【英文教学讲解课件】-HEART

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1、HEARTTHEHEARTNormalPathologyHeartFailure:L,RHeartDiseaseCongenital:LRshunts,RLshunts,ObstrustiveIschemic:Angina,Infarction,ChronicIschemia,SuddenDeathHypertensive:Leftsided,RightsidedValvular:AS,MVP,Rheumatic,Infective,Non-Infective,Carcinoid,ArtificialValvesCardiomyopathy:Dilated,Hypertrophic,Restr

2、ictive,Myocarditis,OtherPericardium:Effusions,PericarditisTumors:Primary,EffectsofOtherPrimariesTransplantsNORMALFeatures6000L/day250-300grams40%ofalldeaths(2xcancer)Wallthicknesspressure(i.e.,awallisonlyasthickasithastobe)LV=1.5cmRV=0.5cmAtria=.2cmSystole/DiastoleStarlingsLawTERMSCARDIOMEGALYDILATA

3、TION,anychamber,orallHYPERTROPHY,andchamber,orallSTRIATIONSNUCLEUSDISCSSARCOLEMMASARC.RETIC.MITOCHONDRIAENDOTHELIUMFIBROBLASTSGLYCOGENA.N.P.S.A.NodeAVNodeBundleofHISL.Bundle,R.BundleAnteriorLateralPosteriorSeptalVALVESAV:TRICUSPIDMITRALSEMILUNAR:PULMONICAORTICSigmoid-shapedventricularseptumDecreased

4、leftventricularcavitysizeIncreasedleftatrialcavitysizeChambersBucklingofmitralleafletstowardtheleftatriumFibrousthickeningofleafletsMitralvalveannularcalcificdepositsAorticvalvecalcificdepositsValvesAtheroscleroticplaqueCalcificdepositsIncreasedcross-sectionalluminalareaTortuosityEpicardialCoronaryA

5、rteriesAmyloiddepositsBasophilicdegenerationLipofuscindepositionBrownatrophyIncreasedsubepicardialfatIncreasedmassMyocardiumCARDIACAGINGCARDIACAGINGAtheroscleroticplaqueElasticfragmentationandcollagenaccumulationSinotubularjunctioncalcificdepositsElongated(tortuous)thoracicaortaDilatedascendingaorta

6、withrightwardshiftAortaBROWNATROPHY,HEARTLIPOFUCSINPathologicPumpPossibilitiesPrimarymyocardialfailure(MYOPATHY)Obstructiontoflow(VALVE)Regurgitantflow(VALVE)Conductiondisorders(CONDUCTIONSYSTEM)Failuretocontainblood(WALLINTEGRITY)CHFDEFINITIONTRIAD1)TACHYCARDIA2)DYSPNEA3)EDEMAFAILUREofFrankStarling

7、mechanismHUMORALFACTORSCatecholamines(nor-epinephrine)ReninAngiotensionAldosteroneAtrialNatriureticPolypeptide(ANP)HYPERTROPHYandDILATATIONHYPERTROPHYPRESSUREOVERLOAD(CONCENTRIC)VOLUMEOVERLOAD(CHF)LVH,RVH,atrial,etc.2Xnormalweightischemia3XnormalweightHTN3XnormalweightMYOPATHY,aorticregurgitationCHF

8、:AutopsyFindingsCardiomegalyChamberDilatationHypertrophyofmyocardialfibers,BOXCARnucleiLeftSidedFailureLowoutputvs.congestionLungspulmonarycongestionandedemaheartfailurecellsKidneyspre-renalazotemiasaltandfluidretentionrenin-aldosteroneactivationnatriureticpeptidesBrain:Irritability,decreasedattenti

9、on,stuporcomaLeftHeartFailureSymptomsDyspneaonexertionatrestOrthopnearedistributionofperipheraledemafluidgradedbynumberofpillowsneededParoxysmalNocturnalDyspnea(PND)LEFTHeartFailureDyspneaOrthopneaPND(ParoxysmalNocturnalDyspnea)BloodtingedsputumCyanosisElevatedpulmonary“WEDGE”pressure(PCWP)RightSide

