（优质医学）ARDS肺复张的临床实施.ppt

ARDSRM的临床实施,1,BP70/50，HR170,cvp8.NE5PHE5FiO270%,PEEP12Ph24SaO290%,ARDS常见的临床综合征,2,内容提要,病理生理特点肺泡塌陷的危害如何实施肺复张?肺复张疗效的判断影响肺复张实施的因素,3,30kg猪肺灌洗复制ARDS模型压力控制通气PCVPaw13cmH2OPEEP5cmH2O,ARDS-肺泡塌陷广泛存在,4,肺容积明显降低(a)肺泡水肿(b)肺泡表面活性物质的消耗或不足(c)肺间质水肿压迫远端细支气管肺顺应性明显降低通气/血流比例失调肺内分流和死腔样通气,ARDS的病理生理,5,CTscan70-80%的肺野呈现高密度区分布：下垂部位(dependentfield)提示：1.参与通气的肺泡区域明显减少(20-30%)2.肺损伤具有不均一性,肺容积减少SmalllungBabyLung,6,肺顺应性明显降低,Reducedrangeofvolumeexcursion:LowcomplianceFlatteningatlowandhighvolumes:Lowerandupperinflectionpoints,Volume,Pressure,NORMAL,ARDS,顺应性曲线明显向右下移位,7,肺内分流增加,肺泡塌陷：ARDS重力依赖区炎症或不张区生理性低氧缩血管反应：障碍,8,HEART,SP,ARDS-Gattinoni分区,1.过度通气区或“干区”“babylung2.可复张区或湿区3.实变区,9,内容提要,病理生理特点肺泡塌陷的危害如何实施肺复张?肺复张疗效的判断影响肺复张实施的因素,10,PEEP肺复张与低氧血症改善,GattinoniL,CaironiP,PelosiP,etal.AmJRespirCritCareMed,2001,164:1701-1711,A.低氧血症,11,Pressure,Volume,Pressurewedge,Shearforce,B.剪切力(Shearforce),12,DR-RM,盐水灌肺制造家兔ARDS模型,低流速法测定LIP水平,肺保护通气3h,Vt6ml/kg,PEEP=LIP,DR后予SI的RM,DR后予PCV的RM,每小时的0、10、20、30、40分钟将呼吸机脱开1分钟制造肺泡的重复去复张(DR),动物处死，取肺病理检查、测湿/干重比、测TNF-mRNA表达、转录因子NF-B的活性、MPO及MDA活性,对照组,ARDS组,LP组,DR组,PCV组,SI组,动物准备,13,1,2,3,4,5,6,1、2、3、4、5和6泳道分别为正常、ARDS、DR、LP、SI和PCV组,肺复张手法对重复去复张ARDS家兔肺组织NF-B活性的影响,14,肺复张手法对重复去复张ARDS家兔肺组织TNFmRNA表达的影响,0,1,2,3,4,5,6,1、2、3、4、5和6泳道分别为Normal、ARDS、LP、DR、SI和PCV组0泳道为分子质量标准,15,肺复张手法对重复去复张ARDS家兔PaO2的影响,16,C.感染与肺不张,全麻-肺不张的发生率90%择期腹部手术：肺不张肺部感染9.6%择期心脏手术：肺不张肺部感染5.7%肥胖病人手术：25%-30%发生肺不张肺部感染,CHEST1997;111:564-71,17,QiuHaibo.ChinJEmergMed,2001,10(5):293-294,气压伤生物伤启动炎症反应,炎症介质移位细菌毒素移位,MODS/MOF,D.气压伤、生物伤与MODS,FromSlusky,18,ARDSmotorofMODS,邱海波.中华急诊医学杂志,2001,10(5):293-294,BiotraumaBarotraumainitiateacascadeofproinflamediators,肺是炎症细胞激活和聚积的重要场所肺实质细胞可释放炎症介质,MediatortranslocationBacteriaandLPStranslocation,MODS/MOF,19,腹部手术后肺不张及增加气道内正压的肺复张作用,将大鼠常规镇静肌松,通气参数:Vt8ml/kg;f3840/min;PEEP1cmH2O;FiO20.21,剖腹术(series1),非剖腹术(series2),复张组:复张方法：(PEEP增加到8cmH2O，10个呼吸周期,每30分钟一次).PEEP降至2cmH2O通气,无复张组:0PEEP不采取任何肺复张手法,DugganM.AmJRespirCritCareMed.2003,167:1633-1640.,肺泡塌陷与复张对预后影响的实验研究,20,DugganM.AmJRespirCritCareMed.2003,167:1633-1640.,21,DugganM.AmJRespirCritCareMed.2003,167:1633-1640.,持续肺泡塌陷-预后不良,22,临床研究:塌陷肺泡越多,病死率越高,NEnglJMed2006;354:1775-86,23,VillarandAmatotrial,VillarJ.CritCareMed2006;34:1311,24,内容提要,病理生理特点肺泡塌陷的危害如何实施肺复张?