EMCrit Podcast 37 – Lactate in Sepsis

When an ED starts providing advanced care for severe sepsis, lactate testing is an absolute requirement. Lactate use brings up a lot of questions, especially if it is not commonly ordered in your department. In this podcast, I discuss all of the lactate questions that have come up in the course of the NYC Sepsis Collaborative.

For the past few months, I have been co-chairing this NYC-wide sepsis collaborative under the auspices of a hospital organization. 56 hospitals have joined the collaborative with the goal of breaking down the barriers to aggressive sepsis care in the ED.

The protocols and educational materials for the project will always be cross-posted here:


Many of the questions we have been getting relate to the use of lactate as a screen and an indicator of adequate treatment. Last week, I discussed these issues during a webinar. This podcast is the recording of that cast.

Here is the Lactate Reference Sheet

Other important info:

The emcrit webtext is now at crashingpatient.com and the blog has moved to http://emcrit.org

Scott Gallagher sent in the comment regarding commotio cordis as a cause of v-fib/v-tach in trauma patients. He is quite right to point out that ACLS works for these folks. Shock and use anti-dysrhythmics.

Here is a reference from the New England Journal:

NEJM 2010;362:917


Another article demonstrating the equivalence of arterial and venous lactates (The American Journal of Emergency Medicine  Volume 31, Issue 7, July 2013, Pages 1118–1120)

A review by some of the Lactate Doubters

A balanced perspective on lactate from NEJM (25494270)

Another article demonstrating the >=4.0 threshold is a good one (10.1097/CCM.0000000000000742)

A small study demonstrates that venous lactate may be even a better prognostic predictor than arterial (Effectiveness of arterial, venous, and capillary blood lactate as a sepsis triage tool in ED patients. Am J Emerg Med. 2014 doi: 10.1016/j.ajem.2014.11.003)


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  1. emcrit says

    A listener writes in:
    Great post !!

    While I listend to the podcast, I thought of Metformin as an often quoted cause for high lactate levels/acidosis. So I pulled up a Cochrane Review (Pubmed ID: 20393934). According to which:

    “Average lactate levels measured during metformin treatment were no different than for placebo or for other medications used to treat diabetes. In summary, there is no evidence at present that metformin is associated with an increased risk for lactic acidosis when prescribed under the study conditions.”

    So no baseline change in lactate in patients on M.
    But what about patients on M who are septic, how much of an elevated lactate could be atributed to the Metformin, potentially misleading our clinical judgment? (i.e. making the patient look worse than he really is) Or should we leave it out of the equation even in a septic patient and just interpret the lactate level as it is?

    I actually wanted to post this on your blog, but I wasnt sure if my e-mail would appear too, that’s why I write my comment per mail. If the e-mail of a blog response stays confidential, maybe a remark next to the box would be helpful!

    Thanks and keep up the great work, very inspiring!


    • emcrit says


      Intriguing thought. I have never seen any lit showing metformin in normal doses should alter the accuracy of lactate for sepsis. Overdose is a different story.


  2. Alex Stoker says

    Stupid question, I know, so I apologise in advance, but when you refer to the “show notes” on the podcast, is this just the entry here (on which I’m commenting), and which appears on my iPod? Or are there notes elsewhere?
    Sorry to be so dim, buty I often hear you talking about references in the handout/shownotes etc., and am never quite sure where I should be looking.



    • emcrit says


      It is a great question because I forgot to put the reference sheet up. It is here now. Show notes refer to the blog post that goes with each episode. So you went to the right place and the reason you could not find it is I had completely forgotten.

      Much thanks–Scott

  3. Alex Stoker says

    I was thinking in particular of the refs for venous vs arterial lactate, which I can’t seem to find. I’m not usre if this is me, the work computer and it’s odd access policies denying me a look at some pages, or something else.

    Thanks for the help!


  4. emcrit says

    Harry Writes:
    Hello Scott
    Great podcast on lactate. However two lurking questions remain.
    Firstly, what happened to the intro music?
    Secondly, carrying the notion of the elderly not being able to generate super high lactates secondary to poor catchecolamine reserve, what about the patient that is on beta blockade.

    intro music will come back in 2011

    your intuition regarding beta blockade is dead-on I think,
    some data supports this, such as
    however, I have no advice on how to lower the lactate cut-off in these pts to account for their beta-blockers

  5. Eric Sauvageau says


    The Lactate FAQ is great, but a nurse asked me if my Lactated Ringer’s (28mEq/L) can cause a false positive. Any knowledge on that?



  6. Li Jia says

    Hi Scott,

    I am going to give a talk regarding lactate as biomarker in sepsis on September 3rd. However, I found this article that raises serious concerns on the application of lactate clearance in sepsis management.

    Marik PE, Bellomo R, Demla V. Lactate clearance as a target of therapy in sepsis: a flawed paradigm. OA Critical Care 2013 Mar 01;1(1):3.

    Are you aware of it? Any comments?


  7. Shahzaib Ahmad says

    Probably a stupid question from a medical student, but if you have a septic patients being treated with inotropes, how do you know whether the lactate is from the drups or from hypo perfusion? Thanks in advance.

    • says

      Iionotropes as far I know won’t increase lactate significantly, you see that more with epinephrine which is more of a pressor, and that too only at higher doses. Basically if all other variables are improving, like MAP, urine output, CO etc. then lactate even if elevated should be down trending and that’s all that matters.

      • says

        lactate increase is from beta stimulation. has nothing to do with alpha/pressor effects of epi. you will see this phenomenon even more commonly with agents like albuterol that are pure beta.


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