10、dHeartFailureEtiologyleftheartfailurecorpulmonaleSymptomsandsignsLiverandspleenpassivecongestion(nutmegliver)congestivespleenomegalyascitesKidneysPleura/PericardiumpleuralandpericardialeffusionstransudatesPeripheraltissuesRIGHTHeartFailureFATIGUE“Dependent”edemaJVDHepatomegaly(congestion)ASCITES,PLE

11、URALEFFUSIONGICyanosisIncreasedperipheralvenouspressure(CVP)HEARTDISEASECONGENITAL(CHD)ISCHEMIC(IHD)HYPERTENSIVE(HHD)VALVULAR(VHD)MYOPATHIC(MHD)CONGENITALHEARTDEFECTSFaultyembryogenesis(week3-8)UsuallyMONO-morphic(i.e.,SINGLElesion)(ASD,VSD,hypo-RV,hypo-LV)Maynotbeevidentuntiladultlife(Coarctation,A

12、SD)Overallincidence1%ofUSAbirthsINCREASEDsimpleearlydetectionvianoninvasivemethods,e.g.,US,MRI,CT,etc.Tricuspidatresia1120Totalanomalouspulmonaryvenousconnection1136Truncusarteriosus4388Transpositionofgreatarteries4388Aorticstenosis4396Atrioventricularseptaldefect5492Coarctationofaorta5577Tetralogyo

13、fFallot7781Patentductusarteriosus8836Pulmonarystenosis101043Atrialseptaldefect424482Ventricularseptaldefect%IncidenceperMillionLiveBirthsMalformationGENETICSGeneabnormalitiesinonly10%ofCHDTrisomies21,13,15,18,XOMutationsofgeneswhichencodefortranscriptionfactorsTBX5ASD,VSDNKX2.5ASDRegionofchromosome2

14、2importantinheartdevelopment,22q11.2deletionconotruncus,branchialarch,faceENVIRONMENTRUBELLATERATOGENSCHDLRSHUNTS:all“Ds”intheirnamesNOcyanosisPulmonaryhypertensionSIGNIFICANTpulmonaryhypertensionisIRREVERSIBLERLSHUNTS:all“Ts”intheirnamesCYANOSIS(i,.e.,“blue”babies)VENOUSEMBOLIbecomeSYSTEMICOBSTRUCT

15、IONSLRASDVSDASVDPDANONCYANOTICIRREVERSIBLEPULMONARYHYPERTENSIONISTHEMOSTFEAREDCONSEQUENCEASDNOTpatentforamenovaleUsuallyasymptomaticuntiladulthoodSECUNDUM(90%):DefectivefossaovalisPRIMUM(5%):NexttoAVvalves,mitralcleftSINUSVENOSUS(5%):NexttoSVCwithanomalouspulmonaryveinsdrainingtoSVCorRAVSDByfar,most

16、commonCHDdefectOnly30%areisolatedOftenwithTETRALOGYofFALLOT90%involvethemembranousseptumIfmuscularseptumisinvolved,likelytohavemultipleholesSMALLonesoftenclosespontaneouslyLARGEonesprogresstopulmonaryhypertensionPDA90%isolatedHARSH,machinery-likemurmurLR,possiblyRLaspulmonaryhypertensionapproachessy

17、stemicpressureClosingthedefectmaybelifesavingKeepingitopenmaybelifesaving(ProstaglandinE).Why?AVSDAssociatedwithdefective,inadequateAVvalvesCanbepartial,orCOMPLETE(ALL4CHAMBERSFREELYCOMMUNICATE)RLTetralogyofFallotTranspositionofgreatarteriesTruncusarteriosusTotalanomalouspulmonaryvenousconnectionTri

