scholarly journals Lactate arterial-central venous gradient among COVID-19 patients in ICU: a potential tool in the clinical practice

2020 ◽  
Author(s):  
Giuseppe Nardi ◽  
Gianfranco Sanson ◽  
Lucia Tassinari ◽  
Giovanna Guiotto ◽  
Antonella Potalivo ◽  
...  
Keyword(s):  
Venous Blood ◽  
Lactate Concentration ◽  
Blood Lactate Concentration ◽  
Lung Cells ◽  
Central Venous ◽  
Arterial Blood ◽  
Arterial Blood Lactate ◽  
Arterial Blood Lactate Concentration ◽  
The Difference ◽  
Potential Tool

ABSTRACTObjectiveIn physiological conditions arterial blood lactate concentration is equal or lower than central venous. The aim of this study was to explore if the COVID-19 induced lung cells damage was mirrored by an arterial lactatemia higher than the central venous one; then if the administration of immunosuppressant drugs (i.e. canakinumab) could normalize such abnormal lactate a-cv difference.MethodsProspective cohort study started on March 25th 2020 for a duration of 10 days, enrolling 21 patients affected by severe COVID-19 pneumonia undergoing mechanical ventilation consecutively admitted to the ICU of the Rimini Hospital, Italy.Arterial and central venous blood samples were contemporary collected to calculate the difference between arterial and central venous lactate (Delta a-cv lactate) concentration within 24 h from tracheal intubation (T0), and 24 hours after canakinumab administration (T1).ResultsAt the T0 19/21 (90.5%) patients showed a pathologic Delta a-cv lactate (median 0.22 mmol/L; IQR 0.07–0.36), suggesting severe inflammation. In the 13 patients undergoing canakinumab administration, at the T1 Delta a-cv lactate decreased in 92.3% of cases, being the decrease statistically significant (T0: median 0.15, IQR 0.07–0.25 mmol/L; T1: median −0.01, IQR 0.09–0.04 mmol/L; p=0.002).ConclusionA reversed Delta a-cv lactate is likely to be one of the effects of COVID-19 related cytokine storm, that could reflect a derangement in the lung cells mitochondrial metabolism induced by inflammation or other uncoupling mediators. Delta a-cv lactate decrease may reflect the anti-inflammatory activity of canakinumab. Our preliminary findings need to be confirmed by larger outcome studies.

scholarly journals Lactate Arterial-Central Venous Gradient among COVID-19 Patients in ICU: A Potential Tool in the Clinical Practice

2020 ◽  
Vol 2020 ◽  
pp. 1-5
Author(s):  
Giuseppe Nardi ◽  
Gianfranco Sanson ◽  
Lucia Tassinari ◽  
Giovanna Guiotto ◽  
Antonella Potalivo ◽  
...  
Keyword(s):  
Blood Lactate ◽  
Venous Blood ◽  
Lactate Concentration ◽  
Blood Lactate Concentration ◽  
Mitochondrial Metabolism ◽  
Lung Cells ◽  
Central Venous ◽  
Central Venous Blood ◽  
Arterial Blood ◽  
Anti Inflammatory

Objective. In physiological conditions, arterial blood lactate concentration is equal to or lower than central venous blood lactate concentration. A reversal in this rate (i.e., higher lactate concentration in central venous blood), which could reflect a derangement in the mitochondrial metabolism of lung cells induced by inflammation, has been previously reported in patients with ARDS but has been never explored in COVID-19 patients. The aim of this study was to explore if the COVID-19-induced lung cell damage was mirrored by an arterial lactatemia higher than the central venous one; then if the administration of anti-inflammatory therapy (i.e., canakinumab 300 mg subcutaneous) could normalize such abnormal lactate a-cv difference. Methods. A prospective cohort study was conducted, started on March 25, 2020, for a duration of 10 days, enrolling 21 patients affected by severe COVID-19 pneumonia undergoing mechanical ventilation consecutively admitted to the ICU of the Rimini Hospital, Italy. Arterial and central venous blood samples were contemporarily collected to calculate the difference between arterial and central venous lactate (Delta a-cv lactate) concentrations within 24 h from tracheal intubation (T0) and 24 hours after canakinumab administration (T1). Results. At T0, 19 of 21 (90.5%) patients showed a pathologic Delta a-cv lactate (median 0.15 mmol/L; IQR 0.07–0.25). In the 13 patients undergoing canakinumab administration, at T1, Delta a-cv lactate decreased in 92.3% of cases, the decrease being statistically significant (T0: median 0.24, IQR 0.09–0.31 mmol/L; T1: median −0.01, IQR −0.08–0.04 mmol/L; p=0.002). Conclusion. A reversed Delta a-cv lactate might be interpreted as one of the effects of COVID-19-related cytokine storm, which could reflect a derangement in the mitochondrial metabolism of lung cells induced by severe inflammation or other uncoupling mediators. In addition, Delta a-cv lactate decrease might also reflect the anti-inflammatory activity of canakinumab. Our preliminary findings need to be confirmed by larger outcome studies.

