CAJ | 학술논문

目的评价末梢灌注指数(TPI)监测地氟醚诱发的患者交感神经兴奋作用.方法择期全麻患者48例,年龄25～60岁,ASA Ⅰ或Ⅱ级,随机分为3组(n=16):七氟醚组(Ⅰ组)、地氟醚组(Ⅱ组)和地氟醚+异丙酚组(Ⅲ组).气管插管后Ⅰ组和Ⅱ组地氟醚或七氟醚呼气末浓度依次快速达到0.5 MAC、1.0 MAC和1.5 MAC,并在每个水平维持5 min.Ⅲ组在气管插管后靶控输注异丙酚.血浆靶浓度至1μg/ml,地氟醚呼气末浓度依次快速达到0.5 MAC、1.0 MAC,并在每个水平维持5 min.分别在给予咪达唑仑后5 min(T0)、麻醉诱导后3 min(T1)、插管后即刻(T2)、呼气末浓度达到0.5 MAC(T3)、0.5 MAC后5 min(T4)、1.0 MAC(T5)、1.0MAC后5min(T6)、1.5MAC(T7)、1.5MAC后5min(T8)时记录心率(HR)、平均动脉压(MAP)、TPI、脑电双频谱指数,并在T0、T1、T2、T5、T7时测定血浆肾素活性和血管紧张素Ⅱ水平.结果与T4时比较,Ⅱ组T5时,IPI降低(P<0.05);与T7时比较,Ⅱ组T4～6、T8时HR、MAP降低,T3～6、T8时TPI降低(P<0.05);与Ⅰ组比较,Ⅱ组T7时HR、MAP升高,TPI降低(P<0.05);Ⅱ组T5和T7时TPI出现变化最大值的时间短于HR、MAP;ATPI与△HR、AMAP呈负相关(r=-0.593,P<0.05;r=-0.591,P<0.05);与Ⅰ组比较,Ⅱ组血浆肾素活性和AT-Ⅱ浓度升高(P<0.05).结论 TPI可灵敏地反映地氟醚诱发的患者交感神经兴奋.
목적 평개말소관주지수(TPI)감측지불미유발적환자교감신경흥강작용.방법 택기전마환자48례,년령25～60세,ASA Ⅰ혹Ⅱ급,수궤분위3조(n=16):칠불미조(Ⅰ조)、지불미조(Ⅱ조)화지불미+이병분조(Ⅲ조).기관삽관후Ⅰ조화Ⅱ조지불미혹칠불미호기말농도의차쾌속체도0.5 MAC、1.0 MAC화1.5 MAC,병재매개수평유지5 min.Ⅲ조재기관삽관후파공수주이병분.혈장파농도지1μg/ml,지불미호기말농도의차쾌속체도0.5 MAC、1.0 MAC,병재매개수평유지5 min.분별재급여미체서륜후5 min(T0)、마취유도후3 min(T1)、삽관후즉각(T2)、호기말농도체도0.5 MAC(T3)、0.5 MAC후5 min(T4)、1.0 MAC(T5)、1.0MAC후5min(T6)、1.5MAC(T7)、1.5MAC후5min(T8)시기록심솔(HR)、평균동맥압(MAP)、TPI、뇌전쌍빈보지수,병재T0、T1、T2、T5、T7시측정혈장신소활성화혈관긴장소Ⅱ수평.결과 여T4시비교,Ⅱ조T5시,IPI강저(P<0.05);여T7시비교,Ⅱ조T4～6、T8시HR、MAP강저,T3～6、T8시TPI강저(P<0.05);여Ⅰ조비교,Ⅱ조T7시HR、MAP승고,TPI강저(P<0.05);Ⅱ조T5화T7시TPI출현변화최대치적시간단우HR、MAP;ATPI여△HR、AMAP정부상관(r=-0.593,P<0.05;r=-0.591,P<0.05);여Ⅰ조비교,Ⅱ조혈장신소활성화AT-Ⅱ농도승고(P<0.05).결론 TPI가령민지반영지불미유발적환자교감신경흥강.
Objective To evaluate the desflurane-induced sympathetic activation with finger tip perfusion index (FTPl). Methods Forty-eight ASA ⅠorⅡ patients aged 25-60 yr undergoing elective surgery under general anesthesia were randomly divided into 3 groups (n=16 each): groupⅠsevoflurane; group Ⅱ desflurane and groupⅢ desthrane + propofol. Anesthesia was induced with midazolam 0.03 mg/kg, propofol 2 mg/kg and fentanyl 2 μg/kg. Tracheal intubatian was facilitated with vecuronium 0.1 mg/kg. The patients were mechanically ventilated (VT 8-10 ml/kg, RR 12 bpm). PETCO2 was maintained at 35-40 mm Hg. In group ⅠandⅡanesthesia was maintained with sevoflurane and desflurane respectively. The end-tidal concentration of sevoflurane and desflurane were rapidly increased to 0.5 MAC, 1.0 MAC and 1.5 MAC and maintained at each level for 5 rain. In group Ⅲanesthesia was maintained with TCI of propofol and destlurane. The target plasma prepofol concentration was set at 1 μg/ml and the end-tidal concentration was rapidly increased to 0.5 MAC and 1.0 MAC and maintained at each level for 5 mitt. MAP, HR, FTPI and BIS were continuously monitored and recorded at 5 rain after midazolam (T0), 3 rain after induction of anesthesia (T1), immediately after tracheal intubation (T2), as soon as the end-tidal concentration of sevoflurane and desflurane reached 0.5 MAC(T3), 1.0 MAC(T5) and 1.5 MAC(T7) and after being maintained at 0.5 MAC (T4), 1.0 MAC (T6) and 1.5 MAC (T8) for5 rain. The plasma renin activity and the levels of angintonin Ⅱwere determined at T0, T1, T2, T5 and T7 by using radioimmuno-ssay. Results FTPI was significantly lower at T5 than at T4 in group Ⅱ HR and MAP were significantly lower at T4-6 and T8 and FTPI were significantly lower at T3～6 and T0 than at T7 in group Ⅱ. HR and MAP were significantlyhigher while FTPI was lower at T7 in groupⅡthan in group Ⅰ The changes in MAP and FTPI between T4 and T5 were significantly less in group Ⅲthan in group Ⅱ. The time when the highest value of FTPI was maintain was significantly shorter than the time when the highest values of HR and MAP were maintained at T5 and T7 in group ⅡΔFTPI was negatively correlated with ΔHR and ΔMAP (r=-0.593, P<0.05;r=-0.591, P<0.05). Conclusion FTPI can reflect the desflurane-induced sympathetic activation promptly and sensitively.