Sodium bicarbonate, Serum Sodium and TCA overdose

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Paseo Del Norte

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I was curious if any body had additional information or knew of good sources that looked at possible mechanisms for why the serum Sodium does not seem to significantly change in at least some patients who are given Sodium bicarbonate (Sodium load) to treat TCA toxicity.

I saw this discussed via emcrit:

http://www.blubrry.com/emcrit/1758033/podcast-98-cyclic-tricyclic-antidepressant-overdose/

A small study shows this apparently does occur in other patients:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3544084/

I've read through the relevant chapters in Goldfrank's and this was not specifically addressed.

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I was curious if any body had additional information or knew of good sources that looked at possible mechanisms for why the serum Sodium does not seem to significantly change in at least some patients who are given Sodium bicarbonate (Sodium load) to treat TCA toxicity.

I saw this discussed via emcrit:

http://www.blubrry.com/emcrit/1758033/podcast-98-cyclic-tricyclic-antidepressant-overdose/

A small study shows this apparently does occur in other patients:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3544084/

I've read through the relevant chapters in Goldfrank's and this was not specifically addressed.

First, I'm not sure if the underlying mechanism really matters, as what's truly important is that we can treat TCA overdoses with NaHCO3 boluses and not worry too much about causing hypernatremia, as opposed to using 3% (which has been done per the literature, but scares me). As sometimes you need a *lot* of amps of this stuff, not having to concern myself for the most part with the effects on the serum Na+ concentration makes me happy. d=)

As a knowlege exercise, however, I'm willing to posit this:
1) Na homeostasis occurs in the kidney - typically filtered out in Henle then reabsorbed throughout.
2) Most reabsorption comes from a NaCl symporter or a Na-K-Cl symporter; however, you're giving NaHCO3 not NaCl so there is a molar incongruity that does not allow the filtered Na to renter the body as you cannot use these proteins without having all the relevant molecules locked into the transport sites. This would seem to be supported by the elevation in serum Na+ when using hypertonic saline, as there is an equimolar amount of Na+ and Cl- in 3%.
3) Furthermore, there is a Na-H antiporter that exists to maintain serum pH; when giving a bicarb load, the kidney will preferentially reabsorb H+ ions to buffer it, at the expense of Na+ ions, to maintain electroneutrality.

Overall, it is possible that the net serum gain of Na+ with NaHCO3 is offset by renal excretion and inability to reabsorb. However, I'm not a nephrologist and I'm not exactly sure. It makes sense from a physiologic standpoint, though, to me.

Cheers!
-d
 
Absolutely, I agree that the mechanism in this case does not change the fact that Sodium bicarbonate can effectively treat TCA toxicity. I agree that my question is more "academic" in the sense that it is simply something I have been thinking about but I do not believe the answer if every found would change the bigger picture.

Thank you for the reply and thank you for your thoughts, they are much appreciated.
 
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