The pathophysiologic effects of PE are caused both by mechanical obstruction of the pulmonary arterial system and by the release of vaso- and bronchoactive mediators. Mechanical obstruction produces the clinical picture of acute cor pulmonale. The trigger for the release of chemical mediators is platelet degranulation in the lung. These mediators—prostaglandins, catecholamines, serotonin, and histamine—cause bronchoconstriction as well as pulmonary artery vasoconstriction. This results in an overall reduction in lung compliance. Vasoconstriction is the predominant effect, leading to a ventilation/perfusion ( ) mismatch. Vasoconstriction may be severe enough to cause pulmonary hemorrhage or infarct, producing an infiltrate on the chest radiograph. The infiltrate of pulmonary hemorrhage usually resolves in 1 to 2 weeks, while that of infarct may take months to disappear.5
PE tend to be multiple and bilateral, with the right lower lobe of the lung being the most commonly involved lung segment. Angiographic evidence of PE generally resolves in 1 to 4 weeks and pulmonary artery (PA) pressure usually normalizes within a month. If the PE fails to resolve, chronic cor pulmonale may occur.
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