呼吸治疗肺保护.ppt

呼吸机治疗的肺保护策略呼吸机治疗的肺保护策略呼吸机相关性肺损伤呼吸机相关性肺损伤acuteparenchymallunginjuryandanacuteinflammatoryresponseinthelung.cytokinesalveoliandthesystemiccirculationmultipleorgandysfunctionmortality呼吸机相关性肺损伤呼吸机相关性肺损伤ventilator-inducedlunginjury容量性损伤容量性损伤Volutrauma（largegasvolumes）压力性损伤压力性损伤Barotrauma（highairwaypressure）不张性损伤不张性损伤Atelectotrauma（alveolarcollapseandre-expansion）生物性损伤生物性损伤Biotrauma（increasedinflammation）肺肺损损伤伤病病理理alveolarstructuraldamagepulmonaryedema、inflammation、fibrosissurfactantdysfunctionotherorgandysfunctionexacerbatethedisturbanceoflungdevelopmentSeminNeonatol.2002Oct;7(5):353-60.ApproachesinthemanagementofacuterespiratoryfailureinchildrenprotectiveventilatoryandpotentialprotectiveventilatorymodeslowertidalvolumeandPEEPpermissivehypercapniahigh-frequencyoscillatoryventilationairwaypressurereleaseventilationpartialliquidventilationimproveoxygenationrecruitmentmaneuverspronepositioningkinetictherapyreduceFiO2andfacilitategasexchangeinhalednitricoxideandsurfactantCurrOpinPediatr.2004Jun;16(3):293-8.Canmechanicalventilationstrategiesreducechroniclungdisease?continuouspositiveairwaypressurepermissivehypercapniapatient-triggeredventilationvolume-targetedventilationproportionalassistventilationhigh-frequencyventilationSeminNeonatol.2003Dec;8(6):441-8小潮气量和呼气末正压小潮气量和呼气末正压lowertidalvolumeandPEEPVentilationwithlowertidalvolumesversustraditionaltidalvolumesinadultsforALIandARDS1202patientslowertidalvolume(7ml/kg)lowplateaupressure30cmH2Oversustidalvolume10to15ml/kgMortalityatday28 long-termmortalitywasuncertainlowandconventionaltidalvolumewithplateaupressure31cmH2OwasnotsignificantlydifferentCochraneDatabaseSystRev.2004;(2):CD003844Higherversuslowerpositiveend-expiratorypressuresinpatientswiththeacuterespiratorydistresssyndrome549patientsacutelunginjuryandARDSlower-PEEPgroup8.33.2cmH2Ohigher-PEEPgroup13.23.5cmH2O(P0.001).tidal-volume6ml/kgend-inspiratoryplateau-pressure30cmH2OTheratesofdeath24.9%27.5%(p=0.48)Fromday1today28,breathingwasunassisted14.510.4days13.810.6days(p=0.5)clinicaloutcomesaresimilarwhetherlowerorhigherPEEPlevelsareused.NEnglJMed.2004Jul22;351(4):327-36.Increasinginspiratorytimeexacerbatesventilator-inducedlunginjuryduringhigh-pressure/high-volumemechanicalventilationSprague-Dawleyratsnegativecontrolgrouplowpressures(PIP=12cmH2O),rate=30,iT=0.5,1.0,1.5secsexperimentalgroupshighpressures(PIP=45cmH2O),rate=10,iT=0.5,1.0,1.5secslungcompliance,PaO2/FiO2ratio,wet/drylungweight,anddrylung/bodyweightasinspiratorytimeincreased,staticlungcompliance(p=.0002)andPao2/Fio2(p=.001)decreased.Wet/drylungweights(p.0001)anddrylung/bodyweights(p0.050.050.050.050.05对照组（对照组（NPM)：应用人工呼吸机限压定时持续气流型，通气模应用人工呼吸机限压定时持续气流型，通气模式为式为IMV，持续脉搏血氧饱和度监测使其维持，持续脉搏血氧饱和度监测使其维持在在8595%，每，每8h监测动脉血气一次，要求血监测动脉血气一次，要求血气维持在正常范围内，气维持在正常范围内，PaO240-70mmHg,PaCO235-45mmHg观察组（观察组（PM组）组）：1、肺肺力力学学监监测测仪仪(BicoreCP100)每每812h监监测测一次机械通气时肺力学参数一次机械通气时肺力学参数2、监监测测时时要要求求患患儿儿与与呼呼吸吸机机完完全全同同步步或或无无自自主呼吸状态（必要时通过药物抑制呼吸）主呼吸状态（必要时通过药物抑制呼吸）3、肺力学监测仪的传感器置于近端接口、肺力学监测仪的传感器置于近端接口4、气管插管气漏率小于、气管插管气漏率小于20%5、每每监监测测一一次次持持续续0.51h至至数数据据稳稳定定后后记记录录监监测的数据测的数据NPM组和组和PM组的评估指标组的评估指标1.疾疾病病极极期期，即即生生后后2448h时时呼呼吸吸机机要要求求最最高高值值，包括包括FiO2、PIP、PEEP、Ti、MAP、VR2.VE、C20/C、TC（限于（限于PM组），组），3.