病理学英文课件：心血管系统疾病

CardiovascularSystemThebloodvesselsTheheartlarge：medium-sized：SmallandarterioleheartelasticmuscularveinscapillariesvesselsarteriesMajorDisordersofCVSAtherosclerosisHypertentionRheumatismAneurysmsInfectiveendocarditisValvularHeartDiseaseCardiomyopathyAtherosclerosis

ArteriosclerosisIntroduction:Arteriosclerosisencompassesanyconditionofarterialvesselsthatresultinathickeningorhardeningofthewallsandaweakeningoftheelascity,itgenerallyincludesthreetypes:Atherosclerosis(ATH)medialcalcificationArteriolosclerosisDefinition:Atherosclerosisisadiseasewhichaffectslargeandmedium-sizearteries,characterizedbyintimalfattydepositsfollowedbyproliferationofsmoothmusclecellsandconnectivetissue,ultimatelywitharteriosclerosis.Asystemicdiseaserelatingtothemetabolismoflipid.Morbidity:AtherosclerosisAtherosclerosis-riskfactorsHyperlipidemiaHypertensionSmokingDiabetesandhyperinsulinemiaGeneticOthersHyperlipidemia

(oneofthemostimportantriskfactors)Hypercholesterolemia-moreresponsiblethanhypertriglyceridemiaforatherosclerosis.HighLDL,VLDL,TGandapoBcausehigherrisk;HDLandapoAactsinreverse,helpspreventatherosclerosisExperimentaldietsinanimalsPlaquesaremostlycholesterolDietary&PharmacologicLoweringofCholesterolHypertensionSmoking:independentriskfactorforMIDiabetesandhyperinsulinemiaGeneticOthers:Age:4-6thdecades;but,thediseasebeginsmuchyoungerage,slowlyprogressive.Sex:MenaremorepronetoATHanditsconsequencesthanarewomen.Aftermenopause,femaleincreaseandby60-70yrsequaltomale.Atherosclerosis-pathogenesisTheresponsetoinjuryhypothesistheroleoflipid:directlyimpairECfunctionthroughincreasedproductionofoxygenfreeradicalincreaseendothelialpermeabilityLDLyieldoxidizedbymacrophagesorEC(ox-LDL)

ox-LDLinduceECdysfunction→increaseexpressionofadhesionmolecule→reinforceadhesionbetweenECandmonocyteincreasemonocyteaccumulation(chemotaxis)inlesioningestedbymacrophages,thusformingfoamcellsstimulatereleaseofGFsandcytokinescytotoxictoECsandFCstheroleofendothelialinjury:earlyendothelialinjury(nondenudingendothelialdysfunction):monocytesandplateletsadhesion→GF→SMCproliferateandelaborateextracellularmatrixendothelialdenudinginjury:plateletsadhesion→GFtheroleofmacrophage:inearlyATH,adheretoendotheliumbymeansofspecificAMsinducedonthesurfaceofdysfunctionalECs→migratebetweenECstolocalizeintheintima→transformintomacrophagesandengulflipid,largelyox-LDL,tobecomefoamcellsgeneratecytokines,chemokines,toxicoxygenspecies,etc.andelaborateGFsthatmaycontributetoSMCsproliferation.theroleofsmoothmusclecellproliferation:severalGFsorchemokinescontributetoSMCproliferateandimmigrateintheintimasecreteGFsPhenotypetransformsecreteECMengulflipidhyperlipidemia--initiatingstep（始动环节）endothelialinjury--originatinglesion（起始病变）monocyteadhesion--earlylesion（早期改变）SMCproliferationandmigration--mainstepinprogressiveATH（进展期主要病变）TheresponsetoinjuryhypothesisAtherosclerosis-morphologylocation:largeandmedium-sizearteriesMorphologyinPathology(*)fattystreaksfibrousplaqueatheromaSubsequentcomplicationThelesionofthemajorarteriesBasicmorphologyFattystreaks:earlystageGrossly:palemultipleyellow,flatspotslessthan1mmindiameterthatcoalesceintoelongatedstreaks.Encounter

since

in

infantsLM:lipid-filledfoamcellsMostofthefoamcellsarisefrommacrophagesandasmallfromsmoothmusclecells

FibrousplaqueGrossly:Paleyellow---palestorwaxandslightlyprotuberantplaqueLM:superficialfibrouscapcomposedofSMCandECMlipidzone:deepisagreatdealoffoamcells,freelipidanddebrisbasalzone:SMC,connectivetissueandinflammatorycells

