Noninvasive Mechanical Ventilation
Antonio M. Esquinas (Editor)
Noninvasive Mechanical Ventilation Theory, Equipment, and Clinical Applications
AntonioM.Esquinas AvenidadelParque,2,3B 30500Murcia MolinaSegura Spain e-mail:
[email protected]
ISBN:978-3-642-11364-2
e-ISBN:978-3-642-11365-9
DOI:10.1007/978-3-642-11365-9 SpringerHeidelbergDordrechtLondonNewYork LibraryofCongressControlNumber:2010925792 ©Springer-VerlagBerlinHeidelberg2010 Thisworkissubjecttocopyright.Allrightsarereserved,whetherthewholeorpartofthematerialis concerned,speci callytherightsoftranslation,reprinting,reuseofillustrations,recitation,broadcasting, reproductiononmicro lmorinanyotherway,andstorageindatabanks.Duplicationofthispublication orpartsthereofispermittedonlyundertheprovisionsoftheGermanCopyrightLawofSeptember9, 1965,initscurrentversion,andpermissionforusemustalwaysbeobtainedfromSpringer.Violations areliabletoprosecutionundertheGermanCopyrightLaw. The use of general descriptive names, registered names, trademarks, etc. in this publication does not imply,evenintheabsenceofaspeci cstatement,thatsuchnamesareexemptfromtherelevantprotective lawsandregulationsandthereforefreeforgeneraluse. Productliability:Thepublisherscannotguaranteetheaccuracyofanyinformationaboutdosageand applicationcontainedinthisbook.Ineveryindividualcasetheusermustchecksuchinformationby consultingtherelevantliterature. Coverdesign:eStudioCalamar,Figueres/Berlin Printedonacid-freepaper SpringerispartofSpringerScience+BusinessMedia(www.springer.com)
Contents
SectionI InterfaceTechnologyinCriticalCareSettings 1 FullMaskVentilation.......................................................................................... FrancisCordovaandManuelJimenez
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2 HelmetContinuousPositiveAirwayPressure:TheoryandTechnology........ GiacomoBellani,StefanoIsgrò,andRobertoFumagalli
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3 HelmetContinuousPositiveAirwayPressure:ClinicalApplications............ 13 AlbertoZanella,AlessandroTerrani,andNicolòPatroniti SectionII V entilatoryModesandVentilators: Theory,Technology,andEquipment 4 PressureSupportVentilation.............................................................................. 21 EnricaBertellaandMicheleVitacca 5 VentilatorsforNoninvasiveMechanicalVentilation........................................ 27 RaffaeleScala 6 N oninvasivePositivePressureVentilationUsingContinuous PositiveAirwayPressure..................................................................................... 39 PedroCaruso 7 HomeMechanicalVentilators............................................................................. 45 FrédéricLofaso,BrigitteFauroux,andHélènePrigent 8 MaintenanceProtocolforHomeVentilationCircuits...................................... 51 MichelToussaintandGregoryReychler 9 NocturnalNoninvasiveMechanicalVentilation................................................ 59 DavidOrlikowski,HassanSka ,andDjillaliAnnane
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SectionIII Patient VentilatorInteractions 10 P atient VentilatorInteractionDuringNoninvasive Pressure-SupportedSpontaneousRespirationinPatients withHypercapnicChronicObstructivePulmonaryDisease........................... 67 WulfPankow,AchimLies,andHeinrichBecker 11 AsynchronyandCyclicVariabilityinPressureSupportVentilation.............. 73 AntoineCuvelierandJean-FrançoisMuir 12 C arbonDioxideRebreathingDuring NoninvasiveMechanicalVentilation.................................................................. 77 FrancescoMojoliandAntonioBraschi 13 C arbonDioxideRebreathingDuringPressureSupport VentilationwithAirwayManagementSystem(BiPAP)Devices..................... 83 FrédéricLofasoandHélènePrigent 14 CarbonDioxideRebreathinginNoninvasiveVentilation................................ 87 DanielSamolskiandAntonioAntón 15 N ewAdaptiveServo-Ventilation DeviceforCheyne StokesRespiration.............................................................. 93 Ken-ichiMaenoandTakatoshiKasai SectionIV MonitoringandComplications 16 N octurnalMonitoringintheEvaluationofContinuous PositiveAirwayPressure.....................................................................................101 OresteMarrone,AdrianaSalvaggio, AnnaLoBue,andGiuseppeInsalaco 17 ComplicationsDuringNoninvasivePressureSupportVentilation.................107 MicheleCarron,UldericoFreo,andCarloOri SectionV C hronicApplicationsofNoninvasive MechanicalVentilationandRelatedIssues 18 E f cacyofContinuousPositiveAirwayPressure inCardiovascularComplicationsofObstructiveSleepApnea.......................121 AhmedS.BaHammamandMohammedK.A.Chaudhry 19 ObstructiveSleepApneaandAtherosclerosis...................................................131 R.Schulz,F.Reichenberger,andK.Mayer 20 T ransnasalInsuf ation ANewApproachin theTreatmentofOSAs........................................................................................135 GeorgNilius,BrianMcGinley,andHartmutSchneider
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21 C ardiopulmonaryInterventionstoProlongSurvival inPatientswithDuchenneMuscularDystrophy..............................................143 YukaIshikawa 22 N oninvasiveVentilationPressureAdjustments inPatientswithAmyotrophicLateralSclerosis................................................149 KirstenL.Gruis 23 N oninvasivePositivePressureVentilation inAmyotrophicLateralSclerosis.......................................................................153 DanieleLoCoco,SantinoMarchese,andAlbinoLoCoco 24 N oninvasiveMechanicalVentilationasanAlternative toEndotrachealIntubationDuringTracheotomy inAdvancedNeuromuscularDisease.................................................................161 DavidOrlikowski,HélènePrigent,andJésusGonzalez-Bermejo 25 N oninvasiveMechanicalVentilationinPatients withMyasthenicCrisis........................................................................................167 CristianeBrennerEilertTrevisan,SilviaReginaRiosVieira, andRenataPlestch 26 P redictorsofSurvivalinCOPDPatientswithChronic HypercapnicRespiratoryFailureReceivingNoninvasive HomeVentilation..................................................................................................171 StephanBudweiser,RudolfA.Jörres,andMichaelPfeifer 27 W ithdrawalofNoninvasiveMechanicalVentilation inCOPDPatientswithHypercapnicRespiratoryFailure...............................179 JacoboSellares,MiquelFerrer,andAntoniTorres 28 N oninvasiveVentilationinPatientswithAcute ExacerbationsofAsthma....................................................................................185 SeanP.Keenan 29 N oninvasivePositivePressureVentilation DuringAcuteAsthmaticAttack.........................................................................191 ArieSoroksky,IsaacShpirer,andYuvalLeonov 30 N oninvasivePositivePressureVentilation forLong-TermVentilatoryManagement..........................................................199 AkikoTokiandMikioSumida 31 HomeVentilationforChronicObstructivePulmonaryDisease......................205 Georg-ChristianFunk
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SectionVI C riticalCareApplicationsofNoninvasiveMechanical VentilationandRelatedIssues 32 C urrentStrategiesandEquipment forNoninvasiveVentilationinEmergencyMedicine.......................................217 KeisukeTomii 33 NoninvasiveVentilationOutsideofIntensiveCareUnits................................223 DavideChiumello,GaetanoIapichino,andVirnaBerto 34 N oninvasivePositiveAirwayPressureandRisk ofMyocardialInfarctioninAcuteCardiogenicPulmonaryEdema...............231 GiovanniFerrari,AlbertoMilan,andFrancoAprà 35 T heRoleofContinuousPositiveAirwayPressureinAcute CardiogenicPulmonaryEdemawithPreservedLeftVentricular SystolicFunction:APreliminaryStudy............................................................237 AndreaBellone 36 N oninvasiveVentilationinAcuteLungInjury/ AcuteRespiratoryDistressSyndrome...............................................................241 RiteshAgarwal 37 N oninvasivePositivePressureVentilationinAcute HypoxemicRespiratoryFailureandinCancerPatients.................................249 S.EgbertPravinkumar 38 NoninvasiveVentilationasaPreoxygenationMethod.....................................257 ChristopheBaillard 39 I n uenceofStaffTrainingontheOutcomeofNoninvasive VentilationforAcuteHypercapnicRespiratoryFailure..................................263 JoséLuisLópez-CamposandEmiliaBarrot SectionVII TheRoleofSedation 40 SedationforNoninvasiveVentilationinIntensiveCare...................................269 Jean-MichelConstantin,RenauGuerin,andEmmanuelFutier 41 UseofDexmedetomidineinPatientswithNoninvasiveVentilation................273 ShinhiroTakeda,ShinjiAkada,andKeikoNakazato SectionVIII W eaningfromConventional MechanicalVentilationandPostextubationFailure 42 E xtubationandDecannulationofUnweanablePatients withNeuromuscularWeakness...........................................................................279 JohnRobertBach
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43 M echanicallyAssistedCoughingandNoninvasive VentilationforExtubationofUnweanablePatients withNeuromuscularDiseaseorWeakness........................................................287 JohnRobertBach 44 N oninvasivePositivePressureVentilationin thePostextubationPeriod...................................................................................295 HasanM.Al-DorziandYaseenM.Arabi 45 NoninvasiveVentilationinPostextubationRespiratoryFailure.....................305 RiteshAgarwal SectionIX I ntraoperativeandPostoperative IndicationsforNoninvasiveMechanicalVentilation 46 IntraoperativeUseofNoninvasiveVentilation.................................................317 FabioGuarracinoandRubiaBaldassarri 47 NoninvasiveVentilationinAdultLiverTransplantation.................................321 PaoloFeltracco,StefaniaBarbieri,andCarloOri 48 N oninvasivePositivePressureVentilation inPatientsUndergoingLungResectionSurgery..............................................327 ChristophePerrin,ValérieJullien,YannickDuval, andFabienRolland SectionX NoninvasiveMechanicalVentilation inNeonatesandChildren 49 E quipmentandTechnologyforContinuousPositive AirwayPressureDuringNeonatalResuscitation..............................................335 GeorgM.SchmölzerandColinJ.Morley 50 A irLeakageDuringContinuousPositiveAirway PressureinNeonates............................................................................................343 GerdSchmalisch 51 TheUseofNoninvasiveVentilationintheNewborn........................................357 DebbieFraserAskin 52 N asalHigh-FrequencyVentilation: ClinicalStudiesandTheirImplications............................................................363 KatarzynaDabrowskaandWaldemarA.Carlo 53 BubbleContinuousPositiveAirwayPressure...................................................369 J.JanePillow
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54 N oninvasiveMechanicalVentilationwithPositive AirwayPressureinPediatricIntensiveCare....................................................377 GiancarloOttonello,AndreaWol er,andPietroTuo 55 H omeMechanicalVentilationinChildren withChronicRespiratoryFailure......................................................................387 SedatOktem,Re kaErsu,andElifDagli Index.............................................................................................................................397
Abbreviations
ACPE AHI AHRF ALI ALS ARDS ARF ASV BiPAP BNP BPD CAD CCHS CF CHF CHRF CO2 COPD CPAP CPE CPF CRF CSA CSR CSR-CSA DMD DR ED EELV EPAP ETCO2
Acutecardiogenicpulmonaryedema Apneahypopneaindex Acutehypercapnicrespiratoryfailure Acutelunginjury Amyotrophiclateralsclerosis Acuterespiratorydistresssyndrome Acuterespiratoryfailure Adaptiveservo-ventilation Bi-levelpositiveairwaypressure Brainnatriureticpeptide Bronchopulmonarydysplasia Coronaryarterydisease Congenitalcentralhypoventilationsyndrome Cystic brosis Congestiveheartfailure Chronichypercapnicrespiratoryfailure Carbondioxide Chronicobstructivepulmonarydisease Continuouspositiveairwaypressure Cardiogenicpulmonaryedema Coughpeak ows Chronicrespiratoryfailure Centralsleepapnea Cheynestokesrespiration Cheyne-stokesrespirationwithcentralsleepapnea Duchennemusculardystrophy Deliveryroom Emergencydepartment Endexpiratorylungvolume Expiratorypositiveairwaypressure CO2attheendofexpiration
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ETI ETO2 EV f f/Vt FAO2 FiCO2 FiO2 FRC Ftot FVC GPB hCO2 HTN HVC ICU IMT IPAP IPPV ITE Leaki LVEF MAC MEP MIC MIP MMRC MRSA MV MWD N NIMV NIPPV NIPSV NIV NMD NNPV NO NPPV NPSV ON OLTx OSA P[A=a]O2
Abbreviations
Endotrachealintubation End-tidalO2 Exhaustvent Respiratoryrate Respiratoryfrequency/tidalvolume Alveolarfractionofoxygen CO2inspiredfraction Inspiratedfractionofoxygen Functionalresidualcapacity Totalgas owpassingthroughthehelmet Forcedvitalcapacity Glossopharyngealbreathing Meancarbondioxideconcentrationinsidethehelmet Hypertension Homeventilationcircuits Intensivecareunit Intimamediathickness Inspiratorypositiveairwaypressure Intermittentpositivepressureventilation Inspiratorytriggeringefforts Differentde nitionsofairleakage(i=1,2,3) Leftventricularejectionfraction Mechanicallyassistedcoughing Maximalexpiratorypressure Maximuminsuf ationcapacity Maximalinspiratorypressure Modi edmedicalresearchconcil MethicillinresistantStaphylococcusaureus Mechanicalventilation 6-minutewalkingdistance Nasal Noninvasivemechanicalventilation Noninvasivepositivepressureventilation Noninvasivepressuresupportventilation Noninvasiveventilation Neuromuscularweakness Noninvasivepositivepressure Nasaloral Noninvasivepositivepressureventilation Noninvasivepressuresupportventilation Oronasal Livertransplantation Obstructivesleepapnea Arterialoxygenpressuregradient
Abbreviations
PaCO2 PaO2 PAP PAV PCV PEEP PPO PSV PTP RASSScore RCPAP RCTs RDI RDS REM RLeak RR SBT SCI SDB SGRQ SINP SMA1 SMT SNIPPV SpO2 Texp TFM Ti Ti/Ttot Ti Tinsp TNI TPPV TV Vinsp VAP V/CO2 V/Q VC VD/VT Vexp VFBA VFBT VT
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Carbondioxidetension Arterialpressureofoxygen Positiveairwaypressure Proportionalassistventilation Pressurecontrolledventilation Positiveendexpiratorypressure Potentiallypathogenicorganism Pressuresupportventilation Dipressuretimeproduct Richmondagitationsedationscalescore ResistanceoftheCPAPinterface Randomizedcontrolledtrials Respiratorydisturbanceindex Respiratorydistresssyndrome Rapideyemovement Airleakageresistance Respiratoryrate Spontaneousbreathingtrial Spinalcordinjury Sleepdisorderedbreathing St.George srespiratoryquestionnaire Sniffnasalinspiratorypressure Spinalmuscularatrophytype1 Standardmedicaltreatment Synchronizednasalintermittentpositivepressureventilation Oxygenhemoglobinsaturation Expiratorytime Totalfacemask Inspiratorytime Inspiratorytime/totaltime Inspiratorytime Inspiratorytime Treatmentwithnasalinsuf ation Tracheostomypositivepressureventilation Tidalvolume Inspiredvolume Ventilation-associatedpneumonia Patient scarbondioxidemetabolicproduction Ventilation/perfusionratio Vitalcapacity Vitalvolumeratio Expiredvolume Ventilator-freebreathingability Ventilatorfreebreathingtime Tidalvolume
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VPat Vmeas VLeak VE δVexp maxVCPAP V Pat, means
QOL WOB
Abbreviations
Air owofthepatient Flowmeasuredbythe owsensor Leakage ow Minuteventilation Volumeerrorofthedisplayedexpiratoryvolume MaximalCPAP ow Measuredpatient ow Qualityoflife Workofbreathing
Section I Interface Technology in Critical Care Settings
Full Mask Ventilation
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FrancisCordovaandManuelJimenez
1.1 Introduction Noninvasivepositivepressureventilation(NPPV)hasbecomeanintegralpartofventilator supportinpatientswitheitheracuteorchronicrespiratoryfailure.NPPVhasbeenshown toavoidtheneedforinvasivemechanicalventilation,it sassociatedcomplicationsand facilitate successful extubation in patients with chronic obstructive pulmonary disease (COPD) who have marginal weaning parameters. In addition, some studies [1 3] have shown that NPPV improves survival compared with invasive mechanical ventilation in patientswithacuterespiratoryfailure.Moreover,NPPVhasbeenshowntobeaneffective modalityforthetreatmentofchronicrespiratoryfailureinpatientswithrestrictiveventilatorydisorders[4 6]andinselectedpatientswithCOPD[7,8].Comparedwithinvasive ventilation,NPPVdecreasedtheriskofventilator-associatedpneumoniaandoptimized comfort.Becauseofitsdesign,successdependslargelyonpatientcooperationandacceptance.SomefactorsthatmaylimittheuseofNPPVaremask-(orinterface-)relatedproblems such as air leaks, mask intolerance due to claustrophobia and anxiety, and poorly ttingmask.Approximately10 15%ofpatientsfailtotolerateNPPVduetoproblems associatedwiththemaskinterfacedespiteadjustmentsinstraptension,repositioning,and trialofdifferenttypesofmasks.Othermask-relatedproblemsincludefacialskinbreakdown,aerophagia,inabilitytohandlecopioussecretions,andmaskplacementinstability. Themostcommonlyusedinterfacesinbothacuteandlong-termsettingsarenasaland nasal-oral(NO)masks.Thefollowingreviewstheapplicationsoffull-facemaskinpatients whoareunabletotolerateaconventionalmaskduringNPPV.
F.Cordova()andM.Jimenez DivisionofPulmonaryMedicineandCriticalCareMedicine, TempleUniversityHospital,3401NBroadStreet,Philadelphia,PA19140-5103,USA e-mail:
[email protected];
[email protected] A.M.Esquinas(ed.), NoninvasiveMechanicalVentilation, DOI:10.1007/978-3-642-11365-9_1,©Springer-VerlagBerlinHeidelberg2010
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1.2 Total-Face Mask During NPPV AwidevarietyofmaskinterfaceshasbecomeavailabletodeliverNPPV.ThemostcommoninusearenasalandNO(orfull-face)masks.AlargerversionoftheNOmask,the total-facemask(TFM;Fig.1.1)couldbeusedasanoptiontoimprovepatientacceptance andpossiblyimprovegasexchangeandavoidintubationandmechanicalventilation.This maskcoversthewholeanteriorsurfaceofthefaceanddeliverseffectiveventilationviathe nasalandoralroutes.Crinerandcolleagues[9]comparedtheef cacyofNPPVviaTFM maskversusnasalorNOmasksinpatientswithchronicrespiratoryfailure.Theirstudy showed that NPPV via TFM in selected patients with chronic respiratory failure may improvecomfort,minimizeairleakfromthemaskinterface,andimprovealveolarventilation.Theyalsosuggestedthatthisformofmaskmaybeeffectiveinpatientssufferingfrom acuterespiratoryfailurewhoarecandidatesfornoninvasivemechanicalventilationina controlledenvironmentsuchastheintensivecareunit(ICU).We[10]alsoreviewedretrospectively13casesofacuterespiratoryfailure;thisanalysisshowedthatNPPVwassuccessfullyaccomplishedviaTFMinpatientswhowerepreviouslyunabletotolerateNPPV viaconventionalnasalorNOmasks.NPPVviaTFMimprovedgasexchangewithincreased pH,improvedgasoxygenationlevels,anddecreasedhypercapnia.Inthemajorityofthe patients,NPPVwaswelltoleratedwithoutdislodgementofthemaskorsigni cantneed forreadjustment.Complicationsfromtreatmentwereminimalandgenerallydidnotlead toaninterruptionintherapy.Thistypeofmaskwasalsoratedbypatientsasmorecomfortablethanthestandardfull-facemaskinapreliminaryreport[11]. BecausetheTFMcoverstheentireface,onewouldthinkthatthiswouldworsenfeelings of claustrophobia rather than improve them. However, Criner and colleagues [9] observedthatthissensationwasavoidedwiththeuseofTFMinsomeofthepatientswho werenotabletotolerateanNOmask.Potentialexplanationsforthisincludeunobstructed eldofvisionforthepatient;theabilitytocommunicateverbally;andthesensationofair owingovertheentirefacewhileusingthemask.
Fig.1.1 Differenttypes ofmaskavailablefor theNPPVinterface. Notethelargersizeof theTFM
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Full Mask Ventilation
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Concerns have been raised about the TFM. Since this form of face mask has much largervolume,ithasasigni cantlygreateramountofdeadspacecomparedwithother commerciallyavailableformsofnasalandNOmasks,butstreamingofair owdirectly fromtheinlettothepatient snoseandmouthappearstominimizethisproblem. Othercomplications,suchaseyeirritationandgastricdistention,wouldbeexpectedto bemorecommonduringNPPVwithaTFM.However,anincreaseintheseproblemshas notbeenreportedinanyofthestudies. The ef cacy of nasal and NO masks has been compared in a controlled trial of 26patientswithCOPDandrestrictivethoracicdisease.TheNOmasksweremoreeffectiveinloweringPaco2,perhapsbecauseofthegreaterairleakassociatedwiththenasal mask[12].Thissupportsthebeliefthat,intheacutesetting,nasal-oralmasksarepreferabletonasalmasksbecausedyspneicpatienttendtobemouthbreathers,predisposingto greaterairleakage.
1.3 Discussion Full-facemaskshavebeenusedmainlyonpatientswithacuterespiratoryfailurebutmay alsobeusefulforchronicventilatorysupport.Full-facemasksmaybepreferredforpatients withcopiousairleakingthroughthemouthduringnasalmaskventilation.Asnoted,the TFMisanoptionforpatientswhofailNPPVviamoreconventionalnasalorNOmasks. Patient traits or preferences may still favor the selection of one particular device over another.Regardlessofthemaskselected,proper tisofparamountimportanceinoptimizingthecomfortandsuccessofNPPV.Practitionersmustbepreparedtotrydifferentmask sizesandtypesinanefforttoenhancepatientcomfort. Insummary,NPPVviaaTFMinselectedpatientswithacuteorchronicrespiratory failure may improve comfort, minimize air leaking from the mask face interface, and improve alveolar ventilation in patients who fail NPPV with conventional oral or NO interface.
Key Recommendations
› › ›
AirleakageandclaustrophobiaassociatedwithNPPVmaybeovercomebyusing afull-facemask. TFMisaninterfaceoptiontoprovideNPPVinpatientswhofailtheuseof conventionaltypesofmasks(nasalornasal-oral). Practitionersmustbepreparedtotrydifferentmasktypesandsizesinaneffortto enhancethecomfortandsuccessofNPPV.
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References 1. AuriantI,JallotA,HervePetal(2001)Noninvasiveventilationreducesmortalityinacute respiratoryfailurefollowinglungresection.AmJRespirCritCareMed164:1231 1235 2. CarlucciA,RichardJC,WysockiM,LepageEetal(2001)Noninvasiveversusconventional mechanicalventilation.Anepidemiologicsurvey.AmJRespirCritCareMed163:874 880 3. BottJ,CarrollMP,ConwayJHetal(1993)Randomizedcontrolledtrialofnasalventilationin acuteventilatoryfailureduetochronicobstructiveairwaysdisease.Lancet341:1555 1557 4. KerbyGR,MayerLS,PingletonSK(1987)Nocturnalpositivepressurevianasalmask.Am RevRespirDis135:738 740 5. BachJR,AlbaAS(1990)Managementofchronicalveolarhypoventilationbynasalventilation.Chest97:148 152 6. LegerP,JennequinJ,GerardMetal(1989)Homepositivepressureventilationvianasalmask for patients with neuromuscular weakness or restrictive lung or chest wall disease. Respir Care34:73 79 7. GayPC,PatelAM,ViggianoRW,HubmayerRD(1991)Nocturnalnasalventilationfortreatmentofpatientswithhypercapnicrespiratoryfailure.MayoClinProc66:695 703 8. CarreyZ,GottfriedSB,LevyRD(1990)Ventilatorymusclesupportinrespiratoryfailurewith nasalpositivepressureventilation.Chest97:150 158 9. CrinerGJ,TravalineJM,BrennanKJetal(1994)Ef cacyofanewfullfacemaskfornon invasivepositivepressureventilation.Chest106:1109 1115 10. BruceRoyMD,CordovaF,TravalineJetal(2007)Fullfacemaskfornoninvasivepositive pressure ventilation in patients with acute respiratory failure. J Am Osteopath Assoc 107(4):148 156 11. LieschingTN,CromierK,NelsonDetal(2003)TotalfacemaskTMvsstandardfullface mask for noninvasive therapy of acute respiratory failure. Am J Respir Crit Care Med 167:A996 12. NavalesiP,FanfullaF,FrigeiroPetal(2000)Physiologicevaluationofnoninvasivemechanicalventilationdeliveredwiththreetypesofmasksinpatientswithchronichypercapnicrespiratoryfailure.Chest28:1785 1790
Helmet Continuous Positive Airway Pressure: Theory and Technology
2
GiacomoBellani,StefanoIsgrò,andRobertoFumagalli
2.1 Introduction Continuouspositiveairwaypressure(CPAP)isadministeredtopatientstomaintainthe airwayataselectedpressure(usuallynamedthepositiveend-expiratorypressure,PEEP) higherthanthatoftheatmosphereone.PEEPapplicationhasseveralwell-knowneffects ontherespiratorysystemandhemodynamics,whosedescriptionisnotamongtheaimsof thischapter.Theappliedpressureiskeptconstantthroughoutthewholerespiratorycycle sothatintrapulmonarypressureswingsaroundthesetlevel.Patientscanbreathspontaneously at the selected pressure without any active support of inspiration; it follows that CPAPcannotbestrictlyconsideredaformof ventilation.
2.2 Helmet Technology Thehelmetinterface[1]wasconceivedtodeliverhighoxygenconcentrationsduring hyperbarictherapy.Sincetheninetiesithasbeenincreasinglyused,particularlyinthe southernEuropeancountries,todelivernoninvasiveventilation.Thehelmetconsistsof asofttransparentplastichoodbuiltonahardplasticring.Asilicon/polyvinylchloride softcollarbuiltontheringprovidesapneumaticsealattheneck,whilethehoodcontainsthepatient sentirehead.Thepresenceoftwoormoreinletsandoutletsenables connectionofstandardventilatortubingfortheexpiratoryandinspiratoryportsofthe circuitandtheinsertionofnasogastrictubesandstraws.Thecollarprovidesagood sealwithoutmajorcompressionatcontactpoints.Thelackofpressurepointsonthe
G.Bellani(),S.Isgrò,andR.Fumagalli DepartmentofExperimentalMedicine,Milano-BicoccaUniversity,Monza,Italyand DepartmentofPerioperativeandIntensiveCareMedicine,SanGerardoHospital,Monza,Italy e-mail:
[email protected];
[email protected];
[email protected] A.M.Esquinas(ed.), NoninvasiveMechanicalVentilation, DOI:10.1007/978-3-642-11365-9_2,©Springer-VerlagBerlinHeidelberg2010
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faceavoidsskinnecrosisandpain,reducesdiscomfort,andimprovespatienttolerance. The seal around the neck allows the use of the helmet also in patients with dif cult anatomicalsituationsthatcommonlydonotallowtheuseofafacemask,suchasin edentulouspatients,patientswithafullbeard,orpatientswithfacialtrauma.Thehelmet allows the patients to see, read, talk, and interact more easily than with other devices. Differentcompaniesproducevariousadult,pediatric,andneonataltypesandsizesof helmets,eachprovidedwithvarious xingandsafetyfeatures.Adulthelmetsareeasily heldinplacebytwostrapspositionedundertheaxillae.Codazzietal.[2]introducedan interestingtechniquetoprovidehelmetCPAPtopreschoolchildrenbyemployinga babybody wornunderthepubicregionasadiaperand xedtotheplasticring.Inasinglecenter prospective study, this system was effective in delivering CPAP and was well tolerated.Amodi edhelmethasbeendevelopedtodeliverCPAPtopreterminfants[3]; thesealedhoodismountedontheupperpartofthebed,towhichtheinspiratorylineofthe circuit is connected. Another port is provided for expiratory exit; a threshold valve is mountedheretogeneratePEEP.Inaddition,intheupperpartofthehoodthereisapressure release valve that prevents excessive pressure in the system. Pressure, inspiratory fractionofoxygen,andtemperatureinthechamberarecontinuouslymonitored.Thepressurechamberiskeptseparatefromtherestofthebedbyatransparent,latex-free,polyurethanemembrane.Thecone-shapedmembranehasaholeinthemiddletoallowthepatient s headtopassthrough.Duetothepressureinthechamber,thesoftmembranebecomesa loosecollararoundtheneck,adheringtotheshouldersofthepatientwithasealingand nontraumaticeffect.
2.2.1 Helmet to Deliver Noninvasive CPAP Whileahelmethasbeenusedtodeliverpressuresupportventilationbyconnectingthe inspiratoryandexpiratorylineofthehelmettoaventilator,theef cacyofsuchasystem indeliveringpressuresupportisquestionable[4].Theanalysisofthepatient ventilator interaction becomes quite complicated and is not the subject of this chapter, which focusesonCPAP. A typical circuit setup to deliver noninvasive CPAP by a helmet consists of an inspiratorybranch thatsuppliesaconstant owoffreshgastothehelmet.Gas ow (typically30 60l/min)isprovidedtypicallythroughanO2/air owmeterwithananalog scalethatallowsthecliniciantoregulateoxygenandair owseparatelyandaccordingly Fio2.The owmeterisinterposedbetweenthesourceoffreshgases(wall,tanks)andthe gasinletofthehelmet.The expiratorybranch disposesthegasthroughathreshold spring-loadedorwater-sealvalve(seeFig.2.1),whichkeepsthesystemunderpressure. ThehelmethasbeensuccessfullyusedtodeliverCPAPinseveralclinicalstudies(see chapter3). Patronitietal.[5]comparedtheef cacyofthehelmetversusthefacemaskindeliveringCPAPtoeighthealthyvolunteers.AcombinationofthreePEEPlevels(5,10,and 15cmH2O)andthreegas owswastestedinrandomorder;theincreaseinend-expiratory
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Helmet Continuous Positive Airway Pressure: Theory and Technology
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Fig. 2.1 Continuous owCPAPsystemwiththresholdspring-loadedPEEP;seetextfordetails
lungvolume,theswingsinairwaypressureduringthebreathingcycle,andtheworkof breathingweresimilarateachPEEPlevelbetweenthetwointerfaces,thusdemonstrating that CPAP delivered by helmet is at least as effective as CPAP by face mask. It shouldbenotedthatduetoitsextremelyhighcompliance,helmetsactasareservoir; evenifthepeakinspiratory owrateofthepatientexceedsthefreshgas owrate,the pressurewillremainalmostconstant.ThisisnotthecasewhenusingafacemaskCPAP, whichrequireseitherthepresenceofareservoirabletodumpthepressureswingorthe presence of a mechanical ventilator able to generate as much ow as the patient demands. The helmet CPAP system is effective, cheap, and easy to set up also outside the intensivecareunits(ICUs),suchasinthehospitalsetting[6],intheemergencydepartment,inthepostanesthesiacareunit[7],andevenintheward.Themaindisadvantages ofthissystemaretheinabilitytoprovideventilatoryassistanceorlungrecruitmentif neededandtheabsenceofanacousticalarmsystemforinadvertentpressure/gasdrop.
2.3 Limitations of the Technique 2.3.1 Carbon Dioxide Rebreathing Oneofthemainconcernswhentheheadofthepatientisinaclosedsystemisthepotential forCO2rebreathing,whichisobviouslyavoidedbyprovidinganadequatefreshgas ow rate.Indeed,incomparisonwithfacemaskCPAP,theuseofthehelmetwasassociated
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withhigherinspiratoryconcentrationofCO2,whichdecreasedatincreasing owrates[5]. Similar ndingswerereportedinabenchandhealthyvolunteersstudywithanincreasein inspiredconcentrationofCO2whenthegas owratewasreducedbelow30l/min.Itis noteworthy that the study also showed the inadequacy of delivering CPAP via helmet employingamechanicalventilator,which,becauseitisonlyaimedatkeepingtheairway pressure constant, lackscontinuousdeliveryofgas owtothehelmetandprovidesa freshgas owtothehelmetequaltoorslightlysuperiorthanthepatient sminuteventilationandwellbelowthelimitof30l/minsuggestedaseffectiveinmaintainingtheinspiratoryconcentrationofCO2inareasonablerange[8]. Forthisreason,wehighlydiscourageconnectingthehelmettoamechanicalventilator to provide CPAP. This result has been con rmed by Racca and coworkers, who also showedthatelevatedCO2rebreathingoccursifthePEEPvalveismountedontheinspiratorybranchasopposedtotheexpiratoryone[9]. Furthermore,astudy[10]byPatronitietal.addressedtheissueofthepotentialdanger derivingfromthediscontinuationoffreshgas ow.Thestudytestedthreedifferenthelmet models;oneofthehelmetsboreanantisuffocationvalve.Afterjust4minfromthedisconnectionofthefreshgas ow,theFio2dropped,andtheinspiratoryCO2rosetoextremely highlevels(upto70mmHg),withafourfoldincreaseintheminuteventilation.These effectsweregreatlydiminishedinthepresenceofanantisuffocationvalve.Theauthors concluded that some features of the helmet design (a high-volume, low-resistance inlet portandtheadjunctofasafetyvalve)caneffectivelylimitanddelaytheconsequencesof freshgassupplyinterruptionandthat,whendeliveringhelmetCPAP,thereisaclearneed to include a monitoring and alarm system along with a clinical control, even in ICU settings.
2.3.2 Noise Cavaliereetal.[11]addressedtheissueofthenoise(arisingfromtheturbulent owat thegasinletduringhelmetCPAP)asapossiblesourceofdiscomfortforpatients.The reportednoiselevelsinthehelmetduringnoninvasiveventilationequal100dB,andthe noise perceived by the subjects (assessed by a visual analog scale) was signi cantly greaterwiththehelmetthanwithafacemask;nonetheless,thehelmetwasoverallbetter tolerated than the face mask. Finally, the presence of a simple lter for heat and moistureexchangeontheinletlinesigni cantlydecreasedthesubjectivenoiseperception.Thesameauthorsreported,after1hofpressuresupportventilationdeliveredby helmettohealthyvolunteers,areversibleincreaseinacousticcompliance(indicatinga less-stiff tympanic membrane) that could predispose the middle and inner ear to mechanicaldamage.Althoughtheclinicalrelevanceofthesedataisunknown,particularlyafterprolongedtreatment,theauthorssuggestedtheuseofprotectivedevicessuch asearplugs.
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2.3.3 Pressure Monitoring and Generators As an important factor affecting the pressure generated into the helmet is the ow rate passingthroughthePEEPvalvegenerator,specialattentionmustbereservedforproviding adequategas owandavoidingmajorleaks.Asimplewaytoassessifthepressureinside thehelmetdoesnotdropbelowthePEEPistoascertainthatgasis owingthroughthe expiratoryvalvethroughouttherespiratorycycle:Ifduringinspirationthegas owstops, thisindicatesthatpressureinthehelmetisbelowthePEEPandthatahigherfreshgas ow rate is necessary. Moreover, it could be recommended to frequently measure pressure insidethehelmet,especiallywhenhelmetCPAPisperformedinahighlytechnological environment(suchasICUs). Somecompaniesemploypressurereliefvalvepressure,whichopenswhenthepressure risesaboveasafetylevel(e.g.,ifthepatientscoughs). Furthermore,togeneratePEEPathreshold(orplateau)valveisusuallyemployed.This valveisdesignedtoopenatathresholdpressureandabovethisleveltogenerateaconstant pressureindependentlyfromvariationsof ow.Themostemployedarespring-loadedand water-seal valves. Several different technologies have been developed to grant the rst kindofvalvesaconstantresistanceinthewiderrangeofgas ow,butdependingonthe manufacturer,when owishightheycouldshowsomedegreeof owdependency,thus increasingthepressuregeneratedinsidethehelmet.Thesecondkindiseasytoprovide alsoinanontechnologicalenviromentandcheap;itneedsaventilatortubetoconnectthe helmetandthewaterrepository.
Key Recommendations
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Duetoitslowinvasivenessandsimplicityofuse,ahelmetshouldbetakeninto considerationwhenconsideringapplicationofnoninvasiveCPAP. Adequatefreshgas ow(certainlynotlowerthan30l/min,buthighermightbe necessary)mustbeprovidedtoavoidrebreathingandpressuredropbelowPEEP. MechanicalventilatorssetinCPAPmodalityshouldnotbeconnectedtohelmets asfreshgas owrateisinadequate. A lterforheatandmoistureexchangeandearplugsmightbeusefultoolsto reducenoiseanddiscomfort. PressuremeasurementinsidethehelmetisrecommendedtotitratethePEEP atthecorrecttherapeuticlevel.Apressure/ ow/CO2alarmingsystemisstill desirabletoimprovesafety. Thepresenceofasafetyvalveavoidstheriskofchokingduetofreshgas owsupplyinterruption.
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References 1. BellaniG,PatronitiN,GrecoMetal(2008)Theuseofhelmetstodelivercontinuouspositive airwaypressureinhypoxemicacuterespiratoryfailure.MinervaAnestesiol74:651 656 2. CodazziD,NacotiM,PassoniMetal(2006)Continuouspositiveairwaypressurewithmodiedhelmetfortreatmentofhypoxemicacuterespiratoryfailureininfantsandapreschool population:afeasibilitystudy.PediatrCritCareMed7(5):455 460 3. TrevisanutoD,GrazzinaN,DoglioniNetal(2005)Anewdeviceforadministrationofcontinuouspositiveairwaypressureinpreterminfants:comparisonwithastandardnasalCPAP continuouspositiveairwaypressuresystem.IntensiveCareMed31:859 864 4. NavalesiP,CostaR,CerianaPetal(2007)Non-invasiveventilationinchronicobstructive pulmonarydiseasepatients:helmetversusfacialmask.IntensiveCareMed33(1):74 81 5. PatronitiN,FotiG,Man oAetal(2003)Headhelmetversusfacemaskfornon-invasive continuous positive airway pressure: a physiological study. Intensive Care Med 29: 1680 1687 6. FotiG,SangalliF,BerraLetal(2009)IshelmetCPAP rstlinepre-hospitaltreatmentof presumedsevereacutepulmonaryedema?IntensiveCareMed35(4):656 662 7. SquadroneV,CohaM,CeruttiEetal(2005)Continuouspositiveairwaypressurefortreatmentofpostoperativehypoxemia arandomizedcontrolledtrial.JAMA293(5):589 595 8. TacconeP,HessD,CaironiPetal(2004)Continuouspositiveairwaypressuredeliveredwith a helmet :effectsoncarbondioxiderebreathing.CriticalCareMed32:2090 2096 9. Racca F, Appendini L, Gregoretti C et al (2008) Helmet ventilation and carbon dioxide rebreathing: effects of adding a leak at the helmet ports. Intensive Care Med 34(8): 1461 1468 10. PatronitiN,SainiM,ZanellaAetal(2007)Dangerofhelmetcontinuouspositiveairwaypressureduringfailureoffreshgassourcesupply.IntensiveCareMed33:153 157 11. CavaliereF,ContiG,CostaR,ProiettiR,SciutoA,MasieriS(2004)Noiseexposureduring noninvasiveventilationwithahelmet,anasalmask,andafacialmask.IntensiveCareMed 30:1755 1760
Helmet Continuous Positive Airway Pressure: Clinical Applications
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AlbertoZanella,AlessandroTerrani,andNicolòPatroniti
3.1 Introduction Duringnoninvasivecontinuouspositiveairwaypressure(CPAP)thepatient srespiratory systemismaintainedthroughoutthewholerespiratorycycleataconstantpressurehigher thantheatmosphericpressure,usuallytermedthepositiveend-expiratorypressure(PEEP). NoninvasiveCPAPisvoidofanyactivesupportforthepatient sworkofbreathingand thereforecannotbeconsideredaformof ventilation. NoninvasiveCPAPisfrequentlyusedtoimprovegasexchangeandrespiratorymechanics in cooperative patients with an intact neuromuscular function with acute respiratory failure(ARF),includingacutecardiogenicpulmonaryedema(ACPE)[1].Ifononehand theuseoftechniqueswithanactivesupporttoinspiration,likepressuresupportventilation, mightdeterminefurtherbene tstopatientswithARF,ontheotherhandCPAPiseasily deliveredbysimplecontinuous owsystemswithouttheneedforamechanicalventilator, evenoutsideintensivecareunits(ICUs). Inthepast,noninvasiveCPAPhasbeenmostlydeliveredbyafacemask,combined either with a traditional CPAP circuit, equipped with a large reservoir bag on the inspiratory limb (with the purpose of minimizing the pressure swings) and a PEEP valve,orcombinedwitha Boussignacvalve. Whenusingafacemask,toavoidleaks (thusmaintainingaconstantairwaypressure),atightsealbetweenthepatient sface andthedeviceiscrucialbutoftenisdif culttoobtain,especiallywithpatientswith peculiarcharacteristics(e.g.,inanedentulouspatientorinthosewithabeard);moreover, the elevated pressure exerted by the mask on the patient s face can potentially lead to patient discomfort and skin lesions, usually limiting the application of this devicetoshort-termtreatmentsorperiodicapplications.Thecorrectapplicationofthe
A.Zanella(),A.Terrani,andN.Patroniti PerioperativeandIntensiveCareMedicine,Milano-BicoccaUniversity,Milan,Italy e-mail:
[email protected];
[email protected];
[email protected]
A.M.Esquinas(ed.),NoninvasiveMechanicalVentilation, DOI:10.1007/978-3-642-11365-9_3,©Springer-VerlagBerlinHeidelberg2010
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facemaskisthereforesomehowdif cultandrequiresanexperiencedteamandacollaborativepatient. The head helmet has been introduced with success as a tool to deliver noninvasive CPAP. It seems to offer some signi cant advantages compared to a face mask, mainly highertolerabilitybythepatient,preventionofpressuresores,andsuperioref ciencyin keepingthePEEPlevelconstantthroughouttherespiratorycycle.
3.1.1 Acute Cardiogenic Pulmonary Edema During ACPE, the application of a CPAP improves the arterial oxygenation and the respiratorymechanicsandmayreducethepatient srespiratorydriveandeffort.Since theinspiratoryeffortdecreasestheintrathoracicpressure,theafterloadoftheleftventricle increases; for example, if the arterial systolic pressure is 120 mmHg and the intrathoracicpressure(surroundingtheheart)is 20mmHg,theventriclehastogenerateapressureof140mmHg.Forthisreason,adecreaseintheinspiratoryeffortimplies areductionoftheleftventricleafterload.Moreover,CPAPreducesthevenousreturn andtheventriclesize,diminishingthewalltensionandmyocardialoxygenconsumption.ProbablybecauseofthesemultiplemechanismsCPAPiseffectiveinreducingthe needforintubationandthedeathofpatientswithACPE.Inaclinicalstudy[2],acohort ofpatientswithARFfollowingACPEwassuccessfullytreatedwithhelmetCPAP,with ameandurationoftreatmentof13h;asigni cantreductioninrespiratoryandpulse rateandanimprovementingasexchangewereobservedafter1hfrominstaurationof treatment. HelmetCPAPhasbeensuccessfullyusedasaprehospitaltherapyinpatientswithpresumedACPE.Inourexperience[3],prehospitalapplicationofhelmetCPAPwasextremely effective in improving the respiratory function and decreased intrahospital mortality in patientswithACPE.PrehospitalhelmetCPAPwasfeasible,safe,andeffectiveasanaddition to standard medical therapy or as a stand-alone treatment. A similar approach to patientswithACPEhasbeendescribedbyPlaisanceandcoworkers[4].
3.1.2 Acute Noncardiogenic Respiratory Failure In patients with acute noncardiogenic respiratory failure, CPAP, increasing the end- expiratorylungvolume(EELV)andpreventingalveolarcollapse,canimprovethegas exchangeandrespiratorymechanics,decreasingtheworkofbreathing.InFig.3.1,curve A represents a normal respiratory system pressure volume relationship, and P1 is the pressureneededtoinspireatidalvolume(TV).Arightwardshiftofthepressure volume curveB,whichmayoccurwithareductioninrespiratorysystemcompliance,resultedin a decrease in functional residual capacity (FRC) and an increase in work of breathing because, to inspire the same TV, a higher pressure (P2) is required. An application of
B
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80
A
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TV P3 TV
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Fig.3.1 CurveArepresentsa normalrespiratorysystem pressure volume relationship,andP1isthe pressureneededtoinspirea tidalvolume(TV).A rightwardshiftofthe pressure volumecurveB resultsinadecreasein functionalresidualcapacity andincreasestheworkof breathingsince,toinspire thesameTV,ahigher pressure(P2)isrequired.An applicationof10cmH2Oof CPAPreestablishesthe normalend-expiratorylung volumeandreducesthe workofbreathing(P3=P1)
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Total lung capacity(%)
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CPAP (in the gure, 10 cmH2O), reestablished the normal EELV and the reduced the workofbreathing(P3=P1). TheeffectivenessofCPAPinpatientswithARFhasbeenproveninmanystudies[5], especiallyinARFcomplicatinghematologicalmalignancy,giventheimportanceinthose patientsofavoidingendotrachealintubation.Principietal.[6]comparedacohortofpatients withhematologicalmalignancywithARFtreatedwithCPAPdeliveredbyhelmetwitha cohortofhistoricalcontrolstreatedbyfacemaskCPAP.Despiteasimilarimprovementin oxygenationat2and6hfromtheinitiationofthetreatment,inthehelmetgroupthemean duration of continuous application of CPAP without disconnection and the total duration ofCPAPwerelongerthaninthefacemaskgroup(28.4±0.2vs7.5±0.4hand34.1±0.1 vs28.1±0.3h,respectively),withbetterpatienttolerance.Theauthorsalsoreportedstatisticallysigni cantlowerratesofdeathandintubationbetweenthetwogroups,whichcan hardlybeexplainedbyagreateref cacyofthehelmet(astheinitialimprovementinoxygenationwassimilar);rather,thesecouldbeattributabletoamorecontinuativetherapy. Despiteitslimitations,thisstudyprovidedastrongsuggestionthattheheadhelmet,allowingtreatmentofpatientsforalongerperiodoftime,mightbearasubstantialadvantagein comparisontothefacemask,atleastinthesubsetofpatientsrequiringlong-term(days ratherthanhours)intervention,likethoseaffectedbyhematologicmalignancies.Thecapabilityofdeliveringnoninvasiveventilationforamoreprolongedperiodwithbetterpatient tolerancehasbeenreportedalsoinsubsequentstudies[7]. AheadhelmethasbeensuccessfullyappliedtodeliverCPAPduringhypoxicrespiratoryfailurefollowingmajorabdominalsurgery[8].PatientswithaPaO2/FiO2lower than300mmHgwhilebreathingoxygenthroughaVenturimaskataninspiratoryfractionof0.3,wererandomlyassignedtobetreatedfor6hwithoxygenthroughaVenturi
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maskatanFiO2of0.5(controlpatients)orwithoxygenatanFiO2of0.5plusaCPAP of 7.5 cmH2O, delivered by the head helmet. The patients treated with head helmet CPAPshowedalowerintubationrate(1%vs10%)andashorterdurationofICUstay. Inthisstudy,thehelmetwasnotcomparedtootherCPAPdevices;however,therateof intoleranceofthehelmetCPAPreportedbytheauthors(4%)waslowerthanwhathas beenreportedforthefacemaskinotherstudies(14%). Finally,inpatientswithchronicobstructivepulmonarydisease(COPD),CPAPisable tosubstantiallydecreasetheworkofbreathingbycompensationforthepatient sintrinsic PEEP.
3.2 Experience with Helmet CPAP at Our Institution Forseveralyearsatourinstitution,thenumberofavailableICUbedswasnoticeably undersized in proportion to the total number of beds of the hospital. To reduce the requirementtotransferpatientstootherhospitalICUsandtopreventtheICUadmission of certain patients categories (e.g., patients affected by hematological malignancies), theuseoftheheadhelmetinthegeneralwards(medicalandsurgical)wasimplemented. The outreach team for intrahospital urgencies and emergencies, including one staff intensivist and one resident, is alerted by the ward physician when a patient might require the application of noninvasive CPAP (nCPAP). If this is considered to be the case,atreatmentwithhelmetCPAPisinstitutedandmanagedbythewardnurses,who arespeci callytrainedfortheuseofthesystem.Decisionsonthetitrationofthetherapy aswellasitsdiscontinuationortheneedforamoreaggressivetherapyaremadebythe wardphysicianandtheoutreachteam,whoevaluatethepatientstwiceaday.Inthelast 15 years, hundreds of patients have been managed in this way at our institution. We reportdatafromacohortof39consecutivepatientswithARF(26ARFand13ACPE) managed by helmet CPAP in general wards [9]. We included patients with hypoxia refractorytoadministrationofoxygenbyreservoirmaskandwithin ltratesonchest X-rays.Patientsneedingimmediateintubation,withahistoryofCOPD,andwithmore thantwoneworganfailureswereexcluded.TheaveragelengthofCPAPtreatmentwas 2.9±2.3dayswithPEEPlevelsbetween8and12cmH2O.Ninepatients(23%)were subsequentlyintubated,andsix(15%)ultimatelydied.Inallpatients,Pao2/Fio2improved after 1 h of CPAP administration (from 113 ± 36 to 200 ± 83 mmHg). Patients who recoveredfromARFwithoutintubationshowed,from1to24hoftreatment,asigni cantimprovementinPao2/Fio2(from205±84to249±98mmHg,p<0.05)andasigni cantdecreaseinrespiratoryratefrom29.2±7.3to26.2±6.5breathsperminute, p < 0.05). On the contrary, patients who needed intubation did not show any further improvementinPao2/Fio2andrespiratoryrate. Again,wedidnotreportanyintoleranceforthehelmet,andwewereabletoeasily obtainagoodairsealinallpatients,whilepatientdiscomfort,facemaskintolerance,and
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Helmet Continuous Positive Airway Pressure: Clinical Applications
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inabilitytoobtainasuf cientsealarethemostimportantcausesoffailureofnoninvasiveCPAPaswellasofnoninvasivepositivepressureventilation(NPPV).Byavoiding thesetwomajorproblems,theuseofthehelmetmayextendtheuseofCPAPtoamuch largerpatientpopulation.Second,tolimitpatientdiscomfortandpossibleskinlesions, facemaskNPPVcannotbeadministeredcontinuouslyforlongperiods.Inastudyby Delclauxetal.[10]thatdidnotshowanybene toffacemaskCPAPcomparedtostandardoxygentherapy,thelengthofCPAPapplicationrequiredbyprotocolwasonly6h perday.TheshortdurationofCPAPtreatmentmayhavegreatlyaffecteditsef cacy, accountingatleastinpartforthelackofef ciencyshowninthisstudy.Theseresults corroboratethe ndingsofPrincipietal.[6]andsuggestthatthepossibilityofapplying CPAPtreatmentwithoutdisconnectionforlongerperiodsisthemostpromisingadvantageofthehelmet.
3.3 Conclusion TheapplicationofCPAPbyhelmetappearstobeeasy,ef cient,andcheap.Someessential monitoringshouldbeprovidedtowarrantsafetystandards.Despiteasimilarpneumatic performance,helmetCPAPmightbesuperiortofacemask,atleastinpatientsrequiring long-termtreatments,giventhepossibilityofdeliveringCPAPmoreeasilyandformore prolonged periods with greater patient tolerance and with less harm for the patients. A largeproportionofhypoxicpatients,includingthosewithACPE,CAP,postsurgicalrespiratoryfailure,ARFinimmunocompromisedpatients,andsoonmaypotentiallybene t fromearlyapplicationofCPAP.
Key Recommendations
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Theheadhelmetisanef cienttooltodelivernoninvasiveCPAP,anditseems tooffersomesigni cantadvantagescomparedtoafacemask. CPAPisveryeffectiveinreducingtheneedforintubationandthedeathof patientswithACPE. PrehospitalapplicationofhelmetCPAPimprovestherespiratoryfunctionand decreasesintrahospitalmortalityinpatientswithACPE. Inpatientswithacutenoncardiogenicrespiratoryfailure,CPAPimproves oxygenationbyincreasingtheEELFandpreventingalveolarcollapse.
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References 1. MasipJetal(2005)Noninvasiveventilationinacutecardiogenicpulmonaryedema:systematicreviewandmeta-analysis.JAMA294(24):3124 3130 2. TonnelierJMetal(2003)Noninvasivecontinuouspositiveairwaypressureventilationusing a new helmet interface: a case-control prospective pilot study. Intensive Care Med 29(11): 2077 2080 3. FotiGetal(2009)IshelmetCPAP rstlinepre-hospitaltreatmentofpresumedsevereacute pulmonaryedema?IntensiveCareMed35(4):656 662 4. PlaisancePetal(2007)Arandomizedstudyofout-of-hospitalcontinuouspositiveairway pressure for acute cardiogenic pulmonary oedema: physiological and clinical effects. Eur HeartJ28(23):2895 2901 5. HilbertGetal(2001)Noninvasiveventilationinimmunosuppressedpatientswithpulmonary in ltrates,fever,andacuterespiratoryfailure.NEnglJMed344(7):481 487 6. PrincipiTetal(2004)Noninvasivecontinuouspositiveairwaypressuredeliveredbyhelmet in hematological malignancy patients with hypoxemic acute respiratory failure. Intensive CareMed30(1):147 150,Epub2003Oct31 7. RoccoMetal(2004)Noninvasiveventilationbyhelmet or face mask in immunocompromisedpatients:acase-controlstudy.Chest126(5):1508 1515 8. SquadroneVetal(2005)Continuouspositiveairwaypressurefortreatmentofpostoperative hypoxemia:arandomizedcontrolledtrial.JAMA293(5):589 595 9. BellaniGetal(2008)Theuseofhelmetstodelivernon-invasivecontinuouspositiveairway pressureinhypoxemicacuterespiratoryfailure.MinervaAnestesiol74(11):651 656 10. DelclauxCetal(2000)Treatmentofacutehypoxemicnonhypercapnicrespiratoryinsuf ciencywithcontinuouspositiveairwaypressuredeliveredbyafacemask:arandomizedcontrolledtrial.JAMA284(18):2352 2360
Section II Ventilatory Modes and Ventilators: Theory, Technology, and Equipment
Pressure Support Ventilation
4
EnricaBertellaandMicheleVitacca
4.1 Introduction Noninvasive ventilation (NIV) refers to the provision of mechanical ventilation (MV) through the patient s upper airway by means of a mask without the use of an invasive arti cialairway(endotrachealtubeortracheostomy)[1]. NIVhaslongbeenusedasthestandardmethodtotreatpatientswithchronicrespiratory failure(CRF)relatedtochestwalldiseases,neuromusculardisorders,orcentralhypoventilation.Ithasbeenshowntobeeffectiveintreatmentofdifferentformsofacuterespiratoryfailure(ARF)[2,3]. Respiratoryfailuredependsontwomainprocesses:lungfailure,whichleadsmainlyto hypoxemia, and pump failure, which leads mainly to hypercapnia. Causes of hypoxemic respiratory failure can be airway collapse, alveolar lling, low ventilation/perfusion ratio (V/Q), and shunt. Causes of hypercapnic respiratory failure can be depression of central inspiratorydrive(centralalveolarhypoventilation,decreasedchemosensitivity,hypothyroidism,useofdiuretics,metabolicalkalosis,narcoticsabuse);increasedinspiratoryload(increased airwayresistance,reducedchestwallorlungcompliance,dynamichyperin ation);orinspiratorymuscleimpairment(staticordynamichyperin ation,muscleweakness). Carbon dioxide (CO2) retention is mainly related to alveolar hypoventilation; thus, hypercapniasuggeststhatalveolarventilationisinadequatetocounterbalanceCO2production.Usually,patientswithCO2retentionhaveahigherrespiratoryrate,shorterinspiratorytime(Ti),andsmallertidalvolume(Vt)thanpatientswithnormalCO2levels. ThemaingoalsofMVare 1. Improvementofarterialbloodgases 2. Improvementofminuteventilation
M.Vitacca()andE.Bertella RespiratoryDivisionandWeaningCenter,FondazioneS.MaugeriIRCCS, Lumezzane(BS),Italy e-mail:
[email protected];
[email protected] A.M.Esquinas(ed.),NoninvasiveMechanicalVentilation, DOI:10.1007/978-3-642-11365-9_4,©Springer-VerlagBerlinHeidelberg2010
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3. Unloadingofinspiratorymuscles 4. Achievingoptimalventilator patientinteractionwithmaximalcomfort DifferentmodesofMVexisttoachievethesegoals;amongtheassistedmodalities,the mostusedispressuresupportventilation(PSV),amodeofpartialventilatorsupportthat duringspontaneousinspiratoryeffortsimposesasetlevelofpositivepressureinapatient withintactrespiratorydrive[4].
4.2 Mechanisms of Action PSVispressurelimitedandpatienttriggered,anditsuseassumesthatthepatientisableto initiateaninspiratoryeffort[5].Expirationispassive. PSV allows patients to control inspiratory and expiratory times while the ventilator providesasetpressure.Thismechanism,inconjunctionwithpatienteffortandrespiratory mechanics,determinestheinspiratory owandVt[6]. Theinspiratoryeffortisdetectedbyapressureor owsensorwithadjustabletrigger sensitivity.Thepressuretriggerrequiresadecreaseinairwaypressurefromend-expiratory leveltoasetthreshold.The owtriggerrequiresa owchangesuf cienttoreachapredeterminedthreshold[5]. Flow-triggered ventilators have been shown to be more sensitive than pressure- triggeredventilators.Triggersensitivityshouldbeoptimizedaccordingtopatientneed; atoosensitivetriggercausesautotriggering;aninsensitivetriggerincreasestheworkof breathing[6]. PSVisgenerally owcycled,meaningthattheexpiratorytriggerisdeterminedbya decreaseininspiratory owandwhen owfallsbelowaventilator-determinedthreshold level,theexhalationstarts[5].Someventilatorshavethepossibilitytosetatimelimitfor inspiration,atwhichtimethedevicewillcycleintoexpirationregardlessofthe ow[6]. PSVhasthemajortargetofassistingrespiratorymuscles,improvingtheef cacyof inspiratoryeffortandreducingworkload. InpatientswithARF,PSVreducestheworkofbreathingbyincreasingtranspulmonary pressure, the in ation of the lungs, the increase of Vt, and the reduction of inspiratory muscleworkload.PSVimprovesgasexchange rstlybyincreasingalveolarventilation and increases functional residual capacity (FRC), opening collapsed alveoli, reducing shunt,andimprovingtheV/Qratio(Fig.4.1). Pressuredeliverycanbeimprovedandtheworkofbreathingdecreasedbyincreasing inspiratorypressuresupportandreducingthepressurerisetime(thetimesettoreachthe presetinspiratorylevelthatcanbeindividuallyadjusted)[6]. Patientswithseverechronicobstructivepulmonarydisease(COPD)mustovercome thepresenceofintrinsicpositiveend-expiratorypressure(PEEP)totriggertheventilator;thus,theworkofbreathingisfurtherreducedbytheadditionofappliedPEEPthat counterbalancestheintrinsicPEEP[5].Theresultsaretheimprovementofdyspnoea
4
Pressure Support Ventilation
Fig.4.1 Fromtoptobottom: effectsofPSVon ow, airwaypressure(Pao), esophagealpressure(Pes), transdiaphragmaticpressure (Pdi),andtidalvolume(Vt). Leftpanel:patientbreathing spontaneously(SB);right panel:underpressure supportventilation(PSV)
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andthereductionoftherespiratoryrate,CO2retention,andsternocleidomastoidmuscle activity[2]. Success with assisted ventilation is critically related to the adaptation of MV to the patient s needs. This is particularly true for NIV because the patient is conscious, and ventilationisineffectiveoruncomfortablewhenthepatientrejectsit. ThevariabilityinresponsetoPSVappearstobeparticularlypronouncedinpatients withCOPDduringARF.Thesepatientsusuallyshowwiderangesofairwayresistance, elastance,andintrinsicPEEP. Quitefewstudieshavebeenperformedtocomparedifferentventilatorymodesapplied noninvasivelyinCOPDpatientswithhypercapnicARF[7,8].Assistcontrolventilation seemstolowerrespiratoryworkloadbetterthanPSV,butitcausesgreaterpatientdiscomfort,morefrequentlossofbreathingcontrol,andlesspossibilitytocompensateformask leaks. Pressure-targeted ventilators have several advantages compared to volume-targeted ventilatorsandarethepreferredNIVdevicesinthetreatmentofARF.
4.3 Patient–Ventilator Interaction Patient ventilatorsynchronyisparamountforthesuccessoftheventilation.Thepresenceofasynchronydeterminesthepatient sdiscomfortandunnecessarilyincreasesthe workofbreathing. Patient ventilatorinteractionhasbeendescribed[9]asanexpressionoftwocontrollers:theventilator(controlledbythephysician)andthepatient srespiratorymusclepump. Thesecontrollersshouldbeinharmonytoobtainventilationappropriateforthepatient.
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Vignauxetal.[10]studiedtheprevalenceofpatient ventilatorasynchronyinpatients receivingnoninvasivePSVforARF.Autotriggeringwaspresentin13%ofpatients,double triggering in 15%, ineffective breaths in 13%, premature cycling in 12%, and late cyclingin23%. Autotriggeringoccurswhenarespiratorycycleisfalselytriggeredbyasignalnotproducedbythepatienteffort.ThemorefrequentcausesofautotriggeringduringPSVare expiratoryleaksfromthemask,settingtoosensitiveatrigger,patientmovement,ormotion ofwaterinthecircuit[4,5,10]. Autotriggeringcanbedif culttodetectonventilatorcurves.Itissuggestedbyasudden increaseorapersistentlyhighrespiratoryrate[4]. Doubletriggeringoccurswhenpatientdemandoreffortexceedsthe owdeliverysetting on the ventilator. If the level of pressure support is not suf cient, one pronounced inspiratoryeffortretriggerstheventilatoraftertheterminationofpressurization.Thishappens if the ventilator setting has not been adjusted to meet the patient s need or if the patient sdemandsuddenlyincreases,exceedingtheventilatorsetting[10,11]. Ineffectivetriggering(orwastedeffort)(Fig.4.2)islikelyinpatientswithCOPDand is most often due to the additional inspiratory threshold load associated with intrinsic PEEP[10].ThepresenceofintrinsicPEEPcreatesagreaterpressuregradientbetween lungpressureandventilatorcircuitpressure.Ifthepatient seffortisnotsuf cienttoovercomethisgradient,itcannotbetransmittedtothesensortotriggertheventilator[11].As explained,thisasynchronycanbereducedbyapplyinganexternalPEEP. Ineffectivetriggeringcanbedetectedonairwaypressureor owcurvesasirregularities duringtheexpiratoryphase. Premature cycling (or short cycling) is mainly related to restrictive pulmonary mechanics.ItischaracterizedbyTilastinglessthanTiduringspontaneousbreathing(ventilatorcyclesoffbeforetheendoftheneuralactivityoftheexpiratorymuscles)[4,11]. Prolonged cycling (or delayed cycling) occurs when there is a difference between patientneuralTiandventilatorsetbreathtermination(ventilatorcyclesoffonlyafterthe activityoftheexpiratorymusclesisinitiated)[11].DuringPSV,leakshavebeenshownto bethemaincausesofdelayedcycling,whileincontrastobstructivemechanicsarelikely tobeacontributingfactorforintubatedpatients[10].
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Fig. 4.2 Representative tracingofineffective triggering(IT)duringPSV (arrow).Upperpanel: patientunderPSV presentingIT;lowerpanel: thesamepatientafterPSV resetting.Pao=pressureat airwayopening,and Pes=esophagealpressure
Pao (cmH2O) 0 20
Pes (cmH2O) Pao (cmH2O)
0
Pes (cmH2O)
4
Pressure Support Ventilation
25
Table 4.1 MorefrequentproblemsobservedduringPSV(Modi edfrom[6]) Problems Mechanisminvolvedandpossiblesolution Ineffectivetriggering
Airleaks(controlcircuitandinterfaces) Insensitivetrigger(adjusttriggersensitivity) Highworkofbreathing(addPEEP,changetoflowtriggerif pressuretriggerisused)
Autotriggering
Toosensitivetrigger(reducesensitivity) Airleaks(controlcircuitandinterfaces) Waterinthecircuit(checkcircuit)
Inappropriate pressurization
Toolongrisetime(reducerisetime)
Delayedcycleto exhalation
Airleaks(checkinterfacesandchangetofacialmaskifnasalisused)
CO2rebreathing
Ventilatorwithsinglecircuit(changetoatwo-linescircuit)
Insuf cientpressuresupport(increasesupport) Highendinspiratory ow(increase ow-cyclingthresholdorset timelimitforinspiration) Notrueexhalationvalve(usenonrebreathervalve) AbsenceofPEEP(addPEEP) Largedeadspaceinthemask(reducedeadspaceorchangemask) Highrespiratoryrate(lookforcausesoftachypnoea)
Pressure-targeted ventilators can compensate for air leaks, but this capability differs markedlybetweendifferentventilators[6]. CO2rebreathingisanotherproblemobservedwithsomehomebilevelventilatorsthat haveasinglegasdeliverycircuitanddonotcontainatrueexhalationvalve.HighrespiratoryrateandlowexternalPEEPthatshortenexpiratorytimeandlowerCO2lavagefrom thecircuitincreasetheriskofCO2rebreathing[6]. Table4.1reportsthemorefrequentproblemsobservedduringPSV.
4.4 Conclusions PSVisabletoreducetheworkloadoftheinspiratorymusclesandimprovethebreathing pattern. PSVisawidelyusedmethodofNIV.
26
E. Bertella and M. Vitacca
Key Recommendations
› ›
ToavoidpatientsdiscomfortandineffectiveeffortsPSVshouldbeused appropriatelyandbyexpertpeople. MonitoringandreadjustmentofPSVsettingareneededtohavesuccess.
References 1. BritishThoracicSocietyStandardsofCareCommittee.BTSguideline(2002)Non-invasive ventilationinacuterespiratoryfailure.Thorax57:192 211 2. HillN(2006)Noninvasivepositivepressureventilation.In:TobinMJ(ed)Principlesandpracticeofmechanicalventilation,chap19,2ndedn.,McGraw-Hill,NewYork,pp433 471 3. InternationalConsensusConferencesinIntensiveCareMedicine(2001)Noninvasivepositive pressureventilationinacuterespiratoryfailure.AmJRespirCritCareMed163:283 291 4. BrochardL,LelloucheF(2006)Pressuresupportventilation.In:TobinMJ(ed)Principlesand practiceofmechanicalventilation.chap9,McGraw-Hill,NewYork,pp221 250 5. Hess DR (2005) Ventilator waveforms and the physiology of pressure support ventilation. RespirCare50(2):166 186 6. SchonhoferB,Sortor-LegerS(2002)Equipmentneedsfornoninvasivemechanicalventilation.EurRespJ20:1029 1036 7. VitaccaM,RubiniF,FoglioK,ScalviniS,NavaSetal(1993)Non-invasivemodalitiesof positivepressureventilationimprovetheoutcomeofacuteexacerbationinCOLDpatients. IntensiveCareMed19:450 455 8. GiraultC,RichardJC,ChevronV,TamionF,PasquisPetal(1997)Comparativephysiologic effects of noninvasive assist-control and pressure support ventilation in acute hypercapnic respiratoryfailure.Chest111:1639 1648 9. Kondili E, Prinianakis G, Georgopoulos D et al (2003) Patient ventilator interaction. Br J Anaesth91(1):106 119 10. VignauxL,VargasF,RoeselerJetal(2009)Patient ventilatorasynchronyduringnon-invasive ventilationforacuterespiratoryfailure:amulticenterstudy.IntensiveCareMed35:840 846 11. NilsestuenJO,HargettK(2005)Usingventilatorgraphicstoidentifypatient ventilatorasynchrony.RespirCare50(2):202 234
Ventilators for Noninvasive Mechanical Ventilation
5
RaffaeleScala
5.1 Introduction Theuseofnoninvasivepositivepressureventilation(NPPV)totreatbothacuterespiratory failure(ARF)andchronicrespiratoryfailure(CRF)hasbeentremendouslyexpandedin thelasttwodecadesintermsofspectrumofdiseasestobesuccessfullymanaged,settings ofapplication/adaptation,andachievablegoals[1 3]. ThechoiceofaventilatormaybecrucialfortheoutcomeofNPPVintheacuteand chronicsettingaspoortoleranceandexcessiveairleaksaresigni cantlycorrelatedwith thefailureofthisventilatorytechnique[4].Patient ventilatordyssynchronyanddiscomfortmayoccurwhentheclinicianfailstoadequatelysetNPPVinresponsetothepatient s ventilatorydemandsbothduringwakefulnessandduringsleep[5,6].Thisobjectivemay bemoreeasilyachievedifthetechnicalpeculiaritiesoftheappliedventilator(i.e.,ef ciency of trigger and cycling systems, speed of pressurization, air leak compensation, CO2 rebreathing, reliable inspiratory fraction of O2, monitoring accuracy) are fully understood. WiththegrowingimplementationofNPPV,awiderangeofventilatorshasbeenproducedtodeliveranoninvasivesupportbothinrandomizedcontrolledtrialsandin reallife scenarios. This chapter examines the key points concerning the technology of ventilatorsforNPPVandtheirmainimpactinclinicalpractice.Duetoconstraintsinspace, ventilators for negative pressure ventilation (i.e., iron lung, cuirass, poncho-wrap) arenotcovered.
R.Scala UnitàOperativadiPneumologiaeUnitàdiTerapiaSemi-IntensivaRespiratoria, AUSL8,OspedaleS.Donato,ViaNenni,20,52100,ArezzoItaly e-mail:
[email protected] A.M.Esquinas(ed.),NoninvasiveMechanicalVentilation, DOI:10.1007/978-3-642-11365-9_5,©Springer-VerlagBerlinHeidelberg2010
27
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R. Scala
5.2 Classification of Ventilators EvenifanyventilatorcanbetheoreticallyusedtostartNPPVinbothARFandCRF,successismorelikelyiftheventilatorisableto(a)adequatelycompensateforleaks;(b)let thecliniciancontinuouslymonitorpatient ventilatorsynchronyandventilatoryparameters due to a display of pressure ow volume waveforms and a double-limb circuit; (c)adjustthefractionofinspiredoxygen(Fio2)withablendertoensurestableoxygenation;and(d)adjustinspiratorytriggersensitivityandexpiratorycyclingasanaidtomanagepatient ventilatorasynchronies[4]. Ventilators may be classi ed in four categories, whose features are summarized [4] inTable5.1. 1. Volume-controlled home ventilators were the rst machines used to deliver NPPV mostlyfordomiciliarycare;evenifwellequippedwithalarms,monitoringsystem,and innerbattery,theirusefulnessforapplyingNPPVislargelylimitedbytheirinabilityto compensateforairleaks.Consequently,theirapplicationistodayrestrictedtohomebasednoninvasivesupportofselectedcasesofneuromusculardisordersandtoinvasive supportofventilatory-dependenttracheostomizedpatients. 2. Bilevelventilatorsaretheevolutionofhome-basedcontinuouspositiveairwaypressure (CPAP) devices and derive their name from their capability to support spontaneous breathingwithtwodifferentpressures:aninspiratorypositiveairwaypressure(IPAP) andalowerexpiratorypositiveairwaypressure(EPAP)orpositiveend-expiratorypressure (PEEP). These machines were speci cally designed to deliver NPPV thanks to theiref ciencyincompensatingforairleaks.Duetotheireasyhandling,transportability,lackofalarmsandmonitoringsystem,andlowcosts,the rstgenerationofbilevel ventilators matched the needs for nocturnal NPPV in chronic patients with a large ventilatoryautonomy.However,traditionalbilevelventilatorsshowedimportanttechnicallimitations(riskofCO2rebreathingduetotheirsingle-limbcircuitinnonvented masks; inadequate monitoring; lack of alarms and O2 blending, limited generating pressures;poorperformancetofacetheincreaseinrespiratorysystemload;lackofbattery),whichhavebeenlargelyovercomebymoresophisticatedmachines.Thenewer generationsofbilevelventilatorshavegainedpopularityinclinicalpracticeforapplicationofacuteNPPVespeciallyinsettingswithhigherlevelsofcareaswellastoinvasivelysupportventilatory-dependentchronicpatientsathome. 3. Intensivecareunit(ICU)ventilatorswereinitiallydesignedtodeliverinvasiveventilation viaacuffedendotrachealtubeortrachealcannulaeithertosickpatientsintheICUorto the theatre room to allow surgery procedures. Despite good monitoring of ventilatory parametersandof ow pressure volumewavesaswellasa nesettingofFio2andof ventilation,performanceofconventionalICUventilatorstodeliverNPPVispoorasthey arenotabletocopewithleaks.So,anewgenerationofICUventilatorshasbeendevelopedtoef cientlyassistacutepatientswithNPPVthankstotheoptionofleakcompensation(i.e., NPPVmode ),whichallowspartialortotalcorrectionofpatient ventilator asynchronyinducedbyairleaks,evenifwithalargeintermachinevariability.
+/
++ ++
Yes
+++
Some
No
+
Yes +++ NewICU ventilators Absent;+/ low/absent;+low;++moderate;+++high
Conventional ICUventilators
Intermediate ventilators
+/ Secondgenerationbilevel ventilators
No
First-generation bilevelventilators
+++
No
Volume-target ventilators
+
Monitoring
Pressometric +++ andvolumetric
Pressometric +++ andvolumetric
Pressometric ++ andvolumetric
Pressometric ++ andvolumetric
Pressometric
Volumetric
Table 5.1 CharacteristicsofthefourcategoriesofventilatorsforNPPV CO2 Blender Adjustment Modality oftrigger ofNPPV rebreathing O2 andcycling
+++
++
+++
+++
+++
+++
+++
++
++
Airleak Alarms compensation
Yes
Yes
Yes
Yes
No
Yes
Battery
+/
+/
++
+++
+++
++
+++
+++
++
++
+
++
Transportability Costs
5 Ventilators for Noninvasive Mechanical Ventilation 29
30
R. Scala
4. Intermediate ventilators combine some features of bilevel, volume-cycled, and ICU ventilators(dual-limbcircuit;sophisticatedalarmandmonitoringsystems;innerbattery; both volumetric and pressometric modes; wide setting of inspiratory and expiratory parameters). These new machines are studied to meet the patient s needs both in the homeandinthehospitalcarecontextaswellastosafelytransportcriticallyillpatients.
5.3 Technologic Issues 5.3.1 Source of Gas and Oxygen Supply ICUventilatorsareequippedwithhigh-pressureairsourcesandwithablenderwhereO2 fromhigh-pressuresourcesandroomairarevariablymixed,makingtheFio2controlled and stable. Conversely, bilevel and several intermediate ventilators are provided with eitheracompressororanelectricallysuppliedturbinepumptopressurizetheroomair, whichmaynotensureaconstantlystablepressurization;moreover,thesemachinesdonot haveablender,soO2isdeliveredfromlow-pressuresources,andtheFio2duringNPPVis noteasilypredictablebecauseitisdependentonseveralvariables:siteofO2enrichment, typeofexhalationport,ventilatorsetting,O2 ow,breathingpattern,andamountofleaks [4].ItwascalculatedthatthehighestFio2isachievedwiththeleakportinthecircuitand O2addedintothemaskbyusinglowIPAPlevels[7](Table5.2).
5.3.2 Circuit RespironicsBiPAP,likemostofthe rst-generationbilevelventilators,isprovidedwitha single-limbcircuit,andtheexhalationoftheexpiredairoccursthroughthewhisperswivel, a xed-resistance,variable- ow,leakportsituatedinthecircuitproximallywithrespectto theinterface.ThisequipmentexposesthepatienttotheriskofCO2rebreathing,which maybedetrimentalwhentreatinghypercapnicpatients[8].Theoptionsthattheclinician hastopreventthisriskare(a)keeptheconventionalwhisperswivelandapplyhighEPAP levels, such as 8 cmH2O, which therefore may be poorly tolerated; (b) use the plateau exhalation valve which, thanks to its diaphragm, limits air leaks during inspiration and allowsunidirectionalair owduringexpiration;(c)applyanonrebreathingvalve( mushroom, diaphragm, balloon valve),whichworkslikea truevalve asduringtheinspirationthediaphragmoritsballoonisin atedwithafullocclusionoftheexpiratorycircuit limb,whileduringtheexpiration,asthevalveisde ated,theairisallowedtobeexhaled throughout. However, even with a large variability, these valves may interfere with the resistanceandtheexpiratoryworkandthereforemayincreaselunghyperin ation(i.e., intrinsicPEEP)[4]. TheCO2rebreathingisalsoin uencedbythesiteoftheexhalationport,beingsigni cantlylowerwhenusingafacialmaskwiththeexhalationportinsidecomparedtoafacial
5 Ventilators for Noninvasive Mechanical Ventilation
31
Table 5.2 KeypointsoftheperformanceofventilatorsforNPPV[4] Sourceofgases Compressedmedicalgases Compressororelectricallysuppliedturbinepump Oxygensupply High-pressuresourceswithablender Low-pressuresourceswithconnectionattheventilator,circuit,mask Circuit Single-limbcircuitwithnonrebreathingvalve,plateauexhalationvalve,orwhisper Double-limbcircuit Inspiratorytriggerwithsensitivitychangeableornot Flow,pressure,volume,mixed Expiratorycycle Flowdependent(withthresholdchangeableornot),timedependent,autofunction Inspiratory owchangeableornot Backuprespiratoryrate Airleakcompensation Humidi cation Heatedhumidi ers,heat moistureexchangers Battery Internal,additionalexternal Alarms Lackorminimal Sophisticated Monitoringsystems Onlysomeinspiratoryparameters Inspiratoryandexpiratoryparameters Flow,volume,pressurecurves Modeofventilation Onlyspontaneousmodeswithout(PSV,PAV)orwithaguaranteedVT(VAPS) Bothspontaneous(PSV,PAV)andmandatorymodes(VCV,PCV) Interface Nasalmask,full-facemask,total-facemask,helmet,mouthpiece PSVpressuresupportventilation,PAVproportionalassistventilation,VAPSvolume-assuredpressuresupportventilation,VCVvolume-controlledventilation,PCVpressure-controlledventilation
32
R. Scala
maskwiththeexhalationportinthecircuitandatotal-facemaskwiththeexhalationport inside[9]. With ventilators that have a dual-limb circuit in which a complete separation exists betweeninspiratoryandexpiratorylines(i.e.,ICU,last-generationbilevel,andintermediate ventilators),thereisnoriskofrebreathing.
5.3.3 Inspiratory Trigger and Expiratory Cycle Theoptimizationofpatient ventilatorinteractionduringNPPVisessentiallybasedonthe technological ef ciency of the machine in detecting the patient s minimum inspiratory effortasquicklyaspossible(i.e.,inspiratorytrigger)andinendingthedeliveryofmechanicalsupportascloseaspossibletothebeginningofthepatient sexpiration(i.e.,expiratory cycling)independentlyfromtherespiratorysystemimpedanceandfromtheairleaks[4]. Ideally,theinspiratorytriggershouldbesetatthehighersensitivitycapableofreducing thepatient seffortneededtoactivatethemechanicalsupport.Bilevelventilatorsequipped with owtriggersareassociatedwithlowerworkofbreathingandshortertriggeringdelay timewithrespecttothoseequippedwithpressuretriggers[10].However,atoosensitive trigger,especiallyif owbased,mayinduceauto-triggeringduringNPPVwithsubstantial airleaksand,consequently,patient ventilatordyssynchronywith wastedefforts. Inspiratory triggerfunctionmaysigni cantlydiffernotonlyamongthedifferentcategoriesofventilators but also within the same category due to the structural features of the circuit (i.e., single-limbcircuitwithhighresistivevalves; incompletedual-limbcircuit ;andaPEEP valveintheshortexpiratorylimb)andtheheterogeneityintheirperformance(pressure timeand ow timewaveforms,triggerdelay,leak-inducedautotriggeringduringNPPV with ow-triggeredventilators). Thecyclingtoexpirationoptimizesthesynchronybetweentheinspiratorytime(Ti)of thepatientandthatofthemachine.Duringpressuresupportventilation(PSV),cyclingto expirationis owdependentandoccursatathreshold,whichisthedecreasein oweither to a default or changeable percentage (usually 25%) of inspiratory peak ow or to an absolute ow[5].Patient ventilatordyssynchronywithexpiratorymuscleactivationand wasted efforts due to incomplete lung emptying may happen under NPPV in case of excessiveairleaks,whichdelayoravoidtheinspiratory owtoreachthethreshold(i.e., inspiratory hang-up ) [5]. Successful strategies in preventing the inspiratory hang-up maybeappliedwithsomeventilators:(a)setasuitablethresholdoramaximumTi;(b) usespecialalgorithms(i.e., autotracksystem );(c)switchtopressure-controlledventilation(PCV)mode,inwhichexpiratorycyclingistimedependent.Thechanceof nely settingthethresholdforexpiratorycyclingthankstothedisplayofmechanicswaveforms availableinsomenewerventilatorsmaybehelpfulclinicallytoimprovepatient ventilator synchrony during NPPV as well as comfort and the possibilities of success [4]. As observedwiththeinspiratorytrigger,thebehaviorofdifferentventilatorsvariesinterms ofcyclingtoexpiration,andamarkedheterogeneityisreportedforagivenventilatorin responsetovariousconditionsofrespiratorymechanicsandairleaks.Generally,mostof
5 Ventilators for Noninvasive Mechanical Ventilation
33
thebilevelventilatorsuseacutoffatahigherfractionofinspiratory owthanmostofthe ICU ventilators to avoid the mask leak-induced deleterious prolongation of Ti. As a matterofafact,newerbilevelventilatorstendtocycleprematurelytoexpirationunder normalrespiratorysystemmechanics,andthistendencyisexaggeratedinrestrictiveconditions. Conversely, under obstructive conditions, most of the bilevel ventilators show delayed cycling, and this behavior is greatly exaggerated by the presence of air leaks. Consequently, at their default setting, bilevel ventilators seem to be better adapted for supportingobstructedpatients[4].Oppositetobilevelventilators,intheabsenceofleaks andattheirdefaultsetting,newerICUventilatorspresentsomedegreeofdelayincycling toexpirationthatisworsenedbyobstructiveconditions,whilerestrictivemechanicslead toprematurecycling.Theadditionofleaksincreasesthedelayedcyclinginnormaland obstructiveconditionsandpartiallycorrectsprematurecyclinginrestrictivestatus.This dyssynchronyinexpiratorycyclingmaybepreventedbyusingNPPVmodesinnormal andobstructivemechanics[4].
5.3.4 Inspiratory Flow It is known that severely dyspneic patients with chronic obstructive pulmonary disease (COPD)copebetterwithhigherinspiratory owandpatientswithneuromuscularproblemsdobetterwithlowerinspiratory ow(i.e.,pressurerisetimeof0.05 0.1sand0.3 0.4s, respectively)[4].Inmostofthebilevelventilators,thisparameterisunchangeable;conversely,inmoreadvancedbilevelventilators,aswellasinmostoftheintermediateand ICUventilators,therisetimemaybesetwithapotentialprofoundeffectonunloadingof respiratorymuscles,tolerance,andleaks.Inaphysiologicstudy,thehighestpressurization ratewasassociatedwithincreasedairleakageandpoorerNPPVtoleranceeventhoughthe diaphragmaticeffortwasincreasinglyreducedcomparedtolowerspeedswithoutsigni cantdifferencesinbloodgasesorbreathingpattern.Asthepatient scomfortwasnotdifferentatthelowerpressurizationspeeds,theauthorssuggestedthattheindividualtitration shouldbetargetedtoachievegoodtoleranceandtominimizeairleaks,keepingarelatively highpressurizationrate[11].
5.3.5 Backup Respiratory Rate Somebilevelventilatorsdonothavetheoptionofsettingabackuprespiratoryratef,which thereforeraisesthecosts.Conversely,thegreatmajorityofnewerbilevelventilatorsand allintermediateandICUventilatorsareequippedwithabackupf.Thisoptionisparticularlyadvantageousinsickerpatientswithinstabilityoftheirrespiratorydriveasitprevents thephenomenaofapneaandofperiodicbreathing,suchasCheyne Stokesinchronicheart failure.Backupfmayalsobeusefulwhencautioussedationisadministeredtoimprove patientcompliancetoNPPV[4].
34
R. Scala
5.3.6 Air Leak Compensation Duetothekindofinterfaceused,airleaksarealmostaconstantfeatureofNPPVandmay interferewiththepatient scomfort,patient ventilatorsynchrony,and,eventually,thelikelihoodofsuccessinbothacuteandchronicpatients[1 6]. Unintendedleaks mayoccur throughthemouthduringnasalventilationorbetweentheinterfaceandtheskinwithboth nasal and oronasal masks. On the other hand, the attempt of tightly tting the straps of headgeartoreduceairleaksshouldbeavoidedbecausethismayreducethepatient stolerance and predispose to skin damage. Consequently, it is important to have a ventilator capable of well compensating air leaks during NPPV. Air leak compensation is greater whenusingbilevelratherthanvolume-targethomeventilators,withthefallintidalvolume VTmorethan50%withthelatter(Fig.5.1).Conversely,thefallinVTislessthan10%and inIPAPlessthan8%withbilevelventilatorsincaseofleaksthankstoanadequateincrease intheinspiratory owandintheTi.However,theeffectsofairleaksduringNPPVaremore complexthanthesimplefallinIPAPandVTduetotheroleplayedbyfurthervariables,such as Ti, expiratory cycling, and inspiratory trigger sensitivity. Mathematical models that
BiPAP (Respironics)
40
Nippy (Friday Medical) Monnal D (Taema)
Change in VT when leak opened %
20
Companin 2801 (Puritan Bennet)
0 −20 −40 −60 −80
−100 0
200
400
600
800
1,000
VT mL
Fig. 5.1 EffectofanadditionalleakonthetidalvolumeVTdeliveredbyfourhomeventilatorstested inalungmodel.TherelationshipbetweenthepercentagechangesinVTwithleakopenedandthe VTdeliveredintheabsenceofaleakshowedthatpressure-target(BiPAP,Nippy)andnotvolumetargethomeventilators(MonnalD,Companion2801)wellcompensatedfortheleak[4]
5 Ventilators for Noninvasive Mechanical Ventilation
35
a nalyzethecomplexinteractionbetweenairleaksandPSVintheobstructiveconditions andtheirpotentialclinicalimplicationhavebeenrecentlyimplemented.Eventhoughall bilevelventilatorsandmostintermediateandnewerICUventilatorsequippedwithNPPV modeswereabletocompensateforairleaks,theirperformancewasnotuniform[4].
5.3.7 Battery ForbothacuteandchronicpatientswithahighlevelofdependencyonNPPV,abattery powersourceismandatoryincaseofelectricitysupplyfailureathomeandincaseofneed totransportthepatientwithinthesamehospitalortoanotherhospital.However,theclinicianmustbeawarethatbatterydurationmaydiffergreatlyamongthedifferentportable ventilatorsandmaybeshorterthanthatreportedintheoperator smanual.Moreover,portableventilatorbatterydurationisaffectedbythesetting,thelungimpedancecharacteristics, andtheventilatorfeatures[4]. As an alternative or in addition to internal batteries for NPPV ventilators, it is also possibletouseexternalbatteriesthatguaranteeprolongedautonomyoftheventilatorin caseofelectricityblackout.Ithastobeconsideredthatexternalbatteriesmaymakethe ventilatortooheavyifitneedstobetransported.
5.3.8 Alarm and Monitoring System The need for sophisticated alarms and monitoring systems during NPPV is essentially basedonclinicalpracticeasuntilnowthereisnoscienti cevidencefortheirclinicalutility.Thisisespeciallytrueforpatientswithhomeventilation,socaremustbetakenwhen settingthealarmsontheventilatortoensurethattheywillonlyfunctionwhenagenuine needarisesasfrequent,oftenspurious,alarmscansigni cantlydisturbthesleepofthe patient.TheprototypeoftheRespironicsBiPAPhasneitheralarmnormonitoringfeatures, withanadvantageincostandtransportabilityforhomecare.Intheacutesetting,theavailabilityofnewerbilevel,intermediate,andICUventilatorswithmoresophisticatedalarms (i.e.,lowandhighpressure,VT,f,Fio2,leaks)andmonitoringgraph(i.e., ow,VT,and pressure curves) may be useful in terms of safety and in improving patient ventilator interaction[4,5].Conversely,tooelaboratealarmsmaybecounterproductiveinclinical practicesincetheyfrequentlyindicateveryminorairleaksduringNPPV. ThekeyparametertobemonitoredistheexpiratoryVTasexcessiveairleaksmaycause asigni cantdiscrepancybetweeninspiratoryandexpiratoryVT.Single-limbcircuitbilevel ventilatorsallowmonitoringonlytheinspiratoryVT,whichcorrespondstothesumofthe patient sVTandtheairleaks;astheinspiratoryVTincreasesforairleakcompensation,it doesnotre ectdirectlytheminuteventilationofthepatient.Moreover,theexpiratoryVT estimated by some bilevel ventilators has not been validated. Dual-limb circuit bilevel ventilators,aswellasmostoftheintermediateandalltheICUventilators,allowclose monitoringofexpiratoryVT,whosevalueismorereliablewithmachinesthatmakethe
36
R. Scala
measurement at the level of the expiratory branch of the Y-tube than with those that measureitattheinletoftheexpiratorytubeintotheventilator[4].
5.4 Controversial Issues
Moderate
Low
PS 5, 10 and 15 cmH2O
5
High
#
#
$
#
$
PB 7200*
Servo 900C*
2
Adult Star*
3
Bird 8400*
4
Bear 1000*
Inspiratory Area at 0.3 sec (cmH2O.sec)
Due to the huge gap between the commercially available increasing number of newer ventilators and their physiologic and clinical careful evaluation, unfortunately we still havenotpublisheddataaboutseveralsophisticatedventilatorsroutinelyusedinclinical practice.Becausetherearefewinvivoinvestigations,themajorityofdataabouttheperformanceofthedifferentavailableventilatorscomesfrominvitrostudiesconductedona lungmodel.Therefore,somedoubtsremainabouttherealclinicalsigni canceofthetechnical differences observed in the bench studies among the various types of ventilators. Consequently,everyextrapolationoftheseexperimentaldatatoclinicalpracticemustbe donecautiouslysincenolungmodelcansimulatetheventilatoryvariabilityobservedin patients.Thisisparticularlytruewhenthe ndingsofinvitrostudieshavetobeappliedto acutepatientsunderNPPVinthepresenceofleaks. Based on the published data, despite a wide heterogeneity found in each category of machines, several bilevel ventilators demonstrated better performance compared to some conventional ICU ventilators (Fig. 5.2) [4]. However, no study has shown greater NPPV clinicalsuccessforonetypeofventilatorthananotherinbothacuteandchronicsettings. Nevertheless,somepointsshouldbeclearwhentheclinicianhastochooseaventilator[4].
#
$
$
1 0 Helia**
Achieva**
Respicare**
O’Nyx**
Quantum**
St 30**
T Bird**
Vision**
Veolar*
PB 740**
Horus
Galileo
PB 840
Evita IV
Servo 300
Evita II dura
-2
Evita II
-1
Fig. 5.2 Pressurizationrateintheearlyinspiratoryphaseevaluatedinalungmodelastheinspiratoryareainthe rst0.3sofinspirationaccordingtothreelevelsofpressuresupport(PS5,10, 15cmH2O)andthreesimulatedlevelsofinspiratoryeffort(low,moderate,high)for22ventilators (fromlefttoright:sevennew-generationICUventilators,sixold-generationICUventilators,and ninepiston-orturbine-drivenhomeventilators).Allnew-generationICUventilators,butalsomost home devices, outperformed old-generation ICU ventilators. * Old-generation ICU ventilators; **Piston-orturbine-drivenhomeventilators;#p<0.05vsallnew-generationICUventilators; $p<0.05vsatleastoneofthenew-generationICUventilators[4]
5 Ventilators for Noninvasive Mechanical Ventilation
37
Key Recommendations
›
›
›
›
Asexcessiveairleaksarecorrelatedwithtreatmentfailure,theclinicianshould chooseventilatorsdesignedforNPPVwithleakcompensationcapability(i.e., bilevel,someintermediate,andnewICUventilators);moreover,thechanceof settingseveralparametersandlookingat ow volume pressurewaveformswith newerventilatorsmaybehelpfulinimprovingpatient ventilatorsynchrony, comfortand,itishoped,clinicaloutcome. Thechoiceofventilatorshouldbetailoredtothepathophysiologyandtheseverity ofARFandCFR.Intheacutesetting,forhypoxemicpatients,ventilatorswithan O2blenderarerecommended,whileinthosewithhypercapnia,ventilatorswitha dual-limbcircuithaveanadvantageinloweringPaco2.InpatientswithmildCOPD exacerbation,theuseofhomeventilatorsmaybeappropriate,particularlyifthe patientisalreadyonhomeNPPV;bycontrast,patientswithlife-threateningARFat riskofintubationshouldbetreatedwithmoresophisticatedmachines.Inthe chronicsetting,conditionsforwhichrespiratorydriveisgood(i.e.,COPD)could useasimpleventilatorthatworksinaspontaneousmode,whereasthoseforwhom respiratorydriveisabsentmusthaveamandatorybackuprate;conversely,inthe caseoffast-progressingneuromusculardiseases,moresophisticatedventilators withadequatemonitoringequipmentandaninnerbatteryarerecommended. Theselectionofaventilatorshouldalsotakeintoaccountcostsandstaff experience.Themoresophisticatedaventilatoris,thelongeristherequired trainingforclinicians.Duetothetremendousgrowthoftheventilatormarketin termsofcomplexity,someofthenewbilevelventilatorsarenotuserfriendly evenfortrainedICUclinicians.Thesmallerthevarietyofdevicesused,the greaterthelikelihoodthatallteammemberswillacquireenoughexperiencein NPPVsetupwithpositiverepercussionsincostsandworkload. Theclinicianshouldbeawareofthemultipleinterferencesoftheaccessoriesfor NPPV(interfaces,exhalationsystems,pressuresettings,andhumidi cation devices)withtheperformanceofthedifferentcategoriesofventilators.For example,concerninghumidi cationduringNPPV,heatedhumidi ersshowgreat clinicalandphysiologicaladvantagescomparedtoheat moistureexchangers, eventhoughtheformerismoretimeconsuming.
References 1. NavaS,HillN(2009July18)Non-invasiveventilationinacuterespiratoryfailure.Lancet 374(9685):250 259 2. OzsancakA,D AmbrosioC,HillNS(2008May)Nocturnalnoninvasiveventilation.Chest 133(5):1275 1286 3. AnnaneD,OrlikowskiD,ChevretSetal(2007Oct17)Nocturnalmechanicalventilationfor chronichypoventilationinpatientswithneuromuscularandchestwalldisorders.Cochrane DatabaseSystRev(4):CD001941
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4. ScalaR,NaldiM(2008Aug)Ventilatorsfornoninvasiveventilationtotreatacuterespiratory failure.RespirCare53(8):1054 1080 5. VignauxL,VargasF,RoeselerJetal(2009May)Patient ventilatorasynchronyduringnoninvasiveventilationforacuterespiratoryfailure:amulticenterstudy.IntensiveCareMed35(5): 840 846 6. FanfullaF,TaurinoAE,LupoNDetal(2007Aug)Effectofsleeponpatient/ventilatorasynchronyinpatientsundergoingchronicnon-invasivemechanicalventilation.RespirMed101(8): 1702 1707 7. SchwartzAR,KacmarekRM,HessDR(2004)Factorsaffectingoxygendeliverywithbi-level positiveairwaypressure.RespirCare49(3):270 275 8. FergusonGT,GilmartinM(1995)CO2rebreathingduringBiPAPventilatoryassistance.Am JRespirCritCareMed151(4):1126 1135 9. SchettinoGP,ChatmongkolchartS,HessDRetal(2003)Positionofexhalationportandmask designaffectCO2rebreathingduringnoninvasivepositivepressureventilation.CritCareMed 31(8):2178 2182 10. NavaS,AmbrosinoN,BruschiCetal(1997)Physiologicaleffectsof owandpressuretriggeringduringnon-invasivemechanicalventilationinpatientswithchronicobstructivepulmonarydisease.Thorax52(3):249 254 11. PrinianakisG,DelmastroM,CarlucciAetal(2004)Effectofvaryingthepressurisationrate duringnoninvasivepressuresupportventilation.EurRespirJ23(2):314 320
Noninvasive Positive Pressure Ventilation Using Continuous Positive Airway Pressure
6
PedroCaruso
6.1 Introduction Continuouspositiveairwaypressure(CPAP)isatechniqueofrespiratorytherapy,ineither invasivemechanicallyornoninvasivemechanicallyventilatedpatients,inwhichairway pressure is maintained above atmospheric pressure at a constant value throughout the inspirationandexpirationbypressurizationoftheventilatorcircuit.Thischapterdiscusses theequipmentandtechnologyavailabletodeliverCPAPinnoninvasivepositivepressure ventilation(NPPV)inthehospitalscenarioanddoesnotdiscusstheequipmenttodeliver CPAP to patients with obstructive sleep apnea-hypopnea or at home care services. The interfacestodeliverCPAParenotdiscussed. CPAPef cacyhasbeencon rmedincommonclinicalconditionssuchascardiogenic pulmonary edema, chronic obstructive pulmonary disease, and chest wall trauma [1]. CPAPcanbeprovidedwithcontinuous owgenerators,intensivecareunit(ICU)ventilators (high-pressure-driven ventilators), ventilators designed to administer noninvasive positivepressureventilation(NPPVventilator)withorwithoutNPPVmodesandother medicaldevices,suchasthebubbleorBoussignacCPAP.
6.2 Equipments 6.2.1 Continuous Positive Pressure Flow Generators Continuous positive pressure ow generators are electricity-independent devices that utilizeanoxygen-drivenventuritoentrainatmosphericair,producinghighfreshgas ows. Theresultantoxygen airmixtureentersasingle-limbbreathingcircuitandexitsthrough P.Caruso UTI RespiratóriadoHospitaldasClínicasda FaculdadedeMedicinadaUniversidadedeSãoPaulo,SãoPaulo,Braziland UTI HospitalACCamargo,SãoPaulo,Brazil e-mail:
[email protected] A.M.Esquinas(ed.),NoninvasiveMechanicalVentilation, DOI:10.1007/978-3-642-11365-9_6,©Springer-VerlagBerlinHeidelberg2010
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a threshold resistor (the CPAP valve) in the mask or helmet (acting as a double-limb circuit).CPAPvalveshaveaspring-loadedvariableori cedesignthatopenatasetpressureandshouldmaintainconstantupstreampressureas owvaries( owindependence). Thegas owrateandO2inspiratoryfractiongeneratedbythecontinuous owgenerator areadjustableusinguncalibrateddials.Themanufacturersallegea owupto140l/min, buthigher owsaredescribed[2].Tomitigatethedecreaseofpressureduringinspiration, a continuous positive pressure ow generator uses an inspiratory reservoir (CF 800, Dräger,Lübeck,Germany). Thecontinuouspositivepressure owgeneratoradvantagesaresimpleuse,highportability,electricityindependence,andlowercosts.Thedisadvantagesarehighnoisetopatients andstaff,lackofmonitoringoralarms,and,mainly,lowperformance(decreaseofpressure duringinspirationorinabilitytoattainthepresetpressure).Twobenchstudies[2,3]demonstratedthatthemultiplepossibleadjustmentsinacontinuous owgenerator(fractionof O2,pipelinesupply,valveload,and owadjustment)maketheperformanceofacontinuous owpositivepressuregeneratorexcessivelyvariableandunpredictable.Besidesthat,the ubiquitousmask/circuitleak,aconditionnottestedinthosestudies,wouldmaketheperformanceofthe owgeneratorsevenmoreunpredictableandcertainlymoreunsuitable.
6.2.2 Intensive Care Unit Ventilators (High-Pressure-Driven Ventilators) The ICU ventilators offer CPAP mode, but they are designed to be used in intubated patients, so air leak, a ubiquitous condition in NPPV, is not contemplated. However, ICU ventilators can provide satisfactory CPAP since major air leaks are not present, and some adjustments are observed: adequate inspiratory ows, triggering sensitivity adjustedtopreventautocycling,andamechanismavailabletolimitinspiratorytimeand avoidinspiratory-to-expiratoryratioinversion[4].Dependingonthecriticalcareventilatorselected,CPAPmaybeadministeredusing demand, ow-by, or continuous ow techniques, with imposed work differing slightly between them in intubated patients[5]. TheICUventilatormanufacturershavebeenofferingICUventilatorsthattheyclaim areabletodeliverNPPVinthepresenceofleaks.However,theseventilatorswerenot testedintheCPAPmode.Astudythatevaluatedtheperformanceofthoseventilatorsin NPPVduringpressuresupportventilationconcludedthatleaksinterferedwithseveralkey functions,andtheNPPVmodecouldcorrectpartorallofthisinterferencebutwithwide variationsbetweenmachinesintermsofef ciency[6].
6.2.3 Ventilators Designed to Administer Noninvasive Positive Pressure Ventilation TheNPPVventilatorsaredesignedtobeusedinthepresenceofairleaks.Theyaremicroprocessedsystems,turbinedrivenandwithasingle-limbcircuitwithnonrebreathingvalve,
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plateauexhalationvalve,orwhisperswivel.Theyofferalarmsandamonitoringsystem.In theory,NPPVventilatorsshouldbebetterthantheotherdevicestoofferCPAPinNPPV. Two studies using lung simulators compared NPPV to continuous positive pressure owgeneratorsorICUventilators.The rststudycomparedanNPPVventilator(BiPAP, RespironicsInc.,Murrysville,PA)withtwocontinuouspositive owgenerators(Adjustable DownsFlowGenerator VitalSign,NewJersey;andWhisperFlow,Respironics-Philips, Murrysville, PA) to deliver CPAP. In that study, adjusted to their better oxygen supply pressure, owgeneratorshadasimilarorbettercapacitytomaintaintheCPAPlevel,but theNPPVventilatorwasmorereliableforattainingthepresetCPAP[2].Thesecondstudy comparedthesameNPPVventilator(BiPAP)tonineICUventilatorsintheNPPVmode. TheNPPVventilatorandoneventilator(ServoI,Maquet,Solna,Sweden)weretheonly ventilatorsthatrequirednoadjustmentsastheyadaptedtoincreasingleaks[7].Theclinicalsigni canceofthedifferencesbetweenNPPVventilatorsandICUventilatorswiththe NPPVmodeisunclear.
6.2.4 Boussignac CPAP TheBoussignacCPAPisasimplesystemforuseonafacemaskandisbasedonthegenerationofpositiveairwaypressurebyajet[8].Pressureisgeneratedbytheinjectionof gases, which pass through four microcapillaries (located all around the CPAP device), increasinginspeedandgeneratingturbulence,thereforecreatinga virtualvalve. The resulting CPAP level ranges from 2.5 to 10 cmH2O according to gas ow. The CPAP devicehastwoports:oneforinjectinggasesandanotherforcontrollingpressurethrough amanometerormonitoringCO2oraddingoxygen. Becauseofitssimplicity,lowweight,andsmallsize,theBoussignacCPAPisaportable device.Itsef cacyduringbronchoscopyinhypoxemicpatients[8]andinthetreatmentof acutecardiogenicpulmonaryedemahasbeenreported. AnimprovementintheBoussignacCPAPwasproposed(theSuper-Boussignac)[9]. InsertingaT-piecebetweentheBoussignacvalveandthefacemaskandconnectingthe T-piecetoareservoirballoonreceivingoxygenbyanindependentsourceallowedasmaller dropinairwaypressureduringinspirationandhighertidalvolumes.
6.2.5 Bubble CPAP The bubble CPAP can be set up with existing equipment (an ICU ventilator or oxygen blender)usingthecircuitofaventilator.Theinterfaceisamaskornasalprong.Pressure isgeneratedbyplacingtheexpiratorylimbunderwater.Thenumberofcentimetersunder waterthetubingisplacedequalstheCPAPlevel.Inthecircuit,aconnectiontoapressuremonitoringdeviceoroxygenanalyzercanbeincorporated.Itsuseisadvocatedinneonates becausethecolumnofwatercausesaslightoscillationinthepressurewaveformthatis thoughttodecreasetheincidenceofbronchopulmonarydysplasia[10].
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6.3 Discussion TherearedifferenttypesofequipmenttodeliverCPAPinNPPV.Theyrangefromvery simpleequipmenttosophisticatedmicroprocessedventilators.Unfortunately,thereareno studiesthatsimultaneouslycomparedtheperformanceofallthesetypesofequipment.The fewstudiesofthisissuecomparedonetypeofequipmenttodeliverCPAPtoanother,and most were bench studies using lung simulators. Clinical trials comparing the different equipmentthatdeliverCPAPinNPPVarerequired. Intheory,theNPPVventilatorsandtheICUventilatorswithNPPVmodeareabetter choicetodeliverCPAPinNPPVbecausetheyarepreparedtodealwithairleaks,butfew studiesweredonetoverifythis.Anobviousadvantageoftheseventilatorsisthepresence ofalarmsandmonitoring.
Key Recommendations
› › ›
Thereareatleast vetypesofequipmenttodeliverCPAPinnoninvasive ventilation.Thechoiceisbasedonavailabilityofequipmentandthestaff s expertise. ICUventilatorswithNPPVmodesandventilatorsdesignedtoadministerNPPV arepreferredbecausetheyarepreparedtodealwithairleaksandhavebetter monitoringandalarms. Ifcontinuouspositivepressure owgenerators,BoussignacorbubbleCPAPsare used,itisrecommendedtoprovideclosemonitoringofthepatientbythestaff andmonitoringofCPAPpressureandoxygenfractionbyaggregateddevices.
References 1. Nava S, Hill N (2009) Non-invasive ventilation in acute respiratory failure. Lancet 374: 250 259 2. FuC,CarusoP,LucattoJJetal(2005)Comparisonoftwo owgeneratorswithanoninvasive ventilatortodelivercontinuouspositiveairwaypressure:atestlungstudy.IntensiveCareMed 31:1587 1592 3. Glover GW, Fletcher SJ (2009) Assessing the performance of the whisper ow continuous positiveairwaypressuregenerator:abenchstudy.BrJAnaesth102:875 881 4. Mehta S, McCool FD, Hill NS (2001) Leak compensation in positive pressure ventilators: alungmodelstudy.EurRespirJ17:259 267 5. SassoonCS,LodiaR,RheemanCHetal(1992)Inspiratorymuscleworkofbreathingduring ow-by,demand- ow,andcontinuous- owsystemsinpatientswithchronicobstructivepulmonarydisease.AmRevRespirDis145:1219 1222 6. VignauxL,TassauxD,JollietP(2007)PerformanceofnoninvasiveventilationmodesonICU ventilatorsduringpressuresupport:abenchmodelstudy.IntensiveCareMed33:1444 1451
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7. FerreiraJC,ChipmanDW,HillNSetal(2009)BilevelvsICUventilatorsprovidingnoninvasiveventilation:effectofsystemleaks:aCOPDlungmodelcomparison.Chest136:448 456 8. Maitre B, Jaber S, Maggiore SM et al (2000) Continuous positive airway pressure during beropticbronchoscopyinhypoxemicpatients.Arandomizeddouble-blindstudyusinganew device.AmJRespirCritCareMed162:1063 1067 9. BellaniG,FotiG,SpagnolliEetal(2009)AnimprovedBoussignacdeviceforthedeliveryof non-invasiveCPAP:theSUPER-Boussignac.IntensiveCareMed35:1094 1099 10. AveryME,TooleyWH,KellerJBetal(1987)Ischroniclungdiseaseinlowbirthweight infantspreventable?Asurveyofeightcenters.Pediatrics79:26 30
Home Mechanical Ventilators
7
FrédéricLofaso,BrigitteFauroux,andHélènePrigent
7.1 Introduction Awidevarietyofpatientsrequiresmechanicalventilation;therefore,itisnotsurprising thatnumerousventilators,ventilationmodes,andequipmentarenecessarytoselectthe mostappropriatenoninvasiveventilationtechnologyforeachpatient.Wevoluntarilylimitedthischaptertopositivepressureventilationmodesconsideringthatnegativepressure ventilationandabdominalpressureventilationareusedmuchlessoftennow,andthatno technologicalbreakthroughhasemergedinpastyearstoimproveorincreasetheuseof thesemethods.Wealsodonotpresentcontinuouspositiveairwaypressure(CPAP)consideringthatthismodedoesnotactivelyproduceorassistinspiration.However,CPAPventilationsharessimilarequipmentwithothermethodsofpositivepressureventilation.
7.2 Technology and Equipment 7.2.1 Ventilators Homecareventilatorshaveimprovedoverthepast20years,andnowtheircharacteristics andperformanceareclosetocriticalcareventilators.Theyofferavarietyofmodesand featuresdesirablefornoninvasiveventilation.Theyhaverealexhalationvalvesthatlimit CO2rebreathing.Moreover,theexhalationvalvecanbelocatedinsidetheventilator,which
F.Lofaso()andH.Prigent AP-HP,RaymondPoincaréTeachingHospital,UniversitéVersailles-StQuentinenYvelines, Physiology FunctionalTesting,E.A.4497andCIC-IT,92380,Garches,France e-mail:
[email protected];
[email protected] B.Fauroux PediatricPulmonaryDepartment,AP-HP,HôpitalArmandTrousseau,Paris,France A.M.Esquinas(ed.),NoninvasiveMechanicalVentilation, DOI:10.1007/978-3-642-11365-9_7,©Springer-VerlagBerlinHeidelberg2010
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allows improvement of monitoring, alarms, and loop regulation. Some ventilators are smallandlightweight,thusportable,andcanoperatefromabattery.Therefore,theycan beeasilytransported(e.g.,onwheelchairs).Theseventilatorsaregenerallyproposedwhen patientsrequirefullventilatorysupport. Besidesthesesophisticateddevices,someverysimpleventilators,bilevelpositiveairwaypressuredevices,areavailablespeci callyfornoninvasiveventilationduringsleep. Theyareblowerdevicesthatmaydelivervariableinspiratoryandexpiratorypressuresin response to the patient s inspiratory effort. Therefore, they provide a pressure-targeted modewithoutavolume-targetedmode.Theseventilatorsuseasinglehosethatdoesnot haveatrueexhalationvalve.Expiredgasespassthroughaholepreferablypositionedatthe maskleveltoreduceasmuchaspossibleCO2rebreathing[1].Leaksthroughthishole depend on the level of airway pressure; to avoid the risk of rebreathing, manufacturers imposeaminimalend-expiratorypressureofabout4cmH2O.
7.2.2 Mechanical Ventilation Modes Positivepressureventilationdependsonthreeimportantvariables:thesignalallowingthe initiationofpositivepressure,thealgorithmthatcontrolshowthegasisdeliveredbythe ventilatorduringinspiration,andthesignalterminatingthegasdeliverybytheventilator.
7.2.2.1 Initiation of Positive Pressure Whenthepatientisabletoproduceaninspiratoryeffort,assistedmodesarepreferredtocontrolledmodes,withthelimitthatassistedmodeshavebeenshowntoinducesleepfragmentation [2]. A controlled mode can be proposed for safety reasons; however, maintaining an assistedmodeandusingabackupratecanbeanalternative.Controlledmodesarealsoproposedwhentheventilatorisnotabletodetecttheinspiratoryeffortorwheninspiratoryeffort detectionissystematicallyassociatedwithautotriggering.Infact,thetriggervariableusedto detectthepatient sinspiratoryeffortcanbepressure, ow,volume,and owwaveform.With apressuretrigger,thepatienttriggerstheventilatorwhenthepatientdecreasesthepressurein theventilatorcircuittoacertainpresetvalue,whereaswith owandvolumetriggerspatients havetoproduceacertaininspiratory oworvolume.Withthe owwaveformmethod,the ventilatordetectstheexpiratory owwaveformdistortioncausedbythepatient sinspiratory effort.Finally,sometriggerscombineboth owandpressure.However,sincethevariations oftheseparametersaremuchsmallerinpediatricpatients,triggersensitivityisfrequently insuf cientforthepediatricpopulation[3].Itcanalsobechallengedinsomesituations,such asairleaking,whichalters owandpressureintotheventilatorcircuitryandfacilitatesautotriggering; or inability to detect the patient s effort [3]; or dynamic hyperin ation, which producesintrinsicpositiveexpiratorypressureandineffectiveefforts.Onealternativesolutioncouldbetodetecttheactivityofthediaphragmusingeitherelectromyography[4]or transdiaphragmaticpressure[5],butthesetoolsarenotyetavailableforhomedevices.
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7.2.2.2 Gas Delivery by the Ventilator During Inspiration Itisusualtoseparatethevolume-targetedventilatorsfrompressure-targetedventilators. Historically,the rstventilatorsusedavolume-targetedmodewithaconstant ow.These devicesusedapistonorabellow.Duringthe1990s,pressure-targetedmodesdeliveringa constantpressure(withadecelerating owoncethesetpressureisreached)byusingturbines,andnowmicroturbines,weredeveloped.Withthismodeofmechanicalventilation, itispossibletoadjustthepressurizationrate(theamountoftimerequiredtoreachthe targetedpressure),andtheclinicianhasto ndacompromisebetweenafasterpressurizationratethatbetterunloadsinspiratoryeffortandalowerpressurizationrate,whichmay decreaseairleaksandimprovetolerance. The advantages of the pressure-targeted modes compared to the volume-targeted modesarethat,forthesameinspiratorytime,thepressure-targetedmodeusuallydelivers morevolumethanthevolume-targetedmodeand,forthesametidalvolume,thepressuretargetedmodeusuallyrequiresalowerpeakinspiratorypressurethanthevolume-targeted mode.Therefore,toleranceisoftenbetterwithpressure-targetedmodes.Moreover,the pressure-targetedmodesareabletocompensateleaks,whereasthevolume-targetedare not.Last,butnotleast,withapressure-targetedmodethetidalvolumedependsonboth theventilatorsettingsandthepatient sinspiratoryeffort(tidalvolumecanincreasewith the patient s inspiratory demand), while with the volume-targeted mode obviously the patientcannotincreasehisorhertidalvolume.Theadvantagesofthevolume-targeted modesarethatpistons,orbellows,canprovidehigherventilatingpressure,whichmaybe requiredinpatientswithhighrespiratorysystemimpedance;thatairstackingispossible with the volume-targeted modes [6]; and that volume-targeted ventilators can operate considerablylongeronbatterypowerthanpressure-targetedventilators,whichgenerally useaturbine. Now,severalventilatorshavetheabilitytocombinetheadvantagesofbothmodesof noninvasive ventilation. Some volumetric ventilators are able to deliver a volume- controlledbreathwithadescending-ramp owwaveformthatapproximatestheshapeof the owwaveformduringpressure-targetedmode,andsomeventilatorsthatuseapressure-targetedmodearealsoabletoensureaminimaltidalvolumedeliveredtothepatients (whichmaydecreasewheninspiratoryactivitydecreases,respiratorysystemimpedance decreases,oraleakoccurs)byincreasingeitherthetargetedpressure[7]ortheinspiratory time[8].Inaddition,thebatteryautonomyhasimprovedovertheyears,anditisnowpossibletoaddasecondbatteryonsomedevices. Proportionalassistventilation(PAV)isanalternativemodeofnoninvasivemechanical ventilation[9].Itdeliversapressureproportionaltoinstantaneous owandvolumewith factorsthattakeintoaccountboththerespiratorysystemcomplianceandresistance.This may approximate the patient s demand except when leaks occur. In this situation, the patient s demand is overestimated, and a runaway may occur. Finally, leaks frequently observedduringnoninvasiveventilationareanimportantlimitofPAVuse.Analternative couldbepressurizationproportionaltotheactivityofthediaphragmusingeitherelectromyography[4]ortransdiaphragmaticpressure[5],butthesetoolsarenotyetavailablefor homedevices.
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7.2.2.3 Cycling Off Variable Thecriterionforcyclingofftheventilatorandthereforeallowingexhalationdependson themodeofsupportandmaybetime,volume,airwaypressure,or ow.Ideally,theendof insuf ationshouldcoincidewiththeendofinspiratoryeffort.However,thisrarelyhappens, demonstratingthatthealgorithmusedtocycleofftheventilatorhastobeimproved.
