tially involving the pericardium and presenting with signs and symptoms of myocarditis and pericardial effusion \[[@REF11]\]. These events can, in turn, cause direct myocardial depression and impaired myocardial contractility with a dilation of the ventricles and reduced EF.

Amitriptyline interferes with the reuptake of norepinephrine and direct myocardial depression, playing a role in decreased myocyte contractility, causing prolongation of the QT interval, and predisposing to torsade de pointes. Furthermore, it has anticholinergic and alpha-adrenergic blockade properties, which can cause hypotension and further worsen systemic perfusion \[[@REF9]-[@REF12]\]. The early initiation of therapy is vital for the retrieval of cardiac function. Typically, sodium bicarbonate has been found to reverse toxicity effects, with an end goal of blood pH of 7.5-7.55 and no regard to arterial pH at presentation. The administration of sodium bicarbonate was associated with volume expansion and improvement in systolic blood pressure, preventing the further development of acidosis. Also, the induction of hypokalemia by bicarbonate causes membrane hyperpolarization. Such an effect can lower the threshold voltage at which sodium channels open, which, in turn, diminishes the effect of sodium channel blockade. These changes can help in narrowing the QRS complex. Additionally, the withdrawal of all cardiotoxic offending agents and QTc prolonging medications in patients with TCA toxicity is very important \[[@REF13]-[@REF15]\].

Our patient is a 21-year-old male with no previous medical comorbidities and at low risk for cardiac sequelae. He claimed to ingest 41 tablets of amitriptyline 50 mg. His weight at admission was 67 kilogram (kg), putting him at a toxicity dose of approximately 30.6 mg/kg. EKG changes correlated with TCA-induced cardiotoxicity. CMR showed no evidence of coronary artery occlusion, and it was thought that the troponin elevation was due to amitriptyline's direct toxic damage on cardiac myocytes. In addition, the pa