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 Table of Contents    
Year : 2017  |  Volume : 59  |  Issue : 3  |  Page : 370-374
Effectiveness of dexmedetomidine as premedication prior to electroconvulsive therapy, a Randomized controlled cross over study

1 Department of Anaesthesia, Yatharth hospital, Noida, Uttar Pradesh, India
2 Department of Anaesthesiology, R.N. Cooper Hospital and H.B.T. Medical College Mumbai, Mumbai, Maharashtra, India
3 University Hospital Coventry, United Kingdom
4 Department of Anaesthesiology, Lokamanya Tilak Municipal Medical College and Lokamanya Tilak Municipal Government Hospital, Mumbai, Maharashtra, India
5 Department of Anaesthesiology, Fortis Hospital, Chandigarh, India

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Date of Web Publication6-Oct-2017


Background: This study evaluated the effect of dexmedetomidine on the acute hyperdynamic response, duration of seizure activity, and recovery profile in patients undergoing electroconvulsive therapy (ECT).
Aims: To study the effectiveness of dexmedetomidine 1 μg/kg intravenous in ECT in terms of attenuation of the hyperdynamic response, seizures duration, and sedation.
Design: This was a prospective, randomized, double-blinded, crossover study.
Materials and Methods: Thirty patients were included in the study and were treated as both cases and controls. The study drug was given 10 min before induction of anesthesia. Vital parameters and recovery scores were recorded.
Results: In Group D, heart rates at 3rd and 5th min after electric stimulus (T6 and T7, respectively) were 94.5 ± 20.1 and 90.4 ± 12.8/min as compared to 111.9 ± 15.5 and 109.0 ± 13.7 in Group N, respectively (P < 0.0001). The systolic blood pressure in Group D and Group N were 116.53 ± 26.09 and 138.03 ± 19.32 at T6, respectively (P < 0.001). Diastolic blood pressure and mean arterial pressure were significantly reduced after induction and electric stimulus in Group D. The seizures duration was similar in both groups. Modified Aldrete's Score and Richmond Agitation-Sedation Score were prolonged in Group D.
Conclusion: Dexmedetomidine, before the induction of anesthesia, prevents the acute hyperdynamic responses to ECT without altering the seizures duration. However, patients may have delayed recovery and delayed discharge.

Keywords: Anesthesia, dexmedetomidine, electroconvulsive therapy, propofol

How to cite this article:
Sannakki D, Dalvi NP, Sannakki S, Parikh DP, Garg SK, Tendolkar B. Effectiveness of dexmedetomidine as premedication prior to electroconvulsive therapy, a Randomized controlled cross over study. Indian J Psychiatry 2017;59:370-4

How to cite this URL:
Sannakki D, Dalvi NP, Sannakki S, Parikh DP, Garg SK, Tendolkar B. Effectiveness of dexmedetomidine as premedication prior to electroconvulsive therapy, a Randomized controlled cross over study. Indian J Psychiatry [serial online] 2017 [cited 2020 Jan 24];59:370-4. Available from:

   Introduction Top

Electroconvulsive therapy (ECT) is a known treatment for psychiatric patients unresponsive to pharmacotherapy. An electrical stimulus is applied to brain to elicit generalized motor seizures.

The cardiovascular response to ECT consists of initial parasympathetic-induced bradycardia followed by a more prominent sympathetic response resulting in tachycardia and hypertension lasting 5 min or longer.[1]

The cardiovascular response is associated with sudden surge of catecholamines and occasional cardiac arrhythmias, myocardial ischemia/infarction.[2] The acute hyperdynamic response elicited poses great risk in patients with cardiovascular and cerebrovascular diseases.

Drugs such as alpha-2 agonists and beta-blockers have been used to attenuate this response.[3],[4],[5] Alpha-2 agonistic activity results in augmentation of cardiovagal activity in brain leading to bradycardia and hypotension. Clonidine is the prototypical alpha-2 agonist that has been reported to have a beneficial effect on the hyperdynamic response to ECT.[6]

Dexmedetomidine, the newer alpha-2 agonist, is being studied for many procedural sedations.[7],[8],[9],[10],[11],[12] Dexmedetomidine decreases the stress-induced sympathoadrenal responses to painful stimuli, improves intraprocedural hemodynamics, and reduces the anesthetic requirements. Hence, we hypothesize that dexmedetomidine may modify the ECT-evoked hyperdynamic response, if administered as premedication.

