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Lecture Summary
• 1. Definition
• 2. Risk factors
• 3. Patho-physiology
• 4. Clinical symptoms
• 5. Diagnosis
• 6. Differential Diagnosis
• 7. Treatment
• a. Management of Stable COPD
• b. Management of Exacerbations
• C. Management of Comorbidities

• 8. Prognosis
 1. Definition

• A common, preventable and treatable disease

• Characterized by persistent airflow limitation that is usually

progressive and associated with an enhanced chronic
inflammatory response in the airways and the lung to noxious
particles or gases.

• Exacerbations and comorbidities contribute to the overall

severity in individual patients.
 The rule of 50

• 50% of COPD patients are underdiagnosed

• COPD is evident by the age of 50

• At the time of diagnosis, FEV1 is < 50% of the

predicted value
• 5-year survival rate: 50%
5
6
The Global Initiative for Chronic Obstructive Lung
Disease (GOLD) works with health care professionals
and public health officials to raise awareness of
Chronic Obstructive Pulmonary Disease (COPD) and to
improve prevention and treatment of this lung disease
for patients around the world.

7
2. Risk Factors for COPD
Genes

Infections

Socio-economic
status

Aging Populations
© 2014 Global Initiative for Chronic Obstructive Lung Disease
 Lungs with COPD

In COPD, less air flows in and out of the airways because of one or more of the
following:
• The airways and air sacs lose their elastic quality.
• The walls between many of the air sacs are destroyed.
• The walls of the airways become thick and inflamed.
• The airways make more mucus than usual, which tends to clog them.
Normal versus Diseased Bronchi
Emphysema
12
Professor Peter J. Barnes, MD
National Heart and Lung Institute, London UK
Professor Peter J. Barnes, MD
National Heart and Lung Institute, London UK
 INFLAMMATION

Small airway disease Parenchymal destruction

Airway inflammation Loss of alveolar attachments
Airway remodeling Decrease of elastic recoil

AIRFLOW LIMITATION
17
 Causes of Airflow Limitation
Reversible

 Accumulation of inflammatory cells, mucus,

and plasma exudate in bronchi

 Smooth muscle contraction in peripheral and

central airways

 Dynamic hyperinflation during exercise

 Causes of Airflow Limitation
Irreversible

 Fibrosis and narrowing of the airways

 Loss of elastic recoil due to alveolar

destruction

 Destruction of alveolar support that maintains

patency of small airways
 4. Clinical Symptoms

•A diagnosis of COPD should be considered in

patients over the age of 35 who have a risk
factor (generally smoking) and who present
with one or more of the following symptoms:

• Exertional breathlessness
• Chronic cough
• Regular sputum production
• Frequent winter 'bronchitis'
• Wheezing
 Physical Examination

Signs of heavy smokers

• Clubbing
• Distended neck vein on expiration
• The presence of barrel chest
• Abdominal breathing
• The use of pursed lips breathing and chest
movement
• Wheezing characteristics of chronic bronchitis
Clubbing
Jugular Vein Distension
Barrel Chest
Pursed Lips Breathing
 The COPD types

• The most frequent COPD type is the bronchitis type,

where environmental factors in the presence of
genetic, infectious or other factors (asthma), trigger
chronic bronchial inflammation, respectively
chronic bronchitis

• Such inflammation, respectively chronic bronchitis, is

located at the level of small airways (bronchiole); it is
a progressive inflammation and it causes small
airways remodelling and permanent bronchial
obstruction at this level
28
 The COPD types
The first and rarest is emphysematous COPD

In this case, damage to alveolar septa and alveolar

walls and replacement of pulmonary elastic tissue
with connective tissue cause the collapse of small
airways during inspiration and bronchial obstruction.

Finally, chronic bronchitis due to environmental

factors, including bronchial infections, is added to
bronchial obstruction, and over time, a bronchial type
COPD component also adds.
30
 The COPD types

• Boththe permanent obstruction but also the

inflammation will cause acinar hyperinflation
and parenchymal destruction, respectively
alveolar walls destruction and decrease in
pulmonary elasticity (elastic recoil).
Pink Puffer vs Blue Bloater
33
 5. Diagnostic tests

• Symptoms
• Physical examination
• Pulse oximetry
• Arterial blood gases test
• Sample of sputum
• Chest x-ray
• High-resolution CT (HRCT scan)
• Pulmonary function test (spirometry)
 Spirometry
• used to assess the severity of airflow obstruction
• the only accurate method of measuring the airflow obstruction
in patients with COPD.
• should be performed at the time of diagnosis
• can be used to guide therapy and predict prognosis.

