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Article

January 2017

Lactate measurement: arterial versus venous blood sampling

By Chris Higgins
Lactate Infection/sepsis
Summary This article evaluates venous blood as an alternative to arterial blood for lactate measurement, highlighting the general considerations related to each of the three types of venous blood which can be used for lactate measurement: peripheral venous blood, central venous blood and mixed venous blood.

Lactate is the end product of the metabolic process of glucose utilization, known as anaerobic glycolysis, which occurs in the cytoplasm of all cells. In well-oxygenated tissues this lactate is metabolized further, but if tissues are inadequately oxygenated, lactate accumulates locally and blood concentration increases. 

As a blood marker of tissue hypoxia, lactate measurement has long-established clinical utility, most notably in the assessment and monitoring of acutely/critically ill patients and major trauma victims in emergency room and intensive care units. 

Arterial blood is the gold standard sample for lactate measurement, but a reading of the literature and current practice suggests that venous blood is considered an acceptable alternative. 

The purpose of this article is to review the evidence base for the notion that venous blood lactate concentration approximates to that in arterial blood, and thereby, that venous blood is an acceptable alternative sample. 

Until fairly recently the evidence base was sparse and somewhat conflicting, but eight relevant studies have been published since 2011, and these will be a focus of this article. 

The article begins with a general discussion of the distinction between arterial blood and three types of venous blood that could be used for lactate measurement: peripheral venous blood, central venous blood and mixed venous blood. 

Blood sampling from different sites – some general considerations


Arterial blood is constant in its lactate concentration irrespective of the site of sampling. It is considered the ”gold standard” sample for assessment of lactate measurement because it is derived from mixed venous blood and thus provides a representative sum of all sources of tissue lactate production.

By contrast, the concentration of lactate in venous blood could, theoretically at least, vary depending on the site of sampling because of variation, both physiological and pathological, in local tissue lactate production.

Early studies [1,2] that established the link between reduced blood perfusion and increased lactate – and thereby the clinical utility of lactate measurement – were conducted on arterial blood; and lactate reference range was first established using arterial blood. 

Arterial blood remains the gold standard sample for assessment of patient acid-base and oxygenation status. The blood gas analyzers used for these assessments now commonly have the capacity for simultaneous measurement of lactate in the same arterial sample.

Arterial blood is usually sampled by needle puncture of a peripheral artery, most commonly the radial artery in the wrist, the brachial artery in the arm or femoral artery in the groin. Compared with venipuncture (the procedure used to obtain peripheral venous blood), arterial puncture is technically more demanding and certainly more painful and hazardous for the patient [3,4]. 
 
Specialist training in arterial blood collection is essential for patient safety and comfort, so that in some countries medically qualified staff have sole responsibility for the procedure. By contrast, venipuncture is a very commonplace procedure that can be easily and safely performed, after minimal training, by ancillary staff with no medical or nursing education. 

In intensive care and operating room settings catheterization of radial or femoral artery, principally for continuous arterial blood pressure monitoring, offers an alternative means of safely and conveniently sampling arterial blood for a small minority of patients. 
 
However, insertion of an arterial catheter is itself a technically difficult procedure [5] associated with risk of serious complications [6,7]. Novel, non-invasive technology for continuous monitoring of arterial blood pressure [8] is set to reduce the necessity for arterial catheterization in the future, so that this mode of sampling arterial blood could well become even less common. 

Given the difficulties and limitations associated with sampling arterial blood, it would be logistically attractive for clinical staff, as well as safer and more comfortable for patients, if venous blood could be used for lactate measurement. 

By far the most common venous blood sample is that obtained by needle puncture of a peripheral (superficial) vein in the forearm (at the antecubital fossa) or back of the hand; this is peripheral venous blood and must be distinguished from central venous blood and mixed venous blood. 
 
Central venous blood is sampled via a central venous catheter (CVC). CVCs are commonly inserted to intensive care patients and less commonly to emergency room patients; they provide vascular access for delivery of drugs, blood transfusion and fluid therapy. 
 
In addition, they allow monitoring of central venous pressure, central venous oxygen saturation and, importantly for this article, the means for easy sampling of venous blood for routine laboratory testing, including measurement of lactate concentration. 

