ARDS進(jìn)展急性呼吸窘迫綜合征施煥中

急性呼吸窘迫綜合征廣西醫(yī)科大學(xué)第一附屬醫(yī)院呼吸內(nèi)科施煥中廣西醫(yī)科大學(xué)第一附屬醫(yī)院危重癥中心NEnglJMed2003;348:683-693.NEnglJMed2003;348:683-693.NEnglJMed2003;348:683-693.MethodsWeevaluated109survivorsoftheacuterespiratory

distresssyndrome3,6,and12monthsafterdischargefromthe

intensivecareunit.Ateachvisit,patientswereinterviewed

andunderwentaphysicalexamination,pulmonary-functiontesting,

asix-minute–walktest,andaquality-of-lifeevaluation.

ResultsPatientswhosurvivedtheacuterespiratorydistress

syndromewereyoung(medianage,45years)andseverelyill

(medianAcutePhysiology,Age,andChronicHealthEvaluation

score,23)andhadalongstayintheintensivecareunit(median,

25days).Patientshadlost18percentoftheirbase-linebody

weightbythetimetheyweredischargedfromtheintensivecare

unitandstatedthatmuscleweaknessandfatiguewerethereasons

fortheirfunctionallimitation.Lungvolumeandspirometric

measurementswerenormalby6months,butcarbonmonoxidediffusion

capacityremainedlowthroughoutthe12-monthfollow-up.No

patientsrequiredsupplementaloxygenat12months,but6percent

ofpatientshadarterialoxygensaturationvaluesbelow88percent

duringexercise.Themedianscoreforthephysicalroledomain

oftheMedicalOutcomesStudy36-itemShort-FormGeneralHealth

Survey(ahealth-relatedquality-of-lifemeasure)increased

from0at3monthsto25at12months(scoreinthenormalpopulation,

84).Thedistancewalkedinsixminutesincreasedfromamedian

of281mat3monthsto422mat12months;allvalueswere

lowerthanpredicted.Theabsenceofsystemiccorticosteroid

treatment,theabsenceofillnessacquiredduringtheintensive

careunitstay,andrapidresolutionoflunginjuryandmultiorgan

dysfunctionwereassociatedwithbetterfunctionalstatusduring

theone-yearfollow-up.

ConclusionsSurvivorsoftheacuterespiratorydistresssyndrome

havepersistentfunctionaldisabilityoneyearafterdischarge

fromtheintensivecareunit.Mostpatientshaveextrapulmonary

conditions,withmusclewastingandweaknessbeingmostprominent.

NEnglJMed2003;348:683-693.定義ALI/ARDS是指由心源性以外的各種肺內(nèi)外致病因素導(dǎo)致的急性、進(jìn)行性缺氧性呼吸衰竭。ALI/ARDS具有性質(zhì)相同的病理生理改變，嚴(yán)重的ALI即被定義為ARDS。ALI/ARDS以肺微血管通透性增加、肺氣容積減少、肺順應(yīng)性降低和嚴(yán)重肺內(nèi)分流及通氣/血流比例失調(diào)為病理生理特點(diǎn)，臨床表現(xiàn)為不易緩解的急性進(jìn)行性缺氧性呼吸衰竭，胸部X線可見肺部浸潤征象。高危因素