The presence of a post-bronchodilator FEV1/FVC <

0.70 confirms the presence of persistent airflow
limitation and thus of COPD.
Spirometry
 Spirometry: Normal and COPD
0
FEV1 FVC FEV1/ FVC
Normal 4.150 5.200 80 %
1 COPD 2.350 3.900 60 %

2
FEV1
Liter

3
COPD
4 FVC
FEV1

5 Normal
FVC
1 2 3 4 5 6 Seconds

Forced expiratory volume in 1 second Forced vital capacity

SPIROMETRY
40
 Puls Oximetry

• Hypoxia
 Arterial Blood Gases
• Patients with mild COPD have mild to moderate hypoxemia
without hypercapnia.
• As the disease progresses, hypoxemia worsens and
hypercapnia may develop, with the latter commonly being
observed as the FEV1 falls below 1 L/s or 30% of the predicted
value.
• Lung mechanics and gas exchange worsen during acute
exacerbations.
 Arterial Blood Gases
• Ingeneral, renal compensation occurs even in chronic
CO2 retainers (ie, bronchitics); thus, pH usually is near
normal.
• Generally, consider any pH below 7.3 to be a sign of
acute respiratory compromise.
 Sputum analysis
• Induction of sputum  inhalation of hypertonic
saline, or isotonic saline in some patients (with prior
B2 agonist admin)
• Inflammatory markers and cellular markers to
indicate the degree and type of inflammation in the
airways of the patient
• These measurements: critical in diagnosis and
prediction of patient responses to specific treatments
 Sputum analysis
• The most common sputum change: neutrophilia and increased
products of neutrophil activation, including proteases,
myeloperoxidase, and elastase

• Incigarette smokers with COPD, the degree of neutrophilia is

loosely related to the degree of chronic airway obstruction

• Eosinophils are also elevated in the sputum

•  COPD patients with eosinophilic sputum are more responsive

to treatment with steroids (prednisone or prednisolone)
Sample of sputum
 Chest X-Ray
• Chronic Bronchitis:
• Nonspecific
• increased bronchovascular markings 
• Cardiomegaly

• Emphysema:
• Hyperinflated lungs
• flattened hemidiaphragms, a small cardiac silhouette,
and possible bullous changes
• “barrel chest” (antero-lateral projection)
Chest X-Ray
 High-Resolution CT Scan
• Chronic bronchitis
• bronchial wall thickening & enlarged vessels
• scarring with broncho-vascular irregularity and fibrosis
(repeated inflamation)
• Emphysema
• Alveolar septal destruction and airspace enlargement
• Centrilobular emphysema (upper lobes)
• Panlobular emphysema (lower lobes)
• Paraseptal emphysema (near lung fissures and pleura).
• Giant bullae  compression of mediastinal structures,
• Spontaneous pneumothorax / pneumomediastinum (Rupture
of pleural blebs )
 High-Resolution CT Scan

Paraseptal amphysema (peripheral emphysema) has developed into

bullae. In addition, marked centrilobular emphysema.
High-Resolution CT Scan

Centrilobular Emphysema
6. Differential Diagnosis
54
Professor Peter J. Barnes, MD
National Heart and Lung Institute, London UK
 7. Treatment

1. Management of stable COPD

2. Management of Exacerbations

3. Management of commorbidities

 7. Treatment

1. Management of stable COPD

 Goals of therapy
 Relieve symptoms
Reduce
 Improve exercise tolerance
symptoms
 Improve health status

 Prevent disease progression

 Prevent and treat exacerbations Reduce
 Reduce mortality risk
 General Measures

•The most important: stop smoking!

• Smoking cessation has the greatest capacity to influence the natural

history of COPD

• Nicotine replacement (nicotine gum, inhaler, nasal spray, transdermal

patch, sublingual tablet) as well as pharmacotherapy (varenicline,
bupropion, and nortriptyline) reliably increase long-term smoking
abstinence rates.
 General Measures
All COPD-patients benefit from
exercise training programs, improving
with respect to both exercise
tolerance and symptoms of dyspnea
and fatigue.

