Induction Agents Flashcards
Etomidate
Etomidate
Class: nonbarbiturate induction agent, carboxyl imidazole derivative
MOA:
increases the affinity of GABA for GABA receptors, mimics the actions of GABA at receptor. Increases chloride condutance, hyperpolarizes post-synaptic membrane, decreasing neuronal transmission, producing hypnosis and sedation.
Pk:
PB: 75% - high
vD 3.5 L/Kg - large
onset: immediate
E1/2T: 2-5 hours
DOA: short 5-10 minutes
Metabolized by liver hydrolysis and plasma esterases.
Metabolis is dependent on hepatic blood flow.
Excreted in urine and bile.
Termination of effect is r/t redistribution.
Dose:
induction: 0.3 mg/kg
sedation: 5 - 8 mcg/kg/min
SE:
No change to HR, BP, SVR, CO.
Increases EEG activity, lowers seizure thresshold.
decreases CBF, decreases cerebral metabolic oxygen demand, decreases ICP.
Adrenocorticosuppression for 4-8 hours
Nausea/vomiting 30-40%
myoclonus
Potentiates NMB
C/I:
Hx of seizures.
Porphyria
Addison’s dx
Caution with hx of PONV, liver impairment
Ketamine
Ketamine
Non-barbiturate phenylcyclidine derivative, NMDA receptor antagonist
MOA:
NMDA receptor antagonist, decreases influx of sodium, calcicum, glutamate.
Ketamine depressues neuronal association areas in the cerebral cortex and thalamus while stimulating the hippocampus - limbic system. This leads to dissociative state.
Also a muscarinic antagonist,
Also an opioid agonist at mu, kappa, delta - some analgesia, sedation.
Also a B2 agonist - some bronchodilation
Inhibits neuronal sodium channels - local anesthetic effect
Inhibits neuronal calcicum channels - cerebral vasodilator effect
Uses:
Non barbiturate induction of anesthesia
Analgesia, sedation.
Pk:
Pb: minimal
Vd: large - 3L/Kg
Onset: immediate
DOA: Short, 5-10 minutes
E1/2T: 2-3 hours
metabolized by CYP450 to active metabolite norketamine (30% potency).
Clearance dependent on hepatic blood flow.
Excreted via kidneys, termination of effect r/t re-distribution.
Dose:
Induction: 0.5 - 2 mg/kg
Induction (iM) 4-6 mg/kg
sedation: 0.2 - 0.5 mg/kg
SE:
Inhibits the reuptake of norepinephrine, so increase in SNS stim leads to increase in HR, BP, CO.
Ketamine is a direct myocardial depressant.
Increase ICP, increase intraocular pressure, increase cerebral metabolic demand, increase EEG activity.
Hallucinations, emergence delerium, myoclonus, nystagmus
Bronchodilation, increased pulmonary vascular resistance
Increases salivation, increased risk for laryngospasm.
potentiates neuromuscular block.
C/I:
Increased ICP, closed head injuries
Psych d/o
CAD, pulm HTN, pheochromacytoma
Aneurysms
eye injuries
caution with MAO-Is, TCAs
Precedex
highly selective, centrally acting alpha-2 adrenergic agonist.
MOA: Binds to alpha-2 adrenergic receptors, GPCR GaI, decreases SNS outflow and decreases release of norepinephrine causing sedation, anxiolysis, decreased neuroendocrine response. Closely mimics sleep and causes analgesia by inhibiting substance P in spinal cord.
Pk:
PB: High 90%
Vd: LARGE 3 L/kg
Onset: 5 minutes
Peak: 30 minutes
DOA: 2 hours
E1/2T: 2-3 hours
Has a longer context sensitive E1/2 t.
Metabolized by liver, excreted in urine and bile.
antagonist: atipamezole
Dose:
1mcg/kg bolus over 15 minutes, then 0.2 to 1 mcg/kg/hr gtt
SE:
Decrease HR, BP, SVR.
Minimal change to RR, small decrease in TV
Decrease in CBF but no change to cerebral metabolic oxygen rate or ICP
Depresses thermoregulation
decreaes doses/MACs of volatiles/other anesthetics
C/I:
afib, heart block, severe bradycardia
pts that cannot tolerater lower BP or HR
Propofol
Propofol
class: non barbiturate induction agent, 2,6-di-isopropyl phenol
Anti-convulsant, anti-emetic, is packaged in propylene glycol so pain on injection.
MOA:
Decreases the dissasociatoin of GABA at GAB receptors. Prolongs chloride condutance, hyperpolarizes membranes, decreases neuronal transmission.
Also inhibits glutamate activity at NMDA receptor
Pk:
PB: High - 90%
VD: Large - 4L/kg
Onset; immediate
E1/2T: 30-90 minutes
DOA: 5-10 mintues
metabolized in the liver by cyp450, also has extra hepatic metabolism in kidneys, lungs, intesintal mucosa.
excreted in urine.
Termination fo effect by rapid distribution.
Dose:
induction: 1-2.5 mg/kg
N/V: 10 mg
sedation: 25-100 mcg/kg
SE:
Decrease CBF, decreases cerebral metabolic oxygen demand, decrease ICP
Decrease intra ocular pressure
Isoelectric EEG, myoclonus
Decrease BP by 25-40%, decrease in SVR, no change to HR
Decrease ventilatory response to CO2
decrease RR and bronchodilation, apnea with induciton doses
C/I:
soy allergy, egg-yolk allergy because lecithin in packaging
decrease dose in elderly, increase dose in pediatrics
also packaged with metabisulfite, r/f bronchospasm
caution in
hypovolemia
hypotension,
CV instability
