外科休克上交大瑞金

SHOCKDepartmentofSurgeryRuijinHospital,MedicalCollege,ShanghaiJiaotongUniversityWesternrecordviolentimpactorblow,1743physiologicinstability,1815Easternrecord厥脫，內(nèi)閉外脫I.HistoricalAspectInitialrecordsofshockInitialExplanationofshockWesternThomasLatta,1831PatientswithCholeraInfusionoffluids→improvementHypovolemiaEastern邪毒內(nèi)陷氣隨血脫陰虧氣脫氣機郁閉陰絕陽脫withtheRiseofPhysiologyBurgeoningofCardiovascularphysiologyintheendof19CN,CrileCVPdroppedafterhemorrhageAnimalsurvivalwasincreasedaftertheinfusionofsalinetheUseofCardiacCatheterizationBloodvolumeloss→fallinCardiacOutputwiththeCombinationof

PhysiologyandBiochemistryToxintheoryofshock,Cannon&Baylissimpairmentofoxygentransportdevelopmentofacidosistoxininseveremuscleinjury→lossofvasomotortone→venoussequestrationofblood→hypotensionAntedatetheEraofCriticalCareMedicineExtensivephysiologicresearchofWigger,inearly1940sintegratingtheConceptsofimpairedoxygendeliveryoxygendebttissueinjury/deaththeconceptofirreversibleshockprogressivesystemiccirculatorydecompensationControversyonLung&KidneyARDS

Introductionoftheflowdirectedpulmonaryarterycatheter,in1970

Noncardiogenicnature

NotduetovolumeoverloadARFMorepromptandaggressiveresuscitationIncidence↓ATNhappens:hypoperfusionARDShappens:DefectsinCellMembraneFunctionandVascularPermeabilityHypovolemia/Toxin/CytokineHypoxiaARDSAsyndromethatresultsfrominadequateperfusionoftissuesinsufficienttomeetmetabolicdemandleadtocellulardysfunction,elaborationofinflammatorymediators,andcelluarinjurywhichmaybelimited,orwidespread

Acontinuum,rangingfromsubclinicaldeficitsinperfusiontoMODSorfrankorganfailure.Tissuehypoxia

duetohypoperfusionDefectsInjuryII.Definitionofshock

A.組織低灌注所致細胞缺氧

B.低血壓

C.酸中毒

D.心功能不全

E.以上都不對休克的根本問題是:ImpairedtissueperfusionWiderspectrumofshockpresentationsRangingfromocculttissuehypoxiatofull-blowncardiovascularcollapseorMultipleorgandysfunctionImplicationalarmearliertreatearlierExplanationTissuehypoperfusiontissuehypoxiaanaerobicmetabolism,acidosisinflammatorymediaterscirculatoryredistributionearlyinvolvementofsplanchniccirculationcellularinjurysepticcomplicationsMODSExplanationO2DebtWhetherDO2critisincreasedinARDS,orsepsisDelivery-dependentoxygenuptake=HypoxiacauseMODSsupranormallevelssupplyofO2preventtheprogressionofMODSProvidingopportunityforinterventionProvidingtimeforthediseasetosubsiderOxygenconsumption(vO)2Oxygendelivery(DO2)O2DebtExplanationCirculatoryredistributionConceptHomeostaticresponsetohypoperfusiontopreserveoxygendeliverytoheartandbrainbyselectivedivertingbloodMechanismcatechols,angiotensionII,Vasopressin,endothelin,TXA2

ConsequenceCellularandorganderangement→MODSBreakdownoftheintestinalepithelialbarrierbacterialandtoxintranslocation→SIRS→MODSExplanationintrinsicobstructionofcap.Bedlow-flowstates,hypothermia,andincreasedviscositycap.Sludging:intravascularcoagulation,plateletaggregation,otherintraluminaldebrispreventingRBCfromreachingthetissuesextrinsicobstructionofcap.Bedlocaltissueinflammation,edema,orhemorrhage,ACSvesselwallpermeabilitydeficitThechangesinMicrocirculatary

