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:
- Part I lays out the background of the quantitative approach
- Part II puts it in mathematical terms to allow calculation of acid base status
- Part III takes you through some real world examples
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.
Articles
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
Podcast: Play in new window | Download (29.4MB) | Embed
Hi, my name is Scott Weingart. 
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; 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?
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 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
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.
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:
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.
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 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!!!!
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 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)
wow, i do admire a bloke who states his thoughts strongly : )
hopefully this will explain:
http://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.
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.
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.