Different effects of propofol and dexmedetomidine sedation on electroencephalogram patterns: Wakefulness, moderate sedation, deep sedation and recovery

Abstract

Sedation induces changes in electroencephalography (EEG) dynamics. However, the distinct EEG dynamic characteristics at comparable sedation levels have not been well studied, resulting in potential interpretation errors in EEG monitoring during sedation. We aimed to analyze the EEG dynamics of dexmedetomidine and propofol at comparable sedation levels and to explore EEG changes with increased sedation levels for each agent. We measured the Bispectral Index (BIS) and 20-channel EEG under dexmedetomidine and propofol sedation from wakefulness, moderate sedation, and deep sedation to recovery in healthy volunteers (n = 10) in a randomized, 2-day, crossover study. Observer’s Assessment of Alertness and Sedation (OAA/S) score was used to assess sedation levels. Despite similar changes in increased delta oscillations, multiple differences in the EEG spatiotemporal dynamics were observed between these two agents. During moderate sedation, both dexmedetomidine and propofol induced increased spindle power; however, dexmedetomidine decreased the global alpha/beta/gamma power, whereas propofol decreased the alpha power in the occipital area and increased the global spindle/beta/gamma power. During deep sedation, dexmedetomidine was associated with increased fronto-central spindle power and decreased global alpha/beta/gamma power, but propofol was associated with increased theta/alpha/spindle/beta power, which was maximized in the frontal area. The transition of topographic alpha/spindle/beta power distribution from moderate sedation to deep sedation completely differed between these two agents. Our study demonstrated that there was a distinct hierarchy of EEG changes with increased sedation depths by propofol and dexmedetomidine. Differences in EEG dynamics at the same sedation level might account for differences in the BIS value and reflect the different sedation mechanisms. EEG-based clinical sedation monitoring should consider the effect of drug types on EEG dynamics.

Predicting the Outcome of Critically Ill Children and Adolescents with Electroencephalography

“…Changes in the EEG background rhythm and EEG reactivity with an increasing level of sedation were also demonstrated in previous reports [12,31]. In our study, sedation alone significantly influenced the EEG background and reactivity, and the EEG background score and reactivity did not predict mortality if EEG was performed in sedated patients but predicted mortality in non-sedated patients.…”

Efficacy of the bispectral index and Observer’s Assessment of Alertness/Sedation Scale in monitoring sedation during spinal anesthesia: A randomized clinical trial

“…It has recently been reported that BIS values are dependent on the variable EEG spectrums observed with specific sedative agents. 12 Rampil et al 27 reported that BIS monitoring was insufficiently sensitive to assess the level of sedation during nitrous oxide administration. The reliability and applicability of BIS monitoring used to guide propofol sedation has previously been reported.…”

Target‐controlled infusion of dexmedetomidine effect‐site concentration for sedation in patients undergoing spinal anaesthesia

“…Dexmedetomidine has been widely used as a sedative for patients undergoing regional anaesthesia because it prolongs the effect of regional anaesthesia and provides arousable sedation with less effects on respiration . The conventional infusion method for dexmedetomidine is zero‐order infusion which is administered as a maintenance infusion of 0.2‐1 µg kg −1 h −1 after a loading dose of 0.5‐1 µg kg −1 h −1 for 10 minutes . However, the conventional infusion process is entirely the clinicians' decision and it is hard to predict the effect of the infusion dose of dexmedetomidine.…”

“…1 The conventional infusion method for dexmedetomidine is zero-order infusion which is administered as a maintenance infusion of 0.2-1 µg kg −1 h −1 after a loading dose of 0.5-1 µg kg −1 h −1 for 10 minutes. 2,3 However, the conventional infusion process is entirely the clinicians' decision and it is hard to predict the effect of the infusion dose of dexmedetomidine.…”