30/4/2016 VentilatorManagement:IntroductiontoVentilatorManagement,ModesofMechanicalVentilation,MethodsofVentilatorySupport

VentilatorManagement
Author:AllonAmitai,MDChiefEditor:ZabMosenifar,MD,FACP,FCCPmore...

Updated:Dec31,2015

IntroductiontoVentilatorManagement
Intubation,withsubsequentmechanicalventilation,isacommonlifesaving
interventionintheemergencydepartment(ED).Giventheincreasinglengthofstay
ofventilatedpatientsinEDs,itisnecessaryforemergencypractitionerstohavea
goodunderstandingoftechniquestooptimizemechanicalventilationandminimize
complications.

Manydifferentstrategiesofpositivepressureventilationareavailabletheseare
basedonvariouspermutationsoftriggeredvolumecycledandpressurecycled
ventilationsandaredeliveredatarangeofrates,volumes,andpressures.Poor
ventilatorymanagementcaninflictseriouspulmonaryandextrapulmonarydamage
thatmaynotbeimmediatelyapparent.

Becausemanyoftheeffectsofventilatorinducedlunginjuryaredelayedandnot
seenwhilepatientsareintheED,muchofourunderstandingoftheadverse
consequencesofvolutrauma,airtrapping,barotrauma,andoxygentoxicityhas
comefromthecriticalcareliterature.Whilethefundamentalprinciplesunderlying
mechanicalventilatorysupporthavechangedlittleoverthedecades,muchprogress
hasbeenmadeinourunderstandingofthesecondarypathophysiologicchanges
associatedwithpositivepressureventilation.

Ventilatorystrategieshavebeendevisedfordifferentdiseaseprocessestoprotect
pulmonaryparenchymawhilemaintainingadequategasexchange,andtheymaybe
responsiblefortheincreasedratesofsurvivalforpathologiessuchasacute
respiratorydistresssyndrome(ARDS).Severalrecentclinicaltrialshave
demonstratedthatoptimizingventilatoryparametersreducesoveralldurationof
mechanicalventilationandorganfailure.Additionally,anupsurgeinutilizationof
noninvasiveventilationhaspermittedmanypatientstoavoidtherisksand
complicationsoftrachealintubation. [1,2]

ModesofMechanicalVentilation
Volumecycledmode
Inhalationproceedsuntilasettidalvolume(TV)isdeliveredandisfollowedby
passiveexhalation.Afeatureofthismodeisthatgasisdeliveredwithaconstant
inspiratoryflowpattern,resultinginpeakpressuresappliedtotheairwayshigher
thanthatrequiredforlungdistension(plateaupressure).Sincethevolumedelivered
isconstant,appliedairwaypressuresvarywithchangingpulmonarycompliance
(plateaupressure)andairwayresistance(peakpressure).

Becausethevolumecycledmodeensuresaconstantminuteventilationdespite
potentiallyabnormallungcompliance,itisacommonchoiceasaninitialventilatory
modeintheED.Amajordisadvantageisthathighairwaypressuresmaybe
generated,potentiallyresultinginbarotrauma.Closemonitoringanduseofpressure
limitsarehelpfulinavoidingthisproblem.Notethatventilatorssettovolumecycled
modefunctionwellasmonitorsofpatients'pulmonarycompliance,whichwillbe
decreasedinphysiologicalstatessuchasworseningARDS,pneumothorax,right
mainstemintubation,chestwallrigidity,increasedintraabdominalpressure,and
psychomotoragitation("fightingthevent").Thesepathophysiologicalstates
increasepeakpressureandshouldbeconsideredwheneverpressurealarmsare
sounded.

Inpressurecycledsettings,bycontrast,suchstatesresultonlyinreduceddelivered
volumesandmaynottriggeralarms.Giventhattheairwayresistanceand
pulmonarycomplianceofthecriticalEDpatientisunknown,theauthors
recommendthevolumecycledmodeforinitialventilationofmostpatients.

Pressurecycledmode

Asetpeakinspiratorypressure(PIP)isapplied,andthepressuredifference
betweentheventilatorandthelungsresultsininflationuntilthepeakpressureis
attainedandpassiveexhalationfollows.Thedeliveredvolumewitheachrespiration
isdependentonthepulmonaryandthoraciccompliance.

Atheoreticaladvantageofpressurecycledmodesisadeceleratinginspiratoryflow
pattern,inwhichinspiratoryflowtapersoffasthelunginflates.Thisusuallyresults
inamorehomogeneousgasdistributionthroughoutthelungs.However,nodefinite
evidenceexiststhatthisresultsinareductionoftherateofventilatorinducedlung
injuryoroverallmortality.Nevertheless,pressurecycledventilationhasachieved
considerablepopularityintheintensivecaresettingformanagementofpatients
withARDS,whoselungsaremostlikelytobecharacterizedbyabroadrangeof

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alveolardysfunctionandarealsomostvulnerabletotheeffectsofbarotraumaand
volutrauma.

Amajordisadvantageisthatdynamicchangesinpulmonarymechanicsmayresult
invaryingtidalvolumes.Thisnecessitatesclosemonitoringofminuteventilation
andlimitstheusefulnessofthismodeinmanyemergencydepartmentpatients.
However,newerventilatorscanprovidevolumeassuredpressurecycledventilation,
whichincreasepeakpressuresasneededtodeliverapresetminimumtidalvolume.

Highfrequencyoscillatorysupport

Inthisventilatorystrategy,ultrahighrespiratoryrates(180900breathsperminute)
arecoupledwithtinytidalvolumes(14mL/kg)andhighairwaypressures(2530
mmH2O). [3]Thisisacommonlyacceptedventilatorysettingforprematureinfants
andhasnowalsobeenusedinsmallcriticalcareunitstudiesonpatientswith
ARDS,withreportsofimprovingoxygenationandlungrecruitment. [4,5]

WhilethissettingcannotcurrentlyberecommendedforroutineEDuse,itmayin
thefuturebefoundappropriateforthemanagementofpatientswithARDS.

Typesofsupport

Mostventilatorscanbesettoapplythedeliveredtidalvolumeinacontrolmodeor
asupportmode.

