英文班内科学心力衰竭培训课件

1、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 though the fil

2、ling pressure of the heart is adequate.Heart failure (HF) Conception Categories of HF1. left, right and whole 2. acute and chronic3. systolic and diastolic Categories of HF1. left, rightstage of HFPre-heart failurePre-clincal heart failureClinical heart failureRefractory end-stage heart failurestage

3、 of HFNew York Heart Association Functional ClassificationClass 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 Less than ordinary activity causes sympto

4、ms Asymptomatic at rest Class Inability to carry out any physical activity without discomfort Sympotoms at restNew York Heart Association FunStage and Class of HF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 Stage and Class of HF心衰分期是NYHA6-min walk distance mild degree

5、： 450mmoderate degree： 150-450msevere degree： 150mEvaluation of chronic HF cardiac function 6-min walk distance Fundamental causesprimary myocardial diseaseincreased burdens to the heartFundamental causesprimary myocFundamental causes1. primary decreased myocardial contractility coronary heart disea

6、se myocarditis ,cardiomyopathymyocardial metabolic disorder Fundamental causes1. primary dFundamental causes2. increased burdens to the heart increased afterload (pressure load): hypertension aortic stenosis pulmonary stenosis pulmonary hypertensionFundamental causes2. increasedFundamental causes 2.

7、increased burdens to the heart increased preload (volume load): mitral incompetence aortic incompetence tricuspid incompetence atrial septal defect (ASD) ventricular septal defect (VSD) patent ductus arteriosus(PDA) hyperthyroidism anemia Fundamental causes 2.increased英文班内科学心力衰竭培训课件Precipitating cau

8、sesinfection ,especially respiratory infectionarrhythmias,AFphysical or emotional excesses e.g. pregnancy and deliveryrapid intravenous infusion , excessive salt taking malpraticeprimary disease deterioration or a new disease happensPrecipitating causesinfection Pathogenesis and pathophysiology1.Com

9、pensate heart failure 2. Ventricular remodeling 3.About diastolic insufficiency4. Humoral factors changePathogenesis and pathophysiolo1.Compensate heart failureFrank-Starling principleneurohumoral activationmyocardial hypertrophy1.Compensate heart failureFran1.Compensate heart failurecardiac dilatat

10、ion, by way of the Frank-Starling principle ,contractile force increases.1.Compensate heart failurecar1 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321 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 正常静息2 正常活动3 心衰活动3 心衰静息心肌收缩性1.Compensate heart failureneurohumoral activation a. Increase in sympathe

11、tic nervous activity b. RAAS activated (rennin angiotension aldosterone system)1.Compensate heart failureneu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

12、心排血量神经体液兴奋RASSASInSP3循环心肌能量消耗胞浆Ca2+cAMP InSP3 心脏心肌松弛性变力效应+心律失常猝死图322 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. RAAS in Heart Failure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 2. RAAS in Heart Failure 2. RAAS in Heart Failure1.Compensate heart failure myocardial hypertrophy Myocardial cell hypertrophy systole power Not inc

13、reased number Myocardial fibre increased number energy Myocardial compliance(顺应性）1.Compensate heart failure my2.Ventricular remodeling 2.Ventricular remodeling 2.Ventricular remodeling heart failure is the result of ventricular remodeling.Reduce the myocardial cells decreaseofthesystolicfunction Inc

14、reased myocardial fibrosis decreaseofthe Ventricular compliance Heart cavity expansionmyocardial hypertrophyextracellular matrixcollagen fibersMyocardial cells Compensated stage Decompensated stage2.Ventricular remodeling heart3.about diastolic insufficiency Characteristic : in these cases ,filling

15、of the left or right ventricle is abnormal. Mechanism:myocardial relaxation is impaired.Myocardial compliance decreasing. outcome :diastolic pressures -venouse return-fluid retention , dyspnea , intolerance3.about diastolic insufficienc4.some cytofactors take part in heart failure ANP (atrial natriu

16、retic peptide) BNP (brain natriuretic peptide) AVP (arginine vassopressin) Endothelin (NE, angiotensin)Urine volumeperipheral vascularsympathetic nervousRAASVentricular remodeling 4.some cytofactors take part i Ventricular remodelingneurohumoral activationheart failure Ventricular remodeChronic hear

