呼吸治療肺保護指南

呼吸機治療的肺保護策略1.呼吸機相關性肺損傷acuteparenchymallunginjuryandanacuteinflammatoryresponse

inthelung.cytokines→alveoli

andthesystemiccirculation→multiple

organdysfunctionmortality↑2.呼吸機相關性肺損傷

ventilator-inducedlunginjury容量性損傷Volutrauma〔largegasvolumes〕壓力性損傷Barotrauma〔highairwaypressure〕不張性損傷Atelectotrauma〔alveolarcollapseandre-expansion〕生物性損傷Biotrauma〔increasedinflammation〕3.肺損傷病理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.小潮氣量和呼氣末正壓

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.新生兒呼吸窘迫綜合征

呼吸機治療的肺保護性策略研究

施麗萍孫眉月杜立中

中華兒科雜志200311.本工程研究的目的通過肺力學參數(shù)的監(jiān)測〔PM〕指導呼吸機參數(shù)的調節(jié)來降低呼吸機相關性肺損傷的發(fā)生探討新生兒RDS最適宜的呼吸機參數(shù)允許性高碳酸血癥對新生兒的影響12.非肺力學監(jiān)測組〔NPM〕：1994~1997年,RDS50例，作為對照組肺力學監(jiān)測組(PM):1998~2001年，RDS60例，作為觀察組肺力學監(jiān)測儀(BicoreCP100〕13.兩組胎齡、體重、病情嚴重程度比較

胎齡（周）體重(kg)日齡(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.對照組〔NPM)：應用人工呼吸機限壓定時持續(xù)氣流型，通氣模式為IMV，持續(xù)脈搏血氧飽和度監(jiān)測使其維持在85~95%，每8h監(jiān)測動脈血氣一次，要求血氣維持在正常范圍內，PaO240-70mmHg,PaCO235-45mmHg15.觀察組〔PM組〕：1、肺力學監(jiān)測儀(BicoreCP100)每8~12h監(jiān)測一次機械通氣時肺力學參數(shù)2、監(jiān)測時要求患兒與呼吸機完全同步或無自主呼吸狀態(tài)〔必要時通過藥物抑制呼吸〕3、肺力學監(jiān)測儀的傳感器置于近端接口4、氣管插管氣漏率小于20%5、每監(jiān)測一次持續(xù)0.5~1h至數(shù)據(jù)穩(wěn)定后記錄監(jiān)測的數(shù)據(jù)16.NPM組和PM組的評估指標1.疾病極期，即生后24~48h時呼吸機要求最高值，包括FiO2、PIP、PEEP、Ti、MAP、VR2.VE、C20/C、TC〔限于PM組〕，3.記錄血pH、PaO2、PaCO2、氧合指數(shù)〔OI〕〔OI=FiO2×MAP/PaO2〕和心率、血壓4.呼吸機應用時間，用氧時間，住院天數(shù)，病死率，PDA，IVH和呼吸機相關性肺損傷的發(fā)生率。17.兩組呼吸機參數(shù)比較

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>0.0518.19.兩組血氣監(jiān)測結果比較

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<0.0520.21.兩組呼吸機相關性肺損傷、PDA、IVH、

呼吸機應用時間、用氧時間、住院天數(shù)、病死率比較

VALI%PDA%IVH%IMV(d)用氧時間(d)住院天數(shù)(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.結論肺力學監(jiān)測能指導正確應用呼吸機，降低呼吸機相關性肺損傷從本研究結果推薦RDS呼吸機應用的參數(shù)為：PIP25cmH2O左右，短Ti0.3~0.5秒，應用適當?shù)腜EEP5-7cmH2O治療RDS，不影響氧合。PaCO2的輕度增高〔PaCO245-60〕，IVH的發(fā)生未見增加。23.允許性高碳酸血癥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.高頻震蕩通氣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