Venous blood lactate concentration as a predictor of intestinal viability in horses with acquired indirect inguinal hernia.

To measure the correlation and agreement between arterial and peripheral venous blood lactate in the emergency room and to assess the predictive value of lactate for the occurrence of cardiac arrest. This was a retrospective cohort study involving 784 patients from January 1, 2020, to July 31, 2021, in the Emergency Room of the First Affiliated Hospital of Xinjiang Medical University. General information, vital signs, clinical symptoms, and laboratory findings of the patient were collected. Linear regression was used to analyze the correlation between arterial and venous blood lactate, Bland–Altman plots were drawn to assess the concordance of (arterial-venous) serum lactate concentrations, and the predictive value of arterial and venous lactate for the occurrence of cardiac arrest was assessed by using the receiver operating characteristic curve (ROC). A total of 784 emergency room patients were included in the study, of whom 384 experienced cardiac arrest and 400 had no cardiac arrest. Arterial and venous lactate univariate linear regression analysis, correlation coefficient r = 0.80, linear equation Y(venous blood lactate) = 0.729 + 0.960*X(arterial blood lactate), and had statistical significance (P < 0.001); arterial blood (lactate) and venous blood (lactate) were -0.548 (95%CI -0.774 ~ -0.322 mmol/L), and the upper and lower limits of the 95% limits of agreement (LoA) were 5.777 (95%CI 5.390 ~ 6.163 mmol/L) and -6.872 (-7.2590 ~ -6.4855 mmol/L), indicating that the consistency of arterial blood lactate and venous blood lactate is poor and statistically significant (P < 0.001). The results of this study show that venous and arterial blood lactate levels are not identical, but are highly correlated and are important predictors of cardiac arrest in emergency room patients.

Fingertip and venous blood lactate concentrations were determined pre-exercise and after 4-min bouts of treadmill running at 2.69, 3.13, 3.58 and 4.03 m s-1 in 14 normal healthy volunteers. A 1-min rest period intervened each exercise period, and was used for the simultaneous sampling of fingertip and venous blood. Compared to pre-exercise, fingertip and venous blood lactate (BLa) concentrations increased significantly (P < 0.05) in a progressive pattern with increasing exercise intensity. Fingertip BLa concentrations were significantly higher (P < 0.05) than venous blood prior to exercise and in response to all four running speeds. Treadmill speed, heart rate and oxygen consumption were significantly lower (P < 0.05) at a BLa concentration of 4 mM when estimated from fingertip blood as compared with venous blood. These results indicate that differences between fingertip and venous blood exist during treadmill exercise and should be considered when lactate determination is employed as a criterion to evaluate and predict performance and when used as a training guide to standardize exercise intensity.

This study assessed the agreement between arterial and venous blood lactate and pH levels in children with sepsis. This retrospective, three-year study involved 60 PICU patients, with data collected from electronic or paper patient records. The inclusion criteria comprised of children (≤17 years old) with sepsis and those who had a venous blood gas taken first with an arterial blood gas taken after within one hour. The lactate and pH values measured through each method were analysed. There is close agreement between venous and arterial lactate up to 2 mmol/L. As this value increases, this agreement becomes poor. The limits of agreement (LOA) are too large (±1.90 mmol/L) to allow venous and arterial lactate to be used interchangeably. The mean difference and LOA between both methods would be much smaller if derived using lactate values under 2.0 mmol/L. There is close agreement between arterial and venous pH (MD = −0.056, LOA ± 0.121). However, due to extreme variations in pH readings during sepsis, pH alone is an inadequate marker.Conclusion: A venous lactate ≤2 mmol/L can be used as a surrogate for arterial lactate during early management of sepsis in children. However, if the value exceeds 2 mmol/L, an arterial sample must confirm the venous result.What is known:• In children with septic shock, a blood gas is an important test to show the presence of acidosis and high lactic acid. Hyperlactataemia on admission is an early predictor of outcome and is associated with a greater mortality risk.• An arterial sample is the standard for lactate measurement, however getting a sample may be challenging in the emergency department or a general paediatric ward. Venous samples are quicker and easier to obtain. Adult studies generally advise caution in replacing venous lactate values for the arterial standard, whilst paediatric studies are limited in this area.What is new:• This is the first study assessing the agreement between arterial and peripheral venous lactate in children with sepsis, with a significant sample of patients.• This study shows that a venous sample with a lactate of ≤ 2 mmol/L can be used as a surrogate measurement for arterial lactate during early management of sepsis in children. However, if the venous lactate is above 2 mmol/L, an arterial sample must be taken to confirm the result.

