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Assessment of Cardiac Baroreflex Function During Fixed Atrioventricular Pacing Using Baroreceptor‐Stroke Volume Reflex Sensitivity
Author(s) -
YASUMASU TOMIYA,
ABE HARUHIKO,
OGINOSAWA YASUSHI,
TAKAHARA KAZUO,
NAKASHIMA YASUHIDE
Publication year - 2005
Publication title -
journal of cardiovascular electrophysiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.193
H-Index - 138
eISSN - 1540-8167
pISSN - 1045-3873
DOI - 10.1111/j.1540-8167.2005.40767.x
Subject(s) - baroreceptor , medicine , reflex bradycardia , baroreflex , supine position , stroke volume , reflex , heart rate , cardiology , anesthesia , blood pressure
The baroreceptor‐heart rate (HR) reflex has prognostic value in cardiovascular medicine. However, it cannot be used in chronotropically incompetent or paced patients. In healthy subjects, the baroreceptor‐stroke volume (SV) reflex, with power spectral analysis of SV and blood pressure (BP) variations in the low‐frequency band, serves as an alternate measure of the baroreceptor‐cardiac reflex. This study examined the baroreceptor‐stroke volume (SV) reflex sensitivity in the supine and 60° upright positions in paced patients. Methods and Results: We studied 16 recipients of dual‐chamber pacemakers paced at a fixed rate. The hemodynamics and baroreceptor‐SV reflex sensitivity were measured during atrioventricular (AV) sequential pacing every 5 minute in the supine and 60° upright positions. Mean SV decreased from 42.0 ± 20.1 mL in the supine to 36.6 ± 16.1 mL in the upright position (P < 0.05), whereas BP and total peripheral resistance did not change. A significant fall in baroreceptor‐SV reflex sensitivity from 29.2 ± 18.0%/mmHg to 19.5 ± 15.5%/mmHg was observed during upright tilt (P < 0.005). Conclusion: Fixed‐rate AV sequential pacing did not blunt the decrease in baroreceptor‐SV reflex sensitivity consistent with the arterial baroreflex gain response to upright posture. The decreased baroreceptor‐SV reflex sensitivity occurring with the upright posture may reflect a baroreflex‐induced inotropic effect secondary to vagal withdrawal and sympathetic activation.