ANESTHESIA FOR ELECTROCONVULSIVE THERAPY

1. ANESTHESIA FOR ELECTROCONVULSIVE THERAPY Husong Li, M.D., Ph.D. Assistant Professor Department of Anesthesiology University of Texas Medical Branch Galveston, Texas

2. ELECTROCONVULSIVE THERAPY

3. INTRODUCTION TO ELECTROCONVULSIVE THERAPY Electroconvulsive therapy (ECT) is a treatment for severe mental illness in which a brief application of electrical stimulus is used to produce a generalized seizure

4. MENTAL HEALTH CARE PRE-1930�S

5. Cerletti and Bini (1934): ECT

7. INTRODUCTION TO ECT ECT has changed substantially during the past decades. The use of general anesthesia has promoted the interest in ECT (Ottoson 1962) ECT become more complex, more precise, and safer procedure (mortality 1/1000 early to 3-4/100,000 now)

8. INTRODUCTION TO ECT Generalized seizures for 30-60 seconds in duration are required for therapeutic effects 75-90% of patients exhibit a dramatic and sustained improvement Transient neurological dysfunction does occur but permanent neuronal injury is questionable

9. TREATMENT PROTOCOL FOR ECT Generalized seizure can be induced by adjusting waveform, frequency, duration of electrical stimuli. Seizure should last at least 30-60 seconds in duration Good therapeutic effect is generally not achieved until 400-700 seizure seconds Treatments are usually given every other days unto 12 sessions Treatment endpoints are based on clinical experience and evaluation seizure involves: brief initial period of muscular contraction within 15 seconds, tonic phase that persists for 20 seconds followed by a rapid, erratic clonic phase lasting from a few seconds to more than one minute. seizure involves: brief initial period of muscular contraction within 15 seconds, tonic phase that persists for 20 seconds followed by a rapid, erratic clonic phase lasting from a few seconds to more than one minute.

10. INDICATIONS FOR ECT Severe depression: if drug treatment fails or is not tolerated ( i.e. elderly with Parkinson's disease ) Bipolar disorder: manic or depressed phase Acute or Catatonic Schizophrenia Patient is severely withdrawn or starving: effects seen in days rather than weeks Depression in pregnancy: with acute mania ECT is used if drugs fail or are not tolerated for depression, SSRI's and reversible MAOI's have much fewer side effects (dysrhythmias/conduction disturbances) that the traditional TCA's and non reversible MAOI's Schizophrenia Neuroleptics are the first line of treatment for schizophrenia. The evidence for the efficacy of ECT in schizophrenia is not compelling but is strongest for those schizophrenic patients with a shorter duration of illness, a more acute onset, and more intense affective symptoms. ECT has not been useful in chronically ill schizophrenic patients. Although ECT is frequently advocated for treatment of patients with schizophreniform psychoses, schizoaffective disorders, and catatonia, there are no adequate controlled studies to document its usefulness for these disorders Other Disorders There are no controlled studies supporting the efficacy of ECT for any conditions other than those designated above (i.e., delusional and severe endogenous depression, acute mania, and certain schizophrenic syndromes).  ECT is used if drugs fail or are not tolerated for depression, SSRI's and reversible MAOI's have much fewer side effects (dysrhythmias/conduction disturbances) that the traditional TCA's and non reversible MAOI's Schizophrenia Neuroleptics are the first line of treatment for schizophrenia. The evidence for the efficacy of ECT in schizophrenia is not compelling but is strongest for those schizophrenic patients with a shorter duration of illness, a more acute onset, and more intense affective symptoms. ECT has not been useful in chronically ill schizophrenic patients. Although ECT is frequently advocated for treatment of patients with schizophreniform psychoses, schizoaffective disorders, and catatonia, there are no adequate controlled studies to document its usefulness for these disorders Other Disorders There are no controlled studies supporting the efficacy of ECT for any conditions other than those designated above (i.e., delusional and severe endogenous depression, acute mania, and certain schizophrenic syndromes).

