11 心衰--简化

HeartFailureandAdvanceZhouXiaoyanPh.D.Dept.PathophysiologyLearningObjectives•Discussthedefinition•Discusstheetiology•Discusstheclassification•Discusstheresponseofbodytoheartfailure•Discussmainmechanisms•Discusstheclinicalmanifestations•DiscussthetreatprinciplesIntroductioncontractilityafterloadpreloadCardiacoutputStrokeVolumeHeartrateDeterminantsofcardiacfunctionLearningObjectives•Discussthedefinition•Discusstheetiology•Discusstheclassification•Discussmainmechanisms•Discusstheresponseofbodytoheartfailure•Discusstheclinicalmanifestations•DiscussthetreatprinciplesHeartfailureistheinabilityofthehearttosupplyadequatebloodflowandgenerateacardiacoutputsufficienttomeetthemetabolicdemandsofthebody.Definition机体需要不能满足心输出量降低心脏收缩舒张功能障碍各种致病因素各种致病因素心脏收缩舒张功能障碍各种致病因素心脏收缩舒张功能障碍各种致病因素心输出量降低心脏收缩舒张功能障碍各种致病因素心输出量降低心脏收缩舒张功能障碍各种致病因素不能满足组织的代谢需求心输出量相对或绝对减少心脏收缩或舒张功能障碍各种致病因素心功能不全:各种原因导致心脏泵血功能降低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。心力衰竭患者出现明显的症状和体征，属于心功能不全的失代偿阶段。Prevalence5million500,000newcases/yearIncidencerate1.9%;65y6-10%;menwomenAmerican(China):24million2millionnewcases/yearAroundtheworld:LearningObjectives•Discussthedefinition•Discusstheetiology•Discusstheclassification•Discussmainmechanisms•Discusstheresponseofbodytoheartfailure•Discusstheclinicalmanifestations•DiscussthetreatprinciplesEtiologydirectimpairmentofmyocardialcontractilityanddiastolicfunctionischemicheartdisease,myocarditis,cardiomyopathyPrimarymyocardialdysfunctionVentricularoverloadresultofexcesspressure,volumeorhigh-outputstateshypertension,aorticstenosis,pulmonaryembolismaorticormitralregurgitationthyrotoxicosis,anemia,pregnancyorinfectionPredisposingcause(90%)SystemicInfectionElectrolyte&Acid-baseDisturbanceArrhythmiaPregnancyLabour&OthersLearningObjectives•Discussthedefinition•Discusstheetiology•Discusstheclassification•Discussmainmechanisms•Discusstheresponseofbodytoheartfailure•Discusstheclinicalmanifestations•DiscussthetreatprinciplesLeftvsRightVentricularLowvsHighOutputSystolicvsDiastolicClassificationDegreeofcardiacfunctionSpeedofheartfailureNYHAClassificationLowvsHighOutputCOisabsoluteinsufficencyCOisrelativeinsufficencyAbnormallyelevateddemandsCO4L/min,cardiacindex2.5L/min/m2COmaybenormalatrestbutmaysimplyfailtorisesufficientlyonexertioncardiacoutputmaybewithinnormalrangeorevenelevated,suchashyperthyroidism,anemia,AVfistulaorberiberi.低输出量型心衰高输出量型心衰前高输出量型心衰正常心输出量正常人LeftventricularrightventricularpulmonarycongestionshortnessofbreathfatigueandcoughingPartinitiallyinvolvedinthepathologicalchangesIntheearlystagesAsheartfailureprogressesbothventriclesfailurefluidbuild-upintheveinsandswellinginthelegsandankleswholeheartfailureRheumaticmyocarditisVeryseriousanemiaInabilityofthehearttorelaxproperlyandfillwithbloodasaresultofstiffeningoftheheartmuscle.DiastolicheartfailureSystolicheartfailureInabilityofthehearttocontractwithenoughforcetopumpadequateamountsofbloodthroughthebody.LearningObjectives•Discussthedefinition•Discusstheetiology•Discusstheclassification•Discusstheresponseofbodytoheartfailure•Discussmainmechanisms•Discusstheclinicalmanifestations•DiscussthetreatprinciplesslightsevereCompensationdecompensationThereactionstotheinitiatingevent,suchasincreasedpreloadandafterloadetc,donotchangethroughthewholeperiod.ResponseofthebodyCardiaccompensationSystemiccompensationNeurohormonalcompensation一．CardiaccompensationHypertrophyIncreaseofheartrateExpansionoftheheart（紧张源性与肌源性扩张）Myocardialcontractilityincrease压力感受器效应：CO↓→BP↓→颈动脉窦和主动脉弓压力感受器↓→心迷走N↓，交感N↑→心率↑容量感受器效应：心力衰竭→心房淤血→容量感受器↑→交感N↑→心率↑化学感受器效应：缺氧→主动脉体和颈动脉体化学感受器↑→心率↑1.Increaseofheartrate心率加快的意义动员迅速，见效快，贯穿始终一定程度的心率加快可以增加心输出量心率过快时（＞180次/分）增加心肌耗氧缩短心脏舒张期，心脏充盈不足、冠脉供血减少Frank-Starling定律1.72.12.22.7m收缩力肌节初长2.ExpansionoftheheartCardiacMusclevenousreturnincreasetorheheartornotejectenoughbloodtoarterypreloadincreasemyocytesstretchingincreaseinforceincreasingSVandCOItmeanstheenlargementorovergrowthofheartduetoanincreaseinsizeofitsconstituentcells.3.HypertrophyDependingonthetypeofhemodynamicloadproducingthefailure,sarcomeresdevelopeitherinparallelorinseries.ConcentrichypertrophyEccentrichypertrophy-Increasethecontractileforceofheart-ReduceventricularwalltensiontowardsnormalandthenreduceoxygenconsumingofheartWhatistheeffectofhypertrophy?PhysiologicalPathologicalAssociatedwithahighriskofcardiacmortalityHowhypertrophyturnsintodecompensation?LopsidedgrowthRemodelingofextracellularmatrixIntrinsicdefectChangeofphenotype心肌生长速度与交感神经肥大心肌细胞与线粒体肥大心肌与毛细血管肥大心肌肌球蛋白ATP酶活性低肥大心肌肌浆网Ca2+处理障碍4.Myocardialcontractilityincrease心肌功能受损交感-肾上腺髓质系统兴奋胞浆cAMP浓度增高激活蛋白激酶A心肌膜钙通道蛋白磷酸化CAs增多激活β受体胞浆钙浓度升高正性肌力作用二．SystemiccompensationIncreaseinbloodvolume(SNSRAASADHANP)（GFR、重吸收）Redistributionofbloodflow(SNS)Increaseoferythrocyte(EPO)Increasedabilityoftissuestoutilizeoxygen（酶、线粒体）三．NeurohormonalcompensationCatecholamines(CAs)VasoconstrictionofperipheralvasculatureRASsystemRetainsNa/waterStimulatesfibrosisPotentvasoconstrictorIncreaseafterloadandpreloadAntidiuretichormone(ADH)WaterretentionandVasoconstrictionEndothelin–1VasoconstrictionStimluatescardia