10/5/2016 Chronicobstructivepulmonarydisease:Definition,clinicalmanifestations,diagnosis,andstagingUpToDate

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Authors: MeiLanKingHan,MD,MS,MarkTDransfield,MD,FernandoJMartinez,MD,MS
SectionEditor: JamesKStoller,MD,MS
DeputyEditor: HelenHollingsworth,MD

ContributorDisclosures

Alltopicsareupdatedasnewevidencebecomesavailableandourpeerreviewprocessiscomplete.
Literaturereviewcurrentthrough:Sep2016.|Thistopiclastupdated:Apr08,2016.

INTRODUCTIONChronicobstructivepulmonarydisease(COPD)isacommonrespiratorycondition
characterizedbyairflowlimitation[1,2].Itaffectsmorethan5percentofthepopulationandisassociatedwith
highmorbidityandmortality[3].ItisthethirdrankedcauseofdeathintheUnitedStates,killingmorethan
120,000individualseachyear[4].Asaconsequenceofitshighprevalenceandchronicity,COPDcauseshigh
resourceutilizationwithfrequentclinicianofficevisits,frequenthospitalizationsduetoacuteexacerbations,and
theneedforchronictherapy(eg,supplementaloxygentherapy,medication)[1].

EstablishingacorrectdiagnosisofCOPDisimportantbecauseappropriatemanagementcandecrease
symptoms(especiallydyspnea),reducethefrequencyandseverityofexacerbations,improvehealthstatus,
improveexercisecapacity,andprolongsurvival[5].Ascurrentandformersmokersarealsoatriskforanumber
ofothermedicalproblemsforwhichtreatmentisverydifferent,respiratorysymptomsshouldnotbeattributedto
COPDwithoutappropriateevaluationanddiagnosis.

Thedefinition,clinicalmanifestations,diagnosticevaluation,andstagingofCOPDarediscussedinthistopic
review.Theriskfactors,naturalhistory,prognosis,andtreatmentofCOPDarediscussedseparately.(See
"Chronicobstructivepulmonarydisease:Riskfactorsandriskreduction"and"Chronicobstructivepulmonary
disease:Prognosticfactorsandcomorbidconditions"and"Managementofstablechronicobstructivepulmonary
disease"and"Managementofexacerbationsofchronicobstructivepulmonarydisease".)

DEFINITIONSThedefinitionofchronicobstructivepulmonarydisease(COPD)anditssubtypes
(emphysema,chronicbronchitis,andchronicobstructiveasthma)andtheinterrelationshipsbetweentheclosely
relateddisordersthatcauseairflowlimitationprovideafoundationforunderstandingthespectrumofpatient
presentations.

SeveralfeaturesofCOPDpatientsidentifyindividualswithdifferentprognosesand/orresponsestotreatment.
Whetherthesefeaturesidentifyseparate"phenotypes"ofCOPDorreflectdiseaseseverityremainsunclear[6].
However,evaluationofthesefeaturescanhelpguideclinicalmanagement,andtheiruseinclassificationof
patientsisnowrecommended[7,8].(See'Staging'below.)

COPDTheGlobalInitiativeforChronicObstructiveLungDisease(GOLD),aprojectinitiatedbytheNational
Heart,Lung,andBloodInstitute(NHLBI)andtheWorldHealthOrganization(WHO),definesCOPDasfollows
[7]:

"Chronicobstructivepulmonarydisease(COPD),acommonpreventableandtreatabledisease,ischaracterized
bypersistentairflowlimitationthatisusuallyprogressiveandassociatedwithanenhancedchronicinflammatory
responseintheairwaysandthelungtonoxiousparticlesorgases.Exacerbationsandcomorbiditiescontribute
totheoverallseverityinindividualpatients."

ChronicbronchitisChronicbronchitisisdefinedasachronicproductivecoughforthreemonthsineachof
twosuccessiveyearsinapatientinwhomothercausesofchroniccough(eg,bronchiectasis)havebeen

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excluded[9].Itmayprecedeorfollowdevelopmentofairflowlimitation[9,10].Thisdefinitionhasbeenusedin
manystudies,despitethearbitrarilyselectedsymptomduration.

EmphysemaEmphysemaisapathologicaltermthatdescribessomeofthestructuralchangessometimes
associatedwithCOPD.Thesechangesincludeabnormalandpermanentenlargementoftheairspacesdistalto
theterminalbronchiolesthatisaccompaniedbydestructionoftheairspacewalls,withoutobviousfibrosis(ie,
thereisnofibrosisvisibletothenakedeye)[11].Exclusionofobviousfibrosiswasintendedtodistinguishthe
alveolardestructionduetoemphysemafromthatduetotheinterstitialpneumonias.However,manystudies
havefoundincreasedcollageninthelungsofpatientswithmildCOPD,indicatingthatfibrosiscanbea
componentofemphysema[12,13].Whileemphysemacanexistinindividualswhodonothaveairflow
obstruction,itismorecommonamongpatientswhohavemoderateorsevereairflowobstruction[7,14].

Thevarioussubtypesofemphysema(eg,proximalacinar,panacinar,distalacinar)aredescribedbelow.(See
'Pathology'below.)

AsthmaTheGlobalInitiativeforAsthmagivesthefollowingdefinitionofasthma:"Asthmaisachronic
inflammatorydisorderoftheairwaysinwhichmanycellsandcellularelementsplayarole.Thechronic
inflammationisassociatedwithairwayresponsivenessthatleadstorecurrentepisodesofwheezing,
breathlessness,chesttightness,andcoughing,particularlyatnightorintheearlymorning.Theseepisodesare
usuallyassociatedwithwidespread,butvariable,airflowobstructionwithinthelungthatisoftenreversibleeither
spontaneouslyorwithtreatment[15]."

Interrelationshipsamongasthma,chronicbronchitis,andemphysemaEarlydefinitionsofCOPD
distinguisheddifferenttypes(ie,chronicbronchitis,emphysema,asthma),adistinctionthatisnotincludedinthe
currentdefinition[1618].However,individualpatientspresentwithaspectrumofmanifestationsofCOPDand
relatedprocesses,sounderstandingthetypesofCOPD,asillustratedinthefigure(figure1),canbehelpful
diagnostically.Importantpointsabouttheirinterrelationshipinclude:

PatientswithasthmawhoseairflowobstructioniscompletelyreversiblearenotconsideredtohaveCOPD
(subsetnineinthefigure).

PatientswithasthmawhoseairflowobstructiondoesnotremitcompletelyareconsideredtohaveCOPD
(subsetssix,seven,andeightinthefigure).TheetiologyandpathogenesisoftheCOPDinsuchpatients
maybedifferentfromthatofpatientswithchronicbronchitisoremphysema.

Chronicbronchitisandemphysemawithairflowobstructioncommonlyoccurtogether(subsetfiveinthe
figure)[19].Someofthesepatientsmayalsohaveasthma(subseteightinthefigure).

Individualswithasthmamaydevelopachronicproductivecough,eitherspontaneouslyorduetoexposure
(eg,cigarettesmoke,allergen).Suchpatientsareoftenreferredtoashavingasthmaticbronchitis,although
thisterminologyhasnotbeenofficiallyendorsedinclinicalpracticeguidelines(subsetsixinthefigure).

