1. COPD
Dr.S.Nandakumar.
Professor of Medicine
FOM, AIMST

2. Pre Test What is COPD ? What is Asthma ?
How to differentiate these two ?
Main etiology for COPD
Symptoms ?
Name two drugs used to treat COPD ?

3. Facts About COPD Cigarette smoking is the primary Cause of COPD.
The WHO estimates 1.1 billion smoker
worldwide, increasing to 1.6 billion by
2025 in low middle-income countries.
In 2000,the WHO estimated 2.74 million
deaths worldwide from COPD.
In 2020 COPD will be the 3rd most common cause of death

4. Chronic Obstructive Pulmonary Disease
(COPD)
COPD is a disease state characterized by airflow limitation that is not fully reversible. The airflow limitation is usually both progressive and associated with an abnormal inflammatory response of the lungs to noxious particles or gases and associated
with systemic manifestations.
This definition does not use the terms chronic bronchitis and emphysema and excludes asthma (reversible airflow limitation).

5. Diagnosis of COPD
It should be considered in patients over the age of 35 who have a risk factor, generally smoking, and who present with exertional dyspnoea, chronic cough, regular sputum production, frequent bronchitis or wheeze.
The presence of airflow obstruction should be confirmed by performing spirometry.

6. Chronic Obstructive Pulmonary Disease
(COPD)
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 and dilatation of the alveoli, is a pathological term that is sometimes (incorrectly) used clinically.
Chronic bronchitis without airflow limitation is not included in COPD

7. Disease Trajectory of a Patients with COPD
Symptoms
Exacerbations
Deterioration
End of Life

8. Risk Factors Cigarette smoking Hyper responsiveness of airways
Infection- ??? childhood
Occupational exposure ???
Air pollution ???
Passive smoking
Alpha 1 anti trypsin deficiency

9. Pathophysiology
Smoking - activates macrophage – cytokines – inflammation
Smoking – mucous gland hyperplasia – metaplasia - excess mucous production – edema – airway narrowing
Reduced surfactant – airway narrowing or collapse
Fibrosis

10. Pathophysiology of COPD
Airflow obstruction – reduced FEV1/FVC ( COPD Vs BA )
Air trapping due to loss of elastic recoiling -– hyperinflation – impaired respiration
Non uniform ventilation leads to ventilation perfusion mismatch -hypoxemia

11. Figure 7. 24 Diagrammatic representation of breath sounds
Figure 7.24 Diagrammatic representation of breath sounds. (A) Vesicular. (B) Bronchial. Note the gap between inspiration and expiration and change in pitch and the blowing, tubular quality of bronchial breath sounds.
© 2005 Elsevier 11

12. Figure 5.48 Timing of vesicular breathing.
© 2005 Elsevier 12 12

13. Figure 5.49 Timing of bronchial breathing.
© 2005 Elsevier 13 13

14. ASTHMA & COPD Asthma COPD Asthma COPD Onset in mid-life.
Symptoms slowly progressive.
Long smoking history.
Dyspnoea during exercise.
Largely irreversible airflow limitation.
COPD
Asthma
COPD
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.
Asthma

15. Comparisons of asthma & COPD
CD 4+ lymphocytes
eosinophils
mast cells
Vary over time and in severity
cough
wheeze
breathlessness
chest tightness
COPD
CD 8+ lymphocytes
macrophages
neutrophils
Persistent and progressive over time
cough
Wheeze
Breathlessness
sputum
Patho- physiology: chronic inflammation
Clinical history: symptoms
Slide 8
• COPD differs from asthma in both the type of inflammation involved and in the pattern
of respiratory symptoms caused

16. Risk factors that lead to asthma development
Predisposing Factors
atopy
gender
indoor allergens - dust mites - pet animal - cockroach - fungi
outdoor allergens - pollens - fungi
occupational sensitizers
Contributing Factors
respiratory infections
diet
air pollution - outdoor - indoor
Smoking - passive - active
Slide 18
GINA, Guidelines 1998

