So I was in the ED a few days ago as overheard a conversation between one of the staff internists and a resident, and how they were planning to correct a lactic acidosis using some bicarb. I cringed under the surface, because the attending was explaining how this would buffer the acidosis, and the resident was nodding. The attending then turned to me and asked me how much I would give in this case.
I had a moment of hesitation because it was a particularly busy day and I hadn’t planned on an impromptu teaching session which I knew would have to happen if I opened my mouth. On the other hand my…academic principles (? – or something like that) wouldn’t allow me to agree…
“I wouldn’t give any at all.”
So I’ll spare you the play by play, but here is the gist of it.
Rewind first to 2001’s SCCM in San Diego and a talk by Dr. John Kellum about acid-base, and my introduction to the Stewart or physicochemical approach to acid base. Somewhere in that hour was one of my few genuine lightbulb moments in medicine, and a sinking realization that a lot of stuff I’d been thought wasn’t really so.
Here’s a simple equation we all know:
CO2 + H20 <-> H2CO3 <-> H+ + HCO3- this is mediated by carbonic anhydrase.
1. we have a LOT of CO2
2. we have a LOT of H2O
3. carbonic anhydrase is pretty ubiquitous…
thus…we have an (almost) endless supply of “bicarb.” What????
Yup. I’m not particularly bright nor a chemist, and although I did read Peter Stewart’s original paper, much of it was over my head. However smarter docs have distilled the principles (http://www.anaesthetist.com/icu/elec/ionz/Findex.htm) to make it palatable to the clinician. It does seem to make a lot of sense, and explains many clinical scenarios which didn’t seem to make physiological sense. In addition, the slow and steady growth of literature using the strong ion difference rather than traditional acid base theories is encouraging.
Most of all, being involved in education, I have had the privilege of exchanging ideas with some really bright people, and all the ones who are particularly physiological have changed their acid base understanding to the Stewart approach.
So, in super-summary, this approach tells us that the only role of HCO3 is to maintain electroneutrality, which is primarily filling the gap between sodium and chloride. Depending on what happens to sodium, chloride, or if there is another anion, HCO3 will either increase or decrease, mediated by carbonic anhydrase. We make as much or as little HCO3 depending on our needs. It is a dependant variable, and has no active role.
In fact, when we are administering “bicarb,” what we are really giving is sodium without chloride, thus increasing our strong ion difference. We can give sodium acetate or citrate and the bicarb will increase just the same – filling the gap.
So what does this mean clinically?
Well, first of all it is important to understand what we are doing if deciding to administer NaHCO3: attempting to change the pH (note that I’m not saying improve, because in varying scenarios, I’m not sure which pH is better…).
One of the common and sometimes almost subconscious beliefs is that bicarb “buffers” acids in a sense of neutralizing them. This is only true in the sense of electroneutrality, and not in a biological sense. The more important thing to realize is that none of these acids are directly “toxic” and require “buffering”… Lactic acid isn’t toxic, it’s cellular fuel. Its the process behind it that can be and that sometimes needs to be excised!
So the question then becomes when is it truly important to increase the pH? When is there actual benefit? I won’t argue that at some levels (<7) I get chicken too, and feel like giving some solo sodium (more commonly known as bicarb). But I think it is pretty clear (permissive hypercapnia data) that pH in the range of 7.20-7.35 is innocuous. How about 7.10-7.20? Or 7.00 to 7.10? I don’t know. But I do know that my DKA patients (6.85-7.20) are definitely not in cardiovascular collapse. Just a little tired from the Kussmauling…
So what am I doing with the NaHCO3? Is increasing pH beneficial to my patient? Certainly to the one who is arresting from hyperkalemia it is, to shift the K a little, but what about my septic patient?
Well, in giving NaHCO3, I am increasing my CO2 load (equation vide supra), which my respiratory system now has to get rid of, else I am worsening my intracellular acidosis (CO2 diffuses freely). I am also interfering with the adaptive response of the hemoglobin dissociation curve and impeding the right shift (below) which helps deliver more oxygen…hmm…and aren’t most of these patients to whom we consider giving “bicarb” having some degree or other of tissue hypoxia…? hmmm… what was the benefit again?
Scott Weingart (emcrit.org) also gives a great podcast about his use of NaHCO3, especially the means (bolus vs infusion) and indications.
Personally, I think it’s reasonable to use in a mixed infusion when facing hyperchloremic acidosis, usually post-resuscitation due to overzealous use of NaCl, but never really in “treatment” of acute metabolic acidosis (especially not with the theory of “buffering”), and it is important to remember what we are trying to do, to what end and possibly at what price.
Now I know some people really, really disagree with this, so please let me know your (physiological) thoughts!