GOLD分析课件-医学-

Global

Initiative

for

ChronicObstructiveLungDiseaseGLOBAL

STRATEGY

FOR

THE

DIAGNOSIS,MANAGEMENT,

AND

PREVENTION

OFCHRONIC

OBSTRUCTIVE

PULMONARY

DISEASENHLBI/WHO

WORKSHOP

REPORTNATIONAL

INSTITUTES

OF

HEALTHNational

Heart,

Lung,

and

Blood

InstituteCHAPTER

1

DEFINITIONDEFINITIONCOPD

is

a

disease

state

characterized

by

airflolimitation

that

is

not

fully

reversible.

Theairflow

limitation

is

usually

both

progressiveand

associated

with

an

abnormal

inflammatoryresponse

of

the

lungs

to

noxious

particles

orgases.Many

previous

definitions

of

COPD

have

emphasizedthe

terms

“emphysema”

and

“chronicbronchitis”,

which

are

no

longer

included

in

thedefinition

in

this

report.

Because

emphysemadescribes

only

one

of

several

structural

abnormalpresent

in

COPD

andchronic

bronchitis

does

notreflect

the

major

impact

of

airflow

limitation

onmorbidity

and

mortality

in

COPD

patients.The

focus

of

this

Report

is

primarily

on

COPDcaused

by

inhaled

particles

and

gases,

themostcommon

of

which

worldwide

is

tobacco

smoke.Poorly

reversible

airflow

limitation

associatwith

bronchiectasis,

cystic

fibrosis,

tubercuor

asthma

is

not

included

except

insofar

as

thesconditions

overlap

with

COPD.StageCharacteristics0:

At

RiskNormal

spirometryChronic

symptoms

(cough,

sputum

production)Ⅰ:

Mild

COPDFEV1/FVC<70%FEV1≥80%

predictedWith

or

without

chronic

symptoms(cough,sputum

production)Ⅱ:

ModerateCOPDFEV1/FVC<70%30%≤FEV1<80%

predicted(ⅡA:50%≤FEV1<80%

predicted,ⅡB:30%≤FEV1<50%

predicted)With

or

without

chronic

symptoms(cough,

sputum

production,

dyspnea)Ⅲ:

Severe

COPDFEV1/FVC<70%FEV1<30%

predicted

or

FEV1<50%

predicted

plusrespiratory

failure

orclinical

signs

of

right

hefailureCLASSIFICATION

OF

SEVERITY:

STAGESOF

COPDCHAPTER

2BURDEN

OF

COPD·

The

imprecise

and

variable

definitions

of

COPhave

made

it

hard

to

quantify

the

morbidity

andmortality

of

this

disease

in

developed

anddeveloping

countries.··

Most

epidemiological

studies

have

found

thatCOPD

prevalence,

morbidity,

and

mortality

haveincreased

over

time.··

The

prevalence

of

COPS

is

highest

in

countrieswhere

cigarette

smoking

has

been,

or

still

is,

vcommon.EPIDEMIOLOGY·

AirwayHyperresponsiveness·

Lung

GrowthCHAPTER

3

RISK

FACTORSHost

Factors

Exposures·

Genes(e.g.,

alpha-1·

Tobacco

Smokeantitrypsin

deficienc·y)

Occupational

Dusts

andChemicalsIndoor

and

Outdoor

AirPollutionInfectionsSocioeconomic

StatusCHAPTER

4:

