资料课件参考病生shock

ShockChapter7Introduction

Inclinics

shockisacommonandcriticalpathologicalprocesscausedbyavarietyofetiologicfactors.Shockmeansviolentcollisionorconcussionorimpact.IntroductionTheterm“shock”derivedfromGreekmeanscollisionorconcussion.In1731,ShockwasusedatfirstbyHenriFrancoisShockisacommonpathologicalprocessratherthanaspecificdisease.ThebasicfeatureofshockisthefailureofperipheralcirculationandthevitalorganwithdysfunctionDescriptionCirculationfailureMicrocirculationobstructionPresentpalefaceorcyanosiscoldandclammyskinrapidandthreadypulseoliguriaapathyhypotensionacutecirculatoryfailure----vasomotorcenterparalyzed→vasodilation→bloodpressure↓.intensiveexcitationofsympatheticadrenalsystem→bloodflow↓.

Shockisdefinedasapathologicprocessundertheeffectofvariousdrasticetiologicalfactors,andcharacterizedbyacutecirculatoryfailureincludingdecreasedECBV,inadequatetissueperfusion,cellularmetabolismimpedimentanddysfunctionofmultipleorgans.ConceptofshockECBVrefertoflowingbloodinvessel,don’tincludestaticblood.ECBV(effectivecirculatingbloodvolume)1.SufficientBV2.Normalfunctionofheartpump3.NormalVofcapillarybedSection1Etiologyandclassificationofshock1.ClassificationofShockbyCausesEtiologyClassificationPathogenesisHemorrhageHemorrhagicshockHypovolemicshockmaldistributiveshockCardiogenicshockAcuteheartfailureCardiogenicshockNervousstimulationNeurogenicshockAnaphylaxisAnaphylacticshockInfectionInfectiousshockTraumaTraumaticshockBurnBurnshockFluidlossFluidlossshock(Vasogenicshock)2.ClassificationofShockbypathogenesisSufficientBV

NormalfunctionofheartpumpNormalVofcapillarybedNormalcirculationBVDysfunctionofheartCapillarybedshockpathogenesisofshockdevelopmentHypovolemicshockvasogenicshockorlow-resistanceshockormaldistributiveshock

Cardiogenicshock2.ClassificationofShockbypathogenesisClassificationPathogenesisHypovolemicshockvasogenicshockCardiogenicshockReductioninbloodvolumeDecreasedECBVIncreasedvascular-bedvolumeDecreasedECBVrelativelyAHF,SeverearrhythmiasDecreasedCODecreasedECBV1.ClassificationofShockbyCausesEtiologyClassificationPathogenesisHemorrhageHemorrhagicshockHypovolemicshockmaldistributiveshockCardiogenicshockAcuteheartfailureCardiogenicshockNervousstimulationNeurogenicshockAnaphylaxisAnaphylacticshockInfectionInfectiousshockTraumaTraumaticshockBurnBurnshockFluidlossFluidlossshock(Vasogenicshock)Section2PathogenesisofshockPathogenesisofshockMicrocirculatorymechanismCellularandmolecularmechanismsNormalmicrocirculationanditsregulationNormalmicrocirculation(MC)Microcirculationreferstothebloodcirculationbetweenarterioleandvenule.Itisthemostessentialstructureofthecirculationsystemandthesmallestunit.Functionofmicrocirculationistotransferthesubstancesbetweenbloodandthetissues.precapillaryresistancevessel:arteriole,smallartery,precapillarysphincter,postcapillaryresistance

vessel:venule

andsmallervein.

Threebloodflowpathway：1.nutritionalpathway;2.preferentialchannel;3.arteriovenousshuntRegulationofmicrociculationMCwasmainlyregulatedbyneurogenicandhumoralfactors.

