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SHOCK Pathophysiology Introduction whatisshock Comatose SectionIOverview Introduction DropinBP SectionIOverview Caseanalysis Chiefcomplaint Male 45yearsofage severelacerationoftheleftleginacaraccident PhysicalExamination Appearspaleandindifferentbutwithclearconsciousness Multiplesofttissuecontusion Leftinguinalbrieflycovered butwithlargeamountofexudation BP105 85mmHg HR96 min Sonogramindicatesruptureofthespleenwithanestimated600mlofbloodaccumulationintheabdomen SectionIOverview Caseanalysis Treatment Alacerationwoundof7cmintheleftinguinal Partialseparationofthefemoralarteryandveinwitharupturedspleen Vascularprosthesisandsplenectomywereconducted 400mlofbloodtransfusionduringoperation 5 GlucosesolutionI V aftersurgery 2hpost surgeryBP80 50mmHg EpinephrineanddopaminearegivenI V butBPremainslow 85 60mmHg Clammyskinandanuria BPdropsto70 40mmHgthenextmorning I V epinephrinewithnoeffect PatientgoesintocomawithB P at7 30 Weakrespirationandheartbeat Pronounceddeadat7 50 SectionIOverview Questions 1 ThispatienthasanormalBPuponadmission WhydoeshisBPdropdramaticallyafterthesurgerytorepairinjuredvessels 2 WhydothevasoconstrictorsfailtorestoreBP 3 Howwouldyoumodifythetreatmentstrategyforthispatient SectionIOverview ThetermwasoriginatedfromGreek Itsinitialmeaningwas Inthe1730s thistermwasre coinedbyaFrenchdoctortodescribe Shock Apathologicalprocesscausedbytrauma Aviolentcollisionoraheavyblowtothehead SectionIOverview Understandingshock aprogressivehistory Fromtheuseofvasoconstrictor restorationofBP totheuseofvasodilator Understandingshock aprogressivehistory microcirculation Acutecirculatoryfailure 3 Microcirculationdisturbancetheeffectsofpro inflammatorymediatorsandanti inflammatorymediators Shock ReductionofECBVInadequateperfusionofvitalorgansCellularmetabolismdisturbanceDysfunctionoforgans Thepathogenesisofshockiscomplex involving Shockisageneralpathologicprocess characterizedby Including SectionIOverview Shocksyndrome Classicclinicalpresentationofshock Shock peripheralvasoconstriction severelydiminishedCOinadequatebloodflowtothebrainandkidneys respiratorycompensationformetabolicacidosis paleandcoldclammyskin hyperventilation oliguria dulledsensoriumrangingfromagitationtostupororcoma tachycardiawithathreadypulse hypotensionwithanarrowedpulsepressure SectionIOverview SectionII EtiologyandClassificationofShock Hypovolemicshock SectionII 1 Basedoncauses 1 LossofbloodorfluidBloodloss HemorrhagicshockFluidloss DehydrationshockBurn Burnshock2 Trauma Traumicshock3 Infection Infectious endotoxic septic shock4 Anaphylaxis Anaphylacticshock5 Acuteheartfailure Cardiogenicshock6 Strongstimulationonnervesystem Neurogenicshock Perfectperfusion 2 Basedonpathogenesis Sufficient bloodvolume heartpumpfunction Normalfunction Vascularbedvolume 3majordeterminantsofeffectiveperfusion SectionII Normalvasoconstrictionandvasodilation Anyoneofthesedeterminantsmayinfluencetheefficiencyofperfusion Effectivecirculatorybloodvolume Referredtoasthevolumeofbloodcirculatingthroughthecardiovascularsystemperunittime excludingbloodstoredinliver spleen andlymphaticsinusoid orretainedincapillarynetwork Determiningfactors sufficientoverallbloodvolume sufficientcardiacoutput normalperipheralvasoactivity SectionII hypovolemicshock LossofbloodLossoffluidburn ECBV InsufficientvenousreturnCardiacoutput BP NegativefeedbackofpressuresensorSNexcitationConstrictionofperipheralvesselsTissueperfusion Dilationofvisceralmicrovesselsduetoinflammationorallergy whichresultsinbloodstasisanddecreaseofECBV vasogenicshock Myocardiogenic myocardialinfarct septalheartdisease