The right ventricular function is crucial for maintaining hemodynamic stability in critically ill patients who suffer from sudden increases of right ventricular pressure overload and/or severely decreased right ventricular contractility. The morphological and functional assessment of the right ventricle is usually performed by bedside echocardiography and hemodynamic measurements with a pulmonary artery catheter. The therapeutic approach to patients with right ventricular failure includes measures to decrease right ventricular afterload and to improve its coronary perfusion and contractility.Key words: right ventricle, failure, systolic function BASIC ANATOMIC, PHYSIOLOGIC AND PATHOPHYSIOLOGIC DATA Sixty years ago, the right ventricle (RV) was considered a passive conduit for blood flow and only a "weak sister" of the strong and powerful left ventricle (1). More than thirty years later, the RV function was revisited and it became clear, that RV failure is responsible for shock in patients with massive pulmonary embolism and RV myocardial infarction (2-4). The thin free wall of the RV forms the anterior and inferior part of the RV and the posterolateral wall represents the intraventricular septum, which normally bulges into the RV. The RV blood supply occurs during systole and diastole; the oxygen extraction is very high, and ATP amount is lower than in the LV. The free wall is very compliant and is capable of maintaining low systemic pressure and preventing pulmonary edema in the case of LV failure. These characteristics make the RV very sensitive to hypoxia. The geometry of the RV is quite complex with clearly separated inflow and outflow tracts. Because of the complex geometry, the LV models are not valid for the RV. The contraction of the RV is less synchronous than that of the LV and occurs as a peristaltic wave starting in the inflow tract and propagating through the apex to the outflow tract. In physiologic conditions, when the pulmonary vascular resistance is low, RV function is indeed of secondary importance. On the other hand, in pathologic conditions with increased pulmonary vascular resistance and/or severely impaired RV contractility, RV function becomes essential for maintaining adequate pulmonary blood flow. The basic consequence of the sudden increase of RV afterload and/ or decreased contractility is RV dilation. Since a dilated RV reduces the LV volume in the rigid pericardial sac, the LV filling is reduced with consequently decreased LV stroke volume and mean arterial pressure. Arterial hypotension provokes RV ischemia that further reduces RV systolic function (5). The RV function is therefore relevant in patients with chronic lung diseases, primary pulmonary vascular disease, pulmonary thrombembolic disorders, sepsis related acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) and after cardiac surgery. Patients with chronic lung diseases frequently present with chronic cor pulmonale, which is characterized by RV free wall hypertrophy and various degrees of dilation w...