport deficits and
problems. Therefore the lCU physical therapist must be Hospitalization particularly in the ICU is associated
capable of integrating large amounts of objective infor­ with a considerable reduction in mobility (i.e., loss of
mation quickly, interpreting this information, and inte­ exercise stimulus), and recumbency (i.e., loss of grav­
grating it to provide the basis for a treatment prescrip­ itational stimulus) (see Chapters 17 and 18). These
tion (i.e., the specific selection, prioritization, and two factors are essential for normal oxygen transport;
implementation of treatment interventions) (Cutler, thus their removal has dire consequences for the pa­
1985). The integration and interpretation of the vast tient with or without cardiopulmonary dysfunction.
amount of multiorgan system data is perhaps the single In terms of a physiological hierarchy of treatment
most important skill in ICU practice and treatment pre­ interventions (see Chapter 16), exploiting the physio-.
scription. With this database, the physical therapist logical effects of acute mobilization, upright position­
must identify the indications for treatment, contraindi­ ing, and their combination, are the most physiologi­
cations, and optimal timing of interventions. The condi­ cally justifiable primary interventions to maximize
tion of the ICU patient can change rapidly. The physical oxygen transport and prevent its impairment.

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 31 Comprehensive Patient Management in the Intensive Care Unit 569

Specialized Expertise and Skill of the lCU Physical Therapist

Detailed, c omprehensive knowledge of cardiopulmonary physiology and pathophysiology, and phar macology .

Thorough working knowledge of the monitoring systems routinely used in the ICU and an understanding of the inter­
pretation of the output of these mon itoring systems ( e. g. , ECG, arterial blood gases, fluid and e lectrolyte balance,
hemodynamic monitoring, chest-tube drainage systems, intracranial pressure m onitoring ). This information is an
integra l component of the physical therapy assessment of the und erlying problems, and for selecting, prioritizing.
and progressing or modifying treatment.

E xte nsive expertise in c ardiopulmonary assessment and treatment presc ription : preferably a minimum of 2 to 3 years
experience in ge ne ral medicine and surgery.

Detailed understanding of multisystem physiology and pathophysiology and the cardiopulm onary manifestations of
systemic disease.

An ability to practice effectively under pressure and in often apparently congested, suboptimal working conditions.

Knowledgeabh:: regarding all emergency procedures including those for respiratory and cardiac aITest, equipment. or
power failure.

K nowledge abl e rega rding the paging system used in the unit for contacting the physical therapist when she or he is
out of the unit and out of the hospital . On-call service, 24 hours a day. 7 days a week is a co mmon practice and
should be considered in units without this service.

Sensiti vity toward each patient's psychosocial situation, culture , and values, and active involvement of the patient
and family in clinical decision making whenever feasible.

Superior communication skills (e.g., ability to work coop era tively with other members of the lCU team ( see Figure
31-2) and give ve rba l prescntations and discuss patients at rounds).

Specificity of Cardiopulmonary Physical Therapy

Recumbency is nonphysiological; it is a position
that all too often is to what most patients are injudi­ Physical therapy interventions must be specifically
ciously confined. Changing the position of the body geared toward the management of each organ sys­
from erect to supine positions results in significant tem, taking into consideration the pathophysiologi­
physiol ogica l changes, which may jeopardize the pa­ cal basic for the patient's signs and symptoms and
tient's already compromised or threatened oxygen rational for each intervention and the physiological
transport system (sec the box on p. 570, at top left) and scientific evidence supporting t h e efficacy of
(see Chapter 18). the intervention (Dean and Ross, 1992). Physical
The culmination of these deleterious effects off­ therapy provides both therapeutic and prophylactic
sets the increased homogeneity of ventilation and interventions for the ICU patient. The use of con­
perfusion and their matching in the supine position. servative, noninvasive measures is the initial treat­
These effects compound the sU[lerimposed factors of ment of choice to avert or delay the need for addi­
immobility, recumbency-induced central fluid shifts, ti onal invasive mo n i t o r i n g and t r e a t m e nt,
prolonged lying without the normal stimulation or supplemental oxygen, pharmacological agents, and
will to turn the body, and underlying pathophysiol­ the need for intubation and mechanical ventilation.
ogy or trauma that may contribute to impaired car­ The physical therapist aims toward avoiding, post­
diopulmonary function and oxygen transport. Theo­ poning, or reducing the need for respiratory support
retically, the more compromised the patient, the for as long as possible. In addition, the physical
greater the priority is to maximize time spent in the therapist h e lp s to prevent the multitude of side ef­
upright position in conjunction with exploiting the fects of immobility and prolonged confinement to
benefits of acute mobilization. bed. A su mm a ry of general information required

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570 PART VI Guidelines for the Delivery of Cardiopulmonary Physical Therapy: Intensive Care

Generallnformatioll Required Before Treating

the ICU Patient
Normal Physiological Changes When Changing
from the Upright to the Supine Position Medical and surgical histories

Cephalad displacement of the visceral contents and Gender and age

diaphragm Premorbid status (e.g., life style. ethnicity. culture,
Compression on the posterior dependent lung work situation. stress, cardiopulmonary condi­
fields tioning, and oxygen transport reserve capacity)

Cephalad tluid shift to the central circulation Smoking history

Stroke volume and cardiac output Hydration and nutritional status: deficiencies. obe­
sity, or asthenia
Total lung capacity
Recency of onset and course of present condition
Vital capacity
Existing or potential medical instability
Functional residual capacity
Indications or necessity for intubation and mechani­
Residual volume
cal ventilation
Forced expiratory volumes
Invasive monitoring, lincs. leads. anel catheters
Airway resistance
Existencc of or potential for complications and mul­
Closing volumes of small airways tiorgan system failure

Restriction of chest wall and diaphragmatic excursions Coma

Arterial oxygen levels Elevated intracranial pressure (lCP) and the need for
ICP monitoring
Cough effectiveness
Risk or presence and site(s) of infection
Preload and afterload and myocardial work
Quality of sleep and rest periods
Myocardial efficiency
Nutritional support during ICU stay
Sympathetic stimulation and decreased peripheral
vascular resistance Pain control regimen

General Physical Therapy Goals Toward Function Optimization in the ICU Patient

Maintain or restore adequate alveolar ventilation and perfusion and their matching in nonaffected and affected lung
fields and thereby optimize oxygen transport overall

Prolong spontaneous breathing (to the extent that is therapeutically indicated) and thereby avoid, postpone, or mini­
mize need for mechanical ventilation

Minimize the work of breathing

Minimize the work of the heart

Design a positioning schedule to maintain comfort and postural alignment (distinct from therapeutic body positioning
to optimize oxygen transport)

Maintain or restore general mobility, strength. endurance, and coordination, within the limitations of the patient's
condition and consistent with the patient's anticipated rehabilitation prognosis (distinct from therapeutic mobiliza­
tion to optimize oxygen transport)

Maximally involve the patient in a daily routine including self-care, changing body position, standing, transferring,
sitting in a chair, and ambulating in patients for whom these activities are indicated

Optimize treatment outcome by interfacing physical therapy with the goals and patient-related activities of other
team members, coordinating treatments with medication schedules. and treating the patient specifically. based on
results of objective monitoring available in the ICU and subjective findings

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 31 Comprehensive Patient Management in the Intensive Care Unit 571

before treating the ICU patient is presented in the scribed in Chapter 17 and relate primarily to the sta­
box on p. 570, at top right. tus of the cardiopulmonary, neuromuscular, and mus­
culoskeletal systems. In the ICU the negative physio­
logical effects of immobility are amplified in severely
Function Optimization
ill and older patients. A primary objective of the
Function optimization refers to promoting optimal physical therapist, therefore, is to avoid or reduce
physiological functioning at an organ system level, as these untoward effects on the patient's recovery and
well as promoting optimal functioning of the patient length of stay in the ICU. Specifically, these goals in­
as a whole. In critical care, primary goals related to clude reducing the deleterious effects of immobility
function optimization are initially focused on car­ and pathology on cardiopulmonary and neuromuscu­
diorespiratory function. With improvement in oxygen lar function and reducing the risk of deformity and
transport, increased attention is given to optimal decubiti. The negative sequelae of relative confine­
functioning of the patient with respect to self-care, ment are largely preventable. Particular care must be
self-positioning, sitting up, and walking. General taken to avoid pressure sores because these signifi­
physical therapy goals related to function optimiza­ cantly increase the risk of infection and deterioration.
tion are shown in the box on p. 570, at bottom. Physical therapists and nurses need to examine rou­
tinely for sites of redness, pressure, and potential skin
lesions in every patient, regardless of expected length
Prophylaxis
of stay in the ICU (Stillwell, 1992). The texture of
General aspects of patient care related to physical bed coverings, their smoothness, bunching of the bed
therapy practice include the role of prophylaxis or gown, or irritation from lines and catheters to the pa­
prevention. The complications of immobility are de­ tient need to be routinely monitored.

Specific Patient Information Required Before Treating the ICU Patient

Detailed knowledge of the patient's history, including the differential diagnosis on admission to the rcu, and rele­
vant past medical. surgical, and social histories

Detailed understanding and knowledge of the medications administered to the patient, their indications. and side ef­
fects, especially those affecting response to physical therapy

Knowledgeable about the stability of vital signs since admission, including heart rate and rhythm, respiration rate and
rhythm. blood pressure, skin color, core temperature, and hemodynamic stability

Detailed knowledge of relevant findings of laboratory tests, procedures, and biopsies, including arterial blood gases,
blood analysis, fluid and electrolyte balance, ECG, x-ray, thoracentesis, central venous pressure (CVP), left arttial
pressure (LAP), pulmonary artery wedge pressure (PAWP), microbiology and biochemistry reports, and urinalysis

If the patient is ventilated, detailed understanding of the rationale for the ventilatory mode and parameters used

With respect to establishing a patient database, do the following: (I) Conduct a thorough, detailed clinical assessment
specific to the patient's condition(s), including inspection, palpation, percussion, and auscultation of the chest, as
well as a neuromusculoskeletal assessment to rule out any secondary effects of cardiopulmonary dysfunction and
to establish rehabilitation prognosis. (2) Establish a physical diagnosis and problem list and prioritize the treatment
goals and overall treatment plan. (3) Determine the optimal assessment and treatment outcome measures and be
knowledgeable about their interpretation. (4) Conduct serial trend measurements to predict the patient's oxygen
transport reserve capacity before treatment and stressing the oxygen transport system

As treatment progresses, record objective and relevant subjective treatmenl outcome measures and revise treatment
goals as indicated by the patient's progress

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572 PART VI Guidelines for the Delivery of Cardiopulmonary Physical Therapy: Intensive Care

Preparation for Treating the ICU Patient

Physical Therapy Uses of Monitoring Systems
Patients in the rcu are generally characterized by in the leU
some degree of life-threatening medical instability. Be­
Establish the indications for and contraindications of
fore treating a give:1 patient in the rcu, the physical cardiopulmonary physical therapy
therapist should be thoroughly familiar with the spe­
Define treatment intensity, duration, and frequency
cific information shown in the box on p. 571. for optimal treatment outcome

Determine the appropriateness of response to a spe­

cific intervention
GENERAL CLINICAL ASPECTS OF THE
MANAGEMENT OF THE ICU PATIENT Assess the need for supplemental oxygen before,
during, and after treatmcnt
Assessment
Determine appropriate patient positioning between.
The fundamental assessment procedures for the car­ during. and after treatments
diorespiratory system are described in detail in Part Establish whether the patient is responding nega­
Two. Laboratory reports, procedures, sputum culture, tively to treatment and whether treatment should

and x-rays supplement the findings of inspection, pal­ be discontinued or modified

pation, percussion, and auscultation of the chest. Of

particular importance are the blood work, arterial blood
gases, ECG, fluid and electrolyte balance, hemody­ pulmonary artery pressure and wedge pressure, which
namic Ilionitoring, and intracranial pressure monitoring. provide an index of myocardial sufficiency and
These are the most commonly monitored parameters in specifically left heart function. Central venous pres­
the ICU in addition to vital signs-respiration rate, sure gives an indication of fluid loading and the abil­
heart rate, temperature, and blood pressure. ity of the right side of the heart to cope with changes
in circulating body fluids. Pressures related to heart
function give the physical therapist an indication of
Monitoring
pulmonary status and help to determine whether heart
Optimal physical therapy treatment depends on opti­ dysfunction is affecting lung function, lung dysfunc­
mal use of the monitoring systems available in the tion is affecting heart function, or both. Existing car­
rcu. Monitoring systems can be used to establish diopulmonary stress alerts the physical therapist to
the indications and contraindications for treatment, appropriately modify workloads or the physical de­
parameters of the treatment prescription and pro­ mands of treatment to keep the patient medically sta­
gression. in addition to assessing the patient. These ble, avoid undue fatigue, and deterioration.
are summarized in the box above. Physical thera­ Changes in ECG may reflect heart disease, lung
pists need to exploit the considerable amount of ob­ disease, altered acid base, and electrolyte and fluid bal­
jective data available to them in patient manage­ ance. The physical therapist is responsible for identify­
ment. A thorough knowledge and routine use of ing the patient's heart rhythm and ECG changes that
monitoring systems for each patient in the lCU can­ might be expected with improvement or deterioration
not be overemphasized in terms of contributing to in oxygen transport, and secondary to medical man­
improved quality of care with less potential risk to agement, drug intervention and changes in the course
the patient. of the disease and response to treatment generally.
The monitoring systems described in Chapter 15
provide essential information with respect to the
Pharmacological Agents
management of the ICU patient. Information regard­
ing acid-base imbalance and fluid and electrolyte bal­ The physical therapist needs a thorough knowledge
ance helps to establish specific treatment goals. The of the common pharmacological agents used in inten­
Swan-Ganz catheter in situ gives the pressures for sive care (Chapter 43). With this knowledge, the

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 31 Comprehensive Patient Management in the Intensive Care Unit 573

physical therapist can augment the effects of these In addition, narcotics tend to have significant multi­
agents and optimize physical therapy treatment re­ system effects rather than localized effects. Because
sponse when treatments are coordinated with medica­ physical therapy is the most physiological and nonin­
tion schedules. Most medications have optimal vasive intervention available to the ICU patient, it be­
dosages for any given patient, optimal sensitivity, and hooves the physical therapist to ensure that all other
peak-response time. Most medications have side ef­ pharmacological agents that are effective and more
fects. Side effects may cause deterioration in the pa­ selective than narcotics in achieving the desired ef­
tient's condition, create apparent signs and symptoms fect have been considered.
suggestive of other disorders, or alter response to
treatment. The physical therapist therefore needs to
TREATMENT PRESCRIPTION IN THE ICU
identify the medications each patient is taking and
their side effects. Physical therapy treatments in the ICU are judiciously
Certain medications, such as bronchodilators, selected in a goal-specific manner. As a general
sedatives, mucolytic agents, antianginal medications, guideline, treatments descend in a physiological hier­
and analgesics, help the patient to be able to cooper­ archy. Mobilization, exercise, and body positioning
ate during treatments. Special consideration must al­ should be exploited first with respect to their direct
ways be given to the different peak-response times of and potent effects on oxygen transport overall. At the
medications used in the ICU. The patient is willing to other end of the hierarchy (i.e., least physiological in­
cooperate more actively in the treatment if pain is re­ terventions that have a more limited effect on the
duced, breathing is easier, and mucus is easier to steps in the oxygen transport pathway) are conven­
clear. A better treatment effect is therefore more tional interventions, such as manual techniques.
likely. These advantages result in more effective use Mobilization and exercise can be prescribed to ef­
of the physical therapist's time, and often a shorter, fect three physiologically distinct outcomes based on
more cost-effective, efficacious treatment. their acute effects, their long-term effects, and their
Certain other medications may prevent close moni­ preventative effects (see Chapter 17). The treatment
toring of patients during exercise and activity. Patients prescription needs to focus on which specific effects
on beta-blocking agents, for example, will not show of mobilization and exercise are required to reverse
the normal changes in heart rate and blood pressure in or mitigate deficits in the oxygen transport pathway
response to exercise. In addition, beta-blockers con­ or prevent impaired oxygen transport. The treatment
tribute to fatigue. Caution must therefore be observed prescription is different in each case.
when prescribing exercise for these patients. Another Unlike other patient care areas, the frequency of
classification of drugs called vasopressor agents help treatments may range from one to several treatments
regulate blood pressure and heart rate. Patients on daily. The frequency depends on the patient's spe­
these agents may also exhibit abnormal exercise re­ cific treatment goals, the aggressiveness of treatment
sponses. Hence monitoring vital signs to assess treat­ indicated, interfering related problems and their man­
ment response may be of limited value for patients on agement, patient cooperation, and tolerance for the
drugs acting on the cardiovascular system. physical therapy treatments prescribed. The patient's
Narcotics is a commonly used classification of oxygen reserve capacity needs to be assessed to en­
drug used in the ICU and are often administered sure that the patient can meet the demands of exercise
jointly with sedatives and tranquilizers. Despite their stress. The physical therapist needs to assess the pa­
beneficial effects on pain relief, narcotics of any clas­ tient's tolerance with respect to duration, intensity,
sification of pharmacological agents and particularly and frequency of treatments, as well as prescribed ex­
in combination with other sedative type drugs antago­ ercise. Objective and subjective measures of the pa­
nize and often prohibit physical therapy treatments tient's tolerance to the initial assessment and the ob­
because of the patient's reduced arousal, monotonous servations of other members of the team help to
ventilation, and inability to cooperate with treatment. establish this baseline.

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574 PART VI Guidelines for the Delivery of Cardiopulmonary Physical Thel'3py: Intensive Care

Treatment goals and interventions are described in progress notes during the ICU stay in order that the team
Part III. Interventions frequently used in the ICU in­ responsible for the patient after discharge is able to con­
clude those related to mobilization and exercise, body tinue management with reduced risk of disruption of
positioning, breathing control and coughing, mucocil­ care or regression of the patient's condition. The patient
iary transport and mucous clearance interventions, should be consulted, if possible, and informed at all
such as deep breathing and coughing maneuvers, times of his or her progress and plans made by the team
chest wall mobilization, postural drainage, percussion, and family. The patient should be given as many
vibration, shaking, rib springing, relaxation, body choices as possible about his or her care and be actively
alignment, and general strengthening exercises. These involved in long-term planning.
interventions are the mainstay of cardiopulmonary
physical therapy. Intensive care physical therapy de­
NONCLINICAL ASPECTS OF THE MANAGEMENT
mands particular skill in selecting, prioritizing, and
OF THE ICU PATIENT
applying the particular interventions that can effect
Team Work
the optimal treatment outcome in the shortest time in a
given critically ill patient. For example, a common Comprehensive patient care in the ICU includes some
scenario in the ICU is the physical therapist's attempt­ nonclinical activities. Team work is the cssence of
ing to reduce or reverse the adverse changes observed optimal patient care, particularly in the ICU. The
in blood gases; that is, falling Pao2 levels and increas­ physical therapist interacts frequently with other team
ing Paco2 levels in the patient for whom intubation is members regarding observations and changes in the
being seriously considered if improvement is not ob­ patient's condition, treatment goals, and treatment re­
served soon. The focus of treatment for such a patient sponse (Figure 31-2). In addition to providing therapy
is delineated into two parts. The physical therapist for patients, the physical therapist is often consulted
first focuses on optimizing oxygen transpOit and car­ regarding ambulation, body positioning, lifting, trans­
diopulmonary function of the involved lung fields and ferring, chair sitting, and self-care.
second on maintaining optimal cardiopulmonary func­
tion of the uninvolved lung fields.
Infection Control
Contraindications and the awareness of potential ad­
verse effects of cardiopulmonary physical therapy are Personal hygiene and good hygienic practice on the
particular concems in the ICU. The physical therapist part of the physical therapist cannot be overempha­
needs to be well-versed about these. Treatments need to sized. Patients in the ICU are usually prone to infec­
be modified to achieve an optimal treatment effect with­ tion. Meticulous hand washing with an antiseptic de­
out posing a hazard to the patient. Herein lies one of the tergent between patients is essential. Soaping for 30
many challenges of intensive care physical therapy. seconds or more with a thorough scrubbing motion and
followed by thorough rinsing should be carried out.
After contact with infected wounds, saliva, wounds,
Discharge from the ICU
blood, pus, vomitus, urine, or stool, the physical thera­
To be recommended for discharge from the ICU, the pist must be particularly conscientious about washing
patient should not require cardiopulmonary physical immediately. Given the concerns regarding HIV infec­
therapy more than every 4 to 6 hours. The patient tion and AIDS, physical protection, including gown­
should be breathing spontaneously and independently ing, gloving, capping, and masking, should be routine.
and elicit a cough with or without assistance, prefer­
ably one that is effective in clearing secretions. If
Recognition of the Patient as a Person
alert, the patient should be moving purposefully in
bed before transfer. Although constraints do exist in the high technology
The physical therapist is responsible for documenting atmosphere of the ICU, the patient's dignity is ob­
the physical therapy treatment priorities and frequent served as much as possible regardless of the reason

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 31 Comprehensive Patient Management in the Intensive Care Unit 575

FIGURE 31-2

Team work in the intensive care unit is essential to facilitate communication and patient

treatment. A, Physical ther<lpist and nurse "bagging" and suctioning the patient. B, Two persons

positioning for dependent, heavy patients prior to portable chest x-ray. C, Respiratory care

practitioners. D, Radiologist. E, Nursing staff.

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576 PART VI Guidelines for the Delivery of Cardiopulmonary Physical Therapy: Intensive Care

THE DYING PATIENT

for admission, the level of consciousness, or belliger­
ent and objectionable behavior directed toward the Anticipation of dying and death are traumatic for the
ICU staff. Gestures, such as using the patient's pre­ patient, family and friends, and the health-care team.
ferred name, explaining aspects of the patient's care, The phases of dying (Andreoli, Fowkes, Zipes, and
continually orienting the patient to person, place, Wallace, 1991; Warner, 1978) that can be anticipated
time, and day, and having an interpreter available if when caring for the dying patient are presented in the
necessary are widely practiced. A supportive caring box on p. 577.
atmosphere is created in which the patient is free to
Principles 01 physical therapy management
make choices and ask questions as much as possible.
The dying patient and his or her family and friends
have special needs that must be included in and in
leu as a Healing Environment
fact constitute an integral parl of the patient's over­
The physical environment of the IC U has a profound all care. In general the physical comfort and per­
effect on the patient's recovery independent of the sonal hygiene of the patient, as well as the quality of
level of care received. Windows with pleasant views, the immediate psychosocial environment, are para­
for example, help to orient the patient, and provide a mount concerns. Compassion, understanding, and
sense of day and night and the passage of time (Fig­ respect for the patient and the family must be forth­
ure 31-3). Other benefits incl\lde reduced number and coming from the ICU team. The ability to be atten­
types of complications and reduced length of stay in tive, comforting, and compassionate are invaluable
the ICU and in hospital overall. Physical therapists personal qualities that need to be developed to a
who are involved in the designing of rcus should high degree in the critical care area. The tcam needs
consider psychosocial, environmental, technological, to attend to how the patient, if sufficiently alert, is
and clinical factors. dealing with the possibility of dying and take their

FIGURE 31-3
An overview of an rcu room. Note large window area and openness of room. Windows help
patients orient to day and night.

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 31 Comprehensive Patient Management in the Intensive Care Unit 577

to the fatigue induced by treatment and by coughing.

Characteristics of the Dying Patient
Facilitated and supported coughing may help reduce
Loss of strength. motion, and reflexes in the legs the effort required to cough productively.
and then in the anm,
The use of human touch may be the single most
Failure of the peripheral circulation and profuse important means of communicating with and provid­
sweating, causing body cooling
ing support to the dying patient who may be unable
The dying patient tends to turn toward the light or disinterested in communicating. Supportive touch­
Decreased sensitivity to touch and deep pressure ing and handholding may be even more important to
and pain tends to remain the patient on life support systems where these may
Often conscious until death be experienced as a physical barrier between the pa­

May experience pain. acute loneliness. and fear tient and those around him or her.

May increase spiritual neeus, particularly at night

an interval of 4uiescence just before death SUMMARY

Cardiopulmonary physical therapy in the ICU is a

From Andreoli KG, Fo\V cs VK. Zipl!s DP, Wallace AG: COl11pre­
specialty in itself. The overriding goals pertain to
hel1.live cardiac care, ed 7, St. Louis. 1991. Mosby.
returning the patient to a premorbid level of func­
tion and in the process minimize morbidity, mortal­
ity, and length of hospital stay. The general goals of
critical care are function optimization and prophy­
cues from the patient with respect to the role they laxis. Specific primary goals are defined by the un­
need to play. If requested by the patient or family, derlying cardiopulmonary pathophysiology and
pastoral care services are summoned, preferably be­ multisystem dysfunction and its sequelae. Specific
fore death is imminent. secondary goals are defined by the presence of or
If life support systems are being continued, the the potential for musculoskeletal and neuromuscll­
physical therapist may provide treatment to keep lar dysfunction. This chapter elaborates on some
the patient as comfortable as possible. Conservative general a s p e c t s of treating ICU p a tients. The
prophylactic cardiopulmonary physical therapy knowledge base and experience of physical thera­
may be provided to reduce the work of breathing. pists working in the area are presented. A broad
Treatments are kept to a minimum in terms of num­ overview of the objectives of treatment and the ra­
ber and duration if death is inevitable. Range of tionale for prioritizing treatments according to a
motion exercises may help to reduce the discomfort physiological hierarchy is described. General clini­
of immobility and facilitate nursing management cal and nonclinical aspects of patient management
and the basic care of the patient. Analgesics may be are discussed. Finally, issues related to the manage­
continued along with other medications to reduce ment of the dying patient are addressed.
pain and sufl'ering and maximize comfort. If so,
these are prudently timed with treatments if appro­
REVIEW QUESTIONS
priate. In the presence of life supports the patient's
needs may have to be anticipated somewhat more I. Describe the elements of evidence-based practice
than without life supports because they severely in cardiopulmonary physical therapy.
limit communication. The dignity and modesty of 2. Describe the general goals and principles of car­
the patient continue to be observed even after death diopulmonary physical therapy in the intensive
has occurred. care unit.
The patient who has had life supports removed re­ 3. Describe the role of monitoring in cardiopul­
ceives the same level of palliative care as the patient monary physical therapy care of the critically-ill
with supports. Weakness and wasting may contribute patient.

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578 PART VI Guidelines for the Delivery of Cardiopulmonary Physical The.-apy: Intensive Care

References
Dean. E" & Ross, J. (1992). Discordance between cardiopulmonary
Andreoli, K.G .. I·owke,. V.K., Zipes , D.P.. & Wallace. A.G. (1991). phy iology and physical therapy. Chest. 101. 1694-1698.
COlllprehensi!'e cardiac care, (7th ed.). St Louis: Mosby. Hi slop. J.H. (1975). Tenth Mary Mc M illain lecture. The not-50-im­
Barluw, D.H .. H ayes. S.c., & Nelson . R.O. (1 984). the scientist possible dream. Physical Thi'rapy. 55. 1069-1080.
practitioner. research and accountability in clinical (lI1d educa­ Riegelm an . R.K. (1991). Millillli illg lII e dico l lIliswkes. The art
tion "ettillgs. New York: Pennagon Press . of lIledical decision II/akillg. Boston: Little_ Brown and
Cutler. P. (1985). Problem soil'ing in clinical medicine. from data Company.
to diagnoSis. (2nd cd.). B altimore : Williams & Wilkins. Ross. J .• & D ean . E. (1989). Integrating physiological princi ples
Dean, E. (1983). Research. The right way. Clinical Mal1af'emcnr, into the comprehensive management or cardiopulmonary dys­
3. 29-33. function. Physica l Tlltrop),. 69. 255-259.
Dean. E. (1985). Psychobiolugical adaptation model fur physical Schon. D.A. (1983). Til" rejleClil'e practitiollel'. HOlV IJruje.uilllwls
therapy practice. Physical Therapy. 65. 1061-1 06R. thillk ill act io ll. New York: Basic Books.
Dean. E. (1994a). Oxygen tran sport : A physiologically-based con­ Stillwell. S. ( 1 992 ) . Mosby's critical care lIursill!; referellce, St
ceptual I'ramework for the practice of ca rdiopulmonary physio­ Louis: Mosby.
ther apy. Physiotherapy. 80, 347-355. Wo rth i ng ham. C. (1960). The de velopment of physical therapy as
Dean. E. (1994b). Physiotherapy skills: Positioning and mobili/.a­ a profession through research and publica tion . Physical Ther­

tion of the patient. In B.A. Webber & J.A. Pryor. (Eds.). Phys­ apy.40. 573-577.
iother(l!I.1' lor Respimtorr and Cardiac Prnhlellls. Edinburgh: Zadai. C.C. (19 86) . Pathokinesiology: The clinical implications
Churchill Livingstone. from a cardiopulmonary perspective. Physica l Therapy. 66
Dean. E. (1994c). Invited cOlllmental), to "Are incentive spirometry. 368-371.
intermittent positive pressure breathing. and deep breathing exer­
cises effectivc in the prevention of pos toperative pull11on ry
complications after upper abdominal surgery? A systematic
ovcrvi w and meta-analysis." Physica l Therapy. 74. 10-15.

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 CHAPTER 32

Intensive Care Unit Management of

Primary Cardiopulmonary Dysfunction

Elizabeth Dean

KEY TERMS Cardiopulmonary failure Primary cardiopulmonary dysfunction

Coronary artery disease Restrictive lung disease
Obstructive lung disease Status asthmaticLls

INTRODUCTION
not treatment prescriptions. Rather, each patient must
This chapter presents the principles of cardiopul­ be assessed and treated individually taking into con­
monary physical therapy in the management of criti­ sideration all factors that contribute to impaired oxy­
cally ill patients with primary cardiopulmonary dys­ gen transport (i.e., immobility, recumbency, extrinsic
function that can lead to cardiopulmonary failure. The factors related to the patient's care, intrinsic factors
categories of conditions presented are obstmctive lung related to the patient, and the underlying pathophysi­
disease, status asthmaticus, restrictive lung disease, ology) (Chapter 1). For examples of treatment pre­
and coronary art ry disease (medical and surgical con­ scriptions for specific patients refer to the companion
ditions). Each category of condition is presented in volume to this book entitled Clinical case studies in
two parts. First, the related pathophysiology and perti­ cardiopulmon(/ry phY.licaltherapy.
nent aspects of the medical management of each con­
dition are pres nted. Second, the principles of physi­
CARDIOPULMONARY FAILURE
cal therapy management are discussed. These are not
Pathophysiology
mutually exclusive for each category because consid­
erable overlap may exist when conditions coexist. The heart and lungs work interdependently; thus fail­
It should be emphasized that these principles are ure of one organ has significant imp] ications for the

579

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580 PART VI Guidelines for the Delivery of Cardiopulmonary Physical Therapy: Intensive Care

TABLE 32-1

Classification of'Respiratory Failure by Cause and Mechanisms

Origin Drugs Metabolic Neoplasms Injections Trauma Other

BRAIN Narcotics Hyponatremia Plimary Meningitis Direct injury Central alveolar
Barbiturates Hypocalcemia Metastatic Encephalitis Increased hypovcntilation
Sedatives Hypercapnia Abscess pressure Obstructive sleep
Poisons Alkalosis Bulbar polio apnea
Anesthetics Hyperglycemia
Myxedema

NERVES AND Curariform drugs Hypophosphatemia Primary Polio Direct injury Motor neuron
MUSCLES Arsenic Hypomagnesemia Metastatic Tetanus disease
Aminoglycosides Myasthenia gravis
Multiple sclerosis
Muscular dystrophy
GuilJain-Barre
syndrome

UPPER Tonsillar Epiglottitis Vocal cord

AIRWAY adenoid LaryngotraCheitis paralysis
hyperplasia Tracheoma­
Goiter lacia
Polyps Cricoarytenoid
Malignant arthritis
tumors Laryngeal
edema

CHEST Flail chest Sclerodenl1a

BELLOWS Burn with Pleural inter­
keloids position (fibrosis,
fluid, tumor, air)
Spondylitis
Scoliosis
Kyphosis

CONTRIBUTING Massive obesity

FACTORS A cites
lleus
Pain
Recumbency

LOWER Malignant Viral Contused Bronchospasm

AIRWAY AND Benign (bronchiolitis, lung Hea11 failure
PARENCHYMA broncho­ congestive restric­
pneumonia) tive OilSlIlJctive
Bacterial COPD
(bronchitis, Rcspiratory distress
pneumonia, syndrome
abscess, Interstitial lung
bronchiectasis) disease
Fungal Atelectasis
Mycoplasma Cystic fibrosis
Pulmonary emboli

From Civelliu JM, Taylor RW, Kirby RR: Crilical care, Philadelphia, 1988, JB Lippincolt.

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 32 Intensive Care Unit Management of Primary Cardiopulmonary Dysfunction 581

function of the other organ (Vincent and Suter, 1987; PATIENT WITH OBSTRUCTIVE LUNG DISEASE
Weber, Janicki, Shroff, and Likoff, 1983). Insuffi­ Pathophysiology and medical management
ciency or failure of the cardiopulmonary system
Obstructive lung disease can result in ventilatory fail­
refers to the inability of this system to maintain ade­
ure and admission of the patient to the intensive care
quate oxygen and carbon dioxide homeostasis.
unit (ICU), or this disease can complicate manage­
Pulmonary failure reflects a gas exchange defect or
defect of the ventilatory pump. Table 32-1 shows the ment if the patient is admitted for other reasons
(Boggs and Wooldridge-King, 1993; Un derhill,
classification of pulmonary failure by specific causes
and the mechanisms involved. Some common predis­ Woods, Froelicher, and Halpenny, 1989). If conserv­

posing conditions include primary cardiopulmonary ative management fails or is unlikely to improve crit­

conditions, (e.g., chronic lung disease, overwhelming ically impaired oxygen transport and gas exchange
and to adequately remove copious and tenacious se­
pneumonia, and myocardial infarction) and secondary
cardiopulmonary conditions (e.g., motor neuron dis­ cretions, intubation and mechanical ventilation are in­
dicated (Chapter 41). Complicating factors include
eases, spinal cord injury, stroke, and muscular dystro­
phy) (Chapter 30). The oxygen and carbon dioxide impaired oxygen delivery, polycythemia, impaired
respiratory mechanics secondary to lung damage and
tensions that have been used to define failure are vari­
increased time constants impairing optimal inhalation
able because they depend on factors such as premor­
and exhalation, flattened hemidiaphragms, rigid
bid status, general health, age, prior blood gas profile,
and the time frame for the development of failure. Ar­
terial blood gases and pH are essential in the assess­
ment of cardiopulmonary failure, which is usually di­
agnosed when the Pa02 falls below 50 to 60 mm Hg
and the PaC02 rises above 50 mm Hg (Shoemaker,
Thompson, and Holbrook, 1984).
Primary cardiac failure reflects failure of the my­
ocardium to pump blood to the pulmonary and sys­
temic circulations and maintain adequate tissue per­
fusion (Austin and Greenfield, 1980). Significant
dysfunction of the left ventricle can lead to pul­
monary vascular congestion and cardiogenic pul­
monary edema ( i . e . , c o n g e s t i v e h e a r t f a i l u r e )
(Matthay, 1985). Diseases o f the heart that can lead
to failure include significant myocardial damage as a
result of infarction or myopathy, valvular heart dis­
ease, and congenital defects.
Both primary pulmonary and cardiac failure can be
classified into acute and chronic stages. The compen­
sation mechanisms that occur in the two stages are
distinct. With adequate physiological comp:nsation,
patients can tolerate some degree of chronic failure.
Patients with a mild degree of failure can live I'eason­
ably independent lives. Moderate failure is signifi­
cantly more limiting, thus these patients may require
home ventilatory support (e.g., supplemental oxygen
and nighttime ventilation), and severe failure requires FIGURE 32-1
hospitalization and mechanical ventilatory support. Patient receiving mechanical ventilation.

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582 PART VI Guidelines for the Delivery of Cardiopulmonary Physical Therapy: Intensive Care

banel-shaped chest wall, increased accessory muscle tion from the oropharyngeal cavity can be reduced by
use and work of breathing, reduced diffusing capac­ suctioning through the airway with the cuff of the air­
ity, impaired mucociJiary transport, secretion accu­ way inflated, in addition to suctioning the oropharynx'
mulation, ineffective cough mechanism, increased after suctioning via the airway.
oxygen consumption, increased work of the heart, Suctioning can be performed frequently in a pa­
and general debility and weakness. tient with an artificial airway and is less traumatic.
The goal of intubation and mechanical ventilation Patients should be suctioned only as indicated be­
is to provide an airway and adequate alveolar ventila­ cause this procedure can produce significant desatu­
tion, which is based on arterial blood gas analysis. A ration (up to 60%), particularly in the ventilated pa­
tidal volume and a respiratory rate that provide satis­ tient (Walsh, Vanderwarf, Hoscheit, and Fahey,
factory blood gas and pH values are established and 1989). Administration of 100% oxygen for 3 minutes
maintained unless the clinical condition changes. The before and after suctioning (i.e., hyperoxygenation)
precise regulation of mechanical ventilation helps to minimizes this desaturation effect. This can be ac­
restore adequate blood gases and cardiopulmonary complished by manually bagging the patient before
function, reduce the work of breathing, rest fatigued treatment (i.e., manual hyperventilation) or by preset­
ventilatory muscles, and provide an optimal fraction ting the mechanical ventilator (Fell and Cheney,
of inspired oxygen (FIo2) and humidification (Figure 1971). Risk of aspiration of gastric contents is re­
32-1) (Wilson, 1992). duced by the use of a nasogastric tube.
Minute ventilation can be seriously impaired with a A common cause of acute rcspiratory failure is ad­
leak in the mechanical ventilator circuitry. The tube vanced chronic airflow limitation (Civetti, Taylor, and
connecting sites are often the sites of air leakage. Com­ Kirby, 1988). The pathophysiological deficits include
plete disconnection at the endotracheal or tracheostomy significant loss of alveolar tissue, increased compli­
connection may occur in those patients with high pul­ ance of alveolar tissue, hyperintlated chest wall, im­
monary resistance. Close monitoring of the exhaled paired respiratory mechanics, flattened hemidi­
tidal volume and end tidal carbon dioxide will ensure aphragms, impaired breathing efficiency, and reduced
the patient is receiving sufficient ventilation. diffusing capacity. Proportional changes in lung vol­
Positive end expiratory pressure (PEEP) is useful umes and capacities in patients with chronic airway
in promoting greater opportunity for gas exchange at limitation compared with healthy persons are pre­
end-cxpiration in mechanically ventilated patients. sented in Figure 8-5, p. I SO. The primary abnormality
However, venous return, myocardial perfusion, and is a significantly increased residual volume and inspi­
cardiac output may be impaired during positive pres­ ratory reserve volume and hence total lung capacity.
sure ventilation with PEEP administration (Jardin, et Failure of oxygen transport ensues secondary to venti­
aI., 1981; Kumar, Pontoppian, Falke, Wilson, and lation and perfusion mismatch, ventilatory muscle fa­
Laver, 1973). Excessive stimulation to cough in these tigue, reactive pulmonary hypertension, and right ven­
ventilated patients shOUld be avoided because this ac­ tricular failure. Correcting the complications of
centuates the cardiovascular side effects of PEEP. respiratory failure, however, is often more problem­
Continuous positive airway pressure (CPAP) can atic than treating the specific cause. Hypoxemia and
maintain airway patency during spontaneous ventila­ hypercapnia are often present. Hypoxemia is usually
tion. This mode of ventilation, however, seems to be improved with supplemental oxygen in the absence of
prcferred in children, whereas PEEP is used more significant diffusion defect or shunt.
commonly in adults. Cardiovascular complications are among the most
Interfcrence with the gag reflex in the patient with prevalent observed in ventilatory failure. Marked hy­
an endotracheal tube increases the risk of aspiration percapnia (increased arterial P(02) with acidemia (re­
of the oropharyngeal and gastric contents and can re­ duced pH) can produce extreme vasodilatation and
sult in pneumonitis and pneumonia. Risk of aspira­ hypotension resulting from the local action on blood

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 32 Intensive Care Unit Management of Primary Cardiopulmonary Dysfunction 583

Nutrition
vessels (Boggs and Wooldridge-King, 1993). Mild
hypercapnia can produce reflex vasoconstriction and Critically ill patients are hypermetabolical. Metaboli­
hypertension. Occasionally systemic hypertension is cal demand and oxygen consumption are increased
observed during weaning from the ventilator with the secondary to healing and repair, increased tempera­
presence of a moderate degree of hypercapnia. ture, altered thermoregulation and after surgery. Pa­
Right heart failure, cor pulmonale, is a well­ tients with chronic cardiopulmonary limitation are
known complication of chronic lung disease and con­ often undernourished because of the effort required to
gestive heart failure. Both hypoxia and reduced pH purchase food, prepare, and consume it. Furthermore,
cause pulmonary vasoconstriction and an increase in these patients have an increased oxygen consumption
pulmonary artery prcssure. Consequently, reversing and energy expenditure secondary to the increased
bronchospa sm, hypoxemia, hypercapnia, a n d work of breathing (Petty, 1985; Rochester and Esau,
acidemia can often reduce pulmonary vasoconstric­ 1984). Without adequate nutrition, patients incur the
tion, lower pulmonary artery pressure, and thereby effects of deconditioning faster, are debilitated, are
improve hemodynamics. less capable of responding optimally to therapy, and
The end stage of respiratory failure results in a pro­ are more susceptible to infection. Intravenous hyper­
gressive increase in airway resistance, work of breath­ alimentation, or external hyperalimentation, is typi­
ing, oxygen consumption, and carbon dioxide produc­ cally instituted early to maintain optimal nutritional
tion. In areas of bronchial obstruction, marked status and to avoid excessive physical wasting and
alveolar hypoventilation results and ventilation and deterioration. If a tracheostomy has been pelformed,
pelfusion are severely mismatched. Hypoxemia and the patient is able to eat normally.
respiratory acidosis produce reactive pulmonary hy­
pertension and further ventilatory failure. Profound
Principles of physical therapy management
carbon dioxide retention, refractory hypoxemia, and The principles of management of acute respiratory
respiratory acidemia may terminate in a fatal dys­ failure are based on interventions that will enhance
rhythmia (Gibson, Pride, Davis, and Loh, 1977; oxygen transport (i.e., oxygen delivery, oxygen
Macklem and Roussos, 1977; Rochester and Arora, consumption, and oxygen extraction), and facilitate
1983; Vincent and Suter, 1987; Weinstein and Skill­ carbon dioxide removal (Gallagher and Civetta,
man, 1980; Wcissman, Kemper, Elwyn, Askanazi, 1980). Thus the steps of the oxygen transport path­
Hyman, and Kinney, 1989). way that have been identified as impaired or threat­
Acidemia from respiratory causes with a pH of ened by the patient's condition (i.e., immobility, re­
less than 7.25 is often harmful with respect to dys­ cumbency, and extrinsic and intrinsic factors in
rhythmia production. Conversely, hypoventilation is addition to the underlying pathophysiology) (Chap­
equally harmful, and pH elevations greater than 7.5 ter I) are the focus of treatment. Based on a de­
may cause neurological and cardiovascular complica­ tailed analysis of these factors, treatments are se­
tions. In acute respiratory failure with profound lected, prioritized, and applied to optimize the steps
acidemia, intravenous use of bicarbonate is used to in the pathway that are affected. These may include
buffer the hydrogen ion concentration until the under­ treatments to maximize the patency of the airways,
lying disorder is corrected. Bicarbonate infusion is increase alveolar ventilation, facilitate mucuciliary
guided by frequent pH measurements. transport, facilitate airway clearance, optimize the
Transport of oxygen and carbon dioxide to and mechanical position of the diaphragm, optimize
. from the tissues depends on adequate pulmonary and ventilation and perfusion matching, optimize pH,
systemic circulation. Frequently, blood volume has to eliminate carbon dioxide, optimize peripheral circu­
be restored by fluids or blood replacement or both. lation and tissue perfusion, and reduce the work of
Inotropic agents are used to maintain adequate circu­ breathing and of the heart. To optimize oxygen
lation by augmenting myocardial contractility. transport, the primary goals of physical therapy

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584 PART VI Guidelines for the Delivery of Cardiopulmonary Physical Intensive Care

include the following: treatments with medications so the

l. To improve or maintain arterial oxygen tension maximal effect is control, and coor­
(Pao2) or prevent its deterioration dinating treatments with peak energy periods and
2, To improve or maintain arterial oxygen satura­ around rest
tion or its deterioration Mobilization and exercise are at the top of the hi­
3, To improve or maintain arterial carbon dioxide erarchy of physiological treatments; thus the potent
levels and pH or prevent its detedoration and direct effects of these interventions are ex­
The means by which these are fulfilled de- first (see Chapter I
on each patient's clinical presentation and into the upright
the factors that contribute t o cardiopul­ promotes cardiopulmonary function and
monary dysfunction. gas exchange. Chairs should be available at the side
of every ICU bed to provide greater opportunity for
Mobilization the Datien! to be upright. The benefits of the upright
Mobilization and ambulation are for normal are different to propped up in
IUIU glCtll functioning of the human body (i.e., to bed. Stretcher chairs are particularly useful in reduc­
stimulate exercise stress and stress and the physical labor of lifting during
thereby optimize oxygen (Dean and transfers. These devices are designed to be
1992b). Although oatients in the ICU are tioned under the patient while recumbent in bed and
to move, sit up, stand, sit in chairs, take a then mechanically configured into a chair. One po­
few and in some circumstances, ambulate tential danger, however, is overreliance on these de­
across the unit even if they are ventilated (Macken­ vices, Even minimal ability of the patient to assist
and Ciesla, mobilization with his or her bed and must
is prescribed to exploit its (I) acute effects, (2) the be exploited, even i f the maneuver takes several
long-term cumulative and (3) the minutes and assistants. These minimal ef­
effects These effects are forts must be exploited. Without so, the pa­
cally distinct and need to be specifically to tient's oxygen transport system deconditions fur-
address each patient's problems. With the monitoring which also reduces the tolerance to be
in the ICU, critically ill patients can move mobilized. What
and be moved within safe limits. cost is the greater outcome that can be
Given that cardiopulmonary physical is expected with passive interventions. The
among those activities that are the most metaboli­ fundamental goal is enhanced recovery, reduced
cally for ICU patients Murphy, reduced morbidity and mortalitv. and re­
Parrent and Weissman and Kem­ duced ICU and hospital stay.
per, 1 Askanazi, Significant benefit can be gained from
and Kinney, the patient'S the ventilated provided there are no absolute
to meet a given increase in oxygen demand must be contraindications to being upright i n terms of car­
determined before treatment. Even car­ diopulmonary neuromuscular and muscu­
therapy stresses the oxygen loskeletal status, and skin Ambulating the
as a means of the func­ ventilated patient is the whenever
tion and efficiency of this system, unnecessary or and Jones, 1972). The potential
excessive energy i s undesirable and Mobilization and
thus should be minimized. Interventions that can exercise must be specifically to ensure that
minimize oxygen demand include relaxation, the exercise stimulus is therapeutic provides an
cious body to facilitate oxygen trans­ stressor to the oxygen transport pathway,
port, coordination of treatments with other inter- is not hazardous),
scheduling treatments at appropriate Standing and even a few steps can be ex­

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 32 Intensive Care Unit Management of Primary Cardiopulmonary Dysfunction 585

Body positioning
tremely strenuous for the ICU patient with respect to
oxygen demand, considering that this patient is hy­ Body positioning is a potent therapeutic intervention

permetabolical. Such activities need to be introduced that promotes optimal oxygen transport and gas ex­

gradually and with continuous monitoring to ensure change in two ways; one, from the physiological

the patient does not exceed the prescribed therapeutic benefits accrued from the specific positions them­

intensity needcd to maximize oxygen transport. selves, and two, from the physiological hcndits ac­

Standing and walking are coordinated with other as­ crued from physically changing from one position to

pects of the patient's care and should be carried out another (see Chapter 18). Body position can be used

in several stages. Monitoring of the ECG and arterial preferentially to augment alveolar volume, alveolar

saturation of the critically ill patient performing ac­ ventilation, ventilation and perfusion matching, res­

tivities such as standing or walking cannot be piratory mechanics, cough effectiveness, eentral and

overemphasized. By disconnecting these monitors, peripheral hemodynamics and fluid shifts, mucocil­

the physical therapist is working blindly and poten­ iary transport, and secretion clearance (see Chapter

tially dangerously because the leads do not reach or 18). Both ventilation and perfusion are enhanced in
becausc of movement artifact. In anticipation of an the inferior lung fields. Thus in postural drainage po­

increased workload, ventilatory parameters for the sitions the superior lung being treated is neither pref­

ventilated patients may require adjusting. A greater erentially ventilated nor perfused. The less affected

concentration of oxygen should be delivered for at lung fields therefore may be contributing more sub­

least 3 to 5 minutes before the activity and continued stantially to improving arterial gases. Hence the

afterward for 10 minutes or so until the patient has physical therapist must consider the goals of treat­

recovered from the increased exertion and the heart ment with respect to pulrnona:-y function in both the

rate and blood pre. sure have returned to within 5% to involved and less-involved lung fields. During pos­

10% of baseline values. tural drainage, the length of time in a given position

Active movement has greater therapeutic effect needs to be monitored to avoid drainage of secre­

on oxygen transport than assisted or passive move­ tions into the less involved, functional, inferior lung

ments; thus the benefits of active movements are ex­ fields and to avoid the possibility of compression at­

ploited first. Movement recruiting large muscle electasis in the inferior lung (Dcan, 1985; Leblanc,

groups minimizes the disproportionate hemodynamic Ruff, and Milic-Emili, 1970).

stress associated with movement of small muscle Although positions can be predicted that will opti­

groups or movements requiring excessive dynamic mize ventilation and pert'usion matching, each patient

stabilization (Hanson and Nagel, 1987). If active will respond differently, depending on such factors as

movements cannot be performed or excessively pathology, age, weight, depth of breathing, and me­

stress the oxygen transport system, then active as­ chanical ventilation (Clauss, Scalabrini, Ray, and

sisted movements arc indicated. Passive movements Reed, 1968; Ray et aI., 1974), Thcrefore the patient's

have a role primarily when the patient is paralyzed response to specific positioning must be observed,

or' so hemodynamically unstable that the patient de­ documented, and objectively monitored with respect

teriorates with active movement. With respect to car­ to the effect on oxygen transport variables.

diopulmonary benefits, passive movement stimulates Another important goal of body positioning is to

changes in ventilatory and circulatory patterns potentiate position-dependent fluid shifts to optimize

(West, 1995). These can be particularly beneficial in cardiovascular function. For this reason the patient

patients who have significant mobility restriction, should be positioned upright as often as possible. In

however, they should not substitute for active and addition, there are other beneficial effects of the up­

active-assisted movements, which are associated right position on pulmonary function (e.g., maximizc

with even greater benefit because they are higher lung volumcs and capacities, minimize alveolar col­

order activities on the physiologically based treat­ lapse, decrcase airway resistance, increase lung eom­

ment hierarchy (see Chapter 16). pliancc and, therchy, reduce ventilator system pres­

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586 PART VI Guidelines for the Delivery of Cardiopulmonary Physical Therapy: Intensive Care

sure). To maximize the effect of gravity on promot­ increased before postural drainage and treatment to
ing fluid shifts, the legs should be positioned depen­ help compensate for any physical stress imposed
dently at frequent intervals. In a patient who is not by treatment. Oxygen, however, should always be
self-supporting with or without assistance, fluid increased to 100% and inspired for at least 3 min­
shifts can be stimulated with a high Fowler's posi­ utes before and after suctioning. Should arterial de­
tion coupled with the use of the bed knee-break. Be­ saturation be apparent during treatment, oxygen
tween sessions of therapeutic body positioning, a may need to be increased. If the patient is sponta­
schedule of four-point turning (supine, left side, neously breathing without oxygen, supplemental
prone, right side) is ideal and should be attempted oxygen may also be indicated during treatment to
even in the ventilated patient if not strictly con­ avoid desaturation in some patients. Oxygen ad­
traindicated (Dean, 1994). ministration must be knowledgeably regulated by
Extreme body positions have been reported to the ICU team based on arterial blood gas results.
have beneficial effects on oxygen transport in pa­ Severe hypoxemia is known to result in irreversible
tients with acute respiratory failure. The head-down tissue damage within minutes, but hyperoxia can
position has been shown to reduce respiratory distress also produce harmful effects within hours. By max­
in some patients with obstructive lung disease imizing alveolar ventilation, gas exchange, and
(Barach and Beck, 1954). The abdominal viscera are ventilation and perfusion matching, supplemental
displaced cephalad, thereby elevating the typically oxygen can be opti mally used and the effects of
flattened hemidiaphragms and placing them in a me­ acidemia minimized.
chanically advantageous position. This effect may be Treatment for respiratory acidosis is aimed at in­
mimicked in other body positions by manual abdomi­ creasing alveolar ventilation to improve the ex­
nal compression and abdominal binders. In some pa­ change of carbon dioxide and oxygen. Because the
tients, however, the additional load imposed by the r e s p i r a t o r y c e n t e r is d e p ressed by i n creased
increased intraabdominal pressure on the underside amounts of carbon dioxide (carbon dioxide narco­
of the diaphragm may inadvertently increase the sis), the lowered oxygen tension of the blood be­
work of breathing and increase respiratory distress. comes the stimulus for respiration. If the patient in­
The prone position has been reported to be beneficial hales high c o n c e n t r a t i on s of oxygen, the
in patients with acute respiratory fai I ure (Douglas, stimulation for respiration may be removed. For
Rehder, Beynen, Sessler, and Marsh, 1977; Piehl and this reason, oxygen is never given to patients with
Brown, 1976). A variant of the prone position, semi­ carbon dioxide narcosis.
prone, may be more beneficial in some patients by re­ Low flow oxygen (I to 3 Llmin) is given to a pa­
ducing intraabdominal pressure. In addition, the tient with chronic pulmonary disease who maintains a
semi-prone position may be safer and more comfort­ chronically elevated arterial Pe02 in the presence of
able for the mechanically ventilated patient. The pre­ arterial hypoxemia. If intermittent positive pressure
scription of any body positioning must be based on breathing is indicated, compressed or room air is used
its anticipated benefits on oxygen transport. The instead of oxygen in this situation.
more extreme positions should be introduced in pro­ Severe hypoxemia usually suppresses cardiac out­
gressive stages and the patient's response monitored put to some degree. Cardiac output may be further
to ensure the response is favorable. compromised immediately after a patient is placed on
a mechanical ventilator because of impaired venous
return by the elevated transpulmonary pressure
Supplemental oxygen
(Jardin et aI., 1981). An attempt is made to carefully
Supplemental oxygen is usually administered con­ balance ventilation with an optimal or adequate car­
tinuously, whether the patient is ventilated or not, diac output by shortening inspiratory time and by
to maintain Pa02 level within an optimal range minimizing transpulmonary pressures by using lower
(Dantzker, 1991). Oxygen concentrations can be tidal volumes.

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 32 Intensh'e Care Unit Management of Primary Cardiopulmonary Dysfunction 587

Bagging
Dean and I 992a), Thus these less
Dr�lctl:ce in some ICUs is bagging, A self­ less physiological conventional proce­
is temporarily connected to manual should be considered
are manually inflated for a few and after other more supported and
breaths, The purpose of the is to pro­ physiological treatments have been Fur-
vide some breaths during treatment, to because of their documented adverse ef­
maintain some degree of end-expiratory fects, it is essential that the patient be continuously
pressure, to assess lung and to facilitate monitored for safety reasons and to establish a favor­
the effect of instillation of a small volume of saline able treatment outcome, For the unconscious or para-
solution into the tracheobronchial tree to loosen se­ patient, the ventilator or self-inflating bag can
cretions, Bagging must be performed Ag­ be used to increase inflation volumes, Research is
can The use needed to examine the role of and the effect
in conjunction with is contro­ of this on mucous removal.
versial. Some clinicians to bag the patient after
suctioning to a void the of the
Instillation
pressure pushing the mucus distally, Others maintain
that because of the adherent quality of the mucus to Instillation is another procedure that should be used
the walls of the and the dilatation of the air­ in A mucolytic effect of saline
ways in response to positive pressure, does has not been well established, Beneficial
not propel the mucus distally, Rather, it is believed however, may be more apparent in neonates,
that before suctioning promotes air entry dis­
tal to the mucous and movement of cen­
Mucociliary transport and secretion clearance
on expiration,
Certain body prob­ The patient in failure needs atten­
lem when a ventilator is used, tion to fluid balance to carefully hydration
The of the ventilator is greatly reduced and fluid volume, Inhaled humidified air is a
when the head is below the hips cant additional source of fluid, Normally the
because of an increase in total pulmonary resistance alveolar gas is saturated with water vapor. The
caused the pressure of the abdominal contents, of the tracheobronchial tree is therefore
Therefore the use of a bag from erosion and potential infection, This is partiCLI­
may be to maintain pressure when larly important in the requmng suc­
from one 10 another and during some pos­ tioning, The effect of humidification can be assessed
tural positions, tidal volume can by the of the secretions, Thick
be maintained an assistant while the pllysical ther­ secretions suggest humidification may be
aids the patient with bronchial With and the patient may be systemically
the use of the the physical therapist If the effects of mobilization on
needs to ensure the is adequately ventilated port and secretion accumulation have been
and takes a than tidal breath every minute or and further secretion clearance is
so, As soon possible, breathing is en­ may be indicated, Postural may be
couraged in conjunction with postural drainage, The contraindicated in patients with unstable vital
small airways dilate on and cause and is usually contraindicated immediately after feed-
mucus to peel away from the walls; thus, during expi­ and meals, In some however, pa­
mucous are moved toward the trachea, tients on continuous 24-hour tube are
to which chest wall percussion, shaking, after has been discontinued for 15 minutes.
and vibration facilitate this movement is l!l The cuff in the artificial
the literature (KiriJloff, and Maz- A sequence

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588 PART VI Guidelines for the Delivery of Cardiopulmonary Physical Therapy: Intensive Care

and vibration may be indicated in conjunction with clearance. Patients should not breathe below the end
postural drainage. Manual techniques have been asso­ of normal tidal ventilation to avoid airway closure.
ciated with desaturation, atelectasis, musculoskeletal
trauma, discomfort, cardiac dysrhythmias, and arrest
Weaning from the mechanical ventilator
(Kirilloff, et aL, 1985); therefore these techniques
must be applied rationally and with attention to all The physical therapist and the respiratory therapist
monitoring systems and changes in signs and symp­ are primarily responsible for weaning the patient off
toms. The precise sequence, the duration, intensity, mechanical ventilation. Thus coordinating their goals
and frequency of treatment is based on treatment out­ and working together to ensure the weaning process
come rather than ti me. The application of manual is carried out expediently and with the least risk of
techniques in the head-down position is contraindi­ weaning complications (e.g., postextubation atelecta­
cated in patients with acute myocardial infarction and sis, aspiration and hypoxemia) is a priority (Marini,
increased intracranial pressure. Relative contraindica­ 1984; Shoemaker et aI., 1984). Blood gas analysis
tions include hemorrhage, bronchopulmonary fistula, and pulmonary function provide the indications for
acute chest trauma, lung abscess, and gastric reflux weaning. Ideally, the patient's spontaneous tidal vol­
(Boggs and Wooldridge-King, 1993). ume should approximate that delivered by the venti­
The specific postural drainage positions to be used lator. Forced vital capacity should be two to three
are determined based on the pathology, x-ray, and times the patient's required tidal volume (Figure
clinical examination. The recommended positions for 32-2). Weaning is not usually indicated if the patient
the bronchopulmonary segments involved should be requires PEEP greater than 5 cm H20 or FIo2 greater
approximated as closely as possible (Chapter 19) and than 0.4. In addition, patients who are unable to gen­
only modified if there are clear indications to do so. erate a negative inspiratory pressure of -20 mm Hg
Frequently, specific positioning in the ICU is com­ or greater are unlikely to be able to generate suffi­
promised as a result of the patient's status, intoler­ cient intrathoracic pressures for deep breathing and
.
ance to lying flat or being tipped, or limitations im­ airway clearance and thus are poor candidates for
posed by the monitoring apparatus or ventilator. weaning. Minute ventilation and maximum voluntary
ventilation can be measured at bedside and contribute
to the decision whether to wean. Although weaning
Breathing and cOl)ghing maneuvers
protocols differ depending on the patient and the ven-
If the patient is nonventilated or recently extubated,
body positioning and breathing and coughing maneu­
vers are emphasized to promote mucociliary transport
and secretion clearance (Bennett, Foster, and Chap­
man, 1990), decrease minute ventilation and respira­
tory. rate, increase tidal volume, and improve arterial
blood gases (Barach, 1974; Casciari, Fairshter, Harri­
son, M o r r is o n, Blackhurn, a n d Wi l s o n, 1981).
Breathing exercises are believed to be most effective
if pursed-lips breathing is performed in conjunction
with mechanical pressure applied over the abdomen
(Irwin and Tecklin, 1985; Mueller, Petty, and Filley,
1970). To derive the maximal benefits, breathing and
coughing maneuvers should be performed in body
positions that are most mechanically and physiologi­ FIGURE 32·2
cally optimal. In addition, they are performed in the Spirometer for bedside measurement of TV, ve, and
postural drainage positions to augment mucociliary minute volume.

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 32 Intensive Care Unit Management of Primary Cardiopulmonary Dysfunction 589

tilatory mode used, general guidelines for this com­ include tachypnea, dyspnea, labored breathing, audi­
mon ICU procedure are outlined in the box below. ble wheezing, tachycardia, cyanosis, anxiety, and
panic. If the patient is able to cooperate wilh spiro­
metric testing, the degree of reduced vital capacity,
PATIENT WITH STATUS ASTHMATICUS
peak flow, and forced expiratory volume provide in­
Pathophysiology and medical management
dices of the severity of airway obstruction (Brunner
Status asthmaticus is a potentially life-threatening sit­ and Wolff, 1988).
uation (Petty, 1982; Gaskell and Webber, 1988). The Medical management is aimed at administering
pathophysiological features include marked airway re­ drugs and fluids to reduce hypoxemia with oxygen,
sistance secondary to bronchospasm, edema, and mu­ decrease airway inflammation and resistance, and
cous secretion and retention. The work of breathing is hence reduce the work of breathing and anxiety. In­
markedly increased, resulting in respiratory distress. travenous sodium bicarbonate helps to reverse respi­
A cycle results in which the patient becomes more hy­ ratory acidosis and possibly m e tabolic acidosis
poxemic and hypercapnic secondary to alveolar hy­ (Civetta, et aI., 1988).
poventilation, 'bronchospasm increases, and reactive
Principles of physical therapy management
pulmonary hypertension may ensue along with a fur­
ther incrcase in the work of breathing and anxiety. The prime objective of physical therapy is to optimize
The classical signs and symptoms of a severe asth­ oxygen transpolt and possibly avoid or delay the need
matic attack that may progress to status asthmaticus for mechanical ventilation. If ventilation becomes

General Steps in Weaning a Patient From the Mechanical Ventilator

1. An individualized weaning schedule is designed for each patient in which periods of time are spent off the venti­
lator and on a T tube thaI delivers appropriate oxygen and humidity

2. The initial time period off the venti lator is carefully selected; mornings are often good times

3. (a) Physical activity should be at a minimum d uring this period (e. g. , not during or after physical therapy. not
after meals. rests, or procedures, and not during family visits) (b) Supplemental oxygen and humidity are given

4. The physical therapist offers support and reassurance

5. Vital signs. and signs and symptoms of respiratory distress are monitored continuously during weaning

6. The patient is not left unattended in the initial weaning sessions until periods off the ventilator are reliably toler­
ated well for several successive minutes

7. (a) Deterioration of vital signs, blood gases. and evidence of distress indicate that the patient will have to return
\0 ventilatory assistance imminently (b) Rest periods of at least an hour are strategi cally interspersed in the
weaning schedule

8. B lood gases are performed at regular intervals (e.g .. 15, 30. 60, 90, and 120 minutes or more or less frequently as
indicated)

9. If blood gases stabilize within acceptable limits during the weaning period and the patient is generally tolerating
the procedure well. the time off the ventilator is increased

10. Patients with underlying cardiopulmonary disease who are older, malnourished, obese, or smoke can be expected
to take longer to be completely weaned from the ventilator

II. Weaning is generally faster in patients who have required a shorter period of mechanical ventilation

12. To hasten the weaning process, intermillent mandatory ventilation (lMV) has been reported to be useful in some
patients. Others, however. have observed that the use of IMV tends to fatigue the patient and delay the patient's
progress in wcaning. Thus IMV must be used cautiously. and individual variability must be considered in terms
of its effectiveness.

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590 PART VI Guidelines for the Delivery of Cardiopulmonary Physical Therapy: Intensive Care

necessary, prognosis for recovery is poorer (Petty, expiration and to maintain the patency of the
I Physical can augment the medical small airways. and relaxed
management of the with status asthmaticus. In emphasized with periodic
an attempt to avert intubation and mechanical ventila­ huffing and avoidance of forced maneu­
tion the physical therapist coordinates treatment with vers Roth, and J Nunn, Cole­
the medications bronchodilators, mus­ man, Sachithanandan, and Laws, 1965).
cle relaxants. steroids. and supolemental oxygen). Despite ve noninvasive management,
control, en­ blood gases may deteriorate and mechanical ventila­
matching, promotes tion may be inevitable, Relaxation, alveo­
mucociiiary and secretion reduces lar ventilation, and reducing airway and ob­
and teaches the patient CO coordinate re- struction continue to be the primary however.
with general movement. Cau­ means of achieving these differ when the patient
tion needs to be observed to avoid stimuli that poten­ is ventilated. Optimal prescriptive body
tiate bronchospasm and deterioration of the positioning is the intervention of choice. Secretion
condition that increase clearance is achieved by judicious suctioning. Suc­
tory distress rather than relieve it, chest wall percus­ tioning is as required because it can con­
forced maneuvers, bag­ tribute to reduced oxygenation, collapse, and
and possibly instillation). Attention to relaxation atelect asis, increased arousal, increased work o f
and reduction of excessive oxygen demands is a and generallv increased respiratory distress,
as was described for the patient with chronic air­
flow limitation. Certain positions may have to '
PATIENT WITH RESTRICTIVE LUNG DISEASE
be avoided, for because of the in­
colerance and exacerbation of symptoms in those po-­
Pathophysiology and medical management
sitions. Because of the relationship of altered pul­ Acute failure can be associated with
positioning mary restnctlve disease interstitial
in patients in distress) must be monary fibrosis). This is distinct from restrictive de­
cautiously within the patient's tolerance. fects secondary to neuromuscular and musculoskeletal
Those body positions that reduce respiratory distress diseases Guillain-Barn
and the work of and maximize alveolar ven­ and neuromuscular
tilation, oxygen saturation and blood gases, are the neuromuscular disorders that can respira­
of choice.
tory failure in the absence of underlying primary
problems in status asthmaticus are alveolar
(Chapter 33). If the will
airway obstruction secondary t o likely be on assistance.
bronchospasm, mucosal edema, and secretions. Thus dysfunction may, the
maximizing alveolar ventilation and mu- management of admitted to the ICU for rea­
transport are priorities 1989). Other sons other than cardiopulmonary disease. The lung
include significantly increased work of the chest or both may be involved.
because of an inefficient breathing pattern The underlying cause of failure may there­
and an ineffective cough. The physical therapist coor­ fore reflect ventilatory failure, gas
dinates treatment with the medications to fa­ failure, or both. The restrictions ro
cilitate mucociliary and clear­ monary function need to be identified and treated in­
a n c e of s e c r e t i o n s w i t h b r e a t hi n g c o n t r o l and dividually t o treatment. Obstructive and re­
modified chest wall percussion. and huff­ stricti ve patterns of cardiopulmonary frequently
Obtaining a productive cough thus the contribution of both types of defects
is a to a patient's oxygen should be determined.
Typically, in restrictive lung disease, all lung volumes

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 32 Intensive Cafe Unit Management of Primary Cardiopulmonary Dysfunction 591

and are tidal volume can the condition and considerations.

be relatively normal p. 150). Patients Movements may be totally assisted but more oftcn
with severe interstitial pulmonary fibrosis have in­ are likely to be active-assisted and active. No mat­
creased pulmonary artery pressures with an associated ter how weak the patient may be, active-assisted
increase in ventricular work and and active movements a r e the mainstay of the
1989). These patients desaturate very movement interventions performed by the physical
particularly if these can be in
Principles of physical therapy management
near-upright positions. Assisted or passive move­
Restrictive ventilatory is commonly as­ ments should not be unless
sociated with both medical and conditions. indicated the is unable to execute these
The principles of management of acute respiratory movements alone). Even modest at­
failure with these differ in that medical tempts at active-assisted movements, with perhaps
conditions are associated with underly only a minimal number of repetitions, benefit the
versible whereas in the pa­ considerably more both in terms of treat­
tient the pulmonary restriction is reversible. The ment related to cardiopulmonary and muscu­
natural course of disease in the medical patient will loskeletal function than assisted movements that do
be determined in part by the patient's sta­ not contribute to muscle endurance, and
tus. The majority of surgical patients, however, will coordination. application of totaUy as­
have had normal function before surgery and sisted movements will contribute to the s
the development of cardiopulmonary complications deconditioning and physical deterioration. Regard­
Chapter 34). of whether mechanical less of the type of mobilization, the patient is ob­
tissue carbon served for arterial discomfort,
regulation of blood pH, and an ef­ and extent of
fective output are priofltles. if ass isted-acti ve and acti v e move­
oxygen is often effective in tissue oxy­ ments are performed.
in conditions associated with restrictive Assisted movements are indicated to promote oxy­
disease in the absence of a right to left shunt. gen via their effects on ventilatory and cir­
In the presence of supplemental oxygen does culatory patterns Additionally, the
is to maintain joint range of motion and
can also be tive of soft tissue in particu­
function, if the lar. Care must therefore be taken to these
is ventilated), reduce risks of movements the complete range of movement
cardiopulmonary compl reduce muscu­ for each joint, with special attention to rotatory com­
loskeletal deformities and skin breakdown, and pro­ ponents of joint movement. Lax joints can maintain
mote comfort. It is essential with body for range with one range of motion daily. Lax
any purpose that the patient is not confined unneces­ joints are and vulnerable to excessive
sarily and does not assume any position for too strain. Protection may best be effected in these joints
Although lines, leads, monitoring dev by the joint more slowly the ex­
catheters may be these are anchored as se­ tremes of joint range and just short of complete
as with sufficient length to allow the range. In the presence of or limb splinting
patient to move spontaneously, be mobilized as much because of discomfort the involved joints will benefit
IJV'''HL!lv, .. . as many positioning as from two or more excursions through full range
and facilitate routine patient care. One that may be particularly beneficial in
Mobilization and body movement, par­ the distribution of ventilation and blood flow
ticularly in upright positions, is always a priority in is body and range of motion particu­
the ICU, as much and as often as given larly of the upper limbs. If the patient is able to

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592 PART VI Guidelines for the Delivery of Cardiopulmonary Physical Therapy: Intensive Care

however, greater cardiopulmonary stress occurs with Optimizing oxygen transport using body positioning
upper limb exercise; thus heart rate, ECG, and blood and then nonphysiological interventions may then
pressure need monitoring. Lower-extremity move­ need to be considered. Furthermore, extreme caution
ments, such as hip and knee flexion, may help to posi­ needs to be observed in positioning these patients and
tion the diaphragm for improved excursion. Lower-ex­ moving their limbs because they are at risk of sublux­
tremity movements will also increase venous return, ations, pressure sores, bruising, and strains.
which may or may not be desirable, depending on the Interventions to promote mucociliary transport and
patient. The goals of upper- or lower-extremity work secretion clearance are applicable to all situations in
must therefore be clearly defined. Possible benefits which secretions, mucosal edema, bronchospasm, or a
and untoward effects must be identified to ensure the combination of these factors occur. If postural drainage
patient benefits optimally from the prescribed exercise. is indicated to further facilitate mucociliary transport
The treatment of choice in all patients is to stimu­ and secretion clearance, caution needs to be exercised
late those conditions that maintain optimal oxygen to avoid inducing bronchospasm and hypoxemia; thus
transport in health or approximate those conditions as the use of percussion should be considered carefully.
closely as possible. That is, the most physiological
interventions are exploited first and the least physio­
PATIENT WITH RESTRICTIVE LUNG DISEASE
logical interventions are exploited last or when more
physiological interventions are not possible. Physio­
Pathophysiology and medical management
logical interventions such as mobilization may be The initial priority of management in the acute phase
contraindicated in patients whose oxygen delivery is of myocardial infarction (MI) is the correction of the
too low. Without some reserve capacity in oxygen immediate problems including dysrhythmias, my­
transport, the patient cannot sustain the additional ocardial insufficiency, reduced cardiac output, hy­
metabolical load that mobilization imposes. Patients poxemia, chest pain, and anxiety followed by imple­
who are this critical are often put on neuromuscular mentation of a progressive rehabilitation program
blocking agents to reduce muscle tone and thereby ranging from the acute medically stable phase to post
reduce oxygen demand. Because these patients are in discharge rehabilitation phase (Andreoli, Fowkes,
induced paralytic states, mobilization is not possible. Zipes, and Wallace, 1991; Froelicher, 1987; Irwin

Means of Reducing Myocardial Work Load in Patients With Cardiopulmollary Disease

1. A quiet environment without excessive noise and stimulation.

2. Low-intensity activity until medical stability has been maintained and patient shows signs of physical improvement.

3. Progressive mobilization begun in conj unction with patient's medical status, ECG stability, and unchanging or re­
solving enzyme levels.

4. Reduce patient's anxiety about his or her condition, self-care activities, and family and work responsibilities.

5. Gentle mobilization exercises, deep breathing, and coughing are usually begun immediately as a prophylactic
measure, although crepitations are frequently audible in the bases of the lungs of coronary patients; treatments
need to minimize pulmonary congestion and cardiac stress.

6. Relaxation is often promoted with low-intensity activity. All levels of activity, including breathing exercises, are
ped'ormed in a coordinated, rhythmic manner. Breath holding. Valsalva maneuvers, and isometric muscle contrac­
tions, (i.e., isometric exercise and exercise involving significant muscle or postural stabilization) are absolutely
contraindicated during all activities in patients with coronary artery disease and should not be performed in any
stage of a rehabilitation program.

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 32 Intensive Care Unit Management of Primary Cardiopulmonary Dysfunction 593

and Tecklin, 1985). Before admission to the coronary cluding generalized or localized pain anywhere over
care unit, continuous monitoring of the heart rate and the thorax, upper limbs, and neck, palpitations, dysp­
rhythm is established. An intravenous line is rou­ nea, lightheadedness, syncope, sensation of indiges­
tinely started for the administration of medications tion, hiccups, and nausea.
and fluids. An arterial line may be started for serial Depending on the degree of myocardial infarction
blood sampling for blood gases and enzyme mea­ and damage, varying lengths of modified mobility
sures. Initially, pain medications, coronary vasodila­ may be recommended (Andreoli, Fowkes, Zipes, and
tors, and diuretics are frequently used to minimize the Wallace, 1991). During this period, the physical ther­
work of the heart, anginal pain, and discomfort. apist concentrates on rhythmic breathing exercises,
Drugs such as morphine serve to depress the respira­ gentle coughing exercises or huffing, modified posi­
tory drive; thus the physical therapist must be aware tioning with the bedhead elevated at least 15 degrees
of corresponding changes in vital signs. Less potent to facilitate the gravity-dependent mechanical action
sedatives and tranquilizers are more routinely pre­ of the heart and thereby reduce myocardial oxygen
scribed. Increascd pain and anxiety potentially demand. The patient is encouraged to perform deep
worsen the patient's cardiac status by increasing my­ breathing and coughing every hour during the day.
ocardial oxygen demand and altering normal breath­ Bed exercises including rhythmic, unresisted, hip and
ing pattern and gas exchange. knee and foot and ankle exercises are usually per­
The primary purpose of oxygen administration to formed every 4 hours or so, or when the patient turns
the cardiac patient is to reduce hypoxemia, myocar­ in bed. The patient is cautioned to exercise one leg at
dial work, and angina. Dyspnea, however, is com­ a time, sliding one heel up and down the bed, guard­
monly observed in the initial phases of myocardial ing against lifting the leg off the bed. These exer­
infarction and can be effectively controlled by sup­ cises; when performed correctly and coordinated with
plemental oxygen administered by nasal cannulae or inspiration and expiration require relatively little ef­
mask. Oxygen may also correct potential ventilation­ fort or additional physical stress to the MI patient.
perfusion mismatching and hypoxemia. Oxygen is Comparable with the management of the postopera­
always administered with humidity to avoid drying tive patient, these exercises are performed prophylac­
the airways. tically to reduce the risk of venous stasis and forma­
Blood gas analysis is performed within an hour of tion of thromboemboli. In addition, they may help to
initiating oxygen therapy to establish a baseline of ar­ regulate more coordinated breathing, encouragc deep
terial saturation. In this way, oxygen dose can be al­ breaths and mucociliary transport, and rcduce atelec­
tered to regulate blood gases and acid base balance. tasis. The patient is cautioned against performing the
VaJsalva maneuver and straining because these activ­
ities increase intrathoracic pressure and reduce car­
MEDICAL CARDIAC PATIENT
diac output.
Principles of physical therapy management
Electrocardiographic (ECG) monitoring of the car­
A primary principle of the management of the patient diac patient is the responsibility of all members of the
after myocardial infarction is to reduce myocardial health-care team involved in the patient's care. The
oxygen demand and workload. The myocardium physical therapist has a special responsibility to be
needs rest to promote optimal healing. Judicious rest proficient in ECG interpretation in the coronary care
of the myocardium is a priority that can often be bal­ unit because physical therapy is one of the most
anced with gentle rhythmic, non static movements. metabolically demanding interventions for patients
The box on p. 592 illustrates several ways of reduc­ (Dean et aI., 1995; Weissman et aI., 1984). The phys­
ing myocardial workload in patients with cardiopul­ ical therapist often has the responsibility of initiating
monary disease. new activities with the cardiac patient, which might
The physical therapist should be watchful at all include sitting over the edge of the bed, engaging in
times for signs of impending or silent infarction, in­ self-care (particularly involving the arms being main­

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594 PART VI Guidelines for the Delivery of Cardiopulmonary Physical Therapy: Intensive Care

tained in a raised position), getting in and out of bed, duration, and frequency of these activities (Bjore,
sitting in a chair, going to the bathroom, walking 1972; Froelicher, 1987). The patient's tolerance and
around the room or in the hallways, and eventually changes in ECG and vital signs are used as indicators
exercising on the treadmill or ergometer. Changes in for establishing and modifying the treatment program.
the ECG must be watched for, particularly when in­ These physiological parameters must be observed
troducing new activities and increasing the intensity carefully as the patient progresses to optimize the po­
of workload in activities. Careful attention to ECG tential benefits of the therapeutic regimens as early as
changes and serum enzyme levels will contribute to possible without endangering the patient.
enhanced physical therapy care of the acute MI pa­ Patient education and prevention of infarction are
tient by optimizing the treatments prescribed and the particularly important for the cardiac patient. As
margin of safety with which activities are performed. soon as the patient is alert and able to cooperate, in­
Congestive heart failure may be unavoidable in formation about his or her condition with guidelines
cases of severe infarction or even milder infarction about activity, diet, and stress management is rein­
coupled with lung disease. Fluid intake and output forced. The more involved and informed the patient
and daily weight measurements promote early detec­
tion of congestive heart fai lure. Routine fluid intake
by an intravenous line should not exceed 20 to 30 ml
per hour. Signs of imminent and established conges­
tive heart failure appear in the box below. The work
of the heart can be significantly reduced in the up­
right position (Levine and Lown, 1952).
All cardiac patients are prone to anxiety about their
conditions and prognoses. The patient is given realis­
tic guidelines at each stage of recovery with respect to
the level of activity that can be safely performed,
which can potentially avert deterioration and promote
recovery. Involving the patient in rehabilitation plan­
ning from the onset facilitates the patient's planning
realistically for the future and may help to reduce the
depression often experienced by the acute MI patient.
The initial rehabilitation program is planned with
the long-range rehabilitation goals in mind. The pro­
gram designed for the cardiac patient is progressive in
terms of types of activities, usually beginning with ac­
tivities of daily living and with respect to the intensity,

Signs of Imminent Congestive Heart Failure

Development of tachydysrhythmias

Development of a ventricular gallop

Pulmonary crackles and other persistent advenlitiae

FIGURE 32-3

Development of dyspnea
Patient following open heart surgery (4 hours

Development of increased jugular venous pressure postoperative). NOTE: patient on mechanical ventilator,

and distention mediastinal drains, receiving blood, IV's, on EKG, CVP,

Swan Ganz, Arterial Blood Gas lines.

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 32 Intensive Care Unit Management of Primary Cardiopulmonary Dysfunction 595

Guidelines to Stages of Physical Therapy in the Open Heart Surgical Patient

Stage I

Patient may be seen in the postanesthesia and recovery room for a physical therapy assessment; the patient is usually
extubated within 24 hours after surgery. Although the patient must be permilled to rest as much as possible in the
initial 24-hour period, judicious body positioning is instituted to stimulate physiologic "stir-up." Usually once ex­
tubated, the patient is positioned side to side for deep breathing and coughing at least four times in the first 24
hours and low-intensity mobilization is initiated. Medications are administered before lreatment to ensure optimal
effect during treatment. Depending on the findings of x-ray, physical examination, and arterial blood gases, the pa­
tient may require vibrations and possibly percussion. Postural drainage positions are modi lied to avoid tipping the
patient head-down and causing increased myocardial strain. A sputum sample for culture and sensitivity testing
may be taken at this time. The patient can usually tolerate being dangled over the edge of the bed for a few min­
utes. Special care is taken for all hem1 patients to avoid the Valsalva maneuver, forced coughing, and huffing and ,

to maintain a semirccumbent or upright position for treatment. Blood pressure is checked before, during, and after
treatment. Mobilization is progressed.

Stage 2

Deep breathing and coughing maneuvers coupled with mobilization are continued. Positioning for enhanced alveolar
ventilation and ventilation and pelfusion matching may be indicated. If secretion accumulation is a problem and
the patient too unstable to be optimally mobilized or positioned, postural drainage and possibly percussion and/or
vibration may be indicated. Upper limb and neck exercises are introduced. Neck exercises are withheld if central
venous pressure lines are still in place in the neck veins. The patient can sit in a chair at bedside as tolerated. The
patient is encouraged to stand erect for a minute or so on transferring back and forth to the chair.

Stage 3

The patient can take ShOl1 walks as tolerated. Ambulation is not begun until arterial lines and the Swan-Ganz catheter
have been capped or removed. Vital signs are monitored before and after standing and walking. Deep breathing
and coughing maneuvers are continued even if the chest is clear, until the patient is up and about within reasonable
limits as tolerated. The patient is encouraged in grooming and self-care.

Stage 4

Deep breathing and coughing should be done by the patient without supervision. The presence of atelectasis on x-ray
or from assessment findings. however, would indicate the need for continuation of mobilization and body position­
ing with breathing exercises. Ambulation is increased as tolerated.

Stage 5

Palient can participate in individual or class activities, concentrating on trunk mobility, upper-extremity range of mo­
tion, coordinated breathing activities, posture. biomechanics, and increasing the patient's endurance gradually.

Stage 6

The palient can attempt six to eight stairs if progress has been satisfactory and as indicated. Aortic repairs in the first
week or so are prone to rupture. Elevation of the blood pressure is therefore avoided to reduce the risk of break­
down of the aortic suture line.

Stage 7

The patient depends primarily on ambulation for maintaining optimal alveolar ventilation and mucociliary transport
rather than brealhing and coughing exercises. The patient is cautioned to balance a period of exertion with a period
of rest. The pat ient may be discharged. The physical therapi st ensures the patient fully understands the specific de­
tails of the home exe rci se progrdm. The emphasis of exercise for cardiac patients conlinues to be
- 011 rhythmic, co­
ordinated dynamic movements on discharge, avoiding isomelric, static exercise. If possible, the patient is invited to
participate in a reconditioning and health promotion program as an oUlpatient in a physical therapy department.

NOTE: The physical therapist must guard againsl excessively intense treatmenl of open heart surgical palienLs or other patients who are on a
prophylactic course of anticoagulants.

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596 PART VI Guidelines for the Delivery of Cardiopulmonary Physical Therapy: Intensive Care

is in self-management, the greater the likelihood of cate different practices, depending on their facilities,
receptivity and adherence to a rehabilitation regimen experience of the surgical and ICU team, and the in­
after discharge. cidence of postoperative complications and survival
for that institution.
The physical therapist must guard against exces­
PATIENT AFTER OPEN HEART SURGERY
sively intense treatment of open heart surgical pa­
Principles of physical therapy management
tients or other patients for whom periods of relatively
Patients scheduled for open heart surgery are treated restricted mobility (4 to 5 days) are anticipated. Tn ad­
as high-risk surgical candidates because of the nature dition to the fact these patients may be hemodynami­
and invasiveness of this type of surgery (Figure cally unstable initially, these patients may be suscep­
32-3), regardless of their general level of health be­ t i b l e to s o f t t i s s u e bruising f r o m being on a
fore surgery (Trekova, Dementyeva, Dzemeshke­ prophylactic course of anticoagulants.
vich, and Asmangulyan, 1994). Whenever possible, Physical therapy follow-up should continue sev­
patients prepare for surgery in advance by decreasing eral months beyond discharge at which point the pa­
or stopping smoking, by avoiding exposure to respi­ tient should be well integrated into a cardiac rehabili­
ratory tract infections, by avoiding stress, by eating a tation program. Continuity and continuation of
balanced diet, and by getting adequate sleep. In addi­ physical therapy throughout the entire rehabilitation
tion, patients can benefit from a modified, prescrip­ period, from acute- to long-term, cannot be overem­
tive exercise program before surgery to maximize phasized given that achieving a maximal recovery
their aerobic capacity and thereby improve their peri­ from surgery is the priority.
operative course.
In the preoperative period the physical therapist
SUMMARY
may spend additional time with patients scheduled
for open heart surgery to provide teaching of the This chapter describes the principles of cardiopul­
basic anatomy and physiology related to surgery to be monary physical therapy in the management of criti­
performed, the effect of anesthesia, the role of intuba­ cally ill patients with primary cardiopulmonary dys­
tion and mechanical ventilation, the incision lines to function. Cardiopulmonary failure secondary to
be expected over the chest and the legs if veins are to chronic lung disease and heart disease are described.
be removed for bypass surgery, the lines, leads, chest Cardiopulmonary physical therapy management is
tubes, and catheters that will be in place after surgery, based on the specific underlying pathophysiological
and the course of recovery the patient might expect mechanisms of these various disorders. Tbese princi­
barring complications (Chapter 26). The emphasis on ples, however, cannot be interpreted to be guidelines
patient education in most open heart surgery units for specific treatment in that each patient is an indi­
may contribute to the generally low incidence of vidual whose condition reflects mUltiple factors con­
complications and mortality. tributing to impaired cardiopulmonary function or
Some guidelines for physical therapy management threatening it (i.e., the effects of restricted mobility,
of the open heart surgical patient appear in the box on recumbency, extrinsic factors related to the patient's
p. 595. These guidelines are to be applied thought­ care, and intrinsic factors related to the patient in ad­
fully and cautiously with regard to each specific pa­ dition to the underlying pathophysiology).
tient's condition and observed recovery. These guide­
lines suggest the upper limit of intensity of physical
REVIEW QUESTIONS
therapy if all is progressing well initially and sh0uld
be reduced if warranted by the patient's condition. 1. With respect to critically ill patients with the fol­
Progression from one stage to the next is based on an lowing conditions, describe the pathophysiology
optimal and reliable treatment response at each level of primary cardiopulmonary dysfunction, car­
before proceeding. Different institutions may advo­ diopulmonary failure, obstructive lung disease,

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 32 Intensive Care Unit Management of Primary Cardiopulmonary Dysfunction 597

status asthmaticus, restrictive lung disease, and Dean, E. (1994). Physiotherapy skills: Positioning and mobiliza­

coronary artery disease. tion of the patient. In B.A. Webber & lA. Pryor. (Eds.). Pfly.l'­
iotherapv for respiratory and cardiac problems. E dinburg h:
2. Relate cardiopulmonary physical therapy treatment
Churchill Livingstone.
interventions to the underlying pathophysiology of Dean, E., Murphy, S., Parrent, L., & Rousseau, M. (1995). Meta­
each of the above conditions in the critically ill pa­ bolic consequences of physical therapy in critically-ill p atients.

tient and provide the rationale for your choice. Proceedings of the world confederation of physical therapy
congress, Washington, De.
Dean, E., & Ross, J. (1992a). Discordance be tween cardiopuitnonary
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 Intensive Care Unit Management
of Secondary Cardiopulmonary
Dysfunction

Elizabeth Dean

KEY TERMS Burns Musculoskeletal trauma

Head injury Neuromuscular dysfunction
Morbid obesity Spinal cord injury

INTRODUCTION
management are not mutually exclusive for each cat­
This chapter describes the principles and practice of egory. Rather, considerable overlap may exist when
cardiopulmonary physical therapy in the manage­ conditions coexist. The principles presented are not
ment of secondary cardiopulmonary dysfunction that treatment prescriptions. Each patient must be as­
can lead to cardiopulmonary failure. Some common sessed and treated individually taking into considera­
categories of conditions described include neuro­ tion the contribution of immobility, recumbency, ex­
muscular disease, morbid obesity, musculoskeletal trinsic factors related to the patient's care, and
trauma, head injury, spinal cord injury, and burns. intrinsic factors related to the individual patient (see
Each category of condition is presented in two parts. Chapter 16), in addition to the underlying pathophys­
First, the related pathophysiology and pertinent as­ iology. For examples of specific treatment prescrip­
pects of the medical management of the condition tions refer to the companion volume to this book en­
are presented. Second, the principles of physical titled Clinical case studies in cardiopulmonary
therapy management are discussed. Guidelines to physical therapy.

