外科休克（surgicalshock）课件

DepartmentofPediatricSurgeryUnionHospitalofHuazhongUniversityofScienceandTechnologyQiangsongTong,M.D.Ph.D.SURGICALSHOCK1DepartmentofPediatricSurgerObjectivesUnderstandwhatisshock？DefinetypesofshockUnderstandpathophysiologyofshockUnderstandhowtotreatshock2ObjectivesUnderstandwhatissDevelopmentoftheconceptofshockAhistoryofthe200yearstorecognizeshock:l“shake”,“attack”lFromsuperficialsyndrometomicrocirculatorylevel,cellularlevel,molecularlevelCirculatorylevel：bloodpressureMicrocirculatorylevel：inadequatetissueperfusionCellularlevelandmolecularlevel：lFrontierlExploratorystage，experimentaltherapies3DevelopmentoftheconceptofWHATISSHOCK?Shockresultsfrompoortissueperfusionandtissuehypoxiafrominadequatecirculatorycompensationsneededtosustainacutelyincreasedbodymetabolism.AbreakdownofeffectivecirculationInadequatetissueperfusionDecreasedoxygensupplyAnaerobicmetabolismAccumulationofmetabolicwasteMultipleorganfailureAclinicalsyndrome4WHATISSHOCK?ShockWhatiseffectivecirculatorybloodvolume?Varioustypesofshockresultfromfailureinoneormoreofthe3majorcomponentsofthecirculatorysystem：BloodvolumePumpPeripheralresistance5WhatiseffectivecirculatoryCausesofShockSevereorsuddenbloodlossLargedropinbodyfluidsMajorinfectionsHighspinalinjuriesMyocardialinfarctionAnaphylaxisExtremeheatorcold6CausesofShock6TypesofShockHypovolemicShock:haemorrhagictraumaticdehydrationOthercausesofshockSepticShockCardiogenicShockNeurogenicShockHypersensitiveShock7TypesofShockHypovolemicShocPathophysiology1.Microcirculatorychanges2.Thechangesofbodyfluidmetabolism3.Mediatorsofinflammationreleaseandischemicalreperfusioninjury4.Secondarylesion8Pathophysiology81.MicrocirculationPrecapillaryresistancevessel：arteriole、metarteriole、precapillarysphincter Postcapillaryresistancevessel：veinuleMicrocirculationperfusion：91.Microcirculation9lIncreasedcatecholaminereleaselIncreaseglucocorticoidandmineralcorticoidreleaselActivationofRenin-angiotensinsystemCompensatorymechanisms(earlyshock)TheHPAandneuroendocrineaxesaretriggeredAdecreaseinbloodvolumeStretchreceptorsinheartbaroreceptorsinaortaandcarotidarteries10Compensatorymechanisms(earlCompensatorymechanismsThebodyattemptstocompensateandrestoreperfusionby:lIncreasingcardiacoutputlStimulationofthesympatheticnervoussystemcausesanincreaseinheartrate,strokevolume,andPVR(peripheralvesselresistance).lRedistributingthecirculatingbloodvolumetovitalorganslVasoconstriction,(periph-andviscero-vessel)lPathologicarteriovenousshuntinglAutotranfused:precapillaryresistancevesseltocontract，todecreasecapilaryhydrostaticpressure.fluidandnoperfusion11CompensatorymechanismsprecapiCompensatorysignificanceKeepingbloodpressurenormalPerfusiontovitalorgans12CompensatorysignificanceKeepiEarlyStage(compensatedshock):CompensatorymechanismsareabletomaintainperfusionofvitalorgansClinicalmanifestationofShockHeartRate:mildtachycardia;boundingpulseLevelofConsciousness:lethargy,confusion,combativenessSkin:delayedcapillaryrefill;coolandclammyBloodPressure:normalorslightlyelevatedRespirations:rapidandshallow13EarlyStage(compensatedshockCompensatorymechanisms（Progressiveshock）plasmashifttointerstitualspacespachyemiaandincreasingbloodviscidityperfusionandnofluidarteriovenousshunt,directpassagewaytoopentissuehypoperfusionanaerobicmetabolismlacticacidbuildsupmetabolicacidosisPre-CRVtodilatePost-CRVtocontractcapillaryhydrostaticpressuretoincrease14Compensatorymechanisms（ProgHeartRate:moderatetachycardia;weakandthreadypulseLevelofConsciousness:confusionorunconsciousnessSkin:delayedcapillaryrefill;cold,clammy,andcyanoticBloodPressure:decreasedRespirations:rapidandshallowUrineoutput:oliguriaMiddleStage(uncompensatedshock):Compensatorymechanismsareunabletomaintainperfusion15HeartRate:moderatetachycarIrreversibleshockHypercoagulablecharactererythrocyteandthrombocytetoaggregateDICCellularhypoxia，lysosomerupturehydrolyticenzymereleasingaqtocytolysisandtodamageothercellsCelldamage,organfailureoccurdeathoccurnoperfusionandnofluid16IrreversibleshockHypercoagulLateShockHeartRate:bradycardia;severedysrhythmiasLevelofConsciousness:comaSkin:pale,cold,markeddiaphoresisBloodPressure:markedhypotensionRespirations:decreasedrateandtidalvolumeUrineoutput:oliguriaoranuriamultiplesystemorganfailure,MSOF17LateShockHeartRate:bradyc2.MetabolicresponsesAnaerobicmetabolismAbnormalenergymetabolism：Increasedproteincatabolism,enzymicproteintoconsume，tocauseMODSIncreasedliverglyconeogenesis，hyperglycaemiallipolysisisanmainenergysourcemetabolicacidosislacticacidaccumulatesDecreased Decreased metaboliccapabilityintheliverdecreasedcatecholamineresponcetocardiovascularsystem182.MetabolicresponsesAnaerob3.IschemicalreperfusioninjuryAnacuterestorationofoxygendeliverycanalsoamplifytheinitialischemicinsult,leadingtofurthercellinjuryDuringthisphaseofshockresuscitation,leukocytesadheretopostcapillaryvenularendotheliumthatisfollowedbythegenerationofreactiveoxygenspecies.Thelatterresponsedamagesproteinsandmembranestructures,andactivatessignaltransductionpathwaysthatcanultimatelyleadtoapoptosis(programmedcelldeath).193.IschemicalreperfusioninjCelldeath1.Hypoxia:intracellularischemiaoccurs;anaerobicmetabolismbegins;lacticacidbuildsupincell;leadingtometabolicacidosis;causesthesodiumpotassiumpumptofail.2.IonshiftoccursSodiumrushesintothecellbringingwaterwithit.20CelldeathHypoxia:intracellul3.Cellswellingoccurs.4.Mitochondrialswellingoccurs;productionofATPceases.5.Intracellulardisruptionreleaseslysosomes,cellmembranebeginstobreak.6.Celldestructionbeginsleadingtotissuedeath.213.Cellswellingoccurs.214.SecondarylesiontoorganLungARDS(acuterespiratorydistresssyndrome)：Capillaryendotheliumcelldamage：Permeabilityincreases,causinginterstitial edema,hyalinization.Alveolarepithelialcelldamage：decreasing alveolarsurfactant，pulmonaryshrinkandatelectasisAtthesametime,thereisveryhighoxygenconsumptionandCO2production V/Q mismatch,shunting,and pulmonary hypertension occur,allleadingtoseverehypoxemia224.SecondarylesiontoorganLuKidneysARF(acuterenalfailure)：nHypotensionandcatecholamineleadstorenalarteryvasoconstriction,reduced GFR,oliguria,and