英文班内科学心力衰竭课件

Heart Failure(HF)HeartFailure(HF)1Heart 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 though the filling pressure of the heart is adequate.Heartfailure(HF)Conception2Categories of HF1.left,rightandwhole2.acuteandchronic3.systolicanddiastolicCategoriesofHF1.left,right3stage of HFA.Pre-heartfailureB.Pre-clincalheartfailureC.ClinicalheartfailureD.Refractoryend-stageheartfailurestageofHF4New York Heart Association Functional ClassificationClass No limitation 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 restClassInability to carry out any physical activity withoutdiscomfortSympotoms at restNewYorkHeartAssociationFun5Stage 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 StageandClassofHF心衰分期是NYHA66-minwalkdistance milddegree：450mmoderatedegree：150-450mseveredegree：150mEvaluationofchronicHFcardiacfunction 6-minwalkdistance7Fundamental causes1.primarymyocardialdisease2.increasedburdenstotheheartFundamentalcausesprimarymyoc8Fundamental causes1.primarydecreasedmyocardialcontractilityA.coronaryheartdiseaseB.myocarditis,cardiomyopathyC.myocardialmetabolicdisorderFundamentalcauses1.primaryd9Fundamental causes2.increasedburdenstotheheartincreasedafterload(pressureload):A.hypertensionB.aorticstenosisC.pulmonarystenosisD.pulmonaryhypertensionFundamentalcauses2.increased10Fundamental causes 2.increasedburdenstotheheartincreasedpreload(volumeload):A.mitralincompetenceB.aorticincompetenceC.tricuspidincompetenceD.atrialseptaldefect(ASD)E.ventricularseptaldefect(VSD)F.patentductusarteriosus(PDA)G.hyperthyroidismH.anemia Fundamentalcauses2.increased11英文班内科学心力衰竭课件12Precipitating causesA.infection,especiallyrespiratoryinfectionB.arrhythmias,AFC.physicaloremotionalexcessese.g.pregnancyanddeliveryD.rapidintravenousinfusion,excessivesalttakingE.malpraticeF.primarydiseasedeteriorationoranewdiseasehappensPrecipitatingcausesinfection13Pathogenesis and pathophysiology1.Compensateheartfailure2.Ventricularremodeling3.Aboutdiastolicinsufficiency4.HumoralfactorschangePathogenesisandpathophysiolo141.Compensate heart failurelFrank-Starlingprinciplelneurohumoralactivationlmyocardialhypertrophy1.CompensateheartfailureFran151.Compensate heart failurecardiacdilatation,bywayoftheFrank-Starlingprinciple,contractileforceincreases.1.Compensateheartfailurecar161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室作功左室作功呼呼 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正常静息2正常活动3心衰活动3心衰静息心肌收缩性171.Compensate heart failureneurohumoralactivationa.Increaseinsympatheticnervousactivityb.RAASactivated(renninangiotensionaldosteronesystem)1.Compensateheartfailureneu18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收缩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19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.RAASinHeartFailure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202.RAASinHeartFailure2.RAASinHeartFailure211.Compensate heart failure myocardial hypertrophy MyocardialcellhypertrophysystolepowerNotincreasednumberMyocardialfibreincreasednumberenergyMyocardialcompliance(顺应性）1.Compensateheartfailuremy222.Ventricular remodeling2.Ventricularremodeling232.Ventricular remodelingheart failure is the result of ventricular remodeling.ReducethemyocardialcellsdecreaseofthesystolicfunctionIncreasedmyocardialfibrosis decreaseoftheVentricularcomplianceHeart cavity expansionmyocardial hypertrophyextracellular matrixcollagen fibersMyocardial cells2.Ventricularremodelingheart243.about diastolic insufficiency Characteristic:inthesecases,fillingoftheleftorrightventricleisabnormal.Mechanism:lmyocardialrelaxationisimpaired.lMyocardialcompliancedecreasing.outcome:diastolicpressures-venousereturn-fluidretention,dyspnea,intolerance3.aboutdiastolicinsufficienc254.some