118a – 2nd handout

CHAPTER II: about the present illness and any symptoms are thoroughly
investigated using the mnemonic NOPQRST (image on the left
RESPONSES TO ALTERED column)
VENTILATORY FUNCTION FOCUSED HEALTH HISTORY
This chapter covers nursing management to a Subjective information about the respiratory history can be taken
critically ill patient that affects the body’s from the patient if they are awake, or from other sources
ventilatory function. It contains relevant 09(e.g.,
– 26 family,
– 21
assessment techniques and findings that will be caregivers, or patient notes).
useful in identifying nursing interventions that
focuses on the emergency relief and prevention of Principal symptoms that should be investigated in more detail
potential complications. commonly include dyspnea, chest pain, sputum production, and
cough, shortness of breath, wheezing, chest pain and sleep
disturbance. An overview of the patient’s past medical history and
INTRODUCTION OF THE LESSON AND LEARNING OUTCOME family’s respiratory history, as well as personal and social history,
may uncover elements that are contributing to the patient’s current
health problem.
This lesson focuses on the different spectrum of respiratory diseases/illnesses requiring
immediate nursing management. This lesson highlights the importance of efficient and
effective comprehensive history and physical assessment allowing the nurse to establish a
baseline level of assessment of patient’s status and provides a framework for detecting
rapid changes in the patient’s condition, as well as effective nursing interventions.
II. PHYSICAL ASSESSMENT
Any respiratory problem can interfere with gas exchange, oxygenation, and tissue
perfusion, progressing to an emergency and death, even with prompt treatment. These
 In most cases, you should begin the physical examination
problems may overwhelm the adaptive responses of the cardiac and blood oxygen after you take the patient’s history. However, you may not
delivery systems be able to take a complete history if the patient develops
LEARNING INPUTS an ominous sign such as acute respiratory distress.
If an actual or potential respiratory abnormality is identified  If your patient is in respiratory distress, establish the
during a general ABCDE assessment or while monitoring the patient, priorities of your nursing assessment, progressing from
a more detailed and focused respiratory assessment can provide the most critical factors (airway, breathing, and
further information to guide clinical management. Patients with
dyspnea or acute respiratory failure will often also manifest systemic circulation [the ABCs]) to less critical factors.
signs and symptoms, including altered consciousness, cardiovascular
compromise, and gastrointestinal dysfunction.
 Physical assessment of the respiratory system is a reliable
means of gathering essential data and is guided by the
ASSESSMENT FOR THE HIGH-RISK information obtained through the history. A thorough
physical assessment includes inspection, palpation,
RESPIRATORY PATIENT percussion, and auscultation. Recall your previous
I. HISTORY AND INTERVIEW subjects.
The clinical history of the respiratory system
is divided into six components: (1) chief III. RESPIRATORY MONITORING
complaint, (2) history of present illness, (3) Keep in Mind.
past health history, (4) family history, (5)  Specific respiratory monitoring may be indicated
personal and social history, and (6) review Build your patient’s health history by
of systems.
asking short, open-ended questions. during the care of a critically ill patient. An
Conduct the interview in several short
sessions if you have to, depending on the understanding of the indications and practices
Begin by asking why your patient severity of your patient’s condition. Ask associated with these monitoring devices will ensure
is seeking care. Because many respiratory his family to provide information, if your
disorders are chronic, ask how the patient’s patient can’t
accuracy of the results. In addition to the respiratory
latest acute episode compares with previous monitoring described in this section, the following
episodes and what relief measures are helpful systems will provide further support for the respiratory
and unhelpful. assessment and care of the patient: chest X-ray,
mechanical ventilation waveform analysis and blood
gas analysis
The patient’s history starts with the chief
complaint and information about the present illness. Often, if the
patient is very ill, a relative or friend provides more information. Data a. PULSE
OXIMETRY:
This provides
continuous,
noninvasive
measurement of
oxygen saturation
in arterial blood (SpO2). Pulse oximetry is used to assess for
hypoxemia, to detect variations from the patient’s oxygenation
baseline (e.g. due to procedures or activity level), and to
support the use of oxygen therapy.

b. ARTERIAL BLOOD GAS (ABG) ANALYSIS

Arterial blood gas (ABG) monitoring is frequently performed
in critically ill patients to assess acid-base balance, ventilation,

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and oxygenation. Here’s a summary of commonly assessed the capnogram indicates the exhalation of alveolar gases
ABG values and what the findings indicate: (AKA alveolar plateau).
 pH measurement of the hydrogen ion (H+) concentration
is an indication of the blood’s acidity or alkalinity. 4. The fourth phase is known as the inspiratory downstroke.
 Partial pressure of arterial carbon dioxide (Paco2) reflects The downward deflection of the waveform is caused by
the adequacy of ventilation of the lungs. the washout of carbon dioxide that occurs in the presence
 Pao2 reflects the body’s ability to pick up oxygen from of the oxygen influx during inspiration.
the lungs.
 Bicarbonate (HCO3 – ) level reflects the activity of the
kidneys in retaining or excreting bicarbonate.

c. CAPNOGRAPHY / END TIDAL CARBON DIOXIDE

(ETCO2) MONITORING
 End-tidal carbon dioxide
(ETCO2) monitoring Because ETCO2 provides
measures the level of continuous estimates of alveolar
carbon dioxide at the ventilation, its measurement is
end of exhalation. useful for monitoring the patient
ETCO2 values are during weaning from a ventilator,
in cardiopulmonary resuscitation,
obtained by monitoring
and in endotracheal intubation
samples of expired gas
from an endotracheal
tube, an oral airway, or
a nasopharyngeal IV. RESPIRATORY DIAGNOSTIC STUDIES
airway.

