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Dyspnea is unpleasant or uncomfortable breathing. It is experienced and described differently by patients depending on the cause.
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.
Dyspnea has many pulmonary, cardiac, and other causes, which vary by acuity of onset (see Table: Some Causes of Acute* Dyspnea, see Table: Some Causes of Subacute* Dyspnea, and see Table: Some Causes of Chronic* Dyspnea).
The most common causes include
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 an MI, a patient with chronic heart failure may develop pneumonia).
Some Causes of Acute* Dyspnea
Some Causes of Subacute* Dyspnea
Some Causes of Chronic* 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 with 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 [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.
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 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.
The history and physical examination often suggest a cause and guide further testing (see Table: Some Causes of Acute* Dyspnea, see Table: Some Causes of Subacute* Dyspnea, and see Table: Some Causes of Chronic* Dyspnea). Several findings are of note. Wheezing (see Wheezing) suggests asthma or COPD. Stridor (see 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 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 Table: Clinical Prediction Rule for Diagnosing Pulmonary Embolism) can help estimate the risk of 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.
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 Table: Clinical Prediction Rule for Diagnosing Pulmonary Embolism) 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 PE in a low-risk patient).
Chronic dyspnea may warrant additional tests, such as CT, pulmonary function tests, echocardiography, and bronchoscopy.
Treatment is correction of the underlying disorder.
Hypoxemia is treated with supplemental O2 as needed to maintain SaO2> 88% or PaO2> 55 mm Hg because 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, where even a small decline in arterial O2 tension can result in a large decline in Hb saturation. O2 saturation should be maintained at > 93% if myocardial or cerebral ischemia is a concern.
Morphine 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 can worsen respiratory acidemia.
Pulse oximetry is a key component of the examination.
Low O2 saturation (< 90%) indicates a serious problem, but normal saturation does not rule one out.
Accessory muscle use, a sudden decrease in O2 saturation, or a 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 patients may also develop new problems.
* This is the Professional Version. *