呼吸窘迫综合征-病历

呼吸窘迫综合征病 例男性,70岁,2001年1月9日入院咳嗽,咳痰12天,发热4天,呼吸困难1天12天前 咳嗽,咳黄粘痰,伴全身乏力4天前寒战高热,体温39.5

CCXR:肺部感染,右上肺膨胀不全头孢呋肟治疗无效1天前 呼吸困难,紫绀,伴血压下降(50/20mmHg)病 例入ICU时BT37.2

CHR130bpmBP84/40mmHg(DA10

g/kg/min)SpO278%双肺散在湿罗音病 例呼吸功能支持(SIMV+PSV)FiO2100%,PEEP10cmH2OSpO292%循环支持羟基淀粉500ml扩容无效DA13

g/kg/min–NE1.2

g/kg/minBP110/70mmHg病 例病 例能否在普通病房及时鉴别此类患者?是否会将ARDS作为诊断之一?如果患者收入ICU,应该进行哪些治疗?预后如何?“AdultRespiratoryDistressSyndrome”“TheacuteonsetofsevererespiratorydistressandcyanosisthatwasrefractorytooxygentherapyandassociatedwithdiffuseCXRabnormalityanddecreasedlungcompliance”Ashbaugh,Bigelow,Petty.Lancet1967WhatisARDS成人呼吸窘迫综合征Adultrespiratorydistresssyndrome急性呼吸窘迫综合征Acuterespiratorydistresssyndrome急性肺损伤AcutelunginjuryWhyisadefinitionimportant?肺损伤评分–Murray项目评分项目评分1.胸片(肺泡实变)3.PEEP(cmH2O)(机械通气时)无050限于1个象限16–81限于2个象限29–112限于3个象限312–1434个象限41542.PaO2/FiO24.呼吸系统顺应性(ml/cmH2O)3000800225–299160–791175–224240–592100–174320–393<1004194肺损伤评分–Murray肺损伤最终评分为评价项目的平均分.肺损伤评分无肺损伤0轻中度肺损伤0.1–2.5严重肺损伤(ARDS)>2.5Source:AdaptedfromMurrayJE,MaubayMA,LuceJM,FlickMR.Anexpandeddefinitionoftheadultrespiratorydistresssyndrome.AmRevRespirDis1988;138:720-723ARDS/ALI的定义综合征标准急性肺损伤急性起病PaO2/FiO2

