The patient described is exhibiting cholinergic toxicity probably from the ingestion of an organophosphate or carbamate. The first rule in management of organophosphate poisoning is to maintain a patent airway. Upper airway obstruction from vomitus and copious secretions may occur. Increased airway resistance from bronchospasm may prove to exceed the respiratory capacity of the weakened muscles of respiration. Hypoxia rapidly ensues from bronchospasm and increased bronchial secretions. Early intubation is paramount in treating the poisoning. The most common cause of treatment failure in severe organophosphate poisoning is inadequate atropinization. The end-point of atropine administration is when drying of secretions occur. Tachycardia after organophosphate poisoning may be secondary to excessive atropinization necessitating a lower infusion rate. Hypoxia caused by increased pulmonary secretions may also produce tachycardia necessitating a higher infusion rate of atropine. 2-PAM should be given early based on the suspicion of cholinesterase poisoning. It is effective in reversing muscle weakness (nicotinic effects) but only if given within 36 hours of exposure. 2-PAM will reactivate acetylcholinesterase by displacing the organophosphate. Because true cholinesterase regenerates at a rate of only 1% a day, it can take months for symptoms to resolve if cholinesterase is not regenerated with 2-PAM.