The Pre-brief
Sodium Bicarbonate (SB) is one of those drugs used in the management of cardiac arrest that has the ability to stay in common practice despite plenty of literature over several years showing little to no benefit and perhaps harm. In the 2005 ACLS guidelines for adults, the American Heart Association made a recommendation that stated, “Giving sodium bicarbonate routinely during cardiac arrest and CPR (especially in out of hospital cardiac arrest) or after ROSC is not recommended.”
Let’s see if we can review the relevant literature and narrow the use of SB in cardiac arrest.
Spoiler alert: SB is probably best used for tricyclic antidepressant overdose and confirmed hyperkalemia (the literature is pretty poor for this as well.)
Theory of Correcting Acidosis
One of the critical pathophysiologic components of cardiac arrest is the generation of both metabolic and respiratory acidosis. Obviously, if you are not breathing to oxygenate your blood and remove CO2, you will generate respiratory acidosis. Also, if your heart is not delivering oxygen-rich blood to the tissues and CO2 is unable to be removed, then metabolic acidosis will ensue.
The hypothesis of using alkalizing agents in cardiac arrest is to scavenge hydrogen ions, thus improving the body’s systemic acidosis to improve cardiovascular function.
In the original 1974 guidelines for cardiac arrest management entitled Standards for Cardiopulmonary Resuscitations and Emergency Cardiac Care of the American Heart Association, SB was listed as the first-line drug in cardiac arrest management. The theory of its use was from the original 1961 Manuscript “Reports of Applications of External Cardiac Massage in 118 Patients” by Jude, Kouwenhoven, and Knickerbocker. They theorized that “Continued cardiac arrest, even though the circulation is artificially maintained, will result in metabolic acidosis. Sodium Bicarbonate is beneficial in maintaining blood pH close to the normal value….”
By the early 1980s, SB was the most frequently used medication in the management of cardiac arrest. According to one study, 84.7% of in-hospital cardiac arrests SB was administered. However, in the mid-1980s, a series of papers questioned the use of sodium bicarbonate. The researchers developed four theories:
- During the very low flow states of CPR, CO2 elimination is determined mainly by tissue perfusion rather than by alveolar ventilation.
- SB administration will result in excessive carbon dioxide production, which cannot be eliminated effectively and will accumulate in the tissues.
- CO2 penetrates cellular membranes more rapidly than bicarbonate ions, and it will accumulate intracellularly and paradoxically aggravate intracellular acidosis by enhancing its hypercarbic component.
- Intracellular (myocardial) hypercarbic acidosis is detrimental, and therefore SB administration might worsen CPR outcomes
By 1986, guidelines started to waver on SB’s use and no longer recommended SB but instead left it to “the discretion of the team leader.”
The Evidence
Let’s look at the evidence from four fairly recent articles that discuss SB’s use in cardiac arrest. The conclusions are borrowed with permission from the Washington University Emergency Medicine Journal Club.
Vukmir RB, Katz L; Sodium Bicarbonate Study Group. Sodium bicarbonate improves outcomes in prolonged prehospital cardiac arrest. Am J Emerg Med. 2006 Mar;24(2):156-61.
Bottom Line: This prospective, randomized controlled trial conducted in Western Pennsylvania found no difference in survival rates to ED admission between groups given sodium bicarbonate and placebo early in the EMS course (relative risk 0.99; 95% CI 0.70 to 1.40. While there was a trend toward improved survival in those patients with prolonged cardiac arrest (> 15 minutes), this did not achieve statistical significance.
Kim J, Kim K, Park J, Jo YH, Lee JH, Hwang JE, Ha C, Ko YS, Jung E. Sodium bicarbonate administration during ongoing resuscitation is associated with increased return of spontaneous circulation. Am J Emerg Med. 2016 Feb;34(2):225-9
Bottom Line: This retrospective, observational, case-control study found an independent association between bicarbonate administration and ROSC within 20 minutes of ED arrival, with an OR of 2.49 (95% CI 1.33 to 4.65). Despite the use of multivariable logistic regression to attempt to balance groups, this study is at high risk of selection bias. Additionally, the outcome measured is not patient-centered, and does not necessarily correlate with more important long-term outcomes that included neurologic function.
Kawano T, Grunau B, Scheuermeyer FX, et al. Prehospital sodium
bicarbonate use could worsen long term survival with favorable neurological
recovery among patients with out-of-hospital cardiac arrest. Resuscitation. 2017 Oct;119:63-69.
Bottom Line: This retrospective review of data collected in a prospective registry found no difference in survival to hospital discharge or discharge with a favorable neurologic outcome among patients who received sodium bicarbonate for OHCA and those who did not receive sodium bicarbonate. When looking at patients with prolonged cardiac arrest (> 22.6 minutes), patients receiving sodium bicarbonate were less likely to survive with good neurologic outcome (AOR 0.33, 95% CI 0.16-0.66).
Bottom Line: This small, pilot study found that the administration of sodium bicarbonate in prolonged OHCA without ROSC after 10 minutes of CPR in the ED was associated with a small (but statistically significant) rise in pH and bicarbonate compared to placebo, but was not associated with any improvement in survival to hospital admission or survival with good neurologic function at 1 or 6 months. Further large trials will be needed to confirm these results.
What about for the suspected hyperkalemia patient? In a paper entitled Treatment of Severe Hyperkalemia: Confronting 4 Fallacies, the author states, ”Sodium bicarbonate fails to lower serum potassium acutely and has no role in the emergent treatment of hyperkalemia.” The author goes on to cite a paper that says, “In 10 cases, 50 mEq (SB) given over 15 minutes produced a 0.5mmol/l (K) drop at 30 minutes.”
I was not able to find a paper that looked specifically at giving SB as a single agent for a hyperkalemic arrest. If you suspect hyperkalemia, your best bet would be providing calcium chloride as well as insulin/glucose.
The Debrief
- There is no definitive evidence that SB works to improve outcomes in cardiac arrest
- If a TCA overdose is suspected, then SB should be administered
- Another potential harm of SB administration is it adds a cognitive load to the team leader, distracting them from interventions that could improve survival.
Indicated in TCA OD, but what about other presentations with metabolic acidosis? DKA? Uremia?
Thanks!