   Materials and Methods Top

The study was approved by the institutional ethics committee. Written informed consent was taken from the respective patients or their legal guardians. Thirty American Society of Anesthesiologists I or II patients of either sex, 18–50 years of age, scheduled for ECT, were included in a prospective, randomized, double-blind, placebo-controlled comparative crossover study. The exclusion criteria were involuntary patient status, pregnancy, lactation, asthma, use of drugs such as beta blockers, calcium channel blockers, digitalis, history of myocardial infarction, congestive cardiac failure in the previous 6 months, significant arrhythmias, and a known family history of reactions to the study drugs.

Two groups consisting of 15 patients each were made and named as Group D and Group N. A computer-generated table of random numbers was prepared and each patient was given a number. In the first setting of ECT, Group D received dexmedetomidine and Group N received normal saline as the study drug. In the following setting, study drugs were interchanged. Vital parameters were noted in either settings and compared. The data thus collected were statistically analyzed.

Patients were kept fasting overnight for the procedure. The study drug was prepared by the anesthesiologist who was not included in the study. Patient's monitoring included electrocardiography, pulse oximetry, respiration, and blood pressure by noninvasive monitoring. Basal parameters were noted. The patient was preloaded with 6 ml/kg of Ringer's lactate solution intravenous (IV).

Patients in Group D received dexmedetomidine 1 μg/kg in 20 ml dilution over 10 min. Similarly, patients in Group N received 20 ml of normal saline. While infusing the study drug, heart rate (HR), systolic blood pressure (SBP), diastolic blood pressure (DBP), mean arterial pressure (MAP), and oxygen saturation were monitored at 0th (T0), 1st (T1), 5th (T2), and 10th (T3) min of infusion. At the end of infusion, injection propofol 1 mg/kg was slowly given till loss of consciousness. To one arm, pneumatic tourniquet was applied to assess of the motor seizures. Succinylcholine 0.5 mg/kg IV was administered. Bag and mask ventilation was with 100% oxygen.

Electric stimulus was delivered through bifrontotemporal electrodes. The duration of the motor seizure was noted as the time from the electric stimulus to cessation of tonic–clonic seizures in the “isolated” arm. The before-mentioned parameters were again noted immediately after induction of anesthesia (T4) and 1st (T5), 3rd (T6), 5th (T7), and 10th (T8) min after the electrical stimulus. After cessation of seizures, patient's recovery was assessed by the time taken to breathe spontaneously, eye opening, follow verbal commands, and to shift to postanesthetic care. For the next 90 min, the patient was monitored in post anaesthetic care (PAC) for vital parameters and sedation. Modified Aldrete's Score and Richmond Agitation-Sedation Score (RASS) score were used to assess the recovery at 0 (T9), 15 (T10), 30 (T11), 45 (T12), 60 (T13), and 90 (T14) min after shifting to PAC.

The data thus obtained were statistically analyzed. The data such as distribution of age and weight were analyzed with Chi-square test. The data such as number of electric stimuli, seizures duration, and vital parameters (HR, SBP, DBP, and MAP) were analyzed with unpaired Student's t-test. Sedation scores were analyzed with Mann–Whitney test. P < 0.05 was considered statistically significant.

   Results Top

Sixty ECT procedures were evaluated involving 19 males and 11 females. The Mean values were age (31.37 ± 9.60 years), height (155.9 ± 5.09 cm), and weight (55.17 ± 9.94 kg).

The HRs in both groups did not differ significantly from T0 to T2. However, from T5 to T8 (from 1st to 10th min after electric stimulus), there was spike in Group N which was not noticed in Group D (P < 0.0001). The highest mean HRs in Group N and Group D were 113.30 and 94.57, respectively [Figure 1].
Figure 1: Comparison of heart rate between two groups

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In Group N, SBP was 124.6 ± 16.85 mmHg at T0 and 140.10 ± 22.5 mmHg at T6. On the contrary, SBP in Group D was 123.27 ± 12.01 mmHg (T0) and 119.8 ± 22.5 mmHg (T6) [Figure 2].
Figure 2: Comparison of systolic blood pressure between study groups

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In Group N, there was no statistically significant reduction in HR, SBP, DBP, and MAP any time during procedure when compared to baseline [Figure 3] and [Figure 4]. In Group D, there was reduction in all vital parameters as compared to baseline. When both the groups were compared with respect to HR, SBP, DBP, and MAP, P value was <0.05 at T5, T6, T7, and T8 (from 1st to 10th min of electric stimulus).
Figure 3: Comparison of diastolic blood pressure between study groups