300mmHg前后位CXR显示双肺浸润影PAWP18mmHg或无左房压升高的证据急性呼吸窘迫综合征急性起病PaO2/FiO2

200mmHg前后位CXR显示双肺浸润影PAWP18mmHg或无左房压升高的证据UnderrecognitionbycliniciansPatientwithautopsy138DADatautopsy42(30.4%)MentionofARDSinchart20(47.6%)FergusonND,Frutos-VivarF,EstebanA,Fernández-SegovianoP,AramburuJA,NájeraL,StewartTE.Acuterespiratorydistresssyndrome:Underrecognitionbycliniciansanddiagnosticaccuracyofthreeclinicaldefinitions.CritCareMed2005;33:2228-2234ChestX-Ray“Itwasfeltthatthechestradiographicinfiltratesshouldbebilateralandshouldbeconsistentwithpulmonaryedema,and,importantly,itwasfeltthattheseinfiltratescouldsometimesbeverymild.”BernardGRetal.AmJRespirCritCareMed1994;149:818X片判读的差异21名专家判读28张胸片43%:完全一致32%:明显差异%符合ALI/ARDS:36–71%Rubenfeldetal.Chest2000;118:566StandardventilatorsettingsandPaO2/FiO2ICUmortality52.9%ICUmortality12.5%FergusonND,KacmarekRM,ChicheJD,SinghJM,HallettDC,MehtaS,StewartTE.ScreeningofARDSpatientsusingstandardizedventilatorsettings:influenceonenrollmentinaclinicaltrial.IntensiveCareMed2004;30:1111–1116ARDS:clinicalcriteriavs.autopsy382ptswhounderwentclinicalautopsyDiffusealveolardamage:112(29%)AECCcriteria:127(33%)EstebanA,Fernandez-SegovianoP,Frutos-VivarF,AramburuJA,NajeraL,FergusonND,AliaI,GordoF,RiosF.ComparisonofClinicalCriteriafortheAcuteRespiratoryDistressSyndromewithAutopsyFindings.AnnInternMed2004;141:440-445.ARDS:clinicalcriteriavs.autopsyClinicalCriteriaforARDSNoClinicalCriteriaforARDSPtsDADNoDADDADNoDADAll(n=382)844328227Withriskfactors(n=284)844327130Pulmonaryriskfactors(n=106)27191743Extrapulmonaryriskfactors(n=178)57241087EstebanA,Fernandez-SegovianoP,Frutos-VivarF,AramburuJA,NajeraL,FergusonND,AliaI,GordoF,RiosF.ComparisonofClinicalCriteriafortheAcuteRespiratoryDistressSyndromewithAutopsyFindings.AnnInternMed2004;141:440-445.ARDS:clinicalcriteriavs.autopsyPtsSenSpe+veLR-veLRAll(n=382)75(66–82)84(79–88)4.7(3.5–6.3)0.3(0.2–0.4)Withriskfactors(n=284)76(67–83)75(68–81)3.0(2.3–4.0)0.3(0.2–0.5)Pulmonaryriskfactors(n=106)61(47–74)69(57–79)2.0(1.3–3.1)0.6(0.4–0.8)Extrapulmonaryriskfactors(n=178)85(75–92)78(70–85)3.9(2.7–5.7)0.2(0.1–0.3)EstebanA,Fernandez-SegovianoP,Frutos-VivarF,AramburuJA,NajeraL,FergusonND,AliaI,GordoF,RiosF.ComparisonofClinicalCriteriafortheAcuteRespiratoryDistressSyndromewithAutopsyFindings.AnnInternMed2004;141:440-445.ARDS:clinicalcriteriavs.autopsyGoldstandard:Diffusealveolardamageby2pathologistsClinicalcriteriaLunginjuryscore(LIS>2.5)AECCcriteriaDephidefinitionFergusonND,Frutos-VivarF,EstebanA,Fernández-SegovianoP,AramburuJA,NájeraL,StewartTE.Acuterespiratorydistresssyndrome:Underrecognitionbycliniciansanddiagnosticaccuracyofthreeclinicaldefinitions.CritCareMed2005;33:2228-2234ARDS:clinicalcriteriavs.autopsyDephidefinitionPaO2/FiO2

200mmHgwithPEEP10cmH2OBilateralairspacediseaseonchestradiographOnsetwithin72hoursNoclinicalevidenceofcongestiveheartfailure5a. PAWP18mmHgorLVEF40%5b. PresenceofarecognizedriskfactorforARDSCriteria1–4and5aand/or5bFergusonND,Frutos-VivarF,EstebanA,Fernández-SegovianoP,AramburuJA,NájeraL,StewartTE.Acuterespiratorydistresssyndrome:Underrecognitionbycliniciansanddiagnosticaccuracyofthreeclinicaldefinitions.CritCareMed2005;33:2228-2234ARDS:clinicalcriteriavs.autopsyPtsSensitivitySpecificityAECCdefinition83(72–95)51(41–61)LIS>2.574(61–87)77(69–86)Delphidefinition69(55–83)82(79–90)FergusonND,Frutos-VivarF,EstebanA,Fernández-SegovianoP,AramburuJA,NájeraL,StewartTE.Acuterespiratorydistresssyndrome:Underrecognitionbycliniciansanddiagnosticaccuracyofthreeclinicaldefinitions.CritCareMed2005;33:2228-2234PathologicalfindingsindefinitionpatientswithoutDADNo.(%)ofpatientsVariableAECC+veLIS+veDelphi+veTotal472217Pneumonia22(46.8)13(59.1)10(58.8)Pulmonaryembolism10(21.3)5(22.7)5(29.4)Cardiogenicpulmonaryedema5(10.6)1(4.5)1(5.9)Nosignificantfindings18(38.3)6(27.3)5(29.4)FergusonND,Frutos-VivarF,EstebanA,Fernández-SegovianoP,AramburuJA,NájeraL,StewartTE.Acuterespiratorydistresssyndrome:Underrecognitionbycliniciansanddiagnosticaccuracyofthreeclinicaldefinitions.CritCareMed2005;33:2228-2234ARDS/ALIDefinition–Bestwecandofornow…综合征标准急性肺损伤急性起病PaO2/FiO2

