- 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.
- It has several uses within the pre-hospital setting including management of severe pain from traumatic origin and sedation of patient’s with abnormal behaviour or a combative TBI.
- Ketamine interacts with N-methyl-D-aspartate receptors, opioid receptors, monoaminergic receptors, muscarinic receptors and voltage sensitive Ca ion channels. Unlike other anaesthetic agents, it doesn’t interact with GABA receptors. It disrupts the neurotransmitter glutamate which is involved with learning, memory, emotion and pain recognition.
- Short term effects: problems with attention, learning and memory, hallucinations, sedation and confusions. Also increased blood pressure, unconsciousness and decreased respiratory effort
- Long term effects: ulcers and pain in bladder, kidney problems, stomach pain, depression and poor memory
- Blocking of NMDA receptors have shown an increase in apoptosis in the brain deficits when used for longer than 3 hours
- Can cause an increase in blood pressure. Thus if increased blood pressure will cause complications, Ketamine should be avoided
- Ketamine interacts with a large range of medication and in some cases reduces the effects of some medications.
- There are no medications that cause severe interactions
- Symptoms of an overdose can include: hallucinations, lethargy, GI symptoms, intense muscle pain, headaches, seizures, loss of coordination, muscle rigidity, chest pain and loss of consciousness.
Pharmacokinetics
- Ketamine absorption is rapid and bioavailability is around 93%. After first pass metabolism 17% of the administered dose is absorbed.
- Distributes rapidly and has a distribution half-life of 1.95 minutes. The volume of distribution of the central compartment and at steady-state are 371.3ml/kg and 4060.3mL/kg respectively.
- Ketamine presents as a mainly hepatic metabolism and its major metabolite is norketamine. The biotransformation of Ketamine corresponds to N-dealkylation, hydroxylation of the cyclohexone ring, conjunction to glucuronic acid and dehydration of the hydroxylated metabolites for the formation of cyclohexene derivatives.
- 85%-95% of Ketamine is eliminated in the urine with a small amount in bile and feces
- When administered intravenously the resultant recovery is distributed by 91% of the administered dose in urine and 3% in faeces
Pharmacodynamics
- Ketamine is a rapid acting general anaesthetic producing anaesthetic state characterised by profound analgesia, normal pharyngeal-laryngeal reflexes, normal skeletal muscle ton, cardiovascular and respiratory stimulation and occasional respiratory depression.
- Ketamine selectively interrupts association pathways of the brain before producing somesthetic sensory blockade. Ketamine can also depress the thalamoneocortical system before significantly obtunding the ancient cerebral centres and pathways
- Immediate onset with a 186 minute reported half life
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