1、SHOCKDepartment of Surgery Ruijin Hospital,Medical College,Shanghai Jiaotong UniversitynWestern recordnviolent impact or blow,1743nphysiologic instability,1815nEastern recordn厥脱，内闭外脱I.Historical Aspect Initial records of shockInitial Explanation of shocknWesternnThomas Latta,1831nPatients with Chole
2、ranInfusion of fluids improvementHypovolemianEasternn邪毒内陷n气随血脱n阴亏气脱n气机郁闭n阴绝阳脱with the Rise of PhysiologynBurgeoning of Cardiovascular physiology in the end of 19CN,CrilenCVP dropped after hemorrhagenAnimal survival was increased after the infusion of salinenthe Use of Cardiac CatheterizationnBlood v
3、olume loss fall in Cardiac Outputwith the Combination of Physiology and BiochemistrynToxin theory of shock,Cannon&Baylissnimpairment of oxygen transportndevelopment of acidosisntoxin in severe muscle injury loss of vasomotor tone venous sequestration of blood hypotensionAntedate the Era of Critical
4、Care MedicinenExtensive physiologic research of Wigger,in early 1940snintegrating the Concepts of nimpaired oxygen deliverynoxygen debtntissue injury/death nthe concept of irreversible shocknprogressive systemic circulatory decompensationControversy on Lung&KidneynARDS nIntroduction of the flow dire
5、cted pulmonary artery catheter,in 1970n Noncardiogenic nature Not due to volume overloadnARF nMore prompt and aggressive resuscitationnIncidence ATN happens:hypoperfusionARDS happens:Defects in Cell Membrane Function and Vascular Permeability Hypovolemia/Toxin/CytokineHypoxiaARDSnA syndrome that res
6、ults from inadequate perfusion of tissues ninsufficient to meet metabolic demandnlead to cellular dysfunction,elaboration of inflammatory mediators,and celluar injuryn which may be limited,or widespreadn A continuum,ranging from subclinical deficits in perfusion to MODS or frank organ failure.nTissu
7、e hypoxia due to hypoperfusionnDefectsnInjuryII.Definition of shock A.组织低灌注所致细胞缺氧B.低血压C.酸中毒D.心功能不全E.以上都不对休克的根本问题是:nImpaired tissue perfusion nWider spectrum of shock presentations nRanging from occult tissue hypoxia to full-blown cardiovascular collapse or Multiple organ dysfunctionnImplication nala
8、rm earlierntreat earliernTissue hypoperfusionntissue hypoxiananaerobic metabolism,acidosisninflammatory mediatersncirculatory redistributionnearly involvement of splanchnic circulationncellular injurynseptic complicationsnMODS nO2 DebtnWhether DO2crit is increased in ARDS,or sepsis?nDelivery-depende
9、nt oxygen uptake=Hypoxiancause MODSnsupranormal levels supply of O2nprevent the progression of MODS?nProviding opportunity for interventionnProviding time for the disease to subsider Oxygen consumption(vO )2Oxygen delivery(DO2)O2 DebtCirculatory redistributionnConceptnHomeostatic response to hypoper
10、fusion to preserve oxygen delivery to heart and brain by selective diverting bloodnMechanismncatechols,angiotension II,Vasopressin,endothelin,TXA2 nConsequencenCellular and organ derangement MODS nBreakdown of the intestinal epithelial barriernbacterial and toxin translocation SIRSMODSnintrinsic obs
11、truction of cap.Bednlow-flow states,hypothermia,and increased viscosityncap.Sludging:intravascular coagulation,platelet aggregation,other intraluminal debrisnpreventing RBC from reaching the tissues nextrinsic obstruction of cap.Bednlocal tissue inflammation,edema,or hemorrhage,ACSnvessel wall perme
12、ability deficitThe changes in Microcirculatary LevelnHypovolemic ShocknHemorrhage-nPlasma losses-nCardiogenic ShocknIntrinsic-nExtrinsicnCompressive-nObstructive-III.Classificaion of Shock TraumaGI BleedingRuptured aneurysmsBurnBowel obstructionMyocardial infarctionCardiomyopathyValvular Heart Disea
13、seCardiac Rhythm disturbanceMyocardial depression Tension pneumothoraxPericardial tamponadeHigh level of positive-pressure ventilationPulmonary embolismnNeurogenic Shockne.g.nVasogenic ShocknSIRS,toxin nSeptic despite adequate fluid resucitationnTraumatic nAnaphylactic and AnaphylactoidnHypoadrenalS
14、pinal cord injurySevere head injurySpinal cord anesthesianThe othersnThere may be a“”to be filled.n 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.各型休克的共同特点是：A.血压下降B.中心静脉压下降C.脉