Personswithchronicbronchitis,emphysema,orbotharenotconsideredtohaveCOPDunlesstheyhave
airflowobstruction(subsetsone,two,andeleveninthefigure)[20,21].

Patientswithairflowobstructionduetodiseasesthathaveaknownetiologyoraspecificpathology(eg,
cysticfibrosis,bronchiectasis,obliterativebronchiolitis)arenotconsideredtohaveCOPD(subset10inthe
figure).However,theseexclusionsarelooselydefined[22].

AsthmaCOPDoverlapsyndromeConsistentwiththeideathatsignificantoverlapexistsamongthe
differenttypesofCOPD,manyindividualshavebronchialinflammationwithfeaturesofbothasthmaandchronic
bronchitis/emphysema[7,23,24].Similarly,thenatureofthebronchialinflammationvarieswidelyevenamong

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individualswithasingletypeofCOPD.Inrecognitionofthisoverlap,GOLDandtheGlobalInitiativeforAsthma
(GINA)issuedaconsensusstatementonAsthma,COPD,andAsthmaCOPDOverlapSyndrome(ACOS)[25],
whichdescribesACOSas"characterizedbypersistentairflowlimitationwithseveralfeaturesusuallyassociated
withasthmaandseveralfeaturesusuallyassociatedwithCOPD.ACOSisthereforeidentifiedinclinicalpractice
bythefeaturesthatitshareswithbothasthmaandCOPD."

FurtherstudyofACOSwillbeneededtodeterminewithcertaintyhowtreatmentalgorithmsshouldbetailoredto
thesepatients[24].Asanexample,asubgroupofpatientswithsputumeosinophiliamayexperiencelung
functionimprovementwithantiinerleukin5receptormonoclonalantibodythatdepletesbloodandsputum
eosinophils[26]andfurtherinvestigationintothismedicationclassisongoing.Similarly,anevolvingliterature
suggestsdifferentialresponsestoinhaledglucocorticoidsinpatientswithorwithoutincreasedcirculating
eosinophils[27,28].

PATHOLOGYThepredominantpathologicchangesofchronicobstructivepulmonarydisease(COPD)are
foundintheairways,butchangesarealsoseeninthelungparenchymaandpulmonaryvasculature.Inan
individual,thepatternofpathologicchangesdependsontheunderlyingdisease(eg,chronicbronchitis,
emphysema,alpha1antitrypsindeficiency),possiblyindividualsusceptibility,anddiseaseseverity[7].While
radiographicmethodsdonothavetheresolutionofhistology,highresolutioncomputedtomographycanassess
lungparenchyma[29],airways[30],andpulmonaryvasculature[31].

AirwaysAirwaysabnormalitiesinCOPDincludechronicinflammation,increasednumbersofgobletcells,
mucusglandhyperplasia,fibrosis,narrowingandreductioninthenumberofsmallairways,andairwaycollapse
duetothelossoftetheringcausedbyalveolarwalldestructioninemphysema[14].Amongpatientswithchronic
bronchitiswhohavemucushypersecretion,anincreasednumberofgobletcellsandenlargedsubmucosal
glandsaretypicallyseen.Chronicinflammationinchronicbronchitisandemphysemaischaracterizedbythe
presenceofCD8+Tlymphocytes,neutrophils,andCD68+monocytes/macrophages(picture1)intheairways
[3236].Incomparison,thebronchialinflammationofasthmaischaracterizedbythepresenceofCD4+T
lymphocytes,eosinophils,andincreasedinterleukin(IL)4andIL5(algorithm1)[23,37,38].Whilethese
paradigmsarehelpfulconceptually,theyarenotdiagnosticandoverlapsexist.Forexample,theremaybeaset
ofasthmaticpatientswhoprogresstodevelopCOPD.

LungparenchymaEmphysemaaffectsthestructuresdistaltotheterminalbronchiole,consistingofthe
respiratorybronchiole,alveolarducts,alveolarsacs,andalveoli,knowncollectivelyastheacinus.These
structuresincombinationwiththeirassociatedcapillariesandinterstitiumformthelungparenchyma.Thepartof
theacinusthatisaffectedbypermanentdilationordestructiondeterminesthesubtypeofemphysema.

Proximalacinar(alsoknownascentrilobular)emphysemareferstoabnormaldilationordestructionofthe
respiratorybronchiole,thecentralportionoftheacinus.Itiscommonlyassociatedwithcigarettesmoking,
butcanalsobeseenincoalworkerspneumoconiosis.

Panacinaremphysemareferstoenlargementordestructionofallpartsoftheacinus.Diffusepanacinar
emphysemaismostcommonlyassociatedwithalpha1antitrypsindeficiency,althoughitcanbeseenin
combinationwithproximalemphysemainsmokers.(See"Clinicalmanifestations,diagnosis,andnatural
historyofalpha1antitrypsindeficiency".)

Indistalacinar(alsoknownasparaseptal)emphysema,thealveolarductsarepredominantlyaffected.
Distalacinaremphysemamayoccuraloneorincombinationwithproximalacinarandpanacinar
emphysema.Whenitoccursalone,theusualassociationisspontaneouspneumothoraxinayoungadult.
(See"Primaryspontaneouspneumothoraxinadults".)

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PulmonaryvasculatureChangesinthepulmonaryvasculatureincludeintimalhyperplasiaandsmooth
musclehypertrophy/hyperplasiathoughttobeduetochronichypoxicvasoconstrictionofthesmallpulmonary
arteries[39].Destructionofalveoliduetoemphysemacanleadtolossoftheassociatedareasofthepulmonary
capillarybedandpruningofthedistalvasculature,whichcanbedetectedradiographically[31].

CLINICALFEATURES

SmokingandinhalationalexposurehistoryThemostimportantriskfactorforchronicobstructive
pulmonarydisease(COPD)iscigarettesmoking.Theamountanddurationofsmokingcontributetodisease
severity.Thus,akeystepintheevaluationofpatientswithsuspectedCOPDistoascertainthenumberofpack
yearssmoked(packsofcigarettesperdaymultipliedbythenumberofyears),asthemajority(about80
percent)ofpatientswithCOPDintheUnitedStateshaveahistoryofcigarettesmoking[40,41].Inthe
developingworld,however,otherexposures,particularlybiomassfueluse,playmajorroles[42].Asmoking
historyshouldincludetheageofstartingandtheageofquitting,aspatientsmayunderestimatethenumberof
yearstheysmoked.Withenoughsmoking,almostallsmokerswilldevelopmeasurablyreducedlungfunction
[5].Whilestudieshaveshownanoverall"doseresponsecurve"forsmokingandlungfunction,someindividuals
developseverediseasewithfewerpackyearsandothershaveminimaltonosymptomsdespitemanypack
years[5].

Theexactthresholdfortheduration/intensityofcigarettesmokingthatwillresultinCOPDvariesfromone
individualtoanother.Intheabsenceofagenetic/environmental/occupationalpredisposition,smokinglessthan
10to15packyearsofcigarettesisunlikelytoresultinCOPD.Ontheotherhand,thesinglebestvariablefor
predictingwhichadultswillhaveairflowobstructiononspirometryisahistoryofmorethan40packyearsof
smoking(positivelikelihoodratio[LR],12[95%CI,2.750])[43,44].

