title: Lactate and glucose metabolism in severe sepsis and cardiogenic shock.
abstract: 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.
authors.affiliation: Surgical Intensive Care Unit, University Hospital, Lausanne, Switzerland.
authors.forename: Jean-Pierre
authors.initials: JP
authors.lastname: Revelly
authors.forename: Luc
authors.initials: L
authors.lastname: Tappy
authors.forename: Alexandro
authors.initials: A
authors.lastname: Martinez
authors.forename: Marc
authors.initials: M
authors.lastname: Bollmann
authors.forename: Marie-Christine
authors.initials: MC
authors.lastname: Cayeux
authors.forename: Mette M
authors.initials: MM
authors.lastname: Berger
authors.forename: René L
authors.initials: RL
authors.lastname: Chioléro
mesh_terms: 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
chemical_list: D019344:Lactic Acid; D005947:Glucose; D019354:Sodium Lactate