OBJECTIVE: Carbon monoxide (CO) is eliminated mainly via the lungs so that exhaled carbon monoxide concentration reflects endogenous production. In this context, we studied the effects of inspiratory oxygen concentration and endotracheal intubation on endtidal CO concentrations.
METHODS: In patients undergoing general anaesthesia, endtidal CO concentrations were measured while breathing room air, oxygen as well as after induction of general anaesthesia and endotracheal intubation. To exclude time-dependent effects, patients were assigned to two groups. Patients in group 1 (n = 20) were preoxygenated for 5 minutes, whereas patients in group 2 (n = 20) were preoxygenated for 10 minutes. We also studied the effects of different inspiratory oxygen concentrations in volunteers (n = 20) breathing room air, 50% and 100% oxygen.
RESULTS: Breathing oxygen for 5 minutes increased endtidal carbon monoxide concentrations in all patients (in group 1 from 7.6+/-4.9 to 12.6+/- 5.0 ppm, p < 0.001; in group 2 from 7.1+/-6.1 to 16.4 +/- 8.6 ppm, p < 0.001). No further change of CO concentration was detected after 10 minutes of preoxygenation (16.4 +/- 9.0 vs. 16.4 +/- 8.6 ppm, p > 0.05). Endtidal CO values however significantly increased with induction of anaesthesia and endotracheal intubation (in group 1 to 21.5 +/- 6.3 ppm, p < 0.001, in group 2 to 26.1 +/- 13.1 ppm, p < 0.001). In volunteers, mean endtidal CO values increased from 10.7 +/-5.9 to 14.8+/-7.3 ppm after breathing 50% oxygen for 3 minutes (p < 0.001). Breathing pure oxygen had no additional effect on endtidal CO values (16.0 +/- 6.0 ppm, p > 0.05).
CONCLUSIONS: Endtidal carbon monoxide levels are influenced by inspiratory oxygen concentrations. Induction of anaesthesia and endotracheal intubation further increases endtidal CO concentrations beyond the effects attributable to preoxygenation alone.