Cardiac insufficiency

Introduction Structure What is the normal cardiac structure and function? Structure

Function pumping blood endocrine

Process of pumping blood excitation contration pumping blood

Cardiac output (CO, minute volume): stroke volume × heart rate Stroke volume: end-diastolic volume (145ml) - end-systolic volume (75ml) Factors of effecting cardiac output: preload, afterload, myocardial contractility, heart rate

Concept Cardiac insufficiency： causes pump function Heart failure： Congestive heart failure： Myocardial failure：

What is the causes and precipitating factors of heart failure？

Ⅰ The cause,precipitating factor and classification of heart failure Ⅰ) Etiology 1. cardiac muscles was injured: ① mycardiopathy: myocardial infarction, myocarditis etc.

② cardiac muscle’s metabolism was disturbanced : ischemia，hypoxia , deficit of vitamin B1 . ▲primary myocardial contractility /diastolic function 2. ventricular load was overweight ① afterload : BP , valvular stenosis ② preload : valvular regurgitation, high dynamic circulation ▲ secondary myocardial contractility /diastolic function

Ⅱ) predisposing factors 3. ventricular fill balk 4. arrhythmia Ⅱ) predisposing factors 1. general infection ① metabolic rate ② endotoxin ③ heart rate ④ infection of respiratory system 2. disorders of acid-base and electrolyte ① acidosis ② hyperkalemia

Cases 3. arrhythmia 4. pregnancy and delivery Case1 患者,女性,36岁。 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。 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6 cm，压痛；脾于肋下3 cm。指端呈杵状，下肢明 显凹陷性水肿。

化验:白细胞18×109/L 中性粒细胞占90% 尿量300-500ml/日, 少量蛋白和细胞, 尿胆红素（++） 血浆总胆红素31.6µmol/L(正常<17.1) 直接胆红素12.8µmol/L (正常<3.4) 血清尿素氮正常 诊断:风湿性心脏病 二尖瓣关闭不全 心力衰竭

1) 诊断该患者存在心力衰竭的根据是什么？ 2) 哪些因素诱发和加重了心力衰竭？ 3) 病人先后出现了哪些形式的呼吸困难？ 4) 病人为什么有下肢水肿和肝功能异常？ Case2 男性患者，75岁。 主诉：间断呼吸困难7年，加重20余天。 现病史：患者7年前劳累后出现胸闷、气短，偶 伴夜间阵发性呼吸困难，诊断“充血性心力衰竭，高 血压病”。出院后可步行400-500米，无夜间阵发性 呼吸困难。

是否发生了心力衰竭？如何诱发的？ 1.为什么会出现劳累后胸闷、气短？ 2.什么是夜间阵发性呼吸困难？有何意义？ 2年来，间断发作胸闷、憋气，多于感冒后或劳累 后发生，严重时走路5米即发生呼吸困难，夜间睡眠 不能平卧，伴双下肢水肿。多次入急诊和病房治疗。 20余天前患者受凉感冒后，咳嗽、咳白粘痰，不 伴发热，有胸闷、憋气症状，活动后加重，夜间不 能平卧，夜间阵发性呼吸困难发作2-3次/夜，伴双 下肢水肿。 是否发生了心力衰竭？如何诱发的？

辅助检查：WBC 11000/mm3, HGB 15.5 g/dL, 既往史：患高血压病8年，血压最高(170-180/ 监测血压。发现2型糖尿病8年，自今年起使用胰岛 素控制血糖，未监测血糖。1年前发现房颤，为阵发 性，未治疗。不吸烟，不喝酒。 查体：BP：170/80mmHg，P：84次/分，双下肺可 闻及细小湿罗音。心界扩大，心律齐，各瓣膜区未 闻及杂音。腹软，无压痛，肝脾肋下未触及，双下 肢轻度凹陷性水肿。 辅助检查：WBC 11000/mm3, HGB 15.5 g/dL, PLT 13.4万/mm3,BUN 6.6 mmol/L

心电图：心房颤动，电轴左偏，重度顺钟向转位, 室内阻滞 胸片：两肺、膈未见异常，心外形饱满，右肺门 角消失 超声心动图：左房左室增大，二尖瓣返流(轻度), 左室舒张功能减低，左室收缩功能减低，LVEF 51%, 左室多条假腱索,LA 42.5mm,LV 63.1mm,IVS 11.8mm 动态心电图：窦性心律,房性早搏,阵发性房性心 动过速，I度房室传导阻滞，室内阻滞，ST-T无异常 诊断：高血压病；心律失常-心房颤动,慢性充血 性心力衰竭 2型糖尿病

Case3 男性患者，54岁。 主诉：12天前剑突下疼痛3天，喘息6天，少尿2天。 现病史：患者12天前晚饭后突发剑突下疼痛，呈 烧灼样，无返酸，无恶心、呕吐，急诊诊断“胃肠 炎”，予654－2解痉治疗，疼痛持续3天逐渐缓解。 6天前患者“感冒”后出现喘息，休息后缓解。2天 前发现足部水肿，自觉尿少。1天前查心电图示急性 前壁心肌梗死。 超声心动图示室壁节段性运动异常（前壁、前间 壁、侧壁中段-心尖）右室舒张功能减低，LVEF33%。

查体：P:88次/分，BP:112/74mmHg。 冠脉造影示LAD6段100％闭塞，对其植入支架。 发病以来，饮食睡眠可，无夜间阵发性呼吸困 难，大便1次/日。 查体：P:88次/分，BP:112/74mmHg。 神清，双肺呼吸音清，左肺中下部散在少量哮鸣 音，左肺底可闻及细湿啰音，心界不大，心率88次/ 分，律齐，A2=P2，心音低钝, 各瓣膜听诊区未闻及 额外心音及杂音，腹软, 肝脾肋下未及，双下肢无 水肿，双侧足背动脉搏动对称、良好。 心电图：窦性心动过速，电轴不偏，肢导低电压, 前壁心肌梗死

