结直肠外科课件.ppt

1、于志伟于志伟 副主任医师副主任医师哈尔滨医科大学附属肿瘤医院，结直肠外科哈尔滨医科大学附属肿瘤医院，结直肠外科休休 克克Shock Syndrome休克休克(Shock)的定义的定义 休克是指任何原因引起有效循环血量减少休克是指任何原因引起有效循环血量减少,导致组织和器导致组织和器官氧合血液灌流不足官氧合血液灌流不足,从而发生的代谢障碍和功能细胞受从而发生的代谢障碍和功能细胞受损的病理过程损的病理过程 Shock is a condition in which the cardiovascular system fails to perfuse tissues adequately.Inade

2、quate tissue perfusion can result in:generalized cellular hypoxia(starvation)widespread impairment of cellular metabolism tissue damage organ failure death 维持有效循环血量维持有效循环血量的必要因素的必要因素:充足的血容量充足的血容量 Sufficient blood volume 有效的心排出量有效的心排出量 Effective cardiac pump 良好的周围血管张力良好的周围血管张力 Upstanding peripheral a

3、ngiotasisEffective circulating blood volumeEffective circulating blood volume休克的分类（休克的分类（Types of Shock）分类分类 疾病举例疾病举例低血容量性休克低血容量性休克 创伤出血、上消化道出血创伤出血、上消化道出血 （hypovolemic shock）烧伤、肠梗阻烧伤、肠梗阻 感染性休克感染性休克 胆道感染等胆道感染等（Septic Shock）心源性休克心源性休克 心梗心梗（Cardiogenic Shock）过敏性休克过敏性休克 青霉素过敏、血清过敏青霉素过敏、血清过敏（Anaphylactic

4、 shock）神经源性休克神经源性休克 疼痛刺激、脊髓损伤疼痛刺激、脊髓损伤（Neurogenic Shock）hemorrhage shock and traumatic shock.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 organsMicrocirculation ChangeDecompensated phaseCompensated phaseIrreversible phaseDeathSympathetic nervous system

5、 activates 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 Decreased renal blood flowRenin released from

6、 kidney arterioleRenin&Angiotensinogen combineConverts to Angiotensin IAngiotensin I converts to Angiotensin II Peripheral vasoconstriction Increased aldosterone release(adrenal cortex)Peripheral capillaries contain minimal bloodStagnationAerobic metabolism changes to anaerobicCompensatory Mechanism

7、s休克的病理生理过程休克的病理生理过程-微循环的变化微循环的变化 微循环收缩期微循环收缩期(休克代偿期休克代偿期)的特点的特点:心跳中枢、血管舒缩中枢、交感神经兴奋心跳中枢、血管舒缩中枢、交感神经兴奋心心跳加快，心排出量增加，儿茶酚胺大量释放跳加快，心排出量增加，儿茶酚胺大量释放 儿茶酚胺的作用：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肌强烈收缩，动静脉短路和直捷通道开放 收缩期结果收缩期结果:外周血管阻力增加和回心血量增加；低灌注外周血管阻力增加和回心血量增加；低灌注、缺氧状态。缺氧状态。Contin

8、ued anaerobic metabolism Relaxation of precapillary sphincters Continued contraction of postcapillary sphincters Peripheral pooling of bloodDecreased blood flow to the tissues causes cellular hypoxia Decreased coronary blood flow Myocardial ischemia Decreased force of contraction Decreased blood pre

9、ssureDecompensated Shock休克的病理生理过程休克的病理生理过程-微循环的变化微循环的变化 微循环扩张期微循环扩张期(休克抑制期休克抑制期)的特点的特点:组织灌流不足，乏氧代谢，酸性物质增多，微动组织灌流不足，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脉和毛细血管前括约肌扩张，但毛细血管后静脉仍收缩缩 肥大细胞释放组胺肥大细胞释放组胺,缓激肽缓激肽,毛细血管扩张范围增毛细血管扩张范围增加加 扩张期结果：扩张期结果：毛细血管多灌少流，容积增加，血液浓缩，回心毛细血管多灌少流，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，

10、血大减，心排血量减少，血压下降，心脑灌注不足，休克加重。休克加重。If Low Perfusion States persists:IRREVERSIBLE DEATH IMMINENT!Decreased perfusion causes tissue damage/necrosis Tissue necrosis triggers diffuse clotting Diffuse clotting consumes clotting factors Fibrinolysis begins Severe,uncontrolled systemic hemorrhage occursDisse