Thechronologicallytakenenvironmental/occupationalhistorymaydiscloseotherimportantriskfactorsfor
COPD,suchasexposuretofumesororganicorinorganicdusts.Theseexposureshelptoexplainthe20
percentofpatientswithCOPD(definedbylungfunctionalone)andthe20percentofpatientswhodiefrom
COPDwhoneversmoked[41,45,46].Ahistoryofasthmashouldalsobesought,asCOPDisoften
misdiagnosedasasthma.Inaddition,asthmamayprogresstofixedairflowlimitationandCOPD[45].(See
"Chronicobstructivepulmonarydisease:Riskfactorsandriskreduction".)

SymptomsandpatternofonsetThethreecardinalsymptomsofCOPDaredyspnea,chroniccough,and
sputumproductionandthemostcommonearlysymptomisexertionaldyspnea.Lesscommonsymptoms
includewheezingandchesttightness(table1A).However,anyofthesesymptomsmaydevelopindependently
andwithvariableintensity.

TherearethreetypicalwaysinwhichpatientswithCOPDpresent[47]:

Patientswhohaveanextremelysedentarylifestylebutfewcomplaintsrequirecarefulquestioningtoelicita
historythatissuggestiveofCOPD.Somepatientsunknowinglyavoidexertionaldyspneabyshiftingtheir
expectationsandlimitingtheiractivity.Theymaybeunawareoftheextentoftheirlimitationsorthattheir
limitationsareduetorespiratorysymptoms,althoughtheymaycomplainoffatigue.

Patientswhopresentwithrespiratorysymptomsgenerallycomplainofdyspneaandchroniccough.The
dyspneamayinitiallybenoticedonlyduringexertion.However,iteventuallybecomesnoticeablewith
progressivelylessexertionorevenatrest.Thechroniccoughischaracterizedbytheinsidiousonsetof
sputumproduction,whichoccursinthemorninginitially,butmayprogresstooccurthroughouttheday.The
dailyvolumerarelyexceeds60mL.Thesputumisusuallymucoid,butbecomespurulentduring
exacerbations.

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Patientswhopresentwithepisodesofincreasedcough,purulentsputum,wheezing,fatigue,anddyspnea
thatoccurintermittently,withorwithoutfever.Diagnosiscanbeproblematicinsuchpatients.The
combinationofwheezingplusdyspneamayleadtoanincorrectdiagnosisofasthma.Conversely,other
illnesseswithsimilarmanifestationsareoftenincorrectlydiagnosedasaCOPDexacerbation(eg,heart
failure,bronchiectasis,bronchiolitis)(table2).Theintervalbetweenexacerbationsdecreasesasthe
severityoftheCOPDincreases.(See"Managementofexacerbationsofchronicobstructivepulmonary
disease".)

Approximately62percentofpatientswithmoderatetosevereCOPDreportvariabilityinsymptoms(eg,
dyspnea,cough,sputum,wheezing,orchesttightness)overthecourseofthedayorweektoweekmorningis
typicallytheworsttimeofday[48].

PatientswithCOPDmayexperienceweightgain(duetoactivitylimitations),weightloss(possiblydueto
dyspneawhileeating),limitationofactivity(includingsexual),coughsyncope,orfeelingsofdepressionor
anxiety.Weightlossgenerallyreflectsmoreadvanceddiseaseandisassociatedwithaworseprognosis.
However,themajorityofCOPDpatientsareoverweightorobese.

ComorbiddiseasesthatmayaccompanyCOPDincludelungcancer,bronchiectasis,cardiovasculardisease,
osteoporosis,metabolicsyndrome,skeletalmuscleweakness,anxiety,depression,andcognitivedysfunction.
PatientsmayalsoreportafamilyhistoryofCOPDorotherchronicrespiratoryillness[7,4954].

PhysicalexaminationThefindingsonphysicalexaminationofthechestvarywiththeseverityoftheCOPD
(table1AB).

Earlyinthedisease,thephysicalexaminationmaybenormal,ormayshowonlyprolongedexpirationor
wheezesonforcedexhalation.

Astheseverityoftheairwayobstructionincreases,physicalexaminationmayrevealhyperinflation(eg,
increasedresonancetopercussion),decreasedbreathsounds,wheezes,cracklesatthelungbases,
and/ordistantheartsounds[55].Featuresofseverediseaseincludeanincreasedanteroposteriordiameter
ofthechest("barrelshaped"chest)andadepresseddiaphragmwithlimitedmovementbasedonchest
percussion.

PatientswithendstageCOPDmayadoptpositionsthatrelievedyspnea,suchasleaningforwardwitharms
outstretchedandweightsupportedonthepalmsorelbows.Thisposturemaybeevidentduringthe
examinationormaybesuggestedbythepresenceofcallousesorswollenbursaeontheextensorsurfaces
offorearms.Otherphysicalexaminationfindingsincludeuseoftheaccessoryrespiratorymusclesofthe
neckandshouldergirdle,expirationthroughpursedlips,paradoxicalretractionofthelowerinterspaces
duringinspiration(ie,Hoover'ssign)[56,57],cyanosis,asterixisduetoseverehypercapnia,andan
enlarged,tenderliverduetorightheartfailure.Neckveindistentionmayalsobeobservedbecauseof
increasedintrathoracicpressure,especiallyduringexpiration.

Yellowstainsonthefingersduetonicotineandtarfromburningtobaccoareacluetoongoingandheavy
cigarettesmoking[58].

ClubbingofthedigitsisnottypicalinCOPD(evenwithassociatedhypoxemia)andsuggestscomorbidities
suchaslungcancer,interstitiallungdisease,orbronchiectasis.

EVALUATIONEvaluationforchronicobstructivepulmonarydisease(COPD)isappropriateinadultswho
reportdyspnea,chroniccough,chronicsputumproductionorhavehadagradualdeclineinlevelofpeak
activity,particularlyiftheyhaveahistoryofexposuretoriskfactorsforthedisease(eg,cigarettesmoking,

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indoorbiomasssmoke)[7,43].Allpatientsareevaluatedwithspirometryandselectedpatientshavelaboratory
testingandimagingstudies.(See"Chronicobstructivepulmonarydisease:Riskfactorsandriskreduction".)

LaboratoryNolaboratorytestisdiagnosticforCOPD,butcertaintestsaresometimesobtainedtoexclude
othercausesofdyspneaandcomorbiddiseases.

Assessmentforanemiaisanimportantstepintheevaluationofdyspnea.Measurementofplasmabrain
natriureticpeptide(BNP)orNterminalproBNP(NTproBNP)concentrationsisusefulasacomponentof
theevaluationofsuspectedheartfailure(HF).Bloodglucose,ureanitrogen,creatinine,electrolytes,
calcium,phosphorus,andthyroidstimulatinghormonemaybeappropriatedependingonthedegreeof
clinicalsuspicionforanalternatediagnosis.(See"Approachtothepatientwithdyspnea",sectionon'Initial
testinginchronicdyspnea'.)

