so, outside of crash carts, we're down to <20 50mEq amps of bicarb.

Apparently there was a TCA overdose over the weekend.

We've been converting bicarb gtt's to sodium acetate on a mEq:mEq basis for other patients.

Any experience using acetate pushes in place of bicarb?

There's also the hypertonic saline +/- hyperventilation idea.

so, outside of crash carts, we're down to <20 50mEq amps of bicarb.

Apparently there was a TCA overdose over the weekend.

We've been converting bicarb gtt's to sodium acetate on a mEq:mEq basis for other patients.

Any experience using acetate pushes in place of bicarb?

There's also the hypertonic saline +/- hyperventilation idea.

We're due to be in that boat shortly. Already have specific blood pH requirements out for allowing IV push outside of a code situation or drips - they have not been well-accepted at all. Lots of notes left blaming any negative outcomes on specific pharmacists (no negative outcomes so far). Our HD MTX patients aren't helping things either.

I'd be very interested in the acetate push - I always thought there was some reason it couldn't be done (might just be the gestalt with acetate). We're also pushing LR on everyone, I feel like people outside of OB and trauma completely forget that it exists.

Our pharmacy is getting compounded bicarb for limited applications like this. Frankly, sodium acetate should work just as well as bicarb. I would actually prefer to use a mixed sodium acetate/chloride solution for resuscitation of most patients.

You can also try glucagon pushes and theory says that lidocaine may help as well. Case reports using intralipid for TCAs are also very interesting however there was a recent animal study that yielded suboptimal results.

There's also the high-dose insulin case report.

We had that discussion here... consensus was to do either NaAc or 3%. NaAc would theoretically be better, but 3% more easily obtained.

Personally, while lidocaine would theoretically work, it trades one poison for another, and if I had no other option, I'd go for it. Same for lipids. The HIE report was interesting, but probably more effect as a general cardiac support method than a true antidote.

Personally, I'm still trying to figure out how to microfilter Arm & Hammer. d=)

-d

I think physicians overuse bicarb. There is minimal to none evidence supporting the use of bicarb (or any buffer) in lactic acidosis or DKA. One could argue that bicarb worsens intracellular acidosis. And bicarb was taken off the ACLS algorithm years ago due to ineffectiveness or even worsening outcomes (increases CO2 after dissociation). I would only use it in a code if I suspected hyperkalemia.

Critical Care 2004, 8:259-265

I think physicians overuse bicarb. There is minimal to none evidence supporting the use of bicarb (or any buffer) in lactic acidosis or DKA. One could argue that bicarb worsens intracellular acidosis. And bicarb was taken off the ACLS algorithm years ago due to ineffectiveness or even worsening outcomes (increases CO2 after dissociation). I would only use it in a code if I suspected hyperkalemia.

Critical Care 2004, 8:259-265

http://pediatrics.aappublications.org/content/122/4/831.abstract

"Common clinical practices often are unsupported by experimental evidence. One example is the administration of sodium bicarbonate to neonates. Despite a long history of widespread use, objective evidence that administration of sodium bicarbonate improves outcomes for patients in cardiopulmonary arrest or with metabolic acidosis is lacking. Indeed, there is evidence that this therapy is detrimental. This review examines the history of sodium bicarbonate use in neonatology and the evidence that refutes the clinical practice of administering sodium bicarbonate during cardiopulmonary resuscitation or to treat metabolic acidosis in the NICU."

http://pediatrics.aappublications.org/content/122/4/831.abstract

"Common clinical practices often are unsupported by experimental evidence. One example is the administration of sodium bicarbonate to neonates. Despite a long history of widespread use, objective evidence that administration of sodium bicarbonate improves outcomes for patients in cardiopulmonary arrest or with metabolic acidosis is lacking. Indeed, there is evidence that this therapy is detrimental. This review examines the history of sodium bicarbonate use in neonatology and the evidence that refutes the clinical practice of administering sodium bicarbonate during cardiopulmonary resuscitation or to treat metabolic acidosis in the NICU."

Thanks - I wasn't aware of the neonatal angle as I only work in adult units.

As others mentioned above, sodium acetate is a nice alternative to sodium bicarb. If I do feel the need to use a buffer (RTA, or hyperchloremic acidoses), I will go for bicarb first.

As others mentioned above, sodium acetate is a nice alternative to sodium bicarb. If I do feel the need to use a buffer (RTA, or hyperchloremic acidoses), I will go for bicarb first.

Note that acetate (Na and K), which we use in neonatal TPN due to renal bicarb wasting has also been intermittently on backorder over the last year or so. Right now it's not as critically short as Na bicarb, but there's no guarantee we won't have another critical acetate shortage in the future.

Note that acetate (Na and K), which we use in neonatal TPN due to renal bicarb wasting has also been intermittently on backorder over the last year or so. Right now it's not as critically short as Na bicarb, but there's no guarantee we won't have another critical acetate shortage in the future.

..great

...and first experience using it as a push today (for hyperkalemia :rolleyes: )

Package insert says to dilute, but gives no further instructions, so went 1:1 with D5W to make 1mEq/mL.

