1

The metabolic response to stress was first described in 1942, by Sir David Cuthbertson, who introduced the terms ebb and flow to describe the phases of hypo-and hypermetabolism that follow traumatic injury. The metabolic response is triggered by multiple stimuli, including arterial and venous pressure and volume, osmolality, pH, arterial oxygen content, pain, anxiety, and toxic mediators from infection and tissue injury (Table 1.1). These stimuli reach the hypothalamus and then stimulate the sympathetic nervous system and the adrenal medulla. Indeed, the metabolic response to stress is a physiological response to an insult that might become pathological, depending on the intensity and duration of injury. Actually, the metabolic response can be seen as the “fight or flight” response to adverse phenomena that can become highly associated with increased morbidity and mortality if perpetuated for long periods. The ultimate goal of the metabolic response is to restore homeostasis. Intermediate goals are to limit further blood loss; to increase blood flow, allowing greater delivery of nutrients and elimination of waste products; to debride necrotic tissue; and to initiate wound healing.