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1、 Heart Failure Department of Department of pathophysiologypathophysiology XiangrongXiangrong Sun Sun2024/9/2Fundamental knowledge Heart is one of the most important organs in body. The main function of heart is to providing impetus for circulation of blood.2024/9/2volumevolume：like left fistlike lef
2、t fistweightweight：500g500gEjection of bloodEjection of blood： 70ml/SV70ml/SV70/min70/min 60min60min24h24h 7056 L/d7056 L/d10.810.8万次万次/ /天天2024/9/2Histology of myocardiumIntercalated disc2024/9/22024/9/2SRmitochondrionCa2+Ca2+ 10-7mol/LCa2+ 10-5mol/LRelease of Ca2+2024/9/2tropomyosincontraction（粗）（
3、粗）myosin（细）（细）actintroponinInteraction pointCa2+ATPase2024/9/2Ca2+ 10-5mol/LSRmitochondrionCa2+Ca2+ 10-7mol/LReuptake of Ca2+2024/9/2relaxationtropomyosin（粗）（粗）myosin（细）（细）actintroponinInteraction pointCa2+ATPase2024/9/22024/9/2AP and contraction of cardiac myocyte2024/9/22024/9/2 冠心病冠心病 (CHD) 高血压高血
4、压 (Hypertension) 心肌病心肌病 (Cardiomyopathy) 瓣膜疾病瓣膜疾病(Valvular heart disease)Heart failureWhat causes heart failure?2024/9/2In addition to those causes above, the following factors also can play a role in determining if heart failure will affect you:1.family history of heart disease(家族史）家族史） 2.diabetes（
5、糖尿病）糖尿病） 3.marked obesity（肥胖）肥胖） 4.heavy consumption of alcohol, or tobacco（酗酒、（酗酒、 吸烟）吸烟）5.large salt intake in diet （高盐饮食）高盐饮食）Other factors2024/9/2 heart failure is the pathological process in which the systolic or/and diastolic function of the heart impaired, and as result , cardiac output decre
6、ase and is unable to meet the metabolic demands of body Concept of heart failure2024/9/2the systolic or/and diastolic function of the heart impairedcardiac output decreaseunable to meet the metabolic demands of bodyheart failure2024/9/2contractilitypreloadStroke VolumeCardiac outputafterloadDetermin
7、ants of cardiac function2024/9/2Myocardial impairmentCardiomyopathies、 Myocarditis 、Toxicity、 Myocardial infarction Metabolic abnormalitiesIschemia 、Hypoxia 、Deficiency of VitB1 EtiologyDecreased myocyte contractility2024/9/2vpressure overload (afterload) Systemic hypertention;Aortic valvular stenos