一、直接肺損傷因素嚴(yán)重肺部感染、胃內(nèi)容物吸入、溺水、吸入有毒氣體、肺挫傷、氧中毒等。二、間接肺損傷因素膿毒癥、休克、嚴(yán)重非胸部創(chuàng)傷、重癥胰腺炎、大量輸血、輸液、體外循環(huán)、DIC等。發(fā)病機(jī)制一、血管內(nèi)皮和氣道上皮損傷二、中性粒細(xì)胞介導(dǎo)的肺損傷三、其他炎癥機(jī)制細(xì)胞因子表面活性物質(zhì)呼吸機(jī)引起的肺損傷其他損傷機(jī)制四、機(jī)化性肺泡炎發(fā)病機(jī)制TheNormalAlveolus(Left-HandSide)andtheInjuredAlveolusintheAcutePhaseofAcuteLungInjuryandtheAcuteRespiratoryDistressSyndrome(Right-HandSide).Intheacutephaseofthesyndrome(right-handside),thereissloughingofboththebronchialandalveolarepithelialcells,withtheformationofprotein-richhyalinemembranesonthedenudedbasementmembrane.Neutrophilsareshownadheringtotheinjuredcapillaryendotheliumandmarginatingthroughtheinterstitiumintotheairspace,whichisfilledwithprotein-richedemafluid.Intheairspace,analveloarmacrophageissecretingcytokines,interleukin-1,6,8,and10,(IL-1,6,8,and10)andtumornecrosisfactor(TNF-),whichactlocallytostimulatechemotaxisandactivateneutrophils.Macrophagesalsosecreteothercytokines,includinginterleukin-1,6,and10.Interleukin-1canalsostimulatetheproductionofextracellularmatrixbyfibroblasts.Neutrophilscanreleaseoxidants,proteases,leukotrienes,andotherproinflammatorymolecules,suchasplatelet-activatingfactor(PAF).Anumberofantiinflammatorymediatorsarealsopresentinthealveolarmilieu,includinginterleukin-1–receptorantagonist,solubletumornecrosisfactorreceptor,autoantibodiesagainstinterleukin-8,andcytokinessuchasinterleukin-10and11(notshown).Theinfluxofprotein-richedemafluidintothealveolushasledtotheinactivationofsurfactant.MIFdenotesmacrophageinhibitoryfactor.發(fā)病機(jī)機(jī)制管狀髓髓磷脂脂發(fā)病機(jī)機(jī)制SurfactantProductionandRecyclingintheNormalAlveolus(PanelA)andChangesinSurfactantMetabolisminAcuteLungInjury(PanelB).Inthenormalalveolus,surfactantissynthesizedandpackagedintolamellarbodiesinthecellcytoplasm.Theselamellarbodiesthenmigratetothecellmembrane,withwhichtheyfuse,andthenarereleasedintotheair––fluidinterfacewithinthealveolus.Theysubsequentlyformanintermediatetubularstageofsurfactantcalledtubularmyelin,whichfinallyproducesthefunctionalcoatinglayer.Surfactantproteinsarealsoinvolvedinthecoatingprocess.Surfactantrecyclingoccursthroughtheendocytosisofsmallvesicles.Alterationsinsurfactantmetabolism(PanelB)mayoccuratanyofthesesteps.TheexactpathophysiologyofsurfactantmetabolisminARDShasnotbeenfullyestablished,butitislikelytoconsistofboththedestructionandthestructuralalterationofsurfactantlipidsandproteincausedbytheinflammatorymilieuoftheinjuredairspace.Inaddition,synthesisandrecyclingofsurfactantarelikelytobereducedanditsfunctionimpairedbytheaccumulationofproteinaceousmaterialwithinthealveolus.TNFdenotestumornecrosisfactor.