上交大外科學課件07休克英語版

shockoutline1、physiopathologyandclinicalmanifestation2、classification3、diagnosisandmonitoring4、treatementhistory1743年法國醫(yī)生年HenriFran?oisLeDran提出概念1815年英國醫(yī)生GeorgeJames用shock一詞來描述生理的不穩(wěn)定狀態(tài)一次世界大戰(zhàn)期間的研究認為組胺可能是導致休克的原因，后來被推翻二戰(zhàn)期間研究認為失血和失液是休克的主要原因越南戰(zhàn)爭期間發(fā)現(xiàn)“休克肺”，原因是細胞膜功能損害和血管滲透性改變現(xiàn)代關于休克的研究：炎癥介質(zhì)（細胞因子、白細胞介素、前列腺素）和休克繼發(fā)的多臟器功能障礙（代謝支持、氧輸送、器官功能支持）DefinitionSabinston：休克是不論任何原因所導致的組織灌注不足而產(chǎn)生的臨床綜合征，即組織灌注難以滿足組織代謝的需要2014歐洲指南：循環(huán)衰竭導致氧輸送障礙引發(fā)的細胞缺氧，不強調(diào)低血壓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總循環(huán)血量降低壓力感受器、兒茶酚胺、腎素-血管緊張素使外周、內(nèi)臟小血管收縮以保證心腦血供少灌少流灌少于流mechanismeThromboxaneA2：vasoconstrictormyocardialdepressivefactor

：收縮內(nèi)臟小血管，心肌收縮減弱EndothelineLeucotrienegoalmaintainAPperiphericresistanceCardiacoutputReturnedbloodvolumeMaintainthecerebralandmyocardialperfusion休克早期的臨床表現(xiàn)及機制致休克的動因交感-腎上腺髓質(zhì)系統(tǒng)興奮心率加快心肌收縮力加強脈搏細速脈壓減少腹腔內(nèi)臟、皮膚等小血管強烈收縮，腹腔內(nèi)臟缺血尿量減少肛溫降低兒茶酚胺分泌皮膚缺血臉色蒼白四肢冰冷汗腺分泌增加中樞神經(jīng)系統(tǒng)高級部位興奮出汗煩躁不安注意:血壓變化，可正常、可降低Principal：hypovolemia、vasoconstrictionReversibleEtiologictreatementFluidresuscitationMiddlestage毛細血管前括約肌舒張微靜脈保持收縮血液滯留、靜水壓高、通透性增加、血液濃縮多灌少流，灌大于流mechanismeAcidosisReleaseofhistamineandpotassiumNOhemoconcentrationminithromboseAutoperfusionstop：augmentationhydrostaticpressionincreaseandcapillaryleakThird-spacefluidlossTips第一間隙：細胞內(nèi)液體重的40%第二間隙：細胞外液體重的20%第三間隙：特殊的細胞外液：組織基質(zhì)中被膠原纖維和彈性蛋白固化的液體主要臨床表現(xiàn)

休克可逆期血壓進行性下降休克淤血性缺氧期的臨床表現(xiàn)及機制微循環(huán)淤血腎淤血回心血量↓

淤血血細胞粘附

心輸出量↓

腎血流量↓

動脈血壓↓

腦缺血缺氧

神志淡漠昏迷

少尿無尿

皮膚紫紺出現(xiàn)花斑

Laterstage微血管麻痹性擴張毛細血管內(nèi)形成血凝塊血流完全受阻不灌不流

PhysiopathologyCatecholamineineffectiveThrombosisofwhiteandredcellsDIC休克分期分期血量血管灌注皮膚意識可逆早期降低毛細血管前括約肌收縮少灌少流灌少于流蒼白躁動是中期繼續(xù)降低括約肌舒張微靜脈收縮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顯著降低前后擴張毛細血管血栓不灌不流淤斑昏迷否MetabolismEnergydeficiencyAnaerobicmetabolismLiverdysfunctionNapumpdysfunctionIntracellularedemacalciumentrylactate休克的臨床表現(xiàn)