599

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600 PART VI Guidelines for the Delivery of Cardiopulmonary Physical Therapy: Intensive Care

PATIENT WITH NEUROMUSCULAR DISEASE

mobility and recumbency, in addition to the patho­
Pathophysiology and medical management
physiological consequences of respiratory failure.
GuiUain-Barre syndrome, myasthenia gravis, muscu­ Provided the patient has some residual muscle
lar d y s t r o p h y , mUl tiple scl e r o s i s, s t r o k e , p o ­ power, the balance between oxygen demand and
liomyelitis, and neuromuscular poisonings are com­ supply will determine the degree to which mobiliza­
mon neuromuscular disorders that can precipitate tion can be exploited to maximize oxygen transport.
respiratory failure in the absence of underlying pri­ The treatment goals for these patients are to maxi­
mary lung disease (Cooper, Trend, and Wiles, 1985; mize oxygen delivery, enhance the efficiency of
Cu rran and Col b e rt , 1 9 8 9; Dean, Ross, Ro ad, oxygen uptake and utilization, and thereby reduce
Courtenay, and Madill, 1991; Fug l-Me yer and the work of breathing. In these patients, minimizing
Grimby, 1984; Griggs and Donohoe, 1982; Lane, oxygen demand overall (i.e., during mobilization as
Hazleman, and Nichols, 1974). If paralyzed, the pa­ well as at rest) is a priority. Mobilization needs to
tient will likely be dependent on ventilatory assis­ be prescribed in body positions that enhance oxygen
tance. Cardiopulmonary physical therapy has a cen­ transport and its efficiency so that the benefits of
tral role in minimizing the need for mechanical mobilization can be exploited more fully without
ventilation in these patients because their prognosis worsening arterial oxygenation (Dean, 1985). The
for weaning is poor. Progressive respiratory insuffi­ patient requires continuous monitoring of oxygen
ciency is best addressed early with the institution of transport and hemodynamic monitoring to ensure
nighttime ventilation at home (Curran, 1981) before the exercise stimulus is optimally therapeutic and
the development of failure and necessity for hospi­ not excessive.
talization. Patients with progressive neuromuscular Although the mechanisms are different, patients
diseases (e.g., muscular dystrophy) are living longer; with neuromuscular dysfunction can benefit from
thus cardiopulmonary insufficiency wil I be com­ body positioning to reduce respiratory distress much
pounded by age-related changes of the cardiopul­ like a patient with chronic airflow limitation (Barach,
monary system (Dean, 1994a; Leblanc, Ruff, and 1974). Upright and lean-forward positions will re­
Milic-Emili, 1970). duce distress to the greatest extent.
Neuromuscular conditions contribute to cardiopul­ The patient's body position and length of time in
monary dysfunction in numerous ways (Chapters 21 any one position must be carefully monitored and
and 22). With progressive deterioration of inspiratory recorded to minimize the risks of positions that are
and expiratory muscle strength and endurance, respi­ deleterious to oxygenation and to ensure that a bene­
ratory insufficiency and failure can ensue (Black and ficial position is not assumed for too long because of
Hyatt, 1971). Depending on the specific pathology, the diminishing benefits over time. This is particu­
such deficits include reduced lung volumes and flow larly important for the patient who is incapable of po­
rates, reduced alveolar ventilation, increased airway sitioning him or herself, who is incapable of commu­
resistance, ventilation and perfusion mismatch, im­ nicating a need to turn, and in whom muscle wasting,
paired mucociliary transport, mucous accumulation, bony prominences, and thinning of the skin may pre­
reduced cough and gag reflexes, relatively unpro­ dispose the patient to skin breakdown.
tected airway secondary to impaired glottic closure Patients who are hypotonic and generally weak
and weakness of the pharyngeal and laryngeal struc­ and debilitated fail to adapt normally to position-de­
tures, and increased work of breathing. pendent fluid shifts and thus are Illore prone to ortho­
static intolerance (Marini and Wheeler, 1989). Gravi­
tational stimulation is essential to maintain the
Principles of physical therapy management
volume regulating mechanisms. Tilt tables should be
A patient with restrictive pulmonary disease sec­ used judiciously given the potential risks in these pa­
ondary to neuromuscular conditions is at consider­ tients, which is compounded by the loss of the lower­
able risk of succumbing to the negative cardiopul­ extremity muscle pump mechanislll. Because of po­
monary and cardiovascular sequelae of reduced tential adverse reactions to fluid shifts and the

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 33 Intensive Care Unit Management of Secondary Cardiopulmonary Dysfunction 601

potential for desaturation. falling Pao2 levels and dys­ sential that these attempts are maximized (i.e., the
rhythmias. the patient's hemodynamic status must be patient optimally rested and medicated le.g., bron­
monitored closely during gravitational challenges. chodilators, analgesia, reduced sedation and nar­
The importance of chest waH mobility to optimize cotics] is physically positioned to optimize length­
three-dimensional chest wall excursion in chronic tension relationship of the diaphragm and abdominal
neurological patients is emphasized in Chapters 2 I muscles, positioned vertically to optimize inspiratory
and 22. This goal is particularly challenging in the lung volumes. and expiratory flows and avoid of as­
neurological patient with acute respiratory insuffi­ piration, and is provided thoracic and abdominal
ciency. The goal is to promote alveolar ventilation, support during expiration to maximize intrathoracic
reduce areas of atelectasis. and optimize ventilation and intraabdominal pressures) (see Chapter 21).
and perfusion matching and breathing efficiency to These supportive measures will ensure that the bene­
augment and minimize reliance on respiratory sup­ fits of the normal physiological cough mechanism,
port (i.e., supplemental oxygen and mechanical venti­ which is the single best secretion clearance tech­
lation) while minimizing respiratory distress. This is nique, is maximized (i.e., the most productive cough
especially important because patients with neuromus­ with the least energy expenditure) (Bennett, Foster,
cular conditions are poor candidates for being and Chapman, 1990; Hasani et aI., 1991; Kirilloff,
weaned off mechanical ventilation (Petty, 1982). In Owens, Rogers, and Mazzocco. 1985; Zinman,
addition these patient are prone to microaspirations. 1984). Forced chest wall compression or forced ex­
Promotion of mucociliary transport is therefore es­ piratory maneuvers are contraindicated (Nunn, Cole­
sential to facilitate clearing of aspirate and minimize man, Sachithanandan, Bergman, and Laws, 1965).
bacterial colonization and risk of infection. Impaired mobility, inability to cough effectively,
Another major problem for patients with restric­ decreased airway diameter, and bronchospasm con­
tive lung disease secondary to generalized weakness tribute to impaired mucociliary transport and secre­
and neuromuscular disease is an ineffective cough. tion accumulation. In addition, impaired glottic clo­
Cough facilitation techniques (e.g., body positioning, sure and increased risk of reflux in this patient
abdominal counter pressure, and tracheal tickle can population exposes the airway to risk of aspiration.
be used to increase intraabdominal and intrathoracic Prophylactically, multiple body positions and fre­
pressures and cough effectiveness. A natural cough, quent position changes will minimize the risk of se­
even when facilitated, is preferable and more effec­ cretion accumulation and stasis. If mechanically
tive in dislodging mucus from the sixth or seventh ventilated. these patients are suctioned as indicated.
generation of bronchi than repeated suctioning. Even If pulmonary secretions become a significant prob­
a weak, facilitated cough may be effective in dis­ lem despite these preventative measures, postural
lodging secretions to the central airways for removal drainage positions are selected to achieve the opti­
by suctioning or for redistributing peripheral secre­ mal effect (i.e., secretion mobilization and optimal
tions (Hasani, Pavia, Agnew. and Clarke, 1991). gas exchange). Given the treatment response. man­
Huffing, a modified cough peJformed with the glottis ual techniques of which manual vibration would
open and with abdominal support. may help to mobi­ have the greatest physiological justification, may
Jize secretions in patients with generalized weakness yield some benefit.
(Hietpas, Roth, and Jensen. 1979). In some cases, Patients with chronic neuromuscular dysfunction
suctioning may be the only means of eliciting a and residual musculoskeletal deformity pose an ad­
cough and clearing secretions simultaneously. ditional challenge to the cardiopulmonary physical
Coughing attempts are usually exhausting for these therapist in that cardiopulmonary function is less
patients. Thus ample rest periods must be inter­ predictable because of altered lung mechanics
spersed during treatment, particularly for the venti­ (Bake, Dempsey, and Grimby, 1976) and possibly
lated patient. Coughing maneuvers need to be strate­ cardiac dynamics. Thus clinical decision making is
gically planned. Even though the patient may be more experiential in these patients who require
only to effect a series of a few weak coughs, it is es­ close monitoring.

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602 PART Vl Guidelines for the Delivery of Cardiopulmonary Physical Therapy: Intensive Care

OBESITY Principles of physical therapy management

Pathophysiology and medical management
The obese patient can be treated aggressively pro­
Restriction of cardiopulmonary function secondary to vided there are no contraindications and he or she is
morbid obesity is called the alveolar hypovenlilalion being fully monitored. Treatments need to be intense,
syndrome or Pickwickian syndrome. In this syndrome to the limits of the patient's tolerance, provided this
the weight of excess adipose tissue over the thoracic is not contraindicated. An aggressive approach is es­
cage and abdominal cavity restricts chest wall move­ sential given that the obese patient is at greater risk of
ment and movement of the diaphragm and abdominal deteriorati ng between treatments than a nonobese
contents, respectively, during respiration. In very counterpart. Recumbency is tolerated poorly by an
heavy individuals, cardiopulmonary function can be obese patient. Positional decrements in Pa02 and
significantly impaired, resulting in hypoxemia and Sa02 can induce dysrhythmias. The weight of the ab­
cardiopulmonary failure. The major pathophysiologi­ dominal viscera limit diaphragmatic descent and ele­
cal mechanisms include significant alveolar hypoven­ vate the resting position of the diaphragm, impeding
tilation, reactive hypoxic pulmonary vasoconstriction, its mechanical efficiency.
increased pulmonary vascular resistance, myocardial These patients need to be aggressively mobilized;
hypertrophy, increased right ventricular work, altered both whole body exercise stress and range of motion
position of the thoracic structures, abnormal compres­ exercises between mobilization sessions. Active and ac­
sion of the heart, lungs, and mediastinal structures, ab­ tive assisted upper-extremity range-of-motion exercises
normal position of the heart, cardiomegaly, increased are associated with increased hemodynamic stress; thus
intraabdominal pressure, elevated hemidiaphragms the patient must be monitored closely. Lower-extremity
with resulting pressure on the underside of the di­ exercise, such as pedaling and hip and knee flexion and
aphragm, impaired cough effectiveness, impaired mu­ extension exercises, may help position and improve the
cociliary transport, mucous obstruction of airways, excursion of the diaphragm. Lower-extremity move­
airway narrowing, bronchospasm, impaired mechani­ ment will augment venous return. Depending on the pa­
cal efficiency of diaphragmatic excursion, and im­ tient and the work of the heal1, the effect of lower-ex­
paired respiratory mechanics and breathing efficiency tremity movement will need monitoring to ensure that
(Bates, 1989). In addition, such patients are likely to myocardial work is not increased excessively.
have poor cardiopulmonary reserve capacity sec­ The erect upright position is optimal to augment
ondary to increased metabolical rate and minute venti­ ventilation and reduce the work of the mechanical
lation at submaximal work rates, increased metabolic ventilator and the risk of barotrauma. The upright po­
cost of breathi ng, and increased work of breathing. sition, coupled with leaning forward, displaces the
Moderately heavy patients whose pulmonary function abdominal contents forward, thereby reducing in­
is normally not compromised may exhibit cardiopul­ traabdominal pressure and facilitating diaphragmatic
monary dysfunction when their oxygen transport sys­ descent. The posterior lung fields, particularly of the
tems are stressed because of illness. bases, are at risk for dynamic airway closure and at­
Mechanical ventilation can be a challenge in that electasis. Numerous positions and position changes
the system pressure required to inflate the lungs may ensure that the dependent alveoli remain open. The
predispose the patient to barotrauma. Furthermore, time spent in the supif!e position should be mini­
high system pressures contribute to reduced stroke mized. In fact, greater emphasis should be placed on
volume and cardiac output. Adequate circulation is nursing these patients in the upright position (i.e., the
essential to fulfill the goals of medical management position of least risk and its variants). In addition to
(i.e., to optimize tissue oxygenation and carbon diox­ its pulmonary benefits, the upright position can re­
ide removal). Thus a delicate balance between ade­ duce compression of the heart and mediastinal struc­
quate alveolar ventilation, cardiac output, and periph­ tures and there is a potential decrease in stroke vol­
eral circulation is maintained. ume and cardiac output. The weight of the chest wall,

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 33 Intensiye Care Unit Management of Secondary Cardiopulmonary Dysfunction 603

in addition to the weight of internal fat deposits in are taught comparable with those described for the
and around the cardiopulmonary unit, can compro­ patient with neuromuscular disease. Body positioning
mise cardiac output and contribute to dysrhythmias. to facilitate coughing and supported coughing need to
Thus during all body position changes the patient be instituted to maximize cough effectiveness. These
should be monitored hemodynamically to ensure the maneuvers should be carried out in conjunction with
position is being tolerated well. Obese patients often hourly extreme position shifts.
slump after being positioned in the upright position. Morbidly obese patients have a high incidence of
It is crucial that the position of these patients is upper airway obstruction and sleep apnea secondary
checked frequently and corrected. The slumped posi­ to floppy compliant pharyngeal tissue. Thus the qual­
tion can be counterproductive in that the benefits of ity of their sleep and rest is suboptimal, and they are
the upright position are significantly reduced and can apt to desaturate significantly while sleeping. These
lead to deterioration. patients are also at high risk for esophageal reflux
Although obese patients do not tolerate the prone and aspiration. The optimal resting position is with
position well, the semi-prone position can be benefi­ the head of bed up.
cial by simulating the benefits of the upright lean-for­
ward position on the displacement of the abdominal
PATIENT WITH MUSCULOSKELETAL TRAUMA
viscera (Ross and Dean, 1992). This position also
Pathophysiology and medical management
simulates the prone abdomen-free position, which is
associated with even greater benefit than the prone Crush and penetrating injuries of the chest are com­
abdomen-restricted position (Dean, 1985). The bene­ monly seen in the ICU (Moylan, 1988). Damage to
fits of the prone position for the obese individual in­ the chest wall, lung parenchyma, and heart contribute
clude increased lung compliance and enhanced gas to the risk of cardiopulmonary failure (see box on
exchange and oxygenation. The full prone abdomen p. 604). Associated injuries of the head, spinal cord,
restricted position is contraindicated in the obese in­ and abdomen may also contribute. Fractures of long
dividual with cardiopulmonary failure, however, be­ bones and pelvis are associated with fat emboli,
cause this position can compromise diaphragmatic which pose the threat of pulmonary embolism. In ad­
descent and contribute to further cardiopulmonary dition, fluid loss in multiple trauma contributes to
distress and failure and possibly cardiac arrest. loss of blood volume, hypovolemia, and hcmody­
Mucociliary transport is slowed and ineffective in namic instability. The more extensive the injuries, the
obese patients with cardiopulmonary failure. Fre­ greater the pain and need for analgesia. Pain con­
quent body positioning will facilitate mucociliary tributes significantly to reduced alveolar ventilation,
transport and lymphatic drainage. The postural airway closure, and inefficient breathing patterns.
drainage positions can be effective in mobilizing se­ Paradoxical motion of the chest wall associated
cretions should accumulation become a problem. with flail chest and rib fractures results from instabil­
Manual techniques are not likely to add much benefit ity of portions of the rib cage after trauma to the
particularly in the morbidly obese patient. Suctioning chest. If severe, patients may require surgical stabi­
is essential to clear pulmonary secretions from the lization of the ribs or stabilization by continuous ven­
central airways. tilatory management. Chest wall injuries and rib frac­
The obese individual is at risk for postextubation tures are particularly painful.
atelectasis. Thus aggressive mobilization and numer­ The presence of blood or air in the chest cavity
ous positions and frequent position changes need to and in the potential spaces of the pericardiai sac and
be continued. intrapleural cavity impairs cardiac distension and
The spontaneously breathing obese patient has a contraction, impairs venti lation, promotes retention
weak ineffective cough, which will be even less ef­ of secretions, interferes with effective clearance, and
fective after a period of intubation and mechanical impairs lymphatic drainage (Marini and Wheeler,
ventilation. Deep breathing and coughing maneuvers 1989). Resolution of effusions can be facilitated with

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604 PART VI Guidelines for the Delivery of Cardiopulmonary Physical Therapy: Intensive Care

sion. A tension pneumothorax results when air col­

Factors COlltributillg to Cardiopulmonary
lects under tension in the pleural cavity. The tension
Failure After Trauma and Their Diagnostic Signs
pneumothorax promotes lung collapse on both the ip­
silateral and contralateral sides, which furlher threat­
Airway Obstruction
ens respiratory failure. Phrenic nerve injuries inhibit
Respiratory insufficiency
diaphragmatic function (Dureuil, Viires, and Canti­
Respiratory distress
neau, 1986). The position of the affected hemidi­
Impaired blood gases aphragm rests higher in the thoracic cavity, which

Inadequate Ventilation may restrict ventilation to the lung base and con­
tribute to airway closure and basal atelectasis. Di­
Reduced thoracic movement
aphragmatic injuries directly affect ventilation in two
Paradoxical thoracoabdominal movement
ways. First, the bellows action of the lungs is com­
Tension Pneumothorax promised. Second, the lung is displaced by herniation
Cyanosis of the abdominal contents into the thoracic cavity.

Unilaterally absent breath sounds Analysis of blood gases in the patient with post­
traumatic injuries of the chest often shows severe hy­
Distended neck veins
poxemia and moderate elevations of arterial PC02.
Subcutaneous emphysema
The presence of acidemia is common, which may
Cardiac Tamponade have both respiratory and metabolical components.
Distended neck veins

Muffled heart sounds

Principles of physical therapy management
Narrowed pulse pressure
Severe restlessness and dysp nea in a patient with
Paradoxical pulse
chest injury are classic indications of respiratory fail­
Open Pneumothorax ure. Auscultation and percussion can usually reveal
Decreased breath sounds an underlying pneumothorax or hemothorax. Tension
Penetration of thoracic wall pneumothorax is confirmed by chest x-ray or aspira­
tion of the chest with a needle and syringe.
Myocardial Contusion
Flail chest refers to fractures involving the chest
Dysrhythmia
cage where there are two or more fractured ribs at
Flail Chest two or more sites. This results in instability of the
Loose segment chest wall. The so-called flail segment is usually ap­
parent on physical examination. Paradoxical move­
Multiple palpable fractured ribs
ment of the flail segment can often be observed. The
Decreased or moist breath sounds
chest is depressed rather than elevated over the site
during inspiration. Rib fractures are indicated by ten­
Modified from Moylan, J. A. (Ed.). (1988). Trauma surgery.
derness and crepitations on physical examination and
Philadelphia: .IB LippincOl1.
from x-ray findings. Nonventilatory management of
chest injuries in the absence of severe hypoxemia is
preferred in these patients.
mobilization and body positioning. These interven­
tions reexpand underlying atelectasis and help restore
Rib Fractures
fluid balance by their effects on lymphatic drainage.
Furthermore, by shifting the effusion fluid, atelectatic Simple uncomplicated rib fractures often receive no
areas can reexpand. The presence of a pneumothorax specific treatment. Pain from complicated fractures
or hemothorax can severely compromise lung expan­ may be treated with intercostal nerve blocks and tran­

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 33 Intensive Care Unit Management of Secondary Cardiopulmonary Dysfunction 605

scutaneous electrical nerve stimulation and analgesia. ventilator. Small leaks can be tolerated and are usu­
Optimizing alveolar ventilation and mucociliary trans­ ally compensated for by a n increase in tidal or
port and avoiding pulmonary complications are pri­ minute ventilation.
mary goals. Strapping the chest is avoided because this
further restricts and compromises chest wall expansion.
Multiple Trauma
The CUITent method of therapy for flail chest is in­
ternal stabilization of the chest and use of a mechani­ The management of multiple trauma is a major chal­
cal ventilator. Slight hyperventilation will usually re­ lenge for the rcu team. Multisystem involvement
duce the respiratory drive of most patients to allow and complications often present a precarious situation
the ventilator to take over the full work of breathing. in which priorities have to be defined for each indi­
The flail segment is then stabilized by internal expan­ vidual situation. Multiple trauma can include head in­
sion of the lungs. The treatment ensures adequate jury, chest wall injuries, fractures, lung contusions,
ventilation with the least pain possible. After 2 diaphragm injury, pleural space disorders, internal in­
weeks, the flail segment is usually stable. juries, thromboemboli, fat emboli, and cardiac contu­
When the patient can maintain a reasonable tidal sions. Shock and adult respiratory distress syndrome
volume and normal blood gases, weaning is begun. may ensue (see Chapter 34). The clinical picture of
As soon as tidal volume and forced vital capacity are the patient with mulliple trauma is compounded by
within acceptable limits, oxygen can be administered the mobilization and positioning restrictions imposed
through an endotracheal tube with a T tube assembly. (Ray et aI., 1974). Positive end-expiratory pressure
Arterial blood gases are monitored closely after the (PEEP) is frequently used to reduce the effects of
ventilator has been discontinued. Once the blood lung congestion secondary to shock or adult respira­
gases are in acceptable ranges over a reasonable pe­ tory distress syndrome (ARDS) (McAslan and Cow­
riod of time (i.e., 12 to 24 hours) the endotracheal ley, 1979). Arterial blood gases are assessed to evalu­
tube is removed. ate the effectiveness of PEEP in effecting improved
oxygen transfer.

Pneumothorax and Hemothorax

Multiple Fractures
Air or blood in the pleural cavity after chest trauma
must be removed through a chest tube. For a pneu­ Multiple trauma patients are assumed to have spinal
mothorax the chest tube is positioned in the second or involvement, particularly of the cervical spine, until
third intercostal space in the midclavicular line. For a ruled out with appropriate scans and x-rays. Mean­
hemothorax the chcsl tube is positioned in the sixth while the physical therapist performs repeated assess­
intercostal space in the posterior axillary line. Usually ments to establish a baseline and recommend posi­
the chest tubes are sutured and taped into position and tions for the patient that will ma ximize oxygen
therefore are not easily dislodged. If the tubes are transport. Treatment to enhance oxygen transport and
pulled out, subcutaneous emphyscma or a pneumotho­ mucociliary lransport is primarily restricted to body
rax results. A pneumothorax will also result if the tube positioning using log rolling maneuvers and a se­
is disconnected from the underwater seal. This is the lected range of motion exercises (i.e., not of the head
reason for securing the collecting reservoirs of a chest and neck, and possibly shoulders).
tube drainage system with tape to the floor. Mobiliz­ Fixation, traction. and casting of fractures and dis­
ing and frequency repositioning the patient facilitates locations of the limbs complicate the management of
chest tube drainage and reexpansion of collapsed alve­ the trauma patient. Restrictions to mobilization and
oli. Care is taken to avoid kinking or straining chest body positioning arc primary concerns of the physical
tubes during patient treatment. therapist (Mackenzic, 1989). Mobilization in the up­
A bronchopulmonary fistula can be responsible right position provides both a gravitational stimulus
for a major loss of the tidal volume delivered by the and an exercisc stimulus, both of which are essential

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606 PART VI Guidelines for the Delivery of Cardiopulmonary Physical Therapy: Intensive Care

to optimize oxygen transport. This is preferable to the trauma patient to reduce excessive oxygen con­
mobilization exercises in the recumbent position. In sumption and promote comfort (Malamed, 1989).
some cases, traction can be transferred from over the Active relaxation refers to relaxing the patient
end of the bed to over a chair. A strict routine of body through participation of the patient in relaxation pro­
positioning is maintained, although severe limitations cedures. Passive relaxation refers to relaxing the pa­
often exist with respect to the specific positions and tient using passive procedures (e.g., body positioning,
the degree of turning permitted. Lower limb traction physical supports, talking slowly and calmly, and tak­
can be maintained when the patient is positioned in a ing adequate time for conducting treatments). Taking
modified sidelying position. Coordinating treatments time to implement mobilization is essential. First,
with analgesia schedules reduces the patient's pain mechanically moving and having patients who have
and fatigue, thereby improving tolerance to and pro­ mUltiple injuries move requires a prolonged period of
longing the treatment. These patients usually tolerate time. In addition, however, the cardiovascular and
the head-down position well provided head injury cardiopulmonary systems of critically ill need time to
does not complicate the clinical picture. adapt to new positions physiologically and to control
The acute effects of mobilization that will benefit concommitant discomfort. Prolonged periods of time
the patient with musculoskeletal trauma include aug­ may be required to turn a patient, dangle him or her
mentation of ventilation, perfusion, ventilation and over the bed, or transfer him or her to chair with con­
perfusion matching, and promotion of mucociliary tinuous monitoring. Every effort is made to maintain
transport and cough effectiveness. General mobiliza­ the patient's spirits, reduce stress, and encourage a
tion exercises and propriocepti ve neuromuscular fa­ positive attitude toward active participation early in
cilitation (PNF) can be used to promote a mobiliza­ the rehabilitation program that begins in the ICU.
tion stimulus. Cycle pedals can be attached to a chair Care must be taken to avoid undertreating or
or the end of the bed to provide a low-intensity exer­ overtreating trauma patients. A clear chest can
cise challenge for some patients. Maximal work out­ rapidly regress because of general immobility and
put can be achieved within the patient's capacity limitations to body positioning imposed by traction
using an interval training type schedule (i.e., schedule and pain. Treatments should always be coordinated
of work to rest periods). A mobilization program that with the patient's analgesics to optimize treatment re­
promotes the long-term effects of exercise can be pre­ sponse and for the patient's comfort. Whenever pos­
scribed that involves as many large muscle groups as sible, the patient should be equipped with slings and
possible in rhythmic, dynamic exercise. pulleys and weights at bedside and a monkey bar
Frequent deep breathing and coughing is continued overhead for bed mobility and upper-extremity exer­
during and between treatments, depending on whether cise. In addition to their cardiopulmonary benefits,
the patient requires mechanical ventilation. Body posi­ PNF patterns are useful in preparation for slings and
tioning is carried out within the limits of the patient's pulleys. The use of PNF patterns for trauma and post­
traction and casts. Impaired mucocil iary transport is operative patients can be well tolerated by these pa­
treated with body positioning and frequent position tients. All activities are taught in conjunction with
changes. Secretion accumulation may require postural breathing control exercises and coordination with the
drainage. Modified positions may be indicated because respiratory cycle.
of the positioning restrictions imposed by the fractures,
traction, and fixation devices. If indicated manual tech­
PATIENT WITH HEAD INJURY
n i q u e s may be c o u p l e d with postu ral drainage
Pathophysiology and medical management
(Mackenzie, Shin, Hadi, and Ilnle, 1980). Care must
be taken to ensure the addition of manual techniques is Hypoxemia is observed in many patients with injury
beneficial and is tolerated by the patient. to the central nervous system (Demling, 1980). This
Relaxation interventions, both active and passive, may reflect primary damage to the cardiopulmonary
should be integrated into the treatment regimen for centers of the brain or secondary effects of associated

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 33 Intensive Care Unit Management of Secondary Cardiopulmonary Dysfunction 607

trauma. Arterial blood gases are therefore closely ICP depend on cerebral blood volume and intracranial
monitored in these patients. compliance. On cerebral stimulation, a chain reaction
Acute cerebral edema with sudden increase in in­ is initiated. Cerebral activity is increased, which in
tracranial pressure (ICP) and reduction in cerebral turn elevates metabolical rate, blood flow, and hence
pelfusion pressure, rapidly affects central control of volume and ICP. Alternatively, increased cerebral
respiration (Borozny, 1987). Advancing cerebral blood volume secondary to gravitational effects, in­
edema is evidenced by deterioration in level of con­ creased ICP, and reduced cerebral perfusion pressure.
sciousness, pupillary reflexes, ocular reflexes, pattern The head of the bed is usually maintained between
of respiration, and exaggerated muscle tone and pos­ 30 and 40 degrees to promote venous drainage and
ture. The sequence of these clinical signs corresponds thereby reduce ICP. The patient's head and neck can be
to progressively increasing ICP from the cortex to­ fixed in a neutral position by halo traction or by sand
ward the medullopontine region. With involvement of bags positioned on either side (Figure 33-1). Mechani­
the brain stem, respiration becomes variable and inco­ cal hyperventilation is used to maintain PC02 below
ordinate. With loss of central control and imminent normal limits but above 20 mm Hg. Arterial blood
cessation of breathing, respiration is shallow and gases are checked during or immediately after hyper­
ataxic. The appearance of the jaw and laryngeal jerk ventilation. Prolonged hyperventilation is avoided.
with each inspiratory effort suggests a poor prognosis. Barbiturate coma may be induced to decrease the
Physical therapy and the patient's normal routine cerebral metabolical rate for oxygen and hence cere­
may have a dramatic effect on the ICP. ICP can be el­ bral blood flow. The reduction in cerebral metaboli­
evated indirectly by an increase in intrathoracic pres­ cal rate exceeds the reduction in blood flow and thus
sure as a result of physical therapy or suctioning. oxygen supply exceeds demand, which is a desirable
Turning and positioning may produce obstruction to treatment outcome. Invasive hemodynamic monitor­
cerebral venous outflow. Noxious stimuli, such as ar­ ing is instituted in conjunction with barbiturate
terial and venous punctures or cleansing wounds, can coma because barbiturates contribute to hemody­
elevate ICP and relatively innocuous stimuli, such as namic instability.
noise or pupil checks. Wbether these factors elevate A complication of head injuries is acute lung in­

--
' ......... IIIft,-
.
' . . . .

FIGURE 33-1
Patient following neurosurgical procedure; head of bed elevated 20 degrees to help reduce ICP.

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608 PART VI Guidelines for the Delivery of Cardiopulmonary Physical Therapy: Intensive Care

jury, specifically, neurogenic pulmonary edema (see may be acceptable provided the pressure returns to
Chapter 34). Antonomical nervous system dysfunc­ normal immediately after the removal of the pres­
tion contributes to hypertension and neurogenic pul­ sure-potentiating stimulus. Prolonged elevation of
monary edema. The endothelial tight junctions in the ICP suggests low cerebral compliance and the possi­
pulmonary capillaries leak protein into the intersti­ bility of potential brain damage unless pressure is re­
tium along with fluid. Constriction of the lymphatic duced. Thus all interventions must be performed
vessels may also contribute to fluid accumulation by guardedly with due consideration being given to cor­
impeding the removal of lung water. Increased fluid responding changes in ICP. Typically, management
accumulation in the interstitium may progress to the of patients with central nervous system trauma in­
alveoli contributing further to impaired gas exchange cludes judicious tracheal suctioning, a stringent turn­
and reduced lung compliance. ing regimen, lung hyperinflation with the manual
breathing bag in the nonventilated patient, or deep
breathing with occasionally increased tidal volumes
Principles of physical therapy management
or sighs in the ventilated patients.
Physical therapy priorities in the management of the If the ICP is unstable and a risk of brain damage
patient with cardiopulmonary dysfunction secondary exists, physical therapy should follow sedation. Ide­
to head injury appear in the box below. ally, treatments should be peIformed when the ICP is
In cases of abnormally elevated ICP, mechanical low and intracranial compliance is satisfactory. The
hyperventilation and maintenance of Pe02 around 25 head-down position is contraindicated. Noise and
mm Hg are effective measures to reduce cerebral noxious stimulation that increases rcp should be kept
edema by reducing blood flow. Intracranial pressure to a minimum.
may increase with treatment and in particular with If the ICP is elevated, all noxious stimuli should
turning or suctioning. An ICP of up to 30 mm Hg be removed. In severe conditions a decision may

Physical Therapy Priorities in the Management of the Patient with

Cardiopulmonary Dysfunction Secondary to Head Injury

I. Prevention of cerebral hypoxia by maintaining a patent airway

2. Reduction of intracranial pressure and optimal cerebml perfusion pressure

3. Position the patient within the limits of fracture stabilization and elevated intracranial pressure to promote alveo­
lar ventilation and ventilation and pert'usion matching

4. Position the patient to reduce pathological patterns of muscle synergy and thereby promote ventilation and re­
duce oxygen consumption

5. Position the patient to reduce myocard ial stress

6. Avoid a ctivities and stimuli that increase ICP

7. Reduce atelectasis

8. Shift lung fluid accumulations and areas of atelectasis

9. Promote lymphatic dr ainage

10. Promote m ucocil i ary transport and reduce pooling of secretions. and risk of chest infection

II. Reduce the work of breathing and improve the efficiency of the muscles of respiration, particularl y if long-term
disability is a risk

12. Perform active, active-assisted, or passive movements as soon as possible to enhance cardiopulmonary function
and secondarily to preserve musculoskeletal and neuromuscular function and reduce the risk of thromboemboli

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 33 Intensive Care Unit Management of Secondary Cardiopulmonary Dysfunction 609

have to be made by the team to limit or withdraw in­ sions, is cardiopulmonary complications. Lung vol­
terventions that lead to an excessive ICP increase that umes are reduced with the exception of residual vol­
does not remit instantly (e.g., physical therapy, posi­ ume that increases. Interestingly, vital capacity in­
tioning, suctioning, or neurologic assessment). creases in the supine compared with the sitting
Movement of the limbs is performed gently and in a position in quadriplegic patients. However, this does
relaxed manner. Patients in a comatose state may expe­ not counter the negative effects of reduced functional
rience passive limb movement noxiously. Intracranial residual capacity (FRC) and increased airway closure
pressure may be elevated as a result. Passive move­ in this position and reduced flow rates.
ments, however, may have the added benefit of pro­ Spinal cord injuries above C3 result in loss of
moting improved tidal ventilation in the nonventilated phrenic nerve i n n e r vati on, necessitating a t ra­
patient by providing afferent stimulation to the respira­ cheostomy and mechanical ventilation. The lower the
tory center via peripheral muscle and joint receptors. level of the spinal cord lesion, the lower the car­
Severe head injury may produce flexor or extensor diopulmonary risk. All patients with spinal cord in­
posturing. These synergies may be inhibited by ap­ juries are at risk for developing atelectasis and pneu­
propriately positioning the patient. Judicious body monia. The coughing mechanics of quadriplegic
positioning, in turn, reduces oxygen consumption and patients are abnormal and contribute to ineffective air­
the patient's overall energy requirements. way clearance (Estenne and Gorino, 1992). In addi­
Neurophysiological facilitation of respiration has tion the quadriplegic patient is at risk for developing
been proposed as a treatment intervention to improve pulmonary emboli. Prophylactic low-dose heparin is
ventilation, coughing, and breathing pattern in the un­ used routinely unless the presence of pulmonary em­
conscious patient (Bethune, 1975). Neurophysiologi­ boli is suspected and higher dosages are indicated.
cal facilitation techniques include cocontraction of Patients with suspected spinal cord injuries usually
the abdominal muscles, vertebral pressure, intercostal undergo immediate spinal fixation on admission. De­
stretch, lifting the posterior basal areas of the lungs, pending on the level of injury detennined by clinical
and perioral stimulation. Although these techniques signs and x-rays, traction, and fixation may be local­
are believed to stimulate reflex involuntary respira­ ized to the head and neck or spinal support and cast­
tory movements, there is no evidence to support their ing may be required in the thoracic or lumbar regions.
efficacy in the management of the unconscious pa­
tient. Comparable with conventional chest physical
Principles of physical therapy management
therapy procedures, reported benefits associated with
neurofacilitation cannot be discriminated from the Because of the need to maintain relative immobility
potent and direct physiological effects of increased in the acute stabilization period of suspected spinal
arousal, body positioning, and mobilization on oxy­ cord injury, therapeutic body positioning rather than
gen transport (Dean, 1994b). These latter effects have mobilization is a primary intervention for optimizing
been well documented. oxygen transport. Although modified body position­
Although arousing the patient and increasing oxy­ ing can be achieved, the provision of optimal care
gen consumption occurs with cardiopulmonary physi­ under these restricted conditions is a singularly im­
cal therapy, arousal and oxygen consumption are pOl'tant challenge to the physical therapist, particu­
generally minimized to reduce hemodynamic and larly with respect to the management of adequate
metabolical demands in head-injured patients. oxygen transport while the patient is in the ICU. Pa­
tients with high spinal cord lesions can be positioned
in all positions within the limits of the cervical trac­
PATIENT WITH SPINAL CORD INJURY
tion device being used, barring head injury. Both
Pathophysiology and medical management
head and foot-tipped positions, however, are intro­
The principal cause of death in the early stages of duced cautiously and with hemodynamic monitoring
acute spinal cord injury, particularly for the high le­ because both positions can have significant car­

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610 PART VI Guidelines for the Delivery of Cardiopulmonary Physical Therapy: Intensive Care

diopulmonary and hemodynamic consequences sec­ respiratory muscles. In some centers, patients are
ondary to spinal nerve loss and hence sympathetic started in the weaning period on respiratory muscle
nerve loss to the peripheral blood vessels. Turning training. The physical therapist must be well versed
frames such as the Stryker frame facilitate turning and practiced in this procedure before using it in con­
and tipping these hemodynamically labile patients in junction with weaning the quadriplegic patient off the
the supine and prone positions (Douglas, Rehder, ventilator. Because of the potential risk of inappropri­
Beynen, Sessler, and Marsh, 1977). ate application and of danger to the patient, respira­
Effective body positioning, despite the need in tory muscle training must be effected knowledgeably
some cases for extensive modification, may be suffi­ to optimize its benefits for each individual patient.
cient to optimize oxygen transport secondary to im­
proved regional ventilation and perfusion to all lung
Respiratory Muscle Training
fields. In the spontaneously breathing patient, deep
breathing and coughing maneuvers need to be cou­ Respiratory muscle weakness and fatigue, two physio­
pled with position changes to optimize mucociliary logically distinct entities, are probably much more
transport (Alverez, Peterson, and Lunsford, 1981; common in the ICU than appreciated. These states
Braun, Giovannoni, and O'Connor, 1984). Some pa­ need to be recognized and detected early because both
tients may not tolerate numerous positions and posi­ can cause respiratory muscle failure (Macklem and
tion changes and thus have impaired mucociliary Roussos, 1977). The distinction between the two con­
transport. If secretion accumulation and stasis de­ ditions is that weakened muscles respond to resistive
velop, postural drainage can be instituted; however, muscle training, whereas fatigued muscles do not. Ex­
tipping must be attempted very cautiously. Patients posing fatigued respiratory muscles to resistive loads
should be monitored closely during and after treat­ can accentuate respiratory failure. The indication for
ment. Because of their well-documented side effects respiratory muscle training, therefore, is weak rather
(Kirilloff et aI., 1985) and the hemodynamic lability than fatigued respiratory muscles. Rest is indicated for
of acute quadriplegic patients, percussion and vibra­ fatigued respiratory muscles. Whether the respiratory
tion are applied cautiously, should they be indicated, muscles are weak or fatigued must be established be­
depending on the severity of any complicating frac­ fore prescribing respiratory muscle training.
ture-dislocation(s), the stability of fixation, the condi­ The combination of immobilization and cardiopul­
tion of the lungs, the presence of chest wall injuries, monary involvement secondary to multiple trauma
and hemodynamic lability. may result in similar disuse atrophy and weakness of
The high-frequency oscillating ventilator may the diaphragm as observed in other skeletal muscles.
have some benefit in the management of mUltiple Respiratory muscle weakness and fatigue can be a
trauma patients with spinal injuries who require ven­ component of both obstructive and restrictive pat­
tilation. The advantages of the high-frequency oscil­ terns of lung disease. Patients with spinal cord in­
lating ventilator include improved spontaneous mu­ juries do not have the same advantage of performing
c o c i l i a r y clearance and r e d u c e d i n c i d e n c e of coordinated general body activity and relaxation ma­
atelectasis (Gross and King, 1984). Weaning quadri­ neuvers to help reduce the work of breathing. This
plegic patients off the ventilator requires special skill contributes to a marked decrease in respiratory mus­
because of the lost function of the respiratory mus­ cle strength and endurance resulting in reduced vital
cles. For these patients, weaning can be particularly capacity, rib cage mobility, and the ability to cough.
fatiguing, frightening, and frustrating. Patients are For these reasons, patients with paralysis and demon­
weaned lying supine when they are alert and able to strated respiratory muscle weakness are particularly
cooperate. Short periods off the ventilator on the T well suited for respiratory muscle training. The quad­
piece are used initially. Use of the accessory muscles riplegic patient has lost the function of the intercostal
of respiration and any other muscular reserves are en­ muscles which are important muscles of inspiration
couraged to compensate for the loss of function of the and are responsible for thoracic cage expansion. In

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 33 Intensive Care Unit Management of Secondary Cardiopulmonary Dysfunction 611

addition, the absence of the abdominal muscles, fatiguing factors as eating a meal, talking, exposure to
which are the primary expiratory muscles, drastically heat and humidity, sitting upright, overcoming a respi­
reduces the ability to cough effectively and to per­ ratory tract infection, and so on.
form a forced expiration. The diaphragm and the ac­ A candidate for respiratory muscle training is
cessory muscles of inspiration, namely the scaleni equipped with an individual resistive breathing pack­
and sternocleidomastoid muscles, then become the age containing the valve, mouthpiece, noseclip, flow
quadriplegic patient's respiratory muscles. regulator, and a series of resistors that attach to the
These factors as well as the effects of heat, humid­ inspiratory side of the valve (Figure 33-2). It is es­
ity, and the vertical position, all predispose the quad­ sential that flow rate is controlled in that patients can
riplegic individual to the development of respiratory negate the training effect of a set resistor by chang­
muscle weakness and failure. The physical therapist ing flow rate.
can help avert the effects of respiratory muscle weak­ An initial pretraining assessment is performed to
ness with respiratory muscle training. determine the appropriate resistor with which to com­
Respiratory muscle training with a regimen of pro­ mence training. The progression to the next level of
gressive resistive breathing has been demonstrated to resistance is based on specific criteria of endurance
improve the strength and endurance of respiratory on the current resistor. Once the resistor has been
muscles (Gross and King, 1980; Loveridge and Dubo, chosen, a typical training session includes the steps
1990; Pardy and Leith, 1984) and improve functional shown in the box on p. 612.
capacity in some patients (Reid and Warren, 1984). Maximum inspiratory mouth pressure and vital ca­
Resistive breathing exercise is aimed at the prevention pacity can be measured routinely to monitor change
of respiratory failure by increasing the strength and in diaphragmatic function. The level of inspiratory
particularly endurance of the key muscle of inspira­ resistance and the duration for which the patient can
tion, the diaphragm. Because the diaphragm is skeletal use each resistor are indications of the endurance of
muscle, it can be reconditioned using a series of inspi­ the inspiratory muscles. Measurement of vital capac­
ratory resistance maneuvers. A stronger, endurance­ ity and maximum inspiratory and expiratory mouth
trained diaphragm will not fatigue as quickly as an un­ pressures provide an index of the strength of the in­
trained diaphragm when exposed to such potentially spiratory muscles.

FIGURE 33-2
Handheld resistive breathing training devices. Left, P-Flex; resistance level is altered by changing
settings on dial. Right, DHD device; resistance level is altered by inserting stopper with different
size orifice into inspiratory port.

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612 PART VI Guidelines for the Delivery of Cardiopulmonary Physical Therapy: Intensive Care

General Steps Involved in Respiratory Muscle Training and Its Prescription

I. The patient is usua lly in the sitting or upright position for training initial l y unless sitting is not yet indicated

2. The noseclip is attached snugly

3. The mouth pi e ce is p l aced securel y in the individual's mouth and a l l ows him or her to select an indi v i dual rate and
pattem of breathing

4. The patient adjusts flow rate to that designated and maintains it with feedback from the flow regulator

5. Breathing is performed comfortably without force

6. The patient is instructed to stop the exercise by letting go of the valve if the resistance becomes too difticu lt or if
lightheadedness or dizziness occur

7. When the individual has adjusted to the resistance in the initial training position. an attempt can then be made to
train at the same load in other positions

8. The parameters of the respiratory muscle training is determined by thc patient" s baseline: specific paramcters of
the prescription include initial resistance, the flow rate, the number of repetitions, the number of sets. the fre­
quency of sessions. and progression

Modified from Hornstein S: Ventilatol), muscle training. A clinical guide for physiotherapis/s, Unpublished manual of the Spinal Cord In­
jury Unit, Shaughnessy Hospital, J 984, Vancouver. Be.

Celtain precautions must be observed with respira­ plicate the clinical picture further and seriously
tory muscle training. Each time a new resistance is threaten tissue oxygenation (Cahalane and Deming,
tried, the physical therapist should be with the patient. 1984; Cane, Shapiro, and Davison, 1990). Hemoglo­
The patient selects his or her own rate and pattern of bin has a higher affinity for binding with carbon
breathing. The inspiratory rate is usually constant. monoxide than oxygen. A carboxyhemoglobin level
Too shallow breathing is inefficient, and too slow, greater than 20% denotes carbon monoxide poison­
deep breathing may result in accumulation of carbon ing. Levels in excess of 50% may produce irre­
dioxide. The patient is cautioned about avoiding hy­ versible neurological damage. The principal danger
perventilation. The physical therapist, or the patient of carbon monoxide poisoning is that arterial Paoz
when he or she is capable, should check the valving can be adequate and tissue oxygen tension inade­
system on the respiratory muscle trainer before each quate. Administration of high levels of oxygen is an
training session to ensure it is functioning properly. initial priority to reduce the half-life of carbon
monoxide to 1 hour from several hours.
Depending on the severity and extent of the burns,
PATIENT WITH BURNS
treatment ranges from conservative medical interven­
Pathophysiology and medical management
tions to multiple surgeries related to progressive de­
Cardiopulmonary complications are common in pa­ bridement and skin grafting. Both second and third
tients with smoke inhalation with or without severe degree burns can result in severe disfigurement and
burns and are a major cause of death (Marini and disability. Second-dcgree burns are partial thickness
Wheeler, 1989). Smoke and chemical inhalation pro­ burns and tend to be painful. Third-degree burns are
duce edema, bronchospasm, cough, mucosal slough­ full thickness burns; these tend to be anesthetic in that
ing, hemorrhage, hoarseness, stridor, and profuse the nerves themselves have been destroyed. Body po­
carbonaceous secretions. Irritation of the alveoli and sitioning to optimize oxygen transport is life-preserv­
acute pulmonary edema can result in a condition re­ ing; however, positioning and limb splinting must also
sembling adult respiratory distress syndrome (see be considered from the outset to minimize defonnity
Chapter 34). Carbon monoxide poisoning may com­ and restore optimal neuromuscular and musculoskele­

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 33 Intensive Care Unit Management of Secondary Cardiopulmonary Dysfunction 613

taJ statllS. in the burn monary circulation in these Treatment of

must address both these aspects of management. pulmonary edema consists typically of di­
Treatment is directed at improving arterial satura­ uretics, and mechanical ventilation. Positive end ex­
tion, fluid and preventing infec­ piratory pressure is usually indicated in the ventilated
tion. is effectively treated with the ad­ burn Mist or aerosol inhalation is also used to
ministration of oxy g e n a n d m a in t a i n i n g c l e a r reduce the thickness of pUlmonary secretions.
airways. I f the is breathing spontaneously, On admission of the burn to hospital, the
oxygen is via nasal cannulae or mask at tlows patency of the airway is assessed In­
of I to 5 L/min, on the arterial oxygen sat­ halation are common in burn
uration. Moisture can be administered through a face ing from smoke heat trauma, and chemical
tent with a heated nebulizer. Fluid balance is and gas inhalation.
larly in the burn patient because of the usually administered Heat may cause
which is essential to the retention and and bronchial edema. If occlusion
compartmentalization of body fluids and in the regu­ from edema threatens, intubation is per­
lation of fluid and electrolyte loss from the body. In formed. If indicated early, intubation may avoid res­
these patients may lose blood because of in­ distress within the critical 24-hour period
at the time of the accident. There is also a after admission. Particular care given to children
without tluid replacement from before the to and older adults with inhalation injury because these
the time medical attention is available and IV tluid have a higher risk of developing secondary
resuscitation commenced. Because of the nature of complications.
even when tluid resuscitation has fluid must be
and balance remains a challenge until con­ tient and nrp'\iPI1fP

siderable healing and has occurred. Fluid and impaired thermoregulation, hypermetabolism and in­
imbalances have considerable implica­ creased energy expenditure, ileus and disten­
tions for hemodynamics and cardiopulmonary func­ sion, pain, and infection. Eschar formation associated
tion 15) and contribute to with circumferential burns of the chest wall mechani­
instability, which necessitates modification of the cally restricts chest wall movement and can lead to
physical management. respiratory failure. Tissue edema that can continue for
An may be inserted initially with burns to a few after the bum contributes to increased tis­
the airway, and in anticipation of progres­ sue pressure and tissue potentiat­
sive which would make the insertion of air­ tissue ischemia and necrosis. Late complications
way considerably more difficult hours or days later. include gastrointestinal bleeding to stress
Ventilatory assistance is indicated with evidence of ulceration and the continued high risk of infection.
to smoke inhala­
and burns of the nose, throat, airway,
PrinCiples of physical therapy management
lungs, and chest wall. A nasotracheal tube i s pre­
ferred to tracheostomy tube because complications physical therapy is often required
with a tracheostomy tube are greater in burn patients. immediately for the with inhalation to
Cardiopulmonary are re­ maintain the of the prevent atelecta­
lated to or tluid overload in the initial stage. sis and retention of and improve or main­
Acute pulmonary edema and are largely tain gas Pulmonary function may be se­
preventable with careful fluid Central ve­ verely i r e d as t h e n e t result of i n halation
nous pressure can be in the burn patient burns and trauma to the chest wall, and
because of severe fluid loss and may remain at low tluid imbalance.
values pulmonary edema. artery physical often has to be
pressure more reflects the status of the modified in the burn 1984). Mobi­

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614 PART VI Guidelines for the Delivery of Cardiopulmonary Physical Therapy: Intensive Care

lization to enhance oxygen transport is exploited as traindicated over freshly grafted skin; however, man­
much as possible, however, because of blood volume ual vibration may be transmitted from a more distal
and hemodynamic problems, orthostatic intolerance site to a lung field that cannot be vibrated directly.
may limit mobilization and positioning alternatives. Risk of aspiration is increased if tube feedings are
With more severe burns and more extensive burn dis­ not discontinued for at least I hour before treatment.
tribution, body positioning is the primary interven­ A nasogastric tube is often used and should be cor­
tion. Positioning to effect an optimal therapeutic ef­ rectly positioned particularly during treatment.
fect on oxygen transport is challenging because of the Stimulating exercise and gravitational stress may
significant physical limitations that may exist. Given initially consist of being in the upright position prefer­
that body positioning profoundly influences ventila­ ably with the legs dependent, performing selected
tion and perfusion matching (Clauss, Scalabrini, Ray, limb movements and dangling over the edge of the
and Reed, 1968), the reduced number of positioning bed for a few minutes if this can be tolerated. how­
alternatives will contribute to shunt, ventilation and ever, in patients with severe burns and significant
perfusion mismatch, and hypoxemia. This effect will fluid imbalance, active and active-assisted movements
be accentuated if the patient is mechanically venti­ in an upright position that can be tolerated, may sub­
lated (see Chapter 32). stitute. As the patient's tolerance increases, free un­
Patients who have skin grafts require particular supported sitting can progress to standing and walk­
care when moving or positioning because of the dan­ ing. Ambulation during ventilator-assisted breathing
ger of sheering forces of the graft, which can disrupt should always be considered for any patient for whom
the circulation, nutrition, and healing of the new skin. this activity is not contraindicated. The upright posi­
Sterile procedures must be observed at all times. The tion and physical activity in the upright position are
physical therapist is usually required to cap, gown, likely to enhance markedly the patient's cardiopul­
mask, and glove before treating the patient with ex­ monary and neuromuscular function, and improve the
tensive exposed areas and to cover the chest with a patient's strength and endurance in preparation for
sterile drape. Facilitating mucociliary transport is a long-term rehabilitation. If sitting up and ambulation
priority if the patient has significant mobility and po­ are not imminent, appropriate limb movements,
sitioning restrictions because of the burn severity. preferably active, can help provide an exercise stimu­
Wherever possible, mobilization in conjunction with lus that can enhance oxygen transport. Passive full
multiple body positions and position changes is at­ range of motion exercises, in addition, are required to
tempted to maximize mucociliary clearance (Wolff, maximize joint range (a distinct goal from that to en­
Dolovich, Obminski, and Newhouse, 1977). If secre­ hance oxygen transport), wherever possible.
tions have accumulated, positioning for postural Positioning to minimize deformity is a priority
drainage requires the same consideration as position­ given the potential consequences for cardiopul­
ing for improved alveolar ventilation and ventilation monary function and oxygen transport, as well as
and perfusion matching. In the spontaneously breath­ musculoskeletal and biomechanical reasons. Position­
ing patient, postural drainage positions can be used ing a burn patient regardless of the goal should con­
selectively to increase alveolar volume in the superior sider alignment, pressure points, muscle balance, and
lung fields and alveolar ventilation to inferior lung effect on healing and grafted skin.
fields, in addition to purposes of drainage of the su­ Certain precautions have to be observed in the
perior bronchopulmonary segments. However, if the management of the burn' patient. First, skin loss con­
patient is mechanically ventilated, the superior lung tributes to substantial fluid loss, often resulting in la­
fields are preferentially ventilated (see Chapter 32). bile fluid and electrolyte imbalance. This situation
Should the addition of manual techniques be indi­ enhances myocardial irritability and the risk of dys­
cated, percussion may not be comfortably tolerated in rhythmia. Hemodynamic and ECG monitoring is per­
the presence of first and second degree burns. Manual formed routinely during physical therapy treatment.
vibration may substitute. Manual techniques are con­ Second, large areas of skin loss increase the risk of

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 33 Intensive Care Unit Management of Secondary Cardiopulmonary Dysfunction 615

infection; therefore the therapist must be fa­

Barach, A.L. (1974). Chronic obstructive lung disease: Postural re
miliar with sterile technique.
of dyspnea. Archives oj Physical Medicine & Rehabilila­
lion, 495-504,
Bates, D.V. (1989). Respiralory JU i leli on (3rd ed.).
SUMMARY
Philadelphia: W.B. Saunders.
This chapter describes the principles and practice of Bennett, W.D., Foster, WM, & Chapman, WF (1990). Cough­
enhnnced mucus clearance in the normal lung. Journal
therapy in the management of cardiopul­
plied Physiology, 69, 1670-1675.
monary secondary to neuromuscular and
Bethune. D.o, (1975). NeurophysiOlogical facilitation of respira­
musculoskeletal conditions that can lead to cardiopul­ tion in unconscious adull patient. Physiotherapy Canada,
monary failure. of conditions included are 27(5),
neuromuscular conditions_ musculoskeletal condi­ Black, L.F., & Hyatt, R.E. (1971). Maximal static respiratory pres­
sures in generalized neuromuscular disease. American Review
tions, morbid obesity, head spinal cord injury,
oJRespiralOJ), Diseases, 103,641-650.
and burns. A detailed of the underly­
M.L. (1987). Intracranial hypertension: Implications for
pathophysiology of these conditions and their the physiotherapist. Physiotherapy Canada, 39, 360-366.
medical management provides a basis for defining Braun, S.R., Giovannoni, R., & O'Connor, M. (1984). Improving
the physical and treatment. the cough in patients with spinal cord injury. American Journal
oj P ilfl ical Medicine, 63, 1-10.
The principles described in this chapter cannot be in­
Cahalane, M., & Deming, R.H. (1984). Early respiratory abnor­
terpreted as treatment in that each pa­
malities from smoke inhalation. .Iournal oj the A m eri can Med­
tient is an individual whose condition reflects multi- ical Associalion, 25,
factors contributing to oxygen transport Cane, R.D., Shapiro, B.A., Davison, R. (1990). Case silidies in
or threat to it the effects of restricted mobility, care me d ic ine (2nd cd.). St. Louis: Mosby.
Clauss, R.H., Scalabnni, BY, Ray, J.F., Ill, Reed, G.E. (1968).
recumbency, extrinsic factors related to the patient's
Effects of changing body position upon improved vemilatio!l­
care, and intrinsic factors related to the in ad­
Circulalion, 37(SuppL 4), 214-217.
perfusion relationships.
dition to the pathophysiology). Cooper, C.B., Trend, P.S., & Wiles, C.M. (1985). Severe di­
aphragm weakness in multiple sclerosis. Thorax, 40, 631-632.
Curran, FJ. (1981). Night vent.ilation body respirators for pa­
REVIEW QUESTIONS tients in chronic respiratory failure due to late stage muscular
dystrophy. Archives oj Physical Medicine Gnd Rehabilitation,
1. With respect to critically ill
62.
lowing describe the Curran, F.J., & Colbcr!, A.P. (1989). Ventilator management in
of cardiopulmonary dysfunction \P{''''IfU/f Duchenne muscular dystrophy and postpoliomyelilis syn­

neuromuscular morbid drome: twelve years' experience. Archives of Physi cal Medi­
cine and Rehabilila/ion, 70, 180-185.
musculoskeletal trauma, head spinal cord
Dean, E, (1985). Effect of body position on pulmonary function.
injury, and burns.
Physical 65, 613-618.
2. Relate cardiopulmonary Dean, E. Cardiopulmonary development. In B.R. Bonder
ment interventions to the underlying &M.B. (Eds.). Philadelphia: FA Davis.

ology of each of the above conditions in the criti­ Dean, E. (l994b). Invited commentary on "Are incentive spirom­
etry, intermittent positive pressure breathing, and deep
cally ill patient and the rationale for
breathing exercises effective in the prevention of postopera­
your choice.
p ul m o n a r y c o m p l i c a t i o n s a f t e r u p p e r a b d o mi n a l
P .. p ,,,·I" A systematic overview and meta-analysis. Physical

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1373-1390

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Douglas, W.W., Rehder, K., Beynen, F.M., Sessler, A.D., & Mackenzie, D.F. (Ed.). (1989). Chest physiolhempv in the in ten­
Marsh, H.M. (1977). Improved oxygenation in patients with sil'e care Llni! (2nd ed.). Baltimore: Williams & Wilkins.
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Dureuil, B., Viires, N., & Cantineau, J.P. (1986). Diaphragmatic A nesthesia & Analgesia, 59. 207-210.
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PhysioioRY. 61.1775-1780. tigue: A cause of respiratory failure? Cli nical Science & Mole­
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Hornstein, S. (1984). VenlilO/ory muscle training. A clinical guide Reid, W.D., & Warren, C.P.W. (1984). Ventilatory muscle
for physiolherapisls. Unpublished manual of the Spinal Corcl strength and endurance training in elderly subjects and patients
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(1985). Chesi. 88, 436-444. Ross, 1., & Dean, E. (1992). Body positioning. In e. Zadai, (Ed.).
Lane, DJ., Hazleman, B., & Nichols, PJ.R. (1974). Late onset res­ Clinics ill physical th era py. pulmonarv managel1lent in phys i­
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Leblam:, P., Ruff, F., & Milic-Emili, J. (1970). Effects of age and Effects of exercise ancl eucapnic hyperventilation on bronchial
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P hys iology, 28, 448-45 I. Wright, P.e. (1984). Fundamentals of acute burn care and physical
Loveridgl:, B., & Dubo, H. (1990). Respiratory muscle train ing therapy management. Physical Therapy, 64. 1217-123\.
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Rellllbilitalion. Review of ReSI) i ralOr y Diseases, 129. 1 82-184.

Copyrighted Material
 Complications, Adult Respiratory
Distress Syndrome, Shock, Sepsis,
and Multiorgan System Failure

Elizabeth Dean

KEY TERMS Acute lung injury Respiratory failure

Adult respiratory distress syndrome Sepsis
Multiorgan system failure Shock
Perioperative complications

INTRODUCTION
physiological deficits in these complex conditions is
The purpose of this chapter is to describe some com­ the basis for efficacious management in addition to re­
mon complications seen in critically ill patients. Com­ ducing the risk of an untoward treatment response and
plications arising from the following conditions are preventing worsening the patient's condition.
included: respiratory failure, surgery, acute lung in­
jury and adult respiratory distress syndrome, shock,
RESPIRATORY FAilURE
sepsis, and multiorgan system failure. Second, the im­
plications for cardiopulmonary physical therapy are
Metabolical Dysfunction
presented. Complications add further complexity to
the diagnosis of the multiple factors contributing to The range of complications associated with respira­
impaired oxygen transport and to the challenge of pre­ tory failure that can further impair tissue oxygenation
scribing effective treatment. Understanding the patho­ are described in the box on p. 619. The metabolical

617

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618 PART VI Guidelines for the Delivery of Cardiopulmonary Physical Therapy: Intensive Care

consequences of these complications and impairment (Fenwick, Dodek, Ronco, Phang, Wiggs, and Russell,
of oxygen transport are lifc threatening for the pa­ 1990). This so-called pathological dependence of
tient. Thus prevention of their development is a prior­ oxygen consumption on oxygen delivery occurs
ity. Should complications develop, however, early when the cells are inadequately extracting and using
detection and definitive management becomes the oxygen even in the presence of supranormal oxygen
priority if the patient is to survive. delivery levels. This phenomenon is observed in pa­
A hallmark of these complications is the impair­ tient with adult respiratory distress syndrome and
ment of multiple steps in the oxygen transport path­ shock (discussed later this chapter).
way, which adds to the complexity of management Given physical therapy is one of the most meta­
(Dantzker, 1991). The three major components of bolically demanding rcu interventions (Dean, Mur­
oxygen transport can be affected individually or in phy, Parrent, and Rousseau, 1995; Weissman and
combination (i.e., oxygen delivery, consumption, and Kemper, 1993), the physical therapist needs to be
extraction) (Pallares and Evans, 1992; Wysocki, Bes­ able to calculate this safety margin to prescribe the
bes, Roupie, and Brun-Buisson, 1992). type of treatment and its parameters (i.e., intensity,
In health the ratio of oxygen consumption to deliv­ duration and frequency) such that treatment is maxi­
ery is low (i.e., 23%, which ensures an over supply of mally beneficial and associated with the least risk to
oxygen as a safety margin) (see Chapter I). This the patient.
safety margin also ensures that most patients are able The ultimate treatment outcome measures are
to recover from insults to the oxygen transport sys­ markers of oxygen tissue metabolism (Dantzker,
tem. However, if the insult is extreme, such as that 1993; Nightingale, 1993; Pallares and Evans, 1992).
resulting from complications of respiratory failure, In addition, hourly assessment of oxygen delivery,
surgery, acute lung injury and adult respiratory dis­ consumption, and extraction provide the basis for di­
tress syndrome, shock, sepsis, and multiorgan system recting management of oxygen transport deficits.
failure, significant metabolical dysfunction secondary
to tissue hypoxia can result (Guiterrez, 1991).
Pulmonary Dysfunction
The relationship between oxygen consumption
and delivery has elucidated our understanding of he­ Complications of the cardiopulmonary system can
modynamic and metabolical changes observed in lead to respiratory failure (see box on p. 619) (Boggs
critical illness (Vincent, 1991). The phenomenon of and Wooldridge-King, 1993; Civetta, Taylor, and
oxygen-delivery dependence of oxygen consumption Kirby, 1988). Some of these relate to being mechani­
occllrs when a patient's oxygen transport system is cally ventilated. Certain technical problems related to
unable to supply sufficient oxygen to meet basal oxy­ the cuffs used in conjunction with artificial airways
gen demand (Phang and Russell, 1993). Oxygen de­ may occur (e.g., overinflation, distortion, and hernia­
livery below 300 ml 02/min/M2 limits the oxygen tion of the orifice of the tube). Mucous plugs can oc­
diffusion gradient and reduces oxygen extraction and clude the endotracheal tube or tracheostomy and im­
utilization at the ceLlular level. This is termed the pede ventilation. The common complications can be
critical/evel of oxygen delivery. When oxygen deliv­ reduced if the tube is changed frequently and if mini­
ery exceeds 300 ml/min/M2, oxygen consumption mal amounts of air are used for cuff inflation.
does not depend on delivery. Thus the greater the de­ Prolonged endotrach al intubation can result in la­
livery in relation to consumption the greater the ryngeal edema, ulceration, and fibrosis. Mechanical
safety margin. When oxygen transport is so severely ventilation may also rupture a bleb on the surface of
compromised that oxygen delivery falls below the the lung and produce a pneumothorax with rapid ten­
critical level, anaerobic metabolism is triggered. sion development. Chest tubes are inserted immedi­
However, anaerobic metabolism may also be trig­ ately to relieve the tension. Blebs occur when alveoli
gered at levels of oxygen delivery that exceed the rupture, causing air to track to subpleural sites.
normal critical threshold for anaerobic metabolism Mechanical ventilators can be a source of infection.

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 34 Complications, Adult Respiratory Distress Syndrome, Shock, Sepsis, and Multiorgan System Failure 619

ated with some complications (see Chapter 15). In­

Complications of Respiratory Failure
fection may lead to bacteremia and septicemia. Judi­
Life-threatening impairment of oxygen transport cious selection and application of any invasive proce­
and tissue oxygenation dure is warranted to minimize undue hazard. The
Fluid ,md electrolyte imbalances presence of these catheters limits head and neck posi­

Cardiac dysrhythmias and hemodyn,lmic instability tions and requires mobilization be carried out cau­
tiously within the patient's hemodynamic tolerance.
Myocardial dysfunction

Metabolical dysfunction

Thromboembolism Acid-Base Abnormalities

Neurological dysfunction Any combination of acid-base imbalance may occur
Gastrointestinal dysfunction either acutely or chronically during respiratory fail­

Renal dysfunction ure. Severe alkalemia associated with potassium and

chloride losses may occur after mechanical ventila­
Metabolical and blood sligar irregularities
tion and can precipitate serious cardiovascular and
Infection
neurological complications (see Chapter 15) (Petty,
Nutritional deficits
1982). Significantly impaired oxygen delivery to pe­
Complications of intubation and mechanical ventila­ ripheral tissue may contribute to increased anaerobic
tion, including increased risk of infection
metabolism and metabolic acidosis (Fenwick, Dodek,
Complications of oxygcn therapy Ronco, Phang, Wiggs, and Russell, 1990).

Fluid and Electrolyte Abnormalities

T':L: physical therapist can help minimize this risk by Fluid retention can occur with prolonged mechanical
not directly handling the ventilator attachments that ventilation in a patient with no evidence of cardiac
communicate with the air flow channels. Condensation failure. Pulmonary edema, weight gain, decreased pul­
from the hose should not be drained toward the venti­ monary compliance, and reduced oxygen transport are
lator or toward the patient. The physical therapist common signs. Fluid overload is a common cause of
should be maskcd and gloved when connecting and this fluid retention. Mechanically ventilated patients
disconnecting the patient to and from the ventilator. are therefore usually maintained underhydrated. Be­
Oxygen toxicity is a significant clinical complica­ cause of a tendency for sodium retention and hence
tion of mechanical ventilation. Mechanical ventila­ fluid retention, intravenous saline solution is kept to a
tors have precise oxygen controls to deliver the low­ minimum. Humidifiers attached to mechanical venti­
est possible inspired oxygen concentration needed to lators are responsible for adding a considerable
maintain arterial oxygen tensions. Because of the ia­ amount of water by absorption through the lungs.
trogenic complications of high FIo2 levels (i.e., deni­
trogen atelectasis and oxygen toxicity) excess oxygen
Cardiac Dysrhythmias
above the patient's needs is never indicated other
than short periods of hyperoxygenation before suc­ Cardiac dysrhythmias are a common complication of
tioning or in preparation for, during, and immediately respiratory failure. In addition, patients in respiratory
after mobilization (Fell and Cheney, 1971; Shoe­ failure tend to be older adults who as a group have a
maker, 1984). greater incidnce of dysrhythmias secondary to cardiac
Flow-directed pulmonary artery catheters (i.e., disease. Electrocardiographic monitoring is therefore
Swan-Ganz catheters), commonly used in the inten­ essential for all patients requiring ventilatory assis­
sive care unit (lCU) for monitoring patients who de­ tance in addition to patients with overt or suspected
velop hemodynamic complications, are also associ­ heart disease. Both atrial and ventricular tachydys­

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620 PART VI Guidelines for the Delivery of Cardiopulmonary Physical Therapy: Intensive Care

rhythmias are seen in acute respiratory failure. Sinus over the lower legs to minimize venous pooling and
tachycardia and premature ventricular contractions, assist venous return (see Chapter 32). JOBST® and
however, are particularly common. With rapid lower­ TED® stockings also may be applied over the feet
ing of arterial Pe02, ventricular fibrillation, or even and legs to increase circulatory transit time in the de­
death may occur. pendent areas and reduce circulatory stasis.
In the presence of respiratory failure and in the ab­
sence of cardiac disease the management of cardiac
Myocardial Dysfunction
dysrhythmias lies predominantly in the correction of
blood-gas abnormalities. Effective supportive man­ As in any clinical situation, acute myocardial infarc­
agement can usually be achieved with pharmaceutical tion can occur during the management of acute respi­
agents. Intravenous injection of lidocaine followed by ratory failure. The risks are increased because pa­
continuous infusion is useful in managing premature tients in respiratory failure tend to be older and more
ventricular contractions, which may be the precursor susceptible to positional hypoxemia. The probability
of potentially fatal tachydysrhythmias and cardiac ar­ of heart failure and associated dysrhythmias is in­
rest. Electrolyte replacement may also be required. creased and significantly compounds the problems of
A thorough understanding of the clinical presenta­ the patient in respiratory failure.
tion, electrocardiographic diagnosis, and correct man­
agement of cardiac dysrhythmias is fundamental to
Gastrointestinal Dysfunction
the optimization of physical therapy treatments in the
ICU and minimizing any risk to the patient. Cardiac Peptic ulcer is commonly associated with chronic
dysrhythmias resulting from any cause necessarily re­ airway obstruction. The stress of respiratory failure
quire ongoing evaluation and therapy. predisposes the patient to peptic ulceration. Pro­
The physical therapist must be able to treat the found hemorrhage may occur and blood replace­
patient optimally and safely within the restrictions of ment is necessitated.
any dysrhythmia in addition to other medical or sur­ Gastric dilation may occur in patients who are re­
gical conditions. The implications of the dysrhyth­ ceiving mechanical ventilation. Gastric dilation is
mia on the patient's clinical presentation and for best managed by means of a nasogastric tube and in­
treatment selection and response must be recognized termittent suction. Care must be exercised to avoid
by the physical therapist and considered in designing hypokalemia and hypochloremia caused by excessive
the treatment plan. gastric suctioning. Special care is also taken to avoid
fecal impaction, particularly in the paralyzed patient.
This risk can be reduced with suitable fluid balance,
Thromboembolism
mobilization, frequent turning in conjunction with ap­
A high incidence of pulmonary thrombosis or em­ propriate trunk and lower limb movements.
bolism exists in patients in acute respiratory failure.
Early diagnosis and management of pulmonary
Neurological Dysfunction
thromboembolism have been greatly facilitated by the
use of serial ultrasound procedures and scans. Physi­ A close correlation exists between the state of con­
cal therapy has a key role in preventing the develop­ sciousness and the arteri 1 P02 and Pe02. In addition,
ment of t hromboemboli by p r o moting f r equent changes occur in alertness, personality, memory, and
changes in position, specific bed exercises, particu­ orientation with altered blood gases. Motor changes
larly of the lower limbs, and passive range of motion also occur, including generalized or localized weak­
exercises if indicated. It is essential that movement ness, tremors, twitching, myoclonic jerks, gross
and repositioning are performed regularly to maxi­ clonic movements, convulsions, and flaccidity. Neu­
mize their cardiopulmonary protective benefits. Pneu­ rological complications of respiratory failure must be
matic extremity cuffs apply pressure intermittently differentiated from those of nonpulmonary origin.

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 34 Complications, Adult Respiratory Distress Syndrome, Shock, Sepsis, and Multiorgan System Failure 621

The physical therapist must be aware of the spectrum teredo The presence or absence of cyanosis may be an
of neurological complications that can result from unreliable sign because peripheral cyanosis can occur
respiratory failure and recognize that apparent im­ despite adequate arterial P02. Morbidity and mortality
provement of neurological signs may reflect im­ has been reported to be reduced in patients with se­
proved cardiopulmonary status. vere respiratory failure and system involvement when
Sllpranormal levels of oxygen delivery was achieved
(Hayes, Yau, Timmins, Hinds, and Watson, 1993;
Renal Dysfunction
Waxman and Shoemaker, 1980; Yu, Levy, Smith,
The development of renal failure greatly compro­ Takiguchi, Miyasaki, and Myers, 1993).
mises the chances of the patient's survival. Renal
failure can result from gastrointestinal bleeding, sep­
sis associated with shock, drug-induced nephrotoxic­
ity, and hypotension, Urinary outputs are maintained Common Postoperative Complications
with adequate fluid and diuretics, with care not to in­
Hypoxemia
duce pulmonary edema. Dialysis may need to be in­
stituted if more conservative management fails Hypercapnia

(Phipps, Long, and Woods, 1991). If dialysis is antic­ Increased work of breathing
ipated, the physical therapist should review existing Increased work of thc heart
treatment goals to mOdify treatment accordingly,
Fluid shifts and third spacing

Fluid and electrolyte imbalances

POSTOPERATIVE COMPLICATIONS Metabolic and blood sugar abnormalities

Reduced blood volume

Pathophysiology and medical management
Cardiac dysrhythmias
Respiratory failure in the postoperative patient is usu­ Reduced cardiac OUlput
ally associated with a low Pao2 and a high Paco2. This
Reduced tissue perfusion and oxygenation
situation is likely to be more common than generally
Anemia
appreciated. If the patient is in good general health
Pain
and is free from underlying cardiopulmonary disease,
recovery is usually rapid. Otherwise, more severe Alveolar hypoventilation

complications and cardiopulmonary failure may result Airway collapse

and progress to a life-threatening situation. The effects Atelectasis
of surgery on oxygen transport and on the varioLls
Physiological shunting
organ systems are described in Chapter 28. Common
Ventilation and ped'usion mismatching
postoperative complications and their causes appear in
Impaired mucociliary t ransport
the box at right and the box on p. 622.
Mucus accumulation and stasis

Pneumonia
Hypoxemia
Thromboemboli
The most common postoperative complication is hy­
Pulmonary embolus
poxemia secondary to alveolar hypoventilation, re­
Coaglliopathies
duced functional residual capacity (FRC), airway clo­
Sepsis
sure, and postsurgical atelectasis (Leblanc, Ruff, and
Milic-Emili, 1970; Marini, 1984; Ray et aI., 1974). Shock

Adequate oxygenation, however, can be present de­ MlIltiorgan system failure

spite hypoventilation when oxygen is being adminis­

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622 PART VI Guidelines for the Delivery of Cardiopulmonary Physical Therapy: Intensive Care

Factors Contributing to Postoperative Complications That Affect Oxygen Transport

Pre morbid cardiopulmonary status

Premorbid oxygen transp0l1 (aerobic) capacity

Premorbid systemic disease

Premorbid general health and immune status

Smoking history

Age and gender

Lifestyle factors-nutlitional status. stress, work situation. family situation, psychosocial support system. and substance abuse

Obesity

Pregnancy

Perioperative pain and anxiety

Perioperative reduced arousal

Perioperative reduced mobility

Perioperative recumbency

Perioperative medications (e.g .. narcotics)

Perioperative nutritional deprivation

Perioperative reduction in normal sleep quality and quantity

Type of surgery

Extent of physical manipulation and compression of lung parenchyma, phrenic nerves, diaphragm. and the heart

Perioperative fever and increased oxygen consumptions

Duration of surgery

Position assumed during surgery

Duration of static positioning during surgery

Type. depth, and duration of anesthesia and sedation

Use of an airway

Use of mechanical ventilation

Oxygen therapy

Neuromuscular blockade

Fluid loss and chest tube drainage

Fluid accumulation and third spacing

Infusion of blood products

Site. number. and extent of incisions

Dressings and binders

Traction and splinting devices

Placement of lines, leads, catheters. and monitoring devices

Invasive monitoring equipment (e.g., Swan-Ganz catheter, Foley catheter, intracranial pressure monitor. central
venous line, arterial lines, intravenous lines, and intraaortic balloon counter pulsation pump)

Need for cardiopulmonary bypass machine

Duration on cardiopulmonary bypass machine

Infection

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 34 Comp,lic:�ti(ms, Adult Respiratory Distress Syndrome, Shock, Sepsis, and .....'''r<mn System Failure 623

Pain
these increase with the magnitude of the op­
in addition to the effects of anesthesia, fre­ erative procedure and of anesthesia required
contributes to alveolar hypoventilation and and the premorbid risk factors. These abnor­
atelectasis after abdominal or thoracic surgery. malities observed in the period are
Rapid, shallow, and monotonous breathing may be and alveolar
spontaneously adopted by the patient to avoid pain FRC, and residual vol­
and minute ventilation is fa- decreased in
alveolar ventilation is compromised by the in­ Because of the
creased ratio of dead space to tidal volume. Further­ crease in FRC (30% o r m o r e), c o m p liance is
more, in the absence of breaths, coughs, and vv"",-,a,,,"u, and therefore the work of is in­
atelectasis may develop in the underventilated creased, Hypoxemia secondary to transpulmonary
portions of the The ventilation-perfusion ratio shunting usually becomes maximal within 72 hours
is disturbed because blood flow to underventilated after surgery, and often is completely resolved with
physiological shunting conservative management within seven days. The
tends to although Peo2 will on the mode of 100% oxygen ad-
may be An abnormally Low oxygen flows and low amounts of
monary pressure is then needed to reinflate these at­ tend to be delivered via nasal cannulae.
electatic alveoli. flows can deliver higher amounts of
masks and masks with reservoir bags.
always be taken into account when arter­
Pulmonary Embolism and Deep Vein Thrombosis
ial blood gases. The is selected to provide ade­
embolism is a potentially life-threatening quate oxygenation with lowest oxygen concentra­
complication. Pulmonary embolism usually results tion possible.
from a thrombus forming in the veins of the lower Based on the assessment, arterial blood
limbs, in the atrium, or in the ven­ gases, fluid and balance, hemodynamic
tricle. Patients may be at risk if have varicose status, and x-ray, a decision is made as to which
chronic heart failure or if are preg­ treatments on the hierarchy will opti­
nant, or oral rr""tr"""nh mize oxygen transport and what will be
The patient with a pulmonary thromboembolism used for each treatment.
usually has a sudden onset of and mobilizing them wherever possible will
chest pain, and apparent Occasionally, maximize FRC and reduce closing volumes and
heart failure follows. are often elevated. hence enhance gas and What
heart strain may be evidenced on ECG. Right these even minimally
bundle branch P waves, and inverted T their lack of alertness which must be explained. If the
waves may be seen. No abnormality may be noted on patient is unable to to treatment because of
chest x-ray. for this can b e discussed at
Treatment consists of primary and cir­ rounds and other medications should be considered
culatory with oxygenation of pe­ so that the is able to .. nl",n'·r f'" more. Thus
ripheral tissues. Anticoagulants, such as are even extreme body positioning will achieve more fa­
infused intravenously to minimize further formation vorable results and Geraghty
of thromboembolic substrates. (1973; Ray, and Reed, 1968; Oou-
Beynen, and 1977;
Piehl and Brown, 1976).
Principles of physical therapy management
Endoctracheal intubation and mechanical ventila­
of lung volume, tion may be indicated if blood gases fail to
and gas uniformly occur after anesthesia with conservative management. The treatment
and tissue dissection. The extent and duration of ties for the ventilated patient before and during

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624 PART VI Guidelines for the Delivery of Cardiopulmonary Physical Therapy: Intensive Care

weaning are presented in Chapter 32. Special atten­ Rest is prescribed as judiciously as treatment inter­
tion in the postoperative patient is given to the pul­ ventions to enable the patient to physiologically restore
monary complications associated with diminished between and within treatments. This is particularly im­
ability to move spontaneously, surgical pain, restric­ portant for ICU patients who are hypermetabolical and
tions imposed by dressings and binders, diminished have increased oxygen demands. Particular care must
ability to cooperate, and to periodically hyperventi­ be observed in prescribing treatment threshold parame­
late the lungs. ters for these patients. Suprathreshold states can be as­
Facilitating mucociliary transport is a primary goal sociated with an inappropriate balance between oxy­
in these patients. Impaired mucociliary transport can gen delivery and oxygen consumption such that the
be precipitated by alveolar hypoventilation, perhaps patient becomes compromised (e.g., hemodynamically
the most common cause of postoperative complica­ unstable, cardiopulmonary distress is precipitated, or
tions. Sufficient impairment can lead to mucous sta­ both). A greater volume of a mobilization stimulus,
sis, airway obstruction, atelectasis, and infection. however, may be delivered to these patients with an in­
Multiple positions, including upright positions and termittent mobilization regimen than with a single pro­
360-degree axial turns, and multiple position changes longed course of mobilization. Thus the benefits that
facilitates mucociliary transport. In the event of mu­ would be accrued would be correspondingly increased.
cous accumulation and difficulty in removing pul­ Prevention of thromboemboli is a major treatment
monary secretions, specific body positions are se­ objective and is best achieved with mobilization, body
lected to optimize postural drainage of the affected positioning, passive movements, and physical devices,
bronchopulmonary segments and to maximize alveo­ such as pneumatic cuff devices and stockings, to aug­
lar volume and ventilation. The addition of manual ment low-dose anticoagulants in patients at risk. Pa­
techniques can be detrimental in severely ill patients tients who develop pulmonary emboli are treated
(Mackenzie, 1989; Poelaert, Lannoy, Vogelaers, medically and physical therapy needs to be corre­
Everaert, D ecruyenaere, Capiau, and Colar dyn, spondingly modified to minimize oxygen consump­
1991), thus their use needs to be considered carefully. tion until the embolus resolves and the patient is in no
Suctioning may be most effective immediately be­ imminent danger.
fore and after position changes. The appropliate oxy­
gen transport variables are monitored to assess treat­
ACUTE LUNG INJURY ANI) ADULT RESPIRATORY
ment outcome and minimally to ensure the patient
DISTRESS SYNDROME
who may be unstable is not deteriorating. If the pa­
tient begins to deteriorate, treatment is discontinued Acute lung injury results from damage to the alveolar
until the patient stabilizes. Why the patient deterio­ epithelium (Gattinoni et aI., 1994). The extent of the
rated is determined so that a decision can be made as damage reflects damage to the type I and type II alve­
to whether treatment can be reintroduced, and if so, olar cells. Damage to the type I cells results in alveo­
what modifications are indicated. lar edema, atelectasis, and loss of lung compliance
Pain management is integral to the management of secondary to loss of structuraJ integrity of the alveoli
the surgical patient. Noninvasive and nonphannacologi­ provided by the type I alveolar cells. Damage to the
cal pain control strategies need to be exploited for all type II cells also contributes to atelectasis and loss of
surgical patients to augment or reduce the need for po­ lung compliance, but the mechanism relates to im­
tent analgesics especially narcotics. Chapter 28 de­ pairment of the production of surfactant and pul­
scribed some physical therapy pain control strategies for monary fluid that covers the alveolar epithelium.
surgical patients that can be applied with modification to Pulmonary edema refers to the accumulation of
the patient with surgical complications. Of these, use of vascular fluid in the interstitial spaces and alveoli. In
electrotherapy modalities, such as transcutaneous elec­ acute lung injury the mechanism of pulmonary edema
trical nerve stimulation, may be limited in the ICU be­ involves increased water movement across the pul­
cause of electrical interference with monitoring devices. monary endothelial cells and increased permeability

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 34 Complications, Adult Re5ioirato:rv and Multiorgan System Failure 625

of the endothelium to protein. This type of pulmonary Acute lung injury is characterized as a clinical spec­
edema is referred to as noncardiogenic pulmonary trum of parenchymal cell dysfunction. Mild injury re­
edema. Pulmonary edema that is in ori­ flects predominantly endothelial cell and
results from left ventricular failure. An increase noncardiogenic edema. Severe injury reflects a progres­
in hydrostatic pressure damages the interstitial sion to both endothelial and cell dysfunction
spaces, which normally provide an effective barrier and adult respiratory distress syndrome The
between the pulmonary circulation and alveoli. The clinical spectrum of acute lung injury and the clinical
critical distinction between the two of pul­ manifestations of mild and severe are shown in
monary edema is that pulmonary edema 34-1. The clinical of moderate in­
primarily involves the movement of water across the jury falls between these two extremes.
alveolar capillary membrane, whereas noncardio­ ARDS results from insult to the and in­
pulmonary edema involves the movement of to the alveolar-capillary membrane. Some of the
and water into the interstitial and alveolar causes of ARDS include shock, severe trauma or in­
spaces. The clinical consequences reflect the location fection, overwhelming and inhaled tox­
of the edema alveolar or and ins. Increased vascular that
the amount of fluid accumulation. of the response is a common feature.

MILD MODERATE SEVERE

AU All All

ARDS Late ARDS

MILD SIGNIFICANT SEVERE HH

LUNG PEEP non·PEEP
resp onsive
COMPLIANCE responsive

MILD SIGNIFICANT SEVERE

HYPOXEMIA O2 responsive PEEP responsive to
02 or

ENDOTHELIAL
CELLS
PERMEABILITY tt METABOLIC METABOLIC
INTERSTITIUM DYSFUNCTION 4+
DYSFUNCTION 1 +

EPTHELIAl CELLS
EDEMA EDEMA ttt EDEMA ttt
TYPE 1

TYPE 2
SLOUGHING ttt SLOUGHING tttt
HYPERMITOSIS METABOLIC

CONSOLIDATION tttt

FIGURE 34-1
manifestations the spectrum of acute injury from mild to
severe disease. (From Shapiro BA, Peruzzi WT: Changing inventilatator management: a
review of the literature and suggest clinical correlates, 117:121-133,1991.)

