Psych/ECT exam 4 Flashcards
SSRI MOA
block re-uptake of serotonin at presynaptic memrbraines
Most common antidepressant
SSRI
SSRI anesthesia consideration
Discontinuation syndrome - continue SSRIs through peri-operative period
SSRI discontinuation syndrome s’sx
N/V
abdominal pain + diarrhea
Sleep disturbance
irritability and mood swings
TCA MOA
- inhibit synaptic reuptake of NE and serotonin
TCA anesthesia considerations - first 4-6 weeks of treatment
- Increased neurotransmitter availability = increased anesthesia requirements
- Increased catecholamines can cause exaggerated response to INDIRECT vasopressors (i.e. ephedrine) - use phenylephrine for hypotension
TCA anesthesia considerations all the time
Increase risk of anticholinergic syndrome (post - op delirium)
especially considering when using anticholinergics such as robinol
Serotonin syndrome: what is it, cause and main features
overstimulation of 5HT receptors
Common cause: 2 or more sertonergic drugs
main features: clonus, hyperreflexia, delerium
Serotonin syndrom treatemtn
- stop drug and supportive care
- cryohetadine
MAOI MOA
Inhibit metabolic breakdown of NE and serotonin (liver)
MAOI anesthesia considertaions
- Indirect hypertension
- May increase MAC
- avoid abrupt changes in SNS activity (i.e. not deep enough or too deep)
With MAOI, avoid
- merperidene (know triggering agent)
- Indirect - acting sympathomimetic (ephederine)
Pre-operative lithium levels should be
Less than 2mEq/L
Sodium and lithium
Sodium depletion reduces renal excretion of lithium
Lithium and neuromuscular blockade
Lithium prolongs NM blockade
Lithium and anesthesia
Lithium decreases anesthetic requirements
Anorexia anesthesia consideration
cardiomyopathy and hypokalemia
need EKG and maybe ECHO
Schizophrenia MAO
domaine dysfunction - treat with dopamine blockers
Antipsychotics act on
dopamine receptors
Neuroleptic Malignant syndrome differential diagnosis
shortly after neuroleptic medication
Main inhibitory neurotransmitter in the brain
GABA
Alcohol MOA
reduces excitatory neurotransmitters (asptarate, glutamate)
Aspatrate and glutamate act through
NMDA receptors (and non)
How does alcohol affect brain function?
disrupts balance between inhibitory and excitatory neurotransmitters
Long term ETOH exposure compensation
Brain attempts to tilt balance back toward equilibrium = tolerance
ETOH withdrawal occurs from
excitation of neurotransmitter system from compensation
Acute ETOH risk
aspiration of gastric contents because laryngeal reflex is blunted
Acute intox ETOH anesthetic effeects
- exaggerated responses to anesthetic agents
- Decreased requirements
- additive depressant effect
Long term ETOH mechanism
change in receptor level of protein composition of receptor –>decreased in GABA-A function –>decreased sensitivity to neurotransmission
Chronic ETOH electrolyte imblanace
Hypomagnesia
delirium tremens begins
2 -4 days after cessation of drinking
Delirium tremens is characterized by
tremor
agitation
fever
tachycardia
confusion
delusions
hallucinations
Anesthesia role in medically-assisted withdrawal
-high dose benzos to counteract sympathetic response
-sympatholytics
-control airway for safe sedation
VTA (what it stands for and association)
Ventral tegmental area
associated with the reward pathway
VTA neurons contain ____ which is released____
dopamine, which is released in the nucleus accumbens
pathway is activated by rewarding stimulus
Illicit drugs anesthetic considerations
all cause NE reuptake blockade
=central and peripheral effects of increased endogenous NE
Smoked drugs and MAC
Acute - decrease MAC
Chronic - increase MAC
Cocaine MOA
Blocks reuptake of endogenous catecholamines presynaptically
= increase BP, HR, Temp
Cocaine use: caution with
beta blockade - can lead to unopposed alpha 1 mediated coronary and peripheral vasoconstriction/spasm
Cocaine HTN treatment:
alpha blockade (phentolamine) and NTG or vasodilator (nitropursside)
Cocaine EKG/cardiac risk
prolonged QT interval and torsades
Cocaine: avoid
- ketamine
- pancuronium
potentiates CV toxicity of cocaine
Cocaine acute intoxication MAC
Increases MAC - they are revved up with lots of catecholamines so you need a lot more
Meth anesthesia considerations
similar to cocaine
Affinity of hemoglobin for CO is
200 x greater tahn oxygen
so CO binds first
ECT anesthesia goals
- provide neuromuscular blockade to prevent fractures and muscle injury
- produce unconsciousness
ECT seizure lasts
minimum 25 seconds to ensure adequate antidepressant efficacy
ECT seizure parasympathetic CV response:
- transient bradycardia
- occasional asystole (hypotension, bradydysrthythmia)
ECT seizure sympathetic CV respsonse:
during clonic phase
1. prominent HTN
2. tachycardia
ECT seizure responses (7)
- Increased CBF
- Raised ICP
- Cardia dysrhythmias
- Myocardial ischemia, infarction
- neurologic vascular events
- increased IOP
- Increased intragastric pressure
ECT side effect on memory
short term memory loss
Most common long term effect associated with ECT
memory impairment
ECT risks and SE (5)
- myalgia
- HA
- Emergence agitation
- staus epilepticus
- sudden death
Absolute ECT contraindications (6)
- pheochromocytoma
- recent MI 4-6 weeks
- Recent CVA (3 month)
- recent intracranial surgery (3 mnths)
- Intracranial mass lesion
- Unstable cervical spine
ECT gold standard induction agent
Methohexital 0.5.- 1 mg/kg
Ketamine and ECT
Ketamine prolongs seizure duration (proconvulsant)
but also has negative effects
Conditions that prolong seizure duration in ECT
Hyerventilation/hypocapnia