ARDS進(jìn)展（急性呼吸窘迫綜合征）-施煥中

1、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N EnglJMed2003;348:683-693.N EnglJMed2003;348:683-693.N EnglJMed2003;348:683-693.MethodsWeevaluated109 survivorsoftheacuterespiratorydistresssyndrome3,6,and12months after dischargefrom theintensivecareunit.Ateach visit,patientswere interviewedandunderwent

2、 aphysicalexamination, pulmonary-functiontesting,a six-minutewalktest,andaquality-of-lifeevaluation.ResultsPatientswhosurvivedthe acute respiratory distresssyndromewere young (medianage,45years)and severely ill(median Acute Physiology, Age,and ChronicHealth Evaluationscore,23) andhadalong stayinthe

3、intensivecare unit(median,25days).Patientshad lost18percentoftheirbase-linebodyweightbythe timetheywere dischargedfromtheintensive careunit andstatedthatmuscleweaknessand fatiguewerethereasonsfortheirfunctionallimitation.Lung volumeandspirometricmeasurementswerenormalby6months, butcarbonmonoxidediff

4、usioncapacityremainedlowthroughoutthe12-monthfollow-up.Nopatientsrequiredsupplementaloxygen at 12 months,but 6percentofpatientshadarterialoxygen saturationvalues below 88 percentduringexercise. Themedianscorefor thephysicalrole domainoftheMedicalOutcomesStudy36-item Short-FormGeneralHealthSurvey(ahe

5、alth-relatedquality-of-life measure) increasedfrom 0at3monthsto25at12months (scoreinthenormal population,84). Thedistancewalkedinsix minutesincreased fromamedianof281mat3 monthsto422mat12months; allvalueswerelowerthan predicted.The absenceofsystemiccorticosteroidtreatment, theabsence of illnessacqui

6、redduring theintensivecare unitstay,and rapid resolutionoflunginjuryandmultiorgandysfunctionwere associatedwithbetterfunctionalstatusduringtheone-yearfollow-up.ConclusionsSurvivorsofthe acute respiratory distress syndromehave persistentfunctionaldisability oneyear after dischargefrom theintensivecar

7、eunit.Most patients haveextrapulmonaryconditions,with musclewasting andweaknessbeingmost prominent.N EnglJMed2003;348:683-693.定義ALI/ARDS是指由心心源性以以外的各各種肺內(nèi)內(nèi)外致病病因素導(dǎo)導(dǎo)致的急急性、進(jìn)進(jìn)行性缺缺氧性呼呼吸衰竭竭。ALI/ARDS具有性質(zhì)質(zhì)相同的的病理生生理改變變，嚴(yán)重重的ALI即被定義為ARDS。ALI/ARDS以肺微血血管通透透性增加加、肺氣氣容積減減少、肺肺順應(yīng)性性降低和和嚴(yán)重肺肺內(nèi)分流流及通氣氣/血流比例例失調(diào)為為病理生生理特點(diǎn)點(diǎn)，臨床床

8、表現(xiàn)為為不易緩緩解的急急性進(jìn)行行性缺氧氧性呼吸吸衰竭，胸部X線可見(jiàn)肺肺部浸潤(rùn)潤(rùn)征象。高危因素素一、直接接肺損傷傷因素嚴(yán)重肺部部感染、胃內(nèi)容容物吸入入、溺水水、吸入入有毒氣氣體、肺肺挫傷、氧中毒毒等。二、間接接肺損傷傷因素膿毒癥、休克、嚴(yán)重非非胸部創(chuàng)創(chuàng)傷、重重癥胰腺腺炎、大大量輸血血、輸液液、體外外循環(huán)、DIC等。發(fā)病機(jī)制制一、血管管內(nèi)皮和和氣道上上皮損傷傷二、中性性粒細(xì)胞胞介導(dǎo)的的肺損傷傷三、其他他炎癥機(jī)機(jī)制細(xì)胞因子子表面活性性物質(zhì)呼吸機(jī)引引起的肺肺損傷其他損傷傷機(jī)制四、機(jī)化化性肺泡泡炎發(fā)病機(jī)制制TheNormal Alveolus (Left-HandSide)and theInjured

