呼吸治疗肺保护施丽萍指南课件

呼吸机治疗的肺保护策略浙江大学医学院附属儿童医院施丽萍呼吸机治疗的肺保护策略浙江大学医学院附属儿童医院1呼吸机相关性肺损伤acuteparenchymallunginjuryandanacuteinflammatoryresponse

inthelung.cytokines→alveoli

andthesystemiccirculation→multiple

organdysfunctionmortality↑呼吸机相关性肺损伤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）呼吸机相关性肺损伤

ventilator-inducedl3肺损伤病理alveolarstructuraldamagepulmonaryedema、inflammation、fibrosissurfactantdysfunctionotherorgandysfunctionexacerbatethedisturbanceoflungdevelopment

SeminNeonatol.2002Oct;7(5):353-60.肺损伤病理alveolarstructurald4

ApproachesinthemanagementofacuterespiratoryfailureinchildrenprotectiveventilatoryandpotentialprotectiveventilatorymodeslowertidalvolumeandPEEPpermissivehypercapniahigh-frequencyoscillatoryventilationairwaypressurereleaseventilationpartialliquidventilationimproveoxygenationrecruitmentmaneuverspronepositioningkinetictherapyreduceFiO2andfacilitategasexchange

inhalednitricoxideandsurfactant

CurrOpinPediatr.2004Jun;16(3):293-8.Approachesinthemanagement5Canmechanicalventilationstrategiesreducechroniclungdisease?

continuouspositiveairwaypressurepermissivehypercapniapatient-triggeredventilationvolume-targetedventilationproportionalassistventilationhigh-frequencyventilation

SeminNeonatol.2003Dec;8(6):441-8Canmechanicalventilationstr6小潮气量和呼气末正压lowertidalvolumeandPEEP小潮气量和呼气末正压7VentilationwithlowertidalvolumesversustraditionaltidalvolumesinadultsforALIandARDS1202patientslowertidalvolume(≤7ml/kg)lowplateaupressure≤30cmH2Oversustidalvolume10to15ml/kgMortalityatday28long-termmortalitywasuncertainlowandconventionaltidalvolumewithplateaupressure≤31cmH2Owasnotsignificantlydifferent

CochraneDatabaseSystRev.2004;(2):CD003844

Ventilationwithlowertidalv8Higherversuslowerpositiveend-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.Higherversuslowerpositivee9Increasinginspiratorytimeexacerbatesventilator-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.Increasinginspiratorytimeex10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2003新生儿呼吸窘迫综合征

呼吸机治疗的肺保护性策略研究11本项目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最合适的呼吸机参数允许性高碳酸血症对新生儿的影响本项目研究的目的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）呼吸治疗肺保护施丽萍指南课件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>0.05两组胎龄、体重、病情严重程度比较

胎龄（周）体重日龄AaDO14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,PaCO235-45mmHg对照组（NPM)：15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观察组（PM组）：16NPM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。NPM组和PM组的评估指标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>0.05两组呼吸机参数比较

FiO2PIP（cmH2O)PE18呼吸治疗肺保护施丽萍指南课件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<0.05两组血气监测结果比较

PHPaO2PaCO2(mmHg)H20呼吸治疗肺保护施丽萍指南课件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>0.05两组呼吸机相关性肺损伤、PDA、IVH、

呼吸机应用时间、用22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。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23允许性高碳酸血症Permissivehypercapnia允许性高碳酸血症24Permissivehypercapnia--roleinprotectivelungventilatorystrategies

First,weconsidertheevidencethatprotectivelungventilatorystrategiesimprovesurvivalandweexplorecurrentparadigmsregardingthemechanismsunderlyingtheseeffectsSecond,weexaminewhetherhypercapnicacidosismayhaveeffectsthatareadditivetotheeffectsofprotectiveventilationThird,weconsiderwhetherdirectelevationofCO2,intheabsenceofprotectiveventilation,isbeneficialordeleteriousFourth,weaddressthecurrentevidenceregardingthebufferingofhypercapnicacidosisPermissivehypercapnia--rolei25

Lung-protectiveventilationinacuterespiratorydistresssyndrome:protectionbyreducedlungstressorbytherapeutichypercapnia?

hypercapnicacidosislung-protectiveventilationrespiratoryacidosisprotected

thelungTheprotectiveeffect

ofrespiratoryacidosisinhibitionofxanthine

oxidasepreventedbybufferingtheacidosis.theprotectionresultedfromtheacidosisratherthanhypercapnia

