Podcast 96 – Acid Base in the Critically Ill – Part V – Enough with the Bicarb Already


This is Part V of the EMCrit Acid-Base Talks. If you haven’t listened to the initial series, you may be better off starting there:

Acid-Base Sheet

EMCrit Acid-Base Sheet

Today’s topic comes from a debate I have been having with Steve Smith of the amazing EKG Blog. The main thrust of the debate started with this question…

Does Bicarb Fix pH if You Can’t Increase Minute Ventilation?


When you can adjust PaCO2 to maintain a certain value (i.e. you increase minute ventilation), bicarb will raise pH as evidenced by this animal study (Crit Care Med 1996; 24:827-834). However, if you can’t blow off the CO2 then the effects on pH will not be there (J Pediatr 1977;91(2):287).

In this study, NaBicarb did not correct the pH, while CarbiCarb did (Carbicarb: an effective substitute for NaHCO3 for the treatment of acidosis. (Surgery 102:835–839).

This review article recommends against bicarb for permissive hypercapnia (Intensive Care Med (2004) 30:347–356).

This study furthers the idea that NaBicarb is not all that great in closed systems (J Pediatr 1972;80(4):671) and then this discussion explores all of the biochemical reasons why administering bicarbonate as a rapid push in a closed system is a bad idea (J Pediatr. 1972 Apr;80(4):681-2.).

Here is a quote from another review article (Anesthesiology 1990;72(6):1064):

The key concept in the equation [above] is that pH is not related to the absolute value of either bicarbonate concentration nor PCo2, but rather to their ratio.
When exogenous bicarbonate is administered during acidemia, bicarbonate reacts with hydrogen ions to form carbonic acid. Physicochemical equilibrium is shifted, favoring dissociation of carbonic acid to C02 and water. C02 partial pressure increases. The degree of alkaliniza- tion resulting from increased [HC03“] is limited by the rise in Pco2* In (open) systems where increases in PCo2 are prevented (by ventilation) alkalination occurs. When CO2 cannot be eliminated, the pH of the system is only minimally changed. Ostrea and Odel demonstrated in vitro that when isotonic sodium bicarbonate was added to whole blood in a (closed) system where generated C02 could not escape, PCo2 increased and pH was unchanged. Only when C02 was eliminated was the system alkalinized. Similarly, Steichen and Kleinman noted in hypoxic acidotic dogs that administration of 2 mEq/kg of sodium bicarbonate over 3 min when ventilation was unchanged resulted in no net change in arterial pH, although PaCo2 rose from 46 to 61 mmHg. If C02 elimination cannot keep pace with increased C02 generation, administration of bicarbonate during acidemia produces hypercarbia (respiratory acidosis) with little net improvement in pH.

pH Equation

How about this quote from a strong-ion approach to the use of buffers (Crit Care 2004;8:259):

When ventilation is fixed, however, as commonly occurs in mechanically ventilated patients, the effect of sodium bicarbonate may be to lower arterial pH, as was seen in patients ventilated with a lung protective strategy [in this study-Am J Resp Crit Care Med 2000;161:1149].

Here is Table 4 from the Am J Resp Crit Care Article:


But don’t believe me, let’s get an expert…

John Kellum, MDI got to interview John Kellum, MD, master of all things acid-base in the critically ill. You’ll hear more from him in upcoming episodes; this time I asked him the following questions:

  • Does giving NaBicarb actually do anything to the patient’s pH if the patient can’t increase their minute ventilation to blow off the generated PaCO2? (Closed System)
  • Let’s say you can actually can increase pH with NaBicarb, Is there any clinical advantage to actually doing this in an Anion-Gap Acidosis?
  • How about in a patient that received a ton of NS in the ED, should we switch them to a bicarb drip to get SID back in balance?

Even when you Fix the pH with Bicarb, have you done any good in patients with SIG Acidosis?

Probably not!

Advocates of NaBicarb discuss its salutary effects on hemodynamics. However based on the available evidence, there is no reason to think there is any additional effects above those you would see giving hypertonic saline.

Small head-to-head study of NaBicarb and NS showed deleterious effects of the Bicarb (Am J Med. 1989 Jul;87(1):7-14.)