9、Alveolus in theAcutePhaseofAcuteLung Injuryandthe Acute Respiratory Distress Syndrome (Right-Hand Side).Intheacutephaseofthe syndrome (right-hand side),thereissloughingofboththebronchial andalveolarepithelial cells,with theformationofprotein-rich hyalinemembranes on thedenuded basement membrane.Neut

10、rophilsareshownadheringtothe injuredcapillary endothelium andmarginatingthrough theinterstitiuminto theairspace, which is filledwith protein-richedemafluid.Inthe airspace,analveloarmacrophage is secretingcytokines, interleukin-1, 6, 8, and10,(IL-1, 6, 8, and10)and tumor necrosis factor(TNF- ), which

11、 actlocally to stimulatechemotaxis andactivateneutrophils.Macrophagesalsosecrete other cytokines,including interleukin-1, 6, and10.Interleukin-1canalsostimulatethe productionofextracellularmatrixbyfibroblasts. Neutrophils canrelease oxidants,proteases,leukotrienes, andotherproinflammatorymolecules,s

12、uch as platelet-activatingfactor (PAF).A numberofantiinflammatorymediatorsare alsopresentinthealveolarmilieu,includinginterleukin-1receptorantagonist,soluble tumor necrosis factorreceptor,autoantibodiesagainst interleukin-8, andcytokinessuchasinterleukin-10and11(notshown). Theinfluxofprotein-rich ed

13、ema fluid intothe alveolus hasledtothe inactivationofsurfactant.MIFdenotesmacrophage inhibitoryfactor.發(fā)病機(jī)制制管狀髓磷磷脂發(fā)病機(jī)制制Surfactant Productionand RecyclingintheNormal Alveolus (PanelA)andChangesinSurfactant MetabolisminAcuteLungInjury(Panel B).Inthenormal alveolus,surfactant is synthesized andpackagedi

14、nto lamellar bodiesinthecellcytoplasm. These lamellar bodiesthen migratetothe cellmembrane, withwhichtheyfuse,andthenarereleasedintotheairfluid interfacewithinthe alveolus.They subsequentlyform an intermediatetubular stage of surfactantcalled tubularmyelin,whichfinally produces thefunctional coating

15、layer. Surfactantproteinsare alsoinvolvedinthe coatingprocess.Surfactantrecyclingoccurs throughtheendocytosisofsmallvesicles.Alterationsinsurfactantmetabolism (PanelB)mayoccuratany of these steps.Theexactpathophysiologyofsurfactant metabolisminARDShasnot beenfullyestablished, butitislikelytoconsisto

16、fboth thedestructionandthe structuralalterationofsurfactant lipidsandproteincausedbythe inflammatorymilieuofthe injuredair space.Inaddition,synthesis andrecyclingofsurfactantarelikely to be reducedand itsfunctionimpairedbytheaccumulation ofproteinaceousmaterialwithinthe alveolus.TNFdenotestumornecro

17、sisfactor.病理2 d14d14d病理4 d14dPanelA shows alung-biopsyspecimenobtainedfroma patienttwo daysafterthe onset of thesyndromeasa resultoftheaspirationofgastric contents.Characteristichyaline membranesareevident(arrow),with associatedintraalveolarredcellsand neutrophils,findingsthat areconsistent withthe

18、pathologicaldiagnosisofdiffusealveolardamage(hematoxylinandeosin, x90). PanelsB andC showlung-biopsyspecimens obtained 14 daysafterthe onset of sepsis-associated acute lunginjury andtheacuterespiratorydistresssyndrome. Panel Bshowsgranulationtissue in thedistalair spaceswith achronicinflammatory-cel

19、linfiltrate (hematoxylinandeosin, x60).TrichromestaininginPanelC revealscollagendeposition(darkblue areas)inthegranulationtissue,a findingthatisconsistent withthe depositionofextracellularmatrixinthe alveolar compartment (x60).PanelD shows aspecimenoflungtissuefroma patientwho diedfourdays after the

