INTERACTION BETWEEN CAROTID BAROREGULATION AND THE PULSATING HEART - A MATHEMATICAL-MODEL

A mathematical model of short-term arterial pressure control by the ca rotid baroreceptors in pulsatile conditions is presented. The model in cludes an elastance variable description of the left and right heart, the systemic (splanchnic and extrasplanchnic) and pulmonary circulatio ns, the afferent carotid baroreceptor pathway, the sympathetic and vag al efferent activities, and the action of several effector mechanisms. The latter mechanisms work, in response to sympathetic and vagal acti on, by modifying systemic peripheral resistances, systemic venous unst ressed volumes, heart period, and end-systolic elastances. The model i s used to simulate the interaction among the carotid baroreflex, the p ulsating heart, and the effector responses in different experiments. I n all cases, there has been satisfactory agreement between model and e xperimental results. Experimental data on heart rate control can be ex plained fairly well by assuming that the sympathetic-parasympathetic s ystems interact linearly on the heart period. The carotid baroreflex c an significantly modulate the cardiac function curve. However, this ef fect is masked in vivo by changes in arterial and atrial pressures. Du ring heart pacing, cardiac output increases with frequency at moderate levels of heart rate and then fails to increase further because of a reduction in stroke volume. Shifting from nonpulsatile to pulsatile pe rfusion of the carotid sinuses decreases the overall baroreflex gain a nd significantly modifies operation of the carotid baroreflex. Finally , a sensitivity analysis suggests that venous unstressed volume contro l plays the major role in the early hemodynamic response to acute hemo rrhage, whereas systemic resistance and heart rate controls are a litt le less important.