1、SHOCKDepartment of Surgery Ruijin Hospital, Medical College, Shanghai Jiaotong UniversitySHOCKDepartment of Surgery RuiWestern recordviolent impact or blow, 1743physiologic instability, 1815Eastern record厥脫，內閉外脫I. Historical Aspect Initial records of shockWestern recordI. Historical AsInitial Explan

2、ation of shockWesternThomas Latta, 1831Patients with CholeraInfusion of fluids improvementHypovolemiaEastern邪毒內陷氣隨血脫陰虧氣脫氣機郁閉陰絕陽脫Initial Explanation of shockWewith the Rise of PhysiologyBurgeoning of Cardiovascular physiology in the end of 19CN, CrileCVP dropped after hemorrhageAnimal survival was in

3、creased after the infusion of salinethe Use of Cardiac CatheterizationBlood volume loss fall in Cardiac Outputwith the Rise of PhysiologyBurwith the Combination of Physiology and BiochemistryToxin theory of shock, Cannon & Baylissimpairment of oxygen transportdevelopment of acidosistoxin in severe m

4、uscle injury loss of vasomotor tone venous sequestration of blood hypotensionwith the Combination of PhysAntedate the Era of Critical Care MedicineExtensive physiologic research of Wigger, in early 1940sintegrating the Concepts of impaired oxygen deliveryoxygen debttissue injury / death the concept

5、of irreversible shockprogressive systemic circulatory decompensationAntedate the Era of Critical CControversy on Lung & KidneyARDS Introduction of the flow directed pulmonary artery catheter, in 1970 Noncardiogenic nature Not due to volume overloadARF More prompt and aggressive resuscitationIncidenc

6、e ATN happens: hypoperfusionARDS happens:Defects in Cell Membrane Function and Vascular Permeability Hypovolemia / Toxin /CytokineHypoxiaARDSControversy on Lung & KidneyARA syndrome that results from inadequate perfusion of tissues insufficient to meet metabolic demandlead to cellular dysfunction, e

7、laboration of inflammatory mediators, and celluar injury which may be limited, or widespread A continuum, ranging from subclinical deficits in perfusion to MODS or frank organ failure.Tissue hypoxia due to hypoperfusionDefectsInjuryII. Definition of shock A syndrome that results from i A. 組織低灌注所致細胞缺

8、氧B. 低血壓C. 酸中毒D. 心功能不全E. 以上都不對休克的根本問題是: A. 組織低灌注所致細胞缺氧B. 低血壓C. 酸中Impaired tissue perfusion Wider spectrum of shock presentations Ranging from occult tissue hypoxia to full-blown cardiovascular collapse or Multiple organ dysfunctionImplication alarm earliertreat earlierExplanationImpaired tissue perfu

9、sion ExplTissue hypoperfusiontissue hypoxiaanaerobic metabolism, acidosisinflammatory mediaterscirculatory redistributionearly involvement of splanchnic circulationcellular injuryseptic complicationsMODS ExplanationTissue hypoperfusionExplanatioO2 DebtWhether DO2crit is increased in ARDS, or sepsis

10、?Delivery -dependent oxygen uptake = Hypoxiacause MODSsupranormal levels supply of O2prevent the progression of MODS ?Providing opportunity for interventionProviding time for the disease to subsider Oxygen consumption(vO )2Oxygen delivery(DO2)O2 DebtExplanationO2 DebtOxygen consumption(vO Circulator

11、y redistributionConceptHomeostatic response to hypoperfusion to preserve oxygen delivery to heart and brain by selective diverting bloodMechanismcatechols, angiotension II, Vasopressin, endothelin,TXA2 ConsequenceCellular and organ derangement MODS Breakdown of the intestinal epithelial barrierbacte

12、rial and toxin translocation SIRSMODSExplanationCirculatory redistributionConcintrinsic obstruction of cap. Bedlow-flow states, hypothermia, and increased viscositycap. Sludging: intravascular coagulation, platelet aggregation, other intraluminal debrispreventing RBC from reaching the tissues extrin