代償期抑制期

程度輕度中度重度神志清楚、不安淡漠模糊、昏迷口渴有較重嚴重膚色稍白蒼白蒼白、青紫肢溫正?；虬l(fā)涼發(fā)涼冰冷血壓正常、脈壓小收縮壓低、脈壓更小血壓更低或測不出脈搏增快、有力更快細速或摸不清呼吸深快淺快表淺、不規(guī)則壓甲1秒遲緩更遲緩頸靜脈充盈塌陷空虛尿量正常少尿少尿或無尿失血量（%）15～203545ClinicalmanifestationhypotensionDICMODSheartbrainlungkidneyIntestinARDSInterstitialedemaAlveolarcollapsusshunting有血無氣Deadspaceincrease有氣無血ProgressivehypoxiaAcutekidneyinjuryHypoperfusionWaterandsodiumreabsorptionOliguriaetanuriaNecrosisofrenalcortexMyocardialdysfunctionLesscoronaryvasoconstrictionatbeginningTachycardiawithdiastolichypotensionMyocardialhypoxemiaMyocardialdysfunctionrelatedtodysfunctionofATPaseAcidosis,hyperkaliemiaandmyocardialdepressivefactorLocalnecrosisCerebraldysfunctionNon-apparentatbegininghypoperfusion（MAP<50mmHg）Store-operatedcalciumentryDIC,cerebraledema,intracranialhypertension,cerebralherniaDigestivedysfunctionerosion,bleeding,mucus,bowelsounddecreaseBacteriatranslocationintobloodsepsisLiverdysfunctionKupffercellactivatedInhibitionofmacrophageMinithromboseinthecentralveinandthehepaticsinusNecrosisofhepaticlobulesMonitoringGeneralSpecialgeneralconsciousnessNormalanxious,somnolence,comaConfusionpulseTachycardiaShockindexArterialpressionNormalatbeginninganddecreaseslaterlybecauseofdecompensationSkinWhite,cold,wet,marbleUrineoutput0.5~1ml/Kg/hOliguriaoranuriaafterfluidresuscitationmalgrémeansAKISpecialCVPPCWPCardiacoutputandcardiacindexOxygendeliveryandoxygenconsumptionBloodgaslactateDICpHintramucusalCVP的影響因素升高右心及左右心室衰竭容量過多導管過淺或進入頸內(nèi)靜脈血管收縮胸腹腔壓力增加膠體應用降低容量過少血管擴張導管位置過深測量系統(tǒng)密閉性喪失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氧輸送氧合心排量攜氧能力$OxygenconsumptionOxygenconsumedinMicrocirculation100-180ml/（min·m2）inpeaceTissularneedsIfoxygenconsumption<tissularneedsmeanshypoxemiaDICthrombocytopeniaPTprolongedmorethan3secondsFibrinogendecreasesRedcellrupture>2%FromhypercoagulabilitytohypocoagulabilityTreatmentHemostasisliftlowerlimbsFluidresuscitationPeripheralandcentralveinaccess：catheterFluidspeeddependsonaccesscalibreOxygenotherapyKeepwarmFluidresuscitationimportant！SpeednotfixedPulmonaryedemaiftoofastLowBPiftooslowNeedprecisedsurveyTypeoffluidCrystalloidandcolloid?SameaccordingtoSAFETRIPSstudyEtiologictreatmentMostimportant！surgicalshockHemostasisInfecticfociBiliarylithiase,ileus,liverabces,pancreatitis,acuteappendicitisMetabolicacidosisVasopressor縮血管擴血管縮血管擴血管+縮血管COMEON!What’sthevascularstate？正常低容量感染性休克血容量正常低低血管狀態(tài)正常收縮收縮/擴張補液后血管擴張正常、擴張正常、擴張張力好好（短時間）差后果血壓正常血壓不升處理擴張內(nèi)臟血管多巴胺增加血管張力去甲腎上腺素Dopamin<5mg/kg/min

:

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