NeurogenicregulationExcitationofsympatheticnervoussystemactontheα-RonsmallvesselsVasoconstrictionBloodflowoftissue↓Neurogenicandhumoralregulation

HumoralfactorsVasoconstrictionfactorsVasodilatationfactorsCatecholamine(CA)HistamineAngiotension-Ⅱ(AngⅡ)KininsVasopressin(VP)Adenosine(ADP)ThromboxaneA2(TXA2)LacticacidEndothelin(ET)prostacyclin(PGI2)EndorphinNeurogenicandhumoralregulationLocalfeedbackregulationPrecapillarysphincterandmetarteriolecontractionBloodflowincapillary↓Accumulationoflocalmetaboliteandhistamine↓ReactivityofsmoothmuscleonsubstanceofvasoconstrictionPrecapillarysphincterandmetarteriolerelaxationBloodflowincapillary↑Eliminationoflocalmetaboliteandhistamine↑ReactivityofsmoothmuscleonsubstanceofvasoconstrictionMicrocirculatorymechanismAccordingtothedifferentalterationsinMC,thedevelopmentofshockmaybedividedintothreestages:

ischemichypoxiastage

stagnanthypoxiastage

refractorystage

ⅠⅡⅢ

Compensatorystage

--Ischemichypoxiastageavarietyofcompensatorymechanismsareevokedandperfusionofvitalorgansismaintained.Ⅰ1.AlterationsofMCandtissueperfusion

Compensatorystage

--IschemichypoxiastageⅠ2.MechanismofMCdisturbance3.CompensatorySignificance4.Clinicalmanifestations

①Arterioleandprecapillarysphincterconstrict②Arteriovenousshuntisopening③Pre-capillaryresistance>Postcapillaryresistance④Inflowofbloodislessthanoutflowfromcapillary⑤Bloodflowslowdown1.AlterationsofMCandtissueperfusionCausesofShockCA↑catecholamine

HumoralfactorsofvasoconstrictionincreasesuchasAG-Ⅱ,ADH,TXA2,ET,etc.2.MechanismofMCdisturbanceα-receptors→constrictionofskin,visceraandkidneyvesselsβ-receptor→arteriovenousshuntopening3.CompensatorySignificance(1)MaintainsBP(2)Maintainsbloodflowoftheheartandbrain(1)MaintainsBPvenousreturn↑2)CO↑3)peripheralresistance

↑venousreturn↑①Autobloodtransfusion②AutofluidinfusionMaintainBP.

(firstdefenselineagainstdecreaseinvenousreturn)①AutobloodtransfusionTheconstrictionofvenulesandvesselofliverandspleenandcausedbyexcitementofsympatheticnervoussystemmadevenousbloodreturntothecirculationandincreasedvenousreturntotheheart.LiverSpleenpre-capillaryresistance↑→BPincapillaries↓→fluidshiftfrominterstitialspacetothevascularcompartmentMaintainBP

(seconddefenselineagainstdecreaseinvenousreturn)VenuleArterioleconstriction②Autofluidinfusion2)CO↑venousreturn↑,cardiaccontractilityandheartrate↑

3)peripheralresistance

↑Arteriolecontractconstrictionoftheskin,visceravessels→bloodflow↓thecerebralvesselandcoronaryarterydon’tchangegreatlyEnsuresadequatebloodflowthroughtheheartandbrain(2)Maintainsbloodflowoftheheartandbrain-----BloodredistributionConstrictionofskinvesselsIschemiaofkidneyConstrictionofvisceravesselsOliguriaIschemiaofskinPallor,coollimbs(+)CNSsober(+)sympatheticadrenalsystemCardiaccontractilityandheartrate↑ThreadypulseBP(N)pulsepressure↓CA↑4.ClinicalmanifestationsCauesofshockItischaracterizedbytissuehypoperfusionandonsetofworseningcirculatoryandmetabolicimbalances.Ⅱ

Decompensatorystage--StagnanthypoxiastageⅡ

Decompensatorystage--Stagnanthypoxiastage1.AlterationsofMCandtissueperfusion2.MechanismofMCStasis

3.ConsequenceofMCStasis

4.Clinicalmanifestations1.AlterationsofMCandtissueperfusion①Theconstrictedvesselsbegintodilate;②Perfusionofcapillary