13、sic obstruction of cap. Bedlocal tissue inflammation, edema, or hemorrhage, ACSvessel wall permeability deficitThe changes in Microcirculatary LevelExplanationintrinsic obstruction of cap. Hypovolemic ShockHemorrhage -Plasma losses -Cardiogenic ShockIntrinsic - ExtrinsicCompressive -Obstructive -III

14、. Classificaion of Shock TraumaGI BleedingRuptured aneurysmsBurnBowel obstructionMyocardial infarctionCardiomyopathyValvular Heart DiseaseCardiac Rhythm disturbanceMyocardial depression Tension pneumothoraxPericardial tamponadeHigh level of positive-pressure ventilationPulmonary embolismSurgical Sho

15、ck 1Hypovolemic ShockIII. ClassifiNeurogenic Shocke.g. Vasogenic ShockSIRS, toxin Septic despite adequate fluid resucitationTraumatic Anaphylactic and AnaphylactoidHypoadrenalSpinal cord injurySevere head injurySpinal cord anesthesiaSurgical Shock 2Neurogenic ShockSpinal cord inThe othersThere may b

16、e a “ ” to be filled. but “cellular shock”, such as poisoning, hypoxia, hypoglycemia, is not the syndrome, continuum, or tissue hypoxia due to hypoperfusion, may be excluded from the category of shock.The others各型休克的共同特點是： A. 血壓下降B. 中心靜脈壓下降C. 脈壓縮小D. 尿量減少E. 有效循環血量銳減各型休克的共同特點是： A. 血壓下降B. 中心靜脈壓Secondar

17、y visceral impairement Microcirculatory changes Metabolic changesIV. Pathophysiologic staging of shockSecondary visceral impairement Microcirculatory StagingMicrocirculatory constrictive phaseMicrocirculatory dilatation phaseMicrocirculatory failure phase Microcirculatory StagingMicro后微A微V前括約肌AV吻合支微

18、動脈微靜脈加重過程 只出不進/只過不進只進不出/進多出少Microcirculatory Structure后微A微V前括約肌AV吻合支微動脈微靜脈加重過程Mic Metabolic Changesenergy metabolic abnormality無氧糖酵解，產能減少metabolic acidosis引起微血管擴張，等barrier function defects of membrane 累及基底膜，細胞膜，溶酶體膜 Metabolic Changesenergy metab Secondary Visceral ImpairmentHeart Kidney LungBrainGas

19、trointestinal tractLiver Secondary Visceral ImpairmenClinical StagingShock compensatory stagenervous, restless, agitation, cool, pale, thirsty, tachycardia, short of breathBP normal or increased, pulse pressure decreased, urinary output normal or decreasedBlood loss 20% ，20% ，800mlShock inhibiting s

20、tage 關于休克代償期微循環改變， 下列那一項是錯誤的： A. 動靜脈短路開放B. 直捷通道開放C. 微動脈收縮D. 微靜脈收縮E. 毛細血管內血液淤積 關于休克代償期微循環改變， 下列那一項是錯誤V. Diagnosis and patient monitoringCauses and PredictionConventional monitoringMental statusSkin temperatureBlood pressure, Pulse rateUrinary output (30ml/hr)Special monitoringCVP (15, 20)Blood routin

21、e test/Arterial blood gas analysis/ElectrolytesPCWP(615mmHg)CO CISerum lactate concentrationArterial blood gas analysisDIC: PLT/FDPV. Diagnosis and patient monitVI. Measurement of Shock一般緊急處理Urgent measurement補充血容量Resuscitation積極處理原發病Treat inciting cause of shock糾正酸堿平衡失調Control electrolytes, and aci

22、d base derangement血管活性藥物的應用Inotropic agent治療DIC，改善微循環 Treat DIC, improve microcirculation皮質類固醇和其它藥物的應用 Corticosteroids心理支持與呵護VI. Measurement of Shock一般緊急處理PCWPCVP15, Volume expansion10cmH2O18, Consider volume 18 Diurese 14 Reestablishment of urinary outputto a rate of 0.5-1.0ml per kg. Per hourA nor