300mmHg前后位CXR显示双肺浸润影PAWP18mmHg或无左房压升高的证据急性呼吸窘迫综合征急性起病PaO2/FiO2

200mmHg前后位CXR显示双肺浸润影PAWP18mmHg或无左房压升高的证据ARDSAsyndromeoftenprogressiveandcharacterizedbydistinctclinical,pathological,andradiographicstagesARDS--incidenceStudiesBeforeTheIntroductionofAECCDefinitionARDS--incidenceStudiesAfterIntroductionofAECCDefinitionYear Nation Incidence Mortality (case/105/yr) (%)1999 Denmark 13.5 41.21995 Finland 4.9 421997 USA 12.6 --ARDS:危险因素直接肺损伤间接肺损伤胃内容物误吸严重感染严重胸部外伤严重非胸部外伤肺挫裂伤多发长骨骨折弥漫性肺部感染低血容量性休克细菌大量输血病毒急性胰腺炎卡氏肺囊虫药物过量有毒气体吸入再灌注损伤溺水肺移植术后心肺旁路术后TraumaShockSyndromes-Sepsis,CardiogenicGastricAspirationBurnsDiffusePneumoniasNearDrowningDrugOverdoseMetabolicEvents-Pancreatitis,UremiaSystemicMediatorReleaseAssociatedDiseasesDisseminatedIntravascularCoagulopathyCardiopulmonaryBypass --AnaphylaxisExtrapulmonaryInfection --TransfusionReactionARDS--riskfactorsARDS--riskfactorFrequencyofARDSAfterClinicalRiskARDS:分期渗出期(急性期) 0–4天增殖期 4–8天纤维化期 >8天恢复期ARDS的发展过程123456708101214911130.51.0EdemaHyalinemembranesInterstitialinflammationInterstitialfibrosisExudativestageProliferativestage回到最初的病例…诊断重症社区获得性肺炎ARDSSIRS最初治疗收入ICU细菌培养输液(200ml/hrNS)氧疗半坐位适当的抗生素ARDS–治疗原则治疗基础疾病!器官支持治疗肺其他器官避免并发症肺(气压伤,VALI…)感染(肺炎,其他…)其他(DVT,营养,应激性溃疡…)治疗基础疾病感染–抗生素,引流误吸–预防复发药物–鉴别并预防骨折–开放固定胰腺炎–支持,NPO,+/-抗生素支持治疗(肺)充分氧合充分通气(清除CO2)预防并发症充分氧合改善血流扩张肺动脉(NO)增加心输出量(液体/其他)改善通气PEEP反比通气复张手法患者体位液体治疗–‘drylungsarehappylungs’AcuteRespiratoryDistressSyndromeCurrentStatusConcerningManagementARDS--reviewTheacuterespiratorydistresssyndrome:definitions,severityandclinicaloutcome--ananalysisof101clinicalinvestigationsbyP.Krafftet.al.atotalof3264patientsIntensiveCareMed1996:22;519-29Ofthe101investigationsmeanmortalityrate 53%±22% (0-95%)meanPaO2/FiO2ratio 118±47 (35-270)meanAPACHEIIscore 21.3±6.6meanLIS 3.1±0.4nocorrelationbetweenLISandmortalityARDS--reviewARDS--reviewr=-0.11,p=0.28ConclusionnostatisticallysignificanttrendtowardsareductioninmortalityinthelatteryearsARDS--reviewPrimaryobjectivesmaintainnormalbloodlevelofoxygencarbondioxidethroughdeliveryofsupraphysiologictidalvolumewithoutrestrictionofairwaypressureSettingsPEEPlevel

