About 300 million tiny air bubbles with their thin, elastic membranes provide for the gas exchange: the absorption of oxygen from the air and the release of carbon dioxide from the body. Without these alveoli, we would gasp like a fish ashore. In chronic lung diseases it can lead to the expansion of these air chambers and damage to the fine membranes. The result is an increasing, irreversible dyspnea.
How does this disease develop?
An estimated 400, 000 people in Germany currently suffer from pulmonary emphysema - with an upward trend. Most of those affected are older than 50 years.
- Almost all cases of lung hyperinflation are preceded by years of smoking and / or chronic bronchitis. Due to the constant irritation of the mucous membrane in the respiratory tract it comes to an inflammatory reaction. As a result, tough mucus is formed and the tissue changes. The result is chronic obstructive pulmonary disease (COPD), in which the bronchi collapse. The air can not be properly exhaled and remains trapped in the air spaces. If the inflammatory processes also spread to the walls between the alveolar septa, they break. This will turn into several small bladders - a pulmonary emphysema. There is less and less space available for gas exchange, so that the affected person has to do more breathing work for the same amount of oxygen or can no longer meet the increased demand for oxygen during physical exertion.
- About 2% of the emphysema patients is due to an inherited enzyme defect, alpha-1-antitrypsin deficiency. This protein is in the blood and protects among other things the alveoli against aggressive substances. In the case of sufferers, its concentration is greatly reduced. This causes inflammation and the processes described above begin.
- Other causes include age-related loss of elasticity (age emphysema), scarred changes in other lung diseases (scar emphysema) and overstretching of the lungs, for example, when one part has been removed and the remaining lung fills the remaining space (overstretching emphysema).