Global Initiative for Chronic

e
uc
Obstructive

od
Lung

pr
re
Disease

or
er
alt
ot
on
-d
ial
ter
ma

POCKET GUIDE
d
hte

TO COPD DIAGNOSIS, MANAGEMENT,

rig

AND PREVENTION
py

A Guide for Health Care Professionals

Co

U P D AT ED 2 0 10
 Global Initiative for Chronic
Obstructive

e
L ung

uc
od
Disease

pr
re
Pocket Guide to COPD Diagnosis, Management,
and Prevention

or
er
GOLD Ex ecu t iv e Co m m it t ee

Roberto Rodriguez-Roisin, MD, Spain, Chair alt

Antonio Anzueto, MD, US (representing ATS)
ot
Jean Bourbeau, MD, Canada
on

Teresita S. DeGuia, MD, Philippines

David Hui, MD, Hong Kong, ROC
Christine Jenkins, MD, Australia
-d

Fernando Martinez, MD, US

Michiaki Mishima, MD, Japan (representing APSR)
ial

Mara Montes de Oca, MD, PhD (representing ALAT)

Robert Stockley, MD, UK
ter

Chris van Weel, MD, Netherlands (representing WONCA)

Jorgen Vestbo, MD, Denmark
ma

Ob s er v er :
Jadwiga Wedzicha, MD, UK (Representing ERS)
d
hte

GOLD Nat io n al L ead er s

Representatives from many countries serve as a network for the dissemination and
rig

implementation of programs for diagnosis, management, and prevention of COPD.

The GOLD Executive Committee is grateful to the many GOLD National Leaders who
py

participated in discussions of concepts that appear in GOLD reports, and for their
comments during the review of the 2006 Global Strategy for the Diagnosis,
Co

Management, and Prevention of COPD.

2010 Global Initiative for Chronic Obstructive Lung Disease, Inc.

 TA B L E O F CON T EN T S
3 P R EFA CE

e
uc
5 K EY P O I N T S
6 W H AT I S CH R O N I C OB S T R U CT I V E

od
P U L M ON A R Y D I S EA S E ( CO P D ) ?
7 R I S K FA CT OR S : WH AT CA U S ES CO P D ?

pr
8 D I A GN O S I N G COP D

re
Figure 1: Key Indicators for Considering a
COPD Diagnosis

or
Figure 2: Normal Spirogram and Spirogram Typical of
Patients with Mild to Moderate COPD

er
Figure 3: Differential Diagnosis of COPD
12

13
CO M P ON EN T S OF CA R E:
alt
A COP D M A N A G EM EN T P R O GR A M
Co m p o n e n t 1 : A s s e s s a n d M o n i t o r D i s e a s e
ot
15 Co m p o n e n t 2 : R e d u ce R i s k F a ct o r s
on

Figure 4: Strategy to Help a Patient Quit Smoking

17 Co m p o n e n t 3 : M a n a g e S t a b l e COP D
Patient Education
-d

Pharmacologic Treatment
Figure 5: Commonly Used Formulations of Drugs for COPD
ial

Non-Pharmacologic Treatment
Figure 6: Therapy at Each Stage of COPD
ter

22 Co m p o n e n t 4 : M a n a g e Ex a ce r b a t i o n s
How to Assess the Severity of an Exacerbation
ma

Home Management
Hospital Management
Figure 7: Indications for Hospital Admission
d

for Exacerbations
hte

24 A P P EN D I X I : S P I R OM ET R Y F OR D I A G N OS I S OF COP D
rig
py
Co
 PREFACE

e
uc
Chronic Obstructive Pulmonary Disease (COPD) is a major cause of

od
chronic morbidity and mortality throughout the world. The Globa l
In it iat iv e f or Ch ro n ic Ob s t r u ct iv e L u n g Dis eas e was created to

pr
increase awareness of COPD among health professionals, public health

re
authorities, and the general public, and to improve prevention and
management through a concerted worldwide effort. The Initiative

or
prepares scientific reports on COPD, encourages dissemination and
adoption of the reports, and promotes international collaboration on

er
COPD research.

alt
While COPD has been recognized for many years, public health officials
are concerned about continuing increases in its prevalence and mortality,
ot
which are due in large part to the increasing use of tobacco products
on

worldwide and the changing age structure of populations in developing

countries. The Global In it iat iv e f or Ch r on ic Obs t r u ct iv e L u n g
Dis eas e offers a framework for management of COPD that can be
-d

adapted to local health care systems and resources. Educational tools,

such as laminated cards or computer-based learning programs, can be
ial

prepared that are tailored to these systems and resources.

ter

The Glob al In it iat iv e f or Ch r on ic Ob s t r u ct iv e L u n g Dis eas e

program includes the following publications:
ma

Global Strategy for the Diagnosis, Management, and Prevention of

COPD. Scientific information and recommendations for COPD
d

programs. (Updated 2010)

hte

Executive Summary, Global Strategy for the Diagnosis, Management,

and Prevention of COPD. (Updated 2010)
rig

Pocket Guide to COPD Diagnosis, Management, and Prevention.

Summary of patient care information for primary health care
py

professionals. (Updated 2010)

Co

What You and Your Family Can Do About COPD. Information booklet
for patients and their families.

