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1、Heart Failure(HF)Heart failure(HF)Conception:heart failure is a final common pathway for many cardiac disorders of diverse etiology and pathogenic mechanisms.It is a clinical syndrome,manifested as a result of the inability of the heart to match its output to the metabolic needs of the body even tho
2、ugh the filling pressure of the heart is adequate.Categories of HF1.left,rightandwhole2.acuteandchronic3.systolicanddiastolicstage of HFA.Pre-heartfailureB.Pre-clincalheartfailureC.ClinicalheartfailureD.Refractoryend-stageheartfailureNew York Heart Association Functional ClassificationClass No limit
3、ation of physical activity No sympotoms with ordinary exertion Class Slight limitation of physical activity Ordinary activity causes symptomsClassMarked limitation of physical activityLess than ordinary activity causes symptomsLess than ordinary activity causes symptoms Asymptomatic at restClassInab
4、ility to carry out any physical activity withoutdiscomfortSympotoms at restStage and Class of HF心衰分期是心衰分期是NYHANYHA分级的补充，但不能分级的补充，但不能替代替代 NYHANYHA分级分级NYHANYHA分级分级 在具体病人在具体病人可上下变动可上下变动 (对治疗的反应和对治疗的反应和/或疾病进程不同或疾病进程不同)分期分期 随心脏重构加重随心脏重构加重只能进展只能进展 6-minwalkdistance milddegree：450mmoderatedegree：150-450mse
5、veredegree：150mEvaluationofchronicHFcardiacfunction Fundamental causes1.primarymyocardialdisease2.increasedburdenstotheheartFundamental causes1.primarydecreasedmyocardialcontractilityA.coronaryheartdiseaseB.myocarditis,cardiomyopathyC.myocardialmetabolicdisorderFundamental causes2.increasedburdensto
6、theheartincreasedafterload(pressureload):A.hypertensionB.aorticstenosisC.pulmonarystenosisD.pulmonaryhypertensionFundamental causes 2.increasedburdenstotheheartincreasedpreload(volumeload):A.mitralincompetenceB.aorticincompetenceC.tricuspidincompetenceD.atrialseptaldefect(ASD)E.ventricularseptaldefe
7、ct(VSD)F.patentductusarteriosus(PDA)G.hyperthyroidismH.anemia Precipitating causesA.infection,especiallyrespiratoryinfectionB.arrhythmias,AFC.physicaloremotionalexcessese.g.pregnancyanddeliveryD.rapidintravenousinfusion,excessivesalttakingE.malpraticeF.primarydiseasedeteriorationoranewdiseasehappens
8、Pathogenesis and pathophysiology1.Compensateheartfailure2.Ventricularremodeling3.Aboutdiastolicinsufficiency4.Humoralfactorschange1.Compensate heart failurelFrank-Starlingprinciplelneurohumoralactivationlmyocardialhypertrophy1.Compensate heart failurecardiacdilatation,bywayoftheFrank-Starlingprincip
9、le,contractileforceincreases.1正常静息正常静息2正常活动正常活动3心衰活动心衰活动3心衰静息心衰静息心肌收缩性心肌收缩性BADC左室舒张末容量左室舒张末容量图图321正正常常和和心心力力衰衰竭竭时时对对机机体体活活动动时时的的代代偿偿情况情况最最 大大 活活动动活动活动静息静息左左室室作作功功呼呼 吸吸 困困难难肺水肿肺水肿E4静息静息致死性心肌受损致死性心肌受损1.Compensate heart failureneurohumoralactivationa.Increaseinsympatheticnervousactivityb.RAASactivated(
10、renninangiotensionaldosteronesystem)心力衰竭心力衰竭神经体液的代偿和失代偿神经体液的代偿和失代偿交感神经激活交感神经激活水、钠潴留水、钠潴留水肿水肿 肺瘀血肺瘀血血流动力学异常血流动力学异常血管收缩血管收缩心肌耗氧量增加心肌耗氧量增加心肌氧供应降低心肌氧供应降低心肌细胞功能心肌细胞功能障碍和坏死障碍和坏死心肌重塑心肌重塑功能恶化功能恶化疾病进展疾病进展血管紧张素血管紧张素儿茶酚胺儿茶酚胺毒性作用毒性作用心肌细胞凋亡心肌细胞凋亡肾素肾素-血管紧张素系统激活血管紧张素系统激活代偿代偿失代偿失代偿心衰症状心衰症状体征加重体征加重治疗目标治疗目标增强心肌收缩增强心肌
