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 CONTENTS

Contributing Authors
Foreword
Preface

CARDIOLOGY
Rachel Frank, Shilpa Sharma, Nino Mihatov, Nilay Patel, Marc S. Sabatine, Michelle
L. O’Donoghue
Electrocardiography
Chest Pain
Noninvasive Evaluation of CAD
Coronary Angiography and Revascularization
Acute Coronary Syndromes
PA Catheter and Tailored Therapy
Heart Failure
Cardiomyopathies
Valvular Heart Disease
Pericardial Disease
Hypertension
Aortic Aneurysms
Acute Aortic Syndromes
Arrhythmias
Atrial Fibrillation
Syncope
Cardiac Rhythm Management Devices
Cardiac Risk Assessment for Noncardiac Surgery
Peripheral Artery Disease

PULMONARY
Miranda Theodore, Jason Maley, Walter J. O’Donnell
Dyspnea
Pulmonary Function Tests
Asthma
Anaphylaxis
Chronic Obstructive Pulmonary Disease
Solitary Pulmonary Nodule
Hemoptysis
Bronchiectasis
Cystic Fibrosis
Interstitial Lung Disease
Pleural Effusion
Venous Thromboembolism
Pulmonary Hypertension
Respiratory Failure
Mechanical Ventilation
Acute Respiratory Distress Syndrome
Sepsis and Shock
Toxicology
Lung Transplant

GASTROENTEROLOGY
Stephanie M. Rutledge, Emily Walsh Lopes, Lawrence S. Friedman
Esophageal and Gastric Disorders
Gastrointestinal Bleeding
Diarrhea
Dysmotility & Nutrition
Disorders of the Colon
Inflammatory Bowel Disease
Intestinal Ischemia
Pancreatitis
Abnormal Liver Tests
Hepatitis
Acute Liver Failure
Cirrhosis
Hepatic Vascular Disease
Ascites
Biliary Tract Disease

NEPHROLOGY
Alexander Blair, Harish Seethapathy, Andrew S. Allegretti
Acid-Base Disturbances
Sodium and Water Homeostasis
Potassium Homeostasis
Renal Failure
Glomerular Disease
Urinalysis
Nephrolithiasis

HEMATOLOGY-ONCOLOGY
Melissa Lumish, Arielle Medford, Tanya E. Keenan, Harshabad Singh, Jean M.
Connors, Daniel J. DeAngelo, David P. Ryan
Anemia
Disorders of Hemostasis
Platelet Disorders
Coagulopathies
Hypercoagulable States
Disorders of Leukocytes
Transfusion Therapy
Myelodysplastic Syndromes
Myeloproliferative Neoplasms
Leukemia
Lymphoma
Plasma Cell Dyscrasias
Hematopoietic Stem Cell Transplantation
Lung Cancer
Breast Cancer
Prostate Cancer
Colorectal Cancer
Pancreatic Tumors
Hepatocellular Carcinoma (HCC)
Oncologic Emergencies
Chemotherapy & Immunotherapy Side Effects

INFECTIOUS DISEASES
Alison C. Castle, Kristen Hysell, Kimon C. Zachary
Pneumonia
Fungal Infections
Infections in Immunosuppressed Hosts
Urinary Tract Infections
Soft Tissue and Bone Infections
Infections of the Nervous System
Bacteremia & Endocarditis
Tuberculosis
HIV/AIDS
Tick-Borne Diseases
Fever Syndromes
ENDOCRINOLOGY
Caitlin Colling, Armen Yerevanian, Michael Mannstadt
Pituitary Disorders
Thyroid Disorders
Adrenal Disorders
Calcium Disorders
Diabetes Mellitus
Lipid Disorders

RHEUMATOLOGY
Isaac D. Smith, Mazen Nasrallah, Robert P. Friday
Approach to Rheumatic Disease
Rheumatoid Arthritis
Adult-Onset Still’s Disease & Relapsing Polychondritis
Crystal Deposition Arthritides
Seronegative Spondyloarthritis
Infectious Arthritis & Bursitis
Connective Tissue Diseases
Systemic Lupus Erythematosus
Vasculitis
IgG4-Related Disease
Cryoglobulinemia
Amyloidosis

NEUROLOGY
Omar Al-Louzi, Leeann Brigham Burton, Kristin Galetta, Morgan Prust, Michael P.
Bowley
Change in Mental Status
Seizures
Alcohol Withdrawal
Dizziness
Stroke
Weakness & Neuromuscular Dysfunction
Headache
Back and Spinal Cord Disease

CONSULTS
Sarah J. Carlson, Jennifer F. Tseng, Katherine T. Chen, Stella K. Kim
Surgical Issues
Ob/Gyn Issues
Ophthalmic Issues

APPENDIX
ICU Medications & Treatment of Hypotension/Shock
Antibiotics
Formulae and Quick Reference

ABBREVIATIONS
INDEX
PHOTO INSERTS
Radiology
Echocardiography & Coronary Angiography
Peripheral Blood Smears & Leukemias
Urinalysis

ACLS
 CONTRIBUTING AUTHORS

Andrew S. Allegretti, MD, MSc

Director of ICU Nephrology, Attending Physician, Nephrology Division, and
Principal Investigator, Kidney Research Center, Massachusetts General Hospital
Instructor of Medicine, Harvard Medical School

Omar Al-Louzi, MD
Neurology Resident, Partners Neurology Residency

Alexander Blair, MD
Internal Medicine Resident, Massachusetts General Hospital

Michael P. Bowley, MD, PhD

Instructor in Neurology, Massachusetts General Hospital
Associate Program Director, Partners Neurology Residency Program

Leeann Brigham Burton, MD

Neurology Resident, Partners Neurology Residency

Sarah J. Carlson
Assistant Professor of Surgery, Boston University of Medicine
Attending Surgeon, Boston Veterans Affairs Healthcare

Alison C. Castle, MD
Internal Medicine Resident, Massachusetts General Hospital

Katherine T. Chen, MD, MPH

Vice-Chair of Ob/Gyn Education, Career Development, and Mentorship
Professor of Obstetrics, Gynecology, and Reproductive Science
Professor of Medical Education
Icahn School of Medicine at Mount Sinai, New York

Caitlin Colling, MD
Internal Medicine Resident, Massachusetts General Hospital

Jean M. Connors, MD
Medical Director, Anticoagulation Management Services
Hematology Division, Brigham and Women’s Hospital & Dana-Farber Cancer
Institute
Associate Professor of Medicine, Harvard Medical School

Daniel J. DeAngelo, MD, PhD

Chief of the Division of Leukemia, Dana-Farber Cancer Institute
Professor of Medicine, Harvard Medical School

Rachel Frank, MD
Internal Medicine Resident, Massachusetts General Hospital

Robert P. Friday, MD, PhD

Chief, Division of Rheumatology, Newton-Wellesley Hospital
Affiliate Physician, Rheumatology Unit, Massachusetts General Hospital
Instructor in Medicine, Harvard Medical School

Lawrence S. Friedman, MD
The Anton R. Fried, MD, Chair, Department of Medicine, Newton-Wellesley Hospital
Assistant Chief of Medicine, Massachusetts General Hospital
Professor of Medicine, Harvard Medical School
Professor of Medicine, Tufts University School of Medicine

Kristin Galetta, MD
Neurology Resident, Partners Neurology Residency

Kristen Hysell, MD
Infectious Disease Fellow, Massachusetts General Hospital

Tanya E. Keenan, MD, MPH

Hematology-Oncology Fellow, Dana-Farber/Partners CancerCare

Stella K. Kim, MD
Joe M. Green Jr. Professor of Clinical Ophthalmology
Ruiz Department of Ophthalmology and Visual Sciences
Robert Cizik Eye Clinic
University of Texas McGovern School of Medicine

Emily Walsh Lopes, MD

Gastroenterology Fellow, Massachusetts General Hospital

Melissa Lumish, MD
Internal Medicine Resident, Massachusetts General Hospital

Jason Maley, MD
Pulmonary Fellow, Massachusetts General Hospital
Michael Mannstadt, MD
Chief, Endocrine Unit, Massachusetts General Hospital
Associate Professor of Medicine, Harvard Medical School

Arielle Medford, MD
Internal Medicine Resident, Massachusetts General Hospital

Nino Mihatov, MD
Cardiology Fellow, Massachusetts General Hospital

Mazen Nasrallah, MD, MSc

Rheumatology Fellow, Massachusetts General Hospital

Walter J. O’Donnell, MD
Staff Physician, Pulmonary/Critical Care Unit, Massachusetts General Hospital
Assistant Professor of Medicine, Harvard Medical School

Michelle L. O’Donoghue, MD, MPH

Senior Investigator, TIMI Study Group
Associate Physician, Cardiovascular Division, Brigham and Women’s Hospital
Affiliate Physician, Cardiology Division, Massachusetts General Hospital
Associate Professor of Medicine, Harvard Medical School

Nilay Patel, MD
Cardiology Fellow, Massachusetts General Hospital

Morgan Prust, MD
Neurology Resident, Massachusetts General Hospital

Stephanie M. Rutledge, MBBCh, BAO, MRCPI

Internal Medicine Resident, Massachusetts General Hospital

David P. Ryan, MD
Clinical Director, Massachusetts General Hospital Cancer Center
Chief of Hematology/Oncology, Massachusetts General Hospital
Professor of Medicine, Harvard Medical School

Marc S. Sabatine, MD, MPH

Chairman, TIMI Study Group
Lewis Dexter, MD, Distinguished Chair in Cardiovascular Medicine, Brigham and
Women’s Hospital
Affiliate Physician, Cardiology Division, Massachusetts General Hospital
Professor of Medicine, Harvard Medical School

Harish Seethapathy, MBBS

Nephrology Fellow, BWH/MGH Joint Nephrology Fellowship Program

Shilpa Sharma, MD
Internal Medicine Resident, Massachusetts General Hospital

Harshabad Singh, MBBS

Instructor, Gastrointestinal Cancer Treatment Center, Dana-Farber Cancer Institute

Isaac D. Smith, MD
Internal Medicine Resident, Massachusetts General Hospital

Miranda Theodore, MD
Internal Medicine Resident, Massachusetts General Hospital

Jennifer F. Tseng, MD, MPH

Utley Professor and Chair, Boston University School of Medicine
Surgeon-in-Chief, Boston Medical Center

Armen Yerevanian, MD
Endocrinology Fellow, Massachusetts General Hospital

Kimon C. Zachary, MD
Assistant Professor of Medicine, Infectious Disease Division, Massachusetts
General Hospital
 FOREWORD

To the 1st Edition

It is with the greatest enthusiasm that I introduce Pocket Medicine. In an era of

information glut, it will logically be asked, “Why another manual for medical house
officers?” Yet, despite enormous information readily available in any number of
textbooks, or at the push of a key on a computer, it is often that the harried house
officer is less helped by the description of differential diagnosis and therapies than
one would wish.
Pocket Medicine is the joint venture between house staff and faculty expert in a
number of medical specialties. This collaboration is designed to provide a rapid but
thoughtful initial approach to medical problems seen by house officers with great
frequency. Questions that frequently come from faculty to the house staff on
rounds, many hours after the initial interaction between patient and doctor, have
been anticipated and important pathways for arriving at diagnoses and initiating
therapies are presented. This approach will facilitate the evidence-based medicine
discussion that will follow the workup of the patient. This well-conceived handbook
should enhance the ability of every medical house officer to properly evaluate a
patient in a timely fashion and to be stimulated to think of the evidence supporting
the diagnosis and the likely outcome of therapeutic intervention. Pocket Medicine
will prove to be a worthy addition to medical education and to the care of our
patients.

DENNIS A. AUSIELLO, MD
Physician-in-Chief, Massachusetts General Hospital
Jackson Professor of Clinical Medicine, Harvard Medical School
 PREFACE

To my parents, Matthew and Lee Sabatine, to their namesake

grandchildren Matteo and Natalie, and to my wife Jennifer

Written by residents, fellows, and attendings, the mandate for Pocket Medicine
was to provide, in a concise a manner as possible, the key information a clinician
needs for the initial approach to and management of the most common inpatient
medical problems.
The tremendous response to the previous editions suggests we were able to
help fill an important need for clinicians. With this seventh edition come several
major improvements. We have updated every topic thoroughly. In particular, we
have included the newest diagnostic algorithms and pharmacotherapy for acute
coronary syndromes, the revolutionary data for transcatheter aortic valve
replacement (TAVR), and distilled the most recent guidelines for the classification
and treatment of hypertension. We have added a dedicated section for the
management of cystic fibrosis and updated the treatment of sepsis and shock. We
continue to revise the approach to malignancies based on molecular classification
and the corresponding biologic therapies, including dedicated sections on
immunotherapy. We have incorporated the paradigm-shifting data for diabetes
medications that lower cardiovascular risk and cover the newest classes of lipid-
lowering therapies. As always, we have incorporated key references to the most
recent high-tier reviews and important studies published right up to the time
Pocket Medicine went to press. We welcome any suggestions for further
improvement.
This edition builds on the work of the many contributors to prior editions of
Pocket Medicine. In addition, we appreciate the advice on specific topics from
additional attendings including Dr. Adam Sperling.
Of course, medicine is far too vast a field to ever summarize in a textbook of
any size. Long monographs have been devoted to many of the topics discussed
herein. Pocket Medicine is meant only as a starting point to guide one during the
initial phases of diagnosis and management until one has time to consult more
definitive resources. Although the recommendations herein are as evidence-based
as possible, medicine is both a science and an art. As always, sound clinical
judgement must be applied to every scenario.
 I am grateful for the support of the house officers, fellows, and attendings at
the Massachusetts General Hospital. It is a privilege to work with such a
knowledgeable, dedicated, and compassionate group of physicians. I always look
back on my time there as Chief Resident as one of my best experiences. I am
grateful to several outstanding clinical mentors, including Hasan Bazari, Larry
Friedman, Nesli Basgoz, Eric Isselbacher, Mike Fifer, and Roman DeSanctis, as well
as the late Charlie McCabe, Mort Swartz, and Peter Yurchak.
This edition would not have been possible without the help of Melinda Cuerda
and Abby Cange, my academic coordinators. They shepherded every aspect of the
project from start to finish, with an incredible eye to detail to ensure that each
page of this book was the very best it could be.
Lastly, special thanks to my parents for their perpetual encouragement and love
and, of course, to my wife, Jennifer Tseng, who, despite being a surgeon, is my
closest advisor, my best friend, and the love of my life.
I hope that you find Pocket Medicine useful throughout the arduous but
incredibly rewarding journey of practicing medicine.

MARC S. SABATINE, MD, MPH

 ELECTROCARDIOGRAPHY

Approach (a systematic approach is vital)

• Rate (? tachy or brady) and rhythm (? P waves, regularity, P &
QRS relationship)
• Intervals (PR, QRS, QT) and axis (? LAD or RAD)
• Chamber abnormality (? LAA and/or RAA, ? LVH and/or RVH)
• QRST changes (? Q waves, poor R-wave progression V1–V6, ST
↑/↓ or T-wave ∆s)

Figure 1-1 QRS axis

Left axis deviation (LAD)

• Definition: axis beyond –30° (S > R in lead II)
• Etiologies: LVH, LBBB, inferior MI, WPW
• Left anterior fascicular block (LAFB): LAD (–45 to –90°) and
qR in aVL and QRS <120 msec and no other cause of LAD (eg,
 IMI)
Right axis deviation (RAD)
• Definition: axis beyond +90° (S > R in lead I)
• Etiologies: RVH, PE, COPD (usually not > +110°), septal
defects, lateral MI, WPW
• Left posterior fascicular block (LPFB): RAD (90–180°) and rS
in I & aVL and qR in III & aVF and QRS <120 msec and no
other cause of RAD

Bifascicular block: RBBB + LAFB/LPFB. “Trifascicular block”: bifascicular block + 1°

AVB.