肺复张疗效的判断影响肺复张实施的因素,25,20,40,60,80,100,PressurecmH2O,10,20,30,40,60,50,TotalLungCapacity%,R=22%,R=81%,R=100%,R=93%,肺复张是压力依赖性过程,0,0,R=0%,R=59%,FromPelosietalAJRCCM2001,1/5of“Recruitable”Units,26,肺复张是压力依赖性过程,40SECONDS,27,肺复张的常用方法,控制性肺膨胀(SI)PEEP递增法压力控制法(PCV),45for40s,35Peak,45/16and1:2for120s,PCVAdvantages-SameRecruitingPressure-RepeatedManeuvers-LowerMeanPressure-PreservedVentilation,28,CPAP模式:PS0,PEEP30-40cmH2O,20-50s2.BIPAP:Ph/PL30-40cmH2O,20-50s3.InspHold:将吸气保持键按住，持续20-40s,控制性肺膨胀(SI)法,29,内容提要,病理生理特点肺泡塌陷的危害如何实施肺复张?肺复张疗效的判断影响肺复张实施的因素,30,肺泡完全复张的临床标准,氧合标准CT标准EIT标准,31,肺泡完全复张的临床标准-PaO2/FiO2,PaO2/FiO2400PaO2+PaCO24002.PaO2/FiO2降低5%,32,PaO2+PaCO2400(at100%oxygen):维持肺开放的可靠指标达到PaO2+PaCO2400时：CT显示只有5%的肺泡塌陷PaO2+PaCO2400对塌陷肺泡的预测：ROC曲线下面积0.943,BorgesJB,AmatoMBP.AmJRespirCritCareMedVol174.pp111,2006,肺泡完全复张的临床标准-CT,33,肺泡完全复张的临床标准-CT,BorgesJB,AmatoMBP.AmJRespirCritCareMedVol174.pp111,2006,动脉氧合与塌陷肺组织重量明显呈负相关(R=0.91),34,LowervshigherPercentageofPotentiallyRecruitableLung,ARDS塌陷肺泡都能重新开放吗?,NEnglJMed2006;354:1775-86,35,PEEP5cmH2OPpla20cmH2O,PEEP17cmH2OPpla40cmH2O,PEEP25cmH2OPpla40cmH2O,PEEP25cmH2OPpla60cmH2O,Correspondence:Amato,NEnglJMed2006,355:319,36,内容提要,病理生理特点肺泡塌陷的危害如何实施肺复张?肺复张疗效的判断影响肺复张实施的因素,37,Prespective,randomizedstudy:EffectofRMonARDS,Prespective,randomizedcrossoverstudy34ICUat19hospRM:CPAPover510sto35cmH2OPEEP:FIO2/PEEPsteptomaintainSpO28895%.,CCM,2003,31(11):2592-7,肺泡复张的决定因素(1):肺内vs肺外源性ARDS,38,ARDSTrialNetwork,CritCareMed2003;31(11):2592-2597,StartingConditionsFortheARDSnetRecruitingTrial,Primary,39,为什么RM改善氧合不明显？,病人的特点：入组时Ppla26.4肺内原因ARDS占65%,PawcmH2O,%,0,5,10,15,20,25,30,35,40,45,50,0,10,20,30,40,50,Crottietal.AJRCCM2001.,PPLAT,PRECRUIT,OpeningPressures:PrimaryARDS,40,RM能够实现ARDS肺完全开放,实现openthelungandkeepthelungopeninthe24/26pats,BorgesJB,AmatoMBP.AmJRespirCritCareMedVol174.pp111,2006,41,麻醉导致的非炎症性肺泡塌陷,肺泡复张的决定因素(2):病理特征,RothenHU.Dynamicsofreexpansionofatelectasisduringgeneralanaesthesia.BrJAnaesth1999;82:5516,42,Superimposed,Pressure,(modifiedfromGattinoni),RegionalSpectrumofOpeningPressures,43,肺泡复张的决定因素(3):压力与时间,实现openthelungandkeepthelungopeninthe24/26pats,BorgesJB,AmatoMBP.AmJRespirCritCareMedVol174.pp111,2006,44,Multiplemaneuvers-获得理想的