Cite this post as:
Scott Weingart, MD FCCM. EMCrit Wee – Is Lactate Clearance a Flawed Paradigm?. EMCrit Blog. Published on June 5, 2013. Accessed on January 17th 2025. Available at [https://emcrit.org/emcrit/lactate-clearance-flawed/ ].
Financial Disclosures:
The course director, Dr. Scott D. Weingart MD FCCM, reports no relevant financial relationships with ineligible companies. This episode’s speaker(s) report no relevant financial relationships with ineligible companies unless listed above.
CME Review
Original Release: June 5, 2013
Date of Most Recent Review: Jul 1, 2024
Termination Date: Jul 1, 2027
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thanks Scott. interesting stuff.
My immediate question on hearing your thoughts is ” if the lactate was going down and you did the echo just for teachng purposes and it looked crappy, would you still put up inotropes or be reassured by the lactate and sit tight?”
Would hold tight as long as all the other variables look good. May check an ICal to see if that is the trouble.
Hi Dr. Weingart, I read the article by Dr. Marik and Dr. Bellomo last week and was happy to see that it caught your eye. It is an excellent review on lactate physiology and brings up some interesting theories why we do or do not clear our lactate burden. What it does not do is provide a convincing argument in changing how we use lactate in every day practice. From the Jones study (2) we know that people who clear their lactate levels do better than those who do not. Whether this is a prognostic factor or an evaluation of… Read more »
Rory,
Fantastic post!
Hi Scott, Definitely, a very interesting discussion, but I feel that Dr. Marik and yourself are saying essentially the same thing……that there is more to Sepsis than meets the eye!. It is essential we understand that the so called ‘Oxygen debt’ may not exist in every patient with a high lactate….the latter may just be reflecting the ton of badness that is already in progress. I don’t think Dr. Marik is implying that high lactate does not have a prognostic implication at all. You said that you would not be averse to trying inotropes if you found the heart to… Read more »
Biju,
I think we disagree on the intent of the article, which is to debase the concept of using lactate clearance as a resuscitation goal. All the rest that you mention is just a lead-up to that. I agree with most of what Dr. Marik has said up until the point where they then conclude b/c of these things, serial lactates can not be used to guide a severe sepsis resuscitation.
I accept that (endogenous) catecholamines are responsible for elevated lactate in many cases and as such represents a stress state and “badness”.
But what does this mean for patients we start exogenous catecholamines on ?
Logically, this would prevent us from using lactate clearance as a marker for effective resuscitation because you would expect lactate to go up instead of down.
For epinephrine we know this to be true, at least for the first day after starting epinephrine infusion (CAT study)
Absolutely, this is why I don’t use epi as a primary pressor if I want to use lactate clearance. Albuterol will also mess with lactate’s value.
Here is a quick search strengthening what Iwan Dierckx posted.
http://www.ncbi.nlm.nih.gov/pubmed/18323749
http://www.ncbi.nlm.nih.gov/pubmed/11901313
I believe we are continuing to misunderstand the Kreb-Cycle and its mechanism. There are several way Lactate is formed to Lactate Dehydrogenase then converted back to a usable form for the cells. For Example, if pyruvic acid was converted by fermentation then we would be thinking more about elevated Ethanol levels in shock states.
Did a lit search and way back in ’99 this was published in the Lancet: http://www.ncbi.nlm.nih.gov/pubmed/10465191
A redux perhaps?
not sure what you mean; this is exactly what I said on the podcast.
Scott, I just listened to this Wee again after having to endure an IHI presentation touting CVP and ScVO2 and slamming lactate clearance. I totally agree with your points. My question to you (topic for a separate Wee), What is the evidence that ScVO2 predicts survival in Severe Sepsis? The Surviving Sepsis Campaign and IHI seem to think the evidence is stronger for ScVO2 than lactate clearance. I would like your perspective.
Len,
The Jones trial established lactate clearance as equivalent if not superior to ScvO2. CVP is laughable and has been debunked by 2 separate meta-analyses by Paul Marik et al. If you meet a staunch defender of CVP and ScvO2, you may want to ask if there is anything in their academic career that biases them to that viewpoint.
I have to contend a bit with Marik and Bellomo’s argument that lactate is disproportionately driven by catecholamine stimulation via beta-receptors. While the citation of adrenergic blockers blunting lactate rise in hemorrhagic shock is somewhat pertinent, the evidence they cite by Levy et al. to extrapolate this model to sepsis is flawed. They claim that beta-receptor agonists are a main driver of lactate production based on an experiment in which ouabain (a Na/K/ATPase pump inhibitor) was given to septic patients with a resultant decrease in lactate production (given that catechoamine beta-agonists drive lactate production through simulation of the Na/K/ATPase pump).… Read more »
Absolutely grand comment Dustin. I have always thought of the lactate of sepsis as a mixed bag of stuff just as you say. The one conclusion I always come back to in my septic and my trauma patients is that when it comes to lactate, if its not getting better things are probably getting worse.
Forgot to add that the evidence using dichloroacetate as a simulator of oxidative metabolism to drive down lactate levels reinforces the mitrochondrial dysfunction hypothesis and further negates the oxygen debt argument- yes epinephrine may accelerate glycolysis and lactate production, but it is the failure of the mitrochondia to keep up in the septic state that is the real trouble, and which will eventually lead to multi-organ failure via mitochondrial shutdown. Septic cardiomyopathy is only a proxy for this process, which is unlikely to be ameliorated with pro-inflammatory beta-agonists. And so I’ve pretty much typed myself into the same conclusion as… Read more »
Lactate not clearing (or increasing), SvO2> 70, Hbg >10, No evidence of LV dysfunction on bedside echo, fluid resuscitation appears adequate (however you prefer to determine that), ABx and source control done (you think, at least) -> Give esmolol trial?
CZ
Intubate if not already
Thiamine if pt malnourished
Ask is there dead gut/tissue somewhere
then if tachycardic, consider esmolol
I had recently a woman with lobar pneumonia, BP 85/50, RR 24, HR 120, a little confusion, lactate of 3…resuscitated with fluid, 30ml/kg, prompt antibiotics, and had serial lactates that over 3 draws dropped to 1.6. She had complete resolution of vital abnormalities and confusion. I left her for the nocturnalist and simply ordered a follow-up lactate the next morning. Did well through the night and looked great, but AM lactate 5??! Carefully examined her. Warm and dry, no mottling, MAP well above 65 on maintenance fluid with no pressors, excellent urine output with normal oxygen sats and respiratory rate,… Read more »
how are family getting access to lab tests?
Nurse’s with loose lips sink ships?