10.9

4.2cmH2Omeantidalvolume

11.5

2.2ml/kgmeanRR

16.8

9bpmmeanPIP

39.4

8.6cmH2OAcuteRespiratoryDistressSyndromeWhynochangeinmortality?lessonsfrompathophysiologicalstudiesARDS--morphologyFRCandEELVreductioninARDSptsFromL.Puybasset,etal.Regionaldistributionofgasandtissueinacuterespiratorydistresssyndrome.I.Consequencesforlungmorphology.IntensiveCareMed2000;26:857-69.ARDS--morphologyTheconceptofBABYLUNGTheproportionoflungwhichcanbeventilatedreducedtoalmost20-30%ofanormallungInARDSthedecreaseinlungvolumedoesnotindicateadecreaseintotalthoracicvolume,butasimplereplacementofgasvolumewithtissuevolumeForm:GattinoniL,etal.Relationshipsbetweenlungcomputedtomographicdensity,gasexchangeandPEEPinacuterespiratoryfailure.Anesthesiology1988;69:824-32.ARDS--PVcurveUIPappearstocorrespondtotheonsetofalveolaroverinflationresultingfromexcessivetidalvolumeorpressure.LIPappearswhensufficientpressureisgeneratedtoopenatelectaticlungunits.Ventilator-InducedLungInjuryEffectof45cmH2Opeakairwaypressureventilationofincreasingdurationonindicesofpulmonaryedemainrats.ExtravascularlungwaterQwl/BW,drylungweightDLW/BW,andthedistributionspaceinlungsofI-labeledalbumin(Alb.Space)progressivelyincreasedasventilationwascontinued.After20minofmechanicalventilation,therewasadramaticincreaseinalledemaindices(p<0.01versusothergroups).Moreover,atthisstage,proteinaceoustrachealfluidwasregularlyfoundinthetrachea.(AdaptedfromDreyfussetal.AmRevRespirDis1985;132:880-884)ARDS--VILIBarotraumaVolutraumaAtelectraumaBiotraumaARDS--barotraumaBarotrauma:referstogrossairleaksduetothedevelopmentofanexcessivepressuredifferencebetweenanalveolusanditsadjacentbronchovascularsheathNormalratlungsPIP45,5minPIP45,20minsARDS--volutraumaVolutrauma:referstoamoresubtletypeoflunginjurythatcanoccursecondarytopulmonaryover-distentioninducedbymechanicalventilationAlveolaroverdistensionratherthanhighproximalairwaypressureperseistheprimarydeterminantofthisformofVALIthecriticalvariableforinjuryisnottheairwaypressureperse,butratherend-inspiratorylungvolumeorstretchDreyfussDP.AJRCCM1988;137:1159ARDS--barovsvolutraumaAtelectrauma:referstothedamagethatcanoccurwhenlungsareallowedtobecomeatelectaticandthenarere-expanded.collapse/re-expansiontobeacriticalfactorcausinginjury.

ARDS--atelectraumaTidalvolumeatlowairwaypressures:lunginjuryMuscedereJG,MullenJBM,GanK,etal.Tidalventilationatlowairwaypressurescanaugmentlunginjury.AmJRespirCritCareMed1994;149:1327–1334.TremblayLN,SlutskyAS.ProcAssocAmPhys1998;110:482ARDS--biotraumaBiotrauma:arelativelynewlydescribedresponsetomechanicalstresses,ischaracterizedbythereleaseofinflammatorymediatorsfromcellswithinthelung.Thesemediatorscancausefurtherinjurytolungtissueandtootherorgansystemsover-stretchingoflungcellsand/orallowingrecruitment/de-recruitmentofthelungcanleadtoanincreaseinlungcytokines.Control:VT7;PEEP3MVZP:VT15;PEEP0MVHP:VT15;PEEP10HVZP:VT40;PEEP0TremblayL.JClinInvest1997;99:944ARDS--biotraumaARDS--VALIIncidenceofbarotraumaARDS--UIPDecreasedFRC

.Lossofsurfaceareaofgasexchange.

Disruptionoflungarchitecture

.Increasedpulmonaryvascularresistance.Increasedsmallairwayresistance.

Diversionofdeliveredtidalvolumetocompliantlungunits.

Regionallunghyperinflation.

Inflammation.CapillaryLeak.Increasedsecretions.

Surfactantdeactivation.

