外科休克(surgicalshock)课件

DepartmentofPediatricSurgeryUnionHospitalofHuazhongUniversityofScienceandTechnologyQiangsongTong,M.D.Ph.D.SURGICALSHOCK1DepartmentofPediatricSurgerObjectivesUnderstandwhatisshock？DefinetypesofshockUnderstandpathophysiologyofshockUnderstandhowtotreatshock2ObjectivesUnderstandwhatissDevelopmentoftheconceptofshockAhistoryofthe200yearstorecognizeshock:“shake”,“attack”Fromsuperficialsyndrometomicrocirculatorylevel,cellularlevel,molecularlevelCirculatorylevel：bloodpressureMicrocirculatorylevel：inadequatetissueperfusionCellularlevelandmolecularlevel：FrontierExploratorystage，experimentaltherapies3DevelopmentoftheconceptofWHATISSHOCK?

Shockresultsfrompoortissueperfusionandtissuehypoxiafrominadequatecirculatorycompensationsneededtosustainacutelyincreasedbodymetabolism.AbreakdownofeffectivecirculationInadequatetissueperfusionDecreasedoxygensupplyAnaerobicmetabolismAccumulationofmetabolicwasteMultipleorganfailureAclinicalsyndrome4WHATISSHOCK?ShockWhatiseffectivecirculatorybloodvolume?Varioustypesofshockresultfromfailureinoneormoreofthe3majorcomponentsofthecirculatorysystem：BloodvolumePumpPeripheralresistance5WhatiseffectivecirculatoryCausesofShockSevereorsuddenbloodlossLargedropinbodyfluidsMajorinfectionsHighspinalinjuriesMyocardialinfarctionAnaphylaxisExtremeheatorcold6CausesofShock6TypesofShockHypovolemicShock:

haemorrhagictraumatic

dehydrationOthercausesofshockSepticShockCardiogenicShockNeurogenicShockHypersensitiveShock

7TypesofShockHypovolemicShocPathophysiology1.Microcirculatorychanges2.Thechangesofbodyfluidmetabolism3.Mediatorsofinflammationreleaseandischemicalreperfusioninjury4.Secondarylesion8Pathophysiology81.MicrocirculationPrecapillaryresistancevessel：arteriole、metarteriole、precapillarysphincter

Postcapillaryresistancevessel：veinuleMicrocirculationperfusion：91.Microcirculation9

Increasedcatecholaminerelease

IncreaseglucocorticoidandmineralcorticoidreleaseActivationofRenin-angiotensinsystem

Compensatorymechanisms(earlyshock)TheHPAandneuroendocrineaxesaretriggered

Adecreaseinbloodvolume

Stretchreceptorsinheartbaroreceptorsinaortaandcarotidarteries

10Compensatorymechanisms(earlCompensatorymechanismsThebodyattemptstocompensateandrestoreperfusionby:IncreasingcardiacoutputStimulationofthesympatheticnervoussystemcausesanincreaseinheartrate,strokevolume,andPVR(peripheralvesselresistance).RedistributingthecirculatingbloodvolumetovitalorgansVasoconstriction,(periph-andviscero-vessel)PathologicarteriovenousshuntingAutotranfused:precapillaryresistancevesseltocontract，todecreasecapilaryhydrostaticpressure.

fluidandnoperfusion11CompensatorymechanismsprecapiCompensatorysignificanceKeepingbloodpressurenormalPerfusiontovitalorgans12CompensatorysignificanceKeepiEarlyStage(compensatedshock):

CompensatorymechanismsareabletomaintainperfusionofvitalorgansClinicalmanifestationofShockHeartRate:mildtachycardia;boundingpulse