Controlmode

Incontrolmode,theventilatordeliversthepresettidalvolumeonceitistriggered
regardlessofpatienteffort.Ifthepatientisapneicorpossesseslimitedrespiratory
drive,controlmodecanensuredeliveryofappropriateminuteventilation.

Supportmode

Insupportmode,theventilatorprovidesinspiratoryassistancethroughtheuseofan
assistpressure.Theventilatordetectsinspirationbythepatientandsuppliesan
assistpressureduringinspiration.Itterminatestheassistpressureupondetecting
onsetoftheexpiratoryphase.Supportmoderequiresanadequaterespiratorydrive.
Theamountofassistpressurecanbedialedin.

MethodsofVentilatorySupport
Continuousmandatoryventilation

Breathsaredeliveredatpresetintervals,regardlessofpatienteffort.Thismodeis
usedmostoftenintheparalyzedorapneicpatientbecauseitcanincreasethework
ofbreathingifrespiratoryeffortispresent.Continuousmandatoryventilation(CMV)
hasgivenwaytoassistcontrol(A/C)modebecauseA/Cwiththeapneicpatientis
tantamounttoCMV.ManyventilatorsdonothaveatrueCMVmodeandofferA/C
instead.

Assistcontrolventilation
Theventilatordeliverspresetbreathsincoordinationwiththerespiratoryeffortof
thepatient.Witheachinspiratoryeffort,theventilatordeliversafullassistedtidal
volume.SpontaneousbreathingindependentoftheventilatorbetweenA/Cbreaths
isnotallowed.Asmightbeexpected,thismodeisbettertoleratedthanCMVin
patientswithintactrespiratoryeffort.

Intermittentmandatoryventilation

Withintermittentmandatoryventilation(IMV),breathsaredeliveredatapreset
interval,andspontaneousbreathingisallowedbetweenventilatoradministered
breaths.Spontaneousbreathingoccursagainsttheresistanceoftheairwaytubing
andventilatorvalves,whichmaybeformidable.Thismodehasgivenwayto
synchronousintermittentmandatoryventilation(SIMV).

Synchronousintermittentmandatoryventilation

Theventilatordeliverspresetbreathsincoordinationwiththerespiratoryeffortof
thepatient.Spontaneousbreathingisallowedbetweenbreaths.Synchronization
betweenpresetmandatorybreathsandthepatient'sspontaneousbreathsattempts
tolimitbarotraumathatmayoccurwithIMVwhenapresetbreathisdeliveredtoa
patientwhoisalreadymaximallyinhaled(breathstacking)orisforcefullyexhaling.
OnedisadvantageofSIMVisincreasedworkofbreathing,thoughthismaybe
mitigatedbyaddingpressuresupportontopofspontaneousbreaths.

Theinitialchoiceofventilationmode(eg,SIMV,A/C)isinstitutionandpractitioner
dependent.A/Cventilation,asinCMV,isafullsupportmodeinthattheventilator
performsmost,ifnotall,oftheworkofbreathing.Thesemodesarebeneficialfor
patientswhorequireahighminuteventilation.Fullsupportreducesoxygen
consumptionandCO2productionoftherespiratorymuscles.Apotentialdrawback
ofA/Cventilationinthepatientwithobstructiveairwaydiseaseisworseningofair
trappingandbreathstacking.

Whenfullrespiratorysupportisnecessaryfortheparalyzedpatientfollowing
neuromuscularblockade,nodifferenceexistsinminuteventilationorairway

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pressureswithanyoftheabovemodesofventilation.Intheapneicpatient,A/C
witharespiratoryrate(RR)of10andaTVof500mLdeliversthesameminute
ventilationasSIMVwiththesameparameters.

Pressuresupportventilation

Forthespontaneouslybreathingpatient,pressuresupportventilation(PSV)has
beenadvocatedtolimitbarotraumaandtodecreasetheworkofbreathing.
PressuresupportdiffersfromA/CandIMVinthatalevelofsupportpressureisset
toassisteveryspontaneouseffort.Airwaypressuresupportismaintaineduntilthe
patient'sinspiratoryflowfallsbelowacertaincutoff(eg,25%ofpeakflow).The
patientdeterminesthetidalvolume,respiratoryrate,andflowrate. [3]Withsome
ventilators,thereistheabilitytosetabackupIMVrateshouldspontaneous
respirationscease.

PSVisfrequentlythemodeofchoiceinpatientswhoserespiratoryfailureisnot
severeandwhohaveanadequaterespiratorydrive.Itcanresultinimprovedpatient
comfort,reducedcardiovasculareffects,reducedriskofbarotrauma,andimproved
distributionofgas.

Noninvasiveventilation

Theapplicationofmechanicalventilatorysupportthroughamaskinplaceof
endotrachealintubationisbecomingincreasinglyacceptedandusedinthe
emergencydepartment.Consideringthismodalityforpatientswithmildtomoderate
respiratoryfailureisappropriate.Thepatientmustbementallyalertenoughto
followcommands.Clinicalsituationsinwhichithasprovenusefulincludeacute
exacerbationofchronicobstructivepulmonarydisease(COPD)orasthma,
decompensatedcongestiveheartfailure(CHF)withmildtomoderatepulmonary
edema,andpulmonaryedemafromhypervolemia.Itismostcommonlyappliedas
continuouspositiveairwaypressure(CPAP)andbiphasicpositiveairwaypressure
(BiPAP).BiPAPiscommonlymisunderstoodtobeaformofpressuresupport
ventilationtriggeredbypatientbreathsinactuality,BiPAPisaformofCPAPthat
alternatesbetweenhighandlowpositiveairwaypressures,permittinginspiration
(andexpiration)throughout.

Reviewsoftheliteraturehaveshownnoninvasivepositivepressureventilation
(NPPV)tobebeneficialforCOPD,reducingtherateoftrachealintubationsandthe
lengthofstay. [2]RecentlydevelopedclinicalguidelinesrecommendthatNPPVbe
consideredasanadjuncttostandardmedicaltherapyinpatientswithsevereCOPD
exacerbations(pH<7.35andrelativehypercarbia),aswellasinpatientswith
cardiogenicpulmonaryedemaandrespiratoryfailurewithoutshockoracute
coronarysyndromerequiringurgentpercutaneouscoronaryintervention. [6]

TheuseofNPPVhasbeenlesswellstudiedinasthma,thougharecentmeta
analysisfoundthatNPPVimprovedsecondaryoutcomessuchasnumberof
hospitaladmissions,lengthofICUstay,andlengthofhospitalstay,aswellashad
afavorableeffectsoncertainlungfunctionparameterssuchaspeakexpiratoryflow,
forcedvitalcapacity,andFEV 1. [7]However,thestudydidnotdemonstratea
definitebenefitofNPPVformortalityorintubationrates.