17. Common occupational agents
flour / grain dust (bakery)
paint, glue or plastic fumes
soldering flux
natural rubber latex
wood dust
Slide 19
• A large number of agents encountered in the workplace may provoke or exacerbate asthma
• Some agents induce allergic asthma through stimulating the formation of a specific
serum IgE (taking many years to cause the disease); some cause an immediate
antigen-antibody response and others result in airway hyperresponsiveness because
of a direct irritant effect on the airway wall
• Typically, PEF measurements improve as soon as the patient is away from the workplace

18. Asthma - an inflammatory disease
Normal
Asthma
Slide 13
• Asthma is a chronic inflammatory disorder of the airways
• This bronchoscopic view of an airway shows the normal appearance of a healthy airway,
contrasted with inflammation (reddening and swelling) and narrowing of the asthmatic airway
• Microscopic examination of biopsy and lavage samples taken through the bronchoscope has
established that inflammatory changes are present in asthma of all grades of severity,
including recently diagnosed asthma

19. Inducers Inflammation Airway Hyperresponsiveness Airflow Limitation
Allergens, Chemical sensitisers,
Air pollutants, Virus infections
Inflammation
Triggers
Allergens,
Exercise
Cold Air, SO2
Particulates
Symptoms
Cough Wheeze
Chest tightness
Dyspnoea
Airway
Hyperresponsiveness
Airflow Limitation
Slide 16
• Inflammation of the airways not only causes symptoms associated with widespread,
variable airflow obstruction, it also results in an increase in airway hyperresponsiveness
to a variety of stimuli (triggers)
• Environmental and genetic influences in asthma (inducers) act mainly by provoking
airway inflammation, rather than directly stimulating airway hyperresponsiveness
• Triggers of bronchoconstriction, which are factors that provoke contraction of the sensitised
airway wall, include a wide range of stimuli, such as exercise, cold air and pollen
• Allergens can act as both inducers and triggers
Barnes PJ

20. Indicators for Considering a COPD Diagnosis
Indicators for Considering a COPD Diagnosis
Chronic cough
Present intermittently or every day. Often present throughout the day; seldom only nocturnal.
Chronic sputum
production
Any pattern of chronic sputum production may indicate COPD.
Acute bronchitis
Repeated episodes.
Dyspnoea that is
Progressive (worsens over time).
Persistent (present every day). Worse on exercise. Worse during respiratory infections.
History of
exposure to
risk factors
Tobacco smoke
…. (including popular local preparations). Occupational dusts and chemicals. Smoke from home cooking and heating fuel.
CLINICAL FEATURES OF COPD

21. Clinical features – physical examination
Early stage – no findings
Barrel chest
Pursed lip breathing
Tripod position
Prolonged expiratory phase & wheeze
Predominant emphysema – pink puffers
Ch. Bronchitis – blue bloaters
Signs of right heart failure

24. Diagnosis Of COPD SPIROMETRY The diagnosis should be confirmed by
When performing spirometry, measure:
Forced Vital Capacity (FVC) and
Forced Expiratory Volume in one second (FEV1).
Calculate the FEV1/FVC ratio.
Patients with COPD typically show :
a decrease in both FEV1 and FEV1/FVC
With limited/no reversibility after bronchodilators
However, both symptoms and spirometry should be considered when developing an individualized management strategy for each patient.

25. Assessment of severity of COPD
MILD AIRFLOW OBSTRUCTION
MODERATE AIRFLOW OBSTRUCTION
SEVERE AIRFLOW OBSTRUCTION
FEV % PREDICTED
FEV % PREDICTED
FEV1 <30% PREDICTED

26. Other tests…
ABG
X ray chest
CT thorax
Alpha 1 AT

27. GOLD Classification of COPD
Stage 0 At Risk normal spirometry
Chronic symptoms (cough and sputum production)
Stage I Mild COPD FEV1 / FVC < 70% but
FEV1 > or equal to 80 % predicted
With or without chronic symptoms cough and sputum production.
Stage II Moderate COPD :FEV1/FVC<70%
30% < or equal FEV1<80% predicted (IIA:50% < or equal FEV1<80% )
(IIB:30% < or equal FEV1<50% )
With or without chronic symptoms (cough, sputum production and dyspnea)
Stage III Severe COPD
FEV1 /FVC < 70%
FEV1 < 30% predicted or
FEV1 <50% predicted +presence of respiratory failure or
clinical signs of right heart failure.
At this stage, quality of life is very impaired and exacerbations
may be life-threatening.

