[Hemodynamics and gas exchange in acute lung embolism]

The main hemodynamic consequence of pulmonary embolism is the acute mechanical reduction of the pulmonary vascular cross-sectional area. This results in a sudden increase of the pulmonary vascular resistance, and if the cardiac output is to be maintained, in an increase in pulmonary artery pressure and right ventricular work. The extent of hemodynamic changes in pulmonary embolism are determined primarily by the size of the emboli and whether or not the patient has underlying cardiopulmonary disease. Although humoral factors and neural reflexes play a role in determining the severity of hemodynamic responses to pulmonary embolism in experimental animals, their role in patients is uncertain. In patients free of preembolic cardiopulmonary disease, the extent of embolic obstruction can be related directly to the mean pulmonary artery pressure. Accordingly, either the extent of obstruction or the mean pulmonary artery pressure may be used as a measure of right ventricular afterload. Obstruction of 25 to 40% leads to an increase in mean pulmonary artery pressure of 20 to 30 mm Hg, massive obstruction over 75% to a pressure of 40 to 45 mm Hg. Continuous hemodynamic monitoring helps to estimate the speed of the resolution of emboli and to a certain extent the adequacy of treatment. Right arterial pressure is consistently elevated by a mean pulmonary artery pressure over 30 mm Hg and provides also a rough estimate of the degree of pulmonary vascular obstruction. A previously normal right ventricle will dilate at a mean pulmonary artery pressure of 40 to 45 mm Hg. which may result in acute tricuspid insufficiency.(ABSTRACT TRUNCATED AT 250 WORDS)