1. Patrick McElhone, CRNA Chief CRNA Hines VA Hospital
Anesthesia for ECT
Patrick McElhone, CRNA
Chief CRNA
Hines VA Hospital

2. Disclosures

3. Anesthesia for ECT History Theories on how ECT works
Indications for ECT
Complications of ECT

4. History of ECT
The concept of inducing convulsions to promote mental wellness has existed since the 16th century
Swiss alchemist Paracelsus gave camphor by mouth to induce convulsions and “cure lunacy”

5. Seizures Cure Catatonic Schizophrenia
In 1934, Ladislaw Meduna, a Hungarian psychiatrist, investigated a hypothetical inverse relationship between seizures and schizophrenia
Lack of glial cells in individuals with schizophrenia
Overgrowth of these cells in people with epilepsy.

6. Seizures Cure Catatonic Schizophrenia
Meduna hypothesized that inducing epilepsy would cure cure patients with schizophrenia
Meduna injected camphor in oil into a patient with catatonic schizophrenia, causing a 60 second grand mal seizure.
The patient went into a full recovery after a short series of such treatments

7. Development of ECT: Camphor to Electricity
Camphor was replaced by Metrazol
Frequent seizures
Vertebral fractures
Pulmonary tuberculosis
Myocardial damages
Hypertension
Alternative methods to induce Seizure
Electricity was recently used to induce seizures in dogs

8. Development of ECT
Italian scientists Cerletti and Bini defined the parameters to applying electricity to the human scalp to induce seizures
1938, 39yo, found delusional at train station electrically induced seizures
Full recovery reported after 11 treatments
Electroconvulsive Therapy was born

9. How Does ECT Work: Psychological Effects
Patient’s expectations
Placebo effect
Force regression
Retrograde amnesia
Proven incorrect

10. How does ECT Work: Neurophysiological Effects
Anticonvulsant
Treatment of Intractable Seizures
Increased Seizure Threshold during treatment course
Decrease Seizure Duration over the treatment course
Increase inhibitory neurotransmitter
Decrease in excitatory neurotransmitters
Post-ictal bioelectrical suppression
All associated with improved clinical improvement

11. How Does ECT Work: Effects on Hippocampus
Promote neurogenesis dentate gyrus
Perera et al.
12 ECT total (3x week/4 weeks) to monkeys
Increase in cell proliferation in the dentate gyrus
Increase lasted for 4 weeks
Meduna saw a lack of glial cells in schizophrenics and an over growth of glial cells in epileptics

12. How Does ECT Work? Decrease Glucocorticoid levels
Chronic Stress leads to decrease cell proliferation in the dentate gyrus
Basis for the animal model of depression
ECT can mitigate this response
Increase in BDNF

13. Indications for ECT
Schizophrenia
Catatonia
Mania
Depression

14. Indications for ECT Increased Clinical Urgency
Depressive Hallucinations
Catatonia
Suicidal Ideations
Intolerance to psychotropic drugs
Failure of drug therapy
Patient Preference
Co-existing Medical Disorders for which psychoactive medication poses a risk
Pregnancy
Cardiac patients-TCAs

15. ECT for Schizophrenia First use of ECT Indications:
Fell out of use with antipsychotic medications in 1950s
Most common indication for ECT in India and other Asian Countries
Indications:
Augment to pharmacotherapy
Rapid improvement is needed
Refractory to medication
Catatonia

16. ECT for Schizophrenia Combined with antipsychotics
Multitude of studies showing improvement when combined with Clozepine
Effects were not persistent and required continuation in treatments

17. ECT for Mania 80% Manic patient had remission or marked improvements
Showed improvement when pharmacotherapy did not
Lower seizure threshold
Improvement seen in few treatments

18. ECT For Depression Treatment Resistant Depression 80% of all ECT in US
50% of patients showed improvements
50% relapse with 12months

19. ECT For Depression compared to medication
20% higher response vs. tricyclic antidepressants
45% higher response vs. MAOIs
“No study has found any treatment to be superior to ECT for the treatment of major depression

20. Complications of ECT Skeletal Injuries Cognitive Decline
Cervical Fractures-Unmodified
Long Bone Fractures-Unmodified
Cognitive Decline
Memory Loss
Concentration and Attention Problems
Confusion
Brain Injury?? TBI?
Why???
Complications from procedure/anesthesia

21. Bilateral vs Uni-lateral Electrode Placement
Most common in use
Better seizures
Memory loss
Uni-lateral
Less impairment of new learning capacity
Less amnesia for remote events
Possible to not trigger seizure

22. "Well, what is the sense of ruining my head and erasing my memory, which is my capital, and putting me out of business? It was a brilliant cure but we lost the patient....” -Ernest Hemingway

23. Anesthesia in ECT aka Modified ECT
1940s Neuromuscular blocking agents (NMB) used to prevent joint/bone injury during treatment
Curare
Succinylcholine
Short acting IV anesthetics were administered to prevent memory of being paralyzed
Unmodified ECT
Done without anesthesia is still practiced in Japan, China and India

24. Anesthesia for ECT Overview
Akinesia #1
Prevent excessive motor activity during seizure
Musculoskeletal Injury
Oxygen consumption
Amnesia
Prevent recall of being paralyzed
Autonomic Stability
Managed parasympathetic and sympathetic effects of ECT
Analgesia
Ensure patient comfort from procedure
Myalgia from succinylcholine
Headaches from ECT

