Merck Manual

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Rebecca Dezube

, MD, MHS, Johns Hopkins University

Reviewed/Revised Sep 2021 | Modified Sep 2022
Topic Resources

Dyspnea is unpleasant or uncomfortable breathing. It is experienced and described differently by patients depending on the cause.

Pathophysiology of Dyspnea

Although dyspnea is a relatively common problem, the pathophysiology of the uncomfortable sensation of breathing is poorly understood. Unlike those for other types of noxious stimuli, there are no specialized dyspnea receptors (although MRI studies have identified a few specific areas in the midbrain that may mediate perception of dyspnea).

The experience of dyspnea likely results from a complex interaction between chemoreceptor stimulation, mechanical abnormalities in breathing, and the perception of those abnormalities by the central nervous system. Some authors have described the imbalance between neurologic stimulation and mechanical changes in the lungs and chest wall as neuromechanical uncoupling.

Etiology of Dyspnea

The most common causes include

The most common cause of dyspnea in patients with chronic pulmonary or cardiac disorders is

  • Exacerbation of their disease

However, such patients may also acutely develop another condition (eg, a patient with long-standing asthma may have a myocardial infarction, a patient with chronic heart failure may develop pneumonia).


Etiology reference

Evaluation of Dyspnea


History of present illness should cover the duration, temporal onset (eg, abrupt, insidious), and provoking or exacerbating factors (eg, allergen exposure, cold, exertion, supine position). Severity can be determined by assessing the activity level required to cause dyspnea (eg, dyspnea at rest is more severe than dyspnea only when climbing stairs). Physicians should note how much dyspnea has changed from the patient’s usual state.

Occupational exposures (eg, gases, smoke, asbestos) should be investigated.

Physical examination

Vital signs are reviewed for fever, tachycardia, and tachypnea.

Examination focuses on the cardiovascular and pulmonary systems.

A full lung examination is done, particularly including adequacy of air entry and exit, symmetry of breath sounds, and presence of crackles, rhonchi, stridor, and wheezing. Signs of consolidation (eg, egophony, dullness to percussion) should be sought. The cervical, supraclavicular, and inguinal areas should be inspected and palpated for lymphadenopathy.

Neck veins should be inspected for distention, and the legs and presacral area should be palpated for pitting edema (both suggesting heart failure).

Heart sounds should be auscultated with notation of any extra heart sounds, muffled heart sounds, or murmur. Testing for pulsus paradoxus Pulsus paradoxus Complete examination of all systems is essential to detect peripheral and systemic effects of cardiac disorders and evidence of noncardiac disorders that might affect the heart. Examination... read more Pulsus paradoxus (a > 12-mm Hg drop of systolic blood pressure during inspiration) can be done by inflating a blood pressure cuff to 20 mm Hg above the systolic pressure and then slowly deflating until the first Korotkoff sound is heard only during expiration. As the cuff is further deflated, the point at which the first Korotkoff sound is audible during both inspiration and expiration is recorded. If the difference between the first and second measurement is > 12 mm Hg, then pulsus paradoxus is present.

Conjunctiva should be examined for pallor.

Red flags

The following findings are of particular concern:

  • Dyspnea at rest during examination

  • Decreased level of consciousness or agitation or confusion

  • Accessory muscle use and poor air excursion

  • Chest pain

  • Crackles

  • Weight loss

  • Night sweats

  • Palpitations

Interpretation of findings

However, the symptoms and signs of life-threatening conditions such as myocardial ischemia and pulmonary embolism can be nonspecific. Furthermore, the severity of symptoms is not always proportional to the severity of the cause (eg, pulmonary embolism in a fit, healthy person may cause only mild dyspnea). Thus, a high degree of suspicion for these common conditions is prudent. It is often appropriate to rule out these conditions before attributing dyspnea to a less serious etiology.

A clinical prediction rule can help estimate the risk of pulmonary embolism. Note that normal oxygen saturation does not exclude pulmonary embolism.

