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1、ChapterVIDiseasesofCardiovascularSystem(心血管系统疾病心血管系统疾病)CardiovascularsystemHeartBlood vessels“Pump” Moremorbidity&mortality - Approximately half of all death caused by disorders of circulatory system - In US, myocardial infarction alone is responsible for 20-25% of all deathSystemicPathologyEtiology
2、,PathogenesisPathologicmorphologyClinico-pathologicalcorrelationConsequenceGeneralpathologySystemicpathologyExample: Myocardial infarctionCoagulative necrosis Granulation tissueScarArrhythmiasmyocardial ruptureVentricular aneurysmContractile dysfunction Heart failureshock, deathMorphologyConsequence
3、sCardiovasculardiseasesHeartBlood vesselsIschemicheartdiseaseAtherosclerosisHypertensionRheumaticHeartDiseaseValvularheartdisease(InfectiveEndocarditis)MyocarditisCardiomyopathyLarge(Elastic):Aorta&largebranches,pulmonaryarteriesMedial(Muscular):Coronary,renalarteriesSmall(=1.0cmstreaks,oilredstaini
4、ng(+)Ostiaofbranches-Fattystreak:foamcells-MayevolveintoadvancedlesionsordisappearMicroscopy2.Fibrousplaqueandatheroscleroticplaque(纤维斑块和粥样斑块纤维斑块和粥样斑块)Gross:whitetoyellow,red-brownwiththrombosisoverthesurface0.31.5cmcancoalescetoformlargermassesThebasicstructureofanatheromatousplaqueMicroscopyMasson
5、trichromestainF:fibrouscapC:acentralnecrotic(lipid)coreL:lumenTheinternalandexternalelasticmembranesaredestroyedThemediaisthinnedunderthemostadvancedplaqueScatteredinflammatorycells,calcification,andneovascularizationatthejunctionofthecapandcoreClinicallyimportantchangesofatheroscleroticplaquesHemor
6、rhageintoaplaqueRupture,ulceration,orerosionthrombusformationAtheroembolismCalcificationAneurysmformation：动脉瘤、夹层动脉瘤PlaqueruptureAcutecoronarythrombosisonaplaquewithfocalrupture,triggeringfatalmyocardialinfarctionHemorrhageintoplaqueAneurysmAbdominalaortaClinicalconsequencesofatherosclerosisAortaAneu
7、rysmCoronaryA.CoronaryHeartDiseaseCerebralA.Thrombosis,Aneurysm,Hemorrhage,AtrophyRenalA.Infarction,Nephrosclerosis,HypertensionFemoral,Popliteal,TibialA.Intermittentcramp,GangreneIschemicHeartDisease(缺血性心脏病缺血性心脏病)(CoronaryArteryDisease)AtherosclerosisNarroworOcclusionofLumenofCoronaryA.Coronaryperf
8、usionMyocardialdemandIschemia,FunctionDisturbance,InfarctionofHeartEpidemiologyLeadingcauseofmorbidityandmortalityinindustrializednationsAnnually,ahalf-millionAmericansdieofIHDCardiacriskfactors:smokingcessationprogramhypertension&diabetictreatmentcholesterol-loweringagentsNormalheart“Pump”Weight:25
9、0270g,240260gWallthickness:leftventricle0.91.0cmrightventricle0.30.4cmatrium0.10.2cmValves：asingledirectionofbloodflowMyocardium：nearlyinexhaustibleBloodsupply:coronaryarteriesCoronaryarteries(冠状动脉冠状动脉)ThefrequenciesofocclusionofvariouscoronaryarteriesandthedistributionoftheresultantinfarctsLeftante
10、riordescendingcoronaryartery40%50%Anteriorandapicalleftventricle;anteriortwothirdsoftheinterventricularseptumRightcoronaryartery30%40%Posteriorwalloftheleftventricle;posterioronethirdoftheinterventricularseptum；rightventricleLeftcircumflexcoronaryartery15%20%lateralwalloftheleftventricleLesionsofCor
11、onaryAtherosclerosisPlaquechanges:thrombosis,hemorrhage,vasospasmCriticalstenosis:=75%Grade of Occlusion: I级级76%PlaqueruptureAcutecoronarythrombosisonaplaquewithfocalrupture,triggeringfatalmyocardialinfarctionMassiveplaquerupturewiththrombus,triggeringafatalmyocardialinfarctionClinicalPresentations1