cytofactors take part in heart failure ANP(atrialnatriureticpeptide)BNP(brainnatriureticpeptide)AVP(argininevassopressin)Endothelin(NE,angiotensin)Urine volumeperipheral vascularsympathetic nervousRAASVentricular remodeling 4.somecytofactorstakeparti26 Ventricular remodelingneurohumoral activationheart failureVentricularremode27Chronic heart failure,CHFChronicheartfailure,CHF28Clinical manifestations1.Left heart failurepulmonarycongestionlesscardiacoutput2.Right heart failuresystemicvenouscongestion3.Whole heart failureClinicalmanifestations1.Left291.Left heart failure 1)dyspnea1.exertional dyspnea2.paroxysmal nocturnal dyspnea3.orthopnea,4.acute pulmonary edema 1.Leftheartfailure1)dyspn301.Left heart failure2)cough,hemoptysis,spit pink sputum 3)fatigue,dizziness,palpitation.4)oliguria,renal dysfunction1.Leftheartfailure2)cough,31signsign 1)pulmonary basal rales bilaterally or right-side2)enlarged left heart pulsus alternans,protodiastolic gallop P2 increasedPulmonaryedemasign1)pulmonarybasalrales32 2.Right heart failuresymptomuabdominaldiscomfortuanorexia(厌食)unausea,vomituexertionaldyspnea2.Rightheartfailuresymptom33 2.Right heart failuresignuliver enlargeduascitesudistention of jugular veinsuhepatojugular reflux(+)uperipheral edema,most mark in dependent partsucyanosisuprotodiastolic gallop,u functional murmurs of tricuspid and pulmonary valve2.Rightheartfailuresignliv343.Whole heart failureLHFRHF3.Wholeheartfailure35laboratory examinationBNP and NT-proBNPlaboratoryexaminationBNPand36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呼吸困难,虚弱,运动受限等症状(NT-proBNP)37laboratory examinationCnTIbloodroutineexaminationroutineurineexaminationbiochemicalexaminationFT3,FT4,TSHlaboratoryexaminationCnTI38ECG(electrocardiogram)lischemialOMIlconductionblocklarrhysmiaECG(electrocardiogram)ischemia39X-rayPulmonarycongestionPleuraleffusionKerlryBRightpulmonaryarterybroadeningPulmonaryhilarbutterflyshapeX-rayPulmonarycongestion40 EchocardiogramlLVEF50%lE/A1.2lLVEDV/LVESVLVEDV/LVESVlLVEDD/LVESDLVEDD/LVESDlventricularwallmotionCardiac magnetic resonance,CMR99MTC-MIBI SPECT(radionuclide)Coronary angiographyEchocardiogramLVEF50%Car41CardiacCatheterizationSwan-GanzPCWP12mmHgCI2.5L/（min.m2）CardiacCatheterizationSwan-Ga42CardiopulmonaryExerciseTesting(CPET)lChronicstableHFlMeasurementofrateofoxygenuptake(VO2),rateofCO2production(VCO2),duringmaximal“symptom-limited”exerciseCardiopulmonaryExerciseTesti43英文班内科学心力衰竭课件44Diagnosis and differential diagnosis1.Diagnosis: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 contraction:LVEF50%b.function of relaxation:E/A1.2 Diagnosisanddifferentialdia452.Differential diagnosis:cardiacasthmaBronchialasthmaHistoryHeartdiseaseallergichistoryageolderyoungtimenightspringHFsignyesnoLungsignpulmonarybasalrales typicalwheezingx-rayPulmonarycongestionLVlargeemphysemaalleviatesymptomsofdyspneaDiureticsdigitalisisosorbidedinitrateaftercoughoutsputumantispasmodic2.Differentialdiagnosis:card462.