3
 These publications are available on the Internet at www.goldcopd.org.
This site provides links to other websites with information about COPD.

e
This Pocket Guide has been developed from the Global Strategy for the

uc
Diagnosis, Management, and Prevention of COPD (2010). Technical
discussions of COPD and COPD management, evidence levels, and specific

od
citations from the scientific literature are included in that source document.

pr
A ck n o w l e d g e m e n t s : Grateful acknowledgement is given for the educational

re
grants from Almirall, AstraZeneca, Boehringer Ingelheim, Chiesi, Dey, Forest
Laboratories, GlaxoSmithKline, Novartis, Nycomed, Pfizer, Philips Respironics, and

or
Schering-Plough. The generous contributions of these companies assured that the
participants could meet together and publications could be printed for wide distribu-

er
tion. The participants, however, are solely responsible for the statements and con-
clusions in the publications.
alt
ot
on
-d
ial
ter
d ma
hte
rig
py
Co

4
 KEY POINTS

e
uc
Ch r o n i c O b s t r u ct i v e P u l m o n a r y D i s e a s e ( COP D ) is a
preventable and treatable disease with some significant extra-

od
pulmonary effects that may contribute to the severity in individual
patients. Its pulmonary component is characterized by airflow limitation

pr
that is not fully reversible. The airflow limitation is usually progressive

re
and associated with an abnormal inflammatory response of the lung
to noxious particles or gases.

or
Worldwide, the most commonly encountered r i s k f a ct o r for COPD

er
is ci g a r e t t e s m o k i n g . A t e v e r y p o s s i b l e o p p o r t u n i t y
i n d i v i d u a l s w h o s m o k e s h o u l d b e e n co u r a g e d t o q u i t . In
alt
many countries, air pollution resulting from the burning of wood and
other biomass fuels has also been identified as a COPD risk factor.
ot
A d i a g n o s i s of COPD should be considered in any patient who has
on

dyspnea, chronic cough or sputum production, and/or a history of

exposure to risk factors for the disease. The diagnosis should be
-d

confirmed by spirometry.

A CO P D m a n a g e m e n t p r o g r a m includes four components:

ial

assess and monitor disease, reduce risk factors, manage stable

ter

COPD, and manage exacerbations.

ma

P h a r m a co l o g i c t r e a t m e n t can prevent and control symptoms,

reduce the frequency and severity of exacerbations, improve health
status, and improve exercise tolerance.
d
hte

P a t i e n t e d u ca t i o n can help improve skills, ability to cope with

illness, and health status. It is an effective way to accomplish smoking
cessation, initiate discussions and understanding of advance directives
rig

and end-of-life issues, and improve responses to acute exacerbations.

py

COPD is often associated with e x a ce r b a t i o n s of symptoms.

Co

5
 WHAT IS CHRONIC
OBSTRUCTIVE

e
uc
PULMONARY DISEASE

od
(COPD)?

pr
re
Ch r o n i c Ob s t r u ct i v e P u l m o n a r y D i s e a s e ( CO P D ) is a preventable

or
and treatable disease with some significant extrapulmonary effects that may
contribute to the severity in individual patients. Its pulmonary component

er
is characterized by airflow limitation that is not fully reversible. The air-
flow limitation is usually progressive and associated with an abnormal
alt
inflammatory response of the lung to noxious particles or gases.
ot
This definition does not use the terms chronic bronchitis and emphysema*
and excludes asthma (reversible airflow limitation).
on

S y m p t o m s o f CO P D i n cl u d e :
-d

Cough
ial

Sputum production
Dyspnea on exertion
ter

Episodes of acute worsening of these symptoms often occur.

d ma

Ch r o n i c co u g h a n d s p u t u m p r o d u ct i o n o f t e n p r e ce d e t h e
hte

d e v e l o p m e n t o f a i r f l o w l i m i t a t io n b y m a n y y e a r s , a l t h o u g h
n o t a l l i n d i v i d u a l s w i t h co u g h a n d s p u t u m p r o d u ct i o n g o o n
t o d e v e l o p COP D .
rig
py
Co

*Chronic bronchitis, defined as the presence of cough and sputum production for at least 3
months in each of 2 consecutive years, is not necessarily associated with airflow limitation.
Emphysema, defined as destruction of the alveoli, is a pathological term that is sometimes
(incorrectly) used clinically and describes only one of several structural abnormalities present
in patients with COPD.

6
 RISK FACTORS:
WHAT CAUSES COPD?

e
uc
Wo r l d w i d e , ci g a r e t t e s m o k i n g i s t h e m o s t co m m o n l y

od
e n co u n t e r e d r i s k f a ct o r f o r CO P D .

pr
The genetic risk factor that is best documented is a severe hereditary

re
deficiency of alpha-1 antitrypsin. It provides a model for how other
genetic risk factors are thought to contribute to COPD.

or
COPD risk is related to the total burden of inhaled particles a person

er
encounters over their lifetime:

alt
To b a cco s m o k e , including cigarette, pipe, cigar, and other types
of tobacco smoking popular in many countries, as well as
ot
environmental tobacco smoke (ETS)
Occu p a t i o n a l d u s t s a n d ch e m i ca l s (vapors, irritants, and
on

fumes) when the exposures are sufficiently intense or prolonged

I n d o o r a i r p o l l u t i o n from biomass fuel used for cooking and
-d

heating in poorly vented dwellings, a risk factor that particularly

affects women in developing countries
Ou t d o o r a i r p o l l u t i o n also contributes to the lungs total burden
ial

of inhaled particles, although it appears to have a relatively small

ter

effect in causing COPD

ma

In addition, any factor that affects lung growth during gestation and
childhood (low birth weight, respiratory infections, etc.) has the potential
for increasing an individuals risk of developing COPD.
d
hte
rig
py
Co

7
 DIAGNOSING
COPD

e
uc
A diagnosis of COPD should be considered in any patient who has dyspnea,

od
chronic cough or sputum production, and/or a history of exposure to risk
factors for the disease, especially cigarette smoking (FF i g u r e 1 ).

pr
re
F i g u r e 1 : K e y I n d i ca t o r s f o r Co n s id e r i n g a COP D D i a g n o s i s

or
Consider COPD, and perform spirometry, if any of these indicators

er
are present in an individual over age 40. These indicators are not
diagnostic themselves, but the presence of multiple key indicators
increases the probability of a diagnosis of COPD.
alt
D y s p n e a that is: Progressive (worsens over time).
ot
Usually worse with exercise.
Persistent (present every day).
on