17、t failure,CHFChronic heart failure,CHFClinical manifestations1.Left heart failure pulmonary congestion less cardiac output 2.Right heart failure systemic venous congestion 3.Whole heart failureClinical manifestations1.Left 1.Left heart failure 1)dyspnea1.exertional dyspnea2.paroxysmal nocturnal dysp

18、nea3.orthopnea,4.acute pulmonary edema 1.Left heart failure 1)dyspn1.Left heart failure 2)cough, hemoptysis, spit pink sputum 3)fatigue,dizziness,palpitation. 4)oliguria,renal dysfunction 1.Left heart failure 2)cough, sign 1) pulmonary basal rales bilaterally or right-side2) enlarged left heart puls

19、us alternans, protodiastolic gallop P2 increasedPulmonary edemasign 1) pulmonary basal rales 2.Right heart failuresymptomabdominal discomfortanorexia(厌食)nausea,vomitexertional dyspnea 2.Right heart failuresymptom 2.Right heart failuresignliver enlargedascitesdistention of jugular veinshepatojugular

20、reflux(+)peripheral edema , most mark in dependent partscyanosisprotodiastolic gallop, functional murmurs of tricuspid and pulmonary valve 2.Right heart failuresignliv3.Whole heart failureLHFRHF3.Whole heart failurelaboratory examination BNP and NT-proBNP心室扩张心衰张力增大BNP释放laboratory examination BNP and

21、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呼吸困难, 虚弱, 运动受限等症状(NT-proBNP)laboratory examination CnTIblood routine examination routine urine examinationbiochemical examinationFT3,FT4,TSHlaboratory examination CnTIECG(electrocardiogram)ischemiaOMIconduction bl

22、ockarrhysmiaECG(electrocardiogram)ischemiaX-rayPulmonary congestion Pleural effusion Kerlry BRight pulmonary artery broadeningPulmonary hilar butterfly shapeX-rayPulmonary congestion EchocardiogramLVEF 50%E/A 1.2LVEDV / LVESVLVEDD / LVESDventricular wall motionCardiac magnetic resonance,CMR99MTC-MIB

23、I SPECT (radionuclide)Coronary angiography EchocardiogramLVEF 50%CarCardiac CatheterizationSwan-Ganz PCWP12mmHg CI2.5L/（min.m2）Cardiac CatheterizationSwan-GaCardiopulmonary Exercise Testing (CPET)Chronic stable HFMeasurement of rate of oxygen uptake (VO2), rate of CO2 production (VCO2), during maxim

24、al “symptom-limited” exerciseCardiopulmonary Exercise Testi英文班内科学心力衰竭培训课件Diagnosis and differential diagnosisDiagnosis: medical history + symptoms + signs + examExam:ECG: rarely normal in systolic HF.x-ray: to detect cardiomegaly and pulmonary congestion.(3) Echocardiogram: It is critical importance

25、 . 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 Diagnosis and differential dia2. Differential diagnosis:cardiac asthma Bronchial asthma HistoryHeart diseaseallergichistoryageolderyou

26、ngtimenightspringHF signyesnoLung signpulmonary basal rales typical wheezing x-rayPulmonary congestion LV largeemphysemaalleviate symptoms of dyspnea Diureticsdigitalisisosorbide dinitrateafter cough out sputum antispasmodic2. Differential diagnosis:card2. Differential diagnosis: Pericardial effusio

27、n, 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. Differential diagnosis: Pe2. D

28、ifferential diagnosis: Hepatocirrhosis with ascites and edema of lower extremity distention of jugular veins (-) hepatojugular reflux(-)2. Differential diagnosis:Treatment of chronic heart failure Principle: alleviate symptoms ,improve life quality.treatment for primary disease and precipitating cau

29、sesAntagonism of neurohumoral activationinhibition of progressive ventricular remodelingreduce mortality and extend life.Treatment of chronic heart faiTreatment of chronic heart failureGeneralPharmacologic treatmentNon-medicine treatmentTreatment of chronic heart faiGeneral treatmentdecreased burden

30、sincreased systole powerAnti-neurohumoral activationGeneral decreased increased AnGeneral treatmentdecreased burdensincreased systole powerAnti-neurohumoral activation1.Lifestyle managementEducationRegulate weightDietary management:salt take2.Rest and action3. Treatment for primary disease and preci

31、pitating General decreased increased AnGeneral treatmentdecreased burdensincreased systole powerAnti-neurohumoral activation1.Rest2. Dietary management:salt take3. Diuretics furosemidedihydrochlorothiazide ( potassium-losing) antistone (potassium-sparing)General decreased increased AnThe main point

