ECT Flashcards
One resource listed 2 (others say none absolute).
What are relative contraindications to ECT?
raised ICP with mass effect
phaeochromocytoma
raised ICP
recent (within 3/12) CVA or MI
untreated cerebral aneurysm
myocardial ischaemia or uncontrolled heart failure
DVT (until anti coagulated)
unstable major fracture
phaeochromocytoma
retinal detachment or glaucoma
cochlear implants (concern re: damage to the pt or implant but could consider in life-threatening psych conditions)
severe osteoporosis
Anaesthetic considerations for ECT?
Location- remote (if ASA II or higher, consider relocating to OT suite); MUST comply with statements regarding facilities & monitoring for safe provision of anaesthesia including recovery facilities & equipment to manage emergencies (INCL cardiac arrest, MH, range of airway equipment) ass’d w GA
Patient- often elderly, multiple comorbidities, multiple medications which may have side-effects or interactions with anaesthetic drugs, need to consider the cardiovascular & cerebral effects of the anaesthetic & procedure
Consent issues/guardianship (eg. involuntary Rx)
Pre-anaesthetic medications:
-headache: most common adverse effect of ECT. peaks 2 hrs post-headache. if the pt has a Hx of it responsive to otc meds, consider prophylactic dose of paracetamol or ibuprofen. if severe, consider IV ketorolac. triptans also effective. cold therapy.
-nausea: in 25%. prophylaxis w ondans. props for induction :)
-anticholinergic: bradycardia (severe, w hypoT) is more common w 1st ECT Rx (greater chance of subconvulsive stimulus leading to PSNS discharge. also excessive secretions may occur. routine anticholinergic not necessary (risks high HR in pts w IHD, memory impairment in elderly, dry mouth). but consider if Hx severe brady or excess salivation w ECT.
Pre-O2: aiming SpO2 100% (incr risk desat if obese or long seizures)
Induction agent: avoid excessive depth (impairs efficacy of ECT Rx). while props has rapid onset & good recovery, it has significant anticonvulsant properties so a higher stimulus dose (voltage) may be required for adequate seizures & seizure duration may be reduced, there may be more severe cognitive side effects. Good for pts w Hx prolonged seizures, postictal agitation, PONV.
Ketamine may be useful if ect seizures are suboptimal (some studies suggest it may enhance seiure duration). analgesic properties. bronchodilating. risks incl postprocedure hallucinations/restlessness, sympathomimetic effects may incr myocardial O2 demand of ECT SNS effects. QTcprol (potential interaction w some psychotrophic meds). incr salivation so use glyco if also ketamine).
ketofol :)
dexmed doesn’t interfere w seizure duration, doesn’t prolong recovery time but IS ass’d w decr in MAP & HR. may attenuate hyperdynamic responses. Reduces post-ect headache, agitation, delirium.
remi: attenuates hypertensive response, may result in longer seizure duration but doesn’t have intrinsic properties to enhance ect seizures. may have dizziness, nausea, headache & doesn’t have intrinsic properties enhancing seizures.
sevo: induction agent of choice if need inhalational (rapid onset, low airway irritation).it may shorten motor seizure but can attenuate by switch to IV post-induction. risks ass’d w inhalational induction).
NMBA: limits physical trauma w uncontrolled tetanic muscle contractions. sux 1mg/kg generally used (rapid onset, short DoA, rapid recovery). consider higher dose in osteoporotic pts. wait until fasciculations ceased & plantar reflex on side sans ankle tourniquet has been abolished.
Roc 0.3-0.6mg/kg alternative if contraindication (eg neuromuscular disorder, prolonged immobilisation). slower onset (consider larger dose), needs neuromuscular monitoring. use sugammadex.
airway: facilitate hyperventilation, hypocapnia & hyperoxia to augment ECT-induced seizure.
biting pressure: can’t abolish forceful jaw clench w NMBA since temporalis, masseter & pterygoids are directly stimulated by the electrodes. Use a bite guard w maximal cushioning over molar area, insert prior to electrical stimulation. MAKE SURE TONGUE inf/posterior.BMV for most, SGA an option if obstruction/obese, rarely I&V.
After pre-O2 & GA induction, hyperventilate to EtCO2 approx 30mmHg; incr seizure intensity & duration, reduces electrical charge required for therapeutic convulsion. ?maintain 100% supplemental O2 & airway control throughout the procedure incl emergence & recovery.
