To the Editor:
Wagenaar et al. 1 report improvement in gas exchange and increased minute ventilation (V′E) in patients with stable, moderately severe chronic obstructive pulmonary disease receiving treatment with acetazolamide and medroxyprogesterone. They estimate a baseline carbon dioxide (CO2) production rate of 400 mL·min−1 from the placebo values for CO2 arterial tension (Pa,CO2) of 6.5 kPa or 49 mmHg and V′E of 9.3 L min−1. Assuming that Pa,CO2 can be substituted for alveolar carbon dioxide tension (PCO2), one can calculate the dead space to tidal volume ratio (VD:VT) using the standard formula 2: where V′CO2 is carbon dioxide production.
The VD:VT calculates to 0.24, a surprisingly low value in patients with advanced airways obstruction. If this value is modified by the increased VT during acetazolamide and medroxyprogesterone treatment and one calculates V′CO2 (Pa,CO2 of 5.3 kPa or 40 mmHg and V′E of 11.2 L·min−1), V′CO2 is 412 mL·min−1, not the 450 mL·min−1 the authors state.
If medroxyprogesterone therapy was associated with a substantial increase in metabolic carbon dioxide production, then an increase in total ventilation would be necessary to prevent an increase in alveolar and arterial carbon dioxide tension production, in part defeating the purpose of the use of respiratory stimulants in this situation.
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