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Chronic Obstructive Pulmonary Disease (COPD) is a chronic respiratory condition characterised by airflow obstruction, most commonly the result of a combination chronic bronchitis and emphysema.
  • Bronchitis – 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.
Unlike asthma, in COPD there is little or no reversibility of the obstruction. 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.
Most cases of COPD are due to smoking, or other exposure to noxious gasses or particles.
COPD is the 4th leading cause of death worldwide. 
  • In the past patients were often diagnosed with “chronic bronchitis” or “emphysema” – dependent on their clinical symptoms. However, it is now best practice to avoid using the terms, and instead to use the umbrella diagnosis of COPD
  • COPD should be distinguished from the other main form of chronic respiratory disease – the restrictive pulmonary diseases. These are a groups of disorders characterised by decreased lung capacity where FEV1 and FVC are both decreased proportionately, resulting in a normal FEV1:FVC.

In COPD the FEV1:FVC ratio is <70%. COPD can also be diagnosed in patients with FEV1:FVC ratio is >70% on the basis of clinical signs and symptoms – such as shortness of breath, or cough. About 30% of cases of COPD will have normal spirometry at diagnosis.

Patients typically follow a slowly progressive course, with recurrent “exacerbations” – short periods of increased shortness of breath, with or without infection.

Long term management often involves combinations of inhaled steroids and bronchodilators, smoking cessation and pulmonary rehabilitation. It is also important to prevent exacerbations with flu and pneumonia vaccination.

Exacerbations are often mild and can be treated in primary care, but COPD also frequently present to hospital with exacerbations. Treatment of exacerbations typically involves oral steroids, increases in doses of inhaled agents, oxygen therapy and in many (but not all cases) antibiotics.

Severe long-term cases may result in the use of home oxygen therapy.


  • Prevalence of about 1.5m in the UK
  • Affects at least 1 in 7 people over 40
  • Mortality is 23,000 /year in the UK
  • It is severely under-diagnosed. Airway obstruction affects 10% off the UK population, but only about 5% of these are diagnosed with COPD – i.e. 50% of patients are undiagnosed
  • The 4th highest cause of death world-wide – and soon likely to be the 3rd
  • Smoking accounts for 90-98% of all cases
    • Symptoms will improve in 90% of patients with smoking cessation
  • Number of cases has stabilised in men, but is rising among women
  • Most commonly seen in ex-smokers > 35 years of age
    • Most patients done show symptoms until in their 50s
  • COPD is unlikely to develop with a smoking history less than 10 pack years
  • The number of deaths from COPD each year has been greatly reduced from 200 per 100 000, to 70 per 100 000 in the last 25 years
  • It is responsible for 1 in 8 hospital admissions
    • It is the second most common cause of preventable hospital admission
  • 25% of patients will die within the first 5 years of diagnosis
  • Associated with other co-morbidities: cardiovascular disease, lung cancer, osteoporosis, depression


  • Smoking
    • 10 – 20% of all smokers will develop COPD
    • Up to 50% of those with a >20 pack year smoking history will get COPD
  • Coal mining
  • Exposure to air pollution – particularly from indoor fires and cooking in the developing world
  • Genetic, i.e. α1 –antitrypsin deficiency causes emphysema
  • Low socioeconomic status and low birth weight are predisposing factors
    • Low birth weight is associated with reduce maximum lung capacity in adulthood
  • Asthma and COPD may also co-exist

