于志伟 副主任医师 哈尔滨医科大学附属肿瘤医院，结直肠外科

1. 休 克Shock Syndrome 于志伟副主任医师 哈尔滨医科大学附属肿瘤医院，结直肠外科

2. 休克(Shock)的定义 • 休克是指任何原因引起有效循环血量减少,导致组织和器官氧合血液灌流不足, 从而发生的代谢障碍和功能细胞受损的病理过程 • Shock is a condition in which the cardiovascular system fails to perfuse tissues adequately. Inadequate tissue perfusion can result in: • generalized cellular hypoxia (starvation) • widespread impairment of cellular metabolism • tissue damage • organ failure • death • 维持有效循环血量的必要因素: • 充足的血容量 Sufficient blood volume • 有效的心排出量 Effective cardiac pump • 良好的周围血管张力 Upstanding peripheral angiotasis Effective circulating blood volume

3. 休克的分类（Types of Shock） 分类 疾病举例 低血容量性休克 创伤出血、上消化道出血 （hypovolemic shock ） 烧伤、肠梗阻 感染性休克 胆道感染等 （Septic Shock） 心源性休克 心梗 （Cardiogenic Shock ） 过敏性休克 青霉素过敏、血清过敏 （Anaphylacticshock） 神经源性休克 疼痛刺激、脊髓损伤 （ Neurogenic Shock） • hemorrhage shock and traumatic shock.

4. PATHOPHYSIOLOGY OF SHOCK SYNDROME • 微循环改变Microcirculation Change • 代谢变化Metabolism Change • 内脏器官的继发性损害Secondary damage on internal organs

5. Microcirculation Change Compensated phase Decompensated phase Irreversible phase Death

6. Compensatory Mechanisms • Sympathetic nervous system activates • Decreased renal blood flow • Renin released from kidney arteriole • Renin & Angiotensinogen combine • Converts to Angiotensin I • Angiotensin I converts to Angiotensin II • Peripheral vasoconstriction • Increased aldosterone release (adrenal cortex) • Cardiac effects Increased force of contractions Increased heart rate Increased cardiac output • Peripheral effects Arteriolar constriction Pre-/post-capillary sphincter contraction Increased peripheral resistance Shunting of blood to core organs • Peripheral capillaries contain minimal blood • Stagnation • Aerobic metabolism changes to anaerobic

7. 休克的病理生理过程--微循环的变化 • 微循环收缩期(休克代偿期)的特点: 心跳中枢、血管舒缩中枢、交感神经兴奋→心跳加快，心排出量增加，儿茶酚胺大量释放 • 儿茶酚胺的作用： 促使外周和内脏小、微血管和毛细血管前括约肌强烈收缩，动静脉短路和直捷通道开放 • 收缩期结果: 外周血管阻力增加和回心血量增加；低灌注、缺氧状态。

8. Decompensated Shock Decreased blood flow to the tissues causes cellular hypoxia Continued anaerobic metabolism • Relaxation of precapillary sphincters • Continued contraction of postcapillary sphincters • Peripheral pooling of blood • Decreased coronary blood flow • Myocardial ischemia • Decreased force of contraction • Decreased blood pressure

9. 休克的病理生理过程--微循环的变化 • 微循环扩张期(休克抑制期)的特点: 组织灌流不足，乏氧代谢，酸性物质增多，微动脉和毛细血管前括约肌扩张，但毛细血管后静脉仍收缩 肥大细胞释放组胺,缓激肽,毛细血管扩张范围增加 • 扩张期结果： 毛细血管多灌少流，容积增加，血液浓缩，回心血大减，心排血量减少，血压下降，心脑灌注不足，休克加重。

10. If Low Perfusion States persists: • IRREVERSIBLE DEATH IMMINENT!!!

11. Disseminated Intravascular Coagulation (DIC) • Decreased perfusion causes tissue damage/necrosis • Tissue necrosis triggers diffuse clotting • Diffuse clotting consumes clotting factors • Fibrinolysis begins • Severe, uncontrolled systemic hemorrhage occurs

12. 休克的病理生理过程--微循环的变化 • 微循环衰竭期（DIC期）的特点： 毛细血管内形成微血栓，DIC，细胞缺氧，组织自溶，由于凝血因子消耗，纤维蛋白溶解系统激活，出现严重的出血倾向

13. 休克的病理生理变化—体液代谢的改变 • 能量不足(Energy deficiency) • 乏氧代谢(Anonic metabolism)致乳酸(Lactic acid)和丙酮酸(Pyruvic acid)积聚，造成酸中毒(Metabolic acidosis) • 钠泵(Sodium-pump)和钙泵(Calcium pump)功能异常，致细胞肿胀 ，甚至死亡

