We undertook this study to test the hypothesis that apneic oxygenation with high flows of intratracheal oxygen may increase carbon dioxide elimination over that with low intratracheal flows. Methods: We anesthetized five conditioned dogs and cannulated the femoral artery for arterial blood sampling. Heart rate was recorded by electrocar-diograph, and tracheal airway pressure was measured by transtracheal catheter. After inserting a 16-gauge plastic catheter through the cricothyroid membrane into the trachea and connecting the catheter to a high-pressure oxygen source, we started apneic oxygenation. Continuous flows of 100% oxygen were delivered under constant driving pressures of 30, 40, and 50 psi, each pressure for a period of 10 minutes. The gas flows leaving the trachea at the three pressures were measured at 19, 27, and 33 L/min, respectively, through an endotracheal tube placed above the transtracheal catheter. During apneic oxygenation, arterial blood gases were analyzed—PaCO2 at the start and thereafter at 2-minute intervals, PaO2 at the start and at the end of each 10-minute period. Before the institution of a different driving pressure, PaCO2 was brought back to baseline by intermittent oxygen insufflation by jet. Results: We found that PaCO2 increased at oxygen-line pressures of 30, 40, and 50 psi and that the amount of the increase did not differ significantly among the three pressures. The PaO2 level after 10 minutes at 30 psi pressure was significantly lower (P < 0.01) than the baseline level, but no such differences were found at pressures of 40 and 50 psi. Airway pressures were 7, 13, and 18 torr, respectively, at 30, 40, and 50 psi driving pressures. No complications occurred in any of the animals, and their recovery was uneventful. Conclusion: We conclude that the clinical value of apneic oxygenation, even with high flows of intratracheal oxygen, is limited by carbon dioxide accumulation. (Respir Care 1985;30:26-29.)