CVCs are usually inserted cutaneously via the jugular vein in the neck or subclavian vein in the upper chest to one of the two largest central veins, called the superior vena cava. This vessel drains all venous blood from the upper half of the body to the right atrium of the heart. 
 
The tip of the CVC, from which blood is sampled, is ideally sited in the superior vena cava close to its junction with the right atrium. Central venous blood is thus the mixed venous blood from the upper half of the body. Since it does not include venous blood from the lower half of the body, which is drained to the right atrium via the inferior vena cava, central venous blood cannot be considered truly mixed venous blood. 

Mixing of venous blood drained from the lower and upper halves of the body occurs in the right atrium and right ventricle. Only blood flowing from the right ventricle to the lungs via the pulmonary artery is truly mixed venous blood. Mixed venous blood can only be sampled by catheterization of the pulmonary artery, a procedure used in critical care for hemodynamic monitoring of selected patients. 
 
The value of pulmonary artery catheterization has been challenged and is now less frequently used than was once the case [9], but for those critically ill patients with a pulmonary artery catheter there remains the option of conveniently sampling venous blood, specifically mixed venous blood, for lactate measurement. 

To summarize, for the vast majority of patients including most in the emergency room, the only available venous sample for lactate measurement is peripheral venous blood. But for critically ill and trauma patients being cared for in intensive care units and occasionally in the emergency room, who have either a central venous line or pulmonary artery catheter fitted, it is more convenient to sample central venous blood or mixed venous blood than to sample peripheral venous blood. 
 

Comparing arterial and venous lactate concentration – study design


A number of studies [11-24] that test the validity of using venous blood in lieu of arterial blood for lactate measurement have been conducted since the first was published in 1987 [10]. More than half of these studies [17-24] are recently published (in the past 5 years), signifying that the issue remains relevant and to some extent, unresolved. 

In essence, all these studies have a common and simple design based on the assumption that arterial blood is the gold standard sample. Lactate concentration of venous blood is compared with lactate concentration of arterial blood collected from the same patient at the same time, among a defined cohort of intensive care or emergency room patients. (One study [17] includes a small cohort of healthy controls.) 

Some of the important differences in detail of the studies are highlighted in Table I, which reveals, for example, that the type of venous blood used to compare with arterial blood differs. Whilst most studies [11,13-15,17,19-24] compare arterial and peripheral venous lactate, four studies [10,16-18] examine the relationship between arterial and central venous lactate, and just two, the relationship between arterial and mixed venous lactate [10,12]. 

Three studies [18,20,23] are retrospective in nature (lactate results being retrieved from laboratory records); all others are prospective in design. The studies vary greatly in terms of the size of study cohort; the smallest is seven pediatric intensive care patients [12] and the largest is 232 adult emergency room patients retrospectively selected on the basis of increased lactate. [20]. 
 
The number of paired lactate results (arterial and venous) available for statistical analysis in each study also varies greatly, ranging from 20 [12] to 673 [18]. The studies vary somewhat in the method used to determine arterial and venous lactate concentration, but in eight of ten studies published since 2000, blood gas analyzers, often sited at the point of care (ICU or ED), were used.
 
TABLE I: Study design and characteristics
 

Study date (Ref)

Retrospective (R) or Prospective (P)

Number of Patients studied

(ICU or ED)

Venous sample

Peripheral (PV) Central (CV) or Mixed (MV)

Number of pairs

Time between sampling arterial and venous blood

Method of lactate measurement

1987 [10]

P

35 adults

ICU

CV & MV

50 for CV

104 for MV

”Simultaneous”

Enzymatic central laboratory

1988 [11]

P

20 adults

ICU

PV

20

”Simultaneous”

Enzymatic central laboratory

1994 [12]

P

7 children

ICU

MV

21

”Simultaneously as possible”

Enzymatic central laboratory

1996 [13]

P

48 adults

ED

PV

48

Mean time 6 ±5.5 mins

“Lactimeter”

1997 [14]

P

69 adults

ED

PV

69

 

<5 mins

Clin Chem analyzer

2000 [15]

P

221 adult trauma victims

ED

PV

221

<2 mins

Blood Gas analyzer

 

2006 [16]

P

110 adult

ICU

CV

167

”Simultaneously as possible”

Blood Gas analyzer

2011 [17]

P

32 adult ICU patients

10 healthy controls

PV & CV

 