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Figure 4: Comparison of mean arterial pressure between study groups

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In the immediate recovery period, except the time taken to breathe spontaneously, there was a significant delay in other three parameters (eye-opening, follow verbal commands, shift to PAC) in Group D (P < 0.05) [Table 1]. Delayed recovery scores were noted as assessed by Aldrete and RASS score in Group D at T9, T10, and T11 (15th and 30th min after shifting to PAC; P < 0.05) [Table 2].
Table 1: Comparison among study groups for recovery parameters

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Table 2: Comparison among study group for Aldrete's score

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   Discussion Top

ECT is associated with autonomic nervous system activation with a sudden surge of catecholamines. This may lead to complications such as transient arrhythmias, myocardial ischemia, cardiovascular, and cerebrovascular accidents.[2] Dexmedetomidine has shown to be promising in various procedures to blunt this catecholamine-induced stress response.[7],[8],[9],[10],[11],[12] Hence, we decided to use dexmedetomidine as premedication in our study.

Fu and White conducted a study on six patients to assess the effect of dexmedetomidine 0.5–1 μg/kg on hyperdynamic response to ECT.[13] It produced dose-related increase in level of sedation but failed to decrease BP and HR. It was concluded that dexmedetomidine was not beneficial in ECT.

Begec et al. in 2008 compared dexmedetomidine 1 μg/kg IV with placebo.[14] They concluded that dexmedetomidine was useful in preventing the acute responses to ECT without altering the seizures and recovery.

A prospective, randomized, double-blind, comparative, crossover study was carried out in thirty patients of either sex between the ages of 18–60 years undergoing ECT. In the first setting of ECT, Group D received dexmedetomidine, and Group N received normal saline as the study drug. In the following setting, study drugs were interchanged. Data thus collected were statistically analyzed. Unpaired t-test was used for comparing demographic parameters, hemodynamic variables, seizures duration, and recovery parameters. Mann–Whitney test was used to analyze the postprocedure sedation.

HR showed a sharp spike from T5 to T8 in Group N which was not noticed in Group D (P value < 0.0001). The highest mean HRs in Group N and Group D were 113.30 and 94.57, respectively. In comparison with baseline (T0), HR was significantly raised in Group N at T5, T6, and T7 (P < 0.05). No such observations were made in Group D. Fu and White [13] had found that maximum HRs were noted at T6 and T7 in both groups in a similar manner.

In our study, there was a significant increase in SBP, DBP, and MAP in Group N after the electric stimulus was given. In Group N, SBP was 124.6 ± 16.85 mmHg at T0 and 140.10 ± 22.5 mmHg at T6. On the contrary, SBP levels in Group D were 123.27 ± 12.01 mmHg (T0) and 119.8 ± 22.5 mmHg (T6). Similar readings were found in Group D from the time of induction till 10 min after electric stimulus (P < 0.05). The P values calculated with respect to DBP and MAP, compared between both groups, were statistically significant (P < 0.05) at T5, T6, T7, and T8. These data are suggestive that dexmedetomidine is highly effective in curbing the hyperacute response to ECT. In a study done by Fu and White, there was concomitant use of glycopyrrolate and labetalol along with dexmedetomidine.[13] These drugs might have confounded their results. Our study did not have such confounding factors.

Ten percent of patients in Group N and 13.3% of Group D required second electric stimulus to elicit convulsions (P = 0.447). In the study conducted by Fu and White,[13] seizures duration was prolonged in Group D. In our study, the duration in Group N was 27.93 ± 7.91 s and in Group D was 24.77 ± 8.17 s (P = 0.133). Hence, it was concluded that dexmedetomidine did not interfere with seizures.

ECT is done as day care procedure; hence, patient's recovery in the postictal period [Table 2] was given a greater importance. Except for the resumption of spontaneous breathing, rest of the parameters, namely eye opening (P = 0.01) and time taken to shift to PAC, were significantly prolonged (P < 0.00001) in Group D. The mean time to readiness to discharge from hospital in Group N was 13.00 ± 5.7 min and in Group D was 46.37 ± 19.67 min (P < 0.0001). However, no patients required monitoring beyond 90 min. No patients required hospitalization. Our study results were similar to the study conducted by Fu and White.[13]

In the postictal period, modified Aldrete's score [Table 2] was prolonged in Group D at T10 (P = 0.001) and T11 (P < 0.0001). In Group N, mean RASS at T10 was “0” (for 28 patients) whereas in Group D it was “1” (for 29 patients) with P < 0.0001. Similar values were recorded even at T9 and T11 (P < 0.05). However, at no point of time, RASS scores in both groups were beyond −1–+1. In nutshell, all 30 patients in Group N could safely be discharged by 45 and 90 min in Group D. Other side effects such as hypotension, bradypnea, dry mouth, and nausea vomiting were closely observed for, but none was encountered. No patient required overnight hospital stay or Intensive Care Unit admission and were successfully managed as outpatients.

