外科急诊创伤英文休克及出血

外科急诊创伤英文休克及出血Sections IntroductiontoHemorrhage

&ShockHemorrhageShockHemorrhageAbnormalinternalorexternallossofbloodHomeostasisTendencyofthebodytomaintainasteadyandnormalinternalenvironmentShockINADEQUATETISSUEPERFUSIONTransitionbetweenhomeostasisanddeathIntroductiontoHemorrhage&ShockSHOCK“amomentarypauseintheactofdeath”“Butamorecarefulexaminationsoonservestoshowthatdeepmischiefislurkinginthesystem;thatthemachineryoflifehasbeenrudelyunhinged,andthewholesystemprofoundlyshocked;inaword,thatthenervousfluidhasbeenexhausted”(ASystemofSurgery,1859)1800’sInjurytoonepartofthebodyresultsinoftenfataleffectStrychninetostimulateNS;seizuresElectricalcurrentalcohol“shockwasnotaprocessofdying,ratheramarshalingofthebodilydefensesinastruggletolive”RealizedafallinBPcouldaccountforallsymptomsofshockRepresentsageneralizedfailureofthebodytodeliversufficientamountsofO2toitstissuesS/SrepresentcompensationmeasuresutilizedbythebodytomaintaindeliveryofO2tovitalorgansDelayofappropriatetherapy,cascadeofeventsresultsindamagetoorgansTreatmentGoalsRecognitionofearlyshockAppropriateairwaymanagementRapidtransportationtoappropriatefacilityHemorrhageCirculatorySystemHemorrhageClassificationClottingFactorsAffectingClottingHemorrhageControlStagesofHemorrhageHemorrhageAssessmentHemorrhageManagementCardiovascularSystemDeliveryofnutrientsandO2totissuesandcellsTransportationofwasteproductsproducedbymetabolismtoliverandkidneysDeliveryofCO2tolungsComponentsHeartorpumpBloodvesselsorpipesBloodorfluidCirculatorySystemReviewTerminologyStrokeVolumePreloadVentricularFillingFrank-StarlingMechanismAfterloadCardiacOutputSVxHR=CO5L/minFickPrincipleHeartParasympatheticNervousSystemSlowsrateVagusNerveSympatheticNervousSystemIncreasesrateCardiacPlexusCardiacOutputVolumeofbloodpumpedin1minute=4-6LSVxHRSV=amountofbloodejectedfromleftventriclewitheachcontractionBloodPressureDirectlyproportionaltotheproductoftheCOmultipliedbySVRBP=COxSVRSVR,resistancetoflowinthesystem(systemicvascularresistance)StrokeVolumePreloadRepresentsfillingoftheventricleVolumeofblooddeliveredtoatriapriortoventriculardiastoleDependentonvenousreturnAfterloadAmountofresistanceheartmustovercometoejectbloodContractilityAbilitytocontract,inotropyFrankStarling’sLawInotropyNegativeScartissue,CHFBetaadrenergicblockersCalciumchannelblockersPositiveBetaadrenergicagonists,B1ListsomeBblockers,Cachannelblockers,BagonistsNamesIndicationsContraindicationsWhatwouldyouexpecttoseeifyouadministeredthismedicationWhyFickPrincipleFactorsnecessaryforsystemicO2deliveryAbilityofO2todiffuseacrossalveolarmembraneintobloodstreamAdequatenumberofRBC’stotransportO2AdequatebloodflowtotransportRBC’sAbilityofRBC’stooff-loadO2O2DeliveryNormalcircumstancesbodyextractsabout20%ofO2and80%returnedtoheartforreoxygenationNormalratioofdeliveredtoconsumed5:1Shockmayincreaseextractionto50%Ratiodropsto2:1CellularMetabolismGlycolysisKreb’sCycleElectronTransportGlycolysisOccursincytoplasmGlucoseconvertedtopyruvicacid2ATPcreatedO2presentfurtheraerobicmetabolismNoO2present,hypoperfusion,pyruvicacidconvertedtolacticacidLiverconvertssomelacticacidGeneralizedshockAmountoflacticacidexceedstheliver’sabilitytoconvertitMuscleandskincanfunctioninaerobicconditionsforshortperiodBrainmostsensitivetohypoxiaKreb’sCycleAerobicconditionspyruvicacidentersmitochondriaProduces6CO2moleculesand4ATPElectronTransportOccursinproteinsboundtomitochondrialmembraneAdditional32ATPproducedPrimarysiteofO2utilizationwithincellProduceverylittleATPonanarerobicconditionsCellularMetabolismTwoStepProcessGlycolysisCellutilizingenergysourceReleasesenergyAerobicMetabolism:95%ofcellularEnergyRequiresoxygenandglucoseKreb’scycle(citricacidcycle)Usescarbohydrates,proteinsandfatstoreleaseenergyOtherProcessesAnaerobicMetabolismInadequateoxygenpathwayByproducts:PyruvicAcidLacticAcidCellulardeatheventuallyoccursduetoinadequateperfusionCirculatorySystemVascularSystemArteriesTunicaAdventitiaTunicaMediaTunicaIntimaArterioleCapillary:7%ofbloodvolumeVenuleVeinConstrictionreturns20%(1L)ofbloodtoactivecirculation13%ofbloodvolume64%ofbloodvolumeBloodVesselsSympatheticinnervationVasoconstrictionAlpha1agonistListsomedrugsthathavealpha1agonsist/blockereffectsNamesIndicationsContraindicationsWhatphysiologicalresponsewouldyouexpectWhyHydrostaticandOncoticPressure

TwoopposingforcesthatcontrolnetflowoffluidandnutrientsoutofproximalcapillariesandflowofwasteproductsandfluidintodistalcapillariesHydrostaticpressurePressureoffluid(BP)servestodrivefluidoutofcapillaryintointerstitialspaceOncoticpressureForceexertedbylargeproteinmoleculesinbloodthatdrawsfluidintovascularsystemProximalcapillaryHydrostaticpressureprevailsAllowsintravascularfluidandnutrientstodiffuseoutofcapillaryDistalcapillaryOncoticpressureisdominantDrawsfluidfrominterstitialfluidandwasteofmetabolismintocapillariesBloodComponentsErythrocyte:45%HemoglobinHematocritOtherFormedElements:<1%PlateletsLeukocytesMonocytes,Basophils,Eosinophils,NeutrophilsPlasma:54%FunctionDeliversO2andnutrientstotissuesandtransportswastetokidneysandliverfordetoxificationRidsbodyofinvadingmicroorganismsAcidosisHgbhasadecreasedaffinityforO2inanacidoticstateTherefore,hgbwillreleasemoreO2intoacidotictissueOxyhgbsaturationwillbelowerAlkolosisCausesHgbtohaveahigheraffinityforO2DecreasedamountofO2releasedintoalkalotictissueHemorrhageClassificationCapillarySlow,evenflowArterialSpurtingbloodPulsatingflowBrightredcolorVenousSteady,slowflowDarkredClottingThreeStepProcessVascularPhaseVasoconstrictionReductionlumensize=reductionbloodlossPlateletPhaseTunicaintimadamagedTurbulentbloodflowFrictionaldamagetoplateletsAgglutinationandaggregationCoagulationPhaseReleaseofenzymesExtrinsic=nearbytissueIntrinsic=damagedplateletsFIBRINreleaseNormalcoagulation=7-10minutesClottingOtherFactorsNatureofWoundTransverseVesselsconstrictanddrawinwardReductionoflumenReductionofbloodlossExample:CleanTearLongitudinalConstrictionofsmoothmuscleEnlargeswoundIncreasedbloodlossExample:CrushingTraumaFactorsAffectingClottingMovementofthewoundsiteAggressiveFluidTherapyIncreasesBPandpushesclotsFluiddilutesclottingfactorsLowBodyTemperatureIneffectiveclotformationMedicationsASA,heparin,warfarin(Coumadin)HemorrhageControlExternalHemorrhageDirectPressure&PressureDressingGeneralManagementDirectPressureElevationIcePressurePointsConstrictingBandTourniquetReleasemaysendtoxinstoheartLacticacid,andelectrolytesTourniquetsareONLYusedasalastresort!HemorrhageControlInternalHemorrhageHematomaPocketofbloodbetweenmuscleandfasciaHumerusorTibia/Fibulafracture:500-750mLFemurfracture:1,500mLUNEXPLAINEDSHOCKisBESTattributedtoabdominaltraumaGeneralManagementImmobilization,Stabilization,ElevationEarlyS/SInternalHemorrhagePain,tenderness,swelling,discolorationBleedingfrommouth,nose,rectum,vaginaHematemesisTender,rigid,distendedLateS/SInternalHemorrhageAnxiety,restlessness,combative,AMSWeak,faint,dizzyPale,cool,clammyDilatedpupils,sluggishThirstShallow,tachypnicrespirationsRapid,weakpulseCaprefill>2secDecreasedBPNausea,vomitingHemorrhageControlInternalHemorrhageEpistaxis:NoseBleedCauses:Trauma,HypertensionTreatment:Leanforward,pinchnostrils,rollgauzeunderupperlipHemoptysisEsophagealVaricesMelenaChronicHemorrhageAnemiaStagesofHemorrhage60%ofbodyweightisfluid7%circulatingbloodvolume(CBV):Male5L(10units)6.5%CBVinwomen4.6L(9-10units)15%lossofCBV70kgpt=500-750mLCompensationVasoconstrictionNormalBP,PulsePressure,RespirationsSlightElevationofPulseReleaseofcatecholaminesEpinephrineNorepinephrineAnxiety,slightlypaleandclammyskinStagesofHemorrhage

