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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 recent 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 CNS. 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, which vary by acuity of onset (see Table 2: Approach to the Patient With Pulmonary Symptoms: Some Causes of Dyspnea).

The most common causes include

• Asthma
• Pneumonia
• COPD
• Myocardial ischemia
• 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 an MI, a patient with chronic heart failure may develop pneumonia).

Table 2
Some Causes of Dyspnea Cause Suggestive Findings Diagnostic Approach* Acute (within minutes) Pulmonary causes Pneumothorax 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 Pulmonary embolism 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 or V/Q scanning Doppler or duplex studies of extremities showing positive findings of DVT 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 bedside peak flow measurement Foreign body inhalation 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 Toxic airway damage (eg, 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 Acute myocardial ischemia or infarction Substernal chest pressure with or without radiation to the arm or jaw, particularly in patients with risk factors for CAD ECG Cardiac enzyme testing 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 Heart failure 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 h after falling asleep (paroxysmal nocturnal dyspnea) Auscultation Chest x-ray BNP measurement Echocardiography Other causes Diaphragmatic paralysis Sudden onset after trauma affecting the phrenic nerve Frequent orthopnea Chest x-ray Fluoroscopic sniff test Anxiety disorder—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 Subacute (within hours or days) Pulmonary causes Pneumonia 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 COPD exacerbation Cough, productive or nonproductive Poor air movement Accessory muscle use or pursed lip breathing Clinical evaluation Sometimes chest x-ray and ABGs Cardiac causes Angina or CAD 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 Pericardial effusion or tamponade Muffled heart sounds or enlarged cardiac silhouette in patients with risk factors for pericardial effusion (eg, cancer, pericarditis, SLE) Possibly pulsus paradoxus Echocardiography Chronic (hours to years) Pulmonary causes Obstructive lung disease Extensive smoking history, barrel chest, and poor air entry and exit Chest x-ray Pulmonary function testing (at initial evaluation) Restrictive lung disease Progressive dyspnea in patients with known occupational exposure or neurologic condition Chest x-ray Pulmonary function testing (at initial evaluation) Interstitial lung disease Fine crackles on auscultation High-resolution chest CT Pleural effusion Pleuritic chest pain and lung field that is dull to percussion with diminished breath sounds Sometimes history of cancer, heart failure, RA, SLE, or acute pneumonia Chest x-ray Often chest CT and thoracentesis Cardiac causes Heart failure Crackles, S3 gallop, and signs of central or peripheral volume overload (eg, elevated neck veins, peripheral edema) Orthopnea or paroxysmal nocturnal dyspnea Auscultation Chest x-ray Echocardiography Stable angina or CAD 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 Sometimes cardiac catheterization Other causes Anemia Dyspnea on exertion progressing to dyspnea at rest Normal lung examination and pulse oximetry measurement Sometimes systolic heart murmur due to increased flow CBC Physical deconditioning Dyspnea only on exertion in patients with sedentary lifestyle Clinical evaluation *Most patients should have pulse oximetry and, unless symptoms are clearly a mild exacerbation of known chronic disease, chest x-ray. BNP = Brain (B-type) natriuretic peptide; CAD = coronary artery disease; DVT = deep venous thrombosis; S3 = 3rd heart sound; V/Q = ventilation/perfusion.

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 produce dyspnea (ie, dyspnea at rest is more severe than dyspnea only with climbing stairs). For patients with baseline dyspnea, the physician 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 [PE], 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, 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 PE

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 wheezes. 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 BP during inspiration) can be done by inflating a BP 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. Rectal examination and stool guaiac testing should be done.

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

Interpretation of findings: The history and physical examination often suggest a cause and guide further testing (see Table 2: Approach to the Patient With Pulmonary Symptoms: Some Causes of Dyspnea). Several findings are of note. Wheezing (see Approach to the Patient With Pulmonary Symptoms: Wheezing) suggests asthma or COPD. Stridor (see Approach to the Patient With Pulmonary Symptoms: 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 signs and symptoms of life-threatening conditions such as myocardial ischemia and PE can be nonspecific. Furthermore, the severity of symptoms is not always proportional to the severity of the cause (eg, PE 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 (see Approach to the Cardiac Patient: Clinical Prediction Rule for Diagnosing Pulmonary Embolism and see Approach to the Cardiac Patient: PE testing algorithm) can help estimate the risk for PE. Note that a normal O₂ saturation does not exclude PE.

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, 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 PE (from the clinical prediction rule—see Approach to the Cardiac Patient: PE testing algorithm and see Approach to the Cardiac Patient: Clinical Prediction Rule for Diagnosing Pulmonary Embolism) should undergo ventilation/perfusion scanning or CT-angiography. Patients who are at low risk may have D-dimer testing (to detect the presence of clot); a normal D-dimer level effectively rules out PE in a low-risk patient.

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

Treatment

Treatment is correction of the underlying disorder.

Hypoxemia is treated with supplemental O₂ as needed to maintain SaO₂ > 88% or PaO₂ > 55 mm Hg, as levels above these thresholds provide adequate O₂ delivery to tissues. Levels below these thresholds are on the steep portion of the O₂–Hb dissociation curve, in which small declines in arterial O₂ tension result in large declines in Hb saturation. O₂ saturation should be maintained at > 93% if myocardial or cerebral ischemia is a concern.

Morphine Some Trade Names
DURAMORPH
MS CONTIN
MSIR
ROXANOL
Click for Drug Monograph
0.5 to 5 mg IV helps reduce anxiety and the discomfort of dyspnea in various conditions, including MI, PE, 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 worsen respiratory acidemia.

Key Points

• Pulse oximetry is a key component of the examination.
• Low O₂ saturation (< 90%) indicates a significant problem, but normal saturation does not rule one out.
• Accessory muscle use, low O₂ saturation, or decreased level of consciousness requires emergency evaluation and hospitalization.
• Myocardial ischemia and PE are relatively common, but symptoms and signs can be nonspecific.
• Exacerbation of known conditions (eg, asthma, COPD, heart failure) is common, but such patients also may develop new problems.

Last full review/revision July 2009 by Noah Lechtzin, MD, MHS

Content last modified July 2009