医学shock休克英文专题课件

shock休克英文What’sshock？sickorunconsciousness？Introductionhypotension？Introductionvasoconstrictivetreatment→vasodilativetreatmentIntroduction

Lartin

GeneralCriticalReaction:strikeandvibration1731,HenriFrancoisLeDranapplytomedicineforthefirsttimeI.ConceptofShockpalefacecyanosiscoldandclammylimbsoliguriafaintconsciousnesshypotension1.Descriptionofsymptoms&signs“shocksyndrome”I.ConceptofShock“sympatheticfailuretheory”sympatheticfailure

→Bp↓→shock2.AcutecirculatorydisorderI.ConceptofShockbloodvolume↓

ECBV（effectivecirculatingbloodvolume）↓

→microcirculationdisturbancessympatheticactivation3.Microcirculation

theoryI.ConceptofShocksystemicinflammatoryresponsesyndrome,SIRS全身炎症反应综合征pro-inflammatory&anti-inflammatoryfactors4.CellularandmolecularlevelI.ConceptofShockRegardlessofcauses,shockisdefinedasaclinicalconditionandpathophysiologicprocesscharacterizedbymicrocirculationdysfunction(inadequatebloodflowvitalorgans,andinabilityofcelltometabolizenormally).

causes→acutecirculatoryfailure→microcirculationdisturbance→ECBV(effectivecirculatorybloodvolume)↓→“lowflowstate”invitalorgans→abnormalcellularmetabolismandfunction,tissueinjury,dysfunctionofvitalorgans→shockI.ConceptofShockII.EtiologyofShock5.Anaphylaxis:allergen→combinationofIgEandmastcells→releaseofhistamineandbradykinin→vasodilationandcapillarypermeability↑→peripheralresistance↓→bloodflowbacktotheheart↓→cardiacoutput↓→Bp↓,plasmaexosmosisallergenII.EtiologyofShock

6.Strongstimulationonnervesystem:

braininjury,thedepressantactionofdrugs,generalanesthesia,hypoxia,orlackofglucose,spinalanesthesiaorspinalcordinjury→

decreasedsympatheticcontrol

7.Heart&largebloodvesselsdiseases:

acutemassivemyocardialinfarction,acutemyocarditis,perimyocarditis,cardiactamponade,seriousarrhythmias,myocardialdiseases,

cardiovalvularproblems,etc.→pumpingfunctionoftheheartisimpaired→

“cardiogenic

shock”coronaryarterydisease,pulmonaryembolism,etc.→

“extracardiacobstructiveshock”

II.EtiologyofShockAccordingtoEtiology:

1、HemorrhagicShock2、DehydrationShock3、TraumaticShock4、BurnShock5、InfectiousShock:endotoxic,septic6、CardiogenicShock7、ExtracardiacObstructiveShock8、AnaphylacticShock9、NeurogenicShockIII.ClassificationofShockAccordingtothepathogenesisofshock:III.ClassificationofShock↓↓↑markedvasodilation

“HypovolemicShock”

“CardiogenicShock”“VasogenicShock”AccordingtotheHemodynamicshyperdynamicshock(高排低阻型休克)cardiacoutput↑peripheralresistance

↓“warmshock”hypodynamicshock(低排高阻型休克)cardiacoutput↓peripheralresistance↑“coldshock”低排低阻型休克cardiacoutput↓peripheralresistance

↓“decompensatory”III.ClassificationofShockMicrocirculation(MC):

Thecapillaries,venules,andmetarteriolesofthecirculatorysystemarecollectivelyreferredtoasthemicrocirculation.

1.Functionofmicrocirculation:

Itisherethatexchangeofgases,nutrients,andmetabolitesmovebetweenthetissuesandthecirculatingblood.

transportofnutrientstothetissuesandremovalofcellularexcretaIV.PathogenesisandMechanismsofShock微动脉Arteriole

后微动脉Metarteriole

毛细血管前括约肌PrecapillarySphincters

真毛细血管Truecapillary

通血毛细血管（直捷通路）Preferentialchannels

微静脉Venule

动静脉短路Arteriovenousanastomosis后微动脉2.Structureofmicrocirculation:IV.PathogenesisandMechanismsofShockIV.PathogenesisandMechanismsofShock(1)precapillary&postcapillaryvessels(resistance)(2)truecapillary:extremelythinstructureswithtubularwallsofsingle-layer,highlypermeableendothelialcells(3)threechannelsforbloodflow