DecreasedFRC.ARDS--MechanismofVALIFroeseAB,CritCareMed1997;25:906ARDS--ventilatorystrategyTherearetwoinjuryzonesduringmechanicalventilationLowLungVolumeVentilationtearsadhesivesurfacesHighLungVolumeVentilationover-distends,resultingin“Volutrauma”Thedifficultyisfindingthe“SweetSpot”LowMortalityassociatedwithLowVolumePressureLimitedVentilationwithPermissiveHypercapneainARDS

[Hicklingetal,IntensiveCareMed1990]70patientswithARDSPatientswithlowlungcompliance:PIPlimitedto30cmH2OVTaslowas350mL(5mL/kg)Volumeventilation(SIMV),highPEEP,spontaneousbreathing;noPSVresultedinhighRRandhigherPaCO2OUTCOMESActualMortality16%PredictedMortality39.6%NoPneumothoraciesARDS--lungprotectionEffectofaprotective-ventilationstrategyonmortalityintheacuterespiratorydistresssyndrome

[Amatoetal,NEnglJMed1998;338:347]53PatientswithearlyARDSRandomlyassignedtoeitherConventionalorProtectiveventilationstrategyAllpatientsweretreatedwithidenticalhemodynamicandgeneralsupport.

ConventionalVentilation

Protective-ventilationstrategyVt 12ml/kg

<6mL/kgPEEP

LowestPEEPtoFiO2

Setfromthelowerinflection pointPVcurvePCO2

35-45mmHg PermissiveHypercapneaPPLAT

38-46cmH2O Limitedto20cmabovePEEPAmatoMBP,NEnglJMed1998;338:347ARDS--studyofAmatoWhetherpreventingpersistingcollapseofrecruitableunits,reducingcycliclungreopeningandoverdistensionstretchwouldlowerratesofpulmonarycomplicationsandmortality.53ARDSpatientsCombinedopenlungapproach,permissivehypercapnea,limitingoverdistension,pressure-limitedmodes,andrecruitmentmaneuverTargetPaO2≧80mmHg,PEEP≧5cmH2OPEEPlevels,ventilatorymodes,andVTalldifferedbetweengroups,preventingassessmentoftherelativeimportanceofandsingleinterventionAmatoMBP,NEnglJMed1998;338:347ARDS--studyofAmatoConventionalApproachMaintainPaCO2:35–38mmHgVT:12ml/kgRR:10to24b/min,accordingtoPaCO2PEEP:adjusttokeepFiO2<0.6VolumecyclewithsquarewaveformProtectiveApproachAllowPaCO2upto80mmHgVT≦6ml/kgRR≦30b/minTotalPEEP:Pflex+2PC-IRV,PSVorVASPDrivingpressure(Pplat–PEEP)andPIP:keptbelow20and40cmH2ORecruitingmaneuverAmatoMBP,NEnglJMed1998;338:347ARDS--studyofAmatoResultsStewartNEnglJMed1998;338:355ARDS--StudyofStewartWhetherastrategyofmechanicalventilationthatplacedspecificlimitsonPIPandVTinpatientsathighriskforARDSwouldaffectin-hospitalmortality120highriskforARDSwithPaO2/FiO2<250atPEEP5,orpatientsofsepsisorburnregardlessofPaO2/FiO2IdealbodyweighttocalculateVTLimited-ventilationPIP≦30cmH2OVT≦8ml/kgConventional-ventilationPIP≦50cmH2OVT≦10to15ml/kgA/Cmodewithdeceleratingwave-formflow,pressure-controlifthresholdforPIPwasreachedPEEPrangefrom5to20cmH2OtomaintainFiO2

≦0.5withSaO289%to93%RR(5to35b/min)adjustedtokeepPaCO235to45mmHgHCO3-infusionifpH<7.0StewartTE,NEnglJMed1998;338:355ARDS--studyofStewartStewartTE,NEnglJMed1998;338:355ARDS--studyofStewartStewartTE,NEnglJMed1998;338:355ARDS--studyofStewartBrochardLAJRCCM1998;158:1831ARDS--studyofBrochardTocompareaconventionalapproachofactualroutinepracticewithastrategyaimedatlimitingtheplateaupressure.HumandataclearlysupportingpermissivehypercapniaislackingHypercapniaandacidosisaswellaspossibleriskofalveolarcollapsecouldbehazardous116ARDSwithoutotherorganfailureActualBWminusestimatedweightgainduetosaltwaterretentionMinimalFiO2usedtomaintainSaO2≧92to95%