12、.Anginapectoris2.Myocardialinfarction3.Chroniccoronaryheartdisease4.SuddencoronarydeathAnginapectoris(心绞痛心绞痛)Anintermittentchestpaincausedbytransient,reversiblemyocardialischemia(1)Stable-Afixedatheroscleroticnarrowing(usually75%)-Occurinthesettingofincreaseddemands-Relievedbyrest(reducingdemand)orb
13、yadministrationofnitroglycerin(vasodilator)(2)Unstable-Afixedatheroscleroticnarrowing(usually90%)-Occurprogressivelyatlesslevelsofexertionorevenatrest(3)Variant-Causedbyvasospasm-OccuratrestAcrushingorsqueezingsubsternalsensation,mayradiatedowntheleftarmMyocardialInfarction(MI，心肌梗死心肌梗死)Necrosisofhea
14、rtmuscleresultingfromischemiaMostMIsarecausedbyacutecoronaryarterythrombosisPlaquedisruptionPlateletaggregation&vasospasmThrombosisOccludingthecoronaryarterylumenIschemiaMyocardialResponsetoIschemiaBiochemistry:Withinsecondsaerobicglycolysis,ATPFunction&morphology:Withinaminuterapidlossofcontractili
15、ty,ultrastructuralchangesreversible2040minutescoagulationnecrosisirreversiblePromptinterventionThrombolysis(溶栓)Angioplasty(血管成形术)Coronary arterial bypass graft(血管搭桥)MORPHOLOGYMItypicallybeginsinthesubendocardialregionMIusuallyreachesitsfullsizewithin3to6hoursPatternsofinfarction Depending on The inv
16、olved vessel The duration of the occlusion Metabolic demands of the myocardium Extent of collateral supply1. Transmuralinfarctions2.Subendocardialinfarctions3.MicroscopicinfarctsGrossMIslessthan12hoursoldusuallyarenotgrosslyapparentBy12to24hoursafterMI,aninfarctusuallycanbegrosslyidentifiedbyared-bl
17、uediscolorationcausedbystagnated,trappedbloodMap-likeMicroscopyCoagulationnecrosis/inflammationFormationofgranulationtissueOrganization&scar-AcuteMI-Rupture-Scar(remoteinfarction，陈旧性梗死)“Irregular”map-likeAreasofnecrosis(arrow);Theanteriorscar(arrowhead);Hemorrhage(asterisk)duetoventricularrupture1da
18、y-coagulationnecrosisedemawavyfibers3-4daysCompletecoagulationnecrosisofmyofibersHeavyneutrophilicinfiltrate7-10daysWell-developedphagocytosis3wkGranulationtissueCollagenfibersScar-Richcollagenfibers-ResiduemyofibersReperfusioninjuryRestorationofbloodflowgreaterdamage Mitochondrial dysfunction; Myoc
19、yte hypercontracture (高度挛缩); Free radicals; Leukocyte aggregation; Platelet and complement activationClinicalFeaturesThechestpaincannotberelieved“Silent”infarctsarecommonindiabeticpatients&elderlypersonsRapid&weakpulseDiaphoretic（出汗）（出汗）&nauseous（恶心）（恶心）,particularlywithposteriorwallMIsElectrocardio
20、graphic abnormalitiesQwaves,STsegmentchanges,&TwaveinversionslethalArrhythmiasLaboratory evaluationTroponins（肌钙蛋白）andCK-MB（肌酸激酶同工酶）havehighspecificityandsensitivityformyocardialdamageConsequences&ComplicationsofMIDependingon-infarctsize-site-fractionalthicknessofthemyocardialwallthatisdamaged1.Contr
21、actiledysfunction Cardiogenic shock:massiveMIs,involving40%oftheleftventricle2.Arrhythmias(心律失常)Myocardial irritability&conduction disturbancesSuddendeath3.MyocardialruptureMostcommonbetweendays3-7afterMIsParticularlyinpapillarymuscleandventricularwallofleftventricle,andventricularseptum4.Pericardit
22、is5.Chamberdilation6.Muralthrombusthromboembolism7.Ventricularaneurysm-AlatecomplicationoflargetransmuralMIs-Thebulgingofthenoncontractilefibrousmyocardiumduringsystole-Athin-walled,fibrousoutpouchingoftheventricularwall-OftenwithamuralthrombusChronicIschemicHeartDiseaseThe development of progressiv
