- Definition
- Causes
- Respiratory System Dyspnea
- Cardiovascular System Dyspnea
- Dyspnea with Normal Respiratory and Cardiovascular Systems
- Pulmonary Edema
Dyspnea, a subjective experience of uncomfortable breathing, is a symptom that typically results from cardiac, pulmonary, and neurologic etiologies that cause an increased drive to breathe, increased work of breathing, and/or stimulation of specific receptors in the heart, lungs, or vasculature. Assessment begins by determining the quality and intensity of the discomfort. Chronic dyspnea is typically defined as symptoms lasting >1 month.
- Airway disease:Asthma and chronic obstructive pulmonary disorder (COPD) are common causes of dyspnea associated with increased work of breathing. Bronchospasm can cause chest tightness and hyperventilation. Hypoxemia and hypercapnia can result from ventilation-perfusion mismatch.
- Chest wall disorders: Chest wall stiffness (e.g., kyphoscoliosis) and neuromuscular weakness (e.g., myasthenia gravis) cause increased work of breathing.
- Lung parenchymal disorders: Interstitial lung diseases (Chap. 136 Interstitial Lung Disease) cause reduced lung compliance and increased work of breathing. Ventilation-perfusion mismatch and pulmonary fibrosis may lead to hypoxemia. Stimulation of lung receptors can cause hyperventilation.
- Left heart disorders: Elevations of left-ventricular end-diastolic and pulmonary capillary wedge pressures lead to dyspnea related to stimulation of pulmonary receptors and hypoxemia from ventilation-perfusion mismatch. Coronary artery disease and cardiomyopathy are examples of diseases affecting left heart function.
- Pulmonary vascular disorders: Pulmonary emboli, primary pulmonary arterial hypertension, and pulmonary vasculitis stimulate pulmonary receptors via increased pulmonary artery pressures. Hyperventilation and hypoxemia also may contribute to dyspnea.
- Pericardial diseases: Constrictive pericarditis and pericardial tamponade cause increased intracardiac and pulmonary arterial pressures, leading to dyspnea.
Dyspnea with Normal Respiratory and Cardiovascular Systems 
Anemia can cause dyspnea, especially with exertion. Obesity is associated with dyspnea due to high cardiac output and impaired ventilatory function. Deconditioning and anxiety may also cause dyspnea in pts with normal respiratory and cardiovascular systems.
| APPROACH TO THE PATIENT | ||
DyspneaHistory: Obtain description of discomfort, including the impact of position, infections, and environmental exposures (Fig. 35-1. Algorithm for the Evaluation of the Pt with Dyspnea). Orthopnea is commonly observed in CHF. Nocturnal dyspnea is seen in CHF and asthma. Acute intermittent dyspnea suggests myocardial ischemia, asthma, or pulmonary embolism. Physical examination: Assess increased work of breathing indicated by accessory ventilatory muscle use or supraclavicular retractions. Determine if chest movement is symmetric. Use percussion (dullness or hyperresonance) and auscultation (decreased or adventitious breath sounds) to assess the lungs. Cardiac examination should note jugular venous distention, heart murmurs, and S3 or S4 gallops. Clubbing can relate to interstitial lung disease or lung cancer. To evaluate exertional dyspnea, reproduce the dyspnea with observation while assessing pulse oximetry. Radiographic studies: Chest radiograph should be obtained as initial evaluation. Chest CT can be used subsequently to assess lung parenchyma (e.g., emphysema or interstitial lung disease) and pulmonary embolism. Laboratory studies: Hematocrit should be assessed for anemia, and a basic metabolic panel (for metabolic acidosis) and brain natriuretic peptide should be considered. ECG should be obtained; echocardiography can assess left ventricular dysfunction, pulmonary hypertension, and valvular disease. Pulmonary function tests to consider include spirometry, lung volumes, diffusing capacity, and tests of neuromuscular function. Methacholine challenge testing can assess for asthma in subjects with normal spirometry. Cardiac stress testing can be performed to assess for coronary artery ischemia, while cardiopulmonary exercise testing can determine whether pulmonary or cardiac disease limits exercise capacity. |
| TREATMENT | ||
DyspneaIdeally, treatment involves correcting the underlying problem that caused dyspnea. Supplemental oxygen is required for significant oxygen desaturation at rest, during sleep, or with exertion. Pulmonary rehabilitation is helpful to improve exercise tolerance in COPD. |
Cardiogenic pulmonary edema results from cardiac abnormalities that cause increased pulmonary venous pressure leading to interstitial edema; with greater pressures, alveolar edema and pleural effusions develop. Symptoms include exertional dyspnea and orthopnea. Physical examination can reveal S3 gallop, elevated jugular venous pressure, and peripheral edema. Chest radiographs show prominent vascular markings in the upper lung zones. CXRs demonstrate perihilar alveolar opacities progressing to diffuse parenchymal abnormalities as pulmonary edema worsens.
Noncardiogenic pulmonary edema results from damage to the pulmonary capillary lining. Hypoxemia relates to intrapulmonary shunt; decreased pulmonary compliance is observed. Clinical impact can range from mild dyspnea to severe respiratory failure. Normal intracardiac pressures are typically observed. Etiologies may be direct injury (e.g., aspiration, smoke inhalation, pneumonia, oxygen toxicity, or chest trauma), indirect injury (e.g., sepsis, pancreatitis, and transfusion-related acute lung injury), or pulmonary vascular (e.g., high altitude and neurogenic pulmonary edema). Chest radiograph typically shows normal heart size and diffuse alveolar infiltrates; pleural effusions are atypical. Hypoxemia in noncardiogenic pulmonary edema often requires treatment with high concentrations of oxygen.