【医学英文精品课件】心脏 heart

HEART THEHEART NormalPathologyHeartFailure L RHeartDiseaseCongenital L Rshunts R Lshunts ObstrustiveIschemic Angina Infarction ChronicIschemia SuddenDeathHypertensive Leftsided RightsidedValvular AS MVP Rheumatic Infective Non Infective Carcinoid ArtificialValvesCardiomyopathy Dilated Hypertrophic Restrictive Myocarditis OtherPericardium Effusions PericarditisTumors Primary EffectsofOtherPrimariesTransplants NORMALFeatures 6000L day250 300grams40 ofalldeaths 2xcancer Wallthickness pressure i e awallisonlyasthickasithastobe LV 1 5cmRV 0 5cmAtria 2cmSystole DiastoleStarling sLaw TERMS CARDIOMEGALYDILATATION anychamber orallHYPERTROPHY andchamber orall STRIATIONSNUCLEUSDISCSSARCOLEMMASARC RETIC MITOCHONDRIAENDOTHELIUMFIBROBLASTSGLYCOGENA N P S A Node AVNode BundleofHIS L Bundle R Bundle AnteriorLateralPosteriorSeptal VALVES AV TRICUSPIDMITRALSEMILUNAR PULMONICAORTIC CARDIACAGING CARDIACAGING BROWNATROPHY HEART LIPOFUCSIN PathologicPumpPossibilities Primarymyocardialfailure MYOPATHY Obstructiontoflow VALVE Regurgitantflow VALVE Conductiondisorders CONDUCTIONSYSTEM Failuretocontainblood WALLINTEGRITY CHF DEFINITIONTRIAD1 TACHYCARDIA2 DYSPNEA3 EDEMAFAILUREofFrankStarlingmechanismHUMORALFACTORSCatecholamines nor epinephrine Renin Angiotension AldosteroneAtrialNatriureticPolypeptide ANP HYPERTROPHYandDILATATION HYPERTROPHY PRESSUREOVERLOAD CONCENTRIC VOLUMEOVERLOAD CHF LVH RVH atrial etc 2Xnormalweight ischemia3Xnormalweight HTN 3Xnormalweight MYOPATHY aorticregurgitation CHF AutopsyFindings CardiomegalyChamberDilatationHypertrophyofmyocardialfibers BOXCARnuclei LeftSidedFailure Lowoutputvs congestionLungspulmonarycongestionandedemaheartfailurecellsKidneyspre renalazotemiasaltandfluidretentionrenin aldosteroneactivationnatriureticpeptidesBrain Irritability decreasedattention stupor coma LeftHeartFailureSymptoms DyspneaonexertionatrestOrthopnearedistributionofperipheraledemafluidgradedbynumberofpillowsneededParoxysmalNocturnalDyspnea PND LEFTHeartFailure DyspneaOrthopneaPND ParoxysmalNocturnalDyspnea BloodtingedsputumCyanosisElevatedpulmonary WEDGE pressure PCWP RightSidedHeartFailure EtiologyleftheartfailurecorpulmonaleSymptomsandsignsLiverandspleenpassivecongestion nutmegliver congestivespleenomegalyascitesKidneysPleura PericardiumpleuralandpericardialeffusionstransudatesPeripheraltissues RIGHTHeartFailure FATIGUE Dependent edemaJVDHepatomegaly congestion ASCITES PLEURALEFFUSIONGICyanosisIncreasedperipheralvenouspressure CVP HEARTDISEASE CONGENITAL CHD ISCHEMIC IHD HYPERTENSIVE HHD VALVULAR VHD MYOPATHIC MHD CONGENITALHEARTDEFECTS Faultyembryogenesis week3 8 UsuallyMONO morphic i e SINGLElesion ASD VSD hypo RV hypo LV Maynotbeevidentuntiladultlife Coarctation ASD Overallincidence1 ofUSAbirthsINCREASEDsimpleearlydetectionvianoninvasivemethods e g US MRI CT etc GENETICS Geneabnormalitiesinonly10 ofCHDTrisomies21 13 15 