Maximal lactic capacity at altitude: effect of bicarbonate loading

1993 ◽  
Vol 75 (3) ◽  
pp. 1070-1074 ◽  
Author(s):  
B. Kayser ◽  
G. Ferretti ◽  
B. Grassi ◽  
T. Binzoni ◽  
P. Cerretelli
Keyword(s):  
Sea Level ◽  
Blood Lactate ◽  
Lactate Concentration ◽  
Blood Lactate Concentration ◽  
Altitude Effect ◽  
Arterial Blood ◽  
Arterial Ph ◽  
Arterial Blood Lactate ◽  
Arterial Blood Lactate Concentration ◽  
Blood Lactate Accumulation

The aim of the present study was to test the hypothesis that the net maximal blood lactate accumulation ([La]max) during heavy exercise in lowlanders acclimatized to chronic hypoxia may be limited by the reduced bicarbonate stores. Six men [age 32 +/- 4 (SD) yr] performed supramaximal exercise until voluntary exhaustion at sea level (204 +/- 54 W) and after sojourning for 1 mo at 5,050 m (175 +/- 23 W), without (C) and with (B) oral sodium-bicarbonate loading (0.3 g/kg body wt). Exhaustion time, arterial blood lactate concentration, arterial pH (pHa), arterial PCO2, and intramuscular pH were measured at rest and after exercise. At sea level, exhaustion time increased from 6.5 +/- 2.8 min in C to 7.5 +/- 2.7 min in B (P < 0.05). At altitude, exhaustion times were similar to the sea level C values and the same in C and B. At sea level, resting pHa increased from 7.41 +/- 0.02 in C to 7.46 +/- 0.03 in B (P < 0.001); the corresponding values at altitude were 7.46 +/- 0.04 and 7.55 +/- 0.03 (P < 0.001). Postexercise pHa at sea level was 7.22 +/- 0.02 in C and 7.25 +/- 0.08 in B (NS). After exercise at altitude, pHa was 7.32 +/- 0.04 and 7.44 +/- 0.03 in C and B, respectively (P < 0.001). [La]max increased from 12.86 +/- 1.45 mM in C to 16.63 +/- 1.76 mM in B (P < 0.01) at sea level and from 6.85 +/- 1.40 mM in C to 7.95 +/- 1.74 mM in B (NS) at altitude.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of cocaine on incremental treadmill exercise in horses

1993 ◽  
Vol 75 (6) ◽  
pp. 2727-2733 ◽  
Author(s):  
K. H. McKeever ◽  
K. W. Hinchcliff ◽  
D. F. Gerken ◽  
R. A. Sams
Keyword(s):  
Right Ventricular ◽  
Blood Lactate ◽  
Venous Blood ◽  
Lactate Concentration ◽  
Blood Lactate Concentration ◽  
Ventricular Pressure ◽  
Mixed Venous Blood ◽  
Work Intensity ◽  
Venous Blood Lactate ◽  
Mixed Venous

Four mature horses were used to test the effects of two doses (50 and 200 mg) of intravenously administered cocaine on hemodynamics and selected indexes of performance [maximal heart rate (HRmax), treadmill velocity at HRmax, treadmill velocity needed to produce a blood lactate concentration of 4 mmol/l, maximal mixed venous blood lactate concentration, maximal treadmill work intensity, and test duration] measured during an incremental treadmill test. Both doses of cocaine increased HRmax approximately 7% (P < 0.05). Mean arterial pressure was 30 mmHg greater (P < 0.05) during the 4- to 7-m/s steps of the exercise test in the 200-mg trial. Neither dose of cocaine had an effect on the responses to exertion of right atrial pressure, right ventricular pressure, or maximal change in right ventricular pressure over time. Maximal mixed venous blood lactate concentration increased 41% (P < 0.05) with the 50-mg dose and 75% (P < 0.05) with the 200-mg dose during exercise. Administration of cocaine resulted in decreases (P < 0.05) in the treadmill velocity needed to produce a blood lactate concentration of 4 mmol/l from 6.9 +/- 0.5 and 6.8 +/- 0.9 m/s during the control trials to 4.4 +/- 0.1 m/s during the 200-mg cocaine trial. Cocaine did not alter maximal treadmill work intensity (P > 0.05); however, time to exhaustion increased by approximately 92 s (15%; P < 0.05) during the 200-mg trial.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Arterialized and venous blood lactate concentration difference during different exercise intensities

2017 ◽  
Vol 15 (1) ◽  
pp. 22-26 ◽  
Author(s):  
Leandro C. Felippe ◽  
Guilherme A. Ferreira ◽  
Fernando De-Oliveira ◽  
Flavio O. Pires ◽  
Adriano E. Lima-Silva
Keyword(s):  
Blood Lactate ◽  
Venous Blood ◽  
Lactate Concentration ◽  
Blood Lactate Concentration ◽  
Concentration Difference ◽  
Venous Blood Lactate

scholarly journals Blood Lactate Is a Useful Indicator for the Medical Emergency Team

