Division of Pulmonology, Department of Internal Medicine,

Medical faculty ,Diponegoro University Semarang

Definition

COPD is a preventable and treatable disease with some

significant extrapulmonary effects that may
contributed 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 with the lung to
noxious particles or gases. (GOLD 2009)
Emphysema :

Is a pathological diagnosis, destruction of the gas-

exchange surfaces of the lung ( alveoli)

Chronic bronchitis :

Is a clinical diagnosis, the presence of cough and

sputum production for least 3 months in each of two
consecutive years.
Epidemiology
Facts Morbidity
 Cigarette smoking is the Year Consultations
primary cause.
 USA - 47.2 million smoke, 1980 6.1 million
♂ 28%,♀ 23% 1985 7.4 million
 WHO estimates 1.1 billion
1990 10.1 million
smokers in world.
 This increases to 1.6 billion 1995 11.8 million
by 2025.
2000 13.9 million
2010 ↑↑↑
Risk factors of COPD
EXPOSURE HOST

 Genes  Exposure to particles

 Tobacco smoke
 Lung growth &  Occupational dusts, organic and
development inorganic
 Indoor air pollution from heating and
 Oxidative stress cooking with biomass in poorly vented
 Gender dwellings
 Outdoor air pollution
 Age  Respiratory infections
 Socioeconomic status
 Nutrition
 Comorbidities
 Risk factors of COPD
Nutrition

Infections

Socio-economic
status

Aging
Populations
Pathogenesis of COPD
NOXIOUS AGENTS
(tobacco smoke, pollutants, occupational exposures)

• GENETICS FACTORS
• RESPIRATORY
INFECTION
• OTHERS

COPD
 Pathogenesis of COPD
Cigarette smoke
Biomass particles
Particulates
Host factors
Amplifying mechanisms

LUNG INFLAMMATION
Anti-oxidants
Anti-proteinases

Oxidative
stress Proteinases

Repair
mechanisms

COPD PATHOLOGY
Source : Barnes PJ
 Pathogenesis of COPD
INFLAMMATION

Small airway disease Parenchymal destruction

Airway inflammation Loss of alveolar attachment
Airway remodeling Decreased of elastic recoil

AIRFLOW LIMITATION
Emphysema

The Journal of Family Practice 2003

 Changes inSmall Airways in COPD Patients

Inflammatory exudate in lumen

Disrupted alveolar attachments

Thickened wall with inflammatory cells

- macrophages, CD8+ cells, fibroblasts

Peribronchial fibrosis
Lymphoid follicle

Source : Barnes PJ
Pathology Microscopic Changes of
Gross Pathological Changes of Emphysema
Emphysema
Natural history
Diagnosis
 Anamnesis
 Physical examination
 Spirometry
 Laboratory examination
 Radiological examination
Anamnesis
 Chronic productive cough
 Dyspnea
 Sputum production
 Limited activation
 History of smoking
 History of exposure to noxious agent
Physical Examination
 Inspection
 Pursed lip breathing
 Barrel chest
 Pink puffer or Blue bloater
 Palpation
 Decreased of fremitus
Physical Examination

Pink puffer Blue bloater Pursed lip breathing

Physical Examination
 Percussion
 Hypersonor emphysema
 Auscultation
 Normal vesiculer or decreased
 Ronchi and or prolong expiration or wheeze
on normal breathing/forced expiration
 Prolong expiration
Radiological examination
Other investigations
 Serial spirometry
 Alpha 1 anti- trypsin levels
 High resonance CT Scanning
 Echocardiography
 Sputum culture
Diagnosis of COPD
EXPOSURE TO RISK
SYMPTOMS FACTORS
cough tobacco
sputum occupation
shortness of breath
indoor/outdoor pollution

Spirometry
Spirometric classification of COPD

 Post-bronchodilator FEV1/forced vital capacity <0.7

confirms the presence of airflow limitation that is
not fully reversible.
Spirometric classification of COPD
Severity Postbrochodilator FEV1 % pred
FEV1/FVC

At risk >0.7 80

Patients who:
smoke or have exposure to pollutants
have cough, sputum or dyspnoea
have family history of respiratory disease

Mild COPD 0.7 80

Moderate COPD 0.7 50–80

Severe COPD 0.7 30–50

Very severe COPD 0.7 <30

Spirometry: Normal and Patients with COPD
High Resonance CT Scanning – HRCT

Normal

COPD
 Differential diagnosis of COPD
Diagnosis Suggestive Features
COPD Onset in mid-life. Symptoms slowly progressive.
Long history of tobacco smoking. Dyspnea during
exercise. Largely irreversible airflow limitation.
Asthma 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.
Congestive Heart Failure Fine basilar crackles on auscultation.
Chest X-ray shows dilated heart, pulmonary edema.
Pulmonary function tests indicate volume restriction,
not airflow limitation.
 Differential diagnosis of COPD
Diagnosis Suggestive Features
Diffuse Most patients are male and nonsmokers.
Panbronchiolitis Almost all have chronic sinusitis.
Chest X-ray and HRCT show diffuse small centrilobular
nodular opacities and hyperinflation.

