Hemodynamic compromise in pulmonary embolism: "A tale of two ventricles"

Abstract

In acute pulmonary embolism (PE), low cardiac output (CO)-hypotension results from disparate ventricular conditions: The left ventricle (LV) is under-filled and contracting vigorously, whereas the right ventricle (RV) is failing and dilated. The proximate cause of LV preload deprivation is thrombus-induced pulmonary vascular obstruction; abruptly increased pulmonary vascular resistance (PVR) induces acute RV systolic dysfunction which further compromises trans-pulmonary flow. "Escalation of Care" interventions (thrombolytics and aspiration thrombectomy) improve systemic hemodynamics by increasing LV preload delivery directly by reducing PVR and indirectly by relief of the strained failing RV.