Signs and symptoms


  • Breathlessness (dyspnoea)
  • Cough – may or may not be productive (of sputum)
  • Regular exacerbations
  • 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
    • Wheeze 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 abnormally narrowed airways.
    • Wheeze is caused by narrowing of the smaller airways
    • A monophonic wheeze is caused by a single airway obstruction, and is more likely to be cancer.
    • Stridor is the name for a sound heard on inspiration. It is typically cause by an upper airway obstruction – such as croup, inhaled foreign body or a mass(cancer) impinging on the upper airway. Colloquially, patients may to differentiate wheeze and stridor. Ask about inspiration vs expiration.
  • Cyanosis
  • Cor pulmonale
  • 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 creates a smaller opening through which air can exit the respiratory system, and as such, keeps the pressure in the airways higher
    • This helps to stop smaller airways from collapsing, and thus creates a larger surface area for gas transfer than in the absence of pursed lip breathing
    • Sometimes we call pursed lip breathing “Auto-PEEP’. PEEP in regards to ventilation stands for Positive End Expiratory Pressure, and is a common technique used with intubated and CPAP/BiPAP patients to improve ventilation. Pursed-lip breathing provides a small amount of PEEP for patients with COPD.
    • Pursed-lip breathing reducing dyspnoea
    • The high pressure in the lungs that is created by pursed lip breathing will mean that the dynamic closure point is moved to a more distal area of the lung (see images below).
    • In COPD, some of the airways will collapse at a point proximal to many of the alveoli – this point is known as the dynamic closure point. I presume this occurs due to the destruction of elastin tissue that occurs in emphysema.
    • Pursed lip breathing keeps the pressure in the lungs higher, and thus the closure point is kept open, and thus ventilation can occur in a greater number of alveoli (more alveoli are ‘recruited’), and the VQ mismatch is reduced.
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.


  • Lung function tests (spirometry)
    • FVC<80% predicted
    • FEV1/FVC<0.7, OR <LLN (lower limit of normal)
    • Increased residual volume
  • CXR
    • Possibly hyperinflation, but often normal
    • Flat hemi-diaphragms
    • Large central pulmonary arteries
    • Decreased peripheral vascular markings
    • Bullae
    • Cylindrical heart
X-ray of patient with COPD
X-ray of patient with COPD during an acute exacerbation. Note the flattened diaphragm (sign of chronic COPD), and the patchy consolidation the right lung – indicative of an infective exacerbation
  • ECG
    • Right atrial and ventricular hypertrophy suggestive of cor pulmonale, leading to large p waves on ECG p pulmonale
  • ABG – often normal, but in advanced disease, there may be:
    • Decreased PaO2
    • Increased PaCO2
  • Full Blood Count
    • Polycythaemia – measure the haematocrit – >45
    • Normocytic normochromic anaemia of chronic disease – prevalence of up to 20%.
    • HB and PCV may be raised
  • Tests for α1-antitrypsin
  • Gas transfer – reduced
    • This is a test to measure the effectiveness of gas transfer across the alveoli. Requires a known Hb value for calibration The patient inhales a known value of carbon monoxide (which has a very high affinity for haemoglobin – higher even than oxygen). In emphysema and severe fibrosis, the gas transfer value is reduced.


Spirometry is required to confirm a diagnosis of COPD. The offical diagnostic cutoff is FEV1/FVC ratio <0.7 (70%). In patients over 65 and those under 45 the FEV1/FVC ration may not be as reliable, and specialist spirometry may be required to clarify the diagnosis in borderline cases.

  • There is no screening programme for COPD
  • COPD cannot be diagnosed on the basis of CXR findings or clinical history alone
  • There are no clinical features that are diagnostic. Be wary of giving a diagnosis of COPD just on the basis of hyperinflation as seen in a CXR. 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.

You should consider a diagnosis of COPD in any of the following:

  • Patients >35 with symptoms of breathlessness and cough and / or sputum production
  • All smokers and ex-smokers >35
The most important information in spirometry is the measure of FEV1 as a % of the FVC. It is important to ensure that both pre and post-bronchodilator spirometry is recorded. Reversibility of post-bronchodilator tests to above these cut-offs suggests asthma is more likely. The cutoffs for the diagnosis of COPD are base on post-bronchodilator levels. 
Is it asthma?
  • An FEV1 increase of >12% and >200mls indicates a “positive bronchodilator response”
  • An FEV1 increase >400mls suggests asthma (or mixed COPD / asthma)
Staging of COPD
It is also possible to clarify the stage of COPD using a slightly different measurement – the measurement of the the predicted FEV (based on age).
StageFEV % PredictedSymptoms
  • Variable
  • Typically few symptoms
  • Breathlessness on moderate exertion
  • No effects on ADLs
  • May be cough and sputum production
  • Breathlessness when walking on flat ground
  • Exacerbations
  • Some limitation of ADLs
  • SOB on minimal exertion
  • Daily activities severely limited
  • Frequent and severe exacerbations

More recent staging systems (such as the COPD Assessment Test, or CAT) also take into account functional ability, and may involve cardiopulmonary exercise testing and cardiac stress testing, as well as measurement of SpO2 (oxygen saturations).

