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, abnormalities in cardiac function or venous return, 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
Dyspnea has many pulmonary, cardiac, and other causes (1), which vary by acuity of onset (see tables Some Causes of Acute Dyspnea, Some Causes of Subacute Dyspnea, and Some Causes of Chronic Dyspnea).
The most common causes include
COPD (chronic obstructive pulmonary disease)
Physical deconditioning
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
1. Pratter MR, Curley FJ, Dubois J, Irwin RS: Cause and evaluation of chronic dyspnea in a pulmonary disease clinic. Arch Intern Med 149 (10): 2277–2282, 1989.
Evaluation of Dyspnea
History
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.
Review of systems should seek symptoms of possible causes, including chest pain or pressure (pulmonary embolism, myocardial ischemia, pneumonia); dependent edema, orthopnea, and paroxysmal nocturnal dyspnea (heart failure); fever, chills, cough, and sputum production (pneumonia); black, tarry stools or heavy menses (occult bleeding, possibly causing anemia); and weight loss or night sweats (cancer or chronic lung infection).
Past medical history should cover disorders known to cause dyspnea, including asthma, COPD, and heart disease, as well as risk factors for the different etiologies:
Smoking history—for cancer, COPD, some interstitial lung diseases, and heart disease
Family history, hypertension, and high cholesterol levels—for coronary artery disease
Recent immobilization or surgery, recent long-distance travel, cancer or risk factors for or signs of occult cancer, prior or family history of clotting, pregnancy, oral contraceptive use, calf pain, leg swelling, and known deep venous thrombosis—for pulmonary embolism
Environmental and 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 (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
The history and physical examination often suggest a cause and guide further testing (1—see tables Some Causes of Acute Dyspnea, Some Causes of Subacute Dyspnea, and Some Causes of Chronic Dyspnea). Several findings are of note:
Stridor suggests extrathoracic airway obstruction (eg, foreign body, epiglottitis, vocal cord dysfunction).
Crackles suggest left heart failure, interstitial lung disease, or, if accompanied by signs of consolidation, pneumonia.
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.
Consideration of pre-test probability and sometimes clinical prediction rules can help estimate the risk of pulmonary embolism. Note that normal oxygen saturation does not exclude pulmonary embolism.
Hyperventilation syndrome 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.
Testing
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 acid-base disorders stimulating hyperventilation, and calculate the alveolar-arterial gradient. Also, basic metabolic panel to measure the bicarbonate level can be useful to assess the chronicity of a respiratory acidosis.
Patients who have no clear diagnosis after chest x-ray and ECG and are at moderate or high risk of having pulmonary embolism (based on 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. If initial workup is inconclusive, cardiopulmonary exercise testing can be considered.
Evaluation reference
1. Parshall MB, Schwartzstein RM, Adams L, et al: An Official American Thoracic Society Statement: Update on the mechanisms, assessment, and management of dyspnea. Am J Respir Crit Care Med 185:435–452, 2012.
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 (1).
Treatment reference
1. Cabello JB, Burls A, Emparanza JI, Bayliss SE, Quinn T. Oxygen therapy for acute myocardial infarction. Cochrane Database Syst Rev 2016;12(12):CD007160. Published 2016 Dec 19. doi:10.1002/14651858.CD007160.pub4
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.
