Hypotensive effect of nimodipine during treatment for aneurysmal subarachnoid haemorrhage.

To determine the incidence of induced systemic hypotension in patients after aneurysmal subarachnoid haemorrhage (SAH) and nimodipine treatment 87 consecutive cases were reviewed. The patients were managed according to the same Nimodipine treatment protocol. After confirmation of SAH the nimodipine treatment was started as a continuous intravenous perfusion at a dosage of 0.5 mg/h and gradually increased every 6 hours if haemodynamically tolerated until the maintenance dose of 2 mg/h was reached. Median systemic pressure was continuously measured and tolerated until a lowest limit of 75 mmHg. In 31 patients (36%) hypotension with values below 75 mmHg during at least 30 minutes was noted and needed Nimodipine reduction. Intravenous Nimodipine administration was responsible for hypotension in 26 cases as compared to 5 cases due to oral administration. 38% of all patients required support by vaso-active agents (Dopamine or Nor-adrenaline). There was no statistically significant difference of incidence of delayed ischaemic deterioration comparing the Nimodipine-reduction group with the normal dose group. This study demonstrates that a considerable risk exists of Nimodipine induced hypotension in intravenous administration despite gradually increasing the doses. Correction of hypotension through further induced hypervolaemia accompanied by vasoactive agents can lead to critical haemodynamic situations. We therefore recommend oral Nimodipine administration.