Abstract

Chronic obstructive pulmonary disease (COPD) is an entity which causes progressive and largely irreversible chronic obstruction. It is caused mainly by smoking, but only 15-20% of regular smokers develob COPD. Tobacco smoke causes an inflammatory response of the central and peripheral airways, and lung parenchyma. This promote neutrophil accumulation in the lung. In addition to this, increased numbers of CD8+ T-cells are present in the airways and lung parenchyma in smokers with COPD. Peribronchiolar inflammation and fibrosis in small airways result in structural narrowing of the lumen, and hence, in air flow limitation. Neutrophil-mediated tissue damage leads to the loss of pulmonary elastic recoil. This results both in decreased pressure to drive expiratory flow, and also in decreased intraluminal pressure to maintain airway patency during forced expiration. Unevenly distributed airway narrowing and emphysema in COPD induce inequalities in V/Q ratios leading to arterial hypoxemia. Lung hyperinflation results in respiratory muscle weakness and reduced ability of diaphragm to generate tension. Consequent alveolar hypoventilation is the cause of hypercapnia. Airflow obstruction is best assessed by FEV1 and FEV1/VC ratio. The obstructive ventilatory defect is associated with a progressive increase in static lung volumes (RV/TLC >40%). Due to the loss of capillary bed and enlargement of the air space in emphysema, diffusion capacity is reduced.