32、of diuretics application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-受体阻滞剂一起使用。（I类建议，证据级别C）。The main point of diuretics ap 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

33、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 applicationThe main point of diuretics apGeneral treatmentdecreased burdensincreased systole powerAnti-neurohumoral activation1.Rest2. Dietary management:salt take3. Diu

34、retics4. Vasodilator sodium nitroprusside(SNP) nitroglecerinregitine(酚妥拉明)General decreased increased AnThe main point of Vasodilator application直接血管扩张剂对于CHF的治疗无特殊作用。（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（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The main point of Vasodilator General treatmentdec

35、reased burdensincreased systole powerAnti-neurohumoral activation1.Digitalis （1）effection:Positive inotropic： inhibit Na+-K+-ATP enzyme introcellular Na+、K+ Na+-Ca2+exchange introcellular Ca2+ myocardial systole power introcellular K+ ，digitalis poisoningGeneral decreased increased AnGeneral treatme

36、ntdecreased burdensincreased systole powerAnti-neurohumoral activation1.Digitalis （1）effection:Positive inotropic：Electrophysiological Inhibit condution system, espicially atriventricular junction. Improve the autorhythmicty of atrium, junction region and ventricle.General decreased increased AnGene

37、ral treatmentdecreased burdensincreased systole powerAnti-neurohumoral activation1.Digitalis （1）effection:Positive inotropic：ElectrophysiologicalParasympathetic stimulating anti-sympathetic nerve exciting General decreased increased AnGeneral treatmentdecreased burdensincreased systole powerAnti-neu

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

39、umoral activation1.Digitalis （2）application indication: chronic congestive heart failure complicated by atrail flutter and fibrillation and a rapid ventricular rateGeneral decreased increased AnGeneral treatmentdecreased burdensincreased systole powerAnti-neurohumoral activation1.Digitalis （2）applic

40、ation contraindication:WPW with AF degree AVB , degree AVBsick sinus syndrome(SSS)Hypertrophic cardiomyopathy (HOCM)severe mitral stenosis(SMS)acute myocardiac infarction(first 24 hGeneral decreased increased AnGeneral treatmentdecreased burdensincreased systole powerAnti-neurohumoral activation1.Di

41、gitalis (3) digitalis poisoningfactors： K+ ,O2 ,RFClincal expression: gastric bowel reaction; arrhythmia; neurological and visual changeDiagnosis： 2.0 ng/mlGeneral decreased increased AnArrhythmia of digitalis poisoningVentricular Premature beatNonparoxysmal atrioventricular junctional tachycardiaAt

42、rial Premature beatAtrial fibrillaton Atrioventricular block ST-T change like fishhookCharacteristic featureArrhythmia of digitalis poisonGeneral treatmentdecreased burdensincreased systole powerAnti-neurohumoral activation1.Digitalis Treatment of digitalis poisoningdrug withdrawaltachycadia:supply

43、K+ , Lidocain ivbradicadia： atropin iv, not suitable for pacemaker not suitable for isoprenaline disable cardioerterGeneral decreased increased AnGeneral treatmentdecreased burdensincreased systole powerAnti-neurohumoral activation 1、 Digitalis2、-excitantDopamine： NE precursor2g/kg.min Dopamine -R(+

44、) 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.min Vasodilate, HR -small effectsGeneral decreased increased AnGeneral treatmentdecreased burdensincreased systole powerAnti-neurohumoral activa

45、tion 1、 Digitalis2、-excitant3、Phosphodiesterase inhibitors 1、effect: restrain activity of phosphodiesterase ， the degradation of cAMP(-) cAMP Ca2+ channel activation Ca2+ -inflowmyocardial contractility General decreased increased AnGeneral treatmentdecreased burdensincreased systole powerAnti-neuro

46、humoral activation 1、 Digitalis2、-excitant3、Phosphodiesterase inhibitors 1、effect:2、indications ：refractory heart failureend-stage heart failure before heart transplantation General decreased increased AnGeneral treatmentdecreased burdensincreased systole powerAnti-neurohumoral activation 1、 Digital

47、is2、-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 decreased increased AnGeneral treatmentdecreased burdensincreased systole powerAnti-neurohumoral activation 1、 Digitalis2、-excitant3、Phosphodiesterase inh