14. 休克的病理生理变化—内脏器官的继发性损害 • 多器官衰竭 (Multiple Organ Systems Failure, MOSF):几个脏器相继或同时受损： • 呼吸窘迫综合征, （ ARDS: Adult respiratory distress syndrome ） • 肾衰 (Renal failure):肾皮质内肾小管上皮变性坏死 3. 心：心肌受损，局灶性坏死 4. 肝功能衰竭 (Hepatic failure)：小叶中央坏死 5. 胃肠道：粘膜糜烂、出血 6. 脑：脑水肿(cerebral edema)、脑疝(cerebral hernia)

15. Stages of Shock • Initial stage - tissues are under perfused, decreased CO, increased anaerobic metabolism, lactic acid is building • Compensatory stage- Reversible. SNS activated by low CO, attempting to compensate for the decrease tissue perfusion. • Progressive stage - Failing compensatory mechanisms: profound vasoconstriction from the SNS ISCHEMIA Lactic acid production is high anaerobic metabolic acidosis • Irreversible or refractory stage - Cellular necrosis and Multiple Organ Dysfunction Syndrome may occur DEATH IS IMMINENT!!!!

16. Generally Clinical Presentation • Hypotension < 90 mmHg (may be normal level or increase due to compensatory mechanism) • Mean arterial pressure (MAP) < 60 mmHg • Tachycardia: weak and thready pulse • Tachypnea: blow off CO2 respiratory alkalosis • Decreased urine output

17. 休克的临床表现 • 休克代偿期： 丧失血容量<20%;交感神经活动增强 1. 神清 (consciousness)，但烦躁 (restlessness)，呼 吸加快 (quicken respiration) 2. 皮肤苍白 (Pale skin)，手足厥冷(Cold hands and feet) 3. 心率快 (Rapid rate)，血压正常 (Normal BP)或稍升高 (Increasing BP)，舒张压 (diastolic blood pressure)升高，脉压缩小 (narrow pulse pressure) 4. 尿量 (urine output)正常或减少

18. 休克的临床表现 • 休克抑制期： 丧失血容量>20% 1. 神志淡漠 (Disturbance of consciousness)→昏迷 (Coma) 2. 口唇 (Oral lip)、肢端 (Limb)发绀 (Cyanosis)，出冷汗 (Cold sweat) 3. 脉细速 (Rapid rate and thread / weak pulse)，血压下降 (Falling BP)，脉压差 (Pulse pressure difference)明显缩小 4. 5. 尿量减少或无尿 (Anuria)

19. 休克的临床表现 • 重度休克： 血容量丧失>40% 1. 昏迷 (Coma) 2. 全身皮肤粘膜紫绀 (Cyanosis)，四肢冰冷 3. 脉搏摸不到，血压测不出 4. 无尿 (Anuria) 5. 器官功能衰竭的表现

20. 休克的诊断Diagnosis of Shock • 早期诊断: 病史：失血、失液、创伤等 临床表现：兴奋或烦躁，出冷汗，心率快，脉压缩小，尿少 • 抑制期诊断：依靠典型表现——神志淡漠，反应迟钝，皮肤苍白或紫绀， 四肢湿冷，脉细速，呼吸浅快，收缩压下降至12kPa（90mmHg）以下，尿少或无尿

21. 休克的监测—一般监测General Monitor 神志状态 (Mental status) 肢体温度、色泽 (Limb temperature and color) 血压 (Blood pressure) 脉率 (Pulse) 尿量 (Urine output)

22. 休克的监测—特殊监测Special Monitor • 中心静脉压(Central Venous Pressure,CVP): 血容量和心功能 正常值：0.49-0.98 kPa (5-10cmH2O) CVP↓，——血容量不足 CVP↑，——心功能不全或过度收缩（﹥1.47 kPa) 充血性心力衰竭 (Congestive Heart Failure)(>1.96 kPa)

23. 休克的监测—特殊监测Special Monitor • 肺动脉楔压 (Pulmonary Capillary Wedge Pressure, PCWP) ：可直接反映肺静脉、左心房和左心室的压力，了解肺循环阻力 正常值：0.8-2.0 kPa ,低于正常值，提示血容量不足， >4.0 kPa，表示肺水肿 • 心排出量和心脏指数：心排出量难以准确测定，临床应用少 • 动脉血气分析 (Arterial Blood Gas Analysis )： 可了解呼吸功能和酸碱平衡的变化。 PaO2 80-100mmHg, PaCO2 36-44mmHg, PaCO2>60mmHg, PaO2<60mmHg,