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626 PART VI Guidelines for the Delivery of Cardiopulmonary Physical Therapy: Intensive Cm'e

Fluid seeps into the interstitial spaces and over­ alveoli open and thereby optimizes gas transfer at
whelms the alveoli, leading to p u lmonary edema. end e xpiration. Arterial oxygenation is usually im­
-

Lung compliance and gas exchange are severely proved with PEEP because the effect of shunting is
compromised. Thus the patient presents with severe reduced and a given Fl02 tends to be more effective.
dyspnea and hypoxemia. Diffuse pulmonary infil­ Although the Fl0 2 may be reduced, which reduces the
trates appear on x-ray. Arterial hypoxemia results pri­ possibility of oxygen toxicity, supranonnal oxygen
marily from underventilated but pelfused lung units delivery can be beneficial in these patients (Bishop et
and right to left shunt. In this situation, hypoxemia is aI., 1993). Survival may be improved and frequency
relatively refractory to increases in Fl0 . of multiorgan system failure reduced.
2
Fibrinogen in the fluids leaking into the alveoli Further monitoring of respiratory status in con­
contributes to fibrosis and reduction of lung compli­ junction with arterial blood gases is essential for fol­
ance associated with ARDS. Increased lung surface lowing the progress of the syndrome. In addition to
tension and alveolar collapse tend to result from an the oxygen transport variables the principal parame­
inactivation of surfactant with the accumulation of ters monitored in ARDS are reduced lung compli­
fluid in the alveolar spaces. Thus reduced lung com­ ance, tachypnea, and the concentration of inspired
pliance produces a significant decrease in FRC in the oxygen needed to maintain acceptable levels of the
patient with ARDS. arterial blood gases.
The signs and symptoms of ARDS may take up to ARDS is characterized by a major pathophysio­
48 hours to be fully manifested. The prognosis for logical restrictive component. Hence the principles of
survival of patients is 40% to 60%. Hypoxemia is a management of restrictive lung disease can be effec­
principal feature of the syndrome, and results from a tively applied. Changes in lung compliance and Fl0
2
right to left shunt, whereby fluid-filled alveoli are in­ requirements provide guidelines to treatment re­
effectively ventilated. Hyperventilation and labored quired, treatment response, and course of the syn­
respiration can be expected in conjunction with hy­ drome. Patients with ARDS require close monitoring
poxemia. Oxygen therapy has little effect in the pres­ and often frequent treatments aimed at promoting op­
ence of shunting. Hypercapnia is not usually a major timal gas exchange because of the severity of the syn­
problem in the ARDS patient. drome and high incidence of mortality associated
The metabolical perturbations that can result in­ with it. Special attention is given to body positioning
clude problems with oxygen delivery, consumption , to promote ventilation and perfusion matching and
and extraction as discussed previously. When oxy­ mucociliary transport and to minimize the effect of
gen delivery falls below the critical level, anaerobic restriction of diaphragmatic and chest wall excursion.
metabolism is triggered resulting in increased lactate Some patients, for example, benefit from side lying
production. Elevated serum lactates are associated in which excursion of the inferior hemidiaphragm is
with a poor prognosis. favored. Other patients, however, seem to detel;orate
from apparent restriction of the inferior lung in side
lying. Each patient's condition and specific areas of
Principles of physical therapy management
lung involvement must be taken into consideration
Intubation and ventilatory support are implemented if when prescribing a turning regimen. The effect of the
arterial blood gases are severely affected and rerspi­ patient's body position on blood gases helps to estab­
ratory distress worsened. An endotracheal tube can lish a suitable regimen on a rational basis.
be placed t h r o u g h t h e n o s e o r mouth or a tra­ The sitting position optimizes lung capacity. The
cheostomy can be performed. The tidal volume is set use of a reclining chair at the bedside perhaps should
at about 10 mUkg of the patient's body weight. The be considered more often in the management of pa­
patient usually establishes the respiratory rate, al­ tients with acute lung inj u ry. Theoretically, the poten­
though it may be rapid. A positive end expiratory tial function of all lung fields will be benefited with
pressure (PEEP) of around 12 cm H20 maintains the the lungs in a more upright position. Patients who are

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 34 Complications, Adult Respiratory Distress Syndrome, Shock, Sepsis, and Multiorgan System Failure 627

too unstable to tolerate upright positions may respond tribute to intracellular digestion and calcium deposi­
favorably to extreme body positions and the prone tion. Once the lysosomes have ruptured and intracel­
position (Albert, Leasa, Sanderson, Robertson, and lular digestion is triggered, irreversible cell damage
Hlastala, 1987; Langer, Mascheroni, Marcolin, and ensues, impairing oxygen extraction and uptake
Gattinoni, ] 988). (Wysocki, Besbes, Roupie, and Brun-Buisson, 1992).
Severely affected patients may require neuromus­ The pathology of shock and the effect on the res­
cular blockade to reduce their oxygen demand and piratory membranes of the mitochondria follow a
enable them to respond to ventilatory assistance more similar course regardless of cause. Swelling of the in­
effectively. Handling and positioning patients on neu­ terstitial tissue disrupts the perfusion of the pul­
romuscular blockade requires particular care because monary capillaries. Congestive atelectasis and pul­
these patients lack muscle tone to protect their mus­ monary edema ensue. In the advanced stages, hyaline
cles and joints. Rotating beds can be extremely bene­ membrane changes and pneumonitis may occur.
ficial for these patients who are either too hemody­
namically unstable or difficult to turn manually.
Principles of physical therapy management
These mechanical beds slow ly rotate side to side
through an arc, thus changing the patient's body posi­ Foremost, the physical therapist must be knowledge­
tion continuously (Gentilello et aI., 1988; Pape, able about the relationship of oxygen delivery and
Regel, Borgman, Sturm, and Tacherne, 1994). consumption in these patients, as well as the implica­
tions of the pathophysiological processes on oxygen
extraction. The type of treatments and their pat'ame­
SHOCK
ters are based on a careful analysis of oxygen trans­
Common causes of shock include hypovolemia, sep­ port variables. Treatments are prescribed within the
ticemia, heart failure, and direct insult to the central patient's safety margin. Physical therapists in the
nervous system. Some of the classical features of ICU must also be knowledgeable about the signs and
shock are hypotension, reduced cardiac output, tachy­ symptoms associated with impending and frank
cardia, hyperventilation, diaphoresis, pallor, confu­ shock. By recognizing and understanding the compo­
sion, nausea, and incontinence. Inadequate tissue per­ nents of the different types of shock and the effect on
fusion results in extracellular acidemia and loss of the cardiopulmonary system, the physical therapist
potassium ions from the cells. The pulmonary blood can better prescribe a rational treatment plan for the
vessels constrict in response to hypoxemia, which short- and long-term management of the patient.
tends to increase pulmonary artery pressures. Although physical therapy may be limited in re­
Failure of cellular function secondary to shock can versing the signs and symptoms of shock, physical
result from a deficiency of substrate for energy pro­ therapy can help to restore and maintain optimal car­
duction, a reduced ability to use the nutrients for en­ diopulmonary function, reduce the risk of complica­
ergy production, or both. The pathophysiological tions associated with immobility and with recum­
mechanisms responsible include hypoperfusion of the bency, and maintain physical status at the best
tissues, hormonal and metabolical cellular changes, possible optimal level during the episode and in an­
and the toxic effects of the metabolical changes. Col­ ticipation of the patient's recovery. The primary ob­
lectively, these produce cellular damage. With hy­ jective, however, is to minimize oxygen demand. A
poperfusion and decreased oxygen delivery and other minimal objective is not to worsen the patient's con­
nutrients, the production of adenosine triphosphate is dition by imposing excessive metabolical demand.
reduced. The maintenance and repair of cell mem­ This is the case in patients whose oxygen delivery is
branes is disrupted, resulting in swelling of the endo­ approaching the critical level with respect to oxygen
plasmic reticular and eventually the mitochondria. consumption dependence. Excessive demands in
Persisting cellular hypoxia contributes to rupture of these patients can be life threatening.
the lysosomes, which releases enzymes that con­ Patients in shock are usually unresponsive. The

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628 PART VI Guidelines for the Delivery of Cardiopulmonary Physical Therapy: Intensive Care

course of the shock episode is often complicated with The fluid is drained after about 30 minutes. Car­
the sequelae of immobility and recumbency. The spe­ diopulmonary physical therapy is most effective if
cific goals related to optimization of cardiopul­ performed after the fluid has been completely drained
monary and musculoskeletal function and prevention from the peritoneum. After drainage of the fluid the
of further complications associated with cardiopul­ diaphragm is at a more optimal functional length for
monary function in particular are priorities. respiration, which potentially can improve treatment
Specific concerns for the patient in shock include response. If hemodialysis is indicated, the patient is
the need for short, efficacious treatments and avoid­ connected to a unit that dialyzes the blood externally.
ance of unnecessary fatiguing of the patient. Treat­ This process takes several hours and is usually re­
ment goals are therefore critically appraised and pri­ peated every few days.
oritized throughout each day to target physical In the end stages of shock, as for other severely ill
therapy treatment only to the very immediate and es­ medically unstable patients, physical therapy may
sential needs of the patients. Prudent patient position­ constitute primarily supportive care and comprehen­
ing is a priority because of the relative immobility sive monitoring.
and reduced spontaneous movement observed in
these patients and recumbency. Approximations to
SEPSIS AND MULTIORGAN SYSTEM FAILURE
the upright position (i.e., head of bed up and foot of
bed down) can augment sympathetic stimulation and Sepsis is the response to bacteremia or other by prod­
improve hemodynamic status and reduce sympath­ ucts of bacteria in the blood. The clinical features of
omimetic medications. In addition, this position sim­ sepsis include fever, tachycardia, tachypnea, and res­
ulates the upright sitting position (although not per­ piratory alkalemia. Metabolical abnormalities are
fectly) with re spect to i t s beneficial effects on also a common feature of sepsis. Sepsis is the most
pulmonary and cardiac function. common predisposing factor contributing to multior­
Late stages of refractory shock leading to renal gan system failure (MOSF), which typically involves
failure may necessitate dialysis. In peritoneal dialysis failure of more than two organ systems (Carrico,
a liter of fluid with a high osmotic fluid content is in­ Meakins, and Marshall, 1993; Vincent, \993). Table
jected into the patient's abdomen to draw fluid out. 34-1 shows the major organs affected and their clini-

TABLE 34-1

Presentation of Multiorgan System Failure

ORGAN CLIN[CAL PRESENTAnON SYNDROME

Lungs Hypoxemia, lung compliance, diffuse infiltrates Acute lung injury/AROS

Kidneys Creatine> 2 mg/dl
Urine output < 500 m1l24 hr Oliguric ARF
Urine output> 500 m1l24 hI' Nonoliguric ARF
Liver Bilirubin 2 mg/dl, SGOT and LOH Jaundice
Intractible hyperglycemia or hypoglycemia Hepatocyte failure
Cholecystitis Acalculous cholecystitis
Gut Upper gastrointestinal bleed Stress ulceration
Coagu lation Thrombocytopenia, prolonged PT and PTT Hypofibrinogenemia DIC
Heart Hypotension, Cl Heat1 failure
CNS Response only to painful stimuli Obtundation

Modified from Civetta. J.M., Taylor, R.W., & Kirby, R.R. (1988). Critical care. Philadelphia: JB Li ppi ncott .

ARF. acute renal failure; SCOT. serum glutamic oxaloacetic transaminase; LDH. lactate, dehydrogenase; DIC, disseminaling intravascular
coagulalion; PT. prothrombin time; PIT. partial prothrombin time; C/, c ardiac index

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 34 Complications, Adult Respiratory Distress Syndrome, Shock, Sepsis, and Multiorgan System Failure 629

cal manifestations (i.e., pulmonary, gastrointestinal, fective Floz. Even though the patient wi II likely bene­
hepatic, renal, cardiovascular, hematological, and fit more from some positions than others, frequent
central nervous systems). The cascade of pathophysi­ body position changes, preferably 360-degree turning
ological features of this MOSF is believed to be pre­ regimen, are still necessary to avoid the sequelae of
cipitated by mUltiple mediator systems. The release static body positioning. Semi-prone positions can
of these mediators impairs oxygen delivery and uti­ substitute well for full prone positions if the patient is
lization of oxygen by the cells. Thus the supply of the too hemodynamically unstable. Semi-prone positions
major energy source to the cell, adenosine triphos­ may be tolerated better by the patient and may be
phate, is reduced which leads to structural and func­ safer. Even though hourly position changes may not
tional damage of the various organ systems. The mor­ be feasible in these severely ill patients, prolonged
tality rate ranges from 60% to 80%. periods in a static position (more than 2 hours) is
Conditions that predispose a patient to MOSF in­ deleterious to the patient. Thus a balance between
clude sepsis, overwhelming infection, multiple these two concerns must be achieved.
trauma and tissue injury, inflammation, and tissue Promoting optimal mucociJiary transport remains a
perfusion deficits. Patients who are older, have priority even in the absence of secretion accumula­
chronic diseases, are immunosuppressed or have a se­ tion. Frequent position changes and numerous posi­
vere initial presentation have an increased risk of fail­ tions ensure pulmonary secretions are continually
ure and mortality. being redistributed to prevent accumulation and en­
hance removal. Should postural drainage be indicated,
these positions may need to be modified. Head-down
Principles of physical therapy management
positions in particular may not be tolerated well.
The patient with sepsis and MOSF, like the patient in Based on a careful assessment, the relative benefits of
shock, is gravely ill and unlikely to be able to cooper­ superimposing manual techniques must be established
ate with treatment. The principles for management in that these procedures are associated with increased
are comparable with those for managing the patient metabolical demand to which the patient is not readily
in shock, however, oxygen delivery is likely to be able to adapt. Increasing the oxygen demand of these
consistently compromised in these patients. If oxygen patients may worsen their condition.
delivery is critically low, oxygen consumption de­
pends on oxygen delivery and the patient is in a state
SUMMARY
of metabolical acidosis (see Chapter I). In this situa­
tion, where oxygen delivery is compromised to the This chapter presents several major complications
point of not meeting tissue oxygen demands, the goal that occur secondary to various conditions in the in­
of treatment is to maximize oxygen delivery (Bishop tensive care unit. Complications add significantly to
et aI., 1993; Yu, Levy, Smith, Takiguchi, Miyasaki, the complexity of the physical therapy diagnoses of
and Myers, 1993) and minimize oxygen demand so the patient'S underlying problems with respect to
that oxygenation of vital organs is threatened to the oxygen transport and cardiopulmonary management.
least extent. Thus the physical therapist must estimate The complications highlighted in the chapter include
the oxygen reserve capacity (i.e., the balance between those that impair multiple steps in the oxygen trans­
oxygen demand and oxygen) in every assessment to port pathway and hence jeopardize metabolism at the
select optimal treatment, which is associated with the cellular level. This sequence of events is most fre­
least risk. Treatments are selected to improve the effi­ quently associated with the complications of respira­
ciency of oxygen transport and utilization a n d tory failure, surgery, adult respiratory distress syn­
thereby reduce the work of the heart and o f breathing. drome, shock, sepsis, and multiorgan system failure.
Above all, treatment should not worsen the patient's Physical therapy treatments in critical care areas
oxygen transport status. Selective body positioning are typically short, frequent, and should always be ef­
can augment oxygen transport and maximize the ef­ ficacious. Patients with the complications, however,

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630 PART VI Guidelines for the Delivery of Cardiopulmonary Physical Therapy: Intensive Care

are usually severely compromised and often unable to

Boggs, R.L., & Wooldridge-King, M. (1993). AACN procedure
cooperate with treatment necessitating particularly
manual for critical care (3 rd ed.). Philadelphia: WB Saunders.
short and frequent sessions. Because of the severity
Cane, R.D., Shapiro, B.A., & Davison, R. (\990). Case sludies ill
of illness, patients with the complications described critical care medicine ( 2nd ed.), St. Louis: Mosby.
often require treatments that are more passive (i.e., Carrico, C.J. , Meakins, 1 ,L., & Marshall, J.e. (1993), Multiple

stress the oxygen transport system minimally, thus organ failure syndrome, The gastrointestinal tract: the motor of
MOF. Archives of Surge/y, 121, 197-208.
are lower on the physiological treatment hierarchy).
Civetta, 1.M., Taylor, R,W., & Kirby, R.R. (1988), CrilicaL care.
These patients require frequent and comprehensive
Philadelphia: 18 Lippincott.
monitoring (often several times daily) of their oxygen Clauss, R.H., Scalabrini, BY. Ray, 1.F, III, & Reed, G.E. (1968).
transport capacity (i.e., the relationship between oxy­ Effects of changing body position upon improved ventilation­

gen delivery and consumption, and oxygen extrac­ perfusion relationships. Circulatioll, 37(Suppl. 4), 214-217.

tion, to establish if and when treatment is indicated, Dean, E" Murphy, S., Parrent, L., & Rousseau, M. (1995), Meta­
bolic consequences of physical therapy in critically-ill patients.
and the specific parameters of treatment. If a patient
Proceedings of the World Confederation of Physical Therapy
is thought to be too unstable for treatment at a given Cogress, Washington, De.
time, continued monitoring of her or his status is es­ Dantzker, D.R. (1991). Cardiopulmonary critical care (2nd ed.).

sential so that small windows of opportunity can be Philadelphia: WB Saunders.

Dantzker, D.R. (1993). Adequacy of tissue oxygenation, Critical
exploited during stable periods. During periods of
Care Medicinc, 21, S40-S43.
monitoring rather than active treatment intervention,
Douglas, W.W., Rehder, K., Beynen, FM., Sessler, A.D., &
the physical therapist continues to have an impoltant Marsh, H,M, (1977), Improved oxygenation in patients with
role in recommending body positions and frequency acute respiratory failure: the prone position, American Review

of body position changes so that these can yield the of Respirato/y Disease, 115, 559-566.
Fell, T, & Cheney, F W. (J 971), Prevention of hypoxia during en­
greatest benefit to oxygen transport.
dotracheal suction. Annals of Surgery, 174, 24-28.
Fenwick, l,e., D odek, P.M., Ronco, 1.1., Phang, P.T" Wiggs, B" &
Russell, 1 , A. (1990), Increased concentrations of plasma lactate
REVIEW QUESTIONS
predict pathologic dependence of oxygen consumption on oxy­

1. Describe the complications associated with respi­ gen delivery in patients with adult respiratory distress syn­
drome, loumal of Crilical Care, 5, 81-86,
ratory failure.
Gattinoni, L., Bombino, M., Pelosi, P., Lissoni, A., Pensenti. A.,
2. Describe the implications for cardio ulmonary
Fumagalli, R., & Tagliabue, M, Lung structure and function in
physical therapy of respiratory failure, surgical different stages of severe adult respiratory distress syndrome,
complications, acute lung injury, adult respira­ loumal of the American MedicaL Association, 2 71 , 1772-1779,

tory distress syndrome, shock, sepsis, and multi­ Gentilello, L, Thompson, D.A., Tonnesen, A,S" Hernandez, D" Ka­
padia, A,S., Allen, S.1., Houtchens, B.A., & Miner, M.E. (1988),
organ system failure.
Effect of a rotating bed on t he incidence of pu I monary complica­
tions in critically ill patients. Crilica! Care Medicine, 16,783-786.

References Gutierrez, G. (1991). Cellular e nergy metabolism during hypoxia.

Critical Care Medicine, 19,619-626.
Albert. R.K., Leasa, D., Sanderson, M., Robertson, H.T., & Hayes, M.A" Yau, E.H.S., Timmins, A.e., Hinds, C.J. . & Watson,
Hlastala, M.P. (1987). The prone position improves arterial oxy­ D. (1993), Response of critically-ill patients to treatment aimed
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jury. American Review of Respiralory Diseases, 135, 626-633. Chesl, 103, 886-895,
Bartlett, R.H., Gazzaniga, A.B., & Geraghty, T.R. (1973). Respira­ Kariman, K., & Burns, S,R, (1985). Regulation of tissue oxygen
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Critical Care Medicine, 21, 56-63. body position on "airway closure" in man, Journal of Applied
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Mackenzie, e.F. (Ed.). (1989). Chest physiotherapy in the inlen­ Roukonen, E., Takala, 1., & Kari, A. (1991). Scrtic shock and mul­
sive care IInil (2nd ed.). Baltimore: Williams & Wilkins. tiple organ failure. Cr itic al Care Medicine, 19,1/46-1151.
Marini, J.J. (1984). Postoperative ateleclasis: pathophysiology, Shapico, B .A., & Peruzzi, WT (1995). Changing practices in ven­
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Care, 29, 516-528. clinical correlates, Surgery, 117, 121-133.
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Pape, H.e., Regel, G., Borgman, W., Sturm, J.A., & Tacherne, H. Vincent, J.L. (1993). Oxygen transport in severe sepsis. Ac l a
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(3rd ed.). Philadelphia Lea & Febiger. Weissman, e., & Kemper, M, (1993). Stressing the critically ill pa­
Ph an g, PT, & Russell, J.A. (1993). When does V02 depend on tient: the cardiopulmonary and metabolic resposnes to an acute
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Phipps, W.J., Long, B.e., & Woods, N.F. (Eds.). (1991). Medical­ 100-108
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4(1),13-14 Wysocki, M., Besbes, M., Roupie, E" & Brun-Buisson, e. (1992),
Poelaert, 1., Lannoy, B., Vogelaers,D., Everaert, 1., Decruyenaere, Modification of oxygen extraction ratio by change in oxygen
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Be/gica, 42, 165-170. Myers, S.A. (1993). Effect of maximizing oxygen delivery on
Ray, J.F., [[[, Yost, L., Moallem, S., Sanoudos, G.M., Villamena, morbidity and mortality rates in critically ill patients: A
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Surgery, 109, 537-541.

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PART VII

Guidelines for the Delivery of

Cardiopulmonary Physical
Therapy: Special Cases

Copyrighted Material
 The Neonatal and Pediatric Patient

Victoria A. Moerchen
Linda D. Crane

KEY TERMS Bronchopulmonary dysplasia Hyaline membrane disease

Chest physical therapy with Patent ductus arteriosus
infants/children Pediatric cardiac rehabilitation
Childhood asthma Pediatric pulmonary rehabilitation
Cystic fibrosis Pulmonary development
Endocardial cushion defect Transitional circulation
Handling for ventilation Trunk-ventilation interaction

INTRODUCTION
(3) present principles and precautions of direct respi­
Pediatrics entails a "special" application of cardiopul­ ratory care; and (4) incorporate these principles into
monary physical therapy. This chapter stresses that suggestions for practice.
cardiopulmonary development and its related vulner­ This chapter begins with a brief description of crit­
abilities form the basis for cardiopulmonary practice ical events and important characteristics of cardiac
with neonatal and pediatric patients. and pulmonary development. Relevant diagnoses are
The objectives of this chapter include to: (l) re­ then presented to build onto this developmental per­
view cardiopulmonary development and related vul­ spective and to stress that cardiopulmonary pathology
nerabilities; (2) relate developmental pathologies to and ventilatory compromise are often related to de­
issues of adequate ventilation and oxygen transport; velopmental vulnerabilities. Finally, treatment ap­

635

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636 PART VII Guidelines for the Delivery of Cardiopulmonary Physical Therapy: Special Cases

proaches are described, including pediatric cardiac men ovale allows right-to-left blood flow through the
rehabilitation, pulmonary care for neonatal and pedi­ atria, bypassing the lungs (Yao, 19H3). Left ventricular
atric patients, pediatric pulmonary rehabilitation, and output (LVO) is well-oxygenated blood that then enters
developmental motor approaches for trunk and venti­ the ascending aorta and flows to the brain and upper
latory muscle function. body. The ductus arteJiosus similarly allows the lungs
A knowledge of cardiopulmonary development, to be bypassed, as most of the right ventricular output
congenital and d evelopmental cardiopulmonary (less well-oxygenated than the LVO) flows to the de­
pathology, and pediatric cardiopulmonary treatment is scending aorta and from there to the lower body.
essential for any therapist serving children. Most pedi­ Fetal blood flow to the lungs is minimal, secondary
atric patients require ongoing attention to respiratory to high pulmonary vascular resistance during fetal cir­
function, whether as a primary focus of physical ther­ culation. Only 10% to 12% of evo goes to the lungs
apy or as an inherent aspect of motor development. (Koff, 1993; Phelan, Olinsky, and Robertson, 1994),
This chapter is relevant to therapists who perform di­ with the function of nourishing the developing lung
rect cardiopulmonary care and to therapists who incor­ tissue rather than providing gas exchange.
porate a cardiopulmonary awareness into developmen­
tal motor therapy.
Neonatal circulation
Adult-like circulation occurs at or shortly after birth,
with separation from the placenta and ventilation of
CARDIOPULMONARY DEVELOPMENT
the lungs resulting in closure of the ductus venosus,
The application of cardiopulmonary physical therapy foramen ovale, and ductus arteriosus. This process,
to infants and children requires a special understand­ referred to as transitional circulation, occurs early in
ing of developmental cardiopulmonary anatomy and neonatal life and increases the efficiency of oxygen
physiology. Knowledge of normal development and uptake and transport (Heyman and Hanley, 1994;
its inherent points of vulnerability will help the Rudolph, 1970).
reader understand some of what is known about car­ The initiation of breathing and the removal of lung
diopulmonary pathology in pediatric patients. fluid increases pulmonary blood flow. Whereas fetal
circulation was characterized by high pulmonary vas­
cular resistance and low systemic resistance, separa­
Cardiac Development
tion from the placenta causes a rise in systemic resis­
Differences in fetal and neonatal gas exchange ac­ tance and a decrease in pulmonary vascular resistance.
count for differences in the anatomy and physiology As this shift in relative pulmonary and systemic resis­
of fetal and neonatal circulation. A basic review of tances occurs, sites of intercommunication (shunts)
developmental circulation is essential for discussion close, and the ventricles shift from working in parallel
of congenital heart defects and the role of pediatric to working in series (Heyman and Hanley, 1994).
cardiopulmonary physical therapy. Closure of Foramen Ovale. The increased left atrial
pressure that occurs during transitional circulation re­
Fetal circulation sults in apposition of the valve of foramen ovale
Placental oxygenation is a major characteristic of against the interatrial septum, functionally closing this
fetal circulation. Additionally, in fetal circulation site of fetal circulatory shunting (Rudolph, 1970). In
blood flow through the right and left sides of the most infants, anatomical closure occurs 2 to 3 months
heart occurs in parallel, such that cardiac output is ac­ later (Emmanouilides and Baylen, 1988; Yao, 1983).
tually combined ventricular output (eVO) (Heyman Closure of Ductus Arterioslls. Functional closure or
and Hanley, 1994). This is possible as a result of constriction of the ductus arteriosus occurs postnatally
shunts in fetal circulation (Parks, 1988). within the first IS to 72 hours in response to increased
Two points of shunting during fetal circulation are at arterial oxygen saturation (Daniels, Hopman, Stoelinger,
the foramen ovale and the ductus arteriosus. The fora­ Busch, and Peer, 1982). Anatomical closure of ductus

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 35 The Neonatal and Pediatric Patient 637

arteriosus occurs by 2 to 3 weeks in most term neonates diaphragm of a newborn has fewer type I (high oxida­
(Rudolph, 1970). It is important to note that the respon­ tive) muscle fibers (25% compared with 50% in adult)
siveness of the ductal smooth muscle to arterial oxygen (Muller and Bryan, 1979). This difference predisposes
tension and to endogenous prostaglandins is impacted an infant to earlier diaphragmatic fatigue when stressed.
by gestational age (Pack, 1988; Yao, 1983). A biomechanical difference between the infant
and child is the circular and horizontal alignment of
the ribs and the concomitant horizontal angle at
Pulmonary Development
which the diaphragm inserts on the ribs during new­
Structural and functional characteristics of pulmonary born and early infant chest development (Massery,
development in infants and children are significant 1991; Muller and Bryan, 1979). This, along with the
because they may contribute to aspects of respiratory more cartilaginous nature of the rib cage, results in
vulnerability (Muller and Bryan, 1979). less efficient chest wall mechanics. The result, again,
is increased work to breathe. (See Chapter 37 for a
Newborn respiration
more complete discllssion of chest development).
The pulmonary anatomy of t h e term i n f a n t i s
Respiration in the child
markedly different from the adult but also different
from the child. An infant's airways are narrower from Two residual strllctural differences exist beyond the
the nares to the terminal bronchioles. This presents a newborn period and have potential implications for
point of pulmonary vulnerability because a smaller pulmonary vulne rabili ty in the child. First, the some­
diameter airway is more easily obstrllcted by mucus, what horizontal angulation of the ribs persists unti I
edema, foreign objects, and enlarged lymphatic tis­ approximately 7 years of age and results in less effi­
sue. The infant also has a high larynx (Laitman and cient chest wall mechanics (Muller and Bryan, 1979).
Crelin, 1980). Although this position of the larynx Secondly, lymphatic tissue (especially adenoids)
enables the newborn to breathe and swallow simulta­ grows rapidly until about 6 years of age (Sinclair,
neously, it may also contribute to predominant pat­ 1978) and can continue to be a potential source of
terns of infant nasal breathing, which can result in in­ upper airway obstruction.
creased work to breathe during any compromise of As infants and children grow and develop, how­
the nasal airway. ever, most structural and functional disadvantages
Even without airway compromise, the work of disappear. An aspect of growth and development that
breathing is increased during the neonatal period. can be protective for infants and younger ch i ld re n is
The initial low compliance of the newborn's lungs alveolar multiplication. This begins in the rirst year
requires increased effort for ventilation, which re­ of lire and continues until approximately 8 years of
sults in a high rate of respiration and increased oxy­ age (Blackburn, 1992; Thurlbeck, 1975).
gen consumption.
Although the process of transitional circulation al­
Cardiopulmonary Considerations
lows more efficient O2 transport in the neonate than
in the Preterm Infant
in the fetus, gas exchange in the newborn is still
somewhat inefficient because of immature alveolar All of the cardiopulmonary structural and functional·
structure and function. The surface area for gas ex­ characteristics of neonates that have been previously
change is 1120 that of an adult (Johnson, Moore, and discussed apply to the premature infant. Additionally,
Jefferies, 1980), and the diffusion distance across the there arc signi["jeant gestationa l characteristics and as­
alveoli-capillary membrane is increa sed as a result of pects or cardiopulmonary vulnerability that are more
thick alveolar walls (Blackburn, 1992). pronounced and create more problems in premature
Functional characteristics of infant pulmonary de­ infants Cfable 35- I).
velopment are also significant to understanding possi­ Recall that the transitional circulation of a term
ble contributions to pulmonary distress in infants. The newborn includes a decrease in pulmonary vascular

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638 PART VII Guidelines for the Delivery of Cardiopulmonary Physical Therapy: Special Cases

TABLE 35-1

Factors Contributing to Cardiopulmonary Dysfunction in the Premature Infant*

ANATOMICAL PHYSIOLOGICAL

Capillary beds not well developed before 26 weeks' gestation Increased pulmonary vascular resistance leading
10 right-to-Ieft shunting

Type II alveolar cells and surfactant production not mature Decreased lung compliance
until 35 weeks' gestation; elastic properties of lung not
well developed; lung space decreased by relative size of
the heart and abdominal distention

Decreased responsiveness of the ductus arteriosus to oxygen Left-to-right shunting

tensions; delayed ductal closure

Type I, high-oxidative fibers compose only 10% to 20% of Diaphragmatic fatigue: respiratory failure
diaphragm muscle

Highly vascular subependymal germinal matrix not resorbed Decreased or absent cough and gag reflexes; apnea
until 35 weeks' gestation, increasing the vulnerability of the
infant to hemorrhage

Lack of fatty insulation and high surface area to body-weight ratio Hypothermia and increased oxygen consumption

*Modified from Crane, L.D. (J 995). Physical Therapy for the Neonate with Respiratory Disease. In S. Irwin & lS. TeckJin (Eds.).
Cardiopulmonary physica/therapy. St. Louis, Mosby.

resistance over the first day. In preterm infants, how­ Most significantly, the immature status of car­
ever, lung immaturity and abnormal surfactant func­ diopulmonary anatomy in preterm infants predisposes
tion (Jobe, 1988) may result in retained high pul­ them to h ypoxia under any conditions that require in­
m o na r y resistance (p o o r lung complia nce), creased oxygen (Blackburn, 1992). Cardiopulmonary
hypoperfusion, and respiratory distress syndrome pathophysiology and/or the stressors inherent to med­
(Walther, Benders, and Leighton, 1992). Persistent ical care often present challenges beyond the adaptive
pulmonary hypertension will reinforce persistent capacities of these fragile little systems.
right-to-Ieft shunting through the ductus arteriosus
(Nude! and Gootman, 1983; Rudolph, 1980). In fact,
COMMON PEDIATRIC DIAGNOSES
respiratory distress syndrome (RDS) has been identi­
fied as the best predictor of prolonged patency of duc­ The sections that follow present and discuss specific
tus arteriosus (Milne, Sung, Fok, and Crozier, 1989). cardiac and pulmonary diagnoses. Common neuro­
As the respiratory distress of the premature infant muscular or developmental diagnoses that have in­
improves with neonatal intensive care, cardiopulmonary herent to them the risk of compromised respiration or
vulnerabilities can then occur in the opposite circulatory associated cardiopulmonary disease are also dis­
direction. Given the gestationally related responsiveness cussed. The diagnoses presented are not all inclusive
of ductus arteriosus to oxygen, some preterm infants re­ but merely represent an attempt to give the reader a
tain patency of the ductus even when pulmonary vascu­ preliminary knowledge of underlying pathologies and
lar resistance falls (Archer, 1993). The result is Ieft-to­ medical management of diagnoses commonly en­
right shunting that may lead to congestive heart failure countered in the practice of pediatric cardiopul­
(Nudel and Grootman, 1983; Parks, 1988). monary physical therapy.

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 3S The Neonatal and Pediatric Patient 639

TABLE 35-2

Common Pediatric Diagnoses and Associated Heart Defects

DlAGNOSIS HEART DEFECTS

Duchenne's muscular dystrophy Cardiomyopathy (adolescence)

Fetal alcohol syndrome Ventricular septal defect

Tetralogy of Fallot
Pulmonary value stenosis
Patent ductus arteriosus

Friedreich's ataxia Ventricular hypertrophy

Congestive heart failure

HIV-l infection Myocarditis

Ventricular dysfunction

Juvenile rheumatoid arthritis Pericarditis

Marfan syndrome Aortic aneurysm

AorticlMitral insufficiency

Noonan's syndrome Dystrophic pulmonary valve (Pulmonary stenosis)

Prematurity Patent ductus arteriosus

Trisomy 13 (Patau's syndrome) Ventricular septal defect

Atrial septal defect
Patent ductus arteriosus

Trisomy 18 (Edwards' syndrome) Ventricular septal defect

Patent ductus arteriosus (large)

Trisomy 21 (Down syndrome) Endocardial cushion defect

Ventricular septal defect
Atrial septal defect
Tetralogy of Fallot

Turner's syndrome Coarctation of the aorta

Williams syndrome Supravalvular aortic stenosis

Supravalvular pulmonary stenosis

Cardiac Diagnoses
the most common heart defect during the neonatal
Patent ductus arteriosus, endocardial cushion defects, period (Musewe and Olley, 1992). In term newborns,
and tetralogy of Fallot are the cardiac defects dis­ however, PDA accounts for 10% of congenital heart
cussed within the limits of this chapter. Additionally, disease (Mitchell, Korones, and Berendes, 197 I).
Table 35-2 provides a summary of common develop­ Gestational age, the presence of lung disease, the
mental diagnoses and their associated cardiac defects. size of the ductus, and the direction of the shunt me­
d i a t e the clini c a l f e a t u r e s of P D A (Gr e e n e ,
Patent ductus arteriosus
Mavroudis, and Backer, 1994; Musewe and O lley,
Patent ductus arteriosus (PDA), already introduced as 1992). The preterm infant with very low birth-weight
a cardiopulmonary complication in preterm infants, is will have the most extreme clinical picture. An infant

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640 PART VII Guidelines for the Delivery of Cardiopulmonary Physical Thempy: Special Cases

or child with a large ductus will also have an obvious of mitral valve regurgitation (Merrill et ai., 1994).
clinical presentation. Tachycardia, an ejection sys­ For infants with complete ECD, early surgical repairs
tolic murmur, bounding peripheral pulses, increased are indicated (Bender, Hammon, Hubbard, Muirhead,
respiratory distress, and poor feeding or poor weight and Graham, 1982; Graham and Bender, 1980).
gain are the classical signs of PDA (Archer, 1993;
Tetralogy of Fallot
Greene et ai., 1994; Musewe and Olley, 1992). In the
term infant, PDA may be more clinically silent, espe­ Tetralogy of Fallot (TOF) is named for its "tetrad" of
cially when the ductus is small (Parks, 1988). defects: ventricular septal defects, right ventricular
Medical management of PDA includes nonsurgi­ outflow obstruction, right ventricular hypertrophy,
cal use of indomethacin or direct surgical closure of and aortic override (Bove and Lupinetti, 1994; Pin­
the PDA (Musewe and Olley, 1992). sky and Arciniegas, 1990). A neonate with TOF will
have symptoms dependent on the extent of right ven­
Endocardial cushion defects and
tricular tract obstruction, which results in decreased
artrioventricular defects
pulmonary blood flow and the presence of right-to­
Endocardial cushion defects (ECD) represent a spec­ left shunting (Bove and Luppinetti, 1994). The clas­
trum of defects characterized by malformation of the sic picture is one of cyanosis, especially with crying
atrial septum, the mitral and tricuspid valves, and/or (EmmanouiIides and Baylen, 1988; Pinsky and
the ventricular septum (Emmanouilides and Baylen, Arciniegas, 1990).
1988). Combinations of these defects are categorized In neonates, initial medical management may in­
as complete, transitionaVintermediate, and partial, de­ clude treatment of hypoxemia by pharmacologically
pending on degree of ventricular septal deficiency maintaining patency or reopening the ductus arterio­
(Merrill, Hoff, and Bender, 1994; Spicer, 1984). In sus for additional pulmonary blood flow (Driscoll,
the complete fOlm of ECD, all of the structures are 1990; Freedom and Benson, 1992). The elimination of
deficient. In the partial form, only an atrial septal de­ conditions that produce hypoxemia may also include
f e c t w i t h a cleft mit ral valve is present ( E m ­ pharmacological agents to increase systemic vascular
manouilides and Baylen, 1988; Merrill e t ai., 1994; resistance and decrease myocardial contractility (Bove
Parks, 1988). and Lupinetti, 1994). Surgical repairs are generally
T h e r e is marked variation in the underlying performed within the first year (Bove and Lupinetti,
anatomy of this class of cardiac defects, such that 1994; Starnes, Luciani, Latter, and Griffin, 1994).
clinical features are equally varied and difficult to in­
clusively summarize. In neonates with a complete de­
Pulmonary Diagnoses
fect, heart failure may manifest in infancy. However,
neonates with milder forms of this defect may not be The section that follows provides a brief discussion
symptomatic until much later in development (Parks, of common pulmonary disorders for which chest
1988). Additionally, endocardial cushion defects are physical therapy is indicated. Additional physical
frequently associated with other cardiac defects (Em­ therapy treatment is described later in this chapter.
manouilides and Baylen, 1988).
Hyaline membrane disease
Although the total incidence of endocardial cush­
ion defects in infancy is 1 % to 4%, the incidence in The most common respiratory disorder in premature
infants and children with Down syndrome is 40% infants is hyaline membrane disease (HMD) or infant
(Freedom and Smallhorn, 1992). In fact, in these chil­ respiratory distress syndrome (IRDS or RDS). Occur­
dren a complete ECD is the most common cardiac ring almost exclusively in preterm infants younger
malformation (Spicer, 1984). than 37 weeks' gestation, HMD results from lung im­
Operative management of infants and children maturity and an inadequate amount and regeneration
with ECD depends on the morphology of the defect, of surfactant (Phelan et ai., 1994). Surfactant func­
the degree of pulmonary hypertension, and the extent tions to decrease alveolar surface tension and thus en­

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 35 The Neonatal and Pediatric Patient 641

abies the neonate to stabilize terminal air spaces (Wal­ with severe BPD (Berman, Katz, Yabek, Dillon,
lis and Harvey, 1979). Surfactant deficiency results in Fripp, and Papile, 1986; Gerhardt, Hehre, Feller, Re­
alveolar collapse and increased effort to breathe. infenberg, and Bancalari, 1987). Right-sided heart
Clinical signs of respiratory distress resulting from failure (cor pulmonale) is a common sequelae of this
HMO occur early (usually within I to 2 hours) and disease, especially in the first few years. Addition­
persist for at least 48 to 72 hours (Farrell and Avery, ally, BPD survivors demonstrate an increased inci­
1975). Respiratory failure is 'common in these infants, dence of neurodevelopmental sequelae, including
necessitating oxygen therapy and assisted ventilation. cerebral palsy and general development delay (North­
Chest physical therapy (CPT) is commonly indi­ way, 1979; Vohr, Bell, and Oh, 1982).
cated in the management of infants with HMO. There Chest physical therapy is an important component
is usually a marked increase in airway secretions in of the management of an infant with BPD. Airway
the "recovery" state of the syndrome (after approxi­ clearance problems are common due to submucosal
mately 2 to 3 days), which is exacerbated by oxygen and peribronchial smooth muscle hyperplasia, in­
therapy and endotracheal intubation (Crane, 1981; creased mucous secretions, oxygen therapy, and fre­
Finer and Boyd, 1978). quent lower respiratory tract infections. Infants with
BPD also frequently have poor growth, which may be
Bronchopulmonary dysplaSia
a consequence of a higher resting V02, such that
As more preterm newborns survive neonatal respira­ caloric needs are greater (Weinstein and Oh, 1981).
tory distress, the prevalence of chronic lung disease
Transient tachypnea of the newborn
or bronchopulmonary dysplasia (BPD) has increased
(Parker, Lindstrom, and Cotton, 1992). Although Transient tachypnea (TTNB) is another neonatal
controversial, the etiology of BPD is usually linked problem considered in the differential diagnosis of
with positive pressure ventilation and oxygen therapy HMD/RDS. It is associated with delayed clearance of
in the treatment of respiratory distress during the amniotic fluid from the lungs, results in early presen­
neonatal period. The risk of BPD is highest in tation of respiratory distress, and is most common in
younger, low-birth-weight premature infants (Abman full-term and postterm neonates (especially if deliv­
and Groothius, 1994). ered by cesarean) (Avery, Garewood, and Brumley,
Northway, Rosan, and Porter's (1967) classic de­ 1966; Emmanouilides and Baylen, 1988). Chest
scription of BPD includes four pathological stages. physical therapy is occasionally indicated for infants
The f irst stage invo lves s ymptoms si milar t o with this problem, but TINB is uSllally self-limited.
HMD/RDS, but b y the fourth stage, BPD has pro­
Meconium aspiration syndrome
gressed to include characteristics of chronic lung dis­
ease (Voyles, 1981). Meconium is the content of fetal and newborn bow­
Clinically, infants with BPD often present with els. Although the cause of meconium passage is
rales, wheezing, cyanosis, hypoxemia, increased inci­ highly debated (Bacsik, 1977), once meconium is
dence of lower respiratory tract infections, and abnor­ present in the uterine environment the risk for aspira­
mal chest radiographs by I month postnatally tion is significant. It is generally accepted that meco­
(Abman and Groothius, 1994). Medical management nium aspiration most frequently occurs with the first
of BPD is primarily supportive. Long-term oxygen postnatal breaths of term or postterm infants (Gre­
therapy is often necessary for infants who exhibit gory, 1977), but it may also occur with gasping in
persistent severe hypoxemia. utero just before delivery (Katz and Bowes, 1992;
The cardiopulmonary outcome of BPD is variable, Wiswell and Bent, 1993). Research has supported tile
ranging from near normal pulmonary function by age contention that meconium aspiration syndrome
3 to 5 in children who had milder forms of BPD, to (MAS) is often preventable if the upper and lower
continued poor cardiopulmonary function, chronic a i r w a ys a r e s u c t i o n e d immedi atel y after b i r t h
distress, and ongoing oxygen dependence in children (Wiswell, Tuggle, and Turner, 1990). The lower air­

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642 PART VII Guidelines for the Delivery of Cardiopulmonary Physical Therapy: Special Cases

ways especially should be suctioned in infants deliv­ i n g c a u s e of s y m p t o ms in ch ildren with HIV

ered through thick, particulate ("pea soup") meco­ (Marold a, Pace, Bonforte, Kotin, Rabinowitz, and
nium in amniotic material (Gregory, 1977). Katlan, 1991). In infants with perinatally acquired
Aspiration of meconium can result in serious and HIV, pneumocyctis carnii pneumonia (PCP) fre­
devastating pathophysiology. Most commonly, the quently occurs within the first 15 months of life
meconium will partially or completely block the (Connor et aI., 1991). The risk of mortality during
peripheral airways (Wiswell and Bent, 1993). At­ the infant's first episode of PCP is high (Bagarazzi,
electasis is the classic finding, but with partial ob­ Connor, McSherry, and Oleske, 1990; Bernstein,
struction, hyperexpanded areas will also be ob­ Bye, and Rubinstein, 1989; Scott et aI., 1989).
served as a result of air that was inspired but then The clinical presentation of PCP includes failure
trapped in distal, small airways. Common compli­ to thrive, cough, dyspnea, tachypnea, fever, hypox­
cations of MAS include tension pneumothorax, per­ emia, and chest radiograph evidence of prominent air
sistent pulmonary hypertension, and bronchiolitis b r onchograms and mUltiple cysts or bullae
and pneumonitis secondary to chemical irritation (Bagarazzi et aI., 1990; Berdon, Mellins, Abramson,
from the components of the meconium (Wiswell and Ruzal-Shapiro, 1993; Bernstein et aI., 1989).
and Bent, J 993). A d d itionally, long-term pul­ PCP is most often diagnosed after bronchoalveolar
monary sequelae have been reported (MacFarlane lavage studies (Phelan et aI., 1994).
and Heaf, 1988; Swaminathan, Quinn, Stabile, Treatment is supportive and includes antibiotic
Bader, Platzker, and Keens, 1989). therapy, antiretroviral therapy, nutritional support,
Medical management of MAS is supportive, with and mechanical ventilation as needed (Bagarazzi et
supplemental oxygen and, if necessary, mechanical aI., 1990; Phelen et aI., 1994).
ventilation. Chest physical therapy is especially advo­
Asthma
cated during the first 8 hours of life, although it may
be necessary for a longer period of time if the infant Although asthma is discussed in detail in Chapter 4, a
requires assisted ventilation. discussion of pediatric pulmonary problems would
not be complete without some discussion of this com­
Pneumonia
mon cause of childhood lung disease. An estimated
Neonatal Pneumonia. The most common organisms 8% to 10% of children in the United States have
producing neonatal septicemia associated with pneu­ asthma, with asthma accounting for the most lost
monia in neonates are group B streptococcus and He­ time from school and 33% of pediatrician visits per
mophilis inJluenzae (Emmanouilides and Baylen, year (Magee, 1991).
1988). Neonatal pneumonia mimics HMD/RDS in Childhood asthma can begin at any age, and its
clinical presentation and chest radiographs. clinical etiology and clinical course are variable.
Aspiration Pneumonia. Aspiration is an unfortunate Children with early medical histories including very
result of small children's "indiscreet curiosity" (War­ low birth weight, bronchopulmonary dysplasia, and
ing, 1975) in exploring their environment and relying respiratory syncytial virus infection may be at in­
on their mouths for sensory learning. Aspiration can creased risk for developing asthma (Pullen and Hey,
also result from gastroesophageal reflux and de­ 1982; Rickards, Ford, Kitchen, Doyle, Lisseden, and
creased upper airway neuromuscular control (Oren­ Keith, 1987; Smyth, Tabachnik, Duncan, Reilly, and
stein and Orenstein, 1988). Levison, 1981).
Bronchial drainage techniques are often indicated Medical management usually includes avoidance
as part of the medical management of infants and of known precipitants, adrenergic drugs, and corti­
children after aspiration to aid with airway clearance costeroids (in chronic, severe cases). Chest physical
and reduce the possibility of bacterial superinfection. therapy for this disease includes patient and family
Pneumocystis Carnii PneumonialHIV-lnJected education in breathing control, relaxation, effective
Children. Pulmonary involvement is often the lead­ coughing, and exercise. Older children, in paJticular,

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 35 The Neonatal and Pediatric Patient 643

may benefit from CPT especially when they are re­ breathing (ACB) technique, use of a positive expira­
sponding slowly to pharmacological treatment alone tory pressure (PEP) mask, autogenic drainage (AD),
(Asher, Douglas, Airy, Andrews, and Trenholme, and use of the flutter device, have been shown to be
1990). Exercise, also highly effective in the treatment effective in assisting sputum expectoration, often in
and management of asthma, is discussed in a later greater amounts and in less time per treatment
section on pulmonary rehabilitation. (Konstan, Stern, and Doershuk, 1994; Mahlmeister,
Fink, Hoffman, and Fifer, 1991; Pryor, 1991; Pryor
Cystic fibrosis
and Webber, 1979; Schoni, 1989).
Cystic fibrosis (CF) is a complex autosomal-reces­ Although postural drainage, percussion, and vibra­
sive disorder that affects the exocrine glands. Defini­ tion remain the treatment of choice for infants and
tive diagnosis of CF includes positive family history, children who are unable to be instructed in tech­
obstructive pulmonary disease, recurrent pulmonary niques that use patterns of voluntary breathing, other
infection, intestinal malabsorption and poor growth, techniques are available for children who can follow
the presence of Slaphylococcus aur eus or specific breathing instructions and who can perform a
Pseudomonas aeruginosa i n the respiratory tract, reliable pulmonary function test. Children as young
and, most importantly, a positive sweat chloride test as 2 to 3 years can be taught to "huff' as part of FET
(Cystic Fibrosis Foundation, 1990). (Pryor, 1991), the PEP mask has been used with chil­
The chronic pulmonary disease in CF is related dren as young as 3Y2 years (Mahlmeister et aI., 1991),
to increased secretion of a b n o rm a lly v i s c o u s and AD can reportedly be taught to children as carly
mucus, impaired mucociliary transport, airway ob­ as 4 to 6 years of age (DeCesare and Graybill, 1990;
struction, bronchiectasis, overinflation, and infec­ Sci1oni, 1989). The benefits of each technique should
tion. Radiographic changes are most pronounced in be carefully considered relative to each child's cogni­
the upper lobes, especially the right (Wood, Boat, tive, respiratory, and motor planning abilities when
and Doershuk, 1976). choosing or modifying the child's program for airway
The early institution of prophylactic pulmonary clearance.
physical therapy, including postural drainage and the Ventilatory muscle training is an important aspect
judicious use of antibiotics, provides effective mea­ of pulmonary treatment in older children with CF.
sures for controll ing or slowing the effects of bron­ Studies have demonstrated that training to improve the
chiolar and bronchial obstruction. Involvement of the endurance of ventilatory muscles decreases dyspnea
child and family in pulmonary care is particularly im­ and increases general exercise tolerance in patients
portant. Family understanding of the nature of the with CF (Keens, Krastins, Wannamaker, Levison,
disease and the purpose of each therapeutic measure Crozier, and Bryan, 1977; Reid and Loveridge, 1983).
promotes successful management of the child. A The role of general exercise in the cardiopul­
home program of CPT should be established for each monary management of children with CF is specifi­
child, taking into consideration the child's ongoing cally discussed within the context of pulmonary reha­
pulmonary needs and the family's unique contribu­ bilitation. However, it is important to realize that
tions and constraints. some debate exists as to whether exercise can replace
Bronchial drainage is an aspect of conventional more traditional airway clearance techniques. Pryor
treatment for CF that in recent years has gained sev­ (1991) has suggested that exercise should be an addi­
eral options that allow both efficacy and patient in­ tional component rather than a substitute for breath­
dependence (Davis, 19(4). Airway clearance tech­ ing techniques. Cerney (1989) in contrast, reported
niques are described in detail in Chapter 20, but that some children with mild disease may be able to
alternatives to traditional percussion and postural use regular exercise in place of bronchial drainage
drainage warrant mention within the context of CPT treatments. The severity of the disease process and
for children with CF. Specifically, the forced-expi­ the child's condition at any one point in time, will
ration technique (FET) as part of the active cycle of clearly mediate the appropriateness and effectiveness

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644 PART VII Guidelines for the Delivery of Cardiopulmonary Physical Therapy: Special Cases

of exercise as either a component or as a primary These deviations and other aspects of ventilatory
means of airway clearance. compromise are discussed with regard to motor diag­
noses common to pediatric practice.
Special respiratory problems associated
with intubation and tracheostomy Cerebral palsy
Once an infant or child develops respiratory failure, Children with cerebral palsy generally have weak trunk
intubation and mechanical ventilation are usually re­ and postural muscles, which, when combined with atyp­
quired. The goals of medical management are then to ical neural mechanisms, produce atypical movement
treat the cause of the respiratory failure as aggres­ pattems and functional alignment deviations. The trunk
sively as possible and to wean the child from me­ and respiration relationshi[ls described in Table 35-3 are
chanical ventilation as quickly as possible. consistent with the clinical picture of external pul­
If a child's condition necessitates long-term me­ monary development in children with cerebral palsy.
chanical ventilation, or if an artificial airway is needed Although the extent of mobility impair ment is
to bypass an upper airway obstruction, a tracheostomy variable between children, hypoventilation, increased
is usually petformed (Scott and Koff, 1993). work to breathe, inefficient cough, increased risk for
Infants and children who have a tracheostomy and aspiration, and poor breath support for vocalization
are intubated for long periods of time require vigorous can occur (Alexander, 1993). Limited active mobility
prophylactic airway management, such as bronchial and the use of habitual patterns with little deviation
drainage and airway suctioning. Chest PT, including
postural drainage and vibration emphasizing right
upper lobe segments, has been shown to significantly
decrease the incidence of postextubation atelectasis in
infants intubated for more than 24 hours (Finer, Mori­
artey, Boyd, Phillips, Stewart, and Ulan, 1979).

Pulmonary Considerations in Neuromuscular

and Motor Diagnoses

Although cardiopulmonary symptoms may not be

the primary reason for referral to physical therapy in
children with neuromuscular and general motor de­
velopmental diagnoses, these children do have motor
involvement that can result in respiratory and pos­
tural muscle weakness, immobile chests, and hy­
p oventilation. Furthermore, many of these children
have had medical histories remarkable for cardiopul­
monary complications or have diagnoses that entail
progressive processes that will result in cardiopul­
monary compromise.
Table 35-3 provides an extensive summary of the
interactions between trunk musculature and ventila­
tion in children with atypical development. Although
the biomechanical deviations noted are frequently
seen in children with atypical tonal presentations, FIGURE 35-1
they are also common in children with scoliosis, ster­ Flattened anterior chest with marked rib flaring in a child
nal deformity, or general immobility of the thorax. with cerebral palsy.

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 35 The Neonatal and Pediatric Patient 645

TABLE 35-3

Functional Relationships of Trunk Control and Respiration

BIOMECHANICAL POSTURAUfRUNK CONTROL RESPIRATORY

COMPONENT CONSEQUENCES CONSEQUENCES

Weak abdominal obliques Passive lumbar lordosis Ineffective cough

Protruding tummy High chest
Lower rib flaring Retained horizontal rib alignment
Decreased trunk rotation
Unable to weight shift Tight rectus abdominis may lead to
Dependence on rectus abdominis pectus excavatum
Child may use diapl1ragm for trunk
control, limiting its function as a
primary muscle of respiration

Decreased support of abdominal

contents under diapmagm

Tight pectoralis minor Forward shoulders Anterior upper chest cannot adequately
Scapula pulled laterally and anteriorly, expand
away from the thoracic wall
Upper thoracic flexion

Weak serratus anterior Wcak upper fibers-medial edge of Decreased structural reinforcement
scapula Icaves the thoracic wall of the posterior chest wall
Interdigitation of the lower fibers of
serratus anterior with the external
abdominal oblique will interact to
affect the dynamic stability of the
rib cage

Decreased active upper Kyphotic upper trunk Approximation of upper ribs -7

thoracic extension Passive overlengthening of the decreased upper chest mobility -7

scapular retractors decreased oxygenation of the upper

lobe -7 abdominal breathing

Decreased rib cage stability Serratus anterior will elevate the ribs Decreased structural support for the
rather than stabilize the scapula respiratory muscles to work from
against the thoracic wall

Modified from Moerchen V A: Respiration and motor development: a systems perspective, Neural Rep 18 (3): 8-10, 1994. Reprinted from
the Neurology Report with the permission of the Neurology Section, APTA.

of the center of gravity beyond the base of support chest excursion and should be incorporated into a
contribute to thoracic stiffness. A high chest, flat­ home program. Mobilization of the ribs and thoracic
tened anteriorly, with excessive rib flaring, is com­ spine are important precursors to improving chest ex­
mon in these children (Figure 35-l). cursion during ventilation.
Therapeutic attention to respiration should first Chest PT may be indicated if the child develops a
identify possible aspiration and suggest modifications primary pulmonary complication. Prophylactic pos­
for positioning during feeding. Additionally, certain tural drainage can also be integrated into many sen­
postures for sleep and play may be less restrictive for sory stimulation programs for more severely involved

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646 PART VII Guidelines for the Delivery of Cardiopulmonary Physical Therapy: Special Cases

children. Additional "handling" to address ventilatory

function will be discussed in a subsequent section on
motor approaches to respiratory treatment.

Myelomeningocele
Myelomeningocele or spina bifida are diagnoses that
physical therapists generally equate with issues of am­
bulation and mobility. However, central ventilatory
dysfunction is prevalent in infants, children, and ado­
lescents who also have an associated Arnold-Chiari
type II malformation (Hays, Jordan, McLaughlin,
Nickel, and Fisher, 1989; Swaminathan et aI., 1989;
Ward, Jacobs, Gates, Hart, and Keens, 1986).
The Arnold-Chiari type II malformation, which oc­
curs in 90% of infants with myelomeningocele, is a
hindbrain malformation consisting of a caudal helllia­
tion of the cerebellum and brain stem into the cervical
canal (Charney, R orke, Sutton, and Schut, 1987).
Ventilatory problems associated with a symptomatic
Arnold-Chiari type II malformation include inspira­
tory stridor (vocal cord paralysis), central apnea, and
respiratory distress (Hays et aI., 1989; Hesz and Wol­
raich, 1985; Oren, Kelly, Todres, and Shannon, 1986).
However, abnormal ventilatory patterns have also
FIGURE 35-2
been observed in asymptomatic infants (Ward et aI.,
An 8nterior cut-out and elastic support in a body
1987) and adolescents (Swaminathan et aI., 1989).
jackel/spinal orthosis aids diaphragm function.
Ventriculoperitoneal shunting (management of hy­
drocephalus) and, if necessary, cervical decompres­
sion are the surgical approaches to treatment of life­
threatening ventilatory complications in this population.
Down syndrome
Other p u lmonary issues in c h ildren with Impaired pulmonary function in children with Down
myelomeningocele warrant discussion. TtUnk weakness syndrome is clearly related to generalized weakness of
and hypotonia are observed early in the motor develop­ trunk musculature (Dichter, Dm·bee, Effgen, and Pal­
ment of infants and toddlers who have shunted hydro­ isano, 1993). The postural deviations common in these
cephalus. Additionally, in children with thoracic and children reflect (Figure 35-3) inefficient muscle func­
high lumbar level lesions, abdominal muscle SUpp0l1 for tion for both ventilation and movement (Moerchen,
diaphragm function may be insufficient. The use of ab­ 1994). Again the ttUnk-ventilation relationships delin­
dominal binders, and spinal othoses/body jackets with eated in Table 35-3 summarize the subtle but significant
(anterior) diaphragm cut-outs and an elastic inse11 are clinical presentation of external pulmonary develop­
indicated to aid in diaphragm function (Figure 35-2). ment in these children. Too often only motor develop­
Although progressive scoliosis is not the natural history ment is addressed by physical therapists who are treat­
of children with spina bifida, it is a symptom of unstable ing children with Down syndrome. Respiration needs to
neurology (tethered cord), and attention to ventilatory be considered if therapy goals include increased vocal­
ability is necessary both for general monitoring and for izations or improved tolerance for exercise.
possible preoperative evaluation. Pulmonary hypoplasia may also challenge the res­

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 35 The Neonatal and Pediatric Patient 647

FIGURE 35·3
A, Characteristic posture of a child with Down syndrome/hypotonia. Note the abdominal protrusion
and sternal retraction. B, Rib flaring with upper extremity movement; the abdominal obliques are
not stabilizing the lower ribs.
Photos from Moerchen, V.A. (1994). Respiration and Motor Development: a Systems Perspective.
Neurology Report, 18(3), 8-10. Reprinted with the permission of the Neurology Section, APTA.

piratory function of these children. Cooney and Thurl­

Muscular dystrophy
beck (1982) observed a consistent combination of de­ Duchenne's muscular dystrophy involves end-stage
creased numbers of alveoli and larger alveolar ducts respiratory failure that results from progressive respi­
in individuals with Down syndrome, not related to age ratory muscle weakness, thoracic deformity, reduced
or incidence of heart disease. Although these re­ lung compliance, retained secretions, ventilation­
searchers had a small sample size, their results do sug­ peIi'usion imbalance, and hypoxemia (Bach, O'Brien,
gest that trisomy 21 may result in lung vulnerability. Krotenberg, an d Alba, 1987; Smith, C alverley,

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648 PART VII Guidelines for the Delivery of Cardiopulmonary Physical Therapy: Special Cases

Edwards, Evans, and Campbell, 1987). In 70% to

niIe rheumatoid arthritis (JRA) may have inflamma­
90(;1(:
tion of thoracic joints or may splint through their
strictive respiratory complications (Bach et aI., 1987;
trunks when they try to move painful extrcmities.
Smith et aI., 1987).
With thcsc children, brcathing exercises will have a
Physical therapists are typically involved in treat­ role both in pulmonary carc and in pain management.
ment of these paticnts for preservation of motor func­ Put simply, children who make cumpensatiuns in
tion. Early attention to ventilation, however, is war­ their movement patterns to accomlllodate pain, weak­
r a n t ed. P r o phyla c t i c spi n a l f u s i o n to pre v e n t ness, or deformity, may limit the mechanics of their
scoliosis-related compromise o f ventilation i n these thoraces. Con versel y. chi I dren who cannot ade­
patients considers both the progrcssion of the spinal quately oxygenate may make compensations in their
curvature and vital capacity (YC) (Rideau, Glorion, movement patterns to SUpp0l1 ventilation. Clearly, at­
Delauber, Tarle, and Bach, 1984). tention to ventilation should be an inherent aspect of
Chest physical therapy should be a component of observing motor development and quality of move­
the overall rhysical therapy management of children ment in all children.
with muscular dystrophy. Deep breathing, coughing,
and activitics to addrcss cndurance arc recommended
PHYSICAL THERAPY TREATMENT APPROACHES
but will require ongoing modification as the disease
progresses. Inspiratory muscle training in these chil­
Postoperative Pediatric Cardiac Rehabilitation
dren remains controversial. Although some researchers
havc del11on. trated improved endurance of ventilatory Postopcrative physical therapy consists largely of
muscles (DiMarco, Kelling, DiMarco, Jacobs, Shields, techniques to increase respiration, mobilize secretions,
and Altose, 1985; Martin, Stern, Yeates, Lepp, and Lit­ and progress physical mobility. Positional rotation for
tle, 1986; Stern, Martin, Jones, Garrett, and Yeates, pulmonary care is pussible if the child has a stabilized
1991), other researchers have suggested that inspira­ sternum. Breathing exercises and coughing will need
tory resistance may over-tax respiratory muscles that to be modified based on the child"s age and cognitive
are all'eady near fatigue due to working against incom­ level. Huckabay and Daderian (1990) reported im­
pliant structures (lungs, thorax) (Smith, Coakley, and proved postoperative cooperation in children 3 to 10
Edwards, 1988). years of age when choice making was incorporated
Respiratory dependence does occur as the disease into a breathing program.
progresses. Protocols for point of initiation and type Immobilization after cardiac surgery is to be
of mechanical ventilation are being studied. There is, avoided as much as medically possible. Passive range
however, agreement that close monitoring of YC and of motion may be initiated immediately, with care to
of nocturnal hypoventilation can allow respi ratory avoid compromising arterial lines. Ambulation is
support to be implemented before the onset of acute generally initiated once the child is extubated and has
respiratory failure (Bach, Alba, Pilkington, and Lee, had atrial and groin lines removed (Johnson, 199 I).
1981; Bach et aI., 1987; Curran, 198 I). Child and family education as part of pediatric
cardiac rehabilitation has been observed to reduce
Miscellaneous conditions parent and child anxiety related to safe levels of
Multiple other pediatric diagnoses and musculoskele­ pllysical activity (Balfour, Drimmer, Nouri, Penning­
tal conditions include clinical presentations (strength, ton, Hemkens, and Harvey, 1991; Calzolar et ai,
alignment, and limited mobility) that should cue the 1990; Mathews et ai, 1983). Although studies of pe­
therapist'S attention to pulmonary function. Syn­ diatric cardiac rehabilitation have been focused on
dromes that involve sternal deformity such as Marfan children older than 6 years, monitored exercise has
syndrome or Poland's syndrome will clearly entail been shown to safely produce an increase in peak
possible ventilatory compromise. Children with juve­ oxygen consumption and a decrease in resting heart

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 35 The Neonatal and Pediatric Patient 649

r a t e (B a l f o u r, Dri m m e r, Nouri, P e n n i n g t o n, of lymph nodes, making it vulnerable to extrinsic

Hemkins, and Harvey, 1991; Calzolari et aI., 1990; compression. Important considerations and essentials
Mathews et aI., 1983). of a positional rotation program for infants are out­
Exercise prescription for cardiopulmonary rehabili­ lined in the box below.
tation of older children who have undergone cardiac re­ It is important to note that premature infants do
pairs at an early age will require careful monitoring. tolerate and benefit from prone positioning. Studies
Lower exercise V02 values, lower cardiac output, and have demonstrated improved oxygenation, tidal vol­
lower values of diffusion capacity of the lung for car­ ume, dynamic lung compliance, and synchrony of
bon monoxide have been observed in response to exer­ chest wall movement when preterm infants are put in
cise in children who have undergone cardiac surgery as prone positions (Hutchinson, Ross, and Russell,
compared with the responses of age-matched controls 1979; Lioy and Manginello, 1988; Martin, Harrell,
(Gildein, Mocellin, and Kaufmehl, 1994; Tomassoni, Rubin, and Fanaroff, 1979).
Galioto, and Vaccaro, 1991). Exercise recommenda­ Positional rotation is generally performed manu­
tions include submaximal performance (Tommassoni et ally every 2 hours, and, although this provides pul­
aI., 1991) and technique training to increase the biome­
chanical efficiency of movement while decreasing the
associated metabolical costs (Gildein et aI., 1994).

Essentials of a Positional ROUl/ion Program

Chest Physical Therapy for Neonates and Infants I. Care should be taken to coordinate any change
in the infant's position with other nursing proce­
The plimary goal of chest physical therapy for neonates
dures to avoid unnecessary stimulation.
and infants is to improve airway clearance. If tech­
2. Infants should never be left unattended when in
niques of bronchial drainage can increase the diameter
a head-down position.
of the airways through secretion mobilization, then
3. Vital signs should be monitored closely by res­
ventilation may also be improved and the work of
piration and heart rate monitors. The alarms
breathing reduced. These techniques should be judi­ should be turned on.
ciously applied for prophylaxis and treatment in infants
4. The infant's chest should be auscultated for ad­
who have or are at risk for developing airway clearance ventitious breath sounds after positioning.
problems. Applying bronchial drainage techniques to
5. While the infant is in a drainage position, secre­
infants requires a thorough understanding of each in­ tions will be more easily mobilized. The infant's
fant's condition and the precautions and considerations trachea or endotracheal tube should be suctioned
inherent to any technique or combination of techniques. as needed.

6. Avoid placing the infant in a head-down posi­

Positional rotation tion for approximately I hour after eating to
avoid aspiration of regurgitated food.
Frequent changing of position will prevent prolonged
dependency of any one portion of the lung, so that 7. Any change in the infant's position should be
done slowly to minimize stress on the cardiovas­
pooling of secretions can be limited/avoided and im­
cular system.
proved ventilation can be achieved (Menkes and
8. Infants with umbilical arterial lines can be
Britt, 1980; Ross and Dean, 1989). Whereas posi­
placed on their abdomens. However, one should
tional rotation programs for adults emphasize the
always check that the line has not been kinked.
lower lobes, positional programs for infants must em­
9. Some infants might require modified drainage
phasize all lung areas (Figures 35-4 to 35-6). The
positions. Infants with severe cardiovascular in­
upper lobes and right middle lobe are common sites stability or suspected intracranial bleeding
of airway collapse and atelectasis in infants, and the should not be placed in a head-down position.
right middle lobe bronchus is surrounded by a collar

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650 PART VII Guidelines for the Delivery of Cardiopulmonary Physical Therapy: Special Cases

J. ��

FIGURE 35-4
Sequence for positional rotation.
Position I.-Segments that come off the left lower bronchus posteriorly are drained by positioning
the infant on his right side, three-foUl1hs prone with a head-down angle. Position 2.-The posterior
segment of the right upper lobe is drained by positioning on the left side, three-fourths prone with
the bed flat. Position 3.-The anterior segments of the upper lobes are drained by positioning
supine with the head of the bed elevated or flat. Position 4.-Segments that come off the right
lower lobe bronchus posteriorly are drained by positioning on the left side, three-fourths prone with
a head down angle.

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 35 The Neonatal and Pediatric Patient 651

4.

5.

FIGURE 35-4-cont'd
Position 5.-The posterior segment of the left upper lobe is drained by positioning on the right
side, three-fourths prone with the head of the bed elevated. Position 6.-Segments that come off
the tracheobronchial tree anteriorly are drained by positioning supine with a head-down angle.
Positu)1Is 7 and 8.-Segments such as the right middle lobe or lingula that come off the
tracheobronchial tree anterolaterally will be drained in a three-fourths spine position, slightly head
dow (see Figure 35-5, p. 652).
NOTE: Babies on ventilators may also be positioned prone. This is usually done by the therapist
rather than in a routine positional rotation (see Figure 35-6, p. 652).

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652 PART VII Guidelines for the Delivery of Cardiopulmonary Physical Therapy: Special Cases

FIGURE 35-5 FIGURE 35-6

Three-fourths supine position for right middle lobe. Lingula Premies (even those on ventilalOrs with numerous
is the same three-fourths supine position with the patient catheters) may be placed prone when care is taken.
lying on his right side.

monary benefit, it may also contribute to the disrup­ ing less than 800 grams) usually require and benefit
tion of homeostasis that has been documented to from modification of the head-down position. Hori­
occur in the course of neonatal intensive care (Long, zontal to slightly elevated positioning of the head may
Philip, and Lucey, 1980; Yeh, Lilien, Leu, and be best (Thoresan, Cowan, and Whitelaw, 1988). This
Pildes, 1984). Use of nursery beds that provide con­ modification primarily is due to the high incidence of
tinuous positional oscillation (from right side to intraventricular hemorrhage in premature infants
supine to left side, and so forth) might provide an op­ (Crane, Zombek, Krauss, and Auld, 1978; Emery and
tion that allows the benefits of position change while Peabody, 1983). Other precautions for Trendelenburg
also minimizing the homeostatic disruption. Murai positioning of infants include but are not limited to
and Grant (1994) demonstrated that continuous posi­ abdominal distention, congestive heart failure, dys­
tional oscillation as part of a total chest physical ther­ rhythmias, hydrocephalus, frequent episodes of apnea
apy program decreased the duration of oxygen sup­ and bradycardia, and acute respiratory distress.
p l e m e n t a ti o n w i t h o u t a d v e r s e ly e f f e c t i n g t h e
cardiopulmonary status o f the neonates.
Chest percussion and vibration
Percussion and vibration are used in conjunction with
Postural drainage postural drainage to augment the effect of gravity in
Postural drainage (PD) positions to promote gravity­ the removal of secretions. There are several ways to
assisted drainage of specific segmental airways can be perform percussion on infants. For a larger infant, it
safely applied to infants and children. In the acute care is possible to use a cupped hand, similarly to per­
setting, however, many of the head-down positions cussing an adult's chest. For a smaller infant, some
are modified according to tolerance and precautions or modification of this technique is needed. Chest per­
contraindications (Table 35-4). The rule for modifica­ cussion for a smaller infant is accomplished by the
tion of any position for PD is that the position used use of tenting three fingers, four fingers, or using any
should be as close to the classical (anatomically cor­ of the commercially available percussion devices
rect) position for that segment as safely possible. Ex­ made for neonates (Figure 35-8). A small anesthesia
amples of the classical PD positions for each bron­ mask or "palm cup" can also be used effectively.
chopulmonary segment are pictured in Figure 35-7. Precautions for chest percussion in the infant in­
Tiny infants (especially premature infants weigh- clude but are not limited to unstable cardiovascular or

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 3S The Neonatal and Pediatric Patient 653

TABLE 35-4

Precautions and Contraindications for Postural Drainage in a Neonate*

POSITION PRECAUTION CONTRAINDICA TlON

Prone Umbilical arterial catheter Untreated tension pneumothorax

Continuous positive airway pressure
·in nose
Excessive abdominal distention
Abdominal incision
Anterior chest tube

Tendelenburg position Distended abdomen Untreated tension pneumothorax

(head down) SEHlIVH* (grades I ancllI) Recent tracheoesophageal fistula repair
Chronic congestive heart failure or Recent eye or intracranial surgery
cor pulmonale Intraventricular hemorrhage (grades III
Persistent fetal circulation and IV)
Cardiac dysrhythmias Acute congestive heart failure or cor
Apnea and bradycardia pulmonale
Infant exhibiting signs of acute
respiratory distress
Hydrocephalus
Less than 28 weeks' gestational age

'Subependymal hemorrhage/intraventricular hemorrhage.

From Crane LD: Physical therapy for the neonate with respiratory disease. ln [rwin S, Tecklin JS, editors: Cardiopulmonary physical
therapy, SI. Loui" 1995, Mosby.

oxygenation status (although percussion may be pro­ bration will depend on the day-to-day medical status of
vided safely if continuous transcutaneous monitoring the infant and the infant's response to treatment.
is available), coagulopathy, subcutaneous emphy­
sema, or intraventricular hemorrhage. Additionally,
Airway suctioning
percussion is generally contraindicated over a healing Sterile airway suctioning is discussed in detail in
thoracotomy incision or if the child displays ilTitabil­ Chapter 42. However, some special considerations
ity and signs of rcspiratory distress with the treatment. for suctioning the a i rway of an infant need to be
Vibration is accomplishcd either through manual vi­ highlighted (Durand, Sangha, Cabal, Hoppenbrowers,
bratory motion of the therapist's fingers on the infant's and Hodgman, 1989; McFadden, 1981; Perlman and
chest wall (Figure 35 -9) or through the use of a me­ Volpe, 1983).
chanical vibrator. An electric toothbmsh can be adapted 1. If possible, suction with a transcutaneous oxy­
by padding the bristle portion with foam (Cun'an and gen monitor in place. These monitors give con­
Kachoyeanos, ) 979). Vibration has been observed to tinuous feedback regarding the infant's oxy­
occasionally increase irritability and may be less well genation status.
tolerated than percussion. The most common precau­ 2. Bagging should be done only with a bag at­
tion for vibration is increased irritability with the devel­ tached to a pressure manometer to ensure that
opment of bradycardia alld respiratory distress. sufficient prcssures are being used without ex­
The decision to use chest percussion and vibration ceeding the maximum safe le v els (these l imits
will depend on the reviewed principles and precautions, should be similar to the ventilator settings).
the medical condition of the infant, and the infant's tol­ 3. Suction for no more than 5 seconds with each
erance to handling. Continuation of percussion and vi­ catheter withdrawal.

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654 PART VII Guidelines for the Delivery of Cardiopulmonary Physical Therapy: Special Cllses

A - --:--- '- B

C :.- D

FIGURE 35-7
Postural drainage with an infant. A, Both upper lobes-apical segments. B, Left upper lobe-­
anterior segment. C, Right upper lobe-anterior segment. D, Lingula.

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 35 The Neonatal and Pediatric Patient 655

E F

G H

FIGURE 35-7-cont'd
E, Right middle lobe. F, Right upper lobe-posterior segment. G, Left Lipper lobe-posterior
segment. H, Both lower lobes-apical (superior) segments.

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656 PART VII Guidelines for the Delivery of Cardiopulmonary Physical Therapy: Special Cases

FIGURE 35-7-cont'd
I, Both lower lobes-anterior basal segments. J, Left lower lobe-lateral basal segment; Right
lower lobe arduac (medial) segment. K, Both lower lobes-posterior basal segments. L, Right
lower lobe-lateral basal segment.

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 35 The Neonatal and Pediatric Patient 657

FIGURE 36-8
'Tenting" of the finger for percussion of premies or small children.

FIGURE 36-9
Manual chest wall vibration of a premie.

4. Infants should be carefully hyperoxygenated tions and imitating a therapist's demonstration of deep
when hyperventilated so as to minimize hyper­ breathing, coughing, and active exercise. Chest physi­
oxia and hypoxia. Bagging usually does not cal therapy in children is focused on improving venti­
need to continue for more than 5 to 10 seconds lation, improving the efficiency of breathing, increas­
to maintain adequate oxygen levels. ing general strength and endurance with an emphasis
5. Monitor the blood pressure of preterm infants be­ on muscles of respiration, improving posture, and ad­
fore, during, and after suctioning. Change in dressing relaxation, breathing control, and pacing.
blood pressure may indicate increased intracra­ The application of chest PT with children often re­
nial pressure and risk for intracranial hemOtThage. quires patience and creative adaptation (Figure 35-
10). The challenge is to make it seem less like a treat­
ment and more like a game. It is important, however,
Chest Physical Therapy for Children
to be honest in your explanations and to speak to the
The goals for chest physical therapy with children (2 child with respect and at a level appropriate to the
years and older) include more than improving airway child's age and development.
clearance. Children are capable of following direc­ Involving the family in PT treatment of a child can

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658 PART VII Guidelines for the Delivery of Cardiopulmonary Physical Therapy: Special Cases

FIGURE 36-10
A, B, C, Few areas of health care delivery require creative adaptation and problem solving to the
extent that pediatrics does.

be invaluable. In some cases the parent may do most tant to have his position changed, changing the loca­
of the "hands-on" and repeat instructions to the child tion of the television may be helpful. Be creative!
under the direct guidance of the therapist. This Young Children. In younger children (18 months to 3
arrangement will also help reinforce parent and fam­ years) deep breathing is usually encouraged by blow­
ily education for carry-over of home therapy. ing bubbles, tissue paper, mobiles. or simple horns. To
achieve maximal chest expansion, the child should be
Positional rotation
positioned on each side while playing blowing games
The goal of positional rotation and postural drainage or singing. The theory behind the side lying position is
is to prevent the accumulation of secretions and to aid that the downside lung ventilates more effectively (see
in their removal. Any child who is immobile, receiv­ Chapter 18). Additionally, if the poorly ventilated
ing artificial ventilation, or not expanding his chest lung is uppermost, stretch techniques can facilitate
adequately should have his position changed at least deeper breathing (see Chapter 22).
every 2 hours. Recall that positional changes will en­ Spontaneous coughing in younger children often
hance oxygen transport and promote pulmonary occurs with a change in position or with crying. For
drainage (Ross and Dean, 1989). If the child is reluc­ the child who does not cough spontaneously or whose

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 35 The Neonatal and Pediatric Patient 659

FIGURE 35-11
Whistles such as these encourage increased inspiration and controlled, sustained expiration to make
the whistle components move (left: a fish with a wheel that moves at its back fin; middle: a race car
that drives around a track making whirling sounds; right: a ball that moves up and down in a train).

cough is inadequate to clear secretions, nasopharyn­ treat ment by therapists helps to decrease the inci­
geal suctioning may be necessary. dence of postoperative complications.
Older Children. School-age children can be more Preoperative teaching is extremely important for
specifically instmcted in various breathing exercises, both the child and the family. Parents can often be
such as diaphragmatic breathing, pursed-lip breathing, more anxious than the child, so patient and family ed­
and segmental lateral costal breathing. They may also ucation is important. The level of preoperative train­
be candidates for using relaxed deep breathing for ing with the child will depend on the child's age.
control and pacing of activity. Cooperation with this If the child is very young (under 2 years), the thera­
age group, however, still remains higher if some as­ pist will meet with the parents and explain the purpose
pect of therapy is fun. Elaborate whistles are available of bronchial drainage treatments, potential airway clear­
that encourage deep breathing as a fun means to an ance problems, and possible complications. The pre­
end of making the whistle components move (Figure ventative nature of these treatments should be stressed,
35-11). Additionally, pediatric incentive spiro meters and procedures that might be done with the child after
are available with cheerfull"cool" pictures to make surgery should be demonstrated and discussed. These
respiration exercises more like a game (Figure 35-12). might include: (I) positioning, (2) chest percussion,
Older children (not infants) can be stimulated to (3) vibration, and (4) airway suctioning. In addition, al­
cough by applying a firm pressure over the trachea in ways allow time for the parents to ask questions.
the suprasternal notch. Beware t h a t coughi ng, If the child is able to understand simple concepts,
whether spontaneous or stimulated, may elicit gag­ the therapist can, in addition to parent orientation, in­
ging and vomiting, especially if airway clearance is stmct the child in various breathing games, use of an
scheduled too soon after a child has eaten. incentive spirometer, coughing, and general upper
and lower extremity exercises.
Preoperative and postoperative care In older children (8 years or older), postoperative
The efficacy of postoperative chest PT is highly re­ procedures can be explained and demonstrated. The
lated to preoperative care. The appropriate applica­ importance of bronchial hygiene should be stressed
tion of preoperative assessment, instruction, and during demonstration of deep breathing and cough­

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660 PART VII Guidelines for the Delivery of Cardiopulmonary Physical Therapy: Special Cases

are atelectasis, infection secondary to pooling of se­

cretions, and airway obstruction. Infants and children
with the following characteristics will be at risk for
developing postoperative pulmonary complications:
(I) preexisting lung disease, (2) thoracic or upper ab­
dominal location of the incision, (3) prolonged post­
operative bedrest or restricted mobility, and (4) neu­
romuscular involvement that affects the ability to be
mobile and to cough and deep breathe.
Postoperative treatments generally focus on in­
creasing ventilation, coughing, and active mobility.
Specific bronchial drainage is used only if the child is
unable to clear his or her airways or is at risk due to
chronic lung disease.
After high abdominal or thoracic surgery, there
may be a tendency for the child to splint on the side
of his or her incision. Arm, shoulder, and trunk
movement should be encouraged to prevent any post­
operative complications. For the younger child, chest
mobility can be encouraged by clapping the hands
overhead or by dramatizing songs such as The Itsy
Bitsy Spider. More conventional exercises may be
taught to the older child.
Children tend to mobilize very quickly (unless
their movement is limited secondary to motor in­
volvement or to a specific surgical procedure). Once
the child is out of bed and moving about, with clear
lungs and an effective cough, postoperative CPT
treatments can generally be discontinued.

FIGURE 35-12
A pediatric incentive spirometer. (Photo provided courtesy Pediatric Pulmonary Rehabilitation
of DHD Medical Products. Used by permission.)
Rehabilitation programs for pediatric patients with
chronic lung disease include the same components
and have essentially the same goals as adult pul­
ing. The child can be shown how to splint the inci­ monary rehabilitation. The major difference is related
sion using a pillow or stuffed animal to assist with to different diagnoses being most prevalent in the
comfort while coughing. Do not tell the child that children versus adult age groups. Asthma and CF are
coughing will not hurt; be honest but reinforce that the most common diagnoses of children who are can­
splinting will help. Teach the child diaphragmatic didates for pulmonary rehabilitation.
and pursed-lip breathing with an inspiratory-hold ma­
neuver, and, if appropriate, teach the child how to use
Exercise and asthma
an incentive spirometer. Exercise and conditioning are very important compo­
Postoperative pulmonary complications may not nents of the treatment of the child with asthma. Im­
be as prevalent in the pediatric age group as in adults, proved chest and trunk mobility, control of breathing,
but they still occur. The most common complications strength, posture, and an increased tolerance to exer­

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 35 The Neonatal and Pediatric Patient 661

cise are all goals that can be addressed in the design oxygen desaturation during exercise in children with
of exercise programs for these children (Magee, CF (Coates, 1992). Loutzenhiser and Clark (1993),
1991; Seligman, Randel, and Stevens, 1970). however, suggested that severity of CF is not the pri­
Part of a pulmonary rehabilitation program may mary limiting factor in the exercise capacity of these
involve providing recommendations for the child's children. Clearly, any aerobic exercise program de­
participation in physical education (PE). Certain as­ signed for older children with CF will require careful
pects of exercise relative to pul monary function in monitoring of pulmonary support during exercise.
children with asthma need to be communicated to the
PE teacher. Running is the form of exercise most
Motor Approaches to Maximize Trunk
likely to aggravate exercise-induced asthma, espe­
and Ventilatory Function
cially if performed in a cool, dry environment. Swim­
ming, by contrast, is an excellent activity. Continuous Attention to pulmonary function is easily accom­
or high burst exercise might induce bronchospasm, plished within any "handling" approach to motor
whereas short periods of exercise (less than 6 contin­ therapy for children with trunk weakness, tightness,
uous minutes) may be beneficial for conditioning alterations in tone, or general immobility. Most "han­
wi thout bronchial aggravation (Magee, 1991). PE dling" consistent with a neurodevelopmental tech­
teachers should also be aware that the child may need nique (NDT) approach lends itself readily to a dual
to use a preexercise aerosol to participate in PE with­ focus on movement quality and ventilation. Extrinsic
out pulmonary consequence (Magee, 1991). pulmonary development is clearly interrelated with
musculoskeletal and motor development of the trunk.
Exercise and cystic fibrosis
Treatment should begin with assessment and ini­
Physical activity designed to improve exercise toler­ tial handling for functional range of motion through
ance helps children with CF to mobilize secretions the trunk. This will typically require elongation of the
and to improve body image. The development of an pectoral, sternocleidomastoid, upper trapezius, and
exercise program for children with CF should be done rectus abdominis muscles. Manual lowering of the rib
on a individualized basis and a preexercise assessment cage will also be necessary to work toward maximiz­
should include but not be limited to the following: ing chest mobility (Figure 35-13).
I. Assessment of range of motion, strength, and Passive elongation of muscles must always be
posture. followed by active elongation. Controlled prone
2. Complete chest evaluation. extension off the ball is both fun for the child and
3. Evaluation of ADL tolerance and limitations. effective for the therapist (Figure 35-14). Manual
4. Inspiratory muscle strength (maximal inspira­ guidance for upper extremity abduction and exter­
tory ncgativc pressure at the mouth) and en­ nal rotation will facilitate active elongation of the
durance testing. This inspiratory endurance pectoral muscles via active firing of the scapular
testing can be done with an inspiratory muscle retractors. The ball can be used to impart move­
training device by having the child breathe for ment and support the lower rib cage. This elon­
a predetermined length of time at progressively gates the anterior trunk (rectus abdominis), length­
increased resistances until tolerance is reached. ens intercostal muscles, and facilitates increased
5. Exercise tolerance testing, performed with upper chest expansion.
ECG, blood pressure, and oxygen monitoring. Handling to achieve proprioceptive input of the
A basic exercise program for children with CF scapulae on the posterior thorax, will help reinforce
should include activities to strengthen the back and active thoracic extension and anterior chest expan­
shoulder extensors, to elongate the trunk t1exors, and sion. The therapist's hands can stabilize the rib cage
to address overall endurance. The role of more vigor­ to reinforce abdominal oblique function during
ous exercise and fitness training in these children is a movement (Figurc 35-15).
issue of debate, based on inconsistent incidence of Activities requiring alternating extension-rotation

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662 PART VII Guidelines for the Delivery of Cardiopulmonary Physical Therapy: Special Cases

FIGURE 35-13

Manual lowering of the rib cage.

NOTE: Arrows indicate direction of therapist's hand movement (caudal and medial).

FIGURE 35-14 FIGURE 35-15

Handling to facilitate active upper thoracic extension, as a Handling to reinforce upper chest expansion and abdominal

means of actively opening the anterior chest and oblique stabilization of the lower ribs.

lengthening rectus abdominis while supporting the lower

rib cage on the ball.

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 35 The Neonatal and Pediatric Patient 663

and flexion-rotation will recruit control of the abdom­ 4. Compare the goals of chest physical therapy for
inal obliques and maintain active upper trunk exten­ infants and older children. What are the similari­
sion. Bubble blowing, whistle toys, and singing are ties and differences?
excellent means o f monitoring the ventilatory 5. When treating infants to improve airway clear­
changes that occur with active use of increased upper ance, what are the precautions/considerations of:
chest expansion. As tidal volume increases, vocaliza­ • positional rotation?
tions should increase in frequency, sound higher, and • postural drainage?
become louder. • percussion?
The concept of functional carry-over is central to • vibration?
the treatment approach presented here. Addressing • airway suctioning?
ventilation and trunk control simultaneously has intu­ 6. How might neuromotor (neuromuscular) dys­
itive appeal based not only on shared musculoskeletal function affect pulmonary development and con­
relationships but also on the necessity of pulmonary , tribute to possible postoperative complications?
tolerance for motor activity. 7. Describe goals, precautions, and suggested monitor­
ing for exercise in children who have the following:
• a history of cardiac surgery
SUMMARY
• asthma
Cardiopulmonary physical therapy with infants and • cystic fibrosis?
children is presented starting with issues related to
development and developmental vulnerabilities. Spe­
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 The Aging Patient

Elizabeth J. Protas

KEY TERMS Aging Exercise changes

Autonomic Pulmonary changes
Cardiovascular changes

INTRODUCTION linear but curvilinear, with changes accelerating after

Cardiopulmonary and autonomic nervous system age 65. Thus many of the physiological studies that
functions are dynamic and undergo changes as people have been done with 60 year olds may not apply to in­
age. It is important for physical therapists to be aware dividuals who are 80, 90, or 100 years old. Most of the
of changes that are to be expected with normal aging studies that are available on exercise in older individu­
to better understand the impact of disease and impair­ als have been conducted with subjects who are under
ment on these functions. In addition, a clear under­ age 65. A vast majority of these studies only used men
standing of how these systems respond to exercise as subjects or had a small number of women in the
training will assist the clinician in prescribing and sample. Gender may be an important variable in rela­
evaluating exercise interventions in elders. tion to exercise and aging, but there is limited data
Unfortunately, aging is a bit more complicated to available on this issue. Another consideration is the
understand than just the issue of chronological age. As composition of study populations. With increasing age,
people age, greater variability occurs between individu­ there is a greater incidence of disease. Latent cardiovas­
als, making predications about any one individual more cular disease and histories of chronic illnesses are com­
difficult. The trends of some changes are probably not mon in older populations. Comorbidities are frequently

669

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670 PART VII Guidelines for the Delivery of Cardiopulmonary Physical Therapy: Special Cases

encountered in elders. It may be more uncommon to characteristics of aging. The impact of various dis­
have a person over age 75 without any problems than to eases is discussed in other chapters. Psychosocial is­
have a healthy older individual. As a physical therapist, sues related to exercise and aging are not discussed.
I may be more interested in the responses of a frail 85­
or 90-year-old woman who has a history of hyperten­
CARDIAC CHANGES WITH AGING
sion, coronary artery disease, and diabetes than some­
one who is healthy at this age because this reflects the
Aerobic Capacity
population who is referred to physical therapy. The oc­
currence of disease states in study populations may im­ The aerobic capacity is the maximum ability to per­
pact the cardiopulmonary responses to exercise. Fi­ form exercise with large muscle groups. This ability
nally, the study of the physiological aspects of exercise is produced by the interaction of the lungs, heart, and
and aging is still evolving. The literature can be confus­ peripheral tissues. The most common indirect mea­
ing and contradictory, making conclusions and general­ sure of the aerobic capacity is the maximum oxygen
izations difficult. An attempt is made to provide some consumption (Vo2ma,), or the maximum oxygen used
direction in this confusing maze of infonnation. during exercise. The Vo2max is directly related to the
An additional issue is a model of aging that might cardiac output (the amount of blood pumped by the
sort out some of the determinants of aging. (Figure heart) and the arteriovenous oxygen difference (the
36-1) The model identifies biological factors, disuse, amount of oxygen extracted in the periphery). The
disease, and psychosocial concerns as determinants of cardiac output is the product of the heart rate times
aging. Biological factors address genetics, gender, cel­ the stroke volume. The aerobic capacity reflects the
lular mechanisms, and metabolical, and physiological central cardiac function and the efficiency of the pe­
responses that influence aging. Disuse is implicated in ripheral tissues to extract and use oxygen.
more sedentary life styles led by many elders, which The Vo2max declines with age between 0.40 to
results in loss of exercise capacity (Bortz, 1993). Ca­ 0.50 ml/kg/min per year in men and between 0.20 to
pacities that decline as a result of disuse should be re­ 0.35 mllkg/min per year in women (Figure 36-2)
versible or attenuated with exercise training. The em­ (Buskirk and Hodgson, 1987). The reduction is ap­
phasis in this chapter is on the biological and disuse proximately 10% per decade. The decline is larger in

V02max
50 (ml/kg/min)
1
45
40
35
30
Disuse 25

I 20
15
10
5
Biological
factors -- L:J --
Psychosocial
factors o 20-29 30-39 40-49 50- 59 60- 75
Age (years)

FIGURE 36-2

Disease Decline in maximum oxygen consumption (Vo2max) from

age 20 to 75 in both men and women. (Redrawn with
FIGURE 36-1 permission Hossack KF, Bruce RA: Maximal cardiac
A model of aging which identifies the major determinants function in sedentary normal men and women: comparison
underlying the aging process. of age-related changes, J App/ Physio/53:799-804, 1982.)