48、ibitors 1、effect:2、indications ：3、drugs： 4、defect ： side-effect ; mortality General decreased increased An 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) Ang II（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ARB AII 产生是通过多种通道 血管紧张素原肾素血管General treatmentdecreased burdensincreased systole powerAnti-neu

49、rohumoral activation 1、 RAAS inhibitorAngiotensin Converting Enzyme Inhibitors(ACEI) dilate blood vessels inhibit RAS, sympathetic system reverse the ventricular remodeling improve artery stiffness and sensitivity Improve endothelial function AT ,Inhibit the degradation of bradykininGeneral decrease

50、d increased AnGeneral treatmentdecreased burdensincreased systole powerAnti-neurohumoral activation 1、 RAAS inhibitorAngiotensin Converting Enzyme Inhibitors(ACEI) Clinical status symptoms , exercise tolerance mortality delay the progress of heart failure reducing hospitalization rates prevent HF af

51、ter myocardial infarction General decreased increased AnGeneral treatmentdecreased burdensincreased systole powerAnti-neurohumoral activation 1、 RAAS inhibitorAngiotensin Converting Enzyme Inhibitors(ACEI) Captopril 6.2525mg 23/d Enalapril 10 mg 2/d Cilazapril 2.5 mg/d Benazepril 2.510 mg/d Perindop

52、ril 24 mg/d Fosinopril 510 mg/d Ramipril 2.5 mg/dGeneral decreased increased AnGeneral treatmentdecreased burdensincreased systole powerAnti-neurohumoral activation 1、 RAAS inhibitorAngiotensin Converting Enzyme Inhibitors(ACEI) application methods starting with small dosesif tolerated , gradually i

53、ncrease the dosemonitoring of renal function and ions renal function change, high potassium, dry cough, angioedema General decreased increased AnGeneral treatmentdecreased burdensincreased systole powerAnti-neurohumoral activation 1、 RAAS inhibitorAngiotensin Converting Enzyme Inhibitors(ACEI) Contr

54、aindication: anuric renal failure pregnancy and brest feeding woman allergeRelative Contraindication: renal artery stenosis bilaterally Cr225 mol/l k+5.5mmol/l hypotensionGeneral decreased increased AnGeneral treatmentdecreased burdensincreased systole powerAnti-neurohumoral activation 1、 RAAS inhib

55、itorAngiotensin Converting Enzyme Inhibitors(ACEI) Angiotensin II receptor antagonist (ARB) AT-AT1 receptor Inhibit RAS No affecting the degradation of bradykininGeneral decreased increased AnGeneral treatmentdecreased burdensincreased systole powerAnti-neurohumoral activation 1、 RAAS inhibitorAngio

56、tensin Converting Enzyme Inhibitors(ACEI) Angiotensin II receptor antagonist (ARB)application methods less dry cough and angioedema when HF , first chose ACEIwhen HF , should not be combined application of ACEI and ARB Losartan 50mg/d;valsartan 80mg/dGeneral decreased increased AnGeneral treatmentde

57、creased burdensincreased systole powerAnti-neurohumoral activation 1、 RAAS inhibitorAngiotensin Converting Enzyme Inhibitors(ACEI) Angiotensin II receptor antagonist (ARB)Aldosteroneantagonists spironolactone(SPI)potassium-sparing diuretic reverse the ventricular remodeling improve prognosisGeneral

58、decreased increased AnGeneral treatmentdecreased burdensincreased systole powerAnti-neurohumoral activation 1、 RAAS inhibitorAngiotensin Converting Enzyme Inhibitors(ACEI) Angiotensin II receptor antagonist (ARB)Aldosteroneantagonists renin inhibitor ACEI/ARB increasingplasmareninactivity renininhib

59、itiorhastheeffectof cardiorenalprotection not ACEI/ARB replacement therapyGeneral decreased increased AnGeneral treatmentdecreased burdensincreased systole powerAnti-neurohumoral activation RAAS inhibitor -blockersympathetic activation b1 receptorsb2 receptorsa1 receptorsmetoprolol bisoprololarrythm

60、iadilate blood vessels;the myocardial O2Cardiac toxicity carvedilolGeneral decreased increased AnGeneral treatmentdecreased burdensincreased systole powerAnti-neurohumoral activation RAAS inhibitor -blockerInhibition of sympathetic activation improve prognosis 1- blocker metoprolol , bisoprolol 1 2