Hemodynamic measurements in human subjects and in experimental animals are generally made in the supine position; not much attention is paid to potential beneficial or harmful effects of right or left lateral positions on cardiac output or other hemodynamic variables. To evaluate the potential influence of such positional changes on cardiac performance, we measured cardiac output and left and right ventricular pressures (with micromanometer catheters) in anesthetized experimental animals (eight dogs and nine pigs) in the supine, right lateral, and left lateral positions. Cardiac output increased from supine to left lateral (mean SD, 2.6 ± 0.9 to 3.1 ± 1.0 liters/min; p < .001) and from supine to right lateral positions (2.6 ± 0.9 to 3.1 ± 1.1 liters/min; p < .001). There was an associated decrease in arteriovenous oxygen saturation difference from supine to left lateral position (31 ± 8% to 24 ± 4%; p < .001) and from supine to right lateral position (32 ± 9% to 25 ± 6%; p < .001). Left ventricular systolic and end-diastolic pressures increased from supine to left lateral (128 17/9 ± 2 to 147 ± 19/16 ± 4 mm Hg; both p < .001) and from supine to right lateral positions (128 ± 19/9 ± 2 to 141 ± 16/16 ± 7 mm Hg; p < .01 and p < .001, respectively). Similarly, right ventricular systolic and end-diastolic pressures also increased from supine to left lateral (30 ± 7/3 ± 2 to 38 ± 7/8 ± 2 mm Hg; both p < .001) and from supine to right lateral positions (31 ± 8/3 ± 2 to 43 ± 8/11 ± 4 mm Hg; both p < .001). Systolic and end-diastolic right ventricular pressures were significantly higher in the right lateral position than in the left (both p < .001). Heart rate did not change with positional maneuvers. Neither the sequence of positional changes nor the species of animal (dog vs pig) had any apparent influence on the results. Roentgenographic analysis of the differences in height of the right ventricle relative to the inferior vena cava suggests that changes in hydrostatic pressure may be entirely responsible for the increases in right ventricular end-diastolic pressure when animals are changed from the supine to the left or right lateral positions. We conclude that a change from supine to lateral position significantly increases intracardiac pressures and cardiac output in experimental animals. If confirmed in humans, these findings may have significant implications for the assessment of hemodynamic status of patients in intensive care unit and catheterization laboratory settings and for the treatment of patients in low-cardiac output states.