Produced by the Royal College of Physicians of Edinburgh and Royal College of Physicians and Surgeons of Glasgow

Chronic Obstructive Pulmonary Disease

  • Dr P Albert, Clinical Research Fellow, University Hospital, Aintree, Liverpool, England
  • Professor P Calverley, Professor of Respiratory and Rehabilitation Medicine, University Hospital, Aintree, Liverpool, England


COPD is a chronic and disabling lung disease which, whilst being common, is also believed to be significantly under-diagnosed. In this article Dr Paul Albert and Professor Peter Calverley provide an overview of COPD and how best to manage this disease.

Key Points

  • Chronic Obstructive Pulmonary Disease results from airflow obstruction which may not be reversible and is the preferred term for patients who may have been labelled as having chronic bronchitis or emphysema in the past.
  • Chronic Obstructive Pulmonary Disease is predominantly caused by cigarette smoking, although occupational exposure can contribute to its development.
  • Symptoms may not be present until the more advanced stages of the disease.
  • Ten to eleven percent of the UK adult population may have COPD.
  • The volume of air that can be forced out in one second after taking a deep breath (FEV1) classifies disease severity.
  • Treatment centres on bronchodilation, steroids and control of infection in the acute presentation.
  • Pulmonary rehabilitation should be offered to all functionally disabled patients.

Declaration of interests: The authors have received speaker fees from GlaxoSmithKline, AstraZeneca and Pfizer.


Chronic Obstructive Pulmonary Disease (COPD) is a disease state characterised by airflow obstruction that is not fully reversible. It is predominantly caused by smoking, although other factors such as occupational exposures also contribute to the development. The obstruction arises from chronic inflammation in the airways and lung parenchyma. COPD produces symptoms, disability and impaired quality of life but significant airflow obstruction may be present before the patient is aware of symptoms. COPD is the preferred term for patients who may have been labelled as having chronic bronchitis or emphysema in the past.

Chronic Obstructive Pulmonary Disease is generally a progressive disease. If the patient stops smoking, the disease may still progress due to the decline in lung function that occurs with the normal aging process. However, ongoing smoking accelerates the process.


The prevalence of COPD is uncertain since many patients are asymptomatic in the early stages or do not seek medical attention. However, in a national study of patients aged 18-65 in the UK, 10% men and 11% women had an abnormally low forced expiratory volume in one second (FEV1); half of these individuals had not previously been diagnosed. Although the prevalence of COPD in men appears to have reached a plateau, it is still rising in women. In the UK, 27,478 people died as a result of COPD in 2004,3 representing 5% of all deaths. Morbidity is also high. In 2002, there were 110,000 hospital admissions for COPD in England and Wales, representing 1•1 million inpatient days (Department of Health, Health Solutions Wales). The annual total direct cost of COPD to the NHS is estimated at £491,652,000.


A diagnosis of COPD should be considered in patients over the age of 35 with a smoking history who present with one or more of:

  • exertional breathlessness
  • chronic cough
  • regular sputum production
  • frequent winter bronchitis
  • wheeze

Spirometry should be performed to confirm the presence of airflow obstruction (FEV1/FVC ratio < 70%) FEV1= forced expiratory volume in 1 second; FVC= forced vital capacity.

Reversibility to bronchodilator or steroids is not usually necessary to make a diagnosis of COPD. However, these investigations may be helpful if there is uncertainty whether the patient has asthma rather than COPD.

More detailed investigations such as total lung capacity (TLC), residual volume (RV), inspiratory capacity (IC), functional residual capacity (FRC) and gas transfer calculations may be carried out to estimate further the degree of airflow obstruction and hyperinflation.

Additionally all patients should have a chest radiograph, full blood count (to exclude anaemia and polycythaemia) and body mass index (BMI) calculated.

The GOLD (Global Initiative for Chronic Obstructive Lung Disease) guidelines (2004) identified five stages of COPD based on the FEV1 (See Table 1).

The ‘at risk’ category is a controversial one and represents patients with a chronic cough and sputum production but normal lung function. It is best seen as a pointer to alert patients to their risk of disease rather than as a true stage in COPD development as not all patients report these symptoms. Indeed, the revised guidelines in 2006 removed stage 0.

The FEV1 is the single best variable to stratify COPD severity. However, it does not accurately predict dyspnoea intensity, exercise tolerance, or mortality. In light of this, the BODE index1 has been devised (Body mass index, Obstruction, Dyspnoea, Exercise capacity) which is a useful prognostic tool (see Table 2).

In a prospective study of 625 COPD patients1, the hazard ratio for death from any cause per one-point increase in the BODE score was 1•34 and the hazard ratio for death from respiratory causes was 1•62.


Smoking Cessation

Chronic Obstructive Pulmonary Disease patients who stop smoking show significantly smaller declines in FEV1, along with less cough, wheeze, chronic phlegm production and dyspnoea than patients who continue to smoke.

All COPD patients who continue to smoke should be encouraged to stop at every opportunity. This is more easily achieved with the help of a support programme and the use of nicotine replacement therapy and/or bupropion (unless contraindicated; such contraindications would include seizure disorders including a current or prior diagnosis of bulimia or anorexia nervosa and concurrent administration of bupropion with a monoamine oxidase (MAO) inhibitor.) A new smoking cessation agent, varenicline, has recently been introduced.

Inhaled bronchodilator therapy
Short acting beta 2 agonists (salbutamol, terbutaline)

These act directly on bronchial smooth muscle