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Anesthesia & Analgesia:
doi: 10.1097/00000539-200012000-00043
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The Comparative Effects of Propofol Versus Thiopental on Middle Cerebral Artery Blood Flow Velocity During Electroconvulsive Therapy

Saito, Shigeru MD; Kadoi, Yuji MD; Nara, Takeshi MD; Sudo, Makoto MD; Obata, Hideaki MD; Morita, Toshihiro MD; Goto, Fumio MD

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Department of Anesthesiology & Reanimatology, Gunma University School of Medicine, Maebashi, Japan

August 11, 2000.

Address correspondence and reprint requests to Shigeru Saito, MD, Department of Anesthesiology & Reanimatology, Gunma University School of Medicine, 3-39-22, Showamachi, Maebashi, 371-8511, Japan. Address e-mail to shigerus@news.sb.gunma-u.ac.jp.

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Abstract

Electroconvulsive therapy provokes abrupt changes in both systemic and cerebral hemodynamics. An anesthetic that has a minor effect on cerebral hemodynamics might be more suitable for patients with intracranial complications, such as cerebral aneurysm. The purpose of our present study was to compare the effects of thiopental and propofol on cerebral blood flow velocity. We continuously compared cerebral blood flow velocity at the middle cerebral artery (MCA) during electroconvulsive therapy, using propofol (1 mg/kg, n = 20) versus thiopental (2 mg/kg, n = 20) anesthesia. Systemic hemodynamic variables and flow velocity at the MCA were measured until 10 min after the electrical shock. Heart rate and arterial blood pressure increased in the thiopental group until 5 min after the electrical shock. In the propofol group, an increase in mean blood pressure was observed to 1 min after the electrical shock. Mean flow velocity at the MCA decreased after anesthesia in both groups, and increased at 0.5–3 min after the electrical shock in the thiopental group and at 0.5 and 1 min after the shock in the propofol group. The flow velocities at 0.5–5 min after the electrical shock were significantly more rapid in the thiopental group compared with the propofol group. {abs}

Implications: Cerebral blood flow velocity change, measured by transcranial Doppler sonography during electroconvulsive therapy, was minor using propofol anesthesia compared with barbiturate anesthesia. Propofol anesthesia may be suitable for patients who cannot tolerate abrupt cerebral hemodynamic change.

Electroconvulsive therapy (ECT) is effective for drug-therapy resistant severe depression. Because the therapy can be completed within 10 min, the anesthetics used for ECT should have a short action and a rapid recovery profile. In addition, because the seizure itself is believed to be important for the efficacy of the therapy, the anesthetics should not interfere with the electrical seizure. Until now, short-acting barbiturates, such as methohexital and thiopental, were the commonly used anesthesia (1). More recently, propofol at <1 mg/kg has also been recommended for ECT anesthesia (2,3). Many studies demonstrated that hemodynamics during ECT using propofol anesthesia were more stable than those using barbiturate anesthesia (2–5).

ECT induces an abrupt change in cerebral hemodynamics and systemic circulation (1,6). In a previous study, we reported that cerebral blood flow velocity at the middle cerebral artery (MCA) is drastically changed by the application of electrical shock (7). This finding was confirmed by Vollmer-Haase et al. (8). Two mechanisms have been proposed for the hyperemia during ECT (6,9): 1) cerebrovascular regulation, which meets the increased cerebral oxygen demand during seizure with the oxygen supply from the cerebral blood stream, and 2) a secondary effect of the systemic hyperdynamic state, which is induced by the excessive release of catecholamines. Although the effects of propofol on seizure and systemic circulation are not identical with those of thiopental, how propofol differs from thiopental regarding changes in cerebral hemodynamics during ECT is unknown. In our present study, we continuously compared cerebral blood flow velocity at the MCA during ECT by using propofol versus thiopental anesthesia. The dose of thiopental we used was 2 mg/kg, as in our previous study. The dose of propofol was 1 mg/kg, which was the minimal dose to induce unconsciousness.

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Methods

Informed consent was obtained from the patient or, when necessary, the appropriate relative. Our study protocol was approved by a local Clinical Study Committee. ECT was prescribed for 40 patients with endogenous depression. The patients ranged from 16 to 69 yr of age, and were in good physical heath. No patient had cardiovascular or cerebrovascular complications, or drug allergy. All patients were treated more than six times (three times per week at 2-day intervals). The data were obtained in the second ECT trial in each case. The selection of thiopental or propofol was determined by a random table. All persons present at the ECT session were blinded to the identity of the study drugs (drugs were given from a foil-covered cylinder and lines). The data obtained were analyzed later by an individual who was also blinded to the treatment regimens.

