Chronic Obstructive Pulmonary Disease (COPD)

Overview

Chronic Obstructive Pulmonary Disease (COPD) is a disease entity that results in long-term irreversible changes in pulmonary function that follow a pattern of obstructive lung disease. The two prototypical pathologies that result in COPD are emphysema and chronic bronchitis which typically co-exist within a single patient. We discuss the etiologies and morphologies of emphysema and chronic bronchitis on their own pages; however, we detail common themes of pathogenesis and clinical manifestation of COPD below, given the fact that most patients display combined features of emphysema and chronic bronchitis.

Pathogenesis

The primary defect in pulmonary function in those with COPD is an irreversible obstruction to airflow which increases airflow resistance. As discussed in their respective pages, the source of this increased resistance is different for emphysema and chronic bronchitis. The obstruction in emphysema occurs dynamically during expiration and results from a reduction in the lung's elastic recoil that decreases traction on the airways during air outflow. The obstruction in chronic bronchitis is due to narrowing of the airways by secretions of respiratory glands and goblet cells. Importantly, obstruction in COPD is irreversible and does not improve significantly with bronchodilators, thus distinguishing this disease process from that of asthma.

The increased airflow resistance observed in patients with COPD will result in a decrease in their Forced Expiratory Volume/Forced Vital Capacity ratio (FEV/FVC) as is common for any obstructive lung disease. At a late stage, the widespread obstruction to airflow can result in trapping of air within the lung and progressive expansion of the total lung capacity, known as hyperinflation. Hyperinflation is more severe in those with a significant component of emphysema because the reduced elastic recoil of the lung in these patients results in a much higher lung compliance and thus less resistance to higher lung volumes. Hyperinflation of the lung pushes the chest wall outward and the diaphragm downward, often rendering inspiration more difficult as their is less distance for these structures to move for air intake. Outward movement of the chest wall can often be observed clinically as a "Barrel-shaped" chest while downward movement of the diaphragm can be seen as a flattening of this structure of chest radiography.

With disease progression, patients with COPD show gradual development of pulmonary hypertension likely due to increased pulmonary Vvascular resistance. The rise in vascular resistance is likely multi-factorial but may be caused by destruction of pulmonary capillaries from emphysematous changes as well as hypoxic vasoconstriction in poorly-ventilated areas. The rise in pulmonary vascular resistance may also be exacerbated by increased blood viscosity from polycythemia, often observed in COPD patients due to chronic hypoxemia. Whatever the case, chronic and progressive pulmonary hypertension in COPD patients may eventually yield right heart failure.

The pathological changes of COPD result in profound ventilation-perfusion defects in the lung. Although the arterial oxygen tension may be normal or near normal early in the disease, with progression hypoxemia often develops. At late stages in the disease patients may begin to display hypercapnia possibly due to hypoventilation as respiratory muscles become exhausted given chronic airway obstruction and lung hyperinflation.

Clinical Consequences

COPD clinically manifests within a wide spectrum whose ends are often characterized by two classic clinical presentations known as the "Pink Puffer" and the "Blue Bloater". Historically, it had been thought that these extremes corresponded to patients whose disease was either dominated by emphysema (Pink Puffer) or chronic bronchitis (Blue Bloater); however, more thorough studies have shown that such a notion is over-simplified. Regardless, the Pink Puffer and Blue Bloater are useful examples of the COPD clinical syndrome although one must keep in mind that an individual patient may display features of both manifestations.

These patients display progressive dyspnea and weight loss with little in the way of a productive cough. Hyperinflation of the lungs often to a barrel-shaped chest with quiet breath sounds and hunching over during expiration to help force air out of their lungs. Individuals may also purse their lips during expiration, which increases pressure within the lungs and thus reduces airways collapse, thus facilitating outward airflow (See "Expiration" section of Airflow Resistance). The term pink-puffer originates from the fact that these patients typically display adequate oxygenation which is maintained through hyperventilate.

These patients also display progressive dyspnea although weight loss tends to be less prominent. Most characteristically, individuals will complain of a long history of progressively worsening productive cough. At presentation, rales and rhonchi will be heard over lung fields whereas hyperinflation will not be prominent. The term blue bloater originates from the fact that these patients often display reduced respiratory drive which results in more prominent hypoxemia that can manifest as frank cyanosis. Patients are also frequently hypercapnic. Finally, for cryptic reasons, these individuals tend to be more prone to right heart failure, thus leading to increased jugular venous pressures and peripheral edema.

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