Described by the patient as an increased

effort to breathe, heaviness, air hunger,
-d

or gasping.
Ch r o n ic co u g h : May be intermittent and may be unproductive.
Ch r o n ic s p u t u m p r o d u ct i o n :
ial

Any pattern of chronic sputum production may

indicate COPD.
ter

H i s t o r y o f e x p o s u r e t o r i s k f a ct o r s :
To b a cco s m o k e ( in cl u d in g p o p u l a r l o ca l
ma

p r e p a r a t io n s ) .
Occupational dusts and chemicals.
Smoke from home cooking and heating fuel.
d
hte

T h e d i a g n o s i s s h o u l d b e co n f i r m e d b y s p i r o m e t r y *
( F i g u r e 2 , p a g e 9 a n d A p p e n d i x I, p a g e 2 4 ) .
rig
py

*Where spirometry is unavailable, the diagnosis of COPD should be made using all
Co

available tools. Clinical symptoms and signs (abnormal shortness of breath and increased
forced expiratory time) can be used to help with the diagnosis. A low peak flow is consistent
with COPD but has poor specificity since it can be caused by other lung diseases and by
poor performance. In the interest of improving the accuracy of a diagnosis of COPD, every
effort should be made to provide access to standardized spirometry.

8
 When performing spirometry, measure:

F orced V ital Capacity (FF V C) and

e
F orced Expiratory V olume in one second (FF EV 1 ).

uc
Calculate the FEV1/FVC ratio.

od
Spirometric results are expressed as % P r e d i ct e d using

pr
appropriate normal values for the persons sex, age, and height.

re
F i g u r e 2 : N o r m a l S p i r o g r a m a n d S p i r o g r a m Ty p i ca l o f

or
P a t i e n t s w i t h M i l d t o M o d e r a t e CO P D *

er
alt
ot
on
-d
ial
ter
d ma
hte

*Postbronchodilator FEV1 is recommended for the diagnosis

and assessment of severity of COPD.
rig
py

P a t i e n t s w i t h COP D t y p ica l l y s h o w a d e cr e a s e in b o t h F EV 1
a n d F EV 1 /F V C. T h e d e g r e e o f s p i r o m e t r ic a b n o r m a l i t y
g e n e r a l l y r e f l e ct s t h e s e v e r i t y o f COP D . H o w e v e r, b o t h
Co

s y m p t o m s a n d s p ir o m e t r y s h o u l d b e c o n s i d e r e d w h e n
d e v e l o p in g a n i n d i v id u a l i z e d m a n a g e m e n t s t r a t e g y f o r
e a ch p a t i e n t .

9
 St a g es o f COP D

St a ge I: Mild COP D - Mild airflow limitation (FEV1/FVC < 70%;

e
FEV1 80% predicted) and sometimes, but not always, chronic cough

uc
and sputum production.

od
At this stage, the individual may not be aware that his or her lung
function is abnormal.

pr
re
St a ge II: Mo de r at e COP D - Worsening airflow limitation
(FEV1/FVC < 70%; 50% FEV1 < 80% predicted), with shortness

or
of breath typically developing on exertion.

This is the stage at which patients typically seek medical attention

er
because of chronic respiratory symptoms or an exacerbation of their
disease. alt
St a ge III: Sev er e COP D - Further worsening of airflow limitation
ot
(FEV1/FVC < 70%; 30% FEV1 < 50% predicted), greater shortness of
on

breath, reduced exercise capacity, and repeated exacerbations which

have an impact on patients quality of life.
-d

St a ge IV: Ver y Sev e r e COP D - Severe airflow limitation

(FEV1/FVC < 70%; FEV1 < 30% predicted) or FEV1 < 50% predicted
ial

plus chronic respiratory failure. Patients may have Very Severe (Stage IV)
ter

COPD even if the FEV1 is > 30% predicted, whenever this complication
is present.
ma

At this stage, quality of life is very appreciably impaired and

exacerbations may be life-threatening.
d
hte

At R is k f or COP D
A major objective of GOLD is to increase awareness among health care providers and the
rig

general public of the significance of COPD symptoms. The classification of severity of COPD
now includes four stages classified by spirometryStage I: Mild COPD; Stage II: Moderate
py

COPD; Stage III: Severe COPD; Stage IV: Very Severe COPD. A fifth categoryStage 0: At
Riskthat appeared in the 2001 report is no longer included as a stage of COPD, as there
Co

is incomplete evidence that the individuals who meet the definition of At Risk (chronic cough
and sputum production, normal spirometry) necessarily progress on to Stage I: Mild COPD.
Nevertheless, the importance of the public health message that chronic cough and sputum are
not normal is unchanged and their presence should trigger a search for underlying cause(s).

10
 D if f e r e n t ia l D i a g n o s i s : A major differential diagnosis is asthma. In
some patients with chronic asthma, a clear distinction from COPD is not

e
possible using current imaging and physiological testing techniques. In these

uc
patients, current management is similar to that of asthma. Other potential
diagnoses are usually easier to distinguish from COPD (FF ig u r e 3 ).

od
pr
F i g u r e 3 : D i f f e r e n t i a l D i a g n o s i s o f CO P D

re
D ia g n o s is Su g g e s t iv e Fe a t u r e s *
COPD Onset in mid-life.

or
Symptoms slowly progressive.
Long smoking history.

er
Dyspnea during exercise.
Largely irreversible airflow limitation.
Asthma
alt
Onset early in life (often childhood).
Symptoms vary from day to day.
Symptoms at night/early morning.
ot
Allergy, rhinitis, and/or eczema also present.
on

Family history of asthma.

Largely reversible airflow limitation.
Congestive Heart Failure Fine basilar crackles on auscultation.
-d

Chest X-ray shows dilated heart, pulmonary edema.