11、收缩心肌细胞死亡心肌细胞死亡心力衰竭心力衰竭心肌细胞死亡心肌细胞死亡+心肌能量消耗心肌能量消耗后负荷后负荷血管收缩血管收缩心排血量心排血量神经体液兴奋神经体液兴奋RASSASInSP3循环循环心肌能量消耗心肌能量消耗胞浆胞浆Ca2+cAMPInSP3心脏心脏心肌松弛性心肌松弛性变力效应变力效应+心律失常心律失常猝死猝死图图322肾素肾素血管紧张素和交感血管紧张素和交感肾肾上腺素能系统激活时对心脏代偿功能的影响上腺素能系统激活时对心脏代偿功能的影响2.RAASinHeartFailure2.RAASinHeartFailure1.Compensate heart failure myocardi
12、al hypertrophy MyocardialcellhypertrophysystolepowerNotincreasednumberMyocardialfibreincreasednumberenergyMyocardialcompliance(顺应性）2.Ventricular remodeling2.Ventricular remodelingheart failure is the result of ventricular remodeling.ReducethemyocardialcellsdecreaseofthesystolicfunctionIncreasedmyoca
13、rdialfibrosis decreaseoftheVentricularcomplianceHeart cavity expansionmyocardial hypertrophyextracellular matrixcollagen fibersMyocardial cells3.about diastolic insufficiency Characteristic:inthesecases,fillingoftheleftorrightventricleisabnormal.Mechanism:lmyocardialrelaxationisimpaired.lMyocardialc
14、ompliancedecreasing.outcome:diastolicpressures-venousereturn-fluidretention,dyspnea,intolerance4.some cytofactors take part in heart failure ANP(atrialnatriureticpeptide)BNP(brainnatriureticpeptide)AVP(argininevassopressin)Endothelin(NE,angiotensin)Urine volumeperipheral vascularsympathetic nervousR
15、AASVentricular remodeling Ventricular remodelingneurohumoral activationheart failureChronic heart failure,CHFClinical manifestations1.Left heart failurepulmonarycongestionlesscardiacoutput2.Right heart failuresystemicvenouscongestion3.Whole heart failure1.Left heart failure 1)dyspnea1.exertional dys
16、pnea2.paroxysmal nocturnal dyspnea3.orthopnea,4.acute pulmonary edema 1.Left heart failure2)cough,hemoptysis,spit pink sputum 3)fatigue,dizziness,palpitation.4)oliguria,renal dysfunctionsignsign 1)pulmonary basal rales bilaterally or right-side2)enlarged left heart pulsus alternans,protodiastolic ga
17、llop P2 increasedPulmonaryedema 2.Right heart failuresymptomuabdominaldiscomfortuanorexia(厌食)unausea,vomituexertionaldyspnea 2.Right heart failuresignuliver enlargeduascitesudistention of jugular veinsuhepatojugular reflux(+)uperipheral edema,most mark in dependent partsucyanosisuprotodiastolic gall
18、op,u functional murmurs of tricuspid and pulmonary valve3.Whole heart failureLHFRHFlaboratory examinationBNP and NT-proBNP阳性阳性阴性阴性NT-proBNP NT-proBNP 临床应用流程图临床应用流程图辅助诊断心衰辅助诊断心衰辅助判断进展期心衰患者预后辅助判断进展期心衰患者预后laboratory examinationCnTIbloodroutineexaminationroutineurineexaminationbiochemicalexaminationFT3,
19、FT4,TSHECG(electrocardiogram)lischemialOMIlconductionblocklarrhysmiaX-rayPulmonarycongestionPleuraleffusionKerlryBRightpulmonaryarterybroadeningPulmonaryhilarbutterflyshape EchocardiogramlLVEF50%lE/A1.2lLVEDV/LVESVLVEDV/LVESVlLVEDD/LVESDLVEDD/LVESDlventricularwallmotionCardiac magnetic resonance,CMR
20、99MTC-MIBI SPECT(radionuclide)Coronary angiographyCardiacCatheterizationSwan-GanzPCWP12mmHgCI2.5L/（min.m2）CardiopulmonaryExerciseTesting(CPET)lChronicstableHFlMeasurementofrateofoxygenuptake(VO2),rateofCO2production(VCO2),duringmaximal“symptom-limited”exerciseDiagnosis and differential diagnosis1.Di