77 for PV

80 for CV

 

”Simultaneous”

Enzymatic central laboratory

2012 [18]

R

188 adults

ICU

CV

673

All <30 mins

Median time 2 mins

Blood Gas analyzer

2013 [19]

P

72 adults

ED

PV

72

<5 mins

Blood Gas analyzer

2014 [20]

R

232 adults

ED

All with raised lactate (³2.0 mmol/L)

PV

232

Median 22 mins

(IQR 13-36 mins)

 

Blood Gas analyzer

2015 [21]

P

103 adults

ED

 

PV

103

Mean time 8 ±2 mins

Point-of-care lactate analyzer

2015 [22]

P

26 adults ICU

PV

102

”Simultaneous”

Blood Gas analyzer

2016 [23]

R

60 children with sepsis

PICU

PV but not made absolutely clear

60

<60 mins

Blood Gas analyzer

 

 

2016 [24]

P

68 adults

with sepsis

ICU

PV

68

Not recorded

Blood Gas analyzer

 

Comparing arterial and venous lactate concentration – study results


There is in general a commonality among these studies in the way the primary data (paired arterial and venous lactate concentrations) are statistically manipulated and presented. In all but three studies, overall correlation between arterial and venous values is determined with generation of Pearson’s correlation coefficient (r or r2) for the data set.
 

The authors of three studies [15,19,24] provide a derived regression equation that allows calculation of arterial lactate concentration from measured venous lactate concentration. 

In common with correlation analysis, nearly all studies employ Bland-Altman analysis to determine agreement between arterial and venous values. This allows generation of mean difference (bias) between venous and arterial values and 95 % limits of agreement (LOA), which defines the precision of the bias. 

Results of studies comparing arterial and peripheral venous lactate are provided in Table II. Results of studies comparing arterial and central venous lactate are provided in Table III; and finally results of studies comparing arterial and mixed venous lactate are provided in Table IV. 

TABLE II: Study results – arterial versus peripheral venous

Study Date [Ref]

No. of pairs

Arterial lactate range and mean

(mmol/L)

Mean difference

Venous – Arterial (mmol/L)

95 % limits of agreement

(mmol/L)

Correlation r, r2

(p-value)

1988 [11]

20 pairs

1.0-10.5

Mean not recorded

Not recorded

Not recorded

r = 0.99

(p<0.001)

1996 [13]

48 pairs

0.3-7.6

only 13 pairs abnormal (>1.6 mmol/L)

0.18

–0.012 to 0.372

Agreement less good at higher concentration

r = 0.71

(p<0.001)

1997[14]

69 pairs

0.5-11.5

Mean 2.8

0.22

–1.3 to 1.7

r = 0.94

r2 = 0.89

2000 [15]

221 pairs

0.5-18.0

Mean 3.11

0.32

Not recorded

 

r = 0.94

(p <0.0001)

Regression eqtn allows prediction of arterial lactate (AL) from venous lactate (VL)

AL = 0.076 + 0.889 × VL)

2011[17]

77 pairs

0.8-4.8

Mean 1.55

0.35

–0.7 to 1.4

r = 0.79

(p<0.0001)

2013 [19]

72 pairs

0.4-15.0

Mean 2.15

(Only 37 of 72 pairs abnormal lactate i.e. >1.6 mmol/L)

0.268

–0.4 to1.1

r2 = 0.94

Regression eqtn allows prediction of arterial lactate (AL) from venous lactate (VL)

AL = –0.259 + 0.997 ×VL

2014 [20]

232 pairs

 

1.0-13.2

Mean 2.45

All abnormal (venous lactate > 2.0 mmol/L)

1.06

–1.53 to 3.66 mmol/L

Not recorded

2015 [21]

103 pairs

 

0.6-10.0

Mean 2.03

0.48

Not recorded

r = 0.96

(p<0.0001)

2015 [22]

102 pairs

1.5-4.3

Mean 2.3

0.3

–1.8 to 2.4

r =0.972

(p<0.001)

2016 [23]

55 pairs

Not recorded

Approx. range 0.5-13.5

0.8

–1.9 to 1.9

Not recorded

2016 [24]

68 pairs

0.5-17.0

(Interquartile range 1.2-4.1)