PATHOGENESIS,

PATHOLOGY,AND

PATHOPHYSIOLGYCOPD

is

characterized

by

chronicinflammation

throughout

the

airways,parenchyma,

and

pulmonary

vasculature.PATHOGENESISCharacteristics

of

Inflammation

in

COPD

and

AsthmaCOPDAsthmaCells·

Neutrophils·maLcarrogpehiangcersease

in·lyImnpchroecaysteeisnCD+

8

TEosinophilsSmall

increase

in

macrophagesIncrease

in

CD+

4

Th2

lymphocyteActivation

of

mast

cellsMediatorsLTB4IL-8TNF-αLTD4IL-4,IL-5(Plus

many

others)Consequences·epSiqtuhaemloiuusmmetaplasiaof·dePsatrreunccthiyomnalMucus

metaplasiaGlandular

enlargemetFragile

epitheliumThickening

of

basement

membranMucus

metaplasiaGlandular

enlargementIn

addition

to

inflammation,

two

otherprocesses

thought

to

be

important

in

thepathogenesis

of

COPD

are

an

imbalance

of

proteinases

and

antiproteinases

inthe

lung,

and

oxidative

stress.Pathological

changes

characteristic

ofCOPD

are

found

in

the

central

airways,peripheral

airways

,

lung

parenchyma,

andpulmonary

vasculature.PATHOLOGYchanges

includes:macrophages

and

CD+8

T

lymphocytes

infiltratingincreasing

epithelial

goblet

and

squamous

cellsdysfunction,

damage

,

and/or

loss

in

ciliaenlarged

mucus-secreting

glandsincreasing

smooth

muscle

and

connectivetissue

in

the

airway

walldegeneration

of

the

airway

cartilagemucus

hypersecretionCentral

AirwaysThe

early

lung

function

decline

is

correlated

wi

inflammatory

changes

in

peripheral

airways,similar

to

those

in

central

airways.However,

the

most

characteristic

change

in

the

peripheral

airways

of

patients

with

COPD

isairway

narrowing.Peripheral

AirwaysThe

most

common

type

of

parenchymaldestruction

in

COPD

patients

is

the

centrilobulform

of

emphysema.Lung

ParenchymaPulmonary

vascular

changes

are

characterized

by

athickening

of

the

vessel

wall.

Thickening

of

theintima

is

the

first

structural

change,

followingincrease

in

smoothmuscle

and

the

infiltration

byinflammatory

cells.Pulmonary

VasculaturePhysiological

changes

include

mucus

hypersecretionciliary

dysfunction,

airflow

limitation,

pulmonaryhyperinflation,

gas

exchange

abnormalities,pulmonary

hypertension,

and

cor

pulmonale.Expiratory

airflow

limitation

is

the

hallmarkphysiological

change.The

irreversible

component

of

airflow

limitation

isprimarily

due

to

remodeling

–fibrosis

and

narrowingof

the

small

airways.PATHOPHYSIOLOGYCHAPTER

5

MANAGEMENT

OF

COPDWhile

disease

prevention

is

the

ultimate

goal,

oCOPD

has

been

diagnosed,

effective

managementshould

be

aimed

at

the

following

goals:Prevent

disease

progressionRelieve

symptomsImprove

exercise

toleranceImprove

health

statusPrevent

and

treat

complicationsPrevent

and

treat

exacerbationsReduce

mortalityCOMPONENT

1:

ASSESS

AND

MONITOR

DISEASE·

Stage

0

and

Stage

I:

chronic

cough

and

sputumproduction.·

Stage

II:

dyspnea

(interfere

daily

activitiesabove

symptoms.·

Stage

III:

dyspnea

worsens,

additional

symptoheralding

complications

may

develop.SymptomsThough

an

important

part

of

patient

care,a

physical

examination

is

rarelydiagnostic

in

COPD.Central

cyanosis,

“barrel-shaped”chest,

reduced

breath

sounds,

wheezingand

inspiratory

crakles.Physical

ExaminationSpirometry

measurements

remains

the

gold

standardfor

diagnosing

and

monitoring.Spirometry

measure:

FVC,

FEV1,

FEV1/FVC

.Postbronchodilator

FEV1<80%

and

FEV1/FVC<70%confirms

airflow

limitation

not

fully

reversible.FEV1/FVC

is

more

sensitive

than

FEV1,

FEV1/FVC<70%

is

considered

an

early

sign

of

airflowlimitation.Measurement

of

Airflow

Limitation(Spirometry)Forpatients

diagnosed

with

Stage

II:

ModerateCOPD

and

beyond,

the

following

additionalinvestigations

may

be

useful.Additional

Investigations

Performed

at

the

time

of

diagnosis,

it’s

usefulhelp

rule

out

asthma

and

to

assess

potentialresponse

to

treatment.