Copyrighted Material
 36 The Aging Patient 671

men than women; however, the capacity of the males ation of the myocardial fibers, sufficient venous re­
is larger than the females (Hossack and Bruce, turn to rapidly fill the heart, and the timing of the
1982). Vo2max is related to body size, which tends to atrial contraction to contribute to the end diastolic
be smaller in women than men. Increases in body volume. Relaxation is hampered possibly by an in­
weight as people age results in reduced V02max even crease in ventricular stiffness, although there is lim­
if the aerobic capacity remains the same, since rela­ ited evidence of this in humans (Lakatta, 1993). The
tive oxygen consumption is related to body weight. period of the isovolumic myocardial relaxation (be­
Reduced physical activity with aging also con­ tween aortic valve closing and mitral valve opening)
tributes to a loss of Vo2ma". is prolonged. Likewise the peak rate of left ventricu­
Considerable disagreement exists about the mecha­ lar filling during early diastole is reduced in older,
nisms that contribute to the decline in V02max with healthy men and women compared with younger in­
age. Both cardiac and peripheral changes contribute to dividuals. Despite the changes in early diastole, the
the loss. A reduction in maximum cardiac output ac­ resting left ventricular end-diastolic volume remains
counts for 50% to 100% of the total reduction in the same because of an enhanced left atrial contribu­
V02max (Dempsey and Seals; Ogawa et aI., 1992; tion to ventricular filling. This is accompanied by an
Saltin, 1986). Decreased maximum arteriovenous enlarged left atrium and an audible fourth heart sound
oxygen consumption accounts for whatever is not due in most older adults (Lakatta, 1993; Fleg, Gersten­
to decreased maximal cardiac output. A major compo­ blech and Lakatta, 1988).
nent to the decline in maximal cardiac output is a de­ Considerable disagreement exists about what hap­
creased maximal heart rate (Ogawa et aI., 1992; Hag­ pens to diastolic function during exercise. Some re­
berg, 1987). The decline in heart rate is linearly cent studies suggest that end-diastolic volume during
related to age and occurs in both sedentary and active exhaustive exercise increases in older men but not it
elders (Sidney and Shephard, 1977). Reduced maxi­ women (Lakatta, 1993). Filling pressures during ex­
mal stroke volume has also been observed as people ercise in men increase with age (Ehrsam, Perruchoud,
age (Ogawa et aI., 1992) Recent studies suggest de­ Oberholzer, Burkhart, and Herzog, 1983). In addi­
creased stroke volume is associated with a decrease in tion, peak left ventricular diastolic filling rate during
total blood volume in healthy older men and women submaximal and maximal exercise decreases with
(Dempsey and Seals, 1995; Davy and Seals, 1994; aging (Levy, Cerqueria, Abrass, Schwartz, and Strat­
Stevenson, Davy, Reiling, and Seals, 1995). Most evi­ ton, 1993; Schulman, Lakatta, Fleg et al. 1992) De­
dence suggests that decreased V02max with aging is re­ creased filling rate is associated with increased ven­
lated to decreased maximal heart rate, stroke volume, tricular stiffness and prolonged relaxation times
and arteriovenous oxygen difference, although each (Ehsani, 1987).
component's contribution varies (Dempsey and Seals, Resting measures of systolic and cardiac pump
1995; Lakatta, 1993), function do not change with aging. The resting end­
systolic volume and stroke volume do not change
with age. Likewise, the ejection fraction at rest (end­
Cardiac Mechanics
diastolic volume - end-systolic volume/end-diastolic
The most consistent cardiac structural change is a volume) is similar in healthy older and younger indi­
modest increase in left ventricular wall thickness in viduals (Lakatta, 1993).
80 year olds compared with 20 year olds (Lakatta, Unlike resting systolic function, the pumping func­
1993), attributed to an increase in size of cardiac my­ tion of the heart changes considerably in response to
ocytes and is exaggerated by hypertension and/or exercise. Myocardial contractility as measured by the
coronary artery disease (Lakatta, 1993). After age 80, ratio of end-systolic volume to systolic arterial pres­
the left ventricular wall thickness again decreases. sure declines during exercise as people age (Lakatta,
The cardiac filling or diastolic properties of the 1993). The end-systolic volume increases, whereas
heart are altered with age. Diastole requires a relax­ the ejection fraction decreases during exercise. These

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672 PART VII Guidelines for the Delivery of Cardiopulmonary Physical Special Cases

changes reduce stroke volume exercise. Re­ catecholamines is most often cited as the reason for
duced contractile performance is related to a decrease "' "<"vu in maximal heart rate with (Rodehef­
in the response to beta-adrenergic stimulation, f e r, Gerste nbl Beck er, W e i sfeld, and
changes in the myocardium, increased blood Lakatta, 1984). Relatively intense endurance training
pressure, a n d v e n t r i c u l a r w a l l abnorma l i t i e s for a year or more can increase stroke volume in
(Dempsey and 1995). Ogawa, Miller, and Jilka, 1991;
Spina, and
Adaptations to exercise training in
Impact of Training on Aerobic Capacity
older women have been attributed to
and Cardiac Mechanics
in arteriovenous oxygen differ­
Older persons who continue to be active reduce the ence rather than central changes in cardiac function
rate of decline in Vo2max to 5% per decade compare (Spina, Kohrt, Martin, Holloszy, and Ehsani,
with an decline of 10% per decade in 1993). This apparently occurs desoite intensive en­
sedentary adults 1987). A recent metaanaly­ durance over a year-long
sis of 29 studies including 1030 men and 466 women The diastolic changes thal occur with can be
between the ages of 61 and 78 and endurance train- reversed by exercise training et al., 1993).
concluded that endurance Levy et al. endurance trained 13 rigor-
increases functional in young elders screened older men 60 to 82 age
and Less improvement was seen with 68) and II younger men in their twenties for 6
increasing age, a shorter length of low months. The training increased submaximal,
Vo2rnax before and short duration of exercise and rates for the older group comparable
sessions. The analysis suggests that a 68- with the seen in the younger group (Levy et
year-old individual who exercises for 30 minutes aI., 1993). End-diastolic peak volume at rest and ex­
three times per week for 4 to 6 months can improve ercise also increase after lengthy endurance training
14% and 1 Similar (Ehsani et 1991). Thus reduces the age­
occur in both men and women (Kohn, associated diastolic changes. The mechanisms of this
1991; Warren et response are uncertain in humans. Studies in rats
The mechanisms underlying in have shown that exercise training increases calcium
Vo2max i n the with endurance are not in cardiac decreases
clear. One consistent finding is greater extraction of relaxation reduces the decline of left ventricular
oxygen in the exercising skeletal which pro­ pressure, enhances fatty acid oxidation, and increases
duces a wider arteriovenous oxygen difference in c oxidase levels
both older men and women 1992; and Stratton, I Taffet,

1 This implies that in the McBride, and Michael, 1990;

skeletal muscles account for some of the and Edington, 1 All of these

increase in in elders. The of exercise have been associated with reduced diastolic

on maximal cardiac i s uncertain

(Ehsani, 1 can either Exercise can also
remain the same or increase after exercise training, mance in older men as reflected by the increase in the
depending on the effect of training on maximal stroke exercise stroke volume. Increased stroke vol­
volume and maximal heart rate. Maximal heart rate ume occurs with an increased exercise frac­
remains the same in older men of activity tion, a decrease in end-systolic volume, and greater
that the decline in maximal heart left ventricular wall mass (Ehsani et Seals et al.,
on factors other than exercise and physi- 1994). These changes apparently do not occur in
Hagberg, and Hol- older, women et 1993).
A decrease in response to circulating Table 36-1 contains a summary of these

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 36 The Aging Patient 673

TABLE 36-1 Blood pressure

160
(mm/Hg)
Cardiac Changes With Aging*
140
BECAUSE AFTER
OF AGING EXERCISE
120
TRAINING

Maximum Exercise 100

Oxygen consumption J, i
Heart rate J, H 80
Stroke volume J, i,H
Arteriovenous oxygen 60
difference J, i --+-Systolic
Cardiac output J, i, H 40 -D-Diastolic
Cardiac function
20
Diastolic

Left ventricular wall o �--�----�--�

thickness i, J, after 80 i 35 40 45 50 55 60 65 70 75
Left ventricular Age
filling rate J, i
End-diastolic volume H i FIGURE 36-3
Changes in systolic and diastolic bl.ood
Systolic age. (Redrawn with permission from Timiras PS:
Myocardial contractility J, i ,Hi Cardiovascular alterations with age: atherosclerosis, coronary
End-systolic volume i J" Ht heart disease and hypertension. In Timiras, PS: Physiological
Ejection fraction J, i,Ht basis of aging and geriatrics. Boca Raton, Fla., 1988, CRe.)

°i increase; J, decr as : H no change;

= = =
over the age of 70 (Lipsitz, 1989). Orthostatic intoler­
tin women
ance is associated with decreased resting diastolic
function, decreased stroke volume, extreme inactiv­
ity, and, in individuals with hypertension, high levels
Vascular and Autonomic Changes with Aging
of systolic blood pressure (Harris, Lipsitz, Kleinman,
Aging results in an increase in arterial stiffness be­ and Cornoni-Huntley, 1991).
cause of a loss of elastin and an increase in collagen There are decreases in baroreceptor and cardiopul­
(Lakatta, 1993; Roach and Burton, 1959). Arterial monary reflexes with aging (Lakatta, 1993; Cleroux,
wall thickness and diameter and resting systolic pres­ et a\., 1989) Arterial and venous dilation are reduced,
sure also increase (Figure 36-3) (Lakatta, 1993). It is but vasoconstriction is relatively spared. The heart
unclear whether peripheral vascular resistance in­ demonstrates an overall decrease in responsiveness to
creases in normotensive older adults. Changes in the autonomic stimulation. Older individuals experience
structure, size, and reactivity of the arteries increase higher central venous and mean arterial pressures, but
the work of the left ventricle and have been directly lower forearm blood flow and forearm vascular resis­
implicated in the increase in cardiac myocyte size. tance in response to passive leg raising (Cleroux et aI.,
Complaints of dizziness when an older patient 1989). During submaximal and maximal exercise, ar­
moves from supine to standing are frequently en­ terial blood pressure is either unchanged or increased
countered by the physical therapist. Postural hypoten­ when comparing younger and older subjects (Seals,
sion, or orthostatic intolerance, generally does not 1993). There also appears to be impaired peripheral
occur in healthy community dwelling elders but is vasodilation in skeletal muscle in response to exercise
common in debilitated, institutionalized individuals (Ogawa et a\., 1992). Redistribution of blood flow

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674 PART VII Guidelines for the Delivery of Cardiopulmonary Physical Therapy: Special Cases

during exercise normally involves the shunting of chest wall (Dempsey and Seals, 1995). The lung's
blood from inactive limbs and viscera. There seems to elastic recoil depends on the composition of the con­
be an enhanced vasoconstriction in inactive muscles nective tissue, the structure of the connective tissue,
during dynamic exercise in healthy older men (Taylor, and alveolar surface tension produced by surfactant
Hand, Johnson, and Seals, 1992). (Dempsey and Seals, 1995). Very limited evidence
suggests that the structure of the connective tissue
may be the primary mechanism for age-associated
Effect of Exercise Training on Vascular
change in elastic recoil. Chest wall stiffness is ac­
and Autonomic Function in Aging
companied by an increase in chest anterioposterior
Exercise training improves peripheral bloodflow in diameter, coastal cartilage calcification, nan'owing of
skeletal muscle in 60-year-old men and women (Mar­ the intervertebral disks, and changes in the rib to ver­
tin, Ogawa, Kohrt, Malley, Korte, and Stoltz, 1991). tebrae articulations (Crapo, 1993).
Systolic and mean arterial blood pressure responses Decreases occur with the alveolar-capillary sur­
to submaximal exercise are lower in physically active face area, the alveolar septal surface area, and the
adults compared with sedentary individuals (Martin total surface area of lung parenchyma (Brody and
et aI., 1991). Endurance training also increases mus­ Thurlbeck, 1985). This reduces the surface area avail­
cle sympathetic nerve activity and plasma norepi­ able for gas exchange.
nephrine concentrations at rest and during a moderate Loss of elastic recoil with aging is directly associ­
isometric handgrip, indicating elevated sympathetic ated with reduced forced expiratory flow. Limitations
nerve activity in response to exercise (Table 36-2) in exhalation are caused by airway narrowing and
(Ng, Callister, Johnson, and Seals, 1994). closure at all lung volumes; thus reducing forced ex­
piratory volume in I second (FEV1) (Dempsey and
Seals, 1995) Early airway closure also produces an
PULMONARY FUNCTION
early closing volume and a relati ve increase in the
total residual volume. The combination of reduced
Structural and Functional Changes With Aging
elastic recoil and increased chest wall stiffness leads
Two major changes with aging of the pulmonary sys­ to a decrease in the forced vital capacity in older indi­
tem are decreased elastic recoil and stiffening of the viduals. Flow rates are also significantly lower in
women and African-Americans than in Caucasian
men at any age (Dempsey and Seals, 1995).
Respiratory muscle strength, as reflected by the abil­
ity to create pressure over a range of lung volumes and
TABLE 36-2 flow rates, is similar when comparing healthy 30 and 70
Vascular and Autonomic Changes With Aging* year olds (Johnson and Dempsey, 1991) This suggests
that respiratory muscle strength does not change with
BECAUSE AFTER
OF AGING EXERCISE aging; however, maximal inspiratory and expiratory
TRAINING pressures have been reported to decrease 15% between
Arterial wall thickness i ? the sixth and eighth decades (Figure 36-4) (Enright,
Systolic blood pressure i t Kronmal, Manolio, Shanker, and Hyatt, 1994). Perhaps
Diastolic blood pressure i and H t these observed differences are similar to the differences
Orthostatic tolerance H ?
observed with submaximal and maximal cardiac re­
Arterial and venous dilation t ?
sponses with the dynamic pressure measures over dif­
Vasoconstriction H H

Central venous pressure i ferent volumes and flows considered submaximal.

Changes in the surface area result in a decrease in
"i = increases; t = decreases; H = unchanged; the diffusion capacity of the lung (Murray, 1986).
? = insufficient data on older adult subjects Both the loss of surface area and a decrease in pul­

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 36 The Aging Patient 675

monary capillary blood volume contribute to reduced mains unchanged as people age, although the vital ca­
and uneven ventilation to perfusion matching in el­ pacity for elders is reduced. Likewise, as exercise and
ders. The resting partial arterial pressure of oxygen the tidal volume increase there is a slight drop in the
declines 5 to 10 mm Hg between ages 25 and 75 ratio of dead space to tidal volume. This drop is not
(Dempsey and Sea Is, 1995). These changes do not af­ effected by aging, although the older person will
fect the arterial oxymyoglobin saturation or oxygen breathe more (have a higher minute ventilation) in re­
content. Paralleling changes in the peripheral vascu­ sponse to submaximal exercise.
lature, pulmonary vascular resistance and pulmonary The work of breathing is increased during exercise
arterial pressure at rest increase (Table 36-3). as people age as a result of a number of factors.
Higher ventilation during exercise requires the devel­
opment of higher pleural pressures; thus increasing
Changes in Pulmonary Responses to
the work required. In addition, an increase in the end­
Exercise With Aging
expiratory lung volume with increasing exercise re­
In addition to the structural and functional changes at sults in breathing that occurs at a stiffer point in the
rest, a number of significant changes occur in breath­ lung-volume relationship. The increased stiffness im-
ing during acute exercise. Expiratory flow limitations
occur at lower exercise intensities as people age. A
normal, healthy 69 year old will begin to experience TABLE 36-3
flow limitations even in response to moderate exercise
Pulmonary Function Changes With Aging*
(Dempsey and Seals, 1995). Practically, this may be
experienced by the individual as having greater diffi­ BECAUSE AFTER
OF AGING EXERCISE
culty "catching his or her breath" during exercise. TRAINING
Normally as people exercise, the tidal volume in­
Structure and Function
creases directly with increasing exercise intensity up
to about 50% to 60% of the vital capacity. This re­ Elastic recoil J,
Chest wall stiffness i
Alveolar-capillary surface area J,
Forced expiratory flow J,
MEP(cmHpl Total residual volume i
200
,--
lD.Women
Men Forced vital capacity J,
180 ,--
Maximum inspiratory and J,
160 r--
-
expiratory pressure
140 Ventilation-perfusion matching J,
120 Partial arterial pressure oxygen J,
100 Oxygen saturation H
80 Pulmonary vascular resistance i
60
Exercise response
40
Expiratory flow limitation i
20
Minute ventilation i
o f--�
65-69 70 - 74 75-79 80-84 Work of breathing i
Age Respiratory muscle oxygen i
consumption
FIGURE 36-4 Arterial hypoxemia H,i
Decrease in maximum expiratory pressures between ages Pulmonary artery pressure i
65 to 84 for both men and women. This is a measure of Pulmonary wedge pressure i
respiratory muscle strength. (Redrawn with permission
from Enright PL, Kronmal RA, Monlio TA, Schenker MB, 'i increases; J,
= = decreases; H = unchanged
Hyatt RE: Respiratory muscle strength in the elderly, Am J Tsubmaximal
Respir Cril Care Med 149:430-438, 1994.) t maximal

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676 PART VII Guidelines for the Delivery of Cardiopulmonary Physical Therapy: Cases

elastic recoil on the ventilatory mus­ diffusion and may contribute to ventilation
greater pressure development by the maldistribution ( Dempsey and 1995)
inspiratory muscles. The increase in expiratory flow
resistance likewise requires greater pressure
Effects of ExerCise Training on Pulmonary Function
ment by the muscles. Both the inspiratory
and changes increase the work of breath­ Aerobic training in elders can reduce some of the
ing. The increase in the work of breathing increases that have been described. There are limited or
the respiratory muscle oxygen consumption so that no studies that address some of the changes, such as
the muscles alone can 10% to chest wall or artery pressure.
12% of the total oxygen during The studies that are available deal with relatively
maximal exercise in a sedentary 70-year-old man young who are 60 to 70 years which does
)""W.N'" and (995). not insights into what exercise might do for
What is also apparent is that the reserves used to the those in their or beyond.
respond to exercise represent a greater percent of the Aerobic training can significantly decrease sub-
available capacity. An older individual can exceed
50% of inspiratory muscle capacity even during mod­ Jones,
erate exercise. This is in contrast to the younger indi­ program with women over a 12­
vidual who exceeds 50% of the capacity with and demonstrated a 7.7% drop in the sub­
exercise and 1 Thus the reserve maximal minute ventilation 36-5) et
capacity to pleural pressure is reduced in eI­ al., 1993). Decreased minute ventilation is accompa­
ders v irtue of the fact that greater caoacitv is nied by a decrease in carbon dioxide production, the
needed even for moderate exercise. respiratory exchange ratio (carbon dioxide produc­
The variability characteristic of exercise r e ­ tion/oxygen consumption), and the blood lactate level
sponses in older individuals is particularly evident for any level of submaximal exercise (Makrides
when gas and et aI., 1986; Warren et aI., 1993). Thus the improved
cular hemodynamics. I n most individuals ventilatory after may have more to
demonstrate only slight in arterial blood-gas do with improved in the rather
but a small number of individuals than an on the pulmonary system Im­
d e m on s t r a t e a r t e r i a l h y p o x e m i a w i t h e x e r c i s e proved metabolical efficiency results in the
and 1995). Some studies suggest production of less carbon dioxide; therefore the
that this response may be a factor of fitness level. do not have to work as hard to eliminate the carbon
More fit older individuals showed progressive arter­ dioxide. The important functional results of these
ial and carbon dioxide retention during changes are that the older adults will less
mild-to-moderate exercise (Prefaut, Anselme, Cail­ experience a lower perceived exertion,
laud, and Masse-Biron, 1994; et aI., 1994). and use a lower of their maximal ventila­
The pulmonary artery pressure is increased with tory capacity during exercise (Jones,
at any oxygen consumption or cardiac output Exercise training also increases maximal ventila-
during exercise (Reeves, and \989). maximal exercise et
In addition, the maximal pulmonary artery pressure at 12-week pro­
maximal exercise is reached at substantially lower oxy­ gram referred to above increased maximum minute
gen consumption and cardiac output in older individu­ ventilation 14% in women Figure
als with younger persons. The pulmonary 36-5) (Jo n e s, I . These w o me n walked 5
pressure also increases with age and can exceed s/week at an of 78% of the maximal
25 mm Hg peak supine exercise (Dempsey and treadmill heart rate or 118 beats/minute on average,
Seals, I Limited data suggest that these pres­ so the program was not very strenuous but IJH;'UWc.C'u

sures may in tum induce pulmonary edema during in­ substantial in maximum ventilation. Exercise
tense exercise in elders. Pulmonary edema would limit training can improve submaximal ventilatorv effi­

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 36 The Aging Patient 677

Ventilation REVIEW QUESTIONS

70 (L/min)
1. What are the which occur
with in the cardiovascular
2. What outcomes will exercise pro­
duce in an older adult's cardiovascular sys­
tem?
3. What are the major that occur with
in the autonomic nervous
sponse to and which of these
can be influenced by execise
4. What are the major that occur in the
pulmonary system with and in reo
to exercise?
5. Describe the possible impact of exercise
on the system.

References

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Copyrighted Material
 The Patient with Neuromuscular or
Musculoskeletal Dysfunction

Mary Massery

KEY TERMS Adverse musculoskeletal changes Paradoxical breathing

Chest development Planes of ventilation
Effects of gravity Pulmonary function tests
Gravity Respiratory impairments
Impaired phonation support Respiratory muscles
Musculoskeletal deficits Sleep disorders
Neuromuscular deficits Triad of ventilation
Nighttime hypoxemia

INTRODUCTION
muscular and/or musculoskeletal deficits and what
It is often observed in a rehabilitation setting that clinicians can do to minimize or eliminate these
patients with neurological deficits continue to ac­ complications. The focus of this treatment approach
quire respiratory problems long after their acute is primarily aimed at the physical therapist (PT).
phases have subsided. Research has repeatedly doc­ Every effort is made to explain specific physical
umented a decrease in pulmonary function for the therapy concepts so that all clinicians, occupational
chronic neurologically impaired patient, yet many therapists (OTs), speech language pathologists
therapists do not appear to fully comprehend why (SLPs), respiratory therapists (RTs), and nurses
this occurs. This section tries to elaborate the causes (RNs), family members, and others can benefit from
of respiratory complications secondary to neuro­ the ideas presented in this chapter.

679

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680 PART VII Guidelines for the Delivery of Cardiopulmonary Physical Therapy: Special Cases

DIAGNOSES ADDRESSED
ing may respond better to techniques that act primarily
The following treatment ideas are applicable for all on the subconscious and require little cognitive partici­
neurological and orthopedic diagnoses including the pation. Finally, the differcnce between rehabilitation
following: spinal cord injuries (SCI), head traumas, and habilitation must be understood. Rehabilitation in­
cerebral vascular accidents (CV A), multiple sclerosis volves restoring function, and habilitation teaches
(MS), amyotrophic lateral sclerosis (ALS), Parkinson's functioning for the first time. Children with acquired
disease, cerebral palsy (CP), muscular dystrophy (MD), deficits in utero or shortly after birth have never expe­
polio myelitis (polio), spina bifida, and neuropathies as rienced normal movement patterns. Therefore they
well as back, neck, and shoulder injuries or dysfunc­ cannot depend on the memory of past motor experi­
tion. However, it is by no means an exhaustive list. The ences to help con'ect abnormal motor patterns the way
primary consideration for application of these treatment adults going through rehabilitation can. This important
techniques is the residual physical deficits left by a neu­ difference must be accounted for when developing
rological or musculoskeletal insult. Therefore a patient their treatment programs.
presenting with hemiplegia will be treated with tech­
niques geared toward promoting increased function on
PLANES OF VENTILATION
the involved side, regardless of how the original deficit
was acquired (e.g., from a CVA, head trauma, or CP). This neuromuscular/musculoskeletal treatment ap­
Likewise, tetraplegia or paraplegia not only refers to proach is based on the premise that ventilation does
patients that have suffered from SCls but any patient not take place in a one-dimensional plane but rather as
that presents with tetraplegic or paraplegic deficits. a three-dimensional activity. The chest expands in an
However, three aspects of neurological/muscu­ anterior-posterior plane, an inferior-superior plane, and
loskeletal disorders must be clarified here to assist the a lateral plane (Figure 37-1). Too often, therapists treat
therapist in discerning which techniques, described patients with neuromuscular and/or musculoskeletal
later, are appropriate for his or her particular patient. dysfunctions with apparent disregard for this ex­
The three aspects follows: (1) progressive vs. nonpro­ tremely important fact. This one-dimensional fallacy
gressive injuries, (2) cerebral vs. noncerebral injuries, has been perpetrated by techniques taught to new ther­
and (3) rehabilitation vs. habilitation. Single-insult in­ apists that describe the patient's breathing program in
juries, such as SCTs, traumatic brain injuries, CVAs, only one or two postures, most often supine and sit­
CPs, or cervical whiplash, are nonprogressive. The ting. To be effective, we must acknowledge this three­
damage was only inflicted once and does not repeat it­ dimensional movement of the thorax and use this con­
self. Progressive diseases, on the other hand, such as cept when determining treatment protocol.
MS, ALS, Parkinson's disease, MD, or scoliosis, show
increasing physical deficits over time. Goals for these
EFFECTS OF GRAVITY
groups will be different, with maximal respiratory
functioning stressed for the single-insult diagnoses and If chest expansion takes place in three planes, the ef­
comfort and ease of ventilation stressed for progres­ fect of gravity on these planes must be considered.
sive diagnoses. Similar treatment consideration is Physical therapists would not exercise a weak muscle
given for patients with detrimentally affected cerebral without taking into account the effect of gravitational
functioning, such as with traumatic brain injuries, pull on that muscle, tbereby making the positioning
CVAs, and Parkinson's disease, versus those whose of the limb in space an important consideration in
deficits are at the spinal level, such as with SCIs, neu­ treatment planning. This same consideration must be
ropathies, myopathies, and polio. Patients with only given for the weakened ventilatory muscles. Gravity
spinal involvement may respond favorably to complex can assist, resist, or have no effect on the movement
techniques and demonstrate better conscious carry­ of the chest wall, according to the chest's position in
over, whereas those with impaired cerebral function­ space. Consider weakened intercostal muscles. Plac­

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 37 TIle Patient with Neuromuscular or MuscuJoskeletal Dysfunction 681

in abdominal tone (many SCIs, Guillian-Barre syn­

drome, or spina bifida), intestinal positioning be­
comes an important factor in respiratory functioning.
The abdominal wall acts as the anterior support
for the intestines, causing the intestines to sit high in
the abdominal cavity (see Chapter 2). This forces the
diaphragm to rest high, at approximately the level of
the fifth rib in an erect posture (Figure 37-2). The di­
aphragm contracts, drawing its origins toward its in­
sertion (concentric contraction). These muscle fibers,
which originate down as low as the tenth rib, must
rise up superiorly and then medially toward the cen­
tral tendon (see Chapter 2). This movement pattern
causes primarily superior and lateral expansion of
the lower chest. Without abdominal wall support, the
intestines shift inferiorly and anteriorly, the "beer­
belly" effect, allowing gravity to position the di­
aphragm lower in the abdominal cavity (Figure 37-
3). This p u t s t h e d i a p h r a g m at an e x t r e m e
mechanical disadvantage. Instead o f having t o rise

••
up and over the intestines, the lateral fibers of the di­
aphragm can now move more horizontally to reach
the central tendon, thereby significantly reducing ex­
cursion in all three planes of expansion. This adverse
positioning may be so significant as to cause a nega­
FIGURE 37-1 tive lower chest expansion on inspiration for patients
Planes of respiration (anterior-posterior, inferior-superior, with tetraplegia. Quantitatively, this may be seen as
and lateral). much as Y2- to I-inch decrease rather than increase in
overall lower chest expansion, measured at the
ing a patient with this deficit in a supine position for xiphoid process, when the patient proceeds from
initial treatment in his or her rehabilitation program maximal expiration to maximal inspiration.
and then asking the patient to "breathe up into your Since gravity causes the intestines to shift, the ef­
hands" is asking the patient to attempt the most diffi­ fect on the diaphragm will be most dramatic in a
cult gravitational posture first (breathing into the an­ gravity-dependent position, such as sitting or stand­
terior plane with gravity resisting the movement). It ing, rather than in a gravity-eliminated position, such
would seem more appropriate to start retraining tech­ as supine. Thus the imponance of providing the pa­
. niques in a gravity-eliminated posture for anterior tient with an external abdominal wall support in these
chest expansion, such as side lying, or a gravity­ upright postures should be undeniably clear. Al­
assisted posture, such as hands-knees, and then though not as effective as the abdominal muscles
progress to gravity-resisted postures, such as supine. themselves, abdominal supports help restore the nat­
Gravity also affects the positioning of the in­ ural mechanical advantage of the diaphragm (see
testines under the diaphragm. In the normal, neuro­ Chapter 22).
logically intact person, this seems to have a minor ef­ In addition to changing muscle effectiveness,
fect on respiratory functioning. However, for many gravity also affects bony structures. Obviously, this
neurologically impaired persons with a marked loss affects a growing child more so than a fully devel­

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682 PART VII Guidelines for the Delivery of Cardiopulmonary Physical Therapy: Special Cases

FIGURE 37-2
Proper mechanical positioning of the diaphragm relative to the abdominal viscera. Note the high
dome shape of the diaphragm.

oped adult, but both will be affected. Bones grow ac­ plays an extremely crucial role in the skeletal devel­
cording to stress laid on them, thus abnormal stresses opment of the chest in the newborn. Normal, neuro­
produce abnormal bony developments. For persons logically intact infants move freely in and out of pos­
with severe neurological deficits, gravity becomes the tures, such as prone, hands-knees, and standing, as
main force acting on the bones and joints, unopposed they progress developmentally, allowing gravity to
by normal muscle action. This can result in many alternately assist or resist the movements. Through
skeletal deformities, such as flattening or flaring o f this, the infant begins to strengthen and develop mus­
the lower anterior rib cage, narrowing of the upper cle groups and learn to interact with the gravitational
chest, loss of normal spinal curves, and chest cavus force in his or her environment.
deformities. Prevention of these deformities, rather This combination of normal movement patterns in
than their cure, must be the aim of a good long-term a gravitational field, along with genetic predisposi­
ventilatory program for the neurologically impaired. tion, accounts for the normal development of the
bones, muscles, and joints that comprise the chest
wall. Conversely, infants with severe neurological
GRAVITY: EFFECTS ON CHEST DEVELOPMENT
impairments do not have that same freedom of move­
Thus far the effects of gravity on the planes of venti­ ment within their environments. This applies to chil­
lation, muscle function, and bony changes in the dren with congenital deficits, such as CP or spina bi­
adult have been discussed. This same force, gravity, fida, or for children who acquire deficits at an early

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 37 The Patient with Neuromuscular or Musculoskeletal Dysfunction 683

FIGURE 37-3
Independent upright posturing in a patient with congenital quadriplegia. Note relationship of rib
cage and abdominal viscera.

developmental age, such as some CY As, head trau­ neck renders the upper accessory muscles nonfunc­
mas, or SCIs. These children become subjugated to tional as a ventilatory muscle. The infant's arms are
the effects of gravity on their growing and develop­ held in flexion and adduction across the chest, signif­
ing bodies because they are unable to independently icantly hampering lateral or anterior movement of the
counteract its constant presence. A variety of reasons chest wall. This all points to underdevelopment of the
may account for their inability to change their own upper chest region in the newborn. The infant, forced
positions in space:(I) muscle weakness, (2) tonal to be a diaphragmatic breather, shows greater devel­
problems (e.g., spasticity or flaCCidity), (3) reflex opment of the lower chest and hence leads to the tri­
dominance, (4) incoordination, or (5) a combination angular shaping of the rib cage.
of the above. Typically, these children spend signifi­ From 3 to 6 months of age, the infant begins to de­
cantly more time in supine than in any other posture, velop more trun k extension tone, they spend more
which can lead to undesirable changes in the thorax. time in a prone on elbows position, and they begin to
Understanding the basic steps and principles in reach out into the environmenr with the upper extrem­
normal chest development is essential for accurately ities. This facilitates development of the anterior
assessing abnormal chest deformities often seen in upper chest. Constant stretching helps to expand the
this physically challenged population. Initially, the anterior upper chest both anteriorly and laterally. An
newborn's chest is triangular in shape, narrow and increase in intercostal and pectoralis muscle strength
flat in the upper portion, and wider and more rounded improves the infant's ability to counteract the force of
in the lower portion (Figure 37-4). The infant's short gravity on the anterior upper chest in supine, leading

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684 PART VII Guidelines for the Delivery of Cardiopulmonary Physical Therapy: Special Cases

FIGURE 37-4
Newborn chest configuration. Note triangular shape.

FIGURE 37-5
A and B, I O-month old infant chest configuration. Note shape of chest changes and angle of ribs.

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 37 The Patient with Neuromuscular or Mu culoskeletal Dysfunction 685

to the development of a slight convex configuration of Children with severe neurological deficits often
the area and a more rectangular shaping of the thorax show a very different picture of chest development.
from a frontal plane. Frequently, they do not develop adequate upper­
The next significant development occurs when extremity and neck muscle control (e.g., weak mus­
the child begins to independently assume erect pos­ cles, tone problems, reflex dominance, or incoordina­
tures (e.g., sitting, kneeling, or standing). Until this tion), causing their upper chests to retain the more
time, the ribs are aligned 'fairly horizontally, with primitive triangular, flattened shape. Inadequate mus­
narrow intercostal spacing (see Figure 37-4). In fact cle control or chronically shortened neck muscles
the newborn's chest only comprises approximately also renders the accessory muscles less able to assist
one tbird of the total trunk cavity. As the child be­ if needed in ventilation. In some cases the child's di­
gins to move up against the pull of gravity, the ribs aphragm remains so strong and unbalanced by the ab­
rotate downward (more so in the lower ribs), creat­ dominal and intercostal muscles that it creates a
ing the sharper angle of the ribs as seen in the adult cavus deformity (pectus excuvatum) at the sternum
(Figures 37-5 and 37-6). This markedly elongates (Figure 37-7). This occurs when the intercostal mus­
the rib cage until it eventually occupies more than cles are incapable of maintaining the anterior chest
half of the trunk cavity. A comparison of chest x­ wall's position against gravity and the abdominal
rays of newborns and adults, as well as pictures of muscles are weak or flaccid, thus not stabilizing the
infants, clearly shows these developmental trends lower borders of the thorax. This may also eventually
(see Figure 37-4 to 37-6). Development trends are cause an anterior flaring of the lower ribs.
summarized in Table 37-1. Most of these children with severe neuromuscular

FIGURE 37-6
Normal adult chest x-ray. Chest shape is rectangular, ribs angled downward, upper and lower chest
equally developed.

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686 PART VII Guidelines for the Delivery of Cardiopulmonary Physical Therapy: Special Cases

impairments require significant assistance to maintain rectus abdominus, as seen in many children with spastic
an upright posture, therefore they spend more time in a tetraplegia CP, the chest will become flattened anteri­
recumbent position. Thus the rib cage tends to show orly, yet flared laterally in the lower ribs (Figure 37-8).
less downward rotation and elongation than that of the These children are unable to stabilize the lower lateral
normally developing child. In some cases of prolonged borders of their rib cage and are unable to counteract
supine posturing combined with hyperactivity of the gravity's influence on the anterior chest wall move-

TABLE 37-1

Chest Development Table

Chest Infant Ad ul t

Size Occupies one third of the trunk cav ity Occupies greater than one half trunk cavity
Shape Triangular frontal plane Rectangular frontal plane
Circular anterior-posterior plane Elliptical anterior-posterior plane
Upper chest Narrow Wide
Flat apex Convex apex
Lower chest Circular Elliptical
Flared lower ribs Integrated with abdominals
Ribs Evenly horizontal Rotated downward; especially inferiorly
Intercostal spacing Narrow Wide
Limits movement of ribs Allows for individual movement of ribs
Diaphragm Adequate Adequate
Minimal dome shape Large dome shape, greater excursion
Accessory muscles Nonfunctional Functional

FIGURE 37-7
Pectus excavation deform i t y (secondary to spinal cord injury and resultant muscle imbalance).

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 37 The Patient with Neuromuscular or Musculoskeletal Dysfunction 687

ments. Thus we see these adverse musculoskeletal occurs because of pressure gradients between the air
changes, which limits the breathing patterns options. outside the lungs and the air inside. These gradients
As long as the neurological deficits are present, are achieved through movements in the chest wall.
these children will never develop normally. However, Muscle contractions provide the power to move the
frequent position changes, inhibition of undesired chest wall. If these muscles do not overcome the ef­
tone, facilitation of weakened chest muscles, promo­ fect of gravity because of weakness, paralysis, abnor­
tion of preferred breathing patterns, and incorporation mal tone, or inadequate muscle control, the chest will
of ventilatory strategies with movement will stimu­ be unable to expand in all three planes of ventilation,
late normal chest development. Optimum respiratory thus limiting pulmonary function. Because of this im­
function cannot be expected from a severely underde­ portant fact, all muscles originating or inserting into
veloped chest. the chest wall become "ventilatory muscler" The box
on p. 688 lists these muscles and how they affect chest
expansion and other specific respiratory function.
MUSCULAR AND TONAL INFLUENCES
They are listed in the following two distinct groups:
ON CHEST DEVELOPMENT
the primary muscles needed for normal ventilation
Adverse effects of gravity are counteracted by func­ (the triad of normal ventilation) and all other acces­
tioning musculature. Recall that inspiration/expiration sory muscles of ventilation. Impairment to any of
these muscles may result in respiratory deficits.
Another factor that determines a muscle's effec­
tiveness as a chest wall mover is neurological tone in
the muscle. Rigidity of movement, as seen in some
patients with head traumas and Parkinson's disease
will render the chest immobile, severely limiting its
ability to expand in any plane. Spasticity, more often
to a lesser degree than rigidity, can render the chest
immobile. Spasticity (i.e., SCI, CP, some head
trauma), is frequently activated by quick movement of
the affected muscle either actively or passively. A
quick activity like coughing may activate this abnor­
mal tone and work against the patient as he or she
tries to produce an effective cough. The other extreme
of abnormal muscle tone is flaccidity or lack of any
muscular tone, as seen with some SCIs, CY As, and
MD. In this case the muscle is entirely unable to move
the chest wall or to counteract the effects of gravity.
Of the three types of abnormal tone, flaccidity is the
most adversely influenced by the effects of gravity.
At the same time, postural reflexes and their effect
on muscle tone must be considered. For instance, the
tonic labrinthyne reflex (TLR) increases extensor
tone when the person is supine and increases flexor
tone when that person is prone. For patients with CP,
for example, this reflex may stay a dominant force in
FIGURE 37-8 their motor control, interfering with their ability to
Musculoskdetal changes secondary to static positioning move freely in supine and prone positions. Because
and neurological deficit. of this, a child with CP with increased extensor tone

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688 PART VII Guidelines for the Delivery of Cardiopulmonary Physical Therapy: Special Cases

Trunk Muscles and Their Function in Ventilation

Muscles of Velltilatioll-Three-Dimensional Movements

Triad of lIormal velltilatioll

Diaphragm

• Major muscle of passive ventilation

• Innervation-phrenic nerve-C3 to C5

• Primary movement-all three planes

• Dependency on intercostal and abdominal muscles

• Concentric contractions--quiet and forceful inhalation

• Eccentric contractions---controlled exhalation and speech

Intercostals

• Primary function-stabilizes rib cage

• Innervation-Tl to T2

• Primary movement-concentric contractions

• Lateral and superior expansion in lower chest during both quiet and forceful inhalation. Anterior expan­
sion occurs to a lesser degree.

• Anterior and superior expansion in upper chest, lateral expansion occurs to a lesser degree.

• Forceful exhalation-primarily medial and inferior compression in lower chest, posterior and inferior
compression in upper chest

• Eccentric contractions-needed for controlled exhalation and speech

Abdominals

• Stabilizes inferior border of rib cage-provides mid trunk control

• Innervation T6 to L I

• Provides visceral support

• Provides positive pressure support for the diaphragm

• Provides necessary intrathoracic pressure for an effective cough

Accessory muscles

Erector spinae

• Stabilizes thorax posteriorly to allow for normal anterior chest wall movement to occur

• Innervated at TI to S3

Pectoralis muscles

• Provides upper chest anterior and lateral expansion

• Innervated C5 to TI

• Can be a substitute rib cage stabilizer after paralysis of the intercostal muscles

Serratus anterior

• Provides posterior expansion of rib cage when upper extremities are fixated

• Innervated C5 to C7

• Only inspiratory muscle that is paired with trunk flexion movements rather than tnlllk extension mo.ements

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 37 The Patient with Neuromuscular or Musculoskeletal Dysfullction 689

Trunk Muscles and Their Function in Ventilation-cont'd

Scalenes

• Provides superior and anterior expansion of the upper chest

• Innervated C3 to C8

Sternocleidomastoid

• Provides sup e ri or and anterior exp ansi on of upper chest

• Innervated C2 to C3 and accessory cranial nerve

Trape zi us

• Provides superior expansion of the upper chest

• Innervated C2 to C4 and accessory crani al ne rve

DECREASED CHEST EXPANSION

will see an even greater increase in that abnormal
tone if placed supine. That will make it more difficult Muscle weakness or abnormal tone, combined with
for the child to attempt any flexion phase of a breath­ the effects of gravity that were previously discussed,
ing pattern in supine (coughing or exhalation). Chil­ serve to decrease the ability of the chest to expand in
dren should not be left supine as the therapist teaches one or all three planes of ventilation. Quantitatively,
them altered breathing patterns. If the goal of that chest expansion can be measured via lung volumes
treatment session is to promote controlled exhalation by taking vital capacity readings and comparing them
maneuvers, the child would have been positioned for with the norms, and it can be measured by taking
failure rather than success. Therefore positioning of chest excursion measurements during inhalation with
the patient and tonal inhibitory or facilatory tech­ a tape measure in three places: under the axilla, just
niques become of vital importance when developing beneath the nipple line, and on the lowest most ribs
a treatment plan for maximizing respiratory function. (8,9, and 10). Although both methods give an objec­
tive measurement, neither technique can assess which
planes of ventilation are being compromjsed. Subjec­
SPECIFIC RESPIRATORY IMPAIRMENTS
tive assessment skills are needed to dctermine limit­
The first half of this chapter discusses the forces that ing factors. The box on p. 690 gives detailed sum­
influence the functioning of the neurologically im­ maries of such assessments for persons with aU levels
paired chest. Understanding these forces allows one of SCls. These characteristics can be extrapolated to
to discern the impairments that will appear as a di­ subjective chest assessments of other neurological
rect or indirect result of those neurological deficits. and/or musculoskeletal disorders, especially where
Decreased chest expansion, abnormal or inefficient weakness is present.
breathing patterns, abnormal bony changes, de­
creased cough effectiveness, decreased coordination
COMPENSATORY BREATHING PATTERNS
of breathing with functional activities, decreased
ability to phonate, and decreased ability to self-main­ Limitations in chest expansion inevitably lead to
tain bronchial hygiene can all be direct results of se­ changes in breathing patterns. Severely involved
vere neurological deficits. These specific impair­ CV As or head trauma patients may show severe ab­
ments are addresseu now in detail. normalities in their breathing patterns in response to

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690 PART VII Guidelines for the Delivery of Cardiopulmonary Physical Therapy: Special Cases

Neuromuscular Effects Oil Respiratory FU1lction in Spi1lal Cord Injuries

Paraplegia: Primarily Tl to T5

I. Weakened and/or absent

• Abdominal

• Intercostal

• Erector spinae

2. Planes of ventilation limited

• Slight decrease in anterior and lateral expansion

3. Resulting in

• Slight to moderate decrease in chest expansion and vital capacity (YC)

• Decreased ability to build up intrathoracic and intraabdominal pressures

• Decreased cough effectiveness

• Possible paradoxical breathing

Tetraplegia: C5 to C8

I. Missing aforementioned muscles and weakened

• Pectoralis

• Sen-atus anterior

• Scale·nes

2. Planes of ventilation limited

• Marked decrease in anterior and lateral expansion

• Slight decrease in posterior expansion

3. Resulting in

• Significant decrease in chest expansion and VC

• Significant decrease in forced expiratory volume (FEY)

• Significant decrease in cough effectiveness

• Paradoxical breathing in acute phase and perhaps longer

Tetraplegia: C4

I. Missing aforementioned muscles and weakened

• SClllenes

• Di aphragl1l

2. Planes of ventilation limited

• Marked decrease in anterior and lateral expansion

• Slight decrease in inferior and superior expansion

3. Resulting in

• More pronounced limitations in all three planes of ventilation

• Possible decrease in tidal volume (TY)

• Possible need for mechanical ventilation

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 37 The Patient with Neuromuscular or Musculoskeletal Dysfunction 691

Neuromuscular Effects on Respiratory Function in Spinal Cord Injuries-cont'd

Tetraplegia: Cl to C3

I. Missing aforementioned muscles and weakened and/or absent, the last of the remaining accessory muscles

• Sternocleidomastoid (SCM)

• Trapezius

2. Planes of ventilation limited

• All severely limited including superior expansion

3. Resulting in

• Significant decrease in TV

• The need for full-time mechanical ventilation (at least in acute phase)

impairments to their respiratory centers in the brain

Possible Compensatory Breathing Patterns after
stem. This chapter focuses on compensatory breathing
a NeurologicallnjurylDisease
patterns that develop as a result of muscular weakness
or paralysis, high tone, or pain. Details of breathing • Paradoxical breathing (see-saw breathing)
pattern changes secondary to brain stem lesions can • Paralyzed intercostals and/or abdomina Is
be found in Chapter 22. The compensatory patterns
• upper chest collapses
discussed here are itemized in the box at right.
• abdomen rises excessively
There are two types of paradoxical, or "see-saw,"
Paralyzed diaphragm
breathing. The first is caused by a strong diaphragm
•

in the absence of the two other triad muscles, inter­ • lower chest collapses

costal muscles and abdominal muscles (e.g., polio, • upper chest rises excessively
tetraplegia, or paraplegia). Normal diaphragmatic ex­ • Diaphragm and upper accessory muscles only
cUl'sion requires the muscular support and function of (paralyzed intercostals)
the intercostal and abdominal muscles to optimize the • Upper accessory muscles only (all three "triad"
diaphragm's contractions. In this type of paradoxical muscles paralyzed)
breathing the diaphragm contracts, the abdomen rises • Asymmetrical breathers (hemiplegia, unilateral
excessively because of flaccid abdominal muscle disorders)
tone, and the upper chest collapses because of a lack • Lateral or "gravity eliminated" breathers (weak­
of the stabilizing contraction of the intercostal mus­ ness not paralysis)
cles (Figure 37-9). This is the more common form of • Shallow breathers (typically associated with high­
paradoxical breathing. tone)
The second type of paradoxical breathing occurs
when there is diaphragm paralysis while the upper
accessory muscles are still intact. The abdominal
muscles may or may not be functional. The see-saw primarily in a superior plane. Anterior and lateral ex­
action here is the opposite motion of that described pansion may also occur if the intercostal and pec­
previously (Figure 37-10). With this type of paradox­ toralis muscles are functioning. Generally, this com­
ical breathing, the abdomen draws inward during in­ pensatory breathing pattern requires some kind of
spiration and the upper chest rises. The upper acces­ assisted ventilation, at least part time, because the di­
sory muscles c o n t r a c t , exp a n d i n g the r i b c a g e aphragm normally supplies most of the expansion

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692 PART VII Guidelines for the Delivery of Cardiopulmonary Physical Therapy: Special Cases

FIGURE 37-9
Paradoxical breathing, strong diaphragm, absent accessory muscles and abdominal muscles.

W((I'
FIGURE 37-10
Paradoxical breathing, diaphragm paralysis.

necessary to maintain adequate oxygenation levels. Another type of compensatory breathing pattern oc­
Total accessory muscle breathing is generally inca­ curs when the intercostal and abdominal muscles are
pable of providing adequate independent long-term paralyzed but the diaphragm and upper accessory mus­
ventilation because of the likelihood of respiratory cles still function (i.e., tetraplegia, Cs to Cs; and para­
muscle fatigue. plegia, T I to T5). These patients learn to counterbal­

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 37 The Patient with Neuromuscular or Musculoskeletal Dysfunction 693

FIGURE 37-11
Shortened neck musculature secondary to accessory muscle breathing pattern.

ance the strength of the diaphragmatic pull by using Neurological insults that affect the chest asymmet­
their sternocleidomastoid muscles and possibly their rically, such as with CV As and some head traumas,
scalene, trapezius, and pectoralis muscles. Allowing show another type of compensatory breathing pattern.
for superior and possibly some anterior and lateral ex­ These patients can still acti vely ex pand their unaf­
pansion of the chest, this compensatory breathing pat­ fected side in all three planes of ventilation. Often,
tern prevents the collapse of the upper chest seen in they accentuate this asymmetry to achieve more ex­
paradoxical breathing. This must be cognitively coor­ pansion on their unaffected sides. This may be seen
dinated with the inspiratory phase and is generally a as increased sidebending toward their involved side
more effective breathing pattern. On subjective breath­ (Figure 37-13). This leads to inadequate venti lation
ing assessment, these patients often present with short­ on the affected side, which puts these patients at a
ened neck muscles (Figure 37-11). Intercostal retrac­ higher risk of developing respiratory complications
tions, or the collapsing of the intercostal spaces on secondary to inadequate ventilation. In addition, the
inspiration, may be seen here. The paralyzed inter­ adverse effects on their posture can lead to undesired
costal muscle tissue will be sucked in toward the lungs musculoskeletal changes over a prolonged period of
during the creation of negative pressure within the time especially for the pediatric patient. Prevention of
chest, thus the observance of the retractions (Figure these secondary changes is of utmost importance.
37-12). This may be the most accurate way of assess­ Patients with generalized weakness, such as with
ing intercostal paralysis without an EMG test. Guillain-Barre syndrome, some myopathies, neu­
If the patient lacks all "triad ventilatory muscles," ropathies, or incomplete SCls, may show a tendency to­
they may be able to breathe using their upper acces­ ward lateral breathing, or breathing that takes place pri­
sory muscles only. Generally they will need mechani­ marily in gravity-eliminated planes. For example, in
cal ventilation to augment their independent effort. supine, patients with weakened chest muscles could not

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694 PART VII Guidelines for the Delivery of Cardiopulmonary Physical Therapy: Special Cases

FIGURE 37-12

Intercostal retractions noted during inspiration.

FIGURE 37-13

A and B, patients with hemiplegia. Note asymmetry of trunk.

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 37 The Patient with Neuromuscular or Musculoskeletal Dysfunction 695

effectively oppose the force of gravity in the anterior disorder with oximeter)' during sleep. Patients show­
plane, thus they alter their breathing pattern to cause ex­ ing deficiencies may need repositioning of their sleep
pansion in the lateral plane where gravity is eliminated. postures, nighttime ventilation, oxygen support, or a
In sitting, these same patients would tend to breathe in­ combination of these. Rigorous exercising or activities
feriorly where gravity would assist the movement. of daily living (ADL) training may be more appropri­
Likewise, in side lying, they would tend to breathe in ately scheduled later in the day for these patients until
an anterior plane. Overall, these patients have the best their sleep problems have been rectified.
prognosis for effective breathing retraining methods be­
cause they have weakness, not complete paralysis.
CHANGES IN PULMONARY FUNCTIONS
The last breathing pattern to be discussed involves
patients with central nervous system deficits resulting The abnormal breathing patterns discussed previously
in high tone, such as MS, Parkinson's disease, and develop secondary to the patient's neurological
some head traumas. Their breathing patterns are altered deficits. However, those new patterns then change the
not so much by muscle weakness as by the following: patient's pulmonary function, which in turn affects
(1) chest immobility because of abnolmally high neuro­ functional respiratory status. Specifically, changes in
muscular tone (spasticity, rigidity, tremors), which se­ respiratory rates (RR), tidal volume (TV), and vital
verely limits chest expansion in any plane, (2) cerebel­ capacity (VC) are addressed here.
lar incoordination, or (3) improper sequencing because Alveolar minute ventilation is the product of TV
of lesions in the brain, most commonly seen with times RR. The optimal relationship between these
medullary lesions. Breathing is usually symmetrical, two parameters is those values that result in minimiz­
shallow, sometimes asynchronous, and frequently ing the mechanical work that the lungs must perform
tachypneic (respiratory rates over 25 breaths/minute). with a particular breathing pattern. In other words, it
Initiation and follow-through of a volitional maximal is the combination of RR and TV that requires the
inspiration is difficult or impossible for these patients. body to put out the least muscular effort per breath.
This will markedly curtail the ability to produce an ef­ Because most of the compensatory breathing patterns
fective cough and to maintain bronchial hygiene. that have been discussed thus far reduce the patient's
TV, the only recourse this patient has is to increase
RR. Normal RR is between 12 to 20 breaths/minute;
SLEEP DISORDERS
however, for this neurological population, it is not
The patients described in this chapter frequently uncommon to see RRs at least twice that figure.
need to use their accessory muscles cognitively, to ar­ Although adjusting RR does bring the patient's res­
rive at a work-efficient, ventilation-efficient, breathing piratory system back to a state of equilibrium, it may
pattern. Because of this, they should be evaJuated for not produce the most efficient pattern in the long run.
nighttime ventilatory assistance. Muscle weakness or The idea of the oxygen cost of breathing in that pat­
breathing inefficiency may cause a state of chronic tern must be considered in its long-term functional
hypoventilation and/or sleep apnea episodes during use. Ideally, TV at rest should be about 10% of one's
sleep. Drowsiness, lack of concentration, disturbed actual Vc. At this level, the able-bodied person needs
sleep, and/or irritability are common complaints of less than 5% of the total oxygen available to the body
this s t ate. In the c l i n i c a l setting, we see m a n y to operate the respiratory mechanisms. When per­
tetraplegic patients and other severely involved neuro­ forming a normaJ physical task or low-level exercise,
logical patients who are lethargic after awakening. this oxygen consumption rate increases slowly, never
Hospital staff may incorrectly label these patients as quite reaching a point where the oxygen cost of oper­
lazy or uncooperative. It should be assessed whether ating the respirator), system outweighs the cost of per­
this behavior is volitional or whether it is due to a forming the activity. However, for patients with im­
state of chronic nighttime hypoxemia. Assessments paired chest functions, such as in this popUlation, the
can be made by screening high-risk patients for this total oxygen consumption level of the respiratory

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696 PART VII Guidelines for the Delivery of Cardiopulmonary Physical Therapy: Special Cases

muscles at rest can be as much as 4 to 10 times that the work of breathing. If VC remains less than 60% of
amount. These patients may have TVIYC ratios that the predicted value, most research indicates that these
are already in the 33% to 67% range at rest, indicating patients will demonstrate inadequate coughs. Similarly,
inefficient breathing patterns, reduced VCs, inade­ a FEV 1 less than 60% indicates lack of sufficient power
quate respiratory reserves, or both. When they attempt behind the cough. When VC remains or decreases to
a mild exercise, they become quickly short of breath. only 25% to 30% of the predicted nonn, then ventila­
They do not have adequate oxygen reserves to supply tion assistance usually becomes necessary.
the respiratory and the nonrespiratory muscles simul­
taneously, thus severely limiting exercise tolerance.
ADVERSE MUSCULOSKELETAL CHANGES
Therefore although these patients may show adequate
maintenance of alveolar minute ventilation at rest, a Neuromuscular wea kness and the compensatory
mild increase in activity level may magnify respira­ breathing patterns may cause adverse musculoskele­
tory insufficiencies. tal changes over a prolonged period of time. Previous
An adequate VC is imperative in restoring a pa­ discussion in this chapter revolved around the ad­
tient's functional status. Without the ability to expand verse effects that gravity can play on the skeleton if
the chest maximally under his or her own muscle the body is unable to counteract its force. Pronounced
power, VC will decrease after a neurological insult. For deformities are more prevalent in children, of course;
example, studies show that tetraplegia resulting from however, both children and adults are effected. Sev­
SCIs may reduce the patient's VC to 33% of the pre­ eral examples of specific changes are presented.
dicted value, increasing the TVIYC ratio to 30%. For A common musculoskeletal deformity secondary
SCIs, an adequate VC is generally considered to be to muscle weakness is seen as a flattened anterior
66% of the expected value. This would restore the c h e s t w all, as s e e n w i t h m a n y p a r a p legic and
TVIYC ratio to approximately 15%, thus decreasing tetraplegic patients. (Figure 37-14) For the patient

FIGURE 37-14
Musculoskeletal changes in adult chest secondary to spinal cord injury (SCi). Note flattening of the
anterior chest wall and narrowing of the upper chest.

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 37 The Patient ith Neuromuscular or Musculoskeletal Dysfunction 697

with weak or paralyzed intercostal muscles, this t1at­ Anterior or lateral t1aring of the lower rib cage
tening often occurs because of prolonged supine posi­ may also be noted. This is usually a result of insuffi­
tioning along with the significant resistance that ante­ cient abdominal strength, thus the lower ribs are not
rior chest expansion meets from gravity. stabilized and integrated into the abdominal area (see
Another common deformity is a pectus excuva­ Figure 37-8, p. 687). In upright, this is seen as a
tum at the base of the xiphoid process. Patients who marked delineation between the rib cage and abdom­
have a strong diaphragm but no muscular support inal area in the mid-trunk region (see Figures 37-3,
from the intercostals and abdominal muscles may p. 683 and 37 -15).
develop this type of musculoskeletal deformity (see Upper chest ad verse m uscu loskeletal changes
Figure 37-7, p. 686). It can result from the di­ occur when the intercostal and/or other upper acces­
aphragm pulling inward so hard that the sternum, sory muscles are impaired. The diaphragm is not po­
without intercostal muscle support, cannot maintain sitioned to assist in expansion of this area. Therefore,
its neutral position. Over time, it caves in, resulting without those accessory muscles, the anterior wall of
in a permanent deformity. the upper chest wiII become flattened and appear

FIGURE 37-15
Independent upright posturing. Adult with tetraplegia. Kyphosis restricts chest movement for
respiration. Note folding at mid-trunk line.

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698 PART VII Guidelines for the Delivery of Cardiopulmonary Physical Therapy: Special Cases

more narrow than that of the normal upper chest (see Proper elongation of the cervical spine cannot occur,
Figure 37-14, p. 696), resembling the more primitive resulting in skeletal changes to that area. Scoliosis,
triangular shaping of the chest seen in the newborn along with thoracic kyphosis, tends to be more pro­
(see Figure 37-4, p. 684). nounced than in the adult.
Spinal curves are not spared deformities. In a
weakened, low-tone patient, scoliosis is common be­
DECREASED COUGH EFFECTIVENESS
cause the patient cannot adequately maintain himself
or herself upright against gravity. Slowly, the spine With decreased chest expansion, the presence of
collapses on itself, seeking stability; therefore scolio­ compensatory breathing patterns, and the adverse
sis is developed. All types of patients with the neuro­ musculoskeletal changes, the patient's ability to
logical diagnoses discussed in this chapter are at risk cough will be drastically reduced. Vital capacity will
for developing scoliosis. The second possible spinal be impaired as will the ability to build up sufficient
change, a lumbar and thoracic kyphosis, can occur as intraabdominal pressure, especially for patients with
well because of the force of gravity on a mobile spine weakened, flaccid, or uncoordinated abdominal mus­
and lack of paraspinal muscle support. Secondary to culature. For many patients with traumatic brain in­
these kyphoses, many patients develop an excessive juries, Parkinson's disease, CP, and CVA, the inabil­
cervical lordosis to maintain eye contact. In sitting ity to coordinate an effective cough will be
the patient hunches over his or her trunk, making eye significantly impaired. This inability may be due to
contact and head righting difficult (see Figures 37-3, cerebellar damage or to high neuromuscular tone
p. 683 and 37-15, p. 697). (spasticity, rigidity, tremors). Frequently, the quick
These spinal changes affect the functioning of the action required to produce an effective cough will be
respiratory system adversely. With a kyphotic thorax the same action that will trigger a sudden increase in
in an upright posture, expansion of the chest in all the abnormal neuromuscular tone. Objectively, when
three planes of ventilation will be impaired. The ribs the patient can not expel at .Ieast 60% of his or her ac­
require a stable base from which to become properly tual vital capacity in 1 second (FEV d, he or she will
mobilized. A kyphotic, weak posterior support does often be incapable of producing an effective cough
not provide the necessary stability for optimal rib without some assistance or retraining.
mobility and function. Therefore proper elevation and
angulation of the ribs becomes impossible. This lim­
MAINTAINING BRONCHIAL HYGIENE
its overall chest expansion and vital capacity.
Musculoskeletal changes in children must be ad­ All these changes in respiratory functioning lead to a
dressed. They are in a state of habilitation rather than decreased ability of the neurologically impaired pa­
rehabilitation. Because of this, the neurological tient to independently maintain bronchial hygiene.
deficit affects their developing chests more severely. Complete expansion of the chest in all three planes
Their rib cages remain more triangular in shape, since of ventilation and in all postures is impaired, so the
the muscles of the upper chest never develop fully or ability to properly aerate all lung segments is im­
normally. The ribs also remain more horizontal than paired. Thus the ability to perform independent
in the normal adult, probably because of less upright bronchial drainage will I ikewise be impaired. Ineffi­
posturing and lack of intercostal and abdominal mus­ cient breathing patterns rl)ay cause them to remain in
cle contractions on the rib frames. Their necks and a state of chronic hypoventilation. Inability to pro­
shoulders do not mature developmentally, often be­ duce an effective cough impairs the ability to clear
cause of overuse of the neck accessory muscles. This the lungs of secretions. Therefore most of these pa­
leads to a permanent shortening of the neck strap tients will require some assistance, either physically
muscles, making the child appear to lack a cervical or through verbal instruction, to achieve adequate
area (see Figures 37-7, p. 686, and 37-8, p. 687). bronchial hygiene.

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 37 TIle Patient with Neuromuscular or Musculoskeletal DysfWlction 699

IMPAIRED PHONATION
provided by the muscles of ventilation (Figure 37-16).
Aphasia, as a secondary impairment to neurological When the respiratory muscles are malfunctioning, as
deficits, is generally recognized by all members of the in the neurological diseases discussed, the patient's
medical team as a problem that necessitates speech ability to regulate the flow of air out of the lungs may
therapy. However, many persons with neurological be impaired. Good eccentric control of the inspiratory
impairments display serious deficits in communica­ muscles (the ability to slowly release these muscle
tion that remain untreated and the deficits remain un­ during exhalat ion) is needed to p r oduce normal
acknowledged. Primarily, that deficit is inadequate lengths of phonation. Otherwise, the air may be ex­
breath support for phonation; in other words the pa­ pelled from the lungs too quickly because of the nat­
tient's inability to control the force and duration of ex­ ural elastic recoil of the diaphragm, rendering that
halation for the purpose of phonation. Duration of volume of air useless for phonation. Therefore both a
phonation and voice intensity are regulated by a deli­ decrease in tidal volume and a decrease in eccentric
cate balance between airway resistance, provided by control of the respiratory muscles will lead to impair­
the laryngeal muscles, and the force of exhalation, ments in functional speech.

FIGURE 37-16
Relationship of air flow and vocal folds.

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700 PART VII Guidelines for the Delivery of Cardiopulmonary Physical Therapy: Special Cases

The average adult breathes at a ratio of 1:1 or 1:2 Airtlow out of the lungs should be as impOitant to
(inhalation time: e x h alation time) d u ring quiet clinicians as airflow into the lungs. An evaluation of
breathing. The average ratio during phonation be­ expiratory eccentric control is nccessary for all neu­
comes I :5, with 8 to 10 syllables per breath being a rological patients regardless of diagnoses. All disci­
comfortable speaking length. Clinically, many pa­ plines should incorporate a phonation facilitation pro­
tients are seen to struggle with two- to thee-syllable gram into their rehabilitation program, especially for
phrases because of inadequate breath support. Often those patients who would otherwise not receive any
these same patients are not referred to speech therapy speech training.
for training because they are not diagnosed as having
a "speech" problem (e.g., many patients with SCIs,
GOALS OF A NEUROMUSCULAR OR
MDs, polio, or spina bifida). Optimally, these pa­
MUSCULOSKELETAL RESPIRATORY PROGRAM
ticnts should be able to phonate (an "ah" or "oh"
sound) for at least I 0 to 12 seconds during a con­ In conclusion, the combination of secondary cfJ'ects
trolled expired vital capacity. Many of their voices that follow a neurological and/or musculoskeletal in­
fade away after 3 to 4 seconds. Without the ability to sult are responsible for leaving the person with residual
communicate with normal speaking lengths and nor­ musculoskeletal or neuromuscular deficits at greater
mal voice intensities, these patients' successful reen­ risk for developing respiratory complications long
try into society's mainstream becomes significantly after their acute phases have subsided. The long-term
more difficult. goal of any respiratory rehabilitation program for these
Another misconception about these patients is that patients is obvious; reduce their risk for developing
they are mentally slow or retarded because they do these complications. First and foremost is the need to
not use all the proper figures of speech. In reality, increase or maintain chest expansion in all three planes
these patients may exclude figures of speech because of ventilation. Second, educating the patient and/or
of the extended time it takes them to communicate family in methods to maintain good bronchial hygiene
something. For them, it is more expedient to forego must be emphasized to prevent infections. Logically,
their inclusion. improving cough effectiveness will improve airway
A marked example of this was seen in our clinic. clearance. Next, increasing the patient's vital capacity
A 3-year-old girl who sustained a complete C4 to C5
spinal cord lesion at birth and had not received prior
rehabilitation was seen. On initial examination, her
Respiratory Rehabilitation Goals
speech was choppy, brief, and grammatically incor­
rect. She rarely initiated conversation and her voice • lncrease or maintain chest expansion in all three

intensity was very low. It was suspected that she per­ pl anes of ventilation

haps suffered some anoxic brain damage to account • Educate the patient and/or family in methods for
for her developmentally delayed speech. After an in­ maintaining good bronchial hygiene

tense breathing retraining program in conjunction • Improve cough effectiveness

with a physical rehabilitation program, her speech • Inc r e a s e the patient's vital capacity and t idal
changed drastically. She spoke fluently, with 8 to 10 volume

syllables/breath, correct inclusion of grammar, and • Reduce high respiratory rates

louder and more varied voice intensities. Instead of • Modify inadequate breathing pattern s
being quiet and more reserved as she had been before
• Improve eccentric control of the diaphragm and
treatment, the mother reported that the child was a other ventilatory muscles for improved phonation
regular chatterbox. Her new communication skills ap­ skills
peared to improve her self-esteem. At that point, it • Incorporate effective ventilatory strategies with all
became understood that her cognitive skills were well motor tasks
underestimated on initial screening.

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 37 The Patient with Neuromuscular or Musculoskeletal Dysfunction 701

and tidal volume, where indicated, will help to im­ Aronson, A. (1985). Clinical voice disorders: An interdisciplinary
approach. (2nd ed.). New York, Thieme Inc.
prove aeration of the lungs. If necessary, reducing high
Ashw0l1h, B. & Hunter, A.R. (1971). Respiratory failure in myas­
respiratory rates to improve pulmonary functions will
thenia gravis. Proc R SocLondon (Bioi) 64:489-90.
be a goal. Other goals include modifying inadequate Bach,J.R. (1991). New approaches in the rehabilitation of the trau­
breathing patterns, which could mean increasing or de­ matic high level quadriplegic. Americal JOllm,,1 of Physical
creasing the use of accessory muscles to achieve maxi­ Medicine and Rehabilitation 70( I):1]-9.
Bach, J.R. (1995). Respiratory muscle aids for the prevention of
mal breathing efficiency, and improving eccentric con­
pulmonary morbidity and mortali t y. Seminar.< in Neurology
trol of the diaphragm and other ventilatory muscles for
15( I):72-82.
improved phonation skills. These concepts lead us to Boehme, R. (1992). Assessment and treatment of the respi rato ry
realize the need for incorporating effective ventilatory system for b realhing, sOllnd production and trunk control.
strategies with all motor tasks. These goals are summa­ Teamtalk 2(4):2-8.

rized in the box on p. 700. When implementing this Borden, G., H a r ris, K. Speech Science Primer: Physiology,
Acoustics, and Perception of Speech, 2nd cd. Baltimore,
program, it is necessary to recall that the patient's res­
Williams & Wilkens, 1984.
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able to apply what they learn from this program into the head i n juried patient in the intensive care unit. TOIJi('s in
all phases of their lives. Thus incorporation of these Acute Care Trauma Rehabilitation 1( 1) : 1-18.
Boyden, E. (1977). Development of the newborn lung. In hudson,
goals into ADL or mUltipurpose activities will yield
W.A. (Ed). Development and growlh oj the airways. New
the most successful results.
York: Marcel Dek.ker.
Braun,N.T. (1982). Force-length rela tionship of the normal human
diaphragm. Journal of Applied Physiologv 53:405-412.
REVIEW QUESTIONS Brown, J.e., Swank, S.M., Matta, J., & brras, D.M. (1984). Lare
spinal deformity in quadriplegic children and adolescents.
l. What differences are noted in patients suf­
Journal of Pediatric Orthopedics 4(4):456-61.
fering deficits acquired as adults versus a Bymn, A.e. Mansell, A.I.. & Levison, H. (1977). Regulation of
c h il d with acquired d e f i c its in u tero or pulmonary alveolar development i n late gestation and the peri­
shortly after birth? natal period. In Hudson, W.A. (Ed). Development and grm4'lh
offhe airways. New York: Marcel Dekker. 399-418.
2. Which orthopedic and neurologic diagnoses
Cartwright, R.D. (1984) Effect of sleep position on sleep apnea
can be associated with cardiopulmonary dys­
severity. Sleep 7(2): 110-14.
function? Cherniak, R.M. Cherniak, L., Naimark, A. (1972). Respiration
3. How should the effect of gravity on ventilation i n heallh and disease. (Second Edition). Philadelphia: PA

be considered during exercise and positioning? Saunders.

4. What factors contribute to normal chest de­ Cherniak, N.S. A bnormal breathing pal/ems: Their mech(lI1isms

and clinical significance. JAMA 230:57-58.

velopment?
Clough, P., Lindenauer. D., Hayes, M., & Zekany, B. (1986).
5. What symptoms would be noted in patients Guidelines for routine respiratory care of patients with spinal
that have sleep disorders? 66(9): 1395-402.
cord injury. Physical Therapy
6. Why should a therapist be concerned about Cooper, e.B., Trend, P.S. & Wiles, e.M. (1985). Severe di­
phonation in patients with neurological dys­ aphragm weakness in multiple sclerosis. Thorax 40:631-32.
Corrado, A., Gorini, M., & De Paola, E. (1995). Alternative tech­
function?
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7. What are the goals of a neuromuscular/mus­ Seminars in Neurologv 15( 1):84-88.
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uals with it history of poliomyelitis. Chest 1991; 100: 118-123.
DeGroodt, W., et al. (1988). Growth of the lung and thorax di­
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 The Transplant Patient

Susan Scherer

KEY TERMS Cardiac rehabilitation Organ rejection

Denervation of the heart Psychosocial
Immunosuppression Pulmonary rehabilitation
Organ donation Secretion management

HISTORY BACKGROUND

The ability to transplant an organ from one individual Early transplant experiments were carried out on ani­
to another is a relatively new phenomenon. Early at­ mals in the early 1900s, with success at maintaining
tempts at transplant were barely successful. New ad­ life for 90 minutes to 8 days (Hosenpud, Cobanoglo
vances in surgical techniques and immunosuppres­ Norman, Starr, 1 991). Medical advances in car­
sive drugs, however, have made transplantation of diopulmonary bypass and immunosuppressive med­
solid organs a viable treatment option. The increased ications provided the opportunity for successful
life expectancy of transplant patients means that transplants. After many trials and failures, the first
physical therapists have many opportunities to treat successful orthotopic heart transplant was performed
patients after transplant in various settings. Trends in in 1967 by Barnard; the first successful lung trans­
patient demographics indicate that a physical thera­ plant was performed in 1963 by Hardy and Webb.
pist may see a transplant patient not only in a re­ Improvements in surgical technique, detection of
gional medical center setting but also in outpatient rejection, and immunosuppressive drugs means trans­
and rural clinics. This chapter contains guidelines for plants are increasing in number. Virtually every solid
treating patients with heart or lung transplants. organ can be transplanted from one individual to an­

703

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704 PART VII Guidelines for the Delivery of Cardiopulmonary Physical Therapy: Special Cases

other of the same species if there are similarities in National I-year survival rates are as follows:*
immune system markers. Kidney transplants are the
simplest and most common, whereas heart-lung block Kidney 93 8%
.

transplants are uncommon. Liver 76.7'k

Heart 82.6%
Heart-lung 57%
Purpose of Transplants Lung 68%

Although transplants are considered an acceptable

Organ Donation
treatment option, a solid organ transplant is usually
considered a last-resort therapeutic intervention. The major limitation of organ transplantation is a
Medical intervention for diseases, such as cardiomy­ supply and demand issue. The number of patients
opathy and interstitial pUlmonary fibrosis, is limited. who could benefit from transplant significantly ex­
When conventional medical therapy has failed, a ceeds the number of organs available. Media cover­
transplant may be considered. Although a transplant age assists with identifying the issues and may play a
offers a patient a second chance at life, the medical role in increasing the number of donors. To become
management of a transplant causes a patient to re­ an organ donor, check with your state about specific
quire medical intervention on a long-term basis. requirements; often a driver's license has a space to
identify you as an organ donor. Make sure that you
discuss your wishes with your family. If you are hos­
Availability of Transplants
pitalized, family members or close personal friends
The number of medical centers who perform trans­ wil I often be approached about donating your organs.
plants has grown to approximately 175 worldwide If your family is confident that you wished your or­
in 1989 (Hosenpud et aI., 1990). Because of the suc­ gans to be donated, they will more likely say "yes" to
cess rates, many types of transplants are no longer organ donation.
considered experimental but are considered appro­
priate treatment for organ failure. In 1994 approxi­
CURRENT TRANSPLANT ISSUES
mately 10,000 kidney transplants were performed
and 2500 heart transplants were completed (Col­ Transplant trends include early detection of rejection,
orado Organ Recovery Systems [CORS], Denver, development of new immunosuppressive medica­
Colorado 1994). tions, and donor management. For donor organs to be
viable, the donor must be managed in a way that pre­
serves organs. In the past, fluids were pushed to pre­
Rejection Issues
serve kidney function for transplant. This extra fluid,
Although transplants are successful, some health pro­ however, made the lungs unusable. New donor man­
fessionals believe that patients are merely exchanging agement techniques are increasing the viability of
one set of problems for another. For a transplant to be multiple organs from the same donor.
successful, a patient must remain on powelful immuno­
suppressive drugs for the remainder of his or her life.
Ethical Considerations
Some of these medications have crippling side effects.
The effects of long-tenn prednisone are well known: Should a p e rson who h a s developed end-stage
osteoporosis, muscle weakness, and glucose intoler­ chronic obstructive pulmonary disease (COPD) from
ance, whereas the long-term effects of cyclosporine and smoking be allowed to receive a lung transplant?
azathioprine impact on the patient's ability to fight in­ Should a heart transplant be given to someone who
fection. Patients also need to manage medication side developed alcoholic cardiomyopathy? Should a pa­
effects on a day to day basis. It is these medications,
however, that make for impressive survival rates. 'Source: CORSo Denver. 1994.

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 38 The Transplant Patient 705

tient with cystic fibrosis receive a double-lung trans­ transplant program. Because of these needs, most
plant even though the donor lungs could go to two transplants are performed at large, regional medical
different individuals with pulmonary fibrosis? These centers, often those associated with a medical school.
are some of the ethical issues with which transplant Because donor organs are viable for only hours after
teams struggle. There are no easy answers nor is there removal from the donor, patients waiting for trans­
unanimous agreement on each case. Despite the diffi­ plant are required to live within a several-hour radius
culty of making wise choices, each team carefully of the transplant center. Some patients may arrange
considers each candidate for transplant. Criteria are air transportation to the medical center, others may
used so that individual preferences of team members relocate themselves and family to temporary housing
are not given priority. When and if health-care re­ within the metropolitan area. Most patients are given
sources become more limited, the decisions may be­ a beeper to maintain contact in a timely manner.
come more difficult. If transplant success improves
and donor organs increase in number, transplants
Psychosocial Implications
could become a mainstream of treatment.
A strong support system is considered an essential
component of a successful transplant. Demands of
Criteria for Being listed on a Transplant Waiting list
waiting and relocation to the transplant city put con­
Virtually every medical center with a transplant siderable stresses on the patient and significant others.
program has developed criteria for patient selec­ The patient is torn between wanting to remain hopeful
tion. Although each center may set its own criteria, that a transplant will provide new life and the reality
there are similarities among the medical centers of knowing that death may come before the transplant.
(see box below). Patients feel these oppositional forces continuously
and struggle to keep a balance between hope and real­
ity. Therapists can assist patients by listening to feel­
Waiting Time
ings, being supportive, and encouraging participation
The time spent waiting for a transplant can vary con­ in support groups. Because most patients experience
siderably. Some patients wait less than a week; others these feelings, support groups offer invaluable inter­
wait up to 18 months. During the waiting period, pa­ vention. Groups which include patients both before
tients struggle with the need to carry on their lives, all and after transplant probably have the most to offcr in
the while knowing that at any moment they may be terms of psychosocial support. Those patients who re­
called to the hospital for transplant. locate to transplant centers may have the most diffi­
The number of transplant centers in the United cult time psychologically, especially as they leave
States is limited. State of the art hospital facilities and family and significant others behind. Feelings of
surgeons are neccssary components of a successful being useless are common because patients waiting in
a foreign city must find something to do.
Spouses and significant others also benefit from
group support. The psychological stresses are some­
what different on spouses. Spouses speak of the
Criteria for Transplant Waiting List struggle to remain hopeful, yet plan for a future that
may not include their loved one. If the patient and
Age: under 65 (60 in some centers)
spouse move to a new city to wait for transplant, they
Terminal illness (expected life span less than I year
may find themselves with more time together than
Nonsmoker
they have ever spent before. ]n this forced retirement,
Adequate social support system new stresses are added to relationships. Transplant
Disease free in other systems teams usually include a psychologist or social worker
to whom patients may be referred for individual or

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706 PART VII Guidelines for the Delivery of Cardiopulmonary Physical Therapy: Special Cases

family counseling if the stresses limit function or par­ fort and function after surgery. The physical therapist
ticipation in pretransplant programs. should be familiar with the surgical incisions and im­
After transplant, patients struggle with conflicting pact on rehabilitation.
feelings. Patients are often emotionally overwhelmed Heart transplants are usually performed through a
with a feeling of gratefulness that they are alive and median sternotomy incision and cardiopulmonary by­
feel guilty that someone else's glief has given them a pass is used. A midline incision from sternal notch
chance to rejoice. Psychological or spiritual support distally allows the sternum to be accessed and split.
may be requested or s u g gested after transplant Although the native heart is excised, a portion of the
(Craven, Bright, and Dear, 1990). right atrium and the SA node is preserved. The donor
heart is sutured to the atrial cuff and the major ves­
sels reattached. After surgery, the two halves of the
Patient Education
sternum are wired together, the new heart defibril­
The waiting period time provides an ideal opportu­ lated, bypass reversed, and the patient awakened.
nity for patient education. Nursing generally provides Lung transplantation surgical incisions depend on
much of the education regarding preoperative proce­ whether a single or double-lung transplant is to be
dures, postoperative course, and medication. Rehabil­ performed. Single lung transplants are performed
itation teaching includes breathing training, airway through a posterolateral thoracotomy incision, with
clearance techniques, and activity progression. the patient side lying on the opposite side. To allow
visual access for the surgeon, the latissimus dorsi and
lower trapezius muscles are cut. The incision through
TRENDS IN TRANSPLANT CARE
the fourth or fifth intercostal space also means the in­
Transplants are being made available to a broader tercostal muscles at this level may be incised. If the
group of patients. Although transplants are only per­ rib at the surgical level fractures, it is resected so that
formed in certain centers, patients from rural areas the bone ends do not rub or puncture the lung. The
are being evaluated at regional centers. Because serratus anterior muscle is preserved if at all possible,
transplant criteria differ slightly from center to center, but the lateral portion of the rhomboid may be cut to
some patients may be evaluated at several centers. allow more access for the surgeon. Postoperative pain
The increased availability of transplants and the relia­ and impaired upper quarter movement patterns may
bility of air transportation means that even patients present significant problems for patients.
from outlying geographical areas may be considered Double-lung transplants are performed through an
for transplant. After transplant, improved medical anterior incision sometimes described as a clamshell
care has led to shorter hospital stays. For the patient approach. A horizontal incision above the level of the
who has relocated to the transplant city this means diaphragm is performed, but the distance needed for
that he may be discharged to an apartment and return adequate visualization means that the pectoralis
to the hospital several times a week for physician fol­ major and minor may be incised bilaterally.
low-up and rehabilitation. Once medically stable, pa­
tients may be allowed to return to their homes as
PHYSICAL THERAPY CONSIDERATIONS
early as 2 to 3 months after transplant, if medical sup­
port and rehabilitation needs can be met. As important members of the transplant team, physi­
cal therapists need an understanding of the physiolog­
ical components of both the pretranspJant disease and
SURGICAL PROCEDURES
posttransplant state, the influence of surgery or physi­
The surgical approach for transplant is chosen to pro­ ology on musculoskeletal structure and function, and
vide the surgeon the optimal working area and visual how medical management may necessitate modifica­
field. The choice of incision may affect patient com­ tion of therapeutic interventions.

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 38 The Transplant Patient 707

Physiology
c1es of respiration is reduced. The physical therapist
The cardiovascular and respiratory systems are criti­ needs to optimize breathing in the preoperative pe­
cal elements of functional ability, in areas of en­ riod, yet prepare the chest and shoulder muscu­
durance and movement. Adequate oxygenation and loskeletal system for normal function.
circulation are needed to provide fuel to perform
daily activities. In the patient awaiting heart trans­
Medical Management
plant, cardiac output is significantly compromised,
and hemodynamics may be unstable. Because of Knowledge of medical management including med­
these limitations, pretransplant exercise is inappropri­ ications, ventilatory support, and hemodynamic mon­
ate. Posttransplant. however. the main interventions itoring assists the therapist in determining whether
will be to restore normal cardiac output. Knowledge modifications are needed during rehabilitation. Table
of physiology allows the therapist to choose appropri­ 38-1 lists suggested areas to monitor during both be­
ate interventions. fore and after transplant rehabilitation. For example,
In patients with terminal lung disease. the primary patients often complain of tremors during rest and ac­
limitation is ventilation. Pulmonary rehabilitation has tivities. Therapists should be knowledgeable enough
been beneficial in improving daily function (Toronto to question other health professionals as to whether
Lung Transplant Group, 1988; Petty, 1980; Moser, the tremors are a result of medications, such as cy­
Bokinsky. Savage, Archibald, Hansen, 1980) and c1osporine, a metabolic abnormality, a seizure disor­
may be used in the pretransplant period. Supplemen­ der, or muscle weakness.
tal oxygen can be lIsed during exercise to maintain
adequate oxygenation. The waiting period before
PHYSICAL THERAPY ASSESSMENT
transplant is an ideal time to optimize muscle func­
tion and flexibility. The purpose of physical therapy before transplant is
to identify baseline function and to screen for impair­
ments that may limit rehabilitation goals. In some in­
Musculoskeletal Considerations
stances, physical therapists will provide treatment in
The musculoskeletal problems of patients with pul­ the pretransplant period; in other cases, the informa­
monary disease are well documented (see Chapter 4). tion gained from early assessment allows the thera­
Patients undergoing lung transplants are unique in pist to identify areas needing attention or modifica­
that after transplant the musculoskeletal system re­ tion after transplant. Physical therapy assessment in
turns to normal structure. The chest wall adapts in the postoperative period addresses specific impair­
size to the new lung. The need to use accessory mus- ments and functional limitations of the individual.

TABLE 38-1

Recommended Monitoring
" = heart x = lung

BLOOD PRESSURE HEART RATE Sa02 RA TING OF PERCEIVED EXERTION

Before exercise x -.J x -.J x

During exercise -.J x -.J x x -.J

After exercise -.J x -.J x

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708 PART V[[ Guidelines for the Delivery of Cardiopulmonary Physical Therapy; Special Cases

Cardiac Patients PRETRANSPLANT REHABILITATION

Pretransplant assessment of the cardiac patient in­

Heart Transplant
cludes functional ambulation (6-minute walk) and
screening for deficits in muscle strength or range of Because the patient awaiting heart transplant has sig­
motion. Exercise training is not generally recom­ nificantly compromised cardiac output and may be
mended pretransplant. Range of motion may be in­ hemodynamically unstable, preoperative rehabilita­
creased or specific muscle strengthening may be ac­ tion is generally not recommended. Some patients
complished, however, if the need is determined to be with moderate congestive heart failure may be able to
significant. All patients will be limited in functional tolerate a mild level of exercise (Roubin, Anderson,
endurance, therefore the results of the 6-minute walk et aI., 1990; Hillegass and Sadowsky, 1994). Most
is compared with posttransplant functional status. patients, however, are unable to tolerate endurance
training.
Some patients may need musculoskeletal interven­
Pulmonary Patients
tion for decreased range of motion, muscle weakness, or
Because rehabilitation in the pretransplant period is general discomfort. If physical intervention is needed,
often indicated in patients waiting for lung transplant, heart rate, blood pressure, and ECG monitoring is used
the physical therapy assessment information may be to guide treatment. If heart rate or blood pressure de­
used to design a more effective rehabilitation pro­ creases during exercise, exercise should be stopped.
gram. Upper and lower extremity muscle strength The main goal in the preoperative period is to pre­
and range of motion is assessed, as well as posture, vent losses of function. Maintenance of range of mo­
shoulder and trunk mobility, breathing pattern, breath tion, soft tissue extensibility, and muscle strength are
sounds, and functional mobility. suggested goals.

Posttransplant Assessment Lung Transplant

(Heart and Lung)
Although each patient is treated individually, there
After transplant, physical therapy assessment ad­ are similarities among patients, resulting in a stan­
dresses all areas of functional limitations and the cor­ dard program for pretransplant rehabilitation (Figure
responding impairments. Patients should be evaluated 38-1). Pretransplant rehabiIi tation resembles pul­
in the immediate postoperative phase, and reevalu­ monary rehabilitation programs in existence for pa­
ated on admission to the outpatient treatment phase. tients with COPD, CF, and restrictive d i seases
Because of the surgical intervention, bed mobility, (Toronto Lung Transplant Group, 1988; Conners and
ventilation, secretion management, range of motion, Hilling, 1993; Malen and Boychuck, 1989).
and pain control are important areas to address.

General Considerations for Rehabilitation

REHABILITATION OF THE TRANSPLANT
Since the primary limitation in pulmonary disease is
PATIENT
ventilatory, oxygen needs are essential to monitor. A
To assist in treatment planning, rehabilitation is cate­ pulse oximeter with finger or ear probe is mandatory
gorized into the following four phases: pretransplant, in a pretransplant pulmonary rehabilitation program.
postoperative acute phase, postoperative outpatient Oxygen saturation should be maintained above 88%
phase, and community- or home-based phase. Al­ at all times. A source of supplemental oxygen is nec­
though the ultimate goal of transplant rehabilitation is essary, whether the patients bring their own oxygen
to improve the patient's function and quality of life, or it is supplied by the center. In patients with severe
each phase of rehabilitation has its own emphasis. disease, oxygen-conserving devices may need to be

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 38 The Transplant Patient 709

loskeletal impairments to function. Using the waiting

time to maximize muscle strength and range of mo­
tion means that less time is needed posttransplant to
return to functional activities. Pretransplant rehabilita­
tion programs have been shown to decrease posttrans­
plant hospital stay (Scherer, 1995). It is reasonable to
set goals to achieve normal muscle strength in lower
extremity musculature, increase upper extremity mus­
cle strength, increase shoulder and chest wall range of
motion to normal or within functional limits, demon­
strate coordinated diaphragmatic breathing with exer­
cise and activities, and improve cardiovascular en­
durance. An example of a preoperative pulmonary
rehabilitation program is in the box on p. 710.

Interventions

Deficits which are found in any of the above areas

may be addressed in the pulmonary rehabilitation
program, except in patients with primary pulmonary
hypertension or Eisenmenger's syndrome. In those
patients, exercise which increases cardiac workload
is contraindicated. However, if cardiac output is
monitored and the physician agrees, range of motion
exercises may be taught and light strengthening ex­
ercises may be performed. For example, a 22-year­
old female with primary pulmonary hypertension
was found to have injured her shoulder 4 weeks pre­
FIGURE 38-1
viously, resulting in decreased range of motion in a
Pre-lung transplant rehabilitation.
capsular pattern. She has been on the lung transplant
waiting list for 3 months. The physician wants her
only to walk as necessary for her daily activities.
used. Patients with COPD should have blood gases With consultation with the physician, joint mobi­
monitored for carbon dioxide retention, since increas­ lization, range of motion activities, and modalities
ing exercise often requires an increase in supplemen­ may be used with few precautions. Strengthening
tal oxygen. Several of our patients has carbon dioxide exercises may be used cautiously, avoiding breath­
levels in the 88 to 100 range. Although heart rate is holding and Valsalva maneuvers.
not a good measure of exercise intensity, patients
with lung disease may demonstrate signs of right
Other Transplants
heart failure and should have heart rate and blood
pressure monitoring on a regular basis. Patients awaiting other organ transplants may also be
referred to physical therapy for treatment of muscu­
loskeletal problems. Because of the level of meta­
Goals
bolic abnormality in patients awaiting liver and kid­
The overall goal of pretransplant pulmonary rehabili­ ney transplants, endurance training is difficult to
tation is to maximize function and reduce all muscu­ perform. Other physical therapy interventions, how­

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710 PART VII Guidelines for the Delivery of Cardiopulmonary Physical Therapy: Special Cases

Preoperative Pulmonary Rehabilitation

Warm-up (group) 10 minute

Active range of motion

Upper body

Lower body

Trunk

Light resistance (5 to 10 reps)

Individualized Endurance Program

Bike (Airdyne) 25 to 30 watts 10 to 20-minute intervals

Treadmill 0.8 to 1.5 mph

0% to 5% grade 10 to 30 minutes

Arm ergometer 0 to 25 watts 10 to 15 minutes forward and backward

Individualized Strength Program 15 to 20 minutes

Pulleys Theraband

Latissimus pull-downs Rhomboids

Diagonal arms Shoulder extension rotation

Pectoral Shoulder flexion

Latissimus

Triceps

Subscapularis

Lower Extremity

Quadriceps

Hip extensors

Hip abductors

Cool-down (group) 10 minutes

Stretching (full-body)

B reathing

Relaxation

ever, m a y be u s e d as appropriate (i.e., muscle and increasing functional abilities in self-care and
strengthening, range of motion). ambulation.