23、mal heart rate and blood pressureAdequate capillary refillNormal sensoriumNormal CVP and PWCPi. Volume Resuscitation & Initial end-pointsFluid resuscitation End-point reachingPCWP15, Volume expansion90% Optimize Cardiac Index Optimize HbSupply supplemental O2 Early hemodynamic monitoring 11-13 g/dlV

24、entilator, if necessary Assess volume status(preload) ReassessKeep: PCWP15-18 mmHg, MAP 60-80mmHg, Delivery independent O2 consumptionGoal meet Goal not meetTreat inciting cause of shockControl SIRSNutritional support Inotropic support beta agonismGoal meetGoal not meetConsider Vasodilator, alpha ag

25、onistInitial resuscitation of patients in ShockPCWP15, Volume expansion18 DiureseOptimize Oxygen DeliveryKeep S A. 心功能不全B. 血容量不足C. 血容量過多D. 血管張力升高E. 以上都不是 休克病人經補液后，血壓仍低。5 10 min內經靜脈注入等滲鹽水250ml，如血壓上升，而中心靜脈壓不變，提示： A. 心功能不全 休克病人經補液后，血壓ShockMODSDisturbanceDeath? Timing & Strategy!Effort & Effectii. Curre

26、nt Strategy for Shock Solution ShockMODSDisturbanceDeath? TimPrevention, early Identification, early and specific treatment for Shock and MODS感染創傷燒傷SAPSIRS代謝紊亂低氧乏氧代謝休克復蘇失敗痊愈MODS好轉MODS第二次打擊心源性、神經源性因素低血容量血管源性PrimarySecondary（感染）(24h)死亡Prevention, early Identificati1. Hypovolemic shockSymptoma decrease

27、 in pulse pressuretachycarida and hypotensionurine output fallsnormal skin turgor is lostmental status changes - in a progressive fashion apprehension, anxiety, complete obtundationCVP decreaseTreatmentResuscitation & Control the inciting cause of shockSpecific1. Hypovolemic shockSpecific2. Traumati

28、c shockTypeVasogenic shock that begins as hypovolemic shockCharacter - refractory to fluid replacement therapyLarger volume losses, greater fluid sequestrationMore intense activation of inflammatory mediatorsDevelopment of SIRSDevastating soft tissue injuriesMachanismincreasing microvascular permeab

29、ility, Excessive fluid requirement Frequently Require mechanical ventilation, Pulmonary artery catheter monitoringCardiovascular supportOperationSpecific2. Traumatic shockSpecific 3. Septic shockTypeVasogenic shock, Refractory to fluid replacement therapyDefinitionSepsis with hypotension despite ade

30、quate fluid resuscitationalong with the presence of manifestations of hypoperfutionsuch as lactic acidosis, obliguria, or acute alteration in mental statusMechanism CytokinesVasodilatation, Increasing microvascular permeability, Excessive fluid requirement Specific 3. Septic shockSpecific Treatment

31、of Septic shockResuscitationControl infectionNormalization of electrolytes, acid base dearangementInotropic agentCorticosteroidsNutritional support, deal with DIC, organ function support Specific Treatment of Septic shockSpec4. Anaphylactic and Anaphylactoid shockMechanismInflammatory mediatorsC3a,

32、C5a, Histamine, Kinnins, ProstaglandinssymptomsVasodilatation, increased capillary permeabilitybronchospasm, airway edema, circulatory collapseTreatmentEpinephrine 0.3-0.5ml s.c. / 0.5-5ug/min / bolus 0.1-0.2ml縮血管Aminophylline CorticosteroidsAntihistamineImmunologically Mediated: byIgE antibodyNot I

33、mmunologically Mediated: Radiographic contrast dyes, narcoticsSpecific4. Anaphylactic and Anaph5. Cardiogenic ShockSymptomWeak or slow pulse ratetachycarida or bradycardiaurine output fallsCough, pink foamy phlegm, dyspnea, cyanosismental status changes fatigue, apathiaBP decrease & CVP normal or increaseTreatmentResuscitation & cardiac s