休克英文课件.ppt

毛细血管无复流现象(capillary no-reflow phenomenon) Concept: large amount of blood transfusion and fluid infusion → Bp↑ but capillary blood flow has no recovery 休克晚期即使大量输血补液，血压回升，有时仍不能恢复毛细血管血流，称为无复流现象。 Mechanism： （1） WBC adhesion and aggregation （2）capillary endothelial cells swelling （3）formation of extensive microthrombi→blockage of capillaries 患者，男，40岁，有多年胃溃疡病史。入院前一天解黑便2次。 入院查体：神志淡漠，血压60/40mmHg,脉搏130次/min，脉细而弱，皮肤冰冷。入院后病人又解黑便1次。以往血常规检查在正常范围。给予止血治疗，输液和输血共500ml。病人24h尿量约50ml. 实验室检查：Hb 90 g/L, pH 7.13，PaCO2 30mmHg ,[HCO3_]16mmol/L, 红细胞压积25%。 1.该患者发生休克了吗？属于哪种类型？处于哪一期？ 2.该患者血压为何降低？ 3.患者尿量为什么减少？ 4.该患者应如何治疗？ 病例2-3的微循环变化分别属于哪一个期？为什么？各应该如何治疗？ vasodilation upper: normal lung tissue lower: lung edema diffused lung edema alveolar hyaline membrane 1. coronary blood volume↓: SAMS(+) → HR↑, myocardial contractility↑ → oxygen consumption↑ → deterioration of myocardial hypoxia 2. water, electrolytes and acid-base disturbance: hyperkalemia, acidosis → HR↓, myocardial contractility↓ 3. production of MDF: ischemic pancreas → production of MDF → myocardial contractility↓ 4. myocardial DIC → myocardial contractility↓ 5. endotoxins → damage myocardium 6. ATP↓ → myocardial contractility↓ (III) Effects on Heart: hypoxia, acidosis→ ATP↓ → impaired Na+-K+ pump → cytotoxic brain edema lysosome injury → brain cell injury activation of complement (C3a,C5a) → histamine, bradykinin↑ → capillary permeability↑ → vasogenic brain edema (IV) Effects on Brain: (V) Effects on Digestive System: enterogenous endotoxemia （肠源性内毒素血症) ischemia stasis barrier function? endotoxin enter blood stress ulcer jaundice hepatic encephalopathy Definition: Dysfunctions of more than two organs occur successively in patients without pre-exist organ dysfunction defined as MODS. (VI) MODS(multiple organ dysfunction syndrome,多器官功能障碍综合征): MSOF ( Multiple System Organ Failure