Mean 2.1

0.66

–2.3 to 3.66

r = 0.934

(p<0.001)

Regression eqtn allows prediction of arterial lactate (AL) from venous lactate (VL)

AL = –0.236 + 0.934 × VL

 

TABLE III: Study results – arterial versus central venous

Study Date [Ref]

No. of pairs

Arterial lactate range and mean

(mmol/L)

Mean difference

Venous – Arterial (mmol/L)

95 % limits of agreement

(mmol/L)

Correlation r, r2

(p-value)

1987 [10]

50 pairs

0.39-9.71

Mean 2.32

0.029

Maximum difference 0.5 mmol/L

Not recorded

 

r = 0.995

(p <0.001)

2006 [16]

167 pairs

0.38-6.51

Mean 1.13

0.08

–0.27 to 0.42

Not recorded

2011 [17]

80 Pairs

0.8-4.8

Mean 1.55

0.08

–1.4 to 1.2

r = 0.84

(p<0.0001)

2012 [18]

673 pairs

 

0.6-26.6

Mean 3.2

0.04

–1.2 to 1.2

r2 = 0.97

(p<0.0001)

 

TABLE IV: Study results arterial versus mixed venous 

Study Date [Ref] 

No. of pairs

Arterial lactate range and mean

(mmol/L)

Mean difference

Venous – Arterial (mmol/L)

95 % limits of agreement

(mmol/L)

Correlation r, r2

(p-value)

1987 [10]

104 pairs

0.46-12.99

Mean 2.63

0.03

Not recorded

Max absolute difference 0.82

r = 0.998

(p <0.0001)

1994 [12]

21 pairs

0.92-11.1

Mean 2.97

0.02

–0.2 to 0.24

r = 0.995

 

 

It is apparent from these tables that venous blood lactate concentration correlates very strongly with arterial lactate concentration. The results of three early studies [10-12] suggest near-perfect correlation (r 0.99) with almost all other studies reporting correlation coefficients in the range of 0.84-0.98. 

All studies reveal a bias, with venous blood lactate tending to be higher than arterial blood lactate. The magnitude of this bias, however, varies significantly between studies, with mean difference (venous lactate – arterial lactate) ranging from 0.02 mmol/L in one study [12] to 1.06 mmol/L in another [20]. Likewise, the 95 % limits of agreement (LOA) vary across studies.

The best agreement in terms of 95 % LOA is –0.22 to 0.24 [12] and the worst, –2.33 to 3.66 [24]. The results of this last study [24] imply that in 95 % of cases arterial lactate could be anywhere between 2.33 mmol/L less than venous lactate value and 3.66 mmol/L greater than that venous value; clearly very poor agreement. 

Comparing the bias and 95 % LOA results for all studies suggest that agreement between arterial lactate and venous depends crucially on the site of venous blood sampling. Peripheral venous lactate agreement appears not as good as that for central venous lactate or mixed venous lactate. 

And there is limited evidence from two early, relatively small studies [10,12] that mixed venous blood lactate reflects arterial blood lactate better than either peripheral or central venous blood lactate. This empirical evidence of very close agreement between mixed venous lactate and arterial lactate is not surprising since arterial blood is derived directly from mixed venous blood. 

Indeed, one of the studies [12] that confirms the closeness of this agreement was conceived and designed over 20 years ago in order to justify the use of arterial blood for lactate measurement in lieu of what the authors considered to be the ideal reference sample, mixed venous blood. 

Variable agreement between peripheral venous and arterial lactate

 

There is evidence from a number of studies [13,17,20,23,24] that agreement between peripheral venous and arterial lactate is satisfactory at normal lactate concentration, but declines as lactate concentration increases. 

Nascente et al [17] investigated the relationship between peripheral venous lactate and arterial lactate in a cohort of 10 healthy individuals with normal lactate and found excellent correlation (r = 0.90) and very close agreement (mean bias 0.07 mmol/L, 95 % LOA –0.3 to +0.2). 

This close agreement between peripheral venous and arterial lactate is not evident in study patients, particularly if the study cohort includes a high proportion of patients with abnormal lactate. The study [20] returning the largest bias and the second broadest LOA is unique in that the patient population studied all had a raised lactate (venous lactate >2.0 mmol/L). 

