To use end-tidal PCO2 as a non-invasive estimate of arterial PCO2, one adds a nominal value, representing the arterial–end-tidal PCO2 difference. How much does one add? We hypothesized that, halving the ventilator rate and simultaneously doubling tidal volume, the immediate change in end-tidal PCO2 would be proportional to the original arterial-end-tidal PCO2 difference. We ventilated 31 patients at 20 breaths per minute (bpm), sampled arterial blood, and changed the rate to 10 bpm. The change in end-tidal PCO2 was, as hypothesized, positively correlated to the original arterial–end-tidal difference at 20 bpm (r = 0.64). End-tidal PCO2 increased in 23 patients. Thus, in theory, this method could offer some improvement in the estimate of arterial PCO2 from end-tidal. However, because of the considerable spread of values, a separate study is needed for verification

Tracheal and arterial CO2 partial pressures were measured simultaneously in 27 laryngectomized patients both while they were awake and during high-frequency jet ventilation. Tracheal gas was sampled during brief interruptions of high-frequency jet ventilation. Agreement between tracheal and arterial CO2 partial pressures was assessed using the Bland–Altman method. The tracheal–arterial CO2 partial pressures gradient during spontaneous breathing was significantly lower (P<0.0002) than during high-frequency jet ventilation. During spontaneous ventilation, the bias was −0.77 kPa (95% CI= −0.99 to −0.55 kPa), and the upper and lower limits of agreement were 0.29 kPa (95% CI= −0.11 to −0.7 kPa) and −1.83 kPa (95% CI= −2.24 to −1.43 kPa). During high-frequency jet ventilation, the bias was −1.61 kPa (95% CI= −1.76 to −1.46 kPa), and the limits of agreement were −0.48 kPa (95% CI= −0.75 to −0.21 kPa) and −2.74 kPa (95% CI= −3.01 to −2.47 kPa). Despite the poor agreement between tracheal CO2 partial pressure and arterial CO2 partial pressure, it is sufficient to allow for adjustment of ventilator settings during jet ventilation.