LevelofConsciousness:lethargy,confusion,combativeness

Skin:delayedcapillaryrefill;coolandclammy

BloodPressure:normalorslightlyelevated

Respirations:rapidandshallow

13EarlyStage(compensatedshockCompensatorymechanisms（Progressiveshock）plasmashifttointerstitualspacespachyemiaandincreasingbloodviscidity

perfusionandnofluidarteriovenousshunt,directpassagewaytoopentissuehypoperfusionanaerobicmetabolismlacticacidbuildsupmetabolicacidosisPre-CRVtodilatePost-CRVtocontractcapillaryhydrostaticpressuretoincrease14Compensatorymechanisms（ProgHeartRate:moderatetachycardia;weakandthreadypulse

LevelofConsciousness:confusionorunconsciousness

Skin:delayedcapillaryrefill;cold,clammy,andcyanotic

BloodPressure:decreased

Respirations:rapidandshallowUrineoutput:oliguriaMiddleStage(uncompensatedshock):Compensatorymechanismsareunabletomaintainperfusion15HeartRate:moderatetachycarIrreversibleshockHypercoagulablecharactererythrocyteandthrombocytetoaggregateDICCellularhypoxia，lysosomerupturehydrolyticenzymereleasingaqtocytolysisandtodamageothercellsCelldamage,organfailureoccurdeathoccurnoperfusionandnofluid16IrreversibleshockHypercoagulLateShockHeartRate:bradycardia;severedysrhythmias

LevelofConsciousness:coma

Skin:pale,cold,markeddiaphoresis

BloodPressure:markedhypotension

Respirations:decreasedrateandtidalvolumeUrineoutput:oliguriaoranuria

multiplesystemorganfailure,MSOF17LateShockHeartRate:bradyc2.MetabolicresponsesAnaerobicmetabolismAbnormalenergymetabolism：Increasedproteincatabolism,enzymicproteintoconsume，tocauseMODSIncreasedliverglyconeogenesis，hyperglycaemialipolysisisanmainenergysourcemetabolicacidosislacticacidaccumulatesDecreasedmetaboliccapabilityintheliverdecreasedcatecholamineresponcetocardiovascularsystem182.MetabolicresponsesAnaerob3.IschemicalreperfusioninjuryAnacuterestorationofoxygendeliverycanalsoamplifytheinitialischemicinsult,leadingtofurthercellinjuryDuringthisphaseofshockresuscitation,leukocytesadheretopostcapillaryvenularendotheliumthatisfollowedbythegenerationofreactiveoxygenspecies.Thelatterresponsedamagesproteinsandmembranestructures,andactivatessignaltransductionpathwaysthatcanultimatelyleadtoapoptosis(programmedcelldeath).193.IschemicalreperfusioninjCelldeathHypoxia:intracellularischemiaoccurs;anaerobicmetabolismbegins;lacticacidbuildsupincell;leadingtometabolicacidosis;causesthesodiumpotassiumpumptofail.2.IonshiftoccursSodiumrushesintothecellbringingwaterwithit.

20CelldeathHypoxia:intracellul3.Cellswellingoccurs.4.Mitochondrialswellingoccurs;productionofATPceases.5.Intracellulardisruptionreleaseslysosomes, cellmembranebeginstobreak.6.Celldestructionbeginsleadingtotissuedeath.213.Cellswellingoccurs.214.SecondarylesiontoorganLung－ARDS(acuterespiratorydistresssyndrome)：Capillaryendotheliumcelldamage：Permeabilityincreases,causinginterstitialedema,hyalinization.Alveolarepithelialcelldamage：decreasing

alveolarsurfactant，pulmonaryshrinkandatelectasisAtthesametime,thereisveryhighoxygenconsumptionandCO2production

V/Qmismatch,shunting,andpulmonaryhypertensionoccur,allleadingtoseverehypoxemia224.SecondarylesiontoorganLuKidneys－ARF(acuterenalfailure)：Hypotensionandcatecholamineleadstorenalarteryvasoconstriction,reducedGFR,oliguria,andazotemiaBloodflowredistributioninkidneys,IschemialeadstoAcuteTubularNecrosis(ATN).