  • Symptom severity does not necessarily correlate with spirometry severity
  • History of previous exacerbations is a good predictor of risk of future risk of exacerbations and advancement of disease
  • Be wary of heart failure in t hose with significant COPD

Differentiating COPD and asthma

Age of onset >35
Age of onset <35
No diurnal variation in FEV1
Diurnal variation in FEV1
Chronic dyspnoea
Acute episodes
Sputum produced
No sputum produced
History of many years of smoking
(generally patients too young to have this)
Neutrophil infiltrate
Eosinophil infiltrate
CD8 mediated
CD4 mediated
Be aware that many patients may have a mixed asthma / COPD picture – especially those who were diagnosed with asthma at a young age and subsequently have smoked.


  • Hypersecretion of mucus due to marked hypertrophy of mucus-secreting glands and hyperplasia of goblet cells. Reduces lumen size and increasing distances for gas diffusion
  • Abnormal dilation of air spaces with destruction of alveolar walls
  • Inflammation and scarring, reducing size of lumen of airways and reducing lung elasticity
  • 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

Chronic Bronchitis

Defined as cough and sputum production on most days for at least 3 months during the last two years.

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 causes enlarged airspaces distal to the terminal bronchioles, with destruction of the elastin alveolar walls causing decreased elastic recoil. 
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.
There are several different types of emphysema that can be identified anatomically – e.g. centrilobular and panlobular are the most common types. But this is not clinically very useful, 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.

Α1-antitrypsin deficiency

α1-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.
The condition is genetic, and is autosomal dominant. You need to be homozygous to have clinical effects, and about 1/5000 people are. 1/10 are carriers of the gene.
The deficiency accounts for about 2% of cases of emphysema in the UK.
The proteinases that act in the lung are often released by inflammatory cells, such as macrophages. Thus, in smoking, there are more of these around, and the effect becomes exaggerated. This also explains the mechanism of emphysema in a normal individual who smokes.

‘Pink Puffers’ and ‘Blue Bloaters’

This terminology is now generally outdated, but you may still come across others using these terms.

  • Pink Puffers – used to refer to patients who have a near normal PaO2, and a normal or low PaCO2 (due to hyperventilation). They ‘puff’ to increase their alveolar ventilation – and by doing so they are able to keep their blood gas values normal. These patients generally have emphysema or at least a higher degree of emphysema than bronchitis. These are likely to enter type I respiratory failure.
  • Blue Bloaters – used to refer to patients who have decreased alveolar ventilation. They have a low PaO2 and a high PaCO2. They are cyanosed but not breathless (because their respiratory centre has become sensitised). They rely on hypoxic drive to maintain adequate ventilation. They often go on to develop cor pulmonale. These patients are more likely to be type II respiratory failure. ‘Bloater’ – due to cor pulmonale.


Acute exacerbations

An exacerbation of COPD is defined as a change in the patients baseline symptoms, such as:

  • Worsening SOB
  • Increase cough
  • Increase sputum

that is beyond normal day-to-day variation and is acute in onset.

Exacerbations are more common in those with:

  • History of previous regular exacerbations
  • History of GORD / reflux
  • More severe disease (low FEV1)

Frequent exacerbations are associated with an increased rate of decline of respiratory function – as measured by FEV1.

  • Mortality is also directly correlated with the frequency of exacerbations.

In patients having frequent exacerbations – consider a written COPD exacerbation action plan to discuss with and give patients a copy.

  • Early recognition of exacerbations can prevent hospital admission. Increasingly, hospital admission is being used as an outcome measure in randomised controlled trials of COPD.