11. CONTRAINDICATIONS TO ECT CV Recent MI < 3 months; Severe angina, CHF Aneurysm of major vessel Pheochromocytoma CNS Cerebral tumor or aneurysm Recent CVA <1 month Respiratory System Severe respiratory failure Pregnancy Thyrotoxicosis Cardiac dysrhythmias Glaucoma Retinal detachment

12. PHYSIOLOGIC EFFECTS OF ECT-INDUCED SEIZURES Initial Parasympathetic Discharge (15 seconds) Bradycardia: marked Bradycardia <30 bpm or transient asystole Increased secretion Increased intragastric and intraocular pressure Sustained Sympathetic Discharge (1-3 min) Tachycardia Hypertension Dysrhythmias and T-wave abnormalities CNS: increased CBF, ICP, O2 consumption autonomic stimulation (CVS effects) follows a pattern of parasympathetic activation followed by sympathetic discharge bradycardia lasts about 15 seconds (attenuated by pre-treatment with anticholinergics) potential for asystole, PVC's or ventricular escape tachycardia/hypertension peaks at 60 seconds and lasts less than three minutes potential for PVC's, VT B-blockers (e.g. Esmolol 0.5 - 1.0 mg/kg) are more effective than vasodilators but may decrease seizure duration Increasing doses of pentothal or IV lidocaine will NOT block the hypertensive response and potentially increase seizure threshold and delay awakening heart rate may slow again before returning to normal values autonomic stimulation (CNS effects) brief vasoconstriction coincident with the electrical stimulus marked increase in cerebral blood flow may last up to several hours following the seizure marked increase in cerebral metabolism returns towards normal within five minutes large transient increase in intraocular pressure autonomic stimulation (CVS effects) follows a pattern of parasympathetic activation followed by sympathetic discharge bradycardia lasts about 15 seconds (attenuated by pre-treatment with anticholinergics) potential for asystole, PVC's or ventricular escape tachycardia/hypertension peaks at 60 seconds and lasts less than three minutes potential for PVC's, VT B-blockers (e.g. Esmolol 0.5 - 1.0 mg/kg) are more effective than vasodilators but may decrease seizure duration Increasing doses of pentothal or IV lidocaine will NOT block the hypertensive response and potentially increase seizure threshold and delay awakening heart rate may slow again before returning to normal values autonomic stimulation (CNS effects) brief vasoconstriction coincident with the electrical stimulus marked increase in cerebral blood flow may last up to several hours following the seizure marked increase in cerebral metabolism returns towards normal within five minutes large transient increase in intraocular pressure

13. ADVERSE EFFECTS TO ECT Muscle contractions: can result in fractures and dislocations; prevented by small doses of muscle relaxants Injury to teeth, tongue or lips: stimulus causes intense contraction of the masseter muscles and forceful movement of the jaw; use a bite block Electrical injury to the staff or patient muscle contractions accompany the grand mal seizure if unmodified, can result in fractures and dislocations; attenuated by small doses of muscle relaxants;approximately 50% of an intubating dose (0.5 mg/kg) detection of the epileptic event can be enhanced by tourniquet isolation of one limb to prevent entry of muscle relaxant employing an EEG recording of the seizure elderly patients or those receiving unilateral stimulation may have minimal signs of seizure discharge injury to teeth, tongue or lips stimulus causes intense contraction of the masseter muscles which results in vigorous clenching of the teeth stimulus causes additional forceful movement of the jaw and tongue due to proximity of stimulating electrodes important to prevent the tongue or the lips of the patient from being positioned between the teeth where serious injuries may occur a soft rubber bite block is used to separate the teeth from the tongue and lips wedging an airway between the molar teeth at the comer of the mouth may be useful in patients with poor dental hygiene electrical injury to the staff or patient careless application of conducting gel along the surface of the forehead may result in short circuit and burns conducting gel on hand surface of operator may lead to problems if hand subsequently touches improperly grounded equipmentmuscle contractions accompany the grand mal seizure if unmodified, can result in fractures and dislocations; attenuated by small doses of muscle relaxants;approximately 50% of an intubating dose (0.5 mg/kg) detection of the epileptic event can be enhanced by tourniquet isolation of one limb to prevent entry of muscle relaxant employing an EEG recording of the seizure elderly patients or those receiving unilateral stimulation may have minimal signs of seizure discharge injury to teeth, tongue or lips stimulus causes intense contraction of the masseter muscles which results in vigorous clenching of the teeth stimulus causes additional forceful movement of the jaw and tongue due to proximity of stimulating electrodes important to prevent the tongue or the lips of the patient from being positioned between the teeth where serious injuries may occur a soft rubber bite block is used to separate the teeth from the tongue and lips wedging an airway between the molar teeth at the comer of the mouth may be useful in patients with poor dental hygiene electrical injury to the staff or patient careless application of conducting gel along the surface of the forehead may result in short circuit and burns conducting gel on hand surface of operator may lead to problems if hand subsequently touches improperly grounded equipment

14. ADVERSE EFFECTS TO ECT Postictal Headache (45%) and muscle ache Short-term memory loss and cognitive deficits Difficult relationship with patients: frightened; withdrawn; suspicious; uncooperative Anesthesia related problem: i.e. air way issue (more pt with OSA); aspiration Line infection and sepsis

15. TREATMENT PROTOCOL Premedicate Glycopyrrolate and Beta blocker ? Patient not intubated Bite block Cuff leg to monitor seizure activity EEG and EMG Length of seizure: 30 sec to 1 min.