病理2d14d14d病理4d14dPanelAshowsalung-biopsyspecimenobtainedfromapatienttwodaysaftertheonsetofthesyndromeasaresultoftheaspirationofgastriccontents.Characteristichyalinemembranesareevident(arrow),withassociatedintraalveolarredcellsandneutrophils,findingsthatareconsistentwiththepathologicaldiagnosisofdiffusealveolardamage(hematoxylinandeosin,x90).PanelsBandCshowlung-biopsyspecimensobtained14daysaftertheonsetofsepsis-associatedacutelunginjuryandtheacuterespiratorydistresssyndrome.PanelBshowsgranulationtissueinthedistalairspaceswithachronicinflammatory-cellinfiltrate(hematoxylinandeosin,x60).TrichromestaininginPanelCrevealscollagendeposition(darkblueareas)inthegranulationtissue,afindingthatisconsistentwiththedepositionofextracellularmatrixinthealveolarcompartment(x60).PanelDshowsaspecimenoflungtissuefromapatientwhodiedfourdaysaftertheonsetofacutelunginjuryandtheacuterespiratorydistresssyndrome;thereisinjurytoboththecapillaryendotheliumandthealveolarepithelium.Thereisanintravascularneutrophil(LC)inthecapillary(C).Vacuolizationandswellingoftheendothelium(EN)areapparent.Lossofalveolarepithelialcellsisalsoapparent,withtheformationofhyalinemembranesontheepithelialsideofthebasementmembrane(BM*).PanelEshowsaspecimenoflungtissueobtainedfromapatientduringthefibrosing-alveolitisphaseinwhichthereisevidenceofreepithelializationoftheepithelialbarrierwithalveolarepithelialtypeIIcells.ThearrowindicatesatypicaltypeIIcellwithmicrovilliandlamellarbodiescontainingsurfactant.TheepithelialcellimmediatelyadjacenttothiscellisintheprocessofchangingtoatypeIcell,withflattening,lossoflamellarbodies,andmicrovilli.Theinterstitiumisthickened,withdepositionofcollagen(C).臨床表表現(xiàn)一、大大多起起病急急劇，，進(jìn)展展快。。二、呼呼吸困困難、、窘迫迫，一一般氧氧療難難以糾糾正。。三、體體格檢檢查：：早期期可無無明顯顯異常常，較較多見見呼吸吸頻數(shù)數(shù)。唇唇指發(fā)發(fā)紺，，心率率增加加，肺肺部聽聽診可可聞及及于羅羅音或或哮鳴鳴音，，后期期出現(xiàn)現(xiàn)濕羅羅音并并呈肺肺實(shí)變變體征征。。四、胸胸部X線表表現(xiàn)：：早期期可無無異常常,或或呈輕輕度間間質(zhì)改改變，，表現(xiàn)現(xiàn)為紋紋理增增多、、邊緣緣模糊糊，繼繼之出出現(xiàn)斑斑片狀狀或大大片狀狀陰影影，后后期兩兩肺可可出現(xiàn)現(xiàn)廣泛泛實(shí)變變。。X線PanelAshowsananteroposteriorchestradiographfroma42-year-oldmanwiththeacuterespiratorydistresssyndromeassociatedwithgram-negativesepsiswhowasreceivingmechanicalventilation.Thepulmonary-arterywedgepressure,measuredwithapulmonary-arterycatheter,was4mmHg.Therearediffusebilateralalveolaropacitiesconsistentwiththepresenceofpulmonaryedema.PanelBshowsananteroposteriorchestradiographfroma60-year-oldmanwithacutelunginjuryandtheacuterespiratorydistresssyndromewhohadbeenreceivingmechanicalventilationforsevendays.Reticularopacitiesarepresentthroughoutbothlungfields,afindingsuggestiveofthedevelopmentoffibrosingalveolitis.PanelCshowsaCTscanofthechestobtainedduringtheacutephase.Thebilateralalveolaropacitiesaredenserinthedependent,posteriorlungzones,withsparingoftheanteriorlungfields.Thearrowsindicatethickenedinterlobularsepta,consistentwiththepresenceofpulmonaryedema.Thebilateralpleuraleffusionsareacommonfinding.PanelDshowsaCTscanofthechestobtainedduringthefibrosing-alveolitisphase.Therearereticularopacitiesanddiffuseground-glassopacitiesthroughoutbothlungfields,andalargebullaispresentintheleftanteriorhemithorax.診斷標(biāo)標(biāo)準(zhǔn)一、有有發(fā)病病的高高危因因素。。二、急急性起起病，，呼吸吸頻數(shù)數(shù)和（（或））呼吸吸窘迫迫。三、低低氧血血癥：：ALI時(shí)時(shí)PaO2/FiO2≤300mmHg；ARDS時(shí)時(shí)PaO2/FiO2≤200mmHg。四、胸胸部X線檢檢查兩兩肺浸浸潤影影響。。五、PCWP≤≤18mmHg或或臨床床上能能除外外心源源性肺肺水腫腫。返符合合以上上5項(xiàng)項(xiàng)者可可診斷斷為ALI或ARDS。。一、不不把是是否行行機(jī)械械通氣氣和行行機(jī)械械通氣氣的時(shí)時(shí)間納納入診診斷標(biāo)標(biāo)準(zhǔn)。。二、不不強(qiáng)調(diào)調(diào)PEEP對氧氧合的的影響響。三、為為了動(dòng)動(dòng)態(tài)觀觀察病病情變變化，，對上上機(jī)患患者應(yīng)應(yīng)盡量量在相相同的的通氣氣條件件下進(jìn)進(jìn)行前前后比比較。。四、PaO2/FiO2難于排除通通氣功能障障礙對氧合合的影響。。在臨床應(yīng)應(yīng)用中以PA～AO2可以更好地地反映ARDS的病病理生理特特點(diǎn)，從而而提高ARDS診斷斷的特異性性，應(yīng)用時(shí)時(shí)宜注意氧氧濃度的影影響。診斷時(shí)應(yīng)注注意以下各各項(xiàng)五、ARDS胸片的的表現(xiàn)缺少少特異性，，在不同的的原發(fā)病和和不同的時(shí)時(shí)期可有不不同的表現(xiàn)現(xiàn)，可以為為間質(zhì)或?qū)崒?shí)質(zhì)，散在在或彌漫，，可輕可重重，但進(jìn)展展迅速。。六、若能除除外左房壓壓高，PAWP對診診斷ARDS并非必必須，但對對無典型胸胸片或不能能完全從臨臨床表現(xiàn)除除外左房高高壓的患者者，必須有有PAWP作為診斷斷條件。。七、有慢性性肺病者（（如肺間質(zhì)質(zhì)纖維化、、結(jié)節(jié)病等等），即使使達(dá)到ARDS的診診斷標(biāo)準(zhǔn)也也不納入ARDS。。診斷時(shí)應(yīng)注注意以下各各項(xiàng)治療一、原發(fā)病病的治療應(yīng)積極尋找找原發(fā)病灶灶并予以徹徹底治療。。感染是導(dǎo)導(dǎo)致ARDS的常見見原因，而而且ARDS易并發(fā)發(fā)感染，所所以對于所所有的病人人都應(yīng)懷疑疑感染的可可能，除非非有明確的的其他導(dǎo)致致ARDS的原因存存在。宜選選擇廣譜抗抗生素。2004-07-272004-08-122004-08-142004-08-152004-08-172004-08-182004-08-202004-08-232004-08-252004-08-272004-08-302004-08-312004-09-012004-09-032004-09-072004-09-152004-09-202004-09-232004-09-272004-09-302004-10-082004-10-172004-10-24治療二、機(jī)機(jī)械通通氣機(jī)械通通氣是是ARDS最為為重要要的支支持治治療手手段。。在掌掌握ARDS呼呼吸力力學(xué)改改變特特點(diǎn)的的基礎(chǔ)礎(chǔ)上，，合理理的使使用機(jī)機(jī)械通通氣技技術(shù)對對于提提高ARDS的的搶救救成功功率具具有重重要意意義。。詳見下下述。。治療三、液液體管管理保持循環(huán)環(huán)系統(tǒng)較較低的前前負(fù)荷可可減少肺水水的含量量，有報(bào)報(bào)道可以以縮短上機(jī)時(shí)間間和降低低死亡率率。建議議在早期可給予予高滲晶晶體液，，此后可可給予膠體液，，同時(shí)限限制入量量，輔以以利尿劑劑，使出出入量保保持一定定水平的的負(fù)平衡衡，有條條件可監(jiān)監(jiān)測PAWP，，在不影影響心輸輸出量和和血壓的的情況下下盡量降降低PAWP。。必要時(shí)時(shí)可使用用多巴胺胺和多巴巴酚丁胺胺等血管管活性藥藥物。CritCareMed2002;30:2175-2182.Figure1.Changeinserumtotalproteinduringthestudy,withthetreatmentperiodidentifiedbytheshadedarea.Pointsrepresentmean,witherrorbarsindicatingsem.Figure3.Changeinoxygenation,asmeasuredbythePao2/Fio2ratio(mean±±sem),withthetreatmentperiodidentifiedbytheshadedarea.