18 XOMutationsofgeneswhichencodefortranscriptionfactors TBX5 ASD VSD NKX2 5 ASDRegionofchromosome22importantinheartdevelopment 22q11 2deletion conotruncus branchialarch face ENVIRONMENT RUBELLATERATOGENS CHD L RSHUNTS all D s intheirnamesNOcyanosisPulmonaryhypertensionSIGNIFICANTpulmonaryhypertensionisIRREVERSIBLER LSHUNTS all T s intheirnamesCYANOSIS i e blue babies VENOUSEMBOLIbecomeSYSTEMICOBSTRUCTIONS L R ASDVSDASVDPDA NONCYANOTICIRREVERSIBLEPULMONARYHYPERTENSIONISTHEMOSTFEAREDCONSEQUENCE ASD NOTpatentforamenovaleUsuallyasymptomaticuntiladulthoodSECUNDUM 90 DefectivefossaovalisPRIMUM 5 NexttoAVvalves mitralcleftSINUSVENOSUS 5 NexttoSVCwithanomalouspulmonaryveinsdrainingtoSVCorRA VSD Byfar mostcommonCHDdefectOnly30 areisolatedOftenwithTETRALOGYofFALLOT90 involvethemembranousseptumIfmuscularseptumisinvolved likelytohavemultipleholesSMALLonesoftenclosespontaneouslyLARGEonesprogresstopulmonaryhypertension PDA 90 isolatedHARSH machinery likemurmurL R possiblyR LaspulmonaryhypertensionapproachessystemicpressureClosingthedefectmaybelifesavingKeepingitopenmaybelifesaving ProstaglandinE Why AVSD Associatedwithdefective inadequateAVvalvesCanbepartial orCOMPLETE ALL4CHAMBERSFREELYCOMMUNICATE R L TetralogyofFallotTranspositionofgreatarteriesTruncusarteriosusTotalanomalouspulmonaryvenousconnectionTricuspidatresia R LSHUNTS TETRALOGYofFALLOTmostCOMMON1 VSD large2 OBSTRUCTIONtoRVflow3 AortaOVERRIDEStheVSD4 RVHSURVIVALDEPENDSonSEVERITYofSUBPULMONICSTENOSISCanbea PINK tetrologyifpulmonicobstructionissmall butthegreatertheobstruction thegreateristheR Lshunt TGA TRANSPOSITIONofGREATARTERIES NEEDSaSHUNTforsurvivalPDAorPFO 65 unstable shuntVSD 35 stable shuntRV LVinthicknessFatalinfirstfewmonthsSurgical switching TRUNCUSARTERIOSIS TRICUSPIDATRESIA HypoplasticRVNeedsashunt ASD VSD orPDAHighmortality TotalAnomalousPulmonaryVenousConnection TAPVC PULMONARYVEINSdoNOTgointoLA butintoL innominatev orcoronarysinusNeedsaPFOoraVSDHYPOPLASTICLA OBSTRUCTIVECHD COARCTATIONofaortaPulmonarystenosis atresiaAorticstenosis atresia COARCTATIONofAORTA M FButXO sfrequentlyhaveitINFANTILEFORM proximaltoPDA SERIOUS ADULTFORM CLOSEDDUCTUS Bicuspidaorticvalve50 ofthetime PULMONICSTENOSIS ATRESIA If100 atretic hypoplasticRVwithASDClinicalseverity stenosisseverity AORTICSTENOSIS ATRESIA VALVULARIfsevere hypoplasticLV fatalSUB valvular subaortic AorticwallTHICKBELOWcuspsSUPRA valvularAorticwallTHICKABOVEcuspsinascendingaorta HEARTDISEASE CONGENITAL CHD ISCHEMIC IHD HYPERTENSIVE HHD VALVULAR VHD MYOPATHIC MHD SYNDROMESofIHD AnginaPectoris Stable UnstableMyocardialInfarction MI AMI ChronicIHD CHF CIHD SuddenCardiacDeath SCD Acute CoronarySyndromes UNSTABLEANGINAAMISCD SuddenCardiacDeath IHDRISK NumberofplaquesDistributionofplaquesSize structureofplaques ACUTECORONARYSYNDROMES Theacutecoronarysyndromesarefrequentlyinitiatedbyanunpredictableandabruptconversionofastableatheroscleroticplaquetoanunstableandpotentiallylife