呼吸治疗肺保护指南

呼吸机治疗的肺保护策略1.呼吸机相关性肺损伤acuteparenchymallunginjuryandanacuteinflammatoryresponse

inthelung.cytokines→alveoli

andthesystemiccirculation→multiple

organdysfunctionmortality↑2.呼吸机相关性肺损伤

ventilator-inducedlunginjury容量性损伤Volutrauma〔largegasvolumes〕压力性损伤Barotrauma〔highairwaypressure〕不张性损伤Atelectotrauma〔alveolarcollapseandre-expansion〕生物性损伤Biotrauma〔increasedinflammation〕3.肺损伤病理alveolarstructuraldamagepulmonaryedema、inflammation、fibrosissurfactantdysfunctionotherorgandysfunctionexacerbatethedisturbanceoflungdevelopment

SeminNeonatol.2002Oct;7(5):353-60.4.

ApproachesinthemanagementofacuterespiratoryfailureinchildrenprotectiveventilatoryandpotentialprotectiveventilatorymodeslowertidalvolumeandPEEPpermissivehypercapniahigh-frequencyoscillatoryventilationairwaypressurereleaseventilationpartialliquidventilationimproveoxygenationrecruitmentmaneuverspronepositioningkinetictherapyreduceFiO2andfacilitategasexchange

inhalednitricoxideandsurfactant

CurrOpinPediatr.2004Jun;16(3):293-8.5.Canmechanicalventilationstrategiesreducechroniclungdisease?

continuouspositiveairwaypressurepermissivehypercapniapatient-triggeredventilationvolume-targetedventilationproportionalassistventilationhigh-frequencyventilation

SeminNeonatol.2003Dec;8(6):441-86.小潮气量和呼气末正压

lowertidalvolumeandPEEP7.VentilationwithlowertidalvolumesversustraditionaltidalvolumesinadultsforALIandARDS1202patientslowertidalvolume(≤7ml/kg)lowplateaupressure≤30cmH2Oversustidalvolume10to15ml/kgMortalityatday28

long-termmortalitywasuncertainlowandconventionaltidalvolumewithplateaupressure≤31cmH2Owasnotsignificantlydifferent

CochraneDatabaseSystRev.2004;(2):CD003844

8.Higherversuslowerpositiveend-expiratorypressuresinpatientswiththeacuterespiratorydistresssyndrome

549patientsacutelunginjuryandARDSlower-PEEPgroup8.3±3.2cmH2Ohigher-PEEPgroup13.2±3.5cmH2O(P<0.001).tidal-volume6ml/kgend-inspiratoryplateau-pressure≤30cmH2OTheratesofdeath24.9%27.5%(p=0.48)Fromday1today28,breathingwasunassisted14.5±10.4days13.8±10.6days(p=0.5)clinicaloutcomesaresimilarwhetherlowerorhigherPEEPlevelsareused.NEnglJMed.2004Jul22;351(4):327-36.9.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(p<.0001)increasedLightmicroscopyrevealedevidenceofintra-alveolaredemaandhemorrhageintheiT=1.0andiT=1.5animalsbutnottheLoPandiT=0.5animals.

CritCareMed.2002Oct;30(10):2295-9.10.新生儿呼吸窘迫综合征

呼吸机治疗的肺保护性策略研究

施丽萍孙眉月杜立中

中华儿科杂志200311.本工程研究的目的通过肺力学参数的监测〔PM〕指导呼吸机参数的调节来降低呼吸机相关性肺损伤的发生探讨新生儿RDS最适宜的呼吸机参数允许性高碳酸血症对新生儿的影响12.非肺力学监测组〔NPM〕：1994~1997年,RDS50例，作为对照组肺力学监测组(PM):1998~2001年，RDS60例，作为观察组肺力学监测仪(BicoreCP100〕13.两组胎龄、体重、病情严重程度比较