*Significantwithin-groupchangefrombaseline;?timepointswithsignificantbetween-groupdifferences.Amaximumof25%ofdatapointsmaybeabsentfromcalculationsrepresentedafterday5.Figure4.Changeinthemeanarterialpressure(mmHg)/heartrate(beats/min)ratio(MAP/HRratio)frombaseline.Thetreatmentperiodisindicatedbytheshadedarea.Pointsrepresentmeanvalues,witherrorbarsdepictingsem(mean±sem)ateachtimepoint.Figure5.Kaplan-Meierplotdepictingthepercentageofpatientsrequiringmechanicalventilationduringthe30-dayfollow-upperiod.Differencesbetweengroupsarenotstatisticallysignificant.CritCareMed2002;30:2175-2182.Patients:Thirty-sevenmechanically-ventilatedpatientswithacutelunginjuryandserumtotalprotein<=5.0g/dL.Interventions:Five-dayprotocolizedregimenof25gofhumanserumalbuminevery8hrswithcontinuousinfusionfurosemide,ordualplacebo,targetedtodiuresis,weightloss,andserumtotalprotein.MeasurementsandMainResults:Measuredoutcomesincludedchangeinweight,serumtotalprotein,fluidbalance,hemodynamics,respiratorysystemcompliance,andoxygenation.Baselinecharacteristicsweresimilarbetweengroups(treatment,n=19;control,n=18),withtraumabeingthemajorcauseofacutelunginjury.Diuresisandweightlossover5days(5.3kgmoreinthetreatmentgroup,p=.04)wasaccompaniedbyimprovementsinthePao2/Fio2ratiointhetreatmentgroupwithin24hrs(from171to236,p=.02).Respiratorymechanicswereunchanged.Meanarterialpressureincreasedfrom80to88mmHg(p=.10),andheartratedecreasedfrom110to95beats/min(p=.008)overtimeinthetreatmentgroup.Nodifferenceinmortalitywasobserved,withfavorabletrendsinmeasuresofintensivecare.Conclusions:Albuminandfurosemidetherapyimprovesfluidbalance,oxygenation,andhemodynamicsinhypoproteinemicpatientswithacutelunginjury.Determiningtheeffectofthissimpletherapyoncost,outcomes,andotherpatientpopulationsrequiresfurtherstudy.NEnglJMed2004;350:2247-2256.6997patientsBackgroundItremainsuncertainwhetherthechoiceofresuscitationfluidforpatientsinintensivecareunits(ICUs)affectssurvival.Weconductedamulticenter,randomized,double-blindtrialtocomparetheeffectoffluidresuscitationwithalbuminorsalineonmortalityinaheterogeneouspopulationofpatientsintheICU.ResultsOfthe6997patientswhounderwentrandomization,3497wereassignedtoreceivealbuminand3500toreceivesaline;thetwogroupshadsimilarbaselinecharacteristics.Therewere726deathsinthealbumingroup,ascomparedwith729deathsinthesalinegroup(relativeriskofdeath,0.99;95percentconfidenceinterval,0.91to1.09;P=0.87).Theproportionofpatientswithnewsingle-organandmultiple-organfailurewassimilarinthetwogroups(P=0.85).Therewerenosignificantdifferencesbetweenthegroupsinthemean(±±SD)numbersofdaysspentintheICU(6.5±6.6inthealbumingroupand6.2±6.2inthesalinegroup,P=0.44),daysspentinthehospital(15.3±9.6and15.6±9.6,respectively;P=0.30),daysofmechanicalventilation(4.5±±6.1and4.3±5.7,respectively;P=0.74),ordaysofrenal-replacementtherapy(0.5±±±2.0,respectively;P=0.41).ConclusionsInpatientsintheICU,useofeither4percentalbuminornormalsalineforfluidresuscitationresultsinsimilaroutcomesat28days.NEnglJMed2004;350:2247-2256.治療四、氧運(yùn)輸輸呼吸、循環(huán)環(huán)和血液系系統(tǒng)的功能能狀態(tài)共同同決定氧運(yùn)運(yùn)輸量的大大小。應(yīng)通通過合理的的液體療法法、氧療、、機(jī)械通氣氣、使用血血管活性藥藥物使氧運(yùn)運(yùn)輸量達(dá)最最佳水平，，而不應(yīng)只只著眼于某某一個(gè)臟器器的功能狀狀態(tài)。目前前尚無充分分證據(jù)表明明使氧運(yùn)輸輸量達(dá)到一一個(gè)超常水水平能降低低ARDS的死亡率率。治療五、肺外臟臟器功能的的支持和營營養(yǎng)支持近年年來來，，呼呼吸吸支支持持技技術(shù)術(shù)的的進(jìn)進(jìn)步步可可使使多多數(shù)數(shù)ARDS患患者者不不再再死死于于低低氧氧血血癥癥，，而而主主要要死死于于MODS。。ARDS可可使使肺肺外外臟臟器器功功能能受受損損，，而而肺肺外外臟臟器器功功能受受損損又又能能反反過過來來加加重重ARDS。。因因此此，，加強(qiáng)強(qiáng)液液體體管管理理，，盡盡早早開開始始腸腸內(nèi)內(nèi)營營養(yǎng)養(yǎng)，，注意意循循環(huán)環(huán)功功能能、、腎腎功功能能和和肝肝功功能能的支支持持對對于于防防止止MODS的的發(fā)發(fā)生生有有重重要意意義義。。AmJRespirCritCareMed,2004,169:638-644.Theaimofthisstudywastoevaluatetheeffectofparenteralnutritioncontainingmedium-andlong-chaintriglyceridesonthefunctionoftherespiratorysystemandtoinvestigatemechanismsinvolvedinthisprocess.Westudied13patientswithacuterespiratorydistresssyndrome(ARDS),8receivinglipidand5placebo,and6withoutARDS,receivinglipid.Bronchoalveolarlavage(BAL)wasperformedbeforeand1hourafteradministrationoflipidorplacebo.InpatientswithARDS,lipidadministrationresultedindeteriorationofoxygenation(PaO2/FIO2:from129±37to95±±42),complianceofrespiratorysystem(from39.2±±12to33.1±±9.2ml/cmH2O),andpulmonaryvascularresistance(from258±±47to321±±58dyne·s·cm-5).IntheBALfluidofthesamegroup,anincreaseintotalproteinandphospholipidconcentrations,phospholipaseactivities,platelet-activatingfactorandneutrophils,aswellasalterationsinBALlipidprofilewereobserved.NosignificantchangeswereobservedinthecontrolorintheARDS-Placebogroups.Inconclusion,thisstudyindicatesthatadministrationofmedium-andlong-chaintriglyceridesinpatientswithARDScausesalterationsinlungfunctionandhemodynamics.Inflammatorycells,possiblyactivatedbylipids,releasephospholipaseA2andplatelet-activatingfactor,enhancingedemaformation,inflammation,andsurfactantalterations.AmJRespirCritCareMed,2004,169:638-644.治療六、其其他藥藥物治治療皮質(zhì)激激素在在中晚晚期應(yīng)應(yīng)用可可能對對防止止肺纖纖維化化有一一定作作用。。對于于脂肪肪栓塞塞綜合合征和和卡氏氏肺囊囊蟲肺肺炎有有預(yù)防防和治治療作作用。。