2016 ◽  
Vol 2016 ◽  
pp. 1-7 ◽  
Author(s):  
Maria Schollin-Borg ◽  
Pär Nordin ◽  
Henrik Zetterström ◽  
Joakim Johansson
Keyword(s):  
Blood Lactate ◽  
Medical Emergency Team ◽  
Lactate Concentration ◽  
Vital Signs ◽  
Blood Lactate Level ◽  
Medical Emergency ◽  
Emergency Team ◽  
Arterial Blood ◽  
Arterial Blood Lactate ◽  
Secondary Referral Hospital

Lactate has been thoroughly studied and found useful for stratification of patients with sepsis, in the Intensive Care Unit, and trauma care. However, little is known about lactate as a risk-stratification marker in the Medical Emergency Team- (MET-) call setting. We aimed to determine whether the arterial blood lactate level at the time of a MET-call is associated with increased 30-day mortality. This is an observational study on a prospectively gathered cohort at a regional secondary referral hospital. All MET-calls during the two-year study period were eligible. Beside blood lactate, age and vital signs were registered at the call. Among the 211 calls included, there were 64 deaths (30.3%). Median lactate concentration at the time of the MET-call was 1.82 mmol/L (IQR 1.16–2.7). We found differences between survivors and nonsurvivors for lactate and oxygen saturation, a trend for age, but no significant correlations between mortality and systolic blood pressure, respiratory rate, and heart rate. As compared to normal lactate (<2.44 mmol/L), OR for 30-day mortality was 3.54 (p<0.0006) for lactate 2.44–5.0 mmol/L and 4.45 (p<0.0016) for lactate > 5.0 mmol/L. The present results support that immediate measurement of blood lactate in MET call patients is a useful tool in the judgment of illness severity.

Measuring tracee turnover from tracer specific activity in the steady state

1988 ◽  
Vol 255 (1) ◽  
pp. E94-E98 ◽  
Author(s):  
S. L. Lehman ◽  
W. C. Stanley
Keyword(s):  
Steady State ◽  
Specific Activity ◽  
Numerical Estimate ◽  
Venous Blood ◽  
Compartment Model ◽  
Tissue Specific ◽  
Tissue Compartment ◽  
Arterial Blood ◽  
The Difference ◽  
Relationship Of

When a substrate appears in and disappears from an unmeasured (tissue) compartment, the proper sites for tracer infusion and sampling to measure tracee turnover become controversial. We analyze a three-compartment model representing arterial blood, tissue, and venous blood. The desired quantity, tracee turnover, is the ratio of the steady-state infusion rate to tissue specific activity. However, specific activity in the tissue compartment is unknown. We assume infusion of tracer into the arterial pool at a constant rate and consider sampling of specific activity of either blood compartment in the steady state. We obtain estimates of tissue specific activity from measurement of concentrations of tracer and tracee in blood samples in two extreme cases. In case I, tracee is assumed to appear in the venous compartment but to disappear from the tissue pool. Then tissue specific activity is equal to arterial specific activity. In case II, both appearance and disappearance are from the tissue pool. Tissue specific activity is then less than arterial or venous specific activity. We give formulas for the difference in each case. We discuss the relationship of our models to actual tracer experiments and define physiological locations for our three compartments. Appearance of substrates is probably intermediate between our extreme cases. A numerical estimate of turnover for the substrate lactate in resting humans reveals an error bound of approximately 30%. We discuss sites of infusion and sampling consistent with our model, the effects of relaxing some of our modeling constraints, and experimental necessities for getting beyond the steady state.

Lactic acid infusion in dogs: effects of varying infusate pH

1983 ◽  
Vol 54 (5) ◽  
pp. 1254-1260 ◽  
Author(s):  
L. B. Gladden ◽  
J. W. Yates
Keyword(s):  
Lactic Acid ◽  
Blood Lactate ◽  
Muscle Blood Flow ◽  
Lactate Concentration ◽  
Blood Lactate Concentration ◽  
Weak Acid ◽  
Muscle Lactate ◽  
Acid Infusion ◽  
Arterial Blood ◽  
Arterial Ph

This study had two purposes: 1) to determine the effects of varying the pH of lactic acid infusion solutions on the acid-base status of anesthetized dogs, and 2) to determine the effect of elevated blood lactate concentration on muscle lactate concentration. The experiments were performed on the in situ gastro cnemius-plantaris muscle group in 14 mongrel dogs. The infusions increased the arterial blood lactate concentration to 11.0 +/- 0.5 (SE) mM after 20 min. Above an infusate pH of 4.4, the arterial pH increased by 0.118–0.167 during infusion; the arterial pH was unchanged when the infusate pH was between 3.4 and 4.0; and the arterial pH decreased as infusate pH decreased below 3.0. The effect of lactic acid infusion on blood pH appears to be the result of two opposing effects: 1) an acidifying effect due to its weak acid properties, and 2) an alkalinizing effect due to the metabolism of sodium lactate. The estimated ratio between intracellular muscle lactate and venous plasma water lactate averaged 0.647 +/- 0.038, indicative of a substantial gradient between blood and muscle. The infusion produced a significant change from lactate output to lactate uptake by the muscles. The infusion also transiently increased muscle blood flow and oxygen uptake.

Sign in / Sign up

Export Citation Format

Share Document