CoronaryCirculation课件专题知识课件

CoronaryCirculationCoronaryArteryDisease

ReadingKlabunde,CardiovascularPhysiologyConceptsChapter7(OrganBloodFlow)pages151-155(SectiononCoronaryCirculation)Chapter4(CardiacFunction)pages85-88CoronaryArteryAnatomyEpicardialVesselSubepicardiumSubendocardiumMyocardiumPericardium(Epicardium)CoronaryVascularResistanceEpicardialconductancevesselsOnlyasmall%ofresistancenormallyStenoticlesionsIntramyocardialvessels(arterioles)ContributemosttototalcoronaryvascularresistanceCapillaryDensityintheHeartDeterminantsofMyocardialOxygenSupplyandDemandVascularResistanceCoronaryBloodFlowHeartRateContractilitySystolicWallTensionO2-CarryingCapacitySUPPLYDEMANDDiastolicPhaseMetabolicControlAutoregulationExtravascularCompressiveForcesNeuralControlEndothelialControlMyocardialOxygenSupplyRestingO2ConsumptionofVariousOrgansCoronaryPerfusionPressurePressuregradientthatdrivesbloodthroughthecoronarycirculation. CoronaryPerfusionPressure=DiastolicBP–LVEDP(orPCWP)MyocardialOxygenSupplyOxygenContentofBloodO2Content=(1.36ccO2/gHgb/100mlbloodxHgbx%Saturation)+(pO2x0.003)O2deliveredtomyocardium=O2contentxcoronarybloodflowMyocardialOxygenSupplyOxygenExtractionTheheartextractsoxygentoagreaterextentthananyotherorganCoronarysinuspO2valueisnormallyinrangeof20-22mmHg(%sat=32-38%)CanonlyminimallyincreaseO2extractionIncreasesinO2demandmustbemetbyincreasedcoronarybloodflowMyocardialOxygenSupplyRegulationofCoronaryBloodFlowCoronaryBloodFlowMetaboliccontrolAutoregulationEndothelialcontrolofcoronaryvasculartoneExtravascularcompressiveforcesNeuralcontrolRegulationof

CoronaryBloodFlowMetabolicControlCoronarycirculationisexquisitelysensitivetomyocardialtissueoxygentensionIncreasedoxygendemandresultsinalowertissueoxygentension.Thiscausesvasodilationandincreasedbloodflow.AdenosineNitricoxideProstaglandinsK+ATPchannelsMetabolicControlofBloodFlowLackofoxygen?Formationofvasodilators?Combinationofboth??MetarteriolePrecapillarySphincterCapillaryRelaxationofsmoothmuscleIncreasedBloodFlowAutoregulationAbilityofavascularnetworktomaintainconstantbloodflowoverarangeofarterialpressures.AutoregulationisanindependentdeterminantofCBFThesetpointatwhichCBFismaintaineddependsonMVO2CoronaryPerfusionPressureFlowAutoregulationNormalAutoregulationMaximalAvailableCoronaryBloodFlowAutoregulationinAnemiaorLVHEndothelialControlofCoronaryVascularToneWhenDamagetoEndotheliumOccursDamagetoendothelialcellswillleadto:DecreasedNitricOxideandProstacyclinproductionIncreasedEndothelinproductionThiswillleadto:VasoconstrictionVasospasmThrombosisNeuralControlCoronarybloodflowiscontrolledpredominantlybylocalmetabolic,autoregulatory,andendothelialfactorsNeuralcontrolofthecoronarycirculationcomplementstheabovelocaleffectsNeuralControlSympatheticControlAlpha=constrictcoronaryvesselsBeta=dilatecoronaryvesselsBeta1inconduitarteriesBeta2inresistancearteriolesParasympatheticControlAcetylcholineVasodilationinhealthysubjectsVasoconstrictioninpatientswithatherosclerosisExtravascularCompressiveForcesTheheartinfluencesitsbloodsupplybythesqueezingeffectofthecontractingmyocardiumonthebloodvesselscoursingthroughtheheartExtravascularCompressiveForcesLeftVentricleEarlySystole>InitialFlowReversalRemainderofSystole>Flowfollowsaorticpressurecurve,butatamuchreducedpressureEarlyDiastole>Abruptpressurerise(80-90%ofLVflowoccursinearlydiastole)RemainderofDiastole>PressuredeclinesslowlyasaorticpressuredecreasesExtravascularCompressiveForcesExtravascularCompressiveForcesRightVentricleLowerpressuregeneratedbythinrightventricleinsystoleNoreversalofbloodflowduringearlysystoleSystolicbloodflowconstitutesamuchgreaterproportionoftotalbloodflowTransmuralDistributionofMyocardialBloodFlowExtravascularcompressiveforcesaregreaterinthesubendocardium(inner)andleastnearthesubepicardiallayer(outer)UndernormalrestingconditionsthisdoesnotimpairsubendocardialbloodflowasincreasedflowduringdiastolecompensatesSubendocardialtosubepicardialratio:1.25/1DuetopreferentialdilatationofthesubendocardialvesselsSecondarytoincreasedwallstressand,therefore,increasedMVO2inthesubendocardiumTransmuralDistributionofMyocardialBloodFlowThesubendocardiumismoresusceptibletoischemiathanthemidmyocardiumorsubepicardiumEpicardialcoronarystenosesareassociatedwithreductionsinthesubendocardialtosubepicardialflowratioCoronaryFlowReserveDifferencebetweenbaselinebloodflowandmaximalflowUsuallymeasuredfollowingpharmacologiccoronaryvasodilationIntheabsenceofcoronaryarterydisease,maximalflowis4–5timesasgreatasatrestCoronaryflowreservedecreaseswithincreasingseverityofcoronaryarterydiseaseMyocardialOxygenDemandMyocardialOxygenConsumptionOxygenconsumptionisdefinedasthevolumeofoxygenconsumedperminute(usuallyexpressedper100gramsoftissueweight)MyocardialOxygenDemand