Younger et al [13] acknowledge that results of their study of 48 patients of whom only 16 had a raised lactate show ”greater spread (less agreement) at higher lactate concentration”. 

Samaraweera et al [23] found close agreement between venous (presumed peripheral) and arterial for those samples with lactate <2.0 mmol/L, but poor agreement above this concentration. 

Theerawith et al [24] found that excluding data for 20 patients with highest lactate (>4.0 mmol/L) had the effect of reducing mean bias from 0.66 to 0.38, and reducing 95 % LOA from (–2.33 to 3.66) to (–1.19 to 1.95). 

Central venous lactate superior to peripheral venous lactate

The poor agreement between peripheral venous lactate and arterial lactate at higher lactate concentration has prompted the authors of a number of recent studies [14,17,20,23,24] to advise caution in the routine substitution of peripheral venous blood lactate for arterial blood lactate. 

To summarize this cautionary view: peripheral venous blood lactate concentration cannot be assumed to be clinically indistinguishable from arterial blood lactate concentration, unless it is normal or only marginally increased (<2.0 mmol/L). 

By contrast authors of all studies comparing central venous lactate and arterial lactate [10,16,17,18] have no reservations in stating that central venous lactate and arterial lactate agree sufficiently well, irrespective of lactate concentration, for them to be considered interchangeable for all practical purposes. 

The study by Nascente et al [17] of 32 ICU patients with severe sepsis/septic shock is unique in comparing agreement of arterial lactate with venous blood from both a peripheral and central venous site in the same patient. Their data, derived from 238 samples, reveals better correlation, smaller bias, and narrower 95 % LOA for central venous compared with that for peripheral venous site samples. 

They demonstrate that in terms of clinical management central venous lactate is more concordant with arterial lactate than peripheral venous lactate. They conclude that ”in septic patients central venous lactate may replace arterial lactate […] the same cannot be said of peripheral venous lactate because despite reasonable correlation with arterial lactate, it tends to overestimate arterial lactate, which may lead to unnecessary therapeutic interventions for such patients”.  

Samaraweera et al [23] suggest that if peripheral venous blood lactate is >2.0 mmol/L, then arterial blood should be sampled to confirm the result.

Although retrospective in design, the study by Reminiac et al [19] provides the most compelling evidence of the notion that central venous lactate and arterial lactate are interchangeable. Their study is one of the largest in terms of patients studied and by far the largest in terms of the number of paired (venous and arterial) samples for lactate measurement. 

The studied population comprises a very high proportion with abnormal lactate, across a wide concentration range. Their analysis clearly indicates that irrespective of the lactate concentration, central venous lactate is sufficiently close to arterial lactate for the two values to be considered clinically interchangeable. 

Summary

Arterial blood is considered the ”gold standard” sample for lactate measurement. For a number of reasons venous blood is a more attractive sample. Justification for current routine use of venous blood at some institutions is based on a few studies conducted over 20 years ago that revealed excellent correlation between arterial and venous lactate concentration. 

Recent study conducted in the past 5 years has confirmed this good correlation, but revealed that the site of venous blood sampling is an important factor in the extent to which venous lactate and arterial lactate concentration agree. If venous blood is sampled from a central vein or pulmonary artery, venous lactate concentration can be considered a clinically acceptable approximation of arterial lactate concentration. 

A more nuanced view is indicated if venous blood is sampled from a peripheral vein. Under these circumstances, evidence suggests that venous blood lactate concentration is probably a clinically acceptable approximation of arterial blood lactate concentration if lactate is normal or marginally increased (<2.0 mmol/L), but may not be if lactate concentration is increased above this level. 

Caution is advised in making the assumption that peripheral venous lactate concentration is the same as arterial lactate concentration, particularly among patients with markedly increased lactate. 

