The duration, severity, and periodicity of dyspnea influence the tempo of the clinical evaluation. Rapid onset or severe dyspnea in the absence of other clinical features should raise concern for pneumothorax, pulmonary embolism, or increased left ventricular end-diastolic pressure (LVEDP). Spontaneous pneumothorax is usually accompanied by chest pain and occurs most often in thin, young males and in those with underlying lung disease. Pulmonary embolism should always be suspected when a patient with new dyspnea reports a recent history (previous 4 weeks) of prolonged immobilization or surgery, estrogen therapy, or other risk factors for deep venous thrombosis (DVT) (eg, previous history of thromboembolism, cancer, obesity, lower extremity trauma) and when the cause of dyspnea is not apparent. Silent myocardial infarction, which occurs more frequently in diabetic persons and women, can result in increased LVEDP, acute HF, and dyspnea.
Although no symptom description is adequately sensitive or specific for identifying a condition, chest "tightness" was found in a study to be unique for asthma and "shallow breathing" was unique for interstitial lung disease. Accompanying symptoms provide important clues to causes of dyspnea. When cough and fever are present, pulmonary disease (particularly infection) is the primary concern; myocarditis, pericarditis, and septic emboli can present in this manner. Chest pain should be further characterized as acute or chronic, pleuritic or exertional. Although acute pleuritic chest pain is the rule in acute pericarditis and pneumothorax, most patients with pleuritic chest pain in the outpatient clinic have pleurisy due to acute viral respiratory tract infection. Periodic chest pain that precedes the onset of dyspnea suggests myocardial ischemia or pulmonary embolism. When associated with wheezing, most cases of dyspnea are due to acute bronchitis; however, other causes include new-onset asthma, foreign body, and vocal cord dysfunction. Interstitial lung disease and pulmonary hypertension should be considered in patients with symptoms (or history) of connective tissue disease. Pulmonary lymphangitis carcinomatosis should be considered if a patient has a malignancy, especially breast, lung, or gastric cancer.
When a patient reports prominent dyspnea with mild or no accompanying features, consider noncardiopulmonary causes of impaired oxygen delivery (anemia, methemoglobinemia, cyanide ingestion, carbon monoxide poisoning), metabolic acidosis, panic disorder, neuromuscular disorders, and chronic pulmonary embolism.
Platypnea-orthodeoxia syndrome is characterized by dyspnea and hypoxemia on sitting or standing that improves in the recumbent position. It may be caused by an intracardiac shunt, pulmonary vascular shunt (including hepatopulmonary syndrome), or ventilation-perfusion mismatch. Hyperthyroidism can cause dyspnea from increased ventilatory drive, respiratory muscle weakness, or pulmonary hypertension.
A focused physical examination should include evaluation of the head and neck, chest, heart, and lower extremities. Visual inspection of the patient can suggest obstructive airway disease (pursed-lip breathing, use of accessory respiratory muscles, barrel-shaped chest), pneumothorax (asymmetric excursion), or metabolic acidosis (Kussmaul respirations). Patients with impending upper airway obstruction (eg, epiglottitis, foreign body) or severe asthma exacerbation sometimes assume a tripod position. Focal wheezing raises the suspicion for a foreign body or other bronchial obstruction. Maximum laryngeal height (the distance between the top of the thyroid cartilage and the suprasternal notch at end expiration) is a measure of hyperinflation. Obstructive airway disease is virtually nonexistent when a nonsmoking patient younger than age 45 years has a maximum laryngeal height greater than 4 cm.
Factors increasing the likelihood of obstructive airway disease include patient history of more than 40 pack-years smoking (adjusted likelihood ratio [LR]+ 11.6; LR– 0.9), patient age 45 years or older (LR+ 1.4; LR– 0.5), and maximum laryngeal height greater than or equal to 4 cm (LR+ 3.6; LR– 0.7). With all three of these factors present, the LR+ rises to 58.5 and the LR– falls to 0.3.
Absent breath sounds suggest a pneumothorax. An accentuated pulmonic component of the second heart sound (loud P2) is a sign of pulmonary hypertension and pulmonary embolism.
Clinical predictors of increased LVEDP in dyspneic patients with no prior history of HF include tachycardia, systolic hypotension, jugular venous distention, hepatojugular reflux, bibasilar crackles, third heart sound, lower extremity edema, and chest film findings of pulmonary vascular redistribution or cardiomegaly. When none is present, there is a very low probability (less than 10%) of increased LVEDP, but when two or more are present, there is a very high probability (greater than 90%) of increased LVEDP.
Causes of dyspnea that can be managed without chest radiography are few: ingestions causing lactic acidosis, anemia, methemoglobinemia, and carbon monoxide poisoning. The diagnosis of pneumonia should be confirmed by chest radiography in most patients, and elevated blood levels of procalcitonin or C-reactive protein can support the diagnosis of pneumonia in equivocal cases or in the presence of interstitial lung disease. Conversely, a low procalcitonin can help exclude pneumonia in dyspneic patients presenting with HF.
