内科学教学课件：心力衰竭Heart Failure (HF)

HeartFailure(HF)

Heartfailure(HF)

Conception:heartfailureisafinalcommonpathwayformanycardiacdisordersofdiverseetiologyandpathogenicmechanisms.Itisaclinicalsyndrome,manifestedasaresultoftheinabilityofthehearttomatchitsoutputtothemetabolicneedsofthebodyeventhoughthefillingpressureoftheheartisadequate.CategoriesofHF1.left,rightandwhole2.acuteandchronic3.systolicanddiastolicstageofHFPre-heartfailurePre-clincalheartfailureClinicalheartfailureRefractoryend-stageheartfailureNewYorkHeartAssociationFunctionalClassificationClassⅠNolimitationofphysicalactivityNosympotomswithordinaryexertionClassⅡSlightlimitationofphysicalactivity

Ordinaryactivitycausessymptoms

ClassⅢ

Markedlimitationofphysicalactivity

Lessthanordinaryactivitycausessymptoms

Asymptomaticatrest

ClassⅣ

Inabilitytocarryoutanyphysicalactivitywithout

discomfort

SympotomsatrestStageandClassofHF心衰分期是NYHA分级的补充，但不能替代

NYHA分级NYHA分级–

在具体病人可上下变动

(对治疗的反应和/或疾病进程不同)分期–

随心脏重构加重只能进展

6-minwalkdistance

milddegree：＞450mmoderatedegree：150-450mseveredegree：＜150mEvaluationofchronicHF

cardiacfunction

FundamentalcausesprimarymyocardialdiseaseincreasedburdenstotheheartFundamentalcauses1.primarydecreasedmyocardialcontractility

coronaryheartdiseasemyocarditis,cardiomyopathymyocardialmetabolicdisorderFundamentalcauses2.increasedburdenstotheheart①increasedafterload(pressureload):hypertensionaorticstenosispulmonarystenosispulmonaryhypertensionFundamentalcauses

2.increasedburdenstotheheart②increasedpreload(volumeload):mitralincompetenceaorticincompetencetricuspidincompetenceatrialseptaldefect(ASD)ventricularseptaldefect(VSD)patentductusarteriosus(PDA)hyperthyroidismanemia

Precipitatingcausesinfection,especiallyrespiratoryinfectionarrhythmias,AFphysicaloremotionalexcessese.g.pregnancyanddeliveryrapidintravenousinfusion,excessivesalttakingmalpraticeprimarydiseasedeteriorationoranewdiseasehappensPathogenesisandpathophysiology1.Compensateheartfailure2.Ventricularremodeling3.Aboutdiastolicinsufficiency4.Humoralfactorschange1.CompensateheartfailureFrank-Starlingprincipleneurohumoralactivationmyocardialhypertrophy1.Compensateheartfailure①cardiacdilatation,bywayoftheFrank-Starlingprinciple,contractileforceincreases.1正常静息2正常活动3’心衰活动3心衰静息心肌收缩性BADC左室舒张末容量图3–2–1正常和心力衰竭时对机体活动时的代偿情况最大活动活动静息左室作功呼吸困难肺水肿E4静息致死性心肌受损1.Compensateheartfailure②neurohumoralactivation

a.Increaseinsympatheticnervousactivityb.RAASactivated(renninangiotensionaldosteronesystem)40年代心衰的概念心衰液体潴留向

