重症急性胰腺炎治疗现状与发展.pptx

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 CholeranInfusion 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 volume 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 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 directed 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 results 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.nTissue 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 nalarm earlierntreat earlierExplanationExplanationnTissue hypoperfusionntissue hypoxiananaerobic metabolism,acidosisninflammatory mediatersncirculatory redistributionnearly involvement of splanchnic circulationncellular injurynseptic complicationsnMODS ExplanationExplanationnO2 DebtnWhether DO2crit is increased in ARDS,or sepsis?nDelivery-dependent 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 DebtExplanationExplanationCirculatory redistributionnConceptnHomeostatic response to hypoperfusion 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 SIRSMODSExplanationExplanationnintrinsic obstruction 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 permeability deficitThe changes in Microcirculatary LevelExplanationExplanationnHypovolemic ShocknHemorrhage-nPlasma losses-nCardiogenic ShocknIntrinsic-nExtrinsicnCompressive-nObstructive-III.Classificaion of Shock TraumaGI BleedingRuptured aneurysmsBurnBowel obstructionMyocardial infarctionCardiomyopathyValvular Heart DiseaseCardiac Rhythm disturbanceMyocardial depression Tension pneumothoraxPericardial tamponadeHigh level of positive-pressure ventilationPulmonary embolismSurgical Shock 1Surgical Shock 1nNeurogenic Shockne.g.nVasogenic ShocknSIRS,toxin nSeptic despite adequate fluid resucitationnTraumatic nAnaphylactic and AnaphylactoidnHypoadrenalSpinal cord injurySevere head injurySpinal cord anesthesiaSurgical Shock 2Surgical Shock 2nThe 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.脉压缩小D.尿量减少E.有效循环血量锐减Secondary visceral impairement Microcirculatory changes Metabolic changesIV.Pathophysiologic staging of shock Microcirculatory Stagingn nMicrocirculatory constrictive phasen nMicrocirculatory dilatation phasen nMicrocirculatory failure phase后微后微A微微V前括约肌前括约肌AV吻合支吻合支微微动动脉脉微微静静脉脉加重过程 只出不进/只过不进只进不出/进多出少Microcirculatory Structure Metabolic Changesnenergy 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 Secondary Visceral Impairmentn nHeart n nKidney n nLungn nBrainn nGastrointestinal tractn nLiverClinical Stagingn nShock compensatory stagen nnervous,restless,agitation,nervous,restless,agitation,n ncool,pale,thirsty,cool,pale,thirsty,n ntachycardia,short of breathtachycardia,short of breathn nBP normal or increased,pulse pressure decreased,BP normal or increased,pulse pressure decreased,urinary output normal or decreasedurinary output normal or decreasedn nBlood loss Blood loss 20%20%，80020%20%，800800mlml 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V.Diagnosis and patient monitoringn nCauses and PredictionCauses and Predictionn nConventional monitoringConventional monitoringn nMental statusMental statusn nSkin temperatureSkin temperaturen nBlood pressure,Pulse rateBlood pressure,Pulse raten nUrinary output(30ml/hr)Urinary output(30ml/hr)n nSpecial monitoringSpecial monitoringn nCVP(5,510cmHCVP(15,20)O,15,20)n nBlood routine test/Arterial blood gas analysis/ElectrolytesBlood routine test/Arterial blood gas analysis/Electrolytesn nPCWP(615mmHg)PCWP(615mmHg)n nCO CICO CIn nSerum lactate concentrationSerum lactate concentrationn nArterial blood gas analysisArterial blood gas analysisn nDIC:PLT/FDPDIC:PLT/FDPVI.Measurement of Shockn n一般紧急处理一般紧急处理n nUrgent measurementUrgent measurementn n补充血容量补充血容量n nResuscitationResuscitationn n积极处理原发病积极处理原发病n nTreat inciting cause of shockTreat inciting cause of shockn n纠正酸碱平衡失调纠正酸碱平衡失调n nControl electrolytes,and acid base derangementControl electrolytes,and acid base derangementn n血管活性药物的应用血管活性药物的应用n nInotropic agentInotropic agentn n治疗治疗DICDIC，改善微循环改善微循环 n nTreat DIC,improve microcirculationTreat DIC,improve microcirculationn n皮质类固醇和其它药物的应用皮质类固醇和其它药物的应用n n Corticosteroids Corticosteroidsn n心理支持与呵护心理支持与呵护PCWPCVP15,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-point 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 meetTreat inciting cause of shockControl SIRSNutritional support Inotropic support beta agonismGoal meetGoal not meetConsider Vasodilator,alpha agonistInitial resuscitation of patients in ShockInitial resuscitation of patients in ShockPCWP15,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?Timing&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1.Hypovolemic shocknSymptomna decrease in pulse pressurentachycarida and hypotensionnurine output fallsnnormal skin turgor is lostnmental status changes-in a progressive fashion apprehension,anxiety,complete obtundationnCVP decreasenTreatmentnResuscitation&Control the inciting cause of shockSpecificSpecific2.Traumatic shocknTypenVasogenic shock that begins as hypovolemic shocknCharacter-refractory to fluid replacement 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 artery catheter monitoringnCardiovascular supportnOperationSpecificSpecific 3.Septic shocknTypenVasogenic 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 alteration in mental statusnMechanism nCytokinesnVasodilatation,Increasing microvascular permeability,Excessive fluid requirement SpecificSpecific Treatment of Septic shocknResuscitationnControl infectionnNormalization of electrolytes,acid base dearangementnInotropic agentnCorticosteroidsnNutritional support,deal with DIC,organ function support SpecificSpecific4.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 0.1-0.2mln缩血管nAminophylline nCorticosteroidsnAntihistamineImmunologically Mediated:byIgE antibodyNot Immunologically Mediated:Radiographic contrast dyes,narcoticsSpecificSpecific5.Cardiogenic ShocknSymptomnWeak or slow pulse ratentachycarida or bradycardianurine output fallsnCough,pink foamy phlegm,dyspnea,cyanosisnmental 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 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 interventionnManipulation possible?nOne dose therapy?nWhat is shock?What is surgical shock?nRecommendationnSpecialist,books and referencesnRecognitionnConfusing,busynDeny,neglectnAggressive,defensivenAffected/affecting nExploration/clarifyingVIII.Before closing,can we draw a conclusion?nPivotal Factor of shock?nExtrinsic or IntrinsicnSolution?nEastern or westernThe END