AmongstableCOPDpatientswithnormalkidneyfunction,anelevatedserumbicarbonatemayindirectly
identifychronichypercapnia.Inthepresenceofchronichypercapnia,theserumbicarbonateistypically
increasedduetoacompensatorymetabolicalkalosis(figure2).Abnormalresultsmustbeconfirmedwith
arterialbloodgasmeasurement.(See"Simpleandmixedacidbasedisorders",sectionon'Respiratory
acidbasedisorders'.)

Testingforalpha1antitrypsin(AAT)deficiencyshouldbeobtainedinallsymptomaticadultswithpersistent
airflowobstructiononspirometry.Especiallysuggestivesubsetsincludethepresenceofemphysemaina
youngindividual(eg,age45years),emphysemainanonsmokerorminimalsmoker,emphysema
characterizedbypredominantlybasilarchangesonthechestradiograph,orafamilyhistoryofemphysema
[59].However,AATdeficiencymaybepresentinapatientwithotherwise"typical"COPD.Aserumlevelof
AATbelow11micromol/L(~57mg/dLbynephelometry)incombinationwithaseveredeficientgenotypeis
diagnostic.(See"Clinicalmanifestations,diagnosis,andnaturalhistoryofalpha1antitrypsindeficiency",
sectionon'Evaluationanddiagnosis'.)

PulmonaryfunctiontestsPulmonaryfunctiontests(PFTs),particularlyspirometry,arethecornerstoneof
thediagnosticevaluationofpatientswithsuspectedCOPD[60].Inaddition,PFTsareusedtodeterminethe
severityoftheairflowlimitation,assesstheresponsetomedications,andfollowdiseaseprogression.(See
'Diagnosis'belowand"Officespirometry".)

SpirometryWhenevaluatingapatientforpossibleCOPD,spirometryisperformedpreandpost
bronchodilatoradministration(eg,inhalationofalbuterol400mcg)todeterminewhetherairflowlimitationis
presentandwhetheritispartiallyorfullyreversible.Airflowlimitationthatisirreversibleoronlypartially
reversiblewithbronchodilatoristhecharacteristicphysiologicfeatureofCOPD.Screeningspirometryisnot
currentlyrecommended.Incontrast,spirometryshouldbeperformedinpatientswithsuggestivesymptoms[42].
(See"Officespirometry",sectionon'Postbronchodilatorspirometry'and'Screening'below.)

Themostimportantvaluesmeasuredduringspirometryaretheforcedexpiratoryvolumeinonesecond(FEV1)
andtheforcedvitalcapacity(FVC).ThepostbronchodilatorratioofFEV1/FVCdetermineswhetherairflow
limitationispresent[7]thepostbronchodilatorpercentpredictedvalueforFEV1determinestheseverityof
airflowlimitationasshowninthetable(table3).

LowerlimitofnormalFEV1/FVCTraditionally,apostbronchodilatorFEV1/FVCratiolessthan0.7has
beenconsidereddiagnosticofairflowlimitation[7].However,theFEV1/FVCratiodecreaseswithage,souseof
thefifthpercentilelowerlimitofnormal(LLN)oftheFEV1/FVCratio,ratherthantheabsolutevalueof<0.7,has
beenadvocatedbysomeasadividingpointforthediagnosisofCOPD[9,6164].However,thedistinction
betweentheLLNandthefixedratioasdividingpointsisunlikelytoleadtomajorclinicalproblemsbecause
currentrecommendationscombinephysiologicassessmentwithassessmentofsymptomsandexacerbationsin

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stagingseverity.Moreover,inastudyof13,847subjects,anincreasedmortalitywasnotedamongthosewithan
FEV1/FVC<0.7,but>LLNFEV1/FVC,whencomparedwiththosewhoseFEV1/FVCwas0.7orhigher[65].
(See"Officespirometry",sectionon'RatioofFEV1/FVC'.)

ForcedexpiratoryvolumeinsixsecondsTheforcedexpiratoryvolumeinsixseconds(FEV6),
obtainedbystoppingtheexpiratoryeffortafter6secondsratherthanatcessationofairflow,isanacceptable
surrogatefortheFVC[6670].TheadvantagesoftheFEV1/FEV6includelessfrustrationbythepatientand
techniciantryingtoachieveanendoftestplateau,lesschanceofsyncope,shortertestingtime,andbetter
repeatability,withoutlossofsensitivityorspecificity.TheappropriateLLNforFEV1/FEV6fromNHANESIII
shouldbeusedtodiagnoseairflowlimitation.(See"Officespirometry",sectionon'Forcedexpiratoryvolumein
sixseconds'and"Officespirometry",sectionon'RatioofFEV1/FVC'.)

PeakexpiratoryflowPeakexpiratoryflow(PEF)isoftenusedasameasureofairflowlimitationin
asthma,butmayunderestimatethedegreeofairflowlimitationinCOPD[7].Inaddition,alowPEFisnot
specificforairflowlimitationandrequirescorroborationwithspirometry.(See"Peakexpiratoryflowrate
monitoringinasthma".)

LungvolumesLungvolumemeasurementisnotneededforallpatientswithsuspectedCOPD.However,
whenareducedFVCisnotedonpostbronchodilatorspirometry,lungvolumemeasurementbybody
plethysmographyisusedtodeterminewhetherthereductioninFVCisduetoairtrapping,hyperinflation,ora
concomitantrestrictiveventilatorydefect.Decreasedinspiratorycapacity(IC)andvitalcapacity,accompaniedby
anincreasedtotallungcapacity(TLC),functionalresidualcapacity(FRC),andresidualvolume(RV)are
indicativeofhyperinflation.AnincreasedFRCwithanormalTLCisindicativeofairtrappingwithout
hyperinflation.(See"Overviewofpulmonaryfunctiontestinginadults",sectionon'Lungvolumes'and"Dynamic
hyperinflationinpatientswithCOPD".)

DiffusingcapacityThediffusingcapacityforcarbonmonoxide(DLCO)isanexcellentindexofthe
degreeofanatomicemphysemainsmokerswithairflowlimitation,butisnotneededforroutineassessmentof
COPD.TheindicationsforperformingaDLCOmeasurementincludehypoxemiabypulseoximetry(eg,PaO2
<92mmHg)andevaluationforlungresectionorlungvolumereductionsurgery.TheDLCOdecreasesin
proportiontotheseverityofemphysemahowever,itcannotbeusedtodetectmildemphysemabecauseitis
neitherasensitivenoraspecifictest.

PulseoximetryandarterialbloodgasesPulseoximetryisanoninvasive,easilyperformedtestthat
assessesbloodoxygensaturation.Ithasreducedthenumberofpatientswhorequirearterialbloodgases
(ABGs),assupplementaloxygenisnotneededwhenthepulseoxygensaturation(SpO2)is>88percent.
However,pulseoximetrydoesnotprovideinformationaboutalveolarventilationorhypercapnia(PaCO2
>45mmHg),andassessmentofoxygenationbypulseoximetrymaybeinaccurateinthesettingofanacute
exacerbationofCOPD[71].(See"Pulseoximetryinadults"and"Arterialbloodgases"and"Theevaluation,
diagnosis,andtreatmentoftheadultpatientwithacutehypercapnicrespiratoryfailure".)

