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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