Bronchiectasis Large volumes of purulent sputum.

Commonly associated with bacterial infection.
Coarse crackles/clubbing on auscultation.
Chest X-ray/CT shows bronchial dilation, bronchial wall
thickening.
Tuberculosis Onset all ages
Chest X-ray shows lung infiltrate.
Microbiological confirmation.
High local prevalence of tuberculosis.
 Differences in Inflammation and its Consequences: Asthma and COPD

ASTHMA COPD
Allergens Cigarette smoke

Ep cells Mast cell Alv macrophage Ep cells

CD4+ cell Eosinophil CD8+ cell Neutrophil

(Th2) (Tc1)

Bronchoconstriction Small airway narrowing

AHR Alveolar destruction

Airflow Limitation
Reversible Irreversible

Source : Barnes PJ
COPD and Co-morbidities
COPD patients are at increased risk for:
o Myocardialinfarction, angina
o Osteoporosis
o Respiratoryinfection
o Depression
o Diabetes
o Lungcancer
COPD and Co-Morbidities
 COPD has significant extrapulmonary (systemic)
effectsincluding:
 Weight loss
 Nutritionalabnormalities
 Skeletalmuscledysfunction
Exacerbation of COPD
 Worsening dyspnoea  Limited activation
 Cough  Respiratory failure
 Increase in sputum  Decreased of awareness
production  Fever
 Increase in sputum
purulence
Triggers of COPD exacerbation
Rhinovirus, influenza,
Viral parainfluenza,
coronavirus

Infective
H. influenza,
S. pneumoniae,
Bacterial
P. aeruginosa,
Mycoplasma

Irritants, air
Noninfective NO2, SO2
pollutants

 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).
Management of
COPD
Goals of COPD management
 Relieve symptoms
 Prevent disease progression
 Improve exercise tolerance
 Improve health status
 Prevent and treat complications
 Prevent and treat exacerbations Goals
 Reduce mortality
Management of COPD
Assess and monitor disease

Reduce risk factors

Manage stable COPD :

• Education
• Pharmacologic
• Non – pharmacologic

Manage exacerbations
Assess and Monitor Disease
Classification of COPD :
 Stage 0 : At Risk
 Stage I : Mild COPD
 Stage II : Moderate COPD
 Stage III : Severe COPD
 Stage IV : Very Severe COPD
Stage 0 At Risk
 Normal spirometry
 +/- Chronic symptoms
 cough
 sputum production
Stage I Mild COPD
 FEV1/FVC <70%
 FEV1 >80% predicted
 With or without chronic
symptoms (cough,
sputum production)
Stage II Moderate COPD
 FEV1/FVC <70%
 50% <FEV1 <80%
predicted
 With or without chronic
symptoms (cough,
sputum production)
Stage III Severe COPD

 FEV1/FVC <70%
 30% <FEV1 <50%
predicted
 With or without chronic
symptoms (cough,
sputum production)
Stage IV Very Severe COPD
 FEV1/FVC <70%
 FEV1 <30% predicted or
FEV1 <50% predicted
plus chronic respiratory
failure
Risk factor reduction
 Smoking cessation (prolongs survival)
 Avoid exposure to second hand cigarette smoke
 Reduction of exposure to indoor and outdoor pollution
 Influenza vaccine
 Pneumococcal vaccine
Manage stable COPD
 Pharmacology
 Bronchodilator : β 2 agonist, anticholinergic,
methylxanthine
 Glucocorticosteroid
 Other pharmacology
 Vaccine, antibiotic, antitussive, immunoregulator,
vasodilator, antioxidant, morphine
 Nonpharmacology
 Pulmonary rehabilitation and education, nutrition
Bronchodilators (Beta2-agonists)
 Short-acting
 Fenoterol
 Salbutamol (albuterol)
 Terbutaline
 Long-acting
 Formoterol
 Salmeterol
Bronchodilators (anticholinergics)
 Mode of Action
 Cholinergic tone is only reversible component of
COPD
 Normal airway have small degree of vagal cholinergic
tone
 Short-acting
 Ipratropium bromide
 Oxitropium bromide
 Long-acting
 Tiotropium
Bronchodilators (combos and methylxanthines)
 Combination beta2-agonists plus anticholinergic in
one inhaler
 Fenoterol/Ipratropium
 Salbutamol/Ipratropium
 Methylxanthines
 Aminophylline (slow release preparations)
 Theophylline (slow release preparations)
 RARELY OF SIGNIFICNAT BENEFIT
 LEVEL 8-12 mcg/ml
Manage stable COPD
(nonpharmacologic : education)