AmJRespirCritCareMed.2000Dec;162(6):2021-2.Lung-protectiveventilation26PermissivehypercapniainARDSanditseffectontissueoxygenationTheright-shiftofthehaemoglobin-oxygendissociationcurvereduceintrapulmonaryshunt(Qs/Qt)bypotentiatinghypoxicpulmonaryvasoconstrictionaffectthedistributionofsystemicbloodflowbothwithinorgansandbetweenorgans

ActaAnaesthesiolScandSuppl.1995;107:201-8PermissivehypercapniainARDS27

Hypercapnicacidosisattenuatesendotoxininducedacutelunginjuryattenuatedthedecrementinoxygenationimprovedlungcompliancereducedalveolarneutrophilinfiltrationandhistologicindicesoflunginjury

AmJRespirCritCareMed.2004Jan1;169(1):46-56Hypercapnicacidosisattenu28Hypercapnicacidosisisprotectiveinaninvivomodelofventilator-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

Hypercapnicacidosisisprotec29EffectsofhighPCO2onventilatedpretermlamblungsPretermsurfactant-treatedlambswithahightidalvolume(Vt)30minacutelunginjury.Vt6-9mL/kg5.5hPCO240-50mmHgaddtotheventilatorcircuitPCO295±5mmHgheartratesbloodpressuresplasmacortisolvaluesoxygenationnodifferent↑whitebloodcells↑hydrogenperoxideproduction↑IL-1beta,IL-8cytokinemRNAexpressionincellsfromthealveolarwashHistopathologylesslunginjury

PediatrRes.2003Mar;53(3):468-72.EffectsofhighPCO2onventil30PermissivehypercapniaforthepreventionofmorbidityandmortalityinmechanicallyventilatednewborninfantsTwotrialsinvolving269newborninfantsnoevidence↓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):CD002061Permissivehypercapniaforthe31Permissivehypercapniainneonates:thecaseofthegood,thebad,andtheugly

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

PediatrPulmonol.2002Jan;33(1):56-64呼吸治疗肺保护施丽萍指南课件32高频震荡通气High-frequencyoscillatoryventilation高频震荡通气33

High-frequencyoscillatoryventilationforacuterespiratorydistresssyndromeinadultpatients148randomized,controlledtrialARDSHFOVPCVPaO2/FiO2<16h(p=0.008)>72hnoThirty-daymortality37%or52%(p=0.102)barotrauma,hemodynamicinstability,ormucuspluggingnodifferentclinicaluseinadultsFiO2>60%andMAP20cmH2OorPEEP>15cmH2OCritCareMed.2003Apr;31(4Suppl):S317-23High-frequencyoscillatoryve34Electivehighfrequencyoscillatoryventilationversusconventionalventilationforacutepulmonarydysfunctioninpreterminfants

updatedinMay20033275RandomizedcontrolledtrialscomparingHFOVandCVinpretermorlowbirthweightinfantswithpulmonarydysfunctionnoevidenceofeffectonCLDandmortalityat28-30daysPre-specifiedsubgroupanalyses

Shorttermneurologicalmorbidity

Grade3or4IVHandPVL(nousinghighvolumestrategy)

CochraneDatabaseSystRev.2003(4):CD000104Electivehighfrequencyoscill35OpenlungventilationimprovesgasexchangeandattenuatessecondarylunginjuryinapigletmodelofmeconiumaspirationProspective,randomizedanimalstudy36newbornpiglets(6salinecontrols)PPV(OLC),HFOV(OLC),PPV(CON)ventilatedfor5hrsbronchoalveolarlavagefluidmyeloperoxidaseactivitylunginjuryscoreAlveolarproteininfluxnodifferentsuperioroxygenationandlessventilator-inducedlunginjury

CritCareMed.2004Feb;32(2):443-9Openlungventilationimproves36ChangesinmeanairwaypressureduringHFOVinfluencescardiacoutputinneonatesandinfants14patients<1yearweight<10kgHFOVstudygroup(n=9)MAP+5and-3cmH2Ocontrolgroup(n=5)CardiacoutputechocardiographyDopplertechniqueCardiacoutputthestudygroup(P=0.02)thegreatestchangeatthehighestPawat-11%(range:-19to-9)comparedwithbaseline.ActaAnaesthesiolScand.2004Feb;48(2):218-23Changesinmeanairwaypressur37Randomizedtrialofhigh-frequencyoscillatoryventilationversusconventionalventilation:effectonsystemicbloodflowinverypreterminfants43infants<29w<1hrwithHFOVorCVAt31024hrsofageEchocardiographySuperiorvenacavaflowRightventricularoutputHypotentionNosignificantadverseeffectsofHFOVonsystemicbloodflow

