Abstract

The single-breath carbon monoxide diffusing capacity (DLCO) is the
product of twomeasurements during breath holding at full inflation:
(1) the rate constant for carbon monoxide uptake from alveolar gas
(kCO [minute21]) and (2) the “accessible” alveolar volume (VA). kCO
expressed permmHg alveolar dry gas pressure (Pb*) as kCO/Pb*, and
thenmultiplied byVA, equalsDLCO; thus,DLCO divided byVA (DLCO/VA,
also called KCO) is only kCO/Pb* in different units, remaining, essentially,
a rate constant. The notion that DLCO/VA “corrects” DLCO for
reduced VA is physiologically incorrect, because DLCO/VA is not constant
as VA changes; thus, the term KCO reflects the physiology more
appropriately. Crucially, the same DLCO may occur with various combinations
of KCO and VA, each suggesting different pathologies. Decreased
KCO occurs in alveolar–capillary damage, microvascular
pathology, or anemia. Increased KCO occurswith (1) failure to expand
normal lungs to predicted full inflation (extrapulmonary restriction);
or (2) increased capillary volume and flow, either globally (left-toright
intracardiac shunting) or from flow and volume diversion from
lost or damaged units to surviving normal units (e.g., pneumonectomy).
Decreased VA occurs in (1) reduced alveolar expansion, (2)
alveolar damage or loss, or (3)maldistribution of inspired gases with
airflow obstruction. KCO will be greater than 120% predicted in case
1, 100–120%in case 2, and 40–120%in case 3, depending on pathology.
KCO and VA values should be available to clinicians, as fundamental
to understanding the clinical implications of DLCO. The diffusing
capacity for nitric oxide (DLNO), and the DLNO/DLCO ratio, provide
additional insights.

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