Chronic Obstructive Pulmonary Disease - COPD

1. CHRONIC OBSTRUCTIVE
PULMONARY DISEASE (COPD)

2. lobal Initiative for Chronic
bstructive
ung
isease
G
O
L
D © Global Initiative for Chronic Obstructive Lung Disease

3. Global Strategy for Diagnosis,
Management and Prevention of COPD
Definition, Classification
Burden of COPD
Risk Factors
Pathogenesis,
Pathology,
Pathophysiology
Management of COPD
Primary Care
Recommendations

4. Definition of COPD
COPD is a preventable and treatable disease with
some significant extrapulmonary effects that may
contribute to the severity in individual patients.
Its pulmonary component is characterized by airflow
limitation that is not fully reversible.
The airflow limitation is usually progressive and
associated with an abnormal inflammatory response
of the lung to noxious particles or gases.

5. Sponsored
Medical Lecture Notes – All Subjects
USMLE Exam (America) – Practice

6. History
COPD has probably always existed but has been called by different names in the past. Bonet
described a condition of “voluminous lungs” in 1679. In 1769, Giovanni Morgagni described
19 cases where the lungs were “turgid” particularly from air. The first description and
illustration of the enlarged airspaces in emphysema was provided by Ruysh in
1721."History of pathologic descriptions of COPD" (PDF).
Matthew Baillie illustrated an emphysematous lung in 1789 and described the destructive
character of the condition. Badham used the word "catarrh" to describe the cough and
mucus hypersecretion of chronic bronchitis in 1814. He recognised that chronic bronchitis
was a disabling disorder.
René Laennec, the physician who invented the stethoscope, used the term "emphysema" in
his book A Treatise on the Diseases of the Chest and of Mediate Auscultation (1837) to
describe lungs that did not collapse when he opened the chest during an autopsy. He
noted that they did not collapse as usual because they were full of air and the airways were
filled with mucus.
In 1842, John Hutchinson invented the spirometer, which allowed the measurement of vital
capacity of the lungs. However, his spirometer could only measure volume, not airflow.
Tiffeneau in 1947 and Gaensler in 1950 and 1951 described the principles of measuring
airflow.
The terms chronic bronchitis and emphysema were formally defined at the CIBA guest
symposium of physicians in 1959. The term COPD was first used by William Briscoe in
1965 and has gradually overtaken other terms to become established today as the
preferred name for this disease.

7. Classification of COPD
Severity
by SpirometryStage I: Mild FEV1/FVC < 0.70
FEV1 > 80% predicted
Stage II: Moderate FEV1/FVC < 0.70
50% < FEV1 < 80% predicted
Stage III: Severe FEV1/FVC < 0.70
30% < FEV1 < 50% predicted
Stage IV: Very Severe FEV1/FVC < 0.70
FEV1 < 30% predicted or
FEV1 < 50% predicted plus

8. “At Risk” for COPD
COPD includes four stages of severity classified by
spirometry.
A fifth category--Stage 0: At Risk--that appeared in the 2001
report is no longer included as a stage of COPD, as there 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.
The public health message is that chronic cough and sputum
are not normal remains important - their presence should
trigger a search for underlying cause(s).

9. Global Strategy for Diagnosis,
Management and Prevention of COPD
Definition, Classification
Burden of COPD
Risk Factors
Pathogenesis,
Pathology,
Pathophysiology
Management
Primary Care
Recommendations

10. Burden of COPD: Key Points
 COPD is a leading cause of morbidity and mortality
worldwide and results in an economic and social
burden that is both substantial and increasing.
 COPD prevalence, morbidity, and mortality vary
across countries and across different groups within
countries.
 The burden of COPD is projected to increase in the
coming decades due to continued exposure to
COPD risk factors and the changing age structure
of the world’s population.

11. Burden of COPD: Prevalence
 Many sources of variation can affect estimates of
COPD prevalence, including e.g., sampling methods,
response rates and quality of spirometry.
 Data are emerging to provide evidence that
prevalence of Stage I: Mild COPD and higher is
appreciably higher in:
- smokers and ex-smokers
- people over 40 years of age
- males

12. COPD Prevalence Study
in Latin America (Platino)
The prevalence
of post-
bronchodilator
FEV1/FVC < 0.70
increases
steeply with age
in 5 Latin
American Cities
Source: Menezes AM et al. Lancet 2005

13. Burden of COPD: Mortality
 COPD is a leading cause of mortality worldwide
and projected to increase in the next several
decades.
 COPD mortality trends generally track several
decades behind smoking trends.
 Between 1999 and 2006, death rates for COPD
have declined among U.S. men; there has been
no significant change among death rates among
U.S. women.