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,CMR the most sensitive specific noninvasive method2.Differentialdiagnosis:Pe472.Differential diagnosis:Hepatocirrhosis with ascites and edema of lower extremity distention of jugular veins(-)hepatojugular reflux(-)2.Differentialdiagnosis:48Treatment of chronic heart failurePrinciple:A.alleviatesymptoms,improvelifequality.B.treatmentforprimarydiseaseandprecipitatingcausesC.AntagonismofneurohumoralactivationD.inhibitionofprogressiveventricularremodelingE.reducemortalityandextendlife.Treatmentofchronicheartfai49Treatment of chronic heart failurelGenerallPharmacologic treatmentlNon-medicine treatmentTreatmentofchronicheartfai50General treatmentdecreased burdensincreased systole powerAnti-neurohumoral activationGeneraldecreasedincreasedAn51General treatmentdecreased burdensincreased systole powerAnti-neurohumoral activation1.LifestylemanagementuEducationuRegulateweightuDietarymanagement:salttake2.Restandaction3.Treatmentforprimarydiseaseandprecipitating GeneraldecreasedincreasedAn52General treatmentdecreased burdensincreased systole powerAnti-neurohumoral activation1.Rest2.Dietarymanagement:salttake3.Diuretics furosemidedihydrochlorothiazide(potassium-losing)antistone(potassium-sparing)GeneraldecreasedincreasedAn53The 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。（I类建议，证据级别C）。Themainpointofdiureticsap54 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 applicationThemainpointofdiureticsap55General treatmentdecreased burdensincreased systole powerAnti-neurohumoral activation1.Rest2.Dietarymanagement:salttake3.Diuretics4.Vasodilator sodium nitroprusside(SNP)nitroglecerinregitine(酚妥拉明酚妥拉明)GeneraldecreasedincreasedAn56The 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 心脏流出道或瓣膜狭窄患者ThemainpointofVasodilator57General treatmentdecreased burdensincreased systole powerAnti-neurohumoral activation1.Digitalis （1）effection:Positiveinotropic：inhibitNa+-K+-ATPenzymeintrocellularNa+、K+Na+-Ca2+exchangeintrocellularCa2+myocardialsystolepowerintrocellularK+，digitalispoisoningGeneraldecreasedincreasedAn58General treatmentdecreased burdensincreased systole powerAnti-neurohumoral activation1.Digitalis （1）effection:Positiveinotropic：Electrophysiological Inhibitcondutionsystem,espiciallyatriventricularjunction.Improvetheautorhythmictyofatrium,junctionregionandventricle.GeneraldecreasedincreasedAn59General treatmentdecreased burdensincreased systole powerAnti-neurohumoral activation1.Digitalis （1）effection:Positiveinotropic：ElectrophysiologicalParasympatheticstimulatinganti-sympatheticnerveexciting GeneraldecreasedincreasedAn60General treatmentdecreased burdensincreased systole powerAnti-neurohumoral activation1.Digitalis （1）effection:Positiveinotropic：ElectrophysiologicalParasympatheticstimulatingRoleintherenaltubulecellsreducingsodiumreabsorptioninhibitthesecretionofrenin GeneraldecreasedincreasedAn61General treatmentdecreased burdensincreased systole powerAnti-neurohumoral activation1.Digitalis （2）applicationindication:chroniccongestiveheartfailurecomplicatedbyatrailflutterandfibrillationandarapidventricularrateGeneraldecreasedincreasedAn62General treatmentdecreased burdensincreased systole powerAnti-neurohumoral activation1.Digitalis （2）applicationcontraindication:WPWwithAFdegreeAVB,degreeAVBsicksinussyndrome(SSS)Hypertrophiccardiomyopathy(HOCM)severemitralstenosis(SMS)acutemyocardiacinfarction(first24hGeneraldecreasedincreasedAn63General treatmentdecreased burdensincreased systole powerAnti-neurohumoral activation1.Digitalis (3)digitalispoisoningfactors：K+,O2,RFClincalexpression:gastricbowelreaction;arrhythmia;neurologicalandvisualchangeDiagnosis：2.0ng/mlGeneraldecreasedincreasedAn64ArrhythmiaofdigitalispoisoninglVentricularPrematurebeatlNonparoxysmalatrioventricularjunctionaltachycardialAtrialPrematurebeatlAtrialfibrillatonlAtrioventricularblocklST-TchangelikefishhookCharacteristicfeatureArrhythmiaofdigitalispoison65General treatmentdecreased burdensincreased systole powerAnti-neurohumoral activation1.Digitalis Treatmentofdigitalispoisoningdrugwithdrawaltachycadia:supplyK+,Lidocainivbradicadia：atropiniv,notsuitableforpacemakernotsuitableforisoprenalinedisablecardioerterGeneraldecreasedincreasedAn66General