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8.5
I. BACKGROUND. Pleuritic chest pain is pain that is referable to the parietal pleura, lining the
inner wall of the thoracic cavity. The character of the pain is typically described as sharp, burn-
ing, or catching but may be perceived as dull (1). It is most appropriate to consider “pleuritic
pain” a descriptor of the source rather than character of the pain. “Pleurisy” is often used syn-
onymously with pleuritic pain.
II. PATHOPHYSIOLOGY
A. Etiology.
The parietal pleura is the primary source of respiratory pain and lines the inner
chest wall, superior surface of the diaphragm, and lateral boundaries of the mediastinum.
It is innervated by somatic intercostal nerves inside the chest wall and along the lateral por-
tions of the diaphragm. Inflammation involving these areas results in localized chest pain.
The parietal pleura at the central portion of the diaphragm is innervated by the phrenic
nerve, and inflammation in this region is frequently referable to the ipsilateral shoulder or
neck. The visceral pleura, or pleura pulmonalis, represents a layer of mesothelial tissue that
is insensate and covers the entire surface of the lung (1–3).
B. Epidemiology. Determining that chest pain is of a pleural origin, rather than from car-
diac or pulmonary vasculature sources, is an important initial distinction. The incidence of
primary care evaluations for chest pain varies from 1% to 3% (4). In an emergency setting
in Belgium, a cardiovascular etiology for chest pain was found 18% of the time and a non-
cardiac etiology was found 30% of the time (5). In contrast, the same study and two others
from the United States and Switzerland found the incidence of a cardiovascular cause of
chest pain in the outpatient primary care setting to be 13–16% and a noncardiac etiology
to be present 68–80% of the time (5–7).
III. EVALUATION
A. History
1. History of Present Illness. The history alone rarely leads to a definitive etiology of
pleuritic chest pain (4, 8). The primary value of the history during an evaluation is to
describe the temporal course and to identify markers that increase the likelihood that
a life-threatening condition is present (8). Acute (minutes to hours) processes of con-
cern include myocardial infarction, pulmonary embolism, pneumothorax, and trauma.
Subacute (hours to days) processes include pneumonia, parapneumonic infections, and
some inflammatory processes such as pericarditis. Chronic (days to weeks) presentations
may be associated with malignancy or connective tissues diseases such as rheumatoid
arthritis or systemic lupus erythematosus.
2. Review of Systems. The review of systems should be used to generate a differential diag-
nosis and establish pretest probabilities for possible etiologies prior to ordering diagnostic
tests. Typical angina symptoms may lead to consideration of acute coronary syndrome
(9); exertional dyspnea may suggest congestive heart failure (10); a Wells score of >2
increases the likelihood of pulmonary embolism (11); and a sudden, ripping or tearing
pain in the chest or back should suggest dissecting aortic aneurysm (4).
3. Past Medical History. Its greatest value is in refining the initial differential diagnosis
that was generated based upon the description of symptoms provided by the patient.
B. Physical Examination. The negative and positive predictive values for most exam find-
ings in pleuritic pain are low (4). A pleural friction rub may be heard in as many as 4%
of patients with either pulmonary embolism or pneumonia (8, 12). Myocardial infarction
may cause diaphoresis, an S3 gallop, or evidence of new valvular dysfunction. Pneumonia,
pleural effusion, or pneumothorax all may be associated with a focal area of decreased breath
Pleuritic Pain
Lisa B. Norton
158
sounds. Pneumonia can be associated with egophony on examination, whereas pleural effu-
sion is not. Pneumothorax may cause tympany with percussion, while pleural effusion and
pneumonia do not.
C. Testing
1. A posteroanterior and lateral chest radiograph should be obtained in all patients being
evaluated for pleuritic chest pain. This may quickly identify, or suggest, life-threatening
conditions such as pneumothorax or thoracic aortic aneurysm. However, the study is
imperfect for all causes of chest pain. Other studies to consider include electrocardiogram,
chest computed tomography, cardiac enzymes, rheumatologic serology studies, or lung
ultrasound. In one study of various diagnostic tests in the bedside evaluation of pleuritic
chest pain in the emergency department with an apparently normal chest radiograph, the
lung ultrasound was found to have better positive predictive value (94.12%), negative
predictive value (98.21%), and area under the curve of receiver operator curve (0.967)
for pain etiology versus the D-dimer or C- reactive Protein (CRP) blood studies (13).
