EMCrit Podcast 50 – Acid Base Part IV – Choose the Solution Based on the Problem

This is Part 4 of the Acid Base saga. In this episode, I discuss the acid base effects of fluids and when and how to use sodium bicarbonate.

If you haven’t checked out the previous episodes, you should definitely do that first:

You may need the EMCrit Acid Base Sheet to follow along

The Acid Base of Fluids

Crystalloids will have acid-base effects by their SID and the dilution of extracellular Atot

“Balanced Fluids” are fluids with a SID just low enough to balance the dilution of the weak acid, albumin (SID of 24-28)

For the effects on a patient with altered pH, any fluid with a SID the same as the pt’s bicarb will keep the patient at the same pH. If the SID is greater than the pt’s bicarb, then the fluid will be alkalotic and if less than the pt’s bicarb–acidotic (Intens Care Med 2011;37:461).

Hypertonic fluids are even more acidifying b/c they draw pure water into the extracellular space

Chart with a bunch more fluids is on crashingpatient.com

Sodium Bicarbonate

If not stored in glass, bicarb containing solutions leech CO2 and become not so much bicarbonate.

If given at all, should be given slowly by push over 5-10 minutes or by drip; never by rapid push

In hyperkalemia, NaBicarb isotonic is essentially a potassium-free, non-acidic fluid that dilutes down the potassium.

NaBicarb can be used as a substitute for hypertonic saline in increased ICP (Neurocrit Care 2010;13:24). They used 85 ml of 8.4% sodium bicarb infused over 30 minutes.


Best Review of the Stewart/Quant Approach to Fluids

Best Review of Sodium Bicarb Use Ever

Balanced solutions (p-lyte) led to lower Cl and higher bicarb (Am J Emerg Med. 2011 Jul;29(6):670-4)

Another incredible review on fluids including the rec. that we use 3 amps of bicarb (J Intens Care Med 2010;25(5):271)

Also of interest may be the previous episode on intubating the patient with the severe metabolic acidosis


Josh Farkas has done a lit review showing that the body may not change gluconate to bicarb, leading plasmalyte to be neutral rather than extremely basic (which is a good thing)

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  1. Andrew Coggins says

    Thanks for a great review of a topic thats been confusing me during my recent term in the ICU.

  2. says

    The only indication we have anymore, with standing orders, for bicarb on the trucks is for cardiac arrest, and now I feel bad for all the bicarb I’ve pushed in arrests!

    We could call for orders in TCA/sodium channel blocker OD, but I don’t think prehospital providers knew just how slow we should be pushing it. Probably needs to be on our cheat sheets.

    We can also call in hyperK+, but we’ve got CaCl and I think given our patient interaction time I should reach for that first. Another consideration is our only options for mixing are NS and LR; with that said is it even worth mixing 50 mEq/mL and starting a drip? From what I’ve gleaned in this podcast and the prior one on hyperK+, I would get more bang for the buck reaching for CaCl, am I on the right track?

    • says

      Chistopher–I pushed a ton as well. If the patient is crashing from tricyclics or seizing, push away maybe over a minute or so. But if you have the 5 minutes, probably better. CaCl is probably the way to go for prehospital hyperKso you are just the right track (as usual)!

  3. Mike Jasumback says


    Thanks for the stellar review. I had already pretty much figured out where this was going but your explanation was more clear than my muddy understanding.


    • Derek says

      Scott: Do you think I should have my EMS providers no longer push sodium bicarb in hyperkalemic arrest? In the ED, it sounds like we should always be using drips rather than pushes. How about in the ESRD patient?

      • says

        I still do it if I suspect or know there is hyperkalemia during arrest b/c there is so much extra acidosis and any rapid push during arrest is the same as a slow push b/c of slow circ times. No evidence either way.

  4. Derek says

    This article appeared in the July issue of AJEM. Hope you don’t mind me copying the abstract. Would love to hear your comments:

    Resuscitation with balanced electrolyte solution prevents hyperchloremic metabolic acidosis in patients with diabetic ketoacidosis
    Simon A. Mahler MD

    Objective: The objective of the study was to determine if balanced electrolyte solution (BES) prevents hyperchloremic metabolic acidosis in patients with diabetic ketoacidosis (DKA).
    Methods: This is a prospective, randomized, double-blind study. A convenience sample of DKA patients aged 18 to 65 years with serum bicarbonate less than or equal to 15 and anion gap greater than or equal to 16 was enrolled at “Louisiana State University Health Sciences Center-Shreveport” an capitalize Emergency Department over a 24-month period (2006-2008). Patients were randomized to
    standardized resuscitation with normal saline (NS) or BES (Plasma-Lyte A pH 7.4). Every 2 hours, serum chloride and bicarbonate were measured until the patient’s anion gap decreased to 12. An intention-to-treat analysis was performed on patients who met inclusion criteria and received at least 4 hours of study fluid.