Chest radiography is fairly sensitive and specific for new-onset HF (represented by redistribution of pulmonary venous circulation) and can help guide treatment of patients with other cardiac diseases. NT-proBNP can assist in the diagnosis of HF; the Acute Diagnostic Cut-Offs in the Emergency Department study defines best diagnostic cutoff points.
Lung ultrasonography is superior to chest radiography in detecting pulmonary edema due to acute decompensated HF among adult patients presenting with dyspnea and in the diagnosis of pneumonia in patients admitted to an acute geriatric ward. End-expiratory chest radiography enhances detection of small pneumothoraces.
A normal chest radiograph has substantial diagnostic value. When there is no physical examination evidence of COPD or HF and the chest radiograph is normal, the major remaining causes of dyspnea include pulmonary embolism, Pneumocystis jirovecii infection (the initial radiograph may be normal in up to 25%), upper airway obstruction, foreign body, anemia, and metabolic acidosis. If a patient has tachycardia and hypoxemia but a normal chest radiograph and electrocardiogram (ECG), then tests to exclude pulmonary emboli, anemia, or metabolic acidosis are warranted. High-resolution chest CT is particularly useful in the evaluation of interstitial and alveolar lung disease. Helical (“spiral”) CT is useful to diagnose pulmonary embolism since the images are high resolution and require only one breathhold by the patient, but to minimize unnecessary testing and radiation exposure, the clinician should first consider a clinical decision rule (with or without D-dimer testing) to estimate the pretest probability of a pulmonary embolism. It is appropriate to forego CT scanning in patients with very low probability of pulmonary embolus when other causes of dyspnea are more likely (see Chapter 9).
Laboratory findings suggesting increased LVEDP include elevated serum B-type natriuretic peptide (BNP or NT-proBNP) levels. BNP has been shown to reliably diagnose severe dyspnea caused by HF and to differentiate it from dyspnea due to other conditions. However, systematic use of BNP in evaluation of dyspnea in the emergency department does not appear to have a clinically significant impact on patient or system outcomes, and it does not conclusively affect hospital mortality rates. Newer cardiac biomarkers such as ST2 may have better prognostic value for mortality and may help titrate medical therapy.
Arterial blood gas measurement may be considered if clinical examination and routine diagnostic testing are equivocal. With two notable exceptions (carbon monoxide poisoning and cyanide toxicity), arterial blood gas measurement distinguishes increased mechanical effort causes of dyspnea (respiratory acidosis with or without hypoxemia) from compensatory tachypnea (respiratory alkalosis with or without hypoxemia or metabolic acidosis) and from psychogenic dyspnea (respiratory alkalosis). An observational study, however, found that arterial blood gas measurement had little value in determining the cause of dyspnea in patients presenting to the emergency department. Carbon monoxide and cyanide impair oxygen delivery with minimal alterations in Po2; percent carboxyhemoglobin identifies carbon monoxide toxicity. Cyanide poisoning should be considered in a patient with profound lactic acidosis following exposure to burning vinyl (such as a theater fire or industrial accident). Suspected carbon monoxide poisoning or methemoglobinemia can also be confirmed with venous carboxyhemoglobin or methemoglobin levels. Venous blood gas testing is also an option for assessing respiratory and acid-base status by measuring venous pH and PCO2 but is unable to provide information on oxygenation status. To correlate with arterial blood gas values, venous pH is typically 0.03–0.05 units lower, and venous PCO2 is typically 4–5 mm Hg higher than arterial samples.
Because arterial blood gas testing is impractical in most outpatient settings, pulse oximetry has assumed a central role in the office evaluation of dyspnea. Oxygen saturation values above 96% almost always correspond with a Po2 greater than 70 mm Hg, whereas values less than 94% may represent clinically significant hypoxemia. Important exceptions to this rule include carbon monoxide toxicity, which leads to a normal oxygen saturation (due to the similar wavelengths of oxyhemoglobin and carboxyhemoglobin), and methemoglobinemia, which results in an oxygen saturation of about 85% that fails to increase with supplemental oxygen. A delirious or obtunded patient with obstructive lung disease warrants immediate measurement of arterial blood gases to exclude hypercapnia and the need for intubation, regardless of the oxygen saturation. If a patient reports dyspnea with exertion, but resting oximetry is normal, assessment of desaturation with ambulation (eg, a brisk walk around the clinic) can be useful for confirming impaired gas exchange.
A study found that for adults without known cardiac or pulmonary disease reporting dyspnea on exertion, spirometry, NT-proBNP, and CT imaging were the most informative tests.
Episodic dyspnea can be challenging if an evaluation cannot be performed during symptoms. Life-threatening causes include recurrent pulmonary embolism, myocardial ischemia, and reactive airway disease. When associated with audible wheezing, vocal cord dysfunction should be considered, particularly in a young woman who does not respond to asthma therapy. Spirometry is very helpful in further classifying patients with obstructive airway disease but is rarely needed in the initial or emergent evaluation of patients with acute dyspnea.