Cardiac Baroreflex during the Postoperative Period in Patients with Hypertension

Parlow, Joel L.; Bégou, Gérard; Sagnard, Pierre; Cottet-Émard, J. M.; Levron, J. C.; Annat, G.; Bonnet, Francis; Ghignone, M.; Hughson, Richard L.; Viale, Jean–Paul; Quintin, Luc

doi:10.1097/00000542-199903000-00008

Cited by 47 publications

(71 citation statements)

References 39 publications

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“…These methods have been validated in previous investigations, and allow the quantification of brainstemmediated sympathovagal influences on the heart under a variety of conditions. 19,[26][27][28][29] General anesthetics have been shown to depress both the sympathetic and parasympathetic influence on the heart, with the resulting level of sympathovagal balance dependent on the agent studied. Most previous studies have documented the effects of induction of general anesthesia on cardiovascular control, while few have explored the effects of graded increases in depth of CNS depression with specific agents.…”

Section: Autonomic Circulatory Controlmentioning

confidence: 99%

Autonomic circulatory and cerebrocortical responses during increasing depth of propofol sedation/hypnosis in humans

Lafreniere

Milne

Brunet

et al. 2000

Can J Anesth/J Can Anesth

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Purpose: To describe the relative effects of graded central nervous system (CNS) depression, using increasing propofol infusion rates, on neurovegetative brainstem-mediated circulatory control mechanisms and higher cortical activity in healthy humans.Methods: Propofol was administered using an infusion scheme designed to achieve three target blood concentrations in ten healthy volunteers. Blood propofol concentrations and sedation scores were determined at baseline, during the three propofol infusion levels, and 30 min into the recovery period. Electroencephalographic (EEG) power was measured in three frequency bands to quantify cortical activity, and autonomic heart rate control was quantified using spontaneous baroreflex assessment and power spectral analysis of pulse interval. Results: Sedation scores closely paralleled propofol blood concentrations (0, 0.53 ± 0.34, 1.24 ± 0.21, 3.11 ± 0.80, and 0.96 ± 0.42 µg·mL -1 at baseline, three infusion levels and recovery respectively), and all subjects were unconscious at the deepest level. Indices of autonomic heart rate control were decreased only at the deepest levels of CNS depression, while EEG effects were apparent at all propofol infusion rates. These EEG effects were frequency specific, with power in the beta band being affected at light levels of sedation, and alpha and delta power altered at deeper levels. Conclusions: The results of this study support a relative preservation of neurovegetative circulatory control mechanisms during the early stages of CNS depression using gradually increasing rates of infusion of propofol. Indices of circulatory control did not reliably reflect depth of sedation.Objectif : Décrire les effets relatifs d'une dépression graduée du système nerveux central (SNC) sur les mécanismes d'origine centrale du contrôle neurovégétatif de la circulation, et l'activité corticale supérieure chez des humains sains, en utilisant des perfusions de propofol à vitesses croissantes. Méthode : Le propofol a été administré, chez dix volontaires en santé, selon un schéma de perfusion conçu pour atteindre trois concentrations sanguines cibles. Les concentrations sanguines de propofol et les scores de sédation ont été déterminés au départ, pendant les trois régimes de perfusion de propofol et à 30 min pendant la récupéra-tion. La puissance électroencéphalographique (EEG) a été mesurée selon trois bandes fréquentielles pour quantifier l'activité corticale, et le contrôle autonome de la fréquence cardiaque a été mesuré à l'aide d'une évaluation baroréflexe spontanée et de l'analyse spectrale de la puissance de l'intervalle pulsé.Résultats : Les scores de sédation ont présenté un étroit parallélisme avec les concentrations sanguines de propofol (0; 0,53 ± 0,34, 1,24 ± 0,21; 3,11 ± 0,80, et 0,96 ± 0,42 µg·mL -1 au début, pendant les trois perfusions et la récupération, respectivement), et tous les sujets ont connu un profond sommeil. Les indices de contrôle autonome de la fréquence cardiaque ont diminué seulement au moment de la plus profonde dépression d...

