End-tidal CO₂ 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 CO₂ elevation was defined as an increase of ≥20% from the baseline end-tidal CO₂ value. The time to initial increase (lag time, T_lag), time to peak (T_peak), and duration of the end-tidal CO₂ 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 CO₂ 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 CO₂ 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 CO₂ pressure as a physiological indicator may be limited.