'Digital Computer Model of the Cardiovascular System and the Effects of Hypertensive Reculation'

This paper presents a digital computer model of the cardiovascular system (CVS) for an integrated open loop, as well as a closed loop, regulator and indicates the results of experimentation to regulate pressure. The results of the mathematical analysis and simulation verify many of the conclusions of previous investigators and develop some new ones related to hypertension. The model is basically developed from the work of Grodins (1-3), and Mc Adam (4), and extended and refined to result in one of the few all digital computer simulations utilizing Starling's law of filling (5). The paper proceeds to develop the CVS model from Starling's law of filling for an isolated ventricle and presents a set of equations which will be utilized to develop a digital computer simulation as well as perform an analytical analysis. A model for the simulation of heart-rate feedback is carefully developed, tested and incorporated in the CVS model in order to study feedback regulation. Both the parameters used for linear and nonlinear operation of the system are extended from experimental data on dogs to those of humans. Experimental results of the digita1 computer model for a human CVS indicate the effects of pressure regulation with and without feedback. The effect of various gain factors on the heartrate feedback equations is carefully analyzed. It is clearly shown that the CVS operating with-cut heart-rate feedtack either delayed or inhibited causes excessively high arterial pressure (hyertension). Utilizing the correct type and kind of regulation causes normal pressure regulation. In addition to the response of the systems pressure the effect of regulation on cardiac output and blood volume are also experimented with. It was observed that for constant cardiac output the blood volume increased and the heart-rate decreased as the arterial pressure increased. Experimentations with the human CVS model also revealed the non-linear relationship between arterial pressure, cardiac output and heart-rate in addition to the linear relationship between arterial pressure and peripheral resistance. The CVS model developed should prove to be a valuable aid to medical doctors and researchers in their attempt to find causes for the nations number one killer - hypertension. This work is a result of more extensive analysis and simulation and represents a condensation of' the more basic work. Some of the more inportant results are presented in this paper.