One of the best reviews is by Forsythe and Schmidt in this article (Chest 2000; 117:260–267). Table 1 demonstrating the intracellular effects is particularly relevant.

The other is by Hindman et al. (Anesthesiology 1990;72(6):1064). Here is a passage from the article:

If you are going to use it, use it by slow infusion while increasing minute ventilation. Boyd et al. agree and say it better than I can (Curr Opin in Crit Care 2008;14:379).

Severe Acidosis in Trauma Patients

Not fantastic evidence, but in this recent trauma paper (J Trauma 2013;74:45) giving bicarb to severely acidotic patients was associated with increased mortality.

Comments and where they Go…

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Here is a bibliography of the Literature Reviewed for this Episode

[1] Arieff AI, Leach, W, Park, R, et al. Systemic effects of NaHCO3 in experimental lactic acidosis in dogs. The American journal of physiology. 1982;242: F586-591.

[2] Bersin RM, Chatterjee, K, Arieff, AI. Metabolic and hemodynamic consequences of sodium bicarbonate administration in patients with heart disease. The American journal of medicine. 1989;87: 7-14.

[3] Boyd JH, Walley, KR. Is there a role for sodium bicarbonate in treating lactic acidosis from shock? Current opinion in critical care. 2008;14: 379-383.

[4] Cuhaci B, Lee, J, Ahmed, Z. Sodium bicarbonate controversy in lactic acidosis. Chest. 2000;118: 882-884.

[5] Dell RB. Acid-base effects of hypertonic sodium bicarbonate solutions: a commentary. The Journal of pediatrics. 1972;80: 681-682.

[6] Forsythe SM, Schmidt, GA. Sodium bicarbonate for the treatment of lactic acidosis. Chest. 2000;117: 260-267.

[7] Gehlbach BK, Schmidt, GA. Bench-to-bedside review: treating acid-base abnormalities in the intensive care unit – the role of buffers. Critical care. 2004;8: 259-265.

[8] Hindman BJ. Sodium bicarbonate in the treatment of subtypes of acute lactic acidosis: physiologic considerations. Anesthesiology. 1990;72: 1064-1076.

[9] Kallet RH, Jasmer, RM, Luce, JM, et al. The treatment of acidosis in acute lung injury with tris-hydroxymethyl aminomethane (THAM). American journal of respiratory and critical care medicine. 2000;161: 1149-1153.

[10] Omron EM, Omron, RM. A physicochemical model of crystalloid infusion on acid-base status. Journal of intensive care medicine. 2010;25: 271-280.

[11] Ostrea EM. The influence of bicarbonate administration on blood pH in a “closed system”: clinical implications. The Journal of pediatrics. 1972;80: 671-680.

[12] Rhee KH, Toro, LO, McDonald, GG, et al. Carbicarb, sodium bicarbonate, and sodium chloride in hypoxic lactic acidosis. Effect on arterial blood gases, lactate concentrations, hemodynamic variables, and myocardial intracellular pH. Chest. 1993;104: 913-918.

[13] Steichen JJ, Kleinman, LI. Studies in acid-base balance. I. Effect of alkali therapy in newborn dogs with mechanically fixed ventilation. The Journal of pediatrics. 1977;91: 287-291.

[14] Wilson RF, Spencer, AR, Tyburski, JG, et al. Bicarbonate therapy in severely acidotic trauma patients increases mortality. The journal of trauma and acute care surgery. 2013;74: 45-50; discussion 50.

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  1. Mathias Tschopp says

    In Podcast 44 you say about Henderson-Hasselbalch: “I find this method to provide no comprehensive explanation for why things are as they are”. But you don’t shy from writing this very same equation on the current podcast as proof that bicarb can’t raise pH when minute ventilation stays the same… Go figure…

    I find this quote from Dorje (http://goo.gl/1QVja) interesting: “One of the interesting questions resulting from Stewart’s approach relates to how sodium bicarbonate corrects the metabolic acidosis. The metabolic acidosis may be corrected not so much by its bicarbonate content but by its sodium content. The increased sodium concentration resulting from bicarbonate therapy corrects the reduced SID toward normal, thereby correcting the acidosis.”

