上交大外科学课件07休克英语版

shockoutline1、physiopathologyandclinicalmanifestation2、classification3、diagnosisandmonitoring4、treatementhistory1743年法国医生年HenriFrançoisLeDran提出概念1815年英国医生GeorgeJames用shock一词来描述生理的不稳定状态一次世界大战期间的研究认为组胺可能是导致休克的原因，后来被推翻二战期间研究认为失血和失液是休克的主要原因越南战争期间发现“休克肺”，原因是细胞膜功能损害和血管渗透性改变现代关于休克的研究：炎症介质（细胞因子、白细胞介素、前列腺素）和休克继发的多脏器功能障碍（代谢支持、氧输送、器官功能支持）DefinitionSabinston：休克是不论任何原因所导致的组织灌注不足而产生的临床综合征，即组织灌注难以满足组织代谢的需要2014欧洲指南：循环衰竭导致氧输送障碍引发的细胞缺氧，不强调低血压DéfinitionOxygendeliverdeficiency,

hypoxemiaettissuedamagemisunderstandingsyncopeSimplelowBPArterialPressionAP=circulationvolume*cardiacejection*vasculartensionClassification

HypovolemicHemorragictraumaticSeptic

CardiogenicNeurgenicanaphylactic外科休克hemodynamicclassification低血容量性休克hypovolemic心源性休克cardiogenic分布性休克distributive梗阻性休克obstructivePhysiopathologyFactor

HypovolemiamicrocirulationdysfonctionEarlystage总循环血量降低压力感受器、儿茶酚胺、肾素-血管紧张素使外周、内脏小血管收缩以保证心脑血供少灌少流灌少于流mechanismeThromboxaneA2：vasoconstrictormyocardialdepressivefactor

：收缩内脏小血管，心肌收缩减弱EndothelineLeucotrienegoalmaintainAPperiphericresistanceCardiacoutputReturnedbloodvolumeMaintainthecerebralandmyocardialperfusion休克早期的临床表现及机制致休克的动因交感-肾上腺髓质系统兴奋心率加快心肌收缩力加强脉搏细速脉压减少腹腔内脏、皮肤等小血管强烈收缩，腹腔内脏缺血尿量减少肛温降低儿茶酚胺分泌皮肤缺血脸色苍白四肢冰冷汗腺分泌增加中枢神经系统高级部位兴奋出汗烦躁不安注意:血压变化，可正常、可降低Principal：hypovolemia、vasoconstrictionReversibleEtiologictreatementFluidresuscitationMiddlestage毛细血管前括约肌舒张微静脉保持收缩血液滞留、静水压高、通透性增加、血液浓缩多灌少流，灌大于流mechanismeAcidosisReleaseofhistamineandpotassiumNOhemoconcentrationminithromboseAutoperfusionstop：augmentationhydrostaticpressionincreaseandcapillaryleakThird-spacefluidlossTips第一间隙：细胞内液体重的40%第二间隙：细胞外液体重的20%第三间隙：特殊的细胞外液：组织基质中被胶原纤维和弹性蛋白固化的液体主要临床表现

休克可逆期血压进行性下降休克淤血性缺氧期的临床表现及机制微循环淤血肾淤血回心血量↓

淤血血细胞粘附

心输出量↓

肾血流量↓

动脉血压↓

脑缺血缺氧

神志淡漠昏迷

少尿无尿

皮肤紫绀出现花斑

Laterstage微血管麻痹性扩张毛细血管内形成血凝块血流完全受阻不灌不流

PhysiopathologyCatecholamineineffectiveThrombosisofwhiteandredcellsDIC休克分期分期血量血管灌注皮肤意识可逆早期降低毛细血管前括约肌收缩少灌少流灌少于流苍白躁动是中期继续降低括约肌舒张微静脉收缩血管通透性增加形成微栓多灌少流灌大于流花斑淡漠是晚期显著降低前后扩张毛细血管血栓不灌不流淤斑昏迷否MetabolismEnergydeficiencyAnaerobicmetabolismLiverdysfunctionNapumpdysfunctionIntracellularedemacalciumentrylactate休克的临床表现