A method for portal venous, aortic, and gastric cannulation in the rat is described. Changes in mean portal venous and aortic blood glucose and lactate concentrations after an intragastric infusion of d-glucose to chronically catheterized rats (after regaining preoperative weight) were compared to those of acutely catheterized rats (1 h after catheter placement). Both portal venous and aortic catheters were patent for blood sampling in 67% of rats 8 days after catheter placement and 42% after 14 days. After intragastric infusion of 10 ml of 0.29 M dextrose, mean aortic blood glucose and lactate concentrations in chronically catheterized rats increased 80 and 73%, respectively, 15 min after infusion and decreased to preinfusion concentrations by 60 min. In acutely catheterized rats, mean aortic glucose and lactate concentrations increased linearly for 60 min. The concentration differences between portal venous and aortic blood glucose and lactate concentrations in chronically catheterized rats were not significantly different than baseline differences. The portal venous glucose concentrations were significantly greater than aortic concentrations in acutely catheterized rats 15, 30, and 45 min after the glucose infusion when compared to baseline differences. These data suggest that the rate of glucose uptake and metabolism to lactate is significantly altered in acutely catheterized rats when compared to chronically catheterized animals.

In recent years the blood lactate level can be easily and quickly measured with a small amount of blood, and the availability of an arterial blood lactate level has been reported as an indicator of oxygen deficit in adults. To determine whether venous blood lactate level can serve as such a marker for determining the indications for transfusion, blood lactate and hemoglobin level were monitored before and after transfusion. The study subjects consisted of 12 very low-birthweight infants admitted to the neonatal intensive care unit and who had transfusion between June 2005 and June 2007. The data on the blood lactate and hemoglobin were collected retrospectively by referring to the clinical records. A total of 18 transfusions was performed. There was no significant relationship between venous blood lactate and hemoglobin concentration before transfusion. The subjects were classified into two groups according to the lactate level before transfusion: > or =3.3 mmol/L and <3.3 mmol/L. In the high-lactate group the lactate decreased significantly after transfusion (P < 0.01) and it continued to decrease thereafter. In the low-lactate group, however, the lactate remained unchanged. Venous blood lactate measurements may offer some additional information regarding the optimal time for performing a transfusion. To the authors' knowledge this is the first report to study the changes in lactate levels using venous blood sampling in red blood cell transfusion in very low-birthweight infants.

To determine whether O2 availability limited diaphragmatic performance, we subjected unanesthetized sheep to severe (n = 11) and moderate (n = 3) inspiratory flow resistive loads and studied the phrenic venous effluent. We measured transdiaphragmatic pressure (Pdi), systemic arterial and phrenic venous blood gas tensions, and lactate and pyruvate concentrations. In four sheep with severe loads, we measured O2 saturation (SO2), O2 content, and hemoglobin. We found that with severe loads Pdi increased to 74.7 +/- 6.0 cmH2O by 40 min of loading, remained stable for 20-30 more min, then slowly decreased. In every sheep, arterial PCO2 increased when Pdi decreased. With moderate loads Pdi increased to and maintained levels of 40-55 cmH2O. With both loads, venous PO2, SO2, and O2 content decreased initially and then increased, so that the arteriovenous difference in O2 content decreased as loading continued. Hemoglobin increased slowly in three of four sheep. There were no appreciable changes in arterial or venous lactate and pyruvate during loading or recovery. We conclude that the changes in venous PO2, SO2, and O2 content may be the result of changes in hemoglobin, blood flow to the diaphragm, or limitation of O2 diffusion. Our data do not support the hypothesis that in sheep subjected to inspiratory flow resistive loads O2 availability limits diaphragmatic performance.

Eight male subjects were studied during incremental bicycle exercise. From the forearm, arterial and venous blood lactate concentrations were measured every minute until exhaustion. There was a statistically significant difference (P<0.01) in the points at which the arterial and venous blood lactates began to increase above the resting level. The onset of increase of lactate in arterial blood occurred at 1.00±0.07 l·min−1 in\(\dot V\)O2 (mean ± SEM), which corresponded to 37.0±1.5% of\(\dot V\)O2max. Its venous counterpart occurred at 1.50±0.17 l·min−1 in\(\dot V\)O2, 55.0±3.8% of\(\dot V\)O2max. The arterio-venous lactate difference became greater after the onset of increase in arterial blood lactate (anaerobic threshold), presumably as consequence of lactate utilization by the forearm muscles.

