[Experimental infarction of the right ventricle. Its natural history]

To elucidate the pathophysiology of severe right ventricular infarction (RVI), isolated RVI was produced in 12 dogs in an open chest preparation with intact pericardium. After RVI; mean right auricle pressure and right ventricular end-diastolic pressure (RVEDP) increased (p < 0.05). A statistical significant decline was observed in cardiac output (43%, p < 0.05). However, for left ventricular systolic and end diastolic pressures (LVEDP) a decline was noted only after 120, or 90 min of the production of the RVI. Hemodynamic findings suggested a decreased preload of left chambers, as consequence of ischemic injury of the RV. This feature contributes to low cardiac output. A depression in right and left ventricular function curves were noted after RVI and this condition was maintained after 180 min of experimental observation. Equalized end-ventricular diastolic pressures were noted soon after RVI, a finding that was sustained over the time course of the experiment. Equalization of ventricular filling pressures was noted with RVEDP of < than 10 mmHg and with normals LVEDP. This features do not support, as a main cause, a restrictive role of the pericardium in the genesis of equalized filling pressures in RVI.