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Sodium Bicarb Increases End-Tidal CO2 Values

January 5, 2024

Written by Samuel Rouleau

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A prospective, observational study demonstrated that giving sodium bicarbonate to patients undergoing mechanical ventilation or CPR resulted in an increase in end-tidal CO2 values in as quickly as 17 seconds and lasted for 7 minutes.

Le Chatelier was right! Bicarb goes in…CO2 comes out!
Both sodium bicarbonate and end-tidal CO2 monitoring are employed commonly in the ED and ICU. While it is known that sodium bicarbonate affects end-tidal CO2 levels, the magnitude of change and temporal parameters have not been well-described. In this single center, prospective observational study, there were 33 adult patients who received sodium bicarbonate if: 1) intubated with severe metabolic acidosis (pH ≤ 7.1 on arterial blood gas) in those with spontaneous circulation, 2) undergoing CPR with an arterial pH ≤ 7.0. Twenty-five patients were intubated with spontaneous circulation; 8 were undergoing CPR. Sodium bicarbonate was delivered at a dose of 1-1.5 mEQ/kg over 3 minutes.

End-tidal CO2 was measured immediately prior to sodium bicarbonate administration and then continuously for 20 minutes. An increase was defined as 20% or greater in end-tidal CO2 value. They calculated the Tlag (time to increase in end-tidal CO2), Tpeak (time to peak value), Tduration (total time end-tidal CO2 remained 20% above baseline).

The median end-tidal CO2 values increased by 100% in all patients (from 21 to 41 mm Hg), yet the increase was more profound in those undergoing CPR with median increase of 160.2% (15 to 41 mm Hg) compared to 89.5% in those with spontaneous circulation (21 to 39 mm Hg). The Tlag across all patients was 17 seconds (IQR 12-21) with the median Tpeak occurring at 35 seconds (IQR 27-52), and the median Tduration was 420 second (IQR 90-639). For Tlag, Tpeak, and Tduration there was no statistically significant difference between the spontaneous circulation and CPR group. Tduration did correlate with the total amount of sodium bicarbonate given, especially for the CPR group. This is likely explained due to the lower cardiac output, even under ideal CPR.

Overall, this study is limited by its small sample size, especially with only 8 patients in the CPR subgroup, which limits the utility and validity of comparative statistics. Also, the authors excluded patients who were under CPR and achieved ROSC within 20 minutes of sodium bicarb administration, which is the subgroup that I would be the most interested in learning about. Nevertheless, this study offers firm data that sodium bicarbonate administration increases end-tidal CO2 in practically all patients who receive it and gives insight into the magnitude and duration of this effect.

How will this change my practice?
My current practice is not to routinely use sodium bicarbonate during CPR, unless there is a clear indication. This study enhances my understanding of how end-tidal CO2 responds after giving sodium bicarb.

  • The indications for sodium bicarbonate are fewer than one might expect: hyperkalemia, toxic ingestion (sodium channel blockers, salicylates, toxic alcohol), and shock with metabolic acidosis in the setting of acute kidney injury (BICAR-ICU trial).
  • After you push sodium bicarb during CPR, the end-tidal CO2 is now unreliable and no longer a useful surrogate for ROSC.
  • If you push sodium bicarbonate, you need to be aware of the expected increase in end-tidal CO2, as I have seen CPR prolonged because the end-tidal CO2 is “improving,” when it’s just the sodium bicarbonate.  
  • If there is no increase in end-tidal CO2 after administering sodium bicarbonate during CPR, this could indicate that your access has gone bad or the quality of CPR is low and not allowing for circulation of the medication.

Source
End-tidal carbon dioxide after sodium bicarbonate infusion during mechanical ventilation or ongoing cardiopulmonary resuscitation. Am J Emerg Med. 2023 Nov 25:76:211-216. doi: 10.1016/j.ajem.2023.11.027. Online ahead of print.