Prolonged QT interval (NEJM 2008;358:169; www.torsades.org)

• Measure QT from start of QRS to end of Tw (use longest QT, often
V2-V3, omit U wave)
• QT varies w/ HR → corrected w/ Bazett formula: QTc = QT/
(RR in sec), overcorrects at high HR, undercorrects at low HR
(nl QTc <450 msec ♂, <460 msec ♀)
• Fridericia’s formula preferred at very high or low HR: QTc = QT/

• QT prolongation a/w ↑ risk TdP (espec >500 msec); establish

baseline QT and monitor if using QT prolonging meds, no estab
guidelines for stopping Rx if QT prolongs
• Etiologies:
Antiarrhythmics: class Ia (procainamide, disopyramide),
class III (amio, sotalol, dofet)
Psych drugs: antipsychotics (phenothiazines, haloperidol,
atypicals), Li, ? SSRI, TCA
Antimicrobials: macrolides, quinolones, azoles, pentamidine,
atazanavir
Other: antiemetics (droperidol, 5-HT3 antagonists), alfuzosin,
methadone, ranolazine
Electrolyte disturbances: hypoCa (nb, hyperCa a/w ↓ QT),
± hypoK, ? hypoMg
Autonomic dysfxn: ICH (deep TWI), Takotsubo, stroke, CEA,
neck dissection
Congenital (long QT syndrome): K, Na, & Ca channelopathies
(Circ 2013;127:126)
Misc: CAD, CMP, bradycardia, high-grade AVB, hypothyroidism,
hypothermia, BBB

Left ventricular hypertrophy (LVH) (Circ 2009;119:e251)

• Etiologies: HTN, AS/AI, HCM, coarctation of aorta
• Criteria (all w/ Se <50%, Sp >85%; accuracy affected by age,
sex, race, BMI)
Sokolow-Lyon: S in V1 + R in V5 or V6 ≥35 mm or R in aVL
≥11 mm (↓ Se w/ ↑ BMI)
Cornell: R in aVL + S in V3 >28 mm in men or >20 mm in
women
Romhilt-Estes point-score system (4 points = probable; 5
points = diagnostic): ↑ volt: limb lead R or S ≥20 mm or S in
V1 or V2 ≥30 mm or R in V5 or V6 ≥30 mm (3 pts)
 ST displacement opposite to QRS deflection: w/o dig (3 pts);
w/ dig (1 pt)
LAA (3 pts); LAD (2 pts); QRS duration ≥90 msec (1 pt)
Intrinsicoid deflection (QRS onset to peak of R) in V5 or V6
≥50 msec (1 pt)
If LAFB present: S in III + max (R+S) in any lead ≥30 mm in
men or ≥28 mm in women
Right ventricular hypertrophy (RVH) (Circ 2009;119:e251; JACC
2014;63:672)
• Etiologies: cor pulmonale, congenital (tetralogy of Fallot, TGA, PS,
ASD, VSD), MS, TR
• Criteria [all insensitive, but specific (except in COPD); all w/ poor
PPV in general population]
R > S in V1, R in V1 ≥6 mm, S in V5 ≥10 mm, S in V6 ≥3 mm,
R in aVR ≥4 mm
RAD ≥110° (LVH + RAD or prominent S in V5 or V6 → consider
biventricular hypertrophy)
Ddx of dominant R wave in V1 or V2
• Ventricular abnl: RVH (RAD, RAA, deep S waves in I, V5, V6);
HCM; Duchenne’s
• Myocardial injury: posterior MI (anterior R wave = posterior Q
wave; often with IMI)
• Abnormal depolarization: RBBB (QRS >120 msec, rSR′); WPW (↓
PR, δ wave, ↑ QRS)
• Other: dextroversion; counterclockwise rotation; lead
misplacement; nl variant
Poor R wave progression (PRWP) (Am Heart J 2004;148:80)
• Definition: loss of anterior forces w/o frank Q waves (V1–V3); R
wave in V3 ≤3 mm
• Possible etiologies (nonspecific):
old anteroseptal MI (usually w/ R wave V3 ≤1.5 mm, ±
persistent ST ↑ or TWI V2 & V3)
 LVH (delayed RWP w/ ↑ left precordial voltage), RVH, COPD
(may also have RAA, RAD, limb lead QRS amplitude ≤5 mm,
SISIISIII w/ R/S ratio <1 in those leads)
LBBB; WPW; clockwise rotation of the heart; lead
misplacement; CMP; PTX
Pathologic Q waves
• Definition: ≥30 msec (≥20 msec V2–V3) or >25% height of R
wave in that QRS complex
• Small (septal) q waves in I, aVL, V5 & V6 are nl, as can be isolated
Qw in III, aVR, V1
• “Pseudoinfarct” pattern may be seen in LBBB, infiltrative dis.,
HCM, COPD, PTX, WPW
ST elevation (STE) (NEJM 2003;349:2128; Circ 2009;119:e241 & e262)
• Acute MI: upward convexity STE (ie, a “frown”) ± TWI (or prior
MI w/ persistent STE)
• Coronary spasm: Prinzmetal’s angina; transient STE in a
coronary distribution
• Pericarditis: diffuse, upward concavity STE (ie, a “smile”); a/w
PR ↓; Tw usually upright
• HCM, Takotsubo CMP, ventricular aneurysm, cardiac
contusion
• Pulmonary embolism: occ. STE V1–V3; classically a/w TWI V1–
V4, RAD, RBBB, S1Q3T3
• Repolarization abnormalities:
LBBB (↑ QRS duration, STE discordant from QRS complex; see
“ACS” for dx MI in LBBB)
LVH (↑ QRS amplitude); Brugada syndrome (rSR′, downsloping
STE V1–V2); pacing
Hyperkalemia (↑ QRS duration, tall Ts, no P’s); epsilon waves
(late afterdepol.) in ARVC
• aVR: STE >1 mm a/w ↑ mortality in STEMI; STE aVR > V1 a/w
left main disease
• Early repolarization: most often seen in V2–V5 in young adults
(Circ 2016;133:1520)
1–4 mm elev of peak of notch or start of slurred downstroke of
R wave (ie, J point); ± up concavity of ST & large Tw (∴
ratio of STE/T wave <25%; may disappear w/ exercise)
? early repol in inf leads may be a/w ↑ risk of VF (NEJM
2009;361:2529; Circ 2011;124:2208)

ST depression (STD)
• Myocardial ischemia (± Tw abnl)
• Acute true posterior MI: posterior STE appearing as anterior
STD (± ↑ R wave) in V1–V3 ✔ posterior ECG leads; manage as
a STEMI with rapid reperfusion (see “ACS”)
• Digitalis effect (downsloping ST ± Tw abnl; does not correlate w/
dig levels)
• Hypokalemia (± U wave)
• Repolarization abnl a/w LBBB or LVH (usually in leads V5, V6, I,
aVL)
T wave inversion (TWI; generally ≥1 mm; deep if ≥5 mm)
(Circ 2009;119:e241)
• Ischemia or infarct; Wellens’ sign (deep, symm precordial TWI) →
critical prox LAD lesion
• Myopericarditis; CMP (Takotsubo, ARVC, apical HCM); MVP; PE
(espec if TWI V1–V4)
• Repolarization abnl in a/w LVH/RVH (“strain pattern”); BBB; nl
variant if QRS predom. ⊖
• Posttachycardia or postpacing (“memory” T waves)
• Electrolyte, digoxin, PaO2, PaCO2, pH/core temp ∆’s, intracranial
bleed (“cerebral Tw”)
Low voltage
• QRS amplitude (R + S) <5 mm in all limb leads & <10 mm in all
precordial leads
• Etiol: COPD, pericard./pleural effusion, myxedema, ↑ BMI,
amyloid, diffuse CAD
Electrolyte abnormalities
• ↑ K: tented Tw, ↓ QT, ↑ PR, AVB, wide QRS, STE; ↓ K: flattened
Tw, U waves, ↑ QT
• ↑ Ca: ↓ QT, flattened Tw & Pw, J point elevation; ↓ Ca: ↑ QT; Tw
∆s
ECG in young athletes (JACC 2017;69:805)
• Normal patterns may incl. LVH, RVH, early repol
• Evaluate if: arrhythmias, HR <30, prolonged QT, ε/δ waves, LBBB,
Brugada pattern, QRS >140 ms, PR >400 ms, Mobitz II, 3˚
AVB, ST depression, TWI

CHEST PAIN

Disorder Typical Characteristics & Diagnostic Studies

Cardiac Causes
ACS Substernal “pressure” (! LR 1.3) → neck, jaw, arm (! LR 1.3–
(15–25% of 1.5)
chest pain in Sharp, pleuritic, positional, or reprod. w/ palp all w/ ⊕ LR
ED) ≤0.35
Diaphoresis (⊕ LR 1.4), dyspnea (⊕ LR 1.2), a/w exertion (⊕
LR 1.5–1.8)
≈ prior MI (⊕ LR 2.2); ↓ w/ NTG/rest (but not reliable; Annals
EM 2005;45:581)
± ECG ∆s: STE, STD, TWI, Qw. ± ↑ Troponin.
Pericarditis Sharp pain → trapezius, ↑ w/ respiration, ↓ w/ sitting forward.
& myo- ± Pericardial friction rub. ECG ∆s (diffuse STE & PR ↓, opposite
pericarditis in aVR) ± pericardial effusion. If myocarditis, same as above +
↑ Tn and ± s/s HF and ↓ EF.
Aortic Sudden severe tearing pain (absence ⊖ LR 0.3). ± Asymm
dissection (>20 mmHg) BP or pulse (⊕ LR 5.7), focal neuro deficit (⊕ LR
>6), AI, widened mediast. on CXR (absence ⊖ LR 0.3); false
lumen on imaging. (JAMA 2002;287:2262)
 Pulmonary Causes
Pneumonia Pleuritic; dyspnea, fever, cough, sputum. ↑ RR, crackles. CXR
infiltrate.
Pleuritis Sharp, pleuritic pain. ± Pleuritic friction rub.
PTX Sudden onset, sharp pleuritic pain. Hyperresonance, ↓ BS. PTX
on CXR.
PE Sudden onset pleuritic pain. ↑ RR & HR, ↓ SaO2, ECG ∆s (sinus
tach, RAD, RBBB, SIQIIITIII, TWI V1–V4, occ STE V1–V3), +
CTA or V/Q, ± ↑ Tn.
Pulm HTN Exertional pressure, DOE. ↓ SaO2, loud P2, RV heave, right S3
and/or S4.

GI Causes
Esophageal Substernal burning, acid taste in mouth, water brash. ↑ by
reflux meals, recumbency; ↓ by antacids. EGD, manometry, pH
monitoring.
Esoph Intense substernal pain. ↑ by swallowing, ↓ by NTG/CCB.
spasm Manometry.
Mallory- Esoph tear precipitated by vomiting. ± Hematemesis. Dx w/
Weiss EGD.
Boerhaave Esoph rupture. Severe pain, ↑ w/ swallow. Mediastinal air
palpable & on CT.
PUD Epigastric pain, relieved by antacids. ± GIB. EGD, ± H. pylori
test.
Biliary dis. RUQ pain, N/V. ↑ by fatty foods. RUQ U/S; ↑ LFTs.
Pancreatitis Epigastric/back discomfort. ↑ amylase & lipase; abd CT.
Musculoskeletal and Miscellaneous Causes
Costochond Localized sharp pain. ↑ w/ movement. Reproduced by
palpation.
Zoster Intense unilateral pain. Pain may precede dermatomal rash.
Anxiety “Tightness,” dyspnea, palpitations, other somatic symptoms

(Braunwald’s Heart Disease, 11th ed, 2018; JAMA 2015;314:1955)

Initial approach
• Focused history: quality, severity, location, radiation;
provoking/palliating factors; intensity at onset; duration, freq,
& pattern; setting; assoc sx; cardiac hx & risk factors
• Targeted exam: VS (incl. BP in both arms); gallops, murmurs,
rubs; signs of vascular dis. (carotid/femoral bruits, ↓ pulses) or
CHF; lung & abd. exam; chest wall for reproducibility
• 12-lead ECG: obtain w/in 10 min; comp to priors & obtain serial
ECGs; consider posterior leads (V7–V9) to ✔ for posterior
STEMI if: hx c/w ACS but stnd ECG unrevealing; ST ↓ V1–V3
(ant ischemia vs. post STEMI) w/ refractory angina; or R/S >1
in V1–V2
• CXR; other imaging (echo, PE CTA, etc.) as indicated based on
H&P and initial testing
• Troponin: >99th %ile w/ rise and/or fall in approp. setting is dx
of AMI (Circ 2018;138:e618)
Detectable 1–6 h after injury, peaks 24 h, may be elevated for
7–14 d in STEMI ✔ at presentation & 3–6 h later; repeat if
clinical or ECG ∆s; ? sex-specific cutpoints If high-sens Tn
(hsTn) assay, can ✔ at presentation & 1 h later; assess level
&Δ
• Causes for ↑ Tn other than plaque rupture (= “type 1 MI”): (1)
Supply-demand mismatch not due to ∆ in CAD (= “type 2 MI”;
eg, ↑↑ HR, shock, HTN crisis, spasm, severe AS), (2) non-
ischemic injury (myocarditis/toxic CMP, cardioversion, cardiac
contusion) or (3) multifactorial (PE, sepsis, severe HF, renal
failure, Takotsubo, infilt dis.)
• CK-MB: less Se & Sp than Tn (other sources: skel. muscle,
intestine, etc.); CK-MB/CK ratio >2.5 → cardiac source. Limited
utility: ? higher bar for post-revasc MI; early reMI.
Early noninvasive imaging
• Low prob of ACS (eg, ⊖ ECG & Tn) & stable → outPt or inPt
noninv. fxnal or imaging test (qv)
• CCTA w/ high NPV, low PPV. ↓ LOS c/w fxnal testing (NEJM
2012;366:1393). In stable outPt w/ CP, CCTA added to standard
 of care ↑ early but not overall angiography/revasc; ↑ use of
preventive med Rx, and ↓ coronary death/MI at 5 y (NEJM
2018;379:924).
• “Triple r/o” CT angiogram sometimes performed to r/o CAD, PE,
AoD if dx unclear

NONINVASIVE EVALUATION OF
CAD

Stress testing (JACC 2012;60:1828; J Nucl Cardiol 2016; 23:606)

