Brand name Ketalar.
Mainly used for starting and maintaining anesthesia.
Approved for induction of anesthesia prior to other general anesthetic agents, sole anesthetic agent the procedure is not requiring skilled muscle relaxtion, and to supplement low potency anesthetic agents.
Known as a dissociative anesthetic their produce is strong analgesia and amnesia.
Its pharmacologic effects include: sedation, analgesia, bronchodilation, and sympathetic nervous system stimulation.
Approved as a sedative, analgesic come and general anesthetic.
Induces a trance-like state while providing pain relief, sedation, and memory loss.
It is a non-competitive N-methyl-D-aspartate (NMDA) receptor antagonist that reduces the neurotransmission of glutamate, the primary excitatory neurotransmitter in the CNS.
It has inhibitory effect on voltage gated sodium and potassium channels and serotonin receptors, and inhibits dopamine reuptake.
The reduction of excitatory neurotransmission reduces pain sensation, resulting in analgesic effect.
Other uses include for chronic pain and for sedation in intensive care.
Has been used in subanesthetic doses for long-term treatment of chronic refractory pain, particularly neuropathic pain, regional complex regional pain syndrome, postherpetic neuralgia, and diabetic neuropathic pain.
It can be used as an active adjuvant that prolongs the duration of analgesic effect of painkillers and pain management.
It has been used in clinical practice to manage major resistant depression, enhance memory function in Alzheimer’s patients, and reduce brain damage after stroke.
When administered intravenously, at subanesthetic doses of 0.5 mg per kilogram has rapid anti-depressant effects in patients with major depressive disorder and treatment resistant major depression.
In a randomized trial of electroconvulsive therapy or ketamine infusion in patients with moderately severe depression: 41% of the patients in the ECT group and 55% of those in the ketamine group reported a 50% of greater reduction in symptoms at the conclusion of the three week trial.
Heart function, breathing, and airway reflexes generally remain functional.
Has a variety of side effects: induction of psychedelic conditions leading to hallucinations and excitation symptoms.
Effects typically begin within five minutes when given by IV injection with the main effects lasting up to 25 minutes.
Routes of administration IV, IM, insufflated, by mouth, intraosseous, intranasal, and topical.
Rapidly passes the blood brain barrier and has a quick onset of analgesic effect.
Produces an analgesic effect at several sites of the nervous system, both sensually and peripherally.
Metabolism by the liver, primarily by CYP3A4.
Onset of action < 5min (IM, IV), < 30min by mouth.
Biological half-life 2.5–3 hours
Duration of action less than one hour.
Excretion Kidney is greater than90%.
Common side effects include psychological reactions as the medication wears off and includes :agitation, confusion, or hallucinations.
Elevated blood pressure and muscle tremors are relatively common.
Hypotension and a decrease in breathing rate rarely affected.
Classified as an NMDA receptor antagonist.
1000mg/10ml vial of ketamine.
May be the sole anesthetic for minor procedures in children or as an induction agent followed by muscle relaxant and tracheal intubation.
Useful in asthmatics or people with chronic obstructive airway disease.
Can be used as a sedative for physically painful procedures in emergency departments, and for emergency surgery in field conditions in war zones
Can be used as a supplement to spinal or epidural anesthesia. as it suppresses breathing much less than most other available anaesthetics,
Because of associated hallucinations that it may cause, it is not typically used as a primary anesthetic.
A single dose of intravenous ketamine significantly reduces suicidal thoughts in patients with depression and suicidal ideation in as little as 1 day. according to a systematic review and meta-analysis.
Ketamine, has potent anti-depressant effects after a single infusion due to its capacity to rapidly increase the number of dendritic spines and to restore aspects of functional connectivity.
It is non-inferior to electro convulsive therapy for treatment, resistant, major depression without psychosis (Anand,S).
Is the anaesthetic of choice when reliable ventilation equipment is not available, and is the drug of choice for people in traumatic shock at risk of hypotension.
It is least likely to cause low blood pressure, often even able to prevent it.
At anesthetic doses, usually stimulates rather than depress the circulatory system.
Considered relatively safe because protective airway reflexes are preserved.
Can be used as a bronchodilator in the treatment of severe asthma.
May be used for postoperative pain management.
At low doses it reduces morphine use and nausea and vomiting after surgery.
High quality evidence in acute pain.
It is insufficient in acute pain.
May be used as an intravenous analgesic with opiates to manage otherwise intractable pain, particularly if this pain is neuropathic.
