PE increases the right ventricular (RV) afterload, resulting in an increase in the RV end-diastolic volume (EDV). The increase in RVEDV adversely affects left ventricular hemodynamics through ventricular interdependence. Specifically, the interventricular septum bows into the left ventricle (LV) and impairs diastolic filling, resulting in decreased LV preload and subsequently diminished cardiac output and hypotension. These physiologic phenomenon are manifested by respiratory
distress, hypoxia, and decreased cardiac output with signs of shock.