 The exhaled carbon dioxide waveform is displayed on the  CHEST RADIOGRAPHY

monitor as a plot of ETCO2 versus time called a This is an essential noninvasive diagnostic tool for evaluating
CAPNOGRAM, which provides the nurse with a respiratory disorders, infiltration, and abnormal lung
continuous graphic reading of the patient’s ETCO2 level shadows, as well as identifying foreign bodies. Chest x-rays
with each exhaled breath. in critical care settings are also used to check and monitor the
effectiveness and placement of tubes and lines such as an
endotracheal tube, chest tubes, and pulmonary artery lines.
 Changes in the waveform indicate clinical abnormalitie s,
mechanical abnormalities, or both and require immediate
assessment by the nurse or other trained professional.  Normal lung fields appear black because they are
air-filled spaces.
 Thin, wispy white streaks are seen as vascular
 On a capnogram, the waveform is composed of markings.
FOUR PHASES, each one representing a specific  Blood vessels can also appear gray. However,
part of the respiratory cycle: grayness in the lung fields usually suggests pleural
effusion. Light white areas indicate fluid, blood, or
exudate.
1. The first phase is the baseline phase, which represents
both the inspiratory phase and the very beginning of the
expiratory phase, when carbon dioxide–free air in the
 VENTILATION–PERFUSION SCANNING
anatomical dead space is exhaled.
Ventilation–perfusion scanning is a nuclear imaging test used
2. The second phase is the expiratory upstroke, which to evaluate a suspected alteration in the ventilation– perfusion
represents the exhalation of relationship. A ventilation– perfusion scan is helpful in
carbon dioxide from the lungs. detecting the percentage of each lung that is functioning
Any process that delays the V scans aren’t commonly normally, diagnosing and locating pulmonary emboli, and
delivery of carbon dioxide from used for patients on assessing the pulmonary vascular supply.
the patient’s lungs to the mechanical ventilators
because the ventilation The ventilation–perfusion scan consists of two parts: a
detector prolongs the expiratory portion of the test is difficult
upstroke. ventilation scan and a perfusion scan. In the ventilation
to perform. (Pulmonary scan, the patient inhales radioactive gas, which follows the
angiography is the preferred same pathway as air in normal breathing. In pathological
3. The third phase begins as test for a critically ill patient
with a suspected pulmonary
conditions, the diminished areas of ventilation are visible on
carbon dioxide elimination the scan.
embolus.)
rapidly continues; a plateau on
You may recall your previous subjects in studying these other tests.

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  Pulmonary angiogram (preferred test with critically ANSWER: The risk of pulmonary embolism increases
ill pt) with prolonged bed rest or immobilization of a limb in
 Sputum culture a cast because as we all know, when there is
 Bronchoscopy Immobilization, this can leads to local venous stasis by
 Pulmonary function test (PFTs) accumulation of clotting factors and fibrin, resulting in
 Thoracentesis blood clot formation.

Nursing Management to patient with Pulmonary

Embolism
PATHOPHYSIOLOGY:
PULMONARY EMBOLUS (PE) refers to the obstruction of
the pulmonary artery or one of its branches by a thrombus (or
thrombi) that originates somewhere in the venous system or in The hazards of PE can be summarized by Virchow’s
the right side of the heart. triad. A patient at highest risk is one who has (1) venous
stasis, (2) injury to blood vessels, and (3) hemoconcentrated
blood.
RISK FACTORS:
Venous stasis can be caused by immobility from bedrest
In critical care, air, fat, amniotic fluid, and septic and bland and riding in the same position in a car, train, or airplane.
thrombotic emboli are the major syndromes of interest. Identify Blood vessels can be injured through any
how the following risk factors contribute to the formation of Pulmonary instrumentation or surgery, especially of the pelvis and
Embolism.
lower extremities such as total knee surgery and
prostatectomy.
1. DEEP VEIN THROMBOSIS (DVT) Hypercoagulability or hemoconcentrated blood can
(Deep vein thrombosis (DVT) is a medical condition that occurs result from pregnancy or dehydration.
when a blood clot forms in a deep vein. These clots usually develop
in the lower leg, thigh, or pelvis, but they can also occur in the arm.) Pulmonary emboli can result in any of the following:
ANSWER: The most serious complication of DVT happens when a  Embolus with infarction: an embolus that causes
part of the clot breaks off and travels through the bloodstream to the infarction (death) of a portion of lung tissue
lungs, causing a blockage called pulmonary embolism (PE).
 Embolus without infarction: an embolus that does not
cause permanent lung injury (perfusion of the affected
*** In most cases, pulmonary embolism is caused by blood clots that lung segment is maintained by the bronchial circulation)
travel to the lungs from deep veins in the legs or, rarely, from veins in  Massive occlusion: an embolus that occludes a major
other parts of the body (deep vein thrombosis). Because the clots
block blood flow to the lungs, pulmonary embolism can be life- portion of the pulmonary circulation (i.e., main
threatening pulmonary artery embolus)
2. POST PARTUM HEMORRHAGE  Multiple pulmonary emboli: multiple emboli may be
chronic or recurrent.
ANSWER: _ If a blood clot forms inside a vein after
childbirth, the body may not be able to dissolve it. Sometimes,  The effect of the obstruction will cause inflammatory
this clot can break free inside the vein and travel to the lung, changes, which will lead to increased pulmonary artery
known as a pulmonary embolism.
vasoconstriction causing pulmonary hypertension and
Pulmonary embolisms (PE) typically occur during or
shortly after the labor and delivery, and may be fatal for the subsequent coronary oedema, and right ventricular
mother if not treated immediately. dilation and afterload. In addition, the obstruction will
cause a ventilation/perfusion mismatch, leading to
3. FRACTURE OF LONG BONE hypoxemia.

ANSWER: a person who breaks a leg may suffer a fat ASSESSMENT:

embolism, then later develop a blood clot in the leg In most cases the clinical manifestations of PE are
because they do not move around much due to their nonspecific; therefore, evaluation of risk factors and
injury. The leg blood clot can then cause a pulmonary
embolism. predisposing factors is an important aspect of diagnosis.
The effect of the embolus depends on the extent of
pulmonary blood flow obstruction, the size of the
4. CENTRAL VENOUS AND PA CATHETERS affected vessels, the nature of the embolus, and the
ANSWER: Thromboemboli can also originate in arm secondary effects.
veins or central veins of the chest (caused by central
venous catheters or resulting from thoracic outlet
syndromes). … also bcause of trauma in the area …

5. IMMOBILITY

3|Page
 MASSIVE EMBOLUS
A more pronounced manifestation of the above signs and
symptoms, plus the ff:

 Cyanosis  Confusion
 Restlessness  Hypotension
 Anxiety  Cool, clammy skin
 Decreased urinary output

 Pleuritic chest pain: associated w/ pulmonary infarction
 Hemoptysis: associated with pulmonary infarction.

