This document provides information on Chronic Obstructive Pulmonary Disease (COPD). It defines COPD as a disease characterized by persistent airflow limitation that is usually progressive. The primary cause of COPD is tobacco smoking. It discusses the characteristics and components of COPD including chronic bronchitis and emphysema. The document also covers the diagnosis, assessment of severity, management including medications, oxygen therapy, pulmonary rehabilitation, and end of life care considerations for COPD patients.

1. COPD
Chronic Obstructive
Pulmonary Disease
By
Mr. Mahadev Prasad KB
Msc Nurse

2. SYNONYMS

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

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Chronic obstructive lung disease (COLD)
Chronic obstructive airways disease (COAD)
Chronic airflow obstruction (CAO)
CHRONIC BRONCHITIS
EMPHYSEMA
Small airways disease
ASTHMA NOT included in COPD

3. Definition
Chronic obstructive pulmonary disease
(COPD) is characterised by airflow
obstruction. The airflow obstruction is
usually progressive, not fully reversible
and does not change markedly over
several months.
1
The disease is predominantly caused by smoking.
1. NICE 2004

4. The Umbrella Disease
COPD – an umbrella term covering
the “irreversible” aspect of chronic
bronchitis, emphysema and asthma
Chronic
bronchitis
Emphysema
COPD
(shaded area)
Airway
obstruction
Chronic severe asthma

5. Umbrella Disease

COPD now preferred term for previous
diagnosis of bronchitis or emphysema,
chronic asthma

Significant airflow obstruction may be
present before individual is aware of it

May also be related to occupational
exposures e.g. asbestos

6. Epidemiology

COPD is the fourth leading cause of death in the USA and Europe.
The leading cause of death worldwide 1

Mortality in females has more than doubled over the last 20 years.
1

Nearly 900,000 people in England and Wales have a
diagnosis of COPD 2

Morbidity data greatly underestimate the total burden of COPD
because the disease is usually not diagnosed until it is clinically
apparent and moderately advanced.
1

COPD is a more costly disease than asthma and, depending on
country, 50–75% of the costs are for services associated with
exacerbations. 1
1 COPD Audit Commission 2 BTS Consortium 2005

7. Characteristic

Changes characteristic of the disease include:

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smooth muscle contraction (bronchoconstriction)
mucus hypersecretion
ciliary dysfunction
pulmonary hyperinflation
gas exchange abnormalities
pulmonary hypertension
cor pulmonale
These abnormalities contribute to the characteristic
symptoms of COPD - chronic cough, sputum production and
dyspnoea 1
1 Pauwels et al, 2001

8. Risk Factors

Tobacco Smoke
Cigarettes,
 Pipes, cigars – lower rates
than cigarette smokers but
higher than non-smokers



Occupational dusts and
chemicals

Vapors, irritants, fumes


Need sufficiently intense or
prolonged exposure
Indoor air pollution

Biomass fuel used for cooking
and heating in poorly vented
dwellings
Outdoor air pollution



Minor risk factor Passive
cigarette smoke exposure
Respiratory infections in early
childhood
Lower socioeconomic status
association with COPD
 May be secondary to
crowding, poor nutrition, etc.


9. WHAT CAUSES COPD?
COPD is usually related to a history of
tobacco smoking,cigarette
smoking,pipe&cigar smoke.
 Breathing in air pollution and chemical
fumes or dust from the environment or
workplace also can contribute to COPD.
 In rare cases a genetic condition called
alpha1-antitrypsin deficiency may play a
role in causing COPD


11. Healthy Respiratory Mucosa
This electron micrograph
shows the respiratory mucosa
in a healthy state
The cells are fully ciliated
The cilia beat in a co-ordinated
fashion to move mucus out of
the airways (mucociliary
transport)
Scanning electron micrograph showing a sheet
of mucus being moved along by the cilia

12. Damaged Respiratory Mucosa


This slide shows the result of
bacterial infection stripping away
the cilia from the mucosa

Scanning electron micrograph showing cilial and
epithelial damage induced by bacteria
Damage to the cilia and
epithelium occur as a result of
disease processes in COPD.
This can also occur as a result of
bacterial damage
The damage to the cilia means
they are less effective in
removing mucus from the
airways

13. Chronic Bronchitis
↑ in mucus glands and goblet cells
– Production of sputum on most days for > 3 months on 2
consecutive years
–
Small airway disease
(structural changes in the small airways 2-5mm)
> 50% of bronchioles may be effected
before any SOB
–↑ airway smooth muscle
– Inflammatory infiltration resulting in
structural narrowing and distortion
Collagen deposition / fibrosis / mucous
plugging

