外科休克.ppt
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外科休克
surgery shock
什么是休克？
Historical aspects
希波克拉底的思考
? 创伤 出血→止血→希波克拉底面容→死亡
? Traumatic wounds hemorrhage→tourniquet to arrest hemorrhage→Hippocraticfacies
? →imminent death
? 赖得朗 ：1743年 首次将shock 翻译成英语而不用法语choc
? Le Dran: first medical use of the term "shock "in 1743 ,he translated "shock"
?into English ,did not use the French word "choc"
休克：冲击 打击 震荡
shock referred to a violent impact or blow
1815年George james
首次shock描述创伤后生理紊乱
in 1815 George James first used the word shock connote physiologic instability after impact
Keith. 1919年
用染料稀释法确定血容量 休克的另一重要机制是低血容量
Keithin 1919
used dye-dilution method to determine blood volume
provided another mechanism namely hypovolemia
was an important determinant of shock
? Wiggers:
不可逆性休克: 进行性系统循环失代偿
氧供减少氧债
组织损伤
in the early 1940s defined for first time the concept of irreversible shock ,a state characterized as progressive systemic circulatory decompensationimpaired DO2oxygen debt tissue injury or death
? 1960年微循环障碍
? 近年 分子生物学发展
炎性介质 ：细胞因子 白三烯
前列腺素等
Recent work spurred on ,by rapid advances inmolecular biology
inflammatory mediators ,such as CytokinesLeukotrienes PG
休克的定义
definition
? 有效循环血量↓↓
? 组织灌注不足
? 细胞代谢紊乱及功能障碍
的病理过程
? Valid circulation blood volume↓insufficient perfusion of tissues derangement in cellular metabolism and dysfunctionreleased inflammatory mediatorsoxygen demand exceeds the oxygen supply
? 现代观点：休克是一序惯性事件 是一个从亚临床阶段的组织灌注不足到多器官功能障碍的病理过程
? Current interpretation:a continuum ,ranging from subclinical deficits in perfusion to MODS
休克分类classification
? 低血容量休克：出血 血浆容量丢失
Hypovolemic shockHemorrhage losses or plasma volume losses
? 血管源性休克内外源性血管活性介质起作用
Vasogenic shock endogenous exogenous vasoactive mediators play a major role
感染性休克 创伤性休克
Septic traumatic shock
? 心源性休克 cardiogenic shock
? 神经源性休克neurogenic shock
病理生理
pathophysioligy
? 休克的共同特点：有效血容量锐减
组织灌注不足
炎症介质释放
? Common feature :valid circulation volume decreased dramatichypoperfusionelaboration of inflammatory mediators
? 组织低灌注Hypoperfusion:
微循环改变 分布异常
alteration on microcirculationmaldistribution
组织缺氧Tissue hypoxia
代谢改变Anaerobic metabolisms
酸中毒acidosis
炎症介质释放 elaboration of inflammatory
mediators
微循环改变
? 微循环收缩期
Microcirculation contraction stage
微循环血流受毛细血管前括约肌舒缩效应控制
Control of flow through capillaries is effected by contraction and relaxation of precapillary sphincters
?↓ ↓
? HR ↑ 胃肠道低灌注
? 心肌收缩力↑ 不可逆休克
? 组织间液重吸收 SIRS
?Irreversible shock
?SIRS
微循环扩张期
microcirculation dilation stage
? 缺氧 hypoxia
? 无氧代谢 anaerobic metabolism
? 乳酸堆积 lactate accumulation
? 酸中毒acidosis
? 血管舒张介质
NO PGE2 PGI2IL-2 BK
? 血管通透性↑permeability ↑
? 血粘度↑ viscosity ↑
? 静脉回流减少venous return ↓CO ↓
? 心 脑缺血 cardiaccerebral ischemia
微循环衰竭期
microcirculation failure stage
? 毛细血管血流淤滞 Capillary sludging
? 酸中毒 acidosis
? 高凝hypercoagulation
? 红细胞 血小板聚集red cellplatelet
aggregation
? DIC
? 水解酶释放 细胞溶解
代谢改变
metabolism derangement
? 缺氧 无氧代谢 酸中毒
Hypoxiaanaerobic metabolism and acidosis
伤害性组织灌注不足导致氧供不能满足氧耗 休克的主要病理机制
Impaired tissue hypoperfusion the primary pathophisiologicmechanismin shocklead
to decreased oxygen delivery relative to needs
? 无氧代谢
Anaerobic metabolism supervenes
丙酮酸(P) → 乳酸(L)+2ATP
Pyruvate lactate +2ATP
高乳酸血症hyperlactatemia
代谢性酸中毒acidosis
L/P>15-20 细胞缺氧
cellular hypoxia
? 能量代谢障碍Bioenergetic failure
糖异生gluconeogenesis (Adr NE)
蛋白质
脂肪分解
急性相蛋白合成(ACTH)
proteolysis lipolysisacute-phase protein
? 生命膜功能障碍vital membrane
