Infusion of 2.5 meq/min of lactic acid minimally increases CO(2) production compared to an isocaloric glucose infusion in healthy anesthetized, mechanically ventilated pigs

INTRODUCTION: Blood acidification by lactic acid infusion converts bicarbonate to CO(2). This effect can be exploited to increase the transmembrane PCO(2) gradient of an extracorporeal membrane lung, resulting in a significant increase of extracorporeal CO(2) removal. Lactic acid, however, is an energetic substrate and its metabolism might increase total body CO(2) production (VCO(2)), limiting the potential beneficial effects of this technique. The aim of our study was to compare VCO₂ during isocaloric infusion of lactic acid or glucose. METHODS: Six pigs (45 ± 5 kg) were sedated and mechanically ventilated. Estimated caloric needs were 2,300–2,400 Kcal/die (95 to 100 Kcal/h). A sequence of two steps lasting four hours each was performed: 1) Glucose, 97 kcal/h were administered as 50% glucose solution, and 2) Lactic Acid, approximately 48.5 kcal/h were administered as lactic acid and approximately 48.5 kcal/h as 50% glucose solution. This sequence was repeated three times with two-hour intervals. Every hour VCO₂, arterial blood gases and lactate were measured. Blood glucose level was kept constant by titrating an insulin infusion, ventilation was adjusted to maintain arterial PCO(2) at 50 mmHg, a normal value for our animal model. RESULTS: During Lactic Acid steps VCO(2) increased less than 5% compared to the Glucose steps (282 vs. 269 ml/min, P <0.05); blood glucose did not differ between the two groups (respectively 101 ± 12 vs. 103 ± 8 mg/dl). Arterial lactate was always lower than 3 mmol/L. Arterial pH was lower during Lactic Acid steps (7.422 vs. 7.445, P <0.05). CONCLUSIONS: Replacing 50% of the caloric input with lactic acid increased total CO(2) production by less than 5% compared to an equal caloric load provided entirely by a 50% glucose solution.