AdverseConsequencesofMechanicalVentilation
Thedeteriorationofintubatedpatientsduetomultiorganfailurehasbeenobserved
fordecades.Inrecentyears,however,muchprogressdelineatingtheadverse
effectsofpositivepressureventilationhasbeenmade. [8]In1993,Tremblayetal
demonstratedincreasedcytokineandinflammatorymRNAexpressioninahigh
stressventilatorymodel,showingthatincreasingvolumesandreducingPEEP
resultedinhighertumornecrosisalphaserumconcentrations.Furtherresearchover
the1990sdemonstratedacascadeofsystemicinflammatoryeffectsofbiochemical
pulmonaryinjurycontributingtodistalorgandysfunction. [9]

Pulmonaryeffects

Barotraumamayresultinpulmonaryinterstitialemphysema,pneumomediastinum,
pneumoperitoneum,pneumothorax,and/ortensionpneumothorax.Highpeak
inflationpressures(>40cmH2O)areassociatedwithanincreasedincidenceof
barotrauma.However,notethatseparatingbarotraumafromvolutraumaisdifficult,
sinceincreasingbarometricpressureisusuallyaccompaniedbyincreasingalveolar
volume.

Experimentalmodelsofhighpeakinflationpressuresinanimalswithhigh
extrathoracicpressureshavenotdemonstrateddirectalveolardamagefrom
increasedpressurewithoutincreasedvolumeaswell.Thus,thestatementthathigh
airwaypressuresresultinalveolaroverdistention(volutrauma)andaccompanying
increasedmicrovascularpermeabilityandparenchymalinjurymaybemoreaccurate.
Alveolarcellulardysfunctionoccurswithhighairwaypressures.Theresultant
surfactantdepletionleadstoatelectasis,whichrequiresfurtherincreasesinairway
pressuretomaintainlungvolumes.

Highinspiredconcentrationsofoxygen(fractionofinspiredoxygen[FiO2]>0.5)
resultinfreeradicalformationandsecondarycellulardamage.Thesesamehigh
concentrationsofoxygencanleadtoalveolarnitrogenwashoutandsecondary
absorptionatelectasis.

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Ithasbeentheorizedthatpulmonarybiophysicalandbiomechanicalinjuryinthe
presenceofbacteriallunginfectionscontributestobacterialtranslocationand
bacteremia.

Cardiovasculareffects

Theheart,greatvessels,andpulmonaryvasculatureliewithinthechestcavityand
aresubjecttotheincreasedintrathoracicpressuresassociatedwithmechanical
ventilation.Theresultisadecreaseincardiacoutputduetodecreasedvenous
returntotherightheart(dominant),rightventriculardysfunction,andalteredleft
ventriculardistensibility.

Thedecreaseincardiacoutputfromreductionofrightventricularpreloadismore
pronouncedinthehypovolemicpatientandinthosewithalowejectionfraction.

Exaggeratedrespiratoryvariationonthearterialpressurewaveformisacluethat
positivepressureventilationissignificantlyaffectingvenousreturnandcardiac
output.Intheabsenceofanarterialline,agoodpulseoximetrywaveformcanbe
equallyinstructive.Areductioninthevariationaftervolumeloadingconfirmsthis
effect.Theseeffectswillmostfrequentlybeseeninpatientswithpreload
dependentcardiacfunction(thatis,operatingontherightsideoftheStarlingcurve)
andinhypovolemicpatientsorinthosewithotherwisecompromisedvenousreturn.

Increasedalveolarcapillarypermeabilitysecondarytopulmonaryinflammatory
changesmay,alternatively,contributetoincreasedcardiacoutput.

ForpatientswithSwanGanzcatheterizationinplaceforwhomcardiacoutputmay
bemeasured(usuallyintheICUsetting),PEEPstudiesmaybeperformed.Thisis
performedbyadjustingPEEP,monitoringoxygenationbyperipheraloxygen
saturationorarterialoxygenmeasurementviabloodgassampling,andmeasuring
theassociatedcardiacoutput.TheprocessisrepeatedatvariousPEEPsettings,
andtheresultsarerecorded.Thepractitionercanthenreviewtheresultsand
determinetheoptimalPEEPforthatpatientatthattime.Thisprocedureisnot
generallyperformedintheEDbutunderliestheassociationofventilationstrategy
andcardiacoutput.

Renal,hepatic,andgastrointestinaleffects

Positivepressureventilationisresponsibleforanoveralldeclineinrenalfunction
withdecreasedurinevolumeandsodiumexcretion.

Hepaticfunctionisadverselyaffectedbydecreasedcardiacoutput,increased
hepaticvascularresistance,andelevatedbileductpressure.

Thegastricmucosadoesnothaveautoregulatorycapability.Thus,mucosal
ischemiaandsecondarybleedingmayresultfromdecreasedcardiacoutputand
increasedgastricvenouspressure.

IndicationsForMechanicalVentilation
Theprincipalindicationsformechanicalventilationareairwayprotectionand
respiratoryfailure.Acompromisedairway,oranairwayatriskofcompromise,may
beidentifiedbyphysicalexaminationandancillarytesting.

RespiratoryfailureintheEDisalmostalwaysandmostappropriatelyaclinical
diagnosis.Thedecisiontointubateandmechanicallyventilateortoinstitute
noninvasiveventilationsupportisgenerallymadepurelyonclinicalgroundswithout
delayforlaboratoryevaluation.