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Section: Autonomic Circulatory Controlmentioning

confidence: 99%

Autonomic circulatory and cerebrocortical responses during increasing depth of propofol sedation/hypnosis in humans

Lafreniere

Milne

Brunet

et al. 2000

Can J Anesth/J Can Anesth

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“…2,9 It also increases cardiac baroreflex sensitivity in hypertensive individuals and stabilize blood pressure. 10 Furthermore clonidine increases perioperative hemodynamic stability in patients undergoing laparoscopic cholecystectomy with enhancement of parasympathetic control of heart rate. 11,12 The effect of preanaesthetic medication on minimum anaesthetic concentration of propofol has been studied earlier.…”

Section: Original Articlementioning

confidence: 99%

Effect of Oral Clonidine Premedication on Propofol Consumption for Patient Undergoing Laparoscopic Cholecystectomy

et al. 2016

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Background: Various goals of premedication includes anxiolysis, sedation, amnesia, analgesia, attenuation of autonomic reflexes, and reduction of anaesthetic dose requirement. Preanaesthetic oral clonidine has been shown to produce anxiolysis, sedation and attenuation of hemodynamic stress response to tracheal intubation. Objective: To investigate the clinical efficacy of oral clonidine on propofol consumption in patients undergoing laparoscopic cholecystectomy. Methods: This was a prospective, randomized, double-blind placebo controlled study conducted in ninety consecutive patients randomly divided into three equal groups (placebo, tab. clonidine 150 mcg and tab. clonidine 300 mcg) meeting inclusion and exclusion criteria who underwent laparoscopic cholecystectomy. Study drug was given 60 minutes before induction of anaesthesia. Anaesthesia was induced with intravenous pethidine 1mg/kg followed by propofol . The dose of propofol for loss of verbal command was recorded. Anaesthesia was maintained with propofol at the rate of 10 mg/kg/h for 10 minutes then to 8 mg/kg/h for 10 minutes and ultimately decreased to 6 mg/kg/h after tracheal intubation. The rate of propofol infusion was adjusted by 2mg/kg/h to obtain adequate depth of anaesthesia (maintaining hemodynamic parameters within 20% of baseline). Results: The propofol induction dose was less in clonidine 150 mcg (1.2±0.2 mg/kg) and clonidine 300 mcg (1.08±0.24 mg/ kg) groups as compared to placebo group ( 1.4±0.3 mg/kg) (p=˂0.001). The rate of propofol infusion in mg/kg/h and in mcg/kg/h was lower in clonidine 150 mcg (6.7±1.6 and 121.3±11.37) and clonidine 300 mcg (7±1.4 and 120.0±9.8) groups as compared to placebo (10±3.2 and 148.0±32.53) group (p =˂ 0.001). Conclusion: oral clonidine premedication reduces propofol requirement for induction and maintenance of anaesthesiain patients undergoing laparoscopic cholecystectomy.

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“…3D in [12]). However, this demonstration [12] was only qualitative. Furthermore, clonidine is nonselective and presents both as a sympatholytic [13] and as a parasympathomimetic [14].…”

Section: Introductionmentioning

confidence: 98%

“…Clonidine reduced pressure lability in hypertensive patients [10,11] following major surgery (see Fig. 3D in [12]). However, this demonstration [12] was only qualitative.…”

Section: Introductionmentioning

confidence: 99%

“…Furthermore, clonidine is nonselective and presents both as a sympatholytic [13] and as a parasympathomimetic [14]. Thus, these data [12] leave open the question of whether pressure lability is linked only to sympathetic inhibition. An alternative explanation could be that reduced pressure lability might be secondary to increased parasympathetic activity to the heart ("cardiac vagal activity"), and increased barorefl ex sensitivity.…”

Section: Introductionmentioning

confidence: 99%

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Effect of catecholamine depletion on increased blood pressure lability upon emergence from halothane anesthesia in rats: the role of sympathetic nervous activity in postanesthetic circulatory instability

et al. 2008

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Cardiac Baroreflex during the Postoperative Period in Patients with Hypertension

Abstract: Patients with hypertension exhibit reduced heart rate control during the recovery period after elective surgery. Clonidine prevents this reduction in heart rate control. This may represent a basis for the improved circulatory stability seen with perioperative administration of clonidine.

Cited by 47 publications

References 39 publications

Autonomic circulatory and cerebrocortical responses during increasing depth of propofol sedation/hypnosis in humans

Autonomic circulatory and cerebrocortical responses during increasing depth of propofol sedation/hypnosis in humans

Effect of Oral Clonidine Premedication on Propofol Consumption for Patient Undergoing Laparoscopic Cholecystectomy

Effect of catecholamine depletion on increased blood pressure lability upon emergence from halothane anesthesia in rats: the role of sympathetic nervous activity in postanesthetic circulatory instability

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