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1、心衰心衰 简化简化(jinhu)第一页，共91页。Learning ObjectivesLearning ObjectivesLearning ObjectivesDiscussthedefinitionDiscusstheetiologyDiscusstheclassificationDiscusstheresponseofbodytoheartfailureDiscussmainmechanismsDiscusstheclinicalmanifestationsDiscussthetreatprinciples第1页/共91页第二页，共91页。IntroductionIntroductio
2、nIntroduction第2页/共91页第三页，共91页。contractilityafterloadpreloadCardiacoutputStrokeVolumeHeartrateDeterminantsofcardiacfunctionDeterminantsofcardiacfunction第3页/共91页第四页，共91页。Learning ObjectivesLearning ObjectivesLearning ObjectivesDiscussthedefinitionDiscusstheetiologyDiscusstheclassificationDiscussmainme
3、chanismsDiscusstheresponseofbodytoheartfailureDiscusstheclinicalmanifestationsDiscussthetreatprinciples第4页/共91页第五页，共91页。Heartfailureistheinabilityofthe heart to supply adequateblood flow and generate acardiacoutputsufficienttomeetthe metabolic demands of thebody.DefinitionDefinition 机体需要(xyo)不能满足 心输
4、出量降低心输出量降低(jingd)(jingd)心脏收缩心脏收缩(shu su)(shu su)舒张舒张功能障碍功能障碍 各种致病因素各种致病因素 各种致病因素各种致病因素 心脏收缩舒张心脏收缩舒张功能障碍功能障碍 各种致病因素各种致病因素 心脏收缩舒张心脏收缩舒张功能障碍功能障碍 各种致病因素各种致病因素 心输出量降低心输出量降低 心脏收缩舒张心脏收缩舒张功能障碍功能障碍 各种致病因素各种致病因素 心输出量降低心输出量降低 心脏收缩舒张心脏收缩舒张功能障碍功能障碍 各种致病因素各种致病因素 不能满足组不能满足组织的代谢需求织的代谢需求心输出量相心输出量相对或绝对减少对或绝对减少 心脏收缩或舒
5、张心脏收缩或舒张功能障碍功能障碍 各种致病因素各种致病因素 第5页/共91页第六页，共91页。心功能不全:各种原因导致心脏泵血功能降低(jingd)包括心脏泵血功能下降但处于完全代偿直至失代偿的整个过程。心力衰竭 患者出现(chxin)明显的症状和体征，属于心功能不全的失代偿阶段。第6页/共91页第七页，共91页。PrevalencePrevalence5million500,000newcases/yearIncidence rate 1.9%;65 y 6-10%;men womenAmerican(China):24million2millionnewcases/yearAround t
6、he world:第7页/共91页第八页，共91页。Learning ObjectivesLearning ObjectivesLearning ObjectivesDiscussthedefinitionDiscusstheetiologyDiscusstheclassificationDiscussmainmechanismsDiscusstheresponseofbodytoheartfailureDiscusstheclinicalmanifestationsDiscussthetreatprinciples第8页/共91页第九页，共91页。EtiologyEtiologydirect
7、impairmentofmyocardialcontractilityanddiastolicfunctionischemicheartdisease,myocarditis,cardiomyopathyPrimarymyocardialdysfunctionVentricularoverloadresultofexcesspressure,volumeorhigh-outputstateshypertension,aorticstenosis,pulmonaryembolismaorticormitralregurgitationthyrotoxicosis,anemia,pregnancy
8、orinfection第9页/共91页第十页，共91页。PredisposingPredisposing cause (90%)cause (90%)Systemic Infection Electrolyte&Acid-base Disturbance Arrhythmia Pregnancy Labour&Others第10页/共91页第十一页，共91页。Learning ObjectivesLearning ObjectivesLearning ObjectivesDiscussthedefinitionDiscusstheetiologyDiscusstheclassification
9、DiscussmainmechanismsDiscusstheresponseofbodytoheartfailureDiscusstheclinicalmanifestationsDiscussthetreatprinciples第11页/共91页第十二页，共91页。LeftvsRightVentricularLowvsHighOutputSystolicvsDiastolicClassificationClassificationDegreeofcardiacfunctionSpeedofheartfailure第12页/共91页第十三页，共91页。NYHA Classification
10、第13页/共91页第十四页，共91页。LowvsHighOutputCO is absolute insufficencyCO is relative insufficencyAbnormally elevated demandsCO4 L/min,cardiac index 2.5 L/min/m2CO may be normal at rest but may simply fail to rise sufficiently on exertioncardiac output may be within normal range or even elevated,such as hyper
