The patient’s marked hyperthermia and respiratory depression suggest severe poisoning by salicylates. This is supported by the lab results indicating mixed respiratory and metabolic acidosis (low pH, increased Pco2 and decreased plasma bicarbonate content). This acid-base disturbance is typical of high salicylate content in the blood. In salicylate poisoning, the initial event (when salicylate concentration in blood is not yet high) is respiratory alkalosis caused by salicylate-induced stimulation of the respiratory center. Partial compensation is achieved, as usual, by increased renal excretion of bicarbonate. Therefore the initial phase of poisoning (or when the poisoning is mild) is characterized by high pH, and decreased plasma levels of CO2 and bicarbonate. In a later phase, when salicylate blood levels become quite high, the respiratory center becomes depressed and respiratory acidosis supervenes. This acidosis is uncompensated since a significant amount of bicarbonate has been already eliminated. Moreover, salicylates cause uncoupling of mitochondrial oxidative phosphorylation (which leads to hyperthermia) and inhibits the enzymes of Krebs cycle, resulting in increased pyruvic and lactic acids. Lipolysis, gluconeogenesis, and glycolysis are also stimulated, leading to hyperglycemia and the production of keto acids. Therefore the final picture is the one of mixed respiratory and metabolic acidosis. Acute alcohol poisoning can cause combative behavior, but hypothermia and hypoglycemia are typical signs of alcohol poisoning and tinnitus is usually absent. Poisoning by NSAIDs other than salicylates does not usually cause profound impairment of acid-base balance.