Bicarbonate for Respiratory Acidosis: Not So Fast

We all like to make the numbers pretty in our critically ill patient. Euboxic is a term that is thrown out there. It’s like there’s a check box in our brains that we need to fill in when turning a lab value back to the default color rather than red in our EMR. But one of those that we should potentially let ride is to provide sodium bicarbonate to patients whose acidosis is driven by an elevated CO2. In other words, providing bicarbonate for a respiratory acidosis.

I must be fully transparent and admit that I use sodium bicarbonate more often than the average clinician. Jaber et al. published a study that showed benefit of providing bicarbonate therapy for patients who had a metabolic acidosis, primarily lactate driven. This study was covered in this post on lactate/lactic acid. The scope of this post, however, is respiratory acidosis and not metabolic acidosis. Also putting it out there that the data is not at all robust. Better yet, it is nonexistent and this is by no means medical advice.

Cite this post as: Eddy J. Gutierrez, “Bicarbonate for Respiratory Acidosis: Not So Fast”, eddyjoemd blog, December 4, 2021. Available at:

Why do patients develop a respiratory acidosis?

This is overly simplified. That’s your disclaimer. But we breathe in oxygen and breathe out carbon dioxide. This is amongst other things but you get the point. Respiratory acidosis is too much carbon dioxide in the bloodstream to be able to breathe out so it stays in your circulation. Generally speaking, the normal CO2 levels on an arterial blood gas are 35-45. Some people who have COPD, OSA, OHS, and other ventilation-impairing diseases may live with CO2 levels that are higher than this. These patients usually have a compensation increase in their serum bicarbonate. I covered how we obtain those numbers in THIS POST. But of course you’re not going to cite this on your dissertation at Yale.

Too much CO2 production or not enough ventilation

If your patient has an elevated arterial CO2, aka PaCO2, that means that either they are producing too much CO2 or they can’t get rid of it. Humans do not like for the CO2 levels to get too high so we’ve developed brainstem chemoreceptors to notice when the level is too high. In turn, we breathe a little faster and/or a little deeper to blow off that extra CO2. Minute ventilation is normally 5-8L/min. One could calculate minute ventilation by multiplying respiratory rate by tidal volume. If you sent a somnolent OSA/OHS patient on BiPAP, for example, and notice that their minute ventilation on the screen is just 4, it’s time to crank up the pressures and/or respiratory rate.

Additional differential diagnoses for respiratory acidosis

Other causes for an increased PaCO2 that are include acute processes that damage the actual alveoli impeding ventilation. Many of us have seen the in COVID. We could also see this in other illnesses that cause ARDS but also in some patients with pulmonary edema, diffuse alveolar hemorrhage, etc. This list could get extensive. It’s always fun to see the patient who is clearly volume overloaded, with wheezing and retaining CO2 be called a COPD exacerbation. I’ll personally treat that “COPD exacerbation” with a slug of furosemide and some non-invasive ventilation (NIV) until we dry out their lungs.

Do we sometimes cause a respiratory acidosis ourselves?

Sometimes, in an iatrogenic nature, we deeply sedate or paralyze patients on the ventilator prohibiting them from being able to compensate themselves via these brainstem chemoreceptors. As an aside, I do not check daily ABGs on my patients who are on mechanical ventilation because, since I typically do not snow them, I allow them to breathe over the vent and compensate themselves. If they’re just riding the vent, fully awake, with no spontaneous breathing, then chances are I am over-ventilating them. If you put that person on pressure support, you can count on them going apneic. They will just look at you while you’re yelling at them to breathe. Their brainstem chemoreceptors are like meh. Any of these can cause an increase in the PaCO2 and therefore a respiratory acidosis if not properly compensated for. This in turn will cause a decrease in pH.

Respiratory Acidosis may be good for our patients!

This whole question of providing bicarbonate for respiratory acidosis has been on my mind for decades but I had never quite found a good answer. There’s a good reason for this. It’s because there are zero clinical trials looking at it. But before we try to make the numbers pretty, we must understand that the respiratory acidosis that we are seeing in our patients may actually be good for them!

Chand et al. published a paper that was the final motivating factor for me to create this post. Unfortunately, it is not free for you to download. They explained the pathophysiology of the benefits in a much better form that I ever can. To make it easy, they explained the following potential benefits of a respiratory acidosis:

  • improve oxygenation via the Bohr effect
  • increase cardiac output by catecholamine mediated increases in venous return and end-systolic volume as well as myocardial contractility
  • decrease in left-ventricular afterload
    • although this can go too far when the pH drops a bit too much
  • causes microvascular vasodilation: this increases oxygen delivery and tissue perfusion
  • improves alveolar ventilation-perfusion

But there could be too much of a good thing.

