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Patrick McElhone, CRNA Chief CRNA Hines VA Hospital
Anesthesia for ECT Patrick McElhone, CRNA Chief CRNA Hines VA Hospital
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Disclosures
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Anesthesia for ECT History Theories on how ECT works
Indications for ECT Complications of ECT
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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”
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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.
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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
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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
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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
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How Does ECT Work: Psychological Effects
Patient’s expectations Placebo effect Force regression Retrograde amnesia Proven incorrect
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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
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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
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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
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Indications for ECT Schizophrenia Catatonia Mania Depression
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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
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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
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ECT for Schizophrenia Combined with antipsychotics
Multitude of studies showing improvement when combined with Clozepine Effects were not persistent and required continuation in treatments
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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
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ECT For Depression Treatment Resistant Depression 80% of all ECT in US
50% of patients showed improvements 50% relapse with 12months
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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
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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
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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
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"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
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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
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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
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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
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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
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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
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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
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GABAergic agents Activate gaba receptors Influx of Cl- Channels
Hyperpolarization of neuron Anticonvulsants Limits effectiveness in ECT Medications Methohexital Etomidate Propofol
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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
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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
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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
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Ketamine NMDA receptor antagonist
Blocks glutamate Decrease seizure duration compared to methohexital Enhances sympathomimetic activity Increases ICP
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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
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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
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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 < )
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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
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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
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Airway Management NMB induce apnea
Ventilatation Oxygenation NMB abolish the airway protective reflexes Increased risk of aspiration
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Apnea Mask Ventilation-most common Supra-glottic airway
Prolonged apnea Difficult mask ventilaiton Endotracheal Intubation High risk for aspiration
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Aspiration Nothing by mouth
Endotracheal tube intubation for high risk patients GERD Hiatal Hernia Delayed gastric emptying Extubate awake and airway reflexes have returned
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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
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Balanced Individualized Anesthesia for ECT
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Experiences? Questions? Thank you
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