Cardiac failure remains a life-threatening complication for certain patients undergoing intracardiac repair. Despite improvements in surgical techniques, methods of myocardial protection, and postoperative care, patients are frequently at risk to develop postoperative low output syndrome. Approximately 1% of cardiac surgical patients cannot be weaned from extracorporeal circulation in spite of adequate volume loading, the use of inotropic support, and initiation of intraaortic balloon pumping. In these cases, ventricular assist devices (VAD) can mechanically aid the failing heart and reverse the low output state. The concept of mechanical support for the failing left ventricle was first proposed by Clauss et al. in 1961. By 1968, Kantrowitz and associates had developed and refined the first intraaortic balloon pump (IABP). Through the efforts of Moulopolous and others, this device evolved into the present-day intraaortic balloon pump (IABP). Clinical evidence for the efficacy of left ventricular assist devices (LVAD) remained questionable until 1980, when the National Heart, Blood and Lung Institute evaluated short-term LVADs by comparing various types of mechanical aids. This report focused attention primarily on the failing left ventricle (LV). As the use of inotropic support, intraaortic balloon pumping, and LVADs improved, a small group of patients emerged who could not be separated from extracorporeal circulation due to a failing right ventricle. The failing right ventricle emerged as a unique clinical entity similar to postcardiotomy left ventricular failure that also benefited from mechanical cardiac assistance. Current therapy at major centers incorporating mechanical assist devices is based on the premise that the low output state will allow the failing heart to recover from a reversible injury. The frequent occurrence of postcardiotomy ischemia may be due to several factors such as poor myocardial protection, overdistension of the LV, emboli, coronary spasm or technical problems. Whatever the etiology, the end product of cardiac failure is a demand for oxygen consumption that cannot be met, thus leading to cardiac demise.
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