↑③Pre-capillaryresistance<Postcapillaryresistance④inflowofbloodismorethanoutflowfromcapillary⑤bloodstasisandtissuehypoxia（1）vasodilatation①Acidosis

②Localaccumulationofmetabolicproducts（2）Stagnationofblood

①WBCadhesioninvenule

②Hemoconcentration2.MechanismofMCStasis

（1）vasodilatation①Acidosisischemiaandhypoxiaanaerobicglycolysislacticacid↑metabolicacidosis

reactivityofSMCtoCA↓vasodilatationvasodilatation

ischemiahypoxiaacidosislocalaccumulationofhistamine,adenosine↑capillarypermeability↑fluidtransudefromcapillariesintotissuesCO↓（1）vasodilatation

②Localaccumulationofmetabolicproducts（2）Stagnationofblood

①WBCadhesioninvenuleHypoxia,acidosis，infection.WBCadhesioninvenulePostresistanceofcapillaries↑stagnationofbloodfluidtransudefromcapillariesintotissuesHemoconcentration

andviscosity↑RBCandplateletaggregationbloodflowslowdown（2）Stagnationofblood

②Hemoconcentrationstagnationofblood3.ConsequenceofMCStasis

(1)venousreturn

↓(2)“Autobloodtransfusionandfluidinfusion”disappear(3)bloodflowofthebrainandheart↓VenousreturnCOAutobloodtransfusiondisappearCap.bloodpressureCap.permeabilityPlasmamoveoutAutofluidinfusiondisappear

Bp

acidosis

Cap.open↑

BloodflowstasisinCap.Tissueperfusion，hypoxiaviciouscycle4.ClinicalmanifestationsThemajormanifestationinthisstageisprogressinglowBpBrainischemiadullorcomacoolorcyanosisbloodflow↓andbloodstasisinthekidneyoliguriaoranuriaStasisinskin

Refractorystage–MicrocirculatoryfailurestageⅢThereisnolongeranyresponsetovasopressordrugsandCOremainsdepressedevenifthebloodvolumeisreturnedtonormal.Therefore,thisconditionisknownasrefractorystageormicrocirculatoryfailurestage.

Refractorystage–MicrocirculatoryfailurestageⅢ1.AlterationsofMCandtissueperfusion2.MechanismofMCdisturbance3.Clinicalmanifestations1.AlterationsofMCandtissueperfusion

①Paralyticdilationofsmallvessels

②AmassivemicrothrombusformationinMC

③“noperfusion,noflow”2.MechanismofMCdisturbanceSeriousacidosisandhypoxiaNoresponsetovasopressordrugs

ParalyticdilatationofvesselsFailureofMCDamageofVECTriggercoagulationFormationthrombusDICDIC(disseminatedintravascularcoagulation)3.Clinicalmanifestations(1)CirculatoryfailureProgressinglowBP,decreasingCVP,rapidandthreadypulse.(2)no-reflowphenomenoninCap.Noreflowphenomenon

is

BPreturnbutbloodperfusionofMCdon’trecoverafterbloodtransfusionandfluidinfusion.Seechapter18(3)Disseminatedintravascularcoagulation(DIC)(4)Multipleorgandysfunctionsyndrome(MODS)Severeischemia,hypoxia,acidosis,humoralfactors,activeoxygenmakeimportantvitalorgans“irreversible”injury,leadingtoMODS3.Clinicalmanifestations（1）alterationofhemorheology（2）coagulationsystemactivated（3）imbalanceTXA2-PGI2MechanismofshockleadtoDICMechanismofshockleadtoDIC

bloodconcentrationandviscosity↑shiftoffluid

BloodflowslowdownRBCandplateletaggregation

DICsevereacidosis

destroyVEC

traumaticshock

ReleasingTFInitiatingextrinsicCoagulationExcessdestructionofRBCImbalanceofTXA2-PGI2PGI2↓,TXA2↑ReleaseofADPplateletreleasereactionExposingcollagenandinitiatingintrinsiccoagulationMicrothrombusblockedMC

