COPD

Summary
COPD is an umbrella term for several diseases characterised by airflow obstruction, most
commonly chronic bronchitis and emphysema, but also including bronchial asthma and
brochiectasis.

COPD is distinguished from restrictive pulmonary disease, a group of disorders characterised

by decreased lung capacity due to either chest wall or skeletal abnormalities.

Epidemiology
 Smoking accounts for 90-98% of all cases
 Number of cases has stabilised in men, but is rising among women
 Most commonly seen in ex-smokers > 35 years of age
 COPD is unlikely to develop with a smoking history less than 10 pack years
 Low socioeconomic status

Causes
 Smoking
 Coal mining
 Genetic, i.e. α1 –antitrypsin deficiency causes emphysema
 

Signs and symptoms

 Tachypnoea
 Use of accessory muscles of respiration
 Hyperinflation caused by gas trapping
 Reduced cricosternaldistance ,<3cm
 Reduced chest expansion
 Resonant chest sounds
 Quiet breath sounds over areas of emphysematous bullae
 Wheeze
 Cyanosis
 Corpulmonale
 Prolonged expiration
 Pursed lip breathing
 Dyspnoea
 Cough, productive or non-productive
 Regular exacerbations
 Weight loss – a sign of very poor prognosis
 

Investigations
 Lung function  - FVC<80% predicted; FEV1/FVC<0.7; increased residual volume
 CXR - possibly hyperinflation, but often normal; flat hemidiaphragms; large central
pulmonary arteries, decreased peripheral vascular markings; bullae; cylindrical heart
 ECG– right atrial and ventricular hypertrophy suggestive of corpulmonale, leading to large p
waves on ECG →p pulmonale
 ABG – in advanced disease decreased Pa O2, increased PaCO2
 Tests for α1-antitrypsin – haematocrit>45; normocytic normochromic anaemia; HB and
PCV may be raised → secondary polycythaemia
 Gas transfer – reduced
 Spirometry– varies from ≥80% in mild disease to <30% in very severe disease
 

 Respiratory failure
 Corpulmonale
 

Treatment of acute exacerbation

 Give controlled O2 therapy beginning at 24%, increasing to 28% if after 20 minutes ABGs
demonstrate a steady or decreased PaCO2. 
 If PaCO2 has risen, assisted ventilation. 
 Give nebulised salbutamol and ipratropium, and if measures are unsuccessful consider non-
invasive ventilation.
 Also give a 5-7 day course of prednisolone 40mg.
 Treat the cause, which is usually a chest infection most commonly caused
by Streptococcus pneumonia or Haemophilus influenza, i.e. give antibiotics  

Management of long-term disease

 Smoking cessation
 Long-term oxygen therapy – give 2L via nasal prongs for at least 15 hours per day
 Known as LTOT – long term oxygen therapy
 Nebulizer -  salbutamol, ipratropium
 Surgery, i.e. bullectomy in those who have large emphysematous bullae,
or lung transplant in those with end-stage emphysema.
 Exercise training
 Diet - to promote weight gain if weight loss experienced
 
 Chronic bronchitis
This is defined as cough and sputum production on most days for at least 3 months during the last
two years.  

Pathology
 Hypersecretion of mucus due to marked hypertrophy of mucus-secreting glands and
hyperplasia of goblet cells
 Initially small airways are affected and this initial inflammation is reversible, whereas in later
stages larger airways become affected and the process is no longer reversible
 Epithelial layer becomes ulcerated and squamous epithelium may be replaced by columnar
cells, resulting in increased gas diffusion distance
 

Emphysema
Emphysema is enlarged airspaces distal to the terminal bronchioles, with destruction of the alveolar
walls causing decreased elastic recoil. 

Pathology
 Abnormal dilation of air spaces with destruction of alveolar walls
 Inflammation and scarring, reducing size of lumen of airways and reducing lung elasticity
 Hypersecretion of mucus, again reducing lumen size and increasing distances for gas
diffusion
  

COPD
COPD is a chronic airways disease with little or no reversibility. The airflow limitation is usually
progressive and is associated with an abnormal inflammatory response of lung tissues to certain
particles. It does not change markedly over several months – i.e it is slowly progressive.

