Clinical significance of pulmonary function tests. Pulmonary function after uncomplicated myocardial infarction.
Derangement of pulmonary function following myocardial infarction is related to the severity of hemodynamic dysfunction. Abnormalities of pulmonary function appear even in patients without clinical or radiologic evidence of congestive failure. There is a reduction in vital capacity and rates of air flow. There is evidence for dysfunction of "small airways" and diminished ventilation to dependent parts of the lung. Total lung capacity may be normal or reduced, and residual volume may be increased slightly in uncomplicated myocardial infarction. Residual volume falls with more pronounced pulmonary congestion and edema. Distribution of pulmonary perfusion is altered after myocardial infarction, with a shift of perfusion away from the dependent parts of the lung (bases) towards the apices. Pulmonary gas exchange is impaired, with hypoxemia (due to both ventilation-perfusion inequality and increased shunting); and the diffusing capacity for carbon monoxide is diminished. Dead space is increased. The basic pathophysiologic mechanism responsible for abnormalities of pulmonary function is increased pulmonary water, which may be very minimal with uncomplicated myocardial infarction and stay primarily in the pulmonary interstitial space, but becomes progressively more severe with eventual alveolar flooding and marked impairment of pulmonary function.
D006801:Humans; D008168:Lung / Q000000981:diagnostic imaging; D008176:Lung Volume Measurements; D009203:Myocardial Infarction / Q000503:physiopathology*; D010366:Peak Expiratory Flow Rate; D011654:Pulmonary Edema / Q000209:etiology; D011859:Radiography; D012129:Respiratory Function Tests; D014692:Ventilation-Perfusion Ratio