ACUTE PHASE REHABILITATION Heart Transplant (Acute)

The acute phase of rehabilitation begins in the inten­ Considerations

sive care unit and continues throughout the patient's In the immediate postoperative period after heart
hospital stay. Interventions are focllsed on facilitat­ transplant, cardiac output is compromised and hemo­
ing normal cardiovascular and pulmonary function dynamic responses slowed. A transplanted heart is

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 38 The Transplant Patient 711

University Hospital Cardiovascular Rehabilitation Supervised Exercise/Activity Plan/Surgical Patients

Physician DX MEDS

Step/Date Exercise Activity

I ICU -Active/Passive ROM, in bed x 5 reps -Partial self care

1/5 METS -Feed self
-Use of bedside commode
I I -Teach hourly ROM exercise -UP in chair for meals as
/ / -Turn, cough, deep breathe & use in-
centive spriometer, q2-4°
-Sitting bed bath

21CU -Active ROM, sit on edge of bed x 5 reps -Sit in chair as tol
1.5-2.0 METS -Teach Rating Perceived Exertion -Partial/complete self care
-Up in chair for meals
-Turn, cough, deep breathe and use
incentive spriometer, q2-4°
-Sitting bed bath

3 FLOOR -Active ROM/warmups, standing x IO reps -Sit in chair 2-3x/day (20 min)
2.0 METS -Walk 100 ft. slow pace -Complete self care
-Sitting bed bath
-Incentive spriometer indep, TID

4FLOOR -Warmups, standing x 10 reps -Complete self care

2.5 METS -Walk 150 ft, average pace -Use of bathroom w/assist
-Teach pulse counting -Walk around room
-May take warm shower after pacer
wire removed
-Incentive spriometer indep, TID

5 FLOOR -Warmups, standing x IO reps -Dressing indep

3METS -Walk 300 ft, average pace -May stand at sink for ADLs

6 FLOOR -Warmups. standing x 10 reps -As above

3.5 METS -Walk 500 ft. average pace -Introduce to phase II
-Walk down flight of stairs
-Instruct in home exercise

7 FLOOR -Warmups, standing x 10 reps -All self care indep

4METS -Walk up flight stairs -As above
-Walk 500 ft average pace
-Schedule sub max ETI
-Enroll in Phase II

Guidelines for Exercise

-Pt HR to be 50-120 bpm -no significant anhythmias

-Exercise HR not more than 20 beats above rest -SBP < 200, DBP < 120 during exercise

-No worsening ST changes -< 10-15 DBP drop during exercise

-RPE of IO or less -no angina or other symptoms

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712 PART VII Guidelines for the Delivery of Cardiopulmonary Physical Therapy: Special Cases

stiff for several days, and the sympathetic nervous the heart is denervated. Because of the lack of sym­
system input to the heart is destroyed in the transplant pathetic input, heart rate cannot increasc quickly and
process. To maintain cardiac output (HR x SV) in a contracti I ity is not under sympathetic control. The
heart with decreased stroke volume a fixed rate pace­ only mechanism by which heart rate can be increased
m a k e r is u s e d at a r a t e of a p p r o x i m a t e l y 120 is by circulating catecholamines, which take 10 to 15
beats/minute for several days. ECG readings may be minutes to influence a response. Therapists working
normal because the donor heal1 has an intact conduc­ with heart transplant patients should allow time for
tion system, although the atrial cuff left from the na­ patients to adapt to changes in position and may want
tive heart may cause the ECG to have two P waves. to use light active bed exercises as a warm-up activity
The therapist working with heart transplant patients (Irwin and Tecklin, 1995 ).
in the ICU should be aware that heart rate cannot in­
crease significantly, therefore blood pressure and pa­ Lung Transplant
tient response should be monitored. Surgical cardiac
rehabilitation guidelines can be used to guide treat­ Considerations
ment, with increases of 0.5 to I metabolic equivalent After lung transplantation, patients are generally me­
(MET) per day (see box on p. 711). Complications of chanically ventilated for 24 to 72 hours. Often, para­
heart transplant include sternum instability, infection lytic agents are lIsed in this period so that ventilation
or pain, and potential nerve or circulatory damage to can be optimized. Patients who received double-lung
the femoral area because of intraaortic balloon pump transplants may be more hemodynamically compro­
(lABP) cardiac assist. Acute rejection episodes are mised if they were on bypass during surgery. Chest
characterized by flu-like symptoms including low­ tubes are likely in place, and patients are medicated
grade fever and muscle achiness and is often accom­ for pain. Infection control is imperative; isolation
panied by dysrhythmias. Rejection episodes can only rooms with negative-pressure ventilation are used
be confirmed by tissue biopsy. and medical personnel at minimum are required to
wash their hands and wear masks when in the pa­
Goals
tient's room. Isolation or reverse-isolation procedures
Goals of the acute phase of rehabilitation include the are followed (the patient wears the mask when leav­
following: (I) regain normal postural cardiovascular ing the room). The primary monitoring is oxygen sat­
responses (no postural hypotension) and (2) increase uration, followed by heart rate and blood pressure. A
functional activities. The former is primarily focused common complication in the immediate postoperative
on the patient being able to tolerate changes in posi­ period is pneumothorax.
tion, increase time in upright sitting, and transfer in­
dependently. Upper and lower extremity range of
Goals
motion and strength need to be adequate to perform In the immediate postoperative period the major goals
activities of daily living. are to increase time out of bed, optimize ventilation­
perfusion ratio, and increase active range of motion on
Exercise Guidelines
the surgical side (Malen and Boychuck, 1989). Major
Deconditioning and lack of sympathetic input to in­ problems and goals are listed in Table 38-2.
crease heart rate response contribute to the possibility
of hypotension. Because of the high incidence of pos­
Interventions
tural hypotension, patients need to change positions The range of therapeutic interventions are many. In
slowly and be given time to adapt to the new posi­ general an intervention may continue until an abnor­
tion. Exercise may be continued during mild-to-mod­ m a l exercise response is reached. Abnormal re­
erate rejection episodes but is not performed during sponses include a decrease in heart rate or blood pres­
periods of severe rejection. The main consideration sure with an increase in exercise, a decrease in
for exercise in patients with heart transplants is that oxygen saturation below recommended levels (88%

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 38 The Transplant Patient 713

TABLE 38-2

Problems and Goals for Acute Posttransplant Rehabilitation: Lung Transplant

PROBLEM GOAL
Decreased secretion clearance Independent secretion management
Because the lungs are denervated, there is decreased
sensation of secret ions.

Incisional pain Pain management

Postoperative pain is related to the surgical incision Pain medication
and decreased movement of muscles

Abnormal postural hemodynamic responses Normalize hemodynamic response

(i.e., postural hypotension and fatigue) (i. e. , no postural hypotension, normal heart rate, respiratory
rate, and blood pressure response to exercise)

Increased oxygen/venWatory requirements Adequate oxygenation without supplemental (Sa02 94%

to 96% on room air)
Diaphragmatic breathing
Normal vital capacity

Decreased runctional mobility Independent activities of daily living (dressing, hygiene,

shower, toilet)
Decreased shoulder range of motion Need adequate shoulder range of motion to perform these
activities

Decreased exercise tolerance Independent transfers

Out of bed most of day
Independent ambulation SOO ft
Bicycle 10 minutes, no resistance

Compromised nutrition No supplemental feedings (IV)

Considerations
to 90%), or symptoms of dizziness and diaphoresis.
Suggested treatments are shown in Table 38-3. As mentioned before, transplanted hearts lack auto­
nomic innervation. Implications for exercise response
are that heart rate increases can only be accom­
POSTOPERATIVE OUTPATIENT REHABILITATION plished, using circulating catecholamines. For the
phase II cardiac rehabilitation patient, this means that
Heart Transplant the warm-up and cool-down portions of exercise
Once the patient leaves the hospital, rehabi litation should be increased to 10 t o 15 minutes and pro­
looks much like phase II cardiac rehabilitation. The gressed slowly. Resting heart rates are close to the in­
overall objective is to increase functional activity to trinsic heart rate of 100, and heart rate should not be
within normal limits. used as an indication of fitness nor to establish exer­
Duration of this phase of rehabilitation generally cise intensity. Rating of perceived exertion is a more
continues for 8 to 12 weeks, at which time the patient appropriate indication of exercise intensity. Recom­
is encouraged to continue exercise on his or her own mended guidelines are 11 to 13 on the 20-point Borg
or at a fitness facility. Many heart transplant patients scale (Irwin and Tecklin, 1995; Hosenpud et aI.,
return to predisease levels at this stage. 1990). Both endurance and strength exercise can be

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714 PART VII Guidelines for the Delivery of Cardiopulmonary Physical Therapy: Special Cases

TABLE 38-3

Acute Rehabilitation Interventions

GOALS INTERVENTIONS
I
Independent secretion management Incentive spirometer I
Secretion removal (positioning, percussion, and vibration)
Assisted cough or instruction

Pain management Active range of motion shoulder girdle

Pain medication Positioning
Mild heat
Massage/soft tissue techniques

Normalize hemodynamic response Sitting on edge of bed

(i.e., no postural hypotension, normal heart rate, Out of bed to chair day 1 or 2
respiratory rate, or blood pressure response to Ambulation to bathroom day 2 or 3
exercise)

Adequate oxygenation without supplemental oxygen Instruction of diaphragmatic breathing

Diaphragmatic breathing with activity Facilitation of diaphragmatic breathing
Normal vital capacity Lateral costa l expansion techniques (surgery side)
Incentive spirometry

Independent activities of daily living (dressing, Encourage and assist with activities of daily living
hygiene, shower, toilet) Active and active-assisted range of motion
Need adequate shoulder range of motion to All motions shoulder girdle
perform these activities Wand exercises
Side lying shoulder abduction

Independent transfers Daily schedule

Out of bed most of day Assisted ambulation in room initially, to hallway within
Independent ambulation 500 ft 2 to 3 days
Bicycle 10 minutes, no resistance Bicycle in room, 2 minutes initially, progress to 10 minutes

No supplemental feedings (IV) Schedule rehabilitation around meals

Medical management of nausea

performed in this rehabilitation stage, although upper should be reported to the physician immediately. Re­
extremity strengthening should only be started after jection episodes are monitored by biopsy. Exercise
the sternum has healed. To protect the sternum, lift­ can continue if the rejection episode is mild or mod­
ing should be limited to Jess than 10 lbs for 6 to 8 erate as determined by biopsy. Summary guidelines
weeks. Treadmill, bike, arm ergometry, and indoor for postoperative rehabilitation for heart transplant
cross-country ski equipment are all appropriate are outlined in the box below.
choices.

Signs of Rejection Lung Transplant

The primary signs and symptoms of rejection include Because patients are discharged from the hospital as
flu-like symptoms including low-grade fever and early as 8 days after transplant, much of their medical
muscle aches. Dysrhythmias and bradycardia below management and rehabilitation occurs on an outpatient
60 or relative bradycardia (decreased compared with basis. In the early stages of this postoperative outpa­
patient's normal resting heart rate) are significant and tient phase, patients are medically labile and need

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 38 The Transplant Patient 715

portable oximeter at home and may report episodes

Summary Cardiac Guidelines
of desaturation. Rejection should be suspected and
Cardiac phase II protocols reported if a decrease in Sa02 of 4% to 5% for the

Heart rate is not intens ity regulator same amount of activity is seen (Malen and Boy­
chuck, 1989).
Increase warm-up and cool-down to 10 to 15 minutes

RPE II to 13 (20-point Borg scale) Goals

No exercise in severe rej ection ( b iops y )
Patients are generally excited about the improvement
Continue exercise in mild rejection in shortness of breath and surprised at the level of
muscle weakness seen especially in the lower extrem­
ities. Once ventilation is no longer a limiting factor in
function, other deficits emerge. In the initial stages of
Once- or twice-a-week monitoring of medical status. outpatient rehabilitation, patients may have multiple
Rehabilitation should progrcss in this phase, but close complaints about the side effects of medications and
communication with medical personnel is recom­ often generally do not feel well. Rehabilitation
mended because of thc many medication changes. should continue through these periods of malaise.
Blood levels of immunosuppressive drugs are moni­ The overall objective of outpatient rehabilitation is to
tored and metabolic function (fluid and electrolyte lev­ improve function to levels appropriate for the pa­
els, kidney and liver function) are followed. tient's age and interests. Generally, patients are
closely followed by the medical staff for 2 to 3
General Considerations months after transplant, and rehabilitation 2 to 3
Patients in the outpatient phase of rehabilitation begin times per week continues throughout this period.
at low levels of function and progress to having few The most common impairments that limit func­
functional limitations. Therapists need to adapt and tion are decreased cardiopulmonary endurance, de­
progress the rehabilitation program appropriately. If creased muscle strength and endurance, range of mo­
rehabilitation is not aggressive, patients may succumb tion limitations, and abnormal movement patterns of
to the effects of prednisone and cyclosporine. Because the shoulder or trunk. Impairments may be caused by
of the debilitating side effects of immunosuppressive the surgical procedure itself or as a result of years of
medications, rehabilitation needs to be aggressive and abnormal muscle mechanics, posture, and decreased
preventive in nature. Rehabilitation can occur in a activity. Cardiopulmonary endurance training is em­
group setting and/or on an individual basis. phasized at this stage of rehabilitation, as is posture
reeducation, range of motion, and upper extremity
Monitoring movement patterns. Lower extremity strengthening
The areas of emphasis in the lung transplant patient can begin early, but upper extremity resistive train­
follow from the physiology and surgery performed. ing should be delayed until wound and tissue healing
The primary limitation pretransplant is ventilatory, is complete, generally about 6 weeks because of the
with the surgery intended to improve ventilation. delays in wound healing caused by prednisone.
Monitoring of ventilatory status should be the pri­ Goals which specifically address impairments may
mary consideration of the therapist. Respiratory rate include normal shoulder range of motion, normal
and oxygen saturation should be followed closely muscle strength in all major muscle groups of upper
during exercise sessions. and lower extremities, and normal thoracic mobility
(Figure 38-2).
Rejection
Interventions
The primary symptoms of acute rejection are short­
ness of breath, exercise intolerance, and desaturation To achieve the goals of rehabilitation and address im­
at rest or with exercise. Patients generally have a pairments, a pulmonary rehabilitation protocol may be

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716 PART VII Guidelines for the Delivery of Cardiopulmonary Physical Therapy: Special Cases

Lung Transplant Guidelines

Keep S a0 2 above 90%

Add supplemental oxygen if necessary during

treated acute rejection episodes

Patient should wear mask when with people

Increase strength program during prednisone bursts

Return to home can occur at this point in time, whether

or not rehabilitation goals have been met. The major
goal of community-based rehabilitation is return to
normal function with minimal limitations. Many pa­
tients feel so good after transplant that return to prior
FIGURE 38-2 level of function, including employment, is a natural
Post-single lung transplant inp atient. phenomenon. Formal rehabilitation may only be neces­
sary in complicated cases or after rejection episodes or
illness. Patients may also seek physical therapy advice
used, or the therapist may creatively design a rehabili­ for musculoskeletal problems unrelated to the trans­
tation program. Except for delaying upper extremity plant. Therapists should be comfortable treating pa­
strengthening for 6 weeks after surgery, no therapeutic tients in many settings, addressing the common com­
interventions are contraindicated. For endurance train­ plications, and watching for signs of rejection.
ing, stationary bicycles, treadmills, arm ergo meters,
indoor nordic ski machines, rowers, and stair climbers
Heart Transplant
may be used. Pulleys, weight equipment, free weights,
resistive elastic bands, or gymnastic balls all may be Ironically, the medications used to prevent rejection
appropriate for strengthening and facilitation of nor­ in transplant patients may increase the incidence of
mal movement patterns. Because of the effects of coronary artery disease. It is recommended that pa­
prednisone, proximal muscle function must be ad­ tients partici pate in a regular exercise program to
dressed, and strengthening programs should be ag­ manage the effects of the medications and to prevent
gressive, keeping the repetitions to 10 or less. Once a coronary artery disease complications. Hospital­
patient has achieved a satisfactory level of function based phase III cardiac rehabilitation programs are
(determined by the therapist and patient), formal reha­ appropriate, or patients may elect to independently
bilitation may be discontinued. exercise in a fitness facility. Some follow-up by the
The general considerations for lung transplant pa­ center is important to encourage compliance in exer­
tients are to monitor oxygen saturation and prevent cise programs.
the patient from contracting respiratory infections. A
summary of lung transplant treatment guidelines are
lung Transplant
listed in the box below.
For patients who have left their home community to
wait for lung transplant, the transition to home fre­
COMMUNITY OR HOME-BASED REHABILITATION
quently occurs at 3 months after transplant. Ideally,
Patients are generally followed at the transplant center rehabilitation goals from the outpatient phase will
until the medical staff is satisfied with patient progress. have been accomplished, and the patient will be able

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 38 The Transplant Patient 717

and needed long-term therapy. A 55-year-old male

had a bowel obstruction after surgery, which length­
ened his recovery time. If the patient is medically sta­
ble but has rehabilitation needs, the patient may be
referred for physical therapy in his or her home town,
possibly away from the transplant center. Other pa­
tients may have multiple episodes of rejection, which
are treated with high-dose steroids, and develop
steroid myopathy, requiring intensive and progressive
strength training.

Goals
Physical therapy assessment is critical to identify
problem areas and evaluate progress toward goals.
Goals at this stage should be primarily guided by spe­
cific patient quality of life issues. Common long-term
impairments are chest wall soreness, abnormal upper
quarter movement patterns, and low back and knee
pain from overuse.

Influence of Medications on Treatment

Patients are on a multitude of medications after trans­

plant, and additional medications may be added to
decrease the side effects of the primary immunosup­
pressive drugs (Miller, 1995). Prednisone, cy­
closporine, and azathioprine (lmuran) are the main­
FIGURE 38-3
stay of immunosuppression, with OKT 3 and FK 506
Post-douhle lung transplant outpatient at approximately 3
months pust-surgery. being additional options.

Prednisone
Because organ rejection is primarily an inflammatory
to return home to pursue his or her own interests. response, corticosteroids are usually used in trans­
Success stories are many. One patient returned home plant patients. Steroid therapy may be delayed until
and progressed to walking 5 miles a day, fishing 4 to primary wound closure is certain (1 to 2 weeks) at
5 times/week, and bow hunting with a 50-lb bow. which time the patient is begun on low-dose oral
One gentleman reported at a 6-month follow-up visit steroids. Acute rejection episodes are treated with
that he was pleased to be riding around his ranch and oral or intravenous steroid pulses. Corticosteroids
checking up on things. The therapist asked if he was work by immobilizing macrophages and decreasing
riding in the truck, and he replied, "no, on my horse." B and T lymphocytes.
A 21-year-old male (130 Ib) with cystic fibrosis re­
sumed weight lifting and bench pressed 1 JO Ibs, 8 Cyclosporine
months after a double-lung transplant (Figure 38-3). Cyclosporine is a very powelful immunosuppressive
Other patients have more rehabilitation needs. For agent that works by inhibiting T lymphocyte growth
example, a 40-year-old single-lung transplant patient factor and T helper cells. Side effects are common
sustained a brachial plexus injury from the surgery and annoying to patients. It is considered a peripheral

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718 PART VII Guidelines for the Delivery of Cardiopulmonary Physical Therapy: Special Cases

ability to analyze movement and function allow reha­

Side Effects of Immunosuppressive Medications
bilitation professionals to maximize a patient's qual­
ity of life. The field of organ transplant is exciting
Prednisone Cyc1osporine
and growing. New advances in long-term manage­
Hypertension Tremors
ment of transplant recipients means that rehabilitation
Glucose intolerance Hypertension
professionals need to continue to develop and evalu­
Osteoporosis Increased cholesterol ate approaches to care.
Muscle weakness Nephrotoxicity

Delayed wound healing

REVIEW QUESTIONS

I. What feelings do patients and family com­

monly experience before and after an organ
nerve irritant. Therapists should watch for muscle
transplant?
tremors and peripheral neuropathy.
2. What is the role of pretransplant pulmonary
rehabilitation?
Azathioprine
3. How does the surgical incision affect the
Azathioprine ({muran) is a powerful drug that inhibits
musculoskeletal function of a posttransplant
RNA and DNA synthesis of most immune system
patient?
cells. Bone marrow suppression (leukopenia, anemia)
4. What are the signs of organ rejection in the
is common as are gastrointestinal symptoms of nau­
cardiac transplant patient? the lung trans­
sea, vomiting, and anorexia.
plant patient?
5. How is the rehabilitation of the heart trans­
New Drugs
plant patient similar and different than tradi­
Research has added drugs such as OKT 3 and FK 506
tional cardiac rehabilitation')
to the immunosuppression regimen. OKT 3 is a mon­
6. How is the rehabilitation of the lung trans­
oclonal antibody that is used for management of
plant patient different than other forms of
acute rej ection and is not used on a daily basis. OKT
pulmonary rehabilitation?
3 blocks all T lymphocyte functions for a short time
7. How do immunosuppressive drugs affect a
after administration and can help remove T cell
patient's neuromuscular function? Muscle
byproducts from the graft site. Because of its dra­
strength? Cardiopulmonary endurance?
matic and potentially dangerous side effects, this
medication is given in a controlled setting where the
patient can be carefully monitored at 15­ or 30­ References
minute intervals. Pulmonary edema, bronchospasm,
Conners, G., & Hilling, L. (1993). AACVPR guidelines for pul­
fever, chills, and hypokalemia are common reactions. rnon{/l)' re/wiJililalion programs. Champaign. 111.: Human Ki­
Rehabilitation should not be given during ad­ netics Publishers.

ministration of these medications. The box above Craven, J.L., Bright, J., & Dear. C.L. (J991). Psychiatric, psy­
chosocial, and rehabilitative aspects of lung transplantation.
summarizes the effects of common immunosup­
Clinics Chesl Medicine, 1/(2),247-57.
pressive medications.
Hillegass, E., & Sadowsky. S.A. (1994). Essenlials of cardiopul­
monary rei1.aiJilirarion. Philadelphia: WB Saunders.
Hosenpud, .I .D., Cobanoglll, A., et al. (199 I). Cardiac rral/splanra­
SUMMARY
liol1. New York: Springer-Verlag.
Irwin, S., & Tecklin, 1.S. (1995). Cardiopulmol/ary physical rher­
Physical therapy has an important role in maintaining
apy. St. Louis: Mosby.
and improving functional levels of patients both be­
Malen, J.F., & Boychllck. J.E. (1989). Nursing perspectives on
fore and after organ transplant. Knowledge of cardio­ lung transplantation. Crilical Care Nursing Clinics of Norlh
vascular and pulmonary physiology along with the America, 1(4),707-722.

Copyrighted Material
 38 The Transplant Patient 719

Moser, K.M., Bokinsky, G.E., et al. (1990). Results of a compre­ Toronto Lung Transplant Group. (1988). Experience with Singlc­

hensive rehabilitation program: physiologic and functional ef­ lung transplantation for pulmonary fibrosis. lAMA, 259(15),

fects on patients with chronic obstructive pulmonary disease. 2258-2262

Archives of Intemal Medicine 140( 12): 1596-1601. Urliversill' Hospital surgical cardiac rehab ilitation proto col.

Scherer, S.A. (1995). Preoperative pulmonary rehabilitation re­ (1994). Denver.

duces pot-operative length of hospita l stay after lung trans­

plant. Denver: International Conference on Pulmonary Reha­
bilitation and Home Ventilation; abstract.

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 The Patient in the Community

Donna Frownfelter

KEY TERMS Assisted living Outpatient

Continuity of care Skilled nursing and rehabiliatation facilities
Home care Subacute hospitals
Managed care Transitional care units

INTRODUCTION
This chapter focuses on patients in the skilled
Physical therapy in the community may take on a nursing home, home care, and alternative long-term
wide variety of forms. The practice has certainly care settings. These concepts and ideas could easily
changed dramatically over the last few years. Diag­ be used in an adult day care or outpatient setting,
nostic related groupings (DRGs) began the trend of senior housing, or a transitional or an assisted liv­
patients leaving the hospital earlier and often in a ing facility. The settings described in this chapter
more acute stage of recovery. Subacute hospitals, will be used only as examples on which to focus the
Medicare skilled nursing, and rehabilitation facili­ discussion.
ties with transitional care units provide therapy and Continuity of care is an essential component of qual­
facilitate patient progression so that he or she will ity health care in light of the trend toward earlier hospi­
be back home within a short (perhaps a month) pe­ tal discharge either to a skilled nursing/rehabilitation fa­
riod of time. Managed care has had a significant cility or to home with nursing and therapy support. A
impact on diagnoses and treatment authorization, colleague in hospital practice recently commented that
which affects the type of diagnosis given to patients she feels more like a triage therapist than a physical
and the number of therapy sessions authorized for therapist. At times the absolute basics of therapy (i.e.,
given diagnoses or symptoms. transfers and gait with an assistive device) are all that a

721

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722 PART VII Guidelines for the Delivery of Cardiopulmonary Physical Thempy: Special Cases

patient is able to receive before leaving the hospital set­ live fuller and more salisfying lives even if they are
ting. An exercise sheet may accompany the patient unable to return home aCLcr rehabilitation. Many
home but, in general, after discharge from the hospital, nursing home chains have developed beautiful, hotel­
most patients do not know their exercise programs. In like atmospheres with a range of services. The resi­
addition, they have poor endurance because they are dents may live in independent apartments and, if a
generally still healing from the insults or injuries for disease or trauma occurs, may return to the skilled
which they were hospitalized. In the geriatric popula­ nursing area to receive rehabilitation services. When
tion the caregiver is often an elderly spouse who also they are able, they transfer to an assisted living area
has medical problems and is limited in the ability to as­ and continue to live there or will transfer back to
sist the patient. their apartments when they are sufficiently recovered.
The types and diagnoses of patients seen in the com­ Even after an acute incident (e.g., a cerebrovascu­
munity may vary; often they are the very young and the lar accident [eV AD, a patient may not be able to re­
very old. With the medical community's ability to save turn home in a month but may continue to make
premature, low-birth-weight infants we have had an in­ gains up to a year or more as strength, balance, and
flux of ventilator-assisted, oxygen-dependent infants endurance improve. Therapists can screen residents
with bronchopulmonary dysplasia (BPD). They may be and continue to try to improve their physical status
slow to develop and need intervention to prevent pul­ and to enable them to live to their fullest capacity.
monary infections and to improve in the natural devel­
opmental sequence. Often they may have difficulty
MANAGED CARE
swallowing, and nutritional issues may delay their
physical gains, as well as their speech and language, Managed care groups are having a significant impact
secondary to poor breath SUppOit. on placement and case management of individuals
Specialty hospitals have been developed to care for who are able to return home. We are seeing many pa­
the medically fragile, ventilator-assisted (dependent) tients in home care 5 days a week with caregivers pre­
patient who is not stable enough to be at home or sent around the clock. Significant cost savings may be
lacks the resources to be at home. Many patients, es­ noted compared with an extended hospitalization or
pecially children on ventilators whose parents can stay in a skilled nursing facility. Most managed care
provide some care and are assisted by nursing staff, companies are willing to listen to suggestions that
are coming home successfully on ventilators. They in­ save money and improve customer satisfaction.
tegrate into the community in school and recreation, When we think of these practice settings, it be­
function well, and perceive a high quality of life. comes obvious that cardiopulmonary concerns are
Elderly patients will often try valiantly to remain highlighted. From the very young to the very old, pri­
at home and independent, amazing the most seasoned mary and secondary cardiopulmonary issues are often
clinician with their inventiveness and family/friend the limiting factor in a patient's rehabilitation progress.
supports. Others will recognize that they no longer Before considering some specific differences in
are able to care for themselves and that the caregiver, community settings, we will look at the commonalities
who is often also elderly (often a frail spouse), cannot in the principles of exercise training and prescription.
continue in that role.
Nursing homes, long thought of as a place "to go
GENERAL PRINCIPLES OF EXERCISE
to die," have become centers of skilled nursing and
TRAINING AND PRESCRIPTION
rehabilitation. The trend is moving toward "transi­
tional care units" where a patient will go for approxi­
Specificity of Training
mately I month to gain strength and practice activi­
ties of daily living, transfers, and gait and develop Exercise programs are ind i viduall y developed to
endurance that will allow them to return home. meet specific goals. To develop muscle strength, a
The focus of long-term care is to help residents high-resistance, low-repetition program (i.e., weight

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 39 The Patient in the Community 723

lifting) is prescribed. To develop muscle endurance, a of resting. Even more troublesome were the results
low-resistance, high-repetition program (i.e., walk­ that it took 10 to 50 days for the values to return to
ing, treadmill) is prescribed. The benefits of exercise the level before resting (Saltin et aI., 1968).
depend on the targeted exercise. Strength training in­ In normal individuals who received ventilatory
creases muscle fibers (white) and endurance training muscle training followed by a month without train­
increases the number of capillaries and mitochondrial ing, the subjects lost the achieved training effect
content (Celli, 1994). (Keens et aI., 1977).
It is noted that a weight lifter is usually not a long­
term runner, and few runners are able to lift heavy
SPECIFIC CARDIOPULMONARY CONCERNS
arm weights. In developing exercise programs, we
IN THE COMMUNITY
must keep in mind the goals for the individual. Gen­
erally, some form of both strength and endurance is Patients in nursing homes, alternative long-term care
desired. However, programs often focus on one or the and independent living facilities, and the home after
other, not both. disease or trauma often have several problems in
common. They may have decreased independence,
mobility level, strength, and endurance, as well as
Intensity and Duration of Training
poor posture, and are at risk for falls 'if:condary to
Both intensity and duration have significant conse­ poor balance and weakness. Often they are poorly
quences on the amount of training effect. Olympians nourished, either from lack of appetite or dysphagia
often train at maximal or near maximal levels to or as a result of depression brought on by their physi­
achieve their "superstar" level of fitness. However, it cal limitations and feelings of being overwhelmed
has been noted that middle-aged, nonathletic individ­ with their situations. At times there is a sense of
uals benefit from lesser levels of exercise. Siegel et hopelessness and a feeling that things will not be the
a!. (1970) demonstrated that training sessions of 30 same again. This depression is especially common
minutes about three times a week significantly im­ when patients are placed in nursing homes when they
proved V021l1a, when the heart rate was raised over wanted to go home but realized they could not take
80% of predicted maximal heart rate. care of themselves or their families insisted on the
Casaburi et al. (1991) studied 19 COPD patients placement.
who could achieve either 50% or 80% of maximal Many patients have a preexisting cardiopulmonary
exercise (anaerobic threshold). They found that pa­ disease, such as asthma, emphysema, bronchitis,
tients who participated in the higher intensity training coronary artery disease, prior myocardial infarction,
program benefited more than the lower intensity hypertension, dysrhythmias, or congestive heart fail­
training patients. However, significant training did ure. In addition to those diagnoses, they often have
occur in the lower intensity group (Casaburi, 1991). fractured hips, knee replacements, or CV A. The car­
The number and length of treatments have a sig­ diopulmonary factors may in fact be the limiting con­
nificant effect on endurance training. An intense pe­ sideration to the progress with therapy. These con­
riod of care followed by a maintenance or managed­ cerns need to be dealt with so that the patient reaches
care period prevents the effects of stopping exercise his or her full rehabilitation potential.
training. Carry-over and maintenance is extremely
important (Make, 1991).
IF YOU CANNOT BREATHE YOU CANNOT FUNCTION

Functioning depends on the ability to breathe. An ex­

Deconditioning Effect
ample of this was seen in a patient that fell in the
Training effect can be lost after the exercise has parking lot of a hospital while going to a pulmonary
stopped. Bed rest in normal individuals was shown to rehabilitation program. She was in a long leg cast at
result in a significant decrease in Vo2max with 21 days home and became very short of breath with sit-to­

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724 PART VII Guidelines for the Delivery of Cardiopulmonary Physical Therapy: Special Cases

stand transfers. Limited by severe shortness of breath, dentures fit or is he or she not eating or chewing
she could barely ambulate across the room with her food because of poor dentition or denture fit? Is he
pick-up walker. When observed using her bron­ or she aspirating? Does he or she have dysphagia?
chodilator metered-dose inhaler (MDI), she was • Is the patient sleeping? Many patients after
found to be using it improperly. After she was in­ surgery, trauma, or a CVA are left supine or in a
structed on how to use it properly, she used the bron­ side-lying position to sleep. They may not have
chodilator before transfer and gait and was like a dif­ ever slept in that position before. However, they
f e r e n t patient. She was able to coordinate h e r do not recognize that may be the reason they are
breathing pattern with control t o match her activity not sleeping. If the patient states he or she cannot
and her endurance was remarkably improved. sleep ask him or her about previous sleep posi­
With these principles in mind, we can look at tions and try to work with the nursing aide staff
some of the considerations in nursing home and on positioning for sleep.
home health settings. • Follow-through of methods of working with
the patient should be consistent so as not to
confuse the patient. For example, breathing ex­
lONG-TERM CARE FACILITIES
ercises in conjunction with activities should be
AND NURSING HOMES
consistent. If the patient is taught in therapy to
As mentioned previously, with the changes in health inspire when extending the trunk, that should
care, much rehabilitation is now taking place in transi­ be communicated to other caregivers and con­
tional care units, Medicare skilled nursing homes, and sistently encouraged. If the goal is for the pa­
assisted living facilities. tient to walk to meals, a coordinated effort
The following are special considerations when should be made to try to have the patient ac­
working in a long-term care setting. complish this as a transition plan. For example,
• There are several layers of care from geriatric when the therapist talks with the aide and a
specialist nurse consultants to head nurses to care plan is established, the patient can start
general floor nurses to aides. walking to one meal or as far as he or she can
• Most patient care is given by aides. toward the dining room. When that is accom­
• Communication and cooperation are the keys to plished, the goal will be to walk to two meals,
achieving patient goals and success. and so on. Then additional goals can be added
• Input and involvement of the patient and family or to walk to activities, social settings, out to the
significant others is essential in developing goals. car to meet the family, and other functional,
• Clear and achievable goals need to be devel­ appropriate goals.
oped and revisited as the patient progresses or • In-services to reinforce the therapy techniques and
regresses in therapy. Is the goal to transition to goals should be done individually and in formal
home, to assisted living, or to living at the classes. Classes are helpful, on a one time basis, to
nursing home? discuss and instruct on a particular topic. How­
• Quality of life issues need to be taken into con­ ever, an ongoing one-on-one therapist/aide pa­
sideration. How mobile is the patient? Is he or tient-specific mini-in-service is essential. The
she independent? Is he or she a morning person? classes need to be repeated on a regular basis for
When is therapy going to be most efficient time­ new staff and as a refresher for some aides who
wise? Will it conflict with his or her other inter­ have not used or practiced the techniques. The
ests and activities, which may give him or her aides may at first feel they are "too busy and un­
moral support or act as a distractor and provide able to do the job," but you can convince them
real recreation? that it will be of benefit to dle aide, as well as the
• Nutritional concerns need to be taken seriously. Is patients. The patient will be able to do more and
the patient losing or gaining weight? Do his or her in the long run, the aide will have less work. In ad­

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 39 The Patient in the Community 725

dition, the family members will be pleased and re­ markable in their patient care follow-through for
gard the work of the aide more highly. This will therapy goals. Be on the look out for ways to
also benefit the nursing home because it will be praise and thank them in a sincere manner. They
known for its individualized, excellent patient will be more willing to help in the future.
care, which will make the director of nursing and • Sponsor open house times in the therapy depart­
the administrator pleased. Most aides would like ment so that the staff come in and can see the ther­
to do the best for their. patients and provide the apists. You can provide educational material for
best care they can render. the staff (and food). Welcome their input and sug­
• Try to get other programs and nursing home ac­ gestions for patients who may benefit from ther­
tivity groups to follow-through with therapeutic apy but are not on the physical therapy caseload.
goals. Talk with the activity department if pa­ • Prepare a bulletin board to show the accom­
tients need extra encouragement or help with plishments of patients in pictures and descrip­
oxygen to participate. If patients need to drink tion. We all love success stories and being part
more water for increased hydration, ask them to of the success. Show pictures of aides, as well as
remind the patient and provide water. therapists, helping the patients.
• As a therapist, be willing to pitch in and help • In addition to chart reviews and talking about pa­
whenever you are able, even if it "isn't in your tients with the nurses, screen patients in the din­
job description." Your willingness to be a ing rooms and activity sessions and walking in
team player will be noticed. If an aide is off the hall. The aides will be a terrific source of pa­
sick and you are available at lunch and see tient referrals; they are with the patients more
there is a problem passing out trays, offer to than anyone else.
help. The next time you ask an aide for help
there will probably be more willingness. If
MONITORING CARDIOPULMONARY STATUS
there is a patient that is difficult to transfer,
IN THE LONG-TERM CARE FACILITY
offer to help in getting the patient up for phys­
ical therapy. This will serve as both a teaching With the increase in patient acuity, it is more impor­
opportunity and as a help to the aide. Look for tant than ever to monitor the patient's response to
ways of blending your therapy with the needs mobilization and exercise. Many long-lerm care and
of the nursing staff. subacute facilities are purchasing pulse oximctcrs and
• Give recognition to aides who have been re­ portable ECG monitors because they have more

FIGURE 39-1
Pulse oximeter.

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726 PART VII Guidelines for the Delivery of Cardiopulmonary Physical Therapy: Special Cases

unstable patients (Figure 39-1). In addition, all thera­ oxygen in the arterial blood) or to relieve the myocar­
pists should be competent in blood pressure monitor­ dial work, such as in a patient with a severe myocardial
ing and taking pulse rates; auscultation training is infarction or other cardiac dysfunction (see Chapters 4
highly recommended (see Chapter 14). and 27).
During the initial evaluation the vital signs and It is important to note that the arterial blood gas
oximetry should be taken. The readings should be is drawn at rest with no patient activity unless
taken at rest in a supine or semi-Fowler's position for specifically noted otherwise (such as an exercise
a baseline. Readings should then be taken in sitting test blood gas). Generally the Medicare guidelines
and standing positions. It is helpful to take the blood require that the patient has a P02 of 55 mm Hg
pressure on both arms to see if there is a difference in (Torr) to be placed on oxygen. This is on the steep
the readings. part of the oxyhemoglobin dissociation curve (see
When the patient begins treatment, vital signs and Chapter 3).
oximetry should be performed before and after the When the patient exercises he or she consumes
mobilization or gait activity. A normal exercise re­ more oxygen than at rest. Consequently if a patient
sponse would be that the blood pressure and pulse is on oxygen at rest and the P02 is 55 or 60 mm Hg
would increase in relation to the activity. An increase he or she may desaturate during exercise. This
of 20% to 30% might be expected and would be means that the red blood cell Hg will give up more
within normal limits. The time the vital signs take to oxygen to supply the exercising muscle. However,
return to normal (recovery time) should be within 5 it is enough oxygen for exercise and the patient will
to 10 minutes. experience i n c reased s h o r tness of b r eath, the
Many patients who are not considered cardiopul­ oximeter will note a drop below 90%, and the blood
monary patients have an abnormal response to exer­ pressure and heart rate may initially increase be­
cise. If we are not observing and measuring objec­ cause of the stress and later drop as the heart cannot
tively, we will not know the cardiopulmonary response compensate for the decrease in oxygen level.
is abnormal, and deleterious effects may occur. The pulse oximetry reading of normals is 97.5%
An example of this was seen in a patient one oxygen saturation. It is clinically acceptable to main­
month after a CV A. The patient was very fatigued tain oxygen saturation at 90% or above. This satura­
and complained that his knees felt like they were tion corresponds with keeping the P02 generally at
going to buckle. This patient had been doing quite above 55 mm Hg. When the P02 drops below 55 mm
well and was not being monitored. However, after the Hg, a dramatic drop in oxygen saturation will occur
patient ex pressed the feeling of weakness the thera­ for a small drop in P02.
pist took the vital signs after the patient rested and If the nursing home does not have an oximeter, the
walked again. The blood pressure and heart rate durable medical equipment company that supplies the
dropped during the exercise. The doctor was in­ oxygen may be called and will bring an oximeter
formed and ordered a blood test that revealed the pa­ when they check the oxygen. However, any patient
tient did not have an appropriate blood level of digi­ on oxygen at rest should be tested for desaturation.
talis. The medication was increased and the patient Another option is to call the patient's doctor to re­
improved. Had the therapist not checked the vital quest an increase in oxygen during exercise. For ex­
signs and continued to push the patient, there could ample, a patient on I Llmin at rest can have a pre­
have been serious consequences. scription written for I Llmin at rest and 2 or 3 I/min
during exercise. The increase in oxygen is no prob­
lem as long as the oxygen is decreased back to the
SPECIAL MONITORING CONSIDERATIONS
resting amount as soon as the patient recovers back to
FOR PATIENTS ON OXYGEN
baseline. This is even true for carbon dioxide retain­
Patients receiving oxygen therapy have usually been ers whose oxygen is carefully titrated to prevent tak­
placed on oxygen because of hypoxemia (low levels of ing away the hypoxic drive to breathe.

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 39 The Patient in the Community 727

DOCUMENTATION CARDIOPULMONARY CONCERNS IN HOME CARE

Functional outcomes are key to documentation. As Home care takes the practice setting one step further
we evaluate patients and write care plans, we set from the hospital. Managed care is having major im­
goals that are both short and long tenn. Each goal pacts on changes in this area of therapy and nursing
should be linked to functional outcomes that enable care. Cost effective yet excellent therapy is the goal
the patient to be more mobile, safe, as independent as of managed care. There is a great deal of creativity;
possible, and functional in. the care setting in which deals can be made if a provider group can demon­
he or she lives. strate that the patient will benefit and a cost savings
Documentation needs to show progress toward to the managed care group will occur. We are seeing
the functional outcomes the therapist has developed coalitions form between' contract service therapy
with the patient. Goals should be attainable and real­ agencies, durable medical equipment companies,
istic. If there is poor or slow progress to a goal, there nursing agencies, and enteral feeding companies to
needs to be documentation and explanation in the provide "one-stop shopping" groups. The managed
notes of what has occurred and how the treatment care companies prefer to make one call that will pro­
program will be modified or how the goals need to vide them with nursing service, therapists, and home
be changed. medical equipment, such as walkers, canes, tub seats,
When the functional outcomes have been met, the raised toilet seats, oxygen, IVs, and enteral feeding.
patient is reasscssed to see if they can accomplish more Home care involves not only seeing more acutely
or if the patient should
. ill patients but also seeing some interesting cardiopul­
a maintenance program. A screening date should be set monary situations. For example, in working with
to check back and monitor the patient to ensure mainte­ major medical centers who perform transplant surgery
nance, improvement, or decline in condition. At times the therapist works with patients before and after heart
patients who have "plateaued" will improve and may and lung and other transplant surgeries. It has been
be picked up on a screening to request a doctor's order demonstrated that patients, even as seriously ill as pre­
to have additional therapy with specific increased goals transplant patients, can improve their functional abili­
defined. If a patient's condition has declined, the pa­ ties, strength, and endurance to be better candidates
tient can be reevaluated to see if the patient's former for surgery. Postoperative care is also improved when
status can be resumed or maintained. the patient is in better physical condition before
It shou ld be remembered that third party payors surgery. Other diagnoses are also being treated effec­
are reading the notes to understand what the evalua­ tively before and after surgery. It makes sense to
tion and treatment plan for the patient is and how begin preoperative orthopedic consults to evaluate pa­
the patient has progressed in meeting functional out­ tients and teach them the exercises they will be doing
comes. Because the patient is receiving long-term after surgery. In addition, any patient facing abdomi­
therapy, the more therapy the patient needs, the nal or thoracic surgery could benefit from a preopera­
more documentation is necessary to tell the story to tive visit if coming to the hospital presents difficulty.
the third party payor or the managed care group. A Consequently, therapists who never thought they
good quote to remember is, "If it wasn't written, it would be required to work with cardiopulmonary pa­
wasn't done!" tients are needing to increase their knowledge bases to
In summary, every patient in a long-term facility treat these patients appropriately.
is a patient with cardiopulmonary concerns. The car­ In the home-care setting the therapist is alone with
diopulmonary system needs to be optimized for full supports through the nursing and home-care agencies.
rehabilitation to occur. Cooperation with the nurses However, in the home they usually must be prepared to
and aides, as well as special activities staff, is essen­ evaluate patients and their progress with very little su­
tial for follow-through of treatment programs and pa­ pervision or consultation. In addition, they must be able
tient success. Teamwork is the key, and communica­ to handle emergencies and crisis situations. AU home­
tion and documentation are vital. care therapists must have a basic CPR certification

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728 PART VII Guidelines for the Delivery of Cardiopulmonary Physical Therapy: Special Cases

renewed annually. Policies and procedures dealing with friends, or a caretakers smokers? Signs need to be
how to handle emergencies, infection control, and posted to warn of danger of smoking and flames
safety are essential for any therapist in the home. around oxygen. Patients who are smokers need to
Therapists need to know how to obtain necessary have this reinforced very clearly.
information and equipment for the patient. They need Does the patient have stairs? I s the bedroom up­
to be creative in adapting equipment and be innova­ stairs? Is there a first floor bathroom? If the bathroom
tive if the patient cannot afford to purchase medical is on the second floor can the patient get up the stairs
equipment. This is not the setting for new graduates, safely and in a timely manner, or does a commode on
but rather for the experienced therapists. the lower level seem more appropriate?
Is the bed the proper height? Are there handrails? I s
i t difficult for the patient to transfer into bed? Is a de­
HOME SETTING
vice needed to help the patient transfer independently?
In the hospital or outpatient center the patient comes to The question of the bed arose with one home-care
your place of business. They come where you work. patients who had a fractured pelvis. When I first vis­
With long-term care and home care, you go to work ited her, I asked how she had broken her pelvis and
where they live. A certain etiquette is required when she replied, "Hopping into bed." I questioned what
going into a patient's residence. Pennission needs to be she meant and she said, "I' JI show you." I followed
requested to enter the residence, alter their living space, her to her bedroom watching her gait with her walker.
put in grab bars, remove scatter rugs and telephone When we got to her bedroom, it was quickly noted
cords that are seen as a safety hazard, or rearrange that this very short patient had a very tall bed. The
rooms that you may consider too cluttered and unsafe. mattress was between her iliac Crest and waist when
The therapist must remember that this is the patient's she backed up to the bed. She stated, "I used to have a
home and must be tactful in the way recommendations stool that I climbed into bed on, but my son thought it
are made. The cluttered room may hold treasures that wasn't safe and took it away. Now I have to hop up
have been accumulated over a lifetime. They may sur­ into bed!" She had returned home to do the same ac­
round themselves with items that are all they have left to tivity that had put her in the hospital with a fractured
remember. It may be true that a path needs to be made pelvis. Looking at the bed, I noted that there were 3-
for safe walker ambulation, but how this is communi­ inch rolling casters and a caster pad under the hed.
cated may make all the difference in developing good The son was called and the casters and pads removed.
rapport between a home-care therapist and the patient. The patient was quite pleased that the bed was 4
I nitially, an evaluation of the patient's home needs inches lower and she could transfer in quite easily.
to be made. What equipment do they have, is it in Is there family support or a caretaker if the patient
working order, do they know how to use it? Often a is not independent? If the spouse needs to work or go
patient borrows "grandpa's cane" and does not real­ out, how long can the patient be safely left alone?
ize that he or she is eight inches shorter than grandpa. Does the patient know how to obtain a caretaker? Are
Modifications may need to be made so that existing they able to financially afford the support?
equipment fits properly and is functional. Most home-care agencies have social worker sup­
Safety is a primary consideration. Are there cords port to help patients discover resources available to
across the floor? Are scatter rugs loose or tacked down them. A physician's referral is needed and the service
with carpet tape? Can the patient pick up his or her foot is generally covered under Medicare.
sufficiently to walk over the scatter rug without trip­
ping? Are there pieces of kitchen linoleum that have
COMMUNICATION AND CROSS REFERRALS
come up and might trip the patient? Are the kitchen
TO OTHER DISCIPLINES
chairs on rollers and the patient's balance poor?
Is the patient on oxygen and you discover that he It is essential that communication take place between
or she h a s a gas stove? Are the close relatives, the members of the home-care team. Communication

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 39 The Patient in the Community 729

is difficult because everyone is on the road and travel­ and is having difficulty swallowing may benefit from
ing to patients' homes. Generally, pager numbers of speech and occupational therapists working on seating
therapists and nurses are exchanged and compliance systems and feeding. The interaction and communica­
with answering pages is good. However, considera­ tion between therapists facilitates ideas for both thera­
tion needs to be given to the realization that we do not pists, provides continuity and follow-through, and
like to be interrupted frequently when seeing patients. helps to optimize patient care.
Generally a system of timing the calls or pages is wel­
comed. A 91 I can be placed after the page number to
MONITORING CARDIOPULMONARY
identify an urgent call if the call is very impOltant or
STATUS AT HOME
information needs to be given immediately.
Physical therapy is the most common therapy. How­ Cardiopulmonary status at home is similar to that in a
ever, at times another therapy will be indicated but not long-term care facility. However, at home there is not
made when the patient is discharged. When a patient usually an oximeter available. This is unfortunate, since
expresses a problem that could be handled better or many more patients are coming home on oxygen and
could provide increased service to a patient, a cross re­ ventilators. This trend should change and home-care
ferral should be made by calling the home-care agency therapists should have oximeters available for evaluation
or the patient's nurse case manager. Identify the prob­ of patient status and exercise desaturation. The durable
lem and why you feel the additional therapy is indi­ medical equipment company has oximeters and the ther­
cated. The physician will be called and the order gener­ apist may reqnest an oximetry study done with a physi­
ally obtained. It would then be helpful for the refelTing cian referral. It is helpful to make an appointment and
therapist to call the new therapist and update rum or her meet the therapist to see the results and to try to reenact
on the patient and reason for the referral. This commu­ the therapy to see if the patient de saturates with exercise.
nication should be documented to show the necessary The same blood pressure and pulse monitoring
communication between the therapists and nurses. should be done at rest on both arms and in sitting,
An example of this was seen in a patient that I re­ standing, and before and after exercise as mentioned
ceived a refelTal on for home care that had been on a previously in this chapter.
ventilator for a month in the hospital. She had been intu­
bated, was very hoarse, and complained that she was
HOME OXYGEN
having trouble swallowing and eating. Liquids espe­
cially were going down the wrong way. The home-care Home oxygen may be supplied by an oxygen concen­
referral said that the patient had a swallowing study in trator, by tanks or as a liquid oxygen system (Figure
the hospital that demonstrated she was aspirating. A 39-2) (Chapter 41). One consistent problem that must
speech language pathologist had been working with her be dealt with in exercise with patients at home on oxy­
on swallowing in the hospital. However, speech therapy gen is the incredibly long oxygen tubing needed to
had not been ordered at home. Nothing had changed on allow patients t o go to the bathroom, out to the
the day the patient had been discharged. Since the pa­ kitchen, and to the living room (Figure 39-3). Often 60
tient was still aspirating, a speech consult was requested. to 90 feet of tubing must be used. The question often
At times it is helpful to do a joint treatment session arises, "Does the patient get the right amount of oxy­
with another discipline. This can be done to coordinate gen with such long tubing?" The answer is yes because
therapy and provide focus and continuity of goals. It the flow meter is a compensated one, which means it
will also lead to success for the patient. For example, a reads what really is occurring. If more tubing is added
physical therapist and a speech language therapist may and a lesser flow was occurring, the flow meter would
meet to focus on a patient with poor posture who lacks drop to indicate that had happened. Then it would be
breath support for phonation. Another patient who is readjusted to the proper liter flow as ordered.
having difficulty feeding because of trunk weakness It has been found that the portable oxygen systems,
and is sitting in flexion with a forward head and neck in particular the demand oxygen system, do not always

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730 PART VII Guidelines for the Delivery of Cardiopulmonary Physical Therapy: Special Cases

·"1
••
jf r-;- .
--

--

f .

FIGURE 39-2 FIGURE 39-3

Oxygen concentrator. Oxygen tubing presents a significant safely hazard.

deliver the exact amount expected (Figure 39-4). It is • Be compliant with medications and health
necessary to use oximetry to determine whether the pa­ precautions.
tient has an appropriate oxygen saturation reading. • Learn preventative care (i.e., prevent pulmonary
Patients need to be taught either to coil the tubing or infections and not increase salt/water intake if
to develop a means to make sure that they do not trip on cardiac precautions or taking steroids).
over the tubing because it creates a safety hazard. • Learn ventilatory strategies to increase comfort
Some patients have more than one tank or concentrator and function (see Chapter 00).
in the home to prevent having long lengths of tubing. • Learn to monitor themselves for signs of im­
pending trouble (i.e., increased shortness of
breath, swelling in ankles, productive cough,
THERAPEUTIC GOALS FOR HOME-CARE PATIENTS
change in mucus, decreased urine Olltput, or
WITH CARDIOPULMONARY DYSFUNCTION
rapid weight gain) (Figure 39-5).
To be independent at home, patients with cardiopul­ • Train to pace activity and use energy conserva­
monary dysfunction need to: tion techniques and rest periods to accomplish
• Understand the dysfunction or disease. more with less stress.

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 39 The Patient in the Community 731

FIGURE 39-4

Portable demand oxygen system.

FIGURE 39-5

Patient monitoring oximeter

with exercise.

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732 PART VII Guidelines for the Delivery of Cardiopulmonary Physical Therapy: Special Cases

FIGURE 39-6
Nasal CPAP unit.

• Maintain proper nutrition and hydration. tion are essential in the progress and maintenance of
• Develop a support network to help when needed patients at home. As health-care practitioners, we
and to check on the patient occasionally. offer helpful suggestions for modification of the pa­
• Maintain walking program and general exercise tient's home environment and life style. However, we
to continue functional gains. cannot force a patient to comply or accept what we
Some patients may need noctural nasal continu­ have proposed. The patient in the home setting is in­
ous positive airway pressure (CPAP) (Fig. 39-6). dependent in his or her judgments and activities. We
This may be ordered to treat sleep apnea or to rest need to respect that and at the same time provide our
the patient and assist with ventilation. A Bt-PAP experience and therapeutic judgment and expertise.
unit allows the patient to rest and let the machine as­ This setting is often the most rewarding a therapist
sist ventilation by providing pressure support on in­ can have, although at times it also may be the most
spiration and exhalation. Often at first, the patient frustrating. One thing is certain, if you ask a patient
may have difficulty adjusting to the nasal CPAP, but where they want to be, the answer sounds like,
in time, the patient will adapt to the assistance and "There's no place like home'"
feel it is beneficial.

REVIEW QUESTIONS
SUMMARY
I. What are some common problems patients in the
Education, self-monitoring, compliance to medica­ community have in common?
tion, reduction of risk factors, nutrition, and hydra­ 2. What role does a preexisting cardiopulmonary

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 39 The Patient in the Community 733

condition play in a new diagnosis or trauma (e.g., Jackson, D.E., & Wilhoire, M.J. (1985). Home health physical
therapy, considerations for the provision of care. Clinical Mun­
CV A, hip fracture)?
agement in Physical Therapy, 5: I O.
3. What are some uniques situations or concerns
May, B.1., ( 1 993 ) . Home health and rehabilitation, Conce pis of
about patient care being delivered in a nursing Ca re, Philadelphia. F.A. Davis.
home, assisted living center, home care? May, B.J. (1990). Principles of exercise for the elderly, In Ba5ma­

4. What role can a physical therapist play in opti­ jian, J.V. & Wolf, S.L. (Eds.). (1990). Therapeutic exercise,

mizing the patient's care in the above settings? (5th ed.). Baltimore: Williams & Wilkins. 1990.
Pfau, J. (1989). Adull exe rc ise inslrllClion sheets: Home exercise
5. How can cardiopulmonary function be monitored
fo r rehabili/{llion therapy skill b uilders. Tucson.
outside the hospital? Polich, C. (1990). The provision of home health care services
6. What special considerations should be taken with through health maintenance organizations: Conflicting roles for

a patient on oxygen') HMOs. Home He alth Care Quarterly, II: 17.

Sallade,J. & Adam, L. (1986). Geriatric exercise booklet, Cli nical
Manageme nt in Physical Therapy. 6:32, 1986.

References Schaefer, K. & Lewis, C. Marketing geriatric programs-A home

care example, Clinit'al Management in Physical The rap y ,
Emlet, c., Cragtree, J., Condon, V., & Tremel, L. (1995). In - ho me 6: \1-17,1986.
aHessmenl of older aduil.\', an inlerdisciplinary approach. Vassif, J.A. (1985). The Home Health Care Solution, New York:
G ithersburg, Md.: Aspen Publishers. Harper & Row.
Harrington, J. (1983). The case for home heallh specialization. Zola. I.K. (1990). Aging, disability and the home care revolution,
Clillical Mallagemenl in Physical Therapy, 3: 17. Archives of Physical Med icine and Rehabilitation, 71:93.
Jackson. B.N. (1984). Home health care and the elderly in the
1980's. Am erican Journal of OccupalirJII(l1 Therapy. 38:717.

Copyrighted Material
PART VIII

Related Aspects of
Cardiopulmonary
Physical Therapy

Copyrighted Material
 Body Mechanics-The Art of
Positioning and Moving Patients

Mary Massery
Donna Frownfelter

KEY TERMS Body mechanics Ventilation related to:

Dependent patients Supine

Lifting and moving Sidelying

Upright

Upright

Neutral alignment of trunk, head

and shoulders

INTRODUCTION
who can move independently and assume any given
Body mechanics may be defined as the efficient use of position with ease. In this chapter, the principles of
one's body as a machine and a locomotive entity. In body positioning and moving dependent patients are
working with critically ill or chronically dependent pa­ discussed.
tients, it is essential that optimal body positioning is ac­
complished to facilitate maximal ventilatory potential.
POSITIONING FOR OPTIMAL VENTILATION
Therapists and nurses attempting to position or move
dependent patients must understand and use proper Because of the three-dimensional nature of breathing,
body mechanics (Neil, 1959; Fuerst and Wolff, 1969). the therapist's goal is to facilitate chest excursion in
This is necessary to reduce stress and trauma and to all three planes of ventilation-anterior-posterior, su­
promote success for both the patient and the nurse or perior-inferior, and lateral (Massery, 1994). This can
therapist. Positioning and moving dependent patients is be accomplished by improving the length-tension re­
an art that is quite different than working with a patient lationships of the muscles used in inspiration (Crosbie

737

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738 PART VIII Related Aspects of Cardiopulmonary Physical Therapy

and Myles; 1985; Kendall, 1993). Massery reasons Upper chest expansion can be increased by remov­
that the success of proper positioning to enhance in­ ing pillows under the patient's head to increase tho­
spiratory muscles will do the following: racic extension. This will increase the length-tension
I. Improve the length-tension relationship of the relationship of the neck accessory muscles (scalene
accessory ventilatory muscles involved in that and sternocleidomastoid muscles). Increased move­
posture ment will be noted in the upper chest in a superior
2. Incorporate a passive stretch of the chest wall and anterior plane. Further anterior expansion can be
3. Use the natural coordination of the trunk-chest achieved by using a towel roll placed longitudinally
wall movement with inspiration and exhalation at the vertebral spine to open the anterior chest of a
patterns to maximize movement patient who tends toward excessive flexion of the
The following are some common improvements that trunk (Figure 40-1).
can be incorporated into normal positioning. If the patient needs some support under his or her
head to achieve a neutral chin tuck to protect his or her
swallowing ability, then a thin pillow or horizontal
Supine Position
towel roll under the occiput, may be used (Figure 40-2).
As mentioned in Chapter 37, all activity is performed External rotation of the shoulders with the scapula
in the field of gravity. Patients in a supine position in a neutral or retracted position will place the pec­
may find breathing difficult because they must over­ toral is and intercostal muscles on stretch. This will
come gravity to move the chest wall with each improve lateral and anterior chest wall movement
breath. Using towel rolls or pillows to facilitate a bet­ (Kendall 1993). If a patient has full range of motion
ter position may significantly improve the patient's (ROM) and is comfortable with the arms placed over­
opportunity for improved respiration. head or in full flexion/abduction/external rotation for

"

//
,'\

\
'.t

FIGURE 40-1
Placement of vertical towel roll.

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 40 Body Mechanics-The Art of Positioning and Moving Patients 739

FIGURE 40-2

Increased openness of anterior chest wall with the vertical thoracic towel roll and the occipital
towel roll combined.

FIGURE 40-3

Buttertly position with thoracic towel rolllO open anterior chest.

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740 PART VIII Related Aspects of Cardiopulmonary Physical Therapy

maximal stretch, this is the optimal po ition for full

excursion of the anterior chest wall (Figure 40-3). If
there are significant shoulder limitations, moderate
shoulder abduction with forearm supination lUay be
the best position available to facilitate chest excur­
sion. Whenever significant limitations are found, the
therapist should try to modify the position to accom­
modate the patient and achieve optimal ventilation.

Sidelying Position

Side lying is an optimal position for improving breath­

ing pattell1s. Gravity is elimi. nated
sion and the diaphragm moves freely. In addition side­
lying is a reflex-inhibiting posture, and some high-tone
patients will be able to relax and breathe more freely.
It is impoltant to consider the shunt effects if a patient
has lung pathology. For example, if a patient has right
lower lobe pneumonia or atelectasis, sidelying on the
good side will improve oxygenation. Conversely, side­
lying with the affected side down will cause a decrease
in oxygenation (differential shunt) because a poorly
ventilated patient receives more perfusion to the down
lung and more shunting will occur. The patient's hip
and knee joints should be flexed and supported for
comfOlt. The upper extremities can be moved up and
away from the body to allow for free movement of the
upper chest wall. A pillow can be used to support the
FIGURE 40-4
upper arm anteriorly, or the patient can be placed in a
Unsupported upright position of patient with Tl paraplegia.
three-quarter supine position and a pillow behind the NOTE: Posterior plevic tilt and excessive thoracic khyphosis
back to support the uppermost arm. If the patient has with resulting collapse of anterior chest wall.
full range of motion and is comfortable, a butterfly po­
sition of the anns can be used. This will automatically
open up the rib cage and facilitate inspiration.
(Woodhall-McNeal, 1992; Borello-France, Burdett,
and Gee, 1988). The anterior tilt of the pelvis will im­
Upright Postures
prove upper-extremity ROM and ventilation poten­
Upright postures create new challenges to breathing tial. Attending to this one consideration may be all
by adding the component of balance and an unsup­ that is necessary to improve the breathing capacity in
ported spinal column. Pelvic alignment is a key com­ some patients, allowing them to continue to advance
ponent. An anteriorly tilted pelvis in healthy flexible in their exercise programs or rehabilitation courses.
adults will tend to do the following: (I) reduce the One simple means of attaining an anterior pelvic
kyphotic curve in the thoracic spine, (2) adduct the tilt in sitting is to have the patient lean forward over
scapula toward a neutral position, (3) produce a more his or her legs, then slide a towel roll horizontally just
neutral or externally rotated upper-extremity position, behind the ischial tuberosities, which will prevent the
and (4) pull the head back into a neutral chin tuck pelvis from rolling back into a posterior tilt (Johnson,

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 40 Body Mechanics-The Art of Positioning and Moving Patients 741

and head back into a more neutral alignment. The an­

terior chest wall will also be more open with this
technique.
A neutral head and neck position is important for
patients with impaired speech volume or endurance
and for patients with swallowing or aspiration dys­
function. A neutral chin tuck will optimize the
length-tension relationship of the vocal folds, mini­
mize vocal strain, and improve protective airway re­
flexes (Massery, 1994).
It is also vital to evaluate the patient's shoulder
positioning. Internal rotation of the shoulders and
scapular protraction tends to block the upper chest
from reaching its full expansion potential. Alter­
n a tely, external rotation of the s h o u l ders will
markedly increase upper chest wall movements and
thoracic extension. Clinically, improved lung vol­
umes will be noted when these positioning considera­
tions are taken into consideration. Often these smail,
seemingly insignificant changes will position the pa­
tient for success with other therapeutic activities. If
unattended, these small factors can impede patient
progress. Positioning has everything to do with in­
creasing ventilation and functional skills.

LIFTING AND MOVING DEPENDENT PATIENTS

There has been a change from earlier concepts and

FIGURE 40-5
principles of lifting. As discussed, the body has
Ischial towel roll to support pelvis in anterior tilt in patient
with Tl parapkgiJ. NmL: ch enges in the thoracic spine and been thought of as a machine. It was believed that
open anterior chest wall as well as improved head and neck improper mechanics of lifting would result in
alignment.. tremendous loads on the disks. The key components
of lifting were to "keep it close," "bend knees," "lift
with the legs." Later the spinal posture was the cen­
ter of attention during lifting (Physical Therapy
1989) (Figures 40-4 and 40-5). This is well tolerated Forum, 1985).
for many patients with intact sensation and a pelvis During observation, lifting seemed to occur "natu­
that is at least minimally mobile. For neurological pa­ rally" from slightly bent knees and then, during the
tients with impaired sensation or less pelvic mobility, raise lift butt-end first, with the patient rearing back­
a wedge may be substituted; however, caution must ward at the start as the therapist started to extend the
be used because some sliding may occur. knees before lifting. The predominance of injuries
seems to occur with the back in flexion. There is a ra­
tionale for strengthening abdominal muscles to pro­
Neutral Alignment of the Head and Shoulders
mote safer lifting. Abdominal strength is necessary to
A vertical or horizontal towel roll may also be used support a pelvic tilt during lifting. Many commer­
with wheelchair positioning to bring the shoulders cially available lumbar and abdominal elastic velcro

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742 PART VIII Related Aspects of Cardiopulmonary Physical Therapy

supports are now available and widely accepted. factors, such as limited space (i.e., small hospital
They provide additional abdominal wall support. rooms), clothing, or degenerative knee joints.
Another current school of thought advocates lift­ The first consideration in body mechanics is the
ing with the lordotic lumbar curve intact. This is the need for maintenance of proper posture and balance
technique used by weight lifters. When these individ­ (body stability). Consideration should he paid to the
uals are questioned about backaches, they usually relationship between gravity, posture, and body sta­
deny any problems. bility (Figure 40-6). It is commonly known that grav­
The lifting technique may be modified by other itational force is always exerted in a vertical direction
toward the center of the emth. In addition, that point
in a patient or object at which all of its mass is cen­
tered is called the (·crller or gravity (the point at
whieh the patient's maximum weight is concen­
trated). In the standing position the human body's

;�" e 0' gm"",

center of gravity is approximately SSG;!., of the body's
total height and in the pelvic cavity, slightly anterior
to the upper part of the sacrum. The lower the center
of gravity, the greater the hody stability. Conse­
quently, when the human body is used as a machine
to lift an object, muscular cffort great enough to
maintain stability and to lift against the force of grav­
ity is necessary, especially when the patient's center
of gravity is fUlthcr removed from your own. There­
fore one way to conserve energy and maintain stabil­
ity is to carry the weight of the patient (or object) as

I
Center of gravity close to one's own centcr of gravity as possible. This
allows maximal conccntration of onc's own energy
toward movement of the patient, with minimal stress
or injury to oneself. To help accomplish this, the bed

I
should be adjusted so the therapist or nurse can reach
the patient comfortably. Usually adjusting the bed to
one's hip level is adequate. This makes the patient
close to the therapist's center of gravity.

)
The majority of lifting should be done with the
legs (knees) and not by straining to lift with the arms
and back (Figure 40-7). Whenever there is a question
about one's ability to lift a patient alone, generally it

4
should not be done, and assistance should be obtained
(Rantz & Courtial, 1977).
Another point to consider is the base of support
while lifting. The base of support is defined as the
area between the feet that provides the body's stabil­
- Base of support

I. ity. It is easily appreciated that the wider the base of

support, the greater the body's stability. To enlarge on
FIGURE 40-6 this concept, one also needs to define the line of grav­
The line of gravity passes through the center of gravity and ity and its relationship to body stability. The line of
the base of support to maintain body stability. gravity is an imaginary line passing through the center

Copyrighted Material
 40 Body Mechanics-The Art of Positioning and Moving Patients 743

of gravity of an object and perpendicular to the sur­ places the center of gravity in the direction of
face on which the object (body) rests (see Figure 40- the weight being lifted. To conserve energy and
6). The closer the line of gravity passes to the center maintain stability, carry the weight as close to
of the base of support, the greater the body's (ob­ your own center of gravity as possible. Lower
ject's) stability. Increased muscular effort needs to be your hips to the level of the surface supporting
exerted in proportion to the distance the line of gravity the weight you plan to lift by flexing your hips
shifts away from the base of support (Rauch, 1971). and knees. Adjust the bed up as high or down
To summarize and apply these concepts, one can as low as you need for comfortable and effi­
list the following guidelines: cient work.
1. The lower the center of gravity, the wider the 3. The effort to petform a given activity depends on
base of support, and the nearer the line of grav­ the weight of the object to be lifted. Know your
ity falls to the center of the base of support, the limits. Do not attempt to lift alone if YOLl have
greater the body's (object's) stability. When any doubts about your ability to do so. Don't be a
lifting, stand with feet well apart, knees slightly hero in a back brace. Obtain assistance for the
tlexed, and one foot forward. Keep head and sake of both the patient and yourself.
trunk in proper alignment. 4. Other general tips for lifting are as follows
2. When our bodies are used as machines, the ex­ (Figure 40-7):
ternal weight on which we are working dis- • Lift with your legs. Keep legs in a position
that permits them to supply most of the force
for shifting your trunk.
• Do not attempt to lift with your arms and back.
• W hen lifting, avoid rotation of the spine.
Shift feet into position for weight shift when
moving or lifting patient.
• Stabilize your body against a stationary ob­
ject whenever possible.
• For best efficiency, coordinate the move by a
synchronized verbal expression understood
by therapists and patient, such as "1-2-3 lift."
One additional consideration mLlst be noted­
moving against the resistance of friction. Friction is
defined as a force that opposes the movement of one
object over the SUlface of another. Friction is reduced
as the amount of surface area contact between two
objects is reduced.
W hen moving a patient side to side or up and
down in bed, the therapist or nurse attempts to reduce
the contact of the patient's body sutface with the bed.
This can be accomplished by several maneuvers­
use a turning sheet (placed just above the patient's
shoulders to just below the patient's hips), cross the
patient's arms over the chest or abdomen, flex the pa­
FIGURE 40-7
Reach work level by bending the knees and hips rather than tient's knees and hips, and ask the patient to flex his

the back. Lift with the legs! This can also be done with a or her neck and raise the head as he or she is lifted (if
full double knee squat similar to techniques by the patient is unable to do this, the therapist or nurse
weightl ifters. will assist) (Figure 40-8).

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744 PART VIII Related Aspects of Cardiopulmonary Physical Thel'apy

MOVING DEPENDENT PATIENTS

r. Moving the patient up or down (Roper, 1973;

Lewis, 1976; Neil, J 976).
A. Using a turning sheet (Figures 40-9 to 40-11).
I. Sheet should cover from shoulders to hips.
\
2. Gather material as close to the patient's
body as possible.
3. Hold at shoulders and hips, with a flexion
pattern (see Figure 40-10).
4. Cross patient's arms over chest, flex knees
and hips.
5. Ask patient to raise head if possibl e.
6. Synchronize action by counting"1 2 3 lift."
- -

7. Shift weight from one leg to the other

rather than lifting up and pulling on back.
B. Without turning sheet (up or down), two people.
I. Follow basic procedurc-cross arms, lift
head, tlex knees and hips.
2. The therapist places his or her hands and
forearms under the patient's shoulders and
hips.
-0.
3. If patient is extremely hea vy or tall, an­
other person can bend knees and assist.
FIGURE 40-8
The patient should be prepared for a position chenge: knees
bent, arms crossed over chest and head lefted up to reduce
friction between the patient's body and the bed.

GIfJ "\

FIGURE 40-9
To insert the drawsheet, the patient is tumed to
his side and the half-rolled drawsheet is tucked
under him (from just above the shoulders to
just below the hips). He rolls over the
drawsheet and it is pulled out behind him.

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 40 Body Mechanics-The Art of Positioning and Moving Patients 745

FIGURE 40-10
The drawsheet should be rolled close to the patient's body.
A flexion hand grip at the patient's shoulders and hip is
most efficient.
FIGURE 40-11
Moving the patient toward the head of the bed. The patient
is prepared. The therapist is positioned to move toward the
II. Moving the patient to the side of the bed. head of the bed in order to shift his body weight to move
A. With turning sheet. the patient.
I. Cross arms, and other body parts, toward
the side to w hich the patient is to be
moved.
2. Therapist's hands at patient's hips and
shoulder on material close to patient's
body. 2. Bring right arm to the side at a 90-degree
3. One therapist pushes, the other pulls. angle up and away from body.
B. Without turning sheet. 3. Place left arm across chest.
I. Both persons stand on the desired side. 4. Place left leg over right leg.
2. One therapist's forearms under patient's 5. Pull sheet at patient's back to turn.
shoulder, the others under patient's hips. B. Without turning sheet (to right side).
3. Synchronize action by counting "1-2-3 I. Move to opposite side (therapist's hands
pull." and forearms under patient's shoulders
III. Turning the patient to his side. and hips).
A. With turning sheet (to right side) (Figures 40- 2. Same steps as 2, 3, and 4 above.
12 and 40-13). 3. Roll to right side using left shoulder and
l. Move patient supine to opposite side of left hip to push or pull.
turn (e.g., if turning to right side, move IV. Turning the patient prone (e.g., roll to right side)
patient to left side of bed). (Figure 40-14).

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746 PART VIII Related Aspects of Cardiopulmonary Physical Therapy

'� ------ J
FIGURE 40-12
Preparation for the patient to turn to his left side: move
patient to the right side of the bed, position his left arm up
to the side at a 90-degree angle, cross the right leg and arm
over his body and turn the patient's head to the left.

FIGURE 40-13
A one-person turn to the right side using a drawsheet. The
patient's body position is the same as for the turn to the side. k!-
The therapist is positioned with one foot forward, the other
back. He pulls the sheet with his hands positioned at the hips
"@:: -

and shoulders of the patient.

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 40 Body Mechanics-The Art of Positioning and Moving Patients 747

physical therapy. It is so often taken for granted and

pelformed with little thought or planning. Therapists
and nurses need to analyze beforehand their physi­
cal activities in relation to the principles of efficient
movement and the proper application of body me­
chanics. A "tube index", counting and identifying
each technical attachment, (e.g., IV, Foley cather,
arterial blood gas stint, or chest tubes) should be
done before moving a patient. Extra care needs to be
taken to prevent dislodging important medical
equipment. This could prove life threatening if ven­
tilator tubing was pulled and a patient was extu­
bated. The practical application of body mechanics
will not only conserve energy and preserve muscles
and joints but will also allow the patient to be
moved with a minimum amount of pain and discom­
fort, with greater safety.

REVIEW QUESTIONS

I. Why is it important to utilize efficient body me­

chanics when positioning and moving dependent
patients?
2. How can changing a patient's position affect

FIGURE 40-14 ventilation?

Positioning pa tient prone (EXM"IPLE: Rolling to the right 3. How can therapist use towel rolls and easily ac­
side). The patient's right arm is tucked in at his side with cessible equipment to improve a patient's posi­
the left arm and leg crossed ove r. tion and potential for improved ventilation?
4. What ventilation/perfusion changes occur when a
patient is turned from the "bad" side down to the
"good" side down?
S. Can positioning alone be considered therapeutic

A. With or without turning sheet. when it accomplishes the plan of treatment goal?

l . Move patient to opposite side of bed from

side toward which he or she is turning.
References
2. Cross left arm and left leg over body.
3. Right hand and arm at body side tucked in B orello-France, D.P., Burdett, R.G., & Gee, Z.L.,(1988). Modifi­
cation of silting posture of patients with hemiplegia using seat
as close as possible.
boards and backboards, Physical Therapy, 68(l), 68-7l.
4. Use hips and shoulders to turn.
Crosbie, W.J., & Myles, S. (1985). An investigation into the effect
S. Free both arms, do not allow patient to lie of postural modification on some aspects of normal pulmonary
on arm or hand. function. Physiolherap)" 7,(7),311-314.

6. May want pillow under hips and lower Fuerst, E., & Wolff, L. (J 959). Fundamel1lals of nursing (4th ed)
Philadelphia: 18 Lippincott.
legs to bend knee and relieve back strain
[s there a right way to lift') ([985). Physical Therapy Forum, 4, 23.
at lumbar spine.
Johnson, G. (1989). Functional Orlhopedics I. San Ansellmo,
To summarize, we find patient positioning and Calif: Institute of Physical Art. Chicago: Course presentation
movement is a necessary and integral function of June 8-11,1989.

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748 PART VIII Related Aspects of Cardiopulmonary Physical Therapy

Kendall, FP., McCreary, E.K., & Provance. P.G. (1993). Muscles Rantz. M. & Comiial, D. Lijiing, moving and Iransferring
lesling am/ flUlellOll. Baltimore: Williams & Wilkins. paliellls: a manual, S . . Louis, Mosby.
Lewis. L (1976). FUlldamellfai skills in patient care Philadelphia:
. Rauch, B. (J 971 L Kinesiology alld app/red allatomy, Philadelphia:
JB LippincotL Lea & Febiger.
Masscry. M. (1994). What's positioning got to do with it? Neuml­ Roper, N. (1973). Principles of (2nd ed). New
Report, /8 (3). 11-14. Churchill Livingstone.
Neil, C. (1959). Body management in nursing. Nursing Times, Woodhall-McNeal, A. P. (19')2). Changes 1I1 posture and balance
55,163. with age, Aging, 4 (3), 219-225.

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 Respiratory Care Practice Review

Michael Wade Baskin

KEY TERMS Aerosol Mechanical ventilation

Humidity Oxygen
rntermittent positive pressure Oxygen delivery
breathing (IPPB)

INTRODUCTION OXYGEN THERAPY

Proper care of the pulmonary patient involves a multi­ The atmosphere around us contains 20.95°/'1 oxygen,
disciplinary approach, and all professionals involved one of the most essential elements needed to sustain
should have a working knowledge of each individual human life. Oxygen exerts a partial pressure of 159.6
profession's scope of care. As respiratory therapists, mm Hg at sea level (dry air) and approximately 97
physical therapists, occupational therapists, and nurses mm Hg in arterial blood. The normal range as mea­
apply their expertise in providing care for pulmonary sured by arterial blood gas analysis is 80 to 100 mm
patienls, it becomes ev ident that coordi nated team Hg. Under normal circumstances, this molecule trav­
work is essential 10 ensure errective treatment pro­ els from the atmosphere to the mitochondria at the
gramming. The purpose of this chapter is to provide cellular level where it is used to produce ATP in a
nonrespiratory therapist health-care professionals with process called aerobic metabolism. The pathway in­
an overview of respiratory care principles and modali­ volves the lungs, blood, circulation, and the muscle
ties frequently encountered in the various settings. It tissue where the mitochondria reside. Any process
is also the intention of this chapter to eliminate the that inhibits the transport of oxygen from the atmos­
anxiety experienced by professionals because of the phere to the cellular level can cause tissue hypoxia
plethora of attachments to the cardiopulmonary pa­ and ultimately death.
tient. Interaction with the various modalities and One of the most common drugs that a respiratory
pieces of equipment is also discussed. therapist uses is oxygen. Patients with cardiopul­

749

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750 PART VIII Related Aspects of Cardiopulmonary Physical Therapy

monary problems frequently need oxygen supple­ The nasal cannula, also called nasal hi-prongs, is
mentation. Respiratory therapists and the nursing one of the most common low now devices encoun­
staff are generally responsible for administration of tered because of its low expense and high patient
this drug under a physician's order. There are several compliance (Figure 4 1-]). This device supplies be­
different methods a therapist may choose to deliver tween 24% and 40% oxygen with flow rates from I
oxygen in the most effective way. Llmin to 6 Llmin. Flow rates above 6 Llmin can
The purpose of oxygen therapy is to treat and to cause nasal mucosa irritation and drying. The approx­
prevent hypoxemia, excessive work of breathing, and imate liter flow and resultant Flo2 values are shown
excessive myocardial work (Kacmarek, Mack, and in Table 41-1.
Dimas, 1 990). Although individual oxygen appli­ Nasal canulas deliver 100% oxygen, however, this
ances offer suggested guidelines regarding oxygen percentage significantly lessens as the oxygen mixes
administration, the only way to ensure effective de­ with inspired air from the room. The amount of oxy­
livery from a given device is blood gas monitoring of gen delivered depends on the now rate and the venti­
Pao2, partial pressure of oxygen in the arterial blood latory pattern of the patient. A larger minute volume
or by monitoring hemoglobin saturation by oximetry. (TV x RR) would dilute the oxygen at any given flow
Oxygen therapy can be administered by one of two rate causing a greater decrease in the percentage de­
methods-low-flow and high-flow systems. livered to the lungs. In other words, the faster and
deeper a patient breathes, the more diluted the oxy­
gen will become. On the other hand, if a patient has a
Low-Flow Systems
low minute volume, the oxygen percentage delivered
A low-flow oxygen system is that which does not in­ will increase (Kacmarek et aI., 1990). If precise con­
tend to meet the total inspiratory requirements of the trol of Flo2 is needed, the nasal cannula should not be
patient. This method of oxygen delivery is not used used (Bazuaye, Stone, Corris, and Gibson, 1992).
when a specific concentration of oxygen is needed Mouth breathing by patients on a nasal cannula
(Burton, Hodgkin, and Ward, 1991). typically causes the attending health-care provider to
switch the patient to a mask; however, this may be un­
necessary. If the nasal passages are unobstructed, then
oxygen is able to collect in the oral and nasal cavity
(anatomical reservoir). On inspiration, the oxygen col­
lected in this area is drawn into the airway system. If a
patient with a nasal cannula is mouth breathing, the
practitioner should ensure the nasal passages are un­
obstructed. If there is concern that the patient is not

TABLE 41-1

Approximate liter flow Hod resultant Fl02 values.

FLOW (Llmin) Flo2(%)

I 24
2 28
3 32
4 36
5 40
FIGURE 41-1 6 44
Oxygen cannula.

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 41 Respiratory Care Practice Review 751

receiving adequate oxygen, an oxygen saturation mea­ cheal oxygen catheters are more efficient than nasal
surement should be obtained. If this is not feasible, or cannulas, and they have a high patient acceptance
if the patient is unable to breathe through the nose, it rate with low complications (Kent, et a!., 1987). Be­
would be appropriate to switch the patient to a mask. cause the oxygen is administered directly into the tra­
Breathing through the nosc should be encouraged chea, 50% less oxygen is needed (Kacmarek et a!.,
to receive maximum benefil from the nasal cannula; (990). For people who use portable oxygen systems,
however, mouth breathing does not mean the patient and for those who require high oxygen flow rates,
is not receiving oxygen (Dunlevy & Tyl, 1992). tracheal oxygen catheters may be beneficial (Jackson,
The simple mask, or open-face mask, is another King, Wells, and Shneerson, 1992). The catheter can
low-flow oxygen delivery device commonly used. It be covered by the patient's clothing, therefore, it is
can deliver from 40% to 60('>(; oxygen, depending on cosmetically appealing.
the flow rate and the patient's ventilatory pattern.
This device requires a flow rate of 5 to 6 Llmin to
HIGH-FLOW SYSTEMS
prevent rebreathing and excessive respiratory work
(Jensen, Johnson, and Sandstedt, 1991). As with the A high-flow oxygen delivery system is that which de­
nasal cannula, this type of oxygen delivery method livers a specific oxygen concentration despite the pa­
should not be used if precise control of oxygen con­ tient's ventilatory pattern. If it is found that a patient
centration (FI02) is required. requires oxygen delivered at an FIo2 of 50% to keep
The partial rebreathing mask is basically a mask the oxygen saturation at a safe level, then a high-flow
with a reservoir bag attached. The oxygen source system would be the method of choice.
supplics the bag with 100% oxygen where it mixes This type of system is also used when there is fear
with exhaled anatomical dead-space-air that has not of administering too much oxygen to a hypercapneic
taken place in gas exchange. This exhaled air is rich patient. The respiratory drive to breath could be re­
in oxygen. The exhaled air that has taken place in gas duced and possibly result in apnea. Precise control of
exchange and contains CO2 is vented through the low-concentration oxygen is warranted in such cases.
open ports on each side of the mask. This mask can
deliver oxygen concentrations from 70% to more
than 80%, and it requires flows between 7 and 10
Llmin to keep the bag from fully collapsing during
inspiration (Kacmarek et a!., (990).
The nonrebreathing mask is another low-flow de­
livery device that also contains a bag reservoir, but it
can deliver up to 100% oxygen. This mask contains
valves at the reservoir bag and the side vents to pre­
vent ambient air mixing on inspiration and exhaled air
mixing on expiration. In order for this mask to operate
effectively, a good seal between the patient's face and
the mask should be achieved. The bag should partially
deflate during inspiration (Figure 41-2).
Another interesting form of low-flow oxygen de­
livery is the transtracheal oxygen calheter. This
method has gradually gained wider acceptance as a
long-term oxygen delivery device. It is surgically FIGURE 41-2
placed into the trachea via a small incision between Left to right, mask without bag, partial rebreathing bag,
the second and third tracheal rings. Generally, these nonbreathing bag. NOTE: the valves on the mask and at the
devices are seen in home-oxygen patients. Transtra­ junction between the mask and bag.

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752 PART VIH Related Aspects of Cardiopulmonary Physical Therapy

The Venturi mask is a common method of deliver­

ing high-flow oxygen concentrations from 24% to
50%. This mask operates via the Venturi principle,
which provides for a mixing of 100% oxygen and en­
trained ambient air. The oxygen flows though a nar­
row orifice at a high velocity causing a subatmos­
pheric pressure. This drop in pressure is what causes
the ambient air to be entrained through a port. The
size of the port determines the amount of air to be en­
trained and thus the percentage of oxygen delivered.
The Venturi mask has a rotating air entrainment port
that allows the health-care provider to "dial in" the
desired FI02 (Figure 4 1-3).
Mechanical aerosol systems also operate via air en­
trai nment, but the mask is connected to the aerosol
unit by large-bore tubing to allow a specific FI02 to be FIGURE 41-3
delivered with high humidity (Figure 41 -4). Although Venturi mask.
drainage bags are usually attached to the tubing to col­
lect condensation, the tubing must be monitored for
possible pooling of water causing flow obstruction to
the patient. If pattial obstruction occurs, a mild back
pressure results in the tubing, causing less air entrain­
ment. This means that a higher concentration of oxy­
gen will result and possibly deliver a higher dosage of
oxygen to the patient than desired.

FIGURE 41-4
A, Heated aerosol. B, Nebulizers.

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 41 Respiratory Care Practice Review 753

HOME AND PORTABLE OXYGEN

Smaller tanks are used for portability and can provide
As health care continues to move out of the hospital set­ up to 3 hours of use. They can be refilled by transfer­
ting and into the home, more health-care practitioners ring gas from the larger reservoir tank.
will be providing care to oxygen patients in their homes. Liquid oxygen is a low-pressure oxygen delivery
Oxygen is most commonly delivered in the home for method, and it tends to be more convenient than
those needing long-term oxygen, usually chronic ob­ using the high-pressure tanks, especially for the ac­
stl1lctive pulmonary disease (COP D) patients. Generally tive oxygen patient. The canisters are lightweight and
I to 2 Llmin is prescribed via nasal cannula, but the allow patients to be away from the home reservoir for
flow rate will depend on the patient's need. up to 8 hours. The down side is that liquid oxygen
Home oxygen-delivery systems can be divided costs more, and the reservoirs need to be filled up to
into three categories: high-pressure oxygen cylinders, twice a week with continuous use. If high flows are
low-pressure liquid oxygen, and oxygen concentra­ needed, these units are not recommended.
tors (Burton et aI., 1991). Oxygen concentrators are commonly seen in the
High-pressure oxygen tanks come in various sizes. home health setting, especially since Medicare offers
The larger ones such as the H and K sizes are used as coverage for these devices (Figure 4 I -5). Generally,
a base unit or reservoir. Long oxygen tubing con­ they tend to be expensive initially but are actually
nected to these tanks allows for patient mobility. less expensive for long-term use. They are electri­
cally powered and create oxygen by drawing ambient
air across a semipermeable membrane, separating
oxygen from nitrogen. They generally operate at 2
Llmin and provide 90% oxygen. Long oxygen tubing,
up to 50 ft, allows patients extra mobility. Patients
using concentrators should have a back-up device,
such as a pOJ1abie tank, in case of a power outage.

RESPIRATORY MODALITIES
Intermittent Positive Pressure Breathing

Intermittent positive pressure breathing (lPPB) is

mentioned here not to educate the reader about its use
but to inform the reader about its declining use. Al­
though this particular modality continues to be used
in some hospital settings, there is little evidence to
supports its efficacy.
This particular technology was developed during
World War II to assist pilots breathing in unpressur­
ized cabins at high altitudes. IPPB subsequently be­
came a very popular respiratory therapy device in the
1960s and I970s (Figure 41 -6). However, its use
began to decline in the 1980s. In 1983 the National
Heart, Lung, and Blood Institute reported that IPPB
has limited therapeutic benefit. This clinical trial is
only one of several studies that show IPPB is an out­
moded medical technology. In fact, research dating
FIGURE 41-5 back to the 19 50s questions the efficacy of this de­
Oxygen concentrator. vice (Duffy and Farley, 1992).

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754 PART VIII Related Aspects of Cal'diopulmonary Physical Therapy

FIGURE 41-6

Left, Bird Mark and righI, Bennett AP-S IPPB machines.