TheindicationsformeasuringABGs(eg,arterialoxygentension[PaO2],carbondioxidetension[PaCO2],and
acidity[pH]),whichmustbeconsideredintheclinicalcontext,includethefollowing:

LowFEV1(eg,<50percentpredicted)

Lowoxygensaturationbypulseoximetry(eg,<92percent)

Depressedlevelofconsciousness

AcuteexacerbationofCOPD

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Assessmentforhypercapniainatriskpatients30to60minutesafterinitiationofsupplementaloxygen(see
"Theevaluation,diagnosis,andtreatmentoftheadultpatientwithacutehypercapnicrespiratoryfailure")

InpatientswithmildtomoderateCOPD,arterialbloodgasesusuallyrevealmildormoderatehypoxemiawithout
hypercapnia.Asthediseaseprogresses,thehypoxemiabecomesmoresevereandhypercapniamaydevelop.
HypercapniabecomesprogressivelymorelikelywhentheFEV1approachesorfallsbelowoneliter.Bloodgas
abnormalitiesworsenduringacuteexacerbationsandmayalsoworsenduringexerciseandsleep.The
compensatoryresponsestoacuteandchronicrespiratoryacidosisareshowninthefigureanddiscussed
separately(figure3).(See"Simpleandmixedacidbasedisorders",sectionon'Respiratoryacidosis'.)

ImagingChestradiographyandcomputedtomography(CT)aretypicallyperformedinpatientswithCOPD
whenthecauseofdyspneaorsputumproductionisunclearandduringacuteexacerbationstoexclude
complicatingprocesses(eg,pneumonia,pneumothorax,heartfailure).Imagingisnotrequiredtodiagnose
COPD.However,inpatientswithsevereCOPD,CTscanningidentifiesindividualswithpredominantlyupper
lobediseasewhomaybecandidatesforlungvolumereductionsurgery.(See'Diagnosis'below.)

ChestradiographyThemainreasontoobtainachestradiographwhenevaluatingapatientforCOPDis
toexcludealternativediagnoses,evaluateforcomorbidities(eg,lungcancerwithairwayobstruction,
bronchiectasis,pleuraldisease,interstitiallungdisease,heartfailure),orwhenachangeinsymptomssuggests
acomplicationofCOPD(eg,pneumonia,pneumothorax).Plainchestradiographshaveapoorsensitivityfor
detectingCOPD.Asanexample,onlyabouthalfofpatientswithCOPDofmoderateseverityareidentifiedas
havingCOPDbyaplainchestradiograph(ie,sensitivityof50percent).

RadiographicfeaturessuggestiveofCOPD(usuallyseeninadvanceddisease)include:

Rapidlytaperingvascularshadows,increasedradiolucencyofthelung,aflatdiaphragm,andalong,
narrowheartshadowonafrontalradiograph(image1).

Aflatdiaphragmaticcontourandanincreasedretrosternalairspaceonalateralradiograph(image2).
Thesefindingsareduetohyperinflation.

Bullae,definedasradiolucentareaslargerthanonecentimeterindiameterandsurroundedbyarcuate
hairlineshadows.Theyareduetolocallyseveredisease,andmayormaynotbeaccompaniedby
widespreademphysema(image3).

WhenadvancedCOPDleadstopulmonaryhypertensionandcorpulmonale,prominenthilarvascular
shadowsandencroachmentoftheheartshadowontheretrosternalspacemaybeseen[72,73].The
cardiacenlargementmaybecomeevidentonlybycomparisonwithpreviouschestradiographs.(See
"Overviewofpulmonaryhypertensioninadults".)

ComputedtomographyComputedtomography(CT)hasgreatersensitivityandspecificitythanstandard
chestradiographyforthedetectionofemphysema.ThisisparticularlytruewithhighresolutionCT(ie,
collimationof1to2mm)[7477].Theuseofexpiratoryscans,particularlywhenusedinconjunctionwiththe
inspiratoryscans,canalsobeusedtoassessnonemphysematousairtrappingasasurrogatemeasurefor
smallairwayabnormality[78](see"Highresolutioncomputedtomographyofthelungs").However,CTscanning
isnotneededfortheroutinediagnosisofCOPD.Usually,itisperformedwhenachangeinsymptomssuggests
acomplicationofCOPD(eg,pneumonia,pneumothorax,giantbullae),analternatediagnosis(eg,
thromboembolicdisease),orwhenapatientisbeingconsideredforlungvolumereductionsurgeryorlung
transplantation.(See"Evaluationandmedicalmanagementofgiantbullae",sectionon'Evaluation'and"Lung
volumereductionsurgeryinCOPD",sectionon'Patientselection'and"Clinicalpresentation,evaluation,and
diagnosisoftheadultwithsuspectedacutepulmonaryembolism".)

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CertainCTscanfeaturescandeterminewhethertheemphysemaiscentriacinar(centrilobular),panacinar,or
paraseptal,althoughthisisusuallynotnecessaryforclinicalmanagement[77,79].

Centriacinaremphysemaoccurspreferentiallyintheupperlobesandproducesholesinthecenterof
secondarypulmonarylobules.Thewallsofemphysematousspacesareusuallyimperceptible,butcentral
vesselsmaybevisible(image4).Incontrast,thewallsofcystsinpulmonaryLangerhanshistiocytosis,
anothercysticlungdiseaseofcigarettesmokers,arethicker(image5).(See'Pathology'above.)

Panacinaremphysemamorecommonlyinvolvesthelungbasesandinvolvestheentiresecondary
pulmonarylobule(image6).Panacinaremphysemacancauseageneralizedpaucityofvascularstructures.
Amongpatientswithalpha1antitrypsindeficiency,panacinaremphysemaisthemorecommonpattern.
(See"Clinicalmanifestations,diagnosis,andnaturalhistoryofalpha1antitrypsindeficiency",sectionon
'Clinicalmanifestations'.)

Paraseptal(distalacinar)emphysemaproducessmall,subpleuralcollectionsofgaslocatedintheperiphery
ofthesecondarypulmonarylobule(image7).Itisconsideredtobetheprecursorofbullae(image8).(See
'Pathology'above.)

NewerCTscannerswithhigherresolutionandnewanalyticalmethodscanresolveairwaydimensions,although
theclinicalsignificanceofthesemeasuresisundefined[77,80,81].Quantitativeparametersbasedonlung
density,asmeasuredbyCTscan,havebeenestablishedtogaugeemphysema,butarecurrentlyusedprimarily
asresearchtools.

DIAGNOSISThepresenceofsymptomscompatiblewithchronicobstructivepulmonarydisease(COPDeg,
dyspneaatrestoronexertion,coughwithorwithoutsputumproduction,progressivelimitationofactivity)are
suggestiveofthediagnosis,especiallyifthereisahistoryofexposuretotriggersofCOPD(eg,tobaccosmoke,
occupationaldust,indoorbiomasssmoke),afamilyhistoryofchroniclungdisease,orpresenceofassociated
comorbidities(table4).ThediagnosisofCOPDisconfirmedbythefollowing[82]:

Spirometrydemonstratingairflowlimitation(ie,aforcedexpiratoryvolumeinonesecond/forcedvital
capacity[FEV1/FVC]ratiolessthan0.7orlessthanthelowerlimitofnormal[LLN]PLUSanFEV1less
than80percentofpredicted)thatisincompletelyreversibleaftertheadministrationofaninhaled
bronchodilator(table1AB).(See'Pulmonaryfunctiontests'above.)