Hypocapnia lowers the seizure threshold.
Hypocapnia ALSO reduces intracranial HTN & incidence of postictal headache & agitation.
risks= coronary & cerebral VC & risk arrhythmias.
conversely, hypercapnia ass’d w HTN, tachy, somnolence & incr post-procedure agitation & headache.
Recovery in PACU facility.
if postictal agitation (acute confusional state, disorientation, restlessness, poor response to vegal requests, amnesia). usually self-limiting. mild cases supportive measures, Bx intervention. if severe, consider IV BZD, propofol, dexmed @ end of seizure.
SS_HN 1.27: What are the cardiovascular effects of the ECT?
-Response is secondary to activation of the ANS; with the electrical stimulus there’s initially a parasympathetic discharge lasting 10-20 seconds (stimulation notor nucleus of vagus nervewhich causes bradycardia (& risks hypotension, atrial arrhythmias, AV block, asystole).
A more prominent SNS response follows w clonic phase of - can get arrhythmias, SBP may increase by 30-40% & HR may increase by 20% or more, generally peaks at 3-5mins; CO may incr 80%. These haemodynamic responses continue into the postictal period, usually resolve within 10-20mins of the seizure. Post-procedure short-acting B blockers (eg. esmolol or labetalol) can be used to quickly treat persistent or severe tachycardia & HTN; alternatives= IV clonidine. For pts @ very high risk of complications of transient HTN, could use short-acting labetalol (5-20mg) or esmolol (10-50mg) IV. if concerned re: bradycardia (incl from the B-blockers), could give prophylactic glyco.
Myocardial O2 consumption therefore increases, as does tissue O2 consumption with the seizure, which may–> myocardial O2 supply:demand mismatch.
What are the cerebral effects of ECT?
cerebral O2 consumption, blood flow & ICP all increase.
IOP increases.
transient ischaemic events, ICH & cortical blindness have occurred.
Cognitive adverse effects are more common, particularly in pts with pre-existing dementia.
What are the major causes of death & major morbidity in ECT?
Cardiovascular (arrhythmia & MI) & to a lesser extent, pulmonary (laryngospasm, aspiration) complications
What’s a complication of lithium use relative to anaesthesia?
nephrogenic diabetes insipidus
What’s the only IV induction agent that reduces seizure threshold?
etomidate. it also results in the longest seizure duration.
what generally happens to seizure threshold over a course of ECT treatment?
it increases
SS_HN 1.26
Describe the evidence supporting the use of electro- convulsive therapy for managing depression
Indicated for major depression refractory to antidepressants, incl MDD w psychotic features, catatonia, persistent suicidal intent, food refusal leading to nutritional compromise/dehydration.
Also can be used for bipolar disorder, schizophrenia, catatonia, NMS
incr risk if:
unstable/severe CVD
space-occupying intracranial lesion w evidence elevated ICP
recent cerebral haemorrhage or stroke
bleeding or unstable vascular aneurysm
severe pulm condition
ASA 4 or 5
Following acute ECT, continuation & maintenance + pharmacotherapy is more effective than pharmacotherapy alone for both unipolar & bipolar major depression & it reduces relapse.
It’s exact mechanism is yet to be elucidated.
human & animal studies show it increases release of monoamine neurotransmitters, esp dopamine, serotonin, norepinephrine. Also enhances monoamine transmission.
may cause hypothalamus or pituitary to release PRL, TSH, ACTH & endorphins, helping depression.
Neurotrophic, so may reverse atrophic brain changes of severe chronic depression.
gray matter volume & cortical thickness increase.
ect pre-procedure evaluation
complete Hx & physical to identify risk factors.
no specific lab tests required in pre-ECT evaluation.
only require electrolytes for pts on diuretics or other meds incr the likelihood of an abnormality OR those w established renal disease or CCF. (*electrolyte disturbances, BZD withdrawal, head trauma, neurol disease & some ABx & preg may predispose to tardive seizures.
12-lead ECG for ALL pts over age of 50.
Particular focus on cardiac ischaemia, arrhythmias, heart failure, brain tumours or neurosurgical issues.
Hx of skull fractures (may affect electrode placement).