Respiratoryfailuremayalsobeeasilyidentifiedwithlaboratoryorpulmonary
functiondata.ObtainingaPaCO2isusefultoconfirmrespiratoryfailurewhena
broaderdifferentialdiagnosisexistsforexample,obtundedpatientswhomaybe
hypercarbicbutmighthaveareversiblemetabolicortoxicologicaletiologyfortheir
conditionsbutadequatestabilizationandventilationofthesepatientsshouldnot
bedelayedtowaitforlaboratoryresults.

Mechanicalventilationisindicatedforbothhypercapnicrespiratoryfailureand
hypoxemicrespiratoryfailure.Itisalsoindicatedfortreatmentofcertaincritical
conditionssuchascorrectionoflifethreateningacidemiainthesettingofsalicylate
intoxication,forintentionalhyperventilationinthesettingofmajorheadinjurywith
elevatedintracranialpressure,forsuspicionofclinicalbrainherniationfromany
cause,orforapatientincriticalconditionwithcyclicantidepressanttoxicity.

Laboratorycriteria

Table.LaboratoryCriteriaforMechanicalVentilation(OpenTableinanewwindow)

LaboratoryCriteriaforMechanicalVentilation
Bloodgases PaO2<55mmHg
PaCO2>50mmHgandpH<7.32
Pulmonaryfunctiontests Vitalcapacity<10mL/kg
Negativeinspiratoryforce<25cmH2O
FEV 1<10mL/kg

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Clinicalcriteria

Seethelistbelow:

Apneaorhypopnea
Respiratorydistresswithalteredmentation
Clinicallyapparentincreasingworkofbreathingunrelievedbyother
interventions
Obtundationandneedforairwayprotection

Othercriteria

Seethelistbelow:

Controlledhyperventilation(eg,inheadinjury).
Severecirculatoryshock

Noabsolutecontraindicationsexisttomechanicalventilation.Theneedfor
mechanicalventilationisbestmadeearlyonclinicalgrounds.Agoodruleofthumb
isifthepractitioneristhinkingthatmechanicalventilationisneeded,thenit
probablyis.Waitingforreturnoflaboratoryvaluescanresultinunnecessary
morbidityormortality.

GuidelinesforVentilatorSettings
Seetheimagebelowforsuggestedinitialsettings.

Initialventilatorsettingsinvariousdiseasestates.

Modeofventilation

Themodeofventilationshouldbetailoredtotheneedsofthepatient.Inthe
emergentsituation,thepractitionermayneedtoorderinitialsettingsquickly.SIMV
andA/Careversatilemodesthatcanbeusedforinitialsettings.Inpatientswitha
goodrespiratorydriveandmildtomoderaterespiratoryfailure,PSVisagoodinitial
choice.

Tidalvolume

Observationsoftheadverseeffectsofbarotraumaandvolutraumahaveledto
recommendationsoflowertidalvolumesthaninyearspast,whentidalvolumesof
1015mL/kgwereroutinelyused.

AninitialTVof58mL/kgofidealbodyweightisgenerallyindicated,withthe
lowestvaluesrecommendedinthepresenceofobstructiveairwaydiseaseand
ARDS.ThegoalistoadjusttheTVsothatplateaupressuresarelessthan35cm
H2O.

Respiratoryrate

Arespiratoryrate(RR)of812breathsperminuteisrecommendedforpatientsnot
requiringhyperventilationforthetreatmentoftoxicormetabolicacidosis,or
intracranialinjury.Highratesallowlesstimeforexhalation,increasemeanairway
pressure,andcauseairtrappinginpatientswithobstructiveairwaydisease.The
initialratemaybeaslowas56breathsperminuteinasthmaticpatientswhen
usingapermissivehypercapnictechnique.

Supplementaloxygentherapy

ThelowestFiO2thatproducesanarterialoxygensaturation(SaO2)greaterthan
90%andaPaO2greaterthan60mmHgisrecommended.Nodataindicatethat
prolongeduseofanFiO2lessthan0.4damagesparenchymalcells.

Inspiration/expirationratio

Thenormalinspiration/expiration(I/E)ratiotostartis1:2.Thisisreducedto1:4or
1:5inthepresenceofobstructiveairwaydiseaseinordertoavoidairtrapping
(breathstacking)andautoPEEPorintrinsicPEEP(iPEEP).UseofinverseI/E
maybeappropriateincertainpatientswithcomplexcomplianceproblemsinthe
settingofARDS.

Inspiratoryflowrates

InspiratoryflowratesareafunctionoftheTV,I/Eratio,andRRandmaybe

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controlledinternallybytheventilatorviatheseothersettings.Ifflowratesareset
explicitly,60L/ministypicallyused.Thismaybeincreasedto100L/mintodeliver
TVsquicklyandallowforprolongedexpirationinthepresenceofobstructiveairway
disease.

Positiveendexpiratorypressure

Positiveendexpiratorypressure(PEEP)hasseveralbeneficialeffectsand,when
usedatoptimallevelsincombinationwithlowtidalvolumes,mayreducethe
incidenceofventilatorinducedlunginjury.Inparticular,thereisasignificantamount
ofongoingresearchevaluatingtheuseofhighlevelsofPEEPinacutelunginjury
(ALI)andARDS.PEEPhasbeenfoundtoreducetheriskofatelectasistraumaby
increasingthenumberof"open"alveoliparticipatinginventilation,thereby
minimizingtraumaduetothecyclicalcollapseandreopeningofalveoli.However,
notethatindiseasestatessuchasARDS,thedegreetowhichalveolifunctionhas
beencompromisedvariestremendouslywithinthelungsandthereisnosingleideal
PEEPappropriateforallalveolirather,acompromisePEEPmustbeselected.

Inadditiontoalveolarrecruitment,anadditionalbeneficialeffectofPEEPistoshift
lungwaterfromthealveolitotheperivascularinterstitialspace.Itdoesnot
decreasethetotalamountofextravascularlungwater.Thisisofclearbenefitin
casesofcardiogenicaswellasnoncardiogenicpulmonaryedema.Anadditional
benefitofPEEPincasesofCHFistodecreasevenousreturntotherightsideof
theheartbyincreasingintrathoracicpressure.

