1、外科休克 surgery shock,什么是休克？ Historical aspects,希波克拉底的思考,創(chuàng)傷 出血止血希波克拉底面容死亡 Traumatic wounds hemorrhagetourniquet to arrest hemorrhage Hippocratic facies imminent death,賴得朗 ：1743年 首次將shock 翻譯成英語(yǔ) 而不用法語(yǔ)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：沖擊 打擊 震蕩shock referred to a violent impact or blow1815年George james首次shock描述創(chuàng)傷后生理紊亂in 1815 George James first used the word shock connote physiologic instability after impact,Keith. 1919年 用染料稀釋法確定血容量 休克的另一重要機(jī)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: 進(jìn)行性系統(tǒng)循環(huán)失代償 氧供減少 氧債 組織損傷 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 微循環(huán)障礙,近年 分子生物學(xué)發(fā)展 炎性介質(zhì) ：細(xì)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,休克的定義definition,有效循環(huán)血量 組織灌注不足 細(xì)胞代謝紊亂及功能障礙 的病理過(guò)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,現(xiàn)代觀點(diǎn)：休克是一序慣性事件 是一個(gè)從亞臨床階段的組織灌注不足到多器官功能障礙的病理過(guò)程 Current interpretation:a continuum ,ranging from subclinical deficits in perfusion to MODS,休克分類classification,低血容量休克 ： 出血

6、血漿容量丟失 Hypovolemic shock Hemorrhage losses or plasma volume losses 血管源性休克 內(nèi)外源性血管活性介質(zhì)起作用 Vasogenic shock endogenous exogenous vasoactive mediators play a major role 感染性休克 創(chuàng)傷性休克 Septic traumatic shock 心源性休克 cardiogenic shock 神經(jīng)源性休克neurogenic shock,病理生理pathophysioligy,休克的共同特點(diǎn)：有效血容量銳減 組織灌注不足 炎癥介質(zhì)釋放 Comm

7、on feature :valid circulation volume decreased dramatic hypoperfusion elaboration of inflammatory mediators,組織低灌注Hypoperfusion: 微循環(huán)改變 分布異常 alteration on microcirculation maldistribution 組織缺氧 Tissue hypoxia 代謝改變 Anaerobic metabolisms 酸中毒 acidosis 炎癥介質(zhì)釋放 elaboration of inflammatory mediators,微循環(huán)改變,微循環(huán)

8、收縮期 Microcirculation contraction stage 微循環(huán)血流受毛細(xì)血管前括約肌舒縮效應(yīng)控制 Control of flow through capillaries is effected by contraction and relaxation of precapillary sphincters,皮膚 皮下 胃腸道 心 腦 Skin subcutaneous gastrointestinal tract heart brain 交感傳出 Sympathetic neurat output CA Ang- VP ET TXA2, HR 胃腸道低灌注 心肌收縮力 不

9、可逆休克 組織間液重吸收 SIRS Irreversible shock SIRS,微循環(huán)擴(kuò)張期microcirculation dilation stage,缺氧 hypoxia 無(wú)氧代謝 anaerobic metabolism 乳酸堆積 lactate accumulation 酸中毒 acidosis 血管舒張介質(zhì) NO PGE2 PGI2 IL-2 BK,血管通透性 permeability 血粘度 viscosity 靜脈回流減少venous return CO 心 腦缺血 cardiac cerebral ischemia,微循環(huán)衰竭期microcirculation failu

10、re stage,毛細(xì)血管血流淤滯 Capillary sludging 酸中毒 acidosis 高凝 hypercoagulation 紅細(xì)胞 血小板聚集 red cell platelet aggregation DIC 水解酶釋放 細(xì)胞溶解,代謝改變metabolism derangement,缺氧 無(wú)氧代謝 酸中毒 Hypoxia anaerobic metabolism and acidosis 傷害性組織灌注不足 導(dǎo)致氧供不能滿足氧耗 休克的主要病理機(jī)制 Impaired tissue hypoperfusion the primary pathophisiologic mech

11、anism in shock lead to decreased oxygen delivery relative to needs,無(wú)氧代謝 Anaerobic metabolism supervenes 丙酮酸(P) 乳酸(L)+2ATP Pyruvate lactate +2ATP 高乳酸血癥hyperlactatemia 代謝性酸中毒acidosis,L/P15-20 細(xì)胞缺氧cellular hypoxia,能量代謝障礙Bioenergetic failure 糖異生 gluconeogenesis (Adr NE) 蛋白質(zhì) 脂肪分解 急性相蛋白合成(ACTH) proteolysi