oliguria(<400ml/d)oranuria(<100ml/d)23Kidneys－ARF(acuterenalfailuCardiacinsufficiencyHeartfailureShockbloodpressure↓heartrate↑Coronalarterybloodflow↓HR↑contraction↑AcidosishyperkaliemiaVO2↑DICmicrothrombusfocalnecrosishaemorrhageIschemicalreperfusioninjurymediatorsHeartEarliershocknormal24CardiacinsufficiencyShockblooBrainearliershock

RedistributingthebloodvolumeKeepperfumetobrainnobraindisorderbraintissueIschemia,hypoxiaLethargicsleepyComashockBp<7kPaDIC

Stressdysphoria25BrainearliershockRedistrAlimentarytractandLiverfunctionIschemia、congestion、DICIntestinefunctionaldisorderdigestivejuicesecretion↓gastrointestinalmotility↓Mucosalerosionulcerintestinalbacteriatobreed

Endotoxin,bacteriatoenterboodhepatosisKupffercellmediatorsofinflammationdetoxicate↓lacticacid→glucoseSIRSacidosis26AlimentarytractandLiverfunHemodynamicmonitoring1.Mentalstatus：braintissueperfusion2.Skinperfusion：warm,normalcolorgoodperfusioncold,pale,moistskinvasoconstriction3.Bloodpressure：importantbutnosensitiveindexEarlydetection:Don’trelyonBPsystolicpressure<12kPa(90mmHg)pulsepressure<2.67kPa(20mmHg)Generalmonitoring（5item）27Hemodynamicmonitoring1.Menta4.Pulserate：

Initialpresentationofshock：increasedpulseratesShockindex：PR/SPmmHg0.5noshock，>1.0-1.5shock，>2.0severeshock5.Urineoutput：themostsensitiveindexoftheadequacyofvitalorganperfusionoliguria：initialshock,initialresuscitationnormalBP,oliguriaandlowspecificgravity：acuterenalfailure(ARF)urineoutput<25ml/h，inadequateperfusionurineoutput>30ml/h：improve284.Pulserate：28

Specialmonitoring（7item）1.CentralVenousPressure(CVP):CVP=rightatrialpressure(RAP)=right-ventricularend-diastolicpressure(RVEDP)(RightVentricularPreload)

avaluableguidetovascularvolumerepalcement

NormalCVP0.49～0.98kPa(5～10cmH2O)

ArisingCVPindicatesfillingofthevenousreservoir

restorationoftotalintravascularvolumeorcardiacfailureAfallingCVPindicatesdepletionofthevenousreservoir

2.PulmonaryCapillaryWedgePressure(PCWP):PCWP=leftatrialpressure(LAP)=left-ventricularend-diastolicpressure(LVEDP)(LeftVentricularPreload)

Normalvolume0.8～2kPa(6～15cmH2O)

29Specialmonitoring（7item）1.CVPANDCIRCULATINGVOLUME?30CVPANDCIRCULATINGVOLUME?30PulmonaryArteryCatheterizationKlkj31PulmonaryArteryCatheterizati3.CardiacOutput(CO)=HR×SV(L/min)NormalCO=4to6L/minItmeasuredwiththeSwan-Ganzbalooncatheter4.CardiacIndex(CI)=CO/BSA(L/min/m2)NormalCI=2.5-3.5L/min/m2Oxygendelivery（DO2）:1.34×HB×CO×10×SaO2Oxygenuptake（VO2):1.34×HB×CO×10×(SaO2-SvO2）323.CardiacOutput(CO)=HR×S5.Arterialbloodgasanalysis：PaO2:10.7～13Kpa(80～100mmHg)PaCO2:4.8～5.8Kpa(36～44mmHg)arterial

pH:7.35～7.45Reflectedrepiratoryreverse,ARDS,acid-basebalance,acidosis,etal6.Serumlactatelevels：asaprognosticguidenormalvalue1～1.5mmol/Lheavypatient2mmol/Lexceed8mmol/L:amortalityrateof100％335.ArterialbloodgasanalysisQuestionWhichoneofthefollowingisthemostcommoncauseofsevereLacticacidosis(bloodlactateconcentration>5mmol/L)? a.Ethanolintoxication b.Severeliverdisease c.Circulatoryshock d.Ischemicbowel e.Acuteasthma34QuestionWhichoneofthefollo7.Disseminatedintravascularcoagulation(DIC)