All medications, including ginkgo, ginseng, st John’s wort, valerian, kava kava (CNS effects that may interfere w ECT). considerations:
-Psychotropic meds: most are synergistic w ECT, continue peri-procedurally.
SSRIs: continue, consider that fluoxetine & sertraline inhibit cholinesterase in serum & the erythrocyte membrane (may extend duration sux!)
fluoxetine inhibit CYP2D6 (may incr plasma [] someantiarrhythmics, antiemetics)
Serotonin syndrome (characterised by hyperreflexia, agitation, akathesia, tremor, muscle rigidity, dilated pupils, dry mucus membranes, diaphoresis, clonus (incl ocular), hyperthermia), rare but potentially lethal: if combine w other drugs w serotoninergic potential (ondans, metoclopramide, fentanyl).
DDx: NMS, sympathomimetic toxicity, MH, meningitis/encephalitis, anticholinergic toxicity).
Adverse effects: rhabdomyolysis, metabolic acidosis, seizures, renal failure, DIC, coma.
Rx: discontinue serotonergic agents, sedate w BZD (aim to eliminate agitation, neuromuscular abnormalities & elevations in HR & BP.
O2 to maintain SpO2>=94%
IVT
continuous cardiac monitoring
any temp >41.1 immediate sedation, paralysis, endotracheal intubation, cool
cyproheptadine IV (1st generation antihistamine which has anti-serotonergic properties)
theophylline may cause status epilepticus after ECT (taper prior to ECT).
TcAs: inhibit reuptake serotonin & norepi. also have antimuscarinic & anti alpha 1 adr effects. avoid abrupt withdrawal.
*may potentiate indirect sympathomimetics (eg. ephedrine metaraminol), amplify effects of catecholamines
MAOIs: interact w vasopressors (indirect sympathomimetics ephetrine & metaraminol contraindicated (MAOIs inhibit their metabolism, exaggerated response. direct-acting (eg. Adr, NAdr, phenylephrine, vasopressin) safe but carefully titrate. AVOID pethidine (may precipitate serotinergic reaction.
remi, fent, alf & morph safe.
Mood stabilisers:
LITHIUM: may prolong sux & NDNMBA effects but generally not clinically significant.
CARBAMAZEPINE: potent inducer of CYP3A4 (may incr anaes requirements).
Antipsychotics:
-may reduce anaesthetic requirements (enhance effects of CNS depressants)
-they may alter B blocker efficacy (CYP2D6 selectivity)
-there may be EPS (eg. tremor, TD)
-NMS (rare but life-threatening; hyperthermia, muscle rigidity, ANS instability (diaphoresis, labile BP), altered mental status (agitation, delirium, coma); may last for hours to weeks! complications incl myoglobinuria, renal failure, cardiac failure, DIC, PE, cognitive sequelae (due to hypox, hyperthermia)
-SOME antipsychotics linked w CM & myocarditis
-BZD: may incr seizure duration, impair seizure induction (anticonvulsant). synergistic w most anaesthetics.
ECT is not formally listed in the ACC-AHC guidelines but it should be treated as low-risk as usually well-tolerated (even in those @ risk), haemodynamic changes are brief & mortality rate is low. It’s therefore difficult to prove a beneficial effect of any intervention reducing cardiovascular risk.
Those with major clinical predictors of coronary risk (decompensated heart failure, unstable angina or arrhythmias, severe valvular disease) should undergo further management/stabilisation, otherwise most can undergo ECT w appropriate medical management, however:
-those who’ve had a MI should have minimum 3/12 prior to ECT (if high risk death due to depression, could be treated sooner w cardiology input; w Hx of MI the longer wait the better but extent of myocardial damage & residual functional status weigh into decision); MACE rare after ECT, <1%, most common diagnoses= acute HF, arrhythmia, APO (APO may be ass’d w hypertensive crisis, cardiogenic cause, neurogenic cause, -ve pressure pulm oedema w airway obstruction). that said, 5-10% of ect pts develop cardiac trop rise.
-pts with unstable HTN must be stabilised (give routine antihypertensives other than diuretics about 2 hrs before ECT; diuretics avoided to limit risk of bladder emptying during procedure). if on longstanding diuretics, ensure electrolytes checked before proceeding, ensure K+ & Mg++ are replete.
