What class of drug is Ketamine?
A. Opioid analgesic
B. Benzodiazepine
C. Phencyclidine-derivative dissociative anesthetic
D. Barbiturate
C. Phencyclidine-derivative dissociative anesthetic
What is the typical induction dose range of Ketamine for adults?
A. 0.5-1 mg/kg
B. 1-2 mg/kg
C. 2-3 mg/kg
D. 3-4 mg/kg
B. 1-2 mg/kg
TxWes Reference
Induction:
0.5-1.5 mg/kg
Maintenance:
0.2 - 0.5 mg/kg IV analgesia
4 - 8 mg/kg IM”
Onset:1 min
Duration: 10 - 20 min
For intramuscular (IM) administration, what is the dose range of Ketamine known as the “Ketamine Dart”?
A. 1-2 mg/kg
B. 2-4 mg/kg
C. 4-6 mg/kg
D. 6-8 mg/kg
B. 2-4 mg/kg
Tx Wes Reference:
4-8 mg/kg IM
What is the infusion dose range of Ketamine for general anesthesia (GA)?
A. 10-30 mcg/kg/min
B. 30-60 mcg/kg/min
C. 30-90 mcg/kg/min
D. 90-120 mcg/kg/min
C. 30-90 mcg/kg/min
TxWes Reference
Induction:
0.5-1.5 mg/kg
Maintenance:
0.2 - 0.5 mg/kg IV analgesia
4 - 8 mg/kg IM”
Onset:1 min
Duration: 10 - 20 min
How is Ketamine typically used for analgesia after induction?
A. 0.5 mg/kg immediately after induction, then 0.25 mg/kg every 2 hours
B. 0.5 mg/kg immediately after induction, then 0.25 mg/kg every hour
C. 1 mg/kg immediately after induction, then 0.5 mg/kg every 2 hours
D. 1 mg/kg immediately after induction, then 0.5 mg/kg every hour
B. 0.5 mg/kg immediately after induction, then 0.25 mg/kg every hour
“We use about 20 mg after induction, then 10 mg Q1H, but not on last hour before closing”
What is the concentration of Ketamine typically used?
A. 1 mg/mL
B. 5 mg/mL
C. 10 mg/mL
D. 20 mg/mL
C. 10 mg/mL
What is the primary mechanism of action (MOA) of Ketamine?
A. NMDA antagonism
B. GABA-A agonism
C. Opioid receptor agonism
D. Serotonin reuptake inhibition
A. NMDA antagonism
Binds noncompetitively to N-methyl-D-aspartate (NMDA) receptors.
-Glutamate (most abundant excitatory neurotransmitter in CNS)
-Glycine is an obligatory co-agonist.
-Inhibits activation of NMDA receptors by glutamate and decreases the presynaptic release of glutamate.
MOA:How does Ketamine affect the NMDA receptor?
A. It enhances glutamate depolarization on the postsynaptic neuron
B. It blocks glutamate depolarization on the postsynaptic neuron
C. It activates glutamate receptors
D. It inhibits acetylcholine release
B. It blocks glutamate depolarization on the postsynaptic neuron
MOA: Which system does Ketamine primarily dissociate by antagonizing NMDA receptors?
A. Thalamocortical and limbic system
B. Corticospinal and somatosensory system
C. Reticular activating system and hypothalamus
D. Limbic and hypothalamic system
A. Thalamocortical and limbic system
NMDA antagonism (block glutamate depolarization on post synapse) causes dissociation of thalamocortical and limbic system and decrease temporal summation,
What are Ketamine’s other MOA?
A. Catecholamine reuptake inhibitor (NE)
B. Mu agonist
C. weak GABAa agonist
D. monoaminergic
E. cholinergic/muscarinic (N&M) –>
hypersalivation
F. subcortical neurons in spinal tract - decrease pain
G. All of the above
A. Catecholamine reuptake inhibitor (NE)
B. Mu agonist
C. weak GABAa agonist
D. monoaminergic
E. cholinergic/muscarinic (N&M) –> hypersalivation
F. subcortical neurons in spinal tract - decrease pain
G. All of the above
What is the typical onset time of Ketamine when administered intravenously (IV)?
