The use of ketamine in anesthesia reflects its characteristics. It is a drug of choice for short-term procedures when muscle relaxation is not required.^[33] The effect of ketamine on the respiratory and circulatory systems is different from that of other anesthetics. It suppresses breathing much less than most other available anesthetics.^[34] When used at anesthetic doses, ketamine usually stimulates rather than depresses the circulatory system.^[35] Protective airway reflexes are preserved,^[36] and it is sometimes possible to administer ketamine anesthesia without protective measures to the airways.^[33] Psychotomimetic effects limit the acceptance of ketamine; however, lamotrigine^[37] and nimodipine^[38] decrease psychotomimetic effects and can also be counteracted by benzodiazepines or propofol administration.^[39] Ketofol is a combination of ketamine and propofol.

Ketamine is frequently used in severely injured people and appears to be safe in this group.^[40] It has been widely used for emergency surgery in field conditions in war zones,^[41] for example, during the Vietnam War.^[42] A 2011 clinical practice guideline supports the use of ketamine as a sedative in emergency medicine, including during physically painful procedures.^[21] It is the drug of choice for people in traumatic shock who are at risk of hypotension.^[43] Ketamine often raises blood pressure upon administration and is unlikely to lower blood pressure in most patients, making it useful in treating severe head injuries for which low blood pressure can be dangerous.^[44][45][46]

Ketamine is an option in children as the sole anesthetic for minor procedures or as an induction agent followed by neuromuscular blocker and tracheal intubation.^[41] In particular, children with cyanotic heart disease and neuromuscular disorders are good candidates for ketamine anesthesia.^[39][47]

Due to the bronchodilating properties of ketamine, it can be used for anesthesia in people with asthma, chronic obstructive airway disease, and with severe reactive airway disease, including active bronchospasm.^[41][39][48]

Ketamine infusions are used for acute pain treatment in emergency departments and in the perioperative period for individuals with refractory or intractable pain. The doses are lower than those used for anesthesia, usually referred to as sub-anesthetic doses. Adjunctive to morphine or on its own, ketamine reduces morphine use, pain level, nausea, and vomiting after surgery. Ketamine is likely to be most beneficial for surgical patients when severe post-operative pain is expected, and for opioid-tolerant patients.^[49][50]

Ketamine is especially useful in the pre-hospital setting due to its effectiveness and low risk of respiratory depression.^[51] Ketamine has similar efficacy to opioids in a hospital emergency department setting for the management of acute pain and the control of procedural pain.^[52] It may also prevent opioid-induced hyperalgesia^[53][54] and postanesthetic shivering.^[55]

For chronic pain, ketamine is used as an intravenous analgesic, mainly if the pain is neuropathic.^[28] It has the added benefit of counteracting spinal sensitization or wind-up phenomena experienced with chronic pain.^[56] In multiple clinical trials, ketamine infusions delivered short-term pain relief in neuropathic pain diagnoses, pain after a traumatic spine injury, fibromyalgia, and complex regional pain syndrome (CRPS).^[28] However, the 2018 consensus guidelines on chronic pain concluded that, overall, there is only weak evidence in favor of ketamine use in spinal injury pain, moderate evidence in favor of ketamine for CRPS, and weak or no evidence for ketamine in mixed neuropathic pain, fibromyalgia, and cancer pain. In particular, only for CRPS, there is evidence of medium to longer-term pain relief.^[28]

This section needs to be updated. The reason given is: Recent (2022–2025) systematic reviews and guideline updates on ketamine and esketamine for depression have not been incorporated.. Please help update this article to reflect recent events or newly available information. (October 2025)

Ketamine is a rapid-acting antidepressant,^[20] but its effect is transient.^[57] Intravenous ketamine infusion in treatment-resistant depression may result in improved mood within 4 hours reaching the peak at 24 hours.^[58][23] A single dose of intravenous ketamine has been shown to result in a response rate greater than 60% as early as 4.5 hours after the dose (with a sustained effect after 24 hours) and greater than 40% after 7 days.^[59] Although only a few pilot studies have sought to determine the optimal dose, increasing evidence suggests that 0.5 mg/kg dose injected over 40 minutes gives an optimal outcome.^[60] The antidepressant effect of ketamine is diminished at 7 days, and most people relapse within 10 days. However, for a significant minority, the improvement may last 30 days or more.^{[23][24][59][61]}