14. Of the six
leading causes
of death in the
United States,
only COPD has
been
increasing
steadily since
1970
Source: Jemal A. et al. JAMA 2005

15. Global Strategy for Diagnosis,
Management and Prevention of COPD
Definition, Classification
Burden of COPD
Risk Factors
Pathogenesis,
Pathology,
Pathophysiology
Management
Primary Care
Recommendations

16. Risk Factors for COPD
Lung growth and development
Oxidative stress
Gender
Age
Respiratory infections
Socioeconomic status
Nutrition
Comorbidities
Genes
Exposure to particles
● Tobacco smoke
● Occupational dusts, organic
and inorganic
● Indoor air pollution from
heating and cooking with
biomass in poorly ventilated
dwellings
● Outdoor air pollution

17. Risk Factors for COPD
NutritionNutrition
InfectionsInfections
Socio-economicSocio-economic
statusstatus
Aging PopulationsAging Populations

18. Global Strategy for Diagnosis,
Management and Prevention of COPD
Definition, Classification
Burden of COPD
Risk Factors
Pathogenesis,
Pathology,
Pathophysiology
Management
Primary Care
Recommendations

20. LUNG INFLAMMATIONLUNG INFLAMMATION
COPD PATHOLOGYCOPD PATHOLOGY
OxidativeOxidative
stressstress ProteinasesProteinases
RepairRepair
mechanismsmechanisms
Anti-proteinasesAnti-proteinasesAnti-oxidantsAnti-oxidants
Host factors
Amplifying mechanisms
Cigarette smokeCigarette smoke
Biomass particlesBiomass particles
ParticulatesParticulates
Source: Peter J. Barnes,
Pathogenesis of
COPD

21. Mucus gland hyperplasia
Goblet cell
hyperplasia
Mucus hypersecretion Neutrophils in sputum
Squamous metaplasia of epithelium
↑ Macrophages
No basement membrane thickening
Little increase in
airway smooth muscle
↑ CD8+
lymphocytes
Changes in Large Airways of COPD PatientsChanges in Large Airways of COPD Patients
Source: Peter J. Barnes,
MD

22. Disrupted alveolar attachments
Inflammatory exudate in lumen
Peribronchial fibrosis
Lymphoid follicle
Thickened wall with inflammatory cells
- macrophages, CD8+
cells, fibroblasts
Changes in Small Airways in COPD Patients
Source: Peter J. Barnes,
MD

23. LUNG INFLAMMATIONLUNG INFLAMMATION
COPD PATHOLOGYCOPD PATHOLOGY
OxidativeOxidative
stressstress ProteinasesProteinases
RepairRepair
mechanismsmechanisms
Anti-proteinasesAnti-proteinasesAnti-oxidantsAnti-oxidants
Host factors
Amplifying mechanisms
Cigarette smokeCigarette smoke
Biomass particlesBiomass particles
ParticulatesParticulates
Pathogenesis of
COPD
Source: Peter J. Barnes,

24. Cigarette smokeCigarette smoke
(and other irritants)(and other irritants)
PROTEASESPROTEASES
Neutrophil elastaseNeutrophil elastase
CathepsinsCathepsins
MMPsMMPs
Alveolar wall destructionAlveolar wall destruction
(Emphysema)(Emphysema)
Mucus hypersecretionMucus hypersecretion
CD8CD8++
lymphocytelymphocyte
Alveolar macrophageAlveolar macrophageEpithelialEpithelial
cellscells
FibrosisFibrosis
(Obstructive(Obstructive
bronchiolitis)bronchiolitis)
FibroblastFibroblast
MonocyteMonocyteNeutrophilNeutrophil
Chemotactic factorsChemotactic factors
Inflammatory Cells Involved in COPD
Source: Peter J. Barnes, MD

