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From the Authors

Dept of Pulmonary Diseases, Dekkerswald, University of Nijmegen, Groesbeek, the Netherlands

From the authors:

We thank R.P. Cole for his interest in our paper. The ventilatory control system consists of two subsystems: 1) the ventilatory response to carbon dioxide (CO₂), representing the controller or controlling system; and 2) the metabolic hyperbola, which represents the controlled system and depends on the metabolic CO₂ production. The actual ventilation and arterial carbon dioxide tension (P_a,CO2) are determined by the intersection of the metabolic hyperbola and CO₂ response.

In the present study, the hypercapnic ventilatory response was assessed by the steady-state method 1. In this way we were informed on the characteristics of the controlling system of the ventilatory control system of our chronic obstructive pulmonary disease (COPD) patients, in the baseline condition as well as during the use of the respiratory drugs acetazolamide and medroxyprogesterone acetate.

However, we did not actually measure the actual CO₂ production or mixed expiratory carbon dioxide tension (P_CO2) values in our patients. As, in spontaneously breathing humans, the working point is the intersection of the ventilatory CO₂ response curve and the metabolic hyperbola, the latter could be estimated by the equation that R.P. Cole cites. Furthermore, as R.P. Cole points out, we had to assume that alveolar P_CO2 equals arterial P_CO2, which may not be true in severe COPD patients.

We agree that this led to an unrealistically low value of dead space to tidal volume ratio (V_D:V_T). Assuming a more realistic value for V_D:V_T in COPD patients of 0.5, this would yield a value for CO₂ production of 264 mL·min^–1. The latter value is rather low for COPD patients.

Therefore, if actual values of CO₂ production, alveolar P_CO2, or mixed expired P_CO2, and dead space ventilation are not actually measured, the various assumptions may not be fully realistic.

R.P. Cole's second point questions the effectiveness of an increase in ventilation by medroxyprogesterone acetate to obtain a decrease in carbon dioxide arterial tension in our patients. As shown in tables 3 and 4 in the paper, a modest but significant increase in ventilation was found (1.9 L·min^–1). Since the arterial carbon dioxide tension range of our patients was in the relatively flat part of the metabolic hyperbola, only a small increase in ventilation was needed to bring about a substantial decrease in carbon dioxide arterial tension, as was also discussed by Teppema and Dahan 2. The net effect in our patients was still a significant decrease in carbon dioxide arterial tension, indicating that even this rather limited increase in ventilation exceeded that needed for compensation of the increased carbon dioxide production.

References

1. Folgering HTM. Studying the control of breathing in man. Eur Respir J 1988;1:651–660.[Abstract]
2. Teppema LJ, Dahan A. Acetazolamide and breathing. Does a clinical dose alter peripheral and central CO(2) sensitivity?. Am J Respir Crit Care Med 1999;160:1592–1597.[Abstract/Free Full Text]

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