Physiological and Pharmacological Interventions on Coupling of Heart and Arterial Load

Summary

Cardiac output (F) increases, but the mean pressure (P) decreases with decreasing peripheral resistance. This inverse relationship is called the pump function graph, which characterizes the heart as a fluid pump. Power output (P × F) depends on the properties of the heart and of the arterial load, and when plotted as a function of cardiac output shows a relative maximum at a certain flow (F_p). This power maximum is relative since it depends not only on flow but also on the “setting of the heart,” i.e., contractility, heart rate, and end-diastolic volume. The actual values of pressure and flow measured in the intact animal define working point (P_w and F_w). A consistent finding in anesthetized, open-thorax cats is that the heart works at the relative maximum of power output (F_w = F_p).

This paper discusses the influence of experimental and pathological conditions on power output. For variations in heart rate and volume loading and under influence of halothane the heart remained working at maximum power output (F_w = F_p). Noradrenalin and the vasodilator Hydralazine caused the working point to shift away from the maximum (F_w > F_p and F_w< F_p, respectively). These results are compatible with the hypothesis that the heart is regulated to work at maximum power output, and that noradrenalin and hydralazine somehow interfere with the regulatory mechanisms.