Blood pressure control with glyceryl trinitrate during electroconvulsive therapy in a patient with cerebral aneurysm

Abstract

EDITOR: Electroconvulsive therapy (ECT) induces abrupt changes in systemic and cerebral haemodynamics that are problematical for patients with cardiovascular or cerebrovascular complications. Although there are no reports of ECT causing rupture of a cerebral aneurysm, excessive haemodynamic changes in such patients must be avoided. Short-acting β-adrenoceptor-blocking agents, e.g. esmolol, are suitable to attenuate hyperdynamic states after ECT. However, this type of drug is sometimes inapplicable for medical or social reasons. We describe a patient with a cerebral aneurysm who was successfully treated with glyceryl trinitrate before undergoing ECT. A 68-yr-old female diagnosed with endogenous depression and resistant to medication needed ECT. Preoperative evaluation with computed tomography revealed a cerebral aneurysm (6 mm in diameter) with a bleb in the middle section of the anterior communicating artery. Her family refused to have surgical clipping performed before the series of ECT. They understood the risks of both the procedure and cerebral aneurysm rupture, and written informed consent was obtained. Atropine 0.01 mg kg−1 intramuscularly (i.m.) was given as a vagolytic premedication. Arterial blood pressure was measured continuously at the right radial artery using a tonometric BP monitor (CBM-7000®; Colin Co Ltd, Komaki, Japan). The tc-Doppler probe (Sonos 5500®; Agilent Technology, Palo Alto, CA, USA) was adjusted to detect the middle cerebral artery flow (right temporal side) using a 2 MHz ultrasonic wave. The Doppler signals were obtained at a depth of 45-55 mm from the surface and the velocity was calculated automatically by tracing the waveforms. General anaesthesia was induced with propofol, 1 mg kg−1, over 15 s through an indwelling intravenous (i.v.) cannula. After consciousness had been lost, succinylcholine chloride (1 mg kg−1) was administered and the lungs inflated with 100% oxygen via a facemask. Glyceryl trinitrate (0.01-0.02 mg kg−1) was administered i.v. immediately after the succinylcholine to prevent excessive hypertension during the ECT. One minute later, an electrical current was applied bilaterally for 5 s at the minimal stimulus intensity, which had been determined in a first ECT trial by increasing the electrical intensity stepwise. The electroshock was delivered by a trained psychologist using an ECT stimulator (CS-1®; Sakai Iryo Co Ltd, Tokyo, Japan). The efficacy of electrical stimulation was determined using a tourniquet. The lungs were then gently inflated and PETCO2 at the nostrils was maintained at 4.0-4.7 kPa and SPO2 > 98%. The patient received ECT three times a week for a total of 20 treatments. Heart rate and blood pressure were largely unchanged after the ECT stimulus. Maximum changes of the averages (average of the 20 ECT sessions) were a 13.6% increase in heart rate (preanaesthesia 109 ± 12 beats min−1, pre-electrical stimulus 107 ± 10 beats min−1, maximum after the shock 122 ± 10 beats min−1, respectively). The increase in mean blood pressure was 8.4% (preanaesthesia 81 ± 12 mmHg, pre-electrical stimulus 71 ± 11 mmHg, maximum after the shock 77 ± 18 mmHg, respectively), 30 s after the electrical stimulus. The mean flow velocity in the middle cerebral artery was increased to a maximum of 12.7% at 30 s after the electrical stimulus (preanaesthesia 67 ± 8 cm s−1, pre-electrical stimulus 65 ± 7 cm s−1, maximum after the shock 73 ± 10 cm s−1, respectively). The patient's mental condition improved gradually, and she was discharged after the completion of the course of treatment without any physical problems. An intracranial aneurysm is listed as a contraindication of ECT, since the abrupt haemodynamic changes during therapy may cause aneurysmal rupture. However, there are several reports describing safe ECT management of patients with a cerebral aneurysm [1,2]. In all reports, some kind of antihypertensive drug was given to prevent excessive hypertension. Esmolol is the antihypertensive agent most used since short-acting β-adrenoceptor-blocking agents were suitable for controlling blood pressure during ECT [1]. Salaris and colleagues reported two patients whose blood pressures were controlled with two kinds of β-adrenoceptor-blocking agents, esmolol and labetalol [2]. Another combination of β-adrenoceptor-blocking agents, i.e. nadolol and propranolol, was reported in a patient with a