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  • History of cigarette smoking or other chronic inhalational exposure.

  • Chronic cough, dyspnea, and sputum production.

  • Rhonchi, decreased intensity of breath sounds, and prolonged expiration on physical examination.

  • Airflow limitation on pulmonary function testing that is not fully reversible and is most often progressive.


The Global Initiative for Chronic Obstructive Lung Disease (GOLD) defines COPD as a common, preventable, and treatable disease state characterized by persistent respiratory symptoms and airflow limitation due to airway and alveolar abnormalities usually caused by significant exposure to noxious particles or gases. Symptoms include cough, dyspnea, and sputum production. COPD is a major cause of chronic morbidity and mortality worldwide.

Most patients with COPD have features of both emphysema and chronic bronchitis. Chronic bronchitis is a clinical diagnosis defined by excessive secretion of bronchial mucus and is manifested by daily productive cough for 3 months or more in at least 2 consecutive years. Emphysema is a pathologic diagnosis that denotes abnormal permanent enlargement of air spaces distal to the terminal bronchiole, with destruction of alveolar walls and without obvious fibrosis. Both of these definitions are no longer included in GOLD because they comprise a minority of patients. Chronic respiratory symptoms also exist in people with normal spirometry, and a number of smokers without airflow limitation will have varying degrees of emphysema.

Cigarette smoking is by far the most important cause of COPD in North America and Western Europe. Nearly all smokers suffer an accelerated decline in lung function that is dose- and duration-dependent. One major study reported yearly decreases in FEV1 of 66.1 mL per year in men and 54.2 mL per year in women who continued to smoke, compared to 30.2 mL per year in men and 21.5 mL per year in women who sustained smoking cessation. Fifteen percent develop progressively disabling symptoms in their 40s and 50s. Approximately 80% of patients seen for COPD have significant exposure to tobacco smoke. The remaining 20% frequently have a combination of exposures to environmental tobacco smoke, occupational dusts and chemicals, and indoor air pollution from biomass fuel used for cooking and heating in poorly ventilated buildings. Outdoor air pollution, airway infection, environmental factors, and allergy have also been implicated in chronic bronchitis, and hereditary factors (most notably, deficiency of alpha-1-antiprotease [alpha-1-antitrypsin]) have been implicated in emphysema. Atopy and the tendency for bronchoconstriction to develop in response to nonspecific airway stimuli may be important risks. Evidence suggests that lung exposures to pollution and allergens early in life can lead to poor lung growth in childhood and expiratory airflow limitation, resulting in lower than predicted spirometric values in midlife. The pathogenesis of emphysema may involve excessive lysis of elastin and other structural proteins in the lung matrix by elastase and other proteases derived from lung neutrophils, macrophages, and mononuclear cells.


A. Symptoms and Signs


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