Physiological basis for human autonomic rhythms.
Oscillations of arterial pressures, heart periods, and muscle sympathetic nerve activity have been studied intensively in recent years to explore otherwise obscure human neurophysiological mechanisms. The best-studied rhythms are those occurring at breathing frequencies. Published evidence indicates that respiratory fluctuations of muscle sympathetic nerve activity and electrocardiographic R-R intervals result primarily from the action of a central 'gate' that opens during expiration and closes during inspiration. Parallel respiratory fluctuations of arterial pressures and R-R intervals are thought to be secondary to arterial baroreflex physiology: changes in systolic pressure provoke changes in the R-R interval. However, growing evidence suggests that these parallel oscillations result from the influence of respiration on sympathetic and vagal-cardiac motoneurones rather than from baroreflex physiology. There is a rapidly growing literature on the use of mathematical models of low- and high-frequency (respiratory) R-R interval fluctuations in characterizing instantaneous 'sympathovagal balance'. The case for this approach is based primarily on measurements made with patients in upright tilt. However, the strong linear relation between such measures as the ratio of low- to high-frequency R-R interval oscillations and the angle of the tilt reflects exclusively the reductions of the vagal (high-frequency) component. As the sympathetic component does not change in tilt, the low- to high-frequency R-R interval ratio provides no proof that sympathetic activity increases. Moreover, the validity of extrapolating from measurements performed during upright tilt to measurements during supine rest has not been established. Nonetheless, it is clear that measures of heart rate variability provide important prognostic information in patients with cardiovascular diseases. It is not known whether reduced heart rate variability is merely a marker for the severity of disease or a measurement that identifies functional reflex abnormalities contributing to terminal dysrhythmias.
Eckberg
D L
DL
Department of Medicine, Medical College of Virginia at Virginia Commonwealth University, and Hunter Holmes McGuire Department of Veteran Affairs Medical Center, Richmond, USA. deckberg@aol.com
D000328:Adult; D000818:Animals; D001145:Arrhythmias, Cardiac / Q000503:physiopathology; D001341:Autonomic Nervous System / Q000502:physiology*; D017704:Baroreflex / Q000502:physiology; D001794:Blood Pressure / Q000502:physiology; D002318:Cardiovascular Diseases / Q000503:physiopathology*; D002320:Cardiovascular Physiological Phenomena; D016757:Death, Sudden, Cardiac / Q000209:etiology; D004285:Dogs; D004562:Electrocardiography; D006339:Heart Rate / Q000502:physiology; D006801:Humans; D008962:Models, Theoretical; D012143:Respiratory Physiological Phenomena; D013564:Sympathetic Nervous System / Q000502:physiology; D014630:Vagus Nerve / Q000502:physiology