18、cuspidatresiaRLSHUNTSTETRALOGYofFALLOTmostCOMMON1)VSD,large2)OBSTRUCTIONtoRVflow3)AortaOVERRIDEStheVSD4)RVHSURVIVALDEPENDSonSEVERITYofSUBPULMONICSTENOSISCanbea“PINK”tetrologyifpulmonicobstructionissmall,butthegreatertheobstruction,thegreateristheRLshuntTGA(TRANSPOSITIONofGREATARTERIES)NEEDSaSHUNTfor

19、survivalPDAorPFO(65%),“unstable”shuntVSD(35%),“stable”shuntRVLVinthicknessFatalinfirstfewmonthsSurgical“switching”TRUNCUSARTERIOSISTRICUSPIDATRESIAHypoplasticRVNeedsashunt,ASD,VSD,orPDAHighmortalityTotalAnomalousPulmonaryVenousConnection(TAPVC)PULMONARYVEINSdoNOTgointoLA,butintoL.innominatev.orcoron

20、arysinusNeedsaPFOoraVSDHYPOPLASTICLAOBSTRUCTIVECHDCOARCTATIONofaortaPulmonarystenosis/atresiaAorticstenosis/atresiaCOARCTATIONofAORTAMFButXOsfrequentlyhaveitINFANTILEFORM(proximaltoPDA)(SERIOUS)ADULTFORM(CLOSEDDUCTUS)Bicuspidaorticvalve50%ofthetimePULMONICSTENOSIS/ATRESIAIf100%atretic,hypoplasticRVw

21、ithASDClinicalseveritystenosisseverityAORTICSTENOSIS/ATRESIAVALVULARIfsevere,hypoplasticLVfatalSUB-valvular(subaortic)AorticwallTHICKBELOWcuspsSUPRA-valvularAorticwallTHICKABOVEcuspsinascendingaortaHEARTDISEASECONGENITAL(CHD)ISCHEMIC(IHD)HYPERTENSIVE(HHD)VALVULAR(VHD)MYOPATHIC(MHD)SYNDROMESofIHDAngi

22、naPectoris:Stable,UnstableMyocardialInfarction(MI,AMI)ChronicIHDCHF(CIHD)SuddenCardiacDeath(SCD)“Acute”CoronarySyndromes:UNSTABLEANGINAAMISCD(SuddenCardiacDeath)IHDRISKNumberofplaquesDistributionofplaquesSize,structureofplaquesACUTECORONARYSYNDROMES“The acute coronary syndromes are frequently initia

23、ted by an unpredictable and abrupt conversion of a stable atherosclerotic plaque to an unstable and potentially life-threatening atherothrombotic lesion through superficial erosion,ulceration,fissuring,rupture,or deep hemorrhage,usually with superimposed thrombosis.”EPIDEMIOLOGYmilliondieofIHDyearly

24、inUSA1millionin1963.Why?PreventionofcontrolcontrollableriskfactorsEarlier,betterdiagnosticmethodsPTCA,CABG,arrythmiacontrol90%ofIHDpatientshaveATHEROSCLEROSIS(nosurprisehere)ACUTECORONARYSYNDROMEFACTORSACUTEPLAQUECHANGE*InflammationThrombusVasoconstriction*MOSTIMPORTANTACUTEPLAQUECHANGERupture/Refis

25、suringErosion/Ulceration,exposingECMAcuteHemorrhageNB:PlaquesdoNOThavetobeseverelystenotictocauseacutechanges,i.e.,50%ofAMIresultsfromthrombosesofplaquesshowingLESSTHAN50%stenosisINFLAMMATIONEndothelialcellsreleaseCAMs,selectinsT-cellsreleaseTNF,IL-6,IFN-gammatostimulateandactivateendothelialcellsan

26、dmacrophagesCRPpredictstheprobabilityofdamageinanginapatientsTHROMBUSTotalocclusionPartialEmbolizationVASOCONSTRICTIONCirculatingadrenergicagonistsPlateletreleaseproductsEndotheliallyreleasedfactors,suchasendothelinOftensmallplateletaggregatesorthrombiand/orthromboemboliFrequentUsuallysevereSuddende