Patients

who

show

significant

improvement

inFEV1

are

more

likely

to

benefit

from

treatmentwith

bronchodilators

and

have

a

positive

responseto

glucocorticosteroids.

Even

patients

not

show

a

significant

FEV1response

may

benefit

symptomatically

from

long-term

bronchodilator

therapy.Bronchodilator

reversibility

testTests

should

be

performed

when

patients

areclinically

stable

and

free

form

respiratoryinfection.Patients

should

not

have

taken

inhaled

short-acting

bronchodilators

in

the

previous

sixhours,

long-acting

b2-agonist

12

hours,

orsustained-release

theophyllines

24

hours.PreparationFEV1

should

be

measuredbefore

and

30-45minutes

after

abronchodilator

is

given.The

bronchodilator

should

be

given

by

MDIthrough

a

spacer

or

by

nebulizer.Suitable

dosage

are

400mg

b2-agonist,

80mganticholinergic,

or

the

two

combined.Spirometry·

An

increase

in

FEV1

that

is

both

greater

than200ml

and

12%

above

the

pre-bronchodilatoris

considered

significant.Results

After

inhaled

glucocorticosteroids

for

6

weeto

3

months,

FEV1

increase

of

200ml

and15%above

baseline

is

considered

significant.

Thipart

of

patients

may

benefit

form

long-terminhaled

glucocorticosteroids.·

The

response

should

be

evaluated

with

respecto

the

post

bronchodilator

FEV1

(be

inaddition

to

treatment

with

a

bronchodilator)Glucocorticosteroid

reversibility

tA

Chest

X-ray

is

seldom

diagnostic

in

COPDunless

obvious

bullous

disease

is

present,

but

iis

valuable

in

excluding

alternative

diagnoses.Chest

X-rayThis

test

should

be

performed

in

patients

withFEV1<40%

predicted

or

with

clinical

signssuggestive

of

respiratory

failure

or

right

heafailure.Arterial

blood

gas

measurementAny

patient

who

has

cough,

sputum

production,

ordyspnea,

and/or

a

history

of

exposure

to

riskfactors

for

the

disease.

Whose

postbronchodilatFEV1<80%

with

FEV1/FVC<70%

confirms

thediagsis.Diagnosis

of

COPDDiagnosisSuggestive

FeaturesCOPDOnset

in

mid-lifeSymptoms

slowly

progressiveLong

smoking

historyDyspnea

during

exerciseLargely

irreversible

airflow

limitationAsthmaOnset

early

in

life(often

childhood)Symptoms

vary

from

day

to

daySymptoms

at

night/early

morningAllergy,

rhinitis,

and/or

eczema

also

presentFamily

history

of

asthmaLargely

reversible

airflow

limitationCongestive

HeartFailureFine

basilar

crackles

on

auscultationChest

X-ray

shows

dilated

heartPulmonary

edemaPulmonary

functiontests

indicatevolume

restriction,

notairflow

limitationBronchiectasisLarge

volumes

of

purulent

sputumCommonly

associated

with

bacterial

infectionCoarse

crackles/clubbing

on

auscultationChest

X-ray/CT

shows

bronchial

dilation,

bronchial

wallthickeningTuberculosisOnset

all

agesChest

X-ray

shows

lung

infiltrateDifferential

Diagnosis

Reduction

exposure

to

tobacco

smoke,

occupational

dusts

andchemicals,

air

pollutants

are

important

goals

to

prevent

the

onand

progression

of

COPD.