Atheroma(*)Grossly:differentsizeandnumberlesionsappearinggrey-yellowimpingedonthelumenoftheartery,havingayellowgrumouscoreoflipidandcoveredbyafirm,whitefibrouscapLM:ThesuperficialisdensefibrouscapcomposedofhyalinedegenerativecollagenandSMCimbeddedinECMBelowfibrouscapispinkamorphousmaterial(necroticcore)---disorganizedmassoflipid,cholesterolclefts,debrisfromdeadcellsandfibrin.Foamcells,Tlymphocytesandneovascularizationcanbeenseearoundtheperipheryoflesion.Thedepositsofcalciumwhichstainblue.Ischemicatrophyoftheunderlyingmedia

Complicationofatheroscleroticplague(*)Hemorrhageintoaplaque:raptureofeithertheoverlyingfibrouscaporthethin-walledcapillariesthatvascularizetheplaque→hematomainplaque→aggravatetheocclusion→infarctionRapture:theplaqueshoulder→producemicroemboli,leavetheplaqueulcerationandinducethrombusformationThrombosis:occurondisruptivelesions→exposureofthrombogenicsubstances→partiallyorcompletelyoccludethelumenAneurysm:atrophyofthemediawithlossofelastictissue→hemmorrhageCalcification:calciumdepositsinthenecroticmaterial→arterialwallbecomehardeningandfragileAneurysmsAnanneurysmisanabnormallocalized,permanentdilationofanarteryortheheartcausedbycongenitaloracquiredweaknessinthemedia.typesTrueaneurysmPseudoaneurysmDissectinganeurysmThelesionofthemajorarteriesaorticatherosclerosisLocation:prominentaroundtheposteriorwallandostia,mostseriousinabdominalaorta

Morphology:Atheroscleroticplaqueanditscomplication(→aneurysm)coronaryarteriesrenalarteriesLocation:ostiaorproximalMorphology:atheroscleroticcontractkidneyMesentericarteriesstenosisocclusioncarotidarteriesandcerebricarteriesLocationLesion:BrainatrophyEncephalomalaciacerebralhemorrhageArteriesoftheexterimitiesLocation:Thelowerexterimities–thepoplitealarteriesLesion:stenosis→spasmodicclaudicationobstruction→drygangreneCoronaryAtherosclerosis

AndCoronaryHeartDisease(CHD)

CoronaryAtherosclerosisLocation:theleft＞theright;thelargerbranches＞thesmallerones;proximal＞distal.leftanteriordescendingcoronaryartery----themostfrequentsiteofCA(40%to50%)Andthentherightcoronaryartery(30%to40%)Leftcircumflexcoronaryartery(15%to20%)CoronaryAtherosclerosisCharactersofmorphologySegmentalchanges,crescent-shaped,eccentricconstrictionGrades

Ⅰ≤25%Ⅱ26-50%Ⅲ51-75%Ⅳ＞76%CoronaryHeartDisease(CHD)Localmyocardiallesioncausedbyinsufficiencyorcessationofthecoronarybloodsupplyduetothecoronaryarteriesstenosis.--ischemicheartdisease(IHD)CardiacdiseaseresultingfromcoronaryatherosclerosisanditscomplicationsisreferredtoasatheroscleroticcoronaryheartdiseaseMorethan95%CHDisduetoatheroscleroticcoronaryarterialobstructionCHD-pathogenesisdiminishedcoronaryperfusionincreaseinmyocardialoxygendemandingCHD--typesanginapectorismyocardialinfarctionmyocardialfibrosis/chronicischemicheartdiseaseSuddencoronarydeathAnginapectorisDefinition:acute,transientandreversiblemyocardialischemiccausedbydiminishedcoronaryperfusionor/andincreaseinmyocardialoxygendemanding.AnginapectorisClinicalfeature:isparoxysmalchestpain,occasionallyradiatingdownthemedialaspectoftheleftarm.Classically,anginaisprecipitatedbyactivitiesincreasingmyocardialoxygendemand,suchasexercise,andisrelievedwithinminutesbyrestornitroglycerinMechanismTypicalorstableanginapectorisUnstableanginapectorisPrinzmetalorvariantpectorisAnginapectoris-typesMyocardialinfarctionDefinition:MIisthedevelopmentofadefinedareaofmyocardialinfarctcausedbylocalischemia.ClinicalFeaturescrushingsubsternalchestpainradiatingtoneck,jaw,shoulder,leftarmNOreliefwithNTGCause:Coronaryatherosclerosis(thrombosis)→Prolongedischemiaofover30to45minutes→myocardialinfarcts(typicallybegininthesubendocardialregion).Location:sametothatofCoronaryAtherosclerosisabout50%--leftanteriordescendingcoronaryartery25-30%--rightcoronaryartery15-20%--leftcircumflexcoronaryThesizeoftheinfarctsThesiteoftheocclusionThedegreeofcollateralcirculationTypes:Transmuralinfarcts:involvemostoftheventricularwall,morecommonSubendocardialinfarcts:restrictedtotheinneronethirdofthemyocardium,MultiplesmalllesionTimeGrossMicro1-4hNoneNone4-12hNoneEarlycoagnecrosis,edema,fewPMNs,minimalbleed18-24hslightpallorormottlingPyknosis,cytoplasmiceosinophilia,24-72hPallorCompletenecrosis,heavyNinfiltration3-7dCentralPallor,softMacrophagesappear,disintegrationandwithhyperemiaphagocytosisofnecroticfibersgranulationtissueattheedgeofinfarct10dMaximalyellow,well-developedphagocytosis,prominentshrunken,purplebordergranulation