BrochardLAJRCCM1998;158:1831ARDS--studyofBrochardPressurelimitation:VT:≦10ml/kg,butnot<6ml/kgor300ml,irrespectiveofPplatPplat:kept≦25cmH20bytitrationofVTRRorPFR:norecommendationHCO3-infusionifpH<7.05StandardtreatmentVT:10to15ml/kgRR:adjustedtokeepPaCO2between38to42mmHgNorequirementforpeakflowI:Eratio≦1ARDS--studyofBrochardARDSnetwork.NEnglJMed2000;342:1301ARDS--studyofARDSnetTodeterminewhethertheuseofalowerVTwouldimproveclinicaloutcomesinARDSUseoflowerVTwithALI/ARDSmayreduceinjuriouslungstretchandreleaseofinflammatorymediatorsThisapproachmaycauserespiratoryacidosis,anddecreasedarterialoxygenationandmayrequirechangesinthepriority(normalPaCO2andpHthanprotectionoflungfromexcessivestretchduringtraditionalapproach)LowerVT:InitialVT:6ml/kgReducedstepwise1ml/kgtokeepinspiratoryPplat≦

30cmH2O,orincreasedstepwise1ml/kgifPplat≦25cmH2OMinimalVT4ml/kgTraditionalVT:InitialVT:12ml/kgReducedstepwise1ml/kgtokeepinspiratoryPplat≦50cmH2O,orincreasedstepwise1ml/kgifPplat≦45cmH2OMinimalVT4ml/kgVolumeassist/controlmodeOxygenation:PaO2:55-80mmHgorSaO2:88-95%RR:6to35b/min,adjustedtokeeppH7.3to7.45ARDS--studyofARDSnetARDS--studyofARDSnetLowertidalvolumeTraditionaltidalvolumePvalueNo.ofpatients387405NATidalvolume(ml/kg)6.2

0.911.8

0.8<.05Plateaupressure(cmH2O)257339<.05Peakinspiratorypressure(cmH2O)3283910<.05Respiratoryrate(bpm)29

716

6<.05Minuteventilation(lpm)12.9

3.612.6

4.5NSPEEP(cmH2O)9.43.68.63.6<.05PaO2/FiO215873176

76<.05PaO2(mmHg)76237719NSPaCO2(mmHg)4010358<.05pH7.38

0.087.410.07<.05LowTidalVolumevs.TraditionalTidalVolumeVariableGroupreceivinglowertidalvolumesGroupreceivingtraditionaltidalvolumesPvalueDeathbeforedischargehomeandbreathingwithoutassistance(%)31.039.80.007Breathingwithoutassistancebyday28(%)65.755.0<0.001No.ofventilator-freedays,days1to28121110110.007Barotrauma,days1to28(%)10110.43No.ofdayswithoutfailureofnonpulmonaryorgansorsystems,days1to28151112110.006Kaplan–MeierCurveTheAcuteRespiratoryDistressSyndromeNetwork.Ventilationwithlowertidalvolumesascomparedwithtraditionaltidalvolumesforacutelunginjuryandtheacuterespiratorydistresssyndrome.NEnglJMed.2000;342:1301-1308ARDS--whyresultsvaryGreaterdifferenceinVTbetweengroupsARDSnet:6.2:11.8;Steward:7.2:10.8;Brochard:7.1:10.3Withadequatestatisticalpower(n=861)todetectthemoderateeffectsoflowerVTTreatmentofacidosisAllowingincreaseinRRandbicarbonateinfusiontocorrectmild-to-moderateacidosis,resultinginsmallerdifferencesinPaCO2andpHbetweengroupsthaninprevioustrialsARDSnet:PaCO2:41.5:35.5;pH:7.38:7.41(goal:7.3to7.45);Steward:54.4:45.7;7.29:7.34(lowlimit:7.0);Brochard:59.5:41.3;7.28:7.4(lowlimit:7.05)ALVEOLIStudy