28. Goals of COPD management
Prevent disease progression .
Relieve symptoms.
Improve exercise tolerance.
Prevent and treat complications.
Reduce mortality.

29. Assess and Monitor Disease
A detailed medical history.
Spirometry.
Chest X-ray.
Arterial blood gas measurement.
Alpha-1 antitrypsin deficiency screening.

30. Smoking cessation is the single most effective And cost-effective –
Reduce Risk Factors
Smoking cessation is the single most effective
And cost-effective –
intervention to reduce the risk of developing COPD and slow its progression – nicotine patch or Bupropion
Smoking Prevention
Avoid occupational Exposures

31. Management of stable COPD
Patient education.
Pharmacologic Treatment.
- Bronchodilators,
- Corticosteroids,
- Antibiotics,
- Mucolytic
-- Respiratory Stimulants
Non-Pharmacologic Treatment
- Rehabilitation,
- Oxygen Therapy,
- Surgical Treatments (Bullectomy)

32. “Bronchodilator medications are central to the symptomatic management of COPD”
GOLD Report 2003

33. How Do Bronchodilators Work?
Reverse the increased bronchomotor tone
Relax the smooth muscle
Reduce the hyperinflation
Improve breathlessness

34. “All guidelines recommend inhaled bronchodilator as first line therapy.
Chest 2000; 117: 23S-28S

35. Mode of Action
Increased cholinergic tone is the only reversible component of COPD
Normal airways have less degree of vagal cholinergic tone

36. Mode of Action (Contd.)
Therefore, the need for anticholinergic drugs that will act as muscarinic receptor antagonist and block the acetylcholine induced bronchoconstriction

37. Mode of Action (Contd.)
Anticholinergics may also reduce mucus hypersecretion
Anticholinergic have no effect on pulmonary vessels, and therefore do not cause a fall in PaO2
Drugs of Today 2002; 38(9):

38. “Combining bronchodilators with different
“Patients with moderate to severe symptoms of COPD require combination of bronchodilators”
“Combining bronchodilators with different
mechanisms and durations of actions may
increase the degree of bronchodilation
GOLD Report 2003

39. Algorithm for the management of COPD
Mild
Short acting bronchodilator – as required
Tiotropium
Long acting beta agonist
assess with symptoms and spirometry
Tiotropium+LABA
LABA + tiotropium
Add
-Inhaled steroids
-Theophylline
Severe

41. Management Of Acute Exacerbation
Home Management
Bronchodilators: Increase dose and/or frequency of existing bronchodilator therapy. Can add anticholinergic until symptoms improve.
Glucocorticosteroids: If baseline FEV1 < 50% predicted, add 40 mg oral prednisolone per day for 10 days to the bronchodilator regimen.
Antibiotics: When symptoms of breathlessness and cough are increased and sputum is purulent and increased in volume, provide antibiotic coverage , taking into account local patterns of antibiotic sensitivity.

42. Indications for Hospital Admission for
Acute Exacerbations
.Marked increase in intensity of symptoms,
such as sudden development of resting dyspnea
Onset of new physical signs (e.g. Cyanosis, peripheral edema)
Failure of exacerbation to respond to initial medical management
Newly occurring arrhythmias
.Older age

43. Management of acute exacerbation
Bronchodilators + anticholinergics
Antibiotics
Corticosteroids
Oxygen
Mechanical ventilation

44. Carry home message.. Definition COPD v ASTHMA Risk factors
Clinical features
Management

45. Thank you