cardiogenicshock Non myocardiogenic AcuteCardiacTamponade pneumothorax PAH Lossofbloodandfluid burn trauma infection allergy StrongstimulationofSNnerve e g pain hypovolemic vasogenic cardiogenic Majorcardiovascularpathologies MajorDeterminantsforEffectivePerfusion Normal Sufficient Bloodvolume Shocktype Initialchanges SectionII Threetypesofshock basedondifferentinitiatingfactors Decrease Hypovolemicshock Adequate Vascularbedvolume Increase Vasogenicshock Heartpumpfunction Cardiogenicshock Disturbance Clinicalexamples HemorrhageBurnsortrauma MI CHFArrhythmias AnaphylaxisSepsis Vasogenic maldistributive PathogenesisofShock theMicrocirculatoryDisturbanceTheory SectionIII bloodflowratherthanbloodpressure stimulationratherthansuppressionofsympathetic adrenalsystem SectionIII theimpairmentofmicrocirculationcausedbydysregulatedstimulationofsympathetic adrenalsystem theMicrocirculatoryDisburbanceTheory ThecommonpathogeniclinkisThepathogenickeypointisThemechanismis 22 SectionIII Microcirculation ThecirculationbetweenmicroarteriesandmicroveinsThebasicstructuralandfunctionalunitformetabolismandexchangebetweenbloodandtissue Itisregulatedbyneural humoralfactors Themakeupofmicrocirculation ResistancevesselsRegulatesBPandallocationofblood ResistancevesselsRegulateBPandallocationofblood CapacityvesselsRegulatevenousreturntotheheat arterioles Arteriovenousshunt ExchangevesselsRegulateexchangeamongvessels microcirculatoin venules Capillarybed arteriole metarteriole Pre capillarysphincter Preferentialchannel Vasoconstriction Vasoconstriction Vasodilation Vasodilation Catecholamines AT IIVasopressin TXA2 ETHistamine Kinins LacticacidAdenosine PGI TNF NO Neuropeptides Endorphin SectionIII Localfeedbackloopofcapillaryperfusion Physiologicalregulationofmicrocirculation Effectofneuro humoralfactorsonSMCofmicrovessels SectionIII Constrictionofpre capillaryDecreasedbloodLocalaccumulationsphincterandpost arteriolesflowintotruemetabolicwasteandcapillarynethistamineDecreasedresponseIncreasedresponseofSMCtoofSMCtovasoconstrictiveagentsvasoconstrictiveagentsIncreasedbloodClearanceofhistamineflowintotrueRelaxationofpre capillaryandmetabolicproductscapillarynetsphincterandpost arterioles Constriction Relaxation Localfeedbackloopofcapillaryperfusion Physiologicalregulationofmicrocirculation StagesofShock SectionIII StageI 3stagesbasedonstructuralandfunctionalalterationsofthemicrocirculationasshockprogresses true capillary arteriovenousshunt pre capillarysphincter 1 AlterationsofMicrocirculationandTissuePerfusion arteriole venule ischemicanoxia Normal StageI SectionIII Persistentperipheralvasoconstriction Pre capillaryresistance openingofarteriovenousshunt inflow outflow Tissueperfusion Truecapillary Excitationofsympatheticadrenalsystem ReleaseofcatecholamineAII vasopressinTXA2 ET MDFleukotriene Excitationofsympatheticadrenalsystem 2 Mechanismsofmicrocirculationdisturbance VasoconstrictionOpeningofarteriovenousshunt SectionIII StageI Septicshock endotoxin Hypovolemicshock Cardiogenicshock B P BurnTraumaticshock pain Maintainarterialpressure Maintainbloodsupplytoheartandbrain 3 Compensation SectionIII StageI Sympatheticexcitation Venousconstriction storedbloodreturnstocirculation selfbloodtransfusion Capillarypressure fluidtransferfrominterstitialspacetocirculation selffluidinfusion Catecholamines cardiaccontractility Arterioleconstriction peripheralvascularresistance Redistributionofblood Decreasedbloodflowtotheskin skeletalmuscle kidneysandabdominalorgans threadypulseandnarrowingofpulsepressure urine anustemperature paleskin coollimbs agitation restlessness sweating clamminess SectionIII