《肌松药的临床应用》课件

第八章第八章 肌松药的临床应用肌松药的临床应用第八章肌松药的临床应用目的与要求目的与要求掌握：掌握：肌松药的应用原则以及残留肌松作用的判断熟悉：熟悉：肌松药的不良反应，影响肌松药作用的因素 肌松药的麻醉期间的应用了解了解：神经肌肉传递功能监测目的与要求掌握：肌松药的应用原则以及残留肌松作用的判断KeynHypnosisnAnalgesianAmnesianRelaxationKeyHypnosisHistoryIn1942GriffithandJohnsonsuggestedthatd-tubocurarine(dTc)Succinylcholine,introducedbyThesleffandFoldesetalin1952In1967BairdandReidfirstreportedpancuroniumintheearly1980softwonewmusclerelaxantsofintermediatedurationatracuriumandvecuronium Theearly1990switnessedpipecuronium,doxacurium,mivacuriumandrocuroniumAnatracuriumisomer,cisatracuriumintroducedin1996 HistoryIn1942GriffithandJClinical UseTracheal intubation OperationICUCure of spasticityClinicalUseTrachealintubatioMolecularFeatures NeuromuscularblockingdrugsarequaternaryammoniumcompoundsNearlyallmusclerelaxantscontaintwopositivecharges MolecularFeaturesNeuromusculMusclerelaxantsaregenerallyquitewater-soluble Thewatersolubilityofrelaxantsinhibitsuptakeintohepatocytes Metabolismand/orexcretionintheliverisusuallynotamajorpathwayofelimination Themusclerelaxantsareeasilyexcretedbyglomerularfiltrationintheurine MusclerelaxantsaregenerallyClassDepolarizingdrugsuccinylcholineImbretil（己氨胆碱、氨酰胆碱）ClassDepolarizingdrugPHARMACOLOGY OF SUCCINYLCHOLINE Rapidhydrolysisbypseudocholinesterase假胆碱酯酶FactorsloweringpseudocholinesteraseconcentrationliverdiseasePregnancyBurnsoralcontraceptivesmonoamineoxidaseinhibitorscytotoxicdrugsneoplasticdiseaseanticholinesterasedrugs胆碱酯酶抑制剂PHARMACOLOGYCardiovascularEffectsstimulatesnicotinicreceptorsonbothsympatheticandparasympatheticgangliaandmuscarinicreceptorsinthesinusnodeoftheheart Inlowdoses,bothnegativeinotropicandchronotropic（负性变力、变频）responsesmayoccur.Thesecanbeattenuatedbyprioradministrationofatropine Withlargedoses,positiveresponses.cardiacarrhythmias CardiovascularEffectsstimulaSinus Bradycardia withhighsympathetictone,suchaschildren inadultsandappearsmorecommonlyafteraseconddoseofthedrugisgivenapproximately5minutesafterthefirstpreventedbythiopental,atropine,ganglion-blockingdrugs,andnondepolarizingmusclerelaxants SinusBradycardiaNodal(Junctional)Rhythms suppressingthesinusmechanismandallowingtheemergenceoftheatrioventricularnodeasthepacemaker preventedbyprioradministrationofdTc Nodal(Junctional)RhythmsVentricular Arrhythmias lowersthethresholdoftheventricletocatecholamine-inducedarrhythmiasCirculatingcatecholamineconcentrationsincrease4-foldandpotassiumincreasesbyone-third