7-8wFirm,GreyFibrosis,thescarwellestablishedMI-MorphologyNormalmyocardialtissueMI18-24hr

lossofnucleus,contractionbands,coagulativenecrosisMI3-4day–Hemorrhage,inflammation.MI1-2w–GranulationtissueMI2-4W-Resorption,fibrosisMI>4-6W-

ScarrepairLaboratoryevaluationCreatinekinase(CK):CKindex(CK-MB/totalCK)Troponins:cardiactroponinT(cTnT)andtroponinⅠ(cTnⅠ)Lactatedehydrogenase(LD)Myocardialinfarct-complication(*)ruptureoftheheartVentricularaneurysmsMuralthrombiAcutepericarditisOthers:Cardiogenicshock,ArrhythmiaandheartfailureChronicischemicheartdiseaseFocalfibrosisofthemyocardiumisthelesionwithachronic,progressivetypeofmyocardialischemia–myocardialfibrosis.Themyocardiallesionisobservedintheheartofpatientswhohavehadahistoryofattacksofanginapectoris.Clinicalfeature:progressivecongestiveheartfailureandarrythmiasMorphologyCoronaryarteriesmoderatetosevereatherosclerosisTheheartenlargedMyocardialfibrosisandremainingmyocardiumhypertrophyLM:extensivemyocardialfibrosisaccompaniedbyremainingmyocytesbothatrophyandhypertrophy;vacuolationofthescaroplasmofsomemyofibersSuddencardiacdeathSuddendeathMostcasesofsuddendeathcausedbycardiacdiseaseThemostcommoncauseofsuddencardiacdeathisischemicheartdiseaseLethalventriculararrhythmiasIHDsuchasAPorMIAcutemyocardialischemiaCoronaryspasmSummaryoftheCHDQuestion1.Atheroma.2.Pathologicalchangesandsubsequentcomplicationofatherosclerosis.3.Complicationofmyocardialinfarct.Definition:Hypertensionisthepersistentelevationofsystemicarterialpressureabovenormallevel.Normalbloodpressure:B.P.≤18.6/12kPa(140/90mmHg)Criteriaofhypertension:B.P.≥18.6/12kPa(140/90mmHg)HypertensionTypesEssentialhypertension:90-95%.Secondaryhypertension:5-10%Renal.Endocrine.CausesofEH:isunknownGeneticFactorsEnvironmentalFactorsSaltintakeStressOthers:obesity,smoking,physicalinactivityandagePathogenesisofEHBP=

CardiacOutput(CO)

×

PeripheralResistance(PR)BloodvolumeHRContractilityVasoconstrictionbloodwallComplianceViscosityNeuro-humoralregulationGeneticfactorsEnvironmentalfactorsSaltintake↑Sodiumhemostasis

↓

SaltandwaterretentionPlasmaandECFvolume↑Cardiacoutput↑Sympatheticnerverennin-angiotensin↑Vascularreactivity↑vasoconstrictionDefectsinvascularsmoothgrowthandstructure

Vascularwallthickness

↑Totalperipheralresistance↑VascularcaliberstenosishypertensionautoregulationAld↑SMChypertrophyandhyperplasia+EssentialhypertensionBenignhypertension:In95%ofEHMalignantHypertension:

In1~5%ofEHBenignhypertension(*)pathologicalstagesFunctionaldisordersArterieschangephaseVisceralchangephaseFunctionaldisordersInearlystage,arteriolesandsmallarteriesconstrictintermittently.Thesymptomsareheadachesordizzyspells.TheB.P.levelislabileanddecreasessignificantlywithbedrest.ChangesofBloodvesselsHyalinearteriolosclerosis:thisvascularlesionconsistsofahomogeneous,pinkhyalinethickeningofthewallsofarterioleswithlossofunderlyingstructuraldetailandwithnarrowingofthelumen.Ofteninvolvedinafferentglomerulararteriole,leincentralarterioleThereddishhomogeneousmaterialfrom……Smallandmedium-sizedarteriesMedialmuscularhypertrophy,proliferationandlaterfibrosisIntimalandmedialcollagenfibersandelasticfiberproliferationoftheelasticlaminaIntimalproliferationLarge-sizedarteries:

gentlyinvolvedinOftenaccompaniedbyatherosclerosisinaortacausedbyhypertensionClinicalfeaturesofthisstage:Thesymptomsincludeheadaches,fatigability,insomnia,dizzyspells,andpalpitation.Thediagnosisisestablishedbymeasurementofthebloodpressure.TheBPishigherandmorefixed.ChangesoforgansHeart

Leftventricularhypertrophy—theheartisenlarged,thewalloftheheartisthickandtheweightexceeds400g→eventuallyleft-sidedcongestiveheartfailuredevelops.Clinicalfeatures:hypertensiveheartdiseaseLeftVentricularHypertrophyLeftVentricularHypertrophyKidneys(hypertensivenephrosclerosis)Grossly:decreasedinsize,lightandfirm,withasurfaceofdiffuse,finegranularity--“primarygranularatrophicofthekidney”.hypertensivenephrosclerosisLM:hyalinearteriolosclerosisGlomerulartuftshyalinedegenerationwiththeircorrespondingtubularatrophyandinterstitialfibrosis.Ascantinterstitiallymphocyticinfiltrate.remainingnephroncompensatoryhypertrophyandtubulardilatationClinicalFeatures:Earlyonlyslightlyimpaired;Later,decreasedconcentratingpowerresultinnocturia,slightpolyuria,andaslightalbuminuria→uremia.Braincerebraledema:hypertensiveencephalopathyandhypertensivecrisisEncephalomalacia:multiplesmallinfarctscerebralhemorrhage:mostsevercomplicationofEHRetina

Funduscopicexaminationrevealsretinalarteriolosclerosis—silerwireappearance;exudates,andpapiledemaOutcomeofEH:Thecourseofbenignhypertensionisprotractedandcoversseveraldecades.MostpatientshavefewsymptomsandeventuallydieofIHD,heartfailureandstroke.MalignantHypertension:Thebloodpressureexceeds200/120mmHg,andthediastolicpressureisusuallyover130mmHg.YoungerthanbenignhypertensionRapidlyprogressiveandorgandamageRenalfailureHypertensiveencephalopathyLeftventricularfailurePathologicalchanges(*)Necrotizingarteriolitis

Hyperplasticarteriolosclerosis:Themajorinjuredorgans:kidneyandbrainFibrinoidnecrosisofafferentarteriole(PASstain)HyperplasticArteriolosclerosisOnionSkinThickeningOfarterioles.NarrowLumenHyperplasticarteriolitis(onoin-skinlesion)Outcome:Thecourseisrapid,anddeathoccurswithin2yearsofonset,theaveragedurationbeing8months,Deathisusuallyduetouremia,congestiveheartfailure,orboth,oroccasionallytocerebralhemorrhage.RheumatismDefinitionalsocalledrheumaticfeverisahypersensitivityinflammatorydiseaserelatingtotheinfectionofgroupAstreptocci.Location:Itaffectstheconnectivetissuesinthewholebody,withthedamageinthe

heart,joints,arteries,brainetal.Incidence:thepeakincidenceisbetween10and15yearsofage,mostcommoninsichuanEtiologyandpathogenesis:notclearEtiology:relatingtotheinfectionofgroupAstreptoccimainlyoccursinautumnandspringTreatmentofpharyngitiswithantibioticiseffective.FollowsanepisodeofgroupAstreptoccalpharyngitisafterof2-3weeksRheumatismisahypersensitivityinflammatorydiseasenoorganismsatthetypicallesionpathogenesisThetheoryofimmunologiccross-reactionhasbeenstressedResistanceandreactivityofthebodyAntigenCAntigenMMorphology:(*)