Managing an acute exacerbation

Exacerbations can be managed in the community or in hospital. Indications for hospital admission might include:

  • Sats <92%
  • Not responsive to outpatient management
  • Inability to eat or sleep to due breathlessness
  • Very low exercise tolerance (e.g. <10m)
  • Confusion (may be due to hypercapnia)
  • Unable to cope at home
  • Co-morbidities suggestive of likely poor outcome

Managing the exacerbation

  • Oxygen therapy – if sats are <88% – beware of CO2 retention
    • Give controlled O2 therapy to maintain sats at 88-92%
    • Monitor for hypercapnia and associated respiratory acidosis
      • Consider repeat ABGs (e.g. every 20 minutes) to assess for a rise in PaCO2
      • If PaCO2 has risen > 1.5kPa consider use of Non-invasive ventilation (NIV) – i.e. CPAP or other assisted ventilation
      • PaCO2 is dependent on VENTILATION – i.e. the volume of air inhaled and exhaled
      • PaO2 is dependent on alveolar gas transfer (“OXYGENATION”) and the percentage of oxygen inhaled
      • VENTILATION and OXYGENATION are not the same!
      • In COPD, the normal respiratory drive, (usually driven by PaCO2) is not longer effective – the feedback mechanism between respiratory rate and PaCO2 has been lost. So, a patient may be adequately oxygenating due to the quality of O2 inhaled, but may not be adequately ventilating to “blow off” CO2
      • Rising PaCO2 can lead to reduced level of consciousness and is a poor prognostic factor
      • Over-oxygenation is assocaited with respiratory failure and death – be careful!
  • Give salbutamol (e.g. 4-8 puffs (400-800mcg) via spacer, or nebulised 2.5-5mg in solution), and ipratropium (e.g. 4 puffs (80mcg) or nebulised 0.5mg)
    • Repeat doses as required
    • Check inhaler technique
    • In the community – if patients are not able to go more than 2 hours between doses – this would be an indication for hospital admission
    • Use of nebulisers seems to be becoming less commonplace. The received dose can be very variable per patient, and there are also concerns about spreading respiratory pathogens. In my own practice, I tend to stick to inhalers via spacer.
  • Give steroids – typically 50mg prednisolone OD for 5 days
    • Tapering is not required after short courses such as these
  • Treat the cause
    • Could be viral
    • Not all exacerbations need antibiotics – only prescribe antibiotics when there is evidence of infection
      • Consider sputum MC+S – but beware of long-term colonisation which may not be indicative of an acute infect organism
      • Sputum culture is typically NOT indicated in the community setting, unless there is failure to respond to treatment
    • If bacterial, most common causes are Streptococcus pneumonia or Haemophilus influenza
      • Streptococcus pneumoniae – this is a Gram-positive diplococcus.
      • Haemophilus influenzae – this is a Gram-negative coccobascillus.
    • Patients thought to have a bacterial infection should be managed the same as pneumonia in non-COPD patients
    • Check local guidelines, but typically; the first line treatment is amoxicillin 500mg tds for 7 days. Second and third line options might include doxycycline (100mg PO for 5-7 days) co-amoxiclav and ciprofloxacin (if penicillin allergy
  • Post-exacerbation care should involved a comprehensive follow-up in primary care (if admitted to hospital this should be within 7 days of discharge) to optimise long-term management. This should include:
    • Review of level of physical activity
    • Pulmonary rehabilitation
    • Repeat spirometry (if not recently done)
    • Medication review – including assessment of adherence and inhaler technique
      • Optimise medication as per the stepwise approach (see below)
    • Smoking cessation advice
    • COPD action plan
    • Assess need for long-term oxygen therapy
    • See below for further details of these interventions under Management of long-term disease

The Lung Foundation Australia suggests the following checklist for management of an exacerbation and subsequent follow-up care:

Managing COPD exacerbation Checklist
Managing COPD exacerbation Checklist – taken from COPD-X Concise Guide 2019.

Management of long-term disease

Think of these in terms of pharmacological and non-pharmacological management strategies. For a small group of patients surgical therapies may also be considered.


All patients should be referred for pulmonary rehabilitation. All smokers should be offered smoking cessation assistance.