treatmentdecreased burdensincreased systole powerAnti-neurohumoral activation 1、Digitalis2 2、-excitant-excitantDopamine：NEprecursor2g/kg.minDopamine-R(+)expandrenalartery2-5g/kg.min12-R(+)myocardialcontractility,Vasodilate5-10g/kg.min-R(+)BP,HRDobutamine：Dopaminederivatives2g/kg.min10g/kg.minVasodilate,HR-smalleffectsGeneraldecreasedincreasedAn67General treatmentdecreased burdensincreased systole powerAnti-neurohumoral activation 1、Digitalis2、-excitant3、Phosphodiesteraseinhibitors1、effect:restrainactivityofphosphodiesterase，thedegradationofcAMP(-)cAMPCa2+channelactivationCa2+-inflowmyocardialcontractilityGeneraldecreasedincreasedAn68General treatmentdecreased burdensincreased systole powerAnti-neurohumoral activation 1、Digitalis2、-excitant3、Phosphodiesteraseinhibitors1、effect:2、indications：refractoryheartfailureend-stageheartfailurebeforehearttransplantationGeneraldecreasedincreasedAn69General treatmentdecreased 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.minGeneraldecreasedincreasedAn70General treatmentdecreased burdensincreased systole powerAnti-neurohumoral activation 1、Digitalis2、-excitant3、Phosphodiesteraseinhibitors1、effect:2、indications：3、drugs：4、defect：side-effect;mortalityGeneraldecreasedincreasedAn71AII 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（1-1-8 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ARBAII产生是通过多种通道血管紧张素原肾素血管72General treatmentdecreased burdensincreased systole powerAnti-neurohumoral activation 1、RAASinhibitor1.AngiotensinConvertingEnzymeInhibitors(ACEI)vdilatebloodvesselsvinhibitRAS,sympatheticsystemvreversetheventricularremodelingvimprovearterystiffnessandsensitivityvImproveendothelialfunctionAT,InhibitthedegradationofbradykininGeneraldecreasedincreasedAn73General treatmentdecreased burdensincreased systole powerAnti-neurohumoral activation 1、RAASinhibitor1.AngiotensinConvertingEnzymeInhibitors(ACEI)Clinicalstatusvsymptoms,exercisetolerancevmortalityvdelaytheprogressofheartfailurevreducinghospitalizationratesvpreventHFaftermyocardialinfarctionGeneraldecreasedincreasedAn74General treatmentdecreased burdensincreased systole powerAnti-neurohumoral activation 1、RAASinhibitor1.AngiotensinConvertingEnzymeInhibitors(ACEI)Captopril6.2525mg23/dEnalapril10mg2/dCilazapril2.5mg/dBenazepril2.510mg/dPerindopril24mg/dFosinopril510mg/dRamipril2.5mg/dGeneraldecreasedincreasedAn75General treatmentdecreased burdensincreased systole powerAnti-neurohumoral activation 1、RAASinhibitor1.AngiotensinConvertingEnzymeInhibitors(ACEI)applicationmethodsustartingwithsmalldosesuiftolerated,graduallyincreasethedoseumonitoringofrenalfunctionandionsrenalfunctionchange,highpotassium,drycough,angioedemaGeneraldecreasedincreasedAn76General treatmentdecreased burdensincreased systole powerAnti-neurohumoral activation 1、RAASinhibitor1.AngiotensinConvertingEnzymeInhibitors(ACEI)Contraindication:anuricrenalfailurepregnancyandbrestfeedingwomanallergeRelativeContraindication:renalarterystenosisbilaterallyCr225mol/lk+5.5mmol/lhypotensionGeneraldecreasedincreasedAn77General treatmentdecreased burdensincreased systole powerAnti-neurohumoral activation 1、RAASinhibitor1.AngiotensinConvertingEnzymeInhibitors(ACEI)2.AngiotensinIIreceptorantagonist(ARB)AT-AT1 receptorInhibitRASNoaffectingthedegradationofbradykininGeneraldecreasedincreasedAn78General treatmentdecreased burdensincreased systole powerAnti-neurohumoral activation 