METABOLIC AND RESPIRATORY EFFECTS OF SODIUM LACTATE DURING SHORT IV NUTRITION IN CRITICALLY ILL PATIENTS

Background: Hyperglycemia and an increased ventilatory demand secondar y to an increased CO2 production are frequent undesirable effects of t otal parenteral nutrition (TPN) in critically ill patients. This study was performed to assess whether sodium lactate as a metabolic substra te may affect these variables. Methods: Five male patients with multip le trauma during the flow phase were studied during two consecutive 3- hour periods of isocaloric (1.1 x resting energy expenditure) TPN. Six ty-five percent of total calories was provided as carbohydrate, 15% as lipids, and 20% as amino acids during the first period (TPN-glucose), whereas 35% carbohydrate, 30% lactate, 20% lipids, and 15% amino acid s (TPN-lactate) were substituted during the second period. Respiratory gas exchanges and net substrate oxidation were assessed by means of i ndirect calorimetry. Glucose kinetics was determined by primed-constan t infusion of U-C-13 glucose. Results: Compared with TPN-glucose, TPN- lactate decreased glycemia by 20%, insulinemia by 43%, net carbohydrat e oxidation (assessed from indirect calorimetry) by 34%, and plasma gl ucose oxidation (assessed from (CO2)-C-13) by 54%. Respiratory oxygen exchanges were increased by 3.7% due to a 20% thermic effect of lactat e, but respiratory CO2 exchanges did not change. PaO2 decreased by 11. 3 mm Hg, indicating that the increased O-2 consumption was not matched by an appropriate increase in spontaneous ventilation. Arterial pH in creased from 7.41 +/- 0.04 to 7.46 +/- 0.05. Conclusion: Sodium lactat e as a metabolic substrate limits hyperglycemia but induces metabolic alkalosis and does not spare the ventilatory demand.