最新心力衰竭 PPT课件PPT课件 40页

'心力衰竭PPT课件 Clinton Precipitatingfactors(诱因)Infectionarrhythmiaspulmonaryembolismpregnancywater,eletrolytesdisturbancesacid-basedisturbancesemotion InfectionfevertachycardiahypoxiatoxinemiaIncreaseddemands Arrhythmias(心律失常)Reducethetimeperiodavailableforventricularfillingandcoronaryperfusionincreasethedemandformyocardialoxygenthedissociationbetweenatrialandventricularcontractions Acidosisandheartfailure(酸中毒和心力衰竭)CompetewithCa2+forcombinationoftroponinInfluencetheCa2+triggermechanism-reducethesensitivityofthesarcoplasmicreticulumtothelocalconcentrationsofCa2+;resultinareducedreleaseofCa2+fromtheSR Compensatorymechanisminheartfailure(心衰的代偿机制)1.TheFrank-starlingmechanism(tonogenicdilatation)2.Increasedreleaseofcatecholamines3.Myocardialhypertrophy4.Increaseofbloodvolumeandredistributionofbloodflow 1.TheFrank-starlingmechanismSarcomerelength(micron)Tension2.2Relationshipbetweenmyofilamentlengthandtensiondevelopmentincardiacmuscle3.65 2.Increasedreleaseofcatecholamines(儿茶酚胺释放增加)Augmentmyocardialcontractility(thepositiveinotropiceffect)increaseheartrate(thepositivechrotropiceffect)elevatetheperipheralvascularresistancepressurereceptor,volumereceptor,chemicalreceptor 3.Myocardialhypertrophy(心肌肥大)VolumeoverloadeccentrichypertrophyPressureoverloadconcentrichypertrophy MyocardialhypertyophyheartfailureIncreasedformationofamyosinisozyme,V3uptakeandreleaseofCa2+bySRmaybeimparieddiminishedactivityofsympatheticnervoussystemproliferationofmitochondriaandcapillariesmyofilamentproliferationincreasedcollageninhypertrophicmyocardiumcanleadtoareducedventricularcomplianceandinterferewiththefillingofventricles? 4.increaseofbloodvolumeandredistributionofbloodflow(血容量增加和血流重分布)WaterandsodiumretensionRedistributionofbloodflow Classificationofheartfailure(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)SarcomereThickfilamentThinfilamentMyosinActinTropomyosinTroponinBasicstructureofsarcomere TnCTnITnTMyosinTroponinActinTropomyosinMyocardialfilamentsliding Pathogenesisofheartfailure(心力衰竭的发生机制)Depressedmyocardialcontractilityaltereddiastolicpropertiesofventriclesasymmetryandasynchronisminventricularcontractionandrelaxation 1.Depressedmyocardialcontractility(心肌收缩功能降低)MyocardialcellularinjuriesMyocardialmetabolicdysfunctionDysfunctionofexcitation-contractioncouplingAlterationsoftheadrenergicnervoussysteminthefailingmyocardium TherelationshipbetweenventriculardysfunctionandprognosisMyocardialinfartedsizeCardiacindexMortality5-10%Normal2%10-20%Slightlydecreased10%20-40%Decreased22%>40%Markedlydecreased60% Energyliberation(ischemia)energystorageenergyutilization(hypertrophy) Myocardialmetabolicdysfunction(心肌代谢障碍)Disordersinliberationofenergyischemicheartdisease;shock;severeanemia;hypoxiaDisordersinutilizationofenergymyocardialhypertrophy Dysfunctionofexcitation-contractioncoupling(兴奋和收缩偶联障碍)ReduceduptakeandreleaseofCa2+bysarcoplasmicreticulum(SR)MitochondriaCa2+isgreatlyincreasedExtracellularCa2+inwardmovementDiturbedcombinationwithtroponin Alterationsoftheadrenergicnervoussysteminthefailingmyocadium(交感神经系统变化)NorepinephrinedepletionDowmregulationofbelta1-receptorsUncouplingofbelta2-receptorsReceptor-operatedchannels 2.Altereddiastolicpropertiesofventricles(舒张功能改变)Dysfunctionofventricularrelaxation--increasedcytosolCa2+concentration;lowlevelsofATPReducedventricularcompliance--Myocardialhypertrophy;inflammation;edema;fiberosis 3.Asymmetryandasynchronisminventricularcontractionandrelaxation(心肌收缩舒张不协调)Hypokinesisorakinesisdyskinesisasynchronism Functionalandmetabolicalterationsinheartfailure(功能代谢变化)1.Alterationsincardiacfunction2.Bloodpressurechange3.Respiratorydistress Alterationsincardiacfunction1.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，不能平卧而住院治疗。检查：重病容，半卧位，颈静脉怒张，呼吸36次/分，两肺底闻湿性罗音，心界向两侧扩大，心率130次分，血压14.6/10.7kPa,心尖部可闻及收缩期吹风样杂音和舒张期雷鸣样杂音Ⅲ级，肝脏在右侧锁骨中线肋下6厘米，压痛，腹部有移动性浊音，骶部及下肢明显指压性水肿，腹腔抽出液体，为漏出液，血浆蛋白22g/L,球蛋白15g/L。1.临床诊断?心衰属何种类型?发生机制?2.水肿及腹水发生机制?端坐呼吸?心界扩大,心率130次/分,血压正常,为什么? Myocardialhypertrophyheartfailure?Organic?Histological?Cellular?Molecular? MyocardialhypertyophyheartfailureMolecular:Increasedformationofamyosinisozyme--V3Cellularandsubcellular:uptakeandreleaseofCa2+bySR;mitochondriaproliferation;uptakeandreleaseofCa2+bymitochondriahistological:diminishedactivityofsympatheticnervoussystemandcapillariesorganic:increasedcollageninhypertrophicmyocardiumcanleadtoareducedventricularcomplianceandinterferewiththefillingofventricles? Coronaryheartdiseaseheartfailure Thankyou '