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Introduction

Ketamine is a dissociative anaesthetic and effective analgesic. It was synthesized in 1962 and was first used in the clinical setting during the Vietnam War following FDA approval in 1970.

Uses within SJA

It has several uses within SJA WA including management of severe pain from traumatic origin and sedation of patient’s with abnormal behaviour or a combative TBI.

Pharmacokinetics

Onset

Peak serum levels are reached within a minute when administered intravenously, and in 5-15 minutes when administered via intramuscular injection.

Distribution & Absorption

Ketamine is rapidly distributed following parenteral administration and absorbed into adipose tissue, lungs, liver and brain. Ketamine is an NMDA-receptor antagonist within the spinal, thalamic, limbic and cortical levels of the CNS, and interferes with sensory input to higher levels of the CNS.

Metabolism

Ketamine is metabolised principally in the liver to Norketamine, a metabolite of approximately one third potency of Ketamine.

Excretion

Ketamine metabolites are principally excreted in urine.

Pharmacodynamics

Desired Effects

  • Analgesia
  • Sedation
  • Milder respiratory and cardiovascular effects than some other anaesthetics and analgesics.

Side Effects

  • Elevated pulse and blood pressure Muscle twitching
  • Rash
  • Transient laryngospasm
  • Transient respiratory depression and apnoea
  • Emergence reactions

Duration of Action

30 minutes to two hours, however emergence reactions can occur up to 24 hours after intramuscular administration.

Other Drug Interactions

Ketamine may increase the effects of other sedatives in a dose dependent manner, including, but not limited to:

  • alcohols
  • benzodiazepines
  • opioids
  • anticholinergics

Other drugs which increase blood pressure may interact with ketamine in having an additive effect on blood pressure including: stimulants, SNRI antidepressants, and MAOIs. Increase blood pressure and heart rate, palpitations, and arrhythmias may be potential effects.


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