Dyspnea is a subjective feeling of difficult, labored, or uncomfortable breathing, which patients often describe as "shortness of breath," "breathlessness," or "not getting enough air."1 Dyspnea is frequently associated with other respiratory symptoms or signs. Tachypnea is rapid breathing. Orthopnea is dyspnea in the recumbent position. It is most often the result of left ventricular failure, but can also be seen with diaphragmatic paralysis or chronic obstructive pulmonary disease. Paroxysmal nocturnal dyspnea is orthopnea that awakens the patient from sleep, prompting an upright posture in order to resolve breathlessness. Trepopnea is dyspnea associated with only one of several recumbent positions. Trepopnea can occur with unilateral diaphragmatic paralysis, with ball-valve airway obstruction, or after surgical pneumonectomy. Platypnea is the opposite of orthopnea: dyspnea in the upright position. Platypnea results from the loss of abdominal wall muscular tone and, in rare cases, from right-to-left intracardiac shunting, as occurs from a patent foramen ovale. Hyperpnea is essentially hyperventilation and is defined as minute ventilation in excess of metabolic demand. Respiratory distress is a term used by the physician, combining the patient's subjective sensation of dyspnea with signs indicating difficulty breathing. Ventilatory or respiratory failure occurs when the lungs and ventilatory muscles cannot move enough air in and out of the alveoli to adequately oxygenate arterial blood and eliminate carbon dioxide.
Dyspnea is a complex sensation that arises from the interaction of multiple pathophysiologic mechanisms.1,2 Sensory information about respiratory activity generated by multiple afferent receptors is integrated within the CNS at both the subcortical and cortical levels. The current explanation for the sensation of dyspnea is when imbalance exists among the inspiratory drive, efferent activity to the respiratory muscles, and feedback from these afferent receptors.
Dyspnea is a feature of several disorders seen in the ED (Table 62-1). The presence or degree of dyspnea is difficult to measure, although categorical scales (e.g., the Borg or Fletcher scales) and visual analog scales can be used to gauge response to therapy.1,3 Assess for evidence of impending respiratory failure: marked tachypnea and tachycardia; stridor; use of the accessory respiratory muscles, including the sternocleidomastoid, sternoclavicular, and intercostals; inability to speak normally as a consequence of breathlessness; agitation or lethargy as a consequence of hypoxemia; depressed consciousness due to hypercapnia; and paradoxical abdominal wall movement when the abdominal wall retracts inward with inspiration, indicating diaphragmatic fatigue. In patients with these signs, give oxygen and be prepared for more advanced measures (discussed elsewhere). Lesser degrees of dyspnea allow for a more detailed medical history, physical examination, and indicated ancillary tests.
TABLE 62-1Common Causes of Dyspnea in the ED ||Download (.pdf) TABLE 62-1 Common Causes of Dyspnea in the ED
Most Common Causes
Obstructive airway disease: asthma, chronic obstructive pulmonary disease
Decompensated heart failure/cardiogenic pulmonary edema
Ischemic heart disease: unstable angina and myocardial infarction
Most Immediately Life-Threatening Causes
Upper airway obstruction: foreign body, angioedema, hemorrhage
Neuromuscular weakness: myasthenia gravis, Guillain-Barré syndrome, botulism
Ask about recent infectious and environmental exposures that may impair respiratory function. Carefully question patients who require daily medications for symptom control about compliance and possible drug interactions.
Dyspnea is a prominent symptom of heart failure,4 and differentiating heart failure from pulmonary causes of dyspnea is an important and frequently difficult task. Treatment and prognosis differ, and embarking down the wrong pathway of treatment can have adverse consequences.5 Several findings can assist in this differentiation, although few of them are definitive by themselves (Table 62-2).6,7,8
TABLE 62-2Factors Supporting Heart Failure as the Cause of Dyspnea6 ||Download (.pdf) TABLE 62-2 Factors Supporting Heart Failure as the Cause of Dyspnea6
|Finding ||LR+ (95% CI) ||LR– (95% CI) |
|Clinical gestalt ||4.4 (1.8–10.0) ||0.45 (0.28–0.73) |
| Heart failure ||5.8 (4.1–8.0) ||0.45 (0.38–0.53) |
| Myocardial infarction ||3.1 (2.0–4.9) ||0.69 (0.58–0.82) |
| Coronary artery disease ||1.8 (1.1–2.8) ||0.68 (0.48–0.96) |
| Paroxysmal nocturnal dyspnea ||2.6 (1.5–4.5) ||0.70 (0.54–0.91) |
| Orthopnea ||2.2 (1.2–3.9) ||0.65 (0.45–0.92) |
| Edema ||2.1 (0.92–5.00) ||0.64 (0.39–1.10) |
| Dyspnea on exertion ||1.3 (1.2–1.4) ||0.48 (0.35–0.67) |
|Physical examination |
| S3 gallop ||11.0 (4.9–25.0) ||0.88 (0.83–0.94) |
| Jugular venous distention ||5.1 (3.2–7.9) ||0.66 (0.57–0.77) |
| Hepatojugular reflex ||6.4 (0.81–51.00) ||0.79 (0.62–1.00) |
| S4 ||1.6 (0.47–5.50) ||0.98 (0.93–1.00) |
| Wheezing ||0.52 (0.38–0.71) ||1.3 (1.1–1.7) |
|Chest x-ray |
| Pulmonary venous congestion ||12.0 (6.8–21.0) ||0.48 (0.28–0.83) |
| Interstitial edema ||12.0 (5.2–27.0) ||0.68 (0.54–0.85) |
| Alveolar edema ||6.0 (2.2–16.0) ||0.95 (0.93–0.94) |
| Cardiomegaly ||3.3 (2.4–4.7) ||0.33 (0.23–0.48) |
| Atrial fibrillation ||3.8 (1.7–8.8) ||0.79 (0.65–0.96) |
| Any abnormal finding ||2.2 (1.6–3.1) ||0.64 (0.47–0.88) |
An S3 gallop on physical examination or pulmonary venous congestion/interstitial edema (especially with concomitant cardiomegaly) on chest x-ray strongly suggest heart failure as the cause of the dyspnea (Figure 62-1).6 The physician's overall gestalt of the diagnosis, the presence of jugular venous distention on examination, and alveolar edema on chest x-ray suggest heart failure. Wheezing, dyspnea on exertion, orthopnea, paroxysmal nocturnal dyspnea, and leg edema are not useful in discriminating between cardiac and pulmonary causes. Conversely, the absence of these findings does not exclude heart failure.