Venous blood lactate concentration was measured during the force velocity exercise test in order to determine whether this test is strictly alactic or whether it draws upon lactic anaerobic metabolism. Nine trained male subjects, aged from 23 to 29 years, participated in this study. Two blood samples were drawn at rest, and then for each work load (1 kg to 10 kg): at the end of each sprint (S1) and at the 5th minute of recovery (S2). From the first braking force, venous blood lactate concentration increased very significantly during the force velocity test (p less than 0.001) and, once the peak of power has been obtained, the venous blood lactate concentration remained steady. The lactate increase for each load (delta[LA]) decreased significantly (p less than 0.01). From the beginning of the exercise to the peak of power, a significant positive correlation between the increase of power and the increase of blood lactate concentration measured at S2 existed (r = 0.71, p less than 0.001), whereas there was a negative correlation between the decrease of delta[LA] and the increase of power (r = -0.45, p less than 0.01). In conclusion, the repetition of sprints during the force velocity test induced a recruitment of lactic anaerobic metabolism. Maximal power must be considered as an alactic and lactic anaerobic power. The consequences of lactate accumulation in muscle may be a limitation of the maximal anaerobic power.

To evaluate the analytical agreement between blood lactate concentrations determined by use of an enzymatic-amperometric bedside system in capillary blood samples from the pinna and in jugular venous blood samples from dogs. 53 dogs. For each dog, venous and capillary blood samples were obtained from a jugular vein and from the ear pinna (by use of a lancing device), respectively, following a randomized sequence of collection. Lactate concentrations in both types of samples were analyzed by use of an enzymatic-amperometric bedside system intended for lactate detection in capillary blood samples from humans that was previously validated in dogs. The Passing-Bablock regression analysis was used to compare venous and capillary blood lactate concentrations; the level of agreement was calculated by use of the Bland-Altman method. Jugular venous blood samples were collected without difficulty from all 53 dogs. A capillary blood sample was obtained from only 47 dogs. The correlation coefficient between lactate concentrations measured in venous and capillary blood samples was 0.58 (slope, 2.0 [95% confidence interval, 1.5 to 3.0]; intercept, -1.2 [95% confidence interval, -3.1 to 0.4]). The mean difference between methods was 0.72 mmol/L (95% confidence interval, 0.38 to 1.06) with limits of agreement of -1.55 to 2.99 mmol/L. Because of the lack of agreement between lactate concentrations determined in capillary and jugular venous blood samples, measurement of capillary blood lactate concentration in dogs performed with the technique used in the study does not appear to be a reliable alternative to jugular venous blood measurements.

The aim of this study was to test the hypothesis that venous blood lactate concentrations ([La-]) would vary from the beginning of brief exercise. Maximal vertical jumping was used as a model of brief intense exercise. Eleven healthy male volleyball players, aged [mean (SE)] 18.5 (0.7) years, performed three exercise tests with different protocols, each separated by quiet seated recovery periods of 45 min. After the first test, consisting of a single maximal jump [lasting approximately equals 0.6 s for the pushing phase, and in which the subjects jumped 64 (2.2) cm], forearm venous [La-] increased significantly with respect to rest at 1 min (t1), 3 min (t3), and 5 min (t5) of recovery. The second test, comprising six maximal jumps, each separated by 20-s recovery periods, resulted in an unchanged [La-] with respect to the baseline value. After the third test [i.e., six consecutive maximal jumps that lasted a total of 7.36 (0.33) s], [La-] increased significantly at t3 and t5 with respect to the pre-test value (F= 10.3, P < 0.001). We conclude that a significant venous [La-] increase occurs after vertical jumping. This result may be explained by the activation of lactic anaerobic metabolism at the very onset of exercise, which participates in energy production and/or in the resynthesis of the phosphocreatine that was used during such brief exercise.

AimsTo assess the level of agreement between Arterial and Venous blood gas pH and Lactate levels in children with sepsis.MethodsThis is a retrospective single centre study involving 60 PICU patients...

Five male subjects performed three successive incremental work tests on an electronically braked cycle ergometer. The first and second tests were separated by thirty minutes of rest, the second and third by three minutes of maximum work. During the third test, venous blood lactate concentrations were still decreasing at work rates where they were increasing during the first two tests. The work rate at which rapid increases in lactate concentrations occurred during the final test coincided with the work rate where rapid increases occurred in the two initial tests. It was concluded that this point represented a threshold where a balance existed between removal and release of lactate from and into the plasma compartment, and did not coincide with the anaerobic threshold. It is postulated that steady state work at levels above this threshold would result in a continuous increase in venous lactate concentration.

Evaluation of serial venous and arterial lactate concentrations in healthy anesthetized sheep undergoing ovariectomy

Capillary and venous point-of-care testing of lactate concentrations in the emergency department: a prospective observational study

Department of Obstetrics and Gynecology, Malmö University Hospital, University of Lund, Malmö, Sweden