Location:connectivetissuesinthewholebody,especiallyinthoseoftheheartandjoint.threephasesindevelopment:degenerativeandexudativestageProliferativephaseorgranulomatousphaseFibrosisphaseorhealedphasedegenerativeandexudativestage:lastonemonthMucoiddegenerationoftheconnectivetissuematrixFibrinoiddegenerationornecrosisofthecollagenousfibersSerousexudationandcellular

infiltration(L,P,N,M)outcomedegenerativeandexudativestage:(1-4weeks)

proliferativephaseorgranulomatousphase:last2-3monthsThehallmark

of

rheumativefever:AschoffbodyCentralfocus:fibrinoidnecrosisSurroundedbyaccumulationof

AschoffcellsdiffuseintertitialinflammatoryinfiltrateLocation:myocardialinterstitial、subendocardial、subcutaneousconnectivetissueAschoffcells:Largecellswithabundantbasophiliccytoplasmandonetofournuclei-containaprominentcentralchromatinmassinlongitudinalsection,thenucleusisserrated--“caterpillar-like”incrosssection,ahaloisobservedaboutthechromatin--“owl-eye”.Fibrosisphaseorhealedphase:last2-3monthsThecytoplasmoftheAschoffCells

(*)isdiminishedinamount,andthecellsbecomespindleshapedfibroblasts,whichcanexcretecollagenousfibersandbecomefibrocytes(fibrosis)→ThefusiformAschoffbodychangeintospindlesmallscars.Rheumatism:naturalcourseisabout4-6monthsRheumaticHeartDiseaseTypesAcuteRheumaticCarditisRheumaticendocarditisRheumaticmyocarditisRheumaticpericarditisRheumaticpancarditisChronicValvularDeformitiesRheumaticendocarditis(valvulitis)Location:thevalvesandtheirneighboringendocardium.Thevalvularinflammationismostoccurredinthemitral,thenbothmitralandaorticvalvesMorphologicalchangesactivestageInactivestageInactivestageGrossly:thickeningandlossoftransparencyofthevalvecusps,followedbytheformationofcharacteristictinyvegetations,seenaswartlikeexcrescences,mainlyalongthelinesofthevalveclosure--“verrucousendocardium”(*).LM:Valvesshowedemaandfibrinoidnecrosis,butAschoffbodiesarenotcommonVerrucousexcrescences:composedofplateletsandfibrin--whitethrombusIninactivedisease:thechangesarefollowedasFibroblasticproliferationandcollagenformation--fibrosisOrganizationofthevegetationsMcCallumpatch:thethicknessoftheleftatrialendocardialsurfaceabovetheposteriormitralleafletRheumaticmyocarditisAdults:localstromalmyocarditisInterventricularseptumorposteriorwallofleftventricle.Aschoffbodiesarefoundnearbythevessels.diffuseinterstitialinflammatoryinfiltratesOutcome:Perivascularscarringmayresult.Children:diffusestromalmyocarditisOutcome:acutecongestiveheartfailureRheumaticpericarditis:Serous/fibrinousinflammationSerousinflammation:pericardialeffusionfibrinousinflammation:“Corvillosum”ClinicalFeaturesRheumaticarthritisLocation:thelargejoints,suchasknee,shoulder,wrist,elbow,coxaLesion:jointsandpericularsofttissuesClinical:Morecommoninadults;migratorypolyarthritisOutcome:completeabsorptionwithoutchronicdeformityRheumaticlesionoftheskinGrossly:inacutestage,taketheformofsubcutaneousnodulesorerythemamarginatum–diagnosisLM:subcutaneousnodules:focallesionsareessentiallycomposedoflargeAschoffbodieserythemamarginatum:exudativeinflammationRheumaticarteritisInvolvingcoronaryarteries,renalarteries,cerebralarteries.FibrinoidnecrosisofvascularwallThewallbecomethick,thelumenbecomenarrow.Rheumaticencephalopathy--Chorea

