外科休克19.ppt

1、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 hemorrhagetourniquet to arrest hemorrhage Hippocratic facies 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

2、use the French word “choc”,休克：冲击 打击 震荡shock referred to a violent impact or blow1815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 Keith in 1919 used dye-dilution method to determine blo

3、od 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 decompensation impaired DO2 ox

4、ygen 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 in molecular biology inflammatory mediators ,such as Cytokines Leukotrienes 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 volumeinsufficient perfusion o

5、f tissues derangement in cellular metabolism and dysfunction released inflammatory mediators oxygen 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

6、血浆容量丢失 Hypovolemic shock Hemorrhage 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 Comm

7、on feature :valid circulation volume decreased dramatic hypoperfusion elaboration of inflammatory mediators,组织低灌注Hypoperfusion: 微循环改变 分布异常 alteration on microcirculation maldistribution 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

8、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,皮肤 皮下 胃肠道 心 脑 Skin subcutaneous gastrointestinal tract heart brain 交感传出 Sympathetic neurat output CA Ang- VP ET TXA2, HR 胃肠道低灌注 心肌收缩力 不

9、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 PGI2 IL-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 cardiac cerebral ischemia,微循环衰竭期microcirculation failu

10、re 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 cell platelet 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 Hypoxia anaerobic 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 pathophisiologic mech

11、anism in shock lead 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/P15-20 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) proteolysi

12、s lipolysis acute-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 shock as well as a lipopolysaccha

13、ride 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 PAF NO oxidants 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 cy

14、tokines 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 PAF PG 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 prote

15、in 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 granulo

16、cytes 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-arginine formerly called endothelium-derived relaxing factor a potent vasodilator and i

17、nhibitor of platelet agg-regation refractory hypotension,过氧化物oxidants,在缺血再灌注时产生 引起缺血再灌注损伤 Oxidants are produced in ischemia-reperfusion injury 缺血时黄嘌呤氧化酶堆积 Under ischemic conditions xanthine oxidase accumulates 再灌注时ATP次黄嘌呤hypoxanthine,H2O2 (xanthine oxidase) SOD Hypoxanthine xanthine + O2- OH 次黄嘌呤 黄嘌

18、呤 Fe,内脏继发性损害,肺 ： 急性肺损伤 肺功能障碍 lung acute lung injury pulmonary dysfunction 肺毛细血管内皮细胞损伤 肺间质水肿 Pulmonary capillary endothelial injury lung interstitial edema 肺泡上皮损伤 肺泡水肿 Alveolar injury edema,表面活性物质减少 肺泡塌陷 Loss of surfactant alveolar collapse ARDS : 难治性低氧血症（refractory hypoxemia),肾renal injury,组织低灌注 Tis

19、sue hypoperfusion 炎性细胞 介质 Inflammatory mediators and cells 血管痉挛 Vasoconstriction 血流分布异常 皮质坏死 Maldistribution cortical ischemia,胃肠道gastrointestinal,缺血损伤及缺血再灌注损伤 Ischemic reperfusion injury 细菌 内毒素移位 Bacteria and endotoxine translocation SIRS MODS,临床表现clinical manifestation,一、有效血容量不足 Inadequate valid b

20、lood volume 1 交感活性增加 Enhanced sympathetic activity 脉压下降 Decrease in the pulse pressure 心率增快 Tachycardia,冷汗 perspiration 四肢发冷extremities cold 焦虑 anxiety,2 灌注不足 hypoperfusion 脉搏微弱 pulselessness 低血压 hypotension 苍白 pallor 静脉瘪馅 venous turgor is lost 毛细血管充盈时间延长2s refilling time prolonged 尿量减少 oliguria (7)

21、 SVO2 乳酸,3组织缺氧tissue hypoxia 酸中毒 Acidosis SVO2 发绀 cyanosis 二 难治性休克refractory shock 1 DIC : 消耗性凝血病 consumptioncoagulopathy PLts Fg FDP PT红细胞碎片 肠出血 gut bleeding 淤斑 livedo 2 ARDS MODS,监测monitoring,常规监测-体格检查及实验室检查 神志 皮肤 BP HR 尿量 HCT ：30-35%是缺氧临界值 动脉血气、乳酸值 2mmol/L 脉搏氧饱和度SPO2 90%,HCT ：30-35%是缺氧临界值 动脉血气、乳酸

22、值 2mmol/L 脉搏氧饱和度SPO2 90% CVP,肺动脉置管监测,PCWP pulmonary capillary wedge pressure 可反映 : 1 肺静脉压 pulmonary venous pressure 2 左房压 left atrium pressure 3 左室舒张末期压left ventricular end-diastolic pressure 4 左室前负荷 left ventricular preload,正常值6-15mmHg 下降 低血容量 hypovolemia 较CVP敏感（反映右室前负荷及血 容量 5-10 cm H 2O 要动态监测） 升高

