I think this is old knowledge. Lactate is produced in the tissues during 
anaerobic conditions and first absorbed in the venous blood from Where it is 
cleared resulting in lower levels after the critical

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17 nov 2012 kl. 16:22 skrev "Nancy Brunner" <[email protected]>:

> We have observed a difference in the peripheral and arterial lactic
> acid-sometimes as much as 6 mm! 
> The ED will do a peripheral as a screen, but if it is elevated it would be
> verified with an arterial prior to subjecting a patient to a central line
> based on lactic acid value alone.
> Bryant Nguyen told me that the lactic acid in the EGDT study were all
> arterial.
> 
> Early Goal-Directed Therapy in the Treatment of Severe Sepsis and Septic
> Shock
> Emanuel Rivers, M.D., M.P.H., Bryant Nguyen, M.D., Suzanne Havstad, M.A.,
> Julie Ressler, B.S., Alexandria Muzzin, B.S., Bernhard Knoblich, M.D.,
> Edward Peterson, Ph.D., and Michael Tomlanovich, M.D. for the Early
> Goal-Directed Therapy Collaborative Group
> N Engl J Med 2001; 345:1368-1377November 8, 2001DOI: 10.1056/NEJMoa01030
> 
> Thanks,
> Nancy
> Nancy Brunner RN CCRN
> Boulder Community Hospital
> Boulder, Co
> vm 303-938-5128
> [email protected] 
> 
> -----Original Message-----
> From: [email protected]
> [mailto:[email protected]] On Behalf Of Kramer,
> George C.
> Sent: Monday, November 12, 2012 3:46 PM
> To: Shawver, Stephanie; [email protected]
> Subject: Re: [Sepsis Groups] Venous vs. Arterial Lactate
> 
> As a physiologist I would expect that venous lactate are almost always the
> same, maybe slightly higher, than arterial lactates.
> 
> Venous lactate could be higher with a very peripheral vein in very severe
> shock. So severe that you would not need a lactate to know you were in
> trouble.
> 
> Since peripheral tissues should not clear lactate much it is hard to imagine
> that peripheral could be lower than arterial.
> 
> Lactate is produced by anaerobic metabolism by many tissues when perfusion
> is inadequate and cleared by primarily be the liver. But on a minute to
> minute basis it changes slowly and should be the same in arterial blood and
> the blood that is coming 'around again' from a peripheral limb.
> 
> The literature supports very close correlation, with only small differences,
> below.  Arterial might be the gold standard, venous lactates should suffice
> and likely not worth the extra cost and extra risk of an arterial stick
> versus a venous blood sample.
> 
> I would be interested to know if anyone ever got lead the wrong way using
> venous lactate.
> 
> George Kramer, PhD
> UTMB
> Galveston
> 
> 
> 
> Ann Emerg Med.<http://www.ncbi.nlm.nih.gov/pubmed/9095008#> 1997
> Apr;29(4):479-83.
> Agreement between peripheral venous and arterial lactate levels.
> Gallagher
> EJ<http://www.ncbi.nlm.nih.gov/pubmed?term=Gallagher%20EJ%5BAuthor%5D&cautho
> r=true&cauthor_uid=9095008>, Rodriguez
> K<http://www.ncbi.nlm.nih.gov/pubmed?term=Rodriguez%20K%5BAuthor%5D&cauthor=
> true&cauthor_uid=9095008>, Touger
> M<http://www.ncbi.nlm.nih.gov/pubmed?term=Touger%20M%5BAuthor%5D&cauthor=tru
> e&cauthor_uid=9095008>.
> Source
> 
> Department of Emergency Medicine, Albert Einstein College of Medicine,
> Bronx, New York, USA. [email protected]
> 
> Abstract
> STUDY OBJECTIVE:
> 
> To test the hypothesis that measurements of peripheral venous lactate
> (V-LACT) can be substituted for arterial lactate (A-LACT) in predicting
> arterial hyperlactacidemia.
> 
> METHODS:
> 
> We conducted a prospective comparison of paired A-LACT and V-LACT
> measurements obtained from a convenience sample of 74 ED patients who
> presented to an urban, public teaching hospital, 70% of whom had abnormal
> A-LACT.
> 
> RESULTS:
> 
> Mean A-LACT and V-LACT were 2.8 mmol/L and 3.0 mmol/L, respectively. A-LACT
> and V-LACT were strongly correlated (r2 = .89). Simultaneous multivariate
> adjustment for tourniquet time and for time elapsed between drawing of
> A-LACT and V-LACT had no effect on this correlation. Although the mean
> difference between V-LACT and A-LACT was only .22 mmol/L, the range that
> included 95% of the disagreement between paired measurements in individual
> patients was-1.3 mmol/L to 1.7 mmol/L. When A-LACT and V-LACT levels were
> each divided into normal and abnormal (elevated) groups, V-LACT showed 94%
> sensitivity (95% confidence interval [CI], 83% to 99%), 57% specificity (95%
> CI, 34% to 78%), a positive likelihood ratio of 2.2, and a negative
> likelihood ratio of .1. A-LACT values were used as the criterion standard
> for these calculations.