7.2.3 Interfaces for the Delivery of Noninvasive Ventilation Thechoiceofinterfacehasamajorimpactonthesuccessofnoninvasiveventilationand thereforeshouldbeoptimal.Differenttypesofinterfacesareavailable.
7.2.3.1 Nasal Interfaces Nasal interfaces include nasal masks, which can be commercially produced or custom made, and nasal pillows. Nasal masks can induce facial side effects (skin injury, facial deformityongrowingfacialstructures)[10].Whenskininjuryoccurswithacommercial nasalmask,theuseofacustom-mademaskmayreduceskininjuryrisks[10].AnalternativecouldbetheuseofnasalpillowsconsideringthataCochranereview[11]suggested thatnasalpillowsinducedfewersideeffectsthannasalmasks.Moreover,itisalsopossible towearglasseswithsomenasalpillows.Leakthroughthemouthiscommonwiththese interfaces.Achinstrapcanreduceairleaks[12];however,whenitisinsuf cient,oronasal interfacesmightbeneeded.
7.2.3.2 Oronasal Interfaces Oronasalmasksandfull-facemaskscanbeproposedwhenleaksoccur.Full-facemasks arealsoanalternativetothenasalmaskwhennasalskinbreakdownoccurs.Thosewithan antiasphyxiavalveandquick-releasefeaturesshouldbepreferred.Helmetsarenotappropriateforhomemechanicalventilationbecauseoftheriskofasphyxiaincaseofpower failure.
7.2.3.3 Mouth Interfaces Fewindividualsusemouthpieces.Thisisthepredominantmethodofdaytimeventilation when noninvasive ventilation must be permanent [13]. The mouthpiece has to be positionedclosetothemouthsothatthepatientcanconnectanddisconnectasheorshewants.
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In this situation, volume-targeted ventilation is preferred, and the ventilator circuit can remain open without alarm because the resistance of the mouthpiece allows a residual inspiratorypeakpressureinsidetheventilator.Thepatientcanreceiveinsuf ationswhen thepatientdecidesbymakingasipeffort.
7.2.4 Humidification Upperairwaydrynesscommonlyoccursduringnoninvasivemechanicalventilation,especiallywhenleakoccurs.Inthepresenceofleaks,aheat-and-moistureexchangerisinef cient.Aheatedhumidi ercanbeproposed(exceptduringtransportation).
7.2.5 Safety Theroleofalarmsandmonitoringfornoninvasiveventilationiscontroversial.Itdepends onpatientrespiratoryautonomy.Nonetheless,disconnectionandpowerfailurealarmsare recommended.Batterybackupisdesirableforpatientswhorequirefullventilatorysupport.Moreover,familyshouldbetrainedintheuseofamanualballoonresuscitator.
7.3 Conclusion Theuseofnoninvasivemechanicalventilationisincreasingwiththeincreasingevidence ofimprovementoflifeexpectancyinsomepopulations.Theselectionofequipmentand thesettingsarebasedonthepatient sneeds,whichmayvarywidelyfromonepatientto another.Thekeystothesuccessofthistherapyarethebedsidecaregiver sunderstanding oftheequipment,theventilationmode sfunctioning,andthetimethecaregivercanto devotetothepatientandthepatient sfamily.
References 1. SaatciE,MillerDM,StellIMetal(2004)Dynamicdeadspaceinfacemasksusedwithnoninvasiveventilators:alungmodelstudy.EurRespirJ23:129 135 2. ParthasarathyS,TobinMJ(2002)Effectofventilatormodeonsleepqualityincriticallyill patients.AmJRespirCritCareMed166:1423 1429 3. FaurouxB,LerouxK,DesmaraisG(2008)Performanceofventilatorsfornoninvasivepositivepressureventilationinchildren.EurRespirJ31:1300 1307 4. SinderbyC,NavalesiP,BeckJetal(1999)Neuralcontrolofmechanicalventilationinrespiratoryfailure.NatMed5:1433 1436
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5. SharsharT,DesmaraisG,LouisBetal(2003)Transdiaphragmaticpressurecontrolofairway pressuresupportinhealthysubjects.AmJRespirCritCareMed168:760 769 6. BachJ(2004)Airstackingforcoughassistance.MuscleNerve30:680 681,authorreply681 7. JanssensJP,MetzgerM,SforzaE(2009)Impactofvolumetargetingonef cacyofbi-level non-invasiveventilationandsleepinobesity-hypoventilation.RespirMed103:165 172 8. OrlikowskiD,MroueG,PrigentHetal(2009)Automaticair-leakcompensationinneuromuscularpatients:afeasibilitystudy.RespirMed103:173 179 9. HartN,HuntA,PolkeyMIet al(2002)Comparisonofproportionalassistventilationand pressuresupportventilationinchronicrespiratoryfailureduetoneuromuscularandchestwall deformity.Thorax57:979 981 10. FaurouxB,LavisJF,NicotFetal(2005)Facialsideeffectsduringnoninvasivepositivepressureventilationinchildren.IntensiveCareMed31:965 969 11. ChaiCL,PathinathanA,SmithB(2006)Continuouspositiveairwaypressuredeliveryinterfacesforobstructivesleepapnoea.CochraneDatabaseSystRev18(4):CD005308 12. GonzalezJ,SharsharT,HartNetal(2003)Airleaksduringmechanicalventilationasacause ofpersistenthypercapniainneuromusculardisorders.IntensiveCareMed29:596 602 13. BachJR,AlbaAS,SaporitoLR(1993)Intermittentpositivepressureventilationviathemouth asanalternativetotracheostomyfor257ventilatorusers.Chest103:174 182
Maintenance Protocol for Home Ventilation Circuits
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MichelToussaintandGregoryReychler
8.1 Introduction Homemechanicalventilationhasbecomeastandardofcaretoeffectivelytreatchronicrespiratoryfailureeitherinpatientswithrestrictivediseasessuchasneuromuscularandthoraxcage disordersorinpatientswithobstructivediseasessuchasselectedcasesoflungandairwaydisorders.Dependingonthegroupofpatients,homeventilationmayimprovesurvivalandquality oflifeinthelongtermandmaydecreasetherateoflowerrespiratorytractinfections[1].
8.2 Equipment for Home Mechanical Ventilation Homemechanicalventilationrequiresequipmentconsistingofapressuregenerator (volume-orpressure-cycledventilator),acircuitwithtubing(withorwithoutexpiratory valve),andaninterfacetodeliverairtothepatient.Inthemajorityofpatients,anasalmask isthemostappropriateinterfacefornocturnaluse.Full-facemasksmaybeusedintherare casesforwhichnasalmasksareuseless.Finally,mouthpiecesarepreferentiallyusedin wakingpatientsfordaytimenoninvasiveventilation.Invasiveventilationviatracheostomy mayberequiredwhenitisnotpossibletoconductfurthernoninvasiveventilation.
M.Toussaint() CentreforNeuromuscularDiseaseandCentreforHomeMechanicalVentilationUZ- VUB-Inkendaal,RehabilitationHospitalInkendaal,Inkendaalstraat,1,1602Vlezenbeek,Belgium e-mail:
[email protected] G.Reychler DepartmentofPhysicalMedicineandRehabilitationandwiththeCentreforCysticFibrosis, CliniquesUniversitairesSaint-Luc,UniversitéCatholiquedeLouvain,AvenueHippocrate10, 1200Brussels,Belgium e-mail:
[email protected] A.M.Esquinas(ed.),NoninvasiveMechanicalVentilation, DOI:10.1007/978-3-642-11365-9_8,©Springer-VerlagBerlinHeidelberg2010
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8.2.1 Dirtiness, Contamination, Colonization Contaminationofcircuitsinfersthetransientpresenceofbacteriainthecircuitsorinthe airways, while colonization infers the multiplication of the germs in the airways of patients,whichmayleadtochronicrespiratoryinfection.Bycontrastwiththehospital setting,transmissionofinfectionbycrosscontaminationisrareinthehomesettingsince patients receiving home mechanical ventilation use their own equipment and have no directorindirectcontactwithotherpatients.Inhomeuse,thequestionistowhatextent homeventilationcircuits(HVCs)mustbedisinfected.IsdirtinessofanHVCariskfactorforHVCcontaminationandapatient sself-colonization?Whatisthebestprotocol forcleaning?Isdisinfectionneeded,andhowoftenisitrecommended?Theaimofthis chapteristoanswerthesequestionsandtosuggestanadequateprotocolformaintenance ofHVCs.
8.2.2 Maintenance Is Empirically Driven Although home ventilation is widely used around the world, maintenance of HVC is empiricallydriven.Instructionsgivenbeforedischargingpatientshomearemostlytaken fromtherecommendedguidelinesfromotherareas,suchaslungfunctiontests,nebulizationtechniques,orrespiratorymonitoring.Theseinstructionsaregenerallybasedontradition rather than scienti c evidence and vary depending on the countries and centers. Instructions are often too elaborate and not speci cally adapted for patients receiving homeventilation.Currentinstructionsoftenincludetheuseofdisinfectantsolution,vinegarmixedwithwater,oraquaternaryammoniumcompoundbutgenerallyfailtoexplain howbasicmaintenancemaybeachievedbysimplecleaningwithsoapandhotwateror withthedishwasher.
8.2.3 A European Survey on Maintenance InaEuropeansurvey[2]includingmorethan20,000patientsreceivinghomeventilation(two-thirdsrestrictive,one-thirdobstructivepatients),only60%oftheparticipating centers provided written instructions on the cleaning and maintenance of the equipment. There was a significant positive correlation between the size of centers andtheproportionofwritteninstructions(p<0.001).Onaverage,only56%ofthe centershadprotocolsforcorrectcleaningandmaintenanceofcircuitsandinterfaces. These findings clearly demonstrate that a huge effort is needed to improve the communication to patients regarding adequate rules of maintenance before home discharge.
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8.2.4 Patients Do Not Clean Their Equipment In a recent study, two-thirds of patients who were taught cleaning instructions prior to dischargedidnotadequatelycleantheirequipmentathome[3].Tubingandmaskswere most commonly found as unacceptably dirty. It was hypothesized that dirtiness of equipmentexposescircuitsandmaskstoahigherriskofcontamination.Indeed,thedirtiest circuits were found signi cantly more contaminated than the cleanest ones [3, 4]. Dirtinessandcontaminationshouldpotentiallyexposepatientstoahigherriskofairway colonization,whichinturnshouldcauserespiratoryinfections.However,thisrelationship hasnotyetbeendemonstratedwithevidence.
8.2.5 Sensitivity to Infections Clearly,regularcleaningappearstobethemostimportantinstructionthatneedstobefollowedbyallpatientsforthemaintenanceofHVCs.Aspreviouslyseen,however,there needstobeconsiderableefforttotargetandinstitutethisbasiceffectivecleaning.Bycontrastwithcleaningrules,theinstructionsforpostcleaningdisinfectionwilldependonthe relativesensitivityofpatientstorespiratorytractinfectionsandtherelatedrisksforbacterialcolonizationoftheairways.Twogroupsofpatientsneedtobeconsideredhere:those withrestrictiveandthosewithobstructivedisease.Clearly,bothgroupsarenotequally sensitivetoinfectionsand,asaconsequence,shouldnotrequireasimilarlyelaboratedisinfectionlevel.
8.3 Analysis and Discussion 8.3.1 Restrictive Disorders Bycontrastwithpatientsaffectedbyobstructiverespiratorydiseases,patientsaffectedby restrictive respiratory diseases or hypoventilation syndrome are a priori at low risk for bacterialcolonizationofairways. Inanuncontrolledstudywithstablepatientsreceivingwrittenandverbalinformation onmaintenanceofHVCs(recommendationwasfordailycleaningwithsoapandwater), aSpanishgroupquestionedpatientsregardingtheircleaninghabits[3].Theyconducted bothvisualinspectionofHVCsandsamplingofmasks(contamination)plusnostrils(colonization)ineachpatient.Asaresult,thefrequencyofcleaningwasfoundasfollows:
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47%cleanedtheirHVCsonceaweek,23%cleanedonceamonth,15%cleanedsporadically,and15%nevercleanedtheirequipment.Intotal,67%ofHVCsweredeemedas verydirty,andapositiverelationshipbetweencircuitcontaminationandnostrilcolonizationwashighlighted.Bacterialcolonizationwasmoreimportantinthosepatientswith dirtierHVCs.Theauthorscouldnotconcludewhethercolonizationprecededorfollowed contamination.However,theysuggestedthatadequatecleaningdecisivelydecreasedthe rateofcontamination.Theseauthorsdidnotprovideaprotocolforadequatemaintenance ofHVCs. Inanotherstudy[4],visualandbacterialinspectionsofHVCswereassessedbefore andaftercleaningina rstexperiment.Inasecondexperiment,theauthorsrandomly comparedeithercleaningwiththehouseholddishwasherorlow-leveldisinfectionwith anammonium chlorhexidinecomplex.Their ndingswereinagreementwiththe ndingsofRodriguezetal.[3].Priortocleaning,circuitswerefounddirtyin69%ofthe cases. HVCs were dirtier in invasive ventilation. There was a signi cant positive correlationbetweenthelevelofvisualdirtinessandbacteriologiccontaminationofHVCs (r=0.56;p<0.001).Bacteriologiccontaminationreached22%ofnoninvasiveHVCs withlittlepresenceoffungi.Nevertheless,bycontrastwithinvasiveHVCs,contaminationofnoninvasiveHVCsdidnotincludepotentiallypathogenicorganisms(PPOs)such as Serratia marcescens, methicillin-resistant Staphylococcus aureus (MRSA), or Pseudomonas aeruginosa. In invasive HVCs, contamination affected 81% of HVCs, includingtheimportantpresenceoffungi;19%ofHVCshadPPOs,includingS.marcescensintwocasesandMRSAinonecase,butnoP.aeruginosacontaminatedHVCsin thisgroup.Inthesecondexperimentofthisstudy,cleaninginthedishwasherwasshown tobesuperiortothechemicalcompoundsforbothcleaninganddisinfectingHVCs.In addition,gram-negativebacteriaandfungisurvivedinthechemicalcomplexbutnotin thedishwasher. Inaccordancewiththe ndingsofEbneretal.[5],wesuggestusingeitheradishwasher at65°CorbasicsoapandhotwaterasthebestmeansofcleaningHVCsusedbyrestrictive patients(Fig.8.1).Nevertheless,adisinfectiveagentmayberecommended(1)forthevery dirtyHVCs,(2)incircuitsfrominvasiveventilation,and(3)inHVCsfrompatientsknown fortheirhighsensitivitytorespiratoryinfections,suchasobstructivepatients.Effective cleaningmustalwaysprecedeanydisinfection.ItisimportanttobesurethatathermostableHVCisusedbeforecleaningordisinfectingattemperaturesabove60°C.Effective disinfectionisdescribedinthenextsection.
8.3.2 Obstructive Disorders The situation regarding hygiene of HVCs is slightly different in obstructive respiratory diseasessuchascystic brosis(CF)andchronicobstructivepulmonarydisease(COPD) comparedtorestrictiverespiratorydiseases.Themajorreasonforthisdifferenceconsists ofahighersensitivitytobacterialcolonizationoftheairwaysinthesepatientpopulations. Therateofairwaycolonizationoftencorrelateswiththeseverityorthespeedofobstructive
8
Maintenance Protocol for Home Ventilation Circuits
Fig. 8.1 Protocolofmaintenanceforhomemechanical ventilationcircuits
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Dirty circuits of Home Mechanical Ventilation
CLEANING: - 65° dishwasher or - brush, detergent and hot water RINSING DRYING Restrictive patient
Diagnosis ?
Obstructive patient
Very dirty circuits or invasive ventilation?
no
yes
NO DISINFECTION -
SPORADIC CONTROL : - cleaning
DISINFECTION: hypochlorite solution (20 minutes of soaking in a concentration of 0.5%) high temperature disinfection (>75°c)
REGULAR CONTROL : -cleaning - bacteriologic sampling in case of doubt
diseaseprogression.Inaddition,thereisevidencethattheneedfornoninvasiveventilation becomesmorefrequentafterairwaycolonizationinthesepatients. Ventilator-associatedpneumoniaiswelldocumented.Inintensivecareunits,theuseof mechanical ventilation is an important risk factor for the development of nosocomial pneumonia.Moreover,currentriskisgreaterwiththeuseofinvasivemechanicalventilation comparedwithnoninvasiveventilation.Unfortunately, the relationship betweenthe use of noninvasive ventilation and an increased risk for nosocomial pneumonia is not demonstrated. Thegreaternumberofmanipulationsandthepresenceofanendotrachealtubeassociated with invasive ventilation contribute to HVC contamination. It can be hypothesized that manipulations related to noninvasive ventilation also represent a potential risk for
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c ontamination.Thisimpliesrigorousimplementationofclassicalnonspeci crulesofhygiene, including hand washing. Nevertheless, the ventilator, the circuit, and the interface do not representmajorriskfactorsforcontaminationandcolonization,butmonitoringpotentialbacterialcontaminationofdevicesandpayingattentiontothebasicrulesofhygieneprobably remainimportantchallenges. There is little published research to support the relationship between hygiene and noninvasiveventilationdevicesinobstructivediseases.Nevertheless,wecanextrapolate ndingsfromtherapiessuchasrespiratoryphysiotherapydevicestoobstructivepatients receivinglong-termnoninvasiveventilation.Indeed,thematerialinvolvedinnoninvasive ventilationispartofthesemicriticaldevicesthatareincontactwithmucousmembranes asde nedbytheCentersforDiseaseControlandPrevention.Fortunately,recommendationsonhygieneofthesedevicesareavailable. InpatientsaffectedbyCFandCOPD,nebulizersareconsideredpotentialvectorsof bacterialcolonizationofairways.Notably,studiesshowedthatnebulizersofCFpatients are frequently contaminated [6]. Similarly, it was suggested that nebulizers can lead to nosocomial disease in COPD patients [7]. The bacterial contamination of an HVC is relatedtothedurationofitsuseandtheairwaycolonizationofthepatient. Basedonthisevidence,severalrecommendationswereproposedandcouldbeappliedto thepiecesofthecircuitinvolvedinnoninvasiveventilationinobstructivediseases.Asshown inFig.8.1,regularcleaningofHVCsandmasksismandatory,atleastasabasichygiene procedureand,morespeci cally,toeliminatethebio lmdepositedonthesurfaces,which furtherdecreasestheef cacyofdisinfectants[8].Thenecessaryfrequencyofcleaningisstill beingdebated.Basedontheresultsofstudiesonnebulizers,adailycleaningcouldtheoreticallybetherecommendedtiming.However,less-regularcleaning(i.e.,onceaweek)could beacceptableinpractice.Thepossibilityofusingtapwaterforcleaningmustbetakeninto accountifHVCsarecontaminatedbyS.marcescensandStenotrophomonasmaltophila. Whenconsideringdisinfection,differentmethodsmaybeproposed.Thechoiceofthe optimalmethodlargelydependsonthematerialchosentodisinfect.Thermaldisinfection (i.e., sterilizer, boiling water) may be not suitable for some nonthermostable pieces of HVCseventhoughitsef cacyisevidentwithallgerms.Thereareanumberofchemical methods,andeachhasitsowncharacteristics.Thedurationofsoakingandtheconcentrationofthechemicalwilldependontheparticularsubstanceused,andtheguidelinesfor eachmustbefollowedcarefully.Aceticacidisnotrecommendedduetoitsinef cacyon gram-positiveandgram-negativebacteria[9,10].Bycontrastwithacidacetic,hypochloritesolution(20minofsoakingina0.5%concentration)maybethebestalternativeof thosereadilyavailablechemicalsolutions. Afterdisinfection,rinsinganddryingisthelastpartofthecleaninganddisinfection sequence.Dryingseemsimportantasahighercontaminationratewasrelatedtonondried nebulizersinCFpatients.Becausethereisapaucityofspeci cdatarelatedtononinvasive ventilation, precise recommendations cannot be made. However, it could justify more studiesonthistopic.Finally,itappearscriticallyimportanttoinvestigatetherelativeeffectivenessofthedifferentestablishedprotocolsforcleaninganddisinfectingofHVCsto maintaintheirintegrity.
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Key Recommendations
› › › ›
›
Cleaningtheventilator,circuits,andinterfacesisrequiredtwotofourtimes permonthinallpatientsreceivingmechanicalventilationathome. Writteninstructionsonhowtocleantheequipmentforhomeventilation isuseful.Regularassessmentofwhethercircuitsandinterfacesarecorrectly cleanedandmaintainedismandatory. Inrestrictivepatients,cleaninginthedishwasheriseffectiveandsuf cient forthermostablecircuitsandinterfaces.Cleaningwithsoapandhotwatermay besuf cientforallpieces.Disinfectionisnotmandatory. Inobstructivepatients,cleaningmustbemorefrequentthanforrestrictive patients.Cleaningalwaysprecedesdisinfection.Aftercleaning,rinsingand dryingareimportant.Aneffectiveweeklydisinfectionmaybeachievedbyusing anhypochloritesolution(20minofsoakingina0.5%concentration). Theexpiratoryvalve must be washed speci cally, with care so that the balloon isnotplacedunderwater.
References 1. Dohna-SchwakeC,PodiewskiP,VoitTetal(2008)Non-invasiveventilationreducesrespiratorytractinfectionsinchildrenwithneuromusculardisorders.PediatrPulmonol43:67 71 2. Farre R, Loyd-Owen SJ, Ambrosino N et al (2005) Quality control of equipment in home mechanicalventilation:aEuropeansurvey.EurRespirJ26:86 94 3. Rodriguez Gonzalez-Moro JM, Andrade Vivero G, Miguel Diez J et al (2004) Bacterial colonizationandhomemechanicalventilation:prevalenceandriskfactors.EurRespirJ40: 392 396 4. ToussaintM,SteensM,VanZeebroeckAetal(2006)Isdisinfectionofmechanicalventilation neededathome?IntJHygEnvironHealth209:183 190 5. EbnerW,EitelA,ScherrerMetal(2000)Canhouseholddishwashersbeusedtodisinfect medicalequipment?JHospInfect45:155 159 6. VassalS,TaammaR,MartyNetal(2000)Microbiologiccontaminationstudyofnebulizers afteraerosoltherapyinpatientswithcystic brosis.AmJInfectControl28:347 351 7. MastroTD,FieldsBS,BreimanRFetal(1991)NosocomialLegionnaires diseaseanduseof medicationnebulizers.JInfectDis163:667 671 8. MerrittK,HitchinsVM,BrownSAetal(2000)Safetyandcleaningofmedicalmaterialsand devices.JBiomedMaterRes53:131 136 9. KarapinarM,GonulSA(1992)Effectsofsodiumbicarbonate,vinegar,aceticandcitricacids ongrowthandsurvivalofYersiniaenterocolitica.IntJFoodMicrobiol16:343 347 10. ReychlerG,AarabK,VanOsselCetal(2005)Invitroevaluationofef cacyof5methodsof disinfectiononmouthpiecesandfacemaskscontaminatedbystrainsofcystic brosispatients. JCystFibros4:183 187
Nocturnal Noninvasive Mechanical Ventilation
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DavidOrlikowski,HassanSka ,andDjillaliAnnane
9.1 Introduction Long-term mechanical ventilation in patients with neuromuscular problems was rst introducedbetween1950and1960inFranceandSwedenasaconsequenceofthepoliomyelitisepidemics.Duringthefollowingdecades,theconceptofhomemechanicalventilation expanded rapidly. Long-term mechanical ventilation was implemented in many othercountriesandformanyotherconditions,includingneuromuscularorchestwalldisorders,spinalcordinjury,andchronicobstructivepulmonarydisease.Atthebeginningof the1990s,therewere26,000peopleinFranceand11,419intheUnitedStatesreceiving long-termrespiratoryassistance.About10%presentedwithneuromuscularorchestwall disorders.AEuropeansurveyconductedbetweenJuly2001andJune2002reportedthe useofhomemechanicalventilationin483centersin16countries.Thatstudyidenti ed 27,118participantswithlong-termmechanicalventilationforlungorneuromusculardiseases related to chronic respiratory failure. Then, the estimated prevalence was 6.6 per 100,000people. Chronic alveolar hypoventilation is a state characterized by reduced arterial oxygen tension(Pao2)andincreasedcarbondioxidetension(Paco2),whichthepatientmaycorrect atleastpartiallybyvoluntaryhyperventilation.Inmostcases,chronicalveolarhypoventilationleadstodaytimefatigue,hypersomnia,andchangesinpsychologicalfunction.The mechanismsunderlyinghypercapniainpeoplewithneuromuscularorchestwalldisorders aremultipleandnotyetfullyunderstood.Theymayinvolveimpairmentoflungmechanicsorairwayfunctionandcough,ventilation perfusionmismatch,bluntedcentralventilatorydrive,orrespiratorymusclefatigue.Abnormalitiesmayoccurwhileawakeorduring sleep.Numerousobservationalanduncontrolledstudiessuggestedthatnocturnalmechanicalventilationatleastpartiallyimproveslungmechanics,respiratorymusclestrength,or
D.Annane(),D.Orlikowski,andH.Ska ServicedeRéanimation,HôpitalRaymondPoincaré(AP-HP), UniversitédeVersaillesSQY,104boulevardRaymondPoincaré,92380Garches,France e-mail:
[email protected]
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respiratorydriveorreducesventilation perfusionmismatch,bydayaswellasnight.A multicenterrandomizedtrialofpreventivenocturnalnoninvasivepositivepressureventilatoryassistancein70participantswithmoderatepulmonaryinsuf ciencyduetoDuchenne musculardystrophyshowedthatsurvivalwassigni cantlyworseinparticipantsreceiving preventivenocturnalventilatoryassistance,althoughdaytimebloodgaseswereimproved. Several other randomized trials, performed on parallel groups or based on a crossover designandsmallsamples,suggestedthatnocturnalventilationhadbene cialeffectson arterial blood gases or sleep parameters. The Consensus Conference of the American CollegeofChestPhysiciansrecommendedtheimplementationoflong-termventilationin patientswithchronichypercapniaduringthedayandinthosewithsymptomaticnocturnal hypercapnia,particularlywhensecondarytoneuromuscularorskeletaldisorders.
9.2 Effect of Nocturnal Mechanical Ventilation A systematic review from the Cochrane collaboration examined the effects of nocturnal mechanicalventilation in patients with chronic alveolar hypoventilation [1]. The primary objectiveofthisreviewwastoexaminetheeffectsofnocturnalmechanicalventilationin peoplewithneuromuscularorchestwalldisordersontheimprovementofchronichypoventilation.Subsidiaryendpointsweretoexaminetheeffectsofrespiratoryassistanceonsleep quality,hospitaladmissions,qualityoflife,andmortalityrelatedtochronichypoventilation. Participantswithstablechronichypoventilation,de nedbyanarterialCO2tensionabove6 kPaduringtheday,orsymptomsofnocturnalhypercapnia(i.e.,anyofthefollowing:diurnal hypersomnia, headaches, nightmares, enuresis), including children and adults with all degreesofseverity,whetherlivingininstitutionsorinthecommunity.Chronichypoventilationduetooneofthefollowingmedicalconditionswasconsideredaccordingtotheclassi cationoftheConsensusConferenceoftheAmericanCollegeofChestPhysicians:Central nervoussystemdisorders,includingArnold Chiarimalformation,centralnervoussystem trauma,cerebrovasculardisorders,disordersofcongenitalandacquiredcentralcontrolof breathing, myelomeningocele, spinal cord traumatic injuries; neuromuscular disorders, includingamyotrophiclateralsclerosis,spinalmuscularatrophy,polioandpostpoliosyndrome,congenitalchildhoodhypotonia,Guillain Barrésyndrome,infantilebotulism,musculardystrophy,myotonicdystrophy,phrenicnerveparalysis,myastheniagravis;andskeletal disorders,includingkyphoscoliosis,thoracicwalldeformities,andthoracoplasty. Typesofinterventionswereanalyzedasfollows[1]: 1. Treatment with nocturnal mechanical ventilation (for at least 3 h per night) versus noventilation. 2. Typeofventilation.Invasivetechniques(i.e.,tracheostomy[intermittentpositivepressure])versusnoninvasivetechniquesusingnegativepressureorpositivepressure.For negative pressure, the four available types of body enclosures were considered: (a) bodytanks(ironlungs),(b)chestshells(rigiddomesthat toverthechestandabdomen),(c)bodywraps(nylonorplasticjacketsthatsurroundthechestandabdomen), and (d) abdominal pneumobelts (in atable rubber bladders held rmly against the
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abdomenbynyloncorsets).Fornoninvasivepositivepressureventilation,nasal,mouthpiece,andoronasalinterfaceswereallconsidered. 3. Modeofventilation.Volume-cycled,pressure-cycledmechanicalventilationorbilevel positiveairwaypressure. Typesofoutcomemeasureswereasfollows:Primaryoutcomewasreversalofdaytime hypoventilation-related clinical symptoms (i.e., diurnal hypersomnia, headaches, nightmares,enuresis).Secondaryoutcomesincludedadmissiontohospital(otherthanroutine visits);mortality;reversalofdaytimehypercapnia(i.e.,arterialCO2tension[onroomair] below6kPa);andlungfunctionmeasurements(i.e.,forcedvitalcapacity,respiratorymusclestrength,ventilation perfusionmismatch,sleepstudies[i.e.,apnea hypopneaindexor meanoxygensaturation],orthetimespentwithanarterialoxygensaturationbelow90%). Theprimaryandthesecondaryoutcomeswererecordedseparatelyforthe rst24h(shorttermeffects)andfor12months(long-termeffects)followingimplementationofmechanicalventilation[1]. The authors concluded that the current evidence about the therapeutic bene t of mechanicalventilationwasweakbutdirectionallyconsistent,suggestingalleviationofthe symptomsofchronichypoventilationintheshortterm.Inthreesmallstudies,survivalwas prolonged, particularly in participants with motor neuron disease. They also concluded thatlargerandomizedtrialsareneededtocon rmpossiblelong-termbene cialeffectsof nocturnal mechanical ventilation on hypoventilation-related symptoms, quality of life, unplannedhospitaladmissionrate,andmortalityandtoevaluateitscost-effectivenessin peoplewithneuromusculardiseasesotherthanmotorneurondiseaseaswellasinpeople withchestwalldisorders.Futuretrialsshouldbestrati edaccordingtothetypeofdisease andtowhetherthecourseisrapidlyprogressiveornot.Thecomparisonsbetweeninvasive andnoninvasiveventilationandbetweenvolume-cycledandpressure-cycledventilation alsorequirewell-designedmulticenterrandomizedtrials[1].
9.3 Equipment Requirements for Nocturnal Ventilation Prolongedmechanicalventilationisalife-supportingtechnologythatcanbedeliveredat home. This therapy can be applied with a variety of interfaces, ventilator settings, and severalreviewshavefocusedonboththetypeofventilatorsandinterfaces[2,3]. Bodyventilatorsareusedrarely,andthegoldstandardisactuallynoninvasivepositive pressureventilation(NPPV)[4].
9.3.1 Type of Ventilator VentilatorsusedforhomeventilationcanprovideNPPVinavolumetric(volume-cycled) orbarometricway(pressurecycled).Inthe rstcase,a xedtidalorminutevolumeis
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deliveredthatwillgenerateapressuresuf cienttoachieveventilation.Inthecaseof highin ationimpedance,ahighpressurewilloccurtoreachthetargetedvolumewitha riskofbarotrauma.Anothermajorproblemisthatanappropriatetidalvolumemaynot be delivered in case of leaks. The volume-cycled mode is useful because it permits breathstackingandcoughassistance.Theseventilatorshavealarms,operatefrombatterypower,andareequippedwithexhalationvalvestooffersecurehomeuseevenin verydependentpatients. Thepressure-cycledventilatorsdeliverapredeterminedpressure,andtheresultingtidal volumedependsontheimpedanceoftherespiratorysystem.Inthecaseofleaks, owis increasedtocompensate,butinthecaseofobstruction,thetidalvolumemaybereduced. Airstackingisusuallynotpossiblewiththistypeofventilators.Theseventilatorscanbe equipped with alarms, battery, and exhalation valves or can be simpler, such as bilevel positiveairwaypressure.TheseportablepressureventilatorsarewelldesignedforNPPV and require a leak and positive expiratory pressure to avoid CO2 rebreathing. They are usuallynotequippedwithabatteryandhavenoexhalationvalve.
9.3.2 Modes of Ventilation Mechanicalventilationcanbecontrolled(respiratoryfrequencyisdeterminedbytheventilator)orassisted(ventilatorcyclesaretriggeredbythepatient sspontaneousbreaths)or amixofbothmodes(assistcontrol[A/C]orspontaneous-timed[S/T]).ModesofventilationusedforNPPVarevolume-controlledventilation(VCV),pressuresupportventilation (PSV), or pressure-controlled ventilation (PCV). Pressure modes are actually the most commonlyused[5].Mixedmodesusingapressingsupporttechnologybutenslavedtoa volumetrictargethavebeendeveloped.Intheory,theyseeminterestingbymixingboth advantagesofpressureandvolumeventilation[6].Inpractice,studiesarestilllackingto recommendtheirbroaduse.
9.3.3 Type of Interface Choiceoftheinterfaceisacrucialissuewhenstartinghomeventilation. Commercialorcustomizedinterfacesmaybeusedandabroadvarietyofmasks(nasal, oronasal,oreventotalfaceorhelmet),mouthpieces,orpillowsareavailable.Theselection oftheinterfaceshouldtakeintoaccountthetypeofdisease;theseverityoftherespiratory weakness;thedurationofventilationper24h(nightonlyoralsouseofdaytimeventilation);thelevelofhandicappingabilityofthepatientforplacingorremovingtheinterface; thepresenceofswallowingimpairment;andpatientmorphology.Intentionalleaksmaybe presentonthemaskifnoexhalationvalveisused.Thetypeofinterfacemaybemodi ed secondarilybytheoccurrenceofnonintentionalleaks(needforachinstraporchangeto anoronasalorfacialinterface)orpresenceofskinsores.
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9.4 Conclusion Nocturnalhomenoninvasiveventilationisacommontreatmentinneuromusculardisease orchestwalldisorders.Actually,positivepressureventilationthatcanbedeliveredviaa broadrangeofinterfacesisthegoldstandardforlong-termventilation.Differentmodes maybeusedandlikelyhavesimilaref cacy.Homeventilatorsoffermorechoicesinterms ofsettingsandmodeofventilation.Theyalsoofferanincreasedpossibilityformonitoring andalarms,providingmoresecureuseeveninthemostdisabledanddependentpatients. Qualitycontroloftheequipmentusedinhomemechanicalventilationisthereforenecessary toensuresafeandaccurateventilatorysupport.
Key Recommendations
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Noninvasivenocturnalventilationisthetreatmentofchoiceforneuromuscular diseaseandchestwalldeformities. Thereisnosuperiorityofonemodeofventilationcomparingtoothers. Aregularfollowupisneededbyspecializedteaminordertoindicateandto verifyef cacyofhomeventilation. Adedicatednetworkofcareincludinghomehealthcarepractitionersisparticularly importantforthispopulation.
References 1. AnnaneD,OrlikowskiD,ChevretS,ChevroletJC,RaphaelJC(2007)Nocturnalmechanical ventilationforchronichypoventilationinpatientswithneuromuscularandchestwalldisorders. CochraneDatabaseSystRev17(4):CD001941 2. HessDR(2006)Noninvasiveventilationinneuromusculardisease:equipmentandapplication. RespirCare51(8):896 912 3. SchonhoferB,Sortor-LegerS(2002)Equipmentneedsfornoninvasivemechanicalventilation. EurRespirJ20(4):1029 1036 4. Lloyd-OwenSJ,DonaldsonGC,AmbrosinoN,EscarabillJ,FarreR,FaurouxBetal(2005) PatternsofhomemechanicalventilationuseinEurope:resultsfromtheEuroventsurvey.Eur RespirJ25(6):1025 1031 5. Janssens JP, Derivaz S, Breitenstein E, De Muralt B, Fitting JW, Chevrolet JC et al (2003) Changing patterns in long-term noninvasive ventilation: a 7-year prospective study in the GenevaLakearea.Chest123(1):67 79 6. OrlikowskiD,MroueG,PrigentH,MoulinC,BohicM,RuquetMetal(2009)Automaticairleakcompensationinneuromuscularpatients:afeasibilitystudy.RespirMed103(2):173 179
Section III Patient–Ventilator Interactions
Patient–Ventilator Interaction During Noninvasive Pressure-Supported Spontaneous Respiration in Patients with Hypercapnic Chronic Obstructive Pulmonary Disease
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WulfPankow,AchimLies,andHeinrichBecker
10.1 Introduction Noninvasivepressuresupportventilation(NPSV)hasbecomeastandardofcareinpatientswith acuteexacerbationsofchronicobstructivepulmonarydisease(COPD).InstableCOPD,hypercapniaiscorrelatedwithlessrespiratorymusclestrengthandgreatermuscleload.Inselected patients,mechanicalventilationwithNPSVmaybeindicatedinadditiontooxygentherapyto preventworseningofhypercapniaandtoimprovesleepqualityandqualityoflife.Epidemiologic studiesonNPSVhaveshownthatpatienttoleranceisakeyfactorpredictingsuccessorfailure. TheobjectiveofNPSVistoimprovebloodgasesandtounloadtherespiratorymuscles. SuccessofNPSVisrelatedtomanyfactors.Oneofthemostimportantistheinteraction ofthepatientandtheventilator.Importantdeterminantsareintrinsicpositiveend-expiratory pressure(PEEPi),pressuregeneratedbytheinspiratorymuscles,triggeringoftheventilator,andpatient ventilatorsynchrony.
10.2 Patient Response to the Ventilator WithNPSV,patient-initiatedbreathsarefollowedbyapresetlevelofpressureassist.Intheory,therespiratorysystemcanrespondtoassistedventilationintwoways.First,ventilator
W.Pankow()andA.Lies VivantesKlinikumNeukölln,Berlin,Germany e-mail:
[email protected];
[email protected] H.Becker AsklepiosKlinikBarmbeck,Hamburg,Germany e-mail:
[email protected] A.M.Esquinas(ed.),NoninvasiveMechanicalVentilation, DOI:10.1007/978-3-642-11365-9_10,©Springer-VerlagBerlinHeidelberg2010
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workisusedtoincreaseventilation,whilerespiratorymuscleactivityisunchanged.Second, ventilatorworkisusedtounloadtherespiratorymusclesataconstantlevelofventilation. SeveralstudiesinpatientswithexacerbatedCOPDandwithseverestableCOPDhave shownthat,inclinicalpractice,botheffectsarecombined.Bloodgasesareimprovedas ventilation increases, while respiratory muscle activity is reduced. Downregulation of respiratorymuscleactivityisattributedtofeedbackmechanisms,whichareactivatedby unloading the muscles (nonchemical feedback) and by reducing Pco2 (chemical feedback). WeinvestigatedthephysiologiceffectsofNPSVinsevenpatientswithstablehypercapnicCOPD[1].Inspiratorypositiveairwaypressure(IPAP)wasappliedwith12 14cmH2O andexpiratorypositiveairwaypressure(EPAP)with3cmH2O.Comparedtospontaneous breathing,ventilationwithNPSVwasincreased,asindicatedbyadropofPaco2from58to 50mmHg.Respiratorymuscleactivity,measuredwiththetransdiaphragmaticpressure timeproduct(PTPdi),wasreducedby33%.Othershavedemonstratedevenstrongereffects whenNPSVwasappliedtopatientswithstableorexacerbatedCOPD[2].Differencesmay dependonalternativeventilatorsettingsandpatientcharacteristics. Behavioralfeedbackmayalsoaffectpatient ventilatorinteraction.InCOPDexacerbation, dyspnea and anxiety cause rapid, shallow breathing. These mechanisms promote dynamichyperin ationandPEEPi,affectingtriggersensitivityandpatientcomfort.Asa result,thepatientmay ghtwiththeventilatorratherthenacceptitssupport.Judicious sedationcanhelptoinitiateNPSV. Duringsleep,breathingdriveisreduced,andthedependenceoftherespiratorycontroller onPco2isincreased.ThepotentialeffectofNPSVtoincreasetidalvolumeandtodecrease Pco2mayinduceapneaandperiodicbreathingwithconsequencesonthepatient ventilator interaction.Indeed,astudyshowedthatineffectiveeffortsarecommonduringnocturnal NPSV, while no patient ventilator asynchrony occurred during daytime [3]. Ventilator settings adjusted during wakefulness may therefore not be appropriate for nocturnal mechanicalventilation.
10.3 Ventilator Response to the Patient Thewayinwhichtheventilatorrespondstoinspiratoryandexpiratoryeffortsisin uenced by the patient s respiratory system mechanics and by machine properties (triggering, cycling,andpressurization). RespiratorymechanicsinsevereCOPDisimpairedbystaticanddynamichyperin ation andPEEPi.PEEPiisthemostcommoncauseofineffectivetriggeringinCOPD.Totrigger theventilator,thepatientmust rstperformacertainamountofinspiratorymuscleactivity tocounterbalancePEEPiandthusinducesubatmosphericalveolarpressure.Thisdelays inspiratorypressureassist,andpatient ventilatorsynchronymaybeseverelydisturbed. Also,extra(ineffective)respiratorymuscleactivityisnecessarytotriggertheventilator. Attimes,apatient seffortmightnotevenbestrongenoughtolowerthepressureatthe airwayopeningbelowPEEPiandtotriggertheventilator(Fig.10.1).
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· V 50 (L/min)
Pmask [cm H2O] 10
Pes [cm H2O] 10
Pdi [cm H2O] 10
5 sec
Fig. 10.1 Recordingsof ow(V¢),maskpressure(Pmask),esophagealpressure(Pes),andtransdiaphragmaticpressure(Pdi)inapatientwithstableCOPDreceivingNPSV.Arrowindicatesineffectivetriggering:Positivede ectionoftransdiaphragmaticpressureisnotfollowedbypositivemask pressure,and owremainsatlowlevel(ReproducedfromPankowetal.[1].Withpermission. ©GeorgThiemeVerlagKG)
PEEPi in stable COPD normally ranges from 1 to 6 cmH2O during spontaneous b reathing. In overweight patients with hypercapnic COPD [1] and in acute respiratory failure,highervaluesupto13cmH2Ohavebeenmeasured.Theapplicationofexternal pressure at the airway opening (PEEPe or EPAP) can effectively reduce the work of breathingandimprovetriggering.EPAPcanbeappliedasmaskCPAP(continuouspositive airway pressure), but tolerance and respiratory muscle unloading are more effective in combination with IPAP. The combination of IPAP and EPAP also increases alveolar ventilation.Inclinicalpractice,PEEPicannotbemeasured,andtheoptimallevelofEPAP isappliedinapragmaticway.Anappropriatewayistostartwith0 2cmH2Oandincrease EPAP slowly until ineffective efforts disappear. In addition, effective bronchodilator therapymayoptimizepatient ventilatorinteractionbyreducingexpiratory owlimitation, dynamichyperin ation,andPEEPi. Therespiratorymuscleactivityrequiredtotriggertheventilatoralsodependsonthe triggersystem.Withpressuretriggering,thepatient seffortdecreasesthepressureinthe ventilatorsystemtoopenthedemandvalve.With owtriggering,apresetinspiratory ow isgeneratedtoactivateinspiratorypressureassist.InpatientswithCOPD, owtriggering reduces inspiratory effort compared to pressure triggering [4]. However, the clinical signi canceofthisdifferenceisunclearandmightbeofminorrelevance.
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Airleakingthroughthemouthoraroundthemasksealmayinterferewithventilator triggering.Inastudyonpatient ventilatorinteraction,severeasynchronywithNPSVwas observedin43%of60patients[5].Thestudypopulationwasheterogeneous:40%sufferedfromCOPD,and55%werehypercapnic.Airleakswereidenti edasamajorcontributingfactortoineffectivebreathsandlatecycling[5].Anintensivecareunit(ICU) ventilatorwasused;therefore,theseresultsmaynotbeapplicabletomodernbilevelventilators. They have the potential to compensate for leaks and thus improve triggering. However, with NPSV generated by a modern bilevel device, ineffective triggering has beenidenti edasthedominantcauseofpatient ventilatordyssynchronyinfouroften patients. In the same study, ineffective triggering was observed in three of ten patients using conventional ventilation [6]. To reduce air leaking, chin straps, tightening of the mask,orreplacementofthenasalmaskbyanoronasalmaskmaybetried. Delayed or premature cycling is another source of patient ventilator asynchrony. Ideally,pressuresupportshouldbetightlycoupledtotheinspiratorydriveofthepatient. The ventilator detects the transition from inspiration to expiration by a predetermined decrease of inspiratory ow. In COPD, delayed cycling is a common problem. Airway obstructionisaccompaniedbya atteningofthe owcurve.The owdeterminedtocycle offisreachedlateinthebreathingcycle.Thisinturnshortensexpiratorytime,decreases lung emptying, and contributes to dynamic hyperin ation and PEEPi. Also, air leaking may prolong the reduction of inspiratory ow to the cycling threshold. Cycling can be improvedwhenthedefault owthresholdischangedtoapresettime.Inacuterespiratory failure,inspiratorytimeshouldbelimitedtobelow1.0s. AnimportantadvantageofNPSV,comparedtoinvasiveventilation,isthatthepatient canbeaskedhowcomfortableheorsheinteractswiththemachine.Doesthepatientget enoughair:pressurization?Isiteasyorexhaustingtoobtainventilatorsupport(trigger threshold)? Does the machine interfere with breathing (cycling, leaks, PEEPi)? Visual evaluation of the patient s breathing effort and breathing rhythm is another important meanstooptimizepatient ventilatorsynchrony.
Key Recommendations
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InseverehypercapnicCOPD,NPSVwithexpiratoryPEEP(PEEPeorEPAP) caneffectivelyreduceapatient srespiratorymuscleeffortandincreasealveolar ventilation.Patient ventilatorsynchronyisaprerequisiteforachievingthis effect. PEEPiisthemostcommoncauseofineffectivetriggering.Tocounterbalance PEEPi,EPAPmaybestartedwith0 2cmH2Oandincreasedslowlyuntil ineffectiveeffortsdisappear. Airleaksalsointerferewithventilatortriggeringandcycling.Toreduceleaking, tighteningofthemask,replacementofthenasalmaskbyanoronasalmask,or chinstrapsmaybeappropriate.
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References 1. PankowW,BeckerH,KöhlerU,SchneiderH,PenzelT,PeterJH(2001)Patient ventilator interactionwithnoninvasivepressuresupportventilationinpatientswithhypercapnicCOPD. Pneumologie55:7 12 2. VitaccaM,NavaS,ConfalonieriMetal(2000)Theappropriatesettingofnoninvasivepressure supportventilationinstableCOPDpatients.Chest118:1286 1293 3. FanfullaF,TaurinoAE,LupoND,TrentinR,D AmbrosinoC,NavaS(2007)Effectofsleep onpatient/ventilatorasynchronyinpatientsundergoingchronicnon-invasivemechanicalventilation.RespirMed101:1702 1707 4. NavaS,AmbrosinoN,BruschiC,ConfalonieriM,RampullaC(1997)Physiologicaleffectsof ow and pressure triggering during non-invasive mechanical ventilation in patients with chronicobstructivepulmonarydisease.Thorax52:249 254 5. VignauxL,VargasF,RoeselerJetal(2009)Patient ventilatorasynchronyduringnon-invasive ventilationforacuterespiratoryfailure:amulticenterstudy.IntensiveCareMed35:840 846 6. Mulqueeny Q, Ceriana P, Carlucci A, Fanfulla F, Delmastro M, Nava S (2007) Automatic detection of ineffective triggering and double triggering during mechanical ventilation. IntensiveCareMed33:2014 2018
Asynchrony and Cyclic Variability in Pressure Support Ventilation
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AntoineCuvelierandJean-FrançoisMuir
Adaptationbetweenthepatientandtheventilatorhasalwaysbeenthe rstgoalofthephysicianfacingwithapatienttreatedbymechanicalventilation.Sedationiscommonlyused underinvasiveventilationtofacilitateit,especiallyindif cult-to-ventilatepatientswith acuterespiratorydistresssyndrome(ARDS).Adaptationtononinvasiveventilation(NIV) isoftendif culttoobtainintheacutephaseasthismodeofventilationisa leaky ventilation,andspontaneousventilationhastoberespected,withcontraindicationofsigni cant sedation.Thus,speci cattentionhasbeenbroughttothisphenomenoncalledsynchrony, which may be de ned as the agreement between the patient respiratory efforts and the inspiratoryandexpiratorytimeoftheventilator.So,asynchronymaybeexplainedbythe inspiratorydriveandtheairwayspressurization,whichissecondarytothemechanicaland technicalcharacteristicsofthemachineandtheinterface,theventilatorysettings,andthe pathophysiologicalabnormalitieslinkedtotheetiologyoftherespiratoryfailure[1].This dyssynchronyisthemismatchbetweenpatientandventilatorinspiratorytimeandsecondarywastedorineffectiveefforts. Withasynchronyasthesourceofdiscomfortforthepatientwithincreasedsensationof dyspneaandimpairmentofthequalityofventilatorysupport,itisimportanttoprovideits precisesemiologytoevaluateitsclinicalrelevanceanditspathophysiologytocorrectit, mainly by an improvement of the settings of the respirator and special attention to the inspiratoryandexpiratorytriggers.Ontheotherhand,dyssynchrony,stilltodaydetected andanalyzedduringdaytime,maysigni cantlyoccurduringnight,generatingsleepfragmentationandthusdaytimefatigueandsomnolence.Itwasnecessarytohavetheopportunitytorecordmoreeasilyandforalongtimesucheventstocorrectthemthroughappropriate respirator setting modi cations. Signi cant improvements in recording and detection of patient ventilatorasynchronyhavebeendevelopedinourlaboratorythatmaybederived fromthepressureand owtracesonthescreenoftherespiratorandthususedintheclinical setting.Thethreemajordeterminantsofthepatient-ventilatorsynchronyaretheventilator triggering,theairwaypressurizationandtheventilatorcycling(passagetoexpiration)[2].
A.Cuvelier()andJ.-F.Muir PulmonaryDepartmentandRespiratoryIntensiveCareUnit, RouenUniversityHospital,Rouen,Franceand UPRESEA3830HopitaldeBois-Guillaume 76130Rouen,Cedex,France e-mail:
[email protected];
[email protected] A.M.Esquinas(ed.),NoninvasiveMechanicalVentilation, DOI:10.1007/978-3-642-11365-9_11,©Springer-VerlagBerlinHeidelberg2010
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Poorpatient ventilatorinteractions,especiallyineffectiveinspiratorytriggeringefforts (ITEs)mayoccurduringnoninvasivepressuresupportventilation(PSV)inpatientswith cystic brosis(CF)[3,4],inpatientswithchronicobstructivelungdisease(COPD)with lungin ationandintrinsicpositiveend-expiratorypressure(PEEPi)[5,6],andinpatients with various other pulmonary diseases [7]. ITEs under PSV are more frequent during sleep[8,9]andwhenincreasingthelevelofventilatoryassistance[10,11].ITEsduringNIV areassociatedwithpoorergasexchangeduringsleep[12]andsleepfragmentation[13]. Moreover, ITEs may be a cause of PSV intolerance and failure in critically ill patients ghting againsttheirventilator.Otherwise,theincidenceofITEanditsimpactonPSV ef cacyandcomfortremainunknown.AsimplenoninvasivemethodtodetectITEduring PSVisthereforehighlydesirable.Esophagealpressure(Pes)monitoringiscommonlyused asthestandardfordetectingtheonsetofinspiratoryefforts,althoughdiaphragmaticelectromyographyhasbeenusedbysomeauthors[14].Thislasttechniquerequiresesophageal orsurfaceelectrodesandcannotbeperformedonaroutinebasisduringsleeporfordomiciliaryassessments.Consequently,moststudiesonITEhaveassessedPesortransdiaphragmaticpressure(Pdi)variationstoidentifytherelationshipbetweenindividualinspiratory effortsandventilatortriggering.However,esophagealrecordingsarenotpracticalasaroutinemeasureinmostcentersandareinadequateforprolongedorlong-termassessmentsin patientstreatedbyhomeventilation,whichrequirearealinvestigationofthefrequencyand duration of such events and which cannot be correctly identi ed, scored, and quanti ed fromshortrecordings.Ontheotherhand,manualscoringofITEistimeconsuming.For thisreason,anewresearchaxisiscurrentlybeingexploredthroughalgorithmsthatintegrate airway pressure and ow variations to automatically detect ITE in real time. This automaticnoninvasivemethodhasbeenvalidatedbycomparingitwiththemanualdetectionofITEusingconventionalPesrecordings[15 17].Thisdetectionmethodology,based onsimplephysiologicaldata,isverysensitiveandspeci ccomparedtothestandardmethod (i.e., measurements of Pes variations). Also, the structure of the phase portraits reconstructedfromthe owtimeseriesappearstobeverysensitivetothedynamicsofunderlying patient ventilatorinteractions[16].Phaseportraitsprovideglobalsignaturesofthequality oftheventilationfromamechanicalpointofview.Dependingonloopdispersionandshape, patients with regular ventilatory patterns could be easily distinguished from patients not adaptedtotheirventilators.Itshouldbenotedthatairleakswereeasilydetectedbythis approachsincetheyinducedloopswithabnormalshapesandusuallywithlargeamplitudes. AparallelapproachwasdevelopedbyMulqueneeyetal.[18].Theybuiltanalgorithmthat wasabletodetectineffectivetriggeringeffortsbasedonsigni cantalterationsoftheexpiratory ow signal. However, their technology was connected to a speci c ventilator and required an electronic signal delivered by this machine to detect the expiratory phase. Conversely,thealgorithmofAchouretal.[15]runswithanynoninvasiveventilatorandhas theabilitytocombinetheanalysisof ow/pressuretimeseriesandtheirmathematicaltransformation according to the nonlinear dynamic system theory. It quanti es the breathing patternandalsoidenti essigni cantinspiratoryeffortvariations.Chenetal.[19]havealso nalizedanalgorithmthatworksbyanalyzingminimalandmaximal owvaluesduringthe expiratoryphaseoftheITE.Bycomparison,thealgorithmofAchouretal.uses owderivativesovereachwholeventilatorycycleandnotonlyduringitssoleinspiratoryorexpiratoryphaseandrepresentsanef cienttooltoidentifyrepeatedITE.
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The standard criteria commonly used to de ne ITE are based on a Pes decrease of morethan1cmH2Owithasimultaneousdropinairwaypressureorchangein ow[8]. Giannoulietal.werethe rsttosuggestthatITEcouldbedetectedexclusivelyfromPaw and owtimeseries[9].Thisapproachisaccurateinintubatedpatients,andanacceptable ITEunderestimationmaybeencounteredincaseofseverepatient ventilatorasynchronies.Thepreviouslycitedarticlesshowedthatasimilarapproachcanbeautomatedand canalsobeappliedtopatientsreceivingnoninvasivePSV.Suchalgorithmscouldbeof potentialclinicalinteresttoidentifyITEduringprolongedrecordingsduringsleeporwhen assessing domiciliary ventilation. This new approach for assessing patient ventilator interactions avoids the inherent dif culties and discomfort associated with esophageal pressureassessments.
References 1. NavaS,CarlucciA,CerianaP(2009)Patient ventilatorinteractionduringnoninvasiveventilation:practicalassessmentandtheoreticalbasis.Breathe5:323 333 2. TobinMJ,JubranA,LaghiF(2001)Patient ventilatorinteraction.AmJRespirCritCareMed 163:1059 1063 3. FaurouxB,LeRouxE,RavillySetal(2008)Long-termnoninvasiveventilationinpatients withcystic brosis.Respiration76:168 174 4. FaurouxB,NicotF,EssouriSetal(2004)Settingofnoninvasivepressuresupportinyoung patientswithcystic brosis.EurRespirJ24:624 630 5. KriegerBP(2009)Hyperin ationandintrinsicpositiveend-expiratorypressure:lessroomto breathe.Respiration77:344 350 6. NavaS,BruschiC,RubiniFetal(1995)Respiratoryresponseandinspiratoryeffortduring pressuresupportventilationinCOPDpatients.IntensiveCareMed21:871 879 7. NavaS,BruschiC,FracchiaCetal(1997)Patient ventilatorinteractionandinspiratoryeffort during pressure support ventilation in patients with different pathologies. Eur Respir J 10:177 183 8. ParthasarathyS(2005)Effectsofsleeponpatient ventilatorinteraction.RespirCareClinN Am11:295 305 9. FanfullaF,DelmastroM,BerardinelliAetal(2005)Effectsofdifferentventilatorsettingson sleepandinspiratoryeffortinpatientswithneuromusculardisease.AmJRespirCritCare Med172:619 624 10. LeungP,JubranA,TobinMJ(1997)Comparisonofassistedventilatormodesontriggering, patienteffort,anddyspnea.AmJRespirCritCareMed155:1940 1948 11. GiannouliE,WebsterK,RobertsDetal(1999)Responseofventilator-dependentpatientsto different levels of pressure support and proportional assist. Am J Respir Crit Care Med 159:1716 1725 12. FanfullaF,TaurinoAE,LupoNDetal(2007)Effectofsleeponpatient/ventilatorasynchrony in patients undergoing chronic non-invasive mechanical ventilation. Respir Med 101: 1702 1707 13. GuoYF(2004)Contributionofpolygraphyandpolysomnographytonocturnalmonitoringof patientswithobesity-hypoventilationsyndrome(OHS)andnon-invasiveventilation(NIV). DepartmentofMedicine.Medicalthesis,UniversityofGeneva,Geneva
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14. Parthasarathy S, Jubran A, Tobin MJ (2000) Assessment of neural inspiratory time in ventilator-supportedpatients.AmJRespirCritCareMed162:546 552 15. AchourL,LetellierC,CuvelierAetal(2007)Asynchronyandcyclicvariabilityinpressure supportnon-invasiveventilation.ComputBiolMed37:1308 1320 16. Rabarimanantsoa H (2008) Qualité des interactions patient ventilateur en ventilation non invasive nocturne. PhD Thesis, University of Rouen. http://www.coria.fr/spip.php? article551.AccessMay3,2010 17. CuvelierA,AchourL,RabarimanantsoaH,LetellierC,MuirJ-F,FaurouxB(2009)Anoninvasivemethodtoidentifyineffectivetriggeringinpatientswithnoninvasivepressuresupport ventilation.Respiration.Dec2(Epubaheadofprint) 18. MulqueenyQ,CerianaP,CarlucciAetal(2007)Automaticdetectionofineffectivetriggering anddoubletriggeringduringmechanicalventilation.IntensiveCareMed33:2014 2018 19. ChenCW,LinWC,HsuCHetal(2008)Detectingineffectivetriggeringintheexpiratory phaseinmechanicallyventilatedpatientsbasedonairway owandpressurede ection:feasibilityofusingacomputeralgorithm.CritCareMed36:455 461
Carbon Dioxide Rebreathing During Noninvasive Mechanical Ventilation
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FrancescoMojoliandAntonioBraschi
12.1 Introduction Partial reinhalation of previously exhaled carbon dioxide (CO2) may impair the ef cacy of noninvasive mechanical ventilation (NIMV) in improving CO2 removal and unloadingventilatorymuscles[1].Atconstantalveolarventilation,anyCO2concentrationabovezeroininhaledgasescausesanincreaseofarterialCO2tensionbyanequal amount.Accordingly,signi cantCO2rebreathingincreasesalveolarventilationrequirementstomaintaindesiredarterialCO2tension.Thiscanlimitthebene cialeffectsof inspiratoryassistanceprovidedby NIMV.Inthischapter, we review general mechanismsofCO2rebreathingandtheeffectofdifferentinterfaces,respiratorycircuits,and ventilatorsettings.
12.2 General Mechanisms of Carbon Dioxide Rebreathing During NIMV, inspiratory and expiratory ows share the distal part of the respiratory circuitandtheinnervolumeofthepatient ventilatorconnectinginterface,beitamaskor ahelmet.ExpiredCO2 llsthis common spaceandispushedbytheventilatoragaininto thepatient sairwaysduringthefollowinginspiratoryphase.Anyway,thisspaceisnot
F.Mojoli()andA.Braschi FondazioneIRCCSPoliclinicoSanMatteo,ServiziodiAnestesiaeRianimazioneI, UniversitàdegliStudidiPavia,CattedradiAnestesiaeRianimazione, PiazzaleGolgi2,Pavia,Italy e-mail:
[email protected];
[email protected]
A.M.Esquinas(ed.),NoninvasiveMechanicalVentilation, DOI:10.1007/978-3-642-11365-9_12,©Springer-VerlagBerlinHeidelberg2010
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reallyequivalenttothedeadspacewedealwithduringinvasivemechanicalventilation. Suchclassic,orstatic,deadspaceis lledbythe nalpartofexpiratorytidalvolume,havingaCO2concentrationequaltomeanalveolarvalue(i.e.,theend-tidalCO2).Apartfrom aminorclearingeffectofbias owwhen ow-basedtriggeringisselected,CO2doesnot leave this static dead space. Thus, reinhalation of this volume does not signi cantly decreasealveolarCO2, nallyresultingineffectiveinremovingcarbondioxide. Thisisnotthecasefornoninvasiveventilation.Duringmaskventilation,highexpiratory owsthroughtheexhalationportandsigni cantairleaksattheinterfacewiththe patient sfacecansubstantiallydecreasetheCO2concentrationbelowthealveolarvalue [2];reinhalationofthispartiallycleared(i.e.,dynamic)deadspaceisthereforenotcompletelyineffectiveinremovingCO2.Duringhelmetventilation,CO2rebreathingisnotdue todeadspaceventilationatall.Expiredgasesfromthepatientareindeeddilutedinaspace thatismuchlargerthantidalvolume,withCO2concentrationinsidethehelmetmostly reducedbythe owoffreshgasesfromtheventilator.Therefore,helmetNIMVcanbe assimilatedtobreathinginasemiclosedenvironment[3,4].Fromwhathasbeenjustmentioned, factors underlying rebreathing during mask and helmet NIMV are substantially different;therefore,theywillbediscussedseparately.
12.3 CO2 Rebreathing During Mask Ventilation The amount of CO2 rebreathed from the mask and respiratory circuit depends on dead spacevolumeanditsCO2content. The volume of dead space may be modi ed by mask and respiratory circuit design, ventilatorsettings,andthepatient srespiratorypattern.Maskswithmajorinnervolume (once xed to the patient s face), like total-face masks, may improve comfort during NIMVbutenhanceCO2rebreathing[2].Regardingcircuitdesign,whenatwo-limbrespiratory circuit is used, dead space volume is limited to the mask inner volume plus the volumeoftherespiratorycircuitdistaltotheY-piece(Fig.12.1a). Anyway,NIMVisoftenputinplaceusingasingle-limbrespiratorycircuit.Inthis case, gases exhaled by the patient are discharged in the environment by one or more exhalationports,thepositionanddesignofwhichcansigni cantlyaffectrebreathing[2]. As owthroughexhalationportsislimited,inthe rstpartofpatient sexpiration(when owreachesitspeak),someexhaledgasescangouptherespiratorycircuit,muchbeyond theexhalationport(Fig.12.1b)[5].Actualdeadspacecanthusbecomelargerthanwhat theoreticallyattended(i.e.,thevolumebetweenthepatient smouthandtheexhalation port).Therefore,largetidalvolumesofthepatientandexhalationportswithhighresistancemayenlargedeadspace[1].Inthesecondpartofexpiration,deadspacemayinstead bereducedbythe owoffreshgasesproducedbytheventilatortomaintainpositiveendexpiratorypressure(PEEP);thisisduetointentionalleaksthroughtheexpirationport andunintentionalleaksbetweenthemaskandthepatient sface.AhigherPEEPleveland alongerexpiratorytimeincrease,respectively,thequantityanddurationofleak ows,
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a Two-limb circuit
b Exhaust port on circuit
c Unidirectional expiratory valve
d Exhaust port within the mask
Fig. 12.1 (a) In a two-limb circuit, theoretical dead space is limited to the volume distal to the Y-piece.Duetounintentionalleaksfromthemask patientinterface,theCO2concentrationinthis volumecanbesubstantiallylowerthanthealveolarmeanvalue(i.e.,end-tidalCO2),makingita dynamic dead space.(b)Inthisparticularvarietyofsingle-limbcircuit,theoreticaldeadspace isthevolumedistaltotheexhaustport.Actualvolumeofdeadspaceisincreasedbylargetidal volumesofthepatientandhighresistanceoftheexhalationport(dashedarrows),anddecreased by PEEP and prolonged expiratory time. The balance between these factors determines actual volume of dead space. (c) The existence of a unidirectional valve on a single-limb circuit can decreaseCO2deadspacevolume.Amajordrawbackisincreasedcircuitresistance.(d)Exhaustion portswithinthemaskdecreasedeadspacevolumeanditsCO2content
thuslimitingdeadspace(Fig.12.1b)[1].Exhalationportscanbeprovidedwithaunidirectional(nonrebreathing)valve;thiscansigni cantlydecreasedeadvolume(Fig.12.1c) [5]butmayincreaseinspiratoryandexpiratorycircuitresistance,leadingtobothlower inspiratorypressurizationandhigherexternalPEEP[1].Exhalationportswithinthemask insteaddecreasedeadspacevolumecomparedwiththoselocatedinthecircuit(Fig.12.1d), withoutadverseeffects[2]. DuringmaskNIMV,theCO2contentofdeadspaceisdirectlyrelatedtothepatient sendtidalCO2.Anyway,CO2concentrationinthemask sdeadspacecanbesubstantiallylowered belowthisvaluebymeansofa washing effectoffreshgasesdeliveredbytheventilator.
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HigherPEEPlevels,leaksbetweenthemaskandthepatient sface,andforsingle-limbcircuits,exhalationportslocatedwithinthemask(especiallyoverthenasalbridge)increasethe owoffreshgasesthroughthedeadspaceandthusdecreaseitsCO2content[1,2]. Therefore,tolimitCO2rebreathingduringmasknoninvasiveventilationthebestoption isprobablytheuseofPEEPand,forsingle-limbcircuits,facemasksprovidedwithexhalationportsoverthenasalbridge.Inthesesettings,rebreathingisnegligible,andmonitoring ofinhaledCO2isnottobeconsideredimperative.
12.4 CO2 Rebreathing During Helmet Ventilation Useofheadhelmetsfornoninvasiveventilationcouldbeadvantageous,comparedtofacemasks, intermsofapatient scomfortandtolerance,withimprovedfeasibility,continuity,andduration ofnoninvasiveventilatoryassistance[6].Ontheotherhand,theseadvantagescanbehindered byCO2rebreathingsigni cantlyhigherthanwhatisobservedduringmasknoninvasiveventilation[6,7].Ateverybreath,expiredcarbondioxidedoesnotcompletelyleavethehelmetbut partlydilutesitselfwithintheinternalvolumeofthedeviceandissubsequentlyinhaledagain.In thissetting,itcanbedemonstratedthattheamountofCO2reinhaledbythepatientdependson justtwofactors:thepatient scarbondioxideproduction(V¢CO )andthetotalgas owpassing 2 throughthehelmet(Ftot)[3,4].Infact,whenasteadystateisreachedandCO2isstableinsidethe helmet,theamountofCO2enteringthehelmetperminute(i.e.,thepatient sV¢CO ),mustbeequal 2 totheamountofCO2leavingthedeviceinthesametime.Becausethelastisafunctionofthe meanCO2concentrationinsidethehelmet(hCO2)andthesumofall owsdirectedfrominside thehelmettooutside(Ftot),theequationofCO2steadystateinsidethehelmetis V'CO2=hCO2× Ftot or,oncerearranged, hCO2=V'CO2 / Ftot Totalgas owpassingthroughthehelmetisequivalenttothevolumedeliveredbytheventilator every minute. This ow can be divided into three components: one reaches the patient srespiratorysystem;anotherintermittentlydistendsthehelmet;thelastcorresponds toleaksattheinterfacebetweenthesoftcollarofthehelmetandthepatient sskinsurface. Thepresenceofa helmetventilation, duetotherelativelyhighcomplianceofthisdevice, isauniquefeatureofthistechnique.ThetheoreticallyderivedequationofhelmetCO2content was fully con rmed by experimental data obtained during both continuous positive airway pressure [3] and pressure support ventilation [4] delivered by helmet. In a bench study,alltestedmanipulationsofthesystemaffectedCO2rebreathinginsofarastheywere abletochangeFtotorV¢CO [4].Therefore,signi cantrebreathingcanbeexpectedwhenthe 2 patient s metabolic requirements are high or the ventilator volume delivery is low. Remarkably,thevolumeofthehelmetandthepatient send-tidalCO2,incontrastwithmask ventilation,donotaffectCO2reinhalation.ToincreaseFtotandlowerCO2insidethehelmet, we can increase pressure support, add an intentional leak device, or implement a helmet
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ow-by.UseofleakdevicesdecreasesCO2rebreathingbuthindershelmetpressurization andthepatient sinspiratoryassistance,whicharecounterproductiveforCO2removal[4,8]. Whenpressureassistancetothepatient sspontaneousactivityisalreadyoptimalbutCO2 rebreathingisnot,theadditionofa ow-bycaninsteadbeconsidered[4].Aninteresting optionistheuseofbias owfromtheventilatorasa ow-by;oncea ow-basedinspiratory triggerisselected,theventilatormustbeconnectedtothehelmetbytwoindependentports, forinspirationandexpiration,toforcethebias owtopassthroughthehelmet.Thistrick effectively decreases rebreathing by increasing the ow inside the helmet, thus clearing awayCO2withoutadverseeffects. DuringhelmetNIMV,CO2rebreathingmustbemonitored.Inmechanicallyventilated patients, rebreathing is usually evaluated by end-inspiratory CO2 value. Unfortunately, inhaledCO2insidethehelmetcanbegrosslyunderestimatedbythisvalueduetotheslow decrease of CO2 concentration during the inspiratory phase of helmet ventilation (Fig.12.2)[4].TheCO2valuemeasuredina quietpoint (notaffectedby owstoand
airway opening, Y-piece and helmet CO2(%)
5
etCO2
4 yCO2 hCO2
hCO2 3
2
1 eiCO2
eiCO2 0
time (s)
Fig. 12.2 ContinuousCO2concentrationrecordingsattheairwayopening(blackline),attheY-piece oftheventilatorcircuit(dottedline),andinsidethehelmet(grayline)duringhelmetventilation with16.5L/minoftotalminuteventilationand350mL/minofCO2production.Atairwayopening,theminimumvalueisend-inspiratoryCO2(eiCO2),andthemaximumvalueisend-expiratory CO2(etCO2).TheCO2concentrationmeasuredattheY-piecerangesfromzeroduringinspiration (duetofreshgas owfromtheventilator)andtheend-expiratoryvalue(yCO2),whichislower thanetCO2becausegasesexpiredbythepatientaredilutedinthehelmetinternalvolume.CO2 concentrationmeasuredata quiet pointinsidethehelmet(hCO2)isconstantduringtheentire respiratorycycleandcorrespondstothemeanCO2concentrationininhaledgases
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from the patient) inside the helmet is instead stable and corresponds exactly to mean inhaledCO2[4].Whenastablevalueinsidethehelmetcannotbeobtained,theend-tidal CO2valuemeasuredattheY-pieceorattheexpiratoryportrepresentsafairestimateof CO2rebreathing[4].
Key Recommendations
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Duringmaskventilation,implementPEEPanduseexhalationportswithinthe masktoreduceCO2rebreathing. Whileventilatingwithahelmet,atotalgas owbelow40L/minisathighrisk ofsigni cantCO2rebreathing.Increasetotalgas owthroughthehelmetby raisingpressuresupportand/orbyaddinga ow-by. CO2rebreathinginthehelmetmustbemonitored,atleastperiodically.
References 1. LofasoF,BrochardL,TouchardDetal(1995)Evaluationofcarbondioxiderebreathingduring pressure support ventilation with airway management system (BiPAP) devices. Chest 108: 772 778 2. SchettinoGPP,ChatmongkolchartS,HessDetal(2003)Positionofexhalationportandmask designaffectCO2rebreathingduringnoninvasivepositivepressureventilation.CritCareMed 31:2178 2182 3. TacconeP,HessD,CaironiPetal(2004)Continuouspositiveairwaypressuredeliveredwith a helmet :effectsoncarbondioxiderebreathing.CritCareMed32:2090 2096 4. MojoliF,IottiGA,GerlettiMetal(2008)Carbondioxide rebreathing during non-invasive ventilationdeliveredbyhelmet:abenchstudy.IntensiveCareMed34:1454 1460 5. FergusonGT,GilmartinM(1995)CO2rebreathingduringBiPAPventilatoryassistance.AmJ RespirCritCareMed151:1126 1135 6. AntonelliM,PennisiMA,PelosiPetal(2004)Noninvasivepositivepressureventilationusing ahelmetinpatientswithexacerbationofchronicobstructivepulmonarydisease:afeasibility study.Anesthesiology100:16 24 7. Navalesi P, Costa R, Ceriana P et al (2007) Non-invasive ventilation in chronic obstructive pulmonarydiseasepatients:helmetversusfacialmask.IntensiveCareMed33:74 81 8. RaccaF,AppendiniL,GregorettiCetal(2008)Helmetventilationandcarbondioxiderebreathing:effectsofaddingaleakatthehelmetports.IntensiveCareMed34:1461 1468
Carbon Dioxide Rebreathing During Pressure Support Ventilation with Airway Management System (BiPAP) Devices
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FrédéricLofasoandHélènePrigent
13.1 Introduction Inthe1980s,thedevelopmentofnoninvasiveventilationusingpressuresupportventilationwithorwithoutpositiveend-expiratorypressure(PEEP)constitutedamajorimprovementinthemanagementofbothacuteandchronicrespiratoryfailure.Meanwhile,the rst bilevelventilatorwasdesigned(BiPAP;Respironics;Murrysville,PA).Initiallyintended toimprovehometreatmentofsleepapneasyndrome,thisdevicelackedalarmsandmonitoringsystemsbutwaseasytohandleandlowpriced.Itwasanasalcontinuouspositive airwaypressuredeviceequippedwithasolenoidmagneticvalvesystemallowingseparationofPEEP(withaminimallevelbelow2cmH2O[1,2])andinspiratorypositiveairway pressure adjustments. Like other nasal continuous positive airway pressure devices designedforhome,itusedasingle-limbcircuitwithaleakport(i.e.,RespironicsWhisper Swivel).Therefore,therewasariskofCO2rebreathing,whichwasinitiallyconsideredan importantlimitationforextendingitsuseinthetreatmentofrespiratoryfailure,especially hypercapnicrespiratoryfailure,whichwasconsideredtohavethebestoutcomewithnoninvasiveventilation.
13.2 Rebreathing Mechanisms Toensurethatnoexhaledgasremainsinthetubingattheendofexpiration( readytobe inhaledagain ),themeanexpiratory ow,thatis,theratiobetweentidalvolumeandexpiratorytimeVT/TE,hastobelowerthantheintentionalleakobtainedthroughtheleakport
F.Lofaso()andH.Prigent AP-HP,RaymondPoincaréTeachingHospital,UniversitéVersailles-StQuentinenYvelines, Physiology FunctionalTesting,E.A.4497andCIC-IT,92380Garches,France e-mail:
[email protected];
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a Inspiration BiPAP device
patient Exhalation port
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Fig. 13.1 BiPAPventilationwithanintentionalleak owoftheWhisperSwivelconnectorofabout 200ml/swhenPEEPissetat5cmH2O.(a)Inspirationperiod.(b)Expirationperiodwitha ow ratelowerthantheintentionalleakthroughtheleakport;noexhaledgasreturnsintothetubingat theendofexpiration.(c)Expirationperiodwitha owratehigherthantheintentionalleakthrough theleakport;someoftheexhaledgasremainsinthetubingattheendofexpirationandcanbe rebreathedduringthenextinspiration
duringexpiration.Therefore,rebreathingdepends rstonthepatternofbreathing:highVT andshortTEexposesahigherriskofrebreathingbyincreasingexpiratory ow.Second,it dependsonthesizeoftheportandthePEEPlevel:AsmallportandlowPEEPlevelconstituteriskfactorsforrebreathing.Forexample,Lofasoetal.[2]observedthattheintentionalleak owoftheWhisperSwivelconnectorwasabout200ml/swhenPEEPwasset at5cmH2O.Therefore,ifapatienthastoexpire500mlin2s,theexpiredvolumeremaininginthecircuitattheendofexpirationwouldbeapproximately100ml(Fig.13.1).
13.3 Bench and Clinical Studies TheinversecorrelationbetweenrebreathingandPEEPwiththeWhisperSwivelwasdemonstrated in a bench study [1] and a clinical study [3]. Moreover, it has been clinically demonstrated that CO2 rebreathing observed with the Whisper Swivel worsened the patients workofbreathing(WOB)[2].Theuseofaplateauexhalationvalveandanonrebreathing valve has been proposed to reduce or avoid CO2 rebreathing. Ferguson and Gilmartin[3]observedthat,withtheiruse,CO2rebreathingbecameminimalinpatients. Theplateauexhalationvalveconsistsofadiaphragmthatlimitsairleaksathighpressure (during inspiration) and works as a larger leak port at low pressure (during expiration),
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whilethenonrebreathingvalveisanantireturnvalvewithalateralintentionalleak.Lofaso etal.[1]con rmedthatthesubstantialrebreathingobservedwiththeWhisperSwiveldisappeared when using a nonrebreathing valve. However, the drawback is that the nonrebreathingvalveinducesadditionalexpiratoryresistance[2],whichmayhavesomeimpact onintrinsicPEEPandthereforeonWOB[4].Incontrast,inacrossoverstudywithseven patientsreceivinglong-termnocturnalnoninvasiveventilation,theplateauexhalationvalve didnotimprovedaytimeornocturnalgasexchangeorsymptomscomparedtotheWhisper Swivel,mostlikelybecauseofairleakageandCO2escapeoccurringviaotherroutes[5].
13.4 Exhalation Port Characteristics Toexplorethein uenceoftheexhalationportpositiononCO2rebreathing,Shettinoetal. [6]performedabenchstudythatobservedthattheCO2rebreathingwassigni cantlylower whentheexhalationportwasplacedwithinthemaskratherthanonthecircuit.Inaddition, thesmallestmaskvolumewasassociatedwithlowerCO2rebreathingthanthelargerone. However,thesedifferencesmayalsobeexplainedbydifferencesinexhalationportsizes.
13.5 Devices Evolution Now,thesedeviceshavebeenimproved;allbilevelventilatorshaveaminimalPEEPsettingof4cmH2Obydefault,andtheintentionalleakthroughtheleakportofmostavailable masksexceeds300ml/swhenPEEPissetat5cmH2O(higherthanwhatwasobserved withtheWhisperSwivelleak[2,7]).Thisgreatlyreducesandevenabolishestheriskof rebreathingduringnoninvasiveventilation,exceptwiththeuseofhelmets[8].Thisnovel interface,aimingtoimprovecomfortandtoreducelocalsideeffects,exposesthepatient toahigherriskofCO2rebreathing[8]andisnotcurrentlyadaptedforhomeventilation.
13.6 Conclusion Theriskofrebreathingduringnoninvasiveventilationisnowlowthankstonotonlythe improvementsachievedsincethe rstbilevelventilatorsandtheirinitialcircuitrybutalso secondarytononintentionalairleakageandCO2escapealmostconstantlyobservedduring noninvasiveventilationandsleep.ThesystematicuseofaminimalPEEPlevelof4cmH2O isusuallyef cientinreducingrebreathingbutcanbealimitationfortheuseofthisdevice forsomepatients.However,CO2rebreathingsystematicallyoccursduringtheuseofhelmetinterfaces.
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Finallytheclinicianshouldbeawareofriskofrebreathing,whichcanbeafactor ofmechanicalventilation,pooref ciencyandthisrebreathingisfacilitedbyhigh respiratoryfrequencyandlowpeeplevel.
References 1. LofasoF,BrochardL,HangTetal(1996)Homeversusintensivecarepressuresupportdevices. Experimentalandclinicalcomparison.AmJRespirCritCareMed153:1591 1599 2. LofasoF,BrochardL,TouchardDetal(1995)Evaluationofcarbondioxiderebreathingduring pressure support ventilation with airway management system (BiPAP) devices. Chest 108: 772 778 3. FergusonGT,GilmartinM(1995)CO2rebreathingduringBiPAPventilatoryassistance.AmJ RespirCritCareMed151:1126 1135 4. LofasoF,AslanianP,RichardJCetal(1998)Expiratoryvalvesusedforhomedevices:experimentalandclinicalcomparison.EurRespirJ11:1382 1388 5. HillNS,CarlisleC,KramerNR(2002)Effectofanonrebreathingexhalationvalveonlongtermnasalventilationusingabileveldevice.Chest122:84 91 6. SchettinoGP,ChatmongkolchartS,HessDRetal(2003)Positionofexhalationportandmask designaffectCO2rebreathingduringnoninvasivepositivepressureventilation.CritCareMed 31:2178 2182 7. LouisB,LerouxK,IsabeyDetal(2010)Effectofmanufacturer-insertedmaskleaksonventilatorperformance.EurRespirJ35:627 636 8. RaccaF,AppendiniL,GregorettiCetal(2008)Helmetventilationandcarbondioxiderebreathing:effectsofaddingaleakatthehelmetports.IntensiveCareMed34:1461 1468
Carbon Dioxide Rebreathing in Noninvasive Ventilation
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DanielSamolskiandAntonioAntón
14.1 Introduction Severalfactorsinnoninvasivepositivepressureventilation(NIPPV)haveprovedtobe potentialcausesoffailurewhenthiskindofmechanicalrespiratoryassistanceisusedin patientswhosufferfromacute(ARF)orchronic(CRF)respiratoryfailure[1 3].Onesuch factoriscarbondioxide(CO2)rebreathing[1 4].Thisphenomenonconsistsofrebreathing partoftheCO2expiredbythepatientduringtheventilatorycycleasaresultofanaccumulationofthisgasinthemaskorthecircuit.Suchrebreathingtakesplacemainlyinsinglelimb circuits (inspiration and expiration into the same tube). Besides the use of such a circuit,therearetechnicalcircumstancesthatplayanactiveroleinthepresenceoreliminationofexpiredCO2:theventilatorymode[4,5],typeofmaskandexpiratoryport[6 12],aswellasthelevelofpositiveend-expiratorypressure(PEEP)used[4,10,11].Since 1995, when Ferguson and his collaborators rst described such a phenomenon, little research has been done on this issue. The development of technological innovations, mainlyininterfaces,hasrestrictedthepotentialclinicalimplicationsofthisdeleterious phenomenon.Likewise,researchworksconductedsofarhavenotcon rmedwhetherCO2 rebreathing does have a signi cant in uence on patients clinical evolution or is just a potentially,butrarely,harmfulphenomenon.
D.Samolski() RespiratoryMedicineDepartment,HospitaldelaSantaCreuiSantPau,Barcelona,Spainand Roosevelt49574°B,CP1431BuenosAires,Argentina e-mail:
[email protected] A.Antón RespiratoryMedicineDepartment,HospitaldelaSantaCreuiSantPau,Barcelona,Spain e-mail:
[email protected]
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14.2 Main Topics Asoutlinedintheintroduction,thereareseveralelementsorcircumstancesthatin uence theCO2rebreathingscope.
Typeofcircuit Typeofmask:internalvolume,exhaustvent(EV),orcontrolledleakholes Devicesattachedtothecircuit(incaseofmaskswithoutanEV):conventionalorantirebreathingexpiratoryports,cylindricalspacers
Levelofexpiratorypressure(expiratorypositiveairwaypressure,EPAP) Patient sfeatures:ARForCRFinnormo-orhypercapnicpatientsandtheirventilatory pattern
14.2.1 Type of Circuit CO2rebreathingisaninherentcharacteristicofthesingle-limbcircuitsystem[1 3]andis lessfrequentintwo-limbcircuits(separateinspiratoryandexpiratorylimbs)orcircuitswith pneumaticexpiratoryvalves(domiciliaryvolumetricventilators).Logically,wecaninfer thatexpirationintothesametubeintowhichthepatientinspiresleadstorebreathingpreviouslyexpiredgasifsuchgasisnotappropriatelyeliminatedfromthetubingormask.
14.2.2 Type of Mask Maskswithhighlevelsofdeadspace[12,13]cangiverisetosigni cantlevelsofrebreathing incaseofinappropriatekineticsofexpiredgaselimination.Technologicaldevelopmenthas createdEVs(controlledleakholes)inmasks,whichallowadequateeliminationofgases beforethenextinspiration.Suchholesarelocatedinthemaskitselfaswellasintheelbowshapedtubejoiningthemaskwiththecircuit.Thekeyissueistocontroltheef ciencyof newmasksineliminatingCO2throughtheirholesasresearchstudiesconductedsofarhave testedonlyareducednumberoftrademodels[10,11]TheexistenceofaninherentphenomenoninNIPPV,suchasleaks,highlyfrequentinnasalmasks,willcertainlyplayakeyrole inpreventingCO2rebreathingbyreducingtheairvolumeexpiredintothecircuit.
14.2.3 Devices Attached to the Circuit Whenhermeticmasks(withoutEVs)andsingle-limbcircuitsareused,itisfundamentalto addexpiratoryports[4,11,12]thatwillallowairreleasebeforethefollowingventilatory
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cycle.Somehow,thesemasksfellintodisuseafterthedevelopmentofEVmasks.However, theyarestillavailableinthemarketduetotheirlowcostanduseindomiciliaryventilators andinrespiratorycareunits.Consequently,weshouldbeawareofhowtousethemappropriately.Therearetraditionalexpiratorydevices,suchastheWhisperSwivel®,ordevices withananti-rebreathingsystem,suchasPlateauvalve®.Furthermore,sometubeshavea built-inleakport. Regardingtheuseofspacers(corrugatedcylindricaltubeswhosefunctionistokeep anykindofpotentiallyannoyingelementawayfromthepatientbecauseofitssizeorform) betweentheventilatorandthepatient,atleastintheorythesecouldincreasethedeadspace andthereforegiverisetorebreathing.Ourgroup[11]hasprovedthatasingle-limbcircuit withitsownpneumaticvalve,evenwithlargeattachedspacers,avoidedrebreathingwhile usingvolumetricventilation.
14.2.4 Level of EPAP Used Acertainlevelofexpiratorypressureimprovestheeliminationofexpiredgaseswithinthe maskandcircuit.AlthoughFerguson sworksuggestedaminimumlevelofEPAPbetween 6and8cmH2Owhenusingtraditionalexpiratoryvalves,theuseofantirebreathingdevices aswellasEVs(leakholes)inthemaskhashelpedreducesuchpressureto4cmH2Oor evenless[11].Inclinicalpractice,theEPAPaveragelevelreaches6 8cmH2O.
14.2.5 Patient Characteristics: Hypercapnia or Normocapnia Hypercapniahasprovedtoberelatedtorebreathinglevels[4].Onlyoneresearchstudy conductedinhypercapnicpatientshasshownazerorebreathinglevelwhenusingnasal maskswithEVsandantirebreathingdevicesduringNIPPV[14].Inaddition,thepatient s ownventilatorypattern(inspiratorytime/totaltimeTi/Ttot;respiratoryfrequency/tidalvolumef/Vt)mayin uenceboththedeadspaceandthedegreeofrebreathing,althoughthis facthasnotbeendemonstrated.
14.3 Discussion CO2rebreathingisapotentiallyharmfulphenomenonwithadirectin uenceonthefailure orsuccessofNIPPV[1 3].Thereareseveralfactorsinvolvedintheexistenceandscopeof thisphenomenon.Manyauthorshavedescribedtheimportanceofsuchfactors,givingrise toopposing ndingsinsomecases.Theactualin uenceofCO2rebreathinginusualclinical practicehasnotbeendulyevidencedbyanyresearch.Hilletal.[15]comparedgaseous
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Fig. 14.1 ContinuousanalysisofCO2insidethemask.Horizontalarrow:ETCO2(end-tidalCO2, mmHg).Verticalarrow:FiCO2(inspiredCO2fraction,%)
interchangeandsymptomsinpatientsunderNIPPVwhousedbothaconventionalexpiratoryportandanantirebreathingone.Nodifferencewasfoundbetweenthetwogroups;even more,theantirebreathingvalvewasconsiderednoisierandbadlookingbypatients.Inaddition,Farréetal.[16]suggestedthatrebreathingcouldbetoodeleteriousincaseofcontinuouspositiveairwaypressure(CPAP)failure,aneventthatcouldbepreventedbyusingan antirebreathingvalve.AnothercontroversialissueisthemomentatwhichtheCO2should bemeasuredintheventilatorycycletoshowtheamountofgasrebreathingaswellasthe place on the patient ventilator unit where such value should be measured (Fig. 14.1). SeveralauthorsallegedthatCO2attheendofexpiration(ETCO2)[7,8,10,15]measurementhasproveduseful,whereasothersarguedthatthevalueofCO2inhaled(CO2inspired fraction, FiCO2) [8, 11] offers more accurate and bene cial information. Other research indicated a preference for measurement of CO2 partial pressure in an arterial blood gas sample(PaCO2)[4,5],transcutaneous[4]CO2,orsimplecontinuousCO2quanti cationin themask[4,6,16].Infact,allthesevaluescouldberegardedasinterdependentvalues. Accordingtoourpointofview,FiCO2isthemostrepresentativevalueinrebreathingasit showstheCO2amountinthepatients nostrilsattheprotoinspiratoryphase.However,this measurementmayundervaluerebreathingattheinitialstageofbreathinginitial. Atpresent,andaccordingtothestudiescarriedout,weshouldtakeintoconsideration severalkeyissueswhensettinguptherespiratory patientsysteminanattempttolimitthe in uenceofCO2rebreathing:
UseofmaskswithEVs,dulytestedthroughtechnicalstudiesthatprovetheirabilityto
eliminate the expired CO2 (only a small number of masks sold presently have been subjecttosuchtests) UseofantirebreathingexpiratoryportsincaseofusingmaskswithoutEVsandsinglelimbcircuits Useofcircuitswithpneumaticvalvesincaseofvolumetricventilators Useofspacerswiththecorrespondingvolumestatedinresearchworks OptimizationoftheexpiratorypressurelevelthatallowsadequateeliminationofCO2 fromthemask Optimizationofeachandeveryparameter,takingintoconsiderationpatients individual characteristics: CO2 level, ventilatory level, other factors for NIPPV success or failure(leaks,asynchrony)
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Key Recommendations
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CO2rebreathingisapotentialfactorforfailureinNIPPV. Whensingle-limbcircuitsareused,thefollowingelementsshouldbeusedto avoidhighlevelsofFiCO2:
Mask with minimum volume or dead space Duly tested masks with EVs – Antirebreathing expiratory ports in hermetic masks – Appropriate EPAP levels –
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KnowledgeofthecurrentclinicalimportanceofCO2rebreathingisstillpending.
References 1. Hill NS (2001) Problems, remedies, and strategies to optimize the success of noninvasive ventilation.In:HillNS(ed)Noninvasivepositivepressureventilation.Futura,Armonk,NY, pp187 213 2. Kacmarek RM, Hill N (2001) Ventilators for NIPPV: technical aspects. Eur Resp Mon 16:76 105 3. Frades SH, Peces Barba G (2007) In: Lucas Ramos P, Jareño Esteban JJ (eds) Ventilacion mecanicanoinvasiva:ine caciaycomplicaciones.Monogra asdelaSociedadMadrileñade Neumologia y Cirugia toracica (NeumoMadrid), volumen IX: Ventilacion no invasiva. Madrid,pp45 61 4. FergusonGT,GilmartinM(1995)CO2rebreathingduringBiPAPventilatoryassistance.Am JRespirCritCareMed151:1126 1135 5. LofasoF,BrochardL,TouchardD,HangT,HarfA,IsabeyD(1995)Evaluationofcarbon dioxide rebreathing during pressure support ventilation with airway management system (BiPAP)devices.Chest108:772 778 6. ZhangX,ChenR,HeG(2000)Modi cationoffacialmaskonthedeadspaceeffectinnon invasivemaskventilation.ZhonghuaJieHeHeHuXiZaZhi23(12):734 736 7. SchettinoGP,ChatmongkolchartS,HessDR,KacmarekR(2003)Positionofexhalationport andmaskdesignaffectCO2rebreathingduringnon-invasivepositivepressureventilation.Crit CareMed31(8):2178 2182 8. TacconeP,HessD,CaironiP,BigatelloLM(2004)Continuouspositiveairwaypressuredeliveredwithahelmet.Effectsoncarbondioxiderebreathing.CritCareMed32(10):2090 2096 9. RaccaF,AppendiniL,GregorettiC(2005)Effectivenessofmaskandhelmetinterfacesto deliver noninvasive ventilation in human model of resistive breathing. J Appl Physiol 99: 1262 1271 10. MedianoO,GarciaRioF,VillasanteC(2006)Comparaciondelareinhalacióndeanhídrido carbónico originada por 3 mascarillas durante la aplicacion de CPAP. Arch Bronconeumol 42(4):189 193 11. SamolskiD,CalafN,GuellR,CasanP,AntonA(2008)Carbondioxiderebreathinginnoninvasive ventilation. Analysis of masks, expiratory ports and ventilatory modes. Monaldi ArchChestDis69(3):114 118 12. Racca F, Appendini L, Gregoretti C et al (2008) Helmet ventilation and carbon dioxide rebreathing:effectsofaddingaleakatthehelmetports.IntensiveCareMed34:1461 1468
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13. SaatciE,MillerDM,StellIM,LeeKC,MoxhamJ(2004)Dynamicdeadspaceinfacemasks usedwithnon-invasiveventilators:alungmodelstudy.EurRespirJ23:129 135 14. SamolskiD,GuellR,CalafNetal.(2006)AnalysisofCO2rebreathinginhypercapnicpatients whileusingdifferentexpiratorydevicesinnon-invasiveventilation.EurRespJ28(S50) 15. HillNS,CarlisleC,KramerN(2002)Effectofanonrebreathingexhalationvalveonlongterm nasalventilationusingabileveldevice.Chest122:84 91 16. FarreR,MontserratJM,BallesterE,NavajasD(2002)PotentialrebreathingafterCPAPfailureduringsleep.Chest121(1):196 200
New Adaptive Servo-Ventilation Device for Cheyne–Stokes Respiration
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Ken-ichiMaenoandTakatoshiKasai
15.1 Introduction Severalstudieshaveshownthatpatientswithcongestiveheartfailure(CHF)oftensufferfrom thecomplicationofsleep-disorderedbreathing(SDB),includingCheyne Stokesrespiration withcentralsleepapnea(CSR-CSA)aswellasobstructivesleepapnea(OSA).Thesetwo typesofSDBoftencoexistinsuchcases.CSR-CSAischaracterizedbycyclicalrecurrenceof centralapneasandhyperpneaswithwaxingandwaningofthe owamplitude,whichresults frominstabilityoftherespiratorycontrolsystemcharacterizedbyatendencytohyperventilate duetotheheartfailurecondition.CentralapneaoccurswhenthePaco2fallsbelowtheapnea thresholdduringsleepduetoventilatoryovershoot.CSR-CSAismodi ablebyseveraltypes ofpositiveairwaypressure(PAP)therapy;however,intheclinicalsetting,CSR-CSApatients withCHFtendtohavepooradherencetotheconventionalPAPtherapies,especiallycontinuousPAP(CPAP),whicharewellestablishedastreatmentsforOSA.Furthermore,theyare wellknowntobe nonresponders toconventionalPAPasatherapyforCSR-CSA.Inthe CANPAP(CanadianContinuousPositiveAirwayPressureforPatientswithCentralSleep ApneaandHeartFailureTrial)study[1],CPAPonlydecreasedtheaverageapnea hypopnea index(AHI)byabout50%(from40to19/h).TheposthocanalysisoftheCANPAP.study[2] showedsubjectswitharesidualCSR-CSAofAHI³15usingCPAPremainedwithapoor prognosis.ThesedatasuggestthatothertreatmentoptionsthatcansuppresstheCSR-CSA moreeffectively(i.e.,AHI<15)andcanproducebettercomplianceareneeded. Adaptiveservo-ventilation(ASV),anovelPAPdevice,hasbeendevelopedasaneffectivetherapeuticalternativetootherconventionalPAPtechnologies.TheASVcansuppress notonlyOSAbutalsoCSR-CSA.WereviewtheASVtherapyforCSR-CSAmainlyin patientswithCHF.
T.Kasai()andK.Maeno SleepCenter,ToranomonHospital,Tokyo,Japanand DepartmentofCardiology,JuntendoUniversity,SchoolofMedicine, 2-2-2Toranomon,Minatoku,Tokyo,105-8470,Japan e-mail:
[email protected] A.M.Esquinas(ed.),NoninvasiveMechanicalVentilation, DOI:10.1007/978-3-642-11365-9_15,©Springer-VerlagBerlinHeidelberg2010
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15.2 Methods WesearchedforEnglisharticlesusingMEDLINE(PubMedandOvid)fromJanuary1996 throughAugust2009usingtherelatedterminologyofASVandCSR(orSDB).Thesearch waslimitedtoclinicaltrial,humans,andalladultsolderthan19years. TheASVisanocturnalPAPtherapythroughamaskandbasicallyissimilartobilevel PAP therapy with a spontaneous/timed mode, which delivers two treatment pressures, inspiratorypositiveairwaypressure(IPAP)toprovide xedpressuresupportandexpiratorypositiveairwaypressure(EPAP)tokeeptheupperairwaypatentandpreventobstructiveapnea,hypopnea,snoring,and owlimitation;thereisatransitiontoatimedmode withbackuprespiratoryrateduringsustainedapnea.However,thecurrentASVhastwo noveltherapeuticalgorithmsforCSR-CSA(Fig.15.1a).Theprimaryalgorithmisanadaptivepressurecontrolsystemthatnormalizespatientventilationlevelsbyadjustingeach amount of pressure support (equal to the pressure difference between IPAP and EPAP) withalmostbreath-by-breathresponsetowardthechangesintidalvolumeofCSR.Brie y, the algorithm rapidly increases pressure support in responsse to hypoventilation and decreases it during hyperventilation by varying the level of IPAP (or pressure support) betweenthetwopresetIPAPs(orpressuresupports):minimumIPAP(pressuresupport) andmaximumIPAP(pressuresupport).Thesecondaryalgorithmisanautomaticbackup systemthatallowsthepatienttotakenaturalpausesininspirationwhilestillproviding pressuresupportassistanceduringtrueapneas.Theautomaticbackupsystemtracksthe patient sspontaneousbreathpattern.Basedonthesedata,abackupbreathwithadjusted rateandpressureisautomaticallydeliveredtothepatientduringacentralapneaevent.
15.3 Results ThereweretenarticlesaboutASVtherapyforCSR-CSAinpatientswithheartfailure;all includedaverysmallsample.The rstwasacrossoverstudybyTeschleretal.in2001, whichwastocomparetheeffectsofasinglenighteachofoxygen(2L/min),CPAP,bilevel PAP,andASVonCSR-CSAandsleepon veconsecutivenightsinrandomorderin14 patients with heart failure [3]. Patients preferred the ASV night to either the CPAP or bilevelPAPtitrationnights.ASVsuppressedCSR-CSAandimprovedsleepqualitybetter thanCPAPornasaloxygen.Thereweretwoothersimilararticles,inwhichheartfailure patientswithCSR-CSAunderwentthreenightsofpolysomnography:baseline,conventionalPAP(CPAPorbilevelPAP)titration,andASVtitration[4,5].Inboth,compared withconventionalPAPtherapy,ASVsigni cantlyreducedCSR-CSAandwaswelltolerated.Oldenburgetal.reportedthatuseofASVfor5.8±3.5monthssigni cantlyimproved left ventricular ejection fraction (LVEF), amino-terminal pro-brain natriuretic peptide (BNP)level,andexercisetolerancetothecardiopulmonaryexercisetestaswellasCSRCSAin29malepatientswithheartfailure[6].
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Fig. 15.1 Polysomnographyduringadaptiveservo-ventilation(ASV)inapatientwithCheyne Stokes respirationwithcentralsleepapnea(CSR-CSA)andheartfailure.(a)InitiationofASVforCSRCSA;notethebackupventilationduringacentralapneawithmaximuminspiratorypositiveairway pressure(insidesolidlineoval)andthereductioninpressuresupportduringthehyperventilation phase(insidedottedlineoval).(b)GradualstabilizationofventilatorystateunderASVtherapy;note theabsenceofbackupventilationandtheadaptationoftheASVwiththeminimumnecessarypressuresupportsonspontaneousbreathing.ContinuingASVinturncorrectsthe uctuationofPaco2and bringsinthestabilizationofbreathing.EOGelectro-oculogram,EMGsubmentalelectromyogram, EEGelectroencephalogram,ECGelectrocardiogram,SO2oxyhemoglobinsaturation
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ThereweretwoprospectiverandomizedcontrolledtrialsofASVforCSR-CSAwithheart failure.Inonestudy,30subjectswithheartfailureandCSR-CSAweretreatedwith4weeks oftherapeuticASV(n=15)orsubtherapeuticASV(n=15)[7].Comparedwithasubtherapeuticcontrol,thereweresigni cantfallsinplasmaBNPlevelandurinarymetadrenaline excretioninthetherapeuticASVgroup.Intheotherstudy,25patientswithheartfailureand CSR-CSA were randomly assigned to either CPAP or ASV [8]. Both CPAP and ASV decreasedAHI,butonlyASVcompletelysuppressedCSA-CSR,withAHIbelow10.At6 months,compliancewithCPAPwassigni cantlylessthanwithASV,theimprovementin qualityoflifewashigherwithASV,andonlyASVinducedasigni cantincreaseinLVEF. TherewereafewreportsofASVforCSR-CSAinpatientswithoutCHF.Somereports showedtheef cacyofASVforcomplexsleepapneasyndrome(i.e.,CPAP-emergedCSA) oridiopathicCSRthatwasunresponsivetoCPAPoroxygen.Ontheotherhand,theresults ofstudiesoftheASVforopioid-inducedSDBwerecontroversial.
15.4 Discussion ASVhasbeendesignedtomoreeffectivelyreducethenumberofCSR-CSAepisodes.In fact,somestudiesshowedthatASVdecreasedtheAHImoreeffectivelythanconventional PAPtherapyinpatientswithCSR-CSAandheartfailure[3 5,8].Moreover,itwasreported thatheartfailurepatientswithCSR-CSAweremorecompliantwithASVthanconventional PAP[3,5,8].TheseresultsseemtobeduetotheuniquealgorithmsofASV,whichcanlead toreducedalterationinthePaco2levelandmaintainingthePaco2abovethehypocapnic apneathreshold,whichcaninturnunspreadtheCSR,stabilizethebreathingpattern,and improvesleeparchitectureandquality(Fig.15.1b).Ontheotherhand,bilevelPAPwasalso effectiveforCSR-CSA,butitcouldbethatthis xedpressuresupportinCSR-CSApatients setupoverventilationduringphasesofnormalbreathingorhyperpnea,whichcausesarousalsanddiscomfortorleadstoafallinthePaco2level,whichmayinducecentralapnea.In practice,suchpatientstendtorequiretheIPAPleveltobesettolowervaluesbecauseofthe perceiveddif cultywithhigher-pressuresupport,andsuchreductioninIPAPoftenleadsto insuf cientmanagementoftheCSR-CSA.TheASVmightbeabletoresolvethisproblem ofbilevelPAPbecausetheIPAPlevelisautomaticallyandappropriatelyadapted. SomestudiesshowedthatASVimprovednotonlytheSDBbutalsocardiacfunctionin patientswithheartfailure[6 8].IncreasedintrathoracicpressurethroughPAPcanreduce preloadduetothedecreaseofthevenousreturnandafterloadduetothedecreaseofthe leftventriculartransmuralpressure.ItwasreportedthatPAPcausesdose-relatedincreases incardiacandstrokevolumeindicesamongpatientswithheartfailurewithelevatedleft ventricular llingpressure[9].Westudiedtheeffectof3-monthASVtherapyonresidual CSR-CSAwithAHI³15onCPAPandusedtenpatientswithheartfailurewhoalready hadundergoneCPAPtherapy[10].Inthestudy,thechangeofCPAPtoASVsigni cantly improvedAHIandsleepquality,increasedLVEF,anddecreasedthelevelsofplasmaBNP andurinenoradrenaline.Remarkably,thecompliancewithASVwassigni cantlybetter thanwithCPAP.Intheory,allkindsofPAPtherapiescanbringinthesebene cialeffects
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New Adaptive Servo-Ventilation Device for Cheyne–Stokes Respiration
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onhemodynamicsinpatientswithheartfailure.However,ASVislikelytomoreeffective thanconventionalPAPoncardiacfunctioninpatientswithheartfailurewithCSR-CSA, which may result from better-suited pressure delivery of ASV, better compliance with ASV,oramoresuppressanteffectontheincreasedsympatheticnerveactivity. Currently,twoASVdevicesareclinicallyavailableonaglobalscale.OneisAutoSet CS2/VPAPAdaptSV manufacturedbyResMed(Sydney,Australia),andtheotheris BiPAP®autoSV byRespironics(Murrysville,PA,USA).Inbothproducts,pressuresupportisdynamicallyadjustedbreathtobreathasnecessarytoensurethatthepatients actual ventilation matches the target value. However, there are some differences between the devices; these are brie y shown in Table 15.1. The main points of difference are the mechanicstoassesstheventilatorystatusanddecidethetargetandthecon gurableparametersandsettingranges.AutoSetCS2/VPAPAdaptSVprovidesvolume-targetedASV, whichsetsaminuteventilationtargetthatis90%oftherecentaverageminutevolumein a3-mincollectionperiodandtriestokeepventilationatthetarget.Tomakethesynchrony withthepatient sventilationbetter,thisdevicealsolearnsthepatient srecent owpattern in an 8-s period. On the other hand, the BiPAP autoSV provides ow-targeted ASV, whichmonitorsthepeakinspiratory owofthepatientoverarecentmoving4-minwindowbycalculatinganaveragepeak owateverypointwithinthiswindowtosetatarget peak ow,comparesittotheinternaltarget,andmaintainsatargetpeakinspiratory ow. Theclinicianhastosetthreetypesofpressurelevels.TheEPAPlevelissettomaintain upperairwaypatencyasamanagementofanyobstructiveSDB.Todeterminetherangeof pressuresupportlevels,minimumIPAPandmaximumIPAPneedtobeset.TheAutoSet CS2/VPAPAdaptSValwaysprovidesapressuresupportofatleast3cmH2O.TheBiPAP autoSVcanconformEPAPtominimumIPAPandapplythesamepressureduringinspirationandexpiration(whichisthesameasCPAP)instablebreathing.Whilebothdevices provideanautomaticbackuprateforsustainedapnea,theBiPAPautoSVcanalsomanuallysetthe xedbackuprate.TherearenostudiescomparingthesetwodifferentASV. Table 15.1 Comparisonbetweentwoadaptiveservo-ventilation(ASV)products Volume-targetedASV Flow-targetedASV Productname
AutoSetCS2orVPAPAdapt SV
BiPAPautoSV
Manufacturer
ResMed
Respironics
Targetparameter
90%ofminuteventilation
Peak ow
Calculationwindow
Recentaverageof3-min window
Recentaverageof4-min window
Backupventilation
Auto(15±a/min)
Automodeor xedmode(off or4 30/min)
EPAP
4 10cmH2O
4 25cmH2O
IPAPmin
3 6cmH2OplusEPAP
EPAPlevel 30cmH2O
IPAPmax 8 16cmH2OplusEPAP IPAPminlevel 30cmH2O EPAPexpiratorypositiveairwaypressure,IPAPmin,minimuminspiratorypositiveairwaypressure,IPAPmax,maximuminspiratorypositiveairwaypressure
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Each manufacturer introduces the recommended methodologies to titrate each ASV device.WewouldemphasizethatthetitrationforASVapplicationunderattendedpolysomnography should be performed because these automatic algorithms do not always workappropriatelyforallpatientswithoutanytitrationstudies. There have been no data to evaluate the effect of ASV on long-term prognosis in patientswithCSR-CSA and heart failure until now. However, a large randomized controlledtrialisongoingmainlyinEurope;itspurposeistoinvestigatethelong-termeffects ofASVonthemorbidityandmortalityofpatientswithstableheartfailurewhohaveSDB predominantlywithCSR-CSA.Theresultsofthisstudyareimportantandmayyieldthe primary evidence and determine the rst-line therapy for CSR-CSA in patients with chronicheartfailure.
References 1. BradleyTD,LoganAG,KimoffRJetal(2005)Continuouspositiveairwaypressureforcentralsleepapneaandheartfailure.NEnglJMed353:2025 2033 2. ArztM,FlorasJS,LoganAGetal(2007)Suppressionofcentralsleepapneabycontinuous positiveairwaypressureandtransplant-freesurvivalinheartfailure:aposthocanalysisofthe Canadian Continuous Positive Airway Pressure for Patients with Central Sleep Apnea and HeartFailureTrial(CANPAP).Circulation115:3173 3180 3. TeschlerH,DöhringJ,WangYMetal(2001)Adaptivepressuresupportservo-ventilation:a noveltreatmentforCheyne Stokesrespirationinheartfailure.AmJRespirCritCareMed 164:614 619 4. KasaiT,NaruiK,DohiTetal(2006)Firstexperienceofusingnewadaptiveservo-ventilation deviceforCheyne StokesrespirationwithcentralsleepapneaamongJapanesepatientswith congestiveheartfailure:reportof4clinicalcases.CircJ70:1148 1154 5. ArztM,WenselR,MontalvanSetal(2008)Effectsofdynamicbilevelpositiveairwaypressuresupportoncentralsleepapneainmenwithheartfailure.Chest134:61 66 6. OldenburgO,SchmidtA,LampBetal(2008)Adaptiveservoventilationimprovescardiac functioninpatientswithchronicheartfailureandCheyne Stokesrespiration.EurJHeartFail 10:581 586 7. PepperellJC,MaskellNA,JonesDRetal(2003)Arandomizedcontrolledtrialofadaptive ventilation for Cheyne Stokes breathing in heart failure. Am J Respir Crit Care Med 168:1109 1114 8. PhilippeC,Stoïca-HermanM,DrouotXetal(2006)Compliancewithandeffectivenessof adaptive servoventilation versus continuous positive airway pressure in the treatment of Cheyne Stokesrespirationinheartfailureoverasixmonthperiod.Heart92:337 342 9. DeHoyosA,LiuPP,BenardDCetal(1995)Haemodynamiceffectsofcontinuouspositive airwaypressureinhumanswithnormalandimpairedleftventricularfunction.ClinSci(Lond) 88:173 178 10. KasaiT,DohiT,MaenoKetal(2009)Impactofadaptiveservoventilationinheartfailure patients with central sleep apnea which is not suf ciently treated with continuous positive airwaypressure[abstract].AmJRespirCritCareMed179:A5336
Section IV Monitoring and Complications
Nocturnal Monitoring in the Evaluation of Continuous Positive Airway Pressure1
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OresteMarrone,AdrianaSalvaggio,AnnaLoBue,andGiuseppeInsalaco
16.1 Introduction Continuous positive airway pressure (CPAP) counterbalances forces leading to upper airway narrowing or collapse during sleep and is the most widely used treatment for obstructivesleepapnea(OSA).InpatientswithOSA,progressivelyhigherCPAPlevels appliedduringsleepturnobstructiveapneasintohypopneas,hypopneasintocontinuous inspiratory owlimitation,withorwithoutsnoring,and owlimitationintounobstructed breathing. When breathing becomes unobstructed, respiratory arousals (i.e., arousals that may follow increased inspiratory efforts associated with obstructed breathing) are eliminated,whilesleepbecomesmorestableandsleepcyclesmoreregular,contributing toimprovementsinsubjectivesleepquality,daytimesleepiness,andqualityoflifeusually observed after just a few nights of CPAP application [1]. Also, relief of upper airway obstruction is associated with resolution of intermittent hypoxemia and hemodynamic swingsthataccompanyobstructiveevents,withaconsequentreductioninlong-termcardiovascularmorbidityandmortality[2]. TheobjectivesofCPAPtreatmentareeliminationofsymptomsandofcardiovascular and,possibly,metabolicriskrelatedtoOSA.Today,thebestwaytoaccomplishtheseaims is usually considered to fully eliminate all degrees of upper airway obstruction during sleep.ThelowestCPAPthateliminatesupperairwayobstructioninallsleepstagesand bodyposturesinapatientisindicatedas optimal CPAP.
This work was supported by the Italian National Research Council, order number ME.P01.014.002.
1
O.Marrone(),A.Salvaggio,A.LoBue,andG.Insalaco ItalianNationalResearchCouncil,InstituteofBiomedicineand MolecularImmunology,Palermo,Italy e-mail:
[email protected];
[email protected];
[email protected];
[email protected]
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ThereismuchcontroversyaboutthemostconvenientprocedurestoadoptbeforeCPAP prescription.Atoneextreme,of cialguidelinesstillconsiderthecomplexmanualCPAPtitrationduringassistedpolysomnographythegoldstandardprocedurebeforeCPAPprescription [3].Attheoppositeextreme,ithasbeenclaimedthatneitherpressuretitrationnoranyinstrumentalmonitoringwithCPAPapplicationisessentialforprescription[4].Inthischapter,we reviewproceduresforinitiationofCPAPtreatmentanddiscusstheireffectiveness.