15、压缩小D.尿量减少E.有效循环血量锐减后微后微A微微V前括约肌前括约肌AV吻合支吻合支微动脉微动脉微静脉微静脉加重过程 只出不进/只过不进只进不出/进多出少Microcirculatory Structurenenergy metabolic abnormalityn无氧糖酵解，产能减少nmetabolic acidosisn引起微血管扩张，等nbarrier function defects of membrane n累及基底膜，细胞膜，溶酶体膜 关于休克代偿期微循环改变，下列那一项是错误的：A.动静脉短路开放B.直捷通道开放C.微动脉收缩D.微静脉收缩E.毛细血管内血液淤积PCWPCVP1
16、5,Volume expansion10cmH2O18,Consider volume 18 Diurese 14 nReestablishment of urinary outputnto a rate of 0.5-1.0ml per kg.Per hournA normal heart rate and blood pressurenAdequate capillary refillnNormal sensoriumnNormal CVP and PWCPi.Volume Resuscitation&Initial end-pointsFluid resuscitation End-po
17、int reachingOptimize Oxygen DeliveryKeep SaO290%Optimize Cardiac Index Optimize HbSupply supplemental O2 Early hemodynamic monitoring 11-13 g/dlVentilator,if necessary Assess volume status(preload)ReassessKeep:PCWP15-18 mmHg,MAP 60-80mmHg,Delivery independent O2 consumptionGoal meet Goal not meetTre
18、at inciting cause of shockControl SIRSNutritional support Inotropic support beta agonismGoal meetGoal not meetConsider Vasodilator,alpha agonistPCWP15,Volume expansion18 Diurese A.心功能不全B.血容量不足C.血容量过多D.血管张力升高E.以上都不是 休克病人经补液后，血压仍低。5 10 min内经静脉注入等渗盐水250ml，如血压上升，而中心静脉压不变，提示：Shock MODSDisturbanceDeath?Ti
19、ming&Strategy!Effort&Effectii.Current Strategy for Shock Solution Prevention,early Identification,early and specific treatment for Shock and MODS感染创伤烧伤SAPSIRS代谢紊乱低氧乏氧代谢休克复苏失败痊愈MODS好转MODS第二次打击心源性、神经源性因素低血容量血管源性PrimarySecondary（感染）(24h)死亡nSymptomna decrease in pulse pressurentachycarida and hypotensio
20、nnurine output fallsnnormal skin turgor is lostnmental status changes-in a progressive fashion apprehension,anxiety,complete obtundationnCVP decreasenTreatmentnResuscitation&Control the inciting cause of shocknTypenVasogenic shock that begins as hypovolemic shocknCharacter-refractory to fluid replac
21、ement therapynLarger volume losses,greater fluid sequestrationnMore intense activation of inflammatory mediatorsnDevelopment of SIRSnDevastating soft tissue injuriesnMachanismnincreasing microvascular permeability,Excessive fluid requirement nFrequently Require nmechanical ventilation,Pulmonary arte
22、ry catheter monitoringnCardiovascular supportnOperationnTypenVasogenic shock,Refractory to fluid replacement therapynDefinitionnSepsis with hypotension despite adequate fluid resuscitationnalong with the presence of manifestations of hypoperfutionnsuch as lactic acidosis,obliguria,or acute alteratio
23、n in mental statusnMechanism nCytokinesnVasodilatation,Increasing microvascular permeability,Excessive fluid requirement Treatment of Septic shocknResuscitationnControl infectionnNormalization of electrolytes,acid base dearangementnInotropic agentnCorticosteroidsnNutritional support,deal with DIC,or
24、gan function support 4.Anaphylactic and Anaphylactoid shocknMechanismnInflammatory mediatorsnC3a,C5a,Histamine,Kinnins,ProstaglandinsnsymptomsnVasodilatation,increased capillary permeabilitynbronchospasm,airway edema,circulatory collapsenTreatmentnEpinephrine 0.3-0.5ml s.c./0.5-5ug/min/bolus 0.1-0.2
25、mln缩血管nAminophylline nCorticosteroidsnAntihistamineImmunologically Mediated:byIgE antibodyNot Immunologically Mediated:Radiographic contrast dyes,narcotics5.Cardiogenic ShocknSymptomnWeak or slow pulse ratentachycarida or bradycardianurine output fallsnCough,pink foamy phlegm,dyspnea,cyanosisnmental
26、 status changes fatigue,apathianBP decrease&CVP normal or increasenTreatmentnResuscitation&cardiac stimulant,diuretics,vesodialatorsVII.Solution of Shock nChain&RingnHeart,Lung,Kidney,Liver,BrainnDilema&OptionnExtended or limited?nEarly or delayed?nIntervention and CarenBalance&AdjustnVolume,osmotic
27、 pressure,compositionnSpecial agent A.E.Baue,the Expert on shock:链子的牢固程度是由最薄弱的环节所决定的。当前一个弱点加固之后，又会出现新的易断点。nCytokine and MediatorsnActivated after severe injury,ischemia,or sepsisnMechanism of SIRS,MODS nParameter of Severity n Prevention of irreversible shock,and MODSntiming of interventionnManipula
28、tion possible?nOne dose therapy?nWhat is shock?What is surgical shock?nRecommendationnSpecialist,books and referencesnRecognitionnConfusing,busynDeny,neglectnAggressive,defensivenAffected/affecting nExploration/clarifying43写在最后写在最后成功的基础在于好的学习习惯成功的基础在于好的学习习惯The foundation of success lies in good habits 结束语当你尽了自己的最大努力时，失败也是伟大的，所以不要放弃，坚持就是正确的。When You Do Your Best,Failure Is Great,So DonT Give Up,Stick To The End演讲人：XXXXXX 时 间：XX年XX月XX日
