Cite this post as:
Scott Weingart, MD FCCM. EMCrit Podcast – Acid Base Ep. 7 – Bicarb Updates, Quantitative Approach, and Prof. David Story. EMCrit Blog. Published on June 28, 2018. Accessed on March 21st 2023. Available at [https://emcrit.org/emcrit/bicar-icu-lactate-debate/ ].
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.
Original Release: June 28, 2018
Date of Most Recent Review: Jan 1, 2022
Termination Date: Jan 1, 2025
You finished the 'cast,
Now Join EMCrit!
As a member, you can...
- Get CME hours
- Get the On Deeper Reflection Podcast
- Support the show
- Write it off on your taxes or get reimbursed by your department
Get the EMCrit Newsletter
If you enjoyed this post, you will almost certainly enjoy our others. Subscribe to our email list to keep informed on all of the Resuscitation and Critical Care goodness.
This Post was by the EMCrit Crew, published 5 years ago. We never spam; we hate spammers! Spammers probably work for the Joint Commission.
On the topic of DKA acidosis Vs Sepsis acidosis. The way we used to talk about the difference at my old shop… where we had a disproportionately high number of young people with electively poorly controlled TIDM is… These DKA patients, particularly the frequent attenders that everyone knows on a first name basis. You know the ones, they have all of the sequelae of diabetes and are even a nightmare to phlebotomise as they have sclerotic IJVs from repeated central access. They live in a perpetual state of acidosis. They control their sugars and thus, their acod-base status, so poorly… Read more »
i have not found this to be the case
these pts are more like asthmatics
they may show up recurrently, but between attacks they are normal if they have access to insulin. (if they don’t then they will be constantly in a state of ketoacidosis. but not sure if there is adaptation so much as the acidosis is not clinically relevant. they come in for dehydration not acidosis and not b/c of tolerance IMO
I agree it is worth noting how well we see DKA patients tolerate severe acidemia with normal BP’s. I’m not so sure, however, that it has to do with habituation to acidemia, as much as the “metabolic mess” underlying the acidemia. Similar to the acute respiratory acidotic with a pH < 7 who is probably obtundation but not in shock or probably even hypotensive. Which brings up the big question for me – is acidemia on its own even a "bad thing" that warrants an attempt at being directly corrected? What tiny amount of human data that exists on the… Read more »
I agree that it is somewhat of a simplistic view to use habituation to acidaemia as a direct causation of this tolerance in DKA. It’s just a way that we came to think about it. The regularity with which this subset of patients tolerate significant acidaemia is impressive. I agree that it definitely lends itself to the argument of how clinically significant isolated acidaemia is. The reality of it is that the confounders are huge, will we ever have a group of people that we can study acidosis in without the major confounders you have already touched on. From my… Read more »
fantastic ?s!! i was right on the fence to give bicarb to renal failure pre-CRRT. my intensivists and nephrologists at both of my EDICU venues both want us to administer and I have held back to do v. little evidence. It could all come down to avoiding HD and we would get just as good outcomes if we just didn’t do HD, but acidosis is an indication at the place I work, so essentially regardless of the reason–bicarb may help my patients (whether it is due to intrinsic benefit or just avoiding CRRT). The reason why not to give it… Read more »
Hi, I was wondering about the assertion that Ringer’s Lactate will cause an immediate acidosis which then converts to a long term alkalosis with proper liver function.
However, in this post by Dr. Farkas (https://emcrit.org/pulmcrit/understanding-lactate-in-sepsis-using-it-to-our-advantage/), he asserts that the lactate in LR is sodium lactate and thus acts more as a buffer than an acid promoting substance.
How do you reconcile these two views?
there is no need for reconciliation–those 2 are the same statement
What is the mechanism for that initial acidosis then?
Because my understanding of Dr. Farkas’ post is that initial administration is pH neutral with a later trend towards alkalosis
lactate is a strong anion that acts as an acid
What I understood so far from your podcasts and the Stewart-book is this: The initial acidosis has nothing to do with lactate acting as an acid (actually its a base), rather the SID of the solution causes the initial acidosis. If lactate is a strong anion (and it is), then the acid-base effects of a lactate solution should be estimated by the SID of that solution. LACTIC ACID leads to acidosis because it decreases SID. On the other hand, Ringer-Lactate/Hartmanns contains SODIUM-LACTATE, not lactic acid, with a SID much lower than the plasma. So if the lactate is not metabolized,… Read more »
lactate is a strong ion that acts in the vernacular as an acid.
yes lactate acts as an acid b/c it reduces the SID. Ringers/Hartmanns has the the exact SID to keep the plasma neutral, (lower than normal plasma SID to make up for dilution of weak acids)–given that the lactate is metabolized. Otherwise it is essentially NS. It doesn’t cause subsequent alkalosis when metabolized, it maintains neutrality.
Great podcast – thanks for the shout-out – and I’m glad that this contributes to clinicians thinking about acid-base..