D. Genetics. Most common causes of pleuritic chest pain are not directly related to identified
genetic abnormalities, although this area of research is evolving rapidly. Notable exceptions
include hypercoagulable states (caused either directly by a genetic abnormality or indirectly
due to a genetically related condition such as some cancers).
IV. DIAGNOSIS
A. Differential Diagnosis.
The differential diagnosis of what clinically appears to be a
pleuritic chest pain syndrome is quite broad. Viral infection, due to the Coxsackie B virus
in particular, is among the most common causes of pleuritic chest pain (8). Some of the
conditions, such as myocardial infarction, in the differential diagnosis are not truly causes of
inflammation of the parietal pleura, but are included in the differential because of similarity
in presentation. Commonly considered causes of a pleuritic chest pain syndrome include (4)
acute coronary syndrome, pulmonary embolism, aortic dissection, pneumonia, lung cancer,
pneumothorax, chest wall syndrome, costochondritis, trauma, fibromyalgia (14), odyno-
phagia, gastroesophageal reflux disease, and psychogenic chest pain. The latter is always a
diagnosis of exclusion (Table 8.5.1).
Disclaimer
The opinions and assertions contained herein are the private views of the author and are not to be
construed as official or as reflecting the views of the U.S. Air Force Medical Service, the U.S. Air
Force or the Department of Defense at large.
TABLE 8.5.1 Differential Diagnosis of Pleuritic Pain
• Acute coronary syndrome
• Pulmonary embolism
• Pneumothorax
• Pneumonia
• Pleural effusion
• Empyema
• Aortic dissection
• Pericarditis
• Costochondritis
• Neoplasm
• Fibromyalgia
• Other known cause: infection, autoimmune disorder, or medications
159
REFERENCES
1. Brims FJH, Davies HE, Lee YC. Respiratory chest pain: diagnosis and treatment. Med Clin N Am
2010;94:217–232.
2. English JC, Leslie KO. Pathology of the pleura. Clin Chest Med 2006;27:157–180.
3. Cagle PT, Allen TC. Pathology of the pleura: what the pulmonologists need to know. Respirology
2011;16:430–438.
4. Yelland M, Cayley WE, Vach W. An algorithm for the diagnosis and management of chest pain in
primary care. Med Clin N Am 2010;94:349–374.
5. Buntinx F, Knockaert D, Bruyninckx R, et al. Chest pain in general practice or in the hospital emer-
gency department: is it the same? Fam Pract 2001;18(6):586–589.
6. Ruigomez A, Rodriguez LA, Wallander MA, et al. Chest pain in general practice: incidence, comor-
bidity and mortality. Fam Pract 2006;23(2):167–174.
7. Nilsson S, Scheike M, Engblom D, et al. Chest pain and ischaemic heart disease in primary care. Br
J Gen Pract 2003;53:378–382.
8. Kass SM, Williams PM, Reamy BV. Pleurisy. Am Fam Physician 2007;75:1357–1364.
9. Gibbons RJ, Balady GJ, Bricker JT, et al. ACC/AHA 2002 guideline update for exercise testing: sum-
mary article: a report of the American College of Cardiology/American Heart Association Task Force
on Practice Guidelines (Committee to Update the 1997 Exercise Testing Guidelines). Circulation
2002;106:1883–1892.
10. Davie AP, Caruana FL, Sutherland GER, et al. Assessing diagnosis in heart failure: which features are
any use? QJM 1997;90:335–339.
11. Wells PS, Anderson DR, Rodger M, et al. Derivation of a simple clinical model to categorize patients
probability of pulmonary embolism: increasing the models utility with the SimpliRED D-dimer.
Thromb Haemost 2000;83:416–420.
12. Miniati M, Prediletto R, Formichi B, et al. Accuracy of clinical assessment in the diagnosis of pulmo-
nary embolism. Am J Respir Crit Care Med 1999;159:864–871.
13. Volpicelli G, Cardinale L, Berchialla P, et al. A comparison of different diagnostic tests in the bedside
evaluation of pleuritic pain in the ED. Am J Emerg Med 2012;30:317–324.
14. Almansa C, Wang B, Achem SR. Noncardiac chest pain and fibromyalgia. Med Clin N Am
2010;94:275–289.
8.6
I. BACKGROUND. Pneumothorax occurs when air collects between the lung and the chest wall
(the pleural space), due to a disruption in either the visceral or parietal pleura. The clinical
manifestations can be asymptomatic, mild, or life-threatening, necessitating immediate inter-
vention.
