Physiological changes characteristic of the disease include mucus hypersecretion, ciliary dysfunction, airflow limitation, pulmonary hyperinflation, gas exchange abnormalities, pulmonary hypertension and cor pulmonale, and they usually develop in this order over the course of disease. Pulmonary hypertension develops late in the course of COPD. It is the major cardiovascular complication of COPD and is associated with a poor prognosis.

No drug treatment has been shown to alter the natural history of COPD. Smoking cessation is the only intervention that can arrest the rapid decline in lung function. Domiciliary oxygen therapy is the only other treatment known to improve prognosis in patients of COPD with hypoxemia.

The best guide to the progression of COPD is the change in FEV₁ over time. FEV₁ declines with normal ageing at about 30 ml/year and this increases to an average of 45 ml/year in smokers.⁸⁴ However, the individual susceptibility to cigarette smoking is very wide. Stopping smoking produces only small improvements in FEV₁, but the subsequent fall in FEV­₁ progressively slows to the nonsmoker rate of about 30 ml/year.

Depending of disease severity, the five-year mortality rate of patients with COPD varies from 40% to 70%.⁸⁵ The three major causes of death have been identified as COPD itself, lung cancer, and cardiovascular disease. The age and the degree of airways obstruction, as reflected by FEV₁, are the most commonly recognized prognostic factors.