Ketamine is a dissociative anesthetic. In medicine it is used for anesthesia, pain control, and procedural sedation, including what clinicians call conscious sedation (more precisely, procedural or dissociative sedation). In that setting the drug produces a trance-like state: pain is blocked, memory of the procedure is often reduced, and the person may have their eyes open and even make sounds, but they are detached from their surroundings. Airway reflexes and blood pressure are often better preserved than with many other sedatives, which is why it is used in emergency departments and for short procedures. The person is not fully unconscious the way they would be under general anesthesia, but ordinary awareness and control are interrupted. The drug’s effect on consciousness does not depend on whether the dose was taken willingly. Ketamine blocks NMDA glutamate receptors and alters signaling in circuits that support awareness, perception, and executive control. Once a sufficient amount is in the system, those circuits are disrupted whether the person chose the drug or not. “Conscious sedation” in the clinical phrase means the patient is sedated but not fully anesthetized. In plain terms, the contents of consciousness—attention, sense of self, ability to track what is happening and decide what to do—are impaired for the duration of the effect. During a single dose, decision-making is already degraded. People commonly show poor judgment, distorted time and body sense, reduced ability to weigh consequences, and suggestibility. They may answer questions or follow simple prompts while being unable to form a reliable plan or refuse something they would normally refuse. Repeated doses make that worse in two ways. Acutely, residual dissociation, slowed processing, and impaired working memory can linger between doses, so choices are made on incomplete information and weaker impulse control. With ongoing heavy use, studies of frequent ketamine users find lasting deficits in executive function: worse cognitive flexibility, poorer planning, weaker inhibitory control, and impaired decision-making on tasks that require weighing risk and reward. Memory, especially episodic memory, is also commonly affected. Those changes are linked to repeated disruption of glutamate signaling and, in heavy users, structural and functional changes in frontal and hippocampal regions. Some recovery is reported after sustained abstinence, but it is often incomplete if use was prolonged and high-dose. Separate from cognition, repeated recreational use is strongly associated with ketamine bladder toxicity (pain, frequency, ulceration), which is unrelated to the sedation question but is the main physical harm of chronic use.