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ARDS肺复张的临床实施课件PPT模板

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ARDS肺复张的临床实施课件PPT模板(Excellenthandouttrainingtemplate)ARDS肺复张的临床实施BP70/50,HR170,cvp8.NE5+PHE5FiO270%,PEEP12Ph24SaO290%ARDS常见的临床综合征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30kg猪肺灌洗复制ARDS模型压力控制通气PCVPaw13cmH2OPEEP5cmH2OARDS--肺泡塌陷广泛存在肺容积明显降低(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...

ARDS肺复张的临床实施课件PPT模板
(Excellenthandouttrainingtemplate)ARDS肺复张的临床实施BP70/50,HR170,cvp8.NE5+PHE5FiO270%,PEEP12Ph24SaO290%ARDS常见的临床综合征 内容 财务内部控制制度的内容财务内部控制制度的内容人员招聘与配置的内容项目成本控制的内容消防安全演练内容 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30kg猪肺灌洗复制ARDS模型压力控制通气PCVPaw13cmH2OPEEP5cmH2OARDS--肺泡塌陷广泛存在肺容积明显降低(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肺顺应性明显降低Reducedrangeofvolumeexcursion:LowcomplianceFlatteningatlowandhighvolumes:LowerandupperinflectionpointsVolumePressureNORMALARDS顺应性曲线明显向右下移位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HEARTSPARDS----Gattinoni分区1.过度通气区或“干区”“babylung"2.可复张区或湿区3.实变区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PEEP—肺复张与低氧血症改善GattinoniL,CaironiP,PelosiP,etal.AmJRespirCritCareMed,2001,164:1701-1711A.低氧血症PressureVolumePressurewedgeShearforceB.剪切力(Shearforce)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=LIPDR后予SI的RMDR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-αmRNA表达、转录因子NF-κB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1234561、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活性的影响肺复张手法对重复去复张ARDS家兔肺组织TNFαmRNA表达的影响01234561、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肺复张手法对重复去复张ARDS家兔PaO2的影响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;111:564-71QiuHaibo.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/MOFD.气压伤、生物伤与MODSFromSluskyARDS-motorofMODS邱海波.中华急诊医学杂志,2001,10(5):293-294Biotrauma—Barotraumainitiateacascadeofproinflamediators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MediatortranslocationBacteriaandLPStranslocationMODS/MOF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;f38~40/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DugganM.AmJRespirCritCareMed.2003,167:1633-1640.DugganM.AmJRespirCritCareMed.2003,167:1633-1640.持续肺泡塌陷-----预后不良临床研究:塌陷肺泡越多,病死率越高NEnglJMed2006;354:1775-86VillarandAmatotrialVillarJ.CritCareMed2006;34:1311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20406080100Pressure[cmH2O]102030406050TotalLungCapacity[%]R=22%R=81%R=100%R=93%肺复张是压力依赖性过程00R=0%R=59%FromPelosietalAJRCCM20011/5of“Recruitable”Units肺复张是压力依赖性过程~40SECONDS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)45for40s35Peak45/16and1:2for120sPCVAdvantages--SameRecruitingPressure--RepeatedManeuvers--LowerMeanPressure--PreservedVentilationCPAP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肺泡完全复张的临床标准氧合标准CT标准EIT标准肺泡完全复张的临床标准----PaO2/FiO2PaO2/FiO2>400PaO2+PaCO2>4002.PaO2/FiO2降低>5%PaO2+PaCO2>400(at100%oxygen):维持肺开放的可靠指标达到PaO2+PaCO2>400时:CT显示只有5%的肺泡塌陷PaO2+PaCO2>400对塌陷肺泡的预测:ROC曲线下面积0.943BorgesJB,…,AmatoMBP.AmJRespirCritCareMedVol174.pp1–11,2006肺泡完全复张的临床标准--CT肺泡完全复张的临床标准---CTBorgesJB,…,AmatoMBP.AmJRespirCritCareMedVol174.pp1–11,2006动脉氧合与塌陷肺组织重量明显呈负相关(R=0.91)LowervshigherPercentageofPotentiallyRecruitableLungARDS塌陷肺泡都能重新开放吗?NEnglJMed2006;354:1775-86PEEP5cmH2OPpla20cmH2OPEEP17cmH2OPpla40cmH2OPEEP25cmH2OPpla40cmH2OPEEP25cmH2OPpla60cmH2OCorrespondence:Amato,NEnglJMed2006,355:319