FIGURE 41-7

Incentive spirometry device in use,

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 41 Respiratory Care Practice Review 755

The purpose of the IPPB machine is to increase rina. This humidification process is important to mu­
alveolar ventilation, to improve the ventilation-pelfu­ COlIS production, ciliary activity, and a healthy respi­
sion ratio, to mobilize and facilitate expectoration of ratory tract. When this normal humidification process
thick secretions, to decrease the work of breathing, is interferred with, other methods of adding moisture
and to deliver aerosolized medications. It is a pres­ to the respiratory system must be employed.
sure-cycled ventilator that, when triggered by a pa­ Humidification is the addition of water vapor in its
tient's inhalation, delivers ambient air or oxygen to molecular form to a gas. When a dry gas is being ad­
the patient until a preset pressure is rcached. It is ba­ ministered to a patient (e.g., via a nasal cannula),
sically a lung expansion device that helps deliver an some type of humidification appliance would be used
increased tidal volume. IPPB is used for a variety of to prevent unneccssary complications. Flows of 2
pulmonary conditions, and treatment scssions usually Llmin or less may not require humidification when
last 10 to 15 minutes. using a nasal cannula. Humidification therapy is also
This modality comes into question in the clinical indicated in the presence of thick tenacious secretions
setting because it has not shown to provide benefits and when an artificial airway is in place. Artificial
over that of other simpler respiratory treatment meth­ airways, such as endotracheal and tracheostomy
ods. It also introduces potential complications and tubes, bypass the normal humidification system (the
hazards that the other treatments do not. Typically, upper airway); therefore, supplementation is essential
IPPB has been used to treat asthma, COPO, and post­ (Frownfelter, 1987).
operative atelectasis; however, other therapies, such There are basically two types of humidifiers. Bub­
as incentive spirometry (IS), postural drainage, and ble-through humidifiers are those which are generally
aerosol therapy, tend to prevai I as the treatment of used with simple oxygen appliances. The pass-over
choice over IPPB. type of humidifier is usually found in conjuction with
Although IPPB is questionable regarding its clini­ a mechanical ventilator. Both bubble-through and
cal efficacy, it may be a beneficial form of treatment pass-over humidifiers are available for ventilators,
in acute asthma or COPO that is refractory to stan­ and they are usually heated to warm the humidified
dard therapy, atelectasis that has not responded to air to body temperature before entering the airway
simpler therapy, and the prevention of respiratory (Kacmarek et ai., 1991).
failure in patients with kyphoscoliosis and neuromus­
cular disorders (Handelsman, 199 I).
Aerosol Therapy

An aerosol is created when a suspension of liquid or

INCENTIVE SPIROMETRY
solid particles exists in a gas. Today, the two most
Incentive spirometry (IS), also called sustained maxi­ common forms of medication aerosol delivery in the
mum inspiration (SMI), is simply a visual and/or clinical setting are the small.
audio feedback device that encourages slow, deep in­ and the metered dose inhaler (MOl). A bland aerosol
spiration (Figure 41-7). Generally, this treatment is is administration of water or saline solution to the pa­
performed frequently, up to every hour, and its pur­ tient's lungs.
pose is to treat and prevent atelectasis, especially in In general the goals of aerosol therapy are to hy­
postoperative thoracic and abdominal patients. drate dried retained secretions, to improve cough effi­
ciency, to restore and maintain function of the mu­
cociliary elevator, to deliver medications, and to
HUMIDITY AND AEROSOL THERAPY
humidify gases delivered through artificial airways.
Humidity Therapy
The MOl is strictly used for medication delivery.
Under normal circumstances, when inhalation takes Other forms of aerosol delivery are the spinning
place, air becomes 100(;'(; saturated with water vapor disk, such as in a room humidifier or mist tent, and
before entering the lower airway tracts below the ca­ the ultrasonic nebulizer. Both of these are electri­

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756 PART VIII Related Aspects of Cardiopulmonary Physical Therapy

ble while taking slow, deep breaths with a short 3- to

4-second inspiratory hold. Mouth breathing is en­
couraged if aerosol therapy is delivered by mask.
Nasal breathing may filter out particles of optimal
size. Of course, not all patients will be able to
achieve this position and ventilatory pattern, and the
therapist must modify accordingly.
In comparing SVN with MOl's ability to deliver
medications, it is found that the MOl is either equal
in efficacy or outperforms nebulizers. Significant cost
savings are also realized by those institutions who
recog nize M O l usage as an effec tive means of
aerosol medication delivery over SVN (Orens,
Kester, Fergus, and Stoller, 1991).
To further enhance the efficacy of the MOl treat­
ment, a spacer or holding chamber may be attached
to trap the aerosol particles before inhalation. This
device allows greater drug particle deposition to the
FIGURE 41-8
airways and reduces oropharyngeal deposition (Ash­
Commonly used spacer device.

worth, Wilson, Sims, Wotton, and Hardy, 1991).

Ventilator patients that are receiving drug aerosol
therapy also receive greater benefit from an in-line
MOl with a holding chamber as compared with a jet
nebulizer (Fuller, Oolvich, Posmituck, Pack, and
cally powered as opposed to the SVN, which is Newhouse, 1990).
pneumatically powered (Figure 41-8) (Branson and
Seger, 1988).
Aerosol-Therapy Precautions
A key element in aerosol delivery is particle size.
The size of the aerosol particle will determine its abil­ It should be mentioned that there are hazards associ­
ity to penetrate into the airway before depositing or ated with aerosol therapy. Bronchospasm may occur
raining out. The therapeutic range is considered I 11 as the smooth muscle of the bronchial passages
with the smaller range of paJticles having the greatest react to foreign particles entering the lung. Short­
penetrating ability. The larger particles deposit sooner. ness of breath and respiratory distress may also
If they are greater than 5 11 then the chances of entry o c c u r as a r e s u l t of d r i e d retained secretions
into the airway are less. The particles may deposit in swelling and occluding portions of the lung. Cross
the nose and proximal airway. The greatest amount of contamination is a concern in that aerosol devices
alveolar deposition (95% to 100%) occurs in the I to may harbor organisms that can be transmitted to pa­
2 11 range. On the other hand, aerosol particles smaller tients. Frequent equipment changes and proper ster­
than I 11 are so stable that they may not deposit at all ilization and cleaning techniques are key in prevent­
(Kacmarek et aI., 1991). ing this occurrence.
Although particle size is important in determining
appropriate deposition, a patient's ventilatory pattern
MECHANICAL VENTILATION
is probably more important in that it is the more vari­
able and controllable of the two. Gravity also plays a The subject of mechanical ventilation is vast and
factor, and it too can be used to benefit particle depo­ highly technical. The purpose of this section is to give
sition. Patients should be sitting up as much as possi­ the reader a concise overview of mechanical venti la­

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 41 Respiratory Care Practice Review 757

FIGURE 41-9
A, Puritan Bennett 7200a microprocessor driven ventilator. B, Bennett MA-I ventilator-bellows
system driven by an electric compressor.

tion and provide a foundation from which to make ap­ tive pressure breaths to a patient. Positive pressure
propriate decisions when working in this environment. ventilation is opposite of normal physiological venti­
Many disease states that lead to cardiac and/or res­ lation in that normal ventilation occurs when negative
piratory failure will require mechanical ventilation to pressure, created by contraction of the diaphragm,
support the patient's effort to ventilate and oxygenate causes air to enter the lungs. Whereas normal inspira­
(Figure 41-9). Today, patients receiving mechanical tion occurs by "pulling" air into the lungs, ventilators
ventilator support can be found in both the hospital "push" air into the lungs. This is important in that the
and the home. Acute exacerbations of disorders such thoracic cavity becomes an area of higher pressure,
as emphysema, COPD, and chronic hronchitis com­ which may create adverse cardiovascular and hemo­
monly require mechanical ventilation and are gener­ dynamic events.
ally seen in hospital rcus. Disorders requiring long­
term ventilation, such as spinal cord injury, brain
Modes of Mechanical Ventilation
injury, and certain neuromusculoskeletal diseases,
may be found receiving mechanical ventilation in the The physician and respiratory therapist have a nev­
home or long-term care facility. erending sea of choices in which to choose the most
Today, mechanical ventilator assistance is pro­ appropriate method of ventilation. This area some­
vided primarily by machines that deliver preset posi­ times presents confusing terminology and a lack of

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758 PART VIII Related Aspects of Cardiopulmonary Physical Therapy

consistency. In fact, choosing the appropriate mode breaths with the patient's spontaneous breaths. In
of ventilation may be considered more of an art than IMV the machine may cycle a breath before the
a science. Before describing the modes of ventilation, patient can completely exhale a spontaneous
the following terms should be defined: breath. If no inspiratory effort is present, the ma­
1. Trigger-Variable that causes a breath to be chine delivers the mandatory breaths.
delivered by the ventilator. A patient may inhale •
Continuous positive airway pressure (CPAP).
causing the ventilator circuit pressure to drop to The patient spontaneously breathes and a preset
a preset number (i.e., less than 1 or 2 em H20). level of pressure is constantly maintained. This
This is called a pressure trigger. Some ventila­ method of ventilation can also be achieved
tors are volume and flow triggered. through use of commercially available pneumati­
2. Flowrate-The speed at which the ventilator cally powered units that hook directly into the
breath is deli vered. This parameter is usually oxygen wall outlet. A tight fitting mask is secured
measured in liters per minute. around the patient's mouth and nose, and a preset
3. Frequency-R e fers to the number of breaths pressure and oxygen percentage is delivered.
delivered over time (e.g., 10 breaths per minute). • Airway pressure release ventilation (APRV).
4. Spontaneous breath-Breathing through the The patient is allowed to spontaneously breathe
ventilator circuit without assistance. with a set amount of CP AP. If additional ventila­
The following is a descri ption of common current tion is required, the CPAP will be dropped period­
ventilator modes: ically, releasing the pressure, causing the patient
•
Controlled mechanical ventilation (CMV). The to exhale. When the exhalation is complete, CPAP
control mode is a lesser used method of ventilation is restored. Proponents of this mode claim that by
and generally requires the patient be sedated and allowing the patient control, patient comfort and
paralyzed. The ventilator delivers all breaths at a compliance are high.
p r e s e t f re q uency, volume or p r e s sure, a n d • Pressure support ventilation (PSV). In using
flowrate. T h e patient cannot take spontaneous pressure support the patient is allowed to breathe
breaths or trigger the machine. spontaneously and receives a preset amount of
•
Assist control (AC). The patient receives a preset inspiratory support until the fIowrate reaches a
pressure or volume, f requency or number of minimal level. The patient controls the fre­
breaths, and fIowrate. In between machine-cycled quency, tidal volume, inspiratory time. This
breaths, the patient can trigger the machine to de­ mode is often used in conjuntion with SIMV.
li ver another breath at the preset parameters. All This mode is also popular due to high patient
breaths are machine delivered. No spontaneous compliance.
breathing can occur. •
Mandatory minute ventilation (MMV). The pa­
•
Assisted mechanical ventilation. This mode is tient is allowed to breathe spontaneously; how­
similar to AC, however, there is no set frequency. ever, a minimal level of minute ventilation will be
The patient triggers the machine at will to deli ver achieved through ventilator-assisted breaths. This
a set pressure or volume at a set fIowrate. is usually accomplished by using PSV.
•
Intermittent mandatory ventilation (lMV). As • Volume-assured pressure support (V APS).
the ventilator delivers a set mandatory frequency This is one of the newest modes of ventilation. It
and volume or pressure, the patient is allowed to allows the patient to breathe spontaneously in the
take spontaneous breaths between cycles. This is a PSV mode and monitors each breath's tidal vol­
former popular mode. ume. If the breath is not going to reach the set
•
Synchronized intermittent mandatory ventila­ volume, the ventilator will hold the fIowrate con­
tion (SIMV). This mode improves on that of IMV stant and increase the pressure until the desired
in that it synchronizes the machine delivered volume is reached (Branson and Chatburn, 1992).

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 41 Respiratory Care Practice Review 759

Alarm Management and Precautions

or excessive water buildup (Figure 41-10). Low
When working around ventilators, it is inevitable that pressure may signify a leak in the ventilator circuitry
alarms will sound. Alarms are important indicators of a or a bad patient connection.
patient's condition or machine malfunction. All alarms If you are unfamiliar with a particular ventilator
should be recognized and valued as excellent sources and an alarm sounds that you are unable to identify
of information. If alarms are silenced or ignored with­ and/or remedy, first ensure the patient is not in any
out interpretation, patient fatalities may result. extra distress. Assess the overall appearance and,
The most common alarms are those which moni­ most of all, rise and fall of the chest as the ventilator
tor high and low pressurc. FI02, apnea, disconnec­ cycles. If the patient does not appear to be receiving
tion, and volume. Generally, if the high-pressure breaths, immediate action should be taken to remove
alarm continucs to sound, the patient should be the ventilator from the patient and to begin manual
checked for secretion buildup. Suctioning can rem­ ventilation with a self-inflating bag. The respiratory
edy this problem. The ventilator tubing should also care practioner should be called to rectify the situa­
be checked for possibJe occlusion from compression tion. When the problem is resolved, the patient
should be returned to the mechanical ventilator.
One primary precaution to keep in mind when
working with a ventilator patient is to watch for con­
densation in the tubing that could accidentally be
poured directly into the patients lungs. When moving
a ventilator patient, plan ahead by securing aJl lines,
wires, and tubing. Follow the appropriate procedure
for emptying any water from the ventilator tubing be­
fore moving the patient. Aspiration of water from
ventilator tubing can be fatal.

SUMMARY

Physical therapists need to understand the basic

equipment and principles of respiratory care in order
to optimize functional outcomes of their patients.

REVIEW QUESTIONS

I. If precise control of oxygen percentage to a pa­

tient is wananted, what type of delivery system
is indicated?
2. Does mouth breathing by a patient on a nasal
cannula indicate that he is receiving no oxygen?
3. Why do low-flow oxygen masks require a certain
minimum liter flow, that is,S to 6 Llmin for a
simple mask?
4. Why is IPPB come into question as an effective
FIGURE 41-10 modality?
Condensation build-up in ventilator tubing-a potential 5. What are two concerns regarding condensation
hazard. collecting in mechanical ventilator tubing?

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 760 PART VIII Related Aspects of Cardiopulmonary Physical Therapy

References
Fuller, H.D., Dolovich, M.B., Posmituck, G., Pack, W.W., & New­
Ashworth, HL, Wilson, CG., Sims, E.E., Wotton, P.K., & Hlirdy, house, M.T. (1990). Pressuril.ed aerosol versus jet aerosol de­
lG. (1991). Delivery of propellant soluble drug from a metered livery to mechanically ventilated patients. Comparison of dose
dose inhaler. Thorax, 46(4),245-247. to the lungs. American Rel'iew of Respiratory Disease. 141(2),
Barharash, R.A., Smith, L.A., GOdwin, J .E., & Sahn, SA (1990). 440-444.
Mechanical ventilation. DICP, The Annals of Pharmacother­ >f' Handelsman, H. (1991). Intermittent positive pressure breathing
apy. 24, 959-970. (IPPB) therapy. Health Technology Assessment Reports. 1. 1-9.
Bazuaye, E.A . , Stone, T.N , Corris, P.A., & Gibson, GJ. (1992) -J Hodgkin, J.E., Connors, G.L., & Bell, e.w. (1993). Pulmonary re­
Variability of inspired oxygen concentration with nasal cannu­ habilitation guidlines to success (2nd ed.). Philadelphia: JB
las. Thorax,4 7(8 ) , 609-611. Lippincotl.
ranson, R.D., & Seger, S.M. (1988). Bronchial hygiene tech­ Jackson, M., King, M.A., Wells, F.e., & Shneerson, J.M. (1992).
niques. In R.M. Kacmarek, & 1.K. Stoller. C urren l respiralory Clnical experience and physiologic resulls with an implantable
care (pp. 24-28). Philadelphia: B.e. Decker. intratracheal oxygen catheter. Chest, 102(5), 1413-8.
Branson, R.D., & Chatburn, R.L. (1992). Technical description and Jensen, A.G., Johnson, A., & Sandstedt, S. (1991). Rebreathing
classification of modes of ventilator operation. Respiralory during oxygen treatment with face mask. The effect of oxygen
Care, 37(9),1026-1044. flow rates on ventilation. Acta Anaesthesiologica Scandinal'­
-*' Burns, S.M. (1990). Advances in ventilatory therapy: high-fre­ ica, 35(4),289-292.
quency, pressure support, and nocturnal nasal positive pressure Kacmarek, R.M., Mack, e.W., & Dimas, S. (1990). The essentials
ventilation. Focus on Critical Care. 17(3),227-237. o{respiratory care (3rd ed.). SI. Louis: Mosby.
f Burton, G.G., Hodgkin, J . E., & Ward, J.J. (1991). Respiratory care Kent, e., et a!. (1987). A program for transtracheal oxygen deliv­
a guide to clinical practice (3rd ed.) (pp. 524-525). Philadel­ ery: Assessment of safety and efficacy. Annals of Internal
phia: J.B. Lippincott. Medicine, 107,802-808.
Duffy S.Q., & Farley, D.E. (1992). The protracted demise of med­ Orens, K.D., Kester, L., Fergus L.e., & Stoller, J.K. (1991). Cost
ical technology: the case of intermittent positive pressure impact of metered dose inhalers vs small volume m:huli/.crs in
breathing. Medical Care, 30(8),718-734. hospitalized patients: the cleveland clinic experience. Resp ira­
..( Dunlevy, e.L., & Tyl, S.E. (1992). The effect of oral versus nasal tory Care, 36( I 0), 1099-1104.
breathing on oxygen concentrations received from nasal cannu­ Pilbeam, S.P. (1992). Mechanical ventilatioll physiological alld
las. Respiratory Care, 37(4),357-60. clinical applirllliol1s. St. Louis: Mosby.
Frownfelter, D.L. (1987). Chest physical therapy and pulmanary ",*, .zadai, e.e. (1992). Pulmonary manogclllcnt in phvsical therapy.
rehabilitation an interdisciplinary approach (2nd ed.). St New York: Churchill Livingstone.
Louis: Mosby.

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 Care of the Patient With
an Artificial Airway

Lisa Sigg Mendelson

KEY TERMS Airway clearance Tracheostomy

Artificial airway Tracheostomy tube/cuff
Suctioning

HISTORICAL PERSPECTIVE
purposes: (I) to bypass upper airway obstruction,
An artificial airway is a tube inserted in the trachea (2) to assist or control respirations over prolonged pe­
either through the mouth or nose or by a surgical in­ riods, (3) to facilitate the care of chronic respiratory
cision. Artificial airways have been known to med­ tract infections, and (4) to prevent aspiration of oral
ical science for 3000 years. George Washington ulti­ and gastric secretions. Multiple disease processes and
mately died of upper airway obstruction because his traumatic problems can require an artificial airway,
p h ysicians could not agree on t h e use of tra­ but each situation, simple or complex, can fit into one
cheostomy. It was not until 1909, when Chevalier or several of these categories (see box on p. 762).
Jackson published his classical paper on tracheotomy,
that this procedure gained some acceptance. The pro­
INDICATIONS OF NEED-OBSERVATION
cedure did not become a highly specialized technique
in patient care until the invention of modern tra­ The respiratory care team can play a vital role in rec­
cheostomy tubes and the development of intermittent ognizing patient need for a tracheostomy from physi­
positive-pressure ventilators. In today's clinical prac­ ological changes that indicate respiratory distress.
tice, artificial airways have the following four basic Cardinal signs of dangerous airway obstruction are

761

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762 PART VIII Related Aspects of Cardiopulmonary Physical Therapy

Disease Processes that CouLd Require all ArtificiaL Airway because of Respiratory Illsufficiency

I. Primary lung disease (e.g.. emphysema. chronic bronchitis, pulmonary fibrosis. cystic fibrosis, severe pneumonia,
burned lung, and toxic inhalation).

2. Systemic disease with secondary lung involvement (e.g.. cardiac failure, renal failure (fluid overload), and Illulti­
organ system failure).

3. Neuromuscular disease (e.g., polio, Guillain-Barre syndrome, my asthenia gravis usc of muscle relaxants. and
,

tetanus).

4. Central nervous system depression (e.g.. drugs, postanesthesia, metabolical coma. cerebrovascular accident,
meningitis. and central nervous system tumors).

5. Trauma (e.g.. head/necklchest surgery or injuries).

6. Diseases complicated by extremes of age (e.g., premature infant or elderly).

7. Mechanical obstmction (e.g., upper airway infection. laryngeal paralysis, tumor. edema. bleeding. foreign body,
and thyroid malignancy).

8. Recurrent aspiration (e.g .. glottic incompetence, occlusive diseases of the esophagus, and swallowing disorders of
various causes).

From Selecky PA: Tracheostomy-a review of present day i ndicat ions complications and
, care, !-Iellrt Lung 3: 272-283, 1974.

stridor and chest wall retractions. Early clinical signs long-term intubation. The nasal tube is more efficient
may include restlessness, agitation, tachycardia, con­ in that it is better secured, the patient may eat, it is
fusion, motor dysfunction, and decreased oxygen sat­ easier to suction, and it is generally more comfortable
uration on pulse oximetry. These signs may be ac­ for the patient.
c o m p a n i e d by h e a d a ch e , f l a p p i n g t r e m o r, a n d There are certain complications with nasotracheal
diaphoresis. Cyanosis from impaired oxygenation of tubes. Among these are sinus blockage and pain,
the blood is a late, ominous sign. vocal cord damage, or pressure necrosis to the carti­
In children, restlessness must be due to lack of laginous structure of the nose. To reduce these com­
oxygen unless another factor (e.g., thirst) is clearly plications, the airway should be evaluated daily. The
evident. Extreme fatigue and an inability to sleep in­ tube should be removed as quickly as possible when
dicate impending danger. Apprehension, restlessness, the indication for intubation is reversed. However, if
and mental confusion at any age may be taken as there appears to be a need for a more long-term air­
early signs of hypoxia. way, a tracheostomy should be considered. The pro­
cedure should not be taken lightly because many ad­
ditional complications may occur.
Complications of Tracheostomy
Complications of tracheostomy can be surgical,
The selection of the appropriate airway is made by postoperative, or physiological. Complications that
the following factors:(I) What is the best means of occur at the time of the operation are more frequently
accomplishing the goal? (2) Is it an emergency or a direct results of the surgical procedure itself. Delayed
controlled, determined situation? (3) Will the airway complications may result directly or indirectly from
be needed for long-term care? In general, oral endo­ surgery, from postoperative care, or from the abrupt
tracheal tubes are inserted in emergencies. They are physiological changes resulting from tracheostomy.
the quickest and easiest tubes to insert even for rela­ Nursing objectives in caring for the patient after a tra­
tively untrained personnel. A nasotracheal tube will cheostomy are to maintain patency of the tube, clean­
generally replace the oral endotracheal tube for a liness of the wound site, and good aeration and to ob­

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 42 Care or the Patient With an Artificial Airway 763

serve any changes in the patient's vital signs and oxy­ A patient with an artificial airway is understand­
genation by pulse oximetry. ably apprehensive and has special communication
In patients with artificial airways the normal phys­ needs. He or she should also be reminded that the in­
iological mechanism for adding moisture to the air ability to phonate is only temporary. The patient must
via the nasal mucosa obviously is bypassed. There­ be reassured that he or she will be attended to con­
fore supplemental humidification is extremely impor­ stantly and will be able to trust and depend fully on
tant to protect the mucosa from drying and crusting, the nursing staff to attend to his or her needs. If alert,
which results in obstruction. the patient must be equipped with a signal light or
The dressing under the tracheostomy tube and tra­ bell, paper and pencil, magic slate, or picture board
cheostomy ties should be changed when they become for communication.
soiled because dried blood and other secretions near Airway obstruction is the foremost complication that
the incision can encourage bacterial growth. The inci­ exists for the postoperative tracheostomy patient. Tra­
sion should be checked frequently for bleeding. The cheal secretions are the major source of obstruction,
skin may be cleaned with half-strength hydrogen per­ particularly if they are excessive or viscous. When
oxide and sterile saline when a new dressing is ap­ using cuffed tube, acute obstruction might occur from
plied. The dressing should be folded into place­ overinflating the cuff, which would allow it to balloon
never cut. This eliminates the possibility of lint or over the end of the tube. Other causes of obstruction are
frayed threads being aspirated. Commercially pre­ dislodgement of the tube into a false tract anterior to the
pared dressings best meet these criteria. tube tracheal opening, occlusion by an overinflated
When changing the tapes that hold the tube in cuff, and kinking of softened plastic cannula.
place, it is best to have one nurse hold the tube in Tracheobronchitis, inflammation of the trachea and
place while another replaces the old tapes. An angle bronchus, is a complication resulting primarily from ir­
is cut at the end of the tape to facilitate its placement ritation resulting from incorrect suctioning technique.
through the flange of one side of the tube. The tape is Crusting is a common and complex problem that
then threaded through the back of the tracheostomy may result from inadequate humidification of inspired
tube and through the other flanged opening and tied air or may result from dehydration. In many instances,
securely with a square knot placed on one side of the ulceration of the tracheal mucosa results from irrita­
patient's neck. One finger should be placed under the tion by the airway or incorrect suctioning. This ulcer­
twill tape while tying to prevent the tape from being ated area becomes infected with various organisms
tied too tight. and is virtually covered by crust. Further suctioning
Pneumothorax can occur immediately after tra­ removes the crust, causing discharge of serum and
cheostomy because of laceration of the mediastinal bleeding. The discharge produces a wet eschar that is
pleura at the time of surgery or within 24 hours (arises covered with mucus. Because of the drying effect of
often in children and patients with chronic obstructive air passing over this mass, a hard crust can form. This
lung disease). Other problems include air embolism, process can compound the difficulty because the de­
aspiration, and subcutaneous and mediastinal emphy­ velopment of this crust in the trachea might eventually
sema. Recurrent laryngeal nerve damage or posterior produce a mass large enough to completely plug the
tracheal penetration may occur but is uncommon. tracheal cannula and almost completely obstruct the
trachea. Cases have been cited where an entire cast of
the tracheobronchial tree has been removed.
Postoperative Physiological Complications
Other physiological complications may be related
Attentive nursing care is the single most essential to the following: (1) hypoxia developing before or
factor in postoperative management. A ratio of one during the procedure and resulting in an uncontrol­
nurse for each patient is the ideal; however, since this lable patient, cardiac arrest, and increased myocardial
is not often possible, increased vigilance by the entire sensitivity to adrenalin; (2) alkalosis developing from
respiratory care team is of vital importance. rapid carbon dioxide wash-out after establishment of

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764 PART VIII Related Aspects of Cardiopulmonary Physical Therapy

the airway, resulting in myocardial fibrillation and tube can be replaced by the nurse on written order of
apnea; (3) cardiac fa i lure resulting in profuse bron­
, the physician.
chorrhea caused by pulmonary edema and shock.
Other chronjc complications cited by Dailey, Simon,
TRACHEOSTOMY TUBES
Young, and Stewalt (1992) include the following: (1) in­
fection at the surgical site, (2) aspiration, (3) aerophagia,
Metal Tubes
(4) persistent stoma, and (5) tracheal stenosis.
Tracheostomy tubes are of two basic types-metal
and polyvinyl chloride (hard and soft). Metal tubes
Postoperative Mechanical Complications
can be made of either stainless steel or sterling silver
Dislocation of the tube may result from unsatisfactory and composed of the following three parts: (I) an
nursing care, poor attention to the airway during posi­ outer cannula that fits into the tracheal incision,
tioning, or ventilator tubing pulling on the airway. If (2) an inner cannula that fits into the outer cannula,
the tracheostomy tube tapes are not kept tight and tied and (3) an obturator. Before the outer cannula is in­
with a square knot or if they become loose as a result serted into the tracheal incision, the obturator is
of cervical emphysema or edema, the tube may be placed inside. The lower end of the obturator pro­
coughed out of the trachea and become lodged in the trudes from the end of the outer cannula and facili­
tissues of the neck and obstruct the airway. tates its insertion into the trachea. This is the only
Stay sutures are useful in tracheostomy patients purpose of the obturator. The protruding end of the
when there is the possibility of tube displacement. obturator obstructs the lumen of the outer cannula.
These sutures are valuable during recannulization of When the obturator is removed, immediately replace
the tube if it comes dislodged before a tract has been it with the inner cannula. When dealing with metal
well established. Stay sutures will prevent entry into tubes, the parts of each set are not interchangeable
a false tract. Advantages of this technique include the and fit only one particular set. If one part is lost or
following: (I) blockage or displaced tubes can be damaged, the entire set is useless. Therefore each
rapidly replaced, (2) exposure of the trachea at surgi­ part, including obturator, is accounted for carefully.
cal intervention is improved, (3) firm anchoring of Plastic tubes generally have interchangeable parts.
the trachea at the moment of incision, (4) decreased Care should be exercised in handling sterling silver
trauma associated with extubation, and (5) uniform tubes, since silver is easily dented.
tracheostomy technique for aJJ ages. Mucus that has dried inside the inner cannula can­
Dislodgement of the outer cannula or required re­ not be cleaned by merely rinsing in water. The can­
moval before a tract has been well established (usu­ nula should be soaked in hydrogen peroxide and
ally 5 to 10 days) again requires diligence and quick scrubbed with a tracheostomy brush and rinsed with
action by the nurse. No attempt at reinsertion should saline to be sure aJJ secretions have been removed. If
be made without adequate light, satisfactory tissue re­ a silver inner cannula becomes discolored, it may be
traction, tracheal hook, and a Trousseau's dilator. A cleaned with silver polish.
Trousseau's dilator and tracheal hook should be read­ The inner cannula should always be inspected to
ily available. A spare tracheostomy tube of the cor­ be sure it is clean and clear of secretions before it is
rect size should be kept at the patient's bedside at all reinserted. Be sure to lock the inner cannula in posi­
.
times. Then, should the tube be coughed out, the tion after reinsertion.
nurse uses the Trousseau's dilator to hold the wound
apart while summoning the physician. Tragedies have
Polyvinyl Chloride (Plastic) Disposable
occurred from inserting the tube into the soft tissues
Tubes and Cuff Inflation
of the neck or mediastinum because of a dislodged
cannula and the frantic efforts to replace it. Once the The development of plastic tracheostomy tubes came
tracheostomy tract has been firmly established, the about for the following three important reasons:

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 42 Care or the Patient With an Artificial Airway 765

(1) application of silicone to the inner sUliace of the fore insertion of the tube into the trachea to be certain
plastic tube minimizes crusting and adherence of se­ that there are no leaks. The Luer valve inflation port
cretions; (2) there is greater ease in attaching a safe, to the pilot balloon is self-sealing. Some Luer valves
dependable, permanent inflatable cuff to the plastic have a relief valve when pressure exceeds 25 mm Hg.
tube that cannot slip off and occlude the tracheal
opening; and (3) lower costs allow the tube to be dis­
Cuff Inflation
posable. Plastic tubes come with and without cuffs.
The cuffed tracheostomy tube is primarily used in There are two commonly used methods of cuff infla­
conjunction with a positive-pressure ventilator to tion. These are the minimal air leak, in which a small
form a closed system (Figure 42-1). It is also used to amount of air escapes on inspiration, and minimal oc­
reduce the possibility of aspiration because of absent, clusive volume, in which just enough air is placed in
protective laryngeal, and pharyngeal reflexes. The in­ the cuff to stop air from escaping on inspiration. Ac­
flatable cuff is located around the lower portion of cording to Crabtree Goodnough (1988), the minimal
the tube and, when inflated, seals the trachea from leak cuff technique may produce less injury than the
most airtlow except through the tube itself (see Fig­ minimal occlusive volume inflation technique. Re­
ure 42-1). The cuff, usually made of pliable plastic, is gardless of which technique is used, the pressure of
inflated by injecting air into the fine-bore tubing. A the cuff should be checked every 4 to 8 hours and the
small pilot balloon is located proximally in the tubing pressures documented. With continued research and
and indicates that the cuff is inflated. The nurse must monitoring of tracheal cuff pressures, potential tra­
check the inflation end of the cuff and the balloon be­ cheal injury can be prevented.

FIGURE 42-1
A, Cuffed adult tracheostomy tubes, uncuffed pediatric tracheostomy tube (far left). B, Cuffed adult
endotracheal tubes, uncuffed pediatric endotracheal tube (far left).

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766 PART VIII Related Aspects of Cardiopulmonary Physical Therapy

Once the cuff is inflated, the only route for air ex­ ideall y every 8 hours but at least once every 24 hours.
change is through the patient's tracheostomy tube; The Communitrache I is a tracheostomy tube that
therefore careful observation of the patient by the permits the removal of secretions above the inflation
nurse is essential. If the patient is on mechanical ven­ cuff without nasotracheal suctioning. The other plus
tilation, observation is essential if there is ventilator factor to this tracheostomy tube is the patient's ability
failure because asphyxiation may occur. Alarms are to communicate, especially while on a ventilator.
always in the "on" position when a patient is being When the patient is weaned from the ventilator, a
mechanically ventilated. Some means of resuscita­ fenestrated tube may be used. Fenestrated comes
tion, such as a manual resuscitating bag with mask, from the French word jenesfre, meaning window.
must be available at the bedside to ventilate the pa­ There is a window (fenestration) in the outer cannula.
tient in case the tracheostomy tube comes out or is When the tube is used for speaking the cuff is down,
dislodged. the inner cannula removed, and an external plug is in­
Considerable emphasis has been given to the inci­ serted to cap the tracheostomy tube to allow the pa­
dence of tracheal ischemia and resulting stenosis tient to speak. The cuff must be deflated when the
from the use of a cuffed tube. This ischemia results cap is in place. If the cuff was inflated, the patient
from the pressure of the cuffed tube against the tra­ would be unable to breathe air into the lungs. The pa­
cheal wall, which heals with scar formation, resulting tient exhibits immediate distress if this mistake is
in subsequent stenosis. This complication can be re­ made. If a patient with fenestrated tube needs to be
duced or eliminated by minimal air leak or minimal suctioned, the inner cannula must be placed so that
occlusive volume. For the minimal occlusive volume, the suction catheter does not enter the fenestration
the cuff must be inflated to eliminate any air leak on and cause injury to the tracheal wal.l mucosa.
inspiration. Cuff pressures should be monitored and
documented every 4 to 8 hours to prevent tracheal in­
Other Airway Devices
jury. The recommended cuff pressure is I S to 2S mm
Hg. Inflate the cuff until there is no air leak between The Olympic tracheostomy button is used as an in­
the wall of the trachea and the cuff, and then release a terim airway after tracheostomy tube removal (Figure
small amount of air to allow only a slight air leak be­ 42-2). This method is another example of weaning a
tween the walls of the trachea and the cuff. This re­ patient from tracheostomy tube but still maintaining
duces the pressure of the cuff, still allows the ventila­ the stoma should a tracheostomy be again needed.
tor to function properly, and reduces the likelihood of The patient that benefited most from the procedure
tracheal ischemia. Any difficullY in properly inflating was the COPD patient. This was one method used to
the cuffed tracheostomy tube should be immediately facilitate secretion removal after hospitalization when
reported to the physician. it became necessary because of the disease proces?
If the tracheotomized patient is conscious, he or The Olympic tracheostomy button allowed the tra­
she may attempt to speak. If the cuff is properly in­ cheostomy patient the opportunity to reestablish an
flated, he or she will be aphonic, since no air can pass unobstructed airway and at the same time allowed the
over the vocal cords. If he or she needs to speak, the patient to speak.
cuff can be deflated, and the patient may be given a The Passy-Muir valve is used for patients with
sterile dressing to hold over the tube. This will allow upper airway obstruclion, and with difficult decannu­
him or her to speak and also simulate a cough by lation (Figure 42-3). The Passy-Muir is a one-way
rapid exhalation to clear secretions. valve, allowing inspiration only and forcing exhala­
Inspired air must be continuously and adequately tion through the upper airway. By using the valve the
humidified by means of nebulizing equipment to pre­ upper airway muscles gradually recover, allowing for
vent the formation of crusts. The equipment used for transition to a fenestrated tube or a smaller size tra­
this purpose can be a possible source of infection. cheostomy tube and preparing the patient for eventual
Therefore the nebulizer and tubing should be changed decannulation (Pierson and Kacmarek, 1992).

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 42 Care of the Patient With an Artificial Airway 767

Basic length 27-40 mm

-I

FIGURE 42-2
Dimensions and actual positiorung of an Olympic tracheostomy button. (From Pierson OJ and Kacmarek
RM: Foundations of respiratory care, Churchill Livingstone, 1992, Edinburgh © David 1. Pierson.)

FIGURE 42-3
The Passy Muir Valve. This valve attaches to a standard lS-mm tracheostomy adapter. It allows
inspriation A, via the valve, but exhilation 8, must occur via the upper airway. (From Pierson OJ
and Kacmarek RM: Foundations of respiratory care, Churchill Livingstone, 1992, Edinburgh
© David J. Pierson.)

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768 PART VIII Related Aspects of Cardiopulmonary Physical Therapy

Airway Care

Normally, the mucociliary escalator and the cough

reflex provide ajrway clearance. When these mecha­
nisms fail, suctioning of the airways is indicated.
Suctioning does have potential hazards, but it should
be a safe procedure with proper guidance and care.

\ Suclioning
I Proper explanation of the suctioning technique to the
patient helps allay apprehension and enhance cooper­
ation. Medicate your postoperative patient before
suctioning to decrease the pain of coughing. Always
maintain a calm and reassuring manner.
Maintain aseptic technique throughout the entire
procedure. Use sterile gloves and a sterile disposable
catheter for each suctioning.
Position the patient properly unless contraindi­
cated. Nasotracheal and/or pharyngeal suctioning
should be done with the patient in Fowler, 60 to 70
degrees, or semi-Fowler position, approximately 45
degrees, with the neck hyperextended (Figure 42-5).
FIGURE 42-4 The supine position is best for the patient with tra­
The Montgomery T-tube. (Reprinted with permission from
cheostomy or endotracheal tubes (Figure 42-6).
Montgomery WW: Manual care of the Montgovery silicone
Pharyngeal suctioning may be necessary before de­
tracheal T-tube. The annals of olOlogy rhinology &
flating the cuffed tracheostomy tube. The nurse should
lQ/yngology (supplement 73) 89(4): 3,1980.)
not suction the pharynx and then the trachea with the
same catheter, but the trachea may be suctioned first
and then the pharynx with the same catheter.
Duration of suctioning is of extreme importance.
Each suctioning procedure should last no longer than
The management of major airway obstruction 5 to 10 seconds to avoid hypoxia.
by tracheal tumor, external compression, or tra­ Prolonged suctioning may result in precipitating a
cheal disease below the thoracic inlet still present dysrhythmia or cardiac arrest. A good way to judge
difficult problems. The Montgomery T tube is a bi­ the elapsed time is to hold one's OWIl breath and be
furcated silicone rubber stent designed to preserve guided by the development of discomfort. This is
patency of the airways in a patient with injury to most important for the patient who depends on venti­
the trachea or main bronchi (Figure 42-4). When latory assistance.
the T tube is in place, the patient breathes normally The lowest possible vacuum settings are to be llsed
through nose and mouth and can speak. The T tube (below 120 mm Hg) that will still support suctioning
is a method in which secretions can be removed if the tracheostomy tube. The higher the setting is
necessary and is helpful in long-term therapy to al­ raised, the greater the risk of trauma to the tracheal
l e v i a t e o b s t r u c t i o n or d u r i n g r e c o n s t r uctive mucosa. Caution should be exercised to avoid kinking
surgery. This device does not cause any adverse the suction tubing or catheter. When negative pressure
tissue reaction on a long-term basis, according to is excessive and released suddenly, inadvertent re­
Montgomery. moval of portions of tracheal mucosa may occur.

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 42 . t With
Care 0 f the Pahen . an Artificial Airway 769

Fowler 60-70 degrees

Seml-Fowler 10- 12"

.

FIGURE 42-5
A, Fowler ' s an
, dB, Semi-Fowler's positions.

FIGURE 42 6
Supine posillon,

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770 PART VIII Related Aspects of Cardiopulmonary Physical Therapy

)(
FIGURE 42-7
The catheter will simulate coughing when it contacts the carina (in a patient with cough reflex).

FIGURE 42-8
The catheter is withdrawn I cm after it reaches the carina, before applying suction.

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 42 Care of the Patient With an Artificial Airway 771

Insertion of the suction catheter should be done Right main-stem bronchus aspiration is the usual
gently, using aseptic technique and sterile gloves. case because of the more direct alignment of this
Goggles are used as part of universal precautions if bronchus with the trachea. This can be carried out al­
there is any danger of coughed-ollt secretions. The most always with a straight tracheal catheter.
catheter should first be moistened in sterile saline or Excessive suctioning can be harmful. Use judg­
with a water-soluble gel. Suction is not applied while ment to determine just how often a patient requires
the catheter is passed down into the trachea. Proper suctioning. Auscultation by stethoscope should be
insertion of the catheter will stimulate coughing when used to determine the thoroughness of suctioning.
it contacts the carina (Figure 42-7). It is then immedi­ Suction only when it is needed (Carroll, 1994). Allow
ately withdrawn I cm before suction is applied (Fig­ the patient to rest and breathe between each insertion
lire 42-8). Do not force the catheter lip and down of the suction catheter and, if necessary, ventilate him
while suctioning. Suction is applied only while the or her for few minutes before further suctioning. Re­
catheter is being wi thdrawn. Rotating the catheter member each suctioning attempt removes air as well
during withdrawal results in suctioning a larger area as secretions. Hyperoxygenation and hyperinflation
and increases the surface contact of the trachea and with 100% oxygen has been suggested with better re­
tracheostomy tube (Figure 42-9). sults and fewer complications. Complications from
Left main-stem bronchus aspiration is more diffi­ tracheal suctioning include the following: (l) hypox­
cult because of the anatomical arrangement of the emia, (2) cardiac dysrhythmia, (3) bronchospasm,
bronchus. It was formerly thought that left bronchial and (4) infection. Suctioning can lead to hypoxemia
aspiration was facilitated by turning the patient's because oxygen is removed from the airways, and
head to the right. Studies by Kirimli et al. (1970) and this could lead to tissue hypoxia. To minimize this
Panacek et £II. (1989) indicate that left bronchial aspi­ problem, preoxygenation is recommended. This can
ration is best accomplished by using a Coude tip be done by hyperinflating the patient with Ilf2 times
catheter. After its insertion into the trachea. the their normal tidal volume on a ventilator and hy­
curved tip should be positioned to point toward the perox-genating with 100% oxygen for 3 to 5 breaths.
left main-stem bronchus. Even so, insertion is diffi­ Cardiac dysrhythmias, such as premature ventricular
cult, and auscultation by stethoscope is necessary to contractures, bradycardia, and tachycardia, can be di­
thoroughly access the suctioning. minished by hyperinflating and hyperoxygenating the

To suction unit

Connection
(
Detall

Air vent I

Catheter

FIGURE 42-9
The catheter is rotated during withdrawal in order to suction a larger surface area.

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772 PART VIII Related Aspects of Cardiopulmonary Physical Therapy

patient with 100% oxygen. If any dysrhythmias occur 18. Discard used equipment and remove gloves.
on the monitor, the suctioning procedure should be 19. Wash your hands.
discontinued. Bronchospasm may be effectively pre­
vented by a few puffs of a bronchodilator, such as al­
Nasopharyngeal Airways
buterol, to the tracheostomy tube before suctioning.
Infection can be decreased by maintaining sterile When frequent, aggressive nasopharyngeal suction­
technique with sterile gloves and sterile catheters ing is indicated in a semicomatose patient, a nasopha­
when suctioning. ryngeal airway (NPA) will lessen the trauma of fre­
quent passage of the catheter. The NPA is a soft latex

Suctioning Artificial Airway material that provides easy access to the trachea for
nasopharyngeal suctioning. The nasal and pharyngeal
Nasotracheal, Endotracheal, and Tracheostomy mucosa are protected and the procedure thus becomes
I. Check equipment, be sure you have all necessary more co mfortable to the patient. In addition, a
equipment and maintain sterile field. fiberoptic bronchoscope may be passed through the
2. Check monitors. airway if the procedure is indicated.
3. Wash your hands.
4. Inform patient of the procedure.
Endotracheal or Tracheostomy Suctioning
5. Hyperoxygenate with 100% oxygen for three to
five breaths with manual resuscitation bag. The procedures are the same except sterile technique
6. Place patient's neck in extension. is followed and no lubrication is usually necessary,
7. Put on sterile gloves. although it may be used if there is difficulty passing
8. Lubricate catheter with sterile saline or water the catheter.
soluble gel.
9. Place catheter (without suction) upward and
Sterile Suctioning
backward in short increments. Continue until an
obstruction (the carina) is reached. The technique for correct sterile suctioning of artifi­
10. When the carina is stimulated, the patient will cial airways is perhaps the most important and vital
generally cough un less his or her reflexes are segment of care for the patient because it removes se­
obtunded. cretions that would otherwise obstruct the airway. If
11. The catheter should be pulled back slightly, from suctioning is not performed properly, it can cause
the carina, then suction applied with no more physiological or psychological trauma to the patient.
than 120 mm Hg pressure as catheter is with­ The equipment necessary for proper sterile suc­
drawn in a rotating motion. tioning includes proper mechanical apparatus, con­
12. The aspiration time should be within 10 to 15 sec­ necting tubing, sterile gloves, sterile saline, suction
onds total. (A good guideline is for the therapist to catheters, dressings, and goggles as indicated with
hold his or her breath during suctioning as the pa­ universal precautions. While suctioning the patient, it
tient is also not breathing. This gives the therapist a should be remembered that the patient's only air pas­
better sensitivity for what the patient experiences.) sage is being partially occluded. Thus the suction
13. The patient should be allowed to rest for several catheter should never be larger than one half the di­
seconds and again be preoxygenated. ameter of the tube opening; if it is larger, it may com­
14. Check the patient's breath sounds and repeat the pletely occlude the patient's air passage.
procedure if necessary to remove more secretions. One method of determining the size of the catheter
15. Suction pharynx. used for suctioning is to double the size of the tra­
16. The monitor is to be watched for any dysrhytlunias. cheostomy tube in place and add two. For example, if
17. Pulse oximetry is to be used for indications of the patient has a #6 tube, the calculation would be as
desaturation. follows: 6 + 6 = 12 + 2 = 14. Therefore a 14-fr catheter

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 42 Care of the Patient With an Artificial Airway 773

the trachea or large bronchi is usually indicated by

TABLE 42-1
coarse rattling sounds. Fine bubbling sounds usually
The Pediatric Trach Card suggest fluid located more peripherally (i.e., in the

TRACHEOSTOMY SIZE RECOMMENDED alveolar spaces). If accumulated secretions are not

CATHETER SIZE cleared, they can cause respiratory and cardiac rates

Pediatric Tubes to increase; effective oxygen and carbon dioxide

transfer is impaired causing cyanosis to appear and
OOPT 6.S FR
OPT 6.S FR
low-grade fever to develop.
I PT 8FR

2 PT 8FR

3 PT 10 FR
Extubalion/Decannulalion
4 PT IOFR

Extubation or decannulation is the removal of the ar­

Neonatal Tubes tificial airway. The patient is helped to gradually re­
00 NT 6.S FR learn normal breathing through his or her upper respi­
ONT 6.S FR ratory tract before the tube is removed. This can be a
I NT 6.S FR time of considerable fear and anxiety for patients be­
SCT-Single Cannula Tracheostomy Tubes cause they have learned they can breathe safely

S seT 10 FR through their tracheostomy, and they may become

6 seT 12 FR apprehensive when asked to breathe in a normal man­
7 seT 14 FR ner. The relearning process can be accomplished
8 seT 14 FR under the physician's direction by reducing the lumen
of the tube for a day or two or by partially obstructing
Reprinted with permission of Janetti Publications, Inc., publisher
the tube's outer opening for increasing lengths of
Pediatric Nursing, Volume 20, Number 2, (March-April, 1994).
time. Eventually, the patient is able to tolerate the
complete occlusion of the tracheostomy opening.
This is sometimes difficult and similar to breathing
through a straw.
would be the largest catheter that could be used to suc­ When occluding the tracheostomy opening with a
tion the #6 tracheostomy. See Table 42-1 for a correla­ cuffed tube, the cuff must be deflated first. Failure to
tion of tracheostomy sizes to catheter sizes. do this will result in total obstruction of the patient's
The catheter used for pharyngeal suctioning airway as the tube opening is occluded.
should never be used for subsequent suctioning of the Fenestrated tubes have also been excellent for
artificial airway, but using an artificial airway suction weaning the patient from the tracheostomy tube. Ac­
catheter for pharyngeal suction is acceptable. Aseptic tually, they do not increase the airway resistance as in
technique is absolutely necessary to minimize the risk the above method and are probably more effective.
of infection and, ideally, only disposable catheters They also allow the patient to talk and attempt to
should be used. cough to mobilize secretions. Other methods used in
Suctioning may be necessary every few minutes decannulation include the Olympic tracheostomy but­
when the patient initially returns from surgery be­ ton and the Passy-Muir valve. The Olympic tra­
cause there is an increase in secretions, which usually cheostomy button allows the airway to remain patent
results from irritation of the endotracheal tube plus a for suctioning and reinsertion of a tracheostomy tube
reflex mechanism initiated by the surgical trauma. should it become necessary. The Passy-Muir valve
Usually by paying attention to the patient's color, res­ allows for normal recovery of the upper airway mus­
piratory rate, lung sounds, and oxygen saturation on cle, making it possible to reduce the size of tra­
pulse oximetry, the nurse or therapist can determine cheostomy tube leading to eventually plugging and
the amount of secretions present. Excessive mucus in decannulating. Careful observation and documenta­

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774 PART VIII Related Aspects of Cardiopulmonary Physical Therapy

tion of the patient's ability to ventilate must be done Goodwell, EW. (1':)34). The story of trach"ostolll)'. Srilish .Iour­
l1al of ('hildren '.\' iJi.l'l'{/se.l', 31(367-36')),167-176.
when either of these devices are used in the decannu­
Goodwell, E.W. (1934). The story of tracheostomy. Srilish Jour­
lating process.
nal of Children's Diseases, 31(370-372),253-27 I.
Close supervision should continue after extuba­ Jackson, C (1909). Tracheostomy. Laryngoscope, 18,285-290.
tion. After a tracheostomy tube is removed, the skin Jackson, C (1921). High tracheostomy and other errors. The chief
edges are usually taped together with butterfly strips causes of chronic laryngeal atenosis. Surgery, CynecoIOfi.Y, Ob­
slelrics, 32, 392-395
for a few days until the wound heals. While healing,
Jackson, D., & Albamonte, S. (1994). Enhancing communication
air will escape through the wound and reduce the ef­
with the Passy-Muir valve. Pedialric Nursing, 20,(2),149-153.
fectiveness of the patient's cough. The patient should Kirchner, J .A. (1980). Tracheostomy and its problems. Surgical
be instructed that the noise from the partially closed Clinics ofNorih America, 60,(5), 1093-1104.

trachea is normal and small secretions should be re­ Kirimli, B., King, lE., & Pfaeffle, H.H. (1970). Evaluation of tra­
cheobronchial suction technique. Journal of Thoracic and Car­
moved from this area. The patient should be taught to
diovascular Surge!)" 59, 340-344.
hold a sterile dressing firmly over the incision when
Lull, J.M, Pierson, OJ., & Tyler, ML (1993). Methods of Air­
coughing until the opening healed. way Maintenance. In Inlellsive respiralOry care. Philadelphia:
WB Saunders.
Mocaluso, S., & Roman, M. (1994). Managing post-intubation in­
REVIEW QUESTIONS juries. Medsurg Nursing, 3(3),192-202.
Montgomery, W.W. (1989). Manual of care or the Montgomery
I. What physiological changes occur with surgical silicone tracheal T-tube. Annals of OlOlof!)" Rhinology and
placement of tracheostomy tube? La!)'ngology (Supp. 73),89(4),3.

2. Discuss possible psycosocial concerns of patients Montanari, 1., & Spearing, C (1986). Of measuring tracheal curf
pressure. Nursing, 86(7),46-49.
with a tracheostomy.
Noll, M.L., Hix, CD" & Scott, G. (1990). Closed tracheal suction
3. List information that you would include in a systems: effectiveness and nursing implications. In ArlCN clin­
teaching plan for the tracheostomized patient. ical issues in crilical care nursing. Philadelphia: JB Lippincott.
4. How does the patient care team prepare the tra­ Panacek, E.A., Albertson, T.E., Rutherford, W.F., Fisher, C.J., &
Foulke, G.E. (1989). Selections left endobronchial suctioning
cheostomized patient for self care?
of the intubated patient. Chesl, 95,885-87.
5. Compare emergency care, acute care, and long
Patton, C (1991). The critical airway classic problems. CurrenI
term care for a patient with upper airway ob­ Reviews for Ihe p(1S! Aneslhesia Care NI/rses, 13(5),33-40.
struction and tracheostomy placement. Pierson, OJ., & Kacmarek, R.M. (1992). In Foundalions of respi­
ralory care. New York: Churchill Livingstone.
Roberts, J.T. (1994). In Clinical Management of the Airway,

References Philadelphia: WB Saunders.

Selecky, P. (1974). TraCheostomy-a review of present day indica­
Carroll, P. (1994). Safe suctioning PRN. RN, May. 32-37. tion, complications and care. Hearl Lung, 3. 272.
Class, P. (1992). Nursing considerations for airway management in Tr acheoslomy lUbe a d u l l homecare guide. (1993). Irvine:
the PAC U . Currenl Reviews for POSI Aneslhesia Care Nurses. MaLlinckrodt Medical TPT.
14(1),1-8. Traver, l.A., Mitchell, IT., & Flodquist-Priestly, d. (1991). Artifi­
Crabtree Goodnough, S.K. (1988). Reducing tracheal injury and cial airway care. In RespiralOry care: a clinical approach.
aspiration. Dimension of Crilical Care Nursing, 7(6),324-331. Gaithersberg, Md.: Aspen Publishers.
Dailey, R.H., Simon. B., Young, G.P., & Stewart, R.D. (1992). Traver, J.A., Mitchell, IT, & Flodquist-Priestly, G. (1991). Suc­
Airway maneuvers. In The airway emergency management. St. lioning. In RespiraIO!), care: a clinical approach. Gaithersberg,
Louis: Mosby. Md.: Aspen Publishers.
Frost, E.A. (1976). Tracing the tracheostomy. Annals of OlOlaryn­ Warnoch, C, & Porpora, K. (1994). A pediatric tmche card: trans­
gology, 85, 618-624. fonning research into practice. Pediatric Nursing, 20(2), 186-188.
Funllll, N.D, Dutcher, P.O., & Roberts, J.K. (1993). The safety and Weilitz, P.B., & Dertenrneier, P.A. (1994). Back to basics test your
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Neck Surgery, (109),707-711. ing, 94(2),46-50.

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 Respiratory and Cardiovascular
Drug Actions

Arthur V. Prancan

KEY TERMS Adrenergic drugs Corticosteroids

Antihistamines Functional reflex
Cardiovascular reflex Metered dose inhalers
Carotid baroreceptors Mucolytics and expectorants
Cholinergic blocking drugs Sympathomimetic drugs
Cholinergic drugs Xanthines

INTRODUCTION
Before a drug can be used effectively, the system
The respiratory and cardiovascular systems have it is to modify must be understood. How the mecha­
many built-in mechanisms for controlling their func­ nism of the drug action relates to the biological sys­
tions during health and disease. In healthy individu­ tem must be clear before an effect can be predicted.
als, both systems act quickly and positively to main­ This chapter describes much of the basic respira­
tain proper functioning under the most complicated tory and cardiovascular physiology that underlies the
conditions. Even during trauma or disease, these sys­ action of the drugs presented. Hopefully, the relation­
tems often overcome distress and regain normal func­ ship between basic physiology and the drug mecha­
tion. The physiology of respiration or circulation is nism of action is also evident.
sometimes altered by a disease so that the homeosta­ All pharmacological interventions for the respi­
tic mechanisms are no longer effective. In such a ratory and cardiovascular systems are not covered.
case, a drug with the appropriate action becomes nec­ Certainly no attempt has been made to describe the
essary to restore normal physiological function. pharmacology of other systems or disease states.

775

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776 PART VIII Related Aspects of Cardiopulmonary Physical Therapy

For further study, one of the books listed in the ref­ tagonistic action of the two components of the auto­
erence section at the end of the chapter is highly nomic nervous systcm.
recommended. Some organs, however, have only one innervation.
Much of the arterial blood vessel network is con­
trolled only by sympathetic nerves. Also, gastric se­
AUTONOMIC PHARMACOLOGY
cretion and gastric motility are primarily regulated by
This section introduces the basic aspects of drug action one system-the parasympathetic.
related to both components of the autonomic nervous
system-the sympathetic and parasympathetic nervous
SYMPATHETIC NEUROTRANSMISSION
systems. For both systems, synthesis, storage, and re­
lease of the chemical neurotransmitter are described to Sympathetic nerves transport impulses from the vaso­
emphasize the places in the metabolical scheme where motor center in the medulla of the brain through the
drugs can intervene. The sites of action for the adrener­ spinal cord and out to the smooth muscle, heart mus­
gic (sympathetic) and cholinergic (parasympathetic) cle, and secretory cells. These tissues have receptor
transmitters and blockers is also described. sites that will accept the norepinephrine released
The autonomic nervous system controls all of the from the nerve ending. Norepinephrine, also called
bodily functions over which you have no voluntary noradrenalin. is synthesized in the nerve ending only
control, and perhaps which you might not control as in the sympathetic neurons. It is stored in the terminal
well if you had the opportunity. The functions in­ until an electric impulse reaches the terminal, then it
clude regulation of respiratory airway diameter, res­ is released into the synapse.
piratory secretions, blood vessel diameter, heart rate, The norepinephrine molecule attaches to a recep­
intestinal motility, pupil size, and many others. It is tor molecule on a cell sUlface in the immediate vicin­
easy to see that it might take more than the talents of ity of its release. This drug-receptor combination
a well-trained expert to keep an active person func­ causes a biological change, such as stimulation of the
tioning day and night. pacemaker cells in the heart to fire more frequently
The sympathetic nervous system is the half of the (increased heart rate). The effect is terminated when
autonomic system that takes a dominant role in the the norepinephrine is reabsorbed into the nerve termi­
cardiovascular and respiratory systems when some nal. About 90% of the released norepinephrine is
sort of bodily activity is necessary. This includes ac­ taken back into the neuron. There, it is either restored
tions such as increasing ventilation capacity, elevat­ into granules for future release or it is destroyed by
ing blood pressure, and shunting blood flow to the the enzyme monoamine oxidase (MAO).
skeletal muscles. Classically, the sympathetic compo­ There are two types of sympathetic receptors­
nent of the autonomic nervous system has been called alpha and beta. The alpha-receptor is found in the
the fight-or-t1ight system. The other half of the auto­ arterioles, and the beta-receptor is found in the arte­
nomic system is called the parasympathetic nervous rioles, heart, and bronchioles. Stimulation of the
system. It is most important in maintaining the less alpha-receptor in the arteriole causes vasoconstric­
exciting functions of the body like digestion, saliva­ tion that results in increased blood pressure. The
tion, and urination. In some organs the two systems beta-receptor in the arterioles causes vasodilation
work against each other to provide very fast and very and a lowered blood pressure. Some drugs stimu­
fine control. For example, the size of the pupil re­ late both receptors, and in those cases the effect
sponds quickly to a change in light intensity. The will be determined by the degree of alpha or beta
parasympathetic system actively functions to de­ activity of the drug. An example is norepinephrine.
crease the size of the opening while the sympathetic It has 90% alpha activity and 10% beta activity, and
system relaxes, thereby causing a quick decrease in it always causes vasoconstriction. Epinephrine is
pupil size. If the light is turned down, the opposite 50% alpha and 50% beta and may cause a rise or
occurs just as fast. This is a good example of the an­ drop in blood pressure.

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 43 Respiratory and Cardiovascular Drug Actions 777

Epinephrine (Adrenalin)
Stimulation of the beta-receptor in the heart results
in increased heart rate (beats per minute) and in­ Epinephrine (Adrenalin) is also a mixed activity drug
creascd stroke volume (number of milliliters of blood (50% alpha, 50% beta). It is naturally produced in the
the left ventricle pumps out into the aorta every time adrenal medulla and can be released during sympa­
it contracts). Incidentally, the combination of these thetic nervous system activation. When this occurs, it
two changes (heart rate [HR] x stroke volume [SV]) acts as a circulating hormone, stimulating both alpha­
is another way of saying cardiac output (CO) (milli­ and beta-receptors. This drug wi II increase heart rate
liter of blood pumped per minute): and stroke volume and may slightly increase or de­
crease total peripheral resistance at the arterioles. In
beats/min(HR) x mllbeat(SV) = mllmin(CO)
any case, cardiac output always goes up; blood pres­
This expression, cardiac output, is a common one sure may go up or down slightly.
and it constitutes half of the blood pressure regulation In the bronchioles, epinephrine exerts a dramatic
equation: CO x TPR = BP, where CO is cardiac out­ dilating effect that is mediated by the beta-receptor.
put, TPR is total peripheral resistance, and BP is Epinephrine can be administered by inhalant aerosol
blood pressure. Total peripheral resistance is deter­ to reverse a bronchoconstrictive episode. It is also
mined by vasoconstriction or vasodilation in the arte­ administered intramuscularly and subcutaneously to
rioles. Vasoconstriction increases resistance so TPR treat asthma, anaphylactic reactions to an allcrgic re­
and BP goes up. sponse, cardiac arrest, heart block, and as a mild
Stimulation of smooth muscle beta-receptors will vasoconstriction to keep local anesthetics at the in­
relax these tissues wherever they are found. Respiratory jection siteo
airway smooth muscle will decrease tension when the
Isoproterenol (Isuprel)
beta-receptor is activated by beta-acting drugs like epi­
nephrine or isoproterenol. The functional result will be Isoproterenol (lsuprel) is a synthetic compound that
an increase in air flow because of a larger airway diam­ has 100% beta activity. This means that it can in­
eter. Likewisc, blood vessels respond to beta-acting crease heart rate and stroke volume to produce a great
drugs by increasing in diameter, allowing a greater rate rise in cardiac output, and it stimulates the beta-recep­
of flow. In this case, TPR has decreased and blood tor on the arterioles to effect a profound vasodilation.
pressure will drop. The final result can be a high cardiac output with low
blood pressure. This drug improves blood circulation
in shock patients by increasing local blood flow (va­
Adrenergic Drugs sodilation) and elevating cardiac output. Isoproterenol
is considered very useful for treating acute asthmatic
Norepinephrine (Levarterenol, Levophed) conditions because of its bronchodilating action.
As mentioned previously, n o repinephrine
Phenylephrine (Isophrin, Neo-Synephrine)
(Levarterenol, Levophed) is a mixed-activity drug
and Metaraminol
(90% alpha, 10% beta). It stimulates beta-receptors in
the heart, which results in an increase of heart rate Both phenylephrine (lsophrin, Neo-Synephrine) and
and stroke volume (increased cardiac output). In the metaraminol are powerful and prolonged stimulators
arterioles, norepinephrine causes vasoconstriction via of alpha-receptors. The action is directly on the re­
the alpha-receptor, resulting in increased total periph­ ceptor site itself. The response to the administration
eral resistance. The total effect, of course, is an in­ of either of these drugs is a rise in blood pressure be­
crease in blood pressure. Norepinephrine has little ef­ cause of vasoconstriction accompanied by a reflex
fect on the bronchioles. This drug is given only bradycardia, which causes a decrease in cardiac out­
intravenously, and it can be used clinically to raise put. Reflex alterations of cardiovascular function are
blood pressure. The natural sympathetic compounds explained later in this chapter. The primary useful­
are known as catecholamines. ness of these drugs is in various hypotensive states.

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778 PART VIII Related Aspects of Cardiopulmonary Physical Therapy

Phenyle phrine is used as a nasal decongestant and asthma. The drugs are metaproterenol (Alupent,
mydriatic and for the relief of paroxysmal atrial Metaprel), terbutaline (Brethine, Bricanyl), albuterol
tachycardia. Phenylephrine affords relief from the (P r o v e n t il, Ven t o l i n ), i s o e t h ar ine ( B r on kosol,
tachycardia because it increases blood pressure and Bronkometer), and salmeterol (Servant).
evokes the cardiovascular reflex that is marked by
high vagal tone and bradycardia. Alpha-Adrenergic Blocking Drugs

Ephedrine Phentolamine (Regitine)

Ephedrine has both alpha and beta activity as direct Phentolamine (Regitine) is a competitive alpha-receptor
effects and it also causes release of epinephrine and blocker. Its action is reversible. This drug prevents the
norepinephrine. Its pharmacological actions are simi­ hypertensive effect of norepinephrine, and it reverses
lar to epinephrine, with the main exception that dura­ the blood pressure elevating effect of epinephrine (epi­
tion of action of ephedrine is longer. Ephedrine in­ nephrine reversal). Epinephrine reversal looks like an
creases cardiac o utput and vascular resistance, isoproterenol effect with high cardiac output and low
resulting in increased blood pressure. Ephedrine also blood pressure. Phentolamine may be used clinically as
causes bronchial muscle relaxation, which is less po­ a vasodilator. It is also useful as a clinical diagnostic
tent than that of epinephrine but has a longer duration. agent in evaluating hypertensive patients who may
This drug is useful in controlling milder cases of bron­ have pheochromocytoma, which is a tumor that grows
choconstriction that require long-term drug therapy. in the gastrointestinal chromaffin tissue. The tumor pro­
duces epinepJu'ine and norepinephrine and may be re­
Amphetamine (Dextroamphetamine, Dexedrine)
sponsible for one aspect of a clinical hypeltension.
Amphetamine (Dextroamphetamine, Dexedrine) drug
Phenoxybenzamine (Dibenzyline)
has pharmacological properties related to the cate­
cholamines because it causes release of norepinephrine Phenoxybenzamine (Dibenzyline) is also an alpha­
from the nerve terminal. Amphetamine has both alpha­ adrenergic blocki ng agent. It has effects similar to
and beta-receptor activity, although indirectly, through phentolamine in the cardiovascular system but it is
its release of norepinephrine. The usual cardiovascular less reversible. This drug is gaining some usefulness
response is an increase in blood pressure often accom­ in the treatment of shock syndromes characterized by
panied by a reflex bradycardia. Amphetamine also has high vascular tone.
potent central nervous system (CNS) activity. It is a
Prazosin (Minipress), Doxazosin (Cardura), and
stimulant of the medullary respiratory center, and it
Terazosin (Hytrin)
can antagonize drug-related central nervous system de­
pression. Respiratory depression often accompanies Prazosin (Minipress), doxazosin (Cardura), and tera­
overdoses of CNS depressant drugs and this effect may zosin (Hytrin) are selective for arterioles and venules
be overcome by amphetamine. This drug is usually and are the most useful against hypertension of the
used for its central nervous system effects and not for drugs in this class. Although they act by vasodilation,
peripheral cardiovascular or respiratory effects. these drugs exert minimal reflex tachycardia because
they do not potentiate the vasomotor center and the
BetarReceptors Stimulants
increased venous capacitance reduces venous return
There are several drugs that act primarily at the beta2 and cardiac output.
smooth muscle receptor site, causing selective actions
in the bronchioles and arterioles but not in the heart. Beta-Adrenergic Blocking Drugs
Thcse drugs will produce a bronchodilation without
increasing cardiac output. This particular lack of car­ Propranolol (/nderal)
diovascular effect makes them safer than isopro­ Propranolol (Inderal) is a beta-adrenergic blocker. This
terenol or epinephrine in treatment of bronchial drug occupies the beta-receptor sites of the heart, the

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 43 Respiratory and Cardiovascular Drug Actions 779

blood vessels, and the bronchioles. It prevents the beta­ crease in catecholamine response to sympathetic stim­
adrenergic effect usually seen with drugs like epineph­ ulation. Blood pressure in humans does not drop dra­
rine, norepinephrine, and isoproterenol. In the arteri­ matically with therapeutic doses of reserpine, but when
oles, when epinephrine is given after propranolol, the reserpine is used in combination with diuretics or other
usual mixed alpha and beta effect is eliminated, leav­ antihypertensive agents, a significant antihypertensive
ing only an alpha-adrenergic action. This causes pro­ effect is obtained. Reserpine is used in this way to treat
found vasoconstriction, allowing greater increase in essential hypertension. One serious side effect related
blood pressure than is normally seen with epinephrine to reserpine use is the behavioral modification that can
alone. In the heart the beta-receptors are blocked and, result in severe depression and suicide.
since there are no alpha-adrenergic receptors in this
organ, all effects of catecholamine drugs on the heart
Guanethidine (Ismelin)

are effectively eliminated, allowing the vagal influence Guanethidine (Ismelin) is an adrenergic neuron­
on the heaJ1 to predominate. Propranolol decreases the blocking agent that works by replacing norepineph­
heart's requirement for oxygen because it blocks the rine in the nerve terminal. Norepinephrine is usually
cardiac stimulant action of norepinephrine. In the res­ taken up by the nerve terminal after its discharge and
piratory system the administration of propranolol re­ i s r e u s e d to m a i n t ain g r a n u l e c o n c e n t r a t i o n s .
sults in bronchoconstriction. This effect is increased Guanethidine takes the place o f norepinephrine i n the
dramatically in patients who are susceptible to asthma. granules and prevents the reuptake of norepinephrine,
The main use for propranolol is in conditions related to thereby causing its metabolism outside of the neuron
hypertension and tachycardia, where a decrease in car­ and its eventual depletion. The result on the cardio­
diac output is beneficial. vascular system of this action is postural hypoten­
sion. The patient is unable to control blood pressure
Metoprolol (Lopressor) and Atenolol (Tenormin)
by sympathetic activity. This drug is used in treat­
Metopolol (Lopressor) and atenolol (Tenormin) are ment of severe hypertension, usually after diuretics
beta-adrenergic antagonists that have been designed and reserpine are shown to be ineffective.
to be cardioselcctive. This offers an advantage in
Methyldopa (Aldomet) and Clonidine (Catapress)
safety when a beta-blocker must be used in asthmatic
patients, in whom this disease would be aggravated if Methyldopa (Aldomet) and c10nidine (Catapress) de­
respiratory beta-receptors were blocked. The natural crease the activity of the sympathetic nervous system
beta-adrenergic agonist, epinephrine, is bronchodilat­ at its control center in the brain. The consequence is a
ing, and an important class of bronchodilating drugs total decrease in sympathetic activity in the heart and
acts at bronchiolar beta-adrenergic receptors. blood vessels leading to a reduction in blood pressure.

SympatholytiC Drugs PARASYMPATHETIC NEUROTRANSMISSION

Reserpine The center for parasympathetic control is the vagal
Reserpine is an alkaloid of Rauwolfia serpentina, also nucleus in the medull a . T h e vagus nerves p a s s
known as the Indian snake root plant. There are many through t h e spinal c o r d a n d out to t h e heart, the
commercial preparations of this compound, but it is smooth m u s c l e , and e x o c r i n e g l a n d s ( s a l i v a r y
widely sold as the simple plant extract. This compound glands and pancreas). In all of these tissues, acetyl­
depletes norepinephrine from the nerve endings in the choline is released from the nerve terminals and
various tissues of the body that produce and store nor­ combines with receptor sites to cause an effect such
epinephrine, including the brain. The depletion takes as bradycardia (slowing of the heart) or an increas­
several days to accomplish, and it may take several ing gastric motility. Acetylcholine is found in many
weeks to restore catecholamine levels to normal after parts of the central and peri pheral nervous system.
therapy is discontinued. During this time, there is a de­ Acetylcholine is the only transmitter used in the

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780 PART VIII Related Aspects or Cardiopulmonary Physical Therapy

parasympathetic system. It is used to transmit im­ acid and choline. The acetic acid is washed away for
pulses from the nerve that comes out of the spinal further metabolism, and the choline is reabsorbed into
cord to the nerve that finally reaches the cells in the the nerve terminal for resynthesis to acetylcholine.
organ being affected. This connection is called a gan­
glion and exists in both sympathetic and parasympa­ Cholinergic Drugs
thetic systems. Acetylcholine is also the neurotrans­
m i t t e r t h a t m a k e s t h e c o n n e c t i o n b e t w e e n the AcetylchOline
voluntary (somatic) nerves and the skeletal muscle. Acetylcholine is the endogenous cholinergic trans­
There are two types of receptors in these systems. mitter that accounts for nicotinic and muscarinic ac­
Acetylcholine affects both, but some drugs affect only tions within the autonomic nervous system. It is
one and not the other. The two types of receptors are rapidly hydrolyzed by acetylcholinesterase and the
called nicotinic and muscarinic. They are named after nonspecific cholinesterase and therefore has a short
the drugs that selectively stimulate them. Nicotine duration of action if administered parenterally. This
stimulates only those receptors in the ganglia and at makes acetylcholine (ACh) a poor drug. Nicotinic ef­
the neuromuscular junction. The muscarinic receptor fects of acetylcholine are (I) stimulation of parasym­
site is found everywhere a parasympathetic nerve ter­ pathetic ganglia, causing occurrence of all muscarinic
mjnal synapses at a tissue. The biological effects usu­ effects, (2) stimulation of sympathetic ganglia, caus­
ally attributed to the parasympathetic nervous system, ing increase in vascular resistance and cardiac output
such as bradycardia, salivation, and bronchoconstric­ to produce hypertension, and (3) stimulation of the
tion, for example, are produced when the muscarinic neuromuscular junction (NMJ) at the skeletal muscle
receptors are stimulated. Of course, it is also possible (muscle contraction and movement). Muscarinic ef­
to stimulate muscarinic receptors indirectly with a fects of acetylcholine are bradycardia, salivation, pin­
nicotinic drug by activating the parasympathetic gan­ point pupils, bronchial constriction, gastric and in­
glia. In fact, in a sirilliar way, it is possible to stimulate testinal hypermotility, increased gastric acid and
the entire sympathetic nervous system. The neuro­ mucous secretion, and facilitated urination. Toxic ef­
transmitter at the sympathetic ganglia is acetylcholine fects of cholinergic stimulation include diarrhea, uri­
and it affects nicotinic receptor sites there. One of the nary incontinence, bradycardia, bronchoconstriction,
toxic effects of acetylcholine and drugs that act like it excessive salivation, CNS excitement, and respiratory
is hypertension with tachycardia because of stimula­ collapse. In all of these toxic effects, atropine, a com­
tion of the sympathetic postganglionic fibers. petitive muscarinic blocker, is the antidote of choice.
To better understand the action of acetylcholine
Bethanecol (Urecholine)
and related drugs, let us consider the synthesis, re­
lease, and inactivation of this transmitter. Acetyl­ Bethanecol (Urecholine) is a synthetic choline ester
choline is synthesized inside the nerve terminal from that is not destroyed as easily as acetylcholine by
acetyl-CoA and choline. The acetylcholine is then cholinesterase enzymes. It is useful in treating patients
stored in granules and is released out into the synapse with urinary retention and paralytic ileus, and it is ad­
when an action potential reaches the terminal. The ministered orally or subcutaneously. The side effects
acetylcholine molecule attaches to a receptor site, and toxicities for this drug are exactly those for ACh.
muscarinic or nicotinic, or to the enzyme that breaks it However, since the drug is not given intravenously,
apart. Combination with the receptor site results in bi­ cardiac and respiratory effects are minimized.
ological action, and coupling with the enzyme ends in
Carbachol (Carcholin)
destruction. The enzyme, acetylcholinesterase, is
found at all cholinergic synaptic sites. A nonspecific Carbachol (Carcholin) is a mixed nicotinic and mus­
variety of the enzyme is also prevalent in many other carinic drug because it releases acetylcholine from the
tissues. It too will break down acetylcholine. The final nerve ending, producing the expected cholinergic ef­
action of either enzyme is the production of acetic fects at all receptor sites. The drug is useful for treat­

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 43 Respiratory and Cardiovascular Drug Actions 781

ment of glaucoma (applied topically), paralytic ileus, cholinesterase, such as diisopropy lfluorophosphate
and urinary retention (orally and subcutaneously). (DFP) or sarin, is ingested, inhaled, or absorbed
across the skin, a great variety of toxic cholinergic ef­
Pilocarpine
fects are seen. The first effects seen after exposure to
Pilocarpine is a cholinomimetic that is useful in oph­ an anticholinesterase are often ocular and respiratory
thalmology as an antiglaucoma agent. Cholinergic effects. In the eyes, marked miosis is produced
compounds decrease intraocular pressure by relieving quickly. In the respiratory system, bronchoconstric­
the obstruction to the canal of Schlemm, a drainage tion and bronchial secretions combine to produce
circuit for the eye. Miosis (pinpoint pupils) is one tightness in the chest and wheezing. Gastrointestinal
feature of cholinergic therapy and may be beneficial symptoms include nausea, vomiting, cramps, and di­
to glaucoma treatment because the muscular base of an·hea. Other muscarinic effects are severe salivation,
the relaxed iris may contribute to the drainage block. involuntary defecation and uri nation, swea ting,
Another use of pilocarpine is to promote salivary lacrimation, bradycardia, and hypotension.
flow in patients with a ganglionic blockade. Further effects are related to nicotinic functions of
acetylcholine. These include skeletal muscle twitch­
ing, weakness, and paralysis. CNS effects include de­
Anticholinesterases
pression of the respiratory and cardiovascular control
Before proceeding to sp ific anticholinesterase drugs, centers, leading to respiratory collapse. At the time of
it is important to understand the basic mechanism of death, respiratory paralysis is evident and it is because
action for these compounds. Acetylcholinesterase is of a combination of bronchoconstriction, bronchose­
the enzyme responsible for destroying acetylcholine at cretions, respiratory muscle paralysis from overstimu­
the various nerve junctions where it is released. The lation, and CNS and control depression. The treatment
class of drugs that intetfere with this function is called of this toxicity is closely related to preserving respira­
anticholinesterascs. These drugs attach to the enzyme tory function. Administration of atropine, a mus­
and thereby block the enzymatic hydrolysis of ACh, carinic blocker, will effectively decrease bronchocon­
causing ACh to accumulate outside of the nerve end­ striction and secretion. Another drug, pralidoxime
ing. This results in a greater response than normal to (Pr o t o p am), is u s e d to re a c t i v a t e the a c e t y l ­
any cholinergic nerve stimulation. Some of these anti­ cholinesterase. I t i s most effective shortly after expo­
cholinesterases are relatively short-acting compounds sure to the toxic agent because it breaks down the an­
and are therapeutically impot1ant, whereas others are ticholinesterase so it can be removed from the enzyme
ext.remely long-lasting and potent compounds that are site. Additional measures are related to physiological
important only as poisons. The long-acting compounds suppOt1 of the patient. Maintenance of an airway, arti­
have been used as insecticides and as nerve gases in ficial respiration, and oxygen administration are im­
chemical warfare. The therapeutically useful anti­ portant therapeutic applications for these patients.
cholinesterases are beneficial in problems related to
Physostigmine (Eserine)
the eye, intestine, and the skeletal neuromuscular junc­
tion (NMJ). In these applications, these drugs increase Physostigmine (Eserine) is useful in glaucoma and in
the amount of ACh available for activity, an effect that selected therapeutic measures where a cholinergic ef­
is es ially impOt1ant in cascs where the synthesis or fect is beneficial. It functions as an indirect choli­
release of acetylcholine is lower than normal, as in nomimetic by blocking the acetylcholinesterase.
myasthenia gravis.
Neostigmine (Prostigmine)
There is also great medical interest in the toxicol­
ogy of the anticholinesterases, especially the ex­ Neostigmine (Prostigmine) is useful in patients with
tremely potent irreversible anticholinesterases. Toxic­ nonobstructive paralytic ileus to increase tone and
ity because of these compounds is not uncommon motility of the small and large intestines. It is also
and is often severe. When a toxic irreversible anti­ useful for stimulating skeletal NMJ. Neostigmine is

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782 PART VIII Related Aspects of Cardiopulmonary Physical Therapy

used for treating gravis because it indi­ and does not counteract the nicotinic 2:aufllionic ef­
increases acetylcholine at the NMJ and it acts fects or the nicotinic effects at the NMJ.
directly at the nicotinic receptor site itself. The dis­ Because heart rate is controlled both sympathetic
ease is marked by subnormal response t o and parasympathetic tone, atropine will eliminate the
resulting i n skeletal muscle weakness. parasympathetic effect on the heart, the sym­
temporarily restores muscle Nrpncrth system to increase heart rate and stroke vol­
ume to cause an increase in cardiac output. In
Edrophonium (Tensilson) may occur after atropine administration. In
This a very anticholinesterase. It is pri­ cases where exists because of high vagal
marily useful as a diagnostic agent in tone, atropine can be used to reverse this depression.
to reveal, for a few minutes, if the dose of In the tract, is a bronchodila­
is appropriate. A longer-acting tor. It is also possible to respiratory depression
w o u ld risk a serious c holinergic if t h e associated with tranquilizing, and anti­
neostigmine dose was alreadv at the therapeutic limit. cholinesterase drugs atropine, either as a
agent or as an antidote
Atropine is used widely as medica­
Cholinergic Blocking Drugs
tion to bronchiolar secretions and laryngeal
antagonists block the various spasm, as well as A more general med­
is a transmitter. There are ical use for atropine exists as an emergency tool. It is
for each type of acetylcholine the antidote of choice for all cholinergic toxicities.
receptor. blocks all cholinergic action right One of the most important clinical uses for at­
at the muscarinic receptor site on smooth muscle, ex­ ropine is in the (Ol) tract as an antiul­
and myocardium. Another cholinergic cer and agent. This acts to de­
curare, works only at the neuromuscular crease in the OI tract so that other antiulcer
to block the nicotinic effect of agents can remain in contact with the OI mucosa
in paralysis of skeletal muscle. Still another and it is possible that it also decreases acid se­
type of nicotinic blocker is the blocker, cretion, Other related to hypermotility of
which blocks both sympathetic and the OJ tract are treated with atropine, to de­
parasympathetic ganglia occupvinfl the crease muscle activity during treatment of
choline receptor there. These conditions such as cramping and diarrhea.
ever sympathetic or tone needs to be In ophthalmology, is useful for
decreased. It is possible to selectively inhibit cholin­ which is dilation. It is contraindi­
effects in the body to produce a desired effect or cated in glaucoma
to eliminate an undesirable effect. Because of this se­ an acute attack.
lectiveness, have Atropine itself is also capable of producing toxic
use in many areas of medicine. effects. These are mydriasis, dry
and urinary retention, Effects related to
Atropine the central nervous are also apparent, and
Atropine is an extract from the these include sedation initially, followed by delirium
ladonna, also known as the deadly An­ and hallucinations, lead to a coma, In severe
other plant extract, scopolamine, has action similar to convulses and severe
atropine, works by establishing a respiratory which may be the final course.
tive at the muscarinic receptor which is Anticholinesterase drugs, such as and
the effector at all tissues innervated the parasym­ are effective antidotes for atropine be­
nervous This blockade is selective cause they increase the amount of acetylcholine that
for the tissue effect of the parasympathetic system will compete with atropine for the rl

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 43 Respiratory and Cardiovascular Drug Actions 783
--------� ----- ------ .----

Homatropine (Novatrin) and

some way this reflex is i a condition
Cyelopentolate (Cyelogyf)
known as orthostatic hypotension will exist. A com
( Novatrin) and cyclopentolate mon manifestation of this condition is fainting on
gyl) are anticholinergic related in action to at­ because of inadequate blood flow to the
ropine. are useful in ophthalmology to brain. This section is devoted to the functional as
mydriasis. of the retlex after a change in blood pressure.

Dicyelomine (Bentyl)
The Carotid Baroreceptors
Dicyclomine (Bentyl) is considered very useful in the
gastrointestinal tract to decrease secretions and motU­ Neuronal elements, known as baroreceptors, exist in
It is sometimes called a chemical vagotomy, the sinus of the carotid arteries supplying the brain.
These are stretch that fire electrical im­
rr;hexyphenidyl HCL (Artane) and
pulses at a rate related to the blood pressure,
Benztropine Mesylate (CogenUn) As the pressure in the the ves:-;el wall
Trihexyphenidyl HCL and me (and stretches, causing an increase in
sylate (Cogentin) are antiparkinson that enter the receptor firing rate. Conversely, a decrease in
the CNS to reverse the imbalance between the cholin blood pressure results in a decrease in stretch receptor
and systems in this disease, They firing rate. This firing rate is sent directly to
have some of the same side effects as the where the vasomotor center and nu­
cleus respond to it.
Penlolinium (Ansolysen) and
Hexamethonium (Methium)
The Functional Reflex
Pentolinium (Ansolysen) and hexamethonium (Me
thium) are nicotinic block the To create an this
acetylcholine receptor site in the ganglia in both the let us assume we have experienced a loss of
sympathetic and blood pressure. The carotid shorten and
are used to control slow their This message is then delivered to
to a tonc, Because of their the brain, and the vasomotor center by in­
action at the sympathetic ganglion, these drugs pro­ sympathetic nerve activity, This control al­
duce a hypotension. They will also decrease ways to information blood pres­
cholinergic effects at the parasympathetic effector sure in the carotid artery by doing the of the
sites because block the for the entire If the pressure had the barore
nervous as well. This means would have increased their rate and the
that a patient may blurred vision, dryness vasomotor center would have responded by slowing
of mouth, and as well as other atropine the sympathetic nerve rate. Since the blood
like peripheral effects. pressure in this example is
increases nerve in in
creased release of norepinephrine from the nerves
THE CARDIOVASCULAR REflEX
that reach the heart and arterioles. Norepinephrine in
The cardiovascular reflex involves many of the com­ creases the heart rate and stroke volume, thereby pro­
ponents of the autonomic nervous system to maintain ducing an increase in cardiac output. In the "rt"rlrllp

a normal blood pressure. This mechanism is impor­ stimulates the pro

tant for blood pressure within certain ducing which results in increased
of physical Even the resistance result in raised blood pressure. A third
from a position component of the sympathetic nervous system can be
by this reflex system, If in involved activation.