动脉泵血障碍静脉回流障碍肾血流静脉压

肾静脉肾微循环

回流障碍障碍水钠排泄障碍

水钠排泄障碍

水肿前向衰竭假说反向衰竭假说

60年代心衰的概念心衰泵功能障碍长期静脉和动脉收缩

周围至中央循环心输出量前后负荷

重新分布

肺血管压力骨骼肌灌注左室肥厚/扩张

肺充血

运动能力近代心衰的概念

心衰神经激素异常长期神经激素激活细胞因子

水钠潴留冠脉及全身血管收缩血管紧张素Ⅱ过度氧化和儿茶酚胺心肌耗氧量毒性作用水肿肺充血心肌细胞功能障碍及坏死血流动力学异常心脏重塑和功能恶化进展细胞凋亡

疾病进展生存率降低心力衰竭——神经体液的代偿和失代偿交感神经激活水、钠潴留水肿肺瘀血血流动力学异常血管收缩心肌耗氧量增加心肌氧供应降低心肌细胞功能障碍和坏死心肌重塑功能恶化疾病进展血管紧张素Ⅱ儿茶酚胺毒性作用心肌细胞凋亡肾素-血管紧张素系统激活代偿失代偿心衰症状体征加重治疗目标增强心肌收缩心肌细胞死亡心力衰竭心肌细胞死亡++↑心肌能量消耗↑后负荷血管收缩↓心排血量神经体液兴奋RASSASInSP3循环↑心肌能量消耗↑胞浆Ca2+cAMPInSP3

心脏↓心肌松弛性↑变力效应+－—心律失常猝死图3–2–2肾素—血管紧张素和交感—肾上腺素能系统激活时对心脏代偿功能的影响2.RAASinHeartFailure心衰时的ＲＡＡＳ系统血管紧张素原非ＡＣＥ肾素ＡＣＥＩ缓激肽径路血管紧张素ⅠＡＣＥ（激肽酶Ⅱ）血管紧张素Ⅱ失活片断

醛固酮ＡＴ１受体ＮＯ螺内酯ＰＧｓ

Na+潴留血管收缩血管扩张心肌纤维化血管肥大生长抑制血管损伤心肌肥大、纤维化抗增生血管功能失调血管保护交感神经激活肾保护

2.RAASinHeartFailure1.Compensateheartfailure③myocardialhypertrophy

MyocardialcellhypertrophysystolepowerNotincreasednumberMyocardialfibreincreasednumberenergyMyocardialcompliance(顺应性）2.Ventricularremodeling

2.Ventricularremodeling

heartfailureistheresultofventricularremodeling.Reducethemyocardialcellsdecrease

of

the

systolic

functionIncreasedmyocardialfibrosis

decrease

of

theVentricularcompliance

HeartcavityexpansionmyocardialhypertrophyextracellularmatrixcollagenfibersMyocardialcells

Compensatedstage

Decompensatedstage3.aboutdiastolicinsufficiency①Characteristic:inthesecases,fillingoftheleftorrightventricleisabnormal.②Mechanism:myocardialrelaxationisimpaired.Myocardialcompliancedecreasing.

③outcome:diastolicpressures↑----venousereturn↓---fluidretention,dyspnea,intolerance4.somecytofactorstakepartinheartfailure

ANP(atrialnatriureticpeptide)BNP(brainnatriureticpeptide)AVP(argininevassopressin)Endothelin(NE,angiotensin)UrinevolumeperipheralvascularsympatheticnervousRAASVentricularremodeling

VentricularremodelingneurohumoralactivationheartfailureChronicheartfailure,CHFClinicalmanifestations1.Leftheartfailurepulmonarycongestionlesscardiacoutput2.Rightheartfailuresystemicvenouscongestion3.Wholeheartfailure1.Leftheartfailure

1)dyspnea1.exertionaldyspnea2.paroxysmalnocturnaldyspnea3.orthopnea,4.acutepulmonaryedema1.Leftheartfailure

2)cough,hemoptysis,spitpinksputum3)fatigue,dizziness,palpitation.4)oliguria,renaldysfunction

sign

1)pulmonarybasalralesbilaterallyorright-side2)enlargedleftheartpulsusalternans,protodiastolicgallopP2increasedPulmonaryedema

2.Rightheartfailuresymptomabdominaldiscomfortanorexia(厌食)nausea,vomitexertionaldyspnea

2.Rightheartfailuresignliverenlargedascitesdistentionofjugularveinshepatojugularreflux(+)peripheraledema,mostmarkindependentpartscyanosisprotodiastolicgallop,functionalmurmursoftricuspidandpulmonaryvalve3.WholeheartfailureLHF＋RHFlaboratoryexamination

