女性患者不同效应室靶浓度罗库溴铵肌松效应的比较

目的 比较女性患者不同效应室靶浓度罗库溴铵的肌松效应.方法 选择女性甲状腺或乳腺手术患者120例,ASA分级Ⅰ或Ⅱ级,年龄40～ 55岁,BMI 18～22 kg/m2.采用随机数字表法,将患者随机分为4组(n=30),A组、B组、C组麻醉诱导时罗库溴铵效应室靶浓度(Ce)为3.5 μg/ml,麻醉维持Ce分别为1.0、1.2、1.4 μg/ml；D组麻醉诱导时Ce为3.8μg/ml,麻醉维持Ce为1.2 μg/ml.记录肌松起效时间、恢复时间、恢复指数、罗库溴铵用量；评估气管插管条件和术中肌松程度.结果 与A组比较,B组、C组和D组肌松程度深,肌松满意率高(p＜0.05),B组、C组、D组间上述指标差异无统计学意义(P＞0.05).与A组、B组和C组比较,D组起效时间最短(P＜0.05).与C组比较,A组、B组和D组罗库溴铵用量、恢复时间、恢复指数降低(P＜0.05).B组和D组罗库溴铵用量、恢复时间、恢复指数比较差异无统计学意义(P＞ 0.05).结论 麻醉诱导时罗库溴铵Ce 3.8 μg/ml,麻醉维持Ce1.2 μg/ml,可产生满意的肌松条件,且有利于术后肌松恢复,是一种适用于女性患者的TCI给药方案.     

肝移植术患者罗库溴铵不同给药方式肌松效果的比较

目的 比较肝移植术患者间断静脉注射(Ⅳ)、静脉输注(CI)和靶控输注(TCI)罗库溴铵的肌松效果.方法 拟行肝移植术的患者36例,性别不限,年龄21～63岁,体重48～80 kg,Child-Pugh评分7～9分,肝功能Child分级B或C级,随机分为3组(n=12):Ⅳ组、CI组和TCI组.采用TOF模式进行肌松监测,Ⅳ组:麻醉诱导时静脉注射罗库溴铵0.6 mg/kg,无肝前期T1恢复至25%时、无肝期和新肝期T4/T1(TOFR)恢复至25%时追加0.15 mg/kg.TCI组:麻醉诱导时靶控输注罗库溴铵,初始效应室靶浓度3μg/ml,调整靶浓度,维持T1 5%～10%;无肝期和新肝期开始时暂停TCI,随后以效应室靶浓度0.1μg/ml再次输注,调整靶浓度,维持T15%～10%.CI组:麻醉诱导时静脉注射罗库溴铵0.6 mg/kg,无肝前期以30μg·kg-1·min-1的速率开始静脉输注,调节输注速率,维持T1 5%～10%,无肝期和新肝期开始时暂停CI,随后以1μg·kg-1·min-1的速率静脉再次输注,调整输注速率,维持T15%～10%.各组于肌松达最大效应时行气管插管,于缝合腹膜后停止给药.记录麻醉诱导时罗库溴铵肌松起效时间、T1最大抑制程度和气管插管条件满意情况;记录各组无肝期T1 25%恢复时间及TOFR 25%恢复时间,新肝期停药后T125%恢复时间、TOFR 25%恢复时间、TOFR 75%恢复时间、TOFR90%恢复时间及恢复指数;记录罗库溴铵总用量.结果 与Ⅳ组比较,TCI组和CI组气管插管条件满意率、罗库溴铵总用量、麻醉诱导时罗库溴铵起效时间、T1最大抑制程度和各期肌松恢复情况差异均无统计学意义(P＞0.05).肌松效应监测图显示Ⅳ组各期罗库溴铵肌松效应波动较大,TCI组和CI组各期肌松效应较为平稳.结论 采用Ⅳ、CI和TCI给药时,肝移植术患者罗库溴铵肌松起效和恢复情况无差异,而采用TCI或CI给药时,肌松效应较Ⅳ更加平稳.     