    Results: Of 52 patients enrolled, 45 (22 in BES group and 23 in NS group) met inclusion criteria and received 4 hours of fluid. The mean postresuscitation chloride was 111 mmol/L (95% confidence interval [CI] = 110-112) in the NS group and 105 mmol/L (95% CI = 103-108) in the BES group (P ? .001). The mean postresuscitation bicarbonate was 17 mmol/L (95% CI = 15-18) in the NS group and 20 mmol/L (95% CI = 18-21) in the BES group (P = .020).

    Conclusions: Resuscitation of DKA patients with BES results in lower serum chloride and higher bicarbonate levels than patients receiving NS, consistent with prevention of hyperchloremic metabolic acidosis

    • says


      this is the article I have referenced at the end of the post and mention on the podcast. Bicarb gets better quicker, but not designed to determine better outcome.

  5. don says

    You have really knocked it out of the park with this acid base series. I am reading like mad and getting it; finally. Never really understood hyperchloremic acidosis-now it makes sense thanks to you.

    BTW….Why do they call 25% albumin salt poor?


  6. Derek says

    Thanks again for this podcast. Last night I had a pt with AKI from dehydration, ph=7.22, K=7.1. I would have given NS in the past but gave isotonic bicarb. The renal guys were impressed that an ED doc came up with that. Thanks again for making me look good

  7. says

    A listener wrote with this question:
    hey Scott,

    Loved your recent fluids talk….

    I have a question that I know I’ll regret asking, but can’t help it.

    In sepsis and low flow states, hyper metabolic states where serial
    lactate trends may be useful, does LACTATED RINGERS contribute to a
    falsely high serum lactate?

    Thanks for not ridiculing!

    it is a fantastic question. So your liver clears 100 mmol of lactate per hour in a normal state. So the lactate you see in sepsis is usually the result of ongoing production in excess of this amount. The lactate in ringers comes in two forms, D and L lactate, only the L is measured. So basically it is a drop in the bucket… except when the patient’s liver is not working up to snuff, whether b/c of preexisting disease or shock; in this case, yes the lactate in LR will raise lactate levels and act as an acid instead of a base buffer. In these cases it is best to use isotonic bicarb drip if the patient is severely acidotic. Plasmalyte or similar won’t raise latate, but will also act as an acidic fluid in these cases.

  8. says

    Hi Scott
    I have a quick question (kind of more related back to parts 1-3 of this series, but it occurred to me when seeing a DKA patient t’other day) regarding calculating SID when the blood glucose is elevvated. Do you correct a low sodium for the high glucose BEFORE calculating the SID?? You may have answered the question somewhere, but I can’t track it down…
    Thanks mate – love your podcasts!

  9. says

    Hmm – just found the answer – doh! – “For the acid base purposes, never correct the sodium, b/c the sodium level is real. Cl drops with the sodium to maintain SID. Correct sodium with hyperglycemia only to find out if the pt has hypo or hypernatremia.”

  10. Anthony says

    I just want to let u know that u create awesome podcasts and I have grown so much as an ER nurse. What’s cool is that lately I have been caring for pt’s with SCAPE, Cardiogenic Shock, Hemorrhagic Shock, Ca Channel blocker OD and so many more. I have been a RN for 10 yrs and I currently work in a Level I Trauma Center where we see a little over 100K patients per year. We are an inner city hospital and we are exposed to a variety of diseases and conditions. The thing I love about you is u seem sincere and I get the impression that you love to teach and want the paople around you to become more knowledgable/skillful and provide the SICK patients with the care they really need as oppsoed to what they regularly receive ( I can’t stand it when the MD states to “We don’t do this in the ED the ICU residents will take care of that upsatirs.”) Thank You, Thank You, Thank You. Pleases keep on with the podcasts and I will keep on listening. This stuff really helps me and I have made the decision to get my NP. You are awesome Scott..keep up the great work!!!!

  11. mohammed says

    in part III you mentioned you have a paper which references the simplified equation you use to work out SIG, however, that paper does not mention ‘minusing’ lactate at all.