It is a collective term used for chronic bronchitis and emphysema.

 COPD - Cough and sputum production on most days for at least 3 months during the last two
years.
 Emphysema - Enlarged airspaces distal to the terminal bronchioles, with destruction of the
alveolar walls.
 

Symptoms will improve in 90% of cases if the patient stops smoking!

  

Chronic Bronchitis
In this, there is:

 An enlargement in mucus secreting glands (hypertrophy)

 An increased number of goblet cells (hyperplasia)
particularly in the larger airways. In extreme cases, the bronchial tissue itself may become inflamed,
and these may be pus excreted into the lumen.

≫ the main cell involved in this reaction is the NEUTROPHIL – in asthma, the main inflammatory
cell involved is the eosinophil. The main leukocyte infiltrate is CD8+ in COPD, as opposed to CD4
in asthma.

After events of inflammation, there will be scarring and fibrosis of the tissue. This thickens the walls
of the airway, and thus reduces the size of the lumen (thus decreasing the amount of air you can get
into and out of the lungs quickly (FEV1),and also increasing the distance that gasses have to travel
in order to diffuse properly.

Also remember that the inflammatory process will also cause bronchoconstriction – thus in some
cases of COPD where bronchoconstriction is a factor, bronchodilators, such as salbutamol may be
of some use for symptom relief.

Initially, the small airways are affected by chronic bronchitis, and this initial inflammation is
reversible if smoking is stopped soon enough. Later, the larger airways become affected, and the
process is no longer reversible.

In the later stages there will be fibrosis, and squamous cell metaplasia, further narrowing the
bronchial lumen.

The epithelial layer can become ulcerated, and when the ulcer heals, the squamous epithelium may
be replaced by columnar cells.

Emphysema
This is essentially enlargement of the alveolar spaces with destruction of the elastin walls. In this you
lose the natural elastic recoil of the lungs, and you may also have collapse of the small airways.

 
 There are several different types of emphysema that can be identified anatomically, but this may not
be of that much use, as often several different types co-exist to different degrees.

About 1/3 of lung tissue has to be destroyed before the clinical consequences of emphysema are
seen. You should also note that after the age of 25, an individual will naturally lose 30ml of functional
lung capacity each year – the process of COPD just massively accelerates this!

Emphysematous bullae will often form, which are essentially just large closed off air spaces with
trapped air inside them.

The three main pathological effects in COPD:

1. Loss of elasticity of the alveoli

2. Inflammation and scarring – reducing the size of the lumen, as well as reducing elasticity
3. Mucus hypersecretion – reducing the size of the lumen and increasing the distance gasses
have to diffuse.
 

Centrilobular and panlobular are the most common types of emphysema.

Α1-antitrypsin deficiency
α 1 antitrypsin is an enzyme that destroys other enzymes! It destroys several proteases, including
trypsin, elastases and collagenases. In the deficiency, these enzymes aren’t destroyed, and they are
allow to happily eat away at the lung tissue, leading to COPD.

Types of respiratory failure

Type one
This is hypoxaemia without hypercapnia. The CO2 level will tend to be normal or low. Common
causes include:

 Pneumonia
 Pulmonary oedema
 PE
 Asthma
 Emphysema
 Fibrosingalveolitis
 ARDS

 Treatment
 Treat the underlying cause
 Give O2 (35-60%) by face mask to correct the hypoxia
 If PaO2 does not rise above 8kPa then give assisted ventilation
 

Type two
This is hypoxaemia with hypercapnia. It is a result of alveolar hypoventilation.  Common causes
include:

 Pulmonary disease (COPD, asthma, pulmonary fibrosis, obstructive sleep apnoea)

 Reduced respiratory drive – can be a result of sedentary drugs, trauma or CNS tumour
 Neuromuscular disease – e.g. cervical cord lesion, diaphragmatic paralysis, polio,
myasthaenia gravis
 Thoracic wall disease
 

Treatment
In type II failure, the respiratory centre is likely to have become desensitised to CO2 levels, and
hypoxia will now be its main driving force, thus oxygen therapy should be given with
care! However, don’t leave the hypoxia untreated!