LevelExplanationHypovolemicShockHemorrhage-Plasmalosses-CardiogenicShockIntrinsic-ExtrinsicCompressive-Obstructive-III.ClassificaionofShockTraumaGIBleedingRupturedaneurysmsBurnBowelobstructionMyocardialinfarctionCardiomyopathyValvularHeartDiseaseCardiacRhythmdisturbanceMyocardialdepressionTensionpneumothoraxPericardialtamponadeHighlevelofpositive-pressureventilationPulmonaryembolismSurgicalShock1NeurogenicShocke.g.VasogenicShockSIRS,toxin

SepticdespiteadequatefluidresucitationTraumatic

AnaphylacticandAnaphylactoidHypoadrenalSpinalcordinjurySevereheadinjurySpinalcordanesthesiaSurgicalShock2TheothersTheremaybea“

”tobefilled.but“cellularshock”,suchaspoisoning,hypoxia,hypoglycemia,isnotthesyndrome,continuum,ortissuehypoxiaduetohypoperfusion,maybeexcludedfromthecategoryofshock.各型休克的共同特點是：

A.血壓下降

B.中心靜脈壓下降

C.脈壓縮小

D.尿量減少

E.有效循環(huán)血量銳減Secondaryvisceralimpairement

Microcirculatorychanges

MetabolicchangesIV.Pathophysiologicstagingofshock

MicrocirculatoryStagingMicrocirculatoryconstrictivephaseMicrocirculatorydilatationphaseMicrocirculatoryfailurephase后微A微V前括約肌A－V吻合支微動脈微靜脈加重過程——只出不進/只過不進

只進不出/進多出少MicrocirculatoryStructure

MetabolicChangesenergymetabolicabnormality無氧糖酵解，產(chǎn)能減少metabolicacidosis引起微血管擴張，等barrierfunctiondefectsofmembrane累及基底膜，細胞膜，溶酶體膜

SecondaryVisceralImpairmentHeartKidneyLungBrainGastrointestinaltractLiverClinicalStagingShockcompensatorystagenervous,restless,agitation,cool,pale,thirsty,tachycardia,shortofbreathBPnormalorincreased,pulsepressuredecreased,urinaryoutputnormalordecreasedBloodloss<20%，<800mlShockinhibitingstagefaint,dullness,confusion,comacyanosis,dyspneaextremitiescoldandwet,pulsefastandweakoliguria,anuriaBPdecreased

Bloodloss>20%，>800ml關(guān)于休克代償期微循環(huán)改變，

下列那一項是錯誤的：

A.動靜脈短路開放

B.直捷通道開放

C.微動脈收縮

D.微靜脈收縮

E.毛細血管內(nèi)血液淤積V.DiagnosisandpatientmonitoringCausesandPredictionConventionalmonitoringMentalstatusSkintemperatureBloodpressure,PulserateUrinaryoutput(30ml/hr)SpecialmonitoringCVP(<5,5~10cmH2O,>15,>20)Bloodroutinetest/Arterialbloodgasanalysis/ElectrolytesPCWP(6~15mmHg)COCISerumlactateconcentrationArterialbloodgasanalysisDIC:PLT/FDPVI.MeasurementofShock一般緊急處理Urgentmeasurement補充血容量Resuscitation積極處理原發(fā)病Treatincitingcauseofshock糾正酸堿平衡失調(diào)Controlelectrolytes,andacidbasederangement血管活性藥物的應用Inotropicagent治療DIC，改善微循環(huán)TreatDIC,improvemicrocirculation皮質(zhì)類固醇和其它藥物的應用Corticosteroids心理支持與呵護PCWPCVP<15,Volumeexpansion<10cmH2O<18,Considervolume<14>18Diurese>14Reestablishmentofurinaryoutputtoarateof0.5-1.0mlperkg.PerhourAnormalheartrateandbloodpressureAdequatecapillaryrefillNormalsensoriumNormalCVPandPWCPi.VolumeResuscitation&Initialend-pointsFluidresuscitationEnd-pointreachingOptimizeOxygenDeliveryKeepSaO2>90%

