EFfects of nimodipine on cerebral blood flow and cerebrospinal fluid pressure after cardiac arrest: correlation with neurologic outcome

• Published in: Anesthesia and analgesia Vol. 68; no. 4; pp. 436 - 443
• Main Authors: FORSMAN, M, AARSETH, H. P, NORDBY, H. K, SKULBERG, A, STEEN, P. A
• Format: Journal Article
• Language: English
• Published: Hagerstown, MD Lippincott 01-04-1989
• Subjects: Aged; Biological and medical sciences; Cardiovascular system; Cerebrospinal Fluid Pressure - drug effects; Cerebrovascular Circulation - drug effects; Consciousness; Female; Heart Arrest - physiopathology; Humans; Intracranial Pressure - drug effects; Male; Medical sciences; Middle Aged; Miscellaneous; Nimodipine - pharmacology; Pharmacology. Drug treatments; Human; Brain; Intensive cardiocirculatory care; Cardiocirculatory arrest; Calcium antagonist; Double blind study; Cardiovascular disease; Hemodynamics; Cerebrospinal fluid; Osmotic pressure
• ISSN: 0003-2999; 1526-7598
• DOI: 10.1213/00000539-198904000-00003

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 g-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.