

Impact of Bolus Administration of Sodium Bicarbonate on Immediate Vasopressor Requirements
Wednesday, May 20, 2026 4:40 PM to 4:48 PM · 8 min. (America/New_York)
International Hall 7: Level I
Abstracts
Critical Care/Resuscitation
Information
Abstract Number
645
Background and Objectives
Since an acidotic state can reduce the sensitivity of adrenergic receptors to epinephrine and norepinephrine (NE), sodium bicarbonate has become a common practice to help rapidly normalize arterial blood gas in patients with septic shock. However, the 2021 SCCM Surviving Sepsis Guidelines only recommend sodium bicarbonate in patients who have severe metabolic acidemia and acute kidney injury (AKI). Overall, the benefits of sodium bicarbonate administration in septic shock remain unclear, and studies comparing benefits versus risks are controversial. This study aimed to explore the impact of bolus administration of sodium bicarbonate on reducing immediate vasopressor requirements for patients in the intensive care unit (ICU).
Methods
This retrospective, observational, multi-center study included adult patients who were admitted to an ICU with diagnosis of septic shock between October 2024 to October 2025 and received at least one sodium bicarbonate bolus after requiring 6 hours of NE or epinephrine. The most recent NE and epinephrine infusion rate prior to administration of sodium bicarbonate was collected, and subsequent rates were collected at 30 minutes, 1 hour, and 3 hours after bicarbonate administration. Primary outcome was the numerical difference in NE equivalent requirements 30 minutes after sodium bicarbonate administration, and secondary outcomes evaluated the difference at 1 hour and 3 hours. Additional outcomes included the difference in requirements in patients with an AKI versus those without. Paired samples t-test were used to assess the difference in NE equivalent requirements, and Mann-Whitney test was used to compare patients with an AKI versus those without.
Results
Among 123 patients included, there was no change in the difference of NE equivalents following administration of sodium bicarbonate at 30 minutes (55.9 vs 55.8 mcg/min, P=0.913). The difference increased after bicarbonate administration at 1 hour (55.9 vs 58.9 mcg/min, P=0.218) and 3 hours (55.9 vs 66.1 mcg/min, P=0.004). When comparing AKI versus no AKI, there was no significant difference in the mean difference of NE equivalent requirements at any observed time point.
Conclusion
Bolus administration of sodium bicarbonate did not result in a decrease of vasopressor requirements in patients with septic shock. Further studies with a larger population would be ideal to confirm the findings of this analysis.
CME
1.25
Disclosures
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