• Indications: dx obstructive CAD, evaluate ∆ in clinical status in
Pt w/ known CAD, risk stratify after ACS, evaluate exercise
tolerance, localize ischemia (imaging required)
• Contraindications (Circ 2002;106:1883; & 2012;126:2465)
Absolute: AMI w/in 48 h, high-risk UA, acute PE, severe sx
AS, uncontrolled HF, uncontrolled arrhythmias,
myopericarditis, acute aortic dissection
Relative (discuss with stress lab): left main CAD, mod
symptomatic valvular stenosis, severe HTN, HCMP, high-
degree AVB, severe electrolyte abnl
Exercise tolerance test (w/ ECG alone)
• Generally preferred if Pt can meaningfully exercise; ECG ∆s w/ Se
~65%, Sp ~80%
• Typically via treadmill w/ Bruce protocol (modified Bruce or
submax if decond. or recent MI)
• Hold anti-isch. meds (eg, nitrates, βB) if dx’ing CAD but give to
assess adequacy of meds
Pharmacologic stress test (nb, requires imaging because ECG not
interpretable)
• Use if unable to exercise, low exercise tolerance, or recent MI. Se
& Sp ≈ exercise.
• Preferred if LBBB, WPW or V-paced, because higher prob of false
⊕ imaging with exercise
• Coronary vasodilator: diffuse vasodilation → relative “coronary
steal” from vessels w/ fixed epicardial dis. Reveals CAD, but not
if Pt ischemic w/ exercise. Regadenoson (↓ side effects),
dipyridamole, adenosine. Side effects: flushing, ↓ HR, AVB,
SOB, bronchospasm.
• Chronotropes/inotropes (dobuta): more physiologic, but longer
test; may precip arrhythmia
Imaging for stress test
• Use if uninterpretable ECG (V-paced, LBBB, resting ST ↓ >1 mm,
digoxin, LVH, WPW), after indeterminate ECG test, or if
pharmacologic test
• Use when need to localize ischemia (often used if prior coronary
revasc)
• Radionuclide myocardial perfusion imaging w/ images
obtained at rest & w/ stress
SPECT (eg, 99mTc-sestamibi): Se ~85%, Sp ~80%
PET (rubidium-82): Se ~90%, Sp ~85%; requires
pharmacologic stress, not exercise
ECG-gated imaging allows assessment of regional LV fxn (sign
of ischemia/infarction)
• Echo (exercise or dobuta): Se ~85%, Sp ~85%; no radiation;
operator dependent
• Cardiac MRI (w/ pharmacologic stress) another option with
excellent Se & Sp
Test results
• HR (must achieve ≥85% of max pred HR [220-age] for exer. test
to be dx), BP response, peak double product (HR × BP; nl
>20k), HR recovery (HRpeak – HR1 min later; nl >12)
• Max exercise capacity achieved (METS or min); occurrence
of symptoms
• ECG ∆s: downsloping or horizontal ST ↓ (≥1 mm) 60–80 ms after
QRS predictive of CAD (but does not localize ischemic
territory); however, STE highly predictive & localizes
• Duke treadmill score = exercise min – (5 × max ST dev) – (4 ×
angina index) [0 none, 1 nonlimiting, 2 limiting]; score ≥5 →
<1% 1-y mort; –10 to + 4 → 2–3%; ≤–11 → ≥5%
• Imaging: radionuclide defects or echocardiographic regional wall
motion abnormalities
reversible defect = ischemia; fixed defect = infarct; transient
isch dilation → ? severe 3VD
false ⊕: breast → ant defect; diaphragm → inf defect. False
⊖: balanced (3VD) ischemia.
High-risk test results (PPV ~50% for LM or 3VD, ∴ consider coronary
angio)
• ECG: ST ↓ ≥2 mm or ≥1 mm in stage 1 or in ≥5 leads or ≥5 min
in recovery; ST ↑; VT
• Physiologic: ↓ or fail to ↑ BP, <4 METS, angina during exercise,
Duke score ≤–11; ↓ EF
• Radionuclide: ≥1 lg or ≥2 mod. reversible defects, transient LV
cavity dilation, ↑ lung uptake
Myocardial viability (Circ 2008;117:103; Eur Heart J 2011;31:2984 &
2011;32:810)
• Goal: identify hibernating myocardium that could regain fxn after
revascularization
• Options: MRI (Se ~85%, Sp ~75%), PET (Se ~90%, Sp ~65%),
dobutamine stress
echo (Se ~80%, Sp ~80%); SPECT/rest-redistribution (Se
~85%, Sp ~60%)
In Pts w/ LV dysfxn, viabil. doesn’t predict ↑ CABG benefit vs.
med Rx (NEJM 2011;364:1617)
Coronary CT/MR angio (NEJM 2008;359:2324; Circ 2010;121:2509;
Lancet 2012;379:453)
• Pts w/ CP: CCTA 100% Se, 54% Sp for ACS, ∴ NPV 100%, PPV
17% (JACC 2009;53:1642). ↓ LOS, but ↑ cath/PCI, radiation vs.
 fxnal study (NEJM 2012;367:299; JACC 2013;61:880).
• Sx outPt: CCTA vs. fxnal testing → ↑ radiation, cath/PCI early; by
5 y, ↓ CHD death/MI w/ similar rates of cath/PCI (NEJM
2018;379:924)
• Unlike CCTA, MR does not require iodinated contrast or radiation,
and can assess LV fxn
Coronary artery calcium score (NEJM 2012;366:294; JAMA
2012;308:788)
• Quantifies extent of calcium; thus, estimates plaque burden (but
not % coronary stenosis)
• CAC sensitive (91%) but not specific (49%) for presence of CAD;
high NPV to r/o CAD
• May provide incremental value to clinical scores for risk
stratification (JAMA 2004;291:210). ACC/AHA guidelines note CAC
assessment is reasonable in asx Pts w/ intermed risk (7.5–
<20% 10-y risk) and selected borderline risk (5– <7.5% 10-y
risk) (Circ 2019;139:e1082).

CORONARY ANGIOGRAPHY AND

REVASCULARIZATION

Indications for coronary angiography in stable CAD, asx Pts,

and others
• CCS class III–IV angina despite med Rx, angina + systolic dysfxn,
or unexplained low EF
• High-risk stress test findings (qv) or uncertain dx after noninv
testing (& info will ∆ mgmt)
• Occupational need for definitive dx (eg, pilot) or inability to
undergo noninvasive testing
• Survivor of SCD, polymorphic VT, sustained monomorphic VT
• Suspected spasm; nonathero cause of ischemia (eg, anomalous
coronary; CCTA preferred)
• Preop workup in select Pts undergoing organ transplant eval
(CCTA reasonable)
Precath checklist & periprocedural pharmacotherapy
• Peripheral arterial exam (radial, femoral, DP, PT pulses; bruits); ✔
palmar arch intact (eg, w/ pulse oximetry & plethysmography).
✔ can lie flat, NPO >6 h.
• ✔CBC, PT, Cr; hold ACEI/ARB if renal dysfxn (see “CIAKI”). Blood
bank sample.
• ASA 325 mg × 1. Timing of P2Y12 inhib debated. ASAP for STEMI.
? preRx NSTEACS if clopi (JAMA 2012;308:2507) or ticagrelor, not
prasugrel. Cangrelor (IV P2Y12 inhib) ↓ peri-
PCI events vs. clopi w/o PreRx (NEJM 2013;368:1303). ? statin
preRx (Circ 2011;123:1622).
Coronary revascularization in stable CAD (NEJM 2016;374:1167;
JACC 2017;69:2212)
• Optimal med Rx (OMT): preferred 1st line if stable disease w/o
critical anatomy & w/ nl EF
• PCI: ↓ angina; no ∆ exercise time (Lancet 2018;391:31) or D/MI
(NEJM 2015;373:1204);
if ≥1 stenosis w/ FFR (qv) ≤0.8, ↓ urg revasc & MI c/w OMT
(NEJM 2018;379:250)
• CABG (NEJM 2016;374:1954): in older studies, ↓ mort. c/w OMT if
3VD, LM, 2VD w/ crit. prox LAD, esp. if ↓ EF; recently
confirmed if multivessel dis. & EF <35% (NEJM 2016;374:1511);
radial artery ↑ patency & ↓ MACE vs. saphenous vein grafts
(NEJM 2018;378:2069); less complete revasc & possibly ↑ mort. w/
off vs. on-pump (NEJM 2016;375:2359 & 377:623)
• If revasc deemed necessary, PCI if limited # of discrete lesions, nl
EF, no DM, poor operative candidate; CABG if extensive or
diffuse disease, ↓ EF, DM or valvular disease; SYNTAX score II:
ID Pts w/ ↑ benefit w/ CABG (Lancet 2013;381:639); if multivessel
disease w/ high complexity or DM, CABG ↓ mortality (Lancet
 2018;391:939); if LM disease, PCI ≈ CABG, but ↑ repeat revasc
w/ PCI (JAMA Cardiol. 2017;2:1079)
PCI and peri-PCI interventions
• Access: radial ↓ bleed/vasc comp (? ↓ death in ACS) vs. fem (Circ
CV Interv 2018;11:e000035)
• Fractional flow reserve (FFR): ratio of max flow (induced by
adenosine) distal vs. prox to stenosis to ID hemodyn. signif.
lesions (≤0.80). Instantaneous wave-free ratio (iFR) similar to
FFR, doesn’t require vasodilator; iFR threshold ≤0.89 (NEJM
2017;376:1813 & 1824).
• Balloon angioplasty by itself rare b/c elastic recoil; reserved for
lesions too narrow to stent
• Bare metal stents (BMS): ↓ restenosis & repeat revasc c/w
angioplasty alone
• Drug-eluting stents (DES): latest DES ↓ cardiac death or MI,
repeat revasc, and stent thrombosis vs. BMS (Lancet
2019;393:2503)
• Antiplt Rx: DAPT (ASA 81 + P2Y12 inhib) in SIHD for 4 wk (BMS)
or ≥6 mo (DES); in ACS (qv) for 12 mo and possibly beyond
(JAMA Cards 2016;1:627). Data emerging for DAPT for just 1 mo,
followed by P2Y12 inhib for 11 mo (Lancet 2018;392:940; JAMA
2019;321:2414 & 2428).
• If need long-term oral anticoag, consider clopi+DOAC and
consider stopping ASA (? after ~1 wk) as ↓ bleed, but trend
small ↑ ischemic risk (Lancet 2013;381:1107 & NEJM 2019;380:1509)
Post-PCI complications (NEJM 2017;377:1513)
• Postprocedure ✔ vascular access site, distal pulses, ECG, CBC, Cr
• Bleeding: if hematoma/overt bleeding → manual
compression, reverse/stop anticoag.
Retroperitoneal bleed: may p/w ↓ Hct ± back pain; ↑ HR & ↓
BP late; Dx w/ abd/pelvic CT (I–); Rx: reverse/stop anticoag
(d/w interventionalist), IVF/PRBC/plts as required.
• Vascular damage (~1% of dx angio, ~5% of transfemoral PCI;
Circ 2007;115:2666)
 Pseudoaneurysm: triad of pain, expansile mass, systolic bruit;
Dx: U/S; Rx (if pain or >2 cm): manual or U/S-directed
compression, thrombin injection, or surgical repair
AV fistula: continuous bruit; Dx: U/S; Rx: surgical repair if large
or sx
LE ischemia (emboli, dissection, clot): cool, mottled extremity,
↓ distal pulses; Dx: pulse volume recording (PVR), angio;
Rx: percutaneous or surgical repair
• Peri-PCI MI: >5× ULN of Tn/CK-MB + either sx or ECG/angio
∆s; Qw MI in <1%
• Contrast-induced AKI: w/in 48 h, peak 3–5 d; pre-hydration
reasonable (see “CIAKI”)
• Cholesterol emboli syndrome (typically in middle-aged &
elderly and w/ Ao atheroma)
renal failure (late and progressive, ± eos in urine); mesenteric
ischemia (abd pain, LGIB, pancreatitis); intact distal pulses
but livedo pattern and toe necrosis
• Stent thrombosis: mins-yrs after PCI, typically p/w AMI. Due to
mech prob. (stent underexpansion or unrecognized dissection,
typically presents early) or d/c of antiplt Rx; espec if d/c both
ASA & P2Y12 inhib (JAMA 2005;293:2126).
• In-stent restenosis: mos after PCI, typically p/w gradual ↑
angina (10% p/w ACS).
Due to combination of elastic recoil and neointimal hyperplasia;
↓ w/ DES vs. BMS.

ACUTE CORONARY SYNDROMES

Ddx (causes of myocardial ischemia/infarction other than atherosclerotic plaque
rupture)
• Nonatherosclerotic coronary artery disease (JACC
2018;72:2231)
Spasm: Prinzmetal’s variant, cocaine-induced (6% of chest pain
+ cocaine use r/i for MI)
Dissection: spontaneous (vasculitis, CTD, pregnancy), aortic
dissection with retrograde extension (usually involving RCA
→ IMI) or mechanical (PCI, surgery, trauma)
Embolism (Circ 2015;132:241): AF, thrombus/myxoma, endocard.,
prosth valve thrombosis
Vasculitis: Kawasaki syndrome, Takayasu arteritis, PAN, Churg-
Strauss, SLE, RA
Congenital: anomalous origin from aorta or PA, myocardial
bridge (intramural segment)
• Ischemia w/o plaque rupture (“type 2” MI): ↑ demand (eg, ↑
HR), ↓ supply (eg, HoTN)
• Direct myocardial injury: myocarditis; Takotsubo/stress CMP;
toxic CMP; cardiac contusion
Clinical manifestations (JAMA 2015;314:1955)
• Typical angina: retrosternal pressure/pain/tightness ± radiation
to neck, jaw, arms; precip. by exertion, relieved by rest/ NTG.
In ACS: new-onset, crescendo or at rest.
• Associated symptoms: dyspnea, diaphoresis, N/V, palpitations
or light-headedness
• Many MIs (~20% in older series) are initially unrecognized b/c
silent or atypical sx
• Atypical sxs (incl N/V & epig pain) ? more common in ♀, elderly,
diabetes, inferior ischemia
Physical exam
• Signs of ischemia: S4, new MR murmur 2° pap. muscle dysfxn,
paradoxical S2, diaphoresis
• Signs of heart failure: ↑ JVP, crackles in lung fields, ⊕ S3, HoTN,
cool extremities
• Signs of other vascular disease: asymmetric BP, carotid or femoral
bruits, ↓ distal pulses
Diagnostic studies (NEJM 2017;376:2053)
• ECG: ST ↓/↑, TWI, new LBBB, hyperacute Tw; Qw/PRWP may
suggest prior MI & ∴ CAD
✔ ECG w/in 10 min of presentation, with any ∆ in sx & at 6–12
h; compare w/ baseline
STEMI dx w/ old LBBB: ≥1 mm STE concordant w/ QRS (Se
73%, Sp 92%), STD ≥1 mm V1–V3 (Se 25%, Sp 96%), STE
≥5 mm discordant w/ QRS (Se 31%, Sp 92%)
Localization of MI
Anatomic Area ECG Leads w/ STE Coronary Artery
Septal V1–V2 ± aVR Proximal LAD
Anterior V3–V4 LAD

Apical V5–V6 Distal LAD, LCx, or

RCA
Lateral I, aVL LCx
Inferior II, III, aVF ± aVR RCA (~85%), LCx
(~15%)
RV V1–V2 & V4R (most Se) Proximal RCA
Posterior ST depression V1–V3 (= STE RCA or LCx
V7–V9 posterior leads, ✔ if
 clinical suspicion)

If ECG non-dx & suspicion high, ✔ leads V7–V9 to assess distal LCX/RCA territory.
✔ R-sided precordial leads in IMI to help detect RV involvement (STE in V4R most
Se). STE in III > STE in II and lack of STE in I or aVL suggest RCA rather than LCX
culprit in IMI. STE in aVR suggests LM or prox LAD occlusion or diffuse ischemia.