16. ECT DEVICE

17. EEG ACTIVITY

18. PRE-ECT EVALUATION Regular anesthesia pre-op evaluation: Esp. airway, CV, CNS Psychotropic medication should be stopped before ECT (antidepressants, benzodiazepine, lithium) for 7 days? Pre-ECT sedation: hydroxyzine or promethazine 25-50 mg, droperidol 2.5-5 mg (promote seizure) Pain medication prior to ECT The pre-ECT evaluation serves several functions. The anesthetist�s goal is to ensure the patient�s safety by identifying risks of anesthesia and recommending appropriate modifications, tests, and consultations (Beyer et al, 1998; Haddad & Benbow, 1993; Kellner et al, 1997). Patients scheduled for ECT may be delusional, paranoid, or uncommunicative. A thorough explanation may alleviate fears and anxiety. The evaluation should include the medical history and physical examination. A review of systems, particularly the neurologic and cardiovascular systems, may identify potential problems. A complete examination, including airway examination, must be performed. The cardiovascular, pulmonary, and neurologic examinations are particularly important for the possible physiologic changes during ECT. Previous anesthetic history, allergies, and current medications used are integral parts of the evaluation (Beyer et al, 1998; Kellner et al, 1997).The pre-ECT evaluation serves several functions. The anesthetist�s goal is to ensure the patient�s safety by identifying risks of anesthesia and recommending appropriate modifications, tests, and consultations (Beyer et al, 1998; Haddad & Benbow, 1993; Kellner et al, 1997). Patients scheduled for ECT may be delusional, paranoid, or uncommunicative. A thorough explanation may alleviate fears and anxiety. The evaluation should include the medical history and physical examination. A review of systems, particularly the neurologic and cardiovascular systems, may identify potential problems. A complete examination, including airway examination, must be performed. The cardiovascular, pulmonary, and neurologic examinations are particularly important for the possible physiologic changes during ECT. Previous anesthetic history, allergies, and current medications used are integral parts of the evaluation (Beyer et al, 1998; Kellner et al, 1997).

19. ANESTHETIC AGENTS SELECTION OBJECTIVE: �To leave the patient unaware of (amnesia) frightening sensations, particularly muscle paralysis and feelings of suffocation and the image of a light flash that may accompany the beginning of the stimulus, without obstructing the seizure� (McCleave & Blackmore, 1975) PRINCIPLE: To provide ultra-brief, light general anesthesia with moderate degree of muscular relaxation (APA, 1990, 2001)