胎龄（周）体重(kg)日龄(天）AaDO2(mmHg)a/ANPM32.6±2.11.76±0.35.6±5.1328±1410.16±0.1PM32.7±2.51.89±0.54.8±4.9345±1240.16±0.1t0.1781.6370.7750.6270.597p>0.05>0.05>0.05>0.05>0.0514.对照组〔NPM)：应用人工呼吸机限压定时持续气流型，通气模式为IMV，持续脉搏血氧饱和度监测使其维持在85~95%，每8h监测动脉血气一次，要求血气维持在正常范围内，PaO240-70mmHg,PaCO235-45mmHg15.观察组〔PM组〕：1、肺力学监测仪(BicoreCP100)每8~12h监测一次机械通气时肺力学参数2、监测时要求患儿与呼吸机完全同步或无自主呼吸状态〔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4、气管插管气漏率小于20%5、每监测一次持续0.5~1h至数据稳定后记录监测的数据16.NPM组和PM组的评估指标1.疾病极期，即生后24~48h时呼吸机要求最高值，包括FiO2、PIP、PEEP、Ti、MAP、VR2.VE、C20/C、TC〔限于PM组〕，3.记录血pH、PaO2、PaCO2、氧合指数〔OI〕〔OI=FiO2×MAP/PaO2〕和心率、血压4.呼吸机应用时间，用氧时间，住院天数，病死率，PDA，IVH和呼吸机相关性肺损伤的发生率。17.两组呼吸机参数比较

FiO2（%）PIP（cmH2O)PEEP（cmH2O)MAP（cmH2O)Ti(sec)VR（次/分）NPM60±1930.5±3.45.6±0.814.9±3.40.75±0.139±9PM62±1826.7±1.75.4±0.611.9±2.00.45±0.142±10t0.1847.5271.3395.81818.101.81p>0.05<0.001>0.05<0.001<0.001>0.0518.19.两组血气监测结果比较

PHPaO2(mmHg)PaCO2(mmHg)HR(次/分）BP(mmHg)OINPM7.31±0.157±1740±10144±840±4.619±13PM7.3±0.0459±1648±6.3145±639±3.614±7.7t0.2890.5164.6630.7980.9422.011p>0.05>0.05<0.001>0.05>0.05<0.0520.21.两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

VALI%PDA%IVH%IMV(d)用氧时间(d)住院天数(d)病死率%NPM3236423.9±1.811±719±1414PM13.333.3404.2±1.713±722±118.3t

0.8671.4741.22

χ²5.570.090.05

0.9p<0.05>0.05>0.05>0.05>0.05>0.05>0.0522.结论肺力学监测能指导正确应用呼吸机，降低呼吸机相关性肺损伤从本研究结果推荐RDS呼吸机应用的参数为：PIP25cmH2O左右，短Ti0.3~0.5秒，应用适当的PEEP5-7cmH2O治疗RDS，不影响氧合。PaCO2的轻度增高〔PaCO245-60〕，IVH的发生未见增加。23.允许性高碳酸血症Permissivehypercapnia24.Permissivehypercapnia--roleinprotectivelungventilatorystrategies

First,weconsidertheevidencethatprotectivelungventilatorystrategiesimprovesurvivalandweexplorecurrentparadigmsregardingthemechanismsunderlyingtheseeffectsSecond,weexaminewhetherhypercapnicacidosismayhaveeffectsthatareadditivetotheeffectsofprotectiveventilationThird,weconsiderwhetherdirectelevationofCO2,intheabsenceofprotectiveventilation,isbeneficialordeleteriousFourth,weaddressthecurrentevidenceregardingthebufferingofhypercapnicacidosis25.

Lung-protectiveventilationinacuterespiratorydistresssyndrome:protectionbyreducedlungstressorbytherapeutichypercapnia?

hypercapnicacidosislung-protectiveventilationrespiratoryacidosisprotected

thelungTheprotectiveeffect

ofrespiratoryacidosisinhibitionofxanthine

oxidasepreventedbybufferingtheacidosis.theprotectionresultedfromtheacidosisratherthanhypercapnia

AmJRespirCritCareMed.2000Dec;162(6):2021-2.26.PermissivehypercapniainARDSanditseffectontissueoxygenationTheright-shiftofthehaemoglobin-oxygendissociationcurvereduceintrapulmonaryshunt(Qs/Qt)bypotentiatinghypoxicpulmonaryvasoconstrictionaffectthedistributionofsystemicbloodflowbothwithinorgansandbetweenorgans

ActaAnaesthesiolScandSuppl.1995;107:201-827.

