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Plasma cholesterol levels, plasma lactate, and total body RQ were measured in septic patients undergoing total parenteral nutrition (TPN) with glucose, fat, and two different branch-chain amino acid admixtures (49% BCAA and 16% BCAA). Mean plasma cholesterol for all measurements (2.61 +/- 0.94 [SD] mmol/L) was lower than normal; however, it was higher with 49% BCAA than with 16% BCAA (2.94 +/- 0.95 vs. 2.27 +/- 0.81 mmol/L, p less than .001) for comparable loads of glucose, fat, and total amino acids. Plasma lactate and RQ were lower with 49% BCAA than with 16% BCAA (p less than .001 for both). Cholesterol was directly related to the absolute dose of BCAA (p less than .001), was unrelated to the dose of non-BCAA, and was inversely related to lactate (p less than .001). These results suggest that BCAA ketoacids contribute to cholesterol synthesis in sepsis, as well as being an oxidative source. The data also suggest that the reduction in alanine in BCAA-enriched amino-acid TPN assists in the lowering of plasma lactate secondary to abnormal septic glucose metabolism.

The effect of the infusion of mixed amino acids with glucose and fat on metabolic rate (MR) in sepsis (S) and in nonseptic trauma (NS) was investigated. The results demonstrated that diet-induced thermogenesis (specific dynamic action) controlled in S and in NS 25% and 18% of the MR variability, respectively (r2 = .25 and .18, p less than .01 for both). Also, diet-induced thermogenesis represented a quantitatively relevant portion of the total MR. There was a larger thermogenic effect of amino acids in S with respect to NS (22.3 vs. 5.7 cal/mg N, p less than .01) with a concomitantly increased thermogenic effect of fat. The results suggest the importance of recognizing the thermogenic effect of administered nutrients as an important determinant of MR during calorimetric measurements. The finding of an enhanced thermogenic effect of amino acids and fat in S also implies the need for more complete investigations of the impact of these substrates in modifying oxidative and energy metabolism in S.

A quantification of the determinants of arterial hypoxemia was performed in 376 cardiorespiratory measurements obtained from 180 critically ill patients. Statistical analysis showed that pulmonary venous admixture (Qsp/Qt) could explain only 48% of the PaO2 variability in the sample of measurements taken (r2 = 0.48), while the effect of central venous O2 tension (PVO2) brought the total explained PaO2 variability up to 82% (total r2 = 0.82). These findings imply that pulmonary function is not the only determinant of PaO2; the PVO2-mediated effect of other cardiovascular and metabolic determinants must be recognized in the clinical setting.