Smoking

cessation

is

the

single

most

effective

and

cost

effectto

reduce

the

risk

of

developing

COPD

and

stop

its

progression.

Practical

counseling,

social

support,

and

social

support

arraoutside

of

treatment

are

especially

effective.

If

counseling

is

not

sufficient

to

help

patients

quit

smoking,effective

pharmacotherapies

for

tobacco

dependence

are

availabCOMPONENT

2:

REDUCE

RISKFACTORSCOMPONENT

3:

MANAGE

STABLECOPDStudies

indicate

that

patient

education

alonedoes

not

improve

exerciseperformance

or

lungfunction

,

but

it

can

play

a

role

in

improvingskills,

ability

to

cope

with

illness,andhealthstatus.EDUCATIONTopics

for

Patient

EducationStage

o:Information

and

advice

about

reducing

risk

factorStage

I

to

Stage

II

:Information

about

the

nature

of

COPDInstruction

on

how

to

use

inhalers

and

othertreatmentsRecognition

and

treatment

of

acute

exacerbationsStrategies

for

minimizing

dyspneaStage

III:Information

about

complicationsInformation

about

oxygen

treatmentAdvance

directives

and

end-of-life

decisionsNone

of

the

existing

medication

for

COPD

has

been

shown

to

modify

the

long-term

decline

inlung

function,

the

pharmacologic

therapy

is

useto

prevent

and

control

symptoms,

reduce

thefrequency

and

severity

of

exacerbations,

improvhealth

status,

and

improve

exercise

tolerance.PHARMACOLOGIC

TREATMENT

Stepwise

increase

in

treatment

depending

onthe

severity

of

the

disease.

Regular

treatment

needs

to

be

maintained

atthe

same

level

for

long

periods

of

time

unlesssignificant

side

effects

occur

or

the

diseaseworsens.

Treatment

response

of

an

individual

patientvariable

and

should

bemonitored

closely

andadjusted

frequently.The

pharmacological

treatment

generprinciples:

Bronchodilator

medications

are

central

to

symptommanagements

in

COPD.Inhaled

therapy

is

preferred.

The

choice

between

b2

–agonist,

anticholinergic,

theophyllicombination

therapy

depends

on

availability

and

individualresponse.Bronchodilators

areusedas-needed

orrular.Long-acting

inhaled

bronchodilators

are

more

convenient.

Combining

bronchodilators

may

improve

efficacy

and

decreasethe

risk

of

side

effects

compared

to

increasing

the

doseof

asingle

bronchodilator.BronchodilatorsThe

principal

action

of

b2-agonists

isto

relax

airway

smooth

muscle

bystimulating

b2-adrenergic

receptors,whichincreases

cyclic

AMP

and

producedfunctional

antagonism

tobronchoconstriction.Adverse

effects

include:

resting

sinustachycardia,

exaggerated

somatic

tremor,hypokalemia,

mild

falls

in

PaO2.b

-agonists2The

most

important

effect

of

anticholinergic

medications

in

COPD

patientsappears

to

be

blockage

of

acetylcholine’seffect

on

M3

receptors.Extensive

use

of

this

class

of

inhaled

agentsi

a

wide

range

of

doses

and

clinical

settingshas

shown

them

to

be

very

safe.AnticholinergicsAll

studies

that

have

shown

efficacy

of

theophyllineCOPD

were

done

with

slow-release

preparation.Common

side

effects

include

headaches,

insomnia,nausea,

and

heartburn.

Some

times

atrial

andventricular

arrhythmias

and

grand

malconvulsions.Theophylline

is

effective

in

COPD

but,

due

to

itspotential

toxicity,

inhaled

bronchodilators

are

prefwhen

available.MethylxanthinesThe

effects

of

oral

and

inhaled

glucocorticosterin

COPD

are

much

less

dramatic

than

in

asthma,and

their

role

in

the

management

of

stable

COPD

ilimited

to

very

specific

indications.Glucocorticosteroidsshort-term:

Recent

studies

find

that

short

couof

oral

glucocorticosteroids

is

a

poor

predictor

oflong-term

response

to

inhaled

glucocorticosteroidCOPD.