Stage115-25%lossofCBV750-1250mLEarlyDecompensationUnabletomaintainBPTachycardia&TachypneaStagesofHemorrhage

Stage2(continued)DecreasedpulsestrengthNarrowingpulsepressureSignificantcatecholaminereleaseIncreasePVRCool,clammyskin&thirstIncreasedanxietyandagitationNormalrenaloutputMAP<70hypoperfusionStagesofHemorrhage

Stage2MAPMeanArterialPressureSystolic+2(diastolic) 3Mapshouldbemaintained>7025-35%lossofCBV1250-1750mLLateDecompensation(EarlyIrreversible)CompensatorymechanismsunabletocopewithlossofBloodVolumeStagesofHemorrhage

Stage3(continued)ClassicShockWeak,thready,rapidPULSENarrowingpulsepressure=<MAPTachypneaAnxiety,restlessnessDecreasedLOCandAMSPale,coolandclammyskinStagesofHemorrhage

Stage3>35%CBVLoss>1750mLIrreversiblePulse:BarelypalpableRespiration:Rapid,shallowandineffectiveLOC:Lethargic,confused,unresponsiveGU:CeasesSkin:Cool,clammyandverypaleUnlikelysurvivalStagesofHemorrhage

Stage4StagesofHemorrhage

>35%4

25-35%3

15-25%2

<15%1Resp.VolumeResp.RateBPPulsePressure/StrengthPulseRateVasocon-strictionBloodLossStageAverageBloodVolume=5LPre-existingconditionRateofbloodlossPatientTypesPregnant>50%bloodvolumethannormalFetalcirculationisimpairedwhenmotheriscompensatingAthletesGreaterfluidandcardiaccapacityObeseCBVisbasedonIDEALweight(lessCBV)StagesofHemorrhage

