心力衰竭--PPT課件Concept(概念)Heartfailure(pumpfailure)maybedefinedastheconditioninwhichtheheartisnolongerabletopumpanadequatesupplyofbloodforthemetabolicneedsofthebody,providedthereisadequateveneousblood.Concept(概念)Myocardialfailure(心肌衰竭)referstotheheartfailurewhichiscausedbyadefectinmyocardiumitself.Congestiveheartfailure(充血性心衰)hasachroniccoursewithanabnormalaccumulationoffluid,whichresultsintheexpansionofintravascularbloodvolumeCardiacinsufficiency(心功能不全)

CausesofHeartFailure(心衰的病因)Dysfunctionofmyocardium(心肌結(jié)構(gòu)破壞)

diffusemyocardialdamage:myocardialinfarction;cardiopathies;myocarditi;myocardialischemiaandhypoxia:

coronaryheartdisease;severeanemia;hypotension;shock;myocardialhypertrophy;vitaminB1deficiency

CausesofHeartfailure(心衰的病因)Overloadformyocardium(心臟負荷過重)

Pressureoverload(afterload):systemichypertension;pulmonaryhypertension;aorticstenosis;pulmonarystenosis;Volumeoverload(preload):mitralandaorticregurgitationforleftventricles;tricuspidandpulmonaryregurgitationforrightventriclesCausesofheartfailure(心衰的病因)Conditionsthatrestrictventricularfilling(心室充盈受限)

mitralstenosis,constrictivepericarditis,restrictivecardiomyopathy

Precipitatingfactors(誘因)Infectionarrhythmiaspulmonaryembolismpregnancywater,eletrolytesdisturbancesacid-basedisturbancesemotionInfectionfevertachycardiahypoxiatoxinemiaIncreaseddemandsArrhythmias(心律失常)ReducethetimeperiodavailableforventricularfillingandcoronaryperfusionincreasethedemandformyocardialoxygenthedissociationbetweenatrialandventricularcontractionsAcidosisandheartfailure(酸中毒和心力衰竭)CompetewithCa2+forcombinationoftroponinInfluencetheCa2+triggermechanism-reducethesensitivityofthesarcoplasmicreticulumtothelocalconcentrationsofCa2+;resultinareducedreleaseofCa2+fromtheSRCompensatorymechanisminheartfailure(心衰的代償機制)1.TheFrank-starlingmechanism(tonogenicdilatation)2.Increasedreleaseofcatecholamines3.Myocardialhypertrophy4.Increaseofbloodvolumeandredistributionofbloodflow

1.TheFrank-starlingmechanismSarcomerelength(micron)Tension2.2Relationshipbetweenmyofilamentlengthandtensiondevelopmentincardiacmuscle

3.652.Increasedreleaseofcatecholamines(兒茶酚胺釋放增加)Augmentmyocardialcontractility(thepositiveinotropiceffect)increaseheartrate(thepositivechrotropiceffect)elevatetheperipheralvascularresistancepressurereceptor,volumereceptor,chemicalreceptor

3.Myocardialhypertrophy(心肌肥大)VolumeoverloadeccentrichypertrophyPressureoverloadconcentrichypertrophyMyocardialhypertyophy

