This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a colleague Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Forsman, M. Articles by Steen, P. A. Search for Related Content PubMed PubMed Citation Articles by Forsman, M. Articles by Steen, P. A.

Effects of Nimodipine on Cerebral Blood Flow and Cerebrospinal Fluid Pressure After Cardiac Arrest

Correlation With Neurologic Outcome

Marianne Forsman, MD, Hans P. Aarseth, MD, PhD^*, Hans K. Nordby, MD, PhD, Andreas Skulberg, MD, PhD, and Petter A. Steen, MD, PhD

Department of Anesthesiology, Ullevaal University Hospital, Oslo, Norway *Department of Internal Medicine, Ullevaal University Hospital, Oslo, Norway Department of Neurosurgery, Ullevaal University Hospital, Oslo, Norway

Abstract

Fifty-one patients were included in a blind randomized study to evaluate whether the Ca-blocker nimodipine could influence cerebral blood flow (CBF) or cerebrospinal fluid pressure (CSFP) during the cerebral hypoperfusion period that follows resuscitation from cardiac arrest and to determine whether changes in CBF correlate with neurologic outcome.

CBF measured 1 to 4 hours after arrest with the use of ¹³³Xe intravenous was significantly greater with nimodipine than with placebo (27 ± 3 versus 13 ± 1 ml. 100 8^–1.min^–1 at 3 hours), but with no significant difference at 24 hours. There was no clinical evidence of seriously increased CSFP in any patient in either group the first 48 hours. Mean arterial pressure was significantly lower (86 ± 4 versus 101 ± 4 mm Hg at 3 hours), and antiarrhythmic drugs were used significantly less frequently in the nimodipine group than in the placebo group. Twelve patients in each group eventually regained consciousness. There was no significant difference in neurologic status between the two groups at any point, and no positive correlation between CBF in the hypoperfusion period and neurologic outcome.

Key Words: BRAIN, CEREBRAL BLOOD FLOW—cardiac arrest • HEART—cardiac arrest • PHARMACOLOGY—CALCIUM CHANNEL BLOCKERS, nimodipine

This article has been cited by other articles:

				R. W. Neumar, J. P. Nolan, C. Adrie, M. Aibiki, R. A. Berg, B. W. Bottiger, C. Callaway, R. S.B. Clark, R. G. Geocadin, E. C. Jauch, et al. Post-Cardiac Arrest Syndrome: Epidemiology, Pathophysiology, Treatment, and Prognostication A Consensus Statement From the International Liaison Committee on Resuscitation (American Heart Association, Australian and New Zealand Council on Resuscitation, European Resuscitation Council, Heart and Stroke Foundation of Canada, InterAmerican Heart Foundation, Resuscitation Council of Asia, and the Resuscitation Council of Southern Africa); the American Heart Association Emergency Cardiovascular Care Committee; the Council on Cardiovascular Surgery and Anesthesia; the Council on Cardiopulmonary, Perioperative, and Critical Care; the Council on Clinical Cardiology; and the Stroke Council Circulation, December 2, 2008; 118(23): 2452 - 2483. [Full Text] [PDF]

				W. T. Longstreth Jr., C. E. Fahrenbruch, M. Olsufka, T. R. Walsh, M. K. Copass, and L. A. Cobb Randomized clinical trial of magnesium, diazepam, or both after out-of-hospital cardiac arrest Neurology, August 27, 2002; 59(4): 506 - 514. [Abstract] [Full Text] [PDF]

				R. O. Roine, J. Launes, P. Nikkinen, L. Lindroth, and M. Kaste Regional Cerebral Blood Flow After Human Cardiac Arrest: A Hexamethylpropyleneamine Oxime Single Photon Emission Computed Tomographic Study Arch Neurol, June 1, 1991; 48(6): 625 - 629. [Abstract] [PDF]