直捷通路（Ａ）thoroughfarechannel

动静脉短路（Ｂ）arteriovenousshunt

迂回通路(营养通路Ｃ)nutrientflow后微动脉ＡＡＡＡＡＡＢＣＣＣＣ“microcirculationdisturbance”

IV.PathogenesisandMechanismsofShockcompensatorystageprogressivestagerefractorystageStageI:compensatorystageMicrocirculationchanges2.Mechanism3.Effectsonbody4.Mainclinicalmanifestations５.TreatmentprincipleIV.PathogenesisandMechanismsofShockAlterationsofMicrocirculationandTissuePerfusion:StageI:compensatorystageStageI:compensatorystage:“ischemichypoxiastage”MechanismsofMicrocirculationDisturbance:vasoconstrictionarteriovenousshuntopeningcauses(hemorrhage,etc)α-receptor:skin,skeletalm.,kidneys,abdominalorgansreleaseofcatecholamineβ-receptor:

arteriovenousshuntSAMS(+)(sympathetic-adrenal-medullasystem)“initiallink”“result”StageI:compensatorystageStageI:compensatorystageMechanismsofMicrocirculationDisturbance:ischemia&hypoxiainpancreas→MDF↑

(myocardialdepressantfactor,心肌抑制因子)vasoconstrictionPGI2

ischemia&hypoxiaendothelialcellsinjuryRAAS(+)AngIIrenalbloodvolume

catecholamineTXA2

plateletET

endothelialcellsvaso-pressin(2)severalhumoralfactors:catecholamine,AngII(angiotensinII),vasopressin,TXA2,ET(endothelin),etc.StageI:compensatorystageMechanismsofMicrocirculationDisturbance:(3)productionofPGI2↓(1)activationofSAMS:vasoconstriction

(4)productionofMDF

AsummaryformechanismofstageIofshock:(1)self-bloodtransfusion:肝脾储血库、静脉收缩、动静脉短路开放

“firstdefenseline”venousconstriction→bloodreturntotheheart↑→cardiacoutput↑aldosterone(ADS)↑&vasopressin(ADH)↑(2)self-fluidinfusion:

“seconddefenseline”precapillaryresistance↑

>postcapillaryresistance↑

→capillarypressure↓→fluidtransferfrominterstitialfluidtocirculation(3)bloodredistribution:

β-adrenoceptor:brain,coronaryA.α-adrenoceptor:skin,skeletalm.,kidneys,abdominalorgans(4)activationofSAMS:

catecholamine↑→myocardialcontractility↑StageI:compensatorystageEffectsonBody:StageI:compensatorystageMainClinicalManifestations:palefacecoolandclammylimbs96/minoliguriaconsciousnessbutrestless105/85mmHgBp?“reversiblecompensatorystage”

eliminatingpathogenicfactors&restoringbloodvolumeandtissueperfusion

尽早消除休克的动因，补充血容量，防止向休克期发展。StageI:compensatorystageTreatmentPrinciple:StageII:progressivestageMicrocirculationchanges2.Mechanism3.Effectsonbody4.Mainclinicalmanifestations５.TreatmentprincipleIV.PathogenesisandMechanismsofShockAlterationsofMicrocirculationandTissuePerfusion:StageII:progressivestageStageII:progressivestage:“stagnanthypoxiastage”precapillaryresistance↓→highperfusionpostcapillaryresistance↑→lowflow→tissuecongestionandhypoxia1.Acidosis:anaerobicglycolysis↑→productionoflacticacid↑→metabolicacidosis→responseofarterioleandmetarterioletocatecholamine↓→vasodilationStageII:progressivestageMechanismsofMicrocirculationDisturbance:2.Localaccumulationofmetabolicproducts:

histamine,adenosine,Kinin3.Endotoxin:→myocardialcontractility↓activatemononuclearcells→productionofIL-1,TNF,andNO→vasodilation,Bp↓5.Alterationofhemorheology:

RBCaggregationandadhesion,WBCrollingandblock,plateletaggregationandadhesion

bloodconcentration&increasedbloodviscosity4.Effectsofhumoralfactors:

endorphin(内啡肽)→vasomotorcenter(-)→vasodilationWBCpenetratecapillary

BlockageofWBC白细胞附壁、滚动、嵌塞组织间胶体venousstasisvasodilationcappermeability↑“self-bloodtransfusion”stopbloodvesselscapacity↑bloodreturn↓StageII:progressivestage(decompensatedstage)Decompensatedchanges:self-bloodtransfusionandself-fluidinfusionstopcapstaticpressure↓plasmaexudation“self-fluidtransfusion”stop