23、e congestive heart failure as a consequence of long-term ischemic myocardial injuryCoronaryarteries:moderatetosevereatherosclerosisHeart:Gross-enlarged,leftventriculardilationandhypertrophy,patchyscars,muralthrombiMicroscopy-myocardialhypertrophy,fibrosis,subendocardialmyocytevacuolizationClinicalfe
24、atures:progressiveanginapectoris,MI,arrhythmiasSuddenCardiacDeathUnexpecteddeathfromcardiaccauses,occurringwithin24hoftheonsetofsymptomsCoronaryarterydiseasesinadultsNon-atheroscleroticcausesinyoungervictimsAlethalarrhythmia,eg.VentricularfibrillationHypertensionAdultbloodpressureGradeSystolicpressu
25、re(mmHg)Diastolicpressure(mmHg)Normal=130=140and/or=90Borderline13013985-89ClassificationofHypertensionEssential(idiopathic):9095%Arterioles/smallarteriesBenign:Malignant=9:1Secondary:diseasesofadrenalglands,renaldiseases,renalarterystenosisEssential(Primary,Idiopathic)HypertensionAchronicdiseasewit
26、hspasm and sclerosis of arteriole and small artery causedby different factors, andeventuallyresultinginthelesions of organsPathogenesisTheBPlevelisdeterminedbytheinteractionofmultiplegenetic,environmental,anddemographicfactorsthatinfluence2hemodynamicvariables:cardiac outputandtotal peripheral resis
27、tanceMORPHOLOGYHyalinearteriolosclerosis(benignhypertension)HyperplasticarteriolosclerosisNecrotizingarteriolitis(malignanthypertension)Thickening of the walls with narrowing of the lumenProcessesofbenignhypertensionStage1:Functionaldisturbance（功能障碍期）（功能障碍期）SpasmofarterioleandsmallarteriesStage2:Cha
28、ngesofvascularsystem（动脉病变期）（动脉病变期）Smallartery&ArteriolehyalinedegenerationLarge&medialarteryatherosclerosisStage3:Lesionsoforgans（器官病变期）（器官病变期）Heart-HypertensiveheartdiseaseLeftventricularhypertrophyEarlystageConcentrichypertrophyLaterAcentrichypertrophydilationofcardiacchambersLM:Myocyteshypertroph
29、y,withprominentnuclearenlargementandhyperchromasia(“boxcarnuclei”)InterstitialfibrosisKidneyArterionephrosclerosisGrosssymmetricallyatrophicdiffuse,finegranularityofsurfaceMicroscopyhyalinearteriolosclerosisischemicatrophycompensatedhypertrophy&dilationArrangedatintervalsBrainHypertensiveencephalopa
30、thyEdema,softening(microinfarct),microaneurysmsHemorrhage:basalganglia基底核（内囊）lenticulostriateartery(豆纹动脉branchingsquarefromarteriaecerebrimedia)MalignanthypertensionNecrotizingarteriolitis:fibrinoidnecrosisHyperplasticarteriolosclerosisonion-skin,concentric,laminatedthickeningofthewallsBenignvsMalig
31、nantHypertensionBenignMalignantIncidencehigh(90%)low(10%)AgemiddleorsenioryoungerormiddleBP140/90mmHg200/120mmHgSymptomlightsevereLesionhyalineofarteriolefibrinoidnecrosisofarteriole&smallarteriesCourse10yr12yrCausesofdeathcerebralhemorrhage,renalfailure,heartfailureuremia(95%)Rheumatism(风湿病）风湿病）Rhe
32、umaticfeverisan acute, immunologically mediated, multisystem inflammatory disease. FollowinganepisodeofgroupA-hemolyticstreptococcalinfections(usuallypharyngitis)afteranintervalofafewweeksOccuringinheart,synovium,joints,bloodvessels,skin,etc.AcuterheumaticcarditisChronicvalvulardeformitiesAfteranini
33、tialattack,thereisincreasedvulnerabilitytoreactivationofthedisease.Just like a crazy dog, licking all over the body and finally biting the heartEtiologyandPathogenesisImprovedsocioeconomicconditionsRapiddiagnosisandtreatmentAhypersensitivityreactioninducedbygroupAstreptococci(1)Symptomstypicallydeve
