异丙酚芬太尼复合不同剂量右美托咪啶麻醉对老年患者血液动力学及脊髓诱发电位的影响

Effects of propofol and fentanil compounded different doses of dexmedetomidine on hymodynamics and intraoperative somatosensory and motor evoked potentials monitoring of senile patient

目的探讨异丙酚芬太尼复合不同剂量右美托咪啶麻醉对老年患者血液动力学及对体感诱发电位（somatosensory evoked potentials，SEPs）、运动诱发电位（motor evoked potentials，MEPs）监测的影响。方法择期全麻颈椎前路手术患者45例，依据右美托咪啶剂量按随机数字表法随机分成C组（对照组）、D1组（右美托咪啶浓度0．3g·kg-1·h-1）；D2组（右美托咪啶浓度0．8μg·kg-1·h-1）。3组麻醉诱导方法相同。麻醉诱导：静脉注射咪达唑仑2mg～3mg、异丙酚Cp1．5mg／L（Marsh药代动力学参数）、芬太尼1．5μg／kg-2．0μg／kg，患者意识消失后经口置入4号喉罩，行机械通气。D1、D2两组患者置入喉罩后给予右美托咪啶0．5μg／kg静脉推注10min完成，两组患者随即分别以0．3μg·kg-1·h-1、0．8μg·kg-1·h-1持续泵注至手术结束；C组患者以生理盐水代替右美托咪啶，其余用药同D组。术中调整异丙酚芬太尼用量维持脑电双频谱指数（BIS）值45-55之间，所有病例均不给入肌肉松弛剂，术中专人持续监测并记录SEPs、MEPs。结果D1、D2组患者应用右美托咪啶后心率减慢，平均动脉压（MAP）无明显变化。3组患者SEPs P15-N20的潜伏期、波幅均无统计学差异（P〉0．05）。D2组患者有3例出现不同程度MEPs波形消失，阳性率为3／15，与D1组及C组（0／14）比较差异有统计学意义，且3例患者停用右美托咪啶20min左右MEPs波形全部恢复。结论右美托咪啶延长苏醒时间，减慢患者心率，其对老年患者SEPs影响轻微，但较大剂量应用对MEPs产生抑制作用。

Objective To evaluate the effects of different doses of dexmedetomidine compounded propofol and fentanil on hymodynamics and intraoperative somatosensory evoked potentials （SEPs） and motor evoked potentials （MEPs） monitoring on the senile people. Methods Forty-five patients undergoing selected anterior spinal fusion surgery were randomly divided into three groups by the dose of dexmedetomidine： group C （normal saline, NS）; group D1 （dexmedetomidine injected by 0.3 μg·kg-1·h-1）; group D2（dexmedetomidine injected by 0.8 μg·kg-1·h-1）. The induction of all patients in three groups：midazolam 2 mg-3 mg, propofol Cp 1.5 mg/L （Marsh model）, fentanil 1.5 μg/kg-2 μg/kg. When the patient＇s consciousness disappeared, a LMA was intubated and mechanical ventilation was made. In group D1 and group D2, dexmedetomidine （0.5 μg/kg over 10 min） was administered and then followed by an infusion of 0.3 μg·kg-1·h-1 or 0.8 μg·kg-1·h-1 until the end of surgery. In group C, the same dose of NS instead of dexmedetomidine was administered. Anesthesia was maintained by target controlled injection of propofol. Bispectral index （BIS） were kept in the range of 45-55 by adjusting the concentration of propofol. Muscle relaxant wasn＇t be used in whole operation. SEPs and MEPs were monitored by a specialist during the operation. Results Heart rate were lower in group D1 and D2 than group C, but mean arterial pressure （MAP） were no different in three groups. The latency and the amplitude of SEPs P15-N20 were also no different in three groups （P〉0.05）. Three patients＇s amplitudes of MEPs were disappeared in different degrees among the group D2. The positive rate is 3/15. There was a significant difference from the cases of group D1 （0/14） and C （0/14）. After dexmedetomidine was stopped about 20 min-30 min, the amplitudes of MEPs recoveried in all the three patients. Conclusions In senile patients, dexmedetomidine possibly prolonged analepsia time and decreased heart rate. Dexmedetomidine does not significantly influence the SEPs, but higher dose of dexmedetomidine depressed MEPs.