8、is;Pulmonary hypertention;Pulmonary valvular stenosisVentricular ejectionOverload for myocardium2024/9/2Mitral or aortic regurgitation;Tricuspid and pulmonary regurgitation;High cardiac output (hyperthyroidism、Arterivenous fistula、anemia)Loading condition of the heart at the end of diastole v volume
9、 overload （preload ） etiology of heart failure2024/9/2Restriction of fillingMitral or/and tricuspid stenosis;Pericardial disease: Constrictive pericarditis, Endomyocardial fibrosis;Infiltrative diseases: AmyloidosisVentricular filling2024/9/2voutputlow-output heart failurehigh-output heart failure(*
10、compared with healthy adult)Classification2024/9/2Low output heart failure before high output heart failurehigh output heart failureNormal output health adult2024/9/2vonsetacute heart failurechronic heart failure2024/9/2vLocationleft-sided heart failureright-sided heart failure whole heart failure 2
11、024/9/2法洛氏四联征法洛氏四联征2024/9/2Compensatory responses2024/9/2vincreased heart ratev cardiac dilationv myocardial hypertrophy Cardiac compensation2024/9/2(一一) Increased heart rate v Mechanismpressure receptorvolume receptorsympathetic nerve excited HR2024/9/2v advantageThis adaptation may increase the ca
12、rdiac outputAnd maintain the perfusion of heart and brainv disadvantageIf heart rate 180times/min, it will:Increase the consumption of oxygen of heartReduce the duration for ventricular fillingInadequate flow of the coronary artery (squeeze, lumen, narrow)2024/9/2(二二) cardiac dilatationFrank-Starlin
13、g lawnormal condition 1.7 2.0 2.2 3.6 mstrength of contractinitial length of musle2024/9/2Frank-Starling law: The more a myocyte or ventricular chamber is stretched ,the more it will contract2024/9/2Ventricular end-diastolic volume (ml) (EDV)Stroke volume (ml)Fig. 13-2 Relationship between EDV and s
14、troke volumeFrank-Staling curve2024/9/2vtonicity dilation: the volume of ventricle increases due to the sarcomere dilation, accompanying the increased cardiac contractility and stoke volumevmyocardiogenic dilation: the stretch of sarcomere does not accompany the increased cardiac contractility.2024/
15、9/2(三三) Myocardial hypertrophy vconceptionincrease in volume and weight2024/9/2concentric hypertrophyeccentric hypertrophy2024/9/2Concentric hypertrophy: is the response to pressure overload. It is associated with increased number of sarcomere arranged in parallel. The increase in wall thickness red
