The goals of administering general anesthesia for electroconvulsive therapy (ECT) are to provide the patient with a lack of awareness of the treatment, to modify the motor effects of the seizure in order to prevent injury, to produce rapid induction and recovery with minimal side effects, to attenuate the physiologic effects of ECT, and to minimize any antagonistic effects on seizure activity.1 In an attempt to better attain these goals, new anesthetic agents and cardiovascular drugs are frequently applied in the ECT setting. In this ai'ticle, the anesthetic agent propofol and two antihypertensive drugs, labetalol and esmolol, will be discussed.
Methohexital and thiopental are the intravenous anesthetic agents most commonly used for ECT. Both are barbiturates with a rapid onset of action and a relatively rapid time to recovery. However, recovery occurs not because of drug metabolism, but because of redistribution within the body, which leads to a decrease in the plasma concentration. Significant concentrations remain in the body for many hours and may cause impairment of mental and psychomotor ability for up to 24 hours after administration.2 This is particularly dangerous in patients undergoing ECT, as they often return quickly to a psychiatric ward where staff supervision may be low and the prolonged effects of anesthetic agents may be unappreciated.3 The hazard increases as the number of patients receiving ECT on an outpatient basis continues to grow.
Propofol is a new rapidly acting intravenous anesthetic agent that is chemically unrelated to other agents. It is widely used in the operating room, particularly for outpatient anesthesia because of its characteristics of rapid emergence from anesthesia and minimal postoperative confusion.4 When compared with methohexital for use in ECT, propofol has been associated with a lower incidence of hypertension.3,56 The temporary impairment of cognitive function associated with ECT has been claimed to correlate highly with the magnitude of the associated elevation in blood pressure.7 Theoretically, the cognitive impairment may be preventable by agents that abolish or attenuate the hypertensive response. Since propofol appears to at least partially blunt the increase in blood pressure, it may have some clinical usefulness for ECT.
In comparison to methohexital, propofol has been found to result in a significant decrease in the duration of seizures when used as an induction agent for ECT.3'5'6'8 Although studies have shown that agents that shorten seizure duration usually have an adverse effect on therapeutic response to ECT,9 other studies have suggested that it is the amount of energy used to induce the seizure, and not the seizure itsel£ that significantly influences the therapeutic outcome of ECTJ0'11
The question of whether therapeutic efficacy is determined by the seizure duration or the amount of current passed remains to be answered. Two studies have assessed the effects of propofol and other induction agents on the therapeutic efficacy of ECT. In one study comparing propofol and thiopental, seizure duration was reduced with propofol, but there was no evidence of reduced efficacy as measured by percentage or absolute reduction in Hamilton and Zung scores over the course of ECT12
In the second study comparing propofol and methohexital, seizure duration was significantly reduced with propofol, but the final Hamilton score was identical regardless of the anesthetic agent used for ECT.1'' There was no significant difference between the propofol group and either the thiopental or methohexital group in total number of treatments.12·13 Until there are more controlled studies of the effect of propofol on the therapeutic efficacy of ECT, its use for ECT will remain controversial, despite its otherwise very desirable characteristics.
NEW BETA-ADRENERGIC RECEPTOR ANTAGONISTS
It is well appreciated that ECT causes intense stimulation of the sympathetic nervous system and an increase in circulating catecholamines, resulting in tachycardia and hypertension. It is not surprising, therefore, that the leading cause of death in ECT is cardiac-related.14 Cardiovascular mortality has been reported to be as high as 0.03%. 15 One study has found that the older-than-65 age group was more likely than younger patients to experience medical complications, and cardiovascular complications were the most important variety, occurring in 9% of the older group but only in 1% of the younger group. Hypertension, arrhythmias, ischemia, and congestive heart failure were the most common cardiovascular complications noted.16 As the population presenting for ECT continues to include greater numbers of elderly patients, many of them with severe chronic medical diseases, hemodynamic control during ECT becomes more important.