To avoid an unfavorable parasympathetic reflex, atropine (0.01 mg/kg IM) was given as premedication. Arterial blood pressure (BP) was measured continuously at the right radial artery by using a tonometric BP monitor (CBM-7000™; Colin Co. Ltd., Komaki, Japan). The tc-Doppler (TC2–64™; EME Co. Ltd., Uberlingen, Germany) probe was adjusted to detect MCA flow from the right temporal side. General anesthesia was induced with thiopental (2 mg/kg) or propofol (1 mg/kg). One of these drugs was administered over 15 s through an indwelling IV catheter. After loss of consciousness, succinylcholine chloride (1 mg/kg) was administered and ventilation was assisted using a face mask and 100% oxygen. One minute after the injection, an electrical current was applied bilaterally for 5 s at the minimal stimulus intensity, which had been determined in the first ECT trial by a stepwise increase in electrical intensity. The electroshock stimulus 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 by the “tourniquet technique”—that is, by observation of convulsive movements of the distal leg, around which an inflated tourniquet was set to block the distribution of muscle relaxant. The end-expiratory CO2 partial pressure (end-tidal CO2) at nostrils and arterial blood oxygen saturation (Spo2) were monitored by a respiration monitor (Capnomac Ultima™; Datex Co. Ltd., Helsinki, Finland), and end-tidal CO2 tension was maintained at 30–35 mm Hg and the Spo2 value (measured at left index) above 98% by manual ventilation assistance throughout the therapy.

The flow velocity at the MCA was measured by using a 2-MHz ultrasonic wave. The Doppler signals were obtained through the right temporal window at a depth of 45–55 mm from the surface. The signal quality was determined from the characteristic high pitch sound and from the waveform of the displayed sonogram. The velocity was calculated automatically by tracing the waveforms every 5 s.

The data were expressed as mean ± sd. Data were compared by analysis of variance for repeated measures with a P value < 0.05 considered statistically significant. For comparison of each mean value, two-way analysis of variance was applied and post hoc testing was performed by using the Scheffé method (StatView 5.0™; SAS Institute, Cary, NC).

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Results

There was no significant difference between the demographics of the patients in the two groups (Table 1). Patients had been prescribed multiple psychiatric medications at various doses in their history (Table 2). However, they were unresponsive to drug therapy, and the medications were interrupted at least 1 day before the start of ECT sessions. Heart rate in the thiopental group significantly increased after the application of electrical shock, and the increase continued until 5 min after the electrical shock (Figure 1). Maximal heart rate was observed 1 min after the electrical shock, and was 31% ± 13% more rapid than the preanesthesia control value. In the propofol group, heart rate did not change significantly throughout the ECT trial. Mean BP in the thiopental group increased by 39% ± 9% at 30 s after the electrical shock (Figure 2). The increase continued until 5 min after the electrical shock. In the propofol group, an increase in mean BP was observed at 1 min after the electrical shock (17% ± 13% more than the preanesthesia value). Mean BP at preanesthesia control measurement and immediately before the electrical shock did not differ significantly between the thiopental and propofol groups. However, the values after the electrical shock (0.5, 1, 2, 3, and 5 min) were significantly increased in the thiopental group compared with the propofol group.

Table 1
Table 1
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Table 2
Table 2
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Figure 1
Figure 1
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Figure 2
Figure 2
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Mean flow velocity at the MCA decreased after anesthesia in both groups (preanesthesia 56 ± 18 cm/s to 43 ± 9 cm/s in the thiopental group, preanesthesia 58 ± 18 cm/s to 45 ± 4 cm/s in the propofol group) (Figure 3). The values at preanesthesia control measurement and immediately before the electrical shock did not differ significantly between groups. The flow velocity increased at 0.5–3 min after the electrical shock in the thiopental group. In the propofol group, an increase in the flow velocity was observed at 0.5 and 1 min after the electrical shock. The flow velocity trend in the thiopental group and that in the propofol group was significantly different (P < 0.01), and the values at 0.5, 1, 2, 3, and 5 min after the electrical shock were significantly increased in the thiopental group compared with the propofol group. Mean seizure duration was 38 ± 18 s in the thiopental group and 27 ± 18 s in the propofol group. The duration in the propofol group was significantly shorter than that in the thiopental group (P < 0.05).

Figure 3
Figure 3
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Discussion

Ideal anesthetics used for ECT should have characteristics that include rapid induction, short duration of action, minimal side effects, rapid recovery, and no interference with the ECT efficacy. Because of its rapid induction and rapid recovery, propofol was recently introduced for ECT anesthesia. Previous studies have compared the use of propofol for ECT with barbiturates, which have long been used for ECT anesthesia (2–5,10). These studies demonstrated that propofol anesthesia reduced seizure duration compared with barbiturates. The approximately 20% shorter seizure duration observed in our propofol group was comparable to a previous report by Boey and Lai (4). Although seizure duration has been considered crucial for ECT therapeutic efficacy, two psychiatric reports conclude that the efficacy of ECT using propofol did not differ significantly from that using barbiturates (5,11). In those reports, which could not demonstrate any difference in outcome, several different types of psychiatric rating methods, such as the Hamilton Scale, Beck Inventory, and Montgomery-Asberg Rating (11,12), were used. Because the dose of propofol and the duration of seizure have an inverse relationship, we tried doses <1 mg/kg to obtain a longer seizure in our preliminary study. However, propofol <1 mg/kg was not enough for many patients to lose consciousness. Fredman et al. (2) reported that patients lost consciousness after a bolus infusion of 0.75 mg/kg of propofol. This discrepancy may be explained by the difference in the premedication protocol and by the racial differences of the subjects.

