Respiratory membrane

Also known as: blood–gas barrier, alveolar–capillary membrane, air–blood barrier

The ultrathin barrier (≈0.2–0.6 µm) separating alveolar air from capillary blood, across which O2 and CO2 diffuse.

Overview

Thickness≈0.2–0.6 µm

Area≈70 m²

Equilibration time (rest)≈0.25 s of ≈0.75 s transit

On the thin side of each alveolar septum the diffusion path consists of: (1) the alveolar fluid layer with surfactant; (2) the alveolar epithelium (type I pneumocyte cytoplasm); (3) the epithelial basement membrane; (4) a very thin interstitial space, which in most places disappears as (5) the epithelial and capillary basement membranes fuse; and (6) the capillary endothelium. Gas then crosses plasma and the red-cell membrane to reach haemoglobin.

The barrier is extraordinarily thin (as little as ≈0.2 µm, averaging ≈0.5–0.6 µm) and vast (≈70 m²), which together give the lung a diffusing capacity far in excess of resting needs. Its thinness also makes it vulnerable: very high capillary pressures can cause stress failure with leakage of fluid or blood.

Location

Thin side of the interalveolar septa throughout the respiratory zone.

Parts & subdivisions

Surfactant/fluid layer

Air–liquid interface lining the alveolus.

Alveolar epithelium

Type I pneumocyte cytoplasm.

Fused basement membranes

Shared basal lamina of epithelium and endothelium; type IV collagen provides strength.

Capillary endothelium

Continuous, non-fenestrated endothelium of pulmonary capillaries.

Function

Permits rapid diffusion of O2 and CO2.

Restricts movement of fluid and protein into the alveoli.

Physiology

By Fick's law, diffusion is proportional to area and partial-pressure gradient and inversely proportional to thickness. At rest, blood equilibrates with alveolar gas within ≈0.25 s of its ≈0.75 s capillary transit. Diffusing capacity for CO (DLCO) quantifies the barrier's function.

Clinical significance

Diffusion impairment

Interstitial fibrosis and oedema thicken the barrier; emphysema and pneumonectomy reduce its area. Patients desaturate on exertion when transit time shortens, and DLCO is reduced. Goodpasture (anti-GBM) disease targets type IV collagen in both alveolar and glomerular basement membranes, causing pulmonary haemorrhage and glomerulonephritis.

High-altitude pulmonary oedema

Uneven hypoxic vasoconstriction exposes some capillaries to very high pressures, causing stress failure of the barrier and protein-rich oedema; treated by descent, oxygen and nifedipine.