Metabolic and nutritional disorders in critically ill cardiac and cardiac surgical patients

Nutritional alteration is frequent in patients with severe chronic heart failure. The determination of body mass, measured in nonedematous state, is the easiest and most cost-effective method; nonintentional loss of 10% of body mass is considered a sign of undernutrition. As for other wasting syndromes, cardiac cachexia is due both to a decrease in nutrient intake (anorexia, malabsorption) and to specific metabolic alterations (hypercatabolism with increased energy expenditure, response to hypoxia, inflammatory status, etc). Among the various mechanisms involved in the pathogenesis of cachexia, cellular hypoxia has long been recognized; in the light of recent findings in chronic hypoxia, several effects of Pot on transcription might be involved. The chronic activation of the endogenous neurohormonal system is a specific feature of such patients; a striking relationship was found between cachexia and hormonal levels which correlate better than the classical parameters of cardiac failure severity. The frequency of inflammatory syndrome is a third important point. Several studies have shown that tumor necrosis factor-alpha was significantly increased in cachectic patients and that chronic activation of the systemic immune response might be a common and unifying factor. Cardiac surgery and cardiopulmonary bypass represent another source for severe metabolic stress and are often responsible for lactate metabolism disturbance. By using a model of the metabolic fate of an exogenous lactate load, we found that 12 to 14 hrs after uncomplicated cardiac surgery lactate clearance was strongly affected while plasma lactate was only moderately increased. This finding could be linked to the endotoxin release that has often been reported during bypass.