Absenceofanalternativeexplanationforthesymptomsandairflowlimitation(table2)[7].Thedifferential
diagnosisofCOPDisdiscussedbelow.(See'Differentialdiagnosis'belowand"Approachtothepatientwith
dyspnea".)

AfterconfirmingthepresenceofCOPD,thenextstepistoconsiderthecause.Forthemajorityofpatients,the
etiologyislongtermcigarettesmoking.However,itisimportanttoreviewwiththepatientwhetherunderlying
asthma,workplaceexposures,indooruseofbiomassfuel,apriorhistoryoftuberculosis,orfamilial
predispositioniscontributory,becausemitigationofongoingexposuresmayreducediseaseprogression.

Inareasofhighprevalenceofalpha1antitrypsin(AAT)deficiency,itisappropriatetoscreenallpatientswith
COPDbyobtaininganAATserumlevel[7].(See'Laboratory'aboveand"Chronicobstructivepulmonary
disease:Riskfactorsandriskreduction".)

DIFFERENTIALDIAGNOSISAmongpatientswhopresentinmidorlaterlifewithdyspnea,cough,and
sputumproduction,thedifferentialdiagnosisisbroad(eg,heartfailure,chronicobstructivepulmonarydisease
[COPD],interstitiallungdisease,thromboembolicdisease)(table2).Typically,thefindingofpersistentairflow
limitationonpulmonaryfunctiontestingandtheabsenceofradiographicfeaturesofheartfailureorinterstitial
lungdiseasedirectthecliniciantoanarrowerdifferentialofCOPD,chronicobstructiveasthma,bronchiectasis,
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tuberculosis,constrictivebronchiolitis,anddiffusepanbronchiolitis[7].Importantly,theseconditionscan
commonlyoccurtogether,forexample,patientswithasthmamaydevelopCOPDandpatientswithCOPDmay
haveconcurrentbronchiectasis.

ChronicobstructiveasthmaInsomepatientswithchronicasthma,acleardistinctionfromCOPDisnot
possible.Asanexample,apatient,whohashadatopicasthmasincechildhoodandsmokedcigarettesfor
15yearsintheirtwentiesandthirtiescouldpresentintheirfiftieswithacombinationofasthmaandCOPD.
Theimportanceofrecognizingthecoexistenceofthesediseasesisindevisingatreatmentplanthatis
adaptedtoreflectbothunderlyingdiseaseprocesses.(See'Interrelationshipsamongasthma,chronic
bronchitis,andemphysema'aboveand"Diagnosisofasthmainadolescentsandadults".)

ChronicbronchitiswithnormalspirometryAsmallportionofcigarettesmokershaveachronic
productivecoughforthreemonthsintwosuccessiveyears,butdonothaveairflowlimitationonpulmonary
functiontests.TheyarenotconsideredtohaveCOPD,althoughtheymaydevelopCOPDiftheycontinue
tosmoke.SometreatmentsforCOPDmayimprovetheircough.(See'Interrelationshipsamongasthma,
chronicbronchitis,andemphysema'above.)

CentralairwayobstructionCentralairwayobstructioncanbecausedbynumerousbenignand
malignantprocessesandcanmimicCOPDwithaslowlyprogressivedyspneaonexertionfollowedby
dyspneawithminimalactivity(table5).Monophonicwheezingorstridormaybepresent.Symptomsare
minimallyimprovedbyinhaledbronchodilator,ifatall.Ahighindexofsuspicionisneededasconventional
chestradiographsarerarelydiagnostic.Thoughinsensitive,flowvolumeloopscanshowthecharacteristic
changesofcentralairwayobstruction,frequentlybeforeabnormalitiesinthespirometricvolumesarenoted
(figure4andfigure5)[83].AhighresolutionCTscanwiththreedimensionalreconstructioncanbehelpful.
Thegoldstandardfordiagnosisisdirectvisualization.(See"Clinicalpresentation,diagnosticevaluation,
andmanagementofcentralairwayobstructioninadults",sectionon'Diagnosticevaluationandinitial
management'.)

BronchiectasisBronchiectasis,aconditionofabnormalwideningofthebronchithatisassociatedwith
chronicorrecurrentinfection,sharesmanyclinicalfeatureswithCOPD,includinginflamedandeasily
collapsibleairways,obstructiontoairflow,andexacerbationscharacterizedbyincreaseddyspneaand
sputumproduction.Bronchiectasisissuspectedonthebasisofprominentsymptomsofcoughanddaily
mucopurulentsputumproduction.Thediagnosisisusuallyestablishedclinicallybasedonthecharacteristic
coughandsputumproductionandthepresenceofbronchialwallthickeningandluminaldilatationonchest
computedtomographic(CT)scans.(See"Clinicalmanifestationsanddiagnosisofbronchiectasisin
adults".)

HeartfailureHeartfailureisacommoncauseofdyspneaamongmiddleagedandolderpatientsand
somepatientsexperiencechesttightnessandwheezingwithfluidoverloadduetoheartfailure.
Occasionally,airflowlimitationisnoted,althougharestrictivepatternismorecommon.Heartfailureis
usuallydifferentiatedbythepresenceoffinebasilarcrackles,radiographicevidenceofanincreasedheart
sizeandpulmonaryedema.Thebrainnatriureticpeptideistypicallyincreasedinheartfailure,butcanalso
beincreasedduringrightheartstrainfromcorpulmonale.(See"Evaluationofthepatientwithsuspected
heartfailure".)

TuberculosisInanareaendemicfortuberculosis,theoverallprevalenceofairflowobstructionwas31
percentamongthosewithapasthistoryoftuberculosiscomparedwith14percentamongthosewithout.
Thisassociationwasunchangedafteradjustmentforrespiratorydiseaseinchildhood,smoking,and
exposuretodustandsmoke[84,85].Thus,tuberculosisisbothariskfactorforCOPDandapotential
comorbidity[7].(See"Clinicalmanifestationsandcomplicationsofpulmonarytuberculosis".)

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ConstrictivebronchiolitisConstrictivebronchiolitis,alsoknownasbronchiolitisobliterans,is
characterizedbysubmucosalandperibronchiolarfibrosisthatcausesconcentricnarrowingofthe
bronchiolarlumen.Constrictivebronchiolitisismostcommonlyseenfollowinginhalationinjury,
transplantation(eg,bonemarrow,lung),orinthecontextofrheumatoidlungorinflammatoryboweldisease
(table6).Symptomsincludeprogressiveonsetofcoughanddyspneaassociatedwithhypoxemiaatrestor
withexercise.Cracklesmaybepresent.Pulmonaryfunctiontestsshowaprogressiveandirreversible
airflowlimitation.FindingsoninspiratoryCTscanincludecentrilobularbronchialwallthickening,bronchiolar
dilation,treeinbudpattern,andamosaicgroundglassattenuationpattern.(See"Bronchiolitisinadults",
sectionon'Bronchiolitisobliterans'.)