JPediatr.2003Aug;143(2):192-8Randomizedtrialofhigh-frequ38气道压力释放通气Airwaypressurereleaseventilation气道压力释放通气39Airwaypressurereleaseventilationinpediatrics33infantsweight>8kgVitalsigns,airwaypressures,minuteventilation,Spo(2),andE(T)CO(2)wererecordedAPRVprovidedsimilarventilation,oxygenation,meanairwaypressure,hemodynamics,andpatientcomfortasSIMVAPRVsignificantlylowerinspiratorypeakandplateaupressuresPediatrCritCareMed.2001Jul;2(3):243-6Airwaypressurereleaseventil40Airwaypressurereleaseventilationasaprimaryventilatorymodeinacuterespiratorydistresssyndrome

58patientsrandomizedAPRVorSIMV

PIPatAPRV-group(25.9±0.6vs.28.6±0.7cmH2O)(P=0.007).nodifferentPEEPandphysiologicalvariables(PaO2/FiO2,PaCO2,pH,minuteventilation,meanarterialpressure,cardiacoutput)Atday28,thenumberofventilator-freedayswassimilar(13.4±1.7,12.2±1.5),themortality(17%and18%)APRVdidnotdifferfromSIMVwithPSinclinicallyrelevantoutcome

ActaAnaesthesiolScand.2004Jul;48(6):722-31Airwaypressurereleaseventil41APRVNoevidencetoindicatethatAPRVisbetterthanconventionalventilationAPRVNoevidencetoindicateth42谢谢谢谢43呼吸机治疗的肺保护策略浙江大学医学院附属儿童医院施丽萍呼吸机治疗的肺保护策略浙江大学医学院附属儿童医院44呼吸机相关性肺损伤acuteparenchymallunginjuryandanacuteinflammatoryresponse

inthelung.cytokines→alveoli

andthesystemiccirculation→multiple

organdysfunctionmortality↑呼吸机相关性肺损伤45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）呼吸机相关性肺损伤

ventilator-inducedl46肺损伤病理alveolarstructuraldamagepulmonaryedema、inflammation、fibrosissurfactantdysfunctionotherorgandysfunctionexacerbatethedisturbanceoflungdevelopment

SeminNeonatol.2002Oct;7(5):353-60.肺损伤病理alveolarstructurald47

ApproachesinthemanagementofacuterespiratoryfailureinchildrenprotectiveventilatoryandpotentialprotectiveventilatorymodeslowertidalvolumeandPEEPpermissivehypercapniahigh-frequencyoscillatoryventilationairwaypressurereleaseventilationpartialliquidventilationimproveoxygenationrecruitmentmaneuverspronepositioningkinetictherapyreduceFiO2andfacilitategasexchange

inhalednitricoxideandsurfactant

CurrOpinPediatr.2004Jun;16(3):293-8.Approachesinthemanagement48Canmechanicalventilationstrategiesreducechroniclungdisease?

continuouspositiveairwaypressurepermissivehypercapniapatient-triggeredventilationvolume-targetedventilationproportionalassistventilationhigh-frequencyventilation

SeminNeonatol.2003Dec;8(6):441-8Canmechanicalventilationstr49小潮气量和呼气末正压lowertidalvolumeandPEEP小潮气量和呼气末正压50VentilationwithlowertidalvolumesversustraditionaltidalvolumesinadultsforALIandARDS1202patientslowertidalvolume(≤7ml/kg)lowplateaupressure≤30cmH2Oversustidalvolume10to15ml/kgMortalityatday28long-termmortalitywasuncertainlowandconventionaltidalvolumewithplateaupressure≤31cmH2Owasnotsignificantlydifferent

CochraneDatabaseSystRev.2004;(2):CD003844

Ventilationwithlowertidalv51Higherversuslowerpositiveend-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.Higherversuslowerpositivee52Increasinginspiratorytimeexacerbatesventilator-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.Increasinginspiratorytimeex53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2003新生儿呼吸窘迫综合征

呼吸机治疗的肺保护性策略研究54本项目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最合适的呼吸机参数允许性高碳酸血症对新生儿的影响本项目研究的目的55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）呼吸治疗肺保护施丽萍指南课件56两组胎龄、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>0.05两组胎龄、体重、病情严重程度比较

胎龄（周）体重日龄AaDO57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,PaCO235-45mmHg对照组（NPM)：58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观察组（PM组）：59NPM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。NPM组和PM组的评估指标60两组呼吸机参数比较

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>0.05两组呼吸机参数比较

FiO2PIP（cmH2O)PE61呼吸治疗肺保护施丽萍指南课件62两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<0.05两组血气监测结果比较