16.2 Analysis and Discussion TheCPAPtitrationprocedureconsistsoftheapplicationofvariousCPAPlevelstoassess their effects and to identify which level may be most appropriate for the correction of upperairwayobstruction(optimalpressure).ManualCPAPtitrationinthesleeplaboratory istheoldestmethodforthedeterminationofoptimalpressure.Itisperformedduringa polysomnographicrecordingwhileatechnicianmanuallymodi espressureadministered byaCPAPdevice.Thetitrationpolysomnographicstudyshouldful lsomeconditions:It shouldhaveanadequateduration(accordingtosomeindications,atleast3hinsubjects whose apnea hypopnea (AHI) index is more than 40 or longer in subjects with milder disease)[5],anditshouldincludetherecordingofsomerapid-eye-movement(REM)sleep and of some sleep time in the supine posture since REM sleep and, even more, supine posturemayrequiretheapplicationofhigherCPAPlevels.Then,thequalityofthetitrationisevaluatedwithanalysisofthecharacteristicsofsleepandrespiration,ineachbody posture,inrelationshiptothepressuresthathavebeenapplied[3].Therefore,allsignals generally recorded during polysomnography have an important role: electroencephalogram, electro-oculogram, and chin electromyogram for recognition of sleep stages and arousals;bodyposition;pressureatthemasktomonitortheCPAPlevelthatisadministered;signalsfordetectionofsnoring,air ow,respiratorymovements,andoxyhemoglobin saturation to observe modi cations in breathing characteristics as CPAP level is changedandtomakesurethatregularunobstructedbreathingisachieved.Inparticular, regardingair ow,monitoringbyapneumotachographisrecommendedasa attenedshape intheinspiratoryportionofthe owsignalrecordedbythismethodisindicativeof ow limitation. Morerecently,identi cationofoptimalpressurebyauto-CPAPdeviceshasbeenintroduced ( autotitration ). Auto-CPAP machines are designed to automatically deliver a variable CPAP level that should correspond to the lowest required pressure in each moment. They are able to record several types of information during their application, includingpressuresdelivered,airleaks,andrespiratoryeventsdetected,andcanusually calculateanAHI. Autotitrationcanbeperformedwiththeapplicationofanauto-CPAPdeviceduringa standard polysomnographic study. A technician may assist autotitration to control the polysomnographic recording and the patient. Analysis of the polysomnographic study allows us to verify the relationship between pressures that have been delivered and breathing characteristics, sleep stages, arousals, and body postures. In this way, it is
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possibletoselecttheCPAPlevelthatprovesmostappropriateforcorrectionofupper airway obstruction. This method is now of cially recognized as a valid alternative to traditional manual titration [6], but differences in costs and time required for the two proceduresarelimited. As an alternative to the search for optimal CPAP with polysomnography, unassisted autotitration without any monitoring, except that provided by the auto-CPAP machine itself, has been introduced. With this method, an auto-CPAP is given to the patient for nocturnalself-application.Datacollectedandelaboratedbythemachinearedownloaded, andperiodswithexcessiveairleaksarediscardedfromanalysis.The90thor95thpercentilepressure(i.e.,thepressurethatisnotexceededfor90%or95%ofthetimeoftheautoCPAPapplication,respectively)isusuallyconsideredequivalenttotheoptimalpressure. Lackofexternalmonitoringduringauto-CPAPapplicationcouldleadtoerrorsintherecognitionofoptimalCPAPlevel.Auto-CPAPdeviceshavedifferentprinciplesofoperation;althoughmostofthemareeffectiveinthecorrectionofupperairwayobstructionand reliableinthevastmajorityofpatients,theiref cacyisvariable.Bothadministrationof excessively high pressures and undercorrection of obstruction are possible. Erroneous pressure administration may be easily recognized during polysomnography, while it is oftenundetectedifnomonitoringinadditiontotheoneperformedwiththeauto-CPAPis done.AHIvaluescalculatedbytheauto-CPAPmachinesmayhelptoidentifysomeunsatisfactoryautotitrations,butalthoughsomestudiesfoundthesevaluesreliableenoughwith somedevices,theymaysubstantiallydifferfromAHIvaluesobtainedwithexternalmonitoringandevaluatedmanually.Otherpossibleerrorsdonotdependonauto-CPAPdevices butonconditionspossiblyoccurringduringautotitration,likeinsuf cientsleeporlackof supinepostureduringtheauto-CPAPapplication.Again,thesecasesmaybeeasilyrecognizedwithappropriatemonitoring[7]. Thestrongestargumentagainstnocturnalmonitoringsforveryprecisedeterminations ofoptimalCPAPisthatpressuresneededbyeachpatientforthecorrectionofrespiratory disorderscanchangefromnighttonight.Reproducibilityofoptimalpressuredetermined with accurate manual titration during polysomnography is limited, with night-to-night changesupto3cmH2O[8].Therefore,theresultsofsingle-nighttitrations,eithermanual orautomatic,couldbequestionable,andcostsforsingle-nightassistedpolysomnographic titrationcouldbedisproportionate,whileanevaluationofoptimalCPAPonseveralnights couldbemorereliable. Aspolysomnographicmonitoringmaynotbeperformedformultiplenightsforpracticalreasons,ithasbeenproposedtoperformunassistedautotitrationwithoutexternalmonitoringforseveralnights.Theaverageofthe90thor95thpercentilepressuresonallnights ofauto-CPAPapplicationcouldrepresentanappropriatepressurefortreatment.Besides, progressiveadaptationofthepatientduringconsecutivenightstosleepwithCPAPcould preventerrorsassociatedwithpoorsleepqualityandminimizeerrorsduetothelackof externalmonitoring.Thenumberofnightsforthisautotitrationmethodisnotstandardized.Asmallnumberofnightscouldmakeitaneconomicalprocedureduetothelackof complexmonitoringsandanalyses,andoftechnicalassistance.Multiple-nightunassisted autotitrationhasbeenrecognizedasapossiblevalidalternativetopolysomnographictitration,butitisrecommendedtorelyonauto-CPAPdevicesthathavebeenbettervalidated andtostrictlykeepintouchwithpatientsafterinitiationofCPAPtreatment[6].Inour
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experience,adisadvantageofunassistedautotitrationisthat,despiteprevioustraining,not allpatientsareabletostartsleepingwithCPAPiftheyhavenoassistanceduringthenight. Besides,somecasesofpoorperformanceoftheauto-CPAPmachinemayremainundetectedifnonocturnalinstrumentalmonitoringisperformedduringorafterautotitration;in our opinion, even simple cardiorespiratory monitorings may be helpful for identifying uncommonbutpossiblecasesofunsatisfactoryautotitrations. IthasbeenproposednottotitrateCPAPbuttoprescribeapressurecalculatedbymeans ofpredictiveequations,possiblymodifyingitthereafter,followingpatients complaintsor indications[9].DifferentpredictiveequationsfortherapeuticCPAPhavebeenelaborated. Calculatedpressurevaluesdiffertosomeextentaccordingtotheequation.Generally,in an OSA population, most calculated pressures are close to the pressure values that are obtainedmostoftenwhentitrationsareperformed;so,forstatisticalreasons,calculated andtitratedpressuresaresimilarinmostpatients.However,agreementbetweencalculatedandtitratedvaluesdropswhenvalueshighlydifferingfromtheaverageandmost common levels are calculated or are required for treatment [10]. Therefore, predictive equationscannotbeconsideredreliablesubstitutesfortitration.Aposteriorievaluationof clinicaleffectsoftheprescribedCPAPandofadherencetotreatmenthasbeenusedto assessef cacyofCPAPtreatmentbasedontheapplicationofpredictiveequations.Infact, clinicalevaluationisessentialtoevaluatetheadequacyofCPAPtreatment.Improvement insleepinessisoneoftheaimsofthetreatment;itisessentialthatpatientsareableto tolerateCPAPandhavegoodcompliancetotreatment;abettercontrolandareductionof bloodpressurearepossibleeffectsofaneffectiveOSAtreatment.However,thesecriteria arenotsuf cienttovalidateaprescribedpressure;improvementinsleepinessmaypartly dependonaplaceboeffect,compliancetotreatmentmaybegoodevenwithsubtherapeutic pressure, and OSA treatment does not always result in effects on blood pressure. IncompletetreatmentofOSAmayexposepatientstopersistenceofincreasedcardiovascularrisk.Changesinbodyweightorsleep-relatedcomplaintsmaysuggesttheneedto reevaluateCPAPtitration.
Key Recommendations
› › › › ›
Aninstrumentalnocturnalmonitoring,eithermanualorautomatic,shouldalways beperformedwhentitratingoptimalCPAP. Thehigherthenumberofsignalsrecordedduringthenocturnalmonitoring,the morereliablethedeterminedtherapeuticCPAPlevelwillbe. Subjectiveandclinical ndingsafterinitiationofCPAPtreatmentshouldbe evaluatedregardlessoftheprocedureadoptedforCPAPprescription. Lackofinstrumentalmonitoringandrelianceonlyonsubjectivereportscanlead toconsideracceptableCPAPlevelsthatinadequatelycorrectrespiratorydisorders. SubjectiveindicationsgivenbypatientsusingpreviouslytitratedCPAPmayhelp tosuspectapoorpreviousCPAPtitrationorachangeinpressurerequirements andcanbetakenintoconsiderationofmakingsmallchangesintheadministered CPAP.
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References 1. GilesT,LassersonT,SmithB,WhiteJ,WrightJ,CatesCJ(2006)Continuouspositiveairways pressure for obstructive sleep apnoea in adults. Cochrane Database Syst Rev 19(3): CD001106 2. MarinJM,CarrizoSJ,VicenteE,AgustìAGN(2005)Long-termcardiovascularoutcomesin men with obstructive sleep apnoea-hypopnoea with or without treatment with continuous positiveairwaypressure:anobservationalstudy.Lancet365:1046 1053 3. KushidaC,ChediakA,BerryRetal(2008)Clinicalguidelinesforthemanualtitrationof positive airway pressure in patients with obstructive sleep apnea. J Clin Sleep Med 4: 157 171 4. StradlingJR,HardingeM,SmithDM(2004)Anovel,simpli edapproachtostartingnasal CPAPtherapyinOSA.RespirMed98:155 158 5. AmericanSleepDisordersAssociationReport(1997)Practiceparametersfortheindications forpolysomnographyandrelatedprocedures.Sleep20:406 422 6. MorgenthalerTI,AuroraRN,BrownT,etal.(2008)Practiceparametersfortheuseofautotitratingcontinuouspositiveairwaypressuredevicesfortitratingpressuresandtreatingadult patientswithobstructivesleepapneasyndrome:anupdatefor2007.AnAmericanAcademy ofSleepMedicineReport.Sleep31:141 147 7. MarroneO,InsalacoG,SalvaggioA,BonsignoreG(2005)RoleofdifferentnocturnalmonitoringsintheevaluationofCPAPtitrationbyautoCPAPdevices.RespirMed99:313 320 8. WiestGH,FuchsFS,HarschIAetal(2001)Reproducibilityofastandardizedtitrationprocedurefortheinitiationofcontinuouspositiveairwaypressuretherapyinpatientswithobstructivesleepapnoea.Respiration68:145 150 9. FitzpatrickMF,AllowayCED,WakefordTMetal(2003)Canpatientswithobstructivesleep apnea titrate their own continuous positive airway pressure? Am J Respir Crit Care Med 167:716 722 10. MarroneO,SalvaggioA,RomanoS,InsalacoG(2008)Automatictitrationandcalculationby predictiveequationsforthedeterminationoftherapeuticcontinuouspositiveairwaypressure forobstructivesleepapnea.Chest133:670 676
Complications During Noninvasive Pressure Support Ventilation
17
MicheleCarron,UldericoFreo,andCarloOri
17.1 Introduction Thetermnoninvasivepressuresupportventilation(NPSV)referstoanyformofventilatorysupportappliedwithouttheuseofaninvasiveconduit[1].GoalsofNPSVincludethe improvementofdyspnoeaandofbloodgasabnormalitiesfromacuterespiratoryfailure (ARF),thereductionofworkofbreathingandtheavoidanceoftrachealintubation.LongtermadvantagesofNPSVarethedecreaseofneedfortrachealintubation,ofnosocomial pneumonia,ofstayintheintensivecareunit(ICU)andinthehospital,and,mostimportantly,oftheoverallmortalityrate[1,2].Thepatientinterfacesmostcommonlyemployed forNPSVareanasalorafacemask(maskNPSV)andahelmet(helmetNPSV).NPSV mayhavecomplications,someofwhicharefrequentandpredictableandsomerareand unpredictable.ThestaffresponsibleforNPSVshouldbeawareandbepreparedtoprevent, detectearly,andcurethesecomplications.NPSVissafeandwelltoleratedwhenapplied optimallyinappropriatelyselectedpatients[1].
17.2 Interface Related Complications Themostfrequentlyencounteredadverseeffectsandcomplicationsareminorandrelated totheNPSVinterface(seesummarizingTable17.1).
M.Carron(),U.Freo,andC.Ori DipartimentodiFarmacologiaedAnestesiologia,ClinicadiAnestesiaeMedicinaIntensiva, UniversitàdegliStudidiPadova,Padova,Italy e-mail:
[email protected]
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Table 17.1 Adverseeventsandcomplicationsofnoninvasiveventilation(NIV)withdifferentinterfaces(IF)andpatientconditions Frequency(%)
IF/Patient condition
Remedy
References
Carbondioxide rebreathing Claustrophobia
50 100
H>FM>NM
2 4,7,8
5 10
FM>NM>H
Discomfort Facialskin erythema Nasalbridge ulceration Armedema andarmvein thrombosis Mechanical malfunction Noise
30 50 20 34
FM>NM>H FM>NM>H
Reducerespiratory rateandIFsize Reduceinspiratory pressure,sedation ChangeIF,sedation CheckIF t
7 100
FM>NM>H
ChangeIF
2,10
<5
H/malnutrition
CheckHarmpits
3
<1
FM=NM=H
Checkequipment
9
50 100
H>FM=NM
11
Patientventilator 50 100 dyssynchrony
H>FM=NM
ChangeIF,use heatandmoisture, earplugs,soundtraps Add/increasePEEP
CheckIF t,reduce pressure Addhumidi ers andemollients, reduceinspiratory pressure Reduceinspiratory pressure
2,4 7,13
FollowNPSV contraindications FollowNPSV contraindications
2
Interfacerelated
1,2 2 4,7,8 2
4,7
AirPressureandFlowRelated Airleaks
18 68
NM>FM>H
Nasalororal drynessand congestion
20 50
FM=NM>H
Gastric Distension
5 50
FM>NM>H
<5
AllIF/ileum
2,10,15
2,16
PatientRelated Aspiration pneumonia Barotrauma
2,17 AllIF/COPD, neuromuscolar disease,cystic brosis Hemodynamic <5 AllIF/highblood FollowNPSV 2,18 effects pressure contraindications COPDchronicobstructivepulmonarydisease;FMfacemask;IFinterface;NMnosemask;NPSV noninvasivepressuresupportventilation;PEEPpositiveend-expiratorypressure. <5
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17.2.1 Arm Edema and Arm Vein Thrombosis ThecomplicationofarmedemaisobservedduringhelmetNPSV.Thehelmetissecured bytwoarmpitbracestoapairofhooksontheplasticringthatjoinsthehelmettoasoft collar.DuringhelmetNPSV,theprolongedcompressionfromthearmpitbracemayproducevenousandlymphaticstasiswithconsequentedema.Thisismorefrequentinpatients withseveremalnutritionandcachexiaandmaypromotedeepvenousthrombosisinthe axillaryveinandanticoagulanttherapy.Fixationofthebracesinseverelymalnourished patientsneedscloseattention[3].
17.2.2 Carbon Dioxide Rebreathing TherespiratorycircuitandtheinterfaceforNPSVrepresentanadditionaldeadspaceand increase chances of carbon dioxide (CO2) rebreathing in proportion to their volumes. Compared with the tidal volume, the dead space of the masks is smaller than that of thehelmet.TheamountofCO2rebreathedisconsequentlysmallerduringmaskNPSV than helmet NPSV. The helmet is less effective than masks in removing CO2 during NPSV[3,4].Further,singlerespiratorycircuitswithnoexhalationvalve,highrespiratory rates, no or low external positive end-expiratory pressure (PEEP), and a reduced expiratorytimemayallincreaseCO2rebreathing[5].TheissueofwhetherCO2rebreathing is clinically relevant remains an open question. According to some authors, CO2 rebreathingisbelow1.5%withbothmaskNPSVandhelmetNPSV,anditisclinically notrelevant[3].Accordingtoothers,however,CO2rebreathingmayimpairCO2elimination and ventilatory muscle unloading [6]. Decreasing the size of the helmet and increasingpressuresupportwillnotnecessarilypreventCO2rebreathingduringhelmet NPSV[4].However,ifarapidincreaseofalveolarventilationisrequiredinpatientswith severe ARF, helmet NPSV reduces hypercapnia less ef ciently than mask NPSV [3]. Usingatwo-linecircuitandanonrebreathervalve,loweringtherespiratoryrate,adding PEEP,andincreasingtheexpiratorytimehavebeenadvocatedasmeasurestoreduceCO2 rebreathing[5].
17.2.3 Claustrophobia Claustrophobiaisthefearofenclosedspaces.Fivepercentto10%ofthegeneralpopulationmaypresentfearofrestrictionandfearofsuffocation.ThedevelopmentofclaustrophobiainvolvestheimpossibilitytobeginortocontinuetheNPSV.Thechoiceofdevice is crucial regarding claustrophobia and discomfort as well. The masks are often poorly toleratedbydistressedpatientscomparedtothehelmet.InthecaseofmaskNPSV,the
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use of manual mask application at rst can minimize the sense of claustrophobia [1]. Theventilatorysupportshouldbeintroducedgradually,startingwithcontinuouspositive airwaypressureandaddinginspiratorypressuresupportasrequired[1].Ventilatorsettings shouldbeadjustedtoprovidethelowestinspiratorypressureneededtoimprovepatient comfort[1].Sedationmaypreventorbehelpfulforclaustrophobicpatients.
17.2.4 Discomfort Discomfortrepresentsanunpleasantsensationthatitisrelatedtothedeviceorpressure valuesadoptedduringNPSV.Inadirectcomparisonamongdifferentmodelsofmaskfor NPSV,thetolerancewaspoorestforthemouthpiecefollowedbythenasalandoronasal masks[7].Althoughallmaskswerereasonablycomfortablefortheeyes,allattachment systemswereconsidereduncomfortablefortheskin[7].Thehelmetwastoleratedbetter thanmasksbecauseoftheabsenceofthefeelingofuncomfortablepressureontheface[3]. It allowed the patients to communicate, drink, and read better than the facial mask; improvedthecollaborationbetweenthepatientandthemedicalstaffduringthetreatment period;andallowedmaintainingcontinuousNPSVforaperiodoftimelongerthaninthe maskgroup[3,8].Thepossibleadvantagesofthehelmetonpatienttolerabilityandcomfortmustbebalancedwithitsinterferencewithventilation,greaterdeadspace,andcompliance compared to the face mask [4]. When pressure support ventilation is adopted, thecomfortlevelsfollowaU-shapedtrendwhenlevelofassistanceismodi ed,andthe extremelevelsofpressuresupport(bothlowestandhighest)arenotassociatedwiththe bestcomfort.Thenasalsalineoremollientsorheatedhumidi cationduringnasalNPSV attenuatestheadverseeffectsofmouthleakoneffectivetidalvolumeandnasalresistance andimprovesoverallcomfort.Sedationmayrepresentacrucialissueforpoorlytolerant patients.
17.2.5 Mechanical Malfunction Avarietyofmechanicalcomplicationscanoccurduringmechanicalventilation,suchas accidentaldisconnection,leakswithintheventilatorcircuit,lossofelectricalpower,and lossofgaspressure.Forthesereason,themechanicalventilatorsystemshouldbechecked frequentlytopreventmechanicalmalfunctions.DuringhelmetNPSV,anaccidentalinterruptionofgas owcauses vemaineffects:theCO2increasesinsidethehelmet;theFiO2 diminishesduetotheinspirationofambientairandtheinspiredpartialpressureofCO2 increases;thePEEPislostinafewseconds;dyspneaofincreasingintensityandasenseof impending suffocation ensue; and a progressive increase in minute ventilation occurs. Somefeaturesofthehelmetdesign,suchasahighvolume,alow-resistanceinletport,and theadjunctofasafetysystemcaneffectivelylimitanddelaytheclinicalconsequencesof fresh gas supply interruption. There is a clear need to include a monitoring and alarm system,andclinicalcontrolisimportant[9].InNPSVathome,thecaregiversmustbe
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preparedtoprovidebag-and-maskventilationtopatientsintheeventofanemergency. Iftheequipmentisavailable,thissimpletechniquemaybelifesavinginthepresenceof mechanicalmalfunctions.
17.2.6 Nasal Bridge Ulceration Nasalpain,eithermucosaloronthebridgeofthenose,andnasalbridgeerythemaorulceration from mask pressure account for a large portion of reported complications of maskNPSV[2].Theincidenceofskinnecrosisorabrasiondependsonthedurationof maskusageandvariesbetween7%and100%after48hofNPSV[10].Themeanpressurerecordedonthebridgeofthenosewasmuchhigherthanthatonthecheek(65vs. 15mmHg,nosevs.cheek),andthispressurecanbeclosetothelowervaluesofnormal diastolicbloodpressure[10].Progressivetighteningoftheharnessandincreasingofthe volumeofairintheoronasalmaskcushionsincreasedthepressureonthebridgeofthe nose,andtheeffectofthesetwofactorswasadditive[10].Thedevelopmentofpressure necrosisisonefactorthatcanlimitthetoleranceanddurationofmaskNPSV.Strategies usedtodecreasetheincidenceofpressurenecrosisduringNPSVincludeminimizingstrap tension,usingforeheadspacers,routinelyapplyingarti cialskintothebridgeofthenose intheacutesetting,applyingaGranu exdressingtotheareasofthefacethatareexposed topressure,usingwaterinsteadofairto llthecushionofafacemask,orswitchingto alternativeinterfacessuchasnasalpillows,newprototypefacemasks,cephalicmasks, andhelmets[2,10].
17.2.7 Noise Noise exposure during NPSV may be underestimated among the factors that in uence patientwell-beingduringtheICUstay.ThenoiseexceedstheusualICUbackgroundnoise, potentiallyincreasingpatientdiscomfort,causingsleepdisruption,andaffectingearfunction.TheintensityofnoiseinsidethehelmetduringNPSVisabout105dBandismostly caused by the turbulent gas ow through the respiratory circuit. By contrast, the noise perceived during mask NPSV is probably mostly caused by the ventilator and is about 65dB,notdifferentfromthebackgroundnoisethatismeasuredatpatients bedsidesinthe ICU[11].Theexcessnoiseinsidethehelmetmayhavesomedetrimentaleffectsonpatient wellness.Noisemayimpairapatient scontactwiththeenvironmentbymaskingsounds andhinderingconversation,andthisinconveniencemayaddtothephysicalbarrierthatthe helmetconstitutes.Suchnoiseintensityhasbeenregardedinthepastasamajorcauseof sleeparousalsincriticallyillpatients.MorerecentstudieshavereportedthatsleepdisruptionintheICUismultifactorial,andthatnoiseisresponsibleforonlyalimitedproportion ofarousalsandawakenings[11].Loudnoisemaydamagetheear.Damagemayresultin permanenthearinglossbutmorefrequentlycausesatemporaryauditorythresholdshift, whichmayrequiredaystorecoverifcausedbyprolongednoiseexposure(days)at100dB.
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Tinnitus,usuallytransitory,mayalsooccurafternoiseexposure,particularlyinpatients with preexisting hearing loss. Noise exposure during helmet NPSV may be attenuated by some devices. Heat and moisture exchanger lters did not affect noise intensity measuredbythesoundlevelmeterbutdecreasethenoiseperceivedbythesubjects[11]. Otherdevicesincludeearplugsandsoundtraps.Earplugsmaybeeffectiveagainstsleep disruption but may also make contact with the environment more dif cult. Conversely, addingsoundtrapstotheinspiratorybranchoftherespiratorycircuitmaypotentiallylimit noiseinsidethehelmetwithoutmajorinconvenience[11].
17.2.8 Patient–Ventilator Dyssynchrony Consideringthatthealgorithmsregulatingthebeginningandtheendofpressuresupport ventilationarepressureand owbased,thecharacteristics(i.e.,deadspace,compliance)of devices for NPSV have in uence on the patient ventilator interaction. Signi cant asynchronybetweenthebeginningandtheendofinspiratorysupportandthebeginningandthe end of patient inspiratory effort is commonly observed during NPSV [4]. Wasted efforts (i.e.,whenapatient sinspiratoryeffortisnotfollowedbyaventilatorcycle),autotriggering (i.e.,whenaventilatorcycleoccurswithoutbeingprecededbyapatient sinspiratoryeffort), andprolongedinspirations(i.e.,wheneachinsuf ationlastslongerthan1.5s)mayalsobe expectedduringNPSV[4,7].Thepatient ventilatordyssynchronyissigni cantlyhigher duringhelmetNPSVthanduringmaskNPSV[4],andamongthedifferentmasks,thedyssynchronyismoreevidentwithamouthpiecethanwithnasalororonasalmasks[7].With regardtoahelmet,thelowelastanceandhighinnervolumeofthedevicecausessigni cant overdampingofpressureassistanceandadeviationofventilator-delivered owfromthe patienttoexpandthecomplianthelmet(inparticularthesoftcollar)duringNPSV[4].These impaired patient ventilator interactions represent underlying mechanisms responsible for thereducedef ciencyofhelmetNPSVinunloadingtherespiratorymusclesinconditionsof increasedrespiratorymuscleworkload[4].AminimumPEEPof6cmH2Omightbehelpful intheclinicalsetting,whiletheuseofhigher owsandhigherpressuresmayreducethe complianceofthehelmetandmayoptimizetheef ciencyofhelmetNPSV[4].Ontheother hand,itmaynotbewelltoleratedbynormalsubjectsandmaybeassociatedtoworseningof patient ventilatorsynchronyanddyspneasensationinpatientwithARF[4].Aproportional assistventilationmayimprovepatient ventilatorinteractionandpatientcomfort[12].
17.3 Air Pressure and Flow Related Complications Airpressureand owarerequiredforNPSVbutarealsopotentialcausesofef ciencyloss andseriouscomplicationsduringNPSV.Theyshouldbemonitoredcloselyinanypatient undergoingNPSV(seesummarizingTable17.1).
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17.3.1 Air Leaks InterfacesforNPSVdonotprovideaperfectsealoftheairway.Someairleakingthrough themouth(withnasalmasks)oraroundtheoronasalmaskorthecollarofthehelmetis virtuallyuniversalwithNPSV.Leaksaresigni cantlylargerwiththemouthpiece,butno differenceisobservedbetweentheothermasks.Theyrangefrom18%(integralfacemask) to68%(mouthpiece).Theleaksoflargeoronasalmaskandsmalloronasalmaskaresimilar(31%versus34%)[3].LeakscannotbequantitatedexactlyduringhelmetNPSVbut theyareestimatedtobeatleastcomparableifnotsmallerthanthoseobtainedwiththe mask[4].Besidesthe ttingofinterface,highvaluesofpeakandplateaupressurescan contribute air leaks during NPSV [2]. Air leaks are important because they can render NPSVineffectiveandbecausetheymayaffecttriggering[13]and,inpatientswithneuromusculardisease,cancausepersistenthypercapnia[6].Forthesereasons,leaksshouldbe monitoredcloselyandtakenintoaccountforthechoiceoftheinterfacebytheNPSVstaff. Forpatientswithnasalmaskmeasurestoreduceairleakingincludeinstructionstokeep themouthclosed,applicationofchinstraps,biteblocksorswitchingtooronasalmaskor helmet.Atighter ttingofthemaskorhelmetandareductionofpressuresmaybenecessarytoprovideadequateventilationinsomepatients[2,4,7].Involume-targetedventilators, small and moderate air leaks can be compensated for by increasing tidal volume whereaslargeleaksaredif culttocompensate.Airleakscanbecompensatedmuchbetter bypressure-targetedventilatorsthankstospeci ccompensatingfeaturesthatarepresent insomemodels[5,14]
17.3.2 Nasal or Oral Dryness and Nasal Congestion Nasalororaldrynessiscausedbyhighair ow,anditisusuallyindicativeofairleaking throughthemouth.Measurestominimizeleaksmaybeuseful,butnasalsalineoremollientsandheatedhumidi ersareoftennecessarytorelievethesecomplaints[2].Generally, gasesdeliveredfrommechanicalventilatorsaretypicallydry.Thephysiologiceffectsof inadequatehumiditycanbeduetoheatlossormoistureloss.Inparticular,moistureloss fromtherespiratorytractandsubsequentdehydrationoftherespiratorytractresultinepithelial damage, particularly of the trachea and upper bronchi, drying of secretions and atelectasis.Itwouldbedesirabletohaveanadequatehumidifyingsystemtoavoidexcessivedehydrationofairwaymucusand,atthesametime,toavoidthecontaminationoflung parenchymabyinfectiousagentsasmuchaspossible.Twohumidifyingdevicesarecommonlyusedwithintensivecareventilators:heatedhumidi ersandheat moistureexchangers.Thelatterarefrequentlyusedbecauseoftheirsimplicityandlowercost.However, duringNPSVtheincreaseddeadspaceofaheat moistureexchangercannegativelyaffect ventilatoryfunctionandgasexchangeinpatientswithARF[15].Nasalcongestionand dischargearealsofrequentcomplaintsandmaybetreatedwithtopicaldecongestantsor steroidsandoralantihistamine/decongestantcombinations.
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17.3.3 Gastric Distension Gastricinsuf ationisreportedinupto50%ofpatientsreceivingNPSVbutisrarelyintolerable.Theloweresophagealsphincterpressureisthepressureattheesophageal-gastricjunction(approximately20 25cmH2O)thatpreventsregurgitationofstomachcontentsintothe pharynxandinsuf ationofairintothegastrointestinaltractduringventilation.Thefrequency ofgastricinsuf ationincreaseswhenhighin ationpressuresareusedandmaybeworsened whenthecomplianceoftheabdomenisgreaterthanthatofthechest.Thisconditioncould occuriftheNPSVventilationsysteminjectsairwhilethepatient sownrespiratorycycleis intheexpiratoryphasesothatthecomplianceofthechestincreaseswhilethatoftheabdomenisrelativelyfreefromtherespiratorycycle[16].Gastricinsuf ation,whichworsensthe patient squalityoflife,canbefatalinseverecases.Gastricdistensioncompressesthelungs, therebydecreasingtheircomplianceanddemandinghigherairwayventilationpressure.The lastisalsoassociatedwithincreasedriskofgastricdistension,thusgeneratingaviciouscycle. Seriouscomplicationsofgastricdistensionareregurgitationofgastriccontents,pulmonary aspiration,intra-abdominalhypertension,andabdominalcompartmentsyndrome.Aconditionclinicallyidenticaltoatensionpneumothoraxhasbeenreportedbutwasrelatedtomassiveintrathoracicdilationofthestomachinapatientwithahiatusherniawhowastreated withNPSV.Airwaypressureshigherthan20cmH2Oshouldbeavoided,andNPSVventilationshouldbeusedinthesittingpositionabouthalfanhourafterameal[2,16].
17.4 Patient Related Complications AcarefulpatientselectioniscrucialforNSPVsuccess.Indicationsandcontraindications, eitherrelativeorabsolute,havebeenproposedforNPSV[1,2]butarebeingreviewedon thebaseofnewstudies(seesummarizingTable17.1).Evenpatientshighlyselectedfor NPSV,however,canpresentunpredictableandseriousorevenlife-threateningcomplicationsbecauseoftheirclinicalconditions.
17.4.1 Aspiration Pneumonia Aspirationpneumoniahasbeenreportedinasmanyas5%ofpatients[2].Ratesofaspirationareminimizedbyexcludingthosewithcompromisedupperairwayfunctionorwith problemsinclearingsecretionsandbypermittingat-riskpatientsnothingbymouthuntil theyarestabilized.Anasogastrictubecanbeinsertedifthepatienthasexcessivegastric distension,anileum,nausea,orvomitingorisdeemedtobeathighriskforgastricaspiration.However,suchpatientsarenotidealcandidatesforNPSV,andnasogastricororogastrictubesshouldnotberoutinelyusedbecausetheyinterferewithmask tting,promoteair leaking,andaddtodiscomfort[2].
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17.4.2 Barotrauma Barotraumaisawell-recognizedcomplicationofpositivepressureventilation.Itisapulmonaryinjuryresultingfromalveolaroverdistensionandcanleadtopulmonaryinterstitial emphysema, pneumomediastinum, subcutaneous emphysema, and pneumothorax. A pneumoperitoneum associated with pneumomediastinum and tension pneumothorax associated with extensive vascular air embolism has also been reported. Barotrauma is thoughttoarisefromahigh-pressuregradientbetweenthealveolusandadjacentvascular sheet,causingruptureoftheoverdistendedalveolus,forcinggasintotheinterstitialtissue and subsequent dissection along the pulmonary vessels. It is likely that the risk of barotraumainpatientsusingNPSVislessthaninthosereceivinginvasiveventilation. Untilnow,ithasbeendescribedinthepresenceofchronicobstructivepulmonarydisease, acutelunginjuryfrompneumonia,cystic brosis,andneuromusculardisorders.During NPSV,thereisusuallyadropinin ationpressureacrosstheupperairway,andthepresenceoftheairleaksactsasasortof securityvalve thatmay,tosomeextent,prevent airway damage from excessive positive pressure. However, the transitory rise of peak pressureintolocalizedalveolaroverdistensionmayberelatedtopatient ventilatordesynchronizationandleadtodisruptionofthealveolarcapillarymembrane.So,itisimportant notonlythatthepeakalveolarpressureiskeptaslowaspossible(i.e.,<30cmH2O)but also that the patient ventilator desynchronization is minimized as much as possible to reduceriskofbarotraumas[2,17].
17.4.3 Hemodynamic effects Ingeneral,NPSViswelltoleratedhemodynamically,presumablybecauseofthelowin ation pressures used compared with invasive ventilation [2]. A short-term use of NPSV reducesheartrate,systolicbloodpressure,andsystemicvascularresistance.Inpatients whoarereceivingoptimaltherapy,thereductionofsystolicbloodpressureisnotsigni cant and may be associated with increase of ejection fraction and cardiac output [18]. On the other hand, signi cant hypotension and reduced cardiac output may occur in patientswithatenuoushemodynamicstatus(i.e.,patientswhoarehypertensiveorhave low uidvolume)orwithanunderlyingcardiacdiseasewithoutadequatepharmacologic therapy.Abilevelventilationinpatientswithacutepulmonaryedemaincreasestherateof myocardialinfarctionassociatedwithagreaterearlydropinbloodpressurecomparedcontinuouspositiveairwaypressurealonethatcouldhaveresultedfromhigherinitialmean intrathoracicpressure,causingagreaterreductioninvenousreturnThus,inthesepatients, clinicians are encouraged to begin with continuous positive airway pressure alone or NPSVusingrelativelylowin ationpressures(i.e.,11 12cmH2Oinspiratory,4 5cmH2O expiratory pressures) while monitoring the clinical response. Also, NPSV should be avoided in patients with uncontrolled ischemia or arrhythmias until these problems are stabilized[2].
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Key Recommendations
›
› › › › ›
DuringNPSV,airleaks,patient ventilatordyssynchrony,andpatientdiscomfort areallcommonproblemsthatdependonpatient ventilatorinteraction.They shouldbelookedforandimprovedwiththeappropriatechoiceand ttingofthe interfaceand,whenpossible,slightreductionofpressure. SkinnecrosisorabrasiondependonandlimitthedurationofmaskNPSV. Alternativeinterfacessuchcephalicmaskorhelmetmaybeconsidered. ThenoiseduringNPSVexceedstheusualICUbackgroundnoiseandcanbe anothercauseofdiscomfort,sleepdisruption,andeardamage.Itshouldbe diminishedwithearplugsandsoundtraps. Gastricinsuf ationfromNPSVincreaseswithventilationpressures,theupper safelimitbeing20cmH2O. BarotraumaisararebutapossibleeventduringNPSVresultingfrompatient ventilatorasynchronywhichshouldbecloselymonitored. Hypotension during NPSV is possible in hemodynamically instable patients. InpatientswithischemiaorarrhythmiasNPSVshouldbeavoidedordelayeduntil theseproblemsarestabilized.
References 1. InternationalConsensusConferencesinIntensiveCareMedicine:noninvasivepositivepressure ventilation in acute Respiratory failure (2001) Organized jointly by the American ThoracicSociety,theEuropeanRespiratorySociety,theEuropeanSocietyofIntensiveCare Medicine,andtheSociétédeRéanimationdeLangueFrançaise,andapprovedbyATSBoard ofDirectors,December2000.AmJRespirCritCareMed163:283 291 2. MehtaS,HillNS(2001)Noninvasiveventilation.AmJRespirCritCareMed163:540 577 3. Antonelli M, Pennisi MA, Pelosi P, Gregoretti C, Squadrone V, Rocco M, Cecchini L, ChiumelloD,SevergniniP,ProiettiR,NavalesiP,ContiG(2004)Noninvasivepositivepressure ventilation using a helmet in patients with acute exacerbation of chronic obstructive pulmonarydisease:afeasibilitystudy.Anesthesiology100:16 24 4. Racca F, Appendini L, Gregoretti C, Stra E, Patessio A, Donner CF, Ranieri VM (2005) Effectiveness of mask and helmet interfaces to deliver noninvasive ventilation in a human modelofresistivebreathing.JApplPhysiol99:1262 1271 5. SchönhoferB,Sortor-LegerS(2002)Equipmentneedsfornoninvasivemechanicalventilation.EurRespirJ20:1029 1036 6. GonzalezJ,SharsharT,HartN,ChaddaK,RaphaëlJC,LofasoF(2003)Airleaksduring mechanical ventilation as a cause of persistent hypercapnia in neuromuscular disorders. IntensiveCareMed29:596 602 7. Fraticelli AT, Lellouche F, L her E, Taillé S, Mancebo J, Brochard L (2009) Physiological effectsofdifferentinterfacesduringnoninvasiveventilationforacuterespiratoryfailure.Crit CareMed37:939 945 8. AntonelliM,ContiG,PelosiP,GregorettiC,PennisiMA,CostaR,SevergniniP,ChiarandaM, ProiettiR(2002)Newtreatmentofacutehypoxemicrespiratoryfailure:noninvasivepressure supportventilationdeliveredbyhelmet apilotcontrolledtrial.CritCareMed30:602 608
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9. Patroniti N, Saini M, Zanella A, Isgrò S, Pesenti A (2007) Danger of helmet continuous positiveairwaypressureduringfailureoffreshgassourcesupply.IntensiveCareMed33: 153 157 10. MuncktonK,HoKM,DobbGJ,Das-GuptaM,WebbSA(2007)Thepressureeffectsoffacemasksduringnoninvasiveventilation:avolunteerstudy.Anaesthesia62:1126 1131 11. CavaliereF,ContiG,CostaR,ProiettiR,SciutoA,MasieriS(2004)Noiseexposureduring noninvasiveventilationwithahelmet,anasalmask,andafacialmask.IntensiveCareMed 30:1755 1760 12. Fernández-Vivas M, Caturla-Such J, González de la Rosa J, Acosta-Escribano J, AlvarezSánchezB,Cánovas-RoblesJ(2003)Noninvasivepressuresupportversusproportionalassist ventilationinacuterespiratoryfailure.IntensiveCareMed29:1126 1133 13. Miyoshi E, Fujino Y, Uchiyama A, Mashimo T, Nishimura M (2005) Effects of gas leak on triggering function, humidi cation, and inspiratory oxygen fraction during noninvasive positiveairwaypressureventilation.Chest128:3691 3698 14. Scala R, Naldi M (2008) Ventilators for noninvasive ventilation to treat acute respiratory failure.RespirCare53:1054 1080 15. JaberS,ChanquesG,MateckiS,RamonatxoM,SoucheB,PerrigaultPF,EledjamJJ(2002) Comparisonoftheeffectsofheatandmoistureexchangersandheatedhumidi ersonventilationandgasexchangeduringnon-invasiveventilation.IntensiveCareMed28:1590 1594 16. YamadaS,NishimiyaJ,KurokawaK,YuasaT,MasakaA(2001)Bilevelnasalpositiveairwaypressureandballooningofthestomach.Chest119:1965 1966 17. CarronM,GagliardiG,MichielanF,FreoU,OriC(2007)Occurrenceofpneumothoraxduringnoninvasivepositivepressureventilationthroughahelmet.JClinAnesth19:632 635 18. AcostaB,DiBenedettoR,RahimiA,AcostaMF,CuadraO,VanNguyenA,MorrowL(2000) Hemodynamiceffectsofnoninvasivebilevelpositiveairwaypressureonpatientswithchronic congestiveheartfailurewithsystolicdysfunction.Chest118:1004 1009
Section V Chronic Applications of Noninvasive Mechanical Ventilation and Related Issues
Efficacy of Continuous Positive Airway Pressure in Cardiovascular Complications of Obstructive Sleep Apnea
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AhmedS.BaHammamandMohammedK.A.Chaudhry
18.1 Introduction Obstructive sleep apnea (OSA) is a form of sleep-disordered breathing (SDB) that is characterizedbyintermittentcompleteorpartialcollapseoftheupperairway.Thispattern of breathing has been considered a cause for several cardiovascular diseases, such as systemichypertension,heartfailure,arrhythmias,myocardialinfarction,andpulmonary hypertension.TheprevalenceofOSAinthemiddle-agedpopulationwas rstestimatedin 1993bytheongoingpopulation-basedWisconsinSleepCohortStudy[1]inasampleof 625employedadults.Theinvestigatorsfoundthat9%ofwomenand24%ofmenhadat least veormoreapneasorhypopneasperhourofsleep[1].Whenthepresenceofextreme daytimesleepinesswasincludedasacriterion,theprevalencewasestimatedtobe2%in womenand4%inmen[1].TheincidenceofSDBisindependentlyin uencedbyage,sex, waist hipratio,andbodymassindex(BMI).ThecorrelationbetweenOSAandcardiovasculardiseaseshasbeenwellstudied,andalinearrelationshipbetweenseverityofOSAand thecomorbiditieshasbeenreported[2,3].ThefamousSleepHeartHealthStudyrevealed thattherelativeoddsofheartfailure,stroke,andcoronaryarterydisease(CAD)(uppervs. lowerapnea hypopneaindex[AHI]quartile)were2.38,1.58,and1.27,respectively[3]. Inthischapter,wereviewthebest-availableevidencesupportingtheuseofcontinuous positiveairwaypressure(CPAP)inOSApatientswithhypertension,CAD,heartfailure, pulmonaryhypertension,andstroke.
18.2 Pathophysiology Thereareanumberofpathophysiologicmechanismsunderlyingcardiovascularcomplications in OSA patients (Fig. 18.1). The most notable immediate mechanisms are (1)
A.S.BaHammam()andM.K.Chaudhry UniversitySleepDisordersCenter,DepartmentofMedicine,CollegeofMedicine, KingSaudUniversity,P.O.Box225503,Riyadh11324,SaudiArabia e-mail:
[email protected];
[email protected] A.M.Esquinas(ed.),NoninvasiveMechanicalVentilation, DOI:10.1007/978-3-642-11365-9_18,©Springer-VerlagBerlinHeidelberg2010
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intermittent swings in blood gas chemistry that range from hypoxia reoxygenation to hypercapnia hypocapnia,(2)arousals,and(3)intrathoracicpressurechanges[4].PathophysiologicalfeaturesthathavebeenassociatedwithOSArangefromfragmentedsleep, todaytimesleepiness,torecurrentepisodesofapnea-relateddesaturationalongwithretention of CO2. All of these factors disrupt the normal structured hemodynamic and autonomic responses to sleep. There is a substantial amount of evidence supporting the conceptionthatintermittenthypoxia reoxygenationisthekeyfeatureofthecardiovascularpathophysiologyofthedisorder[5].Apneasandhypopneascauseintermittenthypoxia andconsecutiveintrathoracicpressureswings.Thistriggerstheautonomicnervoussystem,leadingtosympatheticoveractivation[6].Thishyperactivitypersistsduringthestate ofwakefulness.Thesepatientsthereforehavefasterheartratesduringrestingwakefulness.Thecycleofhypoxia reoxygenationreleasesincreasedquantitiesofreactiveoxygen radicals,triggersoxidativestressmechanisms,andreleasesin ammatorymarkers[7].The endotheliummaintainsharmonybetweenvasodilationandvasoconstrictionandregulates vasoactivemediators.Endothelialdysfunctionleadstoarterialwalldamage.Manystudies haveimplicatedarelationshipbetweenOSAandendothelialdysfunction[8].Figure18.1 showsanalgorithmfortheproposedpathophysiologicmechanisms.
Primary Events Sleep onset
Intermediary Mechanisms
Cardiovascular associations
Hypoxemia / Hypercapnia
Hypertension
Sympathetic activation
Heart Failure
Oxidative stress
Myocardial lschemia
Inflammation
Arrhythmias
Hypercoagulation
Pulmonary HTN
Intrathoracic pressure swings
Stroke
Metabolic dysregulation
Sudden cardiac death
Apneas Hypopneas
Arousals
Reoxygenation
Resumption of airflow
Fig. 18.1 Analgorithmoftheproposedpathophysiologicmechanisms.HTNhypertension
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18.3 Cardiovascular Complications in Patients with OSA Table18.1summarizesthemainstudiesthatexaminedtheeffectsoftreatmentforOSA onoutcomescontributingtocardiovasculardiseases.
18.3.1 Systemic Hypertension ThereiscompellingevidenceshowingthatOSAisanindependentandimportantriskfactorforhypertension[9].ReporteddatafromtheWisconsinSleepCohortStudydocumented acause effectrelationshipbetweenOSAandhypertensionaftercontrollingfordifferent confounders[10].TheyreportedadirectrelationshipbetweentheprevalenceofhypertensionandtheseverityofOSAexpressedastheAHI[11].Afteradjustingforconfounders, theriskofhypertensionwastwofoldforthosewithanAHIof5 15/handthreefoldfor subjectswithanAHIabove15/h[11].
18.3.1.1 CPAP Therapy Effects ControlledtrialsthatstudiedtheeffectofCPAPonbloodpressurelevelinpatientswith OSAshowedcon ictingresults.AllstudiesthatdidnotshowaneffectofCPAPonblood pressurehadsigni cantlimitations.Limitationsincludedunderpower,asmostofstudied subjectswerenormotensive;theshortdurationoftherapy;orinadequatecompliance.A criticalreviewoftheavailableliteratureshowedthatCPAPtherapydropsbloodpressure byaround10mmHgonaverageinpatientswithmoderate-to-severesleepapnea[12,13]. Nevertheless, this effect was less obvious in patients with mild OSA and patients with OSAwhowerenormotensive.
18.3.2 Coronary Artery Disease Ingeneral,theriskofdevelopingacutecoronarysyndrome(ACS)orsuddencardiacdeath increasesduringtheearlymorninghoursafterwakening.ThefactthatpatientswithOSA haveincreasedriskofACSandsuddencardiacdeathduringsleephours(midnightto6 a.m.),whichisthenadirofACSinsubjectswithoutOSA,raisesaconcernabouttherole ofOSAininducingCAD[14].Inaddition,anobservationalprospectivestudythatevaluatedthetimecourseofSDBinpatientswithACSrevealedpersistenceofOSAinthese patients6monthsaftertheacuteevent,suggestingthatOSAmighthaveprecededtheACS eventandhencewasapossiblecausaleffect[15].Studieshaveshownahighprevalence ofCAD(20 68%)inpatientswithOSAreferredtothesleepclinic[16,17].
33
Therapeuticvs.sham CPAP
PulmonaryHTN
Ariasetal.[31]
18weeks
10.1years
7.5years
5years
3months
1month
1month
Mean65days
CPAPtreatmentreducedtherisk offatalandnonfatalcardiovascular events
Deathsfromcardiovasculardisease morecommonintheuntreatedgroup thanintheCPAP-treatedgroup duringfollow-up
Long-termCPAPtreatmentin moderate-to-severeOSAand ischemicstrokeassociatedwitha reductioninexcessriskofmortality
CPAPtreatmentassociatedwith signi cantimprovementsinLVEF
9%increaseinLVEF;10mmHg decreaseinsystolicbloodpressure; decreaseinheartrateof4beats/min
TherapeuticCPAPreducedmean arterialambulatorybloodpressureby 2.5mmHg
10mmHgdecreaseinsystolicand diastolicbloodpressure
Reductionofpulmonarysystolic pressure(from28.9 to24.0mmHg) CPAPcontinuouspositiveairwaypressure,HTNhypertension,LVEFleftventricularejectionfraction,OSAobstructivesleepapnea
1651
TherapeuticCPAP vs.noCPAP
Marinetal.[20]
168
TherapeuticCPAP vs.noCPAP
28
CPAPinsevere OSAvs.noCPAP
Dohertyetal.[21]
55
TherapeuticCPAP vs.noCPAP
Mans eldetal.[26]
Coronaryartery disease
24
TherapeuticCPAP vs.noCPAP
Kanekoetal.[25]
Martinez-Garcia etal.[41]
118
Therapeutic vs.shamCPAP
Pepperelletal.[12]
60
Therapeutic vs.shamCPAP
Beckeretal.[13]
Stroke
Heartfailure
Hypertension
Table 18.1 Summaryofthemainstudiesthatexaminedtheeffectsoftreatmentforobstructivesleepapneaonoutcomescontributingtocardiovasculardiseases Cardiovascular Study Treatment Patient Treatment Treatmentoutcomes association population(n) period
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18.3.2.1 CPAP Therapy Effects EarlyrecognitionandtreatmentofOSAmaybebene cialintermsofCADprevention. Treatment with CPAP reduces angina and nocturnal myocardial ischemia [18]. Drager etal.,inasmallrandomizedcontrolledstudy,reportedimprovementsinpulsewavevelocity, carotid intima wall thickness, and carotid artery diameter after 4 months of CPAP therapy[19].Marinetal.comparedthefatalandnonfatalcardiovasculareventsinpatients withtreatedandnontreatedOSA[20].PatientswithsevereOSA(AHI>30)hadsigni cantlyhigherfatalandnonfatalcardiovascularevents.Amongthepatientswhohadtreated OSA, the incidence of both fatal and nonfatal cardiovascular events approached levels seeninsimplesnorers[20].Along-termfollow-upstudyof168patientswithOSAswho hadbegunreceivingCPAPtherapyatleast5yearspreviouslycomparedthecardiovascular outcomesofthosepatientswhowereintolerantofCPAP(untreatedgroup,61patients) withthosecontinuingCPAPtherapy(107patients)[21].DeathsfromcardiovasculardiseaseweremorecommonintheuntreatedgroupthanintheCPAP-treatedgroupduring follow-up[21].
18.3.3 Heart Failure AnumberofstudiesreportedahighprevalenceofOSAamongpatientswithheartfailure (11 38%),aprevalencehigherthanthatreportedinpatientswithoutOSA[22].Patients withheartfailureandOSAareusuallyoverweightandsnorehabitually,whichisdifferent from the phenotype of patients with heart failure who have central sleep apnea and Cheyne Stokesrespiration.EvenpatientswithmildheartfailurehaveincreasedprevalenceofOSA.Vaziretal.describeda15%incidenceofOSAinpatientswithmildsystolicleftventriculardysfunction[23].HeartfailureinOSApatientscanbebothsystolic anddiastolic.
18.3.3.1 CPAP Therapy Effects CPAP therapy improves both systolic and diastolic functions. In a controlled crossover designstudy,Ariasetal.reportedsigni cantimprovementindiastolicdysfunctionwith CPAPtherapy[24].TworandomizedcontrolledtrialsassessedtheimpactofCPAPtherapy onsystolicdysfunctioninpatientswithOSA.Onestudyreportedanimprovementfrom 27%to36%inleftventricularejectionfraction(LVEF)in24patientsafter4weeksof CPAP therapy [25]. The second study reported an improvement in LVEF from 35% to 40%,areductioninurinarycatecholamines,andimprovedqualityoflifein55patients withCPAPtherapyfor3months[26].Amulticenterrandomizedstudyexploredtheef cacyofCPAPin60OSApatientswithheartfailure(LVEF<45%)[27].Therewasasigni cantimprovementintheLVEFinthegroupofpatientstreatedwithCPAPbutnosuch
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improvementintheshamCPAPgroup.Theimprovementwasmoremarkedinpatients with a LVEF above 30% [27]. On the contrary, a randomized, double-blind, crossover study did not elicit a signi cant change in LVEF after 6 weeks of CPAP use [28]. Nevertheless,CPAPusagewaslow(3.5hpernight)[28].OSAhasbeenassociatedwith highermortalityinpatientswithheartfailure[29].TheimpactofCPAPtherapyonmortalityinpatientswithheartfailurehasnotbeenshown.Currently,therearenoguidelinesfor treatmentofsleepapneainheartfailure.Well-designed,long-termstudiesareneededto seeiftreatmentwithCPAPprolongssurvival.
18.3.4 Pulmonary Arterial Hypertension TheWorldHealthOrganizationrecognizedSDBasasecondarycauseofpulmonaryarterial hypertension (PAH) in its second conference on PAH in 1998 [30]. Studies have shown that mild PAH (mean pulmonary artery pressure of 20 30 mmHg) is relatively commoninpatientswithOSA.Aprevalenceof17 43%hasbeenreportedindifferent studies.HighAHI,lowPao2,highPaco2,lowFEV1,andincreasedBMIhavebeenassociated with PAH in patients with OSA [31]. The clinical signi cance of this mild OSArelatedPAHisnotknown. Thepulmonaryvasculature,incontrasttothesystemicvasculature,respondstohypoxia withvasoconstrictiontomaintainmatchedventilationandperfusion.Sustainedlong-term hypoxiaresultsinchronicallypresentvasoconstrictionthatvariesamongindividuals.Over time,thisleadstoremodelingofpulmonaryvasculature.Experimentalintermittenthypoxia forpartofthedayforafewweekscausedPAH,pulmonaryarterialremodeling,andright ventricularhypertrophyinrodents[32].
18.3.5 CPAP Therapy Effects TreatmentofpatientswithOSAwithCPAPhasbeenshowntoreducepulmonaryartery pressure.Ariasandcolleagues[31]havestudiedpulmonaryhemodynamicsandOSAin their randomized crossover study and found that CPAP treatment compared with sham CPAPsigni cantlyreducedpulmonarysystolicpressure(from29to24mmHg).Patients whorespondedwellweretheoneswhohadPAHatbaselineorwithleftventriculardysfunction.Anumberofstudiesreportedasigni cantdecreaseinpulmonaryarterypressure inpatientswithOSAwithPAHafter3 6monthsofCPAPtherapy[31,33].Onestudy demonstrated reduction in the reactivity of the pulmonary circulation to hypoxia after CPAPtherapy[33].Nevertheless,itisimportanttomentionherethatsomestudiesshowed negativeresults[34]. Basedonavailabledata,itseemsthatadropinpulmonaryarterypressureislikelyto occurinpatientswithsevereOSA;thoseinwhomPAHiscausedbyOSAnotbycomorbid
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conditions;thosewithleftventriculardysfunction;andthosewhoareadherenttotherapeuticCPAP.
18.3.6 Stroke Cross-sectionalstudiesshowedstrongassociationbetweenOSAandstroke.Thestrength ofassociationwassimilartotraditionalriskfactorsforstrokelikehypertensionandsmoking. In addition, even after adjustment for known confounding factors like obesity and hypertension, SDB remains an independent association [3]. Large observational cohort prospectivestudieshaveshownthatOSAincreasestheriskofstrokeandall-causemortalityindependentofknownconfounders[35,36].Moreover,severityofOSAwasassociated withahigherriskofstrokeanddeath[35 37].ThosewithanAHIabove36hadamore thanthreefoldincreasedriskofstrokeanddeath.AstudythatfollowedpatientswithOSA for10yearsshowedthatOSAwassigni cantlyassociatedwithahigherriskofstrokein patientswithCADwhowerebeingevaluatedforcoronaryintervention[38].
18.3.6.1 CPAP Therapy Effects ThereisalwaysaconcernthatindividualswithOSAandstrokemaynottolerateCPAPdue to their acute illness. Studies addressing CPAP tolerance in this group of patients have reportedcon ictingresults.Whilesomeinvestigatorsreportedasimilarimprovementand acceptanceofCPAPtherapyasinpatientswithOSAwithoutstroke[39],othersreported poortoleranceandlackofbene t[40]. AprospectiveobservationalstudyexploredSDBin166patientswithacutestroke [41].CPAPtherapywasofferedwhenAHIwas20/horhigher,andthenpatientswere followedfor5years.PatientswithanAHIof20orhigherwhodidnottolerateCPAP (n=68)showedanincreasedadjustedriskofmortality(hazardsratio[HR]2.69)comparedwithpatientswithanAHIbelow20(n=70)andanincreasedadjustedriskof mortality(HR1.58)comparedwithpatientswithmoderate-to-severeOSAwhotolerated CPAP (n = 28). There were no differences in mortality among patients without OSA, patients with mild disease, and patients who tolerated CPAP therapy [41]. Furthermore,CPAPtherapymayreducetheriskforstrokeindirectlythroughdifferent mechanisms.CPAPtherapyhasbeenshowntoreducebloodpressure;eliminateintermittent hypoxia; decrease platelet aggregation and brinogen levels; reduce risk of atrial brillation; reduce sympathetic nerve activity, ambulatory blood pressure, and arterialwallstiffness;andincreasesensitivityofthearterialbarore exinpatientswith OSA[12,42].TheseeffectsmayreducetheriskofCADandstrokeinthisgroupof patients.
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OSAisaseriousmedicaldisorderthatmaycauseandincreasetheriskformany cardiovasculardisorders. Severalmechanismsmayaccountforthisrisk,includingintermittenthypoxia, sympatheticoveractivity,oxidativestress,endothelialdysfunction,in ammation cascadeoveractivity,intrathoracicpressureswings,metabolicdysregulation,and thrombosis. EarlytreatmentofOSApatientswithCPAPtherapymaypreventcardiovascular complications. CPAPtherapyhasbeeneffectiveinreducinganumberofcardiovascular complicationsandcardiac-relatedmortalityinpatientswithOSA. CliniciansshouldbeawareoftheseriousnessofOSAandhenceshould recognizethisdisorderinitsearlystages,initiateCPAPtherapy,andstressthe importanceofadherencetotheirpatients.
References 1. YoungT,PaltaM,DempseyJ,SkatrudJ,WeberS,BadrS(1993)Theoccurrenceofsleepdisorderedbreathingamongmiddle-agedadults.NEnglJMed328(17):1230 1235 2. NietoFJ,YoungTB,LindBK,ShaharE,SametJM,RedlineSetal(2000)Associationof sleep-disorderedbreathing,sleepapnea,andhypertensioninalargecommunity-basedstudy. SleepHeartHealthStudy.JAMA283(14):1829 1836 3. ShaharE,WhitneyCW,RedlineS,LeeET,NewmanAB,JavierNietoFetal(2001)Sleepdisordered breathing and cardiovascular disease: cross-sectional results of the Sleep Heart HealthStudy.AmJRespirCritCareMed163(1):19 25 4. LavieL(2003)Obstructivesleepapnoeasyndrome anoxidativestressdisorder.SleepMed Rev7(1):35 51 5. SomersV,JavaheriS(2005)Cardiovasculareffectsofsleep-relatedbreathingdisorders.In: KrygerMH,RothT,DementWC(eds)Principlesandpracticesofsleepmedicine,4thedn. Saunders,Philadelphia,pp1180 1191 6. ZieglerMG,MillsPJ,LoredoJS,Ancoli-IsraelS,DimsdaleJE(2001)Effectofcontinuous positiveairwaypressureandplacebotreatmentonsympatheticnervousactivityinpatients withobstructivesleepapnea.Chest120(3):887 893 7. RyanS,TaylorCT,McNicholasWT(2005)Selectiveactivationofin ammatorypathwaysby intermittenthypoxiainobstructivesleepapneasyndrome.Circulation112(17):2660 2667 8. IpMS,TseHF,LamB,TsangKW,LamWK(2004)Endothelialfunctioninobstructivesleep apneaandresponsetotreatment.AmJRespirCritCareMed169(3):348 353 9. YoungT,JavaheriS(2005)Systemicandpulmonaryhypertensioninobstructivesleepapnea. In:KrygerMH,RothT,DementWC(eds)Principlesandpracticesofsleepmedicine,4thedn. Saunders,Philadelphia,pp1192 1202 10. Young T, Peppard P, Palta M, Hla KM, Finn L, Morgan B et al (1997) Population-based study of sleep-disordered breathing as a risk factor for hypertension. Arch Intern Med 157(15): 1746–1752 11. Peppard PE, Young T, Palta M, Skatrud J (2000) Prospective study of the association between sleep-disordered breathing and hypertension. N Engl J Med 342(19):1378–1384
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12. Pepperell JC, Ramdassingh-Dow S, Crosthwaite N, Mullins R, Jenkinson C, Stradling JR et al (2002) Ambulatory blood pressure after therapeutic and subtherapeutic nasal continuous positive airway pressure for obstructive sleep apnoea: a randomised parallel trial. Lancet 359(9302):204–210 13. Becker HF, Jerrentrup A, Ploch T, Grote L, Penzel T, Sullivan CE et al (2003) Effect of nasal continuous positive airway pressure treatment on blood pressure in patients with obstructive sleep apnea. Circulation 107(1):68–73 14. Gami AS, Howard DE, Olson EJ, Somers VK (2005) Day–night pattern of sudden death in obstructive sleep apnea. N Engl J Med 352(12):1206–1214 15. BaHammam A, Al-Mobeireek A, Al-Nozha M, Al-Tahan A, Binsaeed A (2005) Behaviour and time-course of sleep disordered breathing in patients with acute coronary syndromes. Int J Clin Pract 59(8):874–880 16. Hanly P, Sasson Z, Zuberi N, Lunn K (1993) ST-segment depression during sleep in obstructive sleep apnea. Am J Cardiol 71(15):1341–1345 17. Mooe T, Rabben T, Wiklund U, Franklin KA, Eriksson P (1996) Sleep-disordered breathing in men with coronary artery disease. Chest 109(3):659–663 18. Franklin KA, Nilsson JB, Sahlin C, Naslund U (1995) Sleep apnoea and nocturnal angina. Lancet 345(8957):1085–1087 19. Drager LF, Bortolotto LA, Figueiredo AC, Krieger EM, Lorenzi GF (2007) Effects of continuous positive airway pressure on early signs of atherosclerosis in obstructive sleep apnea. Am J Respir Crit Care Med 176(7):706–712 20. Marin JM, Carrizo SJ, Vicente E, Agusti AG (2005) Long-term cardiovascular outcomes in men with obstructive sleep apnoea-hypopnoea with or without treatment with continuous positive airway pressure: an observational study. Lancet 365(9464):1046–1053 21. Doherty LS, Kiely JL, Swan V, McNicholas WT (2005) Long-term effects of nasal continuous positive airway pressure therapy on cardiovascular outcomes in sleep apnea syndrome. Chest 127(6):2076–2084 22. Bradley TD, Floras JS (2003) Sleep apnea and heart failure: part I: obstructive sleep apnea. Circulation 107(12):1671–1678 23. Vazir A, Hastings PC, Dayer M, McIntyre HF, Henein MY, Poole-Wilson PA et al (2007) A high prevalence of sleep disordered breathing in men with mild symptomatic chronic heart failure due to left ventricular systolic dysfunction. Eur J Heart Fail 9(3):243–250 24. Arias MA, Garcia-Rio F, Alonso-Fernandez A, Mediano O, Martinez I, Villamor J (2005) Obstructive sleep apnea syndrome affects left ventricular diastolic function: effects of nasal continuous positive airway pressure in men. Circulation 112(3):375–383 25. Kaneko Y, Floras JS, Usui K, Plante J, Tkacova R, Kubo T et al (2003) Cardiovascular effects of continuous positive airway pressure in patients with heart failure and obstructive sleep apnea. N Engl J Med 348(13):1233–1241 26. Mansfield DR, Gollogly NC, Kaye DM, Richardson M, Bergin P, Naughton MT (2004) Controlled trial of continuous positive airway pressure in obstructive sleep apnea and heart failure. Am J Respir Crit Care Med 169(3):361–366 27. Egea CJ, Aizpuru F, Pinto JA, Ayuela JM, Ballester E, Zamarron C et al (2008) Cardiac function after CPAP therapy in patients with chronic heart failure and sleep apnea: a multicenter study. Sleep Med 9(6):660–666 28. Smith LA, Vennelle M, Gardner RS, McDonagh TA, Denvir MA, Douglas NJ et al (2007) Auto-titrating continuous positive airway pressure therapy in patients with chronic heart failure and obstructive sleep apnoea: a randomized placebo-controlled trial. Eur Heart J 28(10):1221–1227 29. Wang H, Parker JD, Newton GE, Floras JS, Mak S, Chiu KL et al (2007) Influence of obstructive sleep apnea on mortality in patients with heart failure. J Am Coll Cardiol 49(15): 1625–1631 30. Rich S (ed) (1998) Primary pulmonary hypertension: executive summary from the world symposium on primary pulmonary hypertension. World Health Organization, Geneva 31. Arias MA, Garcia-Rio F, Alonso-Fernandez A, Martinez I, Villamor J (2006) Pulmonary hypertension in obstructive sleep apnoea: effects of continuous positive airway pressure: a randomized, controlled cross-over study. Eur Heart J 27(9):1106–1113
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32. Campen MJ, Shimoda LA, O’Donnell CP (2005) Acute and chronic cardiovascular effects of intermittent hypoxia in C57BL/6J mice. J Appl Physiol 99(5):2028–2035 33. Sajkov D, Wang T, Saunders NA, Bune AJ, McEvoy RD (2002) Continuous positive airway pressure treatment improves pulmonary hemodynamics in patients with obstructive sleep apnea. Am J Respir Crit Care Med 165(2):152–158 34. Sforza E, Krieger J, Weitzenblum E, Apprill M, Lampert E, Ratamaharo J (1990) Long-term effects of treatment with nasal continuous positive airway pressure on daytime lung function and pulmonary hemodynamics in patients with obstructive sleep apnea. Am Rev Respir Dis 141(4 Pt 1):866–870 35. Arzt M, Young T, Finn L, Skatrud JB, Bradley TD (2005) Association of sleep-disordered breathing and the occurrence of stroke. Am J Respir Crit Care Med 172(11):1447–1451 36. Yaggi HK, Concato J, Kernan WN, Lichtman JH, Brass LM, Mohsenin V (2005) Obstructive sleep apnea as a risk factor for stroke and death. N Engl J Med 353(19):2034–2041 37. Sahlin C, Sandberg O, Gustafson Y, Bucht G, Carlberg B, Stenlund H et al (2008 Feb 11) Obstructive sleep apnea is a risk factor for death in patients with stroke: a 10-year follow-up. Arch Intern Med 168(3):297–301 38. Valham F, Mooe T, Rabben T, Stenlund H, Wiklund U, Franklin KA (2008) Increased risk of stroke in patients with coronary artery disease and sleep apnea: a 10-year follow-up. Circulation 118(9):955–960 39. Scala R, Turkington PM, Wanklyn P, Bamford J, Elliott MW (2009 Jan) Acceptance, effectiveness and safety of continuous positive airway pressure in acute stroke: a pilot study. Respir Med 103(1):59–66 40. Palombini L, Guilleminault C (2006 Feb) Stroke and treatment with nasal CPAP. Eur J Neurol 13(2):198–200 41. Martinez-Garcia MA, Soler-Cataluna JJ, Ejarque-Martinez L, Soriano Y, Roman-Sanchez P, Illa FB et al (2009) Continuous positive airway pressure treatment reduces mortality in patients with ischemic stroke and obstructive sleep apnea: a 5-year follow-up study. Am J Respir Crit Care Med 180(1):36–41 42. Kohler M, Pepperell JC, Casadei B, Craig S, Crosthwaite N, Stradling JR et al (2008) CPAP and measures of cardiovascular risk in males with OSAS. Eur Respir J 32(6):1488–1496
Obstructive Sleep Apnea and Atherosclerosis
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RichardSchulz,FrankReichenberger,andKonstantinMayer
19.1 Introduction Atherosclerosisisaprogressive,chronicdiseaseoflargearteriesinwhichvariousstagesof vascularremodeling nallyleadtosigni cantnarrowingofthevessellumen.Intheearly phase of atherosclerosis, cholesterol particles are incorporated into the vascular wall (i.e.,foamcellformation,developmentoffattystreaks).Later,plaquesoccurthatareprone torupturewithconsecutivethrombosisandcompletevesselocclusion.Inthiscase,acute clinicalsyndromessuchasmyocardialinfarctionmayresult.Atherosclerosisisviewedasan in ammatoryprocessinwhichcirculatingleukocytesareattachedtotheendothelium,penetrateintothesubendothelialspace,andreleaseawidespectrumofcytokines.Knownrisk factorsforatherosclerosisare,forinstance,smoking,diabetesmellitus,andhyperlipidemia.
19.2 Relation of Obstructive Sleep Apnea to Atherosclerosis Large-scaleepidemiologicalstudiessuchastheSleepHeartHealthStudyandtheWisconsin SleepCohortStudyhaveshownthatpatientswithobstructivesleepapnea(OSA)havean increasedriskforatheroscleroticsequelaesuchasischemicheartandcerebrovasculardisease[1,2].Ofnote,thiseffectwasfoundtobeindependentofconfoundingfactorssuchas obesity,metabolicdisorders(i.e.,diabetesmellitusandhyperlipidemia),andsmoking. MultiplepathwaysmaybeinvolvedinthepathogenesisofatherosclerosisinOSA.First, oxidativestressprobablyplaysanimportantrole.Inthiscontext,neutrophilsfrompatients with OSA have been found to display an enhanced release of free oxygen radicals after invitrostimulationbyvariouscompounds.Theradical uxassociatedwithOSAmaytrigger
R.Schulz(),F.Reichenberger,andK.Mayer, UniversityofGiessen,LungCenter,Giessen,Germany e-mail:
[email protected];
[email protected];
[email protected] A.M.Esquinas(ed.),NoninvasiveMechanicalVentilation, DOI:10.1007/978-3-642-11365-9_19,©Springer-VerlagBerlinHeidelberg2010
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lipid peroxidation and reduce nitric oxide bioavailability. Second, vascular in ammation maycontributetoOSA-associatedatherosclerosis.Thisisre ectedbyanupregulationof in ammatory biomarkers such as C-reactive protein (CRP), interleukin 6 (IL-6), tumor necrosis factor a (TNF-a), and soluble adhesion molecules in the blood of patients with OSA.Furthermore,differentleukocytesubpopulationsareactivatedinthesesubjectsand mayprovokeinjurytothevascularendothelium.Likewise,ratsundergoingrepetitiveair ow limitationsarecharacterizedbyincreasedleukocyte endothelialcellinteractions.Thesame hasbeenfoundinmicesubjectedtochronicintermittenthypoxia(CIH).Third,untreated OSAislinkedwithincreasedinsulinresistanceorimpairedglucosetolerance,whichmaybe equallyimportantfortheemergenceofatherosclerosis.Takentogether,thesechangesprovokeashiftofvascularhomeostasistovasoconstriction,in ammation,andthrombosis(i.e., endothelial dysfunction). This impairment of endothelial-dependent vasorelaxation is an established precursor lesion for atherosclerosis. Vasoreactivity studies employing venous occlusionplethysmographyand ow-mediatedvasodilationhaveclearlyshownthatendothelialdysfunctioncanbeobservedinotherwisehealthy,nonsmokingpatientswithOSA[3]. DirectevidencethatOSAmayinduceatherosclerosiscomesfromstudiesinvestigating subclinicalmarkersofatherosclerosisinpatientswithversuswithoutOSA.Thebestestablishedofthesemarkersisintimamediathickness(IMT).Itisdeterminedbyhigh-resolution ultrasonography,usuallyatthelevelofthecommoncarotidartery,andre ectstheearly phasesofatherosclerosis.VariousstudieshaveshownthatpatientswithOSAhavesigni cantlyincreasedIMTwhencomparedtosubjectswithoutsleep-disorderedbreathing,and thatthisisalsotrueforthosepatientswithoutanycomorbidities[4].Furthermore,itwas observedthatIMTinOSAisrelatedtothedegreeofnocturnalhypoxiaandtheapnea hypopneaindex(AHI).Inaddition,onestudyfoundthatIMTcorrelatedwithserumconcentrationsofin ammatorymarkers(i.e.,CRP,IL-6,andIL-18).Itshouldbenotedthat the ndingsfromthesesleeplab-basedstudieswerenotreplicatedinthepopulation-based SleepHeartHealthStudy.However,inthisstudy,patientswithmoderate-to-severeOSA inwhomanincreaseofIMTcanbeexpectedtooccurwereunderrepresented. Coronaryarteryatherosclerosiscanbevisualizedbyelectronbeamcomputedtomography.Usingthistechnique,Sorajjaandcolleaguesreportedthat,inpatientswithoutclinically overtcoronaryarterydisease,thepresenceandseverityofOSAwasindependentlyassociatedwiththepresenceandextentofcoronaryvesselcalci cations.Afurtherstudyinwhich coronary vessel architecture was evaluated by three-dimensional intravascular ultrasound foundthat,inpatientswithstablecoronaryarterydisease,therewasasigni cantrelationship betweenthefrequencyofapneasorhypopneasandcoronaryatheroscleroticplaquevolume. Theratioofankle-to-brachialsystolicbloodpressure(i.e.,theankle brachialindex)can beusedtoscreenforthepresenceofperipheralvaso-occlusivedisease.Inpatientswith OSA,thisindexhasbeenfoundtobehigherthaninpatientswithoutOSA.Atherosclerosis is characterized by enhanced arterial stiffness, which can be determined by carotid-tofemoralpulsewavevelocitymeasurement.PatientswithOSAhaveincreasedpulsewave velocitiesincomparisonwithmatchedcontrolswithoutsleep-disorderedbreathing. Inadditiontothesehumandata,ananimalexperimentfoundthatratsexposedtoCIH andfedwithahigh-cholesteroldietdevelopedacceleratedatherosclerosis[5].Interestingly, inthismodel,CIHalonewasnotsuf cienttoinduceatherosclerosis,thuspointingtoa ratherpermissiveroleofOSAinthepathogenesisofatherosclerosis.
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P=0.02 P=0.04 Intima-media thickness (µm)
Intima-media thickness (µm)
NS 1200 1100 1000 900 800 700 600 500 400 Baseline 4 months Control group
1200 1100 1000 900 800 700 600 500 400 Baseline 4 months Group receiving CPAP
Fig. 19.1 Effectsof4monthsofcontinuouspositiveairwaypressure(CPAP)therapyonintimamedia thickness(IMT)inobstructivesleepapnea(OSA)intreatedversusuntreatedpatients(n=12ineach group(From[6])
Continuouspositiveairwaypressure(CPAP)therapycanrestorethevascularmicromilieu, improve endothelial function, and prevent deaths from myocardial infarction and strokeinpatientswithOSAwithanAHIabove30/h.Therefore,oneshouldexpectthat thisformoftreatmentisabletoinhibitorevenreverseatherosclerosis.Indeed,onegroup fromBrazilfoundthatshort-termCPAPtherapyledtoamodestdecreaseofIMTinasmall sampleofpatientswithOSA([6];Fig.19.1).However,substantiallymorepatientsshould beinvestigatedoverlongertimeperiodstodetermineifCPAPreallycanreverseatheroscleroticremodelingofthevascularwall.
Key Recommendations
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The vemajorkeymessagesofthisreviewareasfollows: PatientswithuntreatedOSAhaveanincreasedriskforatherosclerosisandits relateddiseasesindependentofconfoundingfactors. Presumably,theunderlyingmechanismisadisturbanceofthevascularmicromilieu (i.e.,endothelialdysfunction)inresponsetotheintermittentnocturnalhypoxia. Studieslookingatdifferentsubclinicalmarkersofatherosclerosishaveclearly shownthatpatientswithOSAhaveacceleratedatherosclerosiswhencompared withcontrolswithoutsleep-disorderedbreathing. RatsexposedtoCIHandfedwithahigh-cholesteroldietdevelopaccelerated atherosclerosis. CPAPtherapyislikelytodecreaseatherosclerosisinOSA;however,long-term studiesenrollinglargernumbersofpatientsarenecessarytode nitivelyprove thisassumption.
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References 1. ShaharE,WhitneyCW,RedlineSetal(2001)Sleep-disorderedbreathingandcardiovascular disease.Cross-sectionalresultsoftheSleepHeartHealthStudy.AmJRespirCritCareMed 163:19 25 2. ArztM,YoungT,FinnLetal(2005)Associationofsleep-disorderedbreathingandtheoccurrenceofstroke.AmJRespirCritCareMed172:1447 1451 3. IpMS,TseHF,LamBetal(2004)Endothelialfunctioninobstructivesleepapneaandresponse totreatment.AmJRespirCritCareMed169:348 353 4. SchulzR,SeegerW,FegbeutelCetal(2005)Changesinextracranialarteriesinobstructive sleepapnoea.EurRespirJ25:69 74 5. SavranskyV,NanayakkaraA,LiJetal(2007)Chronicintermittenthypoxiainducesatherosclerosis.AmJRespirCritCareMed175:1290 1297 6. DragerLF,BortolottoLA,FigueiredoACetal(2007)Effectsofcontinuouspositiveairway pressureonearlysignsofatherosclerosisinobstructivesleepapnea.AmJRespirCritCare Med176:706 712
Transnasal Insufflation — A New Approach in the Treatment of OSAs
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GeorgNilius,BrianMcGinley,andHartmutSchneider
20.1 Introduction Obstructive sleep apnea (OSA) syndrome leads to intermittent hypoxemia, sleep fragmentation,metabolicdysfunction,andincreasedcardiovascularmorbidityandmortality.Currenttreatmentoptions,includingcontinuouspositiveairwaypressure(CPAP),oral appliances,andsurgicalprocedures,areoftenintrusiveorinvasiveandnotwelltolerated, leavingavastnumberofsubjectsuntreated.Therefore,improvedtherapeuticstrategiesare requiredtotreatsleepapneasandhypopneasandtheirassociatedmorbidityandmortality. Currently,CPAPismosteffectiveineliminatingapneasandhypopneas,althoughlongtermeffectivenessiscompromisedbylowadherence,whichisestimatedatonly50 60% andevenlowerinchildrenorpatientswithcomorbidconditionslikechronicobstructive pulmonarydisease(COPD),stroke,orheartfailure.Anopennasalcannulasystem ThestudywassponsoredbyHL72126,P50HL084945-01,SeleonInc.,NHMRC353705. Con ictofInterestDr.SchneiderreceivedconsultingfeesfromTNImedicalin2006 2009andis entitledtoroyaltypaymentsonthefuturesalesofproductsdescribedinthisarticle.UnderaseparatelicensingagreementbetweenDr.SchneiderandTNImedicalandJohnsHopkinsUniversity, Dr. Schneider is entitled to a share of royalty received by the university on sales of products described in this article. The terms of this agreement are being managed by Johns Hopkins Universityinaccordancewithitscon ict-of-interestpolicies.Fundingforthestudydescribedin thisarticlewaspartiallyprovidedbyTNImedical. H.Schneider() DivisionofPulmonaryandCriticalCareMedicine,JohnsHopkinsSleepDisordersCenter, JohnsHopkinsUniversity,5501BayviewBlvd,Baltimore,MD224,USA e-mail:
[email protected] G.Nilius HELIOS-Klinik,Hagen-Ambrock,Germany e-mail:
[email protected] B.McGinley DivisionofPediatricPulmonary,JohnsHopkinsPediatricSleepDisordersCenter, JohnsHopkinsUniversity,Baltimore,MD,USA e-mail:
[email protected] A.M.Esquinas(ed.),NoninvasiveMechanicalVentilation, DOI:10.1007/978-3-642-11365-9_20,©Springer-VerlagBerlinHeidelberg2010
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Fig. 20.1 Studyparticipant wearingthetreatmentwith nasalinsuf ation(TNI) cannula(cannulalengthis 1,800mm,5-mmouter diametercannulaandnasal prongs,3.4-mminner diameter)
deliveringwarmandhumidi edair(Fig.20.1)hasbeenintroducedasamethodforincreasingpharyngealpressure[1].Thischaptersummarizesthestudiesthatwereconductedwith treatment with nasal insuf ation (TNI) in adults and children with OSA and hypopnea acrossaspectrumofdiseaseseverity.
20.2 Mechanism of Actions of Nasal Insufflations 20.2.1 Effect on Upper Airway Upper airway obstruction is due to increased pharyngeal collapsibility, which decreases inspiratoryair ow,asmanifestedbysnoring,obstructivehypopneas,andapnea.Thisdefect inupperairwaycollapsibilitycanbeovercomebyelevatingnasalpressure.Infact,somewhatgreaterlevelsofnasalpressurearerequiredtoabolishapneasthanhypopneasandto restorenormallevelsofinspiratoryair ow.Viceversa,inpatientswithmildformsofupper airwayobstruction,lowlevelsofnasalpressurethroughanasalcannulamaybesuf cient torelievesleep-disorderedbreathing.Severalstudieshavebeenpublishedtocon rmthis hypothesis. ThemechanismofactionofTNIonupperairwayfunctionwas rstdeterminedinadult patientswithvaryingdegreesofupperairwayobstruction[1].Air owdynamicsandsupraglotticpressureresponsestoTNIwereexamined.Atarateof20L/min,TNIincreases nasalpressurebyapproximately2cmH2Oandincreasesinspiratoryair owbyapproximately100mL/s.Thisincreaseinpharyngealpressureandair owcanexplaintheimprovementofsnoringandhypopneasasfollows:Thepeakinspiratoryair owforhypopneasand
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for ow-limitedbreathsaveragesapproximately150 200mL/s.Theadditional owfrom TNIwillincreasetheinspiratoryair owto250 300mL/s,alevelpreviouslyassociated withstabilizationofbreathingpatterns(seeFig.20.2).However,unexpectedly,someindividuals also showed improvements in the event rate of obstructive apneas. The mechanismsfortheseresponsesarenotfullyunderstood.Additionalnonquanti ablefactorsmay havecontributedtothisresponse.First,smallincreasesinpharyngealpressuremayhave increasedlungvolume,whichmayimprovebothoxygenstoresandupperairwaypatency. Second,asventilationimprovesduringsleep,enhancedsleepcontinuity(decreasedarousal frequency)mayfurtherstabilizebreathingandreducetheeventrateofapneasandhypopneas.Finally,additionalbene tsmayhaveaccruedfrominsuf atingairdirectlyintothe nose,producingconcomitantreductionsindeadspaceventilation.
20.2.2 Effect on Ventilation NewevidenceexiststhatTNImayimproveventilationevenintheabsenceofupperairway obstruction.InonestudyinpatientswithamilddegreeofCOPD(GOLDI II:FEV1/FVC= 70%predictedandFEV1 <80%and>50%predicted),theuseofTNIduringsleepwas associatedwithareductioninarterialCO2comparedtoroomair[3].Inanotherstudy[4], TNIwasusedduringwakefulnessinadditiontosupplementaloxygensincepatientshad severeCOPD(GOLDIV-FEV1/FVC<70%predictedandFEV1<30%predicted)requiring oxygen treatment. In these patients, TNI and supplemental oxygen also reduced the respiratoryrate,whichwasassociatedwithareductioninarterialCO2from58to49mmHg, indicatingthatalveolarventilationhadimproved,andventilationhadbecomemoreeffective with TNI. Additional data for ventilator support independent of inspiratory ow
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Fig. 20.3 Polysomnographicrecordingshowingacuteeffectsofnasalinsuf ations(TNI20L/min) onventilationandbreathingpatterninachildwithobesityhypoventilationsyndromeandinspiratory owlimitationduringnon-rapid-eye-movement(NREM)sleep.Atbaseline,arapidshallow breathing pattern was present that was abolished with nasal insuf ations. Note that inspiratory owlimitationwasnotabolished,indicatingthatimprovementsinventilationareindependentof inspiratory owlimitation
limitation were given by the data in children [5]. McGinley et al. demonstrated that, in patients with rapid, shallow breathing, TNI markedly reduced the respiratory rate and inspiratory duty cycle, even if inspiratory ow limitation was not fully restored (see Fig.20.3).Theprecisemechanismforimprovinggasexchangeandef cacyofventilation isnotfullyunderstood.ItispossiblethatTNImayhavereducedCO2productionbyloweringtheworkofbreathing,orithasreducedthedeadspaceventilationbywashingoutthe anatomicdeadspaceofthenasalcavity.Alternatively,TNImayhavereducedintrapulmonarydeadspacebyopeningupatelectasisthroughtheslightincreaseinpositiveend-expiratorypressure(PEEP).Regardlessofthemechanism,thedatainchildrenandinindividuals withCOPDindicatedthatnasalinsuf ationsreducedtheloadofbreathing,particularlyin patientswitharapid,shallowbreathingpattern.Nevertheless,clinicaldataarewarrantedto determinetheeffectivenessofTNIinthesepatients.
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20.3 Predictors for Therapeutic Responses to TNI in Adults with OSA PolysomnographicresponsestoTNIwereexaminedinalargerclinicalsampleofpatients[5]. Theprimarypurposewastoidentifypolysomnographiccharacteristicsinabaselinesleep studythatmaybeusedtopredictTNItreatmentresponses.Inthisstudy,wecon rmedthat TNIreducedtheoverallsleep-disorderedbreathingeventratebelowaclinicallyacceptable thresholdin30 50%ofpatientsreferredtoasleeplaboratoryforCPAPtherapy.Patientswith awiderangeofsleep-disorderedbreathingeventrate(rangingfrom10to80events/h)had similarresponserates,indicatingthattreatmentresponsestoTNIwereindependentofthe sleepapneadiseaseseverity.Moreover,theresponseratewasmarkedlyincreasedinpatients withpredominantlyhypopneasandpatientswithmildupperairwayobstruction.Inaddition, thepresenceofmorethan10%centralapneaspredictedpoorresponse.Thus,TNItreatment responsesdependedontheseveritybutnotthefrequencyofupperairwayobstruction(see Fig.20.4).ThemainconclusionfromthisstudywasthatTNImayofferanalternativetothe standard CPAP therapy in patients with predominantly obstructive hypopneas. In patients withapneas,TNImayalsoincreaseair ow,butthatincreasemaybeinsuf cient.Asaresult, in apneic patients TNI may shift apneas to hypopneas, leaving the overall event rate unchanged.Sincetheef cacyofTNIcanbeeasilyassessedwithinasinglenight,initiation of this treatment should be monitored to ensure treatment ef cacy before recommending hometreatment.Nevertheless,itcanbepredictedthattreatmentef cacyishigherinpatients whosesleep-disorderedbreathingeventsconsistofatleast90%hypopneaandRERAs.Itis ofnotethattheseeventsarepredominantlyseeninchildren,women,andpatientswithcomorbidconditions.Therefore,thesepopulationsmaybeidealforthisformoftherapy.Todate, theeffectofTNIwasdeterminedinchildren.
20.4 Therapeutic Responses in Children with OSA Childrenwithupperairwayobstructionduringsleepdiffermarkedlyinregardtothedistributionofobstructiveevents.Theyhaveobstructiveapneaspredominantlyduringrapideye-movement(REM)comparedtonon-rapid-eye-movement(NREM)sleep.Incontrast toadults,childrencommonlyexhibitperiodsofprolongedstableupperairwayobstruction orhypopneasduringNREMsleep.Thus,theapplicationoflowlevelsofpharyngealpressuremayhavegreatertherapeuticeffectsinchildren.TNIresponseswerecomparedto CPAPandbaselinein12morbidlyobese,otherwisehealthy,childrenwithsleepapnea,for whomadherenceratestoCPAPweresolowthatmostchildreninthisstudywereineffectivelytreated[2].TNItreatedsleepapneaacrossawidespectrumofdiseaseseverityinall buttwochildren(seeFig.20.5).Second,inthemajorityofchildren,thereductioninthe sleep-disordered breathing event rate with TNI was comparable to CPAP. The authors concludedthatTNImayofferanalternativetoCPAPinsomechildrenforwhomstandard treatmentapproachesarenotsuccessful.Thegreatertherapeuticresponserateinchildren maybeduetothemilderdegreeofupperairwayobstructioninchildren.Alternatively,
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Fig. 20.4 Polysomnographic characteristics of the baseline sleep study that predict therapeutic response rates to TNI. A therapeutic response was de ned by a fall in RDI below 10 events/h associated with a 50% reduction in the RDI from baseline sleep study. *Denotes a statistically signi cantdifference(P<0.05)totheexpectednight-to-nightvariabilityinsleepapneaseverity of13%:Leftpanel:sleepapneadiseaseseveritywascategorizedintomild,moderate,andsevere bycalculatingtertilesoftheRDIatthebaselinesleepstudy.Rightpanel:fordegreeofhypopneas, theproportionsofobstructivehypopneastoallobstructiveevents(apneas,hypopneas,andRERAs) foreachpatientduringNREMsleepwerecalculated,andtherapeuticresponseratestoTNIare givenforsubgroupsofpatientswhohadmorethan50%(n=34),morethan2/3(n=23),andmore than90%(n=11)hypopneas.Notethatsubgroupsofpatientsoverlap(e.g.,thosewith>90%are alsorepresentedinthosewith>50%and>66%)
TNImighthaveincreasedpharyngealpressuremoreinchildrenthanadultsduetotherelativelylargersizeofthenasalcannulacomparedtothesizeofthenares. The greater therapeutic response rate in children may be due to the milder degree of upperairwayobstructioninchildren.Alternatively,TNImighthaveincreasedpharyngeal pressuremoreinchildrenthanadultsduetotherelativelylargersizeofthenasalcannula comparedtothesizeofthenares.Perhapsaslightincreaseinpharyngealpressuremight haveincreasedlungvolumestoagreaterdegreeinchildrenasaresultofhigherchestwall andlungcompliance,particularlyduringREMsleepwhenthechestwallmusculatureis hypotonic.Increasesinlungvolumemighthaveimprovedbothoxygenstoresandupper airwaypatency.Finally,itisalsopossiblethatchildren sre exresponsestoinsuf ationof airaregreaterthaninadults,leadingtoimprovementsinupperairwaypatency.Theauthors [2] concluded that, for the majority of children, the response to TNI was comparable to CPAP,thatTNImightultimatelybeamoreeffectivetreatmentoptionthanCPAP,andthat TNImayhaveaparticularroleinyoungerchildren,forwhomtheuseofCPAPcarriesconcernforthepotentialofcompressionofbonyfacialstructures.TNIisanopensystemthatis notdependentonatightlysealednasalmask,obviatingconcernsoffacialcompression.
20 Transnasal Insufflation — A New Approach in the Treatment of OSAs
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Fig. 20.5 Theapnea hypopneaindices(AHIs)aredisplayedforthebaselinecomparedtoTNItreatment night during non-rapid eye movement (NREM; left panel), rapid eye movement (REM; middlepanel),andfortheentirenight(rightpanel).Datapresentedaremean±standarderrorof themean(SEM).*ParticipantswithresidualsleepapneaonTNI, participantswithsuboptimal AHIresponsesonTNIcomparedtocontinuouspositiveairwaypressure(CPAP), childrenwithoutadenotonsillectomy
20.5 Summary An open nasal cannula system delivering warm and humidi ed air at a ow rate of 20L/min(TNI)caneffectivelytreatsleep-disorderedbreathinginasubsetofadultpatients andinamajorityofchildren.TNItreatmentresponsesdependedontheseverity(hypopneasratherthanapneas)butnotthefrequency(eventrate/h)ofupperairwayobstruction. TNImayalsoplayaroleinprotectingpatientswithrespiratoryfailureasitcanreducearterialCO2andalleviaterapid,shallowbreathing,therebyincreasingef cacyofbreathing. Thus,TNImightbeanalternativefornon-invasiveventilationforpatientsatriskfordevelopingrespiratoryfailure.
References 1. McGinleyB,PatilSP,DeRosaPA,KirknessJP,SmithC,SmithPL,SchwartzAR,Schneider H(2007)Anoveltherapeuticapproachforobstructedsleepdisorderedbreathing treatment withnasalinsuf ation(TNI).AmJRespirCritCareMed176:194 200 2. McGinleyB,HalbauerA,PatilSP,SmithC,SmithPL,SchwartzAR,SchneiderH(2009)An opennasalcannulatreatsobstructivesleepapneainchildren.Pediatrics124(1):179 188
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3. BrownCD,HerpelLB,GoringKL,SmithPL,WiseRA,SchneiderH,SchwartzAR(2007) Treatmentofsleep-disorderedbreathinginchronicobstructivepulmonarydiseasewithnocturnalnasalinsuf ation.AJRCCM175(AbstractsIssue)A709 4. NiliusG,DomanskiU,van tHogT,FrankeKJ,RuhleKH,SchwartzAR,SchneiderH(2009) Nasalinsuf ationofair(TNI)decreaseshypoventilationinoxygendependentpatientswith COPD[abstract].ERJ2009;53(Suppl):P842 5. Nilius G, Wessendorf T, Maurer J, Stoohs RA, Patil SP, Schubert N, Schneider H (2009) Predictors for treating obstructive sleep apnea with an open nasal cannula system (TNI) [publishedonlineaheadofprint].Chest2010Mar;137(3):521 528
Cardiopulmonary Interventions to Prolong Survival in Patients with Duchenne Muscular Dystrophy
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YukaIshikawa
21.1 Introduction Duchennemusculardystrophy(DMD)iscausedbymutationsinthedystrophingeneon theXchromosomeatXp21.DMDaffects1ofevery3,500livemalebirths.Progressionof muscularweaknessleadstolossofambulationby12yearsofage,andthedevelopmentof scoliosisismarkedbytheearlyteenageyears. Prior to the availability of effective ventilatory support and cardiac management, in DMDpatientsintheirlateteensorearly20stheleadingcauseofdeathwasrespiratory insuf ciency,andthoseintheirearlytomiddleteensdiedfromcardiaccomplicationssuch asdilatedcardiomyopathyandconductionabnormality. Currenttherapies,includingnoninvasiveventilation(NIV)andcardioprotectionhave improvedsurvivalandqualityoflifeforpatientswithDMD.
21.2 Respiratory Management 21.2.1 NIV for Chronic Respiratory Failure Pulmonaryfunctionisevaluatedannuallyorwhensigns rstappear(Table21.1). Whenthevitalcapacity(VC)decreases,anysymptomofchronicalveolarhypoventilation ismanifested,orhypoxemiaorhypercapniaisnoted,useofhigh-spanbilevelpositiveairway pressure(PAP)oravolume-cycledventilator(withcontrolmode)atnightisconsidered. Forpatientswhodevelopsymptomatichypercapniaandhypoxemiawhenawake,daytimeNIVisgraduallyincreased.Whenthepatientusesamotorizedwheelchair,theventilatorismountedonthewheelchairwitha exibletube,andanasalplugormouthpieceis xed.SomepatientscanhaveamealwhileusingNIV(desirablyusingcontrolmodewith avolume-cycledventilatororthepositiveend-expiratorypressure[PEEP]setatzero). Y.Ishikawa NationalHospitalOrganization,YakumoNationalHospital,Hokkaido,Japan e-mail:
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Table 21.1 CardiopulmonaryevaluationinpatientswithDMD 1.Generalexamination Height(armspan) Weight Scoliosis Chestdeformity Abdominaldistention Symptomsofchronicalveolarhypoventilationorcardiacdysfunction Respiratorysoundandheartsound 2.Pulmonaryfunction Respiratoryrate Abnormalbreathingpattern:Row-a-boatphenomenon,glossopharyngealbreathing,etc. Vitalcapacity(VC) Saturationofpulse-oximetryoxygen(SpO2):daytimeandnighttime TranscutaneousCO2gastension(PtcCO2) orend-tidalCO2gastension(PetCO2):daytimeandnighttime orPaCO2 Coughpeak ow(CPF):unassistedCPF CPFassistedbyairstackingtodeeplungvolumes(CPFair) CPFassistedbyabdominalthrusts(CPFthrust) CPFassistedbybothairstackingandabdominalthrust(aCPF) Maximuminsuf ationcapacity(MIC)when%VCis<50% 3.Cardiacfunction Heartrate Bloodpressure ChestX-ray:CTR ECG,HolterECG Brainnatriureticpeptide(BNP) Echocardiography
21.2.2 Airway Clearance Childrenaged12yearsorolderaretaughthowtoperformmanuallyassistedcoughing when the cough peak ow (CPF) decreases to less than 270 L/min. Children under 12yearsaretaughthowtoperformmanuallyassistedcoughingifanepisodeofdif cult airwayclearanceoccurs.Coughingisperformedafterairstackingwithassistedprocedures
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such as the use of a resuscitator bag, by inhaling several tidal volumes delivered by a volume-cycled ventilator under NIV, by performing glossopharyngeal breathing, or by raisingtheinspiratorypositiveairwaypressure(IPAP)by2 4cmH2O[1]. Once maximum assisted CPF becomes less than 270 L/min or ineffective for airway clearance,patientswithDMDrequiremechanicallyassistedcoughing(MAC)toprevent pneumoniaandacuterespiratoryfailure.MAChasbeende nedastheuseofmechanical insuf ation exsuf ation(CoughAssist,Phillips,Netherlands).Itisusedinconjunctionwith exsuf ation-timedabdominalthruststofurtheraugmentcough owsaspartofMAC.
21.2.3 Management of Chest Colds OncedecreasedVCorCPFisrecognizedinchildrenwithDMD,thosepatientsandfamilies shouldlearnhowtomaintainanSpO2(saturationofpulse-oximetryoxygen)greaterthan 94%usingassistedcoughingandprolongedhoursofNIVifthechildhasachestcold. NIVincombinationwithassistedcoughinghasbeenreportedtoreduceconsultations withageneralpractitionerforrespiratorytractinfections(RTIs),thenumberofantibiotic treatmentsforRTIs,andthenumberofhospitaladmissionsforRTIs[2].
21.2.4 Long-Term Continuous NIV ManypatientswithDMDusingcontinuousNIVfordecadeswithouttracheostomyhave beenreported.NIVhasalwaysbeeneffectiveforcontinuousventilatorysupportaslongas theventilatorsettingsorinterfacesareappropriate,evenwhenpatientsaretoomentally impairedtocooperatewithitorbulbar-innervatedmusculatureistooimpairedtoprotect theairwayfromcontinuoussalivaaspirationthatresultsinoxyhemoglobindesaturation.
21.3 Cardioprotection 21.3.1 Cardiac Evaluation Byadulthood,almostallpatientswithDMDhavecardiacinvolvement,includingcardiomyopathyandarrhythmia.ForpatientswithDMD,cardiacevaluationbyechocardiogram, serumbrainnatriureticpeptide(BNP),andelectrocardiogram(ECG)shouldbeobtained onceortwiceayear(Table21.1). Due to impaired motor function, patients with DMD are less likely to experience inspiratoryloadingandthusinspiratorydif culty.However,whenaloadslightlyhigher than usual is imposed, symptoms are suddenly manifested. Cardiac symptoms include dyspnea,cyanosis,paleness,cough,fatigue,palpitations,sweating,chestandabdominal discomfortorpain,nausea,lossofappetite,headache,frequentnocturnalarousal,frequent
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changesinneedforturningatnight,arthralgias,chills,decreasedurinaryoutput,irritability,dif cultyinconcentration,andedema(weightgain).
21.3.2 Combined Drugs and NIV Preventive management of cardiac involvement with ACEi and beta-blockade in DMD is effective when standard respiratory management with NIV and assisted coughing are also applied.Fifty-twoDMDpatientsreceivedtreatmentforheartfailureduetocardiomyopathy orasymptomaticleftventricular(LV)dysfunctionwithACEiandbeta-blockadeduringthe periodfrom1992to2005[3].The5-and7-yearsurvivalratesofallpatientswere93%and 84%,respectively.Inthetreatmentgroup(n=12,symptomaticheartfailuredueto cardiomyopathy),5-and7-yearsurvivalrateswere81%and71%,respectively.Theprevention group(n=40,asymptomaticLVdysfunction,leftventricularejectionfraction[LVEF]<45%), 5-and7-yearsurvivalrateswere97%and84%,respectively,andthe10-yearsurvivalratewas 72%.Thepreventiongroupshowedabettersurvivalratecomparedwiththetreatmentgroup. TheconsequencesofDMDcardiomyopathyareworsenedbysleep-disorderedbreathingwithhypoxemiaandhypercapnia.Inapatientwithcardiacfailure,reducedpharyngeal muscletoneduringperiodicbreathingandincreasedpharyngealedemaassociatedwith congestion can contribute to the obstructive apneas and hypopnea. Therefore, NIV can havedirectcardioprotectiveeffects.
21.4 Anesthesia and Sedation TherisksrelatedtoanesthesiaandsedationinpatientswithDMDincludepotentiallyfatal reactions to inhaled anesthetics and certain muscle relaxants, upper airway obstruction, hypoventilation,atelectasis,congestiveheartfailure,cardiacdysrhythmias,respiratoryfailure,anddif cultyweaningfrommechanicalventilation.Therefore,expertrecommendations arenecessaryregardingrespiratory,cardiac,gastrointestinal(GI),andanestheticmanagementofpatientswithDMDwhoundergogeneralanesthesiaorproceduralsedation. AccordingtoastatementbytheAmericanCollegeofChestPhysicians,preoperative pulmonaryassessmentshouldbeperformed(Table21.1).Iftheforcedvitalcapacity(FVC) isbelow30%,trainingintheuseofNIVisrecommended[4].IftheCPFislessthan270 L/min,traininginassistedcoughingandemphasisontheuseofMACisapplied. OptimizationofthepreoperativenutritionalstatusmayinvolvetheuseofNIVbecause patientswithuntreatedrespiratoryfailuremaybecomemalnourishedduetotheincreased workofbreathingortheymaybeunabletoeatduetodyspnea. Postoperatively,theSpO2shouldbemonitoredcontinuouslyuntilthecardiopulmonary statusbecomesstable.Wheneverpossible,assesscarbondioxidelevels(e.g.,PtcCO2[transcutaneous CO2 gas tension]). Assess carbon dioxide levels if hypoxemia is caused by hypoventilation,atelectasis,orairwaysecretionsandtreatimmediatelywithNIVandassisted coughing.Supplementaloxygentherapyshouldbeusedwithcautionbecauseoxygentherapy cancorrecthypoxemiawithouttreatingtheunderlyingcause(e.g.,hypoventilation,atelectasis,orairwaysecretions),andoxygentherapymayimpairthecentralrespiratorydrive.
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Inaddition,patientswithDMDmayhavegastroparesis,intestinaldysmotility,andconstipation,allofwhichcanbeexacerbatedpostoperativelybypainmedications.GIdysfunction can impair breathing if abdominal distention and increased intra-abdominal pressure occur, hampering diaphragmatic excursion. Gut dysmotility also increases the likelihoodofgastricdistentionwhenNIVisapplied.Bowelregimensshouldbeemployed to avoid and treat constipation, and selected patients may bene t from pharmacologic therapy with GI smooth muscle prokinetic agents. Appropriate postural management, feedingaids,gastrostomyinsertion,orparenteralnutritionshouldbeindicated.
21.5 The Parent as the “Lifeline” for a Child’s Life Using NIV Individuals with muscular dystrophy had average medical expenditures 10 20 times greaterthanindividualswithoutmusculardystrophy(intheUnitedStatesin2004).But, mostfamiliesfeltthattheyhadmadetherightchoiceinusingNIV. Accordingtoonestudy[5],familylifechangessigni cantlywiththedecisiontoplace achildwithDMDonNIV.Despitebecomingexpertcaregivers,theparentsexperienceda recurrentsenseoflossanduncertainty.Thosewhoperceivedinsuf cientsupportfeltthe weightofresponsibilityassolecareprovidersfortheirchild.Sincetheparents experience wasasthe lifeline fortheirchild slifeandqualityoflife,moresupportbyhealthcare professionalsandthecommunityisneeded.
Key Recommendations
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AsstandardrespiratorycareforindividualswithDMDleadstogreaterlongevity, bothrecognitionandpreventivetreatmentofcardiacinvolvement,including cardiomyopathyandarrhythmia,becomemoreimportant.Thetrendtoward improvingsurvivaltimesofpatientswithDMDcouldberelatedtothesalutary effectofNIVoncardioprotectioninadditiontotheincreasinguseofACEiand beta-blockers[3]. ForchildrenwithDMDwithdecreasedVCorCPF,NIVincombinationwith assistedcoughingreducesthefrequencyandseverityofRTIs[2]. Airstackingwassigni cantlymoreeffectivethanabdominalthrustinincreasing CPF,butthecombinationwasthemosteffective[1]. AlthoughthestatementbytheAmericanCollegeofChestPhysicians[4]includes adviceregardingrespiratoryandcardiacmanagementofpatientswithDMD undergoinganesthesiaorsedation,speci cstudiesneededtodevelopbetter guidelinesthatincludethefollowing:studiesofthespeci csettingsthatoptimize theef cacyofnoninvasivepositivepressureventilation(NPPV)andMACand studiesthatclarifytheroleofalternativemucusmobilizationtechniques. AmultidisciplinaryteamthatworksforoptimalmanagementofDMDusing NIV-speci cmultisystemcomplicationsisessential,andcollaborationinthis speci cclinicalnetworkisrecommendedtosupportfamiliesinmakingtheir choicetouselife-sustainingtechnologies[5].
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References 1. IshikawaY,BachJR,KomaroffE,MiuraT,Jackson-ParekhR(2008)Coughaugmentationin Duchennemusculardystrophy.AmJPhysMedRehabil87:726 730 2. Dohna-SchwakeC,PodlewskiP,VoitT,MelliusU(2008)Non-invasiveventilationreduces respiratory tract infections in children with neuromuscular disorders. Pediatr Pulmonol 43: 67 71 3. OgataH,IshikawaY,IshikawaY,MinamiR(2009)Bene cial effects of beta-blockers and angiotensin-converting enzyme inhibitor in Duchenne muscular dystrophy. J Cardiol 53: 72 78 4. BirnkrantDJ,PanitchHB,BendittJO,BoitanoLJ,CarterER,CwikVAetal(2007)American CollegeofChestPhysiciansconsensusstatementontherespiratoryandrelatedmanagementof patients with Duchenne muscular dystrophy undergoing anesthesia or sedation. Chest 132: 1977 1986 5. MahJK,ThannhauserJE,McNeilDA,DeweyD(2008)Beingthelifeline:theparentexperience of caring for a child with neuromuscular disease on home mechanical ventilation. NeuromuscDisord18:983 988
Noninvasive Ventilation Pressure Adjustments in Patients with Amyotrophic Lateral Sclerosis
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KirstenL.Gruis
Amyotrophiclateralsclerosis(ALS)isaprogressiveneurodegenerativedisorderofmotor neurons.PatientswithALSdevelopdiffuseskeletalmuscleweaknessinadditiontorespiratory muscle weakness, and respiratory failure is the most common cause of death. Tolerancetointermittentuseofnoninvasiveventilation(NIV)for4hormoreadayis associatedwithimprovedsurvivalandqualityoflifeinpatientswithALS[1,5]. NIV decreases the work of breathing by providing bilevel positive airway pressure: inspiratorypositiveairwaypressure(IPAP)and,toalesserextent,expiratorypositiveairway pressure (EPAP). Typically, the positive airway pressure is administered noninvasivelyviaanasal-typemaskinterface.Theamountofsupportprovidedtoweakinspiratory musclesisthedifferencebetweenIPAPandEPAP,termedpressuresupport. AlthoughNIVprovidessupportforweakenedrespiratorymuscles,itdoesnotcompletely replacerespiratorymusclefunctionascanbedonewithairwaycannulationandmechanical ventilation.Inthesettingoffullyassistedmechanicalventilation,themedicalprovidercan titratetheventilatorsettingstocorrectgasexchangeimpairment.However,inadisorderwith progressiverespiratorymuscleweaknesstreatedwithintermittentsupportiveNIV,itisuncertainhowmuchpressuresupporttoprovideandwhentoalterthepressuresupportsettings. InitialstudiesofNIVthatdemonstratedasurvivalbene tinALSusedNIVtitratedto patientcomfortbutdidnotprovideinformationregardingpressuresettings[2].Asurvey ofALSclinicmedicaldirectorsintheUnitedStatesshowedthatthemostfrequentlyused protocolwastoinitiateNIVwith8cmH2OIPAPand4cmH2OEPAPandtoincreasethe IPAPby2 3cmH2Oasneededtoimprovesymptoms[3].Incontrast,otherexpertshave proposedthatallALSpatientsuse high-span NIVwithapressuresupportof10cmH2O orgreaterwithagoalIPAPof16 18cmH2O.
K.L.Gruis MotorNeuronDiseaseCenter,UniversityofMichiganHealthSystem, DepartmentofNeurology,1914/0316TaubmanCenter,1500EastMedicalCenterDrive, AnnArbor,MI48109-0316,USA e-mail:
[email protected]
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Whileprovidinghighlevels(>10cmH2O)ofpressuresupportforallALSpatientsmay appearprudentinaprogressivedisorder,exposingpatientstohighairwaypressuresmay result in signi cant side effects that decrease NIV tolerance and subsequent bene ts of therapy.Inaddition,bythetimeNIVisstartedALSpatientshavelearnedtocompensate for respiratory muscle weakness and small tidal volumes with increased breathing frequency.Therefore,titratingallALSpatientstohighNIVpressurestocorrectreducedtidal volumes and increased breathing frequency may result in patient ventilator asynchrony andintolerancetoNIVtherapy. Importantly,thelackofguidanceinthemedicalliteratureregardingNIVpressuresettingsandadjustmentsforALSpatientsmaycontributetomedicalproviders unwillingness to prescribe NIV therapy. Therefore, we performed a retrospective, single-center, chart reviewassessmentofNIVpressuresettingsusedforsymptomatictreatmentofALSpatients. WeassessedNIVpressuresettingsovertimeandcomparedsurvivalbetweenthoseALS patientstolerant,de nedbymorethan4hofusepernight,andintoleranttoNIV[4]. TheALSpatientsinourstudywerestartedonNIV,andpressuresweretitratedinasimilar fashion to that described [3]. Therefore, the NIV pressures used were the minimum requiredtoimprovebreathingcomfort.Wecompared18patientswhoweretoleranttoNIV therapyand19patientswhowereintolerant.Themajorityoftolerantpatients(67%)used pressuresupport(IPAP EPAP)oflessthan10cmH2Ountiltheirdeaths,whiletheremainingthirdofpatientsrequiredpressuresupportgreaterthan10cmH2Otoimprovesymptoms.Themaximumpressureneededwas19/5cmH2O,while4of18patients(22%)found theoriginalNIVsettingsof8/3cmH2Osuf cienttoimproverespiratorysymptoms[4]. These ndings are similar to a prospective, randomized study of NIV therapy in ALS patientsthatdemonstratedanaveragepressuresupportofonly11cmH2O[5].Awiderange ofNIVpressures(8.2 22.4cmH2O)hasbeenassociatedwithimprovedALSpatientventilationasmeasuredbygasexchange[6].Takentogether,these ndingsdemonstratethat notallALSpatientsneedapressuresupportgreaterthan10cmH2Otoimproveventilation withNIVtherapy. Inourstudy,mostNIVpressurechangesoccurredwithinthe rstyearofNIVtherapy, andonly2of18patients(11%)requiredmorethantwochangesinNIVpressuresettings[4]. ThisiscontrarytothebeliefthatALSpatientswillneedmorefrequentNIVpressure increasesasthediseaseprogresses.Instead,whatlikelyoccurswithprogressiverespiratory muscleweaknessisincreasedhoursofusageofNIVtherapyratherthanmarkedincreasesin NIVpressuresupport.Asigni cantincreaseinNIVusagedurationhasbeendescribedina prospectivestudyofALSpatients,withNIVusagehoursincreasing98 277%,withsome patientseventuallyusingNIVcontinuously[5]. Patients who tolerated NIV had a nearly 1-year increase in survival compared with thosewhowerenottolerantofNIV.Thesurvivalassociationremainedwhenadjustingfor ageandsymptomonsetlocation(bulbarvs.limb) clinicalcharacteristicsassociatedwith poor ALS survival with a hazard ratio of 0.23 (95% con dence interval 0.10, 0.54). These ndingsaresimilartothebene tfoundinaprospective,randomizedclinicaltrial thatdemonstratedamediansurvivalbene tofnearly7monthsinthosepatientstreated withNIVtherapycomparedtothosewhoreceivedstandardmedicalcarewithoutNIV[5]. Thus,ourdatasuggestthatevenrelativelylowNIVpressuresupportisassociatedwithan improvementinsurvival.
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References 1. Kleopa KA, Sherman M, Neal B, Romano GJ (1999) Heiman Patterson T Bipap improves survivalandrateofpulmonaryfunctiondeclineinpatientswithALS.JNeurolSci164:82 88 2. AboussouanLS,KhanSU,BanerjeeM,ArroligaAC,MitsumotoH(2001)Objectivemeasures of the ef cacy of noninvasive positive-pressure ventilation in amyotrophic lateral sclerosis. MuscleNerve24:403 409 3. MeloJ,HommaA,IturriagaEetal(1999)Pulmonaryevaluationandprevalenceofnon- invasive ventilation in patients with amyotrophic lateral sclerosis: a multicenter survey and proposalofapulmonaryprotocol.JNeurolSci169:114 117 4. GruisKL,BrownDL,LisabethLD,ZebarahVA,ChervinRD,FeldmanEL(2006)Longitudinal assessmentofnoninvasivepositivepressureventilationadjustmentsinALSpatients.JNeurol Sci247(1):59 63 5. BourkeSC,TomlinsonM,WilliamsTL,BullockRE,ShawPJ,GibsonGJ(2006)Effectsof non-invasive ventilation on survival and quality of life in patients with amyotrophic lateral sclerosis:arandomisedcontrolledtrial.LancetNeurol5:140 147 6. ButzM,WollinskyKH,Wiedemuth-CatrinescuUetal(2003)Longitudinaleffectsofnoninvasive positive-pressure ventilation in patients with amyotrophic lateral sclerosis. Am J Phys MedRehabil82:597 604
Noninvasive Positive Pressure Ventilation in Amyotrophic Lateral Sclerosis
23
DanieleLoCoco,SantinoMarchese,andAlbinoLoCoco
23.1 Introduction Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disease of unknown origin that affects approximately 1.5 individuals per 100,000 every year; usually,theseindividualsarebetween55and75yearsofage[1].ALScausesprogressiveweaknessofvoluntarymusclegroups,includingrespiratoryones,andrespiratory failureorpneumoniarelatedtorespiratorymuscleweaknessisthemostfrequentcause ofdeath. However,onlyafewpatientspresentwithrespiratorymuscledysfunction,whereas themajorityofthemmaintainanalmostnormalrespiratoryfunctionforlongperiodsof time. Patients thus need to be regularly and progressively evaluated to identify early signs of respiratory muscle weakness so that adequate treatment can be implemented. Furthermore,itisgoodpracticetodiscussrespiratoryissueswellinadvancewiththe patientsandtheirfamilytoavoidemergencydecisionsorunwantedtreatmentsincaseof acrisis.
D.LoCoco() ALSClinicalResearchCenter,DipartimentoUniversitariodiNeuroscienzeCliniche(DiNeC), UniversityofPalermo,ViaG.LaLoggia,1,90129Palermo,Italy e-mail:
[email protected] S.Marchese RespiratoryIntensiveCareUnit,OspedaleCivicoeBenfratelli,ARNAS,ViaC.Lazzaro, 2,90127Palermo,Italy A.LoCoco PulmonaryDepartmentandRespiratoryIntensiveCareUnit,OspedaleCivicoeBenfratelli, ARNAS,ViaC.Lazzaro,2,90127Palermo,Italy
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23.2 Respiratory Function Evaluation Usually,whenpatientswithALSseekmedicalattention,pulmonaryevaluationiswithinthe normalrange,andpatientsdonotreferrespiratorycomplaints.However,duringtheprogressionofthediseaseallpatientseventuallycomplainofdyspneawithexertion,orthopnea, andpoorsleepqualitywithfrequentawakenings,nightmares,earlymorningheadaches,or excessivedaytimesleepiness[2,3].Aclinicalexaminationatthispointmightshowrespiratoryparadox,rapidshallowbreathing,oraccessorymusclecontraction.Nevertheless,the observation that many patients may remain asymptomatic even when there is a marked reductionofvitalcapacitylimitsthereliabilityofthesesignsandsymptoms. Inadditiontorespiratorysymptomsandsigns,manyexamsareusedintheevaluation ofpulmonaryfunctioninALSpatients(Table23.1)[2,3].Themostwidelyavailablemeasurefordetectingrespiratorydeclineisforcedvitalcapacity(FVC)whensittingorsupine. FVCiscorrelatedwithsurvivalandusuallypresentsanalmostlineardecreaseduringthe courseofthedisease,butwithamarkedvariabilityfrompatienttopatient(within2 4%of predictedvaluepermonth). Well-knownlimitationsofFVCarethelowsensitivityinpatientswithbulbarinvolvement,becauseofreducedbuccalstrength,orcognitiveinvolvement,andtherelativeinsensitivitytodetectmildormoderatediaphragmaticdysfunction. Maximal inspiratory and expiratory pressure (MIP and MEP, respectively) are other sensitive measurements, but in many centers these are not routinely executed because manypatientsareunabletoperformthetestwiththeprogressionofdisease. ArterialbloodgasanalysismayalsobeofhelpintheevaluationofpatientswithALS, especiallyinthosewithseverebulbarinvolvementsinceitcouldrevealrestinghypercapnia(Paco2>6.5kPa)orhypoxemia(Pao2<90mmHg).However,theseareusuallyvery latesignsofrespiratoryfailureinALS. Increasing attention has been drawn to measurement of sniff nasal inspiratory pressure (SNIP),whichisregardedasagoodmeasureofdiaphragmaticstrength.SNIPisprobablymore accuratethanFVC,althoughevenSNIPmayunderestimaterespiratoryfunctioninpatients withbulbarinvolvementbecauseofupperairwaycollapse.However,asniffnasalpressuretest below40%ofpredictedvalueisasigni cantpredictorofnocturnalhypoxemiaandmortality. Finally,nocturnalhypoventilationandsleep-disorderedbreathingarealsocommonin ALS with the progression of the disease and can occur even when respiratory muscle functionisonlymildlyaffectedanddaytimegasexchangeremainsnormal.Then,since Table 23.1 Objective measurements of pulmonary function of patients with amyotrophic lateral sclerosis(ALS)inadditiontorespiratorysymptomsandsigns Forcedvitalcapacity(FVC;bothuprightandsupine) Maximalinspiratoryandexpiratorypressure(MIPandMEP,respectively) Sniffnasalinspiratorypressure(SINP) Nocturnaloximetry Arterialbloodgasanalysis
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nocturnaloximetryiseasytoperformandcanbeexecutedinthehome,ithasbecome frequentlyusedinclinicalpracticefortheevaluationofrespiratoryinvolvementinALS patients.Polysomnographyisnotroutinelyrecommended.