复张效应,Fujinoetal,CritCareMed2001;29(8):1579-1586,45,肺泡复张的决定因素(4):ARDS病程(早期vs后期),N=17ARDSwithalungprotectiveventEarlyARDS(n=9)vsLateARDS(n=8,7d)RM:PCV2minatPIP50cmH2O/PEEPPUIP,AmJRespirCritCareMed,2002,165:165170,46,不同RM方法的肺复张效应不同,PCV,Volumeincrementsat15minPost-RMinVILIModel,47,PawcmH2O,%,OpeningandClosingPressures,0,5,10,15,20,25,30,35,40,45,50,0,10,20,30,40,50,5patients,ALI/ARDS,FromCrottietalAJRCCM2001.,SomeunitscantbekeptopenbyanyreasonablePEEP!,肺泡复张的决定因素(5):循环耐受情况,48,AnRMCanProfoundlyDepressCO,AveragedDatafrom3Models,S-CLim,etal2004,49,RMEffectonCOVariesAmongInjuryModels,Averageddatafor3RMMethods,PNM,VILI,S-CLim,CCM2004,50,EffectofRMMethodonCOinPneumoniaModel,SI,PCV,S-CLim,CCM2004,51,肺泡复张的决定因素(6):肺泡过度膨胀,ClinicalexpofGattinonii,低可复张的ARDS患者HigherPEEP:littlebenefitandmayactuallybeharmful.多数肺泡(60%)处于开放状态高PEEP和肺复张对开放的肺泡可能是有害的高可复张的ARDS患者theuseofhigherPEEPlevelsseemsappropriateInourdailypracticePEEP15cmH2OPEEP150mlNonrecruiters:50%LVend-diastolicarea45%Meanarterialpressuredrop20%Ofcourse,hemodynamicstatusreturnstablewithin3min,IntensiveCareMed(2005)31:11891194,57,AnRMCanProfoundlyDepressCO,AveragedDatafrom3Models,S-CLim,etal2004,CO降低的原因ContractilityAfterloadPreload,58,Prospectiverandomizedcross-overstudyPatswithCABGRM(40cmH2OX10s/20s,RM循环干扰的机制：EffectofRMonLVpreload,IntensiveCareMed(2005)31:11891194,TEE:transgastricEDshortaxisviewoftheLVAbeforea10sLRMBattheendofa10-sLRMCbeforea20sLRMDattheendofa20-sLRM,59,RM循环干扰的机制：EffectofRMonRVafterload,IncreaseinRVafterloadAlveolaroverdistentionofaeratedlungareasHypoxicvasoconstrictioninatelectaticlungareas,Atelectasiscausesvascularleakandlethalrightventricularfailureinuninjuredratlungs.AmJRespirCritCareMed2003,167:1633-1640.Ventilationaboveclosingvolumereducespulmonaryvascularresistancehysteresis.AmJRespirCritCareMed1998,158:1114-1119.,60,Randomized,controlled,cross-overstudyPigARDSmodelbylung-lavageRM:12s-sX40cmH2OOR30-sX40cmH2O,RM循环干扰的机制：EffectofRMonLeftwardseptalshift,Echocardiogram:viatheshortaxisend-diastolicviewoftheRVandLV,BeforeRMandattheendofa30-sRM,IntensiveCareMed(2006)32:585594,61,CriticalCare2006,10:R86,EffectofRMonLV,EffectofRMContractilityandAfterload(SVR):NOTPreload:decrease,PigwithARDSbyrepeatedlunglavageConventionalMV(CMV):PEEP5cmH2O+Vt810ml/kg.NoRMOLCventilation:RMforPaO2/FiO260kPa.Vt68ml/kg,62,RMEffectonCOVariesAmongInjuryModels,Averageddatafor3RMMethods,PNM,VILI,S-CLim,CCM2004,突破循环限制血流动力学干扰vsARDS病因(a),63,PigswithBALvsLPS-inducedALIRMfor1minvitalcapacitymanoeuvres(ViCM)atSI30ORSI40cmH2OPCRMwithpeakairwaypressurePIP/PEEP30/15OR40/20Volumeexpansion:dextran8ml/kg,IntensiveCareMed(2005)31:112120,Aorticbloodflow(ABF)Mesentericbloodflow(QPV),突破循环限制血流动力学干扰vsARDS病因(a),64,1.RM使三种ARDS模型CI均明显下降2.CI盐酸组降低37%油酸组19%生理盐水组23%3盐酸组5min后接近RM前水平,不同病因的ARDSvsRM对CI的影响,65,EffectofRMMethodonCOinPneumoniaModel,SI,PCV,S-CLim,CCM2004,突破循环限制血流动力学干扰vsRM方法(b),66,HCI吸入复制模型CI降低程度不同PCV:降低25%SI:降低46%IP:降低39%,RM方法不同对CI的影响,67,PigswithBALvsLPS-inducedALIRMfor1minvitalcapacitymanoeuvres(ViCM)atSI30ORSI40cmH2OPCRMwithpeakairwaypressurePIP/PEEP30/15OR40/20Volumeexpansion:dextran8ml/kg,IntensiveCareMed(2005)31:112120,Aorticbloodflow(ABF)Mesentericbloodflow(QPV),突破循环限制血流动力学干扰vsRM方法(b),68,突破循环限制血流动力学干扰vsRM方法(b),IntensiveCareMed(2006)32:585594,69,突破循环限制血流动力学干扰vsVolumeexpansion(c),VolumestatusinpatswithARDS,IntensiveCareMed(2006)32:585594,70,PigswithARDS,RMfor1minvitalcapacitymanoeuvres(ViCM)atSI30ORSI40cmH2OPCRMwithpeakairwaypressurePIP/PEEP30/15OR40/20Volumeexpansion:dextran8ml/kg,IntensiveCareMed(2005)31:112120,Aorticbloodflow(ABF)Mesentericbloodflow(QPV),突破循环限制血流动力学干扰vsVolumeexpansion(c),71,Randomized,controlled,cross-overstudyPigARDSmodelbylung-lavageRM:12s-sX40cmH2OOR30-sX40cmH2OVolumestatus:underhypovolemia,normovolemiaandhypervolemia,EffectofvolumestatusonLeftwardseptalshift,EchocardiogramScreen:viatheshortaxisend-diastolicviewoftheleftandrightventriclesBeforeRMandattheendofa30-sRM,IntensiveCareMed(2006)32:585594,突破循环限制血流动力学干扰vsVolume/septalshift(d),72,hypovolemia,normovolemiaandhypervolemia,突破循环限制血流动力学干扰vsVolume/septalshift(d),73,AnesthetizedpigsAbronchialblockerwasinsertedintherightlowerlobe,whichwasselectivelylavagedtocreateadenselobarcollapse.RandomizedintotwogroupsSelectivelungRM(usingtheinnerlumenofthebronchialblocker)GenerallungRMRM40cmH2Ofor30s,突破循环限制血流动力学干扰vsSelectiveRM(e),Before(A)andafter(B)selectivelobarrecruitment,ANESTHANALG2006;102:150410,74,突破循环限制血流动力学干扰vsS