16、uces wall tension and cardiac compliance without increasing the internal chamber size. eccentric hypertrophy: the response to volume overload is characterized by dilation of chamber size, as well as relative decreased wall thickness. It is thought to result from increased number of sarcomere arrange
17、d in series. concept2024/9/2Eccentric hypertrophyConcentric hypertrophyCausesPreloadAfterloadReplication forms of sarcomereIn seriesParellel connectionMorphologic changeChambers of heart enlarge obviouslyHeart wall increases obviously Wall thickness /radius of chambers/NSignificanceAlleviating prelo
18、adOvercoming the afterload2024/9/2GPCR胞膜胞膜 Ca2+离子通道离子通道Ca2+IP3DAGGqPLCPKCBiologic responses in hypertrophyCA, Ang等等GsRR肌钙蛋肌钙蛋白结合白结合兴奋兴奋- -收收缩偶联缩偶联心肌收缩心肌收缩基因表达增加，心肌和血管平滑肌增生基因表达增加，心肌和血管平滑肌增生cAMPPKA(+)细胞内细胞内Ca2+库库MAPK家族家族/NHE-1CaM-K2024/9/2Significance of myocardial hypertrophy Enhancing the contractil
19、ity of heart Decreasing wall tension and oxygen consumption2024/9/2v Reduced in the concentration of NE and 1-adrenergic receptor (Tyrosine hydroxylase )v Decreased oxygen and blood supply vAltered of energy metabolism and utilizationvDysfunction of excitation-contraction couplingExcessive cardiac h
20、ypertrophyvDecreased compliance (collagen)2024/9/2(二二) Redistribution of blood flowadvantage？disadvantage ？(四四) Increased ability of cells to use oxygen(三三) Increase in red cells advantage？disadvantage ？(一一) Increased blood volumeadvantage？disadvantage ？Systemic compensation2024/9/2Increased blood v
21、olumev 机制机制 1.肾小球滤过率（ CA ，AGII , PGE2 ,肾血流)2.肾小管对水钠的重吸收肾内血流重分布：皮质髓质水钠的重吸收 肾小球滤过分数=肾小球滤过率/肾血流量.促进水钠重吸收的激素（醛固酮ADH ） 抑制水钠重吸收的激素（PGE2 利钠素）2024/9/22024/9/2v交感肾上腺髓质系统激活交感肾上腺髓质系统激活 (activation of sympathetic-adrenal medulla system) v 肾素肾素- -血管紧张素血管紧张素- -醛固酮系统激活醛固酮系统激活 (activation of renin-angiotensin-aldos
22、terone system, RAAS) Neurohumoral compensation2024/9/2血流重新分布血流重新分布肾肾血管收缩血管收缩GFRRAASAng钠水重吸收钠水重吸收ET心缩力心缩力血管收缩血管收缩RAAS血容量血容量血压血压心衰心衰 心输出量心输出量 压力感受器压力感受器 交感交感 迷走迷走 心缩力心缩力血管收缩血管收缩 缺血缺氧缺血缺氧 化学感受器化学感受器 呼吸深快呼吸深快 回心血量回心血量血压血压sympathetic-adrenal medulla system2024/9/2Renin-angiotensin system and concept of i
23、ts inhibitory actionAngiotensinogenLiverKid-neyLungAngiotensin Angiotensin Vascular contractionAngiotension IIReceptor antangonistsACEInhibitorsAngiotensin converting enzyme(ACE)ReninRenin inhibitorsetc.etc.etc.Receptor2024/9/2心力衰竭与机体的代偿模式图心力衰竭与机体的代偿模式图 心力衰竭心力衰竭 机体代偿机体代偿心脏心脏HR心脏紧张源性扩张心脏紧张源性扩张心肌肥大心肌肥