Pulmonary function tests indicate volume restriction, not airflow
limitation.
ial

Bronchiectasis Large volumes of purulent sputum.

Commonly associated with bacterial infection.
ter

Coarse crackles/clubbing on auscultation.

Chest X-ray/CT shows bronchial dilation, bronchial wall thickening.
ma

Tuberculosis Onset all ages.

Chest X-ray shows lung infiltrate or nodular lesions.
Microbiological confirmation.
d

High local prevalence of tuberculosis.

hte

Obliterative Bronchiolitis Onset in younger age, nonsmokers.

May have history of rheumatoid arthritis or fume exposure.
CT on expiration shows hypodense areas.
rig

Diffuse Panbronchiolitis Most patients are male and nonsmokers.

Almost all have chronic sinusitis.
py

Chest X-ray and HRCT show diffuse small centrilobular

nodular opacities and hyperinflation.
Co

*These features tend to be characteristic of the respective diseases, but do not occur in
every case. For example, a person who has never smoked may develop COPD (especially
in the developing world, where other risk factors may be more important than cigarette
smoking); asthma may develop in adult and even elderly patients.

11
 COMPONENTS OF CARE:
A COPD MANAGEMENT

e
uc
PROGRAM

od
pr
re
The goals of COPD management include:

or
Relieve symptoms
Prevent disease progression

er
Improve exercise tolerance
Improve health status


Prevent and treat complications
Prevent and treat exacerbations
alt
ot
Reduce mortality
Prevent or minimize side effects from treatment
on

Cessation of cigarette smoking should be included as a goal throughout

-d

the management program.

T H ES E G OA L S CA N B E A CH I EV ED T H R OU G H
ial

I M P L EM EN TAT I ON OF A COP D M A N A GEM EN T P R OG R A M

ter

WI T H F OU R COM P O N EN T S :

1 . A s s e s s a n d M o n it o r D is e a s e
ma

2 . R e d u ce R i s k F a ct o r s
d

3 . M a n a g e S t a b l e CO P D
hte

4 . M a n a g e Ex a c e r b a t i o n s
rig
py
Co

12
 Component 1: Assess and Monitor Disease

e
A d e t a i l e d m e d i ca l h i s t o r y of a new patient known or thought to

uc
have COPD should assess:

od
Exposure to risk factors, including intensity and duration.

pr
Past medical history, including asthma, allergy, sinusitis or nasal

re
polyps, respiratory infections in childhood, and other respiratory
diseases.

or
Family history of COPD or other chronic respiratory disease.

er
Pattern of symptom development.
alt
History of exacerbations or previous hospitalizations for
ot
respiratory disorder.
on

Presence of comorbidities, such as heart disease, malignancies,

osteoporosis, and musculoskeletal disorders, which may also
-d

contribute to restriction of activity.

Appropriateness of current medical treatments.

ial
ter

Impact of disease on patients life, including limitation of activity;

missed work and economic impact; effect on family routines; and
ma

feelings of depression or anxiety.

Social and family support available to the patient.

d
hte

Possibilities for reducing risk factors, especially smoking cessation.

rig
py
Co

13
 In addition to s piro m e t r y , the following ot h er t es t s may be considered
for the assessment of a patient with Moderate (Stage II), Severe
(Stage III), and Very Severe (Stage IV) COPD.

e
uc
B ro n ch od ilat o r r e v er s ibilit y t e s t in g: To rule out a diagnosis of
asthma, particularly in patients with an atypical history (e.g., asthma

od
in childhood and regular night waking with cough and wheeze).

pr
Ch es t X - r a y : Seldom diagnostic in COPD but valuable to exclude

re
alternative diagnoses such as pulmonary tuberculosis, and identify
comorbidities such as cardiac failure.

or
Ar t er ia l blo od ga s m ea s u r em e n t : Perform in patients with

er
FEV1 < 50% predicted or with clinical signs suggestive of respiratory

alt
failure or right heart failure. The major clinical sign of respiratory
failure is cyanosis. Clinical signs of right heart failure include ankle
edema and an increase in the jugular venous pressure. Respiratory
ot
failure is indicated by PaO2 < 8.0 kPa (60 mm Hg), with or without
on

PaCO2 > 6.7 kPa (50 mm Hg) while breathing air at sea level.
-d

Alph a - 1 an t it r y p s in def icie n cy s cr een in g: Perform when

COPD develops in patients of Caucasian descent under 45 years or
with a strong family history of COPD.
ial
ter
d ma

COP D is u s u ally a p ro g r es s iv e dis ea s e. L u n g f u n ct io n

hte

ca n b e ex pect ed t o w o r s en o v er t im e, ev en w it h t h e b es t
av aila ble car e. Sy m p t o m s a n d lu n g f u n ct io n s h o u ld be
m o n it o r ed t o f o llo w t h e d ev elo p m en t o f co m plica t ion s , t o
rig

gu ide t r ea t m en t , an d t o f acilit a te d is cu s s io n o f m an a gem en t

o pt io n s w it h pa t ien t s . Co m o r bidit ies a r e co m m o n in COP D
py

an d s h o u ld b e a ct iv ely id en t if ied .
Co

14
 Component 2: Reduce Risk Factors
S m o k i n g ce s s a t i o n i s t h e s i n g l e m o s t e f f e ct i v e a n d co s t -

e
e f f e ct i v e i n t e r v e n t i o n t o r e d u ce t h e r i s k o f d e v e l o p i n g

uc
COP D a n d s l o w i t s p r o g r e s s i o n .

od
Even a brief, 3-minute period of counseling to urge a smoker to
quit can be effective, and at a minimum this should be done for

pr
every smoker at every health care provider visit. More intensive

re
strategies increase the likelihood of sustained quitting (FF i g u r e 4 ).