12、s lipolysis acute-phase protein 生命膜功能障礙vital membrane dysfunction,炎癥介質(zhì)及缺血再灌注損傷inflammatory mediators and ischemia reperfusion injury,內(nèi)毒素endotoxin G的胞壁成分 脂多糖 感染性休克的強(qiáng)效介質(zhì) 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,宿主對(duì)內(nèi)毒素的反應(yīng)host responses to endotoxin,激活巨噬細(xì)胞 補(bǔ)體 凝血系統(tǒng) Activation of macrophages complement and coagulation systems and release of numerous mediators including TNF-a IL-I,6 PAF NO oxidants 巨噬細(xì)胞激活同時(shí)釋放細(xì)胞因子是感染性休克生理紊亂的關(guān)鍵 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,細(xì)胞因子cytokines,白介素interleukins (IL) IL-1 TNF-a IL-6 PAF PG fever acute-phase protein 內(nèi)皮細(xì)胞促凝活性 endothelial procoagulant activity,IL-2 hypotension TNF-a IFN-gamma T 細(xì)胞增殖 T cell proliferation IL-6 急性相蛋白合成 acute-phase prote

15、in synthesis 中性粒細(xì)胞 活性 neutrophil activation,腫瘤壞死因子（TNF-a) Tumor necrosis factors 低血壓 hypotension 乳酸酸中毒 lactic acidosis DIC disseminated intravascular coagulation 血管通透性增加vascular permeability increase 過(guò)氧化物釋放oxidants released,集落刺激因子colony stimulating factors,刺激中性粒細(xì)胞 巨噬細(xì)胞生長(zhǎng) Stimulates growth of granulo

16、cytes macrophages 干擾素（IFN）Interferone 促進(jìn)巨噬細(xì)胞功能 加強(qiáng)TNF的作用 Promotes macrophages function potentiates the TNF,一氧化氮NO nitric oxide,由精氨酸代謝產(chǎn)生 又稱內(nèi)皮細(xì)胞源性舒因子 具強(qiáng)力血管擴(kuò)張 抑制血小板集聚 可引起難治性低血壓 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,過(guò)氧化物oxidants,在缺血再灌注時(shí)產(chǎn)生 引起缺血再灌注損傷 Oxidants are produced in ischemia-reperfusion injury 缺血時(shí)黃嘌呤氧化酶堆積 Under ischemic conditions xanthine oxidase accumulates 再灌注時(shí)ATP次黃嘌呤hypoxanthine,H2O2 (xanthine oxidase) SOD Hypoxanthine xanthine + O2- OH 次黃嘌呤 黃嘌

18、呤 Fe,內(nèi)臟繼發(fā)性損害,肺 ： 急性肺損傷 肺功能障礙 lung acute lung injury pulmonary dysfunction 肺毛細(xì)血管內(nèi)皮細(xì)胞損傷 肺間質(zhì)水腫 Pulmonary capillary endothelial injury lung interstitial edema 肺泡上皮損傷 肺泡水腫 Alveolar injury edema,表面活性物質(zhì)減少 肺泡塌陷 Loss of surfactant alveolar collapse ARDS : 難治性低氧血癥（refractory hypoxemia),腎renal injury,組織低灌注 Tis

19、sue hypoperfusion 炎性細(xì)胞 介質(zhì) Inflammatory mediators and cells 血管痙攣 Vasoconstriction 血流分布異常 皮質(zhì)壞死 Maldistribution cortical ischemia,胃腸道gastrointestinal,缺血損傷及缺血再灌注損傷 Ischemic reperfusion injury 細(xì)菌 內(nèi)毒素移位 Bacteria and endotoxine translocation SIRS MODS,臨床表現(xiàn)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 脈壓下降 Decrease in the pulse pressure 心率增快 Tachycardia,冷汗 perspiration 四肢發(fā)冷extremities cold 焦慮 anxiety,2 灌注不足 hypoperfusion 脈搏微弱 pulselessness 低血壓 hypotension 蒼白 pallor 靜脈癟餡 venous turgor is lost 毛細(xì)血管充盈時(shí)間延長(zhǎng)2s refilling time prolonged 尿量減少 oliguria (7)

21、 SVO2 乳酸,3組織缺氧tissue hypoxia 酸中毒 Acidosis SVO2 發(fā)紺 cyanosis 二 難治性休克refractory shock 1 DIC : 消耗性凝血病 consumptioncoagulopathy PLts Fg FDP PT紅細(xì)胞碎片 腸出血 gut bleeding 淤斑 livedo 2 ARDS MODS,監(jiān)測(cè)monitoring,常規(guī)監(jiān)測(cè)-體格檢查及實(shí)驗(yàn)室檢查 神志 皮膚 BP HR 尿量 HCT ：30-35%是缺氧臨界值 動(dòng)脈血?dú)?、乳酸?2mmol/L 脈搏氧飽和度SPO2 90%,HCT ：30-35%是缺氧臨界值 動(dòng)脈血?dú)?、乳?/p>