14. EMPHYSEMA

15. Emphysema
•Dilation of alveolar wall
•↓ alveolar capillary network, loss of guy rope effect
•↓ lung tissue elasticity
•Caused by smoking » irritation » inflammation »
neutrophils and macrophages » release neutrophil
elastase (type of proteases)
Normal Lung
Emphysema

17. The COPD Patient

Generally over 40 years

A smoker or ex-smoker

Presentation with:
cough
 excessive sputum
production
 shortness of breath


Dyspnoea is the reason
most patients seek
medical attention 3
1. BTS, 1997; 3. GOLD, 2003
1

18. Pathophysiology
Mucus hypersecretion
Ciliary dysfunction
Airflow limitation
Pulmonary hyperinflation
Gas exchange abnormalities
Pulmonary hypertension
Cor pulmonale

Mucus hyperserection & ciliary dysfunction → cough, sputum production

19. Diagnosis
>35 years
 Smoker or ex-smoker
 Spirometry (obstructive pattern)
 Any symptoms :
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Exertional breathlessness
Chronic cough
Regular sputum production
Frequent “winter bronchitis”
Wheeze
+ no clinical features of asthma

20. Assessment of Severity of COPD
Severity of airflow
obstruction
FEV1 % predicted
Mild
Moderate
Severe
50-80%
30-49%
<30%
GOLD state that spirometry is the gold standard for diagnosing
COPD, severity is measured by FEV1(Forced expiratory volume).
1 NICE Guidelines 2004
1

21. Management of COPD (Stable)
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Use short acting bronchodilator PRN
(beta2-agonist or anti-cholinergic)
If still symptomatic try combined therapy
with a short acting beta2 agonist and a
short acting anti-cholinergic.
If still symptomatic use a long acting
bronch-dilator (beta2 agonist or anticholinergic)

22. Management
In moderate or severe COPD

If still symptomatic consider a trial of a combination of a long
acting beta2 agonist and inhaled corticosteroid. (Discontinue if no benefit after 4 – 6
weeks)

If still symptomatic consider adding theophylline.

Offer pulmonary rehab to all patients who consider themselves
functionally disabled (usually MRC 3 and above)

Consider referral for surgery.

End of Life Care (need to start these conversations ,what the future will hold,
discuss issues, worries and concerns with patients at an earlier stage. Palliative
care being part of end of life care)

23. Acute exacerbation of COPD


Sustained worsening of patients symptoms from their
usual stable state, which is beyond normal day-to-day
variations and is acute in onset. 1
Symptoms :


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1 NICE Guidelines 2004
Increased shortness of breath
Increased sputum production and/or change in colour
Increased cough
Increased wheeze/tightness
Decreased exercise tolerance
Increased fatigue
Confusion

24. Annual Review – Primary Care
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Smoking cessation
Spirometry
Need for Oxygen Assessment
Pharmacological Therapy - inhaler technique
Pulmonary Rehabilitation
LVRS / Transplantation
BMI – Need for Dietician Input
Referral to other Services
MRC Scale
Need for Specialist Referral
Chronic NIV
End of Life Care

25. Severe COPD
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Smoking cessation
Oxygen
Pharmacological Therapy
Pulmonary Rehabilitation
Dyspnoea Clinic
LVRS / Transplantation
Chronic NIV
End of Life Care - Palliation

26. Look
magazine ad
from 1951

27. Oxygen Therapy

Long Term Oxygen
Therapy (LTOT)

Short Burst
Oxygen Therapy

Ambulatory
Oxygen Therapy

28. Benefits of LTOT
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Improved survival
Prevention of deterioration of pulmonary
haemodynamics
Reduction in secondary polycythaemia
Neuropsychological benefit
improved sleep quality
Increased renal blood flow
reduction in cardiac arrhythmias
Reduction in dyspnoea, improved exercise tolerance
Should be worn for 15 hrs or more a day to gain these
benefits

29. Short Burst Oxygen Therapy

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Further research is required
Episodic dyspnoea not relieved by other
treatments
Palliative therapy or in emergency
situations
If improvement in dyspnoea or exercise
tolerance can be documented

30. Ambulatory Oxygen Therapy
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Improved exercise tolerance
Reduced dyspnoea
Improved quality of life

31. Medicines Management

Flu and Pneumonia vaccination

Bronchodilators

Coticosteroids

Mucolytics
Pharmacotherapy does not modify long-term decline, but is
used to
–prevent and control symptoms / improve exercise tolerance
–reduce the frequency and severity of exacerbations
–improve health status

32. Long – Acting Inhaled bronchodilators e.g.
Salmeterol / Tiotropium

Significant improvement in lung function

1-3
better sustained improvement in lung function over 12 hours
than ipratropium bromide 1