• Cardiac biomarkers: ✔ Tn (pref. over CK-MB) at presentation &

3–6 h (? 1hr if hsTn); repeat if clinical or ECG ∆s; >99th %ile
w/ rise and/or fall in appropriate clinical setting dx of AMI (see
“Chest Pain”); in CKD, ↑ Tn still portends poor prognosis (NEJM
2002;346:2047)
• If low prob, stress test, CT angio to r/o CAD; new wall motion
abnl on TTE suggests ACS
• Coronary angio gold standard for epicardial CAD
Prinzmetal’s (variant) angina
• Coronary spasm → transient STE usually w/o MI (but MI, AVB, VT
can occur)
• Pts usually young, smokers, ± other vasospastic disorders (eg,
migraines, Raynaud’s)
• Angiography: nonobstructive CAD (spasm can be provoked during
cath but rarely done)
• Treatment: high-dose CCB & standing nitrates (+SL prn), ? α-
blockers/statins; d/c smoking; avoid high-dose ASA (can inhibit
prostacyclin and worsen spasm), nonselect βB, triptans
• Cocaine-induced vasospasm: CCB, nitrates, ASA; ? avoid βB, but
labetalol appears safe
Approach to triage
• If hx, initial ECG & Tn non-dx, repeat ECG q15–30min × 1 h & Tn
3–6 h (? 1hr if hs) later
• If remain nl and low likelihood of ACS, search for alternative
causes of chest pain
• If remain nl, have ruled out MI, but if high suspicion for ACS
based on hx, then still need to r/o UA w/ stress test to assess
for inducible ischemia (or CTA to r/o epicardial CAD);
if low risk (eg, age ≤70; ∅ prior CAD, CVD, PAD; ∅ rest angina)
can do before d/c from ED or as outPt w/in 72 h (0%
mortality, <0.5% MI; Ann Emerg Med 2006;47:427)
if not low risk, admit and initiate Rx for possible ACS and
consider stress test or cath
Acute Anti-Ischemic and Analgesic Treatment
Nitrates (SL or IV) Use for relief of sx, Rx for HTN or HF. No clear ↓ in
0.3–0.4 mg SL q5min mortality.
× 3, then consider IV Caution if preload-sensitive (eg, HoTN, AS, sx RV
if still sx infarct); contraindicated if recent PDE5 inhibitor
use.
β-blockers ↓ ischemia & progression of UA to MI (JAMA
eg, metop 25–50 mg 1988;260:2259)
PO q6h titrate slowly STEMI: ↓ arrhythmic death & reMI, but ↑ cardiogenic
to HR 50–60 IV only shock early (espec if signs of HF) (Lancet
if HTN and no HF 2005;366:1622).
 Contraindic. PR >0.24 sec, HR <60, 2°/3° AVB, severe
bron-chospasm, s/s HF or low output, risk factors
for shock (eg, >70 y, HR >110, SBP <120, late
presentation STEMI)
CCB If cannot tolerate βB b/c bronchospasm
(nondihydropyridines)
Morphine Relieves pain/anxiety; venodilation ↓ preload. Do not
mask refractory sx. May delay antiplt effects of P2Y12
inhib.
Oxygen Use prn for resp distress or to keep SaO2 >90%; no
mortality benefit if SaO2 ≥90% (NEJM 2017;377:1240)

Other early adjunctive therapy

• High-intensity statin therapy (eg, atorva 80 mg qd; PROVE-IT
TIMI 22, NEJM 2004;350:1495); ↓ ischemic events w/ benefit
emerging w/in wks (JAMA 2001;285:1711 & JACC 2005;46:1405); ↓
peri-PCI MI (JACC 2010;56:1099); ? ↓ contrast-induced
nephropathy (NEJM 2019;380:2156)
• Ezetimibe: ↓ CV events when added to statin (IMPROVE-IT,
NEJM 2015;372:1500)
• ACEI/ARB: start once hemodynamics and renal function stable
Strong indication for ACEI if heart failure, EF <40%, HTN, DM,
CKD; ~10% ↓ mortality, greatest benefit in ant. STEMI or
prior MI (Lancet 1994;343:1115 & 1995;345:669)
ARB appear ≈ ACEI (NEJM 2003;349:20); give if contraindic to
ACEI
• IABP: can be used for refractory angina when PCI not available

NSTE-ACS (CIRC 2014;130:e344)

Key issues are antithrombotic regimen and invasive vs. conservative
strategy

Antiplatelet Therapy
Aspirin 50–70% ↓ D/MI (NEJM 1988;319:1105)
162–325 mg × 1, then 81 mg Low dose (~81 mg) pref long term (NEJM
qd 2010;363:930)
(non–enteric-coated, If allergy, use clopi and/or desensitize to ASA
chewable)
P2Y12 (ADP receptor) inhibitor (choose one of the following in addition to
ASA).
Timing (on presentation or at angiography) remains controversial. Some data
for upstream clopidogrel (JAMA 2012;308:2507). See below for specific
recommendations.
• Ticagrelor (preferred More rapid and potent plt inhib c/w clopi
over clopi) 16% ↓ CVD/MI/stroke & 21% ↓ CV death c/w
180 mg × 1 → 90 mg bid clopi; ↑ non-CABG bleeding (NEJM
Reversible, but wait 3–5 d 2009;361;1045)
prior to surg. Antidote Given upstream or at time of PCI
being developed (NEJM Dyspnea (but SaO2 & PFTs nl) & ventricular
2019;380:1825). pauses
Use only with ASA <100
mg qd
• Prasugrel (preferred over More rapid and potent plt inhib c/w clopi
clopi) 19% ↓ CVD/MI/stroke in ACS w/ planned PCI
60 mg × 1 if undergoing vs. clopi, but ↑ bleeding (NEJM
PCI → 10 mg qd 2007;359:2001), incl fatal bleeds
(consider 5 mg/d if In NSTE-ACS, should be given at time of PCI
<60 kg) and not upstream due to ↑ bleeding (NEJM
Wait 7 d prior to surgery 2013;369:999)
Contraindic. if h/o TIA/CVA; ? avoid if >75 y
• Clopidogrel* ASA+clopi → 20% ↓ CVD/MI/stroke vs. ASA
300–600 mg × 1 → 75 mg qd alone ↑ benefit if given hrs prior to PCI
Requires ~6 h to steady state (JAMA 2012;308:2507), but if require CABG,
need to wait >5 d after d/c clopi
• Cangrelor 22% ↓ CV events (mostly peri-PCI MI and
Only IV P2Y12 inhibitor stent thrombosis) vs. clopi 300 mg at time
Rapid onset/offset; t¹⁄² 3–5 of PCI; no significant ↑ bleeding (NEJM
min 2013;368:1303)
Consider for rapidly reversible P2Y12 inhibition
during PCI or as bridge to surgery in high-
risk Pts who need to stop P2Y12
GP IIb/IIIa inhibitors No clear benefit for routinely starting prior to
(GPI) PCI and ↑ bleeding (NEJM 2009;360:2176)
 abciximab; eptifibatide; Consider if refractory ischemia despite optimal
tirofiban Rx while awaiting angio or in high-risk Pts
Infusions given ≤24 h peri & (eg, large clot burden) at time of PCI,
post PCI; shorter (~2 h) espec if using clopi and no preRx.
as effective w/ ↓ bleeding
(JACC 2009;53:837)
*~30% pop has ↓ fxn CYP2C19 → ↑ CV events if PCI on clopi (NEJM
2009;360:354)

Anticoagulant Therapy (choose one)

UFH: 60 U/kg IVB 24% ↓ D/MI (JAMA 1996;276:811)
(max 4000 U) then Titrate to aPTT 1.5–2× control (~50–70 sec)
12 U/kg/h (max 1000 Hold until INR <2 if already on warfarin
U/h initially) × 48 h
or until end of PCI
Enoxaparin (low- ~10% ↓ D/MI vs. UFH (JAMA 2004;292:45,89). Can
molec-wt heparin) 1 perform PCI on enox (Circ 2001;103:658), but ↑
mg/kg SC bid (± 30 bleeding if switch b/w enox and UFH.
mg IVB) (qd if CrCl
<30) × 2–8 d or until
PCI
Bivalirudin (direct No diff in bleeding, MI, or death c/w UFH (NEJM
thrombin inhibitor) 2017;377:1132). Use instead of UFH if HIT.
0.75 mg/kg IVB at
PCI → 1.75 mg/kg/h
Fondaparinux (Xa Rarely used; must supplement w/ UFH if PCI.
inh) 2.5 mg SC qd

Coronary angiography (Circ 2014;130:e344)

• Immediate/urgent coronary angiography (w/in 2 h) if
refractory/recurrent angina or hemodynamic or electrical
instability
• Invasive (INV) strategy = routine angiography w/in 72 h
Early (w/in 24 h) if: ⊕ Tn, ST ∆, GRACE risk score
(www.outcomes-massmed.org/grace) >140 (NEJM
2009;360:2165; Circ 2018;138:2741)
 Delayed (ie, w/in 72 h) acceptable if w/o above features but
w/: diabetes, EF <40%, GFR <60, post-MI angina, TRS ≥3,
GRACE score 109–140, PCI w/in 6 mo, prior CABG
32% ↓ rehosp for ACS, nonsignif 16% ↓ MI, no ∆ in mortality
c/w cons. (JAMA 2008;300:71).
↑ peri-PCI MI counterbalanced by ↓↓ in spont. MI. Mortality
benefit seen in some studies, likely only if cons. strategy w/
low rate of angio.
• Conservative (CONS) strategy = selective angio. Med Rx w/
pre-d/c stress test; angio only if recurrent ischemia or strongly
⊕ ETT. Indicated for: low TIMI Risk Score, Pt or physician pref
in absence of high-risk features, or low-risk women (JAMA
2008;300:71).

Figure 1-2 Approach to UA/NSTEMI

 STEMI
Requisite STE (at J point)
• ≥2 contiguous leads w/ ≥1 mm (except for V2–V3: ≥2 mm in ♂
and ≥1.5 mm in ♀), or
• New or presumed new LBBB w/ compelling H&P, or
• True posterior MI: ST depression V1–V3 ± tall Rw w/ STE on
posterior leads (V7–V9)
Reperfusion (“time is muscle”)
• In PCI-capable hospital, goal should be primary PCI w/in 90
min of 1st medical contact
• In non–PCI-capable hospital, consider transfer to PCI-capable
hospital (see below), o/w fibrinolytic therapy w/in 30 min of
hospital presentation
• Do not let decision regarding method of reperfusion delay time to
reperfusion
Primary PCI (JACC 2013;61:e78 & 2016;67:1235)
• Definition: immediate PCI upon arrival to hospital or transfer for
immediate PCI
• Indic: STE + sx onset w/in <12 h; ongoing ischemia 12–24 h
after sx onset; shock
• Superior to lysis: 27% ↓ death, 65% ↓ reMI, 54% ↓ stroke, 95% ↓
ICH (Lancet 2003;361:13)
• Transfer to center for 1° PCI superior to lysis (NEJM 2003;349:733),
see below
• Routine thrombus aspiration: no benefit, ↑ stroke (Lancet
2015;387:127; 2015;372:1389)
• Consider PCI of non-culprit lesions at time of primary PCI or
planned staged procedure because appears to ↓ MACE vs.
culprit alone (NEJM 2013;369:1115; JACC 2015;65:963); but may
harm if cardiogenic shock (NEJM 2018;379:1699)
Fibrinolysis vs. Hospital Transfer for Primary PCI: Assess Time and
Risk
1. Time required for transport to skilled PCI lab: door-to-balloon <120
min & [door- to-balloon]–[door-to-needle] <1 h favors transfer for PCI
2. high-risk Pts (eg, shock) fare better with mechanical reperfusion
3. Time to presentation: efficacy of lytics ↓ w/ ↑ time from sx onset, espec
>3 h
4. Risk of fibrinolysis: if high risk of ICH or bleeding, PCI safer option

Adapted from ACC/AHA 2013 STEMI Guidelines (Circ 2013;127:529)

Fibrinolysis
• Indic: STE/LBBB + sx <12 h (& >120 min before PCI can be
done); benefit if sx >12 h less clear; reasonable if persist. sx &
STE, hemodynamic instability or large territory at risk
• Mortality ↓ ~20% in anterior MI or LBBB and ~10% in IMI c/w ∅
reperfusion Rx
• Prehospital lysis (ie, ambulance): further 17% ↓ in mortality (JAMA
2000;283:2686)
• ~1% risk of ICH; high risk incl elderly (~2% if >75 y), ♀, low wt.
∴ PCI more attractive

Contraindications to Fibrinolysis
 Absolute Contraindications Relative Contraindications
• Any prior ICH • H/o severe HTN, SBP >180 or DBP
• Intracranial neoplasm, aneurysm, >110 on presentation (?
AVM absolute if low-risk MI)
• Ischemic stroke or closed head • Ischemic stroke >3 mo prior
trauma w/in 3 mo; head/spinal • CPR >10 min; trauma/major surg.
surg. w/in 2 mo w/in 3 wk
• Active internal bleeding or known • Internal bleed w/in 2–4 wk; active
bleeding diathesis PUD
• Suspected aortic dissection • Noncompressible vascular
• Severe uncontrollable HTN punctures
• For SK, SK Rx w/in 6 mo • Pregnancy
• Current use of anticoagulants
• For SK, prior SK exposure

Nonprimary PCI
• Rescue PCI if shock, unstable, failed reperfusion, or persistent sx
(NEJM 2005;353:2758)
• Routine angio ± PCI w/in 24 h of successful lysis: ↓ D/MI/revasc
(Lancet 2004;364:1045) and w/in 6 h ↓ reMI, recurrent ischemia, &
HF compared to w/in 2 wk (NEJM 2009;360:2705);
∴ if lysed at non-PCI-capable hosp., consider transfer to PCI-
capable hosp. ASAP espec if hi-risk (eg, ant. MI, IMI w/ ↓ EF
or RV infarct, extensive STE/LBBB, HF, ↓ BP or ↑ HR)
• Late PCI (median day 8) of occluded infarct-related artery: no
benefit (NEJM 2006;355:2395)

Antiplatelet Therapy
Aspirin 162–325 mg × 1 23% ↓ in death (Lancet 1988;ii:349)
(crushed/chewed) then Should not be stopped if CABG required
81 mg qd
P2Y12 inhibitor Lysis: clopidogrel 41% ↑ in patency, 7% ↓ mort,
Give ASAP (do not wait no ∆ major bleed or ICH (NEJM 2005;352:1179;
for angio) b/c onset Lancet 2005;366:1607); no data for pras or ticag
inhib delayed in w/ lytic
STEMI pts
 Ticagrelor or prasugrel (if PCI: prasugrel and ticagrelor ↓ CV events c/w clopi
PCI) as detailed above (Lancet 2009;373:723 & Circ 2010;122:2131)
Clopidogrel: 600 mg pre- Prehospital ticagrelor may be safe & ? ↓ rate of
PCI; 300 mg if lysis stent thrombosis (NEJM 2014;371:1016)
(no LD if >75 y) → 75
mg qd
GP IIb/IIIa inhibitors Lysis: no indication (Lancet 2001;357:1905)
abciximab, eptifibatide, Peri-PCI: 60% ↓ D/MI/UR (NEJM 2001;344:1895)
tirofiban
Adapted from ACC/AHA 2013 STEMI Guidelines Update (Circ 2013;127:529);
Lancet 2013;382:633

Anticoagulant Therapy (choose one)

UFH No demonstrated mortality benefit
60 U/kg IVB (max 4000 ↑ patency with fibrin-specific lytics
U) Titrate to aPTT 1.5–2× control (~50–70 sec)
12 U/kg/h (max 1000 U/h
initially)
Enoxaparin Lysis: 17% ↓ D/MI w/ ENOX × 7 d vs. UFH × 2 d
Lysis: 30 mg IVB → 1 (NEJM 2006;354:1477)
mg/kg SC bid (adjust PCI: ↓ D/MI/revasc and ≈ bleeding vs. UFH (Lancet
for age >75 & CrCl) 2011;378:693)
PCI: 0.5 mg/kg IVB
Bivalirudin PCI: similar bleeding, ± ↑ MI, ↑ stent thromb
0.75 mg/kg IVB → 1.75 (Lancet 2014;384:599; NEJM 2017;377:1132)
mg/kg/hr IV
Fondaparinux can be used (if CrCl >30 mL/min) in setting of lysis, where superior
to UFH w/ less bleeding (JAMA 2006;295:1519). Adapted from ACC/AHA 2013
STEMI Guidelines (Circ 2013;127:529; Lancet 2013;382:633)

LV failure (occurs in ~25%)

• Diurese to achieve PCWP ~14 → ↓ pulmonary edema, ↓
myocardial O2 demand
• ↓ Afterload → ↑ stroke volume & CO, ↓ myocardial O2 demand.
Can use IV NTG or nitroprusside (although risk of coronary
steal) → short-acting ACEI.
• Inotropes if HF despite diuresis & ↓ afterload; use dopamine,
dobutamine, or milrinone
• Cardiogenic shock (~7%) = MAP <60 mmHg, CI <2.2
L/min/m2, PCWP >18 mmHg.
If not done already, coronary revasc (NEJM 1999;341:625)
Support w/ inotropes or mechanical circulatory support to keep
CI >2
Intraaortic balloon pump (IABP) counterpulsation offers
~0.5 L/min CO and ↑ coronary perfusion, but no survival
benefit if early revasc (NEJM 2012;367:1287)
Axial flow pumps (eg, Impella) offer up to 3–5 L/min
CO, but no data that improves clinical outcomes (JACC
2017;69:278)

