Clinical meaning
Surgery triggers a complex neuroendocrine stress response mediated by afferent neural signals from the surgical site and systemic inflammatory mediators. The hypothalamic-pituitary-adrenal (HPA) axis is activated, increasing cortisol secretion (reaching 75-150 mcg/dL in major surgery vs normal <20 mcg/dL). Sympathetic nervous system activation increases catecholamine release, causing tachycardia, hypertension, increased myocardial oxygen demand, and peripheral vasoconstriction. The overall metabolic response shifts to catabolism: hyperglycemia (from cortisol-mediated insulin resistance and gluconeogenesis, glycogenolysis), protein catabolism, lipolysis, and sodium/water retention (ADH and aldosterone release). These stress responses increase myocardial oxygen demand while surgical blood loss, anemia, and hypotension may simultaneously decrease oxygen supply, creating a dangerous supply-demand mismatch in patients with coronary artery disease. This explains why perioperative myocardial infarction (PMI) occurs in 1-5% of patients undergoing non-cardiac surgery and accounts for the majority of perioperative deaths. The surgical inflammatory response also creates a prothrombotic state through tissue factor release, platelet activation, and impaired fibrinolysis, increasing the risk of deep vein thrombosis and pulmonary embolism. Anesthetic agents affect multiple organ systems: volatile anesthetics cause myocardial depression and vasodilation; neuromuscular blocking agents require adequate...