This would be my practice too. Ron
Dr Ron Daniels Chair: UK Sepsis Trust CEO: Global Sepsis Alliance Sent on the move from my iPhone, excuse brevity! On 16 Nov 2012, at 01:17, "Nancy Brunner" <[email protected]> wrote: > 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! > > > > > > > mg.slrmc.org made the following annotations > --------------------------------------------------------------------- > "This message is intended for the use of the person or entity to which it is > addressed and may contain information that is confidential or privileged, > the disclosure of which is governed by applicable law. If the reader of this > message is not the intended recipient, you are hereby notified that any > dissemination, distribution, or copying of this information is strictly > prohibited. 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