25. Akinesia Neuromuscular Blocking Agents
Competitively block acetylcholine at the neuromuscular junction
Prevent motor end plate activation
2 primary types
Depolarizing
Succinylcholine
Non-deplolarizing
Rocuronium
Vecuroniom
Cis-atricurium

26. Depolarizing neuromuscular blocking agents
Succinylcholine (Anectine)
Activates the motor end-plate
Cause a prolong depolarization
Fasciculations
Relaxation occurs during the relative refractory period
Primary NMB used in ECT
Dose mg/kg
Contraindications
Malignant Hyperthermia
Paralysis/Weakness
Burns
Hyperkalemia

27. Non-deplorazing neuromuscular blocking agents
Block end-plate but do not cause any action
Longer duration of action
Rocuronium
Cisatricurium
Reversible
Neostigmine
Blocks acetylcholinesterase
Allows competitive build-up of Acetylcholine
Sugamadex
Binds to free rocuronium
Rapid, complete

28. Amnesia agents for ECT “Remember why we are here”
Seizure Quality
Advantages
Disadvantages
Methohexital
mg/kg
“Gold Standard”
Long history
Limited availability
Not common anesthetic
Etomidate
mg/kg
Duration prolonged
May reduce threshold
Resistant Seizures
Pronounce sympathetic response
Increased nausea
Longer emergence
Propofol
mg/kg
Shorter duration
Improved CVS stability
Quick emergence
Pain on injection
Ketamine
mg/kg ( mg/kg)
Unclear-shown to both shorten and lengthen
Emergence delirium
Increased ICP

29. GABAergic agents Activate gaba receptors Influx of Cl- Channels
Hyperpolarization of neuron
Anticonvulsants
Limits effectiveness in ECT
Medications
Methohexital
Etomidate
Propofol

30. Methohexital (Brevital)
“Gold Standard”
Barbiturate
No Change on ECT induced seizure duration
Dosage:
mg/kg
Increased dosage
Chronic ETOH
Benzodiazepines
Contraindicated in acute intermittent porphyria

31. Etomidate Gabametic Increases seizure duration Dosage
Compared to methohexital, thiopental, and propofol
Useful seizure <20s
Dosage
0.15–0.3 mg/kg
Hemodynamically stable
Increased sympathetic response

32. Propofol Potent anticonvulsant effects during ECT
1-1.5mg/kg
1.5mg/kg still shown to allow adequate seizure
Minimal hypnotic dosage 0.75mg/kg compares to methohexital

33. Ketamine NMDA receptor antagonist
Blocks glutamate
Decrease seizure duration compared to methohexital
Enhances sympathomimetic activity
Increases ICP

34. Autonomic stability-Initial Response to ECT Hemodynamic Changes with ECT
Parasympathetic Surge
Anticipate bradycardia
Asystole
Increase secretions
Anticholinergics Pretreatment
Glycopyrrolate mg
Less tachycardia
Atropine 0.4mg-1.0mg
Sympathomimetics during arrest
Epinephrine mcg

35. Autonomic Stability-Second Response to ECT
Sympathetic Surge
Increased BP 20-40%
Increase HR >20%
Last 3-5min
Risks:
Myocardial Ischemia
Treatment
Beta receptor antagonists
Labetalol
Esmolol
Vasodilators
Hydralazine

36. rSO2 changed conisently
Regional Cerebral Oxygen Saturation During Electroconvulsive Therapy: Monitoring by Near-Infrared Spectrophotometry Saito, Shigeru MD; Miyoshi, Sohtaro MD; Yoshikawa, Daisuke MD; Shimada, Hitoshi MD; Morita, Toshihiro MD; Kitani, Yasuharu MD Anesthesia & Analgesia:  October Volume 83 - Issue 4 - pp Neurosurgical Anesthesia
43 patients, ECT under GA
Continually monitored
Heart rate (HR)
Mean arterial blood pressure
Regional cerebral oxygen saturation (rSO2)
 rSO2 changed conisently
Initially, -9.4% +/- 0.9%
Later, +8.7%, =?- 0.9%
Demonstrated a close correlation between the increase in rSO2 and the mean blood pressure after the electrical shock (r2 = 0.832, P < )

37. Analgesia in ECT Muscle aches-myalgia Headache-ECT electrodes
Succinylcholine
Headache-ECT electrodes
Treatment
Ketoralac
IV NSAIDs
Acetaminophen
Opioids
Fentanyl 25-50mcg
Best assessed after ECT

38. Complications from ECT
Airway
Difficult airway management
Larygnospasm
Respiratory
Aspiration
Prolonged muscle weakness
Cardiovascular
Effects of ECT
Bradycardia/asystole
Tachycardia
Cardiovascular
Effects of anesthetics
Prolonged seizures
Propofol
Midazolam
Emergence delerium

39. Airway Management NMB induce apnea
Ventilatation
Oxygenation
NMB abolish the airway protective reflexes
Increased risk of aspiration

40. Apnea Mask Ventilation-most common Supra-glottic airway
Prolonged apnea
Difficult mask ventilaiton
Endotracheal Intubation
High risk for aspiration

41. Aspiration Nothing by mouth
Endotracheal tube intubation for high risk patients
GERD
Hiatal Hernia
Delayed gastric emptying
Extubate awake and airway reflexes have returned

42. Equipment for ECT Anesthesia
Machine
Suction
Monitors
Nerve Stimulator!
EKG and BP
Pulse-Oximetry and ETCO2
Airway
Oral Airway
Bite Block
Endotracheal tube IV
Drugs

43. Balanced Individualized Anesthesia for ECT

44. Experiences?
Questions?
Thank you