 Give controlled oxygen therapy, starting at 24% O2

 Recheck the ABG after 20 minutes – if the PaCO2 is steady or lower, then you can increase
the O2 to 28%.
 If the PaCO2 has risen >1.5kPa– consider giving a respiratory stimulant or assisted
ventilation.
 You can also see CO2 retention as physical signs – the patient will become
drowsy and confused
 If this fails consider intubation / ventilation
 

Signs and Symptoms

Signs

 Tachypnoea
 Use of accessory muscles of respiration
 Hyperinflation
 Reduced cricosternal distance (<3cm) – this is the distance between the cricoid cartilage and
the sternal angle – this is reduced because of hyperinflation – thus the thorax is raised in relation to
the cricoid cartilage.
 Reduced chest expansion
 Resonant chest sounds – suggestive of hyperinflation
 Quiet breath sounds – over areas of emphysematous bullae
 Wheeze – this is an abnormal high pitched or low pitched breath sound heard
on expiration. Often a wheeze is polyphonic- this means it is made up of many different notes, and
thus this shows it is caused by many abnormal airways. Wheeze is normally caused by abnormal
small airways. A monophonic wheeze is caused by a single airway obstruction, and is more likely
to be cancer.
 Stridor is the name for a wheeze heard on inspiration. It is caused by abnormal large
airways – and thus not normally heard in COPD. It is more likely to be heard in cancer.
 Cyanosis
 Corpulmonale
 Prolonged expiration – because their FEV1 is low, they have to have a prolonged
expiratory phase to allow for adequate respiration.
 Pursed lip breathing - This is a technique that many COPD patients adopt by themselves,
but it is also taught in pulmonary rehab clinics. It will reduce the respiratory rate, as well as helping
some areas of trapped air in the lungs. There is evidence to suggest it reduces dyspnoea.

 
 As we can also see, COPD leads to gas trapping – which causes an increase in dead space and
leads to hyperinflation. This is not only a problem in its own right as it reduces the amount of air
exchanged with outside air with each breath, but it also reduced chest wall compliance.

Hyperinflation is particularly a problem during exercise as the time for expiration is reduced, and
hyperinflation is exaggerated.

Symptoms
 Breathlessness (dyspnoea)
 Cough – may or may not be productive (just normal sputum)
 Regular exacerbations
 

Weight loss and COPD

This is a bad prognostic sign. It is thought to be caused by the increased energy needs of the body
as a result of the massive amount of energy needed for respiration. A small contributory factor may
also be that patients find it hard to eat because they are too breathless!

Complications
Patients will either basically get respiratory failure or corpulmonale.

Respiratory Failure
 Cardiac output will be normal or slightly increased
 Salt and fluid retention will occur as a result of renal hypoxia
 Respiratory failure occurs when the PaO2 decrease, or the PaCO2 >increase.
 Pink puffers/blue bloaters
 

Corpulmonale
 This is right sided heart failure, as a result of pulmonary hypertension
 The patient is likely to be cyanosed – look at the hands!
 They are also likely to have ankle oedema and ascites due to fluid retention
 Likely to have severe breathlessness
 There may be an especially loud pulmonary heart sound, and there may be a diastolic
murmur, as a result of incompetence of the pulmonary valve.
 

Tests
 Lung function

Chest X-Ray
 However – CXR is very often normal
 Large central pulmonary arteries
 Decreased peripheral vascular markings
 Cylindrical heart due to hyperinflation of lungs – heart appears like a small line down the
middle of the chest

ECG
 Right atrial and ventricular hypertrophy (corpulmonale)
 Corpulmonale lead to large p waves on the ECG – p pulmonale
ABG
These are often normal, but in advanced disease, there may be:

 Decreased PaO2
 Increased PaCO2

Test for α1 anti-trypsin

 Polycythaemia – measure the haematocrit
 Normocytic normochromic anaemia of chronic disease – prevalence of up to 20%.
 HB and PCV may be raised

Blood tests
 -HB and PVC may often be raised – as a result of persistent hypoxaemia – which causes
a secondary polycythaemia.
 