ApplyingphysiologicPEEPof35cmH2Oiscommontopreventdecreasesin
functionalresidualcapacityinthosewithnormallungs.Thereasoningforincreasing
levelsofPEEPincriticallyillpatientsistoprovideacceptableoxygenationandto
reducetheFiO2tonontoxiclevels(FiO2<0.5).ThelevelofPEEPmustbe
balancedsuchthatexcessiveintrathoracicpressure(witharesultantdecreasein
venousreturnandriskofbarotrauma)doesnotoccur.

Sensitivity

Withassistedventilation,thesensitivitytypicallyissetat1to2cmH2O.The
developmentofiPEEPincreasesthedifficultyingeneratinganegativeinspiratory
forcesufficienttoovercomeiPEEPandthesetsensitivity.Newerventilatorsoffer
theabilitytosensebyinspiratoryflowinsteadofnegativeforce.Flowsensing,if
available,maylowertheworkofbreathingassociatedwithventilatortriggering.

MonitoringDuringVentilatorySupport
Cardiacmonitor,bloodpressure,andpulseoximetry(SaO2)arerecommended.The
authorspracticewithstablepatientsistotitratedownFiO2totheminimumvalue
necessarytomaintainmaximalSaO2.Anarterialbloodgas(ABG)measurementis
frequentlyobtained1015minutesaftertheinstitutionofmechanicalventilation.
ThemeasuredarterialPaO2shouldverifythetranscutaneouspulseoximetry
readingsanddirectthereductionofFiO2toavaluelessthan0.5.Themeasured
PaCO2cansuggestadjustmentsofminuteventilationbutshouldbeinterpretedin
lightofthepatient'soverallacidbasestatus.Forexample,fullcorrectionofPaCO2
inachronicallyhypercarbicCOPDpatientwillleadtounopposedmetabolic
alkalosis.

Reasonablealternativestoarterialbloodgasmeasurementinmorestablepatients
includemeasuringthevenousbloodgas,whichwillgivevaluesclosetoarterialpH
andPaCO2ormonitoringanendtidalCO2.Anadditionaladvantageofendtidal
CO 2monitoringisthatitcandetectacuteventilatordysfunctionsuchas
endotrachealtubeobstructionordislodgement. [10]

Peakinspiratoryandplateaupressuresshouldbeassessedfrequently,althoughit
shouldberecognizedthatbothpressureswillbeincreasedbyextrapulmonary
pressure,forexamplefromstiffchestwallsoradistendedabdomen,anddonot
reflectthetrueriskofbarotrauma.Ingeneral,however,parametersmaybealtered
tolimitpressurestolessthan35cmH2O.Expiratoryvolumeischeckedinitially
andperiodically(continuouslyifventilatoriscapable)toensurethatthesettidal
volumeisdelivered.Anyindicationofanairleakmustpromptasearchfor
underinflatedtubecuffs,opentubingports,orworseningpneumothorax.Inpatients
withairwayobstruction,monitorautoPEEP.

InitialVentilatorSettingsinVariousDiseaseStates
IntheEDsetting,patientsfrequentlyrequirefullrespiratorysupport.FormostED
patientswhoareparalyzedasacomponentofrapidsequenceinduction,CMVand
A/Caregoodchoicesasaninitialventilatorymode.SIMVmaybebettertolerated
innonparalyzedpatientswithobstructiveairwaydiseaseandanintactrespiratory
effort.PSVcanbeusedwhenrespiratoryeffortisintactandrespiratoryfailureis
notsevere. [11]

Noninvasiveventilation(CPAP,BiPAP)canbeusedeffectivelyinmanycasesof
severeCOPDandCHFtoavoidtrachealintubation.Initialventilatorsettingsare
guidedbythepatient'spulmonarypathophysiologyandclinicalstatus.Adjustments
canthenbemadetolimitbarotrauma,volutrauma,andoxygentoxicity.CPAPand
BiPAPrequirealert,cooperativepatientscapableofindependentlymaintainingtheir
airwaysandarecontraindicatedinthepresenceoffacialtrauma.
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AsthmaandCOPD

HypoxiacangenerallybecorrectedthroughahighFiO2,butpatientswithairway
obstructionareatriskofhighairwaypressures,breathstackingleadingtointrinsic
PEEP,barotrauma,andvolutrauma.TominimizeintrinsicPEEP,itis
recommendedthatexpiratoryflowtimebeincreasedasmuchaspossibleandthat
tidalvolumesandrespiratoryratesaresetatlowvalues. [12]Permissivehypercapnia
enablesalowrespiratoryrateof68breathsperminutetobeused,aswellasan
increasedI:Eratioof1:1.5or1:2.

PEEPmaybenefitsomeasthmaticpatientsbyreducingtheworkofbreathingand
maintainingopenairwaysduringexpiration,butitseffectsaredifficulttopredictand
mustbecarefullymonitored.PatientswithasthmaandCOPDareatparticularrisk
ofbarotraumaticprogressiontotensionpneumothorax,acomplicationthatcan
initiallyappearsimilartorunawayintrinsicPEEP.Theseconditionsmaybe
distinguishedbytemporarydetachmentofthepatientfrompositivepressure
ventilationifexhalationresultsinarecoveryofpulseornormalbloodpressure,the
diagnosisisintrinsicPEEP.

CPAPandBiPAPwillbenefitsomeasthmaticsandmanypatientswithCOPD.
Thesepatientswillrequirecarefulmonitoringastheycaneasilydeterioratefrom
hypercarbia,intrinsicPEEP,orrespiratoryexhaustion.Nevertheless,a
CochraneDatabaseSystematicReviewanalysisoftrialsincludingpatientswith
severeCOPDexacerbationsdemonstratedthattheuseofnoninvasivepositive
pressureventilationabsolutelyreducedtherateofendotrachealintubationby59%
(95%confidenceinterval[CI]ofrelativerisk[RR]:0.330.53),thelengthofhospital
stayby3.24days(95%CI:2.064.44days),andtheriskofmortalityby48%(95%
CIofRR:0.350.76). [2]

