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PH-RS02

COPD: emphysema and chronic bronchitis

How smoke and inflammation destroy alveolar walls (emphysema) and inflame mucus-filled airways (chronic bronchitis), why airways collapse on breathing out, and how gas exchange and the right heart suffer.

By the end, you can

  • Explain how elastic recoil and radial traction keep small airways open in the normal lung.
  • Describe the protease–antiprotease imbalance and the role of alpha-1 antitrypsin.
  • Distinguish emphysema from chronic bronchitis by structure, mechanism and findings.
  • Relate loss of recoil and airway collapse to air trapping, hyperinflation and breathlessness.
  • Explain how hypoxaemia, hypercapnia and pulmonary hypertension develop in advanced disease.
  • Recognise the classic patterns of emphysema, the GOLD grades and the tests of COPD, and explain how each main treatment acts on its mechanism.

What it is

Chronic obstructive pulmonary disease (COPD) is persistent, usually progressive airflow limitation caused by long-term exposure to noxious particles or gases, above all tobacco smoke. It combines, in varying proportions, emphysema (destruction of alveolar walls) and chronic bronchitis and small-airway disease (mucus hypersecretion and narrowed airways).

2 types to tell apart
Emphysema
Permanent enlargement of airspaces beyond the terminal bronchioles with destruction of their walls: centriacinar in smokers (upper zones), panacinar in alpha-1 antitrypsin deficiency (lower zones).
Chronic bronchitis
A clinical definition: productive cough on most days for at least three months in each of two consecutive years, from mucus hypersecretion and inflamed airways.

Normal function

Elastic lungs and tethered airways

Each alveolar wall is a thin sheet of capillaries and connective tissue rich in elastin. Stretched on inspiration, the store energy like a spring; their elastic recoil, with surface tension, pushes air out during quiet expiration without muscle work.

The same walls hold the small airways open. Bronchioles under about 2 mm across have no cartilage; alveolar walls attached around them pull outwards (radial traction), like guy ropes on a tent, so they stay open as the lung empties.

The is a fine sponge of small alveoli with a vast surface for gas exchange, roughly 50–100 m² in an adult.

Point to it on the model