英文班内科学心力衰竭课件.ppt

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,right and whole 2.acute and chronic3.systolic and diastolic stage of HFA.Pre-heart failureB.Pre-clincal heart failureC.Clinical heart failureD.Refractory end-stage heart failureNew York Heart Association Functional Classificati

3、onClass No limitation of physical activity No sympotoms with ordinary exertion Class Slight limitation of physical activity Ordinary activity causes symptoms Class Marked limitation of physical activity Asymptomatic at rest Class Inability to carry out any physical activity without discomfort Sympot

4、oms 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-min walk distance mild degree：450mmoderate degree：150-450msevere degree：150mEvaluation of chronic HF cardiac function

5、Fundamental causes1.primary myocardial disease2.increased burdens to the heartFundamental causes1.primary decreased myocardial contractility A.coronary heart disease B.myocarditis,cardiomyopathyC.myocardial metabolic disorder Fundamental causes2.increased burdens to the heart increased afterload(pre

6、ssure load):A.hypertension B.aortic stenosisC.pulmonary stenosis D.pulmonary hypertensionFundamental causes 2.increased burdens to the heart increased preload(volume load):A.mitral incompetence B.aortic incompetence C.tricuspid incompetence D.atrial septal defect(ASD)E.ventricular septal defect(VSD)

7、F.patent ductus arteriosus(PDA)G.hyperthyroidismH.anemia Precipitating causesA.infection,especially respiratory infectionB.arrhythmias,AFC.physical or emotional excesses e.g.pregnancy and deliveryD.rapid intravenous infusion,excessive salt taking E.malpraticeF.primary disease deterioration or a new

8、disease happensPathogenesis and pathophysiology1.Compensate heart failure 2.Ventricular remodeling 3.About diastolic insufficiency4.Humoral factors change1.Compensate heart failurelFrank-Starling principlelneurohumoral activationlmyocardial hypertrophy1.Compensate heart failurecardiac dilatation,by

9、way of the Frank-Starling principle,contractile force increases.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 正常和心力衰竭时对机体活动时的代偿正常和心力衰竭时对机体活动时的代偿情况情况最 大 活最 大 活动动活动活动静息静息左室作功左室作功呼 吸 困呼 吸 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 failureneurohumoral activation a.Incr

10、ease in sympathetic nervous activity b.RAAS activated(rennin angiotension aldosterone system)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

11、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+cAMP InSP3 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.RAAS in Hear

12、t Failure 2.RAAS in Heart Failure1.Compensate heart failure myocardial hypertrophy Myocardial cell hypertrophy systole power Not increased number Myocardial fibre increased number energy Myocardial compliance(顺应性）2.Ventricular remodeling 2.Ventricular remodeling heart failure is the result of ventri

13、cular remodeling.Reduce the myocardial cells decrease of the systolic function Increased myocardial fibrosis decrease of the Ventricular compliance Heart cavity expansionmyocardial hypertrophyextracellular matrixcollagen fibersMyocardial cells Compensated stage Decompensated stage3.about diastolic i

14、nsufficiency Characteristic:in these cases,filling of the left or right ventricle is abnormal.Mechanism:l myocardial relaxation is impaired.l Myocardial compliance decreasing.outcome:diastolic pressures-venouse return-fluid retention,dyspnea,intolerance4.some cytofactors take part in heart failure A

15、NP(atrial natriuretic peptide)BNP(brain natriuretic peptide)AVP(arginine vassopressin)Endothelin(NE,angiotensin)Urine volumeperipheral vascularsympathetic nervousRAASVentricular remodeling Ventricular remodelingneurohumoral activationheart failureChronic heart failure,CHFClinical manifestations1.Lef

16、t heart failure pulmonary congestion less cardiac output 2.Right heart failure systemic venous congestion 3.Whole heart failure1.Left heart failure 1)dyspnea1.exertional dyspnea2.paroxysmal nocturnal dyspnea3.orthopnea,4.acute pulmonary edema 1.Left heart failure 2)cough,hemoptysis,spit pink sputum

17、3)fatigue,dizziness,palpitation.4)oliguria,renal dysfunction signsign 1)pulmonary basal rales bilaterally or right-side2)enlarged left heart pulsus alternans,protodiastolic gallop P2 increasedPulmonary edema 2.Right heart failuresymptomuabdominal discomfortuanorexia(厌食)unausea,vomituexertional dyspn

18、ea 2.Right heart failuresignuliver enlargeduascitesudistention of jugular veinsuhepatojugular reflux(+)uperipheral edema,most mark in dependent partsucyanosisuprotodiastolic gallop,u functional murmurs of tricuspid and pulmonary valve3.Whole heart failureLHFRHFlaboratory examination BNP and NT-proBN

