اثر آرام بخش در الکتروانسفالوگرافی کمی پس از ایست قلب Effect of sedation on quantitative electroencephalography after cardiac arrest

Introduction Cardiac arrest (CA) affects over 500,000 Americans annually [1]. Most patients with return of spontaneous circulation are comatose on hospital arrival. For these patients, sequelae of ischemic brain injury are the most common cause of morbidity and mortality [2]. Electroencephalography (EEG) has clinical and prognostic importance in this population. In addition to assessing reactivity to external stimuli, EEG is helpful to detect seizures and can guide therapeutic decision making [3–5]. EEG interpretation may be qualitative or quantitative (qEEG), but interest in qEEG analysis has recently grown. Continuous or reactive patterns predict favorable recovery, while patterns such as burst suppression and attenuation, with qEEG analogues of suppression ratio (SR) and amplitudeintegrated EEG (aEEG), are known predictors of poor outcomes [5–8]. Sedation and analgesia use is almost ubiquitous in post cardiac arrest care [9–11]. In healthy individuals and non-brain injured patients, it is known that sedative and anesthetic administration can cause burst suppression and generalized slowing of EEG, however few studies describe sedation effects on EEG in patients with severe global ischemic brain injury [12]. In particular, quantitative effects of sedation and analgesia on EEG are unknown in the post-cardiac arrest population, and sedation may be an important confounder in clinical prognostication using EEG [5]. Coma after global ischemic brain injury is associated with functional reduction of thalamo-cortical connectivity [2,13,14]. In patients with some preservation of cortical function, sedation may further reduce connectivity, increasing EEG suppression and altering EEG component frequencies. Specifically, sedation would decrease EEG amplitude and alpha/delta ratio (ADR) and increase suppression ratio (SR). In this study, we describe sedation-induced changes in qEEG of post-cardiac arrest patients, and we explore the association of response to sedation with functional recovery.We hypothesize that sedation would: 1) significantly increase SR and decrease both ADR and EEG amplitude, and 2) the magnitude of sedation effects on qEEG will be associated with outcome at hospital discharge.