EEG-Assisted Titration of Propofol Infusion During Neuroanesthesia

Hiraoka

British Journal of Anaesthesia

et al. 2006

Section: Discussionmentioning

confidence: 99%

Changes in the effect of propofol in response to altered plasma protein binding during normothermic cardiopulmonary bypass

Hiraoka

British Journal of Anaesthesia

et al. 2006

Southern African Journal of Anaesthesia and Analgesia

“…Singh et al 15 reported smoother recovery and early tracheal extubation in the N 2 Obased group when compared with what was achieved with isoflurane-only anesthesia. Similarly, Hemelrijck et al 14 found that time to awakening was shorter when a EEG-titrated propofol infusion was used together with N 2 O (24 ± 13 minutes, compared to 34 ± 18 minutes in the propofol-only group).…”

Section: Resultsmentioning

confidence: 86%

“…Our patients received intravenous fentanyl prior to induction, which could have blocked the centrally mediated β-adrenergic stimulation of N 2 O. 20 The haemodynamic and recovery profile, with and without N 2 O, in patients receiving EEGtitrated propofol infusion during neuroanaesthesia, was compared in the study by Hemelrijck et al 14 They found that the use of N 2 O with propofol produced more hypotension during induction (p < 0.050). However, improved haemodynamic stability was observed during the maintenance period compared to that achieved in the propofol-only group.…”

Section: Resultsmentioning

confidence: 97%

A prospective, randomised, controlled clinical trial to evaluate the effect of nitrous oxide on propofol requirement in elective craniotomy in which entropy was used to measure depth of anaesthesia

Nanda

Prakash

Choudhury

et al. 2016

Open Access article distributed under the terms of the Creative Commons License [CC BY-NC-ND 4.0] http://creativecommons.org/licenses/by-nc-nd/4.0 A prospective, randomised, controlled clinical trial to evaluate the effect of nitrous oxide on propofol requirement in elective craniotomy in which entropy was used to measure depth of anaesthesia Background: Propofol is known to have a favourable effect on cerebral haemodynamics. The role of nitrous oxide (N 2 O) in neurosurgical anaesthesia is still being debated. The primary aim of this study was to assess the dose-sparing effect of N 2 O on propofol infusion maintenance dosing. Method: Fifty American Society of Anesthesiology (ASA) grade I and II adults scheduled for elective craniotomies for supratentorial tumours were enrolled in the study. The patients received a standard anaesthetic comprising a fentanyl 2 μg/kg bolus prior to propofol induction. Anaesthesia was maintained with an infusion of fentanyl (2 μg/kg/hour), atracurium and propofol. The patients were randomised into two groups. Group A received 67% N 2 O. Group B did not receive N 2 O concomitantly with the propofol infusion. Entropy was used to guide the titration of the propofol infusion in both groups. Results: The propofol maintenance dose requirements were 47% lower in Group A (54.30 ± 11.47 μg/kg/minute) vs. Group B (102.30 ± 14.00 μg/kg/minute), (p < 0.001). Conclusion: The use of supplemental N 2 O significantly decreased propofol infusion rate requirements, compared with the propofol infusion alone, in ASA I and II patients undergoing elective supratentorial tumour excision.

“…At even higher infusion rates, propofol can achieve EEG burst suppression [4]. To achieve BS during neuroanesthesia, blood propofol concentrations of 6.3 ± 1.4 mg ml -1 were required [5]. It is known, from previous studies, that to induce an isoelectric EEG much higher doses of propofol are required [6].…”

Section: Discussionmentioning

confidence: 99%

Abnormally low bispectral index and isoelectric electroencephalogram observed after administration of small doses of propofol during induction of anesthesia

2005

We describe a case in which an unexpectedly, abnormally low bispectral index value (BIS = 4) and an almost isoelectric electroencephalogram (EEG) pattern were observed during typical induction of anesthesia with propofol. Starting 2 min after the beginning of propofol administration (1.26 mg kg(-1)), the EEG recordings showed burst and suppression pattern for the next 12 min. The EEG during this period was characterized by gradual prolongation of suppression periods until the appearance of the isoelectric line. After that, burst activity returned and eventually the burst suppression pattern disappeared. We excluded the possibility of ischemic brain damage, and the evidence increasingly points toward a greater sensitivity to propofol. The findings described in this case report support the thesis that there is a wide variability in the responses of patients to propofol that cannot be detected without continuous monitoring of cortical electrical activity.