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, resulting in a shrunken brain, and hence lower
intracranial 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. About 60% of the glucose and oxygen used by the brain is meant for its electrical activity and the rest for all other activities such as metabolism. When barbiturates are given to brain injured patients for induced coma, they act by reducing the electrical activity of the brain, which reduces the metabolic and oxygen demand. Their action limits oxidative damage to lipid membranes and may scavenge free radicals. They also lead to reduced vasogenic edema, fatty acid release and intracellular calcium release. Once there is improvement in the patient's general condition, the barbiturates are withdrawn gradually and the patient regains consciousness. Controversy exists over the benefits of using barbiturates to control
intracranial hypertension. Some studies have found that barbiturate-induced coma can reduce intracranial hypertension but does not necessarily prevent brain damage.
intracranial aneurysm rupture,
intracranial hemorrhage, ischemic
stroke, and
status epilepticus. If the patient survives, cognitive impairment may also follow recovery from the coma. Due to these risks, barbiturate-induced coma should be reserved for cases of refractory intracranial pressure elevation. == See also ==