One of the main challenges with ketamine treatment can be the length of time that the antidepressant effects last after finishing a course of treatment. A possible option may be maintenance therapy with ketamine, which usually runs twice a week to once every two weeks.^[23][24][25] Ketamine may decrease suicidal thoughts for up to three days after the injection.^[62]

An enantiomer of ketamine – esketamine – was approved as an antidepressant by the European Medicines Agency in 2019.^[63] Esketamine was approved as a nasal spray for treatment-resistant depression in the United States^[64] and elsewhere in 2019. The Canadian Network for Mood and Anxiety Treatments (CANMAT) recommends esketamine as a third-line treatment for depression.^[24]

A Cochrane review of randomized controlled trials in adults with major depressive disorder^[20] found that when compared with placebo, people treated with either ketamine or esketamine experienced reduction or remission of symptoms lasting 1 to 7 days.^[65] There were 18.7% (4.1 to 40.4%) more people reporting some benefit and 9.6% (0.2 to 39.4%) more who achieved remission within 24 hours of ketamine treatment. Among people receiving esketamine, 12.1% (2.5 to 24.4%) encountered some relief at 24 hours, and 10.3% (4.5 to 18.2%) had few or no symptoms. These effects did not persist beyond one week, although a higher dropout rate in some studies means that the benefit duration remains unclear.^[65]

Ketamine may partially improve depressive symptoms^[20] among people with bipolar depression at 24 hours after treatment, but not three or more days.^[66] Potentially, ten more people with bipolar depression per 1000 may experience brief improvement, but not the cessation of symptoms, one day following treatment. These estimates are based on limited available research.^[66]

In February 2022, the US Food and Drug Administration (FDA) issued an alert to healthcare professionals concerning compounded nasal spray products containing ketamine intended to treat depression.^[67]

Ketamine is used to treat status epilepticus^[68] that has not responded to standard treatments, but only case studies and no randomized controlled trials support its use.^[69][70]

Ketamine has been suggested as a possible therapy for children with severe acute asthma who do not respond to standard treatment.^[71] This is due to its bronchodilator effects.^[71] A 2012 Cochrane review found there were minimal adverse effects reported, but the limited studies showed no significant benefit.^[71]

Some major contraindications for ketamine are:^[28][49]

• Severe cardiovascular disease such as unstable angina or poorly controlled hypertension
• Increased intracranial or intraocular pressure (however these remain controversial, with recent studies suggesting otherwise)^[49]
• Poorly controlled psychosis
• Severe liver disease such as cirrhosis
• Pregnancy
• Active substance use disorder (for serial ketamine injections)
• Age less than 3 months^[10]

At anesthetic doses, 10–20% of adults and 1–2% of children^[10] experience adverse psychiatric reactions that occur during emergence from anesthesia, ranging from dreams and dysphoria to hallucinations and emergence delirium.^[73] Psychotomimetic effects decrease when adding lamotrigine^[37] and nimodipine^[38] and can be counteracted by pretreatment with a benzodiazepine or propofol.^[73][39] Ketamine anesthesia commonly causes tonic-clonic movements (greater than 10% of people) and rarely hypertonia.^[14][73] Vomiting can be expected in 5–15% of the patients; pretreatment with propofol mitigates it as well.^[10][73] Laryngospasm occurs only rarely with ketamine. Ketamine, generally, stimulates breathing; however, in the first 2–3 minutes of a high-dose rapid intravenous injection, it may cause a transient respiratory depression.^[73]

At lower sub-anesthetic doses, psychiatric side effects are prominent. The most common psychiatric side effects are dissociation, visual distortions, and numbness. Also common (20–50%) are difficulty speaking, confusion, euphoria, drowsiness, and difficulty concentrating. hallucinations are described by 6–10% of people. Dizziness, blurred vision, dry mouth, hypertension, nausea, increased or decreased body temperature, or flushing are the common (>10%) non-psychiatric side effects. All these adverse effects are most pronounced by the end of the injection, dramatically reduced 40 minutes afterward, and completely disappear within 4 hours after the injection.^[74]

Urinary toxicity occurs primarily in people who use large amounts of ketamine routinely, with 20–30% of frequent users having bladder complaints.^[28][75] It includes a range of disorders from cystitis to hydronephrosis to kidney failure.^[76] The typical symptoms of ketamine-induced cystitis are frequent urination, dysuria, and urinary urgency sometimes accompanied by pain during urination and blood in urine.^[77] The damage to the bladder wall has similarities to both interstitial and eosinophilic cystitis. The wall is thickened and the functional bladder capacity is as low as 10–150 mL.^[76] Studies indicate that ketamine-induced cystitis is caused by ketamine and its metabolites directly interacting with urothelium, resulting in damage of the epithelial cells of the bladder lining and increased permeability of the urothelial barrier which results in clinical symptoms.^[78]