II. PATHOPHYSIOLOGY. Pneumothorax can be classified into two major categories—spontane-
ous and nonspontaneous. Spontaneous pneumothoraces occur without any obvious precipitat-
ing cause and are further subclassified as primary or secondary. Nonspontaneous pneumotho-
races are traumatic and can be either iatrogenic or noniatrogenic.
A. Spontaneous Pneumothorax
1. Primary spontaneous pneumothorax (PSP) occurs in previously healthy individuals
without a history of lung disease. It is found more frequently in tall, slender young
adults (age 20–30 years) and is uncommon in those older than 40 years (1, 2). PSP is
often caused by a rupture of alveolar apical blebs or bullae. Cigarette smoking increases
the possibility of PSP in a dose-dependent fashion. Light smokers (1–12 cigarettes a
day) have a seven times higher lifetime relative risk, while heavy smokers (>22 cigarettes
per day) have greater than 100 times increased risk (1). The estimated annual incidence
Pneumothorax
Carlton J. Covey
160
of PSP is 7.4–18 cases per 100,000 men and 1.2–6 cases per 100,000 women (3).
Patients who have had a PSP have an approximate 30% rate of recurrence. However,
the consensus remains that these patients should not undergo definitive preventive treat-
ment (1, 4).
2. Secondary spontaneous pneumothorax (SSP) occurs as a complication in individuals
with underlying pulmonary disease and therefore can be a much more serious entity.
A multitude of lung disorders have been described as etiologies for SSP, but chronic
obstructive pulmonary disease (COPD) is by far the most commonly associated condi-
tion (5). SSP can also be seen in individuals with pulmonary infections, particularly
Pneumocystis carinii pneumonia and tuberculosis, as well as with primary lung neoplasms
or metastatic tumors. The incidence is similar to that of PSP, with an estimated
15,000 cases per year in the United States (1). Patients who have had an SSP have an
approximately 40–80% rate of recurrence. This high recurrence rate, and the increased
clinical severity of a pneumothorax in this subset of patients, has led to the consensus
that these patients should receive immediate definitive therapy for recurrence prevention,
even after the first episode (1, 4).
B. Traumatic Pneumothorax
1. Iatrogenic pneumothorax is more common than PSP and SSP combined and, by defini-
tion, occurs as a complication of medical procedures (6). The leading cause of iatrogenic
pneumothorax is transthoracic needle biopsy, but it can also occur during other proce-
dures such as central venous catheter placement, thoracentesis and bronchoscopy, or as
a complication of mechanical ventilation.
2. Penetrating and Blunt Trauma. Penetrating trauma, such as a stab wound, allows
air to enter through the chest wall wound. Pneumothorax can also be a result of blunt
trauma (e.g., when a rib fracture pierces the visceral pleura). However, the majority of
nonpenetrating trauma and resultant pneumothorax lack a preceding rib fracture (1).
The decelerating force of blunt chest trauma and subsequent thoracic compression leads
to an increase in alveolar pressure that can cause a pneumothorax.
III. EVALUATION
A. History
1. Spontaneous Pneumothorax. Sudden ipsilateral chest pain or discomfort, most often
pleuritic, is the most common symptom. In PSP, symptom onset is usually at rest, and
patients often do not immediately seek medical attention (2). Dypsnea may be pres-
ent but is often mild in PSP. In patients with underlying lung disease (SSP) who have
impaired pulmonary reserve, symptoms are generally more severe and dyspnea is the
most prominent clinical feature.
2. Traumatic Pneumothorax. The symptoms are preceded by a medical procedure or a
traumatic event and are similar to those seen in spontaneous pneumothorax. In cases
of iatrogenic pneumothorax, symptoms may not occur for 24 hours or more after the
diagnostic or therapeutic procedure (2). Any mechanically ventilated patient with acute
deterioration should always be evaluated for pneumothorax and is more likely in venti-
lated patients with acute respiratory distress syndrome, aspiration pneumonia, COPD,
or interstitial lung disease (1, 2).
B. Physical Examination. Vital signs can be normal with small pneumothoraces, but
tachycardia is the most common sign of spontaneous pneumothorax (3). In larger pneu-
mothoraces, or in patients with SSP, significant tachypnea, cyanosis, and hypoxemia can
occur and deterioration can be rapid and fatal. These symptoms can also be accompanied by
hypotension in patients with tension pneumothorax, a life-threatening medical emergency.
