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Войти в исследования Journal of neurosurgical anesthesiology · 2023
The Effect of Oral Nimodipine on Cerebral Metabolism and Hemodynamic Parameters in Patients Suffering Aneurysmal Subarachnoid Hemorrhage.
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Moser Miriam, Schwarz Yannik, Herta Johannes, Plöchl Walter, Reinprecht Andrea, Zeitlinger Markus, Brugger Jonas, Ramazanova Dariga, Rössler Karl, Hosmann Arthur
Аннотация
INTRODUCTION: Nimodipine is routinely administered to aneurysmal subarachnoid hemorrhage patients to improve functional outcomes. Nimodipine can induce marked systemic hypotension, which might impair cerebral perfusion and brain metabolism.
METHODS: Twenty-seven aneurysmal subarachnoid hemorrhage patients having multimodality neuromonitoring and oral nimodipine treatment as standard of care were included in this retrospective study. Alterations in mean arterial blood pressure (MAP), cerebral perfusion pressure (CPP), brain tissue oxygen tension (pbtO 2 ), and brain metabolism (cerebral microdialysis), were investigated up to 120 minutes after oral administration of nimodipine (60 mg or 30 mg), using mixed linear models.
RESULTS: Three thousand four hundred twenty-five oral nimodipine administrations were investigated (126±59 administrations/patient). After 60 mg of oral nimodipine, there was an immediate statistically significant (but clinically irrelevant) drop in MAP (relative change, 0.97; P <0.001) and CPP (relative change: 0.97; P <0.001) compared with baseline, which lasted for the whole 120 minutes observation period ( P <0.001). Subsequently, pbtO 2 significantly decreased 50 minutes after administration ( P =0.04) for the rest of the observation period; the maximum decrease was -0.6 mmHg after 100 minutes ( P <0.001). None of the investigated cerebral metabolites (glucose, lactate, pyruvate, lactate/pyruvate ratio, glutamate, glycerol) changed after 60 mg nimodipine. Compared with 60 mg nimodipine, 30 mg induced a lower reduction in MAP (relative change, 1.01; P =0.02) and CPP (relative change, 1.01; P =0.03) but had similar effects on pbtO 2 and cerebral metabolism ( P >0.05).
CONCLUSIONS: Oral nimodipine reduced MAP, which translated into a reduction in cerebral perfusion and oxygenation. However, these changes are unlikely to be clinically relevant, as the absolute changes were minimal and did not impact cerebral metabolism.
METHODS: Twenty-seven aneurysmal subarachnoid hemorrhage patients having multimodality neuromonitoring and oral nimodipine treatment as standard of care were included in this retrospective study. Alterations in mean arterial blood pressure (MAP), cerebral perfusion pressure (CPP), brain tissue oxygen tension (pbtO 2 ), and brain metabolism (cerebral microdialysis), were investigated up to 120 minutes after oral administration of nimodipine (60 mg or 30 mg), using mixed linear models.
RESULTS: Three thousand four hundred twenty-five oral nimodipine administrations were investigated (126±59 administrations/patient). After 60 mg of oral nimodipine, there was an immediate statistically significant (but clinically irrelevant) drop in MAP (relative change, 0.97; P <0.001) and CPP (relative change: 0.97; P <0.001) compared with baseline, which lasted for the whole 120 minutes observation period ( P <0.001). Subsequently, pbtO 2 significantly decreased 50 minutes after administration ( P =0.04) for the rest of the observation period; the maximum decrease was -0.6 mmHg after 100 minutes ( P <0.001). None of the investigated cerebral metabolites (glucose, lactate, pyruvate, lactate/pyruvate ratio, glutamate, glycerol) changed after 60 mg nimodipine. Compared with 60 mg nimodipine, 30 mg induced a lower reduction in MAP (relative change, 1.01; P =0.02) and CPP (relative change, 1.01; P =0.03) but had similar effects on pbtO 2 and cerebral metabolism ( P >0.05).
CONCLUSIONS: Oral nimodipine reduced MAP, which translated into a reduction in cerebral perfusion and oxygenation. However, these changes are unlikely to be clinically relevant, as the absolute changes were minimal and did not impact cerebral metabolism.