Dyspnea

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[edit] Dyspnea

John J.W. Fangman

David H. Roberts

Dyspnea, an uncomfortable awareness of breathing, is a common problem in primary care. Although the exact frequency of dyspnea complaints is not known, it is the presenting complaint in many common disorders such as congestive heart failure (CHF), acute myocardial ischemia, chronic obstructive pulmonary disease (COPD), and asthma. The sensation of dyspnea may result from activation of the cerebral cortex, from central and peripheral chemoreceptors, or from an array of mechanoreceptors in the upper airway, lung, and chest wall.^[1] Afferent traffic is processed in higher brain centers and is influenced by context and behavior. The pathophysiology of dyspnea may involve dissociation of incoming afferent information and central respiratory motor activation. This mismatch may heighten or even produce the sensation of dyspnea. Dyspnea may also result when the level of ventilation and O₂ consumption is increased (e.g., exercise). It is important to note that behavioral style and emotional state can contribute markedly to the sensation of dyspnea.

Dyspnea resulting from cardiac disease is characterized by inadequate cardiac output to meet cellular oxygen demand. Although most often the result of decreased cardiac output and elevated pulmonary capillary wedge pressure, dyspnea can also result from high-output states (e.g., anemia, hyperthyroidism) and normal output states (e.g., diastolic dysfunction). Dyspnea secondary to pulmonary disease may result from a sensation of increased respiratory drive, chest wall movement, hyperinflation, bronchoconstriction, or impaired gas exchange.

[edit] History

[edit] Timing and Setting.

Even when not disabling or life threatening, rapidly progressive dyspnea demands aggressive evaluation (see C). A sudden increase in severity of chronic dyspnea should also prompt a search for additional causes of shortness of breath.^[2] The setting in which dyspnea occurs often provides important clues to its etiology. Shortness of breath in a young person after exercise, exposure to cold or dry air, or inhalation of irritants suggests bronchospasm. Although anxiety often accompanies dyspnea of any cause, agoraphobia, peripheral paresthesias, and hyperventilation suggest panic attacks or other anxiety disorders. Dyspnea associated with cough that is more prominent at night or worse after meals suggests reflux. Dyspnea after surgery may indicate diaphragmatic injury, pneumonia, or pulmonary embolism. Although a nonspecific complaint, severe exertional dyspnea most often results from pulmonary vascular disease, severe obstructive disease, or left ventricular (LV) dysfunction. Orthopnea (shortness of breath when lying flat) and paroxysmal nocturnal dyspnea are also signs of left-sided heart failure. Platypnea (shortness of breath when upright) suggests intracardiac, vascular, or pulmonary shunt.

[edit] Risk Factors.

It is important to quantify tobacco use and assess for other risk factors for coronary artery disease when evaluating the patient with dyspnea. Risk factors include occupational exposures, environmental exposures or allergens, and a family history of congenital heart disease or hereditary pulmonary diseases (e.g., cystic fibrosis).

[edit] Description.

Careful attention should be paid to the patient's description of dyspnea. Patients with bronchospasm or myocardial ischemia often complain of chest tightness or constriction. Patients with interstitial lung disease or conditions that result in excessive load on the respiratory muscles (e.g., neuromuscular disease, severe airway obstruction) often describe an increased work of breathing. Air hunger, the exaggerated urge to breathe, may signal the increased respiratory drive associated with conditions such as acute hypercapnia, pregnancy, anemia, pulmonary embolism, acidosis, or CHF. Finally, patients who have normal cardiac and respiratory function but who are deconditioned often complain of heavy or rapid breathing with exertion. Patients whose dyspnea is multifactorial may complain of several different types of dyspnea.

[edit] Medical Conditions.

A detailed review of the patient's history of cardiac or pulmonary disease is an important first step. Pregnancy, malignancy, and anemia also are often associated with dyspnea. The patient's current medication list and medical record should be reviewed for exposure to drugs that produce acute or chronic lung disease (see D). Psychiatric disease, especially panic attacks and other anxiety disorders, are associated with dyspnea. In dyspneic immunocompromised patients, evaluation focuses on infectious and toxic risk factors particular to the immunodeficiency and its treatment. Finally, it is important to assess the patient's cardiovascular conditioning by clarifying both baseline level of activity and ability to perform activities of daily living (ADLs).

[edit] Physical Examination

[edit] General.

The physical examination should first establish the severity of respiratory distress.^[3] Measurement of vital signs, including temperature, heart rate, blood pressure, respiratory rate, and oxygen saturation, is the first step. The respiratory pattern (e.g., muscle use, chest wall movement, pursed-lip breathing) and the degree of cyanosis should be assessed. The patient's level of anxiety, affect, mobility, respiratory effort, and use of supplemental oxygen are noted.