ConcomitantFactors(continued)StagesofHemorrhage

ConcomitantFactorsChildrenCBV8-9%ofbodyweightPoorcompensatorymechanismsTREATAGGRESIVELYElderlyDecreasedCBVMedications:BP,&AnticoagulantsHemorrhageAssessmentSceneSize-upIsitSafeBSIBloodLossLawEnforcementMechanismofInjury/NatureofIllnessNumberofPatientsNeedforAdditionalResourcesHemorrhageAssessmentInitialAssessmentGeneralImpressionObviousBleedingMentalStatusCABCInterventionsManageasyougoO2BleedingControlShockBLSbeforeALS!HemorrhageAssessmentFocusedH&PRapidTraumaAssessmentFullHeadtoToeConsiderAirMedicalifStage2+BloodLossFocusedPhysicalExamGuidedbyc/cVitals,SAMPLE,&OPQRSTAdditionalAssessmentOrthostaticHypotensionTiltTest:20BPorPfromsupinetosittingPelvicfracture: 2,000mLFemurfracture:

1,500mLTibia/Fibulafracture: 500-750mLHematomas&Contusions:500mLHemorrhageAssessment

FracturesandBloodLossHemorrhageAssessmentOngoingAssessmentReassessVitals&MentalStatusQ5min:UNSTABLEpatientsQ15min:STABLEpatientsReassessInterventionsOxygenETIVMedicationActionsTrending:ImprovementvsDeteriorationHemorrhageManagementABC’sO2,ET,IV,CMProtectC-SpineFullimmobilizationBestsplintisthebodyCPR:BLS&ALScareIfmultiplecasualties,donotbeginunlessadequateresourcesareavailableBleedingControlPASGAnyinjurytotheheadortorsoisALSOconsideredaninjurytothespine.HeadWoundsPresentationSeverebleedingSkullFractureManagementGentleDirectPressureFluiddrainagefromEarsandNoseDONOTPackCoverandbandagelooselySpecificWoundConsiderationsNeckWoundsPresentationLargevesselcanentrainair.ManagementConsiderdirectdigitalpressureOcclusivedressingGapingWoundsPresentationMultiplesitesGapingpreventsuniformpressureManagementBulkyDressingTraumaDressingSterile,non-adherentsurfacetowoundCompressiondressingSpecificWoundConsiderationsCrushInjuryPresentationDifficulttolocatesourceofbleedingNormalhemorrhagecontrolmechanismnon-functionalManagementConsideranair-splintandpressuredressingConsiderconstrictingbandortourniquetTransportConsiderationsConsiderRapidTransportSuspectedseriousbloodlossSuspectedseriousinternalbleedingDecompensatingShockAMS,pulse,NarrowingpulsepressureWHENINDOUBTTRANSPORTOtherConsiderationsSympatheticResponseAnxietySHOCKis…

INADEQUATE

TISSUE

PERFUSIONInaNutshell…..CirculationSystolicPressureStrengthandvolumeofcardiacoutputDiastolicPressureMoreindicativeofthestateofconstrictionofthearteriolesMeanArterialPressure1/3pulsepressureaddedtothediastolicpressureTissuePerfusionPressureCompensationRespiratoryCardiovascularSympatheticNSactivationNeuroendocrineResponseTranscapillayrrefillRespiratoryCompensationChemoreceptorslocatedincarotidbodyandaorticarchCommunicaterespiratorycenterviaCNIX,XPaO2<50mmHg,hypoxemiaPaCo2increased,hypercarbiaacidosisIncreasedrate,depthorrespirationsCirculationVascularControlIncreasedsympathetictoneresultsinincreasedvasoconstrictionMicrocirculationBloodflowinthearterioles,capillariesandvenulesSphincterFunctioningMostorgantissuerequiresbloodflow5to20%ofthetimeSphincterFunctioningSphinctersConstrictO2returnsCO2removedpHnormalDropinpHSphinctersDilateCO2increasesO2fallsMASTCellsHISTAMINEReleaseMASTCellsStopReleasingHISTAMINERespiratoryControlIncreasedbloodCO2DecreasedbloodO2DecreaseCSFpH(acidosis)MastcellsreleasehistamineVasodilationIncreaseO2/decreaseCO2/pHHistaminereleasehaltedStopvasodilationHistamineReleaseEventually:VasodilationIncreasedvenouscapacitanceBloodpoolingIncreasedvascularpermeabilityLeakingintotissuesEdemaCirculationThoracoabdominalPumpRespirationsassistbloodreturntotheheartChangingintrathoracicpressureChangingpressuresdrawbloodbacktoheartBloodVolume:5L7%heart13%majorarteries7%capillaries64%venoussystem9%pulmonarycirculationInshock,thebloodreturntotheheartisdiminishedPreloadandAfterloadParasympathetic

