Emphysema is characterised by large permanently inflated alveolar air spaces due to the destruction of the alveolar walls and septae. The primary cause of emphysema is cigarette smoking and to a lesser extent other air pollutants. A genetic factor has also been identified as a contributor to early development of the condition in non-smokers. Below is an outline of the differing mechanisms in which the alveoli become damaged.

  1. Cigarette smoking and exposure to other air pollutants triggers an immune response by the body which amongst other things increases the amount of neutrophils (white blood cells) in the alveoli. Neutrophils play an essential role in the immune response however in this case they also have a damaging effect as they release protease, a destructive group of enzymes that begin protein catabolism. The most damaging of these enzymes is called elastase which is responsible for breaking down elastic fibres. What further compounds the problem and accelerates the damaging effects of the protease enzymes  is that cigarette smoke and other air pollutants decrease the effect of alpha-1-antripsyin, a substance which usually fights and removes the protease enzymes. Therefore an imbalance is created with a large amount of protease enzymes being present in the alveoli which greatly contributes to the loss of proteins responsible for keeping the lungs elastic and also for destroying the tissue separating the alveoli from one another.
  2. Mucous and other secretions cannot be cleared from the airways as effectively due to cigarette smoke and other air pollutants temporarily disrupting the cilia (fine “hairs” which line the airways and clear fluids through a sweeping action). Long term exposure to cigarette smoke causes the cilia to disappear from the cells lining the airways and mucous and other secretions begin to build up. The accumulation of mucous is also accelerated as smoking and some other air pollutants cause mucous production to increase. Mucous is a good medium for bacteria and other organisms to proliferate and may lead to infection. Infection leads to the release of more neutrophils to the alveolar with some types releasing proteases. This leads to an even greater number of protease enzymes to be present and thus further contributing to the breakdown of the alveolar.
  3. In some individuals a genetic deficiency of alpha-1-antitrypsin can also contribute to the destruction of alveolar tissue. People with alpha-1-antitrypsin deficiency cannot fight the destructive effects of the protease enzymes once it is released in the lung causing alveolar destruction at an even greater rate (as described above in point one).

The damage to the alveoli and other changes to the lungs have many negative effects on lung function as described below:

Alveolar wall breakdown

The breakdown in the alveolar walls (as demonstrated in figure 2) will result in the following:

  • Decrease in the surface area available for gas exchange
  • Loss of pulmonary capillaries which leads to a decrease in perfusion and the diffusion of gasses
  • The loss of elastic fibres causes a loss in elastic recoil on expiration
  • Decreased support for structures within the lungs (such as the small bronchi) which may lead to collapse of the walls and obstruction of airflow during expiration.
  • Pulmonary hypertension

Fibrosis and thickening of the bronchial walls

This occurs due to chronic irritation and frequent infections associated with smoking and the increased mucous production. The effects that this has on lung function are:

  • Narrowed airways (figure 2)
  • Weakened walls
  • Interference with passive expiratory airflow


Figure 2: The breakdown of alveoli in emphysema and thickening of bronchial walls

Difficulty with expiration

Alveolar breakdown and thickening of the bronchial walls causes progressive difficulty with expiration. Over time this will lead to:

  • Air trapping and increased residual  volume
  • Over inflation of the lungs
  • Fixation of the ribs in an inspiratory position, and an increased anterior-posterior diameter of the thorax (barrel chest)
  • Increased intrathoracic pressure

Advanced Emphysema and significant loss of tissue

If emphysema continues to progress (may happen rapidly if avoidance of respiratory irritants does not occur) the fore mentioned effects will gradually worsen leading to a significant loss of lung tissue. The following processes occur with these patients:

  • Adjacent damaged alveoli combine forming very large air spaces called blebs or bullae (figure 2)
  • The tissue and pleural membrane surrounding large blebs near the surface may rupture, resulting in pneumothorax
  • Carbon dioxide (CO2) retention (Hypercapnia) becomes marked and hypoxic drive for inspiration develops as the patient’s respiratory control adapts to a chronic elevation of CO2 levels. (see drive to breath on page 6)

In the late stages pulmonary hypertension and cor pulmonale (enlargement of the right side of the heart) occurs due to pulmonary blood vessels being destroyed coupled with vasoconstriction caused by hypoxia. The increased pressure in pulmonary circulation puts a large strain on the right ventricle leading the patient to display signs of heart failure. 

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