Effect of neuromuscular blockade on energy expenditure in patients with severe head injury.

BACKGROUND: The purpose of this study was to determine the effect of neuromuscular blockade on energy expenditure in severely head-injured patients; to determine the effects of body temperature, nutrition support, and morphine use on metabolic rate; and to compare measured energy expenditure with values from predictive equations. METHODS: Energy expenditure was measured using indirect calorimetry in 2 groups of ventilated patients-18 with severe head injury during and after administration of pancuronium bromide and morphine, and second, 14 severely traumatized patients without severe head injury (trauma group) who received morphine without neuromuscular blockade. RESULTS: The mean energy expenditure of head-injured patients increased significantly once pancuronium was discontinued, ie, from 24.2 +/- 3.1 to 28.7 +/- 4.6 kcal/kg (p = .002). This effect was independent of other relevant variables such as morphine dose, body temperature, and nutrition support. When compared with the Harris-Benedict and World Health Organization predictive equations, neuromuscular blockade resulted in a stress factor of only 0.96 and 0.95, respectively, which increased to 1.19 and 1.18, respectively, once blockade was discontinued. Head-injured patients not on neuromuscular blockade had a significantly greater energy expenditure when compared with the trauma group (p = .02). CONCLUSIONS: Neuromuscular blockade in severely head-injured patients decreases energy expenditure to basal levels, independent of morphine use, body temperature, and feeding. Levels of hypermetabolism in both the head-injured and trauma groups were relatively low, at 19% and 5% above predicted values, respectively. This study provides useful information for the management of nutrition support in severely traumatized patients.

Conditioned nutritional requirements: therapeutic relevance to heart failure.

BACKGROUND: The advent of disease, genetic predisposition or certain drug therapies may significantly alter the nutritional demands of specific organs. Several specific metabolic deficiencies have been found in the failing myocardium: (1) a reduction in L-carnitine, coenzyme Q10, creatine, and thiamine--nutrient cofactors important for myocardial energy production; (2) a relative deficiency of taurine, an amino acid integral to intracellular calcium homeostasis; (3) increased myocardial oxidative stress and a reduction of antioxidant defenses. Deficiencies of carnitine or taurine alone are well documented to result in dilated cardiomyopathy in animals and humans. Each of these deficiencies is amenable to restoration through dietary supplementation. A variety of nutrients have been investigated as single therapeutic agents in pharmacologic fashion, but there has been no broad-based approach to nutritional supplementation in congestive heart failure to correct this complex of metabolic abnormalities. METHOD AND RESULTS: We have demonstrated deficiencies in carnitine, taurine and coenzyme Q10 in cardiomyopathic hamster hearts during the late stage of the cardiomyopathy. In another study, we randomized placebo diet against a supplement containing taurine, coenzyme Q10, carnitine, thiamine, creatine, vitamin E, vitamin C, and selenium to cardiomyopathic hamsters during the late stages of the disease. Supplementation for 3 months markedly improved myocyte sarcomeric structure, developed pressure, +dp/dt, and -dp/dt. We also documented carnitine, taurine and coenzyme Q10 in biopsies taken from human failing hearts, the levels correlating with ventricular function. A double-blind, randomized, placebo-controlled trial of a supplement containing these nutrients, given for 30 days, restored myocardial levels and resulted in a significant decrease in left ventricular end-diastolic volume. CONCLUSION: These experiments suggest that a comprehensive restoration of adequate myocyte nutrition may be important to any therapeutic strategy designed to benefit patients suffering from congestie heart failure. Future studies in this area are of clinical importance.