Effects of three anesthetic induction techniques on heart rate variability

Latson, Terry W.; McCarroll, S. M.; Mirhej, M. Andrew; Hyndman, V; Whitten, Charles W.; Lipton, James M.

doi:10.1016/0952-8180(92)90127-m

Cited by 100 publications

(64 citation statements)

References 44 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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“…Several studies have also described marked reduction of all components of the HRV power spectra following anesthesia induction with inhaled and iv anesthetics. [27][28][29] Changes in cardiac autonomic neural output are largely depended on anesthetic depth, surgical stimulation and opiate dosage. Using a lower dose opioid-benzodiazepine regimen, Kortly et al demonstrated that vagal activity, -but not cardiac sympathetic neural drive -, could be further increased as indicated by baroreflex mediated HR changes in response to PHE and NTG.…”

Section: Limitations Of the Studymentioning

confidence: 99%

Cardiovascular responses to anesthetic induction in patients chronically treated with angiotensin-converting enzyme inhibitors

Licker¹,

Schweizer²,

Hohn³

et al. 2000

Can J Anesth/J Can Anesth

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Purpose: To investigate the effects of chronic ACE inhibition on cardiac neural function following induction of general anesthesia in patients with underlying coronary artery disease. Method:In a prospective case-control study, heart rate variability (HRV) and baroreflex control were compared preoperatively and 30 min after anesthesia induction in patients receiving, or not, ACEI (n=16, control group and n=16, ACEI group). All patients had normal cardiac function and anesthesia consisted of a fixed dose regimen of fentanyl and midazolam. Anesthesia-related hypotension was defined by systolic blood pressure < 90 mmHg. Spectral density of HRV was calculated for low frequency and high frequency bands (LF, from 0.05 to 0.15 Hz and HF, from > 0.15 to 0.6 Hz). Baroreflex sensitivity was estimated after blood pressure changes induced by injections of phenylephrine (PHE) and nitroglycerin (NTG). Results:The HRV parameters and baroreflex sensitivity were not different between groups, during the awake and anesthesia periods. Anesthesia produced similar reduction in total HRV in the Control and ACEI groups (-93 ± 28% vs -89 ± 32%,) and in baroreflex sensitivity during NTG (-64 ± 21% vs -54 ± 17%) or PHE tests (-74 ± 25% vs -72 ± 22%). Anesthesia-related hypotension occurred in nine patients in the ACEI group (vs two controls). Although the hypertensive response to phenylephrine was greater after anesthesia in both groups, the sensitivity to phenylephrine was attenuated in those patients experiencing hypotension in the ACEI group. Conclusions: Chronic preoperative treatment with ACEIs does not influence cardiac autonomic regulation and anesthetic-induced hypotensive episodes are mainly attributed to decreased -adrenergic vasoconstrictive response.Objectif : Rechercher les effets d'une inhibition chronique de l'ECA sur la fonction neurale cardiaque à la suite de l'induction d'une anesthésie générale chez des patients qui présentent une cardiopathie ischémique sous-jacente.Méthode : Lors d'une étude prospective cas-témoins, la variabilité de la fréquence cardiaque (VFC) et le contrôle baroréflexe ont été comparés avant l'opération et 30 min après l'induction de l'anesthésie chez des patients qui reçoivent, ou non, un IECA (groupe témoin : n = 16, groupe IECA : n = 16). Tous les patients présentaient une fonction cardiaque normale et l'anesthésie comprenait un schéma posologique fixe de fentanyl et de midazolam. On a défini l'hypotension reliée à l'anesthésie comme la tension artérielle systolique < 90 mmHg. La densité spectrale de la VFC a été calculée pour des bandes de basses et de hautes fréquences (BF, de 0,05 à 0,15 Hz et HF, de > 0,15 à 0,6 Hz). La sensibilité baroréflexe a été évaluée après les changements de pression sanguine induits par les injections de phényléphrine (PHE) et de nitroglycérine (NTG).Résultats : Les paramètres de la VFC et la sensibilité baroréflexe n'ont pas présenté de différence intergroupe pendant les périodes d'éveil et d'anesthésie. L'anesthésie a produit une réduction similaire de la VFC total...

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“…Endüksiyon sonrası ANİ hariç diğer parametrelerde saptanan istatistiki anlamlı düşme, kullanılan ajanların sistemik baskılayıcı etkisine bağlıdır (27)(28)(29)(30). ANİ'de ise değişiklik saptanmamış olup preoperatif yeterli sedatize edilen ve ek ağrılı uyaran verilmeyen hastalarda bu bulgu doğaldır.…”

Section: Discussionunclassified

Prediction of Hemodynamic Reactivity during Sevoflurane Remifentanyl Anesthesia for Laparoscopic Cholecystectomy Using Analgesia Nociception Index

Köprülü¹,

Toptaş²,

Gül³

et al. 2016

Haseki

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Effects of three anesthetic induction techniques on heart rate variability

Cited by 100 publications

References 44 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

Cardiovascular responses to anesthetic induction in patients chronically treated with angiotensin-converting enzyme inhibitors

Prediction of Hemodynamic Reactivity during Sevoflurane Remifentanyl Anesthesia for Laparoscopic Cholecystectomy Using Analgesia Nociception Index

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