Low blood pressure is dangerous for people with severe head injury and ketamine is unlikely to lower blood pressure — conversely, often raising blood pressure, making it often the best suited for those with severe head injury.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 In particular, children with cyanotic heart disease and neuromuscular disorders are good candidates for ketamine anesthesia.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. Pain
Ketamine infusions are used for acute pain treatment in emergency departments and in the perioperative period in individuals with refractory pain. The doses are lower than those used for anesthesia; they are 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.Ketamine is especially useful in the prehospital setting, due to its effectiveness and low risk of respiratory depression. Ketamine has similar efficacy to opioids in a hospital emergency department setting for management of acute pain and for control of procedural pain. It may also prevent opioid-induced hyperalgesia and postanesthetic shivering.For chronic pain, ketamine is used as an intravenous analgesic, particularly, if the pain is neuropathic.
However, multiple other NMDA receptor antagonists, including memantine, lanicemine, rislenemdaz, rapastinel, and 4-chlorokynurenine, thus far have failed to demonstrate sufficient effectiveness for depression. 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 a  potent alpha-7 nicotinic receptor antagonist may have antidepressive action. It is now argued that NMDA receptor antagonism may not be primarily responsible for the antidepressant effects of ketamine. Molecular targets
Ketamine principally acts as an antagonist of the NMDA receptor, an ionotropic glutamate receptor. 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.Ketamine may interact with and inhibit the NMDAR via another allosteric site on the receptor.With a couple of exceptions ketamine actions at other receptors are far weaker than ketamines antagonism of the NMDA receptor (see the activity table to the right).Although ketamine is a very weak ligand of the monoamine transporters (Ki > 60 μM), it has been suggested that it may interact with allosteric sites on the monoamine transporters to produce monoamine reuptake inhibition. 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.