Doufas A G, Wadhwa A, Shah Y M, Lin C-M, Haugh G S, Sessler D I
Outcomes Research Institute and Department of Anesthesiology, University of Louisville, KY 40202, USA.
Br J Anaesth. 2004 Aug;93(2):228-34. doi: 10.1093/bja/aeh192. Epub 2004 Jun 25.
Neuraxial anaesthesia produces a sedative and anaesthetic-sparing effect. Recent evidence suggests that spinal cord anaesthesia modifies reticulo-thalamo-cortical arousal by decreasing afferent sensory transmission. We hypothesized that epidural anaesthesia produces sensory deafferentation-dependent sedation that is associated with impairment of brainstem transmission. We used brainstem auditory evoked potentials (BAEP) to evaluate reticular function in 11 volunteers.
Epidural anaesthesia was induced with 2-chloroprocaine 2%. Haemodynamic and respiratory responses, sensory block level, sedation depth and BAEP were assessed throughout induction and resolution of epidural anaesthesia. Sedation was evaluated using verbal rating score (VRS), observer's assessment alertness/sedation (OAA/S) score, and bispectral index score (BIS). Prediction probability (PK) was used to associate sensory block with sedation, as well as BIS with other sedation measures. Spearman's rank order correlation was used to associate block level and sedation with the absolute and interpeak BAEP latencies.
Sensory block level significantly predicted VRS (PK=0.747), OAA/S score (PK=0.748) and BIS. BIS predicted VRS and OAA/S score (PK=0.728). The latency of wave III of BAEP significantly correlated with sedation level (rho=0.335, P<0.01) and sensory block (rho=0.394, P<0.01). The other BAEP parameters did not change during epidural anaesthesia. Haemodynamic and respiratory responses remained stable throughout the study.
Sedation during epidural anaesthesia depends on sensory block level and is associated with detectable block-dependent alterations in the brainstem auditory evoked responses. Sensory deafferentation may reduce CNS alertness through mechanisms related to brainstem neural activity.
椎管内麻醉具有镇静和节省麻醉药物的作用。最近的证据表明,脊髓麻醉通过减少传入感觉传导来改变网状丘脑皮质觉醒。我们假设硬膜外麻醉会产生与脑干传导受损相关的感觉传入阻滞依赖性镇静。我们使用脑干听觉诱发电位(BAEP)来评估11名志愿者的网状功能。
用2%的氯普鲁卡因诱导硬膜外麻醉。在硬膜外麻醉诱导和消退过程中,评估血流动力学和呼吸反应、感觉阻滞平面、镇静深度和BAEP。使用语言评分量表(VRS)、观察者的警觉/镇静评估(OAA/S)评分和脑电双频指数评分(BIS)评估镇静情况。预测概率(PK)用于将感觉阻滞与镇静以及BIS与其他镇静措施相关联。使用Spearman等级相关分析将阻滞平面和镇静与BAEP的绝对潜伏期和峰间潜伏期相关联。
感觉阻滞平面显著预测VRS(PK=0.747)、OAA/S评分(PK=0.748)和BIS。BIS预测VRS和OAA/S评分(PK=0.728)。BAEP的波III潜伏期与镇静水平(rho=0.335,P<0.01)和感觉阻滞(rho=0.394,P<0.01)显著相关。在硬膜外麻醉期间,其他BAEP参数没有变化。在整个研究过程中,血流动力学和呼吸反应保持稳定。
硬膜外麻醉期间的镇静取决于感觉阻滞平面,并且与脑干听觉诱发电反应中可检测到的阻滞依赖性改变有关。感觉传入阻滞可能通过与脑干神经活动相关的机制降低中枢神经系统的警觉性。