25. Anti-proteases
SLPI α1-AT
Proteolysis
OO22
--
, H, H220022
OHOH..
, ONOO, ONOO--
↑ Mucus secretion
Plasma leak Bronchoconstriction
NF-NF-κκBB
IL-8IL-8
NeutrophilNeutrophil
recruitmentrecruitment
TNF-TNF-αα
IsoprostanesIsoprostanes
↓↓ HDAC2HDAC2
↑↑InflammationInflammation
SteroidSteroid
resistanceresistance
Macrophage Neutrophil
Oxidative Stress in COPD
Source: Peter J. Barnes,
MD

26. NormalNormal
Inspiration
Expiration
alveolar attachments
Mild/moderateMild/moderate
COPDCOPD
loss of elasticity
SevereSevere
COPDCOPD
loss of alveolar attachments
closure
smallsmall
airwayairway
Dyspnea
↓ Exercise capacity
Air trappingAir trapping
HyperinflationHyperinflation
↓↓ HealthHealth
statusstatus
Air Trapping in COPD
Source: Peter J. Barnes,

27. Chronic hypoxiaChronic hypoxia
Pulmonary vasoconstrictionPulmonary vasoconstriction
MuscularizationMuscularization
IntimalIntimal
hyperplasiahyperplasia
FibrosisFibrosis
ObliterationObliteration
Pulmonary hypertensionPulmonary hypertension
Cor pulmonaleCor pulmonale
Death
EdemaEdema
Pulmonary Hypertension in
COPD
Source: Peter J. Barnes, MD

28. Macrophages
TNF-α IL-8 IL-6
Bacteria Viruses Non-infective
Pollutants
Epithelial
cells
Oxidative stressOxidative stress
Neutrophils
Inflammation in COPD Exacerbations
Source: Peter J. Barnes,

29. Alveolar wall destruction
Loss of elasticity
Destruction of pulmonary
capillary bed
↑ Inflammatory cells
macrophages, CD8+
lymphocytes
Source: Peter J. Barnes, MD
Changes in Lung Parenchyma in
COPD

30. Chronic hypoxiaChronic hypoxia
Pulmonary vasoconstrictionPulmonary vasoconstriction
MuscularizationMuscularization
IntimalIntimal
hyperplasiahyperplasia
FibrosisFibrosis
ObliterationObliteration
Pulmonary hypertensionPulmonary hypertension
Cor pulmonaleCor pulmonale
Death
EdemaEdema
Pulmonary Hypertension in COPD
Source: Peter J. Barnes,
MD

31. YYYY
YY
Mast cellMast cell
CD4+ cellCD4+ cell
(Th2)(Th2)
EosinophilEosinophil
AllergensAllergens
Ep cellsEp cells
ASTHMAASTHMA
BronchoconstrictionBronchoconstriction
AHRAHR
Alv macrophageAlv macrophageEp cellsEp cells
CD8+ cellCD8+ cell
(Tc1)(Tc1)
NeutrophilNeutrophil
Cigarette smokeCigarette smoke
Small airway narrowingSmall airway narrowing
Alveolar destructionAlveolar destruction
COPDCOPD
Reversible Irreversible
Airflow LimitationAirflow Limitation
Source: Peter J. Barnes, MD

32. Symptoms of COPD
One of the most common symptoms of COPD is
shortness of breath (dyspnea). People with
COPD commonly describe this as: "My breathing
requires effort," "I feel out of breath," or "I can't
get enough air in". People with COPD typically
first notice dyspnea during vigorous exercise
when the demands on the lungs are greatest.
Over the years, dyspnea tends to get gradually
worse so that it can occur during milder,
everyday activities such as housework. In the
advanced stages of COPD, dyspnea can become
so bad that it occurs during rest and is constantly
present.

33. Symptoms of COPD
Other symptoms of COPD are a persistent cough,
sputum or mucus production, wheezing, chest
tightness, and tiredness.
People with advanced (very severe) COPD
sometimes develop respiratory failure. When
this happens, cyanosis, a bluish discoloration of
the lips caused by a lack of oxygen in the blood,
can occur. An excess of carbon dioxide in the
blood can cause headaches, drowsiness or
twitching (asterixis). A complication of advanced
COPD is cor pulmonale, a strain on the heart
due to the extra work required by the heart to
pump blood through the affected lungs.
Symptoms of cor pulmonale are peripheral
edema, seen as swelling of the ankles, and
dyspnea.