> 
> CONCLUSION:
> 
> Correlation between A-LACT and V-LACT was high in this cohort of patients,
> but agreement is imperfect. The odds of arterial hyperlactacidemia appear to
> be reduced substantially by the finding of a normal V-LACT but are only
> marginally increased if the V-LACT is increased. Caution should be used in
> the routine substitution of V-LACT for A-LACT.
> 
> ----
> 
> Comparison between values of central venous and arterial lactate and
> standard base excess in shocked patients
> 
> VRP Pizzo, ASM Machado, A Toledo-Maciel, M Park and IT Velasco
> 
>   *
> 
> Author Affiliations<http://ccforum.com/content/9/S2/P44#>
> 
> Clinical Intensive Care Unit, School of Medicine, University of São Paulo,
> Brazil
> 
> For all author emails, please log on<http://ccforum.com/logon>.
> 
> Critical Care 2005, 9(Suppl 2):P44 doi:10.1186/cc3588
> 
> 
> The electronic version of this article is the complete one and can be found
> online at: <http://ccforum.com/content/9/S2/P44>
> 
> Published:      9 June 2005
> 
> 
> ©
> 
> Introduction
> 
> Hemodynamic optimization based on tissue perfusion markers is a strategy
> considered adequate for the management of patients in shock in ICUs.
> 
> Objectives
> 
> To evaluate the variability and correlation between venous and arterial
> standard base excess (SBE) and lactate samples.
> 
> Materials and methods
> 
> The analysis of lactate levels was performed and the SBE obtained from the
> same blood of central venous and arterial samples of 115 patients. We
> compared these measurements (Wilcoxon signed rank test), and determined the
> correlation between these variables (Spearman rank order correlation).
> 
> Results
> 
> There was a statistically significant difference between the value of venous
> SBE: -4.3 mEq/l (-7.4 to -0.9) as compared with the arterial value: -3.2
> (-6.9 to 0), P < 0.001; but there was no difference between the venous
> lactate: 1.67 mmol/l (1.22–2.22) as compared with the arterial lactate: 1.56
> (1.22–2.22), P = 0.792. The correlation coefficients were 0.929 to venous
> and arterial SBE (bias: 0.09) and 0.826 to lactate (bias: -0.024).
> 
> Discussion
> 
> The agreement between venous and arterial samples permits one to use the
> central venous lactate level similar to the arterial level and their
> variations. For SBE, the module value was different between the
> measurements, otherwise their variation has good correlation. As these
> variations guide the clinical decision, we can use it as a goal of
> hemodynamic monitoring.
> 
> Conclusion
> 
> It is possible to guide hemodynamic monitoring in shock patients using
> values of central venous lactate and variations of SBE.
> 
> From: <Shawver>, Stephanie
> <[email protected]<mailto:[email protected]>>
> Date: Friday, November 9, 2012 10:15 AM
> To:
> "[email protected]<mailto:[email protected].
> org>"
> <[email protected]<mailto:[email protected].
> org>>
> Subject: [Sepsis Groups] Venous vs. Arterial Lactate
> 
> Colleagues,
> 
> Our facility has recently implemented point of care arterial lactate testing
> as an extension of point of care ABG’s. However, all of our sepsis protocols
> are built around the assessment of venous lactate. We are starting to see
> practitioners rely on the arterial lactate rather than the venous lactate
> and / or reassess an elevated arterial lactate with a venous lactate or vice
> versa. It is a concern of mine that if a practitioner sees a normal arterial
> lactate and doesn’t assess the venous lactate as well – it could be missed
> that the venous lactate is elevated (as I understand it, in sepsis the
> venous lactate will be elevated before the arterial lactate becomes
> elevated). We have had a couple cases where the practitioner did not
> activate the sepsis protocols based on a normal arterial lactate, only to
> find out later the venous lactate was elevated and EGDT was delayed.
> 
> I have looked into the research and cannot find much about the use of
> arterial lactates in sepsis & all the SSC / EGDT studies focus on the use of
> venous lactate levels. Have any of you ran into this in your sepsis programs
> and if so, how did you address it? And if anyone out there can point me to
> research about arterial vs. venous lactate in sepsis? Any
> thoughts/feedback/suggestions are welcome! Thank you!
> 
> 
> Stephanie Shawver BSN, RN
> SLMV Sepsis  and Stroke Coordinator
> St. Luke's Magic Valley
> 801 Pole Line Road West  | Twin Falls, ID 83301
> Office: (208) 814.4030   |  Email:
> [email protected]<mailto:[email protected]>
>  Suspect stroke? Think FAST!
> Facial droop, Arm drift, Speech impairment, Time is brain - this is an
> emergency!
> 
> 
> 
> 
> 
> 
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