临床科室急救、备用药品及高危药品检查记录

1Chapter12.Shock2ThetermwasoriginatedfromGreece,itsinitialmeaningwas:About200yearsago,itwasusedfirsttimebyaFrancedoctortodescribeShockApathologicprocessCausedbytraumaAviolentcollisionoraheavyblow；Theeffectofsuchacollisionorblow2Introduction3AcutecirculatoryfailureIntroduction3Microcirculationdisturbanceandtheeffectsofpro-inflammatorymediatorsandanti-inflammatorymediatorsShockReductionofECBVInadequateperfusionofvitalorgansCellularmetabolismdisturbanceDysfunctionoforgansThepathogeniciscomplex,involving:Shockisageneralpathologicprocess,charactrizedby:Including:4ShocksyndromeClassicclinicalpresentationofshock:5IntroductionShockperipheralvasoconstrictionseverelydiminishedCOinadequatebloodflowtothebrainandkidneysrespiratorycompensationformetabolicacidosispaleandcoldclammyskinhyperventilationoliguriadulledsensoriumrangingfromagitationtostupororcomatachycardiawithathreadypulsehypotensionwithanarrowedpulsepressure5Section1.EtiologyandClassificationofShock6Hypovolemicshock6Section1.1.EtiologyandClassificationofshock(1)Accordingtocauses1)LossofbloodorfluidBloodlossHemorrhagicshockFluidlossDehydrationshock2)BurnBurnshock3)TraumaTraumicshock4)InfectionInfectious(endotoxic,septic)shock5)AnaphylaxisAnaphylacticshock6)AcuteheartfailureCardiogenicshock7)StrongstimulationonnervesystemNeurogenicshock7(2)AccordingtotheinitialchangesofshockdevelopmentSufficientbloodvolumeheartpumpNormalfunctionVascularbedvolumeNormalvasoconstrictionandvasodilation3majordeterminantsofeffectiveperfusion:Perfectperfusion2Section1.8ConditionsnecessaryforeffectiveperfusionShocktypeInitialchanges×3213Section1.3typesofshockaccordingtodifferentinitialchangesSufficientbloodDecreasedHypovolemicvolumeshockAdequatecapacityIncreasedVasogenicofvascularbedshockNormalfunctionDisturbedCardiogenicofheartpumpshock9Section2.StagesandPathogenesisofShock10MicrocirculationTheory3Section2.012345678910BPPRCABFPresentedbyLilleheiin1964.Shockisasyndromemainlyofmicrocirculationimpairment.Thesympathetic-adrenalsystemisconsecutiveexcitedalltimeduringshockdevelopment,leadingtodecreasedtissueperfusionbyvasoconstriction.11microcirculationimpairmentcausedbyintensiveexcitationofsympathetic-adrenalsystembloodflowratherthanbloodpressureintensiveexcitationratherthanfailureornumbnessofsympathetic-adrenalsystem3ShockThecommonpathogeniclinkisThepathogenickeypointisThemechanismisSection2.“MicrocirculationTheory”of12VasoconstrictionVasoconstrictionVasodilationVasodilationEffectofneuro-humoralfactorsonSMCofmicrovasculatureCatecholamines,AT-IIVasopressin,TXA2,ETHistamine,Kinins,LacticacidAdenosine,PGI,TNF,NONeuropeptides(Endorphin)5Section2.51Microcirculation:Thecirculationbetweenmicroarteryandmicrovein.Thebasicstructuralandfunctionalunitofmaterialmetabolismandexchangebetweenbloodandtissue.Itisregulatedbyneural-humoralfactors.13Section2.Localfeedbackregulationofcapillaryperfusion：ConstrictionofPre-capillaryDecreasedbloodLocalaccumulationofsphincterandPost-arterioleflowofproductsandhistaminetruecapillarynetIncreasedresponseDecreasedresponseofSMCtoofSMCtoVasoconstrictiveagentsVasoconstrictiveagentsIncreasedbloodClearanceofhistamineandflowofRelaxationofpre-capillarymetabolicproductstruecapillarynetsphincterandpost-arterioleConstrictionRelaxation14shockcanbedividedinto3stages:1.Ischemicanoxiaphaseofshock(compensatorystageofshock)2.Stagnantanoxiaphaseofshock(reversibledecompensatorystage)3.RefractoryshockstageAccordingtothechangesinmicrocirculationandtakehemorrhagicshockasanexampleStagesofShock1.Ischemicanoxiaphaseofshock(compensatorystageofshock)2.Stagnantanoxiaphaseofshock(reversibledecompensatorystage)3.Refractoryshockstage1Section2.StageI115(1)Microcirculationandtissueperfusionpre-capillarysphincterpre-capillarysphincterarteriovenousshuntture-capillaryture-capillaryarteriolevenuleischemicanoxiaNormalarteriovenousshuntPersistentperipheralvasoconstriction→Pre-capillaryresistance↑,Openingofarteriovenousshunt→inflowoutflow→Tissueperfusion↓5StageISection2.16(2)Mechanismofmicrocirculationimpairment5Section2.StageIHypovolemicshock↘excitationofCardiogenicshock→B.P.↓sympatheticBurnTraumaticshock→pain-adrenalvasoconstrictionSepticshock→endotoxinarteriovenous→releaseofcatecholamineshuntopenOthersAII,Vasopressin,TXA2,ET,MDF,leukotriene17①Venousconstriction→storedbloodreturntocirculation(selfbloodtransfusion)(60~70%)Maintain②Capillarypressure→fluidtransferfrominterstitialarterialspacetocirculation(selffluidinfusion)(1500ml)pressureCatecholamines,AII→cardiaccontractilityperipheralvascularresistance③Redistributionofblood→Decreasebloodflowtotheskin,skeletalmuscle,kidneysandabdominalorgansmaintainbloodsupplyingtoheartandbrain①②③(3)Compensatoryeffects→2Section2.StageI18(4)Clinicalmanifestationsheartratethreadypulseandcardiaccontractilitynarrowingofpulsepressuresympatho-adrenalvasoconstrictionandischemiaurinemedullaofabdominalorgansanustemperatureexcitationischemiaofskinpaleface,coollimbscatecho-laminessweatglandsecretionsweating,clamminessexcitationofagitate,restlessseniorregionofCNS(awa