Anesth Analg 2002;95:400-402
© 2002 International Anesthesia Research Society
ANESTHETIC PHARMACOLOGY
Intravenous Verapamil Blunts Hyperdynamic Responses During Electroconvulsive Therapy Without Altering Seizure Activity
Zen’ichiro Wajima, MD PhD*,
Tatsusuke Yoshikawa, MD PhD*  ,
Akira Ogura, MD PhD*,
Kazuyuki Imanaga, MD*,
Toshiya Shiga, MD PhD ,
Tetsuo Inoue, MD PhD*, and
Ryo Ogawa, MD PhD||
*Department of Anesthesia, Chiba Hokusoh Hospital, Nippon Medical School, Chiba, Japan; Department of Anesthesia, Hakujikai Memorial Hospital, Tokyo, Japan; Department of Anesthesiology, Tokyo Jikeikai Medical School, Tokyo, Japan; Center for Anesthesiology Research, The Cleveland Clinic Foundation, Cleveland, Ohio; and ||Department of Anesthesiology, Nippon Medical School, Tokyo, Japan
Address correspondence and reprint requests to Zen’ichiro Wajima, MD, PhD, Department of Anesthesia, Chiba Hokusoh Hospital, Nippon Medical School, 1715, Kamagari, Inba-mura, Inba-gun, Chiba 270-1694, Japan. Address e-mail to HFB01245{at}nifty.com
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Abstract
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IMPLICATIONS: A dose of 0.1 mg/kg of verapamil, administered immediately before anesthesia, significantly reduces the increase in peak heart rate and mean arterial blood pressure after electroconvulsive therapy. Furthermore, the administration of verapamil does not reduce the duration of the seizure.
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Introduction
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Electroconvulsive therapy (ECT) is often associated with acute hyperdynamic responses, including transient hypertension and tachycardia, immediately after the ECT stimulus is delivered. Attenuation or blockade of the acute hemodynamic and myocardial consequences of ECT may be desirable in patients with brain tumors, cardiac conduction defects or ectopy, hypertension, recent myocardial infarction or hemorrhagic stroke, and aortic or cerebral aneurysms (1). Many drugs, such as nitroglycerine (2,3), nitroprusside (4),1 nifedipine (5–7), nicardipine (8), ß-adrenergic blockers (8–17),1 clonidine (18),1 and diltiazem (19) attenuate the hyperdynamic responses to ECT.
There have been no reports on the use of verapamil, a calcium channel-blocking drug, for ECT, and we hypothesized that verapamil could also be used to blunt the hyperdynamic response to ECT. The aim of this study was to investigate the effect of IV verapamil administration on heart rate (HR), arterial blood pressure, and seizure duration during ECT.
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Methods
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After obtaining approval from our IRB and obtaining written informed consent, 16 ASA physical status I, II, or III patients undergoing ECT treatments for chronic depression were investigated by using a randomized, double-blinded, placebo-controlled crossover study design. Patients with unstable cardiovascular diseases, those receiving ß-adrenergic or other calcium channel-blocking drugs, and those with second- or third-degree atrioventricular blockage, arrhythmia, hypotension, sinus bradycardia, chronic obstructive pulmonary disease, and renal or hepatic failure were excluded from this study. Each patient received one of two different medications on different days, 48 h apart: a placebo (normal saline) (control group) or verapamil (verapamil group). The anesthesiologists were unaware of the treatment being administered.
Mean arterial blood pressure (MAP), electrocardiographic data, HR, and oxygen saturation values were recorded before the anesthesia induction. Tonometric blood pressure was measured with a continuous, noninvasive blood pressure-monitoring instrument (20–22). None of the patients was premedicated. The control group was given saline at a rate of 2.4 x body weight mL/h for a 10-min period, and the verapamil group was given 0.1 mg/kg of verapamil (0.025% verapamil solution) at a rate of 2.4 x body weight mL/h for a 10-min period. Just after verapamil was injected, unconsciousness was induced with propofol (1.5 mg/kg IV). Before the administration of succinylcholine (SCC), a tourniquet applied to the upper arm was inflated to isolate the circulation to the arm and permit an accurate assessment of the motor seizure. On loss of consciousness, a blood pressure cuff was applied to isolate the circulation to the arm so as to assess the duration of motor seizure activity (cuff method); SCC (1.5 mg/kg IV) was then administered, and ventilation was assisted via a face mask and oxygen. The electrical stimulus was delivered via bitemporal electrodes by using a Sakai CS-1 apparatus (Sakai Medical Instruments, Tokyo, Japan) at a 110-V setting for 7 s. The magnitude of the electrical stimulus was held constant during the two ECT treatments performed on each patient.