threateningatherothromboticlesionthroughsuperficialerosion ulceration fissuring rupture ordeephemorrhage usuallywithsuperimposedthrombosis EPIDEMIOLOGY milliondieofIHDyearlyinUSA1millionin1963 Why PreventionofcontrolcontrollableriskfactorsEarlier betterdiagnosticmethodsPTCA CABG arrythmiacontrol90 ofIHDpatientshaveATHEROSCLEROSIS nosurprisehere ACUTECORONARYSYNDROMEFACTORS ACUTEPLAQUECHANGE InflammationThrombusVasoconstriction MOSTIMPORTANT ACUTEPLAQUECHANGE Rupture RefissuringErosion Ulceration exposingECMAcuteHemorrhage NB PlaquesdoNOThavetobeseverelystenotictocauseacutechanges i e 50 ofAMIresultsfromthrombosesofplaquesshowingLESSTHAN50 stenosis INFLAMMATION EndothelialcellsreleaseCAMs selectinsT cellsreleaseTNF IL 6 IFN gammatostimulateandactivateendothelialcellsandmacrophagesCRPpredictstheprobabilityofdamageinanginapatients THROMBUS TotalocclusionPartialEmbolization VASOCONSTRICTION CirculatingadrenergicagonistsPlateletreleaseproductsEndotheliallyreleasedfactors suchasendothelin ANGINAPECTORIS Paroxysmal sudden Recurrent15sec 15min Reducedperfusion butNOinfarctionTHREETYPESSTABLE relievedbyrestornitroPRINZMETAL SPASMismainfeature respondstonitro S TelevationUNSTABLE crescendo PRE infarction Q waveangina perhapssomethrombosis perhapssomenontransmuralnecrosis perhapssomeembolization butDISRUPTIONofPLAQUEisuniversallyagreedupon MYOCARDIALINFARCTION Transmuralvs Subendocardial inner1 3 DUH EXACTSAMEriskfactorsasatherosclerosisMostareTRANSMURAL andMOSTarecausedbycoronaryarteryocclusionInthe10 oftransmuralMIsNOTassociatedwithatherosclerosis VasospasmEmboliUNexplained MYOCARDIALRESPONSE PROGRESSIONOFNECROSIS TIMINGofGrossandMicroscopicFindings 1day 3 4days 7days weeks months RE PERFUSION ThrombolysisPTCACABGReperfusionCANNOTrestorenecroticordeadfibers onlyreversiblyinjuredonesREPERFUSION INJURY FreeradicalsInterleukins AMIDIAGNOSIS SYMPTOMSEKGDIAPHORESIS 10 ofMIsare SILENT withQ waves CKMBgoldstandardenzymeTroponin I Troponin TbetterCRPpredictsriskofAMIinanginapatients COMPLICATIONS WallmotionabnormalitiesArrhythmiasRupture 4 5days PericarditisRVinfarctionInfarctextensionMuralthrombusVentricularaneurysmPapillarymuscledysfunction regurgitation CHF CIHD aka ischemic cardiomyopathy ProgresstoCHFoftenwithnopathologicorclinicalevidenceoflocalizedinfarctionExtensiveatherosclerosisNoinfarctH Dpresent SUDDENCARDIACDEATH 350 000inUSAyearlyfromatherosclerosisNON atheroscleroticsuddencardiacdeathincludes CongenitalcoronaryarterydiseaseAorticstenosisMVPMyocarditisCardiomyopathy suddendeathinyoungathletes PulmonaryhypertensionConductiondefectsHTN hypertrophyofUNKNOWNetiology AUTOPSYfindingsinSCD 75 narrowingof1 3vesselsHealedinfarcts40 ARRHYTHMIA isoftenaveryconvenientconclusionwhennoanatomicfindingsarepresent i e wastebasket diagnosis HEARTDISEASE CONGENITAL CHD ISCHEMIC IHD HYPERTENSIVE HHD VALVULAR VHD