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&cauthor=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=true&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]>" <[email protected]<mailto:[email protected]>> 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! 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