azotemianBloodflowredistributioninkidneys,IschemialeadstoAcute Tubular Necrosis(ATN).oliguria(400ml/d)oranuria(100ml/d)23KidneysARF(acuterenalfailuCardiacinsufficiencyHeartfailureShockbloodpressureheartrateCoronalarterybloodflowHRcontractionAcidosishyperkaliemiaVO2DICmicrothrombusfocalnecrosishaemorrhageIschemicalreperfusioninjurymediatorsHeartEarliershocknormal24CardiacinsufficiencyShockblooBrainearliershockRedistributingthebloodvolumeKeepperfumetobrainnobraindisorderbraintissueIschemia,hypoxiaLethargicsleepyComashockBp7kPaDICStressdysphoria25BrainearliershockRedistrAlimentarytractandLiverfunctionIschemia、congestion、DICIntestinefunctionaldisorderdigestivejuicesecretiongastrointestinalmotilityMucosalerosionulcerintestinalbacteriatobreedEndotoxin,bacteriatoenterboodhepatosisKupffercellmediatorsofinflammationdetoxicatelacticacidglucoseSIRSacidosis26AlimentarytractandLiverfunHemodynamicmonitoring1.Mentalstatus：braintissueperfusion2.Skinperfusion：warm,normal color good perfusion cold,pale,moist skin vasoconstriction3.Bloodpressure：importantbutnosensitiveindexlEarlydetection:DontrelyonBPlsystolicpressure12kPa(90mmHg)pulsepressure1.0-1.5shock，2.0severeshock5.Urineoutput：themostsensitiveindexoftheadequacyofvitalorganperfusionloliguria：initialshock,initialresuscitationlnormalBP,oliguriaandlowspecificgravity：acuterenalfailure(ARF)lurineoutput30ml/h：improve284.Pulserate：28Specialmonitoring（7 item）1.CentralVenousPressure(CVP):CVP=rightatrialpressure(RAP)=right-ventricularend-diastolicpressure(RVEDP)(RightVentricularPreload)a valuable guide to vascular volume repalcementa valuable guide to vascular volume repalcement Normal CVP 0.49Normal CVP 0.490.98kPa(510cmH2O)A rising CVP indicates filling of the venous reservoirA rising CVP indicates filling of the venous reservoir restoration of total intravascular volume or cardiac failurerestoration of total intravascular volume or cardiac failure A falling CVP indicates depletion of the venous reservoir A falling CVP indicates depletion of the venous reservoir 2.PulmonaryCapillaryWedgePressure(PCWP):PCWP=leftatrialpressure(LAP)=left-ventricularend-diastolicpressure(LVEDP)(LeftVentricularPreload)Normalvolume0.82kPa(615cmH2O)29Specialmonitoring（7item）1.CVPANDCIRCULATINGVOLUME?30CVPANDCIRCULATINGVOLUME?30PulmonaryArteryCatheterizationKlkj31PulmonaryArteryCatheterizati3.CardiacOutput(CO)=HRSV(L/min)NormalCO=4to6L/minItmeasuredwiththeSwan-Ganzbalooncatheter4.CardiacIndex(CI)=CO/BSA(L/min/m2)NormalCI=2.5-3.5L/min/m2lOxygendelivery（DO2）:1.34HBCO10SaO2lOxygenuptake（VO2):1.34HBCO10(SaO2-SvO2）323.CardiacOutput(CO)=HRS5.Arterialbloodgasanalysis：lPaO2:10.713Kpa(80100mmHg)PaCO2:4.85.8Kpa(3644mmHg)arterialpH:7.357.45lReflected repiratory reverse,ARDS,acid-base balance,acidosis,etal6.Serumlactatelevels：asaprognosticguidelnormalvalue11.5mmol/Llheavypatient2mmol/Llexceed8mmol/L:amortalityrateof100335.ArterialbloodgasanalysisQuestionWhichoneofthefollowingisthemostcommoncauseofsevereLacticacidosis(bloodlactateconcentration5mmol/L)?a.Ethanolintoxicationb.Severeliverdiseasec.Circulatoryshockd.Ischemicbowele.Acuteasthma34QuestionWhichoneofthefollo7.7.Disseminatedintravascularcoagulation(DICDIC)DICisdiagnosedinthreeormoreofthe5items bloodplateletscount3second；plasmafibrinogen2%。