 EMBOLUS WITH INFARCTION: an embolus that

causes infarction (death) of a portion of lung tissue SIGNS of PULMONARY EMBOLISM in
 EMBOLUS WITHOUT INFARCTION: an embolus INTENSIVE CARE PATIENTS
that does not cause permanent lung injury (perfusion  Worsening hypoxemia or hypocapnia in a patient on
of the affected lung segment is maintained by the spontaneous ventilation.
bronchial circulation)  Worsening hypoxemia and hypercapnia in a sedate patient
 MASSIVE OCCLUSION: an embolus that occludes on controlled mechanical ventilation.
a major portion of the pulmonary circulation (i.e.,  Worsening dyspnea, hypoxemia and a reduction in
main pulmonary artery embolus) PaCO2 in a patient with chronic lung disease and known
 MULTIPLE PULMONARY EMBOLI: multiple carbon dioxide retention.
emboli may be chronic or recurrent.  Unexplained fever]
  Sudden elevation in pulmonary artery pressure or central
venous pressure in a hemodynamically monitored patient.
The effect of the obstruction will cause inflammatory changes,
which will lead to increased pulmonary artery vasoconstriction
causing pulmonary hypertension and subsequent coronary DIAGNOSTIC ASSESSMENT:
oedema, and right ventricular dilation and afterload. In
 Worsening hypoxemia and hypercapnia with respiratory
addition, the obstruction will cause a ventilation/perfusion
acidosis.
mismatch, leading to hypoxemia.
 Chest x-ray to rule out pulmonary edema or tumor. It often
shows pulmonary infiltration and occasionally pleural
effusion.
ASSESSMENT:  ECG to rule out MI. ECG findings commonly associated
with pulmonary embolism include tachycardia and
In most cases the clinical manifestations of PE are nonspecific T wave changes.
nonspecific; therefore, evaluation of risk factors and  Chest CT with contrast is the principal test used to
predisposing factors is an important aspect of diagnosis. The diagnose pulmonary embolism. Chest CT effectively
effect of the embolus depends on the extent of pulmonary shows large, central PE; newer generation scanners also
blood flow obstruction, the size of the affected vessels, the can detect peripheral emboli.
nature of the embolus, and the secondary effects.  Plasma D-dimer levels are highly specific to the presence
of a thrombus. D-dimer is a fragment of fibrin formed
during lysis of a blood clot; elevated blood levels
indicate thrombus formation and lysis
 Pulmonary angiogram where dye is injected into the heart
is the definitive test, but it has a high mortality rate.
 Exhaled carbon dioxide (ETCO2) may be measured to
evaluate alveolar perfusion. The normal ETCO2 reading
Signs & Symptoms of Pulmonary Embolism: is 35 to 45 mmHg; it is decreased when pulmonary
perfusion is impaired.
SMALL to MODERATE EMBOLUS
 Apprehension NURSING DIGNOSIS: The priority NANDA-I nursing
 Dyspnea  Cough diagnoses and collaborative problems for patients with PE
 Tachypnea  Diaphoresis include:
 Tachycardia  Decreased breath sounds
 Chest pain over affected area
 Mild fever  Rales 4|Page
 Hypoxemia  Wheezing
 IMPAIRED GAS EXCHANGE: Pulmonary embolism
results in areas of the lung that are ventilated but not
perfused; they receive no capillary blood flow.
 DECREASED CARDIAC OUTPUT: Pressures in the
pulmonary vascular system and right heart increase; blood
return to the left heart and cardiac output may
significantly decrease.
 INEFFECTIVE PROTECTION: Thrombolytics and
anticoagulant therapy impair normal clotting mechanisms,
increasing the risk for bleeding and hemorrhage. This risk 3. Preventing Reembolization: Several strategies are
is particularly acute during the first 24 to 48 hours employed to prevent the likelihood of future embolization
following thrombolytic drug administration. and cardiopulmonary compromise:
 ANXIETY: Pulmonary embolism is a physiologic and a. limiting activity to prevent dislodgement of
psychologic threat to safety and integrity. It is a major additional clots.
physiologic stressor, eliciting a strong neuroendocrine b. Use of anticoagulation therapy with
stress response. The feeling of suffocation and inability to unfractionated heparin to maintain a PTT 1.5 to
catch one’s breath that accompanies a pulmonary embolus 2.5 times the control when no contraindication
is also a strong psychologic stressor. Fear, anxiety, and exists.
apprehension are common responses. c. Insertion of vena cava filters to prevent emboli
from legs, pelvis, and inferior vena cava from
migrating to pulmonary circulation if
anticoagulation therapy is contraindicated.
NURSING INTERVENTIONS:
The key to preventing morbidity and mortality from 4. PREVENTING VENOUS THROMBOEMBOLISM
PE is primarily prevention and secondarily early diagnosis and (VTE): An important recommendation for the prevention
treatment to prevent reembolization. Objectives include the of VTE is awareness and access to a hospital prevention
improvement of oxygenation and ventilation, improvement of policy including risk assessment
cardiovascular function, prevention of reembolization, and
prevention of pulmonary embolus. 5. MINIMIZING ANXIETY: Interventions for reducing
anxiety in those with PE include oxygen therapy,
1. IMPROVING OXYGENATION AND VENTILATION: communication, and drug therapy.
Oxygen therapy is usually very effective in relieving
hypoxemia associated with PE. When cardiopulmonary 6. MANAGING HYPOTENSION: In addition to the
compromise is severe, mechanical ventilation may be interventions used for hypoxemia, IV fluid therapy and
required to achieve optimal oxygenation. drug therapy are used to increase cardiac output and
maintain blood pressure.
2. Improving Cardiovascular Function: Controversy exists as
to the benefit of vasoactive drug administration (such as
norepinephrine and/or inotropic agents) to improve NURSING MANAGEMENT TO PATIENT WITH
myocardial perfusion of the right ventricle. In severe ACUTE RESPIRATORY DISTRESS SYNDROME/ ACUTE
embolic events, where cardiac failure is profound, LUNG INJURY:
additional therapy to hasten clot resolution, such as use of
thrombolytic agents and/or interventional removal of ACUTE RESPIRATORY DISTRESS SYNDROME (ARDS)
massive emboli may be warranted represents a complex clinical syndrome (rather than a single
disease process) and carries a high risk for mortality. ARDS is
defined as a type of acute, diffuse, inflammatory lung injury
a) For patients with blood clots, anticoagulation that leads to increased pulmonary vascular permeability and
with low molecular weight heparin (enoxaparin loss of aerated lung tissue
[Lovenox]), I.V. unfractionated heparin (UFH),
subcutaneous unfractionated heparin, or
subcutaneous fondaparinux (Arixtra) inhibits the
formation of more thrombi. It’s followed by
warfarin (Coumadin) for 3 to 6 months,
depending on risk factors.

