The most appropriate next step in treatment is to begin intravenous sodium bicarbonate therapy. The combination of progressive somnolence, hypotension, widening of the QRS interval, seizure, and anticholinergic signs (fever, tachycardia, mydriasis, reduced bowel sounds) is concerning for severe tricyclic antidepressant overdose. Tricyclic antidepressants inhibit fast sodium channels in the myocardium and conduction system, resulting in decreased ventricular function and increased duration of repolarization that predisposes to ventricular arrhythmias. Electrocardiographic findings in tricyclic overdose include nonspecific changes in QRS morphology and QRS prolongation that predisposes to ventricular arrhythmia; a QRS duration of greater than 100 ms is often used as an indicator of significant tricyclic cardiotoxicity. Sodium bicarbonate increases the serum pH, which inhibits the ionized form of the drug that binds sodium channels, making it less available. Sodium bicarbonate also increases extracellular sodium, which increases the electrochemical gradient across myocardial cell membranes and minimizes the effect of blockade of rapid sodium channels. Clinically, this improves myocardial contractility and results in a reduction in the risk of arrhythmias.

Intravenous calcium gluconate is used in the management of calcium channel blocker overdose, which is a possibility given this patient's baseline use of amlodipine, her hypotension, and the possibility of hypotension-associated encephalopathy. Verapamil and diltiazem poisoning is associated with bradycardia, but this is not typically seen in the case of poisoning with dihydropyridines like amlodipine. Amlodipine poisoning would not explain this patient's anticholinergic signs, widened QRS interval, and seizure.

Fomepizole is an alcohol dehydrogenase inhibitor that prevents the breakdown of methanol and ethylene glycol into toxic metabolites. This patient's somnolence and history of depression raise the possibility of methanol and ethylene glycol poisoning, but the normal osmolal gap, QRS interval widening, and anticholinergic signs would not be expected.

Physostigmine is a potential antidote for anticholinergic toxicity and may be particularly helpful in the management of associated agitated delirium. Although this patient has anticholinergic symptoms, her somnolence, widened QRS interval, and baseline use of amitriptyline are more compatible with tricyclic antidepressant overdose. Physostigmine has reportedly precipitated asystole when used in the setting of tricyclic overdose and should not be given to this patient.