Otherstimuli,suchasendotrachealintubation,hypoxia,hypercarbia,andsurgery,areprobablyadditivetotheeffectofsuccinylcholine VentricularArrhythmiasComplications Hyperkalemia Burns Trauma ClosedHeadInjury Intra-AbdominalInfections RenalFailure MetabolicAcidosis ComplicationsHyperkalemiaIncreasedIntraocularPressure IncreasedIntragastricPressure PregnancyAscitesBowelobstructionHiatusherniaIntracranialPressureMusclePains IncreasedIntraocularPressureNondepolarizing drugSteroidalCompoundsPancuronium,Pipecuronium,Vecuronium,RocuroniumandRapacuronium无组胺释放作用，主要经肾排泄，可松弛迷走神经松弛迷走神经中度Pancuronium,Rapacuronium轻度Rocuronium无Pipecuronium,VecuroniumNondepolarizingdrug亲脂/亲水的水平决定肝脏摄取亲脂性强Vecuronium，RocuroniumandRapacuronium中短效、效能低、作用快、肝脏摄取代谢比例大，Vecuronium3040%经肝去乙酰基代谢亲脂性弱Pancuronium长效、效能高、作用慢、肝脏摄取代谢比例小，1520%经肝代谢亲脂/亲水的水平决定肝脏摄取Benzylisoquinolinium（苄基异喹啉）Compoundsd-Tubocurarine，Metocurine，Doxacurium，Atracurium，CisatracuriumandMivacurium有组胺释放作用，可经肾排泄，不松弛迷走神经组胺释放作用显著d-Tubocurarine中度Metocurine甲筒箭毒轻度Atracurium，Mivacurium无Doxacurium，Cisatracurium给予组胺受体(H1和H2受体)阻滞药Benzylisoquinolinium（苄基异喹啉）无Pipecuronium,VecuroniumVecuronium肝疾病、饥饿、妊娠末期及产褥期，此酶量减少或活性降低Circulatingcatecholamineconcentrationsincrease4-foldandpotassiumincreasesbyone-thirdShort-ActingRelaxants重症肌无力病人用药应十分谨慎抗惊厥药及精神药RenalFailure监测肌松药的起效、维持和消退过度肥胖、严重胸部创伤、严重肺部疾病及呼吸功能受损已近临界水平、术后需充分恢复肌力的病人肌颤搐抑制90以上可顺利完成气管插管和大部分腹部手术恩氟烷和异氟烷可促使琥珀胆碱较早演变为II相阻滞Maintenance假性胆碱酯酶异常长时效肌松药后加用中时效或短时效肌松药，前者使后者的作用时效延长Dosage(mg/kg)preventedbythiopental,atropine,ganglion-blockingdrugs,andnondepolarizingmusclerelaxantsIntubation(att=+2.ClassificationbyDurationofAction Long-ActingRelaxants RelaxantsofIntermediateDuration Short-ActingRelaxants 无Pipecuronium,VecuroniumClLong-ActingRelaxantsd-Tubocurarine，Metocurine，Doxacurium，Pancuronium，Pipecuronium，Gallamine36min起作用1.52倍ED95剂量插管80120min肌颤搐恢复25%需谨慎拮抗绝大部分经肾以原型排泄Long-ActingRelaxantsd-TubocurRelaxantsofIntermediateDurationVecuronium，Rocuronium，Atracurium，Cisatracurium22.5min起效维持3060min4590min95%肌颤搐恢复Vecuronium,Rocuronium经肝、肾双通道排泄Atracurium,CisatracuriumHofmann效应RelaxantsofIntermediateDuraShort-ActingRelaxantsMivacurium2min起效维持1220min2535min95%肌颤搐恢复血浆假性胆碱酯酶催化水解Short-ActingRelaxantsMivacuriRapacuronium1min起效维持1520min2550min95%肌颤搐恢复经胆汁、肾排泄代谢产物仍有活性可有蓄积作用RapacuroniumPharmacokineticsandPharmacodynamics PharmacokineticsandPharmacod肌松药的临床应用课件肌松药的临床应用课件DosageforTrachealIntubation