11、thyroidism,anemia,AV fistula or beriberi.第14页/共91页第十五页，共91页。低输出量型心衰高输出量型心衰前高输出量型心衰正常正常(zhngchng)心输出心输出量量正常人第15页/共91页第十六页，共91页。Leftventricularrightventricularpulmonarycongestionshortnessofbreathfatigueandcoughing Partinitiallyinvolvedinthepathologicalchanges Intheearlystages Asheartfailureprogresses
12、bothventriclesfailurefluidbuild-upintheveinsandswellinginthelegsandankles第16页/共91页第十七页，共91页。wholeheartfailure Rheumaticmyocarditis Veryseriousanemia 第17页/共91页第十八页，共91页。Inabilityofthehearttorelaxproperlyandfillwithbloodasaresultofstiffeningoftheheartmuscle.DiastolicheartfailureSystolicheartfailureIna
13、bilityofthehearttocontractwithenoughforcetopumpadequateamountsofbloodthroughthebody.第18页/共91页第十九页，共91页。Learning ObjectivesLearning ObjectivesLearning ObjectivesDiscussthedefinitionDiscusstheetiologyDiscusstheclassificationDiscusstheresponseofbodytoheartfailureDiscussmainmechanismsDiscusstheclinicalm
14、anifestationsDiscussthetreatprinciples第19页/共91页第二十页，共91页。slight severeCompensation decompensationThe reactions to the initiating event,such as increased preload and afterload etc,do not change through the whole period.第20页/共91页第二十一页，共91页。ResponseofthebodyResponseofthebody Cardiac compensation System
15、ic compensation Neurohormonal compensation第21页/共91页第二十二页，共91页。1Cardiac compensationn Hypertrophyn Increase of heart raten Expansion of the heart（紧张(jnzhng)源性与肌源性扩张）n Myocardial contractility increase第22页/共91页第二十三页，共91页。压力感受器效应压力感受器效应(xioyng)(xioyng)：COBPCOBP颈动脉窦和主动脉弓压力感受器颈动脉窦和主动脉弓压力感受器心迷心迷走走NN，交感，交感
16、N N 心率心率 容量感受器效应容量感受器效应(xioyng)(xioyng)：心力衰竭心力衰竭心房淤血心房淤血容量感受器容量感受器交感交感NN心率心率 化学感受器效应化学感受器效应(xioyng)(xioyng)：缺氧缺氧主动脉体和颈动脉体化学感受器主动脉体和颈动脉体化学感受器 心率心率 1.Increase of heart rate第23页/共91页第二十四页，共91页。心率加快(ji kui)的意义 动员迅速，见效快，贯穿动员迅速，见效快，贯穿(gunchun)(gunchun)始终始终一定程度的心率加快可以增加心输出量一定程度的心率加快可以增加心输出量心率过快时（心率过快时（1801
17、80次次/分）增加心肌分）增加心肌(xnj)(xnj)耗氧耗氧缩短心脏舒张期，心脏充盈不足、冠脉供血减少缩短心脏舒张期，心脏充盈不足、冠脉供血减少第24页/共91页第二十五页，共91页。Frank-Starling定律(dngl)1.7 2.1 2.2 2.7 m收缩收缩(shu su)力力肌节初长肌节初长2.Expansion of the heart 第25页/共91页第二十六页，共91页。CardiacMuscle第26页/共91页第二十七页，共91页。venous return increase to rhe heart or not eject enough blood to art
18、erypreload increasemyocytes stretching increase in force increasing SV and CO第27页/共91页第二十八页，共91页。It means the enlargement or overgrowth of heart due to an increase in size of its constituent cells.3.Hypertrophy第28页/共91页第二十九页，共91页。Depending on the type of hemodynamic load producing the failure,sarcom
19、eres develop either in parallel or in series.Concentric hypertrophyEccentric hypertrophy第29页/共91页第三十页，共91页。-Increase the contractile force of heart-Reduce ventricular wall tension towards normal and then reduce oxygen consuming of heartWhatistheeffectofhypertrophy?uPhysiologicaluPathologicalAssociat
20、ed with a high risk of cardiac mortality 第30页/共91页第三十一页，共91页。Howhypertrophyturnsintodecompensation?LopsidedgrowthRemodelingofextracellularmatrix Intrinsicdefect Changeofphenotype 心肌生长速度与交感神经心肌生长速度与交感神经(jiogn-(jiogn-shnjng)shnjng)肥大心肌细胞与线粒体肥大心肌细胞与线粒体 肥大心肌与毛细血管肥大心肌与毛细血管 肥大心肌肌球蛋白肥大心肌肌球蛋白ATPATP酶活性低酶活性低
