Dyspnea is unpleasant or uncomfortable breathing. It is experienced and described differently by patients depending on the cause.
Pathophysiology
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
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
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COPD (chronic obstructive pulmonary disease)
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Physical deconditioning
The most common cause of dyspnea in patients with chronic pulmonary or cardiac disorders is
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).
Some Causes of Acute* Dyspnea
Cause |
Suggestive Findings |
Diagnostic Approach† |
Pulmonary causes |
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Asthma, bronchospasm, or reactive airway disease |
Wheezing and poor air exchange that arise spontaneously or after exposure to specific stimuli (eg, allergen, URI, cold, exercise) Possibly pulsus paradoxus Often a preexisting history of reactive airway disease |
Clinical evaluation Sometimes pulmonary function testing or peak flow measurement |
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Sudden onset of cough or stridor in a patient (typically an infant or young child) without URI or constitutional symptoms |
Inspiratory and expiratory chest x-rays Sometimes bronchoscopy |
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Abrupt onset of sharp chest pain, tachypnea, diminished breath sounds, and hyperresonance to percussion May follow injury or occur spontaneously (especially in tall, thin patients and in patients with COPD) |
Chest x-ray |
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Abrupt onset of sharp chest pain, tachypnea, and tachycardia Often risk factors for pulmonary embolism (eg, cancer, immobilization, DVT, pregnancy, use of oral contraceptives or other estrogen-containing drugs, recent surgery or hospitalization, family history) |
CT angiography Less often, V/Q scanning and possibly pulmonary arteriography |
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Toxin-induced airway damage (eg, due to inhalation of chlorine or hydrogen sulfide) |
Sudden onset after occupational exposure or inappropriate use of cleaning agents |
Inhalation usually obvious by history Chest x-ray Sometimes ABGs and observation to determine severity |
Cardiac causes |
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Substernal chest pressure or pain that may or may not radiate to the arm or jaw, particularly in patients with risk factors for CAD |
ECG Cardiac enzyme testing |
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Papillary muscle dysfunction or rupture |
Sudden onset of chest pain, new or loud holosystolic murmur, and signs of heart failure, particularly in patients with recent MI |
Auscultation Echocardiography |
Other causes |
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Anxiety disorder causing hyperventilation |
Situational dyspnea often accompanied by psychomotor agitation and paresthesias in the fingers or around the mouth Normal examination findings and pulse oximetry measurements |
Clinical evaluation Diagnosis of exclusion |
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Diaphragmatic paralysis |
Sudden onset after trauma affecting the phrenic nerve Frequent orthopnea |
Chest x-ray Fluoroscopic sniff test |
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* Acute dyspnea occurs within minutes of triggering event. |
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† Most patients should have pulse oximetry and, unless symptoms are clearly a mild exacerbation of known chronic disease, chest x-ray. |
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ABG = arterial blood gas; BNP = brain (B-type) natriuretic peptide; CAD = coronary artery disease; COPD = chronic obstructive pulmonary disease; DVT = deep venous thrombosis; ECG = electrocardiography; MI = myocardial infarction; S3 = 3rd heart sound; URI = upper respiratory infection; V/Q = ventilation/perfusion. |
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Some Causes of Subacute* Dyspnea
Cause |
Suggestive Findings |
Diagnostic Approach† |
Pulmonary causes |
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COPD exacerbation |
Cough, productive or nonproductive Poor air movement Accessory muscle use or pursed lip breathing |
Clinical evaluation Sometimes chest x-ray and arterial blood gas measurement |
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Fever, productive cough, dyspnea, sometimes pleuritic chest pain Focal lung findings, including crackles, decreased breath sounds, and egophony |
Chest x-ray Sometimes blood and sputum cultures WBC count |
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Cardiac causes |
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Substernal chest pressure with or without radiation to the arm or jaw, often provoked by physical exertion, particularly in patients with risk factors for CAD |
ECG Cardiac stress testing Cardiac catheterization |
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Crackles, S3 gallop, and signs of central or peripheral volume overload (eg, elevated neck veins, peripheral edema) Dyspnea while lying flat (orthopnea) or appearing 1–2 hours after falling asleep (paroxysmal nocturnal dyspnea) |
Chest x-ray BNP measurement Echocardiography |
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Muffled heart sounds or enlarged cardiac silhouette in patients with risk factors for pericardial effusion (eg, cancer, pericarditis, SLE) Possibly pulsus paradoxus Orthopnea |
Echocardiography |
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* Subacute dyspnea occurs within hours or days. |
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† Most patients should have pulse oximetry and, unless symptoms are clearly a mild exacerbation of a known chronic disease, chest x-ray. |
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CAD = coronary artery disease; COPD = chronic obstructive pulmonary disease; SLE = systemic lupus erythematosus; S3 = 3rd heart sound; WBC = white blood cell. |
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Some Causes of Chronic* Dyspnea
Etiology reference
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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
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:
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Smoking history—for cancer, COPD, some interstitial lung diseases, and heart disease
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Family history, hypertension, and high cholesterol levels—for coronary artery disease
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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
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
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:
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 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 any acid-base disorders 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
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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
Treatment is correction of the underlying disorder.
Hypoxemia 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
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Pulse oximetry is a key component of the examination.
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Low oxygen saturation (< 90%) indicates a serious problem, but normal saturation does not rule one out.
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Accessory muscle use, a sudden decrease in oxygen saturation, or a decreased level of consciousness requires emergency evaluation and hospitalization.
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Myocardial ischemia and pulmonary embolism are relatively common, but symptoms and signs can be nonspecific.
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Exacerbation of known conditions (eg, asthma, chronic obstructive pulmonary disease, heart failure) is common, but patients may also develop new problems.
