COPD is a preventable and treatable lung disease defined by airflow limitation that is usually progressive and not fully reversible. It has two main components: chronic bronchitis and emphysema. It is a leading cause of death worldwide, with over 3 million deaths annually. Risk factors include tobacco smoke, air pollution, and genetics. Clinically, it presents with dyspnea, cough, and sputum production. Diagnosis involves spirometry showing an FEV1/FVC ratio of less than 70%. Management focuses on smoking cessation, vaccinations, bronchodilators, pulmonary rehabilitation, and treating exacerbations with antibiotics and steroids.

1. COPD
Dr. Shashikiran Umakanth
Professor of Medicine

2. COPD
Chronic obstructive lung disease (COLD)
Chronic obstructive airway disease (COAD)
Chronic airflow limitation (CAL)
Chronic obstructive respiratory disease (CORD)
Synonyms

3. Agenda - COPD
Definition
Components
Epidemiology
Risk factors
Pathology
Clinical features
Investigations
Management

4. Definition
 COPD is a preventable and treatable lung
disease with significant extrapulmonary
effects
 Pulmonary component
 airflow limitation
 not fully reversible
 usually progressive
GOLD Definition
http://goldcopd.org

5. Raising COPD Awareness Worldwide
15 November 2018

6. COPD
 Associated with
 Abnormal inflammatory response of the lungs
 To noxious particles and gases
 Severe COPD leads to
 Respiratory failure
 Repeated hospitalization
 Death

7. Airflow
Limitation
COPD
Components

8. Chronic Bronchitis
 Productive cough, for
 at least 3 months
 at least 2 consecutive years
 Absence of any other identifiable cause of
excessive sputum production
 Airflow limitation that is not fully reversible
 Abnormal inflammatory response to noxious
agent - e.g., smoking

9. Emphysema
 Alveolar wall destruction
 Irreversible enlargement of air spaces
 Distal to the terminal bronchioles
 Without evidence of fibrosis

10. Burden of Disease: Epidemiology
 In 2010, estimated 384 million patients
 Leading cause of morbidity and mortality
 Induces substantial economic and social burden
 Second leading cause of death
 Annual deaths due to COPD
 About 3 million
 4.5 million by 2030

11. Mortality due to COPD – 2005 & 2016

12. Risk factors
 Exposure
 Tobacco smoke
 Bio mass fuel smoke, open fires
 Chronic uncontrolled asthma
 Occupational dusts and chemicals
 Infections, overcrowding, damp
 Low socioeconomic status
 Host Factors
 Genes (alpha1- anti-trypsin↓)
 Hyper responsiveness
 Lung growth, low BW
 Advanced age

13. COPD Increasing Worldwide
Increase in exposure to risk factors (especially
tobacco) in developing countries & in women
Changing demographics globally, with more
people living into the COPD age range

16. PREGNANT SMOKERS

17. Pathology of COPD

18. Pathogenesis
Small Airway Disease
Cellular infiltration
Airway Remodeling
Parenchymal Destruction
Loss of alveolar attachments
Decreased elastic recoil

19. Airway Pathology
Normal bronchial architecture
1. Mucous gland hypertrophy
2. Smooth muscle hypertrophy
3. Goblet cell hyperplasia
4. Inflammatory infiltrate
5. Excessive mucus
6. Squamous metaplasia
COPD

20. Parenchymal Pathology
Normal parenchymal architecture Emphysematous lung architecture

21. Clinical Features of COPD

22. Chronic Bronchitis
 Mild dyspnea
 Cough is prominent
 Copious, purulent sputum
 More frequent infections
 Cor pulmonale common

23. Emphysema
 Severe dyspnea
 Cough after dyspnea
 Scant sputum
 Less frequent infections
 Terminal respiratory failure
 Cor pulmonale rare

24. mMRC Grading of Dyspnoea
Grade Description
0 Dyspnea only with strenuous exercise
1 Dyspnea when hurrying or walking up a slight hill
2
Walks slower than people of the same age because of
dyspnea or has to stop for breath when walking at own pace
3 Stops for breath after walking 100 m or after a few minutes
4 Too dyspneic to leave house or breathless when dressing

25. Physical Examination
 Physical exam may be normal in some
 Hyper-inflated chest, barrel chest
 Wheezes or quiet breathing
 Pursed lip / accessory muscles resp.
 Peripheral edema
 Cyanosis, ↑ JVP
 Cachexia
 Cough, wheeze, dyspnea, sputum

