Sodium bicarbonate during a cardiac arrest is widely debated and used in many cases. In a 2018 PULMCrit post, Dr. Josh Farkas reviews much of the data and concludes that use of sodium bicarbonate is a “source of eternal disagreement.” A 2013 EMCrit article and podcast by Dr. Scott Weingart also details some of the controversy. The 2020 ACLS Guidelines state that routine use of sodium bicarbonate is not recommended in cardiac arrest [1]. Despite this recommendation, sodium bicarbonate is still often administered during resuscitations if a metabolic (or respiratory) acidosis is suspected or after a prolonged downtime. A recent study evaluated the effect of pre-arrest acid-base status on response to sodium bicarbonate and achievement of return of spontaneous circulation (ROSC) [2].


This was a retrospective review of in-hospital cardiac arrests (IHCA) in patients with pre-arrest serum bicarbonate levels ≤21 mmol/L compared to >21 mmol/L. Pre-arrest bicarbonate levels were obtained <24 hours prior to the arrest. Similarly, post-arrest bicarb levels were obtained <24 hours following the arrest. Bicarbonate levels were recorded from basic chemistry panels rather than blood gases. All patients received a median sodium bicarbonate dose of 100 mEq. The groups were relatively well-matched, with the only major difference being the time to first bicarb administration was faster in the ‘acidotic’ group (6.9 vs. 9.2 minutes). Initial ECG rhythms were similar between the groups.

  • 102 patients in ‘acidotic’ group with a median pre-arrest bicarb level of 17 mmol/L
  • 123 patients in ‘non-acidotic’ group with a median pre-arrest bicarb level of 27 mmol/L
  • There was no difference in ROSC (53.9% vs 48.8%, p=0.44) or survival to discharge (8.8% vs 5.7%, p=0.36) between the acidotic group versus the nonacidotic group

Thoughts and Limitations

  • A meta-analysis found no difference in sustained ROSC or survival to discharge with sodium bicarbonate (Alshahrani 2021).
  • In the current study, prearrest bicarb levels could have resulted up to 24 hours prior to the arrest and the authors don’t comment on when exactly they were drawn. The timing limits the ability to know true acid-base status just prior to the arrest. And, that really limits applying this to out-of-hospital cardiac arrest where patients may have more significant acidemia if resuscitation is delayed.
  • A median bicarbonate concentration of 17 mmol/L isn’t really that low, relatively speaking, to indicate a potential impact from administering sodium bicarbonate.
  • Retrospective cardiac arrest studies are challenging. Many interventions happen around the same, making it impossible to connect any one of them with a specific outcome.
  • The study that would be more helpful is taking patients with metabolic/respiratory acidosis and giving have bicarb and the other placebo.

Bottom Line

  • In this cohort of IHCA patients, sodium bicarbonate administration did not improve the chances of ROSC or survival to hospital discharge, irrespective of pre-arrest acid-base status. In other words, attempting to correct ‘acidosis’ does not seem to change rate of ROSC.
  • Sodium bicarbonate use in cardiac arrest should be targeted (e.g., hyperkalemia with metabolic acidosis, sodium channel blockade secondary to an overdose).

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  1. Panchal AR, Bartos JA, Cabañas JG, et al. Part 3: adult basic and advanced life support: 2020 american heart association guidelines for cardiopulmonary resuscitation and emergency cardiovascular care. Circulation. 2020;142(16_suppl_2):S366-S468. doi: 10.1161/CIR.0000000000000916. PMID: 33081529.
  2. Mclean H, Wells L, Marler J. The effect of prearrest acid-base status on response to sodium bicarbonate and achievement of return of spontaneous circulation. Ann Pharmacother. Published online August 5, 2021:10600280211038392. doi: 10.1177/10600280211038393. PMID: 34353142.
Bryan D. Hayes, PharmD, DABAT, FAACT, FASHP

Bryan D. Hayes, PharmD, DABAT, FAACT, FASHP

Leadership Team, ALiEM
Creator and Lead Editor, Capsules and EM Pharm Pearls Series
Attending Pharmacist, EM and Toxicology, MGH
Associate Professor of EM, Division of Medical Toxicology, Harvard Medical School
Bryan D. Hayes, PharmD, DABAT, FAACT, FASHP


EM Pharmacist & Toxicologist @MassGeneralEM | Asst Prof @HarvardMed/@EMRES_MGHBWH | @ALiEMteam leadership | Capsules creator, ALiEMU | President, ABAT | #FOAMed