Administration of sodium bicarbonate successfully reversed life-threatening doxepin-induced cardiotoxicity that was initially masked by clonidine-induced bradycardia in a 27-year-old woman.
Case Report (n=1)
Clonidine-induced bradycardia can mask the expected tachycardia of tricyclic antidepressant cardiotoxicity, highlighting the critical role of ECG in diagnosing and guiding sodium bicarbonate therapy in complex polypharmacy overdoses.
Abstract Introduction Drug overdoses that involve multiple ion-channel toxins demand rapid interpretation and decisive therapy. When toxidromes conflict, the electrocardiogram (ECG) becomes the most reliable diagnostic compass. This case demonstrates how bradycardia from clonidine masked life-threatening tricyclic antidepressant (TCA) cardiotoxicity until the ECG revealed the true mechanism. Case A 27-year-old woman was found altered and bradycardic after a reported clonidine ingestion. She was intubated for airway protection and started on an epinephrine infusion for persistent bradycardia and hypotension in the emergency department (ED). Initial laboratory evaluation, including electrolytes and toxicology screens, was normal, and she was admitted to the intensive care unit (ICU). While preparing for transfer from the ED to the ICU, serial ECGs showed rapid progression from sinus bradycardia to QRS 130 ms, QTc 730 ms, and a terminal R wave in aVR, consistent with combined sodium and potassium-channel blockade. Review of an alternate medical record revealed prescribed doxepin, raising concern for TCA-type cardiotoxicity initially masked by clonidine’s central α2-adrenergic agonism. Given the ECG progression, a sodium bicarbonate challenge (three 50-mEq boluses) was administered, resulting in prompt narrowing of the QRS and improved QTc. An isotonic sodium bicarbonate infusion maintained alkalemia (arterial pH 7.52). Magnesium sulfate, calcium gluconate, and potassium repletion were provided to mitigate dysrhythmic risk, and vasopressor support was transitioned to norepinephrine. The patient’s ECG and hemodynamics normalized with continued ICU care. Discussion This case illustrates the intersection of emergency medicine, critical care, and medical toxicology. Clonidine blunted the expected tachycardia of the TCA’s anticholinergic poisoning, creating a diagnostic trap. Doxepin is a TCA class agent that blocks fast sodium and delayed rectifier potassium channels, leading to QRS widening and QTc prolongation in overdose. The ECG exposed the underlying threat: sodium-channel blockade producing conduction delay, compounded by potassium-channel blockade prolonging repolarization. Several teaching points emerge from this case. First, clonidine-induced bradycardia can conceal TCA cardiotoxicity, delaying diagnosis. Second, ECG findings, especially QRS widening, QTc prolongation, and a terminal R in aVR, serve as early diagnostic clues even when toxicology screens are negative. Third, sodium bicarbonate reverses sodium-channel blockade and decreases toxin-protein binding through systemic alkalinization. Finally, cross-disciplinary collaboration among ED, ICU, and toxicology teams is vital for rapid recognition and coordinated management of complex polypharmacy overdoses. This abstract is funded by: None
Sherman et al. (Fri,) conducted a case report in Clonidine and doxepin overdose (n=1). Sodium bicarbonate, magnesium sulfate, calcium gluconate, potassium, norepinephrine was evaluated. Administration of sodium bicarbonate successfully reversed life-threatening doxepin-induced cardiotoxicity that was initially masked by clonidine-induced bradycardia in a 27-year-old woman.