In the COPD patient, routine pulmonary function tests depict the characteristic pattern of volume-dependent airway obstruction. Spirometry typically reveals a reduction in the FEV1/FVC ratio and an even greater relative decline in FEV, which may decrease between 25% and 75% of vital capacity (Table 1). As airflow obstruction worsens, a normal volume of gas can no longer be exhaled in the time available, and vital capacity declines. Measurement of lung volume consistently reveals an increased residual volume (RV) and a normal-to-increased functional residual capacity (FRC). The RV may be 2 to 4 times higher than normal, because as the expiratory airflow slows, gas becomes trapped in airways that close prematurely. The FRC may become increased by 2 mechanisms: dynamic hyperinflation and activation of inspiratory muscles during exhalation. Hyperinflation flattens the diaphragm, which increases the work of breathing, diminishes the capacity for exercise, and increases dyspnea. Hyperinflation becomes worse with exercise, causing dynamic hyperinflation, which adds to the load of inspiratory muscles.
As a result of these processes, tidal breathing may take place at lung volumes as high as 1 to 2 L above normal levels. In the patient who has significant airflow obstruction, an increased FRC provides the benefits of an enlarged airway diameter -- which provides greater radial support and thus less airway resistance -- and an increased driving pressure (ie, elastic recoil) required for exhalation. The cost to the patient of an increased FRC is the greater work of breathing incurred at the higher lung volume.
Abnormalities in Gas Exchange
It has long been recognized that the pattern of gas exchange abnormalities in COPD may differ greatly among patients with airflow obstruction of identical severity. Early in the course of disease, when expiratory flow is only slightly reduced, mild hypoxemia may be the only blood gas abnormality. However, in advanced stages of COPD, 2 distinct patterns emerge (Table 2).
Table 2. Clinical Findings in Emphysema and Chronic Bronchitis
|Dominant symptom||Dyspnea||Productive cough|
|Signs||Thin build; hyperinflated,
|Stocky build, wheezy,
right heart failure
|Chest radiograph||Normal or hyperinflation,
|Normal or only increased
|Arterial blood gas|
|PaO2||Slightly reduced||Markedly reduced|
|Spirometry||Decreased FEV1||Decreased FEV1|
|Total lung capacity||Increased||Normal or slightly
|Exercise||Severe desaturation||May improve|
DLCO = diffusing capacity of the lung for carbon monoxide; FEV1 = forced expiratory volume in 1 second; Pao2 = partial pressure of arterial oxygen; PaCO2 = partial pressure of arterial carbon dioxide
Two clinical patterns. Patients with the type A pattern have dyspnea and only mild-to-moderate hypoxemia (partial pressure of arterial oxygen[PaO2] is usually > 65 mm Hg). In addition, these patients maintain normal or even slightly reduced partial pressure of arterial carbon dioxide (PaCO2). These patients are sometimes referred to as pink puffers -- they tend to be thin, to experience hyperinflation at total lung capacity, and to be free of signs of right heart failure. The pink puffer usually has emphysema.
Patients with the type B pattern are characterized by marked hypoxemia and peripheral edema resulting from right heart failure. These patients, sometimes called blue bloaters, typically exhibit cough and sputum production. They have frequent respiratory tract infections, experience chronic carbon dioxide retention (PaCO2 > 45 mm Hg), and have recurrent episodes of cor pulmonale. Type B patients may have pathologic evidence of severe emphysema, as well as inflammation of large and small airways and possible defects in ventilatory control. These patients usually meet the criteria for chronic bronchitis.
Many patients have features of both clinical types, giving rise to either mixed or intermediate clinical presentations.
Differing effects on the cardiovascular system. The 2 clinical types also have very different consequences for the cardiovascular system. In the type B patient, both alveolar hypoxia and acidosis (secondary to chronic hypercapnia) stimulate pulmonary arterial vasoconstriction, and hypoxemia stimulates erythrocytosis. Increased pulmonary vascular resistance, increased pulmonary blood volume, and possibly increased blood viscosity from secondary erythrocytosis all contribute to pulmonary arterial hypertension. In response to long-term pulmonary hypertension, cor pulmonale generally develops: The right ventricle becomes hypertrophic, and increases in cardiac output are achieved by abnormally high filling pressure in the right ventricle. Additional hemodynamic loads may cause the right ventricle to fail, with the consequent development of systemic venous hypertension, which is manifested by jugular venous distention, peripheral edema, passive hepatic congestion, and sometimes ascites. It should be noted that, in the absence of left heart failure, pleural effusion is not a manifestation of cor pulmonale. In type B patients, echocardiographic evaluation of right heart function and estimation of pulmonary artery systolic pressure are useful in quantifying the degree of pulmonary hypertension.
The emphysematous lung destruction characteristic of type A patients leads to a restricted vascular bed because of the loss of pulmonary capillaries from the destroyed alveolar walls. This condition is reflected in the reduced diffusing capacity of the lung for carbon monoxide (DLCO) observed in type A (but not type B) patients. However, because PaO2 levels are only mildly depressed in type A patients, pulmonary vasoconstriction is minimal and secondary erythrocytosis does not develop. Cardiac output may be slightly reduced. As a result, pulmonary hypertension in type A patients is milder than that in type B patients, and cor pulmonale develops infrequently, usually only in the terminal phase of the illness.
Differing degrees of oxygen saturation on exertion. Differences in gas exchange during exercise also distinguish the 2 clinical types. Type A patients develop oxygen desaturation during exercise, whereas type B patients may exhibit increases in oxygen saturation during exercise.
Medscape Internal Medicine © 2009 Medscape, LLC
Cite this: Gerald W. Staton. Chronic Obstructive Pulmonary Disease - Medscape - Sep 01, 2009.