最新心力衰竭PPT课件PPT课件.ppt

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1、心力衰竭心力衰竭 PPT PPT课件课件Precipitating factors (诱诱因因)Infectionarrhythmiaspulmonary embolismpregnancywater,eletrolytes disturbancesacid-base disturbancesemotionInfectionfevertachycardiahypoxiatoxinemiaIncreased demandsArrhythmias(心律失常心律失常)Reduce the time period available for ventricular filling and corona

2、ry perfusionincrease the demand for myocardial oxygenthe dissociation between atrial and ventricular contractions Acidosis and heart failure (酸中毒和心力衰竭酸中毒和心力衰竭)Compete with Ca2+for combination of troponinInfluence the Ca2+trigger mechanism-reduce the sensitivity of the sarcoplasmic reticulum to the l

3、ocal concentrations of Ca2+;result in a reduced release of Ca2+from the SRCompensatory mechanism in heart failure (心衰的代偿机制心衰的代偿机制)1.The Frank-starling mechanism(tonogenic dilatation)2.Increased release of catecholamines 3.Myocardial hypertrophy4.Increase of blood volume and redistribution of blood f

4、low 1.The Frank-starling mechanismSarcomere length(micron)Tension2.2Relationship between myofilament length andtension development in cardiac muscle 3.652.Increased release of catecholamines (儿茶酚胺释放增加儿茶酚胺释放增加)Augment myocardial contractility(the positive inotropic effect)increase heart rate(the posi

5、tive chrotropic effect)elevate the peripheral vascular resistancepressure receptor,volume receptor,chemical receptor 3.Myocardial hypertrophy (心肌肥大心肌肥大)Volume overload eccentric hypertrophyPressure overload concentric hypertrophyMyocardial hypertyophy heart failureIncreased formation of a myosin iso

6、zyme,V3uptake and release of Ca2+by SR may be imparieddiminished activity of sympathetic nervous systemproliferation of mitochondria and capillaries myofilament proliferationincreased collagen in hypertrophic myocardium can lead to a reduced ventricular compliance and interfere with the filling of v

7、entricles?4.increase of blood volume and redistribution of blood flow (血容量增加和血流重分布血容量增加和血流重分布)Water and sodium retensionRedistribution of blood flowClassification of heart failure (心力衰竭的分类心力衰竭的分类)Right-sided versus left-sided heart failureacute versus chronic heart failurehigh-output versus low-outp

8、ut heart failure high out-put heart failure:hyperthyrodism,anemia,arterioveneous fistulas and beriberi(any other factors that decrease the total resistance chronically will also increase the cardiac output)beriberiLack of this vitamin causes diminished ability of the tissues to utilize cellular neut

9、rients,which in turn causes marked peripheral vasodilation.The total peripheral resistance decreases sometimes to as little as one-half normal.consequently,the long time level of cardiac output also increases to as much as 2 times normal.Pathogenesis of heart failure (心力衰竭的发生机制心力衰竭的发生机制)SarcomereThi

10、ck filamentThin filamentMyosinActinTropomyosinTroponinBasic structure of sarcomereTnCTnITnTMyosinTroponinActinTropomyosinMyocardial filament slidingPathogenesis of heart failure (心力衰竭的发生机制心力衰竭的发生机制)Depressed myocardial contractilityaltered diastolic properties of ventriclesasymmetry and asynchronism

11、 in ventricular contraction and relaxation1.Depressed myocardial contractility(心肌收缩功能降低心肌收缩功能降低)Myocardial cellular injuriesMyocardial metabolic dysfunctionDysfunction of excitation-contraction couplingAlterations of the adrenergic nervous system in the failing myocardiumThe relationship between ven

12、tricular dysfunction and prognosisMyocardial infarted sizeCardiacindexMortality5-10%Normal 2%10-20%Slightly decreased 10%20-40%Decreased 22%40%Markedly decreased 60%Energy liberation(ischemia)energy storageenergy utilization(hypertrophy)Myocardial metabolic dysfunction (心肌代谢障碍心肌代谢障碍)Disorders in lib

