Barbiturates reduce the metabolic rate of brain tissue, as well as the cerebral blood flow. With these reductions, the blood vessels in the brain narrow, decreasing the amount of volume occupied by the brain, and hence the intra-cranial pressure. The hope is that, with the swelling relieved, the pressure decreases and some or all brain damage may be averted. Several studies have supported this theory by showing reduced mortality when treating refractory intracranial hypertension with a barbiturate coma.
Controversy exists, however, over the benefits of using barbiturates to control intracranial hypertension. Some studies have shown that barbiturate-induced coma can reduce intracranial hypertension but does not necessarily prevent brain damage. Furthermore, the reduction in intracranial hypertension may not be sustained. Some randomized trials have failed to demonstrate any survival or morbidity benefit of induced coma in diverse conditions such as neurosurgical operations, head trauma, intracranial aneurysm rupture, intracranial hemorrhage, ischemic stroke, and status epilepticus. If the patient survives, cognitive impairment may also follow recovery from the coma.
About 55% of the glucose and oxygen utilisation by the brain is meant for its electrical activity and the rest for all other activities like metabolism. This is recognised by something such as an Electro encephalogram (EEG), which measures electrical activity in the brain. When barbiturates are given to brain injured patients for Induced coma, they act by reducing the electrical activity of the brain, which in theory reduces the metabolic and oxygen demand. Once there is improvement in the patient's general condition, the barbiturates are withdrawn gradually and the patient regains consciousness.