1、RAASinhibitor1.AngiotensinConvertingEnzymeInhibitors(ACEI)2.AngiotensinIIreceptorantagonist(ARB)applicationmethodsulessdrycoughandangioedemauwhenHF,firstchoseACEIuwhenHF,shouldnotbecombinedapplicationofACEIandARBLosartan50mg/d;valsartan80mg/dGeneraldecreasedincreasedAn79General treatmentdecreased burdensincreased systole powerAnti-neurohumoral activation 1、RAASinhibitor1.AngiotensinConvertingEnzymeInhibitors(ACEI)2.AngiotensinIIreceptorantagonist(ARB)3.Aldosteroneantagonistsspironolactone(SPI)vpotassium-sparingdiureticvreversetheventricularremodelingvimproveprognosisGeneraldecreasedincreasedAn80General treatmentdecreased burdensincreased systole powerAnti-neurohumoral activation 1、RAASinhibitor1.AngiotensinConvertingEnzymeInhibitors(ACEI)2.AngiotensinIIreceptorantagonist(ARB)3.Aldosteroneantagonists4.renininhibitorTACEI/ARBincreasingplasmareninactivityTrenininhibitiorhastheeffectofcardiorenalprotectionTnotACEI/ARBreplacementtherapyGeneraldecreasedincreasedAn81General treatmentdecreased burdensincreased systole powerAnti-neurohumoral activation 1.RAASinhibitor2.-blockersympathetic activation 1 1 receptors receptors 2 2 receptors receptorsa a a a1 1 receptors receptorsmetoprololmetoprololbisoprololbisoprololarrythmiadilatebloodvessels;themyocardialO2Cardiac toxicityCardiac toxicitycarvedilolcarvedilolGeneraldecreasedincreasedAn82General treatmentdecreased burdensincreased systole powerAnti-neurohumoral activation 1.RAASinhibitor2.-blockerInhibitionofsympatheticactivationimproveprognosis 1-blockermetoprolol,bisoprolol 1 1 2 2-blokercarvedilolapplicationmethodsstartingwithsmalldosesiftolerated,graduallyincreasethedosemonitoringofBp,HR,ECGGeneraldecreasedincreasedAn83General treatmentdecreased burdensincreased systole powerAnti-neurohumoral activation 1.RAASinhibitor2.-blockerContraindication:bronchospasmseverebradycardia。atrioventricularblocksevereperipheralvasculardiseaseacuteheartfailureGeneraldecreasedincreasedAn84Treatment of chronic heart failureTherecentadvancesaboutthetreatmentofHFMicturitionrestrainthesympatheticnervoussystemdilatebloodvesselsrhBNPlevosimendanIncreasetheCa2+sensitivitymyocardialcontractilityMediateATP-K+channeldilatebloodvesselsivabradineInhibiteSANIfcurrenttolvaptanCombineV2receptorH2O2reabsoptionTreatmentofchronicheartfai85Treatment of chronic heart failureNon-medicine treatmentTreatmentofchronicheartfai86CardiacResynchronizationTherapy(CRT)CardiacResynchronizationTher87LeftVentricularAssistDevice（LAVD）TransitedtreatmentforhearttransplantationhearttransplantationAdjuvanttherapyforacuteHFLeftVentricularAssistDevice88Treatment of chronic heart failureNon-medicine treatmenthearttransplantationcellreplacementtherapy-SCT(stemcelltransplantation)Treatmentofchronicheartfai89Acuteheartfailure,AHFAcuteheartfailure,AHF90Categories of AHF1.Acuteleftheartfailure2.Acuterightheartfailure3.non-cardiacacuteheartfailureCategoriesofAHF1.Acuteleft91Categories of AHF1.Acuteleftheartfailureudecreasedmyocardialcontractilityuincreasedburdenstothehearttightmitralstenosis,especiallyinpresenceofrapidheartrateextensiveAMIhypertensiontachyarrhythmiaandseverebradyarrhythmiarapidintravenousinfusionCategoriesofAHFAcutelefthe92Categories of AHF2.AcuterightheartfailurelrightventricularinfarctionlpulmonaryembolismlrightheartvalvediseaseCategoriesofAHF2.Acuterigh93Categories of AHF3.non-cardiacacuteheartfailurelhighcardiacoutputsyndromelheart-kidneysyndromelpulmonaryhypertensionCategoriesofAHF3.non-cardia94Killip Classification for acute myocardial infactionClass No sympotoms and signsClass Has sympotoms and signs rales 50%,S3 gallop,X-ray pulmonary congestion Classsever pulmonary edema,rales 50%,Classcardiac shockKillipClassificationfora95Clinical manifestation1.extreme degree of breathl