formationofviciouscyclecapstaticpressure↑cappermeability↑plasmaexudationbloodconcentrationRBCaggregationmicrocirculationstasisvasodilationbloodstasis,bloodreturn↓C.O.,Bp↓,sympatheticN.(+)tissueperfusion↓↓ischemia,hypoxia,acidosisStageII:progressivestage(decompensatedstage)Decompensatedchanges:Heart——

heartfailureKidneys——oliguraoranuriaSkin——cyanosisBp↓↓Brain——

dullorcoma80/50mmHgStageII:progressivestageMainClinicalManifestations:StageIII:refractorystageMicrocirculationchangesandmechanism2.Effectsonbody3.MechanismofrefractoryshockIV.PathogenesisandMechanismsofShockAlterationsofMicrocirculationandTissuePerfusionanditsMechanism:StageIII:refractorystageStageIII:refractorystage:“microcirculationfailurestage”后微动脉noanyresponsetovasoactivedrugs:bloodflowstop→noperfusionandnoflow血细胞聚集成团块，似淤泥状，在血管内摆动StageIII:refractorystageDIC(disseminatedintravascularcoagulation)（1）alterationofhemorheology:bloodstasis,concentration,viscosity,bloodcellsaggregation“hypercoagulablestate”（2）acidosis（3）impairmentofmono-macrophagessystem（4）imbalanceofTXA2andPGI2(3)MODS

(multipleorgansdysfunctionsyndrome,

多器官功能障碍)

“circulatoryfailure”

(1)DIC

shock(2)capillaryno-reflowphenomenon(无复流现象)(4)SIRS（systemicinflammatoryresponsesyndrome,全身炎症反应综合征）EffectsonBody:StageIII:refractorystage毛细血管无复流现象(capillaryno-reflowphenomenon)Concept:

largeamountofbloodtransfusionandfluidinfusion→Bp↑butcapillarybloodflowhasnorecovery

休克晚期即使大量输血补液，血压回升，有时仍不能恢复毛细血管血流，称为无复流现象。Mechanism：（1）WBCadhesionandaggregation

（2）capillaryendothelialcellsswelling

（3）formationofextensivemicrothrombi→blockageofcapillariesStageIII:refractorystageMechanismofrefractoryshock:DIC,SIRS后微动脉后微动脉后微动脉后微动脉ABCDSummaryfortheMechanismofShockneural-humeralcellularmicrocirculationtheorySAMS(+)→microcirculationdisturbances→cellinjuries,organdysfunction

“concept”Pro-inflammatory&anti-inflammatoryfactorsimbalance

“SIRS”causes→cellinjuries(structure,metabolism&functionchanges)

“cellularlevel”

Neural-humeralmechanism:SAMSHypothalamus-pituitary-adrenocorticalsystem(下丘脑-垂体-肾上腺皮质系统)RAASendothelin（ET，内皮素）

vasoconstrictorscatecholamine(CA)include：epinephrine(EP)andnorepinephrine(NE)

angiotensinⅡ（AngⅡ，血管紧张素）

vasopressin（ADH，血管升压素）

TXA2（thromboxane,血栓素A2）

Neural-humeralmechanism:CGRP（calcitoningene-relatedpeptide,降钙素基因相关肽）atrialnatriureticpeptide（ANP,心房钠尿肽）endogenousopioidpeptide（内源性阿片肽）kinin

NO

vasodilatorshistamineβ-endorphinearly:improveischemia；↑myocardialcontractility;↑C.O.later:hypotension;I-RI.7

Neural-humeralmechanism:Cellinjury:

Cellularandmolecularmechanism:glycolysisATPlacticacidimpairedNa+-K+pump

celledemahyperkalemiametabolicacidosishypoxiaMitinjuryATPlysosomeinjuryproteasereleaseCellinjury:

Cellularandmolecularmechanism:Metabolismdisturbances:

Cellularandmolecularmechanism:causeschangesresultATP↓，NapumpimpairedNaandwaterinflowcelledemaATP↓，NapumpimpairedextracellularK+↑hyperkalemiaanaerobicglycolysislacticacidmetabolicacidosisearly:ventilation

