[Effects of sedative agents on metabolic demand]

Literature about the effects of sedative drugs on the metabolic demand of critically ill patients is relatively old and of relatively poor quality. Most are experimental or observational studies. Level of evidence is therefore relatively low corresponding to "expert opinion". The effects of analgesics and hypnotics on tissue metabolic demand associated remain difficult to be adequately quantified. They are essentially related to a decreased neuro-humoral response to stress. This response involves principally the sympathetic system, which could be effectively blocked by most of the anesthetic agents. Other factors could participate to the observed reduction in tissue metabolic demand, as a decrease in spontaneous muscular activity, a reduction in work of breathing and/or a decrease in body temperature. The relative contribution of these different factors will depend on the clinical situation of the patient. Proper effects of anesthetic agents on cellular metabolism are limited as they can only decrease the functional component of this metabolism especially at the level of the heart and to some extent, at the level of the brain. Although the control of the sympathetic activity may be beneficial in critically ill patient, complete sympathetic blockade could be detrimental. Indeed, when oxygen transport to the tissues is acutely reduced, the sympathetic system plays an important role in the redistribution of blood flow according of local metabolic demand. The complete blunting of the neuro-humoral response to stress and therefore of the sympathetic system alters this physiological mechanism and results in a decrease in tissue oxygen extraction capabilities. An imbalance between tissue oxygen demand and delivery could appear with the development of cellular hypoxia. The institution of sedation in a critically ill patient requires careful evaluation of the sedation level using an appropriate scale. In patients in whom a reduction in metabolic demand is specifically requested, but also in patients with limited oxygen transport, the effects of sedative agents on the oxygen consumption-oxygen delivery relationship must also be monitored. The choice of the different agents to be administered will depend on the predefined objectives. As far as intravenous agents are concerned, there is no evidence than one association is more efficient in reducing patient's metabolic demand.