21、肥大心肌肌浆网肥大心肌肌浆网Ca2+Ca2+处理障碍处理障碍第31页/共91页第三十二页，共91页。4.Myocardial contractility increase心肌心肌(xnj)功功能受损能受损交感交感-肾上腺髓质肾上腺髓质系统系统(xtng)兴兴奋奋胞浆胞浆cAMP浓度浓度(nngd)增高增高激活蛋白激酶激活蛋白激酶A心肌膜钙通道蛋心肌膜钙通道蛋白磷酸化白磷酸化CAs 增多增多激活激活受体受体胞浆钙浓度升高胞浆钙浓度升高正性肌力作用正性肌力作用第32页/共91页第三十三页，共91页。2Systemic compensation Increase in blood volume (S
22、NS RAAS ADH ANP)（GFR、重吸收）、重吸收）Redistribution of blood flow(SNS)Increase of erythrocyte (EPO)Increased ability of tissues to utilize oxygen（酶、线粒体）（酶、线粒体）第33页/共91页第三十四页，共91页。3Neurohormonal compensationCatecholamines(CAs)VasoconstrictionofperipheralvasculatureRASsystemRetainsNa/waterStimulatesfibrosisP
23、otentvasoconstrictorIncreaseafterloadandpreload第34页/共91页第三十五页，共91页。Antidiuretichormone(ADH)WaterretentionandVasoconstriction Endothelin1VasoconstrictionStimluatescardiacfibrosis第35页/共91页第三十六页，共91页。BaroreceptorsSympatheticnerves(SNS)Renin-angiotensinsystem(RAS)Antidiuretichormone(ADH)Atrialnatriureti
24、cpeptide(ANP)VasoconstrictionIncreasedbloodvolumeMaintainBPIncreasedbackflow第36页/共91页第三十七页，共91页。OverloadofheartIncreaseoxygenconsumingArrhythmiaInjurybycytokinesMyocardialremodelingRetentionofwaterandsodiumAdverseeffects第37页/共91页第三十八页，共91页。MyocardialremodelingChangesinshapeandsizeofthechamberinvolve
25、schangesinthestructure,function,andgeneexpressionofthemyocardialcell.第38页/共91页第三十九页，共91页。The heart is composed of Cardiac myocytesNonmyocyte cellsExtracellular matrix(ECM)第39页/共91页第四十页，共91页。u心肌细胞的凋亡、坏死、肥大、延u 长、心肌肥厚u心肌间质纤维胶原合成和降解动态(dngti)平 u 衡破坏 Fibrosis心室(xnsh)重塑第40页/共91页第四十一页，共91页。Sympatheticnervou
26、ssystemHormonalalterationsHemodynamicalterationsWhy ventricular remodeling occurs?ACEI(angiotensin converting enzyme inhibitors)and Beta blockers have a direct antagonistic effect on the remodeling process第41页/共91页第四十二页，共91页。第42页/共91页第四十三页，共91页。Learning ObjectivesLearning ObjectivesLearning Objectiv
27、esDiscussthedefinitionDiscusstheetiologyDiscusstheclassificationDiscusstheresponseofbodytoheartfailureDiscussmainmechanismsDiscusstheclinicalmanifestationsDiscussthetreatprinciples第43页/共91页第四十四页，共91页。CardiacMuscle第44页/共91页第四十五页，共91页。第45页/共91页第四十六页，共91页。MolecularBasisofContractionMolecularBasisofCont
28、raction 第46页/共91页第四十七页，共91页。WeakenofcontractilityAbnormityofdiastolicpropertiesofventricleAsynergiaofventricularcontractionandrelaxationMechanismsforheartfailureMechanismsforheartfailure第47页/共91页第四十八页，共91页。(1)Damage of myocardial cells(2)Myocardial metabolic dysfunction(3)Dysfunction of EC coupling(
29、4)HypertrophyWeakenofcontractility第48页/共91页第四十九页，共91页。各种因素各种因素Cell damage收缩收缩(shu su)力下降力下降XCell deathNecrosisApoptosishomeostasis第49页/共91页第五十页，共91页。Cellswellsandruptures.Cellcontentsspillout.Necrosis第50页/共91页第五十一页，共91页。MyocardialInfarction心肌梗死MyocardialischemiaHypoxiaVirusorbacterialinfectionAthero
30、sclerosisofthelargercoronaryarteries 第51页/共91页第五十二页，共91页。Active Energy-requiring Gene-directed Signal-dependent Apoptosis第52页/共91页第五十三页，共91页。DNA ladderDetection of DNA fragmentationApoptosisindex35.5%第53页/共91页第五十四页，共91页。(1)Damage of myocardial cells(2)Myocardial metabolic dysfunction(3)Dysfunction o