IMI complications (Circ 1990;81:401; NEJM 1994;330:1211; JACC

2003;41:1273)
• Heart block: ~20%, occurs in part because RCA typically
supplies AV node
40% on present., 20% w/in 24 h, rest by 72 h; high-grade AVB
can develop abruptly
Rx: atropine, epi, aminophylline (100 mg/min × 2.5 min), temp
pacing wire
• RV infarct: proximal RCA occlusion → ↓ flow to RV marginals
Angiographically present in 30–50% of cases, but only ~1/2
clinically significant
HoTN; ↑ JVP, ⊕ Kussmaul’s; ≥1 mm STE in V4R; RA/PCWP
≥0.8; RV dysfxn on TTE
Rx: optimize preload (RA goal 10–14 mmHg; BHJ 1990;63:98);
↑ contractility (dobutamine); maintain AV synchrony (pacing
as necessary); reperfusion (NEJM 1998;338:933); mechanical
support (IABP or RVAD); pulmonary vasodilators (eg,
inhaled NO)
Mechanical complications (incid. <1% for each; typically occur a few
days post-MI)
• Free wall rupture: ↑ risk w/ lysis, large MI, ↑ age, ♀, HTN; p/w
PEA or hypoTN, pericardial sx, tamponade; Rx: volume resusc.,
? pericardiocentesis, inotropes, surgery
• VSD: large MI in elderly; AMI → apical VSD, IMI → basal
septum; 90% w/ harsh murmur ± thrill (NEJM 2002;347:1426);
Rx: diuretics, vasodil., inotropes, IABP, surgery, perc. closure
• Papillary muscle rupture: more common after IMI (PM pap m.
supplied by PDA alone) than AMI (AL supplied by OMs &
diags); 50% w/ new murmur; ↑ v wave in PCWP tracing;
asymmetric pulmonary edema on CXR. Rx: diuretics,
vasodilators, IABP, surgery.
Arrhythmias post-MI (treat all per ACLS protocols if unstable or
symptomatic)
• AF (10–16% incidence): βB or amio, ± digoxin (particularly if
HF), heparin
• VT/VF: lido or amio × 6–24 h, then reassess; ↑ βB as tol., replete
K & Mg, r/o ischemia;
VT <48 h post-MI does not worsen prognosis; >48 h, consider
ICD (see below)
• Accelerated idioventricular rhythm (AIVR): slow VT (<100 bpm),
often seen after
successful reperfusion; typically asx, self-terminates, and does
not require treatment
• Backup transcutaneous or transvenous pacing if: 2° AVB
type II; BBB + AVB
• Transvenous pacing if: 3° AVB; new BBB + 2° AVB type II;
alternating LBBB/RBBB
Other Post-MI Complications
Complication Clinical Features Treatment
LV thrombus ~30% incid. (espec lg Anticoagulate × 3–6 mo
antero-apical MI)
Ventricular Noncontractile outpouching Surgery or perc repair if
aneurysm of LV; 8–15% incid. (espec HF, thromboemboli,
ant); persist STE arrhythmia
 Ventricular Rupture (narrow neck) → Urgent surgery (or
pseudoaneurysm sealed by thrombus and percutaneous repair)
pericardium (esp in inf).
Pericarditis 10–20% incid.; 1–4 d post- High-dose ASA,
MI ⊕ pericardial rub; ECG colchicine, narcotics;
∆s rare minimize anticoag
Dressler’s <4% incid.; 2–10 wk post- High-dose aspirin,
syndrome MI fever, pericarditis, NSAIDs
pleuritis

Prognosis
• In registries, in-hospital mortality is 6% w/ reperfusion Rx (lytic or
PCI) and ~20% w/o
• TIMI Risk Score for STEMI (includes age, time to Rx, anterior MI
or LBBB, Killip class, tachycardia, HoTN) defines 30-d mortality
after STEMI (JAMA 2001;286:1356)

CHECKLIST AND LONG-TERM POST-ACS

MANAGEMENT
Risk stratification
• Stress test if anatomy undefined; consider stress if signif residual
CAD post-PCI of culprit
• Assess LVEF prior to d/c; EF ↑ ~6% in STEMI over 6 mo (JACC
2007;50:149)

Medications (barring contraindications)

• Aspirin: 81 mg daily (no clear benefit to higher doses)
• P2Y12 inhib (ticagrelor or prasugrel preferred over clopi): treat
for at least 12 mo
Prolonged Rx >12 mo → ↓ MACE & CV death, ↑ in bleeding,
but no ↑ ICH. Beyond 1st 12 mo, ticag 60 bid preferred to
90, b/c better tolerability (NEJM 2015;372:1791; EHJ 2016;37:390).
PPIs ↓ GI complic; some PPIs ↓ antiplt effect, but no clear ↑ in
CV risk (NEJM 2010;363:1909)
• β-blocker: 23% ↓ mortality after MI
• LDL-C management: benefit with lowering LDL-C to <<40 mg/dl
(Lancet 2017;390:1962)
Statin: high-intensity (eg, atorva 80 mg, PROVE-IT TIMI 22,
NEJM 2004;350:1495)
Ezetimibe: ↓ CV events when added to statin (IMPROVE-IT,
NEJM 2015;372:1500)
PCSK9 inhibitor: ↓ CV events when added to statin (NEJM
2017;376:1713; 2018;379:2097)
• ACEI: lifelong if HF, ↓ EF, HTN, DM; 4–6 wk or at least until hosp.
d/c in all STEMI
? long-term benefit in CAD w/o HF (NEJM 2000;342:145 &
2004;351:2058; Lancet 2003;362:782)
• Aldosterone antag: 15% ↓ mort. if EF <40% & either s/s of HF
or DM (NEJM 2003;348:1309)
• Nitrates: standing if symptomatic; SL NTG prn for all
• Ranolazine: ↓ recurrent ischemia, no impact on CVD/MI (JAMA
2007;297:1775)
• Oral anticoag: if needed (eg, AF, LV thrombus), consider DOAC
instead of warfarin; some data for reduced-dose DOAC but
unclear if ischemic stroke prevention adeq. (NEJM 2016; 375:2423
& 2017;377:1513). Clopi (not ticag or pras). Stopping ASA (? after
~1 wk) ↓ bleed risk by 40–50%, but trend small ↑ MI & stent
thromb. (Lancet 2013;381:1107; NEJM 2019;379:1509).
• In Pts w/o indic. for anticoag, once DAPT completed, rivaroxaban
2.5 bid + ASA ↓ MACE & CV death and ↑ bleeding vs. ASA
monoRx (NEJM 2017;377:1319)
ICD (NEJM 2008;359:2245; Circ 2014;130:94)
• Sust. VT/VF >2 d post-MI w/o revers. isch; ? ↓ death w/ wearable
defib (NEJM 2018;379:1205)
• 1° prevention of SCD if post-MI EF ≤30–40% (NYHA II–III) or
≤30–35% (NYHA I); wait 40 d after MI (NEJM 2004;351:2481 &
2009;361:1427)

Risk factors and lifestyle modifications (Circ 2014;129(Suppl 2):S1

& S76)
• Low chol. (<200 mg/d) & fat (<7% saturated) diet; ? Ω-3 FA.
• LDL-C at least <70 mg/dl (& ≥50% ↓ in LDL-C) (Circ
2019;139:e1082)
• BP <130/80 (JACC 2018;71:e127); quit smoking
• If diabetic, tailor HbA1c goal based on Pt (avoid TZDs and saxa if
HF); GLP1-RA & SGLT2i ↓ MACE & SGLT2i ↓ hospitalization for
HF (Lancet 2019;393:31 & Circ 2019;139:2022)
• Exercise (30–60′ 5–7×/wk) 1–2 wk after revasc; cardiac rehab;
BMI goal 18.5–24.9 kg/m2
• Influenza & S. pneumo vaccines (JAMA 2013;310:1711; NEJM
2018;378:345); ✔ for depression