DICisdiagnosedinthreeormoreofthe5items

①bloodplateletscount<80×109/L；②prothrombintime>3second；③plasmafibrinogen<1.5g/L④SP(+)；⑤brokenerythrocyteinbloodfilm>2%。357.DisseminatedintravascularcPrinciple:EarlyRecognition-DonotrelayonBP!(30%fluidloss)ControlhemorrhageRestorecirculatingvolumeOptimizeoxygendeliveryDO2>600ml/min.m2VO2>170ml/min.m2CI>4.5L/min.m2VasodilatorifBPstilllowaftervolumeloadingTreatmentofShock36Principle:TreatmentofShock361.GeneralmanagementofShockControlactivitybleedingAssureairwayPositionpatienttoassistperfusion.(elevateheadandshouldersifpulmonaryedema.)Keeppatientwarm.AdministeroxygenAdjustO2,GainIVaccess,ECGmonitor,PulseOximetry.371.GeneralmanagementofShockC2.RestorebloodvolumeCrystalloids:(ex:LRor0.9%NS)–Greatwhenlossfromvomitting,intestinalobstruction,diarrhea–2-3Lcanrapidlyrestorevolume–CanbegivenwhilebloodiscrossmatchedColloids:(ex:albumin)–Willincreaseosmoticpressure,watchforpulmedema–Remaininvascularspacelonger(severalhrs)Plasmaexpanders:(ex:Dextran)–ProteinorstarchcontainingBlood:–Increasesoxygencarryingcapacity–500mlwholebloodincreasesHct2-3%,250mlPRBC’sincreasesHct3-4%–Usedwithacutehemorrhaging(mntnHct30%andHgb7g/dL)382.RestorebloodvolumeCrystal3.SurgicaltreatmentofprimarydiseaseControllingofhemorrhageExcisionofnecrosisbowelsRepairofperforatedalimentarytractDrainageandsurgicaldebridementAnti-shockandsurgicaltreatmentatthesametime393.Surgicaltreatmentofprima4.Correctacidbaseimbalance

Earlystageofshock：

nottoutilizealkalicmedicineLatestageofshock:

5％Sodiumbicarbonate,containingNa+andHCO3-60mlper100ml,inputahalfin2～4hrsTherapeuticprinciple：ratheracidnobase404.Correctacidbaseimbalance5.ApplicationofvasoactivedrugsVasoactivedrugsareanimportantpharmacologicdefenseinthetreatmentofshock.MayberequiredtosupportBPintheearlystagesofshock.Theseagentsmaybeneededto:EnhanceCOthroughtheuseofinotropicagentsIncreaseSVRthroughtheuseofvasopressors415.ApplicationofvasoactivedrSeldomuseonlyvasoconstrictorVasodilatorandvolumeexpansiontherapyCombinedapplicationofvasodilatorandvasoconstrictorCurrentPharmacotherapyofshock:42Seldomuseonlyvasoconstricto6.EffectsofinotropicagentsandvasodilatorsEpinephrinea1,b1,(b2)0.02–0.5Norepinephrinea1,b10-0.2–2mgDopamineb1,DR,(a)10ug/min.kgDobutamineb1,b210ug/min.kgMetaraminolb1,b20-2–5mgIsoprenalinb0.1–0.2mgPhentolamine

a0.1-0.5mg/KgDrug Receptor CO SVRDoseRange436.EffectsofinotropicagentsAnendogenousprecursorofnorepinephrinewith

multipledose-relatedeffectsLowDose(<10μg/min.kg)b1

anddopaminergic(DR)effectsPositiveinotropiceffectsEnhancedbloodflowtorenalandsplanchnicbedsHighDose>15μg/min.kg)a-actions(vasoconstriction)Dopamine44AnendogenousprecursorofnorAnticholinergicagents：Atropine,AnisodamineandDaturineTorelievesmoothmuscle