During chest and lung examinations, patients may be found to have unilateral enlargement
of the chest cavity, loss of tactile fremitus, hyperresonance to percussion, and decreased, or
absent, breath sounds on the affected side (1, 5).
C. Testing
1. Chest x-ray is paramount in the diagnosis, with visualization of the visceral pleural line
and the absence of lung markings distal to this line. The radiographical pleural line is
defined by air density on either side of the line and should be sharp and well demarcated.
161
This is best seen on an upright inspiratory posteroanterior film (7). There is no value of
adding additional expiratory films and this is not recommended for diagnosis. Lateral
decubitus films (with the affected side up) may be helpful when the diagnosis is in ques-
tion or in critically ill patients who cannot sit upright (1, 7).
2. Arterial blood gas typically reveals hypoxia and occasionally hypocarbia secondary to
hyperventilation (1). The hypoxia is due to both the creation of low ventilation-perfu-
sion ratios and absent ventilation (creating a shunt) in affected areas of the lung.
3. Computed tomography (CT) can be useful when the chest x-ray is not diagnostic, but is
not routinely recommended for patients with a first-time pneumothorax (4). In patients
with SSP, the radiographic appearance of the pneumothorax can be altered by the
underlying lung abnormalities, making the chest x-ray more difficult to interpret. These
complicated patients may need a CT scan for diagnosis. Utilization of CT can also be
important when diagnosing traumatic pneumothoraces as up to 40% are not detected
by chest x-ray alone (8). More recently, bedside ultrasound has been utilized to diagnose
pneumothoraces, especially in the emergency department setting. Unfortunately, there
is a high rate of false-positive scans, especially in patients with underlying COPD, and
most patients will require a confirmatory CT scan (8).
IV. DIAGNOSIS
A. Differential Diagnosis
1. The differential diagnosis of pleuritic chest pain and dyspnea includes other life-threat-
ening conditions such as myocardial infarction, COPD exacerbation, aortic dissection,
pericarditis, pneumonia, and pulmonary embolism (9). PSP can be diagnosed by the
clinical history and physical examination in tall, thin patients who have had acute onset
of chest pain and mild dyspnea and confirmed with a chest radiograph visualizing the
visceral pleural line.
2. SSP can be more complicated to diagnose. Although the symptoms are more prominent,
the signs on physical examination are often subtle, especially in patients with COPD
who tend to have decreased breath sounds and decreased tactile fremitus, because of their
underlying disease. As previously addressed, radiographic evaluation can also be more
difficult. Because of the lack of interstitial markings in the emphysematous lung, little
difference is seen in the appearance proximal and distal to the visceral line.
B. Clinical Manifestations
1. Symptoms of a pneumothorax can range from being mild to life-threatening. Most
healthy individuals never seek care for their PSP. A high index of suspicion for a
spontaneous pneumothorax should be kept for young, tall, slender males with acute-
onset chest pain occurring at rest. Patients with pleuritic chest pain and dyspnea after
a diagnostic or therapeutic procedure, and all patients with significant blunt trauma
to the chest, should be evaluated for pneumothorax, including all patients with rib or
scapula fractures. All patients with underlying lung conditions, especially COPD, have
an increased risk of spontaneous pneumothorax and usually present with more signifi-
cant clinical symptoms.
2. Tension pneumothorax is a rare but life-threatening entity that occurs when a condi-
tion exists that allows air into, but not out of, the pleural space. As pressure in the
pleural space exceeds the atmospheric pressure, the ipsilateral lung, mediastinum, and
contralateral lung are compressed. The diagnosis of tension pneumothorax must be
made clinically and appropriate treatment rendered promptly. Diagnosis should never
be delayed for radiographic confirmation. The diagnosis can be confirmed by treatment:
insert a large bore needle (14–16 G) through the second anterior intercostal space at
the clavicular midline. A rush of air and rapid improvement of symptoms confirms the
diagnosis (1).
Disclaimer
The opinions and assertions contained herein are the private views of the author and are not to be
construed as official or as reflecting the views of the U.S. Air Force Medical Service, the U.S. Air
Force or the Department of Defense at large.
162
REFERENCES
1. Light RW, Lee YC. Pneumothorax, chylothorax, hemothorax, and fibrothorax. In: Murray and Nadel’s
textbook of respiratory medicine, 5th ed. Philadelphia, PA: Saunders, 2010:1764–1778.
