Baroreceptor Unloading at Rest and During Exercise in Heart Failure Exacerbates Ventricular‐Vascular Coupling

Abstract

The arterial baroreflex is the primary reflex controlling arterial blood pressure on a beat-by-beat basis via modulation of autonomic output to change cardiac output and systemic vascular resistance. This moment-to-moment control of arterial pressure is well maintained with the transition from rest to exercise. However, in systolic heart failure (HF) baroreflex dysfunction can occur. Effective control of cardiac output occurs in part via efficient energy transfer from the left ventricle to the systemic circulation; known as ventricular-vascular coupling. Ventricular-vascular coupling can be evaluated by changes in stroke work and the relationship between effective arterial elastance to left ventricular maximal elastance. We investigated if the effects of baroreceptor unloading (via bilateral carotid occlusion) on effective arterial elastance and stroke work at rest, and during exercise were altered in HF, in conscious chronically instrumented canines. We hypothesized that in healthy subjects the baroreflex maintains ventricular-vascular coupling whereas in HF, exacerbated increases in effective arterial elastance as a result of baroreceptor unloading would cause decoupling of the ventricular-vascular interaction. We observed in healthy subjects that baroreceptor unloading significantly increased effective arterial elastance (Ea) and stroke work (SW) at rest (Ea: +1.6 ± 0.2 mmHg/ml) (SW: +1.8 ± 0.1 L/mmHg) and during exercise (Ea: +1.4 ± 0.2 mmHg/ml) (SW: +1.6 ± 0.2 L/mmHg) thus maintaining ventricular-vascular coupling. In HF, ventricular-vascular uncoupling is already apparent with higher effective arterial elastance and reduced maximal ventricular elastance. Baroreceptor unloading in HF further worsens ventricular-vascular coupling at rest and during exercise by eliciting ~2-3 fold increases in effective arterial elastance (EaΔREST +4.3 ± 0.3 mmHg/ml) (EaΔEX +2.5 ± 0.5 mmHg/ml) unaccompanied by much improvement in stroke work (SWΔREST +0.1 ± 0.5 L/mmHg) (SWΔEX +0.5 ± 0.1 L/mmHg). We conclude that the ability of the arterial baroreflex to raise cardiac output in heart failure is impaired in part due to further reflex induced uncoupling of the ventricular-vascular relationship. This likely contributes to impaired reflex control of arterial pressure during hypotensive challenges in HF.