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Dyspnea is unpleasant or uncomfortable breathing. It has multiple components and is experienced and described differently depending on the cause.

Dyspnea has multiple pulmonary, cardiac, and other causes (see Table 1: Approach to the Patient With Pulmonary Symptoms: Causes of Dyspnea). Often, more than one mechanism underlies the sensation.

Table 1
Causes of Dyspnea Acute onset (within minutes) Pulmonary Pneumothorax Pulmonary embolism Bronchospasm Asthma (with previous history) Reactive airway disease (with previous exposure) Foreign body Toxic inhalation (eg, chlorine, hydrogen sulfide) Cardiac Acute myocardial ischemia or infarction Papillary muscle dysfunction or rupture Ventricular dysfunction Cardiogenic pulmonary edema Other Diaphragmatic paralysis Anxiety disorder—hyperventilation Subacute onset (within hours or days) Same as acute onset, with addition of: Pneumonia Acute bronchitis Poisoning Salicylate Ethylene glycol Nonacute onset (hours–years) Pulmonary Obstructive lung disease Restrictive lung disease Interstitial lung disease Pleural effusion Cardiac Ventricular dysfunction Pericardial effusion and tamponade Other Anemia Physical deconditioning

The basis for the sensation of discomfort of dyspnea is unclear but may be a centrally perceived discrepancy between respiratory muscle tension (the need to take a deep breath) and length (the ability to take a deep breath). This mechanism partially explains why some forms of breathlessness and hyperpnea, such as with metabolic acidosis (Kussmaul's respirations), in CNS disease (Biot's and Cheyne-Stokes respirations), and during exercise among trained athletes, are not experienced as dyspnea.

Evaluation

History: Reports of shortness of breath or of being unable to take a deep breath are more common among patients with COPD exacerbation. Chest tightness or increased effort to breathe suggests asthma or an obstructive ventilatory disorder. A feeling of suffocation is characteristic of pulmonary edema. Heavy breathing on exertion is common in physical deconditioning, whereas air hunger, or an urgent sense of a need to breathe in more air, has been linked to hypercapnia, restricted chest wall excursions, and pulmonary edema. Phrases such as “out of breath” and “hard to breathe” are nonspecific.

Abrupt onset of dyspnea with or without sharp chest pain suggests spontaneous pneumothorax or pulmonary embolism; concomitant leg pain and swelling or recent immobility support pulmonary embolism. Abrupt onset of productive cough and fever suggests bacterial pneumonia, particularly that caused by Streptococcus pneumoniae if it is accompanied by pleuritic chest pain. Severe dyspnea that appears 1 to 2 h after falling asleep (paroxysmal nocturnal dyspnea) is pathognomonic for left ventricular dysfunction, but it must be distinguished from nocturnal awakening by cough from asthma or mucus hypersecretion. Dyspnea while recumbent (orthopnea) also implies left ventricular dysfunction or, less commonly, pericardial effusion, respiratory muscle weakness, or diaphragmatic paralysis. Dyspnea that worsens when sitting upright and resolves when recumbent (platypnea) is unusual and suggests pulmonary arteriovenous malformation or the hepatopulmonary syndrome; it may also occur after pneumonectomy, in recurrent pulmonary embolism, and in chronic pulmonary diseases that preferentially affect the lower lobes, such as aspiration pneumonia and α₁-antitrypsin deficiency. Dyspnea accompanied by paresthesias in the fingers or around the mouth suggests hyperventilation. Exertional dyspnea in the absence of objective findings on examination or testing may indicate anemia, primary pulmonary hypertension (if it occurs in a young woman), or, more likely, physical deconditioning.

Physical examination: Absent or markedly diminished breath sounds on only one side suggest pneumothorax or pleural effusion; these can be distinguished by increased resonance and dullness to percussion, respectively. 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 in the dyspneic patient suggest left heart failure or interstitial lung disease. Rhonchi suggest COPD.