23、15 左房压升高 : 肺水肿,心输出量监测（CO） 热稀释法(thermodilution method) 混合静脉血氧饱和度监测（SVO 2 ） Mixed venous oxygen saturation 分光光度测定法(spectrophotometry) 正常值 75% 表示氧供 氧耗平衡 balance between oxygen delivery and consumption,下降 : 氧供不足inadequate oxygen delivery 低心排low cardiac output Hb SaO 2 氧耗增加 increase in oxygen consumption

24、,氧供与氧耗,非氧供依赖性氧耗 independent VO 2 on DO 2 氧 供 依 赖 性 氧 耗 反映组织缺氧 dependent VO 2 on DO 2,氧供DO2 = CaO2 CO = (1.34 Hb SaO2 ) CO = 800 - 1200 ml 氧耗VO2 VO2=（ CaO2 - CvO2 ) CO =(SaO2-SvO2) 1.34 Hb CO =200-400ml CO=4-6L/min CI =2.5-3.5L/min/m,休克的治疗treatment,最终目标：恢复组织灌注及氧供 Ultimate goals:restore perfusion and

25、adequate oxygen delivery to tissue 达到氧供非依赖性氧耗 超常值氧供：DO2i600ml VO2i170ml C I 4.5L/min/m,休克：氧供不足inadequate oxygen delivery SaO 2 Hb 低心排low cardiac output,维持适当的CO maintain reasonable cardiac output (1)适当的前负荷 preload 血容量 (2)后负荷 afterload-调节外周血管张力 (3)心肌收缩强心药物,To reach these goals,上氧 oxygenation 扩容/估计血容量

26、volume expansion/ Assessment of volume status (preload) 维持适当的CO maintain reasonable cardiac output (1)前负荷 preload (2)后负荷 afterload (3)心肌收缩,达到氧供非依赖性氧耗,SaO2 90% Hb 100g/L 理想心输出量Optimize CO: 血流动力学监测,补充血容量volume expansion,失血量估计 7-8%Wkg 血浆 5% 红细胞 2.5% 动脉 1L 静脉 3.5L 毛细血管 0.5L 30%(1500ml)- HRBP 尿量减少 skin t

27、urgor lost mental status change,扩容volume expansion the key of restoring hypoperfusion and hypoxia,液体选择 晶体 3-4 times 胶体 1:1 高渗盐 3-7.5% 输血 血浆 plasma 浓红packed red cell 全血whole blood,Ordinarily : 林格氏液 Ringers bolus 1-2L/30min 低血压持续存在（活动性出血） 胶体colloids solution 1:1 3-7.5%NaCI(+colloid) HCT30% Hb110-130 (

28、全血whole blood/浓红 packed red cell) ,HCT正常时 输晶体 胶体液 失血量 30% 血容量时： 输全血及浓缩红细胞各半加晶胶体液 失血量 50%时 ：应补充特殊成分如血小 板、凝血因子,达到临床反应组织灌注的指标正常 尿量 0.5-1.0ml/kg/hr HR BP ：Normal MAP= 60-80mmHg 毛细血管充盈良好 反映良好,改善心功能improve cardiovascular function,目标： 氧供非依赖性氧耗 independent VO2 on DO2 理想心输出量Optimize CO:,达到理想CO的方法,1理想的前负荷：扩容

29、2理想的后负荷：血管活性药物 3 良好的心肌收缩力：强心药物 PCWP15 CVP5 volume expansion ,血管扩张剂Vasodilators 硝酸甘油nitroglycerin 硝普纳nitroprusside 血管收缩剂 + 多巴胺 Alpha-agonist + dopamine 3ug/kg/min 提高心肌收缩力 : dobutamine 2-15ug/kg/min dopamine 5-10ug/kg/min,多巴胺dopamine 正性肌力作用 5-10ug/kg/min 扩张肠细膜小动脉2-5ug 直接的血管收缩15ug 多巴丁酚胺dobutamine 心肌收缩力

30、cardiac contrictile force 2.5-15ug/kg/min: CO SAP PCWP Urine ,使用血管活性药物的理想目标,感染性休克septic shock sepsis with 1 hypotension 2 lactic acidosis3 oliguria 4 acute mental status change,病理演变过程 Inflection SIRS Sepsis(26%/16% ) septic shock(4%/46%) MODS,SIRS systemic inflammatory response syndrome,Temperature

31、38 , 90bpm PaO212,000 10%,临床特点clinical features,发热fever 心动过速tachycardia 低血压hypotension 尿少oliguria 神志改变altered mental status,暖休克warm phase,高动力反应： CO SVR 外周动静脉容量血管扩张而内脏低灌注 四肢温暖 vasodilatation occurs in peripheral arterial and venous capacitance vessels while the splanchnic circulation may remain under- perfused patients extremities feel warm to touch,原因,血流分布异常 功能性分流 maldistribution functional shunt SVR 下降 : NO PGE PGI I