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Drug Cards > Ketamine > Flashcards

Ketamine Flashcards

Please note that the drug card information is for Educational Use ONLY, and the source is from Carrie Bowman's glossary of drug cards permitted by use of Georgetown NAP students. No permission is given to use these cards for anything other than as a study resource for our program.

1
Q

What are the trade names for Ketamine?

A

Ketalar or Ketaject

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2
Q

What is the formal drug class of Ketamine?

A
  • General anesthesia induction agent; phencyclidine derivative
  • N-methyl-D-aspartate (NMDA) receptor antagonist
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3
Q

What are the uses of Ketamine?

A

Causes intense analgesia at subanesthetic doses and produces prompt induction of anesthesia when administered IV at higher doses

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4
Q

What is the MOA of Ketamine?

A
  • Ketamine’s CNS effects are dose dependent and are related to its antagonistic activity at the NMDA receptor
  • Glutamate and NMDA are excitatory amino acids. When glutamate binds to the NMDA subtype of the glutamate receptor, the channel opens and allows Na, K, Ca to either enter or leave the cell. Flux of these ions depolarize the POSTsynaptic neuron and initiate an action potential. ***Ketamine blocks this open channel and prevents further ion influx, thus inhibiting the excitatory response to glutamate
  • dissociative anesthesia
  • evidence that Ketamine depresses transmission of impulses in the medial medullary reticular formation, which is important for transmission of the affective-emotional components of nocioception from the spinal cord to higher brain centers
  • it also binds with opioid, cholinergic, and monoaminergic(involves descending inhibitory pathways for antinocioception) receptors
  • Ketamine inhibits neuronal sodium channels (producing a modest local anesthetic action) and calcium channels (causing cerebral vasodilation)
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5
Q

How does Ketamine produce “dissociative anesthesia”?

A

there is depression of neuronal function in association areas of the cerebral cortex and thalamus while stimulation of the hippocampus (limbic systems) producing a marked sensory loss and analgesia, as well as amnesia; basically you are getting the information to the thalamus, but you are not integrating the info appropriately! ie pt sees the light in the OR as falling bricks….

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6
Q

How is Ketamine metabolized?

A

Hepatic microsomal enzymes

  • an important pathway in metabolism is demethylation of Ketamine by CYP450 enzymes to form NORKETAMINE. Norketamine is eventually hydroxylatedand then conjugated to form more water-soluble and inactive glucuronide metabolites that are excreted by the kidneys
  • 1st pass effect!!
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7
Q

After IV administration of Ketamine, where do you see Ketamine being eliminated?

A

< 4% of a dose can be recovered from the urine unchanged

Fecal excretion accounts for < 5% of an injected dose

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8
Q

Why does Ketamine cross the BBB so rapidly (3)?

A
  • has low-molecular weight
  • a pKa near the physiologic pH, and
  • relatively high lipid solubility
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9
Q

What is the onset of action of Ketamine?

A

30-60 seconds

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10
Q

When does the maximal effect of Ketamine occur?

A

within 1 minute of IV administration

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11
Q

What is the volume of distribution of Ketamine?

A

large distribution volume (3 L/kg) ; 2 compartment model-> high lipid solubility-> large Vd!
redistribution is a factor!!

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12
Q

What is the E 1/2 life of Ketamine?

A

2 - 3 hours

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13
Q

Is Ketamine protein bound?

A

approximately 12% protein bound

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14
Q

What is the major drawback to Ketamine administration?

A

Hallucination and

Emergence Delirium

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15
Q

What are the CNS side effects of Ketamine?

A
  • Increased ICP and IOP
  • increases CBF, CMRO2
  • dose related depression of LOC
  • Seizure like activity
  • Nystagmus, pupil dilation
  • SALIVATION, lacrimation
  • Myoclonic activity
  • SNS stimulation
  • Emergence delirium
  • Vivid dreaming
  • Extracorporeal experiences
  • Illusions
  • Hallucinations
  • Nightmares
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16
Q

What are the CV side effects of Ketamine?

A
  • Direct Myocardial depressant but does cause intense SNS stimulation resulting in Tachycardia, HTN, Increased CO in those with normal catecholamine stores
  • increases BP, HR, CO
  • Inhibits reuptake of NE
  • increases myocardial work and O2 consumption
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17
Q

What are the Respiratory side effects of Ketamine?

