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SHOCKShenHongZhejiangUniversitySchoolofMedicine.2003.2.17HistoricalAspectsTheconceptofshockhasevolvedoverthecenturiesfromtheearliestdescriptioninantiquityoftraumaticwoundsandhemorrhage.Hippocraticfacies(460~380B.C.):tourniguet.BloodlettingGalen(A.D.130~200):erroneousknowledgeofanatomy.LigationofbleedingvesselsVesalius.WilliamHarvey(16centuries):anatomyandcirculationofthecardiovascularsystemAFrenchmilitarysurgeon:theuseofsimplebandagesThomasLatta:in1831.infusionofintravenousfluidsintohypo-volemicpatientsinflictedwithcholeracausedclinicalimprovent.Pathogenesis:a.vasomotorexhaustion:neurogenictheoryb.traumatictoxemia:cannon.Bay(WorldWarI)c.hypovolemia:Keith,Blalock(experimentsondogs)d.fatembolism;e.acidosisf.adrenaldysfunctionPathogenesis:resuscitation,individualargandysfunction,cellularderangements(Korean,Vietnamconflict).Shocklung.ARDSmolecularbiology,inflammatorymediator,metabolicsupport,oxygendelivery,organischemia,sepsis.II.DefinitionofshockAsyndromeresultsfrominadequateperfusionoftissuesalterationsincellularmetabolism,cellulardysfunctionandcellularinjury,MODSduetotissuehyperfusion,hypoxia.Oxygendelivery;oxygendebt;oxygendemandexceedstheoxygensupply.III.Cause,classificationofshock1.hypovolemicshock1)hemorrhagiclosses:trauma,gastrointestinalbleedingrupturedaneurysm.2)plasmavolumelosses:extravascularfluidsequestration,pancreatitis,burns,bowelobstruction.2.cardiogenicshockdinminishedcardiacoutputintrinsiccauseextrinsiccausemyocardialinfarctioncardiacrhythmdisturbances.Tensionpneumothoraxpericardialtamponade3.neurogenicshockfailureofthesympatheticnervoussystemtomaintainnormalvasculartone.Spinalcordinjury,severeheadinjury.Spinalanesthesia4.vasogenicendogenousorexogenousvaso-activemediatorssystemicinflammatoryresponsesyndrome(SIRS)sepsis(infectious)noninfectiousAnaphylacticHypoadrenaltraumaticIV.PathophysiologyofshockImpairedtissueperfusionTissuehypoxiaAnaerobicmetabolismAcidosisCellulardysfunctionSIRS/SepsisMultipleorgandysfunctionsyndromeInflammatoryMediatorsCirculatoryredistributionIschemia/ReperfusionPathophysiology:RoleofhypoxiaAnaerobicmetabolismandacidosisHyperlactatemiaCirculatoryredistributionImpairmentofgutperfusionAnaerobicmetabolismandacidosisGlucoseGlycogenlactatePyruvateAcetylCoACitricAcidcyclemitochondriacytosolAerobicglycolysisAnaerobicglycolysisCirculatoryredistributionVaso-constrictivefactors:Catechol,angiotensinII,vasopressin,endothelin,thromboxanA2Vaso-dilatory:Nitricoxide,prostaglandinE2,prostacyclin,interleukin-2,bradykinin.Impairmentofgutperfusion:SubsequentbacterialortoxintranslocationSystemicinflammatoryresponse,MODSI.baroreceptorsVasomotorcenter(medulla)SympatheticneuraloutputIncreasedsystemicvascularresistanceIncreasedvenousreturntotheheartArteriolarvasoconstriction(cutaneoustissue.Skeletalmuscle.Renalandsplanchnicvascularbeds)II.adrenalmedullaryoutput↑tachycardia,enhancedcardiaccontractilityIII.Antidiuretichormone(posteriorpituitary)VasoconstrictionWaterreabsorptioninthedistaltubuleofthekidneyIV.rennin(kidney)AngiotensinI(liver)AngiotensinII(lungs)vasoconstrictoraldosterone(adrenalcortex)→reabsorptionofsodiumV.microcirculatoryautoregulationMediatorofshockandsepsisEndotoxinComplementfragmentsEicosanoidsLeukotrienes,Prostaglandins,ThrobomxanesCytokines:Interleukins(IL1,IL2,IL6);TNF-a;CSF,GCSF,GM-CSF;IFN-rNeuroendocrinemediators:catechols,cortisol,glucagonsV.diagosisandmanagementofshock:GeneralapproachKeepSaO290%OptimizecardiacindexOptimizeHbsupplysupplementalO2mechanicalventilation,ifnecessaryMayneedearlyhemodynamicmonitoring11-13g/dlAssessvolumestatus(preload)PCWP15volumeexpansionPCWP15considervolumeifPCWP18diuresesifPCWP18Reassesstokeep:PCWP15-18mmHgMAP60-80mmHgSvO265-70%DeliveryindependentO2consumptionGoalsmetGoalsnotmetTreatincitingcauseofshockcontrolinflammatoryresponsenutritionalsupportInotropicsupport(bagonism)DobutamineDopamineEpinephrine注:此图表太大,一个幻灯页面不能全部显示ConsidervasodilatorsNitroglyceninNitroprussideConsideraagonistNorepinephrineEpinephrineNeosynephrinePlusDopamineGoalsmetGoalsnotmetReassessTreatincitingcauseofshockcontrolinflammatoryresponsenutritionalsupport注:此图表太大,一个幻灯页面不能全部显示SPECIFICSHOCKSYNDROMESClinicalsignsandsymptomsofhemorrhagicshockbasedonseverityofbloodlossPercentlossofcirculatingbloodvolume(volumelossfor70kgmale)PulserateSystolicpressurePulsepressureCapillaryrefillRespirationsCentralnervoussystemUrineoutput15%(750ml)15%-30%(750-1500ml)30%-40%(1500-2000ml)40%(2000ml)normal100120140nonpalpablenormalnormalweakdecreasedmarkeddecreasednormaldecreaseddecreasedmarkeddecreasednormaldelayeddelayedabsentNormalMildtachypneaMarkedtachypneaMarkedtachypneanormalanxiousconfusedlathargicnormal20-30ml/hr20ml/hrnegligible注:此图表太大,一个幻灯页面不能全部显示TraumaticshockHypovolemicshockwith1.largervolumelosses2.greaterfluidsequestrationintheextravascularcompartments3.moreintenseactivationofinflammatorymediatorsdevelopmentofSIRS4.microcirculatoryderangements5.MODSfrequentlyoccurTraumaticshocktreatment1.exces
本文标题:shock
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