Most effective when used with a low-dose opioid.
May be a viable option for treatment-refractory cancer pain, and in the treatment of complex regional pain syndrome (CRPS).
Ketamine use as a recreational drug has been implicated in accidental poisonings, drownings, traffic accidents, suicides and deaths.
It is very short-acting,taking effect within about 10 minutes.
Its hallucinogenic effects last 60 minutes when insufflated or injected and up to two hours when ingested orally.
At anesthetic doses produces a dissociative state, characterized by a sense of detachment from one’s physical body and the external world.
Side effects include: arrhythmias, bradycardia, tachycardia, hypertension, hypotension, increased intracranial pressure, transient erythema, transient morbiliform rash, anorexia, nausea, increased salivation, vomiting. pain or exanthema of the injection site, increased skeletal muscle tone, double vision, increased intraocular pressure, nystagmus, tunnel vision, airway obstruction, apnea, increased bronchial secretions, respiratory depression, and laryngospasm.
In 10-20% of patients at anesthetic doses have adverse reactions that occur during emergence from anesthesia, manifesting as hallucinations and delirium.
These reactions can occur up to 24 hours postoperatively
Such severe reactions may require treatment with a small dose of a short- or ultrashort-acting barbiturate.
At higher anesthetic doses tonic-clonic movements at occur in 10% of patients.
Infrequent use of ketamine does not cause cognitive deficits
Acute effects cause cognitive impairment, including reductions in vigilance, verbal fluency, short-term memory, and executive function, as well as schizophrenia-like perceptual changes.
Drugs which increase blood pressure may interact with ketamine in having an additive effect on blood pressure including: stimulants, SNRI antidepressants, and MAOIs.
It may increase the effects of other sedatives.
Acts primarily as an antagonist of the NMDA receptor.
Known actions of ketamine include:
Non-competitive antagonist of the NMDA receptor (NMDAR)
Inhibits the reuptake of serotonin, dopamine, and norepinephrine.
NMDAR antagonism is responsible for the anesthetic, amnesic, dissociative, and hallucinogenic effects.
NMDAR antagonism results in analgesia by preventing central sensitization in dorsal horn neurons, interfering with pain transmission in the spinal cord.
Inhibition of nitric oxide synthase lowers production of nitric oxide, which is a neurotransmitter involved in pain perception, contributing to analgesia.
It blocks voltage-dependent calcium channels and sodium channels, attenuating hyperalgesia.
It alters cholinergic neurotransmission, and inhibits the reuptake of serotonin and norepinephrine, which are involved in descending antinociceptive pathways.
Affects catecholaminergic transmission producing measurable changes in peripheral organ systems, including the cardiovascular, gastrointestinal, and respiratory systems
Inhibits the reuptake of catecholamines, stimulating the sympathetic nervous system, resulting in cardiovascular symptoms.
Its serotonin reuptake inhibition is thought to underlie nausea and vomiting.
Absorbable by intravenous, intramuscular, oral, and topical routes.
After oral administration it undergoes first-pass metabolism, where it is biotransformed in the liver into norketamine and norketamine.
Norketamine is the major metabolite of ketamine, and is one-third to one-fifth as potent anesthetically, and plasma levels of this metabolite are three times higher than ketamine following oral administration.
Bioavailability through the oral route reaches 17–20%; bioavailability through other routes are: 93% intramuscularly, 25–50% intranasally, 30% sublingually, and 30% rectally.
Peak plasma concentrations are reached within a minute intravenously, 5–15 min intramuscularly, and 30 min orally.
Its duration of action in a clinical setting is 30 min to 2 h intramuscularly and 4–6 h orally.
Plasma concentrations of ketamine are increased by diazepam and other CYP3A4 inhibitors due to inhibition of conversion to norketamine.
It is usually injected intravenously or intramuscularly.
Ketamine can be started using the oral route.
Can be used as a subcutaneous infusion.
Oral bioavailability is around 20%
40-minute infusion of ketamine rapidly improves suicidal ideation in patients with major depressive disorder, showing better results than midazolam.
Ketamine is a glutamate N-methyl-D-aspartate receptor antagonist that can be used to treat major depressive disorder by single or repeated infusions.
All studies report significant improvement following oral ketamine administration.
Ketamine was well tolerated without serious adverse events.
Ketamine dosage varied from 0.5 to 1.25 mg/kg. The frequency of administration was daily to monthly.
Preliminary evidence suggests the potential for antidepressant effect of oral ketamine.