Friday, January 21, 2011



Dyspnea refers to difficulty with breathing and can occur with a wide variety of cardiac, pulmonary, and systemic conditions [see Table 5]. Dyspnea can be classified as occurring (1) at rest, (2) with exertion, (3) during the night, awakening a patient from sleep (paroxysmal nocturnal dyspnea), or (4) during episodes of recumbency (orthopnea). Paroxysmal nocturnal dyspnea and orthopnea result from similar mechanisms. Specifically, the recumbent position augments venous return to the right heart. This increase in cardiac filling further increases the pulmonary capillary pressure and results in interstitial (and possibly intra-alveolar) pulmonary edema. Patients find relief by sitting upright, which reduces venous filling and transiently decreases the pulmonary interstitial pressure.
Table 5 Causes of Dyspnea
Valve disease
Aortic stenosis
Aortic regurgitation
Mitral stenosis
Mitral regurgitation
Myocardial disease
Dilated cardiomyopathy
Restrictive cardiomyopathy
Hypertrophic cardiomyopathy
Pericardial disease
Constrictive pericarditis
Pericardial tamponade
Pericardial effusion
Coronary disease
Myocardial infarction and ischemia
Ventricular and supraventricular arrhythmias
Congenital heart disease
Reactive airway disease
Chronic obstructive lung disease (chronic bronchitis and emphysema)
Interstitial lung disease
Infection (acute bronchitis and pneumonia)
Pulmonary embolism
Chest wall disease
Pleural effusion
Anxiety and panic disorders

Dyspnea may be acute or chronic. An acute presentation suggests a pulmonary embolism, acute asthma exacerbation, pneumothorax, or rapidly developing pulmonary edema, as occurs with ischemic mitral regurgitation. Chronic dyspnea suggests heart failure resulting from systolic or diastolic dysfunction.
The history will often exclude less likely conditions and establish the etiology of dyspnea. A history of reactive airway disease, bronchodilator use, or corticosteroid use suggests asthma. Reactive airway disease tends to occur in children and young adults; therefore, in older patients given this diagnosis, a cardiac cause for dyspnea (e.g., new onset of congestive heart failure) should be considered. A significant history of tobacco use, wheezing, chronic cough, and sputum production suggests obstructive airway disease.19 A recent history of fever, chills, and productive cough may indicate bronchitis or pneumonia. The acute onset of dyspnea associated with pleuritic chest pain after a period of immobilization suggests pulmonary embolism. Paroxysmal nocturnal dyspnea, orthopnea, nocturia, recent weight gain, and lower extremity edema suggest a cardiac cause for dyspnea. Patients with chronic obstructive pulmonary disease may also awaken at night with dyspnea, but they usually have a history of sputum production and expectoration that improves with the patient in the upright position. Occasionally, on the basis of the history alone, it may not be possible to determine whether a cardiac or pulmonary cause of dyspnea is present.20 In up to one third of patients being evaluated, dyspnea may have more than one cause.21 In elderly patients, dyspnea may be the only symptom of a myocardial infarction. Hemoptysis may indicate the presence of severe underlying pulmonary disease (e.g., pulmonary embolism or lung cancer) but must be differentiated from hematemesis and nasopharyngeal bleeding.
Several findings on physical examination can assist in excluding a cardiac cause for dyspnea. These findings include a normal level of the jugular venous pressure, a normal point of maximal cardiac impulse, the lack of a third heart sound or cardiac murmurs, the absence of rales on lung examination, and the absence of peripheral edema. Alternatively, elevated jugular venous pressure, a displaced point of maximal cardiac impulse, a third heart sound, a holosystolic murmur of mitral regurgitation, basilar rales, and peripheral edema suggest congestive heart failure. A positive abdominojugular reflux maneuver may also identify dyspnea of cardiac origin.22
Obese patients and those with chest wall deformities may experience dyspnea secondary to the increased workload of breathing from the mechanical limitation imposed on the chest wall. Patients with emphysema frequently have an increased anteroposterior chest diameter, prolonged expiratory phase, expiratory wheezes, and diminished breath sounds. Central cyanosis, a normal anteroposterior chest diameter, and expiratory wheezes or rhonchi on lung examination suggest chronic bronchitis. Expiratory wheezing can occur in both cardiac and pulmonary conditions and is therefore not helpful in establishing an etiology. Stridor may result from an upper airway obstruction or vocal cord paralysis and at times may resemble wheezing. Tachypnea, a loud pulmonic component of the second heart sound, and calf tenderness suggest a pulmonary embolism.
An ECG and a chest roentgenogram should be the initial tests in the evaluation of dyspnea. Pertinent ECG findings include Q waves (prior myocardial infarction), a bundle branch block (structural heart disease), left ventricular hypertrophy (aortic stenosis, hypertension), and evidence of atrial chamber enlargement (valvular heart disease). Notable chest roentgenogram findings include an enlarged cardiac silhouette; interstitial or alveolar edema (congestive heart failure); aortic valve calcification (valvular heart disease); lung mass (lung cancer); focal infiltrate (pneumonia); pleural effusion (congestive heart failure, infectious process); and hyperinflation, bullae, and flattened hemidiaphragms (emphysema). Screening laboratory tests may be useful to exclude anemia as a potential cause of dyspnea.
If the diagnosis of dyspnea remains unclear, additional testing can be pursued [see Figure 2]. For patients with cardiovascular risk factors, with findings on physical examination that suggest structural heart disease, or with abnormal ECGs, echocardiography is indicated to exclude valvular heart disease and assess systolic and diastolic ventricular function. Patients with a presumed pulmonary etiology for dyspnea that remains undiagnosed should undergo pulmonary function testing to exclude reactive airway and restrictive and chronic obstructive pulmonary disease. Stress-ECG may be useful to objectively evaluate the degree of limitation and may be particularly helpful for patients with presumed deconditioning, malingering, or a psychogenic cause for dyspnea. For patients who may have a component of dyspnea from both a cardiac and a pulmonary source, cardiopulmonary exercise testing can be considered. Serum brain natriuretic peptide (BNP) levels are useful in distinguishing cardiac from noncardiac causes of dyspnea; a BNP greater than 100 pg/ml has a sensitivity of 90% but a specificity of only 73% for establishing the diagnosis of heart failure.23 Other factors that affect BNP levels include renal failure, acute coronary syndrome, and female gender.

Figure 2. Evaluation of Patients with Dyspnea
Evaluation of patients with dyspnea. (ECG—electrocardiogram)

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