20、onsetofacutelung injuryandthe acute respiratory distress syndrome;thereisinjurytoboththecapillary endothelium andthealveolarepithelium.Thereisanintravascularneutrophil (LC)inthe capillary(C). Vacuolizationand swelling of theendothelium(EN) areapparent.Lossofalveolarepithelial cells is alsoapparent,

21、withthe formationofhyaline membranesontheepithelialside of thebasementmembrane(BM*).PanelEshowsa specimen of lungtissue obtained fromapatient duringthefibrosing-alveolitisphaseinwhichthereisevidenceofreepithelializationoftheepithelialbarrier withalveolarepithelialtype II cells.Thearrowindicates atyp

22、icaltype II cellwithmicrovilliandlamellarbodies containingsurfactant.The epithelialcellimmediatelyadjacenttothis cellisinthe processofchangingtoatype Icell,withflattening,loss of lamellar bodies,andmicrovilli. Theinterstitiumisthickened, withdepositionofcollagen(C).臨床表現(xiàn)現(xiàn)一、大多多起病急急劇，進(jìn)進(jìn)展快。二、呼吸吸困難、窘迫，一般

23、氧氧療難以以糾正。三、體格格檢查：早期可可無(wú)明顯顯異常，較多見(jiàn)見(jiàn)呼吸頻頻數(shù)。唇唇指發(fā)紺紺，心率率增加，肺部聽(tīng)聽(tīng)診可聞聞及于羅羅音或哮哮鳴音，后期出出現(xiàn)濕羅羅音并呈呈肺實(shí)變變體征。四、胸部部X線表現(xiàn)：早期可可無(wú)異常常,或呈輕度度間質(zhì)改改變，表表現(xiàn)為紋紋理增多多、邊緣緣模糊，繼之出出現(xiàn)斑片片狀或大大片狀陰陰影，后后期兩肺肺可出現(xiàn)現(xiàn)廣泛實(shí)實(shí)變。X線PanelA shows ananteroposteriorchestradiograph froma42-year-oldmanwiththeacuterespiratorydistresssyndromeassociatedwith gram-nega

24、tivesepsis whowasreceiving mechanicalventilation. Thepulmonary-artery wedge pressure,measuredwith apulmonary-arterycatheter,was 4mmHg. There arediffuse bilateralalveolaropacitiesconsistentwith thepresenceofpulmonaryedema. Panel Bshowsananteroposteriorchestradiograph froma60-year-oldmanwithacutelung

25、injuryandthe acute respiratory distress syndrome whohadbeenreceivingmechanicalventilationforsevendays.Reticular opacitiesarepresentthroughout bothlungfields, afindingsuggestive of thedevelopmentoffibrosingalveolitis. Panel CshowsaCTscan of thechestobtainedduringthe acute phase.Thebilateral alveolar

26、opacitiesaredenser in thedependent, posteriorlung zones,with sparingofthe anterior lungfields.Thearrows indicate thickenedinterlobularsepta, consistentwiththepresenceofpulmonary edema.Thebilateral pleuraleffusions area commonfinding.PanelD shows aCTscanofthechestobtainedduring thefibrosing-alveoliti

27、sphase.Thereare reticularopacitiesand diffuseground-glass opacitiesthroughout bothlungfields, anda large bulla is presentinthe leftanteriorhemithorax.診斷標(biāo)準(zhǔn)準(zhǔn)一、有發(fā)發(fā)病的高高危因素素。二、急性性起病，呼吸頻頻數(shù)和（或）呼呼吸窘迫迫。三、低氧氧血癥：ALI時(shí)PaO2/FiO2300 mmHg；ARDS時(shí)PaO2/FiO2200 mmHg。四、胸部部X線檢查兩兩肺浸潤(rùn)潤(rùn)影響。五、PCWP18 mmHg或臨床上上能除外外心源性性肺水腫腫。返符合以以