2. Baumann MH, Noppen M. Pneumothorax. Respirology 2004;9:157–164.
3. Sahn SA, Heffner JE. Spontaneous pneumothorax. N Engl J Med 2000;342:868–874.
4. Baumann MH, Strange C, Heffner JE, et al. Management of spontaneous pneumothorax: an American
College of Chest Physicians Delphi consensus statement. Chest 2001;119:590–602.
5. Noppen M. Spontaneous pneumothorax: epidemiology, pathophysiology and cause. Eur Respir Rev
2010;19:217–219.
6. Gordon CE, Feller-Kopman D, Balk EM, Smetana GW. Pneumothorax following thoracentesis. Arch
Intern Med 2010;170(4):332–339.
7. O’Connor AR, Morgan WE. Radiologic review of pneumothorax. BMJ 2005;330:1493–1497.
8. Rowen KR, Kirkpatrick AW, Liu D, et al. Traumatic pneumothorax detection with thoracic US: cor-
relation with chest radiography and CT-initial experience. Radiology 2002;225:210–214.
9. Kass SM, Williams PM, Reamy BV. Pleurisy. Am Fam Physician 2007;75:1357–1364.
8.7
I. BACKGROUND. Shortness of breath, or dyspnea, is defined as “a subjective experience of
breathing discomfort that is comprised of qualitatively distinct sensations that vary in intensity.
The experience derives from interactions among multiple physiologic, psychological, social, and
environmental factors and may induce secondary physiologic and behavioral responses” (1).
Given the potential for patient distress when experiencing dyspnea, it is common for dyspneic
patients to present to the emergency department (ED) or acute care clinic. In 2009, dyspnea was
the chief complaint in 2.7% of the more than 136 million ED visits in the United States. Dyspnea-
related complaints such as cough and chest pain accounted for 8.8% of ED visits in 2009 (2).
II. PATHOPHYSIOLOGY. The respiratory system is responsible for maintaining appropriate gas
exchange and acid–base regulation within the body. Factors that impair oxygenation or cause
acidemia, whether they originate in the heart, lungs, or elsewhere, can lead to the sensation of
breathing difficulty or shortness of breath.
Dyspnea can be the primary manifestation of various life-threatening conditions
(Table 8.7.1), but the vast majority of patients who experience dyspnea have one of the
following five chronic conditions (3, 4):
• Asthma
• Chronic obstructive pulmonary disease (COPD)
• Interstitial lung disease
• Myocardial dysfunction
• Obesity/deconditioning
The most common diagnoses for elderly patients (age >65 years) who present to the
ED with shortness of breath and the signs of respiratory distress (respiratory rate > 25, Spo
2
< 93%) are (5)
• Decompensated heart failure
• Pneumonia
• COPD
• Pulmonary embolism
• Asthma
III. EVALUATION. Cardiac disease remains the leading cause of death in the United States.
Shortness of breath is one of the hallmark symptoms, and occasionally the only symptom, of
Shortness of Breath
David K. Gordon II
163
myocardial infarction and angina (6). As such, heart disease must remain on the top of the dif-
ferential diagnosis when beginning the workup of a patient with dyspnea.
A. History. Knowing how to differentiate between respiratory system causes of dyspnea
and cardiovascular system causes of dyspnea is essential for accurate diagnosis. Health-care
TABLE 8.7.1 Life-Threatening Causes of Dyspnea
Upper airway
• Tracheal foreign objects
• Angioedema
• Anaphylaxis
• Infections of the pharynx and neck
• Airway trauma
Pulmonary/lower airway
• Pulmonary embolism
• Chronic obstructive pulmonary disease
• Asthma
• Pneumothorax/hemothorax and pneumomediastinum
• Pulmonary infection
• Noncardiogenic pulmonary edema
• Direct pulmonary injury
• Acute Respiratory Distress Syndrome
• Pulmonary hemorrhage
Cardiac
• Acute coronary syndrome
• Acute decompensated heart failure
• Flash pulmonary edema
• High-output heart failure
• Cardiomyopathy
• Cardiac arrhythmia
• Valvular dysfunction
• Cardiac tamponade
Neurologic
• Stroke
• Neuromuscular disease
Toxic and metabolic
• Poisoning, e.g., salicylates and carbon monoxide
• Toxin-related metabolic acidosis
• Diabetic ketoacidosis
• Sepsis
• Anemia
• Acute chest syndrome
164
providers should approach the evaluation of dyspneic patients in much the same way that
they approach the evaluation of pain, by asking the patient to use descriptive words to
explain their shortness of breath. Several causes of dyspnea have been found to have com-
mon terms used in the description of the patients’ symptoms:
• COPD patients report an increased “effort to breathe,” a sensation of “unsatisfying
breaths,” and a feeling that they “cannot get a deep breath” (7).
