Esmolol Blunts the Cerebral Blood Flow Velocity Increase During Emergence from Anesthesia in Neurosurgical Patients Philippe Grillo, MD*, Nicolas Bruder, MD*, Pascal Auquier, MD†, Daniel Pellissier, MD*, and Franc ¸ois Gouin, MD* *De ´partement d’Anesthe ´sie-Re ´animation and †Service de Sante ´ Publique et de Biostatistiques, Marseille, France Cerebral hyperemia has been demonstrated during emergence from anesthesia in neurosurgical patients, but its mechanism is speculative. We performed this study to test the hypothesis that this could be attrib- uted to sympathetic overactivity. Thirty neurosurgi- cal patients were included in a prospective, random- ized, double-blinded study comparing esmolol, a short-acting -blocker, and a placebo. Esmolol (0.3 mg · kg -1 · min -1 ) was infused from the end of anesthesia to 15 min after extubation. Cerebral blood flow velocity (CBFV), mean arterial blood pressure, and heart rate were recorded before anesthesia, dur- ing anesthesia after surgery, at extubation, and 5– 60 min after extubation. Cardiac output (COe) was estimated by using an esophageal Doppler from an- esthesia to 60 min after extubation. CBFV, COe, and heart rate were significantly lower in the esmolol group. Mean arterial blood pressure was comparable between the groups. There was no correlation be- tween CBFV and COe at any time point during the study. In conclusion, esmolol blunted the CBFV in- crease during emergence, confirming that sympa- thetic overactivity contributes to cerebral hyperemia during neurosurgical recovery. (Anesth Analg 2003;96:1145–9) R ecovery from general anesthesia and extubation is a period of intense physiological stress for patients. Oxygen consumption, catecholamine blood concentration, blood pressure, and heart rate (HR) increase after intracranial surgery (1). Cerebral hyperemia was also demonstrated at extubation by a concomitant increase in cerebral blood flow velocity (CBFV) and jugular venous bulb saturation in oxygen (2). There was a 60%– 80% increase in CBFV in the middle cerebral artery from preinduction value on extubation that persisted at a lower level for 1 h. This observation occurred after anesthesia with propofol or isoflurane. The mechanism of this cerebral hyperemic response was unclear. In this study, we hypothesized that the stress associated with emergence and re- sultant sympathetic stimulation could explain this finding. To test this hypothesis, we performed a prospective, randomized, double-blinded study, us- ing esmolol, a short-acting -blocking drug, to blunt the effects of sympathetic stimulation. Because es- molol may decrease cardiac output (CO), the rela- tionship between CBFV and CO changes was also studied. Materials and Methods After IRB approval and written informed consent, 30 patients, ASA physical status I or II, scheduled for elective intracranial surgery, were included in this study. The intracranial lesions were 16 meningiomas, 3 grade 0 aneurysms, 6 gliomas, 3 metastatic tumors, and 2 arteriovenous fistulas, and were equally distrib- uted between the 2 groups. Patients requiring emer- gency surgery, with clinical symptoms of intracranial hypertension, treated for systemic hypertension, or having contraindications for -blocking therapy, were not included in the study. Patients were ran- domly allocated into two groups: Group P (placebo: saline), n = 15, or Group E (esmolol), n = 15. The medication was prepared in equivalent volumes by a nurse who did not participate in the study. The anesthesiologist was blinded to the medication in- fused. Anesthesia was maintained with IV fentanyl (5–10 /kg), desflurane (5% expired), nitrous ox- ide (N 2 O) in oxygen (Fio 2 = 0.5), and atracurium. The end-tidal CO 2 value was maintained between 30 This study was supported by an institutional grant from the Assistance Publique–Ho ˆ pitaux de Marseille. Accepted for publication December 26, 2002. Address correspondence and reprint requests to Pr Nicolas Bruder, De ´partement d’anesthe ´sie-re ´animation, CHU Timone, 264 Rue Saint-Pierre 13385 Marseille Cedex, France. Address e-mail to nicolas.bruder@ap-hm.fr. DOI: 10.1213/01.ANE.0000055647.54957.77 ©2003 by the International Anesthesia Research Society 0003-2999/03 Anesth Analg 2003;96:1145–9 1145