dosageintherangeoftwotothreetimestheED95isusuallygivenwithin1to3minutes Ifthetracheahasalreadybeenintubatedwithoutarelaxantorwithsuccinylcholineandthepurposeissimplytoproducesurgicalrelaxation,adoseslightlylessthantheED95 DosageforTrachealIntubationMaintenanceDosage Supplemental(maintenance)dosesofnondepolarizersrangefrom20to30percentoftheinitialdoseinthecaseoflong-actingdrugsto35to50percentoftheinitialdoseinthecaseofintermediate-andshort-actingrelaxants MaintenanceDosageSupplementaControlofDepthofNeuromuscularBlockade tomaintain90to95percentblockofthetwitch(onetwitchvisibleonTOFstimulation)Infusiondosageisusuallydecreasedbyabout30to50percentinthepresenceofpotentinhaledanestheticsRelaxationisgenerallyinadequateformostsituationsifallfourresponsesareclearlyvisibleorpalpableduringTOFmonitoringControlofDepthofIfoneortworesponsesarevisibleorpalpable,relaxationshouldbesufficientforabdominalsurgeryunderadequatedepthofanesthesiaIfonlyonetwitchisfaintlyvisibleorpalpable,relaxationshouldbedeepenoughtopermitintubationofthetracheaunderalready-establishedgeneralanesthesia IfoneortworesponsesareviDosageforPriming asmallsubparalyzingdoseofthenondepolarizer(about20%oftheED95orabout10%oftheintubatingdose)begiven2to4minutesbeforegivingasecondlargedosefortrachealintubation.Thisprocedure,termedprimingDosageforPrimingasmallsubhasbeenshowntoacceleratetheonsetofblockofmostnondepolarizingrelaxantsbyabout30to60secondswiththeresultthatintubationcanbeperformedwithinapproximately90secondsfollowingtheseconddose RocuroniumandRapacuronium起效快不需预给量5倍ED95剂量以上的初始量后不需预给量hasbeenshowntoacceleratetPancuronium Dosage(mg/kg)Clinical Duration(min)ED950.06-0.07Intubation(att=+23min)0.08-0.1260-120Relaxation(N2O/O2)0.05-0.0630-60Relaxation(Vapor)0.0330-60Maintenance0.01-0.01530-40PancuroniumDosage(mg/kg)Clistimulationofthesympatheticnervoussystemusuallycauseanincreaseinheartrate,bloodpressure,andcardiacoutputPancuroniumisclearedlargelybythekidneyAsmallamount(1020%)isdeacetylatedatthe3-positionintheliver stimulationofthesympathetiPipecuronium Dosage(mg/kg)Clinical Duration(min)ED950.04-0.05Intubation(att=+23min)0.08-0.1280-120Relaxation(N2O/O2)0.04-0.0640-60Relaxation(Vapor)0.2-0.340-60Maintenance0.005-0.0130-45PipecuroniumDosage(mg/kg)Clpipecuroniumdoesnotblockautonomicganglia,nordoesitreleasehistamine Themajorexcretorypathwayisthekidney Onlyaverysmallamountofthedrug(5%)maybedeacetylatedatthe3-position