其他他抗炎炎制劑劑，如如PGE1抗內(nèi)毒毒素抗抗體、、IL-1受體體抗體體、PAF受體體拮抗抗劑、、抗TNF抗體體等，，均需需進(jìn)一一步研研究。。NEnglJMed2004;351:884-892.NEnglJMed2004;351:884-892.Figure1.Mean(±±SE)PaO2:FiO2ValuesintheControlGroupandtheSurfactantGroup.ThemeanPaO2:FiO2value,ameasureoftheblood-oxygenatingabilityofthelung,wassignificantlygreaterfrom4to24hoursaftertreatmentinthesurfactantgroupthaninthecontrolgroup.Figure2.NumberofVentilator-freeDaysintheControlGroupandtheSurfactantGroup.Patientswith0ventilator-freedaysincludedthosewhowereneverfreefrommechanicalventilationandthosewhodiedwithin28daysaftertreatment,regardlessoftheirneedformechanicalventilation.Therewerenosignificantdifferencesbetweenthetwogroups.Figure3.Nonpulmonary-OrganFailureduringthe28DaysafterTreatmentamongPatientswithARDSasaResultofDirectorIndirectLungInjury.DirectARDSwasdefinedasARDSduetopneumonia,aspiration,orboth.Thenumberofnonpulmonaryorgansthatfailed(withfailureofanorgandefinedasascoreof3or4SOFA)wassignificantlygreateramongpatientswithindirectARDSthanamongthosewithdirectARDS(P=0.02).NEnglJMed2004;351:884-892.MethodsIntwomulticenter,randomized,double-blindtrialsinvolving448patientswithARDSfromvariouscauses,wecomparedstandardtherapyalonewithstandardtherapyplusuptofourintratrachealdosesofarecombinantsurfactantproteinC––basedsurfactantgivenwithinaperiodof24hours.ResultsTheoverallsurvivalratewas66percent28daysaftertreatment,andthemediannumberofventilator-freedayswas0(68percentrange,0to26);therewasnosignificantdifferencebetweenthegroupsintermsofmortalityortheneedformechanicalventilation.Patientsreceivingsurfactanthadasignificantlygreaterimprovementinbloodoxygenationduringtheinitial24hoursoftreatmentthanpatientsreceivingstandardtherapy,accordingtobothunivariateandmultivariateanalyses.ConclusionsTheuseofexogenoussurfactantinaheterogeneouspopulationofpatientswithARDSdidnotimprovesurvival.Patientswhoreceivedsurfactanthadagreaterimprovementingasexchangeduringthe24-hourtreatmentperiodthanpatientswhoreceivedstandardtherapyalone,suggestingthepotentialbenefitofalongertreatmentcourse.NEnglJMed2004;351:884-892.ARDS的的機(jī)械通氣氣一、ARDS的呼吸吸力學(xué)特點(diǎn)點(diǎn)1．肺氣容容積減少2．病變的的非均一性性3．肺順應(yīng)應(yīng)性降低心臟SPARDS的的機(jī)械通氣氣二、呼吸機(jī)機(jī)所致肺損損傷1．肺氣壓壓傷(barotrauma)2．肺容積積傷(volutrauma)3．肺萎陷陷傷(atelectauma)4．肺生物物傷(biotrauma)ARDS的的機(jī)械通氣氣三、機(jī)械通通氣的策略略1．高呼氣氣末正壓策策略2．小潮氣氣量策略3．長吸氣氣策略4．肺開放放策略ARDS的的機(jī)械通氣氣四、通氣參參數(shù)的調(diào)節(jié)節(jié)1．吸氧濃濃度(FiO2)2．PEEP3．潮氣量量4．呼吸頻頻率的調(diào)節(jié)節(jié)5．吸呼比比(I／E)的調(diào)節(jié)節(jié)0204060VT（L）LIPUIPNEnglJMed1998;338:347-354.NEnglJMed1998;338:347-354.BackgroundInpatientswiththeacuterespiratorydistresssyndrome,

