• Jan Claassen, Stephan A Mayer, Neeraj Badjatia, J Michael Schmidt, Sang-Bae Ko, Amanda M Carpenter, H Alex Choi, Emily Gilmore, E Sander Connelly, and Myunghee Paik.
• Division of Neurocritical Care, The Neurologic Institute of New York, Columbia University College of Physicians and Surgeons, Milstein Hospital Building 8 Center, 177 Fort Washington Ave, New York, NY 10032, USA.
• Neurocrit Care. 2012 Jun 1;16(3):363-7.

BackgroundNimodipine is the only medication shown to improve outcomes after aneurysmal subarachnoid hemorrhage (SAH). Preliminary theories regarding the mechanism by which it prevents vasospasm have been challenged. The acute physiologic and metabolic effects of oral Nimodipine have not been examined in patients with poor-grade SAH.MethodsThis is an observational study performed in 16 poor-grade SAH patients undergoing multimodality monitoring who received oral Nimodipine as part of routine clinical care. A total of 663 doses of Nimodipine were observed. Changes in physiologic measurements including MAP, CPP, ICP, P(bt)O(2), and CBF were examined.ResultsAdministration of oral Nimodipine was associated with a 1.33 mmHg decrease in MAP (P < 0.001) and a 1.22 mmHg decrease in CPP (P < 0.001). When administration of Nimodipine was associated with MAP decreases, P(bt)O(2) (1.03 mmHg; P < 0.001) and CBF (0.39 ml/100 g/min; P = 0.002) also decreased.ConclusionsDespite CPP targeted therapy with vasopressor medication, oral Nimodipine was associated with a decrease in MAP and CPP. When Nimodipine administration was associated with a decrease in MAP, there were concomitant drops in P(bt)O(2) and CBF. These findings suggest that MAP support after oral Nimodipine may be important to maintain adequate CBF in patients with poor-grade subarachnoid hemorrhage.

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