BNPandNT-proBNP心室扩张心衰张力增大BNP释放呼吸困难,虚弱,

运动受限等症状(NT-proBNP)

慢性心衰

转至心脏专科继续下一步诊断阳性阴性NT-proBNP临床应用流程图辅助诊断心衰辅助判断进展期心衰患者预后laboratoryexamination

CnTIbloodroutineexaminationroutineurineexaminationbiochemicalexaminationFT3,FT4,TSHECG(electrocardiogram)ischemiaOMIconductionblockarrhysmiaX-rayPulmonarycongestionPleuraleffusionKerlryBRightpulmonaryarterybroadeningPulmonaryhilarbutterflyshapeEchocardiogramLVEF＞50%E/A＞1.2LVEDV/LVESVLVEDD/LVESDventricularwallmotionCardiacmagneticresonance,CMR99MTC-MIBISPECT(radionuclide)CoronaryangiographyCardiacCatheterizationSwan-GanzPCWP＜12mmHgCI＞2.5L/（min.m2）CardiopulmonaryExerciseTesting(CPET)ChronicstableHFMeasurementofrateofoxygenuptake(VO2),rateofCO2production(VCO2),duringmaximal“symptom-limited”exerciseDiagnosisanddifferentialdiagnosisDiagnosis:medicalhistory+symptoms+signs+examExam:ECG:rarelynormalinsystolicHF.x-ray:todetectcardiomegalyandpulmonarycongestion.(3)Echocardiogram:Itiscriticalimportance.①todeterminetheunderlyingcausesofHF②toassesstheseverityofventriculardysfunctiona.functionofcontraction:LVEF>50%b.functionofrelaxation:E/A≥1.2

2.Differentialdiagnosis:cardiacasthmaBronchialasthmaHistoryHeartdiseaseallergichistoryageolderyoungtimenightspringHFsignyesnoLungsignpulmonarybasalralestypicalwheezingx-rayPulmonarycongestionLVlargeEmphysema(肺气肿）alleviatesymptomsofdyspneaDiuretics（利尿剂）Digitalis（洋地黄）isosorbidedinitrateaftercoughoutsputumAntispasmodic(解痉）2.Differentialdiagnosis:②Pericardialeffusion,Constrictivepericarditis:distentionofjugularveins,hepatojugularreflux(+)liverenlarged,ascitesperipheraledema,mostmarkindependentparts

medicalhistorysignsofheartandperivascularechocardiogram,CMR…themostsensitive…specificnoninvasivemethod2.Differentialdiagnosis:③Hepatocirrhosiswithascitesandedemaoflowerextremitydistentionofjugularveins(-)hepatojugularreflux(-)患者男性，23岁。半年前于“感冒”后出现逐渐加重的胸闷、心悸、气急，近一月经常出现夜间阵发性呼吸困难，昨晚大便后又出现呼吸困难并加重，不能平卧，咳嗽，咳泡沫样痰及粉红色血色痰而就诊入院。病例分析病例分析

T37.50C、P130次/分、BP120/70mmHg，R30次/分,明显发绀，大汗，端坐呼吸。颈静脉怒张，心界扩大，第一心音减低和心动过速；心尖区可闻及Ⅲ～Ⅳ级收缩期杂音及舒张期奔马律；双肺布满中小水泡音及哮鸣音；肝肿大、肝颈静脉返流征阳性；双下肢轻度水肿。实验室检查：血、尿、粪常规均正常；肝、肾功能正常心电图提示有窦性心动过速伴不同程度的ST-T缺血性改变，同时伴有频发室性早搏；X胸片呈普大型心脏，心胸比率0.66；心脏多普勒检查示心腔均扩大，其中左室扩大最明显，心脏搏动明显减弱；EF（心脏输出量）在29%病例分析病例分析

