医学ppt课件：英文班内科学心力衰竭.ppt

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 though the filling pressure of the heart is adequate.,Categories of HF,1.left,right and whole 2.acute and chronic3.systolic and diastolic,stage of HF,Pre-heart failurePre-clincal heart failureClinical heart failureRefractory end-stage heart failure,New York Heart Association Functional Classification,Class 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 symptoms Asymptomatic at rest Class Inability to carry out any physical activity without discomfort Sympotoms at rest,Stage 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,6-min walk distance,mild degree：450mmoderate degree：150-450msevere degree：150mEvaluation of chronic HF cardiac function,Fundamental causes,primary myocardial diseaseincreased burdens to the heart,Fundamental causes,1.primary decreased myocardial contractility coronary heart disease myocarditis,cardiomyopathymyocardial metabolic disorder,Fundamental causes,2.increased burdens to the heart increased afterload(pressure load):hypertension aortic stenosis pulmonary stenosis pulmonary hypertension,Fundamental causes,2.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,Precipitating causes,infection,especially respiratory infectionarrhythmias,AFphysical or emotional excesses e.g.pregnancy and deliveryrapid intravenous infusion,excessive salt taking malpraticeprimary disease deterioration or a new disease happens,Pathogenesis and pathophysiology,1.Compensate heart failure 2.Ventricular remodeling 3.About diastolic insufficiency4.Humoral factors change,1.Compensate heart failure,Frank-Starling principleneurohumoral activationmyocardial hypertrophy,1.Compensate heart failure,cardiac dilatation,by way of the Frank-Starling principle,contractile force increases.,1.Compensate heart failure,neurohumoral activation a.Increase in sympathetic nervous activity b.RAAS activated(rennin angiotension aldosterone system),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 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,2.RAAS in Heart Failure,心衰时的系统,血管紧张素原非肾素 缓激肽径路 血管紧张素（激肽酶）血管紧张素失活片断醛固酮受体 螺内酯 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.RAAS in Heart Failure,1.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 ventricular remodeling.Reduce the myocardial cells decreaseofthesystolicfunction Increased myocardial fibrosis decreaseofthe Ventricular compliance,Heart cavity expansion,myocardial hypertrophy,extracellular matrix,collagen fibers,Myocardial cells,Compensated stage,Decompensated stage,3.about diastolic insufficiency,Characteristic:in these cases,filling of the left or right ventricle is abnormal.Mechanism:myocardial relaxation is impaired.Myocardial compliance decreasing.outcome:diastolic pressures-venouse return-fluid retention,dyspnea,intolerance,4.some cytofactors take part in heart failure,ANP(atrial natriuretic peptide)BNP(brain natriuretic peptide)AVP(arginine vassopressin)Endothelin(NE,angiotensin),Urine volume,peripheral vascular,sympathetic nervous,RAAS,Ventricular remodeling,Ventricular remodeling,neurohumoral activation,heart failure,Chronic heart failure,CHF,Clinical manifestations,1.Left heart failure pulmonary congestion less cardiac output 2.Right heart failure systemic venous congestion 3.Whole heart failure,1.Left heart failure,1)dyspnea,1.exertional dyspnea,2.paroxysmal nocturnal dyspnea,3.orthopnea,4.acute pulmonary edema,1.Left heart failure,2)cough,hemoptysis,spit pink sputum 3)fatigue,dizziness,palpitation.4)oliguria,renal dysfunction,sign,1)pulmonary basal rales bilaterally or right-side2)enlarged left heart pulsus alternans,protodiastolic gallop P2 increased,Pulmonary edema,2.Right heart failure,symptom,abdominal discomfortanorexia(厌食)nausea,vomit,exertional dyspnea,2.Right heart failure,sign,liver enlargedascites,distention of jugular veinshepatojugular reflux(+),peripheral edema,most mark in dependent parts,cyanosis,protodiastolic gallop,functional murmurs of tricuspid and pulmonary valve,3.Whole heart