27、athWidelyvariable,maybeabsent,partial/complete,orlysedVariableVariableSubendocardialmyocardialinfarctionOcclusiveFrequentVariableTransmuralmyocardialinfarctionNonocclusive,oftenwiththromboemboliFrequentVariableUnstableanginaNoNo75%StableanginaPlaque-AssociatedThrombusPlaqueDisruptionStenosesSyndrome

28、CoronaryArteryPathologyinIschemicHeartDiseaseANGINAPECTORISParoxysmal(sudden)Recurrent15sec.15min.Reducedperfusion,butNOinfarctionTHREETYPESSTABLE:relievedbyrestornitroPRINZMETAL:SPASMismainfeature,respondstonitro,S-TelevationUNSTABLE(crescendo,PRE-infarction,Q-waveangina):perhapssomethrombosis,perh

29、apssomenontransmuralnecrosis,perhapssomeembolization,butDISRUPTIONofPLAQUEisuniversallyagreeduponMYOCARDIALINFARCTIONTransmuralvs.Subendocardial(inner1/3)DUH!EXACTSAMEriskfactorsasatherosclerosisMostareTRANSMURAL,andMOSTarecausedbycoronaryarteryocclusionInthe10%oftransmuralMIsNOTassociatedwithathero

30、sclerosis:VasospasmEmboliUNexplainedMYOCARDIALRESPONSE1hrMicrovascularinjury2040minIrreversiblecellinjury40minto10%ofnormal10minto50%ofnormalATPreduced2moIncreasedcollagendeposition,withdecreasedcellularityGray-whitescar,progressivefrombordertowardcoreofinfarct28wkWell-establishedgranulationtissuewi

31、thnewbloodvesselsandcollagendepositionRed-graydepressedinfarctborders1014daysWell-developedphagocytosisofdeadcells;earlyformationoffibrovasculargranulationtissueatmarginsMaximallyyellow-tanandsoft,withdepressedred-tanmargins710daysBeginningdisintegrationofdeadmyofibers,withdyingneutrophils;earlyphag

32、ocytosisofdeadcellsbymacrophagesatinfarctborderHyperemicborder;centralyellow-tansoftening37daysCoagulationnecrosis,withlossofnucleiandstriations;interstitialinfiltrateofneutrophilsMottlingwithyellow-taninfarctcenter13daysOngoingcoagulationnecrosis;pyknosisofnuclei;myocytehypereosinophilia;marginalco

33、ntractionbandnecrosis;beginningneutrophilicinfiltrateDarkmottling1224hrBeginningcoagulationnecrosis;edema;hemorrhageOccasionallydarkmottling412hrUsuallynone;variablewavinessoffibersatborderNone4hr1day,3-4days,7days,weeks,monthsRE-PERFUSIONThrombolysisPTCACABGReperfusionCANNOTrestorenecroticordeadfib

34、ers,onlyreversiblyinjuredonesREPERFUSION“INJURY”FreeradicalsInterleukinsAMIDIAGNOSISSYMPTOMSEKGDIAPHORESIS(10%ofMIsare“SILENT”withQ-waves)CKMBgoldstandardenzymeTroponin-I,Troponin-TbetterCRPpredictsriskofAMIinanginapatientsCOMPLICATIONSWallmotionabnormalitiesArrhythmiasRupture(4-5days)PericarditisRV

35、infarctionInfarctextensionMuralthrombusVentricularaneurysmPapillarymuscledysfunction(regurgitation)CHFCIHD,aka,ischemic“cardiomyopathy”ProgresstoCHFoftenwithnopathologicorclinicalevidenceoflocalizedinfarctionExtensiveatherosclerosisNoinfarctH&DpresentSUDDENCARDIACDEATH350,000inUSAyearlyfromatheroscl