In an attempt to prevent or to attenuate the hemodynamic response to ECT, numerous pretreatment regimens have been studied. Due to the usually very short duration of hypertension and tachycardia during ECT, the therapeutic effect of many of the antihypertensive agents may extend beyond this period and lead to prolonged and severe episodes of hypotension. Also, the administration of cardiovascular drugs may shorten seizure duration, thereby potentially decreasing the therapeutic effectiveness of ECT.17
Labetalol and esmolol are two new beta-adrenoceptor antagonists that have gained widespread use in the operating room and intensive care unit. Labetalol has both selective alpha, and nonselective beta, and beta., adrenergic receptor blocking activity.18 In humans, the ratio of alpha-to-beta receptor blockade is 1:7 after intravenous administration.1*' Its elimination half-time is five to eight hours,11' so its therapeutic effect tends to last longer than necessary for most ECT patients, but there have been no reports of prolonged or severe hypotension after ECT. Labetalol pretreatment has been found to effectively reduce the hypertension, tachycardia, and arrhythmias associated with ECT in both healthy patients and those with cardiovascular dis'ease.17,20,22 However, in one study, labetalol significantly reduced seizure duration when compared with control.17
With the brief need for cardiovascular protection during ECT, the pharmacokinetic and pharmacodynamic characteristics of esmolol provide advantages over the use of other antihypertensive agents. Esmolol is an ultrashort-acting beta, adrenergic blocking agent with an elimination half-time of approximately nine minutes.20 Administered either as a bolus dose or as an infusion prior to ECT, it effectively blunts the increase in heart rate and blood pressure that occurs with EGT.17,23-25 As opposed to labetalol, esmolol significantly attenuates ECT-induced norepinephrine and epinephrine secretion.26
Esmolol's effect on seizure duration is less clear. It has been reported that esmolol either has no significant effect on seizure duration17,24-25 or significantly decreases the length of seizures.2'' One study suggests that when administered as a bolus dose, esmolol may have a doserelated effect on seizure duration. 2n Seizure duration was significanti}' shorter with 200 mg esmolol compared with placebo, whereas 100 mg esmolol resulted in no significant difference.25 It should be noted, however, that for both 100-mg and 200-mg bolus doses, seizure durations monitored by electroencephalogram were longer (40 and 45 seconds, respectively) than the recommended 30-second minimum.27 With its short duration of action, ability to effectively blunt the hemodynamic response to ECT, and its lack of effect on seizure duration when used at low doses, esmolol should become a popular adjunct agent for the anesthetic management of patients undergoing ECT
As the applications for ECT broaden and the number of relatively high-risk patients undergoing ECT increases, anesthesiologists and psychiatrists must work together to make ECT as safe and effective as possible. It is with this goal in mind that new drugs that have been useful in the operating room are applied to ECT It is therefore beneficial to investigate these new drugs in order to find the most efficacious interaction between the physiologic and psychologic effects of ECT, anesthetic considerations, and ECT requirements.
1. Selvin BL. Electroconvulsive therapy - 1987. Anesthesiology. 1987; 67:367-385.
2. Dundee JW, Wyant GW. Intravenous Anesthesia. London: Churchill Livingstone; 1974.
3. Dwyer R, McCaughey W, Lavery J, McCarthy G, Dundee JW. Comparison of propofol and methohexitone as anaesthetic agents for electroconvulsive therapy. Anaesthesia. 1988; 43:459-462.
4. Johnston R, Noseworthy T, Anderson B, Konopad E, Grace M. Propofol versus thiopental for outpatient anesthesia. Anesthesiology. 1987: 67:431-433.
5. Rampton AJ, Griffin RM. Stuart CS, Durcan JJ. lluddy NC. Abbott MA. Comparison of methohexital and propofol for electroconvulsive therapy: effects on hemodynamic responses and seizure duration. Anesthesiology. 1989; 70:412-417.
6. Rouse EC. Propofol for electroconvulsive therapy: a comparison with methohexitone; preliminary report. Anaesthesia. 1988; 43(suppl 1:61-64.
7. Hamilton M, Stocker MJ, Spencer CM. PostECT cognitive defect and elevation of blood pressure. Br J Psychiatry. 1979: 135:77-78.
