Dyspnea is an uncomfortable awareness of breathing. It is a common symptom of cardiac and pulmonary diseases, and may also result from neurological conditions, chest wall problems, and anxiety states.

Differential Diagnosis of dyspnea (see Table 2-1)

Cardiac causes of dyspnea predominantly relate to increased pressure in the left ventricle and/or atrium.

This pressure is transmitted back to the lungs where it results in transudation of fluid into the interstitial and alveolar spaces, and interferes with alveolar gas exchange. This can occur as a result of:

  •   valvular heart disease (mitral or aortic regurgitation or stenosis)
  • left ventricular systolic dysfunction (ischemic or non-ischemic cardiomyopathies)
  •   left ventricular diastolic dysfunction (e.g., left ventricular hypertrophy, acute myocardial ischemia, infiltrative cardiomyopathy)
  •   pericardial diseases (pericardial constriction or tamponade)

Pulmonary causes of dyspnea may result from abnormalities of the tracheobronchial tree, alveolae, pulmonary vasculature, or pleura. These include:

  • pneumoma
  • chronic obstructive pulmonary disease (COPD)
  • asthma
  • Pulmonary embolism (PE)
  • pneumothorax
  • pulmonary fibrosis
  • pulmonary hypertension
  • pleural effusion
  • airway obstruction
  • diaphragmatic paralysis

Dyspnea may also be a feature of anemia, hyperthyroidism, obesity, neurological disorders that effect the respiratory muscles, physical deconditioning, and anxiety.

Clinical Manifestations

Several historical features may help differentiate between causes of dyspnea. The sudden onset of dyspnea may occur with angina, pulmonary edema, pneumothorax, or PE. Slowly progressive dyspnea may result from COPD, pleural effusions, anemia, or chronic congestive heart failure (CHF). Other historical features that implicate specific causes of dyspnea include:

  • chest pain (angina, myocardial infarction (MI), pneumonia, PE, pneumothorax)
  • cough (pneumonia, bronchitis, asthma)
  • fever (pneumonia, bronchitis)
  • hemoptysis (PE, bronchitis)
  • history of smoking (COPD)
  • cardiac risk factors (angina, MI)
  • chest wall trauma (pneumothorax)

It is also important to note the pattern of dyspnea.

Dyspnea is frequently precipitated by exertion irrespective of its cause. Dyspnea that occurs at rest usually indicates severe cardiac or pulmonary disease. Paroxysmal nocturnal dyspnea suggests left heart failure; this usually occurs 2 to 4 hours into sleep and requires that the patient sit up or get out of bed to obtain relief. Orthopnea is often a symptom of heart failure, but can also occur as a result of pulmonary disorders.

Physical Examination
The physical examination of the person with dyspnea usually demonstrates tachypnea. Patients may also be cyanotic, reflecting poor oxygenation or low cardiac output. In patients with cardiac diseases causing dyspnea, examination may reveal evidence of valvular heart disease (e.g., murmurs, opening snap of mitral stenosis (MS), widened pulse pressure of aortic regurgitation) or evidence of CHF (S1, pulmonary rales, elevated jugular venous pressure). Patients with pneumonia may have fever and focal lung findings, whereas patients with COPD may have diffusely reduced air entry and wheezes. Decreased breath sounds may indicate pleural effusion or pneumothorax, whereas a pleural rub indicates pleuritis associated with PE or pneumonia. Wheezes may be heard with heart failure or bronchospasm, while stridor indicates upper airway obstruction.

Diagnostic Evaluation

The approach to patients with dyspnea depends in part on the acuity of the problem. Patients with acute dyspnea require a rapid evaluation to exclude life-threatening causes, whereas patients with chronic dyspnea require less urgent evaluation.

The initial test of choice for most patients with dyspnea is the chest x-ray. This can be diagnostic in a variety of settings including:

  • pneumonia (focal infiltrate)
  • CHF (Kerley B lines, vascular cephalization, cardiomegaly, pulmonary edema)
  • pleural effusion (blunted costophrenic angle)
  • pneumothorax (mediastinal shift, loss of lung markings)

The chest x-ray may also suggest the diagnosis in the setting of:

  • PE (peripheral infiltrate, loss of vascular markings)
  • COPD (hyperinflation, bullous changes)
  • Cardiac tamponade (large, “water bottle” -shaped cardiac silhouette

If dyspnea is associated with chest pain, or the patient has known or suspected coronary artery disease (CAD), an ECG should be obtained to exclude acute ischemia as the cause. Suspected cardiac causes of dyspnea should be evaluated with an echocardiogram to evaluate ventricular systolic and diastolic function, and to exclude valvular heart disease.

A complete blood count should be obtained to evaluate for anemia. Arterial blood gas analysis rarely clarifies the underlying diagnosis, but it can be helpful in assessing physiological significance and severity of the disease. An elevated serum brain natriuretic peptide (BNP) level during an acute episode of dyspnea suggests CHF as the cause.

The extent to which dyspnea is attributable to lung disease can be assessed with pulmonary function tests (PFTs). With PFTs, flow-volume loops, lung volumes, and diffusion capacity can be measured to assess for restrictive or obstructive lung diseases. CT scanning is appropriate to evaluate patients suspected of having interstitial lung disease or pulmonary emboli, the latter of which may also be diagnosed with a ventilation-perfusion lung scan.

Often it is not clear if a patient’s dyspnea is the result of cardiac or pulmonary disease. In this setting, metabolic exercise testing or invasive assessment of intracardiac and pulmonary vascular pressures with a pulmonary artery catheter (Swan-Ganz catheter) may help distinguish between the two possibilities.

1. Dyspnea is the uncomfortable awareness of breathing.
2. Dyspnea most commonly results from cardiac or pulmonary disease.
3. Life-threatening causes of dyspnea include Pulmonary embolism, pneumothorax, pneumonia, and myocardial ischemia/infarction.

Provided by ArmMed Media
Revision date: July 4, 2011
Last revised: by Andrew G. Epstein, M.D.