Contribution of Autonomic Reflexes to the Hyperadrenergic State in Heart Failure

Figures

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  Figure 1. Representative tracings of muscle sympathetic nerve activity (MSNA), blood pressure (BP) and respiration rate (RR) in a healthy subject, a patient with heart failure with preserved ejection fraction (HFpEF) and a patient with heart failure with reduced ejection fraction (HFrEF), at rest. Note the difference in the discharge patterns of the sympathetic outflow between healthy control subjects vs. HFpEF vs. HFrEF patients. Representative tracings of MSNA, BP and RR are unpublished material.

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  Figure 2. Classical schematic diagram of arterial baroreflex control (A), cardiopulmonary reflex (B), cardiac sympathetic afferent reflex (C), and arterial chemoreflex (D). NTS, nucleus tractus solitarii; NA, nucleus ambiguus; DMV, dorsal motor nucleus of the vagus; CVLM, caudal ventrolateral medulla; RVLM, rostral ventrolateral medulla; PVN, paraventricular nucleus of the hypothalamus; A5, noradrenergic neurons of the ventrolateral pons; RTN/pFRG, retrotrapezoid nucleus/parafacial respiratory group; VRC, ventral respiratory column; BötC, Bötzinger complex; pre-BötC, pre-Bötzinger complex; Rvrg, rostral ventral respiratory group; eSN, efferent sympathetic nerve; PN, phrenic nerve; VN, vagus nerve.

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  Figure 3. Hypothetical representation of the reflex mechanisms considered as “controller units,” and their complex and dynamic interaction in a physiological condition (A) and during heart failure (B). CSAR, cardiac sympathetic afferents reflex; PVN, paraventricular nucleus of the hypothalamus; SN, sympathetic nerve; VN, vagus nerve. Note that the sustained hyperadrenergic state in patients with HF occurs due to the predominance of inputs of excitatory mechanisms on inhibitory mechanisms.