21、agnosis:medical history+symptoms+signs+examExam:(1)ECG:rarely normal in systolic HF.(2)x-ray:to detect cardiomegaly and pulmonary congestion.(3)Echocardiogram:It is critical importance.to determine the underlying causes of HF to assess the severity of ventricular dysfunction a.function of contractio
22、n:LVEF50%b.function of relaxation:E/A1.2 2.Differential diagnosis:cardiacasthmaBronchialasthmaHistoryHeartdiseaseallergichistoryageolderyoungtimenightspringHFsignyesnoLungsignpulmonarybasalrales typicalwheezingx-rayPulmonarycongestionLVlargeemphysemaalleviatesymptomsofdyspneaDiureticsdigitalisisosor
23、bidedinitrateaftercoughoutsputumantispasmodic2.Differential diagnosis:Pericardial effusion,Constrictive pericarditis:distention of jugular veins,hepatojugular reflux(+)liver enlarged,ascitesperipheral edema,most mark in dependent parts medical history signs of heart and perivascular echocardiogram,C
24、MR the most sensitive specific noninvasive method2.Differential diagnosis:Hepatocirrhosis with ascites and edema of lower extremity distention of jugular veins(-)hepatojugular reflux(-)Treatment of chronic heart failurePrinciple:A.alleviatesymptoms,improvelifequality.B.treatmentforprimarydiseaseandp
25、recipitatingcausesC.AntagonismofneurohumoralactivationD.inhibitionofprogressiveventricularremodelingE.reducemortalityandextendlife.Treatment of chronic heart failurelGenerallPharmacologic treatmentlNon-medicine treatmentGeneral treatmentdecreased burdensincreased systole powerAnti-neurohumoral activ
26、ationGeneral treatmentdecreased burdensincreased systole powerAnti-neurohumoral activation1.LifestylemanagementuEducationuRegulateweightuDietarymanagement:salttake2.Restandaction3.Treatmentforprimarydiseaseandprecipitating General treatmentdecreased burdensincreased systole powerAnti-neurohumoral ac
27、tivation1.Rest2.Dietarymanagement:salttake3.Diuretics furosemidedihydrochlorothiazide(potassium-losing)antistone(potassium-sparing)The main point of diuretics applicationl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）l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。l如能耐受，利尿剂始终应与ACEI和-受体阻滞剂一起使用。
28、（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（类，B级）。The main point of diuretics applicationGeneral treatmentdecreased burdensincreased
29、 systole powerAnti-neurohumoral activation1.Rest2.Dietarymanagement:salttake3.Diuretics4.Vasodilator sodium nitroprusside(SNP)nitroglecerinregitine(酚妥拉明酚妥拉明)The main point of Vasodilator applicationl直接血管扩张剂对于CHF的治疗无特殊作用。（类类，A级）l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（类，B级）l禁忌证：血容量不足，低血压、肾功能衰竭 心脏流出道或
30、瓣膜狭窄患者General treatmentdecreased burdensincreased systole powerAnti-neurohumoral activation1.Digitalis （1）effection:Positiveinotropic：inhibitNa+-K+-ATPenzymeintrocellularNa+、K+Na+-Ca2+exchangeintrocellularCa2+myocardialsystolepowerintrocellularK+，digitalispoisoningGeneral treatmentdecreased burdensi