23.3 Noninvasive Positive Pressure Ventilation Inthelast10years,therehasbeenarevolutioninrespiratoryassistanceandventilatory supportinALSthathashadasigni cantimpactonthenaturalhistoryofthedisorder.The application of ventilatory assistance, most frequently noninvasively, has been shown to alleviaterespiratorysymptoms,toextendsurvivalconsiderably,andtoimprovequalityof lifeandcognitivefunctionsinmostpatients[1 3].Atpresent,noninvasivepositivepressure ventilation (NIPPV), usually via nasal mask with bilevel positive airway pressure (BiPAP)machines,isthemosteffectivetreatmentavailableforpatientswithALS[4].A proposedrespiratorymanagementalgorithmforpatientswithALSisshowninFig.23.1. AllpatientswithALScanbene tfromNIPPVtherapy,andatrialwiththisappliance should never be discouraged, but marked bulbar involvement could be associated with reducedtoleranceandmaybesurvival.Indeed,theincreasedriskofaspirationinpatients withbulbaronsetandproblemsbecauseofdif cultiesinclearingsecretionsorobstructions, such as those related to abnormal function of the vocal cords, should be considered.
offer NIPPV
periodic respiratory evaluations (FVC, SNIP, nocturnal oxymetry)
ALS onset
- Respiratory symptoms - FVC < 80% - SNIP < 40cmH2O - nocturnal desaturation - morning pCO2 > 6.5 kPa
monitor NIPPV compliance and coughing efficacy
progressive skeletal muscles weakness and atrophy
diagnosis
chronic hypoventilation
respiratory insufficiency
tracheostomy ventilation
death
Fig. 23.1 Schematicrepresentationoftheprogressiverespiratorydysfunctioninamyotrophiclateral sclerosis (ALS) over time and recommended respiratory management. FVC forced vital capacity,NIPPVnoninvasivepositivepressureventilation,SNIPsniffnasalinspiratorypressure
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Inourexperience,NIPPVcanbewelltoleratedbybothpatientsandcaregivers,evenin patientswithbulbarinvolvement[5].Specialimportanceshouldbegiventoadaptation andcomplianceduringthe rstfewweeksofNIPPVusesincethiscouldbeacrucialstep indeterminingtheef cacyofthetreatment. Factors predicting survival following NIPPV include advanced age, airway mucus accumulation,andlowerbodymassindex. The mechanisms by which NIPPV therapy could affect survival in ALS are not perfectlyknown,andithasbeensuggestedthatmostofitseffectscouldberelatedto aslowingoftherateofrespiratoryimpairment,thusmodifyingthenaturalcourseof thedisease.Amongthehypothesesthathavebeengeneratedtoexplainthesustained improvementinrespiratoryfunctionandgradualresolutionofsymptomsassociated withNIPPV,ithasbeenpostulatedthatNIPPVrestschronicallyfatiguedrespiratory muscles,therebyimprovingdaytimerespiratorymusclefunction.Anotherhypothesis suggeststhatNIPPVimprovesrespiratorysystemcompliancebyreversingmicroatelectasis, thus diminishing daytime work of breathing. Finally, a third theory proposes that NIPPV improves central respiratory drive and the arousal mechanism (chronically depressed by habitual exposure to hypoventilation), leading to better ventilationduringbothwakingandsleepinghours.Allthesetheoriesarenotmutually exclusive,witheachpossiblycontributingtotheameliorationsobservedinpatients undergoingNIPPV. Notwithstanding the effects on respiratory symptoms, quality of life, and survival, manystudiessuggestedthattheemploymentofNIPPVinALSispoorworldwide,witha needformoreeducationofcliniciansandpatientsregardingthebene tsofNIPPVearlier inthecourseofthedisease[6].ThereasonsforsuchlowuptakeofNIPPVaremultifactorialbutarein uencedbydifferencesintheexperienceofphysicians,itsavailabilityand cost,uncertaintyofthebene tsandtimingforstartingventilation,andconcernsthatventilatorysupportmightprolongsuffering,renderhomecarelessfeasible,andleadtodependencyorventilatorentrapment[1]. Moreover, there is still debate about the optimal timing to introduce ventilation in thesepatientsandwhetherearlyNIPPVinitiationcouldactuallyleadtoincreasedsurvivalrates. Atpresent,worldwideacceptedguidelinesproposeNIPPVinitiationinthepresence of respiratory symptoms or evidence of respiratory muscle weakness (FVC £ 80% of predictedorSNIP£40cmH2O),evidenceofsigni cantnocturnaldesaturationonovernightoximetry(<90%for>5%ofthetimeasleep),oramorningarterialPaco2above6.5 kPa[1]. NIPPVisusuallyinitiallyusedforintermittentnocturnalsupporttoalleviatesymptoms of nocturnal hypoventilation, although as respiratory function worsens, patients tend to requireincreasingdaytimesupportandeventuallycontinuoussupport.However,thedisorderwilleventuallyprogresstothestageatwhichNIPPVwillnotbeabletocompensate forrespiratoryimpairment,andinthesecircumstancesonlyinvasiveventilationbytracheostomyisabletoprolongsurvival[1 3]. Whenplacedoninvasiveventilation,patientsaresupportedfromarespiratorypoint ofview;however,thelossofmotorneuronsgoesonprogressively,leadingtocomplete paralysis and muscular atrophy. Some patients may eventually reach a locked-in
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stateinwhichtheycannotcommunicateatallbecausethereisalsototalparalysisof theextraocularmuscles.Despitethis,whenconnectedtotracheostomytubespatients maysurviveformanyyears,withrespiratorytractinfectionsthemostfrequentcause ofdeath. Notwithstandingitseffectonsurvival,onlyaminorityofALSpatientsreceiveinvasive mechanical ventilation, at least in the Western countries. On the contrary, in Japan the frequencyofinvasiveventilationisconsiderablyhigher. Furthermore, many patients undergo tracheostomy in emergency without advance planningbecauseofarespiratorycrisis,whereasthenumberofpatientswhoelectively choosethistreatmentislow.SocioeconomicreasonsmaybeoneofthepossibleexplanationsforthelowprevalenceofinvasiveventilationinALSsincethetreatmentiscostly. Moreover,thereisaneedfor24-hcaregiving,whichcouldbeperceivedasextremely burdensomeforthewholefamily.Theattitudesofthetreatingphysicianhavealsogreat in uence,andthereisconcernthattracheostomyventilationwillprolonglifebeyondthe pointthatthepatientcancommunicateorinteractwithothersorabouttheprocedureto withdrawcare. Despitethesemanydoubtsandconcerns,themajorityofpatientswhounderwentinvasiveventilationwerepositiveabouttheirchoice,reportedasatisfyingqualityoflife,and indicated that they would repeat the choice again in the same situation. Caregivers weremorefrequentlyburdenedanddistressedbythisintervention,andtheyfrequently witnessedamarkedreductionofsociallifeactivities[1 3]. It is important to underline that unplanned and unwanted tracheotomy could beavoidedbyearlydiscussionoftheoptionsforrespiratorysupportandthroughadvance directives.Indeed,onceintubated,patientsarerarelyfreefromtheventilator.Advance directives should also be reviewed periodically during the course of the disease. On thecontrary,emergencyintubationandtracheostomyshouldbeavoided[1 3].
23.4 Supportive Care Apartfromsustainingrespirationwithmechanicaldevices,specialconsiderationhasto begiventopreventionofaspirationanddevelopmentofpneumonia[1 3].Inthisregard, itisoffundamentalimportancetoreducetheamountofsalivarysecretionsthroughthe use of several medications (such as amitriptyline and botulinum toxin injections), to devoteadequatetimeinteachingproperswallowingtechnique,andtomaintainhydration.Itisalsousefultoprovideaportablemechanicalhomesuctiondevice.Inaddition, when dysphagia worsens, placement of a percutaneous endoscopic gastrostomy tube shouldbethepreferredoption,especiallywhentherespiratoryfunctionisnottoomuch compromised. Anotheraspectofthepatient scarethatneedsspecialattentionisphysiotherapy,which is a useful aid for the management of respiratory secretions [1 3]. Indeed, during the courseofthedisease,progressiveinspiratoryandexpiratorymuscleweaknessandbulbar innervated muscle dysfunction result in the cough re ex becoming ineffective, causing
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dif cultiesintheclearanceofmucus.Thisislargelydependentonthemagnitudeofpeak cough ows(PCFs),andaPCFbelow2.7L/sindicatesanineffectivecough.However, sincePCFdecreasesduringrespiratorytractinfections,whenthepressuregeneratedby expiratorymusclesisreduced,ithasbeensuggestedthatonceapatient sPCFisbelow4.5 L/s,particularlyinthepresenceofbulbardysfunction,thereisariskforpulmonarycomplications,andthatthresholdcouldbeanappropriatetimetoimplementassistedcough techniques. Methodstotreatofrespiratorysecretionsincludebreathingexercises,posturaldrainage,exerciseregimens,andtheuseofassistedcoughtechniques.However,ithastobe pointedoutthatpatientswithlimitedmobilityandmuscleweaknesshavedif cultywith postural drainage and generally do not bene t from chest physical therapy. Moreover, intensivecyclesofphysiotherapymaybeexhaustingformanypatients,particularlythose withadvanceddisease,andmaycausearterialdesaturation. Amongnoninvasiveexpiratoryaids,manuallyassistedcoughingtechniques,suchas anteriorchestcompression and abdominal thrust, have been effective in facilitating the elimination of airway secretions in patients with neuromuscular diseases, even if these maneuversarelaborintensiveandoftendif cultfornonprofessionalcaregivers. Themechanicalin-exsuf ator(MI-E)isadevicethatassistspatientsclearbronchial secretions. It consists of a two-stage axial compressor that provides positive pressure (whichcausesadeepinsuf ation),therebygeneratingaforcedexpirationinwhichhigh expiratory owratesandahighexpiratorypressuregradientaregeneratedbetweenthe mouthandthealveoli.Itisusuallyappliedviaafacemask.TheuseofMI-Eissimple andsafeenoughforapplicationbynonprofessionalcaregiversandisconsideredacomplement to manually assisted coughing in the prevention of pulmonary morbidity in patientswithneuromusculardiseases.Moreover,theuseofMI-Eprolongsnoninvasive respiratoryaidsanddelaystheneedfortracheostomyinpatientswithALS.However, thisdeviceseemstobeineffectiveinpatientswithseverebulbardysfunction,perhaps becausetheapplicationoftheexsuf ationcycleofMI-Eforthosepatientswithweaknessofthegenioglossusmusclemightproduceadynamic,total,orpartialcollapseofthe upperairway. Itcanbeusefultorememberthat,forpatientswhosevitalcapacitiesarelessthannormal,manuallyassistedcoughingisnotoptimallyeffectiveunlessprecededbymaximal lunginsuf ation,andMI-Eisnotoptimalunlessanabdominalthrustisappliedduringthe exsuf ation.AbdominalthrustsandMI-Earenotmutuallyexclusive,andtheyshouldbe combined for effective prevention of lower respiratory tract infection and respiratory insuf ciency. Failure to correctly administer physical medicine aids continues to make respiratory failure inevitable for the great majority of people with neuromuscular diseases. Finally, high-frequency chest wall oscillation (HFCWO) is another airway-clearance technique that has been tested on ALS patients. HFCWO is a technique that, throughgenerationofhigh owinthesmallairways,isthoughttomobilizesecretions from the distal airways to the larger airways, from where they can be more easily removed.Althoughwedonothavespeci cknowledgeaboutit,HFCWOseemstobe well tolerated and helpful to a great proportion of patients, decreasing symptoms of breathlessness.
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Conclusion and Key Recommendations
› ›
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›
› ›
Recentpublicationshavemadeimportantcontributionsinparticulartosome aspectsofrespiratorycareforpatientswithALS,suchasnoninvasiveventilation andassistedcough. Thereisaneedforregularassessmentandfollow-upofrespiratoryfunction,and investigationsshouldincludedaytimeassessmentofrespiratoryfunction (includingFVCandSNIP)aswellasasleepstudiestoensureearlyrecognition ofpatientswithrespiratorymuscleimpairment. NIPPVtreatmentalleviatesrespiratorysymptoms,prolongssurvivalforlonger thananyavailablepharmaceuticalagent,improvesqualityoflife,andmay probablymodifythediseasecourse.Forthisreason,NIPPVshouldbeconsidered mandatoryinanypatientatriskofhypoventilationorinwhomrespiratoryfailure hasbecomeevidentduringsleepdespitenormaldiurnalrespiration. ThedegreeofhypoventilationthatshouldpromptintroductionofNIPPVmustbe de nedfurther,evenifthereisgrowingevidencefromliteratureshiftingthe evidence-basedindicationforNIPPVtowardearlierintervention.Nocturnal hypoventilationcouldbeparticularlyusefulforthispurpose. EveryeffortshouldbemadetoimproveNIPPVimplementationinthe managementworldwideofpatientswithALSsinceitisstillunderutilized. Preventionofaspirationandpneumoniaandadequatemanagementofbronchial secretionsaretwoimportantissues.Adequatetreatmentofsialorrheaand dysphagiaisimportantinthereductionofpneumoniarisk.Insuf cientcough isaconditionthatcanbediagnosedbymeasuringpeakcough owandshould, wheneverpresent,betreatedinpatientswithALS.Thereissomeevidencethat mechanicalcough-assistingdevicescouldbeofhelpincoughassistance,except forpatientswithseverebulbardysfunction,butfurtherresearchisneeded.
References 1. RadunovićA,MitsumotoH,LeighPN(2007)Clinicalcareofpatientswithamyotrophiclateral sclerosis.LancetNeurol6:913 925 2. Beneditt JO, Boitano L (2008) Respiratory treatment of amyotrophic lateral sclerosis. Phys MedRehabilClinNAm19:559 572 3. Heffernan C, Jenkinson C, Holmes T et al (2006) Mangement of respiration in MND/ALS patients:anevidencebasedreview.AmyotrophLateralScler7:5 15 4. Heiman-PattersonTD,MillerRG(2006)NIPPV:atreatmentforALSwhosetimehascome. Neurology67:736 737 5. LoCocoD,MarcheseS,PescoMC,LaBellaV,PiccoliF,LoCocoA(2006)Noninvasivepositive-pressureventilationinALS.Predictorsoftoleranceandsurvival.Neurology67:761 765 6. MillerRG,AndersonF,BrooksBR,MitsumotoH,BradleyWG,RingelSP,ALSCAREStudy Group(2009).Outcomesresearchinamyotrophiclateralsclerosis:lessonslearnedfromthe amyotrophiclateralsclerosisclinicalassessment,research,andeducationdatabase.AnnNeurol 65(Suppl1):S24 S28
Noninvasive Mechanical Ventilation as an Alternative to Endotracheal Intubation During Tracheotomy in Advanced Neuromuscular Disease
24
DavidOrlikowski,HélènePrigent,andJésusGonzalez-Bermejo
24.1 Introduction 24.1.1 Difficulties for intubation and invasive procedures in neuromuscular disease Tracheotomyisamajorstepforpatientswithneuromusculardiseaseasitrequiresahigher levelofcare,whichaffectsqualityoflifeandincreasesdependence.Intoleranceornonfeasibilityofnoninvasiveventilation(NIV)isthemostcommonreasonfortracheotomyof patientswithneuromusculardisease.Otherreasonsincludeworseningofrespiratoryfailurewithalowvitalcapacity(VC),persistenthypercarbia,andtheneedtoincreaseventilationtime.Onemajorconditiontorealizetracheotomyistobeabletomaintainef cient ventilation throughout a procedure while providing efficient analgesia. Due to their severely impaired pulmonary function, respiratory management of patients with neuromusculardif cultiesisverychallenging.Theseindividualsareatriskofseverecomplicationswhentheyrequiredeepsedationoranesthesiawithendotrachealintubation.They present many factors that can lead to dif cult intubation: skeletal deformities, tracheal deviationrelatedtokyphoscoliosis,reducedneckmobilityduetocervicalfusionormyopathy,tonguehypertrophy,andreducedmouthopening.Themainriskincaseofdif cult intubationisadelayinef cientairwayprotection;adverseeventsinthissettinginclude desaturation,hypoxemia,aspirationpneumonia,andprolongedstaysintheintensivecare D.Orlikowski() IntensiveCareUnitandHomeVentilationUnit,RaymondPoincaréTeachingHospital, UniversityVersaillesSQY,104boulevardRaymondPoincaré,92380Garches,France e-mail:
[email protected] H.Prigent PhysiologyLaboratoryandNewTechnologyInvestigationCenter,RaymondPoincaréTeaching Hospital,UniversityVersaillesSQY,104boulevardRaymondPoincaré,92380Garches,France J.Gonzalez-Bermejo RespiratoryUnit,PitiéSalpêtrièreTeachingHospital,Paris,France A.M.Esquinas(ed.),NoninvasiveMechanicalVentilation, DOI:10.1007/978-3-642-11365-9_24,©Springer-VerlagBerlinHeidelberg2010
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unit(ICU)orhospital.Musclerelaxantsandsedativeanestheticagentsmayinducesevere respiratorydepressionandinef cientcough;moreover,musclerelaxantsmaycauserhabdomyolysiswithfatalhyperkalemia[1].Aheightenedmaximaleffectofvecuroniumhas beenreportedinpatientswithDuchennemusculardystrophy(DMD),resultinginalarge increaseoftimetorecovery.Sedativeagentscaninduceseverehypotensioninpatients withcardiacinvolvement,asseeninDMD;thepotentialdepressiveeffectofsedativeson cardiaccontractilitymustbeconsideredwhenusedinpatientswithcardiacdysfunction andatriskoflife-threateningcardiacdysrhythmia. The dif culties and risks associated with endotracheal intubation in patients with advancedneuromusculardiseasepromptedustocompareourexperienceoftwotracheotomyprocedures:conventionaltracheotomywithsedationandintubationtotracheotomy withlocalanesthesiaandNIVasproposedforthegastrostomyprocedureinDMDorin amyotrophiclateralsclerosis(ALS)[2]. We publishedtheresultsofaretrospectivestudy[3] comparing an initial period when patientswithadvancedneuromusculardiseaseweredeeplysedatedandintubatedfortracheotomytoaperiodwhenpatientsunderwenttracheotomywithlocalanesthesiaandNIVbut withoutsedation.Conventionaltracheotomywasperformedin7patientsandwithNIVand localanesthesiain13patients.Allbut3patientshadriskfactorsfordif cultintubation.We showedthatthenumberofrespiratorycomplicationssuchaspneumoniawashigherinthe conventionalgroup(fourvs.one)despiteasimilarhospitalstay.Weconcludedthatinpatients withneuromusculardiseasewhorequiretracheotomy,useofNIVcombinedwithlocalanesthesiamaybehelpfultoavoidendotrachealintubationandreducemorbidity(Table24.1). Progressinmedicalmanagementofneuromusculardisordershasresultedinincreased survival.Peoplewithadvancedneuromusculardisease,suchasmusculardystrophy,more frequentlyrequireinvasiveandpainfulproceduresandthereforedeepsedationoranesthesia.Someneuromusculardiseasesareassociatedwithmajorskeletaldeformities:limited neckextension,macroglossia,andreducedmouthopening(Fig.24.1).Norecommendation is available for intubation of patients with neuromuscular disease. The American SocietyofAnesthesiologistsTaskForceonDif cultAirwayManagementpublishedan updateofpracticeguidelines[1,4].Factorspredictiveofdif cultintubationincludedan interincisordistancesmallerthan3cm,aMallampaticlasshigherthanII,decreasedmandibularspacecompliance,andashort,thickneckwithimpossibleextension.Mostofour patientshadsuchriskfactors.Therelativeriskfordif cultintubationincreaseswiththe Mallampaticlass.NIVdeliveredthroughseveralinterfaces(i.e.,nasalmask,facemask,or mouthpieceortolaryngealmask)hasbeenproposedinchildrenwithfacialdeformities, cervical spine rigidity, and neuromuscular disease who are undergoing several invasive medicalorsurgicalprocedurestoprovidesaferespiratorysupportduringdeepsedationor anesthesia[2].Thesetechniquesrequirewell-trainedphysiciansabletoadapttheventilatorsettinginresponsetothelossofspontaneousbreathingduetosedationortochangethe methodofventilationduringtheprocedure.Nochangeinventilatorsettingswasnecessary inourpatients.NIVmayexposepatientstothelackofef cientairwayprotectionduring theprocedure,whichmustbecounterbalancedwiththeriskslinkedtoendotrachealintubationinthesepatients.Regionalanesthesiaisusedtoeliminatehazardsassociatedwith general anesthesia and to facilitate chest physiotherapy in patients with DMD [1]. Advantagesinavoidinggeneralanesthesiaincludemaintenanceoftheabilitytocoughand
DMD
7
11
DMD
6
DMD
Acidmaltasede ciency
5
10
DMD
4
DMD
DMD
3
DMD
DMD
2
8
DMD
1
9
Neuromusculardisease
DMD
NIV
Tonguehypertrophy Reducedmouthopening Reducedneckmobility
Tonguehypertrophy Reducedmouthopening Reducedneckmobility
Tonguehypertrophy Reducedmouthopening Neckimmobility
Neckimmobility
Reducedmouthopening Neckimmobility
None
Tonguehypertrophy Reducedmouthopening Neckimmobility
Neckimmobility
Neckimmobility
Neckimmobility
Tonguehypertrophy Reducedmouthopening Neckimmobility
Riskfactorsfordif cultintubation
IV
IV
IV
III
IV
II
IV
III
III
III
IV
Mallampatiscore
20
20
30
11
36
63
21
27
30
20
10
Hospitalstay(days)
None
(continued)
SeizurePneumonia
None
None
None
Earlydecannulation
None
None
None
None
None
Complication
Table 24.1 Comparisonofgroupsintermsofrespiratoryfailureseverity,riskfactorsfordif cultintubation,andcomplicationsoftracheotomy
24 Noninvasive Mechanical Ventilation as an Alternative to Endotracheal Intubation 163
LGMD2C
DMD
CMD1C(FKRPde cit)
DMD
LGMD2C
3
4
5
6
7
Reducedneckmobility
Tonguehypertrophy Reducedmouthopening Neckimmobility
Tonguehypertrophy Reducedmouthopening Neckimmobility
Tonguehypertrophy Dif cultiestoopenthemouth Neckimmobility
Tonguehypertrophy Kyphoscoliosiswithtrachealdeviation
Tonguehypertrophy Reducedmouthopening Neckimmobility
Kyphoscoliosiswithtrachealdeviation Reducedmouthopening Neckimmobility
Dif cultiesforintubation
Tonguehypertrophy Reducedmouthopening Neckimmobility
Reducedneckmobility
Riskfactorsfordif cultintubation
II
IV
25
15
35
21
IV
IV
15
11
41
Hospitalstay(days)
20
21
Hospitalstay(days)
III
IV
IV
Mallampatiscore
IV
II
Mallampatiscore
Pneumonia
Dif cultintubation
None
Dif cult intubationPneumonia
Pneumonia
Failedintubation
Failed intubationPneumonia
Complication
None
None
Complication
DurationofhospitalizationandnumberofpatientswithaMallampattiscoregreaterthan2weresimilarinbothgroups.TheincidenceofpneumoniawaslowerintheNIVcompared totheconventionalgroup.DMDDuchennemusculardystrophy,BMDBeckermusculardystrophy,LGMDlimbgirdlemusculardystrophy,CMDcongenitalmusculardystrophy, FKRPFukutin-relatedprotein
DMD
Neuromusculardisease
Conventional
2
DMD
13
DMD
BMD
12
1
Neuromusculardisease
NIV
Table 24.1 (continued)
164 D. Orlikowski et al.
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Fig.24.1 ChestX-ray: congenitalmuscular dystrophypresentingsevere kyphoscoliosisandtracheal deviation
to swallow as well as to breathe spontaneously, even in the event of decannulation in patients with low VC and low respiratory reserve. Patients with neuromuscular disease oftenpresentpiecemealdeglutitionandimpairmentofthebreathing swallowinginteraction[5].Swallowingdisordersandinabilitytocleartheairwaymaybeworsenedbythe useofsedativedrugs,anesthetics,andmusclerelaxants,increasingtheriskofaspiration pneumonia[1].Consideringthatintubationisoftendif cultandhazardousinpatientswith advancedneuromusculardisease,thisadditionalfactormayexplainthehighrateofaspirationpneumoniaobservedintheintubationgroup.Ontheotherhand,theNIVprocedure allowedpatientstoremainconscious,thereforepreservingvoluntarybreathing,swallowing,coughing,andsuctioningoforopharyngealsecretions,ifneeded,andreducingtherisk ofaspiration. Tracheotomyisasurgicalprocedurethatshouldbeperformedonlybyexperienced physicians. Recently introduced techniques include percutaneous tracheotomy; to be performed, these methods do not require in-depth knowledge of neck anatomy comparedtosurgicaltracheotomy.Thesetechniquesarenotrecommendedinpatientswith cervicaldeformityandthereforedonotseemsuitableforpatientswithneuromuscular diseases;furtherevaluationofthesetechniquesarenecessaryinthispopulation.Cannula malpositionhasbeenreportedinupto25%ofcases,andbleedingduetobloodvessel injurycanoccur. However,regardlessofcomplicationsduringorafteraprocedure,theposttracheotomy periodisdedicatedtotheeducationofpatientsandtheirfamilyregardingofthetracheostomytube,suctioningtechniques,andsoon.Dischargefromthehospitaldependsdirectly ontheacquisitionofthesetechniquesandontheorganizationofthepatient senvironment. Therefore,thelengthofhospitalstayisnotsolelyin uencedbythecomplicationsofthe procedures,whichmightaccountforthelackofdifference.
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24.2 Conclusion 24.2.1 Use of NIV may decrease complications during invasive procedures in neuromuscular disease NIVtracheotomywithlocalorlocoregionalanesthesiaisanacceptableoptionforpatients withneuromusculardiseasewhoareathighriskofcomplicationsfromendotrachealanesthesia.Thisnewprocedurecouldbefavoredoveraprocedureusingintubationandgeneral anesthesiainpatientswithadvancedneuromusculardiseases.
Key Recommendations
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Useoflocalorloco-regionalanesthesiashouldbepreferredincaseofinvasive procedureinneuromusculardiseaseinordertolimitthenumberofcomplications. UseofNIVshouldbeaddedtolocalorloco-regionalanesthesieorslight sedationincaseofrespiratoryinsuf ciencyandifpossibleintubationavoided. Thistechniquesrequirewellskilledcareteamwithhighknowledgeofneuromuscular disease.
References 1. LeCorreF,BenoitP(1998)Neuromusculardisorders.CurrOpinAnaesthesiol11(3):333 337 2. BirnkrantDJ,PanitchHB,BendittJO,BoitanoLJ,CarterER,CwikVAetal(2007)American CollegeofChestPhysiciansconsensusstatementontherespiratoryandrelatedmanagementof patients with Duchenne muscular dystrophy undergoing anesthesia or sedation. Chest 132(6):1977 1986 3. OrlikowskiD,PrigentH,Gonzales-BermejoJ,AubertP,LofasoF,RaphaelJCetal(2007) Noninvasive ventilation as an alternative to endotracheal intubation during tracheotomy in advancedneuromusculardisease.RespirCare52(12):1728 1733 4. Practiceguidelinesformanagementofthedif cultairway(2003)Anupdatedreportbythe AmericanSocietyofAnesthesiologistsTaskForceon Management of the Dif cult Airway. Anesthesiology98(5):1269 1277 5. TerziN,OrlikowskiD,AegerterP,LejailleM,RuquetM,ZalcmanGetal(2007)Breathing swallowinginteractioninneuromuscularpatients:aphysiologicalevaluation.AmJRespirCrit CareMed175(3):269 276
Noninvasive Mechanical Ventilation in Patients with Myasthenic Crisis
25
CristianeBrennerEilertTrevisan,SilviaReginaRiosVieira, andRenataPlestch
Myastheniagravisisanautoimmuneneuromusculartransmissiondisordercharacterized bymuscleweakness.Thisserious,buttreatable,diseaseisthemostfrequentprimaryneuromusculardisorder. Inthisclinicalentity,theimmunesystemproducesantibodiesthatattackthereceptors inthemuscleendplatesoftheneuromuscularjunction,andtheacetylcholinereceptorsthat receivethenervesignalaredamaged(Fig.25.1).Itisunknownwhattriggerstheimmune reactionoftheorganismagainstitsownacetylcholinereceptors,butgeneticpredisposition playsanessentialroleinit. Myastheniagravishasanestimatedprevalenceof0.5 12.5/100,000,anincidenceof 0.4/100,000amongthegeneralpopulation,andamale-to-femaleratioof2:3. Thediagnosisofmyastheniagraviscanoftenbecon rmedusingcurrentlyavailable methods,suchasteststodetectanti-AChR(acetylcholinereceptor)antibodiesand electromyography. The most common symptoms are eyelid ptosis, ocular muscle weakness that causes diplopia,andexcessivefatigueofcertainmusclesafterexercise.In40%oftheindividuals withmyastheniagravis,theocularmusclesarethe rsttobeaffected,andwithtime,85% ofthepatientshavethissymptom.Dif cultiesinspeakingandswallowingandweakness ofupperandlowerextremitiesarealsocommon. About 17 20% of the patients with myasthenia gravis will eventually have a myastheniccrisis(MC),de nedasasuddenworseningofrespirationinwhichmuscleweaknessissoseverethatitmakesbreathingimpossibleorimpairstheadequatefunctioningof airways.Thereasonsforrespiratoryfailurearedysfunctionofupperairways,weaknessof inspiratoryandexpiratorymuscles,andassociatedcomplications. C.B.E.Trevisan() Physiotherapistandassociatedprofessor,PhysiotherapyDepartament,UniversityHospital, UniversidadeLuteranadoBrasil(ULBRA),Canoas,RioGrandedoSul,Brazil e-mail:
[email protected] S.R.R.Vieira Associatedprofessor,InternalMedicineDepartment,FacultyofMedicine,UFRGSandCritical CareDivision,HospitaldeClínicasdePortoAlegre,RioGrandedoSul,Brazil R.Plestch Physiotherapist-Hospital sPhysiotherapyteam,MãedeDeusHospital,PortoAlegre,RioGrande doSul,Brazil A.M.Esquinas(ed.),NoninvasiveMechanicalVentilation, DOI:10.1007/978-3-642-11365-9_25,©Springer-VerlagBerlinHeidelberg2010
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Fig. 25.1 [1]
Respiratoryfailurehasseveralconsequences,asdescribedinTable25.1.Oneofthem isthereductioninthecapacitytoexpandthethoraciccavityandoflungin ation. Whenrespiratorymuscleweaknessismildormoderate,hyperventilation,normalblood pH,lowerthannormalPco2,andnormalorreducedPao2areusual ndings.However,in moreadvancedstagesofthedisease,hypercapniamaydevelopbecauseofhypoventilation secondarytorespiratorymusclefatigue,whichmakesitdif culttomovetheribcageand decreasesnormallungcompliance. Asaresultofrespiratoryfailure,manypatientsmayrequiretheuseofventilatorysupport. Beforemechanicalventilationwasavailable,70%ofpatientsinMCdiedofrespiratory failure.Asintensivecareunitsimproved,thisratedecreasedto30%inthe1950sandto Table 25.1 Consequencesofrespiratoryfailureonlungmechanics Reducedcapacitytoexpandribcage Decreasedlunginflation Decreasedlungcompliance Increasedworkofbreathing Alteredventilationtoperfusionratio Diffuselungmicroatelectasis
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15%inthe1960s.Theadventofmechanicalventilationinassociationwiththegeneralized useofimmunotherapyhassubstantiallychangedtheprognosisofpatientswithanMC, whichisre ectedinamortalityratethatisnow4 8%. Becauseofpossiblecomplicationsofmechanicalventilation,suchaspneumonia,as wellasothersystemiccomplications,noninvasivemechanicalventilationhasbeenusedas analternativetopreventreintubationandavoidtherisksassociatedwithintubation. Seneviratneetal.[2]conductedastudywithpatientsinMCwhoadaptedwelltononinvasiveventilatorysupportbecausetheyremainedcapableofinitiatingbreaths.However,those patientsbecameincapableofachievingasatisfactory owvolume,whichincreasedtherisk ofmicroatelectasisandcollapseofupperairwaysanddidnotensureef cientgasexchange. Inthiscontext,noninvasiveventilatorysupportisthe rstchoiceforpatientsinMC becausethemajorconcernistoavoidtrachealintubationanditscomplications. The decision to use noninvasive mechanical ventilation depends on several factors. AccordingtoAgarwaletal.[3],theuseofnoninvasivemechanicalventilationdependson theseverityofacuterespiratoryfailure,thepresenceofbulbarinvolvement,andtheassociationwithotheref cacioustreatments.Severeanomaliesingasexchangeandseverebulbar involvementthatcompromisesthemanagementofairwaysareabsolutecontraindications. PatientstreatedwithnoninvasivemechanicalventilationduringMCshouldbeunder carefulcardiacmonitoringbecausetheymayhavecardiacarrhythmias. Duringtheuseofnoninvasivemechanicalventilation,clinicalevaluationandarterial gasmeasurementsshouldbemadeinthe rst6 8htoevaluatetheef cacyofthemethod andthepossibleneedtouseconventionalmechanicalventilation. Two studies were optimistic about results despite the different intubation rates in patients who received noninvasive mechanical ventilation. According to Wu et al. [4], 57.1%ofthepatientsdidnotrequireintubation,andRabinsteinetal.[5]founda70%rate of success. However, their studies did not nd any improvement in hyperventilation of patientswithelevatedPaco2 and dyspnea.Thiscon rms that patients withhypercapnia haveamoreseveredegreeofneuromuscularrespiratoryfailurethatcannotbetreatedonly withpositivepressureandrequirestheuseofcontrolledvolumeventilation. Inpatientswhorequireinvasivemechanicalventilation,trachealextubationfailureis associatedwithhighhospitalmorbidity,longerdurationofventilatorysupport,andhigh incidenceofventilation-associatedpneumonia(VAP).Therefore,studieshaveinvestigated predictorsofsuccessofnoninvasiveventilationwhenusedasaweaningstrategy.Adequate maximalexpiratorypressure(PEmax)andstrengthtocougharesigni cantlycorrelated withtrachealextubationsuccess.Otherpredictorsofnoninvasiveventilationsuccessare young age, low disease score, and good neurological score. Wu et al. [4] reported that patientswithalowAPACHEIIscoreandalesserdegreeofmetaboliccompensationfor respiratoryacidosisbene tthemostfromnoninvasivemechanicalventilation.
25.1 Conclusion TheuseofnoninvasivemechanicalventilationinpatientswithMCmaypreventintubation, helpweaningfrominvasivemechanicalventilation,andavoidtrachealextubationfailure.
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References 1. HamptonT(2007)Trialsassessmyastheniagravistherapies.JAMA298:29 30 2. Seneviratne J, Mandrekar J, Wijdicks EF, Rabinstein AA (2008) Noninvasive ventilation inmyastheniccrisis.ArchNeurol65(1):54 58 3. WuJY,KuoPHetal(2009)Theroleofnon-invasiveventilationandfactorspredictingextubationoutcomeinmyastheniccrisis.NeurocritCare10:35 42 4. AgarwalR,ReddyC,GuptaD(2006)Noninvasiveventilationinacuteneuromuscularrespiratoryfailureduetomyastheniccrisis:casereportandreviewofliterature.EmergMedJ23(1):e6 5. RabinsteinA,WijdicksEF(2002)BiPAPinacuterespiratoryfailureduetomyastheniccrisis maypreventintubation.Neurology59(10):1647 1649
Predictors of Survival in COPD Patients with Chronic Hypercapnic Respiratory Failure Receiving Noninvasive Home Ventilation
26
StephanBudweiser,RudolfA.Jörres,andMichaelPfeifer
26.1 Introduction Amongthesevererespiratorydisordersthatleadtochronichypercapnicrespiratoryfailure (CHRF), chronic obstructive pulmonary disease (COPD) is of major importance. EpidemiologicalsurveyshavedemonstratedthatCOPDisoneoftheleadingindications forlong-termnoninvasiveventilation(NIV).Nonetheless,theavailabledataarestillnot fullyconclusivewithregardtothelong-termbene tsofNIVinsevereCOPD.Themajorityofrandomizedcontrolledtrialshaveyieldedmoreorlessdisappointingresults,while some of the more recent, although predominantly observational, clinical investigations providedevidenceforpositiveeffectsonhealth-relatedqualityoflife(HRQL),thefrequencyofhospitaladmissions,orlong-termsurvival. Someofthesediscrepanciescanbetracedtomethodologicalfactors,especiallydifferencesintheeffectivenessofventilation,includinginadequateventilatorsettingsorinsufcient adherence to NIV therapy in the randomized trials. This is supported by the observationthat,inmostinstances,highinspiratorypressurelevelswereassociatedwith highNIVsuccessrates.Ofsimilarrelevanceappeartobetheselectioncriteriaforchoosing patientsfortheinitiationofNIV,particularlywhenthelong-termcourseofthediseaseand survivalaretakenasanoutcomemeasure.Owingtothepathophysiologicalmechanisms involved in the development of chronic ventilatory failure, persistently elevated arterial carbon dioxide tension (Paco2) is currently considered the major objective measure to
S.Budweiser() CenterforPneumology,DonaustaufHospital,Ludwigstraße68,93093Donaustauf, Germany e-mail:
[email protected] R.A.Jörres InstituteandOutpatientClinicforOccupational,SocialandEnvironmentalMedicine, Ludwig-Maximilians-University,Munich,Germany M.Pfeifer DepartmentofInternalMedicineII,UniversityofRegensburg, Regensburg,Germany A.M.Esquinas(ed.),NoninvasiveMechanicalVentilation, DOI:10.1007/978-3-642-11365-9_26,©Springer-VerlagBerlinHeidelberg2010
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decideontheinitiationofNIV.However,theassociationbetweenchronicpersistenthypercapnia and long-term outcome in COPD is far from uncontroversial. Moreover, when adopting the modern perspective of COPD as a multicomponent, systemic disease, it appearsadequatenottorelyonasinglemeasurebuttotakeapaneloffactorsknownto affectseverityandcourseofthediseaseasabasisfortherapeuticdecisionsorascandidate measuresformonitoringpurposes.
26.2 Predictors of Long-Term Survival in Patients with COPD and CHRF Basedonthescienti cbackgroundoutlined,weperformedanumberofstudiestoevaluate predictorsoflong-termsurvivalinlargepopulationsofpatientswithsevereCOPDreceivinglong-termNIVduetoCHRF.Inoneofthesestudies,whichcoveredanobservation periodofupto10years[1],awholesetofmeasures,includinganthropometricdata,nutritional status in terms of body mass index (BMI), spirometric, body plethysmographic, laboratory,andbloodgasdata,wereconsidered.Inviewofthefactthattheprognostic valueofthePaco2isnotclear,wealsoanalyzedthepotentialroleofbaseexcess(BE)(i.e., thedeviationofnormalbufferbase)asanobviousmarkeroflong-termmetabolicresponses tochronichypercapniathatisnotaspronetoapotentialbiasfromshort-termchangesin ventilatorypatternasPaco2. Whenanalyzedseparatelyinunivariateanalyses,quiteanumberofdimensionsofthe disease,includingage,BMI,hemoglobinconcentration,forcedexpiratoryvolumein1s (FEV1), speci c airway resistance, lung hyperin ation in terms of the ratio of residual volumetototallungcapacity(RV/TLC),pH,andBE(butnotPaco2),weresigni cantly associatedwithlong-termsurvival.Itisnoteworthy,however,thatsubsequentmultivariate analysesrevealedthatamongthesemeasuresonlyBMI,RV/TLC,andBEwerestatistically independentpredictors.
26.3 Implications for the Assessment and Monitoring of Patients with COPD and CHRF Despitethelimitationsposedbytheretrospectivedesign,thestudy[1]suggestedsome potentialconsequencesforclinicalpractice.First,itsupportedtheviewthattheprognosis ofpatientswithsevereCOPDandCHRFisre ectedinabroadpanelofanthropometric, physiological,andfunctionalmeasures.Althoughthispanelbecamesmallerinthemultivariate analysis, at least three different predictors remained. Thus, the establishment of individualriskpro lesinsuchpatientsislikelytobeimprovedbyacomprehensiveassessment.Accordingtothesedata,asaminimumthismightincludebloodgasvalues(inparticularBE),lungfunction(preferablybodyplethysmography),andnutritionaldata.The basicnutritionalstatusissimpletoassessbyBMI,buttherearestudiesindicatingthatfatfreemassindex(FFMI)mightbeevenbetterforthispurpose(Table26.1).
26
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Table 26.1 Proposed measures for the multidimensional assessment of patients with chronic obstructivepulmonarydisease(COPD)andchronichypercapnicrespiratoryfailurebasedontheir prognosticvalue Candidatemeasuresforlong-termassessmentandprognosis Nutritionalstatus(bodymassindex,BMI;fat-freemassindex,FFMI)asintegrativemeasure offunctionalandmetabolicreserves Chronicarterialhypoxemia(Pao2)asmarkerofgasexchangeef ciencyandorganstress Baseexcess(BE)asmarkerofthelong-termmetabolicresponsetochronichypercapnia Lungfunction(hyperin ationasratioofresidualvolumetototallungcapacity,RV/TLC; forcedexpiratoryvolumeinonesecond,FEV1)asmeasureoforgan-speci cfunctional reserves Six-minutewalkingdistance(6-MWD)asintegrativemeasureoffunctionalreserves I n ammatory(C-reactiveprotein,CRP)orcardiac(brainnatriureticpeptide,BNP)as systemicmarkersfromperipheralblood Anemiaasre ectedinlowhemoglobinandhematocritlevels M odi edMedicalResearchCouncil(MMRC)DyspneaScaleasintegrativemeasureof thesubjectivestatus M outhocclusionpressureat100msrelativetomaximalinspiratorypressure(P0.1/PImax) asameasureoftheload-to-capacityratioregardingrespiratorymuscles Cardiovascular,metabolic,andmentalcomorbiditiesasimportantconfounders
Inlinewiththeliterature,thedataalsoindicatedthatthepresenceofanemiaintermsof low hematocrit or hemoglobin levels should be considered for long-term survival in patientswithCOPDandCHRF.ThiswasalsofoundintheBODEcohort,whichpredominantlycomprisedpatientswithless-severedisease[2].Moreover,the6-minwalkingdistance (6-MWD) and the Modi ed Medical Research Council (MMRC) Dyspnea Scale areknownasvaluabletoolstoimprovetheindividualpictureoffunctionalcapacity (Table26.1).Thesedata were not included in the study [1] but at least for 6-MWD an independentpredictivevalueforlong-termsurvivalhasbeendemonstrated.Italsoappears reasonabletotakeintoaccountindicesthatmorecloselyre ectthepathophysiologyof CHRF.Forexample,mouthocclusionpressure100msafterstartofinspirationrelativeto maximalinspiratorypressure(P0.1/PImax)isknownasanoninvasiveestimateoftheloadto-capacityratioofrespiratorymuscles.Indeed,thisratiowasidenti edasafurtherindependentpredictoroflong-termprognosisinpatientswithNIVandCHRF[3]. Therefore,anadequateassessmentofadvancedstagesofthediseaseshouldprobably movebeyondexistingscoringsystemsandcovervariousdimensionsofthedisease, includingcomorbiditiesorsystemicmarkers,suchasC-reactiveprotein(CRP),brain natriureticpeptide(BNP),orhypoxemia,asmajorpredictorsinsevererespiratorydiseases (Table 26.1). Future studies should address the appropriate de nition and validation of suchcomprehensive,multidimensionalscoresaswellasthequestionofareasonablebalancebetweeninformationcontentandaffordability. Second,itwasreassuringthatthechangesofBMI,RV/TLC,orBEobserved6months after initiation of NIV were also linked to survival, at least in patients who showed an elevatedriskfordeathaccordingtotheirbaselinevalues[1].Besidesindicatingthatthe measureswerestatisticallyconsistent,thisobservationalsosuggeststhattheymightbe usefulinlong-termmonitoring,irrespectiveofthefactthatinthestudytheeffectofNIV
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wasinextricablymingledwiththatoftheoveralloptimizationofmedicaltreatment.Asan interestingaspect,thedataespeciallycon rmedthatpatientsshowingweightlosswithin 6 monthsexperienced an increased risk for death. These patients might be primary candidatesfornutritionalsupport. AnumberofstudieshaveprovidedevidencethatNIVcouldhaveadditionalpositive effectsthroughmodi cationofknownriskfactors.Therearebothshort-termrandomized and long-term observational physiological investigations that found a reduction in lung hyperin ation after initiation of NIV, presumably due to a change in breathing pattern. Moreover,thebene cialeffectofNIVonhypercapnia,providedthateffectiveventilation isguaranteed,isanestablishedfact.Furthermore,thereareobservationaldataindicatinga weightgaininpatientswithCOPDandcachexiaafterinitiationofNIV. Takentogether,theobservationsfromthisstudy,whichcomprisedbothbaselinedata andthelongitudinalmodi cationofriskfactors,wereinsupportofthehypothesisthaton averageNIViscapableofimprovingthelong-termprognosisinpatientswithCOPDand CHRF.Atleastformally,however,thishypothesisstillhastobeveri edbyrandomized controlledtrialsinappropriatepopulations.GreatcarehastobetakenthatthesepopulationsmatchthoseactuallytreatedinclinicalpracticewithNIV,soitmightturnouttobe extremelydif culttocircumventmajorethicalproblems.
26.4 Impact of the Decision to Initiate NIV in Severe COPD Third,inadditiontotheimplicationsregardingassessmentandmonitoring,theremight alsobeimplicationsfortherapeuticdecisionsthatareworthconsidering,particularlythe initiationofNIV.Accordingtointernationalguidelines,theindicationforlong-termNIV insevereCOPDismainlybasedonsymptomsofCHRFandthelevelofchronichypercapnia.AcriticalPaco2limitof55mmHg(7.3kPa)ormorehasbeenspeci edtojustifyNIV insevereCOPD[4].Ithastobestated,however,thatthecriteriaofchronichypercapnia havenotbeenvalidatedinlargeprospectivetrials,anditiscommonknowledgethatPaco2 often exhibits large intraindividual and intraday variability, depending on the patient s conditionandventilatorystate.Comparedtothis,thelong-termmetaboliccompensation ofhypercapniaandrespiratoryacidosisasre ectedinBEisaslowprocess.Accordingly, BEseemstobeafairlystablemeasureofCHRFanddiseaseseverity,asindicatedbythe nding that BE but not Paco2 had relevant and independent prognostic information on long-termsurvival(Fig.26.1).However,toestablishtheprognosticuseofthisspeci c measureinclinicalroutine,furtherstudiesonBEincomparisontodaytimeandnocturnal Paco2undervariousconditionsseemtobedesirable. Accordingtotheconsensusstatement[4],NIVisalsorecommendedwhenPaco2ranges below55(50 54)mmHgbuttwoormorehospitalizationsduetorecurrentepisodesof hypercapnicrespiratoryfailureoccurredwithin12months.Asknown,patientswhosurviveacutehypercapnicrespiratoryfailureandsubsequentlyrequireNIVhaveahighrisk forreadmission,furtherlife-threateningevents,ordeath.Althoughstudiedprimarilywith regardtotheirlong-termprognosticvalue[1],themarkersidenti edcouldalsobehelpful inestimatingtheriskforrespiratorydecompensationorinstabilityduringoraftersevere
26
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175
Probability of survival (%)
100 80 BE < 9 mmol/I paCO2 < 56 mmHg
60 40
paCO2 ≥ 56 mmHg BE ≥ 9 mmol/I
20 0 0
24
48 72 Time (months)
96
120
Fig. 26.1 Prognosticvalueofbaseexcess(BE)versusthatofcarbondioxidetension(Paco2).The gureillustratesthesuperiorityofBE(HR0.399;95%CI0.230 0.658;p=0.0004)overPaco2 (hazards ratio 0.787; 95% con dence interval 0.467 1.317; p = 0.359) in predicting long-term survivalfrombaselinemeanvaluesinpatientswithseverechronicobstructivepulmonarydisease (COPD),chronichypercapnicrespiratoryfailure,andnoninvasiveventilation(Datafrom[1]but plottedinadifferentway)
exacerbationsofCOPD.Someofthesemeasurescouldbeimplementedinthedecisionfor NIVevenundertheseconditions.Thisviewissupportedbyanobservationalstudythat showedthatpatientspresentingwithawholesetofriskfactorsinthisconditionbene ted mostfromNIV.Suchanapproachisnotunusualsinceconsiderationofapanelofinformationondiseaseseverityiseverydaypracticeintherapeuticdecisions,beyondtheformal evidenceprovidedbyclinicaltrials.Thisindividualapproachis,forexample,already customaryindecisionsonlungvolumereductionsurgeryorlungtransplantation. Irrespectiveoftheclinicalusefulnessoflong-termNIV,thequestionarisesregarding which mechanisms could underlie its lifesaving role, in particular if the bene t is only partiallyre ectedinPaco2levels.Sophisticatedphysiologicalandclinicalstudieshave demonstratedthatNIVinducesacomplexinterplayamongunloadingofrespiratorymuscles,restorationofchemosensitivity,andimprovementofalveolarventilation.Thebene cial effects are re ected in changes in breathing pattern, including an increase of tidal volumeandadecreaseofrespiratoryfrequency[5].Mostimportant,theyarenotlimited totheperiodofapplicationofNIVbutaremaintainedduringsubsequentperiodsofspontaneousbreathing.IfNIVpreservesorevenimprovesfunctionalreservesviathesemechanisms,itisreasonabletoexpectapositiveimpact,especiallyinconditionsrequiring augmentedventilation,andtoassumelowervulnerabilityinepisodesofacutedeteriorationorduringexacerbations.Thisviewissupportedbyclinicalstudiesthatdemonstrated lowerratesofhospitalizationduetoexacerbationsofCOPDaftertheinitiationoflongtermNIV.Despitetheadditionalexpensesfortheventilator,thisreductionwasassociated withloweroverallhealthcarecosts.
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Table 26.2 Possibleindicationsforlong-termnoninvasiveventilationinpatientswithseverechronic obstructivepulmonarydisease(COPD)(Modi edfrom[5]) Indicationsfornoninvasiveventilation S ymptomaticchronichypercapnia(afteroptimizationofstandardtherapy,includingoxygen) andcarbondioxidetensionlevels(Paco2)of55mmHgormore Recurrentacutehypercapnicrespiratorydecompensations(³2within12months)requiring ventilatorysupportifPaco2rangesbetween50and54mmHg High-riskpro leforlong-termmortalitybasedonestablishedprognosticfactors Stateafterprolongedinvasivemechanicalventilationoradif cultweaningprocedure
AsimilarargumentprobablyappliestopatientswithsevereCOPDwhoundergoadif cultweaningprocedureoranepisodeofprolongedinvasivemechanicalventilation.Basedon thehighriskforrespiratorydecompensationandreintubationafterinvasivemechanicalventilation,NIVhasbecomeanimportantinstrumentinthemanagementofrespiratoryfailure duringweaningintheintensivecareunitsetting.However,thevalueofNIVasalong-term treatmentafterweaninghasnotbeendemonstratedatahighlevelofevidence.Retrospectively collecteddataindicatedasurvivalbene tinpatientswhoweredischargedwithNIVaftera prolongedperiodofweaningcomparedtopatientswhodidnotreceiveNIVformaintenance athome.Inanalogytotheargumentsgiven,patientspresentingwithspeci criskpro lesare likelytobene tmostfromthistreatment.Ofcourse,theapplicationofNIVunderthisconditiondoesnotabolishtheneedforacarefulreevaluationaftersometimetoassesswhether NIVbecamedispensableowingtosuf cientrestorationofphysiologicalstrength.According totheseconsiderations,possibleindicationsforNIVaresummarizedin(Table26.2)
Key Recommendations
› › › ›
›
PatientswithsevereCOPDandCHRFshowanumberofindependentrisk factorsformortalityandthusneedamultidimensionalassessmentandlong-term monitoringoftheirclinicalstate. BEisameasureofthelong-termmetabolicresponsetochronichypercapniaand ispromisingasaneasilyaccessible,integrativemarkerofCHRF. Nutritionalstatus,lunghyperin ation,andBEhavebeenidenti edasstatistically independentpredictorsoflong-termsurvival.Othermarkersbearfurther, althoughrelated,information. ThedecisiononinitiationofNIVshouldprobablynotrelysolelyonsymptomsand persistentlyelevatedPaco2levels.Itshouldbebasedonanintegratedanalysisofa wholespectrumofriskfactorsthatarerelevantforlong-termsurvival.Thisapproach willnaturallytakeintoaccountthewell-knownheterogeneityofthedisease. OwingtothephysiologicaleffectsofNIV,patientswithCOPDandrecurrent hypercapnicrespiratorydecompensationandpatientsexperiencingprolonged mechanicalventilationordif cultweaningcouldbesuitablecandidatesfor successfullong-termNIV.
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References 1. Budweiser S, Jorres RA, Riedl T et al (2007) Predictors of survival in COPD patients with chronic hypercapnic respiratory failure receiving noninvasive home ventilation. Chest 131: 1650 1658 2. CoteC,ZilberbergMD,ModySH,DordellyLJ,CelliB(2007)HaemoglobinlevelanditsclinicalimpactinacohortofpatientswithCOPD.EurRespirJ29:923 929 3. BudweiserS,JorresRA,CrieeCPetal(2007)Prognosticvalueofmouthocclusionpressurein patientswithchronicventilatoryfailure.RespirMed101:2343 2351 4. Clinicalindicationsfornoninvasivepositivepressureventilationinchronicrespiratoryfailure duetorestrictivelungdisease,COPD,andnocturnalhypoventilation aconsensusconference report.(1999)Chest116:521 534 5. BudweiserS,JorresRA,PfeiferM(2008)Noninvasivehomeventilationforchronicobstructivepulmonarydisease:indications,utilityandoutcome.CurrOpinPulmMed14:128 134
Withdrawal of Noninvasive Mechanical Ventilation in COPD Patients with Hypercapnic Respiratory Failure
27
JacoboSellares,MiquelFerrer,andAntoniTorres
27.1 Introduction Recentinvestigationsinnoninvasivemechanicalventilation(NIMV)havefacilitatedthe increasinguseofthistypeofventilationworldwide.IndicationsofNIMVarebetterestablished,andthebene tofitsusehasbeendemonstratedinseveralstudies,especiallyin acutehypercapnicrespiratoryfailure(AHRF).However,someaspectsoftheuseofNIMV stillremainunclearandareundercontroversy.Thisisthecaseforwhichmethodisthebest towithdrawNIMV.Thepaucityofinformationinde ningastrategytowithdrawNIMV contrastswithalltheinformationandstudiesrelatedtoweaningfrominvasivemechanical ventilation(IMV).ThereisamarkedvariabilityinthemethodsusedtowithdrawNIMV inthenumerousstudiesofNIMVpublished,whichre ectstheabsenceofaprospectively validatedprotocol.Inthischapter,wereviewthecurrentrecommendationstowithdraw NIMV,andwesuggestnovelpotentialstrategies.Weespeciallyfocusonthewithdrawal ofNIMVinAHRFasthisindicationisthebestestablishedinNIMV,althoughsomepoints ofourreviewmayalsobeextrapolatedtootherindicationsofNIMV.
J.Sellares(),M.Ferrer,andA.Torres UnitatdeCuresIntensivesiIntermèdiesRespiratòries,ServeidePneumologia, InstitutClínicdelTòrax,HospitalClinic,Institutd InvestigacionsBiomèdiques AugustPiiSunyer(IDIBAPS),UniversitatdeBarcelona,Villarroel170, 08036Barcelona,Spainand CentrodeInvestigaciónBiomedicaEnRed-EnfermedadesRespiratorias (CibeRes,CB06/06/0028),Sabadell,Barcelona,Spain e-mail:
[email protected]
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27.2 Use of NIMV in Acute Hypercapnic Respiratory Failure Different studies have established the use of NIMV in patients who develop AHRF. Although chronic obstructive pulmonary disease (COPD) is the most frequent cause of AHRF,NIMVcouldalsobeusefulinothertypesofchronicrespiratorydisorders,suchas thosecausedbyobesityandchestwalldeformities.Whenapatientwitharespiratorydisorderisassessedintheacutesetting,NIMVisinitiatedwhenthereisaworseningofthe respiratorystatus,themeasurementsofarterialbloodgastensionsshowrespiratoryacidosis,andnocriteriaforintubationorexclusionarepresent[1]. OncetheNIMVisstarted,carefulmonitoringofthepatientsisnecessarytoensurean optimalprognosisforthepatient.MonitoringofpatientsonNIMVshouldincludeclinical assessment combined with pulse oximetry and arterial blood gas. Clinical features that shouldberoutinelyassessedduringNIMVareasfollows: 1. Chestwallmovement 2. Coordinationofrespiratoryeffortwiththeventilator 3. Accessorymusclerecruitment 4. Heartrate 5. Respiratoryrate 6. Patientcomfort 7. Mentalstate ContinuouscontrolofoxygensaturationincombinationwithperiodicanalysisofpH,Paco2, andPao2arenecessarytoassessthecorrectapplicationofNIMV.Theclinicalandphysiologic analysiswillbeusefultoassesstheadaptationoftheNIMVtothepatientandtodetectearly failureofNIMV.Differentfactorshavebeendescribed[1]toestablishthefailureofNIMV: 1. Deteriorationinpatient scondition 2. Failuretoimproveordeteriorationinarterialbloodgastensions 3. Developmentofnewsymptomsorcomplicationssuchaspneumothorax,sputumretention,nasalbridgeerosion 4. Intoleranceorfailureofcoordinationwiththeventilator 5. Failuretoalleviatesymptoms 6. Deterioratingconsciousnesslevel 7. Patientandcaregiverwishtowithdrawtreatment DifferentoptionscouldbeconsideredtooptimizetheNIMV,whichincludebetterconditioningoftheinterfacesandventilationsettings.Oncethepatientisclinicallystable,the recommendationisthatNIMVshouldbeprolongedforatleast24h[1],withsmallperiods offtheventilatorformedicationasnebulizersandformeals.IfpatientswithNIMVclinicallyimprovedandnosignsoffailuredevelop,physiciansdecidetowithdrawtheNIMV after24h.However,althoughtothispointtheclinicalapplicationofNIMVisrelativelywell described,noclearvalidatedprotocolsarede nedregardingthediscontinuationofNIMV.
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27.3 Rationale for Designing a Protocol to Withdraw NIMV AlthoughnumerousprotocolsareestablishedforweaningfromIMV,theabsenceofprospectivestudiescomparingdifferentprotocolstowithdrawNIMVisastonishing.InweaningfromIMV,weaningprotocolsarewellde nedandhavedemonstratedanimprovement insurvivalofmechanicallyventilatedpatients[2].InanalogytoweaningfromIMV,we havetodifferentiatetwostagesinthewithdrawalofNIV:Ina rststage,wedeterminethe readiness to withdraw NIMV, and in a second stage, we use a method to discontinue NIMV.
27.3.1 Determining the Readiness to Withdraw NIMV in Hypercapnic Respiratory Failure DuringweaningfromIMV,thereadinesstoweanapatientisdecidedbyassessingdifferent clinical and respiratory functional parameters [2]. Similarly, during IMV, we could decidetheinitialwithdrawalofNIMVusingtheclinicalandfunctionalvariablesavailable inthecaresetting.However,de nedparameterstowithdrawNIMVarevariableinthe differentstudiespublished.Inadditiontoresolutionoftheacuterespiratoryepisodethat wasthecauseforinitiatingNIMV,differentfunctionalparametershavebeensuggestedto decideonthediscontinuationofventilatorysupport[1](Fig.27.1):
Resolution of the acute respiratory episode Readiness to withdrawNIMV
Potential methodsto withdrawNIMV
+ Clinical signs: •respiratoryrateof<24breaths/min •heartrate<110beats/min. •compensatedpH>7.35(H+<45nmol/l) •SpO2>90%onFiO2<4l/min
•DirectdiscontinuationofNIMV •DirectdiscontinuationofNIMV+nocturnalsupport •Gradualdiscontinuation: -ProgressivereductionoftimeapplyingNIMV -Progressive reduction of pressure support
Fig. 27.1 Methodstowithdrawnoninvasivemechanicalventilation(NIMV)inhypercapnicrespiratoryfailure
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1. Respiratoryratebelow24breaths/min 2. Heartratelessthan110beats/min 3. CompensatedarterialpHabove7.35(H+<45nmol/l) 4. Spo2above90%onFio2lessthan4l/min
27.3.2 Methods to Withdraw NIMV in Hypercapnic Respiratory Failure ThecurrentrecommendationforNIMVwithdrawalistograduallyreducetheperiodsof ventilatorysupportwhenpatientstabilityisachieved.However,nostudieshavevalidated thisoption,thespeci cpointsoftheseprotocolsdifferbetweencenters,andnocomparisonswithotherapproacheshavebeenundertaken.Fromourpointofview,threedifferent approachesarepossibleasmethodstowithdrawNIMV: 1. DirectdiscontinuationofNIMV:TheNIMVisstoppedwhenpatientsful llthecriteria for withdrawal. Oxygen is supplied as necessary. Afterward, the patient is clinically assessed during the next hours in spontaneous breathing. Periodic arterial blood gas analysesareperformed.IfthepatientisclinicallystableandarterialpHisover7.35and Paco2isstablewithrespecttothepreviousdetermination,NIMVisnotrestarted.No studiesareavailablethatassessedthisstrategy. 2. Direct discontinuation of NIMV with nocturnal support: NIMV is withdrawn in the samewayasoption1,butnocturnalNIMViskeptforafewdays.Therationalefor usingnocturnalNIMVisthat,inpatientswithchronicrespiratorydisorders,especially COPD,typicallythereisthedevelopmentofperiodsoftransienthypoxemiaassociated withepisodesofhypoventilation,whicharemorefrequentduringrapid-eye-movement (REM)sleepstages.Theseepisodescouldhaveclinicalimplicationsinpatientswho arerecoveringfromanepisodeofhypercapnicrespiratoryfailure.Theapplicationof nocturnalNIMVforafewdayscouldavoidtheseepisodesofhypoventilation,which couldbedeleteriousfortheventilatedpatient.Nostudiesareavailablethatassessed thisstrategy. 3. GradualdiscontinuationofNIMV:Inthiscase,wecouldfollowtwostrategies: (a) Progressive reduction of time applying NIMV: The period of the duration of NIMVisgraduallyreduceduntilthepatientcanbreathespontaneously.Damas etal.[3]reportedtheirexperienceusingthismethodofgradualwithdrawal fromNIMVinpatientswithacuteexacerbationofchronicrespiratoryfailure.In theirprotocol,theyprogressivelyreducedNIMVperiodsover3days,maintaining continuous NIMV during the night. While the patients were not receiving NIMV,supplementaryoxygenwasdelivered.Fromthe65patientswhoachieved clinicalstabilitytobeginthewithdrawalofNIMV,nopatientshadtobereconnected to NIMV or required invasive ventilations during the hospital stay. The mainlimitationofthisstudyisthatitwasmerelydescriptiveandonlyrepresents thepersonalexperienceofasinglecenter.However,therearenootherreported studies that have focused on comparing this strategy with other methods to withdrawNIMV.
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(b) Progressivereductionofinspiratoryandexpiratorypressuresupport:Similartothe useofpressuresupportasaweaningmethodinIMV,someauthorssuggestedthe progressivedecreaseofinspiratorypositiveairwaypressure(IPAP)andexpiratory positive airway pressure (EPAP), assessing the patient s capability for sustaining ventilationineachstepofcorrespondingpressure.Althoughthisapproachisinteresting,nostudiesareavailablethatusedthisparticularmodeofwithdrawingNIMV. ThesedifferentstrategiesshowdifferentviewsforapproachingNIMVwithdrawal.The rst strategy has the bene t of expending less time in the process of withdrawal, but patientsmayhaveanincreasedriskofanewepisodeofhypercapnicrespiratoryfailure, especiallyduringthenight.ThelaststrategypotentiallycouldbethesafestwaytowithdrawNIMV,butitcouldrepresentanunnecessaryprolongationofNIMVandanincreased riskoflateraleffects(nasalulcers,intoleranceofNIMV,etc.).Infact,Damasetal.reported intheirstudyalongerdurationofNIMVcomparedtootherstudies[3].Futurestudies mustclarifywhichisthebestmethodtowithdrawNIMVthatdoesnotrepresentincreased morbidityforthepatientandhasaminimumdurationofNIMVandhospitalstay.
27.4 Long-Term Dependency on NIMV AlthoughNIMVcouldusuallybediscontinued,somepatientsareconsideredfordomiciliaryNIMVafteranepisodeofhypercapnicrespiratoryfailure.Cuvelieretal.[4]de ned this situation as long-term dependency (LTD)-NIMV, requiring the presence of all the criteriafromTable27.1.Moreover,physiciansmustconsiderlong-termNIMVinthefollowingclinicalsituations[1]: 1. AHRFsecondaryto
(a) Spinalcordlesion (b) Neuromusculardiseases (c) Chestwalldeformity(e.g.,scoliosis,thoracoplasty) (d) Morbidobesity
2. COPDwith (a) Recurrentepisodesofhypercapnicrespiratoryfailure(>3episodes)requiringtreatmentwithNIMV (b) Intoleranceofsupplementaryoxygen(becauseofCO2retention)withsymptomatic sleepdisturbance Table 27.1 Criteriaforlong-termdependency(LTD)onnoninvasiveventilation(allrequired) 1. Stableresolutionofthetriggeringfactor 2. Inability to stop NIMV for at least 8 consecutive days (after two attempts) because of worseningclinicalstatus,ariseinPaco2withrespiratoryacidosis(pH 7.35)orrecurrent hypercapnicrespiratoryfailurewithoutanyidenti ablecause 3. DischargehomewithdomiciliaryNIMV
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However,LTD-NIMVismorecommoninpulmonaryrestrictivedisordersthaninCOPD. TheincidenceofLTD-NIVMisestimatedat31%inpatientsnoninvasivelyventilateddue toAHRF[4].InanItaliansurveyof26respiratoryintensivecareunits[5],LTD-NIMV wasevidentin22%ofthepopulationofnoninvasivelyventilatedpatients.Inhypercapnic respiratoryfailure,LTD-NIMVwasindependentlyassociatedwithadecreaseofbaseline pH6monthspriortotheindicationofNIMV(oddsratio1.32,con denceinterval[CI] 1.27 1.54)andwithanoninfectiouscauseofAHRF(oddsratio5.1,CI1.8 14.0).The de nitionandstandardizationofprospectivelyvalidatedprotocolsofwithdrawalofNIMV arenecessaryalsoforearlyidenti cationofthosepatientswithLTD-NIVM.
Key Recommendations
› › › › ›
Nostandardizedprospectivelyvalidatedprotocolsarede nedforwithdrawing NIMVinAHRF. Clinicalsignsandgasexchangevaluesmustbemonitoredduringtheapplication ofventilationtodecidethemomentforwithdrawingNIMV. DifferentstrategiesarepossibleasmethodsofwithdrawingNIMV:direct discontinuation,partialventilationduringthenight,orgradualdiscontinuationof NIMV. Futurestudiesmustde newhichmethodtodiscontinueNIMVisoptimalin reducinglengthofstayandavoidingcomplications. The identi cation of LTD-NIVM patients during the process of withdrawal of NIMViscrucialforearlydetectionofthepatientswhomustcontinuewithhome noninvasiveventilation.
References 1. British Thoracic Society Standards of Care Committee (2002) Non-invasive ventilation in acuterespiratoryfailure.Thorax57:192 211 2. BolesJM,BionJ,ConnorsAetal(2007)Weaningfrommechanicalventilation.EurRespirJ 29(5):1033 1056 3. DamasC,AndradeC,AraujoJP,AlmeidaJ,BettencourtP(2008)Weaningfromnon-invasive positivepressureventilation:experiencewithprogressiveperiodsofwithdraw.RevPort Pneumol14(1):49 53 4. CuvelierA,ViacrozeC,BenichouJetal(2005)Dependencyonmaskventilationafteracute respiratoryfailureintheintermediatecareunit.EurRespirJ26:289 297 5. ConfalonieriM,GoriniM,AmbrosinoN,MollicaC,CorradoA,Scienti cGrouponRespiratory Intensive Care of the Italian Association of Hospital Pneumonologists (2001) Respiratory intensive care units in Italy: a national census and prospective cohort study. Thorax 56:373 378
Noninvasive Ventilation in Patients with Acute Exacerbations of Asthma
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SeanP.Keenan
28.1 Introduction Asthma remains a common respiratory disorder, and despite advances in its outpatient management,patientscontinuetopresenttotheemergencyroomdepartmentasaresultof anacuteexacerbation.Whilethevastmajorityofcasesaremanagedwithinhaledbronchodilatorsandsystemicsteroids,somepatientspresentwithsevererespiratorydistressand require ventilatory support. Traditionally, the only option beyond medical therapy has been endotracheal intubation and conventional mechanical ventilation. However, care becomesmorecomplicatedafterintubatingapatientwithsevereasthmaduetothepotentialforseveredynamichyperin ationandcardiovascularcollapse.Whileitisnotthepurpose of this chapter to discuss the approach to invasive mechanical ventilation of the asthmaticpatient,itissuf cienttosaythatgreatcareandattentionarerequiredbythose skilledintheseareas,andeventhisdoesnotprecludesigni cantmorbidity.Theuseof noninvasive ventilation (NIV) for patients with severe acute exacerbations of chronic obstructive pulmonary disease (COPD) associated with respiratory failure has become increasinglyrecognizedas rst-linetherapyafterusualmedicaltherapyandoxygen[1,2]. TheevidencesupportingtheuseofNIVinacuteexacerbationsofasthmaismorelimited. Theobjectiveofthischapteristoprovideareviewofthecurrentliteratureandsummary recommendationsfortheuseofNIVinthissetting.
S.P.Keenan DivisionofCriticalCare,DepartmentofMedicine,UniversityofBritishColumbian ProgramMedicalDirectorforCriticalCareMedicine,FraserHealthAuthority, BritishColumbia,Canadaand RoyalColumbianHospital,SherbrookeBuilding-Of ceM-02(MainFloor) 260SherbrookeStreet,NewWestminster,BritishColumbia, V3L3M2,Canada e-mail:
[email protected]
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Before reviewing the literature on the use of NIV in acute exacerbations of asthma presentingtotheemergencyroom,itisimportanttorecognizethatasthmaticexacerbationsrepresentacontinuumofdiseaseseverity.Attheextremeistheentityreferredtoas near-fatalasthmaorstatusasthmaticus.Thesepatientspresentwithseveredyspneaand signs of dynamic hyperin ation with tachycardia, pulsus paradoxus, marked accessory muscleuse,andatitsmostsevere,signsofhypercarbia,includingalteredlevelofconsciousness.Patientswithrefractoryhypoxemia,persistentorworseninghypercarbia,signs ofexhaustion,worseningmentalstatus,orhemodynamicinstabilityrequireurgentendotrachealintubationandshouldnotbeconsideredascandidatesforNIV.Studiesontheuse ofNIVinthesettingofacuteasthmavaryintheseverityofpatientsenrolled,andthiswill behighlightedastheliteratureisreviewed.Selectedcaseserieswillbediscussed rstfollowedbyrandomizedcontrolledtrials(RCTs).
28.2 Case Series The rststudyspeci callyreportingontheuseofNIVinpatientswithacuteasthmatic exacerbationswaspublishedin1996byMeduriandcolleagues[3].Theyretrospectively reviewed all patients admitted to their intensive care unit (ICU) with severe asthmaovera3-yearperiod(1992 1995).Ofthe26patientspresentingwithsevere asthma, 4 were intubated (2 respiratory arrest, 1 exhaustion, 1 hypotension), 7 respondedwelltomedicaltherapyalone,and17underwentatrialofNIV.Thepatients receivingNIVwereseverelyill,withameanpHof7.25±0.7andPaco2of65±11 mmHg and respiratory rate of 29 breaths/min. Of the 17 patients, 2 (12%) required intubationandconventionalmechanicalventilation;therestdemonstratedanimprovementinrespiratoryrateandbloodgasesinthe rstcoupleofhoursandcontinuedto improveover24h. Fiveyearslater,Fernandezandcoworkerspublishedasimilarstudyoftheirexperience overa7-yearperiod(1992 1998)[4].Duringthatperiod,58patientspresentedwithsevere asthmawithmarkedrespiratoryacidosis,similartothoseseeninthestudyofMeduriand associates.Theauthorsde nedcriteriapriortoreviewingthedataforpatientstheyfelt werecandidatesforNIV:inclusioncriteriaincludedatleasttwoof(1)severedyspneaat rest,(2)respiratoryrateabove30breaths/min,(3)Pao2below60mmHgwhilebreathing roomairorlessthan80mmHgwithadditionaloxygen,(4)Paco2of50mmHgormore, (5)pH7.30orless,and(6)activecontractionofaccessorymusclesorparadoxicalmovement of abdominal muscles. Patients were excluded if there was a need for immediate intubationforrespiratoryorcardiaccompromise.Ofthe58patients,11requiredimmediateendotrachealintubationforrespiratoryarrest,and14respondedwelltomedicaltherapy alone.Ofthe33patientswhometcriteriaforNIV,11wereintubatedwithoutatrialofNIV, and22receivedNIVastheirinitialventilatorysupport.Ofthe22patientsreceivingNIV, 3(14%)wereintubated.Overthe7-yearperiod,therewasanincreaseduseofNIVandless useofinvasiveventilation,suggestingbothanincreasedfamiliaritywithNIVandcon denceinitseffectiveness.Whiletherewassigni cantvariabilityinthenumberofpatients
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seenyeartoyearandoverallnumbersweresmall,thestudysuggestedtheNIVwasable todecreasethenumberofpatientsreceivinginvasiveventilation.
28.2.1 The Randomized Controlled Trials The rstRCTwasreportedin2001byHolleyandcolleagues,whorandomizedpatients presentingwithacuteexacerbationsofasthmatotheiremergencyroomtoeithernasalNIV andstandardtherapyorstandardtherapyalone[5].Theyhadestimatedasamplesizeof 336patientspergrouptohavesuf cientpowertodetecta5%reductioninratesofendotracheal intubation. Unfortunately, they were only able to enroll 35 patients due to an increasingbiastouseNIVforthesepatientsoutsidethestudy.Theyalsohadnotrealized thenumberofrepeatadmissionsbythesamepatients.Asaresultofthismajorselection bias,thevalidityofthestudyresultsissigni cantlycompromised.Theyfoundnosigni cantdifferencebetweenthetwogroupsinanyoutcomemeasures.FromTable28.1,itis clearthattheirpatientswerenotasseverelyillasthosepresentinginthetwocaseseries, althoughtheyclearlyweresick,withapHtowardtheacidoticrangeandahighrespiratory rate.Thisisalsosuggestedbytheneedforintubationin3of35patients(1intheNIVarm and2inthecontrol). ThesecondRCTwaspublishedbySorokskyandcolleaguesin2003andwasuniquein itsdesign[6].Theseauthorsrandomized30patientstoeithernasalNIVor sham NIV. The latter included a subtherapeutic pressure of 1 cmH2O, holes cut in the tubing, and encouragementofmouthbreathing.Itispossiblethattheshamcontrolpatientshadincreased
Table 28.1 Summaryofstudiesonuseofnoninvasiveventilation(NIV)inasthma Study Study Numberof pHofNIV Paco2 Respiratory design patients ofNIV rate
Intubation rate
Case series
26(17NIV)
7.26±0.05
65±11
29±5
2/17(12%)
Fernandez Case series etal.[4]
58(22NIV)
7.28±0.008
63±24
32±6
3/22(14%)
Meduri etal.[3]
Holley etal.[5]
RCT
35(19NIV)
7.35±0.04
40±11
28±5
1/19(5%)
Soroksky etal.[6]
RCT
30(15NIV)
7.41±0.04
33.6±3
34.8±1.8
0/15(0%)
Soma etal.[7]
RCT (three arms)
40(26NIV)
na
na
20±6
0/26(0%)
36.5±11.1
49.8±14.6 1/20(5%) (trans cutaneous)
20children na RCT (crossover) RCTrandomizedcontrolledtrial,nanotavailable Thill etal.[8]
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workofbreathingrelatedtotheshamNIV.Regardless,theauthorsreportedamorerapid reduction in FEV1 (forced expiratory volume in 1 s) and in need for hospital admission (3/17 in NIV group vs. 10/16 in control group). From Table 28.1, it is clear that these patientshadmilderexacerbationsofasthmaasmanydidnotrequirehospitalization,and nonerequiredintubation.TheirbaselinepHwasnormal,andtheywerehypocarbic,unlike thepatientsinthecaseseriesstudies,whopresentedwithacuterespiratoryacidosis. ThemostrecentRCTbySomaandassociatesdifferedinafewwaysfromtheearlier studies[7].Theauthorsrandomizedpatientstothreearms:14toaninspiratorypositive airwaypressure(IPAP)of8cmH2Oandexpiratorypositiveairwaypressure(EPAP)of 6cmH2O,12toIPAPof6cmH2OandEPAPof4cmH2O,and14tooxygentherapy alone.Allreceivedotherstandardtherapy,includingoxygen.Theauthorsreportedamore rapidreductioninbreathlessness,usingtheBorgscale,inbothNIVarmsandamorerapid improvementinFEV1inthehigherpressureNIVarmcomparedtocontrols.Thisstudy usedverylowlevelsofpressuresupportventilation(2cmH2O)andwasalmostmoreofa studyofcontinuouspositiveairwaypressure(CPAP)alone.Thepatientsstudiedhadvery mildasthmawithrespiratoryratesofabout20breaths/minonpresentation,andnopatients requiredintubation. The nalstudythatshouldbementionedwasconductedinchildrenwithlowerairway obstruction;thestudyusedarandomizedcrossoverdesign[8].Childrenreceivedboth2h ofnasalorfull-facemaskNIVand2hofconventionaltherapyappliedinarandomorder andwereassessedattheendofeach2-hperiod.Theyfoundsigni cantlylesswheezing, dyspnea,andaccessorymuscleuseattheendofa2-htrialofNIVcomparedtocontrol.
28.3 Summary Fromthisreviewoftheliterature,the rstconclusiontobedrawnisthatwedonothave adequatedatatomakestrongrecommendations.Todate,twosmallcaseseriesandfour smallRCTshavebeenpublished.InformationfromtheRCTssuggeststhatNIVisassociatedwithareductioninbreathlessnessandamorerapidimprovementinlungfunction(see Table28.2)inmild-to-moderateexacerbationsofasthma.Todate,wehaveonlycaseseries datasuggestingthatNIVmaybeofbene tinpatientswithsevereexacerbations.Suggesting that a large, multicenter trial in acute exacerbations of asthma should be conducted to provide a de nitive answer generally follows when confronted with such a gap in the Table 28.2 Summaryofrandomizedcontrolledtrial(RCT)results Somaetal. Study Halleyetal.[5] Sorosky [7] etal.[6] Breathlessness FEV1/PEFR Hospitalization FEV1forcedexpiratoryvolumein1s;PEFRpeakexpiratory owrate
Thilletal.[8]
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e vidence.However,suchastudywillbechallengingforanumberofreasons.First,severe exacerbationsofasthmaoccurwithlessfrequencythesedaysduetoimprovingoutpatient management. Second, those patients who do present with such an exacerbation tend to account for a large number of repeat admissions and can only be enrolled once. Third, thereisapotentialbiastouseNIVbasedoncurrentliterature,successinotherpatient groupssuchasthosewhohaveCOPDandcardiogenicpulmonaryedema,andanecdotal experience. Finally, to recruit a larger number of patients there will be temptations to includethosewhopresentinlargernumberswithmild-to-moderateexacerbations,which willmakeithardertodetectdifferencesinintubationratesasthesemilderpresentations rarelyrequireintubation. Intheinterim,itmaybemoreusefultoaskthequestion:WhynotuseNIVinacute exacerbations of asthma? To date, we have good evidence of effectiveness in patients withacuteexacerbationsofCOPD,whoarephysiologicallyrelated.Wehaveevidenceto suggest that it helps reduce breathlessness and improves lung function more rapidly. However,webelievethatwaitingtoolongtointubatehypoxemicpatientsreceivingatrial ofNIVcanleadtoharm.Thebalanceofevidencefromtheliteratureandtheexperience ofexpertswouldsuggestthatitisreasonabletoofferatrialofNIVtopatientswithacute exacerbationsofasthma,butthatthesepatientsareamongthosewhoneedtobeextremely closelymonitoredinanICUsettingtoensurerapidrecognitionofdeteriorationandintubationifnecessary.
Key Recommendations
› › ›
ThereislittlepublishedevidencesupportingtheuseofNIVinpatientswith acuteexacerbationsofasthma. NIVdoesappeartoreducebreathlessnessandimprovelungfunctionmore rapidlyinpatientswithmild-to-moderateexacerbationsofasthma. UseofNIVinsevereexacerbationsrequiresintensivemonitoringandpersonnel availableforimmediateintubationifdeteriorationoccurs.
References 1. KeenanSP,SinuffT,CookDJ,HillN(2003)Whichpatientwithacuteexacerbationofchronic obstructivepulmonarydiseasebene tfromnoninvasivepositive-pressureventilation?Asystematicreviewoftheliterature.AnnInternMed138:861 870 2. Nava S, Hill N (2009) Non-invasive ventilation in acute respiratory failure. Lancet 374:250 259 3. MeduriGU,CookTR,TurnerRE,CohenM,LeeperKV(1996)Noninvasivepositivepressure ventilationinstatusasthmaticus.Chest110:767 774 4. FernandezMM,VillagraA,BlanchL,FernandezR(2001)Non-invasivemechanicalventilationinstatusasthmaticus.IntensiveCareMed27:486 492
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5. HolleyMT,MorrisseyTK,SeabergDC,AfessaB,Wears RL(2001)Ethicaldilemmas ina randomized trial of asthma treatment: can Bayesian statistical analysis explain the results? AcadEmergMed8:1128 1135 6. SoroskyA,StavD,ShpirerI(2003)Apilotprospective,randomized,placebo-controlledtrial ofbilevelpositiveairwaypressureinacuteasthmaticattack.Chest123:1018 1025 7. SomaT,HinoM,KidaK,KudohS(2008)Aprospectiveandrandomizedstudyforimprovement of acute asthma by non-invasive positive pressure ventilation (NPPV). Intern Med 47:493 501 8. ThillPJ,McGuireJK,BadenHP,GreenTP,ChecchiaPA(2004)Noninvasivepositive-pressure ventilationinchildrenwithlowerairwayobstruction.PediatrCritCareMed5:337 342
Noninvasive Positive Pressure Ventilation During Acute Asthmatic Attack
29
ArieSoroksky,IsaacShpirer,andYuvalLeonov
29.1 Introduction Asthmaischaracterizedbyreversibleairwayobstructioncausedbyatriadofbronchial smoothmusclecontraction,airwayin ammation,andincreasedsecretions. In most patients, control of disease activity is easily achieved. However, in a small minority,asthmamaybefatal.Inbetweenthetwoextremes,somepatientswithsevere asthmaticattacksrefractorytostandardtreatmentaresteroiddependentandtypicallyhave frequentadmissionstoemergencyroomdepartmentsandconsequentlyareasubstantial burdenonhealthcaresystems.Afewofthesepatientshaveahistoryofsevereasthmatic attacksthatnecessitatedmechanicalventilation. Theseandotherfactorsareknownpredictorsofrecurrentsevereattacks.Thesemandateextracautionbythephysician,withneedforclosermonitoring,intensivecareunit (ICU)admission,andasalastresortinvasivemechanicalventilation. Invasivemechanicalventilationofasthmaticpatients,inadditiontotheusualcomplications of mechanical ventilation, is associated with other risks. These patients are often dif culttoventilate,havelowcompliancewithhighinspiratorypressures,andhavefrequentpatient ventilatorasynchrony. Asaresult,mechanicalventilationoftheasthmaticpatientisachallengetotheintensivistandoftennecessitatespermissivehypercapnea,deepsedation,andattimesneuromuscularblockade. Inspitetheseprotectiveapproaches,mechanicallyventilatedasthmaticpatientsareat higherriskforbarotraumawithresultantpneumothoraxandprolongedICUstay.
A.Soroksky(),I.Shpirer,andY.Leonov GeneralIntensiveCareUnit, AssafHaRofeMedicalCenter, Zeri n70300,Israel e-mail:
[email protected],
[email protected]
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Invasivemechanicalventilationisthereforeameasureoflastresort.Nevertheless,it shouldbeappliedpromptlywhenneeded.Hence,patientsrefractorytostandardtreatment whoareatriskforrespiratoryfailureshouldbeidenti edsoonerratherthanlater.These patientshavethepotentialtobene tfromearlyrespiratorysupportintheformofnoninvasivepositivepressureventilation(NPPV). NPPVhasgainedwideacceptanceandisnowusedmorefrequently.Ithasbeenshown tobebene cialforavarietyofclinicalconditions.Prospective,randomized,controlled trialshavedemonstratedtheef cacyofNPPVinacuteexacerbationofchronicobstructive pulmonarydisease(COPD),acutecardiogenicpulmonaryedema,hypoxemicrespiratory failure,immunocompromisedpatients,andasanadjuncttoweaninginpostoperative patientsandinpatientswithCOPD. However, reports of NPPV in asthmatic patients are scarce, and its use in asthmatic attacksisthereforestillcontroversial.
29.2 Evidence for Use of NPPV in Asthmatic Attacks Evidence for application of NPPV in asthma has been sparse. Only a few reports have appearedoverthelastdecade.Otherreportsdatingbacktothe1980sand1990saremore scarceandarecaseseries. Table 29.1 summarizes recent reports of noninvasive ventilation in asthmatic attack. Thesearemostlywithsmallnumberofpatientsandwithproblematicmethodology.[1 4]. Mostexacerbationsofasthmaareeasilycontrolled,andonlyaminorityarerefractory to standard treatment, with even fewer patients deteriorating to the point of respiratory failurewithneedformechanicalventilation.Thiscouldexplainthepaucityofreportsand thesmallnumberofpatientsinthesetrials. Nevertheless,thereportsthatdoexistclearlyindicatethatselectedpatientswithsevere asthmaticattackscanbene tfromacarefullyandcloselymonitoredtrialofNPPV. ThekeytosuccessfulNPPVapplicationischoosingtherightpatient.Patientswitheasilycontrolleddiseaseprobablydonotneedanyrespiratorysupport.Attheotherextreme are patients with severe status asthmaticus with pending respiratory failure and on the vergeofendotrachealintubation.AtrialofNPPVinthesepatientsmightdelayinevitable endotrachealintubationandsubjectthemtounnecessaryrisks.Therefore,thesepatients shouldbeconsideredforendotrachealintubationsoonerratherthanlater. Inbetweenthesetwogroupsarepatientswithsevereasthmaticattackwho,ifnottreated aggressively,mayprogresstorespiratoryfailure.Thesearethepatientswhocouldbene t fromacloselymonitoredtrialofNPPV. Table29.2summarizesthecontraindicationstoNPPVandthesubgroupofpatientsat riskofrespiratoryfailurewhocouldbene tfromanNPPVtrial.Theseareusuallythe patientswhobyde nitionareconsideredtohaveasevereasthmaattack. ContraindicationsforNPPVinrespiratoryfailurearesubjectfordebate.Overthelast decade,NPPVhasgainedwideacceptanceforvariousindications.Withtheincreaseduse of NPPV, we gained new knowledge and experience. We therefore believe that under
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Noninvasive Positive Pressure Ventilation During Acute Asthmatic Attack
Table 29.1 RecentreportsofNPPVinasthmaticpatients Typeof No.of Studydesign study patients
193
Modeof ventilatory support/ durationof application
Outcome
Meduri etal.[1]
Prospective observational
17
Reportof 17episodes ofstatus asthmaticus treatedwith NPPVover 3years
CPAPmask withpressure supportusing commercial ventilator for16h
NPPV improvedgas exchangein status asthmaticus
Fernández etal.[2]
Retrospective observational
33
Retrospective comparison of22patients treatedwith NPPVvs. 11patients treatedwith invasive mechanical ventilation
CPAPwith orwithout pressure supportusing commercial ventilators for12h
Improvedgas exchangein bothgroups, withthe possibilityof preventionof endotracheal intubationin NPPVgroup
Soroksky etal.[3]
Prospective, randomized, sham controlled
30
Fifteenpatients onBiPAP comparedto shamBiPAP withstandard treatment
BiPAP circuitfor 3h
Improved FEV1and decreased hospitalizationratein NPPVgroup
Improved BiPAP Prospective FEV1with circuitfor comparisonof 1h low-and increasing high-pressure pressure groupsto support standard medicalgroup BiPAPbilevelpositiveairwaypressure,CPAPcontinuouspositiveairwaypressure,FEV1forced expiratoryvolumein1s,NPPVnoninvasivepositivepressureventilation Soma etal.[4]
Prospective randomized trial
44
appropriate conditions and with experienced respiratory teams, NPPV use can now be extendedtonewdiseasessuchasasthmaandbeusedinconditionsthatpreviouslywere consideredcontraindications. Signi canthypoxiaorhypercapnea,whilepreviouslyconsideredacontraindicationfor NPPV,isnownolongerconsideredbyusasanabsolutecontraindication.Itisourimpressionthat,withexperiencedpersonnelandintheappropriateenvironment(e.g.,admission toanICU),thesepatientscansafelybetreatedwithacloselymonitoredNPPVtrial. Patientswithunstablehemodynamicswhocannotbestabilizedwithvasopressorsor patients with worsening hemodynamic instability necessitating increasingly higher
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Table 29.2 Indicationsandcontraindicationsfornoninvasivepositivepressureventilation(NPPV)trial ContraindicationsforNPPVtrial Patientsatriskforrespiratoryfailurewho couldbene tfromNPPVtrial Absolutecontraindications Needforimmediateendotrachealintubation Decreasedlevelofconsciousness E xcessrespiratorysecretionsandriskof aspiration Pastfacialsurgeryprecludingmaskfitting Relativecontraindications: Hemodynamicinstability S everehypoxiaand/orhypercapnea (PaO2/FiO2ratioof<200,PaCO2>60) Poorpatientcooperation Severeagitation Lackoftrainedorexperiencedstaff
Diagnosticcriteriaforsevereasthma(atleast oneofthefollowingcriteria): Useofaccessorymuscles Paradoxicalpulseabove25mmHg Heartrateabove110beats/min Respiratoryrateabove25 30breaths/min Limitedabilitytospeak PEForFEV1lessthan50%ofpredicted Arterialoxygensaturationlessthan91 92% Riskfactorsforsevereasthmaexacerbation Recenthospitalization P riorICUadmissionwithmechanical ventilation Pooradherencetotherapy Highallergenexposure
FEV1 forcedexpiratoryvolumein1s, ICU intensivecareunit
vasopressordosesshouldprobablybeintubated.However,unstablepatientswhocanbe rapidly stabilized with uids and low doses of a vasopressor could probably bene t fromanNPPVtrialaswell. Agitationandpoorcooperationcanbecontrolledwithlowdosesofbenzodiazepines and,aspublishedrecently,withdexmedetomidine.Thesemeasuresmayrelieveagitation andpromotepatientcooperation,thuspreventingendotrachealintubation.However,sound clinicaljudgmentshouldbeapplied,andthesemeasuresshouldbepursuedonlytoacertainlimit.Endotrachealintubationshouldnotbedelayedmorethannecessary. Theyieldofroutinechestradiographyisquestionable;however,insevereasthmatic attacksadditionalpathologiesshouldbeconsidered,includinglungin ltrates,pneumothorax,orlungcollapse.Therefore,insevereandrefractoryasthmaticattacks,chestradiographyshouldprobablybeobtained.
29.3 Pathophysiology and Mechanism of Action ThemechanismbywhichNPPVimprovestheforcedexpiratoryvolumein1s(FEV1)and clinicaloutcomeinacuteasthmaisnotexactlyunderstood.Acombinationoffactorscould explainatleastsomeofthebene t.Asearlyas1939,BarachandSwenson[5]showedthat gasunderpositivepressure(continuouspositiveairwaypressure[CPAP]of7)candilate small-to-moderatesizebronchi.Similar ndingswerelaterreproducedbyshowingthat CPAPapplicationresultedinbronchodilationanddecreasedairwayresistance.Furthermore,
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aerosolizedbronchodilatorsdeliveredthroughabilevelpositiveairwaypressure(BiPAP) circuitresultedinimprovedFEV1andPEFR,suggestingthatperhapspositiveairwaypressurecoulddispersethebronchodilatorstomoreperipheralairways.These ndingsstrongly suggestthatNPPVapplicationmayresultinbronchialdilationbymechanicaleffect. Promotingbronchialdilationdecreasesairwayresistance,expandsatelectaticregions, andfacilitatesclearanceofsecretions. FEV1andpeakexpiratory owrateareusedasmeasuresofair owobstruction.These measurescanascertainseverityofdiseaseandquantifytheresponsetotreatment.Ithas beenshownthatprogressivereductioninFEV1isassociatedwithaproportionalincrease intheworkofbreathing. Concomitantly,expiratoryair owlimitationincreasesandresultsinadynamicincrease in end-expiratory lung volume. This phenomenon is called dynamic hyperinflation. Increasingobstructionandtachypnearesultinarelativelyshortexpiratorytime.Asaresult, therespiratorysystemdoesnotreachstaticequilibriumvolumeattheendofexpiration. Thisresultsinpositiveend-expiratorypressure(PEEP),termedintrinsicorauto-PEEP. Theresultantdynamichyperin ationinterfereswithinspiratorymusclefunctionand reduces the mechanical ef ciency of the muscles, which further contributes to muscle fatigue.Thisresultsinincreasedphysiologicdeadspaceandeventuallyventilatoryfailure. Asairwayobstructionworsensandtheworkofbreathingincreases,CO2productionisin excess of what can be eliminated by the decreased alveolar ventilation. This has been showntooccurwithaconcomitantreductionofFEV1tolessthan25%ofpredicted.
29.4 Setting Up Ventilatory Support and Patient–Ventilator Interaction NoninvasiveventilatorysupportmaybeappliedbydedicatedCPAPorBiPAPcircuitsor bycommerciallyavailableventilators. WedonotrecommendtheuseofCPAPaloneinasthmaasthismodeisineffectexternalPEEPthatisusedmainlyforimprovingoxygenation.Inaddition,CPAPhasnopressure support and therefore does not possess the added bene t of increased ventilation. Adding pressure support to CPAP increases tidal volume and helps to unload fatigued respiratorymuscles.Therefore,werecommendtheuseofcommerciallyavailableBiPAP circuitsorcommerciallyavailableventilatorswithpressuresupport. WhenusingBiPAP,werecommendstartingwithmild-to-moderatesupport;thiswill enhancepatientcomfortandcooperation.Whensettinguptheexpiratorypositiveairway pressure(EPAP)value,weaimatcounterbalancingauto-PEEP.PreviousreportshaveindicatedthatmostobstructedpatientshaveintrinsicPEEP,whichresultsinincreasedworkof breathing.WeusuallystartwithanEPAPof3cmH2Oandincreasegraduallyto5cm.This isconsideredtobeamild-to-moderateexternallyappliedPEEP.Wedonotapplymore than5cmH2Ounlessthereisgoodclinicalevidenceofahigherauto-PEEP.Settingupthe inspiratorypositiveairwaypressure(IPAP)isbasedonarbitraryvalues;weoftenstartwith 7cmH2Oandtitrateittorespiratoryrateandpatientcomfort.WeincreaseIPAPgradually to15cmH2Oorlessuntiltherespiratoryrateislessthan25 30breaths/min.Thisapproach
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wasusedbyourgroupinapilotstudyofNPPVinsevereasthmaticattack[3].Wefound ittobesafeandcomfortableinmostpatients.Furthermore,onceNPPVwasapplied,we observedthatinmostpatientstachypneadecreasedandanxietyresolved(datanotreported). WepresumethistobeduetomusclefatiguethatwasalleviatedwithNPPVapplication. Weusenasalorfacialmasks.Duetothetight t,facialmasksaremoreeffective;however,nasalmasksarepreferredbysomepatientsasthisallowsthemtospeakandtoclear secretions.
29.5 Cycling in Commercial Ventilators SettingupacommercialventilatorisbasedonthesameprincipleasaBiPAPcircuitbut withsomedifferences.WhenwesetupPEEP,weusethesameconsiderationaswithEPAP onaBiPAPcircuit.However,theequivalenttoIPAP(e.g.,pressuresupport)isdifferent andmoreadvancedonthecommercialventilator. Mostmoderncommerciallyavailableventilatorscandeliverpressuresupportbreaths withtwotypesofcyclingorexpiratorytriggers(e.g.,timecyclingor owcycling).By settingupappropriateexpiratorycriteria,weenhancepatientcomfortandsynchronywith theventilator.Theusualcriterionusedinmostpressuresupportventilatorsisadecreasein inspiratory owfromapeaktoathresholdvalue(usually25%ofpeak ow).Previous reportshaveindicatedthatbyincreasingthe owthresholdfromtheusual25%ofpeak owto50%orevento70%shortensinspiratorytime. AcommonproblemwithanyNPPVisleaksfromthemaskthatmayimpairtheexpiratory triggeror owcyclingwheninspiratorypressuresupportventilationisused.Inthepresence ofairleaks,modernventilatorsdonotdecreaseinspiratory owduetoleakcompensation.As thereisnodecreasein ow,theventilatorwillnotcycletoexpiration.Thisleadstoprolonged inspiratory time and patient ventilator asynchrony. An alternative to ow cycling is time cycling.Limitinginspiratorytimeindependentofairleaksallowsashorterinspiratorytime. Weusuallysettheinspiratorytimeto1 1.3s.However,thisshouldbeadjustedonanindividualbasis,andattimesshorterinspiratorytimesareneededinseverelyobstructedpatients. Modernventilatorsallowadjustable owcycling,which,inthecaseofleaks,canalso betimelimited.Thisisprobablytheidealwayforanexpiratorytriggerinnoninvasive ventilation. Therefore,inthepresenceofairleakswepreferanadjustable ow-cycledexpiratory triggerthatcanbelimitedbytime.Thisprovidesbetterpatient ventilatorinteractionthan asimple ow-ortime-cycledexpiratorytrigger.
29.6 Possible Risks and Side Effects of NPPV in Asthma Pneumothorax has been reported previously when NPPV was applied in acute asthma. However,acuteasthmainitselfcarriesanincreasedriskforpneumothorax.Therefore,these reportsaresporadicanddonotnecessarilyindicateanincreasedriskwiththeuseofNPPV.
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With the use of NPPV, there is always a risk of delay in endotracheal intubation. Therefore, NPPV should be applied in an ICU environment, preferably by experienced personnel.PatientswhoareonthevergeofendotrachealintubationorwithpendingrespiratoryfailureshouldprobablybeintubatedwithoutNPPVtrial. Finally,inadvertentapplicationofextrinsicPEEPthatishigherthanauto-PEEPcould contributefurthertodynamichyperin ation.Inaddition,acombinationofrelativehypovolemia and auto-PEEP decreases venous return and subjects the patient to the risk of hemodynamiccompromise.
29.7 Conclusion TheadvantageofNPPVissupportedbyevidencethatNPPVmayhaveadirectbronchodilatingeffect,offsetintrinsicPEEP,recruitcollapsedalveoli,improveventilation perfusionmismatch,andreducetheworkofbreathing.NPPVshouldprobablybeapplied inselectpatientswhohaveorareatriskforsevereasthmaattack. No doubt, a multicenter and perhaps an international effort has to be conducted to answersomeofthesequestionsbeforewecanconclusivelyrecommendtheroutineuseof NPPVinasthma.
References 1. MeduriGU,CookTR,TurnerRE,CohenM,LeeperKV(1996)Noninvasivepositivepressure ventilationinstatusasthmaticus.Chest110(3):767 774 2. FernándezMM,VillagráA,BlanchL,FernándezR(2001)Non-invasivemechanicalventilationinstatusasthmaticus.IntensiveCareMed27(3):486 492 3. SorokskyA,StavD,ShpirerI(2003)Apilotprospective,randomized,placebo-controlledtrial ofbilevelpositiveairwaypressureinacuteasthmaticattack.Chest123(4):1018 1025 4. SomaT,HinoM,KidaK,KudohS(2008)Aprospectiveandrandomizedstudyforimprovement of acute asthma by non-invasive positive pressure ventilation (NPPV). Intern Med 47:493 501 5. BarachAL,SwensonP(1939)Effectofgasesunderpositivepressureonlumensofsmalland mediumsizedbronchi.ArchInternMed63:946 948
Noninvasive Positive Pressure Ventilation for Long-Term Ventilatory Management
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AkikoTokiandMikioSumida
30.1 Introduction Inthischapter,wediscussnoninvasivepositivepressureventilation(NPPV)forpatientswith respiratoryparalysisduetohigh-levelspinalcordinjuries(SCIs).Especiallyintheacute phase,84%ofthosewithSCIswithalevelofC1 C4andFrankelgradeA,B,Csuffered from respiratory complications such as pneumonia, ventilator failure, and atelectasis [1]. Anotherstudy[2]reportedthatthe1-yearsurvivalrateofventilator-dependentpersonswith SCIswas25.4%.However,amongthosewhosurvivedthe rstyear,cumulativesurvival overthenext14yearswas61.4%.Werecommendthemthistechnology,whichdoesnot havecomplicationsandmaintainstheirlong-termqualityoflife.
30.2 Patients Who Need This Technology and Equipment Patientswithhigh-levelSCIscannotventilateeffectivelybecausetheirrespiratorymuscles,whichincludethediaphragmandtheintercostalmuscles,areparalyzedduetoSCIs. Hypoventilationinducesnotonlyrespiratoryinsuf ciencybutalsoatelectasisandpneumonia.Iftheydidnothaverespiratorydiseasesbeforeonset,thistechnologyplaysabig partintheirhealthylife.
A.Toki()andM.Sumida DepartmentofRehabilitationMedicine,KansaiRosaiHospital, AmagasakiCity,Japan e-mail:
[email protected]
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DysphagiaandlackofcooperationarethemaincontraindicationsforNPPVforthese patients[3].Itwasreportedthatage,tracheostomyandmechanicalventilation,andspinal surgeryviaananteriorcervicalapproacharethreesigni cantpredictorsofriskfordysphagia[4].InNPPV,wecannotpreventaspiration,andwecannotsuctionsputumviaa tracheostomytube. The cooperation and comprehension of the patients are important for safe NPPV. In tracheostomy positive pressure ventilation (TPPV), patients are ventilated passively; in NPPV,theyhavetomasterhowtoinhaleairfromtheventilator.Theyalsohavetomaster howtocougheffectivelybythismethod.
30.3 Purpose of This Technology NPPVtechnologyconveysthesepatientsmorebene tsthanTPPV. First,NPPVcanprovideef cientventilationtomaintaingoodgasexchangewithoutatracheostomy.Therefore,thecomplicationsduetouseofatracheostomytube(e.g.,atelectasis, pulmonaryinfections,cardiacarrhythmia,mucousplug,granulationformation,stomalinfection,tracheomalacia,trachealperforation,hemorrhageandtrachealstenosis,etc.)decrease[5]. Second,NPPVmaintainslungandchestwallcompliance.Inthismethod,theycanair stackbyventilatortoreachtheirmaximuminsuf ationcapacity(MIC).Somepatientscan doairstackingbyglossopharyngealbreathing(GPB).TheycanobtainMICbythesemethods.Iftheyarecontrolledbyatracheostomy,theycannotairstackanddoGPB. A strong cough is made by air stacking and chest thrusting. For most cases, airway secretionsdramaticallydecreaseafterremovingthetracheostomytube.Inaddition,these individualscancoughstronglybyassistedchestthrustafterairstackingbyNPPVorGPB. Usually,theirpeakcough owsexceed270L/minbythesemethods.Theycanexpeltough sputumwhentheyhaveacoldorpneumonia[6]. PatientscanvocalizenaturallywhenusingNPPV.Afterinhalingairfromaventilator, theyvocalize.Iftheywanttospeaklouderorlonger,theyshouldvocalizeafterairstacking. ByNPPV,individuals ventilator-freebreathingtime(VFBT)usuallyincreasesmore thaniftheyareventilatedwithatracheostomytube.Iftheyareventilatedwithtracheostomytube,theycannottraintheirinspiratorymusclesbythemselveswithouttheassistance ofremovalfromtheventilators.Otherwise,iftheyareventilatedbyNPPVandthemouthpiecesaresetinarangethatthemouthcanreach,theycaneasilybetrainedtoventilateby theirinspiratorymuscles.GPBalsosecuresVFBT.
30.4 How to Introduce This Technology Intheacutephase,mostpatientswithSCIwhoneedventilatorsupportareventilatedvia cuffedtracheostomytube.Wechangetheirventilatorsettingtolargetidalvolumeanda cuf esstubeaccordingtotheclinicalpracticeguidelineoftheConsortiumforSpinalCord Medicine[7](Table30.1).
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Table 30.1 Ventilatorsetting Onadmission MODE
A/CorCMV
VT
Setperprevioushospitalsetting
RR
12
FiO2
TitrateO2tomaintainsaturationgreaterthan92%
PEEP
Sameasprevioushospitalsetting
Day2andthereafter MODE
A/CorCMV
VT
Ifpeakpressureisunder40cmH2O,thenVTisincreasedby100cc/day until20cc/kgidealbodyweight
RR
12
PEEP
PEEPisdecreasedby2cm/dayuntilthePEEPisentirelyremoved
Fio2
IfO2saturationisgreaterthan92%,theFio2maybedecreasedvia titrationtomaintainSao2ofgreaterthan92%
Fio2 fraction of inspired air, PEEP positive end-expiratory pressure, A/C assist/control, CMV continuousmandatoryventilation,VTtidalvolume,RRrespiratoryrate,SaO2saturation
Afterchangingthesesettings,patientsaretrainedtouseNPPV.Duringtraining,tracheostomytubesareplugged,andpatientsareventilatedbyNPPVviamouthpieces,nose masks, or nose plugs. The time for training is gradually increased. If patients can use NPPValldaylong,weremovetheirtracheostomytubesandclosetheirtracheostomies. ToassurethepatientsofthesafetyofNPPV,wemustcoachthemhowtoremovetheir sputumandhowtoincreasetheirVFBTusingtheirreservedrespiratorymusclesorGPB.
30.5 Ventilators and Ventilator Setting IntheNPPVmethod,weuseportablevolume-controlledventilators.Thereasonswhywe usevolume-controlledventilators,notpressure-controlledventilators,areasfollows:First, airstackingisachievedeffectivelybyvolume-controlledventilators.Thepeakinspiratory pressureafterMICismorethan40cmH2O,upto70cmH2O.Iftheyusepressure-controlled ventilators,theycannotperformef cientairstackingthatreachestheMIC.Therefore,itwill bedif culttomaintainlungandchestwallcomplianceandtocoughstrongly.Second,many usemouthpieceNPPVduringmealsorexceptforsleep.Theyholdthemouthpieceinthe mouthandreleaseitaccordingtotheirneeds.Pressure-controlledventilatorsdonotallow suchamethod. Assist/controlorcontrolmodesareapplied.Therespiratoryrateissetto10 15times/min, usually12times/min.Tidalvolumeis20mL/kgidealbodyweight.Peakpressureisunder 40cmH2O.Wedonotusepositiveend-expiratorypressure(PEEP).TheInspiratory/Expiratory (I/E)ratioissetbetween1/1.5and1/2.0.Oxygenationisnotnecessaryformostcases.
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30.6 Interfaces Therearemanyshapesandsizesofinterfaces.Theyaredividedmostlyintothreecategories:mouthpiece,nosemask,andnoseplug.Inararecase(e.g.,increasedairleakfromthe mouth),thefull-facetypeisselected.Toobtainef cientairstacking,theexpiratoryports ofnoseplugsandnosemasksareclosed. Fitismostimportant.Theshapesofthefaceandnosearediverse.High-volumeleakage due to bad t causes dyspnea and other dif culties. Leakage to the eyes must be avoided because it causes dry eyes. In the case of a nose mask, pressure ulcers on the bridgeofthenosearecommon.Noseplugssometimesmakeapressureulceronthewall betweenthebilateralnares.ThesetroublesoccurwhenNPPVisintroducedandresultin rejectionofNPPV. Situationsforusearethesecondimportantpointinchoosinganinterface:Willtheybe usedonlyduringsleeporallthetime,athomeorinthecommunity?WhileusingNPPV, willtheindividualbeabletouseacomputersoranenvironmentcontrolsystems?Wemust choosebetterinterfacesthataresuitableforeachpatient slifestyleandtheabilitiesoftheir respiratorysystems.
30.7 Surrounding Machines Werecommendpatientsandtheirfamilyhavemonitorsforavoidingaccidentalventilator troublesanddisconnection.Ventilatorshavesomealarmsystems,buttheycannotbecome awareofalltypesofventilatoraccidents.Therefore,westronglyrecommendpreparinga pulseoximeterforthesecondalarmsystem. If the patients cannot cough strongly enough, they should use mechanically assisted coughing(MAC).Thismachinedeliversdeepinsuf ationsandimmediatelydeliversdeep exsuf ations.Acombinationwithassistedchestthrustintheexsuf ationperiodwillbe moreeffectiveforremovingairwaysecretions.
Key Recommendations
› › ›
NPPVwillreducecomplicationsthatlong-termarti cialrespiratorymanagement withatracheostomytubecause.Patientswillhaveahealthierandhigher-qualitylife. TointroduceNPPVsafely,wemuststrictlyevaluatetheindicationforit. Dysphagiaandlackofcooperationarethemostimportantcontraindications. HowtoremoveairwaysecretionsandhowtoobtainVFBTaslongaspossibleare taughttopatientsandtheircaregivers.
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References 1. JacksonAB,GroomesTE(1994)Incidenceofrespiratorycomplicationsfollowingspinalcord injury.ArchPhysMedRehabil75:270 275 2. DeVivoMJ,IvieCSIII(1995)Lifeexpectancyofventilator-dependentpersonswithspinal cordinjuries.Chest108:226 232 3. BachJR,AlbaAS(1990)Noninvasiveoptionsforventilatorysupportofthetraumatichigh levelquadriplegicpatient.Chest98:613 619 4. Kirshblum S, Johnston MV, Brown J et al (1999) Predictors of dysphagia after spinal cord injury.ArchPhysMedRehabil80:1101 1105 5. BachJR(1991)Newapproachesintherehabilitationofthetraumatichighlevelquadriplegic. AmJPhysMedRehabil70:13 19 6. BachJR(1999)Guidetotheevaluationandmanagementofneuromusculardisease.Hanley andBelfus,Philadelphia,pp89 122 7. ConsortiumforSpinalCordMedicine(2005)Respiratorymanagementfollowingspinalcord injury:aclinicalpracticeguidelineforhealth-careprofessionals.ParalyzedVeteransof America,Washington,DC,pp34 35
Home Ventilation for Chronic Obstructive Pulmonary Disease
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Georg-ChristianFunk
31.1 Introduction Severechronicobstructivepulmonarydisease(COPD)isconsideredthemostcommon causeofchronicrespiratoryfailure,althoughexactestimationsofincidenceandprevalencearenotavailable.Thestandardtreatmentofthisconditionislong-termoxygentherapy(LTOT),whichimprovessurvival[1,2].Patientswithhypoxemiawhothendevelop hypercapniatendtohavetheworstprognosis[2 7].Inaddition,patientswithCOPDwho remain hypercapnic after surviving an acute episode of ventilatory failure that requires mechanicalventilationhaveaworseprognosisthanpatientswithonlyhypoxemia[8]. Thebene tofnoninvasiveventilation(NIV)forthetreatmentofacuterespiratoryfailureinCOPDhasbeenwelldocumentedbymultiplestudiesandmeta-analyses[9].However, thebene tofNIVfortreatmentofchronicrespiratoryfailureinpatientswithCOPDhas notbeenestablisheddespitevariousrandomizedandnonrandomizedstudies.Thisreview highlightssomepathophysiologicpeculiaritiesofNIVforthisindicationandsummarizes theavailableevidence.Finally,somepracticalaspectsofhomeNIVarediscussed,suchas tohowtoidentifypatientswithCOPDwhoarelikelytobene tfromhomeNIV.
31.2 Physiologic Effects of NIV in COPD InchronicrespiratoryfailuresecondarytoCOPD,hypoxemiacanbeviewedasaconsequence ofventilation/perfusionmismatchanddiffusiveimpairment.Hypercapnia,ontheotherhand, isamarkerofalveolarhypoventilation.InstableCOPD,hypercapniaisincreasinglyregarded astheresultofacompensatorymechanismaimedatunloadingtheventilatorymusclepump. Morespeci cally,theeffectiveworkofbreathingisreducedduetorapidshallowbreathing,
G.-C.Funk DepartmentofRespiratoryandCriticalCareMedicineandLudwigBoltzmannInstitute forChronicObstructivePulmonaryDisease,OttoWagnerHospital,Vienna,Austria e-mail:
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thuspreventingventilatorymusclefatigue.Thecostofthisbreathingpatternishypercapnia, whichresultsfromlowertidalvolumesandincreaseddeadspaceventilation[10,11]. Theexactmagnitudeandmechanismsofthephysiologiceffectsoflong-termmechanicalventilationinCOPDareunclear.Insomestudies,hypercapniawasreduced[12 14], whileinothersitwasnot[15 19].Thisdiscrepancyislikelydependentontheeffective ventilatory pressure applied during NIV. Nocturnal application of NIV decreases Paco2 andmayresetthePaco2sensitivityofthebluntedrespiratorycentersinCOPDwithsubsequentincreasesindiurnalrespiratorydrive[20].ImprovementofnocturnalPao2mayalso improvediurnaloxygenationduetoimprovedcomplianceofthechestwallandthelungs [21]andanincreasedrespiratorydrive[20]. ItisunclearwhetherandtowhatextenthomeNIVimprovesrespiratorymusclefunction,reducesoxygenconsumptionoftheventilatorypump,increasesrespiratorymuscle ef ciency,orreduceschronicrespiratorymusclefatigue[22,23].NIVreducedtheactivity oftheventilatorymusclesinmanystudies[12,23 28].However,onlyonestudyshoweda sustainedimprovementinmaximuminspiratoryforce[29].Otherstudiesshowedonlya trendtowardimprovementornochange[15 18,27,30 32]. NIVreducedpulmonaryhyperin ationintwostudies,buttheexactmechanismwas unclear[12,33].Additionalbene cialeffectsofNIVinCOPDincludeareductioninpulmonaryarterialpressure[34]andimprovednutritionalstatus[35].
31.3 Summary of Available Clinical Evidence 31.3.1 Mortality and Hospital Admissions Todate,threeprospectiverandomizedstudieshaveinvestigatedtheeffectofhomeNIVon thesurvivalofpatientswithCOPD.Casanovaetal.[17]andClinietal.[18]investigated patientsover1and2years,respectively.Bothwereunabletodemonstrateimprovedsurvivalinthosepatients.However,thestudybyCasanovaetal.alsoincludednormocapnic patients,suggestingabsenceofchronicventilatoryfailure.Currently,thelargest(n=144) and longest (mean follow-up 2.2 years) randomized study was undertaken by McEvoy etal.[19]inAustralia;thisstudyshowedasmallsurvivalbene tofNIVonlyafteradjustmentofbaselinegasexchangeandsymptoms.Inallthreestudies,rathersmalllevelsof effectiveventilatorypressuresupportwereapplied. ThestudiesbyClinietal.[18]andMcEvoyetal.[19]showednoreductionsinhospital admissionintheNIVgroupcomparedtotheLTOTgroup.Incontrast,Casanovaetal.[17] observedareductioninthenumberofhospitaladmissionsafter3months;however,this ndingwasnotsustainedafter1year.Inanolderstudy,Tuggeyetal.showedthatdomiciliaryNIV,appliedinpatientswithCOPDwithrecurrentadmissionsforacute-on-chronic respiratoryfailurerequiringNIV,reducedhospitaladmissions[36]. Asmall,randomized,pilotstudyofhomeNIVinpatientswhoremainedhypercapnic after acute-on-chronic respiratory failure showed an increased probability of clinical
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worsening (i.e., death, intubation, resumption of NIV, progressive hypercapnia, or intolerabledyspnea)whenNIVwaswithdrawn[37].