年龄对罗库溴铵靶控输注时效的影响

目的 探讨靶控输注(TCI)罗库溴铵时年龄对其药效学的影响.方法 选择ASA Ⅰ或Ⅱ级、无神经肌肉疾患、接受丙泊酚-NzO/O2-芬太尼复合麻醉的患者30例,根据年龄分为老年组和青壮年组,每组15例.在静脉注入罗库溴铵0.6 mg/kg后用加速度仪采用四个成串刺激(TOF)方式监测拇内收肌的收缩反应.待T1恢复至10%时开始TCI罗库溴铵,靶控血浆浓度为2μg/ml.记录神经肌肉阻滞的最大阻滞时间及起效时间、恢复时间,并记录罗库溴铵的用药量.结果 老年组的平均输注速率为(7.6±0.9)μg·kg-1·min-1,青壮年组的平均输注速率为(8.2±0.8)/μg·kg-1·min-1.单次注入罗库溴铵0.6 mg/kg后的起效时间,两组间差异无统计学意义.青壮年组的肌松恢复过程明显快于老年组,表现为单次注药后老年组的无反应期明显长于青壮年组(P<0.01);停止TCI后T1恢复到25%、50%和75%的时间及恢复指数,老年组都明显长于青壮年组(P<0.01).但老年组罗库溴铵的平均用药量明显少于青壮年组(P<0.01).两组术中肌松均维持平稳.结论 罗库溴铵采用TCI在老年患者用药量虽然相应减少,但其恢复过程仍较青壮年组延长.     

活体肝移植术供体右半肝切除后罗库溴铵用量的变化

目的 探讨活体肝移植术供体右半肝切除术后罗库溴铵用量的变化.方法 择期拟行右半肝切除术的肝移植术供体病人16例,年龄21～49岁,体重51～86 kg,ASA Ⅰ级.麻醉诱导:静脉注射咪达唑仑和芬太尼,靶控输注异丙酚和罗库溴铵(血浆靶浓度3 μg/ml),采用肌松监测,待T1/Tc=0时进行气管插管,机械通气.气管插管后罗库溴铵血浆靶浓度降至1.0 μg/ml,调整罗库溴铵浓度,维持0相似文献   

罗库溴铵对不同丙泊酚镇静水平脑电双频指数和脑状态指数的影响

目的 观察罗库溴铵对丙泊酚不同镇静水平脑电双频指数(BIS)和脑状态指数(CSI)的影响.方法 选择ASA Ⅰ或Ⅱ级气管插管全麻行择期手术患者70例.分为罗库溴铵组(L1、L2 组,n=20)和生理盐水组(C1、C2组,n=15),L1、C1组效应室浓度(Ce)设定为2.5～g/ml,L2、C2组Ce设定为4.0μg/ml.比较麻醉诱导前(To)、气管插管前(T1)、气管插管即刻(T2)、气管插管后3 min(T3)、5 min(T4)、注射罗库溴铵/生理盐水前(T5)、注射罗库溴铵/生理盐水后最大作用强度时(T6)及肌颤搐恢复时(T7)的HR、MAP,并记录T5～T7时的BIS、CSI.结果 L1组BIS、CSI T6时较T5、T7时下降(P<0.05).结论 丙泊酚Ce为2.5～μg/ml时,罗库溴铵会导致BIS、CSI 下降.     