Influenza and pneumococcal

vaccination (COPD patients ≥ 65 years
and for COPD patients < 65 years with
an FEV1< 40% predicted).
 General Measures
Reduction of indoor
pollution

Reduction of
occupational
exposure
 Pharmacologic therapy

• I. Bronchodilators
• Short-acting: Albuterol, Ipratropium
• Long-acting: Salmeterol, Formoterol
Teophylline
Tiotropium
• II. Corticosteroids
• Inhaled: Budesonide, Fluticasone
• Oral: Prednisone

• III. Phosphodiesterase-4 Inhibitors

• Roflumilast
7.1 Management of Stable COPD
I. Bronchodilators

central to the symptomatic management of COPD to prevent or

reduce symptoms.

prescribed on as-needed or on a regular basis to prevent or reduce

symptoms (inhaled therapy is preferred).
7.1 Management of Stable COPD

I. Bronchodilators
Long-acting inhaled bronchodilators are convenient and
more effective for symptom relief than short-acting
bronchodilators.
Long-acting inhaled bronchodilators reduce
exacerbations and related hospitalizations and improve
symptoms and health status.
Combining bronchodilators of different pharmacological
classes may improve efficacy and decrease the risk of
side effects compared to increasing the dose of a single
bronchodilator.
7.1 Management of Stable COPD
The principal bronchodilator treatments are:
Beta2-agonists
Anticholinergics
Methylxanthines
 7.1 Management of Stable COPD
II. Corticosteroids - inhaled

 improve symptoms, lung function and quality of life and reduce

frequency of exacerbations for COPD patients with an FEV1< 60%
predicted.

Do NOT modify the long term decline in FEV1

Long-term treatment with inhaled corticosteroids is recommended for:

patients with severe and very severe airflow limitation
patients with frequent exacerbations that are not controlled by long-term
bronchodilators
 7.1 Management of Stable COPD
II. Corticosteroids - inhaled

 Long-term monotherapy with inhaled corticosteroids is NOT recommended

(less efficient than combining a beta2-agonist + inhaled corticoid)

 Inhaled corticosteroid therapy is associated with an increased risk of

pneumonia.

 Withdrawal from treatment with inhaled corticosteroids may lead to

exacerbations in some patients.
 7.1 Management of Stable COPD
II. Corticosteroids - oral

Variable results in patients with COPD

Long-term oral treatment with oral corticosteroids is NOT recommended

(adverse systemic side effects)

Useful for the treatment of exacerbations

↓ treatment failure rate
improve subjective dyspnea
rapid improvement in lung function and symptome scores
↓ in hospital days
 7.1 Management of Stable COPD
I + II. Combination therapy

 An inhaled corticosteroid + a long-acting beta2-agonist

more effective than the individual components in improving lung function and
health status and reducing exacerbations in moderate to very severe COPD.
Combination therapy is associated with an increased risk of pneumonia.
Addition of a long-acting beta2-agonist/inhaled glucorticosteroid
combination to an anticholinergic (tiotropium) appears to provide additional
benefits.
7.1 Management of Stable COPD

III. Phosphodiesterase 4 inhibitors

 Roflumilast

Reduce exacerbations in patients with chronic bronchitis, severe and very

severe airflow limitation (GOLD 3 and GOLD 4) and frequent exacerbations
that are not adequately controlled by long-acting bronchodilators.
 7.1 Management of Stable COPD
• Oxygen therapy
• The long-term administration of oxygen (> 15 hours per day)
to patients with chronic respiratory failure has been shown
to increase survival.

• Ventilatory Support
• Combination of noninvasive ventilation (NIV)
with long-term oxygen therapy may be of some
use in a selected subset of patients, particularly in
those with pronounced daytime hypercapnia.
 Surgical Treatment
• Lung volume reduction surgery (LVRS)

• more efficacious than medical therapy among patients with upper-lobe

predominant emphysema and low exercise capacity

• is costly relative to health-care programs not including surgery.

