Barry J Ruijter1, Michel J A M van Putten2, Walter M van den Bergh3, Selma C Tromp4, Jeannette Hofmeijer5. 1. Department of Clinical Neurophysiology, Technical Medical Centre, University of Twente, Enschede, the Netherlands. Electronic address: b.j.ruijter@utwente.nl. 2. Department of Clinical Neurophysiology, Technical Medical Centre, University of Twente, Enschede, the Netherlands; Departments of Neurology and Clinical Neurophysiology, Medisch Spectrum Twente, Enschede, the Netherlands. 3. Department of Critical Care, University Medical Center Groningen, University of Groningen, Groningen, the Netherlands. 4. Departments of Neurology and Clinical Neurophysiology, St. Antonius Hospital, Nieuwegein, the Netherlands. 5. Department of Clinical Neurophysiology, Technical Medical Centre, University of Twente, Enschede, the Netherlands; Department of Neurology, Rijnstate Hospital, Arnhem, the Netherlands.
Abstract
OBJECTIVE: To quantify the effects of propofol on the EEG after cardiac arrest and to assess their influence on predictions of outcome. METHODS: In a prospective multicenter cohort study, we analyzed EEG recordings within the first 72 h after cardiac arrest. At six time points, EEGs were classified as favorable (continuous background), unfavorable (generalized suppression or synchronous patterns with ≥50% suppression), or intermediate. Quantitative EEG included measures for amplitude, background continuity, dominant frequency, and burst-suppression amplitude ratio (BSAR). The effect of propofol on each measure was estimated using mixed effects regression. RESULTS: We included 496 patients. The EEG after propofol cessation had no additional value over EEG-based outcome predictions during propofol administration at 12 h after cardiac arrest. Propofol was associated with decreased EEG amplitude, background continuity and dominant frequency, and increased BSAR. However, propofol did neither increase the chance of unfavorable EEG patterns (adjusted odds ratio (aOR) 0.95 per increase of 2 mg/kg/h, 95%-CI: 0.81-1.11) nor decrease the chance of favorable EEG patterns (aOR 0.98, 95%-CI: 0.89-1.09). CONCLUSIONS: Propofol induces changes of the postanoxic EEG, but does not affect its value for the prediction of outcome. SIGNIFICANCE: We confirm the reliability of EEG-based outcome predictions in propofol-sedated patients after cardiac arrest.
OBJECTIVE: To quantify the effects of propofol on the EEG after cardiac arrest and to assess their influence on predictions of outcome. METHODS: In a prospective multicenter cohort study, we analyzed EEG recordings within the first 72 h after cardiac arrest. At six time points, EEGs were classified as favorable (continuous background), unfavorable (generalized suppression or synchronous patterns with ≥50% suppression), or intermediate. Quantitative EEG included measures for amplitude, background continuity, dominant frequency, and burst-suppression amplitude ratio (BSAR). The effect of propofol on each measure was estimated using mixed effects regression. RESULTS: We included 496 patients. The EEG after propofol cessation had no additional value over EEG-based outcome predictions during propofol administration at 12 h after cardiac arrest. Propofol was associated with decreased EEG amplitude, background continuity and dominant frequency, and increased BSAR. However, propofol did neither increase the chance of unfavorable EEG patterns (adjusted odds ratio (aOR) 0.95 per increase of 2 mg/kg/h, 95%-CI: 0.81-1.11) nor decrease the chance of favorable EEG patterns (aOR 0.98, 95%-CI: 0.89-1.09). CONCLUSIONS:Propofol induces changes of the postanoxic EEG, but does not affect its value for the prediction of outcome. SIGNIFICANCE: We confirm the reliability of EEG-based outcome predictions in propofol-sedated patients after cardiac arrest.
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