[edit] Respiratory.

Examination of the upper airway should rule out obstruction (e.g., nasal or pharyngeal obstruction, neck mass, stridor). Similarly, the patient should be examined for chest wall deformities (e.g., kyphoscoliosis, pectus excavatam, increased anteroposterior diameter, traumatic injury)

that may affect ventilation. Percussion of the back may reveal hyperinflation (low-lying diaphragm with minimal expansion), whereas dullness to percussion of the lung fields suggests pleural disease or parenchymal consolidation. Auscultation helps assess the focality of any pulmonary process and the volume of air movement. Rales, the short high-pitched sounds that result from the rapid opening of collapsed alveoli, may indicate interstitial lung disease, pneumonia, or CHF. Whispered pectoriloquy and egophony suggest consolidation. Rhonchi, the result of turbulent flow in large airways, often indicate increased mucus production associated with such disorders as chronic bronchitis. Although classically associated with diseases such as asthma and COPD, wheezing may also indicate LV dysfunction.

[edit] Cardiac.

Auscultation of the heart may reveal murmurs, rhythm disturbances, or evidence of reduced LV compliance or overload (S₄ and S₃, respectively). Palpation of the precordium should identify both the point of maximum impulse (PMI) and abnormalities of cardiac impulses that suggest right ventricular (RV) or LV dysfunction (e.g., RV heave, pulmonary artery tap, and loud pulmonic component of S₂ suggesting pulmonary hypertension; diffuse, laterally displaced PMI suggesting LV dilation). Examination of peripheral and carotid pulses may reveal vascular disease or suggest valvular abnormalities, dysrhythmia, shunt, or heart failure. Jugular venous distention suggests right-sided or left-sided heart failure, pericardial disease, or restrictive heart disease.

[edit] Additional Findings.

Other findings that suggest an etiology for dyspnea include abnormalities in the neck, abdomen, and extremities. A large goiter with a bruit suggests hyperthyroidism. Tense ascites may limit movement of the diaphragm and, along with hepatomegaly and peripheral edema, may suggest right-sided heart failure. Painful unilateral limb swelling should prompt evaluation for deep venous thrombosis and pulmonary embolus. Examination of the nail beds may reveal signs of decreased perfusion, cyanosis, or even clubbing. Since anemia may both mask significant hypoxemia and produce significant dyspnea, pallor is also important to note.

[edit] Acute Dyspnea.

The differential diagnosis of acute dyspnea includes hyperventilation secondary to anxiety, bronchospasm, pulmonary edema, pulmonary embolism, and pleural/chest wall injury (e.g., rib fracture, hemothorax/pneumothorax, pulmonary contusion).^[4] Pneumonia, pleural effusion, fibrosing lung disease, and toxic inhalation can also produce rapidly progressive dyspnea. When confronted with the patient with acute dyspnea, the evaluation should include a focused history and examination with chest radiograph, electrocardiogram (ECG), and arterial blood gases (ABGs). Patients with severe or rapidly progressive dyspnea should be treated according to the American Heart Association Advanced Cardiac Life Support (ACLS) protocol for acute dyspnea. Acute hyperventilation occurs as both a primary manifestation of anxiety and an appropriate response to cardiorespiratory pathology. The evaluation of an initial episode of acute dyspnea should usually occur in a monitored setting (e.g., emergency department).

[edit] Medications.

A broad array of medications may trigger anaphylaxis, but the list of drugs that typically produce isolated dyspnea is limited. β-Blockers, adenosine, nonsteroidal antiinflammatory drugs (NSAIDs), and aspirin may trigger wheezing in patients predisposed to bronchospasm. Amiodarone, a commonly used antidysrhythmic, can produce a dose-related interstitial lung disease. Many chemotherapeutic agents produce pulmonary toxicity; bleomycin is the most common offender, but cyclophosphamide, chlorambucil, melphalan, nitrosoureas, and methotrexate all can produce lung disease. The effects of these agents are often magnified when administered with radiation therapy.

[edit] Basic Diagnostic Testing.

Data collected in the history, physical examination, and basic laboratory evaluation may allow the physician to categorize the patient's shortness of breath as either cardiovascular or respiratory. Recognizing that some individuals experience a multifactorial dyspnea, this division allows the physician to focus further evaluation and to limit unnecessary testing.

