In this episode, I’ll discuss the alternatives to sodium bicarbonate given the current drug shortage.
This isn’t the first time we’ve had to deal with a sodium bicarbonate shortage. Back in 2012 there was also a bicarb shortage…but this time it is more complicated. The two alternatives to sodium bicarbonate – sodium acetate and THAM are in short supply and discontinued, respectively.
I reviewed the use of sodium bicarbonate in critical care in episode 138.
The good news is that actual legitimate uses of sodium bicarbonate in critical care are few and far between.
The bad news is that sodium bicarbonate is frequently given in circumstances where it has no to little effect.
The habit of using sodium bicarb for cardiac arrest, DKA, contrast-induced nephropathy, rhabdomyolysis, hyperkalemia, or respiratory acidosis can be difficult to break. But the possibility of not having any sodium bicarb available when it is actually needed might be enough to change practice.
Perhaps the toughest practice to change is giving sodium bicarbonate in the setting of cardiac arrest. A review of literature and ACLS guidelines concluded:
Although many studies have shown little/no benefit and perhaps harm from administration of sodium bicarbonate (SB) for rapid correction of acidemia accompanying cardiac arrest, and the latest ACLS guidelines published by the AHA do not recommend routine administration, SB is still used as part of resuscitation in cardiac arrest. Additional research is needed to elucidate further the effects of SB on organ function, on the likelihood of ROSC and on survival in patients resuscitated from cardiac arrest. An objective reappraisal of the use of SB or other buffer agents and perhaps on an appropriate “therapeutic window” for use of SB in cardiac arrest patients is warranted.
When sodium bicarb is not available, sodium acetate can be given instead. 1 mEq sodium acetate can be used to replace 1 mEq sodium bicarbonate. However, sodium acetate needs to be given slowly – over 15 to 20 minutes – to avoid the risk of hypotension and cardiac instability. The slow rate of infusion limits the usefulness of sodium acetate in critical scenarios such as cardiac arrhythmias or toxicologic emergencies.
In order to get through this period of shortage, conserve sodium bicarb by seeking alternatives for the following conditions:
Metabolic, respiratory, or diabetic acidosis; treat the underlying cause.
Rhabdomyolysis; use normal saline instead.
Hyperkalemia; use calcium gluconate or chloride to stabilize myocardium, insulin+dextrose to hide potassium from the heart, then remove excess potassium from the body.
Prevention of contrast-induced nephropathy; use normal saline instead.
Cardiac arrest; follow ACLS protocols instead.
Reserve sodium bicarbonate and sodium acetate supplies for tricyclic, aspirin, methotrexate, and phenobarbital toxicity.
If you are completely out of sodium bicarb and sodium acetate, consider the following alternatives for drug toxicity:
Cardiac arrhythmias from tricyclic toxicity: Use Hypertonic saline. 1 mL of 8.4% sodium bicarb contains the same amount of sodium as about 2 mL of 3% saline. Use 3% NaCl 2-4 mL/kg per dose, giving approximately 1-2mEq of sodium per kg.
Methotrexate or phenobarbital toxicity: Consider acetazolamide, 500 mg every 6 hours followed by enteral sodium bicarbonate.
Quinidine-induced torsades: No other treatment will alkalize the serum quickly beside sodium bicarb/acetate. Use other treatments for torsades such as magnesium and electricity.
If you like this post, check out my book – A Pharmacist’s Guide to Inpatient Medical Emergencies: How to respond to code blue, rapid response calls, and other medical emergencies.
Joe,
Another Great podcast.
When you bring up using 3% sodium chloride for TCA toxiticy, via what route are you administering this? The current hospital I am working at is working on a policy for 3% to determine routes it can be administered. Previous hospitals I’ve worked at only allow administration via a Central line, but in the ED, typically we aren’t going to have that option. Do you happen to have a recommended bore size that tends to be safe?
Thanks
Thank you!
My motto is:
If you do not have immediate central line or IO access, then I would use the smallest bore in the largest vein possible.
Hi. Really enjoying your podcasts. Are you able to attach references to the info you supply in the podcasts?
Thanks!
Thanks Breanne! Most references are linked within the show notes. Links appear in red like this. A few statements in this episode are supported by references in episode 138.
Dear Pharmacy Joe,
Thank you for your podcasts. I really enjoy them. I have hesitation with using acetazolamide with salicylate poisoning based on the reference below:
http://pediatrics.aappublications.org/content/pediatrics/47/4/658.full.pdf
In brief, the authors investigated acetazolamide use in salicylate-poisoned rats. Acetazolamide use was associated with lower serum pH, higher tissue concentrations and increased toxicity.
If in the clinical situation of no sodium bicarbonate, I would lean towards no treatment vs. treatment with acetazolamide in a salicylate-poisoned patient.
Thanks again for your podcasts.
That is a great point, I’ve edited the post to remove aspirin from that section. Thank you!
Agree with everything but… likely there’s a benefit to an infusion of sodium bicarb with metabolic acidosis (previously reviewed HyperK mgmt. with NaBicarb discussion — https://emcrit.org/pulmcrit/management-of-severe-hyperkalemia-in-the-post-kayexalate-era/) — certain circumstance but wouldn’t promote ‘no use’ as there’s some evidence.
Thank you for the comment!
Here’s my take on bicarb in the setting of hyperkalemia+metabolic acidosis from episode 34:
In the setting of a shortage, I’d rather reserve bicarb for other uses.
Great stuff, thank you! My question is, when forced to use sodium acetate for DKA patients (provider insists), what are your recommendations for dilution, volume, and rate of administration? Thank you!