22、值 2mmol/L 脈搏氧飽和度SPO2 90% CVP,肺動(dòng)脈置管監(jiān)測(cè),PCWP pulmonary capillary wedge pressure 可反映 : 1 肺靜脈壓 pulmonary venous pressure 2 左房壓 left atrium pressure 3 左室舒張末期壓left ventricular end-diastolic pressure 4 左室前負(fù)荷 left ventricular preload,正常值6-15mmHg 下降 低血容量 hypovolemia 較CVP敏感（反映右室前負(fù)荷及血 容量 5-10 cm H 2O 要?jiǎng)討B(tài)監(jiān)測(cè)） 升高

23、15 左房壓升高 : 肺水腫,心輸出量監(jiān)測(cè)（CO） 熱稀釋法(thermodilution method) 混合靜脈血氧飽和度監(jiān)測(cè)（SVO 2 ） Mixed venous oxygen saturation 分光光度測(cè)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、,氧供與氧耗,非氧供依賴性氧耗 independent VO 2 on DO 2 氧 供 依 賴 性 氧 耗 反映組織缺氧 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,休克的治療treatment,最終目標(biāo)：恢復(fù)組織灌注及氧供 Ultimate goals:restore perfusion and

25、adequate oxygen delivery to tissue 達(dá)到氧供非依賴性氧耗 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,維持適當(dāng)?shù)腃O maintain reasonable cardiac output (1)適當(dāng)?shù)那柏?fù)荷 preload 血容量 (2)后負(fù)荷 afterload-調(diào)節(jié)外周血管張力 (3)心肌收縮強(qiáng)心藥物,To reach these goals,上氧 oxygenation 擴(kuò)容/估計(jì)血容量

26、volume expansion/ Assessment of volume status (preload) 維持適當(dāng)?shù)腃O maintain reasonable cardiac output (1)前負(fù)荷 preload (2)后負(fù)荷 afterload (3)心肌收縮,達(dá)到氧供非依賴性氧耗,SaO2 90% Hb 100g/L 理想心輸出量Optimize CO: 血流動(dòng)力學(xué)監(jiān)測(cè),補(bǔ)充血容量volume expansion,失血量估計(jì) 7-8%Wkg 血漿 5% 紅細(xì)胞 2.5% 動(dòng)脈 1L 靜脈 3.5L 毛細(xì)血管 0.5L 30%(1500ml)- HRBP 尿量減少 skin t

27、urgor lost mental status change,擴(kuò)容volume expansion the key of restoring hypoperfusion and hypoxia,液體選擇 晶體 3-4 times 膠體 1:1 高滲鹽 3-7.5% 輸血 血漿 plasma 濃紅packed red cell 全血whole blood,Ordinarily : 林格氏液 Ringers bolus 1-2L/30min 低血壓持續(xù)存在（活動(dòng)性出血） 膠體colloids solution 1:1 3-7.5%NaCI(+colloid) HCT30% Hb110-130 (

28、全血whole blood/濃紅 packed red cell) ,HCT正常時(shí) 輸晶體 膠體液 失血量 30% 血容量時(shí)： 輸全血及濃縮紅細(xì)胞各半加晶膠體液 失血量 50%時(shí) ：應(yīng)補(bǔ)充特殊成分如血小 板、凝血因子,達(dá)到臨床反應(yīng)組織灌注的指標(biāo)正常 尿量 0.5-1.0ml/kg/hr HR BP ：Normal MAP= 60-80mmHg 毛細(xì)血管充盈良好 反映良好,改善心功能improve cardiovascular function,目標(biāo)： 氧供非依賴性氧耗 independent VO2 on DO2 理想心輸出量Optimize CO:,達(dá)到理想CO的方法,1理想的前負(fù)荷：擴(kuò)容

29、2理想的后負(fù)荷：血管活性藥物 3 良好的心肌收縮力：強(qiáng)心藥物 PCWP15 CVP5 volume expansion ,血管擴(kuò)張劑Vasodilators 硝酸甘油nitroglycerin 硝普納nitroprusside 血管收縮劑 + 多巴胺 Alpha-agonist + dopamine 3ug/kg/min 提高心肌收縮力 : dobutamine 2-15ug/kg/min dopamine 5-10ug/kg/min,多巴胺dopamine 正性肌力作用 5-10ug/kg/min 擴(kuò)張腸細(xì)膜小動(dòng)脈2-5ug 直接的血管收縮15ug 多巴丁酚胺dobutamine 心肌收縮力

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

31、38 , 90bpm PaO212,000 10%,臨床特點(diǎn)clinical features,發(fā)熱fever 心動(dòng)過(guò)速tachycardia 低血壓hypotension 尿少oliguria 神志改變altered mental status,暖休克warm phase,高動(dòng)力反應(yīng)： CO SVR 外周動(dòng)靜脈容量血管擴(kuò)張而內(nèi)臟低灌注 四肢溫暖 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,血流分布異常 功能性分流 maldistribution functional shunt SVR 下降 : NO PGE PGI I