34. Symptoms of COPD
There are a few signs of COPD that a healthcare worker may detect
although they can be seen in other diseases. Some people have
COPD and have none of these signs. Common signs are:
tachypnea, a rapid breathing rate
wheezing sounds or crackles in the lungs heard through a
stethoscope
breathing out taking a longer time than breathing in
enlargement of the chest, particularly the front-to-back distance
(hyperaeration)
active use of muscles in the neck to help with breathing
breathing through pursed lips
increased anteroposterior to lateral ratio of the chest (i.e. barrel
chest).

35. Spirometry - Introduction
Spirometry is the gold standard for COPD
diagnosis
Underuse leads to inaccurate COPD
diagnosis
Widespread uptake has been limited by:
Concerns over technical performance of
operators
Difficulty with interpretation of results
Lack of approved local training courses

36. What is Spirometry?
Spirometry is a method of
assessing lung function by
measuring the total volume of
air the patient can expel from
the lungs after a maximal
inhalation.

37. Why Perform Spirometry?
Measure airflow obstruction to help make a
definitive diagnosis of COPD
Confirm presence of airway obstruction
Assess severity of airflow obstruction in COPD
Detect airflow obstruction in smokers who may
have few or no symptoms
Monitor disease progression in COPD
Assess one aspect of response to therapy
Assess prognosis (FEV1) in COPD
Perform pre-operative assessment

38. Spirometry – Additional
Uses
Make a diagnosis and assess severity in a
range of other respiratory conditions
Distinguish between obstruction and
restriction as causes of breathlessness
Screen workforces in occupational
environments
Assess fitness to dive
Perform pre-employment screening in certain
professions

39. Types of Spirometers
Bellows spirometers:
Measure volume; mainly in lung
function units
Electronic desk top spirometers:
Measure flow and volume with real
time display
Small hand-held spirometers:
Inexpensive and quick to use but no
print out

40. Volume Measuring Spirometer

41. Flow Measuring Spirometer

42. Desktop Electronic
Spirometers

43. Small Hand-held Spirometers

44. Standard Spirometric Indicies
FEV1 - Forced expiratory volume in one second:
The volume of air expired in the first second of
the blow
FVC - Forced vital capacity:
The total volume of air that can be forcibly
exhaled in one breath
FEV1/FVC ratio:
The fraction of air exhaled in the first second
relative to the total volume exhaled

45. Criteria for Normal
Post-bronchodilator Spirometry
FEV1: % predicted > 80%
FVC: % predicted > 80%
FEV1/FVC: > 0.7 - 0.8, depending
on age

46. Normal Trace Showing FEV1 and
FVC
1 2 3 4 5 6
1
2
3
4
Volume,liters
Time, sec
FVC5
1
FEV1 = 4L
FVC = 5L
FEV1/FVC = 0.8

47. SPIROMETRY
OBSTRUCTIVE
DISEASE

48. Spirometry: Obstructive
Disease
Volume,liters
Time, seconds
5
4
3
2
1
1 2 3 4 5 6
FEV1 = 1.8L
FVC = 3.2L
FEV1/FVC = 0.56
Normal
Obstructive

49. Spirometric Diagnosis of COPD
COPD is confirmed by post–
bronchodilator FEV1/FVC < 0.7
Post-bronchodilator FEV1/FVC
measured 15 minutes after 400µg
salbutamol or equivalent

50. Bronchodilator Reversibility
Testing
Provides the best achievable FEV1
(and FVC)
Helps to differentiate COPD from
asthma
Must be interpreted with clinical
history - neither asthma nor COPD
are diagnosed on spirometry alone

51. Bronchodilator Reversibility
Testing
Can be done on first visit if no diagnosis
has been made
Best done as a planned procedure: pre-
and post-bronchodilator tests require a
minimum of 15 minutes
Post-bronchodilator only saves time but
does not help confirm if asthma is present
Short-acting bronchodilators need to be
withheld for at least 4 hours prior to test