dysfunction
炎症介质及缺血再灌注损伤
inflammatory mediators and ischemia reperfusion injury
? 内毒素endotoxin
G的胞壁成分 脂多糖 感染性休克的强效介质
A cell wall component of gram-negative bacteria and a potent mediator in the development of septic shockas well as a lipopolysaccharide molecule
宿主对内毒素的反应
host responses to endotoxin
? 激活巨噬细胞 补体 凝血系统
Activation of macrophages complement and coagulation systems and release of numerous mediators including TNF-a IL-I,6 PAFNOoxidants
? 巨噬细胞激活同时释放细胞因子是感染性休克生理紊乱的关键
The activation of macrophages by endotoxin with subsequent release of cytokines appears to be a key factor in the physiologic derangement of septic shock
细胞因子
cytokines
? 白介素interleukins (IL)
IL-1→TNF-a IL-6 PAFPG
fever
acute-phase protein
内皮细胞促凝活性↑
endothelial procoagulant activity↑
IL-2→hypotension
TNF-a
IFN-gamma
T 细胞增殖 T cell proliferation
IL-6→ 急性相蛋白合成
acute-phase protein synthesis
中性粒细胞 活性↑
neutrophil activation
? 肿瘤坏死因子(TNF-a)
Tumor necrosis factors
↓
低血压hypotension
乳酸酸中毒lactic acidosis
DIC disseminated intravascular
coagulation
血管通透性增加vascular permeability increase
过氧化物释放oxidants released
? 集落刺激因子
colony stimulating factors
刺激中性粒细胞 巨噬细胞生长
Stimulates growth of granulocytes macrophages
? 干扰素(IFN)Interferone
促进巨噬细胞功能 加强TNF的作用
Promotes macrophages function potentiates the TNF
一氧化氮NO nitric oxide
由精氨酸代谢产生 又称内皮细胞源性舒因子 具强力血管扩张 抑制血小板集聚 可引起难治性低血压
NO is produced from the metabolism of L-arginineformerly called endothelium-derived relaxing factora potent vasodilator and inhibitor of platelet agg-regationrefractory hypotension......（后略) ......
外科休克
surgery shock
什么是休克？
Historical aspects
希波克拉底的思考
? 创伤 出血→止血→希波克拉底面容→死亡
? Traumatic wounds hemorrhage→tourniquet to arrest hemorrhage→Hippocraticfacies
? →imminent death
? 赖得朗 ：1743年 首次将shock 翻译成英语而不用法语choc
? Le Dran: first medical use of the term "shock "in 1743 ,he translated "shock"
?into English ,did not use the French word "choc"
休克：冲击 打击 震荡
shock referred to a violent impact or blow
1815年George james
首次shock描述创伤后生理紊乱
in 1815 George James first used the word shock connote physiologic instability after impact
Keith. 1919年
用染料稀释法确定血容量 休克的另一重要机制是低血容量
Keithin 1919
used dye-dilution method to determine blood volume
provided another mechanism namely hypovolemia
was an important determinant of shock
? Wiggers:
不可逆性休克: 进行性系统循环失代偿
氧供减少氧债
组织损伤
in the early 1940s defined for first time the concept of irreversible shock ,a state characterized as progressive systemic circulatory decompensationimpaired DO2oxygen debt tissue injury or death
? 1960年微循环障碍
? 近年 分子生物学发展
炎性介质 ：细胞因子 白三烯
前列腺素等
Recent work spurred on ,by rapid advances inmolecular biology
inflammatory mediators ,such as CytokinesLeukotrienes PG
休克的定义
definition
? 有效循环血量↓↓
? 组织灌注不足
? 细胞代谢紊乱及功能障碍
的病理过程
? Valid circulation blood volume↓insufficient perfusion of tissues derangement in cellular metabolism and dysfunctionreleased inflammatory mediatorsoxygen demand exceeds the oxygen supply
? 现代观点：休克是一序惯性事件 是一个从亚临床阶段的组织灌注不足到多器官功能障碍的病理过程
? Current interpretation:a continuum ,ranging from subclinical deficits in perfusion to MODS
休克分类classification
? 低血容量休克：出血 血浆容量丢失
Hypovolemic shockHemorrhage losses or plasma volume losses
? 血管源性休克内外源性血管活性介质起作用
Vasogenic shock endogenous exogenous vasoactive mediators play a major role
感染性休克 创伤性休克
Septic traumatic shock
? 心源性休克 cardiogenic shock
? 神经源性休克neurogenic shock
病理生理
pathophysioligy
? 休克的共同特点：有效血容量锐减
组织灌注不足
炎症介质释放