HR and MAP were measured before the start of the experiment to establish a baseline and before SCC administration, before ECT, and at the peak response after ECT. The electroencephalographic (EEG) seizure length was also recorded with a two-channel EEG after the electrical stimulus.
Intragroup comparisons of HR and MAP were performed by using a two-way analysis of variance with repeated measures and paired Student’s t-tests with Bonferroni’s correction. Between-group comparisons of HR, MAP, and recovery time were made by using unpaired Student’s t-tests. Between-group comparisons of motor and EEG seizure duration time were made by using Mann-Whitney U-tests. A P value of <0.05 was considered to be statistically significant.
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Results
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Five men and 11 women completed the study (32 ECT treatments); the average (mean ± SD) age of the subjects was 52 ± 16 yr (range, 24–76 yr), the average weight was 52 ± 9 kg (range, 40–72 kg), and the average height was 160 ± 8 cm (range, 148–176 cm). No significant differences in the baseline HR and MAP values were observed between the groups (Table 1).
In the control group, the HR before SCC and before ECT and the peak HR after ECT were significantly more rapid than the baseline HR. In the verapamil group, the HR was significantly more rapid after medication, before SCC, before ECT, and at its peak after ECT compared with the baseline HR. The increase in the HR after the electrical stimulus was significantly smaller after the verapamil treatment, compared with the placebo (P < 0.01) (Table 1).
In the control group, the peak MAP after ECT was significantly higher than the baseline MAP (P < 0.01). In the verapamil group, MAP was significantly lower after medication, before SCC, and before ECT than at baseline; the peak MAP after ECT was significantly higher than the baseline MAP. MAP was significantly lower in the verapamil group after medication, before SCC, before ECT, and at its peak value after ECT than in the control group (Table 1).
Recovery time, indicated by spontaneous respiration, eye opening, and the ability to follow commands, did not differ significantly between the control and verapamil groups. The motor and EEG seizure durations were similar in both groups (Fig. 1).
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Figure 1. Motor seizure duration (left) and electroencephalographic (EEG) seizure duration (right). The lower and upper borders of the box represent the 25th to 75th percentiles; the horizontal line within the box represents the median value, marking the 50th percentile; the rectangular symbol within the box represents the mean; error bars represent the 10th and 90th percentiles.
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Discussion
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The results of this study show that 0.1 mg/kg of verapamil, administered immediately before anesthesia, significantly reduces the increases in peak HR and MAP after ECT. Furthermore, the administration of verapamil did not reduce the duration of the seizure. Attenuation of the cardiovascular response is brought about by two effects: the reduction of baseline hemodynamic values and a blunting of their increases after ECT. We selected an IV dosage of 0.1 mg/kg of verapamil because this dosage attenuates the hypertensive responses to laryngoscopy, tracheal intubation, and tracheal extubation (23,24).
Beta-adrenergic blockers are probably the most useful and widely used drugs for ECT (1). McCall et al. (11) found that 5- and 10-mg doses of labetalol safely and effectively decreased blood pressure and the rate-pressure product (but not HR) without shortening the duration of seizure. Weinger et al. (15), however, showed that labetalol does shorten seizure duration. Esmolol also blunted the maximal HR response and the blood pressure response (12,13,15,17) (or rate-pressure product) (12). However, esmolol shortened the seizure duration (12,13,15,17) except in one study (14). Oral clonidine produced a dose-related decrease in MAP before and after ECT and produced no significant changes in the duration of either motor or EEG seizure activity or the recovery times after anesthesia. However, clonidine did not produce significant changes in HR (18). We recently reported that IV diltiazem (10 mg), another calcium channel blocker that has pharmacological characteristics similar to those of verapamil, can blunt acute hyperdynamic responses after ECT, but the seizure duration was also significantly reduced, possibly making this therapy less effective (19). We do not know why diltiazem shortens the seizure duration but verapamil does not. In view of these findings, we believe that IV verapamil is an ideal prescription for ECT because it reduces both tachycardia and hypertension after ECT without shortening the seizure duration.
In summary, a 0.1 mg/kg IV dose of verapamil, administered immediately before anesthesia, significantly reduces the increases in peak HR and MAP seen after ECT but does not affect seizure duration. Verapamil may be useful for attenuating hemodynamic responses in patients at risk of cardiovascular complications. Because verapamil does not affect seizure duration, nor is it likely to interfere with the psychotherapeutic efficacy of ECT, the routine administration of verapamil may be advisable and ideal.
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Footnotes
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1 1Liu WS, Petty WC, Jeppsen A, et al. Attenuation of hemodynamic and hormonal responses to ECT with propranolol, Xylocaine, sodium nitroprusside or clonidine [abstract]. Anesth Analg 1984;63:244. 
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Accepted for publication April 30, 2002.
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Abstract
Introduction