Excessive PaCO2 causes tissue acidosis that could impair tissue perfusion. We could also see CO2 narcosis in those who aren’t adapted to having elevated PaCO2 levels. Don’t forget that if the patient is on catecholamine-based vasopressors, these will not work very well in patients with an acidosis. I’ll dig into this more at a later date. If it gets too high then we’re stuck looking for an exit strategy.

So if you have an acid which is problematic, then why not add a base?

It seems like a no brainer to go ahead and add bicarbonate when the respiratory acidosis becomes a problem. Baby Doctor Eddy used to think this would make sense, especially in lieu of evidence suggesting the contrary. But now that Baby Doctor Eddy has had more time to take deep dives into these concepts, it’s easier to understand why the easy solution isn’t the solution at all.

When we give bicarbonate our best intention is to make the acidic intracellular and extracellular spaces non-acidic. The problem with this, which is better explained in other sources so I will not break down the organic chemistry reaction, is that sodium bicarbonate (NaHCO3), when metabolized ends up producing molecules of CO2. So if your initial problem was that you had too much CO2 because one cannot ventilate the patient, then adding more CO2 to the mix doesn’t seem like the brightest of ideas.

What is your exit strategy for your patient?

If one has the ability to adjust the settings on the ventilator to compensate for this increased CO2 in serum, then it may not be such a big deal. But if they reason why you’re pushing amps of bicarbonate to get the hemodynamics stable enough to switch the patient to a transport ventilator to attempt to get them to an ECMO center, then you may have waited a bit too long to make the call to get them out of your shop.

Chand et al. commented on how bicarbonate therapy can help in patients who have a respiratory acidosis from severe asthma exacerbations or COPD exacerbations. The thought process there is that the acidosis in those patients actually increases the bronchoconstriction. In addition, I suspect that those patients also have a metabolic acidosis that forms due to their acute, extreme work of breathing. A sprinkle of bicarbonate may help out there.

What should we be doing if the patient has a respiratory acidosis and we won’t use bicarbonate?

Team, here is where we need to step up our mechanical ventilation game and have a low threshold to call for ECMO. Every institution has their preferred mode of mechanical ventilation that is their “set it and forget it mode”. I have worked at several institutions and it has been hilariously different with each one convinced that their mode is the best. If COVID has taught us one thing, it’s to learn to be a bit more flexible. I can honestly admit that I had never spent as much time tinkering in front of the ventilator with my respiratory therapist friends to try to improve oxygenation and ventilation in these patients. They are challenging. There’s no doubt about that.

Call for an escalation of care if you cannot correct the respiratory acidosis

If despite all the best tricks one has up their sleeves: paralytics, proning, APRV, oscillators, and other strategies, if you’re thinking about using bicarbonate but have not called for an ECMO evaluation, chances are you’ve waited too long to make that call. For those of us who do not have ECMO in-house, remember that the transport ventilators are not as potent (for lack of a better term) that the ones we have in our unit. Not to mention that moving these patients or even disconnecting them from one ventilator circuit to place them on another ventilator circuit could be deadly. This is particularly true if there’s no wiggle room for the slightest human variable that could throw a wrench in it all.

If your patient is not an ECMO candidate or beds are not available, try what you need to try. But informing the family of the fact that there’s no evidence to support what you are trying to do to save their loved one is necessary. Transparency is the key here. After all, there’s no definitive trial nor in vivo data about all this. It’s all theoretical.

Citations looking at Bicarbonate for Respiratory Acidosis

Jaber S, Paugam C, Futier E, Lefrant JY, Lasocki S, Lescot T, Pottecher J, Demoule A, Ferrandière M, Asehnoune K, Dellamonica J, Velly L, Abback PS, de Jong A, Brunot V, Belafia F, Roquilly A, Chanques G, Muller L, Constantin JM, Bertet H, Klouche K, Molinari N, Jung B; BICAR-ICU Study Group. Sodium bicarbonate therapy for patients with severe metabolic acidaemia in the intensive care unit (BICAR-ICU): a multicentre, open-label, randomised controlled, phase 3 trial. Lancet. 2018 Jul 7;392(10141):31-40. doi: 10.1016/S0140-6736(18)31080-8. Epub 2018 Jun 14. Erratum in: Lancet. 2018 Dec 8;392(10163):2440. PMID: 29910040.
Link to Article

Chand R, Swenson ER, Goldfarb DS. Sodium bicarbonate therapy for acute respiratory acidosis. Curr Opin Nephrol Hypertens. 2021 Mar 1;30(2):223-230. doi: 10.1097/MNH.0000000000000687. PMID: 33395037.
Link to Article (NOT FREE)

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