Prospective,Randomized,Multi-CenterTrialofHigherPEEP/LowerFiO2versusLowerPEEP/HigherFiO2VentilationinAcuteLungInjuryandAcuteRespiratoryDistressSyndromeNIHNHLBIARDSNetworkALVEOLIStudyAssessmentofLowtidalVolumeandelevatedEnd-expiratoryvolumetoObviateLungInjuryAprospective,randomized,multicentertrialcompareclinicaloutcomesofptswithALI/ARDStreatedwithahigherEELV&lowerFIO2vsalowerEELV&higherFIO2Planforamaximumof750pts,withinterimanalysesat250and500ptsALVEOLIStudyThestudyhaltedinFeb2002afterenrollmentof550ptsafterthe2ndinterimanalysisNodifferencesdetectedinmortality,durationofMV,barotrauma,fluidbalance,orhemodynamicinstabilityinflammatorymeasures(IL-6,ICAM1,andSPD)BaselinedifferencestreatmentgroupolderandmorehypoxicButnotchangetheconclusionARDSNetwork–ALVEOLITrialAssessmentofLowtidalVolumeandelevatedEnd-expiratoryvolumetoObviateLungInjuryRCTof6ml/kgPBWvs.6ml/kgPBWPEEPsetbyPEEP/FiO2scaleNHLBIARDSClinicalTrialNetwork.HigherversusLowerPositiveEnd-ExpiratoryPressuresinPatientswiththeAcuteRespiratoryDistressSyndrome.NEnglJMed2004;351:327-36.ALVEOLI:

PaO2=55–80mmHgorSpO2=88–95%ControlPEEP558810121416–1820–24FiO2.3.4.4.5.5–.7.7.7–.9.91.0HigherPEEPPEEP121414161618202224FiO2.3.3.4.4.5.5.5–.8.8–.91.0NHLBIARDSClinicalTrialNetwork.HigherversusLowerPositiveEnd-ExpiratoryPressuresinPatientswiththeAcuteRespiratoryDistressSyndrome.NEnglJMed2004;351:327-36.ARDSnetAlveoliAtEntryPEEPLowHighPvalueAge48

154

1<0.0003PaO2/FiO2149

4137

40.056NHLBIARDSClinicalTrialNetwork.HigherversusLowerPositiveEnd-ExpiratoryPressuresinPatientswiththeAcuteRespiratoryDistressSyndrome.NEnglJMed2004;351:327-36.ALVEOLI–mortalitybeforehospitaldischargeUnadjustedP=0.58AdjustedP=0.44NHLBIARDSClinicalTrialNetwork.HigherversusLowerPositiveEnd-ExpiratoryPressuresinPatientswiththeAcuteRespiratoryDistressSyndrome.NEnglJMed2004;351:327-36.ALVEOLIStudyHigherPEEPorelevatedEELVdonotimproveoutcomeforALI/ARDSpatientsARDS--pronepositionExactmechanismunclearARDS--pronepositionAmulticenter,randomizedtrialproneposition(n=152)6ormorehoursdailyx10dayssupineposition(n=152)conventionaltreatmentGattinoniL,TognoniG,PesentiA,etal.Effectofpronepositioningonthesurvivalofpatientswithacuterespiratoryfailure.NEnglJMed2001;345:568-73OxygenationImprovedModestlyProneGattinoniL,TognoniG,PesentiA,etal.Effectofpronepositioningonthesurvivalofpatientswithacuterespiratoryfailure.NEnglJMed2001;345:568-73MeanChangeVariableSupinePronePvaluePaO28.526.815.026.40.04FiO2-7.617.6-12.718.70.02P/Fratio44.6