b) Patients with massive pulmonary embolism and

shock may need fibrinolytic therapy with
streptokinase (Streptase) or alteplase (Activase)
to enhance fibrinolysis of the pulmonary emboli
and remaining thrombi

RISK FACTORS:
DRUG ALERT
Risk factors for the development of ARDS include
Thrombolytic therapy is only numerous illnesses and injuries, both pulmonary and
recommended for patients
with acute massive 5|Page
pulmonary embolism who are
 systemic with pneumonia being the most common risk infiltrate, blood, fluid, and surfactant dysfunction.
factor (Sweeney & McAuley, 2016). Pneumonia and Small airways are narrowed because of interstitial
aspiration have the highest associated mortality in fluid and bronchial obstruction.
ARDS.
 Lung compliance may markedly decrease, resulting in
decreased functional residual capacity and severe
hypoxemia. The blood returning to the lung for gas
exchange is pumped through the nonventilated,
nonfunctioning areas of the lung, causing shunting. This
means that blood is interfacing with nonfunctioning
alveoli and gas exchange is markedly impaired, resulting
in severe, refractory hypoxemia.

CAUSES AND PREDISPOSING CONDITIONS

for Acute Respiratory Distress Syndrome (ARDS)

Figure 1. (From McCance KL, Huether SE.

Pathophysiology: The Biologic Basis for Diseases in
Adults and Children. 6th ed. St. Louis: Mosby; 2010.)

PATHOPHYSIOLOGY:

 The clinical presentation consists of hypoxemia,

bilateral lung opacities, increased physiological dead
space, and decreased lung compliance. The acute
phase is characterized by diffuse alveolar damage (i.e.
edema, inflammation, or hemorrhage).

 Inflammatory triggers initiate the release of cellular

and chemical mediators, causing injury to the alveolar
capillary membrane in addition to other structural
damage to the lungs. Severe V./Q. mismatching
occurs. Alveoli collapse because of the inflammatory

6|Page
 with increased airway pressure and development of
pneumothorax management difficulties, with increased
airway pressure and development of pneumothoraces.

ASSESSMENT: DIAGNOSIS:

The 2012 Berlin definition of ARDS changed the terminology Refractory hypoxemia (hypoxemia that does not improve
and diagnostic criteria that had previously been used. The
with oxygen administration) is the hallmark of ARDS.
phrase ‘acute lung injury’ is no longer to be used, and ARDS
is now categorized as mild, moderate, or severe.
 Arterial blood gases initially show hypoxemia with a
Initially, ARDS closely resembles severe pulmonary
PO2 of less than 60 mmHg and respiratory alkalosis due
edema.
to tachypnea. (NORMAL PaO2 is 80–100 mmHg)
 Chest x-ray changes may not be evident for as long as
Recognizing the dynamic nature of the morphological 24 hours after the onset of ARDS. Diffuse, bilateral
changes involved with ARDS enables the nurse to understand pulmonary infiltrates without increased cardiac size are
the changes in physical assessment, mechanical ventilation
strategies, treatment, and management that occur throughout seen initially, progressing to a “white out” pattern.
the patient’s critical care stay.  Chest CT scan provides a better illustration of the
pattern of alveolar consolidation and atelectasis in
ARDS (Fishman et al., 2008).
 In STAGE 1, diagnosis is difficult because the signs of  Pulmonary function testing shows decreased lung
impending ARDS are subtle. Clinically, the patient compliance with reduced vital capacity, minute volume,
exhibits increased dyspnea and tachypnea, but there and functional vital capacity
are few radiographic changes. At this point,  Pulmonary artery pressure monitoring shows normal
neutrophils are sequestering; however, there is no pressures in ARDS, helping distinguish ARDS from
evidence of cellular damage. cardiogenic pulmonary edema.
 In STAGE 2 (within 24 hours, a critical time for early
treatment), the symptoms of respiratory distress NURSING DIAGNOSES:
increase in severity, with cyanosis, coarse bilateral
crackles on auscultation, and radiographic changes
consistent with patchy infiltrates. A dry cough or chest  IMPAIRED GAS EXCHANGE related to refractory
pain may be present. It is at this point that the hypoxemia and pulmonary interstitial/alveolar leaks
found in alveolar capillary injury states.
mediator-induced disruption of the vascular bed results
 INEFFECTIVE AIRWAY CLEARANCE related to
in increased interstitial and alveolar edema. The increased secretion production and decreased ciliary
endothelial and epithelial beds are increasingly motion.
permeable to proteins. This is referred to as the  INEFFECTIVE BREATHING PATTERNS related to
“EXUDATIVE” STAGE. The hypoxemia is resistant to inadequate gas exchange, increased secretions,
supplemental oxygen administration, and mechanical decreased ability to oxygenate adequately, fear, or
ventilation will most likely be commenced in response exhaustion.
to a worsening ratio of arterial oxygen to fraction of  ANXIETY related to critical illness, fear of death, role
changes, or permanent disability.
inspired oxygen (PaO2:FiO2 ratio).
 RISK FOR INFECTION related to invasive
monitoring devices and endotracheal tube.
 In STAGE 3, the “PROLIFERATIVE” STAGE,
develops from the 2nd to the 10th day after injury.
Evidence of SIRS (Systemic Inflammatory Response MANAGEMENT:
Syndrome) is now present, with hemodynamic
instability, generalized edema, possible onset of The primary focus in the management of ARDS includes
nosocomial infections, increased hypoxemia, and lung identification and treatment of the underlying condition.
involvement. Air bronchograms may be evident on Treatment is supportive; that is, contributing factors are
chest radiography as well as decreased lung volumes corrected or reversed, and while the lungs heal, care is taken so
and diffuse interstitial markings. that treatment does not further damage.