bloodreturntoheart↓↓

fibrindegradationproduct(FDP)↑

vascularpermeability↑

ECBV↓thecomplementsystemisactivatedExtensivebleedingMyocardialcontractility↓histamineand5-HT↑shockDICcanpromotedevelopmentofshockIschemichypoxiastageStagnanthypoxiastage(b)RefractorystageTheConstrictedvesselsbegintodilate.Bloodflowthroughnotonlyarteriovenousshunt,butalsotruecapillaryinflowofbloodismorethanoutflowfromcapillarybloodflowisslowdownfluidshiftfromvascularcompartmenttotheinterstitialspacebloodstasisandtissuehypoxiaArterioleandprecapillarysphincterconstrictionArteriovenousshuntopeningTissueperfusionreducedPre-capillaryresistance>PostcapillaryresistanceinflowofbloodislessthanoutflowfromcapillaryBloodflowisslowdownⅠⅡⅢParalyticdilatationofsmallvesselsAmassivemicrothrombusformationinMC“noperfusion,noflow”PathogenesisofshockMicrocirculatorymechanismCellularandmolecularmechanismsCellularandmolecular

mechanismsSeveralfactshavebeenfoundthatprimarycausesofshockmayalsodamagecellsdirectly,whilethedamagedcellsmayinduceMCdisorderororgandysfunction.a)OutwardofK+b)InwardofNa+c)InwardofCa2+

(3)Thealterationsof

lysosome(2)Thealterationsof

mitochondria(1)ThealterationsofcellmembraneCellularandmolecular

mechanisms(1)Thealterationsofcellmembrane

Cellinjuryandapoptosis(2)Thealterationsofmitochondrion(3)Thealterationsoflysosome(1)Thealterationsofcellmembrane

hypoxia,acidosis,hyperkalemia,lysozymeoxygenfreeradicalsandhumoralfactorsInjurycellmembranelackofATPhypoxiaDysfunctionofsodium-potassiumpumpaccumulationofsodiumandwatercelledema(2)Thealterationsofmitochondrion(3)Thealterationsoflysosomecelledema

mitochondrionswellinghypoxia,ischemiaandacidosisintracellulardeteriorationreleasinglysozymeSection3AlterationofmetabolismandfunctioncauseschangesResultsATP↓→dysfunctionofNa+-K+-ATPpumpRetentionofNa+↑,H2OCelledemaExtracellularK+↑Hyperkalemiaanaerobicglycolysis↑

lacticacid↑Metabolicacidosisventilation↑inearlystagePaCO2↓RespiratoryalkalosisVentilationandgasdiffusion↓PaCO2

↑Respiratoryacidosis1.water,electrolytesandacid-basedisturbance1.Alterationsofmetabolisminshock(1)Glycolysis↑Temporalhyperglycemiaorglucosuria(2)Catabolismoffat↑Freefattyacidandketonebodies↑(3)Catabolismofprotein↑Urinarynitrogen↑andnegativenitrogenbalance2.Organdysfunctioninshock(1)Acuterespiratoryfailure--------shocklungInlaterstageofsevereshock,thelungofshockpatientsrepresentsaseriesofseriouspathologicalprocesssuchasincreasedtheweightoflung,congestion,edema,thrombosis,pulmonaryhemorrhageetc.Theincidenceisabout83~100%2.Organdysfunctioninshock(2)Acuterenalfailure--------shockkidneyItreferstoARFtobeproducedduringshock,calledshockkidney.ItincludesfunctionalrenalfailureandparenchymalrenalfailureManifestaions:oliguria,azotemia,hyperkalemiaandmetabolicacidosis2.Organdysfunctioninshock(3)DisturbanceofcardiacfunctionHypotensionandcoronaryarterialbloodflow↓.Acidosisandhyperkalemia.DICincoronaryartery.Effectofbacterialtoxinandendotoxinespecially.2.Organdysfunctioninshock(4)Multipleorgandysfunctionsyndrome(MODS)Dysfunctionofmorethantwoorgansoccursuccessivelyinpatientswithoutpre-exitorgandysfunctionisdefinedasMODSNumberoffailureorganmortality115%～30%245%～55%3＞80%4SeldomsurvivalSection4Featuresofseveralcommontypesofshock1.HypovolemicshockConcept:

acutelossof15~20%ofcirculatingbloodvolumeMaincause:

Externallossofwholebloodplasma,orextracellularfluid,internalhemorrhageMaincomplications:

shockkidney,endotoxemia2.SepticshockMaincause:Immunesystemdeficiency,invasionofbacteriaHighmortalityrate(40~50%)Mechanisms:Releaseofcytokines;Activationofneutrophils,monocytes,neuroendocrinereflexesandplasmaproteincascadesystemsActivationofintrinsicandextrinsicpathwaysofcoagulation(Chapter8)3.Anaphylactic

shock

Itresultsfromasystemichighallergicreactioninwhichthecardiacoutputandbloodpressureoftendecreasedrasticallyduetoextensivevasodilation.E.g.allergicreactiontopenicillinEtiologicfactorsAntigen-antibodyreactionHistamineVenousdilationVenousreturn↓↓arterioledilationBP↓↓Cap.permeability↑Lossoffluid4.NeurogenicshockDefinition:Itisavasogenicshockcausedbydecreasedsympatheticcontrolofbloodvesseltoneduetoadefectinthevasomotorcenteroradecreaseinsympatheticoutflowtothebloodvessel,resultinginvasodilatation,increasedvolumeofvascularlumenandpoolingofbloodintheveins.Commoncauses:Brainorspinalcordinjury,deepgeneralanesthesia,drugintoxication,hypoxia,etc..4.CardiogenicshockDefinition:Itoccurswhentheheartfunctionisacutelyimpairedtosuchaseveredegreethatthecardiacoutputisinadequatetomeetthedemandsofeffectivetissueperfusionandcellularmetabolism..Commoncauses:Extensiveinfarctionoftheleftventricle,primarymyocardialdisease,severearrhythmia,valvulardysfunction.Section6Pathophysiologicbasisofpreventionandtreatment

ImprovemicrocirculationBlockageofhumoralfactorsCellprotectionOrganprotectionPathophysiologicbasisofpreventionandtreatment

ImprovemicrocirculationVolumereplacementRestoringbloodvolumeisanessentialmeasureofenhancingCOandimprovingperfusionoftissuebecausethereareabsoluteorrelativelackofECBVinvarioustypesofshock(transfusionofwholeblood,plasmaorelectrolytesolution)Monitoringindex:BP,urinevolume,pulsepressureandCVPVasoactivedrugsapplicationDrugsofvasodilatation:atropine,anisodamine,isoprenalineThepreconditionofapplication:sufficientfluidreplacementDrugsofvasoconstriction:noradrenaline,dopamineThepreconditionof

application:anaphylacticandneurogenicshock;BP<50mmHgImprovemicrocirculationBecauseofmyocardialinhibition,decreaseofvascularresponsibilityandDICformation,acidosiscorrectionwithalkalinesolutionsisabasictreatmentforimprovingmicrocirculation.AcidosiscorrectionTreatmentofDICImprovemicrocirculationCasepresentation

Ayoungmanisbroughttotheemergencydepartmentbyambulanceonthenextdayafteraseveretrafficaccident．Heisunconscious．Hisbloodpressureis78/48mmHg，heartrate130beatsperminute．Thereisnoevidenceofheadtrauma．Thepupilsare2mmandreactive．Hewithdrawstopain．Cardiacexaminationrevealsnomurmurs，gallops，orrubs．Thelungsarecleartoauscultation．Theabdomenistense,withdecreasedbowelsounds．Thepatientshowscyanosis，withthreadypulses．Questions：1.Whatarethethreemajorpathophysiologiccausesofshock?Whichwaslikelyinthispatient?Why?2.Whatarethethreegeneralstagesofshockaccordingtothedifferentchangesinmicrocirculation?Whichwaslikelyinthispatient?Why?3.Whatpathogeneticmechanismaccountsforthispatient’sunresponsivenessandcyanosis?4.Whattherapeuticmeasuresareessentialforthispatient?Whichofthefollowingpathophysiologicalchangeinischemichypoxiastageofshockiswrong?()

