Cite this post as:
Scott Weingart, MD FCCM. SMACC-Back – On Marik and Lactate. EMCrit Blog. Published on May 21, 2016. Accessed on January 20th 2025. Available at [https://emcrit.org/emcrit/smacc-back-marik-lactate/ ].
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: May 21, 2016
Date of Most Recent Review: Jul 1, 2024
Termination Date: Jul 1, 2027
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Scott,
Thanks for the wee. Mandatory listening for my crews. I’ve spent the last 8 months trying to get folks to understand that, while the biochemistry of lactate is really cool, It’s a marker of disease. Not a pathogen in itself!
Mike
Hi Scott, Totally agree with you that using an initial lactate as a screen for a sick patient who is at high risk of death is useful. However, most clinicians still equate lactate with a poison, the level of which is to be treated like a toxin level, and getting it down with large amounts of fluids is seen as a goal in itself. The logical fallacy follows like this: the lactate is high in sepsis because there is global tissue hypoxia (lactate is produced by anaerobic respiration); I must increase tissue perfusion and the best way of doing this… Read more »
“most clinicians still equate lactate with a poison” That is probably a misrepresentation of the reasoning. The problem is that we have previously given excessive weight to Hypoperfusion/Type A Lactic-associated acidosis as the likely cause of the abnormality without considering other unrelated processes of altered cellular biochemistry (Type B Lactic-associated acidosis). The examples given seem mainly based on Sepsis Pathophysiology where a number of factors are associated with persistent hyperlactataemia long after circulation is restored. We have now a more refined view that the cause to this is not just one of Distributive Shock. However, the same factors may not… Read more »
Thanks Scott for the necessary and overdue counterbalance to Dr. Marik’s talk. These issues are far from settled in the physiological literature – eg recent debates not only in the pages of AJP as outlined in your wee, but also in JAP 2006, 2008 and 2011 amongst others. (The 2008 point:counterpoint debate and comments are particularly relevant to your podcast). Given the lack of scientific agreement and the nuanced arguments I would guess many clinicians without a graduate degree in biochemistry and physiology are as confused as I am about the truth of the matter and its relevance. From the… Read more »
Adam, Thanks for those citations! Yes–totally agree. I hope I was clear, the extra anions that lactate contributes may or may not result in acidemia depending on all else that is going on. But lactic acidosis can indeed exist is the take home message from the piece.
Cool. I think you were clear, though I am not sure I was – it’s all about the “what else is going on”. Let’s make it straight. In simplest terms, and this is merely a hypothetical, if for example it were found that the only way endogenously produced lactate could get extracellularly was via a transporter that imported a Cl anion in exchange (and that there was no associated movement of water), given the anion balance in this process, I don’t think it would make sense to say that endogenously produced lactate causes an acidosis. Just as lactate is administered… Read more »
think we are confusing the terms acidemia and acidosis. what you are describing is lactate contributing to acidosis, but inside a package that could contribute to acidemia, alkalemia, or neutrality.
I was saddened to read Dr. Marik’s Discussion of lactate in sepsis. The need to abandon the dogma in sepsis science is unequivocal. I have enjoyed his antidogmatic views. However the importance of lactic acidosis, a low bicarbonate, and often a high anion gap as a marker for late sepsis is fundamental to sepsis detection on the wards. The patterns of phenotypes of sepsis have been known since the late 1960s. http://dx.doi.org/10.1097/00000658-196710000-00004 Young house officers should be taught to watch for a fall in venous bicarbonate which at times is the first solid clue that sepsis is evolving. At first… Read more »
you must understand that marik is not saying lactate is not a sign of sepsis he has been arguing for years that using lactate as a marker for hypoxemia caused by hypoperfusion is false therefore trending it or using interventions ie fluid boluses to bring it down is devoid of evidence, which is important especially in an age where doctors live behind a screen and worship numbers on that screen. whether or not it causes acidosis is up for debate–we have all seen pts with elevated lactate who do not have acidosis and vice versa. if you are using someone’s… Read more »
whether it causes acidosis in plasma has never been up for debate. You’ve never seen a patient whose lactate has not caused acidosis, you’ve seen patients where the elevated lactate did not cause acidemia. Whether you use Stewart approach or H&H, lactate causes anion-gap or SIG acidosis. This is not speculation, this is mathematics and p-chem. If the pt’s chloride or albumin has gone down, then you will not see an acidemia with an elevated lactate, the met acidosis remains though.
One point about sepsis phenotype detection and tracking of transition states. In the management of the phenotypes of sepsis it is pivotal to detect transition states. The “sepsis transition states” comprises; worsening, recovery, superinfection, conversion to a different sepsis phenotype, and other events. Thresholds cannot be used to detect transitions so we look for other dynamic markers. One marker of transition is the dynamic pattern of the platelet count. Another is the pattern of the venous or arterial bicarbonate and the lactate. Of course the pKa of lactate is lower than the pKa of bicarbonate so bicarbonate is consumed (converted… Read more »
Scott I very much appreciate your courageous post here. The reason I responded so much to this post is that I am concerned that easily influenced house officers may misunderstand the role of Lactate and bicarbonate measurement in common phenotypes of sepsis. All experienced clinicians understood the arguments in the web cast which presented on partial aspects of the pathophysiology as volitional hyperbole…..i.e. A kick from a brilliant scientist for the widespread promulgation of dogma which contends that a high lactate always means “give more fluid”. Long before the webcast we arrived on a case of a young man with… Read more »
After a lengthy discussion with my fiancé who is an Anesthesia/ Emergency physican and adamantly in camp Weingart on this issue (I am more of a Marik supporter on this topic) I had a thought. I am probably overlooking something really obvious here which will totally debunk my argument, but I thought I’d write it here anyway. The question at hand is “does hypovolemia/hypoperfusion/hypoxia cause an increase in Lactate and does an increase in Lactate mean that the patient needs fluids? Also does an increase in Lactate cause lowered pH and acidosis?” I stand by Dr. Marik’s teaching that hypoperfusion… Read more »