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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 (AUDIO 9–4) (AUDIO 9–11).

  • Airflow limitation on pulmonary function testing that is not fully reversible and is most often progressive (eFigure 9–1).

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Audio 09–11. Breath sound from a patient with severe long-term chronic obstructive lung disease.

The patient was in respiratory distress because of a cyst on his larynx, causing stridor. The stridor can be distinguished by the inspiratory extenuation of the higher-pitched continuous noise. (Reproduced, with permission, from Self-Assessment on Sounds of the Chest, narrated by Raymond Murphy, Jr., MD [vinyl record distributed by ACCP at 43rd Annual Scientific Assembly, Las Vegas, 1977].)

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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. The term “COPD” has evolved from an umbrella term for chronic bronchitis and emphysema to one that refers to a clinical syndrome of chronic respiratory symptoms, structural pulmonary abnormalities (airways or alveoli), and impaired lung function arising from multiple causes that result in airflow limitation that is not fully reversible. Symptoms include cough, dyspnea, and sputum production. COPD is a major cause of chronic morbidity and is the third leading cause of death worldwide.

The most important causes of COPD are cigarette smoking in the developed world and biomass fuel cooking in the developing world. The majority of smokers suffer an accelerated decline in lung function that is dose- and duration-dependent. One major study of active smokers reported yearly decreases in FEV1 of 66 mL per year in men and 54 mL per year in women compared to 30 mL per year in men and 22 mL per year in women who sustained smoking cessation. Fifteen percent of smokers develop progressively disabling symptoms in their 40s and 50s. Approximately two-thirds of patients seen for COPD have significant exposure to tobacco smoke. The remaining one-third may 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, along with hereditary factors (most notably, deficiency of alpha-1-antiprotease [alpha-1-antitrypsin]). Atopy and bronchoconstriction in response to nonspecific airway stimuli may be important risk factors. There is evidence 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.


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