休克-英语解读.ppt

SHOCK,DepartmentofSurgeryRuijinHospital,MedicalCollege,ShanghaiJiaotongUniversity,Westernrecordviolentimpactorblow,1743physiologicinstability,1815Easternrecord厥脱，内闭外脱,I.HistoricalAspect,Initialrecordsofshock,InitialExplanationofshock,WesternThomasLatta,1831PatientswithCholeraInfusionoffluidsimprovement,Hypovolemia,Eastern邪毒内陷气随血脱阴亏气脱气机郁闭阴绝阳脱,withtheRiseofPhysiology,BurgeoningofCardiovascularphysiologyintheendof19CN,CrileCVPdroppedafterhemorrhageAnimalsurvivalwasincreasedaftertheinfusionofsalinetheUseofCardiacCatheterizationBloodvolumelossfallinCardiacOutput,withtheCombinationofPhysiologyandBiochemistry,Toxintheoryofshock,Cannon&Baylissimpairmentofoxygentransportdevelopmentofacidosistoxininseveremuscleinjurylossofvasomotortonevenoussequestrationofbloodhypotension,AntedatetheEraofCriticalCareMedicine,ExtensivephysiologicresearchofWigger,inearly1940sintegratingtheConceptsofimpairedoxygendeliveryoxygendebttissueinjury/deaththeconceptofirreversibleshockprogressivesystemiccirculatorydecompensation,ControversyonLung&Kidney,ARDSIntroductionoftheflowdirectedpulmonaryarterycatheter,in1970NoncardiogenicnatureNotduetovolumeoverloadARFMorepromptandaggressiveresuscitationIncidence,ATNhappens:hypoperfusion,ARDShappens:,DefectsinCellMembraneFunctionandVascularPermeability,Hypovolemia/Toxin/Cytokine,Hypoxia,ARDS,Asyndromethatresultsfrominadequateperfusionoftissuesinsufficienttomeetmetabolicdemandleadtocellulardysfunction,elaborationofinflammatorymediators,andcelluarinjurywhichmaybelimited,orwidespreadAcontinuum,rangingfromsubclinicaldeficitsinperfusiontoMODSorfrankorganfailure.TissuehypoxiaduetohypoperfusionDefectsInjury,II.Definitionofshock,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:,ImpairedtissueperfusionWiderspectrumofshockpresentationsRangingfromocculttissuehypoxiatofull-blowncardiovascularcollapseorMultipleorgandysfunctionImplicationalarmearliertreatearlier,Explanation,Tissuehypoperfusiontissuehypoxiaanaerobicmetabolism,acidosisinflammatorymediaterscirculatoryredistributionearlyinvolvementofsplanchniccirculationcellularinjurysepticcomplicationsMODS,Explanation,O2DebtWhetherDO2critisincreasedinARDS,orsepsis?Delivery-dependentoxygenuptake=HypoxiacauseMODSsupranormallevelssupplyofO2preventtheprogressionofMODS?ProvidingopportunityforinterventionProvidingtimeforthediseasetosubsider,Oxygenconsumption(vO),2,Oxygendelivery(DO2),O2Debt,Explanation,Circulatoryredistribution,ConceptHomeostaticresponsetohypoperfusiontopreserveoxygendeliverytoheartandbrainbyselectivedivertingbloodMechanismcatechols,angiotensionII,Vasopressin,endothelin,TXA2ConsequenceCellularandorganderangementMODSBreakdownoftheintestinalepithelialbarrierbacterialandtoxintranslocationSIRSMODS,Explanation,intrinsicobstructionofcap.Bedlow-flowstates,hypothermia,andincreasedviscositycap.Sludging:intravascularcoagulation,plateletaggregation,otherintraluminaldebrispreventingRBCfromreachingthetissuesextrinsicobstructionofcap.Bedlocaltissueinflammation,edema,orhemorrhage,ACSvesselwallpermeabilitydeficit,ThechangesinMicrocirculataryLevel,Explanation,HypovolemicShockHemorrhage-Plasmalosses-CardiogenicShockIntrinsic-ExtrinsicCompressive-Obstructive-,III.ClassificaionofShock,Trauma,GIBleeding,Rupturedaneurysms,Burn,Bowelobstruction,Myocardialinfarction,Cardiomyopathy,ValvularHeartDisease,CardiacRhythmdisturbance,Myocardialdepression,Tensionpneumothorax,Pericardialtamponade,Highlevelofpositive-pressureventilation,Pulmonaryembolism,SurgicalShock1,NeurogenicShocke.g.VasogenicShockSIRS,toxinSepticdespiteadequatefluidresucitationTraumaticAnaphylacticandAnaphylactoidHypoadrenal,Spinalcordinjury,Severeheadinjury,Spinalcordanesthesia,SurgicalShock2,TheothersTheremaybea“”tobefilled.but“cellularshock”,suchaspoisoning,hypoxia,hypoglycemia,isnotthesyndrome,continuum,ortissuehypoxiaduetohypoperfusion,maybeexcludedfromthecategoryofshock.,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,Secondaryvisceralimpairement,Microcirculatorychanges,Metabolicchanges,IV.Pathophysiologicstagingofshock,MicrocirculatoryStaging,MicrocirculatoryconstrictivephaseMicrocirculatorydilatationphaseMicrocirculatoryfailurephase,后微A,微V,前括约肌,AV吻合支,微动脉,微静脉,加重过程只出不进/只过不进只进不出/进多出少,MicrocirculatoryStructure,MetabolicChanges,energymetabolicabnormality无氧糖酵解，产能减少metabolicacidosis引起微血管扩张，等barrierfunctiondefectsofmembrane累及基底膜，细胞膜，溶酶体膜,SecondaryVisceralImpairment,HeartKidneyLungBrainGastrointestinaltractLiver,ClinicalStaging,Shockcompensatorystagenervous,restless,agitation,cool,pale,thirsty,tachycardia,shortofbreathBPnormalorincreased,pulsepressuredecreased,urinaryoutputnormalordecreasedBloodloss800ml,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.Diagnosisandpatientmonitoring,CausesandPredictionConventionalmonitoringMentalstatusSkintemperatureBloodpressure,PulserateUrinaryoutput(30ml/hr)SpecialmonitoringCVP(15,20)Bloodroutinetest/Arterialbloodgasanalysis/ElectrolytesPCWP(615mmHg)COCISerumlactateconcentrationArterialbloodgasanalysisDIC:PLT/FDP,VI.MeasurementofShock,一般紧急处理Urgentmeasurement补充血容量Resuscitation积极处理原发病Treatincitingcauseofshock纠正酸碱平衡失调Controlelectrolytes,andacidbasederangement血管活性药物的应用Inotropicagent治疗DIC，改善微循环TreatDIC,improvemicrocirculation皮质类固醇和其它药物的应用Corticosteroids心理支持与呵护,Reestablishmentofurinaryoutputtoarateof0.5-1.0mlperkg.PerhourAnormalheartrateandbloodpressureAdequatecapillaryrefillNormalsensoriumNormalCVPandPWCP,i.VolumeResuscitation&Initialend-points,Fluidresuscitation,End-pointreaching,OptimizeOxygenDelivery,KeepSaO290%OptimizeCardiacIndexOptimizeHbSupplysupplementalO2Earlyhemodynamicmonitoring11-13g/dlVentilator,ifnecessary,Assessvolumestatus(preload),Reassess,Keep:PCWP15-18mmHg,MAP60-80mmHg,DeliveryindependentO2consumption,GoalmeetGoalnotmeet,TreatincitingcauseofshockControlSIRSNutritionalsupport,Inotropicsupportbetaagonism,Goalmeet,Goalnotmeet,ConsiderVasodilator,alphaagonist,InitialresuscitationofpatientsinShock,PCWP,15,Volumeexpansion,18Diurese,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。510min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：,?Timing&Strategy,!,!,!,Effort&Effect,ii.CurrentStrategyforShockSolution,Prevention,earlyIdentification,earlyandspecifictreatmentforShockandMODS,感染创伤烧伤SAP,SIRS,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,Primary,Secondary,（感染）,(24h),死亡,1.Hypovolemicshock,Symptomadecreaseinpulsepressuretachycaridaandhypotensionurineoutputfallsnormalskinturgorislostmentalstatuschanges-inaprogressivefashionapprehension,anxiety,completeobtundationCVPdecreaseTreatmentResuscitation&Controltheincitingcauseofshock,Specific,2.Traumaticshock,TypeVasogenicshockthatbeginsashypovolemicshockCharacter-refractorytofluidreplacementtherapyLargervolumelosses,greaterfluidsequestrationMoreintenseactivationofinflammatorymediatorsDevelopmentofSIRSDevastatingsofttissueinjuriesMachanismincreasingmicrovascularpermeability,ExcessivefluidrequirementFrequentlyRequiremechanicalventilation,PulmonaryarterycathetermonitoringCardiovascularsupportOperation,Specific,3.Septicshock,TypeVasogenicshock,RefractorytofluidreplacementtherapyDefinitionSepsiswithhypotensiondespiteadequatefluidresuscitationalongwiththepresenceofmanifestationsofhypoperfutionsuchaslacticacidosis,obliguria,oracutealterationinmentalstatusMechanismCytokinesVasodilatation,Increasingmicrovascularpermeability,Excessivefluidrequirement,Specific,TreatmentofSepticshock,ResuscitationControlinfectionNormalizationofelectrolytes,acidbasedearangementInotropicagentCorticosteroidsNutritionalsupport,dealwithDIC,organfunctionsupport,Specific,4.AnaphylacticandAnaphylactoidshock,MechanismInflammatorymediatorsC3a,C5a,Histamine,Kinnins,ProstaglandinssymptomsVasodilatation,increasedcapillarypermeabilitybronchospasm,airwayedema,circulatorycollapseTreatmentEpinephrine0.3-0.5mls.c./0.5-5ug/min/bolus0.1-0.2ml缩血管AminophyllineCorticosteroidsAntihistamine,ImmunologicallyMediated:byIgEantibody,NotImmunologicallyMediated:Radiographiccontrastdyes,narcotics,Specific,5.CardiogenicShock,SymptomWeakorslowpulseratetachycaridaorbradycardiaurineoutputfallsCough,pinkfoamyph