Shortness of breath, or dyspnea, is a common problem in the outpatient primary care setting. Establishing a diagnosis can be challenging because dyspnea appears in multiple diagnostic categories. Underlying disorders range from the relatively simple to the more serious, which are best addressed in an emergency department. Timely assessment, diagnosis, and initiation of appropriate therapy play an important role in controlling the commonly associated anxiety. Family physicians should be prepared and equipped to triage, manage, and stabilize patients with acute dyspnea.
Dyspnea is described as faster breathing accompanied by the sensations of running out of air and of not being able to breathe fast or deeply enough. The sensations are similar to that of thirst or hunger (i.e., an unignorable feeling of needing something). Dyspnea results from multiple interactions of signals and receptors in the autonomic nervous system, motor cortex, and peripheral receptors in the upper airway, lungs, and chest wall.1 Various disease states can produce dyspnea in slightly different manners, depending on the interaction of efferent signals with receptors of the central nervous system, autonomic system, and peripheral nerves. The actual sensation of muscular effort and breathlessness results from the simultaneous activation of the sensory cortex at the time the chest muscles are signaled to contract.2 Good evidence demonstrates that increased carbon dioxide partial pressure (Pco2) levels stimulate the feeling of breathlessness independent of the effects of ventilation or the oxygen partial pressure (Po2) level.2
Clinical Presentation and Triage
At presentation, an adult patient usually describes a sensation of difficult or uncomfortable breathing. Triage begins with determining the degree of urgency by assessing the duration of the condition, whether it is acute or chronic, and the severity of symptoms. Studies have shown that the type and severity of an underlying lung or heart disease correlates well with the way the patient describes the dyspnea.3 The first communication with the physician's office, especially for established patients, may be by telephone. Telephone triage is an important initial step in management. Protocols and clearly written office procedures for staff are recommended to provide proper care and minimize risk.4 A triage algorithm (Figure 1) can be used by office nurses.
Recognition and Management of Unstable Patients
Definitive care, which must follow stabilization, depends on the specific diagnosis. An initial quick assessment will help the physician determine if a patient is unstable (Table 1).
Unstable patients typically present with one or more symptom patterns:
Hypotension, altered mental status, hypoxia, or unstable arrhythmia.
Stridor and breathing effort without air movement (suspect upper airway obstruction).
Unilateral tracheal deviation, hypotension, and unilateral breath sounds (suspect tension pneumothorax)
Respiratory rate above 40 breaths per minute, retractions, cyanosis, low oxygen saturation.
The same initial treatment process should be applied for any of these symptom patterns. First, administer oxygen. Consider intubation if the patient is working to breathe (gasping), apneic, or nonresponsive, following advanced cardiac life support (ACLS) guidelines.5
Next, establish intravenous line access and start administration of fluids. Perform needle thoracentesis in patients with tension pneumothorax. Administer a nebulized bronchodilator if obstructive pulmonary disease is present. Administer intravenous or intramuscular furosemide if pulmonary edema is present.
|Assess airway patency and listen to the lungs.|
|Observe breathing pattern, including use of accessory muscles.|
|Monitor cardiac rhythm.|
|Measure vital signs and pulse oximetry.|
|Obtain any history of cardiac or pulmonary disease, or trauma.|
|Evaluate mental status.|
Disposition and transfer of the patient depends on the diagnosis or differential diagnosis. Unstable patients should be transported to the closest emergency department for further evaluation and treatment. Trained health care personnel should accompany the patient in the ambulance and continue management until supervision is transferred to the emergency department team.
Further Assessment of Stable Patients
Once an emergent situation has been excluded, obtain a history to determine the level of acuity. Reassess the patient's airways, mental status, ability to speak, and breathing effort. Check vital signs, and question the patient (or a family member) about the duration of the dyspnea and any underlying cardiac or pulmonary disease. Include a focused history of medication use, cough, fever, and chest pain. Ask about any history of trauma and continue the focused physical examination by listening to breath sounds and observing skin color.