36、erosisNON-atheroscleroticsuddencardiacdeathincludes:CongenitalcoronaryarterydiseaseAorticstenosisMVPMyocarditisCardiomyopathy(suddendeathinyoungathletes)PulmonaryhypertensionConductiondefectsHTN,hypertrophyofUNKNOWNetiologyAUTOPSYfindingsinSCD75%narrowingof1-3vesselsHealedinfarcts40%“ARRHYTHMIA”isof

37、tenaveryconvenientconclusionwhennoanatomicfindingsarepresent,i.e.,“wastebasket”diagnosisHEARTDISEASECONGENITAL(CHD)ISCHEMIC(IHD)HYPERTENSIVE(HHD)VALVULAR(VHD)MYOPATHIC(MHD)HHD(Left)DEFINITION:Hypertrophicadaptiveresponseoftheheart,whichcanprogress:MyocardialdysfunctionCardiacdilatationCHFSuddendeath

38、NEEDEDforDIAGNOSIS:LVH(LV2.0and/orHeart500gm.)HTN(140/90)PREVALENCE:WHAT%ofUSApeoplehavehypertension?PREVALENCE:WHAT%ofUSApeoplehavehypertension?Answer:25%HISTOPATHOLOGYINCREASEDFIBER(MYOCYTE)THICKNESSINCREASEDnuclearsizewithincreased“blockiness”(boxcarnucleus)CLINICALEKGSummaryofLVHCriteria1)R-I+S-

39、III25mm2)S-V1+R-V535mm3)ST-Tsinleftleads4)R-L11mm5)LAE+othercriteriaPositiveCriteria:1=possible2=probable3=definiteATRIALFIBRILLATIONWhy?*CHF,cardiacdilatation,pulmonaryvenouscongestionanddilatationCOURSE:NORMALlongevity,deathfromothercausesProgressiveIHDProgressiverenaldamage,hemorrhagicCVA(Whichar

40、teries?)CHFHHD(Right)=CORPULMONALEACUTE:MassivePECHRONIC:COPD,CRPD,Pulmonaryarterydisease,chestwallmotionimpairmentDiseases of the Pulmonary ParenchymaChronicobstructivepulmonarydiseaseDiffusepulmonaryinterstitialfibrosisPneumoconiosesCysticfibrosisBronchiectasisDiseases of the Pulmonary VesselsRecu

41、rrentpulmonarythromboembolismPrimarypulmonaryhypertensionExtensivepulmonaryarteritis(e.g.,Wegenergranulomatosis)Drug-,toxin-,orradiation-inducedvascularobstructionExtensivepulmonarytumormicroembolismDisorders Affecting Chest MovementKyphoscoliosisMarkedobesity(pickwickiansyndrome)Neuromusculardiseas

42、esDisorders Inducing Pulmonary Arterial ConstrictionMetabolicacidosisHypoxemiaChronicaltitudesicknessObstructiontomajorairwaysIdiopathicalveolarhypoventilationHEARTDISEASECONGENITAL(CHD)ISCHEMIC(IHD)HYPERTENSIVE(HHD)VALVULAR(VHD)MYOPATHIC(MHD)ValvularHDOpeningproblems:StenosisClosingproblems:Regurgi

43、tationorIncompetence70%ofallVHDASCalcificationofadeformedvalve“Senile”calcificASRheum,HeartDis.MSRheumaticHeartDiseaseAORTICSTENOSIS2XgradientpressureLVH,ischemiaCardiacdecompensation,angina,CHF50%diein5yearsifanginapresent50%diein2yearsifCHFpresentMITRALANNULARCALCIFICATIONCalcificationofthemitral“

44、skeleton”UsuallyNOdysfunctionRegurgitationorStenosispossibleFMREGURGITATIONSARRheumaticInfectiousAorticdilatationsSyphilisRheumatoidArthritisMarfanMRMVPInfectiousFen-PhenPapillarymuscles,chordaetendinaeCalcificationofmitralring(annulus)MitralValveProlapse(MVP)MYXOMATOUSdegenerationofthemitralvalveAs

