Chronic Obstructive Pulmonary Disease: Clinical and Laboratory Manifestations, Pathophysiology, and Prognosis

Andrew L. Ries

Chronic obstructive pulmonary disease (COPD) typically appears later in life. Although characterized primarily by airway obstruction and reduced expiratory airflow, COPD is increasingly recognized as a systemic disease with significant extrapulmonary manifestations as well resulting from systemic inflammation.

Dyspnea is the hallmark symptom that brings the patient to medical attention and leads to a diagnosis. A careful history of the insidious onset of breathlessness on exertion, with or without a history of cough, sputum, or frequent lung infections, often provides the clue to diagnosis.

Because of the slow, progressive course of disease and the large reserve in lung function, a long preclinical period typically elapses during which the person who has smoked for years “without a problem” begins to note breathlessness with physical activities previously accomplished without difficulty. This may be attributed to “getting older” or “being out of shape.” Reduced expiratory flow rates may be detected at this stage. Later, the patient may come to medical attention after a critical event, such as a winter cold from which recovery has been slow. Disease onset is often attributed to this time; in reality, however, this event just pushed the patient over the clinical edge of recognition, much like a rope weakened by progressive fraying breaks when only a small weight is attached.

Cough is a frequent symptom, often attributed as a “smoker’s cough” early in disease. It is usually productive; sputum is described as mucoid. Often, there is a history of frequent respiratory infections associated with increased cough, purulent sputum, and breathlessness. The patient may note that it takes longer than usual to recover from these infections.

Some patients with COPD develop abnormal gas exchange with hypoxemia or hypercapnia. Hypoxemia can be associated with cognitive or personality changes, polycythemia, and cyanosis. Chronic hypercapnia can cause headache, particularly on arising, and increased somnolence. During exercise, the arterial Po₂ may change significantly and unpredictably from the resting level. In many patients, the Pao₂ decreases with physical activity; in others, it does not change or may actually increase.

On physical examination, decreased maximal expiratory flow may be apparent even in early disease. Therefore, it is important to assess maximal expiratory flow in persons at high risk (e.g., smokers). In early disease, the examination may be normal, but later, prolonged expiration or wheezing can be detected on forced exhalation. This can be assessed easily with the forced expiratory time, a useful screening test for expiratory obstruction. In this maneuver, the patient exhales with maximal effort through an open mouth after a full inspiration. The examiner listens with the bell of the stethoscope over the trachea in the suprasternal notch and records the time in seconds until airflow ceases. Normal persons can exhale completely within 4 seconds. A forced expiratory time greater than 6 seconds signifies significant expiratory obstruction.

Other physical signs of COPD often are not present until the disease becomes moderate to severe. Overinflation of the lungs can result in an increased anteroposterior diameter of the thorax and a low, flat diaphragm with reduced respiratory excursion. The flattened diaphragm contributes less to inspiration, placing more burden on the accessory breathing muscles (neck and intercostals) and producing greater respiratory movement in the upper chest. With severe hyperinflation, the diaphragm can even become inverted and move paradoxically—up on inspiration, down on expiration. This can be detected best with the patient supine, noting the inward movement of the lower rib cage and abdomen during inspiration. With advanced emphysema, the breath sounds are diminished because of reduced flow and increased lung inflation. Signs of pulmonary hypertension and right-sided heart failure (e.g., peripheral edema and hepatic congestion) are not usually detected until an advanced stage of disease.

The central diagnostic feature of COPD is reduced expiratory airflow, resulting from increased airway resistance due to airway narrowing. Spirometry is the standard pulmonary function test for measuring maximal airflow and is relatively simple, reliable, and reproducible. It is useful for detecting airflow obstruction, staging severity, and following the disease course. A reduction in the forced expiratory volume in 1 second (FEV₁) in relation to the forced vital capacity (FVC)—the FEV₁:FVC ratio—is a standard measure of obstruction. The FEV₁ is the best measure of disease severity; it correlates with exercise tolerance and survival. Other measures of expiratory airflow can also be helpful.

Measures of lung volumes reveal hyperinflation with an increase in residual volume, functional residual capacity, and, sometimes, total lung capacity. These tests can help to confirm the diagnosis suggested from spirometry. Emphysema causes a greater increase in total lung capacity than other obstructive diseases, as well as a reduced carbon monoxide diffusing capacity (DLCO), primarily because of the loss of alveolar–capillary surface area. However, DLCO is neither specific nor sensitive for emphysema.

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