诊断：扩张型心肌病全心衰竭急性左心衰发作诊断依据

①有扩张性心脏病基础②有全心衰竭表现③有引起急性发作的诱因④有急性左心衰的临床表现女性患者，36岁。病例主诉：因发热、呼吸急促及心悸3周入院。现病史：4年前病人开始于劳动时自觉心慌气短，近半年来症状加重，同时下肢出现浮肿。1个月前，经常被迫采取端坐位并时常于晚间睡眠时惊醒，气喘不止，经急诊抢救好转。近三周来，出现恶寒发热，咳嗽，痰中时有血丝，心悸气短加重。既往史：患者于儿童时期曾因患咽喉肿痛而做扁桃体摘除术，以后时有膝关节肿痛史。病例体检：T39.6℃，P161次/分，R33次/分，BP110/80mmHg。重症病容，口唇发紫，半卧位，嗜睡；颈静脉怒张，心界向两侧扩大，心尖区可听到明显收缩期杂音，肺动脉瓣第二音亢进。两肺可闻广泛湿性罗音.腹膨隆，可闻移动性浊音。肝于肋下6cm，压痛；脾于肋下3cm。指端呈杵状，下肢明显凹陷性水肿。

。病例实验室检查：红细胞3.0×1012/L白细胞18×109/L中性粒细胞占90%尿量300-500ml/日少量蛋白和红细胞尿胆红素（++）血浆总胆红素31.6µmol/L（正常<17.1）直接胆红素12.8µmol/L(正常<3.4)血清尿素氮正常病例上述化验检查正常吗？有何意义？诊断：风湿性心脏病二尖瓣关闭不全心力衰竭病例

该患者心功能不全的原因是什么？病例引起本次心力衰竭加重的诱因有哪些？该病人先后出现了哪些形式的呼吸困难？该病人出现下肢水肿的机制是什么？患者的肝脏功能为什么不正常？你认为病人发生了哪种类型的心力衰竭？常用心功能指标：

容量指标：

心排出量（CO）正常值5～6L／min

心脏指数（CI）正常值2.6～4.0L／min／m2

心搏出量（SV）正常值60～70ml／beat

心搏指数（SI）正常值41－51ml／m2LVEDV正常值90－100ml

LVESV正常值30～35ml

LVEFEF=VEDV-VESV/VEDV

正常约为>50%压力指标：

LVEDP正常值0.67~1.60Kpa（5～12mmHg）

LAP正常值0.27~1.60Kpa（2～12mmHg）

PAP正常值1.60～3.34／0.54～1.73KPa

（12~25／4~13mmHg）平均压10.67~25.3KPa（8~19mmHg）PCWP正常值0.67～1.60KPa（5～12mmHg）

13～20mmHg（轻度增高）

21~30mmHg（中度增高）＞30mmHg（重度增高）通常PCWP＞18mmHg（＞2.4KPa）肺底出现涅罗音

PCWP＞25mmHg（＞3.3KPa）湿罗音＞1／2肺野

PCWP＞30mmHg（＞4KPa）肺水肿若无二尖瓣狭窄时，PCWP=LAP=LVEDPTreatmentofchronicheartfailure

Principle:alleviatesymptoms,improvelifequality.treatmentforprimarydiseaseandprecipitatingcausesAntagonismofneurohumoralactivationinhibitionofprogressiveventricularremodelingreducemortalityandextendlife.TreatmentofchronicheartfailureGeneralPharmacologictreatmentNon-medicinetreatmentGeneraltreatmentdecreasedburdensincreasedsystolepowerAnti-neurohumoralactivationGeneraltreatmentdecreasedburdensincreasedsystolepowerAnti-neurohumoralactivation1.LifestylemanagementEducationRegulateweightDietarymanagement:salttake2.Restandaction3.Treatmentforprimarydiseaseandprecipitating