45、sociatedwithconnectivetissuedisorders“Floppy”valve3%incidence,FMEasilyseenonechocardiogramMVP:CLINICALFEATURESUsuallyasymptomaticMid-systolic“click”Holosystolicmurmurifregurg.presentOccasionalchestpain,dyspnea97%NOuntowardeffects3%Infectiveendocarditis,mitralinsufficiency,arrythmias,suddendeathRHEUM

46、ATICHeartDiseaseFollowsagroupAstrepinfection,afewweekslaterDECREASEin“developed”countriesPANCARDITISACUTE:-Inflammation-Aschoffbodies-Anitschkowcells-Pancarditis-VegetationsonchordaetendinaeatleafletjunctionCHRONIC:THICKENEDVALVESCOMMISURALFUSIONTHICK,SHORT,CHORDAETENDINAECLINICALFEATURESMigratoryPo

47、lyarthritisMyocarditisSubcutaneousnodulesErythemamarginatumSydenhamchoreaINFECTIOUSENDOCARDITISMicrobesUsuallystrepviridansOftenStaphaureusinIVDusersEnterococciHAEK(normaloralflora)HemophilusinfluenzaeActinobacillusCardiobacteriumEikenellaKingellaFungi,rickettsiae,chlamydiaINFECTIOUSENDOCARDITISAcut

48、e:50%mortality(course=days)SUB-acute:LOWmortality(course=weeks)VEGETATIONSINFECTIVE5mmNON-Infective5mmDIAGNOSIS=MMm,Mmmm,mmmmmMAJORPositivebloodculture(s)indicatingcharacteristicorganismorpersistenceofunusualorganismEchocardiographicfindings,includingvalve-relatedorimplant-relatedmassorabscess,orpar

49、tialseparationofartificialvalveNewvalvularregurgitationminorPredisposingheartlesionorintravenousdruguseFeverVascularlesions,includingarterialpetechiae,subungual/splinterhemorrhages,emboli,septicinfarcts,mycoticaneurysm,intracranialhemorrhage,JanewaylesionsImmunologicphenomena,includingglomerulonephr

50、itis,Oslernodes,Rothspots,rheumatoidfactorMicrobiologicevidence,includingsinglecultureshowinguncharacteristicorganismEchocardiographicfindingsconsistentwithbutnotdiagnosticofendocarditis,includingnewvalvularregurgitation,pericarditisNON-infectiveVEGETATIONS5mmPETrousseausyndrome(migratorythrombophle

51、bitiswithmalignancies)s/pSwan-GanzLibman-SakswithSLE(bothsidesofvalve)CarcinoidSyndromeEpisodicskinflushingCrampsNausea&VomitingDiarrheaserotonin,5HIAAinurineFIBROUSINTIMALTHICKENINGRV,Tricuspidvalve,Pulmonicvalve(allRIGHTside)SimilartowhatFen-PhendoesontheLEFTsideARTIFICIALVALVESMechanicalXenograft

52、s(porcine)60%havecomplicationswithin10yearsHEARTDISEASECONGENITAL(CHD)ISCHEMIC(IHD)HYPERTENSIVE(HHD)VALVULAR(VHD)MYOPATHIC(MHD)PERICARDIALDISEASECARDIOMYOPATHIESInflammatoryImmunologicMetabolicDystrophiesGeneticIdiopathicDILATED(DCM)SY-stolicdysfunctionHYPERTROPHIC(HCM)DIA-stolicdysfunctionRESTRICTIVE(RCM)DIA-stolicdysfunctionFunctionalPatternLVEF*MechanismsofHeartFailureCausesIndirectMyocardialDysfunction(NotCardiomyopathy)Dilated60%CARDIACTRANSPLANTPATHOLOGY