    Anyways, I’ve always wondered why there is debate about an issue that is so easily verifiable at the bedside. All it takes is an intubated patient (take a cardiac surgery patient that has received plenty of normal saline during surgery and has hyperchloremic acidosis), a blood gas sample before and after administration of 100mL of Bicarb 8.4% (in 15 minutes). I’ve never found a situation where the pH (and metabolic acidosis) didn’t improve (at the cost of a few mmHg of raised PaCO2, but the net effect is still in favor of improving the pH), even with the minute ventilation being exactly the same. Easy to reproduce, works every time, pretty safe, if not beneficial to the patient.

    Not EBM, let’s call this Bedside-Experiment-Based Medicine (BEBM).

    • says

      The equation is there because it was mentioned in one of the quotes. If you go by the Stewart approach this is a non-issue. I’m not sure where I used it as proof. The folks that follow Henderson-Hasselbach approach are the main progenitors of bicarb use as they argue, the patient’s bicarb is too low, so it makes sense to replete it. The equation demonstrates the futility of this.

      I’m not sure what the placement of the Dorje quote here is , that is exactly what was stated in the podcast.

      As to the bedside observation, it is easy: either the pt is increasing their own ventilation by spont. ventilations above set rate or the CO2 is going intracellularly, so plasma numbers get better and nothing good is achieved.

      • Mathias Tschopp says

        I totally agree that the benefit to the patient is at best debatable and totally unproven. My disagreement was about the net effect on pH and the need for the patient to vent off the ‘added’ CO2 that comes with bicarb. If you apply the Stewart approach, the argument that the patient must vent the additional CO2 is less of an issue.

        It’s always helpful to remind the advocates of the ‘bicarbonate does nothing good’ theory that they usually don’t think twice when they prescribe renal replacement therapy to a patient with renal failure and severe metabolic acidosis. The way the renal replacement therapy corrects the acidosis is by infusing bicarb (either directly and by giving a lactate solution that will be converted to bicarb), but strangely nobody ever tells the nephrologist not to use bicarb…

        • DocXology says

          Renal failure is usually a mixture of wide AG and normal AG acidosis. The latter is due to actual bicarb loss/depletion and will respond to bicarbonate.

          The approach is simple:
          With all biochemical abnormalities – always address the cause
          For all metabolic acidoses = treat the cause rather than the pH
          If normal AG you can give bicarb.

  2. says

    Hi Scott, in support of your discussion I just finished listening to EMRAP for this month. Please check out the segment on a recent TCA overdose in which the patient was intubated and received 20amps of NaBicarb IVP in the ED in rapid succession. Now in this situation of course the goal is to effectively compete with TCA molecules at the sodium channel receptors in the myocardium, but as an aside it was noted that the pH after 20amps only ended up slightly above 7.5 and this was with large minute ventilation to avoid acidemia from hypercapnea. I’m not sure why this debate continues. I’m thinking too many baking soda and vinegar volcano science projects as children, people just need to let go of the Bicarb for correcting pH….

  3. O C says

    Hi Scott thanks for the great podcasts
    A couple of comments: hyperchloraemic/renal acidosis and lactic acidosis are different conditions but you seemed to be lumping them together in the podcast. (This is from an ICU perspective, Not ED / acute resus)
    I would think its reasonable to approach the former at least with isotonic bicarb as one part of your maintenance fluid thus giving the sodium and volume while creating a more favorable strong ion difference, but without stressing the kidneys with excessive chloride to get rid of. This probably wont help in the lactic acidosis.
    Secondly the emphasis on increasing minute ventilation on vented patients with any bicarb given: Great idea and probably what most of us do, but even if you dont then with each breath the patient will be getting rid of more CO2 than previously so there should be more weak acid loss.
    Keep up the great work Scott and many thanks again from New Zealand

    • says


      You may want to see the previous acid/base podcasts linked above to see that I am not lumping these together at all. This will be further emphasized in next week’s cast as well. Now as to the greater CO2 elimination with each breath as PaCO2 rises–that is very interesting. I’ve always thought of it as directly proportional to minute ventilation, but the fact that ETCO2 rises would indicate that more CO2 is being blown off. But as to how much extra and whether that amount is clinically relevant, that is a great question. I suppose you would need some form of volumetric CO2 to test this. Do you have any papers? The simple equations (PaCO2 Equation) don’t answer this question.