19、P心室扩张心室扩张心衰心衰张力增大张力增大BNP释放释放呼吸困难呼吸困难,虚弱虚弱,运动受限等症状运动受限等症状(NT-proBNPNT-proBNP)慢性心衰慢性心衰 转至心脏专科转至心脏专科继续下一步诊断继续下一步诊断阳性阳性阴性阴性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 examination CnTI blood routine examination routine urine examination biochemical examination FT3,F

20、T4,TSHECG(electrocardiogram)lischemialOMIlconduction blocklarrhysmiaX-rayPulmonary congestion Pleural effusion Kerlry BRight pulmonary artery broadeningPulmonary hilar butterfly shape Echocardiograml LVEF 50%l E/A 1.2l LVEDV/LVESVLVEDV/LVESVl LVEDD/LVESDLVEDD/LVESDl ventricular wall motionCardiac ma

21、gnetic resonance,CMR99MTC-MIBI SPECT(radionuclide)Coronary angiographyCardiac CatheterizationSwan-Ganz PCWP12mmHg CI2.5L/（min.m2）Cardiopulmonary Exercise Testing(CPET)lChronic stable HFlMeasurement of rate of oxygen uptake(VO2),rate of CO2 production(VCO2),during maximal“symptom-limited”exerciseDiag

22、nosis 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

23、dysfunction a.function of contraction:LVEF50%b.function of relaxation:E/A1.2 2.Differential diagnosis:cardiac asthma Bronchial asthma HistoryHeart diseaseallergichistoryageolderyoungtimenightspringHF signyesnoLung signpulmonary basal rales typical wheezing x-rayPulmonary congestion LV largeemphysema

24、alleviate symptoms of dyspnea Diureticsdigitalisisosorbide dinitrateafter cough out sputum antispasmodic2.Differential diagnosis:Pericardial effusion,Constrictive pericarditis:distention of jugular veins,hepatojugular reflux(+)liver enlarged,ascitesperipheral edema,most mark in dependent parts medic

25、al history signs of heart and perivascular echocardiogram,CMR 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 failure Principle:A.alleviate

26、 symptoms,improve life quality.B.treatment for primary disease and precipitating causesC.Antagonism of neurohumoral activationD.inhibition of progressive ventricular remodelingE.reduce mortality and extend life.Treatment of chronic heart failurelGenerallPharmacologic treatmentlNon-medicine treatment

27、General treatmentdecreased burdensincreased systole powerAnti-neurohumoral activationGeneral treatmentdecreased burdensincreased systole powerAnti-neurohumoral activation1.Lifestyle managementuEducationuRegulate weightuDietary management:salt take2.Rest and action3.Treatment for primary disease and

28、precipitating General treatmentdecreased burdensincreased systole powerAnti-neurohumoral activation1.Rest2.Dietary management:salt take3.Diuretics furosemide dihydrochlorothiazide (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

29、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）。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25 mg/d，呋塞米20 mg/d，托塞米10 mg/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

30、用剂量大和联合用药时（类，B级）。The main point of diuretics applicationGeneral treatmentdecreased burdensincreased systole powerAnti-neurohumoral activation1.Rest2.Dietary management:salt take3.Diuretics4.Vasodilator sodium nitroprusside(SNP)nitroglecerinregitine(酚妥拉明酚妥拉明)The main point of Vasodilator applicationl

31、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General treatmentdecreased burdensincreased systole powerAnti-neurohumoral activation1.Digitalis （1）effection:Positive inotropic：inhibit Na+-K+-ATP enzyme introcellular Na+、K+Na+-Ca2+exchange i

32、ntrocellular Ca2+myocardial systole power introcellular K+，digitalis poisoningGeneral treatmentdecreased burdensincreased systole powerAnti-neurohumoral activation1.Digitalis （1）effection:Positive inotropic：Electrophysiological Inhibit condution system,espicially atriventricular junction.Improve the

33、 autorhythmicty of atrium,junction region and ventricle.General treatmentdecreased burdensincreased systole powerAnti-neurohumoral activation1.Digitalis （1）effection:Positive inotropic：ElectrophysiologicalParasympathetic stimulating anti-sympathetic nerve exciting General treatmentdecreased burdensi

34、ncreased systole powerAnti-neurohumoral activation1.Digitalis （1）effection:Positive inotropic：ElectrophysiologicalParasympathetic stimulatingRole in the renal tubule cells reducing sodium reabsorption inhibit the secretion of renin General treatmentdecreased burdensincreased systole powerAnti-neuroh

35、umoral activation1.Digitalis （2）application indication:chronic congestive heart failure complicated by atrail flutter and fibrillation and a rapid ventricular rateGeneral treatmentdecreased burdensincreased systole powerAnti-neurohumoral activation1.Digitalis （2）application contraindication:WPW with

36、 AF degree AVB,degree AVBsick sinus syndrome(SSS)Hypertrophic cardiomyopathy(HOCM)severe mitral stenosis(SMS)acute myocardiac infarction(first 24 hGeneral treatmentdecreased burdensincreased systole powerAnti-neurohumoral activation1.Digitalis (3)digitalis poisoningfactors：K+,O2,RFClincal expression