  12. 988Thierry Bégin says

    Hi Scott,

    Thank you for this great stuff on acid base podcast.

    I have one question for you:
    In the equation: Atot /-\ A- + AH, can you please let me know where is Albumin, Atot or A- ?

    thierry from Québec

  13. Antony Ashton says

    Whoa there Scotty.
    I like your podcasts and find them very educational as a UK intensivist/anaesthetist
    But at 8:15 in this cast you started saying stuff that made no sense and I suspect may be crap.
    The significance of the SID of a fluid is, when given, how it will affect the SID of the extra cellular fluid.
    So D5w I hope is 5% Glucose, which you say has a SID of 0 and therefore is profoundly acidic. This makes no sense. I get that the glucose is rapidly metabolised leaving you with water, but, erm, water is neutral. It will dilute the albumin and may have an alkalotic effect, but the effect on the cation and anion concentration in extra cellular fluid will be equal, and thus nil effect to electroneutrality.
    The reason why infusing fluids with ions in them alters the pH of extra cellular fluid is because they alter the relative concentrations of the ions in extra cellular fluid.
    So 5% glucose will have net zero effect on relative ion concentrations and thus is neutral, hypertonic saline causes acidosis because of the relatively higher concentration of chloride to sodium when compared with extracellular fluid ( just like normotonic saline) and the effect on drawing out intracellular water is nil (or are you really saying that it will improve intracellular acidosis because acidic water is leaving? TFIC)

        • Antony Ashton says

          Hang on.
          The water is going to dilute the weak acids to the same extent, so although you are reducing the SID you are also reducing the Atot.

          • says

            absolutely, but that is a less prevalent effect and that is the case with all fluids except albumin. Basically, D5W acts the same way as NS in terms of acid base. If you want to add still another level of complexity, water will cause more intracellular acidosis and have less of an effect on the ECF than saline b/c saline will keep more of the fluid in the intravascular space than D5W.

  14. L.W. says

    one thing that some people may not understand or remember from freshman chemistry is that water undergoes autoprotolysis…It protonates itself at a rate of 1×10^-7 in a 25 degree environment. This autoprotolysis becomes a factor at low concentrations of other weak acids (hence the systematic treatment in part 1). Also remember that any weak acid (HA) plus water becomes the conjugate base in solution (A-) plus a Hydrogen ion (or hydronium for us chemists) just as the addition of any conjugate base plus water results in the acid forming in solution (A- +H20—–HA plus OH)

  15. lrock says

    Strictly awesome series. I love it. I was going to try to sell my colleagues on quantitative method and I want to be sure I understand:

    Essentially, by looking at the SID, lactate and SIG you will identify the presence and nature of any mixed metabolic disorders so you don’t need the old gap-gap calculation. Sound right?

    Thank you!

  16. Matteo says

    Scott, sorry if I’m going to be a little bit OT, but as an Italian EM resident I’m starting to become very confused about how to think acid-base of fluids. I’m very fond of this argument (I find it very fascinating) and I’m intensively studying it. Every kind of conference I’ve been or book I’ve read minimize the SID theory: even one of our greatest ED/intensivist (Fernando Schiraldi) doesn’t really “believe” in it and thinks that we can live good without it. Now, after reading this article about the acid/base of fluids I’m thinking: am I doing it right to ignore SID? And if your answer is “no”, why I should consider it?

    PS: in my ED we use liters of normal saline (in Italy is called “Physiological solution” – and that explain it all) and only a few thinks about its acidification
    power. Ringer is almost forgotten and apparently we’re still in the colloids vs cristalloids battle.

    • says

      There is really no room not to believe in it, it is physical chemistry. But Dr. Schiraldi is absolutely right, if you correct for albumin and perform a delta-gap then you will get exactly the same results.

      As to Normal Saline, see this post.

  17. Geoffrey Warnock says


    Love the website and am really getting into the acid-base lectures.
    Just 2 questions about some of the bicarb.

    1 – what is the mechanism behind fluid SID and patient’s bicarb affecting pH.
    2 – why do the balanced/alkalotic fluids need something that will form bicarb?

    Keep up the amazing work.

    • says

      pH is a measure of how much H+ is present; H+ is destroyed or generated depending on the relative concentration of the components of SID.

      The balanced solutions need buffer base to allow a difference between the anions and cations–bicarbonate or bicarbonate surrogates are the only things that will allow that as bicarb is dependent and forms and disappears depending on the other strong ions.

      • Geoffrey Warnock says

        Can you just expand on that slightly.