28、上5項(xiàng)者可診診斷為ALI或ARDS。一、不把把是否行行機(jī)械通通氣和行行機(jī)械通通氣的時(shí)時(shí)間納入入診斷標(biāo)標(biāo)準(zhǔn)。二、不強(qiáng)強(qiáng)調(diào)PEEP對(duì)氧合的的影響。三、為了了動(dòng)態(tài)觀觀察病情情變化，對(duì)上機(jī)機(jī)患者應(yīng)應(yīng)盡量在在相同的的通氣條條件下進(jìn)進(jìn)行前后后比較。四、PaO2/FiO2難于排除除通氣功功能障礙礙對(duì)氧合合的影響響。在臨臨床應(yīng)用用中以PAAO2可以更好好地反映映ARDS的病理生生理特點(diǎn)點(diǎn)，從而而提高ARDS診斷的特特異性，應(yīng)用時(shí)時(shí)宜注意意氧濃度度的影響響。診斷時(shí)應(yīng)應(yīng)注意以以下各項(xiàng)項(xiàng)五、ARDS胸片的表表現(xiàn)缺少少特異性性，在不不同的原原發(fā)病和和不同的的時(shí)期可可有不同同的表現(xiàn)現(xiàn)，可以以為間質(zhì)質(zhì)或?qū)嵸|(zhì)質(zhì)，散在在或彌

29、漫漫，可輕輕可重，但進(jìn)展展迅速。六、若能能除外左左房壓高高，PAWP對(duì)診斷ARDS并非必須須，但對(duì)對(duì)無(wú)典型型胸片或或不能完完全從臨臨床表現(xiàn)現(xiàn)除外左左房高壓壓的患者者，必須須有PAWP作為診斷斷條件。七、有慢慢性肺病病者（如如肺間質(zhì)質(zhì)纖維化化、結(jié)節(jié)節(jié)病等），即使使達(dá)到ARDS的診斷標(biāo)標(biāo)準(zhǔn)也不不納入ARDS。診斷時(shí)應(yīng)應(yīng)注意以以下各項(xiàng)項(xiàng)治療一、原發(fā)發(fā)病的治治療應(yīng)積極尋尋找原發(fā)發(fā)病灶并并予以徹徹底治療療。感染染是導(dǎo)致致ARDS的常見(jiàn)原原因，而而且ARDS易并發(fā)感感染，所所以對(duì)于于所有的的病人都都應(yīng)懷疑疑感染的的可能，除非有有明確的的其他導(dǎo)導(dǎo)致ARDS的原因存存在。宜宜選擇廣廣譜抗生生素。2004-07

30、-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)械械通氣機(jī)械通氣氣是ARDS最為重要要的支持持治療手手段。在在掌握ARDS呼吸力學(xué)學(xué)改變特特點(diǎn)的基基礎(chǔ)上，合理的的使用機(jī)機(jī)械通氣氣技術(shù)對(duì)對(duì)于提高

31、高ARDS的搶救成成功率具具有重要要意義。詳見(jiàn)下述述。治療三、液體體管理保持循環(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(cè)PAWP，在不影響響心輸出出量和血血壓的情情況下盡盡量降低低PAWP。必要時(shí)可可使用多多巴胺和和多巴酚酚丁胺等等血管活活性藥物物。Crit CareMed 2002; 30:2175-2182.Figure1. Changeinserumtotalprotein duringthes

32、tudy, withthe treatmentperiodidentifiedbytheshadedarea.Pointsrepresentmean,witherrorbarsindicatingsem.Figure3. Changeinoxygenation,asmeasuredbythe Pao2/Fio2ratio(meansem),with thetreatmentperiod identifiedbytheshadedarea. *Significantwithin-groupchange frombaseline; time pointswith significant betwe

33、en-groupdifferences. Amaximumof25%ofdatapointsmay be absentfrom calculationsrepresentedafterday5.Figure4. Changeinthemeanarterialpressure(mmHg)/heart rate(beats/min)ratio(MAP/HRratio)frombaseline.The treatmentperiodisindicated by theshadedarea.Pointsrepresentmeanvalues, witherrorbarsdepictingsem(mea