  • Smoking cessation is important in reducing the speed of disease progression
Chart showing decline of pulmonary function over time. Blue line indicates patients who have never smoked. The brown line indicated a regular smoker. Red and green lines indicate the altered trajectory than can be achieved by stopping smoking. Ages on the x-axis are very variable and a guide only for reference.
  • Pulmonary rehabilitation is the most effective treatment after smoking cessation
    • It reduces the risk of hospital admission for exacerbations by about 55%
    • Typically involves a combination of physiotherapy breathing exercises, and regular physical activity
    • There may be COPD pulmonary rehab clinics available in your area. If not – consider referral to a general physiotherapist
    • The exercise guidelines are not different from those advised for the general population – which is – at least 30 minutes on at least 5 days of the week of moderate intensity physical activity. This could involve a brisk walk for 30 minutes a day. Patients should be advised to continue exercising until they feel too breathless to continue, at which point they should rest for several minutes before continuing.
    • Patients may be wary of increased exercise – given that they may already feels short of breath!
    • There is very good evidence to support pulmonary rehabilitation – it has been shown to rescue dyspnoea, improve exercise capacity, decrease hospitalisation and improve quality of life and it has very few adverse effects and is very cost-effective.
    • Pulmonary rehabilitation has not been proven to alter life-expectancy

Pharmacological management

  • Drugs – see below!
  • Vaccinations – all patients with COPD should be offered annual flu vaccination and pneumococcal vaccination boosters
    • Pneumococcal schedules vary by jurisdiction – check your local guidelines. Typically this might involve a booster at the time of diagnosis, and subsequent boosters every 5 years until a total of three doses has been given.
  • Treat co-morbidities – particularly important are:
    • Diabetes
    • Cardiovascular disease
    • Hypertension
    • Dyslipidaemia
    • Osteoporosis

Other considerations

  • Long-term oxygen therapy – give 2L via nasal prongs for at least 15 hours per day
    • Known as LTOT – long term oxygen therapy
    • Generally reserved for severe cases
    • Smoking cessation and LTOT are the only two things that can prolong the life expectancy in COPD
  • Surgery, i.e. bullectomy in those who have large emphysematous bullae, or lung transplant in those with end-stage emphysema.
  • Diet – to promote weight gain if weight loss experienced


The goals of pharmacological management are:

  • To reduce the rate of exacerbations
  • To provide symptomatic relief

The medications themselves do not directly alter prognosis, but reducing the frequency of exacerbations can reduce the rate of declines of lung function.

Despite the fact that airway reversibility is not a typical feature of COPD, the use of bronchdilating medications reduces breathlessness in patients with COPD, even though an improvement of FEV1 often cannot be detected.

There are over 100 different inhaled medications for COPD and asthma on the market. To make things even more confusing, many of these are combination therapies that are often referred to by brand name. The RightBreathe website and app (UK based, but many brands are the same in Australia and NZ) are really useful at navigating the world of inhalers!

  • Just like with asthma, correct inhaler technique is important – especially for the MDI (aerosol) based inhalers
  • Powder based inhalers efficacy is less dependent on technique
  • It is also important to consider the environmental impact of inhalers. It is thought that 4% of the NHS carbon footprint is the result of aerosol inhalers – please consider prescribing powder based alternatives where clinically appropriate

There are essentially 3 main types of inhaled medications used, and two of these have long and short acting variations.

  • SABA – Short acting beta agonist – i.e. salbutamol – 200μg every 4-6 hours
  • LABA – Short acting beta agonist – i.e. salmeterol
  • SAMA – Short acting muscarinic agent – i.e. ipratropium – 40μg 4x a day
  • LAMA – Long acting muscarine agent – i.e. tiotropium
  • ICS – inhaled corticosteroids – i.e. beclomethasone, fluticasone

We typically use a stepwise approach when using inhaled medications. Decisions about stepping up or stepping down treatment are usually based on clinical symptoms.

