End-tidal carbon dioxide after sodium bicarbonate infusion during mechanical ventilation or ongoing cardiopulmonary resuscitation.

End-tidal CO 2 is used to monitor the ventilation status or hemodynamic efficacy during mechanical ventilation or cardiopulmonary resuscitation (CPR), and it may be affected by various factors including sodium bicarbonate administration. This study investigated changes in end-tidal CO2 after sodium bicarbonate administration. This single-center, prospective observational study included adult patients who received sodium bicarbonate during mechanical ventilation or CPR. End-tidal CO 2 elevation was defined as an increase of ≥20% from the baseline end-tidal CO 2 value. The time to initial increase (lag time, T lag), time to peak (T peak), and duration of the end-tidal CO 2 rise (T duration) were compared between the patients with spontaneous circulation (SC group) and those with ongoing resuscitation (CPR group). Thirty-three patients, (SC group, n = 25; CPR group, n = 8), were included. Compared with the baseline value, the median values of peak end-tidal CO 2 after sodium bicarbonate injection increased by 100% (from 21 to 41 mmHg) in all patients, 89.5% (from 21 to 39 mmHg) in the SC group, and 160.2% (from 15 to 41 mmHg) in the CPR group. The median T lag was 17 s (IQR: 12–21) and the median T peak was 35 s (IQR: 27–52). The median T duration was 420 s (IQR: 90–639). The median T lag , T peak , and T duration were not significantly different between the groups. T duration was associated with the amount of sodium bicarbonate for SC group (correlation coefficient: 0.531, p = 0.006). The administration of sodium bicarbonate may lead to a substantial increase in end-tidal CO 2 for several minutes in patients with spontaneous circulation and in patients with ongoing CPR. After intravenous administration of sodium bicarbonate, the use of end-tidal CO 2 pressure as a physiological indicator may be limited. [ABSTRACT FROM AUTHOR]