26. Investigations
 Blood counts
 Spirometry
 Chest X-ray
 Arterial Blood Gases
 CT Scan of Thorax

27. Investigations
 Hematocrit
 Chronic bronchitis - 50-60%
 Emphysema - 35-45%
 Arterial blood gases
PaO2 PaCO2
Chronic bronchitis 45-60 mmHg 50-60 mmHg
Emphysema 65-75 mmHg 35-40 mmHg

28. Spirometry
 Decreased FEV1
 Decreased FVC
 FEV1 < 80%
 FEV1 / FVC < 70%
 Post bronchodilator – no change in FEV1
 PEFR is decreased
 V Max - decreased
Low
Reversibility

29. COPD & Asthma: Reversibility
COPD Asthma

30. Chest X-ray
Normal Chest X-ray Emphysema

31. CT Scan of thorax

32.  Which of the following is NOT a component of
COPD?
1. Chronic bronchitis
2. Emphysema
3. Bronchiectasis
4. Bronchial asthma
Question time

33. Management
 Risk reduction
 Smoking cessation:
 Reduces the rate of decline in lung
function
 Results in clinical improvement

34. Goals of Management
Reduce
Risk
Reduce
Symptoms
 Relieve symptoms
 Improve exercise tolerance
 Improve health status
 Prevent disease progression
 Prevent and treat complications
 Reduce mortality

35. Principles of Management
 Stable COPD
 Inhalation treatment is preferred
 LAMA (long acting antimuscarinic agent) is the FIRST choice
 LABA (long acting beta agonists) are the SECOND best choice
 ICS (inhaled corticosteroids) are the THIRD choice
 SABA and SAMA (salbutamol, ipratropium) for short bursts
 NO systemic steroids in stable COPD

36. Pharmacotherapy
 Short acting relievers
 Short-acting beta agonists (SABA)
 Salbutamol, levosalbutamol,
terbutaline
 Short-acting antimuscarinic (SAMA)
 ipratropium
 Long acting relievers & controllers
 Long-acting beta agonists (LABA)
 Salmeterol, formoterol
 Long-acting antimuscarinin (LAMA)
 tiotropium
 Inhaled corticosteroids (ICS)
 Beclomethasone, budesonide, fluticasone

37. Inhaled therapy
 The mainstay of COPD therapy
 Drugs are delivered as aerosols or powders
 delivered direct to the airways
 first-pass metabolism in the liver is avoided
 lower doses are necessary
 unwanted systemic effects are minimized

38. Delivery systems
 Metered dose inhalers
 Dry powder inhalers (Rotahaler)
 Spacers / Holding chambers
 Nebulisers

39. How to use MDI with spacer

40. Nebulization

41. Remember mMRC grading?
 mMRC grading is for assessing the severity of
1. Breathlessness
2. Angina
3. Chest pain
4. Fatigue
Grade Description
0 Dyspnea only with strenuous exercise
1 Dyspnea when hurrying or walking up a slight hill
2
Walks slower than people of the same age because of
dyspnea or has to stop for breath when walking at own
pace
3
Stops for breath after walking 100 m or after a few
minutes
4
Too dyspneic to leave house or breathless when
dressing

42. Assessment & Management of COPD
Gold 1
Gold 2
Gold 3
Gold 4
FEV1 (%pred)
> 80
50 - 79
30 - 49
<30
Grade
Assessment of
Airflow limitation
Assessment of Symptoms
ExacerbationHistory
mMRC 0-1 mMRC 2+
> 2 or > 1
requiring
admission
0 or 1
NOT
requiring
admission
C D
A B
Diagnosis
FEV1 / FVC
< 0.7

43. C D
A B
Smoking cessation + Pulmonary rehabilitation
Physical activity
Influenza & Pneumococcal vaccine
Regular follow up and spirometry
Bronchodilator
salbutamol - SABA
ipratropium - SAMA
Long acting bronchodilator
LABA - salmeterol, formoterol
LAMA - tiotropium
LABA + LAMA
LAMA
LAMA + LABA
LAMA + ICS
Budesonide, fluticasone
LAMA + LABA + ICS
Roflumilast (if FEV1 < 50%)
Macrolides (if smoker)

44. Management of exacerbations
 Most common causes
 infections of the bronchial
tree
 air pollution
 increase in smoking
 In ~35%, unknown cause
 Treatment
 Antibiotics
 Systemic steroids
 Mechanical ventilation, if
required
 Oxygen*
 Avoid high flow oxygen!

45. Management of complications
 Respiratory failure
 Pulmonary hypertension
 Cor pulmonale
 Cardiac failure
 Pneumothorax

46. Summary - COPD
Definition
Components
Epidemiology
Risk factors
Pathology
Clinical features
Investigations
Management

47. COPD is a complicated illness
Prefer prevention