Cite this post as:
Scott Weingart, MD FCCM. EMCrit Podcast 50 – Acid Base Part IV – Choose the Solution Based on the Problem. EMCrit Blog. Published on June 26, 2011. Accessed on July 6th 2022. Available at [https://emcrit.org/emcrit/acid-base-4-use-of-fluids/ ].
Financial Disclosures:
Dr. Scott Weingart, Course Director, reports no relevant financial relationships with ineligible companies.
This episode’s speaker(s), (listed above), report no relevant financial relationships with ineligible companies.
CME Review
Original Release: June 26, 2011
Date of Most Recent Review: Jan 1, 2022
Termination Date: Jan 1, 2025
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Thanks for a great review of a topic thats been confusing me during my recent term in the ICU.
My pleasure, Andrew.
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;… Read more »
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)!
Scott,
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.
Mike
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?
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.
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… Read more »
Derek,
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.
Hello Scott!
Great as usual.
The link for other fluids chart on crashingpatient.com is not working. Were will I be able to access that data?
Thank you,
Miguel
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?
don
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
fantastic, Derek!
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… Read more »
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!
D
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.”
Scott, 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… Read more »
Anthony, thank you so much for that feedback. With your attitude, you will be an incredible NP!
any more references on the metabolism of bicarb and/or lactate or acetate?
Hi,
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.
I have found these acid-base podcasts very helpful but I can’t access IV?
this is IV
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
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… Read more »
wow, i do admire a bloke who states his thoughts strongly : )
hopefully this will explain:
https://emcrit.org/wp-content/uploads/2012/08/photo.jpg
if this picture is not worth enough words just shoot me another comment. “Water being pH Neutral” is an ex-vivo concept, not applicable to intra-vascular acid-base; look to the SID of the fluid to understand the acid-base effects of a fluid.
I love it. That is a beautifully simple explanation. Nice one.
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.
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.
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)
an excellent scientific underpinning for this episode
Hi.
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!
That’s it exactly.
Not sure I follow how the Stewart quantitative method helps to identify a mixed acid-based disorder. Might you conjure up an example of mixed metabolic acidosis/metabolic alkalosis so that we might see how the Steward method both identifies the problem and maybe even gives some insights into the fluids one would use during treatment.
Let me propose one: an anorectic-bulemic patient who is abusing laxatives AND diuretics and also has been vomiting. What might we see in that circumstance?
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… Read more »
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.
Scott,
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.
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.
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.
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.
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… Read more »
Try these:
Current Opinion in Critical Care 1999;5(6):443-447
and
Crashing Patient Link
Let me know if they clear things up or muddy the waters
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).
Addressed in part 6. Nevermind!
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?
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.)
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
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.
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?
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
Dean
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.
Hello, I really appreciate this podcast. Although it was posted a long time ago, it is extremely useful for me. You are correct, it can be confusing at first (for a while), but with practice and time, gets better. I have a question about a case that I had. After going home to go over the calculations, I was a bit confused and wanted to know if you can look over the numbers. We had a intoxicated patient who was signed out pending sobriety and labs. His labs returned as Na 129, K 2.1, Cl 81, Bicarb 30, BUn 14,… Read more »
Hi Dawn,
I presume Scott can’t see/isn’t reading your comment because this podcast has been moved to the archives.
Your mistake is that you already get BD when substracting bicarb from 24 and not BE. In your example the patient has BD=24 – 30= -6 and a BE of 6 and not the other way round. I hope your calculation is working better now. 😉
Benjamin Danowski
Resident in anesthesia/critical care
Skövde, Sweden
Can Bicarb to the patient increase Carbon Dioxide in blood gas My answer No practically Explanation Bicarbonate is a molar solution so 100 ml of bicarb contains 100 millimoles Because 1 mol bicarb produces 1 mol Carbon Dioxide 100 ml Bicarb soln contains 100 millimoles of Carbon Dioxide molar weight of carbon dioxide = 44.01 g/mol so 100 millimoles of Carbon Dioxide contains 4.4 gr Carbon Dioxide density of carbon dioxide at STP = 1.977 gr/l 2.24 lt of Inspired air contains this 4.4 gr Carbon Dioxide but expired air contains 100 times higher Carbon Dioxide So 2.24/100 = 0.022… Read more »
Hey Scott,
Just a small note.
Above you write
“Hypertonic fluids are even more acidifying b/c they draw pure water into the extracellular space”
More correct with be to say into the intravascular space because hypertonic fluids draw water out of both intracellular and interstitial spaces.
Tx
Miguel Oliveira