A. 30 seconds
B. 1 minute
C. 2 minutes
D. 5 minutes
B. 1 minute
How long does it typically take for Ketamine to take effect when given intramuscularly (IM)?
A. 1 minute
B. 2 minutes
C. 4 minutes
D. 6 minutes
C. 4 minutes
What is the usual duration of action for Ketamine when administered IV?
A. 1-3 minutes
B. 5-10 minutes
C. 15-20 minutes
D. 30-45 minutes
B. 5-10 minutes
Tx Wes Reference:
10-20 min
How long does the duration of Ketamine’s effects typically last when administered IM?
A. 5-10 minutes
B. 10-15 minutes
C. 12-25 minutes
D. 30-45 minutes
C. 12-25 minutes
(overall up to 60 min for full recovery)
What explains the rapid onset and relatively quick offset of Ketamine’s effects?
A. Fast metabolism by the liver
B. Rapid uptake into the brain and redistribution to fat/muscle
C. High rate of renal excretion
D. Immediate hydrolysis in the bloodstream
B. Rapid uptake into the brain and redistribution to fat/muscle = dec in blood concent; not d/t metabolism!)
What is the typical elimination half-life of Ketamine?
A. 0.5-1 hour
B. 1-2 hours
C. 2-4 hours
D. 4-6 hours
C. 2-4 hours
What is the protein binding percentage of Ketamine?
A. 2%
B. 12%
C. 50%
D. 80%
B. 12%
(all other inductions >80%)
How is Ketamine primarily metabolized in the body?
A. By esterases to inactive metabolites
B. Through phase I conjugation reactions
C. By CYP450 enzymes to the norketamine metabolite
D. Via direct renal excretion
C. By CYP450 enzymes to the norketamine metabolite
What is the potency of the metabolite norketamine compared to Ketamine?
A. 1/10th potency
B. 1/3rd potency
C. 1/2 potency
D. Full potency
B. 1/3rd potency
causes prolonged analgesia
Where does the primary excretion of Ketamine occur?
A. Liver
B. Lungs
C. Kidneys
D. Sweat glands
C. Kidneys
Which condition is a contraindication for the use of Ketamine?
A. Systemic or pulmonary hypertension
B. Increased ICP
C. MAOIs
D. Methamphetamines
E. Cocaine (increases epi)
F. Ca2+ depletion
G. Neuro trauma (CNS stimulation)
H. SNS depression
I. All of the above
A. Systemic or pulmonary hypertension
B. Increased ICP
C. MAOIs
D. Methamphetamines
E. Cocaine (increases epi)
F. Ca2+ depletion
G. Neuro trauma (CNS stimulation)
H. SNS depression
I. All of the above
What precaution should be taken when using Ketamine in combination with volatile anesthetics?
A. Monitor for hyperkalemia
B. Be cautious of hypotension due to blunted sympathetic nervous system response
C. Administer additional opioids to prevent bradycardia
D. Increase fluid intake to prevent dehydration
B. Be cautious of hypotension due to blunted sympathetic nervous system response
How does Ketamine affect free calcium concentration and what is the implication?
A. Increases free calcium concentration, which decreases neuromuscular block
B. inhibits free calcium concentration, which increases neuromuscular block
C. No effect on free calcium concentration
D. Decreases free calcium concentration, which decreases neuromuscular block
B. Inhibits free calcium concentration, which increases neuromuscular block
Why might the neuromuscular block be prolonged when Ketamine is used in conjunction with succinylcholine?
A. Due to increased plasma cholinesterase activity
B. Due to decreased plasma cholinesterase activity
C. Due to increased calcium concentration
D. Due to enhanced sympathetic nervous system stimulation
B. Due to decreased plasma cholinesterase activity