In addition, extensive work has gone into creating “bundles,”

 STAGE 4, the “FIBROTIC” STAGE, develops after 10 which are elements of care considered core to the management
days and is typified by few additional radiographic and treatment of specific critical illnesses in intensive care
changes. There is increasing multiorgan involvement, units (ICUs). The image lists essential critical care bundles
SIRS, and increases in the arterial carbon dioxide tension that apply to managing ARDS.
(PaCO2) as progressive lung fibrosis and emphysematous
changes result in increased dead space. Fibrotic lung
changes result in ventilation management difficulties,

7|Page
1. IMPROVING OXYGENATION: Administer high Fio2 4. FLUID THERAPY. Conservative fluid therapy involves
levels with high-flow system or rebreathing mask. A infusing smaller amounts of IV fluid and the use of
constant positive airway pressure (CPAP) mask may be diuretics to maintain fluid balance (Ferri, 2013).
tolerated in alert, cooperative patients. NOTE: Research shows that patients with ARDS who
Continuous, vigilant monitoring for receive conservative fluid therapy have improved lung function
contraindications of noninvasive CPAP (decreased loss and a shorter duration of mechanical ventilation and ICU
of consciousness, nausea/vomiting, increased dyspnea or length of stay compared with those who receive more liberal
panic) is imperative. fluid therapy (Ferri, 2013).

5. NUTRITION THERAPY: The patient with ARDS is at

2. IMPROVING VENTILATION: risk for malnutrition, which further reduces respiratory
a. Intubation and mechanical ventilation if cardiovascular muscle function and the immune response.
instability is present, severe hypoxemia persists, or if NOTE: Patients with ARDS require 35 to 45
fatigue develops. The best treatment is to initiate PEEP kcal/kg/day to meet caloric requirements. ENTERAL
after mechanical ventilation. FEEDING is the first consideration; however, parenteral
nutrition also may be required.
b. Humidified oxygen delivery through a tightfitting mask 6. PRONE POSITIONING is probably the most established
and using CPAP may be adequate. ET intubation and of interventions because it may enable limitation of tidal
mechanical ventilation are commonly required. PEEP volumes
may prevent alveolar collapse. High frequency jet
ventilation is sometimes used. 7. IMPROVING REST. Rest is essential to limit oxygen
consumption and reduce oxygen needs. The patient is
Suctioning as necessary removes accumulated secretions extremely anxious and agitated because of the increasing
from the tracheobronchial tree Suctioning as necessary hypoxemia and dyspnea. It is important to reduce the
removes accumulated secretions from the patient’s anxiety because anxiety increases oxygen
tracheobronchial tree expenditure by preventing rest.
c. Ventilation is usually started with Lung-protective
ventilation strategies such as low tidal volumes (<6 ml/kg
predicted body weight) and the use of adequate positive end- NURSING MANAGEMENT to patient with
expiratory pressure (PEEP) to reduce the risk of using a high Respiratory Failure
FiO2 and precipitating oxygen toxicity
d. Sedation and analgesia may be necessary after
intubation to maximize gas exchange and minimize Respiratory failure can be viewed as a failure in gas exchange due to
oxygen consumption. either heart or lung failure, or both. It is not a specific disease but can
occur in the course of a number of conditions that impair ventilation,
compromise the matching of ventilation and perfusion, or impair gas
3. PHARMACOLOGIC THERAPY continues to be diffusion.
explored.
Respiratory failure is a condition in which the respiratory
i Low-dose corticosteroids may improve survival in system fails in one or both of its gas exchange functions—
selected individuals but needs further investigation oxygenation of mixed venous blood and elimination of carbon
dioxide. The function of the respiratory system can be
b. Antibiotics are used to treat infections when said to consist of two aspects: gas exchange (movement
organisms are identified. Currently, no treatments of gases across the alveolar–capillary membrane) and
reverse the pathologic changes in the lungs, ventilation (movement of gases into and out of the
although many interventions are under alveoli due to the action of the respiratory muscles,
investigation. respiratory center in the CNS, and the pathways that
connect the centers in the CNS with the respiratory
c. Vitamins C and E, N-acetylcysteine – used as muscles).
antioxidant
Thus, respiratory failure is commonly divided into two
types:
d. Nitric oxide – is an effective treatment for
pulmonary hypertension
1. TYPE I / HYPOXEMIC RESPIRATORY
FAILURE
e. surfactant replacement. These include agents that
modify the inflammatory responses and reduce
due to failure of the gas exchange function of the
oxidative stress lung (usually caused by Chronic obstructive
pulmonary disease, Interstitial (restrictive) lung
disease, Severe pneumonia, Atelectasis)

8|Page
 In people with hypoxemic respiratory failure, two major CLINICAL MANIFESTATIONS:
pathophysiologic factors contribute to the lowering of:
Note: Assessment of the patient with ARF begins
with the neurological system resulting from hypoxia and
a. ARTERIAL PO2–VENTILATION–PERFUSION hypercapnia.
MISMATCHING. The mismatching of ventilation and
perfusion occurs when areas of the lung are ventilated
but not perfused or when areas are perfused but not
ventilated; this is commonly seen to patients with severe  Acute respiratory failure is usually manifested by
or advanced COPD. varying degrees of hypoxemia and hypercapnia.

b. IMPAIRED DIFFUSION. Impaired diffusion describes a  There is no absolute definition of the levels of PO2 and
condition in which gas exchange between the alveolar air PCO2 that indicate respiratory failure.
and pulmonary blood is impeded because of an increase  RESPIRATORY FAILURE is conventionally defined
in the distance for diffusion or a decrease in the by an arterial PO2 of less than 50 mm Hg, an
permeability or surface area of the respiratory arterial PCO2 of more than 50 mm Hg, or both
membranes to the movement of gases. It most commonly when prior blood values have been normal.
occurs in conditions such as Interstitial Lung Disease
(ILD), ALI/ARDS, pulmonary edema, and pneumonia.  Hypoxemia is accompanied by increased respiratory
drive and increased sympathetic tone. Potential
2. TYPE II / HYPERCAPNIC/HYPOXEMIC signs of hypoxemia include cyanosis, restlessness,
RESPIRATORY FAILURE confusion, anxiety, delirium, fatigue, tachypnea,
hypertension, cardiac arrhythmias, and tremor.
In the hypercapnic form of respiratory failure, people are
unable to maintain a level of alveolar ventilation  The initial cardiovascular effects are tachycardia
sufficient to eliminate CO2 and keep arterial O2 levels with increased cardiac output and increased blood
within normal range. pressure.

