Nutrition for the patient with respiratory failure: glucose vs. fat.

Abstract

High glucose intakes given during administration of total parenteral nutrition (TPN) have been demonstrated to increase CO2 production. The workload imposed by the high CO2 production may precipitate respiratory distress in patients with compromised pulmonary function. Changes in CO2 production and O2 consumption induced by TPN using either glucose as the entire source of non-protein calories, or fat emulsions as 50 per cent of the non-protein calories, have been analyzed either in patients with chronic nutritional depletion or in acutely ill patients secondary to injury and infection. In patients with chronic nutritional depletion, shifting from the lipid to the glucose system caused a 20 per cent (P less than 0.025) increase in CO2 production which resulted in a 26 per cent increase in minute ventilation (P less than 0.01). In the acutely ill patients receiving the glucose system, CO2 production was significantly higher than in those receiving the lipid system (179 vs. 147 ml.min-1.m-2; P less than 0.01. Fat emulsions can serve as a source of non-protein calories and are associated with lesser degrees of CO2 production than isocaloric amounts of glucose.