PA CATHETER AND TAILORED

THERAPY

Rationale
• Cardiac output (CO) = SV × HR; optimize SV (and thereby CO) by
manipulating preload/ LVEDV (w/ IVF, diuretics), contractility
(w/ inotropes), & afterload (w/ vasodilators)
• Balloon at catheter tip inflated → floats into “wedge” position.
Column of blood extends from tip of catheter, through pulm
venous circulation to a point just prox to LA. Under conditions
of no flow, PCWP ≈ LA pressure ≈ LVEDP, which is proportional
to LVEDV.
• Situations in which these basic assumptions fail:
(1) Catheter tip not in West lung zone 3 (and ∴ PCWP =
alveolar pressure ≠ LA pressure); clues include lack of a &
v waves and if PA diastolic pressure < PCWP
(2) PCWP > LA pressure (eg, mediastinal fibrosis, pulmonary
VOD, PV stenosis)
(3) Mean LA pressure > LVEDP (eg, MR, MS)
Other documents randomly have
different content
infinitesimal spores. That they elude observation does not seem
strange, when we consider that some infusoria are only ⅟240000 of
an inch in length.
It is ascertained that fungi produce seed which contains the
properties of germination; and that vegetable corruption is suited to
effect it. When we contemplate the fineness and volatility of the
germs, the hypothesis will not appear unreasonable that they are
conveyed by the rains into the earth, and are absorbed by
vegetables; that with the sap they are disseminated throughout the
whole body, and begin to germinate as soon as the vegetable has
proceeded to corruption. Whatever, therefore, may be the
appearance or situation of the fungus producing the dry rot, or from
whatever substance it originates, that substance must be in a
corrupt state.
Fungi result from, or are attendant on, vegetable corruption,
assisted by an adequate proportion of heat and moisture. The sap,
or principle of vegetation, brought into activity, is, according to the
‘Quarterly Review,’ No. 15, the cause of dry rot, in as far as it is
favourable to the growth of fungi, as it would seem to be when in a
state of fermentation.
Vegetable corruption invariably presupposes fermentation.
Fermentation is a state of vegetable matter, the component parts
of which have acquired sufficient force to produce an intestinal
motion, by which the earthy saline, the oily and aqueous particles
therein contained, exert their several peculiar attractive and
repulsive powers, forming new combinations, which at first change,
and at length altogether destroy the texture of the substance they
formerly composed.
There are two things essential towards creating and supporting
the intestinal motion, namely, heat and humidity; for without heat,
the air, which is supposed to be the cohesive principle of all bodies,
cannot be so rarefied as to resume its elasticity; and without
humidity there can be no intestinal motion.
 According to Baron Liebig, the decay of wood takes place in the
three following modes:—First, oxygen in the atmosphere combines
with the hydrogen in the fibre, and the oxygen unites with the
portion of carbon of the fibre, and evaporates as carbonic acid: this
process is called decomposition. Second, we have to notice the
actual decay of wood which takes place when it is brought in contact
with rotting substances; and the third process is called putrefaction.
This is stated by Liebig to arise from the inner decomposition of the
wood in itself: it loses its carbon, forms carbonic acid gas, and the
fibre, under the influence of the latter, is changed into white dust.
The fungus occasioning the dry rot is of various appearances,
which differ according to the situation in which it exists. In the earth,
it is fibrous and perfectly white, ramifying in the form of roots;
passing through substances from the external surface, it somewhat
differs from that form; here it separates into innumerable small
branches.
Mr. McWilliam observes, “If the fungi proceed from the slime in the
fissures of the earth, they are generally very ramous, having round
fibres shooting in every direction. If they arise from the roots of
trees, their first appearance is something like hoar frost; but they
soon assume the mushroom shape.”
Hence it appears that we frequently build on spots of ground
which contain the fundamental principle of the disease, and thus we
are sometimes foiled in our endeavours to destroy the fungus by the
admission of air. In this case the disease may be encouraged by the
application of air as a remedy. When workmen are employed in
buildings which contain dry rot, and when they are working on
ground which contains the symptoms of this disease, their health is
often affected. A London builder informs us, that a few years since,
while building some houses at Hampstead his men were never well:
he afterwards ascertained that the ground was affected with rot, and
that within one year after the house was erected, all the basement
floor was in a state of premature decay. Sir Robert Smirke, architect,
remarked in 1835, that he had noticed “there are certain situations
in which dry rot prevails remarkably.”
The fungus protruded in a very damp situation is fibrous, of
moderate thickness, feels fleshy. From the spot whence it arises it
extends equally around, wholly covering the area of a circle. This
form would possibly continue in whatever situation it might
vegetate, if the air had no motion, and every part of the substance
on which it grew were equally supplied with a matter proper to
encourage the expansion. The surface of this fungus is pursed, and
of various colours, the centre is of a dusky brown, mixed with green,
graduated into a red, which degenerates into yellow, and terminates
in white.
One of the most formidable of the tribe of fungi is the Merulius
lachrymans (often called the Dry Rot) of which the following
description is given by Dr. Greville: “Whole plant generally
resupinate, soft, tender, at first very light, cottony, and white. When
the veins appear, they are of a fine yellow, orange, or reddish brown,
forming irregular folds, most frequently so arranged as to have the
appearance of pores, but never anything like tubes, and distilling,
when perfect, drops of water.” Hence the term lachrymans, from
lacrymo, Lat., I weep: the Merulius lachrymans is often dripping with
moisture, as if weeping in regret for the havoc it has made. In the
genus Merulius, the texture is soft and waxy, and the hymenium is
disposed in porous or wavy toothed folds. Berkeley, in his
‘Fungology,’ gives the following description, which is similar to Dr.
Greville’s: “Large, fleshy but spongy, moist, ferruginous yellow,
arachnoid and velvety beneath; margin tomentose, white; folds
ample, porous, and gyroso-dentate.” The Merulius is found in cellars
and hollow trees, sometimes several feet in width, and is the main
cause of dry rot.
Another formidable fungi, which attacks oak in ships, is the
Polyporus hybridus (the dry rot of our oak-built vessels). It is thus
described by Berkeley: “White, mycelium thick, forming a dense
membrane, or creeping branched strings, hymenium breaking up
into areæ, pores long, slender, minute.”
From the slow progress dry rot makes in damp situations, it
appears that excessive damps are inimical to the fungus, for its
growth is more rapid in proportion as the situation is less damp, until
arrived at that certain degree of moisture which is suited both to its
production and vegetation. When further extended to dry situations,
its effects are considerably more destructive to the timber on which
it subsists: here it is very fibrous, and in part covered with a light
brown membrane, perfectly soft and smooth. It is often of much
greater magnitude, projecting from the timber in a white spongeous
excrescence, on the surfaces of which a profuse humidity is
frequently observed: at other times, it consists only of a fibrous and
thin-coated web irregularly on the surface of the wood. Excrescences
of a fungiform appearance are often protruded amidst those already
described, and are evidences of a very corrupt matter peculiar to the
spots whence they spring. According to the situation and matter in
which they are produced, they are dry and tough, or wet, soft, and
fleshy, sometimes arising in several fungiforms, each above the
other, without any distinction of stem; and when the matter is
differently corrupted, it not unfrequently generates the small acrid
mushroom.
Mr. McWilliam observes, “The fungi arising from oak timbers are
generally in clusters of from three to ten or twelve; while those from
fir timber are mostly in single plants: and these will continue to
succeed each other until the wood is quite exhausted.”
Damp is not only a cause of decay, but is essential to it; while, on
the other hand, absolute wet, especially at a low temperature,
prevents it. In ships this has been particularly remarked, for that
part of the hold of a ship which is constantly washed by the bilge-
water is never affected with dry rot. Neither is that side of the
planking of a ship’s bottom which is next the water found in a state
of decay, even when the inside is quite rotten, unless the rot has
penetrated quite through the inside.
 It matters little whether wet is applied to timber before or after
the erection of a building. Timber cannot resist the effect of what
must arise in either case; viz. heat and moisture, producing putrid
fermentation; for instance, in basement stories with damp under
them, dry timber is but little better than wet, for if it is dry it will
soon be wet; decay will only be delayed so long as the timbers are
absorbing sufficient moisture, therefore every situation that admits
moisture is the destruction of timber.
In a constancy and equality of temperature timber will endure for
ages. Sir Christopher Wren, in his letter to the Bishop of Rochester,
inserted in Wadman’s ‘History of Westminster Abbey,’ notices “That
Venice and Amsterdam being both founded on wooden piles
immersed in water, would fall if the constancy of the situation of
those piles in the same element and temperature did not prevent the
timber from rotting.” Nothing is more destructive to woodwork than
partial leaks, for if it be kept always wet or always dry, its duration is
of long continuance. It is recorded that a pile was drawn up sound
from a bridge on the Danube, that parted the Austrian and Turkish
dominions, which had been under water 1500 years.
The writer of an article on the decay of wood, in the
‘Encyclopædia Britannica,’ 1855, observes, “If a post of wood be
driven into the ground, the decay will commence at the surface of
the ground; if driven into the earth through water, the decay will
commence at the surface of the water; if used as a beam let into a
damp wall, rot will commence just where the wood enters the wall.”
Humboldt observes in his ‘Cosmos,’ with reference to damp and
damp rooms, that anyone can ascertain whether a room is damp or
not, by placing a weighed quantity of fresh lime in an open vessel in
the room, and leaving it there for twenty-four hours, carefully closing
the windows and doors. At the end of the twenty-four hours the lime
should be reweighed, and if the increase exceeds one per cent. of
the original weight, it is not safe to live in the room.
Decay of timber will arise from the effects of continued dryness or
continued wetness, under certain conditions; or it may also arise
from the effect of alternate dryness and moisture, or continued
moisture with heat.
At one time dry rot appears to have made great havoc amongst
the wooden ships of the British Navy. In the Memoirs of Pepys, who
was Secretary to the Admiralty during the reigns of Charles II. and
James II., reference is made to a Commission which was appointed
to inquire into the state of the navy, and from which it appears that
thirty ships, called new ships, “for want of proper care and attention,
had toadstools growing in their holds as big as one’s fists, and were
in so complete a state of decay, that some of the planks had
dropped from their sides.”
In the ‘European Magazine’ for December, 1811, it is stated that,
“about 1798, there was, at Woolwich, a ship in so bad a state that
the deck sunk with a man’s weight, and the orange and brown
coloured fungi were hanging, in the shape of inverted cones, from
deck to deck.”
Mr. William Chapman, in his ‘Preservation of Timber from
Premature Decay,’ &c., gives several instances of the rapid decay of
the ships of the Royal Navy, about the commencement of the
present century. He mentions three ships of 74 guns each, decayed
in five years; three of 74 guns each, decayed in seven years; and
one of 100 guns, decayed in six years. Mr. Pering, also, in his ‘Brief
Enquiry into the Causes of Premature Decay,’ &c., says that ships of
war are useless in five or six years; and he estimates the average
duration to be eight years, and that the cost of the hull alone of a
three-decker was nearly 100,000l. Mr. Pering was formerly at the
dockyard, Plymouth, and therefore a good authority, if he availed
himself of the opportunities of studying the subject. He has stated
that he has seen fungi growing so strong betwixt the timbers in a
man-of-war, as to force a plank from the ship’s side half an inch.
No doubt a great deal of this decay was attributable to the use of
unseasoned timber, and defective ventilation; but there is too much
reason to believe that it was principally owing to the introduction of
an inferior species of oak (Quercus sessiliflora) into the naval
dockyards, where, we imagine, the distinction was not even
suspected. The true old English oak (Quercus robur) affords a close-
grained, firm, solid timber, rarely subject to rot; the other is more
loose and sappy, very liable to rot, and not half so durable.
One cause of the decay of wood in ships is the use of wooden
treenails. A treenail is a piece of cleft wood (made round), from 1
foot to 3 feet 6 inches in length and 1½ inch in diameter. As the
treenails are also made to drive easy, they never fill the holes they
are driven into; consequently, if ever it admits water at the outer
end, which, from shrinking, it is liable to do, that water immediately
gets into the middle of the plank, and thereby forms a natural
vehicle for the conveyance of water. The treenail is also the second
thing which decays in a ship, the first, generally, being the oakum.
Should any part of the plank or timbers of a ship be in an incipient
state of decay, and a treenail come in contact with it, the decay
immediately increases, while every treenail shares the same fate,
and the natural consequence is, the ship is soon left without a
fastening. Treenails in a warm country are sure to shrink and admit
water.
Mr. Fincham, formerly Principal Builder in Her Majesty’s dockyard,
Chatham, considers that the destruction of timber by the decay
commonly known as dry rot, cannot occur unless air, (?) moisture,
and heat are all present, and that the entire exclusion of any of the
three stays the mischief. By way of experiment, he bored a hole in
one of the timbers of an old ship built of oak, whose wood was at
the time perfectly sound; the admission of air, the third element, to
the central part of the wood (the two others being to a certain
degree present) caused the hole to be filled up in the course of
twenty-four hours with mouldiness, which very speedily became so
compact as to admit of being withdrawn like a stick.
The confinement of timber under most circumstances is attended
with the worst consequences, yet a partial ventilation tends to fan
the flame of decay.
 The admission of air has long been considered the only means of
destroying the fungus, but as it has frequently proved ineffectual, it
must not be always taken as a certain remedy. If dry air be properly
admitted, in a quantity adequate to absorb the moisture, it will
necessarily exhaust and destroy the fungus; but care should be
taken lest the air should be conveyed into other parts of the
building, for, after disengaging itself from the fungus over which it
has passed, it carries with it innumerable seeds of the disease, and
destroys everything which offers a bar to its progress. Air, in passing
through damps, will partake of their humidity; it therefore soon
becomes inadequate to the task for which it is designed. Owing to
this circumstance, air has been frequently admitted into the affected
parts of a building without any ultimate success; too often, instead
of injuring the fungus, it has considerably assisted its vegetation,
and infected with the disease other parts of the building, which
would otherwise probably have remained without injury. The timber,
which is in a state of decomposition by an intestinal decay, is little
affected by the application of air, as this cannot penetrate the
surrounding spongeous rottenness which generally forms the
exterior of such timber, and protects the action which the humid
particles have acquired in the exterior: as the extent and progress of
the disease is therefore necessarily concealed, it is difficult to
ascertain correctly the effect produced by the admission of dry air.
Under these circumstances of necessity and danger, it will require
considerable skill to effect the purpose without increasing the
disease, and, as each case has its own peculiar characteristics, it is
necessary before one attempts to admit air as a remedy, to
previously estimate the destructive consequences which may result
from so doing, and ascertain whether it will be injurious or beneficial
to the building. The joists of the houses built by our ancestors last
almost for ever, because they are in contact with an air which is
continually changing. Now, on the contrary, we foolishly enclose
them between a ceiling of plaster (always very damp to begin with)
and a floor; they frequently decay, and then cause the most serious
disasters, of which it is impossible to be forewarned.
 Damp, combined with warmth, is as a destroying agent, still more
active than simple damp alone—the heat being understood as
insufficient to carry off the moisture by evaporation; and the higher
the temperature with a corresponding degree of moisture, the more
rapid the decay. If the temperature to which wood is exposed, whilst
any sap remains in it, is too elevated, the vegetable fluids ferment;
the tenacity is diminished, and when the action is carried to its full
extent, the wood quickly becomes affected by the dry rot. Exposure
to the atmosphere in positions where rain can lodge in quantity,
contact with the ground, and application in damp situations deprived
of air, will render wood liable to the wet rot; and however well
seasoned it may have been previously to being brought within the
influence of any of these causes, it will infallibly suffer. Air should
therefore have free access to the wood in every direction:
… “for without in the wall of the house he made
narrowed rests round about, that the beams should
not be fastened in the walls of the house.”—1 Kings vi.
6.
Rondelet says, “The woodwork of the church of St. Paul, outside
the city walls, which was destroyed by fire in 1823, was erected as
far back as the fifth century.” Although the atmosphere surrounding
the framework was often at once warm and damp, yet it was never
stagnant. It should be remembered that 500 people in a church
during two hours give off fifteen gallons of water into the air, which,
if not carried away, saturates everything in the building after it has
been breathed over and over again in conjunction with the impurities
it contains collected from each individual.
Fever, scrofula, and consumption arise in many instances from
defective ventilation.
The signs of decay in timber are, as has been stated, fungi. Some
of them now and then are microscopic, and owe their existence to
the sporules deposited on the surface; while fermentation,
generated by prolonged contact with warm, damp, and stagnant air,
is as a soil where seeds sow and nourish themselves.
 Mr. McWilliam, in his work on dry rot, states that if the
temperature be very low or very high, the effects are the same with
respect to the growth of fungi. At 80° dry rot will proceed rapidly, at
90° its progress is more slow; at 100° it is slower still, and from
110° to 120° it will in general be arrested. It will proceed fast at
50°; it may be generated at 40°; its progress will be slow at 36°;
and is arrested at 32°, yet it will return if the temperature is raised
to 50°.
Dry rot externally first makes its appearance as a mildew, or
rather a delicate white vegetation, that looks like such. The next
step is a collecting together of the fibres of the vegetation into a
more decided form, somewhat like hoar frost; after which it speedily
assumes the leathery, compact character of the fungus, forming into
leaves, spreading rapidly in all directions, and over all materials, and
frequently ascending the walls to a considerable height, the colour
variable—white, greyish white, and violet, light or decided brown,
&c.
In the section of a piece of wood attacked by dry rot a microscope
reveals minute white threads spreading and ramifying throughout its
substance; these interlace and become matted together into a white
cottony texture, resembling lint, which effuses itself over the surface
of the timber; then in the centre of each considerable mass a
gelatinous substance forms, which becomes gradually of a yellow,
tawny hue, and a wrinkled, sinuated porous consistence, shedding a
red powder (the spores) upon a white down; this is the resupinate
pileus, the hymenium being upwards, of Merulius lachrymans, in its
perfect and matured state. Long before it attains to this, the whole
interior of the wood on which it is situated has perished; the sap
vessels being gradually filled by the cottony filaments of the fungus;
no sooner do these appear externally than examination proves that
the apparently solid beam may be crumbled to dust between the
fingers; tenacity and weight are annihilated.
Dr. Haller says that seven parts in eight of a fungus in full
vegetation are found by analysis to be completely aqueous.
 The strength of fungi is proportionate to the strength of the
timber the cohesive powers and nutritive juices of which they
absorb; and according to the food they receive so they are varied
and modified in different ways, and are not always alike. Different
stages of corruption produce food of different qualities, and hence
many of the different appearances of fungi. One takes the process of
corruption up where another leaves it off, and carries it forward and
farther forward to positive putrefaction.
The forms which fungi assume are extremely diversified; in some
instances we have a distinct stem supporting a cap, and looking
somewhat like a parasol; in others the stem is entirely absent, and
the cap is attached either by its margin, and is said to be dimidiate,
or by its back, or that which is more commonly its upper surface,
when it is called resupinate. In some species the form is that of a
cup, in others of a goblet, a saucer, an ear, a bird’s nest, a horn, a
bunch of coral, a ball, a button, a rosette, a lump of jelly, or a piece
of velvet.
Decomposition takes place without fungus where the timber and
the situation are always moist, as in a close-boarded kitchen floor,
where it is always dry, or very nearly so, and where it is alternately
wet and dry, cold and hot. When the decomposition is affected with
very little moisture, and no fungus, the admission of air will generally
prevent further contamination; but where there is abundance of
moisture, rottenness, and fungus, a small quantity of air will hasten
the destruction of the building.
In timber which has been only superficially seasoned this disease
is produced internally, and has been known to convert the entire
substance of a beam, excepting only the external inch or two of
thickness to which the seasoning had penetrated, into a fine, white,
and threadlike vegetation, uniting in a thick fungous coat at the
ends, the semblance being that of a perfectly sound beam. In this
internal rot a spongy fungous substance is formed between the
fibres. This has often been observed in large girders of yellow fir,
which have appeared sound on the outside, but by removing some
of the binding joists have been found completely rotten at the heart.
An instance of this kind occurred at Kenwood (the seat of the Earl of
Mansfield) in 1815. Major Jones, R.E., states that on one occasion he
was called upon to report on the state of a building in Malta; that
the timbers had every external appearance of being sound, but on
being bored with an auger they were found internally in a total state
of decay. It is on this account that the practice of sawing and bolting
beams is recommended, for when timber is large enough to be laid
open in the centre this part is laid open to season; so that when a
tree is large enough to be cut through to make two or more beams,
decomposition is impeded.
The first symptoms of rottenness in timber are swelling,
discoloration, and mouldiness, accompanied with a musty smell; in
its greater advance the fibres are found to shrink lengthways and
break, presenting many deep fissures across the wood; the fibres
crumble readily to a fine snuff-like powder, but retain, when
undisturbed, much of their natural appearance.
In whatever way boughs are removed from trees, the effect of
their removal is, however, very frequently to produce a rotting of the
inner wood, which indicates itself externally by a sudden abnormal
swelling of the trunk a little above the root; sometimes the trunk
becomes hollow at the part affected, and this particular description
of rot will almost invariably be found to exist in those trees whose
roots are much exposed. The rot itself is either of a red, black, or
white colour in the timber when felled, and when either of the two
last-named colours prevail, it will be found that the decay does not
extend very far into the tree; but if, on the contrary, the colour of
the parts most visibly affected should be decidedly red, the wood
should be rejected for any building purposes. Sometimes small
brown spots, indicative of a commencement of decay, may be
observed near the butt or root end of trees, and though they do not
appear to be connected with any serious immediate danger to the
durability of the wood, it is advisable to employ the material so
affected only in positions where it would not be confined in anything
like a close, damp atmosphere.
 Great hesitation may be admitted as to the use of timber which
presents large bands of what are supposed to be indefinitely-marked
annual growth, because the existence of zones of wood so affected
may be considered to indicate that the tree was not in a healthy
state when they were formed, and that the wood then secreted
lacked some of the elements required for its durability, upon being
subsequently exposed to the ordinary causes of decay.
In many cases when timber trees are cut down and converted for
use, it is found that at the junction of some of the minor branches
with the main stem, the roots, as it were, of the branches traverse
the surface wood in the form of knots, and that they often assume a
commencement of decay, which in the course of time will extend to
the wood around them. This decay seems to have arisen in the
majority of cases from the sudden disruption of the branch close to
its roots, with an irregular fracture, and with such depressions below
the surface as to allow the sap to accumulate, or atmospheric
moisture to lodge in them. A decomposition of the sap takes place—
in fact, a wound is made in the tree-and what are called “druxy
knots” are thus formed, which have a contagious action on the
healthy wood near them.
There is this particular danger about the dry rot; viz. that the
germs of the fungi producing it are carried easily, and in all
directions, in a building wherein it once displays itself, without
necessity for actual contact between the affected or the sound
wood; whereas the communication of the disease resulting from the
putrefactive fermentation, or the wet rot, only takes place by actual
contact.
 Timber Beams,—rotten at the heart.