Hypoventilation or ventilatory failure occurs when the  Serious arrhythmias may be triggered. The
volume of “fresh” air moving into and out of the lung is pulmonary vasculature constricts in response to low
significantly reduced. It is commonly caused by alveolar PO2.
conditions outside the lung such as:
- depression of the respiratory center (e.g., drug  If severe, the pulmonary vasoconstriction may result
overdose, brain injury), in acute right ventricular failure with manifestations
- diseases of the nerves supplying the respiratory such as jugular vein distention and dependent
muscles (e.g., Guillain-Barré syndrome, spinal cord edema.
injury),
 Profound acute hypoxemia can cause convulsions,
- disorders of the respiratory muscles (e.g., muscular
retinal hemorrhages, and permanent brain damage.
dystrophy),
Hypotension and bradycardia often are preterminal
- exacerbation of chronic lung disease (e.g., COPD),
events in people with hypoxemic respiratory failure,
or
indicating the failure of compensatory mechanisms.
- thoracic cage disorders (e.g., severe scoliosis or
crushed chest).
 Many of the adverse consequences of hypercapnia
Hypoventilation has two important effects on arterial are the result of respiratory acidosis.
blood gases.
o Direct effects of acidosis include depression
- First, it almost always causes an increase in PCO2 . of cardiac contractility, decreased respiratory
The rise in PCO2 is directly related to the level of muscle contractility, and arterial vasodilation.
ventilation; reducing the ventilation by one half o Raised levels of PCO2 greatly increase
causes a doubling of the PCO2 . Thus, the PCO2 cerebral blood flow, which may result in
level is a good diagnostic measure for headache, increased cerebrospinal fluid
hypoventilation. Second, it may cause hypoxemia, pressure, and sometimes papilledema. The
although the hypoxemia that is caused by headache is due to dilation of the cerebral
hypoventilation can be readily abolished by the vessels.
administration of supplemental oxygen.
 Additional indicators of hypercapnia are warm and
NOTE: It may also have caused impairment of diffusion flushed skin and hyperemic conjunctivae.
such as pulmonary edema or ARDS. Hypercapnia has nervous system effects similar to
those of an anesthetic— hence the term carbon
dioxide narcosis.

9|Page
 perfusion. This decreases the efficiency of the
 There is progressive somnolence, disorientation, respiratory gas exchange process
and, if the condition is untreated, coma.

 Mild to moderate increases in blood pressure are NURSING DIAGNOSIS:

common.
 IMPAIRED GAS EXCHANGE related to alveolar
 Air hunger and rapid breathing occur when alveolar
hypoventilation, intrapulmonary shunting, V/Q
PCO2 levels rise to approximately 60 to 75 mm Hg;
as PCO2 levels reach 80 to 100 mm Hg, the person
becomes lethargic and sometimes semi-comatose. CAUSES OF ACUTE RESPIRATORY FAILURE IN
ADULT

INTERPRETING DIAGNOSTIC RESULTS

 ABGs are examined closely to determine ARF.

 The chest x-ray will change from clear to white and
cloudy (patchy infiltrates) if ARF is due to
aspiration, heart failure, or fluid in the chest cavity.

PATHOPHYSIOLOGY
Regardless of the specific underlying cause, the
pathophysiology of ARF can be organized into four main
components:

1. IMPAIRED VENTILATION: Conditions that disrupt

the muscles of respiration or their neurologic control
can impair ventilation and lead to ARF

2. IMPAIRED GAS EXCHANGE: Conditions that

damage the alveolar capillary membrane impair gas
exchange. Direct damage to the cells lining the
alveoli causing a) an increase in alveolar
permeability, increasing the potential for interstitial
fluid to leak into the alveoli and causing noncardiac
pulmonary edema and b) decrease in surfactant mismatch, and diffusion impairment as evidenced by
hypoxemia and/or hypercapnia
production by alveolar type II cells, increasing
alveolar surface tension, which leads to alveolar
collapse.  INEFFECTIVE AIRWAY CLEARANCE related to
excessive secretions, decreased level of
consciousness, presence of an artificial airway,
3. AIRWAY OBSTRUCTION: Conditions that obstruct
neuromuscular dysfunction, and pain as evidenced by
airways increase resistance to airflow into the lungs,
difficulty in expectorating sputum, presence of
causing alveolar hypoventilation and decreased gas
rhonchi or crackles, ineffective or absent cough
exchange. Airway obstructions can be due to
conditions that: (1) block the inner airway lumen (eg.
excessive secretions or fluid in the airways, inhaled  INEFFECTIVE BREATHING PATTERN related to
foreign bodies) (2) increase airway wall thickness neuromuscular impairment of respirations, pain,
(eg. edema or fibrosis) or decrease airway anxiety, decreased level of consciousness, respiratory
circumference (eg, bronchoconstriction) as occurs in muscle fatigue, and bronchospasm as evidenced by
asthma or (3) increase peribronchial compression of respiratory rate <12 or >24 breaths/min, altered I : E
the airway (eg. enlarged lymph nodes, interstitial ratio, irregular breathing pattern, use of accessory
edema, tumors) muscles, paradoxic breathing, wheezing, and apnea

4. VENTILATION-PERFUSION ABNORMALITIES: TREATMENT:

Conditions disrupting alveolar ventilation or capillary
The goals of treating patients with ARF are fivefold and
perfusion lead to an imbalance in ventilation and include (1) maintaining a patent airway, (2) optimizing O2

