Glycopyrrolate prevents extreme bradycardia and cerebral deoxygenation during electroconvulsive therapy.

The stimulation phase of electroconvulsive therapy (ECT) induces bradycardia. We evaluated the effect of this bradycardia on cerebral perfusion and oxygenation by administration of the anticholinergic drug glycopyrrolate (Glp). Cerebral perfusion was estimated by transcranial ultrasound in the middle cerebral artery reporting the mean flow velocity (middle cerebral artery [MCA] V(mean)), and cerebral oxygenation was determined by near-infrared spectroscopy of the frontal lobe. Before ECT, heart rate (HR) was 84 beats min(-1) (66-113; median and range) and decreased to 17 (7-85) beats min(-1) during the stimulation phase of ECT (P < 0.001). Middle cerebral artery V(mean) decreased 43% (9%-71%; P < 0.001), and frontal lobe oxyhemoglobin (O(2)Hb) concentration decreased from 0.6 (0.0-25.3) to 0.1 (-1.9 to 7.6) microM, whereas the deoxyhemoglobin concentration increased from -0.2 (-13.9 to 0.8) to 0.0 (-4.2 to 0.8) microM (P < 0.001). Pretreatment with Glp largely eliminated these effects during the stimulation phase of ECT, maintaining HR at 78 (40-94) beats min(-1), MCA V(mean) at 53 (37-77) cm s(-1), and O(2)Hb at 5.6 (10.6-38.5) microM (P < 0.05). After ECT, HR, cerebral perfusion and oxygenation normalized over approximately 3 minutes, whereas the electroencephalogram was unaffected by Glp. The results demonstrate that ECT is associated with hemodynamic effects severe enough to affect cerebral oxygenation and perfusion, and that these effects can be attenuated by Glp treatment.