StageI 4 Clinicalmanifestationsheartrate cardiaccontractility sympatho adrenalvasoconstrictionandischemiamedullaofabdominalorgansexcitationischemiaofskincatecho lamine sweatglandsecretion excitationofseniorregionofCNS StagesofShock SectionIII StageII SectionIII StageII 1 AlterationofMicrocirculationandtissueperfusion Althoughstimulationofthesympathetic adrenalmedullaaxismayexertcompensatoryeffectsduringtheischemicanoxiastage prolongedexcitationwillrenderthecompensationmaladapativeandevendetrimental Atthisstage Theresponsivenessofmicrovasculaturetocatecholamine ThebloodflownotonlytravelsthrougharteriovenousshuntbutalsoenterstruecapillarybloodflowslowesdownRBCaggregation WBCrollingandobstructionofvesselsplateletaggregationandadhesioninflow outflowbloodstasisorsludgestagnantanoxia SectionIII StageII SectionIII StageII 2 mechanismsunderlyingmicrocirculatoryalterations Acidosisischemia hypoxialeadstotheaccumulationofCO2andlacticacids TheensuingacidosisdesensitizestheSMCstocatecholamines Localaccumulationofvasodilators SMCRelaxationandcapillarydilation ischemiahypoxiaacidosis Mastcell histamine Celldestruction K ATPhydrolysis adenosine 6aggregationofplatelets7aggregationofRBC8adhesionofleukocytestovenules9blockageofcapillarybyleukocytes microthrombosis Increaseofmicrocirculatoryresistance alterationsinhemorheology SectionIII StageII 2 mechanismsunderlyingmicrocirculatoryalterations 1 Prolongedtissueischemiaandhypoxia acidosis decreasedresponseofSMCtocatecholamine2 Localaccumulationofmetabolicproductshistamine adenosine K Kinin3 AlterationofhemorheologyRBCandplateletaggregation Plasmaexudation bloodviscosity 4 Enteralendotoxinentersintoblood activatingmacrophage TNF NO5 Effectsofhumoralfactorshistamine endorphin IL 1 TXA2 LTB4 VasodilationBloodstasis SectionIII StageII 1 2 3 4 5 2 mechanismsunderlyingmicrocirculatoryalterations Selfbloodtransfusion selffluidtransfusion ceasetofunction Waterintheinterstitialspaceexistsinacolloidalform StasisofcapillarybloodHydrostaticpressure IncreasedcapillarypermeabilityBloodexudationandconcentration 3 Consequencesfollowingmicrocirculationdecompensation SectionIII StageII selfbloodtransfusion ceases Acidicmetabolitesduringshockenhancetheaffinityofinterstitialcolloidforwater Dilationofcapacityvessels selfbloodtransfusion ceases Increaseofvascularbedcapacityanddecreaseofvenousreturn Selfbloodtransfusion selffluidtransfusion ceasetofunction 3 Consequencesfollowingmicrocirculationdecompensation SectionIII StageII formationofaviciouscycle Capillaryhydrostaticpressure Capillarypermeability Bloodexudationandconcentration AggregationofRBCandmicrocirculatorydisruption Openingofmicrovessels Bloodstasisandvenousreturn DecreaseofCOandBPleadstoexcitationofSN Furtherdecreaseintissueperfusion Ischemia hypoxia acidosis 3 Consequencesfollowingmicrocirculationdecompensation SectionIII StageII BloodstasisinthekidneyRenalbloodflow Venousreturn Cardiacoutput B P brainischemiaBloodstasisintheskin BloodstasisinMicrocirculation Oliguria 400ml d orAnuria 100ml d DullorComa Cyanosis Clamminess Maculation SectionIII StageII 4 Clinicalmanifestations StagesofShock 1 SectionIII StageIII pivotalpathologicalprocesses DeficiencyofO2andNutrition Death graduallyprogresses MODS DIC OnsetofShock Recovery BF bloodflow SectionIII StageIII SectionIII StageIII DICformation ThecardiacoutputremainsdepressedevenifthebloodvolumereturnstoNormal ThisstageisalsocalledmicrocirculatoryfailurestageasSMCsceasetorespondtoVasoactivereagents SectionIII StageIII 5 Heterotypicbloodtransfusion hemolysis DIC pronefactors 4 Traumaticshock tissuefactorrelease initiatingtheextrinsicclottingpathway 