CHF can cause dyspnea as pulmonary capillary pressure rises and fluid accumulates in the interstitium, leading to a fall in pulmonary compliance and a sense of difficulty in breathing. The earliest symptom is often dyspnea on exertion. More severe failure is manifested by orthopnea and finally paroxysmal nocturnal dyspnea. Basilar crackles (rales) and a third heart sound (S3) are important signs of left-sided heart failure and pulmonary venous hypertension; the S₃ is one of the most specific signs of CHF; a documented S₃ has been reported to have a positive likelihood ratio (LR+) for heart failure of 24 (see Chapter 2). Peripheral edema and jugular venous distention are common manifestations of right-sided heart failure, but these findings, particularly leg edema, are very nonspecific (see Chapter 22). Jugular venous distention has LR+ of 8.5. Contributing and precipitating factors include fever, acute ischemia, excessive dietary sodium intake, dysrhythmias, concurrent use of agents that are negatively inotropic (e.g., beta-blockers, disopyramide, verapamil), and poor compliance with medical regimen (see Chapter 32).

Community studies have demonstrated a high prevalence of preclinical CHF, including approximately equal numbers of people with diastolic dysfunction and systolic dysfunction. Besides CHF, a number of other causes of pulmonary venous hypertension result in increased pulmonary capillary pressure and dyspnea. Mitral stenosis is the most important.

Airway obstruction at any level of the respiratory tract can lead to difficulty breathing. Tracheal stenosis resulting from intrinsic disease or extrinsic compression is characterized by dyspnea in conjunction with stridor and inspiratory retraction of the supraclavicular space. Chronic obstructive pulmonary disease (see Chapter 47) is the leading cause of airway obstruction. Chronic bronchitis is a subcategory of COPD that is defined as cough and sputum production persisting for 3 months or more in 2 consecutive years. Characteristically, these patients have a long history of smoking, productive cough, and a slowly progressive decline in exercise capacity. In advanced stages, they may become plethoric and cyanotic and cough incessantly; the term “blue bloater” has been applied to such patients. Tobacco-stained fingers, wheezes, coarse rales, rhonchi, and a prolonged expiratory phase of respiration are often present on examination. Signs of cor pulmonale (right ventricular heave, jugular venous distention, leg edema) are late findings indicative of severe, advanced disease.

Another group of COPD patients are those with emphysema. Sputum production is minimal compared with that in patients with bronchitis, and mismatching of ventilation and perfusion is less pronounced; consequently, hypoxia and cyanosis are less prominent. Gradual deterioration in exercise capacity takes place over many years. Patients with advanced emphysema appear thin and barrel chested. They may purse their lips during expiration to keep their poorly supported airways from collapsing. The chest is hyperresonant, breath sounds are distant, and a few end-expiratory wheezes may be noted; expiration is prolonged.

Patients with COPD and bronchiectasis have a clinical presentation similar to that of patients with chronic bronchitis, except that their physical findings are more localized, the clinical course is punctuated by more frequent episodes of pneumonia, and their sputum tends to be more copious and sometimes bloody.

Asthma is another of the obstructive airway diseases. It usually produces attacks of acute dyspnea, but airway obstruction may persist for a prolonged period after an acute episode and result in more chronic respiratory complaints, including exercise intolerance, cough, and sputum production. At times, sputum production may be the predominant early symptom and mistaken for infection. Diffuse wheezes are commonly noted on examination; severe cases are characterized by the use of accessory muscles, retraction, and pulsus paradoxus. Exerciseinduced asthma is common in young people and may contribute to recurrent dyspneic episodes (see Chapter 48).

Diffuse interstitial lung disease alters pulmonary compliance and may lead to a disturbance in the balance between ventilation and perfusion. The process is usually very gradual, and often patients have few symptoms when pulmonary involvement is mild or even moderate; however, tachypnea and cyanosis ensue in severe cases. Diffuse, “dry” midexpiratory crackles are often heard on auscultation. As the interstitial process progresses, dyspnea and hypoxia worsen and exercise tolerance deteriorates (see Chapter 51).

Kyphoscoliosis is the major chest wall deformity capable of seriously impairing pulmonary musculoskeletal mechanics. Advanced cases can even terminate in cor pulmonale and respiratory failure. With the increase in prevalence of obesity in the United States, it has become one of the more common causes of dyspnea even in the absence of pulmonary disease. Other extrapulmonary conditions hindering lung mechanics are marked ascites (see Chapter 71) and large pleural effusions (see Chapter 43). Dyspnea is often the chief complaint in such patients.

Pulmonary hypertension is a serious cause of chronic dyspnea and has a poor prognosis. It may be primary or secondary and is characterized by a fixed elevation in pulmonary artery pressure and resultant strain on the right side of the heart. Common physical findings include an accentuated pulmonic component of S₂, a right ventricular S₃, the murmur of tricuspid regurgitation, and peripheral edema.

Secondary pulmonary hypertension occurs with conditions that chronically elevate pulmonary artery pressure, such as recurrent pulmonary embolization, chronic hypoxemia, pulmonary parenchymal disease, and left-sided heart failure. Some forms of secondary disease have subtle presentations and can easily be mistaken for primary disease. For example, pulmonary hypertension resulting from recurrent pulmonary embolization typically
occurs in patients with few symptoms of embolization. Except for recalling perhaps a single episode of pleuritic chest pain and acute dyspnea, most patients report few symptoms before the onset of pulmonary hypertension. In those with symptomatic, recurrent embolization, significant pulmonary hypertension rarely develops. The reason for this paradox is unclear. The source of emboli is believed to be the proximal deep veins of the legs.

Primary pulmonary hypertension is a diagnosis of exclusion. It occurs most commonly in women between the ages of 20 and 40 years. The mean age is about 35 years, and the ratio of women to men is 1.7:1. Dyspnea is the most frequently reported symptom, followed by fatigue, near-syncope, and Raynaud phenomenon. An immunologic basis for the condition is suspected because of the high frequency of antinuclear antibody seropositivity in many of these patients, especially women. Immunologically mediated endothelial damage is postulated. Hyperventilation may result and be mistakenly attributed to anxiety.

Anxiety attacks are often confused with more serious conditions because the patient may appear to be in severe respiratory distress. Patients often report chest tightness or claim that they cannot take in enough air. The florid, acute case is represented by the hyperventilation syndrome (see Chapter 226), but more common is a less dramatic, chronic feeling of dyspnea and fatigue that is affected little by exertion. Frequent sighing, multiple bodily complaints, nervousness, and normal physical examination findings are typical of such patients.

Patients with cardiopulmonary disease often limit their physical functioning, with the resulting sedentary state creating deconditioning and worsening the effects of dyspnea on exertion. Skeletal muscle atrophy is a common finding among patients with either COPD or CHF and has been linked to low-level systemic inflammation and oxidative stress. The muscle atrophy and sedentary behavior combine to create a vicious cycle of declining function in the setting of increasing dyspnea.