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Historical Development of HRV Analysis
Published in Herbert F. Jelinek, David J. Cornforth, Ahsan H. Khandoker, ECG Time Series Variability Analysis, 2017
Cardiovascular homeostasis is maintained by input from baroreceptors in the carotid sinus and aortic arch (the “high pressure baroreceptors”) and cardiopulmonary volume receptors in the atria, great veins, and ventricles (the “low pressure baroreceptors”). An increase in blood pressure inhibits efferent sympathetic outflow to the heart and peripheral vasculature and promotes efferent parasympathetic activity to the heart. This leads to a decrease in HR, systemic vascular resistance, and blood pressure. In contrast, a fall in blood pressure leads to an increase in HR and blood pressure (Fritsch et al. 1986; Andresen 1984).
Device profile of the MobiusHD EVBA system for the treatment of resistant hypertension: overview of its mechanism of action, safety and efficacy
Published in Expert Review of Medical Devices, 2020
Mark C. Bates, Gregg W. Stone, Chao-Yin Chen, Wilko Spiering
Carotid baroreceptor physiology was first described in landmark animal studies by Hering in the 1920s and led to the discovery and mapping of the afferent nerve to a branch of the glossopharyngeal nerve (Hering’s nerve, also termed the carotid sinus nerve [CSN]) [19]. In the simplified primary arc of the central baroreflex network in regulating sympathetic activities, an increase in systemic blood pressure (BP) results in increasing afferent signaling from carotid sinus (CS) baroreceptors and subsequent inhibition of sympathetic outflow to lower BP via inhibiting neurons in the rostral ventral lateral medulla [20]. Please note that an exhaustive overview baroreceptor physiology is beyond the scope of this review but can be found in the excellent expert summary authored by Manci G and Mark AL. in 1983 [21].