OptimizeCardiacIndex

OptimizeHbSupplysupplementalO2Earlyhemodynamicmonitoring11-13g/dlVentilator,ifnecessaryAssessvolumestatus(preload)ReassessKeep:PCWP15-18mmHg,MAP60-80mmHg,DeliveryindependentO2consumptionGoalmeetGoalnotmeetTreatincitingcauseofshockControlSIRSNutritionalsupportInotropicsupportbetaagonismGoalmeetGoalnotmeetConsiderVasodilator,alphaagonistInitialresuscitationofpatientsinShockPCWP<15,Volumeexpansion<18,Considervolume;>18Diurese

A.心功能不全B.血容量不足C.血容量過多D.血管張力升高E.以上都不是休克病人經(jīng)補液后，血壓仍低。5~10min內(nèi)經(jīng)靜脈注入等滲鹽水250ml，如血壓上升，而中心靜脈壓不變，提示：ShockMODSDisturbanceDeathTiming&Strategy!!!Effort&Effectii.CurrentStrategyforShockSolutionPrevention,earlyIdentification,

earlyandspecifictreatmentforShockandMODS感染創(chuàng)傷燒傷SAPSIRS代謝紊亂低氧乏氧代謝休克復蘇失敗痊愈MODS好轉(zhuǎn)MODS第二次打擊心源性、神經(jīng)源性因素低血容量血管源性PrimarySecondary（感染）(24h)死亡1.HypovolemicshockSymptomadecreaseinpulsepressuretachycaridaandhypotensionurineoutputfallsnormalskinturgorislostmentalstatuschanges-inaprogressivefashionapprehension,anxiety,completeobtundationCVPdecreaseTreatmentResuscitation&ControltheincitingcauseofshockSpecific2.TraumaticshockTypeVasogenicshockthatbeginsashypovolemicshockCharacter-refractorytofluidreplacementtherapyLargervolumelosses,greaterfluidsequestrationMoreintenseactivationofinflammatorymediatorsDevelopmentofSIRSDevastatingsofttissueinjuriesMachanismincreasingmicrovascularpermeability,ExcessivefluidrequirementFrequentlyRequiremechanicalventilation,PulmonaryarterycathetermonitoringCardiovascularsupportOperationSpecific3.SepticshockTypeVasogenicshock,RefractorytofluidreplacementtherapyDefinitionSepsiswithhypotensiondespiteadequatefluidresuscitationalongwiththepresenceofmanifestationsofhypoperfutionsuchaslacticacidosis,obliguria,oracutealterationinmentalstatusMechanismCytokinesVasodilatation,Increasingmicrovascularpermeability,ExcessivefluidrequirementSpecific

TreatmentofSepticshockResuscitationControlinfectionNormalizationofelectrolytes,acidbasedearangementInotropicagentCorticosteroidsNutritionalsupport,dealwithDIC,organfunctionsupportSpecific4.Anaphylactic

andAnaphylactoidshockMechanismInflammatorymediatorsC3a,C5a,Histamine,Kinnins,ProstaglandinssymptomsVasodilatation,increasedcapillarypermeabilitybronchospasm,airwayedema,circulatorycollapseTreatment縮血管AminophyllineCorticosteroidsAntihistamineImmunologicallyMediated:byIgEantibodyNotImmunologicallyMediated:Radiographiccontrastdyes,narcoticsSpecific

5.CardiogenicShockSymptomWeakorslowpulseratetachycaridaorbradycardiaurineoutputfallsCough,pinkfoamyphlegm,dyspnea,cyanosismentalstatuschangesfatigue,apathiaBPdecrease&CVPnormalorincreaseTreatmentResuscitation&cardiacstimulant,diuretics,vesodialatorsVII.SolutionofShockChain&RingHeart,Lung,Kidney,Liver,BrainDilema&OptionExtendedorlimitedEarly