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Right arrow Neuroanesthesia and Intensive Care
Canadian Journal of Anesthesia 47:767-774 (2000)
© Canadian Anesthesiologists' Society, 2000

Reports of Investigation

Reduction of cerebral hyperemia with anti-hypertensive medication after electroconvulsive therapy

Shigeru Saito, MD, Yuji Kadoi, MD, Nobuhisa Iriuchijima, MD, Hideaki Obata, MD, Ken-ichi Arai, MD, Toshihiro Morita, MD and Fumio Goto, MD

From the Department of Anesthesiology & Reanimatology, Gunma University School of Medicine, 3-39-22, Showamachi, Maebashi, 371-8511, Japan.

Address correspondence to: Shigeru Saito MD. Phone: +81-27-220-8454; Fax: +81-27-220-8473; E-mail: shigerus{at}news.sb.gunma-u.ac.jp

Purpose: Several different anti-hypertensive regimens have been introduced for the prevention of systemic hyperdynamic responses after electrically induced seizures. In the present study, the effects of anti-hypertensive medications on cerebral circulation were studied.

Methods: Systemic blood pressure was controlled by several anti-hypertensive medications, nicardipine, prostaglandin E1, alprenolol and nitroglycerin, in 30 patients (150 electroconvulsive therapy trials). Changes in cerebral blood flow velocity were measured by transcranial Doppler sonography of the right middle cerebral artery from the start of anesthesia to 10 min after the electrical shock.

Results: Administration of a Ca2+ antagonist, nicardipine, or prostaglandin E1 did not alter the augmented cerebral blood flow velocity after the seizure. However, a ß-adrenergic blocking agent, alprenolol (P < 0.05) or nitroglycerin (P < 0.01) partially inhibited the increase in cerebral blood flow velocity. Maximal blood flow velocity was 133% larger than the pre-anesthesia value in the control group, 109% in the nicardipine group, 113% in the prostaglandin E1 group, 72% in the alprenolol group, and 45% in the nitroglycerin group, respectively. The increase in cerebral blood flow velocity after electrically induced seizure was independent of systemic blood pressure. Internal jugular venous saturation (SjO2) was increased, and difference in arterial and venous concentrations of lactate was not altered in all groups.

Conclusions: Cerebral hemodynamics is altered by ECT, even when systemic hemodynamics are stabilized by antihypertensive medication. Although the effects of antihypertensive medicine on cerebral hemodynamics are variable, systemic blood pressure control by these agents does not induce cerebral ischemia after ECT.




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