pipecuroniumdoesnotblockauVecuronium Dosage(mg/kg)Clinical Duration(min)ED950.5Intubation(att=+1.53min)0.1-0.245-90Relaxation(N2O/O2)0.0525-40Relaxation(Vapor)0.03-0.0425-40Maintenance0.01-0.0215-30Infusion0.8-2.0g/kg/minVecuroniumDosage(mg/kg)Clinmorefaciletrachealintubationwithnondepolarizerseasieradministrationbyinfusionformaintenanceofblockadeduringsurgeryfasterandmorecompleteantagonismofresidualblockadeattheendofthecase lackofcardiovascularresponsesthroughoutawideclinicaldoserangefromonetoeighttimestheED95theliveristheprincipalorganofeliminationforvecuronium morefaciletrachealintubatioRocuronium Dosage(mg/kg)Clinical Duration(min)ED950.3-0.4Intubation(att=+6090s)0.6-1.035-75Relaxation(N2O/O2)0.3-0.430-40Relaxation(Vapor)0.2-0.330-40Maintenance0.1-0.1515-25Infusion8-12g/kg/minRocuroniumDosage(mg/kg)ClinfasteronsetItisseventoeighttimeslesspotentthanvecuronium rocuroniumproducespainoninjection Rocuroniumiseliminatedprimarilybytheliver,withasmallfraction(10%)eliminatedintheurine fasteronsetRapacuronium Dosage(mg/kg)Clinical Duration(min)ED951.0-1.3Intubation(att=+6090s)1.5-2.515-35Relaxation(N2O/O2)1.0-1.515-20Relaxation(Vapor)0.6-1.015-20Maintenance0.2-0.515-20Infusiona129g/kg/minaCumulationandslowedrecoverytendtodevelop.RapacuroniumDosage(mg/kg)Clowpotency(ED901.15mg/kg)，afastonset，andshort-to-intermediatedurationlittlecardiovasculareffectThedoseof3mg/kgwasassociatedwithanincreaseofplasmahistamine Renalexcretionamountsto22percentofanadministereddoseitispossiblethatitsprincipalrouteofeliminationmaybeviatheliver lowpotency(ED901.15mg/kg)，Atracurium Dosage(mg/kg)Clinical Duration(min)ED950.23Intubation(att=+23min)0.5-0.630-45Relaxation(N2O/O2)0.3-0.430-45Relaxation(Vapor)0.2-0.330-45Maintenance0.1-0.1515-20Infusion4-12g/kg/minAtracuriumDosage(mg/kg)ClinHofmannelimination dosesofmorethan0.5mg/kg(morethantwotimesED95)causethereleaseofhistamineathighdosageHofmanneliminationCisatracurium Dosage(mg/kg)Clinical Duration(min)ED950.05Intubation(att=+1.53min)0.15-0.240-75Relaxation(N2O/O2)0.0530-45Relaxation(Vapor)0.03-0.0430-45Maintenance0.01-0.0215-20Infusion1-2g/kg/minCisatracuriumDosage(mg/kg)CCisatracuriumisaboutfourtimesmorepotentthanatracuriumandhasminimalcardiovascularsideeffects intermediatedurationofaction Hofmannelimination CisatracuriumisaboutfourtiMivacurium Dosage(mg/kg)Clinical