A
  • Increased PulmVR
  • Bronchodilation (SNS Stimulation)
  • Respiratory depression especially in children when given as a bolus
  • Causes increased salivation which has cause upper respiratory obstruction and can promote laryngospasm
  • MINIMAL
  • NO alteration in CO2 response
18
Q

What are the contraindication for use of Ketamine? (6)

A
  • Patients with increased ICP or reduced cerebral compliance
  • Ketamines preservative, chlorobutanol, is neurotoxic; this formation of Ketamine for subarachnoid or epidural administration is CONRAINDICATED
  • patients with open eye surgery or other ophthalmic disorders
  • in patients with significant CAD, pulmonary HTN, or elevation of BP and in those who have shown hypersensitivity to the drug
  • as sole anesthetic in ischemic heart disease/CAD
  • patients with severe psychiatric disorders such as schizophrenia
  • avoid in DTs b/c of emergence delirium
19
Q

What drug should you consider giving with Ketamine? Why?

A

Benzodiazepine to reduce the incidence of hallucinations and emergence reactions

20
Q

What can happen if Ketamine is administered in the presence of volatile anesthetics?

A

may result in hypotension

21
Q

Name the drugs that cause an interaction with Ketamine….we will go in to detail lataaa

A 
Volatile Anesthetics
Verapamil
NDMR
Succinylcholine
Aminophylline
22
Q

What drug interaction occurs between Ketamine and Verapamil?

A

the blood pressure-elevating effects of Ketamine may be attenuated, whereas drug induced increases in HR are enhanced

23
Q

What drug interaction occurs between Ketamine and NDMRs?

A

Ketamine-induced enhancement of non-depolarizing neuromuscular-blocking agents may reflect interference by Ketamine with Calcium ion binding

24
Q

What drug interaction occurs between Ketamine and Succinylcholine?

A

The duration of apnea after administration of succ is prolonged

25
Q

What drug interaction has been reported with Ketamine and Aminophylline?

A

Seizures have been described in asthmatic patients receiving aminophylline followed by administration of ketamine

26
Q

What routes can Ketamine be administered?

A

IV, IM, transcutaneously, PO, nasally, PR, and as a preservative-free solution epidurally or intrathecally (most clinical use is by IV or IM)

27
Q

What is the premedicant dose of Ketamine?

A

Preventative analgesia: 0.15 - 0.25 mg/kg

28
Q

What is the sedative dosage of Ketamine?

A

0.2 - 0.5 mg/kg

29
Q

What is the IV and IM induction of GA dosage of Ketamine?

A

0.5 - 2 mg/kg IV; 4 -6 mg/kg IM

30
Q

What is the maintenance dose of Ketamine?

A

1-2 mg/kg/hr

31
Q

what is Ketamine derived from?

A

Phencyclidine derivative

32
Q

How is Ketamine prepared? Which enantiomers are prepared? Which one is a more potent analgesic?

A
  • prepared in acidic solution
  • Racemic mixture of equal parts R- and S- enantiomer
  • S enantiomer is more potent analgesic, and undergoes faster metabolism and has lower incidence of emergence delirium
33
Q

is Ketamine lipid soluble?

A

VERY lipid soluble

34
Q

Talk about the NMDA receptor associated with Ketamine?

A
  • Activation of the NMDA receptor results in the opening of an ion channel which is nonselective to cations. This allows flow of Na, small amounts of Ca ions into the cell and K out of the cell
  • Calcium influx through the NMDA receptors is thought to play a critical role in synaptic plasticity, a cellular mechanism for learning and memory
  • the NMDA receptor is BOTH ligand-gated and voltage-dependent
35
Q

What is clearance of Ketamine dependent on?

A

total body clearance is roughly equal to LIVER BLOOD FLOW!!!!!
Changes in liver blood flow affect clearance

36
Q

What is an effect that is not very prominent in Ketamine, but higher and seen more in Benzos?

A

Amnesia! not as prominent as the benzos!

37
Q

Why is the termination of effect of Ketamine rapid?

A

Termination of effect is rapid after single bolus- 15 minutes- due to redistribution

38
Q

What are the effects of Ketamine on CBF, CMRO2, and ICP and IOP?

A

Ketamine increases CBF, CMRO2, ICP and IOP

39
Q

How is Ketamine producing spinal analgesia? (the mechanism…)

A

Mu receptor activity?- S enantiomer has some mu activity

NMDA antagonism? -S isomer has high affinity for the excitatory NMDA receptor in the dorsal horn

40
Q

Does ketamine have sympathomimetic effects? How?

A

yes, NMDA effect: this is NOT a peripheral effect, probably occurs b/c of NMDA receptor ativity in nucleus tractus solitarus

41
Q

What drug interaction occurs with Lithium and Ketamine?

A

Lithium prolongs the DOA of Ketamine

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