        You mention that depending on the patient’s bicarb level and the SID of the fluid it can either keep pH the same or make them more acidotic or more alkalotic.

        How does that happen? Is it dilutional effect on plasma SID + the direct effect of the low fluid SID.

        All the best.

        • says

          It is the relation of the fluid SID to the pt’s BE (or the pt’s bicarb–they are linked). In an acidotic pt, a neutral solution like lactated ringers will make their pH higher.

  18. Steve Phillips says

    Hey there Scott.

    Your podcasts (via Tony Asthon) enlightened me to the bedside utility of the simplified Fencl-Stewart approach to acid-base disturbances. I calculate the SIG on almost every ABG I ever see in critical care for no good reason other than because I can!

    In have, like many others here I suspect, attempted to re-trace the chemistry right back to the original Stewart literature to facilitate my understanding of this fascinating theory.

    As one begins to explore this however, there seems to be a distinct conflict of this theory with much of literature concerning renal physiology. Researching the pathophysiology of renal tubular acidosis, for example, results in many descriptions of altered ion-transport mechanisms, particularly pertaining to the retention/excretion of hydrogen and bicarbonate ions.

    This is obviously entirely at odds with the idea of these acting only as dependent variables in acid-base balance. Whilst one can personally conceptualise the associated movement of strong ions underlying the true renal physiological cause, I can find only very minimal published work theorising along those lines.

    It seems odd to me that the physicochemical approach potentially represents such a paradigm shift in our understanding of acid-base balance, but such little discussion exists attempting to apply this to theoretical and experimental models of renal physiology at a cellular level.

    Have you any examples in the literature of this sort of theoretical application?

  19. Eric says

    Do we really need to increase the respiratory rate to blow off the CO2 from the bicarb? From the OR example in the podcast (and the few sentences prior) it sounds like the EtCO2 will pop up on its own, which would be a sign of compensation/increased excretion without a change in rate (and in most cases that patient wouldn’t be breathing on their own).

  20. Dean says

    Hi Scott

    I’ve just listened to Acid Base Part IV and just wanted to clarify the volume of fluid in your 8.4% amps. What volume constitutes an ampoule?

    • says

      in the US, all amps are 50 ml. The difference lies in whether they have 50 meq or 44.6 meq of Bicarb (ours are the latter, the former is better b/c 3 amps makes an isotonic fluid.)

  21. Dean Burns says

    Hi Scott

    Thanks for this great podcast on fluids. My question relates to my institution’s choice of maintenance fluid on the ICU.

    We’re currently using glucose 4%/0.18% NaCl for the last 2 years.

    If I’m understanding the principles outlined, it would seem that this fluid would be acidotic but the hypotonicity of the 0.18% saline would offset this slightly, making it slightly less so?

    Could you advise/explain where this fluid would sit relative to its relatives 0.9% saline and 5% dextrose?

    Thank you kindly

    • says

      any form of saline has a SID of 0–so they are all equivalent in their acid base effects. D5W has a SID of 0 and it is the same.

      • Dean Burns says

        Maintenance fluid with a SID of zero would seem a curious choice, no?

        What are you currently using for maintenance in your ICU? Any preference on the LR vs Plasmalyte, or are you tailoring to each individual patient?

  22. Dean Burns says

    Hi Scott

    A quick question on bicarb – based on the Strong Ion Theory.

    If bicarb is basic, what effect does the hypertonicity have on that basic solution effect? Presumably the overall effect is still basic, despite the drawing in of free water, which behaves as an acid in vivo. How much is the basic effect reduced by the hypertonicity which behaves like an acid?

    Does that make sense?

    Hope so – thanks for these tutorials


    • says

      On the right track, Dean. By strong ion, biacarb is not basic, Na is. Free water is acidotic when clear of any ions. In the case of hypertonic bicarb, free water will move into the plasma space and dilute some of the Na (and other ions). So the basic effect is diminished to whatever extent the Na concentration is brought down by the addition of the free water.


  1. […] by emcrit on April 11, 2011 I have spoken about it for a while, but I’ve finally gotten it done: the acid-base podcast. The podcast is going to be in 3 or 4 parts. They are segmented from a lecture I gave to my residents recently. Part II discusses the mathematics of acid base and Part III goes through actual problems. Part IV then discusses the acid-base of administered solution. […]

  2. […] är ett betydligt enklare sätt att tänka. Se, lyssna och lär från emcrit del I, II, III och IV Share this:TwitterFacebookGillaGillaBe the first to like this. This entry was posted in […]

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