Hyperventilation syndrome Hyperventilation Syndrome Hyperventilation syndrome is anxiety-related dyspnea and tachypnea often accompanied by systemic symptoms. Hyperventilation syndrome most commonly occurs among young women but can affect either... read more is a diagnosis of exclusion. Because hypoxia may cause tachypnea and agitation, it is unwise to assume every rapidly breathing, anxious young person merely has hyperventilation syndrome.


Pulse oximetry should be done in all patients, and a chest x-ray should be done as well unless symptoms are clearly caused by a mild or moderate exacerbation of a known condition. For example, patients with asthma or heart failure do not require an x-ray for each flare-up, unless clinical findings suggest another cause or an unusually severe attack.

Most adults should have an ECG to detect myocardial ischemia (and serum cardiac marker testing if suspicion is high) unless myocardial ischemia can be excluded clinically.

In patients with severe or deteriorating respiratory status, arterial blood gases (ABGs) should be measured to more precisely quantify hypoxemia, measure PaCO2, diagnose any acid-base disorders Acid-Base Disorders Acid-base disorders are pathologic changes in carbon dioxide partial pressure (Pco2) or serum bicarbonate (HCO3) that typically produce abnormal arterial pH values. Acidemia is serum... read more stimulating hyperventilation, and calculate the alveolar-arterial gradient.

Patients who have no clear diagnosis after chest x-ray and ECG and are at moderate or high risk of having pulmonary embolism (from a clinical prediction rule) should undergo CT angiography or ventilation/perfusion scanning. Patients who are at low risk may have D-dimer testing (a normal D-dimer level effectively rules out pulmonary embolism in a low-risk patient).

Chronic dyspnea may warrant additional tests, such as CT, pulmonary function tests, echocardiography, and bronchoscopy.

Evaluation reference

Treatment of Dyspnea

Treatment is correction of the underlying disorder.

Hypoxemia (in the absence of compensatory hyperventilation) is treated with supplemental oxygen as needed to maintain oxygen saturation > 88% or PaO2 > 55 mm Hg (> 7.3 kPa) because levels above these thresholds provide adequate oxygen delivery to tissues. Levels below these thresholds are on the steep portion of the oxygen–hemoglobin dissociation curve, where even a small decline in arterial oxygen tension can result in a large decline in hemoglobin saturation. Oxygen saturation should be maintained at > 93% if myocardial or cerebral ischemia is a concern, although data suggest that supplemental oxygen is not beneficial in the treatment of acute myocardial infarction unless the patient has hypoxia.

Morphine 0.5 to 5 mg IV helps reduce anxiety and the discomfort of dyspnea in various conditions, including myocardial infarction, pulmonary embolism, and the dyspnea that commonly accompanies terminal illness. However, opioids can be deleterious in patients with acute airflow limitation (eg, asthma, COPD) because they suppress the ventilatory drive and can worsen respiratory acidemia.

Key Points

  • Pulse oximetry is a key component of the examination.

  • Low oxygen saturation (< 90%) indicates a serious problem, but normal saturation does not rule one out.

  • Accessory muscle use, a sudden decrease in oxygen saturation, or a decreased level of consciousness requires emergency evaluation and hospitalization.

  • Myocardial ischemia and pulmonary embolism are relatively common, but symptoms and signs can be nonspecific.

  • Exacerbation of known conditions (eg, asthma, chronic obstructive pulmonary disease, heart failure) is common, but patients may also develop new problems.

Drugs Mentioned In This Article

Drug Name Select Trade
ARYMO ER, Astramorph PF, Avinza, DepoDur, Duramorph PF, Infumorph, Kadian, MITIGO, MORPHABOND, MS Contin, MSIR, Opium Tincture, Oramorph SR, RMS, Roxanol, Roxanol-T
NOTE: This is the Professional Version. CONSUMERS: View Consumer Version
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