Influence of the baroreflex on the evolution of ventriculo arterial coupling (681.3)

Abstract

The Baroreflex is a negative feedback mechanism that controls arterial blood pressure, as sensed by the baroreceptors, increasing or decreasing sympathetic and parasympathetic activity to restore arterial blood pressure. It is an important component of arterial blood pressure and circulatory regulation and therefore a fundamental mechanism in the pathogenesis of Hypertension and Congestive Heart Failure, that is further stressed by the multiple therapeutic approaches designed to influence it. As the Baroreflex influences the heart rate, cardiac contractility and vascular resistance, we hypothesised that it must influence the mechanical interaction between the left ventricle and the arterial tree as well as cardiac energy consumption and efficiency.The ventriculoarterial coupling was evaluated on a beat‐per‐beat basis, upon the application of a left‐carotid sinus baroreflex stimulus in rabbits. The left ventricle end‐systolic elastance and arterial elastance were calculated and the coupling ratio was then related to the indexes of cardiac energetics. Upon the application of the baroreflex, the coupling ratio showed an approximately linear increase, attributed to the rise in ventricular elastance. Stroke work and cardiac efficiency both increased, indicating that not only was the stroke work greater, but it was obtained at a lower oxygen cost. The coupling ratio increased indicating that it was moving towards an optimal stroke work.In conclusion the baroreflex is a control mechanism of the cardiovascular system that exerts a feedback modulation on the arterial pressure through a balanced increase in cardiac contractility and arterial input impedance which results in an improvement in ventriculo arterial coupling, mechanical and energetic efficiency.This approach can now be applied to test acute interventions on the circulatory system, including the short term reflexes as mechano reflexes and chemoreflexes, diseases such as myocardial infarction, drug and device therapy.Grant Funding Source: Fundaçao Ciencia e Tecnologia