Testing: A chest x-ray should be taken in most patients. Acute dyspnea also warrants pulse oximetry, which provides a noninvasive measure of O₂ saturation. An ECG to detect cardiac ischemia is mandatory unless cardiac ischemia can be excluded clinically. In patients with severe or deteriorating respiratory status, an ABG should be performed to more precisely quantify hypoxemia, measure Pco₂, and measure any acid-base disorders stimulating hyperventilation and to calculate the alveolar-arterial gradient (see Tests of Pulmonary Function (PFT): Arterial Blood Gas Sampling). Patients suspected of having pulmonary embolism should undergo ventilation/perfusion scanning or CT angiography.

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

Treatment

Treatment is correction of the underlying cause. Hypoxemia is addressed 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 (see Fig. 4: Tests of Pulmonary Function (PFT): Oxyhemoglobin dissociation curve). O₂ saturation should be maintained at > 93% if myocardial or cerebral ischemia is a concern. Morphine Some Trade Names
DURAMORPH
MS CONTIN
MSIR
ROXANOL
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0.5 to 5 mg IV helps reduce anxiety and the discomfort of dyspnea in various conditions, including MI, pulmonary embolism, and the dyspnea that commonly accompanies terminal illnesses (see The Dying Patient: Dyspnea). However, opioids can be deleterious in patients with acute airflow limitation (eg, asthma, COPD) because they suppress the ventilatory drive and worsen respiratory acidemia.

Hyperventilation Syndrome

Hyperventilation syndrome is anxiety-related dyspnea and tachypnea often accompanied by systemic symptoms.

Hyperventilation syndrome is common in young women but can affect either sex at any age. It is sometimes precipitated by emotionally stressful events. Hyperventilation syndrome is separate from panic disorder (see Anxiety Disorders: Panic Attacks and Panic Disorder), although the 2 conditions overlap; about ½ of patients with panic disorder have hyperventilation syndrome and ¼ of patients with hyperventilation syndrome have panic disorder.

History: Patients with acute hyperventilation syndrome present with dyspnea sometimes so severe as to feel like suffocation. It is accompanied by agitation and a sense of terror or by somatic symptoms of chest pain, paresthesias (peripheral and perioral), peripheral tetany, and presyncope or syncope or sometimes by a combination of all of these. Tetany occurs because respiratory alkalosis causes both hypophosphatemia and hypocalcemia. Patients with chronic hyperventilation syndrome present far less dramatically and often escape detection; they sigh deeply and frequently and often have nonspecific somatic symptoms in the context of mood and anxiety disorders and emotional stress.

Physical examination: Physical examination is normal in both acute and chronic hyperventilation syndrome, although patients may be tachypneic and appear anxious or agitated.

Testing: Hyperventilation syndrome is a diagnosis of exclusion; the challenge is to use tests and resources judiciously to distinguish this syndrome from more serious diagnoses. Basic testing includes pulse oximetry, chest x-ray, and ECG. Pulse oximetry in hyperventilation syndrome shows O₂ saturation at or close to 100%. Chest x-ray is normal. ECG is performed to detect cardiac ischemia, although hyperventilation syndrome itself can cause ST-segment depressions, T-wave inversions, and prolonged QT intervals. ABGs are needed when other causes of hyperventilation are suspected, such as metabolic acidosis. Occasionally, acute hyperventilation syndrome is indistinguishable from acute pulmonary embolism, and tests for pulmonary embolism (eg, d-dimer, ventilation/perfusion scan, helical CT) may be necessary.

Treatment

Treatment is reassurance. Some physicians advocate teaching the patient maximal exhalation and diaphragmatic breathing. Most patients require treatment for underlying mood or anxiety disorders that includes cognitive therapy, stress reduction techniques, and/or drugs (anxiolytics, antidepressants, or lithium Some Trade Names
ESKALITH
LITHOBID
LITHONATE
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).

Last full review/revision November 2005

Content last modified November 2005