Ventilatory equivalents for carbon dioxide and oxygen are measures of ventilatory efficiency and not of pulmonary gas exchange efficiency

Sin et al. (2010) have compared ventilatory equivalents for carbon dioxide and oxygen (V̇E/V̇CO2 and V̇E/V̇O2 , respectively) at two different breathing rates in healthy control subjects and patients with permanent cardiac pacemakers. In the healthy control group, reduction of breathing frequency from 15 to 6 breaths min−1 resulted not only in a 2.5-fold increase in respiratory sinus arrhythmia (RSA), but also in a significant reduction of V̇E/V̇CO2 and V̇E/V̇O2 . In subjects with permanent cardiac pacemakers and therefore fixed-rate pacing, while there was no RSA, the reduction in V̇E/V̇CO2 and V̇E/V̇O2 with reduction in breathing rate was similar to that in the healthy control subjects. The conclusion, therefore, is that there is improvement in gas exchange efficiency at the lower breathing rate, and this improvement is not contingent upon an enhancement of RSA. Our opinion is that V̇E/V̇CO2 and V̇E/V̇O2 reflect ventilatory performance and not gas exchange efficiency. It is evident that these ratios will decrease with slow breathing (compared with a higher breathing rate) in any individual, irrespective of RSA, if the individual is asked to maintain end-tidal CO2 at a given value at both breathing rates (normocapnic range of 5–6% in this study), owing to an improved ratio of alveolar-todead space ventilation, resulting in lower minute ventilation. The effect of ventilation to perfusion ratio (V̇/Q̇ ratio) mismatch on gas exchange in a subject without RSA can be appreciated only by measuring the alveolar– arterial PO2 difference (A–a PO2 difference) and not by the parameters mentioned in the study. The authors themselves have stated that they chose not to study the three standard parameters for measuring gas exchange efficiency, including A–a PO2 difference, because these involve invasive procedures such as arterial or mixed venous blood sampling. It is clear, therefore, that the mechanism they refer to as pulmonary gas exchange is indeed the one assessed by A–a PO2 difference. However, V̇E/V̇CO2 cannot serve as a measure of gas exchange efficiency, in the sense conveyed in the paper, because carbon dioxide elimination will not be affected by temporal changes in V̇/Q̇ ratios, as long as total ventilation and perfusion remain unchanged. Ventilation (V̇E) is a function of the arterial PCO2 , and arterial PCO2 is equal to end-tidal CO2. If the subjects are allowed to breathe voluntarily so as to maintain endtidal CO2, as has been done in this study, reduction in breathing rate will not change V̇CO2 , but will lead to lowering of V̇E because of less dead space ventilation at the lower breathing rate (Ganong, 2005), irrespective of the presence or absence of RSA. When V̇E decreases, the ventilatory equivalents estimated in this study will decrease. A decrease in A–a PO2 difference may occur in control subjects as a result of improved RSA when breathing rate is reduced, which may not be seen in the paced subjects. A reduction in A–a PO2 difference will lead to an increase in arterial PO2 and probably an increase in arterial and venous oxygen saturation in the control subjects. The lack of such an increase in oxygen saturation with slow breathing in paced subjects without RSA will not translate into any reduction in V̇E/V̇O2 because oxygen consumption is a function of metabolic rate, and tissues can extract the required oxygen even from less saturated arterial blood.