DiffusepanbronchiolitisDiffusepanbronchiolitisispredominantlyseeninmalenonsmokersofAsian
descent.Almostallhavechronicsinusitis.Onpulmonaryfunctiontesting,anobstructivedefectiscommon,
althoughamixedobstructiverestrictivepatternmayalsobeseen.Chestradiographsandhighresolution
CTscansshowdiffusecentrilobularnodularandlinearopacitiescorrespondingtothickenedanddilated
bronchiolarwallswithintraluminalmucousplugs.(See"Diffusepanbronchiolitis",sectionon'Diagnosis'.)

LymphangioleiomyomatosisLymphangioleiomyomatosis(LAM)isseenprimarilyinyoungwomenof
childbearingage.Pulmonaryfunctiontestingfrequentlyrevealsmildairflowobstruction,althoughamixed
obstructiverestrictivepatternmaybeseen.CTscanstypicallydemonstratesmall,thinwalledcyststhatcan
attimesbeconfusedwithemphysema.However,theairspacesinemphysemaarenotactuallycystsbut
arecausedbythedestructionofalveolarwallsandpermanentenlargementofdistalairspaces,sothe
"walls"aretypicallyinapparent.(See'Diagnosis'aboveand"Sporadiclymphangioleiomyomatosis:
Epidemiologyandpathogenesis".)

SCREENINGRoutinescreeningspirometryisgenerallynotindicatedforadultswhohavenoneofthe
featuressuggestiveofchronicobstructivepulmonarydisease(COPDeg,nodyspnea,cough,sputum
productionorprogressivedeclineinactivity),asasymptomaticmildairflowobstructiondoesnotrequire
treatment[43,86].Asymptomaticandnonsmokingsubjectswithmildairflowobstruction,butnohistoryof
asthma,donothavethesameprogressivedeclineinlungfunctionthatisobservedamongindividualswhohave
asimilardegreeofairflowobstructionandaresymptomaticorcontinuetosmoke[87].

Ontheotherhand,waitingforpatientstoreportsymptomsmaymissalargenumberofpatientswhohave
COPD,as20percentofindividualswithsevereairwayobstructionduetosmokingorasthmawillnotreport
symptoms.Decrementsinforcedexpiratoryvolumeinonesecond(FEV1),evenwithinthenormalrange,are
associatedwithincreasedriskofacutecardiaceventsindependentofage,gender,andsmokinghistory[49].
Thus,performanceofspirometryseemsreasonablewheneverCOPDisadiagnosticconsideration.The
diagnosisofCOPDmayaltermanagementofconcurrentconditionsandmayaffecttheapproachtoexercise.
ExclusionofCOPDcanoftencontributetoclinicalmanagementasmuchasitsdiagnosisbyleadingto
alternativediagnoses.

STAGINGTheinitialGlobalInitiativeforChronicObstructiveLungDisease(GOLD)guidelinesusedthe
forcedexpiratoryvolumeinonesecond(FEV1expressedasapercentageofpredicted)tostagedisease
severity.However,theFEV1onlycapturesonecomponentofchronicobstructivepulmonarydisease(COPD)
severity:twopatientswiththesamepercentpredictedFEV1canhaveasubstantiallydifferentexercise
toleranceandprognosis.Otheraspectsofdisease,suchastheseverityofsymptoms,riskofexacerbations,and
thepresenceofcomorbidities,areimportanttothepatient'sexperienceofthediseaseandprognosisandare
includedinnewerstagingsystems,suchastherevisedGOLDclassification[7,88].

Severaltoolsforevaluatingsymptomseverityhavebeenproposed.TheGOLDguidelinessuggestusing
instrumentssuchastheClinicalCOPDQuestionnaire(table7)ortheCOPDAssessmentTool(CAT)[7,8993].
ThemodifiedMedicalResearchCouncil(mMRC)dyspneascale(table8)maybeusedbutdoesnotassess
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COPDrelatedsymptomsotherthanbreathlessness.Themostwidelyusedresearchtool,theSt.George's
RespiratoryQuestionnaire(SGRQ),isa76itemquestionnairethatincludesthreecomponentscores(ie,
symptoms,activity,andimpactondailylife)andatotalscore.Whilevaluableforresearchpurposesinpatients
withCOPD,asthma,andbronchiectasis,itistoolongandcomplicatedforuseinroutineclinicalpractice[9496].

GOLDsystemTheGOLDtherapeuticstrategysuggestsusingacombinationofanindividual'ssymptoms,
historyofexacerbations,hospitalizationsduetoexacerbationsandFEV1toassesstheexacerbationriskand
guidetherapy[7].SymptomseverityisassessedusingtheCATormMRC.Lungfunctioninadditiontothe
numberofexacerbationsandhospitalizationsforexacerbationsintheprevious12monthscanbeusedto
predictfuturerisk.TheseverityoflungfunctionimpairmentisstratifiedbasedonthepostbronchodilatorFEV1,
usingtheGOLDclassification(table3).Ahistoryofzerooroneexacerbationinthepast12monthsandGOLD
1or2spirometriclevelsuggestsalowfutureriskofexacerbations,whiletwoormoreexacerbationsora
hospitalizedexacerbationorGOLD3or4spirometriclevelsuggestahighfuturerisk[7].Thesethree
componentsarecombinedintofourgroupsasfollows:

GroupA:Lowrisk,lesssymptoms:TypicallyGOLD1orGOLD2(mildormoderateairflowlimitation)and0
to1exacerbationperyearandnohospitalizationforexacerbationandCATscore<10ormMRCgrade0to
1.

GroupB:Lowrisk,moresymptoms:TypicallyGOLD1orGOLD2(mildormoderateairflowlimitation)and
0to1exacerbationperyearandnohospitalizationforexacerbationandCATscore10ormMRCgrade
2

GroupC:Highrisk,lesssymptoms:TypicallyGOLD3orGOLD4(severeorverysevereairflowlimitation)
and/or2exacerbationsperyearor1hospitalizationforexacerbationandCATscore<10ormMRC
grade0to1.

GroupD:Highrisk,moresymptoms:TypicallyGOLD3orGOLD4(severeorverysevereairflowlimitation)
and/or2exacerbationsperyearor1hospitalizationforexacerbationandCATscore10ormMRC
grade2.

OthersystemsforassessingdiseaseseverityintheCOPDpatienthavebeenproposed.TheBODEindex,
whichiscalculatedbasedonweight(BMI),airwayobstruction(FEV1),dyspnea(mMRCdyspneascore),and
exercisecapacity(sixminutewalkdistance)(calculator1),hasbeenusedtoassessanindividualsriskofdeath.
ThisindexprovidesbetterprognosticinformationthantheFEV1aloneandcanbeusedtoassesstherapeutic
responsetomedications,pulmonaryrehabilitationtherapy,andotherinterventions[97100].(See"Chronic
obstructivepulmonarydisease:Prognosticfactorsandcomorbidconditions",sectionon'BODEindex'.)