Duration(min)ED950.07-0.08Intubation(att=+2.03.0min)0.2-0.2515-20Relaxation(N2O/O2)0.110-15Relaxation(Vapor)0.0810-15Maintenance0.05-0.15-10Infusion3-15(average6)g/kg/minMivacuriumDosage(mg/kg)ClinhydrolyzedbyplasmacholinesteraseTheshortdurationofactionenablesmaintenanceofrelaxationbycontinuousinfusionrapidinjectionofdosesof0.2to0.25mg/kgcausehistaminerelease hydrolyzedbyplasmacholinestRelaxation(N2O/O2)亲脂性弱Pancuronium长效、效能高、作用慢、肝脏摄取代谢比例小，1520%经肝代谢PHARMACOLOGYOFSUCCINYLCHOLINE及时使用拮抗药，逆转肌松药的残余作用了解：神经肌肉传递功能监测低温可以减少肌肉的血流量，也可降低血浆蛋白结合肌肉松弛药的能力，使药物不易从神经肌肉接头部位转运至肝肾等器官代谢和排泄Intubation(att=+1.07mg/kg合用可减少心率变化所引起的危险，这适用于心肌缺血和心脏瓣膜疾病病人Vecuronium,Rocuronium经肝、肾双通道排泄Thedoseof3mg/kgwasassociatedwithanincreaseofplasmahistaminefasterandmorecompleteantagonismofresidualblockadeattheendofthecase非去极化肌松药的复合应用 前后复合前后复合应用用 长时效肌松药后加用中时效或短时效肌松药，前者使后者的作用时效延长短时效肌松药后加用长时效或中时效肌松药，前者将使后者的作用时效缩短 Relaxation(N2O/O2)非去极化肌松药的复合应同同时复合复合应用用化学结构为同一类的两肌松药复合应用其作用相加不是同一类的两肌松药复合应用其作用协同 同时复合应用影响肌松药的药代动力学因素影响肌松药的药代动力学因素 增加肌松药与蛋白的结合量，可增加其在体内分布容积，延缓其由肾排泄增加细胞外液量可增加肌松药在体内分布容积肝疾病引起体液潴留可增加肌松药分布容积，肝脏功能下降可引起经肝脏代谢消除延缓，作用时效延长。肾功能衰竭病人不宜应用经肾排泄的肌松药影响肌松药的药代动力学因素增加肌松药与蛋白的结合量，可增影响肌松影响肌松药的的药效效动力学因素力学因素 水、水、电解解质和酸碱平衡和酸碱平衡 呼吸性酸中毒增加氯筒箭毒碱和泮库溴铵的肌松作用，且使其作用不易为新斯的明拮抗代谢性酸中毒抑制新斯的明拮抗上述两肌松药低钾血症和高钠血症可增强非去极化肌松药的作用低钙血症和高镁血症减少乙酰胆碱释放，增强非去极化肌松药作用 影响肌松药的药效动力学因素水、电解质和酸碱平衡低温低温 低温可以减少肌肉的血流量，也可降低血浆蛋白结合肌肉松弛药的能力，使药物不易从神经肌肉接头部位转运至肝肾等器官代谢和排泄低温也影响肝脏和肾的血流量，降低代谢酶的活性低温还可影响乙酰胆碱的合成、释放，并能影响神经肌肉接头部位的敏感性 低温年年龄 新生儿体液量相对较大，分布容积增加，消除半衰延长，因此追加次数应减少老年人体液量减少和肾排泄减慢，肌松药用量应减少神神经肌肉疾病肌肉疾病重症肌无力病人用药应十分谨慎肌无力综合征病人对去极化肌松药和非去极化肌松药都十分敏感肌强直综合征病人易发生术后呼吸抑制年龄假性胆碱假性胆碱酯酶异常异常肝疾病、饥饿、妊娠末期及产褥期，此酶量减少或活性降低有机磷、六甲溴铵、新斯的明、单胺氧化酶抑制剂和某些抗癌药均可抑制该酶活性非典型性假性胆碱酯酶是由于遗传上的缺陷引起酶性质异常假性胆碱酯酶异常药物相互作用药物相互作用 吸入全麻吸入全麻药 吸入麻醉药增强非去极化肌松药作用的顺序是，最强为异氟烷、恩氟烷和地氟烷，其次是氟烷，最弱为氧化亚氮吸入麻醉药增强长时效非去极化肌松药如氯筒箭毒碱、泮库溴铵和哌库溴铵的作用比较明显，1/2-1/3 药物相互作用吸入全麻药吸入麻醉药对中时效非去极化肌松药如维库溴铵和阿曲库铵的增强作用较弱，仅减少其药量的1/4吸入全麻药对去极化肌松药的影响相对较弱，其中以异氟烷的作用最强恩氟烷和异氟烷可促使琥珀胆碱较早演变为II相阻滞 吸入麻醉药对中时效非去极化肌松药如维库溴铵和阿曲库铵的增强作局麻局麻药大剂量局麻药本身就可阻滞神经肌肉接头较小剂量的局麻药能增强非去极化肌松药和去极化肌松药作用 局麻药机制机制局麻药作用于接头前膜，减少乙酞胆碱囊胞的含量直接作用于接头后膜阻断钠通道，从而降低接头后膜对乙酞胆碱的敏感性可直接作用于肌纤维膜的离子通道，降低肌肉的收缩能力抑制血浆假性胆碱酯酶的活性，使琥珀胆碱和米库氯铵的分解减慢，时效延长机制抗心律失常抗心律失常药奎尼丁具有局部麻醉作用，可与非去极化肌松药和去极化肌松药产生协同作用，增强肌松药的强度和作用时效-受体阻滞药、钙通道阻滞药有可能影响神经肌肉接头的离子传导而增强肌松药作用抗心律失常药抗生素抗生素 多粘菌素的神经肌肉接头阻滞作用是所有抗生素中最强者，其效应逆转困难，钙离子和新斯的明对其拮抗的效应均很差氨基甙类抗生素中以新霉素和链霉素抑制神经肌肉传递的功能最强，还有妥布霉素、庆大霉素，丁胺卡那霉素，均可增强非去极化肌松药和去极化肌松药作用抗生素机制有接头前和接头后双重效应。作用于接头前膜有类似镁离子作用，影响乙酞胆碱的释放。作用于接头后有膜稳定作用。