Download - 心力衰竭 Heart failure , HR
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心力衰竭Heart failure , HR
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不要忽略“心”的健康预防心衰从青壮年做起
首位致死和致残原因:心衰( 2% )与脑卒中急诊: 45/8-9 ( 2% )老年人的健康杀手: 360 万 ( 中 )/250 万(美)心衰“年轻化”老年病“年轻化”男性 > 女性猝死的主要原因
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概述心衰时机体的代偿反应心衰发病机制心衰临床表现的病理生理学基础防治原则
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概述概念病因诱因分类
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收缩
舒张
射血
充盈
CO
CO = HR SV5250L=75 次 / 分 70ml/ 分
CO:Cardiac outputSV:Stroke volumeHR:Heart rate
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收缩
舒张
射血
充盈
CO病因
静脉系统淤血
动脉系统缺血
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心力衰竭心肌收缩和(或)舒张功能障碍引起心泵功能下降,导致 CO 绝对或相对减少,不能满足机体组织代谢需要的一种病理过程。
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病因
病因
收缩和(或)舒张功能障碍
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心肌结构 能量代谢
正常负荷
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心肌结构受损
能量代谢障碍
负荷
收缩、舒张功能障碍
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心肌结构受损心肌病变
心肌炎,心肌病心肌梗死
心肌能量代谢障碍贫血、 VitB1冠状动脉粥样硬化
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病毒性心肌炎 扩张型心肌病
心肌梗死
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心肌结构受损心肌病变
心肌炎,心肌病心肌梗死
心肌能量代谢障碍贫血、 VitB1冠状动脉粥样硬化
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心室负荷过重压力负荷左心压力负荷
高血压主动脉瓣狭窄
右心压力负荷肺动脉高压肺动脉瓣狭窄
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心室负荷过重
容量负荷瓣膜返流
主闭 / 肺闭心内分流
F4- 室间隔缺损高动力循环
1
3
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诱因( 90% )
本质是加重心脏负荷感染(最常见)酸中毒、高钾血症心律失常妊娠和分娩
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分类病情轻重起病及病情发展速度
心输出量( CO )发病部位心肌收缩和舒张功能障碍
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慢性、低心输出量性、全心衰
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概述心衰时机体的代偿反应心衰发病机制心衰临床表现的病理生理学基础防治原则
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CO
维持 CO 正常代偿的实质
代偿
病因
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心脏代偿心外代偿神经 - 体液的代偿反应
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CO = HR SV
射血
收缩
1 2
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HR
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HR机制(神经 - 体液机制)腔静脉和心房淤血房内压 (压力? / 容
量?)感受器传入冲动 心交感 N 紧张性 HR BP
COBP 压力感受器传入冲动 心交感N 紧张性 HR BP
缺血、缺 O2 化学感受器传入冲动 呼吸和心血管中枢兴奋
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HR机制意义利
CO =HRSV维持 BP
弊(> 170-180 次 / 分)耗氧冠脉灌注,心室
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机制Frank-Starling 定律(心肌定律)
紧张源性扩张
心脏扩张(异长调节)
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正常和衰竭心脏心功能曲线和肌节长度的关系
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机制Frank-Starling 定律(心肌定律)
紧张源性扩张
心脏扩张(异长调节)
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意义耗氧肌源性扩张(失代偿)
心脏扩张(异长调节)
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心室舒张末期容量( VEDV )
心输出
量耗氧
量
A
B
VEDV 增加对耗氧量( A )和心输出量( B )的影响
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机制SNS 兴奋和 CA 的正性肌力作用
心肌收缩力(等长调节)
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儿茶酚胺 腺苷酸环化酶
ATP 3` , 5`-cAMP
非蛋白活性激酶 蛋白活性激酶
促使肌浆网对 Ca2+
的摄取、储存和释放心肌收缩
- 受体
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CO = HR SV
异长调节
1 2
等长调节
心肌收缩
急性期、快速、有限
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心肌肥大( mycardial hypertrophy )
全心重量> 500g ,左心重量> 200g
数量?体积?
