The carbon monoxide transfer factor (TL,CO) is the product of the two prima
ry measurements during breath-holding, the CO transfer coefficient (KCO) an
d the alveolar volume (VA). KCO is essentially the rate constant for alveol
ar CO uptake (Krogh's kCO), and in healthy subjects, increases when PA is r
educed by submaximal inflation, or when pulmonary blood flow increases. Rec
ently, new reference values mere proposed for clinical use which included t
he observed Va at full inflation; this was claimed to "eliminate the need f
or KCO".
In this commentary, some mechanisms e.g. respiratory muscle weakness, lung
resection, diffuse alveolar damage and airflow obstruction, which decrease
or increase total lung capacity (TLC) are reviewed.
Even when alveolar structure and function are normal, the change in KCO at
a given VA varies according to the underlying pathophysiological mechanism.
The advantages and disadvantages of normalizing KCO and TL,CO to prediseas
e predicted TLC or to the patient's actual VA (using lack of expansion or l
oss of alveolar units models) are considered.
Examination of carbon monoxide transfer coefficient and alveolar volume sep
arately provides information on disease pathophysiology which cannot be obt
ained from their product, the carbon monoxide transfer factor.