Interplay among cardiac chambers. Left and right ventricular performance during changes in contractility, afterload and during simultaneous atrio-ventricular contraction.

Abstract

1. Only a slight increase in stroke volume is observed during a selective left-sided inotropic stimulation of the in situ pig heart. Decreased left ventricular preload during left-sided inotropic stimulation reduces activation of the Frank-Starling mechanism and hence explains the rather small increase in stroke volume. We suggest that left-sided inotropic stimulation redistributes blood from the pulmonary circulation toward the systemic circulation causing a fall in pulmonary artery pressure and increased right ventricular output because of this afterload-reduction. 2. A rise in stroke volume during selective right-sided inotropic stimulation is not attenuated by a concomitant reduction in right ventricular preload. On the contrary, right ventricular preload rises in response to inotropic stimulation of the right atrium. Right-sided inotropic stimulation redistributes blood toward the pulmonary vascular bed and the left side of the heart. Left ventricular function is improved by this redistribution. 3. Both left ventricular end-systolic and end-diastolic volumes are better maintained by thoracic aortic occlusion during left-sided inotropic stimulation than at control inotropy. The concomitantly better preserved dimensions in the right ventricle can be explained by reduced pressure in the pulmonary circulation and a decrease in right-ward septal bulging. The rise in stroke volume by aortic occlusion during intravenous isoproterenol infusion is mainly due to a greater redistribution volume than at control inotropy. 4. Prolongation of the diastolic interval may reduce the end-diastolic pulmonary artery pressure to such an extent that right atrial contraction could eject blood into the pulmonary artery during late ventricular diastole.(ABSTRACT TRUNCATED AT 250 WORDS)