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784 PART VIII Related Aspects of Cardiopulmonary Physical Therapy

released from the adrenal medulla also increases car­ creasing release of histamine, and in a broader ap­
diac output. proach, the general stabilization of cells that can re­
Meanwhile, the vagal nucleus is responding to the lease mediators of the disease, thereby lowering the
decreased baroreceptor firing by decreasing its own ac­ severity of the disease.
tivity. The vagus nerve to the heart will release less
acetylcholine, allowing the sympathetic effect to pre­ Sympathomimetic Drugs
dominate. The total effect becomes an increase in
blood pressure, which is the response required to re­ Isoproterenol (Isuprel) and
turn the systemic pressure to normal. If the original Epinephrine (Adrenalin)
pressure alteration had been an increase above normal, The muscle relaxant bronchodilator effect attributed to
the opposite reflexive actions would have occurred to the beta-adrenergic sympathomimetic compounds is
return pressure to a normal range. In this case the pre­ most commonly required for asthmatic or allergic
dominant effect would have been an increase in vagal emergencies. Isoproterenol (Isuprel) is often self-ad­
nerve tone, releasing high amounts of acetylcholine at ministered by inhalation to reverse mild-to-moderate
the heart, causing a dramatic slowing of heaJ1 rate, ac­ obstructive episodes. However, during a severe acute
companied by a decrease in stroke volume. This com­ obstruction, the airway is unable to pass the drug to the
bination produces a decrease in cardiac output. The alveoli, and the intramuscular or subcutaneous routes
sympathetic system would have responded to the in­ for epinephrine (adrenaline) and isoproterenol are
creased baroreceptor firing by decreasing firing in all used. Isoproterenol is a purely beta compound. Epi­
sympathetic nerves, thereby decreasing norepinephrine nephrine has 50% beta-adrenergic activity and also ex­
and epinephrine release. All of these factors combine erts a great bronchodilating effect. Both of these agents
to decrease blood pressure to normal. are useful when given parenterally or by inhalation.
The most common side effects of isoproterenol are
flushing of the skin, headache, palpitation, and tachy­
DRUGS USED IN AIRWAY OBSTRUCTIVE DISEASE
cardia. Epinephrine may cause an anxiety reaction in a
Patients suffering from asthma, emphysema, and patient along with headache, palpitations, and respira­
chronic bronchitis may have an obstructed airway for tory difficulty. Both drugs can cause serious cardiac
several reasons. Acute asthmatic obstruction and reactions (dysrhythmias), which have resulted in death.
some chronic airway obstruction are due to bronchial
Metaproterenol (Alupent), Isoetharine
smooth muscle contraction, resulting in a smaller di­
(with Phenylephrine, Bronkosol-2),
ameter airway. Inflamed passageways, wh ich are
and Salmeterol (Servant)
swollen because of edema, may also constitute an air­
way obstruction. A further complication seen in Metaproterenol (Alupent), isoetharine (with Phenyle­
many respiratory diseases is the thickening and col­ phrine, Bronkosol-2), and salmeterol (Servant) are
lection of secretions that cannot be eliminated from isoproterenol analogs that exert most of their action
the respiratory tree and subsequently block the air­ on respiratory or vascular smooth muscle but have lit­
way. In this section the various drugs that can reverse tle effect on the heart. They are useful compounds for
smooth muscle contraction, inflammatory edema, and selectively relaxing bronchial smooth muscles without
collection of secretions are presented. directly affecting the heart. The major advantage of
A variety of therapeutic mechanisms are useful these drugs is that their action on the heart is minimal
against this collection of obstructive conditions. The or absent, and their potential for inducing cardiac toxi­
single most effective mechanism for relief of smooth cities is correspondingly reduced. However, because
muscle spasm is the beta2 activity that is available in vascular smooth muscle responds much like respira­
some of the adrenergic agents. Other useful mecha­ tory smooth muscle to these drugs, arterial resistance
nisms aim at potentiating the beta activity of adrener­ can be decreased, leading to a drop in blood pressure
gic agents, decongesting the inflamed airway, de­ and a reflexive tachycardia. The beta agonists are

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 43 Respiratory and Cardiovascular Drug Actions 785
-... --.--- --�----------------.-----

often inhalation, which minimizes their sys­

temic absorption and potential for side effects,
variety of antiinflammatory pOltenCle:s.
Ephedrine of corticosteroids in
is a sympathomimetic that acts by liberat­ on the ability of these the symp­
and from toms of inflamed tissue. The mechanism of action for
sites in addition to having a possible direct effect on the drugs, however, has not clearly been defined. Some
<>,""··c> ,,,'
<tT,r receptors. Its usefulness and side effects specific effects of corticosteroids that relate to the anti­
are similar to those of epinephrine. One beneficial inflammatory action are decreased dilation
factor in ephedrine use is that it can be administered and and stabilization of I"Q.-'Q(";,<n"

orally for convenient branes in white blood cells, In

pounds decrease the synthesis of that can
nr"<n,rot., broncho-obstl11ctive disease- prostaglandins
Xanthines
and ieukotrienes. The use of the corticos­
XanthineI' have effects similar to the catecholamines in teroids is recommended
the respiratory and cardiovascular systems. This simi­ The reason for this caution is that they produce serious
in effect may be due to the elevation of side effects and permanent if used for 2 weeks
AMP. Both the catecholamines and xanthines are or After I week of corticosteroid therapy, be­
known to elevated AMP levels in the tis­ havioral and acute ulcers may be ob­
sues they stimulate. The catecholamines activate served. However, when is instituted and
ate cyclase, the enzyme that converts A TP to adrenal suppression occurs, the patient requires supple­
AMP. The formed cyclic AMP exelts its effects mental corticosteroid until normal adrenal cor­
on the local tissue (e.g., bronchial muscle relaxation) tex function is restored. This state of
and is inactivated by the enzyme last for as long as several months after
The xanthines inhibit Most who receive corticosteroids for long-term
AMP and promoting its effects. Addi­ therapy develop a condition called syn­
tional actions of xanthines may be direct smooth muscle drome. It is characterized by of muscles be­
relaxation that cou Id increase cause of the breakdown of redistribution
tagonism of adenosine, which is brC)fIctlo(;on of fat from the extremities to the face and the trunk,
Eventually these patients develop osteoporosis and dia­
Theophylline and Aminophylline betes. Other serious complications are ulcers,
Theophylline and aminophylline are structurally very intercranial and
similar to caffeine. They are llsed to control asthma retardation. The time to onset of side effects can
when given or is be prolonged and the
often used orally for long-term maintenance of mild-to­ applying dosing antiin­

moderate disease. One of the most common uses for m!m"t",I"V benefit in the at low systemic doses.

aminophylline is the treatment of acute asthmatic air­ COiticosteroids can be at low doses in alternate

way obstruction, in cases that do not administration or can be inhalation in

to epinephrine alone. Intravenous administration of this a form that is not systemically absorbed.
drug increases the opportunity for serious side
which are hypotension and cardiac dysrhythmias, Antihistamine

Cromolyn Sodium (intal) and

Corticosteroids Nedocromil Sodium (Ti/ade)

The antiinflammatory steroids are related to the natu­ Cromolyn sodium (Intal) and nedocromil sodium
glucocorticoid, cortisol (Prednisone, have limited usefulness with the

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786 PART VIII Related Aspects of Cardiopulmonary Physical Therapy

other drugs presented here-they can only prevent an torants that are usually used in mixtures or adminis­
asthmatic episode. The mechanism of action is proba­ tered as cough syrups are ammonium chloride, syrup
bly the stabilization of the mast cell that synthesizes, of ipecac, and glyceryl guaiacolate. These are useful
stores, and releases histamine. Since histamine can for patients who cannot tolerate the iodide salts.
precipitate broncho-obstructive reactions, these drugs
are useful by preventing its release. They are admin­
DRUG INHALATION DEVICES
istered by inhalation.
Most drugs given by inhalation in respiratory disease

Mucolytics and Expectorants are deli vered by pressurized metered-dose inhalers

(MDI). These devices rely on pressurized chlo­
Acetylcysteine (Mucomyst) and roflurocarbon propellants to deliver very small drug
Pancreatic Dornase (Dornavac) particles (less than 5 micron diameter) into the air­
Acetylcysteine (Mucomyst) and pancreatic dornase way. Each activation of the metered valve allows an
(Dornavac) act by breaking the chemical bonds that accurately determined volume (dose) of propellant
hold together the large protein structure that con­ and drug mixture to be released at a high velocity.
tributes to the viscosity of mucus. Mucolytics are in­ The delivery of drugs to the site of action in the
haled to liquify mucus so that it can be moved out of airway by any type of inhalation is inefficient, and
the bronchial tract to prevent airway obstruction. Side therefore, correct technique in use of the MDI is an
effects associated with these drugs are bronchospasm, important concern. The MDI will allow delivery of
nausea, and vomiting. Acetylcysteine also inactivates 20% of the metered drug to the airway if the pa­
the penicillin antibiotics and is contraindicated in tient correctly coordinates the proper rate of inhala­
their presence. tion with activation of the device and then ade­
quately holds the breath before exhalation. It is
Trypsin (Tryptar)
estimated that 50% or fewer patients manage the
Trypsin (Tryptar) is a proteolytic enzyme that may drug delivery correctly. In response, patient educa­
also be useful for liquefying respiratory secretions. It tion on correct MDI technique is an important part
can be administered by inhalation, although it can of therapy, and additional devices, called spacers,
cause irritation to the eyes, nose, and throat. An addi­ have been developed to allow success with varia­
tional problem with this drug is a possible anaphylac­ tions in technique. The spacers come in various
tic reaction in sensitized patients. There is a variety configurations, but they all provide a chamber be­
of other enzymes with specific actions on protein that tween the patient and the MDI, which can be
may be useful in liquefying secretions. charged with the drug-propellant mixture that is
then inhaled without concern for critical timing.
Sodium Iodide and Potassium Iodide
Patients with poor MDI technique should benefit
Sodium iodide and potassium iodide are expectorants from the addition of a spacer.
that act by increasing the amount of respiratory secre­ An alternative to the MDI, in patients who have
tion so that is relatively less viscous and can be more difficulty with inhalation technique, is the single-dose
easily removed. The iodide salts are often used in late or multi-dose powder inhaler. This device offers a
bronchitis, bronchiectasis, and asthma, and they break drug compounded into a fine powder, which is deliv­
up especially tough bronchial secretions by attracting ered from a container on simple inhalation by the pa­
fluid to the respiratory tract. Characteristic side effects tient. Coordination of drug delivery is simple and not
with these compounds are gastric irritation, nausea, a pl'Oblem, because only inspiration by the patient
and vomiting. More serious complications occasion­ drives powder delivery to the airway. The method of­
ally involve the respiratory tract. These patients fers the same or lower efficacy of drug delivery (69'c
wheeze and experience bronchial spasm. Other expec­ to 20%), compared with MDI.

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 43 Respiratory and Cardiovascular Drug Actions 787

REVIEW QUESTIONS References

1. Why is it important to have an understanding of Clark, TJ.H., Godfrey, S., & Lee, T.H., (Eds.). (1992). Asthm({.
the system a drug is to modify? London: Chapman and Hall.
Hardman, J., Gilman, A.G., Limbird, L., & Rail, T.W., (Eds.).
2. What are the primary and secondary effects of
(1995). The pharmacological basis of therapeutics. New York:
the commonly used bronchodilators, Ventolin McGraw-HilI.
and Alupent? Kaliner, M.A. (1993). How the current understanding of the patho­
3. What is the cardiovascular reflex and why is it physiology of asthma influences our approach to therapy. .lour-

important to physical therapists? 1101 afAllergy and Clinical Immunology, 92( I pI. 2), 144-147.
Katzung, B.G., (Ed.). (1995). Basic and clinical pharmacology.
4. What is the pharmacologic rationale for treat­
East Norwalk, CT: Appleton & Lange.
ment of patients with chronic obstructive airways O'Brien-Ladner, A. (1994). Asthma: new insights in the manage­
disease. (COPD)? ment of older patients. Geriatrics, 49( 11),20-25,30-32.
5. Why is patient compliance with their medica­ Powell, C.Y. (1993). Management of ac ute asthma in

tions a concern of the physical therapist? ch ildhood.British .lournal ( fHospil{/1 Medicine, 50(5),272-275.
Whelan, A.M., & Hahn, N.W. (1991). Optimizing drug delivery
from metered-dose inhalers. Drug Intelligence and Clinical
Pharmacology, 25, 638-645.

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 GLOSSARY

Acid-base balance: a condition existing when the net surgery, gram-negative sepsis, multiple blood
rate at which the body produces acids or bases equals transfusions, oxygen toxicity, trauma, pneumonia, or
the net rate at which acids or bases are excreted. The other respiratory infection.
result of acid-base balance is a stable concentration Aerosol: nebulized particles suspended in a gas or air.
of hydrogen ions in body fluids. The amount of acid Airway clearance: the removal of mucus and foreign
or base in the arterial blood is measured by pH. material from the airways.
Acidosis: a process causing acidemia, which is a Airway-clearance deficits: deficits in the ability to
blood pH of less than 7.38. remove mucus and foreign material from the airways.
Acute exacerbation of chronic airflow Alveolar proteinosis: a disorder marked by the
limitation: an increase in the severity of the signs accumulation of plasma proteins, lipoproteins, and
and symptoms of chronic airflow limitation usually other blood components in the alveoli of the lungs.
triggered by infection, inflammation, or increased The cause is unknown and clinical symptoms vary,
sputum production. although only the lungs are affected. Some patients
Acute lung injury: injury to the lung characterized by are asymptomatic, whereas others show dyspnea and
a clinical spectrum of parenchymal lung dysfunction an unproductive cough.
resulting from multiple etiologies and leading to Alveolar ventilation: the volume of inspired air that
alveolar capillary membrane leaking (high protein reaches the alveolar level and participates in gas
content). Mild-to-moderate lung injury results in exchange, measured by Peo2.
noncardiogenic edema and severe injury results in Alveolitis: an allergic pulmonary reaction to the
adult respiratory distress syndrome. The hallmarks of inhalation of antigenic substances characterized by
worsening lung injury include refractory hypoxemia, acute episodes of dyspnea, cough, sweating, fever,
right-to-left shunt, and reduced lung compliance. weakness, and pain in the joints and mnscles
Adult respiratory distress syndrome (ARDS): a lasting from 12 to 18 hours. Recurrent episodes
respiratory syndrome characterized by respiratory may lead to chronic obstructive lung disease with
insufficiency and hypoxemia. Triggers include weight loss, increasing exertional dyspnea, and
aspiration of a foreign body, cardiopulmonary bypass interstitial fibrosis.

G-1

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G-2 Glossary

Anesthesia: the absence of normal sensation, especially bronchodilators, beta-adrenergic drugs,

sensitivity to pain, as induced by an anesthetic methylxanthines, and sh0l1-term use of corticosteroids.
substance or by hypnosis or as occurs with traumatic Atelectasis: an abnormal condition characterized by
or pathophysiological damage to nerve tissue. the collapse of lung tissue, preventing the respiratory
Angina: angina pectoris, the paroxysmal chest pain exchange of carbon dioxide and oxygen. Symptoms
caused by anoxia of the myocardium. may include diminished breath sounds, a mediastinal
Angina pectoris: a paroxysmal thoracic pain caused shift toward the side of the collapse, fever, and
most often by myocardial anoxia as a result of increasing dyspnea.
atherosclerosis of the coronary arteries. The pain Atherosclerosis: a common arterial disorder
usuall.y radiates down the inner aspect of the left arm characterized by yellowish plaques of cholesterol,
and is frequently accompanied by a feeling of lipids, and cellular debris in the inner layers of the
suffocation and impending death. Attacks of angina walls of large and medium-sized arteries. The vessel
pectoris are often related to exertion, emotional walls become thick, fibrotic, and calcified, and the
stress, and exposure to intense cold. lumen narrows, resulting in reduced blood flow to
Ankylosing spondylitis: a chronic inflammatory organs normally supplied by the artery.
disease of unknown origin, first affecting the spine Antilipidemic agents do not reverse atherosclerosis,
and adjacent structures and commonly progressing to but a diet low in cholesterol, calories, and saturated
eventual fusion (ankylosis) of the involved joints. In fats, adequate exercise, and the avoidance of
addition to the spine the joints of the hip, shoulder, smoking and stress may help prevent the disorder.
neck, ribs, and jaw are often involved. Physical
therapy aids in keeping the spine as erect as possible Blood: the liquid pumped by the heart through all the
to prevent flexion contractures. In advanced cases, arteries, veins, and capillaries. The blood is
surgery may be performed to straighten a badly composed of a clear yellow tluid, called plasma, and
deformed spine. the formed elements, and a series of cell types with
Arrhythmia: an abnormal heart rhythm represented different functions. The major function of the blood
by an irregularity of the timing or the appearance of is to transport oxygen and nutrients to the cells and to
the ECG tracing. This term is often used remove from the cells carbon dioxide and other
synonymously with dysrhythmia. waste products for detoxification and elimination.
Arterial blood gas: a test to evaluate the acid-base Body mechanics: using one's body effectively to
balance and panial pressures of oxygen and carbon prevent injury.
dioxide in the anerial blood. Bradycardia: an abnormally slow heart rate.
Arteriovenous-oxygen difference (a-vo2 Bradypnea: a decreased respiratory rate under 10
difference): the difference between the oxygen breaths per minute.
content of arterial blood and the amount in venous Bronchiectasis: an abnormal condition of the
blood. bronchial tree, characterized by irreversible dilatation
Artifact: extraneous detlection of the ECG waveform and destruction of the bronchial walls. Symptoms of
caused by movement or electrical interference. bronchiectasis include a constant cough productive
Artifact may be mistaken for a dysrhythmia. of copious purulent sputum, hemoptysis, chronic
Artificial airway: a plastic or rubber device that can sinusitis, clubbing of fingers, and persistent moist,
be inserted into the upper or lower respiratory tract to coarse rales. Treatment includes mobilization,
facilitate ventilation or the removal of secretions. frequent postural drainage, antibiotics, and, rarely,
Assessment: an evaluation or appraisal of a condition. surgical resection of the affected part of the lungs.
Assisted cough: the physical assistance of a cough, Bronchiolitis: an acute viral infection of the lower
either by the patient or an assistant. respiratory tract that occurs primarily in infants under
Asthma: a respiratory disorder characterized by 18 months of age, characterized by expiratory
recurring episodes of paroxysmal dyspnea, wheezing wheezing, respiratory distres , inflammation, and
on expiration/inspiration because of constriction of the obstruction at the level of the bronchioles.
bronchi, coughing, and viscous mucoid bronchial Bronchitis: an acute or chronic inflammation of the
secretions. Treatment may include elimination of the mucous membranes of the tracheobronchial tree.
causative agent, hyposensitization, aerosol or oral Acute bronchitis is characterized by a productive

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 Glossary G-3

cough, fever, hypertrophy of mucous-secreting present at birth or shortly thereafter. Early

structures, and back pain. Most common in adults, it identification of the disorder facilitates the handling

is uften a complication of cystic fibrosis in children. of infants with cerebral palsy and the initiation of an

Treatment includes the cessation of cigarette exercise and training program. Treatment is

smoking, avoidance of airway irritants, the use of individualized and may include the use of braces,

expectorants, and postural drainage. Currently, surgical correction of deformities, speech therapy,

prophylactic antibiotics, steroids, and desensitization and various indicated drugs, such as muscle rel.
À
therapy are not recummended. and anticonvulsants.

Bronchopulmonary dysplasia: an iatrogenic condition Childhood asthma: reversible airway hyperreactivity

observed in neonates that resembles chronic airflow and edema affecting children that is often triggered
limitation and is associated with positive pressure by dust or animals; hallmarked by narrowing of the
mechanical ventilation and oxygen therapy. airways, wheezing, shortness of breath, accessory
Burns: an injury to tissues of the body caused by heat, muscle use, and impaired oxygenation.
electricity, chemicals, radiation, or gases in which the Chronic bronchitis: a lung condition characterized
extent of the injury is determined by the amount of by the presence of a chronic productive cough for at
exposure of the cell to the agent and to the nature of least 3 months in each of 2 successive years.
the agent. The treatment of burns includes pain relief, Chronic renal insufficiency: impaired function of the
careful asepsis, prevention of infection, maintenance kidneys manifested by impaired blood urea nitrogen,
of the balance in the body of fluids and electrolytes, creatinine clearance, and reduced urinary output.
and good nutrition. Severe bUllls of any origin may Renal insufficiency may precipitate renal failure.
cause shock, which is treated before the wound. Chronic airflow limitation: a more precise term for
chronic obstructive pulmonary disease (e.g., chronic
Cardiac output (Q): the amount of blood ejected bronchitis and emphysema).
from the heart into the aona each minute. Clinical decision making: the process of making
Cardiac rehabilitation: a supervised program of decisions based on a thorough history, assessment,
progressive exercise, psychological support, and integration of the results of laboratory tests and
education or training to enable a myocardial investigations, and the patient's needs and wants.
infarction patient to resume the activities of daily Complications with coughing: Complications
living on an independent basis. Special training may associated with an impaired cough (e.g., impaired
be needed to adapt the patient to a new occupation mucociliary transport, mucous accumulation,
and lifestyle. pulmonary aspiration, and increased risk of infection).
Cardiopulmonary failure: progressive insufficiency Congestive heart failure (CHF): an abnormal
of cardiopulmonary function resulting in significant condition that reflects impaired cardiac pumping,
impairment of cardiac output and/or ventilation that caused by myocardial infarction, ischemic heart
cannot be adequately compensated without disease, or cardiomyopathy. Failure of the ventricle to
ventilatory support. eject blood efficiently results in volume overload,
Cardiopulmonary function: the integrated function chamber dilatation, and elevated intracardiac pressure.
of the heart and lungs. Retrograde transmission of increased hydrostatic
Cardiopulmonary physical therapy: see p. ix. pressure from the left heart causes pulmonary
Cardiopulmonary unit: the heart and lungs, which congestion; elevated right heart pressure causes
function interdependently as a unit. systemic venous congestion and peripheral edema.
Catabolic: relating to catabolism, which is the Connective tissue dysfunction: impaired function of
breaking down in the body of complex chemical connective tissue observed in connective tissue and
compounds into simpler ones, often accompanied by vascular collagen conditions.
the liberation uf energy. Continuity of care: the provision of continuous care
Cellular respiration: the processes involved with from one setting to another (e.g., inpatient to
cellular metabolism, including energy transfer, outpatient facilities).
oxygen utilization, and carbon dioxide production. Controlled breathing: teaching a patient ventilatory
Cerebral palsy: a motor function disorder caused by strategies to exert cognitive control over ineffective
a permanent, nonprogrcssive brain defect or lesion breathing patterns.

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G-4 Glossary

Control of breathing: the central and peripheral constituents of saliva, and overactivity of the
regulation and control mechanisms of breathing. autonomic nervous system. The glands most affected
Control of the heart: the central and peripheral are those in the pancreas, the respiratory system, and
regulation and control mechanisms of the heart. the sweat glands. Because there is no known cure,
Coronary artery disease: any one of the abnonual treatment is directed at the prevention of respiratory
conditions that may affect the arteries of the heart infections, which are the most frequent cause of
and produce various pathological effects, especially death. Mucolytic agents and bronchodilators are used
the reduced flow of oxygen and nutrients to the to help liquefy the thick, tenacious mucus. Physical
myocardium. Any of the coronary artery diseases, therapy measures, such as exercise, postural
such as coronary atherosclerosis, coronary arteritis, drainage, and breathing exercises, can also dislodge
or fibromuscular hyperplasia of the coronary arteries, secretions. Life expectancy in cystic fibrosis has
may produce the common characteristic symptom of improved markedly over the past several decades,
angina pectoris. Studies over the last 30 years and with early diagnosis and treatment, most patients
confirm that coronary atherosclerosis occurs most can be expected to reach adulthood.
frequently in populations with regular diets high in
calories, total fat, saturated fat, cholesterol, and Dead space: the amount of lung in contact with
refined carbohydrates. Other risk factors include ventilating gases but not in contact with pulmonary
cigarette smoking, hypertension, serum cholesterol blood tlow. Alveolar dead space refers to alveoli
levels, coffee intake, alcohol intake, deficiencies of that are ventilated by the pulmonary circulation but
vitamins C and E, water hardness, hypoxia, carbon are not perfused. The condition may exist when
monoxide, social overcrowding, heredity, climate, pulmonary circulation is obstructed, as by a
and viruses. thromboembol.us. Anatomical dead space is an area
Cough: a sudden, audible expulsion of air from the in the trachea, bronchi, and air passages containing
lungs. Coughing is preceded by inspiration, the air that does not reach the alveoli during respiration.
glottis is partially closed, and the accessory muscles As a general rule the volume of air in the
of expiration contract to expel the air forcibly from anatomical dead space in millimeters is
the respiratory passages. Coughing is an essential approximately equal to the weight in pounds of the
protective response that serves to clear the lungs, involved individual. Certain lung disorders, such as
bronchi, or trachea of irritants and secretions or to emphysema, increase the amount of anatomical
prevent aspiration of foreign material into the lungs. dead space. Physiological dead space is an area in
It is a common symptom of diseases of the chest and the respiratory system that includes the anatomical
larynx. Because the function of coughing is to clear dead space together with the space in the alveoli
the respiratory tract of secretions, it is important that occupied by air that does not contribute to the
the cough bring out accumulated debris. Where it oxygen-carbon dioxide exchange.
does not, because of weakness or inhibition of the Denervation of heart: the transplanted heart initially
force of the cough caused by pain, instruction and loses its innervation (i.e., it is deriervated and relies
assistance in effective coughing and deep-breathing on exogenous catecholamines for cardiac
exercises are required. acceleration and deceleration).
Cough pump: the integrated thoracic and abdominal Dependent patients: patients unable to help
mechanisms involved in cough resulting in forced themselves.
expiration and evacuation and clearance of the airways. Depolarization: the changes in ionic concentrations
Cough stages: the stages of cough include maximal across muscle cell membranes leading to contraction
inspiration, closure of the glottis, increased of the cell.
intraabdominal pressure, opening of the glottis, and Diabetes: a clinical condition characterized by the
forced expiration. excessive excretion of urine. The excess may be
Cystic fibrosis: an inherited disorder of the exocrine caused by a deficiency of antidiuretic hormone
glands, causing those glands to produce abnormally (ADH), as in diabetes insipidus, or it may be the
thick secretions of mucus, elevation of sweat polyuria resulting from the hyperglycemia OCCUlTing
electrolytes, increased organic and enzymatic in diabetes mellitus.

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 Glossary G-5

Diaphragmatic breathing pattern: involves teaching Endocrine function: the function of the endocrine
patients with CO PO how to relax the accessory glands responsible for normal physiological function.
muscles and to pelform controlled diaphragmatic Evidence-based practice: practice based on evidence
breathing. from the physiologic and scientific literature.
Diflusion: the process in which solid, particulate Exercise: (I) The petformance of any physical
matter in a t1uid moves from an area of higher activity for the purpose of conditioning the body,
concentration to an area of lower concentration, improving health, or maintaining fitness or as a
resulting in an even distribution of the particles in the means of therapy for correcting a deformity or
fluid. No energy is required. restoring the organs and bodily functions to a state of
Documentation: written material associated with the health. (2) Any action, skill, or maneuver that exerts
history, the compilation of laboratory reports and the muscles and is performed repeatedly in order to
investigations, and the results of the clinical develop or strengthen the body or any of its parts.
assessment. (3) To use a muscle or part of the body in a repetitive
Dyspnea: the sensation of difficulty in breathing. way to maintain or develop its strength. The physical
therapist constantly assesses the patient's needs and
ECG monitoring: electrocardiographic monitoring provides the proper type and amount of exercise,
involving electrode placement on the chest wall and taking into account the patient's physical or mental
on the limbs for a 12-lead ECG; such monitoring limitations. Exercise has a beneficial effect on each
provides a tracing of the electrical activity of the of the body systems, although in excess it can lead to
heart. the breakdown of tissue and cause injury.
Echocardiography: evaluation of cardiac structure Exercise blood gases: blood gases taken before,
and function by using the properties of sound. during, and after exercise to determine the effect of
Quantitative and qualitative measurements can be exercise on oxygen transport.
derived. The most common types include two­ Exercise stress: the physical stress imposed by
dimensional, Doppler, and transesophageal echoes. movement (i.e., mobilization and exercise.)
Ejection fraction: a measure of myocardial function, Expiratory reserve volume (ERV): the maximum
it is the amount of ventricular volume ejected with volume of gas that can be expired from the resting
each heart beat. Expressed as a percent, the ejection expiratory level.
fraction = (end-diastolic volume - end-systolic Extrinsic factors: factors related to the patient's care
volume) x 100 end-diastolic volume. that contribute to cardiopulmonary dysfunction and
Electrocardiogram (ECG): the tracing produced by impaired gas exchange.
the sequential depolarization and repolarization of
myocardial cells as detected by sutface electrodes Fluid and electrolyte status: the status of blood
placed on the skin. volume and distribution, and the status of electrolyte
Electromechanical coupling: the coupling of balance in the body; fluid balance often has a direct
electrical and mechanical events of the heart to effect effect on electrolytes.
cardiac output. Forced expiratory volume in one second (FEV I): the
EMG power spectrum: electromyography is the amount of air expired in I second during a forced
process of recording the electrical activity of muscle exhalation after a maximal inhalation.
on a cathode-ray oscilloscope. The Forced vital capacity (FVC): the total amount of air
electromyographic (EMG) power spectrum is the full exhaled during a forced exhalation after a maximal
range of electrical activity of the muscle. inhalation.
Emphysema: a lung condition characterized by an Functional residual capacity: the volume of gas in
abnormal permanent enlargement of the air spaces the lungs at the end of a normal expiration. The
distal to the terminal bronchioles, accompanied by functional residual capacity is equal to the residual
destruction of their walls. volume plus the expiratory reserve volume.
Endocardial cushion defect: any cardiac defect Function optimization: optimal functioning of the
resulting from the failure of the endocardial cushions in patient as a whole person based on optimal
the embryonic heart to fuse and form the atrial septum. physiological functioning at an organ system level.

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G-6 Glossary

Gas exchange: the movement of oxygen and carbon temperature. The percentage is usually represented in
dioxide between the pulmonary capillary blood and terms of relative humidity, with 100% being the
the alveolar tissue and between the systemic capillary point of air saturation or the level at which the air can
blood and peripheral tissue cells. absorb no additional water.
Gastrointestinal dysfunction: abnormal function of Hyaline membrane disease: disease of the newborn,
the gastrointestinal system. characterized by airless alveoli, inelastic lungs, more
Gravitational stress: stress imposed on the human than 60 respirations a minute, nasal flaring,
body by gravity and its physiological effects. intercostal and subcostal retractions, grunting on
Gravity: the heaviness or weight of an object resulting expiration, and peripheral edema. The condition
from the universal effect of the attraction between any occurs most often in premature babies. The disease is
body of matter and any planetary body. The force of self-limited; the infant dies in 3 to 5 days or
the attraction depends on the relative masses of the completely recovers with no after-effects. Treatment
bodies and on the distance between them. includes measures to corTect shock, acidosis, and
hypoxemia and use of positive airway pressure to
Head injury: any traumatic damage to the head prevent alveolar collapse. This is also called
resulting from blunt or penetrating trauma of the respiratory distress syndrome (RDS) olthe newborn.
skull. Blood vessels, nerves, and meninges can be Hypercapnia: the presence of an abnormally large
torn; bleeding, edema, and ischemia may result. amount of carbon dioxide in the circulating blood.
Health behavior: an action taken by a person to Hyperpnea: rapid shallow breathing.
maintain, attain, or regain good health and to prevent Hypertension: a common, often asymptomatic
illness. Health behavior reflects a person's health disorder characterized by elevated blood pressure
beliefs. Some common health behaviors are persistently exceeding 140/90 mm Hg. Patients with
exercising regularly, eating a balanced diet, and high blood pressure are advised to follow a low­
obtaining necessary inoculations. sodium, low-saturated-fat diet, to reduce calories to
Heart: the muscular, cone-shaped organ, about the control obesity, to exercise, to avoid stress, and to
size of a clenched fist, that pumps blood throughout take adequate rest.
the body and beats normally about 70 times per Hypoxemia: a low level of oxygen in the blood, often
minute by coordinated nerve impulses and muscular characterized by a Pa02 of less than 80 mm Hg.
contractions. Enclosed in pericardium, the heart rests
on the diaphragm between the lower borders of the Immune function: function of the immunological
lungs, occupying the middle of the mediastinum. The system and its components in effecting optimal
sinoatrial node of the heartbeat sets the rate. Other immunological protection.
factors affecting the heartbeat are emotion, exercise, Immunological dysfunction: abnormal function of
hormones, temperature, pain, and stress. the immunological system.
Heart-lung interdependence: the heart and lung are Immunosuppression: of or peI1.aining to a suhstance or
structurally and functionally interdependent and form procedure that lessens or prevents an immune response.
a cardiopulmonary unit. Inspiratory capacity (Ie): the maximum volume of
Hemiplegia: paralysis of one side of the body. gas that can be inhaled from the resting expiratory
Hemodynamic status: status of the heart and its level. Equal to the sum of the tidal volume and the
capacity to effect blood movement to perfuse the inspiratory reserve volume, it is measured with a
tissues of the body. spirometer.
Hibernating myocardium: contractile dysfunction of Inspiratory muscle training: resistance ventilatory
the myocardium as a result of prolonged ischemia, training designed to increase the strength and
appearing as a regional wall motion abnormality. endurance of the inspiratory muscles.
Home care: a health service provided in the patient's Inspiratory resistance breathing: a method of
place of residence for the purposes of promoting, respiratory muscle training that includes normal
maintaining, or restoring health or minimizing the ventilation with added external threshold loading
effects of illness and disability. on inspiration consisting of 15 to 30 minutes of
Humidity: pertaining to the level of moisture in the training 5 days per week. External loading is
atmosphere, the amount varying with the increased from 30% of maximal inspiratory pressure

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 Glossary G-7

to 60% of maximal inspiratory pressure as patient's nephrons. All the blood in the body passes through
tolerance increases. the kidneys about 20 times every hour but only about
Inspiratory reserve volume: The maximum volume one fifth of the plasma is filtered by the nephrons
of gas that can be inspired from the end-tidal during that period. The kidneys remove water as
inspiratory level. urine and return water that has been filtered to the
Intermittent positive pressure breathing (IPPB): a blood plasma, thus helping to maintain the water
form of assistive or controll.ed respiration produced baJance of the body. Hormone, especially the
by a ventilatory apparatus in which compressed gas antidiuretic hormone (ADH), produced by the
is delivered under positive pressure into the person's pituitary gland, control the function of the kidneys in
airways unti I a preset pressure is reached. Passi ve regulating the water content of the body.
exhalation is allowed through a valve, and the cycle Kyphoscoliosis: an abnormal condition characterized
begins again as the flow of gas is triggered by by an anteroposterior curvature and a lateral
inhalation. This is also called i11lermillent positive curvature of the spine. It occurs in children and
pressure ventilation (IPPV). adults and can be associated with cor pulmonale.
Interstitial pulmonary fibrosis: a classification of
restrictive lung disease including conditions that Late sequelae of poliomyelitis: the late effects of
result in a final common pathway of bouts of chronic poliomyelitis that may occur in poliomyelitis
lung infection and irreversible fibrosis. survivors 30 to 35 years after onset. These effects
Intraaortic balloon counter pulsation: procedure for include disproportionate fatigue, weakness, pain,
assisting left ventricular function and coronary reduced endurance, choking and swallowing
petfusion involving the insertion of a balloon in the problems, altered temperature sensitivity, and
femoral artery. The inflation and deflation of the psychological problems.
balloon is synchronized with the ECG such that it Learning theory: a group of concepts and principles
inflates during diastole and deflates during systole. that attempts to explain the learning process. One
Intracardiac pressures: pressures within the concept, Guthrie's contiguous conditioning premise,
chambers of the heart. Optimal movement of blood postulates that each response becomes permanently
through the heart depends on pressure gradients linked with stimuli present at the time so that
throughoLlt the heart. Normal pressures within each contiguity rather than reinforcement is a part of the
heart chamber are within a restricted range. learning process.
Intracranial pressure monitoring: invasive Liver: the largest gland of the body and one of its
monitoring instituted to measure changes in cranial most complex organs. More than 500 of its functions
pressure usually resulting from increased volume of have been identified. It is divided into four lobes,
the brain because of injury. bleeding, fluid contains as many as 100,000 lobules, and is served
accumulation, or an intracranial mass. by two distinct blood supplies. Some of the major
Isocapnic hyperpnea: a method of respiratory muscle functions performed by the liver are the production
training that includes high ventilation with low of bile by hepatic cells, the secretion of glucose,
external loading consisting of sustained periods of proteins, vitamins, fats, and most of the other
hyperpnea lasting 15 to 30 minutes daily for several compounds used by the body, the processing of
weeks with the addition of carbon dioxide to hemoglobin for vital use of its iron content, and the
maintain a normal level. conversion of poisonous ammonia to area.
Lung cancer: a pulmonary malignancy attributable to
Jacobsen's progressive relaxation exercise: a cigarette smoking in 50% of cases. Lung cancer
technique involving contraction followed by develops most often in scalTed or chronically diseased
relaxation to progressively relax muscle groups. lungs and is usual.
because metastases may precede the detection of the
Kidneys: a pair of bean-shaped urinary organs in the primary lesion in the lung. Symptoms of lung cancer
dorsal part of the abdomen, one on each side of the include persistent cough, dyspnea, purulent or blood­
vertebral column. The kidneys produce and eliminate streaked sputum, chest pain, and repeated attacks of
urine through a complex filtration network and bronchitis or pneumonia. Surgery is the most
reabsorption system comprising more than 2 million effective treatment, but only one half of cases are

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G-8 Glossary

operahle at the time of diagnosis and of these 50% are Metabolical demand fluctuates depending on the
not resectable. Thoracotomy is contraindicated if activity level of the individual, the presence of illness
metastases are found in contralateral or scalene lymph and increascd temperature, and the requirements of
nodes. In"adiation is used to treat localized lesions and healing and repair.
unresectable intrathoracic tumors and as palliative Method: a technique or procedure for producing a
therapy for metastatic lesions. Radiotherapy may also desired effect, such as a surgical procedure, a
be administered after surgery to destroy remaining laboratory test, or a diagnostic technique.
tumor cells and may be combined with chemotherapy. Minute ventilation (VE): the amount of air inspired
Lung capacities: lung volumes that consist of two or in I minute. It is the product of tidal volume and
more of the four primary nonoveriapping volumes. respiratory rate.
Functional residual capacity is the sum of residual Minute ventilation: the total expired volume of air
volume and expiratory reserve volume. Inspiratory per minute.
capacity is the sum of the tidal volume and Mobilization: the therapeutic and prescriptive
inspiratory reserve volume. Vital capacity is the sum application of low-intensity exercise in the
of the expiratory reserve volume, the tidal volume, management of cardiopulmonary dysfunction usually
and the inspiratory reserve volume. Total lung in acutely ill patients. The primary goal of
capacity, at the end of maximal inspiration, is the mobilization is to exploit the acute eflects or exercise
sum of the functional residual capacity and the to optimize oxygen transport.
inspiratory capacity. Morbid obesity: an excess of body fat that threatens
Lung compliance: the volume change per unit of normal body functions, such as respiration.
pressure change in the lungs. Mucous blanket: the normal layer of mucous lining
Lungs: a pair of light, spongy organs in the thorax, the bronchopulmonary tree. This blanket provides a
constituting the main component of the respiratory medium through which foreign material and bacteria
system. The two highly elastic lungs are the main can be wafted centrally by the cilia for eventual
mechanisms in the body for inspiring air from which removal by coughing or swallowing.
oxygen is extracted for the arterial blood system and Multiple sclerosis (MS): a progressi ve discase
for exhaling carbon dioxide dispersed from the characterized by disscminated demyelination of
venous system. nerve fibers of the brain and spinal cord. It begins
Lung volume: the volume of the lungs that may be slowly, usually in young adulthood, and continues
compartmentalized into component volumes and throughout life with periods of exacerbation and
capacities. remission. As the disease progresses, the intervals
between exacerbations grow shorter and disabil ity
Malnutrition: any disorder of nutrition. It may result becomes greater. There is no specific treatment for
from an unbalanced, insufficient, or excessive diet or the diseasc; corticosteroids and other drugs are
from the impaired absorption, assimilation, or use of used to treat the symptoms accompanying acute
foods. episodes. Physical therapy may help to postpone
Managed care: a health care system in which there is or prevent specific disabilities. The patient is
administrative control over primary health care encouraged to live as normal and active a life
services in a medical group practice. Redundant as possible.
facilities and services are eliminated and costs are Multisystem assessment: the assessment of
reduced. Health education and preventive medicine multiple organ systems based on clinical examination
are emphasized. Patients may pay a flat fee for basic and investigative laboratory reports. Such assessment
family care but may be charged additional fees for helps identify all factors that contribute to deficits in
secondary care services of specialists. oxygen transport.
Measurement: the determination, expressed Muscle endurance: the ability to sustain repetitive
numerically, of the extent or quantity of a substance, contraction against a given load.
energy, or time. Muscle strength: the maximum force that a muscle
Mechanical ventilation: the use of artificial can develop with maximal stimulation.
mechanical means to support ventilation. Muscular dystrophy (MD): a group of genetically
Metabolical demand: the energy and oxygen transmitted diseases characterized by progressive
demands of the body required to support metabolism. atrophy of symmetrical groups of skeletal muscles

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 Glossary G-9

without evidence of involvement or degeneration of Oxygen (02): a tasteless, odorless, colorless gas
neural tissue. [n all forms of muscular dystrophy, essential for human respiration.
there is an insidious loss of strength with increasing Oxygen consumption (Vo2): the difference between
disability and deformity, although each type differs oxygen that is inspired and the amount of oxygen
in the groups of muscles affected, the age of onset, exhaJed. The difference between inspired and expired
the rate of progression, and the mode of genetic oxygen is a primary measure of aerobic fitness.
inheritance. The basic cause is unknown but appears Oxygen delivery (Do2): the delivery of oxygen to the
to be an inborn error of metabolism. Treatment of the tissues of the body. an essential component of
muscular dystrophies consists primarily of supportive oxygen transport.
measures, such as physical therapy and orthopedic Oxygen desaturation: the desaturation of oxygen
procedures to minimize deformity. from the hemoglobin molecule in the blood in
Myocardial infarction: necrosis of a portion of response to a reduction of tissue oxygen levels.
cardiac muscle caused by obstruction in a coronary Oxygen transport: the process by which oxygen is
artery from either atherosclerosis or an embolus. absorbed in the lungs by the hemoglobin in
Also called a heart attack. circulating deoxygenated red cells and carried to the
peripheral tissues. The process is made possible
Needs assessment: assessment of the patient's specific because hemoglobin has the ability to combine with
physical, functional, and psychological needs. oxygen present at a high concentration, such as in the
Nocturnal ventilation: the selective use of lungs, and to release this oxygen when the
mcchanical ventilation during the night. Patients with concentration is low, such as in the peripheral tissues.
cardiopulmonary dysfunction are at greater risk Oxygen transport pathway: the pathway for oxygcn
during the night when they are recumbent and the delivery to the tissues from the ambient air, through
respiratory drive is depressed. the airways and lungs, across the alveolar capillary
membrane, into the pulmonary circulation through
Obesity: an abnormal increase in the proportion of fat the chambers of the heart, via the peripheral and
cells. mainly in the viscera and subcutaneous tissues regional circulation to the tissues and the
of the body. Obesity may be exogenous or mitochondria where oxygen is used in cellular
endogenous. Hyperplastic obesity is caused by an respiration.
incrcase in the number of fat cells in the increased Oxygen saturation: a measurement of the amount of
adipose tissue mass. Hypertrophic obesity results oxygen attached to a hemoglobin molecule.
from an increase in the size of the fat cells in the Oxyhemoglobin dissociation: the dissociation of
increase adipose tissue mass. oxygen from the hemoglobin molecule in peripheral
Objective: (I) A goal. (2) Of or pertaining to a tissues when the concentration of oxygen is low.
phenomenon or clinical finding that is observed; not
subjective. An objective finding is often described in Parenchyma: the tissue of an organ as distinguished
health care as a sign, as distinguished from a from supporting or connective tissue.
symptom, which is a subjcctive finding. Parkinson's disease: a slowly progressive,
Obstructive lung disease: a classification of lung degenerative, neurological disorder characterized by
disease referring to airflow limitation secondary to resting tremor, pill rolling of the fingers, a masklike
obstruction and increased airway resistance (e.g., expression, shuffling gait, forward flexion of the
chronic bronchitis and emphysema). trunk, loss of postural reflexes, and muscle rigidity
Osteoporosis: a disorder characterized by abnormal and weakness. It is usually an idiopathic disease of
rarefaction of bone, occurring most frequently in people over 60 years of age, although it may occur in
postmenopausal women, in sedentary or immobilized younger people, especially after acute encephalitis or
individuals, and in patients on long-term steroid carbon monoxide or metallic poisoning, particularly
therapy. The disorder may cause pain, especially in by reserpine or phenothiazine drugs.
the lower back, pathological fractures, loss of stature, Partial pressure of gases: the pressure exerted by an
and various deformities. individual gas, a percent of the total pressure of gases.
Outpatient: a patient, not hospitalized, who is being Patent ductus arteriosus (PDA): an abnormal
treated in an olTiec, clinic, or other ambulatory care opening between the pulmonary artery and the aorta
facility. caused by failure of the fetal ductus arteriosus to

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G-10 Glossary

close after birth. The defect, which is seen primarily Prevention: any action directed toward preventing
in premature infants, allows blood from the aorta to illness and promoting health to avoid the need for
flow into the pulmonary artery and to recirculate secondary or tertiary health care.
through the lungs, where it is reoxygenated and Primary cardiopulmonary dysfunction:
returned to the left atrium and left ventricle, causing cardiopulmonary dysfunction resulting from a primary
an increased workload on the left side of the heart condition of the heart, lungs, or both.
and increased pulmonary vascular congestion and Pulmonary rehabilitation: rehabilitation of
resistance. cardiopulmonary dysfunction including the acute,
Pediatric cardiac rehabilitation: specialized cardiac subacute, and chronic phases of the disease or after
rehabilitation for children instituted in the chronic thoracic surgery. The long-term management
stage of heart disease or after cardiovascular surgery includes a comprehensive program of exercise,
when the patient is through the acute phase. ventilatory support, additional airway clearance
Pediatric pulmonary rehabilitation: specialized interventions as needed, nutrition, stress reduction,
pulmonary rehabilitation for children instituted in the smoking cessation, pacing and energy
subacute or chronic stages of lung disease or after conservation, vocational rehabilitation, sexual
thoracic surgery when the patient is through the acute rehabilitation, and education.
phase. Pulmonary development: the anatomical and
Perfusion: the passage of a fluid through a specific physiological development of the cardiopulmonary
organ or an area of the body. system during nom1al growth and development.
Perioperative complications: complications before, Pulmonary circulation: the blood flow through a
during, and after surgery. network of vessels between the heart and the lungs
Peripheral circulation: the systemic circulation, for the oxygenation of blood and removal of carbon
which excludes the circulation to the heart and lungs dioxide.
(the central circulation).
Peripheral vascular disease: any abnormal condition Quality care: the provision of holistic care in which
that affects the blood vessels outside the heart and the needs and wants of the patient are considered.
the lymphatic vessels.
Pneumonia: an acute inflammation of the lungs, Recumbency: the state of lying down or leaning
usually caused by inhaled pneumococci of the against something.
species Streptococcus pneumoniae. The alveoli and Reflex cough: a cough stimulated reflexively.
bronchioles of the lungs become plugged with a Reliability: the extent to which a test measurement or
fibrous exudate. Pneumonia may be caused by a device produces the same results with different
other bacteria, as well as by viruses, rickettsiae, investigators, observers, or administration of the test
and fungi. over time. If repeated use of the same measurement
Positron emission scans: tomographic scans using tool on the same sample produces the same consistent
positron emitting radionuclides. The tracers used are results, the measurement is considered reliable.
often taken up in the metabolical pathways of the Residual volume: the volume of air remaining in the
tissues being studied (e.g., oxygen metabolism or lung after a maximal expiration.
gluclose metabolism). Resources: services, personnel, and treatment options
Prescription: an order for medication, therapy, or a that can be drawn on to maximize treatment delivery
therapeutic device given by a properly authorized and effectiveness.
person to a person properly authorized to dispense or Respiratory muscle fatigue: a loss in the capacity of
perform the order. A prescription is usually in written a muscle underload to develop force or velocity that
form and includes the name and address of the is reversible by rest.
patient, the date, the [4]+ symbol (superscription), Respiratory muscles: the muscles that produce
the medication prescribed (inscription), directions to volume changes of the thorax during breathing. The
the pharmacist or other dispenser (subscription), inspiratory muscles include the hemidiaphragms,
directions to the patient that must appear on the label, external intercostals, scaleni, sternomastoids,
the prescriber's signature, and, in some instances, an trapezius, pectoralis major, pectoralis minor,
identifying number. subclavius, latissimus dorsi, serratus anterior, and

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 Glossary G-11

muscles that extend the back. The expiratory muscles Sclerodenna: a relatively rare autoiuunune disease
are the external intercostals, abdominals, and the affecting the blood vessels and connective tissue. The
muscles that flex the back. disease is chaJ'acterized by fibrous degeneration of lhe
Respirator), muscle weakness: a chronic loss in the connective tissue of the skin, lungs, and intemal organs,
capacity of a rested muscle to generate force. especially the esophagus, digestive tract, and kidneys.
Respiratory mechanics: the physical properties of Scleroderma is most common in middle-aged women.
the lung including resistance and compliance Secretion management: management of airway
characteristics. secretions.
Respiratory failure: the inability of the cardiac and Sedation: an induced state of quiet, calmness, or sleep,
pulmonary systems to maintain an adequate as by means of a sedative or hypnotic medication.
exchange of oxygen and carbon dioxide in the lungs. Sepsis and multiorgan system failure: overwhelming
Respiratory failure may be oxygenation or systemic infection and pathogens leading to failure
hypcrcapniac. Treatment of respiratory fai lure within multiple organ systems.
includes maximizing ventilation, clearing the airways Shock: an abnormal condition of inadequate blood
by suction, bronchodilators, or tracheostomy, flow to the body s peripheral tissues, with life­
antibiotics for infections usually present, threatening cellular dysfunction, hypotension, and
anticoagulants for pulmonary thromboemboli, and oliguria. The condition is usually associated with
electrolyte replacement in fluid imbalance. Oxygen inadequate cardiac output, changes in peripheral
may be administered in some cases; in others it may blood flow resistance and distribution, and tissue
further decrease the respiratory reflex by removing damage. Causal factors include hemorrhage,
the stimulus of a decreased elevated level of oxygen. vomiting, diarrhea, inadequate fluid intake, or
Restrictive lung disease: a category of lung disease excessive renal loss, resulting in hypovolemia.
involving restriction of the lung parenchyma and Skilled nursing and rehabilitation facilities: an
characterized by stiffness (reduced compliance) and institution or part of an institution that meets criteria
reduced lung volume. for accreditation established by the sections of the
Rheumatoid arthritis: a chronic, destructive, sometimes Social Security Act that determine the basis for
deforming collagen disease that has an autoimmune Medicaid and Medicare reimbursement for skilled
component. Rheumatoid aJthritis is characterized by nursing care, including rehabilitation and various
symmetric inflammation of the synovium and increased medical and nursing procedures.
synovial exudate, leading to thickening of the synovium Spinal cord injury: any one of the traumatic
and swelling of the joint. Rheumatoid arthritis usually disruptions of the spinal cord, often associated with
first appears in early middle age, between 36 and 50 extensive musculoskeletal involvement. Common
years of age, and most commonly in women. The spinal cord injuries are vertebral fractures and
course of the disease is variable but is frequently dislocations, such as those commonly suffered by
marked by remissions and exacerbation. individuals involved in car accidents, airplane
Risk factors: factors that cause a person or a group of crashes, or other violent impacts. Such trauma may
people to be particularly vulnerable to an unwanted, cause varying degrees of paraplegia and
unpleasant, or unhealthful event, such as quadriplegia. Treatment of spinal cord injuries varies
immunosuppression, which increases the incidence considerably and involves numerous approaches,
and severity of infection, or cigarette smoking, which such as exercise, ambulatory techniques, and special
increases the risk of developing a respiratory or physical and psychological therapy.
cardiovascular disease. Stable angina: anginal pain that is well-controlled,
Routine body positioning: the routine use of body medically stable, and has a predictable
positioning in the management of patients to activity/exercise threshold.
minimize the negative effects of static positioning Status asthmaticus: an acute, severe, and prolonged
and maximize comfort. The purposes of routine body asthma attack. Hypoxia, cyanosis, and
positioning are distinct from the specific goals of unconsciousness may follow. Treatment includes
prescriptive body positioning, which are related to bronchodilators given intravenously or by aerosol
optimizing particular components of inhalation, corticosteroids, controlled positive
cardiopulmonary function and gas exchange. pressure ventilation, sedation, frequent therapy,

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G-12 Glossary

and emotional support. A bronchodilator may be myocardium based on perfusion of the area. This
given by aerosol inhalation from a ventilator. agent can be used for rest studies, exercise stress
Stroke volume (SV): the amount of blood ejected studies, and pharmacological stress studies.
from the ventricles during systole. Thoracic cavity: the cavity enclosed by the ribs, the
Stunned myocardium: contractile dysfunction of the thoracic portion of the vertebral column, the sternum,
myocardium as a result of an acute episode of the diaphragm, and associated muscles.
ischemia that persists even after perfusion has Thoracic surgery: the branch of medicine that deals
returned to normal. with disease and injuries of the thoracic area by
Subacute hospitals: hospitals that specialize in the manipulative and operative methods.
management of nonacute conditions. Throat clearing: the spontaneous elicitation of a
Subjective: (I) Pertaining to the essential nature of an coughlike maneuver to clear secretions or an
object as perceived in the mind rather than to a thing obstruction from the oropharynx that may be
in itself. (2) Existing only in the mind. (3) That threatening the upper airway.
which arises within or is perceived by the individual, Tidal volume (TV): the amount of air inhaled and
as contrasted with something that is modified by exhaled during normal ventilation. Inspiratory
external circumstances or something that may be reserve volume, expiratory reserve volume, and tidal
evaluated by objective standards. volume make up vital capacity.
Suctioning: the use of mechanical airway suctioning Total lung capacity (TLC): the volume of gas in the
that uses a catheter and negative pressure to remove lungs at the end of a maximum inspiration. It equals
oropharyngeal or airway secretions when the patient the vital capacity plus the residual capacity.
is unable to spontaneously or voluntarily take deep Tracheobronchial tree (TBT): an anatomic complex
breaths and cough effectively. that includes the trachea, the bronchi, and the
Supraventricular: pertaining to a feature or event bronchial tubes. It conveys air to and from the lungs.
occurring superior to the ventricles of the heart. Tracheostomy: an opening through the neck into the
Surgery: the branch of medicine concerned with trachea through which an indwelling tube may be
diseases and trauma requiring operative procedures. inserted.
Syncytium: the arrangement of cells, as in the Tracheostomy tube/cuff: a tube/cuff that is
myocardium, such that stimulation of one cell causes positioned directly through the trachea in the neck to
stimulation of adjacent cells, thus causing an action provide a functioning airway that bypasses the nares
potential to spread from the initial focus. and oropharynx.
Systemic disease: dysfunction or condition affecting Transitional care units: settings that specialize in
one or more systems. providing care between the acute, subacute, and
Systemic lupus erythematosus (SLE): a chronic long-term stages of a patient's illness.
inflammatory disease affecting many systems of the Transitional circulation: a transition from one type
body. The pathophysiology of the disease includes of blood vessel to another on moving peripherally
severe vasculitis, renal involvement, and lesions of through the circulation.
the skin and nervous system. The primary cause of Treatment selection and prioritization: the process
the disease has not been determined; viral infection of selecting treatments and then prioriti7.ing the order
or dysfunction of the immune system has been in which these treatments are administered. This
suggested. Adverse reaction to certain drugs also process is based on the relati ve contribution of the
may cause a lupus like syndrome. SLE occurs four pathogenesis that each treatment addresses with
times more often in women than in men. respect to oxygen transport deficiencies.
Trunk-ventilation interaction: the interrelationship of
Tachycardia: an abnormally rapid heart rate. the shape and movement of the trunk or chest wall on
Tachypnea: an increased respiratory rate over 20 alveolar ventilation. Trunk and ventilation interaction
breaths per minute. depends on body positioning and movement.
Thallium-20l scan: a radionuclide scan that evaluates Tuberculosis: a chromic granulomatous infection
myocardial perfusion. The tracer is taken up in the callsed by an acid-fast baci Ilus, mycobacterium

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 Glossary G-13

tuberculosis, generally transmilled by the inhalation with high, intermediate, or low probability of
or ingestion or infected droplets and usually affecting pulmonary embolus.
the lungs, although infection of multiple organ Ventilation and perfusion matching: the matching
systems occurs . of ventilation and perfusion in the lungs. Optimal
Type I fibers: a type of skeletal muscle fiber that is ventilation and perfusion matching occurs in the
also called slow-twitch and is suitable for sustained mid zones of the upright lung where the ratio is
tonic activity (e.g., the maintenance of posture or 0.8 to 1.0.
breathing, which require resistance to fatigue). Vital capacity (Ve): a measurement of the amount of
Type IlA fibers: a type of skeletal muscle fiber that is air that can be expelled at the normal rate of
also called fast-twitch; this type of fiber is used for exhalation after a maximum inspiration, representing
short-term, fast, powerful activity in which the greatest possible breathing capacity. The vital
endurance to fatigue is not required. capacity equals the inspiratory reserve volume plus
the tidal volume plus the expiratory reserve volume.
Validity: the extent to which a test measurement or The average normal values of 4000 to 5000 ml are
other kind of device measures what il is intended affected by age, physical dimensions of the chest
to measure. cage, posture, and gender. The vital capacity may be
Valvular heart disease: an acquired or congenital reduced by a decrease in functioning lung tissue,
disorder of a cardiac valve, characterized by stenosis resulting from atelectasis, edema, fibrosis,
and obstructed blood flow or by valvular pneumonia, pulmonary resection, or tumors; by
degeneration and regurgitation of blood. limited chest expansion, resulting from ascites, chest
Ventilation: the process by which gases are moved deformity neuromuscular disease, pneumothorax, or
into and out of the lungs. pregnancy; or by airway obstruction.
Ventilatory strategies: teaching patients to control
breathing with the utilization of ventilatory patterns Work of breathing: the total amount of effort
(e.g., combining inspiration with trunk extension and required to expand and contract the lungs; the
exhalation with trunk l1exion). physiological "cost" of breathing. Generally, quiet
Ventilation-perfusion scan: two scans which are breathing consumes 2% to 3% of the oxygen
used to assess patients for the presence of consumption and requires 10% of the vital capacity.
pulmonary emboli. Criteria (BIELLO or PIOPED) If a greater amount is used, one would say the work
are used to determine if matched defects present of breathing is increased.

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 I N D E X

A bronchiOlitis, 477

bronchitis, 476--477

Abscesses
chronic airflow limitation, 478--481
radiography of, 164, 164

chronic bronchitis, 476--477

respiratory failure and, 579,580t, 581

cystic fibrosis, 483--486

AC; see Assisted control (AC)

emphysema, 478--481

ACB; see Active cycle of breathing (ACB)

hypertension, 488

Acetylcholine, pharmacology of, 780

interstitial pulmonary fibrosis, 486

Acetylcysteine (Mucomyst), pharmacology of, 786

myocardial infarction, 490-491

Acid base balance

pneumonias, 472--476

in arterial blood gases, 153,154

tuberculosis, 487--488

ICU, and, 236, 2361

Acute surgical conditions, primary dysfunction secondruy to, 495-508

respiratory failure and, 619

cardiovascular surgery, 501-502

symptoms of, 236t

extrinsic factors, 500

Acidosis, anaerobic metabolism and, 6

intrinsic factors, 500

Acquired immunodeficiency syndrome (AIDS); see AIDS

mobility/recumbency, 500

Active assistivc cough techniques; sec Airway clearance

pathophysiology, 500

techniques (ACT)

perioperative course, 496, 496-500, 498

Active cycle of breathing (ACB)

postoperative management, 502,502-505, 506, 507

in airway clearance, 325-326

preoperative management, 502

clinical applications of, :149-352, 350, 35 I

surgical effects, 500

Acute dyspnea, patient history and, 130

surgical prep, 499

Acute heart failure, pathophysiology of, 93

thoracic, 500--502
Acute medical conditions, primary dysfunction secondary to,
AD; see Autogenic drainage (AD)

469-492

Adenosine, for stress testing, 199

alveolar proteinosis, 478

Adenosine triphosphate (ATP)

alveolitis, 477-478

nuclear imaging and, 203

angina, 488-490

in oxygen transport, 4, 6-11,13,18

asthma, 481-483

i
Adenosinetriphosphatase pump, tha lium 20 I'and, "200--20 I

atelectasis, 470--472,471

1-1

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1-2 Index

Adolescents, myelomeningocele in, 646, 646

anterior chest compression, 375, 375

Adrenal runetion
co stoph renic, 373, 373-374

cardiopulmonary effects of, 109-110, 110

counter rotation, 375, 376,377

laboratory tests in,193t, 194

hands-knees rocking,38 I -382

Adrenergic drugs, pharmacology of,777-778

Heimlich, 374, 374-375

Adult respiratory distress syndrome (ARDS); see also Respiratory long silting self, 379, 379-380, 380

distress syndrome (RDS) prone on elbows, 378, 378-379

management of, 625, 625--627 self, 377-382

Adventitious breath sounds, patient assessments and,219-220

associated with eating/drinking, 368

Aerobic capacity, cardiac aging changes and, 671,671--674,673,673t

complications, 368-369

Aerobic metabolism, in oxygen transport, 6-8, 10-11

evaluations, 369-371

Aerosol therapy infants, 653, 657

defined, 755-756, 756

patient instruction, 371-372

for oxygen transport treatment, 259-260,260

pumps, 368

precautions in, 756

stages of, 369-371

Afterload physiology and, 321-334

cardiopulmonary physiology of. 65

active cycle of breathing, 325-326

oxygen transport and, 13

assessments,334

Aging changes autogenic drainage,326-327

cardiac, 670, 670-671

contraindications. 330, 330-334

aerobic capacity, 671,671--674,673, 673t

exercise, 329-330

vascular/autonomic, 673, 673-675, 674t

factors affecting, 332, 332-334

pulmonary, 674--677, 675, 675t

The Flutter"", 328

exercise, 675-677, 677, 677t

high frequency chest compression. 328-329

AIDS; see also HIV indications, 322-323

cardiopu Imonary effects of, 110

manual hyperventilation, 325

galliu III scintigraphy for, 206

percussion, 323-324

Air, ambient; see Ambient air

positive expiratory pressure,327-328

Air-conditioned environments, oxygen transport and, 16

postural drainage, 323, 324

Air flow measurements

shaking, 325

airway closure volume, 149,149-150

vibration, 324-325

flow volume curve, 147, 148,149

Airway closure volume tests, 149, 149-150

forced expiration, 147

Airway obstructive diseases,drugs for, 784-785

Airway clearance techniques (ACT) Airway p re s sure release v e ntila t i o n (APR V), defined, 758

clinical applications of, 339-365,365t Airway resistance,physiology of,58-59, 59

active cycle breathing,349-352, 350, 35 I

Airways, al1ificial; see Artificial airways
assessments, 364
Akinesia, nuclear imaging of, 200

autogenic drainage, 352-354, 355

Albumin
costs,363
laboratory tests of, 190, 191t

dynamic air therapy bed,363-364

in oxygen transport, 15

effectiveness, 362
for plasma volume, 234

exercise,359-361, 361t Albulerol (Proventil, Ventolin), pharmacology of, 778

future trends, 363

Alkaline phosphatase, laboratory teSls and, 194, 194t

high frequency chest compression, 358. 358-359

Alkalosis, intensive care of, 579, 580t, 581

intrapulmonary percussive ventilator, 363,364

Allergies, treatment of, 784

manual hyperinflation, 348, 348-349

Alpha-adrenergic blocking drugs, pharmacology of, 778-779

percussion, 344-346,345
Alternative long-term care facilities; see Long-term care facilities

positive expiratory pressure, 354-358,355

Alveolar diseases,radiography of, 162, 162

postural drainage, 340, 340-344, 341,342

Alveolar ducts, anatomy of, 42t, 44

selection of,361,361
Alveolar proteinosis
support, 362-363
management of, 478

utilization of,340
pathophysiology of,86, 86-87,478

vibration/shaking,346-349, 347, 348

Alveolitis

cough/suction for, 367-382

management of,478

active assistive, 373-382

pathophysiology of, 477-478

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 Index 1-3

Ambient air, oxygen transport and, 15-16 chronic secondary dysfunction and
threats/treatment, 261 management of, 558
Aminoglycusides, intensive care and, 579,580t,581 pathophysiology of, 557-558
Aminophylline, pharmacology of, 785 Anorexia nervosa, cardiopulmonary effects 0 1', 1 10-11 1 , II I
Amphctnminc (Dextroilmphetamine, Dexedrine), pharmacology ANS; see Automatic nervous system (ANS)
uL 77R Anterior chest compression, 375, 375
Amylase, lahoratory tcsts of, 193t, 193-194, 194t Antianginal agents, for reus, 572-573
Anaerobic Illcwh"lism. in oxygen transport, 6-8, 10-11. 13 Anticholinesterases, pharmacology of, 781
Analgesic Antihistamines, corticosteroids and, 785-786
for leUs, 572-573 Antiinflammatory agents
fur oxygen transport treatment 259-260, 260 for oxygen transport treatment, 259-260, 260
Anaphylactic rc·actions. trcatment of.777 treatment with, 784
Anatomy Anxiety, oxygen transport threats and, 255
bronchopulmonary segment, 4 I, 42t, 43. 44 Aortic volume, cardiopulmonary physiology of, 66, 66
canliupulmonary.2-'-50 Apnea
circulation. 48--50 cardiopulmonary effects of, 109
heart. 44-4R,45,46,47,48 patient asseSSlnents for, 216
fetal,6Je) respiratory failure and, 579, 580t, 581
lungs.40-A4. 41. 42t, 43 Appearance, patient assessments and, 212-213
lymphatic circulation, 50 APRY; see Airway pressure release ventilation CAPRY)
muscle" 26--40 Arrhythmias
diaphragm, 26, 2li28. 27, 28 electrocardiograms and, 177, 178, [79-184,179-184
erector spi nac 30. 3 I
, supraventricular. 177, 178, 179,179,180,181
expiration, 27. 31-32 ventricular, 180-184, 182, [83, 184
inspiration, 26 intensive care of, 236, 236t, 239
intercostal>. 2R, 29 pathophysiology of, 91-92
larynx. 35. 1536 Arsenic, respiratory failure and, 579, 580t,581
lower airways. 36--40, 37,39t Arterial blood gase s 153-157
,

nose, 32-34, 33, 34 acid base balance and, 153- [54

pectoralis major, 29, 30 assessment purpose in, 153, 157
pe<:toralis minor, 30 chemoreceptorslhypoxemia response and, [55
pharynx, 33, 34-35 excess/deficit in, 154
ribs. 24-25, 25y factors affecting, 156-157
scalenes, 29, 29 hemoglobin and, 155
serratus antcrior. 29-30 interpretation of, 155-156
sternocleidomastoid, 28-29.29 normal values in, 154
trapezius. 30. 30 partial pressure of, 154-155
nerve system, 47,47--48. 48 renal buffering and, 154
patient assessments and, 210-211, 21 I, 212, 213 respiratory failure and, 156
pediatric, 1,36-637 in secondary dysfunction, 427
thorax, 23-25. 24, 25 Arteritis, cardiopulmonary effects of, 102-103, 103
Anesthetics Artificial airways,761-774
cpinephrine and, 777 care of, 768
respiratory failurc and, 579. 580t, 581 endotracheal,772
Angina extubationldecannulation and, 773-774
chronic primary history of, 76 I
management of, 525-526 Montgomery T tubes and, 768
pathophysiolugy of, 525 nasopharyngeal,772
management of, 489--490 Olympic tracheostomy buttons and, 766, 767,768, 768
pathophysiology of. 90-91. 488--489 Passy-Muir valves and, 766, 767,768, 768
Angiography postoperative complications of, 763-764
cardiovascular, 20 [t, 205 mechanical, 764
respiratory, 206 suctioning of, 768,769-771,77 1 ,772, 773, 773t
Ankylosing spondylitis tracheostomy tubes and,764-766, 765,767-771, 768,
cardiopu lmonary effects of. 102-103, [03 77 [-774, 773t

Copyrighted Material
1-4 Index

use of, 761-764, 762

B
Aspiration

Bacterial pneumonias

GI dysfunction and, 107

management of, 475-476

infant aspiration pneumonia in, 642

pathophysiology of, 474-475

meonium aspiration syndrome (MAS), management of, 641-642

Bagging, obstructive lung disease and, primary/lCU, 587

Aspiration pneumonia, pediatric, 642

Barbiturates, respiratory failure and, 579, 580t,581

Assessments; see also specific value being tested, e.g., Blood

Baroreceptors, defined, 783

gases, arterial
Barrel chest, patient assessments for, 214-2 I 6,216

multisystem laboratory, J 89-195

Basal metabolic rate (BMR), in oxygen transport, 19

Assisted control (AC), defined, 758

Beclomethasone, pharmacology of, 785

Assisted mechanical ventilation, defined, 758

Bed rest
Asthma

alternatives to, 293-294

chronic primary
hazards of, 293

management of, 5 I 9-520

indications for, 294

pathophysiology of,S I 9

as therapy, 291-292

pathophysiology of, 77-80, 78, 79, 80,481-483

Benztropine mesylate (Cogent in), pharmacology of, 783

pediatric, 642-M3

Beta-adrenergic blocking drugs, pharmacology of, 778-779

exercise for, 660--66 I

Beta-blocking agents, for ICUs, 572-573

primary, management of, 483

Beta2-receptor stimulants, pharmacology of, 778

primary/ICU, 589-59 I

Bethanechol (Urccholine), pharmacology of, 780

management of, 589-590

Blood
pathophysiology of, 589

complete count, 190--192, 191t

treatment of, 777,784

desaturated, 19

beta2-receptors stimulants for, 778

laboratory tests of, 190-- I 92, 191t

Asymmetrical dysfunction, facilitation and, 405-406

oxygen transport and, I 1-15

Atelectasis

cardiopulmonary physiology of, 67-68,68

differential diagnosis of, 227t

flow, 12, IS

management of, 472

hematocrit, 14

pathophysiology of, 470-472,471

hemoglobin, 11-12,14-15,155

radiography of, 164-165, 165,166

plasma, 11-12,15

respiratory failure and, 579, 580t, 58 I

threats/treatment, 261

Atenolol (Tenormin), pharmacology of, 779

viscosity, 14

Atherosclerosis, pathophysiology of, 89-90

volume, 13-15

Atmospheric air content, oxygen transpol1 and, 15-16

Blood gases, arterial, 153-157

ATP; see Adenosine triphosphate (ATP)

acid/base balance of, 153-154

ATPase pump, thallium 201 and, 200--201

assessments of, 153, 157

Atrial pressure, left, ICU measurement of, 24 I -243

base excess/deficit of, 154

Atrioventricular (A V) conduction, electrocardiograms and, 170-172

chellloreceptors/hypoxemia responses in, 155

Atropa belladonna, extract of, 782

factors affecting, 156-157

AU'opine, pharmacology of, 782

hemoglobin in, 155

Auscultation, 217,217-221, 2J8, 219

ICUs and, 236-237

breath sounds, 218-220, 219

interpretation of, 155-156

chest sounds, 217-218

normal values in, 154

heart sounds, 221-222

partial pressure of, 154-155

secondary dysfunction and, 427

renal buffering and, 154

stethoscope use in, 2 I 7,217

respiratory failure and, 156

techniques for, 217, 218

Blood loss, dextran for, 234

Autogenic drainage (AD)

Blood pressure, oxygen transport threats and, 254

in airway clearance, 326-327

Blood urea nitrogen (BUN), laboratory tests of, 192, 192t

clinical applications and, 352-354, 355

BMR; see Basal metabolic rate (BMR)

Automatic nervous system (ANS), oxygen transport and, 19

Body mechanics; see Positioning, body mechanics

Autonomic nervous system, systemic disease effects on, 106-107

Body positioning; see Positioning

A V conduction; see Atrioventricular (AV) conduction

BPD; see Bronchopulmonary dysplasia (BPD)

Azathioprine, for organ transplants, 718

Bradydysrhythmias, intensive care of, 239, 240t-241 t

Copyrighted Material
 Index 1-5

Bradypnea, patient assessments for, 216 future trends in, 363

Breath sounds, patient assessments and, 218-220, 219 high frequency chest compression, 358, 358-359
abnormal, 219 intrapulmonary percussive venti lators, 363, 364
adventitious. 219-220 manual hyperinflation, 348,348-349
bronchial, 218 percussion, 344-346, 345
bronchovesitular,218 positive expiratory pressure,354-358, 355
extrapulmonary,220 postural drainage, 340, 340-344, 341, 342
vesicular, 218-219 selection of,361, 361
voice. 220 support, 362-363
Breathing utiliwtion of, 340
control in, 53-55,54 vibration/shaking, 346-349. 347,348
exercise testing/training in cough/suction, 367-382
primary dysfunction, 420, 420-421 anterior chest compression, 375, 375
seconoary dysfunction,435-436 complications of, 368-369
glossopharyngeal, 410-412,412 costophrenic, 373,373-374
laterRI costal facilitation of, 396, 397, 399, 399 counter rotation,375, 376, 377
mechanical function 01',56-59,57,58,59 eating/drinking type, 368
oxygen transport treatment and, 261 evaluation of, 369-371
patient assessments and, 216 hands-knees rocking,381-382
patterns Heimlich, 374, 374-375
musculoSKeletal/neuromuscular disorders,689, 691-693, long sitting, 379, 379-380, 380
692,693,694,695 patient instruction and, 371-372
paced,435-436 prone on elbows, 378, 378-379
paradoxical. 438-439 pumps, 368
physiology of, 321-334 self, 377-382
active cycle of breathing,325-326 stages of, 369-371
assessments in, 334 Bronchi, radiography of, 162, 162
autogenic drainage, 326-327 Bronchial breath sounds, patient assessments and,218
contraindications for,330,330-334 Bronchial muscle relaxants
exercise, 329-330 ephedrine as, 778
factors affecting, 332,332-334 inhaler treatment and,784, 785
The F1utterT", 328 Bronchiectasis
high frequency chest compression, 328-329 chronic primary
indications for, 322-323 management of, 520-521
manual hyperventilation and, 325 pathophysiology of, 520
percussion and, 323-324 pathophysiology of, 80, 80-83, 81
positive expiralOry pressure, 327-328 mdiography of, 162, 163, 164
postural drainage and, 323, 324 Bronchiolitis
shaking and, 325 acute medical conditions, primary secondary to, 477
vibration and, 324-325 cardiopulmonary effects of, 102-103, 103
repattcrning in, 393 management of, 477
secondary dysfunction pathophysiology of,477
exercise testing/training and, 435-436 Bronchitis
paced,435-436 chronic
systemic disease effects on, 104 differential diagnosis of,227t
Breathing clearance techniques management of, 515-516
active assistive, 373-382 pathophysiology of, 72-73,76-77, 514-515
airway (ACT), 339-365, 365t chronic primary
active cycle breathing, 349-352, 350,351 management of, 476-477
assessments of, 364 pathophysiology of, 476-477
autogenic drainage, 352-354, 355 Bronchodilators
costs, 363 betarreceptors stimulants as, 778, 779
dynamic air therapy bcd, 363-364 for leUs, 572-573
effectiveness of, 362 metered-dose inhalers, 723-724
exercise, 359-361, 361t for oxygen transport treatment, 259-260, 260

Copyrighted Material
1-6 Index

Bronchograms,radiography of,162, 162

arrhythmias,91-92

Bronchopulmonary dysplasia (BPD),preterm infants and,641

chronic hean failure,93-94

Bronchopulmonary segments, anatomy of,41,42t, 43,44

compensated/decompensated heart failure, 94

Bronchovesicular bn:ath sounds, patient assessments and,218

congestive heart failure, 93

Buildings,health issues and,16

coronary artery disease, 89-90, 91-94

Burns myocardial infarction, 91-93

respiratory failure and, 579,580t,581

patient classification and,133

secondary dysfunction and

patient history and, 133

management of,613-615
pediatric,639t,639-640

pathophysiology of, 612--{)13

respiratory failure and,620

BUlleLfly techniques,ventilation facilitation and,408,409,410 systemic, 100-101

fluid balancc effects of,101

c
ischemic, 109

II C acetate,for cardiovascular testing,201t,203

Cardiac function

CAD; see Coronary artery disease (CAD)

afterload in,13

Cameras, for nuclear imaging,198-202

aortic volume and,66, 66

Capillary function,in oxygen transport,18

cardiopulmonary physiology of, 65,65-67,66, 67t

Carbachol (Carcholin),pharmacology of,780-781

electrocardiograms and, 169-187

Carbohydrates,laboratory tests of,194, 194t

arrhythmias, 177,178,179-184,179-184

Carbon dioxide
conduction, 170-172,171

ambient air/oxygen transport and,15-16

blocks, 184--186, 185, 186

transport physiology of,68-69

evaluation of, 174, 174--177,175,176,177

Carbonic anhydrase,in C02/H02 reactions, 14

myocardial infarction, 186-187, 187

Cardiac aging changes

rate, 174, 174-176, 175, 176

aerobic capacity,671, 671-674, 673,673t

recording, 172, 172-174,17,1

defined,670, 670-671
rhythms, 176- 177, 177

vascular/autonomic, 673, 673-675, 674t

use of, 169-170

Cardiac arrest, treatment of, 777

heartbeat physiology and, 66

Cardiac aLThythmias
left atrial pressure, 241-243

electrocardiograms and, 177, 178, 179-184, 179-184

myocardial contractility in, 13

supraventricular, 177,178, 179, 179, 180, 181

myocardial viability and, 202-203

ventricular, 180-184, 182, 183, 184

myocardial workload reduction and,592, 59l-594, 596

intensive care of, 236, 236t,219

nuclear imaging of,200

pathophysiology of, 91-92

output in, 11,12,14,17,636

respiratory failure and,619-620

patient assessments in,220-221

Cardiac development preload, Il

anatomy of,44-48,45,46,47,48
septal defects/ICU and,245

fetal, 636
ventricular

neonatal,636
diastole/systole,66

Cardiac disorders
left assist devices/lCU,245

dyspnea/patient history and,134

left ejection fraction, 200

exercise testing/training in, primary dysfunction,419

left end diastolic volume, 13

fluid balance effects of,101

left fetal anatomy of,636

functional/therapeutic classification of, 133

left output,636

ischemic,109
left pressure/ICU, 241-243, 245

left ventricular assist devLces,245

right ejection fraction, 200

myocardial infarction
right pressure/1CU,241-243

chronic primary dysfunction and,526-528

Cardiac sounds,patient assessments and,221-222

management of,490-491
Cardiac surgery

pathophysiology of,91-93,490
ICUs and, 245

myocardial ischemia,245
open heart, 595,596

oxygen transport threats and,254

CaJdiac transplants

treatment,261
acute phase care in,710-7 I 1,714

pathophysiology of
assessments in,708

acute heart failure, 93

considerations jn

Copyrighted Material
 Index 1-7

availability. 704 lCUs and

ethical. 704-705 monitoring systems, 229-246
organ donation, 704 patient management, 565-577
organ preservation, 704 primary dysfunction, 579-596
patient education, 706 incentive spirometry and, 754, 755
p ychosocial impl icat ions, 705-706 intermittent positive pressure breathing and, 753-755
purpose of. 704 laboratory assessment and, 189-195
trcnds in. 706 lung injury and, 625, 626
waiting list criteria. 705. 705 measurements and, I 17-123
waiting time. 705 mechanical ventilation and, 756-759
when to lise, 704 musculoskeletal/neuromuscular disorders and. 679-701
equipmcnt/monitoring in, 708-709 neonatal, 635--{i63
cxercise guidelines in. 712 nuclear imaging/radiopharmaceuticals and. 197-207
facility vs. home based rehabilitation in, 716-718 organ failure and, 628t, 628--{i29
goals in. 712 oxygen thera py and, 749-753
history of. 704 oxygen transport in, 3-20
interventions in. 710-711, 714 pathophysiology of, 71-95, 251-263
medication in. 716-718 patient assessments in. 209-228
other tr lI1splants and, 709-710 patient education and, 453-463
outpatient care in, 713-714, 714 patient history in, 127-142
pos t-transplant care in , 70S pediatric, 635-663
pre-transplant care in. 70H physical therapy role in, 3-20
rej ec tion signs in, 714, 715, 716 physiology in, 53--{i9
surgery and, 706 positioning and, 299-318, 737-747
therapy in postoperative complications and, 621, 621-624, 622
assessments, 707-708 primary dysfunction and
tlefined, 708-709, 710. 710-713 acute medical conditions and, 469-492
medical management. 707, 707t acute surgical conditions and. 495-508
musculoskeletal considerations, 707, 709-710 chronic, 513-535
physiology and, 707 ex e rcise testing/training in,417-423
therapist rt' quiremcnts, 706 rcus and, 579-596
Cardiogenic shock. ICUs and, 245 pulmonary aging changes and, 674-677
Cardiopulmonary failure, primary. intensive care of, 579, 580t, 581 pulmonary function tests and, 145-151
Cardiopulmonary function respiratory failure and, 617--{i30
acute medical conditions and, 469-492 respiratory muscle fatigue and, exercise training,443-451
acute surgical conditions and, 495-508 secondary dysfunction in
aerosol therapy and, 755-756, 756 chronic, 537-561
airway clearance techniques and, 339-365, 365t exercise testing/training in, 425-441
cough/suction, 367-382 lCUs, 599-615
physiology,321-334 sepsi:; and, 628t, 628-629
anatomy in. 23-50 shock and, 627--{i28
arterial blood gases in, 153-157 systemic diseases and, 99-112
artificial airways and, 761-774 transplant patients and, 703-718
cardiac aging changes and. 671--{i74 treatment in, 256-263, 257,258-259,260,261,262
chronic primary dysfunction and. 513-535 ventilation facilitation and, 383-415, 756-759
chronic secondary dy sfunction and, 537-561 x-ray interpretation, 159-167
documentation and, 12:1-126 Cardiovascular disease, chronic primary
drug and,775-7R6 management of, 525-535
exercise/mobility and. 265-296 pathophysiology of, 525-535
exercise testing/training in Cardiovascular reflex, defined, 783-784
pri mary dysfunction. 417-423 Cardio va:;cular su rgery , p rimary dysfunction secondary to,
secondary dysfunction,425-441 501-502
horne-based/facility care and, 721-732 Carotid barorece ptors, defined. 783
humidity therapy and, 755 Carrying, primary dysfunction and, 4 I 9-420

Copyrighted Material
1-8 Index

Cascade oxygen, defined, 12, 12

ventilation facilitation and,392

Case studies
Chest tubes, in ICUs, 235, 235-236

exercise testing/training in, secondary dysfunction, 437--440. Chest walls

438,439 oxygen transport and, 16-17

patient assessments and, 225-228

patient assessments and, 214-216, 216

Catecholamines, laboratory tests of,194

restriction effects on, 102-103, 103

Catheters,in (CUs
Chloroflurocarbon propellants, for metered-dose inhalers, 786

Swan Ganz,233,241-243, 243

Cholesterol,laboratory tests of, 191, 191 t

two-lumen, 241-242
Cholinergic blocking drugs,pharmacology of, 782

CBC; see Complete blood count (CBC) Cholinergic drugs,pharmacology of,780-781

Cellular respiration Chronic airflow limitation

oxygen transport and, 3, 4-8, 10
management of, 481

oxyhemoglobin dissociation and, 15

pathophysiology of, 478--480.514

Cellular responses, exercise and. 269-270

Chronic airway obstruction disease (COA), pathophysiology of,

Central chemoreceptors, cardiopulmonary physiology of,54

71-72

Central nervous system (CNS)

Chronic bronchitis
amphetamines and,778
differential diagnosis of, 227t

oxygen transport and, 253

management of, 515-516

treatment of, 261

pathophysiology of, 72-73,76-77,514-515

systemic disease effects on, 103,105-106

primary
Central venous pressure (CYP), ICUs and,243-244
management of, 476--477

Cerebral palsy
pathophysiology of,476--47 7

cardiopulmonary effects of, 104

Chronic heart failure (CHF),pathophysiology of, 93-94

chronic secondary dysfunction and

Chronic obstructive airway di se a se (COAO), pathophysiology of,

management of, 546-547

71-72

pathophysiology of, 546

Chronic obstructive lung disease (COLD), 71-72

Cerebrospinal fluid (CSF), cardiopulmonary physiology of, 54

pathophysiology of, 71-72

CF; see Cystic fLbrosis (CF)

Chronic obstructive pulmonary disease (COPO)

Chemical vagotomy, defined, 783

patient assessments in, 214-2 J 5,222,224

Chemoreceptors respiratory failure and, 579, 580t.581

cardiopulmonary physiology of
Chronic primary dysfunction
central, 54
angina,525-526

peripheral, 54-55
asthma,519-520

response to hypoxemia and, 155

bronchiectasis, 520-521

Chest development, in musculoskeletaVneuromuscular disorders,

chronic airflow limitation, 514

682-689,684-689,686t
chronic bronchitis, 514-516

Chest pain, patient history and, 137-138

cystic fibrosis, 521-522

esophageal, 139
diabetes mellitus, 533-535

pericardial,139
emphysema, 516-518

pleuritic,138
hypertension, 531-533

pulmonary hypertension, 139

interstitial lung disease, 522-523

Chest radiographs, lateral, 159-160

lung cancer,523-524

Chest sounds, patient asse ssments and, 217-218

myocardial infarction,526-528

Chest therapy
obstructive patterns in, 514-522

child, 657-660, 658

peripheral vascular disease,529-531

positional rotation, 658-659,659, 660

primary cardiovascular disease, 525-535

pre/postoperative, 659-660
restrictive patterns in, 522-523

compression
valvular disease, 528-529

anterior, 375, 375

Chronic renal insufficiency, chronic secondary dysfunction and

high freq uenc y, 358, 358-359

management of,560-561

infant pathophysiology of, 560

airway suctioning, 653, 657

Chronic secondary dysfunction

percussion, 652---{i53, 657

ankylosing spondylitis and, 557-558

positional rotation, 649,649,650-651

cerebral pal sy and, 546-547

postural drainage, 652,653t, 654---{i56

chronic renal insufficiency and, 560-561

Copyrighted Material
 Index 1-9

L ollagen v<ls u"lIkonn ctivc tissue diseases and, 555-556

' ischemic heart disease and, 109
hemiplegia and. 541-543 pathophysiology of, 93
Intc sequelae or poliomyd itis and. 550-552 pleural effusions and, 101
lllltitirk sL'icrosis and, 544-546 primary/lCU, 594, 594, 596
l11usL'lIlar dystrophy and, 5]8-5]9 radiography of, 164 165, 166,167
,

osteoporosis and, 553-555 Connective tissue disorders

P<lrkinson's disease and, 543-544 chronic secondary dysfunction and
rheum atoid arthrilis and, 558-560 management of, 555-556
scleroderma <Ind. 556-557 pathophysiology of, 555
spinal L'Ilrd injury and. 54t\-550 systemic, cardiopulmonary effects of, 103, 103
systemic lupus erythematosus ancl. 555-556 Consumption, oxygen; see Oxygen, consumption
thoracic JdUllllitics and, 552-553 Content, oxygen; see Oxygen,content
Circul'ltion Continuous positive airway pressure (CPAP)
anatomy in. 40-49 defined, 758
fetal. 636 for oxygen transport treatment, 259-260, 260
neo nata l, 636-6]7 Controlled mechanical ventilation (CMV), defined, 758
peripheral Contused lung, respiratory failure, 579, 580t, 581
anatomy in. 4R-49 COPD; see Chronic obstructive pulmonary disease (COPD)
in oxygen tJ'ansrort, 18 Coronary artery disease (CAD)
physiology of, fl7, 67t associated conditions of, 90-94
threats/trealment,262 cholesterol and, 191, 191 t
pulmonary. threats/treatment, 261 pathophysiology of, 71,89-90,91-94
Clol1idine (Catarrcss), pharmacology of, 779 primary/lCU
Closing volumL'fairway closure, pulmonary function tests and, 149, management of, 593-596
1 49 150 pathophysiology of, 592-593
Closure of ductus arterimus, pediatric anatomy and, 636---63 7 single photon emission tomography (SPECT) for, 199
Closure or' foramen ovale, pediatric anatomy and,636---637 transplant medication and, 716
Clubbing Corticosteroids
Crohn's disease and, 214, 214 Cushing's syndrome and, 785
hepatic fibrosis and. 214, 214 pharmacology of, 785
patient assessments for, 214, 214 Costophrenic assist techniques, 373, 373-374
CMY; see Controlled mechanical ventilation (CMY) Costs, airway clearance techniques and, 363
CNS; see Central nervous system (CNS) Cough
COA; see Chronic airway obstruction disease (COA) active assistive, 373-382
COAD; see Chronic obstructive airway disease (COAD) anterior chest compression, 375, 375
Co gulation, laboratory tests and, 190, 191t costophrenic, 373, 373-374
Cognition, oxygen trans port threats and, 255 counter rotation, 375, 376, 377
COLD; see Chronic obstructive lung disease (COLD) hands-knees rocking, 381-382
Collagen vascular/connective tissue diseases. chronic secondary Heimlich, 374, 374-375
dysfunction and long sitting self, 379, 379-380, 380
management of, 555-556 prone on elbows, 378, 378-379
pathorhysiology of, 555 self, 377-382
Collimatol.s. Jcfined, 19R complications of, 368-369
Combined ventriL'ular output (CVO), fetal anatomy of, 636 eating/drinking and, 368
Community concerns. home-based/facility care, 721-7]2 evaluation of,369-371
Complete blood count (CBC), laboratory tests and, 190-192 191t
, in museuloskeletalfneuromuscular disorders, 698
Comrliance, cardiopulmonary physiology or. 56-57, 57 obstructive lung disease and, primary/lCU, 588
Computerized tomography (CT), for respiratory use, 206-207 patient history and, 135, 136t, 137
Conduction, ck troeardiograrns and, 1 70- 172 171
, patient instruction and, 371-372
blocks, 184-186, 1 5, 186 pumps and, 368
CongenitaJ. IKart disC'asc reflex physiology of, 55
neonate s and, 6.\9-640 stages of,369-371
patent ductus arterio>lIs and, 639-640 suction and, 367-382
Congestive hemt failure (CHF) Counter rotation
intensive carc or. 2]5, 245 assist techniques,375, 376, 377

Copyrighted Material
1-10 Index

for ventilation, 407-408. 409

chronic primary dysfullction and

CP; see Creatine phosphate (CP) management of, 533-535

CPAP; see Continuous positive airway pressure (CPAP)

pathophysiology of, 533

Crackles,defined, 219-220
Diaphragm
Craniosacral therapies, secondary dysfunction and, 437
anatomy of. 26,26-28, 27, 28

Creatine phosphate (CP), in energy transfer, 8

contractilit y and, 444-448

Creatinine, laboratory tests of, 1 92t. 192-193

movement and, 222, 223

Crepitus, defined, 223

ventilation facilitation and

Cricoarytenoid arthritis. respiratory failure and, 579. 580t, 581

breathing, 389, 390, 391,392.394,394, .105, 396, 396

Critically ill patients

inhibition, 402-405, 404. 405

acidosis/anaerobic metabolism in, 6

Diastole, ventricular physiology of. 66

arterial blood gases in, 156

Dicyc10mine (Bentyl), pharmacology or, 783

oxygen consumption in, 13

Di fferential diagnosis, patient assessments and. 227t

oxygen transport in, 3

Diffuse interstitial pneUillonitis, cardiopulmonary effects of,

respiratory failure and, 156

102-103, 103

Crohn's disease, clubbing and, 214, 214

Diffuse interstitial pulmonary fibrosis, pathophysiology of, 83-85

Cromolyn sodium (Intal), pharmacology of, 785-786

Diffusion
Cross-referrals, in home-based care, 728-729
cardiopulmonary physiology of, 60, 60-61

Crystal cameras, for Duclear imaging, 198

oxygen transport and,5. 12, 17

CSF; see Ccr\!brospinal fluid (CSF) Diphosphoglycerate (DPG), in oxygen transport, 15

CT; sec Computerized tomography (CT) Dipyridamole, for pharmacologic stress testing. 199

Curariform drugs,respiratory failure and, 579, 580t, 581

Discharge, from ICUs, 574

Cushing's syndrome, corticosteroids and, 785

Disseminated intravascular coagulation, pulmonary hemorrhage

Cyanosis and, 108

intensive care of, 240

Disseminated intravascular coagulation (DIC), laboratory tcsts of,
patient assessments and, 214
190,191t
Cyclopentolate (Cyclogyl), pharmacology of, 783
D02; see Oxygen, delivery
Cyclosporin, for organ transplants, 717-7 J 8
Documentation, 123-126

side effects of. 718

assessments and. 1 25- J 26

Cystic fibrosis (CF) content for, 124

management of, 484-486. 521-522

exercise testing/training and, secondary dysfunction,426-432

pathophysiology of, 483-484, 521

in homellong-term care facilities, 727

patient assessments and. 225. 227

objective. 125

pediatric
plans and. 126

exercise for. 661

pur'pose of, 123

pathophysiology of, 643

recording electrocardiograms and. 172, 172-174, 173

Pseudomonas aeruginosa and, 643--&14

subjective, '124-125

respiratory failure and. 579, 580t, 581

types of, 123-124

Doppler echocardiography, defined, 20 It, 204

D
Down syndrome

2D echocardiography, defined, 201t. 203-204. 205

cardiology of, 639t
Dead space. defined,145-146
managcment of. 645t, 646--647. 647

Death Doxazosin (Cardura), pharmacology of, 778

exercise and dying patients, 576-577, 577

DPG; see Diphosphoglycerate (DPG)