20. INDUCTION AGENTS An ideal agent: rapid unconsciousness, painless on injection, no hemodynamic effects, no anticonvulsant properties, rapid recovery, and inexpensive (APA1990, 2001; Folk et al, 2000) Brevital Sodium : 0.5-1 mg/kg thiopental: 2-4 mg/kg ketamine: 0.5-2 mg/kg propofol: 1.5-3 mg/kg etomidate: 0.15-0.3 mg/kg An ideal induction agent for ECT would ensure rapid unconsciousness, be painless on injection, have no hemodynamic effects, have no anticonvulsant properties, provide rapid recovery, and be inexpensive (APA1990, 2001; Folk et al, 2000) Commonly used induction agents 1. Methohexital has a rapid action, short duration of action, low cardiac toxicity (Mokriski et al, 1992), minimal anticonvulsant effects (dose-related), and is associated with pain on injection. Other possible side effects include hypotension, shivering, hiccoughing, and necrosis of soft tissue at the injection site. The APA Task Force on ECT recommends its use as an induction agent of choice (APA, 1990). The typical dose is 0.5-1 mg/kg. 2. Thiopental has greater anticonvulsant effects and longer duration of action than methohexital (APA, 1990). Patients with cardiovascular disease whom induced with thiopental may have a greater incidence of postictal electrocardiographic abnormalities, compared with methohexital (Pitts, 1982). As with methohexital, thiopental can induce hypotension and cause possible necrosis at the injection site. Typical dose is 2-4 mg/kg (APA, 1990). 3. Ketamine is a derivative of phencyclidine, which inhibits the N-methyl-D-aspartate (NMDA) subtype of glutamate receptor (Huettner & Bean, 1988). Compared with methohexital, ketamine had slower onset, delayed recovery, and increased incidence of nausea, hypersalivation, �bad trips�, and ataxia during recovery (McInnes & James, 1972). It is recommended for patients with increased seizure threshold so that seizure elicitation is difficult, and typical dose is 0.5-2 mg/kg (APA, 1990, 2001). 4. Propofol has rapid onset, short duration of action, and is commonly associated with pain on injection. It has potent anticonvulsant properties (APA, 1990), as evidenced by a number of studies. Propofol (dose 0.75-1.5 mg/kg) resulted in: 1) markedly decreased the intensity and the duration of seizure (Avramov et al, 1995; Boy & Lai, 1990; Chanpattana, 2000; Kirkby et al, 1995; Rampton et al, 1989; Rouse, 1988), 2) a need for more numbers of treatment (Mitchell et al, 1991), 3) attenuation of ECTinduced hypertension and tachycardia (Villalonga et al, 1993), 4) a decrease in seizure-induced prolactin and ACTH release (Mitchell et al, 1990), and 5) successful use in the treatment of status epilepticus (Chilvers & Laurie, 1990; Wood et al, 1988). Nevertheless, randomized trials between propofol and either methohexital or thiopental do not demonstrate a difference in the therapeutic outcome or the speed of postictal recovery (Martensson et al, 1994; Matters et al, 1995). Other side effects include hypotension, apnoea, bradycardia, etc. 5. Etomidate is associated with pain on injection, as with methohexital, and causes prominent myoclonic activity during induction. Etomidate offers the advantage of having minimal effects on myocardial contractility and cardiac output (Morgan & Mikhail, 1996). It is recommended in patients with decreased cardiac output as well as patients with increased seizure threshold (APA, 1990). Typical dose is 0.15- 0.3 mg/kg. An ideal induction agent for ECT would ensure rapid unconsciousness, be painless on injection, have no hemodynamic effects, have no anticonvulsant properties, provide rapid recovery, and be inexpensive (APA1990, 2001; Folk et al, 2000) Commonly used induction agents 1. Methohexital has a rapid action, short duration of action, low cardiac toxicity (Mokriski et al, 1992), minimal anticonvulsant effects (dose-related), and is associated with pain on injection. Other possible side effects include hypotension, shivering, hiccoughing, and necrosis of soft tissue at the injection site. The APA Task Force on ECT recommends its use as an induction agent of choice (APA, 1990). The typical dose is 0.5-1 mg/kg. 2. Thiopental has greater anticonvulsant effects and longer duration of action than methohexital (APA, 1990). Patients with cardiovascular disease whom induced with thiopental may have a greater incidence of postictal electrocardiographic abnormalities, compared with methohexital (Pitts, 1982). As with methohexital, thiopental can induce hypotension and cause possible necrosis at the injection site. Typical dose is 2-4 mg/kg (APA, 1990). 3. Ketamine is a derivative of phencyclidine, which inhibits the N-methyl-D-aspartate (NMDA) subtype of glutamate receptor (Huettner & Bean, 1988). Compared with methohexital, ketamine had slower onset, delayed recovery, and increased incidence of nausea, hypersalivation, �bad trips�, and ataxia during recovery (McInnes & James, 1972). It is recommended for patients with increased seizure threshold so that seizure elicitation is difficult, and typical dose is 0.5-2 mg/kg (APA, 1990, 2001). 4. Propofol has rapid onset, short duration of action, and is commonly associated with pain on injection. It has potent anticonvulsant properties (APA, 1990), as evidenced by a number of studies. Propofol (dose 0.75-1.5 mg/kg) resulted in: 1) markedly decreased the intensity and the duration of seizure (Avramov et al, 1995; Boy & Lai, 1990; Chanpattana, 2000; Kirkby et al, 1995; Rampton et al, 1989; Rouse, 1988), 2) a need for more numbers of treatment (Mitchell et al, 1991), 3) attenuation of ECTinduced hypertension and tachycardia (Villalonga et al, 1993), 4) a decrease in seizure-induced prolactin and ACTH release (Mitchell et al, 1990), and 5) successful use in the treatment of status epilepticus (Chilvers & Laurie, 1990; Wood et al, 1988). Nevertheless, randomized trials between propofol and either methohexital or thiopental do not demonstrate a difference in the therapeutic outcome or the speed of postictal recovery (Martensson et al, 1994; Matters et al, 1995). Other side effects include hypotension, apnoea, bradycardia, etc. 5. Etomidate is associated with pain on injection, as with methohexital, and causes prominent myoclonic activity during induction. Etomidate offers the advantage of having minimal effects on myocardial contractility and cardiac output (Morgan & Mikhail, 1996). It is recommended in patients with decreased cardiac output as well as patients with increased seizure threshold (APA, 1990). Typical dose is 0.15- 0.3 mg/kg.