-CONTINUE anti-anginals, B-blockers (consider glyco w induction)
-pts with severe valvular disease should have cardiology consultation prior to ECT & goals of tight BP control, limiting significant preload or afterload reductions and avoiding tachyarrhythmia should be adhered to. cardiology consult for decomp HF.
-pts with remote history of HF should have a baseline echo.
-if compensated systolic dysfunction, goal= minimise volume overload.
-diastolic dysfunction= aim to control BP to limit flash pulmonary oedema: Prompt Rx of post-seizure HTN.
-pacemakers & ICDs: CAN have ECT. should have in-date device check. magnet over pulse generator for NON pacing dependent pts puts pacemaker in asynchronous mode or disable anti-tachyarrhythmia therapy. if pacing dependent, consult cardiology & have techs reprogram. Reactivate device after seizure. Continuous ecg monitoring while defib deactivated, prepare to defib if unstable rhythm (ie. pads on).
-pulmonary status must be optimised; airway manipulation during ECT risks bronchospasm. consider risk of desat (eg. OSA; consider SGA or even tube in extreme circumstances)
-While ECT raises CBF, space occupying lesions aren’t absolute contraindications to ECT PROVIDED THERE IS NO EVIDENCE OF ELEVATED ICP. available safety data is from case reports/series so decision should be made on case-by-case basis, w neurosurg opinion. seek evidence on Hx (nausea, headache, visual changes, altered GCS); exam (HTN/bradycardia, focal/general neuro deficit, papilledema) & Ix (brain imaging (CT/MRI), ecg). Neurologists may consider steroids if ect Rx urgent & elevated ICP can’t be ruled out. Structural brain abnormalities (eg. chiari 1) likely to be safe provided no evidence of incr ICP but neurosurgical evaluation prior to ECT essential.
-Stroke: ideally delay 3/12, BP control important.
-*Todd phenomenon= rare transient postictal focal neuro deficit, has complete spontaneous recovery after ECT but must rule out other causes of focal neuro dysfunction (cerebrovascular ischaemia, ruptured aneurysm)
-neuromuscular diseases: avoid sux (risk severe hyperK, use short-acting NDMR). Can have ECT if PD but incr risk post-procedure delirium.
-epilepsy: CAN have ECT but anticonvulsants may interfere w efficacy; continue anticonvulsants, consider reducing dose/witholding evening before in liaison w Neurology if seizures difficult to elicit.
-metallic objects in brain: consult neurosurgeon; in general, inert metals shouldn’t heat up surrounding tissue. Should avoid ECT immediately (ie. within 2-3 months) after any neurosurgical procedure. DBS: most manufacturers recommend not having ECT w functioning electronic medical devices in head or neck (concern re: heating or movement of electrodes w seizure motor activity); none of these effects have been reported. periprocedural management of the device in consult w NSx team & device manufacturer; some may disable the device during Rx.
-diabetes medication management individualised but in general, give half usual total morning dose (immediate & long-acting) as long-acting but if brekky delayed due to very early am ect, consider delaying insulin until after ect, before eating.
-anticoagulants: consider INR (should not be supratherapeutic) & BP control; case-by-case discussion with anticoagulation prescriber.
-pregnancy: ECT generally safe (particularly as psychotropic medications may have significant side effects for mother & foetus, ECT no evidence of adverse developmental effects. most common adverse effects in mother are prem contractions & labour, in foetus bradyarrhythmmia.
-Should perform at a facility w access to obstetricians & foetal monitoring equipment, anaesthetists experienced in providing anaesthesia to pregnant pts for ECT & psychiatrists experienced in the situation. Should be @ a facility resourced for Rx obstetric & neonatal emergencies.
-should NOT hyperventilate (decreases placental blood flow & reduces dissociation of O2 from Hb)
-should hydrate the pt w IVT prior to each ECT
-FHR documented before & after Rx if 12-23wks gestation.
-beyond 20 wks, place wedge beneath pts R) hip.
-continuous FHR & uterine activity monitoring from >=24wks gestation, before & after each Rx, by someone experienced in placing & interpreting these tracings.
-incr GORD risk; may consider witholding glyco (reduces LOS tone) if safe for brady risk, sodi-citrate 30mL 30mins before procedure. consider intubation if 25wks gestation + (obviously inherent risks w this)