|Cardiac: congestive heart failure, coronary artery disease, arrhythmia, pericarditis, acute myocardial infarction, anemia|
|Pulmonary: chronic obstructive pulmonary disease, asthma, pneumonia, pneumothorax, pulmonary embolism, pleural effusion, metastatic disease, pulmonary edema, gastroesophageal reflux disease with aspiration, restrictive lung disease|
|Psychogenic: panic attacks, hyperventilation, pain, anxiety|
|Upper airway obstruction: epiglottitis, foreign body, croup, Epstein-Barr virus|
|Endocrine: metabolic acidosis, medications|
|Central: neuromuscular disorders, pain, aspirin overdose|
|Pediatric: bronchiolitis, croup, epiglottitis, foreign body aspiration, myocarditis|
In children, the most common causes of acute dyspnea are acute asthma, pulmonary infections, and upper airway obstruction. Some conditions associated with dyspnea, such as epiglottitis, croup, myocarditis, asthma, and diabetic ketoacidosis, are serious and may be fatal. In children, always consider foreign body aspiration, croup, and bronchiolitis caused by respiratory syncytial virus.8,9
A complete history should emphasize any coexisting cardiac and pulmonary symptoms. Cardiac and pulmonary problems are the most common causes of dyspnea. Determine onset, duration, and occurrence at rest or exertion. The presence of cough may imply asthma or pneumonia; cough combined with a change in the character of sputum may be caused by exacerbation of chronic obstructive pulmonary disease (COPD). In adults, epiglottitis should be ruled out when severe sore throat is associated with acute dyspnea.10 In children, fever associated with dyspnea usually implies an infectious cause, such as pneumonia, croup, or bronchiolitis.10
Chest pain during dyspnea may be caused by coronary or pleural disease, depending on the quality and description of the pain. Pleuritic chest pain could be caused by pericarditis, pneumonia, pulmonary embolism, pneumothorax, or pleuritis. Dyspnea or tachypnea with pleuritic chest pain occurs in 97 percent of patients who have clinically apparent pulmonary embolism, although some researchers have questioned reliance on clinical presentation as an accurate indicator of pulmonary embolism.11
Sudden shortness of breath at rest is suggestive of pulmonary embolism or pneumothorax. Severe respiratory distress continuing over one to two hours suggests congestive heart failure or asthma. Consider nonrespiratory causes of dyspnea (e.g., anemia, acidosis, drug poisoning).
Chest pain is almost universal in spontaneous pneumothorax, while dyspnea is the second most common symptom.12 Anginal chest pain accompanied by shortness of breath may signify ischemia associated with left ventricular dysfunction. Paroxysmal dyspnea or pulmonary edema may be the only clinical presentation in 10 percent of patients with myocardial infarction.13
Consider spontaneous pneumothorax in patients with COPD, cystic fibrosis, or acquired immunodeficiency syndrome.14 Spontaneous recurrent or nonrecurrent pneumothorax in young females in conjunction with menstruation is an uncommon condition referred to as catamenial pneumothorax.15 A history of scuba diving may suggest barotrauma. Vehicle airbag trauma has been reported to cause pneumothorax; note any history of penetrating or nonpenetrating trauma.16
Inquire about indigestion or dysphagia, which may indicate gastroesophageal reflux or aspiration.17 Anxiety symptoms may imply psychogenic causes of dyspnea, but organic etiologies always should be considered first. A diagnosis of hyperventilation syndrome cannot be made before organic disease is ruled out.18 When obtaining the history, note smoking habits, secondhand smoke exposure, and pertinent medication use (give particular attention to agents that have potential adverse cardiopulmonary effects, such as beta blockers, ophthalmologic drops). A history of orthopnea, pedal edema, or nocturnal paroxysmal dyspnea is suggestive of congestive heart failure.19 Table 3 summarizes clues in the history that help in the diagnosis of dyspnea.
|Symptoms or features in the history||Possible diagnosis|
|Severe sore throat||Epiglottitis|
|Pleuritic chest pain||Pericarditis, pulmonary embolism, pneumothorax, pneumonia|
|Orthopnea, nocturnal paroxysmal dyspnea, edema||Congestive heart failure|
|Tobacco use||Chronic obstructive pulmonary disease, congestive heart failure, pulmonary embolism|
|Indigestion, dysphagia||Gastroesophageal reflux disease, aspiration|
General Appearance and Vital Signs
To determine the severity of dyspnea, carefully observe respiratory effort, use of accessory muscles, mental status, and ability to speak. Pulsus paradoxus may exist in COPD, asthma, or cardiac tamponade. Stridor is indicative of an upper airway obstruction.10 It may be necessary to obtain a rectal temperature to detect fever, since oral airflow may decrease the oral temperature.
Distention of the neck veins may imply cor pulmonale caused by severe COPD, congestive heart failure, or cardiac tamponade. Check the thyroid for enlargement because congestive heart failure may result from hyperthyroidism or hypothyroidism. Ensure that the trachea is in the midline. Auscultate for stridor.
Cardiac and Pulmonary Examination
Palpate the chest for subcutaneous emphysema and crepitus, and percuss for dullness, an indication of consolidations or effusions. Hyper-resonance on percussion suggests pneumothorax or bullous emphysema.