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Prespective,randomizedstudy:EffectofRMonARDSPrespective,randomizedcrossoverstudy34ICUat19hospRM:CPAPover5–10sto35cmH2OPEEP:FIO2/PEEPsteptomaintainSpO288–95%.CCM,2003,31(11):2592-7肺泡复张的决定因素(1):肺内vs肺外源性ARDSARDSTrialNetwork,CritCareMed2003;31(11):2592-2597StartingConditionsFortheARDSnetRecruitingTrialPrimary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%Paw[cmH2O]%0510152025303540455001020304050Crottietal.AJRCCM2001.PPLATPRECRUITOpeningPressures:PrimaryARDSRM能够实现ARDS肺完全开放实现openthelungandkeepthelungopeninthe24/26patsBorgesJB,…,AmatoMBP.AmJRespirCritCareMedVol174.pp1–11,2006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;82:551±6Lim,et,al.Anesthesiology2003;99:71ARDS导致的炎症性肺泡塌陷SuperimposedPressureOpeningPressureInflated0AlveolarCollapse(Reabsorption)20-60cmH2OSmallAirwayCollapse10-20cmH2OConsolidation(modifiedfromGattinoni)RegionalSpectrumofOpeningPressures肺泡复张的决定因素(3):压力与时间实现openthelungandkeepthelungopeninthe24/26patsBorgesJB,…,AmatoMBP.AmJRespirCritCareMedVol174.pp1–11,2006Multiplemaneuvers---获得理想的复张效应Fujinoetal,CritCareMed2001;29(8):1579-1586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/PEEP>PUIPAmJRespirCritCareMed,2002,165:165–170不同RM方法的肺复张效应不同PCVVolumeincrementsat15minPost-RMinVILIModelPaw[cmH2O]%OpeningandClosingPressures0510152025303540455001020304050OpeningpressureClosingpressure5patients,ALI/ARDSFromCrottietalAJRCCM2001.Someunitscan’tbekeptopenbyanyreasonablePEEP!肺泡复张的决定因素(5):循环耐受情况AnRMCanProfoundlyDepressCOAveragedDatafrom3ModelsS-CLim,etal2004RMEffectonCOVariesAmongInjuryModelsAverageddatafor3RMMethodsPNMVILIS-CLim,CCM2004EffectofRMMethodonCOinPneumoniaModelSIPCVS-CLim,CCM2004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theuseofhigherPEEPlevelsseemsappropriateInourdailypracticePEEP>15cmH2OPEEP<10cmH2OGattinoniL.EurRespirJSuppl2003;47:15s-25s.GrassoS.AmJRespirCritCareMed2005;171:1002-8.预测:ARDS肺复张效应N=19ARDSHigherPEEPvslowerPEEPonRVAmJRespirCritCareMedVol171.pp1002–1008,2005HigherPEEPstrategyinducedalvrecruitmentRecruiters:>150mlNonrecruiters:<150ml影响ARDS肺复张效应的因素AmJRespirCritCareMedVol171.pp1002–1008,2005影响复张响应的预测因素(原发病 Noeffect)PEEP-----PaO2/FiO2PEPP-----ComplPEEP-----Stressindex(b)内容提要RM的病理生理基础与实施RM造成的循环问题突破RM的循环限制RM导致的血流动力学改变ARDSpatsn=10SI的实施:30cmH2O,20sSI时PAP、CVP、PAWP、PVRI和RVSWI均显著增加(P<0.05)MAP:4例患者略升高,3例降低,3例不变邱海波,谭焰.江苏医药,2003,29:84-87Prospectiverandomizedcross-overstudyPatswithCABGRM(40cmH2OX10s/20sAdministeredimmediatelyaftersurgeryandSVV>12%RM面临的循环困境LMRs:40cmH2Ofor10sor20sCOreduction>50%LVend-diastolicarea>45%Meanarterialpressuredrop>20%Ofcourse,hemodynamicstatusreturnstablewithin3minIntensiveCareMed(2005)31:1189–1194AnRMCanProfoundlyDepressCOAveragedDatafrom3ModelsS-CLim,etal2004CO降低的原因ContractilityAfterloadPreloadProspectiverandomizedcross-overstudyPatswithCABGRM(40cmH2OX10s/20sRM循环干扰的机制:EffectofRMonLVpreloadIntensiveCareMed(2005)31:1189–1194TEE:transgastricEDshortaxisviewoftheLVAbeforea10sLRMBattheendofa10-sLRMCbeforea20sLRMDattheendofa20-sLRMRM循环干扰的机制:EffectofRMonRVafterloadIncreaseinRVafterloadAlveolaroverdistentionofaeratedlungareasHypoxicvasoconstrictioninatelectaticlungareasAtelectasiscausesvascularleakandlethalrightventricularfailureinuninjuredratlungs.AmJRespirCritCareMed2003,167:1633-1640.Ventilationaboveclosingvolumereducespulmonaryvascularresistancehysteresis.AmJRespirCritCareMed1998,158:1114-1119.RM效应Randomized,controlled