COPD (summary)

Dr Jeremy Jones et al.
This is a basic article for medical students and other non-radiologists

COPD (chronic obstructive pulmonary disease) is defined as a condition characterised by persistent air flow limitation that is usually progressive and associated with an enhanced chronic inflammatory response in the airways and the lung to noxious particles or gases 1.

It is worth noting that the current definition of COPD does not include the terms chronic bronchitis or emphysema

  • chronic bronchitis is defined as the presence productive cough for three months in each of two successive years in a patient in whom other causes of chronic cough (e.g. bronchiectasis) have been excluded; patients with chronic bronchitis are not considered to have COPD unless they have airflow obstruction
  • emphysema is a pathological term defined as destruction of the alveoli walls; this is one of the structural abnormalities that can be present in patients with COPD but can also be found in persons with normal lung function 1

COPD is a common disease, with a highest prevalence among those over 60 years old. Estimated worldwide prevalence is 10% 2. There is currently an increased prevalence amongst men, although the numbers of women who have COPD has been rising over recent years. A severe genetic form is seen in younger females.


The most commonly encountered risk factor for COPD is cigarette smoking although other types of tobacco and marijuana are also risk factors. Occupational exposure to dust and chemicals and indoor air pollution from biomass fuel burning also increase the risk of developing COPD.

The best known genetic risk factor is hereditary deficiency of alpha-1 antitriprysin, these patients typically develop emphysema earlier; other genetic risk factors are also thought to contribute to COPD 1.


Chronic irritants such as cigarette smoke cause an inflammatory response in the respiratory tract which is amplified in COPD-prone patients. Chronic inflammation leads to structural changes which occur predominantly in the peripheral airways but also in the large airways, lung parenchyma and pulmonary vasculature. 

The individual pattern of change varies between patients and can include narrowing and reduction in number of the small airways, destruction of the lung parenchyma or emphysema, enlarged mucous glands with mucus hypersecretion and hyperplasia of the wall of the small pulmonary arteries 1.


The main symptoms of COPD are dyspnoea (exertional dyspnoea is the most common early symptom), chronic cough and sputum production. Less common symptoms are wheezing and chest tightness. Symptoms usually start in mid-life and are slowly progressive. 

Patients with COPD can present with chronic daily respiratory symptoms, recurrent acute exacerbations or with relatively little respiratory complaints but an extremely sedentary lifestyle due to the exertional dyspnea 1.


Spirometry is required to establish the diagnosis of COPD. A post-bronchidialtor FEV1/FVC ratio less than 0.7 confirms the presence of persistent airflow limitation, which in the absence of an alternative explanation for the symptoms and airflow limitation is diagnostic of COPD 1.

Treatment and prognosis

Smoking cessation has the greatest impact on the evolution of the disease. 

The pharmacologic treatment of stable symptomatic COPD includes bronchodilators (beta agonists, anticholinergics, teophylline) alone or in combination with inhaled glucocorticoids +/- phosphosterase 4 inhibitors. Pulmonary rehabilitation as well as oxygen therapy in patients with chronic hypoxemia at rest also have an important role. In appropriately selected patients with severe emphysema lung volume reduction surgery (removing an area of emphysematous lung to allow the rest of the lung to expand better when breathing) can be a treatment option. 

Oxygen therapy, short-acting bronchodilators, systemic corticosteroids and in specific situations antibiotics are the main treatments for exacerbations 1,3.

The natural history and prognosis of COPD are variable but usually there is a slow gradual decline with increasing symptoms, leading to a reduction in life expectancy which depends on the severity of the disease 4.

A chest x-ray should be performed at the time of initial diagnosis to exclude alternative diagnosis or evaluate for co-morbidities (e.g. interstitial lung disease, lung cancer with airway obstruction), and during acute exacerbations to exclude complicating processes (e.g. pneumonia, cardiac failure, pneumothorax).

CT chest can be useful to investigate symptoms that seem disproportionate to the spirometry results, or to assess suitability for lung volume reduction surgery. CT chest can also be necessary when the chest x-ray shows abnormalities that need further investigation 5.


Plain chest radiographs have a poor sensitivity to detect COPD and usually only show features suggestive of COPD in advanced disease. Possible findings include 1:

  • flattened diaphragmatic contour due to hyperinflation as a consequence of the expiratory airflow limitation
  • decreased peripheral bronchovascular markings and increased radiolucency of the lung, due to lung parenchyma destruction
  • bullae (a bulla is defined as a rounded focal lucency > 1cm demarcated by a thin wall and is often associated with emphysematous changes in the rest of the lung)
  • prominence of the hilar vessels if there is pulmonary hypertension

CT can determine the presence, pattern and extent of emphysema. According to the location within the lung parenchyma emphysema can be classified as:

  • centrilobular emphysema: this is the most common type of smoking related emphysema; it is called centrilobular because the destruction of parenchyma is centred around the terminal bronchiole, which is in the centre of the secondary pulmonary lobule, and it tends to be more marked in the upper zones
  • panlobular emphysema: this type of emphysema is associated to alpha-1-antitripsin deficiency but can also be seen in smoking related emphsyema, usually mixed with centrilobular emphysema; it is called panlobular because it affects all the areas of the lung lobule more or less equally
  • paraseptal emphysema: this term is used to describe emphysematous lesions in the parenchyma adjacent to the pleural surfaces

Other possible findings in patients with COPD are 6:

  • bronchial wall thickening
  • air trapping on expiratory scans reflecting small airways obstruction
  • narrowing of the trachea in the coronal plane (saber sheath trachea)
  • enlargement of the pulmonary artery in patients with pulmonary hypertension 

Typically the finding of irreversible airflow limitation on spirometry in a patient with risk factors (smoking history) and clinical symptoms of COPD is diagnostic. The chest radiograph can help to exclude other possible diagnosis as heart failure or interstitial lung disease.

Conditions such as asthma, bronchiectasis and scarring from previous tuberculosis sometimes need to be considered in the differential diagnosis, and it has to be taken into account that these can also occur together with COPD 1,2.

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Article Information

rID: 39654
System: Chest
Synonyms or Alternate Spellings:
  • Chronic obstructive pulmonary disease (basic)

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    Alpha-1-antitrypsine deficiency: panlobular emphysema
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