右美托咪定镇静时唤醒状态下的脑电图模式
Electroencephalographic Arousal Patterns Under Dexmedetomidine Sedation
在无唤醒状态下，难以评估右美托咪定镇静的深度。本研究探讨并证明了额叶脑电图（EEG）可作为右美托咪定镇静深度的客观测量指标。本试验的目的为：在不同剂量的右美托咪定镇静过程中脑电图的反应模式，并确定哪种谱率与评估右美托咪定的最佳镇静水平相关。
本试验纳入了16名健康志愿者，Sedline脑电图传感器置于前额， 在250Hz 频率下收集EEG数据。使用计算机把控输注泵输注右美托咪定：4个15分钟的目标血浆浓度分别为0.3、0.6、1.2和2.4ng/mL。在输注前以及不同浓度右美托咪定输注结束时测量镇静和唤醒状态下右美托咪定血浆浓度。EEG信号用于估计连续4秒数据段中的谱率，对于3个功率带具有75％重叠分别为δ波：0.5-1.5Hz，α波：9-14Hz，β波：15-24Hz。分析右美托咪定的血浆浓度、镇静水平和各种EEG参数之间的关系。
随着右美托咪定浓度的增加，EEG的值也增加，高频率（β）的逐渐减弱，α和δ的频率增强。β波谱率最能预测右美托咪定的镇静深度（R =-0.60,95％CI：-0.43～ -0.75）。δ和α波谱率预测右美托咪定的镇静深度相关性的相应值分别为：R = 0.28（95％CI：0.03～0.45）、R = 0.16（95％CI，-0.09～0.38）。当β波谱率降至-16 dB以下或增量率超过15 dB时，受试者显示中度至深度镇静。当受试者处于唤醒状态时，在0.6、1.2和2.4ng / mL的右美托咪定水平下，δ和α波中频率降低（P <0.001）。在β波中，快速觉醒的波谱率增加（P <0.001），然后缓慢下降到基线值。在唤醒受试者后，EEG波谱率恢复到基线值的时间显著慢于受试者的临床观察清醒时间。
不同剂量的右美托咪定镇静下，本研究发现脑电图β波谱率小于-16 dB和/或增量波谱率超过15 dB与中度至深度镇静状态相关，并且EEG波谱率恢复到基线值的时间显著慢于受试者的临床观察清醒时间。但本研究结果尚不完全适用于临床。
Sleigh J W, Vacas S, Flexman A M, et al. Electroencephalographic Arousal Patterns Under Dexmedetomidine Sedation[J]. Anesthesia & Analgesia, 2018:1.
BACKGROUND: The depth of dexmedetomidine-induced sedation is difficult to assess without
arousing the patient. We evaluated frontal electroencephalogram (EEG) as an objective measure of dexmedetomidine-induced sedation. Our aims were to characterize the response patterns of EEG during a wide range of dexmedetomidine-induced sedation and to determine which spectral power best correlated with assessed levels of dexmedetomidine-induced sedation.
METHODS: Sedline EEG sensor was positioned on the forehead of 16 volunteers. Frontal EEG
data were collected at 250 Hz using the Sedline monitor. A computer-controlled infusion pump
was used to infuse dexmedetomidine to four 15-minute target plasma concentrations of 0.3,0.6, 1.2, and 2.4 ng/mL. Arterial blood samples for dexmedetomidine plasma concentration and sedation (self-reported numerical rating scale) and arousal were measured at baseline and at the end of each infusion step. The EEG signal was used to estimate spectral power in sequential 4-second data segments with 75% overlap for 3 power bands: delta = 0.5–1.5 Hz,alpha = 9–14 Hz, beta = 15–24 Hz. We quantified the relationships among the plasma concentrations of
dexmedetomidine, level of sedation, and various EEG parameters.
RESULTS: EEG data at the end of the dexmedetomidine infusion steps show progressive loss of high frequencies (beta) and increase in alpha and delta powers, with increasing dexmedetomidine
concentrations. Beta prearousal spectral power was best in predicting dexmedetomidineinduced
level of sedation (R = −0.60, 95% CI, −0.43 to −0.75). The respective values for delta and alpha powers were R = 0.28 (95% CI, 0.03–0.45) and R = 0.16 (95% CI, −0.09 to 0.38). When the beta power has dropped below −16 dB or the delta power is above 15 dB, the subjects show moderate to deep levels of sedation. When awakening the subject, there is a reduction in power in the delta and alpha bands at the 0.6, 1.2, and 2.4 ng/mL dexmedetomidine target levels (P < .001 for all). In beta band, there is a rapid awakening-induced increase in power (P < .001) followed by a slow return toward baseline values. After arousing the subjects, the EEG powers returned toward baseline values significantly slower than our clinical observation of the subjects’ wakefulness would have suggested.
CONCLUSIONS: Using a wide range of dexmedetomidine doses, we found that frontal EEG beta power of less than −16 dB and/or a delta power of over 15 dB was associated with a state of moderate to deep sedation and that poststimulus return of EEG powers toward baseline values took significantly longer than expected from observation of the arousal response. It is unclear whether these observations are robust enough for clinical applicability.