Well stated 

Thanks, 

Mary Ann Daly, RN BSN CCRN DC 
Regional Clinical Initiative Lead-Sepsis and ICU Liberation (ABCDE)
Gordon and Betty Moore Foundation Grant 
Sutter Health Sacramento Sierra Region 
E-mail: [email protected] 
Blackberry: 916.200.5604   Office: 916.614.6370
‎"Every worthwhile accomplishment, big or little, has its stages of drudgery 
and triumph: a beginning, a struggle , and a victory" - Mahatma Gandi

-----Original Message-----
From: [email protected] 
[mailto:[email protected]] On Behalf Of Arnold, Ryan
Sent: Monday, November 19, 2012 7:36 AM
To: [email protected]
Subject: Re: [Sepsis Groups] Venous vs. Arterial Lactate


The majority of the subsequent effectiveness trials summarizing implementation 
of protocoled care utilized venous lactate alone as a trigger without 
verification of arterial lactate.  Additionally, targets of lactate clearance 
with serial assessments of lactate were and continued to be performed on venous 
samples.  

I think we need to evaluate the potential implications and unintended 
consequences of requiring a further invasive test (arterial sampling for 
lactate verification) and what effect that would have on multiple levels in the 
care of these patients. This could delay the initiation of timely resuscitation 
but more importantly, I fear this would serve as a further impediment to many 
clinicians even initiating testing.  

Unless there is a compelling study I am unaware of regarding the false 
elevation of venous lactate, I don't think we should advocate for a required 
arterial sampling to initiate such measures at this point.  

Ryan Arnold
Cooper University Hospital
Camden, NJ USA

> 
> 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&c
>> author=
>> true&cauthor_uid=9095008>, Touger
>> M<http://www.ncbi.nlm.nih.gov/pubmed?term=Touger%20M%5BAuthor%5D&caut
>> hor=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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