Lactate and glucose metabolism in severe sepsis and cardiogenic shock.
OBJECTIVE
To evaluate the relative importance of increased lactate production as opposed to decreased utilization in hyperlactatemic patients, as well as their relation to glucose metabolism.


METHODS
Prospective observational study.


METHODS
Surgical intensive care unit of a university hospital.


METHODS
Seven patients with severe sepsis or septic shock, seven patients with cardiogenic shock, and seven healthy volunteers.


METHODS
C-labeled sodium lactate was infused at 10 micromol/kg/min and then at 20 micromol/kg/min over 120 mins each. H-labeled glucose was infused throughout.


RESULTS
Baseline arterial lactate was higher in septic (3.2 +/- 2.6) and cardiogenic shock patients (2.8 +/- 0.4) than in healthy volunteers (0.9 +/- 0.20 mmol/L, p < .05). Lactate clearance, computed using pharmacokinetic calculations, was similar in septic, cardiogenic shock, and controls, respectively: 10.8 +/- 5.4, 9.6 +/- 2.1, and 12.0 +/- 2.6 mL/kg/min. Endogenous lactate production was determined as the initial lactate concentration multiplied by lactate clearance. It was markedly enhanced in the patients (septic 26.2 +/- 10.5; cardiogenic shock 26.6 +/- 5.1) compared with controls (11.2 +/- 2.7 micromol/kg/min, p < .01). C-lactate oxidation (septic 54 +/- 25; cardiogenic shock 43 +/- 16; controls 65 +/- 15% of a lactate load of 10 micromol/kg/min) and transformation of C-lactate into C-glucose were not different (respectively, 15 +/- 15, 9 +/- 18, and 10 +/- 7%). Endogenous glucose production was markedly increased in the patients (septic 14.8 +/- 1.8; cardiogenic shock 15.0 +/- 1.5) compared with controls (7.2 +/- 1.1 micromol/kg/min, p < .01) and was not influenced by lactate infusion.


CONCLUSIONS
In patients suffering from septic or cardiogenic shock, hyperlactatemia was mainly related to increased production, whereas lactate clearance was similar to healthy subjects. Increased lactate production was concomitant to hyperglycemia and increased glucose turnover, suggesting that the latter substantially influences lactate metabolism during critical illness.
Revelly
Jean-Pierre
JP
Surgical Intensive Care Unit, University Hospital, Lausanne, Switzerland.
Tappy
Luc
L
Martinez
Alexandro
A
Bollmann
Marc
M
Cayeux
Marie-Christine
MC
Berger
Mette M
MM
Chioléro
René L
RL
D000328:Adult; D016022:Case-Control Studies; D005947:Glucose / Q000378:metabolism*; D006801:Humans; D019344:Lactic Acid / Q000378:metabolism*; D010084:Oxidation-Reduction; D011446:Prospective Studies; D018805:Sepsis / Q000378:metabolism*; D012770:Shock, Cardiogenic / Q000378:metabolism*; D019354:Sodium Lactate / Q000493:pharmacokinetics
D019344:Lactic Acid; D005947:Glucose; D019354:Sodium Lactate