Pain in the critically ill patient is undesirable for reasons other than humanistic ones. By stimulation of respiration, pain exacerbates tachypnea and interferes with ventilator weaning; thoracoabdominal pain causes reflex splinting of the respiratory musculature resulting in a restrictive respiratory defect; there is also a reflex loss of diaphragmatic contractility. Through excitement of the stress response, pain triggers protein catabolism and worsens nitrogen imbalance; nitrogen imbalance is further exacerbated by a pain-mediated paralytic ileus causing a delay in reinstitution of enteral nutrition and a potential loss of enterocyte integrity. Stress response activation also causes fluid and electrolyte derangements via antidiuretic hormone (ADH) and corticotropin (ACTH) release, and immune dysfunction. Stress can increase blood coagulability and may predispose a patient to deep venous thrombosis. Although neuraxial blockade with local anesthetics has been shown to be more reliable at obtunding this neurohumoral response, the provision of effective analgesia by the intravenous route has been demonstrated to significantly reduce at least some of the detrimental effects of pain.