• Heart failure patients commonly report feelings of “air hunger” and “suffocation” (8).
• Cardiovascular deconditioning is commonly associated with “heavy breathing” (9).
• Bronchospasm is frequently described as chest tightness.
• Interstitial disease often corresponds to rapid, shallow breathing.
Other historical questions should also be asked such as past medical history, prescribed
medication compliance, symptom duration, allergens or toxin exposure, preceding events,
recent onset of cough or fever, recent surgical history or immobilization that could increase
the risk of pulmonary embolism, or recent trauma.
B. Physical Examination. The physical examination begins with your first observation of
the patient and within the first minute you should be able to assess the patient for signs of
significant respiratory distress.
• Signs of impending respiratory arrest
o Cyanosis
o Decreased ability to sustain respiratory effort
o Depressed mental status
• Signs of severe respiratory distress
o Chest retractions
o Use of accessory muscles to maintain respiratory effort
o Extreme diaphoresis
o Staccato, disjointed speech
o Nervousness, anxiety
o Refusal to lie supine
o Altered mental status
If the patient is deemed to be stable after the quick initial assessment, the examiner contin-
ues with a more detailed and thorough examination with the aim of determining whether
the patient’s dyspnea is due to a respiratory or cardiac disease. Begin with a review of the
vital signs—specifically the respiratory rate and pulse oximetry reading. Next, proceed with
an examination of the face and neck where you should look for nasal flaring, postnasal drip,
pharyngeal inflammation/infection, foreign bodies, tracheal deviation, and jugular venous
distension.
Moving down to the chest, observe for symmetric chest rise and fall, retractions, acces-
sory muscle use, tripod seated position, general shape of the chest/thorax (e.g., barrel-shaped
chest commonly seen in COPD). Listen for abnormal breath sounds:
• Inspiratory stridor—obstruction above the vocal cords (e.g., epiglottitis, foreign body).
• Expiratory stridor—obstruction below the vocal cords (e.g., croup, bacterial tracheitis,
foreign body).
• Wheezing—obstruction below the trachea (e.g., asthma, anaphylaxis, foreign body in
bronchus).
• Crackles (rales)—fluid accumulation in the interalveolar space (e.g., pneumonia, acute
decompensated heart failure [ADHF]).
• Decreased breath sounds—any source that prevents air entry into the lung (e.g., pneumo-
thorax, tension pneumothorax, hemothorax).
There are several possible findings in the heart exam that can reveal the etiology of the
patient’s dyspnea. An abnormal rhythm, such as atrial fibrillation in a heart failure patient,
may cause dyspnea. Cardiac tamponade produces muffled or distant heart sounds and the
impaired function of the heart with this condition leads to a systemic decrease in oxygen
delivery and resultant dyspnea. S3 and S4 heart sounds are suggestive of left ventricular
dysfunction. Jugular venous distension can be seen in patients with ADHF and cardiac
tamponade.
165
Next, the examiner should perform an abdominal exam to assess for an intraab-
dominal mass that may be compressing the diaphragm and decreasing the intrathoracic
space and total lung volume or compressing the inferior vena cava and decreasing blood
return to the heart. Finally, a close inspection of the patient’s skin and extremities
should be performed looking for discoloration suggestive of poor perfusion or hypoxia
and peripheral edema suggesting ADHF.
C. Testing
1. A chest x-ray (CXR) and pulse oximetry are useful in evaluating a variety of cardiac and
pulmonary causes of dyspnea. Cardiomegaly, pleural effusion, and cephalization of blood
vessels are indicative of acute heart failure. Pulmonary infiltration is diagnostic of pneu-
monia and a pneumothorax can be identified as an area of increased lucency, typically at
the lung apices, on CXR. COPD and asthma are identified by increased lung volumes
and flattening of the diaphragm. All of these conditions will result in a decreased pulse
oximetry reading.