31、ncreased systole powerAnti-neurohumoral activation1.Digitalis （1）effection:Positiveinotropic：Electrophysiological Inhibitcondutionsystem,espiciallyatriventricularjunction.Improvetheautorhythmictyofatrium,junctionregionandventricle.General treatmentdecreased burdensincreased systole powerAnti-neurohu
32、moral activation1.Digitalis （1）effection:Positiveinotropic：ElectrophysiologicalParasympatheticstimulatinganti-sympatheticnerveexciting General treatmentdecreased burdensincreased systole powerAnti-neurohumoral activation1.Digitalis （1）effection:Positiveinotropic：ElectrophysiologicalParasympatheticst
33、imulatingRoleintherenaltubulecellsreducingsodiumreabsorptioninhibitthesecretionofrenin General treatmentdecreased burdensincreased systole powerAnti-neurohumoral activation1.Digitalis （2）applicationindication:chroniccongestiveheartfailurecomplicatedbyatrailflutterandfibrillationandarapidventricularr
34、ateGeneral treatmentdecreased burdensincreased systole powerAnti-neurohumoral activation1.Digitalis （2）applicationcontraindication:WPWwithAFdegreeAVB,degreeAVBsicksinussyndrome(SSS)Hypertrophiccardiomyopathy(HOCM)severemitralstenosis(SMS)acutemyocardiacinfarction(first24hGeneral treatmentdecreased b
35、urdensincreased systole powerAnti-neurohumoral activation1.Digitalis (3)digitalispoisoningfactors：K+,O2,RFClincalexpression:gastricbowelreaction;arrhythmia;neurologicalandvisualchangeDiagnosis：2.0ng/mlArrhythmiaofdigitalispoisoninglVentricularPrematurebeatlNonparoxysmalatrioventricularjunctionaltach
36、ycardialAtrialPrematurebeatlAtrialfibrillatonlAtrioventricularblocklST-TchangelikefishhookCharacteristicfeatureGeneral treatmentdecreased burdensincreased systole powerAnti-neurohumoral activation1.Digitalis Treatmentofdigitalispoisoningdrugwithdrawaltachycadia:supplyK+,Lidocainivbradicadia：atropini
37、v,notsuitableforpacemakernotsuitableforisoprenalinedisablecardioerterGeneral treatmentdecreased burdensincreased systole powerAnti-neurohumoral activation 1、Digitalis2 2、-excitant-excitantDopamine：NEprecursor2g/kg.minDopamine-R(+)expandrenalartery2-5g/kg.min12-R(+)myocardialcontractility,Vasodilate5
38、-10g/kg.min-R(+)BP,HRDobutamine：Dopaminederivatives2g/kg.min10g/kg.minVasodilate,HR-smalleffectsGeneral treatmentdecreased burdensincreased systole powerAnti-neurohumoral activation 1、Digitalis2、-excitant3、Phosphodiesteraseinhibitors1、effect:restrainactivityofphosphodiesterase，thedegradationofcAMP(-
39、)cAMPCa2+channelactivationCa2+-inflowmyocardialcontractilityGeneral treatmentdecreased burdensincreased systole powerAnti-neurohumoral activation 1、Digitalis2、-excitant3、Phosphodiesteraseinhibitors1、effect:2、indications：refractoryheartfailureend-stageheartfailurebeforehearttransplantationGeneral tre
40、atmentdecreased burdensincreased systole powerAnti-neurohumoral activation 1、Digitalis2、-excitant3、Phosphodiesteraseinhibitors1、effect:2、indications：3、drugs：氨力农(Amrinone)VD5-10g/kg.min米力农(Milrinone)VD0.5g/kg.minGeneral treatmentdecreased burdensincreased systole powerAnti-neurohumoral activation 1、D
