The air you can’t blow out
No matter how hard you blow, the lungs never fully empty — what stays behind is the residual volume. Because spirometry only sees the air that moves, it is blind to this leftover air and to the total lung capacity that includes it. To measure those, we need lung-volume measurement, most accurately by body plethysmography — sitting in a sealed clear booth while gentle pressure changes reveal exactly how much gas is inside the chest.
These volumes finally distinguish two things spirometry can confuse. A genuinely small lung — true restriction — shows a low total lung capacity. But in COPD the opposite happens: damaged airways let air in but trap it on the way out, so residual volume and functional residual capacity climb. This is air trapping and hyperinflation — the chest becomes over-full, and that is why severe COPD gives the “barrel chest” look.
How well the surface transfers gas: DLCO
Volumes tell you the size and mechanics, but not whether the delicate surface where blood meets air is doing its job. The DLCO — also called the transfer factor — measures exactly that. You inhale a tiny, harmless trace of carbon monoxide, hold your breath for about ten seconds, and breathe out; the test calculates how much of that gas crossed into the blood. A low number means the gas-exchange surface is reduced or thickened.
DLCO is wonderfully complementary to spirometry. In emphysema the alveolar walls are destroyed, so DLCO falls even when much air still moves. In scarring lung disease the membrane thickens, so DLCO falls alongside the small volumes. By contrast, in asthma the surface is intact, so DLCO is typically normal or even high — a handy way to separate asthma from COPD when both show obstruction. A combination like restrictive spirometry plus a low DLCO is a strong nudge toward interstitial lung disease.