Pathophysiology
Clinical meaning
Acute alcohol poisoning occurs when blood alcohol concentration (BAC) rises to dangerous levels, typically from rapid binge drinking. Ethanol is a central nervous system depressant that enhances GABA-A receptor activity and inhibits NMDA glutamate receptors, producing dose-dependent CNS depression. At BAC 0.08% (legal intoxication limit), judgment and coordination are impaired. At 0.20-0.30%, confusion, vomiting, and stupor develop. At 0.30-0.40%, loss of consciousness, hypothermia, and respiratory depression occur. BAC > 0.40% is potentially lethal from respiratory arrest, aspiration, and cardiovascular collapse. The liver metabolizes ethanol at approximately 15-20 mg/dL/hour via alcohol dehydrogenase. Risk of aspiration is high in unconscious patients due to loss of protective airway reflexes. Methanol and ethylene glycol (antifreeze) are toxic alcohols that produce metabolic acidosis with an osmol gap; fomepizole or ethanol infusion inhibits their conversion to toxic metabolites.