spasm,improvemicrocirculation,cellularmembranestabilizerusage：

654－2：10mgiv,onceper15minute45Anticholinergicagents：usage：CardiacstimulantDopamineandDobutamine：

aandβ-actions,enhanceCOandSVRCedilanid:

enhancemyocardialcontractility，decreaseheartrate46CardiacstimulantDopamineand7.Modifymicrocirculationlesion：Heparin,2500-5000unitsaregivenintravenouslyevery4-6hoursAntifibrinolytics:AminomethylbenzoicAcidtopreventtheformationofbrinaseAspirin,persantine,lowmolecularweightdextranhasusedtodecreasebloodviscosityandtendencytowardredcellsludgingandplateletaggregation477.Modifymicrocirculationlesi

8.CorticosteroidSepticshock、severeshockMassive(10-20timestheclinicaldoses)Therapymustbeinitiated,oncegivenintravenouslyTostabilizecellmembranes488.CorticosteroidSepticshockShockresultingfromfluidloss:blood,plasma,orbodywaterCauses:Hemorrhagic:bloodloss.(classicshock)TraumaDehydration:fluidloss.Thirdspacing:intestinalobstruction,pancreatitis,cirrhosis.Mostcommoncauses:HemmorhageTraumaHypovolemicShock

49ShockresultingfromfluidlosHypovolaemicShockHaemorrhage:OvertoroccultNonhaemorrhagichypovolaemiaSevereburns,vomitinganddiarrheaReductionincirculatingvolumeReductioninvenousreturnandCOO2supply-demandimbalanceLacticacidosisReductioninvenousoxygensaturationPathophysiology50HypovolaemicShockHaemorrhage:ChangesinCOandMAPinhaemorrhage51ChangesinCOandMAPinhaemoCO,MAPandSvO252CO,MAPandSvO252ClinicalPresentation

HypovolemicShockTachycardiaandtachypneaWeak,threadypulsesHypotensionSkincool&clammyMentalstatuschangesDecreasedurineoutput:dark&concentrated53ClinicalPresentation

HypovoleHemorrhagicshockCommomcause：ruptureofgreatvesselsruptureofspleenandliverGIbleeding

rupturedaneurysmshemorrhagicpancreatitisectopicpregnancy54HemorrhagicshockCommomcause：Traumaticshock①bloodandplasmaloss②vasoactivesubstanceandinflammatoryfactorfromnecrosistissue③pain：toaffectcardiovascularfunction④directinfluence：thoracicinjury,paraplegia,craniocerebralinjuryPathophysiology55Traumaticshock①bloodandplTreatment1.Estimationofbloodloss：Mildshock：upto20%bloodvalumeloss(<800ml)Moderateshock：20～40％bloodvalumeloss(800～1,600ml)Severeshock：40％ormorebloodvalumeloss(>1,600ml)

56Treatment1.Estimationofbl2.FluidadministrationTwotypesoffluids:crystalloidsandcolloidsOtherbloodproductsmaybenecessaryAfter2-3Landrecognizedpossiblehemorrhage,bloodproductsshouldbereadyforuse(Hb70g/L,HCT30%)

MaintenanceofCVPbetween5and15mmHg,Aurineoutputabove0.5ml/kg/h

Treatment572.FluidadministrationTreatmeAdvancedCareLargeboreIV:Minimum18gage Preferably14or16gageUsebloodtubingifavailableormacrotubingapplypressuretobagtospeedinfusionFluidReplacement: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：－systemicresponsetoinfection

tachycardia,tachypnea,alterationsintemperatureleukocytosis－organ-systemdysfunctioncardiovascular,respiratory,renal,hepatichematologicabnormalitiesAsystemicinflammatoryresponse63SepticShockThemortalityrate

