The other day, the supervising Consultant asked me to look up the difference between arterial and venous lactate. This was a direct result of my big mouth as I was the one who raised this point, since a lot of the articles that talked about lactate made a point to mention that it was “arterial” lactate, whereas some articles just said “lactate”.
The question is, are they really any different?
To answer this question, I googled it! (sorry pubmed lovers, I’m a “google” chick!)
And Here is what I got:
There are 3 studies that compare arterial and central venous lactate in patients in shock/cardiac arrest (J Resuscitation 2008;03:055 , Emerg Med J 2006;23:622-624, Crit Care 2005;9:44). They all came to the same conclusion; the levels are closely correlated. The first one even added that the levels more closely correlated if arterial lactate value was >5mmol/L.
I also came across a nice website (that is Google’s benefit ), called www.emedmag.com , in which there’s an article discussing the most important differences in values of ABGs and VBG, AGs, and finally, lactate.
This website came to the conclusion that since an elevated venous lactate (1.6 mmol/L or greater) is 100% sensitive and 89% specific in predicting elevated arterial lactate level, then a normal venous lactate should be enough, but an elevated venous lactate necessitates that an arterial lactate should be obtained. It cites a 1996 study by Younger of 48 ED patients as a basis for this conclusion. These results were bolstered by a 2000 study by Lavery on 375 hypovolemic patients.
While discussing the findings of my mini-search with my colleagues and seniors, we came to a discussion; is lactate higher in arterial blood or venous blood?
Logic says that it should be higher in venous blood than in arterial, as it is always a result of poor tissue perfusion, and is cleared by the liver, right?
NOT EXACTLY!
According to “The ICU Book” by Paul Marino; Lactate level is not indicative of poor tissue perfusion, but rather is a method of detecting global dysoxia. However, it sometimes indicates other things, such as hepatic insufficiency, thiamine deficiency, severe sepsis (as a direct result of endotoxins rather than O2 deprivation) and, finally, intracellular alkalosis.
It’s interesting how a discussion can clarify some of your most basic concepts!
Friday, April 23, 2010
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