3 SepticShock bacteriaandtoxin mono macrophagesecretingcytokines monocyteandendotheliumreleasingtissuefactor 2 Severeacidosis injuryofvascularECs 1 bloodconcentrated fibrinogen RBCandplateletaggregation bloodviscosity bloodflowslowdown ThemechanismsofDICinthisstage 1 PathogenesisofDIC Section3 StageIII TheconsequencesofDIC 1 Themicrocirculationpathwaycompletelyblockedbymicrothrombosis bloodreturntoheartreducedsharply2 Fibrindegradationproduct FDP andcomplement vascularpermeability aggravatingmicrocirculationimpairment3 Extensivebleeding ECBVfurtherdecreased4 Embolismandinfarctionoforgans aggravatingacuteorganfailure Importantvitalorgansirreversiblyinjured Prolongedandsevereischemiaandhypoxicacidosis Varioushumoralfactors lysosomalenzymes activeoxygenspecies andcytokines MODS SectionIII StageIII 2 Multipleorgandysfunctionsyndrome MODS SectionIV PathogenesisofShock Neural HumoralandTissue CellularMechanisms Neuro humoraltheory Cellulartheory Microcirculationtheory ExcitationoftheSN AMaxisandinsufficientmicrocirculatoryperfusionleadtocellinjuryandtissuedysfunction Excessivepro andanti inflammatorymediatorsresultinmicrocirculatorydisorderandcauseinjuriestocellsandtissues shock causativefactorsact directlyorindirectly ontissuesandcells Asaconsequence structural metabolic andfunctionalalterationsensue Progressinunderstandingshock ThemicrocirculationimpairmentcausedbyintensiveexcitationofsympatheticnervesystemisthecommonpathogenicbasisofshockHowever hypovolemiaandotherpathologicconditionscauseamarkedincreaseinthecirculatinglevelsofhumoralfactors Thesefactorsmayalsobeinvolvedinpathogenesisofshockatvariousdegreesindifferentstages 1 Neural HumoralMechanisms NeuralMechanism HumoralMechanism 1 Neural humoralmechanism Manyhumoralfactorsaregeneratedwhenconfrontedbyinfectiousandnon infectiousfactors Sympathetic Adrenomedullaryaxis RAAaxis Hypothalamus pituitarygland adrenocortexaxis 1 Vasoactiveamines 2 Regulatorypeptides SectionIV 2 Histamineand5 hydroxytryptamine 5 HT 1 Endothelin ET 2 AngiotensinII AngII 3 Vasopressin4 Atrialnatriureticpeptide ANP Threetypesoffactorsmaybeinvolved 5 Vasoactiveintestinalpeptide VIP 6 Calcitoningene relatedpeptide CGRP 7 Kinin8 Endogenousopioidpeptide 1 Catecholamines CAs Systemicinflammatoryresponsesyndrome SIRS Compensatoryanti inflammatoryresponsesyndrome CARS Mixedantagonistresponsesyndrome MARS Threetypesoffactorsmaybeinvolved Extensiveactivationofinflammatorycells 3 Inflammatorymediators VECdamage PermeableedemaImpairedoxygenutilization Numerousinflammatorymediators MODSandrefractoryshockstage SectionIV Categorizationofhumoralfactors 1 Vasoactiveamines catecholamines a receptor b receptor vasoconstriction Openingofthearterial venousshunt catecholamines Including dopamine epinephrine norepinephrine histamine Antigenpresentation histamine 1 Vasoactiveamines leukotrienes PAF PGD2 CapillarydilationIncreasedpermeabilityIncreasedsecretionofglandsSMCcontraction IgEproduction Mastcellsensitization Mastcellactivation Releaseofinflammatorymediators serotonin 5 HT Majorsources mastcells SMCfunction constrictionofsmallveins increasesvesselpermeability exacerbateDIC 5 HTtransporter 1 Vasoactiveamines 2 Regulatorypeptides Apowerfulvasoconstrictorandpositiveregulatorofmyocardium endothelin ET Compensatoryeffects Cardio toxiceffects Angiotensin Ang RAAS 2 Regulatorypeptides Vasopressin ReleasedwhenthereisadecreaseinECBVoranincreaseinplasmacrystalloidosmoticpressure Increaseswaterre absorption Alsoactsasavasoconstrictor 2 Regulatorypeptides brain hypothalamus Pituitarygland atrialnatriureticpeptide ANP Asodium excretingdiuretic Increasesduringshock