代偿期抑制期

程度轻度中度重度神志清楚、不安淡漠模糊、昏迷口渴有较重严重肤色稍白苍白苍白、青紫肢温正常或发凉发凉冰冷血压正常、脉压小收缩压低、脉压更小血压更低或测不出脉搏增快、有力更快细速或摸不清呼吸深快浅快表浅、不规则压甲1秒迟缓更迟缓颈静脉充盈塌陷空虚尿量正常少尿少尿或无尿失血量（%）15～203545ClinicalmanifestationhypotensionDICMODSheartbrainlungkidneyIntestinARDSInterstitialedemaAlveolarcollapsusshunting有血无气Deadspaceincrease有气无血ProgressivehypoxiaAcutekidneyinjuryHypoperfusionWaterandsodiumreabsorptionOliguriaetanuriaNecrosisofrenalcortexMyocardialdysfunctionLesscoronaryvasoconstrictionatbeginningTachycardiawithdiastolichypotensionMyocardialhypoxemiaMyocardialdysfunctionrelatedtodysfunctionofATPaseAcidosis,hyperkaliemiaandmyocardialdepressivefactorLocalnecrosisCerebraldysfunctionNon-apparentatbegininghypoperfusion（MAP<50mmHg）Store-operatedcalciumentryDIC,cerebraledema,intracranialhypertension,cerebralherniaDigestivedysfunctionerosion,bleeding,mucus,bowelsounddecreaseBacteriatranslocationintobloodsepsisLiverdysfunctionKupffercellactivatedInhibitionofmacrophageMinithromboseinthecentralveinandthehepaticsinusNecrosisofhepaticlobulesMonitoringGeneralSpecialgeneralconsciousnessNormalanxious,somnolence,comaConfusionpulseTachycardiaShockindexArterialpressionNormalatbeginninganddecreaseslaterlybecauseofdecompensationSkinWhite,cold,wet,marbleUrineoutput0.5~1ml/Kg/hOliguriaoranuriaafterfluidresuscitationmalgrémeansAKISpecialCVPPCWPCardiacoutputandcardiacindexOxygendeliveryandoxygenconsumptionBloodgaslactateDICpHintramucusalCVP的影响因素升高右心及左右心室衰竭容量过多导管过浅或进入颈内静脉血管收缩胸腹腔压力增加胶体应用降低容量过少血管扩张导管位置过深测量系统密闭性丧失Swan-ganzPCWP0.8-1.6KPaLeftheartfunctionandprecharge<0.8KPa：hypovolemia>2.4KPa：leftheartdysfunction>4.0Kpa：pulmonaryedemaCOEjectionvolumeperminute:4-6L/minStrokevolume×heartrateLeftheartfunctioncardiacindexCO/bodysurface:2.5-3.2<2.5L/min·m2heartdysfunction<1.8L/min·m2cardiogenicshockSystemicVascularResistanceIndexpostcharge(MAP-CVP)/COCOencreaseswhenSVRIdecreasesArterialoxygendelivery520-720ml/(min·m2)CO×arterialoxygencontent（saturationandhemoglobin）Transportd’oxygène氧输送氧合心排量携氧能力$OxygenconsumptionOxygenconsumedinMicrocirculation100-180ml/（min·m2）inpeaceTissularneedsIfoxygenconsumption<tissularneedsmeanshypoxemiaDICthrombocytopeniaPTprolongedmorethan3secondsFibrinogendecreasesRedcellrupture>2%FromhypercoagulabilitytohypocoagulabilityTreatmentHemostasisliftlowerlimbsFluidresuscitationPeripheralandcentralveinaccess：catheterFluidspeeddependsonaccesscalibreOxygenotherapyKeepwarmFluidresuscitationimportant！SpeednotfixedPulmonaryedemaiftoofastLowBPiftooslowNeedprecisedsurveyTypeoffluidCrystalloidandcolloid?SameaccordingtoSAFETRIPSstudyEtiologictreatmentMostimportant！surgicalshockHemostasisInfecticfociBiliarylithiase,ileus,liverabces,pancreatitis,acuteappendicitisMetabolicacidosisVasopressor缩血管扩血管缩血管扩血管+缩血管COMEON!What’sthevascularstate？正常低容量感染性休克血容量正常低低血管状态正常收缩收缩/扩张补液后血管扩张正常、扩张正常、扩张张力好好（短时间）差后果血压正常血压不升处理扩张内脏血管多巴胺增加血管张力去甲肾上腺素Dopamin<5mg/kg/min

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vasodilatation5~10mg/kg/min:inotropic>15mg/kg/min:vasoconstrictionNoradrenalina1:peripheralvasoconstrictionb1:heartcontractionEspeciallyinsepticshockDose：0.03~1mg/kg·minLactateaccumulationleadingfromoverdoseadrenalinCPRVasopressinifnoradrenalindoesn’twork0.04u/minDobutaminAgonistenonselectiveofb

receptorb1:inotropicb2:redistributiondusangdesintestinAssociatedwithnoradrenalinincaseofsepticshockwithheartfailure2.5~10mg/kg·minAnticoagulationunfractionatedheparinLowmolecularweightheparinhemorragicshockBloodlose>20%HypovolemiawithvasoconstrictionPaleCVPdecreasetreatmentResuscitationandhemostasisPlasmaandredcellspeed：QuickatbeginningRegulationbyresponseAvoidhypertensionhemostasisCompressionOperationtraumaticshockbleedingLocalorsystemicinflammationCapillaryleakneuro-endocrinologicresponsetreatmentresuscitationevaluationCTscanLifesupportPulmonarycontusion,ARDSOp