34、lopabout23weeksafterinfection.(2)Streptococciareabsentfromthelesions.AntibodiesdirectedagainsttheMproteinsofgroupAstreptococcicross-reactwithnormalproteinspresentintheheart,joints,andothertissues.TheincidenceandmortalityAnautoimmuneresponseagainstself-antigensGeneticsusceptibilityRheumaticfeveroccur
35、sinonlyabout3%ofpatientswithgroupAstreptococcalpharyngitisMORPHOLOGYBasicpathologicchanges3phases Necrotic&exudativephaseFibrinoidnecrosis,inflammatoryinfiltrates Regeneration(proliferativephase)Rheumaticgranuloma(rheumaticbody,Aschoffbody) FibrosisreoccurFibrinoidnecrosis（纤维素样坏死）Rheumaticbody(Ascho
36、ffbody)-Oftenlieincloseproximitytoasmallvessel-Acentralfocusoffibrinoidnecrosissurroundedbyachronicmononuclearinflammatoryinfiltrate-AschoffcellsAschoffcellsRheumaticHeartDisease1.Acute“Pancarditis ”（全心炎）（全心炎）(1)RheumaticendocarditisMitral(二尖瓣)50%;Mitral+Aortic(二尖瓣+主动脉瓣)50%Edematous,thickened,fibrin
37、oidnecrosis,verrucae(疣状物)(vegetation(赘生物),mayresolveorprogress)(2)Rheumaticmyocarditis:Aschoffbodies(3)Rheumaticpericarditis:Fibrinousexudate(corvillosum(绒毛心),generallyresolvewithoutsequelae)Rheumaticendocarditis主动脉瓣二尖瓣Rheumaticmyocarditis风湿小体Rheumaticpericarditis纤维蛋白性渗出浆液性渗出2.ChronicCharacterizedby
38、organizationoftheacuteinflammation&subsequentscarringFibrousscarThemitralvalvesexhibitleafletthickening,commissuralfusionandshortening,andthickeningandfusionofthechordaetendineae.Valvularstenosis,regurgitationMicroscopy:neovascularization,diffusefibrosisthickening,commissuralfusionandshorteningofval
39、vesFishmouth(mitralvalve)InflammatoryneovascularizationPathologicChangesinOtherOrgans Rheumaticarthritis(风湿性关节炎)Largerjoints,migratorypolyarthritisWithoutsequelae SkinErythemaannularecentrifugum(离心性环形红斑)subcutaneousnodules(皮下结节) Rheumaticarteritis(风湿性动脉炎) BrainNeurondegeneration,gliacellproliferatio
40、nextrapyramidal(椎体外系)involved,choreaminor(小舞蹈病)ClinicalFeatures AntibodiestooneormorestreptococcalenzymesAnti-StreptolysinO SignsPericardialfrictionrubsWeakheartsoundsTachycardia(心动过速)orotherarrhythmiasCongestiveheartfailure5%deathInfectiveEndocarditisDefinitionInfectionofthecardiacvalvesormuralsurf
41、aceoftheendocardium,resultingintheformationofbulky, friablevegetationCauseAnytypeofmicroorganism,mostbybacteriaAntibiotictherapyblursthedistinction.Aparticularlydifficultinfectiontoeradicatebecauseoftheavascularnatureoftheheartvalves.ClassificationFormsOrganismValvesAcuteHighvirulencePreviouslynorma
42、lSubacuteLowvirulencePreviouslyabnormalPathogenesis Conditionsthatincreasetherisk(1)Preexistingcardiacabnormalities:rheumaticheartdisease(2)Prostheticheartvalves(瓣膜修复后):nodifferencebetweenmechanicalandbio-prostheticvalves(3)Hostfactors:DM,immunodeficiency,intravenousdrugabuse BacteremiaAninfectionel
43、sewhereApreviousdental,surgicalorotherinterventionalprocedure,e.g.urinarycatheterization(导尿管插入)IntravenousdrugabusersMORPHOLOGYThehallmarkisthepresenceofvalvular vegetationscontainingbacteriaorotherorganisms.Aorticandmitralvalvesarethemostcommonsitesofinfection.SBESBE“repair”“repair”ABEABE“damage”“d
44、amage” Causativeorganismlowvirulencea-hemolyticstreptococcihighvirulencestaphylococcusaureusPathogenesisPreexistingabnormalityNativevalvesCommonsitesmitral/aorticvalvesaorticvalvesFriable , bulky vegetationscontainbacteria,single/multiple,1valveInfluence:typeoforganisms,degreeofhostreaction,previous
