![]() 4), decreased left ventricle output, and therefore decreased supply to the coronary arteries (2) right ventricular intramuscular pressure increases, straightening normal muscular folds, impeding coronary blood flow in the right heart wall (Fig. With acute increases in afterload, the compliant right ventricle cannot unload sufficiently and dilates which gives rise to three important outcomes: (1) the dilated RV pushes the interventricular septum toward the left ventricle, impinging on the left ventricle, resulting in underfilling of the left ventricle (Fig. When there are acute incremental increases in afterload, there are drastic decreases in stroke volume, or forward flow of blood (Fig. In chronic thromboembolic pulmonary hypertension (CTEPH), RV dilatation and wall hypertrophy increase oxygen demand to which the coronary artery blood flow cannot meet, resulting in ischemia, necrosis, and fibrosis of the RV wall.īecause the right ventricle is thin-walled and compliant, it is ill-equipped for acute increases in afterload compared to the muscular thick-walled noncompliant left ventricle. ![]() Patients with submassive PE are systemically normotensive with evidence of myocardial dysfunction and ischemia. Massive pulmonary embolus (PE) is defined as PE with sustained hypotension (systolic BP < 90 for at least 15 min), need for inotropic support, or persistent bradycardia (HR < 40 bpm with signs or symptoms of shock). With increases in afterload, the right ventricle cannot unload sufficiently resulting in dilatation of the compliant right ventricle, impinging on the left ventricle resulting in decreased left ventricle output and supply to the coronary arteries. The right ventricle (RV) as part of a low-pressure system with a low-resistance afterload (the pulmonary artery) is thin-walled, compliant, and crescent-shaped. The anatomic construct of the right heart is suitable for its task. We review here the pathophysiology of right ventricular (RV) failure in acute massive and submassive PE and CTEPH. It is important to understand the pathophysiology of these diseases as it provides the rationale for therapeutic intervention by the Interventional Radiologist. The purpose of this educational manuscript is to instruct on the pathophysiology of RV failure in massive and submassive PE and CTEPH. Increases in afterload from acute massive and submassive PE and CTEPH may markedly compromise the RV function leading to hemodynamic collapse and death. The right ventricle (RV) is constructed to accommodate a low-resistance afterload. About 45% of patients with acute PE will have acute right ventricular failure, and up to 3.8% of patients will develop chronic thromboembolic pulmonary hypertension (CTEPH) with progressive, severe, chronic heart failure. ![]() Pulmonary embolus (PE) is the third most common cause of cardiovascular death with more than 600,000 cases occurring in the USA per year. ![]()
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