or
Pharmacotherapy (nicotine replacement, buproprion/nortryptiline,
and/or varenicline) is recommended when counseling is not sufficient

er
to help patients stop smoking. Special consideration should be
given before using pharmacotherapy in people smoking fewer than
alt
10 cigarettes per day, pregnant women, adolescents, and those
with medical contraindications (unstable coronary artery disease,
ot
untreated peptic ulcer, and recent myocardial infarction or stroke
for nicotine replacement; and history of seizures for buproprion).
on
-d

F ig u r e 4 : S t r a t e g y t o H e l p a P a t ie n t Qu it Sm o k in g

1. A S K : Systematically identify all tobacco users at every visit.

ial

Implement an office-wide system that ensures that, for EVERY patient

at EVERY clinic visit, tobacco-use status is queried and documented.
ter

2. A D V I S E: Strongly urge all tobacco users to quit.

In a clear, strong, and personalized manner, urge every tobacco user
ma

to quit.
3. A S S ES S : Determine willingness to make a quit attempt.
Ask every tobacco user if he or she is willing to make a quit attempt
d

at this time (e.g., within the next 30 days).

hte

4. A S S I S T: Aid the patient in quitting.

Help the patient with a quit plan; provide practical counseling;
rig

provide intra-treatment social support; help the patient obtain

extra-treatment social support; recommend use of approved
py

pharmacotherapy if appropriate; provide supplementary materials.

5. A R R A NG E: Schedule follow-up contact.
Co

Schedule follow-up contact, either in person or via telephone.

15
S m o k i n g P r e v e n t i o n : Encourage comprehensive tobacco-control
policies and programs with clear, consistent, and repeated nonsmoking
messages. Work with government officials to pass legislation to establish

e
smoke-free schools, public facilities, and work environments and

uc
encourage patients to keep smoke-free homes.

od
Occu p a t i o n a l Ex p o s u r e s : Emphasize primary prevention, which
is best achieved by elimination or reduction of exposures to various

pr
substances in the workplace. Secondary prevention, achieved through

re
surveillance and early detection, is also important.

or
I n d o o r a n d O u t d o o r A i r P o l l u t i o n : Implement measures to reduce
or avoid indoor air pollution from biomass fuel, burned for cooking and

er
heating in poorly ventilated dwellings. Advise patients to monitor public
announcements of air quality and, depending on the severity of their
alt
disease, avoid vigorous exercise outdoors or stay indoors altogether
during pollution episodes.
ot
on
-d
ial
ter
d ma
hte
rig
py
Co

16
 Component 3: Manage Stable COPD
M a n a g e m e n t o f s t a b l e CO P D s h o u l d b e g u i d e d b y t h e

e
f o l l o w i n g g e n e r a l p r i n ci p l e s :

uc
Determine disease severity on an individual basis by taking into

od
account the patients symptoms, airflow limitation, frequency and
severity of exacerbations, complications, respiratory failure,

pr
comorbidities, and general health status.

re
Implement a stepwise treatment plan that reflects this assessment of
disease severity.

or
Choose treatments according to national and cultural preferences,
the patients skills and preferences, and the local availability of

er
medications.

alt
P a t i e n t e d u ca t i o n can help improve skills, ability to cope with illness,
and health status. It is an effective way to accomplish smoking cessation,
ot
initiate discussions and understanding of advance directives and end-of-
life issues, and improve responses to acute exacerbations.
on

P h a r m a co l o g i c t r e a t m e n t (FF i g u r e 5 ) can control and prevent

-d

symptoms, reduce the frequency and severity of exacerbations, improve

health status, and improve exercise tolerance.
ial

B r o n ch o d i l a t o r s : These medications are central to symptom

ter

management in COPD.
ma

Inhaled therapy is preferred.

Give as needed to relieve intermittent or worsening symptoms, and
on a regular basis to prevent or reduce persistent symptoms.
d

The choice between 2-agonists, anticholinergics, methylxanthines,

hte

and combination therapy depends on the availability of medications

and each patients individual response in terms of both symptom
relief and side effects.
rig

Regular treatment with long-acting bronchodilators, including nebu-

lized formulations, is more effective and convenient than treatment
py

with short-acting bronchodilators.

Combining bronchodilators of different pharmacologic classes may
Co

improve efficacy and decrease the risk of side effects compared to

increasing the dose of a single bronchodilator.

17
 Figure 5. Formulations and Typical Doses of COPD Medications*
Drug Inhaler Solution for Oral Vials for Duration of
(g) Nebulizer Injection Action (hours)

e
(mg/ml) (mg)

uc
2-agonists
Short-acting

od
Fenoterol 100-200 (MDI) 1 0.05% (Syrup) 4-6
Levalbuterol 45-90 (MDI) 0.21, 0.42 6-8

pr
Salbutamol (albuterol) 100, 200 (MDI & DPI) 5 5mg (Pill), 0.024%(Syrup) 0.1, 0.5 4-6
Terbutaline 400, 500 (DPI) 2.5, 5 (Pill) 4-6

re
Long-acting
Formoterol 4.5-12 (MDI & DPI) 0.01 12+

or
Arformoterol 0.0075 12+
Indacaterol 150-300 (DPI) 24

er
Salmeterol 25-50 (MDI & DPI) 12+
Anticholinergics
Short-acting
Ipratropium bromide 20, 40 (MDI) 0.25-0.5
alt 6-8
ot
Oxitropium bromide 100 (MDI) 1.5 7-9
Long-acting
on

Tiotropium 18 (DPI), 5 (SMI) 24+

Combination short-acting 2-agonists plus anticholinergic in one inhaler
-d

Fenoterol/Ipratropium 200/80 (MDI) 1.25/0.5 6-8

Salbutamol/Ipratropium 75/15 (MDI) 0.75/0.5 6-8
Methylxanthines
ial

Aminophylline 200-600 mg (Pill) 240 mg Variable, up to 24

ter

Theophylline (SR) 100-600 mg (Pill) Variable, up to 24

Inhaled glucocorticosteroids
ma

Beclomethasone 50-400 (MDI & DPI) 0.2-0.4

Budesonide 100, 200, 400 (DPI) 0.20. 0.25, 0.5
Fluticasone 50-500 (MDI & DPI)
Combination long-acting 2-agonists plus glucocorticosteroids in one inhaler
d
hte