Acuterespiratorydistresssyndrome

ARDSlungsaretypicallyirregularlyinflamedandhighlyvulnerabletoatelectasisas
wellasbarotraumaandvolutrauma.Theircomplianceistypicallyreduced,andtheir
deadspaceincreased.Thestandardofcarefortheventilatorymanagementof
patientswithARDSchangeddramaticallyin2000withthepublicationofalarge
multicenter,randomizedtrialcomparingpatientswithARDSinitiallyventilatedwith
eitherthetraditionaltidalvolumeof12mL/kgoralowerTVof6mL/kg.Thistrial
wasstoppedearlybecausethelowertidalvolumewasfoundtoreducemortalityby
anabsolute8.8%(P=0.007).Intriguingly,plasmainterleukin6concentrations
decreasedinthelowTVgrouprelativetothehighTVgroup(P<0.001),suggesting
adecreaseinlunginflammation. [13,14,15,16]

TheauthorsrecommendinitiatingventilationofpatientswithARDSwithA/C
ventilationatatidalvolumeof6mL/kg,withaPEEPof5andinitialventilatoryrate
of12,titrateduptomaintainapHgreaterthan7.25.Thereisnotyetadequate
evidencetoroutinelyrecommendPEEPgreaterthan5cmH2O,but,in
appropriatelymonitoredcircumstances,itmaybeattempted. [17]IntrinsicPEEPmay
occurinpatientswithARDSathighventilatoryratesandshouldbewatchedforand
treatedbyreducingtherateofventilationunderdirectobservationuntilplateau
pressuresdecrease.Theauthorsrecommendatargetplateaupressureoflessthan
30cmH2O.Onceapatienthasbeenstabilizedwithadequatetidalvolumesata
plateaupressureoflessthan30cmH2O,consideringatrialofpressurecycled
ventilationisreasonable.

Severalrecruitmentmaneuvershavebeendevisedtoincreasetheproportionof
alveoliventilatedinARDS.Thesetechniquestypicallyattemptshorttermincreased
PEEPorvolumetoopenoccludedorcollapsedalveoli.Gattinonietal,forexample,
foundthatamongARDSpatientsundergoingwholelungCT,applying45cmH2O
PEEPrecruitedameanof13%newlungtissue. [18]

ArecentmetaanalysisthatcomparedhighversuslowlevelsofPEEPinpatients
withALIandARDSfoundnodifferenceinmortalitybeforehospitaldischarge
amongststudiesthatusedthesametidalvolumeinbothcontrolandintervention
arms. [17]Inasubsequentsubgroupanalysisthatassessedlungprotective
ventilation(lowtidalvolume,highPEEP)versusconventionalmechanical
ventilation,theauthorsfoundadecreaseinmortalitywiththeuseofalung
protectiveventilationstrategy.Thesamereviewalsofoundthathighlevelsof
PEEPdoimproveoxygenationinpatientswithALIandARDS.

Inarecentprospective,randomized,controlledtrial,Guerinetalexaminedwhether
earlypronepositioningduringmechanicalventilationcanimproveoutcomesin
patientswithsevereARDS.Theauthorsfoundthatboththe28dayandunadjusted
90daymortalitiesinthepronegroupweresignificantlylower(16%and23.6%,
respectively)thaninthesupinegroup(32.8%and41%,respectively). [19]Although
theyfoundnodifferencebetweenthegroupswithregardtodurationofinvasive
mechanicalventilationorlengthofstayintheICU,theyfoundahigherincidenceof
cardiacarrestinthesupinegroup(31%vs16%inthepronegroup).

Permissivehypercapniaisaventilatorystrategythathaswonparticularfavorinthe
managementofpatientswithARDSandCOPD/asthmawhowouldotherwise
requiredangerouslyhightidalvolumesandairwaypressures.Inpatientswithout
contraindicationssuchasheadinjury,cerebrovascularaccident(CVA),elevated
intracranialpressure,orcardiovascularinstability,permissivehypercapniahas
permittedmuchdecreasedtidalvolumes,airwaypressures,andrespiratoryrates,
thoughevidenceforadecreaseinmortalityratesisincomplete. [20]Thetypically

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recommendedtargetpHis7.25.

Noninvasiveventilatorystrategieshavemetwithlittlesuccessinthetreatmentof
patientswithARDS.Theauthorsrecommendgreatcautionandclosemonitoringif
noninvasivepositivepressureventilation(NIPPV)isattemptedamongpatientswith
ARDS.

IntrialsofNIPPVamongpatientswithundifferentiatedhypoxemia,thepresenceof
pneumoniaorARDSwasassociatedwithsignificantlyincreasedriskoffailure.
SomesubgroupsofpatientswithARDSmaybenefitfromNIPPVhowever,
Antonellietaldemonstratedgreatersuccessinapplyingnoninvasivepositive
pressureventilationtopatientswithlowersimplifiedacutephysiologyscoresand
higherPaO2/FiO2ratios. [21]

Congestiveheartfailure

CHFrespondsverywelltopositivepressureventilation,whichservesthedualrole
ofopeningalveoliandreducingpreload.ManypatientswithCHFbenefitfromatrial
ofnoninvasiveCPAPorBiPAP.Someofthesepatientswillclinicallyimproveso
rapidlythatadmittingservicesmayrequestdiscontinuationofnoninvasive
ventilatorysupport,butgreatcautionmustbemaintainedifthisisattempted,as
fluidmayunpredictablyreaccumulate,resultinginhypoxiaandrespiratoryfailure.

Intubatedpatientsusuallymanagetoadequatelyoxygenate.PEEPcanbe
increasedastoleratedtoimproveoxygenationandreducepreload.However,in
somepatients,cardiacoutputcanbeparticularlydependentonpreloadandsuch
patientsmayeasilydeveloppostintubationhypotension.Managementofthis
commoncomplicationincludesacombinationoffluidtherapy,discontinuationof
nitroglycerinorothermedicaltherapies,and,ifnecessary,medicalormechanical
hemodynamicsupportinterventions. [22]

Traumaticbraininjury

Hyperventilationwastraditionallyrecommendedinthemanagementofsevere
traumaticbraininjury,butrecentstudieshavedemonstratedpooroutcomesthought
tobesecondarytoexcessivecerebralvasoconstrictionandreducedcerebral
perfusion.However,retrospectivedatahavedemonstrateddecreasedmortality
amongtraumaticbraininjuryventilatedtoPCO2between30and39mmHg,
thoughthishasnotbeenprospectivelyvalidated. [23,24]

VentilatorTroubleshootingManaging
ComplicationsintheED
Thedifferentialdiagnosisoftheclinicallydeteriorating,mechanicallyventilated
patientiswideandincludesendotrachealtubeorventilatordysfunction,improper
ventilatorsettings,pain,anxiety,andpulmonaryorextrapulmonarydisease
processes. [10]ThecomplicationsmostcommonlyencounteredintheEDinclude
hypoxia,hypotension,highpressurealarms,andlowexhaledvolumealarms.

