BACKGROUND: In critically ill patients, elevation in the plasma lactate concentration has traditionally been interpreted as indicating a deficiency in oxygen availability and is often an impetus to increase oxygen delivery clinically. However, another possible basis for increased lactate concentrations may be simply a mass effect from increased pyruvate availability (i.e., accelerated glycolysis). METHODS: In six hypermetabolic burned patients, the rates of glucose production and oxidation were quantified using a tracer infusion of 6,6 d2 glucose combined with indirect calorimetry. Measurements were obtained after a 9-hour fast and after a 3-hour infusion of unlabeled glucose at 30 micromol/kg/min. No patient was overtly septic, hypoxic, or hypovolemic. RESULTS: The infusion of glucose significantly increased the arterial glucose concentration and rate of glucose oxidation, with a corresponding increase in the arterial plasma concentration of lactate and pyruvate. Resting energy expenditure and oxygen consumption were not affected by the infusion of glucose. CONCLUSIONS: These findings show that elevations in plasma lactate in severely injured patients may, in part, be related to increases in glucose flux and not entirely a reflection of any deficit in oxygen availability. Such findings highlight a potential pitfall for interpreting plasma lactate concentrations as an index of tissue oxygen availability in hypermetabolic patients.
BACKGROUND: In critically illpatients, elevation in the plasma lactate concentration has traditionally been interpreted as indicating a deficiency in oxygen availability and is often an impetus to increase oxygen delivery clinically. However, another possible basis for increased lactate concentrations may be simply a mass effect from increased pyruvate availability (i.e., accelerated glycolysis). METHODS: In six hypermetabolic burned patients, the rates of glucose production and oxidation were quantified using a tracer infusion of 6,6 d2 glucose combined with indirect calorimetry. Measurements were obtained after a 9-hour fast and after a 3-hour infusion of unlabeled glucose at 30 micromol/kg/min. No patient was overtly septic, hypoxic, or hypovolemic. RESULTS: The infusion of glucose significantly increased the arterial glucose concentration and rate of glucose oxidation, with a corresponding increase in the arterial plasma concentration of lactate and pyruvate. Resting energy expenditure and oxygen consumption were not affected by the infusion of glucose. CONCLUSIONS: These findings show that elevations in plasma lactate in severely injured patients may, in part, be related to increases in glucose flux and not entirely a reflection of any deficit in oxygen availability. Such findings highlight a potential pitfall for interpreting plasma lactate concentrations as an index of tissue oxygen availability in hypermetabolic patients.
Authors: Marc G Jeschke; Gabriela A Kulp; Robert Kraft; Celeste C Finnerty; Ron Mlcak; Jong O Lee; David N Herndon Journal: Am J Respir Crit Care Med Date: 2010-04-15 Impact factor: 21.405
Authors: Marc G Jeschke; Celeste C Finnerty; David N Herndon; Juquan Song; Darren Boehning; Ronald G Tompkins; Henry V Baker; Gerd G Gauglitz Journal: Ann Surg Date: 2012-02 Impact factor: 12.969
Authors: Marc G Jeschke; Robert Kraft; Fatemeh Emdad; Gabriela A Kulp; Felicia N Williams; David N Herndon Journal: Ann Surg Date: 2010-09 Impact factor: 12.969
Authors: Ricki Y Fram; Melanie G Cree; Robert R Wolfe; Ronald P Mlcak; Ting Qian; David L Chinkes; David N Herndon Journal: Crit Care Med Date: 2010-06 Impact factor: 7.598
Authors: Marc G Jeschke; David L Chinkes; Celeste C Finnerty; Gabriela Kulp; Oscar E Suman; William B Norbury; Ludwik K Branski; Gerd G Gauglitz; Ronald P Mlcak; David N Herndon Journal: Ann Surg Date: 2008-09 Impact factor: 12.969
Authors: Marc G Jeschke; Ronald P Mlcak; Celeste C Finnerty; William B Norbury; Gerd G Gauglitz; Gabriela A Kulp; David N Herndon Journal: Crit Care Date: 2007 Impact factor: 9.097