Monitoring and management of right ventricular function following cardiac transplantation

In cardiac transplantation postoperative right ventricular dysfunction is a major cause of morbidity and mortality. Recipients with pulmonary hypertension due to end-stage heart failure and a donor heart, fragile because of ischemia-reperfusion injury, and not previously adapted to an elevated pulmonary resistance are the causes of right ventricular dysfunction, that unless aggressively treated may progress to overt right ventricular failure. Dysfunctional pulmonary vascular endothelium with diminished release of NO and increased expression of endothelin-1 is considered to be the primary pathophysiology that induces pulmonary hypertension. New therapeutic approaches are aimed at ameliorating endothelial dysfunction. How extensively pulmonary hypertension has to be treated depends on the degree of functional impairment of the right ventricle resulting from the acute increase of right ventricular afterload at heart transplantation. Mainstays in the treatment of pulmonary hypertension are optimizing right ventricular preload, increasing contractility, lowering right ventricular afterload, improving coronary perfusion and failing these therapeutic interventions mechanical circulatory support. Judicious use of volume therapy is mandatory to avoid volume overload in the postoperative setting. As a general rule to explore right ventricular preload reserve volume should only be carefully administered by observing filling pressures up to a maximum of a central venous pressure of 10 mm Hg. Volume administration is not indicated if it only increases right atrial filling pressure without subsequently increasing cardiac output. In most cases relative volume overload is the clinical problem and not hypovolemia. In this situation aggressive diuretic therapy and in cases of acute renal failure renal replacement therapy is mandatory.Positive inotropic therapy is indicated to treat consecutive right ventricular dysfunction. Dobutamine may be a choice in the presence of a low cardiac index but preserved systemic pressures and epinephrine in cases of low cardiac output syndrome and systemic hypotension. A useful adjunct to catecholamine therapy is phosphodiesterase-III-inhibitors in the absence of arterial hypotension. Most importantly, pulmonary arterial pressures and right ventricular afterload have to be lowered in pulmonary hypertension compromising right ventricular function. Systemic vasodilators to treat pulmonary hypertension are non-selective and may induce arterial hypotension. This also applies to intravenously administered prostanoids. Inhaled NO in therapeutic