Callie M Drohan1, Alessandra I Cardi1, Jon C Rittenberger2, Alexandra Popescu3, Clifton W Callaway2, Maria E Baldwin4, Jonathan Elmer5. 1. University of Pittsburgh School of Medicine, 3550 Terrace Street, Pittsburgh, PA 15213, USA. 2. Department of Emergency Medicine, University of Pittsburgh School of Medicine, Iroquois Building Suit 400A, 3600 Forbes Avenue, Pittsburgh, PA 15213, USA. 3. Department of Neurology, University of Pittsburgh School of Medicine, Kaufmann Medical Building, 3471 Fifth Avenue, Pittsburgh, PA 15213, USA. 4. Department of Neurology, University of Pittsburgh School of Medicine, Kaufmann Medical Building, 3471 Fifth Avenue, Pittsburgh, PA 15213, USA; Neurology Division, VA Pittsburgh Health System, 4100 Allequippa Street, Pittsburgh, PA 15213, USA. 5. Department of Emergency Medicine, University of Pittsburgh School of Medicine, Iroquois Building Suit 400A, 3600 Forbes Avenue, Pittsburgh, PA 15213, USA; Department of Critical Care Medicine, University of Pittsburgh School of Medicine, 3550 Terrace Street, Pittsburgh, PA 15213, USA. Electronic address: elmerjp@upmc.edu.
Abstract
BACKGROUND: Electroencephalography (EEG) has clinical and prognostic importance after cardiac arrest (CA). Recently, 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 after anoxic injury are poorly characterized. We hypothesize that sedation increases suppression ratio (SR) and decreases alpha/delta ratio (ADR) and amplitude-integrated EEG (aEEG), and that the magnitude of sedation effects will be associated with outcome. METHODS: We routinely monitor comatose post-arrest patients with EEG for 48-72h. We included comatose EEG-monitored patients after CA who had protocolized daily sedation interruptions. We used Persyst v12 to quantify qEEG parameters and calculated medians for 10min immediately prior to sedation interruption and for the last 5min of interruption. We used paired t-tests to determine whether qEEG parameters changed with sedation cessation, and logistic regression to determine whether these changes predicted functional recovery or survival at discharge. RESULTS: 78 subjects were included (median age 56, 65% male). Interruptions occurred a median duration of 34h post-arrest and lasted a median duration of 60min. Prior to interruption, higher aEEG predicted survival, while lower SR predicted both survival and favorable outcome. During interruption, SR decreased (p<0.001), aEEG increased (p=0.002), and ADR did not change. Larger decreases in SR predicted decreased survival (OR=1.04 per percent change; 95% CI 1.00-1.09). CONCLUSION: Higher aEEG and lower SR predict survival after CA. Sedation alters aEEG and SR, but importantly does not appear to affect the relationship between these parameter values and outcome.
BACKGROUND: Electroencephalography (EEG) has clinical and prognostic importance after cardiac arrest (CA). Recently, 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 after anoxic injury are poorly characterized. We hypothesize that sedation increases suppression ratio (SR) and decreases alpha/delta ratio (ADR) and amplitude-integrated EEG (aEEG), and that the magnitude of sedation effects will be associated with outcome. METHODS: We routinely monitor comatose post-arrestpatients with EEG for 48-72h. We included comatose EEG-monitored patients after CA who had protocolized daily sedation interruptions. We used Persyst v12 to quantify qEEG parameters and calculated medians for 10min immediately prior to sedation interruption and for the last 5min of interruption. We used paired t-tests to determine whether qEEG parameters changed with sedation cessation, and logistic regression to determine whether these changes predicted functional recovery or survival at discharge. RESULTS: 78 subjects were included (median age 56, 65% male). Interruptions occurred a median duration of 34h post-arrest and lasted a median duration of 60min. Prior to interruption, higher aEEG predicted survival, while lower SR predicted both survival and favorable outcome. During interruption, SR decreased (p<0.001), aEEG increased (p=0.002), and ADR did not change. Larger decreases in SR predicted decreased survival (OR=1.04 per percent change; 95% CI 1.00-1.09). CONCLUSION: Higher aEEG and lower SR predict survival after CA. Sedation alters aEEG and SR, but importantly does not appear to affect the relationship between these parameter values and outcome.
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