24. 休克的监测—特殊监测Special Monitor • 动脉血乳酸盐测定：反映细胞血液灌流情况。正常值：1-2 mmol/L，浓度越高，休克越严重。>8 mmol/L, 死亡率100%。 • DIC的实验室检查—确诊依据： Plat <80×109/L; 纤维蛋白原<1.5g/L PTT延长>3`, 副凝实验(+);3P试验阳性；血涂片中破碎红细胞超过2%。

25. 休克的治疗Treatment of Shock • 一般紧急措施 控制活动性大出血 休克体位: 头和躯干抬高20-30度, 下肢抬高5-20度 吸氧，6-8L/min；保持呼吸道通畅 保持安静，避免搬动 保暖，可用休克服

26. 休克的治疗Treatment of Shock • 补充血容量 (Restore circulating volume and tissue perfusion) ：是抗休克的根本措施 补充量：可根据CVP调节，应补充丧失量和已扩大的毛细血管床容量 • 积极处理原发病 (Treat Reversible Causes) ：在恢复有效血容量后积极手术处理外科原发病。在原发病不除，休克不能纠正时，应抗休克的同时，积极手术处理，以免丧失抢救时机

27. Shock treatment “A rude unhinging of the machinery of life” “A brief pause in the act of dying”

28. 休克的治疗Treatment of Shock • 纠正酸碱平衡失调：主要是酸中毒 酸中毒的纠正有赖于休克的根本好转 补充血容量，改善组织灌流， 休克严重者，应给予碱性药物如碳酸氢钠 • 心血管药物的应用 (Circulatory Support)Vasoconstrictor：去甲肾上腺素；间羟胺；苯肾上腺素；苯苄胺；苄胺唑啉；多巴胺；异丙肾上腺素；西地兰等 • 治疗DIC改善微循环 • 皮质类固醇和其他药物的应用

29. In summary, Treatment of Shock • Identify the patient at high risk for shock • Control or eliminate the cause • Implement measures to enhance tissue perfusion • Correct acid base imbalance • Treat cardiac dysrhythmias

30. 失血性休克的治疗(Treatment of Hemorrhagic Shock) • 补充血容量：根据情况输入晶体或/和胶体溶液 出血量少，无活动性出血者，输入晶体液 出血量大，有活动性出血者，先输晶体液，后输血 根据中心静脉压调整输液量和速度 • 止血：在补充血容量的同时积极止血 要处理好休克和止血手术间的辨证关系

31. 中心静脉压和补液的关系 CVP BP原因 处理原则 低 低 血容量严重不足 充分补液 低 正常 血容量不足 适当补液 高 低 心功能不全 强心药，纠酸， 或血容量相对过多 舒血管 高 正常 容量血管过度收缩 舒张血管 正常 低 心功能不全 补液实验 或血容量不足

32. 损伤性休克的治疗(Treatment of Traumatic Shock) • 补充血容量：应根据监测指标的变化来决定补液量 • 纠正酸碱平衡失调：碱中毒→酸中毒 适当应用碱性药物 • 手术治疗：应根据病情判断是否需要手术以及手术时机的选择 • 药物治疗：大量抗生素，复合维生素等

33. Hypovolemic Shock • Management goal: • Restore circulating volume and tissue perfusion: • Control hemorrhage • Restore circulating volume • Optimize oxygen delivery • Vasoconstrictor if BP still low after volume loading

34. Aimed at improvement tissue hypoperfusion • Insert Foley catheter to monitor the urine flow; • Augment systolic bp to ›100mmHg: 1. Place in reverse Trendelenburg position; 2. IV volume infusion (500-1000ml bolus), unless cardiogenic shock suspected (begin with normal saline, then whole blood, dextran, or packed RBCs, if anemic), continue volume replacement as needed to restore vascular volume; • Add vasoactive drugs after intrvascular volume is opmtimized; administer vasopressors if systemic vascular resistance is decreased. • If severe metabolic acidosis is presented (pH<7.15), administer NaHCO3; • Identify and treat the underlying cause of shock.

35. 感染性休克的特点Characteristics of Septic Shock • 内毒素性休克 • 微循环变化的不同阶段常同时存在 • 微循环变化和内脏损害比较严重 • 全身炎症反应综合征

36. 感染性休克的类型Types of Septic Shock • 高排低阻型（高动力型）： “Warm” shock hyperdynamic response, 原因：感染灶释放扩血管物质 特点：周围血管阻力降低，心排出量增加 • 低排高阻型（低动力型） “Cold” shock hypodynamic response 原因：血容量减少+继发感染 活性因子：儿茶酚胺、5-羟色胺、组织胺、缓激肽 特点：周围血管阻力增加，心排出量降低

