1、YouEmergency Department the First Affiliated Hospital of NanChang University Development of the concept of shock A history of the 200 years to recognize shock:l“shake”,“attack”lFrom superficial syndrome to microcirculatory level,cellular level,molecular level Circulatory level：blood pressure Microci
2、rculatory level：inadequate tissue perfusion Cellular level and molecular level：lFrontierlExploratory stage，experimental therapiesSimply.oxygen requirementoxygen delivery低血容量低血容量性休克性休克血液分布性休克血液分布性休克心源性休心源性休克克 阻塞性休克阻塞性休克Distributive(hyperdynamic)ShockHyperdynamic state with high cardiac outputNormal t
3、o low filling pressuresDecreased systemic vascular resistanceMixed venous oxygen may be normal or increasedDistributive(hyperdynamic)Shockcauses:SIRS(sepsis,burns,trauma,pancreatitis)neurogenic(spinal trauma)anaphylaxis/anaphylactoidendocrine(thyroid,myxoedema,adrenal)pharmacologic(vasodilators,benz
4、odiazepines)Hypovolaemic ShockLV preload is too low to support adequate stroke volumecompensatory mechanisms:tachycardia,increased venous tone,increased vascular resistance,increased contractility,decreased urine output and Na+reabsorption may help compensate for up to 1.5 L of blood lossshock devel
5、ops when blood loss exceeds 20-25%of normal circulating volumeprolonged hypovolaemic shock leads to metabolic acidosis,then cardiogenic shockHypovolaemic Shockcauses:blood losspolyuriaGI lossburnsvasodilationthird space lossesvascular permeabilityObstructive Shockcauses:tension pneumothoraxpulmonary
6、 emboli(thrombo-,air-,amniotic)mediastinal tumourspericardial tamponade,constrictive pericarditisacute pulmonary hypertensionaortic dissectionvalvular(mitral stenosis,aortic stenosis)vena-caval compressionCardiogenic Shockcardiac index below 2 L/min/m2PCWP greater than 17-20 mmHgCardiogenic Shockcau
7、ses:ischaemiamyocardial contusionvalvular diseasecardiomyopathymyocarditisdysrhythmiassepticaemiapharmacologicvarious shock states may interrelate clinically to produce a mixed picturehypovolaemic shock may lead to acidosis and result in cardiogenic shockseptic shock may lead to hypovolaemia as a re
8、sult of microbial toxins,cytokines,and capillary permeabilityThe Shock CycleThe Shock CycleConsequences of Shockhypothermiacoagulopathyacid-base disturbanceselectrolyte abnormalitiescellular injury and Multi-System Organ Failuredeath微循环的组成微循环的组成n微动脉、后微动脉微动脉、后微动脉n毛细血管前括约肌毛细血管前括约肌n真毛细血管真毛细血管n通血毛细血管（直捷
9、通通血毛细血管（直捷通路）路）n动动-静脉吻合支静脉吻合支n微静脉。微静脉。直捷通路直捷通路：微动脉：微动脉 后微后微动脉和通血毛细血管动脉和通血毛细血管 微微静脉静脉迂回通路迂回通路：微动脉：微动脉 后微后微动脉动脉 毛细血管前括约肌毛细血管前括约肌 真毛细血管网真毛细血管网 微静脉微静脉动静脉短路动静脉短路：微动脉：微动脉 动动静脉吻合支静脉吻合支 微静脉微静脉前、后阻力血管的特点前、后阻力血管的特点两点同：两点同：1.对儿茶酚胺的敏感性不同对儿茶酚胺的敏感性不同2.对缺氧酸中毒的耐受性不同对缺氧酸中毒的耐受性不同fluid and no perfusion 减压反射减压反射窦弓反射窦弓反
10、射血管血管收缩收缩前阻前阻力大力大于后于后阻力阻力灌少灌少流多流多动静脉吻合支开放动静脉吻合支开放大出血大出血血容量血容量减少减少心输出心输出量下降量下降血压下血压下降降缺血缺血缺氧缺氧交感肾上交感肾上腺（腺（+）儿）儿茶酚胺释茶酚胺释放放血管紧张素血管紧张素管加血压素管加血压素血栓素血栓素A2心肌抑制因子心肌抑制因子 l Increased catecholamine release l Increase glucocorticoid and mineralcorticoid releasel Activation of Renin-angiotensin system Compensato