NervousSystemDecrease

HeartratestrengthofcontractionsbloodpressureIncreaseDigestivesystemKidneysCardiovascularSystemRegulationSympatheticNervousSystemIncreaseBodyactivityHeartrateStrengthofcontractionsVascularconstrictionBowel&DigestiveVisceraDecreasedurineproductionRespirationsBronchodilationIncreasesskeletalmuscleperfusionCardiacInnervationPrimarilyinnervatedbysympatheticNSParasympatheticinnervatesatriaVagalresponseVagalstimulationPNS&SNSalwaysactinbalanceBaroreceptors:MonitorBPLocationAorticArchCarotidSinusesSendImpulsestotheMedullaCardioacceleratoryCenterSNS:controlsreleaseofEandNECardioinhibitoryCenterPNS:controlsthevagusnerveVasomotorCenterArterialandVenoustoneCardiovascularSystemRegulationChemoreceptorsMonitorslevelofCO2inCSFpHCSFMonitorslevelofO2inbloodCardiovascularSystemRegulationSympatheticNSActivationBaroreceptorsmonitorBPCommunicatewithbrainCNIXCarotidarchthruCNXIncreasedactivityofSNS,decreasedvagalactivityAccountformanyS/SassociatedwithshockCompensateforinadequateO2deliveryCatecholaminesEpinephrineNorepinephrineActionsAlpha1Alpha2Beta1Beta2CardiovascularSystemRegulation

HormoneRegulationAlpha1VasoconstrictionIncreasedperipheralvascularresistanceIncreasedpreloadAlpha2RegulatesreleaseofNEBeta1PositiveinotropyPositivechronotropyPositivedromotopyBeta2BronchodilationSmoothmuscledilationinbowelActivationA1VasoconstrictionBloodshuntedfromnon-vitaltissuesSkin-pale,cool,clammyGI-nausea,vomitingActivationB1Increasedchronotropy,inotropy,maintainBPStimulationB2BronchodilationImproveoxygenationAntidiureticHormone(ADH)aka:ArginineVasopressin(AVP)ReleasedPosteriorPituitaryDropinBPorIncreaseinserumosmolarityActionIncreaseinperipheralvascularresistanceIncreasewaterretentionbykidneysDecreaseurineoutputSplenicvasoconstriction200mLoffreebloodtocirculationCardiovascularSystemRegulation

HormoneRegulationAngiotensinIIReleasedPrimarychemicalfromKidneysLoweredBPanddecreasedperfusionActionConvertedfromReninintoAngiotensinIModifiedinlungstoAngiotensinII20minuteprocessPotentsystemicvasoconstrictor1hourdurationCausesreleaseofADH,AldosteroneandEpiCardiovascularSystemRegulation

HormoneRegulationAldosteroneReleaseAdrenalCortexStimulatedbyAngiotensinIIActionMaintainkidneyIONbalanceRetentionofsodiumandwaterReducesinsensiblefluidCardiovascularSystemRegulation

HormoneRegulation(continued)CardiovascularSystemRegulation

HormoneRegulationGlucagonReleaseAlphaCellsofPancreasTriggeredbyEpiActionCausesliverandskeletalmusclestoconvertglycogenintoglucoseGluconeogenesisInsulinReleaseBetaCellsofPancreasActionFacilitatestransportofglucoseacrosscellmembraneCardiovascularSystemRegulation