GeneraltreatmentdecreasedburdensincreasedsystolepowerAnti-neurohumoralactivation1.Rest2.Dietarymanagement:salttake3.Diuretics

furosemidedihydrochlorothiazide(potassium-losing)antistone(potassium-sparing)Themainpointofdiureticsapplication对于有症状的心衰，当液体负荷过重已表现为肺淤血或外周水肿时，利尿剂是基本的治疗。应用利尿剂可迅速改善呼吸困难并增加运动耐量（I类建议，证据级别A）尚无大型随机对照试验评估这类药物对症状和生存的影响。如能耐受，利尿剂始终应与ACEI和β-受体阻滞剂一起使用。（I类建议，证据级别C）。

襻利尿剂应作为首选。噻嗪类仅适用于轻度液体潴留、伴高血压和肾功能正常的心衰患者(I类，B级)。利尿剂通常从小剂量开始(氢氯噻嗪25mg/d，呋塞米20mg/d，托塞米10mg/d),逐渐加量。一旦病情控制即以最小有效量长期维持。每日体重变化是最可靠检测利尿剂效果和调整利尿剂剂量的指标。长期服用利尿剂应严密观察不良反应的出现如电解质紊乱、症状性低血压，以及肾功能不全，特别在服用剂量大和联合用药时（Ⅰ类，B级）。ThemainpointofdiureticsapplicationGeneraltreatmentdecreasedburdensincreasedsystolepowerAnti-neurohumoralactivation1.Rest2.Dietarymanagement:salttake3.Diuretics4.

Vasodilator

sodiumnitroprusside(SNP)nitroglecerinregitine(酚妥拉明))ThemainpointofVasodilatorapplication直接血管扩张剂对于CHF的治疗无特殊作用。（Ⅲ类，A级）血管扩张剂可用于不能耐受ACEI或ARBs的患者；伴有心绞痛或高血压可考虑应用（Ⅰ类，B级）禁忌证：血容量不足，低血压、肾功能衰竭

心脏流出道或瓣膜狭窄患者GeneraltreatmentdecreasedburdensincreasedsystolepowerAnti-neurohumoralactivation1.Digitalis

（1）effection:Positiveinotropic：

inhibitNa+-K+-ATPenzyme

introcellularNa+、K+Na+-Ca2+exchange

introcellularCa2+myocardialsystolepower

introcellularK+，digitalispoisoningGeneraltreatmentdecreasedburdensincreasedsystolepowerAnti-neurohumoralactivation1.Digitalis

（1）effection:Positiveinotropic：Electrophysiological

Inhibitcondutionsystem,espiciallyatriventricularjunction.

Improvetheautorhythmictyofatrium,junctionregionandventricle.GeneraltreatmentdecreasedburdensincreasedsystolepowerAnti-neurohumoralactivation1.Digitalis

（1）effection:Positiveinotropic：ElectrophysiologicalParasympatheticstimulatinganti-sympatheticnerveexciting

GeneraltreatmentdecreasedburdensincreasedsystolepowerAnti-neurohumoralactivation1.Digitalis

（1）effection:Positiveinotropic：ElectrophysiologicalParasympatheticstimulatingRoleintherenaltubulecellsreducingsodiumreabsorptioninhibitthesecretionofrenin

GeneraltreatmentdecreasedburdensincreasedsystolepowerAnti-neurohumoralactivation1.Digitalis

（2）application

indication:chroniccongestiveheartfailurecomplicatedbyatrailflutterandfibrillationandarapidventricularrateGeneraltreatmentdecreasedburdensincreasedsystolepowerAnti-neurohumoralactivation1.Digitalis

（2）application

contraindication:WPWwithAFⅡdegreeAVB,ⅢdegreeAVBsicksinussyndrome(SSS)Hypertrophiccardiomyopathy(HOCM)severemitralstenosis(SMS)acutemyocardiacinfarction(first24hGeneraltreatmentdecreasedburdensincreasedsystolepowerAnti-neurohumoralactivation1.Digitalis