Intubatedpatientswhodevelophemodynamicinstabilitywithrespiratory
compromiseshouldimmediatelybedisconnectedfromtheventilatorandmanually
ventilatedwith100%FiO2.

Oneofthefirstdiagnosesthatshouldbeconsideredinanyhemodynamically
unstablepatientundergoingpositivepressureventilationistensionpneumothorax.
Thisisaclinicaldiagnosisandshouldbedetectedandtreatedwithneedle
decompressionpriortoobtainingachestradiograph.

Aseconddiagnosistoexclude,particularlyinpatientswithasthmaorCOPD,is
intrinsicPEEP.Asdiscussed,intrinsicPEEPoccursasaresultofincomplete
exhalation,whichsubsequentlyleadstohyperinflation,increasedintrathoracic
pressure,decreasedvenousreturn,anddecreasedpreload.Thediagnosisof
intrinsicPEEPmaybemadebyperforminganendexpiratoryholdorbydetectinga
nonzeroendexpiratoryflowontheventilator.ThetreatmentforintrinsicPEEPis
toallowforlungdeflation,thentoaltermechanicalventilationsettingstoallowfor
longerexpiratorytimesbydecreasingtherespiratoryrate,decreasingthetidal
volume,orchangingtheinspiratorytoexpiratoryratio.

Otherdiagnosestoconsiderareanobstructedendotrachealtubeandan
endotrachealtubecuffleak.Inthecaseofendotrachealtubeobstruction,attempts
tomanuallyventilatethepatientaremetwithasignificantamountofresistanceand
highpressurealarmsmaysound.Endotrachealtubeobstructionmaybecausedby
extrinsiccompressiontubeplugswithmucus,blood,orforeignbodiestubekinks
ortubebiting.Tubesuctioningandadequatepatientsedationarerecommended
afterothercausesofobstructionareruledout.

Measurementofpeakpressuresandplateaupressuresmaybehelpfulinidentifying
thelocationofresistance,especiallyifgraphicalrepresentationofairwaypressures
isavailable.Peakpressure,whichreflectsresistancetoairflow,ismeasuredbythe
ventilatorduringinspiration.Plateaupressureisthoughttoreflectpulmonary
complianceandcanbemeasuredbyapplyingabriefinspiratorypauseafter
ventilation.Highpeakpressurewithnormalplateaupressuresindicatesincreased
resistancetoflow,suchasendotrachealtubeobstructionorbronchospasm.An
increaseinbothpeakandplateaupressuressuggestdecreasedlungcompliance,
whichmaybeseenindiseasestatessuchaspneumonia,ARDS,pulmonary

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30/4/2016 VentilatorManagement:IntroductiontoVentilatorManagement,ModesofMechanicalVentilation,MethodsofVentilatorySupport
edema,andabdominaldistention.

Lowexhaledvolumealarmsaretriggeredbyairleaks.Thesearemostfrequently
secondarytoventilatorytubingdisconnectfromthepatient'strachealtubebutwill
alsooccurintheeventofballoondeflationortrachealtubedislodgement.Tube
placement,ballooninflation,andconnectiontotheventilatorshouldbecarefully
verified.

Hypoxiaafterintubationmayoccursecondarytohypoventilation,worseningcardiac
shunting,inadequateFiO2,mainstemintubation,aspiration,tubedislodgement,or
pulmonaryedema.Thecausesofhighairwaypressuresandlowexhaledvolumes
describedabovecanresultinhypoxiaiftheycausehypoventilation.Despitetheuse
ofnumeroussafetyprecautions,casesareoccasionallydocumentedofventilators
beingconnectedtocompressedairornitrousoxideratherthanoxygen.Increasing
FiO2andadjustingventilatorysettingstoincreasePEEPorrespiratoryrateare
usefulfirststepsafterexcludingequipmentfailureandmechanicalcausesof
hypoxia.

Hypotensionafterintubationisusuallyattributabletodiminishedcentralvenous
bloodreturntotheheartsecondarytoelevatedintrathoracicpressures.Thiscanbe
treatedwithfluidinfusionsand/oradjustmentofventilatorysettingstolower
intrathoracicpressure(reducingPEEP,tidalvolume,and,ifairtrappingis
suspected,respiratoryrate).Hypotensionmayalsobesecondarytovasovagal
reactiontointubation,rapidsequenceinduction,sedation,andtension
pneumothorax.

SupportiveCare
Whiletheroleoftheemergencyphysicianhastraditionallybeenlimitedto
intubationandinitiationofmechanicalventilation,intubatedpatientsarespendinga
greaterportionoftheirhospitalstayintheEDsecondarytodecreasedavailabilityof
ICUbeds.Inthissetting,itbecomesimportanttoinitiatepreventativemeasuresto
decreasetheincidenceofthesecondarycomplicationsofmechanicalventilation,
suchasventilatorassociatedpneumonia(VAP),venousthromboembolism(VTE),
andstressrelatedmucosalinjury.

VAPisdefinedaspneumoniainamechanicallyventilatedpatientthatisnot
clinicallypresentatthetimeofintubation. [25]Thetimeframefordevelopmentof
VAPistypically48hoursormoreafterintubation,asthisiswhenthedisease
typicallymanifestsitselfclinically.VAPhasbeenimplicatedasthemostcommon
infectiouscomplicationoccurringinICUpatientsandresultsinprolongedICUand
hospitallengthsofstay,prolongeddurationofmechanicalventilation,andoverall
increasedcostofcare. [10]

EvidencesuggeststhatprehospitalandEDintubation,inadditiontoEDlengthof
stay,areindependentriskfactorsforthedevelopmentofVAP. [10,26]These
findings,whencombinedwiththesignificantmorbidityandmortalityassociatedwith
VAP,conferupontheEDphysicianaresponsibilitytoimplementmeasuresto
reducetheriskofVAPintheED.Theseinterventionsareaimedatreducingthe
riskofaspirationanddecreasingbacterialcolonization.