failure,LHFRHF,laboratory examination,BNP and NT-proBNP,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,laboratory examination,CnTIblood routine examination routine urine examinationbiochemical examinationFT3,FT4,TSH,ECG(electrocardiogram),ischemiaOMIconduction blockarrhysmia,X-ray,Pulmonary congestion Pleural effusion Kerlry BRight pulmonary artery broadeningPulmonary hilar butterfly shape,Echocardiogram,LVEF 50%E/A 1.2LVEDV/LVESVLVEDD/LVESDventricular wall motion,Cardiac magnetic resonance,CMR99MTC-MIBI SPECT(radionuclide)Coronary angiography,Cardiac Catheterization,Swan-Ganz PCWP12mmHg CI2.5L/（min.m2）,Cardiopulmonary Exercise Testing(CPET),Chronic stable HFMeasurement of rate of oxygen uptake(VO2),rate of CO2 production(VCO2),during maximal“symptom-limited”exercise,Diagnosis and differential diagnosis,Diagnosis: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.to determine the underlying causes of HF to assess the severity of ventricular dysfunction a.function of contraction:LVEF50%b.function of relaxation:E/A1.2,2.Differential diagnosis:,2.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 method,2.Differential diagnosis:,Hepatocirrhosis with ascites and edema of lower extremity distention of jugular veins(-)hepatojugular reflux(-),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,有扩张性心脏病基础 有全心衰竭表现有引起急性发作的诱因 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，BP 110/80mmHg。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3 cm。指端呈杵状，下肢明显凹陷性水肿。,病例,实验室检查：红细胞3.01012/L白细胞18109/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31.6mol/L（正常17.1）直接胆红素12.8mol/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56Lmin 心脏指数（CI）正常值2.64.0Lminm2 心搏出量（SV）正常值6070mlbeat 心搏指数（SI）正常值4151 mlm2 LVEDV 正常值90100ml LVESV 正常值3035ml LVEF EF=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 3.340.541.73KPa（12 25413mmHg）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）2130mmHg（中度增高）30mmHg（重度增高）通常 PCWP18mmHg（2.4KPa）肺底出现湿罗音 PCWP25mmHg（3.3KPa）湿罗音12肺野 PCWP30mmHg（4KPa）肺水肿 若无二尖瓣狭窄时，PCWP=LAP=LVEDP,Treatment of chronic heart failure,Principle:alleviate symptoms,improve life quality.treatment for primary disease and precipitating causesAntagonism of neurohumoral activationinhibition of progressive ventricular remodelingreduce mortality and extend life.,Treatment of chronic heart failure,GeneralPharmacologic treatmentNon-medicine treatment,General treatment,1.一般患者应采取高枕位睡眠；较重者采取半卧位或坐位。2.限制体力活动，心力衰竭较重的患者以卧床休息为主；心功能改善后，应适当下床活动，以免下肢血栓形成和肺部感染。3.一定要戒烟、戒酒，保持心态平衡，同时还要保证充足的睡眠。4.少量多餐，低盐饮食,每日食盐不宜超过5克。5.按医嘱服药；预防呼吸道感染；育龄妇女要做好避孕。,General treatment,decreased burdens,increased systole power,Anti-neurohumoral activation,General treatment,decreased burdens,increased systole power,Anti-neurohumoral activation,1.Lifestyle managementEducationRegulate weightDietary management:salt take2.Rest and action3.Treatment for primary disease and precipitating,General treatment,decreased burdens,increased systole power,Anti-neurohumoral activation,1.Rest2.Dietary management:salt take3.Diuretics,furosemidedihydrochlorothiazide(potassium-losing)antistone(potassium-sparing),The main point 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）。,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，特别在服用剂量大和联合用药时（类，B级）。,The main point of diuretics application,General treatment,decreased burdens,increased systole power,Anti-neurohumoral activation,1.Rest2.Dietary management:salt take3.Diuretics4.Vasodilator,sodium nitroprusside(SNP)Nitroglcerin（硝酸甘油）regitine(酚妥拉明),The 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,General treatment,decreased burdens,increased systole power,Anti-neurohumoral activation,1.Digitalis,（1）effection:Positive inotropic：inhibit Na+-K+-ATP enzyme introcellular Na+、K+Na+-Ca2+exchange introcellular Ca2+myocardial systole power introcellular K+，digitalis poisoning,General treatment,decreased burdens,increased systole power,Anti-neurohumoral activation,1.Digitalis,（1）effection:Positive inotropic：Electrophysiological Inhibit condution system,espicially