31.3.2 Quality of Life, Exercise Capacity, and Sleep BecausetheeffectofhomeNIVonmortalityandhospitalizationrateisuncertain,changes inqualityoflife(QOL)arebecomingevermoreimportanttreatmentgoals[38 40]. MeasuringQOLisachallengebecauseitisdeterminednotonlybyfunctionalstatusbut alsobypsychological,social,andsexualfactors[41].Thedisease-speci cSt.George s RespiratoryQuestionnaire(SGRQ)isusuallyusedtoquantifyQOLinpatientswithrespiratorydiseases.Inaddition,theMaugeriFoundationRespiratoryitemset(MRF-28)was developed as a more sensitive instrument to measure disease-speci c QOL treatment effectsinpatientswithrespiratoryfailure[18,42].Inmoststudies,includingtherandomizedstudies,QOLwasimprovedbyNIV[14,18,29].Incontrast,McEvoyetal.didnot observe any change in the SGRQ as a consequence of home NIV [19]. In this study, patientstreatedwithNIVhadevenpoorergeneralandmentalhealth(asmeasuredbythe Shortform36(SF36)healthsurveyquestionnaire)andreportedlessvigorandmoreconfusionandbewilderment.ThereasonsforworseningofmoodandQOLinthisstudywere unclear.Thesecon icting ndingsimplicatedtheneedtocloselymeasureQOLinfuture randomized,controlledtrialsinthispatientgroup. WhetherexercisecapacityisaffectedbyhomeNIVisalsounclear.Whilesomestudies showedanimprovementinthe6-minwalkingtest[13,29],othersdidnot[14,18].Similar considerationsapplytothequalityofsleepduringNIV.Somestudiesfoundimprovements [14,18,43],whileothersdidnot[15,16,29].
31.4 Practical Aspects of Home NIV in COPD 31.4.1 Ventilators and Interfaces VentilatorsforhomeNIVinpatientswithCOPDshouldbereliableandsimpletouse.A battery-operatedsystemisonlyrequiredwhenventilationisneededmorethan12h/day. Alarmsmustbesettodetectair owobstruction,disconnection,orventilatorfailure.With regard to the mode of ventilation, volume-preset and pressure-preset ventilation modes appeartobeequivalent[44 46]. Frequently, pressure support ventilation is the primary mode of choice because it is easiertoadjustandsynchronizewiththepatient.Ifpressuresupportisineffectiveornot welltolerated,pressure-controlledor ow-presetventilatorsmaybeused,dependingon individualpatientconditions[47].Newerpressuresupportventilatorscandeliverrealvolumeventilationwiththeaveragevolume-assuredpressuresupport(AVAPS)mode[48].
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Whenestablishingpressuresupportventilation,thelevelofinspiratoryaidisincreasinglyraisedfrom10cmH2Otoapproximately20cmH2Owithalevelofexpiratorypositiveairwaypressurearound5cmH2O.TheseventilatorsettingsallowoptimalCO2removal withsimultaneouscontrolofautopositiveend-expiratorypressure,accordingtoindividual patienttolerance. Levels of inspiratory pressure aid that are too low may be associated withlong-termfailureofNIV[32].Theinspiratorydurationisgenerallysettobeasshort aspossibleandlimitedatamaximumof1.3stoavoidleak-inducedprolongationofinspiration.Thefractionofinspiredoxygenisadjustedtocorrectfornocturnalhypoxemia,as ascertainedbynocturnaloximetry.Subjectivepatientcomfortiskeyforlong-termcompliancewiththetherapy.Strategiesusingpatientcomfortatacceptablebloodgasesareequivalenttostrategiesusingmorerigorousphysiologiccontrolalgorithms[49].Thechoiceof theinterfaceispersonal.Inprinciple,thesamenasalorfacialmasksthatareusedinsleep medicinearealsoaptforventilatingpatientswithCOPD.
31.4.2 NIV Initiation and Follow-Up in COPD Patients TheinitiationphaseofhomeNIViscrucialforthepatienttoadapttothenewtherapy. Well-informedpatientsaremotivatedandmorelikelytohavegreaterfuturecompliance withthetherapy.PatientswithCOPDarebesttrainedtouseNIVduringa3-to5-daystay in a specialized respiratory care center. This stay allows doctors to optimize patient ventilatorinteractionsandtoobtainandreacttonocturnaloximetryaswellasserialarterial bloodgases.SuccessfulhomeNIVrequiresabasicamountofintellectualcapacity;patients whoareunabletounderstandtheintentionandproceduresofNIVareunlikelytouseand bene tfromhomeNIV.Duringaninitiationphaseinthehospital,variousobstaclestosuccessful usage of home NIV can be identi ed and removed. In addition, this phase also allowsfortheidenti cationofpatientswhowillbeunabletosuccessfullyusehomeNIV. AfteraprimaryinitiationofhomeNIV,patientsshouldhaveregularfollow-upvisitsat thehospitalevery3 6months.Atthesevisits,thefunctionalstatusofthepatientaswell asthehourmeterandhygienicconditionsoftheventilatorarereassessedandreadapted,if needed.Technicalsupervisionathomeisusuallyprovidedbyhomerespiratorycareorganizationsandventilatormanufacturers. Althoughstudyresultscon ictwithregardtotheusefulnessofhomeNIVandNIValso conveyspotentialdiscomfort,almostallstudiesfoundahighcompliancewithhomeNIV onceitwassuccessfullyestablished[14,15,17 19,31,50].
31.5 Selection of Patients for Home NIV ThegenerallyhighpatientacceptanceofhomeNIVandsomeclinicalevidencesuggest thathomeNIVcanbebene cialforpatientswithCOPDwithchronicrespiratoryfailure. Thedif cultyliesinidentifyingindividualpatientswhoaremostlikelytobene tfromit.
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ThemostrecentTheAmericanCollegeofChestPhysicians(ACCP)guidelinesonclinical indicationsfornoninvasivepositivepressureventilationinchronicrespiratoryfailuresuggestusinghomeNIVinthepresenceofwell-documentedandwell-treateddiseaseassociatedwithcertainsymptomsandphysiological ndings(Table31.1)[51].However,these recommendationsdonotdescribeappropriatelyclinicalproblemsofpatientswithCOPD [52].Inaddition,stableoligosymptomatichypercapniaisprobablynotanindicationfor homeNIV. Theprogressivedeteriorationanddestabilizationofaformerlystablepatient,basedon clinical and biological criteria, has been suggested as an indication for home NIV in patientswithCOPDwithchronicrespiratoryfailure[52].Typicalcandidatesarepatients withchronichypercapnicrespiratoryfailurewhoexperiencerepeatedlife-threateningepisodesofacute-on-chronicrespiratoryfailure.TheseepisodesareassociatedwithworseningofhypercapniaandfrequentlyrequireacuteNIV[53].Patientswhoremainhypercapnic aftersuchanacuteepisodeandrequireNIVhaveaparticularlydismalprognosisandmay bene tfromNIV[8,37].ItalsoappearsreasonablethathomeNIVshouldbeinitiatedin patients who cannot be totally weaned off acute NIV but stabilize in the hospital with nocturnalNIVonly[54,55].Thesepatientswouldalternativelybecandidatesfortracheotomy,whichmaybeavoidedbyhomeNIV. Apart from the scenario of repeated acute-on-chronic respiratory failure, alternative indicatorsofinstabilitymaybeslowandprogressiveworseningofhypercapniaassociated withincreasingsymptomsdespiteoptimalmedicaltherapy.IfatrialofNIVinthehospital
Table 31.1 ClinicalindicatorsfortheintroductionofhomeNIVinpatientswithCOPD(Adapted from[51]) Diseasedocumentation 1. EstablishanddocumentanappropriatediagnosisofCOPDusinghistory,physicalexamination,andresultsofdiagnostictests 2. Assure optimal management of COPD (inhalative treatment, rehabilitation,including smokingcessationandoxygentherapywhenindicated) 3. Optimalmanagementofotherunderlyingdisorders(e.g.,multichannelsleepstudytoexclude associatedsleep-disorderedbreathing,ifclinicallyindicated) Indicationsforusage 1. Symptoms:fatigue,dyspnea,morningheadache,etc. 2. Physiologicalcriteria(oneofthefollowing):
Paco 55mmHgorabove Paco between50and54mmHgwithnocturnaldesaturation(Sao bypulseoximetry£ 2 2
2
88%for5mincontinuouslywhilereceivingoxygentherapy³2L/min)
Paco between 50 and 54 mmHg with hospitalization related to recurrent episodes of 2
hypercapnicrespiratoryfailure(morethantwoina12-monthperiod)
COPDchronicobstructivepulmonarydisease
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appears promising in such a patient with improved symptoms and gas exchange, home NIVshouldbeconsidered. Associatedcomorbidities,suchasobstructivesleepapneasyndrome,congestiveheart failure with Cheyne Stokes breathing, or obesity, are conditions that also in uence the decisiontoestablishhomeNIVinCOPDpatientswithchronicrespiratoryfailure.
Key Recommendations
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Long-termdomiciliarynoninvasiveventilation(homeNIV)maybeconsidered inCOPDpatientswithchronichypercapnicrespiratoryfailurewhoexperience progressivedestabilizationdespiteoptimalnon-ventilatorytreatment. TheindicationforhomeNIVshouldbasedonbothsymptomsandbloodgases. Inordertoavoidtracheotomy,homeNIVmaybeinitiatedinpatientswhocannot beweanedoffacuteNIVbutstabilizeinhospitalwithnocturnalNIV. Thelong-termsuccessofhomeNIVrequiresamotivatedandwell-informed patient. InitiationofhomeNIV,patienteducationandregularfollow-upvisitsshouldbe providedbyaspecializedrespiratorycarecentre.
References 1. Nocturnal Oxygen Therapy Trial Group (1980) Continuous or nocturnal oxygen therapy inhypoxemicchronicobstructivelungdisease:aclinicaltrial.AnnInternMed93:391 398 2. Longtermdomiciliaryoxygentherapyinchronichypoxiccorpulmonalecomplicatingchronic bronchitisandemphysema.ReportoftheMedicalResearchCouncilWorkingParty.(1981) Lancet1:681 686 3. Burrows B, Earle RH (1969) Course and prognosis of chronic obstructive lung disease. Aprospectivestudyof200patients.NEnglJMed280:397 404 4. BoushySF,ThompsonHKJr,NorthLB,BealeAR,SnowTR(1973)Prognosisinchronic obstructivepulmonarydisease.AmRevRespirDis108:1373 1383 5. PostmaDS,BuremaJ,GimenoFetal(1979)Prognosisinseverechronicobstructivepulmonarydisease.AmRevRespirDis119:357 367 6. Kawakami Y, Kishi F, Dohsaka K, Nishiura Y, Suzuki A (1988) Reversibility of airway obstructioninrelationtoprognosisinchronicobstructivepulmonarydisease.Chest93:49 53 7. Cooper CB, Waterhouse J, Howard P (1987) Twelve year clinical study of patients with hypoxiccorpulmonalegivenlongtermdomiciliaryoxygentherapy.Thorax42:105 110 8. ChuCM,ChanVL,LinAWN,WongIWY,LeungWS,LaiCKW(2004)Readmissionrates andlifethreateningeventsinCOPDsurvivorstreatedwithnon-invasiveventilationforacute hypercapnicrespiratoryfailure.Thorax59:1020 1025 9. RamFS,PicotJ,LightowlerJ,WedzichaJA(2004)Non-invasivepositivepressureventilationfortreatmentofrespiratoryfailureduetoexacerbationsofchronicobstructivepulmonary disease.CochraneDatabaseSystRevCD004104
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10. RochesterDF(1991)Respiratorymuscleweakness,patternofbreathing,andCO2retentionin chronicobstructivepulmonarydisease.AmRevRespirDis143:901 903 11. PurroA,AppendiniL,PolilloCetal(2008)MechanicaldeterminantsofearlyacuteventilatoryfailureinCOPDpatients:aphysiologicstudy.IntensiveCareMed34:2035 2043 12. DiazO,BeginP,TorrealbaB,JoverE,LisboaC(2002)Effectsofnoninvasiveventilationon lunghyperin ationinstablehypercapnicCOPD.EurRespirJ20:1490 1498 13. DiazO,BeginP,AndresenMetal(2005)PhysiologicalandclinicaleffectsofdiurnalnoninvasiveventilationinhypercapnicCOPD.EurRespirJ26:1016 1023 14. MeechamJonesDJ,PaulEA,JonesPW,WedzichaJA(1995)NasalpressuresupportventilationplusoxygencomparedwithoxygentherapyaloneinhypercapnicCOPD.AmJRespir CritCareMed152:538 544 15. StrumpfDA,MillmanRP,CarlisleCCetal(1991)Nocturnalpositive-pressureventilationvia nasalmaskinpatientswithseverechronicobstructivepulmonarydisease.AmRevRespirDis 144:1234 1239 16. LinCC(1996)Comparisonbetweennocturnalnasalpositivepressureventilationcombined withoxygentherapyandoxygenmonotherapyinpatientswithsevereCOPD.AmJRespir CritCareMed154:353 358 17. CasanovaC,CelliBR,TostLetal(2000)Long-termcontrolledtrialofnocturnalnasalpositivepressureventilationinpatientswithsevereCOPD.Chest118:1582 1590 18. CliniE,SturaniC,RossiAetal(2002)TheItalianmulticentrestudyonnoninvasiveventilationinchronicobstructivepulmonarydiseasepatients.EurRespirJ20:529 538 19. McEvoyRD,PierceRJ,HillmanDetal(2009)Nocturnalnon-invasivenasalventilationin stablehypercapnicCOPD:arandomisedcontrolledtrial.Thorax64:561 566 20. FleethamJA,MezonB,WestP,BradleyCA,AnthonisenNR,KrygerMH(1980)Chemical controlofventilationandsleeparterialoxygendesaturationinpatientswithCOPD.AmRev RespirDis122:583 589 21. GrassinoAE,LewinsohnGE,TylerJM(1973)Effectsofhyperin ationofthethoraxonthe mechanicsofbreathing.JApplPhysiol35:336 342 22. AmbrosinoN,NavaS,BertoneP,FracchiaC,RampullaC(1992)Physiologicevaluationof pressuresupportventilationbynasalmaskinpatientswithstableCOPD.Chest101:385 391 23. NavaS,AmbrosinoN,RubiniFetal(1993)Effectofnasalpressuresupportventilationand external PEEP on diaphragmatic activity in patients with severe stable COPD. Chest 103: 143 150 24. Belman MJ, Soo Hoo GW, Kuei JH, Shadmehr R (1990) Ef cacy of positive vs. negative pressureventilationinunloadingtherespiratorymuscles.Chest98:850 856 25. CarreyZ,GottfriedSB,LevyRD(1990)Ventilatorymusclesupportinrespiratoryfailurewith nasalpositivepressureventilation.Chest97:150 158 26. LienTC,WangJH,ChangMT,KuoCD(1993)ComparisonofBiPAPnasalventilationand ventilationviaironlunginseverestableCOPD.Chest104:460 466 27. Renston JP, DiMarco AF, Supinski GS (1994) Respiratory muscle rest using nasal BiPAP ventilationinpatientswithstablesevereCOPD.Chest105:1053 1060 28. MasaJimenezJF,SanchezdeCosEJ,DisdierVC,HernandezVM,FuentesOF(1995)Nasal intermittentpositivepressureventilation.Analysisofitswithdrawal.Chest107:382 388 29. GarrodR,MikelsonsC,PaulEA,WedzichaJA(2000)Randomizedcontrolledtrialofdomiciliary noninvasive positive pressure ventilation and physical training in severe chronic obstructivepulmonarydisease.AmJRespirCritCareMed162:1335 1341 30. ElliottMW,MulveyDA,MoxhamJ,GreenM,BranthwaiteMA(1991)DomiciliarynocturnalnasalintermittentpositivepressureventilationinCOPD:mechanismsunderlyingchanges inarterialbloodgastensions.EurRespirJ4:1044 1052 31. WindischW,VogelM,SorichterSetal(2002)NormocapniaduringnIPPVinchronichypercapnicCOPDreducessubsequentspontaneousPaCO2.RespirMed96:572 579
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32. WindischW,KosticS,DreherM,VirchowJCJr,SorichterS(2005)Outcomeofpatientswith stableCOPDreceivingcontrollednoninvasivepositivepressureventilationaimedatamaximalreductionofPa(CO2).Chest128:657 662 33. BudweiserS,HeinemannF,FischerW,DobroschkeJ,PfeiferM(2005)Long-termreduction of hyperin ation in stable COPD by non-invasive nocturnal home ventilation. Respir Med 99:976 984 34. SchonhoferB,BarchfeldT,WenzelM,KohlerD(2001)Longtermeffectsofnon-invasive mechanical ventilation on pulmonary haemodynamics in patients with chronic respiratory failure.Thorax56:524 528 35. BudweiserS,HeinemannF,MeyerK,WildPJ,PfeiferM(2006)Weightgainincachectic COPDpatientsreceivingnoninvasivepositive-pressureventilation.RespirCare51:126 132 36. TuggeyJM,PlantPK,ElliottMW(2003)Domiciliarynon-invasiveventilationforrecurrent acidoticexacerbationsofCOPD:aneconomicanalysis.Thorax58:867 871 37. FunkGC,BreyerMK,BurghuberOC,KirchheinerK,SchmidtI,HartlS(2008)Nocturnal non-invasivepositivepressureventilation(NIPPV)instablehypercapnicCOPDpatients a randomizedcontrolledtrial.EurRespirJ359:4 8 38. CrieeCP(2002)[Ishomerespirationeffective?].Pneumologie56:591 592 39. WindischW,CrieeCP(2006)[Qualityoflifeinpatientswithhomemechanicalventilation]. Pneumologie60:539 546 40. WindischW,FreidelK,MatthysH,PetermannF(2002)[Health-relatedqualityoflife(HRQL) inpatientsreceivinghomemechanicalventilation].Pneumologie56:610 620 41. SchonhoferB,VonSK,BucherTetal(2001)Sexualityinpatientswithnoninvasivemechanicalventilationduetochronicrespiratoryfailure.AmJRespirCritCareMed164:1612 1617 42. CaroneM,BertolottiG,AnchisiF,ZottiAM,DonnerCF,JonesPW(1999)Analysisoffactorsthatcharacterizehealthimpairmentinpatientswithchronicrespiratoryfailure.Qualityof LifeinChronicRespiratoryFailureGroup.EurRespirJ13:1293 1300 43. Elliott MW, Simonds AK, Carroll MP, Wedzicha JA, Branthwaite MA (1992) Domiciliary nocturnal nasal intermittent positive pressure ventilation in hypercapnic respiratory failure duetochronicobstructivelungdisease:effectsonsleepandqualityoflife.Thorax47: 342 348 44. MeechamJonesDJ,WedzichaJA(1993)Comparisonofpressureandvolumepresetnasal ventilatorsystemsinstablechronicrespiratoryfailure.EurRespirJ6:1060 1064 45. RestrickLJ,FoxNC,BraidG,WardEM,PaulEA,WedzichaJA(1993)Comparisonofnasal pressuresupportventilationwithnasalintermittentpositivepressureventilationinpatients withnocturnalhypoventilation.EurRespirJ6:364 370 46. SmithIE,ShneersonJM(1997)SecondaryfailureofnasalintermittentpositivepressureventilationusingtheMonnalD:effectsofchangingventilator.Thorax52:89 91 47. SchonhoferB,SonnebornM,HaidlP,BohrerH,KohlerD(1997)Comparisonoftwodifferentmodesfornoninvasivemechanicalventilationinchronicrespiratoryfailure:volumeversuspressurecontrolleddevice.EurRespirJ10:184 191 48. Storre JH, Seuthe B, Fiechter R et al (2006) Average volume-assured pressure support in obesityhypoventilation:arandomizedcrossovertrial.Chest130:815 821 49. VitaccaM,NavaS,ConfalonieriMetal(2000)TheappropriatesettingofnoninvasivepressuresupportventilationinstableCOPDpatients.Chest118:1286 1293 50. JonesSE,PackhamS,HebdenM,SmithAP(1998)DomiciliarynocturnalintermittentpositivepressureventilationinpatientswithrespiratoryfailureduetosevereCOPD:long-term followupandeffectonsurvival.Thorax53:495 498 51. (1999)Clinicalindicationsfornoninvasivepositivepressureventilationinchronicrespiratory failureduetorestrictivelungdisease,COPD,andnocturnalhypoventilation aconsensus conferencereport.Chest116:521 534
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52. MuirJF,MolanoC,CuvelierA(2008)NIVandobstructivelungdiseases.EurRespirMonogr 41:203 223 53. MuirJF,Levi-ValensiP(1987)WhenshouldpatientswithCOPDbeventilated?EurJRespir Dis70:135 139 54. UdwadiaZF,SantisGK,StevenMH,SimondsAK(1992)Nasalventilationtofacilitateweaninginpatientswithchronicrespiratoryinsuf ciency.Thorax47:715 718 55. GiraultC,DaudenthunI,ChevronV,TamionF,LeroyJ,BonmarchandG(1999)Noninvasive ventilationasasystematicextubationandweaningtechniqueinacute-on-chronicrespiratory failure:aprospective,randomizedcontrolledstudy.AmJRespirCritCareMed160:86 92
Section VI Critical Care Applications of Noninvasive Mechanical Ventilation and Related Issues
Current Strategies and Equipment for Noninvasive Ventilation in Emergency Medicine
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KeisukeTomii
32.1 Introduction Growingevidenceindicatesthatnoninvasiveventilation(NIV)isthestandard rst-line therapyforcardiogenicpulmonaryedema(CPE)andchronicobstructivepulmonarydisease(COPD).NIVisalsostartingtobetriedoutintheemergencydepartment(ED)for otherdiseases,suchasasthma,acuteexacerbationofothertypesofhypercapnicfailure, pneumonia,andacuterespiratorydistresssyndrome(ARDS).Furthermore,sincerespiratorydistressduetoCPEcanberapidlyretrievedevenwithcontinuouspositiveairway pressure(CPAP),whichhasthegreatadvantageofeasyapplication,prehospitalCPAPfor presumedCPEisconsideredtobeatthecuttingedgeofemergencymedicine.
32.2 Analysis of Main Topics 32.2.1 NIV Trial in the ED Inemergencymedicine,NIVhasbeenappliedformorethan10yearsincasesofrespiratory distress regardless of the etiology. One study by Wood et al. in 1998 [1], which randomlyallocated27patientswithvarioustypesofacuterespiratorydistresstoeither NIVorconventionalmedicaltherapyintheED,wasunabletoproduceanybene tand showedatrendtowardagreaterhospitalmortalityrate,probablyduetoadelayinperformingintubation.In1999,however,aprospectivenonrandomizedpilotstudybyThys etal.[2]revealedrapidimprovementinclinicalandlaboratoryparametersinalmostall
K.Tomii DepartmentofRespiratoryMedicine,KobeCityMedicalCenterGeneralHospital, 4 6MinatojimanakamachiChuo-ku,Kobe650-0046,Japan e-mail:
[email protected] A.M.Esquinas(ed.),NoninvasiveMechanicalVentilation, DOI:10.1007/978-3-642-11365-9_32,©Springer-VerlagBerlinHeidelberg2010
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oftheir62patients,whohadvariousetiologiesandwhohadnodeleteriouseffectsfrom NIVwhenimplementedforshortperiodsoftime.Thus,thiswasthe rststudytosupport anNIVtrialstrategyintheED. In2002,Thysetal.[3]performedaprospective,randomized,placebo-controlledstudy inwhichtheearlyapplicationofNIVinpatientswithsevereacuterespiratoryfailure(ARF) duetoCPEorCOPDrevealedarapidandsigni cantimprovementinclinicalparameters, pH,andcarbondioxidetensioninarterialblood;respiratoryfrequency;andsternocleidomastoidelectromyogramactivity.Parketal.[4]reportedonarandomizedcontrolledtrial of patients with severe CPE in a tertiary hospital emergency room and demonstrated a lowerrateofendotrachealintubationandnocardiacischemiccomplicationswiththis rstlineNIVstrategy.In2006,Collinsetal.[5]reportedonameta-analysisof494patientsand theuseofNIVintheEDforacuteCPEandfoundthatNIVsigni cantlyreducedhospital mortality(relativerisk[RR]0.61,95%con denceinterval[CI]0.41 0.91). Asmentioned,NIVwasusedforARFofvariousetiologiesotherthanCPEandCOPD; however,noevidentsurvivalbene twasshown.Anewlyreportedretrospectivecohort study by Tomii and colleagues [6] was the rst to demonstrate an overall reduction in mortalityafterintroducingNIVtrialstrategyintheEDforthewholepopulationofARF, excludingrecurrentaspirationpneumonia(RR0.51,95%CI0.31 0.84).
32.2.2 Prehospital CPAP Aswehaveshown,NIVorCPAPisclearlyeffectiveasthe rst-linetreatmentforCPEand willincreasinglybesoifwecandeliveritbeforethepatient sarrivalatthehospital.Kosowski etal.[7] rstreportedacaseseriesof19patientsin2001;prehospitaluseofCPAPwasfeasibleandmayhaveavertedtheneedforendotrachealintubationinpatientswithARFpresumablyduetoCPE.In2008,Thompsonetal.[8]performedarandomizedcontroltrialof out-of-hospitalmaskCPAP(Fig.32.1)in71patientswithsevererespiratoryfailuremainly duetoCPE,COPD,andasthmaandrevealeda30%reductioninintubationanda21%reductioninmortality.HelmetCPAPs(Fig.32.2)havebeenwidelyusedinItaly,andpreliminary datafortheiruseas rst-lineprehospitaltreatmentwerereportedin2009.Prehospitalhelmet CPAPwithanoxygen owofatleast30L/minwasapplied,withorwithoutstandardmedical treatment, to 121 patients with mostly presumed CPE and resulted in no prehospital intubationandsigni cantimprovementinoxygenationandhemodynamics[9].
32.3 Discussion TherearetwodirectionsinwhichNIVcanmakefurtherprogressinemergencymedicine. Oneisinincreasingitsindications,andtheotherisitsmorerapidapplication.NIVtrial strategy,meaningits rst-lineuseforallpossibleindications,shouldbepromotedmore widelyintheED,wherecausesofARFcannotbeeasilyde nedinashortspaceoftime.
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Fig. 32.1 Noninvasivehigh- owCPAP(continuouspositiveairwaypressure)systemforprehospitalandemergencycare.(a)Flowgenerator(WhisperFlowVariable,RespironicsInc.,Murrysville, PA). (b) Flow generator and other parts; mask, positive end-expiratory pressure (PEEP) valve, tubing,and lter(WhisperPak,Respironics)
a
b
c
Fig. 32.2 Helmets for continuous positive airway pressure (CPAP). (a) 4Vent (Rusch GmbH, Kernen, Germany). (b) HelmHar (Harol, Via Marcora, Italy). (c) CaStar (StarMed, Mirandola, Italy).Thickarrowsindicatelocationstoconnectpositiveend-expiratorypressure(PEEP)valves. Thinarrowsindicatelocationsofantisuffocationdevicesorportofconnectingsafetyvalves:(a) twoconnectorsoneachsidefortheconnectionofPEEPandsafetyvalves,(b)integratedantisuffocationdeviceandpop-offvalve,(c)bidirectionalantiasphyxiavalvewithautomaticopening
The equipment for such broadly indicated NIV should not only have both CPAP and bilevel mode but also a high-level oxygen blender that can produce up to 100% Fio2. Moreover,sinceacertainamountofmaskleakageisinevitableintheinitialphaseofmask NIVintheED,NIV-compatibleintensivecareunit(ICU)ventilators,whichcanbarely
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tolerateunexpectedmaskleakageandoftenproducepatient ventilatorasynchronyinthat situation,shouldbeavoided.Therefore,Bipap-Vision(RespironicsInc.,Murrysville,PA) hasbeenfrequentlyusedforthispurposetodate,andthenewlyintroducedCarina(Dräger MedicalAG&Co.KG,Lubeck,Germany)wouldbeanotherchoice. SimpleCPAPwithoxygenationcanrapidlyamelioratetherespiratorydistressofCPE; hence, equipment for administering constant positive pressure and variable Fio2 up to 100%intheambulancewouldcontributegreatlytothecareofemergentpatients.Ahighow CPAP system composed of a mask with positive end-expiratory pressure (PEEP) (CPAP) valve and a specialized ow generator (Fig. 32.1), which enables stable CPAP (5.0,7.5,10cmH2O);variableFio2(30 100%);andmaximum140L/min owisnow available.Anotherdevicethatisapossibilityforout-of-hospitalCPAPishelmetCPAP. Sincethehelmetactsasacompliancechamber,theairwaypressureiskeptabovePEEP throughouttherespiratorycycle,providedthatgas owthroughtheexpiratoryvalveis alwayspresent[10].Itdoesnotrequirecritical ttingandiseasilyapplied,evenbyacrew with minimal training. It does, however, require a high ow of oxygen (>30 L/min) to preventaccumulationofCO2insidethehelmetandrebreathing.Forbothsystemsofprehospital CPAP, an antisuffocation safety device and a dedicated monitoring and alarm systemarecrucial(Figs.32.1and32.2).DatafromprehospitalCPAPforCPEarebeing accumulated[7 9],whilethatforotheretiologies,althoughstilllacking,mightprovetobe promising[8].
Key Recommendations
› › › ›
TryNIV rstforCPEintheED. NIVtrialstrategyforothervarietiesofARFshouldbepromotedmorewidelyin theED. PrehospitalCPAPcouldbeappliedas rstaidtreatmentforCPE. Ambulances should be equipped with prehospital CPAP systems: high- ow maskCPAPorhelmetCPAP.
References 1. WoodKA,LewisL,VonHarzBetal(1998)Theuseofnoninvasivepositivepressureventilation in the emergency department: results of a randomized clinical trial. Chest 113: 1339 1346 2. ThysF,RoeselerJ,DelaereSetal(1999)Two-levelnon-invasivepositivepressureventilation intheinitialtreatmentofacuterespiratoryfailureinanemergencydepartment.EurJEmerg Med6:207 214 3. Thys F, Roeseler J, Reynaert M et al (2002) Noninvasive ventilation for acute respiratory failure:aprospectiverandomisedplacebo-controlledtrial.EurRespirJ20:545 555 4. ParkM,SangeanMC,VolpeMdeSetal(2004)Randomized,prospectivetrialofoxygen, continuous positive airway pressure, and bilevel positive airway pressure by face mask in acutecardiogenicpulmonaryedema.CritCareMed32:2407 2415
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5. CollinsSP,MielniczukLM,WhittinghamHAetal(2006)Theuseofnoninvasiveventilation in emergency department patients with acute cardiogenic pulmonary edema: a systematic review.AnnEmergMed48:260 269,269.e1 4Epub2006Apr25 6. TomiiK,SeoR,TachikawaRetal(2009)Impactofnoninvasiveventilation(NIV)trialfor varioustypesofacuterespiratoryfailureintheemergencydepartment;decreasedmortality anduseoftheICU.RespirMed103:67 73 7. KosowskyJM,StephanidesSL,BransonRDetal(2001)Prehospitaluseofcontinuouspositive airway pressure (CPAP) for presumed pulmonary edema: a preliminary case series. PrehospEmergCare5:190 196 8. ThompsonJ,PetrieDA,Ackroyd-StolarzSetal(2008)Out-of-hospitalcontinuouspositive airwaypressureventilationversususualcareinacuterespiratoryfailure:arandomizedcontrolledtrial.AnnEmergMed52:232 241,241.e1Epub2008Apr3 9. FotiG,SangalliF,BerraLetal(2009)IshelmetCPAP rstlinepre-hospitaltreatmentof presumedsevereacutepulmonaryedema?IntensiveCareMed35:656 662 10. PatronitiN,FotiG,Man oAetal(2003)Headhelmetversusfacemaskfornon-invasive continuous positive airway pressure: a physiological study. Intensive Care Med 29: 1680 1687
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DavideChiumello,GaetanoIapichino,andVirnaBerto
33.1 Introduction Whenindividualswithacuterespiratoryfailurebecameunresponsivetostandardmedical therapy,theymayrequireinvasivemechanicalventilation.However,endotrachealintubationincreasestheriskofnosocomialinfection,inducesairwaytrauma,andrequirestheuse ofsedation. Noninvasive ventilation (NIV), which avoids endotracheal intubation and its related complications,hasbeenshowninseveralstudiestobeaneffectivetreatmentinselected patientswithrespiratoryfailureduetoanacuteexacerbationofchronicobstructivepulmonarydisease(COPD),hypoxemicrespiratoryfailure,community-acquiredpneumonia,or cardiogenicpulmonaryedemaandinimmunocompromisedpatients[1 3]. Althoughinrandomizedtrialsthereductioninintubationratesanddeatharetheprimaryendpoint,ineverydayclinicalpractice,thereliefofdyspnea,palliation,andcomfort arealsoacceptablegoalsofNIV,especiallyinpatientswithapoorprognosisorwhorefuse advancedlifesupport. Traditionally,allformsofventilatoryassistancehavebeenmanagedinintensivecare units (ICUs), where personnel, knowledge, skills, and monitoring capabilities amply exceedthoseofageneralward.Now,however,withtheshortageofintensivecarebeds andthegrowingeaseofapplication,NIVisfrequentlystartedoutsidetheICUnotonlyin theemergencydepartmentundertheindicationsanddirectmanagementofthedutyanesthesiologist, but also in general wards with scant monitoring facilities and usually inadequatemedicalornursingknowledgeandskills[4].
D.Chiumello()andV.Berto U.O.AnestesiaeRianimazione,DipartimentodiAnestesia,Rianimazione(Intensivae Subintensiva)eTerapiadelDolore,FondazioneIRCCSCa Granda-OspedaleMaggiore Policlinico,Milan,Italy e-mail:
[email protected] G.Iapichino IstitutodiAnestesiologiaeRianimazione,UniversitàdegliStudidiMilano, Milano,Italy A.M.Esquinas(ed.),NoninvasiveMechanicalVentilation, DOI:10.1007/978-3-642-11365-9_33,©Springer-VerlagBerlinHeidelberg2010
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33.2 NIV Outside Intensive Care ThemostcommonreportedlocationsfortheinitiationofNIVaretheICUs,followedby theemergencydepartmentsandthegeneralhospitalwards[5].Inaddition,NIVnotonly isinitiatedbutalsoismaintainedforhoursanddaysoutsidetheICU. The recent British Thoracic Society guidelines Non-invasive Ventilation in Acute RespiratoryFailure suggestedthatNIVcanbeprovidedinanumberoflocationsoutside theICU,includingthehigh-dependencyunitsandtherespiratorywards[1]. However,to optimizetheef cacyandnottoharmthepatients,eachhospitalshouldhaveaspeci c designatedareawithanavailablestaffcohortwithappropriateexperience,togetherwith structurestoensurethatpatientsrequiringNIVcanbetransferredtothisareawithaminimumdelay [1]. ApossibleadvantageofapplyingNIVoutsidetheICUisthepossibilityofstartingNIV withmorepatientsatanearlierstageoftheacuterespiratoryfailure,whichisassociated withminorutilizationofmedicalresources. ABritishsurveyconductedfrom268hospitalsin1998showedthatNIVwasavailable inonly48%ofthesehospitals,inparticularin34%oftheintensivecareandin16%ofthe generalwards[6].Inaddition,thecriteriausedtoselectthepatientsrequiringNIVvaried fromdifferentbloodgasanalysisvaluestoasimpleclinicaljudgment,suchasexhaustion orfailuretoimproveduringstandardtreatment[6].AstudyconductedatauniversityhospitalinCanadafoundthatNIVwasmostoftenbegunintheemergencydepartment,and themostcommonindicationsfortheapplicationwereacutecardiogenicpulmonaryedema andtheexacerbationofCOPD[7]. Duringaperiodof1year,Antroetal.foundthat190patientswereadmittedforacute respiratoryfailure,andforthese200NIVtrialsweredelivered[8].Themainindications werecardiogenicpulmonaryedema(70%),acuteexacerbationofCOPD(39%),andpneumonia(48%);therewasanoverallsuccessrateofabout60%. AprospectivestudyconductedinatypicalBritishdistrictgeneralhospital(i.e.,coveringapopulationof727,000inhabitants)aimedtoidentifytherateofacuteexacerbationof COPD;itfoundthat983patientswereadmittedduringaperiodof1year[9].Inmorethan 90%ofthepatients,anarterialbloodgasanalysiswasrecorded:46%ofthesewerehypercapnic;only20%presentedarespiratoryacidosis.However,20%normalizedtheirpHon arrivalintheward,leaving16%tomeetcriteriaforNIV.Acidosiswastheonlyvariable associatedwiththesubsequentICUadmission.Basedonthesedata,theauthorshypothesizedthat,forageneralhospitalcoveringapopulationof250,000inhabitants,everyyear 90 patients should be admitted for acute exacerbations of COPD, and 72 of these will requireNIV. AsingleretrospectivelystudyreportedthatingeneralsurgicalpatientsNIVwasadministeredin40%directlyonsurgicalwards.ThemajorityofthepatientsreceivedNIVfollowinganemergencysurgery,andtheprimaryreasonswerechestinfection,acuterespiratory distresssyndrome,andheartfailure[10].
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33.3 Evidence of NIV Success Outside the Intensive Care Unit ThemostcommonlyreportedlocationsforstartingNIVoutsideICUsandhigh-dependency unitsweretheemergencydepartmentandmorerecentlyageneralhospitalward[5,11], particularlyarespiratorywardstaffedbystandardcaregivers[1,9].However,tooptimize theef cacyandavoidharmtopatients,eachhospitalshouldhaveaspeci cdesignated areastaffedbypersonnelwithappropriateexperienceandwithstructurestoensurethat patientsrequiringNIVcanbetransferredtothisareawithminimumdelay.
33.3.1 Acute Exacerbation of COPD TheacuteexacerbationofCOPDisoneofthemostfrequentlycitedreasonsforrequiring theuseofNIV. InaseminalstudycomparingNIVwithconventionaltreatmentinpatientswithCOPD admittedtothehospitalwithrespiratoryfailureandpresentingarterialoxygenationless than7.5kPaandacarbondioxidevaluehigherthan6kPa,Bottetal.showedthatNIV improvedgasexchangeat1handsurvivalrateat30days[12].Thevisualanalogscores over the rst 3 days showed signi cantly lower scores for breathlessness for the NIV group.AlthoughtheapplicationofNIVoutsidetheICUcansometimesbeadif cultand atime-consumingprocedure,theauthorsdidnot ndanydifferenceinthenursingcare required.Thus,theauthors(severalyearsago)suggestedofferingNIVforeveryacidotic and hypercapnic compliant patients without a face abnormality for whom conventional therapydoesnotproduceapromptclinicalresponse. Similarly,inamulticenterstudyofpatientswithCOPDwithmild-to-moderateacidosis withapHbetween7.25and7.35andwithacarbondioxidevaluehigherthan6kPa,Plant etal.showeddecreasedneedforintubationandhospitalmortality[13].TheNIVledto morerapidcorrectionofacidosisandagreaterdecreaseinrespiratoryratecomparedwith thestandardgroup.Inaddition,15%ofthepatientsmetthecriteriaforintubation,andthe subgroupofpatientsthatpresentedatenrollmentwithapHbelow7.30hadasigni cantly higherfailurerateandhospitalmortalitythanpatientswithapHhigherthan7.30.Hence, itisimportanttorapidlyrecognizethenecessityforstartinginvasiveventilation.IncontrasttotheBottetal.study[12],thegrouptreatedwithNIVcausedamodestbutsigni cantincreaseinnursingworkloadinthe rst8hofadmissioncomparedtothosereceiving aconventionaltreatment. Twofurtherstudies,withsimilaradmissioncriteria,didnotshowanystatisticaldifferenceforgasexchange,rateofendotrachealintubation,lengthofstay,ormortalitybetween theNIVandconventionaltreatments[14,15]Comparedtothetwopositivestudies[12], inthesethepatientswereenrolledrelativelylaterafterthehospitaladmission,andtheNIV wasonlyusedforonlyafewhourseveryday.
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Concerning the clinical predictors for NIV success at hospital admission in patients treated with NIV, Poponick et al. found only an improvement in pH and PaCO2 during 30minofclinicaltrials[16].Thefailuretoimproveafter30minofNIVshouldbeanindication for the discontinuation and initiation, if indicated, of controlled mechanical ventilation. However,itisimportanttonotethatthesestudiesexcludedpatientswithapHlower than7.25becausetheprognosiswithoutNIVisverypoor.Itwouldhavebeenunethical nottoadministertheNIVandnottoadmitthesepatientsdirectlytotheICU[17].
33.3.2 Acute Cardiogenic Pulmonary Edema Acutecardiogenicpulmonaryedemaisacommonmedicalemergencyandhasahospital mortalityvaryingfrom10%to20%[18].SimilartopatientswithCOPD,therationalefor usingNIVinacutecardiogenicpulmonaryedemaistonotonlyimprovegasexchangeand respiratorymechanicsbutalsodecreaseleftventricularafterload[19,20].However,the besttherapyfortreatinganepisodeofacuterespiratoryfailureduetoacutecardiogenic pulmonaryedemaisstillacontroversial,andthepotentialforharmusingNIVhasnot beencompletelyexcluded[21 28].Inalargerandomizedprospectivestudyofpatients with acute cardiogenic pulmonary edema presenting with severe arterial hypoxemia (aPao2/FiO2ratiolessthan250withanoxygen owofatleast10L/min)andarespiratory ratehigherthan30breaths/minandtreatedintheemergencydepartmentwithNIV,nodifferencesintherateofendotrachealintubationorhospitalmortalitycomparedtoconventional medical therapy were found [22]. However, the percentage of patients needing intubation was signi cantly lower in those with a PaCO2 greater than 45 mmHg. After 30 min, patients receiving NIV had signi cantly higher oxygenation, lower respiratory rate,andbetterhemodynamics. Subsequently, Gray et al. performed a multicenter study of 26 emergency departments, enrollingmorethan1,000patientswithacutecardiogenicpulmonaryedemarandomizedto threetreatmentgroups:standardoxygentherapy,NIVdeliveredascontinuouspositiveairway pressure(CPAP),andNIVaspressuresupportventilation[29].Therewerenodifferencesin 7-and30-daymortalityandintubationratesbetweenthethreegroups.However,NIVwas associatedwithgreaterreductionsindyspnea,heartrate,acidosis,andhypercapniathanthe standardoxygentherapy.PatientsreceivingCPAPorpressuresupportventilationpresented similarratesoftrachealintubation,admissiontointensivecare,andmyocardialinfarction. Theonlystudiesthatgaveusefulinformationarethosethatenrolledpatientsunresponsivetofullmedicaltreatment,testingNIV,orcomparingNIVwithinvasiveventilation.A prospectivetrialinemergencydepartmentswithnoninvasivepressuresupportventilation byamaskonpatientswithacutepulmonaryedemaunresponsivetofullmedicaltreatment (morphine,oxygenmask,diuretics,nitrates)[30]showedthat90-minNIVwasenoughto restorerespiratorycompetenceintheoxygenmask,thusavoidingtheneedforICUadmittance.Thisispossibleifthemeanarterialpressureatemergencydepartmentadmissionis 95mmHgorabove(heartresponsetostressreaction)andthepatientdoesnothaveCOPD. Allotherpatientshavetobegiveninvasiveventilatorysupportwithoutdelay.
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33.3.3 Hematological Malignancy and Mixed Etiology Especiallyinimmunosuppressedpatients,itisfundamentaltolimittheriskofnosocomial infectionasmuchaspossible.Consequently,NIVcanplayasigni cantrole.Principietal., inasmallgroupofhypoxemicpatientswithhematologicalmalignancies,foundthatNIV delivereddirectlyinthehematologydepartmentwithahelmetachievedbetteroxygenation withlongerdurationofapplicationandhighersurvivalratescomparedtoahistoricalgroup of patients [31]. However, in this study the hematologist and intensivists collaborated closelyintreatingthepatients,illustratingtheimportanceofinterdisciplinarycollaborationtoensuretheef cacyofNIVandcarefullyevaluatingthedurationoftreatment.
33.4 Monitoring TheminimumsuggestedmonitoringforNIVpatientsshouldincluderegularassessmentof therespiratory,hemodynamic,andneurologicfunctionsbyadequatelytrainedpersonnel 24h/day[1,32,33].Thisimplies
Arterialbloodgasesafter1hofNIVandatleastevery2h,withcontinuousmonitor-
ing of cutaneous oxygen saturation. Caregivers need to know the factors that can influencethis[34]:anemia,ambientlight,motionartifacts,skinpigmentation,orskin perfusion. Circulatory assessment: noninvasive blood pressure every 5 10 min, skin perfusion (cold,clammy,cyanotic),andurinaryoutput. Electrocardiogram(EKG):continuousmonitoringofrhythmatthesecondleadandif possibleSTanalysis. Overallcontinuousoverallclinicalevaluation:adequacyofrespiratorymechanics,use ofaccessorymusclesand,aboveall,neurologicalstatus. Astandardizedsupervisionsystemregardinglengthoftreatmentisneeded(callifoxygensaturationin1hdoesnotreach90%orfallsbelowthislevel).Completematerialfor emergencyintubationshouldbeimmediatelyavailable.
33.5 Conclusion
NIVcanbedeliveredoutsideICUinselectedpatientswithrespiratoryfailure. Minimum NIV monitoring showed include regular assessment of the respiratory, hemodynamic,andneurologicalfunctions.
Carefullycheckpatientsinthe rst30-90minutesafterstartingNIV. ConsideraprecociousadmissioninIntensiveCareinnon-responsiveNIVpatients.
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References 1. British Thoracic Society Standards of Care Committee (2002) Non-invasive ventilation in acuterespiratoryfailure.Thorax57(3):19 211 2. EvansTW(2001)InternationalConsensusConferencesinIntensiveCareMedicine:non-invasivepositivepressureventilationinacuterespiratoryfailure.OrganizedjointlybytheAmerican ThoracicSociety,theEuropeanRespiratorySociety,theEuropeanSocietyofIntensiveCare Medicine,andtheSocietedeReanimationdeLangueFrancaise,andapprovedbytheATS BoardofDirectors,December2000.IntensiveCareMed27(1):166 178 3. Liesching T, Kwok H, Hill NS (2003) Acute applications of noninvasive positive pressure ventilation.Chest124(2):699 713 4. ElliottMW,ConfalonieriM,NavaS(2002)Wheretoperformnoninvasiveventilation?Eur RespirJ19(6):1159 1166 5. MaheshwariV,PaioliD,RothaarR,HillNS(2006)Utilizationofnoninvasiveventilationin acutecarehospitals:aregionalsurvey.Chest129(5):1226 1233 6. DohertyMJ,GreenstoneMA(1998)Surveyofnon-invasiveventilation(NIPPV)inpatients withacuteexacerbationsofchronicobstructivepulmonarydisease(COPD)intheUK.Thorax 53(10):863 866 7. SinuffT,CookD,RandallJ,AllenC(2000)Noninvasivepositive-pressureventilation:autilizationreviewofuseinateachinghospital.CMAJ163(8):969 973 8. AntroC,MericoF,UrbinoR,GaiV(2005)Non-invasiveventilationasa rst-linetreatment foracuterespiratoryfailure: reallife experienceintheemergencydepartment.EmergMed J22(11):772 777 9. PlantPK,OwenJL,ElliottMW(2000)OneyearperiodprevalencestudyofrespiratoryacidosisinacuteexacerbationsofCOPD:implicationsfortheprovisionofnon-invasiveventilationandoxygenadministration.Thorax55(7):550 554 10. Badiger R, Green M, Hackwood H, Palin C, Shee CD (2004) Non-invasive ventilation in surgicalpatientsinadistrictgeneralhospital.Anaesthesia59(10):967 970 11. Browning J, Atwood B, Gray A (2006) Use of non-invasive ventilation in UK emergency departments.EmergMedJ23(12):920 921 12. BottJ,CarrollMP,ConwayJH,KeiltySE,WardEM,BrownAMetal(1993)Randomised controlledtrialofnasalventilationinacuteventilatoryfailureduetochronicobstructiveairwaysdisease.Lancet341(8860):1555 1557 13. PlantPK,OwenJL,ElliottMW(2000)Earlyuseofnon-invasiveventilationforacuteexacerbations of chronic obstructive pulmonary disease on general respiratory wards: a multicentrerandomisedcontrolledtrial.Lancet355(9219):1931 1935 14. BardiG,PierotelloR,DesideriM,ValdisserriL,BottaiM,PallaA(2000)Nasalventilationin COPDexacerbations:earlyandlateresultsofaprospective,controlledstudy.EurRespirJ 15(1):98 104 15. BarbeF,TogoresB,RubiM,PonsS,MaimoA,AgustiAG(1996)Noninvasiveventilatory supportdoesnotfacilitaterecoveryfromacuterespiratoryfailureinchronicobstructivepulmonarydisease.EurRespirJ9(6):1240 1245 16. PoponickJM,RenstonJP,BennettRP,EmermanCL(1999)Useofaventilatorysupportsystem (BiPAP) for acute respiratory failure in the emergency department. Chest 116(1): 166 171 17. American Thoracic Society (1995) Standards for the diagnosis and care of patients with chronicobstructivepulmonarydisease.AmJRespirCritCareMed152(5Pt2):S77 S121
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18. GirouE,Brun-BuissonC,TailleS,LemaireF,BrochardL(2003)SeculartrendsinnosocomialinfectionsandmortalityassociatedwithnoninvasiveventilationinpatientswithexacerbationofCOPDandpulmonaryedema.JAMA290(22):2985 2991 19. OrganizedjointlybytheAmericanThoracicSociety,theEuropeanRespiratorySociety,the European Society of Intensive Care Medicine, and the Société de Réanimation de Langue Française, and approved by ATSBoard of Directors, December 2000. (2001) International ConsensusConferencesinIntensiveCareMedicine:noninvasivepositivepressureventilation inacuterespiratoryfailure.AmJRespirCritCareMed163(1):283 291 20. Mehta S, Hill NS (2001) Noninvasive ventilation. Am J Respir Crit Care Med 163(2): 540 577 21. Guidelines 2000 for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care (2000).Part7:theeraofreperfusion:section1:acutecoronarysyndromes(acutemyocardial infarction).TheAmericanHeartAssociationincollaborationwiththeInternationalLiaison CommitteeonResuscitation.Circulation102(8Suppl):I172 I203. 22. NavaS,CarboneG,DiBattistaN,BelloneA,BaiardiP,CosentiniRetal(2003)Noninvasive ventilationincardiogenicpulmonaryedema:amulticenterrandomizedtrial.AmJRespirCrit CareMed168(12):1432 1437 23. Guidelinesfortheevaluationandmanagementofheartfailure(1995)ReportoftheAmerican CollegeofCardiology/AmericanHeartAssociationTaskForceonPracticeGuidelines(Committee onEvaluationandManagementofHeartFailure).JAmCollCardiol26(5):1376 1398 24. Thetreatmentofheartfailure(1997)TaskForceoftheWorkingGrouponHeartFailureofthe EuropeanSocietyofCardiology.EurHeartJ18(5):736 753 25. PeterJV,MoranJL,Phillips-HughesJ,GrahamP,BerstenAD(2006)Effectofnon-invasive positivepressureventilation(NIPPV)onmortalityinpatientswithacutecardiogenicpulmonaryoedema:ameta-analysis.Lancet367(9517):1155 1163 26. BerstenAD,HoltAW,VedigAE,SkowronskiGA,BaggoleyCJ(1991)Treatmentofsevere cardiogenic pulmonary edema with continuous positive airway pressure delivered by face mask.NEnglJMed325(26):1825 1830 27. MasipJ,BetbeseAJ,PaezJ,VecillaF,CanizaresR,PadroJetal(2000)Non-invasivepressuresupportventilationversusconventionaloxygentherapyinacutecardiogenicpulmonary oedema:arandomisedtrial.Lancet356(9248):2126 2132 28. KellyCA,NewbyDE,McDonaghTA,MackayTW,BarrJ,BoonNAetal(2002)Randomised controlledtrialofcontinuouspositiveairwaypressureandstandardoxygentherapyinacute pulmonaryoedema;effectsonplasmabrainnatriureticpeptideconcentrations.EurHeartJ 23(17):1379 1386 29. GrayA,GoodacreS,NewbyDE,MassonM,SampsonF,NichollJ(2008)Noninvasiveventilationinacutecardiogenicpulmonaryedema.NEnglJMed359(2):142 151 30. GiacominiM,IapichinoG,CigadaM,MinutoA,FacchiniR,NotoAetal(2003)Short-term noninvasivepressuresupportventilationpreventsICUadmittanceinpatientswithacutecardiogenicpulmonaryedema.Chest123(6):2057 2061 31. PrincipiT,PantanettiS,CataniF,EliseiD,GabbanelliV,PelaiaPetal(2004)Noninvasive continuouspositiveairwaypressuredeliveredbyhelmetinhematologicalmalignancypatients withhypoxemicacuterespiratoryfailure.IntensiveCareMed30(1):147 150 32. Nava S, Navalesi P, Gregoretti C (2009) Interfaces and humidi cation for noninvasive mechanicalventilation.RespirCare54(1):71 84 33. HillNS(2009)Whereshouldnoninvasiveventilationbedelivered?RespirCare54(1):62 70 34. JubranA(1999)Inspiratory owrate:moremaynotbebetter.CritCareMed27(4):670 671
Noninvasive Positive Airway Pressure and Risk of Myocardial Infarction in Acute Cardiogenic Pulmonary Edema
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GiovanniFerrari,AlbertoMilan,andFrancoAprà
34.1 Introduction Acutecardiogenicpulmonaryedema(ACPE)isacommoncauseofrespiratoryfailure. While many patients respond to conventional medical treatment with diuretics, vasodilators,morphine,andoxygen,asubsetofpatientsdevelopssevererespiratory failureandrequiresventilatorysupportandendotrachealintubation(ETI).Noninvasive ventilation,administeredeitherwithcontinuouspositiveairwaypressure(nCPAP)or withpressuresupportventilation(nIPSV),hasbeenemployedinpatientswithsevere respiratorydistress,avoidingtheneedforETIandreducingthecomplicationsrelated tointubation. BothnIPSVandnCPAPhavebeensuccessfullyusedinACPE,improvinggasexchange and vital signs; however, it remains controversial whether one mode is superior to the other.Moreover,forseveralyearsmanyconcernsexistedabouttheuseofnIPSVinACPE because a higher percentage of myocardial infarction was observed in patients treated withnIPSV. Theobjectiveofthischapteristoanalyze,accordingtorecentdataexistinginliterature, therelationship,ifany,betweennoninvasiveventilationanddevelopmentofnewcasesof acutemyocardialinfarctioninpatientswithACPE.
G.Ferrari()andF.Aprà HighDependencyUnit,S.GiovanniBoscoHospital,PiazzaDonatoredelSangue3, Torino,Italy e-mail:
[email protected] A.Milan DepartmentofMedicineandExperimentalOncology,UniversityofTorino,Italy A.M.Esquinas(ed.),NoninvasiveMechanicalVentilation, DOI:10.1007/978-3-642-11365-9_34,©Springer-VerlagBerlinHeidelberg2010
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34.2 Rationale for the Use of Noninvasive Ventilation in Acute Cardiogenic Pulmonary Edema ACPEisacommoncauseofacuterespiratoryfailure.Inthesepatients,themainpriorityisto achieveadequateoxygenationlevelstopreventorgandysfunctionandtheonsetofmultiple organfailure.Themaintenanceofanoxygensaturation(SpO2)inthenormalrangeisimportant tomaximizeoxygendeliverytothetissues.Notwithstandingoptimalmedicaltreatmentwith vasodilators,diuretics,morphine,andsupplementaloxygen,asubsetofpatientswithsevere respiratorydistressisnotabletoimprovegasexchangeandrequiresETI.ETIisassociated withsigni cantmorbidity,increasedhospitallengthofstay,andupperairwaycomplications. Inseveralrandomizedtrials,theapplicationofpositiveintrathoracicpressure(ITP),by either nCPAP or nIPSV, has been employed for the treatment of patients who do not respond to standard medical treatment (SMT) and require respiratory assistance for the severerespiratoryfailureduetotheACPE,avoidingtheneedforETI. WithnCPAP,positivepressureisconstantlyappliedtotheairwaythroughouttheentire respiratorycycletoaspontaneouslybreathingpatient.nIPSVisamodeofpartialventilatorassistanceinwhichthepositivepressureincreasesduringtheinspiratoryphase;however,theairwaypressureismaintainedpositivealsoduringexpiration,althoughtoalesser extent,theso-calledpositiveend-expiratorypressure(PEEP).ComparedtonCPAP,nIPSV hasthepotentialtounloadtherespiratorymusclesmoreeffectivelyandtoreverseorto prevent more effectively ventilatory failure, alveolar hypoventilation, and hypercapnia. However,nIPSV,tothebestofourknowledge,hasnoadvantageasopposedtonCPAPin patientswithACPEinimprovinggasexchangeandclinical physiologicalparameters. Themechanismsresponsibleforimprovementofclinicalparametersinpatientswith pulmonaryedemamaybemorerelatedtotheapplicationofanintrathoracicpositivepressurethantotheventilatorytechniqueitself.ByincreasingITP,theapplicationofpositive pressure to the airways has both respiratory and hemodynamic effects. The respiratory effects are reduced oxygen cost of breathing and improvement in functional residual capacityandpulmonarycompliancethroughrecruitmentofatelectaticalveoli.Thehemodynamic effects are reduced venous return and lower left ventricle transmural pressure (i.e.,afterload),whichisprimarilyduetothereductioninthenegativeswingsoftheITP duringinspiration.Infact,inpatientswithACPE,theincreasedamplitudeofinspiratory swingsleadstoalowerITP.AdecreasedITPcontributestotheincreaseinleftventricle afterloadbyincreasingleftventricletransmuralpressure(i.e.,thedifferencebetweenthe insideandtheoutsideoftheheart).Theincreaseintransmuralpressureleadstoagreater preloadandafterloadoftheheartduringdiastoleandsystole,respectively.So, llingofthe leftventricleisincreasedwhileemptyingisreduced;theresultisanincreasedleftventricle afterloadandpulmonaryvascularcongestion.Instead,reductioninintrathoracicinspiratorypressureswings(byeithernCPAPornIPSV)reducesleftventricletransmuralpressureandthusleftventricleafterloadandpulmonarycongestion.Thesemechanismsmay explainwhytheapplicationofapositiveITP(evenwithoutpressuresupport)improves pulmonary compliance and respiratory mechanics and optimizes left ventricle function, providingef cacyintreatingpatientswithACPE.
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34.3 Noninvasive Ventilation and Risk of Acute Cardiogenic Myocardial Infarction AlthoughnCPAPandnIPSVarebotheffectiveinimprovinggasexchangeandclinical physiologicalparametersinACPE,forseveralyearsmanyconcernsexistedabouttheuse ofnIPSVinACPE.In1997,Mehtaandcoworkers[1]interruptedprematurelyarandomizedstudycomparingnCPAPtonIPSVbecauseahigherpercentageofmyocardialinfarctionratewasdetectedinpatientsenrolledinthenIPSVgroup.Theauthorspointedoutthe possiblehazardofthehigherintrapulmonarypressuredeliveredbynIPSVasopposedto nCPAP;infact,theydeliverednIPSVwithaventilatornotprovidedwithasophisticated expiratorytriggersystem,sothatairleaks,whenpresent,couldinterferewithcyclingoff thesystem(so-calledinspiratoryhangup).However,themostimportantissueinthisstudy wasthat71%ofpatientsinthenIPSVgroup,ascomparedto31%ofpatientsinthenCPAP group,hadchestpainonstudyentry,suggestingthattheobserveddifferenceinmyocardial infarctionratewasprobablyconsequenttoabiasintheselectionandallocationofpatients ratherthantotheventilatorytreatmentassigned. nCPAPhasbeenshowntobesafeandeffectiveinpatientswithACPEwithoutincreasing the myocardial infarction rate. Several studies have compared nCPAP to SMT in patientswithACPE.AsassessedinarecentreviewoftheCochraneCollaboration[2],no differenceinmyocardialinfarctionriskwasevidentbetweenthetwogroups.Moreover,in 1998, Takeda and coworkers [3] showed that nCPAP was safe and effective in treating patientswithacutemyocardialinfarctioncomplicatedbyACPE.Inthisstudy,22patients withmyocardialinfarctionassociatedwithACPEwererandomizedtonCPAPortoSMT. TheETIrateandhospitalmortalityweresigni cantlylowerinthenCPAPgroup. Inthefollowingyears,otherstudiessuggestedcautionintreatingACPEwithnIPSV.In 2000,Sharonandcoworkers[4]compared,inpatientswithACPE,theef cacyandsafetyof nIPSVplusalowdoseofisosorbidedinitrateversusnoventilatorytreatmentplushighdoses ofisosorbidedinitrate.FortypatientswererandomizedtoreceivenIPSVplusstandarddose isosorbidedinitrateversusoxygenplushigh-doseisosorbidedinitrate.Patientstreatedwith nIPSVhadsigni cantlymoreadverseevents;infact,theauthorsreportedahighpercentage ofmyocardialinfarctionanddeathsinthe rstgroupcomparedtopatientstreatedwithmedicaltherapyonly.However,itshouldbenotedthattheamountofinspiratoryandexpiratory pressuresappliedtotheairwayinthenIPSVgroupwereextremelylow(withameanof9.3 [2.3]cmH2Oofpressuresupportand4.2[3.1]cmH2OofPEEP),andthatmedicaltreatment wassigni cantlydifferentinthetwogroups,whichmakescomparisonunfair.Moreover,the treatmentwasdeliveredinaprehospitalphasebymobileintensivecareunits,whichcould haveaffectedthecorrectapplicationofnoninvasivepressuresupportventilation. Inanuncontrolledstudy,Rusterholtz[5]observedahigherpercentageofmyocardial infarctioninpatientswithACPEwhofailednIPSVtreatment,suggestingtheneedtoavoid nIPSVinpatientswithacutemyocardialinfarction. Inanotherstudy,Craneandcoworkers[6]didnotobserveasigni cantdifferencein myocardial infarction rate between patients treated with nCPAP as opposed to nIPSV, althoughanonsigni canttrendtowardhighermedianpeakcreatinekinasewasobserved inthenIPSVgroupascomparedtothenCPAPgroup.
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Otherrandomizedcontrolledstudies[7 9]comparednCPAPtonIPSVandfoundno increasedincidenceofnewonsetofmyocardialinfarctioneventhoughthenewonsetof myocardialinfarctionwasnottheprimaryendpointinthesestudies. InstudiescomparingnIPSVtoSMT,noassociationbetweennIPSVandmyocardial infarctionwasobserved.InfactinthestudiesofMasipandcoworkers[10]andNava[11] andcoworkers,theauthorsfoundasimilarproportionofpatientswithmyocardialinfarctioninbothgroups. Finally,thestudiesdidnotdistinguishclearlybetweenmyocardialinfarctionatrandomization or evolving during or after ventilatory treatment (with either nCPAP or nIPSV).Moreover,inmanystudies,myocardialinfarctioncriteriawerenotclearlyestablished,anditwasnotspeci edifmyocardialnecrosiswasprimaryoriftheincreasein cardiacmarkers,whichsometimesisobservedinpatientswithACPE,issecondarytoan imbalancebetweenmyocardialoxygendemandandsupply,eveninabsenceofcoronary stenosis. Cardiac markers, in fact, re ect myocardial necrosis but do not indicate its mechanism. ToclarifythepotentialharmofnIPSVintreatingpatientswithACPE,tworandomized controlledstudies[12,13]analyzedtherelationbetweenthetwoventilatorymodalities (nCPAPandnIPSV)andtheincidenceofnewonsetofmyocardialinfarction.Toavoid anypotentialconfoundingfactor,bothstudiesexcludedallpatientswithahistoryofchest pain, electrocardiogram (ECG) modi cations such as ST segment elevation or depression,T-waveinversion,newonsetofleftbundle-branchblock,andelevatedmarkersof cardiac ischemia at presentation. In both studies, myocardial infarction was de ned accordingtotheinternationalguidelines[14],whenchestpain,modi cationsof12-lead ECG,andincreaseincardiacmarkers(troponinI)wereallpresent.Themaindifference betweenthesetwostudiesisthatwhilethestudyofBellone[12]includedpatientswho hadanairwaytractinfectionasthemainprecipitatingcauseofACPE,inourstudy[13] weincludedonlypatientswithacardiogenicprecipitatingfactor.BothstudiesdemonstratedthannIPSVisaseffectiveasnCPAPinimprovingclinical physiologicalparameters,andthattherateofnew-onsetmyocardialinfarctionisnotdifferentwiththetwo techniques. Accordingtoameta-analysispublishedin2006[15],therewasnodifferenceinmyocardialinfarctionriskbetweenpatientstreatedwithnCPAPandSMT.However,results comparing nCPAP to nIPSV showed a not signi cant trend toward an increase in new onset of acute myocardial infarction in patients treated with nIPSV (relative risk [RR] 2.10,95%con denceinterval[CI]0.91 4.84;p=0.08;I2=25.3%).But,thismeta-analysisdidnotincludethreestudies[9,13,16],twoofthempublishedin2007andonein2008. TherelativeriskgraphofacutemyocardialinfarctionafterinclusionofallstudiescomparingnCPAPandnIPSVisshowninFig.34.1. Figure34.1showsthattheriskratioforacutemyocardialinfarctionwasnotsigni cantly different between patients treated with nIPSV and patients treated with nCPAP (RR1.31,95%CI0.70 2.45;p=0.40;I2=34%). Wecanconcludethatthereisnoevidenceoftheincreaseofnew-onsetacutemyocardialinfarctionduringtreatmentwithnIPSVplusSMTascomparedtonCPAPplusSMT.
34
Noninvasive Positive Airway Pressure and Risk of Myocardial Infarction in Acute Cardiogenic Pulmonary Edema
nIPSV nCPAP Study or Subgroup Events Total Events Total Weight Bellone 2004 Crane 2004 Ferrari 2007 Mehta 1997 Moritz 2007 Park 2004 Rusterholtz 2008
2 9 4 10 3 0 3
24 20 25 14 50 27 17
3 3 8 4 2 0 4
22 20 27 13 59 27 19
10.7% 18.6% 20.3% 25.2% 10.2% 15.1%
Risk Ratio M-H, Random, 95% CI
235
Risk Ratio M-H, Random, 95% CI
0.61 [0.11, 3.32] 3.00 [0.95, 9.48] 0.54 [0.19, 1.57] 2.32 [0.96, 5.60] 1.77 [0.31, 10.18] Not estimable 0.84 [0.22, 3.22]
Total (95% CI) 1.31 [0.70, 2.45] 117 187 100.0% 31 24 Total events 2 2 2 Heterogeneity: Tau = 0.20; Chi = 7.56, df = 5 (P = 0.18); I = 34% 0.01 0.1 1 10 100 Test for overall effect: Z = 0.85 (P = 0.40) Favours experimental Favours control
Fig. 34.1 RiskratioofacutemyocardialinfarctioninthestudiescomparingnIPSV(noninvasive pressure support ventilation) versus nCPAP (noninvasive continuous positive airway pressure). (Note:Intheirstudy,Rusterholtzandcoworkersusedproportionalassistedventilation[PAV]and notpressuresupportventilation)
Key Recommendations
› › › › ›
nCPAPandnIPSVareequallyeffectiveintreatingpatientswithsevereacute respiratoryfailuresecondarytoACPE. nCPAPisrecommended,inadditiontoSMT,inpatientswithsevererespiratory distressduetocardiogenicpulmonaryedema(classIIarecommendation,level ofevidenceA). Nodifferenceinmyocardialinfarctionriskhasbeenshownbetweenpatients treatedwithnCPAPversusoxygenplusSMTorpatientstreatedwithnIPSV versuspatientstreatedwithoxygenplusSMT[2]. nCPAPcanbeconsideredthe rst-lineinterventioninpatientswithACPE becauseoftheeaseofuseandofthelowercostandbecausenIPSVdidnot showbetteref cacy. Inconclusion,theanalysisofthecurrentliteratureshowedthat noninvasiveventilationwasnotharmful,andthattherateofacutemyocardial infarctionwasnotdifferentwithbothnCPAPandnIPSV.
References 1. MehtaS,JayGD,WoolardRHetal(1997)Randomized,prospectivetrialofbilevelversus continuouspositiveairwaypressureinacutepulmonaryedema.CritCareMed25:620 628 2. VitalFMR,SaconatoH,LadeiraMTetal(2008)Non-invasivepositivepressureventilation (CPAPorbilevelNPPV)forcardiogenicpulmonaryedema(review).CochraneDatabaseSyst Rev16.doi:10.1002/14651858.CD005351
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3. TakedaS,NejimaJ,TakanoTetal(1998)Effectofnasalcontinuouspositiveairwaypressure onpulmonaryedemacomplicatingacutemyocardialinfarction.JpnCircJ62:553 558 4. SharonA,ShpirerI,KaluskiEetal(2000)High-doseintravenousisosorbide-dinitrateissafer andbetterthanBi-PAPventilationcombinedwithconventionaltreatmentforseverepulmonaryedema.JAmCollCardiol36:832 837 5. Rusterholtz T, Kempf J, Berton C et al (1999) Noninvasive pressure support ventilation (NIPSV)withfacemaskinpatientswithacutecardiogenicpulmonaryedema(ACPE).Intensive CareMed25:21 28 6. Crane SD, Elliott MW, Gilligan P et al (2004) Randomised controlled comparison of continuouspositiveairwayspressure,bilevelnon-invasiveventilation,andstandardtreatmentin emergencydepartmentpatientswithacutecardiogenicpulmonaryoedema.EmergMedJ21: 155 161 7. ParkM,Lorenzi-FilhoG,FeltrimMIetal(2001)Oxygentherapy,continuouspositiveairway pressure,ornoninvasivebilevelpositivepressureventilationinthetreatmentofacutecardiogenicpulmonaryedema.ArqBrasCardiol76:221 230 8. ParkM,SangeanMC,VolpeMdeSetal(2004)Randomized,prospectivetrialofoxygen, continuous positive airway pressure, and bilevel positive airway pressure by face mask in acutecardiogenicpulmonaryedema.CritCareMed32:2407 2415 9. RusterholtzT,BollaertPE,FeisselMetal(2008)Continuouspositiveairwaypressurevs. proportional assist ventilation for noninvasive ventilation in acute cardiogenic pulmonary edema.IntensiveCareMed34:840 846 10. Masip J, Betbesé AJ, Páez J et al (2000) Non-invasive pressure support ventilation versus conventional oxygen therapy in acute cardiogenic pulmonary oedema: a randomised trial. Lancet356:2126 2132 11. NavaS,CarboneG,DiBattistaNetal(2003)Noninvasiveventilationincardiogenicpulmonaryedema:amulticenterrandomizedtrial.AmJRespirCritCareMed168:1432 1437 12. BelloneA,MonariA,CortellaroFetal(2004)Myocardialinfarctionrateinacutepulmonary edema:noninvasivepressuresupportventilationversuscontinuouspositiveairwaypressure. CritCareMed32:1860 1865 13. FerrariG,OlliveriF,DeFilippiGetal(2007)Noninvasivepositiveairwaypressureandrisk ofmyocardialinfarctioninacutecardiogenicpulmonaryedema:continuouspositiveairway pressurevsnoninvasivepositivepressureventilation.Chest132:1804 1809 14. The Joint European Society of Cardiology/American College of Cardiology Committee (2000)Myocardialinfarctionrede ned:aconsensusdocumentoftheJointEuropeanSociety ofCardiology/AmericanCollegeofCardiologyCommitteefortherede nitionofMyocardial Infarction.EurHeartJ21:1502 1513 15. HoKM,WongK(2006)Acomparisonofcontinuousandbi-levelpositiveairwaypressure non-invasiveventilationinpatientswithacutecardiogenicpulmonaryoedema:ameta-analysis. CritCare10:R49.doi:10.1186/cc4861 16. MoritzF,BrousseB,GelléeBetal(2007)Continuouspositiveairwaypressureversusbilevel noninvasive ventilation in acute cardiogenic pulmonary edema: a randomized multicenter trial.AnnEmergMed50:666 675
The Role of Continuous Positive Airway Pressure in Acute Cardiogenic Pulmonary Edema with Preserved Left Ventricular Systolic Function: A Preliminary Study
35
AndreaBellone
35.1 Introduction Manypatientspresentingwithacutecardiogenicpulmonaryedema(ACPE)havepreserved leftventricular(LV)systolicfunctionandareaffectedbydiastolicdysfunction.Inthese patients,survivalissimilartothatofpatientswithreducedejectionfraction[1,2]. Theaimofourpreliminarystudywastoevaluate,intheemergencysetting,theeffects ofcontinuouspositiveairwaypressure(CPAP)inpatientswithACPEandpreservedLV systolicfunctionwithregardtoresolutiontime.
35.2 Methods PatientsdiagnosedwithACPEintheemergencyroomwererecruitedandenrolled.All patientsunderwentamorphologicalechocardiographicinvestigationshortlybeforeCPAP. Two-dimensionalechocardiogramwasperformedtoqualitativelyestimatetheLVsystolicfunction.PatientswereconsideredtohaveLVsystolicdysfunctioniftheejection fractionwasestimatedaslessthan45%.Intheabsenceofthisconditionandsigni cant valvularabnormalities,patientswereconsideredtohavepreservedsystolicfunction.The competency of emergency physician ultrasonographers was demonstrated through multiplesteps.
A.Bellone DepartmentofEmergency-OspedaleValduce,22100Como,Italy e-mail:
[email protected] A.M.Esquinas(ed.),NoninvasiveMechanicalVentilation, DOI:10.1007/978-3-642-11365-9_35,©Springer-VerlagBerlinHeidelberg2010
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35.3 Study Design PatientswithpreservedsystolicfunctionACPE(groupA=18patients)andsystolicdysfunctionACPE(groupB=18patients)wereimmediatelysubmittedtoechocardiographic evaluationjustbeforetheybegantreatmentwithnitrates,furosemide,morphine,andCPAP. Patientswere ttedwithanoronasalmaskandwereconnectedtoCPAPadjustedto10cm H2O.Thefractionofinspiredoxygen(Fio2)wasdeliveredtoachieveanSpo2of96%. When the goal Spo2 of 96% was reached, the Fio2 was maintained constant. Standard medicaltreatmentwasstartedandconsistedofthefollowing:continuousinfusionofglyceryltrinitrate(15mg/250mLofsaline)atarateof50mL/handsubsequentlyaccordingto thearterialbloodpressureresponse,60mgfurosemideIV,and2mgmorphinesulfateIV asneeded.Weusedasystemicsystolicpressureof90mmHgasthelower-limitcriterion forstoppingglyceryltrinitrate. Resolution of acute pulmonary edema was de ned as evident clinical improvement withbotharespiratoryrateoflessthan30breaths/minandSpo2of³96%withoxygen (Fio2=0.35).Thetimeforthesecriteriatobemetwascalledtheresolutiontime.
35.4 Results TheresultsarereportedinTables35.1 35.3.
35.5 Discussion Theresultsofthepresentpreliminarystudyshowedthat,inpatientswithACPEandpreserved LV systolic function, resolution time was not signi cantly different in comparison withpatientsaffectedbysystolicdysfunction.Thus,thismightsuggestthatCPAPinpatients withACPEwithpreservedordepressedsystolicventricularfunctionisequallywelltolerated. Diastolicdysfunctionisdeterminedbyabnormalpassiveelasticpropertiesoftheleftventricle andanimpairedprocessofactiverelaxation[3].Underthesecircumstances,anelevatedarterialbloodpressure,myocardialischemia,tachyarrythmia,orrespiratoryinfectionmayresult inacutepulmonaryedemabyanincreaseinatrialandvenouspulmonarypressures[3]. Thediagnosisofdiastolicheartfailurecanbemadeonthebasisofclinicalevidenceof heart failure in a patient has a normal LV ejection fraction, no valvular abnormalities and abnormalLVrelaxation,diastolicdistensibility,ordiastolicstiffnessonechocardiography[3].
35 The Role of Continuous Positive Airway Pressure in Acute Cardiogenic Pulmonary Edema
239
Table 35.1 Baseline characteristics of the patients, history, and causes of acute pulmonary edema(dataexpressedasabsolutenumberormean±standarddeviationornumber[%]) GroupA(n=18) GroupB(n=18) Age
80.1±6.8
75.2±11.2
Sex,male/female
5/13
11/7
APACHEIIscore[4]
17.3±2.4
16.8±3
Arterialhypertension
15(83%)
8(44%)*
OSAS
1(5%)
1(5%)
Diabetes
11(61%)
9(50%)
Atrial brillation
3(16%)
4(22%)
Chronicrenalfailure
3(17%)
5(28%)
Chronicheartfailure
0
2(11%)
Ischemicheartdisease
7(39%)
13(72%)*
COPD
1(5%)
0
Hypertension
12(67%)
6(33%)*
Myocardialinfarction
5(28%)
4(22%)
Lowerairwayinfection
7(39%)
6(33%)
History
CausesofACPE
Atrial brillation 3(17%) 5(28%) COPDchronicobstructivepulmonarydisease,OSASobstructivesleepapneasyndrome *p<0.05(Fishertest)
Aurigemmaandcolleagues[3]suggestedthattheeffectsofpositivepressuretherapy compromisevenousreturnanddecreaseLVenddiastolicvolume,furtherlimitingstroke volumeandhencecardiacoutputbecauseofthesteepcurveforLVdiastolicpressurein relationtovolumewithresultantdeteriorationinhemodynamics.Incontrast,ourresults seemtodemonstratethatCPAPisequallyassafeandeffectiveinpatientswithimpaired systolicanddiastolicventricularfunctionandACPE. Inconclusion,theresultsofthispreliminarystudyshowedthatACPEresolvesasfast in patients with preserved systolic function as in those with systolic heart dysfunction. CPAPresultswelltoleratedinbothclinicalconditions.
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Table 35.2 Physiologicaldataatstudyentryandprogression GroupA(n=18) GroupB(n=18) Studyentry After1h Studyentry
After1h
pH
7.26±0.13
7.35±0.06*
7.27±0.09
7.36±0.05*
Paco2
51±12.5
41.6±7.8*
51.7±10.2
42±4.2*
Pao2/Fio2
182.2±34.9
231±72*
177.9±39.9
232±68*
Spo2
76±11.4
93.4±4.1*
80.9±9.3
92.5±7.6*
HCO3
21.8±4.1
22.7±3.4*
21.8±3.5
23.1±2.5*
Heartrate
111±15
91±17*
106±19
88±16*
Respiratoryfrequency
44±4
24±6*
41±6
27±6*
Systolicpressure
195±22
128±24*
170±38**
134±22*
Diastolicpressure
102±15
67±11*
86±18**
75±10*
Ejectionfraction
>45%
31%±5%**
Glycemia
226±67
236±75
BNP 1142±643 1566±1317 BNPbrainnatriureticpeptide *p<0.05(Studentttest)ingroupbetweenstudyentryandafter1h **p<0.05(Studentttest)betweengroupsatstudyentry Table 35.3 Patients outcome pvalue
GroupA(n=18)
GroupB(n=18)
CPAPtreatment failure
1
1
In-hospitaldeaths
0
0
Endotrachealintubation
1(5%)
0
0.99*
80±33.4min
0.17
Resolutiontime 64±25min CPAPcontinuouspositiveairwaypressure *Fisher sexactp,twotailed a n=15,Mann WhitneyUtest a
References 1. Owan TE, Hodge DO, Herges RM et al (2006) Trends in prevalence and outcome of heart failurewithpreservedejectionfraction.NEnglJMed355:251 259 2. BhatiaRS,TuJV,LeeDSetal(2006)Outcomeofheartfailurewithpreservedejectionfraction inapopulation-basedstudy.NEnglJMed355:260 269 3. AurigemmaGP,GaaschWH(2004)Diastolicheartfailure.NEnglJMed351:1097 1105 4. KnausWA,DraperEA,WagnerDPetal(1985)APACHEII:aseverityofdiseaseclassi cation system.CritCareMed13:818 829
Noninvasive Ventilation in Acute Lung Injury/Acute Respiratory Distress Syndrome
36
RiteshAgarwal
36.1 Introduction The acute respiratory distress syndrome (ARDS) is a clinical syndrome of lung injury characterizedbyseveredyspnea,refractoryhypoxemia,andbilateralradiographicopacities.Itisclinicallyde nedbythefollowingcriteria:acuteonset(lessthan7days),bilateral alveolaropacitiesconsistentwithpulmonaryedema,Pao2/Fio2<200,pulmonaryartery occlusionpressurelessthan18mmHg,ornoclinicalevidenceofleftatrialhypertension [1].Itisnowrecognizedthatthereisagradationoftheseverityofclinicallunginjury: patientswithless-severehypoxemia(de nedbyaPao2/Fio2ratioof300orless)areconsideredtohaveacutelunginjury(ALI),andthosewithmoreseverehypoxemia(de ned byaPao2/Fio2ratioof200orless)areconsideredtohaveARDS[1].Themainstayoftreatment for patients with ALI/ARDS is intubation and mechanical ventilation. However, endotrachealintubationisassociatedwithsigni cantmorbidity,includingupperairway trauma,barotrauma,andpneumonia[2 4].Asaresult,anyinterventionthatobviatesthe needforendotrachealintubationinALI/ARDSiswelcome. Noninvasiveventilation(NIV)istheapplicationofventilatorysupportwithoutaninvasiveendotrachealairway.Ithasrevolutionizedthemanagementofdiversecausesofacute respiratoryfailure(ARF)[5].Itnotonlyavoidstheneedforendotrachealintubationbut alsoreducesothercomplications,suchasoccurrenceofnosocomialinfections,durationof intensivecareunit(ICU)stay,andtheoverallcostofhospitalization[6].ThetermNIV encompassesarangeofmodestoaugmentalveolarventilationwithoutanarti cialairway; continuouspositiveairwaypressure(CPAP)andnoninvasivepositivepressureventilation (NIPPV)arethemostcommonlyusedmodes.InNIPPV,twodifferentpressuresareused: inspiratory positive airway pressure (IPAP) and expiratory positive airway pressure (EPAP), whereas CPAP maintains a constant positive airway pressure throughout the respiratorycycle.Theoretically,NIPPVmayconferanadvantageoverCPAPbyreducing theworkofbreathingduringinspirationbyprovidingadditionalinspiratorypressure[7].
R.Agarwal DepartmentofPulmonaryMedicine,PostgraduateInstituteofMedical EducationandResearch,Sector-12,Chandigarh160012,India e-mail:
[email protected] A.M.Esquinas(ed.),NoninvasiveMechanicalVentilation, DOI:10.1007/978-3-642-11365-9_36,©Springer-VerlagBerlinHeidelberg2010
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RelativelylittledebatesurroundsitsuseforARFduetoexacerbationsofchronicobstructivepulmonarydisease[8].However,itsappropriateusetotreathypoxemicrespiratory failure,particularlyregardingpatientswithALI/ARDS,remainsunclear.
36.2 Physiological Basis for NIV in ALI/ARDS ThereisastrongphysiologicalbasisfortheuseofNIVinALI/ARDS.Inastudyonthe physiologicaleffectsofNIVinARDS,L Heretal.measuredbreathingpattern,neuromusculardrive,inspiratorymuscleeffort,arterialbloodgases,anddyspneawithNIPPVand CPAP.AlthoughtheoxygenationincreasedwithCPAP,tidalvolumeincreasedonlywith NIPPVbutnotwithCPAPalone.Theworkofbreathingwasloweranddyspneareliefwas signi cantlybetterwiththeNIPPV.InpatientswithALI/ARDS,NIPPVcanthusreduce inspiratorymuscleeffortanddyspnea,andtheapplicationofoptimallevelsofCPAPcan improveoxygenation[9].However,onehastobalanceCPAPtoimproveoxygenationon theonehandandincreasethepressuresupportabovetheCPAPtoaugmentthetidalvolume,relievedyspnea,anddiminishrespiratorymuscleeffortontheother. Patients with ALI/ARDS have diffuse alveolar damage and represent those with the mostsevereformofhypoxemicrespiratoryfailure.ThemaingoalsofNIVinpatientswith ALI/ARDSaretoimproveoxygenation,unloadtherespiratorymuscles,andrelievedyspnea.Alltheseeffectswouldtranslateintoclinicalendpointsofdiminutionofintubation rates.InpatientswithhypoxemicARF,NIPPVisaseffectiveasconventionalventilation incorrectinggasexchange[10].However,onlylimiteddataarecurrentlyavailableinthe literatureontheroleofNIVinARDS(Table36.1)[11 19],andmanyrecentstudieshave suggestedthatALI/ARDSisanindependentfactorofNIVfailureinpatientswithhypoxemicARF[13,20,21].Currently,theroleofNIVinALI/ARDSisatbestcontroversial. In ARDS, transient loss of positive end-expiratory pressure (PEEP) during ventilation leadstolungderecruitmentandmayseriouslycompromisegasexchange.Asystematic reviewsuggestedthattheadditionofNIPPVtostandardmedicaltherapyinpatientswith hypoxemicARFreducestherateofendotrachealintubation,ICUlengthofstay,andICU mortality.However, the trial results were signi cantly heterogeneous [22]. Further, this reviewdidnotspeci callyreportoutcomesinpatientswithALI/ARDS.
36.3 Studies Investigating the Use of NIV in ALI/ARDS NIVhasbeensuccessfullyusedincasesofALI/ARDS,whicharerapidlyreversiblewith treatment[23,24].Onlythreerandomizedcontrolledtrialswithatotalof111patientshave studiedtheeffectsofNIVinALI/ARDS[11,20,25].Ameta-analysisofthesethreestudiessuggestedthattheadditionofNIVtostandardcareinpatientswithALI/ARDSdidnot reducetherateofendotrachealintubationorICUmortality[26].
354
24
20
54
147
47
40
P
P
P
P
P
R
P
Antonelli [13]
Confalonieri [14]
Cheung [15]
Rana[16]c
Antonelli [17]
Yoshida [18]
Agarwal [19]
21
47
147
54
20
24
86
64
40
41.5(23.9)
69(11)
53(17)
60 (46.2 83.7)
51.4(14.2)
37(9)
45(16)
60(18 88)
12(57.1)
13(28)
54(37)
21(39)
9(45)
29(45)
23(39)
14.9(2.9) APACHEII
17.5(8) APACHEII
35(9)SAPS II
55.5(43 103.5) APACHE III
37(9) SAPSII
56(16) SAPSII
32(6 87) SAPSII
48.3(9.1)
29(6)
36(5)
7.42(0.06)
7.35(0.07)
7.4(0.08)
131.2 (45.7)
123.5(47)
110.5 (33.5)
112 (70 209)
23 (21 39)
122(44)
128(32)
140 (59 288)
137.5 (51.6) 7.37 (7.26 7.45)
7.44(0.06)
7.42 (7.21 7.62)
28.9 (6.2)
35(7)
34 (20 60)
Pao2/Fio2 ratio, mean (SD)
32.2(7.3)
38(10)
40(13)
36(32 48)
33.9(4.6)
29(7)
37(23 61)
PaCO2, mean (SD)
Noninvasive Ventilation in Acute Lung Injury/Acute Respiratory Distress Syndrome
ALI/ARDSacutelunginjury/acuterespiratorydistresssyndrome,APACHEAcutePhysiologyandChronicHealthEvaluation,NIVnoninvasiveventilation, Pprospective,Rretrospective,SAPSSimpli edAcutePhysiologyScore,SDstandarddeviation a DetailsofthewholegroupreceivingNIVandnotspeci callyALI/ARDSpatients b Allvaluesinthisstudywereexpressedasmedian(5th 95thpercentile) c Allvaluesinthisstudywereexpressedasmedian(range)
64
P
Hilbert [12]
40
P
Delclaux [11]a,b
Table 36.1 BaselinecharacteristicsofthepatientsincludedinstudiesinvestigatingtheuseofNIVinALI/ARDS Respiratory pH,mean Severity Age,mean Female No.of No.of Study Type rate,mean (SD) score, (SD) gender, patients ALI/ of (SD) mean(SD) No.(%) ARDS study
36 243
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R. Agarwal
Antonellietal.investigatedtheuseofNIVforARFinpatientsundergoingsolidorgan transplantationandobservedmorepatientsintheNIVgroupimprovingtheirPaO2/Fio2 ratios.Alsotherewassigni cantreductioninintubationratesandICUmortalityoverall, butthiswasnotsigni cantifonlythesubgroupofpatientwithALI/ARDSwasincluded [25].Delclauxetal.foundthat,despiteearlyphysiologicimprovement,theapplication ofCPAPneitherreducedtheneedforintubationnorimprovedoutcomesinpatientsin ALI/ARDS[11].InalargemulticenterstudyinvestigatingpredictorsofNIVfailurein thosewithhypoxemicARF,theintubationratewas30%overallbutwas51%inpatients withARDS.Thestudyidenti edthefollowingpredictorsofNIPPVfailure:agemore than40years,Pao2/Fio2ratiolessthan146,Simpli edAcutePhysiologyScore(SAPS) II score more than 34, and the ARDS/pneumonia as an etiology of hypoxemic ARF. Confalonierietal.,inaseriesofseverepneumocystispneumonia-relatedARF,foundthat NIPPVavoidedintubationintwothirdsofpatients.Notonlywastheavoidanceofintubationassociatedwithimprovedsurvival(100%vs.38%),butalsoNIPPVdecreasedthe needforinvasivedevicesandICU-relatedworkload[14].Inaninterestingobservational study,Ranaetal.observedNIVfailureinallpatientswithARDSandconcomitantshock. InthesubgroupofpatientswithARDSbutwithoutshock,metabolicacidosisandsevere hypoxemia predicted NIPPV failure [16]. In a multicenter study of 147 patients with ARDS,NIPPVdecreasedintubationratesin54%ofpatients.ASAPSIIscoremorethan 34andaPao2/Fio2scorelessthan175after1hofNIPPVwereindependentlyassociated withNIPPVfailureandneedforendotrachealintubation[17].Ourexperiencehasalso been almost similar. In a prospective study of 40 patients with hypoxemic ARF, we observedNIVfailurein57.1%(12/21)intheALI/ARDSgroupand36.8%(7/19)patients inthegroupwithAHRFduetoothercauses.Intheunivariatelogisticregressionmodel, theonlyfactorassociatedwithNIPPVfailurewasthebaselinePao2/Fio2ratio[19]. IfwecombineallthestudiesinTable36.1,theintubationandICUmortalityrateswith theuseofNIPPVinALI/ARDSare47%(95%con denceinterval[CI]37 58)and33% (95%CI22 44),respectively(Figs.36.1and36.2).
36.4 Practical Application of NIPPV in ALI/ARDS NIPPV is de nitely bene cial in selected patients with ALI/ARDS and can potentially preventintubationinalmost50%ofpatients.Theissueisthechoiceoftherightpatient whowillbene tfromNIV.Theidenti cationofpatientswithALI/ARDSwhoshouldbe managedwithNIVischallenging,partlybecausetherearefewreliableselectioncriteria. Overall, the ndings of various studies (Table 36.1) suggest a prudent approach, and it seemssensibletoexcludepatientswhohavemultiorgandysfunctionorarepoorcandidatesforNIVbyvirtueofinabilitytocooperateorprotecttheairwayorbecauseofexcessivesecretions.Clearly,NIVshouldbeavoidedinpatientswithshock,severehypoxemia, oracidosis.Themoredif cultissueistodecidethethresholdofseverityforhypoxemia and acidosis beyond which NIV should be considered contraindicated. There are no answersforthis,andtheapplicationofNIPPVinthosewithALI/ARDSshouldbelimited
36
Noninvasive Ventilation in Acute Lung Injury/Acute Respiratory Distress Syndrome
245
Fig. 36.1 IntubationratesinpatientswithALI/ARDS(acutelunginjury/acuterespiratorydistress syndrome)managedwithnoninvasiveventilation(randomeffectsmodel).Theintubationratesin theindividualstudiesarerepresentedbyasquare(percentage)throughwhichrunsahorizontal line(95%con denceinterval).Thediamondatthebottomrepresentsthepooledintubationrates fromthestudies.*Immunocompromisedpatients
Fig. 36.2 MortalityratesinpatientswithALI/ARDS(acutelunginjury/acuterespiratorydistress syndrome)managedwithnoninvasiveventilation(randomeffectsmodel).*Immunocompromised patients
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Table 36.2 PracticalapproachtotheuseofnoninvasiveventilationinpatientswithALI/ARDS 1.Usejudiciously. 2.Likelytobene tselectedpatientswithALI/ARDS,especiallyearlyduringthecourse: (a) Absenceofseverehypoxemiaattheoutset (b) Nomajororgandysfunction[12](suchasacuterenalfailurerequiringdialysis) (c) Absenceofhypotension[16]orcardiacarrhythmias (d) Simpli edAcutePhysiologyScore(SAPS)IIof34ormore[17] 3.UseofNIPPVpreferredoverCPAP[9]. 4.Useofcriticalcareventilatorwithoxygenblenderpreferredoverdomiciliaryventilator withexternaloxygensupply. 5.Position:headendelevatedat45°angle. 6.Interface:oronasalmask. 7.Protocol:startwithIPAP/EPAPof8/4cmH2O.IPAPisincreasedinincrementsof2 3cm H2O(maximum20cmH2O)toobtainanexhaledtidalvolumeof6mL/kgandarespiratory rateof30breaths/min.EPAPisincreasedinincrementsof1 2cmH2O(maximum10cm H2O)toensureanoxygensaturationof92%withthelowestFio2possible[17]. 8.TrialofNIPPVfor1 4h: (a) Monitorrespiratoryrate,pH,Pao2/Fio2ratios (b) HighlikelihoodoffailureifPao2/Fio2is175orlessafter1h[17]:closeobservation 9.Weaning:duringtheinitialperiod,continuouslyadministerNIPPV,thenformajorityofthe timeuntiloxygenationandclinicalstatusimproved.ProgressivelyreducetheuseofNIPPV inaccordancewiththedegreeofclinicalimprovement.OnceEPAPrequirementsdecrease to5cmH2O,evaluatewhilethepatientisbreathingsupplementaloxygenwithout ventilatorysupportfor15min.NIPPVisdiscontinuedifthepatientmaintainsarespiratory rateof30breaths/minorlessandaPao2of60mmHgwithanFio2of0.3without ventilatorysupportandactivationoftheaccessorymusclesofrespiration[28]. 10.Watchforlatefailuresevenifpatientsshowearlyimprovement. 11.Closemonitoringofrespiratory,cardiovascular,andarterialbloodgasparameters. 12.Facilitiesforintubationandinvasiveventilationmustbereadilyavailable. ALI/ARDSacutelunginjury/acuterespiratorydistresssyndrome,CPAPcontinuouspositiveairway pressure, EPAP expiratory positive airway pressure, IPAP inspiratory positive airway pressure, NIPPVnoninvasivepositivepressureventilation
tohemodynamicallystablepatientswhocanbecloselymonitoredintheICU,whereendotrachealintubationispromptlyavailable.Areasonableclinicalapproachwouldbetouse NIVjudiciouslyinpatientswithALI/ARDS(Table36.2).Althoughtheoptimalduration oftheinitialNPPVtrialremainsuncertain,aresponsewithin1 4hofinitiationisareasonableexpectation.Finally,patientswhoarefailingNIVtrialshouldbepromptlyintubatedandmechanicallyventilatedasdelaysinendotrachealintubationinpatientsmanaged withNIVhavebeenassociatedwithdecreasedsurvival[27].
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36.5 Conclusions ARDSrepresentsonetheultimatefrontiersininvestigatingtheapplicationofNIPPVin patients with ARF, and achieving a 50% reduction in intubation rate would positively affectARDSoutcome.Thechallengingissueistheproperidenti cationofpatientswho are likely to bene t from NIPPV and avoiding potential complications of a delayed intubation.
References 1. Bernard GR, Artigas A, Brigham KL et al (1994) The American European Consensus ConferenceonARDS.De nitions,mechanisms,relevantoutcomes,andclinicaltrialcoordination.AmJRespirCritCareMed149:818 824 2. Stauffer JL, Olson DE, Petty TL (1981) Complications and consequences of endotracheal intubationandtracheotomy.Aprospectivestudyof150criticallyilladultpatients.AmJMed 70:65 76 3. Pingleton SK (1988) Complications of acute respiratory failure. Am Rev Respir Dis 137: 1463 1493 4. FagonJY,ChastreJ,HanceAJetal(1993)Nosocomialpneumoniainventilatedpatients:a cohortstudyevaluatingattributablemortalityandhospitalstay.AmJMed94:281 288 5. Brochard L (2002) Noninvasive ventilation for acute respiratory failure. JAMA 288: 932 935 6. Brochard L, Mancebo J, Elliott MW (2002) Noninvasive ventilation for acute respiratory failure.EurRespirJ19:712 721 7. AgarwalR,AggarwalAN,GuptaDetal(2005)Non-invasiveventilationinacutecardiogenic pulmonaryoedema.PostgradMedJ81:637 643 8. RamFS,WellingtonS,RoweBHetal(2005)Non-invasivepositivepressureventilationfor treatment of respiratory failure due to severe acute exacerbations of asthma. Cochrane DatabaseSystRev.CD004360 9. L HerE,DeyeN,LelloucheFetal(2005)Physiologiceffectsofnoninvasiveventilationduringacutelunginjury.AmJRespirCritCareMed172:1112 1118 10. AntonelliM,ContiG,RoccoMetal(1998)Acomparisonofnoninvasivepositive-pressure ventilationandconventionalmechanicalventilationinpatientswithacuterespiratoryfailure. NEnglJMed339:429 435 11. DelclauxC,L HerE,AlbertiCetal(2000)Treatmentofacutehypoxemicnonhypercapnic respiratoryinsuf ciencywithcontinuouspositiveairwaypressuredeliveredbyafacemask:a randomizedcontrolledtrial.JAMA284:2352 2360 12. HilbertG,GrusonD,VargasFetal(2000)Noninvasivecontinuouspositiveairwaypressure inneutropenicpatientswithacuterespiratoryfailurerequiringintensivecareunitadmission. CritCareMed28:3185 3190 13. Antonelli M, Conti G, Moro ML et al (2001) Predictors of failure of noninvasive positive pressureventilationinpatientswithacutehypoxemicrespiratoryfailure:amulti-centerstudy. IntensiveCareMed27:1718 1728
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14. ConfalonieriM,CalderiniE,TerracianoSetal(2002)Noninvasiveventilationfortreating acute respiratory failure in AIDS patients with Pneumocystis carinii pneumonia. Intensive CareMed28:1233 1238 15. CheungTM,YamLY,SoLKetal(2004)Effectivenessofnoninvasivepositivepressureventilation in the treatment of acute respiratory failure in severe acute respiratory syndrome. Chest126:845 850 16. RanaS,JenadH,GayPCetal(2006)Failureofnon-invasiveventilationinpatientswithacute lunginjury:observationalcohortstudy.CritCare10:R79 17. AntonelliM,ContiG,EsquinasAetal(2007)Amultiple-centersurveyontheuseinclinical practice of noninvasive ventilation as a rst-line intervention for acute respiratory distress syndrome.CritCareMed35:18 25 18. YoshidaY,TakedaS,AkadaSetal(2008)Factorspredictingsuccessfulnoninvasiveventilationinacutelunginjury.JAnesth22:201 206 19. AgarwalR,HandaA,AggarwalANetal(2009)Outcomesofnoninvasivepositivepressure ventilationinacutehypoxemicrespiratoryfailureinarespiratoryICUinNorthIndia.Respir Care54:1679 1687 20. Ferrer M, Esquinas A, Leon M et al (2003) Noninvasive ventilation in severe hypoxemic respiratoryfailure:arandomizedclinicaltrial.AmJRespirCritCareMed168:1438 1444 21. AddaM,CoquetI,DarmonMetal(2008)Predictorsofnoninvasiveventilationfailurein patients with hematologic malignancy and acute respiratory failure. Crit Care Med 36: 2766 2772 22. Keenan SP, Sinuff T, Cook DJ et al (2004) Does noninvasive positive pressure ventilation improveoutcomeinacutehypoxemicrespiratoryfailure?Asystematicreview.CritCareMed 32:2516 2523 23. Agarwal R, Gupta D, Handa A et al (2005) Noninvasive ventilation in ARDS caused by Mycobacterium tuberculosis: report of three cases and review of literature. Intensive Care Med31:1723 1724 24. AgarwalR,NathA,GuptaD(2007)NoninvasiveventilationinPlasmodiumvivaxrelated ALI/ARDS.InternMed46:2007 2011 25. Antonelli M, Conti G, Bu M et al (2000) Noninvasive ventilation for treatment of acute respiratory failure in patients undergoing solid organ transplantation: a randomized trial. JAMA283:235 241 26. AgarwalR,ReddyC,AggarwalANetal(2006)Istherearolefornoninvasiveventilationin acuterespiratorydistresssyndrome?Ameta-analysis.RespirMed100:2235 2238 27. Festic E, Gajic O, Limper AH et al (2005) Acute respiratory failure due to pneumocystis pneumoniainpatientswithouthumanimmunode ciencyvirusinfection:outcomeandassociatedfeatures.Chest128:573 579 28. WysockiM,TricL,WolffMAetal(1995)Noninvasivepressuresupportventilationinpatients with acute respiratory failure. A randomized comparison with conventional therapy. Chest 107:761 768
Noninvasive Positive Pressure Ventilation in Acute Hypoxemic Respiratory Failure and in Cancer Patients
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S.EgbertPravinkumar
37.1 Introduction Acuterespiratoryfailure(ARF)isacommonoccurrenceincancerpatientsandisassociated withahighmortalityrate.TheroleofNPPVinimmunosuppressed,hematologicalmalignancies,andsolidtumorisanareathatinterestsresearchersandcliniciansalike.Several randomizedcontrolledtrialsandsystematicreviewshavecon rmedthebene tsofnoninvasive positive pressure ventilation (NPPV) in patients with exacerbation of chronic obstructivepulmonarydisease(COPD).Bene tsachievedfromNPPVinCOPDpatients arelargelyduetoavoidanceofinvasivemechanicalventilation(IMV)anditscomplications including worsening of preexisting infections, morbidity and mortality, ventilator associatedpneumonia(VAP),ventilatorassociatedlunginjury,increasedneedforsedation resultinginprolongedventilation,ventilatordependence,andupperairwaycomplications relatedtoendotrachealtube[1].TheuseofNPPVinCOPDwithhypercapneicARFisno longerdebatedandisnowconsideredas rst-lineinterventionbeforeconsideringendotrachealintubation(ETI)andIMV. TheroleofNPPVhasbeenmostrecentlystudiedinhypoxemicARF.Inthisgroupof patients,severalstudieshaveshownthatNPPVnotonlyreducedmechanicalventilation, lengthofintensivecareunit(ICU)staybutwasassociatedwithfewercomplications[2]. Sinceoneofthemajorbene tsofNPPVisthereductionofnosocomialinfection,patients whoareathighrisksuchasimmunosuppressed,hematologicalmalignancies,chemotherapyinducedneutropenia,andorgantransplantationpatientsmaybeparticularlylikelyto bene tfromNPPV.RecentguidelinespublishedbytheAmericanThoracicSocietyand theInfectiousDiseasesSocietyofAmericainthemanagementofnosocomialinfections hasprovidedhighgradeevidencebasedrecommendationsinthepreventionofnosocomial infections.TheguidelinerecommendstheuseofNPPVwheneverappropriateinthemanagementofARFandtheavoidanceofETIandIMVwheneverpossible[3].
S.E.Pravinkumar DepartmentofCriticalCare,Unit112,UT-M.D.Anderson CancerCenter,Houston,TX77030,USA e-mail:
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37.2 Epidemiology of Hypoxemic ARF HypoxemicARFisthemostcommonreasonforICUadmissionandventilatorysupport. Anepidemiologicalprospectivesurvey(Carlucci)of42ICUsinEurope(26universityand 16 nonuniversity hospitals) looked at 1,337 admissions over a period of 3 weeks; 689 patients required ventilatory support. ETI and IMV was the mode of treatment in 581 (84%)andNPPVwasusedas rst-linetreatmentin108(16%).Theconditionsprecipitating ARF were hypoxemic ARF, including acute cardiogenic pulmonary edema (55%), coma(30%),andhypercapneicARF(15%). InthisepidemiologicalstudyofpatientswhoneededETIandIMV,mortalityrateswere muchhigherinthehypoxemicARFgroupthanhypercapneicARF(47%vs27%).The28-day hospitalmortalitywas41%inthosewhoneededETIandIMV,comparedto22%inthosewho receivedNPPV(p<0.001).TheincidenceofVAPwas2%inthosewhoweresuccessfully managedwithNPPVcomparedto19%inthosewhoneededIMV(p<0.002)[4].
37.3 NPPV in Hypoxemic ARF Studiesinacutehypoxemicrespiratoryfailure(ARF)usingnoninvasivepositivepressure ventilation(NPPV),hasshownvariedresultsandtheoutcomeisdependentonselective population.Moreandmoretrialsareemerginglookingatthebene tsofNPPVinselected groupswithhypoxemicARF.Systematicreviewrandomizedcontrolledtrials(RCTs)of NPPVuseinhypoxemicARF[5]showsconvincingevidencethatNPPVdecreasedthe needforETIandIMV.NPPValsodecreasedtheICUlengthofstayandmortality.However, unlikehypercapneicARF,hypoxemicARFencompassesseveraldiagnosesandcomprises aheterogeneouspopulation.Thisheterogeneitywasobservedinmultiplestudies.Hence, itwouldbemisleadingtoconcludethatNPPVisbene cialforallpatientswithhypoxemic ARF. Notably NPPV has had limited success in patients with acute respiratory distress syndrome(ARDS)andlobarconsolidation.Furtherstudyofspeci cpatientgroupswith hypoxemicARFwillprovideinsightinthemanagementofARFusingNPPV[5]. AwellconductedsystematicreviewassessedtheeffectsofNPPVforpatientswith HypoxemicARFnotduetoCPE.ThestudylookedateightRCTsfromsixcountriesthat comparedNPPVplus standard therapy versus standard therapy alone in 366 patients. Thestudyresultsareasfollows;NPPVwasassociatedwithasigni cantlylowerrateof ETIandIMV(RR0.23,95%CI:0.10,0.35),reductioninlengthofICUstayof1.9days (95%CI:1,2.9),reducedICUmortalityof17%(95%CI8,26)andnostatisticallysigni canteffectonhospitalmortality.Basedoncurrentlyavailableevidence,routineuse ofNPPVforhypoxemicARFisnotrecommended.Howeverbasedonselectedpopulation analysis, NPPV should be strongly considered for immunosuppressed and post-thoracotomypatientsandtheiruseinothergroupsshouldbecarefullymonitoredto ensurebene cialeffect[1].
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37.4 ARF in Imunosuppressed and Cancer Patients HypoxemicARFisacommonoccurrenceinimmunocompromisedandinmalignancies,both hematologicalmalignancyandsolidtumor.Itisoftenthedreadedconditionincancerpatientsdue toassociatedhighmortalityrelatedtoETIandIMV.Newtypesandmodalitiesofchemotherapy andradiationtherapy,circulatingpluripotenthematopoieticcellgraftsandbonemarrowtransplantationhavecontributedtotheincreaseinsuccessfultreatmentofsolidandhematologicmalignancies.However,theseregimensmaypredisposepatientstovariouslife-threateningcomplic ations,suchasinfection,hemorrhage,capillaryleaksyndrome,radiationtoxicity,ordrug-related toxicity.Thelungisthetargetorganmostfrequentlyinvolvedinthesecomplications. Sincemostofthecancerpatientshavemusclefatigue,diffusepulmonaryin ltrates, anddepressedorganfunctionandreserveduetotreatment,theyaremorevulnerableto rapidclinicaldeteriorationanddevelopingARF.Thecommonesttypeofrespiratoryfailureinthisgroupofpatientsis lung failure,althoughitisnotuncommontosee ventilatorypump failureasthecauseofARF.Severalstudies[6]havelookedattheoutcomeof patientswithacutemyelogenousleukemiaandrecipientsofbonemarrowtransplantation, whoneededETIandIMV.OnlytwovariableshavebeenshowntobeindependentlyassociatedwithmortalityofcancerpatientsintheICUandneitherthetypeofcancer(i.e.,solid orhematologicmalignancy)northepresenceorabsenceofneutropeniawasindependently associatedwithmortality.The rstindependentpredictorofICUmortalityistheseverity ofthepatient sclinicalconditiononadmissionasrecordedbyvariousscores,suchasthe Simpli edAcutePhysiologicScore(SAPSIandSAPSII)andtheAcutePhysiologicand ChronicHealthEvaluation (APACHE II and APACHE III). The second and stronger independentpredictivefactorofmortalityistheneedforETIandIMV,sinceVAPand worseningofapreexistinginfectionaresigni cantcomplicationsinintubatedpatients.
37.5 NPPV in Cancer Patients InaretrospectivestudyofpatientswithsolidorhematologiccanceradmittedtoICUfor ARF,thesurvivalrateforcancerpatients(n=105)intheperiod1996 1998wassigni cantlyhigherthanthose(n=132)admittedbetween1990and1995(39%vs18%,respectively;p=0.0003).Multivariateanalysisshowedthat,theuseofNPPVinthelaterperiod wasassociatedwithamarkedimprovementinsurvival[7].OtherstudiesusingNPPVin cancerpatientsaresummarizedinTable37.1.
37.6 Indications and Contraindications The immediate goals of NPPV therapy should be aimed at relieving patient symptoms and reducingtheworkofbreathing.Theintermediategoalsshouldbetoimproveandstabilizegas
Cancerpatientswithdo-not-intubateorders Solidtumor(ST)andHM
ImmunosuppressedandHM
Fever,neutropenia,AHReF,HM
Meduri1994
Conti1998
Hilbert2000
HelmetNPPVvsMaskNPPV
Rocco2004
Meert2003
Pulmonaryin ltrate,HMMaskvshelmetNPPV
Principi2004
SolidtumorsandHM NPPVforhypoxemicARF
Fever,immunosuppressed,organ transplant,pulmonaryin ltrates,HM
RCT,NPPVvsstandardcare(SC)fever,pulmonary in ltrate,immunosuppresed,HMn=52
Hilbert2001
IntermittentCPAP
Hematologicalmalignancies(HM)
Tognet1994
Table 37.1 NPPVincancerpatientswithhypoxemicARF[6] Study Patientpopulationandintervention
ICUsurvival:57% ETI:25%
HelmetNPPVvsMaskNPPV ETI:36%vs63% ICUMortality:(31%)vs(47%) Hospitalmortality:37%vs53%
NPPVintolerance:helmetNPPV(0%)vsmaskNPPV(50%)
ReducedETI,complications,ICUdeath,andhospitaldeath inNPPVgroup
CPAPavoidedETIin25%CPAPsuccess:allsurvived
Improvementinbloodgasesandrespiratoryrate<1hof NPPV 68%survivedtodischarge
ImprovedsurvivalandhospitaldischargeinNPPVgroup
ICUmortality:IMVvsNPPV:100%vs55%signi cantly lowermortalityinNPPVgroup
Outcome
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exchange,optimizepatientventilatorcomfortandsynchrony,andtheultimategoalisavoidance ofETIandIMV.Thesuccessofthetherapydependsonahighlymotivated,committedand knowledgeable team, and careful patient selection with the help of a well structured NPPV guideline(Table37.2).ApplicationofNPPVearlyintheprocessofARFalongwithcarefuland rigorousmonitoringisvitaltothesuccessofNPPVtherapy.Otherfactorsinclude;location, availabilityofwidevarietyofinterfacestosuitthepatientsmorphologicalandcomfortneeds. NPPVfailureshouldbeidenti edearlyoninordertoavoidunnecessarydelayinETI andIMV.ForthisreasonseveralcentersofferNPPVtherapyintheICU,highdependency careunitsandrespiratoryintermediarycareunits.Staf ngratiosand24hphysiciancover isalsoimportantinconsideringNPPVoutsidetheICU.SomeofthepredictorsofNPPV failureinclude;elevatedICUseverityofillnessscores,presenceofARDSorlobarconsolidation, PaO2/FiO2 ratio <150 even after 1 h of NPPV, pH <7.30 on initiation, and failureofpHimprovementin1 2h Table 37.2 NPPV for cancer patients (©The University of Texas M.D. Anderson Cancer Center NPPVguideline) Eligibilitycriteria Contraindications Clinical(all)
Absolute(any)
– Acuterespiratoryfailure
– Cardiopulmonaryarrest
– Dyspnea
– pH<7.25
– AccessoryResp.muscleuse
– Upperairwayobstruction
– Paradoxicalabdominalmovement
– Facialtrauma
– RR³25
– Uncontrolledarrhythmia
– Adequateairwayprotection
– UntreatedSBP£90mmHg
Adequatesecretionclearance
– GCS£8 – Undrainedpneumothorax
Gasexchangecriteria(any)
Relative
– FiO2³0.60
– Copioussecretions
– PaO2£60mmHgonroomair
– Confusion/agitation
– PaO2£75mmHgonanyFiO2
– GCS9 13
– PaO2:FiO2<200
– Twoormoreorganfailure
– PaCO2³50
– FocalconsolidationonCXR
– pH³7.30 Radiologicalcriteria(any) – PulmonaryInfiltrates Nopneumothorax
– Bowelobstruction – R ecent facial/ upper airway/GI surgery – Pregnancy Thoracicsurgery<6weeks (continued)
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Table 37.2 (continued) Bloodgases1and4hpostNPPV
Bloodgases1and4hPostNPPV
NPPVsuccess
NPPVfailure
Clinicalcriteria(twoormore)
Clinicalcriteria(any)
– PatienttoleratesNPPV
– PatientintoleranttoNPPV
– Toleratesperiods off NPPV
– Persistentdyspnea
– Dyspneareduced(score)
– RR³35
– RR£35
– UrgentneedforETI
Awakeandalert
– Developmentofcontraindications GCS£8(worseningmentalstatus)
Gasexchangecriteria(2ormore)
Gasexchangecriteria(any)
– ImprovementinABG
– FailureofABGimprovement
– FiO2£0.7andSpO2>92
– FiO2³0.7andSpO2£92
– PaO2³65onFiO2<0.6
– PaO2£65onFiO2>0.6
– pH³7.30
– pH£7.30
PaO2:FiO2³100frombaseline
PaO2:FiO2£100frombaseline
37.7 Complications of NPPV Complications of NPPV are predominantly interface related, such as, facial discomfort (30 50%),skinerythema(20 35%).Lesscommon(5 10%)problemsinclude;claustrophobia,nasalulceration,andacneiformrash.Complicationsrelatedtopressureand ow include; nasal congestion (20 50%), sinus/ear pain (10 30%), nasal/oral dryness (10 20%),eyeirritation(10 20%),gastricdistension(5 10%).Majorcomplicationssuch asaspirationpneumonia,hypotension,andpneumothoraxarelessthan5%.
Key Recommendations
› › › ›
NPPVcanbeeffectivelyusedinthemanagementofARF. Ithasseveralbene tsincluding;decreasedrateofETIandIMV,decreasedVAP, decreasedmortality,decreasedICU,andhospitallengthofstay. Patientselectionandearlyapplicationarecrucial. Highlycommittedandmotivatedteamalongwithastructuredguidelineis importantinNPPVsuccess.
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References 1. KeenanSP,SinuffT,CookDJ,HillNS(2004)Doesnoninvasivepositivepressureventilation improveoutcomeinacutehypoxemicrespiratoryfailure?Asystematicreview.CritCareMed 32:2516 2523 2. BrochardL(2002)Noninvasiveventilationforacuterespiratoryfailure.JAMA288:932 935 3. AmericanThoracicSociety/InfectiousDiseasesSocietyofAmerica(2005)Guidelinesforthe managementofadultswithhospital-acquired,ventilator-associated,andhealthcare-associated pneumonia.AmJRespirCritCareMed171:388 416 4. CarlucciA,RichardJC,WysockiM,LepageE,BrochardL(2001)SRLFCollaborativeGroup onMechanicalVentilation.Noninvasiveversusconventionalmechanicalventilation:anepidemiologicsurvey.AmJRespirCritCareMed163:874 880 5. Keenan SP, Sinuff T, Cook DJ, Hill NS (2003) Which patients with acute exacerbation of chronicobstructivepulmonarydiseasebene tfromnoninvasivepositivepressureventilation? Asystematicreviewoftheliterature.AnnInternMed138:861 870 6. NavaS,CuomoAM(2004)Acuterespiratoryfailureinthecancerpatient:theroleofnoninvasivemechanicalventilation.CritRevOncolHematol51:91 103 7. Azoulay E, Alberti C, Bornstain C, Leleu G, Moreau D, Recher C, Chevret S et al (2001) Improvedsurvivalincancerpatientsrequiringmechanicalventilatorysupport:impactofnoninvasiveventilatorysupport.CritCareMed29:519 525
Noninvasive Ventilation as a Preoxygenation Method
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ChristopheBaillard
38.1 Introduction Usually,preoxygenation(3minofspontaneousventilationwithbagandmaskwith100%O2) isrecommendedindelayingarterialdesaturationduringtheapnearelatedtoendotracheal intubation(ETI)procedures[1].Inahealthyapneicadultpatient,thetimecoursetoreachan oxygenhemoglobinsaturation(SpO2)<90%after3minpreoxygenationisabout6 8min. Numerousfactorsareinvolvedintheoxygenloadingprocessduringpreoxygenation,suchas those able to interfere with alveolar, arterial, tissue, and venous compartments and those interactingwiththedeliveredinspiredfractionofoxygen(Fio2).Theextentofoxyhemoglobindesaturationalsodependsonthedurationofapnea,whichcorrespondstothetimeelapsed betweentheonsetofapneaandsuccessfulintubationwiththesubsequentoxygenprovision. The dif culties encountered during airway management prolong the duration of apnea. Finally,thecapacityforoxygenloadingandtheconditionofintubationwillbedeterminants oftheef ciencyofpreoxygenation. Toconsiderthefactorsaffectingtherateofoxyhemoglobindesaturationduringapnea, FarmeryandRoedevelopedamodel[2].Ofnote,thismodelwasadaptedtoapostoperative scenariotopredicttheconsequencesofsuchanonphysiologicalconditiononthetimecourse ofarterialoxyhemoglobindesaturation.Theauthorsstatedthatitrepresentedtosomeextent aworst-casescenarioinwhichthecombinedeffectofhypovolemia(4L),reducedcardiac output(4L/min),anemia(10g/dL),increasedV/Q(ventilation/perfusionratio)mismatch andincreasedshunt(0.1),preapneahypoventilation,andreducedalveolarvolume(2L)are involved.Thecombinationofsuchabnormalities(whichareusualincriticallyillpatients) dramaticallyacceleratedtherateofoxyhemoglobindesaturation.Withoutpreoxygenation, theoxyhemoglobinsaturationreached85%only23saftertheonsetofapnea.
