17-ARDS-PP-李文雄

首都医科大学北京朝阳医院SICU李文雄LorraineB.NEnglJMed.2000,342:1334-1349.diffusealveolardamagewithneutrophils,macrophages,erythrocytes,hyalinemembranes,andproteinrichedemafluidinthealveolarspaces,capillaryinjury,anddisruptionofthealveolarepitheliumApatchyperipheraldistributionProgresstodiffusebilateralinvolvementwithgroundglasschangesBilateralpatchyopacitiesinmostlymiddleandlowerlungzonesAlveolarfilling,consolidation,andatelectasisoccurpredominantlyindependentlungzones,whereasotherareasmayberelativelyspared.itprogressestofibrosingalveolitiswithpersistenthypoxemia,increasedalveolardeadspace,andafurtherdecreaseinpulmonarycompliance.Pulmonaryhypertension,owingtoobliterationofthepulmonarycapillarybed,maybesevereandmayleadtorightventricularfailureSchemarepresentationofspongemodel.InARDSthe“tissue,”likelyedemaintheearlyphase,isalmostdoubledineachlunglevelcomparedwithnormal,indicatingthenongravitationaldistributionofedema.Theincreasedmass,however,causesanincreasedsuperimposedpressure(SP;cmH2O),whichinturnleadstoa“gassqueezing”fromthemostdependentlungregions.SuperimposedpressureisexpressedascmH2O.PelosiP,D’AndreaL,VitaleGetal(1994)Verticalgradientofregionallunginflationinadultrespiratorydistresssyndrome.AmJRespirCritCareMed149:8–13附加压力与胸膜腔内压PelosiPetal.AmJRespirCritCareMed2001;164(1):122-30.SuperimposedPressureOpeningPressureNormal0AlveolarCollapse(Reabsorption)20-30cmH2OSmallAirwayCollapse10-20cmH2OConsolidationTheARDSLungRoubyIntensiveCareMed2000MV可导致肺的形态学和生理学变化StressandstrainShearforcestress=PLPL=PAW-PplStrain=dV/V0dV：肺容积的变化（Vt）Vo：静息肺容积（FRC）Stress(PL)=K(specificlungeleastance)×strain(dV/Vo)DynamicStrain=Vt/FRCStaticStrain=Vpeep/FRCGlobalstrain=(Vt+Vpeep)/FRCSlutsky,AS.NEnglJMed2013;369:2126-36.大VT的危害肺过度膨胀抑制或使表面活性物质失活牵张肺泡上皮细胞和血管内皮细胞—激活炎症反应诱发MODSVT降低的后果肺泡萎陷膨胀不全的肺泡和末端小气道周期性开放与闭合▪Shearforce：主要发生在充气与非充气肺单位的连接处PhuaJ.AmJRespirCritCareMed2009,179:220–227.OecklerRA.EurRespirJ2007,30:1216–1226.TheAcuteRespiratoryDistressSyndromeNetworkNEnglJMed2000,342(18):1301–1308.PelosiP,etal.AmJRespirCritCareMed2001,164:122–130.30cmH2OALVEOLARAIRWAY140cmH2OMeadJ.JApplPhysiol1970;28:596–608.Theinterstitialpressurewasamplifiedupto140cmH2O(V0/V=1/10)Betweenthehyperinflatedandthenormalalveoliandbetweenthecontinuouslyrecruited-derecruitedalveoliandthenormallyexpandedregionsF=PLx(V0/V)2/3F=PLx(V0/V)2/3Whenventilationoccursatlowlungvolumes,lunginjurycanbecausedbytheopeningandclosingoflungunits(atelectrauma)aswellasbyothermechanisms.Thisinjuryismagnifiedwhenthereisincreasedlunginhomogeneity,asshownoncomputedtomography(PanelA),especiallyinpatientswiththeacuterespiratorydistresssyndrome(ARDS)whohavesurfactantdysfunction,pulmonaryedema,andatelectasis.Inaddition,ventilationmaybeveryinhomogeneous,astatusthatmaybepartiallyorfullyreversedbytheuseofpositiveend-expiratorypressure(PEEP),asshowninaventilatedexvivoratlung.Athighlungvolumes,overdistentioncanleadtogrossbarotrauma(airleaks)(PanelB).Intactratsweremechanicallyventilatedwitheitheranormaltidalvolume(left)orwithahightidalvolumefor5min(middle)or20min(right).After5min,therewereonlyfocalcongestivezones.After20min,lunglesionsaresevereasshownbymarkedenlargementandcongestion.Trachealedemafluidfillsthecannula.IntensiveCareMed(2015)41:2076–2086.UpperPercentageofinspiratorycapacity(blacklines;solidblacklinealsopercentageofrecruitment)andpercentageofderecruitment(dashedgrayline)asfunctionofairwaypressure.LowerFrequencydistributionofopeningpressureasfunctionofairwaypressure(solidline)andofclosingpressure(dashedline).VerticallinesExampleofairwaypressuresusedduringmechanicalventilation,plateaupressure25cmH2O(solidline)andPEEP10cmH2O(dashedline).At25cmH2Oairwaypressurenearly60%inspiratorycapacity,40%oflungunitsarestillclosed.At10cmH2OPEEPnearly35%undergoesopeningandclosing.(DatafromCrottietal.)CrottiS,MascheroniD,CaironiPetal(2001)Recruitmentandderecruitmentduringacuterespiratoryfailure:aclin-icalstudy.AmJRespirCritCareMed164:131–140肺保护性通气策略▪吸氧浓度(FiO2）▪小潮气量▪限制气道平台压▪小VT和限制Pplat预防肺和远隔脏器损伤▪恰当的呼气末正压（PEEP）▪PEEP的设置—适当的PEEP降低shearforce▪高PEEPvs低PEEP的作用不确定▪允许性高碳酸血症▪限制驱动压（＜15cmH2O）？PP改善氧合降低肺内Qs/Qt改善VA/Q过去的想法Qs/Qt下降▪血流转向通气好的区域或通气重新转向灌注好的区域▪仰卧位：由于重力效应，Qs/Qt沿着腹侧→背侧方向梯度增加，在背侧区域最大化▪PP：通过逆转重力效应，降低背侧区域Qs/Qt（目前的非重力依赖区）PP：近期的研究结果背侧区域血流依然丰富均质性更好：肺密度分布均匀Qs/Qt降低不能以如下理由解释▪通气好的区域更多的灌注或通气差的区域低灌注ARDS：仰卧位转为俯卧位▪非重力依赖区胸膜腔内压的负压变小，重力依赖区的胸膜腔正压也变小▪净效应：胸膜腔压力梯度显著降低▪胸膜腔压力均质性更好▪跨肺压朝向腹侧→背侧方向▪背侧VA/Q改善，而腹侧无显著变化▪背侧Qs/Qt显著降低▪通气增加、灌注得以维持TawhaiMH.JApplPhysiol2009(107):912–920.Zone1:PAPaPvZone2:PaPAPvZone3:PaPvPAThezonesofthelungdividethelungintothreeverticalregions,basedupontherelationshipbetweenthepressureinthealveoli(PA),inthearteries(Pa),andtheveins(Pv):肺动脉和静脉压力与肺部区域有关肺尖最低肺底最高直立位肺顶部Pa很可能低于PAWestJ,DolleryC,NaimarkA(1964).Distributionofbloodflowinisolatedlung;relationtovascularandalveolarpressures.JApplPhysiol19:713–24.全肺PA=0±2cmH2O直立位肺尖与肺底动脉压差=20mmHg受重力影响全肺静脉压=5mmHg肺尖部静脉压=-5mmHg肺底部静脉压=+15mmHgPAP=25/10mmHg（Mean=15mmHg）肺尖部mPAP=5mmHg肺底部mPAP=25mmHg正常人群全部肺区PaPAZone1正常情况下不存在正压通气时可以存在PAPa受肺泡压力影响区域血管彻底塌陷▪血