Management of ketamine-induced cystitis involves ketamine cessation as the first step. This is followed by NSAIDs and anticholinergics and, if the response is insufficient, by tramadol. The second line treatments are epithelium-protective agents such as oral pentosan polysulfate or intravesical instillation of hyaluronic acid. Intravesical botulinum toxin is also useful.^[76]

Liver toxicity of ketamine involves higher doses and repeated administration. In a group of chronic high-dose ketamine users, the frequency of liver injury was reported to be about 10%.^[79] There are case reports of increased liver enzymes involving ketamine treatment of chronic pain.^[76] Chronic ketamine abuse has also been associated with biliary colic,^[80] cachexia, gastrointestinal diseases, hepatobiliary disorder, and acute kidney injury.^[81]

Most people who were able to remember their dreams during ketamine anesthesia report near-death experiences (NDEs) when the broadest possible definition of an NDE is used.^[82] Ketamine can reproduce features that commonly have been associated with NDEs.^[83] A 2019 large-scale study found that written reports of ketamine experiences had a high degree of similarity to written reports of NDEs in comparison to other written reports of drug experiences.^[84]

Although the incidence of ketamine dependence is unknown, some people who regularly use ketamine develop ketamine dependence. Animal experiments also confirm the risk of misuse.^[22] Additionally, the rapid onset of effects following insufflation may increase potential use as a recreational drug. The short duration of effects promotes bingeing. Ketamine tolerance rapidly develops, even with repeated medical use, prompting the use of higher doses. Some daily users reported withdrawal symptoms, primarily anxiety, tremor, sweating, and palpitations, following the attempts to stop.^[22]

Despite the balance of palliative benefits which planned course(s) of therapy can confer when patients face serious medical conditions, ongoing ketamine use is known to cause brain damage, including reduction in both white and grey matter seen on MRI imaging and atrophy seen on CT scans.^[85] Cognitive deficits as well as increased dissociation and delusions were observed in frequent recreational users of ketamine.^[86]

Ketamine potentiates the sedative effects of propofol^[87] and midazolam.^[88] Naltrexone potentiates psychotomimetic effects of a low dose of ketamine,^[89] while lamotrigine^[37] and nimodipine^[38] decrease them. Clonidine reduces the increase of salivation, heart rate, and blood pressure during ketamine anesthesia and decreases the incidence of nightmares.^[90]

Clinical observations suggest that benzodiazepines may diminish the antidepressant effects of ketamine.^[91] It appears most conventional antidepressants can be safely combined with ketamine.^[91]

Ketamine is a mixture of equal amounts of two enantiomers: esketamine and arketamine. Esketamine is a far more potent NMDA receptor pore blocker than arketamine.^[11] Pore blocking of the NMDA receptor is responsible for the anesthetic, analgesic, and psychotomimetic effects of ketamine.^[92][93] Blocking of the NMDA receptor results in analgesia by preventing central sensitization in dorsal horn neurons; in other words, ketamine's actions interfere with pain transmission in the spinal cord.^[14]

The mechanism of action of ketamine in alleviating depression is not well understood, but it is an area of active investigation. Due to the hypothesis that NMDA receptor antagonism underlies the antidepressant effects of ketamine, esketamine was developed as an antidepressant.^[11] However, multiple other NMDA receptor antagonists, including memantine, lanicemine, rislenemdaz, rapastinel, and 4-chlorokynurenine, have thus far failed to demonstrate significant effectiveness for depression.^[11][94] Furthermore, animal research indicates that arketamine, the enantiomer with a weaker NMDA receptor antagonism, as well as (2R,6R)-hydroxynorketamine, the metabolite with negligible affinity for the NMDA receptor but potent alpha-7 nicotinic receptor antagonist activity, may have antidepressant action.^[11][95] This furthers the argument that NMDA receptor antagonism may not be primarily responsible for the antidepressant effects of ketamine.^[11][96][94] Acute inhibition of the lateral habenula, a part of the brain responsible for inhibiting the mesolimbic reward pathway and referred to as the "anti-reward center", is another possible mechanism for ketamine's antidepressant effects.^[97][98][99]