C.Baillard DepartmentofAnesthesiologyandCriticalCareMedicine,AvicenneHospital, Paris13University-AP-HP,125,routedeStalingrad, 93009Bobigny,France e-mail:
[email protected] A.M.Esquinas(ed.),NoninvasiveMechanicalVentilation, DOI:10.1007/978-3-642-11365-9_38,©Springer-VerlagBerlinHeidelberg2010
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Theexpecteddurationofapneaincriticallyillpatientsrequiringintubationisalsoofinterest.Inaprospectivestudyinvestigatingemergencytrachealintubationsoutsidetheoperating room(n=297),Schwartzandcoworkersshowedthatmorethantwoattemptsatintubation were required in 11% of cases [3], with most intubations performed in critical care units (78%).Jaberandcolleaguesreporteddataon253intubationscarriedoutinsevenintensive careunits(ICUs)[4].Theyobservedthat13%oftheintubationsstillrequiredtwoattemptsfor success.Whennowconsideringboththerateofoxyhemoglobindesaturationandcomplexity ofintubation,itisnotsurprisingtoobservethatseverehypoxemia(SpO2<80%)occurredin morethan25%ofpatientsduringtheintubationperformedinICUs[4].Thereisalsoevidence forastrongrelationshipbetweenthedif cultyofintubationandhypoxemicevents.Inalarge prospective cohort of 2,833 patients requiring emergency intubation outside the operating room,Mortetal.foundthattherelativeriskofseverehypoxemiaoccurrence(de nedasSpO2 <70%)wasmultipliedby14whentheprocedurerequiredmorethantwoattempts[5].Two majordeterminantscanbeindividualized:theamountofoxygenthatcanbestoredbeforethe onsetofapneaandthecomplexityofintubation.Wenowfocusonthepreoxygenation.
38.2 Preoxygenation in Critically Ill Patients Whereas the complications associated with airway management in critically ill patients havebeenwellidenti edforseveraldecades,theeffectivenessofpreoxygenationinthe ICUwasevaluatedforthe rsttimeonly4yearsago.WehaveMorttothankforthecomprehensivestudythatbegantheinvestigationintopreoxygenation[6,7].Inthatprospective andobservationalstudy,theeffectivenessofpreoxygenationwasassessedin42critically ill ICU patients requiring invasive ventilation (unstable patients). At the same time, 34 American Society of Anesthesiologists class IV patients scheduled for cardiac surgery were investigated as a control group (stable patients). Unstable patients were already receivingarangeof60 100%oxygentherapyinconcertwithcontinuouspositiveairway pressure(CPAP)asaventilatorysupport(n=16)orwithanonrebreathingdevice.The preoxygenationconsistedofuseofamanualresuscitatorbagwithreservoir(tube)connectedtohigh- owoxygeninthe ushmode(20L/min).(Suchamethodwasconsistent with the preoxygenation consideration discussed.) The effectiveness of preoxygenation wasde nedastheabilitytoimprovePao2,thearterialpressureofoxygen(ETO2,end-tidal O2,wasnotmonitoredinthisstudy).Amongunstablepatients,4minofpreoxygenation resultedinlittlechangeintheirbaselinePao2(+37mmHg)comparedtothestablepreoperativepatients(+325mmHg).Moreover,intheunstablepatients,twopopulationswere individualizedaccordingtothediagnosisofventilatoryfailure.Inthoserequiringintubationforairwayprotection,thepreoxygenationimprovedPao2by105mmHg,whereasin thosesufferingfromcardiopulmonarydisease(themostseverehypoxemicpatients)preoxygenationwasmarginallyeffective,withonly+22mmHgincreaseinPao2. Theresultsarequitealarmingandareopentocriticism.Consideringthattheamountof oxygenalreadydelivereddidnotcorrectlyoxygenatethepatient,thelittleeffectofthesubsequentpreoxygenationonPao2wasexpected.However,thetechniqueofpreoxygenation
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describedwaswelldesigned,evenprobablyoptimizedregardingtheoxygendelivery(highowoxygenat20L/mininthe ushmode)andthattheDr.Mort spatientsarerepresentativeof true criticallyillpatientsusuallymanagedintheICU.Moreover,conversionfrom CPAP to a bag-mask system was unlikely to improve Pao2. Again, the conversion from noninvasiveventilation(CPAP)toabag-masksystemforthepurposeofpreoxygenation wasunlikelytobeeffective,butsuchaconversionisstillusedthroughoutICUs[4]. Atelectasisisacommonproblemincriticallyillpatients.Whenpreoxygenationisinitiatedtomanagepatientswhomanifestacuterespiratoryfailure,thelimitedalveolarvolume andtheenhancedshuntfractionareimportantdeterminantsintheunderlyinglungdisease. The use of high Fio2 delivery is also a well-known contributing factor affecting early atelectasis formation during preoxygenation. This phenomenon, called absorption atelectasis,occurswhentherateofthealveolargasabsorptionintothebloodexceedsthe ow gas delivered to the alveoli. Complete airway occlusion and very low ventilation/ perfusionratioarethetwosituationspromotingabsorptionatelectasis[8].
38.3 Noninvasive Ventilation as a Preoxygenation Method Theabilityofnoninvasiveventilation(NIV)topreventatelectasisformationinhealthy andobesepatientsduringpreoxygenationandsubsequentinductionofanesthesiainthe operatingroomhasbeenwellinvestigatedbyMagnussonandcoworkers[8]. Toaddressthisproblem,weconductedaprospective,randomizedstudyincriticallyill patientsrequiringtrachealintubationforinvasiveventilation.Patientsmanifestedhypoxemicacuterespiratoryfailurebeforeinclusion[9].Wecomparedpreoxygenationpriorto ETI with the use of NIV to a bag-valve mask device for 3 min. For the control group (n = 26), preoxygenation was performed using a nonrebreather bag-valve mask with a reservoirdrivenby15L/minoxygen.Patientswereallowedtobreathespontaneouslywith occasionalassistance(usualorconventionalpreoxygenationmethod).FortheNIVgroup (n=27),pressuresupportventilation(PSV)wasdeliveredbyanICUventilatorthrougha facemaskadjustedtoobtainanexpiredtidalvolumeof7 10mL/kg.TheFio2was100%, andapositiveend-expiratorypressure(PEEP)levelof5cmH2Owasused.Thebaseline characteristics of the two groups were similar in term of age (62 years) and Simpli ed AcutePhysiologicScore(52).Pneumoniawasthemaindiagnosisonadmission(68%). ThemeanPao2valuewasbelow70mmHgunder15Loxygen owinbothgroups. PreoxygenationimprovedSpO2inthecontrolgroupfrom90%±5%to93%±6%andin NIVgroupfrom89%±6%to98%±2%(mean±standarddeviation[SD],p<0.05).However, SpO2wasstatisticallyhigherintheNIVgroup,andpreoxygenationfailedtoimproveSpO2in 6patientsreceivingtheconventionalmethod(p<0.05).Duringintubation,12patientsinthe controlgroupand2intheNIVgrouphadafallinSpO2below80%(p<0.01).Conventional preoxygenationfailedtoimprovethemeanPao2valuewhereasPao2increasedsigni cantly intheNIVgroup.Attheendofpreoxygenation,thePao2wasstatisticallyhigherintheNIV group compared with the control group (203 [116 276] vs. 97 [66 163] mmHg; median [InterquartileRange],p<0.01),andthisdifferencepersistedat5and30minafterETI.
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TheresultofthisstudywasopenedtocriticismbecausetheFio2deliveredinthecontrol groupwasnotmeasured.IftheFio2deliveredwassuboptimal,thissimplefactcouldhave explainedthedifferencereported.Inacuterespiratoryfailure,similartoinvasiveventilation, NIV improves oxygenation by delivering a high oxygen concentration, unloading respiratorymuscleefforts,recruitingalveoli,andincreasinglungvolumes[10].Byrecruitingalveoli,positivepressureventilationnotonlyenhanceslungvolume(thestore)butalso reducestrueshunt.ThelattereffectimprovesthePao2/Fio2ratio,resultinginmorecomplete hemoglobin saturation in hypoxemic patients. Prevention of atelectasis formation during preoxygenationcanbepreventedwithaCPAPof6cmH2O,whereasreexpansionusually requires a higher level of pressure [8]. Further studies are required to ascertain whether short-durationNIV,asusedforthepreoxygenation,iseffectiveatreducingtrueshunt. NIVasapreoxygenationmethodincreasesboththecontents(Fio2/FAO2[alveolarfractionofoxygen])andthecontainer(FRC,functionalresidualcapacity)andcouldbeview as one of the best ways to enhance the oxygen stores before apnea. However, little is knownaboutthetimenecessarytoloadtheoxygenstores,and3or5minmaybeshort. El-Khatibandcolleaguesdescribedthebene cialeffectofnoninvasivebilevelpositive airway pressure (BiPAP) for the purpose of preoxygenation in a critically ill morbidly obesepatient[11].FromabaselineSpO2andPao2of79%and51mmHg,respectively,the conventionalpreoxygenation(3minusingacirclesystem,tidalvolumebreathingatan oxygen owrateof5L/min)improvedtheSpO2andPao2onlyto90%and60mmHg, respectively.After3minofBiPAPapplication(inspiratorypositiveairwaypressure[PAP] of17cmH2OandexpiratoryPAPof7cmH2O,oxygen owrateof5L/min),theSpO2and Pao2valuesincreasedto95%and81mmHg,respectively.Finally,achangefrom5to10 L/minoxygen owfurtherimprovedtheSpO2andPao2upto99%and95mmHg,respectively.Inourstudy,3minofnoninvasivepositivepressureventilationwasadequateto improveoxygenationandtoreducehypoxemiaduringintubation[9].Moreover,thebene cialeffectonPao2wasstillobserved30minlater.Oneexplanationcouldbetheresidual effectofNIVinrecruitingalveoliandincreasinglungvolume. PSVunloadstherespiratorymusclesthroughchemicalorload-relatedre exfeedback [12].Inawakepatients,thereductionofPaco2,animportantdeterminantofrespiratory motoroutput,causesareductioninthesenseofdyspneaandgreateracceptabilityofNIV. However,3minofpreoxygenationusingNIV(PSV+PEEP)failedtoimprovethePaco2 valueincriticallyillpatients[9].
38.4 Noninvasive Ventilation Complications and Outcome Criticallyillpatientsareusuallyconsideredtohaveafullstomach,andpulmonaryaspirationofgastriccontentsduringETIisfrequentlyencounteredinthisclinicalsetting[3]. Facial mask positive pressure ventilation may increase the gastric air content and may hencepromotepulmonaryaspiration.Thisriskisenhancedwhentheinsuf ationpressure isabove20cmH2O,avalueeasilyobtainedwhenusingmanualventilation.Inourstudy, NIVwasusedinapressure-limitedmode,andnoneoftheNIVgroupofpatientsreceived
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aninsuf ationpressurehigherthan20cmH2O[9].Inaddition,theNIVpreoxygenation wasfollowedbyarapidsequenceinductionknowntoavoidtheregurgitationofgastric contents. Overall, regurgitation was observed in 3 patients, and new in ltrates were observedonthechestradiographobtainedafterintubationin4of53patients.NIVdidnot increaseregurgitationornewin ltrates.Durationofmechanicalventilation,ICUlengthof stay,andICUmortalitywerenotdifferentbetweengroups.However,theconclusionon morbidity and outcome was limited, and it is still uncertain whether NIV will improve clinicaloutcomes.Fromtheresultofthatstudy,aFrenchconsensusguidelinesuggested thattheuseofNIVasapreoxygenationmethodcouldbeusedinhypoxemiccriticallyill patients [13]. A multicenter study is currently under way to nd out whether NIV as a preoxygenationmethodismoreeffectiveatreducingthedegreeoforgandysfunctionor failurethanstandardpreoxygenationfollowingETI[14].Theresultsofthisstudycould haveapositiveimpactonairwaymanagementincriticallyillpatients.
38.5 Discussion and Recommendations Criticallyillpatientsarepredisposedtosevereoxyhemoglobindesaturationduringintubation[4,5].Fortheintubationofhypoxemicpatients,theusualpreoxygenationismarginallyeffective[6,7].Theoretically,becauseNIVincreasesboththecontents(Fio2/FAO2) andthecontainer(FRC),itcouldbeviewedasoneofthebestwaytoenhancetheoxygen stores before apnea. A short application (3 min) of NIV is more effective at reducing arterial oxyhemoglobin desaturation than using a nonrebreather bag-valve mask with reservoir[9].However,itisalsoimportanttoconsiderthatNIVmaypromotepulmonary aspirationbyincreasingthegastricaircontent.TheimpactofNIVonmorbidityormortalityiscurrentlyunderinvestigation.Carefulanalysisoftherisksandbene tsonanindividual basis should hence be made until further studies are available for the intensivist dealingwithhypoxemiccriticallyillpatients. Acknowledgment I would like to thank Sadek Beloucif for his critical and editorial assistance.
References 1. Benumof JL (1999) Preoxygenation: best method for both ef cacy and ef ciency. Anesthesiology91:603 605 2. FarmeryAD,RoePG(1996)Amodeltodescribetherateofoxyhaemoglobindesaturation duringapnoea.BrJAnaesth76:284 291 3. SchwartzDE,MatthayMA,CohenNH(1995)Deathandothercomplicationsofemergency airwaymanagementincriticallyilladults.Aprospectiveinvestigationof297trachealintubations.Anesthesiology82:367 376 4. JaberS,AmraouiJ,LefrantJYetal(2006)Clinicalpracticeandriskfactorsforimmediate complicationsofendotrachealintubationintheintensivecareunit:aprospective,multiplecenterstudy.CritCareMed34:2355 2361
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5. MortTC(2004)Emergencytrachealintubation:complicationsassociatedwithrepeatedlaryngoscopicattempts.AnesthAnalg99:607 613 6. MortTC(2005)Preoxygenationincriticallyillpatientsrequiringemergencytrachealintubation.CritCareMed33:2672 2675 7. MortTC,WaberskiBH,CliveJ(2009)Extendingthepreoxygenationperiodfrom4to8mins incriticallyillpatientsundergoingemergencyintubation.CritCareMed37:68 71 8. MagnussonL,SpahnDR(2003)Newconceptsofatelectasisduringgeneralanaesthesia.BrJ Anaesth91:61 72 9. BaillardC,FosseJP,SebbaneMetal(2006)Noninvasiveventilationimprovespreoxygenationbeforeintubationofhypoxicpatients.AmJRespirCritCareMed174:171 177 10. MehtaS,HillNS(2001)Noninvasiveventilation.AmJRespirCritCareMed163:540 577 11. El-KhatibMF,KanaziG,BarakaAS(2007)Noninvasivebilevelpositiveairwaypressurefor preoxygenationofthecriticallyillmorbidlyobesepatient.CanJAnaesth54:744 747 12. KalletRH,DiazJV(2009)Thephysiologiceffectsofnoninvasiveventilation.RespirCare 54:102 115 13. French Consensus Guideline. Non invasive ventilation in acute respiratory failure (2006) http://www.srlf.org/Data/ModuleGestionDeContenu/application/375.pdf2006 14. Clinicaltrials.gov.PreoxygenationusingNIVinhypoxemicpatients.http://clinicaltrials.gov/ ct2/show/NCT00472160?term=preoxygenation&rank=2:
Influence of Staff Training on the Outcome of Noninvasive Ventilation for Acute Hypercapnic Respiratory Failure
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JoséLuisLópez-CamposandEmiliaBarrot
39.1 Introduction The education and training of medical personnel in noninvasive ventilation (NIV) is essentialinimprovingoutcomes,reducingfailures,andavoidingcomplicationsassociated with the use of ventilation [1]. Furthermore, adequate training of staff provides a cost reductioninpatientcare.Inthisregard,apropertrainingperiodshouldbepartoftheeducationofrespiratoryhealthcareprofessionswhoarepartofthemultidisciplinaryrespiratoryteamdealingwiththeNIV. Respiratoryphysiciansarekeycomponentsofthismultidisciplinaryrespiratoryteam. Theyshouldbefamiliarwiththedifferentdiseasesunderlyingtherespiratoryfailure,treatments,andknowledgeofhowandwhentoinitiateandcontrolNIV. Nurses are key actors in the management of patients under NIV. They provide 24-h patientcarewithinthehospitalsetting,andtheircontributionisessentialforthemultidisciplinaryrespiratoryteam.Thequalityofthenurse srelationshipwithpatientsandtheir relativesmayalsobeakeyfactorforthesuccessoftheventilation.Asakeyinthecoordinationofpatientcare,nursesmaycontributetothecollaborativecost-effectiveapproach forpatientsunderNIV. Physiotherapists need to work closely with other members of the multidisciplinary respiratoryteamtopromotethebestcareforthepatientonNIV.Physiotherapisttreatment isachievedthroughacombinationofeducationandintervention.Themaingoalsarenot onlytomobilizesecretionsandaidexpectorationbutalsotoreducefearandanxiety,dyspnea,andworkofbreathing[2].
J.L.López-Campos()andE.Barrot UnidadMédico-QuirúrgicadeEnfermedadesRespiratorias, HospitalUniversitarioVirgendelRocío,Seville,Spain e-mail:
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39.2 Influence of Staff Training Regarding Where NIV Occurs ThebestlocationforanNIVtreatmentwilldependonseveralfactors,includingparticularlytheskilllevelsofdoctors,nurses,andtherapistsinthistechnique.Iftherearerelatively few patients per month, NIV is best performed in a single location within every centertofacilitatestafftrainingandtomaximizetheresults.Interestingly,whendeciding where to start NIV, staff training and experience are more important than the location itself.AnadequatenumberofNIV-skilledstaffmustbeavailable24haday.Ideally,NIV usuallyisbestcarriedoutinasinglelocationwithonenurseresponsiblefornomorethan atotalofthreetofourpatientseveryshift[3].
39.3 Use of Staff to Initiate NIV NIVhasbeenreportedtobeatime-consumingprocedure,especiallyatthebeginningof thetrainingperiod.Anumberofstudiesontheintensivecareunithaveshownthatasigni cant amount of time is required in the initial stages to establish the patient on NIV. However,thereisalearningcurve,andwithtime,theserequirementssmoothout,withno differenceinworkloadbetweenskillednursesanddoctorsapplyingNIVandthosewhodo not.Obviously,asmoresophisticatedventilatorsbecomeavailable,muchmoretraining wouldbeneeded.However,eveninthiscase,thiswillbecompensatedwithtimeandthe plateauofthelearningcurve.So,althoughaconsiderableamountoftimeisneededwhen aunit rststartstoprovideNIV,aslongasacriticalmassofnursesandtherapistsremains, newstaffwillgainthenecessaryskillsfromtheircolleagues,andthisamountoftimewill besimilartootherunitsthereafter.
39.4 Importance of Training in NIV ItiswellknownthataproportionofpatientswillfailwithNIV,requiringintubationand invasivemechanicalventilation.Inthisregard,itisimportantthatpersonnelandthefacilityforintubationarerapidlyavailableifneeded.Thisisessentialforarespiratoryunitto avoidanincreasedmortalitytrendwithNIV. SeveralvariablesrecordedatthetimeNIVisinitiatedandafterashortperiodofventilationhavebeendescribedaspredictiveofthelikelihoodofsuccessorfailurewithareasonabledegreeofprecision.OneofthemostimportantonesisthelevelofpHafterafew hoursofventilation[4].Thisre ectstheimportanceofwell-adaptedventilationfromthe beginning.Accordingly,thereareseveralprognosticfactorsthatdependonstafftraining, likeleakminimization,coordinationwiththeventilation,andcompliance. Inonestudy,agroupofconsecutivepatientsrequiringNIVduetoacutehypercapnic respiratory failure (AHRF) were included in a prospective observational cohort study
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performedinconventionalwardsaimingtoanalyzevariablesrelatedtoNIVoutcomefor AHRF[5].Althoughthenumberofpatientswassmall,theauthorswereabletoidentifyan inadequateuseofNIVduetolackofpersonneltraininginallpatientsinwhichNIVfailed (p=0.007).Someoftheerrorsdetectedwerethattherewasabad- ttingmaskwithexcessiveleaks,thepersonneldidnotknowhowtodealwithventilatoralarms,thepersonnel didnotknowhowtocontroloxygentherapyusinghigh owrates,orsimplytheventilator wasnotusedduringthatshiftbecausethestaffdidnotknowhowtooperateit.Theauthors concludedthatstafftrainingisakeyfactorin uencingNIVoutcome.Centersattending patientswithacuterespiratoryproblemsshouldhaveanareaoffocusinwhichthisrequirementisful lled.TheapplicationofNIVbyatrainedandexperiencedteam,withcareful patientselection,shouldoptimizepatientoutcomes.
39.5 Training Programs Trainingprogramsshouldbuildknowledgeinaprogressivemannertoensureknowledge aboutvarioustopicsregardingNIV.Thistrainingshouldbecompulsoryforallhealthcare professionalsdealingwithNIVatanytime,includingnotonlyrespiratoryandintensive carephysiciansbutalsonursesandphysiotherapists. Discussion of the training time needed for adequate training of health personnel involvedintheNIVisvariablebetweenstudies,andtherearecurrentlynoagreedstandards.Thereareguidelinesandtrainingprotocolsforarecommendationfortrainingtailoredtothetypeofschoolthatarebasedmainlyontheplacewhereventilationisapplied. Someauthors[1]havesuggestedthataninitialsessionof2hthreetimesamonthmaygive a basis to start using NIV safely. These sessions can distance themselves in time with increasingexperienceofstaff.Althoughthecontentsmayvaryslightlydependingonthe targetaudience(doctors,nurses,physiotherapists),generallytheyshouldincludeatleast thosetopicsinTable39.1.
Table 39.1 Minimumrequirementsforatrainingprogramfornoninvasiveventilation(NIV)inthe acutesetting Respiratorysystem: Physiology Symptomsandsignsofrespiratoryfailure MainrespiratorydiseasesleadingtoNIV NIVtechnique: Typesofventilators De nitionandselectionoftheventilatormode Initialoperationoftheequipment Selectionofmasks Ventilatorcircuit Monitoringtechnique: Noninvasivecardiorespiratorymonitoring ComplicationsofNIV Problemsolving
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Theeducationandtrainingofmedicalpersonnelisessentialinimproving outcomes,reducingfailures,andavoidingcomplicationsassociatedwiththeuse ofventilation. WhendecidingwheretostartNIV,stafftrainingandexperiencearemore importantthanthelocationitself. TheapplicationofNIVbyatrainedandexperiencedintensivecareunitteam, withcarefulpatientselection,shouldoptimizepatientoutcomes. Centersattendingpatientswithacuterespiratoryproblemsshouldhaveanarea offocusinwhichstafftrainingisakeyelement. Thetrainingtimeneededforadequatetrainingofhealthpersonnelinvolvedinthe NIVisvariablebutshouldincluderepetitivesessionsdependingonthedegreeof expertise.
References 1. Esquinas Rodríguez A, Martín UJ, Cordova FC, Criner GJ, González Díaz G (2006) Organizaciónhospitalariayformaciónclínicaenventilaciónmecánicanoinvasiva.In:Esquinas RodríguezA(ed)Tratadodeventilaciónmecánicanoinvasiva.Prácticaclínicaymetodología. AulaMedica,Madrid,pp1129 1134 2. SimondsAK(2001)Non-invasiverespiratorysupport:apracticalhandbook,2ndedn.Arnold, London,pp230 245 3. Miller SDW, Latham M, Elliott MW (2008) Where to perform NIV. Eur Respir Mon 41: 189 199 4. ConfalonieriM,GarutiG,CattaruzzaMS,OsbornJF,AntonelliM,ContiG,KodricM,RestaO, Marchese S, Gregoretti C, Rossi A (2005) Italian noninvasive positive pressure ventilation (NPPV)studygroup.AchartoffailureriskfornoninvasiveventilationinpatientswithCOPD exacerbation.EurRespirJ25:348 355 5. Lopez-CamposJL,GarciaPoloC,LeonJimenezA,ArnedilloA,Gonzalez-MoyaE,Fenandez BerniJJ(2006)Stafftrainingin uenceonnon-invasiveventilationoutcomeforacutehypercapnicrespiratoryfailure.MonaldiArchChestDis65:145 151
Section VII The Role of Sedation
Sedation for Noninvasive Ventilation in Intensive Care
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Jean-MichelConstantin,RenauGuerin,andEmmanuelFutier
40.1 Introduction At the end of the rst decade of the 21st century, noninvasive ventilation (NIV) is increasingly being used to manage patients with acute respiratory failure (ARF). NotwithstandingtheadvantagesofNIVincriticallyillpatients,NIVisassociatedwitha high risk of failures, including patient refusal to continue the often-uncomfortable sessions.Comparedwiththosewhoavoidintubation,patientswhofailNIVhaveworseoutcomes, including death, so maintenance of patient comfort to optimize the chances of successduringNIVisanimportantgoaloftherapy.SincethedescriptionofARFandits treatmentwithNIVandsedationwithmorphineandmidazolambyRockeretal.[1],the conventionalapproachtoventilationhasbeentousetrachealintubationincasesoflow tolerance.Someauthorshaveproposedtheuseofsedationtoincreasepatientcomfortand NIVtolerance.InaworldsurveyonsedationforNIV[2],thephysicianswhoresponded reportedusingsedationoranalgesiainlessthan25%ofpatients.Currentsedationpracticeswereheterogeneousandmainlydeterminedbyclinicalexperience.Theseobservationsemphasizethelackofevidence-basedinformationorrecommendationsfortheuseof sedationduringNIV.Notwithstanding,ifsedationcoulddecreaseNIVfailure,itshouldbe usedwithcautionbyatrainedteamwithsomerecommendations.
40.2 Which Drug for Sedation? IntheworldsurveybyDevlinetal.,sedationandanalgesiaweremorecommonlyusedby NorthAmericansthanEuropeans(41%vs.24%forsedation,48%vs.35%foranalgesia). InNorthAmerica,benzodiazepinealonewasthepreferredagent(33%),followedbyan
J.-M.Constantin(),R.Guerin,andE.Futier, GeneralICU,EstaingHospital,UniversityHospitalofClermont-Ferrand, 63000Clermont-Ferrand,France e-mail:
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opioidalone(29%).Europeanswerelesslikelytouseabenzodiazepinealone(25%)but morelikelytouseanopioidalone(37%).Sedationwasusuallyadministeredasanintermittentintravenousbolus,outsideaprotocol,andwasassessedbynursesusingclinical endpointsratherthanasedationscale[2]. Onarationalpointofview,theidealdrugforsedationduringNIVshouldbeshortacting, haveaconstanthalf-life,andhavenoaccumulationincaseofrenalorliverfailure.Italso shouldnotdecreaserespiratorydriveorhemodynamicsstatus.Attheend,itshouldhaveanxiolyticandanalgesicproperties.Obviously,thisdrugdoesnotexist.Butsomedrugs,aloneor inassociation,havepharmacologicalpropertiesthatarenotsofarfromtheidealdrug. Remifentanilisanopioidwithpharmacodynamicpropertiessimilartothoseofother opioidsbutwithauniquepharmacokineticpro le.Itisapotent,short-actingopioidwith a m-selectivity. Its metabolism is not in uenced by hepatic or renal dysfunction; it is metabolized by nonspeci c blood and tissue esterases into a pharmacology-inactive metabolite.Theeliminationhalf-lifeofremifentanilislessthan5min,whichisindependentofinfusionduration.Sinceitinteractsalmostexclusivelywithm1-receptors,remifentanilhasbeenusedinpatientsunderpressuresupportventilation.Atlowdose,remifentanil increasescomfortwithoutdecreasingrespiratorydrive.Ourgrouphasconductedastudy ofremifentanil-basedsedationincaseofNIVfailure[3].Inthispilotstudy,continuous administration of remifentanil was associated with an increase in NIV tolerance. RemifentanildidnotincreasePaco2.Noaspirationpneumoniaoccurredafter1,200hof sedationduringNIV. Dexmedetomidine,ana2-agonist,isanewsedativeagentusedintheUnitedStates.It currentlylacksapprovalinEurope.Dexmedetomidinestimulatesa2-adrenergicreceptors inthelocusceruleustoprovidesedationandinthespinalcordtoenhanceanalgesia.Italso causessympatholysisviacentralandperipheralmechanisms.Continuousinfusionmaintains unique sedation (patients appear to be asleep but are readily roused), analgesic- sparingeffect,andminimaldepressionofrespiratorydrive.Ithasbeenusedforsedation duringNIVintenpatientsinARFwhoweresubsequentlyuncooperative(ratedas1onthe Ramsayscoreand 1ormoreontheRichmondAgitation SedationScale[RASS])[4]. Allpatientssatis edthetargetcriteriaofaRamsayscoreof2ormoreandaRASSscore of0orlesswithin1h,experiencingadequatesedationevenatlowinitialloadingdoseor without an initial loading dose. Although this study showed no substantial changes in hemodynamicsinanypatient,aninitialloadingdoseofdexmedetomidinemaycausecardiovascular adverse drug reactions such as hypertension, hypotension, or bradycardia. Resultsofthisstudysuggestthat,foragitation,dexmedetomidineinitiatedatalowinitial loading dose followed by continuous infusion can provide adequate sedation and safer controlforpatientsonNIV. Propofol,awidelyuseddrugforsedationintheintensivecareunit(ICU),hassomeinterestingpropertiesforsedationduringNIV.Target-controlledinfusion(TCI)allowsrapidand preciseadjustmentofthepropofolconcentrationaccordingtotheclinicalresponseofthe patient.Physiologicalstudiesontheeffectsofsubhypnoticconcentrationsofpropofolon respiratorymechanics,pharyngealfunction,andairwayprotectionhavesuggestedthepossibilityofcarryingoutNIVwhilepatientsareundersedation.Unfortunately,nodatahave yetbeenpublishedregardingthisdrug.TCIisavailableforremifentanilandshouldbean interestingadministrationmodeforthisindication.
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Benzodiazepinesdonothavethesamepharmacokineticpropertiesasthepreviously described drugs, and continuous administration should be discouraged. However, anxiolyticpropertiesmaybeattractiveinthisindication.Asingle-shotadministrationofbenzodiazepinesfollowed,ornot,byanothersedativedrug(remifentanilorpropofol)should beavaluablecompromise.
40.3 Monitoring Sedation During NIV Several articles have shown that too much NIV will kill NIV. Monitoring sedation decreasesmortalityinmechanicallyventilatedpatients.MonitoringsedationduringNIV isakeypointofasuccessfulprocedure. AsforallICUpatients,evaluationofsedationshouldbeperformedbynursesandothers according to a scale. Moreover, sedation for NIV should be included in a sedation protocolusedintheICU. In the protocol, we could recommend an evaluation of pain and consciousness. Evaluation of pain should be performed by numeric or analogic scale in self-reporting patients.Inpatientsunabletoself-reportpainduetodeepsedationordelirium,anewtool hasbeenpublished.Itseemsthatthisscale,proposedbyChanquesetal.[5],istheonly waytoevaluatesedationofnoninvasivelyventilatedpatientsunabletoself-report. Many scales have been published to evaluate consciousness. There is a lack of data comparingthesedifferentscales.Wecouldrecommenduseofthescaleroutinelyusedinthe ICU.IfnosedationprotocolexistsintheICU,the rstpointistoimplementascoringsystem.SedationusedforNIVisoftenamoderatesedation,called awake sedation.So,we couldrecommenduseofamodernscalewithprecisedescriptionoflowsedationlevels.
40.4 Conclusion SedationforNIVcanreduceNIVfailureandsodecreasemorbidityinselectedpatients.It shouldbehighlightedthatthisprocedureisahigh-riskone.ItmustbeperformedinanICU withtrainedindividualsandwithalltheconventionalmonitoring.Asedationprotocolmust beimplementedintheICU.Evaluationofsedationandadministrationofdrugscouldbeef cientlydonebynursesandothersaccordingtotheprotocol.Theidealdrugdoesnotexist today.Wecouldrecommendtheuseofremifentanilorpropofol.Inacountrywheredexmedetomidineisavailable,itcouldrepresentaninterestingalternative.Thecontinuousadministrationofbenzodiazepinesshouldbediscouraged,buttheanxiolyticpropertiesofthesedrugs may be used in a single-shot administration. Nonpharmacological sedation, like hypnosis, couldincreaseNIVtolerancewithfeweradverseeventsandcouldbeencouraged[6]. SedationforNIVcouldbehelpfulinthemanagementofARFwithNIV,butduringthe procedure,thebene t/riskratiomustbecarefullyevaluated.
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SedationforNIVmustbeincludedinasedationprotocol. Evaluationofpainandconsciousnessmustbeperformedbyspeci csscale. Onlyshortactingwithoutaccumulationdrugsshouldbeusedinacontinuous administrationmode. Bene t/riskratiomustbecarefullyevaluatedallalongprocedure.
References 1. Rocker GM, Mackenzie MG, Williams B, Logan PM (1999) Noninvasive positive pressure ventilation:successfuloutcomeinpatientswithacutelunginjury/ARDS.Chest115:173 177 2. DevlinJW,NavaS,FongJJ,BahhadyI,HillNS(2007)Surveyofsedationpracticesduring noninvasivepositive-pressureventilationtotreatacuterespiratoryfailure.CritCareMed35: 2298 2302 3. ConstantinJM,SchneiderE,Cayot-ConstantinSetal(2007)Remifentanil-basedsedationto treatnoninvasiveventilationfailure:apreliminarystudy.IntensiveCareMed33:82 87 4. AkadaS,TakedaS,YoshidaYetal(2008)Theef cacyofdexmedetomidineinpatientswith noninvasiveventilation:apreliminarystudy.AnesthAnalg107:167 170 5. ChanquesG,PayenJF,MercierGetal(2009)Assessingpaininnon-intubatedcriticallyill patients unable to self report: an adaptation of the Behavioral Pain Scale. Intens Care Med 35:2060 2067 6. ConstantinJM,PerbetS,FutierEetal(2009)Impactofsophrologyonnon-invasiveventilation toleranceinpatientswithacuterespiratoryfailure.AnnFrAnesthReanim28:215 221
Use of Dexmedetomidine in Patients with Noninvasive Ventilation
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ShinhiroTakeda,ShinjiAkada,andKeikoNakazato
41.1 Introduction Agitationanddeliriumarerelativecontraindicationsfornoninvasiveventilation(NIV)in acutecare[1].Thesecauseseriouscomplications,andevenifindicated,NIVsometimes failswiththesecomplications.Althoughsedationtherapycanplayanimportantrolein NIVsuccess,itisalsopotentiallydangerousbecauserespiratorydepressionisaconcern whenusingpotentanalgesicsorsedatives.Routineuseofsedativessuchasopioidsand benzodiazepinescanleadtoafataloutcomewhenoverdosed. Ahighconcentrationofalpha-2receptorsisfoundinthelocusceruleus,whichisinvolved inregulatingsleep.Dexmedetomidineisconsideredafullagonistofthealpha-2receptor, withanalpha-2/alpha-1bindingaf nityratioof1,620:1,whichappearstopromotesedation,hypnosis,analgesia,sympatholysis,neuroproteciton,andinhibitionofinsulinsecretion [2].Incontrasttoinfusionsofopioids,benzodiazepines,orpropofol,dexmedetomidineis abletoachieveitssedative,hypnotic,andanalgesiceffectswithoutcausinganyclinically relevantrespiratorydepression.Ithasbeenusedsuccessfullytofacilitatetrachealextubation inpatientswhohadpreviouslyfailedextubationbecauseofexcessiveagitation[3,4]. Dexmedetomidine would be effective as a sedative during NIV and could be used withoutadverselyaffectingtherespiratorystateofpatientsonNIV.
41.2 Analysis Main Topics Devlinetal.investigatedpracticesandattitudesregardingsedationduringNIV[5].The mostin uentialfactorsforchoiceofsedationwereclinicalexperiencewiththeagentand lackofeffectonrespiratorydrive.Benzodiazepinesalone(33%)oropioidsalone(29%)
S.Takeda(),S.Akada,andK.Nakazato DepartmentofAnesthesiologyandIntensiveCareMedicine,NipponMedicalSchool, 1-1-5Sendagi,Bunkyo-ku,Tokyo,113-8603,Japan e-mail:
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weremostfrequentlychosenaspreferringthesedationregimenofchoice.Lorazepamalone (18%)wasnextinfrequencyofuse,followedbymidazolam(15%),morphine(21%),and fentanyl(8%).Propofol-containingregimens(7%)anddexmedetomidine-containingregimens(5%)wererarelychosenasa rstline.Fifteenpercentand6%ofphysiciansnever usedsedationoranalgesia,respectively,forpatientswithacuterespiratoryfailurepatients treatedwithNIV.Furthermore,physiciansusedsedationtherapyoranalgesictherapymore than25%ofthetimeinonly45%and26%ofpatients,respectively. Akadaetal.haveshowntheef cacyofdexmedetomidineinpatientstreatedwithNIV inapreliminarystudy[6].ThisstudypopulationconsistedoftenpatientswithacutehypoxemicrespiratoryfailurewhowerereceivedNIV.Inclusioncriteriawerepatientsreceiving NIVwhosubsequentlyexperiencednoncooperationratedas1ontheRamsayscoreand+1 orgreaterontheRichmondAgitation SedationScale(RASSscore).Aftercon rmationof responselevel,administrationofdexmedetomidinewasstartedeitherataninitialloading dosage of 3 mg/kg/h over 5 min followed by continuous infusion at a dosage range of 0.2 0.7mg/kg/horbycontinuousinfusionatadosageof0.7mg/kg/h.Theinfusionratewas adjustedtomaintainatargetsedationlevelofRamsayscore2 3andRASSscoreof0to 2. At baseline, all patients showed response levels of Ramsay score 1 and RASS score 1.5±0.8.MaintenanceoftheRamseyscoreandtheRASSscoreat2.94±0.94and 1.23 ±1.30,respectively,andobtainmentofeffectivesedationweredemonstratedinallcases during dexmedetomidine infusion. Oxygenation improved signi cantly, and all patients weresuccessfullyweanedfromNIV,withnoneintubated,andallweredischargedfromthe intensivecareunit(ICU)alive.Allpatientscouldcoughandexpectoratewithoutassistance. NonewasnewlycomplicatedwithpneumoniaduringthestayintheICU. AcasereportdemonstratedtwocasesinwhichdexmedetomidinefacilitatedtheinductionofNIVwithoutinducingrespiratorydepressionforthetreatmentofacuterespiratory failure caused by severe asthma [7]. In the rst case, because of frequent complaints of dyspneawithprogressiveagitationafterapplicationofNIV,dexmedetomidinewasgiven intravenouslyforsedation.OnehouraftertheinstitutionofNIV,respiratorysymptomswere markedlyimproved.Thepatientwascooperativewiththemaskventilationwiththecontinuousdexmedetomidineinfusion,whichwasadjustedbymaintainingtheRamsaysedationscaleat2or3.Inthesecondcase,assoonasparadoxicalrespiratorymovementwith agitationdeveloped,thepatientwastreatedwithNIVanddexmedetomidineadministered intravenously.OnehouraftertheinstitutionofNIVwithdexmedetomidine,theparadoxical respiratorymovementhadalmostdisappeared,andthegasexchangehadimproved.With thecontinuousdexmedetomidineinfusion,theRamsaysedationscalewasmaintainedat 2or3,andthepatientwasabletocoughsuf cientlytoexcreteinfectioussputum.
41.3 Discussion Most physicians infrequently use sedation and analgesic therapy for NIV to treat acute respiratoryfailure.Thesedationandanalgesicregimensthatphysiciansprefertouseduring NPPV are quite varied. The choice of sedation is also heavily in uenced by perceived respiratorydepressanteffectsoftheagent.Mostphysicianswanttouseasedationagent
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thatdoesnotdepressrespirationorhypoxicdrive.Dexmedetomidineisacentrallyacting alpha-2-adrenergicreceptoragonistthatproducesclinicallyusefulsedationdosedependentlywithoutrespiratorydepression.Thereisnoevidenceofrespiratorydepressionwhen dexmedetomidineisadministeredbyintravenousinfusionatdoseswithintherecommended doserangeof0.2 0.7mg/kg/h.Sedationinducedbydexmedetomidinehastherespiratory patternandelectroencephalogramchangescommensuratewithnaturalsleep[8]. AstudyuseddexmedetomidineinpatientswhobecameagitatedduringNIV,andits ef cacy for sedation was demonstrated [6]. In this study, all patients were successfully weanedfromNIVanddischargedfromtheICUwithoutexperiencingaggravationofthe respiratorystate.Allpatientssatis edthetargetcriteriaofaRamsayscoreof2orgreater andRASSscoreof0orlesswithin1h,experiencingadequatesedationevenatlowinitial loadingdoseorwithoutaninitialloadingdose.Afterintravenousinjection,dexmedetomidinehasanonsetofactionafterapproximately15min.Peakconcentrationsareusually achieved within 1 h after continuous intravenous infusion [2]. The most frequently observed treatment-emergent adverse events are cardiovascular. Although this study showednosubstantialchangesinhemodynamicsinanypatient,aninitialloadingdoseof dexmedetomidinemaycausecardiovascularadversedrugreactionssuchashypertension, hypotension,orbradycardia.Resultsofthisstudysuggestthatdexmedetomidineinitiated atalowinitialloadingdoseandacontinuousinfusioncanprovideadequatesedationand safercontrol.Dexmedetomidinealsoblocksbronchoconstrictionindogs,butthiseffect has not been con rmed in humans [9]. Dexmedetomidine, a sedative unlikely to cause respiratorydepression,providesthepossibilityofachievingeffectivesedationduringNIV, ultimatelyleadingtoanincreaseintherateofNIVsuccess.
Key Recommendations
› › ›
Dexmedetomidinehasfavorablerespiratorypharmacologicpropertiesat therapeuticdoses. Dexmedetomidineisagoodcandidatefortheidealsedationofpatientswith agitationwhoaresupportedbyNIV. Thesebene cialeffectsareexpectedinpatientswithmild(notsevere)agitationor deliriumwithaRamsayscoreand+1or+2asaRASSscore.
References 1. Nava S, Hill N (2009) Non-invasive ventilation in acute respiratory failure. Lancet 374: 250 259 2. PanzerO,MoitraV,SladenRN(2009)Pharmacologyofsedative-analgesicagents:dexmedetomidine,remifentanil,ketamine,volatileanesthetics,andtheroleofperipheralmuantagonists. CritCareClin25:451 469 3. ArpinoPA,KalafatasK,ThompsonBT(2008)Feasibilityofdexmedetomidineinfacilitating extubationintheintensivecareunit.JClinPharmTher33:25 30
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4. SiobalMS,KalletRH,KivettVAetal(2006)Useofdexmedetomidinetofacilitateextubation insurgicalintensive-care-unitpatientswhofailedpreviousweaningattemptsfollowingprolongedmechanicalventilation:apilotstudy.RespirCare51:492 496 5. Devlin JW, Nava S, Fong JJ et al (2007) Survey of sedation practices during noninvasive positive-pressureventilationtotreatacuterespiratoryfailure.CritCareMed35:2298 2302 6. AkadaS,TakedaS,YoshidaYetal(2008)Theef cacyofdexmedetomidineinpatientswith noninvasiveventilation:apreliminarystudy.AnesthAnalg107:167 170 7. TakasakiY,KidoT,SembaK(2009)Dexmedetomidinefacilitatesinductionofnoninvasive positive pressure ventilation for acute respiratory failure in patients with severe asthma. JAnesth23:147 150 8. HsuYW,CortinezLI,RobertsonKMetal(2004)Dexmedetomidinepharmacodynamics:part1: crossovercomparisonoftherespiratoryeffectsofdexmedetomidineandremifentanilinhealthy volunteers.Anesthesiology101:1066 1076 9. VennM,NewmanJ,GroundsM(2003)AphaseIIstudytoevaluatetheef cacyofdexmedetomidineforsedationinthemedicalintensivecareunit.IntensiveCareMed29:201 207
Section VIII Weaning from Conventional Mechanical Ventilation and Postextubation Failure
Extubation and Decannulation of Unweanable Patients with Neuromuscular Weakness
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42.1 Introduction 42.1.1 Respiratory Muscle Aids Thethreerespiratorymusclegroupsaretheinspiratorymuscles,expiratorymuscles,and bulbar-innervatedmuscles.Theinspiratoryandexpiratorymusclescanbeassistedorsupported inde nitely by applying pressure to the body or airways such that no extent of dysfunctionshouldresultinrespiratoryfailureorneedtoresorttotracheotomy.Inspiratory andexpiratorymuscleaidsaredevicesandtechniquesthatinvolvethemanualormechanicalapplicationofforcestothebodyorpressurechangestotheairwaytoassistorsubstitute forinspiratoryorexpiratorymusclefunction.Negativepressureappliedtotheairwayduringexpirationassiststheexpiratorymusclesforcoughing,justaspositivepressureapplied to the airway during inhalation (noninvasive intermittent positive pressure ventilation [IPPV])assistsinspiratoryfunction[4].Amanualthrustappliedtotheabdomenduring expirationorexsuf ation,especiallywhenincombinationwithmildchestcompression, assists expiratory muscle function and increases cough ows. Patients with little or no measurablevitalcapacity(VC)oranyabilitytoautonomouslysustainalveolarventilation or cough can be managed without invasive tubes using these methods. However, even wheninspiratoryandexpiratorymusclesarefunctional,patientswithbulbar-innervated muscledysfunctiontotheextentthatcontinuousaspirationofairwaysecretionsresultsin decrease in an oxyhemoglobin saturation (SpO2) baseline below 95% need to undergo tracheotomytosurvive[15].Atthepointthatthisoccurs,thepatienthasusuallyalready
J.R.Bach DepartmentofPhysicalMedicineandRehabilitation, UniversityofMedicineandDentistryofNewJersey(UMDNJ) theNewJerseyMedicalSchool, B-403,150BergenStreet,Newark,NJ07103,USA e-mail:
[email protected]
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losttheabilitytospeakandswallowfood.Thisessentiallyonlyoccursforpatientswith advancedbulbaramyotrophiclateralsclerosis(ALS)andtheoccasionalpatientwithspinalmuscularatrophytype1(SMA1).
42.1.2 Acute Respiratory Decompensation and Conventional Management Inspiratoryandexpiratorymuscleaidscanbeusedathomeorinthehospitaltoprevent episodesofpneumoniaandrespiratoryfailurethatwouldotherwiseoccurduringintercurrentupperrespiratorytractinfections(URIs)andepisodesofbronchitisduetoineffective coughing.Bothmechanicallyassistedcoughing(MAC)anduptocontinuousnoninvasive ventilatory(NIV)supportareoftenneededduringtheseepisodeswhenquitepossiblynot requiredatothertimes[5,14 16,21].Extremelyimportantisthefeedbackobtainedby usinganoximeterduringacuteURIstoguideintheuseofNIVand,especially,MACto keeptheSpO2over94%ortoreturnittoover94%quicklyifitshoulddecreasebelow 95%.ThisisbecausetheSpO2isonlynormalwhen95%orgreater.Itisimpossibleto developrespiratoryfailurewithSpO2greaterthan94%inambientair.AnySpO2below 95%mustindicatesomecombinationofhypoventilation,airwaysecretioncongestion,and intrinsic lung disease such as atelectasis or pneumonia. When the SpO2 cannot be kept above 94%, then patients usually require hospitalization for pneumonia and perhaps impendingrespiratoryfailure[21]. Typically,thedyspneicpatientarrivesattheemergencyroomofalocalhospitaland immediatelyreceivessupplementaloxygen.HisorheralreadyelevatedCO2levelfurther increases,andCO2narcosisresultsinventilatoryarrest,intubation,andthenfailuretowean frominvasiveventilatorysupportviaatranslaryngealtube;atracheotomyisdonebefore extubation,andpatientsareleftwithalifetimeofinvasiveventilatorysupport.Onceatracheostomytubeisplaced,thepatientoftenlosesallventilator-freebreathingability(VFBA). Thismostoftenoccursbecausethetracheostomytubecausesairwaysecretionsthatblock the respiratory exchange membrane, ventilation via the tube causes inspiratory muscle deconditioning[23],andchronicallyandinvasivelyventilatedpatientstendtobehypocapnic and thereby tolerate less ventilator-free breathing [22]. Their demand for increased ventilatorvolumesandpressuresmayberelatedtobypassingupperairwaysensoryinput. SupplementaloxygenshouldnotbegivenuntilattemptsaremadetonormalizeSpO2(>94%) byusingfull-settingNIVtonormalizeventilation(Paco2)andMACtocleartheairwaysof secretions.IntubationbecomesappropriatewhenoptimaluseofNIVandMACfailtomaintain normalSpO2andthepatientdevelopsrespiratorydistress,mostusuallyduetopneumonia.
42.1.3 Conventional Outcomes of Acute Respiratory Failure Intubated patients who fail spontaneous breathing trials (SBTs) are conventionally told thattracheostomyistheironlyoption.Conventionally,unweanableintubatedpatientsare only extubated following tracheotomy. Once a tracheostomy is placed, the majority of
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patientswilleventuallydiefromcomplicationsdirectlyattributabletothetube,including hemorrhage, tracheoesophageal stulae, respiratory infection, trachectasis, pneumonia, accidental disconnection from the ventilator, and ventilator failure. In a review of four articlesdiscussingoutcomesoftracheostomyventilationforDuchennemusculardystrophy(DMD)intheliterature[18 20,24],17patientssurvivedmorethan2years,including onefor18years.Threediedfromcomplicationsofthetubeinlessthan2years,andtwo diedafter2yearsofuse.Inarelativelylargestudy,Bachetal.reportedmeansurvivalfor 17DMDtracheostomyIPPVusersof7.3±8years(range7daysto12years).Atleast4 ofthepatientsdiedfromcomplicationsassociatedwiththetube[10].Thus,onlytwostudiesreportedmeanprolongationsofsurvivalofover6yearsbytracheostomyIPPV.
42.2 Extubation of Unweanable Patients to NIV/MAC Therearenoguidelinesforextubatingunweanablepatientswithneuromusculardisease (NMD)orwithcriticalcareventilatoryfailure.Despitethis,manysuchpatientsmayhave been continuously NIV dependent with no autonomous breathing ability for decades beforebeinghospitalizedandintubated,whetherforgeneralanesthesiaoranintercurrent pneumonia.ThesepatientstypicallydonotdesiretoswitchfromcontinuousNIVtotracheostomyventilation[3].In1996,adifferentapproachtoextubationanddecannulation wasdescribed.Insteadofventilatorweaningwithoxygensupplementation,thenextubationtosupplementaloxygenandcontinuouspositiveairwaypressure(CPAP)orbilevel positiveairwaypressure(BiPAP),theinvasivetubewasremovedandthepatientsetup withamouthpieceornasalNIV(Fig.42.1)toweanhimselforherselfinambientairby takingfewerandfewerIPPVsviaa15-mmangledmouthpieceornasalinterface[9].All patientswithassistedcoughpeak ows(CPFs)greaterthanorequalto160L/minwere
Fig. 42.1 Ten-year-old girlwithneuro bromatosisstatus post-spinalcordtumor resection,extubated withavitalcapacity (VC)of180mLand noventilator-free breathingability,using 15-mmangled mouthpiece (Malincrodt-PuritanBennett,Pleasanton, CA)forventilatory support
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successfully extubated to NIV and MAC [9]. Subsequently, we successfully extubated over 140 unweanable NMD patients with ALS, myopathies and muscular dystrophies, criticalcaremyopathy,postpolio,myastheniagravis,spinalmuscularatrophy,andspinal cordhightetraplegia.OncesatisfyingtheextubationcriterianotedinTable42.1,100%of thepatientswithCPFsgreaterthan160L/minand85%withCPFlessthan160L/minsucceeded with extubation despite having failed extubation or SBTs in other institutions. Thesepatientshadbeentoldthattheycouldonlysurvivebyundergoingtracheotomy. Successfulextubationofcontinuouslyventilator-dependentpatientswithnoVFBAwas achievedbyusingthefollowingprotocol:Normalalveolarventilationwasmaintainedand MACused(pressures40 60cmH2Oto 40to 60cmH2Owithexsuf ation-timedabdominalthrust)viathetranslaryngealtubeasneededuntilSpO2remained95%oraboveinambient air for 12 h or more. Once SBTs were failed but extubation criteria were met, the nasogastrictubewasremovedifpresenttofacilitateimmediatepostextubationNIV.The VCwasmeasured.ThepatientwasthenextubateddirectlytoNIVonpressurecontrolof 18 20cmH2Oorassist/controlmodeof800 1,500mLdeliveredvolumesandbackuprate of10 12/min.TheNIVwasprovidedviamouthpiece[12],nasal,ororonasalinterface.The patientsusingmouthpieceNIVkept15-or22-mmangledmouthpiecesaccessibletotheir mouths(Fig.42.1).Patientsweanedthemselves,whenpossible,bytakingfewerandfewer mouthpieceIPPVsastolerated.DiurnalnasalIPPVwasusedforchildrenandforthosewho couldnotgraborretainamouthpiecebecauseoforalmuscleweakness,inadequatejaw opening,orinsuf cientneckmovement.Beingopensystems,thepatientstookasmuchof thedeliveredvolumesasneededforcomfortablealveolarventilation.Nosupplementaloxygenwasused.ForepisodesofSpO2below95%,thefollowingwereevaluated:ventilator positiveinspiratorypressure(PIP),interfaceairleak,CO2,andventilatorsettings. ThesuccessinextubatingpatientswithlittleornomeasurableCPFwasduetoavariety offactorsbutmostimportantlytotheexperienceofourrespiratorytherapistswithNIV andMACandrelianceonfamilymemberstoprovideMACevery20 30minasneeded postextubationuntiltheSpO2nolongerdippedbelow95%.Sucharegimensimulatesthe normalcoughingfrequencyduringepisodesofbronchitisorpneumonia.Theaggressive useofMACviatheendotrachealtubewasthemaininterventionthatresultedinnormalizationofSpO2inambientair,themostimportantcriterionforextubation. Table 42.1 Extubationcriteriaforcontinuouslyventilator-dependentpatients D iagnosisofneuromuscularweakness(includingcriticalcareventilatoryfailure)with inabilitytopassSBTsorautonomouslybreathe Afebrile Normalwhitebloodcellcount Someresidualbulbar-innervatedmusclefunction O xyhemoglobinsaturation(SpO2)³95%for12hormoreinambientair Alloxyhemoglobindesaturationsbelow95%reversedbyMACviatranslaryngealtube Fullyalertandcooperative,receivingnosedativemedications Chestradiographabnormalitiesclearedorclearing Suf cientairleakageviaupperairwayforverbalizationaftertubecuffde ation NormalPaco2atpeakinspiratorypressureslessthan35cmH2Owiththecuffde ated
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Fig. 42.2 Twenty-six-year-old man with Duchenne muscular dystrophy (DMD) transferred for extubationafterfailingthreeextubationsovera26-dayperiod.Heuseda15-mmangledmouthpiece,asinFig.42.1,fordaytimeventilatorysupportandalip-sealphalangewithnasalprongs (Hybrid,Tele exMedical,ResearchTrianglePark,NC)fornocturnalventilatorysupport
Generally,pressuresof40 60cmH2Oto 40to 60cmH2Owerealsousedwithan exsuf ation-timedabdominalthrustpostextubation.Thus,thehospitalstaffandpatients careprovidersusedoximetryasfeedbacktomaintainSpO2of95%orabovebyMACand NIV.Extubationwasonlyconsideredsuccessfulifthepatientwasdischargedhomewithoutrequiringreintubation. Ventilator-dependentpatientswithNMDcanachievesuccessfulextubationusingfullNIV andMAC.BecauseoftheseextubationsuccessratesforunweanableNMDpatients,weno longerconsidertracheotomyforventilator-dependentNMDpatientswhohavesomeresidual bulbar-innervatedmusclefunctionandwhocanbemadetosatisfyTable42.1criteria.We nowofferextubationanddecannulationeventothosewithCPFslessthan160L/min.
42.3 Decannulation of Unweanable Patients Anypatientwithanindwellingtracheostomytubewhohasunderstandablespeechwhen thetubecuffisde atedisevaluatedfordecannulation.Patientswithoutseverespeechand swallowingimpairmentareusuallygoodcandidates.Theabilitytoeffectglotticclosure andthentomaintainairwaypatencyduringthecoughiscriticalforsuccessfuldecannulation.AnyunweanablepatientforwhomCPFcanapproach160L/minbyMACwiththe tracheostomytubecappedandthepatientusingNIVisastrongcandidatefordecannulationevenifinspiratoryandexpiratorymusclesarecompletelyparalyzed(VC=0mL).If PCFsaremuchlowerthan160L/minwiththetubeinplace,itisremoved,atleasttemporarily,andthesitecovered.Thisdecreasesobstructiontoupperairwayair ows,allowing
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moreaccuratemeasurementofassistedCPFandfacilitatingtheuseofnoninvasiveIPPV aswellasautonomousbreathing.Ifdespiteairstackingandcoordinatedabdominalthrusts levels still fail to approach 160 L/min, vocal cord paralysis, hypopharyngeal collapse, tracheal stenosis, or other reasons for xed airway obstruction are considered, and the patientisreferredfor ber-opticevaluationoftheupperairway. Anynasogastrictubethatmaybepresentisremovedbeforedecannulation.Thepatient isdecannulateddirectlytofullNIVandapressuredressingplacedovertheostomyuntil theskinisclosed(Tegaderm,3MCompany,St.Paul,MN)[2,7,8,25,26]. Ondecannulation,mostcontinuouslyandinvasivelyventilator-dependentpatientswith VCsgreaterthan250mLweantonocturnal-onlyNIV[9,17].Allpatientstransferredfrom continuousinvasiveventilatorysupportviaatracheostomytubetoNIVwithoutoneprefer it for safety, convenience, swallowing, speech, appearance, comfort, and overall [3]. Noninvasive management also minimizes cost and facilitates return to the community ratherthanlong-terminstitutionalization[11].Whereastracheostomizedventilatorusers willalwaysbeafraidofasphyxiafromventilatorfailureandaccidentaldisconnection,two thirdsofNIVuserswithnoinspiratoryorexpiratorymusclefunctionandlittleornomeasurableVCcanbetaughttoglossopharyngealbreatheforsecurityintheeventofventilator malfunctionorlossofaccesstotheNIVinterface[18,19,23].Theneedtodecannulate tracheostomizedventilatoruserstoNIVcanbeavoided,however,if(unweanable)ventilator-dependentpatientscanbeextubatedwithoutresorttotracheotomy.Wehavedecannulatedover100continuouslyventilator-dependentpatientswithoutasinglefailure[3,15, 18, 19]. In all, 31 patients temporarily regained partial independent respiration before returningtocontinuous(noninvasive)ventilatorysupportwithadvancingdisease.Insome cases, our decannulated and extubated continuously ventilator-supported cases have dependedonNIVforover30yearsforprolongedsurvival.Unfortunately,veryfewcentersdecannulatecontinuouslyventilator-dependentpatients[2,25,26]. Finally,afteryearsofdebateandconsensusconferencesof experts whoseknowledge of NIV is limited to CPAP and the use of low-span BiPAP for patients with sleep- disorderedbreathing, aCentersforDiseaseControlpanelofrespiratoryexpertshasrecommendedthatNIVbeusedforuptoandincluding24-h/dayventilatordependencelong termforDMDpatients[1].Despitethefactthatourcenterhasmanagedover100NIVdependentDMDpatientsandhasnotneededtoresorttotracheotomytopreventrespiratory mortalityforDMDpatientsinover25years,ithastakenthislongforrecognitionofthe factthat,evenintheabsenceofinspiratoryorexpiratoryfunction,patients,eventhosewith minimal bulbar-innervated muscle function, can be managed using NIV and MAC (Fig.42.2).Unfortunately,eventhisexpertconsensusreferstoresortingtotracheotomyfor (1)patientandclinicianpreference,(2)lackofsuccesswithNIV,(3)inabilityofthemedicalsystemto support NIV,(4)threeextubationfailurestoNIV,and(5)failureofNIV andMACtopreventSpO2decreasesbelow95%.Yet,wehaveshownthatnoinformed DMD patient trained in NIV and MAC prefers to undergo tracheotomy [3], virtually noneofourover1,000symptomaticpatientsrefusedNIV[6],theequipmentneededfor NIVissimplerthanforinvasiveventilation,andwiththerequiredfamilyandcaregiver involvementforprovidingNIVandMAC,hospitalizationsandstrainonmedicalfacilities longtermisdiminished[13].Noneofthusfar148consecutivepatientswhofailedextubationorventilatorweaningandweretransferredtoourunitsfailedsuccessfulextubationto
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NIVandMAC.Theonlyappropriateoneofthe ve indications forpossibletracheotomy isthelast[2],thefactthatfailureofNIVandMACtomaintainnormalSpO2canbean indicationfortracheotomy.However,inourexperience,thisonlyoccursforpatientswith advancedbulbarALS.Paradigmsshiftslowly.
References 1. Birnkrant D, Bushby K, Amin R, Bach JR, Benditt J, Eagle M, Finder J, Kalra M, Kissel J, KoumbourlisA,KravitzR.TherespiratorymanagementofpatientswithDuchennemuscular dystrophy:aDMDcareconsiderationsworkinggroupspecialtyarticle.PedPulmonol(inpress) 2. BachJR(1991)Newapproachesintherehabilitationofthetraumatichighlevelquadriplegic. AmJPhysMedRehabil70:13 20 3. BachJR(1993)Acomparisonoflong-termventilatorysupportalternativesfromtheperspectiveofthepatientandcaregiver.Chest104:1702 1706 4. BachJR(1994)Updateandperspectivesonnoninvasiverespiratorymuscleaids:part1 the inspiratorymuscleaids.Chest105:1230 1240 5. BachJR(2002)Amyotrophiclateralsclerosis:prolongationoflifebynoninvasiverespiratory aids.Chest122:92 98 6. BachJR(2004)Themanagementofpatientswithneuromusculardisease.Elsevier,Philadelphia, p414 7. BachJR,AlbaAS(1990)Noninvasiveoptionsforventilatorysupportofthetraumatichigh levelquadriplegic.Chest98:613 619 8. BachJR,GoncalvesM(2004)Ventilatorweaningbylungexpansionanddecannulation.Am JPhysMedRehabil83:560 568 9. Bach JR, Saporito LR (1996) Criteria for extubation and tracheostomy tube removal for patientswithventilatoryfailure.Adifferentapproachtoweaning.Chest110:1566 1571 10. BachJR,O BrienJ,KrotenbergR,AlbaA(1987)ManagementofendstagerespiratoryfailureinDuchennemusculardystrophy.MuscleNerve10:177 182 11. BachJR,IntintolaP,AlbaAS,HollandI(1992)Theventilator-assistedindividual:costanalysisofinstitutionalizationversusrehabilitationandin-homemanagement.Chest101:26 30 12. BachJR,AlbaAS,SaporitoLR(1993)Intermittentpositivepressureventilationviathemouth asanalternativetotracheostomyfor257ventilatorusers.Chest103:174 182 13. Bach JR, Rajaraman R, Ballanger F, Tzeng AC, Ishikawa Y, Kulessa R, Bansal T (1998) Neuromuscular ventilatory insuf ciency: the effect of home mechanical ventilator use vs. oxygentherapyonpneumoniaandhospitalizationrates.AmJPhysMedRehabil77:8 19 14. BachJR,BairdJS,PloskyD,NevadoJ,WeaverB(2002)Spinalmuscularatrophytype1: managementandoutcomes.PediatrPulmonol34:16 22 15. BachJR,BianchiC,Au eroE(2004)Oximetryandindicationsfortracheotomyforamyotrophiclateralsclerosis.Chest126:1502 1507 16. Bach JR, Saltstein K, Sinquée D, Weaver B, Komaroff E (2007) Long term survival in Werdnig-Hoffmanndisease.AmJPhysMedRehabil86:339 345 17. BachJR,BianchiC,Vidigal-LopesM,TuriS,FelisariG(2007)Lungin ationbyglossopharyngeal breathing and air stacking in Duchenne muscular dystrophy. Am J Phys Med Rehabil86:295 300 18. BaydurA,GilgoffI,PrenticeW,CarlsonM,FischerDA(1990)Declineinrespiratoryfunction and experience with long-term assisted ventilation in advanced Duchenne s muscular dystrophy.Chest97:884 889
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19. FukunagaH,OkuboR,MoritoyoT,KawashimaN,OsameM(1993)Long-termfollow-upof patients with Duchenne muscular dystrophy receiving ventilatory support. Muscle Nerve 16:554 558 20. GatinG(1983)Inretdelaventilationassisedanslesdystrophiesmusculaires.AnnReadapt MedPhys26:111 128 21. Gomez-Merino E, Bach JR (2002) Duchenne muscular dystrophy: prolongation of life by noninvasiverespiratorymuscleaids.AmJPhysMedRehabil81:411 415 22. HaberII,BachJR(1994)Normalizationofbloodcarbondioxidelevelsbytransitionfrom conventional ventilatory support to noninvasive inspiratory aids. Arch Phys Med Rehabil 75:1145 1150 23. LevineS,NguyenT,TaylorN,FrisciaME,BudakMT,RothenbergP,ZhuJ,SachdevaR, SonnadS,KaiserLRetal(2008)Rapiddisuseatrophyofdiaphragm bersinmechanically ventilatedhumans.NEnglJMed358:1327 1335 24. Splaingard ML, Frates RC, Harrison GM, Carter RE, Jefferson LS (1984) Home positivepressureventilation:twentyyears experience.Chest4:376 382 25. Viroslav J, Sortor S, Rosenblatt R (1991) Alternatives to tracheostomy ventilation in high levelSCI[abstract].JAmParaplegiaSoc14:87 26. ViroslavJ,RosenblattR,Morris-TomazevicS(1996)Respiratorymanagement,survival,and qualityoflifeforhigh-leveltraumatictetraplegics.RespirCareClinNorthAm3:313 322
Mechanically Assisted Coughing and Noninvasive Ventilation for Extubation of Unweanable Patients with Neuromuscular Disease or Weakness
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JohnRobertBach
43.1 Introduction ThereisjustonepointIwouldliketomention,whichhasjustcomealongwhich,Ithink, makesit[noninvasivepositivepressureventilation]evenmorefeasible.Itissosimplethat whyitwasn tthoughtoflongagoIdon tknow.Actually,someofourphysicaltherapists, instrugglingwiththepatients,noticedthattheycouldsimplytakethepositivepressure attachment,applyasmallplasticmouthpiece ,andallowthattohanginthepatient s mouth.YoucantakehimtotheHubbardtankbysuchmeansandyoucandoanynursing procedure,ifthepatientisontherockingbedandhasazerovitalcapacity[VC],ifyou wanttostopthebedforanyreason,orifyouwanttochangehimfromthetankrespirator tothe bed,orput the cuirass respirator on, or anything to stop the equipment, you can simplyattachthis,hangitbythepatient,hegripsitbyhislips,andthusitallowsforthe excesstoblowoffwhichhedoesn twant. Itworksverywell.Weevenhadonepatientwhohasnobreathingabilitywhohasfallen asleepandbeenadequatelyventilatedbythisprocedure,sothatitappearstoworkvery well,andIthinkdoesawaywithalotofcomplicationsofdif cultyofusingpositivepressure.Youjusthangitbythepatientsandtheygripitwiththeirlips,whentheywantit,and whentheydon twantit,theyletgoofit. Itisjusttoosimple. Dr. John Affeldt, Rwd Table Conference on Poliomyelitis Equipment, Roosevelt Hotel, NewYorkCity,sponsoredbytheNationalFoundationforInfantileParalysisIncorporated, May28-29,1953
J.R.Bach DepartmentofPhysicalMedicineandRehabilitation,UniversityofMedicineand DentistryofNewJersey(UMDNJ) theNewJerseyMedicalSchool, B-403,150BergenStreet,Newark,NJ07103,USA e-mail:
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Sincetheuseofnoninvasiveventilatory(NIV)supportviaamouthpiecewasdescribedin 1953,manyhundredsofpatientswithsevereneuromusculardisease,weakness,orparalysis (NMD) and no ability to autonomously sustain their alveolar ventilation have used strictlynoninvasivemethodsofventilatorysupportwithnoneedtoresorttotracheotomy [1].Thishasbeenrealizedbyconsideringtherespiratorymusclesandhowtoevaluateand supportthemandbyunderstandinghowtoextubateordecannulatethesepatientsbackto noninvasiverespiratorymuscleaidsasneeded.
43.2 The Respiratory Muscle Groups Thethreerespiratorymusclegroupsareinspiratorymuscles,expiratorymuscles,and b ulbar-innervatedmuscles.Theinspiratoryandexpiratorymusclescanbeassistedorsupported inde nitely by applying pressures to the body or airways such that no extent of dysfunctionshouldresultinrespiratoryfailureorneedtoresorttotracheotomy.Inspiratory andexpiratorymuscleaidsaredevicesandtechniquesthatinvolvethemanualormechanicalapplicationofforcestothebodyorpressurechangestotheairwaytoassistorsubstitute forinspiratoryorexpiratorymusclefunction.Negativepressureappliedtotheairwayduringexpirationassiststheexpiratorymusclesforcoughing,justaspositivepressureapplied to the airway during inhalation (noninvasive intermittent positive pressure ventilation [IPPV])assistsinspiratoryfunction.Amanualthrustappliedtotheabdomenduringexpirationorexsuf ation,especiallywhenincombinationwithmildchestcompression,assists expiratorymusclefunctionandincreasescough ows.Patientswithlittleornomeasurable vitalcapacity(VC)oranyabilitytoautonomouslysustainalveolarventilationorcoughcan bemanagedwithoutinvasivetubesusingthesemethods.However,evenwheninspiratory andexpiratorymusclesarefunctional,patientswithbulbar-innervatedmuscledysfunction totheextentthatcontinuousaspirationofairwaysecretionsresultsindecreaseinanoxyhemoglobinsaturation(SpO2)baselinebelow95%needtoundergotracheotomytosurvive [2].Atthepointthatthisoccurs,thepatienthasusuallyalreadylosttheabilitytospeakand swallowfood. Inspiratoryandexpiratorymuscleaidscanbeusedathomeorinthehospitaltoprevent episodesofpneumoniaandrespiratoryfailurethatwouldotherwiseoccurduringintercurrent respiratory tract infections and episodes of bronchitis due to ineffective coughing. Bothmechanicallyassistedcoughing(MAC)anduptocontinuousNIVsupportareoften needed during these episodes when quite possibly not required at other times [2 6]. Sometimes,however,patientswithorwithoutaccesstoNIVorMACdeveloppneumonia andacuterespiratoryfailure.Typically,thedyspneicpatientarrivesattheemergencyroom ofalocalhospitalandimmediatelyreceivessupplementaloxygen.HisorheralreadyelevatedCO2furtherincreases,andCO2narcosisresultsinventilatoryarrest,intubation,and thenfailuretoweanfrominvasiveventilatorysupportviaatranslaryngealtube;tracheotomyisdonebeforeextubation,andpatientsareleftwithalifetimeofinvasiveventilatory support. Once a tracheostomy tube is placed, the patient often loses all ventilator-free breathingability(VFBA).Thismostoftenoccursbecausethetracheostomytubecauses
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airwaysecretionsthattheblockrespiratoryexchangemembrane,ventilationviathetube causes inspiratory muscle deconditioning [7], and chronically and invasively ventilated patientstendtobehypocapnicandtherebytoleratelessventilator-freebreathing[8].Their demandforincreasedventilatorvolumesorpressuresmayberelatedtobypassingupper airwaysensoryinput. Whateverthereasons,mostcontinuouslyandinvasivelyventilator-dependentpatients withVCsgreaterthan250mLweantonocturnal-onlyNIVoncetheirtracheostomytubes areremovedandtheyareconvertedtoNIV[9].Unfortunately,fewcentersdecannulate continuously ventilator-dependent patients [10 13]. If done, though, all patients transferredfromcontinuousinvasiveventilatorysupportviaatracheostomytubetoNIVwithoutonepreferitforsafety,convenience,swallowing,speech,appearance,comfort,and overall [14]. Noninvasive management also minimizes cost and facilitates return to the communityratherthan long-term institutionalization [15]. The need to decannulate tracheostomizedventilatoruserstoNIVcanbeavoided,however,if(unweanable)ventilatordependentpatientscanbeextubatedwithoutresorttotracheotomy. Conventionally,unweanableintubatedpatientsareonlyextubatedfollowingtracheotomy.Allconventional ventilator-weaningparameters assesslunghealthandabilityto autonomously sustain alveolar ventilation. Spontaneous breathing trials (SBTs) must alsobepassedbeforeextubationattemptsareundertaken.Sincethisisoftenimpossiblefor thepatientwithNMD,criticalcarestudiesreportveryfew,ifany.NMDpatients(i.e.,18 of162[14];17of900[16]),andtheycompletelyexcludethesepatientsunlesstheyare weanable[17,18].WhilemostcriticalcareNIVtrialseitherexcludedpatientswithNMD [19]orfailedtomentionany[20,21],arandomizedtrialconductedin37centersbyEsteban etal.thatdidinclude7patientswithNMDof221failedtoshowthatNIVpreventedneed forreintubationorreducedmortality[22].Further,anothermulticenterprospectiverandomizedstudybyConfaloniereetal.comparingstandardtreatmentplusNIVversusstandardtreatmentaloneforacuterespiratoryfailureinseverecommunity-acquiredpneumonia excluded patients on home mechanical ventilation and did not have any patients with NMD[23].The NIV inallstudieswaseithernotspeci edoritwascontinuouspositive airwaypressure(CPAP)orbilevelpositiveairwaypressure(PAP)atspansthatprovide lessthanfullventilatorysupport,andnoneofthemreportedtheuseofassistedcoughing orairstacking[17]. Patients with NMD typically have ineffective cough peak ows (CPFs), which can resultinextubationfailureduetoairwaysecretionaccumulation[18,19],butnostudies reportedCPFortheuseofMAC[16].Indeed,therearenoventilator-weaningparameters thataddresstheabilitytocough.Thus,therearenoguidelinesforextubatingunweanable patientswithNMDorcriticalcareventilatoryfailure.Yet,manysuchpatientsmayhave been continuously NIV dependent with no autonomous breathing ability for decades beforebeinghospitalizedandintubatedwhetherforgeneralanesthesiaoranintercurrent pneumonia.ThesepatientstypicallydonotdesiretoswitchfromcontinuousNIVtotracheostomyventilation[14]. In1996,adifferentapproachtoextubationwasdescribed.Insteadofventilatorweaning with oxygen supplementation, then extubation to supplemental oxygen and CPAP or BiPAP,thenewparadigmconsistedofinvasivetuberemovalandthenallowingthepatient toweanhimselforherselfinambientairbytakingfewerandfewerIPPVsviaa15-mm
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Table 43.1 Extubationcriteriaforcontinuouslyventilator-dependentpatients Age4yearsandolder Diagnosisofneuromusculardisease(NMD;includingcriticalcareventilatoryfailure) Afebrile Normalwhitebloodcellcount VClessthan20%ofnormal Paco2of40mmHgorlessonfullventilatorysupport Oxyhemoglobinsaturation(SpO2)95%orabovefor12hormoreinambientair Alloxyhemoglobindesaturationsbelow95%reversedbymechanicallyassistedcoughing (MAC)viatranslaryngealtube Fullyalertandcooperative,receivingnosedativemedications Chestradiographabnormalitiesclearedorclearing Suf cientairleakageviaupperairwayforverbalizationontubecuffde ation NormalPaco2atpeakinspiratorypressureslessthan35cmH2Owiththecuffde ated
angledmouthpieceornasalinterface[24].AllpatientswithassistedCPFgreaterthanor equalto160L/minweresuccessfullyextubatedtoNIVandMAC,whereasallpatients withlessthan160L/minfailed[24]. SubsequenttoourearlierdataondecannulationtoNIV,weextubated146unweanable patientswithNMDwithamyotrophiclateralsclerosis(ALS),myopathiesandmuscular dystrophies,criticalcaremyopathy,postpolio,myastheniagravis,spinalmuscularatrophy (SMA),andspinalcordhightetraplegia.Oncesatisfyingtheextubationcriterianotedin Table43.1,100%of94consecutivelyreferredpatientswhohadfailedextubationorSBTs andweretoldthattheycouldonlysurvivebyundergoingtracheotomyweresuccessfully extubatedtofullNIVandMACandfoundtohaveassistedCPFgreaterthanorequalto 160L/min.Likewise,47of53extubationsalsosucceededonpatientswhoturnedoutto haveCPFslessthan160L/min.Successfulextubationofcontinuouslyventilator-dependent patientswithnoVFBAwasachievedbyusingtheprotocolthatfollows.
43.3 Extubation Protocol NormalalveolarventilationwasmaintainedandMACused(pressures40 60cmH2Oto 40to 60cmH2Owithexsuf ation-timedabdominalthrust)viathetranslaryngealtube asneededuntilSpO2remainedat95%orhigherinambientairfor12hormore.Once SBTswerefailedbutextubationcriteriaweremet,thenasogastrictubewasremovedif presenttofacilitateimmediatepostextubationNIV.TheVCwasmeasured.Thepatient wasthenextubateddirectlytoNIVonpressurecontrolat18 20cmH2Oorassist/control modeat800 1,500mLdeliveredvolumesandbackuprateof10 12/min.TheNIVwas providedviamouthpiece[25],nasal,ororonasalinterface.Foramouthpiece,NIVpatients kept 15- or 22-mm angled mouthpieces accessible to their mouths (Fig. 43.1). Patients
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Fig.43.1 Ten-year-oldgirl withneuro bromatosis statuspostspinalcordtumor resection,extubatedwitha VCof180mLandno ventilator-freebreathing ability,using15-mmangled mouthpiece(MalincrodtPuritan-Bennett,Pleasanton, CA)forventilatorysupport
weanedthemselves,whenpossible,bytakingfewerandfewermouthpieceIPPVsastolerated.DiurnalnasalIPPVwasusedforchildrenandforthosewhocouldnotgraborretain amouthpiecebecauseoforalmuscleweakness,inadequatejawopening,orinsuf cient neckmovement.Beingopensystems,thepatientstookasmuchofthedeliveredvolumes as needed for comfortable alveolar ventilation. No supplemental oxygen was used. For episodes of SpO2 less than 95%, the following were immediately evaluated: ventilator positiveinspiratorypressure(PIP),interfaceairleak,CO2,andventilatorsettings.Patients withmorethan2minofVFBApostextubationwereexcluded. ThecareprovidersweretrainedinandprovidedMACviaanoronasalinterfaceevery 30 60minpostextubationuntilairwaysecretionexpulsionwasnolongeraproblemand theSpO2nolongerdippedbelow95%.Generally,pressuresof40 60cmH2Oto 40to 60cmH2Owerealsousedwithanexsuf ation-timedabdominalthrustpostextubationas well.Thus,thehospitalstaffandpatients careprovidersusedoximetryasfeedbackto maintainSpO2at95%orabovebyMACandNIV. Extubationwasonlyconsideredsuccessfulifthepatientwasdischargedhomewithout requiringreintubation.When,postextubation,theSpO2decreasedandcouldnotbereturned to and maintained over 90% by full NIV via mouthpiece or nasal IPPV and MAC as needed, the patient was switched to using a closed system, often of nasal prongs with lipseal (Fig. 43.2). Continued desaturation could necessitate supplemental oxygen to approachSpO2to95%andreintubation.Ifreintubated,thepatientwasagainpreparedto achieve the Table 43.1 criteria for reextubation. Only patients with bulbar ALS failed extubation. Postextubation weaning from continuous ventilator dependence took 3 21 daysandinmostcaseswasaccomplishedathome. The success of our protocol, especially in patients with CPF less than 160 L/min, stemmedfromthefactthatMACwasuseduptoevery30minandwasappliedbyfamily membersandpersonalcareattendants,ratherthanonlyonceortwiceanursingshift,to maintain ambient air SpO2 over 94%. Such a regimen simulates the normal coughing
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Fig.43.2 Twenty-six-year-old manwithDuchenne musculardystrophy(DMD) transferredforextubation afterfailingthree extubationsovera26-day period.Heuseda15-mm angledmouthpiece,asin Fig.43.1,fordaytime ventilatorysupportanda lip-sealphalangewithnasal prongs(Hybrid,Tele ex Medical,ResearchTriangle Park,NC)fornocturnal ventilatorysupport
frequencyduringepisodesofbronchitisorpneumonia.TheaggressiveuseofMACviathe endotracheal tube was the main intervention that resulted in normalization of SpO2 in ambientair,themostimportantcriterionforextubation. The87%(47of53) rstattemptextubationsuccessrateonpatientswithmaximum CPFlessthan160L/miniscomparabletothe82.4%(61of74)successratereportedfor extubatingventilator-dependentinfantsandsmallchildrenwithSMAtype1accordingto analmostidenticalprotocol(46).Thedifferenceismostlikelyduetotheabilityofthese patients,asopposedtobabies,tofullycooperatewithNIVandMAC.ThehigherpneumoniariskandextubationfailurerateintheSMA1populationisinlargepartduetothesevere bulbar-innervatedmuscledysfunctionassociatedwiththeirunmeasurableCPF.Thismakes theextubationfailureriskcomparabletothatofouradultswithCPFbelow160L/min. Thus, it is not surprising that the extubation success rates for adult patients with CPF below160L/minwerehigherthanthoseforacomparablepediatricpopulationbutnot nearlysogoodasforpatientswithCPFgreaterthan160L/m.Thelowerthemaximum assistedCPF,thelesslikelythatanypatientcanmaintainairwaypatencyforeffectiveuse ofMACbecauseofglotticdysfunction. Thegeneralnotionthatearlytracheotomyafterintubationsomehowfacilitatesventilatorweaning[26]shouldbereassessedforpatientswithNMD.Inmostinstances,onextubation, patients with VC of 250 mL or more eventually weaned from continuous to nocturnal-onlyaidbytakingfewerandfewermouthpieceIPPVs.Thus,theparadigmof weaningthenextubationcanbechangedtoextubationthenweaning.Employingnoninvasiveratherthaninvasivemechanicalventilationhasalsobeenreportedtodecreaseriskof ventilator-associatedpneumoniaby75%orgreater[27]andothercomplicationsassociatedwithinvasiveairwaytubes.Useofmouthpiecesratherthanothermethodsofventilatory support also facilitated speech, oral intake, comfort, and air stacking to deep lung insuf ationstomaintainpulmonarycompliance[25],diminishatelectasis,andaugment CPF[28 30].Nasalinterfaceskinpressurewasalsoavoided. Thus,ventilator-dependentpatientswithNMDcanachievesuccessfulextubationusing fullNIVandMAC.Noninvasivemanagementofbothacuteandchronicventilatoryfailure
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maintainsqualityoflife,maximizesventilator-freebreathing,facilitatescommunitymanagement,andshouldbemorewidelyoffered.Becauseoftheseextubationsuccessratesfor unweanablepatientswithNMD,wenolongerconsidertracheotomyforventilator-dependentpatientswithNMDwhohavesomeresidualbulbar-innervatedmusclefunctionand whocanbemadetosatisfyTable43.1criteria;wenowofferextubationeventothosewith CPFlessthan160L/m.
References 1. Bach JR (2004) The management of patients with neuromuscular disease. Elsevier, Philadelphia 2. BachJR,BianchiC,Au eroE(2004)Oximetryandindicationsfortracheotomyforamyotrophiclateralsclerosis.Chest126:1502 1507 3. Gomez-Merino E, Bach JR (2002) Duchenne muscular dystrophy: prolongation of life by noninvasiverespiratorymuscleaids.AmJPhysMedRehabil81:411 415 4. BachJR(2002)Continuousnoninvasiveventilationforpatientswithneuromusculardisease andspinalcordinjury.SeminRespirCritCareMed23:283 292 5. BachJR,BairdJS,PloskyD,NevadoJ,WeaverB(2002)Spinalmuscularatrophytype1: managementandoutcomes.PediatrPulmonol34:16 22 6. BachJR(2002)Amyotrophiclateralsclerosis:prolongationoflifebynoninvasiverespiratory aids.Chest122:92 98 7. LevineS,NguyenT,TaylorN,FrisciaME,BudakMT,RothenbergP,ZhuJ,SachdevaR, SonnadS,KaiserLRetal(2008)Rapiddisuseatrophyofdiaphragm bersinmechanically ventilatedhumans.NEnglJMed358:1327 1335 8. HaberII,BachJR(1994)Normalizationofbloodcarbondioxidelevelsbytransitionfrom conventional ventilatory support to noninvasive inspiratory aids. Arch Phys Med Rehabil 75:1145 1150 9. BachJR,GoncalvesM(2004)Ventilatorweaningbylungexpansionanddecannulation.Am JPhysMedRehabil83:560 568 10. BachJR,AlbaAS(1990)Noninvasiveoptionsforventilatorysupportofthetraumatichigh levelquadriplegic.Chest98:613 619 11. BachJR(1991)Newapproachesintherehabilitationofthetraumatichighlevelquadriplegic. AmJPhysMedRehabil70:13 20 12. Viroslav J, Sortor S, Rosenblatt R (1991) Alternatives to tracheostomy ventilation in high levelSCI[abstract].JAmParaplegiaSoc14:87 13. ViroslavJ,RosenblattR,Morris-TomazevicS(1996)Respiratorymanagement,survival,and qualityoflifeforhigh-leveltraumatictetraplegics.RespirCareClinNAm3:313 322 14. BachJR(1993)Acomparisonoflong-termventilatorysupportalternativesfromtheperspectiveofthepatientandcaregiver.Chest104:1702 1706 15. BachJR,IntintolaP,AlbaAS,HollandI(1992)Theventilator-assistedindividual:costanalysisofinstitutionalizationversusrehabilitationandin-homemanagement.Chest101:26 30 16. Frutos-VivarF,FergusonND,EstebanA,EpsteinSK,ArabiY,ApezteguiaC,GonzalezM, HillNS,NavaS,D EmpaireGetal(2006)Riskfactorsforextubationfailureinpatientsfollowingasuccessfulspontaneousbreathingtrial.Chest130:1664 1671 17. CaplesSM,GayPC(2005)Noninvasivepositivepressureventilationintheintensivecare unit:aconcisereview.CritCareMed33:2651 2658 18. Smina M, Salam A, Khamiees M, Gada P, Amoateng-Adjepong Y, Manthous CA (2003) Coughpeak owsandextubationoutcomes.Chest124:262 268
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19. FerrerM,ValenciaM,NicolasJM,BernadichO,BadiaJR,TorresA(2006)Earlynoninvasive ventilationavertsextubationfailureinpatientsatrisk:arandomizedtrial.AmJRespirCrit CareMed173:164 170 20. AntonelliM,ContiG,MoroML,EsquinasA,Gonzalez-DiazG,ConfalonieriM,PelaiaP, PrincipiT,GregorettiC,BeltrameFetal(2001)Predictorsoffailureofnoninvasivepositive pressureventilationinpatientswithacutehypoxemicrespiratoryfailure:amulti-centerstudy. IntensiveCareMed27:1718 1728 21. NavaS,GregorettiC,FanfullaF,SquadroneE,GrassiM,CarlucciA,BeltrameF,NavalesiP (2005) Noninvasive ventilation to prevent respiratory failure after extubation in high-risk patients.CritCareMed33:2465 2470 22. EstebanA,Frutos-VivarF,FergusonND,ArabiY,ApezteguiaC,GonzalezM,EpsteinSK, HillNS,NavaS,SoaresMAetal(2004)Noninvasivepositive-pressureventilationforrespiratoryfailureafterextubation.NEnglJMed350:2452 2460 23. ConfalonieriM,PotenaA,CarboneG,PortaRD,TolleyEA,UmbertoMeduriG(1999)Acute respiratoryfailureinpatientswithseverecommunity-acquiredpneumonia.Aprospectiverandomizedevaluationofnoninvasiveventilation.AmJRespirCritCareMed160:1585 1591 24. Bach JR, Saporito LR (1996) Criteria for extubation and tracheostomy tube removal for patientswithventilatoryfailure.Adifferentapproachtoweaning.Chest110:1566 1571 25. BachJR,AlbaAS,SaporitoLR(1993)Intermittentpositivepressureventilationviathemouth asanalternativetotracheostomyfor257ventilatorusers.Chest103:174 182 26. BlotF,MelotC(2005)Indications,timing,andtechniquesoftracheostomyin152French icus.Chest127:1347 1352 27. KollefMH(1999June)Avoidanceoftrachealintubationasastrategytopreventventilatorassociatedpneumonia.IntensiveCareMed25(6):553 555 28. Bach JR, Kang SW (2000) Disorders of ventilation: weakness, stiffness, and mobilization. Chest117:301 303 29. KangSW,BachJR(2000)Maximuminsuf ationcapacity.Chest118:61 65 30. IshikawaY,BachJR,KomaroffE,MiuraT,Jackson-ParekhR(2008)Coughaugmentationin Duchennemusculardystrophy.AmJPhysMedRehabil87(9):726 730
Noninvasive Positive Pressure Ventilation in the Postextubation Period
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HasanM.Al-DorziandYaseenM.Arabi
44.1 Introduction Noninvasivepositivepressureventilation(NPPV)hasbeendemonstratedtobeeffectivein varioustypesofacuterespiratoryfailure.LevelIevidencehasbeenestablishedforitsuse foracuterespiratoryfailureduetoacuteonchronicobstructivepulmonarydisease(COPD) exacerbations [1, 2] or cardiogenic pulmonary edema [3], and in immunocompromised hosts[4].Byavoidingintubation,NPPVhasmanyadvantagesandbene ts.Theseinclude theeaseofapplication;preservationoftheairwaydefensemechanisms;maintenanceofthe patient sabilitytospeak,eat,andcough;andreductionofcomplicationsrelatedtointubation,especiallyventilator-associatedpneumonia[5].ThesereasonsswayphysicianstoutilizeNPPVinothersettings,includingthepostextubationperiod[6,7].Inacross-sectional postalsurvey,approximately40%of385attendingphysiciansandresidentsinfourspecialtiesat15CanadianteachinghospitalsusedNPPVforpostextubationrespiratoryfailure,whichwasthethirdmostfrequentindicationafterCOPDandcongestiveheartfailure (CHF)[6].AtMassachusettsGeneralHospital,458patientsweretreatedwithNPPVfor acuteoracute-on-chronicrespiratoryfailurein2001,theindicationin21%ofthembeing postextubationrespiratoryfailure[7].Thischapterdiscussestheevidencerelatedtotheuse ofNPPVinthepostextubationperiod,whichhappensinoneofthreesettings: 1. Facilitationofweaningfrominvasiveventilationandextubation 2. Preventionofpostextubationrespiratoryfailureandreintubation 3. Treatmentofpostextubationrespiratoryfailure
Y.M.Arabi()andH.M.Al-Dorzi IntensiveCareDepartment,KingAbdulazizMedicalCityand CollegeofMedicine,KingSaudBinAbdulazizUniversityforHealthSciences, MC1425,P.O.Box22490,Riyadh,11426,SaudiArabia e-mail:
[email protected],
[email protected]
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Table 44.1 Evidence-basedgradingsystemusedtorankrecommendations Gradeofrecommendation Bene tsversusrisks Supportingevidence Grade1A,strong recommendation,high-quality evidence
Benefitsclearlyoutweigh risksorviceversa
RCTswithoutimportant limitationsoronexceptionally strongobservationalstudies
Grade1B,strongrecommenda- Bene tsclearlyoutweigh risksorviceversa tion,moderate-quality evidence
RCTswithimportantlimitationsoronverystrong observationalstudies
Grade1C,strongrecommenda- Bene tsclearlyoutweigh tion,low-qualityevidence risksorviceversa
Observationalstudies,case series,orRCTswithmajor limitationsorindirectevidence
Grade2A,weakrecommendation,high-qualityevidence
Bene tscloselybalanced withrisks
RCTswithoutimportant limitationsoronexceptionally strongobservationalstudies
Grade2B,weakrecommendation,moderate-quality evidence
Bene tscloselybalanced withrisks
RCTswithimportantlimitationsoronverystrong observationalstudies
Grade2C,weakrecommendation,low-qualityevidence
Bene tscloselybalanced withrisks
Observationalstudies,case series,orRCTswithmajor limitationsorindirectevidence
RCT randomized controlled trial
Inourevaluationoftheevidence,weusedanevidence-basedgradingsystemadoptedfrom theAmericanCollegeofChestPhysiciansEvidence-BasedClinicalPracticeGuidelines forantithromboticagents[8]assummarizedinTable44.1.
44.2 NPPV to Facilitate Weaning and Extubation Thissectionappliestopatientsoninvasiveventilationwhoarenotreadyforextubationasper extubationcriteriaandareextubatedandsupportedwithNPPV.In1992,Udwadiaandcolleagueswerethe rsttoreportthatdif cult-to-weanpatientscouldbefreedfrommechanical ventilation after extubation with a brief period of NPPV [9]. This was followed by other uncontrolled studies [10, 11]. Nava et al. performed the rst randomized controlled trial (RCT)inwhichNPPVwasusedtoweanpatientswithCOPD(n=50)withhypercapnic respiratoryfailurewhohadbeenintubatedforlongerthan48handfailedspontaneousbreathingtrials(SBTs)usingaT-piece[12].Twenty- vepatientswereextubatedtoNPPV,andthe other25patientswerekeptonpressuresupportventilation(PSV)withintermittentSBTsand wereextubatedwhenready.Comparedtoconventionalweaning,extubationtoNPPVwas associatedwithshorterdurationofmechanicalventilation(10.2±6.8vs.16.6±11.8days, p=0.021)andintensivecareunit(ICU)stay(15.1±5.4vs.24.0±13.7days,p=0.005),
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lower incidence of nosocomial pneumonia (0% vs. 28%) and higher 60-day survival rate (92%vs.72%,p=0.002). Giraultetal.evaluatedtheroleofNPPVin33patientswhofaileda2-hT-pieceweaning trial.Thesepatientshadacute-on-chronicrespiratoryfailure;17patientshadCOPD,8had restrictivelungdisease,and8hadcombinedobstructiveandrestrictivelungdisease.Patients wererandomizedtoreceiveeitherinvasivepressuresupportventilation(IPSVgroup,n=16) orintermittentNPPVwithanasalorfacemaskappliedimmediatelyafterextubation(NPPV group,n=17)[13].ComparedtotheIPSVgroup,theNPPVgrouphadshorterdurationof endotrachealmechanicalventilation(4.6±1.9vs.7.7±3.8days,p=0.004)butsimilarneed forreintubation(23%vs.25%),ICUandhospitalstay,andin-hospitaldeath. Ferrer et al. conducted a prospective RCT of 43 mechanically ventilated patients whohadfailedaweaningtrialfor3daysconsecutively[14].Mostofthepatients(58%) had COPD. Twenty-one patients were extubated and immediately received bilevel NPPVcontinuouslyforatleast24h.Theother22patientsremainedintubatedandhad dailyweaningattempts.Therewasnodifferenceintheprevalenceofchronicpulmonary disease in the two groups. Compared with the conventional weaning group, the NPPVgrouphadshorterdurationofinvasiveventilation(9.5±8.3vs.20.1±13.1days, p=0.003)andICU(14.1±9.2vs.25.0±12.5days,p=0.002)andhospitalstays(28.8 ±15.6vs.40.8±21.4days,p=0.026),lessneedfortracheotomytowithdrawventilation(1.5%vs.13.6%,p=0.001),andlowerincidenceofnosocomialpneumonia(5.2% vs.13.6%,p=0.042).ItwasalsoassociatedwithincreasedICUsurvival(90%vs.59%, p=0.045). Trevisanandcolleaguesrandomized65patientswhowereintubatedforlongerthan48h andthenfailedaT-pieceweaningtrialtoeitherbilevelNPPVbyfacemask(n=28)orcontinuedweaningwithinvasiveventilation(n=37)[15].COPDexacerbation,postoperativeacute respiratoryfailure,andheartdiseasewerethemostcommonindicationsforinvasiveventilationinbothgroups.Althoughbothgroupshadsimilardurationofmechanicalventilationafter randomization,ICUlengthofstay,andmortality,theNPPVgrouphadlowerincidenceof pneumonia(3.6%vs.45.9%,p<0.001)andtracheotomy(0%vs.18.9%,p=0.01). Burns et al. conducted a systematic review of 12 randomized and quasi-randomized controlledtrialsenrolling530participantsandexaminingearlyextubationwithimmediate applicationofNPPVcomparedwithcontinuedinvasiveweaningonimportantoutcomes inintubatedadultswithrespiratoryfailure[16].Comparedwithinvasiveweaning,NPPV weaningwassigni cantlyassociatedwithreducedmortality(relativerisk[RR]0.55;95% con denceinterval[CI]0.38 0.79),ventilator-associatedpneumonia(0.29;95%CI0.19 0.45), length of stay in ICU (weighted mean difference 6.27 days; 95% CI 8.77 to 3.78)andhospital( 7.19days;95%CI 10.80to 3.58),totaldurationofventilation, anddurationofinvasiveventilation.Thebene tsformortalityandweaningfailureswere nonsigni cantlygreaterintrialsthatexclusivelyenrolledpatientswithCOPDcomparedto mixedpopulations. Therefore,thebestofcurrentevidencesupportstheuseofNPPVasaweaningmodalityfor earlyextubationinpatientswithCOPD(recommendation1B).TheevidenceforusingNPPV tofacilitateweaninginpatientswithoutCOPDwhofailSBTislessconvincing(recommendation2C),andfurtherresearchisrequiredbeforeitcanbeadoptedforgeneralapplication.
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44.3 NPPV for Prevention and Treatment of Postextubation Respiratory Failure Extubationfailureiscommonlyde nedastheinabilitytotoleratespontaneousbreathing withouttranslaryngealventilatorysupportwithin48 72hofextubation[17 19].Approximately12.5%ofextubatedpatientsdevelopextubationfailurerequiringreintubation[20]. This rate varies depending on the type of patient population, with the rate being higher (12 20%)inpediatric,medical,andneurologicalICUsandlower(5 8%)insurgicaland traumaICUs[21].Extubationfailurecanoccurbecauseofimbalancebetweenrespiratory musclecapacityandloadthatbecameapparentafterextubation[22],persistenceoftheprimaryprocessthatledtointubation,postextubationcardiacischemiaorfailure,postextubationCOPDexacerbation,upperairwayobstruction,excessiveorinabilitytoclearsecretions, aspiration,respiratorymuscleweakness,andneurologicdysfunction[23]. Predictors for extubation failure have been sought. Large endotracheal secretions [24 26],weakcough[24,25],depressedmentalstatus[24,25],andhypercapnia[27] areassociatedwiththerequirementforreintubationafterasuccessfulbreathingtrial. A retrospective evaluation of 900 patients on mechanical ventilation for longer than 48h,13%ofwhomrequiredreintubation,showedthatincreasingrapidshallowbreathingindex(RSBI)(oddsratio[OR]1.01perunit;95%CI1.003 1.015),positive uid balance (OR 1.70; 95% CI 1.15 2.53), and pneumonia as the reason for initiating mechanical ventilation (OR 1.77; 95% CI 1.10 2.84) were independent predictors of extubationfailure[28]. ExtubationfailureisassociatedwithhigherICUandhospitalmortalitycomparedto patientswhodonotrequirereintubationwithin48 72h[29,30].Italsoleadstoincreased durationofmechanicalventilation,lengthofICUandhospitalstay,needforpostacutecare hospitalization,andtheneedfortracheostomy[29].Thisincreasedmorbidityandmortalitycompelsintensiviststo ndwaystoavoidreintubation.NPPVhassuchpotentialbecause ithasbeenshowntoimproveoxygenationandventilationandtoreducerespiratorydistressandworkofbreathinginpatientswithpersistentacuterespiratoryfailureafterearly extubation[31].
44.3.1 NPPV to Prevent Postextubation Respiratory Failure Thisdiscussionappliestopatientsextubatedfrommechanicalventilationaftersuccessful weaninginwhomNPPVisusedprophylacticallytoavoidpostextubationrespiratoryfailureandreintubation. JiangandcolleaguesstudiedtheeffectofprophylacticNPPVusein93patients,40% ofwhomhadunplannedextubation[32].ThesepatientsrandomlyreceivedeitherNPPV (n=47)orunassistedoxygentherapy(n=46).Therewasnosigni cantdifferenceinthe reintubationrateinthetwogroups(27.7%vs.15.2%,respectively,p=0.14). Navaetal.carriedoutamulticenterstudyof97patientswhorequiredinvasivemechanical ventilation for more than 48 h and were thought to be at risk of extubation failure
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(hypercapnia, CHF, ineffective cough, excessive secretions, more than one failure of a weaningtrial,morethanonecomorbidcondition,andupperairwayobstruction)[33].The patientswererandomizedafterasuccessfulweaningtrialtoNPPVbyfull-facemaskfor longerthan8h/dayinthe rst48h(n=48)orstandardmedicaltherapy(SMT)(n=49). NPPVsigni cantlyreducedtheneedforreintubation(8%vs.24%,p=0.03)andresulted inriskreductionofICUmortalityby10%(p<0.01). Severely obese patients are at increased risk of respiratory complications that might occurinthepostextubationperiod[34,35].ElSolhetal.studied62consecutiveseverely obesepatients(bodymassindex³35kg.m 2)treatedwithbilevelpositiveairwaypressure (PAP)vianasalmaskforatleast48himmediatelypostextubationandcomparedwith62 historicallymatchedcontrolswhoweretreatedwithconventionaltherapy[36].Compared withtheconventionallytreatedgroup,NPPVresultedina16%absolutereductioninthe riskofrespiratoryfailure(10%vs.26%,p=0.03)andreducedstayintheICU(12±8vs. 18±11days,p<0.001)andinthehospital(21±11vs.26±11days,p=0.007).Theuse ofNPPVwasassociatedwithsigni cantlylowerhospitalmortality(16%vs.50%,p=0.03) inthesubgroupofpatientswithhypercapniaduringSBT. Basedonthisinformation,thereislimitedevidencetosupporttheroutineuseofNPPV topreventpostextubationfailure(recommendation2C).High-riskpatientsforextubation failure,likethosewithCOPD,CHF,obesity,andpatientswhohadweaningdif culty,may bene tfromNPPVtopreventpostextubationfailure(recommendation1B).
44.3.2 NPPV to Treat Postextubation Respiratory Failure ThissectiondiscussestheuseofNPPVtotreatpatientssuccessfullyweanedfrommechanicalventilationanddevelopedrespiratoryfailurewithin48 72h. TwoclinicaltrialsinthissettingwereconductedingeneralICUpatientswithpostextubationfailure.Keenanetal.randomized81patientswhorequiredventilatorysupportfor longerthan48horhadahistoryofeitherCHForchroniclungdiseaseanddeveloped respiratory distress within 48 h of extubation to receive either SMT alone (n = 42) or NPPVbyfacemaskplusSMT(n=39)[37].Inthetwogroups,therewerenodifferences intherateofreintubation(72%vs.69%,p=0.79),durationofICUandhospitalstayor ICUandhospitalmortality. Estebanandcoworkerscarriedoutarandomizedtrialat37centersineightcountries andevaluated221patientswhowereonmechanicalventilationformorethan48hthen developedpostextubationrespiratoryfailurewithin48hofelectiveextubation[38].The patientswereassignedtoeitherfacemaskNPPV(n=114)orSMT(n=107).Therateof reintubation was similar in both groups (48%). ICU mortality was higher in the NPPV groupthanintheSMTgroup(25%vs.14%;RR1.78;95%CI1.03 3.20,p=0.048).This differenceinICUmortalityseemedtobeduetoahighmortalityrateinthepatientson NPPVwhorequiredreintubation(38%).Asthemediantimefromrespiratoryfailureto reintubationwaslongerintheNPPVgroup(12h)thanintheSMTgroup(2h30min, p=0.02),thedelayinintubationmayhavebeendeleterious.Thetrialincludedmainly patientswithoutCOPD;only10%hadCOPD.
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Hilbertetal.conductedanRCTonpatientswithCOPDwhohadpostextubationhypercapnicrespiratoryfailure(de nedasrespiratorydistress,RR>25,increaseinPco2>20%, pH<7.35)within72hofextubation[39].ThepatientswererandomizedtoNPPVbyfullfacemaskfor30minorlongerevery4h(n=30)orSMT(n=30).Comparedtothoseon SMT,theNPPVgrouphadalowerreintubationrate(20%vs.67%,p<0.001)andashorter durationofventilatorsupport(6±4vs.11±8days,p<0.01)andICUstay(8±4vs.14±8 days,p<0.01).TherewasnodifferenceinICUmortalityinthetwogroups. NPPVhasalsobeenstudiedforthemanagementofpostextubationrespiratoryfailurein specialpatientpopulations,includingthoseinvolvingburns,cardiacsurgery,lungresection surgery,andpatientswithDo-Not-ResuscitateorDo-Not-Intubateorders.Inaretrospective review,SmailesreportedontheuseofNPPVin30patientswithsevereburninjurieswho experienced respiratory insuf ciency postextubation [40]. Twenty two patients avoided endotracheal intubation, seven patients were reintubated, and one patient died. De Santo etal.reportedtheresultsofanobservationalstudyontheuseofNPPVin43patientswho developed extubation failure after cardiac surgery. The investigators reported that NPPV preventedreintubationin74.4%ofthepatients,withthebestresultsinthoseaftercardiopulmonarybypasslunginjuryandthosewithcardiogenicdysfunction(reintubationrates9.5% and30.8%respectively)andpoorresults(55%reintubationrate)inthosetreatedforpneumonia.However,thestudydesignandthelackofcontrolgroupmakethegeneralizabilityof theresultsdif cultwithoutfurtherstudy[41].Auriantetal.comparedSMT(n=12)with nasalmaskNPPVplusSMT(n=12)inpatientswithacutehypoxemicpostextubationrespiratoryfailurefollowinglungresectionsurgery[42].ComparedtoSMT,NPPVwasassociatedwithasigni cantdecreaseintherequirementforintubation(50%vs.21%,p=0.035) andmortality(37.5%vs.12.5%,p=0.045).Aspecialgroupofpatientsincludesthosewith ordersnottointubateafterdiscontinuationofmechanicalventilation.Iftheydeveloppostextubation respiratory failure, NPPV might be an acceptable option to alleviate respiratory distress.Onestudyshowedthatsuchpatientshaveahighhospitalmortalityof77%[43]. Hence,theavailableliteraturesuggeststhattheindiscriminateuseofNPPVingeneral ICU patients without COPD with postextubation respiratory failure should be avoided (recommendation1A).InpatientswithCOPD,NPPVmightbeuseful(recommendation 1B).Inothersettings,includingburns,cardiacsurgery,lungresectionsurgery,andpatients with orders not to intubate, the use should be individualized considering the limited evidence(recommendation1C).
44.4 Conclusions CurrentevidencesuggeststhatNPPVhasaroleinthecareofpatientsinthepostextubationperiodbasedontheindicationandpatientpopulation.Figure44.1isa owchartofan evidence-based decision algorithm for the use of NPPV in the postextubation period. NPPV is bene cial in facilitating extubation in patients who fail SBT, especially those withCOPDexacerbation.NPPVmayalsobene tpatientswithCOPDexacerbationand severelyobesepatientswhoareextubatedaftersuccessfulSBTtopreventpostextubation
Extubate and apply NPPV.
YES
YES
Apply NPPV if no contraindications with appropriate medical therapy.
Reintubate if no improvement after medical therapy. NPPV might be harmful.
Cause of respiratory failure is COPD?
YES
Extubate and apply NPPV prophylactically.
YES
NO
Continue standard therapy.
NO
Patient develops post-extubation respiratory distress?
Extubate; no need to use NPPV prophylactically.
NO
High risk for extubation failure? e.g. COPD, CHF, severe obesity
YES
Noninvasive Positive Pressure Ventilation in the Postextubation Period
Fig. 44.1 Evidence-baseddecisionalgorithmfortheuseofnoninvasivepositivepressureventilation(NPPV)inthepostextubationperiod
Continue weaning trials and Extubate when weaning is successful.
NO
Patient has COPD ?
NO
Successful spontaneous breathing trial in a patient on invasive ventilation?
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respiratoryfailure.ItmightbeusefulinpatientswithCOPDexacerbationwhodevelop postextubationrespiratoryfailure.However,itsindiscriminateuseisnotbene cial,and might be harmful, in general ICU patients without COPD who develop postextubation respiratoryfailure,anditshouldbeavoidedinthissetting.Furtherresearchisrequiredto betterde nepatientswhoaremostlikelytobene tfromNPPV.
Key Recommendations
› › › › › ›
NPPVshouldbeconsideredtofacilitatediscontinuationofinvasivemechanical ventilationinpatientswithCOPDexacerbationwhofailedSBTs(Grade1B). NPPVmaybeusedtofacilitatediscontinuationofmechanicalventilationin otherhigh-riskpatientswhofailSBTs(Grade2C). NPPVshouldbeconsideredtopreventpostextubationrespiratoryfailurein high-riskpatients,likethosewithCOPD,CHForobesityandpatientswhohad weaningdif culty(Grade1B). NPPVshouldnotberoutinelyusedingeneralICUpatientswithpostextubation respiratoryfailure(Grade1A). NPPVshouldbeconsideredinCOPDpatientswithpostextubationrespiratory failure(Grade1B). In settings such as burn, cardiac surgery, lung resection surgery and patients withDo-Not-Intubateorders,NPPVuseforpostextubationrespiratoryshouldbe individualized(Recommendation1C).
References 1. Lightowler JV, Wedzicha JA, Elliott MW, Ram FS (2003) Non-invasive positive pressure ventilationtotreatrespiratoryfailureresultingfromexacerbationsofchronicobstructivepulmonarydisease:Cochranesystematicreviewandmeta-analysis.BMJ326(7382):185 2. Keenan SP, Sinuff T, Cook DJ, Hill NS (2003) Which patients with acute exacerbation of chronic obstructive pulmonary disease bene t from noninvasive positive-pressure ventilation?Asystematicreviewoftheliterature.AnnInternMed138(11):861 870 3. MasipJ,RoqueM,SanchezB,FernandezR,SubiranaM,ExpositoJA(2005)Noninvasive ventilation in acute cardiogenic pulmonary edema: systematic review and meta-analysis. JAMA294(24):3124 3130 4. Hilbert G, Gruson D, Vargas F et al (2001) Noninvasive ventilation in immunosuppressed patientswithpulmonaryin ltrates,fever,andacuterespiratoryfailure.NEnglJMed344(7): 481 487 5. Mehta S, Hill NS (2001) Noninvasive ventilation. Am J Respir Crit Care Med 163(2): 540 577 6. BurnsKE,SinuffT,AdhikariNKetal(2005)Bilevelnoninvasivepositivepressureventilationforacuterespiratoryfailure:surveyofOntariopractice.CritCareMed33(7):1477 1483 7. SchettinoG,AltobelliN,KacmarekRM(2008)Noninvasivepositive-pressureventilationin acuterespiratoryfailureoutsideclinicaltrials:experienceattheMassachusettsGeneralHospital. CritCareMed36(2):441 447
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8. GuyattGH,CookDJ,JaeschkeR,PaukerSG,SchunemannHJ(2008)Gradesofrecommendation for antithrombotic agents: American College of Chest Physicians Evidence-Based ClinicalPracticeGuidelines(8thedition).Chest133(6Suppl):123S 131S 9. UdwadiaZF,SantisGK,StevenMH,SimondsAK(1992)Nasalventilationtofacilitateweaninginpatientswithchronicrespiratoryinsuf ciency.Thorax47(9):715 718 10. RestrickLJ,ScottAD,WardEM,FeneckRO,CornwellWE,WedzichaJA(1993)Nasalintermittent positive-pressure ventilation in weaning intubated patients with chronic respiratory diseasefromassistedintermittent,positive-pressureventilation.RespirMed87(3):199 204 11. GregorettiC,BeltrameF,LucangeloUetal(1998)Physiologicevaluationofnon-invasive pressuresupportventilationintraumapatientswithacuterespiratoryfailure.IntensiveCare Med24(8):785 790 12. NavaS,AmbrosinoN,CliniEetal(1998)Noninvasivemechanicalventilationintheweaning ofpatientswithrespiratoryfailureduetochronicobstructivepulmonarydisease.Arandomized,controlledtrial.AnnInternMed128(9):721 728 13. GiraultC,DaudenthunI,ChevronV,TamionF,LeroyJ,BonmarchandG(1999)Noninvasive ventilationasasystematicextubationandweaningtechniqueinacute-on-chronicrespiratory failure: a prospective, randomized controlled study. Am J Respir Crit Care Med 160(1): 86 92 14. Ferrer M, Esquinas A, Arancibia F et al (2003) Noninvasive ventilation during persistent weaningfailure:arandomizedcontrolledtrial.AmJRespirCritCareMed168(1):70 76 15. TrevisanCE,VieiraSR(2008)Noninvasivemechanicalventilationmaybeusefulintreating patientswhofailweaningfrominvasivemechanicalventilation:arandomizedclinicaltrial. CritCare12(2):R51 16. Burns KE, Adhikari NK, Keenan SP, Meade M (2009) Use of non-invasive ventilation to weancriticallyilladultsoffinvasiveventilation:meta-analysisandsystematicreview.BMJ 338:b1574 17. BrochardL,RaussA,BenitoSetal(1994)Comparisonofthreemethodsofgradualwithdrawalfromventilatorysupportduringweaningfrommechanicalventilation.AmJRespir CritCareMed150(4):896 903 18. EstebanA,FrutosF,TobinMJetal(1995)Acomparisonoffourmethodsofweaningpatients from mechanical ventilation. Spanish Lung Failure Collaborative Group. N Engl J Med 332(6):345 350 19. EpsteinSK(1995)Etiologyofextubationfailureandthepredictivevalueoftherapidshallow breathingindex.AmJRespirCritCareMed152(2):545 549 20. Epstein SK (2006) Preventing postextubation respiratory failure. Crit Care Med 34(5): 1547 1548 21. EpsteinSK(2002)Decisiontoextubate.IntensiveCareMed28(5):535 546 22. Rothaar RC, Epstein SK (2003) Extubation failure: magnitude of the problem, impact on outcomes,andprevention.CurrOpinCritCare9(1):59 66 23. EpsteinSK,CiubotaruRL(1998)Independenteffectsofetiologyoffailureandtimetoreintubationonoutcomeforpatientsfailingextubation.AmJRespirCritCareMed158(2):489 493 24. Coplin WM, Pierson DJ, Cooley KD, Newell DW, Rubenfeld GD (2000) Implications of extubationdelayinbrain-injuredpatientsmeetingstandardweaningcriteria.AmJRespirCrit CareMed161(5):1530 1536 25. SalamA,TilluckdharryL,Amoateng-AdjepongY,ManthousCA(2004)Neurologicstatus, cough,secretionsandextubationoutcomes.IntensiveCareMed30(7):1334 1339 26. KhamieesM,RajuP,DeGirolamoA,Amoateng-AdjepongY,ManthousCA(2001)Predictors ofextubationoutcomeinpatientswhohavesuccessfullycompletedaspontaneousbreathing trial.Chest120(4):1262 1270 27. MokhlesiB,TulaimatA,GluckmanTJ,WangY,EvansAT,CorbridgeTC(2007)Predicting extubationfailureaftersuccessfulcompletionofaspontaneousbreathingtrial.RespirCare 52(12):1710 1717
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28. Frutos-VivarF,FergusonND,EstebanAetal(2006)Riskfactorsforextubationfailurein patientsfollowingasuccessfulspontaneousbreathingtrial.Chest130(6):1664 1671 29. EpsteinSK,CiubotaruRL,WongJB(1997)Effectoffailedextubationontheoutcomeof mechanicalventilation.Chest112(1):186 192 30. EstebanA,AliaI,GordoFetal(1997)Extubationoutcomeafterspontaneousbreathingtrials withT-tubeorpressuresupportventilation.TheSpanishLungFailureCollaborativeGroup. AmJRespirCritCareMed156(2Pt1):459 465 31. KilgerE,BriegelJ,HallerMetal(1999)Effectsofnoninvasivepositivepressureventilatory support in non-COPD patients with acute respiratory insuf ciency after early extubation. IntensiveCareMed25(12):1374 1380 32. JiangJS,KaoSJ,WangSN(1999)Effectofearlyapplicationofbiphasicpositiveairwaypressureontheoutcomeofextubationinventilatorweaning.Respirology4(2):161 165 33. NavaS,GregorettiC,FanfullaFetal(2005)Noninvasiveventilationtopreventrespiratory failureafterextubationinhigh-riskpatients.CritCareMed33(11):2465 2470 34. El-SolhA,SikkaP,BozkanatE,JaafarW,DaviesJ(2001)MorbidobesityinthemedicalICU. Chest120(6):1989 1997 35. BercaultN,BoulainT,KuteifanK,WolfM,RungeI,FleuryJC(2004)Obesity-relatedexcess mortalityrateinanadultintensivecareunit:arisk-adjustedmatchedcohortstudy.CritCare Med32(4):998 1003 36. El-SolhAA,AquilinaA,PinedaL,DhanvantriV,GrantB,BouquinP(2006)Noninvasive ventilationforpreventionofpost-extubationrespiratoryfailureinobesepatients.EurRespirJ 28(3):588 595 37. KeenanSP,PowersC,McCormackDG,BlockG(2002)Noninvasivepositive-pressureventilationforpostextubationrespiratorydistress:arandomizedcontrolledtrial.JAMA287(24): 3238 3244 38. EstebanA,Frutos-VivarF,FergusonNDetal(2004)Noninvasivepositive-pressureventilationforrespiratoryfailureafterextubation.NEnglJMed350(24):2452 2460 39. HilbertG,GrusonD,PortelL,Gbikpi-BenissanG,CardinaudJP(1998)Noninvasivepressure support ventilation in COPD patients with postextubation hypercapnic respiratory insuf ciency.EurRespirJ11(6):1349 1353 40. SmailesST(2002)Noninvasivepositivepressureventilationinburns.Burns28(8):795 801 41. DeSantoLS,BanconeC,SantarpinoGetal(2009)Noninvasivepositive-pressureventilation forextubationfailureaftercardiacsurgery:pilotsafetyevaluation.JThoracCardiovascSurg 137(2):342 346 42. AuriantI,JallotA,HervePetal(2001)Noninvasiveventilationreducesmortalityinacute respiratoryfailurefollowinglungresection.AmJRespirCritCareMed164(7):1231 1235 43. Schettino G, Altobelli N, Kacmarek RM (2005) Noninvasive positive pressure ventilation reversesacuterespiratoryfailureinselect do-not-intubate patients.CritCareMed33(9): 1976 1982
Noninvasive Ventilation in Postextubation Respiratory Failure
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RiteshAgarwal
45.1 Introduction Endotracheal intubation and mechanical ventilation is a lifesaving intervention used in patientswithrespiratoryfailure.Weaning,theentireprocessofliberatingthepatientfrom theendotrachealtube,mustbalancetheriskofcomplicationsnotonlyduetounnecessary delaysinextubationbutalsoduetoprematurediscontinuationandtheneedforreintubation [1]. In the vast majority, once there is improvement of the underlying indication, mechanical ventilation can be withdrawn abruptly [2, 3]. Even once successfully extubated,theneedforreintubationinthenext48 72hrangesfrom13%to19%becauseof postextubationrespiratoryfailure[4 6].Patientswhorequirereintubationhavebeennoted tohaveasigni cantlyhigherrateofcomplicationsthanthosewhoaresuccessfullyextubatedonthe rstattempt. Noninvasiveventilation(NIV)isaneffectivetoolinpreventingendotrachealintubationandimprovingtheclinicaloutcomeofpatientswithdifferentetiologiesofacuterespiratoryfailure,especiallyexacerbationsofchronicobstructivepulmonarydisease(COPD) [7] and cardiogenic pulmonary edema [8, 9]. Noninvasive positive pressure ventilation (NIPPV)hasbeentriedforfacilitationofweaningandextubation[10].Ameta-analysisby Burns et al. suggested that NIPPV can facilitate weaning in mechanically ventilated patients,especiallythesubgroupofpatientswithchronicobstructivelungdisease[11]. Theaimofthischapteristospeci callyreviewtheroleofNIPPVinthemanagementand preventionofrespiratoryfailureafterextubation.