I hung around because I was curious and RN pushed it like she normally would bicarb in this situation. Patient specifically told us it did not burn (but whined about the D50). About 2 minutes later he turned bright red - looked just like a Niacin flush - and complained of feeling hot through his face/neck/chest. No hypotension or tachycardia. Right then he went up to the floor and I checked on him 10 minutes later and it was resolving, they did give him some IV Benadryl when he got upstairs.

Quick lit search reveals that in large doses (back when it was used as the major fluid in HD baths) it causes vasodilation and potential hemodynamic instability.

...and first experience using it as a push today (for hyperkalemia :rolleyes: )

Why does bicarb for hyperK+ engender rolleyes?

Why does bicarb for hyperK+ engender rolleyes?

if there aren't EKG changes and the patient is 28 and dehydrated from vomiting for the last couple days and he's already getting D50/insulin I'm not sure what more we're getting from the bicarb.

When the bicarb shortage discussion was first starting I discussed this with our nephrologists who admitted that bicarb for hyper-K isn't as efficacious as the insulin/glucose, and felt it is done more as a gesture to show the value was addressed rather than efficiently shifting K+ intracellularly.

I think physicians overuse bicarb. There is minimal to none evidence supporting the use of bicarb (or any buffer) in lactic acidosis or DKA. One could argue that bicarb worsens intracellular acidosis. And bicarb was taken off the ACLS algorithm years ago due to ineffectiveness or even worsening outcomes (increases CO2 after dissociation). I would only use it in a code if I suspected hyperkalemia.

Critical Care 2004, 8:259-265

I would hope most of us aren't still using it for those two conditions.
However, for sodium channel problems it still is pretty easy to get a hold of compared to 3% or the mythical sodium acetate.

if there aren't EKG changes and the patient is 28 and dehydrated from vomiting for the last couple days and he's already getting D50/insulin I'm not sure what more we're getting from the bicarb.

When the bicarb shortage discussion was first starting I discussed this with our nephrologists who admitted that bicarb for hyper-K isn't as efficacious as the insulin/glucose, and felt it is done more as a gesture to show the value was addressed rather than efficiently shifting K+ intracellularly.

So it doesn't work as well, or doesn't work at all? In either case, it's still just moving it around.

So it doesn't work as well, or doesn't work at all? In either case, it's still just moving it around.


It works, just not as well as insulin+glucose. But, the only study I've seen that proved that was specifically in renal failure +acidosis+ Hyper K. (Blumberg A, in Am J Med 1988).

Also Bicarb binds calcium, so you don't want to push it after calcium if do have a wide QRS.

It works, just not as well as insulin+glucose. But, the only study I've seen that proved that was specifically in renal failure +acidosis+ Hyper K. (Blumberg A, in Am J Med 1988).

Also Bicarb binds calcium, so you don't want to push it after calcium if do have a wide QRS.

They're additive, though - not competitive. To make it sound like it's one or the other, but you can't do both, is not correct.

The kidney docs that I know tell me that bicarb has no more effect on serum potassium than an equal amount of normal saline. So, if it does have an effect it is just from the fluid load.

Plus with bicarb you are giving them a Co2 load etc etc.

Here is a good general hyperK review that draws the same conclusion.

http://www.thecochranelibrary.com/userfiles/ccoch/file/CD003235.pdf

The kidney docs that I know tell me that bicarb has no more effect on serum potassium than an equal amount of normal saline. So, if it does have an affect it is just from the fluid load.

Plus with bicarb you are giving them a Co2 load etc etc.

Here is a good general hyperK review that suggest the same conclusion.

http://www.thecochranelibrary.com/userfiles/ccoch/file/CD003235.pdf

I drew a different conclusion than you from the same material. Bicarb is equivocal, and not recommended as monotherapy. However, in conjunction with everything else, I am not going to necessarily withhold it. It's not my first choice, but it's not in the trash. And, as CYA has been ingrained, with my luck, another hyper-K pt that has an untoward event will sue and their attorney will cite Ngugi 1997 - the study that did show bicarb decreasing (temporarily, as most of the interventions do).

The concern for the increased CO2 load is noted, although I don't know that I've ever seen an alkalotic hyperkalemic (although I am not claiming the "fallacy of anecdote" - "I've never seen it, so I don't believe it"). Likewise, the HCO3 <==> CO2 conversion is nearly instantaneous, and a breathing patient can blow off the excess (or it can be ventilated out).

I agree. I would note that 7.1 and below is where bicarb becomes an effective buffer. Above 7.1 it is just a CO2 load.

And a bump
http://emcrit.org/podcasts/enough-with-the-bicarb-already/

Enough with the Ca++, too.

I've never given HCO3 for hyperK – either they're ESRD and the sodium load will worsen the pulmonary edema or they're dehydrated and they really just need resuscitation. I don't do anything more aggressive than insulin/D50/albuterol for folks without significant EKG changes (e.g., more than just peaked T waves).

Forgive me if this has already been discussed, but I'm sleep deprived from the newborn baby. :)

I think there is a role for bicarb in hyperkalemia. The alkalosis causes potassium to shift intracellularly, but it's only temporary (10-20 minutes duration if I remember correctly). If someone has research to suggest otherwise, please post it.