MYOPATHIC MHD HHD Left DEFINITION Hypertrophicadaptiveresponseoftheheart whichcanprogress MyocardialdysfunctionCardiacdilatationCHFSuddendeath NEEDEDforDIAGNOSIS LVH LV 2 0and orHeart 500gm HTN 140 90 PREVALENCE WHAT ofUSApeoplehavehypertension PREVALENCE WHAT ofUSApeoplehavehypertension Answer 25 HISTOPATHOLOGY INCREASEDFIBER MYOCYTE THICKNESSINCREASEDnuclearsizewithincreased blockiness boxcarnucleus CLINICAL EKG SummaryofLVHCriteria1 R I S III 25mm2 S V1 R V5 35mm3 ST Tsinleftleads4 R L 11mm5 LAE othercriteriaPositiveCriteria 1 possible2 probable3 definite ATRIALFIBRILLATIONWhy CHF cardiacdilatation pulmonaryvenouscongestionanddilatation COURSE NORMALlongevity deathfromothercausesProgressiveIHDProgressiverenaldamage hemorrhagicCVA Whicharteries CHF HHD Right CORPULMONALE ACUTE MassivePECHRONIC COPD CRPD Pulmonaryarterydisease chestwallmotionimpairment DiseasesofthePulmonaryParenchymaChronicobstructivepulmonarydiseaseDiffusepulmonaryinterstitialfibrosisPneumoconiosesCysticfibrosisBronchiectasisDiseasesofthePulmonaryVesselsRecurrentpulmonarythromboembolismPrimarypulmonaryhypertensionExtensivepulmonaryarteritis e g Wegenergranulomatosis Drug toxin orradiation inducedvascularobstructionExtensivepulmonarytumormicroembolism DisordersAffectingChestMovementKyphoscoliosisMarkedobesity pickwickiansyndrome NeuromusculardiseasesDisordersInducingPulmonaryArterialConstrictionMetabolicacidosisHypoxemiaChronicaltitudesicknessObstructiontomajorairwaysIdiopathicalveolarhypoventilation HEARTDISEASE CONGENITAL CHD ISCHEMIC IHD HYPERTENSIVE HHD VALVULAR VHD MYOPATHIC MHD ValvularHD Openingproblems StenosisClosingproblems RegurgitationorIncompetence 70 ofallVHD ASCalcificationofadeformedvalve Senile calcificASRheum HeartDis MSRheumaticHeartDisease AORTICSTENOSIS2XgradientpressureLVH ischemiaCardiacdecompensation angina CHF50 diein5yearsifanginapresent50 diein2yearsifCHFpresent MITRALANNULARCALCIFICATION Calcificationofthemitral skeleton UsuallyNOdysfunctionRegurgitationorStenosispossibleF M REGURGITATIONS ARRheumaticInfectiousAorticdilatationsSyphilisRheumatoidArthritisMarfanMRMVPInfectiousFen PhenPapillarymuscles chordaetendinaeCalcificationofmitralring annulus MitralValveProlapse MVP MYXOMATOUSdegenerationofthemitralvalveAssociatedwithconnectivetissuedisorders Floppy valve3 incidence F MEasilyseenonechocardiogram MVP CLINICALFEATURES UsuallyasymptomaticMid systolic click Holosystolicmurmurifregurg presentOccasionalchestpain dyspnea97 NOuntowardeffects3 Infectiveendocarditis mitralinsufficiency arrythmias suddendeath RHEUMATICHeartDisease FollowsagroupAstrepinfection afewweekslaterDECREASEin developed countriesPANCARDITIS ACUTE Inflammation Aschoffbodies Anitschkowcells Pancarditis Vegetationsonchordaetendinaeatleafletjunction CHRONIC THICKENEDVALVESCOMMISURALFUSIONTHICK SHORT CHORDAETENDINAE CLINICALFEATURES