Cerebral metabolic suppression

Hypnotic agents, such as propofol, barbiturates, or etomidate, depress cerebral oxidative metabolism and hence lower cerebral blood flow and volume, and ICP. The brain depends on ATP to uphold its structural integrity (~40% of O2 consumption) and to produce electrical activity (60% of O2 consumption). Only electrical activity can be suppressed with these drugs. Barbiturates are commonly used for this purpose. Cerebral electrical activity and normal coupling mechanisms between metabolism and flow must be present if barbiturates are to lower ICP.21,22,65 Flow-metabolism coupling mechanisms may be assessed by the cerebrovascular response to carbon dioxide and barbiturates are only effective if some carbon dioxide reactivity is retained.22 For thiopentone repeated boluses of 250 mg (up to 3-5 g) are recommended followed by an infusion of 4-8 mg/kg/h. Barbiturate therapy should be targeted to a predefined EEG burst suppression ratio. Unfortunately all agents that depress cerebral metabolism have side effects. For propofol and barbiturates the most relevant is systemic hypotension, which is often exacerbated by hypovolaemia. Etomidate has very little effect on haemodynamics but interferes with endogenous steroid synthesis and its prolonged use in intensive care has been abandoned. Synergy with even moderate hypothermia may be helpful provided mean arterial pressure is maintained.65 After initial reports of the effectiveness of short acting barbiturates in lowering ICP after head injury, three controlled trials have failed to show any overall significant improvement of outcome or reduction in a number of patients dying with intracranial hypertension.149-151 Such trials involved heterogeneous groups of patients, however, and a treatment benefit in a subgroup may have been missed. The ideal hypnotic agent awaits development. Elimination of thiopentone takes several days and interferes with establishing brain death.

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