 The overall approach to managing stable COPD should

be individualized to address symptoms and improve
quality of life.
 For patients with COPD, health education plays an
important role in smoking cessation (Evidence A) and
can also play a role in improving skills, ability to cope
with illness and health status.
 None of the existing medications for COPD have been
shown to modify the long-term decline in lung function
that is the hallmark of this disease (Evidence A).
Therefore, pharmacotherapy for COPD is used to
decrease symptoms and/or complications.
Manage stable COPD
(pharmacotherapy : bronchodilators)

 Bronchodilator medications are central to the

symptomatic management of COPD (Evidence A).
They are given on an as-needed basis or on a regular
basis to prevent or reduce symptoms and
exacerbations.
 The principal bronchodilator treatments are ß2
agonists, anticholinergics and methylxanthines used
singly or in combination (Evidence A).
 Regular treatment with long-acting bronchodilators is
more effective and convenient than treatment with
short-acting bronchodilators (Evidence A).
Manage stable COPD
(pharmacotherapy : glucocorticosteroids)

 The addition of regular treatment with inhaled

glucocorticosteroids to bronchodilator treatment is
appropriate for symptomatic COPD patients with
an FEV1 < 50% predicted (Stage III: Severe COPD
and Stage IV: Very Severe COPD) and repeated
exacerbations (Evidence A).
 An inhaled glucocorticosteroid combined with a
long-acting ß2-agonist is more effective than the
individual components (Evidence A).
Manage stable COPD
(pharmacotherapy : glucocorticosteroids)

 The dose-response relationships and long-term safety

of inhaled glucocorticosteroids in COPD are not
known.
 Chronic treatment with systemic glucocorticosteroids
should be avoided because of an unfavorable benefit-
to-risk ratio (Evidence A).
Manage 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).
Manage stable COPD
(other pharmacologic treatments)
 Antibiotics : Only used to treat infectious
exacerbations of COPD
 Antioxidant agents: No effect of n-acetylcysteine on
frequency of exacerbations, except in patients not
treated with inhaled glucocorticosteroids
 Mucolytic agents, antitussives, vasodilators 
not recommended in stable COPD
Manage stable COPD
(nonpharmacologic treatments)
 Rehabilitation: All COPD patients benefit from
exercise training programs, improving with respect
to both exercise tolerance and symptoms of
dyspnoea 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).
Manage stable COPD
(pulmonary rehabilitation)
 Pulmonary rehabilitation is a multidisciplinary
programme of care that is individually tailored and
designed to optimise physical and social performance
and autonomy.
 Pulmonary rehabilitation programmes include:
 exercise training, education,

 psychosocial/behavioural intervention,

 nutritional therapy,

 outcome assessment,

 promotion of long-term adherence

to the rehabilitation recommendations.

Manage stable COPD
(long-term oxygen therapy) - 1

 Long-term oxygen therapy (LTOT) improves survival,

exercise, sleep and cognitive performance.
 Reversal of hypoxemia supersedes concerns about
carbon dioxide (CO2) retention.
 Arterial blood gas (ABG) is the preferred measure and
includes acid-base information.
 Oxygen sources include gas, liquid and concentrator.
 Oxygen delivery methods include nasal continuous
flow, pulse demand, reservoir cannulas and
transtracheal catheter.
ERS-ATS COPD Guidelines
Manage stable COPD
(long-term oxygen therapy) - 2

 Physiological indications for oxygen include an arterial oxygen

tension (Pa,O2) <7.3 kPa (55 mmHg). The therapeutic goal is
to maintain Sa,O2 >90% during rest, sleep and exertion.
 Active patients require portable oxygen.
 If oxygen was prescribed during an exacerbation, recheck
ABGs after 30–90 days.
 Withdrawal of oxygen because of improved Pa,O2 in patients
with a documented need for oxygen may be detrimental.
 Patient education improves compliance.

ERS-ATS COPD Guidelines