TheCentersforDiseaseControlandPreventionpublishedGuidelinesfor
PreventingHealthCareAssociatedPneumoniain2003,inwhichtheyrecommend
placingthepatientinasemiuprightposition,withtheheadofthebedelevated30
45o,inordertoreducetheriskofaspiration. [27]Othermeasuressuchasearly
placementofanasogastrictubeandoralcarewithasofttoothbrushand
chlorhexidinerinsesmayalsobeconsidered. [25]Lastly,endotrachealcuffpressures
shouldbemonitoredinitiallyafterintubationandevery4hoursthereafter,withgoal
pressuresof2030cmH2O,asincreasedriskofpneumoniahasbeenassociated
withcuffpressureslessthan20cmH2O.

InadditiontoVAP,mechanicallyventilatedICUpatientsarealsoathighriskfor
developmentofVTEandstressrelatedinjuryofthegastrointestinalmucosa.In
patientswithoutcontraindications,unfractionatedorlowmolecularweightheparin
shouldbeconsideredinthesepatientsforVTEprophylaxis.Astheincidenceof
gastricmucosalerosionshasbeenfoundtobegreaterthan75%inICUpatients
within24hoursofadmission,gastrointestinalprophylaxiswithaprotonpump
inhibitor,sucralfate,orhistaminereceptorantagonistshouldbeconsideredin
patientswhoareathighriskofgastrointestinalhemorrhage. [10]Thesehighrisk
patientshavebeenidentifiedasthosewithcoagulopathy,historyofgastrointestinal
bleeding,historyofgastritisorpepticulcer,ormechanicalventilationformorethan
48hours.

ContributorInformationandDisclosures
Author
AllonAmitai,MDInternationalEmergencyMedicineFellow,RhodeIslandHospitalConsultingStaff,Memorial
HospitalofRhodeIslandDoctoringPreceptor,BrownUniversityMedicalSchool

AllonAmitai,MDisamemberofthefollowingmedicalsocieties:AmericanCollegeofEmergencyPhysicians

Disclosure:Nothingtodisclose.

Coauthor(s)
RichardHSinert,DOProfessorofEmergencyMedicine,ClinicalAssistantProfessorofMedicine,Research

http://emedicine.medscape.com/article/810126overview#showall 9/11
30/4/2016 VentilatorManagement:IntroductiontoVentilatorManagement,ModesofMechanicalVentilation,MethodsofVentilatorySupport
Director,StateUniversityofNewYorkCollegeofMedicineConsultingStaff,ViceChairinChargeofResearch,
DepartmentofEmergencyMedicine,KingsCountyHospitalCenter

RichardHSinert,DOisamemberofthefollowingmedicalsocieties:AmericanCollegeofPhysicians,Society
forAcademicEmergencyMedicine

Disclosure:Nothingtodisclose.

AllisonRegan,MDResidentPhysician,DepartmentofEmergencyMedicine,StateUniversityofNewYork
DownstateMedicalCenter,KingsCountyHospitalCenter,Brooklyn

AllisonRegan,MDisamemberofthefollowingmedicalsocieties:AmericanCollegeofEmergencyPhysicians,
AmericanMedicalAssociation,EmergencyMedicineResidents'Association

Disclosure:Nothingtodisclose.

AshikaJain,MDAssistantProfessor,DepartmentofEmergencyMedicine,StateUniversityofNewYork
DownstateCollegeofMedicineSurgicalIntensivist,DepartmentofSurgery,DivisionofTraumaCriticalCare,
KingsCountyHospitalCenter,Brooklyn

AshikaJain,MDisamemberofthefollowingmedicalsocieties:AmericanCollegeofEmergencyPhysicians,
SocietyofCriticalCareMedicine,AmericanAssociationofPhysiciansofIndianOrigin

Disclosure:Nothingtodisclose.

SpecialtyEditorBoard
FranciscoTalavera,PharmD,PhDAdjunctAssistantProfessor,UniversityofNebraskaMedicalCenterCollege
ofPharmacyEditorinChief,MedscapeDrugReference

Disclosure:ReceivedsalaryfromMedscapeforemployment.for:Medscape.

PaulBlackburn,DO,FACOEP,FACEPAttendingPhysician,DepartmentofEmergencyMedicine,Maricopa
MedicalCenter

PaulBlackburn,DO,FACOEP,FACEPisamemberofthefollowingmedicalsocieties:AmericanCollegeof
EmergencyPhysicians,ArizonaMedicalAssociation,AmericanCollegeofOsteopathicEmergencyPhysicians,
AmericanMedicalAssociation

Disclosure:Nothingtodisclose.

ChiefEditor
ZabMosenifar,MD,FACP,FCCPGeriandRichardBrawermanChairinPulmonaryandCriticalCareMedicine,
ProfessorandExecutiveViceChairman,DepartmentofMedicine,MedicalDirector,Women'sGuildLung
Institute,CedarsSinaiMedicalCenter,UniversityofCalifornia,LosAngeles,DavidGeffenSchoolofMedicine

ZabMosenifar,MD,FACP,FCCPisamemberofthefollowingmedicalsocieties:AmericanCollegeofChest
Physicians,AmericanCollegeofPhysicians,AmericanFederationforMedicalResearch,AmericanThoracic
Society

Disclosure:Nothingtodisclose.

AdditionalContributors
StevenAConrad,MD,PhDChief,DepartmentofEmergencyMedicineChief,MultidisciplinaryCriticalCare
Service,Professor,DepartmentofEmergencyandInternalMedicine,LouisianaStateUniversityHealthSciences
Center

StevenAConrad,MD,PhDisamemberofthefollowingmedicalsocieties:AmericanCollegeofChest
Physicians,AmericanCollegeofCriticalCareMedicine,AmericanCollegeofEmergencyPhysicians,American
CollegeofPhysicians,InternationalSocietyforHeartandLungTransplantation,LouisianaStateMedical
Society,ShockSociety,SocietyforAcademicEmergencyMedicine,SocietyofCriticalCareMedicine

Disclosure:Nothingtodisclose.

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