11、minated Intravascular Coagulation(DIC)休克的病理生理过程休克的病理生理过程-微循环的变化微循环的变化 微循环衰竭期（微循环衰竭期（DIC期）的特点：期）的特点：毛细血管内形成微血栓，毛细血管内形成微血栓，DIC，细胞缺氧，细胞缺氧，组织自溶，由于凝血因子消耗，纤维蛋组织自溶，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白溶解系统激活，出现严重的出血倾向休克的病理生理变化休克的病理生理变化体液代谢的改变体液代谢的改变 能量不足能量不足(Energy deficiency)乏氧代谢乏氧代谢(Anonic metabolism)致乳酸致乳酸(Lac

12、tic acid)和丙酮酸和丙酮酸(Pyruvic acid)积聚，积聚，造成酸中毒造成酸中毒(Metabolic acidosis)钠泵钠泵(Sodium-pump)和钙泵和钙泵(Calcium pump)功能异常，致细胞肿胀功能异常，致细胞肿胀，甚至死亡，甚至死亡休克的病理生理变化休克的病理生理变化内脏器官的继发性损害内脏器官的继发性损害多器官衰竭多器官衰竭(Multiple Organ Systems Failure,MOSF):几个脏器相继或同时受损：几个脏器相继或同时受损：1.呼吸窘迫综合征呼吸窘迫综合征,（ARDS:Adult respiratory distress syndro

13、me）2.肾衰肾衰(Renal failure):肾皮质内肾小管上皮变性坏死肾皮质内肾小管上皮变性坏死3.心：心肌受损，局灶性坏死心：心肌受损，局灶性坏死4.肝功能衰竭肝功能衰竭(Hepatic failure)：小叶中央坏死：小叶中央坏死5.胃肠道：粘膜糜烂、出血胃肠道：粘膜糜烂、出血6.脑：脑水肿脑：脑水肿(cerebral edema)、脑疝、脑疝(cerebral hernia)Stages of ShockInitial stage-tissues are under perfused,decreased CO,increased anaerobic metabolism,lacti

14、c 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 acidosisIrreversibl

15、e or refractory stage-Cellular necrosis and Multiple Organ Dysfunction Syndrome may occur DEATH IS IMMINENT!Hypotension 90 mmHg(may be normal level or increase due to compensatory mechanism)Mean arterial pressure(MAP)60 mmHgTachycardia:weak and thready pulseTachypnea:blow off CO2 respiratory alkalos

16、isDecreased urine outputGenerally Clinical Presentation休克的临床表现休克的临床表现 休克代偿期：休克代偿期：丧失血容量丧失血容量20%1.神志淡漠神志淡漠(Disturbance of consciousness)昏迷昏迷(Coma)2.口唇口唇(Oral lip)、肢端、肢端(Limb)发绀发绀(Cyanosis)，出冷汗，出冷汗(Cold sweat)3.脉细速脉细速(Rapid rate and thread/weak pulse)，血压下降，血压下降(Falling BP)，脉压差，脉压差(Pulse pressure diffe

17、rence)明显明显缩小缩小 4.5.尿量减少或无尿尿量减少或无尿(Anuria)休克的临床表现休克的临床表现重度休克：重度休克：血容量丧失血容量丧失40%1.昏迷昏迷(Coma)2.全身皮肤粘膜紫绀全身皮肤粘膜紫绀(Cyanosis)，四肢冰冷，四肢冰冷 3.脉搏摸不到，血压测不出脉搏摸不到，血压测不出 4.无尿无尿(Anuria)5.器官功能衰竭的表现器官功能衰竭的表现休克的临床表现休克的临床表现休克的诊断休克的诊断Diagnosis of Shock 早期诊断早期诊断:病史：失血、失液、创伤等病史：失血、失液、创伤等 临床表现：兴奋或烦躁，出冷汗，心率快，脉临床表现：兴奋或烦躁，出冷汗，

18、心率快，脉压缩小，尿少压缩小，尿少 抑制期诊断：抑制期诊断：依靠典型表现依靠典型表现神志淡漠，反神志淡漠，反应迟钝，皮肤苍白或紫绀，应迟钝，皮肤苍白或紫绀，四肢湿冷，脉细速，四肢湿冷，脉细速，呼吸浅快，收缩压下降至呼吸浅快，收缩压下降至12kPa（90mmHg）以下，尿少或无尿以下，尿少或无尿 神志状态神志状态 (Mental status)肢体温度、色泽肢体温度、色泽(Limb temperature and color)血压血压(Blood pressure)脉率脉率(Pulse)尿量尿量(Urine output)休克的监测休克的监测一般监测一般监测General Monitor 休克的