Formoterol/Budesonide 4.5/160, 9/320 (DPI)

Salmeterol/Fluticasone 50/100, 250. 500 (DPI)
25/50, 125, 250 (MDI)
rig

Systemic glucocorticosteroids
Prednisone 5-60 mg (Pill)
py

Methyl-prednisolone 4, 8, 16 mg (Pill)
Phosphodiesterase-4 inhibitors
Co

Roflumilast 500 mcg (Pill) 24

MDI=metered dose inhaler; DPI=dry powder inhaler
*Not all formulations are available in all countries; in some countries, other formulations may be available.
Formoterol nebulized solution is based on the unit dose vial containing 20 gm in a volume of 2.0ml

18
 Inhaled Glucocorticosteroids: Regular treatment with inhaled
glucocorticosteroids does not modify the long-term decline in FEV1 but
has been shown to reduce the frequency of exacerbations and thus
improve health status for symptomatic patients with an FEV1 < 50%

e
predicted and repeated exacerbations (for example, 3 in the last three

uc
years). The dose-response relationships and long-term safety of inhaled
glucocorticosteroids in COPD are not known. Treatment with inhaled glu-

od
cocorticosteroids increases the likelihood of pneumonia and does not
reduce overall mortality.

pr
An inhaled glucocorticosteroid combined with a long-acting 2-agonist is

re
more effective than the individual components in reducing exacerbations
and improving lung function and health status. Combination therapy

or
increases the likelihood of pneumonia and has no significant effects on
mortality. In patients with an FEV1 less than 60%, pharmacotherapy with

er
long-acting 2-agonist, inhaled glucocorticosteroid and its combination

alt
decreases the rate of decline of lung function. Addition of a long-acting
2-agonist/inhaled glucocorticosteroid to an anticholinergic (tiotropium)
appears to provide additional benefits.
ot
Oral Glucocorticosteroids: Long-term treatment with oral glucocorticosteroids
on

is not recommended.
Phosphodiesterase-4 inhibitors: In patients with Stage III: Severe COPD or
-d

Stage IV: Very Severe COPD and a history of exacerbations and chronic
bronchitis, the phosphodiesterase-4 inhibitor, roflumilast, reduces exacerba-
ial

tions treated with oral glucocorticosteroids. These effects are also seen
when roflumilast is added to long-acting bronchodilators; there are no
ter

comparison studies with inhaled glucocorticosteroids.

ma

Vaccines: Influenza vaccines reduce serious illness and death in COPD

patients by 50%. Vaccines containing killed or live, inactivated viruses
are recommended, and should be given once each year. Pneumococcal
d

polysaccharide vaccine is recommended for COPD patients 65 years and

hte

older, and has been shown to reduce community-acquired pneumonia in

those under age 65 with FEV1 < 40% predicted.
rig

An t ibiot ics : Not recommended except for treatment of infectious

exacerbations and other bacterial infections.
py

M u co ly t ic (Mu co k in et ic, Mu cor e gu lat or ) Agen t s: Patients with

Co

viscous sputum may benefit from mucolytics, but overall benefits are very
small. Use is not recommended.

An t it u s siv e s: Regular use contraindicated in stable COPD.

19
 Non - P h ar m acolo gic Tr e at m en t includes rehabilitation, oxygen
therapy, and surgical interventions.
Rehabilitation: Patients at all stages of disease benefit from exercize

e
training programs improvements in exercise tolerance and symptoms of

uc
dyspnea and fatigue. Benefits can be sustained even after a single pulmo-
nary rehabilitation program. The minimum length of an effective rehabili-

od
tation program is 6 weeks; the longer the program continues, the more
effective the results. Benefit does wane after a rehabilitation program

pr
ends, but if exercise training is maintained at home the patient's health

re
status remains above pre-rehabilitation levels.

Th e go a ls of pu lm on a r y r eh ab ilit at io n a r e t o r ed u ce s y m pt o m s ,

or
im pr o v e qu a lit y o f life, a n d in cr ea s e pa r t icipa t io n in ev er y da y
a ct iv itaties
Patients all. stages of disease benefit from exercise training programs,

er
alt
Ox y gen Th e r apy : The long-term administration of oxygen (>15 hours
per day) to patients with chronic respiratory failure increases survival and
has a beneficial impact on pulmonary hemodynamics, hematologic
ot
characteristics, exercise capacity, lung mechanics, and mental state.
on

Initiate oxygen therapy for patients with Stage IV: Very Severe COPD if:
-d

PaO2 is at or below 7.3 kPa (55 mm Hg) or SaO2 is at or below

88%, with or without hypercapnia; or
PO2 is between 7.3 kPa (55 mm Hg) and 8.0 kPa (60 mm Hg)
ial

or SaO2 is 88%, if there is evidence of pulmonary hypertension,

ter

peripheral edema suggesting congestive heart failure, or

polycythemia (hematocrit > 55%).
ma

Th e go a l o f lo n g- t er m o x y gen t h er a py is t o in cr ea s e t h e ba s e-
lin e P a O2 a t r es t t o a t lea s t 8.0 k P a (60 m m Hg) a t s ea lev el,
d

a n d/o r pr o du ce Sa O2 a t lea s t 90% , w h ich w ill p r es er v e v it al

hte

o r ga n f u n ct io n b y en s u r in g an ad equ at e d eliv er y of o x y gen .

rig

Su r gical Tr e at m en t s : Bullectomy and lung transplantation may be

py

considered in carefully selected patients with Stage IV: Very Severe

COPD. There is currently no sufficient evidence that would support the
Co

widespread use of lung volume reduction surgery (LVRS).