该类药物的神经肌肉接头阻滞作用可被钙离子和抗胆碱酯酶药部分拮抗林可霉素和氯霉素增强非去极化肌松药的效应，而对去极化肌松药的效应影响很小。其作用机制同样涉及接头前和接头后双重作用，并可部分被钙和新斯的明拮抗机制有接头前和接头后双重效应。作用于接头前膜有类似镁离子作用抗惊厥抗惊厥药及精神及精神药 苯妥英钠与泮库溴铵、氯二甲箭毒和维库溴铵合用时，可影响后者的肌肉松弛效应，但对氯筒箭毒碱及阿曲库按无影响锂离子可取代体内的钾离子和钠离子，产生低钾血症和增强非去极化阻滞。对用锂治疗的躁狂抑郁症病人，泮库溴铵和琥珀胆碱的效应增强抗惊厥药及精神药肌松药的拮抗肌松药的拮抗 机制机制使乙酰胆碱在神经肌肉接头部位的浓度相对提高，使更多的胆碱受体从与肌松药结合状态中解离出来而使神经肌肉接头恢复正常增加乙酰胆碱浓度或延长乙酰胆碱作用时间，均能拮抗非去极化肌松药的作用 肌松药的拮抗机制抗胆碱酯酶药新斯的明、吡啶斯的明和依酚氯铵使较多的乙酰胆碱在神经肌肉接头部位积聚，与非去极化肌松药竞争受体。新斯的明还可作用于接头前膜增加乙酰胆碱释放量，且可直接兴奋胆碱受体钾通道阻滞剂4-氨基吡啶延长突触前神经的去极化作用，增加神经内Ca2+，从而增加乙酰胆碱释放量和延长乙酰胆碱释放时间为消除抗胆碱酯酶药所引起的毒蕈碱样不良反应，常需伍用抗胆碱药，如阿托品或格隆溴铵抗胆碱酯酶药新斯的明、吡啶斯的明和依酚氯铵使较多的乙酰胆碱在时机机肌松药应用达其维持效果后有微弱呼吸动作TOFratiotomorethan0.7 单次肌颤搐刺激恢复25%以上时机剂量量neostigmine0.02mg/kg-0.04mg/kg阿托品0.01mg/kg-0.02mg/kg格隆溴铵7g/kg与新斯的明0.0350.07mg/kg合用可减少心率变化所引起的危险，这适用于心肌缺血和心脏瓣膜疾病病人剂量影响抗胆碱影响抗胆碱酯酶药的作用的作用酸碱和酸碱和电解解质失衡失衡呼吸性酸中毒不仅加强非去极化肌松药的阻滞作用，且影响抗胆碱酯酶药的作用。当动脉血二氧化碳分压（PaCO2）超过50mmHg时，抗胆碱酯酶药几乎不可能拮抗残余肌松代谢性碱中毒、低钾血症和高镁血症时，残余肌松也同样难以为抗胆碱酯酶药所逆转 影响抗胆碱酯酶药的作用低温低温肌松药难以从神经肌肉接头部移出抗胆碱酯酶药也难以进人神经肌肉接头 老年人老年人应用抗胆碱用抗胆碱酯酶药应谨慎，尤其是慎，尤其是对应用了心血管系用了心血管系统药物的病人，如洋地黄、物的病人，如洋地黄、-受体阻滞受体阻滞药和三和三环类抗抑郁抗抑郁药的病人，抗的病人，抗胆碱胆碱酯酶药易引起心易引起心动过缓和心律紊乱和心律紊乱 低温神经肌肉传递功能监测神经肌肉传递功能监测 监测肌松药的起效、维持和消退科学合理正确地使用肌松药，减少不良反应的发生及时使用拮抗药，逆转肌松药的残余作用 神经肌肉传递功能监测监测肌松药的起效、维持和消退经验判断Head-liftfor5secondsmaximumnegativeinspiratorypressureof35cmH2OHand-gripEyesopenTongue-stretchVTVASPO2经验判断Head-liftfor5seconds外周神经刺激器外周神经刺激器singletwitch stimulation，SS肌颤搐抑制90以上可顺利完成气管插管和大部分腹部手术拮抗非去极化肌松药作用一般应在肌颤搐恢复到25以上肌颤搐的幅度由25恢复到75的时间称恢复指数，反映肌肉收缩功能的恢复速率singletwitchstimulation，SStetanic stimulation,TS强直刺激引起的衰减与其后的易化用于鉴别肌松药阻滞性质和判断阻滞程度用于评定术后残余肌松时的常用频率为50Hz，持续刺激时间为5秒，如果不出现衰减，可作为临床上随意肌张力恢复的指标tetanicstimulation,TStrain-of-four stimulation，TOFT4/T1的比值来评定阻滞程度有无衰减来确定阻滞性质T4、T3、T2和T1依次消失相当于单刺激肌颤搐抑制75、80、90和100T4T10.75时提示肌张力已基本恢复train-of-fourstimulation，TOFpost tetanic count，PTC完全抑制了单刺激和四个成串刺激引起的肌颤搐时，可进一步用PTC来估计阻滞深度double-burst stimulation，DBS术后测定肌松消退及在恢复室判断残余肌松posttetaniccount，PTC监测的临床应用 肝肾功能障碍或全身情况差、疾病严重以致肌松药的药代动力学或药效动力学可能受影响的病人重症肌无力和肌无力综合征等肌松药药效有异常者支气管哮喘、严重心脏病，及其他需要避免在手术结束时使用抗胆碱醋酶药拮抗残余肌松的病人过度肥胖、严重胸部创伤、严重肺部疾病及呼吸功能受损已近临界水平、术后需充分恢复肌力的病人长时间应用或持续静脉滴注肌松药的病人 监测的临床应用肝肾功能障碍或全身情况差、疾病严重以致肌松药SummaryThemaingoalshouldbetousethelowestpossibledosethatwillprovideadequaterelaxationforsurgeryStimulatingaperipheralnerveisthemostcommonlyadvocatedmethodofmonitoringneuromuscularfunctionclinicallyChoiceofRelaxantandTestingofRecovery SummaryThemaingoalshouldbeTHANKSTHANKS肌松药的临床应用课件80