Ventilation-perfusion abnormalities in experimental pulmonary embolism.

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Abstract
After experimental pulmonary thromboembolism due to autogenous thrombi there is a redistribution of ventilation away from nonperfused to perfused lung segments. This airshift is not of sufficient magnitude to prevent an increase in alveolar dead space and significant arterial-alveolar carbon dioxide tension difference. The airshift cannot be explained on the basis of the measured mechanical changes that follow autogenous thromboembolism. Arterial hypoxemia was observed only in the presence of massive thromboembolism. One important mechanism is right-to-left shunting. A small decrease in diffusing capacity for carbon monoxide was observed after thromboembolism, which did not account for the degree of hypoxemia observed. Not all pulmonary thromboemboli result in complete cessation of blood flow to the involved lung segment. Acute thromboembolism as produced in these studies does not lead to any ultrastructural change in the lung for periods up to 3 hours.