Possible biochemical mechanisms of ketamine's antidepressant action include direct action on the NMDA receptor and downstream effects on regulators such as BDNF and mTOR.^[97] It is not clear whether ketamine alone is sufficient for antidepressant action or its metabolites are also important; the active metabolite of ketamine, hydroxynorketamine, which does not significantly interact with the NMDA receptor but nonetheless indirectly activates AMPA receptors, may also or alternatively be involved in the rapid-onset antidepressant effects of ketamine.^{[92][97][100]} In NMDA receptor antagonism, acute blockade of NMDA receptors in the brain results in an increase in the release of glutamate, which leads to an activation of α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors (AMPA receptors), which in turn modulate a variety of downstream signaling pathways to influence neurotransmission in the limbic system and mediate antidepressant effects.^{[59][97][101]} Such downstream actions of the activation of AMPA receptors include upregulation of brain-derived neurotrophic factor (BDNF) and activation of its signaling receptor tropomyosin receptor kinase B (TrkB), activation of the mammalian target of rapamycin (mTOR) pathway, deactivation of glycogen synthase kinase 3 (GSK-3), and inhibition of the phosphorylation of the eukaryotic elongation factor 2 (eEF2) kinase.^{[59][97][102][103]}

Ketamine principally acts as a pore blocker of the NMDA receptor, an ionotropic glutamate receptor.^[120] The S-(+) and R-(–) stereoisomers of ketamine bind to the dizocilpine site of the NMDA receptor with different affinities, the former showing approximately 3- to 4-fold greater affinity for the receptor than the latter. As a result, the S isomer is a more potent anesthetic and analgesic than its R counterpart.^[121]

Ketamine may interact with and inhibit the NMDAR via another allosteric site on the receptor.^[122]

With a couple of exceptions, ketamine actions at other receptors are far weaker than ketamine's antagonism of the NMDA receptor (see the activity table to the right).^[7][123]

Although ketamine is a very weak ligand of the monoamine transporters (K_i > 60 μM), it has been suggested that it may interact with allosteric sites on the monoamine transporters to produce monoamine reuptake inhibition.^[105] However, no functional inhibition (IC₅₀) of the human monoamine transporters has been observed with ketamine or its metabolites at concentrations of up to 10,000 nM.^[111][120] Moreover, animal studies and at least three human case reports have found no interaction between ketamine and the monoamine oxidase inhibitor (MAOI) tranylcypromine, which is of importance as the combination of a monoamine reuptake inhibitor with an MAOI can produce severe toxicity such as serotonin syndrome or hypertensive crisis.^[124][125] Collectively, these findings shed doubt on the involvement of monoamine reuptake inhibition in the effects of ketamine in humans.^{[124][120][111][125]} Ketamine has been found to increase dopaminergic neurotransmission in the brain, but instead of being due to dopamine reuptake inhibition, this may be via indirect/downstream mechanisms, namely through antagonism of the NMDA receptor.^[120][111]

Whether ketamine is an agonist of D₂ receptors is controversial. Early research by the Philip Seeman group found ketamine to be a D₂ partial agonist with a potency similar to that of its NMDA receptor antagonism.^{[110][126][127]} However, later studies by different researchers found the affinity of ketamine of >10 μM for the regular human and rat D₂ receptors,^{[105][111][112]} Moreover, whereas D₂ receptor agonists such as bromocriptine can rapidly and powerfully suppress prolactin secretion,^[128] subanesthetic doses of ketamine have not been found to do this in humans and in fact, have been found to dose-dependently increase prolactin levels.^[129][130] Imaging studies have shown mixed results on inhibition of striatal [¹¹C] raclopride binding by ketamine in humans, with some studies finding a significant decrease and others finding no such effect.^[131] However, changes in [¹¹C] raclopride binding may be due to changes in dopamine concentrations induced by ketamine rather than binding of ketamine to the D₂ receptor.^[131]

