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The carbon monoxide transfer factor (TL,co) is the product of the two primary measurements during breath-holding, the CO transfer coefficient (Kco) and the alveolar volume (VA). Kco is essentially the rate constant for alveolar CO uptake (Krogh's kco), and in healthy subjects, increases when VA is reduced by submaximal inflation, or when pulmonary blood flow increases. Recently, new reference values were proposed for clinical use which included the observed VA at full inflation; this was claimed to "eliminate the need for 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 predisease predicted TLC or to the patient's actual VA (using lack of expansion or loss of alveolar units models) are considered. Examination of carbon monoxide transfer coefficient and alveolar volume separately provides information on disease pathophysiology which cannot be obtained from their product, the carbon monoxide transfer factor.

In defence of the carbon monoxide transfer coefficientKCO(TL/VA)

In defence of the carbon monoxide transfer coefficientK_CO(T_L/V_A)