357.DisseminatedintravascularcPrinciple:EarlyRecognition-DonotrelayonBP!(30%fluidloss)ControlhemorrhageRestorecirculatingvolumeOptimizeoxygendelivery DO2600 ml/min.m2 DO2600 ml/min.m2 VO2170 ml/min.m2 VO2170 ml/min.m2 CI4.5L/min.m2 CI4.5L/min.m2VasodilatorifBPstilllowaftervolumeloadingTreatmentofShock36Principle:TreatmentofShock361.GeneralmanagementofShockControlactivitybleedingAssureairwayPositionpatienttoassistperfusion.(elevateheadandshouldersifpulmonaryedema.)Keeppatientwarm.AdministeroxygenAdjustO2,GainIVaccess,ECGmonitor,PulseOximetry.371.GeneralmanagementofShockC2.RestorebloodvolumeuCrystalloids:(ex:LRor0.9%NS)Greatwhenlossfromvomitting,intestinalobstruction,diarrhea2-3LcanrapidlyrestorevolumeCanbegivenwhilebloodiscrossmatcheduColloids:(ex:albumin)Willincreaseosmoticpressure,watchforpulmedemaRemaininvascularspacelonger(severalhrs)uPlasmaexpanders:(ex:Dextran)ProteinorstarchcontaininguBlood:Increasesoxygencarryingcapacity500mlwholebloodincreasesHct2-3%,250mlPRBCsincreasesHct3-4%Usedwithacutehemorrhaging(mntnHct30%andHgb7g/dL)382.RestorebloodvolumeCrystal3.SurgicaltreatmentofprimarydiseaselControllingofhemorrhagelExcisionofnecrosisbowelslRepairofperforatedalimentarytractlDrainageandsurgicaldebridementnAnti-shockandsurgicaltreatmentatthesametime393.Surgicaltreatmentofprima4.Correctacidbaseimbalance Earlystageofshock：nottoutilizealkalicmedicineLatestageofshock:5Sodiumbicarbonate,containingNa+andHCO3-60mlper100ml,inputahalfin24hrsTherapeuticprinciple：ratheracidnobase404.Correctacidbaseimbalance5.ApplicationofvasoactivedrugspVasoactivedrugsareanimportantpharmacologicdefenseinthetreatmentofshock.pMayberequiredtosupportBPintheearlystagesofshock.pTheseagentsmaybeneededto:EnhanceCOthroughtheuseofinotropicagentsIncreaseSVRthroughtheuseofvasopressors415.ApplicationofvasoactivedrlSeldomuseonlyvasoconstrictorlVasodilatorandvolumeexpansiontherapylCombinedapplicationofvasodilatorandvasoconstrictorCurrentPharmacotherapyofshock:42Seldomuseonlyvasoconstricto6.EffectsofinotropicagentsandvasodilatorsEpinephrinea a1 1,b,b1 1,(b,(b2 2)0.020.5Norepinephrine a a1 1,b,b1 10-0.22mgDopamineb b1 1,DR,(a),(a)10ug/min.kgDobutamineb b1 1,b,b2 210ug/min.kgMetaraminolb b1 1,b,b2 20-25mgIsoprenalinb b0.10.2mgPhentolaminea a0.1-0.5mg/KgDrugReceptorCO SVRDoseRange436.EffectsofinotropicagentsAnendogenousprecursorofnorepinephrinewithmultipledose-relatedeffectsLowDose(101515g/min.kg)ua a-actions(vasoconstriction)Dopamine44AnendogenousprecursorofnorAnticholinergicagents：Atropine,AnisodamineandDaturineTorelievesmoothmuscle spasm,improve microcirculation,cellularmembranestabilizerusage：6542：10mgiv,onceper15minute45Anticholinergicagents：usage：CardiacstimulantDopamine and and