Abstract 17847: Sedation Use Alters Quantitative Electroencephalography in Comatose Post Cardiac Arrest Patients
Introduction: Electroencephalography (EEG) has clinical and prognostic importance for comatose survivors of cardiac arrest. Recent interest in quantitative EEG (qEEG) analysis has grown. The qualitative effects of sedation on EEG are well known, but potentially confounding effects of sedatives on qEEG are poorly characterized in anoxic injury.
Hypothesis: Sedation decreases amplitude-integrated EEG (aEEG) and alpha/delta ratio (ADR), increases suppression ratio (SR), and the magnitude of this change will predict neurological recovery.
Methods: We routinely monitor comatose post-arrest patients with EEG for 48-72h, or until death or awakening. In this prospective study, we included consecutive EEG-monitored patients who had protocolized sedation interruptions, excluding those with contraindications to interruption such as seizure or hemodynamic instability. We used Persyst v12 to quantify SR, aEEG, and ADR and calculated medians for 10min immediately prior to sedation interruption and the last 5min of interruption. We used nonparametric tests to determine if the qEEG signal changed pre- to post- and whether this differed by outcome (Cerebral Performance Category 1-2 at hospital discharge vs 3-5).
Results: Of 101 screened subjects, 22 met inclusion criteria (median age 58 years, 73% male). Sedation regimens varied (18 propofol; 13 fentanyl; 5 midazolam). Median duration of sedation interruption was 35min, and did not differ by sedative type. Pre-interruption, higher ADR and aEEG and lower SR predicted favorable outcome. Post-interruption, SR decreased (median change -0.85, IQR: -12.0 to 0), aEEG increased (0.38, IQR +0.02 to 1.07), but ADR did not change. SR decreased more among those with a poor outcome (P=0.01), but aEEG and ADR changes did not differ by outcome.
Conclusions: In acute anoxic brain injury, sedation increases SR and decreases aEEG. Larger decreases in SR with sedation interruption predict worse outcomes, which may reflect a susceptibility of deafferentated cortex to suppress in response to sedation.
Author Disclosures: C.M. Drohan: None. A. Cardi: None. J.C. Rittenberger: None. C.W. Callaway: None. M. Baldwin: None. J. Elmer: Research Grant; Modest; NIH 5K12HL109068.
- © 2016 by American Heart Association, Inc.