R.Agarwal DepartmentofPulmonaryMedicine,PostgraduateInstitute ofMedicalEducationandResearch,Sector-12,Chandigarh160012,India e-mail:
[email protected],
[email protected] A.M.Esquinas(ed.),NoninvasiveMechanicalVentilation, DOI:10.1007/978-3-642-11365-9_45,©Springer-VerlagBerlinHeidelberg2010
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45.2 Pathophysiology of Postextubation Respiratory Failure Postextubationrespiratoryfailureisde nedastheappearanceofsignsofrespiratorydistresswithin48 72hafterplannedextubation.Itisbroadlyidenti edbyoneormoreofthe followingfeatures:increaseinrespiratoryratemorethan50%frombaselinewithuseof accessorymusclesofrespirationorabdominalparadox,pHlessthan7.35withPaco2more than45mmHg,pulseoximetricsaturationlessthan90%orPao2lessthan80mmHgon Fio2morethanorequalto50%.Itisobviouslydifferentfromweaningfailureinwhicha patientdevelopssignsofrespiratoryorhemodynamicintoleranceduringaspontaneous breathing trial. Postextubation respiratory failure can arise from airway and nonairway causes,withthelattermorecommon,andisassociatedwithincreasedmortality[12,13]. Airwaycausesincludeupperairwayobstruction,aspiration,andexcesspulmonarysecretions; nonairway causes are congestive heart failure, encephalopathy, and others. Importantly,reintubationduetoextubationfailureisanindependentriskfactorfornosocomialpneumoniaandincreasedhospitallengthofstayandhospitalmortality[14,15]. Certain risk factors are associated with increased propensity for extubation failure and includeneurologicalimpairment;olderage;severityofillness;morethanonecomorbid illness.includingcardiacfailure;longdurationofventilationpriortoextubation;useof continuoussedation;anemia;obesity;andothers[14,16 18].
45.3 Physiological Basis for the Use of NIV in Postextubation Respiratory Failure Duringaspontaneousbreathingtrial,thereisanincreaseinrespiratoryfrequencyanda decreaseinthetidalvolume.Thiscausesalveolarhypoventilationandventilation perfusion mismatch [19]. Further, patients who fail weaning develop a decrease in mixed venous oxygensaturationduetoanincreaseinoxygenextractionbytissuesandfailuretoincrease thecardiacoutput;thisisincontrasttopatientswhotolerateaspontaneousbreathingtrial whenitisassociatedwithincreasedcardiacindex[20].Hence,itcanbehypothesizedthat similareventswouldoccurduringtheprocessofrespiratoryfailurefollowingextubation. NIVaugmentstheinspiratoryandexpiratory owandpressure,therebyincreasingthe tidalvolumeandunloadingtheinspiratorymuscles[21,22].Thisleadstoaccomplishment of an ef cient breathing pattern and improvement in hypoxemia and hypercapnia [23]. Furthermore,ithasbeenshowninmechanicallyventilatedpatientsthatpressuresupportis associated with prevention of ventilation perfusion mismatch while weaning patients from positive pressure ventilation [24]. Finally, in ventilator-dependent patients with chronicrespiratorydisorders,invasiveandnoninvasivepressuresupportareequallyeffectiveindecreasingtheworkofbreathingandimprovingthearterialbloodgases,butthe breathingpatternandtherespiratorypumpimprovebetterwithNIPPV[25]. Thus,basedonindirectevidence,onecanhypothesizethatNIVwouldbeeffectivein management of postextubation respiratory failure and could potentially be tried in two
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differentscenarios:managementofestablishedpostextubationrespiratoryfailureandpreventionofpostextubationrespiratoryfailureinpatientsathighriskforreintubationfollowingsuccessfulextubation.
45.4 Noninvasive Ventilation in Postextubation Respiratory Failure NIVhasbeenbene cialinweaning,thatis,inpatientsreceivingmechanicalventilation whofailasuccessfulspontaneousbreathingtrial,aresystematicallyextubated,andwho receiveNIPPV[26 29].Infact,Burnsetal.,inameta-analysis,demonstratedthat,comparedtoinvasiveventilation,weaningusingNIVdecreasedmortality,ventilator-associated pneumonia,andthetotaldurationofmechanicalventilation,butallthestudiesweremainly ofpatientswithCOPD[30]. NIVwasconsideredapromisingmodalityforpostextubationrespiratoryfailureinthe internationalconsensusconference[31],primarilybasedonresultsofobservationalstudies[32,33].Inastudyof30patientswithCOPDwithpostextubationhypercapnicrespiratory failure insuf ciency, the use of NIV was compared conventional treatment of 30 historically matched control patients. NIPPV was effective not only in correcting gas exchangeabnormalitiesbutalsosigni cantlyreducedtheneedforendotrachealintubation (20/30[67%]inthecontrolgroupvs.6/30[20%]intheNIVgroup)[32].In15patients withoutCOPDpatientsafterprolongedmechanicalventilation(morethan72h)withacute respiratoryinsuf ciencyafterearlyextubation,NIPPVimprovedpulmonarygasexchange andbreathingpattern,decreasedintrapulmonaryshuntfraction,andreducedtheworkof breathing[33].Inanotherobservationalstudyof43patientswithpostextubationfailure aftercardiacsurgery,NIPPVrelievedhypoxemiaandhelpedavoidreintubationin75%of patientswhoalreadymetstandardintubationcriteriaatstudyentry[34]. However,tworandomizedcontrolledtrials(RCTs)havenotshownbene tsfromNIV inpreventingreintubationinpatientswithpostextubationrespiratoryfailure(Table45.1) [35,36].The rsttrialbyKeenanetal.included81patientsrandomizedtoreceivestandardmedicaltherapy(SMT;supplementaloxygentomaintainoxygensaturationbypulse oximetrymorethanorequalto95%)aloneorNIPPVbyfacemaskplusSMT.Thestudy foundnodifferenceintherateofreintubation(28/39[72%]NIVvs.29/42[69%]control), hospital mortality, duration of mechanical ventilation, or length of intensive care unit (ICU)orhospitalstay.Theothertrialincluded221patientswithpostextubationrespiratoryfailurerandomlyallocatedtoreceiveNIPPV(114patients)orstandardtherapy(107 patients). There was no difference between the two groups in the need for reintubation (48%inbothgroups).TheICUmortalitywashigherintheNIVgroupthaninthestandard therapygroup(25%vs.14%),andthetimefromrespiratoryfailuretoreintubationwas longerintheNIVgroup.Ifwecombinethetwostudies,thereisnobene twithNIPPVin decreasingeitherthereintubationrates(relativerisk[RR]1.03,95%con denceinterval [CI]0.84 1.25)orICUmortality(RR1.14,95%CI0.43 3.0)[37]. DoesthismeanthatNIPPVshouldnotbeusedinpostextubationrespiratoryfailure? BeforerejectingNIVcompletelyinpatientswithpostextubationrespiratoryfailure,one
Twoormoreofthe following:pHbelow 7.35withPaco2more than45mmHg, respiratorymuscle fatigueorincreased respiratoryeffort, respiratoryratemore than25/minfor2h consecutively,Sao2less than90%orPao2less than80mmHgonFio2 morethan0.5
221patients:acute respiratoryfailure(pneumonia,sepsis,postoperative respiratoryfailure,trauma, cardiacfailure,ARDS, others)187patients; acute-on-chronicrespiratory failure(COPD,asthma)27 patients;andneuromuscular disease7patients;SAPSII (NIPPV37±13,control 36±10)
Titratedto achieveatidal volumemorethan 5mL/kgbody weightandpatient comfort
Esteban etal.[36], multicenter
DNRorder,prior obstructivesleep apnea,cervicalspine injury,upperairway obstruction,language barrier,respiratory distressoutside intensivecareunit
Atleastoneofthecriteriafor1h orless:lackofimprovementin pHorPaco2;alteredmentalstatus withpatientunabletotolerate NIPPV;Sao2lessthan85% despitehighFio2;lackof improvementinrespiratory musclefatigue;SBPlessthan90 mmHgformorethan30min despiteadequatevolume challenge,vasopressors,orboth; copioussecretionsassociatedwith acidosis,orhypoxemia
Cardiacorrespiratoryarrest, apnea,respiratorydistressin extremis,inabilitytoprotect airway,psychomotoragitation requiringsedatives,heartrateless than50/min,SBPlessthan70 mmHg
APACHEAcutePhysiologyandChronicHealthEvaluation,ARDSacuterespiratorydistresssyndrome,COPDchronicobstructivepulmonarydisease,DNR donotresuscitate,EPAPexpiratorypositiveairwaypressure,IPAPinspiratorypositiveairwaypressure,SAPSSimpli edAcutePhysiologyScore,SBPsystolic bloodpressure
Respiratoryrateabove 30ormorethan50% increasefrombaseline, useofaccessorymuscles ofrespiration,or abdominalparadox
81patients,heterogeneous population(cardiac 28, COPD 9,others); APACHEII(NIPPV 22.5 ±7.1;control 24±7.9)
10.2±2/5.1±1.2
Keenan etal.[35], singlecenter
Table 45.1 Randomizedcontrolledtrialsemployingnoninvasivepositivepressureventilation(NIPPV)inpost-extubationrespiratoryfailure Study IPAP/EPAP Patientcharacteristics Inclusioncriteria Exclusioncriteria Reintubationcriteria
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shouldalsounderstandthelimitationsoftheindividualtrials.TherewasalimitedexperiencewiththeuseofNIPPVbythephysiciansinthetrialsbyKeenanandEstebanetal., andboththetrialsuseddifferentde nitionsforpostextubationrespiratoryfailure[35,36]. Also,inthestudybyEstebanetal.[36],28patientsinthestandardtherapygroupcrossed overtoreceiverescueNIPPV.Ifthesepatientsareconsideredtohavehadtreatmentfailure andincludedwiththeotherpatientsinthatgroupwhowerereintubated,thenthestandard therapygrouphadasigni cantlyhigherriskofaneedforreintubationthantheNIPPV group. Finally, there is also the criticism that the trial was stopped early [38]. Another approachtouseNIPPVinallpatientsafterextubationinasinglestudyalsoshowedno bene twiththeuseofNIPPV[39].Thus,NIPPVshouldbeusedjudiciouslywhenlikely tobene t,suchasforthosewithCOPDorhypercapnicpulmonaryedema.Thetrialof NIPPVshouldnotexceed2h.Thereshouldbeclosemonitoringofrespiratory,cardiovascular,andarterialbloodgasparameterswithfacilitiesforintubationandinvasiveventilationreadilyavailable.However,becauseofpaucityofdata,morestudiesarerequiredto preciselyidentifythepatientslikelytobene tfromNIPPVinthissetting.
45.5 Noninvasive Ventilation in Patients at Risk for Respiratory Failure After Extubation NIVmaybemorebene cialinpatientswhoare atrisk forpostextubationrespiratoryfailurein contrasttoestablishedpostextubationrespiratoryfailure.TwoRCTs[40,41](Table45.2)andone observationalstudy[42]investigatedtheuseofNIPPVinpatientsathighriskforpostextubation respiratoryfailure.Intheobservationalstudy,62patientswithabodymassindexif35kg/m2or morewereassignedtoNIVvianasalmaskimmediatelyfollowingextubationandwerecompared to62historicalcontrolstreatedwithconventionaltherapy.Comparedtoconventionaltherapy,the institutionofNIVresultedinsigni cantreduction(10%vs.26%)intherateofrespiratoryfailure and the ICU and hospital lengths of stay. Subgroup analysis of hypercapnic patients showed reducedhospitalmortalityintheNIVgroupcomparedtothecontrolgroup[42]. Inthe rstmulticenterRCT,97consecutivepatientsrequiringmorethan48hofmechanical ventilationandconsideredatriskofdevelopingpostextubationrespiratoryfailurewererandomizedtoreceiveNIV(8hormoreadayinthe rst48h)orSMT.ComparedwiththeSMT group,theNIVgrouphadalowerrateofreintubation(4/48vs.12/49)andreducedICUmortality[40].IntheotherRCT,162patientswererandomlyallocatedafterextubationtoreceive NIVfor24h(n=79)orSMT(n=83).IntheNIVgroup,postextubationrespiratoryfailurewas lessfrequent(13/79vs.27/83),theICUmortalitywaslower,butthereintubationrateswere similar[41].PooledanalysisofthetwoRCTsshowedthatNIPPV,whencomparedtoconventionaltherapy,signi cantlydecreasedthereintubationrates(RR0.46,95%CI0.28 0.76)and theICUmortality(RR0.26,95%CI0.1 0.66)butnotthehospitalmortality(RR0.71,95%CI 0.42 1.20).Thenumberneededtotreat(NNT)(95%CI)was9(5 29),9(6 21),and16bene t (32harmto7bene t)forreintubationrates,ICU,andhospitalmortality,respectively[37]. From these studies, it can be inferred that the use of NIPPV following extubation decreasesthereintubationratesandICUmortalityinpatientswhoareatriskforpostextubation respiratory failure but not once they develop respiratory failure. Several reasons
162patients:chronic respiratoryfailure82, chronicheartdisease 53,diabetesmellitus 32,immunosuppression 17,neoplasms18, cirrhosis7,chronic renalfailure14; APACHEII(NIPPV14 ±3,control13±3)
14±2/5±1
Ferrer etal.[41], twocenters
Atleastonemajor(pH<7.35 withPaco2>45mmHgorif hypercapnicPaco2increase morethan15%);(Sao2<90% onFio2>50%)ortwominor criteria(increasein respiratoryratemorethan 20%ormorethan35breaths/ min);clinicalsignsof respiratorymusclefatigue; severedyspnea;inabilityto removesecretions;coma, cardiac,orrespiratoryarrest; severehypotension Anyofthefollowing: respiratoryorcardiacarrest, massiveaspiration,apnea withlossofconsciousness, psychomotoragitation, persistentinabilitytoremove respiratorysecretions,heart ratebelow50/minwithloss ofalertness,severehemodynamicinstabilitywithout responseto uidsand vasopressors
Coma,inabilitytoprotect theairways,cervicalspine injury,neuromuscular diseases,lackofinformed consent,agitatedor uncooperativestate, anatomicalabnormalities interferingwiththemaskfit, uncontrolledcardiac ischemiaorarrhythmias, failureofmorethantwo organs,BMI30orabove, sleepapnea,homeNIPPV Facialorcranialtraumaor surgery,recentgastricor esophagealsurgery,active uppergastrointestinal bleeding,excessive respiratorysecretions,lack ofcooperation,do-not-resuscitateorder
Patientsintubatedmore than48hwithsuccessful weaningplusoneormore ofthefollowing:more thanoneconsecutive failureofweaningtrial, chronicheartfailure, Paco245mmHgormore afterextubation,more thanonecomorbidity (excludingchronicheart failure),weakcough, stridoratextubation Patientsintubatedfor48h orlongerwhotolerateda spontaneousbreathing trialplusatleastoneof thefollowing:ageabove 65years,cardiacfailure asthecauseofintubation, APACHEIIscoremore than12onthedayof extubation
APACHEAcutePhysiologyandChronicHealthEvaluation,ARDSacuterespiratorydistresssyndrome,BMIbodymassindex,COPDchronicobstructive pulmonary disease, EPAP expiratory positive airway pressure, IPAP inspiratory positive airway pressure, SAPS Simpli ed Acute Physiology Score, SBP systolicbloodpressure
97patients:acute respiratoryfailure (pneumonia, postoperative respiratoryfailure, trauma,cardiacfailure, ARDS,others)57 patients;acute-onchronicrespiratory failure(COPD)32 patients;neurosurgery 8patients;APACHEII (NIPPV22.5±7.1, control24±7.9)
13.2±4.5/5.3±1.6
Nava etal.[40], multicenter
Table 45.2 Randomized controlled trials employing noninvasive positive pressure ventilation (NIPPV) in patients at high-risk for post extubation respiratoryfailure Study IPAP/EPAP Patient Inclusioncriteria Exclusioncriteria Reintubationcriteria characteristics
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mayexplainthesedifferences.First,whereasthestudiesbyKeenan[35]andEstebanetal. [35]appliedNIPPVafterpatientshaddevelopedrespiratoryfailure,thetwostudiesby Nava[40]andFerreretal.[41]appliedNIPPVimmediatelyafterextubationinhigh-risk patients. Because longer time from extubation to reintubation is associated with worse outcome[13],thedelayinreintubationcorrelateswithworsesurvivalratesinpatientswho receivedNIPPVforestablishedpostextubationrespiratoryfailure[35,36].Second,asigni cantlyhigherproportionofpatientswithchronicrespiratorydisorderswereincludedin at-risk studies (145/383), whereas the postextubation respiratory failure trials enrolled onlyaround10 11%ofpatientswithchronicpulmonarydisease,theetiologyshownto havethebestresponsetoNIPPV[43].
45.6 Conclusions TheuseofNIPPVfollowingextubation,comparedtostandardtherapy,decreasesthereintubationratesandICUmortalitybutnotthehospitalmortalityinpatientswhoareatrisk forpostextubationrespiratoryfailurebutnotoncerespiratoryfailurefollowingextubation isestablished.Infact,thereisatrendtowardworseoutcomeswithapplicationofNIPPV inpatientswithpostextubationrespiratoryfailure.NIPPVshouldbeusedjudiciouslyin patientswithestablishedpostextubationrespiratoryfailure(Table45.3).Aprotocolneeds tobedevelopedbywhichNIPPVisusedprophylacticallyinpatientswhoareathigh-risk fordevelopingpostextubationrespiratoryfailure.EarlyapplicationofNIPPVseemscrucialtoavoidrespiratoryfailureafterextubationandconsequentlyreintubation. Table 45.3 PracticalapproachtotheuseofnoninvasivepositivepressureventilationNIPPVinthe postextubationsetting NIPPVin at-risk patientsforpostextubationrespiratoryfailure PreferredapproachfortheuseofNIPPVinthepostextubationsetting Identifyhigh-riskfeatures Elderlypatients Morethanoneconsecutivefailureofweaningtrial Chronicheartfailure Paco2morethan45mmHgafterextubation Morethanonemedical/surgicalcomorbidillness Poorcoughre ex Upperairwaystridoratextubationnotrequiringimmediatereintubation Higherseverityofillness Severelyobesepatients(BMI>35kg/m2) NIPPVinestablishedpostextubationrespiratoryfailure Usejudiciously Likelytobene tinselectedpatients(acuteCOPD,hypercapnicpulmonaryedema,etc.) T rialofNIPPVfor2hwithclosemonitoringofrespiratory,cardiovascular,andarterial bloodgasparameters Facilitiesforintubationandinvasiveventilationreadilyavailable COPDchronicobstructivepulmonarydisease
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References 1. BolesJM,BionJ,ConnorsAetal(2007)Weaningfrommechanicalventilation.EurRespirJ 29:1033 1056 2. BrochardL,RaussA,BenitoSetal(1994)Comparisonofthreemethodsofgradualwithdrawalfromventilatorysupportduringweaningfrommechanicalventilation.AmJRespir CritCareMed150:896 903 3. EstebanA,FrutosF,TobinMJetal(1995)Acomparisonoffourmethodsofweaningpatients from mechanical ventilation. Spanish Lung Failure Collaborative Group. N Engl J Med 332:345 350 4. ElyEW,BakerAM,DunaganDPetal(1996)Effectonthedurationofmechanicalventilation ofidentifyingpatientscapableofbreathingspontaneously.NEnglJMed335:1864 1869 5. EstebanA,AliaI,GordoFetal(1997)Extubationoutcomeafterspontaneousbreathingtrials withT-tubeorpressuresupportventilation.TheSpanishLungFailureCollaborativeGroup. AmJRespirCritCareMed156:459 465 6. EstebanA,AliaI,TobinMJetal(1999)Effectofspontaneousbreathingtrialdurationon outcomeofattemptstodiscontinuemechanicalventilation.SpanishLungFailureCollaborative Group.AmJRespirCritCareMed159:512 518 7. Ram FSF, Picot J, Lightowler J et al (2004) Non-invasive positive pressure ventilation for treatmentofrespiratoryfailureduetoexacerbationsofchronicobstructivepulmonarydisease. CochraneDatabaseSystRev3:Pub3 8. AgarwalR,AggarwalAN,GuptaDetal(2005)Non-invasiveventilationinacutecardiogenic pulmonaryoedema.PostgradMedJ81:637 643 9. Agarwal R, Aggarwal AN, Gupta D (2009) Is noninvasive pressure support ventilation as effectiveandsafeascontinuouspositiveairwaypressureincardiogenicpulmonaryoedema? SingaporeMedJ50:595 603 10. Ferrer M, Bernadich O, Nava S et al (2002) Noninvasive ventilation after intubation and mechanicalventilation.EurRespirJ19:959 965 11. BurnsKE,AdhikariNK,MeadeMO(2006)Ameta-analysisofnoninvasiveweaningtofacilitateliberationfrommechanicalventilation.CanJAnaesth53:305 315 12. EpsteinSK(1995)Etiologyofextubationfailureandthepredictivevalueoftherapidshallow breathingindex.AmJRespirCritCareMed152:545 549 13. EpsteinSK,CiubotaruRL(1998)Independenteffectsofetiologyoffailureandtimetoreintubationonoutcomeforpatientsfailingextubation.AmJRespirCritCareMed158:489 493 14. EpsteinSK,CiubotaruRL,WongJB(1997)Effectoffailedextubationontheoutcomeof mechanicalventilation.Chest112:186 192 15. TorresA,GatellJM,AznarEetal(1995)Re-intubationincreasestheriskofnosocomialpneumoniainpatientsneedingmechanicalventilation.AmJRespirCritCareMed152:137 141 16. VallverduI,CalafN,SubiranaMetal(1998)Clinicalcharacteristics,respiratoryfunctional parameters, and outcome of a two-hour T-piece trial in patients weaning from mechanical ventilation.AmJRespirCritCareMed158:1855 1862 17. VallverduI,ManceboJ(2000)Approachtopatients who fail initial weaning trials. Respir CareClinNAm6:365 384 18. EpsteinSK(2002)Decisiontoextubate.IntensiveCareMed28:535 546 19. TorresA,ReyesA,RocaJetal(1989)Ventilation perfusionmismatchinginchronicobstructivepulmonarydiseaseduringventilatorweaning.AmRevRespirDis140:1246 1250 20. Jubran A, Tobin MJ (1997) Pathophysiologic basis of acute respiratory distress in patients who fail a trial of weaning from mechanical ventilation. Am J Respir Crit Care Med 155:906 915
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21. AppendiniL,PatessioA,ZanaboniSetal(1994)Physiologiceffectsofpositiveend-expiratory pressureandmaskpressuresupportduringexacerbationsofchronicobstructivepulmonary disease.AmJRespirCritCareMed149:1069 1076 22. Hess DR (2004) The evidence for noninvasive positive-pressure ventilation in the care of patients in acute respiratory failure: a systematic review of the literature. Respir Care 49: 810 829 23. DiazO,IglesiaR,FerrerMetal(1997)Effectsofnoninvasiveventilationonpulmonarygas exchangeandhemodynamicsduringacutehypercapnicexacerbationsofchronicobstructive pulmonarydisease.AmJRespirCritCareMed156:1840 1845 24. FerrerM,IglesiaR,RocaJetal(2002)Pulmonarygasexchangeresponsetoweaningwith pressure-supportventilationinexacerbatedchronicobstructivepulmonarydiseasepatients. IntensiveCareMed28:1595 1599 25. Vitacca M, Ambrosino N, Clini E et al (2001) Physiological response to pressure support ventilationdeliveredbeforeandafterextubationinpatientsnotcapableoftotallyspontaneous autonomousbreathing.AmJRespirCritCareMed164:638 641 26. NavaS,AmbrosinoN,CliniEetal(1998)Noninvasivemechanicalventilationintheweaning ofpatientswithrespiratoryfailureduetochronicobstructivepulmonarydisease.Arandomized,controlledtrial.AnnInternMed128:721 728 27. Girault C, Daudenthun I, Chevron V et al (1999) Noninvasive ventilation as a systematic extubationandweaningtechniqueinacute-on-chronicrespiratoryfailure:aprospective,randomizedcontrolledstudy.AmJRespirCritCareMed160:86 92 28. Chen J, Qiu D, Tao D (2001) Time for extubation and sequential noninvasive mechanical ventilation in COPD patients with exacerbated respiratory failure who received invasive ventilation.ZhonghuaJieHeHeHuXiZaZhi24:99 100 29. Ferrer M, Esquinas A, Arancibia F et al (2003) Noninvasive ventilation during persistent weaningfailure:arandomizedcontrolledtrial.AmJRespirCritCareMed168:70 76 30. BurnsKE,AdhikariNK,MeadeMO(2003)Noninvasivepositivepressureventilationasa weaning strategy for intubated adults with respiratory failure. Cochrane Database Syst Rev:CD004127 31. American Thoracic Society (2001) International Consensus Conferences in Intensive Care Medicine:noninvasivepositivepressureventilationinacuterespiratoryfailure.AmJRespir CritCareMed163:283 291 32. HilbertG,GrusonD,PortelLetal(1998)NoninvasivepressuresupportventilationinCOPD patientswithpostextubationhypercapnicrespiratoryinsuf ciency.EurRespirJ11:1349 1353 33. KilgerE,BriegelJ,HallerMetal(1999)Effectsofnoninvasivepositivepressureventilatory support in non-COPD patients with acute respiratory insuf ciency after early extubation. IntensiveCareMed25:1374 1380 34. DeSantoLS,BanconeC,SantarpinoGetal(2009)Noninvasivepositive-pressureventilation forextubationfailureaftercardiacsurgery:pilotsafetyevaluation.JThoracCardiovascSurg 137:342 346 35. KeenanSP,PowersC,McCormackDGetal(2002)Noninvasivepositive-pressureventilation forpostextubationrespiratorydistress:arandomizedcontrolledtrial.JAMA287:3238 3244 36. EstebanA,Frutos-VivarF,FergusonNDetal(2004)Noninvasivepositive-pressureventilationforrespiratoryfailureafterextubation.NEnglJMed350:2452 2460 37. AgarwalR,AggarwalAN,GuptaDetal(2007)Roleofnoninvasivepositive-pressureventilationinpostextubationrespiratoryfailure:ameta-analysis.RespirCare52:1472 1479 38. Tarnow-Mordi WO, Gebski V, Cust A (2004) Noninvasive ventilation. N Engl J Med 351:1257 1259;authorreply1257 1259 39. JiangJS,KaoSJ,WangSN(1999)Effectofearlyapplicationofbiphasicpositiveairwaypressureontheoutcomeofextubationinventilatorweaning.Respirology4:161 165
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40. NavaS,GregorettiC,FanfullaFetal(2005)Noninvasiveventilationtopreventrespiratory failureafterextubationinhigh-riskpatients.CritCareMed33:2465 2470 41. FerrerM,ValenciaM,NicolasJMetal(2006)Earlynoninvasiveventilationavertsextubation failureinpatientsatrisk:arandomizedtrial.AmJRespirCritCareMed173:164 170 42. El Solh AA, Aquilina A, Pineda L et al (2006) Noninvasive ventilation for prevention of postextubationrespiratoryfailureinobesepatients.EurRespirJ28(3):588 595 43. MehtaS,HillNS(2001)Noninvasiveventilation.AmJRespirCritCareMed163:540 577
Section IX Intraoperative and Postoperative Indications for Noninvasive Mechanical Ventilation
Intraoperative Use of Noninvasive Ventilation
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46.1 Introduction Noninvasivepositivepressureventilationreferstothedeliveryofassistedmechanicalventilationwithouttheneedforaninvasivearti cialairway.Inthelastdecade,noninvasiveventilation(NIV)hasbeenrecognizedasusefulfortreatmentofpatientsaffectedbymoderate-to-severe respiratoryfailure[1].Thistechniquehasbeenlargelyusedforlong-termtreatmentofpatients withadvancedchronicobstructivepulmonarydisease(COPD).IfNIVisperformedinthe veryearlyphaseofpulmonaryimpairment,itcanreducemorbidityandmortality,avoiding moreaggressiveinterventionssuchasendotrachealintubationandmechanicalventilation. NIVcanalsobeappropriatefortreatmentofacuterespiratoryfailureduetoeitherpulmonary or cardiac dysfunction or in patients with severe hypoventilation secondary to neurodegenerativeormetabolicaffections.Forallthesereasons,thiskindofventilatory supporthasbeenexpanding. AfewstudieshavereportedontheapplicationofNIVforintraoperativeairwaymanagement[2 5].Inpatientswhoareathighriskformechanicalventilationorgeneralanesthesiaduetopulmonarydisease(i.e.,COPDandrecurrentpneumothorax)andinpatients affectedbyrespiratoryfailure,whocansufferfromprolongedmechanicalventilationas wellasfromgeneralanesthesia,intraoperativeNIVcanbebene cial.
46.2 The Rationale Avoidingintubationshouldbeanimportantobjectiveinthemanagementofpatientswith respiratorydiseasetopreventcomplicationsfromtrachealintubationandmechanicalventilation,andNIVmayhelpachievethatgoal.Patientswhoareseverelydebilitateddueto
F.Guarracino(),R.Baldassarri DepartmentofCardiothoracicAnaesthesiaandIntensiveCareMedicine, AziendaOspedalieraUniversitariaPisana,Pisa,Italy e-mail:
[email protected] A.M.Esquinas(ed.),NoninvasiveMechanicalVentilation, DOI:10.1007/978-3-642-11365-9_46,©Springer-VerlagBerlinHeidelberg2010
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cardiacandrespiratorydiseaseareoftenscheduledforpalliativesurgeryforconditionssuch aspersistentpneumothoraxandrecurrentpleuralorpericardialeffusions,forsurgeryfor malignancies,orforpercutaneouscardiacprocedures.Surgeryandanesthesiainthesesick patientscanbefatal.Whensurgeryunderthesecircumstancesishighlydesirable,every effortmustbemadetominimizethesigni cantrisks. Therespiratorydepressionassociatedwiththemostcommonanestheticagentsandthe highairwaypositivepressurerelatedtomechanicalventilationandendotrachealintubationcanworsenapreexistingpathologicconditionand,aboveall,candetermineprolonged or dif cult weaning from mechanical ventilation in the postoperative phase. Although improving peripheral anesthetic procedures used with more con dence have given a chancetothesehigh-riskpatients,respiratoryfunctioncanbeworsenedbyneuralblockin regionalanesthesiatechniques. NIVprovidesanadequaterespiratoryperformancethroughtheoperationevenwhena supinepositionisnecessaryforthesurgeryandallowsthesepatientstomaintainspontaneousbreathing,normalswallowing,andcoughmechanisms. ThesurgicalprocedurecanbesafelyperformedcombiningNIVandperipheralanesthetictechnique,andtheuseofNIVcanalsosigni cantlyreduceeithertheperioperative respiratorycomplicationsortherisksassociatedwithprolongedmechanicalventilation.
46.3 Technical Aspects and Clinical Intraoperative Scenario IntraoperativeNIValsopresentslimitsandrisksthatmustbeconsideredforanysinglepatient. Amongthecomplications,themostcommonarethedamagetofacialtissuescausedbythe localpressureofthemask,thegastricdistensionduetoairinsuf ation,andeyeirritation.Also, thepatient stolerancetothefacemaskshouldbetakenintoaccount;eachpatient sadaptabilitytotherhythmicairinsuf ationscannotbethesameandcanevenchangeintime.Some patientsrequiremildsedationtoacceptventilationuntiltheendofthesurgicalprocedure. Continuousmonitoringoftherespiratoryparameterstoassesstheadequacyofventilation ismandatory.Thesettingoftheventilatormustbeadaptedtothepatient sbodycharacteristicsandclinicalfeaturesandeventuallymodi edonthebasesofthefunctionalparameters andmonitoringinformation.Theventilatorisusuallyconnectedwithconventionaltubingto afull-facemaskwithanin atablesoftcushionseal.Themaskissafelysecuredwithhead straps.Ahydrocolloidsheetcanbeappliedoverthenasalbridge.Forpatientswithanasogastrictube,asealconnectorinthedomeofthemaskisusedtominimizeairleakage. Pressuresupportisincreasedtoobtainanexhaledtidalvolumeof8 10mL/kg,arespiratoryratebelow25/min,andthedisappearanceofaccessorymuscleactivity.Positiveend-expiratorypressure(PEEP)canbeincreasedinincrementsof2cmH2Oupto10cmH2Ountilthe Fio2requirementis0.6orlesstomaintainanSao2above95%onpulseoximetry.Ventilator settingsareadjustedbasedoncontinuousoximetryandmeasurementsofarterialbloodgases. NIVisreducedprogressivelyandisdiscontinuedoncethepatientmaintainsarespiratoryrateoflessthan30/minandaPao2greaterthan70mmHgwithanFio2of0.5without ventilatorysupport.
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Fig. 46.1 Noninvasive ventilation(NIV) duringendovascular aorticvalveimplantationinapatient unsuitableforsurgical treatment.Notethe transesophagealecho (TEE)probethrough themask
WeuseNIVintraoperativelyinpatientssubmittedtoendovascularaorticvalveimplantationinthecatheterizationlab(Fig.46.1)andforpalliativethoracicsurgery. In2008atourInstitution,53patientsaffectedbysevereaorticstenosis,classi edas III IV,accordingtoNewYorkHeartAssociation(NYHA)classi cation,andatveryhigh risk for an open heart surgical procedure according to the EUROSCORE system, were scheduledfortheminimallyinvasivepercutaneoustechnique.Amongthem,therewere patientsforwhomsevererespiratorydysfunctioncontraindicatedmechanicalventilation evenfortherelativeshortperiodofthepercutaneousprocedure.Inorthopneicpatients, NIV was started and maintained for 15 min in the sitting position. Subsequently, this allowedthepatientstomovetothesupinepositionand,stillunderNIV,totolerateitfor thedurationoftheprocedure. Insomecases,wemanagedtointroduceatransesophagealecho(TEE)probethrougha holeinthemasktoguidetheimplantationprocedurebyechocardiography(Fig.46.1)[6]. Carefulhemodynamicandrespiratorymonitoringwasperformedduringthesurgicalprocedure.Inallcases,theNIVwassuccessful,andnoperioperativecomplicationoccurred. WehaveappliedNIVinpatientswithsevererespiratoryinsuf ciencyundergoingpalliativethoracicsurgery.Inthosecases,wecombinedNIVwithperipheralanesthesiaor light sedation. This allowed us to operate on patients for whom general anesthesia and mechanicalventilationwouldplacethematriskformajorperioperativecomplications.
46.4 Conclusion Inconclusion,thisapproachmaybeapplicabletoanumberofdifferentsurgicalproceduresonthechestandabdomeninpatientswhoareconsideredtohaveconditionsthatare inoperableduetosevererespiratoryinsuf ciencyortocontraindicationstotrachealintubationandmechanicalventilation.TheadministrationofNIViswelltoleratedandallows
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preventionofrespiratorycomplications.Wesuggestthatsurgicalandanestheticprograms shouldthereforeconsiderNIVinthetreatmentofsuchhigh-riskandsickpatients.
Key Recommendations
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Itshouldbesupportedinpatientswithrespiratorycontraindicationstogeneral anesthesiaandmechanicalventilationandinhigh-riskpatientswhohave conditionsthatareconsideredinoperableduetorespiratoryinsuf ciency. Preoperativeadequatepatientinformationandacomprehensiveexplanationof howtheNIVwillwork(i.e.,byshowingthepatientthemaskandallowingthe patienttotryitonhisorherface)areimportantforintraoperativefeasibility. IntraoperativeNIVisfeasibleonlyforacooperatingpatient. Inorthopneicpatients,NIVshouldbestartedinthesittingposition. Intraoperativeinteractionbetweentheanesthetistandthesurgeonispivotal duringthoracicprocedures.
References 1. Lightowler JV, Wedzicha JA, Elliott MW, Ram FSF (2003) Non-invasive positive pressure ventilationtotreatrespiratoryfailureresultingfromexacerbationsofchronicobstructivepulmonarydisease:cochranesystematicreviewandmeta-analysis.BMJ326:185 2. FerrandiereM,HazouardE,AyoubJetal(2006)Non-invasiveventilationcorrectsalveolar hypoventilationduringspinalanesthesia.CanJAnaesth53:404 3. BapatPP,AndersonJA,BapatS,SuleA(2006)Useofcontinuouspositiveairwaypressure during spinal anaesthesia in a patient with severe chronic obstructive pulmonary disease. Anaesthesia61:1001 4. WarrenJ,SharmaSK(2006)Ventilatorysupportduringneuraxialblockadeusingbilevelpositiveairwaypressureinapatientwithsevererespiratorycompromise.AnesthAnalg102:910 5. GuarracinoF,GemignaniR,PratesiG,Mel F,AmbrosinoN(2008)Awakepalliativethoracic surgeryinahigh-riskpatient:one-lung,non-invasiveventilationcombinedwithepiduralblockade.Anaesthesia63(7):761 6. Guarracino F, Cabrini L, Baldassarri R, Cariello C, Covello RD, Landoni G, Petronio S, AmbrosinoN.Non-invasiveventilation-aidedtransoesophagealechocardiographyinhigh-risk patients:apilotstudy.EurJEchocardiogr.2010Feb25
Noninvasive Ventilation in Adult Liver Transplantation
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PaoloFeltracco,StefaniaBarbieri,andCarloOri
47.1 Introduction Noninvasiveventilation(NIV)withpositivepressure,consolidatedtreatmentofbothacute andchronicrespiratoryfailure,hasproveneffectiveinthemanagementofnumerousmedicalandsurgicaldiseases. Clinical experience has shown that intubation and reintubation, rather than the total durationofrespiratorysupport,aredeterminantsfortheriskoflungcomplications.NIV, considereda gentle, nonaggressivemethodofairwaymanagement,isthereforeincreasinglyappliedtoavoidthesideeffectsofconventionalinvasivemethods. AgrowinginteresthasemergedinadoptionofNIVforventilatoryassistanceinimmunocompromisedpatients,suchasthoseundergoingbonemarrow,liver,lung,cardiac,and kidneytransplantation. Theobligatoryimmunosuppressionconsistentlyincreasestheriskofventilator-associated pneumonia (VAP) in invasively ventilated liver transplant patients. Nosocomially acquiredinfectionsintheserecipientshaveanimportanteffectontheearlyoutcomesince theyincreasemorbidity,lengthoftheintensivecareunit(ICU)stay,andmortality.
47.2 Pathophysiology of Respiratory Failure in Liver Recipients Some degree of respiratory failure and abnormalities of pulmonary gas exchange are common ndingsofend-stageliverdisease.Causesofgasexchangeabnormalitiesfollowingorthotopiclivertransplantation(OLTx)arenumerousandincludethepersistence
P.Feltracco(),S.Barbieri,andC.Ori DepartmentofPharmacologyandAnesthesiology,UniversityHospitalofPadova, ViaGiustiniani267,Padova,Italy e-mail:
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ofpreoperativeintrapulmonaryshunting,postoperativeventilation perfusionmismatching,failureofthehypoxicvasoconstrictorresponse,andleftventricularfailure.Almost 70% of patients undergoing pretransplant assessment of pulmonary function present a widened A-a (alveolar arterial) oxygen gradient. Unpredictable changes in the neural drivetotherespiratorymusclesmaybeinducedbytheintraoperativeanesthetics,poor recovery of the graft, and various drugs administered in the immediate postoperative period. Hypoventilation in liver recipients may be a consequence of decreased overall activityandlackofcoordinationofrespiratorymuscles.Inaddition,pleuraleffusions, abdominaldistension,interstitiallungdisease,andpneumoniaareoftenresponsiblefor restrictiverespiratorydisorders. Livertransplantpatientsfrequentlyhavereducedlungvolumes,elevationofboth hemidiaphragms,andlower-lobeatelectases.Theseconditionsconsistentlyincrease the work of breathing, making it difficult to achieve and maintain postoperative ventilatoryautonomy.
47.3 NIV as a Tool to Facilitate Early Extubation After OLTx Thepersistenceofpreoperativeneurologicdisorders,patchylungin ltrates,lungimbibition, pleural effusion, sputum retention, and unsuccessful weaning attempts sometimes requireprolongedtrachealintubationandmechanicalventilationafterOLTx. Rapidweaningfrommechanicalventilationishighlyrecommendedinlivertransplant patientsforatleastthefollowingreasons:(1)theaugmentedriskforventilatory-induced complications,(2)thepotentialnegativehemodynamiceffectsofahighintrathoracicpressureongraftperfusion,and(3)theneedforrapidavoidanceofsedatives. Earlyremovaloftheendotrachealtubeintheposttransplantcourseisessentialinpreventingtrachealmucosainjuries,impairmentofairwayciliaryfunction,bacterialcolonization,sinusitis,anddevelopmentofnosocomialpneumonia;aprolongeddependenceon invasive airways is, in fact, associated with ventilator-associated complications and increasedmortality.However,lackofimprovementofpreoperativeventilatorydisorders alongwithpostoperativerespiratorymuscledysfunction,poornutritionalstatus,andsuboptimalchestX-rayimagesmakerapiddiscontinuationofmechanicalventilationsometimeschallenging. The introduction of noninvasive mechanical ventilation in the postoperative care of livertransplantpatientshasbeenofgreathelptocliniciansduringthistransitionphase oftencriticalfortheremovalofarti cialairways.Rapidextubationfollowedbyprompt NIVapplicationshouldbeconsideredinthissettingasameanstoshortenandaccelerate theweaningprocess. Anoninvasivetechnique, prophylactically appliedsoonafterwithdrawalofinvasive airways,representsamethodofventilatoryassistanceparticularlyeffectiveinthoserecipientswhodonotcompletelyful llthecriteriaforsafeextubation. Noninvasivepressuresupport(PS)modeplusacontinuouspositiveend-expiratory pressure (PEEP) could prevent severe lung derecruitment and the loss of vital
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capacityfollowingremovaloftheendotrachealtube.SinceNIVwithPEEPavoids the additional respiratory resistance imposed by the tracheal tube, it contributes to reduceinspiratoryeffort. By limiting diaphragm elevation, NIV will also prevent basal atelectases in case of abdominaldistension. Prolongedinvasiveventilationinthepostoperativeperiodmayalsonegativelyaffect graft perfusion. Since mechanical ventilation decreases the extra intrathoracic venous pressure gradient, it may increase inferior vena cava pressure and decrease portal vein ow.Loweringtheintrathoracicpressurebyrapidavoidanceofpositivepressureventilationisanimportantstrategytoreducetheback owpressuretotheliverandpromotebetter oxygendeliveryduringearlyrecoveryofthegraft. Noninvasivetechniquesareassociatedwithmorefavorableintrathoracichemodynamic balancecomparedtoconventionalinvasivemethods.Thisislikelyduetothefactthatthe lungin ationpressurereachedwithNIVislowerthanwhenapatientisventilatedthrough anendotrachealtube. ThisadvantagemakesNIVparticularlysuitableforventilatoryassistanceofhemodynamicallyunstabletransplantedpatients.Lessneed,ornoneed,forsedativesalongwitha morephysiologicvenousreturnmaydecreasetheuseofinotropicandvasoactiveagents, thusimprovingsplanchniccirculationandgraftperfusion. Majorbene tsafterextubationareobservedwhenNIVisappliedcontinuouslyrather thanintermittently.DiscontinuingNIVseveraltimesadaymayresultinlimitedclinical ef cacy. ThesuccessofNIVinpreventingalveolarcollapseandmicroatelectasesandmaintainingrespiratorysystemcompliancehasbeendiffuselydemonstrated. Incaseofmoderatesedation,sometimesnecessaryforagitationorinvasiveprocedures, therecipientsmayexperienceadecreaseininspiratorymusclestrength,somedegreeof lungderecruitment,lossoflungvolumes,andimpairmentofgasexchange.NIVshould alwaysbeconsideredinthesecircumstancestopreventhypoventilation. NocturnalventilationinNIVisfrequentlyindicatedformoderatelyhypoxicliverrecipientswhorequiresedativestofacilitatenightsleep. Anincreaseinintrathoracicbloodvolumeandinterstitiallungwater,oftenunavoidable consequences of massive intraoperative uid loading, can at times lead to respiratory fatigue and hypoxia. If lung congestion is responsible for ventilatory distress, an early NIV plus PEEP is useful to reduce extravascular lung uid when diuretics alone are ineffective. NIVcanbemaintainedforaslongasthepatientrequiresit.Oncethepatientnolonger requirestheNIV-PSmode,intermittentCPAP(continuouspositiveairwaypressure)by facialmaskorahelmetsystemcanbesafelyappliedtopreservethepatencyofperipheral airwaysinspontaneousventilation. InthebeginningofitsuseinsolidorgantransplantationNIVwasmainlydeliveredwith afullfacialmask.However,therearenumeroussideeffectsassociatedwithprolongeduse ofafullfacialmask,suchaserythema,ulcerationsofthenoseandface,conjunctivalirritation, discomfort on speaking, claustrophobia, and air leaks. Now we prefer the helmet system,moresuitableforlongapplicationofNIV.Antonellietal.[1]demonstratedthat thehelmetsystemisassociatedwithalowerfailureratethanthefacialmask.
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47.4 NIV in the Prevention of Posttransplant Infectious Diseases Prolonged anesthesia and surgery may impair the function of lung cells, which could increasesusceptibilitytopostoperativeinfections. Theriskofpostoperativepneumoniaisgreatlyin uencedbythetimetoextubation.In astudybyMedurietal.[2]thepersistenceoftheendotrachealtubeemergedasthesingle mostimportantpredisposingfactorforVAP.Afterabdominalsepsis,VAPrepresentsthe mostimportantcauseofmorbidityandmortalityfollowingOLTx,withahighcostinterms ofeconomicresourcesandtimedemandsonmedicalpersonnel. Asmentioned,anearlyextubationfollowedbyrapidimplementationofNIVshouldbe consideredtopreventVAPincaseofinadequateventilatoryautonomy. Nourdineetal.[3]reportedalowerincidenceofpulmonaryandextrapulmonaryinfectionsaswellasalowermortalityinpatientstreatednoninvasivelycomparedwithpatients intubatedandconventionallyventilated.Hilbertetal.[4]comparedearlyNIVwithstandardtreatmentinimmunosuppressedhematologicalpatients.NIV-treatedpatientshada signi cantly lower death rate in the ICU, and fewer individuals developed infections; pneumoniaandsinusitisoccurredonlyinpatientswhorequiredintubation. The rst application of NIV in solid organ transplant recipients was described by Antonelliandcoworkers[5].Theyrandomizedpatientswithrespiratoryfailurefollowing transplantationtoreceiveeitherNIVorstandardtherapy.PatientsassignedtoNIVshowed a trend toward fewer VAPs and a signi cant reduction of severe sepsis or septic shock episodes. NIVisparticularlyattractiveinpreventingposttransplantinfectiousdiseasesasitleaves theupperairwaysintact,reducesbacterialcolonizationandnosocomiallyacquiredinfections, and avoids the bleeding complications of invasive airways in such immunosuppressedthrombocytopenicrecipients.
47.5 NIV in the Prevention of Tracheal Reintubation After OLTx Reintubationoftenbecomesnecessaryinthepostoperativeperiodofacomplicatedliver transplant, either within the rst few days or at any time later. Respiratory distress can occurbecauseofpulmonaryedema,aspirationpneumonia,inadequatecough,excessive respiratorysecretions,encephalopathy,infectiousdiseases,andcardiacdysfunction. Patientswhodevelopsevererespiratoryfailureintheposttransplantcoursehavebeen generallymanagedwithtrachealintubationandmechanicalventilation.However,many respiratorydisordersfollowingOLTxmayrespondtospeci ctreatments,suchashemo ltration,pleuraldrainage,bronchialtoilette,abdominaldrainage,andsoonandareexpected toimproveoveraperiodofhoursordays.Intubation,deepsedation,andmechanicalventilationmayleadtomuscleweaknessinsuchdebilitatedpatients,thereforeincreasingthe susceptibilitytoadditionalepisodesofventilatoryfailure.
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Ithasbeenrecognizedthattheimmunocompromisedrecipientswithhypoxemicrespiratoryinsuf ciencyareathighriskofpulmonaryinfectionsandsepsiswhileintubated. Iftheseverityofventilatoryfailuredoesnotrequireimmediateintubation,NIVmaybe cautiouslyattemptedbeforeproceedingtoinvasiveairways. NIVrepresentsaneffectivemeansofventilatoryassistanceespeciallywhentheneed for respiratory support will presumably be short lived. Supporting the failing recipient withanoninvasivetechniquemayreducetheworkofbreathingandmaintaingasexchange whileawaitinganimprovementinspontaneousventilation. Institutingthisstrategyatamoreadvancedstagemayimplytheapplicationofbothan increased level of pressure support and a long time of dependency on NIV. This may increasepatientdiscomfortandsideeffects. ClearadvantagesofNIVinsevereimmunodepressedortransplantedpatientssuffering fromacuterespiratoryfailurehavealreadybeendemonstrated[5].InthestudybyAntonelli andcolleagues[5],patientswhoreceivedNIV(vs.standardtreatment)hadareducedneed forreintubationandalowerICUmortalityrate. NIVdoesnotseemtobebene cialinavoidingreintubationwhenthesepatientshave developedovertrespiratoryfailureassociatedwithlife-threateninghypoxemia,anditdoes notrepresentareplacementforendotrachealintubationinrecipientswhorequireairway protection. AlongdelayinNIVinstitution,frankmuscleexhaustion,verylowarterialbloodpH, andamarkedalterationofthepatient smentalstatusreducethelikelihoodofsuccess.In thepresenceofsevereabnormalitiesinrespiratorymechanics,neurologicdisordersimpairingrespiratorydrive,andseverecomorbidconditions,NIVmaybefutileintryingtoavoid reintubation.
47.6 Conclusion NIVandCPAPbyahelmetsystemhavegainedincreasedacceptanceinposttransplant ventilatoryassistance. Recognitionofseriouscomplicationsassociatedwithprolongedintubationandstandardmechanicalventilation,abetterunderstandingofrespiratoryfailureinthissetting, and the development of ventilatory modalities that allow more patient ventilator synchronystronglypromoteNIVfollowingOLTx. ClinicalexperiencehasshownthatproperlydeliveredNIVmostlybene tsmoderately dyspneicrecipientsinacuterespiratoryfailure,whileitappearslesspromisingandef cientintheweaningprocessofpatientsventilatedforextendedperiodsoftime. The improvements in arterial oxygenation, decreased ventilatory demand provided with an inspiratory support, as well as the scarcity of hemodynamic repercussions are amongthemajorbene tsofthismethod. NumerousstudiesandmulticentertrialswillbeneededtoverifywhetherNIVhasa clearpositiveimpactonalargescaleinreducingpostoperativemorbidity,graftcomplications,lengthofICUstay,costs,andmortalityfollowingOLTx.
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TheintroductionofNIVinthepostoperativecareoflivertransplantpatientshas beenofgreathelptocliniciansduringthetransitionphase,oftencritical,ofthe removalofarti cialairways. Rapidweaningfrommechanicalventilationishighlyrecommendedinliver transplantpatientsforatleastthefollowingreasons:(1)theaugmentedriskfor ventilatory-inducedcomplications,(2)thepotentialnegativehemodynamic effectsofahighintrathoracicpressureongraftperfusion,and(3)theneedfor rapidavoidanceofsedatives. Loweringtheintrathoracicpressurebyrapidavoidanceofpositivepressure ventilationisanimportantstrategytoreducetheback owpressuretotheliver andpromotebetteroxygendeliveryduringearlyrecoveryofthegraft. NIVisparticularlysuitableforventilatoryassistanceofhemodynamically unstabletransplantedpatients.Lessneed,ornoneed,forsedativesalongwitha morephysiologicvenousreturnmaydecreasetheuseofvasoactiveagents,thus improvingsplanchniccirculationandgraftperfusion. NIVisparticularlyattractiveasitleavestheupperairwaysintact,reducesbacterial colonization,decreasestheincidenceofVAP,andavoidsthebleedingcomplications ofinvasiveventilationinsuchimmunosuppressedthrombocytopenicrecipients.
References 1. Antonelli M, Conti G, Pelosi P et al (2002) New treatment of acute hypoxemic respiratory failure:noninvasivepressuresupportventilationdeliveredbyhelmet apilotcontrolledtrial. CritCareMed30:602 608 2. Meduri GU, Estes RJ (1995) The pathogenesis of ventilator associated pneumonia. II. The lowerrespiratorytract.IntensiveCareMed21:452 461 3. Nourdine K, Combes P, Carton MJ, Beuret P, Cannamela A, Ducreux JC (1999) Does noninvasiveventilationreducetheICUnosocomialinfectionrisk?Aprospectiveclinicalsurvey. IntensiveCareMed25:567 573 4. Hilbert G, Gruson D, Vargas F et al (2001) Noninvasive ventilation in immunosuppressed patients with pulmonary in ltrates, fever, and acute respiratory failure. N Engl J Med 344: 481 487 5. AntonelliM,ContiG,Bu Metal(2000)Noninvasiveventilationfortreatmentofacuterespiratoryfailureinpatientsundergoingsolidorgantransplantation.JAMA12(283):235 241
Noninvasive Positive Pressure Ventilation in Patients Undergoing Lung Resection Surgery
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ChristophePerrin,ValérieJullien,YannickDuval,andFabienRolland
48.1 Introduction Lungresectionsurgeryisoftencomplicatedbysigni cantpulmonarydysfunctionthatpersistsforafewdaysaftersurgery[1 3].Alterationofventilatoryfunctionismultifactorial, withallfactorscontributing(Fig.48.1):re exinhibitionofthephrenicnerve,depressionof therespiratorydrivebynarcotics,chestpain,closureofdistalairways,andthelossoffunctioningparenchyma[2,3].Pleuralairleaksmayfurtherdeterioratepulmonarygasexchange andincreasetheworkofbreathing[2,3].Finally,hemodynamicinstabilitymayoccurand participateingastransferdecreasewithinthelungsandoxygentransporttotissues[2,3]. Thispulmonaryfunctionimpairmentmayleadtopostoperativepulmonarycomplications suchassputumretention,atelectasis,pneumonia,andrespiratoryfailure[4]. Postoperativemortalityandmorbidityafterlungresectionsurgeryremainimportant.A studyfound30-daymortalityandmorbidityratesof4%and23.8%,respectively,afterlobectomyandof11.5%and25.7%,respectively,afterpneumonectomy[5].Postoperativepulmonarycomplicationsremaintheleadingcauseofdeath;forexample,acuterespiratoryfailure afterlungresectionmaybefatalinupto60 80%ofcases[6].Thesehighmortalityand morbidityratesaremainlylinkedtocomplicationsofendotrachealmechanicalventilation [7].Indeed,prolongedinvasivemechanicalventilationincreasestheriskofbronchialsuture disruption,bronchopleural stula,persistentairleakage,andpneumonia[8,9]. Noninvasivepositivepressureventilation(NPPV)isappliedusingamaskormouthpieceratherthananendotrachealortracheostomytube.AlthoughNPPVisoftenusedfor long-term nocturnal or continuous support in patients with chronic respiratory failure,
C.Perrin(),V.Jullien,Y.Duval,andF.Rolland ServicedePneumologie,CentreHospitalierdeCannes, 15,avenuedesBroussailles,06401,Cannes,France e-mail:
[email protected]
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Reflex inhibition of the phrenic nerve
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NPPVisalsousefulinpatientswithacuterespiratoryfailure[10].Indeed,NPPVimproves gas exchange in patients with various cause of acute respiratory failure [10 13]. Furthermore,NPPVissafeandmayavoidendotrachealmechanicalventilationinpatients with acute respiratory failure from various causes [14 19]. As a consequence, NPPV reducestheriskoflowerrespiratorytractinfectionandpneumonia,therebyreducinginhospitalmorbidityandmortality[13,14,17]. Ontheotherhand,continuouspositiveairwaypressure(CPAP)hasalsobeendemonstratedtobeusefulintheprevention[20,21]andtreatment[22]ofpulmonaryatelectasis afterupperabdominalsurgery. Takingallofthisintoaccount,whetherNPPVmaybeusefulinpatientsundergoing lungresectionsurgeryhasbeenassessed.Althoughfewarticleshavebeenpublishedon thetopic,thischapterreviewscontrastingapproachesofNPPVinthis eld.
48.2 NPPV Improves Gas Exchange After Lung Resection Surgery Regardingmechanismsofpostoperativepulmonaryfunctionimpairmentinpatientswho are candidates for lung resection surgery, NPPV may improve arterial blood gases by openingpreviouslyclosedlungunits[11,12].Ontheotherhand,NPPVmaycauseadverse sideeffects,suchasincreasingtheratioofdeadspacetotidalvolume(VD/VT)andthe pulmonary-to-pleuraairleaks.Further,bydecreasingvenousreturn,NPPVmayreduce cardiacoutput[23]andinterferewithoxygentransport. Aguiloetal.[24]designedaprospective,randomized,controlled,andparalleltrialto investigatetheshort-termeffectsofNPPVonpulmonarygasexchange,ventilatorypattern,systemichemodynamics,andpleuralairleaksin19patientssubmittedtoelective lungresection.Medicaltherapy,includingchestphysiotherapy,wasstandardizedforall patients.TensubjectsreceivedNPPVwithanasalventilatorsupportsystem(studygroup). Theremainingnineindividualsconstitutedthecontrolgroup.Inthestudygroup,NPPV signi cantly increased Pao2 and also signi cantly decreased alveolar-to-arterial oxygen pressure gradient (P[A-a]o2). By contrast, Pao2 and P[A-a]o2 remained unchanged
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throughoutthestudy.Paco2,theventilatorypattern,andsystemichemodynamicsdidnot changesigni cantlythroughoutthestudyinanygroup.NPPVdidnotincreasetheratioof deadspacetotidalvolumeorsigni cantlyworsenpleuralairleaks.
48.3 NPPV Reduces Mortality in Acute Respiratory Failure Following Lung Resection Pulmonarycomplicationsaretheleadingcauseofpostoperativedeathinpatientsfollowing lungresection.Auriantetal.[25]conductedarandomizedcontrolledtrialofusualcarewith orwithoutNPPVin48patientswithacutehypoxemicrespiratoryfailureafterlungresection. Patientswereenrollediftheymetatleastthreeofthefollowingcriteria:dyspneaatrest(respiratoryrate>25breaths/min),activecontractionoftheaccessoryrespiratorymuscles,ratioof Pao2tofractionofinspiredoxygen(Pao2/Fio2)below200mmHg,andchestX-rayabnormalities(alveolarconsolidation,atelectasis,orinterstitialpulmonaryedema).Usualcareconsisted ofoxygensupplementationtoachieveanarterialoxygensaturationabove90%,bronchodilators,patient-controlledanalgesia,andchestphysiotherapy.Theprimaryoutcomevariablewas theneedforendotrachealmechanicalventilation,andthesecondaryoutcomevariableswere in-hospitaland120-daymortalityrates,durationofstayintheintensivecareunit,andduration ofin-hospitalstay.Halfofthepatientsassignedtotheno-NPPVgrouprequiredintubation versusonly5of24patients(20.8%)intheNPPVgroup(p=0.035).Ofthe17patientswho requiredintubation,9intheno-NPPVgroupand1intheNPPVgroupwerestartedonendotrachealmechanicalventilationduringthe rst48hafterlungresection.Ninepatientsinthe no-NPPVgroupdied(37.5%)comparedtoonlythree(12.5%)intheNPPVgroup(p=0.045). Theothersecondaryoutcomesweresimilarinbothgroups.
48.4 Prophylactic Use of NPPV Following Lung Resection Although surgical resection is the treatment of choice for non-small-cell bronchogenic carcinoma,asigni cantnumberofpatientscannotundergosurgicalresectionbecauseof associated comorbidities that increase operative mortality and postoperative morbidity [26].Potentialpatient-relatedriskfactorsthatmaycontributetotheriskofpostoperative pulmonarycomplicationsincludesmoking,poorgeneralhealthstatus,olderage,obesity, and chronic obstructive pulmonary disease (COPD) [4]. Furthermore, it has been suggestedthatamajorriskofpostoperativecomplicationsmaybeassociatedwithapreoperativeimpairmentofpulmonaryfunctionde ning themarginalpatient [26].Themarginal patienthasaforcedexpiratoryvolumeat1s(FEV1)oflessthan1.2L/min;amaximum voluntaryventilationof35 40%predicted;aforcedexpiratoryvolumeof0.6to1L/min; adiffusioncapacityforcarbonmonoxideof30 40%predicted;andaPaco2greaterthan 45mmHg[26].AlthoughCPAPhasbeentestedinaprophylacticmannerafterabdominal surgeryandseemstobemoreeffectivethanroutinechestphysiotherapy[27],itsbene ts areunfortunatelynotsustained,andfunctionalresidualcapacitydeterioratesafewminutes
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afterinterruptionofCPAP[28].IncomparisontoCPAP,relativelyhighinspiratorypressureisusedwithNPPV.Asaresult,NPPVmaystronglyimprovethedistributionofventilationbyrecruitingzonesofalveolarcollapse[29].Thus,prophylacticuseofNPPVmay promotebetterrecoveryofarterialbloodgasesandpulmonaryfunctionafterlungresectionandperhapsmayavoidpostoperativepulmonarycomplications. Inaretrospectivestudy,Lumbierresetal.[30]studied20stablepatientsonNPPVfor chronic respiratory failure secondary to kyphoscoliosis (8), morbid obesity (6), thoracoplasty(4),andneuromusculardiseases(2)whounderwentsurgicalprocedureswithgeneral anesthesia.Thesepatientswerecomparedtosubjectswithoutrespiratorydiseasewhowere submittedtothesametypeofsurgicalprocedures(gastroplasty,mastectomy,septoplasty, hip prosthesis, cholecystectomy, Gasserian ganglion thermocoagulation, hysterectomy, endoscopicretrogradecholangiopancreatography).Themeanpostoperativeintubationtime was3.8±3.2h,andonlyonepatientremainedintubatedformorethan12h.Themeanstay inthepostsurgicalreanimationunitwas19±9h(vs.19±6hinthegeneralpopulation, pnotsigni cant). Perrinetal.[31]examinedtheprophylacticuseofNPPVadministeredpre-andpostoperativelyassociatedwithchestphysiotherapyforreducingpostoperativepulmonaryfunctionimpairment.Thirty-ninepatientswithapreoperativeFEV1below70%ofthepredicted valuescheduledforelectivelobectomyrelatedtolungcancerwereenrolled.Sevenpatients wereexcludedafterenrollment.Arandomized,controlled,andparalleltrialwasdesigned. Patientswererequiredtofollowstandardtreatmentwithout(controlgroup,n=18)orwith NPPV(studygroup,n=14)for7dayspreoperativelyathomeandfor3dayspostoperativelyinthehospital.Standardtreatmentincludedchestphysiotherapy,performedwiththe sameregimenduringthepre-andpostoperativeperiod,twiceaday.NPPVwasprovided viaafacialmask,inthespontaneousmode,for1h vetimesaday.Theprimaryoutcome variablewasthechangeinarterialbloodgasesonroomair.Pulmonaryfunctiontesting, lobar or supralobar atelectasis requiring a ber-optic bronchoscopy, and duration of inhospitalstaywerealsorecorded.ThisstudydemonstratedthatpreventiveNPPVtherapy usedpre-andpostoperativelyinpatientswithapreoperativeFEV1below70%ofthepredictedvaluesubmittedtoelectivelungresectionimprovestheoverallperioperativeevolution of arterial blood gas values and pulmonary function parameters. Also, this study showedthatthepreoperativeuseofNPPVmayreducetheimmediatepostoperativehypoxemiaandpulmonaryfunctionimpairment.Thehospitalstaywassigni cantlylongerinthe controlgroupthaninthestudygroup.Theincidenceofmajoratelectasiswas14.2%in theNPPVgroupand38.9%intheno-NPPVgroup,butthedifferencewasnotsigni cant.
48.5 Conclusions Indeed,short-termpostoperativeuseofNPPVimprovestheef ciencyofthelungasagas exchangerwithoutassociatedunwantedsideeffectsinpatientssubmittedtolungresection surgery.Furthermore,NPPVmayberecognizedasasafeandeffectivemeansofreducing theneedforendotrachealmechanicalventilationandimprovingsurvivalinpatientswith acuterespiratoryfailureaftersuchasurgery.AlthoughprophylacticuseofNPPVreduces
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pulmonarydysfunctionafterlungresection,furtherstudiesarerequiredtoassessthereal impactofNPPVinapreventivemanneronpostoperativepulmonarycomplications.
References 1. AliJ,WeiselRD,LayugAB,KripkeBJ,HechtmanHB(1974)Consequencesofpostoperative alterationsinrespiratorymechanics.AmJSurg128:376 382 2. Nunn JF (1987) Respiratory aspects of anaesthesia. In: Nunn JF (ed) Applied respiratory physiology,3rdedn.Butterworth,Cambridge,pp350 378 3. BrownLK(1986)Surgicalconsiderations:effectsofsurgeryonlungfunction.In:BrownLK (ed)Pulmonaryfunctiontestsinclinicalandoccupationallungdisease.GruneandStratton, Orlando,pp341 351 4. SmetanaGW(1999)Preoperativepulmonaryevaluation.NEnglJMed340:937 944 5. Harpole DH, Decamp MM, Daley J, Hur K, Oprian CA, Hendrson WG, Khuri SF (1999) Prognostic models of 30-day mortality and morbidity after major pulmonary resection. J ThoracCardiovascSurg117:969 979 6. KutluCA,WilliamsEA,EvansTW,PastorinoU,GoldstrawP(2000)Acutelunginjuryand acuterespiratorydistresssyndromeafterpulmonaryresection.AnnThoracSurg69:376 380 7. Harpole DH, Liptay MJ, Decamp MM, Mentzer SJ, Swanson SJ, Sugabaker DJ (1996) Prospective analysis of pneumonectomy: risk factors for major morbidity and cardiac dysrhythmias.AnnThoracSurg61:977 982 8. WrightCD,WainJC,MathissenDJ,GrilloHC(1993)Postpneumonectomybronchopleural stula after sutured closure: incidence, risk factors and management. J Thorac Cardiovasc Surg112:1367 1371 9. KirschMM,RotmanH,BehrendtD,OrringerM,SloanH(1975)Complicationsofpulmonaryresection.AnnThoracSurg20:215 236 10. MehtaS,HillNS(2001)Noninvasiveventilation.AmJRespirCritCareMed163:540 577 11. MeyerTJ,HillNS(1994)Noninvasivepositivepressureventilationtotreatrespiratoryfailure.AnnInternMed120:760 770 12. HillNS(1993)Noninvasiveventilation:doesitwork,forwhom,andhow?AmRevRespir Dis147:1050 1055 13. WysockiM,TricL,WolffMA,GertnerJ,MilletH,HermanB(1993)Noninvasivepressure supportventilationinpatientswithacuterespiratoryfailure.Chest103:907 913 14. BrochardL,IsabeyD,PiquetJetal(1990)Reversalofacuteexacerbationsofchronicobstructivelungdiseasebyinspiratoryassistancewithafacemask.NEnglJMed323:1523 1530 15. BrochardL,ManceboJ,WysockiMetal(1995)Noninvasiveventilationforacuteexacerbationsofchronicobstructivepulmonarydisease.NEnglJMed333:817 822 16. MeduriGU,TurnerRE,Abou-ShalaN,WunderinkR,TolleyE(1996)Noninvasivepositive pressureventilationviafacemask: rstlineinterventioninpatientswithacutehypercapnic andhypoxemicrespiratoryfailure.Chest109:179 193 17. CarlucciA,RichardJC,WysockiM,LepageE,BrochardL;SRLFCollaborativeGroupon MechanicalVentilation(2001)Noninvasiveversusconventionalmechanicalventilation:an epidemiologicsurvey.AmJRespirCritCareMed163:874 880 18. DemouleA,GirouE,RichardJC,TailléS,BrochardL(2006)Increaseduseofnoninvasive ventilationinFrenchintensivecareunits.IntensiveCareMed32:1747 1755 19. MasipJ,RoqueM,SanchezB,FernandezR,SubiranaM,ExpositoJA(2005)Noninvasive ventilation in acute cardiogenic pulmonary edema: systematic review and meta-analysis. JAMA294:3124 3130 20. DehavenCBJr,HurstJM,BransonRD(1985)Postextubationhypoxemiatreatedwithcontinuouspositiveairwaypressuremask.CritCareMed13:46 48
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21. StockMC,DownsJB,GauerPK,AlsterJM,ImreyPB(1985)Preventionofpostoperative pulmonarycomplicationswithCPAP,incentivespirometry,andconservativetherapy.Chest 87:151 157 22. DuncanSR,NegrinRS,MihmFG,GuilleminaultC,Raf nTA(1987)Nasalcontinuouspositiveairwaypressureinatelectasis.Chest92:621 624 23. AmbrosinoN,NavaS,TorbickiA,RiccardiG,FracchiaC,OpasichC,RampullaC(1993) HaemodynamiceffectsofpressuresupportandPEEPventilationbynasalrouteinpatients withstablechronicobstructivepulmonarydisease.Thorax48:523 528 24. AguiloR,TogoresB,PonsS,RubiM,BarbéF,AgustiAGN(1997)Noninvasiveventilatory supportafterlungresectionalsurgery.Chest112:117 121 25. AuriantI,JallotA,HervéPetal(2001)Noninvasiveventilationreducesmortalityinacute respiratoryfailurefollowinglungresection.AmJRespirCritCareMed164:1231 1235 26. BurkeJR,DuarteIG,ThouraniVH,MillerJI(2003)Preoperativeriskassessmentformarginalpatientsrequiringpulmonaryresection.AnnThoracSurg76:1767 1773 27. RickstenSE,BengtssonA,SoderbergC,ThordenM,KvistH(1986)Effectsofperiodicpositiveairwaypressurebymaskonpostoperativepulmonaryfunction.Chest89:774 781 28. StockMC,DownsJB,CorkranML(1984)Pulmonaryfunctionbeforeandafterprolonged continuouspositiveairwaypressure.CritCareMed12:973 974 29. Al-Saady N, Bennett ED (1985) Decelerating inspiratory ow waveform improves lung mechanicsandgasexchangeinpatientsonintermittentpositive-pressureventilation.Intensive CareMed11:68 75 30. LumbierresM,PratsE,FarreroE,MonasterioC,GraciaT,ManresaF,EscarrabillJ(2007) Noninvasivepositivepressureventilationpreventspostoperativepulmonarycomplicationsin chronicventilatorsusers.RespirMed101:62 68 31. PerrinC,JullienV,VénissacN,BerthierF,PadovaniB,GuillotF,CoussementA,MourouxJ (2007) Prophylactic use of noninvasive ventilation in patients undergoing lung resectional surgery.RespirMed101:1572 1578
Section X Noninvasive Mechanical Ventilation in Neonates and Children
Equipment and Technology for Continuous Positive Airway Pressure During Neonatal Resuscitation
49
GeorgM.SchmölzerandColinJ.Morley
49.1 Introduction Immediatelyafterbirth,thelungsofnewlyborninfantshavetoclearlungliquid,createa functional residual capacity (FRC), and establish regular spontaneous breathing [1, 2]. However,manypreterminfantsdonotachievethiswithoutassistance.Thelungsofpreterminfantsareimmature,aresurfactantde cient,arepronetocollapseatendexpiration, and have dif culty establishing and maintaining FRC [1]. Current guidelines do not providerecommendationsabouttheinitialrespiratorysupportofverypreterminfants[3]. However,thereisagrowingbodyofevidencethatcontinuouspositiveairwaypressure (CPAP) and positive end-expiratory pressure (PEEP) might be bene cial during initial respiratory support in the delivery room (DR) [4 7]. CPAP is a continuous pressure deliveredthroughamaskornasalinterface.PEEPisanend-expiratorypressureapplied duringpositivepressureventilation.WhenCPAPorPEEPisused,adistendingpressureis appliedtotheairwaystoenhancelungexpansion,promotearesiduallungvolume,prevent alveolarcollapseandpreserveendogenoussurfactant,reduceventilation perfusionmismatchandairwayresistance,improveoxygenationandlungcompliance,reducethework ofbreathing,andstabilizethebreathingpattern[8,9].
G.M.Schmölzer() DepartmentofNewbornResearch,TheRoyalWomen sHospital,20FlemingtonRoad, Parkville3052,Victoria,Australiaand TheRitchieCentre,MonashInstituteforMedicalResearch,Melbourne,Australia, MurdochChildrenResearchInstitute,Melbourne,Australiaand DepartmentofPaediatrics,MedicalUniversityGraz,Austria e-mail:
[email protected] C.J.Morley NeonatalServices,RoyalWomen sHospital,Melbourne,Australiaand MurdochChildrenResearchInstitute,Melbourne,Australia e-mail:
[email protected]
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Despitethisinformation,theroleofCPAPandPEEPintheresuscitationofverypretermnewborninfantsisyettobepreciselyde ned.ThischapterdescribesdifferentequipmentandtechniquesfortheadministrationofCPAPintheDR.
49.2 CPAP Interface TherearenumerousdevicesavailabletodelivernasalCPAP,butnoneofthemhasbeen identi edastheoptimalinterface.Forpracticalreasons,bothnasalprongsandfacemask areusedtodelivernasalCPAPintheDR.Interfacessuchasaheadboxwithseal,anegativepressurebox,oranosepieceareusedintheneonatalintensivecareunitsbutarenot applicableforDRresuscitation.
49.2.1 Nasal Prongs NasalprongsarethemosteffectivetechniqueofdeliveringnasalCPAP.Oneortwoprongs insertedashortdistanceintothenostrilsandattachedtoapressure-generatingdevicecan beusedtodeliverCPAP[8,10].Neitherdoubleprongsnorasinglepronghasbeenshown tobesuperiorinapplyingnasalCPAPintheDR,althoughithasintheneonatalintensive careunit[11].DuringstabilizationintheDR,asinglenasalprongcanbeinsertedeasily intoonenostriltodelivernasalCPAP(seeFig.49.1).Thisisusuallyalessthan5-cmcut down 2.5- or 3-mm endotracheal tube that is passed 1 2 cm into one nostril [8, 10]. ApplicationofCPAPbyasinglenasalprongneedsconstantattentionbecausetheprong becomeseasilydislodgedorkinked,resultinginlossofpressure.Thecontralateralnostril andthemouthhavetobeoccludedtoreduceanyleak,andthegas owhastobehigh enough to maintain the level of PEEP (see Fig. 49.1) [8, 10]. However, the Columbia experiencehasshownthatbilateralnasalHudsonprongscanbeeasilyusedtoapplyCPAP andPEEPimmediatelyafterbirth[12].Applicationofbinasalprongsneedsconstantattentionbecausetheycaneasilydislodge,resultinginlossofpressure.
49.2.2 Face Mask AfacemaskwilldeliverCPAPtotheentireairway,notlimitingittothenose.Nolossof pressurethroughthemouthisanadvantageofthisinterface,althoughachievingagood facemasksealisdif cult(seeFig.49.2).Everytimethefacemaskisliftedtoassessthe infant,thepressureislost.Inaddition,thegas owhastobehighenoughtopreventloss ofPEEPduringinspiration(seeFig.49.3)[8,10]andtocompensateforleaks.
49
Equipment and Technology for Continuous Positive Airway Pressure During Neonatal Resuscitation
30
1second Nasal CPAP with occluded contralateral nostril
Ventilation Pressure [cm H2O]
0
337
50
Nasal CPAP with open contralateral nostril
Inspiratory flow
Gas Flow [mL/sec]
No expiratory Flow
30
Tidal Volume [mL]
−50 Expiratory Flow
VTi VTe
Leak
0
Fig. 49.1 Continuouspositiveairwaypressure(CPAP)withsinglenasalprongandaT-piecedevice. Expiratory breath holds in a spontaneous breathing infant with nasal prong CPAP support of 7cmH2O.Afterinspiration,theinfantholdshisbreathbetween1and2sbeforeexpirationoccurs. Initially,thecontralateralnostrilisoccluded.Thisisre ectedinthegas owpatternandtidalvolumecurveandnoleak.Suddenly,theresuscitatorreleasestheocclusionand100%leakoccurs
49.3 CPAP Device Currently,thereislittleevidencetoguideclinicians choiceofCPAPpressure-generating device.However,tofacilitatethedevelopmentofFRCimmediatelyafterbirth,toimprove oxygenation,andtopreventlungcollapse,thedevicemustprovidecontinuousPEEPor CPAP.Arangeofdevicesisavailable[13 15].Aself-in atingbagdoesnotprovidePEEP orCPAP(seeFig.49.4)[16].AnattachedPEEPvalveprovidesinconsistentPEEPduring positive pressure ventilation but cannot deliver CPAP [15 17]. Variable and operatordependentPEEPisprovidedbya ow-in atingbag[15,16].Itcannotbeusedtoprovide CPAP.T-piecedevicesallowoperatorstodeliverapredeterminedandmeasuredlevelof PEEPandCPAP[14,16].AneonatalventilatorinCPAPmodecouldbeusedtoprovide CPAP,andinventilatormodealsoprovidesPEEP.
338
G.M. Schmölzer and C.J. Morley
30
1second
Ventilation Pressure [cm H2O]
0
50
Flow towards the infant
Gas Flow [mL/sec]
15
Almost no flow away from the infant
−50
Tidal Volume [mL] 90% Leak
90% Leak
0
Fig. 49.2 Leakduring(continuouspositiveairwaypressure)CPAPwithafacemaskandaT-piece device.SpontaneouslybreathingpreterminfantwithCPAPsupportof9cmH2OthroughaT-piece device.Theareaunderneaththein ation owcurveisgreaterthanthatundertheexpiratory ow curves.Leakisdisplayedasastraightlineinthetidalvolumecurve
49.4 Problems with the Use of CPAP AmajorproblemduringDRCPAPisfacemaskleak.Duringstabilization,agoodmask sealisessentialtomaintainthepressure(seeFigs.49.2and49.3).Inourexperience,operatorsareoftenunabletoachieveadequatemasksealduringmaskCPAPandtendtoliftthe maskfromthefacetoassesstheinfant;hence,thepressureislost.Incomparison,asingle nasalprongmightbemorereliabletodeliverleak-freeCPAPwhileoccludingtheother nostril(seeFig.49.1);however,thisstillneedstobestudied.
49
Equipment and Technology for Continuous Positive Airway Pressure During Neonatal Resuscitation
30
1second PEEP of 9 cm H2O
Ventilation Pressure [cm H2O]
0
339
50
Decrease of PEEP to 5 cm H2O during inspiration
Flow towards the infant
Gas Flow [mL/sec]
−50 15
Flow away from the infant
Tidal Volume [mL]
0
Fig. 49.3 Continuous positive airway pressure (CPAP) with a face mask and a T-piece device. SpontaneouslybreathingpreterminfantwithCPAPsupportof9cmH2OthroughaT-piecedevice.The pressurecurveshowsadropto5cmH2Oduringinspiration.Thetidalvolumecurveshowsanequal volumeofgasenteringandleavingthelungandnoleak
49.5 Limitations of CPAP and PEEP in the Delivery Room DespitethefrequentuseofCPAPandPEEPintheDR,anumberofsigni cantgapsinour knowledgeremainunanswered:(1)WhatistheoptimaldevicetodeliverCPAPorPEEP? (2)Whatpressureisoptimalduringtransition?(3)Howdoweidentifyinfantsmostlikely tobene tfromCPAPandPEEP?
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30 tI
tE
Ventilation Pressure (cm H2O) PEEP of 0.8 cm H2O
0 50
Flow towards the infant
Gas Flow (mL/sec)
15
Flow away from the infant
-50
1 second Tidal Volume (mL)
VTi
VTe
0
Fig. 49.4 Continuouspositiveairwaypressure(CPAP)withafacemaskandaself-in atingbag. SpontaneouslybreathingpreterminfantswithCPAPsupportthroughaself-in atingbag.Theselfin atingbagdoesnotdeliverpositiveend-expiratorypressure(PEEP).Thetidalvolumecurve showsanequalvolumeofgasenteringandleavingthelungandnoleak
Key Recommendations
› › ›
CPAPorPEEPshouldbedeliveredtofacilitatetheearlydevelopmentofFRC, reduceatelectrauma,andimproveoxygenationduringthetransitionfrom intrauterinetoneonatallifeinpreterminfantsimmediatelyafterbirth. BothnasalprongsandfacemaskcanbeusedasinterfacestodeliverCPAPand PEEP.Thenasalprongprovidesbetteraccesstotheinfantfaceduring stabilization. Currently,aT-piecedevicedeliversmorereliableCPAPandPEEPcomparedtoa ow-in atingbag.Aself-in atingbagdoesnotprovideconsistentPEEPand doesnotprovideCPAP.
49
Equipment and Technology for Continuous Positive Airway Pressure During Neonatal Resuscitation
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References 1. Te Pas AB, Davis PG, Hooper SB et al (2008) From liquid to air: breathing after birth. J Pediatr152(5):607 611 2. TePasAB,WongC,KamlinCOetal(2009)Breathingpatternsinpretermandterminfants immediatelyafterbirth.PediatrRes65(3):352 356 3. International Liaison Committee on Resuscitation (2005) International Consensus on CardiopulmonaryResuscitationandEmergencyCardiovascularCaresciencewithTreatment Recommendations.Part7:neonatalresuscitation.Resuscitation67(2 3):293 303 4. GregoryGA,KittermanJA,PhibbsRHetal(1971)Treatmentoftheidiopathicrespiratorydistress syndrome with continuous positive airway pressure. N Engl J Med 284(24): 1333 1340 5. FinerNN,CarloWA,DuaraSetal(2004)Deliveryroomcontinuouspositiveairwaypressure/ positive end-expiratory pressure in extremely low birth weight infants: a feasibility trial. Pediatrics114(3):651 657 6. MorleyCJ,DavisPG,DoyleLWetal(2008)NasalCPAPorintubationatbirthforverypreterminfants.NEnglJMed358(7):700 708 7. GittermannMK,FuschC,GittermannARetal(1997)Earlynasalcontinuouspositiveairway pressure treatment reduces the need for intubation in very low birth weight infants. Eur J Pediatr156(5):384 388 8. MorleyC(1999)Continuousdistendingpressure.ArchDisChildFetalNeonatalEd81(2): F152 F156 9. MorleyC,DavisP(2004)Continuouspositiveairwaypressure:currentcontroversies.Curr OpinPediatr16(2):141 145 10. DavisPG,MorleyCJ,OwenLS(2009)Non-invasiverespiratorysupportofpretermneonates withrespiratorydistress:continuouspositiveairwaypressureandnasalintermittentpositive pressureventilation.SeminFetalNeonatalMed14(1):14 20 11. DavisP,DaviesM,FaberB(2001)Arandomisedcontrolledtrialoftwomethodsofdelivering nasalcontinuouspositiveairwaypressureafterextubationtoinfantsweighinglessthan1000 g: binasal (Hudson) versus single nasal prongs. Arch Dis Child Fetal Neonatal Ed 85(2): F82 F85 12. AveryME,TooleyWH,KellerJBetal(1987)Ischroniclungdiseaseinlowbirthweight infantspreventable?Asurveyofeightcenters.Pediatrics79(1):26 30 13. LeoneTA,RichW,FinerNN(2006)Asurveyofdeliveryroomresuscitationpracticesinthe UnitedStates.Pediatrics117(2):e164 e175 14. O DonnellCP,DavisPG,MorleyCJ(2004)Positivepressureventilationatneonatalresuscitation: review of equipment and international survey of practice. Acta Paediatr 93(5): 583 588 15. DawsonJ,GerberA,KamlinCOFetal(2008)ProvidingPEEPduringneonatalresuscitation: whichdeviceisbest?JPaediatrChildHealth44(Suppl1):A31 16. Bennett S, Finer NN, Rich W et al (2005) A comparison of three neonatal resuscitation devices.Resuscitation67(1):113 118 17. HussainF,DawsonJ,DavisPGetal(2008)UseofaPEEPvalvewithneonatalself-in ating device.JPaediatrChildHealth44(Suppl1):A93
Air Leakage During Continuous Positive Airway Pressure in Neonates
50
GerdSchmalisch
50.1 Introduction Sincetheimplementationofcontinuouspositiveairwaypressure(CPAP)technologyby Gregoryandcolleaguesin1971[1],CPAPhasbeenincreasinglyusedasamodeofnoninvasiverespiratorysupportforneonatesworldwidetoassistinthetreatmentofabroadrange ofneonatalrespiratorydiseases(e.g.,respiratorydistresssyndrome,apneasofprematurity, andtracheomalacia).CPAPhelpstostabilizeairwaysandthediaphragm,todecreasedead spaceventilation,toincreasecomplianceandfunctionalresidualcapacityleadingtoarise inarterialoxygenpressure(Pao2),andtopreventalveolarcollapseattheendofexpiration. Severalstudieshaveshownthat,inneonates,CPAPdecreasestheriskofadverseoutcomes comparedtointubationandmechanicalventilation[2 4].Eveninmechanicallyventilated infants,CPAPreducestheincidenceofadverseclinicalincidents(apnea,respiratoryacidosis,increasedoxygenrequirement,andreintubation)afterextubation[5]. CPAPwasinitiallyusedintheendotrachealmode,andavarietyofcommercialCPAP systemsandinterfacesbecameavailable[6,7].CPAPcanbeappliedviaafacialmaskor headbox,usingmono-orbinasalprongs,orviapharyngealorendotrachealtubesemploying eitheraconstantoravariabledriving ow[8].Independentofwhichinterfaceor owdriver isused,somedegreeofairleakageoccurs,causedbyleakage owbetweenthepatientand interface or in tubing within the patient, which may reduce treatment ef cacy and cause adverseeffects(e.g.,impairmentofthenasalorupperairwaymucosa[9]).Especially,oralair leakagethatoccurswiththeuseofnasalprongscanleadtohighlyvariableleakage ows. AlthoughtheeffectofairleakageonCPAPtreatmenthasbeenwidelyinvestigatedin adults[9 12],onlyafewstudieshaveexaminedtheeffectofsuchleakageinneonates[13, 14]becauseofthetechnicaldif cultiesassociatedwithairleakagemeasurements.Inneonates,leakagemeasurementsdependsmainlyontheinterfaceused,asshowninFig.50.1.
G.Schmalisch ClinicofNeonatology,Charité UniversitätsmedizinBerlin,Charitéplatz1, 10117,Berlin,Germany e-mail:
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a Flow driver P(t)
Flow
Humidifier
FiO2
CPAP valve
0.21-1.0
V’(t)) Flowsensor
Air
O2 - Oro- /nasopharyngeal tube - Face mask
To the patient interface
b Flow driver Flowsensor1
Flow
Humidifier
P(t)
Flowsensor2 CPAP valve
FiO2 0.21-1.0
Air
V’2(t))
V’1(t)) Binasal prongs
O2
c P(t)
Flow driver Flowsensor
Flow
Humidifier
FiO2 0.21-1.0
V’(t))
E.g. Benveniste valve Defined leakage
Air
O2
Fig. 50.1 Methodsofventilatorymeasurementduringcontinuouspositiveairwaypressure(CPAP) inneonatesusingtubesorfacemasks(a),binasalprongs(b),orspecialCPAPdeviceswithde ned leakageattheinterface(c).Ifthereisnoairleak,thebaselineofthemeasured ow(a)or owdifference(b)iszero,whereasinthemethodincthebaselineispermanentlyshiftedby owthrough thede nedleakageintheinterface
Furthermore, air leakage is mostly characterized by leakage ow per se in adults [15], whereasinneonatesairleakageisusuallycharacterizedbyleakage owrelatedtopatient owandisrepresentedasapercentage.Dependingonwhichmeasureofpatient owis used,differentleakagede nitionsarepossible[14]. Theairleakagegivenasapercentageisnoteasytointerpret,andtheuseofdifferent leakagede nitionsmakescomparisonsbetweenstudiesdif cult.Therefore,theaimofthis study was to theoretically investigate the relationship between air leakage and leakage owusingdifferentleakagede nitionsandtovalidatethemodelingbyinvitromeasurementsusingacommerciallyavailableCPAPdevice.
50
Air Leakage During Continuous Positive Airway Pressure in Neonates
345
50.2 Air Leakage Measurements During CPAP Treatment of Neonates 50.2.1 Theory of Air Leakage Measurements During CPAP Inadults,airleakageduringCPAPiscommonlycharacterizedbytheleakage owderived fromthe owoftheblowerthataimstokeeptheCPAPofthefacemaskconstant.An unintendedleakage owiscompensatedbyanincreasein owgeneratedbytheblowerso thatblower owgivesinformationonairleakage[16].Inneonates,however,aconstant driving ow is commonly used, and air leakage is usually calculated as the difference between inspired and expired volume, related to the measured volume. Three different de nitionsarepossible: Leak1 (%) = 100·
Leak 2 (%) = 200·
Leak 3 (%) = 100·
Vinsp −Vexp Vinsp
(50.1a)
Vinsp − Vexp Vinsp + Vexp
(50.1b)
Vinsp − Vexp Vexp
(50.1c)
whereVinspandVexparethemeasuredinspiratoryandexpiratoryvolumes,respectively. Ifthereisnoairleakage,VinspandVexpshouldbeidentical.However,ifthereisanyair leakageata owresistanceRLeakbetweenthepatient slungandthe owmeter,themeasuredair owofthepatient V&Pat, meas willbereduced(usingthecurrentdividerrule)by V&Pat, meas =
RLeak V&Pat RCPAP + RLeak
(50.2)
where V&Pat istherealair owofthepatient,andRCPAPisthe owresistanceoftheCPAP system(interface+ owmeter).RCPAPisde nedasthemaximal owthroughtheCPAP interface: CPAP max V&CPAP = RCPAP
(50.3)
providedthatthe owdriverallowssuchahigh ow.Fortheleakage ow,weobtain V&Leak =
CPAP RLeak + RCPAP
(50.4)
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G. Schmalisch
Assumingthattheleakageresistanceisconstantduringthebreathingcycleandthatthe inspiratoryandexpiratoryvolumesofthepatientareequal, Tinsp
Tinsp + Texp
0
Tinsp
∫ V&Pat dt= −
∫
V&Pat dt = VT
(50.5)
andweobtainthemeasuredinspiredandexpiredvolumesusingEqs.50.2 50.5:
Tinsp V&Leak Vinsp, meas = ∫ V&meas (t )·dt = 1_ VT + V&Leak ·Tinsp 0 maxV&CPAP
Vexp, meas = −
(50.6a)
+ Texp V&Leak VT − V&Leak ·Texp ∫ V&meas (t )·dt = 1_ Tinsp V&CPAP max
Tinsp
(50.6b)
where V&meas isthe owmeasuredbythe owsensor.Thus, V&Leak canbemeasuredbreath bybreathby V&Leak =
Vinsp, meas − Vexp, meas Tinsp + Texp
(50.7)
Withade nitionoftheminuteventilation V&E ofthepatientas V&E =
VT Tinsp + Texp
(50.8)
weobtainthefollowingforthethreeleakagede nitions: Leak1 (%) = 100
V&Leak V&Leak 1 − maxV &
Leak 2 (%) = 200
Leak 3 (%) = 100
Tinsp & & VE + VLeak · T + T CPAP insp exp
(50.9a)
V&Leak & T −T VLeak & 2· 1 − VE + V&Leak · insp exp & Tinsp + Texp max VCPAP
(50.9b)
V&Leak V&Leak 1 − maxV&
Tinsp & & VE − VLeak · T + T CPAP insp exp
(50.9c)
Asshownbyequations50.9a-c,thereisanonlinearandcomplexrelationshipbetween theleakagegiveninpercentageandleakage ow,patientventilation,andtheperformance oftheCPAPdeviceasgivenbymax V&CPAP.However,ifV&Leak << max V&CPAP andTinsp=Texp, thentheformulasareconsiderablysimpli ed:
50
Air Leakage During Continuous Positive Airway Pressure in Neonates
Leak1 (%) = 100
V&Leak V& E
Leak 3 (%) = 100
(50.10a)
V&Leak V&E + 0.5 · V&Leak
Leak 2 (%) = 100
347
V&Leak V&E − 0.5 · V&Leak
(50.10b)
(50.10c)
andweobtainasimplerelationshipbetweenthethreeleakagede nitions:
Leak1 (%) = 100
Leak 2 (%) Leak 3 (%) = 100 100 + 0.5 · Leak 2 (%) 100 + Leak 3 (%)
(50.11)
However,thisrelationshipbreaksdownwithincreasingleakage oworuneveninspiratoryandexpiratorytimes.
50.2.2 Computer Simulation Toinvestigatetherelationshipbetweenthethreeleakagede nitionsandtoidentifythe most important factors in uencing measured leakage, a computer simulation was performedusingMathcad14(MathSoft,Cambridge,MA). Therelationshipbetweenthedisplayedairleakageusingthethreeleakagede nitions andtheleakage owrelatedtopatientventilationisshowninFig.50.2.Forsmallleakages, the differences between the three leakage de nitions are small, but they increase notably with increasing leakage ow. Both Leak2 and Leak3 rise to in nity before the maximalleakage owisreached.OnlyLeak1islimitedinmagnitudeandattainsthe nal 500 %
Leak3
Leak2
Fig. 50.2 Relationship betweenthedisplayed leakageandleakage owrelatedtothe minuteventilationof thepatientusingthe threede nitions (Leak1 3)
Air leak (%)
400 %
. . VLeak = max VCPAP
300 % 200 %
Leak1 100 %
. . VLeak = VE
0% 0
1
2
3
4 5 . . VLeak/VE
6
7
8
9
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G. Schmalisch
value 100*(Tin + Tex)/Tin at the maximal leakage ow given by max V&CPAP . Thus, for onitoring of high leakage ows, only the calculation of Leak1 is useful, and this was m consideredinfurtherinvestigationsasdiscussednext. AdisadvantageofleakagemonitoringusingLeak1isthedependencyofLeak1onbreathing pattern. As shown in Fig. 50.3, the displayed leakage varies distinctly with the 140% RR = 30/min
Air leak (%)
120% 100%
RR = 60/min
80%
RR = 90/min
60% 40% 20% 0% 0
200
400
600 800 1000 Leak flow (mL/min)
1200
1400
140% Tin= 20%
120%
Tin= 40%
Air leak (%)
100%
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Fig. 50.3 Effectof respiratoryrate(RR; topleft),inspiratory time(topright),and maximalcontinuous positiveairway pressure(CPAP) owonLeak1
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35 Displayed inspired and expired volume (ml)
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Fig. 50.4 Dependenceofthemeasuredinspiratoryandexpiratoryvolumeontheleakage owfor differentrespiratoryrates(RRs),assumingatidalvolumeof15mL.Notethatforhighleakage owsandlowrespiratoryratesthedisplayedexpiratoryvolumecanbecomenegative
respiratoryrate(RR).Thein uenceofTin/Texonthedisplayedleakageissmallforleakage ows in the range of patient ventilation but increases continuously with rising leakage ow.Comparedtothetimingparametersofthebreathingcycle,themeasuredleakageisonlyminimallyaffectedbychangesinmax V&CPAPcausedbychangesintheCPAP. Aleakage owleadstoanoverestimationofinspiratoryvolumeandanunderestimationofexpiratoryvolume,andthevolumeerrordependsontheRR,asshowninFig.50.4. DependingontheRRwithincreasingleakage ow,themeasuredexpiratoryvolumecan evenbecomenegative,whichmaybedif cultforacliniciantointerpret.Therefore,in mostdevices,themeasuringscaleforairleakageislimitedtolessthan90%sothatnegativevolumevaluesareexcluded.
50.2.3 In Vitro Experiments To validate the modeling, in vitro measurements were performed using a commercial CPAPdevice(Leoni;Heinen&Löwenstein,BadEms,Germany)andamechanicallung model(VT=15mL)withanadjustableRR,asdescribedbyFischerandcolleagues[17]. Leaksweresimulatedusingopensilicontubes(3.2-mminnerdiameter)ofvaryinglengths (16 170 cm) connected between the ow sensor and lung model. For all simulated air leaks,CPAPwasvariedbetween3and9cmH2O,andtheRRwasintheinterval30 90/ min. Leakage ow was measured using differential pneumotachography (the method showninFig.50.1b),asdescribedbyFoitzikandassociates[18]. TheLeonicanprovideCPAPtherapyforprematurebabies,neonates,andinfantsanduses ahot-wireanemometer,locatedbetweentheY-piece,forair owmeasurement.Thedisplayed
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volumeoftheLeoniisthemeasuredexpiredvolumeVexp,andthedisplayedleakageiscalculatedusingthede nitionofLeak1givenbyEq.50.1a.Themaximumdisplayedleakageof thedeviceissetat90%,andhigherleakagescannotbemeasured.TheLeonidoesnotdisplay leakage ow.However,ourmodelingpermitsleakage owtobecalculatedusingEqs.50.6a, 50.8,and50.9aby V&Leak =
Vexp Leak1 100 − Leak1 Tin + Texp
(50.12)
Measured Leak flow (mL/min)
AsshowninFig.50.5,therewasastrongcorrelation(r=0.984)betweenmeasured leakage ow and that calculated using Eq. 50.12. The difference between the measurementswas16.5mL/min;thisisnegligiblefromtheclinicalviewpoint.AnAltman Bland plot showed relatively wide measurement scatter, but the residuals were randomly distributed.
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Fig. 50.6 Relationship betweenthevolume erroroftheLeoni ventilatorandthesize ofthesimulatedair leak
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Withincreasingairleakage,thedisplayedvolumedecreased,asshowninFig.50.6. Accordingtoourmodeling,theleakage-dependentvolumeerrorcanbecalculatedusing Eq.50.6bby
δVexp (%) = 100
V&Leak Vexp, meas − VT V&Leak · Texp = −100 + VT VT maxV&CPAP & VLeak · Texp ≈ − 100 VT
(50.13)
wheretheapproximationassumesthat V&Leak << max V&CPAP .ThecorrelationbetweenthecalculatedandthemeasuredvolumeerrorisshowninFig.50.7.Therewasalsoastrongcorrelation(r=0.995)betweenthemeasuredandthepredictedvolumeerror,andthebiasof 1.1%wasverysmall.However,theAltman Blandplotshowedthat,withincreasingvolumeerror,therewasanoverestimationofcalculatedvolumeerror.Thismaybecausedby neglectofsomenonlinearitiesinourmodelingofvolumeandairleakagemeasurements.
50.3 Discussion Thepresentstudyshowedthat,duringCPAP,thedisplayofanairleakageasapercentage ofmeasuredpatientventilationisnotadequatelyinformativebecauseleakagedependsnot onlyonthesizeoftheleakandtheresultingleakage ow,butalsoonpatientventilation, thatis,thetidalvolume,RR,andinspiratory/expiratorytimeratio.AsshowninFig.50.3 forlowRRs,evenmoderateleakage owscancausethedisplayedleakagetoriseto90%, andthisiscommonlytheupperlimitofthemeasuringrange[17].ForhigherRRs,leakage measurementsarestillpossibleevenwithmuchmoreseriousleaks.Thedependenceof
352 −100% Measured volume error (%)
Fig. 50.7 Correlationbetween thecalculatedandthe measuredvolumeerrorofthe Leoniventilator(above)and thecorrespondingAltman Blandplot(below)
G. Schmalisch
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thedisplayedleakageonbreathingpatternhampersmonitoringoftheairtightnessofa CPAPsystem,especiallyconsideringthatthebreathingpatternofnewbornswithchronic lungdiseasemaybeveryvariable[19],thuscausinghighly uctuatingleakagedisplays. Furthermore,thepresentsimulationstudyshowedlargedifferencesinleakageresults depending on the various possible leakage de nitions. This makes comparison of displayedleakagesbetweendifferentdevicesdif cultbecausetheleakagecalculationusedis often not described in detail by the manufacturers. If the leakage ow exceeds patient ventilation,onlyacalculationusingLeak1willbeofpracticalvaluebecauseallotherde nitionscanattainin nity. However,themeasuringrangeofairleakageiscommonlylimited(e.g.,to<90%of monitored patient ventilation). This may be adequate for ventilated patients in whom endotracheal tube leakages are commonly relatively small [20], but not during CPAP, whenairleakageismuchhigher.Inparticular,withnasalCPAP,oralleakscancauseleakage owsthatclearlyexceedpatientminuteventilation[21]. Incontrasttothedisplayofairleakageasapercentageofthemeasuredventilation,a displayofleakage owinmillilitersperminutemaybebetterforcomparisonsandiscommonlyusedinadultstudies[15].Theleakage owdependsonlyonleakresistanceand
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theCPAPinstrumentemployedandisgenerallyindependentofthebreathingpatternofthe patient.Adverseeffectsofleakage ow(e.g.,irritationoftheskinorimpairmentofthe nasalorupperairwaymucosabymouthleaks[9])arein uencedbythemagnitudeofleakage owandareindependentofpatientventilation. Theeffectofaleakage owduringCPAPiscontradictory.Smallleakage owsmay improvealveolargasexchangebyCO2washoutofairwaydeadspace(includingapparatus dead space) [22]. However, with increasing leakage ow, ventilatory measurements becomemoredif cultbecauseofashiftin owbaseline[18,23].Furthermore,theeffectiveCPAPforthepatientwillbereducedbythepressuredropacrosstheCPAPinterface ( ∆CPAP = V&Leak · RCPAP ).Ahighleakage owcreatesadditionalnoise,whichimpairsthe identi cationofthebeginningandendofinspirationandexpiration[23,24].Thisisan importantpointinthetriggeringofbilevelCPAP. Largeleaksalsocauseahigherrorinmeasurementofpatientventilation,asshownin Fig.50.6.Towhatextentafaultyreadingcanbenumericallycorrectedisstillunknown. Thepresentstudyshowedgoodagreementbetweenmodelingandinvitromeasurements, sothatnumericalcorrectionofthedisplayedvolumemayindeedbepossible.Inaprevious invitrostudy,successfulvolumecorrectionswereachievedwhenleakagewasupto90% [14],butthiscouldnotbecon rmedbyinvivomeasurements[21].Nevertheless,leakage owmeasurementalone,whichisindependentofmeasurementofpatientventilation,may behelpfulinassessmentofCPAPtreatment.Irrespectiveofwhichmeasuringprincipleof Fig.50.1isused,leakage owmeansashiftinthemeasured owbaseline.Forleakage monitoringduringCPAPinneonates,neweffortsarenecessarytodevelopwell-adapted algorithmstoseparatethebaselinefromthemeasured owsignal. Currently,fordevicesusedinneonatesthatpresentleakageasapercentageofpatient ow, leakage ow measurements are possible only by numerical calculation using the displayed leakage and volume. The low bias between calculated and measured leakage ow and volume errors (Figs. 50.5 and 50.7) demonstrates the adequacy of the model used; however, the relatively wide scatter of the calculated leakage ows indicates the technicalproblemsassociatedwithleakagemeasurementsbasedonthedifferencebetween inspiredandexpiredvolumes.Suchleakagemeasurementsareaffectedbyseveraltechnical(e.g.,differencesinthetransfercharacteristicsofthepneumotachbetweeninspiration andexpiration,qualityofbreathdetection[24])andphysiologicalfactors(e.g.,instability ofend-expiratorylungvolume[25],changesingascompositionbetweeninspirationand expiration[26]).BubbleCPAPiswidelyusedandmaybeadvantageous[8,27];however, thetechniqueisassociatedwithseveretechnicaldif culties,mainlywithrespecttoair ow measurementsandbreathdetectionasaresultofthenoisy owsignal[24]. AlthoughtheeffectsofairleaksonCPAPeffectiveness[9,16],sideeffects[15],triggeringfunction,humidi cation,andinspiratoryoxygenfraction[28]havebeeninvestigatedinadults,fewsuchstudieshavebeenperformedinneonatesbecauseofthedif culties associatedwithventilatoryandleakagemeasurementsduringCPAP.Inadults,leakages over24L/minarede nedasexcessiveandcancompromisetheeffectivenessoftreatment [15].Ifweassumeatenfoldlowerventilationrequirementinneonates,thenanexcessive leakage owwouldbe2.4L/min,whichiscommonlyhigherthanpatientventilationand outsidethemeasuringrangeofmostdevices.Suchhighleakage owsarenotuncommon, especially during nasal CPAP. Hückstädt and colleagues [13] performed leakage ow
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measurementsinneonatesduringnasalCPAPusingdifferentialpneumotachography(the methodshowninFig.50.1b).Leakagemeasurementswerenotpossiblein49of69infants astheleakage owwashigherthanonethirdoftheCPAP ow(4 6L/min),whichwas theupperlimitofthemeasuringrangeoftheequipmentused[18]. In conclusion, the display of air leakage as a percentage of measured ventilation is unsuitableforleakagemonitoringduringCPAPbecausesuchameasurementoftenfails forhighleakage ows,whicharenotuncommon.Furthermore,thedifferencesinresults obtainedwiththeuseofvariousleakagede nitions,andthedependenceofthedisplayed leakageonbreathingpattern,hamperscomparisonsbetweendifferentmeasuringconditionsandvariousCPAPdevices.Asuperiormethodwouldbetodisplaytheleakage ow measuredbyasuitabletechniquesothattheeffectofairleakageonCPAPtreatmentof neonatescanbeinvestigatedinmoredetail.
Key Recommendations
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VerylittleisknownabouttheeffectofairleakageonCPAPtreatmentof neonates,andnewclinicalairleakagestudiesarenecessary.However,withthe measurementequipmentavailabletoday,onlysmallleakagescanbemeasured. Highleakagesarenotuncommon,especiallywhenthewidelyusednasalCPAP isemployed,andmeasurementofsuchleakagesrequiresnewmethodological andtechnicaldevelopments. Thecurrentdisplayofairleakageasapercentageofmeasuredpatientventilation hasseveraldisadvantagesandshouldbereplacedbydirectmeasurementand displayofleakage ow.Newalgorithmsarenecessarytoreliablyseparate leakagefrommeasured owsignal. Therelationshipbetweenairleakageandvolumeerrorcanbeadequatelydescribed bymodeling.However,todate,itremainsunknowntowhatextentanumerical correctionofmeasuredpatient owandvolumeispossibleinthepresenceofair leakage.Thisshouldbeaddressedinfutureclinicalstudies.
Acknowledgments TheauthorswouldliketothankMr.HendrikFischerfortheperformedinvitromeasurements,andDr.ScottButlerofEnglishManagerScienceEditing,Sydney,Australia, forlinguisticrevision.
References 1. GregoryGA,KittermanJA,PhibbsRH,TooleyWH,HamiltonWK(1971)Treatmentofthe idiopathicrespiratory-distresssyndromewithcontinuouspositiveairwaypressure.NEnglJ Med284:1333 1340 2. JobeAH,KramerBW,MossTJ,NewnhamJP,IkegamiM(2002)Decreasedindicatorsof lung injury with continuous positive expiratory pressure in preterm lambs. Pediatr Res 52:387 392
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3. MorleyCJ,DavisPG,DoyleLW,BrionLP,HascoetJM,CarlinJB(2008)NasalCPAPor intubationatbirthforverypreterminfants.NEnglJMed358:700 708 4. DaniC,BertiniG,PezzatiM,CecchiA,CaviglioliC,RubaltelliFF(2004)Earlyextubation andnasalcontinuouspositiveairwaypressureaftersurfactanttreatmentforrespiratorydistresssyndromeamongpreterminfants<30weeks gestation.Pediatrics113:e560 e563 5. Dimitriou G, Greenough A, Kavvadia V, Laubscher B, Alexiou C, Pavlou V et al (2000) Electiveuseofnasalcontinuouspositiveairwayspressurefollowingextubationofpreterm infants.EurJPediatr159:434 439 6. DePaoliAG,DavisPG,FaberB,MorleyCJ(2002)Devicesandpressuresourcesforadministrationofnasalcontinuouspositiveairwaypressure(NCPAP)inpretermneonates.Cochrane DatabaseSystRev(4):CD002977 7. RoehrCC,SchmalischG,KhakbanA,ProquitteH,WauerRR(2007)Useofcontinuouspositiveairwaypressure(CPAP)inneonatalunits asurveyofcurrentpreferencesandpracticein Germany.EurJMedRes12:139 144 8. GuptaS,SinhaSK,TinW,DonnSM(2009)Arandomizedcontrolledtrialofpost-extubation bubblecontinuouspositiveairwaypressureversusinfant owdrivercontinuouspositiveairwaypressureinpreterminfantswithrespiratorydistresssyndrome.JPediatr154:645 650 9. HayesMJ,McgregorFB,RobertsDN,SchroterRC,PrideNB(1995)Continuousnasalpositiveairwaypressurewithamouthleak-effectonnasalmucosalblood uxandnasalgeometry. Thorax50:1179 1182 10. RichardsGN,CistulliPA,UngarRG,Berthon-JonesM,SullivanCE(1996)Mouthleakwith nasalcontinuouspositiveairwaypressureincreasesnasalairwayresistance.AmJRespirCrit CareMed154:182 186 11. RanderathWJ,SchraederO,GaletkeW,FeldmeyerF,RuhleKH(2001)AutoadjustingCPAP therapybasedonimpedanceef cacy,complianceandacceptance.AmJRespirCritCareMed 163:652 657 12. NiliusG,HappelA,DomanskiU,RuhleKH(2006)Pressure-reliefcontinuouspositiveairwaypressurevsconstantcontinuouspositiveairwaypressure:acomparisonofef cacyand compliance.Chest130:1018 1024 13. HückstädtT,FoitzikB,WauerRR,SchmalischG(2003)ComparisonoftwodifferentCPAP systemsbytidalbreathingparameters.IntensiveCareMed29:1134 1140 14. SchmalischG,FischerH,RoehrCC,ProquitteH(2009)Comparisonofdifferenttechniques tomeasureairleaksduringCPAPtreatmentinneonates.MedEngPhys31:124 130 15. Rabec CA, Reybet-Degat O, Bonniaud P, Fanton A, Camus P (2004) Leak monitoring in noninvasiveventilation.ArchBronconeumol4011:508 517 16. TeschlerH,StampaJ,RagetteR,KonietzkoN,Berthon-JonesM(1999)Effectofmouthleak on effectiveness of nasal bilevel ventilatory assistance and sleep architecture. Eur Respir J 14:1251 1257 17. FischerHS,RoehrCC,ProquitteH,WauerRR,SchmalischG(2008)Assessmentofvolume andleakmeasurementsduringCPAPusinganeonatallungmodel.PhysiolMeas29:95 107 18. FoitzikB,SchmidtM,WindstetterD,WauerRR,SchmalischG(1998)Leakmeasurementsin spontaneouslybreathingprematurenewbornsbyusingthe ow-throughtechnique[Special communication].JApplPhysiol85:1187 1193 19. SchmalischG,WilitzkiS,WauerRR(2005)Differencesintidalbreathingbetweeninfants withchroniclungdiseasesandhealthycontrols.BMCPediatr5:36 20. MahmoudR,FischerH,ProquitteH,ShalabyHA,SchmalischG(2009)Relationshipbetween endotracheal tube leakage and under-reading of tidal volume in neonatal ventilators. Acta Paediatr98:1116 1122 21. FischerH,RöhrCC,ProquittéH,HammerH,WauerRR,SchmalischG(2009)Messungvon Atemlecks bei mononasaler CPAP-Therapie im Neugeborenenalter. Z Geburtsh Neonatol 213(Suppl1):S104
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22. ClaureN,D UgardC,BancalariE(2003)Eliminationofventilatordeadspaceduringsynchronizedventilationinprematureinfantspressureinpretermlambs.JPediatr143:315 320 23. BatesJH,SchmalischG,FilbrunD,StocksJ(2000)Tidalbreathanalysisforinfantpulmonary functiontesting.ERS/ATSTaskForceonStandardsforInfantRespiratoryfunctiontesting. EuropeanRespiratorySociety/AmericanThoracicSociety.EurRespirJ16:1180 1192 24. SchmidtM,FoitzikB,WauerRR,WinklerF,SchmalischG(1998)Comparativeinvestigationsofalgorithmsforthedetectionofbreathsinnewbornswithdisturbedrespiratorysignals. ComputBiomedRes31:413 425 25. SchmalischG,WauerRR,FoitzikB,PatzakA(2003)In uenceofpretermonsetofinspiration on tidal breathing parameters in infants with and without CLD. Respir Physiol Neurobiol 135:39 46 26. FoitzikB,SchmalischG,WauerRR(1994)Effectofphysicalpropertiesofrespiratorygason pneumotachographic measurement of ventilation in newborn infants. Biomed Tech (Berl) 39:85 92 27. PillowJJ,HillmanN,MossTJ,PolglaseG,BoldG,BeaumontCetal(2007)Bubblecontinuouspositiveairwaypressureenhanceslungvolumeandgasexchangeinpretermlambs.AmJ RespirCritCareMed176:63 69 28. MiyoshiE,FujinoY,UchiyamaA,MashimoT,NishimuraM(2005)Effectsofgasleakon triggeringfunction,humidi cation,andinspiratoryoxygenfractionduringnoninvasivepositiveairwaypressureventilation.Chest128:3691 3698
The Use of Noninvasive Ventilation in the Newborn
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DebbieFraserAskin
51.1 Introduction Noninvasiveventilation(NIV)intheformofnasalcontinuouspositiveairwaypressure (CPAP) was rst introduced for use in newborns in the early 1970s. When mechanical ventilationforinfantsbecameavailableinthelate1970s,theuseofCPAPdeclined.More recently,recognitionthatexposuretomechanicalventilationsigni cantlyincreasesaprematureinfant sriskfordevelopingchroniclungdiseasehasresultedinrenewedinterestin theuseofNIV. ThereisagrowingbodyofresearchsupportingtheuseofNIVasatreatmentforneonatalapneaandrespiratorydistressandforfacilitatingextubationfollowingmechanical ventilation.ThereisavarietyofdevicesandstrategiesforusingNIVinnewborninfants. ThesuccessfulapplicationofNIVreliesonknowledgeablehealthcareproviderswhoare familiarwiththeequipmentandbene tsandlimitationsofvarioustypesofNIV. ThisworkprovidesabriefoverviewofthetypesofNIVavailableforuseinnewborns andsummarizestheavailableresearchsupportingitsuseinthispopulation.AbriefdescriptionofthecareofnewbornsreceivingNIVconcludesthisreview.
