By first adjusting the ventilator settings until phasic respiratory muscle output disappears, one imposes a high level of background inhibition on the respiratory pump. The measurement loses its uniqueness, however, if PaC02 is raised by lowering ventilator rate or tidal volume instead of supplementing C02 to the inspired gas. Prechter et al considered C02RT to be an estimate of the transition zone between a C02 responsive and a C02 unresponsive region of the ventilatory C02 response curve. As such, any increase in PaC02 above C02RT represents an error signal that induces a compensatory increase in respiratory drive.
In a study of eight normal volunteers, Prechter et al2 found that on average C02RT exceeded C02SB by 1 mm Hg, but this difference did not reach statistical significance. In a similar experiment, Simon et al reported up to 6 mm Hg differences between C02RT and C02SB and explained this observation on the basis of inhibition of respiratory motor output from mechanical lung inflation. We do not know whether differences in the sensitivity of recruitment criteria account for the discrepancy in findings. The hypothesis that mechanical inhibition raises C02RT above C02SB in the absence of respiratory failure is consistent with our observations in three of five patients in group 1.