? Common feature :valid circulation volume decreased dramatichypoperfusionelaboration of inflammatory mediators
? 组织低灌注Hypoperfusion:
微循环改变 分布异常
alteration on microcirculationmaldistribution
组织缺氧Tissue hypoxia
代谢改变Anaerobic metabolisms
酸中毒acidosis
炎症介质释放 elaboration of inflammatory
mediators
微循环改变
? 微循环收缩期
Microcirculation contraction stage
微循环血流受毛细血管前括约肌舒缩效应控制
Control of flow through capillaries is effected by contraction and relaxation of precapillary sphincters
?↓ ↓
? HR ↑ 胃肠道低灌注
? 心肌收缩力↑ 不可逆休克
? 组织间液重吸收 SIRS
?Irreversible shock
?SIRS
微循环扩张期
microcirculation dilation stage
? 缺氧 hypoxia
? 无氧代谢 anaerobic metabolism
? 乳酸堆积 lactate accumulation
? 酸中毒acidosis
? 血管舒张介质
NO PGE2 PGI2IL-2 BK
? 血管通透性↑permeability ↑
? 血粘度↑ viscosity ↑
? 静脉回流减少venous return ↓CO ↓
? 心 脑缺血 cardiaccerebral ischemia
微循环衰竭期
microcirculation failure stage
? 毛细血管血流淤滞 Capillary sludging
? 酸中毒 acidosis
? 高凝hypercoagulation
? 红细胞 血小板聚集red cellplatelet
aggregation
? DIC
? 水解酶释放 细胞溶解
代谢改变
metabolism derangement
? 缺氧 无氧代谢 酸中毒
Hypoxiaanaerobic metabolism and acidosis
伤害性组织灌注不足导致氧供不能满足氧耗 休克的主要病理机制
Impaired tissue hypoperfusion the primary pathophisiologicmechanismin shocklead
to decreased oxygen delivery relative to needs
? 无氧代谢
Anaerobic metabolism supervenes
丙酮酸(P) → 乳酸(L)+2ATP
Pyruvate lactate +2ATP
高乳酸血症hyperlactatemia
代谢性酸中毒acidosis
L/P>15-20 细胞缺氧
cellular hypoxia
? 能量代谢障碍Bioenergetic failure
糖异生gluconeogenesis (Adr NE)
蛋白质
脂肪分解
急性相蛋白合成(ACTH)
proteolysis lipolysisacute-phase protein
? 生命膜功能障碍vital membrane
dysfunction
炎症介质及缺血再灌注损伤
inflammatory mediators and ischemia reperfusion injury
? 内毒素endotoxin
G的胞壁成分 脂多糖 感染性休克的强效介质
A cell wall component of gram-negative bacteria and a potent mediator in the development of septic shockas well as a lipopolysaccharide molecule
宿主对内毒素的反应
host responses to endotoxin
? 激活巨噬细胞 补体 凝血系统
Activation of macrophages complement and coagulation systems and release of numerous mediators including TNF-a IL-I,6 PAFNOoxidants
? 巨噬细胞激活同时释放细胞因子是感染性休克生理紊乱的关键
The activation of macrophages by endotoxin with subsequent release of cytokines appears to be a key factor in the physiologic derangement of septic shock
细胞因子
cytokines
? 白介素interleukins (IL)
IL-1→TNF-a IL-6 PAFPG
fever
acute-phase protein
内皮细胞促凝活性↑
endothelial procoagulant activity↑
IL-2→hypotension
TNF-a
IFN-gamma
T 细胞增殖 T cell proliferation
IL-6→ 急性相蛋白合成
acute-phase protein synthesis
中性粒细胞 活性↑
neutrophil activation
? 肿瘤坏死因子(TNF-a)
Tumor necrosis factors
↓
低血压hypotension
乳酸酸中毒lactic acidosis
DIC disseminated intravascular
coagulation
血管通透性增加vascular permeability increase
过氧化物释放oxidants released
? 集落刺激因子
colony stimulating factors
刺激中性粒细胞 巨噬细胞生长
Stimulates growth of granulocytes macrophages
? 干扰素(IFN)Interferone
促进巨噬细胞功能 加强TNF的作用
Promotes macrophages function potentiates the TNF
一氧化氮NO nitric oxide
由精氨酸代谢产生 又称内皮细胞源性舒因子 具强力血管扩张 抑制血小板集聚 可引起难治性低血压
NO is produced from the metabolism of L-arginineformerly called endothelium-derived relaxing factora potent vasodilator and inhibitor of platelet agg-regationrefractory hypotension......（后略) ......
附件资料：
相关资料1：
- 创伤性休克早期液体复苏的临床研究.pdf
- 230例严重创伤并休克患者的体液复苏及麻醉管理分析.pdf
- 休克的概念与治疗.pdf
- 非控制性出血性休克的液体治疗新进展.pdf
- 低血容量休克复苏指南.pdf
- 低血容量休克复苏指南(2007).pdf
- AMI合并心源性休克的研究进展.PDF
- 失血性休克复苏的新认识.pdf
- 成人严重感染与感染性休克血流动力学监测与支持指南_2006_.pdf
- 失血性休克的研究与治疗进展.pdf
- 最新“休克的早期液体复苏”.pdf
- 创伤性休克液体复苏的探讨.pdf
- 2008年成人严重脓毒症和脓毒性休克治疗指南解读_2_.pdf
- 2008年严重脓毒症和脓毒性休克治疗指南简读.pdf
- 血管外肺水指数对感染性休克患者预后的评价.pdf