MigratoryPolyarthritisMyocarditisSubcutaneousnodulesErythemamarginatumSydenhamchorea INFECTIOUSENDOCARDITIS MicrobesUsuallystrepviridansOftenStaphaureusinIVDusersEnterococciHA EK normaloralflora HemophilusinfluenzaeActinobacillusCardiobacteriumEikenellaKingellaFungi rickettsiae chlamydia INFECTIOUSENDOCARDITIS Acute 50 mortality course days SUB acute LOWmortality course weeks VEGETATIONS INFECTIVE 5mmNON Infective 5mm DIAGNOSIS MMm Mmmm mmmmm MAJORPositivebloodculture s indicatingcharacteristicorganismorpersistenceofunusualorganismEchocardiographicfindings includingvalve relatedorimplant relatedmassorabscess orpartialseparationofartificialvalveNewvalvularregurgitationminorPredisposingheartlesionorintravenousdruguseFeverVascularlesions includingarterialpetechiae subungual splinterhemorrhages emboli septicinfarcts mycoticaneurysm intracranialhemorrhage JanewaylesionsImmunologicphenomena includingglomerulonephritis Oslernodes Rothspots rheumatoidfactorMicrobiologicevidence includingsinglecultureshowinguncharacteristicorganismEchocardiographicfindingsconsistentwithbutnotdiagnosticofendocarditis includingnewvalvularregurgitation pericarditis NON infectiveVEGETATIONS 5mmPETrousseausyndrome migratorythrombophlebitiswithmalignancies s pSwan GanzLibman SakswithSLE bothsidesofvalve CarcinoidSyndrome EpisodicskinflushingCrampsNausea VomitingDiarrhea serotonin 5HIAAinurineFIBROUSINTIMALTHICKENINGRV Tricuspidvalve Pulmonicvalve allRIGHTside SimilartowhatFen PhendoesontheLEFTside ARTIFICIALVALVES MechanicalXenografts porcine 60 havecomplicationswithin10years HEARTDISEASE CONGENITAL CHD ISCHEMIC IHD HYPERTENSIVE HHD VALVULAR VHD MYOPATHIC MHD PERICARDIALDISEASE CARDIOMYOPATHIES InflammatoryImmunologicMetabolicDystrophiesGeneticIdiopathic DILATED DCM SY stolicdysfunctionHYPERTROPHIC HCM DIA stolicdysfunctionRESTRICTIVE RCM DIA stolicdysfunction DILATEDcardiomyopathy Chamberthickness notjustLVH AdultsProgressivelydecliningLVEFLVEF prognosis50 diein2years3MaincausesMyocarditisETOHAdriamycin Path 4chamberdilatationHypertrophyInterstitialFibrosis DCM ArrhythmogenicRightVentricularCardiomyopathy ArrhythmogenicRightVentricularDysplasia ThisisanuncommondilatedcardiomyopathypredominantlyRIGHTventricle SoisNAXOSsyndrome HYPERTROPHICcardiomyopathy AlsocalledIHSS IdiopathicHypertrophicSubaorticStenosis GENETICdefectsinvolving Beta myosinheavychainTroponinTAlpha tropomyosinMyosinbindingproteinCPATHOLOGY Massivehypertrophy Asymmetricseptum DISARRAYofmyocytes INTERSTITIALfibrosisCLINICAL chambervolume SV diastolicfilling RESTRICTIVEcardiomyopathy idiopathic ventricularcomplianceChieflyaffectsDIASTOLENORMALchambersizeandwallthicknessTHREEsimilardiseasesaffectingpredominantlytheSUBENDOCARDIALarea EndomyocardialFibrosis Africanchildren LoefflerEndomyocarditis eosinophilicleukemia EndocardialFibroelastosis infants MYOCARDITIS INFLAMMATIONofMYOCARDIUMChieflymicrobialCOXACKIEA B CMV HIVTrypanosomacruzi Ch