HormoneRegulationErythropoietinReleaseKidneysHypoperfusionorhypoxiaActionIncreasesproductionandmaturationofRBC’sinthebonemarrowNeuroendocrineResponseACTH(adrenocorticotropichormone)secretedbypituitaryStimulatesadrenalcortextoproducealdosteroneandcortisolAldosteronecausesreabsorptionofNa&H2OinkidneyKidneyreleasesreninwhencellsofjuxtaglomerularapparatus(JGA)arehypoperfusedReninacceleeratesconversionangiotensintoangiotensinILungtissueconvertsangiotensinItoangiotensinII,potentvasoconstrictorandstimulatesreleasealdosteroneCortisolStimulatesproteinsynthesisAdrenalmedullasecretesepiandNEVasopressin(ADH)releasedbyposteriorpituitaryinresponsetoincreasedosmolalityCausesdistalrenaltubulestoincreaseH2OabsorptionGreaterLossCellularIschemiaCapillaryMicrocirculationPossibilityofCapillaryWashoutBuildupoflacticacidandCO2RelaxationofpostcapillarysphinctersReleaseofbyproductsintocirculationPROFOUNDMETABOLICACIDOSISTheBody’sResponse

toBloodLossSystemicResponsetoShockSympatheticNSresponseHormonereleaseResultofhemorrhageRatriumdoesnotfillcompletelyVentriclenotfilledDecreasedcontractilityDecreasedSVDecreasedSBPReducedperfusionofcapillarybedsBaroreceptorssignalmedullaIncreasedPVRIncreasedvenoustoneIncreasedHRIncreasedcontractilityBPreturnstonormalIfbloodlossiscontrollednoilleffectsCellularIschemiaBloodlosscontinuesVenousconstrictionPVRincreasesmaintainingSBPDBPalsorisesresultinginnarrowingpulsepressurePulseweakensLessblooddirectedtonon-criticalorgansSkin-pale,cool,clammyAnaerobicmetabolismensuesCO2andlacticacidproducedandaccumulateCellularhypoxialeadstocellularischemiaHRincreasesBloodbecomesmoreacidoticChemoreceptorsincreaseRR/depthCirculatingcatecholaminesandacidosisresultsinAMSArterioleshypoxicandfatiguedHemestasisoccursbloodisdrawnfrominterstitium1L/hrErythropoietenincreasesRBCproductionRecoverypossibleSympatheticstimulation,reducedperfusiontokidneys,pancreas,livercausehormonereleaseAngiotensinIIincreasesPVRreducesbloodflowLacticacidbuildupHydrostaticpressureforcesfluidintointerstitiumCompensatorymechanismsfailInterstitialedemadecreasesabilitytoprovideO2andremoveCO2CapillarycellmembranesbreakdownRBC’sclump,rouleaxBuildupofacidsresultsinrelaxationofpostcapillarysphinctersByproducts,K+releasedbycells,agglutinatedRBC’sreleasedinvenouscirculationResultsinprofoundmetabolicacidosisandmicroscopicemboliCO=0,PVR=0,decreaseBP,decreasecellularperfusiontocriticalorgansirreversibleTranscapillaryRefillFollowinghypovolemiaosmosisallowsmovementoffluidfromintracellularandinterstitialspacesintointravascularspace<2LselflimitingHgb,HctvaluesinaccurateinactivelybleedingpatientsAnemiapresentwithhemodilutionduetoresuscitation,transcapillaryrefillStagesofShockCompensatedShockMinimalChangeDecompensatedShockSystembeginningtofailIrreversibleShockIschemiaanddeathimminentDecompensationBody’scompensatorymechanismsoverwhelmedO2deliveryfallsagainHostFactorsMaylimitabilitytocompensateAge:Neonate,infantsMechanismundevelopedGeriatricsUnderlyingdiseaseMedicationsBblockers,CachannelblockersAlc