COPD

Chronic Obstructive
Pulmonary Disease
 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
 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

 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
 Characteristic
 Changes characteristic of the disease include:
 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

Asthma Is A Disease Of The Large
& COPD The Small Airways
Asthma Bronchitis

trachea

Emphysema Bronchitis

bronchi

alveoli
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
Damaged Respiratory Mucosa
 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

 This slide shows the result of

bacterial infection stripping away
the cilia from the mucosa

 The damage to the cilia means

they are less effective in
removing mucus from the
airways

Scanning electron micrograph showing cilial and

epithelial damage induced by bacteria
 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
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

The COPD Patient
 Generally over 40 years 1

 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

Diagnosis

 >35 years
 Smoker or ex-smoker
 Spirometry (obstructive pattern)
 Any symptoms :
 Exertional breathlessness
 Chronic cough
 Regular sputum production
 Frequent “winter bronchitis”
 Wheeze
 + no clinical features of asthma
 Clinical features
of Asthma vs. COPD
Assessment of Severity of COPD
Severity of airflow FEV1 % predicted 1

obstruction
Mild 50-80%
Moderate 30-49%
Severe <30%

GOLD state that spirometry is the gold standard for diagnosing

COPD, severity is measured by FEV1.
1 NICE Guidelines 2004
 Spirometry - The Sixth Vital
Sign
Indications: Symptoms or >10 pack year smoker

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
Impact of Chronic Disease

 Impairment

 Disability

 Handicap
COPD Therapy
Prolong Life Symptomatic

 Smoking Cessation  MDI Therapy

 Oxygen  SA beta-2 agonists
 Reduce exacerbations  LA beta-2 agonists
 SA and LA
 Pulmonary Anticholinergics
Rehabilitation  Theophylline
 LVRS (selected  Corticosteroids
patients) (inhaled or oral)
 Lung Transplantation  Combination
Preparations
 SABA and anticholinergic
 LABA and corticosteroids
Management of COPD (Stable)

 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 anti-
cholinergic)
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)
 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 :
 Increased shortness of breath
 Increased sputum production and/or change in colour
 Increased cough
 Increased wheeze/tightness
 Decreased exercise tolerance
 Increased fatigue
 Confusion

1 NICE Guidelines 2004

 COPD Exacerbation
Pathophysiology - Current Hypothesis

Chronic Inflammation

Viral Unknown
Infection 20%
25%

Bacterial Air
Infection Pollution
50% Acute 5%

Inflammation

Exacerbation
Natural History
Oxygen Therapy
 Long Term Oxygen
Therapy (LTOT)

 Short Burst
Oxygen Therapy

 Ambulatory
Oxygen Therapy
Benefits of LTOT
 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
Short Burst Oxygen Therapy

 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
Ambulatory Oxygen Therapy

 Improved exercise tolerance

 Reduced dyspnoea
 Improved quality of life
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
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 1,3

 Reduce risk of exacerbations vs. placebo 1

 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. Mahler et al, 1999, 2. Mahler et al, 2001, 3. Boyd et al, 1997, 4. Jones et al, 1997, 5. Cox et al, 2000
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
Inhaled Corticosteroids
 Inhaled steroids now limited to moderate
symptomatic disease with 2
exacerbations per year to reduce
admission rates1

 Emerging evidence of enhanced effect of

xanthines when combined with
corticosteroid
1 NICE (2004)
Mycolytics
Carbocisteine

 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
COPD Therapy - New
Horizons
 Newer anti-inflammatory agents
 Matrix metalloproteinase inhibitors
 Specific phosphodiesterase (PDE4) inhibitors
 Cilomilast
 Rofumilast
 Piklanilast
 Anabolic steroids
 Repair agents
 Retinoic acid
 Long-acting anti-muscarinic agents
 tiotropium
 Lung Reduction In Emphysema

Remove hyperinflated areas of lung:

Improve V/Q matching
Reduce resting length of respiratory muscles
Reduce Dynamic Hyperinflation
 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