References
  1. Broder G, Weil MH. Excess lactate: an index of reversibility of shock in human  patients. Science 1964; 143: 1457-59.
  2. Cady L, Weil M, Afifi A et al. Quantitation of severity of critical illness with special reference to blood lactate. Crit Care Med 1973; 1,2: 75-80.
  3. Okeson G, Wullbrecht P. The safety of brachial artery puncture for arterial blood sampling. Chest 1998; 114: 748-51.
  4. Giner J, Casan P, Belda J et al. Pain during arterial puncture. Chest 1996; 110: 1443-45. 
  5. Eisen L, Miami T, Berger J et al. Gender disparity in failure rate of arterial catheter attempts. J Intensive Care 2007; 22: 166-72.
  6. Scheer B, Perel A, Pfeifer U. Clinical review: complications and risk factors of peripheral arterial catheters used for haemodynamic monitoring in anaesthesia and intensive care medicine. Crit Care 2002; 6: 199-204.
  7. Garland A, Connors A. Indwelling arterial catheters in the intensive care unit: necessary and beneficial, or a harmful crutch? Am J Respir Crit Care Med 2010; 182: 133-37
  8. Jagadeesh A, Singh N, Mahankali S. A comparison of a continuous noninvasive arterial pressure monitor with an invasive arterial blood pressure monitor in the cardiac surgical ICU. Annals of Cardiac Anaesthesia 2012; 15,3: 180-84.
  9. Marik P. Obituary: pulmonary artery catheter 1970 to 2013. Ann Intensive Care  2013; 3: 38.
  10. Weil M, Michaels S, Rackow E. Comparison of blood lactate concentrations in central venous, pulmonary artery, and arterial blood. Crit Care Med 1987; 15,5: 489-90.
  11. Adams J, Hazard P. Comparison of blood lactate concentrations in arterial and peripheral venous blood. Crit Care Med 1988;16,9: 913-14.
  12. Murdoch I, Turner C, Dalton R. Arterial or mixed venous lactate measurement in critically ill children. Is there a difference? Acta Paediatr 1994; 83: 412-13.
  13. Younger J, Falk J, Rothrock S. Relationship between arterial and peripheral venous lactate levels. Acad Emerg Med 1996; 3,7: 730-34
  14. Gallagher E, Rodriguez K, Touger M. Agreement between peripheral venous and arterial lactate levels. Ann Emerg Med 1997; 29,4: 479-83.
  15. Lavery R, Livingston D, Tortella B. The utility of venous lactate to triage injured patients in the trauma center. J Am Coll Surg 2000; 190: 656-64.
  16. Middleton P Kelly A-M Brown J et al. Agreement between arterial and central venous values for pH, bicarbonate, base excess, and lactate. Emerg Med J 2006; 23: 622-24 
  17. Nascente A, Assuncao M, Janaina A et al. Comparison of lactate values obtained from different sites and their clinical significance in patient with severe sepsis. Sao Paulo Med J 2011; 129,1: 11-16.
  18. Reminiac F, Saint-Etienne C, Runge I et al. Are central venous and arterial lactate interchangeable. A human retrospective study. Anesth Analg 2012; 115,3: 605-10.
  19. Mikami A, Ohde S, Deshpands G et al. Can we predict arterial lactate from venous lactate in the ED. Am J Emerg Med 2013; 31: 118-20.
  20. Bloom B Pott J Freund M et al. The agreement between abnormal venous and arterial lactate in the ED: a retrospective chart review. Am J Emerg Med 2014; 32: 596-600.
  21. Contenti J, Corraze H, Lemoel F et al. Effectiveness of arterial, venous and capillary blood lactate as a sepsis triage too in ED patients. Am J Emerg Med 2015; 33: 167-72.
  22. Matti Y, De Freitas F et al. Is venous blood drawn from femoral access adequate to estimate the central venous oxygen saturation and arterial lactate levels in critically ill patients? Rev Bras Ter Intensiva 2015; 27,4: 340-46.
  23. Samaraweera S, Gibbons B, Gour A et al. Arterial vs lactate: a measure of sepsis in children. Arch Diseases in Childhood 2016;101,Suppl 1: A292-293 (poster abstract only)
  24. Theerawit P, Petvicharn C, Tahngsujaritvigit V et al. The correlation between arterial lactate and venous lactate in patients with sepsis and septic shock. J Intensive Care Med 2016. Published on line (ahead of print publication) August 8th 2016. doi: 10.1177/0885066616663169.
+ View more
References
  1. Broder G, Weil MH. Excess lactate: an index of reversibility of shock in human  patients. Science 1964; 143: 1457-59.