52. Bronchodilator Reversibility Testing
Bronchodilator* Dose FEV1 before
and after
Salbutamol 200 – 400 µg via large
volume spacer
15 minutes
Terbutaline 500 µg via Turbohaler® 15 minutes
Ipratropium 160 µg** via spacer 45 minutes
* Some guidelines suggest nebulised bronchodilators can be given but the doses
are not standardised. “There is no consensus on the drug, dose or mode of
administering a bronchodilator in the laboratory.” Ref: ATS/ERS Task Force :
Interpretive strategies for Lung Function Tests ERJ 2005;26:948
** Usually 8 puffs of 20 µg

53. Global Strategy for Diagnosis,
Management and Prevention of COPD
Definition, Classification
Burden of COPD
Risk Factors
Pathogenesis,
Pathology,
Pathophysiology
Management
Primary Care
Recommendations

54. Four Components of COPD
Management
1. Assess and monitor
disease
2. Reduce risk factors
3. Manage stable COPD
Education
Pharmacologic
Non-pharmacologic
4. Manage exacerbations

55. • Relieve symptoms
• Prevent disease progression
• Improve exercise tolerance
• Improve health status
• Prevent and treat complications
• Prevent and treat exacerbations
• Reduce mortality
GOALS of COPD
MANAGEMENT
VARYING EMPHASIS WITH DIFFERING
SEVERITY

56. Four Components of COPD
Management
1. Assess and monitor
disease
2. Reduce risk factors
3. Manage stable COPD
Education
Pharmacologic
Non-pharmacologic
4. Manage exacerbations

57. Management of Stable COPD
Assess and Monitor COPD: Key Points
A clinical diagnosis of COPD should be
considered in any patient who has dyspnea,
chronic cough or sputum production, and/or a history
of exposure to risk factors for the disease.
The diagnosis should be confirmed by spirometry.
A post-bronchodilator FEV1/FVC < 0.70 confirms
the presence of airflow limitation that is not fully
reversible.
Comorbidities are common in COPD and should
be actively identified.

58. SYMPTOMS
cough
sputum
shortness of breath
EXPOSURE TO RISK
FACTORS
tobacco
occupation
indoor/outdoor pollution
SPIROMETRY
Diagnosis of COPD

59. Differential Diagnosis:Differential Diagnosis:
COPD and AsthmaCOPD and Asthma
COPD ASTHMA
• Onset in mid-life
• Symptoms slowly
progressive
• Long smoking history
• Dyspnea during exercise
• Largely irreversible airflow
limitation
• Onset early in life (often
childhood)
• Symptoms vary from day to day
• Symptoms at night/early morning
• Allergy, rhinitis, and/or eczema
also present
• Family history of asthma
• Largely reversible airflow
limitation

60. COPD and Co-Morbidities
COPD patients are at increased risk for:
• Myocardial infarction, angina
• Osteoporosis
• Respiratory infection
• Depression
• Diabetes
• Lung cancer

61. Four Components of COPD
Management
1. Assess and monitor
disease
2. Reduce risk factors
3. Manage stable COPD
Education
Pharmacologic
Non-pharmacologic
4. Manage exacerbations

62. Management of Stable COPD
Reduce Risk Factors: Key Points
Reduction of total personal exposure to
tobacco smoke, occupational dusts and
chemicals, and indoor and outdoor air
pollutants are important goals to prevent the
onset and progression of COPD.
Smoking cessation is the single most effective
— and cost effective — intervention in most
people to reduce the risk of developing COPD
and stop its progression (Evidence A).

63. Brief Strategies to Help the
Patient Willing to Quit Smoking
• ASK Systematically identify all
tobacco users at every visit
• ADVISE Strongly urge all tobacco
users to quit
• ASSESS Determine willingness to
make a quit attempt
• ASSIST Aid the patient in quitting
• ARRANGE Schedule follow-up contact.

64. Management of Stable COPD
Reduce Risk Factors: Smoking
Cessation
 Counseling delivered by physicians and other
health professionals significantly increases quit
rates over self-initiated strategies. Even a brief
(3-minute) period of counseling to urge a smoker to
quit results in smoking cessation rates of 5-10%.
 Numerous effective pharmacotherapies for
smoking cessation are available; pharmacotherapy
is recommended when counseling is not sufficient
to help patients quit smoking.