Improve shortness of breath day and night

Reduce risk of exacerbations vs. placebo

Clinically significant improvements in quality of life 4,5
 unlike ipratropium bromide, Salmeterol significantly increased
the percentage of patients showing a clinically relevant
improvement in health status compared with placebo 5
1,3
1
1. Mahler et al, 1999, 2. Mahler et al, 2001, 3. Boyd et al, 1997, 4. Jones et al, 1997, 5. Cox et al, 2000

33. Xanthines - e.g. theophylline
Less commonly used than other
bronchodilators
 Only modest bronchodilators
 Side effects within therapeutic range
 Many drug interactions
 Smoking can affect the metabolism of
theophylline

34. Inhaled Corticosteroids

Inhaled steroids now limited to moderate
symptomatic disease with ≥2
exacerbations per year to reduce
admission rates
1

Emerging evidence of enhanced effect of
xanthines when combined with
corticosteroid
1 NICE (2004)

35. Mycolytics
Carbocisteine
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
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Reduces sputum viscosity to aid expectoration
Reduces exacerbations of COPD in those with chronic
productive cough
(caution in peptic ulceration / can cause gastrointestinal
irritation)
Erdotin - Short course during acute exacerbation
GOLD guidelines (2007) suggest there is not enough evidence to support there use.
However, there are a group of patients in which it works well in

36. Lung Reduction In Emphysema
↑
↑
↓
↓
↑
↓
↑
↓
↑
↑
↓
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Remove hyperinflated areas of lung:
Improve V/Q matching
Reduce resting length of respiratory muscles
Reduce Dynamic Hyperinflation

37. Pulmonary Rehabilitation

The goal of PR are to reduce the symptoms, disability and handicap to
improve functional independence in COPD 5

Programme incorporates a programme of physical training, disease
education, nutritional, psychological, social and behaviour intervention 5

Provided by a inter professional team, with attention to individual goals
and needs.

Improves exercise tolerance and function / reduces dyspnoea / improves
QOL 1,2

Empowerment for patients to manage their own condition recognition of
exacerbations.
1 Ries et al. 1995, 2 De Paepe et al. 2000 3, Griffiths at al.2000, 4, Troosters et al, 2000 5 BTS 2001

38. Pulmonary Rehabilitation
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Introduction
Benefits of exercising
Anatomy, Physiology
and Pathology
Medication
Chest Clearance
techniques
Dyspnoea
management
OT pacing/aids
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Age Concern Benefits
system
Exacerbation
Nutrition
Psychosocial factors Coping/Anxiety/Panic
Breath easy
Expert patient
What next? – Health
improvement team

40. PREVENTION

43. IF NOT
PREVENTED

45. Chronic Non-Invasive Ventilation

Domiciliary NIV for a highly
selected group of COPD
patients with recurrent
admissions requiring
assisted ventilation is
effective at reducing
admissions and minimizes
costs from the perspective
of the acute hospital
1

1 Tuggey JM, Plant PK, Elliott MW. Thorax. 2003

46. When does COPD become Palliative?
(1 of 2)

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Primary clinical indicators
FEV1 < 30% pred
History of >2 acute exacerbations in last 12
months
Frequent admissions to hospital
Progressive shortening of of the intervals
between admissions
Limited improvement following admission
1

47. When does COPD become Palliative?
(2 of 2)
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Supporting clinical Indicators
On maximum therapy- no other intervention is
likely to alter the conditions progression
Dependence on oxygen therapy
Severe unremitting dyspnoea (MRC Dyspnoea
Scale grade 5)
Severe co morbidities e.g. heart failure, diabetes
Housebound – unable to carry out normal ADL

48. Dyspnoea 
Symptomatic Treatment
Opioids
Mechanism unclear

 respiratory drive,  sensation of respiratory muscle
fatigue, cognitive changes, central effect, cough
suppressant 2
– Oral morphine 2.5 4 hourly (dose maybe escalated if well tolerated)
No evidence to support nebulised morphine
1 Watson et al 2006 2 Jenner 1991
1

49. Dyspnoea related to Anxiety

Benzodiazepines
Examples include
- Diazepam 2 – 5mgs BD and PRN
- Lorazepam 1 – 2 mgs p.r.n
1 Watson et al 2006
1

50. Oxygen Therapy

Some patients do derive good benefit if not already on
LTOT

But: Beware the CO2 retainers

Also:

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Risk of psychological dependence
Paradoxical restriction to activity
Dry mouth / nose
Isolation and communication problems
Consider open window, fan, cool flannel, heliox

51. Intractable Cough

Steam inhalation

Nebulisation -

Oral morphine 2.5 - 5mg, 4 hourly
(0.9% sodium chloride. Consider nebulised
bronchodilation and steroid)
1 Watson et al 2006
1

52. Terminal Breathlessness
 Non-pharmacological
management
Touch
 Relaxation
 Environment
 Modelling of behaviour

 Subcutaneous
Route may be necessary

54. Thank – You
Any Questions?