21. MUSCLE RELAXANTS Succinylcholine: 0.3-1.5 mg/kg. Atracurium, 0.3-0.5 mg/kg (Hickey et al, 1987) Mivacurium, 0.15-0.2 mg/kg (Kelly & Brull, 1994) Rocuronium, 0.45-0.6 mg/kg (Motamed et al, 1997) Objective: To prevent injuries to the musculoskeletal system and to improve airway management (APA, 1990). Principle: To provide the moderate degree of muscular relaxation (APA, 1990, 2001). In general, complete paralysis is neither necessary nor desirable since it may be associated with prolonged apnea. In addition, the intensity and the duration of ictal motor movements should be observed and monitored (Beyer et al, 1998). Muscle paralysis not only facilitates oxygenation, but also decreases oxygen utilization by muscles during the seizure (APA, 1990). Consideration should be given to higher dosage of muscle relaxants for patients with Harrington rods, or at risk for developing pathologic bone fracture (APA, 1990; Coffey et al, 1986; Milstein et al, 1992). The adequacy of muscular relaxation should be ascertained before applying the ECT stimulus. This process is done by testing for a reduction in deep tendon reflexes and muscle tone (APA, 1990). In patients receiving high dose of succinylcholine, a peripheral nerve stimulator should be used (APA, 1990; Beyer et al, 1998; Kellner et al, 1997). Common side effects of succinylcholine include arrhythmia, increased intraocular or intraabdominal pressure. Since succinylcholine has been associated with malignant hyperthermia and hyperkalemia, nondepolarizing muscle relaxants have been developed. The dosage of these agents should be determined individually and clinically. Typically, the succinylcholine dose is 0.5-1 mg/kg. Atracurium, 0.3-0.5 mg/kg (Hickey et al, 1987); mivacurium, 0.15-0.2 mg/kg (Kelly & Brull, 1994); rocuronium, 0.45-0.6 mg/kg (Motamed et al, 1997); and rapacuronium, 1-2 mg/kg (Szenohradszky et al, 1999) are alternatives to succinylcholine (Savarese et al, 2000). These nondepolarizing muscle relaxants produce more prolonged paralysis, and both the onset and duration of action should be monitored with a nerve stimulator (APA, 2001). Objective: To prevent injuries to the musculoskeletal system and to improve airway management (APA, 1990). Principle: To provide the moderate degree of muscular relaxation (APA, 1990, 2001). In general, complete paralysis is neither necessary nor desirable since it may be associated with prolonged apnea. In addition, the intensity and the duration of ictal motor movements should be observed and monitored (Beyer et al, 1998). Muscle paralysis not only facilitates oxygenation, but also decreases oxygen utilization by muscles during the seizure (APA, 1990). Consideration should be given to higher dosage of muscle relaxants for patients with Harrington rods, or at risk for developing pathologic bone fracture (APA, 1990; Coffey et al, 1986; Milstein et al, 1992). The adequacy of muscular relaxation should be ascertained before applying the ECT stimulus. This process is done by testing for a reduction in deep tendon reflexes and muscle tone (APA, 1990). In patients receiving high dose of succinylcholine, a peripheral nerve stimulator should be used (APA, 1990; Beyer et al, 1998; Kellner et al, 1997). Common side effects of succinylcholine include arrhythmia, increased intraocular or intraabdominal pressure. Since succinylcholine has been associated with malignant hyperthermia and hyperkalemia, nondepolarizing muscle relaxants have been developed. The dosage of these agents should be determined individually and clinically. Typically, the succinylcholine dose is 0.5-1 mg/kg. Atracurium, 0.3-0.5 mg/kg (Hickey et al, 1987); mivacurium, 0.15-0.2 mg/kg (Kelly & Brull, 1994); rocuronium, 0.45-0.6 mg/kg (Motamed et al, 1997); and rapacuronium, 1-2 mg/kg (Szenohradszky et al, 1999) are alternatives to succinylcholine (Savarese et al, 2000). These nondepolarizing muscle relaxants produce more prolonged paralysis, and both the onset and duration of action should be monitored with a nerve stimulator (APA, 2001).