34、nsem) at eachtimepoint.Figure5. Kaplan-Meierplot depictingthepercentageofpatientsrequiringmechanicalventilationduringthe 30-dayfollow-upperiod.Differencesbetween groupsarenot statisticallysignificant.Crit CareMed 2002; 30:2175-2182.Patients:Thirty-seven mechanically-ventilated patients withacutelung

35、injuryand serum total protein=5.0g/dL.Interventions:Five-dayprotocolizedregimen of 25 gofhumanserumalbuminevery8 hrswith continuousinfusionfurosemide, or dualplacebo,targetedtodiuresis, weightloss,andserumtotalprotein.Measurementsand MainResults:Measuredoutcomesincludedchange in weight,serumtotalpro

36、tein,fluidbalance,hemodynamics, respiratory systemcompliance,andoxygenation. Baseline characteristicswere similarbetweengroups(treatment,n= 19;control,n =18),with traumabeingthemajorcauseofacutelunginjury.Diuresisandweight lossover5 days(5.3kgmore in thetreatmentgroup,p= .04)was accompanied by impro

37、vementsinthePao2/Fio2ratiointhetreatment group within24hrs(from171 to 236,p= .02). Respiratory mechanicswere unchanged.Meanarterialpressureincreasedfrom80to88mmHg(p= .10), andheartrate decreasedfrom 110to95beats/min(p= .008) overtimeinthetreatment group.Nodifference in mortalitywasobserved, withfavo

38、rable trendsinmeasuresofintensivecare.Conclusions:Albuminandfurosemidetherapy improves fluid balance, oxygenation,andhemodynamicsinhypoproteinemicpatientswith acute lunginjury.Determiningtheeffect of thissimple therapyoncost,outcomes, andotherpatient populations requires furtherstudy.N EnglJMed2004;

39、350:2247-2256.6997 patientsBackgroundItremains uncertainwhether thechoiceofresuscitationfluidforpatientsinintensive careunits(ICUs) affectssurvival.Weconductedamulticenter, randomized, double-blindtrialtocompare theeffectoffluidresuscitationwith albuminorsalineonmortalityinaheterogeneous populationo

40、fpatientsintheICU.ResultsOfthe6997patientswhounderwent randomization, 3497were assigned to receivealbuminand3500toreceive saline;thetwo groupshadsimilarbaselinecharacteristics. There were726deaths in thealbumin group,ascomparedwith 729deathsinthesaline group (relativerisk of death,0.99;95percentconf

41、idence interval,0.91 to 1.09; P=0.87). Theproportion ofpatientswith newsingle-organand multiple-organ failurewassimilar in thetwogroups (P=0.85).Therewere no significantdifferencesbetween thegroupsinthe mean(SD)numbersofdays spent in theICU(6.56.6inthe albumingroupand6.26.2inthesaline group,P=0.44),

42、days spentinthehospital(15.39.6 and15.69.6,respectively;P=0.30),days of mechanicalventilation(4.56.1and4.35.7,respectively; P=0.74), or daysofrenal-replacementtherapy (0.52.3 and0.42.0,respectively; P=0.41).ConclusionsInpatientsintheICU,useofeither 4percentalbumin or normalsalinefor fluid resuscitat

43、ionresultsinsimilar outcomes at 28 days.N EnglJMed2004;350:2247-2256.治療四、氧運(yùn)運(yùn)輸呼吸、循循環(huán)和血血液系統(tǒng)統(tǒng)的功能能狀態(tài)共共同決定定氧運(yùn)輸輸量的大大小。應(yīng)應(yīng)通過(guò)合合理的液液體療法法、氧療療、機(jī)械械通氣、使用血血管活性性藥物使使氧運(yùn)輸輸量達(dá)最最佳水平平，而不不應(yīng)只著著眼于某某一個(gè)臟臟器的功功能狀態(tài)態(tài)。目前前尚無(wú)充充分證據(jù)據(jù)表明使使氧運(yùn)輸輸量達(dá)到到一個(gè)超超常水平平能降低低ARDS的死亡率率 。治療五、肺外外臟器功功能的支支持和營(yíng)營(yíng)養(yǎng)支持持近年來(lái)，呼吸支支持技術(shù)術(shù)的進(jìn)步步可使多多數(shù)ARDS患者不再再死于低低氧血癥癥，而主主要死于