A.ContractionofvenularsmoothmuscleB.ConstrictionofarteriolesmoothmuscleC.ClosureofagreatnumberofcapillariesD.IncreaseofcapillaryhydrostaticpressureE.DecreaseofbloodflowperfusionincapillariesD2.Themaincauseoftherefractorystageofshockis()A.Acid-basedisturbancesB.FailureofvasoconstrictionresponseorDICC.CardiacdysfunctionD.SeriousrenaldysfunctionE.LungedemaB3.Whichoneofthefollowingmanifestationsdoesnotoccurinthestagnanthypoxiastageofshock?()A.DullnessB.DecreaseinbloodpressureC.AnincreaseinpulsepressureD.CyanosisE.AnuriaC4.Whichofthefollowingdoesnotbelongtothecauseofhypovolemicshock()A.BloodlossB.BurnC.AnaphylaxisD.CrushtraumaE.DehydrationC5.Whichofthefollowingmanifestationsmaybedonotoccurintheearlystageofhemorrhageshock?()A.AprogressivedecreaseinbloodpressureB.ThreadypulseC.IrritableandrestlessD.PalenessE.OliguriaA6.Thecharacteristicchangeofmicrocirculatoryperfusioninischemichypoxiastageis()A.Lowinflowandhighoutflowandinflowislowerthan«outflowB.Bothinflowandoutflowarelowandinflow<outflowC.Highinflowandlowoutflowandinflowismorethan»outflowD.Bothinflowandoutflowarehighandinflow<outflowE.Bothinflowandoutflowarelowandinflow>outflowB7.Themostcommontypeofacid-basedisturbanceoccurringinshockis()A.MetabolicalkalosisB.RespiratoryacidosisC.NormalAGmetabolicacidosisD.HighAGmetabolicacidosisE.MixedacidosisD8.Hypovolemicshockbeginstodevelopwhenintravascularbloodvolumelosesbyabout()A.30%B.20%C.35%D.10%E.50%9.Inischemichypoxiastage,theperfusionofheartandbrainis()A.RemarkablyincreasedB.RemarkablydecreasedC.KeptinnormalityorincreasedD.ThatthebrainperfusionisincreasedandtheheartperfusionhasnoremarkablealterationE.AtfirstdecreasedandthenincreasedBC10.Dysfunctionofsodium-potassiumpumpinshockisdueto()A.Augmentedactivityofphosphorylase.B.AugmentedactivityofhexokinaseC.Obviousincreaseofanaerobicglycolysis,andincreaseoflacticacidD.Inefficientaerobicoxidation,significantdecreaseinproductionofATPE.ObviousincreaseofglycogenolysisD11.Whichoneofthefollowingcompensatoryresponsesinischemichypoxiastageofshockis-wrong?()A.VenuleandsmallveinintenseconstrictionB.Auto-bloodtransfusionC.IncreaseoflocalvasodilatingsubstanceD.BloodredistributionE.AutofluidtransfusionC12.Theprincipleofvolumereplacementintreatmentforshockis()A.Thatitisunnecessarytogivevolumereplacementifbloodpressure(Bp)isnormalB.ThatthevolumegivenisequaltothevolumeneededC.Thatthevolumegivenisthevolumelost.D.Thatthelessvolumeis,thebetterthecurativeeffectisE.Thatthemorevolumeis,thebetterthecurativeeffectisB13.Themostimportantprincipleoftreatingtheshockis()A.ToimprovethemicrocirculationB.TokeepcellmembranesandorganelleinstabilityC.Tob