超声心动图：室壁节段性运动异常（前壁、前间 壁、侧壁中段－心尖段），左房增大，二尖瓣返流 （轻度），左室增大，心包少量积液，左室收缩功 能减退，LVEF 33% 诊断： 冠状动脉粥样硬化性心脏病 急性广泛前壁心肌梗死 急性左心衰竭

Ⅲ) classification of heart failure left heart failure： right heart failure： whole heart failure： diastolic heart failure: systolic heart failure: low output heart failure: high output heart failure: acute heart failure chronic heart failure

normal 8 Cardiac 7 output 6 (L/min) 5 4 3 2 1 low output heart failure low output heart failure before high output heart failure after high output heart failure normal

Ⅱ Compensatory/adaptive responses during cardiac insufficiency Ⅰ) activation of mechanism of neuro-humoral regulation 1. excitation of sympathetic nervous system (1) mechanism of excitation cardiac injury cardiac output baroreceptors

ischemia, hypoxia CO2 , H+ chemoreceptors (2) Compensatory effect 1) release of pump repertory A. diastolic efficiency “Frank - Starling mechanism” B. systolic efficiency sympathetic nerve noradrenalin(NE) NE β-receptor cAMP Ca2+ inflow

noradrenalin β-receptor heart rate 2) blood redistribution C. heart rate noradrenalin β-receptor heart rate 2) blood redistribution 3) myocardial remodeling (3) bad effects oxygen consumption pre- and after load catecholamine arrhythmia NE, angiotensinⅡ myocardial remodeling

2. Activation of renin-angiotensin-aldosterone system(RAS) excitation of SNS, cardiac output renin-angiotensin-aldosterone system 3. Other humoral factors endothelin, ADH, atrial natriuretic peptide(ANP), PGI2, nitric oxide

Ⅱ) increase of cytokines and oxygen free radical 1. tumor necrosis factor-α(TNF-α)/other cytokine overload, damage expression of TNF-α myocardial remodeling contractility (表15-5) other cytokine (IL-1,IL-6,TGF-β, PDGF)

Ⅲ) myocardial remodeling and ventricular remodeling 2. oxidative stress overload, damage, ischemia oxygen free radical myocardial injury Ⅲ) myocardial remodeling and ventricular remodeling concept of ① myocardial hypertrophy myocardial ②intercellular substance remodeling ③capillary

concept of ① ventricular hypertrophy ventricular ② chambers heart expanding remodeling ③ disfiguration chambers heart

1. Mechanism of myocardial remodeling damange neuro-humoral overload alteration signal transductive pathway gene expression alteration of (C-myc、C-fos) molecular phenotype molecular remodeling

2. Manifestions of myocardial remodeling 1) concentric hypertrophy after load parallel growth of the sarcomere 2) eccentric hypertrophy preload series-wound growth

3) reactive hypertrophy 3. Compensatory meaning of myocardial remodeling and ventricular remodeling total contractility Laplace law: S=pr/2h S：室壁应力；p：室内压； r：心室半径；h：室壁厚度

4. Disadvantages of myocardial remodeling and ventricular remodeling isoform switch of the proteins in myocardial cells; unbalance of constituent in myocardial cell

Ⅲ mechanism of decrease of cardiac function Ⅰ) decrease of myocardial contractive constituent 1. myocardial cells necrosis ischemia, hypoxia myocarditis myocardiopathy necrosis TNF-α oxygen free radical (OFR)

TNF-α signal pathway apoptosis OFR inflammation ischemia hypoxia TNF-α signal pathway apoptosis OFR inflammation 3. unbalance of constituent of hypertrophy myocardia myofibril , mitochondria

Ⅱ) myocardial energy metabolic disorders 1. production of energy hypoxia, ischemia absence of vitamine B1 ATP

2. impediment of energy of transform and reperdory myocardial hypertrophy myocardial remodeling inhibition of creatine CPK phosphatic kinase(CPK) 3.utilization of energy V1 V3 , activity of ATPase ATP CP C ADP

Ⅲ) impediment of excitation-contraction coupling 1. reduction of responsivity to sympathetic nervous system 1) decrease of NE in myocardial tissue exhaustion of NE tyrosine hydrozylase distribution of sympathetic nerve

3) functional impediment of G-protein Gs Gi 2) sensitivity of β-receptor 3) functional impediment of G-protein Gs Gi 2. impediment of Ca2+ transport 1) impediment of Ca2+ transport in cellular membrane and sarcoplasmic reticulum myocardial remodeling Ca2+ channel 2) Ca2+ ATPase 3) functional impediment of troponin action of hypoxia and acidosis

TNF-α, oxygen free radical damage of cellular membrane Ca2+ inflow diastolic function impediment

Ⅳ) myocardial fibrosis and reduction of myocardial compliance injury of myocardia myocardial fibrosis and ventricular hypertrophy collagenⅠ / collagen Ⅲ normal compliance

Ⅴ) ventricular filling limited and lower coronary blood flow Ⅵ) ventricular activity out of line

Ⅳ effects Ⅰ) cardiac output Ⅱ) venous stagnation 1. systemic venous stagnation neck vein digestive system cardiac edema

2. pulmonary circulatory stagnation pulmonary stagnation pulmonary edema dyspea Mechanism: pulmonary compliance trachea resistance J-receptor chemoreceptor

Forms of dyspnea ： 1) dyspnea on exertion 2) orthopnea 3) paroxysmal nocturnal dyspnea