24、大收缩力收缩力舒缩功能舒缩功能心外心外血容量血容量血液重分配血液重分配红细胞、肌红蛋白红细胞、肌红蛋白心血供心血供有效循环血量有效循环血量供血供氧供血供氧利用氧能力利用氧能力细胞线粒体数细胞线粒体数 、呼吸酶活性、呼吸酶活性SVCO心肌舒缩功能降低心肌舒缩功能降低R x SV = CO 组织细胞缺血缺氧组织细胞缺血缺氧神经神经-体液体液交感交感-肾上腺髓质系统肾上腺髓质系统ARRS血容量血容量血液重分配血液重分配收缩力收缩力2024/9/2v infection ( pulmonary infection) precipitating factors Precipitating factors
25、2024/9/2infection heart rate diastolic phase shortenfeverendotoxinrespiratory infection2024/9/2v cardiac dysrhythmia precipitating factors2024/9/2 尤其是快速型心律失常尤其是快速型心律失常 心率心率 舒张期缩短舒张期缩短 心肌耗氧量心肌耗氧量 冠脉血流冠脉血流 心肌缺血、缺氧心肌缺血、缺氧 心室充盈心室充盈 心泵功能心泵功能 心输出量心输出量房室活动协调性紊乱2024/9/2 water-electrolytes and acid-base dist
26、urbance precipitating factors Ca2+ inflow , SR released Ca2+ binding to troponin activity of ATP enzymesensitivity of Cap to CA acidosis (H+)Hyperpotassaemia(Hyperkalemia)myocardial conductibility autorhythmicity cardiac contractilitymyocardial excitability2024/9/2vpregnancy and delivery precipitati
27、ng factors2024/9/2 妊娠期血容量妊娠期血容量（临产期（临产期） 分娩时疼痛、精神紧张、分娩时疼痛、精神紧张、 稀释性贫血稀释性贫血 交感一肾上腺髓质系统兴奋交感一肾上腺髓质系统兴奋 高动力循环状态高动力循环状态 静脉回流静脉回流 小血管收缩小血管收缩 心脏前负荷心脏前负荷 （左室）后负荷（左室）后负荷 心肌耗氧量心肌耗氧量和冠脉流量和冠脉流量 心输出量心输出量 2024/9/2Excessively labor and spiritual burden; infusion precipitating factors2024/9/2(一一) loss of cardiomyoc
28、yte(二二) metabolic dysfunction of myocardium(三三) dysfunction of excitation-contraction couplingPathogenesisDecreased myocardial contractility2024/9/2(一一) loss of cardiomyocyteDecreased myocardial contractilityvcardiomyocyte necrosis vcardiomyocyte apoptosiscontractility decreased2024/9/22024/9/22024/
29、9/2myocardial cell apoptosis : apoptotic index 35.5%oxidative stresscytokinesmitochondria dysfunctionischemia hypoxiamyocardial cell apoptosismyocardial cell heart failurecalcium homeostasis disequilibrium2024/9/2(二二) metabolic dysfunction of myocardiumv impaired energy production v reduced energy r
30、eserve v impaired energy utilization Decreased myocardial contractility2024/9/21.impaired energy production myocardialmyocardial ischemia ischemia hypoxiahypoxia ATP : Contractility decreased Ca2+mitochondria dysfunctionSynthesis of contractile proteinDisorder of myocardial energy metabolism2024/9/2
