SOME FACTORS IN THE REGULATION OF THE STROKE VOLUME

Abstract

Three important mechanisms are recognized for regulation of the stroke volume: (1) change in diastolic size of the ventricles as evidenced by change in filling pressure; (2) change in the resistance to ejection (aortic pressure); and (3) change in the degree of cardiac stimulation. Expts. on intact dogs indicated that an acute increase in the arterial pressure against which the heart must eject blood, tended to reduce the stroke volume and usually to reduce the external cardiac work. This maneuver caused the heart to dilate, but when the pericardium was intact, the dilation was not sufficient to produce a significant increase in cardiac function. Under some circumstances removal of the pericardium might allow sufficient dilatation to improve the pumping action of the heart, but under other circumstances this was not true. Decreasing the arterial pressure tended to increase the stroke volume and external work. This increase might occur immediately, i.e., before reflex adjustments or changes in filling pressure had time to take place. The fact that the response might occur immediately necessitates the assumption that there is residual blood in the ventricle at the end of systole. A part of this blood can be ejected by a more complete emptying of the ventricle when the pressure is suddenly reduced. The responses to increased and decreased arterial pressure were regarded as simple mechanical results of varying the resistance to ejection in the face of a relatively unchanging contractile process. Sympathetic and sympathomimetic stimulation of the heart increased its contractile activity. This might result in an increased stroke volume and an increase in external cardiac work, if the peripheral resistance was not so greatly elevated as to give rise to an overwhelming increase in arterial pressure. In this case out- put and work might be reduced. In these expts., changes in resistance to ejection (aortic pressure) and in myocardial stimulation were more important than changes in diastolic size (filling pressure) in the regulation of the stroke volume. The responses studied were to acute changes and hence not relevant to the results of prolonged strain which give rise to cardiac enlargement and hypertrophy.