41、igitalis2、-excitant3、Phosphodiesteraseinhibitors1、effect:2、indications：3、drugs：4、defect：side-effect;mortalityAII AII 产生是通过多种通道产生是通过多种通道 血管紧张素原血管紧张素原肾素肾素血管紧张素血管紧张素 I(1-10)I(1-10)Ang IIAng II（1-81-8）ACEACEAT1AT1AT2AT2血管收缩血管收缩 增殖增殖醛固酮增加醛固酮增加血管扩张血管扩张 抗增殖抗增殖Ang1-7Ang1-7受体激活受体激活血管扩张血管扩张 抗增殖抗增殖ARBGeneral t
42、reatmentdecreased burdensincreased systole powerAnti-neurohumoral activation 1、RAASinhibitor1.AngiotensinConvertingEnzymeInhibitors(ACEI)vdilatebloodvesselsvinhibitRAS,sympatheticsystemvreversetheventricularremodelingvimprovearterystiffnessandsensitivityvImproveendothelialfunctionAT,Inhibitthedegrad
43、ationofbradykininGeneral treatmentdecreased burdensincreased systole powerAnti-neurohumoral activation 1、RAASinhibitor1.AngiotensinConvertingEnzymeInhibitors(ACEI)Clinicalstatusvsymptoms,exercisetolerancevmortalityvdelaytheprogressofheartfailurevreducinghospitalizationratesvpreventHFaftermyocardiali
44、nfarctionGeneral treatmentdecreased burdensincreased systole powerAnti-neurohumoral activation 1、RAASinhibitor1.AngiotensinConvertingEnzymeInhibitors(ACEI)Captopril6.2525mg23/dEnalapril10mg2/dCilazapril2.5mg/dBenazepril2.510mg/dPerindopril24mg/dFosinopril510mg/dRamipril2.5mg/dGeneral treatmentdecrea
45、sed burdensincreased systole powerAnti-neurohumoral activation 1、RAASinhibitor1.AngiotensinConvertingEnzymeInhibitors(ACEI)applicationmethodsustartingwithsmalldosesuiftolerated,graduallyincreasethedoseumonitoringofrenalfunctionandionsrenalfunctionchange,highpotassium,drycough,angioedemaGeneral treat
46、mentdecreased burdensincreased systole powerAnti-neurohumoral activation 1、RAASinhibitor1.AngiotensinConvertingEnzymeInhibitors(ACEI)Contraindication:anuricrenalfailurepregnancyandbrestfeedingwomanallergeRelativeContraindication:renalarterystenosisbilaterallyCr225mol/lk+5.5mmol/lhypotensionGeneral t
47、reatmentdecreased burdensincreased systole powerAnti-neurohumoral activation 1、RAASinhibitor1.AngiotensinConvertingEnzymeInhibitors(ACEI)2.AngiotensinIIreceptorantagonist(ARB)AT-AT1 receptorInhibitRASNoaffectingthedegradationofbradykininGeneral treatmentdecreased burdensincreased systole powerAnti-n
48、eurohumoral activation 1、RAASinhibitor1.AngiotensinConvertingEnzymeInhibitors(ACEI)2.AngiotensinIIreceptorantagonist(ARB)applicationmethodsulessdrycoughandangioedemauwhenHF,firstchoseACEIuwhenHF,shouldnotbecombinedapplicationofACEIandARBLosartan50mg/d;valsartan80mg/dGeneral treatmentdecreased burden
49、sincreased systole powerAnti-neurohumoral activation 1、RAASinhibitor1.AngiotensinConvertingEnzymeInhibitors(ACEI)2.AngiotensinIIreceptorantagonist(ARB)3.Aldosteroneantagonistsspironolactone(SPI)vpotassium-sparingdiureticvreversetheventricularremodelingvimproveprognosisGeneral treatmentdecreased burd
50、ensincreased systole powerAnti-neurohumoral activation 1、RAASinhibitor1.AngiotensinConvertingEnzymeInhibitors(ACEI)2.AngiotensinIIreceptorantagonist(ARB)3.Aldosteroneantagonists4.renininhibitorTACEI/ARBincreasingplasmareninactivityTrenininhibitiorhastheeffectofcardiorenalprotectionTnotACEI/ARBreplac