Metabolic and Respiratory Effects of Sodium Lactate During Short IV Nutrition in Critically III Patients

Background: Hyperglycemia and an increased ventilatory demand secondary to an increased CO₂ production are frequent undesirable effects of total parenteral nutrition (TPN) in critically ill patients. This study was performed to assess whether sodium lactate as a metabolic substrate may affect these variables. Methods: Five male patients with multiple trauma during the flow phase were studied during two consecutive 3-hour periods of isocaloric (1.1 x resting energy expenditure) TPN. Sixty-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 acids (TPN-lactate) were substituted during the second period. Respiratory gas exchanges and net substrate oxidation were assessed by means of indirect calorimetry. Glucose kinetics was determined by primed-constant infusion of U-¹³C glucose. Results: Compared with TPN-glucose, TPN-lactate decreased glycemia by 20%, insulinemia by 43%, net carbohydrate oxidation (assessed from indirect calorimetry) by 34%, and plasma glucose oxidation (assessed from ¹³CO₂) by 54%. Respiratory oxygen exchanges were increased by 3.7% due to a 20% thermic effect of lactate, but respiratory CO₂ exchanges did not change. Pao ₂ decreased by 11.3 mm Hg, indicating that the increased O₂ consumption was not matched by an appropriate increase in spontaneous ventilation. Arterial pH increased from 7.41 ± 0.04 to 7.46 ± 0.05. Conclusion: Sodium lactate as a metabolic substrate limits hyperglycemia but induces metabolic alkalosis and does not spare the ventilatory demand. (Journal of Parenteral and Enteral Nutrition 20:257-263, 1996)