13、eration of energy ischemic heart disease;shock;severe anemia;hypoxiaDisorders in utilization of energy myocardial hypertrophyDysfunction of excitation-contraction coupling (兴奋和收缩偶联障碍兴奋和收缩偶联障碍)Reduced uptake and release of Ca2+by sarcoplasmic reticulum(SR)Mitochondria Ca2+is greatly increasedExtracel

14、lular Ca2+inward movementDiturbed combination with troponinAlterations of the adrenergic nervous system in the failing myocadium (交感神经系统变化交感神经系统变化)Norepinephrine depletionDowmregulation of belta 1-receptorsUncoupling of belta 2-receptors Receptor-operated channels2.Altered diastolic properties of ve

15、ntricles(舒张功能改变舒张功能改变)Dysfunction of ventricular relaxation-increased cytosol Ca2+concentration;low levels of ATPReduced ventricular compliance-Myocardialhypertrophy;inflammation;edema;fiberosis3.Asymmetry and asynchronism in ventricular contraction and relaxation(心肌收缩舒张不协调心肌收缩舒张不协调)Hypokinesis or a

16、kinesisdyskinesisasynchronismFunctional and metabolic alterations in heart failure (功能代谢变化功能代谢变化)1.Alterations in cardiac function2.Blood pressure change3.Respiratory distressAlterations in cardiac function1.Decreased cardiac output and cardiac index(CI)2.Decreased ejection fraction(EF):stroke volum

17、e/end diastolic volume3.Increased intracardiac pressure:LVEDP-PCWP;RVEDP-CVP4.Alterations in myocardial contractility and its diastolic properties:Vmax and dp/dt max5.Blood pressure change Respiratory distress(呼吸困难呼吸困难)Dyspnea-exertional dyspneaOrthopnea-reduced pooling of fluid in the extremities a

18、nd abdomen;elevation of diaphragmParoxysmal nocturnal dyspnea-reduced adrenergic drive to the left ventricle during sleep;elevation of thracic blood volume during recunbency;normal nocturnal depression of the respiratory center;elevation of diaphragm病例病例 患者，女，患者，女，3636岁。主诉心慌，气闷，浮肿，腹岁。主诉心慌，气闷，浮肿，腹胀三月

19、余。患者有风湿性心脏病十年病史。近三月胀三月余。患者有风湿性心脏病十年病史。近三月来又出现心慌气闷加重，不能平卧而住院治疗。来又出现心慌气闷加重，不能平卧而住院治疗。检查：重病容，半卧位，颈静脉怒张，呼吸检查：重病容，半卧位，颈静脉怒张，呼吸3636次次/分，两肺底闻湿性罗音，心界向两侧扩大，心率分，两肺底闻湿性罗音，心界向两侧扩大，心率130130次分，血压次分，血压14.6/10.7kPa,14.6/10.7kPa,心尖部可闻及收缩期心尖部可闻及收缩期吹风样杂音和舒张期雷鸣样杂音吹风样杂音和舒张期雷鸣样杂音级，肝脏在右侧级，肝脏在右侧锁骨中线肋下锁骨中线肋下6 6厘米，压痛，腹部有移动性浊

20、音，厘米，压痛，腹部有移动性浊音，骶部及下肢明显指压性水肿，腹腔抽出液体，为漏骶部及下肢明显指压性水肿，腹腔抽出液体，为漏出液，血浆蛋白出液，血浆蛋白22g/L,22g/L,球蛋白球蛋白15g/L15g/L。1.1.临床诊断临床诊断?心衰属何种类型心衰属何种类型?发生机制发生机制?2.2.水肿及腹水发生机制水肿及腹水发生机制?端坐呼吸端坐呼吸?心界扩大心界扩大,心率心率130130次次/分分,血压正常血压正常,为什么为什么?Myocardial hypertrophy heart failure?Organic?Histological?Cellular?Molecular?Myocardia

21、l hypertyophy heart failureMolecular:Increased formation of a myosin isozyme-V3Cellular and subcellular:uptake and release of Ca2+by SR;mitochondriaproliferation;uptake and release of Ca2+by mitochondriahistological:diminished activity of sympathetic nervous system and capillaries organic:increased collagen in hypertrophic myocardium can lead to a reduced ventricular compliance and interfere with the filling of ventricles?Coronary heart disease heart failure