休克病理生理(英文版)課件

休克病理生理ShockPathophysiology休克病理生理1Shockisapathologicalprocessofdecreasedeffectivecirculatingbloodvolume,tissueperfusion,cellmetabolismdisorderandimpairedfunction.Itisasyndromecausedbyavarietyofetiologies.Shockisapathologicalproces2

normalcircumstances

（1）Thearteriovenousanastomosisisclosed.

（2）Only20%ofcapillariesopenalternately,withhemoperfusion.

（3）Capillaryopeningandclosingareregulatedbytherelaxationandcontractionoftheanteriorsphincterofthecapillary.

normalcircumstan3phaseofmicrocirculationischemia：

（1）Sympatheticexcitementandadrenalin,norepinephrinesecretionincreased，

Arterioles,arterioles,posteriorarterioles,anteriorsphincterconstrictionofcapillaries

（2）Arteriovenousanastomosisisopenandbloodflowsdirectlyfromthearterioletothevenules.

（3）Insufficientcapillaryhemoperfusion,hypoxia.phaseofmicrocirculationisch4（1）Arteriolesandarteriolescontract,arteriovenousanastomosesremainopen,andlittlebloodenterscapillaries.（2）Asaresultofhypoxia,histamine,bradykinin,hydrogenionandothervasomotorsubstancesincrease,afterthearterioleandcapillaryanteriorsphincterrelaxation,capillaryopening,vascularvolumeexpansion,bloodflowintothecapillaryisveryslow.Ecchymosisperiodofmicrocirculation：（1）Arteriolesandarterioles5（3）Asaresultofsympatheticexcitement,adrenalineandnorepinephrinesecretionincreased(andperhapshistaminerole),sovenulesandvenulescontraction,capillaryresistanceincreased,resultingintelangiectasiacongestion.Ecchymosisperiodofmicrocirculation：（3）Asaresultofsympathetic6

（1）Duetoseverehypoxiaandacidosisoftissues,capillarywallisdamagedandpermeabilityincreases,bloodconcentrationincapillaries,bloodflowstagnation;Inaddition,bloodcoagulationincreased,resultingindisseminatedintravascularcoagulationinthemicrocirculation.

Microcirculationclottingperiod：（1）Duetoseverehypoxiaan7

（2）Duetotheformationofmicrothrombus,anoxiaandmetabolicdisordersaremoreseriousintissues,intracellularlysosomesrupture,tissuecellnecrosis,resultinginseriousdysfunctionoforgans.

Microcirculationclottingperiod：Microcirculationclottingper8

（3）Asaresultofcoagulation,coagulationfactors(suchasthrombin,fibrinogen,etc.)andplateletsareconsumedinlargequantities,fibrindegradationproductsincrease,andbloodcoagulationisreduced;Thewallsofthebloodvesselsaredamagedandextensivebleedingoccurs.Microcirculationclottingperiod：（3）Asaresultofcoagula9ReleaseofinflammatorymediatorsandgenerationofO2-afterischemiareperfusioninjuryReleaseofinflammatorymediat10

Aftertheruptureoflysosomemembrane,inadditiontoreleasingmanyhydrolasesthatcausecellautolysisandtissuedamage,itcanalsoproducemyocardialinhibitoryfactor(MDF),bradykininandothertoxicfactors.Aftertheinjuryofmitochondrialmembrane,thedegradationofmembranelipidproducestoxicproductssuchasthrombinandleukotriene,presentingmitochondrialswelling,disappearanceofmitochondrialcristae,andimpairedoxidativephosphorylationofcells,whichaffectsenergyproduction.Aftertheruptureoflysosom11Releaseofinflammatorymediatorsandischemia-reperfusioninjury,severetrauma,infectionandshockcanstimulatethebodytoreleaseexcessiveinflammatorymediatorstoforma"waterfall"chainamplificationreaction.Releaseofinflammatorymediat12SecondstrikeofmultipleorgandysfunctionsyndromeSecondstrikeofmultipleorga13休克病理生理(英文版)ppt課件14Hypoxiadamagespulmonarycapillaryendothelialcellsandalveolarepitheliumandreducessurfaceactivesubstances.休克時(shí)內(nèi)臟器官的繼發(fā)性損害(肺)Secondarydamagetointernalorgansduringshock(lungs)Hypoxiadamagespulmonarycapi15Duringresuscitation,ifalargeamountofstoredbloodisused,moremicroaggregatesmaycausepulmonarymicrocirculationembolization,resultinginpartialalveolarcollapse,atelectasisandedema,partialpulmonaryvascularocclusionorhypoperfusion,resultinginincreasedpulmonaryshuntanddeadventilation,andinseverecases,acuterespiratorydistresssyndrome(ARDS).休克時(shí)內(nèi)臟器官的繼發(fā)性損害(肺)Secondarydamagetointernalorgansduringshock(lungs)Duringresuscitation,ifalar16Becausethebloodpressuredrops,catecholaminessecreteincreases,causesthekidneyenterstheballvasospasmandtheeffectivecirculationvolumetoreduce,thekidneyfilterrateobviouslydropsandproducestheoliguria.休克時(shí)內(nèi)臟器官的繼發(fā)性損害(腎)Secondarydamagetointernalorgansduringshock(kidney)Becausethebloodpressuredro17Duringshock,renalbloodflowredistributesandredirectstothemedulla,leadingnotonlytodecreasedurinefiltration,butalsotorenaltubularnecrosisincorticalareasandacuterenalfailure.休克時(shí)內(nèi)臟器官的繼發(fā)性損害(腎)Secondarydamagetointernalorgansduringshock(kidney)Duringshock,renalbloodflow18

Cerebralhypoxiamayresultfromdecreasedcerebralperfusionpressureandbloodflow.Ischemia,CO2retentionandacidosiscancausebraincellswelling,increasedvascularpermeability,resultingincerebraledemaandincreasedintracranialpressure.Thepatientcanappearconsciousnessobstacle,seriouspersoncanproduceencephalopathy,coma.休克時(shí)內(nèi)臟器官的繼發(fā)性損害(腦)Secondarydamagetointernalorgansduringshock(brain)Cerebralhypoxiamayresultf19

Bloodflowinthecoronaryarteriesdecreases,leadingtoischemiaandacidosis,whichcandamagetheheartmuscleandcausefocalnecrosiswhenbloodclotsforminthemicrocirculation.Myocardiumisvulnerabletoischemiaandreperfusioninjury,andelectrolyteabnormalitieswillaffectthesystolicfunctionofmyocardium休克時(shí)內(nèi)臟器官的繼發(fā)性損害(心)Secondarydamagetointernalorg