10 | P a g e
delivery, (3) minimizing O2 demand, (4) treating the cause of
ARF, and (5) preventing complications.  ADMINISTER MEDICATION:
NOTE: The main therapeutic goal in acute hypoxemic  BICARBONATE to correct acidosis according to
respiratory failure is to ensure adequate oxygenation of vital the ABG values
organs, which is generally accomplished by mechanical  NEUROMUSCULAR BLOCKADE to minimize
ventilation. oxygen demand and allow rest
 PAIN CONTROL MEDICATIONS if
neuromuscular blockade to prevent pain from
 MAINTAINING A PATENT AIRWAY: Some causes of immobility
acute respiratory failure such as COPD, cardiogenic
pulmonary edema, pulmonary infiltrates in  DIURETICS LIKE FUROSEMIDE to remove fluid
immunocompromised patients, and palliation in the if heart failure
terminally ill may be effectively treated with noninvasive  BRONCHODILATORS/STEROIDS to dilate
positive-pressure ventilation (NPPV). airways and decrease inflammation in acute COPD
- However, if a patient is unable to maintain a patent  STOMACH ACID BLOCKERS to prevent ulcers
airway, intubation and mechanical ventilation may from stress
be required for treatment.
 PREVENTING COMPLICATIONS: Finally, the
- Improve ventilation with the administration of critical care nurse must be alert to the potential
bronchodilators and other airway management complications that the patient with ARF may
modalities (suctioning, positioning, mobilization) as encounter. Preventive measures must be taken to
indicated. prevent the complications of immobility, adverse
effects from medications, fluid and electrolyte
- The routine use of chest physiotherapy has not been
shown to be supported by the literature and is not imbalances, development of gastric ulcers, and the
recommended. hazards of mechanical ventilation.

 OPTIMIZING O2 DELIVERY: Optimizing O2 delivery can

be achieved in many ways, depending on the needs of the NURSING MANAGEMENT to Patient with
patient. The first is to provide supplemental O2 via nasal Pulmonary Hypertension:
cannula or face mask to maintain the PaO2 above 60
mm Hg or the SaO2 above 90%. Pulmonary Arterial hypertension (PAH) is a progressive,
life-threatening disorder of the pulmonary circulation
characterized by high pulmonary artery pressures (> 25
a. Patients are positioned for comfort and to mm Hg) leading from the right side of the heart to the lungs.
enhance V./Q. matching. Some patients who are This persistent high pulmonary artery pressure ultimately
alert and dyspneic are able to oxygenate more leads to right ventricular failure. Patients with PAH are
effectively in the semi-Fowler to high Fowler often on a chronic regimen of therapy that should not be
position. interrupted during hospitalization. Abrupt cessation of therapy
can lead to rebound pulmonary hypertension that can be fatal.
b. Patients with unilateral lung disease should be
positioned on their side with the better
functioning “good” lung down. This allows
gravity to perfuse the lung that has the best
ventilation.
c. Other methods to optimize O2 delivery include
red blood cell transfusion to ensure adequate
hemoglobin levels to transport O2, and
enhancing cardiac output and blood pressure to
deliver sufficient O2 to the tissues.
 MINIMIZING O2 DEMAND: Decreasing the
patient’s O2 demand begins with providing adequate
rest. Unnecessary physical activity is avoided in the
patient with ARF. Agitation, restlessness, fever,
sepsis, and patient-ventilator dyssynchrony must be
addressed because they all contribute to increased
O2 demand and consumption.

 TREATING THE CAUSE OF ARF: While the

patient’s hypoxia is being treated, efforts must be
made to identify and reverse the cause of the ARF.

11 | P a g e
CLINICAL PRESENTATION adventitial and intimal proliferation [thickening of the wall],
and advanced vascular lesion formation).
Normally, the pulmonary vascular bed can handle the
blood volume delivered by the right ventricle. It has a low
resistance to blood flow and compensates for increased blood
volume by dilation of the vessels in the pulmonary circulation.
However, if the pulmonary vascular bed is
destroyed or obstructed, as in pulmonary
hypertension, the ability to handle whatever flow or volume of
blood it receives is impaired, and the increased blood flow
then increases the pulmonary artery pressure.
As the pulmonary arterial pressure increases, the pulmonary
vascular resistance also increases. Both pulmonary artery
constriction (as in hypoxemia or hypercapnia) and a reduction
of the pulmonary vascular bed (which occurs with pulmonary
emboli) result in increased pulmonary vascular resistance and
pressure. This increased workload affects right ventricular
function. The myocardium ultimately cannot meet the
increasing demands imposed on it, leading to right ventricular
hypertrophy (enlargement and dilation) and failure. Passive
hepatic congestion may also develop.

DIAGNOSTIC TESTS
 Chest x-ray: Enlarged hilar and pulmonary arterial
shadows and enlargement of the right ventricle.
 12-lead ECG: Right ventricular strain, right
ventricular hypertrophy, and right axis deviation.
 CTPA, ventilation-perfusion scan, or pulmonary
angiogram: These are done to rule out
thromboembolism.
 CT chest: Assess for presence or absence of
Signs and symptoms include pallor, dyspnea, fatigue, parenchymal lung disease.
chest pain, and syncope.  6-minute-walk test: Measurement of distance used
Cor pulmonale or enlargement of the right ventricle can to monitor exercise tolerance, response to therapy,
be a result of pulmonary hypertension and may lead to and progression of disease.
right ventricular failure.  Right-heart cardiac catheterization: Gold standard
for diagnosis with vasodilator (adenosine, nitric
The diagnostic strategy is related to both establishing the
oxide, epoprostenol) testing for benefit from long-
diagnosis of pulmonary hypertension and if possible the term therapy with calcium channel blockers. Positive
underlying cause. The image on the right shows the
response is a decrease in mean PAP of 10 to 40 mm
World Health Organization classification of pulmonary
Hg with an increased or unchanged CO from
hypertension.
baseline values.
 Serology testing: Antinuclear antibodies.
 Pulmonary function testing: Used to rule out any
PATHOPHYSIOLOGY
other diseases contributing to shortness of breath.
The pathophysiology is multifactorial with evidence  Sleep study: Done as a screen for sleep apnea,
that endothelial dysfunction leads to remodeling of the which may also contribute to the pulmonary
pulmonary artery vessel wall causing exaggerated
hypertension.
vasoconstriction and impaired vasodilatation. This results in
decreased blood flow and return of deoxygenated blood to the
lungs.
Pulmonary hypertension associated with lung
respiratory disease or hypoxia, or both, is a serious GENERAL INTERVENTIONS:
complication of many acute and chronic pulmonary disorders,
such as COPD and hypoventilation associated with obesity General therapies for PAH include:
(shown below). These conditions are complicated by hypoxic
pulmonary vasoconstriction, which further increases  administration of oxygen, diuretics, and
pulmonary artery pressure. anticoagulants and
Vascular injury occurs with endothelial dysfunction  avoidance of contributing factors, such as air
and vascular smooth muscle dysfunction, which leads to travel, decongestant medications,
disease progression (vascular smooth muscle hypertrophy, nonsteroidal anti-inflammatory medications,
pregnancy, and tobacco use.
12 | P a g e
NEWER MEDICAL TREATMENT OPTIONS: NURSING MANAGEMENT to patient with
A. PROSTACYCLIN THERAPY is a potent PNEUMOTHORAX
vasodilator of both the systemic and pulmonary It is the presence of air or gas in the pleural space caused by
arterial vascular beds and is an inhibitor of a rupture in the visceral pleura (which surrounds the lungs)
platelet aggregation. Patients must be or the parietal pleura and chest wall. As air separates the
preapproved through their insurance prior to visceral and parietal pleurae, It destroys the negative
starting these costly medications and be able to pressure of the pleural space and disrupts the equilibrium
self-administer. between elastic recoil forces of the lung and chest wall. The
lung then tends to recoil by collapsing toward the hilum
 Remodulin (treprostinil sodium) is given PATHOPHYSIOLOGY
continuous subcutaneous or intravenous A. Primary (spontaneous) pneumothorax
infusion. It causes reduction in pulmonary
artery pressure through direct vasodilation occurs unexpectedly in healthy individuals
of the pulmonary and systemic arterial (usually men) between 20 and 40 years of
vascular beds, thereby improving systemic age and is caused by the spontaneous
oxygen transport and increasing cardiac
output with minimal alteration of the heart rupture of blebs (blister-like formations) on
rate the visceral pleura. Bleb rupture can occur
during sleep, rest, or exercise. The ruptured
 Veletri (epoprostenol sodium room blebs are usually located in the apexes of
temperature stable): Epoprostenol has 2
major pharmacological actions: (1) direct
vasodilation of pulmonary and systemic
arterial vascular beds, and (2) inhibition of
platelet aggregation. It is a continuous
intravenous infusion.