  • Step 1 – SABA or SAMA – short acting drugs that are bronchodilators – Typically corresponds with mild disease
  • Step 2 – Add LABA or LAMA – for longer acting bronchodilation – typically corresponds with moderate disease
    • Some studies have shown that LAMAs – particularly tiotropium – are more effective than LABAs
      • About a 35% reduction in risk of hospital admission compared to LABAs
    • DO NOT USE SAMA WITH LAMA. The SAMA should be ceased when LAMA is initiated. SABA+LAMA is however safe (and recommended)
    • Consider using a LAMA+LABA combination
  • Step 3 – Add ICS – a single inhaler combined LABA/LAMA/ICS may be appropriate – typically corresponds with severe disease

It is typically recommended to reassess the effectiveness of any changes in regimens at 6 weeks.

Benefits of inhalers:
  • Bronchodilators relieve breathlessness
  • Inhaled steroids reduce the frequency and severity of exacerbations. However, high doses have been associated with an increased risk of pneumonia

Some selected examples of inhalers. You will NOT be expected to know all of these, but knowing a bit about one or two from each category would be useful:

TypeNameExample DoseFurther Info
  • Salbutamol (100mcg)
  • 2-8 puffs PRN
  • Brands: Ventolin
  • Ipratropium (20mcg)
  • 2 puffs daily (preventative), 4 puffs STAT (exacerbation)
  • In Australia, it comes as 21mcg MDI not 20mcg (!)
  • Salmeterol (25mcg)
  • Formoterol
  • 50-100mcg BD
  • 12-24mcg BD
  • Tiotropium
  • Glycopyronium
  • Umeclinidium
  • 10mcg OD
  • 55mcg OD
  • 65mcg OD
  • Tiotropium preparations vary by brand and may be 13mg or 18mg listed on the product – but there are equivalent to 10mg tiotropium dose. Brand: Spiriva (18mcg)
  • Glycopyronium and Umeclinidium are less widely used, but commonly found in combination therapies.
  • DO NOT USE SAMA WITH LAMA. The SAMA should be ceased when LAMA is initiated. SABA+LAMA is however safe (and recommended)
  • Ultibro
  • Indacterol + glycopyronium
  • With combination therapies, brand names may be more memorable (and are considered appropriate in use of generic names by most clinicians). Be aware that brand names vary by country. I have only included brands that are the same in the UK and Australia in this table.
  • Fluticasone
  • Beclomethasone
  • Budesonide
  • Ciclesonide
  • 100-500mcg BD**
  • 50-200mcg BD
  •  100-400mcg OD
  • 80-320mcg OD
  • Brand: Flixotide
  • Brand: QVAR
  • Brand: Pulmicort
  • Brand: Alvesco
  • Trelegy Elipta
  • Fluticasone, umeclidinium, vilanterol

*Note that in the UK, ICS inhalers outside of combination preparations are NOT licensed for COPD. Similarly – in Australia – although they can be prescribed, this should ALWAYS be in conjunction with a stepwise approach, and concurrent use of LAMA (+/- LABA) and a SABA. 

**For fluticasone propionate. An alternative preparation fluticasone furoate is 100-200mcg OD.  

Oral steroids

  • Typically reserved for acute exacerbations
  • Aim to keep courses as short as possible (3-5 days)
LTOT – long term oxygen therapy
This is indicated for patients with proven hypoxaemia. An initial screening test for hyperaemia is O2 saturations <92% on pulse oximetry, although a true diagnosis of hypoxaemia requires evidence of low PaO2 on blood gas.
LTOT can prolong the life expectancy of COPD patients. The longer it is used, the greater the increase in life-expectancy. It is typically prescribed @ 2L via nasal prongs for at least 15 hours a day. This aims to keep oxygen saturation above 90%.
  • Only 30% of those with hyperaemia who are NOT receiving LTOT survive more than 5 years after diagnosis.
  • By giving the LTOT you reduce the pulmonary arterial pressure. Moderate reduction is pressure is achieved after 15 hours, and a larger reduction after 19 hours a day.

