How Many Nonprotein Calories Does a Critically Ill Patient Require? A Case for Hypocaloric Nutrition in the Critically Ill Patient.

Calculation of energy and protein doses for critically ill patients is still a matter of controversy. For more than 40 years of nutrition support, the total amount of nutrients to be delivered to these patients has been calculated based on expert recommendations, and this calculation is based on the administration of nonprotein calories in one attempt to ameliorate catabolic response and avoid the weight loss. New evidence suggests protein delivery is the most important intervention to improve clinical and metabolic outcomes. This article describes the metabolic rationale and the new evidence supporting a change in the approach of metabolic support of the critically ill, proposing a physiological-based intervention supported by the recognition of ancillary characteristics of the metabolic response to trauma and injury. A moderate dose of calories around 15 kcal/kg/d with a delivery of protein of 1.5 g/kg/d appears to be the new recommendation for many hypercatabolic patients in the first week following injury.

Longitudinal and radial gradients of PO(2) in the hamster cheek pouch microcirculation.

OBJECTIVES: The aim of this study was to determine longitudinal and radial gradients in oxygen tension (PO(2)) in microvessels of the hamster cheek pouch. METHODS: We measured PO(2) using the phosphorescence-quenching method in two orders of arterioles (45.8 +/- 5.5 and 19.9 +/- 1.8 micro m diameter), capillaries, and two orders of venules (50.5 +/- 3.4 and 21.4 +/- 2.0 micro m diameter) in order to determine the longitudinal PO(2) gradient. At the arteriolar and venular sites, we also measured PO(2) at four different sites for an analysis of radial PO(2) gradients: centerline, inside wall (larger arteriole and venule only), outside wall, and interstitium. We used 10 hamsters weighing 115 +/- 27 g anesthetized with pentobarbital intraperitoneally and maintained with alpha-chloralose intravenously. The cheek pouch was everted and a single-layered preparation was studied by intravital microscopy. Albumin-bound Pd-porphyrin was infused into the circulation and excited by flash illumination at 10 Hz, with a rectangular diaphragm limiting the excitation field to 5 x 25 micro m. RESULTS: In the longitudinal direction, intravascular PO(2) decreased significantly (P < 0.01) from large arterioles (39.5 +/- 2.3 mmHg) to small arterioles (32.2 +/- 0.3 mmHg), then to capillaries (30.2 +/- 1.8 mmHg), and on to small venules (27.3 +/- 2.1 mmHg) and large venules (25.5 +/- 2.2 mmHg). In the radial direction, PO(2) decreased significantly (P < 0.01) in and around larger arterioles, and to a lesser extent, around the smaller ones (P < 0.05). There was no significant PO(2) gradient, longitudinal or radial, associated with venules. The PO(2) difference from the centerline to the outside wall in large arterioles was 8.3 +/- 1.4 mmHg, and most of the decline in PO(2) in the radial direction was contributed by the intravascular difference (4.7 +/- 2.1 mmHg) and only about 1.0 +/- 2.7 mmHg by the transmural difference. CONCLUSIONS: Our data show that there are large intra-arteriolar radial PO(2) gradients, but no large transmural PO(2) differences, suggesting that the oxygen consumption of the microvessel wall is not exceptionally high.

Microvascular blood flow and oxygenation during hemorrhagic hypotension.

Understanding microvascular oxygen transport requires the knowledge of microvessel topology and geometry, blood flow and oxygen levels. Microvascular hemodynamic responses to hemorrhagic hypotension (HH) such as size-dependent vasoconstriction and blood flow reduction could lead to increased longitudinal oxygen partial pressure (PO(2)) gradients. However, the mesenteric microvascular PO(2) has never been evaluated during HH. Therefore, we studied hemodynamic variables and PO(2) distribution in 165 mesenteric microvessels from 39 anesthetized rats to investigate whether HH-induced vasoconstriction and blood flow reduction were associated with changes in longitudinal PO(2) gradients. Vessels were analyzed according to their position in the network, as well as a few interstitial PO(2) areas. We found that during baseline a small PO(2) gradient exists, but HH is accompanied by more pronounced microvascular longitudinal PO(2) gradients. Decreased blood flow did not seem to completely explain these findings, since blood flow was uniformly diminished in arterioles and venules, independent of diameter and position in the network. During HH, some microvessels presented higher PO(2) than during baseline despite blood flow reduction, possibly due to a combination of systemic hyperoxia and low oxygen consumption of mesentery. The data suggest that blood flow measurements may be a poor indicator of the oxygenation status in some regions of the mesentery. The enhanced mesenteric longitudinal PO(2) gradient may lead to regions with different levels of other physiologically active compounds.