Dissociation and psychotomimetic effects are reported in people treated with ketamine at plasma concentrations of approximately 100 to 250 ng/mL (0.42–1.1 μM).^[92] The typical intravenous antidepressant dosage of ketamine used to treat depression is low and results in maximal plasma concentrations of 70 to 200 ng/mL (0.29–0.84 μM).^[57] At similar plasma concentrations (70 to 160 ng/mL; 0.29–0.67 μM) it also shows analgesic effects.^[57] In 1–5 minutes after inducing anesthesia by rapid intravenous injection of ketamine, its plasma concentration reaches as high as 60–110 μM.^[132][133] When the anesthesia was maintained using nitrous oxide together with continuous injection of ketamine, the ketamine concentration stabilized at approximately 9.3 μM.^[132] In an experiment with purely ketamine anesthesia, people began to awaken once the plasma level of ketamine decreased to about 2,600 ng/mL (11 μM) and became oriented in place and time when the level was down to 1,000 ng/mL (4 μM).^[134] In a single-case study, the concentration of ketamine in cerebrospinal fluid, a proxy for the brain concentration, during anesthesia varied between 2.8 and 6.5 μM and was approximately 40% lower than in plasma.^[135]

Ketamine can be absorbed by many different routes due to its water and lipid solubility. Intravenous ketamine bioavailability is 100% by definition, intramuscular injection bioavailability is slightly lower at 93%,^[7] and epidural bioavailability is 77%.^[9] Subcutaneous bioavailability has never been measured but is presumed to be high.^[136] Among the less invasive routes, the intranasal route has the highest bioavailability (45–50%)^[7][10] and oral – the lowest (16–20%).^[7][10] Sublingual and rectal bioavailabilities are intermediate at approximately 25–50%.^[7][11][10]

After absorption ketamine is rapidly distributed into the brain and other tissues.^[93] The plasma protein binding of ketamine is variable at 23–47%.^[12]

In the body, ketamine undergoes extensive metabolism. It is biotransformed by CYP3A4 and CYP2B6 isoenzymes into norketamine, which, in turn, is converted by CYP2A6 and CYP2B6 into hydroxynorketamine and dehydronorketamine.^[92] Low oral bioavailability of ketamine is due to the first-pass effect and, possibly, ketamine intestinal metabolism by CYP3A4.^[17] As a result, norketamine plasma levels are several-fold higher than ketamine following oral administration, and norketamine may play a role in anesthetic and analgesic action of oral ketamine.^[7][17] This also explains why oral ketamine levels are independent of CYP2B6 activity, unlike subcutaneous ketamine levels.^[17][137]

After an intravenous injection of tritium-labelled ketamine, 91% of the radioactivity is recovered from urine and 3% from feces.^[15] The medication is excreted mostly in the form of metabolites, with only 2% remaining unchanged. Conjugated hydroxylated derivatives of ketamine (80%) followed by dehydronorketamine (16%) are the most prevalent metabolites detected in urine.^[29]

(S)-ketamine

(R)-ketamine

In chemical structure, ketamine is an arylcyclohexylamine derivative. Ketamine is a chiral compound. The more active enantiomer, esketamine (S-ketamine), is also available for medical use under the brand name Ketanest S,^[138] while the less active enantiomer, arketamine (R-ketamine), has never been marketed as an enantiopure drug for clinical use. While S-ketamine is more effective as an analgesic and anesthetic through NMDA receptor antagonism, R-ketamine produces longer-lasting effects as an antidepressant.^[20]

The optical rotation of a given enantiomer of ketamine can vary between its salts and free base form. The free base form of (S)‑ketamine exhibits dextrorotation and is therefore labelled (S)‑(+)‑ketamine. However, its hydrochloride salt shows levorotation and is thus labelled (S)‑(−)‑ketamine hydrochloride.^[139]

Ketamine may be quantified in blood or plasma to confirm a diagnosis of poisoning in hospitalized people, provide evidence in an impaired driving arrest, or assist in a medicolegal death investigation. Blood or plasma ketamine concentrations are usually in a range of 0.5–5.0 mg/L in persons receiving the drug therapeutically (during general anesthesia), 1–2 mg/L in those arrested for impaired driving, and 3–20 mg/L in victims of acute fatal overdosage. Urine is often the preferred specimen for routine drug use monitoring purposes. The presence of norketamine, a pharmacologically active metabolite, is useful for confirmation of ketamine ingestion.^{[140][141][142]}

Ketamine was first synthesized in 1962 by Calvin L. Stevens,^[20] a professor of chemistry at Wayne State University and a Parke-Davis consultant. It was known by the developmental code name CI-581.^[20] After promising preclinical research in animals, ketamine was tested in human prisoners in 1964.^[29] These investigations demonstrated ketamine's short duration of action and reduced behavioral toxicity made it a favorable choice over phencyclidine (PCP) as an anesthetic.^[143] The researchers wanted to call the state of ketamine anesthesia "dreaming", but Parke-Davis did not approve of the name. Hearing about this problem and the "disconnected" appearance of treated people, Mrs. Edward F. Domino,^[144] the wife of one of the pharmacologists working on ketamine, suggested "dissociative anesthesia".^[29] Following FDA approval in 1970, ketamine anesthesia was first given to American soldiers during the Vietnam War.^[145]