2. An electrocardiogram (ECG) is necessary to assess for cardiac ischemia/infarction,
cardiomegaly, pulmonary embolism, cardiac arrhythmia, and pericardial tamponade. It
should be noted that a normal ECG upon initial presentation does not rule out myocar-
dial infarction. A normal initial ECG is found in nearly 20% of patients subsequently
diagnosed with myocardial infarction and only 33% of initial ECGs are diagnostic (10).
Echocardiography should be considered in dyspneic patients with cardiomegaly on CXR
to further assess for left ventricular heart failure.
3. Pulmonary function tests (PFTs) should be performed in a stable patient in whom lung
disease is suspected as part of an evaluation for restrictive and obstructive lung disease. If
the initial PFTs are normal and the suspicion still remains high that lung disease is pres-
ent, a methacholine challenge test can be performed to help identify asthma in patients
who have intermittent dyspnea symptoms.
4. A variety of other tests should also be considered in order to accurately identify the
source of the patient’s dyspnea symptoms:
• Blood tests:
o Elevated cardiac biomarkers indicate cardiac ischemia or infarction.
o An elevated brain natriuretic peptide is helpful in confirming suspected ADHF.
o A positive D-dimer is useful if the patient’s pretest probability of pulmonary
embolism is high.
o A complete blood count will identify anemia as well as possible sepsis and
subsequent ARDS.
• Imaging:
o Chest computed tomography (CT) and ventilation-perfusion (VQ) scan can be used
to identify pulmonary embolism, pneumonia, malignancy, and pulmonary edema.
• Other:
o Negative inspiratory pressure and forced vital capacity measurements are helpful
bedside tests in dyspneic patients suspected of having neuromuscular disorders such
as myasthenia gravis or Guillain-Barré syndrome. Electomyogram and nerve conduc-
tion studies should be performed to confirm a diagnosis of a neuromuscular disorder.
IV. DIAGNOSIS. The underlying disease causing the patient’s dyspnea can be identified 70%
of the time using the clinical evaluation, CXR, and pulse oximetry (11). If the disease is not
identified using these three modalities, the examiner must proceed with a systematic evaluation,
focusing primarily on the pulmonary and cardiac systems.
A. 75% of dyspnea cases are caused by pulmonary disease (3). CXR and pulse oximetry should
be followed by PFTs and chest CT/VQ scan if indicated by the historical and exam findings.
B. If a pulmonary etiology has been ruled out or if the history and physical are more indica-
tive of a cardiac etiology, a cardiac workup should be initiated immediately. A CXR, pulse
oximetry, ECG, and cardiac biomarkers should all be performed. Once immediate life-
threatening causes have been ruled out, the examiner should proceed with echocardiogram
and arrhythmia evaluation as indicated by history, physical, and study findings.
166
Disclaimer
The opinions and assertions contained herein are the private views of the author and are not to be
construed as official or as reflecting the views of the U.S. Air Force Medical Service, the U.S. Air
Force or the Department of Defense at large.
REFERENCES
1. Dyspnea. Mechanisms, assessment, and management: a consensus statement. American Thoracic
Society. Am J Respir Crit Care Med 1999;159:321.
2. American College of Emergency Physicians. Accessed at http://www.acep.org/uploadedFiles/ACEP/
newsroom/NewsMediaResources/StatisticsData/2009%20NHAMCS_ED_Factsheet_ED.pdf on
July 17, 2012.
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8.8
I. BACKGROUND. Stridor is a harsh, noisy breath sound produced by turbulent air flow created
by partial airway obstruction. Though most commonly found in early childhood, stridor may
present at any age (1, 2).
II. PATHOPHYSIOLOGY. Stridor is usually inspiratory, indicating an obstruction at or above the
larynx. Biphasic stridor can occur with obstruction at or below the larynx in the upper trachea
and suggests a fixed obstruction. Expiratory stridor suggests obstruction in the distal trachea
or mainstem bronchi. The vocal cords are likely involved when hoarseness or aphonia is
present (1, 2).
III. EVALUATION. Stabilize the patient first. Some patients with stridor are in respiratory distress
and require immediate emergency intervention.
A. History
1. To rapidly narrow the differential diagnosis (Table 8.8.1), first identify whether or not
the patient is febrile and if the stridor is acute (new), persistent, or recurrent. Also ask
about recent upper respiratory infection (URI) symptoms and positioning or activities
that relieve or exacerbate the symptoms. Further inquire about feeding difficulties, failure
Stridor
Dillon J. Savard
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