Early effects of nimodipine on intracranial and cerebral perfusion pressures in cerebral anoxia after out-of-hospital cardiac arrest.

Some calcium entry blockers seem to improve the neurological survival of anoxic comas. The early monitoring of intracranial pressure shows the frequency of intracranial hypertension. A calcium channel blocker has been shown to increase the cerebral blood flow which can potentially lead to deleterious increases of the intracranial pressure. This study presents 39 out-of-hospital cardiac arrests resuscitated with success. The intracranial pressures were registered by means of an extra dural screw set up as soon as possible. Nineteen patients received an early continuous 5 days nimodipine treatment (0.58 gamma/kg weight/min. after a 12.3 gamma/kg weight bolus). The other 20 patients did not receive any calcium entry blocker. The two groups were similar in terms of age, origin and electrical type of cardiac arrest, duration of cardiac arrest before BLS and before ACLS, principles of the treatment, initial neurological status and biological values. The maximum and mean intracranial pressures of the nimodipine group were always lower than the intracranial pressure of the control group. The cerebral perfusion pressure was never significantly different in both groups. If the nimodipine treatment proves to be efficient on neurological survival, it would be all the more interesting because it seems to limit the intracranial hypertension phenomenon which aggravates the neurological prognosis.