The discovery of antidepressive action of ketamine in 2000^[146] has been described as the single most important advance in the treatment of depression in more than 50 years.^[61][11] It has sparked interest in NMDA receptor antagonists for depression,^[147] and has shifted the direction of antidepressant research and development.^[148]

While ketamine is marketed legally in many countries worldwide,^[149] it is also a controlled substance in many countries.^[7]

• In Australia, ketamine is listed as a Schedule 8 controlled drug under the Poisons Standard (October 2015).^[150]
• In Canada, ketamine has been classified as a Schedule I narcotic since 2005.^[151]
• In December 2013, the government of India, in response to rising recreational use and the use of ketamine as a date rape drug, added it to Schedule X of the Drug and Cosmetics Act requiring a special license for sale and maintenance of records of all sales for two years.^[152][153]
• In the United Kingdom, it was labeled a Class B drug on 12 February 2014.^[154][155] In 2025, the Home Office requested a review of the classification with a view to changing it to Class A, based on an increase in recreational use and the negative health consequences.^[156]
• The increase in recreational use prompted ketamine to be placed in Schedule III of the United States Controlled Substances Act in August 1999.^[157][158]

At sub-anesthetic doses, ketamine produces a dissociative state, characterised by a sense of detachment from one's physical body and the external world that is known as depersonalization and derealization.^[159] At sufficiently high doses, users may experience what is called the "K-hole", a state of dissociation with visual and auditory hallucination.^[160] John C. Lilly, Marcia Moore, and D. M. Turner (among others) have written extensively about their own entheogenic and psychonautic experiences with ketamine.^[161] Turner died prematurely due to drowning during presumed unsupervised ketamine use.^[162]

Recreational ketamine use has been implicated in deaths globally, with more than 90 deaths in England and Wales in 2005–2013.^[163] They include accidental poisonings, drownings, traffic accidents, and suicides.^[163] The majority of deaths were among young people.^[164] Several months after being found dead in his hot tub, actor Matthew Perry's October 2023 apparent drowning death was revealed to have been caused by a ketamine overdose, and, while other factors were present, the acute effects of ketamine were ruled to be the primary cause of death.^[165] Due to its ability to cause confusion and amnesia, ketamine has been used for date rape.^[166][145]

Ketamine, in the form of esketamine, is approved in the United States for treating treatment-resistant depression.^[167] In vivo, ketamine rapidly activates the mTOR pathway, promoting synaptogenesis and reversing stress-related synaptic deficits in the prefrontal cortex, which might underlie its fast-acting antidepressant effects in treatment-resistant depression.^[168] A 2023 meta-analysis found that racemic ketamine, particularly at higher doses, is more effective than esketamine in reducing depression severity, with more sustained benefits over time.^[30]

Ketamine has shown potential for rapid and tolerable symptom relief in obsessive-compulsive disorder, but evidence is limited and inconsistent.^[169][170]

The British critical psychiatrist Joanna Moncrieff has critiqued the use and study of ketamine and related drugs like psychedelics for treatment of psychiatric disorders, highlighting concerns including excessive hype around these drugs, questionable biologically-based theories of benefit, blurred lines between medical and recreational use, flawed clinical trial findings, financial conflicts of interest, strong expectancy effects and large placebo responses, small and short-term benefits over placebo, and their potential for difficult experiences and adverse effects, among others.^[171]

In veterinary anesthesia, ketamine is often used for its anesthetic and analgesic effects on cats,^[172] dogs,^[173] rabbits, rats, and other small animals.^[174][175] It is frequently used in induction and anesthetic maintenance in horses. It is an important part of the "rodent cocktail", a mixture of drugs used for anesthetising rodents.^[176] Veterinarians often use ketamine with sedative drugs to produce balanced anesthesia and analgesia, and as a constant-rate infusion to help prevent pain wind-up. Ketamine is also used to manage pain among large animals. It is the primary intravenous anesthetic agent used in equine surgery, often in conjunction with detomidine and thiopental, or sometimes guaifenesin.^[177]

Ketamine appears not to produce sedation or anesthesia in snails. Instead, it appears to have an excitatory effect.^[178]