ABSTRACT
The hemodynamic results of acute emboli are a reduction in the cross-sectional area of the pulmonary circulation resulting in increased resistance to blood flow through the lungs. Physiologically, PE increases right ventricular work or afterload, best measured by assessing mean pulmonary artery pressure or calculating pulmonary vascular resistance with a pulmonary artery catheter. This increase in mean pulmonary artery pressure is directly related to the extent of embolization. In the absence of pre-existing underlying cardiopulmonary disease, patients with emboli have marked levels of pulmonary hypertension when at least 50% of pulmonary vasculature is occluded. Mean pulmonary artery pressure begins to rise at 25% obstruction of the vascular tree, and continues to rise with increased degrees of obstruction to reach a maximum value of about 40 mmHg in the absence of preexisting pulmonary hypertension. Normally, the RV being a thin-walled chamber cannot accommodate high pulmonary artery pressures (PAP) and increased RV work. Therefore, it predisposes to rapid contractile failure. Right ventricular dysfunction becomes even more apparent when there is an elevation in the mean right atrial pressure. It is usually associated with a mean PAP of 30 mmHg and obstruction of at least 35-40% of the pulmonary vascular tree. As right atrial pressure increases concomitantly with PAP, an initial compensatory cardio-vascular response is an increase in heart rate to maintain cardiac output. When the right atrial pressure rises by 10 mmHg and mean PAP is greater than 30-40 mmHg, right ventricular failure occurs and cardiac output will decrease.
