[Effects of analgesia and sedation on cerebrovascular circulation, cerebral blood volume, cerebral metabolism and intracranial pressure]

Abstract

Cerebral blood flow autoregulation, CO2 reactivity and the pressure-volume relationship may be impaired or abolished in patients with intracranial mass lesions, brain trauma, cerebral vasospasm or increased cerebral elastance. Sedatives, analgetics, and anesthetics may induce major changes in cerebral blood flow, cerebral metabolism and intracranial pressure (ICP). The inadequate use of these drugs may aggravate the preexisting intracranial pathology and may worsen outcome. Thus it is important to understand the effects of sedatives, analgetics, and anaesthetics on intracranial hemodynamics and metabolism during physiological and pathological conditions. Hypnotics (barbiturates, etomidate, propofol), benzodiazepines, opioids (fentanyl, alfentanil, sufentanil) and alpha-2-adrenergic agonists (clonidine, dexmedetomidine) reduce cerebral blood flow. With ketamine, cerebral blood flow changes in a regionally specific fashion, with some territories showing increases and others showing decreases in cerebral blood flow. Cerebral metabolism is decreased during sedation and analgesia with hypnotics, benzodiazepines, and opioids, while infusion of ketamine produces stimulation as well as suppression of cerebral metabolism. This suggests that the changes in cerebral blood flow seen with these drugs occur secondary to their cerebral, metabolic effects. Alpha-2-adrenergic agonists produce no significant changes in cerebral metabolism. However, cerebral blood flow is decreased with clonidine or dexmedetomidine. This suggests uncoupling between cerebral metabolism and flow due to decreases in central catecholamine turnover. Hypnotics and benzodiazepines decrease ICP due to decreases in cerebral blood volume. However, these drugs may also decrease mean arterial blood pressure, which may result in a critical reduction in cerebral perfusion pressure. ICP remains unchanged with the use of opioids as long as mean arterial pressure is maintained constant. However, decreases in mean arterial pressure during infusion of opioids induce autoregulatory cerebral vasodilation, which in turn increases cerebral blood volume and ICP. Ketamine may increase ICP specifically in subjects with spontaneous ventilation. With mechanical hyperventilation and constant systemic hemodynamics, ketamine fails to increase ICP in most of the patients. Alpha-2-adrenergic agonists produce no significant changes in ICP, although there may be a transient decrease in ICP with lower doses.