心力衰竭-课件教学提纲

心力衰竭--PPT课件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(心肌结构破坏)

diffusemyocardialdamage:myocardialinfarction;cardiopathies;myocarditi;myocardialischemiaandhypoxia:

coronaryheartdisease;severeanemia;hypotension;shock;myocardialhypertrophy;vitaminB1deficiency

CausesofHeartfailure(心衰的病因)Overloadformyocardium(心脏负荷过重)

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

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

3.652.Increasedreleaseofcatecholamines(儿茶酚胺释放增加)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(心力衰竭的分类)Right-sidedversusleft-sidedheartfailureacuteversuschronicheartfailurehigh-outputversuslow-outputheartfailurehighout-putheartfailure:hyperthyrodism,anemia,arterioveneousfistulasandberiberi(anyotherfactorsthatdecreasethetotalresistancechronicallywillalsoincreasethecardiacoutput)beriberiLackofthisvitamincausesdiminishedabilityofthetissuestoutilizecellularneutrients,whichinturncausesmarkedperipheralvasodilation.Thetotalperipheralresistancedecreasessometimestoaslittleasone-halfnormal.consequently,thelongtimelevelofcardiacoutputalsoincreasestoasmuchas2timesnormal.Pathogenesisofheartfailure(心力衰竭的发生机制)SarcomereThickfilamentThinfilamentMyosinActinTropomyosinTroponinBasicstructureofsarcomereTnCTnITnTMyosinTroponinActinTropomyosinMyocardialfilamentslidingPathogenesisofheartfailure(心力衰竭的发生机制)Depressedmyocardialcontractilityaltereddiastolicpropertiesofventriclesasymmetryandasynchronisminventricularcontractionandrelaxation1.Depressedmyocardialcontractility(心肌收缩功能降低)MyocardialcellularinjuriesMyocardialmetabolicdysfunctionDysfunctionofexcitation-contractioncouplingAlterationsoftheadrenergicnervoussysteminthefailingmyocardiumTherelationshipbetweenventriculardysfunctionandprognosisMyocardialinfartedsizeCardiacindexMortality5-10%Normal2%10-20%Slightlydecreased10%20-40%Decreased22%>40%Markedlydecreased60%Energyliberation(ischemia)

energystorageenergyutilization(hypertrophy)Myocardialmetabolicdysfunction(心肌代谢障碍)Disordersinliberationofenergy

ischemicheartdisease;shock;severeanemia;hypoxiaDisordersinutilizationofenergy

myocardialhypertrophyDysfunctionofexcitation-contractioncoupling(兴奋和收缩偶联障碍)ReduceduptakeandreleaseofCa2+bysarcoplasmicreticulum(SR)MitochondriaCa2+isgreatlyincreasedExtracellularCa2+inwardmovementDiturbedcombinationwithtroponinAlterationsoftheadrenergicnervoussysteminthefailingmyocadium(交感神经系统变化)NorepinephrinedepletionDowmregulationofbelta1-receptorsUncouplingofbelta2-receptors

Receptor-operatedchannels2.Altereddiastolicpropertiesofventricles(舒张功能改变)Dysfunctionofventricularrelaxation--increasedcytosolCa2+concentration;lowlevelsofATPReducedventricularcompliance--Myocardialhypertrophy;inflammation;edema;fiberosis3.Asymmetryandasynchronisminventricularcontractionandrelaxation(心肌收缩舒张不协调)HypokinesisorakinesisdyskinesisasynchronismFunctionalandmetabolicalterationsinheartfailure(功能代谢变化)1.Alterationsincardiacfunction2.Bloodpressurechange3.RespiratorydistressAlterationsincardiacfunction1.Decreasedcardiacoutputandcardiacindex(CI)2.Decreasedejectionfraction(EF):strokevolume/enddiastolicvolume3.Increasedintracardiacpressure:LVEDP-PCWP;RVEDP-CVP4.Alterationsinmyocardialcontractilityanditsdiastolicproperties:Vmaxanddp/dtmax5.Bloodpressurechange

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

患者，女，36岁。主诉心慌，气闷，浮肿，腹胀三月余。患者有风湿性心脏病十年病史。近三月来又出现心慌气闷加重，不能平卧而