31、2. reduced energy reservephosphocreatine kinaseATPcreatineCPMyocardial hypertrophy activity of phosphocreatine kinase CP Disorder of myocardial energy metabolism2024/9/23. impaired energy utilizationActivity of myosin Activity of myosin ATPaseATPase V1 (): V2 (): V3 ():Myocardial hypertrophy activit
32、y of ATPase decreaseDisorder of myocardial energy metabolism2024/9/2能量生成能量生成能量利用能量利用脂肪酸脂肪酸 乳酸乳酸 丙酮酸丙酮酸 葡萄糖葡萄糖 氨基酸氨基酸三羧酸三羧酸循环循环氧化磷氧化磷酸化酸化ATPADP+PiCa2+与肌钙与肌钙 蛋白结合蛋白结合心肌收缩心肌收缩心衰时的能量代谢障碍心衰时的能量代谢障碍CP能量储存能量储存冠脉阻塞冠脉阻塞 休克休克 严重贫血严重贫血VitB1缺乏缺乏ATPase心肌肥大心肌肥大乙酰乙酰 CoACoA2024/9/2(三三) dysfuncion of excitation-cont
33、raction couplingDecreased myocardial contractility1. Altered of Sarcoplasmic reticulum (SR) handling Ca2+2. Reduced influx of extracellular Ca2+3. Dysfunction of Ca2+ binding to troponin 2024/9/22024/9/21.Sarcoplasmic reticulum (SR) mishandling Ca2+vReduced Ca2+ uptake by SR myocardial ischemia Ca2+
34、pump -R PLN phosphorylation Ca2+pumpImpaired excitation-contraction coupling2024/9/2v Reduced Ca2+ reserved by SR Mitochondria uptake Ca2+ Na+ - Ca2+ exchange Ca2+ excretionSR mishandling Ca2+2024/9/2vReduced Ca2+ released by SR Ryanodin receptor (Ry-R) or Ry-R mRNA decreased A Acidosis reduced rele
35、ase of Ca2+ by SRSR mishandling Ca2+2024/9/22. Reduced influx of extracellular Ca2+Ca2+ inflowvoltage dependence - receptor dependenceNa+/Ca2+ exchangeImpaired excitation-contraction coupling2024/9/2L型通道亚单位型通道亚单位2024/9/2G蛋白蛋白ATPcAMP肌膜肌膜激活激活钙备用钙备用通道通道腺苷酸环化腺苷酸环化酶（酶（AC）受体受体蛋白蛋白NE胞外胞外 Ca2+内流障碍内流障碍2024/9
36、/2Na+/Ca2+ exchange：Depolarization Na+ outward Ca2+ inwardRepolarization Na+ inward Ca2+ outwardReduced influx of extracellular Ca2+2024/9/2v K+ impaired influx of Ca2+ (Hyperkalemia)v Reduction of 1-receptor densityv Norepinephrine depletionvH+ depress the sensitivity of receptorCauses of Ca2+ infl
37、ux decreased in heart failure:Reduced influx of extracellular Ca2+v Acidosis decrease the m，L-Ca2+ cannel 2024/9/23. Dysfunction of Ca2+ binding to troponin troponinH+Ca2+Impaired excitation-contraction coupling2024/9/2v Reduced in the concentration of NE and 1-adrenergic receptorv Decreased oxygen
38、and blood supply vAltered of energy metabolism and utilizationvDysfunction of excitation-contraction couplingExcessive cardiac hypertrophyvDecreased compliance2024/9/22024/9/2v Delayed reposition of Ca2+ Ca2+ 10-5 mol/L 10-7 mol/LCa+ATP酶CaCa+CaCa+CaCa+Na+Ca+肌浆网肌浆网ATP 与CaCa+亲和力Diastolic dysfunction20