闭环靶控输注罗库溴铵在患儿麻醉中的应用

目的比较闭环靶控与传统持续两种不同药物输注方法,输注罗库溴铵在患儿麻醉中的效果。方法择期行下腹部手术的患儿86例,男53例,女33例,年龄1～3岁,BMI 14～21 kg/m~2,ASAⅠ或Ⅱ级。用随机数字表法分为闭环组(C组)和持续组(S组),每组43例。诱导时两组均给予罗库溴铵0.6 mg/kg,当四个成串刺激中第一次肌颤搐(T1)到达最大阻滞时气管插管。麻醉维持C组使用T1闭环肌松模式,设置T1=20%为增药条件,增药速度30μg·kg~(-1)·min~(-1),维持速度1.60μg·kg~(-1)·min~(-1),自动调整罗库溴铵用量。S组恒速泵注罗库溴铵5μg·kg~(-1)·min~(-1),肌松不满意时单次追加罗库溴铵0.2 mg/kg。记录术中丙泊酚总用量、瑞芬太尼总用量和罗库溴铵总用量,罗库溴铵追加次数。记录两组肌松恢复指数(RI)、罗库溴铵停药至术毕时间、手术时间、麻醉时间、拔管时间和PACU停留时间。记录术后呼吸抑制、低氧血症等麻醉并发症发生情况。结果 C组RI明显低于S组(P0.05)、罗库溴铵追加次数明显低于S组(P0.05),拔管时间明显短于S组(P0.05)。两组丙泊酚总用量、瑞芬太尼总用量、罗库溴铵总用量、罗库溴铵停药至术毕时间、手术时间、麻醉时间和PACU停留时间差异无统计学意义。两组均未见术后呼吸抑制,低氧血症等麻醉相关并发症。结论与持续输注法比较,闭环靶控输注罗库溴铵用于1～3岁患儿下腹部手术的恢复指数明显降低,肌松恢复更快速,术中患儿肌松效果更加确切,稳定。     

罗库溴铵和顺式阿曲库铵用于肝部分切除术肌松效应的比较

目的比较罗库溴铵和顺式阿曲库铵用于肝部分切除术的肌松效应。方法择期全麻下行剖腹单纯肝部分切除术患者40例,随机均分为罗库溴铵组(R组)和顺式阿曲库铵组(C组)。全麻肌松药诱导量R组和C组分别为2倍ED95的罗库溴铵0.6mg/kg及顺式阿曲库铵0.1mg/kg,采用TOF监测肌松程度,当TOFr至25%时追加肌松药。观察两组肌松药起效时间、气管插管条件、临床作用时间、术毕恢复指数、气管拔管时间及不良反应。结果 R组起效时间明显快于、临床作用时间及术毕恢复指数明显长于C组(P0.05);两组气管拔管时间差异无统计学意义。当TOFr为0时,R组气管插管条件为优的例数明显多于C组(P0.05)。R组静脉注射痛发生率为16例(80%),明显高于C组的3例(15%)(P0.05)。两组患者围术期均未发生皮肤潮红、BP降低、HR增快及支气管痉挛等不良反应,未观察到拔管后的肌松残余作用。结论与顺式阿曲库铵比较,应用罗库溴铵具有起效快,作用时间长,虽恢复指数略长,但对拔管时间并无影响,同时未有明显的肌松残余作用,可以安全用于肝部分切除术的患者。     

罗库溴铵预注和麻黄碱预处理对小儿罗库溴铵肌松起效的影响

目的 观察小儿在罗库溴铵预注、麻黄碱预处理和罗库溴铵预注复合麻黄碱预处理对罗库溴铵起效时间、插管条件和肌松时效的影响.方法 选择全麻下行择期手术的患儿80例,ASA Ⅰ或Ⅱ级,随机均分为四组.在麻醉诱导前预先静注:Ⅰ组生理盐水O.5 ml,Ⅱ组罗库溴铵0.06 mg/kg,Ⅲ组麻黄碱70 μg/kg,Ⅳ组罗库溴铵0.06 mg/kg和麻黄碱70 μg/kg.预注和预处理4min后,Ⅰ、Ⅲ组静注罗库溴铵0.6 mg/kg,Ⅱ、Ⅳ组静注罗库溴铵0.54 mg/kg.待四个成串刺激(TOF)第1个颤搐反应高度(Th)达最大阻滞程度后行气管插管.记录肌颤搐抑制75%、90%和达最大阻滞程度的时间,并评估气管插管条件,同时观察HR、BP变化.结果 Ⅰ、Ⅱ、Ⅲ、Ⅳ组的最大阻滞起效时间分别为(196±43)、(140±43)、(144±35)和(100±33)s,Ⅱ、Ⅲ、Ⅳ组的起效时间明显短于Ⅰ组(P＜0.05),Ⅳ组的起效时间较Ⅱ、Ⅲ组短(P＜0.05).各组气管插管条件均达到6～9分,优良率100%.各组麻醉诱导期间均无明显的心血管不良反应.各组的临床肌松作用时间和恢复指数差异均无统计学意义.结论 罗库溴铵预注和麻黄碱预处理分别使用均能缩短小儿罗库溴铵的肌松起效时间,而两种方法复合使用可进一步加快肌松起效,但该方法对罗库溴铵的肌松时效无明显的影响.     

