Intracranial pressure during induction of anaesthesia and tracheal intubation with etomidate-induced EEG burst suppression
Abstract
This study was designed to determine if induction of anaesthesia with etomidate titrated to an early EEG burst suppression pattern would produce minimal changes in cerebral perfusion pressure, and prevent increases in intracranial pressure (ICP) associated with tracheal intubation. Eight patients, 18–71 yr, with intracranial space-occupying lesions, were studied. In each patient ICP was monitored via a lateral ventriculostomy catheter placed preoperatively. In the operating room, an ECG, a radial arterial line, and a two-channel computerized EEG were placed. Control (awake) measurements of MAP (mmHg), ICP (mmHg), CPP(mmHg), heart rate (HR-bpm), EEG power(picowatts-pW), and spectral edge frequency (SEF, Hz) were obtained. Anaesthesia was induced with etomidate, 0.2 mg · kg−1 iv, followed immediately by an etomidate infusion, 20 mg · min−1, iv, and vecuronium 0.2 mg · kg−1 iv. When early burst suppression was achieved, the etomidate infusion was stopped and tracheal intubation performed. The etomidate dose (bolus plus infusion) required to reach burst suppression was 1.28 ± 0.11 mg · kg−1. Compared with awake control values (mean ± SE), the period from induction to burst suppression was associated with a 50% decrease in ICP (22 ± 1 vs 11 ± 1 mmHg, P < 0.01), but there were no changes in MAP, CPP, or HR. The decrease in ICP was maintained during the first 30 sec and the following 60 sec after intubation as MAP and HR remained unchanged. Our results suggest that when etomidate was administered to early burst suppression pattern on EEG, minimal changes in CPP occurred during induction of anaesthesia and a marked reduction in ICP was maintained following tracheal intubation.
Key words
Anaesthetics, Intravenous: etomidate Intubation: endotracheal Measurement Techniques: blood pressure, electroencephalography, intracranial pressure, cerebral perfusion pressureAbstract
Cette étude a été entreprise afin de déterminer si l’induction de l’anesthésie avec l’étomidate, dosé pour provoquer un début de suppression des ondes à l’EEG, produirait des changements minimes de la pression de la perfusion cérébrale, et préviendrait les augmentations de tension intrâcrdnienne (ICP) associées à l’intubation endotrachéale. Huit patients agés de 18 à 71 ans et avec une lésion intracrânienne expansive, ont été étudiés. Dans chaque cas, la tension intracrânienne, était surveillée à l’aide d’un cathéter inséré avant la chirugie à l’aide d’une ventriculostomie latérale. Après l’installation en salle d’opération d’un ECG, d’une ligne artérielle radiale et d’un EEG informatisé à deux canaux, des mesures de contrôle (à l’état d’éveil) de la tension artérielle moyenne (MAP) (mmHg), de la pression de la perfusion cérébrale (CPP) (mmHg), de la fréquence cardiaque (HR — bpm), de la puissance de l’EEG (picowatts-p W) et de la fréquence de l’extrémité du spectre («spectral edge») (SEF, Hz) était obtenues. L’anesthésie était induite avec l’étomidate à raison de 0,2 mg · kg−1 iv, suivie d’une perfusion d’étomidate à 20 mg · kg−1 iv.et de vécuronium à 0,2 mg · kg−1 iv. Lorsque la suppression des ondes de l’EEG était obtenue, la perfusion d’étomidate était cessée et on procédait à l’intubation endotrachéale. La dose d’étomidate (bolus et perfusion) requise pour supprimer les ondes à l’EEG était de 1,28 ± 0,11 mg · kg−1. Comparativement aux valeurs de contrôle à l’état d’éveil (moyenne ± SE), la période entre l’induction et la suppression des ondes de l’EEG était associée à une diminution de 50% de l’ICP (22 ± 1 vs 11 ± 1 mmHg, P < 0,01), mais il n’y avait aucun changement de MAP, CPP, ou HR. La diminution de l’ICP était maintenue pendant les 30 premières secondes, et une minute après l’intubation, alors que la MAP et le HR demeuraient inchangés. Nos résultats suggèrent que lorsque l’étomidate est administré et dosé jusqu’ à la suppression des ondes à l’EEG, des changements minimes dans la CPP apparaissent avec l’induction de l’anesthésie et une réduction marquée de l’ICP est maintenue suite à l’intubation trachéale.
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