65. Management of Stable COPD
Reduce Risk Factors: Indoor/Outdoor Air
Pollution
Reducing the risk from indoor and outdoor
air pollution is feasible and requires a
combination of public policy and protective
steps taken by individual patients.
Reduction of exposure to smoke from
biomass fuel, particularly among women
and children, is a crucial goal to reduce the
prevalence of COPD worldwide.

66. Four Components of COPD
Management
1. Assess and monitor
disease
2. Reduce risk factors
3. Manage stable COPD
Education
Pharmacologic
Non-pharmacologic
4. Manage exacerbations

67. Management of Stable COPD
Pharmacotherapy: Bronchodilators
 Bronchodilator medications are central to the
symptomatic management of COPD (Evidence A).
 Bronchodilators are prescribed on an as-needed or on a
regular basis to prevent or reduce symptoms.
 The principal bronchodilator treatments are ß2- agonists,
anticholinergics, and methylxanthines used singly or in
combination (Evidence A).
 Long-acting bronchodilators are more effective and
convenient than treatment with short-acting
bronchodilators (Evidence A).

68. Management of Stable COPD
Pharmacotherapy: Glucocorticosteroids
 Regular treatment with inhaled
glucocorticosteroids reduces frequency of
exacerbations for symptomatic COPD
patients with an FEV1 < 50% predicted
(Stage III: Severe COPD and Stage IV: Very
Severe COPD) and repeated exacerbations.
 Treatment with inhaled glucocortciosteroids
increases the likelihood of pneumonia and
does not reduce overall mortality.

69. Management of Stable COPD
Pharmacotherapy: Combination Therapy
Glucocorticosteroids and Long-Acting ß2-agonist
 An inhaled glucocorticosteroid combined with a
long-acting ß2-agonist is more effective than the
individual components in reducing exacerbations
and improving lung function (Evidence A).
 Combination therapy increases the likelihood of
pneumonia and has no impact on mortality.
 Addition of a long-acting ß2-agonist /inhaled gluco-
Corticosteroid comgination to an anticholinergic
(tiotropium) appears to provide additional benefits.

70. Management of Stable COPD
Pharmacotherapy: Systemic
Glucocorticosteroids
 Chronic treatment with systemic
glucocorticosteroids should be avoided
because of an unfavorable benefit-to-risk
ratio (Evidence A).

71. Management of Stable COPD
Pharmacotherapy: Phosphodiesterase-4
Inhibitors
 In patients with Stage III: Severe COPD or
Stage IV: Very Severe COPD and a history
of exacerbations and chronic bronchitis, the
phospodiesterase-4 inhibitor, roflumilast,
reduces exacerbations treated with oral
glucocorticosteroids.

72. Management of Stable COPD
Pharmacotherapy: Vaccines
 In COPD patients influenza vaccines can reduce
serious illness (Evidence A).
 Pneumococcal polysaccharide vaccine is
recommended for COPD patients 65 years and
older and for COPD patients younger than age 65
with an FEV1 < 40% predicted (Evidence B).
 Influenza, not pneumococcal vaccination is
associated with reduced risk of all-cause mortality
in COPD (Evidence B).

73. Management of Stable COPD
All Stages of Disease Severity
Avoidance of risk factors
- smoking cessation
- reduction of indoor pollution
- reduction of occupational exposure
Influenza vaccination

74. IV: Very SevereIII: SevereII: ModerateI: Mild
Therapy at Each Stage of COPD*
 FEV1
/FVC < 70%
 FEV1
> 80%
predicted
 FEV1
/FVC < 70%
 50% < FEV1
< 80%
predicted
 FEV1
/FVC < 70%
 30% < FEV1
<
50% predicted
 FEV1
/FVC < 70%
 FEV1
< 30%
predicted
or FEV1
< 50%
predicted plus
chronic respiratory
failure
Add regular treatment with one or more long-acting
bronchodilators (when needed); Add rehabilitation
Add inhaled glucocorticosteroids if
repeated exacerbations
Active reduction of risk factor(s); influenza vaccination
Add short-acting bronchodilator (when needed)
Add long term
oxygen if chronic
respiratory failure.
Consider surgical
treatments
*Postbronchodilator FEV1 is recommended for the diagnosis
and assessment of severity of COPD