ICUs and, 576-577, 577

Dressing techniques, ventilation Lrcilitation and, 389

patient fear in, 577, 577

Drinking, coughs associated with, 368

Debt. oxygen; see Oxygen, debt Drugs, 775-786

Deep vein thrombosis, management of, 623-624

for airway obstructive disease,784-785

Delivery, oxygen; see Oxygen,delivery

autonomic pharmacology of, 776

Demand, oxygen; see Oxygen. demand

rcus and, 572-573

Desaturated blood/C02, oxygen transport and, 19

immunosuppressive,717-718, 718

Dextran, for blood loss, 234

in intensive care, 572-573

Diabetes mellitus pharmacology of

cardiopulmonary effects of, 109
adrenergic agents,777-778

Copyrighted Material
 Index 1-11

anticholineSterascs.781 E
antihistamines, 785-786

Eating. coughs associated with, 368

antiinflammatory agents, 784

Eccentric resistance techniques. ventilation facilitation and. 414

beta- Ad rene rg ic blocking dru!!s. 778-779

ECD; sec Endocardial cushion defects (ECD)

bet32-receptors stimul ants, 77 8

ECG; see Electrocardiograms; Elect r ocardiograms (ECG)

bronchial muscle re l a x ants. 778

Echocardiography
bronchodilators. 778, 779

defined, 20 I t, 203-205

cholinerg i c blockin g drugs, 782

M -mode, 20 I t, 203-204, 205

cholinergic d rugs. 78{}-78 I

Edem a
cort icos tcroi C\s . 785

patient assessments and. 223

cxpeetor'lnts. 785, 786

patient history and, 14{}-141

inhalers. 777, 786

r adiogra phy of, 165, 166

mucolytics, 786

Edrophonium (Tensilson), pharmacology of, 782

sympaiholytic drugs. 779

Education, patient, 453-463

sympathomimctic drugs, 7R4-7X5

defined, 454-456

vasa Iilators, 777. 778

Down syndrome, 645t, 646-647, 647

xanthines. 785

effectiveness in, 461-462

rcspiratorylcardiovascular systems and. 775-776

fundamentals of, 454-456

sympathetic ncurotransmission of, 776

interdisciplinary care and, 463

for trans plant pa tients

leaming needs assessments and, 457, 459

cardiac, 716-- 718

,Ireas, 457,457.459

pulmonary . 717-718

findings, 459

Dry environments. oxygen transport and, 16

goals, 459

DTPA (Tel; see Tcchnetium-99M-diethylcne triamine penta-acetic

tools. 457

(DTPA) aerosol
methods in, 459-461, 460t, 461

D uchcn ne ' s musc ular dystrop hy

needs-based, 456

card io logy of. 639t

patient adherence and, 462

management oj', 647--648

teacher-learner relationship and, 462

Dynamic activitics, ventilation facilitation and, 388·-389

Edward's syndr o m e, cardiology of, 639t
Dynamic a ir therapy bed. clinical applications of, 363-364

EEG; see Electroenc e phalograms (EEG)

Dynamic ail ther a py l " beLl. clinical a p p l ications and. 363-364

Elect r oc ardiograms (ECG), 169-187

Dys func tion; see speci fic typcs, e.g . . Primary dysfun ction.
arrhythmias and. 177, 178, 179-184, 179-184

Secondary dysfunction
conduction and, 170-172, 171

Dyskinesia. nucie,lr imaging of. 200

blocks, 184--186, 185, 186

Dyspnea
evaluation of, 174. 174-177, 175, 176, 177

pat ient assessments and. 216

in lCUs, 238. 239-241, 240t-241t

patient history and. 128-·130. 129. 134-135

myocardial int'arction and, 186-187. 187

acute, UO

recording of, 172, 172- I 74, 173

in cardiac patient s . 134

use of, 169-170

exercise limiting, 1 31t

Electroencephalo grams (EEG), in IC U s, 246

on exertion. 13{}-131. 131t. 132, 132t. 133.133, 134

Electrolyte abnormalities, respiratory failure and, 6 I 9

fu nc tio n al, 135

El ect rolyte balance

onhopnea. 134

ICUs and, 23{}-231, 234t, 234-235

paroxysmal noctumal. 134-135

laborato r y tests and, 191t, 191-192

platypnea. 135

oxygen transport and, 13-14

trcpoplH:a. 135

Elevations, high; see High elevation environments

Dysrhyt h mias
Embolism. pulmonary, differential diagnosis of, 227t
ca rd iopulmona r y effects or. 101

Emotional stress

electrocardiograms and. 177, 17X. 179-184. 179-184

fight/f1ighUfright and, 20

supraventricular . 177. 178. 179. 179, ISO, 181

oxygen transport and, 3

ventricular. 180-184. 182, 183. 184

Emphyse ma
i nte n si vc care or. 236, 236t. 239

chronic primary
pathophysiology oc. 91-92

management of. 517-518

Copyrighted Material
1-12 Index

pathophysiology of, 5 16-5 17

dyspnea and
differential diagnosis of, 227t
on exertion, 130- 13 1. 13lt. 132. 132t,133. 133, 134

management of, 478-481

limiting, J3 l t
pathophysiology of, 73,73-77,74. 75,76,77,478-48 1
intensity/duration of, 723

patient assessments and, 227-228

long term respons s of. 278-280,279

radiography of. 162, 163

monitoring and, 275, 285-286, 288, 289, 290. 29 1-292

Endocardial cushion defects (ECD), management of, 640

multisystem effects of. 278-280, 279

Endocrine disorders
oxygen transport and. 8. 10- 12, 13. 19

cardiopulmonary effects of, 109- 1 10, 110

oxygen transporUmetabolic demand and. 267-268,268. 270

laboratory tests and, 193, 193t

pathophysiological conditions and. 270-271. 27 I

Endotracheal artificial airways, 772

for pediatric asthma. 660-661

Energy transfer, oxygen transport and, 4. 6--8,8, II

prescription for, 266--267. 268, 270-276. 273. 274t. 276. 278t

Enhancement ratio, oxygen; see Oxygen, enhancement ratio

preventive effects of. 291-292. 295

Environment
pulmonary aging changes and, 675-677,677. 677t

ICU, 576, 576y stimulus in. 277-278, 278

oxygen transport and. 15- 16

stress and. 20

Eosinophilia, pulmonary, pathophysiology of, 85

testing/training and
Eosinophilic granulomas, pathophysiology of, 85-86
prescriptions in, 274,274. 276--277,280-285,281. 282t,

Ephedrine, pharmacology of, 778, 785

283t. 284--286, 290,290-29 1

Epiglottitis, respiratory failure and, 579,580t,58 1

primary dysfunction, 417-423

Epinephrine
breathing, 420,420-421

laboratory tests and. 194

guidelines, 42 1-422

pharmacology of, 777. 778, 784

heart disease. 419

reversal of. 778

lung disease, 4 17-4 18

Eq uipment traditional, 422-423

for active cycle breathing (ACB), 349-352. 350, 351

upper/lower extremity, 4 19-420

for autogenic drainage, 352

secondary dysfunction, 425-441

for exercise airway clearance, 359-361, 36 1 t

breathing training, 435-436

for high frequency chest compression, 358,358-359

case studies, 437-440. 438. 439

for manual hyperinflation, 348. 348-349

evaluation, 426-432

for percussion, 344

patient history. 428,428. 429, 430

for positive expiratory pressure, 354--355 patient management. 432-433. 435

for postural drainage, 340,340-344,34 1,342

psychological factors. 425-426,426

for shaking, 346--349. 347, 348

testing guidelines, 430-43 I

for transplant patients therapeutic options, 436-437

cardiac, 708-709
training guidelines. 43 1-432,432

pulmonary, 708-709, 7 15
training and prescription for, 722-723

for vibration. 346--349, 347, 348

for transplant patients,cardiac, 7 I 2

Erector spinae. anatomy of, 30, 3 1

Exercise stress testing, nuclear/cardiovascular. 199

Ergometers, for oxygen transport treatment. 259-260. 260

Expectorants, pharmacology of. 785. 786

Erythrocyte disorders. cardiopulmonary effects of, 108

Expiration

Escherichia coli, in bacterial pneumonias, 474-475

forced. 147

Esophageal chest pain, patient history and. 139

muscle anatomy in. 27, 31-32

Ethical considerations. transplant patients and. 704-705

ventilation facilitation and, 388

Eupnea. patient assessments and. 2 1 6

External thorax manipUlation, contraindications for,331, 331-332

Exercise. 8 , 10- 12. 1 3 , 1 9

Extrapulmonary breath sounds, patient assessments and, 220

acute responses to. 270-271. 27 1. 272. 273, 274. 274t

F
airway clearance teChniques and. 329-330. 359-36 1. 361 t

assessment of. 295-296

18F-f1uoro-deoxyglucose (FOG), for cardiovascular testing. 20 1t. 203

bed rest and. 291. 29 1-295

Facility-based care

cardiac aging changes and. 671, 67 I -674,673. 673t

concerns in, 723

cellular responses to. 269-270

documentation in, 727

deconditioning effects and, 723

monitoring in

defined. 265-266
cardiopulmonary, 725. 725-726

dying patients and, 576--577. 577

oxygen, 726--727

Copyrighted Material
 Index 1-13

for transplant patients

Friedreich's ataxia, cardiology of. 639t

cardiac, 716--718
Fright/flight/fight reactions; see Fight or flight syslCms

pulmonary, 716--718 Function optimization, defined, 570, 571

work consideratIons in, 724-725

Functional reflex, defined. 783-784

FAD; see Flavin adenine dll1uclcotide (FAD)

G
Family history, patients and, 142

Fatigue. patient history and, 140

Gallium scintigraphy, for respiratory testing,206

FDG; sec 18F-fluoro-deoxyglucose (FDG) Gallops, patient assessments and, 221

Fear Gamma cameras,defmed, 198

dying patients and, 577, 577

Ganglionic blockade,defined,781

oxygen transport threats and, 255

Gas exchange
FET; see Forced expiratory techniques (FET) cardiopulmonary physiology of

Fetal alcohol syndrome (FAS), cardiology of, 639t

diffusion, 60, 6 61

Fetal development, circulatory, 636

perfusion, 6 J -65,62, 63,64

Fetal disorders exercise testing/training in,primary dysfunction, 418

fetal alcohol syndrome, 639t in oxygen transport, 5,16

meconium aspiration syndrome,641-642

diffusion,5,12, 17

Fibrinogen, oxygen transport and, 15

perfusion, 17

Fibrobullous disease, cardiopulmonary effects of, 102-103, 103

ox ygen transport threats and, 254

Fibrosis
Gaseous vapors, environmental effects of, 16

cardiopulmonary effects of, 102-103, 103

Gases, arterial blood; see Arterial blood gases

diffuse interstitial pulmonary, pathophysiology of, 83-85

Gastrointestinal disorders

Fight or flight systems

respiratory failure and,620

oxygen transport and, 20

systemic effects and, 107, 107

parasympathetic system and, 776

Glaucoma,treatment of, 78 781
First pass radionuclide testing, cardiovascular, 199, 20 It
Glossopharyngeal breathing, ventilation facilitation and,
Fixed position radiographs. interpretation of, 159-160
410--412,412
FK 506, for organ transplants, 718
Goals
Flail chest, patient assessments and, 214-216, 216
for home-based care,73 732, 731, 732

Flavin adenine dinucleotide (FAD), in energy transfer, 8

for lCU patient management, 568-572,570

Flight or fight systems

for musculoskeletal/neuromuscular disorders, 70 70 I

ox ygen transport and, 2 0

for transplant care, 709,712, 713t, 715

parasympathetic system and. 776

Gravitational flow, physiology of, 61-65, 62, 63, 64

Flow Gravitational stress, oxygen transport and, 19-20

blood in oxygen transport,12, 15

Gravity

gravitational, 61-65, 62,63, 64

body positioning and,300-301, 301

volume curve, 147, 148, 149

in musculoskeletal/neuromuscular disorders, 68 687,
Fluid balance 682-687,686t
cardiac effects on, 101
Guanethidine (lsmelin), phalmacology of, 779

cardiopulmonary physiology of, 67,67t

Guillain-Barre syndrome, respiratory failure and,579, 580t, 581

hematologic conditions and, 108

H
ICUs and, 230-231, 234t, 234-235

oxygen transpol1 and, 13-14, 17

Hands-knees rocking assist techniques, 381-382

plasma protein disorders and, 109

Hct; see Hematocrit (Hct)

respiratory failure and,619

HDL; see High-density lipoproteins (HDL)
systemic disease effects on, 101-102
Head down body positioning,312

Fluid collection, in ICUs, 235, 235-236

Head injuries, secondary dysfunctionlICU

Fluid volume, oxygen transport threats and, 255

management of, 606-609, 608

FluLlerrM, for airway clearance, 328

pathophysiology of, 606--609, 607

Flutter valves, for oxygen transport treatment, 259-260, 260

Health issues, oxygen transport and, 16

Forced expiration, pulmonary function tests and, 147

Heart anatomy, 44--48, 45,46, 47,48

Forced expiratory techniques (FET), active cycle breathing and, Heart block, treatment for, 777

349-352,350,351 Heart disorders

Fractures, secondary dysfunctionllCU and, 605-606
exercise testing/training in, primary dysfunction,419

Friction rub, defined, 220

fluid balance effects of, 101

Copyrighted Material
1-14 Index

ischemic. 109
left ejection fraction,200

myocardial dysfunctionlrespiratory failure and, 620

left end diastolic volume, 13

myocardial infarction
left output, 636

chronic primary dysfunction and,526-528

left pressure, 241-243

management of,490-49 j
Heart sounds,patient assessments and, 221-222

pathophysiology of, 91-93,490,526

Heart surgery

myocardial ischemia,245
ICUs and,245

myocardial perfusion, 202-203

open,595,596

oxygen transport threats and. 254

Heart transplants

treatment,261
acute phase care in. 7 J07 ll, 714

pathophysiology of
assessments in, 708

acute heart failure,93

considerations in

arrhythmias. 91-92
availability, 704

chronic heart failure, 93-94

ethical, 704-705

compensated/decompensated heart failure, 94

organ donation,704

congestive heart failure, 93

organ preservation, 704

myocardial infarction, 91-93

patient education, 706

patient classifIcation and, 133

psychosocial implications,70S-706

patient history and,1:l3

purpose of,704

Heart failure
trends in, 70G

acute,pathophysiology of,93
waiting list criteria, 70S,70S

compensated/decompensated. pathophysiology of, 94

waiting time,705

congestive
when to use,704

intensive care of,235,245

equipment/monitoring in,70S-709

ischemic heart disease and,109

exercise guidelines in, 712

pathophysiology of, 93
facility vs. home based rehabilitation in,716-718

pleural effusions and,101

goals in. 712

primary/lCU, 594,594,596
history of, 704

radiography of,164, 165, 166, 167

interventions in, 7 J0 711, 7 I 4

respiratory failure and,579, 580t,58 I

medication in,716-718

Heart function
other transplants and,709-710

afterload in,13
outpatient care in, 713-714, 714

anatomy and, 44-48, 45, 46, 47, 48

post-transplant care in,708

aortic volume and,66,66

pre-transplant care in, 70S

cardiopulmonary physiology of, 65,65-67, 66, 67t

rejection signs in,714, 715, 716

electrocardiograms and, 169-187

surgery and, 70G

arrhythmias, J 77,178, 179-184,179-184

therapy in

conduction,170-172, 171
assessments,707 -70S

blocks,184-186,185, 186
defined,70S-709, 710,710--713

evaluation of. 174, 174-177. 175, 176,177

medical management, 707,707t

myocardial infarction, 186-187. 187

musculoskeletal considerations,707,709-710

rate, 174,174-176, 175, 176

physiology and,707

recording,172, 172- t 74,173

therapist requirements, 706

rhythms, 176-177, 177

Heartbeat, cardiopulmonary physiology and, 66

use of, 169-170

Heimlich assist techniques,374. 374-375

heartbeat physiology and,66

Hematocrit (Hct)

left atrial pressure,241-243

laboratory tests of,190-192, J 9 J t

myocardial contractility and,13

in oxygen transport, 14

myocardial viability and, 202-203

Hematologic disorders,cardiopulmonary effects of

myocardial workload reduction, 592, 593-594, 596

malignant. 109

output in, I I, 12, 14,17,636

systemic, !O8-109, J09

preload,13
Hematology,oxygen transport and,S

ventricular
Hemiplegia,chronic secondary dysfunction and

diastole physiology,66
management of,541-543

fetal anatomy of, 636

pathophysiology of,541

Copyrighted Material
 Index 1-15

Hemoglobin (Hgb) respiratolY failure and, 579, 580t,581

ancri 1 blood gases and,155

Hyperglycemia, respiratory failure and,579, 580t, 581

laboratory tests of,190-192,191 t

Hyperinflation, manual, 348,348-349

in oxygen transport, 11-12, 14-15

Hyperoxia, ICUs and, 238

Hemophilia,pulmonary hemorrhage and, 108

Hypertension

Henull,hilis il(/ll/enlOe, pneumonia in neonates, 642

chronic primary dysfunction and management of, 531-533

Hemophilus inj7uelllOe, in bactcrial pneumonias, 474--475

pathophysiology of,531

Hemoptysis, patient history and, 140

management of,488

Hemorrhages pathophysiology of,488

anticoagulants and, 108

preterm infants and, 637-638, 638t

disseminated intravascular coagulation. 108

treatment of,777, 778, 779

electrolyte balance and,230

Hyperrhyroidism, cardiopulmon8lY effects of, 109-1 10, I 10

hepatic failure and,108

Hyperventilation, manual airway clearance and, 325

Hcmosiderosis. pathophysiology of, 87

Hypocalcemia, respiratory failure and, 579, 5801., 581

Hemostasis, laboratory tests in, 190,191t

Hypocapnia, ICUs and, 238-239

Hemothorax, secondary dysfunctionllCU and, 605

Hypokinesia, nuclear imaging of, 200

Hepatic fibrosis,clubbing and, 214, 214

Hypomagncsemia, respiratory failure and, 579,580t, 581

Hering-Breuer reflex, cardiopulmonary physiology of, 55

Hyponatremia, respiratory failure and, 579, 5801, 581

Hexamethonium (Methium), pharmacology of,783

Hypophosphatemia, respiratory failure and, 579, 580t, 581

HFCC; sec High frequency chest compression (HFCC) Hypothyroidism, cardiopulmonary effects of, 109-110, 110

Hgb; see Hemoglobin (Hgb) Hypoxemia

High-dcnsity lipoproteins (HOL), cholesterol and, 191, 191t

cardiopulmonary cl'fects of, 101

High elevation environments, oxygen transport and, 16

ICUs and,237t, 237-238

High frcljuency chest comprcssion (HFCC), 328-329, 358, 358-359

management of,621

High-resolution computerized tomography (HRCT), for respiratory symptoms of, 236t

tcsting, 206-- 207
Hypoxia, critical facts relating to, 252

Hip mobilization, secondary dysfullction and, 436

History

of artificial airways. 761

IABP; see Intraaortic balloon counter pulsation (IABP)
of organ transplants, 704
[CP; see Intracranial pressure (ICP)
of patients/family, 142
ICS; see Intercostal space (ICS)
HIY; see also AIDS ICUs; see Intensive care units (ICUs)
associated cardiology of,639t Idiopathic pulmonary hemosiderosis, pathophysiology of, 87

cardiopulmonary effects of, 110

Immobility/recumbency,intensive care units and, 568

HMO; see Hyaline membrane disease (HMO)

Immunological disorders, systemic,cardiopulmonary effects of, I 10

Hoarseness, patient history and, 141

Immunological function, laboratOIY tests in, [94t, 194-195

Hodgkin's disease, cardiopulmonary effects of, 109

Immunosuppressive drugs

Homatropine (Novatrin),pharmacology of, 783

for organ transplants, 717-718

Home-based care
side effects of, 7J 8

concerns in, 727-728

IMT; see Inspiratory muscle training
goals for, 730-732, 731, 732
IMY; see Intermittent mandatory ventilation (IMY)

management of,722
Incentive spirometry (IS), defined, 754, 755

monitoring in, 729

Indices/measures, oxygen transport and, 5

oxygen, 729-730, 730

Indirect percussion; see Mediate percussion
setting requirements in, 728
Indium III antimyosin, for cardiovascular testing,201t, 203

team communication in,728-729

Individualized education plan (lEP), Oowo syndrome and, 645t,
for transplant patients 646--647,647
cardiac, 716--718 Indoor environments,oxygen transport and, 16

pulmonary, 716--718 Infants

Home environments, oxygen transport and, 16

airway clearance techniques (ACT) for, 653, 657

Human immunodeficiency virus (HIY); see HIY

aspiration pneumonia in, 642

Humidity therapy, defined, 755

chest therapy for
Hyaline membrane disease (HMO), preterm infants and, 640-641
airway suctioning, 653,657

Hypercapnia
percussion/vibration,652---653, 657

ICUs and,239
pOsitional rotation, 649, 649, 650-651

Copyrighted Material
1-16 Index

postural drainage,652, 653t, 654-656

Swan Ganz catheter. 233, 241-243, 243

intubation tracheostomy and, 644

patient management in. 565-577

myelomeningocele in,646, 646

assessments,572

Infarct avid scans,defined. 20 I t. 202

death, 576-577,577

Infection
discharge, 574

ICUs and,574
environment, 576. 576y
oxygen transport threats and,255
function optimization,570,571

Inflammatory bowel disease,cardiopulmonary effects of. 107

goals, 568-572,570

Information, ICU patients and, 571-572,572

immobility/recumbency, 568

Inhaled materials, toxic. 16

infection, 574

Inhalers monitoring,572,572

metered-dose. 777,778
patient information,571-572,572

bronchodilators,723-724
personal recognition,574--575

defined,755-756,756
pharmacological agents,572-573

for oxygen transport treatment,259-260,260

preventive care,571-572

pharmacology of,777. 786

team work,574, 575

precautions in. 756

therapist expertise, 568,569

spacers for, 786

treatment in. 569-571, 570, 572-574

powder,pharmacology of,786
upright to supine position,570

Injuries
primary dysfunction and,579-596

head, secondary dysfunctionllCU and

asthma, 589-591

management of,606-609, 608

cardiopulmonary failure,579,580t, 581

pathophysiology of,606-609. 607

congestive heart failure,594,594,596

respiratory failure and,579,580t. 58 I

coronary artery disease,592-596

Inspiration myocardial workload reduction, 592, 593-594,596

exercise for fatigue in. 444--448, 448-450, 450

obstructive lung disease, 581-589, 589

muscle anatomy in,26

open heart surgery,595,596

positioning and. 387-388

restrictive lung disease, 590-592

sustained maximum, 754, 755

secondary dysfunction and,599--615

Inspiratory muscle training (lMT), fatigue and, 444-448,

burns, 612--615

448-450.450
fractures, 604--606
lnspired air head injuries, 606-609, 607,608

in ambient air, 15-16

hemothorax.605

in oxygen transport,5, 15-16

musculoskeletal trauma,603-604,694

Instillation therapy, obstructive lung disease and,primary

neuromuscular disease,600--602

dysfunction/lCU,587
obesity, 602--603

Insulin production,laboratory tests of. 193,193t pneumothorax,605

Intensive care units (ICUs) respiratory muscle training,610--612,6 I 1,612

monitoring systems for. 229-246, 572. 572t
rib fractures, 604--605
acid base balance. 236.236t
spinal cord injuries, 609--612
blood gases, 236-237
trauma, 605

central venous pressure. 243-244

Intercostal muscles, anatomy of, 28,29

chest tubeslfluid collection, 235.235-236

Intercostal space (lCS). defined, 220

description of,229-230, 230,231,232.233

Intermittent mandatory ventilation (IMY), defined, 758

ECG, 238, 239-24 I, 240t-24 I t

Intermittent positive pressure breathing (IPPB),defined.753, 754,755

EEG,246 Interstitial lung disease

fluid/electrolyte balance, 230-231, 234t, 234-235

gallium scintigraphy for, 206 .

hypercapnia. 239
management of, 486-487, 523

hyperoxia.238 pathophysiology of, 486, 522-523

hypocapnia, 238-239
radiography of, 162,163

hypoxemia,237t, 237-238
respiratory failure and,579, 580t. 581

intra-arterial I ines,24 I. 242

Interviews

intraaortic balloon counter pulsation, 244, 244-245

patient assessments and,209-210

intracranial pressure, 245-246

for patient history, 127-128

intravenous lines. 243

Intra-arterial lines, in ICUs, 241,242

Copyrighted Material
 Index 1-17

Intraaortic balloon counter pulsation (IABP), in ICUs, 244, 244-245

liver, 194, 194t
Intracranial pressure (ICP), ICU monitoring of,245-246
multisystem, 190- I 95

Intrapulmonary percllssive ventilators (IPV), 363, 364

pancreatic, 193,193t

Intravascular echocardiography, 204

peripheral vascular, 192, 192t

Intravenous lines. in ICUs, 243

thyroid,193t, 194

Invasive cardiac testing. 205-207

Lactic aci d. laboratory tests of, 190, 19 I t

Iodine, laboratory tests of. 194

Laryngeal edema, respiratory failure and, 579, 580t. 581

IPPB; see Inte.rmiltent positive pressure breathing (JPPB) Larynx, anatomy of, 35, 35-36

IPV; see Intrapulmonary percussive ventilators (IPV) Late sequelae of poliomyelitis, chronic secondary dysfunction and

IS; see Incentive spirometry (IS) management of, 550-552

Ischemia, myocardial; see Myocardial infarction

pathophysiology of,550

Isocapnic hyperpnea, for respiratory muscle fatigue. 450-451

Lateral chest radiographs, interpretation of, 159-160

Isocapnic hyperventilation, for respiratory muscle fatigue, 449-450

Lateral costal breathing, ventilation facilitation and, 396, 397, 399

lsoetharine (Bronkosol, Bronkometer, Servant), pharmacology of,

LOL; see Low-density lipoproteins (LOL)

778,784-785 Left atrial pressure (LAP), ICU measurement of, 241-243

Isoproterenol (Isuprel), pharmacology of,777,784 Left ventricular assist devices, ICUs and, 245

Left ventricular ejection fraction (LVEF), nuclear imaging of, 200

J Left ventricular end diastolic volume (LVEOV), oxygen transport

.IRA; see Juvenile rheumatoid arthritis (JRA) and, 13

Jugular venous distension (1VO), patient assessments and,214

Left ventri cu l ar output (LVO), fetal anatomy of, 636

Jugular venous pressure,electrolyte balance and. 231

Left ventricular pressure (LVP), intensive care units measurement
Jugular venous pulse, patient assessments and, 214
of,241-243
Juvenile rheumatoid arthritis (1RA) Leukemia, cardiopulmonary effects of, 109

cardiology of, 639t

Lifting, primary dysfunction and, 419-420

management of. 648

Lipoprotei ns, cholesterol and, 191, 191 t

JVO; see Jugular venous distension (1VO) Listening skills, secondary dysfunction and,428,429, 430 428

Liver disorders, systemic, cardiopulmonary effects of, 107-108, 108

K
Liver function, laboratory tests in, 194, 194t

Kidney disorders Long sitting self assist techniques. 379, 379-380, 380

acid base imbalances and, 154

Long-term care facilities

cardiopulmonary effects of, 108, 108

concerns in, 723

chronic secondary dysfunction and, 560-561

documentation in, 727

effects of systemic types of, 108, 108

monitoring in

organ damage and, 108

cardiopulmonary, 725, 725-726

pathophysiology of, 560

oxygen, 726-727

respiratory failure and,620

work considerations in, 724-725

Kidney function Low-density lipoproteins (LOL), cholesterol and, 191, 19 I t

arterial blood gases and, 154

Low elevation environments, oxygen transport and,16

laboratory tests in, 192t,192- I 93

Lower airways, anatomy of, 36-40, 37, 39t

Knees-hands rocking assist techniques, 381-382

Lower/upper extremity exercise. testing/training in, primary

Krebs cycle, in aerobic transport, 8-9, 18

dysfunction, 419-420

Kyphoscoliosis
Lung anatomy,40-44, 41, 42t, 43

patient asscssments and, 216, 216

Lung cancer,chronic primary dysfunction and management of, 524

poliomyelitis and, exercise training for, 437-440, 438, 439

pathophysiology of, 523-524

radiography of, 167, 167

Lung disorders
Kyphosis, respiratory failure and, 579, 580t, 581
contused, respiratory failure and, 579, 580t, 581

exercise testing/training in, primary dysfunction, 417-418

L
oxygen transport threats and, 253

Laboratory assessments, 189-195

treatment, 261

adrenal,193t,194
Lung function

blood, 190-192, 191t

oxygen transport and, 16-17

endocrine, 193, 193t

pulmonary function tests and, 146, 146-147

immunological, 194t,194-195
Lung injury, management of, 625. 626

insulin production, 193, 193t

Lung transplants
kidney,192t, 192-193

Copyrighted Material
1-18 Index

assessments in, 708

cardiology of, 639t
considerations in
pediatric management of, 648

availability, 704
MAS; see Meconium aspiration syndrome (MAS)
ethical, 704--705
Maximal voluntary ventilation, pulmonary function tests and, 149,

organ donation,704
149-150

organ preservation, 704--706

MOl; see Metered-dose inhalers (MOl)

patient education,706
Mean oxygen pressure, defined,12

psychosocial implications,705-706
Mean oxygen tension, defined, 12

rejection,704
Measurements, I 17-123

trends, 706
characteristics of, I 18-122

waiting list criteria, 705, 705

documentation and, 123-126

waiting time, 705

electrocardiograms and, 169-187

when to, 704

interpreting, 122-123

equipment/monitoring in, 708-709, 715

interval, I 19

facility vs. home based rehabilitation in, 716--718

nominal, 118

goals in, 709, 712, 713t, 715

nuclear-derived,199-200

history of, 704

objective/subjective, 121, 121-122

interventions in, 709,712-713, 713t, 7 I 5-716,716

ordinal, 118-119

medication for, 7 I 7-718

performing, 122

other transplants and,709-710

ratio,119

outpatient care in, 714--7 I 6, 716

reliability and, I 19-120

post-transplant care and, 708, 7 I 2-7 I 3, 7 I 3t

selecting, 122

pre-transplant care and, 708-709, 710

validity and, 120-121

rejection signs in, 7 I 5

Measures/indices, oxygen transport and, 5

surgery and,706
Mechanical body positioning, 316

therapy in Mechanical breathing function, cardiopulmonary physiology in,

assGssments,707-708 56--59,57,58,59
defined, 708-709, 710, 710-7 I 3
Mechanical ventilation
medical management,707, 7071
assisted, 758

musculoskeletal considerations, 707, 709-7 I 0

controlled, 758

physiology, 707
Meconium aspiration syndrome (MAS), management of, 641-642

pre/post assessments, 707-708

Mediate percussion, patient assessments and, 222

therapist req uirement s , 706

diaphragmatic movement,222, 223

Lupus erythematosus,systemic (SLE)

techniq ues, 222

cardiopulmonary effects of, 103, 103

Medical conditions
pathophysiology of, 88-89
chronic primary dysfunction and
LVEOV; sec Left ventricular end diastolic volume (LYEOV) angina,525-526

LYEF; see Left ventricular ejection fraction (L YEF) asthma,5 I 9-520

Lymphatic circulation bronchiectasis,520-521

anatomy of, 50
chronic airflow I imitation,5 I 4

in oxygen transport,16-17
chronic bronchitis,514--5 I 6

systemic disorders and, fluid imbalance,101

cystic fibrosis, 521 -522
diabetes mellitus, 533-535

M
emphysema, 516-518

M-mode echocardiography, defined, 201t, 203-204,205

hypertension, 531-533

MAB scans, defined, 20 I 1,206

interstitial lung disease, 522-523

Magnetic resonance imaging (MRI),defined, 207

I ung cancer, 523-524

Malignancies
myocardial infarction, 526-528

hematologic, cardiopulmonary effects of,109

obstructive pallerns in, 514--522

lung, chronic primary dysfunction and, management of,524

peripheral vascular disease, 529-531

radiography of,163, 165,166

primary cardiovascular disease, 525-535

respiratory failure and, 579, 580t, 58 I

restrictive pallerns in, 522-523

Managed ca re , defined, 722

valvular disease,528-529

Mandatory minute ventilation (MMY), defined, 758

chronic secondary dysfunction in

Marfan syndrome
ankylosing spondylitis, 557-558

Copyrighted Material
 Index 1-19

cer ebral palsy , 546--547 bronchodi lators, 723-724

chronic renal insufficil'llcy, 560--561 defined, 755-756, 756

collagen vascular/connective tissue diseases, 555-556

for oxygen transport treatment, 259-260, 260

hemiplegia, 541-54
pharmacology of, 777, 786

latc sC4udae of poliomyditis, 550--552

precautions in, 756

multiple sclerosis, 544-546

spacers for, 786

muscular dystrophy, 538-539

Methyldopa ( Aldome t) , pharmac ology of, 779

os teoporos is, 551-555

Methylprednisolone, pharmacology of, 785

Parkinson's disease, 543-544

Metoprolol (Lopressor), pharmacology of, 779

rheumatoid "rthritis, 558-560

MI; see Myocardial infarction

scleroderma, 556-557
M ic rocircu lation

spinal cord inj ury, 548-550

cardiopulmonary physiology and, 67, 67t

systemi c lu pus erythematosus, 555-556

in oxygen transport, 18

thoracic deformities, 552-553

MMV; see Mandatory minute ventilation (MMV)
primary dysfu nction secondary to, 469-492
Mobility
alveolar protcinosis, 478
acute responses to, 270-- 271, 271, 272, 273, 274, 274t

alvcolitis, 477-478
assessment of, 295-296

angina, 488-490
bed rest and, 291, 291-295

asthma, 481-483
cellular response to, 269-270

atelectasis, 470-472, 471

defined, 265-266

bronchiolitis, 477
long term responses of, 278-280, 279

chronic airflow limitation, 478-481

monitoring of, 275,285-286,288,289,290, 291-292

chronic bronchitis, 476-477

motor t h erapy, pediatric, 661-663, 662

cy stic fihrosis, 48 -4R6

mu ltisystem effects of, 278-280, 279

emphysema, 478-481
obstructive lun g disease and, primary dysfunction/ICU,
hypertension, 488
584-585

intcrstitial pulmonary fibrosis, 486

oxygen transportfmetabol ic demand and, 267-268, 268, 270

myocardial infarction, 490-491

oxygen transport threats and, 256, 256

pneu monias, 472-476

pathophysiological conditions and, 270--271, 271

tuberculosis, 487-488
prescription for, 266-- 267, 270--276, 273, 274t, 278t

Medical su rgical con d itions, primary dysfunction secondary to, preventive effects of, 291-292, 295

495-508
secon dary dysfunction and, 436

cardiovascular surgery, 501-502

stimulus in, 277-278, 278

extrinsic factors , 500

surgery and, 500

intrinsic factors, 500

testing/training and, 274, 274, 276--277, 280-285, 281, 282t,

mObilitylrecumbency,500
283t, 284, 285, 286,290, 290-291

pathophysiology, 500
Monitoring
perio[Xrative course, 496, 496--500, 498
of body positioning, 317-3 I 8

postoperative management, 502, 502-505, 506, 507

exercise and, 275, 285-286, 288, 289, 290, 291-292

preoperative management, 502

in fa cility-based care

su rgical effects, 500

cardiopu lmonary, 725, 725-726

surgical prep, 499

oxygen, 726-727

thoracic, 500--502 in home-based care

Medication; see Drugs cardiopulmonary, 729

Med ullary respiratory center, cardiopulmonary physiology of, 54

oxygen, 729-730, 730

Men ingitis, re spirato ry failure and, 579, 580t, 581

in ICUs, 572, 572

Metabolic acidosis, intensive care of, 236, 236t in transplant patients

Metabolic alkalosis, intensive care of, 236, 236t cardiac, 708-709

Metabolic disorders
pulmonary, 708-709, 715

cardiopulmonary effects of, 109

Monoamine oxidase (MAO), 776

respiratory failure and, 580t, 617-618

Montgomery T tubes, 768

Metabolism, muscle, 10--11

Motion radiographs, interpretation of, 159-160

Metaproterenol (Alupent), pharmacol ogy of, 778, 784-785

Motor neuron disease, respiratory failure and, 579, 580t, 581

Metaraminol, pharmacology of, 777-778

Motor therapy, pedi atric, 661-663, 662

Metered-dose inhalers (MOl) MS; see M u ltiple sclerosis (MS)

Copyrighted Material
1-20 Index

99mTcOTPA; see Technetium-99M-diethylene triamine penta­ chest development in,682-689, 684---{i89,686t

acetic COTPA) aerosol compensatory breathing patterns in,689,691---{i93,692,
Mucolytic agents 693,694,695
for intensive care units, 572-573 di agno sis in, 680
for oxygen transpOlt treatment, 259-260, 260 gravity in, 680---{i87,682---{i87,686t
pharmacology of,786 impaired
MUGA; see Multiple uptake gated scans (MUGA) chest expansion, 689
Multicrystal cameras,for nuclear imaging, 198 cough effectiveness, 698
Multiple fractures,secondary dysfunctionllCU, 605-606 function,689
Multiple sclerosis (MS) phonation, 699-700
cardiopulmonary effects of,104 muscle/tonal effects in, 687-689,688, 689
chronic secondary dysfunction and planes of ventilation and, 680
management of, 544--546 program goals for, 700--701
pathophysiology of, 544 pulmonary changes in,695-696
respiratory failure and, 579,580t,581 systemic,cardiopulmonary effects of,102,102-103
Multiple trauma,secondary dysfunction/ICU and, 605 transplant patients and,707,709-710
Multiple uptake gated scans (MUGA), defined, 199,20 I t Musculoskeletal trauma, secondary dysfunction/ICU and,
Muhisystem assessment, laboratory,189-195 603-606,604
Murmurs,patient assessments and,221 management of,604
Muscarinic blockers, defined, 779-781 pathophysiology of, 603-604,604
Muscarinic receptors, defined, 780 Myasthenia gravis
Muscle contraction respiratory failure and,579,5801,581
emotional stress and,20 treatment of, 781-782
oxygen lranspolt and, 9,10, 10--1 2 Myelomeningocele, pediatric management of, 646,646
Muscle fatigue, exercise test i ng/traini ng in, primar y dysfunction, Myocardial contractility, oxygen transport and, 13
418-419 Myocardial dysfunction,respiratory failure and,620
Muscles Myocardial infarction
oxygen transport threats and,254 chronic primary dysfunction and
in respiration anatomy management of,526-528
diaphragms,26,26-28, 27, 28 pathophysiology of,526
erector spinae, 30, 3 I electrocardiograms and,186-187, 187
expiration,27,31-32 management of,490-491
inspiration,26 pathophysiology of,91-93, 490
intercostals,28,29 Myocardial ischemia,ICUs and,245
pectoralis major, 29, 30 Myocardial perfusion
pectoralis minor, 30 nuclear imaging for,202-203
scalenes, 29, 29 oxygen transport threats and, 254
serratus anterior, 29-30 Myocardial viability, testing for,202-203
sternocleidomastoid, 28-29, 29 Myocardial workload reduction, primary dysfunctionllCU and,
trapezius, 30,30 592,593-594,596
in secondary dysfunction, 427-428,432-433, 435 Myoglobin, in oxygen transport, 18
ventilation facilitation and, 401-405,402, 404,405 Myxedema,respiratory failure and, 579, 580t, 581
Muscular dystrophy
N
cardiology of, 639t
chronic secondary dysfunction and NAO; see Nicotinamide adenine dinucleotide
management of,538-539 Narcotics
pathophysiology of, 538 for ICUs, 572-573
management of,647-648 respiratory failure and,579,580t,581
pediatric management of,647-648 Nasopharyngeal suctioning,772
respiratory failure and,579,580t, 581 NOT; see Neurodevelopmental (NOT) treatment
Musculoskeletal conditions Nebulizers,for oxygen transport treatment, 259-260,260
chronic secondary dysfunction and,552-555 Neck
neuromuscular disorders and, 679-701 mobilization in secondary dysfunction and,436
adverse changes in, 696,696-698, 697 patient assessments and,214,215
bronchial hygiene and,698 Nedocromil sodium (Tilade),pharmacology of,785-786

Copyrighted Material
 Index 1-21

Neonates phonation, 699-700

chest therapy fo r muscle/tonal effects in, 687-689, 688,689

airway suctioning, 653, 657

planes of vemilation and, 680

chest percussion/vibration,652-653,657
program goals for, 700-701

positional rotation, 649, 649, 650-651

pulmonary changes in,695-696

postural drainage, 652,653t, 654--656

secondary dysfunction and,436

development in
chronic,538-543

ca rd iac, 636-637
ICU,600-602

prelenn respiration,637, 1i38, 6381

management of. 600-60 I

pulmonary, 637-63tl pathophysiology of, 600

endocardial cushion defects in,640

Neuromuscular ju ncti on (NMJ), defined, 780-781

intubation tracheostomy in,644

Neurotransmission, drugs and, 776-777,778, 779-784

meconium aspiration syndrome in, 641-642

Nicotinamide adenine dinucleotide (NAO), in energy transfer, 8

myelomeningocele in, 646, 646

Nicotinic receptors, defined, 780

patent ductus arteriosus in, 639--640 Nitrogen, ambient air co ntent of, 15-16

pneumonia in, 642

NMJ; sce Neuromuscular junction (NMJ)
preterm Nocturnal ventilation, secondary dysfunction and,432-433, 435

associated cardiology of, 639t Noncardiogenic pulmonary edema, management of,625, 625

bronchopulmonary dysplasia in, 641

N onsmoking, environments, 16

chest therapy for Noonan's syndromc, cardiology or. 6391

airway suctioning,653, 657

Noradrenalin, in neurotransmission, 776

postural drainage, 652,6531, 654-656

Norepinephrine,laboratory tests of,194

dysfunction factors in, 638t Norepinephrine (Leval1erenol, Levophed),pharmacology of', 777

hyaline membrane disease in,640--641

Normal blood gas values, 154

patent ductus arteriosus in,639-640

Nose,anatomy of,32-34, 33, 34

respiration in, 637-638, 638t

Nuclear imaging
tetmlogy of fallot in, 640
for cardiovascular t"sting, 199-204,20 I t

transient tachypnea of the new born in, 641

angiography, 205

Neoplasms,respiratory failure and, 579, 580t, 581

echocardiography, 197, 203-205

Neostigmine (Prostigminc),pharmacology of,781-782

with exercise stress,199

Nervous systems 18F-fluoro-deoxyglucose (FOG), 203

drug interaction and,776-777

gatedlungnted,199

in heart anatomy, 47,47-48, 48

Indium II I antimyosin, 203

systemic, 103-107,104
in vasi ve, 205-207

Neurodevclopmental (NOT) treatment, pediatric motor therapy

myocardial viability, 202-203

and, 661-663,662
noninvasive, 199-205

Neurological disorders nuclear-derived measurements,199-200

respiratory failure and,620-621

perfusion, 199-200

systemic,103-107, 104
with pharmacologic stress, 199

autonomic nervous system, 106-107

Technetium-99M-pyrophosphate, 203

central nervous system,103,105-106

Technetium-99M-sestamibi,202

peripheral nervous system,106

Technetium-99M-teboroxime,202

Neuromuscular disorders Thallium 201, 200-202, 20lt

musculoskeletal,679-70 I
planar, 198-199

advcrse changes in, 696,696-698,697

respiratory,205-207

bronchial hygiene and,698

angiography,206

chest development in, 682-689,684-689,686t

computerized tomography,206-207

compensatory breathing patterns in,689,691-693, 692,

gallium scintigraphy,206

693,694,695
magnetic resonance imaging, 207

diagnosis in,680
ventilation-perfusion lung scan,206

gravity in,680-687, 682-687,686t

tomographic/SPECT,198-199

impaired Nursing homes

chest expansion, 689
concerns in,723

cough effectiveness, 698

documentation in,727

function,689
monitoring in

Copyrighted Material
1-22 Index

cardiopulmonary, 725, 725-726

content,11-12

oxygen, 726-727
debt,13

work considerations in,724-725

delivery, 4, 6, II, 12. 13,14, 14. 19

Nutrition
demand,4, 13

obstructive lung disease and, primary dysfunctionflCU, 583

enhancement ratio,4, 6, 13

oxygen transport threats and, 255

gravitational stress. 19-20

Nutritional disorders, systemic, cardiopulmonary effects of. hyperoxia and, 238

110-111,111 mean pre.,sure defined, 12

mean tension defined, 12

o
myocardial function, 17-18

Obesity for oxygen transport treatment, 259-260, 260

cardiopulmonary effects of. 110-111,III

tissue extraction, 18-19

respiratory failure and, 579, 580t,581

transport, 3-20,4,5, 6

secondary dysfunction/ICU,602-603
airways, 16

management of, 602-603

desaturated blood/C02, 19

pathophysiology of,602
diffusion,S, 12,17

Obstructive lung diseases inspired/ambient,S, 15-16

COPO patient assessments and, 214-215, 222, 224

lungs/chest walls,16-17

pathophysiology of,71-72
measures/indices. 5

primary/le U perfusion, 17

bagging,587
peripheral circulation, 18

body positioning, 585-586

Oxygen therapy

breathing,588
basics of, 749,750, 750t, 751,752

coughing, 588
high-flow systems in, 750, 751-752

management of, 583-589

home/portab le,751, 753

mobilization, 584-585
low-flow systems in,750. 750. 750t,751

nutrition,583
obstructive lung disease and. primary dysfullctionlICU, 5g6

oxygen, 586
Oxygen transport

pathophysiology of, 581-582

airways, 16

secretion ckarance,587-588
threats,253

selective instillation, 587

treatment, 261

ventilator withdrawal, 588, 588-589, 589

analysis schematic of. 129

pulmonary function tests and, diagnosis, 150, 150-151

cardiopulmonary physiology or. blood, 67-68, 68

Obstructive sleep apnea, respiratory failure and,579,580t, 581

exercise/metabolic demand and, 267-268. 268. 270

Occupational history,patient,141
mobilization and,270

OER; sec Oxygen, enhancement ratio pathophysiology of, 251-263

OKT 3, for organ transplants, 718

critical problem-solving Sleps, 252,252

Olympic tracheostomy buttons, 766, 767, 768, 768

deficits/threats, 253-255,256

Open heart surgery, primary dysfunction/ICU and, 595. 596

extrinsic, 256

Organ damage, renal conditions and, 108

fundamental knowledge, 252, 252

Organ donation, 704-706

indirect dclicits,255,256

Organ failure, management of,628t, 628-629

problem list, 252, 253, 254, 255

Orthopnea,dyspnea/patient history and,134

restricted mobilitylrecumbency,256

Orthostatic hypotension,defined,783
treatment,256-263,257, 258-259, 260,261. 262

Osteoporosis, chronic secondary dysfunction and management of, Oxyhemoglobin,cardiopulmonary physiology and. 67-68,68

553-555
Oxyhemoglobin dissociation, cellular respiration and, 15

pathophysiology of, 553-554

p
Outdoor environments, oxygen transport and, 16

Outpatient care; see Home-based care, Facility-based care

Pain
Oxygen management of, 623

cascade, 12, 12
oxygen transport threats <Lilli, 255

consumption,4,6, II, 13
respiratory failure and,579, 5801, 581

IABP and, 244, 244-245

Palpation, patient asscssments and, 222-225

supply-dependent, 13, 14
chest wall, 224, 224

vs. delivery , 14, 14, 19

edema, 223

Copyrighted Material
 Index 1-23

tactile fremitus, 225, 225, 226 intcrdisciplinary care and, 46J

tenderness, 223 learning needs asse.SSlllcnts, 457. 459
tracheal d viation, 225, 226 areas, 457, 45 7, 459
Pancreatic disorders, cardiopulmonary ef fe ct s of, 107, 109 findings, 45 9
Pancreatic dornase (Dornavac),pharmacology of, 786 goals, 459
Pancreatic function. laboratory tests in, 193, 193t tools, 457
Paradoxical breathing patterns, poliomyelitis and, exercise training methods in, 459--461, 460t, 461
for, 438--439 needs-based,456
Parasympathctic neurotransmission patient adherence and, 462
defined,779-783 secretion mobilization, 371-372,372
fight or fl ig ht system and,776 teacher-learner relationship and, 462
Parkinson" disease for transpl a nt patients, 706
cardiopulmonary <:Ffeets of, 104 Patient history, 127-142
chronic secondary dysfunction and c h es t pain , 137-138
management of, 543-544 cardiac, 138-139
pathophysiology of, 543 c hest wall, 139
treatment of, 783 esop hageal , 139
Paroxysmal nocturnal dyspnca . patient hi s tory and, 134-135 pericardial, 139
Partial thromboplastin (PTT), laboratory tests of, 190, 191t pleuritic, 138
Particulate matter, in ambient air, 16 pulmonary hyper tension, 139
Passy - Muir valves, 766,767, 768, 768 cough, 135,136(,137
Pa tau ' s sy nd ro me , card iology of. 639t dyspnea,128-130,129
Patient assessments,209-228 acute, 130
anatomic features in,210-211, 211, 212, 213 in cardiac pa l ients, 134
auscultation and, 217, 217-221, 218,219 exercise limiting,131t
breath sounds, 218-220,219 on exerlion, 130--131, 131.
chest sou n ds,217-218 functional, 135
heart sounds, 221-222 orth opnea, 134
techniques in, 217, 218 paroxysmal nocturnal, 134-135
for barrel chest, 214-216, 216 platypnea, 135
breathing patterns and, 216 trepopnea, J 35
case studies and, 225-228 exerc ise testing/training in, secondary dy sfullction , 428, 428,
chart review/interview in, 209-210 429,430
chest wall cunfi gura lion in. 214-216, 216 family, 142
differential diagnosis in,227t fatigue/weakness, 140
general appearance in, 212-213 heart discasc classification, 133
jugular venous distension and, 214, 215 hemoptysis, 140
medi a te percussion in, 222, 222 hoarseness, 141
diaphragmatic movement, 222, 223 interview, 127-128
techniques in, 222, 222 occupational, 141
neck and, 214, 215 pedal edema, 140--141
palpation prior treatment,142
chest wall, 224, 224 questionnaires, 128
edema. 223 smoking,141-142
tactile fremitus, 2 5. 22<;, 2:!6 wheezing, 135
tcnde rn e s s, 22] Patient management
tracheal de v i ation, 225, 226 exercise testing/training in, secondary dysfunction, 432--433,435
palpation and, 222-225 in leUs, 565-577
physical cxams in, 210 assessments, 572
skin in, 214,214 death,576-577,577
vi " ual inspl!ction in,211-214, 214 discharge,574
Patient education, 453--463 environment, 576, 576y
defined,454--456 function optimization, 570,571
effectivenl!SS in, 461--462 goals, 568-572, 570
fundamentals of, 454--456 immobility/recumbency, 568

Copyrighted Material
1-24 Index

infection, 574
Perfusion
monitoring,572, 572
cardiopulmonary physiology of, 61-65,62,63,64

patient information, 571-572, 572

ventilation matching,61-65,62. 63. 64

personal recognition, 574-575

myocardial,199-200,201t

pharmacological agents,572-573
in oxygen transport, 17

preventive care, 571-572

Pericardial chest pain, patient history and. 139

team work, 574,575

Perioperative management,primary dysfunction/acute surgical

therapist expertise,568, 569

conditions and, 496, 496-500, 498

treatment in,569-571,570,572-574
Peri phera I chemoreceptors

upright to supine position, 570

arterial blood gases and,response to hypoxemia,155

transplant,703-718
cardiopulmonary physiolugy of,54-55

PD; see Postural drainage (PD) Peripheral circulation

Pectoralis facilitation,ventilation and, 401-402,402
anatomy 01',48-49
Pectoralis major, anatomy of, 29. 30
in dying patients, 577,577

Pectoralis minor, anatomy of, 30

laboratory tests in, 192,192t

Pectus carinatum,patient assessments and. 214-216, 216

in oxygen transport, 18

Pectus excavatum,patient assessments and,214-216,216

threats/treatment, 262

Pedal edema,patient history and,140--141

Peripheral nervous system, systemic disease effects on, 106

Pediatrics Peripheral vascular disease, chronic primary

asthma in,642 43, 660--661

management of,530--531

bronchopulmonary dysplasia in,64 I

pathophysiology of, 529-531

cardiac development in, 636-638

Peritoneal cavity,oxygen transport and,17-18

cerebral palsy in,644,644-646, 645t

PET imaging; see Positron emission tOl1lography (PET)

chest physical therapy in

PFT; see Pulmonary function tests (I'I'T)

for children,657 60,658

Pharmacologic stn.:ss testing,cardiovascular,199

positional rotation,658-659, 659,660

Pharmacological agents; see Dl1Jgs

pre/postoperative,659-660
Pharynx,anatomy of, 33,34-35

for infants,649,649,650--651, 652

Phenoxybenzamine (Dibenzyline), pharmacology of, 778

airway suctioning,653,657
Phentolamine (Regitine)

chest percussion/vibration,652 53,657

for epinephrine reversal, 778

positional rotation,649,649,650--651
pharmacology of,778

postural drainage,652,653r,654 56
Phenylephrine (lsophrin,Neo-Synephrine), pharmacology of,
common diagnoses in, 638t,638 48
777-778

cardiac,639t, 639 40
Pheochromocytoma, phentolamine and,778

pulmonary,64 48
Phonation, musculoskeletal/neuromuscular disorders and,699-700

cystic fibrosis in,643 44, 661

Physical exams,patient assessments and,210

Down syndrome in,645t,646-647, 647

Physical therapist requirements, in ICUs,568, 569

endocardial cushion/artrioventricular defects in,640

Physical therapy
hyaline membrane discase in, 64 41
body positioning,299-318

intubation tracheostomy in, 644

considerations in,316-317

motor therapy in, 661 63,662

gravity/physiology and, 300-301,30 I

muscular dystrophy in,647 8 head down,312

myelomeningocele in,646,646
mechanical, 316

patent ductus arteriosus in, 639 0 monitoring of,317-318

pneumonia in,642
physiological effects of,301-313, 302

pulmonary development in,637,638,638t

frequent changes,313,315

rehabilitation in, 660--661

prescription for,313-316.314

tetralogy of fallot in, 640

vs. routine,301

transient tachypnea in, 641

prone,312-313

Pelvis mobilization, secondary dysfunction and,436

side-lying positions, 311,311-312

Pentolinium (Ansolysen),pharmacology of,783

supine,308-309,309, 310

PEP; see Positive expiratory pressure (PEP)

upright, 302-308, 303, 304,305, 306,307, 308

Percussion
exercise/mobility,265-296

in airway clearance,323-324
acute responses to, 270--271,271,272,273,274, 274t

clinical applications of,344-346,345

assessment of, 295-296

Copyrighted Material
 Index 1-25

bed rest and, 291, 291-295 Pneumotaxic centers, cardiopul monary physiology of. 54
cellular responses to 269 -270
. Pneumothorax
de fined 265-266
, different ial diagnosis of, 227t
long term responses of, 278-280,279 radiography of. 164. 165
monitoring and. 275, 285-286,288, 289,290, 291-292 secondary dysfunctiun/ICU and. 605
multi syst em effects of. 278-280,279 Point of maximum impulse (PM!), defined, 220
oxyge.n transport/metabolic d em and and, 267-268,268,270 Poisons, respiratory failure and, 579, 580t,581
pathophysiological c on d iti ons. 270--271,271 Poland's syndrome, pediatric management of, 648
prescription for. 266-267. 268. 270--276. 273, 274t,276,278t Polio, respiratory failure and,579,580t,581
preventivc crfc(,ts or. 291 292 . 295
- Poliomyelitis
stimulus in, 277-27R. 278 chronic secondary dysfunction and
impact of sy temic diseases on, 99-100 management of, 550--552
oxygen ll'llnsport and, 3-20 pathophysiology of, 550
pediatric, 648--663 with s econdary kyphoscoliosis, exercise training for 437-440,

cardiac,648 - 649 438,439

positional release therapies,secondary dysfunction and 437
. Pontine respiratory center, c ardiopulmonary physiology of, 54
shock,627-628 Positional release therapies. secondary dys function and. 437
Physiology Positioning, 299-318
cardiopulmonary, 53-69
b ody mechanics. 737-747
blood transport of oxygen,67--68,68
lifting, 741-743. 742, 743, 744
breathing control, 53-55. 54
moving, 744, 744-745. 745, 746. 747, 747
carbon diuxide transport. 68--69
uptimal ventilation, 737-738. 740-741
cardiac. 65,65--67,66. 67t
side lying. 740
diffusion, 60,60--61 supine, 738. 739, 740
mechanical, 56-59, 57,58,59
upright, 740,740--741,741
perfusion,61--65. 62. 63, 64
considerations in, 316--317

reflexes, 55, 55-56

cough/suction,367-382

ventilation, 59--60 active assistive, 373-382

in tra n splant patients,707

anterior chest compression, 375,375

Physostigmine (Eserine), pharmacology of, 781

costophrenic, 373,373-374

Pilocarpine,pharmacology of, 781

counter rotation, 375, 376, 377

Planar imaging. defincd, 198-199, 201t hands knees rocking,381-382

Plasma, in oxygen transport, 11-12,15 long sitting self, 379, 379-380, 3S0

Plasma volume. albumin for,234

prone on elbows, 378, 378-379

Platelet count. laboratory tests of, 190, 191 t

self, 377-382

Platelet inhibitors, pulmonary hemorrhage and, 108

gravity/physiology and, 300--30 I, 30 I

Platypnea, patient history and, 135

head down, 312

Pleural effusions mechanical 316

cardiopulmonary effects uf, f02-I03, 103, 109

moni toring of,317-318

congestive heart failure and, 101

obstructive lung disease, primary/ICU, 585-586

differential diagnosis of, 227t physiological effects of, 301-313,302

patient a"",,ments and,2 27·- 228 frequent changes, 3 I 3,315

radiography of, 164, 165, 166

prescripti on for, 313-316,314
Pleural tluids, imbalance dkcts of, 101
vs. routine, 30 I

Pleuritic chest pain, paticnt history and. 138

prone, 312-313

PMI; sec Point uf maximum impulse (PMI)

rotation for infants,649,649, 650--651

Pneumonias side-lying positions, 311, 311-312

di f ferential diagno sis of, 227t

supine, 308-309,309,310

management of, 472476

upright,302-308,303,304,305,306,307,308

pathophysiology of, 472-473

ventilation facilitation and, 383-415

patient assessments and 227

. asymmetrical dysfunction and,405-406

pediatric, 642
butterfly techniques and, 408,409, 410

radiograph s of, 162,162,163, 164, 164,167

chest/shoulders and, 392

respiratory failure and, 579,580t,581

counter rota tion 407-408, 409

Copyrighted Material
1-26 Index

diaphragm inhibition and, 402-405,404,405 Preoperative management

diaphragmatic breathing and,389,3'10,391,392,394 pediatric chest physical thelapy,659-660
395,396 primary dysfunction/acute .surgical conditions anu, 502
dressing techniques and, 389 Pressure gradients (P)
dynamic activities and,388-389 in blood now, 15
eccentric resistance techniques and,414 Pressure support ventilation (PSY),ucfJllcd, 7. X
expiration and,388 Pressure/volume, cardiopulmonary physiology and,57-58, 58,66
glossopharyngeal breathing and, 410-4 I 2,4 I 2 Preterm infants
inspiration and,387-388 associated cardiology of, 639t
lateral costal breathing and,396, 397,399 bronchopulmonary dysplasia and,641
manual. 413-414 chest therapy for
mobilizing the thorax in,399-401,400 airway suctioning,653, 657
muscles and,401-405,402,404,405 postural drainage, 652, 653t,654-656
normal timing and,399 dysfunction factors in, 638t
postural inhibition, 406 hyaline membrane disease in,640-641
primary vs. secondary dysfunction and, 390,391 patent ductus arteriosus in,63lJ-MO
pursed-lip breathing,410 respiration in,637-638, 638t
repatterning, 393 Preventive care, ICUs and, 571-572
rolling,388 Primary cardiovascu.lar disease. chronic primmy dysfunction and
sitting, 388 management of,525-535
snifli ng, 392 pathophysiology of,525-535
standing,389 Primary dysfunction
strategies for,387-389 chronic
symmetrical,405-406 angina, 525-526
verbal,414-415 asthma, 519-520
vocalization enhancement, 412-41.5 bronchiectasis, 520-521
Positive expiratory pressure (PEP) chronic airnow limitation, 514
in airway clearance,327-328 chronic bronchitis,514-516
clinical applications and,354--358,355 cystic fibrosis,521-522
Positron emission tomography (PET), defined,199,20 I t diabetes mellitus,533-535
Posteroanterior (PA) radiographs,interpretation of, 159-160 emphysema,516-518
Postoperative complications,621,621--624, 622 hypertension,531-533
in artificial airways,763-764 interstitial lung disease,522-523
mcchanical, 764 lung cancer, 523·- 524
hypoxemia and, 621 myocardial infarction, 526-528
management of, 621, 621-624 obstructive patterns in,514-522
pain and, 623 peripheral vascular disease,529-531
pulmonary embolism and,623-624 primary cardiovascular disea,,:, 525-535
Postoperative manngcment restrictive patterns in, 522-523
pediatric,659--660 valvular diseasc, 528-529
primary/acute surgical conditions and,502, 502-505,506,507 exercise testingitraining in, 417-423
Postural drainage (PD) intensive calC of,579-596
clinical applications and,343-344,345 asthma,589-591
contraindications for,330-331 caruiopulll1onary failule,579,580l, 581
for infants. 652, 653t,654-656 congestive heart failure, 594, 594,596
Postural inhibition, ventilation facilitation and,406 coronary artery disease,592-596
Potassium iodide, pharmacology of,786 myocardial workload redLtction,592, 593-594, 596
Powder u inhalers, spacers for,786 obstructive lung disease, 581--589,589
Prazosin (Miniprcss),pharmacology of, 778 open heart surgery, 595,596
Precapillary arteriole function,in oxygen transport,18 restrictive lung uiseasc, 590-592
Prednisone primary vs . secondary,390,39 I
for organ transplants,717 secondary to acute medical conditions,469-492
side effects,7 I 8 alveolar proleinosis,478
pharmacology of, 785 alveolitis,477-478
Preload, cardiopulmonary physiology of,65 angina,488-490
Preload function, in oxygen transport, 13 asthma, 481-483

Copyrighted Material
 Index 1-27

atelectasis, 470-472, 471 Pulmonary deVelopment

bronchiolitis, 477 in rmr cllloskclctal/neuromuscul"r disorders, 695-696
chronic airl10w limitation, 478-41:1 I pediatric, 637--638, 63 t
chronic bronchitis, 476-477 cardiac, 636-637
cy stic fibrosis, 483-486 Pulmonary disorders
em phy se ma , 478-481 respiratory failure and, 618-619, 619
hypL'rlellsion, 488 sy:;temie, cardiac diseases and, 10 I-I 02
intL'rstitial pulmonary fibrosi" 486 Pulmonary edema, noncardiogenic, defined. 625, 625
myocardial inrarction, 490-491 Pulmonary embolism
pn ulllonias, 472-47/i differential d i agnosis of, 227t
tuherculosis, 4 7-4gS management of, 623--624
sectlillidry to a utc surgical conditions, 495-508 respiratory failure and, 579, 580t, 581
c'ardiovascu idr sur»cry. 501-502 Pulmonary eosinophilia, palhorhysiology of, 85
extrinsic' ractors. SOO Pulmonary functio n tests (PFf), 145-151
intnnsiL' ract,llS. SOli air flow measurements, 147, J 48, 149
11\(,bility!rclulllhency. SOO flow volume cu rve , 147, 148, 149
pathophysiology, SOli forced expira tion . 147
peri<>pcrativc course, 4l)(,. 4Sl6-501l, 4t)K c lo sing volume/airway closure, 149, 149-150
postoperative manageillent, 502, 5()2-, ()5. 5116,507 maximal voluntary ventilation, 149, 149-1 SO
prL()p r;Jliyc 1ll00Ilagl:IllL'llt, 50'2 ckad space. 145-140
surgical errects ..'iOO clel'ineel, 145
surgical prcp, 499 diagnosis and
thoracic, 500-502 obstructive lung disease. 150, 150-ISI
Progressive systemic s clerosis (sclerodcrma), pathophysiology oL 89 restrictive lung disease. 150, 15(),-151
Pronc positioning, 312-31 lung capacities, 14 6. 147
on elbows assist techniqucs, 371:\, 378-379 lung volumes. 146, 1 46 - 1 47
infant positional rotation. 64Sl, 649, 650-651 Puirllonary hemorrhages
Propranolol (Inderal), pharmacology of. 778-779 anticoagulant.s and. 108
Proteins, laboratory tests or, 190, 19 1 t, 194, 194t hematologic conditions and, lOS
Pseudomonas acruginosa Pulmonary hemosiderosis, idiopathic, p athophy si 'log y 01.
'
in bacterial pneumonias, 474-475 Pulmonary hypertension
pediatric cystic fibrosis and, 643-644 exercise testing/training for, primary dysfunction, 41 X
PSV: see Pressurc support vcntilation (PSV) patient history and, 139
Psychological considerations, exercise testing/training and, Pulmonary scans, defined. 20 I t, 205-207
secondary elysfunction, 425-426, 426 Pulmonary thrombocmboli, hematologic conditions and, lOS
Psychosocial considerations Pulmonary Lransplants
oxygen transrorr thrcats and, 255 assessments in, 708
transplant paticnts "nel, 705-706 considerations in
PTT: see Panial thromboplastin (PIT) availability, 704
Pulleys, for oxygen transport treatment. 259-260, 260 ethical,704-705
Pulmonary aging c hanges organ donation. 704
exercise and, 675-677, 677, 677t organ preservation, 704-706
structural/functional, 674-677,675, 675t patieot education, 706
Pulmonary alveolar proteinosis. pathophysiology of, 86, 86--87 psychosocial implications, 705-706
Pulmonary aneritis, cardiopulmonary ef fects of, 102-103, 103 rejection, 704
Pulmonary ,u1cry balloon Ilotation catheters: see Swan Ganz catheters trends, 706
Pulmonary artery occlusion prcssure (PAOP). intensive care units wai ting list criteria, 705, 705
measurement of, 241-243 w a it ing time, 70S
Pulmomuy artery pressure (PAP), intensive care units measurement when to, 704
of. 241-241 equipment/monitoring in, 708-709, 715
Pulmonary artcry wedge pressure (PA WP), intensive c<lre units facility vs. horne based rehabilitation in, 716-718
measurement of, 241-243 goals in, 709, 7J2, 713t, 7J5
Pulmonar'Y circulation h istor y of, 704
anatomy of. 4Sl-50 interventions in, 709, 712-713,713t, 715-716, 716
oxygen transport threats and, treatment, 261 medication in, 717-718

Copyrighted Material
1-28 Index

other transplants and, 709-710

metabolic demand and, 267

outpatient care in, 714-716, 716

RBC; see Red blood count (RBC)
post-transplant care in, 708. 712-713, 713t
Recording, electrocardiograms and, 172, 172-174. 173

pre-transplant care in. 708-709. 710

Recumbency

rejection signs in, 715

intensive care units and, 568

surgery and. 706

respiratory failure and. 579, 580t, 581

therapy in Red blood count (RBC), laboratory tests of, 190-192, 191t

assessments. 707-708
Ret1exes, cardiopulmonary physiology of, 55, 55-56

defined. 708-709. 710, 710-713

Rejection

medical management, 707, 707t

cardiac signs of. 714. 715, 716

musculoskeletal considerations. 707, 709-710

of organ transplants. 704

physiology, 707
pulmonary signs of, 715

therapist requirements, 706

Renal disorders

Pumps, cough, 368

acid base imbalances and, 154

Pursed-lip breathing
cardiopulmonary effects of, 108, 108

for primary dysfunction, 420-421

chronic secondary dysfunction and, 560-561

ventilation facilitation and. 410

management of. 560-561

Push-ups. serratus, 405

pathophysiology, 560

effects of, 108, 108

Q organ damage and, 108

Quadriplegic patients, chronic secondary dysfunction and.

pathophysiology of, 560

management of, 548-550

respiratory failure and. 620

Questionnaires. for patient histOlY, 128

systemic, J08, 108

Repatteming techniques, ventilation facilitation and, 393

R
Reserpine, pharmacology of. 779

RA; see Rheumatoid arthritis (RA) Respiratory centers, cardiopulmonary physiology of, 54-55

Radiography
Respiratory distress syndrome (RDS); see also Adult respiratory

abscesses. 164, 164

distress syndrome (ARDS)

alveolar disease, 162, 162

preterm infants and. 637-638, 638t

atelectasis, 164-165, 165, 166

respiratory failure and, 579, 580t, 58 I

basic structures/shapes, 160

Respiratory fai lure, 617-630

bronchi, 162, 162

acid-based abnormalities and, 6 I 9

bronchiectasis, 162, 163, 164

arterial blood gases and. 156

bronchograms in, 162. 162

cardiac dysrhythmias and. 619--Q20

congestive heart failure,164. 165, 166, 167

complications of, 618--Q19, 619

description of, 159-161,160

fluid/electrolyte abnormalities and, 6 I 9

edema, 165,166
gastrointestinal dysfunction and, 620

emphysema, 162, 163

metabolic dysfunction and, 617--Q I 8

fixed position, 159-160

myocardial dysfunction and, 620

interstitial pulmonary disease, 162, 163

neurological dysfunction and. 62O--Q2 I

kyphoscoliosis, 167, 167

primary dysfunction and. 579, 580t, 58 I

lateral chest, 159-160

pulmonary dysfunction and, 618--Q19, 619

malignancies. 163, 165, 166

renal dysfunction and, 620

motion, 159-160
thromboembolism. 620

pleural effusions. 164, 165, 166

Respiratory muscles

pneumonias. 162, 162, 163. 164,167

defined, 26--40

pneumothorax. 164, 165

exercise training for fatigue, 443-451

posteroanterior (PA), 159-160

assessments in, 447

requirements for. 159-160. 161-162

etiology of, 444-447

routine exams, 160-161

inspiration. 444-448, 448-450. 450

suspended motion, 159-160

isocapnic hyperpnea, 450-451

uremia. 165, 166

isocapnic hyperventilation, 449-450

Radiopharmaceuticals, nuclear imaging and. 197-207

primary dysfunction, 418-419

Rales, defined, 219-220

treatment for, 447-448

Range of motion (ROM) exercises

oxygen transport thn;ats and, 254

dying patients and, 577, 577

secondary dysfunction and, 427-428, 432-433, 435

Copyrighted Material
 Index 1-29

secondary dysfunctionllCU,training for, 610-- 612, 61 I, 612 Sclerosis (scleroderma)

Rest, bed pathophysiology of, 89
alternatives to,293-294 progressive systemic,pathophysiology of,89
hazards of, 293 SCM; see Sternocleidomastoid (SCM)
indications for, 294 Scoliosis, respiratory failure and, 579, 580t,581
as therapy, 291-292 Secondary dysfunction
Restrictive lung diseases chronic
pathophysiology of, 83-89 ankylosing spondylitis and, 557-558
diffuse interstitial pulmonary fibrosis, 83-85 cerebral palsy and,546--547
eosinophilic granuloma, 85-86 chronic renal insufficiency and,560--561
idiopathic pulmonary hemosiderosis,87 collagen vascular/connective tissue diseases and, 555-556
progressive systemic sclerosis (scleroderma),89 hemiplegia and, 541-543
pulmonary alveolar proteinosis, 86,86--87 late sequelae of poliomyelitis and, 550--552
pulmonary eosinophilia,85 multiple sclerosis and, 544-546
pulmonary infiltrates, 85 muscular dystrophy and,538-539
rheumatoid arthritis,88 osteoporosis and, 553-555
sarcoidosis, 87-88, 88 Parkinson's disease and, 543-544
systemic lupus erythematosus (SLE), 88-89 rheumatoid arthritis and,558-560
primary/ICU,590--592 scleroderma and. 556--557
management of, 591--592 spinal cord injury and,548-550
pathophysiology of, 590--591 systemic lupus erythematosus and, 555-556
pulmonary function tests and, diagnosis, 150,150-151 thoracic deformities and,552-553
Rheumatoid arthritis (RA) ICUs, 599-615
chronic secondary dysfunction and burns, 612-615
management of,558-560 fractures,605-606
pathophysiology of,558-560 head injuries, 606--609, 607, 608
pathophysiology of, 88 hemothorax, 605
Rhonchi, defined, 219-220 musculoskeletal trauma, 603-604, 694
Rhythms, electrocardiograms and, 176--177, 177 neuromuscular disease, 600--602
Ribs obesity,602-603
anatomy of,24-25, 25y pneumothorax, 605
secondary dysfunction and. cage mobilization,436 respiratory muscle training, 610-- 612,611, 612
secondary dysfunctionfICU,fractures,604-605 rib fractures, 604-605
Right ventricular ejection fraction (RVEF'), nuclear imaging of, 200 spinal cord injuries, 609-612
Right ventricular pressure (RVP),intensive care units measurement trauma, 605
of,241-243 vs. primary, 390, 391
Rocking assist techniques, knees-hands, 381-382 Secretions
Rolling techniques, ventilation facilitation and,388 obstructive lung disease and,primary dysfunctionfICU,587-588
ROM exercises, metabolic demand and, 267 treatment of, 782,783, 786
Rowing machines, for oxygen transport treatment, 259-260,260 Sedatives
Rural environments,oxygen transport and, 16 for ICUs, 572-573
RVEF; see Right ventricular ejection fraction (RVEF) respiratory failure and, 579, 580t,581
Self assist techniques, 377-382
s
Sepsis, management of, 628t,628-629
SA; see Sinoatrial node (SA) Serratus
Sacrum mobilization,secondary dysfunction and, 436 anterior anatomy of, 29-30
Salmeterol (Servant), pharmacology of,778 push-ups for, 405
Sarcoidosis, pathophysiology of,87-88,88 Shaking
Scalenes in airway clearance, 325
anatomy of,29, 29 clinical applications of,346--349, 347, 348
ventilation and, 402 Shock
Scintillation detectors,defined, 198 cardiogenicfICU and, 245
Scleroderma management of, 627-628,777,778
chronic secondary dysfunction and,556--557 Shoulders
progressi ve systemic, 89 mobilization, 436
respiratory failure and, 579,580t, 581 ventilation facilitation and,392

Copyrighted Material
1·30 Index

Sickle anemia, cardiopulmonary of, 108

Stretch reflex, cardiopulmonary physiology of, 55-56

Side-lying body positioning, 311, 31 12

Stroke, cardiopulmonary effects of, 104

SIMV; ,ce Synchronized intermittent mandatory ventilation (SIMV)

Suctioning, of artificial airways, 768, 769-77 I, 77!, 772, 773, 773t

Single crystal cameras, for nuclear imaging, 198

Supine positioning. 308-309, 309, 310

Single photon emission tomography (SPECT), defined, 198-199,

ICUs and, 570

201 t, 202-203
Supraventricular arrhythmias, In electrocardiograms, 177,
I
Sinoatrial node (SA)
179,179,180,181

electrocardiograms and, 170-172

Surfactants, for transport treatment, 259-260, 260

oxygen transpOl1 and, 18

Surgery

Sitting techniques, 379,379-380, 380

open heal1, primary dysfunction/ICU, 595, 596

for primary dysfunction, 421

organ transplant, 706

ventilation facilitation and, 388

primary dysfunction secondary to, 495-508

Skin, patient assessments and, 214, 214

cardiovascular surgery, 501-502

SLE; see Systemic lupus erythematosus (SLE)

extrinsic factors, 500

Sleep apnea
intrinsic factors, 500

cardiopulmonary effects of, 109

mobilnylrecumbency, 500

respiratory failure and, 579, 580t. 581

pathophysiology, 500

Sleep di:;turbance, oxygen transport threats and, 255

perioperative course, 496, 496-500, 498

SI\1I; Sustained maximum inspiration (SMI)

postoperative management,
502-505,506, 507

Smoking
preoperative management, 502

oxygen transport 16
;,urgical effects, 500

patient history and, .141-142

surgical prep, 499

Sniffing techniques, ventilation facilitation and, 392

thoracic, 50( 502

Sodium iodide, pharmacology of, 786

Suspended motion nldiographs, interpretation of. 159-160

Soft tissue therapies, secondary dysfunction and,

Sustained maximum im:piration (SMI), defined,
755

Spacers, for metered-dose inhalers (MDI), 786

Swan Ganz catheters, in ICUs, 233, 241-243, 243

SPECT imaging; Single photon emission tomography (SPECT)

Symmetrical positioning, ventilation facilitation and, 405-406

Spinal cord injuries

Sympatholytic drugs, pharmacology of, 779

chronic secondary dysfunction and

Sympathomimetic drugs, pharmacology of. 784-785

management of, 548-550

Synchronized intermittent mandatory ventilation (SI\1V), defined,

pathophysiology of,
Systemic circulation, anatomy of, 48-49

secondary dysfunction/ICU, 609-612

Systemic diseases. cardiopulmonary effects of. 99-112

management of, 609-610

cardiac, 100-10 I

pathophysiology of, 609

connective tissue, !O3,103

Spirometers, f1uner, for oxygen transport treatment, 259-260. 260

endocrine. J 09····110. I 10

Spondylitis, respiratory failure and, 579, 580t, 581

gastrointestinal, 107, 107

Standing techniques, ventilation facilitation and, 389

hematologic, 108-109, 109

S/aph)loCliccus Glireus, pediatric cystic fibrosis and, 643

immunological, J 10

Starling effect
liver, 107-108, 108

cardiac effects on, 101

musculoskeletal, 102,102-1 m

cardiopulmonary physiology of, 65

neurological, 103-107, 104

plasma protein disorders and, 109

nutritional, 110- I I I, I J I

Sternocleidomastoid faciliwtion, ve-lltilalion and, 402

phy:;ical impact, 99-100

Sternocleidomastoid (SCM), anatomy of, 28-29, 29

pulmonary, 101-102

Sternum, anatomy of, 24

rellal, 108, 108

Stethoscopes, auscultation and, 217, 217

Systemic lupus erythematosus (SLE)

Sirepiococcus B, pneumonia in neonates, 642

cardiopulmonary effects of, 103, 103

StreplOcoccUS pyogenes, in bacterial pneumonias, 474-475

chronic semndary dysfunction and

Stress
management of, 555-556

emotional, 3
pathophysiology of, 555

oxygen transport threats and, 255

pathophysiology of, 88-89

Stress testing, nuclear/cardiovascular

Systemic sclerosis (sclerode!ma), progressive, pathophysiology of, 89

exercise, 199
Systole, ventricular. cardiopulmonary physiology of, 66

pharmacologic, 199

Copyrighted Material
 Index 1-31

T Thorax
anatomy of, 23-25, 24. 25
T3; sec Triiodothyronine (T3)
mobilization of, 399-401,400
T4; ec Thyroxine (T4)
secondary dysfullcl"ion and. 436
Tachycardia, trc.<ltmem of, 777-778, 779
Thromboembolism
Tachyuysrhythmias. intensive care of, 239, 240t-241t
cardiopulmonary effects of, 108
Tachypnea. patient assessments and, 216
respiratory failure and, 620
Tactile fremitlls. patient assessments and, 225, 225,226
Thrombosis, deep vein, management of, 623--624
Tc-99M-macroaggregated albumin; see Technetium-99M-
Thyroid function, laboratory tests of,193t,194
Illacroaggregatcc\ albumin
Thyroid stimulating hormone (TSH), laboratory tests of. 194
Tc-99M-Pyp; scc Technctiulll-99M-pyrophosphate (TcPyp)
Thyroxine (T4), laboratory tests of, 194
Tc-99M-sl)stamibi; sec Ted1l1etium-99M-sestamibi
TI A; see Transient ischemic attack (TI A)
Tc-99M-teboroximc, Technctium-99M-tcboroxime
Tidal volume (TV),systemic disease effects on, 106
Tc-99mDTPA; see Technetium-99M-diethylene triamine penta-
Timing
acetic (DTPA) aerosol
asymmetrical dysfunction and, 406
Teams
ventilation facilitation and, 399
home-based care communication in, 728-729
Tissue assessments, in oxygen transport treatment, 262
in ICUs, 574, 575
Tissue extraction, oxygen transport and, 18-19
Tec hnct ium-99M-die t hy l ene triamine pe nta-ac etic (DTPA)
Tissue perfusion
aerosol,for ventilation-perfusion scans,20 It, 206
in oxygen transport,S
Technetium-99M-mncroaggregated albumin, for ventilation-
oxygen transpOIt threat.s
perfusion scans, 20 It, 206
TLC; see Total lung capacity (TLC)
Technetiull1-99M-pyrophosphate (TcPyp),defined, 20 I t,203
TLSO; see Total contact thoracic lumbar sacral orthosis (TLSOs)
Technetium-99M-sestamibi, defined,20 I t, 202
TOF; see Tetralogy of fallot (TOF)
Technetium-99M-teboroxime, defined,20 I t, 202
Total contact thoracic lumbar sacral orthosis (TLSOs), defined,
TEE; see Transesophagcal echocardiography (TEE)
384-385
Tenderness. patient assessments and, 223
Total lung capacity (TLC)
Tcrazosin (Hytrin), pharmacology of,778
sickle cell anemia and, 109
Terbutaline (Brethine, Bricanyl), pharmacology of,778
systemic disease effects on, 106
Testing
Toxic-inhaled materials,oxygen transport and, 16
arterial blood gases and, 153-157
Tracheas
documentation and, 123-126
anatomy of, 36-40, 37, 39t
electrocardiograms, 169-187
deviation assessments and,225, 226
exercise
TracheomaJacia, respiratory failure and,579, 580t, 581
pre scriptions and,274, 274, 276-277, 280--285, 281, 282t,
Tracheostomy tubes, artificial airways, 764-766, 765,767-771,
283t, 284-286,290, 290--291
768,771-774,773t
training and, secondary dysfunction, 426-432
cuff inhalation, 765-766
ICU unit monitoring systems,229-246
metal,764
measurements and, 117-123
plastic, 764-765, 765
multisystem laboratory assessments and, 189-195
Training,exercise and, 274,274, 276-277, 280--285, 281,282t,
nuclear imaging/radiopharmaceuticals, 197-207
283t,284, 285, 286. 290, 290-291
patient assessments and, 209-228
Tranquilizers, for I CUs, 572-573
pulmonary function, 145-15 I
Transesophageal echocardiography (TEE), defined, 197, 20 It,
routine radiographs, 16(}-161
204, 205
x-ray interpretation, 159-167
Transient ischemic attack (TI A), transesophogeal
Tetanus, respiratory failure and, 579, 580t, 581
echocardiography (TEE) for, 205
Tetralogy of fallot (TOF), pediatric management of,640
Transient l<lchypnea of the new horn (TINB), pediatric
ThAIRapy (TM), clinical applications and, 358, 358-359
management of, 641
Thallium 20 I, for cardiovascular testing, 200-202, 20 It
Transplant patients, 703-718
The Flutter (TM), for airway clearance, 328
cardiac, 708
Theophylline,phannacology of, 785
acute phase care, 710--711,714
Thempist requirements
assessment, 708
in I CUs, 568, 569
equipment/monitoring, 708-709
for transplant patients, 706
exercise guidelines, 712
Therapy, physical; see Physical therapy
facility vs. home based rehabilitation, 716-718
Thoracic disorders, primary dysfunction secondary to, 500--502
goals, 7 J 2

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1-32 Index

interventions, 710-711,714
Tumors,respiratory failure and,579, 580t, 581

medication, 716-718
Turner's syndrome, associated cardiology of,639t

outpatient care, 713-714, 714

TV; see Tidal volume (TV)

post-transplant,708
Two-lumen catheters, in ICUs, 241-242

pre-transplant, 708

u
rejection signs, 714, 715,716

considerations for
Upper airways, anatomy of,32-36,33, 34, 35

availability,704
Upper/lower extremity exercise,testing/training and,primary

ethical, 704-705
dysfunction,419-420

organ donation,704
Upright body positioning,302-308,303,304,305,306, 307,308

organ preservation, 704-706

to supine positions, lCUs and, 570

patient education, 706

Urban environments, oxygen transport and, 16

psychosocial implications, 705-706

Uremia, radiography of, 165,166

rejection,704
Urinary retention, treatment of,780-781

trends, 706

waiting list criteria,705, 705

waiting time,705
Valves
when to,704
flutter,259-260,260

history of, 704

in heart anatomy, 45,45-47, 46

other transplants and,709-7.10 Valvular disease

pulmonary chronic primary dysfunction and

assessments in, 708

management of,528-529

equipment/monitoring in, 708-709,715

pathophysiology of, 528

facility vs. home based rehabilitation in,716-718

chronic secondary dysfunction and

goals in,709, 712, 713t, 715

management of, 528-529

interventions in,709, 712-713,713t,715-716,716

pathophysiology of,528

medication in, 717-718

VAPS; see Volume-assured pressure support (VAPS)

outpatient in,714-716, 716

Vascular resistance (R), in blood flow,15

post-t.ransplant in,708,712-713,713t
Vascular systems
pre-transplant in,708-709, 710
aging changes in,673,673-675, 674t

rejection signs in, 715

peripheral laboratory tests and,192, 192t

surgery and,706
Vasodilators, treatment with, 777, 778

therapy in Vasopressor agents, for lCUs,572-573

assessments, 707-708
Ventilation facilitation,3 3-415

defined, 708-709, 710, 710-7!3

asymmetrical dysfunction and,405-406

medical management,707,707t buttertly techniques and,408, 409,410

musculoskeletal considerations, 707, 709-710

cardiopulmonary physiology of,59-60

physiology, 707
chest/shoulders and, 392

therapist requirements,706
diaphragm inhibition and,402-405, 404, 405

Trapezius
diaphragmatic breathing and,389,390,391, 392,394,394,

anatomy of, 30,30

395,396,396
ventilation and, 402
dressing techniques and,389

Trauma, secondary dysfunctionllCU and, 605

dynamic activities and, 388-389

Treadmill, for oxygen transport treatment, 259-260, 260

eccentric resistance techniques and,414

Trepopnea, patient history and,135

expiration and,388

Trihexyphenidyl HCL (Artane), pharmacology of, 783

glossophMyngeal breathing and,410-412,412

Triiodothyronine (T3),laboratory tests of, 194

inspiration and,387-388

Trisomy 13, associated cardiology of, 639t intrapulmonary percussive, 363, 364

Trisomy 18, associated cardiology of,639t lateral costal breathing and, 396, 397, 399,399

Trisomy 21, associated cardiology of,639t manual, 413-414

Trypsin (Tryptar), pharmacology of, 786

mobilizing the thorax in,399-40 1,400
TSH,Thyroide stimulating hormone (TSH) muscles and,401-4D5, 402, 404, 405

TINB; see Transient tachypnea of the new born (TINB) musculoskeletal/neuromuscular disorders and, 680

Tuberculosis
normal timing and, 399

management of,488
oxygen rransport and,5,16

pathophysiology of,487-488
to perfusion ratio, 17

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 Glossary G-33

positioning in, 383-385,385, 386, 392,413

Vital capacity (VC), Duchenne's muscular dystrophy and, MH
primary vs. secondary dysfunction and, 390,39 J
Vitamin-K deficiency, pulmonary hem orrh age and, lOR
pursed-lip breathing and,410
Vo,: see Oxygen, consumption
repalterning and, 393
Vocalization enhancement, ventilation facilitation and, 412-415

rolling,388
Voice breath sounds,patient assessments and, 220

sitting, 388
Volume-assured pressure support (YAPS), defined, 758

sniffing, 392
Volume/pressure, cardiopulmonary physiology and 57-58, 58,
, 66

standing, 389

w
strategies for, 387-389

verbal, 414-415
Waiting lists,for transplant patients, 705, 705

voc liz tion enhancement,412-415

time of,705

Ventilation-perfusion lung scans, defined,201t, 206

Walking,primary dysfunction and, 421

V.:ntilator withdrawal, obstructive lung discas.: and, primary

Wall motion,nuclear imaging of,200

dysfunction/ICU, 588,5RH-589,589
WBC; see White blood count (WBC)

Ventricular function
Weights, for oxygen transport treatment, 259-260, 260

al'tcrload in, 13
Wheezing
cardiopulmonary physiology of, 65, 65--67, 66,67t
defined,219-220

diastol.: physiology of,66

patient history and,135

electrocardiograms and, 180-184, 182, 183,184

White blood count (WBC),laboratory tests of, 190-192,1911

alThythmias, 177, 178, 179-184,179-184

Williams syndrome, associated cardiology of, 639t

conduction, 170--172, 171

Work environments
blocks, 184-186,185,186
facility-based care and,724-725

evaluation of,174, 174-177, 175, 176, 177

oxygen transport and, 16

myocardial infarction, 186-187, 187

ratc,174, 174-176, 175, 176

recording, 172, 172-174, 173

X-ray testing
rhythms,176-177, 177
abscesses. 164,164

use of,169-170
alveolar disease, 162, 162

left
atelectasis, 164-165, 165,166

assist devices/ICU,245
basic structures/shapes, 160

ejection fraction,200
bronchi, 162, 162

end diastolic volume, 13

bronchiectasis, 162,163, 164

output,636
bronchograms in,162, 162

pressurenCU, 241-243,245
congestive heart failure,164, 165,166,167

left atrial pressure, 241-243

description of, 159-161, 160

output and, II, 12, 14,17,636

edema, 165,166

patient assessments and,220--221

emphysema, 162,163

preload, 13
fixed position, 159-160

right
interstitial pulmonary disease, 162, 163

ejection fraction, 200

kyphoscoliosis, 167,167

prcssurenCU,241-243
lateral chest, 159-160

septal defects/ICU and,245

malignancies,163, 165,166

Venue function, oxygen transport and, 18

motion,159-160

Verbal techniques, ventilation facilitation and, 414-415

pleural effusions, 164,165, 166

Vesicular breath sounds, patient assessments and,218-219

pneumonias, 162, 162, 163, 164, 164, 167

Vibration th.:rapy
pneumothorax, 164,165

in airway clearance, 324-325

posteroanterior (PA), 159-160

clinical applications and, 346-349,347, 348

requirements for, 159-160, 161-162

for infants, 652--653,657

routine exams, 160-- 16 J

Viral p ncumo nias in secondary dysfunction, 426-427

management of, 474

suspended motion, 159-160

pathophysiology of,473-474
uremia, 165,166

Viscosity,of blood, 14
Xanthines, pharmacology of,785

Visual inspection, pntient assessments and,211-214,214

133Xe gas, for perfusion testing,20 It, 206

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