Abstract
Based on a cinefluoroscopic analysis of the left heart during excessive peripheral blood pooling and roentgenological studies of heart size at rest and during exercise, the following picture of cardiodynamics is presented. During excessive peripheral pooling of blood the left ventricle actively defends arterial homeo-stasis regardless of venous return. By calling upon the pulmonary blood reservoirs and sacrificing its end-systolic volume it pays for the deficit between failing return and normal output. Only after the central volume reserves are exhausted in about 5-6 seconds, does cardiac output become a linear function of venous return. Even during this period the ventricle by changing its motion pattern tries to actively accelerate venous inflow. The immediate reaction of the heart to muscular exercise shows a similar pattern. The increase of heart size during adaptation to chronic stress, such as hard physical training, A-V fistulas or myocardial failure is a slow process. One should expect that in the normal heart the presystolic size of the ventricle is adjusted to the available force of the muscle fiber and the work load. The most important factors which determine this ventricular volume are the total blood volume and its distribution as determined by vascular tone particularly the venous tone, and the "give" of the ventricular walls. One mechanism by which this adjustment of ventricular size could be initiated would be reflexly from receptors in the heart itself, particularly in the atria.