PE may cause hemodynamic alterations to varying degrees. When less than 20% of the pulmonary vascular bed is occluded by thromboemboli, patients without pre­existing cardiopulmonary disease are able to elicit compensatory mechanisms to support near-normal hemodynamics [101]. PE-induced hypoxemia causes neuro­hormonal activation of thromboxane A2 and serotonin, leading to initial vasocon­striction and increased PVR. When 30–40% of the pulmonary bed is occluded, PAP increases, and the RV adapts by increasing the stroke volume to maintain cardiac output (CO). This compensatory mechanism temporarily improves ow through the obstructed pulmonary vascular bed and stabilizes systemic blood pressure. However, the effect is short-lived as the thin-walled RV cannot generate a consistent mean PAP >40mmHg. When pulmonary obstruction exceeds 50–60%, or when the com­pensatory mechanism is overwhelmed, drastic cardiovascular collapse can ensue. The increase in PVR leads to RV dilation, increased RV wall tension, and attening of the interventricular septum, which alter the contractility of the myocardium. Ultimately, abrupt RV failure and desynchronization of the ventricles result in LV lling impedance, reduction in CO, and hemodynamic instability [101]. RV failure is attributed as the main cause of death in severe PE [59]. Patients with preexisting cardiopulmonary disease may have an exaggerated response to smaller degrees of pulmonary vascular occlusion, leading to severe pulmonary hypertension dispro­portionate to the degree of obstruction from acute PE [101].