isRelatedtoWallStressLaPlace’sLawWallStressPrWallStresshFactorsIncreasing

MyocardialOxygenConsumptionIncreasedHeartRateIncreasedInotropy(Contractility)IncreasedAfterloadIncreasedPreloadChangesinpreloadaffectmyocardialoxygenconsumptionlessthandochangesintheotherfactorsOxygenCostofMyocardialWorkPressureworkismuchmorecostlythanvolumeworkfortheheartPressurework=increasingarterialpressureataconstantcardiacoutputVolumework=increasingcardiacoutputwhilemaintainingaconstantpressureCoronaryArteryDiseaseCoronaryArteryDiseaseMyocardialischemiaoccurswhenmyocardialavailabilityisinadequatetomeetmetabolicrequirements.EffectsofCoronaryStenosesCoronaryFlowReserve30%90%DegreeofStenosisR50%70%80%CoronaryStenosisandResistanceMyocardialIschemiaH+H+Na+Na+3Na+Na+3Na+Na+2K+2K+Ca++Ca++Na/HExchangerNa-KATPaseNa/CaExchangerOutsideInsideH+H+Na+Na+3Na+Na+3Na+Na+2K+2K+Ca++Ca++Na/HExchangerNa-KATPaseNa/CaExchangerOutsideInsideIncreasedactivityIschemiaIncreasedintracellularNaDecreasedactivityDecreasedactivityIncreasedintracellularCaMyocardialIschemiaIncreasedNa/HExchangeDecreasedNa-KATPaseActivityIntracellularAcidosisIncreasedIntracellularNaIncreasedHExtrudedDecreasedNa/CaExchangeIntracellularCa++OverloadIMPAIREDMYOCARDIALCONTRACTIONANDCELLDEATHEffectsofMyocardialIschemiaSystolicdysfunctionNormalmyocardiumthickensandshortensduringsystoleIschemiacausesalterationsthatmayrangefromminimalimpairmenttoabsenceofmovement(akinesis)tosystoliclengtheningandpost-systolicshortening(dyskinesis)MayhavecompensationbysurroundingareasofnormalmuscleEffectsofMyocardialIschemiaDiastoleSystoleNormalIschemicEffectsofMyocardialIschemiaDiastolicDysfunctionWhenasufficientamountofmyocardiumisrenderedischemic,thenLVEDPrisesRelaxationisimpaired,andmyocardialcompliancedecreasesMyocardialIschemiaMyocardialStunningAfterabriefepisodesevereischemia,prolongedmyocardialdysfunctionwithgradualreturnofcontractileactivityoccurs.MyocardialHibernationPresenceofimpairedrestingLVfunction,owingtoreducedCBFthatcanberestoredtowardnormalbyrevascularization.MyocardialIschemiaMyocardialInfarctionChronicIschemiawithoutInfarctionAcuteIschemiaNoReturnofContractileFunctionReturnofContractileFunctionHibernatingMyocardiumMyocardialStunningReliefofIschemiaMyocardialIschemiaSystolicanddiastolicdysfunctionAnginaCHForPulmonaryEdemaArrythmiasMyocardialInfarctionVentricularRuptureorVSDCardiogenicShockDeathDrugsUsedforTreatmentofIschemiaOxygenBeta-BlockersNitratesAntiplatelet/AnticoagulantDrugsAnalgesicsCalcium-ChannelBlockersInterventionsfortheTreatmentofMyocardialIschemiaCoronaryarterybypasssurgery(CABG)PercutaneousCoronaryInterventionsCoronaryBalloonAngioplastyBare-metalCoronaryStentsDrug-elutingStentsHowlongshouldyouwaitbeforedoingelectivesurgeryafterPCI?Bare-metalStentCardiaccomplicationsarelowestafter90daysDrug-elutingStent1yearisrecommendedPerioperativeMedicalTherapyVolatileanestheticagentsmaybepreferredAnestheticPreconditioningBeta-blockersStatinsStabilizeplaqueAnti-inflammatoryPerioperativeMedicalTherapyAlpha-2-agonistsClonidineUsefulinpatientsnotabletotakeBeta-blockers(e.g.,asthmatic)CalciumchannelblockersTheuseofNitroglycerinasaprophylacticdrugduringanesthesiaisunclear.Nostudyhasclearlydemonstratedachangeinoutcomefromitsroutineuse.CollateralBloodFlowCollateralBloodFlowCoronarycol