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心肌肥大( mycardial hypertrophy )
定义类型和机制
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Concentric hypertrophy eccentric hypertrophy
向心性肥大:•压力负荷肌节并联性增生心肌纤维变粗室壁增厚离心性肥大:•容量负荷肌节串联性增生心肌纤维变长心腔扩大
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心肌肥大( mycardial hypertrophy )
定义类型和机制意义
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意义:心肌总收缩力 SV CO 不利:心肌收缩、舒张性能心肌缺血,缺氧能量代谢障碍
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心脏代偿心外代偿神经 - 体液的代偿反应
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血容量•肾小球滤过率( GFR )↓
•肾小管重吸收↑
水钠潴留
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肾小球滤过率( GFR )↓ 有效循环血量↓:心衰
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球—管失平衡基本形式示意图
H2O
Na+
球 - 管平衡
球 - 管失平衡
1 2 3
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血容量↑肾小球滤过率( GFR )↓肾小管重吸收↑
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肾血流重新分布
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血容量↑肾小球滤过率( GFR )↓肾小管重吸收↑
肾血流重新分布肾小球滤过分数 (FF) ↑
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GFR(125ml/min)
肾血浆 (660ml/min)FF =
= 19%
GFR(80ml/min)
肾血浆 (330ml/min)FF =
FF↑ = 24%
心衰
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肾小球滤过分数↑( FF )
FF =GFR
肾血浆流量
肾小管周围血液浓缩,血胶压↑毛压↑ 水钠重吸收↑
Pr
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血容量↑肾小球滤过率( GFR )↓肾小管重吸收↑
肾血流重新分布肾小球滤过分数( FF )↑ RAAS : Aldo ↑ ADH ↑ ( 生成↑灭活↓ ) PGE2 ↓ANP↓
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Aldosterone
ADH
肾小管重吸收水钠
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血容量血液重新分布红细胞促红细胞生成素氧离曲线右移
组织对氧利用能力线粒体:数量、表面积酶活性
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PaO2 ( mmHg )
SO2
( % )
100
20 100
2 , 3DPGH+ , CO2温度
氧合血红蛋白解离曲线及其影响因素
40 60 80
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心脏代偿心外代偿神经 - 体液的代偿反应
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交感 -肾上髓质系统兴奋心血管RAAS : AngII
缩管物质↑: ADH 、内皮素
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利:外周阻力 维持 BP,器官血流灌注水钠潴留血容量
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不利:心脏负荷耗氧心律失常水钠潴留体液因子的损伤作用
细胞因子氧自由基
心肌重构
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心肌重构
心脏在结构、功能、代谢及遗传表型的变化神经 - 内分泌系统过度激活RAAS体液因子持续释放: TGF-β 、 A
ngII , ET-1
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心肌重构
心脏在结构、功能、代谢及遗传表型的变化心肌肥大心肌细胞表型的改变
肌球蛋白重链α- MHC (高 ATPE )→ β- MHC (低 ATPE )
心肌间质重构
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非心肌细胞增生和细胞外基质重建
组成实质细胞( 1/3 )间质细胞( 2/3 ,成纤维细胞)ECM
功能:胶原( I 、 III ) AngII/AT1
间质金属蛋白酶 I正常心肌纤维
肥大心肌纤维
—
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心脏代偿CO = HR SV心肌肥大
心外代偿神经 - 体液的代偿反应
代偿反应小结
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CO
维持 CO 正常代偿的实质
代偿 心衰
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概述心衰时机体的代偿反应
心衰发病机制心衰临床表现的病理生理学基础防治原则
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收缩
舒张
射血
充盈
CO
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正常心肌舒缩的分子基础
收缩蛋白
ATP
Ca 2+
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心肌收缩能力降低心肌收缩蛋白破坏 / 数量心肌细胞坏死(质)心肌细胞凋亡(量)
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1.正常心肌纤维
2.心肌梗塞(第 1天)
3.心肌梗塞( 1-2天)
4.心肌梗塞( 3-4天)心肌细胞的坏死