45、antibiotictherapyMicroscopicallyPlatelet,fibrin,inflammatoryinfiltrates,bacteriaGranulation,fibrosis,calcification,chronicinflammatoryinfiltratesdestructionofthevalves&vicinity,ringabscesses(inperivalvulartissue)Sequelaechronicvalvulardisease,regurgitationRupture,suddendeath,chronicvalvulardiseaseSB
46、ESBE“repair”“repair”ABEABE“damage”“damage”SitesotherthanheartSystemicemboli,anemicinfarcts,GNSystemicemboli,septicinfarcts(suppuration),ConsequenceHealing,chronicvalvulardiseaseDeath,SBEABEofaorticvalveTricuspidvalve,rightatriumOftennotedinintravenousdrugabusersABEofaorticvalve,multipleabscessesEmbo
47、lizationviacoronaryarterySterile&nomicroorgnismsSmalltomedium-sized,bland,nondestructivevegetationsatthelineofvalveclosure UsuallyfoundonpreviouslynormalvalvesPathogenesis?Subtle endothelial abnormalities; Hypercoagulable states; malignancies particular adenocarcinoma, SLE, etc.NonbacterialThromboti
48、cEndocarditis(NBTE,非细菌性栓塞性心内膜炎)Gross:Singleormultiplenodules,alongthevalveclosure,5mmMicroscopy:Platelet,fibrin&otherbloodcomponentsConsequences:ResolvespontaneouslyLamblsexcrescences(delicate strands of fibrous tissue)Clinicalfeatures:Asymptomatic,systemicemboli&infarctsApotentialnidusforbacteriale
49、ndocarditisnon-bacterialthromboticendocarditisNBTEComparisonBetweenDiverseValvularVegetationsSmall,warty(疣状),inflammatoryvegetations,alongthelinesofvalveclosureIrregular,large,briskdestructionofchordaetendineaeEmbolizeSmalltomedium,sterile,non-destructive,atthelineofvalveclosureEmbolizeRheumaticendo
50、carditisInfectiveendocarditisValvularHeartDiseasesAdiversegroupofacquiredorcongenitallesionsStenosis:thick,rigid,commissuralfusion,obstructionIncompetence(insufficiency):thick,rolling,shorteningcommissuralfusionregurgitationCombinedvalvulardisease(multivalvulardisease)Stenosisandregurgitationcoexist
51、Anatomyofheart&bloodflowMitralStenosis(二尖瓣狭窄二尖瓣狭窄)Cause:rheumaticheartdiseaseHemodynamicandheartchanges:Earlystage：hypertrophy&dilationofleftatriumLatestage：edemaandcongestionofpulmonaryhypertrophyanddilationoftherightheartrightHeartfailureClinicalfeatures:Diastolicmurmurattheauscultationareaofmitra
52、lvalvePinkcoloredfoamysputumMuralthrombus,embolizeCongestionofmanyorgans二尖瓣狭窄二尖瓣狭窄附壁血栓形成附壁血栓形成“PyriformHeart”（梨形心）（梨形心）MitralRegurgitation(二尖瓣关闭不全二尖瓣关闭不全) Cause:rheumaticheartdisease Hemodynamicandheartchanges:HypertrophyanddilationofthefourchambersLeftandRightHeartFailureEdemaandcongestionofpulmona
53、ryPulmonaryhypertensionClinicalfeatures:SystolemurmurattheauscultationareaofmitralvalveGlobalHeart（球形心）（球形心）AorticStenosis(主动脉瓣狭窄主动脉瓣狭窄) Cause:rheumaticheartdisease Hemodynamicandheartchanges:HypertrophyanddilationofthefourchambersLeftandrightHeartFailureEdemaandcongestionofpulmonaryPulmonaryhyperte
54、nsionClinicalfeatures:SystolemurmurattheauscultationareaofAorticValve;anginapectoris(心绞痛)AorticRegurgitation(主动脉瓣关闭不全主动脉瓣关闭不全) Cause:rheumaticheartdisease,infectiveendocarditis;syphiliticarteritis Hemodynamicandheartchanges:Hypertrophyanddilationofthefourchambers,especiallytheleftventricleLeftandRig
55、htHeartFailureEdemaandcongestionofpulmonaryPulmonaryhypertensionClinicalfeatures:Diastolicmurmurattheauscultationareaofaorticvalveanginapectoris;widepulsepressureBoot-shapedHeart（靴型心）（靴型心）Myocarditis(心肌炎心肌炎) DefinitionAgroupofinflammatoryprocessesprimarilytargetingthemyocardium Cause:(1)Infections:C