Pulmonary edema. Cardiomegaly is present, the pulmonary vasculature is engorged, and cephalization of flow is present.
LABORATORY TESTING AND IMAGING
Pulse oximetry provides a rapid assessment of arterial oxygen saturation but is an insensitive screening test for disorders of gas exchange. Arterial blood gas analysis is more sensitive for detecting impaired gas exchange but cannot evaluate the work of breathing. Arterial blood gas testing can find the rare patient with dyspnea or tachypnea who exhibits no evidence of hypoxemia or pulmonary disease, suggesting hyperventilating from metabolic acidosis.
Bedside spirometric analysis (e.g., peak expiratory flow), especially if performed before and after bronchodilator therapy, can be used to diagnose dyspnea resulting from asthma or chronic obstructive pulmonary disease, but spirometry requires voluntary effort that might be difficult for dyspneic patients.
Negative inspiratory force can assess strength of the diaphragm and inspiratory muscles. Other potentially useful tests include an ECG and measuring the hemoglobin level. In most ED patients, the cause of dyspnea can be identified by the history, the physical examination, and these ancillary tests.
B-type natriuretic peptide (BNP) is a polypeptide secreted by ventricular myocytes in response to volume expansion and pressure overload; BNP elevates with any cause of overload, including heart failure, myocardial ischemia, pulmonary embolism, sepsis, chronic obstructive pulmonary disease, or any right heart strain. Serum levels of BNP or its precursor, N-terminal pro-BNP, are measured using two methods: an enzyme-linked immunosorbent assay and a radioimmunoassay; the enzyme-linked immunosorbent assay is more accurate than the radioimmunoassay.9
A normal BNP (<100 picograms/mL) or N-terminal pro-BNP (<500 picograms/mL) excludes heart failure in low and moderate pretest probability patients outside of "flash" settings.6,9,10 A high level (BNP >500 picograms/mL or N-terminal pro-BNP >2000 picograms/mL) is moderately useful for establishing the diagnosis of heart failure, although these elevations are rarely unsuspected after a careful history, exam, and chest radiograph.10,11 Overall, BNP measurement offers limited real help in assessing dyspneic patients,12 especially when values between 100 and 500 picograms/mL occur, which is common in the patient without a clear clinical syndrome.11,13,14
A chest radiograph may find a pulmonary abnormality, infiltrate, effusion, and pneumothorax.
Bedside lung US is an important tool in the assessment of acute dyspnea. It can differentiate acute decompensated heart failure from noncardiac causes of acute dyspnea with a sensitivity and specificity of about 97% and is superior to chest x-ray and natriuretic peptide determination.15,16 Bedside US can identify pleural effusion, pneumothorax, cardiac tamponade, cardiac functional abnormalities, pulmonary consolidation, and intravascular volume status (Figures 62-2,62-3,62-4).17,18
B lines of pulmonary edema. [Reproduced with permission from Silva FR, Mills L: Chapter 7. Pulmonary, in Ma OJ, Mateer JR, Reardon RF, et al (eds): Ma and Mateer's Emergency Ultrasound, 3rd ed. New York: McGraw-Hill Education; 2014. Fig. 7-4, Part B, p. 176.]
Pleural effusion. [Reproduced with permission from Silva FR, Mills L: Chapter 7. Pulmonary, in Ma OJ, Mateer JR, Reardon RF, et al (eds): Ma and Mateer's Emergency Ultrasound, 3rd ed. New York: McGraw-Hill Education; 2014. Fig. 7-4, Part D, p. 177.]
Arrows point to areas of pulmonary consolidation. [Reproduced with permission from Silva FR, Mills L: Chapter 7. Pulmonary, in Ma OJ, Mateer JR, Reardon RF, et al (eds): Ma and Mateer's Emergency Ultrasound, 3rd ed. New York: McGraw-Hill Education; 2014. Fig. 7-4, Part C, p. 177.]
In severe dyspnea, the initial treatment goal is maintenance of the airway and oxygenation, seeking a partial pressure of alveolar oxygen (PaO2) > 60 mm Hg and/or arterial oxygen saturation (SaO2) ≥90%. Next, or in those with lesser dyspnea, treat the underlying disorder. Rarely are opioids or benzodiazepines used as dyspnea therapy, except in near terminal states for patient comfort.1,19