,cross-overstudyPigARDSmodelbylung-lavageRM:12s-sX40cmH2OOR30-sX40cmH2ORM循环干扰的机制:EffectofRMonLeftwardseptalshiftEchocardiogram:viatheshortaxisend-diastolicviewoftheRVandLVBeforeRMandattheendofa30-sRMIntensiveCareMed(2006)32:585–594CriticalCare2006,10:R86EffectofRMonLVEffectofRMContractilityandAfterload(SVR):NOTPreload:decreasePigwithARDSbyrepeatedlunglavageConventionalMV(CMV):PEEP5cmH2O+Vt8–10ml/kg.NoRMOLCventilation:RMforPaO2/FiO2>60kPa.Vt6–8ml/kgRMEffectonCOVariesAmongInjuryModelsAverageddatafor3RMMethodsPNMVILIS-CLim,CCM2004突破循环限制血流动力学干扰vsARDS病因(a)PigswithBALvsLPS-inducedALIRMfor1minvitalcapacitymanoeuvres(ViCM)atSI30ORSI40cmH2OPCRMwithpeakairwaypressurePIP/PEEP30/15OR40/20Volumeexpansion:dextran8ml/kgIntensiveCareMed(2005)31:112–120Aorticbloodflow(ABF)Mesentericbloodflow(QPV)BAL-ARDSLPS-ARDS突破循环限制血流动力学干扰vsARDS病因(a)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△△▲△▲▲▲△EffectofRMMethodonCOinPneumoniaModelSIPCVS-CLim,CCM2004突破循环限制血流动力学干扰vsRM方法(b)△*△*#△*#△*#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PigswithBALvsLPS-inducedALIRMfor1minvitalcapacitymanoeuvres(ViCM)atSI30ORSI40cmH2OPCRMwithpeakairwaypressurePIP/PEEP30/15OR40/20Volumeexpansion:dextran8ml/kgIntensiveCareMed(2005)31:112–120Aorticbloodflow(ABF)Mesentericbloodflow(QPV)BAL-ARDSLPS-ARDS突破循环限制血流动力学干扰vsRM方法(b)突破循环限制血流动力学干扰vsRM方法(b)IntensiveCareMed(2006)32:585–594突破循环限制血流动力学干扰vsVolumeexpansion(c)VolumestatusinpatswithARDSIntensiveCareMed(2006)32:585–594PigswithARDS,RMfor1minvitalcapacitymanoeuvres(ViCM)atSI30ORSI40cmH2OPCRMwithpeakairwaypressurePIP/PEEP30/15OR40/20Volumeexpansion:dextran8ml/kgIntensiveCareMed(2005)31:112–120Aorticbloodflow(ABF)Mesentericbloodflow(QPV)BAL-ARDSLPS-ARDS突破循环限制血流动力学干扰vsVolumeexpansion(c)Randomized,controlled,cross-overstudyPigARDSmodelbylung-lavageRM:12s-sX40cmH2OOR30-sX40cmH2OVolumestatus:underhypovolemia,normovolemiaandhypervolemiaEffectofvolumestatusonLeftwardseptalshiftEchocardiogramScreen:viatheshortaxisend-diastolicviewoftheleftandrightventriclesBeforeRMandattheendofa30-sRMIntensiveCareMed(2006)32:585–594突破循环限制血流动力学干扰vsVolume/septalshift(d)hypovolemia,normovolemiaandhypervolemia突破循环限制血流动力学干扰vsVolume/septalshift(d)AnesthetizedpigsAbronchialblockerwasinsertedintherightlowerlobe,whichwasselectivelylavagedtocreateadenselobarcollapse.RandomizedintotwogroupsSelectivelungRM(usingtheinnerlumenofthebronchialblocker)GenerallungRMRM40cmH2Ofor30s突破循环限制血流动力学干扰vsSelectiveRM(e)Before(A)andafter(B)selectivelobarrecruitmentANESTHANALG2006;102:1504–10突破循环限制血流动力学干扰vsSelectiveRM(e)ANESTHANALG2006;102:1504–10HemodynamiceffectSelectiveRM:nocirculatorychangesGenerallungRM:mABPdecreasedsignificantlyby36(21,41)mmHgCOdecreasedby2.1(1.6,2.5)L/minLVEDareadecreasedby4.4(3.5,4.5)cm2.Transthoracicend-diastolicshortaxisviewoftheLVatbaseline(A),afterrecovery(B),attheendofaselectiveLRM(C),andattheendofageneralLRM(D)突破循环限制血流动力学干扰vsSelectiveRM/Lowvolume(e)AnesthAnalg2007;105:729–34HemodynamiceffectNormovolemiaand20%hypovolemia:nocircchanges40%hypovolemia:CO:unchangedmABP(mmHg)BeforeRM:48EndofRM:40(P<0.05)3minafterRM:47AnesthetizedpigsAbronchialblockerwasinsertedintherightlowerlobeS-LRM40cmH2Ofor30satnormovolemia,aftervenesectionof20%ofthebloodvolume,aftervenesectionof40%ofthebloodvolume,塌陷肺泡一定要用肺复张打开吗?全身麻醉可导致肺泡塌陷MorbidlyobeseNon-obese肺泡塌陷24h后明显改善AnesthAnalg2002;95:1788–92演讲结速,谢谢观赏!Thankyou. 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