CORRELATION OF JUGULAR VENOUS BULB LACTATE AND ARTERIAL LACTATE IN THE NEUROLOGICAL CRITICAL PATIENT

2002 ◽  
Vol 30 (Supplement) ◽  
pp. A78
Author(s):  
Monica Guedes ◽  
Diamantino Salgado ◽  
Marcus Vinicius Negri ◽  
Giuseppe Chindamo ◽  
Juan Carlos Verdeal ◽  
...  
1991 ◽  
Vol 11 (3) ◽  
pp. 479-484 ◽  
Author(s):  
Emanuel P. Rivers ◽  
Norman A. Paradis ◽  
Gerard B. Martin ◽  
Mark E. Goetting ◽  
Jack A. Rosenberg ◽  
...  

Animal studies have shown cerebral lactate uptake under conditions of anoxia and ischemia. Cerebral lactate uptake in humans during cardiopulmonary resuscitation (CPR) has not been previously reported in the literature. Forty-five patients receiving CPR underwent simultaneous sampling through jugular venous bulb, right atrial, and central aortic catheterization. The mean net cerebral lactate uptake (central aortic minus jugular venous bulb) was 0.76 ± 1.86 and 0.80 ± 2.03 m M on initial measurement and 10 min later, respectively. Both measurements were statistically significant (p = 0.01) compared to normal controls who have net cerebral output of lactate of −0.18 ± 0.1 m M. Seventy-one percent of all patients had a cerebral uptake on initial sampling and this gradient persisted upon sampling 10 min later in 68% of the remaining 40 patients who did not have a return of spontaneous circulation. Among multiple variables measured, patients who exhibited a cerebral lactate uptake were 13.2 years younger (p = 0.004), received an additional 7.6 min of CPR (p = 0.05), and had a mean arterial lactate concentration of 4.8 m M higher (p = 0.005) than the nonuptake group. The pathophysiologic explanation of cerebral lactate uptake during CPR is multifactorial and includes utilization and/or diffusion.


2003 ◽  
Vol 83 (3) ◽  
pp. 171-176 ◽  
Author(s):  
Floris Groenendaal ◽  
Caroline Lindemans ◽  
Cuno S.P.M. Uiterwaal ◽  
Linda S. de Vries

2003 ◽  
Vol 284 (1) ◽  
pp. E193-E205 ◽  
Author(s):  
G. van Hall ◽  
M. Jensen-Urstad ◽  
H. Rosdahl ◽  
H.-C. Holmberg ◽  
B. Saltin ◽  
...  

To study the role of muscle mass and muscle activity on lactate and energy kinetics during exercise, whole body and limb lactate, glucose, and fatty acid fluxes were determined in six elite cross-country skiers during roller-skiing for 40 min with the diagonal stride (Continuous Arm + Leg) followed by 10 min of double poling and diagonal stride at 72–76% maximal O2 uptake. A high lactate appearance rate (Ra, 184 ± 17 μmol · kg−1 · min−1) but a low arterial lactate concentration (∼2.5 mmol/l) were observed during Continuous Arm + Leg despite a substantial net lactate release by the arm of ∼2.1 mmol/min, which was balanced by a similar net lactate uptake by the leg. Whole body and limb lactate oxidation during Continuous Arm + Leg was ∼45% at rest and ∼95% of disappearance rate and limb lactate uptake, respectively. Limb lactate kinetics changed multiple times when exercise mode was changed. Whole body glucose and glycerol turnover was unchanged during the different skiing modes; however, limb net glucose uptake changed severalfold. In conclusion, the arterial lactate concentration can be maintained at a relatively low level despite high lactate Ra during exercise with a large muscle mass because of the large capacity of active skeletal muscle to take up lactate, which is tightly correlated with lactate delivery. The limb lactate uptake during exercise is oxidized at rates far above resting oxygen consumption, implying that lactate uptake and subsequent oxidation are also dependent on an elevated metabolic rate. The relative contribution of whole body and limb lactate oxidation is between 20 and 30% of total carbohydrate oxidation at rest and during exercise under the various conditions. Skeletal muscle can change its limb net glucose uptake severalfold within minutes, causing a redistribution of the available glucose because whole body glucose turnover was unchanged.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Pierre Bay ◽  
Guillaume Lebreton ◽  
Alexis Mathian ◽  
Pierre Demondion ◽  
Cyrielle Desnos ◽  
...  

Abstract Background Systemic rheumatic diseases (SRDs) are a group of inflammatory disorders that can require intensive care unit (ICU) admission because of multiorgan involvement with end-organ failure(s). Critically ill SRD patients requiring extracorporeal membrane oxygenation (ECMO) were studied to gain insight into their characteristics and outcomes. Methods This French monocenter, retrospective study included all SRD patients requiring venovenous (VV)- or venoarterial (VA)-ECMO admitted to a 26-bed ECMO-dedicated ICU from January 2006 to February 2020. The primary endpoint was in-hospital mortality. Results Ninety patients (male/female ratio: 0.5; mean age at admission: 41.6 ± 15.2 years) admitted to the ICU received VA/VV-ECMO, respectively, for an SRD-related flare (n = 69, n = 38/31) or infection (n = 21, n = 10/11). SRD was diagnosed in-ICU for 31 (34.4%) patients. In-ICU and in-hospital mortality rates were 48.9 and 51.1%, respectively. Nine patients were bridged to cardiac (n = 5) or lung transplantation (n = 4), or left ventricular assist device (n = 2). The Cox multivariable model retained the following independent predictors of in-hospital mortality: in-ICU SRD diagnosis, day-0 Simplified Acute Physiology Score (SAPS) II score ≥ 70 and arterial lactate ≥ 7.5 mmol/L for VA-ECMO–treated patients; diagnosis other than vasculitis, day-0 SAPS II score ≥ 70, ventilator-associated pneumonia and arterial lactate ≥ 7.5 mmol/L for VV-ECMO–treated patients. Conclusions ECMO support is a relevant rescue technique for critically ill SRD patients, with 49% survival at hospital discharge. Vasculitis was independently associated with favorable outcomes of VV-ECMO–treated patients. Further studies are needed to specify the role of ECMO for SRD patients.