31、f EC coupling(4)HypertrophyWeaken of cardiac contractility第54页/共91页第五十五页，共91页。Energymetabolismofcardiacmyocyteliberation storingutilizationpumpFreeCa2+CombinedCa2+Actin-myosineH2Ocitricacid-ketoglutaricacid oxaloaceticacid succinicacid acetyl 第55页/共91页第五十六页，共91页。DisordersinliberationofenergyOccursin
32、 ischemicheartdisease,shock,severeanemiaandhypoxia.ThereducedcontractilityismainlybecauseofthedecreasedlevelofATP.第56页/共91页第五十七页，共91页。Disordersinstoringofenergycreatinephosphatekinase磷酸(lnsun)肌酸激酶第57页/共91页第五十八页，共91页。Disordersinutilizationofenergyu Key problem is how much the efficiency of actomyosin
33、-ATPase is.u This enzyme reduces its activity in heart failure.u Myosin isozyme V3 is increased especially during hypertrophy.肌球蛋白同工酶比较V1V2V3组成活性最高较低最低第58页/共91页第五十九页，共91页。(1)Damage of myocardial cells(2)Myocardial metabolic dysfunction(3)Dysfunction of EC coupling(4)HypertrophyWeaken of cardiac cont
34、ractilityWeaken of cardiac contractility第59页/共91页第六十页，共91页。正正常常心心肌肌(x x n nj j)兴兴奋奋-收收缩缩偶偶联联心肌cell兴奋去极化Ca与肌钙蛋白TnG结合，使其构型改变2+肌球蛋白头部偏转，细肌丝向肌节中央滑行Tnl从肌动蛋白移开肌节缩短，心肌收缩肌动蛋白作用点暴露，与肌球蛋白头部接触形成横桥同时激活肌球蛋白头部Ca依赖的ATP酶水解ATP供能2+胞浆内Ca从10上升到102+-7-5mol/L第60页/共91页第六十一页，共91页。Dysfunctionofexcitation-contractioncoupling
35、DysfunctionofCalciumhandlingbySR （肌浆网）Ca2+bindingtotroponin Calciuminflux第61页/共91页第六十二页，共91页。Howistheprocessofcalciuminfluxchangedinheartfailure?TwomainpathwaysCalciumchannelNa+-Ca2+exchangerDysfunctionofcalciuminflux第62页/共91页第六十三页，共91页。CalciumchannelCalcium Channel第63页/共91页第六十四页，共91页。nThedensityof-
36、adrenoceptorandgenerationofnorepinephrine(NE)decreased.nAcidosisbluntedsensitivityofNEto-adrenoceptor.nHyperkalemiainhibitedthecalciuminflux.Whathappenedtothechannelinheartfailure?肥大心肌-R密度相对NE 酸中毒时，H+降低(jingd)-R对NE的敏感高钾血症第64页/共91页第六十五页，共91页。Re-uptakeStoringReleaseMSRHandlingofcalciumbySRDysfunctiono
37、fcalciumhandlingbySR第65页/共91页第六十六页，共91页。Inheartfailure Expression of pump ATP supply-adrenoceptor activationRe-uptake calcium of SRATP-dependentpump Phospholamban 第66页/共91页第六十七页，共91页。Ca2+-inducedCa2+release(CICR)Ryanodinereceptor(RyR)Protein and mRNA level of RyR are both found to reduce in heart fa
38、ilure.Ca2+content of SR decrease in heart failure.Hydrogen(H)increases the affinity of calcium and its binding protein,so it is difficult to be released.In heart failureRelease calcium from SR第67页/共91页第六十八页，共91页。Concentration of cytosolic calciumNormal affinity of troponin to calcium第68页/共91页第六十九页，共
39、91页。(1)Damage of myocardial cells(2)Myocardial metabolic dysfunction(3)Dysfunction of EC coupling(4)HypertrophyWeaken of cardiac contractilityWeaken of cardiac contractility第69页/共91页第七十页，共91页。WeakenofcontractilityAbnormityofdiastolicpropertiesofventricleAsynergiaofventricularcontractionandrelaxation
40、MechanismsforheartfailureMechanismsforheartfailure第70页/共91页第七十一页，共91页。Myocardial relaxation is an active process,not merely an intermittent rest period between systolic periods.Up to 15%of myocardial energy may be expended for that relaxation.Diastolic stage is important to blood supply for heart it