37. 感染性休克的两种临床表现 临床表现 冷休克(高阻力型) 暖休克(低阻力型) 神志 躁动、淡漠或嗜睡 清醒 皮肤色泽 苍白、紫绀或花斑样紫绀 淡红或潮红 皮肤温度 湿冷或冷汗 温暖、干燥 毛细血管充盈时间 延长 1-2秒 脉搏 细速 慢、有力 脉压（kPa） <4 >4 尿量(每小时) <25ml >30ml

38. Septic Shock Treatment: • Prevention • Find and kill the source of the infection • Fluid resuscitation • Vasoconstrictors • Inotropic drugs • Maximize O2 delivery Support • Nutritional Support

39. Treatment of Septic Shock • Antibiotic treatment; • Removal or drainage of a focal source of infection: Remove indwelling intravascular catheters and send tips for quantitative culture; replace Foley and other drainage catheters; • Hemodynamic, respiratory, and metabolic support: ⑴. Maintain intravascular volume with IV fluids. Initiate treatment with 1-2L of normal saline administered over 1-2 h, keeping pulmonary capillary wedge pressure at 12-16 mmHg or central venous pressure at 8-12 cmH2O, urine output at>30ml per hour, mean arterial blood pressure at >65mmHg.

40. Treatment of Septic Shock Add inotropic and vasopressor therapy if needed. Maintain central venous oxygen saturation at >70%. ⑵. Maintain oxygenation with ventilator support as indicated. • Other treatments: Antiendotoxin, anti-inflammatory, and anticoagulant drugs are being studied in severe sepsis treatment. • Anticoagulant recombinant activated protein C (aPC): constant infusion of 24ug/kg per hour for 96 h.

41. 感染性休克的治疗 • 补充血容量：以平衡盐溶液为主，配合适量的血浆和全血；并根据CVP 调节输液量和速度 • 控制感染：处理原发感染灶；应用抗菌药物；改善病人的一般状况；维持呼吸功能等 • 纠正酸中毒：酸中毒发生早，严重，及早应用碱性药物 • 心血管药物应用：西地兰；B-受体兴奋剂和a受体抑制剂联合应用 • 减轻细胞损害：皮质类固醇，大剂量应用；SOD，抑肽酶，PGI2，试用中

42. THE END

43. Clinical examples-1 • An 82-year-old man was brought to the emergency room by his grandson, who reported that the man had been eating poorly for 2 days and had been difficult to arouse that morning. The patient had no specific complaints. On exam, the patient would open his eyes and mumble incoherently in response to pain. His temperature was 38.6℃, BP 75/40, HR 124 regular, respirations 26. His lungs were clear. No murmurs or extra sounds were appreciated on cardiac exam.

44. Clinical examples-1 • His skin was warm, with bounding peripheral pulses. His chest radiograph and EKG were normal. Laboratory data: white blood cell count 19500 (normal less than 10000). A bladder catheter was inserted (with difficulty) and yielded cloudy urine, which was noted to contain many white cells and bacteria. Urine was sent for culture.

45. Clinical examples-2 • An 35-year-old woman presented to an emergency room complaining of a headache present since a myelogram which had been performed 4 days before. Her past medical history was unremarkable and her physical examination was normal. She was given an injection of meperidine for her pain. After the injection she began to complain of numbness and tingling in her fingertips, lightheadedness, shortness of breath and diffuse itching.

46. Clinical examples-2 • Her pulse was noted to be 140 and blood pressure was palpable at 70/0 mmHg. Faint wheezes were noted throughout the lungs. Although she had initially denied drug allergies, she now remembered similar symptoms which had followed an injection of ‘pain medicine” 2 years before.

47. Clinical examples-3 • An 67-year-old female arrived in the emergency room complaining of chest pain and severe weakness for 12 hours. These symptoms had been preceded by several days of nausea and vomiting, poor appetite, and subjective fever. On examination, she had a pulse rate of 110 and BP 85/50. There was no jugular venous distension. Her lungs were clear and no murmur or gallop were heard on auscultation of the heart. There was no extremity edema.

48. Clinical examples-3 • EKG showed new ST elevation in the inferior leads, suggesting an evolving inferior myocardial infarction. Right precordial leads did not show evidence of RV infarction at that time. • The patient was given sublingual nitroglycerin and within minutes became confused and unable to response to questions. Systolic blood pressure dropped to 60 and pulse slowed to 70. her legs were elevated and rapid infusion of intravenous fluids was begun.

49. Clinical examples-3 • Her mental status improved but she remained hypotensive. The decision was made to place a pulmonary artery catheter to help with management of cardiogenic shock. • Initial Hemodynamic Data: • BP: 80/50, mean 60 • RA: 4mmHg, RV 22/3, PA 22/10, PAOP 6 • Cardiac output: 1.9 liters/min • SVR: 2350 dynes-cm-5-sec (normal 400-1900)