Device-Guided Breathing to Lower Blood Pressure: Case Report and Clinical Overview

William J. Elliott, MD, PhD; Joseph L. Izzo, Jr, MD

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In This Article

Potential Mechanism of Action

Inappropriately high sympathetic nervous outflow from the central nervous system is believed to be an important component in the pathophysiology of acute and chronic hypertension, which increases cardiac output and peripheral resistance. Elevated sympathetic activity is often associated with desensitization of arterial and cardiopulmonary baroreceptors, which leads to increased BP fluctuations and sustained elevations in resting BPs.

Slow breathing (< 10 bpm), especially with prolonged exhalation, appears to reduce sympathetic nerve traffic and thus causes arteriolar dilatation. The process is believed to be initiated by activated pulmonary mechanoreceptors, which respond to the increased tidal volume that accompanies slow breathing, and act in concert with cardiac mechanoreceptors to inhibit sympathetic outflow.[17,18]

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