Trunet P, Dreyfuss D, Bonnet J L, Teisseire B, Becker J, Rapin M
Presse Med. 1983 Dec 17;12(46):2927-30.
The influence of increased enteral caloric intakes on respiratory gas exchanges was evaluated in 6 patients (5 men, 1 woman; mean-age: 54 years) in steady state and requiring continuous ventilatory support. Oxygen consumption (VO2), carbon dioxide production (VCO2), respiratory quotient (R), determined using an open circuit indirect calorimetric method, and arterial blood gases were measured on two consecutive days while ventilation conditions were unchanged. On the first day, the patients received a water diet only and on the following day an enteral caloric load (1491 +/- 65 Kcal/m2/24 h). The results showed a significant increase in VO2 (p less than 0.05) and R (p less than 0.001) and a rise in VCO2 from 106 +/- 4 to 139 +/- 9 ml/mn/m2 (p less than 0.01). The rise in VCO2 induced an increase of arterial carbon dioxide tension (PaCO2) from 26.3 +/- 1.6 to 34.4 +/- 2.4 mmHg (p less than 0.001). This study showed that because of the constancy of alveolar ventilation, the enteral nutrition-related increase of VCO2 is responsible for a PaCO2 increase and emphasized the need for adjusting artificial ventilation to any change in caloric intake in patients supported with mechanical ventilation.