44、于MODS。ARDS可使肺外外臟器功功能受損損，而肺肺外臟器器功能受損又又能反過(guò)過(guò)來(lái)加重重ARDS。因此，加強(qiáng)液體體管理，盡早開(kāi)開(kāi)始腸內(nèi)內(nèi)營(yíng)養(yǎng)，注意循環(huán)環(huán)功能、腎功能能和肝功功能的支持對(duì)對(duì)于防止止MODS的發(fā)生有有重要意義。AmJ RespirCrit CareMed,2004,169: 638-644.Theaim of thisstudywas to evaluate theeffectofparenteralnutritioncontainingmedium- andlong-chain triglyceridesonthefunctionofthe respiratory system

45、andtoinvestigatemechanismsinvolvedinthis process. We studied13patientswithacuterespiratorydistresssyndrome(ARDS), 8receiving lipid and5 placebo, and6 withoutARDS,receiving lipid.Bronchoalveolarlavage(BAL)was performedbeforeand 1hourafteradministrationoflipidorplacebo.Inpatientswith ARDS, lipid admin

46、istrationresultedindeterioration of oxygenation (PaO2/FIO2: from129 37 to 95 42),compliance of respiratory system(from39.2 12to33.1 9.2ml/cmH2O),andpulmonaryvascularresistance(from25847to32158dynescm-5).IntheBAL fluid of thesamegroup,anincreaseintotalproteinandphospholipid concentrations,phospholipa

47、se activities, platelet-activatingfactor andneutrophils,aswell as alterations in BALlipidprofile wereobserved. Nosignificantchanges wereobservedinthe controlorinthe ARDS-Placebogroups. In conclusion, thisstudyindicates thatadministrationofmedium- andlong-chain triglyceridesinpatientswithARDScausesal

48、terationsinlungfunctionandhemodynamics.Inflammatorycells,possiblyactivated by lipids,releasephospholipase A2andplatelet-activatingfactor, enhancingedemaformation, inflammation,andsurfactantalterations.AmJ RespirCrit CareMed,2004,169: 638-644.治療六、其他他藥物治治療皮質(zhì)激素素在中晚晚期應(yīng)用用可能對(duì)對(duì)防止肺肺纖維化化有一定定作用。對(duì)于脂脂肪栓塞塞綜合征征和卡

49、氏氏肺囊蟲(chóng)蟲(chóng)肺炎有有預(yù)防和和治療作作用。其其他抗炎炎制劑，如PGE1抗內(nèi)毒素素抗體、IL-1受體抗體體、PAF受體拮抗抗劑、抗抗TNF抗體等，均需進(jìn)進(jìn)一步研研究。N EnglJMed2004;351:884-892.N EnglJMed2004;351:884-892.Figure1.Mean (SE) PaO2:FiO2Valuesinthe ControlGroupand theSurfactant Group.ThemeanPaO2:FiO2value,ameasure of theblood-oxygenatingability of thelung,wassignificantlyg

50、reater from4to24hoursaftertreatmentinthe surfactantgroupthaninthecontrolgroup.Figure2.NumberofVentilator-free Daysinthe ControlGroupand theSurfactant Group.Patientswith 0ventilator-free daysincludedthosewho wereneverfreefrom mechanicalventilationand those whodied within28days after treatment,regardl

51、essoftheirneed formechanical ventilation.Therewere no significant differences betweenthe twogroups.Figure3.Nonpulmonary-OrganFailureduringthe 28 DaysafterTreatment among Patients withARDSasa ResultofDirectorIndirectLungInjury. DirectARDS wasdefined as ARDSdue to pneumonia,aspiration,orboth.The numbe

