Acute right heart failure. Etiology--pathophysiology--diagnosis--therapy

Abstract

Impaired right ventricular (RV) function may be caused by pulmonary hypertension or myocardial ischemia. It is characterized by a dilation of the RV, which is followed by an increase of wall tension and O2-consumption and a decrease of RV ejection fraction (RV 'dysfunction'). If a drop of arterial pressure occurs this my precipitate RV failure and shock (RV 'insufficiency'). Diagnosis of RV failure and monitoring of RV function is difficult. Sometimes, even a severe impairment of RV function goes undetected or is misinterpreted. Patients in the operating room or on intensive care units seem to be especially prone to RV dysfunction and failure. Since a causative therapy often is not readily available, adequate symptomatic therapy is of utmost importance. Four basic principles have to be considered: 1) Optimizing preload: The failing RV requires adequate filling for preservation of stroke volume. On the other hand, overdistension of the RV may result in RV ischemia, thereby further deteriorating RV function Hence, volume loading is important, but requires continuous monitoring. 2) Maintenance of aortic pressure: Vasopressors are indicated if there is a critical drop of coronary perfusion pressure. Norepinephrine presently is the drug of choice for this purpose. 3) Reduction of RV afterload: Whereas intravenous vasodilators are limited in their efficacy in dilating pulmonary vessels due to systemic side effects, inhaled vasodilators result in selective pulmonary vasodilation and may improve RV function. 4) Increase of RV contractility: In RV failure and shock, norepinephrine and epinephrine are the drugs of choice. Inodilators are well suited for reducing pulmonary vascular resistance due to their positive inotropic and vasodilating effects. Since systemic vasodilation may occur, these drugs must only be used in hemodynamically stable patients.