11、ry mechanisms(early shock)The HPA and neuroendocrine axes are triggered A decrease in blood volumeStretch receptors in heart baroreceptors in aorta and carotid arteries 1 1）血容量增加）血容量增加 组织液回流加速组织液回流加速 2 2）心输出量增加）心输出量增加 回心血量增加回心血量增加 心肌收缩增强心肌收缩增强 心率加速心率加速3 3）维持动脉血压）维持动脉血压 心输出量增加心输出量增加 外周阻力增加外周阻力增加4 4）血
12、流重新分布）血流重新分布Compensatory mechanismsThe body attempts to compensate and restore perfusion by:lIncreasing cardiac outputlStimulation of the sympathetic nervous system causes an increase in heart rate,stroke volume,and PVR(peripheral vessel resistance).lRedistributing the circulating blood volume to vi
13、tal organslVasoconstriction,(periph-and viscero-vessel)l Pathologic arteriovenous shuntinglAutotranfused:precapillary resistance vessel to contract，to decrease capilary hydrostatic pressure.fluid and no perfusion 儿茶酚胺儿茶酚胺 CNS 烦燥不安烦燥不安神志清楚神志清楚 汗腺分泌汗腺分泌 出汗出汗 肾血管收缩肾血管收缩 尿量尿量 皮肤缺血皮肤缺血脸色苍白脸色苍白四肢冰冷四肢冰冷 休克
14、病因休克病因 交感肾上腺髓质交感肾上腺髓质 心率心率 心收缩力心收缩力 脉搏脉搏 脉差脉差（交感交感-肾上腺髓质系统兴奋和儿茶酚胺大量释放是肾上腺髓质系统兴奋和儿茶酚胺大量释放是不同类型休克的共同通路。不同类型休克的共同通路。缺血缺氧期的临床表现缺血缺氧期的临床表现 （mild tachycardia;bounding pulse Level of Consciousness:lethargy,confusion,combativeness Skin:delayed capillary refill;cool and clammy Blood Pressure:normal or slight
15、ly elevated Respirations:rapid and shallowEarly Stage(compensated shock):Compensatory mechanisms are able to maintain perfusion of vital organsThe ischemic hyoxia stage is a reversible com-pansatory stage.Eliminating pathogenic factors and restoring blood volume and tissue perfusion are re-commended
16、.Otherwise,it may progress to a more advanced stage.1.Alteration淤血缺氧淤血缺氧组织胺组织胺 激肽类激肽类腺苷腺苷 内毒素等内毒素等缺血缺血缺氧缺氧 酸中酸中毒毒前阻力血管前阻力血管对儿茶酚胺对儿茶酚胺反应性降低反应性降低前阻力前阻力血管扩血管扩张张灌灌多多流流少少后阻力后阻力血管收血管收缩缩后阻力血管后阻力血管对酸中毒耐对酸中毒耐受性强受性强血管扩血管扩张通透张通透性性血 液 浓 缩血 液 浓 缩流速缓慢流速缓慢微循环微循环淤血淤血微血管微血管扩张通扩张通透性透性心输心输出量出量下降下降血压血压下降下降 缺氧酸缺氧酸中毒组中毒组
17、织胺激织胺激肽肽 内内毒素腺毒素腺苷内啡苷内啡肽等肽等回回心心血血量量急急剧剧下下降降滤出滤出大于大于回流回流 更严重缺氧更严重缺氧毛细血毛细血管压增管压增高高 微循环淤血微循环淤血血压血压回心血量减少回心血量减少 脑缺血脑缺血 血压血压 肾血流量减少肾血流量减少心输出量减少心输出量减少皮肤淤血皮肤淤血 肾淤血肾淤血皮肤紫绀皮肤紫绀出现花斑出现花斑神智淡漠、昏迷神智淡漠、昏迷少尿无尿少尿无尿心博无力心音低钝心博无力心音低钝脉搏细速静脉塌陷脉搏细速静脉塌陷 Middle Stage(uncompensated shock):Compensatory mechanisms are unable t
18、o maintain perfusion Heart Rate:moderate tachycardia;weak and thready pulse Level of Consciousness:confusion or unconsciousness Skin:delayed capillary refill;cold,clammy,and cyanotic Blood Pressure:decreased Respirations:rapid and shallow Urine output:oliguria PAF、TXA2LTB4 LPS、IL-1、TNFICAM-1 1.Alter
19、ation血管内皮血管内皮损伤血小损伤血小板激活血板激活血液浓缩流液浓缩流速缓慢等速缓慢等血液高血液高凝状态凝状态血液低血液低凝状态凝状态微血栓微血栓形成形成回心血量急剧减少回心血量急剧减少心输出量急剧下降心输出量急剧下降血压急剧下降血压急剧下降大脑缺血大脑缺血出血出血3.淤血性缺氧期的临床症状淤血性缺氧期的临床症状（Late Shock Heart Rate:bradycardia;severe dysrhythmias Level of Consciousness:coma Skin:pale,cold,marked diaphoresis Blood Pressure:marked hy
20、potension Respirations:decreased rate and tidal volumeUrine output:oliguria or anuria multiple system organ failure,MSOF （Irreversible shockHypercoagulable character erythrocyte and thrombocyte to aggregateDICCellular hypoxia，lysosome rupturehydrolytic enzyme releasingaqtocytolysis and to damage oth