  2. Cady L, Weil M, Afifi A et al. Quantitation of severity of critical illness with special reference to blood lactate. Crit Care Med 1973; 1,2: 75-80.
  3. Okeson G, Wullbrecht P. The safety of brachial artery puncture for arterial blood sampling. Chest 1998; 114: 748-51.
  4. Giner J, Casan P, Belda J et al. Pain during arterial puncture. Chest 1996; 110: 1443-45. 
  5. Eisen L, Miami T, Berger J et al. Gender disparity in failure rate of arterial catheter attempts. J Intensive Care 2007; 22: 166-72.
  6. Scheer B, Perel A, Pfeifer U. Clinical review: complications and risk factors of peripheral arterial catheters used for haemodynamic monitoring in anaesthesia and intensive care medicine. Crit Care 2002; 6: 199-204.
  7. Garland A, Connors A. Indwelling arterial catheters in the intensive care unit: necessary and beneficial, or a harmful crutch? Am J Respir Crit Care Med 2010; 182: 133-37
  8. Jagadeesh A, Singh N, Mahankali S. A comparison of a continuous noninvasive arterial pressure monitor with an invasive arterial blood pressure monitor in the cardiac surgical ICU. Annals of Cardiac Anaesthesia 2012; 15,3: 180-84.
  9. Marik P. Obituary: pulmonary artery catheter 1970 to 2013. Ann Intensive Care  2013; 3: 38.
  10. Weil M, Michaels S, Rackow E. Comparison of blood lactate concentrations in central venous, pulmonary artery, and arterial blood. Crit Care Med 1987; 15,5: 489-90.
  11. Adams J, Hazard P. Comparison of blood lactate concentrations in arterial and peripheral venous blood. Crit Care Med 1988;16,9: 913-14.
  12. Murdoch I, Turner C, Dalton R. Arterial or mixed venous lactate measurement in critically ill children. Is there a difference? Acta Paediatr 1994; 83: 412-13.
  13. Younger J, Falk J, Rothrock S. Relationship between arterial and peripheral venous lactate levels. Acad Emerg Med 1996; 3,7: 730-34
  14. Gallagher E, Rodriguez K, Touger M. Agreement between peripheral venous and arterial lactate levels. Ann Emerg Med 1997; 29,4: 479-83.
  15. Lavery R, Livingston D, Tortella B. The utility of venous lactate to triage injured patients in the trauma center. J Am Coll Surg 2000; 190: 656-64.
  16. Middleton P Kelly A-M Brown J et al. Agreement between arterial and central venous values for pH, bicarbonate, base excess, and lactate. Emerg Med J 2006; 23: 622-24 
  17. Nascente A, Assuncao M, Janaina A et al. Comparison of lactate values obtained from different sites and their clinical significance in patient with severe sepsis. Sao Paulo Med J 2011; 129,1: 11-16.
  18. Reminiac F, Saint-Etienne C, Runge I et al. Are central venous and arterial lactate interchangeable. A human retrospective study. Anesth Analg 2012; 115,3: 605-10.
  19. Mikami A, Ohde S, Deshpands G et al. Can we predict arterial lactate from venous lactate in the ED. Am J Emerg Med 2013; 31: 118-20.
  20. Bloom B Pott J Freund M et al. The agreement between abnormal venous and arterial lactate in the ED: a retrospective chart review. Am J Emerg Med 2014; 32: 596-600.
  21. Contenti J, Corraze H, Lemoel F et al. Effectiveness of arterial, venous and capillary blood lactate as a sepsis triage too in ED patients. Am J Emerg Med 2015; 33: 167-72.
  22. Matti Y, De Freitas F et al. Is venous blood drawn from femoral access adequate to estimate the central venous oxygen saturation and arterial lactate levels in critically ill patients? Rev Bras Ter Intensiva 2015; 27,4: 340-46.
  23. Samaraweera S, Gibbons B, Gour A et al. Arterial vs lactate: a measure of sepsis in children. Arch Diseases in Childhood 2016;101,Suppl 1: A292-293 (poster abstract only)
  24. Theerawit P, Petvicharn C, Tahngsujaritvigit V et al. The correlation between arterial lactate and venous lactate in patients with sepsis and septic shock. J Intensive Care Med 2016. Published on line (ahead of print publication) August 8th 2016. doi: 10.1177/0885066616663169.
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Chris Higgins

has a master's degree in medical biochemistry and he has twenty years experience of work in clinical laboratories.

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