Anesthetics are used to depress the peripheral and central nervous systems (CNS) by blocking nerve conduction in order to facilitate surgical and other noxious procedures.1 Anesthetics can be divided into general (inhalation and parenteral) and local types, the former inducing a loss of waking consciousness in humans similar in many respects to sleep while the latter block local nerve conduction. Parenteral anesthetics are also termed intravenous hypnotics or intravenous induction agents and can be used alone or in combination with other agents.

General anesthesia can be defined in terms of a functional deafferentation reflecting a global loss of response to, and perception of, all external stimuli, e.g., a surgical incision. Additional facets of general anesthesia include: blunting of hemodynamic and endocrine responses, respiratory paralysis, and a lack of awareness and memory.2 It involves sites in both the brain and spinal cord and has been defined as artificially (drug)-induced sleep. In the mid twentieth century, inhalation or volatile anesthetics were defined on the basis of their ability to induce a loss of righting reflex (motor tone) that was frequently referred to as 'sleep time,' and the amount of time required to induce an anesthetic state. Motor atonia can be dissociated from loss of wakefulness while controlled sedation can be equated with 'light sleep.'3 The intertwining of anesthesia with sleep-state physiology is controversial4 and reflects the complexity of the state of consciousness. While both conditions involve a common hypothalamic locus,4 they can be distinguished by the fact that a sleeping individual can be aroused rapidly while an anesthetized individual can only be aroused when the drug is cleared from the brain.


Diethyl ether Chloroform Nitrous oxide

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