39、24/9/2ATPCa2+ ATPaseCa2+outflowuptake of Ca2+ by SR Affinity of Ca2+ and Ca2+-Na+ Ca2+ excretionDelayed reposition of Ca2+2024/9/2v Impaired dissociation of the actin-myosin complexImpaired myocardial diastolic propertiesATP2024/9/2v Decreased ventricular diastolic potential Systolic tension decreas
40、edPerfusion of coronary artery decreasedImpaired myocardial diastolic properties2024/9/2v Reduced ventricular compliance myocardial hypertrophy; fibrosis; edema dv/dpImpaired myocardial diastolic properties2024/9/2心室顺应性心室顺应性(ventricular compliance)：心室在：心室在单位压力变化下所引起的容积改变单位压力变化下所引起的容积改变(Dv/dp) PV曲线左移
41、曲线左移PV曲线曲线 V P正常正常降低降低升高升高100 110（ml）30 18 13 10（mmHg）正常正常 V 100 P 10 V 110 P 13心梗心梗（顺顺） V 100 P 18V 110 P 30V稍有增加稍有增加 P增加很多增加很多2024/9/2三、三、 Inconsistent behavior in systolic and diastolic function of the heart2024/9/2SRtin钙库钙库钠钠 钙交换体钙交换体电压依赖性钙通道电压依赖性钙通道受体操纵性钙通道受体操纵性钙通道Ca2+RyRRyR钙释钙释放通放通道道Ca2+Ca2+Ca
42、2+钙泵钙泵Ca2+2024/9/2Summary of the etiology of heart failureHeart failureContractility Loss of cardiomyocyteMetabolic dysfunctionDysfunction of excitation-contraction couplingAltered of SR handling Ca2+Reduced influx of extracellular Ca+Dysfunction of Ca+ binding to troponinDiastolic dysfunction Delay
43、 of Ca+ repositionImpaired dissociation of actin-myocin complexCardiac diastolic potential energy Impaired ventricular complianceInconsistent behavior in systolic and diastolic function 2024/9/2Questions:严重心肌缺血通过哪些机制使心肌收缩力减弱？严重心肌缺血通过哪些机制使心肌收缩力减弱？酸中毒是如何影响心肌收缩力的？酸中毒是如何影响心肌收缩力的？2024/9/2( (一一) ) 肺循环淤血肺循
44、环淤血 (Pulmonary congestion) 当当PCWP18 mmHg时，即出现时，即出现肺循环淤血征，见于左心衰竭。肺循环淤血征，见于左心衰竭。Clinical manifestations2024/9/2 左心衰竭能导致肺淤血、肺水肿；因此主要的左心衰竭能导致肺淤血、肺水肿；因此主要的临床表现是呼吸困难临床表现是呼吸困难 肺水肿肺水肿心力衰竭细胞心力衰竭细胞2024/9/21、呼吸困难呼吸困难 (dyspnea)表现形式表现形式: :v劳力性呼吸困难劳力性呼吸困难: : 活动时发生活动时发生, ,休息减轻休息减轻 (dyspnea on exertion)v端坐呼吸端坐呼吸: :
45、平卧呼吸困难而被迫采取端坐位平卧呼吸困难而被迫采取端坐位 (orthopnea)v夜间阵发性呼吸困难夜间阵发性呼吸困难: :左心衰竭的典型表现左心衰竭的典型表现 (paroxysmal nocturnal dyspnea) 2024/9/2劳力性呼吸困难的发生机制劳力性呼吸困难的发生机制:v回心血量增多，加重肺淤血回心血量增多，加重肺淤血v心率加快，舒张期缩短心率加快，舒张期缩短v机体活动时需氧量增加机体活动时需氧量增加2024/9/2肺活量肺活量胸腔容积胸腔容积端坐呼吸端坐呼吸机制机制肺肺淤血减轻淤血减轻利于气体交换利于气体交换 端坐位端坐位膈肌下移膈肌下移水肿液吸收水肿液吸收回回心血量心血
46、量肺肺淤血减轻淤血减轻缺氧缓解缺氧缓解气体交换气体交换减轻呼吸困难减轻呼吸困难2024/9/2睡眠时睡眠时迷走神经兴奋性迷走神经兴奋性支气管收缩支气管收缩气道气道阻力阻力呼吸费力呼吸费力突感突感呼吸困难呼吸困难平卧位平卧位回回心血心血量量膈肌上移膈肌上移肺活量肺活量肺肺淤血淤血气体交换障碍气体交换障碍PaO2呼吸呼吸肺肺淤血淤血神经反射神经反射敏感性敏感性刺激呼吸中枢刺激呼吸中枢呼吸呼吸夜间阵发性呼夜间阵发性呼吸困难机制吸困难机制2024/9/2 1) 毛细血管压毛细血管压 左心衰左心衰左室舒张末期压力左室舒张末期压力肺毛细血管压肺毛细血管压 超过其代偿能力超过其代偿能力肺水肿肺水肿 2) 毛