Dobutamine：aand-actions,enhanceCOandSVRCedilanid:enhancemyocardialcontractility，decreaseheartrate46CardiacstimulantDopamineand7.Modifymicrocirculationlesion：Heparin,2500-5000unitsaregivenintravenouslyevery4-6hoursAntifibrinolytics:AminomethylbenzoicAcidtopreventtheformationofbrinaseAspirin,persantine,lowmolecularweightdextranhasusedtodecreasebloodviscosityandtendencytowardredcellsludgingandplateletaggregation477.Modifymicrocirculationlesi8.CorticosteroidSepticshock、severeshockMassive(10-20timestheclinicaldoses)Therapymustbeinitiated,oncegivenintravenouslylTostabilizecellmembranes488.CorticosteroidSepticshockShockresultingfromfluidloss:blood,plasma,orbodywaterCauses:Hemorrhagic:bloodloss.(classicshock)TraumaDehydration:fluidloss.Thirdspacing:intestinalobstruction,pancreatitis,cirrhosis.Mostcommoncauses:HemmorhageTraumaHypovolemicShock 49ShockresultingfromfluidlosHypovolaemicShockHaemorrhage:OvertoroccultNonhaemorrhagichypovolaemiaSevereburns,vomitinganddiarrheaReductionincirculatingvolumeReductioninvenousreturnandCOO2supply-demandimbalanceLacticacidosisReductioninvenousoxygensaturationPathophysiology50HypovolaemicShockHaemorrhage:ChangesinCOandMAPinhaemorrhage51ChangesinCOandMAPinhaemoCO,MAPandSvO252CO,MAPandSvO252ClinicalPresentationHypovolemicShockTachycardiaandtachypneaWeak,threadypulsesHypotensionSkincool&clammyMentalstatuschangesDecreasedurineoutput:dark&concentrated53ClinicalPresentationHypovoleHemorrhagicshockCommomcause：lruptureofgreatvesselslruptureofspleenandliverlGIbleedinglrupturedaneurysmslhemorrhagicpancreatitislectopicpregnancy54HemorrhagicshockCommomcause：Traumaticshock bloodandplasmalossvasoactivesubstanceandinflammatoryfactorfromnecrosistissuepain：toaffectcardiovascularfunctiondirectinfluence：thoracicinjury,paraplegia,craniocerebralinjuryPathophysiology55TraumaticshockbloodandplTreatment1.Estimationofbloodloss：Mildshock：upto20%bloodvalumeloss(1,600ml)56Treatment1.Estimationofbl2.FluidadministrationlTwotypesoffluids:crystalloidsandcolloidslOtherbloodproductsmaybenecessarylAfter2-3Landrecognizedpossiblehemorrhage,bloodproductsshouldbereadyforuse(Hb70g/L,HCT30%)MaintenanceofCVPbetween5and15mmHg,Aurineoutputabove0.5ml/kg/hTreatment572.FluidadministrationTreatmeAdvancedCareLargeboreIV:Minimum18gagePreferably14or16gageUsebloodtubingifavailableormacrotubingapplypressuretobagtospeedinfusionFluidReplacement:LactatedRingersorNormalSaline(MakesurefluidsarewarmNeed3literfluidtoreplace1literbloodloss,titratefluidinfusiontotheB/P.58AdvancedCareLargeboreIV:3.CorrectacidosisMetabolicacidosiswillusuallyrespondtofluidreplacementaloneHowever,severecasesmayrequireadditionofbicarbonate(0.5-1mEq/kg)MyocardialresponsetoendogenousorexogenouscatecholaminesdependsonanormalpH593.CorrectacidosisMetabolicaTreatment4.PressoragentsMosthypovolemicpatientsarealreadymaximallyphysiologicallystimulatedDopamineandEpinephrineareprobablythemostusefulagentsinhypovolemicshock,astheyproducevasoconstriction60Treatment4.Pressoragents60Treatment5.SurgeryOften,surgicalrepairisthedefinitiveanswertotraumaticshockproblemsControllingofbleedingSurgicaldebridement61Treatment5.Surgery61Treatment6.RecognizeandtreatsitesofbleedingExternalbleeding:directpressureisusuallysufficientInternalbleeding