Indications for LTOT

  • PaO2 <7.3kPa
  • PaO2 <8kPa, and patient also has polycythaemia, hypoxaemia, peripheral oedema or pulmonary hypertension
Patients should be asses for LTOT when they have:
  • FEV1 30-49% predicated
  • Cyanosis
  • Sats <92% when well on pulse oximetry


  • Some patients who have a large emphysematous bullae may benefit form a bullectomy. This enables adjacent areas of collapsed lung to re-expand into the space, and function again. This improves VQ mismatch.
    • Another option – you can put a valve in on bronchoscopy – this will allow air out of an emphysematous bullae, but not allow air in, and this eventually allows the bullae to collapse.
  • Another option is lung volume reduction surgery. This aims to increase the elastic recoil of the lung. Patients have to be carefully selected, and have an FEV1 <1L. it improves symptoms, but does not improve mortality.
  • Lung transplant can be performed on certain patients with end stage emphysema. It has a 3-year survival of 75%, and again, the treatment improves symptoms, but does not really affect quality of life.


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.

When to refer to a specialist?

  • Diagnosis is uncertain (including asthma / asthma overlap)
  • Haemoptysis
    • An urgent referral for work-up for lung cancer
  • Rapid decline in function
  • Symptoms not responsive to management
  • Onset of peripheral oedema
  • Large bullous disease visible on x-ray
    • For consideration for surgery
  • COPD at age <40
    • To assess for a1-antitrypsin deficiency


Patient support

  • Involving family members in consultations and management plans can increase compliance
  • Offer written advice about COPD, and offer written exacerbation management plans
  • Offer referral to patient support gourds – either online or in person – e.g. in Australia via the Lung Foundation
  • In Australia – offer patients a GP management plan and Team care arrangements as indicated

Palliative care and advanced care directives

  • Encourage patients to think about the long-term implications and to consider an advanced care directive
  • Consider involving patients for palliative care if they have a very low level of functioning and / or are declining rapidly

Air travel

Commercial airliners have a cabin pressure equal to an altitude of 2750m. At this level PaO2 will fall from 13.5kPa to 10kPa – and oxygen saturation will fall by 3%. In normal healthy individuals this has no effect, but in patients with even moderate COPD, this can reduce their O2 saturation to around 6.5kPa and oxygen therapy may be needed. As a result, patients with COPD should consult their doctor / airline before travelling.

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!


Patients will either basically get respiratory failure or cor pulmonale.

Respiratory Failure

  • Cardiac output will be normal or slightly increased
  • Salt and fluid retention will occur as a result of renal hypoxia
  • Technically, respiratory failure occurs when the PaO2 <8kPa, or the PaCO2 >7kPa.

Type one respiratory failure

This is hypoxaemia without hypercapnia. The CO2 level will tend to be normal or low. It is caused by a VQ mismatch. Common causes include:
  • Pneumonia
  • Pulmonary oedema
  • PE
  • Asthma
  • Emphysema
  • Fibrosing alveolitis
  • ARDS


  • 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 respiratory failure

This is hypoxaemia with hypercapnia. It is a result of alveolar hypoventilation. There is not VQ mismatch. 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


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– then consider giving a respiratory stimulant such as doxapram (1.5-4mg/min IV) 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

Cor pulmonale

  • 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.



  • Murtagh’s General Practice. 6th Ed. (2015) John Murtagh, Jill Rosenblatt
  • Oxford Handbook of General Practice. 3rd Ed. (2010) Simon, C., Everitt, H., van Drop, F.
  • Beers, MH., Porter RS., Jones, TV., Kaplan JL., Berkwits, M. The Merck Manual of Diagnosis and Therapy
  • COPD-X Concise Summary – June 2020

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Dr Tom Leach

Dr Tom Leach MBChB DCH EMCert(ACEM) FRACGP currently works as a GP and an Emergency Department CMO in Australia. He is also a Clinical Associate Lecturer at the Australian National University, and is studying for a Masters of Sports Medicine at the University of Queensland. After graduating from his medical degree at the University of Manchester in 2011, Tom completed his Foundation Training at Bolton Royal Hospital, before moving to Australia in 2013. He started almostadoctor whilst a third year medical student in 2009. Read full bio

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