47、细血管通透性毛细血管通透性 肺循环淤血肺循环淤血 肺泡通气血流失调肺泡通气血流失调缺氧缺氧 毛细血管通透性毛细血管通透性 肺水肿肺水肿 肺泡表面活性物质破坏肺泡表面活性物质破坏肺泡表面张力肺泡表面张力 毛细血管通透性毛细血管通透性 肺水肿肺水肿2、肺 水 肿2024/9/2( (二二) ) 体循环淤血体循环淤血(Systemic congestion) 当当CVP16 cmH2O时，即出现体循时，即出现体循环淤血征，见于环淤血征，见于右心衰竭右心衰竭及及全心全心衰竭。衰竭。2024/9/2主要表现主要表现v颈静脉充盈或怒张颈静脉充盈或怒张v肝肿大及肝功能损害肝肿大及肝功能损害v胃肠道淤血所致的
48、食欲不振等胃肠道淤血所致的食欲不振等 消化道症状消化道症状v心性水肿心性水肿2024/9/2体循环淤血体征：肝大水肿颈静脉怒张食欲不振、恶心、腹胀肝颈静脉返流征皮下水肿、腹水、胸水2024/9/2全心左心衰右心衰2024/9/2 槟榔肝2024/9/2( (三三) ) 心输出量不足心输出量不足(low cardiac output )2024/9/2v 心输出量心输出量 (cardiac output,CO)减少减少 v 心脏指数心脏指数 (cardiac index,CI)降低降低 v 射血分数射血分数 (ejection fraction)降低降低v 心室充盈心室充盈(ventricula
49、r filling)受损受损v 心率心率(heart rate)增快增快 亦称低排出量综合征亦称低排出量综合征 (syndrome of low output)或或前向衰竭前向衰竭( forward failure) 特点为特点为: 2024/9/2q临床表现临床表现疲乏无力、失眠、疲乏无力、失眠、嗜睡嗜睡 皮肤苍白或发皮肤苍白或发绀绀 尿量减少尿量减少 心源性休克心源性休克 表现形式表现形式表现形式表现形式2024/9/2皮肤肌皮肤肌肉供血肉供血不足不足皮肤皮肤苍白苍白疲乏疲乏无力无力脑供脑供血不血不足足失眠失眠头痛头痛头晕头晕水水肿肿肾血肾血流流减减少少钠水钠水潴留潴留少少尿尿合成合成Pr
50、灭灭活活功功能能 肝功肝功肝肝大大压压痛痛劳劳力力性性呼呼吸吸困困难难端端坐坐呼呼吸吸夜间夜间阵发阵发性呼性呼吸困吸困难难 心力衰竭心力衰竭心心输出量不足输出量不足肺循环淤血肺循环淤血(左衰）左衰）体循环淤血体循环淤血(右衰右衰)肝肝淤血淤血静脉静脉压压呼吸困难呼吸困难肺肺水水肿肿2024/9/2防治的病理生理基础Pathophysiologic basis of prevention and treatment2024/9/2着眼点着眼点从传统的改善血流动力学，减轻症状从传统的改善血流动力学，减轻症状“强心、利尿、扩血管强心、利尿、扩血管”到改善预后，降低总死亡率到改善预后，降低总死亡率针对
51、过度激针对过度激活的神经、内分泌系统（交感神经、肾素活的神经、内分泌系统（交感神经、肾素-血管紧张素血管紧张素-醛固酮系统），进行醛固酮系统），进行“修复修复”药物药物强心甙地位强心甙地位 利尿剂、转化酶抑制剂、利尿剂、转化酶抑制剂、-阻滞剂地位阻滞剂地位 2024/9/220032003年在法国召开的以心衰为主题的国际年在法国召开的以心衰为主题的国际会议上，欧洲心脏学会心衰指南委员会的会议上，欧洲心脏学会心衰指南委员会的主席之一主席之一K. Swedberg建议：应向医生们广建议：应向医生们广泛宣传泛宣传阻滞剂在心衰治疗中的效用阻滞剂在心衰治疗中的效用20062006在西班牙召开的国际会议上
52、再次被强在西班牙召开的国际会议上再次被强调调2024/9/2病史：患风湿性心脏病病史：患风湿性心脏病10余年。近余年。近3月来月来出现心慌、闷气出现心慌、闷气, , 伴浮肿、腹胀，不能平伴浮肿、腹胀，不能平卧。卧。体查：重病容体查：重病容, 半坐卧位半坐卧位, 颈静脉怒张颈静脉怒张, 呼呼吸吸36次次/ /分分, 两肺底可闻湿性罗音。心界向两肺底可闻湿性罗音。心界向左右两侧扩大左右两侧扩大, 心率心率130次次/ /分分, 血压血压(110/80mmHg) 。Clinical example2024/9/2心尖部可闻心尖部可闻IV级收缩期吹风样及舒张期级收缩期吹风样及舒张期雷鸣样杂音。肝脏在右
53、肋下雷鸣样杂音。肝脏在右肋下6 6cmcm可触及，可触及，有压痛，腹部有移动性浊音，骶部及下有压痛，腹部有移动性浊音，骶部及下肢明显凹陷性水肿。肢明显凹陷性水肿。 试分析患者发生了哪些病理生理变化？试分析患者发生了哪些病理生理变化？其发生机制是什么其发生机制是什么? ?2024/9/2111 掌握心力衰竭概念掌握心力衰竭概念; ;心力衰竭发生机制心力衰竭发生机制; ;心心力衰竭时心脏的代偿方式（包括几个重要力衰竭时心脏的代偿方式（包括几个重要概念）概念）熟悉心力衰竭原因及分类熟悉心力衰竭原因及分类; ;心力衰竭时心外心力衰竭时心外代偿反应；心力衰竭临床表现的病理生理代偿反应；心力衰竭临床表现的病理生理基础基础了解心力衰竭时神经了解心力衰竭时神经- -体液的代偿反应，防体液的代偿反应，防治原则治原则本章要求本章要求2024/9/2