atriventricular junction.Improve the autorhythmicty of atrium,junction region and ventricle.,General treatment,decreased burdens,increased systole power,Anti-neurohumoral activation,1.Digitalis,（1）effection:Positive inotropic：ElectrophysiologicalParasympathetic stimulating anti-sympathetic nerve exciting,General treatment,decreased burdens,increased systole power,Anti-neurohumoral activation,1.Digitalis,（1）effection:Positive inotropic：ElectrophysiologicalParasympathetic stimulatingRole in the renal tubule cells reducing sodium reabsorption inhibit the secretion of renin,General treatment,decreased burdens,increased systole power,Anti-neurohumoral activation,1.Digitalis,（2）application indication:chronic congestive heart failure complicated by atrail flutter and fibrillation and a rapid ventricular rate,General treatment,decreased burdens,increased systole power,Anti-neurohumoral activation,1.Digitalis,（2）application contraindication（禁忌症）:WPW with AF degree AVB,degree AVBsick sinus syndrome(SSS)Hypertrophic cardiomyopathy(HOCM)severe mitral stenosis(SMS)acute myocardiac infarction(first 24 h,General treatment,decreased burdens,increased systole power,Anti-neurohumoral activation,1.Digitalis,(3)digitalis poisoningfactors：K+,O2,Clincal expression:gastric bowel reaction;arrhythmia;neurological and visual changeDiagnosis：2.0 ng/ml,Arrhythmia of digitalis poisoning,Ventricular Premature beatNonparoxysmal atrioventricular junctional tachycardia非阵发性房室交界性心动过速Atrial Premature beatAtrial fibrillaton Atrioventricular block ST-T change like fishhook,Characteristic feature,General treatment,decreased burdens,increased systole power,Anti-neurohumoral activation,1.Digitalis,Treatment of digitalis poisoningdrug withdrawaltachycadia:supply K+,Lidocain ivbradicadia：atropin iv,not suitable for pacemaker not suitable for isoprenaline disable cardioerter,General treatment,decreased burdens,increased systole power,Anti-neurohumoral activation,1、Digitalis2、-excitant,Dopamine：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.min Vasodilate,HR-small effects,General treatment,decreased burdens,increased systole power,Anti-neurohumoral activation,1、Digitalis2、-excitant3、Phosphodiesterase inhibitors,1、effect:restrain activity of phosphodiesterase，the degradation of cAMP(-)cAMP Ca2+channel activation Ca2+-inflowmyocardial contractility,General treatment,decreased burdens,increased systole power,Anti-neurohumoral activation,1、Digitalis2、-excitant3、Phosphodiesterase inhibitors,1、effect:2、indications：refractory heart failureend-stage heart failure before heart transplantation,General treatment,decreased burdens,increased systole power,Anti-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.min,General treatment,decreased burdens,increased systole power,Anti-neurohumoral activation,1、Digitalis2、-excitant3、Phosphodiesterase inhibitors,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),Ang II（1-8）,ACE,AT1,AT2,血管收缩 增殖醛固酮增加,血管扩张 抗增殖,Ang1-7,Ang1-7受体激活,血管扩张 抗增殖,General treatment,decreased burdens,increased systole power,Anti-neurohumoral activation,1、RAAS inhibitor,Angiotensin Converting Enzyme Inhibitors(ACEI),dilate blood vessels inhibit RAS,sympathetic system reverse the ventricular remodeling improve blood flow dynamics Improve endothelial function,AT,Inhibit the degradation of bradykinin,General treatment,decreased burdens,increased systole power,Anti-neurohumoral activation,1、RAAS inhibitor,Angiotensin Converting Enzyme Inhibitors(ACEI),Clinical status symptoms,exercise tolerance mortality delay the progress of heart failure reducing hospitalization rates prevent HF after myocardial infarction,General treatment,decreased burdens,increased systole power,Anti-neurohumoral activation,1、RAAS inhibitor,Angiotensin Converting Enzyme Inhibitors(ACEI),Captopril 6.2525mg 23/d Enalapril 10 mg 2/d Benazepril 510 mg/d Perindopril 24 mg/d Fosinopril 510 mg/d Ramipril 5 mg/d,General treatment,decreased burdens,increased systole power,Anti-neurohumoral activation,1、RAAS inhibito