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Review
. 2019 Dec 10;74(23):2939-2947.
doi: 10.1016/j.jacc.2019.10.027.

Blood Pressure Management in Afferent Baroreflex Failure: JACC Review Topic of the Week

Affiliations
Review

Blood Pressure Management in Afferent Baroreflex Failure: JACC Review Topic of the Week

Italo Biaggioni et al. J Am Coll Cardiol. .

Abstract

Afferent baroreflex failure is most often due to damage of the carotid sinus nerve because of neck surgery or radiation. The clinical picture is characterized by extreme blood pressure lability with severe hypertensive crises, hypotensive episodes, and orthostatic hypotension, making it the most difficult form of hypertension to manage. There is little evidence-based data to guide treatment. Recommendations rely on understanding the underlying pathophysiology, relevant clinical pharmacology, and anecdotal experience. The goal of treatment should be improving quality of life rather than normalization of blood pressure, which is rarely achievable. Long-acting central sympatholytic drugs are the mainstay of treatment, used at the lowest doses that prevent the largest hypertensive surges. Short-acting clonidine should be avoided because of rebound hypertension, but can be added to control residual hypertensive episodes, often triggered by mental stress or exertion. Hypotensive episodes can be managed with countermeasures and short-acting pressor agents if necessary.

Keywords: autonomic nervous system; baroreflex; carotid sinus; hypertension; orthostatic hypotension.

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Figures

Central Illustration
Central Illustration. Diagram of the Baroreflex.
An increase in blood pressure activates baroreceptors located in the carotid sinus. Afferent signals are sent through the glossopharyngeal nerve (IX) to activate the nucleus tractus solitarii (NTS) of the brainstem. This in turn activates neurons in the caudal ventrolateral medulla (CVLM) which provides inhibitory input to the rostral ventrolateral medulla (RVLM) where sympathetic activity originates. This results in a decrease in sympathetic tone that is carried through preganglionic efferent fibers in the intermediolateral column of the spinal cord (IML), and a decrease in postganglionic efferent fibers innervate the heart and blood vessels, to restore blood pressure to normal values.
Figure 1.
Figure 1.. Pathophysiological and Clinical Differences Between Afferent Baroreflex Failure and Autonomic Failure.
Normal baroreflex function, shown in the Central Illustration, maintains blood pressure under relatively narrow range. Afferent baroreflex failure (Panel A) is due to loss of inhibitory input from the carotid sinus, the nucleus tractus solitarii (NTS) and the caudal ventrolateral medulla (CVLM), leaving cortical input (mental stress) to the rostral ventrolateral medulla (RVLM) unopposed, resulting in paroxysmal surges in muscle sympathetic nerve traffic (MSNA) and parallel increases in blood pressure and heart rate. In primary Autonomic Failure (Panel B) autonomic regulation is impaired because of neurodegeneration of central autonomic pathways (multiple system atrophy, MSA) or efferent autonomic fibers (pure autonomic failure, PAF,). In either case the clinical picture is characterized by supine hypertension and orthostatic hypotension; patients also have impaired baroreflex function leading to hypersensitivity to pressor agents or depressor stimuli, but do not have the paroxysmal hypertensive surges seen in afferent baroreflex failure.

References

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