Before dry rot has time to destroy the principal timbers in a

building, it penetrates behind the skirtings, dadoes, and
wainscotings, drawing in the edges of the boards, and splitting them
both horizontally and vertically. When the fungus is taken off, they
exhibit an appearance similar both in back and front to wood which
has been charred; a light pressure with the hand will break them
asunder, even though affected with the rot but a short time; and in
taking down the wainscot, the fibrous and thin-coated fungus will
generally be seen closely attached to the decayed wood. In timber
of moderate length the fungus becomes larger and more destructive,
in consequence of the matter congenial to its growth affording a
more plentiful supply.
It is a great characteristic of fungi in general that they are very
rapid in growth, and rapid in decay. In a night a puff-ball will grow
prodigiously, and in the same short period a mass of paste may be
covered with mould. In a few hours a gelatinous mass of Reticularia
will pass into a bladder of dust, or a Coprinus will be dripping into
decay. Many instances have been recorded of the rapidity of growth
in fungi; it may also be accepted as an axiom that they are in many
instances equally as rapid in decay.
In considering the liability of any particular description of foreign
timber to take the dry rot, attention must be paid to the
circumstances under which it is imported. Sometimes the timber is a
long while coming here, whilst at other times it is imported in a very
short period. The length of time consumed in the voyage has a great
deal to do with its likelihood of taking the rot: it may have a very
favourable passage, or a very wet one, and the ship is frequently, in
some degree, affected with the disease. It perhaps begins in the
ship, and it may often be seen between the timber or deals, when it
will impregnate the wood to a great depth. Whether it is inherent in
the timber or not, of this we may be certain, that where there is a
fetid atmosphere it is sure to grow. Canadian yellow wood pine
timber is more subject to rot than Baltic or Canadian red wood
timber, although the latter will sometimes decay in four or five years.
Turpentine is a preventive against dry rot, and Canadian timber is
sometimes largely impregnated with it, especially the red wood
timber; the yellow wood is very subject to dry rot. Very few cargoes
of timber in the log arrive from Canada in which in one part or other
of nearly every log you will not see a beginning of the vegetation of
the rot. Sometimes it will show itself only by a few reddish,
discoloured spots, which, when scratched by the finger nail to the
extent of each spot, it will be seen that the texture of the timber to
some little depth is destroyed, and will be reduced to powder; and
on these spots a white fibre may generally be seen growing. If the
timber has been shipped in a dry condition, and the voyage has
been a short one, there may be a few logs without a spot; but
generally speaking very few cargoes arrive from Canada in which
there are many logs of timber not affected. But if the cargo has been
shipped in a wet condition, and the voyage has been a long one,
then a white fibre will be seen growing over nearly every part of the
surface of every log; and in cargoes that have been so shipped, all
the logs of yellow pine, red pine, and of oak, are generally more or
less affected on the surface.
Nearly every deal of yellow pine that has been shipped in Canada
in a wet state, when it arrives here is also covered over with a
network of little white fibres, which are the dry rot in its incipient
state. There is no cargo, even that which is shipped in tolerably dry
condition, in which, upon its arriving here, may not be found some
deals, with the fungus beginning to vegetate on their surface. If they
are deals that have been floated down the rivers of America or
Canada, and shipped in a wet state, on their arrival here they are so
covered with this network of the fungus, that force is often
necessary to separate one deal from another, so strongly does the
fungus occasion them to adhere. They grow together again, as it
were, after quitting the ship, while lying in the barges, before being
landed. Accordingly, if a cargo has arrived in a wet condition, or late
in the year, or if the rain falls on the deals before they are landed,
and they are then piled in the way in which Norwegian and Swedish
deals are piled, that is, flatways, in six months time, or even less,
the whole pile of deals become deeply affected with rot; so that,
whenever a flat surface of one deal is upon the flat surface of
another, the rot penetrates to the depth of ⅛ of an inch. Its
progress is then arrested by repiling the deals during very dry
weather, and by sweeping the surface of each deal before it is
repiled: but the best way is to pile the deals in the first instance
upon their edges; by which means the air circulates freely around
them, the growth of the fungus is arrested, and the necessity of
repiling them prevented. If the ship is built of good, sound, and well-
seasoned oak, the rot would perhaps not affect it, but in order to
prevent its doing so, the precaution is usually taken to scrape the
surface as soon as the hold is clear of the cargo of timber. Were the
cargo not cleared, and the hold not ventilated, a ship that was
permanently exposed to this fungus would, no doubt, be affected. It
is easy, however, to prevent its extending by washing the hold with
any desiccating solution.
Anyone who wishes to know how timber is occasionally shipped to
this country should read the report of a trial, in the ‘Times,’ 22nd
Feb., 1875 (Harrison v. Willis), relative to a cargo of pitch pine
shipped from Sapelo, in the Isthmus of Darien, for Liverpool. This
cargo, however, never arrived at Liverpool: it was lost at sea.
The motto of the Worshipful Company of Shipwrights is, “Within
the ark, safe for ever.” We suggest it should be altered to, “Within
the ark which is free from dry rot, safe for ever.”
There are two descriptions of European deals very liable to take
the dry rot; viz. yellow Petersburgh deals, and yellow and white
battens, from Dram, in Norway. When Dram battens, which have
been lying a long time in bond in this country, have not been repiled
in time, they have been found as much affected with the dry rot as
many Canadian deals; though this has not happened in so short a
time as has been sufficient to rot Canadian deals. The fungus
growing on the Petersburgh deals and Dram battens has all the
characteristics and effects of dry rot as exhibited in the Canadian
deals, the detection of dry rot being in most cases the same.
It should be remembered that white deal absorbs more water than
yellow; and yellow more water than red; and the quantity of water
absorbed by the white accounts for its more rapid decay in external
situations; as the greater the quantity of water absorbed the quicker
is the timber destroyed. Mr. John Lingard, in his work on timber
(1842), states that he has proved that 4½ oz. of water can be
driven off from a small piece of fir, weighing only 10 oz. when wet,
which is nearly half. This timber was on a saw-pit, and going to be
put into a building.
The most general, and the most fatal cause of decay, viz. the wet
rot, has attracted less attention than the more startling, but less
common evils, the dry rot, and the destruction by insects.
Sir Thomas Deane, in 1849, related before the Institution of Civil
Engineers of Ireland, an extraordinary instance of the rapid decay of
timber from rot, which occurred in the church of the Holy Trinity at
Cork.
On opening the floors under the pews, a most extraordinary
appearance presented itself. There were flat fungi of immense size
and thickness, some so large as almost to occupy a space equal to
the size of a pew, and from 1 to 3 inches thick. In other places fungi
appeared, growing with the ordinary dry rot, some of an unusual
shape, in form like a convolvulus, with stems of from a quarter to
half an inch in diameter. When first exposed, the whole was of a
beautiful buff colour, and emitted the usual smell of the dry-rot
fungus.
During a great part of the time occupied in the repairs of the
church, the weather was very rainy. The arches of the vaults having
been turned before the roof was slated, the rain water saturated the
partly decayed oak beams. The flooring and joists, composed of
fresh timber, were laid on the vaulting before it was dry, coming in
contact at the same time with the old oak timber, which was
abundantly supplied with the seeds of decay, stimulated by moisture,
the bad atmosphere of an ill-contrived burial-place, and afterwards
by heat from the stoves constantly in use. All these circumstances
account satisfactorily for the extraordinary and rapid growth of the
fungi.
Many instances might be mentioned of English oak being affected
with dry rot, under particular circumstances. There was a great deal
at the Duke of Devonshire’s, at Chiswick, about 60 years ago. Needy
builders, who work for contract, sometimes use American oak, and
call it wainscot: it is a bad substitute for wainscot, being very liable
to warp and to be affected with dry rot. “I know of one public
building,” observed the late Mr. Henry Warburton, M.P., “in which it
has been introduced, and, I suppose, paid for under that name.”
Another serious instance of the decay of timber from rot occurred
some time since in Old St. Pancras Church, London. When the dry
rot made its appearance, it spread with amazing rapidity. Sometimes
in the course of a night, a fungus of about the consistence of newly-
fallen snow, and of a yellowish-white unwholesome colour, would be
found to have spread over a considerable surface. The fungus was
without shape, but in some cases it rose to a height of 2, 3, or 4
inches above the planks or other surfaces on which it grew. It could
be cut with a knife, leaving a clear edge on each side, and there did
not seem to be any covering or membrane over the outer or under
surface. The smell of those matters was unpleasant, and seemed like
the concentration of the smell which had pervaded the church for so
long a time before; and, in a short time, beams, planks of flooring,
railings, &c., were reduced to rottenness: the colour changed, and a
heavy dark-brown dust fell, and represented the once solid timber.
On making an examination with a view of discovering the cause of
the attack, it was found that in the graveyard, near the church, there
were graves, and several vaults: there were also vaults in the inside
of the church. Most of them were filled, or nearly so, with water,
which had run from the overcrowded graves.
In the interior there were water-logged vaults, and the walls were
saturated with damp. It was also seen that from want of proper
spouts and drains, near the outer walls, the drip from the large pent
roof had fallen into the foundations. In this situation, when the
window frames were properly arranged, a drain dug round and from
parts of the church, and other alterations, which should long before
have been made, were completed, the dry rot vanished, and no
more complaints of the foulness of the air have since been heard.
 We could quote many cases of rot which have been caused from
the want of proper drains and spouts. Architects should remember
that the feet of Gothic collar roofs have to bear the whole weight of
the roof, and unless well seasoned, and carefully protected from
damp, leaks, &c., premature decay and dry rot will be sure to occur.
It is surprising what injury leaks from gutters will sometimes do. In
1851, Professor T. L. Donaldson stated that “a brestsummer of
American timber was used some time since at a house in London:
after an expiration of three years cracks began to appear in the front
wall. A friend of mine, an architect, was called in to find out the
cause; and after examining different parts of the house, was almost
giving up his search in despair, when he thought he would have the
shop cornice removed and look at the brestsummer. He then
discovered that some water had been admitted by accident, and
penetrating the brestsummer, had caused it to rot, and crack the
wall.”
Dry rot was found in the great dome of the Bank of England,
London, as originally built by Sir Robert Taylor: it also existed in the
Society of Arts building, in the Adelphi, London. It was also found in
the domes of the Panthéon, and Halle-au-Blé, Paris; but we hope
there is no dry rot in the dome of St. Paul’s Cathedral, London,
which is constructed entirely of timber, covered externally with lead.
The decayed state of a barn floor attacked by rot is thus described
by Mr. B. Johnson: “An oak barn floor which had been laid twelve
years began to shake upon the joists, and on examination was found
to be quite rotten in various parts. The planks, 2½ inches in
thickness, were nearly eaten through, except the outsides, which
were glossy, and apparently without blemish. The rotten wood was
partly in the state of an impalpable powder, of a snuff colour; other
parts were black, and the rest clearly fungus. No earth was near the
wood.” This oak was probably of the Quercus sessiliflora species;
and there was no ventilation to the floor.
Mr. John Armstrong, carpenter, employed for many years at
Windsor Castle, observed: “I was employed a few years back at a
house where I found a floor rotten. We took it up; it was yellow
pine; it was laid in the damp, but on sleepers, and the sleepers were
not rotten: they were of a different description of wood.” Probably
the sleepers were of Baltic red wood.
Dr. Carpenter relates an instance of the expansive power resulting
from the rapid growth of the soft cellular tissue of fungi. About the
commencement of this century the town of Basingstoke was paved;
and not many months afterwards the pavement was observed to
exhibit an unevenness which could not easily be accounted for. In a
short time after, the mystery was explained, for some of the heaviest
stones were completely lifted out of their beds by the growth of
large toadstools beneath them. One of these stones measured 22
inches by 21 inches, and weighed 83 lb., and the resistance afforded
by the mortar which held it in its place would probably be even a
greater obstacle than the weight. A similar incident came under the
notice of Mr. M. C. Cooke (the author of ‘British Fungi’), of a large
kitchen hearthstone which was forced up from its bed by an under-
growing fungus, and had to be relaid two or three times, until at last
it reposed in peace, the old bed having been removed to the depth
of 6 inches, and a new foundation laid. A circumstance recorded by
Sir Joseph Banks is still more extraordinary, of a cask of wine which,
having been confined for three years in a cellar, was, at the
termination of that period, found to have leaked from the cask, and
vegetated in the form of immense fungi, which had filled the cellar,
and borne upwards the empty wine cask.
Timber decay in contact with stone is a subject deserving
consideration. This decay is entirely obviated by inserting the wood
in an iron shoe, or by placing a thin piece of iron between the wood
and the stone. It is said that a hard crust is formed on the timber in
contact with the iron, which seems effectually to preserve it; it is, of
course, necessary that a free circulation of air round the ends of the
timber be provided. The most notable instance of timber decay in
contact with stone with which we are acquainted occurred at the
coronation of George IV. Westminster Hall was then fitted up, and
they began by laying sleepers of yellow pine. The coronation was
suspended for twelve months, and when the sleepers were taken up
from the floor of Westminster Hall, they were in a rotten state.
Timber in contact with brickwork is in Suffolk and in some parts of
England covered with sheet lead to preserve it from the effects of
the damp mortar. Fungi will arise in mortar, if made with road-drift,
and water from stagnant ponds, &c., and it may be traced through
the mortar joints, and will thus appear on both sides of a wall.
Mortar composed of unwashed sand will generate fungi; sea sand,
even if washed, should never be used. It is considered that the
system of grouting contributes to the early decay of timber; wood
bond timber for walls has been consequently replaced by hoop iron
bond. In Manchester wood bond is frequently used, and is said to
answer well, but the high temperature of the buildings may be a
preventive against the decay of timber, as the walls are soon dried.
The practice is a bad one.
When timber used as posts inserted in the ground is placed in the
inverted position to that in which it stood when growing, it is said to
be very much more durable than if placed in its natural or growing
position. This is easily accounted for in the valves of the sap vessels
of the growing timber opening upwards; but when that position is
inverted, the valves of the sap vessels become reversed in their
action; and, therefore, when timber is used as posts inserted in the
ground, the valves being so reversed prevent the ascent of moisture
from the soil in the wood. Mr. W. Howe relates an experiment made
to test the comparative durability of posts set as they grew. He says,
“Sixteen years ago I set six pairs of bar posts all split out of the butt
end of the same white oak log. One pair I set butts down; another
pair, one butt down, the other top down; the others top down. Four
years ago those set butt down were all rotted off, and had to be
replaced by new ones. This summer I had occasion to reset those
that were set top down: I found them all sound enough to reset. My
experiments have convinced me that the best way is to set them
tops down.” Other instances might be given in favour of placing
posts in an inverted position in the ground. Posts will sometimes
decay, for the following reason: The ends are often sawn off with a
coarse implement and left spongy, with the longitudinal fibres
shaken or broken a considerable way within the extremity of the
wood. In this state the ends of the posts must be apt to absorb from
the ground the moisture, which, being retained, and speedily
pervading the whole internal surface, especially if painted, appears
to cause decay.
With respect to the preservation of wooden fences, Mr.
Cruikshank, of Marcassie, gives in detail various experiments from
which it appears that—1st. When larch or pine wood is to be
exposed to the weather, or to be put in the ground, no bark should
be left on. 2nd. When posts are to be put in the ground, no earth
should be put round them, but stones. 3rd. When a wooden fence is
to be put up, a No. 4 or No. 5 wire should be stretched in place of,
or alongside the upper rail.
Mr. G. S. Hartig, in the ‘Revue Horticole,’ gives the results of
experiments made with great care and patience, upon woods buried
in the earth. Pieces of wood of various kinds 3⅛th inches square,
were buried about one inch below the surface of the ground, and
they decayed in the following order: the lime, American birch, alder,
and the trembling-leaved poplar, in three years; the common willow,
horse-chestnut, and plane, in four years; the maple, red beech, and
common birch, in five years; the elm, ash, hornbeam, and Lombardy
poplar, in six years; the oak, Scotch fir, Weymouth pine, and silver fir,
were only decayed to the depth of half an inch in seven years; the
larch, common juniper, red cedar, and arbor vitæ, at the end of the
last-mentioned period remained uninjured. The duration of their
respective woods greatly depends on their age and quality;
specimens from young trees decaying much quicker than those from
sound old trees; and, when well seasoned, they, of course, last
much longer than when buried in an unseasoned state. In
experiments with the woods cut into thin boards, decay proceeded
in the following order: the plane, horse-chestnut, poplar, American
birch, red beech, hornbeam, alder, ash, maple, silver fir, Scotch fir,
elm, Weymouth pine, larch, locust oak.
 Before quitting the subject of decay of timber when buried in the
earth, it will not be out of place to allude to the decay of railway
sleepers, taking for example those in India: English and American
sleepers will be dealt with more in detail hereafter.
Dr. Cleghorn, Conservator of Forests, Madras Presidency, India,
considers the decay of sleepers to arise in a great measure from the
inferior description of wood used. Mr. Bryce McMaster, Resident
Engineer, Salem, considers that the native wood sleepers in India
have hitherto been found for the most part to fail on the Madras
Railway, between 30 and 40 per cent. requiring to be renewed
annually. Mr. McMaster undertook an investigation with a view of
ascertaining the causes of this deterioration, and whether those
causes could be overcome so as to render available the vast
resources of India. Thirteen hundred sleepers of sixteen different
woods were submitted to careful examination and scrutiny twice at
an interval of one year. The sleepers were variously placed, both on
embankments and in cuttings; in some cases they were entirely
covered with ballast to a depth of 4 inches; while in others they
were as much as possible uncovered, and completely so from the
rails to the ends—the ballast being only raised 2 inches in the middle
of the way, and sloped off so as to carry away the water under the
rails. From these observations it appeared that only five woods,
Chella wungé, Kara mardá, Palai, Karúvalem, and Ilupé, were sound
at the end of two years, the other eleven not lasting even that time.
Also, that when the sleepers were uncovered, decay was less rapid
than when they were buried in the ballast. The plan of leaving the
sleepers partially uncovered had many advantages; it effected a
saving of the ballast, allowed the defects to be more quickly
detected, and kept the sleepers drier. It had been urged that the
heat of the sun would split the sleepers and cause the keys and
treenails to shrink; but from experience it was found that while
among the “uncovered” sleepers there was a large proportion
“beginning to split,” or “useless from being split,” there was on the
other hand, among the “covered” sleepers, a still larger proportion
“beginning to rot,” or “useless from being rotten.” It was also noticed
that of the sleepers “beginning to rot,” 19 per cent. had commenced
under one or both chairs. This was due to the retention of moisture
under them, and might be remedied by tarring the seats of the
chairs. As regarded the treenails where the sleepers were rotten, the
treenails were invariably found to be in the same state; while, when
the heads were exposed to the sun, they were not loosened by
shrinking. Another objection was, that the road would be more likely
to buckle and twist, but this was not found in practice to be the
case. Treenails made in India cost 2l. 10s. to 4l. per 1000, and the
woods generally used for the purpose are Vengé, Kara mardá, Erul,
Porasa, or satin wood, and Trincomalee. The three woods first
named are also extensively employed for keys, but teak keys seem
to be the best, and their cost does not exceed 6l. per 1000. From
the experience of the Indian engineers it appears that Teak, Saul,
Sisso, Pedowk, Kara mardá, Acha, Vengé, Chella wungé, Palai, Erul,
Karúvalem, will make very good sleepers to be used plain.
The sleepers which have failed on the Madras Railway might well
be divided into two classes,—those which were originally of
perishable woods, and were therefore unfit for the purpose; and
those which although of good wood had been cut from young trees,
and not been allowed to stand until old enough. The first arose from
want of experience of the nature of Indian woods: the second from
the absence of a proper system of working the jungles.
The wooden sleepers on the Indian railways should be tarred
under the seats of the chairs, be laid in dry ballast, and raised
slightly in the middle, and sloped off so as to throw the water under
the rails. About two-thirds of the Indian woods are practically useless
owing to the want of proper artificial means for preserving those of a
perishable nature.
The subject of the decay of wood in India and tropical climates is
too extensive to be further considered here; but is of sufficient
importance to demand a volume to itself; the renewal of decayed
wooden sleepers to railways forming annually a most important item
in foreign railway budgets.
 We have heard that some of our fortifications which have been
erected within the last few years to protect our English coast from
invasion, have already been invaded by dry rot. If this be true, some
one well acquainted with the subject should at once be appointed to
find out the cause, and recommend the remedy in each case.
Professional men, if they wish their works to “live for ever,” should
consider the after consequences of neglecting to provide against dry
rot. If the fungi could speak from under floors, ceiled-up roofs,
behind wainscots, girders, &c., we should often hear them exclaim,
“A nice moist piece of wood! Surely this belongs to us.” On the
beams of a building at Crawley, a carpenter many years ago cut a
few words; they are full of meaning in connection with our subject,
and they run as follows:
“Man of weal, beware; beware before of what
cometh behind.”
 CHAPTER III.
FELLING TIMBER.

