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

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

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?

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… Read more »

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

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.… Read more »

I have found these acid-base podcasts very helpful but I can’t access IV?

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… Read more »

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)

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!

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.

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.

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… Read more »

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).

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?

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

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

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, Cr 0.7, albumin 3.7, lactate 2.9. Unfortunately we did not have blood gas. But I used 24-bicarb (30) to get base excess of -6 (BD of 6) and calculated a SID of 48 then I calculated a s SIG of 14.35, which means he has excess acids which may be due to ketoacids that were unmeasured from alcoholic issues. Im confused though bc his bicarb was 30 on the chemistry and his SOD was 48 which means SID alkalosis and not acidosis. So how is he alkalotic but has 14.35 excess unmeasured acids? Please help me with this problem so… Read more »