22. ADJUNCTIVE AGENTS Caffeine 0.25-1.5 gm IV Flumazenil: 0.2-1 mg IV (benzodiazepine antagonist) Benzodiazepine: Valium 5-10 mg IV (status epilepticus) Anticholinergics: atropine 0.4-0.8 mg IV or glycopyrrolate 0.2-0.4 mg IV Beta blockers: Labetalol and Esmolol Nitroglycerine Antihypertensives: Labetalol, Trimethaphan, Nicardipine Anticholinergics Objective: To protect against the parasympatheticinduced bradycardia or asystole (Altschule, 1950; Bankhead et al, 1950). Principle: To decrease the effects of ECT-induced vagal stimulation (APA, 1990). Vagal reflex occurs immediately following the ECT stimulus regardless of the amount of electrical charge, and may be associated with transient bradycardia or asystole. If the electrical charge is near or above the seizure threshold, tonic-clonic motor seizures may occur with accompanying sympathetic stimulation. This sympathetic surge counteracts the effects from vagal stimulation. But if the electrical stimulus fails to elicit the seizure (subconvulsive stimulation), the bradycardia immediately following the stimulus is of graver concern, since the protection afforded by the ictal tachycardia is absent (Bellet et al, 1941). Indications 1. Patients undergoing an estimation of seizure threshold by dose-titration method, especially at the first ECT session (APA, 1990; Bouckoms et al, 1989). 2. Patients receiving sympathetic blocking agents (APA, 1990). 3. Situations when the occurrence of vagal bradycardia should be prevented: e.g., pre-existing cardiac disease, hypodynamic cardiac functions (APA, 2001; Bouckoms et al, 1989). Agents modifying cardiovascular response Objective: To attenuate the ECT-induced cardiovascular responses (Gravenstein et al, 1965; Perrin, 1961). Principle: The risks of ECT are well recognized. The peritreatment mortality rate is about 0.002% (or 1: 80,000 [APA, 2001]). Cardiovascular complications, arrhythmias, myocardial infarction, congestive heart failure, and cardiac arrest, are among the most common causes of death (APA, 1990). At the present time there is no consensus on the indications for use of these agents. The APA Task Force on ECT suggests that indiscriminant use should be avoided (APA, 2001). During ECT-induced seizures, cerebral blood flow increases up to 300%, oxygen use and glucose metabolism increase up to 200% (Ackerman et al, 1986). Therefore, the peripheral hemodynamic surge appears to be necessary to sustain this demand, and provides adequate supply of oxygen and carbohydrates to the brain. Given these concerns, judgment is needed about when to use these agents (APA, 2001). 1. Beta blockers. The literature on beta blockers is extensive. The major side effect is their anticonvulsant properties. Labetalol is the most commonly used �-blockers at present. It selectively blocks a1 and nonselectively blocks �1 and �2 adrenergic receptors. The starting dose is 5-10 mg given intravenously. Its onset of action is 2-5 minutes with duration of action about 4-6 hours. Esmolol has a faster onset (30-90 seconds) and much shorter duration of action (~10 minutes), has more effect on blood pressure than heart rate, and decrease more cardiac work load, compared to labetalol (APA, 2001; Castelli et al, 1995). 3. Trimethaphan, a ganglionic blocking agent, is among the first intravenous antihypertensive recommended for ECT (APA, 1990). It inhibits both sympathetic and parasympathetic nervous systems with effect on arterioles, and promotes peripheral vasodilation without inducing reflex tachycardia. It is only available in parenteral form and has onset of action within minutes. Trimethaphan boluses attenuated blood pressure and heart rate during ECT without rebound hypertension, prolonged hypotension, arrhythmias, or effects on seizure duration (Petrides et al, 1996). Anticholinergics Objective: To protect against the parasympatheticinduced bradycardia or asystole (Altschule, 1950; Bankhead et al, 1950). Principle: To decrease the effects of ECT-induced vagal stimulation (APA, 1990). Vagal reflex occurs immediately following the ECT stimulus regardless of the amount of electrical charge, and may be associated with transient bradycardia or asystole. If the electrical charge is near or above the seizure threshold, tonic-clonic motor seizures may occur with accompanying sympathetic stimulation. This sympathetic surge counteracts the effects from vagal stimulation. But if the electrical stimulus fails to elicit the seizure (subconvulsive stimulation), the bradycardia immediately following the stimulus is of graver concern, since the protection afforded by the ictal tachycardia is absent (Bellet et al, 1941). Indications 1. Patients undergoing an estimation of seizure threshold by dose-titration method, especially at the first ECT session (APA, 1990; Bouckoms et al, 1989). 2. Patients receiving sympathetic blocking agents (APA, 1990). 3. Situations when the occurrence of vagal bradycardia should be prevented: e.g., pre-existing cardiac disease, hypodynamic cardiac functions (APA, 2001; Bouckoms et al, 1989). Agents modifying cardiovascular response Objective: To attenuate the ECT-induced cardiovascular responses (Gravenstein et al, 1965; Perrin, 1961). Principle: The risks of ECT are well recognized. The peritreatment mortality rate is about 0.002% (or 1: 80,000 [APA, 2001]). Cardiovascular complications, arrhythmias, myocardial infarction, congestive heart failure, and cardiac arrest, are among the most common causes of death (APA, 1990). At the present time there is no consensus on the indications for use of these agents. The APA Task Force on ECT suggests that indiscriminant use should be avoided (APA, 2001). During ECT-induced seizures, cerebral blood flow increases up to 300%, oxygen use and glucose metabolism increase up to 200% (Ackerman et al, 1986). Therefore, the peripheral hemodynamic surge appears to be necessary to sustain this demand, and provides adequate supply of oxygen and carbohydrates to the brain. Given these concerns, judgment is needed about when to use these agents (APA, 2001). 1. Beta blockers. The literature on beta blockers is extensive. The major side effect is their anticonvulsant properties. Labetalol is the most commonly used �-blockers at present. It selectively blocks a1 and nonselectively blocks �1 and �2 adrenergic receptors. The starting dose is 5-10 mg given intravenously. Its onset of action is 2-5 minutes with duration of action about 4-6 hours. Esmolol has a faster onset (30-90 seconds) and much shorter duration of action (~10 minutes), has more effect on blood pressure than heart rate, and decrease more cardiac work load, compared to labetalol (APA, 2001; Castelli et al, 1995). 3. Trimethaphan, a ganglionic blocking agent, is among the first intravenous antihypertensive recommended for ECT (APA, 1990). It inhibits both sympathetic and parasympathetic nervous systems with effect on arterioles, and promotes peripheral vasodilation without inducing reflex tachycardia. It is only available in parenteral form and has onset of action within minutes. Trimethaphan boluses attenuated blood pressure and heart rate during ECT without rebound hypertension, prolonged hypotension, arrhythmias, or effects on seizure duration (Petrides et al, 1996).