51.2 Materials and Methods This work is based on a search of PubMed, CINHAL (Cumulative Index of Nursing and AlliedHealthLiterature),andtheCochranedatabases.Thefollowingsearchtermswereused: prematureinfant,newborn,CPAP,NCPAP(nasalcontinuouspositiveairwaypressure),noninvasiveventilation,apnea,respiratorydistresssyndrome,andchroniclungdisease.
D.F.Askin CentreforNursingandHealthStudies,AthabascaUniversity,Athabasca,Alberta,Canada e-mail:
[email protected] A.M.Esquinas(ed.),NoninvasiveMechanicalVentilation, DOI:10.1007/978-3-642-11365-9_51,©Springer-VerlagBerlinHeidelberg2010
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51.3 Types of NIV TherearetwomaintypesofNIVusedinnewborninfants:CPAPusingeithercontinuous- ow or variable- ow devices and phasic ventilation. CPAP is the application of continuouspositivepressureacrosstherespiratorycycle,whilephasicventilationprovides continuous positive pressure with the addition of periods of increased airway pressure(orbreaths)[1].Continuous- owCPAPmaybedeliveredbyaneonatalventilatororthroughbubbleCPAP,asimpledevicethatprovidesasupplyoffreshgaswhile submergingtheexpiratorytubingofthesystemunderwater.Theamountofpositive airwaypressureiscontrolledbythelevelofwaterintheout owchamber.Inphasic NIV,breathsmaybedeliveredatregularintervalsornonsynchronized(nasalintermittentpositivepressureventilation[NIPPV])ormaybesynchronizedwiththeinfant s inspiratory efforts (synchronized nasal intermittent positive pressure ventilation or SNIPPV).
51.4 Benefits of NIV in Newborns Theuseofpositivepressureinnewbornshasbeenshowntoprovideanumberofphysiologicalbene ts,including[2]
Stabilizationoftheairways,diaphragm,andchestwall Increasedlungvolumes Decreasedairwayresistanceandworkofbreathing
51.5 Indications for NIV Innewborninfants,NIVhasbeenshowntofacilitateextubationfrommechanicalventilation [3]; reduce the incidence and severity of apnea and bradycardia [4]; and improve survivalininfantsweighinglessthan1,500gwithrespiratorydistresssyndrome(RDS) [5]. More recent research has examined the role of NIV in the prevention of bronchopulmonarydysplasia(BPD).Whilenotaspromisingaswashoped,thereissome evidencethatNIVreducesthelengthoftimeonmechanicalventilationandinturnreduces theincidenceofBPD[6].WhathasemergedintherecentstudiesofNIVinnewbornswith RDSisthecombinedbene tofsurfactantandNIV[7].
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51.6 Comparison of Different Modes of NIV Limited research has been done comparing various types of NIV. Some studies of bubble CPAPhaveshownthatbubbleCPAPgenerateschestwallvibrationssimilartothoseseenin high-frequencyventilationthatmayincreasegasexchange[8].StudiescomparingCPAPto NIPPV and SNIPPV have found that, in particular, both modes of phasic ventilation may conferadditionalbene tsnotseeninCPAPalone[9].Theseincludeagreaterdecreasein workofbreathing,greaterreductioninapnea,andgreatersuccessinpreventingreintubation.
51.7 Contraindications to NIV SomenewbornsarenotcandidatesforNIV.Theseincludepatientswithcongenitalairway anomalies;gastrointestinalanomaliesorsigni cantgastrointestinaldistension;signi cant centralapnea;hemodynamicinstabilityinconditionssuchasshock,patentductusarteriosus,orsepsis;anduntreatedsurfactantde ciency[10].
51.8 Side Effects ReportedsideeffectsofNIVincludegastricdistensionandfeedingintolerance,damageto thenasalseptumandmucosa,pneumothorax,andoverdistensionofthelungs[1].Insome cases,itmaybedif culttodetermineifthesymptomsofgastricdistensionarebenign ndingsofNIVormoreearlysignsofnecrotizingenterocolitis.Necrotizingenterocolitis ismorelikelytobeaccompaniedbyotherclinical ndings,includingskindiscoloration overtheabdomen,lossofbowelsounds,andsignsofsystemicillness[1].
51.9 Failure Criteria Some infants cannot be successfully managed with NIV; however, criteria identifying thoseinfantsthatrequireintubationandmechanicalventilationhavenotbeende ned.The infant sbirthweight,gestationalage,andunderlyingmedicalconditionmustbeconsidered indeterminingwhenaninfanthas failedNIV. Persistentandsigni cantapnea,anarteriallevelofcarbondioxideexceeding60mmHg,andtheneedformorethan60%inspired oxygensuggeststheneedformechanicalventilation[11].
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51.10 Weaning from NIV Anevidence-basedapproachtoweaninganinfantfromNIVhasnotbeendetermined.Itisgenerallyacceptedthatareductioninthenumberandseverityofapneicspells,thelevelofsupplementaloxygenrequiredforacceptablesaturationlevels,andareturntonormalworkofbreathing signalsthataninfantmaybereadytowean.ForinfantsonphasicNIV,therateisusuallyreduced andtheinfantswitchedtoCPAP.OnceCPAPpressuresarereducedtolessthan5mmHg,atrial withoutNIVmaybeconsidered.Nopublishedtrialshavesupportedthesecriteria[12].
51.11 Patient Care ThesuccessfulmanagementofanewborninfantreceivingNIVisdependentonattention todetail.CaringforanewbornonNIVrequirestimeandattentionaswellasathorough knowledgeoftheequipmentused.Theselectionofappropriateprongsandcarefulpositioning of the infant are critical in avoiding complications such as damage to the nasal mucosa.Shortbinasalprongshavebeenshowntobemoreeffectivethansingleorlong prongs[13].Selectionoftheappropriatesizeprongsandhatisalsoimportant.Excessive movementandtensionoftheprongsandtubingareassociatedwithanincreasedriskof mucosalinjury.Infantsshouldbeswaddledand,whenmonitored,placedpronewiththe neckslightlyextended[12].Thedeliveryofpositivepressureisenhancedwhentheinfant s mouthisclosed.Apaci erorchinstrapmaybeusedtofacilitatedelivery.
Key Recommendations
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NIVisaneffectivestrategyformanagingnewborninfantswithapneaorRDS andthosebeingextubatedfrommechanicalventilation. Growingevidencesuggestsitmayalsohelpreducetheincidenceandseverity ofBPD. ThesuccessofNIVintheclinicalsettingisdependentonattentiontothedetails ofcare,includingtheselectionofequipment,positioningoftheinfant,and ongoingpatientassessment.
References 1. Askin DF (2007) Noninvasive ventilation in the neonate. J Perinat Neonatal Nurs 21(4): 349 358 2. LockeR,GreenspanJS,ShafferTHetal(1991)EffectofnasalCPAPonthoracoabdominal motioninneonateswithrespiratoryinsuf ciency.PediatrPulmonol11:259 264
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3. DavisPG,Henderson-SmartDJ(2003)Nasalcontinuouspositiveairwaypressureimmediatelyafterextubationforpreventingmorbidityinpreterminfants.CochraneDatabaseSyst Rev2:CD0001 43 4. Lemyre B, Davis PG, de Paoli AG (2002) Nasal intermittent positive pressure ventilation (NIPPV)versusnasalcontinuouspositiveairwaypressure(NCPAP)forapneaofprematurity. CochraneDatabaseSystRev(1):CD002272 5. HoJJ,SubramaniamP,Henderson-SmartDJ,DavisPG(2002)Continuousdistendingpressure for respiratory distress syndrome in preterm infants. Cochrane Database Syst Rev (2):CD002271 6. Ramanathan R, Sardesai S (2008) Lung protective ventilatory strategies in very low birth weightinfants.JPerinatol28(Suppl1):S41 S46 7. DunnMS,ReillyMC(2003)Approachestotheinitialrespiratorymanagementofpreterm neonates.PaediatrRespirRev4(1):2 8 8. Lee KS, Dunn MS, Fenwick M, Shennan AT (1998) A comparison of underwater bubble continuouspositiveairwaypressurewithventilator-derivedcontinuouspositiveairwaypressureinprematureneonatesreadyforextubation.BiolNeonate73(2):69 75 9. Lemyre B, Davis PG, De Paoli AG (2002) Nasal intermittent positive pressure ventilation (NIPPV)versusnasalcontinuouspositiveairwaypressure(NCPAP)forapneaofprematurity. CochraneDatabaseSystRev1:CD002272.DOI:10.1002/14651858.CD002272 10. Hutchison AA, Bignall S (2008) Non-invasive positive pressure ventilation in the preterm neonate:reducingendotraumaandtheincidenceofbronchopulmonarydysplasia.ArchDis ChildFetalNeonatalEd93:F64 F68 11. de Paoli AG, Morley C, Davis PG (2003) Nasal CPAP for neonates: what do we know in 2003?ArchDisChildFetalNeonatalEd88(3):F168 F172 12. MorleyC,DavisP(2004)Continuouspositiveairwaypressure:currentcontroversies.Curr OpinPediatr16(2):141 145 13. dePaoliAG,DavisPG,FaberBetal(2002)Devicesandpressuresourcesforadministration ofnasalcontinuouspositiveairwaypressure(NCPAP)inpretermneonates.CochraneDatabase SystRevCD0029772002
Nasal High-Frequency Ventilation: Clinical Studies and Their Implications
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KatarzynaDabrowskaandWaldemarA.Carlo
52.1 Introduction Duringthelastthreedecades,therehasbeenanincreaseinthesurvivalrateofinfantswith verylowbirthweight(VLBW)[1,2].However,thisimprovementinsurvivalhasbeen accompaniedbytheincreasedrateoflong-andshort-termmorbidities,withbronchopulmonary dysplasia (BPD) one the most common adverse outcomes [3]. Introduction of surfactantandwidespreaduseofantenatalsteroidschangedtheclinicalcourseofrespiratory distress syndrome (RDS) as well as the histological picture and natural history of BPD.TheincidenceofBPDintheVLBWinfantsvariesbetweencenters,rangingfrom 3%to43%evenwhenusingstandardizedde nitions[1].Severecasesoriginallydescribed by Northway ( old BPD ) are rarely seen now. The new BPD remains an important problem. The etiology of so-called new BPD is unclear and probably multifactorial. AvailableevidencesuggeststhatBPDdevelopsasaresultofabnormalgrowthandrepair oftheimmaturelungsexposedtorepetitivestressofmechanicalventilation(namely,volutraumaandbarotrauma),especiallyviaendotrachealtube,aggravatedbyrecurrentinfectionsandchronicin ammation[4].Itisbelievedthatthemerepresenceofanendotracheal tubemaycontributetothedevelopmentofBPDbyimpairingnaturalairwaydefensesand increasingtheriskofinfectionandin ammationoftheupperandlowerairways[5].Yet, alargeproportionofpretermandillterminfantsrequiresrespiratorysupportatsomepoint duringtheirhospitalstay.
W.A.Carlo()andK.Dabrowska DivisionofNeonatology,UniversityofAlabamaatBirmingham, 619South20thStreet,525NewHillmanBuilding,Birmingham, AL,35233-7335,USA e-mail:
[email protected];
[email protected]
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52.2 Noninvasive Modes of Ventilation Continuous positive airway pressure (CPAP), delivered by noninvasive means such as withnasalprongs,maybeagentlermodeofrespiratorysupport.CPAPisfrequentlyused asanalternativetherapyinanattempttopreventordecreasetheuseofendotrachealintubationandmechanicalventilation.CPAPimprovesoxygenationbystabilizingsurfactantde cientalveoli.Ameta-analysispublishedintheCochranedatabaseindicatedthatCPAP iseffectiveinpreventingextubationfailurewhencomparedtooxygensupplementation via a hood [6]. However, the effect of CPAP on the incidence of BPD is inconclusive. Avery et al. were the rst ones to suggest that use of CPAP might be associated with decreasedriskofdevelopingBPD[7].Aretrospectiveanalysisshowedthat,amongeight centers,thelowestBPDratewasreportedinthecenterthatusedCPAPpreferablyrather than intubation and mechanical ventilation. Many other retrospective studies have also suggestedthatCPAPmaydecreasetheincidenceofBPD.Thepublishedcontinuouspositiveairwaypressureorintubationatbirth(COIN)trial,whichcomparedinfantsrandomizedatdeliverytoCPAPorintubationandmechanicalventilation,showednosigni cant differenceinBPD/deathat36weeksbutapositivetrend(CPAPgroup34%vs.intubation group39%,95%relativerisk[RR]0.8,con denceinterval[CI]0.6 1.1)[8].However,the rateofpneumothoraxwasthreefoldhigherintheCPAPgroup.Othersmallerrandomized controlledtrialsofearlyCPAP(Finer,Thomson)alsoshowednosigni cantreductionof BPD[9,10].However,ameta-analysisofrelativelysmallstudiescomparingearlysurfactantadministrationandpromptextubationtoCPAPversusselectivesurfactantandcontinuedmechanicalventilationshowedasigni cantreductionofBPDinthegroupwithearly CPAP(RR0.51,95%CI0.26 0.99)[11]. Yet,manyinfantsfailnasalcontinuouspositiveairwaypressure(NCPAP)[6].For thoseinfantswhofailCPAP,otherformsofnoninvasiveventilation,likenasalintermittent positive pressure ventilation (NIPPV), may be bene cial. Available data indicate thatNIPPVimprovesalveolarventilationandcarbondioxide(CO2)eliminationandis moreeffectivethanCPAPintreatingapneaofprematurity[12].Ameta-analysisofthree trialscomparingNIPPVwithCPAPshowedthatNIPPVsigni cantlyandconsistently reducedextubationfailure(RR0.21,95%CI0.10 0.45)[13].InthestudyofBhandari etal.,NIPPVwasassociatedwithalowerincidenceofBPDat36weekswhencompared toconventionalventilation(52%vs.20%,p<0.05)[14].Also,whencomparedwith CPAP,NIPPVseemstohaveafavorableeffectontheincidenceofBPD,asillustrated bytheresultsoftheretrospectivecase-controlstudyconductedbyKulkarnietal.[15]. Data from the study of Garland et al. suggested that NIPPV may be associated with increasedriskofgastrointestinalperforation,butinthemostrecentreportsnoclinically signi cant gastrointestinal side effects were observed [13, 16]. Currently, NIPPV is beingusedinabout50%oftheneonatalintensivecareunits(NICUs)inEngland[15]. EventhoughNIPPVseemstobemoreeffectivethanCPAPaloneinpreventingreintubation,asigni cantpercentageofpatients(45%inthestudyofBhandarietal.)willfail becauseofCO2retentionorworseningoxygenation.Thatgroupofpatientsmaypotentiallybene tfromnasalhigh-frequencyventilation(nHFV).
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52.3 Nasal High-Frequency Ventilation Nasalhigh-frequencyventilationisaless-well-studiednoninvasivemethodofassistedventilation,butthereissomerationalesupportedbylimiteddatathatthismodeofventilation may decrease the need for intubation and incidence of BPD. Endotracheal HFV (high- frequencyventilation)iseffectiveineliminatingCO2,probablyduetoseveralmechanisms thatenhancegasexchange[18].Animaldatasuggestthatwhencomparedtointermittent mandatoryventilation,nHFVinpretermlambspromotesalveolarizationbypreservingthe balancebetweenmesenchymalcellapoptosisandproliferation[19].Recentmeta-analysis of15trialsshowedthathighfrequencyoscillatoryventilation(HFOV)wasassociatedwith reductionofdeathorBPDofborderlinesigni cance(RR0.93,95%CI0.86 1.00)[20]. However,therearelimiteddataonnHFV. VanderHoevenetal.werethe rsttopublishtheirexperiencetreatingneonateswith nHFV.Theyreportedagroupof21patientswhofailedCPAPbecauseofCO2retention (medianvalue62mmHg),acidosis(medianpH7.24),orincreasingoxygenrequirement (medianFio20.42)[21]andwastreatedwithnHFV.Thiswasanuncontrolledobservational studythatincludedpatientswithvariousrespiratorydiseases,includingRDS,transienttachypnea of the newborn (TTN), air leak, or apnea. Nasal CPAP was applied via a single nasopharyngealtube.Themedian(range)gestationalagewas29weeks(27 32weeks)and median(range)birthweightwas1,010g(750 2,170g).Ofthe21patients,15(72%)were switchedtonHFVearlyinthecourseoftherespiratorydisease(medianageof17h;range 2 36h),andin6(28%)nHFVwasinitiatedlate(median9days;range9 21days).nHFV wasinitiatedwithameanairwaypressureequaltoorhigherthanthatonCPAP,afrequency of10Hz,andanamplitudethatwasadjusteduntiltheinfant schestshowedadequatevibration.Themeanairwaypressuresweresigni cantlyhigherafterinitiationofnHFV.Median (range) amplitude was 37 cmH2O (29 46 cmH2O). Only ve patients (23%; three with severeRDSintheearlygroupandtwointhelategroup,onewithairleaksyndromeandone with apnea associated with sepsis and necrotizing enterocolitis) failed nHFV (pH < 7.2, Pco2>64mmHg,Fio2>0.8,orsevereapnea)andsubsequentlyrequiredendotrachealintubation.ThemediandurationofnHFVwas35h(range2 144h)intheearlygroupand40h (range17 126h)inthelategroup.AfterinitiationofnHFV,smallbutsigni cantreductions inPco2wereobservedcomparedwithvaluesrecordedbeforenHFV(p<0.01).Thus,nHFV might be a valuable addition to the ventilatory management of the newborn infant and mightreducetheneedforsubsequentmechanicalventilation. Colaizy et al. reported the results of short-term use of nHFV in 14 VLBW infants requiring nasal CPAP support [22]. Just like van der Hoeven et al., they used a single nasopharyngealtubetodeliverbothnasalCPAPandnHFV.Infantswereswitchedfrom nasalCPAPtonHFVandventilatedwiththatmodefora xedperiodof2h.Thepositive end-expiratorypressure (PEEP) during nHFV was the same as during nasal CPAP, and frequencywaskeptconstantat10Hz.Theamplitudewasadjustedbasedonthepresence of visible chest wall or upper airway (anterior neck) vibration. The amplitude, which rangedfrom29to60cmH2O,wasadjustedevery30minby4 6cmH2Oasnecessaryto maintainanappropriatechestwalloranteriorneckvibration.Median(range)gestational
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agewas27weeks(26 30weeks),andmedian(range)birthweightwas955g(438 1,374g). AllinfantshadahistoryofRDSearlyintheneonatalcoursebutwerestudiedatamedian (range)of30days(18 147days).nHFVresultedinasigni cantdecreaseinPco2(from50 to45Torr,p=0.01)andahigherpH(7.37to7.40,p=0.04).TherewasnoeffectonFio2 oroxygensaturation.Sideeffectswerenotreported.ChestX-raysobtainedafter1hof nHFVdidnotshowevidenceofgastrapping.
52.4 Discussion Clinical studies suggested that CO2 elimination during nHFV is superior to that during CPAP,andthatnHFVdecreasestheneedforendotrachealintubationandmechanicalventilationinpatientswithmild-to-moderaterespiratoryfailureduetoCO2retention.However, severallimitationsinbothstudieshavetobeconsidered.InthestudyofColaizyetal., infantswererelativelystable[22].Formanyclinicians,bloodgasvalueswithPco2inthe rangeof50TorrandaveragepHof7.37thatwereusedasentrycriteriaforthestudywould havebeenacceptableforthepatientstableonCPAP.InthestudyofvanderHoevenetal., thePco2andpHvaluesbeforetheinterventionwereprobablyclosertothewidelyaccepted de nitionofmild-to-moderaterespiratoryfailure,butithastobepointedoutthatthestudy groupwasdiverse[21].Forexample,theageattheentryintothestudyrangedfrom4to 480h.ValuesofPco2,thatwouldbeconsideredasanindicatorofimpendingrespiratory failureearlyafterbirthmightbeacceptableandinlinewitha permissivehypercapnia protocolinanolderinfant. TheeffectsofnHFVonBPDormeasuresoflunginjurywerenotstudied,andtheonly controlledstudyhadacrossoverdesignwithashortperiodofstudy.Randomizedcontrolled trialsarenecessarytodetermineifnHFVimprovespulmonaryoutcomes.Also,theeffect ofthenHFVonsevereapneaintheprematureinfantsneedstobeinvestigatedfurther. Itisimportantthatneitherofthetwostudieswasdesignedtoassessthesideeffectsof nHFV.EventhoughrandomizedtrialsofNIPPVhavenotreportedanincreasedriskofside effects,nHFVmaypresentadditionalproblems,likeoverdistentionandgastrapping.Inthe studyofColaizyetal.,chestradiographstaken1hafterinitiationofthestudydidnotshow evidenceofgastrappinginanyofthepatients[22].However,itisimportanttonoticethatthe pressureamplitudeusedinbothstudieswasrelativelyhigh.Althoughitiswellknownthat the high-frequency signal is dampened by the circuit, nasopharyngeal tubes, and airways, thedegreeofdampeningisvariableanddif culttoestimateclinically[19].Thepresenceof chestoscillationsduringnHFVobservedinpatientsinbothstudiesindicatesthatthedelivery ofthepressuretothealveoliwasprobablysubstantial,andthereisconcernaboutgastrapping andoverdistentionwhileusingthismodeofventilation.Withvariable-pressuretransmission secondarytoleakageandvaryingairwaypatency,asuddendecreaseorincreaseinthepressuredeliveredmayputthepatientsatriskforacutelossoflungvolumeorairleak. OnepotentialadvantageofnHFVoverNIPPVisthatsynchronizationisnotnecessary. Morettietal.reportedaveryhighrateofsynchronizationintheirstudy[23].However,outside thestudyprotocolinthebusyNICU,itmaybedif culttoachievesynchrony.Thepresence
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ofavariableinspiratoryleakthroughthenasalprongsduringNIPPVmakessynchronization of the patient s respiratory effort with respirator cycling dif cult, especially with the new ventilatorsthatrelyoninspiratory owtotriggertheventilator.Yet,lackofsynchronization mayimpairtheventilationandlimitthebene tsofnoninvasiveventilation.Duringsynchronizedbreaths,positivepressureventilatorbreathsaredeliveredwhentheglottisisopen.With nonsynchronized breaths, re exes originating probably from bronchopulmonary receptors maysometimescausepartialclosureoftheglottis,resultinginincreasedairwayresistanceand variations in delivered tidal volumes [24]. Some authors postulated that this is one of the mechanismsdesignedtoprotectthelungsfromoverin ation.Thus, ne-tuningoftheventilatorsupport,includingnoninvasivemethods,isimportant[25].
Key Recommendations
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Nasalhigh-frequencyventilationcanimproveCO2elimination. Nasalhigh-frequencyventilationhasapotentialtodecreasetheneedfor endotrachealintubationandmechanicalventilationinthegroupofinfantswith mild-to-moderaterespiratoryfailure. FurtherresearchontheeffectivenessofnHFVinsickerpatientsisnecessary. BeforenHFVtherapycanberecommendedforwidespreaduse,furtherstudies ofsafetyarerequired.
References 1. LemonsJA,BauerCR,OhWetal(2001)VerylowbirthweightoutcomesoftheNational InstituteofChildhealthandhumandevelopmentneonatalresearchnetwork,January1995 throughDecember1996.NICHDNeonatalResearchNetwork.Pediatrics107:E1 2. StoelhorstGM,RijkenM,MartensSEetal(2005)Changesinneonatology:comparisonof twocohortsofverypreterminfants(gestationalage<32weeks):theProjectonPretermand Small for Gestational Age Infants 1983 and the Leiden Follow-Up Project on Prematurity 1996 1997.Pediatrics115:396 405 3. StJohnEB,CarloWA(2003)RespiratorydistresssyndromeinVLBWinfants:changesin management and outcomes observed by the NICHD Neonatal Research Network. Semin Perinatol27:288 292 4. BhandariA,BhandariV(2003)Pathogenesis,pathologyandpathophysiologyofpulmonary sequelaeofbronchopulmonarydysplasiainprematureinfants.FrontBiosci8:e370 e380 5. JobeAH,KramerBW,MossTJetal(2002)Decreasedindicatorsoflunginjurywithcontinuouspositiveexpiratorypressureinpretermlambs.PediatrRes52:387 392 6. DavisPG,Henderson-SmartDJ(2003)Nasalcontinuouspositiveairwayspressureimmediatelyafterextubationforpreventingmorbidityinpreterminfants.CochraneDatabaseSyst RevCD000143 7. AveryME,TooleyWH,KellerJBetal(1987)Ischroniclungdiseaseinlowbirthweight infantspreventable?Asurveyofeightcenters.Pediatrics79:26 30 8. MorleyCJ,DavisPG,DoyleLWetal(2008)NasalCPAPorintubationatbirthforverypreterminfants.NEnglJMed358:700 708
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9. FinerNN,CarloWA,DuaraSetal(2004)Deliveryroomcontinuouspositiveairwaypressure/ positive end-expiratory pressure in extremely low birth weight infants: a feasibility trial. Pediatrics114:651 657 10. ThomsonM(2002)Earlynasalcontinuouspositiveairwaypressure(nCPAP)withprophylacticsurfactantforneonatesatriskofRDS.PediatrRes51:379A 11. Stevens TP, Harrington EW, Blennow M et al (2007) Early surfactant administration with brief ventilation vs. selective surfactant and continued mechanical ventilation for preterm infants with or at risk for respiratory distress syndrome. Cochrane Database Syst Rev CD003063 12. LinCH,WangST,LinYJetal(1998)Ef cacyofnasalintermittentpositivepressureventilationintreatingapneaofprematurity.PediatrPulmonol26:349 353 13. DePaoliAG,DavisPG,LemyreB(2003)Nasalcontinuouspositiveairwaypressureversus nasalintermittentpositivepressureventilationforpretermneonates:asystematicreviewand meta-analysis.ActaPaediatr92:70 75 14. BhandariV,GavinoRG,NedrelowJHetal(2007)ArandomizedcontrolledtrialofsynchronizednasalintermittentpositivepressureventilationinRDS.JPerinatol27:697 703 15. KulkarniA,EhrenkranzRA,BhandariV(2006)Effectofintroductionofsynchronizednasal intermittentpositive-pressureventilationinaneonatalintensivecareunitonbronchopulmonarydysplasiaandgrowthinpreterminfants.AmJPerinatol23:233 240 16. GarlandJS,NelsonDB,RiceTetal(1985)Increasedriskofgastrointestinalperforationsin neonates mechanically ventilated with either face mask or nasal prongs. Pediatrics 76: 406 410 17. OwenLS,MorleyCJ,DavisPG(2008)Neonatalnasalintermittentpositivepressureventilation:asurveyofpracticeinEngland.ArchDisChildFetalNeonatalEd93:F148 F150 18. BoyntonB,CarloWA(1994)Pulmonarygasexchangeduringhigh-frequencyventilation.In: BoytonBR,CarloWA,JobAH(eds)Newtherapiesforneonatalrespiratoryfailure.Aphysiologicalapproach.CambridgeUniversityPress,Cambridge,pp218 244 19. ReyburnB,LiM,MetcalfeDBetal(2008)Nasalventilationaltersmesenchymalcellturnover and improves alveolarization in preterm lambs. Am J Respir Crit Care Med 178: 407 418 20. Henderson-SmartDJ,CoolsF,BhutaT,OffringaM(2007)Electivehighfrequencyoscillatoryventilationversusconventionalventilationforacutepulmonarydysfunctioninpreterm infants.CochraneDatabaseSystRevCD000104 21. vanderHoevenM,BrouwerE,BlancoCE(1998)Nasalhighfrequencyventilationinneonateswithmoderaterespiratoryinsuf ciency.ArchDisChildFetalNeonatalEd79:F61 F63 22. ColaizyTT,YounisUM,BellEFetal(2008)Nasalhigh-frequencyventilationforpremature infants.ActaPaediatr97:1518 1522 23. MorettiC,GizziC,PapoffPetal(1999)Comparingtheeffectsofnasalsynchronizedintermittentpositivepressureventilation(nSIPPV)andnasalcontinuouspositiveairwaypressure (nCPAP)afterextubationinverylowbirthweightinfants.EarlyHumDev56:167 177 24. Moreau-BussiereF,SamsonN,St-HilaireMetal(2007)Laryngealresponsetonasalventilationinnonsedatednewbornlambs.JApplPhysiol102:2149 2157 25. RoyB,SamsonN,Moreau-BussiereFetal(2008)Mechanismsofactivelaryngealclosure during noninvasive intermittent positive pressure ventilation in nonsedated lambs. J Appl Physiol105:1406 1412
Bubble Continuous Positive Airway Pressure
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J.JanePillow
53.1 Introduction SincetheinitialreportfromGregoryetal.describingtheuseofendotrachealcontinuouspositiveairwaypressure(CPAP)tosupporttheventilationofspontaneouslybreathingnewborn infants [1] and the subsequent development of a head box for noninvasive CPAP delivery, CPAP has gained widespread popularity for respiratory support of the nonintubated infant. Whereastheseinitialmodesofdeliveryassumedthataleak-freeapplicationwasessentialfor effectivetherapeuticdeliveryofCPAP,improvedeaseofapplicationandaccesstoinfantswas achievedwhenthemethodwassubsequentlysuccessfullyadaptedtogeneratenasalCPAP[2]. Currently,therearethreemainformsofnasalCPAPcommonlyappliedtoinfantswith respiratorydistresssyndrome(RDS):Agostino sadaptation[2]usesaneonatalventilator togenerateaconstantbiasgas owwhilstCPAPwasachievedthroughprovisionofavariable resistance to exhalation. This approach created constant positive pressure that fell belowthedesiredvalueduringspontaneousinspirations.TheemergenceofbubbleCPAP, asdescribedbyWungetal.in1975[3],representedasimplebutsigni cantchangetothis initialnasalCPAPcircuit.Wungetal.suppliedaheatedandhumidi edconstant owto thebabyandcreatedthepositiveairwaypressurebyimmersingtheexpiratorylimbofthe circuitinacolumnofwaterinsteadofavariableresistor.Morerecently,athirdapproach has utilized a variable- ow CPAP system (Infant Flow®, Viasys, USA). The proposed advantagesofthislatestapproachincludelowextrinsicworkofbreathing[4],improved thoracoabdominal synchrony [5], and maintenance of constant pressure throughout the respiratory cycle (including during inspiration) aided by a unique uidic ip action. A variation on the variable- ow CPAP system includes a biphasic CPAP (Infant Flow SiPAP ,Viasys),whichfacilitatesalternatinghighandlowlevelsofCPAPpressurewhilst maintainingtheotherpotentialbene tsofvariable owandthe uidic ipmechanics.
J.J.Pillow SchoolofWomen sandInfants Health,UniversityofWesternAustralia, c/-KEMH,374BagotRd,Subiaco6008,Perth,WesternAustralia,Australia e-mail:
[email protected] A.M.Esquinas(ed.),NoninvasiveMechanicalVentilation, DOI:10.1007/978-3-642-11365-9_53,©Springer-VerlagBerlinHeidelberg2010
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Althoughusedclinicallyforinexcessof30years,itisonlyoverthelastdecadethat researcheffortshavefocusedonimprovingourunderstandingofwhetherbubbleCPAP offersaspeci cphysiologicalandclinicaladvantageoverotherformsofnasalCPAPand, ifso,de ningthemechanismsunderlyingthatbene t.ThisreviewsummarizestheevidencesupportingtheuseofbubbleCPAPwithaspeci cfocusonunderstandingtheprinciples and application of bubble CPAP and how it may differ from the two other main modesofneonatalnasalCPAP.
53.2 Bubble CPAP Circuits, Lung Mechanics, and Their Influence on Delivered CPAP ThebasicbubbleCPAPcircuitused rstbyWungetal.in1975[3](Fig.53.1)remainsin use around the world today, with a commercially marketed version (Fisher & Paykel Healthcare, Auckland, NZ) now available in some countries. Rather than achieving a constantpressure(ventilator-derivedCPAPandvariable- owCPAP),bubbleCPAPgenerates,atthenares, pressure waveforms with broadband frequency composition (up to ~60Hz)andoscillatoryamplitudesthatareontheorderof4cmH2Oaroundthemean pressuredependingontheapplied owandphysicalpropertiesoftheexpiratorylimb. Thisnoisypressurewaveformgeneratedbythebubblescreatedwhenbias owescapes fromthedistalendoftheexpiratorylimbcreatesvibrationsthataretransmittedviathe Blender & Flow meter
Expiratory Limb
Inspiratory Limb Nasal Prongs
Safety valve O2analyzer
Humidifier
Pressure Port CPAP Generator
Fig. 53.1 Equipmentrequiredforbubblecontinuouspositiveairwaypressure(CPAP).Medical oxygenandairareblended,anda owmeterisusedtogenerateasetinspiratory ow(6 10L/ min),whichisheatedandhumidi edpriortodeliverytothenasalprongs.Anoxygenanalyser and pressure safety limit valve can be incorporated into the inspiratory limb to prevent the deliveryofinadvertentlyhighairwaypressuresintheeventofblockageintheexpiratorylimb. The tip of the expiratory limb is submerged within a calibrated vessel (jar) lled with uid (normally water). The depth to which the tip is submerged is the main determinant of mean pressuredeliveredtothenares.Flowisadjustedtoensure bubbling occurs,indicatingthatthe circuitisfreeofsigni cantleaksandthatthedesiredmeanpressurewillbeachieved.Thebubblingcreatespressureoscillationsthataretransmittedbackthroughtheexpiratorylimbtothe patient snares
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nasalprongstotheinfant schestwallandlungs,providingtheexpiratorytubingissufcientlyrigid. AdjustingthedepthofinsertionoftheexpiratorylimbalterstheaverageCPAPapplied. Itisimportantthatthemeanpressuremeasuredatthenaresmayexceedtheanticipated meanpressureestimatedfromthedepthofthetipoftheexpiratorylimbduetopressure dropbetweenthenaresandthesubmergedpointatwhich owescapesintothebubblegenerating uid[5].Themagnitudeofthispressuredifferenceincreaseswithincreasing appliedbias ow[6],highlightingtheimportanceofmeasurementofmeanpressureatthe narestogainanaccurateimpressionofdeliveredpressure. Otherfactorsmayin uencethefrequencycontentandamplitudeofthegeneratedpressurewaveformdeliveredtothenares.Thegeometryofthetipoftheexpiratorytubeisan importantdeterminantofbothofthesefactors,withbothfactorsreportedgreatestwhena funnelwitha30-mmdiameterand90°anglerelativetoanormallineprojectedonthe watersurfaceisused[7].Adeviceincorporatinga135°angleintheterminalendofthe expiratory limb was noted to increase amplitude and decrease frequency content of thepressurewaveform[8].Thishigh-amplitudeCPAPdevicewasabletoachieveacceptablegasexchangeinhealthyandsaline-lavagedjuvenilerabbits[9]andmayhavebeen associatedwithreducedworkofbreathingcomparedtoconventionalbubbleCPAP[10], although equivalence of mean airway pressure was not shown. Increased viscosity and surfacetensioncoef cientofthe uidattheair uidinterfacewillresultinlargerbubbles andalterthespeedofbubbleformation[11]. Whereas owmagnitudemayin uencetheamplitudeofthepressurewaveformatthe nares,thereisminimaleffectof owontheamplitudeofthepressurewaveformdelivered tothelung.Rather,asshownpreviouslyforhigh-frequencyoscillatoryventilation,thereis markeddampingofthepressurewaveformbetweenthenaresandthelungduringbubble CPAP [6, 12]. A major determinant of the extent of damping is lung compliance with transmissionofthepressureoscillationstothelungdecreasingexponentiallywithincreasingcompliance.Thus,thepoorlycompliantsurfactant-de cientlungwillexperiencemuch greater uctuationsinCPAPpressurethanthehighlycompliantlung,inwhichpressure oscillationsareminimal.Invitrostudiesfurthersuggestthatthepoorlycompliantlung also ltersoutlessofthefrequencycontentofthewaveformdeliveredtothenares[13], likelyduetohighercornerfrequency.
53.3 Clinical Studies BubbleCPAPhasattractedgrowinginterestamongstneonatalpractitionersoverthelast two decades following the reports of Avery [14] and, more recently, van Marter [15] highlightingthelowincidenceofchroniclungdiseaseinpreterminfantsattheColumbia Presbyterian Medical Center. Avery showed that the reasons for low bronchopulmonary dysplasia(BPD)ratesatColumbiaPresbyterianMedicalCenterweremultifactorial,including tolerance of permissive hypercapnea and minimal sedation, handling, and postnatal
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steroiduse.Inaddition,however,Wungetal.hadincludedearlyuseofbubblenasalCPAP asaprimaryfocusoftheclinicaltreatmentstrategysincetheirinitialreportin1975[3]. Despitetheextendedperiod,clinicaldatacomparingtheef ciencyofbubbleCPAPtoother formsofnasalCPAPremainlimitedtoanecdotalreports.Inoneofthemoredetailedhistorical comparisons following a change of clinical practice, Narendran and colleagues showedthatdeliveryroomintubations,daysonmechanicalventilation,anduseofpostnatal steroidsdecreasedafterintroductionofearlybubbleCPAPininfantswithextremelylow birthweight,whilemeandaysonCPAP,numberofbabiesonCPAPat24h,andmean weightat36weeksofgestationincreasedcomparedtohistoricalcontrols[16].Compared toasimilarhospitalinstitutingearlyventilator-derivedCPAP,bubbleCPAPwasassociated withatrendtowardsdecreasedBPD[17]. The rstprospectiverandomizedcontrolledtrialcomparingbubbleCPAPtoanalternativenasalCPAPstrategywaspublishedin2009[18].Onehundredandfortypreterminfants at24 29weeksofgestationorwithbirthweightsof600 1,500gventilatedatbirthforRDS were randomized to receive either variable- ow CPAP (Infant Flow Driver®, Viasys) or bubbleCPAP.Althoughtheproportionsofinfantswhoachievedsuccessfulextubationfor 72hand7daysweresimilarbetweengroups,themediandurationofCPAPsupportwas50% shorter in infants on bubble CPAP. Analysis of the major subgroup (those ventilated for 14daysorless,n=127)showedthatinfantsmanagedwithbubbleCPAPhadasigni cantly higherrateofsuccessfulextubation.Thisintriguingresultsuggestedthat,forsubgroupsof infants,advantagesofthebubble-generatedpressureoscillationsoutweighanypotentialdisadvantageofconstant- owCPAPgenerationwhencomparedwithavariable- owdevice. Whiletheclinicaldatatosupportapotentialclinicalbene tofbubbleCPAPoverother formsofnasalCPAPtherapyinneonatesareclearlylimited,theyprovidejusti cationfor researchfocusedonunderstandingtherelevanceofthebubbleoscillationsinachievingthe observedclinicaleffect.
53.4 Theory and Discussion CurrentevidencesuggeststhatbubbleCPAPmayenhancephysiologicalresponsesthrough increasedairwaypatencyandrecruitment,augmentationofgasmixingandCO2clearance, andconsequentdampingofthein ammatorycascade.
53.4.1 Airway Recruitment: Power Laws, Avalanches, and Stochastic Resonance Theavoidanceofatelectasisandearlyestablishmentofan openlung viavolumerecruitment are now acknowledged as fundamental goals of noninjurious ventilation. The recruitment of terminal airspaces is governed by power law distributions, arising from avalanchesofairspaceopeningevents,astheappliedpressurerisesaboveairwaypressure thresholds and propagates down the branching airway tree [19]. This recruitment
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process bene ts from the superimposition of noise on the applied driving pressure, exploiting a phenomenon known as stochastic resonance [19]. Pressure uctuations abovethemeanpressurewillpromotegreaterlungvolumerecruitmentthanthosepressure uctuationsfallingbelowthemeanpressure,providedtheupperlimitofthepressure uctuationsliesabovethepointofthelowerin exureofcollapsedlungunitsonthepressurevolumecurve. Stochastic resonance may partially explain the bene ts of bubble CPAP in neonatal RDS[12,13]:TheoscillatorycomponentofthebubbleCPAPpressurewaveformissuperimposedonthedesiredmeanCPAPandthelow-frequencypressure uctuationsimposed bythesubject sspontaneousrespiratoryefforts.Whilethenetvolumeoutputofthesuperimposedoscillationsisessentiallyzerobecausetheseareappliedtoanonlineardynamic system, the noisy nature of the pressure waveform generated from the bubbling in the expiratorylinemayactuallypromoteairway-openingeventsandconsequentlylungvolumerecruitmentifsuperimposedonsubthresholdrespiratoryeffort.Giventhatthetransmittedpressureamplitudeisgreaterinthepresenceoflowcompliance[12,13],reopening ofatelecticairspacesresultingfromstochasticeffectsofthebubbleCPAPwaveformis likelytobegreatestduringneonataltransitionwhen uidmustbeclearedfromthelung andfunctionalresidualcapacityisestablishedandinthepresenceofacuteneonatalRDS whenlungvolumeandcompliancearelow.Thisbene t,comparedtoventilator-derived CPAP,wasevidentinself-ventilatingpretermlambswithsurfactant-de cientlungdisease treatedwithbubbleCPAP[12]. Theprinciplesofstochasticresonancesuggestthattheamplitudeandfrequencyofthe superimposed noise can be optimized to achieve the most favorable ampli cation (i.e., volumerecruitmentevents).Therewasnoevidenceofsigni cantshort-termphysiological consequences of 8 L/min versus 12 L/min in preterm lambs treated with bubble CPAP [12]. Increased amplitude of the generated pressure oscillations was associated with improvedoxygenationinsurfactant-de cientrabbits[10].
53.4.2 Gas Mixing and CO2 Clearance Thenoisynatureofthepressurewaveformdeliveredtotheairwayopeningduringbubble CPAPmayaugmentgasmixinginasimilarfashiontomechanismspresentduringhighfrequencyoscillatoryventilation.Nekvasilandcolleaguesobservedthathigh-frequency bubbleoscillationachievedeffectivegasexchangewhenusedtotreatrespiratoryfailurein threeneonatesweighing1,250 2,700g[7].Subsequently,Leeandcolleagues[20]randomizedagroupofinfantsreadyforextubationtoreceiveeitherbubbleCPAPorventilator-derivedCPAPfor15minpriortocrossovertothealternativetreatment.Whilstthere werenodifferencesinpartialpressureofarterialcarbondioxide(Paco2)betweentreatmentgroups,babieshadlowerrespiratoryratesandlowerminutevolumeswhileonbubble CPAP compared to ventilator-derived CPAP, indicating more ef cient ventilation. Likewise,bubbleCPAPinpretermlambsisassociatedwithlowerPaco2anddecreased ventilationinhomogeneitycomparedtoventilator-derivedCPAP[12].
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53.4.3 Inflammation and Surfactant Metabolism ThereissomelimitedevidencetosuggestthattheuseofbubbleCPAPmayreducethe in ammatory response to noninvasive ventilation. Preterm lambs treated with bubble CPAPtendedtohavelowerlevelsofproteininbronchoalveolarlavage uidcomparedto thosetreatedwithventilator-derivedconstant- owCPAP[12]. Thesuperimpositionofnoiseonthedistendingpressurewaveformmayalsopromote increasedsurfactantsecretion.PretermlambstreatedwithbubbleCPAPtendedtohave highersaturatedphosphatidylcholinelevelsinbronchoalveolarlavage uidcomparedto lambsreceivingventilator-derivedCPAP[12].However,thisdifferencewasnotstatisticallysigni cantandremainstobeproven.
53.5 Conclusions The initial attraction of the bubble CPAP method related primarily to its simplicity and signi cantcostadvantage,facilitatingitsusethroughouttheWesternanddevelopingworld. EvidenceismountingthattheuseofbubbleCPAPisassociatedwithdistinctclinicaloutcomes,includingimprovedoxygenation,increasedairwaypatency,improvedlungmechanics and lung volume, reduced ventilation inhomogeneity, more ef cient CO2 exchange, increased extubation success, and possibly improved surfactant secretion and reduced in ammation.Futureresearchneedstofocusonthekeyrecommendationspresentednext.
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dditionalwell-designedandadequatelypoweredclinicaltrialsareneeded A comparingbubbleCPAPtootherformsofnasalCPAPthatincludetheoutcomes ofseverityoflungdiseaseandlong-termneurologicaloutcomes. Thereneedstobeequipmentdevelopmenttofurtherevaluatethebene tsor otherwiseofspeci cfrequenciesandamplitudesofbubble-generatedpressure oscillationsandhowthismaybeoptimizedtomeettheneedsoftheindividual patient. ItmustbeestablishedwhetherapplicationofbubbleCPAPimpedesthemagnitude ofthein ammatoryresponseinthesettingofacuterespiratorydistress. Discoverymustbemaderegardingwhethersimilaroscillationspresentduring positiveend-expiratorypressureinroutinemechanicalventilationmayprovide clinicalandphysiologicalbene tsintheintubatedinfant. It should be found if there are relevant applications of bubble CPAP in older paediatricandadultpatients.
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References 1. GregoryGA,KittermanJA,PhibbsRHetal(1961)Treatmentoftheidiopathicrespiratorydistresssyndromewithcontinuouspositiveairwaypressure.NEnglJMed284:1333 1340 2. AgostinoR,OrzalesiM,NodariSetal(1973)Continuouspositiveairwaypressure(CPAP)by nasalcannulaintherespiratorydistresssyndrome(RDS)ofthenewborn.PediatrRes7:50 3. WungJT,DriscollJMJr,EpsteinRAetal(1975)AnewdeviceforCPAPbynasalroute.Crit CareMed3:76 78 4. DePaoliAG,MorleyCJ,DavisPGetal(2002)Invitrocomparisonofnasalcontinuouspositiveairwaypressuredevicesforneonates.ArchDisChildFetalNeonatalEd87:F42 F45 5. Courtney SE, Barrington KJ (2007) Continuous positive airway pressure and noninvasive ventilation.ClinPerinatol34:73 92 6. PillowJJ,TravadiJN(2005)BubbleCPAP:isthenoiseimportant?Aninvitrostudy.Pediatr Res57:826 830 7. NekvasilR,KratkyJ,PenkovaZetal(1992)[Highfrequency bubble oscillationventilation intheneonatalperiod].CeskPediatr47:465 470 8. Richardson CP, DiBlasi RM, Zignego JC et al (2009) A novel device for delivering high amplitude bubble CPAP (HAB-CPAP) to infants in respiratory failure [Abstract]. Pediatric AcademicSocietiesAnnualMeeting,Baltimore,MD,E-PAS2009:3858.116 9. DiBlasiRM,ZignegoJC,SmithCV,HansenTN,RichardsonCP(2009)Gasexchangewith conventional ventilation and high-amplitude bubble CPAP (HAB-CPAP) during apnea in healthy and surfactant-de cient juvenile rabbits. Pediatric Academic Societies Annual Meeting,Baltimore,MD,E-PAS2009:4735.8 10. RichardsonCP,DiBlasiRM,ZignegoJCetal(2009)Gasexchangeandworkofbreathing(WOB) in surfactant-de cient rabbits receiving nasal high amplitude bubble CPAP (HAB-CPAP) [Abstract].PediatricAcademicSocietiesAnnualMeeting,Baltimore,MD,E-PAS2009:4515.12 11. QuanS,HuaJ(2008)Numericalstudiesofbubbleneckinginviscousliquids.PhysRevEStat NonlinSoftMatterPhys77:066303 12. PillowJJ,HillmanN,MossTJetal(2007)Bubblecontinuouspositiveairwaypressureenhances lungvolumeandgasexchangeinpretermlambs.AmJRespirCritCareMed176:63 69 13. PillowJJ,StocksJ,SlyPDetal(2005)Partitioningofairwayandparenchymalmechanicsin unsedatednewborninfants.PediatrRes58:1210 1215 14. AveryME,TooleyWH,KellerJBetal(1987)Ischroniclungdiseaseinlowbirthweight infantspreventable?Asurveyofeightcenters.Pediatrics79:26 30 15. Van Marter LJ, Allred EN, Pagano M et al (2000) Do clinical markers of barotrauma and oxygen toxicity explain interhospital variation in rates of chronic lung disease? The NeonatologyCommitteefortheDevelopmentalNetwork.Pediatrics105:1194 1201 16. NarendranV,DonovanEF,HoathSBetal(2003)EarlybubbleCPAPandoutcomesinELBW preterminfants.JPerinatol23:195 199 17. NarendranV,DonovanEF,HoathSVetal(2002)ComparisonbetweenearlybubbleCPAP andconventionalCPAPinreducingtheincidenceofchroniclungdisease[Abstract].Pediatric AcademicSocietiesMeeting,Baltimore,MD,E-PAS2002:1960 18. GuptaS,SinhaSK,TinWetal(2009)Arandomizedcontrolledtrialofpost-extubationbubblecontinuouspositiveairwaypressureversusInfantFlowDrivercontinuouspositiveairway pressureinpreterminfantswithrespiratorydistresssyndrome.JPediatr154:645 650 19. SukiB,AlencarAM,SujeerMKetal(1998)Life-supportsystembene tsfromnoise.Nature 393:127 128 20. LeeKS,DunnMS,FenwickMetal(1998)Acomparisonofunderwaterbubblecontinuous positiveairwaypressurewithventilator-derivedcontinuouspositiveairwaypressureinprematureneonatesreadyforextubation.BiolNeonate73:69 75
Noninvasive Mechanical Ventilation with Positive Airway Pressure in Pediatric Intensive Care
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GiancarloOttonello,AndreaWol er,andPietroTuo
54.1 Introduction Inrecentyears,theuseofnoninvasivepositivepressureventilation(NIPPV)inpediatric intensivecareunits(PICUs)hasbeenincreased.Althoughitsuseiswidelyacceptedfor chronic respiratory conditions such as neuromuscular weakness and obstructive sleep apnea[1 3],theuseofNIPPVintheacutesettinginpediatricpatientsisstilluncommon. Because of the lack of adequate devices and of trained staff, several PICUs do not yet considerNIPPVamongtheirstrategiesforventilation[4,5]. FewreportshaveaddressedtheuseofNIV(noninvasiveventilation)inpatientswithacute respiratoryfailure(ARF)inthePICU[6],andadditionalstudiesareneededtoevaluatethe speci cindications,contraindications,andpossibleadverseeffectsofthistypeofventilation. TheuseofNIPPVcanbebene cialornot,dependingontheetiologyofrespiratory failure.Insomecases,itmightcauseadelayedtimetointubation.Inotherspeci csituations,suchasforimmunocompromisedchildrenandthoseaffectedbycystic brosis(CF), itoffersmajorbene tsbyavoidingtrachealintubation,whichmaybecounterproductive intheseparticulardiseases,andpotentiallycouldimprovethesurvivalrate[7 9].
54.2 The Equipment Differentmanufacturershavecreateddifferentequipmenttoconnectthemechanicalventilatortothepatient;theseminimizeairleaks,improvepatientcomfort,andallowpatient synchronywithmechanicalventilation[10].
G.Ottonello()andP.Tuo Anaesthesia,NeonatalandPediatricIntensiveCareUnit,GGasliniChildrenHospital, Genoa,Italy e-mail:
[email protected] A.Wol er AnaesthesiaandPediatricIntensiveCareUnit,BuzziChildrenHospital,Milan,Italy A.M.Esquinas(ed.),NoninvasiveMechanicalVentilation, DOI:10.1007/978-3-642-11365-9_54,©Springer-VerlagBerlinHeidelberg2010
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54.2.1 The Masks Unlikeresultsinadultstudies,pediatricstudiesshowedthatnasalmasksseemtobepreferredforNIPPVinchildren,bothinthechronicandacutesettings,despitethefactthat childrenenrolledinthesestudieswereoftenpasttheageofobligatorynosebreathing[11,12]. Intheclinicalsetting,itisrecommendedtohaveavailabledifferentmodelsandtypesof masksto ndthebest tforeachpatient[13].
54.2.2 The Helmet AlthoughthemaskisthemostcommoninterfaceusedtodeliverNIPPV,atthesametime itmayberesponsibleofacertainnumberofNIPPVfailures.Thesearerelatedtopressure necrosisoftheskin,airleaks,anddiscomfortassociatedwiththemask.Ahelmetrepresentsanalternativewithbetteracceptanceintheacutesetting[14].Ahelmetiscurrently availableforcontinuouspositiveairwaypressure(CPAP)andforbilevelpositiveairway pressure(BiPAP)ventilation.ForCPAPuse,acontinuousfreshgas owofatleast35L/min isneededtoachievewashoutofexhaledCO2fromthesystem.ThehelmetforNIPPVis smallerthanthatusedforCPAPandcanbeconnectedtothemechanicalventilator.The volumeofthehelmetmaydecreasethesensitivityoftheinspiratorytriggeringmechanism ofthemechanicalventilator,causingasynchronybetweenthepatientandtheventilator [15].Thehelmetistransparent,whichallowsthechildtoseeandinteractwithparents, nurses,andtheenvironment(Fig.54.1).Inchildren,thehelmetcanminimizeairleaks,and threedifferentsizes talargeportionofthepediatricpopulationolderthan1month[10]. AnumberofstudieshavereportedtheroleofhelmetCPAPandhelmetventilationinthe PICU.Codazziandcolleaguesreportedasmallseriesof15youngchildren(from1month to 5 years) with ARF treated with CPAP ventilation with a helmet. No adverse events relatedtothedevicewerereported,andtheauthorsdescribedanincreaseinoxygenation
Fig. 54.1 Thehelmet: treatmentofbronchiolitis
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abovebaselineafter2h.TheyconcludedthatthehelmetisasuitabledeviceforCPAP deliverytoinfantsandpreschoolchildrenwithhypoxicARF[16].
54.3 The Choice of the Mechanical Ventilator Noneoftheventilatorsavailabletodayisperfectandabletoadequatelyventilateallthe different patient types who could need NIPPV. The sensitivity triggering inspiration of mostoftheventilatorsisinsuf cientforinfants[17].ForNIPPV,themechanicalventilator musthave 1. AblenderforFiO2upto1 2. Theabilitytocompensateforlargeairleaks 3. Ahighmaximalinspiratory ow 4. T hepossibilitytosilencealarmsofapnea,lowexhaledtidalvolume,highinspiratory volume(becauseininfantsthepresenceofairleaksoftencauseszeroingofexpired tidalvolume) 5. T heavailabilityofdifferentmodesofventilation,includingtimecycled,pressurelimited
54.4 Humidification NIPPVwithunidirectional owincreasestheneedforhumidi cationduetothehigh ow offreshairusedbytheventilator.Thenasalmucosaloseswaterdeliveredtotheinspiratorygas,leadingtoanincreaseinnasalairwayresistance,whichinadultshasbeenshown toincreaseuptosixtimesthebaselinevalue[18].Becausetheolderchildisnolongeran obligatorynosebreather,thiscouldleadtomouthbreathingandassociatedairleaks[18]. Heatedhumidi ersaretheonlytypeusefulforNIPPV.Thepresenceofahumidi er willaddresistancetothatofthecircuitandwilltendtointerferewithtriggeringandpossiblypressuredelivery.
54.5 Timing of NIV Initiation TherearenoclearindicationsaboutthebesttimingforthebeginningofNIPPVinchildren affected by ARF, but NIPPV should be anticipated in critical patients. Since NIPPV requirespatienteffort,waitingtoolongtobeginthetherapyriskshavingafatiguedpatient whocannoteffectivelyuseNIPPVandmayleadtotreatmentfailureandneedforconventionalventilation.
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54.6 Monitoring NIPPVoftenrequiresmoremonitoringandcarethaninvasivemechanicalventilation.Sincethe possiblefailureofNIPPVhastobepromptlydetectedtoavoidthedelayinstartingconventional ventilation,closebedsideassessmentofitseffectivenessbytherespiratorycareteamisessential. Quali ed professional staff must observe children treated with NIPPV through the use ofcardiacandrespiratorymonitors,pulseoximetry,and,whennecessary,bloodgasanalyses.
54.7 Contraindications ThemaincontraindicationsforNIPPVareacuteneurologicalimpairment,inabilitytoprotecttheairway,hemodynamicfailurewithshock,massivehemoptysis,facialorairway abnormalities,facialtraumaorburns,anduppergastrointestinalsurgeryduetotheriskof gastricdistension.Althoughtheinabilitytohandleairwaysecretionsislistedasarelative contraindicationtoNIPPVinadultpatients,childrenwithcerebralpalsyandspasticlaryngealdysfunctionhavebeentreatedsuccessfullywithNIPPV.
54.8 Side Effects 54.8.1 Gastric Distension Gastricdistensionduetoairiscommonandmightincreasetheriskofacuteemesisof gastriccontentsintothenasal oralmask.Forthisreason,useofnasal oralmasksrequires carefulattentiontofeedingpracticesandahighlymonitoredsetting.
54.8.2 Skin Injury Skininjuryisverycommon.Thespectrumofthisproblemcanrangefromtransienterythematoskinnecrosis[19].
54.8.3 Major Complications Major complications are unusual. Tension pneumothorax, depressed cardiac output, and progressive hypercarbia have been described in acutely ill children. Other
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described complications are secretions obstructing the upper airways and severe gastricdistension[20].
54.9 Factors Predicting Success or Failure Thelackofclearclinicalimprovementafterthe rsthoursoftreatmentshouldmakethephysicianthinkaboutchangingthetechniqueofrespiratorysupport.AnFio2greaterthan0.8after1 hoftreatmenthasbeenassociatedwiththefailureofthetechnique[20].APco2valuehigher than55mmHgduringthe rst24hmaycorrelatewithanincreasedriskoffailure[21].
54.10 Application of NIV in the Acute Setting Intheacutesetting,NIPPViseffectiveinimprovinghypoxemiaandthesignsandsymptomsofARFofdifferentorigin(asthma,bronchiolitis,lungcontusion,pneumonia,etc.). TheuseofNIPPVhasreportedlyledtoareducedneedforintubation[22].Thelargest seriesofpediatricpatientswithARFtreatedwithNIPPVtodatehasbeenreportedby Essourietal.[23].SuccessintheuseofNIPPVwaslargelydependentonthecauseof respiratoryfailureaswellasonseverityofillness,asre ectedbytheirPediatricRisk ofMortality(PRISM)andPediatricLogisticOrganDysfunction(PELOD)scoresonday 1ofPICUstay.Theworstresultswerefoundinpatientswithacuterespiratorydistress syndrome(ARDS)[23].InapopulationofchildrenwithARFmainlyrelatedtoparenchymallungdisease,NIPPVenableddecreasedoxygenrequirement,Pco2levels,respiratory rate, and need for intubation [21]. Even among children with acute moderate hypercapnicrespiratoryinsuf ciency,NIPPVwasabletoimproveclinicaloutcome.It allowedanincreaseintidalvolumeandminuteventilationandadecreaseinesophageal anddiaphragmaticpressuretimeproduct,reducingthemeanpartialpressureincarbon dioxide[24].
54.10.1 Cystic Fibrosis NIPPVisusedinpatientswithCF,mainlyduringacuteexacerbationofchronicrespiratory failure.Itavoidsintubationanditspossiblecatastrophicconsequences.Nevertheless,NIPPV isnotuniformlyusedinCFcenters,andpoorpatienttoleranceandincreasedincidenceof side effects, when compared to other treated diseases, have been reported [25, 26]. To enhancetoleranceandcompliancetoNIPPVforCFpatients,someauthorshavesuggested theuseofinvasivemethods,likemeasuringesophagealpressures,tode neoptimalsettingsofthemechanicalventilator[27].
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54.10.2 Lower Airway Obstruction Asthmaandbronchiolitisareamongthemostcommoncausesofhospitaladmissionsin infancy and childhood. Patients with more severe forms need tracheal intubation and mechanical ventilation, which is often a dif cult task and is associated with signi cant complications, such as barotrauma, hemodynamic instability, infections, and increased lengthofhospitalstay[28]. NIPPVhasbeenevaluatedtoreduceintubationrateandtoimproveclinicalscoresof asthmaandbronchiolitis.Thilletal.reporteddatafrom20childrenagedbetween2months and14yearswithacutelowerairwayobstruction.Theyfoundthatthechildrenreceiving NIPPVhadasigni cantlydecreasedrespiratoryrateandalowerClinicalAsthmaScore (CAS)[29].Beersetal.analyzedretrospectivelyagroupof73patientsaged2 17years withstatusasthmaticusandindicationforadmissioninanintensivecareunit(ICU).The useofNIPPVimprovedoxygenation,andonlytwopatientsprogressedtotrachealintubationandmechanicalventilation[30].Air owlimitationisalwaysassociatedwithsevere asthma exacerbation. If severe gas trapping occurs, the application of NIPPV might increasetheamountofgasinspiredduringeachbreath,butthelowexpiratory owwill preventtheexhalationoftheentireinspiredvolume.Inthiscondition,invasiveventilation withverylongexpiratorytimemayberequired[31]. NasalCPAPimprovestheclinicalscoreandtheCO2eliminationininfantswithrefractorybronchiolitis.Thesepositiveeffectsaresigni cantlyenhancedwhennasalCPAPis combinedwithhelioxinsteadofairandoxygen.Bothtechniquesarenoninvasive,seem safe,andmayreducetheneedforendotrachealintubation[32].
54.10.3 Upper Airway Obstruction The presence of upper airway obstruction is a common challenge in the PICU. Laryngomalacia, tracheomalacia, tracheal hypoplasia, and Pierre Robin sequence are commoncongenitalcauses,whilecroupisthemostfrequentacquiredcondition.NIPPV has been used in these patients, but the problem of synchronization is common since patientswithobstructedairwaysoftenfailtotriggerthemechanicalventilator[33].
54.10.4 Acute Respiratory Distress Syndrome VeryfewstudieshaveevaluatedtheroleofNIPPVinARDSinpediatricpatients.Essouri etal.treatedless-severeARDS(Pao2/Fio2>150)withNIPPVasthemoreseverepatients weresystematicallyintubatedandmechanicallyventilated.Nevertheless,theyreporteda verylowsuccessrateofNIPPVintheirgroupofpatientswiththediagnosisofARDS: 78%wereeventuallyintubated.MultivariateanalysisshowedthatadiagnosisofARDS
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wasanindependentpredictorforNIPPVfailure[23].Theabsenceofclinicalimprovement after1hofNIPPVinARDSpatientsshouldindicatetheneedforintubationandmechanicalventilationtoavoiddangerousdelays[34].
54.10.5 Postextubation Respiratory Failure/Weaning from Extubation ThelargestseriesofpediatricpatientswasthatofEssourietal.Nevertheless,thepopulationwastoosmalltodrawclearconclusions.Theyreportedthat33%ofpatientstreated withNIPPVafterextubationrequiredreintubation,and11%ofthesepatientsdied.They excludedthosedeathsthatwererelatedtotheuseofBiPAPortodelayedreintubation. This ndingissimilartothosefortheadults.Ithasbeenshownthatarequirementfor reintubationafterfailedextubationinadultsisassociatedwithapooroutcomeandahigher mortalityrate[35].
54.10.6 Immunocompromised Patients ARFinimmunocompromisedpatientsoffersaninterestingopportunityfortheuseof NIPPV.TherearedifferentpediatriccasereportsonthesuccessfulutilizationofNIPPV in hematological malignancies with ARF. These encouraging results could be effectivelyrelatedtoareductionininfectiousandbleedingcomplicationsduetoinvasive ventilationtogetherwiththereductioninsedationandlengthofICUstayandincrease in the use of enteral nutrition [36, 37]. Moreover, the avoidance of a translaryngeal deviceallowsthepatienttomaintaintheabilitytocommunicateverbally,tocough,and toswallow[38].
54.11 NIV in Patients Under 1 Year of Age Itisdif culttosynchronizespontaneousbreathingwithmechanicalventilators,particularlyinthepresenceoflargeleaksandthehighrespiratoryrateinchildrenlessthan1year ofage.Themechanicalventilatormustbesetinatime-cycled,pressure-controlledmode, witharespiratoryratemoderatelyhigherthanthespontaneousrespiratoryrateofthechild. Bilevel home ventilators might be inadequate since they do not reach respiratory rates higher than 30/min. Few masks are available for small infants, and sometimes custom circuitsandinterfacesareneededforparticularsituations[39].Criticalsituationssecondarytocardiacsurgery,suchasparalysisofthediaphragm,mayrequireprolongedperiods ofmechanicalventilation,whichcouldbetreatedwithNIV[40].
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Key Recommendations
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NIPPVhasakeyroleinthePICU.Forsomepatientswhoare immunocompromisedandpatientswithCFandneuromusculardiseases, itshouldbeavailablebecauseitsuseoffersapossiblereductioninmortality andanimprovementinqualityofcareandoflife. Speci ctrainingisneededtoachievesatisfactoryuseandoutcomeofthe technique.Trainingmustinvolveallthestaff:physiciansandnurses. Mechanicaldevicesandequipmentarecrucial.Mostmechanicalventilatorsare suitedforNIPPVinadults,butonlyafewcanbeappliedinthepediatric population. Greatattentionmustbegiventotheselectionofthemask;allthepossible interfacesmustbeavailable:nasal,oronasal,nasalprongs,helmets. NIPPVisanimportanttreatmentoption,butinthepresenceofworseningof, ortheabsenceof,clinicalimprovement,itmaycauseadelayintheinstitutionof trachealintubationandmechanicalventilation.
References 1. Bonekat HW (1998) Noninvasive ventilation in neuromuscular disease. Crit Care Clin 14(4):775 797 2. KurzH,SternisteW,DremsekP(1999)Resolutionofobstructivesleepapneasyndromeafter adenoidectomy in congenital central hypoventilation syndrome. Pediatr Pulmonol 27(5): 341 346 3. SimondsAK(2003)Homeventilation.EurRespirJSuppl47:38s 46s 4. HeckmattJZ,LohL,DubowitzV(1990)Night-timenasalventilationinneuromusculardisease.Lancet335:579 582 5. PeterJV,MoranJL,Phillips-HugesJ,WarnD(2002)Noninvasiveventilationinacuterespiratoryfailure.Ametaanalysisupdate.CritCareMed30:555 562 6. PadmanR,LawlessS,VonNessenS(1994)UseofBiPAPbynasalmaskinthetreatmentofrespiratoryinsuf ciencyinpediatricpatients:preliminaryinvestigation.PediatrPulmonol17:119 123 7. AntonelliM,ContiG,EsquinasA,MontiniL,MaggioreSM,BelloG,RoccoM,MavigliaR, Pennisi MA, Gonzalez-Diaz G, Meduri GU (2007) A multiple-center survey on the use in clinical practice of noninvasive ventilation as a rst-line intervention for acute respiratory distresssyndrome.CritCareMed35(1):18 25 8. Hess DR, Fessler HE (2007) Respiratory controversies in the critical care setting. Should noninvasive positive-pressure ventilation be used in all forms of acute respiratory failure? RespirCare52(5):568 578 9. CarvalhoWB,FonsecaMC(2004)Noninvasiveventilationinpediatrics:westilldonothave aconsistentbase.PediatrCritCareMed5(4):408 409 10. deCarvalhoWB,JohnstonC(2006)Thefundamentalroleofinterfacesinnoninvasivepositivepressureventilation.PediatrCritCareMed7(5):495 496 11. BachJR,NiranjanV,WeaverB(2000)Spinalmuscularatrophytype1.Anoninvasiverespiratorymanagementapproach.Chest117:1100 1105
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12. NørregaardO,GellettS(1997)Non-invasivehomemechanicalventilationinyoungandvery youngchildren.EurRespirJ10(Suppl25):A375 13. Noizet-Yverneau O, Leclerc F, Santerne B, Akhavi A, Pomédio M, Saad S, Dessioux E, MorvilleP(2008)Interfacesforpediatricnoninvasiveventilation(excludingneonate).Arch Pediatr15(10):1549 1559 14. ChiumelloD(2006)Isthehelmetdifferentthanthefacemaskindeliveringnoninvasiveventilation?Chest129(6):1424 1431 15. PiastraM,AntonelliM,CarestaE,ChiarettiA,PolidoriG,ContiG(2006)Noninvasiveventilation in childhood acute neuromuscular respiratory failure: a pilot study. Respiration 73:791 798 16. CodazziD,NacotiM,PassoniM,BonanomiE,SpertiLR,FumagalliR(2006)Continuous positiveairwaypressurewithmodi edhelmetfortreatmentofhypoxemicacuterespiratory failure in infants and a preschool population: a feasibility study. Pediatr Crit Care Med 7(5):455 460 17. Fauroux B, Leroux K, Desmarais G, Isabey D, Clement A, Lofaso F, Louis B (2008) Performance of ventilators for noninvasive positive-pressure ventilation in children. Eur RespirJ31:1300 1307 18. HayesMJ,McGregorFB,RobertsDN,SchroterRC,PrideNB(1995)Continuousnasalpositive airway pressure with a mouth leak: effect on nasal mucosal blood ux and geometry. Thorax50:1179 1182 19. FaurouxB,LavisJ-F,NicotF,PicardA,BoelleP-Y,ClémentA,VazquezM-P(2005)Facial sideeffectsduringnoninvasivepositivepressureventilationinchildren.IntensiveCareMed 31:965 969 20. BernetV,HugMI,FreyB(2005)Predictivefactorsforthesuccessofnoninvasivemaskventilation in infants and children with acute respiratory failure. Pediatr Crit Care Med 6(6):660 664 21. JoshiG,TobiasJD(2007)A ve-yearexperiencewiththeuseofBiPAPinapediatricintensivecareunitpopulation.JIntensiveCareMed22(1):38 43 22. YañezLJ,YungeM,EmilforkM,LapadulaM,AlcántaraA,FernándezC,LozanoJ,ContrerasM, ContoL,ArevaloC,GayanA,HernándezF,PedrazaM,FeddersenM,BejaresM,MoralesM, MalleaF,GlasinovicM,CavadaG(2008)Aprospective,randomized,controlledtrialofnoninvasiveventilationinpediatricacuterespiratoryfailure.PediatrCritCareMed9(5):484 489 23. EssouriS,ChevretL,DurandP,HaasV,FaurouxB,DevictorD(2006)Noninvasivepositive pressureventilation: veyearsofexperienceinapediatricintensivecareunit.PediatrCrit CareMed7:329 334 24. EssouriS,DurandP,ChevretL,HaasV,PerotC,ClementA,DevictorD,FaurouxB(2008) Physiologicaleffectsofnoninvasivepositiveventilationduringacutemoderatehypercapnic respiratoryinsuf ciencyinchildren.IntensiveCareMed34(12):2248 2255 25. SmythA(2006)Updateontreatmentofpulmonaryexacerbationsincystic brosis.CurrOpin PulmMed12(6):440 444 26. FaurouxB,BurgelPR,BoellePY,CracowskiC,Murris-EspinM,Nove-JosserandR,StremlerN, DerlichL,GiovanettiP,ClémentA;ChronicRespiratoryInsuf ciencyGroupoftheFrench NationalCysticFibrosisFederation(2008)Practiceofnoninvasiveventilationforcystic brosis:anationwidesurveyinFrance.RespirCare53(11):1482 1489 27. FaurouxB,NicotF,EssouriS,HartN,ClémentA,PolkeyMI,LofasoF(2004)Settingof noninvasive pressure support in young patients with cystic brosis. Eur Respir J 24(4): 624 630 28. ManselJK,StognerSW,PetriniMF,NormanJR(1990)Mechanicalventilationinpatients withacutesevereasthma.AmJMed89:42 48 29. ThillPJ,McGuireJK,BadenHP,GreenTP,ChecchiaPA(2004)Noninvasivepositivepressureventilationinchildrenwithlowerairwayobstruction.PediatrCritCareMed5:337 342
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30. BeersSL,AbramoTJ,BrackenA,WiebeRA(2007Jan)Bilevelpositiveairwaypressurein thetreatmentofstatusasthmaticusinpediatrics.AmJEmergMed25(1):6 9 31. ShapiroJM(2002)Managementofrespiratoryfailureinstatusasthmaticus.AmJRespirMed 1(6):409 416 32. Martinón-TorresF,Rodríguez-NúñezA,Martinón-SánchezJM(2008)Nasalcontinuouspositiveairwaypressurewithhelioxversusairoxygenininfantswithacutebronchiolitis:acrossoverstudy.Pediatrics121(5):e1190 e1195 33. EssouriS,NicotF,ClementA,GarabedianEN,RogerG,LofasoFetal(2005)Noninvasive positivepressureventilationininfantswithupperairwayobstruction:comparisonofcontinuousandbilevelpositivepressure.IntensiveCareMed31:574 580 34. FerrerM,EsquinasA,LeonM,GonzalezG,AlarconA,TorresA(2003)Noninvasiveventilation in severe hypoxemic respiratory failure: a randomized clinical trial. Am J Respir Crit CareMed168:1438 1444 35. EpsteinSK,CiubotaruRL(1998)Independenteffectsofetiologyoffailureandtimetoreintubation on outcome for patients failing extubation. Am J Respir Crit Care Med 158: 489 493 36. JacobeSJ,HassanA,VeysP,MokQ(2003)Outcomeofchildrenrequiringadmissiontoan intensivecareunitafterbonemarrowtransplantation.CritCareMed31:1299 1305 37. GiraultC,BrielA,HellotMF,TamionF,WoinetD,LeroyJetal(2003)Noninvasivemechanicalventilationinclinicalpractice:a2-yearexperienceinamedicalintensivecareunit.Crit CareMed31:552 559 38. PiastraM,AntonelliM,ChiarettiA,PolidoriG,PolidoriL,ContiG(2004)Treatmentofacute respiratoryfailurebyhelmet-deliverednoninvasivepressuresupportinchildrenwithacute leukemia.IntensiveCareMed30:472 476 39. ChinK,UemotoS,TakahashiK,EgawaH,KasaharaM,FujimotoY,SumiK,MishimaM, SullivanCE,TanakaK(2005)Noninvasiveventilationforpediatricpatientsincludingthose under1-year-oldundergoinglivertransplantation.LiverTranspl11(2):188 195 40. ChinK,TakahashiK,OhmoriK,ToruI,MatsumotoH,NiimiA,DoiH,IkedaT,NakahataT, KomedaM,MishimaM(2007)Noninvasiveventilationforpediatricpatientsunder1yearof ageaftercardiacsurgery.JThoracCardiovascSurg134(1):260 261
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55.1 Introduction Use of noninvasive ventilation (NIV) in the treatment of chronic respiratory failure advanced rapidly in the paediatric population. This may be due to further advances in technology and increasing reports of success with NIV. The major advantages of NIV, comparedtoinvasiveventilationwithtracheostomy,includegreaterpatientcomfort;simplerapplication,use,andcare;andreducedincidenceofcomplications,hospitalcost,and sedationrequirement.NIVprovidesatechniquemoreamenabletodomiciliaryuse.But, theuseofNIVcanbeproblematicinchildrenbecauseofthedif cultiesin ndingproper size,well-acceptedmasksandsynchronizingthepatientwiththeventilator[1,2].
55.2 Methods of NIV 55.2.1 Negative Pressure Ventilation Negativepressureventilationwasthe rstmodeofdeliveringNIV;however,nowitisonly availableinafewcentersintheworld.Negativepressurecanbeappliedtothelungsusing aspeciallydesignedairtightrigidchamberthatenclosesthethoraxandupperabdomen. Thereareanumberoffactorsthatlimittheuseofthesedevicesinthehome,includingthe cumbersomenatureoftheequipment,signi cantrestrictionsplacedonthesleepingposition,dif cultyinperformingpersonalcare,thenoisedisturbancetothehousehold,and problemswithupperairwaycollapse[2].
S.Oktem(),R.Ersu,andE.Dagli DivisionofPediatricPulmonology,MarmaraUniversity,Istanbul,Turkey A.M.Esquinas(ed.),NoninvasiveMechanicalVentilation, DOI:10.1007/978-3-642-11365-9_55,©Springer-VerlagBerlinHeidelberg2010
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55.2.2 Positive Ventilation via Mask NIVisbasedonthecyclicalapplicationofapositivepressure(orvolume)totheairways. Volume-targetedventilatorsdeliveraset owtotheusers airwaysforatimedintervaland at a speci ed frequency or in response to an inspiratory effort. This terminates when a presetvolumehasbeendelivered.Usingapressure-targetedrespiratoryassistdevice,the ventilationachievedfromapresetairwaypressurevarieswithusereffortandthemechanicalcharacteristicsoftherespiratorysystem,suchascompliance,resistance,autopositive end-expiratorypressure,theventilatoryfrequency,andpotentialleakage.Whenapplying respiratoryassist,thetriggerfunction,usuallysensedaseitherpressureor owchangesin thesystem,isoffundamentalimportance.Inthecaseofasmallorweakchild,inspiratory ows generated by the child may be insuf cient to activate the trigger. This is further complicatedbythevolumeaddedbythehumidi er,whichinchildrenisofteninterposed. Forthisreason,someauthorshavechosenprotocolsbywhichthesettingoftherateofthe ventilatorisslightlyhigherthanthechild sspontaneousrate,thuseffectivelyinstitutinga controlledmodeofventilation.
55.3 Clinical Scenarios for Home Noninvasive Ventilation with Positive Pressure Long-termNIVathomehasbeenusedinawiderangeofpaediatricconditions(Table55.1).
55.3.1 Obstructive Sleep Apnea Syndrome Obstructivesleepapneasyndrome(OSAS)isnotasingleentitybutisaspectrumofdisordersrangingfromprimarysnoringwithoutimpairmentofgasexchangetochronicrespiratoryfailurewithnocturnalhypoxaemiaandhypoventilation.Enlargementoftheadenoids andtonsilsisatleastoneimportantmechanismofOSASinchildren,butitisnotunusual forchildrenwithOSAStohavenocturnalderangementsinrespiratorygasexchangefollowingadenotonsillectomy.Ithasbeenshownthattreatmentofthesechildrenwithsupplementaloxygenaloneissafebutdoesnotpreventhypoventilationassociatedwithupper airwaynarrowing.Nasalcontinuouspositiveairwaypressure(nCPAP)hasbeenfoundto behighlyeffectiveinschool-agechildrenandevensometoddlerswithOSAScomplicated byhypoxaemiabutwithnormalCO2elimination.Noninvasivepositivepressureventilation(NPPV)isindicatedfortheolderchildwithOSAScomplicatedbybothhypoventilation andhypoxaemia.ThesleeplaboratoryisanidealsitetoinitiateNPPVorCPAPasameans bothtoinitiatetheappropriatepressuresettingsandtoassessthebene torlackthereofof adenotonsillectomyinthechildwithcomplicatedOSAS[3].TheAmericanAcademyof Pediatrics published guidelines on the diagnosis and management of childhood OSAS, recommendingthefollowing:Allchildrenshouldbescreenedforsnoring,complexcases
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Table 55.1 Clinicalconditionsassociatedwiththeuseoflong-termnoninvasiveventilationathome Commonindications Obstructivesleepapneaorhypopnoea Craniofacialsyndromes Obesityhypoventilationdisorders Metabolicdisorders Cerebralpalsy Neuromusculardisorders Kyphoscoliosis Possibleindications Cystic brosis Bridgetotransplantation Tracheobronchomalacia Centralhypoventilation Congenitalcentralhypoventilationsyndrome Downsyndrome Myelomeningocoele Chroniclungdiseaseofinfancy
shouldbereferredtoaspecialist,polysomnography(PSG)isthediagnosticgoldstandard, andadenotonsillectomyisthe rst-linetreatment.NPPVisanoptionforthosewhoarenot candidatesforsurgeryorwhodonotrespondtosurgery[4].
55.3.2 Neuromuscular Diseases Themostcommonindicationforlong-termNIVinchildrenisrespiratoryfailuredueto neuromusculardisorders[5].Mostchildrenwithneuromusculardisease(NMD)eventuallyrequireassistancewithairwayclearanceandbreathing,especiallyduringsleep.The onsetofpulmonarysymptomsinchildrenwithNMDsdependsinlargepartonthetypeof underlyingdisease.ChildrenwithDuchennemusculardystrophymaynotexperienceany respiratoryproblemsuntilmidadolescence,whereasaninfantwithspinalmuscularatrophytypeIislikelytodeveloprespiratorycompromisewithinthe rstyearoflife.Ineither case, there is a typical sequence of events that leads to respiratory insuf ciency and ultimately to respiratory failure. Firstly, respiratory muscle weakness leads to impaired airwayclearanceandcough,sothesepatientsarepronetorecurrentatelectasisandchest infections.Secondly,progressiveinspiratorymuscleweaknesscausesnocturnalrespiratory
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dysfunction, which is manifested by frequent arousals, sleep fragmentation, and sleeprelatedhypoventilation.Finally,hypercapniaextendsintothedaytime,andfrankrespiratoryfailureensues.Thedurationofthistimelinecanbeexpandedbyinterventionssuchas assistancewithclearanceofrespiratorysecretionsandnocturnalmechanicalventilation. Thecriteriaforhomemechanicalventilation(HMV)ofchildrenwithneuromuscular weaknesshaveevolvedsincePSGbecameavailable.Beforethis,patientswhowerecandidates for HMV were generally those with frequent, prolonged, or severe episodes of lower respiratory tract infection or those who had complications secondary to chronic hypoxaemiaorhypoventilation.PSGallowsfortheearlydetectionofpatientswhohave hypoxaemiaorhypoventilationduringsleepandprovidesopportunitiestoinitiateHMV beforeseriouscomplications. TheappropriatetimetointroduceNIVdependsonwhatoneisattemptingtoachieve. Forexample,thereareanumberofpotentialpathophysiologicalproblemsinNMDone mightwishtotackle. Thesepossibilitiesinclude
Preventionofrespiratorydecompensation Reductioninfrequencyofchestinfection,physiotherapyuse Facilitationofpulmonaryrehabilitationandexerciseprograms Controlofnocturnalhypoventilation,symptoms Alterationofchestwallandlungcharacteristics Treatmentofestablishedhypercapnicventilatoryfailure[6] NIV,appliedintermittentlyandpreferablyduringsleep,relievesrespiratorymusclesfrom theworkofbreathingandaugmentsalveolarventilation. However,NIVtherapyisproblematicinpatientswithseverebulbarweaknessleading toaspiration,ifarterialbloodgastensionscannolongerbecontrolled,ifthereareinsuperableinterfacedif culties,orifthereisfailuretothrive.Inthesesituations,atransferto ventilationviatracheotomyisanextstep.However,someindividualswithprogressive conditions elect to continue with NIV therapy and cough assistance and forgo invasive ventilation.
55.3.3 Central Hypoventilation Congenitalcentralhypoventilationsyndrome(CCHS)isafailureofautomaticcontrolof breathing. Patients have absent or negligible ventilatory sensitivity to hypercapnia and hypoxaemiaduringsleepandwakefulness.Managementconsistsofventilatorysupport whilstasleeptoovercomethelackofcentraldrive.Traditionally,thishasbeensupplied viaatracheostomyandpositivepressureventilation,especiallyforinfantsandyounger children.Astracheostomyisviewedunfavourablybymanyfamilymembersofchildren withCCHS,thereisatrendtowardsutilizationofNPPVasanalternatemeansofnocturnal ventilatoryassistance[7].Thereisgrowinginterestinthepossibilityofusingnoninvasive meanstodeliverthisnighttimesupportandfreethechildofatracheostomyduringtheday
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whentherespiratorydriveisvoluntary.SomecentersintheUnitedStatesalsooffersupplementaldiaphragmaticpacingtobeappliedduringthedayasanadjuncttomechanical ventilationatnight.TherearesomeinstanceswhenNPPValoneisusedastheprimary treatmentofCCHSasameansofavoidingtracheostomy.Thesuccessofthisapproach mustbecheckedbycarefulobservationandsleepstudiesalongwithregularassessments ofthechild sdevelopmentalprogressandechocardiographyofthestatusofthepulmonary hypertension. TheroleofNPPVinotherdisorderscharacterizedbycentralmechanismsofhypoventilationisalsoevolving.NPPVhasbeenusefulinmildhypoventilationassociatedwiththe Arnold Chiarimalformation,suchasinchildrenwithmyelomeningocele.Theimportant principleintheuseofNPPVinthesedisordersistobesurethatthedeviceusedcanfunctioninatimedmodetodeliverbackupmachine-deliveredin ationsintheeventofaprolongedcentralrespiratorypause. Anecdotal reports of the successful introduction of mask support from diagnosis in infancyareemerging,althoughtheyarenotuniversallyencouraging.Moreencouragingis increasingexperienceinthesuccessfultransferofolderchildrenoradolescentsfroman invasivetoanoninvasiveinterface.Somestudiesdemonstratedbene cialeffectsfromthe long-termuseofNIVinCCHS,includingchildrenfromtheageof7weekstoteenagers, whointhelattercasewereconvertedfrominvasiveventilation.Ingeneral,NIVisbest startedafter5 6yearsofage,whentheclinicalcourseofCCHSisusuallymorestable[8] (Fig.55.1).
55.3.4 Cystic Fibrosis Severalshort-termphysiologicstudiesfoundthatNPPVimprovesgasexchangeinchildren,bothawakeandasleep,withcystic brosis(CF)[9].Treatmentofnocturnalhypoxaemia in CF with supplemental oxygen alone may aggravate hypoventilation, a complication
Fig. 55.1 Childwith congenitalcentralhypoventilationsyndromereceiving noninvasiveventilation (NIV)withanasalmask
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preventedbyNIV.NIVef cientlyunloadstherespiratorymusclesinCFpatientswitha comparableleveloflungfunction. LungtransplantationisaneffectivetreatmentoptionforselectedCFpatientswithend-stage respiratoryfailure.InadvancedCF,NPPVhasbeensuccessfullyusedasa bridge treatment to facilitate survival before lung transplantation or at least helped these individuals to be dischargedfromthehospitalincountrieswherelungtransplantationisnotanoption[10]. The indication for long-term NIV is diurnal hypercapnia or sleep disturbance. Data fromtheFrenchnationalCFObservatorywerethe rsttoindicatethatNIVisassociated withstabilizationoflungfunctiondeclineinpatientswithsevereCFlungdisease[11].
55.4 Relative Contraindications Contraindicationshavenotbeende ned.However,thereareanumberofclinicalsituationsinwhichNIVmaynotbesuitable.Severecraniofacialmalformations,severelaryngomalacia or tracheomalacia, inadequate nasal passages, ventilatory support for 24 h a day,severelearningdisabilities,markedbulbarimpairment,profusesecretions,inabilityto ventilatesuf ciently,andthechild sorparents inabilitytocooperatewouldseemtobe possiblecontraindications[2].
55.5 The Interface in NIV 55.5.1 Nasal Versus Full-Face Mask Full-facemasksminimizeleakage;however,theyalsohavesigni cantdrawbacks,including increasedriskofgastricdistensionwithair,dif cultiesinfeeding,worseninggastroaesophagealre ux,andevenaspiration.Nonetheless,somechildrenpreferthefull-facemasks,and theycanbeusedsafelyprovidedtherecanbeareasonablelevelofmonitoring.Intheacute setting,full-facemaskshaveclearadvantagesovernasalmasksinreducingoralleaks.
55.5.2 New Masks The desirable characteristics of an interface should include low amount of dead space, adequate transparency, easy adaptability, good seal with low pressure on skin, and low cost.Thecorrectsizeshouldbechosenconsideringabalanceamongpatient sphysiognomy, the least dead space possible, and the possibility of avoiding leaks. Newer interfaces designedtoprovideNPPVtochildrenincludethehelmetdevice,nasalpillowsorplugs, andmodi edwide-boresoftnasaltubingsystems.Whereasthesenewerinterfacesshow promiseinthepaediatricpopulation,experiencewiththemispreliminary.
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55.6 Complications of NIV via Mask TwoimportantfactorsinpatientadherencewithNIVarethe tandcomfortoftheinterface. Complications are poor mask t, skin irritation, mucosal drying, air ow-induced arousals,dyssynchrony,carbondioxideretentionassociatedwithlargedeadspace,aspiration,abdominaldistention,andmidfacialdeformity.
55.6.1 Poor Mask Fit and Skin Irritation TheinterfaceisacrucialdeterminantofthesuccessofNIVbecausethepatientcannot tolerateandacceptNIVinthecaseoffacialdiscomfort,skininjury,orsigni cantairleak. Often,becauseofpoor- ttinginterfacesorinadequateheadgear,nasalmasksareplaced rmlyonachild sface,andinjurytotheunderlyingskinoccurs.Someheadgearsystems have been adapted for smaller children so the systems can t adequately into systems designedforadults.Theprophylacticuseoftapeorhydrocolloiddressingtoprotectthe skinandchangingofmaskdesignmayrelievetheaffectedareaandaidrecovery.
55.6.2 Midfacial Deformity There is evidence that the chronic use of tight- tting masks may affect facial growth, resultinginmidfacialhypoplasiainsomechildren[1].Thisseemsmorelikelyifthechild startsNIVbeforetheageof8yearsandhasweaknessofthefacialmuscles.Regularevaluationoffacialdevelopmentisadvisable.Alternationamongfacemasks,nasalmasks,and nasal plugs, together with the use of customized masks, may distribute pressure more widelyoverthefacialskeletoninthelongterm,therebyreducingthisproblem.
55.7 Initiation of Home Ventilation TheprimaryindicationfortheuseofNIVischronicalveolarhypoventilationwithassociated respiratory failure as indicated by hypoxaemia and hypercapnia. Hypoxaemia is de nedasoneofthefollowing:
Hypoxemia three standard deviations below normal whilst breathing room air and adjustedforageinasteadystateinaninfantoryoungchild Nocturnalhypoxia,de nedasSpo2below90%formorethan5%ofnight The presence of pulmonary hypertension or right ventricular hypertrophy or polycythemiaduetochronichypoxaemiaascited
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Hypercapniaisde nedasPaco2above45mmHg.IndicationsforelectiveNIVinclude symptomsofnocturnal hypoventilation (suchas sleepdisruption, night sweats, fatigue, morningheadaches,anddaytimesleepiness)inpatientswithOSAS,CF,andNMD. Othersymptomssuchasseveredyspnoea,rightheartfailure,andarterialpulmonary hypertensionorotherconditionssuchastransitionfromatracheostomytoNIVcouldalso justifyNIVinpatientswithrestrictivedisorders[5,10,12].
55.7.1 Initial NIV Adjustments in Children NPPVshouldbebasedonspeci cgoals,suchastoassisttherespiratorymuscles,decrease nocturnalhypercarbia,improvedaytimerespiratorygasexchange,preventatelectasis,and improveupperairwaypatency.Thepeakinspiratorypressure(PIP)shouldbesetatalevel suf cient to unload the respiratory muscles, increase tidal volume, and restore alveolar ventilation[3].ChildrenmaygetuncomfortableatPIPsettingsabove20cmH2O,although thismayvary.AreasonablestartingPIPintheclinicalsettingis8cmH2O,withtheexpectationtoraisethisinincrementsasnecessarytoreducetheworkofbreathing.PIPlevels of8 18cmH2Osuf ceformostchildren.Thepositiveend-expiratorypressure(PEEP) settinggenerallyadjustsintherangeof4 10cmH2OwithNIV,dependentonthespeci c processinvolved[3].
55.8 Discharging the Pediatric Patient on NIV Severalimportantaspectsofsuccessfulapplicationoflong-termNIVinchildreninclude careful preparation of the patient and family, comfortable interface selection, and a strong commitment by both the physician and family towards the success of the intervention. Achildmaybeconsideredsuitablefordischargeonlong-termNIVathomeif 1. Themedicalconditionisstable;thiswouldbeaclinicaldecisionandwouldgenerally imply
Thepresenceofastableairway StableO requirements(ifrequired),usuallylessthan40% Pco levelsthatcanbemaintainedwithinsafelimitsonventilatoryequipmentthatis 2
2
operablebythefamilyintheirhome
Nutritionalintakeadequatetomaintainexpectedgrowthanddevelopment Allothermedicalconditionswellcontrolled 2. Parentsunderstandthelong-termprognosisandarewillingandcapableofmeetingthe specialneedsoftheirchildinthehomesetting. 3. Itispracticaltoprovidethelevelofsupportandinterventionthatthechildrequiresat home[13,14].
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55.9 Follow-Up ChildrentreatedwithNIVonalong-termbasisshouldbefollowedbyateamofclinicians experienced in the assessment and management of paediatric respiratory diseases. Respiratory gas exchange, pulmonary function, state of mask, lateral projection of the skull,bloodpressure,developmentalmilestones,growth,andpatientsatisfactionshould be monitored carefully. Echocardiography for pulmonary hypertension should be performed annually. Each patient should have an annual sleep study that includes a brief periodofunassistedbreathingandtitrationofrelevantventilatorpressuresandoxygen. Depending on the condition, follow-up could take place typically every 3 6 months. Generally,atthebeginningoftheNIVathome,theyoungerorthemoreunstablethechild is,theshortertheintervalsshouldbebetweenhospitalvisits[10].
Key Recommendations
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ThemajoradvantagesofNIV,comparedtoinvasiveventilationwith tracheostomy,includegreaterpatientcomfort;simplerapplication,use,andcare; andreducedincidenceofcomplications,hospitalcost,andsedationrequirement. CommonindicationsfortheuseofNIVinchildrenincludeOSAS,NMDs,CF, andcentralhypoventilation. TherearenocontraindicationsforNIV.However,thereareanumberofclinical situationsforwhichNIVmaynotbesuitable.Severecraniofacialmalformations, severelaryngomalaciaortracheomalacia,inadequatenasalpassages,ventilatory supportfor24haday,severelearningdisabilities,markedbulbarimpairment, profusesecretions,inabilitytoventilatesuf ciently,andchild sorparents inabilitytocooperatewouldseemtobepossiblecontraindications. TheinterfaceisacrucialdeterminantofthesuccessofNIVbecausethepatient cannottolerateandacceptNIVinthecaseoffacialdiscomfort,skininjury,or signi cantairleak. Commoncomplicationsarepoormask t,skinirritation,mucosal drying,dyssynchrony,aspiration,andmidfacialdeformity.
References 1. FaurouxB,LavisJF,NicotFetal(2005)Facialsideeffectsduringnon-invasivepositivepressureventilationinchildren.IntensiveCareMed31:965 969 2. WallisC(2000)Non-invasivehomeventilation.PaediatrRespirRev1:165 171
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3. Teague WG (2005) Non-invasive positive pressure ventilation: current status in paediatric patients.PaediatrRespirRev6:52 60 4. AmericanAdademyofPediatrics(2002)Clinicalpracticeguideline:diagnosisandmanagementofchildhoodobstructivesleepapneasyndrome.Pediatrics109:704 712 5. Fauroux B, Boffa C, Desguerre I, Estournet B, Trang H (2003) Long-term noninvasive mechanicalventilationforchildrenathome:anationalsurvey.PediatrPulmonol35:119 125 6. SimondsAK,WardS,HeatherS,BushA,MuntoniF(2000)Outcomeofpaediatricdomiciliarymaskventilationinneuromuscularandskeletaldisease.EurRespirJ16(3):476 481 7. TeagueWG,VanderlaanM,KirkbyS,HayesR,WashingtonG,RobertsN(2002)Transition to NPPV in children with congenital central hypoventilation syndrome (CCHS): caregiver perceptions. Proceedings of the Fifth International Congress on Pediatric Pulmonology. EditionsE.D.K,Paris,p270 8. VillaMP,DottaA,CastelloDet al(1997)Bilevelpositive airway pressure (BiPAP) in an infantwithcentralhypoventilationsyndrome.PediatrPulmonol24:66 69 9. MilrossMA,PiperAJ,NormanMetal(2001)Low- owoxygenandbilevelventilatorysupport. Effects on ventilation during sleep in cystic brosis. Am J Respir Crit Care Med 163(1):129 134 10. OktemS,ErsuR,UyanZSetal(2008)Homeventilationforchildrenwithchronicrespiratory failureinİstanbul.Respiration76:76 81 11. FaurouxB,LeRouxE,RavillyS,BellisG,ClémentA(2008)Long-termnoninvasiveventilationinpatientswithcystic brosis.Respiration76(2):168 174 12. UyanZS,OzdemirN,ErsuRetal(2007)Factorsthatcorrelatewithsleepoxygenationin childrenwithcystic brosis.PediatrPulmonol42:716 722 13. American Thoracic Society (1990) Home mechanical ventilation of pediatric patients. Am RevRespirDis141:258 259 14. JardineE,WallisC(1998Sept)CoreguidelinesforthedischargehomeofthechildonlongtermassistedventilationintheUnitedKingdom.UKWorkingPartyonPaediatricLongTerm Ventilation.Thorax53(9):762 767
Index
A Acute,3,13,21,27,41,67,73,83,87,123, 131,138,145,169,174,179, 185,191 197,199,205,217,223, 231 235,237 247,249 254,259, 263 265,269,273,280,288,295, 305,317,321,327,366,373, 377,392 Acutecardiogenicpulmonaryedema(ACPE), 13,14,16,17,41,192,224,226, 231 235,237 240,250 Acuterespiratorydistresssyndrome(ARDS), 73,217,224,241 247,250,253, 308,310,381 383 Acuterespiratoryfailure,3 5,13,27,69,70, 107,145,169,218,223,224,226, 232,235,241,249,253,259,260, 269,274,280 281,288,289,295, 297,298,308,310,317,325, 327 330,377 Adaptiveservo-ventilation(ASV),93 98 Adult,8,60,94,121,136,139 141,257,292, 297,321 326,343 345,352,353, 374,378 380,383,384,393 Airleakage,5,33,85,282,290,318,327, 343 354 Airwaypressure,9,10,22 24,39,41,46,48, 74,75,114,150,220,232,358, 365,370,371,388 Airways,52 54,56,73,77,158,167,169, 195,232,279,280,288,310, 322 327,336,343,358,363,366, 381,382,388 Amyotrophiclateralsclerosis(ALS), 149 150,153 159,162,280, 282,285,290,291 Anesthesiology,
ARDS.SeeAcuterespiratorydistress syndrome Assistedcoughing,144 147,158,202,289 Asthma,185 189,191 197,217,218,274, 308,381,382 Asthmaticattack,191 197 ASV.SeeAdaptiveservo-ventilation Asynchrony,23,24,28,68,70,73 75,90, 116,150,191,196,220,378 Atherosclerosis,131 133 Averagevolume-assuredpressuresupport (AVAPS)mode,207 B Bi-level,25,28 30,32 37,46,61,62,70,83, 85,94,96,115,143,149,155,193, 195,219,260,281,289,297,299, 353,378,383 Bilevelpositiveairwaypressure(BiPAP),30, 34,35,41,83 86,97,155,193, 195,196,220,260,281,284,289, 378,383 Breathing,9,13,22,28,39,60,68,74,78, 84,90,93,101,107,121,132,136, 144,149,154,162,167,174,182, 186,195,200,205,232,241,251, 258,263,280,287,298,306,318, 322,327,335,346,358,369, 378,389 BubbleCPAP,41,42,353,358,359, 369 374 C Cancer,249 254,330 Carbondioxide(CO2),9 10,21,59,77 91, 109,146,171,175,176,218,225, 359,364,373,381,393 397
398 Cardiogenicpulmonaryedema(CPE),39,189, 217,218,220,223,224,235,250, 295,305 Cardiovascular,101,121 128,135,173,185, 246,275,311 Cheyne Stokesrespiration,93 98,125,210 Children,8,60,135,136,138 141,144,145, 147,162,187,188,282,291,292, 377 383,387 395 Chronicheartfailure,33,239,310,311 Chronichypercapnicrespiratory,171 176, 209,210 Chronicobstructivehypercapnic,67 70 Chronicobstructivepulmonarydisease (COPD),3,5,16,22 24,33,37, 54,56,67 70,74,135,137,138, 171 176,179 185,189,192, 205 210,217,218,223 226,239, 249,295 300,302,305,307 311, 317,329 Chronicrespiratoryfailure(CRF),3 5,21,27, 28,59,83,87,88,143,182,205, 206,208 210,295,297,308,310, 321,327,330,381,387 395 Circuits,7,8,13,24,25,28,30,32,35,37, 39 41,46,49,51 57,77 79,81, 83 85,87 90,109 112,193,195, 196,265,366,369,370,379,383 Colonization,52 56,324,326 Complications,3 5,93,107 116,121 128, 143,147,162 167,169,180,184, 199,200,202,218,223,231,232, 241,247,249,251,252,254,258, 260 261,263,265,266,273,281, 287,292,295,299,305,317 322, 324 329,331,360,380 383,387, 390,391,393,395 Contamination,52 56,113 Continuouspositiveairwaypressure(CPAP), 7,13,28,39,45,69,80,83,90,93, 101 104,110,121 128,133,135, 188,193,217,226,237 241,252, 258,281,289,323,328,335,343, 357,364,369,378,388 Conventionalmechanicalventilation, 169,185,186 COPD.SeeChronicobstructivepulmonary disease CPAP.SeeContinuouspositiveairway pressure
Index CPE.SeeCardiogenicpulmonaryedema CRF.SeeChronicrespiratoryfailure Criticalcare,40,45,246,258,281,282, 289,290 Critically,23,30,56,74,111,257 261,269 Cyclic-variability,73 74 D Decannulation,163,165,279 285,290 Device,5,8,10,13,16,22,23,28,36,37, 39,41,42,46,47,56,70,80,81, 83 86,88 89,93 98,102,103, 109,110,112,113,157 159,219, 220,244,258,259,279,288,336, 337,339,340,344,346,349, 350,352 354,357,358,371,372, 377 379,383,384,387,388, 391,392 Disease,3,16,21,27,39,51,59,67 70,74, 102,115,121,131,135,150,153, 161 167,171,180,185,191,199, 205 210,217,223,239,242,249, 258,263,280,287 293,295,305, 317,321,329,343,357,365,371, 377,389 Disinfection,52 54,56,57 Duchenne,60,143 147,162,164,281,283, 292,389 Dystrophy,60,143 147,162,164,165,283, 292,389 E Ef cacy,4,5,8,15,17,22,39,41,56,63, 74,77,96,103,104,121 128, 138,139,141,147,156,169, 192,224,225,227,233,235, 274,275,323,343 Emergencydepartment(ED),217 220, 223 226 Emergencymedicine,217 220 Endotrachealintubation,15,161 166,185, 186,192 194,197,218,223, 225,226,231,240 242,244, 246,257,300,305,307,325, 366,367,382 Equipment,30,37,39 42,45 49,51 54, 61 63,111,199 200,217 220, 265,284,287,335 340,354, 357,360,370,374,377 379, 384,387,394
Index Equipmentandsupplies,40,41,358 Evidence,35,49,52,53,55,56,61,89,98, 121 123,132,137,156,159,171, 174 176,185,189,192 195,197, 205 208,217,225 227,234,235, 238,241,249,250,258,269,275, 295 297,299 301,306,335,337, 358,360,363,366,372 374,393 Exacerbations,37,67,175,182,185 189, 192,194,217,223 226,242,249, 295,297,298,300,302,305,381, 382 Extubation,3,169,273,279 285,287 293, 295 300,305 307,309,311, 322 324,343,357,358,364, 372 374,383 F Failure,3,13,21,27,48,51,59,67,73,83, 87,93,107,121,135,143,149, 153,163,167,171 176,179 185, 192,199,205,217,223,231,238, 241,249 254,258,263 265,269, 274,279,288,295,305 311,317, 321,327,359,364,373,377, 387 395 H Helmet,7 11,13 17,31,40,48,62,77, 78,80 82,85,107,109 113, 218 220,252,323,325, 378 379,384,392 High-frequencynasalventilation,363 367 Homemechanicalventilation,48,51 53,55, 59,63,289,387 395 Homeventilation,35,51 57,61 63,74,85, 171 176,205 210,393 394 Homeventilator,28,34,36,37,63,383 Hygiene,54,56 Hypercapnic,23,30,205,206,225,309 311, 381,390 Hypercapnicrespiratoryfailure,21,83, 171 176,179 184,209,210, 263 266,296 Hypoxemia,21,101,135,143,146,154,161, 173,182,186,205,208,226,241, 244,246,258,260,306 308,325, 381,393 Hypoxemicrespiratoryfailure,21,192,223, 242,249 254,329
399
I ICUventilator,28 30,33,35 37,40 42,70, 219,259 Injuries,48,59,60,115,132,165,169, 241 247,249,300,308,310, 322,360,366,380,393,395 Inspiratorypositiveairwaypressure(IPAP), 28,30,34,68,69,83,94 97,145, 149,150,183,188,195,196,241, 246,260,308,310 Instrumentation,104,176,207,353 Intensivecare,113,223,224,226,227,265, 269 272,377 384 Intensivecareunit(ICU),4,10,16,28 30, 32,33,35 37,39 42,70,107,111, 116,162,186,189,191,193,194, 197,219,223 227,241,242,244, 246,249 254,258,259,261,270, 271,274,275,296 300,302,307, 309,311,321,324,325,382,383 Interactionspatient-ventilator,8,22 25,32, 34,35,37,67 70,74,75,77,112, 116,195 196,208 Interface,3 5,7,9,25,30,31,34,37,39, 41,48 49,51,56,57,61 63,73, 77 80,85,87,109,111,113,116, 145,149,162,180,202,207 208, 246,253,254,281,282,284, 290 292,336 337,340,343 345, 353,371,378,383,384,390 395 Intraoperative,317 320,322,323 Intubation,4,14 17,37,107,157,161 166, 169,180,185 189,192 194,197, 207,217,218,223,225 227,231, 240 242,244 247,249,257 261, 264,269,280,288,292,295, 298 300,305,307,309 311,317, 321,322,324,325,329,330,343, 359,364 367,377,381 384 IPAP.SeeInspiratorypositiveairway pressure L Leftventricularsystolicfunction,237 240 Livertransplant,321 326 Longtermnoninvasiveventilatorysupport, 56,171,172,174 176,388,389, 391,392,394,395 Lunginjury,115,241 247,249,300,366 Lungresectionalsurgery,300,327 331
400
M MAC.SeeMechanicallyassistedcoughing Maintenance,51 57,162,176,232,269,274, 295,369 Managementsystem,83 86 Mask,3 5,8 10,13 17,21,23 25,28, 30 34,40,41,46,48,51,53,56, 62,69,70,77 80,85,87 91,94, 102,107 114,116,140,149,155, 158,162,188,193,194,196,201, 202,208,218 220,226,238,246, 252,257,259 261,265,274,297, 299,300,307,309,310,318 320, 323,327,330,336 340,343 345, 378,380,383,384,387,388, 391 393,395 Measurements,11,36,61,74,90,132,154, 169,180,284,318,343 351,353, 354,371 Mechanicalinsuf ation exsuf ation,145,158 Mechanicallyassistedcoughing(MAC), 145 147,202,280 285,288 292 Mechanicalventilation,3,21,27 37,45,51, 59 63,67,73,77 82,86,110,146, 149,157,161 169,176,179,185, 191,200,205,223,241,249,261, 264,289,296,305,317,322,327, 343,357,363,372,377 384, 387 395 Medicaldevices,39 Monitoring,10,11,17,25,27 31,35 37, 40 42,46,49,52,56,63,74,80, 83,101 104,110,115,169, 172 174,176,180,189,191,220, 223,227,246,253,265,309,311, 318,319,348,352 354,371,380, 392 Muscular,60,143 147,156,162,165, 280 283,290,292,389 Myastheniccrisis,167 169 Myocardialinfarction,115,121,131,133, 231,233 235,239 N Nasalhigh-frequencyventilation,363 367 Neonatal,8,335 340,343,357,358,364, 366,369 371,373 Neonates,41,343 354,365,372,373 Neonatology, Neuromuscular,13,21,28,33,37,51,59 61, 63,115,158,161 167,169,183,
Index 191,242,279 285,287 293,308, 310,330,377,384,389 390 Neuromusculardisease,37,59,61,63,113, 158,161 166,183,281,287 293, 308,310,330,384,389 390 Newborn,336,352,357 360,365,369 niPSV.SeeNon-invasivepressuresupport ventilation NIV.SeeNon-invasiveventilation Nocturnal,28,51,59 63,68,85,94,101 104, 125,132,133,145,154 156,159, 174,182,206,208 210,283,284, 289,292,323,327,388 391, 393,394 Noninvasivemechanicalventilation, 4,27 37,47,49,59 63, 77 82,161 169,179,181, 322,377 384 Non-invasivepositivepressureventilation (NPPV),3,17,27,39 42,61,87, 147,153 159,191 197,199 202, 209,241,246,249 254,260,274, 287,295 302,305,317,327 331, 377,386 Non-invasivepressuresupportventilation (niPSV),67,74,107 116,226, 231 235 Non-invasiveventilation(NIV),7,10,15,21, 42,45 49,51,61,73,78,80,83, 85,87 91,141,143,149 150,159, 161,169,171,181,185 189,192, 196,205,217 220,223 227, 231 235,241,257 261,263 266, 269 275,287,305 311,317 326, 357 360,364,374,377,387 NPPV.SeeNon-invasivepositivepressure ventilation O Obstructivesleepapnea(OSA),93,101,104, 121 128,131 133,135,136, 139 141,388,389 Oncologycritically,281,282 Outcome,25,27,37,61,83,123 125,171, 172,187,193,194,240,242,244, 247,250 252,260 261,263 265, 269,273,280 281,297,305,311, 321,329,330,343,363,366,374, 381,383,384 Outside,9,13,80,187,223 227,232,253, 258,270,308,353,366
Index
P Patient/machineinterfaces,23,28,34,37,67, 68,70,73,112,325 Patient ventilatorinteraction,8,23 25,32, 35,67 70,74,75,112,,116, 195 196,208 Pediatric,8,46,292,298,377 384,388,394 Positiveairwaypressure,7 11,13 17,28, 39 42,45,61,83,88,93,101 104, 110,121 128,133,135,143,149, 155,183,188,194,208,217,226, 231 235,237 241,258,281,289, 299,323,335 340,343 354,357, 364,369 374,377 384,388 Positive-pressurerespiration,3,22,27,87, 192,199,209,232,249 254,295, 306,308,318,321 Positivepressureventilation,3,17,27, 39 42,45,46,61,63,87,115, 147,153 159,191 197,199 202, 209,241,249 254,260,279,287, 288,295 302,305,306,308,310, 311,317,323,326 331,336,337, 358,364,377,388,390 Postextubation,282,283,290,291,295 302, 305 311,383 Postoperative,146,147,192,257,297,308, 310,318,322 331 Predictors,139,154,169,171 176,191,200, 226,244,251,253,298,383 Pre-hospital,14,17,217 220,233 Prematureventilation,24,33,70,233, 305,357 Preoxygenation,257 261 Pressure-cycledventilators,51,61,62 Pressuresupportventilation(PSV),8,10, 13,21 25,31,32,35,40,62,67, 73 75,80,83 86,107 116,188, 196,207,208,226,231,233,235, 259,260,270,296,297 Preterminfants,8,335,338 340,371,372 Protocol,17,51 57,149,179 184,246, 265,270 272,282,290 293, 311,366,388 Pulmonaryedema,13,14,39,41,115,189, 192,217,223,224,226,231 235, 237 241,250,295,305,309,311, 324,329 Q Quadriplegia,
401
R Rebreathing,9 11,25,27 30,32,45,46,62, 77 91,109,220 Respiratoryfailure,3,13,21,27,51,59,69, 73,83,87,107,141,143,149,153, 161,167,171 176,179 185,192, 205,218,223,231,241,249 254, 259,263 265,269,274,279,288, 295,305 311,317,321,327,366, 373,377,387 395 Respiratoryparalysis,156,157,199 Resuscitation,335 340 Risk,3,11,25,28,46,52,62,82,83,101, 104,114,123,131,141,146,155, 161,169,172,183,191,200,218, 223,231 235,249,258,269,292, 296,305,317,321,327,343,357, 363,379,392 S Sedation,33,68,73,108,110,146 147,161, 162,166,191,223,249,269 275, 306,318,319,323,324,371,383, 387,395 Sleep,27,39,46,59,67,73,83,93,101,111, 121 128,131 133,135,146,154, 182,201,207,239,273,308,323, 377,388 389 Spinalcord,59,60,183,199,200,270,281, 282,290,291 Spontaneousrespiration,67 70 Strategies,32,111,135,169,179,182 184, 208,217 220,323,325,326,357, 360,372,377 Survival,3,51,60,61,126,143 147,149, 150,154 157,159,162,171 176, 181,199,205,206,218,225,227, 237,244,246,251,252,281,284, 297,311,330,358,363,377,392 T Technology,7 11,27,39,45 49,61,62, 74,93,147,199 201,335 340, 343,387 Tidalvolume(TV),14,15,21,23,34,41,47, 62,68,78,79,83,89,94,109,110, 113,145,150,175,195,200,201, 206,242,246,259,260,306,308, 318,328,329,337 340,349,351, 367,379,381,394 TitrationCPAPauto-CPAP,102 104
402
Index
Tracheotomy,157,161 166,209,210,279, 280,282 285,288 290,292,293, 297,390 Training,37,104,146,201,220,263 266,384
250,258,280,281,283,284, 288 292,298,299,317,318, 390,392,395 Volume-cycledventilators,30,61,62,143,145
U Units,4,9,13,28,39,40,55,70,89,90,107, 162,168,176,184,186,191,219, 223 227,233,241,249,253,258, 264,266,270,274,284,296,298, 307,308,321,328 330,336,364, 373,377,382 Unweanable,279 285,287 293
W Weakness,21,62,143,149,150,153, 156 158,167,168,279 285, 287 293,298,324,377,389, 390,393 Weaning,3,146,169,176,179,181,183,192, 246,281,284,289,291,292, 295 299,305 307,310,311,318, 322,325,326,360,383 Workofbreathing,9,13 16,22,23,25,32, 69,84,107,138,146,149,156, 168,188,195,197,205,241, 242,251,263,298,306,307, 322,325,327,336,358 360, 369,371,390,394
V Ventilatorymodes,23,87 Ventilatorysupport,5,46,49,63,73,107, 110,143,145,155,156,168,169, 176,181,182,185,186,193, 195 196,226,231,241,246,