COPDFoundationsystemTheCOPDFoundationhasintroducedastagingsystemthatincludesseven
severitydomains,eachofwhichhastherapeuticimplications(figure6)[8,43].Thesedomainsarebasedupon
assessmentofspirometry,regularsymptoms,numberofexacerbationsinthepastyear,oxygenation,
emphysemaoncomputedtomographyscan,presenceofchronicbronchitis,andcomorbidities.Withinthese
domains,theCOPDFoundationusesfivespirometricgrades:

SG0:Normalspirometry
SG1:Mild,postbronchodilatorFEV1/forcedvitalcapacity(FVC)ratio<0.7,FEV160percentpredicted
SG2:Moderate,postbronchodilatorFEV1/FVCratio<0.7,30percentFEV1<60percentpredicted
SG3:Severe,postbronchodilatorFEV1/FVCratio<0.7,FEV1<30percentpredicted
SGU:Undefined,postbronchodilatorFEV1/FVCratio>0.7,FEV1<80percentpredicted

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Anadvantageofthisstagingsystemisthatitsimplifiestheinterpretationofspirometryanyspirometricfinding
resultsinaclassification,whichisnotthecaseinGOLD.

WhileFEV1isusedtogaugeseverity,theFEV1/FVCratioisnotusedforthispurposebecausemeasurementof
FVCbecomeslessreliableasthediseaseprogresses(thelongexhalationsaredifficultforthepatients),thus
makingtheratiolessaccurate.(See"Chronicobstructivepulmonarydisease:Prognosticfactorsandcomorbid
conditions",sectionon'Forcedexpiratoryvolumeinonesecond'.)

INFORMATIONFORPATIENTSUpToDateofferstwotypesofpatienteducationmaterials,TheBasicsand
BeyondtheBasics.TheBasicspatienteducationpiecesarewritteninplainlanguage,atthe5thto6thgrade
readinglevel,andtheyanswerthefourorfivekeyquestionsapatientmighthaveaboutagivencondition.
Thesearticlesarebestforpatientswhowantageneraloverviewandwhoprefershort,easytoreadmaterials.
BeyondtheBasicspatienteducationpiecesarelonger,moresophisticated,andmoredetailed.Thesearticles
arewrittenatthe10thto12thgradereadinglevelandarebestforpatientswhowantindepthinformationand
arecomfortablewithsomemedicaljargon.

Herearethepatienteducationarticlesthatarerelevanttothistopic.Weencourageyoutoprintoremailthese
topicstoyourpatients.(Youcanalsolocatepatienteducationarticlesonavarietyofsubjectsbysearchingon
patientinfoandthekeyword(s)ofinterest.)

Basicstopics(see"Patienteducation:Chronicobstructivepulmonarydisease(COPD),including
emphysema(TheBasics)"and"Patienteducation:Chronicbronchitis(TheBasics)"and"Patienteducation:
Medicinesforchronicobstructivepulmonarydisease(COPD)(TheBasics)")

BeyondtheBasicstopics(see"Patienteducation:Chronicobstructivepulmonarydisease(COPD),
includingemphysema(BeyondtheBasics)")

SUMMARYANDRECOMMENDATIONS

TheGlobalInitiativeforChronicObstructiveLungDisease(GOLD)definesCOPDasfollows:"Chronic
obstructivepulmonarydisease(COPD),acommonpreventableandtreatabledisease,ischaracterizedby
persistentairflowlimitationthatisusuallyprogressiveandassociatedwithanenhancedchronic
inflammatoryresponseintheairwaysandthelungtonoxiousparticlesorgases.Exacerbationsand
comorbiditiescontributetotheoverallseverityinindividualpatients."(See'Definitions'above.)

SubstantialoverlapexistsbetweenCOPDandtheotherdisordersthatcauseairflowlimitation(eg,
emphysema,chronicbronchitis,asthma,bronchiectasis,bronchiolitis)asillustratedinthefigure(figure1).
(See'Interrelationshipsamongasthma,chronicbronchitis,andemphysema'above.)

CommonpresentationsofCOPDincludepatientswithfewcomplaints,butanextremelysedentarylifestyle
patientswithchronic,dailyrespiratorysymptoms(eg,dyspneaonexertion,cough)andpatientswith
recurrentacuteexacerbations(eg,wheezing,cough,dyspnea,fatigue).Thephysicalexaminationofthe
chestvarieswiththeseverityoftheCOPD,butisoftennormalinmilddisease(table1AB).(See'Clinical
features'above.)

ThediagnosisofCOPDshouldbeconsideredandspirometryperformedinallpatientswhoreportany
combinationofdyspnea,chroniccough,orchronicsputumproduction,especiallyifthereisahistoryof
exposuretotriggersofCOPD(eg,tobaccosmoke,occupationaldust,indoorbiomasssmoke),afamily
historyofchroniclungdisease,orpresenceofassociatedcomorbidities(table4).(See'Pulmonaryfunction
tests'aboveand'Diagnosis'above.)

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COPDisconfirmedwhenapatientwithcompatiblesymptomsisfoundtohaveirreversibleairflowlimitation
(ie,apostbronchodilatorforcedexpiratoryvolumeinonesecond[FEV1]/forcedvitalcapacity[FVC]ratio
lessthan0.7[orlessthanthelowerlimitofnormal]andanFEV1<80percentpredicted)andnoalternative
explanationforthesymptomsandairflowobstruction.(See'Pulmonaryfunctiontests'aboveand
'Diagnosis'above.)

Inareasofhighprevalenceofalpha1antitrypsin(AAT)deficiency,allsymptomaticadultswithfixedairflow
obstructiononspirometryshouldbetestedforAATdeficiencywithanAATserumlevel.(See'Laboratory'
aboveand"Clinicalmanifestations,diagnosis,andnaturalhistoryofalpha1antitrypsindeficiency",section
on'Evaluationanddiagnosis'.)

IntheevaluationofpatientswithCOPD,chestradiographyistypicallyperformedtoexcludealternative
diagnoses,evaluateforcomorbidities,orassessachangeinsymptomsthatsuggestsacomplicationof
COPD.Chestcomputedtomographyisperformedtoevaluateabnormalitiesseenontheconventionalchest
radiograph,toexcludecertaincomplicationsofCOPD(eg,thromboembolicdisease),orwhenapatientis
beingconsideredforlungvolumereductionsurgery.(See'Imaging'above.)

TheoriginalFEV1basedGOLDstagingsystemisshowninthetable(table3).Althoughwellrecognized
andcommonlyused,ithasbeencriticizedforunderestimatingtheimportanceoftheextrapulmonary
manifestationsofCOPDinpredictingoutcome.TherevisedGOLDstrategyusesacombinationofan
individual'ssymptoms,historyofexacerbationsandhospitalizationsduetoexacerbations,andFEV1to
assessexacerbationriskandguidetherapy.OthermultidimensionalstagingsystemsincludetheBODE
index(calculator1)andtheCOPDFoundationsystem.(See'Staging'above.)

ThemanagementofCOPDandstrategiesforsmokingcessationarediscussedseparately.(See
"Managementofstablechronicobstructivepulmonarydisease"and"Overviewofsmokingcessation
managementinadults".)

ACKNOWLEDGMENTTheeditorialstaffatUpToDatewouldliketoacknowledgeStephenRennard,MD,
whocontributedtoanearlierversionofthistopicreview.

UseofUpToDateissubjecttotheSubscriptionandLicenseAgreement.

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