Sympathetic Muscle Nerve Activity, Peripheral Blood Flows, and Baroreceptor Reflexes in Humans during Propofol Anesthesia and Surgery

Sellgren, Johan; Ejnell, Hasse; Elam, Mikael; Pontén, Johan; Wallin, B. Gunnar

doi:10.1097/00000542-199403000-00009

Cited by 146 publications

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“…Propofol has been shown to depress sympathetic neuronal activity and cardiac baroreflex sensitivity after induction doses. 4,7,9,30 In addition, a shift to sympathetic predominance has been shown after induction, as evidenced by an increase in low frequency relative to high frequency power. 31,32 However, during steady state infusions at 54 and 108 µg·kg·min -1 propofol did not decrease baroreflex sensitivity in humans.…”

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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“…Propofol and thiopental are both popular anesthetic induction agents. 11,12 We previously reported that tracheal intubation induced less hypertension and tachycardia when propofol was used for induction. Thiopental did not inhibit hypertension or tachycardia induced by tracheal intubation.…”

Section: Response To Intubationmentioning

confidence: 99%

“…Thiopental did not inhibit hypertension or tachycardia induced by tracheal intubation. 9 Although cardiac inhibition and vasodilation from propofol may produce hypotension and bradycardia, [11][12][13] other commonly used general anesthetics, including thiopental, are similar. 11,14,15 For example, Mouren et al reported that propofol did not inhibit the myocardial performance of a blood-perfused isolated heart, but that thiopental did.…”

Section: Response To Intubationmentioning

confidence: 99%

Propofol ensures a more stable A-line ARX index than thiopental during intubation

Hsu

Yang

See

et al. 2005

Can J Anesth/J Can Anesth

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“…Other mechanisms include inhibition of volume-sensitive chloride channels in coronary artery smooth muscle cells [Masuda et al 2003], a property which may cause depolarization and block adenosine triphosphate channels in rat cardiomyocytes [Kawano et al 2004] or polymorphic ventricular tachycardia in rabbits with long QT syndrome type 2 [Odening et al 2008]. Propofol has also been shown to inhibit sympathetic neuronal activity and decrease baroreflex sensitivity, mechanisms that are believed to predispose other sedative agents to QTc prolongation [Sellgren et al 1994]. Yet, formal evaluations of propofol on QTc interval changes among ICU patients are lacking.…”

Section: Introductionmentioning

confidence: 99%

Propofol-associated QTc prolongation

Scalese

Herring

Rathbun

et al. 2016

Therapeutic Advances in Drug Safety

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Objectives: Propofol is a preferred agent for sedation in patients in the intensive care unit (ICU) due, in part, to its established safety profile. Despite this, recent case reports have suggested a potential for prolongation of the corrected QT interval (QTc) in ICU patients receiving propofol, though limited empirical work has been conducted to evaluate this association. As such, the purpose of this study was to assess the relationship between propofol infusion and QTc prolongation in a historical cohort of ICU patients. Methods: A single-center, historical, observational, pre-post cohort analysis of medical records from admitted patients ⩾18 years old with cardiovascular disease was conducted, involving cases who received propofol infusion for ⩾3 hours with sequential electrocardiogram monitoring from 2006 to 2012. A multivariable, generalized linear model regression was employed to assess the primary outcome of on-propofol QTc interval (QTc 2 ), controlling for various demographic and clinical factors. Results: A total of 96 patients met inclusion criteria, averaging 56.1 ± 14.1 years of age and 86.1 ± 25.0 kg, with 37.5% being female. A mean prolongation in QTc interval of 30.4 ± 55.5 ms (p < 0.001) was observed during the propofol infusion, with 43.8% of cases exhibiting an on-infusion QTc 2 of ⩾ 500 ms. Regression analyses suggested that prolongation in on-propofol QTc was independently associated with baseline QTc interval and amiodarone use, while weight as inversely associated with QTc 2 (p < 0.05). Conclusion:This historical cohort analysis of adult ICU patients receiving propofol suggests that on-infusion QTc prolongation was associated with increasing baseline QTc interval and with amiodarone use. Further research is needed to evaluate the clinical significance and cause-and-effect relationship between potential QTc changes and propofol use in the ICU.

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Sympathetic Muscle Nerve Activity, Peripheral Blood Flows, and Baroreceptor Reflexes in Humans during Propofol Anesthesia and Surgery

Cited by 146 publications

References 0 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

Propofol ensures a more stable A-line ARX index than thiopental during intubation

Propofol-associated QTc prolongation

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