From the Department of Anaesthesia, Waikato Clinical Campus, University of Auckland, Hamilton, New Zealand.
Department of Anesthesia and Perioperative Medicine, University of California, Los Angeles, California.
Anesth Analg. 2018 Oct;127(4):951-959. doi: 10.1213/ANE.0000000000003590.
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.
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.
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 dexmedetomidine-induced 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.
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.
在不唤醒患者的情况下，很难评估右美托咪定诱导的镇静深度。我们评估了额部脑电图（EEG）作为右美托咪定诱导镇静的客观测量方法。我们的目的是描述在广泛的右美托咪定诱导镇静范围内 EEG 的反应模式，并确定哪个频谱功率与评估的右美托咪定诱导镇静水平相关性最佳。
将 Sedline EEG 传感器放置在 16 名志愿者的额头上。使用 Sedline 监视器以 250 Hz 的频率采集额部 EEG 数据。使用计算机控制的输注泵将右美托咪定输注至四个目标血浆浓度 0.3、0.6、1.2 和 2.4ng/mL 的 15 分钟。在基线和每个输注步骤结束时测量动脉血样的右美托咪定血浆浓度和镇静（自我报告的数字评分量表）和觉醒。使用 EEG 信号估计连续 4 秒数据段的频谱功率，重叠率为 75%，用于 3 个功率带：delta = 0.5-1.5 Hz，alpha = 9-14 Hz，beta = 15-24 Hz。我们量化了右美托咪定血浆浓度、镇静水平和各种 EEG 参数之间的关系。
在右美托咪定输注步骤结束时的 EEG 数据显示，随着右美托咪定浓度的增加，高频（beta）逐渐丧失，alpha 和 delta 功率增加。右美托咪定预激前的 beta 频谱功率最能预测右美托咪定诱导的镇静水平（R = -0.60，95%CI，-0.43 至-0.75）。Delta 和 alpha 功率的相应值分别为 R = 0.28（95%CI，0.03-0.45）和 R = 0.16（95%CI，-0.09 至 0.38）。当 beta 功率降至-16dB 以下或 delta 功率超过 15dB 时，受试者表现出中度至深度镇静。当唤醒受试者时，在 0.6、1.2 和 2.4ng/mL 的右美托咪定目标水平下，delta 和 alpha 波段的功率会降低（所有 P <.001）。在 beta 波段中，唤醒诱导后会迅速增加功率（P <.001），然后缓慢恢复到基线值。唤醒受试者后，EEG 功率恢复到基线值的速度明显比我们从观察受试者的清醒状态中所预期的要慢。
使用广泛的右美托咪定剂量，我们发现额部 EEG 的 beta 功率小于-16dB 和/或 delta 功率超过 15dB 与中度至深度镇静状态相关，并且 EEG 功率从刺激后恢复到基线值所需的时间明显长于从唤醒反应的观察中预期的时间。这些观察结果是否足够稳健以用于临床应用尚不清楚。