罗库溴铵复合麻黄碱预先给药对全麻患者罗库溴铵肌松效应的影响

目的 探讨罗库溴铵复合麻黄碱预先给药对罗库溴铵肌松效应的影响.方法 择期全麻手术患者100例,ASAⅠ或Ⅱ级,年龄23～64岁,体重42～88 kg,身高150～181 cm,随机分为5组(n=20):罗库溴铵组(C组)、罗库溴铵预先给药组(R组)、麻黄碱预先给药组(E组)、罗库溴铵复合麻黄碱预先给药组(RE组)和琥珀酰胆碱组(S组).麻醉诱导前R组、E组和RE组分别静脉注射罗库溴铵0.06 mg/kg、麻黄碱70 μg/kg、罗库溴铵0.06 mg/kg复合麻黄碱70 μg/kg,C组和S组无预先给药.麻醉诱导后4 min时C组和E组静脉注射罗库溴铵0.6 mg/kg,R组和RE组静脉注射罗库溴铵0.54 mg/kg,S组静脉注射琥珀酰胆碱1 mg/kg.采用Cooper法评分标准评定气管插管条件.记录从麻醉诱导时静脉注射罗库溴铵完毕至肌颤搐(Th)降至25%、10%、0的时间(分别为T25、T10、T0)和Th恢复至25%、50%的时间(分别为RT25、RT50)、肌松维持时间(从T0至RT25的时间),麻醉诱导期间每分钟记录1次心率、收缩压、舒张压和平均动脉压.结果 各组气管插管条件差异无统计学意义(P＞0.05);与C组比较,其余4组T25、T10、T0均缩短,S组RT25、RT50缩短(P＜0.05);与RE组和S组比较,R组和E组T0延长(P＜0.05);与S组比较,C组、R组、E组和RE组肌松维持时间延长(P＜0.05).结论 罗库溴铵复合麻黄碱预先给药后罗库溴铵肌松起效时间短于单独预先给药,但对肌松程度和维持时间无明显影响.     

不同剂量罗库溴铵对甲状腺手术喉返神经功能监测的影响

目的观察不同剂量罗库溴铵对甲状腺手术喉返神经(RLN)功能监测的影响。方法择期甲状腺手术患者90例,ASAⅠ或Ⅱ级,随机均分为三组,采用静-吸复合全身麻醉。麻醉诱导:丙泊酚1.5~2.0mg/kg、芬太尼4μg/kg和罗库溴铵0.3mg/kg(A组)、罗库溴铵0.6mg/kg(B组)和罗库溴铵0.9mg/kg(C组),吸入2%~3%七氟醚维持麻醉。采用TOF监测肌松。观察并记录给药前60s、给药后60s及插管后60s的BP、HR及体动变化、TOF出现第一个、第二个肌颤搐的时间及RLN振幅。结果与给药前60s比较,给药后60sB组和C组HR明显减慢,三组SBP和DBP明显降低(P0.05),气管插管后60sA组HR明显增快,SBP和DBP明显升高(P0.05)。与给药后60s比较,气管插管后60s三组HR明显增快,SBP和DBP明显升高(P0.05)。与A组比较,气管插管后60sB组和C组HR明显减慢、SBP、DBP明显降低(P0.05),C组术中未监测到RLN例数明显增加、等待时间明显延长(P0.05),B组和C组术中体动例数明显减少、TOF出现第一个肌颤搐时的RLN振幅明显降低(P0.05),三组监测时间、TOF出现第二个肌颤搐时的RLN振幅差异无统计学意义。结论 2倍ED95的罗库溴铵(0.6mg/kg)诱导复合七氟醚麻醉适用于甲状腺手术喉返神经功能的监测。     

Burdened by training not by anaesthesia

Editor—Larsson and colleagues¹ have investigated importantbut often ignored aspects of anaesthetic practice. However,they imply that specialist anaesthetists experience reducedlevels of stress when compared with trainees because they havedeveloped successful coping mechanisms over the years. Thisconclusion cannot be drawn because the specialists' attitudesto work were identified at a particular time and cannot showa progression in learned coping abilities. To demonstrate thedevelopment of these skills, the specialists would have hadto be interviewed     

Bladder carcinoma treated by preoperative radiotherapy followed by cystectomy

Summary In 1969 a clinical trial was started where patients with bladder carcinoma stage T2 and grade 3 were subjected to preoperative radiotherapy followed by cystectomy. The survival rate in this series was higher than in a previous series of comparable patients who were given full irradiation without cystectomy.     