Th er e is n o con v in cin g ev iden ce t h at m ech an ical v en t ilat or y

su ppor t h as a role in t h e rou tin e m an agem en t of stable COP D.

20
 A summary of characteristics and recommended treatment at each stage
of COPD is shown in F i g u r e 6 .

e
uc
Figure 6: Therapy at Each Stage of COPD*

od
pr
I: Mild II: Moderate III: Severe IV: Very Severe

re
FEV1/FVC < 0.70

or
FEV1/FVC < 0.70 FEV1 < 30% predicted
or FEV1 < 50%

er
FEV1/FVC < 0.70 predicted plus chronic
respiratory failure
FEV1/FVC < 0.70 30% FEV1 < 50%

alt
50% FEV1 < 80% predicted

FEV1 8 0% predicted predicted

ot
Active reduction of risk factor(s); influenza vaccination

Add short-acting bronchodilator (when needed)

on

Add regular treatment with one or more long-acting bronchodilators

(when needed); Add rehabilitation
-d

Add inhaled glucocorticosteroids if

repeated exacerbations
ial

Add long term oxygen if

ter

chronic respiratory
failure
Consider surgical
ma

treatments
d
hte

*Postbronchodilator FEV1 is recommended for the diagnosis and

assessment of severity of COPD.
rig
py
Co

21
 Component 4: Manage Exacerbations

An exacerbation of COPD is defined as a n e v e n t in t h e n a t u r a l

e
uc
co u r s e o f t h e d i s e a s e ch a r a ct e r i z e d b y a ch a n g e i n t h e
p a t i e n t s b a s e l i n e d y s p n e a , co u g h , a n d /o r s p u t u m t h a t i s

od
b e y o n d n o r m a l d a y - t o - d a y v a r i a t i o n s , i s a cu t e i n o n s e t ,
a n d m a y w a r r a n t a ch a n g e i n r e g u l a r m e d i ca t i o n i n a

pr
p a t i e n t w i t h u n d e r l y i n g CO P D .

re
The most common causes of an exacerbation are infection of the
tracheobronchial tree and air pollution, but the cause of about one-third

or
of severe exacerbations cannot be identified.

er
alt
H o w t o A s s e s s t h e S e v e r i t y o f a n Ex a ce r b a t i o n
ot
Arterial blood gas measurements (in hospital):
on

PaO2 < 8.0 kPa (60 mm Hg) and/or SaO2 < 90% with or without
PaCO2 > 6.7 kPa, (50 mmHg) when breathing room air indicates
respiratory failure.
-d

Moderate-to-severe acidosis (pH < 7.36) plus hypercapnia (PaCO2

ial

> 6-8 kPa, 45-60 mm Hg) in a patient with respiratory failure is an

indication for mechanical ventilation.
ter

Chest X-ray: Chest radiographs (posterior/anterior plus lateral) identify

ma

alternative diagnoses that can mimic the symptoms of an exacerbation.

ECG: Aids in the diagnosis of right ventricular hypertrophy, arrhythmias,

and ischemic episodes.
d
hte

Other laboratory tests:

Sputum culture and antibiogram to identify infection if there is
rig

no response to initial antibiotic treatment.

py

Biochemical tests to detect electrolyte disturbances, diabetes,

and poor nutrition.
Co

Whole blood count can identify polycythemia or bleeding.

22
 Hom e Car e o r Ho s pit al Car e f o r En d - St a ge COP D P at ien t s ?
Th e r is k of dy in g f ro m a n ex acer ba t io n o f COP D is clos ely r ela t ed
t o t h e dev elo p m en t o f r es pir a t o r y acido s is , t h e p r es en ce o f

e
s er iou s com o r b idit ies , a n d t h e n eed f o r v en t ila t o r y s u pp o r t .

uc
P at ien t s lack in g t h es e f eat u r es a r e n o t at h igh r is k o f dy in g , bu t
t h o s e w it h s ev er e u n der ly in g COP D o f ten r eq u ir e h o s p ita lizat io n

od
in a n y ca s e. At t em p t s at m a n ag in g s u ch p at ien t s en t ir ely in t h e
co m m u n it y h av e m et w it h lim it ed s u cces s , b u t r et u r n in g t h em

pr
t o t h eir h om es w it h in cr ea s ed s o cia l s u p po r t an d a s u p er v is ed
m edica l car e p ro g r am af t er an in it ia l em er gen cy r o om as s es s m en t

re
h as b een m u ch m o r e s u cces s f u l. Ho w ev er, d et ailed co s t - ben ef it
a n a ly s es o f t h es e ap p ro a ch es h av e n o t b een r ep o r t ed .

or
H om e Ma n age m e n t
B ron ch odila t o r s: Increase dose and/or frequency of existing short-

er
acting bronchodilator therapy, preferably with 2-agonists. If not already
used, add anticholinergics until symptoms improve.
alt
Glu cocor t ico st er oids : If baseline FEV1 < 50% predicted, add 30-40
ot
mg oral prednisolone per day for 7-10 days to the bronchodilator regimen.
Budesonide alone may be an alternative to oral glucocorticosteroids in the
on

treatment of exacerbations and is associated with significant reduction

of complications.
-d

H os pit a l Man agem en t

Patients with the characteristics listed in Figu r e 7 should be hospitalized.
ial

Indications for referral and the management of exacerbations of COPD

in the hospital depend on local resources and the facilities of the local
ter

hospital.
ma

Figu r e 7: In dica t io n s fo r Ho s pit al Adm is s ion fo r Ex acerb at ion s

Marked increase in intensity of Failure of exacerbation to respond
symptoms, such as sudden develop- to initial medical management
d

ment of resting dyspnea Significant comorbidities

hte

Severe underlying COPD Frequent exacerbations

Onset of new physical signs (e.g., Newly occurring arrhythmias
cyanosis, peripheral edema) Diagnostic uncertainty
rig