massivealveolarcollapseandcycliclungreopeningandoverdistention

duringmechanicalventilationmayperpetuatealveolarinjury.

Wedeterminedwhetheraventilatorystrategydesignedtominimize

suchlunginjuriescouldreducenotonlypulmonarycomplications

butalsomortalityat28daysinpatientswiththeacuterespiratory

distresssyndrome.

MethodsWerandomlyassigned53patientswithearlyacuterespiratory

distresssyndrome(including28describedpreviously),allof

whomwerereceivingidenticalhemodynamicandgeneralsupport,

toconventionalorprotectivemechanicalventilation.Conventional

ventilationwasbasedonthestrategyofmaintainingthelowest

positiveend-expiratorypressure(PEEP)foracceptableoxygenation,

withatidalvolumeof12mlperkilogramofbodyweightand

normalarterialcarbondioxidelevels(35to38mmHg).Protective

ventilationinvolvedend-expiratorypressuresabovethelower

inflectionpointonthestaticpressure–volumecurve,

atidalvolumeoflessthan6mlperkilogram,drivingpressures

oflessthan20cmofwaterabovethePEEPvalue,permissive

hypercapnia,andpreferentialuseofpressure-limitedventilatory

modes.

ResultsAfter28days,11of29patients(38percent)inthe

protective-ventilationgrouphaddied,ascomparedwith17of

24(71percent)intheconventional-ventilationgroup(P<0.001).

Theratesofweaningfrommechanicalventilationwere66percent

intheprotective-ventilationgroupand29percentintheconventional-ventilation

group(P=0.005);theratesofclinicalbarotraumawere7percent

and42percent,respectively(P=0.02),despitetheuseof

higherPEEPandmeanairwaypressuresintheprotective-ventilation

group.Thedifferenceinsurvivaltohospitaldischargewas

notsignificant;13of29patients(45percent)intheprotective-ventilation

groupdiedinthehospital,ascomparedwith17of24inthe

conventional-ventilationgroup(71percent,P=0.37).

ConclusionsAscomparedwithconventionalventilation,theprotective

strategywasassociatedwithimprovedsurvivalat28days,a

higherrateofweaningfrommechanicalventilation,andalower

rateofbarotraumainpatientswiththeacuterespiratorydistress

syndrome.Protectiveventilationwasnotassociatedwithahigher

rateofsurvivaltohospitaldischarge.

NEnglJMed1998;338:347-354.NEnglJMed2000;342:1301-1308,NEnglJMed2000;342:1301-1308,BackgroundTraditionalapproachestomechanicalventilationusetidalvolumesof10to15mlperkilogramofbodyweightandmaycausestretch-inducedlunginjuryinpatientswithacutelunginjuryandtheacuterespiratorydistresssyndrome.Wethereforeconductedatrialtodeterminewhetherventilationwithlowertidalvolumeswouldimprovetheclinicaloutcomesinthesepatients.ResultsThetrialwasstoppedaftertheenrollmentof861patientsbecausemortalitywaslowerinthegrouptreatedwithlowertidalvolumesthaninthegrouptreatedwithtraditionaltidalvolumes(31.0percentvs.39.8percent,P=0.007),andthenumberofdayswithoutventilatoruseduringthefirst28daysafterrandomizationwasgreaterinthisgroup(mean[±SD],12±11vs.10±±±0.8mlperkilogramofpredictedbodyweight(P<0.001),respectively,andthemeanplateaupressureswere25±6and33±8cmofwater(P<0.001),respectively.ConclusionsInpatientswithacutelunginjuryandtheacuterespiratorydistresssyndrome,mechanicalventilationwithalowertidalvolumethanistraditionallyusedresultsindecreasedmortalityandincreasesthenumberofdayswithoutventilatoruse.N