• In appropriately selected patients with very severe COPD, lung

transplantation has been shown to improve quality of life and functional
capacity.
 7. Treatment

2. Management of Exacerbations

7.2 Management of Exacerbations
• An exacerbation of COPD = an acute event defined by a worsening of the
patient’s respiratory symptoms beyond normal daily variations and leads to
a change in medication.

• Exacerbations of respiratory symptoms requiring medical intervention are

important clinical events in COPD.
7.2 Management of Exacerbations

• The most common causes of an exacerbation are viral upper

respiratory tract infections and infections of the tracheobronchial
tree, but the cause of about one-third of severe exacerbations is
not known.

• The best predictor of having frequent exacerbations (2 or more

per year) is a history of previously bronchodilator treated events;
the risk of exacerbations also increases with the worsening of
airflow limitation.
7.2 Management of Exacerbations
 Diagnosis relies exclusively on the clinical presentation of the
patient complaining of an acute change of symptoms that is
beyond normal day-to-day variation.

 The goal of treatment is to minimize the impact of the current

exacerbation and to prevent the development of subsequent
exacerbations.
 Assessments
Arterial blood gas measurements (in hospital): PaO2< 60 mmHg
±PaCO2> 50 mmHg when breathing room (respiratory failure).
Chest radiographs: useful to exclude alternative diagnoses.
ECG: may aid in the diagnosis of coexisting cardiac problems.
Whole blood count: identify polycythemia, anemia or bleeding.
Purulent sputum during an exacerbation: indication to begin
empirical antibiotic treatment.
Biochemical tests: detect electrolyte disturbances, diabetes, and
poor nutrition.
Spirometric tests: not recommended during an exacerbation.
 Indications for Hospital Admission

 Marked increase in intensity of symptoms

 Severe underlying COPD
 Onset of new physical signs
 Failure of an exacerbation to respond to initial medical
management
 Presence of serious comorbidities
 Frequent exacerbations
 Older age
 Insufficient home support
© 2014 Global Initiative for Chronic Obstructive Lung Disease
 Treatment Options

Oxygen: titrate to improve the patient’s hypoxemia with a target

saturation of 88-92% (max 4l/min).
 
Bronchodilators: Short-acting inhaled beta2-agonists with or
without short-acting anticholinergics are preferred.
 
Systemic Corticosteroids: Shorten recovery time, improve lung
function (FEV1) and arterial hypoxemia (PaO2), and reduce the risk
of early relapse, treatment failure, and length of hospital stay. A
dose of 40 mg prednisone per day for 5 days is recommended .

© 2014 Global Initiative for Chronic Obstructive Lung Disease

 Treatment Options

Antibiotics should be given to patients with:

 Three cardinal symptoms: increased dyspnea,

increased sputum volume, and increased sputum
purulence.
 Who require mechanical ventilation.

© 2014 Global Initiative for Chronic Obstructive Lung Disease

 Treatment Options
Noninvasive ventilation (NIV)

• for patients hospitalized for acute exacerbations of COPD

 Improves respiratory acidosis, decreases respiratory rate, severity of dyspnea,

complications and length of hospital stay.

 Decreases in-hospital mortality and the need for mechanical ventilation and
intubation.

© 2014 Global Initiative for Chronic Obstructive Lung Disease

 7. Treatment

3. Management of commorbidities

7.3 Management of Commorbidities
• Cardiovascular disease

• Ischemic heart disease, Heart Failure, Atrial Fibrillation, and Hypertension

• a major comorbidity in COPD and probably both the most frequent and most
important disease coexisting with COPD.
• Benefits of cardioselective beta-blocker treatment in heart failure outweigh
potential risk even in patients with severe COPD.
7.3 Management of Commorbidities
• Osteoporosis and anxiety/depression: often under-diagnosed and
associated with poor health status and prognosis.
• Lung cancer: frequent in patients with COPD; the most frequent cause of
death in patients with mild COPD.
• Serious infections: respiratory infections are especially frequent.
• Metabolic syndrome and manifest diabetes: more frequent in COPD and
the latter is likely to impact on prognosis.  
 8. Prognosis

• Prognostic factors:
• Smoking
• Pulmonary hypertension
• Declining lung function  
• Bronchiectasis
8. Key Points
8. Key Points
COPD