1983 ◽  
Vol 55 (4) ◽  
pp. 1178-1186 ◽  
Author(s):  
M. P. Yeh ◽  
R. M. Gardner ◽  
T. D. Adams ◽  
F. G. Yanowitz ◽  
R. O. Crapo

Despite the popularity of the concept of “anaerobic threshold” (AT), the noninvasive detection criteria remain subjective, and invasive validations of AT have been based on lactate data of arterial, mixed venous, venous, and capillary blood samples without any concern for the possible lactate differences from these sources. Eight normal subjects underwent two exercise tests on a bicycle ergometer. The protocol consisted of 3 min of rest, 3 min of 0 work load, and a 20 W/min ramp (1 W/3 s) until exhaustion. Simultaneous arterial and venous blood samples were drawn during the second test. Noninvasive gas response data were measured using a computerized breath-by-breath stress test system. Threshold phenomenon of the lactate accumulation was not found. The arterial lactate levels increased continuously after the start of the exercise ramp. The rise in venous lactate lagged behind the rise of the arterial lactate by about 1.5 min, and therefore venous lactate was not considered suitable for AT detection. Four independent exercise physiologists determined AT from the gas response data. The reviewer variability (avg range 16%) of AT for a given subject was representative of AT values reported for untrained and trained individuals (40-70% maximum O2 consumption). We concluded that 1) AT is not detectable using invasive methods (arterial and venous lactates); and 2) the noninvasive gas response determination has such a large range of reviewer variability that it is unsuitable for clinical use.


1977 ◽  
Vol 43 (2) ◽  
pp. 204-210 ◽  
Author(s):  
A. Capderou ◽  
J. Polianski ◽  
J. Mensch-Dechene ◽  
L. Drouet ◽  
G. Antezana ◽  
...  

An impairment of gluconeogenesis has been proposed to explain the low arterial blood glucose of highlanders. Therefore, we studied splanchnic blood flow, splanchnic uptake of oxygen and lactate, and output of glucose in nine normal and six anemic highlanders at an altitude of 3,750 m. Splanchnic blood flow, arteriovenous difference for oxygen, and oxygen consumption were comparable at rest in both groups and in lowlanders from the literature, whereas splanchnic output of glucose, and uptake of lactate were approximately twice those in lowlanders. After 10 min of mild exercise in 12 subjects (7 normals, 5 anemic), no significant changes in splanchnic hemodynamics and metabolism were found. During 29% oxygen breathing in 8 subjects (5 normals, 3 anemics), arterial lactate, splanchnic uptake of lactate and output of glucose fell to normal sea-level values. We concluded that splanchnic hemodynamics are similar in adapted highlanders and in lowlanders, and that there is no evidence of an impaired gluconeogenesis at the altitude of the present study.


1984 ◽  
Vol 247 (3) ◽  
pp. E362-E369 ◽  
Author(s):  
M. A. Davis ◽  
P. E. Williams ◽  
A. D. Cherrington

The present experiments were undertaken to assess lactate and gluconeogenic precursor metabolism in the 30 h following consumption of a mixed meal by the overnight-fasted, conscious dog. The arterial glucose level rose by a maximum of 13 mg/dl 4 h after the meal and had returned to control levels by 12 h. Hepatic glucose production was suppressed for 12 h after feeding, but net hepatic glucose uptake did not occur. The arterial lactate level rose from 0.55 +/- 0.10 to 1.28 +/- 0.14 mM within 1 h of feeding and remained elevated for 12 h. Net hepatic lactate production, measured with an A-V difference technique, rose from 3.5 +/- 2.8 to 19.4 +/- 3.1 mumol X kg-1 X min-1 h after the meal and declined slowly over the next 22 h. The liver then began to consume lactate so that at 30 h net hepatic uptake was 5.7 +/- 0.5 mumol X kg-1 X min-1. The total hepatic uptake of the gluconeogenic amino acids (alanine, glycine, serine, threonine) increased from 5.3 +/- 0.8 to 11.5 +/- 2.5 mumol X kg-1 X min-1 at 1 h and remained elevated for 4 h. The arterial alanine level rose from 0.36 +/- 0.03 to 0.51 +/- 0.04 mM at 2 h and remained elevated for 18 h. Insulin increased from 11 +/- 2 microU/ml to a maximum of 44 +/- 5 4 h after the meal, and the glucagon level rose from 59 +/- 8 pg/ml to a maximum of 150 +/- 22 1 h after feeding.(ABSTRACT TRUNCATED AT 250 WORDS)


2015 ◽  
Vol 41 (11) ◽  
pp. 2029-2030 ◽  
Author(s):  
Sameer Jog ◽  
Shirish Prayag ◽  
Prasad Rajhans ◽  
Kapil Zirpe ◽  
Subhal Dixit ◽  
...  

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