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Division of Respiratory Medicine, National Heart and Lung Institute, Imperial College School of Medicine, Hammersmith Hospital Campus, London, UK
CORRESPONDENCE: J.M.B. Hughes, Division of Respiratory Medicine, Imperial College School of Medicine, Hammersmith Hospital Campus, Ducane Road, London, W12 0NN, UK. Fax: 44 2088789681
Keywords: carbon monoxide, diffusing capacity, gas exchange, pulmonary function, transfer coefficient, transfer factor
Received: February 17, 2000
Accepted June 26, 2000
Abstract
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.
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