52、rofnonpulmonaryorgansthatfailed(withfailureofanorgandefined as ascoreof3or4 SOFA) wassignificantly greateramongpatientswithindirectARDS thanamongthosewithdirectARDS(P=0.02).N EnglJMed2004;351:884-892.MethodsIntwomulticenter, randomized, double-blindtrialsinvolving448 patients withARDSfrom variouscau

53、ses,wecomparedstandardtherapy alone withstandardtherapyplus up to fourintratrachealdosesofa recombinant surfactantproteinCbasedsurfactant given withina periodof24hours.ResultsTheoverallsurvivalrate was66percent 28 daysaftertreatment, andthemedian numberofventilator-freedayswas0 (68percent range,0 to

54、 26);therewas no significant differencebetween thegroupsintermsofmortality or theneed formechanicalventilation.Patientsreceiving surfactanthad asignificantlygreater improvement in blood oxygenation duringtheinitial24hoursoftreatmentthanpatientsreceivingstandardtherapy,accordingtobothunivariateandmul

55、tivariate analyses.ConclusionsTheuse of exogenoussurfactant in aheterogeneouspopulation of patients withARDSdidnot improvesurvival. Patientswhoreceivedsurfactanthadagreater improvement in gasexchangeduringthe 24-hourtreatment periodthan patients whoreceivedstandardtherapy alone,suggesting thepotenti

56、albenefitofa longertreatmentcourse.N EnglJMed2004;351:884-892.ARDS的機(jī)械通通氣一、ARDS的呼吸力力學(xué)特點(diǎn)點(diǎn) 1肺氣容容積減少少2病變的的非均一一性3肺順應(yīng)應(yīng)性降低低 心臟SPARDS的機(jī)械通通氣二、呼吸吸機(jī)所致致肺損傷傷 1肺氣壓壓傷(barotrauma)2肺容積傷傷(volutrauma)3肺萎陷傷傷(atelectauma)4肺生物傷傷(biotrauma)ARDS的機(jī)械通通氣三、機(jī)械械通氣的的策略 1高呼氣氣末正壓壓策略2小潮氣氣量策略略3長(zhǎng)吸氣氣策略4肺開(kāi)放放策略ARDS的機(jī)械通通氣四、通氣氣參數(shù)的的調(diào)節(jié) 1吸氧濃濃

57、度(FiO2)2PEEP3潮氣量4呼吸頻頻率的調(diào)調(diào)節(jié)5吸呼比比(IE)的調(diào)節(jié)0204060VT（L）LIPUIPN EnglJMed1998;338:347-354.N EnglJMed1998;338:347-354.BackgroundInpatientswith theacuterespiratorydistresssyndrome,massive alveolar collapse andcycliclungreopeningandoverdistentionduringmechanicalventilationmayperpetuatealveolarinjury.

58、Wedetermined whetheraventilatorystrategydesignedtominimizesuch lunginjuriescouldreduce notonly pulmonarycomplicationsbutalsomortalityat28daysinpatientswith theacuterespiratorydistresssyndrome.MethodsWerandomlyassigned53patientswith early acute respiratorydistresssyndrome(including 28 describedprevio

59、usly),all ofwhom werereceiving identicalhemodynamicandgeneralsupport,toconventionalorprotectivemechanical ventilation.Conventionalventilationwasbasedonthe strategy of maintaining thelowestpositiveend-expiratorypressure(PEEP)for acceptableoxygenation,with atidalvolume of 12 ml perkilogramofbody weigh

60、tandnormalarterialcarbon dioxidelevels (35to38mmHg). Protectiveventilationinvolvedend-expiratorypressuresabovethe lowerinflection point on thestaticpressurevolume curve,a tidal volumeofless than6mlperkilogram, drivingpressuresofless than20cmofwaterabovethe PEEPvalue, permissivehypercapnia, andprefer