41、self and it is also necessary for the venous return.Diastolic properties of ventricleDiastolic properties of ventricle第71页/共91页第七十二页，共91页。(1)Delayedcalciumdecrease(2)Impaireddissociationoftheactin-myosincomplex(3)Decreaseddiastolicpotentialenergy ofventricles(4)ReducedcomplianceofmyocardiumAbnormity
42、 of diastolic properties of ventricleAbnormity of diastolic properties of ventricle第72页/共91页第七十三页，共91页。After each systole,the concentration of myoplasmic Ca2+need to decrease from 10-5mol/L to 10-7mol/L,allowing separating of the actin-myosin cross-bridges.Without adequate ATP,Ca2+is delayed uptaked
43、 by SR and delayed efflux from the myocyte.Thus,Ca 2+still combines with troponin and myocardium can not relax fully.Delayedcalciumdecrease第73页/共91页第七十四页，共91页。Myocardial relaxation is not a passive,but rather is an energy-requiring activity.ATP is needed for actin-myosin complex to dissociate,So ina
44、dequate ATP supply may lead to impairment of actin-myosin decoupling.Obviously,any pathologic factor with disorders in energy metabolism may result in heart failure via diastolic dysfunction.Impaireddissociationoftheactin-myosin第74页/共91页第七十五页，共91页。Early diastolic recoil of the ventricular walls in c
45、onjunction with release of elastic potential energy stored during systole deformation,generating suction and thus contributing to diastolic filling.DecreaseddiastolicpotentialenergyofventriclesMany pathologic factors accounted for depressed myocardial contractility may lead a limited loading of vent
46、ricle as well as diastolic potential energy.第75页/共91页第七十六页，共91页。ReducedcomplianceofmyocardiumThe ability of a blood vessel or a cardiac chamber to change its volume in response to changes in pressure has important physiological implications.C=V/P 第76页/共91页第七十七页，共91页。WeakenofcontractilityAbnormityofd
47、iastolicpropertiesofventricleAsynergiaofventricularcontractionandrelaxationMechanismsforheartfailureMechanismsforheartfailure第77页/共91页第七十八页，共91页。q部分心肌收缩性减弱部分心肌收缩性减弱q部分心肌没有部分心肌没有(mi yu)收缩性收缩性q部分心肌收缩性膨出部分心肌收缩性膨出q心脏各部收缩不协调心脏各部收缩不协调第78页/共91页第七十九页，共91页。Learning ObjectivesLearning ObjectivesLearning Objec
48、tivesDiscussthedefinitionDiscusstheetiologyDiscusstheclassificationDiscussmainmechanismsDiscusstheresponseofbodytoheartfailureDiscusstheclinicalmanifestationsDiscussthetreatprinciples第79页/共91页第八十页，共91页。ClinicalManifestations 低排出量综合征（前向衰竭）静脉淤血综合征（后向衰竭）第80页/共91页第八十一页，共91页。(一)呼吸困难(h x kn nn)劳力(lol)性呼吸困
49、难 端 坐 呼 吸 夜间(y jin)阵发性呼吸困难 一、肺循环淤血轻度心衰患者，仅在体力活动时出现呼吸困难，休息后症状消失重症心衰患者，安静时感到呼吸困难，被迫采取坐位或半卧位方减轻呼吸困难重症心衰患者，常在入睡后突然感到气闷而惊醒，并立即坐起喘气和咳嗽第81页/共91页第八十二页，共91页。劳力(lol)性呼吸困难发生的机制 第82页/共91页第八十三页，共91页。端坐呼吸(hx)发生的机制 端坐位时，症状(zhngzhung)可减轻，故病人被迫坐起。端坐呼吸可以见于左心衰、右心衰及呼衰。第83页/共91页第八十四页，共91页。夜间阵发性呼吸困难发生(fshng)的机制 平卧时静脉回流及水
50、肿液吸收 肺淤血、肺水肿入睡后迷走神经 支气管收缩 通气阻力入睡后CNS抑制 对外周传入刺激不敏感，当肺淤血很严重时才刺激呼吸中枢 突然(trn)惊醒第84页/共91页第八十五页，共91页。（二）肺水肿1、肺毛细血管(mo x xu un)压升高 2、肺毛细血管(mo x xu un)壁通透性增高 第85页/共91页第八十六页，共91页。二、体循环淤血(yxu)主要主要(zhyo)(zhyo)表现表现颈静脉充盈或怒张颈静脉充盈或怒张肝肿大及肝功能损害肝肿大及肝功能损害胃肠道淤血所致的食欲不振等消化道症状胃肠道淤血所致的食欲不振等消化道症状心性水肿心性水肿第86页/共91页第八十七页，共91页。