   Conclusion Top

Dexmedetomidine 1 μg/kg can safely be used as premedication before the ECT to effectively control the hemodynamic responses.

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Conflicts of interest

There are no conflicts of interest.

   References Top

Ding Z, White PF. Anesthesia for electroconvulsive therapy. Anesth Analg 2002;94:1351-64.  Back to cited text no. 1
López-Gómez D, Sánchez-Corral MA, Cobo JV, Jara F, Esplugas E. Myocardial infarction after electroconvulsive therapy. Rev Esp Cardiol 1999;52:536.  Back to cited text no. 2
Wells DG, Davies GG, Rosewarne F. Attenuation of electroconvulsive therapy induced hypertension with sublingual nifedipine. Anaesth Intensive Care 1989;17:31-3.  Back to cited text no. 3
Figiel GS, DeLeo B, Zorumski CF, Baker K, Goewert A, Jarvis M, et al. Combined use of labetalol and nifedipine in controlling the cardiovascular response from ECT. J Geriatr Psychiatry Neurol 1993;6:20-4.  Back to cited text no. 4
Castelli I, Steiner LA, Kaufmann MA, Alfillé PH, Schouten R, Welch CA, et al. Comparative effects of esmolol and labetalol to attenuate hyperdynamic states after electroconvulsive therapy. Anesth Analg 1995;80:557-61.  Back to cited text no. 5
Fu W, Stool LA, White PF, Husain MM. Is oral clonidine effective in modifying the acute hemodynamic response during electroconvulsive therapy? Anesth Analg 1998;86:1127-30.  Back to cited text no. 6
Venn RM, Grounds RM. Comparison between dexmedetomidine and propofol for sedation in the Intensive Care Unit: Patient and clinician perceptions. Br J Anaesth 2001;87:684-90.  Back to cited text no. 7
Dere K, Sucullu I, Budak ET, Yeyen S, Filiz AI, Ozkan S, et al. A comparison of dexmedetomidine versus midazolam for sedation, pain and hemodynamic control, during colonoscopy under conscious sedation. Eur J Anaesthesiol 2010;27:648-52.  Back to cited text no. 8
Gupta K, Jain M, Gupta PK, Rastogi B, Saxena SK, Manngo A. Dexmedetomidine premedication for fiberoptic intubation in patients of temporomandibular joint ankylosis: A randomized clinical trial. Saudi J Anaesth 2012;6:219-23.  Back to cited text no. 9
[PUBMED]  [Full text]  
Cooper L, Candiotti K, Gallagher C, Grenier E, Arheart KL, Barron ME. A randomized, controlled trial on dexmedetomidine for providing adequate sedation and hemodynamic control for awake, diagnostic transesophageal echocardiography. J Cardiothorac Vasc Anesth 2011;25:233-7.  Back to cited text no. 10
Koroglu A, Demirbilek S, Teksan H, Sagir O, But AK, Ersoy MO. Sedative, haemodynamic and respiratory effects of dexmedetomidine in children undergoing magnetic resonance imaging examination: Preliminary results. Br J Anaesth 2005;94:821-4.  Back to cited text no. 11
Aantaa RE, Kanto JH, Scheinin M, Kallio AM, Scheinin H. Dexmedetomidine premedication for minor gynecologic surgery. Anesth Analg 1990;70:407-13.  Back to cited text no. 12
Fu W, White PF. Dexmedetomidine failed to block the acute hyperdynamic response to electroconvulsive therapy. Anesthesiology 1999;90:422-4.  Back to cited text no. 13
Begec Z, Toprak HI, Demirbilek S, Erdil F, Onal D, Ersoy MO. Dexmedetomidine blunts acute hyperdynamic responses to electroconvulsive therapy without altering seizure duration. Acta Anaesthesiol Scand 2008;52:302-6.  Back to cited text no. 14

Correspondence Address:
Deepa Sannakki
W/O Dr. Ansh Garg, # 3A, Shanti Road, Professor Colony, Yamuna Nagar - 135 001, Haryana
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/psychiatry.IndianJPsychiatry_33_17

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