So

there’s

insufficient

evidence

torecommend

a

therapeutic

trial

with

oralglucocorticosteroids

in

COPD

patients.Long-term:

It

is

notrecommendedin

COPDbecause

lack

of

evidence

of

benefit,

and

the

largebody

of

evidence

on

side

effects.Oral

glucocorticosteroidsFour

large

studies

show

that

regulartreatment

with

inhaled

glucocorticosteroids

ionly

appropriate

patients

with

a

documentedspirometric

response

to

inhaledglucocorticosteroids

or

in

those

with

andFEV1<50%

predicted

and

repeated

exacerbations

requiring

treatment

withantibiotics

or

oral

glucocorticosteroids.Inhaled

glucocorticosteroidsNON-PHARMACOLOGIC

TREATMENTRehabilitationA

comprehensive

pulmonary

rehabilitationprogram

includes

exercise

training,

nutritiocounseling

,

and

education.Administering

methods:

long-term

continuous

therduring

exercise,

and

to

relieve

acute

dyspnea

.Goal:

Increase

the

baseline

PaO2

to

at

lease

8.0kPsea

level

and

rest,

and/or

produce

an

SaO2

at

least90%.Long-term

oxygen

therapy(>15

hours

per

day)

hasbeen

shown

to

increase

survival.

It

can

also

have

abeneficial

impact

on

hemodynamics,

hematologiccharacteristics,

exercise

capacity,

lung

mechanicmental

state.Oxygen

TherapyIndications

for

long

term

oxygen

therapy:PaO

at

or

below

7.3kPa

(55mmHg)

or

SaO

at

or

below2

288%,

with

or

without

hypercapniaPaO

between

7.3kPa

(55mmHg)

and

8.0kPa

(6mmHg)

,2or

SaO2

of

89%,

if

there

is

evidence

of

pulmonaryhypertension

,

peripheral

edema

suggesting

congesticardiac

failure,

or

polycythemia

(hematocrit>55%)Oxygen

TherapyThere

is

no

convincing

evidence

that

thistherapy

has

a

role

in

the

management

of

stableCOPD.

But

the

combination

of

noninvasiveintermittent

positive

pressure

ventilation(NIPPV)

with

long-termoxygen

therapy

may

beof

some

use

in

those

with

pronounced

daytimehypercapnia.Ventilatory

SupportBullectomy:

In

carefully

selected

patients

thisprocedure

is

effective

in

reducing

dyspnea

andimproving

lung

function.Lung

volume

reduction

surgery:

Although

there

aresome

encouraging

reports,

it

is

still

and

experimentapalliative

surgical

procedure.Lung

transplantation:

In

appropriately

selectedpatients

with

very

advanced

COPD,

lung

transplantatihas

been

shown

to

improve

quality

of

life

and

functioncapacity.Surgical

TreatmentsStageCharacteristicsRecommended

treatmentALLAvoidance

of

risk

factor(s)Influenza

vaccination0:At

RiskChronic

symptoms(cough,

sputum)Exposure

to

risk

factor(s)Normal

spirometryI

:

MildCOPDFEV1/FVC<70%FEV1≥80%

PREDICTEDWith

or

without

symptomsShort-acting

bronchodilator

when

neededII

:ModerateCOPDIIA:

FEV1/FVC<70%50%≤FEV1<80%predictedWith

or

without

symptomsRegular

treatmentWith

one

or

morebronchodilatorsRehabilitationInhaled

glucocorticosteroidsignificant

symptoms

and

lfunction

responseIIB:

FEV1/FVC<70%30%≤FEV1<50%predictedRegular

treatmentWith

one

or

morebronchodilatorsRehabilitationInhaled

glucocorticosteroidsignificant

symptoms

and

lfunction

response

or

if

repexacerbationsIII

:

SevereCOPDFEV1/FVC<70%FEV1<30%

predictedor

presenceof

respiratory

failure

or

rightheart

failure

or

right

heartfailureRegular

treatment

with

one

or

more

bronchodilatorsInhaled

glucorticosteroids

if

significant

symptomsfunction

response

or

if

repeated

exacerbationTreatment

of

complicationsRehabilitationLong-term

oxygen

therapy

if

respiratory

failureConsider

surgical

treatmentsTherapy

at

Each

Stage

of

COPDThe

most

common

causes

ofan

exacerbationare

infection

of

the

tracheobronchial

tree

andair

pollution,

but

the

cause

of

about

one-thirdof

severe

exacerbations

cannot

be

identified.COMPONENT

4:

MANAGEEXACERABATONSDIGANOSIS

AND

ASSESSMENT

OFSEVERITYIncreased

breathlessness

is

the

main

symptomof

an

exacerbation,

and

often

accompanied

bywheezing

andchest

tightness,

increasedcoughand

sputum,

change

of

the

color

and/or

tenacityof

sputum

,

and

fever.An

increase

in

sputum

volume

and

purulence

points

to

a

bacterial

cause.Medical

HistoryThe

most

important

sign

of

a

severeexacerbation

is

a

change

of

alertness.In

general

a

PEF<100L/min

or

anFEV1<1.00

L

indicates

a

severe

exacerbation.A

PaO2<6.7kPa,

PaCO2>9.3kPa,

andpH<7.30

point

toward

a

life-threateningepisode

that

needs

ICU

management.Assessment

of

SeverityChest

radiographs

are

useful

in

identifying

alternative

diagnoses

that

canmimic

the

symptoms

of

and

exacerbation.An

ECG

aids

in

the

diagnosis

of

right

heart

hypertrophy,

arrhythmias,

andischemic

episodes.Chest

X-ray

and

ECGStreptococcus

pneumoniae,Hemophilis

influenzae,Moraxella

catarrhalis

are

the

mostcommon

bacterial

pathogens

involved

inCOPD

exacerbations.Other

laboratory

testsHOSPITAL

MANAGEMENTIndications

for

Hospital

Assessment

or

Admissfor

Acute

Exacerbations

of

COPD

Marked

increase

in

intensity

of

symptoms,

suchas

sudden

development

of

resting

dyspneaSevere

background

COPD

Onset

of

new

physical

signs(e.g.,

cyanosis,peripheral

edema)

Failure

of

exacerbation

to

respond

to

initialmedical

managementSignificant

comorbiditiesNewly

occurring

arrhythmiasDiagnostic

uncertaintyOlder

ageInsufficient

home

supportIndications

for

ICU

Admission

of

Patients

wiAcute

Exacerbations

of

COPD

Severe

dyspnea

that

responds

inadequately

to

initiemergency

therapyConfusion,

lethargy,

coma

Persistent

or

worsening

hypoxemia

(PaO2<6.7kPa),and/or

severe/worsening

hypercapnia(PaCO2>9.3kPa,),

and/or

severe

worseningrespiratory

acidosis

(pH<7.30)

despite

supplementoxygen

and

NIPPVOxygen

therapy

is

the

cornerstone

ofhospital

treatment

of

COPD

exacerbationsVenturi

masks

are

more

accurate

sourced

of

controlled

oxygen

than

are

nasal

prongs.Controlled

oxygen

therapyShort-acting

inhaled

β2-agonists

are

usually

thepreferred

bronchodilators

for

exacerbations.If

a

prompt

response

does

not

occur,

the

addition

ofanticholinergic

is

recommended.In

more

severe

exacerbations,

addition

of

an

oral

orin