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SHOCKDepartmentofSurgeryRuijinHospital,MedicalCollege,ShanghaiJiaotongUniversityWesternrecordviolentimpactorblow,1743physiologicinstability,1815Easternrecord厥脱,内闭外脱I.HistoricalAspectInitialrecordsofshockInitialExplanationofshockWesternThomasLatta,1831PatientswithCholeraInfusionoffluids→improvementHypovolemiaEastern邪毒内陷气随血脱阴亏气脱气机郁闭阴绝阳脱withtheRiseofPhysiologyBurgeoningofCardiovascularphysiologyintheendof19CN,CrileCVPdroppedafterhemorrhageAnimalsurvivalwasincreasedaftertheinfusionofsalinetheUseofCardiacCatheterizationBloodvolumeloss→fallinCardiacOutputwiththeCombinationofPhysiologyandBiochemistryToxintheoryofshock,Cannon&Baylissimpairmentofoxygentransportdevelopmentofacidosistoxininseveremuscleinjury→lossofvasomotortone→venoussequestrationofblood→hypotensionAntedatetheEraofCriticalCareMedicineExtensivephysiologicresearchofWigger,inearly1940sintegratingtheConceptsofimpairedoxygendeliveryoxygendebttissueinjury/deaththeconceptofirreversibleshockprogressivesystemiccirculatorydecompensationControversyonLung&KidneyARDSIntroductionoftheflowdirectedpulmonaryarterycatheter,in1970NoncardiogenicnatureNotduetovolumeoverloadARFMorepromptandaggressiveresuscitationIncidence↓ATNhappens:hypoperfusionARDShappens:DefectsinCellMembraneFunctionandVascularPermeabilityHypovolemia/Toxin/CytokineHypoxiaARDSAsyndromethatresultsfrominadequateperfusionoftissuesinsufficienttomeetmetabolicdemandleadtocellulardysfunction,elaborationofinflammatorymediators,andcelluarinjurywhichmaybelimited,orwidespreadAcontinuum,rangingfromsubclinicaldeficitsinperfusiontoMODSorfrankorganfailure.TissuehypoxiaduetohypoperfusionDefectsInjuryII.DefinitionofshockA.组织低灌注所致细胞缺氧B.低血压C.酸中毒D.心功能不全E.以上都不对休克的根本问题是:ImpairedtissueperfusionWiderspectrumofshockpresentationsRangingfromocculttissuehypoxiatofull-blowncardiovascularcollapseorMultipleorgandysfunctionImplicationalarmearliertreatearlierExplanationTissuehypoperfusiontissuehypoxiaanaerobicmetabolism,acidosisinflammatorymediaterscirculatoryredistributionearlyinvolvementofsplanchniccirculationcellularinjurysepticcomplicationsMODSExplanationO2DebtWhetherDO2critisincreasedinARDS,orsepsis?Delivery-dependentoxygenuptake=HypoxiacauseMODSsupranormallevelssupplyofO2preventtheprogressionofMODS?ProvidingopportunityforinterventionProvidingtimeforthediseasetosubsiderOxygendelivery(DO2)O2DebtExplanationCirculatoryredistributionConceptHomeostaticresponsetohypoperfusiontopreserveoxygendeliverytoheartandbrainbyselectivedivertingbloodMechanismcatechols,angiotensionII,Vasopressin,endothelin,TXA2ConsequenceCellularandorganderangement→MODSBreakdownoftheintestinalepithelialbarrierbacterialandtoxintranslocation→SIRS→MODSExplanationintrinsicobstructionofcap.Bedlow-flowstates,hypothermia,andincreasedviscositycap.Sludging:intravascularcoagulation,plateletaggregation,otherintraluminaldebrispreventingRBCfromreachingthetissuesextrinsicobstructionofcap.Bedlocaltissueinflammation,edema,orhemorrhage,ACSvesselwallpermeabilitydeficitThechangesinMicrocirculataryLevelExplanationHypovolemicShockHemorrhage-Plasmalosses-CardiogenicShockIntrinsic-ExtrinsicCompressive-Obstructive-III.ClassificaionofShockTraumaGIBleedingRupturedaneurysmsBurnBowelobstructionMyocardialinfarctionCardiomyopathyValvularHeartDiseaseCardiacRhythmdisturbanceMyocardialdepressionTensionpneumothoraxPericardialtamponadeHighlevelofpositive-pressureventilationPulmonaryembolismSurgicalShock1NeurogenicShocke.g.VasogenicShockSIRS,toxinSepticdespiteadequatefluidresucitationTraumaticAnaphylacticandAnaphylactoidHypoadrenalSpinalcordinjurySevereheadinjurySpinalcordanesthesiaSurgicalShock2TheothersTheremaybea“”tobefilled.but“cellularshock”,suchaspoisoning,hypoxia,hypoglycemia,isnotthesyndrome,continuum,ortissuehypoxiaduetohypoperfusion,maybeexcludedfromthecategoryofshock.各型休克的共同特点是:A.血压下降B.中心静脉压下降C.脉压缩小D.尿量减少E.有效循环血量锐减SecondaryvisceralimpairementMicrocirculatorychangesMetabolicchangesIV.PathophysiologicstagingofshockMicrocirculatoryStagingMicrocirculatoryconstrictivephaseMicrocirculatorydilatationphaseMicrocirculatoryfailurephase后微A微V前括约肌A-V吻合支微动脉微静脉加重过程——只出不进/只过不进只进不出/进多出少MicrocirculatoryStructureMetabolicChangesenergymetabolicabnormality无氧糖酵解,产能减少metabolicacidosis引起微血管扩张,等barrierfunctiondefectsofmembrane累及基底膜,细胞膜,溶酶体膜SecondaryVisceralImpairmentHeartKidneyLungBrainGastrointestinaltractLiverClinicalStagingShockcompensatorystagenervous,restless,agitation,cool,pale,thirsty,tachycardia,shortofbreathBPnormalorincreased,pulsepressuredecreased,urinaryoutputnormalordecreasedBloodloss20%,800mlShockinhibitingstagefaint,dullness,confusion,comacyanosis,dyspneaextremitiescoldandwet,pulsefastandweakoliguria,anuriaBPdecreasedBloodloss20%,800ml关于休克代偿期微循环改变,下列那一项是错误的:A.动静脉短路开放B.直捷通道开放C.微动脉收缩D.微静脉收缩E.毛细血管内血液淤积V.DiagnosisandpatientmonitoringCausesandPredictionConventionalmonitoringMentalstatusSkintemperatureBloodpressure,PulserateUrinaryoutput(30ml/hr)SpecialmonitoringCVP(
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