Auscultate the heart and lungs for murmurs or extra heart sounds; absent breath sounds may be consistent with pneumothorax or pleural effusion. Wheezing usually is consistent with obstructive lung disease but can be caused by pulmonary edema or pulmonary embolism. Rales are present in pulmonary edema and pneumonia.20
Rapid or irregular pulse may signify a dysrhythmia. An S3 gallop suggests a left ventricular systolic dysfunction in congestive heart failure. An S4 gallop suggests left ventricular dysfunction or ischemia. A loud P2 may be heard in patients with pulmonary hypertension or cor pulmonale. Murmurs can be an indirect sign of congestive heart failure, and distant heart sounds can point to cardiac tamponade.21
Look for hepatomegaly and ascites. Assessing for hepatojugular reflux is a valid bedside maneuver in the diagnosis of congestive heart failure in patients with acute dyspnea.
Check the lower extremities for edema and any signs suggestive of deep venous thrombosis.22 Examine the digits for clubbing or cyanosis.
Table 4 summarizes physical findings in the diagnosis of dyspnea.
|Wheezing, pulsus paradoxus, accessory muscle use||Acute asthma, COPD exacerbation|
|Wheezing, clubbing, barrel chest, decreased breath sounds||COPD exacerbation|
|Fever, crackles, increased fremitus||Pneumonia|
|Edema, neck vein distension, S3 or S4 hepatojugular reflux, murmurs, rales, hypertension, wheezing||Congestive heart failure, pulmonary edema|
|Wheezing, friction rub, lower extremity swelling||Pulmonary embolism|
|Absent breath sounds, hyperresonance||Pneumothorax|
|Inspiratory stridor, rhonchi, retractions||Croup|
|Stridor, drooling, fever||Epiglottitis|
|Stridor, wheezing, persistent pneumonia||Foreign body aspiration|
|Wheezing, flaring, intercostal retractions, apnea||Bronchiolitis|
Pulse oximetry determines a patient's level of oxygenation. In the evaluation of acute dyspnea, obtain chest radiographs to rule out conditions such as pneumothorax, pneumonia, COPD, pulmonary edema, or congestive heart failure.23 Obtain lateral neck radiographs when stridor is present or when upper airway obstruction, such as foreign body aspiration, epiglottitis, or croup, is suspected. Subglottic edema (appearing as a narrowed anteroposterior tracheal air column on radiograph) suggests croup, whereas radiographic enlargement of the epiglottis is pathognomonic for epiglottitis.24
|Possible diagnosis||Radiography||Pulse oximetry/spirometry||Other tests|
|Acute asthma, chronic obstructive pulmonary disease exacerbation||Hyperinflated lungs||Decreased oxygen saturation, decreased peak expiratory flow rate and forced expiratory volume in 1 second||—|
|Pneumonia||Infiltrates, effusion, consolidation||Decreased or normal oxygen saturation||Normal or high white blood cell count|
|Congestive heart failure||Interstitial edema, effusion, cardiomegaly||Decreased oxygen saturation||Left ventricular hypertrophy, ischemia, or arrhythmia on ECG; low hemoglobin|
|Pulmonary embolism||Normal, atelectasis, pleural effusion, wedge-shaped density||Decreased oxygen saturation||Right bundle branch block on ECG; tachycardia|
|Pneumothorax||Collapsed lung, mediastinal shift||Decreased oxygen saturation||—|
|Croup||Subglottic narrowing by AP plain film or computed tomography||Decreased or normal oxygen saturation||—|
|Epiglottitis||Enlarged epiglottis||Decreased or normal oxygen saturation||High white blood cell count|
|Foreign body aspiration||Visualized foreign body, air trapping, hyperinflation||Decreased or normal oxygen saturation||Normal or high white blood cell count|
|Bronchiolitis||Hyperinflation, atelectasis||Decreased or normal oxygen saturation||Normal white blood cell count; RSV swab|
d-Dimer testing, although not an office procedure, can be useful in the hospital setting to check for suspected pulmonary embolism. Negative rapid and standard enzyme-linked immunosorbent assay (ELISA) d-Dimer tests can help exclude pulmonary embolism, whether performed alone or in conjunction with normal alveolar dead-space fraction.7,25 Spiral computed tomography (CT) also has a role in the diagnostic work-up of pulmonary embolism in a hospitalized patient, especially when the ventilation-perfusion scan is nondiagnostic. Spiral CT may eventually replace pulmonary angiography.26 Bilateral venous Doppler imaging should be ordered simultaneously with spiral CT and, if findings are suggestive of deep venous thrombosis, treatment for pulmonary embolism should be initiated. A right-heart strain pattern on echocardiogram may be one finding in a patient with acute pulmonary embolism.