75. Management of Stable COPD
Other Pharmacologic Treatments
 Antibiotics: Only used to treat infectious
exacerbations of COPD
 Antioxidant agents: No effect of n-acetyl-
cysteine on frequency of exacerbations,
except in patients not treated with inhaled
glucocorticosteroids
 Mucolytic agents, Antitussives,
Vasodilators: Not recommended in stable
COPD

76. Management of Stable COPD
Non-Pharmacologic Treatments
 Rehabilitation: All COPD patients benefit from
exercise training programs, improving with
respect to both exercise tolerance and
symptoms of dyspnea and fatigue (Evidence A).
 Oxygen Therapy: The long-term administration
of oxygen (> 15 hours per day) to patients with
chronic respiratory failure has been shown to
increase survival (Evidence A).

77. Four Components of COPD
Management
1. Assess and monitor
disease
2. Reduce risk factors
3. Manage stable COPD
Education
Pharmacologic
Non-pharmacologic
4. Manage exacerbations

78. Management COPD Exacerbations
Key Points
An exacerbation of COPD is defined as:
“An event in the natural course of the
disease characterized by a change in the
patient’s baseline dyspnea, cough, and/or
sputum that is beyond normal day-to-day
variations, is acute in onset, and may
warrant a change in regular medication in
a patient with underlying COPD.”

79. Management COPD Exacerbations
Key Points
The most common causes of an exacerbation
are infection of the tracheobronchial tree and
air pollution, but the cause of about one-third of
severe exacerbations cannot be identified
(Evidence B).
Patients experiencing COPD exacerbations with
clinical signs of airway infection (e.g., increased
sputum purulence) may benefit from antibiotic
treatment (Evidence B).

80. Manage COPD Exacerbations
Key Points
 Inhaled bronchodilators (particularly
inhaled ß2-agonists with or without
anticholinergics) and oral glucocortico-
steroids are effective treatments for
exacerbations of COPD (Evidence A).

81. Management COPD Exacerbations
Key Points
 Noninvasive mechanical ventilation in
exacerbations improves respiratory acidosis,
increases pH, decreases the need for endotracheal
intubation, and reduces PaCO2, respiratory rate,
severity of breathlessness, the length of hospital
stay, and mortality (Evidence A).
 Medications and education to help prevent future
exacerbations should be considered as part of
follow-up, as exacerbations affect the quality of life
and prognosis of patients with COPD.

82. Global Strategy for Diagnosis,
Management and Prevention of COPD
Definition, Classification
Burden of COPD
Risk Factors
Pathogenesis,
Pathology,
Pathophysiology
Management
Primary Care
Recommendations

83. Translating COPD Guidelines into Primary Care
KEY POINTS
Better dissemination of COPD guidelines and
their effective implementation in a variety of
health care settings is urgently required.
In many countries, primary care practitioners
treat the vast majority of patients with COPD
and may be actively involved in public health
campaigns and in bringing messages about
reducing exposure to risk factors to both
patients and the public.

84. Translating COPD Guidelines into Primary Care
KEY POINTS
Spirometric confirmation is a key
component of the diagnosis of COPD and
primary care practitioners should have
access to high quality spirometry.
Older patients frequently have multiple
chronic health conditions. Comorbidities
can magnify the impact of COPD on a
patient’s health status, and can complicate
the management of COPD.

85. Global Strategy for Diagnosis,
Management and Prevention of COPD
SUMMARY
Definition, Classification
Burden of COPD
Risk Factors
Pathogenesis,
Pathology,
Pathophysiology
Management
Primary Care

86. Global Strategy for Diagnosis, Management
and Prevention of COPD: Summary
 COPD is increasing in prevalence
in many countries of the world.
 COPD is treatable and preventable.
 The GOLD program offers a
strategy to identify patients and to
treat them according to the best
medications available.

87.  COPD can be prevented by avoidance of
risk factors, the most notable being
tobacco smoke.
 Patients with COPD have multiple other
conditions (comorbidities) that must be
taken into consideration.
 GOLD has developed a global network to
raise awareness of COPD and disseminate
information on diagnosis and treatment.
Global Strategy for Diagnosis, Management
and Prevention of COPD: Summary

88. WORLD COPD DAY
November 16, 2011
Raising COPD Awareness Worldwide