To delineate the determinants of right ventricular performance with acute right ventricular dysfunction, surgical electrical isolation of the right ventricular free wall was produced in 13 dogs. During atrioventricular (AV) pacing, hemodynamic and wall motion measurements were normal. When not paced, the right ventricular free wall became asystolic, resulting in a depressed and bifid right ventricular systolic pressure (33 ± 5 to 18 ± 4 mm Hg) and decreased left ventricular systolic pressure (100 ± 18 to 80 ± 18 mm Hg) and stroke volume (14 ± 4 to 10.3 ± 3.5 ml) (all p < 0.05). Ultrasound demonstrated right ventricular free wall dyskinesia, increased right ventricular enddiastolic size (13 ± 13% of control), but decreased left ventricular size (69 ± 11% of control) (both p < 0.05). Right atrial pressure increased (5.8 ± 2.5 to 7.6 ± 2.8 mm Hg, p < 0.05) with an augmented A wave and blunted Y descent, indicating pandiastolic right ventricular dysfunction. The septum demonstrated reversed curvature in diastole and paradoxically into the right ventricle during early systole, generating the initial peak of right ventricular pressure and reducing its volume. Later, posterior septal motion coincided with maximal left ventricular pressure and the second peak of the right ventricular waveform. Left ventricular pacing alone led to further decreases in right ventricular systolic pressure and size, left ventricular systolic pressure and stroke volume. The previously augmented A wave was replaced by a prominent V wave. Therefore, when contractility of its free wall is acutely depressed, right ventricular performance is dependent on left ventricular-septal contractile contributions transmitted by the septum. Augmented right atrial contraction and intact AV synchrony enhance ventricular filling and performance and are important determinants of cardiac output.