8. Simpson KH, Halsall PJ, Carr CME. Stewart KG. Propofol reduces seizure duration in patients having anaesthesia for electroconvulsive therapy. BrJAnaesth. 1988; 61:343-344.
9. Cronholm B, Ottosson J-O. Experimental studies of the therapeutic action of electroconvulsive therapy in endogenous depression. The role of the electrical stimulation and of the seizure studied by variation of stimulus intensity and modification by lidocaine of seizure discharge. Acta Psyehiatr Sconci. 1960; 35(suppl)145:69-102.
10. Deakin JFW. Antidepressant effects of electroconvulsive therapy: current or seizure? Br Med J. 1983; 286(i): 1083- 1084. Editorial.
11. Robin A, DeTissera S. A double-blind controlled comparison of the therapeutic effects of low and high energy electroconvulsive therapies. Br J Psychiatry. 1982; 141:357-366.
12. Mitchell P, Smithe G, Torda T. Effect of the anesthetic agent, propofol on hormonal responses to ECT. Biol Psychiatry. 1990; 28:315-324.
13. Maisch E, Gratz I. Mani S. Efficacy of electroconvulsive therapy (ECT) after propofol (P) or methohexital (M) anesthesia. Anesth Analg. 1992; 74:S192.
14. Maclay WS. Death in treatment. Proc R Soc Med. 1982; 46:13-20.
15. Abrams R. Electroconvulsive therapy. New York: Oxford University Press; 1988.
16. Alexopoulos GS. Shamoian CA. Lucas J. Weiser N, Berger H. Medical problems of geriatric psychiatric patients and younger controls during electroconvulsive therapy. J Am GeriatrSoc. 1984; 32:651-654.
17. Weinger MB, Partridge BL, Hauger R, Mirow A. Prevention of the cardiovascular and neuroendocrine response to electroconvulsive therapy; I: effectiveness of pretreatment regimens on hemodynamics. Anesth Analg. 1991; 73:556-562.
18. MacCarthy EP, Bloomfield SS. Labetalol: a review of its pharmacology, pharmacokinetics, clinical uses and adverse effects. Pharmacotherapy. 1983;3:193-219.
19. Sloelting RK. Pharmacology and physiology in anesthetic practice. 2nd ed. Philadelphia: JB Lippincott Company; 1991.
20. Knos GB, Sung YF, Stoudemire A. Gladson M, Cooper R. Markwalter H. Use of labetalol to control cardiovascular responses to electroconvulsive therapy. Anesth Analg. 1990; 70:S210.
21. Stoudemire A, Knos G, Gladson M. et al. Labetalol in the control of cardiovascular responses to electroconvulsive therapy in high-risk depressed medical patients. J Clin Psychiatry. 1990; 51:508-512.
22. Sum CY. Yacobi A, Kartzinel R, Stampili H, Davis CS, Lai C-M. Kinetics of esmolol. an ultrashort-acting beta blocker, and of its major metabolite. Clin Pharmacol Ther. 1984; 34:427-434.
23. Howie MB, Black HA, Zvara D. McSweeney TD, Martin D-J. ('oilman JA. Esmolol reduces autonomic hypersensitivity and length of seizures induced by electroconvulsive therapy. Anesth Analg. 1990:71:384-388.
24. Kovac AL, Goto H. Arakawa K, Pardo MP. Esmolol bolus and infusion attenuates increases in blood pressure and heart rate during electroconvulsive therapy. Can J Anaesth. 1990; 37:58-62.
25. Kovac AL, Goto H, Pardo MP. Arakawa K. Comparison of two esmolol bolus doses on the haemodynamic response and seizure duration during electroconvulsive therapy. Can J Anaesth. 1991: 38:204-209.
26. Weinger MB. Partridge BL, Haugher R, Mirow A. Brown M. Prevention of the cardiovascular and neuroendocrine response to electroconvulsive therapy: IL effects of pretreatment regimens on catecholamines, ACTH. vasopressin, and Cortisol. Anesth Analg. 1991; 73:563-569.
27. O'Connell RA. A review of the use of electroconvulsive therapy. Hasp Comm Psychiatry. 1982; 33:469-473.