 Ventavis (iloprost sodium) and Tyvaso

(treprostinil sodium) are intermittent
inhalation treatments using medication
specific nebulizers but cannot be
administered during invasive mechanical
ventilation. Both drugs, dilate systemic and
pulmonary arterial vascular beds the lungs. The cause of bleb formation is not
known, although more than 80% of these
B. ENDOTHELIN RECEPTOR individuals have been found to have
ANTAGONISTS block the neurohormone emphysema-like changes in their lungs even
endothelin from binding in the endothelium and
vascular smooth muscle. if they have no history of smoking or no
 Tracleer (bosentan) and Letairis (ambrisentan) known genetic disorder.
are oral agents. B. Secondary pneumothorax can be caused by
chest trauma (such as a rib fracture or stab
C. PHOSPHODIESTERASE and bullet wounds that tear the pleura;
INHIBITORS blocks phosphodiesterase type 5
which is responsible for the degradation of cyclic rupture of a bleb or bulla [larger vesicle], as
guanosine monophosphate (cGMP). Increased occurs in emphysema; or mechanical
cGMP concentration results in pulmonary ventilation, particularly if it includes positive
vasculature relaxation; vasodilation in the
pulmonary bed and the systemic circulation (to a
endexpiratory pressure [PEEP]). Iatrogenic
lesser degree) may occur. pneumothorax is most commonly caused by
a. Revatio (sildenafil) and Adcirca (tadalafil) are transthoracic needle aspiration.
oral agents specific for use in patients with NURSING ALERT: TENSION PNEUMOTHORAX
pulmonary hypertension.
Tension pneumothorax occurs when the intrapleural pressure
NOTE: The most effective treatment for pulmonary exceeds atmospheric pressure. It is a life-threatening condition
hypertension associated with lung respiratory disease or and occurs when injury to the chest or respiratory structures
hypoxia, or both, is treatment of the primary disorder. permits air to enter but not leave the pleural space. This results
in a rapid increase in pressure within the chest that causes

13 | P a g e
compression atelectasis of the unaffected lung, a shift in the The physician inserts a 14-gauge needle into the
mediastinum to the opposite side of the chest, and second intercostal space at the midclavicular line (this space is
compression of the vena cava, which results in a decrease in used because it is the thinnest part of the chest wall, minimizes
venous return to the heart and reduced cardiac output. the danger of contacting the thoracic nerve, and less visible
Although tension pneumothorax can develop in people with scar) on the injured side.
spontaneous pneumothoraces, it is seen most often in people
with traumatic pneumothoraces. It also may result from This procedure converts a tension pneumothorax to a
barotrauma caused by mechanical ventilation due to high tidal simple pneumothorax.
volume on people on the ventilator Subsequent definitive treatment is required with
placement of a chest tube that is attached to a water-seal
drainage system with suction or a small-bore catheter with a
CLINICAL MANIFESTATIONS one-way valve.

The manifestations of pneumothorax depend on its size and

the integrity of the underlying lung.
 Elevated temperature if from empyema or
malignant pleural effusion (lung fluid)
 Fatigue
 Cough
 Pleuritic chest pain
 decreased or absence of breath sounds in the area of
the pneumothorax
 Dull or flat sound when percussed
 Possible pleural friction rub
Assessment findings with tension pneumothorax
include:
 Asymmetry of the thorax
 Tracheal movement away from midline toward the
unaffected side
 Extreme respiratory distress
 Absence of breath sounds on one side
 Distended neck veins
 Cyanosis
 Hypertympanic sound on percussion over the affected
side
 Hemodynamic instability

DIAGNOSTIC TESTS
 Chest x-ray (color will be blacker than black),
computed tomography (CT), or ultrasound will
indicate presence of fluid buildup causing a
pneumothorax.
 ABGs will indicate a respiratory alkalosis if the
patient is in the early stages and a respiratory acidosis
if the patient develops hypercarbia (later).

EMERGENCY MANAGEMENT
Medical management of pneumothorax depends on its cause
and severity. The goal of treatment is to evacuate the air or
blood from the pleural space.

Treatment is never delayed to confirm the diagnosis

with a chest x-ray study.
Immediate decompression of the intrathoracic
pressure is accomplished by needle thoracostomy.

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