21、er cellsCell damage,organ failure occurdeath occurno perfusion and no fluid3.（身遍瘀斑身遍瘀斑呼吸困难；无尿；大脑缺血：神志不清呼吸困难；无尿；大脑缺血：神志不清休克休克期期 休克休克期期 休克休克期期特点特点痉挛、收缩；痉挛、收缩；前阻力前阻力 后阻力；后阻力；缺血，少灌少流。缺血，少灌少流。前阻力后阻力；前阻力后阻力；扩张，淤血；扩张，淤血；“灌灌”“流流”。麻痹性扩张；麻痹性扩张；微血栓形成；微血栓形成；不灌不流。不灌不流。交感交感-肾上腺髓肾上腺髓质系统兴奋；质系统兴奋；缩血管体液因缩血管体液因子释放。子释放
22、。H H+，平滑肌对，平滑肌对CACA反应性反应性；扩张血管的体液因扩张血管的体液因子释放；子释放；WBCWBC嵌塞，血小嵌塞，血小板、板、RBCRBC聚集。聚集。血管反应性丧失；血管反应性丧失；血液浓缩；血液浓缩；DICDIC形成；形成；血液流变性质恶化。血液流变性质恶化。机制机制 影响影响代偿作用重要；代偿作用重要；维持血压；维持血压；血流重分布血流重分布组织缺血、缺氧组织缺血、缺氧失代偿：回心血量失代偿：回心血量减少；血压进行性减少；血压进行性下降；血液浓缩。下降；血液浓缩。比休克期的影响更严比休克期的影响更严重；重；器官功能衰竭；器官功能衰竭；休克转入不可逆。休克转入不可逆。decre
23、ase in BP 600 ml/min.m2 DO2600 ml/min.m2 VO2170 ml/min.m2 VO2170 ml/min.m2 CI4.5L/min.m2 CI4.5L/min.m2Vasodilator if BP still low after volume loadingTreatment of Shockl Seldom use only vasoconstrictorl Vasodilator and volume expansion therapyl Combined application of vasodilator and vasoconstrictor
24、Current Pharmacotherapy of shock:Hemodynamic monitoring 1.Mental status：brain tissue perfusion2.Skin perfusion：warm,normal color good perfusion cold,pale,moist skin vasoconstriction3.Blood pressure：important but no sensitive indexlEarly detection:Dont rely on BPlsystolic pressure12 kPa(90 mmHg)pulse
25、 pressure1.0-1.5 shock，2.0 severe shock5.Urine output：the most sensitive index of the adequacy of vital organ perfusionl oliguria：initial shock,initial resuscitationl normal BP,oliguria and low specific gravity：acute renal failure(ARF)l urine output 30ml/h：improve Special monitoring（6 item6 item）1.C
26、entral Venous Pressure(CVP):CVP=right atrial pressure(RAP)=right-ventricular end-diastolic pressure(RVEDP)(Right Ventricular Preload)a valuable guide to vascular volume repalcement Normal CVP 0.490.98kPa(5 10cmH2O)A rising CVP indicates filling of the venous reservoir restoration of total intravascu
27、lar volume or cardiac failure A falling CVP indicates depletion of the venous reservoir 2.Pulmonary Capillary Wedge Pressure(PCWP):PCWP=left atrial pressure(LAP)=left-ventricular end-diastolic pressure(LVEDP)(Left Ventricular Preload)Normal volume 0.82kPa(6 15 cmH2O)CVP AND CIRCULATING VOLUME?Pulmon
28、ary Artery CatheterizationKlkj 3.Cardiac Output(CO)=HR SV(L/min)Normal CO=4 to 6 L/min It measured with the Swan-Ganz baloon catheter4.Cardiac Index(CI)=CO/BSA(L/min/m2)Normal CI=2.5-3.5 L/min/m2l Oxygen delivery（DO2）:1.34HBCO10SaO2l Oxygen uptake（VO2):1.34HBCO10(SaO2-SvO2）5.Arterial blood gas analy
29、sis：lPaO2:10.713Kpa(80100mmHg)PaCO2:4.85.8Kpa(3644mmHg)arterial pH:7.357.45lReflected repiratory reverse,ARDS,acid-base balance,acidosis,et al6.Serum lactate levels：as a prognostic guidelnormal value 11.5 mmol/Llheavy patient 2 mmol/Llexceed 8 mmol/L:a mortality rate of 100低血容量性休克低血容量性休克（hypovolemichypovolemic shock shock）休克指数脉搏/收缩压，0.5，说明正常或失血量为10%；1.0，说明失血量约为20%30%；1.5，说明失血量约为30%50%；收缩压80mmHg，失血量约在1500ml以上；凡有以下一种情况，失血量约在1500ml以上：苍白、口渴；颈外静脉塌陷；快速输平衡液1000ml，血压不回升；一侧股骨开放性骨折或骨盆骨折。sorry,I am not good at English.Thank you very much!