The end to be attained in the management of timber trees is to

produce from a given number the largest possible amount of sound
and durable woods. When a tree, under conditions favourable to its
growth, ceases increasing the diameter of its trunk, and loses its
foliage earlier in the autumn than it is wont to do, and when the top
of the tree brings forth no leaves in spring, these facts may be
considered as indications of decline, and that the tree is of sufficient
age to be felled. The state of the upper branches of a tree may be
considered to be amongst the best indications of its soundness, and
provided they be in a healthy condition, the withering of the lower
branches is a matter of comparatively small importance.
Trees may be considered as tall, middle rank, and low, and the
size to which they will attain depends on many different
circumstances. Some trees, the stems of which are short on the
average, as the lime, are virtually of tall growth, from the manner in
which a number of vertical branches of large size ascend from the
stem. And other trees, again, whose branches are comparatively
short, are of tall growth, in consequence of the length of the stems
—like the beech.
The average duration of trees differs, as is well known, in different
species, and they exhibit different symptoms of decay. There are
oaks in Windsor Great Park, certainly nearly one thousand years old,
and which exhibit even now no appearance of approaching the end
of their life. Mr. Menzies, the surveyor, in his work on Windsor Great
Park, describes some of the indications of incipient decay which are
peculiar to the several kinds of trees. “When a beech begins to fail,”
he says, “fungi appear either at the roots or on the forks, the leaves
curl up as if they had been scorched, and the tree quickly perishes.
In an elm, a great limb first fails, while the rest of the tree continues
green and vigorous, but in a few years the whole tree suddenly dies.
Coniferous trees die gradually, but quickly. The oak shows the first
symptoms at the points of its highest branches, while the rest of the
tree will remain healthy and sound for years.” This peculiarity of the
oak did not escape the eye of Shakespere, that universal observer,
who describes the monarch of the woods as not only having its
boughs mossed with age, but its

“High top bald with dry antiquity.”

The age for felling trees is a subject which calls for the deepest
consideration, but does not always receive that attention which is
due to its importance. Timber growers in their haste to supply the
market, too often fell trees that have not arrived at maturity, the
heart-wood being therefore imperfect, with much sap-wood, and, of
course, little durability; but unfortunately they are the more readily
led to do so on account of the increase in size being very slow after
a certain age. Builders are sensible of the inferior quality of young
timber in respect to duration, and it is their province to check this
growing evil, by giving a better price for timber that has acquired a
proper degree of density and hardness; but, unfortunately, this is an
age for cheap building, without much regard being given as to
durability.
Felling should not be too early, for the reasons above mentioned;
neither should it be in the decline of the tree, when its elasticity and
vigour are lost, and the wood becomes brittle, tainted, and
discoloured, with the pith gone, and the heart in progress of decay.
Maturity is the period when the sap-wood bears a small proportion,
and the heart-wood has become uniform and compact. Sir John
Evelyn writes, “It should be in the vigour and perfection of trees,
that a felling should be celebrated.” It must be obvious, however,
that it is a worse fault to fell wood before it has acquired thorough
firmness, than when it is just in the wane, and its heart may exhibit
but the first symptoms of decay; for in the former there is no perfect
enduring timber to be got, while in the latter the greater part is in
the zenith of its strength.
Although there are certain symptoms by which it may be
ascertained when a tree is on the decline, it is somewhat difficult to
decide just when a tree is at maturity. From the investigations of
naturalists, however, it may be safe to consider that hard-wood
trees, as oak and chestnut, should never be cut before they are sixty
years old, the average age for felling being from eighty to ninety
years, and the average quantity of timber produced by a tree of that
age is about a load and a half, or about 75 cubic feet.
Daviller states (see ‘Cours d’Architecture’) “that an oak should not
be felled at a less age than sixty years.” Belidor considers (see
‘Sciences des Ingénieurs’) “that one hundred years is the best age
for the oak to be felled.”
It should be remembered that the times mentioned are by no
means arbitrary, for situation, soil, &c., have much to do with it. For
the soft woods, as the Norway spruce and Scotch pine in Norway,
the proper age is between seventy and one hundred years. The ash,
larch, and elm, may be cut when the trees are between fifty and
ninety years old; and between thirty and fifty years is a proper age
for poplars.
The felling of timber was looked upon by ancient architects as a
matter of much moment. According to Vitruvius, the proper time for
felling is between October and February, and he directs that the
trees should be cut to the pith, and then suffered to remain till the
sap be drained out. The effusion of the sap prevents the decay of
the timber, and when it is all drained out, and the wood becomes
dry, the trees are to be cut down, when the wood will be excellent
for use. A similar effect might be produced by placing the timber on
its end as soon as it is felled, and it would, no doubt, compensate
for the extra expense by its durability in use. In France, so long ago
as 1669, a royal order limited the felling of naval timber from the 1st
October to 15th April, when the “wind was at north,” and “in the
wane of the moon.” Buonaparte directed that the time for felling
naval timber should be “in the decrease of the moon, from 1st
November to 15th March,” in order to render it more durable. In
England, in the first year of James I., there was an Act of Parliament
prohibiting every one from cutting oak timber, except in the barking
season, under a severe penalty.
James I. was not the only English sovereign who has been
concerned with timber trees; for King John was obliged to cancel at
Runnemede the cruel forest laws enacted by his father, William the
Conqueror, especially those restricting the people from fattening
their hogs.
Up to a recent period large droves of hogs were fattened upon the
acorns of the New Forest in Hampshire. At the present time the hogs
of Estremadura are principally fed upon the acorns of the Ballota
oak; and to this cause is assigned the great delicacy of their flesh.
A Berkshire labourer, living near Windsor Forest, thus speaks of
the delicacy of acorn-fed pork: “Well, that be pretty like the thing. I
hadn’t tasted the like o’ that this many a day. It is so meller—when
you gets your teeth on it, you thinks you has it; but afore you knows
where you is, ain’t it wanished!”
There is another point in connection with the time of felling
timber, which ought to be noticed. It is a widespread opinion that
trees should be felled during the wane of the moon. This planetary
influence is open to doubt, but the opinion prevails wherever there
are large forests. Columella, Cato, Vitruvius, and Pliny, all had their
notions of cutting timber at certain ages of the moon. The wood-
cutters of South America act upon it, so do their brethren in the
German forests, in Brazil, and in Yucatan. It was formerly interwoven
in the Forest Code of France, and, we believe, is so still. Vitruvius
recommends this custom, and we find Isaac Ware writing of the
suggestion: “This has been laughed at, and supposed to be an
imaginary advantage. There may be good in following the practice;
there can be no harm: and therefore, when I am to depend upon my
timber, I will observe it.” The Indian wood-cutters believe that timber
is much more liable to decay, if cut when the moon is in crescent.
An American writer, in 1863, thus writes of his experience in the
matter: “Tradition says that the ‘old’ of the moon, in February, is the
best time to cut timber; but from more than twenty years of
observation and actual experience, I am fully convinced it is about
the worst time to cut most, if not all kinds of hard-wood timber.
Birch, ash, and most or all kinds of hard wood will invariably powder-
post if cut any time in the fall after the tree is frozen, or before it is
thoroughly leaved out in the spring of the year. But if cut after the
sap in the tree is used up in the growth of the tree, until freezing
weather again comes, it will in no instance produce the powder-post
worm. When the tree is frozen, and cut in this condition, the worm
first commences its ravages on the inside film of the bark, and then
penetrates the wood until it destroys the sap part thereof. I have
found the months of August, September, and October, to be the
three best in the year to cut hard-wood timber. If cut in these
months, the timber is harder, more elastic, and durable than if cut in
winter months. I have, by weighing timber, found that of equal
quality got out for joiners’ tools is much heavier when cut and got
out in the above-named months than in the winter and spring
months, and it is not so liable to crack. You may cut a tree in
September, and another in the ‘old’ of the moon in February
following, and let them remain, and in one year from the cutting of
the first tree, you will find it sound and unhurt, while the one last cut
is scarcely fit for firewood, from decay. Chestnut timber for building
will last longest, provided the bark be taken off. Hemlock and pine
ought to be cut before being hard frozen, although they do not
powder-post; yet if they are cut in the middle of winter, or in the
spring of the year, and the bark is not taken off, the grub will
immediately commence its ravages between the bark and the wood.
I have walnut timber on hand which has been cut from one to ten
years, with the bark on, which was designed for ox-helves and ox-
bows, and not a worm is to be found therein; it was cut between 1st
August and 1st November. I have other pieces of similar timber cut
in the winter months, not two year’s old, and they are entirely
destroyed, being full of powder-post and grub-worms.”
What shall we say when doctors disagree? The theory given to
account for what is assumed to be a fact, is, that as the moon grows
the sap rises, and the wood, therefore is less dense than when the
moon is waning, because at that time the sap in the tree diminishes.
No evidence whatever can be offered in support of the theory, and
one would certainly imagine that the rise or fall of the sap would
depend on the quantity of heat which reaches the foot of the tree,
and not at all on attraction.
All investigations tend to prove that the only proper time for felling
timber is that at which the tree contains the least sap. There are two
seasons in each year when the vessels are filled. One is in spring,
when the fluid is in motion to supply nutriment to the leaves, and
deposit material for new wood; the other is in the early part of
autumn, when, after the stagnation which gives the new wood time
to dry and harden, it again flows to make the vegetable deposits in
the vessels of the wood. At neither of these times should trees be
felled; for, if the pores be full of vegetable juices, which being acted
upon by heat and moisture may ferment, the wood will decay. Of the
two periods, the spring must be the worst, because the wood then
contains the greatest quantity of matter in a state fit for
germination.
The results of a series of experiments made in Germany show that
December-cut wood allows no water to pass through it
longitudinally; January-cut wood passed in forty-eight hours a few
drops; February-cut wood let two quarts of water through its
interstitial spaces in forty-eight hours; March-cut wood permitted the
same to filter through in two and a half hours. Hence the reasons
why barrels made from wood cut in March or April are so leaky, as
the sap is then rising, and the trees are preparing to put forth their
leaves.
It thus happens that the time for felling is midsummer or
midwinter. The best time for felling, according to some, is
midsummer, when the leaves are fully expanded, and the sap has
ceased to flow, and the extraneous vegetable matter intended for
the leaves has been dislodged from the trunk of the tree by the
common sap, leaving it in a quiescent state, and free from that
germinative principle which is readily excited by heat and moisture,
and if the timber were cut while it remained, would subject it to
rapid decay and to operations of worms. Midwinter, amongst some,
is chosen as a time for felling, as it is stated that winter-felled heart-
wood is less affected by moisture, and likely to be the best and most
durable; but as the only peculiar recommendation which that time
possesses is the facility which it affords for gradual seasoning, by
which timber is rendered less liable to split and get distorted, and
slow drying being generally available at any season under shade and
shelter, midsummer appears for many obvious reasons the most
expedient. In general, all the soft woods, such as elm, lime, poplar,
willow, should be felled during winter. In some kinds of trees a little
after midsummer appears to be decidedly the best time for felling.
Alder felled at that time is found to be much more durable; and Ellis
observes, that beech when cut in the middle of summer is bitter, and
less liable to be worm-eaten, particularly if a gash be cut to let out
the sap some time before felling. Mr. Knowles states that, “About
Naples, and in other parts of Italy, oaks have been felled in summer,
and are said to have been very durable.” Most of the trees in
southern Italy are felled in July and August, and the pines in the
German forests are cut down mostly in summer time, and it is stated
that their wood is sound.
The following are advocates for winter felling, viz. Cato, Pliny,
Vitruvius, Alberti, Hesiod, De Saussure, Evelyn, Darwin, and
Buonaparte. Some of them consider that winter-felled timber, which
has been barked and notched in the previous spring, loses much of
that half-prepared woody matter, containing seeds of fungi, &c., that
there is no doubt of its superiority to summer-felled timber.
The age at which trees should be felled, and the most suitable
time for the work having been determined, there are two other
things which claim attention.
 The first of these is the removal of the bark from the trunk and
principal branches of the tree. For, in oak trees, the bark is too
valuable to be lost; and as the best period for the timber is the worst
for the bark, an ingenious method has been long partially practised,
which not only secures the bark at the best season, but also
materially improves the timber. This method consists in taking the
bark off the standing tree early in the spring, and not felling it till
after the new foliage has put forth and died. This practice has been
considered of inestimable value; for by it the sap-wood is rendered
as strong and durable as the heart-wood; and in some particular
instances experiments have shown it to be four times as strong as
other wood in all respects similar, and grown on the same soil, but
felled with the bark on and dried in sheds. Buffon, Du Hamel, and, in
fact, most naturalists, have earnestly recommended the practice.
Evelyn states, “To make excellent boards, bark your trees in a fit
season, and let them stand naked a full year before felling.”
In regard to the time that should elapse between the removal of
the bark and the felling of a tree, a variety of opinions exist. It was
the usual custom of early architects to remove the bark in the
spring, and fell the trees during the succeeding winter. Later
investigations seemed to have proved that it is better to perform the
work three or even four years in advance, instead of one, although
Tredgold appears to think one year too long. Trees will, in most
situations, continue to expand and leaf out for several seasons after
the bark has been removed. The sap remaining in the wood
gradually becomes hardened into woody substance, thereby closing
the sap vessels and making it more solid. As bark separates freely
from the wood in spring, while the sap is in motion, it should be
taken off at that period. When the above method is not adopted, it is
well either to pierce the trunk some time before felling to drain out
the sap, or immediately on its being felled to set it on end.
The second suggestion is, to cut into and around the entire trunk
of the tree, near the roots, so that the sap may be discharged; for in
this manner it will be done more easily than it can be by evaporation
after the tree is felled. In addition to this, if it be permitted to run
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