23. POST-ECT RECOVERY Headache: Up to 45 % (Devanand et al. 1995; Freeman and Kendell 1980) N/V: 1.4% - 23% (Gomez 1975; Sackeim et al. 1987d) Muscle ache Post-ECT confusion Headache is a common side effect of ECT and is observed in as many as 45% of patients during and shortly following the postictal recovery period (Devanand et al. 1995; Freeman and Kendell 1980; Gomez 1975; Sackeim et al. 1987d: Tubi et al. 1993; Weiner et al. 1994). However, the precise incidence of postECT headache is difficult to determine due to methodological issues such as the high baseline (preECT) occurrence of headache in patients with depression, the potential effects of concurrent medication or medication withdrawal, and differences between studies in the assessment of headache. PostECT headache appears to be particularly common in younger patients (Devanand et al. 1995) and especially in children and adolescents (Rey and Walter 1997; Walter and Rey 1997) It is not known whether pre-existing headache syndromes (e.g., migraine) increase the risk of postECT headache, but ECT may exacerbate a previous headache condition (Weiner et al. 1994). The occurrence of postECT headache does not appear to be related to stimulus electrode placement (at least bifrontotemporal vs. right unilateral) (Fleminger et al. 1970; Sackeim et al. 1987d; Tubi et al. 1993; Devanand et al. 1995), stimulus dosage (Devanand et al. 1995), or therapeutic response to ECT (Sackeim et al. 1987d; Devanand et al. 1995).In most patients the postECT headache is mild (Freeman and Kendell 1980; Sackeim et al. 1987d), although a sizable minority will report severe pain associated with nausea and vomiting. Typically the headache is frontal in location and has a throbbing character.The etiology of postECT headache is not known. Its throbbing character suggests a similarity with vascular headache, and ECT may be associated with a temporary change in quality of headache from muscle-contraction type to vascular type (Weiner et al. 1994; Weinstein 1993). Indeed, ECT upregulates 5-HT2 receptors and 5-HT2 receptor sensitization has been associated with development of vascular headache (Weiner et al. 1994). Other suggested mechanisms include electrically induced temporalis muscle spasm or acute increase in blood pressure and cerebral blood flow (Abrams 1997a; Weiner et al. 1994).Treatment of postECT headache is symptomatic. Aspirin, acetaminophen, or non-steroidal anti-inflammatory drugs (NSAIDs) typically are highly effective, particularly if given promptly after the onset of pain. Sumatriptan, a serotonin 5HTID receptor agonist, has also been effective at doses of 6 mg subcutaneously (DeBattista and Mueller 1995) or 25 - 100 mg orally (Fantz et al. in press). Some patients will require more potent analgesics (e.g. codeine), although narcotics may contribute to associated nausea. Most patients also benefit from bed rest in a quiet, darkened environment.PostECT headache may occur after any ECT treatment in a course, irrespective of its occurrence at any prior treatment. Patients who experience frequent postECT headache may benefit from prophylactic treatment, such as aspirin, acetaminophen, or NSAIDs given as soon as possible after ECT, or even immediately prior to the ECT treatment. Subcutaneous sumatriptan 6 mg given several minutes prior to ECT was also found to provide effective prophylaxis in a patient with severe, refractory postECT headache (DeBattista and Mueller 1995). Headache is a common side effect of ECT and is observed in as many as 45% of patients during and shortly following the postictal recovery period (Devanand et al. 1995; Freeman and Kendell 1980; Gomez 1975; Sackeim et al. 1987d: Tubi et al. 1993; Weiner et al. 1994). However, the precise incidence of postECT headache is difficult to determine due to methodological issues such as the high baseline (preECT) occurrence of headache in patients with depression, the potential effects of concurrent medication or medication withdrawal, and differences between studies in the assessment of headache. PostECT headache appears to be particularly common in younger patients (Devanand et al. 1995) and especially in children and adolescents (Rey and Walter 1997; Walter and Rey 1997) It is not known whether pre-existing headache syndromes (e.g., migraine) increase the risk of postECT headache, but ECT may exacerbate a previous headache condition (Weiner et al. 1994). The occurrence of postECT headache does not appear to be related to stimulus electrode placement (at least bifrontotemporal vs. right unilateral) (Fleminger et al. 1970; Sackeim et al. 1987d; Tubi et al. 1993; Devanand et al. 1995), stimulus dosage (Devanand et al. 1995), or therapeutic response to ECT (Sackeim et al. 1987d; Devanand et al. 1995).