Treatment of hemospermia caused by dilated seminal vesicles by direct drug injection guided by ultrasonography

Bilateral seminal vesicle puncture and injection of drugs with ultrasound guidance were performed in patients with hemospermia resistant to conservative therapy and with dilated seminal vesicles. Of 7 patients 6 had resolution of hemospermia for 2 to 3 months and then relapse. No side effect was noted.     

Amplification by hyperoxia of coronary vasodilation induced by propofol

We tested the hypothesis that in vitro coronary and myocardial effects of propofol (10-300 microM) should be significantly modified in an isolated and erythrocyte-perfused rabbit heart model in the absence (PaO(2) = 137 +/- 16 mm Hg, n = 12) or in the presence (PaO(2) = 541 +/- 138 mm Hg, n = 12) of hyperoxia. The induction of hyperoxia provoked a significant coronary vasoconstriction (-13% +/- 7%). Propofol induced increased coronary vasodilation in the presence of hyperoxia. Because high oxygen tension has been reported to induce a coronary vasoconstriction mediated by the closure of adenosine triphosphate-sensitive potassium channels, we studied the effects of propofol in 2 additional groups of hearts (n = 6 in each group) pretreated by glibenclamide (0.6 microM) and cromakalim (0.5 microM) in the absence and presence of hyperoxia, respectively. The pretreatment by glibenclamide induced a coronary vasoconstriction (-16% +/- 7%) which did not affect propofol coronary vasodilation. The pretreatment by cromakalim abolished the amplification of propofol coronary vasodilation in the presence of hyperoxia. Propofol induced a significant decrease in myocardial performance for a concentration >100 micro M both in the absence and presence of hyperoxia. We conclude that propofol coronary vasodilation is amplified in the presence of hyperoxia. This phenomenon is not explained by the previous coronary vasoconstriction induced by glibenclamide. However, the pretreatment of hearts by cromakalim abolished the amplification of propofol coronary vasodilation in the presence of hyperoxia. The myocardial effects of propofol were not affected by the presence of hyperoxia. IMPLICATIONS: Propofol induced a coronary vasodilation that was amplified in the presence of hyperoxia. This phenomenon does not seem to be related to previous coronary vasoconstriction. The myocardial effects of propofol were not significantly modified in the presence of hyperoxia.     

Tracheal constriction by morphine and by fentanyl in man

The effects of morphine and fentanyl on tracheal smooth muscle tone were studied in 38 patients during induction of anesthesia. Endotracheal tube cuff pressure was used to measure tracheal tone. Anesthesia was maintained with nitrous oxide, 70 per cent in oxygen, and pancuronium and ventilation was controlled with a respirator. Morphine, 0.5 mg/kg, produced a biphasic response, initially causing tracheal dilatation and then tracheal constriction. Ten minutes after morphine injection, cuff pressure increased to significantly (21 +/- 8 per cent) above control. Morphine-induced tracheal constriction could be completely blocked by the prior administration of atropine, 0.5 mg. Fentanyl, 0.006 mg/kg, also produced significant tracheal constriction, cuff pressures increasing to 44 +/- 11 per cent above control at 10 min. Fentanyl-induced tracheal constriction could be blocked by pretreatment with droperidol, 0.25 mg/kg. At equianalgesic doses, morphine and fentanyl produced similar tracheal constriction.     

Reversal by nalbuphine of respiratory depression caused by fentanyl

In 60 ASA class I or II patients given intravenous fentanyl for elective operations in doses large enough to produce postoperative respiratory depression, the intravenous administration of 20 mg nalbuphine resulted in prompt reversal of respiratory depression without loss of analgesia.