ExertsmostlyregionaleffectsandhascrosstalkswithRAASandADH 2 Regulatorypeptides Vasoactiveintestinalpeptide VIP Calcitoningenerelatedpeptide CGRP VIPalleviatesintestinalischemiaduringtheearlystagesofshock Duringlatephases VIPcontributestodecreasedBP Apowerfulvasodilator Regulatesintestinalbloodflow 2 Regulatorypeptides Kinin Endogenousopioidpeptide Animportantinflammatorymediatorandvasodilator Increasesvascularpermeability Decreasesbloodpressure cardiacoutput andheartrate 7 8 2 Regulatorypeptides 3 Inflammatorymediators Itwasbelievedthatinflammatoryresponseduringshockwascausedbybacterialinfection Shock aninflammation induceddisease Itisnowclearthatnotallshockpatientshavebacterialinfection Instead thecommonlinkisanincreaseofinflammatorymediatorsintheplasma sepsis septicemia septicshock InflammatoryCells MacrophagesMf neutrophil acidophil platelet VEC Inflammatorycellsareactivatedduringvariousstagesofshockandsecreteahostofpro inflammatorycytokines whichincludeTNFa IL 1 IL 2 IL 6 IL 8 IFN LT andPAF Inflammatorycellscanalsorelease asacompensatoryresponse acohortofanti inflammatorymediators whichincludeIL 4 IL 10 IL l3 PGE2 PGI2aswellassolublereceptorsforpro inflammatorycytokines forinstancesTNFR Inflammatorymediators Examiningthemechanismofshockfromacellularperspective Alterationofcellmembraneelectricpotentialisamongthefirstseriesofchangesinducedbyshock Medicationsthatpromotenormalcellularmetabolismarebeneficialintreatingshock Restorationofcellularfunctionhelpsamelioratesmicrocirculatorydysfunction Restorationofmicrocirculationtotissuesdoesnotnecessarilycorrelatewithnormalizedfunction shockcellconstitutesthebasisoftissuedysfunction Thealterationsofcellsandmoleculesinshockcouldbesecondarytotheimpairmentofmicrocirculationand orasadirectconsequenceofshock PrimaryCauseofShock MicrocirculationImpairment OrganDysfunction alterationsofcellsandmolecules 2 Tissue Cellularmechanisms SectionIV Theseprimaryorsecondaryalterationsinturnmayinduceorexacerbatemicrocirculatorydisorderandorgandysfunction Activationofinflammatorycellscytokines inflammatorymediatorsandoxygenfreeradicalsvascularendothelium PMNs macrophages lymphocytesandparenchymalcellsofvariousorgansdenaturation apoptosisornecrosis Cell Tissue Organdysfunction secreteorrelease attack 1 CellInjuryandApoptosis VariousInjuriousSignals SectionIV biomembranes mitochondria lysosome 2 ImpairmentofCellularMetabolism Na H2Oinflux swelling Anaerobicmetabolism Localacidosis ProductionofATP Energydeficiency Sodiumpumpdysfunction VasodilationHypotension Microvascularhypoperfusion OxygendeficiencyMitochondriadysfunctionUncouplingofoxidativephosphorylation VariousInjuriousSignals Cell Tissue Organdysfunction SectionIV FunctionalAlterationsofOrgans SectionV OrganInjuries lung kidney liver gastrointestinaltract heartandbrain SectionV Dysfunctionoccurssimultaneouslyinmorethan2organsinpatientswithnopre existingorgandysfunction MODSisthemostfrequentcauseofdeathinshockpatients MODS Prolongedandsevereischemiahypoxia andacidosisuncontrolledinflammatoryresponse Rapidsingle phasedMODS Induceddirectlybytheinjuriousfactor Injuriesoccursimultaneouslyorsequentially Progressesrapidlywithonephaseandonepeakofinjury Delayedtwo phasedMODS Alagphaseafterthefirsthit Thesecondhitoccursin1 3weeks Progresseswithtwophasesandtwopeaksofinjury CategorizationofMODS DisturbanceofMicrocirculation InappropriateInflammatoryResponse MetabolicAlteration MultipleOrganDysfunction Vasodilation Cellswelling NegativeNitrogenBalance SectionV Functionalrenalfailure parenchymalrenalfailure MODS persistentsho

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