Dynamic Assessment of Baroreflex Control of Heart Rate During Induction of Propofol Anesthesia Using a Point Process Method

Heart rate is a vital sign, whereas heart rate variability is an important quantitative measure of cardiovascular regulation by the autonomic nervous system. Although the design of algorithms to compute heart rate and assess heart rate variability is an active area of research, none of the approaches considers the natural point-process structure of human heartbeats, and none gives instantaneous estimates of heart rate variability. We model the stochastic structure of heartbeat intervals as a history-dependent inverse Gaussian process and derive from it an explicit probability density that gives new definitions of heart rate and heart rate variability: instantaneous R-R interval and heart rate standard deviations. We estimate the time-varying parameters of the inverse Gaussian model by local maximum likelihood and assess model goodness-of-fit by Kolmogorov-Smirnov tests based on the time-rescaling theorem. We illustrate our new definitions in an analysis of human heartbeat intervals from 10 healthy subjects undergoing a tilt-table experiment. Although several studies have identified deterministic, nonlinear dynamical features in human heartbeat intervals, our analysis shows that a highly accurate description of these series at rest and in extreme physiological conditions may be given by an elementary, physiologically based, stochastic model.

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Abstract 477: Chronic Baroreflex Activation Improves Baroreflex Control of Heart Rate In Obesity

Hypertension ◽

10.1161/hyp.60.suppl_1.a477 ◽

2012 ◽

Vol 60 (suppl_1) ◽

Author(s):

Radu Iliescu ◽

Ionut Tudorancea ◽

Eric Irwin ◽

Thomas Lohmeier

Keyword(s):

Heart Rate ◽

Pulse Interval ◽

Vagal Activity ◽

Fat Intake ◽

High Fat ◽

Baroreflex Control ◽

Systolic Blood Pressure Variability ◽

Body Weight Increase ◽

Obesity Hypertension ◽

Fat Feeding

Impaired baroreflex control of heart rate (BRS) and attendant risk for cardiac arrhythmias are associated with sympathetically-mediated obesity hypertension. Since both global and renal-specific sympathoinhibition have sustained antihypertensive effects in obesity, we compared BRS in obese dogs subjected to 7 days of electrical baroreflex activation (BA) and, after recovery (REC), to bilateral surgical renal denervation (RDX). After control (C) measurements and 4 weeks of high fat diet, fat intake was reduced (RF) to maintain a body weight increase of ∼ 50%, which led to an increase in mean arterial pressure (MAP) from 100±2 to 117±3 mmHg and heart rate (HR) from 86±3 to 130±4 bpm. Obesity hypertension was associated with decreased sensitivity of 24h spontaneous BRS (determined by the sequence technique from daily beat-to-beat time series) and pulse interval (PI) variability (24h SD). While both BA and RDX abolished hypertension, only BA diminished tachycardia and normalized BRS, consequently improving HR variability. Short-term systolic blood pressure variability (5 min SD) also decreased with high fat feeding and was restored to control upon reduction of fat intake (RF) during established obesity hypertension, suggesting a vasoplegic effect of fat. These data suggest that in addition to the antihypertensive effects of sympathoinhibition, BA corrects cardiac baroreflex dysfunction in obesity hypertension, presumably by enhancing cardiac vagal activity. This in turn markedly improves depressed HR variability, a known risk factor for cardiac arrhythmic events.

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Effects of central venous blood volume shifts on arterial baroreflex control of heart rate

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1981.241.4.h571 ◽

1981 ◽

Vol 241 (4) ◽

pp. H571-H575 ◽

Cited By ~ 5

Author(s):

G. E. Billman ◽

D. T. Dickey ◽

K. K. Teoh ◽

H. L. Stone

Keyword(s):

Heart Rate ◽

Blood Volume ◽

Volume Expansion ◽

Body Position ◽

Venous Blood ◽

Receptor Blockade ◽

Baroreflex Control ◽

Beta Receptor ◽

Blood Volume Expansion ◽

Beta Receptor Blockade

The purpose of this study was to investigate the effects of anesthesia, body position, and blood volume expansion on baroreflex control of heart rate. Five male rhesus monkeys (7.0-10.5 kg) were given bolus injection of 4.0 micrograms/kg phenylephrine during each of the following situations: awake sitting, anesthetized (AN) (10 mg/kg ketamine-HCl) sitting, AN recumbent, AN 90 degrees head down tilt, and AN 50% blood volume expansion with normal saline. beta-Receptor blockade was also performed on each treatment after anesthesia. Four additional animals were similarly treated after 20% blood volume expansion. R-R interval was plotted against systolic aortic pressure, and the slope was determined by linear regression. Baroreflex slope was significantly (P less than 0.05) reduced by 90 degrees head down tilt and 50% volume expansion both before and after beta-receptor blockade. A similar trend was seen after 20% volume expansion. These data are consistent with the thesis that baroreflex control of heart rate is reduced by central blood volume shifts.