:significantbloodlosscanoccurinfemurorpelvicfractures,retroperitoneum,peritoneum,chestcavity,andintracraniallyLookforreversiblecausesofshock62Treatment6.RecognizeandtreaSepticShockThemortalityrateinpatientswithsepticshockrangesfrom20to80percentThemanifestationsofsepsisinclude：systemicresponsetoinfectiontachycardia,tachypnea,alterationsintemperatureleukocytosisorgan-systemdysfunctioncardiovascular,respiratory,renal,hepatichematologicabnormalitiesAsystemicinflammatoryresponse63SepticShockThemortalityrateSepticShockAnytypeofmicroorganismcancausesepsisbutgram-negativebacteriaismostcommonEscherichiacoliKlebsiellaEnterobacterSerratiaPseudomonasaeruginosaBacteroidesproteus64SepticShockCommonoriginsofsepsisLungbacteremiaassociatedwithnosocomialpneumoniaAbdomen(Intraabdominalinfections)GenitourinarytractPostoperativewoundinfectionsPrimarybloodstreaminfectionviaintravascularlines65Commonoriginsofsepsis65PathophysiologyInitiatedbygram-negative(mostcommon)orgrampositivebacteria,fungi,orvirusesCellwallsoforganismscontainEndotoxinsEndotoxinsreleaseinflammatorymediators(systemicinflammatoryresponse)causes.Vasodilation&increasecapillarypermeabilityleadstoShockduetoalterationinperipheralcirculation&massivedilation66PathophysiologyInitiatedbygPathophysiologySIRS67PathophysiologySIRS67SystemicInflammatoryResponseSyndrome(SIRS)SIRStoavarietyofsevereclinicalinsultsmanifestedby2ofthefollowingconditionsTemperature38Cor90beats/minRespiratoryrate20breaths/minorPaCO2,32torr(12,000cells/mm3,10%immature(band)cells68SystemicInflammatoryResponseClassificationHyperdynamicState：HypodynamicState：69ClassificationHyperdynamicSta“Warm”shock-earlyphasehyperdynamicresponsehyperdynamicresponseMassivevasodilationPink,warm,flushedskinIncreasedHeartRateFullboundingpulseTachypneaIncreasedCO&CIDecreasedSVR*SVO2willbeabnormallyhighCrackles70“Warm”shock-earlyphaseIncrVasoconstrictionSkinispale&coolSignificanttachycardiaDecreasedBPChangeinLOCDecreasedCOIncreaseSVRDecreasedUOPMetabolic&respiratoryacidosiswithhypoxemia“Cold”shock-latephasehypodynamicresponse71VasoconstrictionDecreasedCO“CTherapiesofSepsis/SepticShock72TherapiesofSepsis/SepticSho1.FluidresuscitationHemodynamicsupportRestoretissueperfusionNormalizecellularmetabolismLarge,rapidvolumes250-1000mLper15minutes10Liters/24hrsUsuallyneedcolloidsHb100g/L,HCT30%-35%CVPmonitoring731.FluidresuscitationHemodyna2.ControllingthesourceofinfectionRemovalofinfectedandnecrotictissueAntibiotics(earlyadministration)Nutritionalsupport:blood,plasma,albumintransfusion742.Controllingthesourceofi3.3.Electrolyte/acidbaseimbalance -5SodiumbicarbonateSupplementaloxygen(treatmentofacuterespiratorydistresssyndrome,ARDS)753.Electrolyte/acidbaseimbal4.VasoactivedrugslCombinedapplycationofvasodilatorandvasoconstrictornDopamine,dobutamine+norepinephrine,lCardiacstimulant：nCedilanid+dobutamine764.VasoactivedrugsCombineda5.5.AdrenalAdrenalCorticosteroidTorelieveSIRSMassive(10-20timestheclinicaldoses)short-term,48hour775.AdrenalCorticosteroidToreThankyou!Email:qs_Google:童强松童强松orQiangsongTong78Thankyou!78