Hypercapnicacidosisattenuatesendotoxininducedacutelunginjuryattenuatedthedecrementinoxygenationimprovedlungcompliancereducedalveolarneutrophilinfiltrationandhistologicindicesoflunginjury

AmJRespirCritCareMed.2004Jan1;169(1):46-5628.Hypercapnicacidosisisprotectiveinaninvivomodelofventilator-inducedlunginjury12rabbitsventilator-inducedlunginjury(VILI)PaCO240mmHgn=6PaCO280-100mmHgn=6respiratorymechanics(plateaupressures)27.0±2.520.9±3.0p=0.016gasexchange(PaO2)165.2±19.477.3±87.9p=0.02wet:dryweight9.7±2.36.6±1.8p=0.04bronchoalveolarlavagefluidproteinconcentration1350±228656±511p=0.03cellcount6.86x1052.84x105p=0.021injuryscore7.0±3.30.7±0.9p<0.0001AmJRespirCritCareMed.2002Aug1;166(3):403-8

29.EffectsofhighPCO2onventilatedpretermlamblungsPretermsurfactant-treatedlambswithahightidalvolume(Vt)30minacutelunginjury.Vt6-9mL/kg5.5hPCO240-50mmHgaddtotheventilatorcircuitPCO295±5mmHgheartratesbloodpressuresplasmacortisolvaluesoxygenationnodifferent↑whitebloodcells↑hydrogenperoxideproduction↑IL-1beta,IL-8cytokinemRNAexpressionincellsfromthealveolarwashHistopathologylesslunginjury

PediatrRes.2003Mar;53(3):468-72.30.PermissivehypercapniaforthepreventionofmorbidityandmortalityinmechanicallyventilatednewborninfantsTwotrialsinvolving269newborninfantsnoevidence↓theincidenceofdeathorCLDat36weeks(RR0.94,95%CI0.78,1.15)noevidence↑IVH3or4(RR0.84,95%CI0.54,1.31)noevidence↑PVL(RR1.02,95%CI0.49,2.12).noevidence↑LongtermneurodevelopmentaloutcomesOnetrialreportedthatpermissivehypercapniareducedtheincidenceofCLDinthe501to750gramsubgroup

CochraneDatabaseSystRev.2001;(2):CD00206131.Permissivehypercapniainneonates:thecaseofthegood,thebad,andtheugly

PaCO2levelsof45-55mmHginhigh-riskneonatesare"safe"and"welltolerated"

PediatrPulmonol.2002Jan;33(1):56-6432.高频震荡通气High-frequencyoscillatoryventilation33.

High-frequencyoscillatoryventilationforacuterespiratorydistresssyndromeinadultpatients148randomized,controlledtrialARDSHFOVPCVPaO2/FiO2<16h(p=0.008)>72hnoThirty-daymortality37%or52%(p=0.102)barotrauma,hemodynamicinstability,ormucuspluggingnodifferentclinicaluseinadultsFiO2>60%andMAP

20cmH2OorPEEP>15cmH2OCritCareMed.2003Apr;31(4Suppl):S317-2334.Electivehighfrequencyoscillatoryventilationversusconventionalventilationforacutepulmonarydysfunctioninpreterminfants

updatedinMay20033275RandomizedcontrolledtrialscomparingHFOVandCVinpretermorlowbirthweightinfantswithpulmonarydysfunctionnoevidenceofeffectonCLDandmortalityat28-30daysPre-specifiedsubgroupanalyses

Shorttermneurologicalmorbidity

Grade3or4IVHandPVL(nousinghighvolumestrategy)

CochraneDatabaseSystRev.2003(4):CD00010435.OpenlungventilationimprovesgasexchangeandattenuatessecondarylunginjuryinapigletmodelofmeconiumaspirationProspective,randomizedanimalstudy36newbornpiglets(6salinecontrols)PPV(OLC),HFOV(OLC),PPV(CON)ventilatedfor5hrsbronchoalveolarlavagefluidmyeloperoxidaseactivity

lunginjuryscore

Alveolarproteininfluxnodifferentsuperioroxygenationandlessventilator-inducedlunginjury

CritCareMed.2004Feb;32(2):443-936.ChangesinmeanairwaypressureduringHFOVinfluencescardiacoutputinneonatesandinfants14patients<1yearweight<10kgHFOVstudygroup(n=9)MAP+5and-3cmH2Ocontrolgroup(n=5)CardiacoutputechocardiographyDopplertechniqueCardiacoutputthestudygroup(P=0.02)thegreatestchangeatthehighestPawat-11%(range:-19to-9)comparedwithbaseline.ActaAnaesthesiolScand.2004Feb;48(2):218-2337.Randomizedtrialofhigh-frequencyoscillatoryventilationversusconventionalventilation:effectonsystemicbloodflowinverypreterminfants43infants<29w<1hrwithHFOVorCVAt31024hrsofageEchocardiographySuperiorvenacavaflowRightventricularout