(3)digitalispoisoningfactors：K+,O2,RFClincalexpression:gastricbowelreaction;arrhythmia;neurologicalandvisualchangeDiagnosis：>2.0ng/mlArrhythmiaofdigitalispoisoningVentricularPrematurebeatNonparoxysmalatrioventricularjunctionaltachycardiaAtrialPrematurebeatAtrialfibrillatonAtrioventricularblockST-TchangelikefishhookCharacteristicfeatureGeneraltreatmentdecreasedburdensincreasedsystolepowerAnti-neurohumoralactivation1.Digitalis

Treatmentofdigitalispoisoningdrugwithdrawaltachycadia:supplyK+

,Lidocainivbradicadia：atropiniv,notsuitableforpacemakernotsuitableforisoprenalinedisablecardioerterGeneraltreatmentdecreasedburdensincreasedsystolepowerAnti-neurohumoralactivation

1、Digitalis2、β-excitantDopamine：NEprecursor2g/kg.min

Dopamine

-R(+)

expandrenalartery2-5g/kg.min

β1

β2-R(+)myocardialcontractility,Vasodilate5-10g/kg.min

α-R(+)BP,HRDobutamine：Dopaminederivatives

2g/kg.min

10g/kg.min

Vasodilate,HR--smalleffectsGeneraltreatmentdecreasedburdensincreasedsystolepowerAnti-neurohumoralactivation

1、Digitalis2、β-excitant3、Phosphodiesteraseinhibitors

1、effect:restrainactivityofphosphodiesterase

，thedegradationofcAMP(-)

cAMPCa2+

channelactivationCa2+

-inflowmyocardialcontractility

GeneraltreatmentdecreasedburdensincreasedsystolepowerAnti-neurohumoralactivation

1、Digitalis2、β-excitant3、Phosphodiesteraseinhibitors

1、effect:2、indications

：refractoryheartfailureend-stageheartfailure

beforehearttransplantation

GeneraltreatmentdecreasedburdensincreasedsystolepowerAnti-neurohumoralactivation

1、Digitalis2、β-excitant3、Phosphodiesteraseinhibitors

1、effect:2、indications

：3、drugs：氨力农(Amrinone)VD5-10g/kg.min

米力农(Milrinone)VD0.5g/kg.minGeneraltreatmentdecreasedburdensincreasedsystolepowerAnti-neurohumoralactivation

1、Digitalis2、β-excitant3、Phosphodiesteraseinhibitors

1、effect:2、indications

：3、drugs：4、defect

：

side-effect;mortality

AII产生是通过多种通道血管紧张素原肾素血管紧张素I(1-10)

AngII（1-8）ACEAT1AT2血管收缩增殖醛固酮增加血管扩张抗增殖Ang1-7Ang1-7受体激活血管扩张抗增殖ARBGeneraltreatmentdecreasedburdensincreasedsystolepowerAnti-neurohumoralactivation

1、RAASinhibitorAngiotensinConvertingEnzymeInhibitors(ACEI)

dilatebloodvessels

inhibitRAS,sympathetic

systemreversetheventricularremodeling

improvearterystiffnessandsensitivity

Improveendothelialfunction

ATⅡ↓,Inhibitthedegradationof

bradykininGeneraltreatmentdecreasedburdensincreasedsystolepowerAnti-neurohumoralactivation

1、RAASinhibitorAngiotensinConvertingEnzymeInhibitors(ACEI)

Clinicalstatus

symptoms↓,exercisetolerance

↑

mortality↓

delaytheprogressofheartfailure

reducinghospitalizationrates

preventHFaftermyocardialinfarction

GeneraltreatmentdecreasedburdensincreasedsystolepowerAnti-neurohumoralactivation

1、RAASinhibitorAngiotensinConvertingEnzymeInhibitors(ACEI)

Captopril6.25～25mg2～3/dEnalapril10mg2/dCilazapril2.5mg/dBenazepril2.5～10mg/dPerindopril2～4mg/dFosinopril5～10mg/dRamipril2.5mg/dGeneraltreatmentdecreasedburdensincreasedsystolepowerAnti-neurohumoralactivation

