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

Surgical Intensive Care Unit, Department of Anesthesiology, Centre Hospitalier Universitaire Vaudois, Lausanne, Switzerland

Philippe Schneiter, PHD

Institute of Physialogy, Faculty of Medicine, University of Lausanne, Switzerland

Christine Cayeux, RN

Surgical Intensive Care Unit, Department of Anesthesiology, Centre Hospitalier Universitaire Vaudois, Lausanne, Switzerland

Evelyne Temler, BS

Division of Endocrinology and Metabolism, Centre Hospitalier Universitaire Vaudois, Lausanne, Switzerland

Eric Jéquier, MD

Institute of Physialogy, Faculty of Medicine, University of Lausanne, Switzerland

Charles Schindler, PHD

Central Pharmacy, Centre Hospitalier Universitaire Vaudois, Lausanne, Switzerland

Luc Tappy, MD

Institute of Physialogy, Faculty of Medicine, University of Lausanne, Switzerland

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)

Journal of Parenteral and Enteral Nutrition, Vol. 20, No. 4, 257-263 (1996)
DOI: 10.1177/0148607196020004257


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