记录血记录血pH、PaO2、PaCO2、氧合指数（、氧合指数（OI）（OI=FiO2MAP/PaO2）和心率、血压和心率、血压4.呼呼吸吸机机应应用用时时间间，用用氧氧时时间间，住住院院天天数数，病病死死率率，PDA，IVH和和呼呼吸吸机机相相关关性性肺肺损损伤伤的的发发生生率。率。两组呼吸机参数比较两组呼吸机参数比较FiO2（%）PIP（cmH2O)PEEP（cmH2O)MAP（cmH2O)Ti(sec)VR（次（次/分）分）NPM601930.53.45.60.814.93.40.750.1399PM621826.71.75.40.611.92.00.450.14210t0.1847.5271.3395.81818.101.81p0.050.050.0010.05两组血气监测结果比较两组血气监测结果比较PHPaO2(mmHg)PaCO2(mmHg)HR(次次/分）分）BP(mmHg)OINPM7.310.1571740101448404.61913PM7.30.045916486.31456393.6147.7t0.2890.5164.6630.7980.9422.011p0.050.050.050.050.05两组呼吸机相关性肺损伤、两组呼吸机相关性肺损伤、PDA、IVH、呼吸机应用时间、用氧时间、住院天数、病死率比较呼吸机应用时间、用氧时间、住院天数、病死率比较VALI%PDA%IVH%IMV(d)用氧时用氧时间间(d)住院天住院天数数(d)病死率病死率%NPM3236423.91.8117191414PM13.333.3404.21.713722118.3t0.8671.4741.225.570.090.050.9p0.050.050.050.050.050.05结论结论肺肺力力学学监监测测能能指指导导正正确确应应用用呼呼吸吸机机，降降低低呼呼吸吸机相关性肺损伤机相关性肺损伤从从本本研研究究结结果果推推荐荐RDS呼呼吸吸机机应应用用的的参参数数为为：PIP25cmH2O左左右右，短短Ti0.30.5秒秒，应应用用适适当当的的PEEP5-7cmH2O治疗治疗RDS，不影响氧合。，不影响氧合。PaCO2的的轻轻度度增增高高（PaCO245-60），IVH的的发生未见增加。发生未见增加。允许性高碳酸血症允许性高碳酸血症PermissivehypercapniaPermissivehypercapnia-roleinprotectivelungventilatorystrategiesFirst,weconsidertheevidencethatprotectivelungventilatorystrategiesimprovesurvivalandweexplorecurrentparadigmsregardingthemechanismsunderlyingtheseeffectsSecond,weexaminewhetherhypercapnicacidosismayhaveeffectsthatareadditivetotheeffectsofprotectiveventilationThird,weconsiderwhetherdirectelevationofCO2,intheabsenceofprotectiveventilation,isbeneficialordeleteriousFourth,weaddressthecurrentevidenceregardingthebufferingofhypercapnicacidosisLung-protectiveventilationinacuterespiratorydistresssyndrome:protectionbyreducedlungstressorbytherapeutichypercapnia?hypercapnicacidosislung-protectiveventilationrespiratoryacidosisprotectedthelungTheprotectiveeffectofrespiratoryacidosisinhibitionofxanthineoxidasepreventedbybufferingtheacidosis.theprotectionresultedfromtheacidosisratherthanhypercapniaAmJRespirCritCareMed.2000Dec;162(6):2021-2.PermissivehypercapniainARDSanditseffectontissueoxygenationTheright-shiftofthehaemoglobin-oxygendissociationcurvereduceintrapulmonaryshunt(Qs/Qt)bypotentiatinghypoxicpulmonaryvasoconstrictionaffectthedistributionofsystemicbloodflowbothwithinorgansandbetweenorgansActaAnaesthesiolScandSuppl.1995;107:201-8HypercapnicacidosisattenuatesendotoxininducedacutelunginjuryattenuatedthedecrementinoxygenationimprovedlungcompliancereducedalveolarneutrophilinfiltrationandhistologicindicesoflunginjuryAmJRespirCritCareMed.2004Jan1;169(1):46-56Hypercapnicacidosisisprotectiveinaninvivomodelofventilator-inducedlunginjury12rabbitsventilator-inducedlunginjury(VILI)PaCO240mmHgn=6PaCO280-100mmHgn=6respiratorymechanics(plateaupressures)27.02.520.93.0p=0.016gasexchange(PaO2)165.219.477.387.9p=0.02wet:dryweight9.72.36.61.8p=0.04bronchoalveolarlavagefluidproteinconcentration1350228656511p=0.03cellcount6.86x1052.84x105p=0.021injuryscore7.03.30.70.9p0.0001AmJRespirCritCareMed.2002Aug1;166(3):403-8EffectsofhighPCO2onventilatedpretermlamblungsPretermsurfactant-treatedlambswithahightidalvolume(Vt)30minacutelunginjury.Vt6-9mL/kg5.5hPCO240-50mmHgaddtotheventilatorcircuitPCO2955mmHgheartratesbloodpressuresplasmacortisolvaluesoxygenationnodifferentwhitebloodcellshydrogenperoxideproductionIL-1beta,IL-8cytokinemRNAexpressionincellsfromthealveolarwashHistopathologylesslunginjuryPediatrRes.2003Mar;53(3):468-72.PermissivehypercapniaforthepreventionofmorbidityandmortalityinmechanicallyventilatednewborninfantsTwotrialsinvolving269newborninfantsnoevidencetheincidenceofdeathorCLDat36weeks(RR0.94,95%CI0.78,1.15)noevidenceIVH3or4(RR0.84,95%CI0.54,1.31)noevidencePVL(RR1.02,95%CI0.49,2.12).noevidenceLongtermneurodevelopmentaloutcomesOnetrialreportedthatpermissivehypercapniareducedtheincidenceofCLDinthe501to750gramsubgroupCochraneDatabaseSystRev.2001;(2):CD002061Permissivehypercapniainneonates:thecaseofthegood,thebad,andtheuglyPaCO2levelsof45-55mmHginhigh-riskneonatesaresafeandwelltoleratedPediatrPulmonol.2002Jan;33(1):56-64高频震荡通气高频震荡通气High-frequencyoscillatoryventilationHigh-frequencyoscillatoryventilationforacuterespiratorydistresssyndromeinadultpatients148randomized,controlledtrialARDSHFOVPCVPaO2/FiO272hnoThirty-daymortality37%or52%(p=0.102)barotrauma,hemodynamicinstability,ormucuspluggingnodifferentclinicaluseinadultsFiO260%andMAP 20cmH2OorPEEP15cmH2OCritCareMed.2003Apr;31(4Suppl):S317-23ElectivehighfrequencyoscillatoryventilationversusconventionalventilationforacutepulmonarydysfunctioninpreterminfantsupdatedinMay20033275RandomizedcontrolledtrialscomparingHFOVandCVinpretermorlowbirthweightinfantswithpulmonarydysfunctionnoevidenceofeffectonCLDandmortalityat28-30daysPre-specifiedsubgroupanalyses Shorttermneurologicalmorbidity Grade3or4IVHandPVL(nousinghighvolumestrategy)CochraneDatabaseSystRev.2003(4):CD000104OpenlungventilationimprovesgasexchangeandattenuatessecondarylunginjuryinapigletmodelofmeconiumaspirationProspective,randomizedanimalstudy36newbornpiglets(6salinecontrols)PPV(OLC),HFOV(OLC),PPV(CON)ventilatedfor5hrsbronchoalveolarlavagefluidmyeloperoxidaseactivity lunginjuryscore Alveolarproteininfluxnodifferentsuperioroxygenationandlessventilator-inducedlunginjuryCritCareMed.2004Feb;32(2):443-9ChangesinmeanairwaypressureduringHFOVinfluencescardiacoutputinneonatesandinfants14patients1yearweight10kgHFOVstudygroup(n=9)MAP+5and-3cmH2Ocontrolgroup(n=5)CardiacoutputechocardiographyDopplertechniqueCardiacoutputthestudygroup(P=0.02)thegreatestchangeatthehighestPawat-11%(range:-19to-9)comparedwithbaseline.ActaAnaesthesiolScand.2004Feb;48(2):218-23Randomizedtrialofhigh-frequencyoscillatoryventilationversusconventionalventilation:effectonsystemicbloodflowinverypreterminfants43infants29w8kgVitalsigns,airwaypressures,minuteventilation,Spo(2),andE(T)CO(2)wererecordedAPRVprovidedsimilarventilation,oxygenation,meanairwaypressure,hemodynamics,andpatientcomfortasSIMVAPRVsignificantlylowerinspiratorypeakandplateaupressuresPediatrCritCareMed.2001Jul;2(3):243-6Airwaypressurereleaseventilationasaprimaryventilatorymodeinacuterespiratorydistresssyndrome58patientsrandomizedAPRVorSIMV PIPatAPRV-group(25.90.6vs.28.60.7cmH2O)(P=0.007).nodifferentPEEPandphysiologicalvariables(PaO2/FiO2,PaCO2,pH,minuteventilation,meanarterialpressure,cardiacoutput)Atday28,thenumberofventilator-freedayswassimilar(13.41.7,12.21.5),themortality(17%and18%)APRVdidnotdifferfromSIMVwithPSinclinicallyrelevantoutcomeActaAnaesthesiolScand.2004Jul;48(6):722-31APRVNoevidencetoindicatethatAPRVisbetterthanconventionalventilation