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Compensatory recovery of parasympathetic control of heart rate after unilateral vagotomy in rabbits

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1992.262.4.h1122 ◽

1992 ◽

Vol 262 (4) ◽

pp. H1122-H1127 ◽

Cited By ~ 1

Author(s):

D. D. Lund ◽

G. A. Davey ◽

A. R. Subieta ◽

B. J. Pardini

Keyword(s):

Heart Rate ◽

Arterial Pressure ◽

Nerve Stimulation ◽

Vagal Stimulation ◽

Acetylcholinesterase Inhibition ◽

Baroreflex Control ◽

Recovery Mechanism ◽

Vagal Innervation ◽

Increased Sensitivity ◽

Parasympathetic Control

Compensatory recovery by the intact vagal innervation after unilateral vagotomy was investigated by measuring parasympathetic-mediated control of heart rate in beta-adrenergic-blocked rabbits. Direct contralateral vagal nerve stimulation produced greater bradycardia in anesthetized rabbits with chronic vagotomy compared with acutely vagotomized controls. Vagal stimulation during acetylcholinesterase inhibition by physostigmine and direct neuroeffector stimulation by methacholine indicated that a change in metabolism of the neurotransmitter or an increased sensitivity of the tissue to acetylcholine were not responsible for augmentation of vagal responses. Baroreflex control of heart rate in response to an increase in arterial pressure was also tested in urethan-anesthetized rabbits. There was a significant reduction in the prolongation of the R-R interval during baroreflex activation acutely after midcervical vagotomy. These values were subsequently above control levels in rabbits 28 days after vagotomy. In conscious rabbits, the decrease in baroreflex control of heart rate progressively recovered to control levels within 6 days. These results suggest that the recovery mechanism after unilateral vagotomy may be related to peripheral and central compensatory changes in the intact contralateral vagus nerve.

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Characterization of baroreflex impairment in conscious dogs with pacing-induced heart failure

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1993.265.5.r1132 ◽

1993 ◽

Vol 265 (5) ◽

pp. R1132-R1140 ◽

Cited By ~ 14

Author(s):

N. B. Olivier ◽

R. B. Stephenson

Keyword(s):

Heart Failure ◽

Blood Pressure ◽

Heart Rate ◽

Cardiac Output ◽

Peripheral Resistance ◽

Open Loop ◽

Ventricular Pacing ◽

Baroreflex Control ◽

Rapid Ventricular Pacing ◽

Reflex Control

Open-loop baroreflex responses were evaluated in eight conscious dogs before and during congestive heart failure to determine the effects of failure on baroreflex control of blood pressure, heart rate, cardiac output, and total peripheral resistance. Heart failure was induced by rapid ventricular pacing. Baroreflex function was determined by calculation of the range and gain of the open-loop stimulus-response relationships for the effect of carotid sinus pressure on blood pressure, heart rate, cardiac output, and total peripheral resistance. The range and gain of blood pressure responses were substantially reduced as early as 3 days after induction of heart failure (161 +/- 6 to 99 +/- 8 mmHg and -2.7 +/- 0.3 to -1.5 +/- 0.1, respectively) and remained depressed for the 21 days of heart failure. This depression in baroreflex control of blood pressure was associated with similar depressions in reflex range and gain for heart rate (125 +/- 9 to 78 +/- 11 beats/min and -2.05 +/- 0.2 to -1.16 +/- 0.2 beats/min, respectively) and cardiac output (1.74 +/- 0.2 to 0.46 +/- 0.2 l/min and -0.81 +/- 0.02 to -0.027 +/- 0.008 l/min, respectively). The group-averaged range and gain for reflex control of vascular resistance were not altered by heart failure. In three dogs, discontinuation of rapid ventricular pacing led to resolution of heart failure within 7 days and partial restoration of the range and gain of reflex control of blood pressure. We conclude that heart failure reversibly depresses baroreflex control of blood pressure principally through a concurrent reduction in reflex control of cardiac output, whereas reflex control of vascular resistance is not consistently affected.

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Isoflurane Depresses Baroreflex Control of Heart Rate in Decerebrate Rats

Anesthesiology ◽

10.1097/00000542-200205000-00026 ◽

2002 ◽

Vol 96 (5) ◽

pp. 1214-1222 ◽

Cited By ~ 24

Author(s):

Jong S. Lee ◽

Don Morrow ◽

Michael C. Andresen ◽

Kyoung S. K. Chang

Keyword(s):

Central Nervous System ◽

Heart Rate ◽

Nervous System ◽

Baroreflex Sensitivity ◽

Baroreflex Control ◽

Beta Adrenoceptor ◽

Reflex Bradycardia ◽

Reflex Tachycardia ◽

Map Data ◽

Regulatory Sites

Background Isoflurane inhibits baroreflex control of heart rate (HR) by poorly understood mechanisms. The authors examined whether suprapontine central nervous system cardiovascular regulatory sites are required for anesthetic depression. Methods The effects of isoflurane (1 and 2 rat minimum alveolar concentration [MAC]) on the baroreflex control of HR were determined in sham intact and midcollicular-transected decerebrate rats. Intravenous phenylephrine (0.2-12 microg/kg) and nitroprusside (1-60 microg/kg) were used to measure HR responses to peak changes in mean arterial pressure (MAP). Sigmoidal logistic curve fits to HR-MAP data assessed baroreflex sensitivity (HR/MAP), HR range, lower and upper HR plateau, and MAP at half the HR range (BP50). Four groups (two brain intact and two decerebrate) were studied before, during, and after isoflurane. To assess sympathetic and vagal contributions to HR baroreflex, beta-adrenoceptor (1 mg/kg atenolol) or muscarinic (0.5 mg/kg methyl atropine) antagonists were administered systemically. Results Decerebration did not alter resting MAP and HR or baroreflex parameters. Isoflurane depressed baroreflex slope and HR range in brain-intact and decerebrate rats. In both groups, 1 MAC reduced HR range by depressing peak reflex tachycardia. Maximal reflex bradycardia during increases in blood pressure was relatively preserved. Atenolol during 1 MAC did not alter maximum reflex tachycardia. In contrast, atropine during 1 MAC fully blocked reflex bradycardia. Therefore, 1 MAC predominantly depresses sympathetic components of HR baroreflex. Isoflurane at 2 MAC depressed both HR plateaus and decreased BP50 in both groups. Conclusions Isoflurane depresses HR baroreflex control by actions that do not require suprapontine central nervous system sites. Isoflurane actions seem to inhibit HR baroreflex primarily by the sympathetic nervous system.

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