Regulation of cardiac output by stroke volume and heart rate in conscious dogs.

Abstract

The relative importance of increases in stroke volume and heart rate in mediating increases in cardiac output in response to elevations in preload, inotropic state or a combination of these factors in 15 conscious dogs with low, physiological heart rates were examined. Elevating preload by volume with saline increased left atrial pressure by 15 mm Hg, cardiac output by 147 .+-. 7% from a control of 2340 .+-. 80 ml/min, and heart rate by 143 .+-. 7% from a control of 62 .+-. 2 beats/min, but did not alter stroke volume. Volume loading with blood increased cardiac output by 100 .+-. 5% and heart rate by 108 .+-. 10%, while stroke volume did not change significantly. Hemorrhage in conscious dogs reduced cardiac output by 49 .+-. 4% and stroke volume by 75 .+-. 2% while increasing heart rate by 113 .+-. 15%. In dogs anesthetized with pentobarbital Na, and with an open chest, volume loading increased stroke volume by 243 .+-. 89% but did not alter heart rate. In conscious dogs, isoproterenol increased cardiac output solely by increasing heart rate, failing to increase stroke volume, whereas dobutamine, a sympathomimetic amine with less positive chronotropic action than isoproterenol, raised stroke volume by approximately 25%. Infusion of both sympathomimetic amines in the volume-loaded state increased stroke volume by a slightly greater amount than either volume loading or sympathomimetic amine infusion by itself. Severe exercise also increased stroke volume by 27 .+-. 2%, whereas cardiac output rose by 402 .+-. 24%. In the conscious dog with a low physiological heart rate, stroke volume is relatively large at rest and does not increase at all, even with maximally tolerable volume loading, and only modest increases were observed with exercise or combined sympathomimetic amine infusion and volume loading.