Girlsaremorethanboys,5-12yearsoldlesion:Rheumaticarteritis→occlusionofartery→cerebromalaciaSubcortexencephalitis:degenerationofnervecellsandhyperplasiaofcolloidcells;severelyinvolvedinbasipodite,substantianigraInfectiveEndocarditisDefinitionItdesignatesinfectionoftheendocardium,esp.cardiacvalves,causedbymicroorganism.Microorganism:anytypeofmicroorganism,butmostcasesarecausedbybacteriaClassification:AcuteendocarditisSubacuteendocarditisAcuteinfectiveendicarditisHighvirulenceorganismsaffectnormalendocardium,mostcommoninaorticandmitralvalvesCauserapidlyprogressiveinfectionPathologicchangesBulkyandfriablevegetations,dirty,dry,aslargeasseveralcentimeters,singleormultipleRapiddestructionofvalveleafletsValvularvegetationscontainingmicroorganismsandadmixedwithplatelets,fibrinandbloodcells.Systemicembolizationmorethan50%ofpatientsaredead,despiteofantibioticsandsurgerySubacuteinfectiveendocardiumLowervirulenceorganismsMoreslowlyaffectspreviouslyabnormalvalves

MitralandAorticmostcommonLesion:FirmerthaninacuteSmalltolarge,singleormultipleCauselessvalvedamageThevegetationaredistinguishedfromthoseofacutediseasebythepresenceofgranulationtissueatbaseoflesionsEventualfibrosis,chronicinflammatoryinfiltrateandcalcificationmayoccurSystemicemboliOutcome:bylowvirulenceorganisms,weekstomonthsandrecoverafterappropriatetreatmentClinicalFeaturesCardiaccomplicationsAorterialemboliumRenalLesionsSepticemiaOutcomeHealingofthevalvularlesionsoccurswhentheorganismsareeliminatedbyprolongedantibiotictherapy.Variousdegreesofscarringanddistortionofthecuspmayresultthesubsequentdangerofheartfailure.

ChronicvalvularvitiumoftheheartDefinitionThevalvesarestructurallydeformedcausedbycongenitaldysplasiaorlaterdiseases,appearingthevalvularstenosis,insufficiencyorboth.Stenosis:Thevalveleafletsarethick,rigidandinteradherent→Thevalveleafletscannotproperlyopenandthemitralorificeisnarrow→bloodhasdifficultytopassthroughthevalvesInsufficiency:Thevalveleafletsarethickening,convolutingandretractionorperforationandrupture→Thevalveleafletscannotproperlyclose→bloodregurgitatesthroughthevalve.CauseMostcasesarecausedbyrheumaticendocarditisandinfectiveendocarditis.Thelesionofaorticvalvescommonlycausedbyatherosclerosisandsyphiliticaortitis.Calcificationandaplasiaareuncommon.LocationMostpronouncedinmitral&aorticvalves(sometimescombinedaorticandmitralvalvemaybepresent)LesionsoftricuspidandpulmonicvalveslesscommonthanthoseofmitralandaorticMitralstenosisThevalveleafletsarethickening,adhesionsandretraction→narrowingofthevalve.Cause:mostcasesarecausedbychronicrheumaticmitralvalvulitis,afewbyinfectiveendocarditisStenosismorecommonthanregurgitationMorphologyThickenedandrigidvalveleafletsandchordaetendineaeTheorificereducedto1~2c㎡,even0.5c㎡(normal5c㎡)Hypertrophyanddilationofrightventricleandatriuminlongstandingcases,Theleftventricleisnormalorsmallinsize.“fish-mouth”deformityChangesofthehemodynamicsIncreasedworkoftheleftatriumwillcompensateforamildmitralstenosis→formationofturbulentflow→theleftatrialendocardiumisthickenedandmuralthrombimaybepresentAnuncompensatedstenosisresultsinincreasedpressureandstasisinthepulmonarycirculaionandincreasetheworkoftherightventricle→leftatrialdilatation,chronicpassivecongestionofthelungs→rightventricularhypertrophy.Theleftventricleisnormalorsmallinsize.二尖瓣狭窄左房血流入左室受阻左房代偿性扩张、肥大左房血液淤积肺静脉回流受阻肺内小动脉收缩肺动脉压升高心尖部舒张期隆隆样杂音肺淤血水肿漏出性出血呼吸困难，咳嗽咳粉红色泡沫样痰右室代偿性肥大右室扩张导致右房扩张腔静脉回流受阻体循环淤血颈静脉怒张、肝脾肿大、下肢浮肿血液流经狭窄口引起漩涡

二尖瓣狭窄的血流动力学变化ClinicalfeaturesX-ray:aninverted“pearshapedheart”Auscultation:boomingmurmuduringdiastoleatthearea