1、RAASinhibitorAngiotensinConvertingEnzymeInhibitors(ACEI)

applicationmethods

startingwithsmalldosesiftolerated,gradually

increasethedosemonitoringofrenalfunctionandions

renalfunctionchange,highpotassium,drycough,angioedema

GeneraltreatmentdecreasedburdensincreasedsystolepowerAnti-neurohumoralactivation

1、RAASinhibitorAngiotensinConvertingEnzymeInhibitors(ACEI)

Contraindication:

①anuricrenalfailure

②pregnancyandbrestfeedingwoman

③allergeRelativeContraindication:①renalarterystenosisbilaterally②Cr>225µmol/l③k+>5.5mmol/l④hypotensionGeneraltreatmentdecreasedburdensincreasedsystolepowerAnti-neurohumoralactivation

1、RAASinhibitorAngiotensinConvertingEnzymeInhibitors(ACEI)AngiotensinIIreceptorantagonist(ARB)ATⅡ-AT1receptor↓InhibitRASNoaffectingthedegradationof

bradykininGeneraltreatmentdecreasedburdensincreasedsystolepowerAnti-neurohumoralactivation

1、RAASinhibitorAngiotensinConvertingEnzymeInhibitors(ACEI)AngiotensinIIreceptorantagonist(ARB)applicationmethods

lessdrycoughandangioedema

whenHF,firstchoseACEIwhenHF,shouldnotbecombinedapplication

of

ACEIandARB

Losartan50mg/d;valsartan80mg/dGeneraltreatmentdecreasedburdensincreasedsystolepowerAnti-neurohumoralactivation

1、RAASinhibitorAngiotensinConvertingEnzymeInhibitors(ACEI)AngiotensinIIreceptorantagonist(ARB)Aldosterone

antagonists

spironolactone(SPI)potassium-sparingdiureticreversetheventricularremodeling

improveprognosisGeneraltreatmentdecreasedburdensincreasedsystolepowerAnti-neurohumoralactivation

1、RAASinhibitorAngiotensinConvertingEnzymeInhibitors(ACEI)AngiotensinIIreceptorantagonist(ARB)Aldosterone

antagonists

renininhibitorACEI/ARB

increasing

plasma

renin

activityrenin

inhibitior

has

the

effect

of

cardiorenal

protectionnotACEI/ARBreplacementtherapyGeneraltreatmentdecreasedburdensincreasedsystolepowerAnti-neurohumoralactivation

RAASinhibitor

-blockersympatheticactivation↑b1receptorsb2receptorsa1receptorsmetoprololbisoprolol↓arrythmiadilatebloodvessels;↓themyocardialO2Cardiactoxicity

carvedilolGeneraltreatmentdecreasedburdensincreasedsystolepowerAnti-neurohumoralactivation

RAASinhibitor

-blockerInhibitionofsympatheticactivation

improveprognosis1-

blockermetoprolol,bisoprolol

12α-

blokercarvedilolapplicationmethods

startingwithsmalldosesiftolerated,gradually

increasethedosemonitoringofBp,HR,ECGGeneraltreatmentdecreasedburdensincreasedsystolepowerAnti-neurohumoralactivation

RAASinhibitor

-blocker

Contraindication:

bronchospasm

severebradycardia

≥Ⅱ。atrioventricularblock

severeperipheralvasculardisease

acuteheartfailure

TreatmentofchronicheartfailureTherecentadvancesaboutthetreatmentofHF

MicturitionrestrainthesympatheticnervoussystemdilatebloodvesselsrhBNPlevosimendanIncreasetheCa2+sensitivity→myocardialcontractilityMediateATP-K+channel→dilatebloodvesselsivabradineInhibiteSANIfcurrenttolvaptanCombineV2receptor→H2O2reabsoption↓TreatmentofchronicheartfailureNon-medicinetreatmentCardiacResynchronizationTherapy(CRT)L