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PH-RS17

Atelectasis: collapse of the lung

Why alveoli stay open, how blocked airways, pressure from outside, scarring and lost surfactant make parts of the lung collapse, why collapse lowers oxygen through shunt, and how the X-ray shows which lobe has collapsed.

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  • 6 steps · 10 questions
  • 3D anatomy, affected parts marked

By the end, you can

  • Describe what keeps alveoli open: negative pleural pressure, surfactant, the nitrogen in alveolar gas, collateral ventilation and regular deep breaths.
  • Explain resorption, compression, contraction and patchy (surfactant-loss) atelectasis and give typical causes of each.
  • Explain why collapsed lung causes shunt and hypoxaemia that responds poorly to extra oxygen.
  • Predict whether the mediastinum moves towards or away from a white hemithorax, and recognise the X-ray signs of each lobar collapse.
  • Explain why atelectasis is so common after surgery and how each main treatment reopens the lung or removes the cause.

What it is

Atelectasis is incomplete expansion of the lung, or collapse of lung that was expanded, so that a region loses its air and its volume. It can affect a few alveoli (microatelectasis), a segment, a lobe or a whole lung. Acquired atelectasis is grouped by mechanism: resorption behind a blocked airway, compression from outside the lung, contraction by scarring and patchy collapse from loss of surfactant. Failure of a newborn’s lungs to expand fully is neonatal atelectasis.

4 types to tell apart
Resorption (obstructive)
Gas beyond a completely blocked airway is absorbed into the blood: a mucus plug, tumour, foreign body or misplaced breathing tube. The region shrinks and pulls the mediastinum towards it.
Compression (passive or relaxation)
Air, fluid or a mass in the pleural space, or a raised diaphragm, lets the lung recoil or squeezes it; a large collection pushes the mediastinum away.
Contraction (cicatricial)
Scarring in the lung or the pleura stops it expanding; unlike the other forms, it does not reverse.
Patchy (adhesive)
Loss or inactivation of surfactant lets small alveoli collapse, as in neonatal respiratory distress syndrome and the acute respiratory distress syndrome (ARDS).

US spelling: fibres → fibers.

Normal function

What keeps the alveoli open

Left to itself, each would collapse: the in its wall and the surface tension of the thin fluid lining it both pull inwards. Two things oppose them. The pressure in the pleural space is below atmospheric, so the lung is held stretched against the chest wall; and surfactant, made by , lowers surface tension, most of all in small alveoli, so they do not empty into larger ones.

Breathing itself keeps the lung open. Regular sighs and deep breaths reopen alveoli that have begun to close and spread fresh surfactant, and coughing clears the airways. Small pores between neighbouring alveoli (pores of Kohn) and channels to nearby bronchioles let air reach alveoli from the side (collateral ventilation), so one blocked small airway seldom collapses the alveoli beyond it.

Most of the gas in an alveolus is nitrogen, which the blood takes up only very slowly, so it acts as a scaffold that keeps alveoli inflated between breaths. Blood flowing past each alveolus picks up oxygen, and ventilation and blood flow are normally well matched.

Point to it on the model