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PH-RS18

Acute respiratory distress syndrome

How a direct or indirect injury inflames the alveolar barrier of both lungs, why protein-rich fluid, hyaline membranes and lost surfactant cause shunt and stiff lungs, how the lung heals or scars, and why gentle ventilation and lying prone help.

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  • 4 steps · 10 questions
  • 3D disease scene

By the end, you can

  • Distinguish direct from indirect causes of ARDS and explain how both converge on neutrophil-driven injury of the alveolar barrier.
  • Describe the exudative, proliferative and fibrotic phases of diffuse alveolar damage, including hyaline membranes and why they form.
  • Explain how surfactant loss, flooding and collapse cause shunt, refractory hypoxaemia and stiff lungs with a small aerated "baby lung".
  • Apply the Berlin definition and its PaO2/FiO2 bands, and know that newer definitions extend it.
  • Explain how lung-protective ventilation, PEEP, prone positioning and a conservative fluid strategy act on the mechanism.

What it is

Acute respiratory distress syndrome (ARDS) is acute, diffuse, inflammatory injury of both lungs, triggered by a direct or indirect insult, in which a leaky alveolar-capillary barrier floods the alveoli with protein-rich fluid, causing severe hypoxaemia and bilateral shadowing that heart failure or fluid overload does not fully explain. Its tissue pattern is diffuse alveolar damage.

2 types to tell apart
Direct (pulmonary) ARDS
The insult reaches the alveoli through the airways and injures the epithelium first: pneumonia, aspiration of gastric contents, inhaled smoke or toxic gases, lung contusion, near-drowning.
Indirect (extrapulmonary) ARDS
The insult arrives through the blood and injures the capillary endothelium first: sepsis, major trauma with shock, acute pancreatitis, transfusion, burns, cardiopulmonary bypass.

US spelling: hypoxaemia → hypoxemia, oedema → edema.

Normal function

A two-cell barrier, kept open by surfactant

Each is lined mostly by thin, flat type I pneumocytes, which cover almost all its surface and form the air side of the barrier; the capillary endothelium forms the blood side. Scattered cuboidal make surfactant, pump salt and water out of the airspace, and act as the stem cells that replace type I cells after injury. patrol the surface.

A film of water lines every alveolus, and its surface tension pulls inwards. By the law of Laplace, the pressure needed to keep a bubble open rises as its radius falls, so without help small alveoli would empty into large ones and collapse at the end of each breath. Surfactant, a phospholipid and protein film, lowers surface tension most as alveoli shrink, keeping them open, the lungs compliant and the airspaces dry.

How fluid is filtered and drained across this barrier, and why high pressure from a failing heart floods it, is covered in the lesson on pulmonary oedema. ARDS is the other route: the barrier itself is broken.

Point to it on the model