18.3 The Respiratory Membrane: Where Air Meets Blood

Time To Read

4–6 minutes

Date Last Modified

Ages 45


Corticosteroids

1

Recurrent Unilateral Pleuritic Pain

2

Normal Airway Function Between Attacks

3

Intact Gas Exchange During Pleurisy

4

Reduced Tidal Volume from Pain-Limited Excursion

5

Preserved Acid-Base Balance Between Attacks

6

Serositis of the Pleura

7

The FMF Serositis Triad

Shrink to the size of an oxygen molecule and ride one of Stina’s breaths to its destination: a moist, rounded chamber — an alveolus — one of roughly three hundred million bubbles that together spread to the area of a tennis court inside her chest. The wall ahead is almost nothing: a single flat cell of alveolar epithelium, a shared basement membrane, and a single flat cell of capillary endothelium — the respiratory membrane, about half a micrometer thick.

Gases cross this membrane by simple diffusion, which needs nothing but a gradient. Freshly inhaled air is rich in oxygen and poor in carbon dioxide; blood arriving from the body’s veins is the mirror image. So oxygen slides from air into blood and carbon dioxide slides from blood into air, each molecule rolling from where it is crowded to where it is sparse. The membrane is built for it: vast in area, vanishingly thin, always wet. Anything that thickens it — fluid, scar, or amyloid — slows the trade.

Stina’s pleurisy spares this delicate surface entirely; her inflammation is one layer out, on the pleura wrapping the lung, not on the membrane deep inside it. That is why her oxygen holds even while she is splinting in pain. (TEMPI watch: intrapulmonary shunting — blood bypassing ventilated alveoli — is the ‘I’ of the TEMPI differential opened by her erythrocytosis; note it here as a gas-exchange clue distinct from her pleural serositis.)

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