37、:gastric bowel reaction;arrhythmia;neurological and visual changeDiagnosis：2.0 ng/mlArrhythmia of digitalis poisoninglVentricular Premature beatlNonparoxysmal atrioventricular junctional tachycardialAtrial Premature beatlAtrial fibrillaton lAtrioventricular block lST-T change like fishhookCharacteri

38、stic featureGeneral treatmentdecreased burdensincreased systole powerAnti-neurohumoral activation1.Digitalis Treatment of digitalis poisoningdrug withdrawaltachycadia:supply K+,Lidocain ivbradicadia：atropin iv,not suitable for pacemaker not suitable for isoprenaline disable cardioerterGeneral treatm

39、entdecreased burdensincreased systole powerAnti-neurohumoral activation 1、Digitalis2 2、-excitant-excitantDopamine：NE precursor2g/kg.min Dopamine-R(+)expand renal artery2-5 g/kg.min 1 2-R(+)myocardial contractility,Vasodilate5-10 g/kg.min -R(+)BP,HR Dobutamine：Dopamine derivatives 2g/kg.min 10g/kg.mi

40、n Vasodilate,HR-small effectsGeneral treatmentdecreased burdensincreased systole powerAnti-neurohumoral activation 1、Digitalis2、-excitant3、Phosphodiesterase inhibitors 1、effect:restrain activity of phosphodiesterase，the degradation of cAMP(-)cAMP Ca2+channel activation Ca2+-inflowmyocardial contract

41、ility General treatmentdecreased burdensincreased systole powerAnti-neurohumoral activation 1、Digitalis2、-excitant3、Phosphodiesterase inhibitors 1、effect:2、indications：refractory heart failureend-stage heart failure before heart transplantation General treatmentdecreased burdensincreased systole pow

42、erAnti-neurohumoral activation 1、Digitalis2、-excitant3、Phosphodiesterase inhibitors 1、effect:2、indications：3、drugs：氨力农(Amrinone)VD 5-10 g/kg.min 米力农(Milrinone)VD 0.5 g/kg.minGeneral treatmentdecreased burdensincreased systole powerAnti-neurohumoral activation 1、Digitalis2、-excitant3、Phosphodiesteras

43、e inhibitors 1、effect:2、indications：3、drugs：4、defect：side-effect;mortality AII 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 treatmentdecreased burdensincreased

44、 systole powerAnti-neurohumoral activation 1、RAAS inhibitor1.Angiotensin Converting Enzyme Inhibitors(ACEI)v dilate blood vesselsv inhibit RAS,sympathetic systemv reverse the ventricular remodeling v improve artery stiffness and sensitivity v Improve endothelial function AT,Inhibit the degradation o

45、f bradykininGeneral treatmentdecreased burdensincreased systole powerAnti-neurohumoral activation 1、RAAS inhibitor1.Angiotensin Converting Enzyme Inhibitors(ACEI)Clinical status v symptoms,exercise tolerance v mortality v delay the progress of heart failure v reducing hospitalization rates v prevent

46、 HF after myocardial infarction General treatmentdecreased burdensincreased systole powerAnti-neurohumoral activation 1、RAAS inhibitor1.Angiotensin Converting Enzyme Inhibitors(ACEI)Captopril 6.2525mg 23/d Enalapril 10 mg 2/d Cilazapril 2.5 mg/d Benazepril 2.510 mg/d Perindopril 24 mg/d Fosinopril 5

47、10 mg/d Ramipril 2.5 mg/dGeneral treatmentdecreased burdensincreased systole powerAnti-neurohumoral activation 1、RAAS inhibitor1.Angiotensin Converting Enzyme Inhibitors(ACEI)application methods ustarting with small dosesuif tolerated,gradually increase the doseumonitoring of renal function and ions

48、 renal function change,high potassium,dry cough,angioedema General treatmentdecreased burdensincreased systole powerAnti-neurohumoral activation 1、RAAS inhibitor1.Angiotensin Converting Enzyme Inhibitors(ACEI)Contraindication:anuric renal failure pregnancy and brest feeding woman allergeRelative Con

49、traindication:renal artery stenosis bilaterally Cr225 mol/l k+5.5mmol/l hypotensionGeneral treatmentdecreased burdensincreased systole powerAnti-neurohumoral activation 1、RAAS inhibitor1.Angiotensin Converting Enzyme Inhibitors(ACEI)2.Angiotensin II receptor antagonist(ARB)AT-AT1 receptor Inhibit RA

50、S No affecting the degradation of bradykininGeneral treatmentdecreased burdensincreased systole powerAnti-neurohumoral activation 1、RAAS inhibitor1.Angiotensin Converting Enzyme Inhibitors(ACEI)2.Angiotensin II receptor antagonist(ARB)application methods uless dry cough and angioedema uwhen HF,first