carotid artery aneurysm. Recently, the use of the postsynaptic α1-adrenergic antagonist urapidil was proposed as an alternative for β-adrenoceptor antagonists in ECT. In our patient, glyceryl trinitrate was successfully used to minimize the systemic and cerebral haemodynamic changes. We did not use esmolol because it was clinically unavailable in the country where the patient was treated. Gardner and Kellner reported the use of a nitroglycerin spray to control blood pressure during ECT [3]. Viguera and colleagues reported a patient whose blood pressure was controlled by sodium nitroprusside and atenolol, and they suggested that esmolol alone might be insufficient to attenuate haemodynamic changes during ECT [4]. Several other reports have demonstrated that pretreatment with glyceryl trinitrate prevented excessive hypertension after the electrical shock in patients without cerebral aneurysm. We have also reported that glyceryl trinitrate is effective in suppressing the increase in systemic blood pressure and cerebral blood flow velocity during ECT [5]. Recent neurophysiological observations confirmed that glyceryl trinitrate decreased cerebral blood flow velocity without changes in cerebral blood flow [6]. Since the suppression of changes in cerebral haemodynamics is considered effective in the prevention of aneurysmal rupture, use of glyceryl trinitrate or other types of nitric oxide donor may be suitable for haemodynamic management during ECT in patients with a cerebral aneurysm. When the use of β-adrenoceptor-blocking agents is considered inappropriate, e.g. in patients with bronchial asthma, glyceryl trinitrate is recommended instead. The side-effects of glyceryl trinitrate include increases in intracranial pressure or tachycardia; however, we did not observe these side-effects in our patient. There was no excessive hypotension because we injected the drug 1 min before the application of the electrical stimulus. It has been suggested that the peak heart rate after the electrical stimulus is a means of quantifying the quality of seizures and can provide feedback on the intensity of future stimuli. Since the use of an antihypertensive drug modifies the effect of the electrical stimulus on heart rate (HR), the use of antihypertensive medication during ECT might be restricted to cases with complications. We used propofol as the anaesthetic agent, although previous reports for ECT in patients with cerebral aneurysm used methohexital [1-4]. Haemodynamic changes during ECT were less when anaesthesia was induced with propofol when compared with methohexital or thiopental. Changes in cerebral blood flow velocity are reduced and shorter when propofol is used when compared with thiopental [7]. There was no significant HR change when propofol was used. An increase in mean blood pressure was only observed at 1 min after the electrical stimulus (17 ± 13%), and an increase in the middle cerebral artery blood flow velocity was observed at 0.5 and 1 min after the stimulus (maximally 78 ± 21%). Propofol might be more suitable than methohexital or thiopental when trying to minimize systemic and cerebral haemodynamic changes during ECT. To our knowledge, there has been no study that compared the haemodynamic effects of antihypertensive medication for ECT during propofol anaesthesia. However, since the use of antihypertensive medication - such as a β-adrenoceptor antagonist or glyceryl trinitrate - stabilizes haemodynamic changes during ECT with thiopental, it is possible that appropriate use of such medication during ECT under propofol anaesthesia further stabilizes haemodynamics. In the present case, the change in haemodynamics during ECT was considered to be smaller than with thiopental with glyceryl trinitrate. Psychological observations (using the Hamilton Depression Rating Scale and the Beck Depression Inventory) and electroencephalographic analysis (using the postictal suppression index and integrated amplitude) demonstrate that the therapeutic efficacy of ECT when using propofol does not differ significantly from when barbiturates or methohexital are used - despite the duration of seizures being slightly shorter with propofol. The use of short-acting opioids, e.g. remifentanil, at the induction of anaesthesia may be another option when haemodynamic stability is required during ECT management. C. Ogawa-Okamoto S. Saito F. Nishihara N. Yuki F. Goto Departments of Anesthesiology and Reanimatology, and Psychiatry; Gunma University School of Medicine; Maebashi, Japan