Acute right ventricular failure, pathophysiology and treatment

Abstract

Right ventricular (RV) failure is now accepted as a pathophysiological entity. This acceptance has stemmed from the increasing facility of bedside assessment of pump function using thermodilution techniques. The subsequent improvement in the assessment of RV volume changes has allowed existing theories to be confirmed. The anatomical disposition and geometry of the right ventricle allow it to adapt very well to wide variations in preload, but poorly to increases in afterload. In the presence of increased afterload, RV stroke volume decreases linearly with increasing resistance and the ventricle eventually dilates. This dilation is then responsible for further RV failure, due to decreased right coronary artery flow (from systolo-diastolic to diastolic only) at a time when myocardial oxygen consumption is increased. Furthermore, RV dilation shifts the interventricular septum to the left, decreasing left ventricular preload and, hence, the cardiac output. An often lethal vicious circle is induced. The main therapeutic goals aimed at breaking this circle are restoration of adequate oxygen delivery to the myocardium and diminution of RV afterload.