PHPaO2PaCO2(mmHg)H63呼吸治疗肺保护施丽萍指南课件64两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>0.05两组呼吸机相关性肺损伤、PDA、IVH、

呼吸机应用时间、用65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。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66允许性高碳酸血症Permissivehypercapnia允许性高碳酸血症67Permissivehypercapnia--roleinprotectivelungventilatorystrategies

First,weconsidertheevidencethatprotectivelungventilatorystrategiesimprovesurvivalandweexplorecurrentparadigmsregardingthemechanismsunderlyingtheseeffectsSecond,weexaminewhetherhypercapnicacidosismayhaveeffectsthatareadditivetotheeffectsofprotectiveventilationThird,weconsiderwhetherdirectelevationofCO2,intheabsenceofprotectiveventilation,isbeneficialordeleteriousFourth,weaddressthecurrentevidenceregardingthebufferingofhypercapnicacidosisPermissivehypercapnia--rolei68

Lung-protectiveventilationinacuterespiratorydistresssyndrome:protectionbyreducedlungstressorbytherapeutichypercapnia?

hypercapnicacidosislung-protectiveventilationrespiratoryacidosisprotected

thelungTheprotectiveeffect

ofrespiratoryacidosisinhibitionofxanthine

oxidasepreventedbybufferingtheacidosis.theprotectionresultedfromtheacidosisratherthanhypercapnia

AmJRespirCritCareMed.2000Dec;162(6):2021-2.Lung-protectiveventilation69PermissivehypercapniainARDSanditseffectontissueoxygenationTheright-shiftofthehaemoglobin-oxygendissociationcurvereduceintrapulmonaryshunt(Qs/Qt)bypotentiatinghypoxicpulmonaryvasoconstrictionaffectthedistributionofsystemicbloodflowbothwithinorgansandbetweenorgans

ActaAnaesthesiolScandSuppl.1995;107:201-8PermissivehypercapniainARDS70

Hypercapnicacidosisattenuatesendotoxininducedacutelunginjuryattenuatedthedecrementinoxygenationimprovedlungcompliancereducedalveolarneutrophilinfiltrationandhistologicindicesoflunginjury

AmJRespirCritCareMed.2004Jan1;169(1):46-56Hypercapnicacidosisattenu71Hypercapnicacidosisisprotectiveinaninvivomodelofventilator-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

Hypercapnicacidosisisprotec72EffectsofhighPCO2onventilatedpretermlamblungsPretermsurfactant-treatedlambswithahightidalvolume(Vt)30minacutelunginjury.Vt6-9mL/kg5.5hPCO240-50mmHgaddtotheventilatorcircuitPCO295±5mmHgheartratesbloodpressuresplasmacortisolvaluesoxygenationnodifferent↑whitebloodcells↑hydrogenperoxideproduction↑IL-1beta,IL-8cytokinemRNAexpressionincellsfromthealveolarwashHistopathologylesslunginjury

PediatrRes.2003Mar;53(3):468-72.EffectsofhighPCO2onventil73PermissivehypercapniaforthepreventionofmorbidityandmortalityinmechanicallyventilatednewborninfantsTwotrialsinvolving269newborninfantsnoevidence↓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):CD002061Permissivehypercapniaforthe74Permissivehypercapniainneonates:thecaseofthegood,thebad,andtheugly

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

PediatrPulmonol.2002Jan;33(1):56-64呼吸治疗肺保护施丽萍指南课件75高频震荡通气High-frequencyoscillatoryventilation高频震荡通气76

High-frequencyoscillatoryventilationforacuterespiratorydistresssyndromeinadultpatients148randomized,controlledtrialARDSHFOVPCVPaO2/FiO2<16h(p=0.008)>72hnoThirty-daymortality37%or52%(p=0.102)barotrauma,hemodynamicinstability,ormucuspluggingnodifferentclinicaluseinadultsFiO2>60%andMAP20cmH2OorPEEP>15cmH2OCritCareMed.2003Apr;31(4Suppl):S317-23High-frequencyoscillatoryve77Electivehighfrequencyoscillatoryventilationversusconventionalventilationforacutepulmonarydysfunctioninpreterminfants

updatedinMay20033275RandomizedcontrolledtrialscomparingHFOVandCVinpretermorlowbirthweightinfantswithpulmonarydysfunctionnoevidenceofeffectonCLDandmortalityat28-30daysPre-specifiedsubgroupanalyses

Shorttermneurologicalmorbidity

Grade3or4IVHandPVL(nousinghighvolumestrategy)