56、hlamydia,rickettsia,bacteria,fungi,etc.(2)Immune-mediatedreactions postviral;postbacteria;systemiclupuserythematosus;drughypersensitivity(e.g.methyldopa,sulfonamides),transplantrejection(3)Unknown:giantcellmyocarditisViralMyocarditis(病毒性心肌炎病毒性心肌炎)CauseCoxsackievirusesAandB,andotherenteroviruses(most
57、common)Direct damage to myocardium Immune-mediated injuryMorphologyGross:Heartisdilated.Myocardiumisflabbyandoftenmottledwithpaleandhemorrhagicareas.Microscopy:EdematousAdiffuselymphocyticinfiltrateMyocytedegenerationand/ornecrosisClinicalfeaturesBroadspectrumFromanasymptomaticstatetoseverecongestiv
58、eheartfailureSelf-limited,somemaydevelopchroniccongestiveheartfailureCardiomyopathies(心肌病心肌病)Heartdiseasesresultingfromaprimaryabnormalityinthemyocardium “Heart muscle diseases”DilatedHypertrophicRestrictiveDilatedCardiomyopathy(扩张性心肌病扩张性心肌病)Progressivecardiachypertrophy,dilationandcontractile(systo
59、lic)dysfunctionCauseAlargenumberofdifferentmyocardialinsults Genetic; alcohol; peripartum; myocarditis; hemochromatosis; chronic anemia; doxorubicin (Adriamycin); sarcoidosis; idiopathic MorphologyGrossEnlargedandflabbywithweightsoftenexceeding900gDilationandhypertrophyofallchambersFragilemuralthrom
60、bi&subsequentemboliMicroscopyMyocytehypertrophyInterstitialfibrosisWavyfiberchangeScantymononuclearinflammatoryinfiltrate心腔扩大，心尖圆钝Masson三色染色显示间质纤维组织增生ClinicalFeaturesThemostcommonformofcardiomyopathy(90%)Thefundamentaldefectisineffective contractionejectionfractionfreewalloftheleftventricleAsymmetri
61、cseptalhypertrophyassociatedwithobstructionduringsystoleMicroscopyMarkedmyocytehypertrophyHaphazardarrangementofhypertrophied,abnormallybranchingmyocytesInterstitialfibrosisClinicalfeaturesAninabilitytofillahypertrophicleftventricleduringdiastoleEjectionisforcefulbutineffectivelimitationofcardiacout
62、put,asecondaryincreaseinpulmonaryvenouspressureAharshsystolicejectionmurmurMyocardialischemiaiscommon,andanginalpainisfrequentVentriculararrhythmias,suddendeathInfectiveendocarditisincreased.Restrictivecardiomyopathy(限制性心肌病限制性心肌病)Aprimarydecreaseinventricularcompliance,resultinginimpaired,ventricula
63、rfillingdiastole(diastolic dysfunction)CauseRadiationfibrosis,amyloidosis,sarcoidosis,orproductsofinbornerrorsofmetabolismGrossFirmmyocardiumLMInterstitialfibrosisCongenitalheartdisease(先天性心脏病先天性心脏病)AbnormalitiesoftheheartorgreatvesselsthatarepresentatbirthArisesfromfaultyembryogenesisduringgestatio
64、nalweeks3through8Threemajortypes:1,malformationscausingaleft-to-rightshunt2,malformationscausingaright-to-leftshunt3,malformationscausingobstructionAtrialseptaldefect,ASD（房间隔缺损）Ventricularseptaldefect,VSD（室间隔缺损）Patentductusarteriosus,PDA（动脉导管未闭）TetralogyofFallot（法洛四联症）马方综合征非发绀型发绀型左心打开,见房间隔有一个圆形的大孔At
65、rialseptaldefect,ASD（房间隔缺损）小儿心脏,右心室打开,室间隔上方有一个小孔Ventricularseptaldefect,VSD（室间隔缺损）心脏标本正面为左心室，见室间隔上部的膜部有一个很大的圆形缺损空洞（红色箭头），缺损口的上方正对着主动脉的开口大部分，而主动脉瓣最里面一个瓣叶内移到右心室（黄色箭头），形成主动脉骑跨，左心室略有扩张，从标本背面观察，可见右心室扩大。TetralogyofFallot（法洛四联症）PrinciplesofCardiacDysfunction1.Failureofthepumpitself2.Anobstructiontoflow3.Regurgitation4.Disordersofcardiacconduction5.DisruptionofthecontinuityofthecirculatorysystemThanks for your attention!QuizAtheromaAshcoffbody