      • Owen Callender says

        Thanks Scott
        Apologies my name is Owen, in the middle of a night shift I defaulted to not putting my name on the web form.. Thanks for clarifying, I am looking forward to your future podcasts.
        I am not aware of any papers on the volume of CO2, its just been my understanding of it (ETCO2 X effective tidal volume (ie minus circuit and physiological dead space) seems a reasonable estimate of expired volume of CO2) but from a quick google search it looks like ventilator companies are going to start to use volumetric CO2 monitoring to sell their new machines at some point.

  4. Chris says

    Think you have a typo at the top of this post: “When you can adjust PaCO2 to maintain a certain value (i.e. you increase minute ventilation), bicarb will lower pH as evidenced by this animal study (Crit Care Med 1996; 24:827-834). ” Shouldn’t this read “raise” pH?
    Thanks as always for great free education.

  5. says

    Dear Scott,
    I listened to your excellent discussion on acid-base treatment with Dr Kellum. I would like to provide an alternate opinion on many of your key points.
    Forsythe et al: Chest. 2000;117: 260-267. manuscript reviewed Hyperosmolar NaBicarbonate administrations in various populations of critical ill patients without a clear physicochemical endpoint (pH is not a physical-chemical endpoint) , prior to the development of early goal directed therapies, the importance of increasing O2 delivery/minimizing O2 consumption during the golden hours, early antibiotic administration, and adequate resuscitation endpoints were ignored. Many of the patients did not have any meaningful change in acid-base status despite the administration of hyperosmolar NaHCO3.
    These studies were clearly poorly designed from 2013 perspective and their clinical relevance is historical but not clinical.
    Severe intracellular acidosis was certainly noted with hyperosmolar Nabicarbonate buffering given the physiologic fact that the large intracellular compartment must buffer the smaller interstitial and vascular compartments to restore standard state acid-base status (i.e. via Na/K/CL exchange). How harmful is this event given the average intracellular pH is 6.8 to 6.9 to begin with? Activation of the enzyme phosphofructosekinase by NaHCO3 actually increases lactate synthesis. Current day isotonic sodium bicarbonate solutions do not significantly change intracellular pH or increase serum lactate.
    Modern day intensivists use isotonic bicarbonate solutions with various SID’s to optimize the resuscitation to a desired endpoint. Hyperosmolar solutions in the absence of brain injury are strongly discouraged.
    Isotonic NaBicarbonate (SID 150), 1/2NS with 75 mEq NaHCO3 (SID 75), Lactated Ringers (SID 28), and Normal Saline (SID = 0) form the core resuscitation solutions to manipulate a patients pH and standard base excess/deficit in any direction desired. If serum HCO3 = 24.5 then administering a solution whose SID is > than 24.5 mEq/L will alkalinize the plasma solution (NaBicarbonate). Administering a solution with SID < 24.5 mEq/L with acidify the plasma solution (Normal Saline), and administering a hypothetical solution whose SID = 24.5 mEq/L will result in no change in pH. This approach to managing Fluids, Acid-Base Status, and Electrolytes simultaneously during resuscitation in critically ill patient is called a dynamic physicochemical resuscitation. This approach is in contrast to shotgun NaBicarbonate, or Normal Saline. Remember LR fixes nothing but preserves the status quo. With this approach one can fully resuscitate shock but at the same time restore and maintain the standard state physiologic milieu. The endpoint being SBE = O, HCO3 = 24.5…. while concurrently providing early goal resuscitation with appropriate physiologic endpoints.

    Kind Regards,
    Ed Omron MD, MPH, FCCP
    Morgan Hill, CA 95037

  6. Sandi Sellers MSN, RN, CCRN, CNP says


    Is there a specific increase in minute ventilation that should be used in conjunction with sodium bicarbonate administration? Thank you for the podcast.



  7. Austin Johnson says

    Just a bit more fodder for the “bicarb restraint” folks out there:

    Kim, H. J., Son, Y. K., & An, W. S. (2013). Effect of Sodium Bicarbonate Administration on Mortality in Patients with Lactic Acidosis: A Retrospective Analysis. (J. I. F. Salluh, Ed.)PLoS ONE, 8(6), e65283. doi:10.1371/journal.pone.0065283.t004

    Many limitations to this study, but keeps us wanting real prospective data for fluid resuscitation.


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