Ethanol is a selective CNS depressant at low doses and a general depressant at high doses. At the highest blood alcohol levels there is loss of protective reflexes, coma and increased risk of death from respiratory depression. There is a narrow margin between the anesthetic and fatal dose; deeply intoxicated patients are near death and must be managed aggressively. Chronic alcoholics with a developed tolerance may appear sober at a level of 300 mg/dl; whereas, an adolescent with a level of 200 mg/dl may present with respiratory arrest.

A “standard drink” (equivalent to a glass of wine, a shot or a 12 oz. Beer) increases the blood alcohol by 25-35mg/dl. Lethal doses of ethanol are reported to be 5-6mL/kg in adults and 3mL/kg for children. The LD 50 (the “lethal dose” level at which half of those patients with this level would die) in the non-habituated patient is approximately 500 mg/dL. More than 90% of ethanol ingested is eliminated by enzymatic oxidation, with only 5-10% excreted unchanged by the kidneys and lungs. The alcohol dehydrogenase system is the main pathway for ethanol metabolism in the body and is the rate limiting step. Ethanol is metabolized initially by first-order kinetics. As the system is saturated it moves to zero-order kinetics (fixed amount metabolized per unit time). At that point, the level will fall by 15-45 mg/dl/hour depending on the chronicity of ethanol use. The EP can reasonably assume the rate of metabolism will be in the higher range (25-45mg/dl/hr) for known habituated drinkers. Ethanol is a dialyzable substance in cases of potentially lethal ingestion. There is no antagonist to alcohol currently available. Neither naloxone or flumazenil have been shown to reduce the effects of alcohol. Since there is no single receptor, it is unlikely that an ethanol antagonist will ever be discovered .