Gas Transfer
This is a test to measure the effectiveness of gas transfer across the alveoli. You should test the Hb
first, as you need to know this value to work out your transfer value. The patient inhales a known
value of carbon monoxide (which has a very high affinity for haemoglobin – higher even than
oxygen). In normal patients, the transfer test is a good way of measuring transfer efficiency, but in
patients with disease, will alter the results. To help make the results more accurate, the amount of
carbon monoxide inhaled is related to the lung volume.

In emphysema and severe fibrosis, the gas transfer value is reduced.

Diagnosis
This can be done by spirometry, the test needed for clinical diagnosis.
 If there is no history of cigarette smoking then a tentative diagnosis of asthma is usually
given instead of COPD. UNLESS, there is also a family history of lung disease suggestive of α1-
antitrypsin deficiency.
 There are no clinical features that are diagnostic. Be wary of giving a diagnosis
of emphysema just on the basis of hyperinflation. Asthma may also cause this. Also be aware that
in elderly patients, there may appear to be a barrel chest, but in actual fact, it is just curvature of the
spine as a result of osteoporosis.
 

Vaccination
COPD patients should receive an annual flu vaccine, and a one-off vaccine of polyvalent
pneumococcal polysaccharide – which provides life-long immunity.

Air travel
Commercial airliners have a cabin pressure equal to an altitude of 2750m. Patients with COPD
should consult their doctor / airline before travelling.

Exacerbations
These are most commonly caused by:

 Streptococcus pneumoniae – this is a Gram-positive diplococcus.

 Haemophilusinfluenzae – this is a Gram-negative coccobascillus.
Because these two organisms are by far the most common causes, you do not need to take a
sputum sample in an exacerbation of a known COPD patient – the first line treatment
is amoxicillin 500mg tds for 7 days. Second and third line options are co-amoxiclav and
ciprofloxacin respectively. These have almost identical dose regimens as amoxicillin, as
does clarithromycin which is given in penicillin allergic individuals.  

Treatment

Acute exacerbation
Give controlled oxygen therapy, starting at 24% O2
Smoking cessation – whatever stage the disease is at, this can slow down the
progression. Smoking cessation and LTOT are the only two things that can prolong the life
expectancy in COPD.
 
 Drugs – in many cases these are similar to those used in asthma, despite the fact that on paper, it
appears they shouldn’t work. However, in practice, many patients get great symptom relief from
these drugs:
 Short acting beta agonist or anti-cholinergic – i.e. salbutamol – 200μgevery 4-6 hours
 Long acting beta agonist or anti-cholinergic – i.e. ipratropium – 40μg 4x a day
Exacerbations – if they have 2 or more each year, then they are eligible to try inhaled steroids.

Steroids – a trial of these is indicated in virtually any patient with symptoms. The trial is
typically 40mg prednisolone for 2 weeks. 
Antibiotics –
Diuretics – 

Things you don’t give in COPD:

 Moteleucast – this is a leukotriene receptor antagonists, and prevent bronchoconstriction by

leukotriene mediated means. In COPD there is very little bronchoconstriction in this manner.
 Antibiotic prophylaxis – the risk of resistant organisms is too great

Surgery
 Lung volume reduction surgery. This aims to increase the elastic recoil of the lung. .
 Lung transplant can be performed on certain patients with end stage emphysema.
 

Pulmonary rehabilitation
This basically just involves exercise training – and the aim is to improve symptom control. The
exercises usually involve walking / climbing stairs, and can be arranged at clinic or in the home.
These exercises are often in conjunction with physiotherapy and education classes. Breathing
exercises are of little use.

Diet
Patients can lose weight – this is a particularly bad prognostic sign – because it shows that they are
expending a huge amount of energy trying to breathe – you have to encourage them to try and gain
weight – but you can lose muscle mass, and this will make it even more difficult to breathe.