heartfailureIncreasedformationofamyosinisozyme,V3uptakeandreleaseofCa2+bySRmaybeimparieddiminishedactivityofsympatheticnervoussystemproliferationofmitochondriaandcapillariesmyofilamentproliferationincreasedcollageninhypertrophicmyocardiumcanleadtoareducedventricularcomplianceandinterferewiththefillingofventricles?4.increaseofbloodvolumeandredistributionofbloodflow(血容量增加和血流重分布)WaterandsodiumretensionRedistributionofbloodflowClassificationofheartfailure(心力衰竭的分類)Right-sidedversusleft-sidedheartfailureacuteversuschronicheartfailurehigh-outputversuslow-outputheartfailurehighout-putheartfailure:hyperthyrodism,anemia,arterioveneousfistulasandberiberi(anyotherfactorsthatdecreasethetotalresistancechronicallywillalsoincreasethecardiacoutput)beriberiLackofthisvitamincausesdiminishedabilityofthetissuestoutilizecellularneutrients,whichinturncausesmarkedperipheralvasodilation.Thetotalperipheralresistancedecreasessometimestoaslittleasone-halfnormal.consequently,thelongtimelevelofcardiacoutputalsoincreasestoasmuchas2timesnormal.Pathogenesisofheartfailure(心力衰竭的發(fā)生機制)SarcomereThickfilamentThinfilamentMyosinActinTropomyosinTroponinBasicstructureofsarcomereTnCTnITnTMyosinTroponinActinTropomyosinMyocardialfilamentslidingPathogenesisofheartfailure(心力衰竭的發(fā)生機制)Depressedmyocardialcontractilityaltereddiastolicpropertiesofventriclesasymmetryandasynchronisminventricularcontractionandrelaxation1.Depressedmyocardialcontractility(心肌收縮功能降低)MyocardialcellularinjuriesMyocardialmetabolicdysfunctionDysfunctionofexcitation-contractioncouplingAlterationsoftheadrenergicnervoussysteminthefailingmyocardiumTherelationshipbetweenventriculardysfunctionandprognosisMyocardialinfartedsizeCardiacindexMortality5-10%Normal2%10-20%Slightlydecreased10%20-40%Decreased22%>40%Markedlydecreased60%Energyliberation(ischemia)

energystorageenergyutilization(hypertrophy)Myocardialmetabolicdysfunction(心肌代謝障礙)Disordersinliberationofenergy

ischemicheartdisease;shock;severeanemia;hypoxiaDisordersinutilizationofenergy

myocardialhypertrophyDysfunctionofexcitation-contractioncoupling(興奮和收縮偶聯(lián)障礙)ReduceduptakeandreleaseofCa2+bysarcoplasmicreticulum(SR)MitochondriaCa2+isgreatlyincreasedExtracellularCa2+inwardmovementDiturbedcombinationwithtroponinAlterationsoftheadrenergicnervoussysteminthefailingmyocadium(交感神經(jīng)系統(tǒng)變化)NorepinephrinedepletionDowmregulationofbelta1-receptorsUncouplingofbelta2-receptors

Receptor-operatedchannels2.Altereddiastolicpropertiesofventricles(舒張功能改變)Dysfunctionofventricularrelaxation--increasedcytosolCa2+concentration;lowlevelsofATPReducedventricularcompliance--Myocardialhypertrophy;inflammation;edema;fiberosis3.Asymmetryandasynchronisminventricularcontractionandrelaxation(心肌收縮舒張不協(xié)調(diào))HypokinesisorakinesisdyskinesisasynchronismFunctionalandmetabolicalterationsinheartfailure(功能代謝變化)1.Alterationsincardiacfunction2.Bloodpressurechange3.RespiratorydistressAlterationsincardiacfunction1.Decreasedcardiacoutputandcardiacindex(CI)2.Decreasedejectionfraction(EF):strokevolume/enddiastolicvolume3.Increasedintracardiacpressure:LVEDP-PCWP;RVEDP-CVP4.Alterationsinmyocardialcontractilityanditsdiastolicproperties:Vmaxanddp/dtmax5.Bloodpressurechange

Respiratorydistress(呼吸困難)Dyspnea-exertionaldyspneaOrthopnea-reducedpoolingoffluidintheextremitiesandabdomen;elevationofdiaphragmParoxysmalnocturnaldyspnea-reducedadrenergicdrivetotheleftventricleduringsleep;elevationofthracicbloodvolumeduringrecunbency;normalnocturnaldepressionoftherespiratorycenter;elevationofdiaphragm病例

患者，女，36歲。主訴心慌，氣悶，浮腫，腹脹三月余。患者有風(fēng)濕性心臟病十年病史。近三月來又出現(xiàn)心慌氣悶加重，不能平臥而