In the present study, heart rate and mean BP increased after electrical shock in the thiopental group. This phenomenon and the degree of alterations were comparable with our previous observation (7). In contrast, these systemic circulatory changes were mostly abolished in the propofol group. The stable systemic hemodynamics during ECT using propofol were described previously (2–5). Boey and Lai (4), who compared ECT using thiopental and propofol as in the present study, demonstrated no alteration in either heart rate or BP after electrical shock using propofol. Several other studies have compared methohexital and propofol, and demonstrated minor hemodynamic changes during ECT using propofol compared with methohexital (2–5). Fredman et al. (2) reported that 0.75 mg/kg propofol, which is smaller than the doses used in other studies, could ensure stable hemodynamics by using labetalol before the electrical shock.

Flow velocity at the MCA doubled after electrical shock in the thiopental group. This observation was comparable with our previous report (7), and the phenomenon was confirmed by Vollmer-Haase et al. (8). The flow velocity increase was also observed in the propofol group; however, the degree of increase was modest and the duration was shorter compared with those in the thiopental group. Flow velocity at the MCA is considered an indicator of cerebral blood flow (13,14). This idea is based on the premise that the diameter of an insonicated vessel remains constant. Previous studies have demonstrated that the diameter of the MCA is not significantly affected by changes in carbon dioxide tension (15), BP (16), or the administration of anesthetic or vasoactive drugs (17). However, Jansen et al. (18) recently reported that in a pathologic condition such as brain tumor, the correlation between cerebral blood flow and cerebral blood flow velocity at the MCA should be interpreted with caution. Although it is possible that an electrical current of ECT directly induces vessel diameter changes, as observed during in vitro experiments (19), this response is tentative. Most alterations in systemic and cerebral hemodynamics after the electrical shock have been thought to be derived from humoral and neuronal factors (1), and these factors may not induce vessel diameter change at the MCA. Therefore, it is possible that the changes in cerebral blood flow velocity in the present study reflect changes in cerebral blood flow.

Propofol induces cerebral vasoconstriction, and reduces cerebral blood flow and intracranial pressure (20). Cerebral metabolic rate is also reduced by the administration of propofol (21). In the present study, flow velocity at the MCA decreased immediately after anesthesia induction both in the thiopental and propofol groups (23% ± 18% in the thiopental group and 22% ± 18% in the propofol group, respectively). This finding suggests that 1 mg/kg propofol and 2 mg/kg thiopental decreases cerebral blood flow to the same extent, and supports the notion that the effects of propofol on cerebral blood flow appear to be similar to those of barbiturates (20). This observation is consistent with the report by Thiel et al. (22), who compared the effects of induction doses of propofol and thiopental on cerebral blood flow velocity. Also, according to the pharmaceutical information, rate constants of the distribution phase of propofol and thiopental are very similar (23).

Two hypotheses have been proposed to explain hyperemia after electrical shock (6,9). One states that cerebral blood flow is augmented to meet the increased cerebral tissue oxygen and energy demand during seizure. The second states that cerebral hemodynamics may be influenced by drastic changes in systemic hemodynamics after the electrical shock. We have reported that the regional oxygen saturation change detected by a near-infrared cerebral oxymeter correlated with the changes in systemic hemodynamics after electrical shock (24). In the present study, seizure duration was shorter in the propofol group. The potent anticonvulsive property of propofol might be a potential mechanism for the minor reaction to electrical stimulus (23). This shorter seizure, and the probable smaller energy demand change, may have been a cause of the minor increase in cerebral blood flow velocity in the propofol group. Also, in the propofol group, the systemic hemodynamic change was small. This smaller change in systemic hemodynamics may have been another cause of the minor change in cerebral hemodynamics. In the present study, we examined the effect of propofol and thiopental at singular doses, simply because the doses we used were often used in clinical settings. To compare the pharmacologic actions of propofol and thiopental on cerebral hemodynamics extensively, further examination at the other doses is required.

Viguera et al. (25) reported about a patient who had an intracerebral aneurysm and was safely treated by ECT using methohexital anesthesia. In several previous case reports including this one, antihypertensive medications such as β-blocker and sodium nitroprusside, were used to attenuate the expected intracranial hemodynamic change. Considering systemic and cerebral hemodynamic stability during ECT, propofol anesthesia might be more suitable than barbiturates as anesthesia for patients who have intracranial complications.

The authors thank Dr. Takushirou Akada (Department of Psychiatry, Gunma University) for his cooperation with this study, and Forte Inc. (Tokyo) for English editing.

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