COPD Pathophys

COPD Pathophys - chial walls are thickened, and bronchial...

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Pathophysiology Despite known causative factors, such as cigarette smoking and occupational exposure, the de- termination of clinical onset and progression toward patterns related to emphysema or chronic bronchitis remains uncertain. The central element in the pathophysiology of chronic airflow ob- struction is increased resistance or decreased caliber in the small bronchi or bronchioles which leads to impedance in airflow. Airway secretions, mucosal edema, bronchospasm, and bron- choconstriction or a combination may lead to airflow obstruction. Increased airway resistance re- duces total minute ventilation or increases respiratory work. Hypoxemia and hypercapnia result from alveolar hypoventilation or ventilation-perfusion mismatching. Chronic bronchitis is defined by presence of cough and sputum production due to over-secretion or mucus and inflammation caused by irritation of the airways. Ciliary function is reduced, bron-
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Unformatted text preview: chial walls are thickened, and bronchial lumen narrows. Therefore, leading to mucus plugs in the airways. Damage to the alveoli adjacent to bronchioles occurs resulting in altered function of al-veolar macrophages. This causes an increased susceptibility to respiratory infection. In emphysema, impaired gas oxygen and carbon dioxide exchange is the result from distention of air spaces beyond terminal bronchioles and destruction of alveoli. The walls of the alveoli are destroyed leading to a decrease in direct contact with pulmonary capillaries, causing an increase in dead space and impaired oxygen diffusion. As a result, hypoxemia occurs. In the later stages, carbon dioxide elimination is impaired which results in respiratory acidosis. Further damage to alveolar walls leads to an increase in pulmonary blood pressure leading to right sided heart fail-ure....
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