SepticShock

Anytypeofmicroorganismcancausesepsisbutgram-negativebacteriaismostcommon–Escherichiacoli–Klebsiella–Enterobacter–Serratia–Pseudomonasaeruginosa–Bacteroides–proteus64SepticShockCommonoriginsofsepsis•Lung–bacteremiaassociatedwithnosocomialpneumonia•Abdomen(Intraabdominalinfections)•Genitourinarytract•Postoperativewoundinfections•Primarybloodstreaminfectionviaintravascularlines65Commonoriginsofsepsis65Pathophysiology

Initiatedbygram-negative(mostcommon)orgrampositivebacteria,fungi,orvirusesCellwallsoforganismscontainEndotoxinsEndotoxinsreleaseinflammatorymediators(systemicinflammatoryresponse)causes…...Vasodilation&increasecapillarypermeabilityleadstoShockduetoalterationinperipheralcirculation&massivedilation66PathophysiologyInitiatedbygPathophysiologySIRS

67PathophysiologySIRS67SystemicInflammatoryResponseSyndrome(SIRS)SIRStoavarietyofsevereclinicalinsultsmanifestedby≥2ofthefollowingconditions●Temperature>38ºCor<36ºC●Heartrate>90beats/min●Respiratoryrate>20breaths/minorPaCO2,<32torr(<4.3kPa)●Whitebloodcellcount>12,000cells/mm3,<4000cells/mm3,or>10%immature(band)cells68SystemicInflammatoryResponseClassificationHyperdynamicState：HypodynamicState：69ClassificationHyperdynamicSta“Warm”shock-earlyphasehyperdynamicresponseMassivevasodilationPink,warm,flushedskinIncreasedHeartRate FullboundingpulseTachypnea

IncreasedCO&CIDecreasedSVR*SVO2willbeabnormallyhighCrackles70“Warm”shock-earlyphaseIncrVasoconstrictionSkinispale&coolSignificanttachycardiaDecreasedBPChangeinLOCDecreasedCOIncreaseSVRDecreasedUOPMetabolic&respiratoryacidosiswithhypoxemia“Cold”shock-latephasehypodynamicresponse

71VasoconstrictionDecreasedCO“CTherapiesofSepsis/SepticShock72TherapiesofSepsis/SepticSho1.FluidresuscitationHemodynamicsupport●Restoretissueperfusion●NormalizecellularmetabolismLarge,rapidvolumes250-1000mLper15minutes~10Liters/24hrs

UsuallyneedcolloidsHb>100g/L,HCT30%-35%CVPmonitoring731.FluidresuscitationHemodyna2.Controllingthesourceofinfection–Removalofinfectedandnecrotictissue–Antibiotics(earlyadministration)–Nutritionalsupport:

–

blood,plasma,albumintransfusion742.Controllingthesourceofi3.Electrolyte/acidbase

imbalance

-5％SodiumbicarbonateSupplementaloxygen(treatmentofacuterespiratorydistresssyndrome,ARDS)753.Electrolyte/acidbaseimbal4.VasoactivedrugsCombinedapplycationofvasodilatorandvasoconstrictorDopamine,dobutamine+norepinephrine,Cardiacstimulant：Cedilanid+dobutamine764.VasoactivedrugsCombineda5.Adrenal

CorticosteroidTorelieveSIRSMassive(10-20timestheclinicaldoses)short-term,<48hour775.AdrenalCorticosteroidToreThankyou!Email:qs_tong@126.comGoogle:童强松orQiangsongTong78Thankyou!78DepartmentofPediatricSurgeryUnionHospitalofHuazhongUniversityofScienceandTechnologyQiangsongTong,M.D.Ph.D.SURGICALSHOCK79DepartmentofPediatricSurgerObjectivesUnderstandwhatisshock？DefinetypesofshockUnderstandpathophysiologyofshockUnderstandhowtotreatshock80ObjectivesUnderstandwhatissDevelopmentoftheconceptofshockAhistoryofthe200yearstorecognizeshock:“shake”,“attack”Fromsuperficialsyndrometomicrocirculatorylevel,cellularlevel,molecularlevelCirculatorylevel：bloodpressureMicrocirculatorylevel：inadequatetissueperfusionCellularlevelandmolecularlevel：FrontierExploratorystage，experimentaltherapies81DevelopmentoftheconceptofWHATISSHOCK?