24. SUGGESTED REGIME Preoperative Evaluation Fasting Preoperative Medications IV placement Monitors EKG, SpO2 Blood Pressure

25. SUGGESTED REGIME- INDUCTION Preoxygenation Inform MD and RN for the readiness of induction Methohexital or others /Succinylcholine Hyperventilate until fasciculation completed Insertion of bite block or part of oral airway for tooth protection Ascertain the muscle relaxation with stimulator ECT hypoxemia may result from inadequate preoxygenation, airway obstruction, inadequate ventilation, increased metabolic demand arising from the seizure. aspiration is a rare event amnesia is usually created by the seizure although induction agent recommended in case there is malfunction of machine or inadequate seizure activity after administration of succinylcholinehypoxemia may result from inadequate preoxygenation, airway obstruction, inadequate ventilation, increased metabolic demand arising from the seizure. aspiration is a rare event amnesia is usually created by the seizure although induction agent recommended in case there is malfunction of machine or inadequate seizure activity after administration of succinylcholine

26. SUGGESTED REGIME Emergence Hyperventilate with 100% O2 until normal vital signs obtained, then slow assisted breaths until spontaneous ventilation resumes. Turn patient on side and transport to PACU Drugs ready to use Atropine or glycopyrrolate, esmolol or labetalol, ephedrine, phenylephrine Equipment ready to use Laryngoscopes, ETT, stylet, airways, suction, defibrillator, alternative airway devices

27. BURST SUPRESSION THERAPY (BST) Induction Intubation Hyperventilation Emergence Recovery

28. SEVOFLURANE BST