19、监测休克的监测特殊监测特殊监测Special Monitor 中心静脉压中心静脉压(Central Venous Pressure,CVP):血容量和心功能血容量和心功能正常值：正常值：0.49-0.98 kPa(5-10cmH2O)CVP，血容量不足血容量不足 CVP，心功能不全或心功能不全或过度收缩（过度收缩（1.47 kPa)充血性心力衰竭充血性心力衰竭(Congestive Heart Failure)(1.96 kPa)休克的监测休克的监测特殊监测特殊监测 Special Monitor 肺动脉楔压肺动脉楔压(Pulmonary Capillary Wedge Pressure,PC

20、WP)：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：正常值：0.8-2.0 kPa,低于正常值，提示血容量不足，低于正常值，提示血容量不足，4.0 kPa，表示肺水肿表示肺水肿 心排出量和心脏指数：心排出量和心脏指数：心排出量难以准确测定，临床应用少心排出量难以准确测定，临床应用少 动脉血气分析动脉血气分析(Arterial Blood Gas Analysis)：可了解呼吸功能和酸碱平衡的变化。可了解呼吸功能和酸碱平衡的变化。PaO2 80-100mmHg,PaCO2 36-44mmHg,PaCO260mmHg,PaO

21、28 mmol/L,死亡率死亡率100%。DIC的实验室检查的实验室检查确诊依据：确诊依据：Plat 80109/L;纤维蛋白原纤维蛋白原3,副凝实验副凝实验(+);3P试验阳性；试验阳性；血涂片中破碎红细胞超过血涂片中破碎红细胞超过2%。休克的治疗休克的治疗Treatment of Shock 一般紧急措施一般紧急措施 控制活动性大出血控制活动性大出血 休克体位休克体位:头和躯干抬高头和躯干抬高20-30度度,下肢抬高下肢抬高5-20度度 吸氧，吸氧，6-8L/min；保持呼吸道通畅保持呼吸道通畅 保持安静，避免搬动保持安静，避免搬动 保暖，可用休克服保暖，可用休克服休克的治疗休克的治疗 T

22、reatment of Shock 补充血容量补充血容量(Restore circulating volume and tissue perfusion)：是抗休克的根本措施：是抗休克的根本措施 补充量：可根据补充量：可根据CVP调节，应补充丧失量和已调节，应补充丧失量和已扩大的毛细血管床容量扩大的毛细血管床容量 积极处理原发病积极处理原发病(Treat Reversible Causes)：在恢复有效血容量后积极手术处理：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，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，以免丧失抢应抗休克的同时，积

23、极手术处理，以免丧失抢救时机救时机Shock treatment“A rude unhinging of the machinery of life”“A brief pause in the act of dying”休克的治疗休克的治疗Treatment of Shock 纠正酸碱平衡失调：主要是酸中毒纠正酸碱平衡失调：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，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 心血管药物的应用心血管药物的应用(Circulatory Suppo

24、rt)Vasoconstrictor：去甲肾上腺素；间羟胺；苯肾上腺：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；西地素；苯苄胺；苄胺唑啉；多巴胺；异丙肾上腺素；西地兰等兰等 治疗治疗DIC改善微循环改善微循环 皮质类固醇和其他药物的应用皮质类固醇和其他药物的应用In summary,Treatment of Shock Identify the patient at high risk for shock Control or eliminate the cause Implement measures to enhance tissue perfusion C

25、orrect acid base imbalance Treat cardiac dysrhythmias失血性休克的治疗失血性休克的治疗(Treatment of Hemorrhagic Shock)补充血容量：根据情况输入晶体或补充血容量：根据情况输入晶体或/和胶体溶液和胶体溶液 出血量少，无活动性出血者，输入晶体液出血量少，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

26、间的辨证关系要处理好休克和止血手术间的辨证关系中心静脉压和补液的关系中心静脉压和补液的关系CVP BP 原因原因 处理原则处理原则 低低 低低 血容量严重不足血容量严重不足 充分补液充分补液 低低 正常正常 血容量不足血容量不足 适当补液适当补液 高高 低低 心功能不全心功能不全 强心药，纠酸，强心药，纠酸，或血容量相对过多或血容量相对过多 舒血管舒血管 高高 正常正常 容量血管过度收缩容量血管过度收缩 舒张血管舒张血管 正常正常 低低 心功能不全心功能不全 补液实验补液实验 或血容量不足或血容量不足 损伤性休克的治疗损伤性休克的治疗(Treatment of Traumatic Shock)

