不同剂量氯胺酮对右美托咪啶辅助镇静病人BIS影响

EFFECT OF DIFFERENT DOSAGE OF KETAMINE ON BISPECTRAL INDEX IN PATIENTS SEDATED WITH DEXMEDETOMIDINE

目的比较不同剂量的氯胺酮对右美托咪啶镇静期间脑电双频指数(BIS)的影响。方法选择80例择期硬膜外麻醉下行妇科手术的病人,ASA分级Ⅰ或Ⅱ级,随机分为K1、K2、K3组和生理盐水组(N组)。在硬膜外麻醉达到预定平面后,开始泵注负荷量(0.5μg.kg-1)右美托咪啶,继以0.5～1.0μg/(kg.h)的速度持续泵注,待BIS降至≤60并稳定10min后,K1、K2、K3组分别静注氯胺酮0.2、0.4和0.6mg/kg,N组给相同容量的生理盐水。记录各组给氯胺酮前及后0、3、6、9、12及15min时点的BIS、警觉/镇静(OAA/S)评分、心率(HR)和平均动脉压(MAP)。结果与静注氯胺酮前比较,K1组静注氯胺酮后各时点HR、MAP、BIS差异无显著意义(P>0.05),OAA/S评分降低(F=3.66,q=4.472～5.367,P<0.05);K2组给予氯胺酮后HR、MAP无明显变化(P>0.05),BIS值在用药后3min明显升高(F=2.60,q=4.642,P<0.05),6min时又恢复至用药前水平,OAA/S评分给予氯胺酮后明显降低(F=18.65,q=11.424,P<0.05);K3组MAP给予氯胺酮前后无明显变化(P>0.05),HR静注氯胺酮后不同时点均明显升高(F=7.46,q=5.530～7.604,P<0.05),BIS值在静注氯胺酮后3～9min明显升高(F=10.39,q=5.280～6.865,P<0.05),而OAA/S评分明显降低(F=71.36,q=22.350,P<0.05)。与N组相比,K1组各时间点OAA/S评分、HR、MAP、BIS无明显差异(P>0.05);K2组静注氯胺酮后3min时BIS明显升高(F=7.72,q=4.788,P<0.05),0～15min时点的OAA/S评分明显降低(F=18.64～44.90,q=6.828～12.213,P<0.05),而HR、MAP无明显差异(P>0.05);K3组BIS在静注氯胺酮后3～9min时点明显升高(F=3.34～7.72,q=3.787～5.267,P<0.05),在0～15min时点OAA/S评分明显降低(q=9.454～12.932,P<0.05),而HR、MAP无明显变化(P>0.05)。结论在右美托咪啶镇静期间单次小剂量应用氯胺酮时,BIS值不能反映病人的真正镇静深度,氯胺酮可显著加深病人的麻醉深度。

Objective To compare the effect of different dosage of ketamine on bispectral index （BIS） in patients sedated with dexmedetomidine （DEX）. Methods Eighty ASA class Ⅰ orⅡ patients scheduled for gynecologic operation under epidural anesthesia were evenly randomized to ketamine groups K1, K2, K3 and normal saline group （group N）. When the expected anesthetic plane was obtained, Dex was then given to patients in all four groups with a loading dose of 0.5μg · kg^- 1, and then continuing medication with Dex at the rate of 0.5- 1.0μg/（kg · h）. When BIS declined to 60 and stabilized for 10 min, intravenous ketamine 0.2, 0.4 and 0.6 mg/kg was offered to patients in groups K1, K2 and Ka, respectively, to those in group N, isovolume of normal saline was given. Heart rate （HR）, mean arterial blood pressure （MABP）, BIS and OAA/S were recorded before and 0 min, 3 min, 6 min, 9 min, 12 min and 15 min after the infusion of ketamine. Results The differences of HR, MAP, and BIS between before administration of ketamine and in group K1 were not significant （P〉0.05）, but OAA/S was lower in group K1 （F=3.66,q=4. 472-5. 367,P〈0.05）. In group K2, the HR and MAP did not change obviously after ketamine was given （P〉 0.05）, BIS increased after three minutes of ketamine infusion （F=2.60,q=4. 642,P〈0.05）, and returned to its before ketaminemedication level at six minutes, and OAA/S decreased significantly （F= 18.65, q= 11. 424, P〈0.05）. In group K3, MAP did not show much changes before and after giving ketarnine （P〉0.05）, and HR increased at different time points （F=7.46 ,q=5. 530- 7. 604,P〈0. 05）, BIS increased significantly at 3-9 minutes after ketamJne infusion, OAA/S lowered significantly （F= 71. 36, q=22. 350,P〈0.05）. Compared with group N, the differences of OAA/S, HR, MAP and BIS in group K1 were not significant （P〉0.05） ; the BIS in group K2 elevated dramatically at three minutes after injection of ketamine （F=7.72 ,q=4. 788 ,P〈0.05）, OAA/S lowered significantly at 0-15 minutes after injection of ketamine （F= 18.64-44.90 ,q= 6. 828-12. 213, P〈0.05）, butthe differences of HR and MAP were not significant （P〉0.05） ; BIS increased significantly in group K3 at 3-9 minutes after ketamine injection （F=3. 34 7. 72,q=3. 787-5. 267,P〈0. 05）, OAA/Slowered significantly at 0-15 minutes （q= 9. 454-12. 932 ,P〈0.05）, but HR and MAP did not change obviously （P〉0.05）. Conclusion A single small dose of ketamine used during the stage of sedation with dexmedetomidine, BIS does not reflect the patient＇s real depth of sedation, but will notably deepen the patient＇s depth of anesthesia.