Desaturation while performing limited exercise, such as walking down the office hall, suggests severely limited respiratory reserve and should prompt aggressive evaluation and treatment. If acute in onset or rapidly progressive, such a workup is often best accomplished in the hospital. Dyspnea secondary to anemia is rare when the hemoglobin is more than 10 gm/dl. Indirect measurement of hemoglobin saturation with a pulse oximeter is an important screening tool. Its utility is limited, however, because it is an insensitive tool for detecting subtle changes in arterial oxygenation. In cases of unexplained dyspnea, it is important to calculate the alveolar-arterial gradient using the alveolar gas equation. ABGs identify patients with COPD who retain carbon dioxide and those with significant acidosis.

Radiographic examination should assess abnormalities of the ribs and chest wall, large airways, lung parenchyma, pulmonary vasculature, pleura, diaphragm, and cardiac silhouette. If possible, previous films should be examined to assess for interval change. ECG analysis demonstrates abnormalities of cardiac rhythm, evidence of ischemia or past injury, and abnormalities of voltage that suggest ventricular hypertrophy or pericardial disease. Again, a review of previous tracings can provide insight into a patient's changing cardiorespiratory status. Simple office spirometry evaluates basic flow rates (FEV₁) and forced vital capacity (FVC) and can document obstructive lung disease when FEV₁/FVC is less than 70%. Full pulmonary function tests (PFTs), including measurement of the lung diffusing capacity for carbon monoxide (D_LCO), are necessary when spirometry is nondiagnostic.

[edit] Cardiovascular Dyspnea.

Dyspneic patients with chest pain, significant cardiac risk factors, or suggestive ECG changes should be evaluated for ischemic heart disease (see Chapter 63 ). The patient with a murmur or evidence of CHF should receive an echocardiogram to rule out heart failure, valvular disease, or pericardial disease (see Chapters 65 , 66 , and 68 ). Patients with documented CHF and either normal cardiac output or a dilated, diffusely hypokinetic left ventricle may require cardiac catheterization to define the etiology of their cardiomyopathy. Dyspnea secondary to intracardiac shunt may be confirmed with echocardiography (with or without agitated saline or “bubble study”) and cardiac catheterization. Shortness of breath secondary to dysrhythmia (arrhythmia) often requires correlation with symptoms during ambulatory monitoring (see Chapter 61 ).

[edit] Respiratory Dyspnea.

Dyspneic patients with or without chest pain and with nondiagnostic studies should be evaluated for pulmonary embolus using d-dimer, ventilation/perfusion scan, and pulmonary angiography (see Chapter 80 ). Upper airway obstruction is suggested by the contour of the flow volume loop seen during PFTs and can be confirmed by high-resolution computed tomography (HRCT) of the chest and bronchoscopy. Chest wall abnormalities are generally apparent on examination and radiographs, and neuromuscular disease is characterized by decreased respiratory muscle forces and normal gas exchange/D_LCO. Pleural disease is often identified in the initial evaluation and confirmed with further imaging and thoracentesis (see Chapter 79 ). Both asthma and COPD are characterized by wheezing, hyperinflation, and an obstructive pattern on PFTs and can be distinguished by D_LCO and chest imaging (see Chapters 72 and 75 ). When bronchospasm is suspected but FEV₁ is normal, bronchial provocation testing (methacholine challenge) may establish the diagnosis. Pneumonia is suggested by cough, fever, and sputum production and is confirmed by microbiologic evaluation and imaging (see Chapter 73 ). Although patients with interstitial lung disease may have only subtle radiographic findings, PFTs demonstrate decreased FEV₁, FVC, and D_LCO. HRCT often reveals parenchymal or mediastinal abnormalities as well (see Chapter 76 ).

[edit] Unexplained Dyspnea.

When a dyspneic patient's initial evaluation does not suggest an etiology or produces inconsistent results, further evaluation is indicated. In studies of patients referred to pulmonary clinics for evaluation of unexplained dyspnea, occult bronchospasm is diagnosed most often.^[5] If not done previously, PFTs with bronchial provocation should be performed. In such referral populations, gastroesophageal reflux disease is another common cause of dyspnea, and some experts recommend an empiric trial of acid suppression with or without motility agents (see Chapter 24 ). If an etiology for a patient's dyspnea still has not emerged, referral to a pulmonologist for cardiopulmonary exercise testing (CPEX) is indicated. Such testing can both clarify a patient's functional status and assess the relative contribution of coexisting cardiovascular and respiratory disease.

After evaluation fails to disclose a convincing cardiac or respiratory etiology for a patient's dyspnea, psychiatric causes must be considered. Generalized anxiety disorder, panic attacks, obsessive-compulsive disorder, and hyperventilation syndromes all may produce significant dyspnea (see Chapter 49 ).

[edit] REFERENCES