Shockresultsfrompoortissueperfusionandtissuehypoxiafrominadequatecirculatorycompensationsneededtosustainacutelyincreasedbodymetabolism.AbreakdownofeffectivecirculationInadequatetissueperfusionDecreasedoxygensupplyAnaerobicmetabolismAccumulationofmetabolicwasteMultipleorganfailureAclinicalsyndrome82WHATISSHOCK?ShockWhatiseffectivecirculatorybloodvolume?Varioustypesofshockresultfromfailureinoneormoreofthe3majorcomponentsofthecirculatorysystem：BloodvolumePumpPeripheralresistance83WhatiseffectivecirculatoryCausesofShockSevereorsuddenbloodlossLargedropinbodyfluidsMajorinfectionsHighspinalinjuriesMyocardialinfarctionAnaphylaxisExtremeheatorcold84CausesofShock6TypesofShockHypovolemicShock:

haemorrhagictraumatic

dehydrationOthercausesofshockSepticShockCardiogenicShockNeurogenicShockHypersensitiveShock

85TypesofShockHypovolemicShocPathophysiology1.Microcirculatorychanges2.Thechangesofbodyfluidmetabolism3.Mediatorsofinflammationreleaseandischemicalreperfusioninjury4.Secondarylesion86Pathophysiology81.MicrocirculationPrecapillaryresistancevessel：arteriole、metarteriole、precapillarysphincter

Postcapillaryresistancevessel：veinuleMicrocirculationperfusion：871.Microcirculation9

Increasedcatecholaminerelease

IncreaseglucocorticoidandmineralcorticoidreleaseActivationofRenin-angiotensinsystem

Compensatorymechanisms(earlyshock)TheHPAandneuroendocrineaxesaretriggered

Adecreaseinbloodvolume

Stretchreceptorsinheartbaroreceptorsinaortaandcarotidarteries

88Compensatorymechanisms(earlCompensatorymechanismsThebodyattemptstocompensateandrestoreperfusionby:IncreasingcardiacoutputStimulationofthesympatheticnervoussystemcausesanincreaseinheartrate,strokevolume,andPVR(peripheralvesselresistance).RedistributingthecirculatingbloodvolumetovitalorgansVasoconstriction,(periph-andviscero-vessel)PathologicarteriovenousshuntingAutotranfused:precapillaryresistancevesseltocontract，todecreasecapilaryhydrostaticpressure.

fluidandnoperfusion89CompensatorymechanismsprecapiCompensatorysignificanceKeepingbloodpressurenormalPerfusiontovitalorgans90CompensatorysignificanceKeepiEarlyStage(compensatedshock):

CompensatorymechanismsareabletomaintainperfusionofvitalorgansClinicalmanifestationofShockHeartRate:mildtachycardia;boundingpulse

LevelofConsciousness:lethargy,confusion,combativeness

Skin:delayedcapillaryrefill;coolandclammy

BloodPressure:normalorslightlyelevated

Respirations:rapidandshallow

91EarlyStage(compensatedshockCompensatorymechanisms（Progressiveshock）plasmashifttointerstitualspacespachyemiaandincreasingbloodviscidity

perfusionandnofluidarteriovenousshunt,directpassagewaytoopentissuehypoperfusionanaerobicmetabolismlacticacidbuildsupmetabolicacidosisPre-CRVtodilatePost-CRVtocontractcapillaryhydrostaticpressuretoincrease92Compensatorymechanisms（ProgHeartRate:moderatetachycardia;weakandthreadypulse

LevelofConsciousness:confusionorunconsciousness

Skin:delayedcapillaryrefill;cold,clammy,andcyanotic

BloodPressure:decreased

Respirations:rapid