27、补充血容量：应根据监测指标的变化来补充血容量：应根据监测指标的变化来决定补液量决定补液量 纠正酸碱平衡失调：碱中毒纠正酸碱平衡失调：碱中毒酸中毒酸中毒 适当应用碱性药物适当应用碱性药物 手术治疗：应根据病情判断是否需要手手术治疗：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，复合维生素等药物治疗：大量抗生素，复合维生素等Hypovolemic Shock Management goal:Restore circulating volume and tissue perfusion:Control hemorrhage Restore circulati

28、ng volume Optimize oxygen delivery Vasoconstrictor if BP still low after volume loadingAimed 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 card

29、iogenic 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 se

30、vere metabolic acidosis is presented(pH7.15),administer NaHCO3;Identify and treat the underlying cause of shock.感染性休克的特点感染性休克的特点Characteristics of Septic Shock 内毒素性休克内毒素性休克 微循环变化的不同阶段常同时存在微循环变化的不同阶段常同时存在 微循环变化和内脏损害比较严重微循环变化和内脏损害比较严重 全身炎症反应综合征全身炎症反应综合征感染性休克的类型感染性休克的类型Types of Septic Shock 高排低阻型（高动力型）

31、：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）低排高阻型（低动力型）“Cold”shock hypodynamic response 原因：血容量减少原因：血容量减少+继发感染继发感染 活性因子：儿茶酚胺、活性因子：儿茶酚胺、5-羟色胺、组织胺、缓激肽羟色胺、组织胺、缓激肽 特点：周围血管阻力增加，心排出量降低特点：周围血管阻力增加，心排出量降低感染性休克的两种临床表现感染性休克的两种临床表现临床表

32、现临床表现 冷休克冷休克(高阻力型高阻力型)暖休克暖休克(低阻力型低阻力型)神志神志 躁动、淡漠或嗜睡躁动、淡漠或嗜睡 清醒清醒皮肤色泽皮肤色泽 苍白、紫绀或花斑样紫绀苍白、紫绀或花斑样紫绀 淡红或潮红淡红或潮红皮肤温度皮肤温度 湿冷或冷汗湿冷或冷汗 温暖、干燥温暖、干燥毛细血管充盈时间毛细血管充盈时间 延长延长 1-2秒秒脉搏脉搏 细速细速 慢、有力慢、有力脉压（脉压（kPa）4尿量尿量(每小时每小时)30mlSeptic ShockTreatment:Prevention Find and kill the source of the infection Fluid resuscitati

33、onVasoconstrictorsInotropic drugsMaximize O2 delivery SupportNutritional SupportTreatment 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 catheter

34、s;Hemodynamic,respiratory,and metabolic support:.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 at30ml per hour,mean arte

35、rial blood pressure at 65mmHg.Add inotropic and vasopressor therapy if needed.Maintain central venous oxygen saturation at 70%.Maintain oxygenation with ventilator support as indicated.Other treatments:Antiendotoxin,anti-inflammatory,and anticoagulant drugs are being studied in severe sepsis treatme

36、nt.Anticoagulant recombinant activated protein C(aPC):constant infusion of 24ug/kg per hour for 96 h.Treatment of Septic Shock感染性休克的治疗感染性休克的治疗 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；并根据全血；并根据CVP 调节输液量和速度调节输液量和速度 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；维持呼吸功能等人的一般状况；维持呼吸功能等 纠正酸

37、中毒：酸中毒发生早，严重，及早应用碱性药纠正酸中毒：酸中毒发生早，严重，及早应用碱性药物物 心血管药物应用：西地兰；心血管药物应用：西地兰；B-受体兴奋剂和受体兴奋剂和a受体抑制受体抑制剂联合应用剂联合应用 减轻细胞损害：皮质类固醇，大剂量应用；减轻细胞损害：皮质类固醇，大剂量应用；SOD，抑抑肽酶，肽酶，PGI2，试用中试用中THE ENDClinical examples-1 An 82-year-old man was brought to the emergency room by his grandson,who reported that the man had been eati

38、ng 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 soun

39、ds were appreciated on cardiac exam.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 n

40、oted to contain many white cells and bacteria.Urine was sent for culture.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 exami

41、nation 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.Clinical examples-2 Her pulse was noted to be 140 and blood pressure was palpable at 70

42、/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.Clinical examples-3 An 67-year-old female arrived in the emergency room complaining of chest pain

43、 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 auscu

44、ltation of the heart.There was no extremity edema.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

45、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.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:uBP:80/50,mean 60uRA:4mmHg,RV 22/3,PA 22/10,PAOP 6uCardiac output:1.9 liters/minuSVR:2350 dynes-cm-5-sec(normal 400-1900)