6863.068.00.02NoImprovementinSurvivalGattinoniL,TognoniG,PesentiA,etal.Effectofpronepositioningonthesurvivalofpatientswithacuterespiratoryfailure.NEnglJMed2001;345:568-73ARDS--pronepositionLimCM,KimEK,LeeJS,etal.Comparisonoftheresponsetothepronepositionbetweenpulmonaryandextrapulmonaryacuterespiratorydistresssyndrome.IntensiveCareMed2001;27:477-85Markedresponserateproneposition0.5hrARDSp 23%(7/31)ARDSexp 63%(10/16)proneposition2.0hrARDSp 29%(9/31)ARDSexp 63%(10/16)ARDS--pronepositionLimCM,KimEK,LeeJS,etal.Comparisonoftheresponsetothepronepositionbetweenpulmonaryandextrapulmonaryacuterespiratorydistresssyndrome.IntensiveCareMed2001;27:477-85**ARDSnetStudySummariesOngoingstudiesLateSteroidRescueStudyALVEOLIStudyHigherEELV/LowerFiO2vsLowerEELV/HigherFiO2VentilationPACStudyPACvsCVC"FluidConservative"vs."FluidLiberal"ARDS--pharmacologictxCorticosteroidsnotusefulintheacutemanagementofsepsisandARDSnooverallchangeinthemortalityofsepsisnoreductionintheincidenceofARDSsecondarytosepsisnoimprovementofphysiologicparameterspossibleroleofMIFARDS--pharmacologictxCorticosteroidsestablishedroleinfatembolismsyndromePneumocystiscariniipneumoniapotentialtreatmentforlate“fibroproliferative”phasesofARDS?LessonsfromMeduri’sstudyTreatmentofLate-PhaseARDSWithCorticosteroidsEntrycriteriaDiagnosisofARDS7daysofMVwithLIS2.5or<1reductionfromday1NountreatedinfectionMeduriGU,HeadleyAS,GoldenE,etal.Effectofprolongedmethylprednisolonetherapyinunresolvingacuterespiratorydistresssyndrome:arandomizedcontrolledtrial.JAMA.1998;280:159-165TreatmentofLate-PhaseARDSWithCorticosteroidsOutcomemeasuresonstudyday10MPplaceboPvalueNo.ofpatients168NAPaO2/FiO2262(19)148(35)<.001Lunginjuryscore1.7(0.1)3.0(0.2)<.001Patientswith>1-pointreductioninLIS,No.(%)16(100)2(25)<.001CrossedoverbecauseoffailuretoimproveLIS04.007Pulmonaryarterypressure22.5(3.2)30(2.7).01Successfulextubation,No.(%)7(44)0(0).05MODSscore0.7(0.2)1.8(0.3)<.001Infectionsper100patient-daysoftx87.99Newventilator-associatedpneumonia61.70Survivors,No.(%)16(100)6(75).10MeduriGU,HeadleyAS,GoldenE,etal.Effectofprolongedmethylprednisolonetherapyinunresolvingacuterespiratorydistresssyndrome:arandomizedcontrolledtrial.JAMA.1998;280:159-165TreatmentofLate-PhaseARDSWithCorticosteroidsMeduriGU,HeadleyAS,GoldenE,etal.Effectofprolongedmethylprednisolonetherapyinunresolvingacuterespiratorydistresssyndrome:arandomizedcontrolledtrial.JAMA.1998;280:159-165OutcomeMeasuresMPPlaceboPvalueSurvivorsofICUadmission,No.(%)16(100)3(37).002Survivorsofhospitaladmission,No.(%)14(87)3(37).03DeathassociatedwithunresolvingARDS,No.0of25of5NAMODS-freedaysbystudyday28,mean(SEM)16(2)6(2).005Durationofmechanicalventilaiton,median,d11.523.001TreatmentofLate-PhaseARDSWithCorticosteroidsComplicationsMPPlaceboPvaluePatientswithanewinfection12(75)6(75)NSNewinfections2410NSPneumonia9(38)1(10)NSSinusitis2(8)0(0)NSCatheter-relatedinfection3(12)3(30)NSUrinarytractinfection4(17)0(0)NSBacteremia2(8)4(40)NSCandidemia2(8)0(0)NSOthers2(8)2(20)NSNewpneumothorax2(12)4(50)NSReductioninhemoglobin>0.201(6)4(50)NSNewhyperglycemia(glucose>250mg/dL)5(31)4(50)NSMeduriGU,HeadleyAS,GoldenE,etal.Effectofprolongedmethylprednisolonetherapyinunresolvingacuterespiratorydistresssyndrome:arandomizedcontrolledtrial.JAMA.1998;280:159-165LateRescueStudyTheobjectiveiftheadministrationofcorticosteroidsinseverelate-phase