PaCO2↓respiratoryalkalosislater:shocklungventilation↓respiratoryacidosisV.OrganDysfunction1.Causes:

renalperfusion↓endoxins→renaldamage2.Mainclinicalmanifestations:

oliguria,metabolicacidosis,hyperkalemia,azotemia(I)EffectsonKidneys:“shockkidney”休克时最易损害的脏器之一renalperfusion↓GFR↓oliguriaAcutefunctionalrenalfailure

earlystage:

laterstage:Acuteparenchymalrenalfailurepersistentrenalischemiaandthrombosisoliguriaanuriaacuterenaltubularnecrosisrenaltubulardilationupper:microthrombilower:macrophages(II)EffectsonLungs:“shocklung”1.pulmonaryedema:histamine,kinin,adenosine,etc→capillarypermeability↑vasodilation→fluidtransudefromcapillariestotissue2.pulmonaryatelectasis:pulmonaryperfusion↓→productionofsurfactant(DPL)bytypeIIalveolarcell↓→alveolarcollapse3.pulmonaryhemorrhage:DIC→continuousbleeding4.alveolarhyalinemembraneformation:capillarypermeability↑→plasmaproteinsdepositinalveolarcavityALI

（acutelunginjury）ARDS（acuterespiratorydistresssyndrome）lungedemavasodilationupper:normallungtissuelower:lungedemadiffusedlungedemaalveolarhyalinemembrane1.coronarybloodvolume↓:SAMS(+)→HR↑,myocardialcontractility↑→oxygenconsumption↑→deteriorationofmyocardialhypoxia2.water,electrolytesandacid-basedisturbance:hyperkalemia,acidosis→HR↓,myocardialcontractility↓3.productionofMDF:ischemicpancreas→productionofMDF→myocardialcontractility↓4.myocardialDIC→myocardialcontractility↓5.endotoxins→damagemyocardium6.ATP↓→myocardialcontractility↓(III)EffectsonHeart:hypoxia,acidosis→ATP↓→impairedNa+-K+pump→cytotoxicbrainedemalysosomeinjury→braincellinjuryactivationofcomplement(C3a,C5a)→histamine,bradykinin↑→capillarypermeability↑→vasogenicbrainedema(IV)EffectsonBrain:(V)EffectsonDigestiveSystem:enterogenousendotoxemia（肠源性内毒素血症)ischemiastasisbarrierfunction

endotoxinenterbloodstressulcerjaundice&hepaticencephalopathy

Definition:Dysfunctionsofmorethantwoorgansoccursuccessivelyinpatientswithoutpre-existorgandysfunctiondefinedasMODS.(VI)MODS(multipleorgandysfunctionsyndrome,多器官功能障碍综合征):MSOF

(MultipleSystemOrganFailure,多系统器官衰竭)highincidence；greatexpense；highmortality

Causes:1.infectiouscauses:70％septicemia2.non-infectiouscauses:

bigoperationseveretraumacausesincidenceseveretraumaabout10%afterbigoperation8%～22%massiveburnabout30%septicemia30%～50%organsfailuremortality115%~30%245%~55%3>80%4100%

Clinicalclassification:1.速发单相型

(immediate

monophaseMODS,rapidsingle-phasetype)2.迟发双相型

(delayed

dualphaseMODS,

delayedtwo-phasestype)

速发单相型(rapidsingle-phase)“原发型（primarytype）”“一次打击型（onehittype）”

▲causedbyshock,trauma,etcdirectly由损伤因子直接引起▲organsinjuryoccuratthesametimeorsimultaneously

器官损害同时或者相继▲developrapidly,onlyonephase,onlyonepeak病情发展快，只有一个时相，损伤只有一个高峰ThiskindofMODSoftentakesplacerapidlyaftertheoccurrenceofshockandtrauma.ThiskindofMODSisonlyonephase,i.e.,thereisonlyonepeakoforganfailureduringthepathologicalprocesses.

迟发双相型(delayedtwo-phase)“继发型（secondarytype）”“二次打击型（doublehittype）”

▲remssionafterthefirsthit第一次打击后出现一个缓解期▲secondhit其后1～3周又受到第二次打击发生MODS▲dual-phase,twopeaks病情发展呈双相，出现两个损伤高峰Thefirstpeakoforganfailureofpatientswithtrauma,shockorhemorrhageusuallyappearsinashorttime.Iftheconditionofthosepatientscouldnotbeeffectivelycontrolled,asecondorganfailurepeakwillappearin3to5daysduetoarapidlyhappenedsepticemia.ThecourseoftheMODSdescribedaboveshowsadual-phaseprogressionwithtwopeaksoforganfailures.(I)Treatmentofprimarydiseases

(II)Symptomatictreatment:“improvemicrocirculation”

1.Acidosiscorrection:alkalinesolution(NaHCO3)

2.Volumereplacement:transfusionofwholebloodorplasmaadministrationoftheappropriateelectrolytesolutionVI.PathophysiologicBasisofPreventiona