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心肌细胞凋亡
氧化应激细胞因子Ca 2+
线粒体功能异常
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心肌收缩能力降低
心肌收缩蛋白破坏 / 数量心肌能量代谢障碍( ATP )能量生成、释放障碍能量储存障碍能量利用障碍
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心肌能量生成障碍缺血、缺氧VitB1
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心肌能量储备障碍磷酸肌酸激酶( CPK )活性
ATP CPCPK
肌酸 +
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心肌能量利用障碍ATP酶活性
V1 型 ATPE (,高活性) V3 型 ATPE (,低活性)
ATP ADP Pi+ATPE
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CPK
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心肌收缩能力降低
心肌收缩蛋白结构的破坏 /数量心肌能量代谢障碍心肌兴奋 - 收缩耦联障碍
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2
3
1
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抑制 SR 对 Ca2+摄取、储存和释放
肌浆网 (SR)的 ATP酶活性降低;线粒体对 Ca2+摄取增加,释放 Ca2+缓慢 SR储存 Ca2+细胞内酸中毒肌浆网和钙结合牢固 Ca2+释放缓慢
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抑制 SR对 Ca2+摄取、储存和释放
线粒体
抑制 Ca2+ 的内流
CA
Ca2+
H+ 、 K+
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儿茶酚胺
腺苷酸环化酶
ATP 3` , 5`-cAMP
- 受体
Ca 2+通道激活
↓
↓
心肌肥大
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抑制 Ca2+ 与肌钙蛋白结合
酸中毒 H+与 Ca 2+竞争肌钙蛋白的结合位置 抑制 SR释放 Ca 2+ 高钾血症 破坏线粒体
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心肌收缩能力降低心肌结构的破坏心肌收缩蛋白(质、量)心肌能量代谢障碍心肌兴奋 - 收缩耦联障碍心肌肥大的不平衡生长
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心肌肥大的不平衡生长心肌交感神经分布密度能量代谢障碍:毛细血管密度心肌缺血心肌线粒体数量相对心肌肌球蛋白 ATP酶活性
兴奋 - 收缩耦联障碍
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心肌肥大的不平衡生长
心肌交感神经分布密度能量代谢障碍:毛细血管密度心肌缺血心肌线粒体数量相对心肌肌球蛋白 ATP酶活性
兴奋 - 收缩耦联障碍
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心室舒张功能异常
Ca 2+复位延迟肌球蛋白与肌动蛋白复合体解离障碍心室舒张势能减少心室顺应性
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心脏各部舒缩功能不协调心梗
心律失常
舒缩失调
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心肌收缩心肌舒缩不协调心肌舒张
心肌结构受
损 心肌兴奋-
收
缩耦联障碍
能量代谢障
碍 钙离子复位延
迟 肌球-
肌动蛋
白复合体解离障
碍 心肌顺应性下
降心肌舒张势能减
弱
心律失常
心衰
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对机体的影响
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收缩
舒张
射血
充盈 CO
静脉系统淤血
动脉系统缺血2
2
1
对机体的影响
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CO↓
心泵功能CO 和心脏指数( CI ) 搏出量( SV )和射血分数( EF ) 心室舒张末压( LVEDP )HR 心悸
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心泵功能
器官血流重新分配皮肤、骨骼肌、肾、腹腔
脏器血流明显减少心源性休克
紫绀
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静脉淤血综合征
体循环淤血右心衰与全心衰肺循环淤血左心衰
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静脉淤血和静脉压↑颈静脉充盈或怒张
体循环淤血
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体循环淤血静脉淤血和静脉压↑肝肿大 , 压痛
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体循环淤血静脉淤血和静脉压↑肝肿大 , 压痛心性水肿
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肺循环淤血肺水肿呼吸困难 - 左心衰最早的表现机制:肺淤血,肺水肿
肺顺应性(肺通气 / 血流比值 , V/Q ) 缺氧气道阻力肺间质压力 肺泡毛细血管感受器
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肺循环淤血呼吸困难 - 左心衰最早的表现机制:肺淤血,肺水肿表现形式:
劳力性呼吸困难端坐呼吸夜间阵发性呼吸困难
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肺循环淤血肺水肿呼吸困难 - 左心衰最早的表现肺水肿毛细血管血压↑毛细血管通透性↑
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心衰的防治
防治原发病及消除诱因改善心脏泵血功能减轻心脏前、后负荷改善心脏舒缩功能改善心肌能量代谢
调整神经 - 内分泌活动及干预心室重建替代疗法:干细胞移植
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THE ENDTHANK YOU