Older age
Insufficient home support
py

An t ibio t ics: Antibiotics should be given to patients:

Co

With the following three cardinal symptoms: increased dyspnea,

increased sputum volume, increased sputum purulence
With increased sputum purulence and one other cardinal symptom
Who require mechanical ventilation

23
 APPENDIX I:

e
SPIROMETRY FOR

uc
DIAGNOSIS OF COPD

od
pr
Spirometry is as important for the diagnosis of COPD as blood

re
pressure measurements are for the diagnosis of hypertension.
Spirometry should be available to all health care professionals.

or
Wh a t is S p i r o m e t r y ?

er
S p i r o m e t r y is a simple test to measure the amount of air a
alt
person can breathe out, and the amount of time taken to do so.
A s p i r o m e t e r is a device used to measure how effectively, and
ot
how quickly, the lungs can be emptied.
on

A s p i r o g r a m is a volume-time curve.
Spirometry measurements used for diagnosis of COPD include
-d

(see Figure 2, page 9):

ial

F V C (Forced Vital Capacity): maximum volume of air that

ter

can be exhaled during a forced maneuver.

F EV 1 (Forced Expired Volume in one second): volume expired in
ma

the first second of maximal expiration after a maximal inspiration.

This is a measure of how quickly the lungs can be emptied.
d

F EV 1/F V C: FEV1 expressed as a percentage of the FVC,

hte

gives a clinically useful index of airflow limitation.

rig

The ratio FEV1/FVC is between 70% and 80% in normal adults; a

value less than 70% indicates airflow limitation and the possibility
py

of COPD.
Co

FEV1 is influenced by the age, sex, height and ethnicity, and is

best considered as a percentage of the predicted normal value.
There is a vast literature on normal values; those appropriate for
local populations should be used1,2,3.
24
 W h y d o S p i r o m e t r y f o r CO P D ?
Spirometry is needed to make a firm diagnosis of COPD.

e
uc
Together with the presence of symptoms, spirometry helps stage
COPD severity and can be a guide to specific treatment steps.

od
A normal value for spirometry effectively excludes the diagnosis
of clinically relevant COPD.

pr
The lower the percentage predicted FEV1, the worse the

re
subsequent prognosis.

or
FEV1 declines over time and faster in COPD than in healthy
subjects. Spirometry can be used to monitor disease progres-

er
sion, but to be reliable the intervals between measurements must
be at least 12 months.
alt
ot
W h a t Yo u N e e d t o P e r f o r m S p i r o m e t r y
on

Several types of spirometers are available:

-d

relatively large bellows or rolling-seal spirometers (usually only

available in pulmonary function laboratories). Calibration
should be checked against a known volume e.g. from a 3-litre
ial

syringe on a regular basis.

ter

smaller hand-held devices, often with electronic calibration

systems.
ma

A hard copy of the volume time plot is very useful to check

optimal performance and interpretation, and to exclude errors.
d
hte

Most spirometers require electrical power to permit operation of

the motor and/or sensors. Some battery operated versions are
rig

available that can dock with a computer to provide hard copy.

py
Co

25
 I t i s e s s e n t i a l t o l e a r n h o w y o u r m a ch i n e i s ca l i b r a t e d
a n d w h e n a n d h o w t o cl e a n i t .

e
uc
H o w t o P e r f o r m S p ir o m e t r y

od
Spirometry is best performed with the patient seated. Patients may
be anxious about performing the tests properly, and should be

pr
reassured. Careful explanation of the test, accompanied by a
demonstration, is very useful. The patient should:

re
Breathe in fully.

or
Seal their lips around the mouthpiece.

er
Force the air out of the chest as hard and fast as they can
until their lungs are completely empty.
Breathe in again and relax. alt
ot
Exhalation must continue until no more air can be exhaled, must
on

be at least 6 seconds, and can take up to 15 seconds or more.

Like any test, spirometry results will only be of value if the

-d

expirations are performed satisfactorily and consistently. Both

FVC and FEV1 should be the largest value obtained from any of
ial

3 technically satisfactory curves and the FVC and FEV1 values in

ter

these three curves should vary by no more than 5% or 100 ml,

whichever is greater. The FEV1/FVC is calculated using the maxi-
ma

mum FEV1 and FVC from technically acceptable (not necessarily

the same) curves.
d

Those with chest pain or frequent cough may be unable to

hte

perform a satisfactory test and this should be noted.

rig
py
Co

26
 Wh e r e t o f in d m o r e d e t a i l e d i n f o r m a t i o n o n
s p ir o m e t r y

e
1 . A m e r i ca n T h o r a ci c S o ci e t y

uc
http://www.thoracic.org/adobe/statements/spirometry1-30.pdf

od
2. A u s t r a l i a n /N e w Z e a l a n d T h o r a ci c S o ci e t y
http://www.nationalasthma.org.au/publications/spiro/index.htm

pr
re
3. B r i t i s h T h o r a ci c S o ci e t y
http://www.brit-thoracic.org.uk/copd/consortium.html

or
4. G O L D
A spirometry guide for general practitioners and a teaching slide

er
set is available:
http://www.goldcopd.org
alt
ot
on
-d
ial
ter
d ma
hte
rig
py
Co

27
28
Co
py
rig
hte
d
NOTES

ma
ter
ial
-d
on
ot
alt
er
or
re
pr
od
uc
e
 The Global Initiative for Chronic Obstructive Lung Disease
is supported by educational grants from:

e
uc
od
pr
re
or
er
alt
ot
on
-d
ial
ter
d ma
hte
rig
py
Co

Visit the GOLD website at www.goldcopd.org

www.goldcopd.org/application.asp
Copies of this document are available at www.us-health-network.com
2009 Medical Communications Resources, Inc.