Propafenone is a class IC anti-arrhythmic agent with potent fast sodium channel blockade whose overdose may result in profound intraventricular conduction delay and malignant ventricular arrhythmias. Management strategies are largely derived from isolated case reports, and consensus guidelines are lacking. We describe a case of a young man with a history of supraventricular tachycardia who presented following intentional polysubstance ingestion, including at least 600 mg of propafenone. On presentation, he was hypoxemic, acidotic, and minimally responsive. Electrocardiography revealed sustained wide complex tachycardia with marked QRS widening. Initial laboratory testing demonstrated normal electrolyte levels with a modestly elevated troponin, along with severe anion-gap metabolic acidosis, elevated lactate levels, acute kidney injury, and toxic acetaminophen concentrations. Intravenous sodium bicarbonate was initiated to achieve mild alkalemia, along with aggressive electrolyte correction and supportive intensive care. Within 1 h of bicarbonate therapy, the ventricular tachycardia resolved with rapid narrowing of the QRS complex and restoration of sinus rhythm. Serial electrocardiograms over the ensuing 24 h showed continued normalization of conduction. This case highlights the electrophysiologic manifestations of propafenone toxicity and underscores the value of QRS duration as a dynamic marker of toxicity severity and treatment response. Early alkalinization with intravenous sodium bicarbonate may rapidly correct conduction disturbances and stabilize malignant arrhythmias in severe class IC anti-arrhythmic overdose.

The majority of patients presenting to the emergency department with a stable, regular, monomorphic, wide complex tachycardia will be diagnosed with ventricular tachycardia, with a minority of these patients being diagnosed with supraventricular tachycardia (SVT) with aberrant conduction. Vagal maneuvers may be performed as a first-line treatment for these patients, primarily for the treatment of potential SVT with aberrant conduction.

We report a 52-year-old man with coronary artery disease, reduced left ventricular ejection fraction, and a cardiac resynchronization therapy-defibrillator (CRT-D), admitted to the emergency department for palpitations. Surface ECG showed a wide-complex tachycardia with a 2:1 ventricular-to-atrial (V:A) relationship. Device interrogation revealed episodes detected in the ventricular tachycardia monitor zone, according to the atrioventricular discrimination algorithms. Detailed analysis of surface ECG and device intracardiac electrograms was performed, followed by an electrophysiological study and catheter ablation of the responsible circuit of the tachycardia. This case illustrates the diagnostic complexity and differential diagnosis of tachycardias presenting with a 2:1 V:A relationship and highlights the importance of integrating surface ECG, device tracings, and electrophysiological findings to correctly identify the underlying mechanism, to avoid misclassification by device algorithms, and to treat the arrhythmia effectively.

An 11-year-old male neutered Birman cat was referred for investigation of pyelonephritis. On physical examination, gallop sounds and bradycardia were noted. There was mild azotaemia and marked neutrophilia, attributed to the pyelonephritis. Transthoracic echocardiography revealed a non-specific cardiomyopathy phenotype with biatrial enlargement. Electrocardiography showed wide QRS complexes, bradycardia and synchronous dissociation between atrial and ventricular activity. During the first examination, the synchronisation appeared mostly fixed, with consistent PR intervals; on subsequent evaluations, the PR intervals appeared to vary on a beat-to-beat basis. The diagnosis was of isorhythmic atrioventricular dissociation type I, with an initial long phase of fixed synchronisation, mimicking an isorhythmic atrioventricular dissociation type II, and concomitant ventricular depolarisation with a left bundle branch block morphology.

We report a 69-year-old woman with persistent palpitation, a history of myocardial infarction. ECG showed irregular wide QRS tachycardia with positive precordial concordance and flutter waves, initially misdiagnosed as atrial flutter with accessory pathway. Direct current cardioversion restored sinus rhythm but failed to terminate tachycardia, revealing ventricular tachycardia (VT). Amiodarone resolved VT. This case highlights the challenge of differentiating wide QRS tachycardias, emphasizing QRS morphology and atrioventricular (AV) relationship analysis for accurate diagnosis.

We report a 27-year-old man presenting with paroxysmal palpitations due to alternating wide and narrow QRS tachycardias that transitioned without termination. Based on Coumel's law, an accessory pathway-mediated mechanism was initially suspected for both tachycardias. However, the wide QRS tachycardia was ultimately confirmed to be ventricular tachycardia. Although Coumel's law may aid in the diagnosis of tachycardias with alternating QRS widths, potential confounding factors must be carefully considered to prevent misdiagnosis.

Wolff-Parkinson-White syndrome, though previously diagnosed and without prior arrhythmic events, may remain clinically quiescent until atrial fibrillation with rapid antegrade conduction over an accessory pathway precipitates a potentially life threatening arrhythmia. We present a teaching case of a 46-year-old man who developed abrupt onset wide-complex tachycardia with ventricular rates exceeding 280 beats per minute on postoperative day three following thoracic surgery. Electrocardiography demonstrated an irregularly irregular rhythm with marked beat-to beat QRS variability and very short RR intervals, favoring atrial fibrillation with preexcitation rather than ventricular tachycardia or rate-related aberrancy. This case is used to illustrate key electrocardiographic features that distinguish pre-excited atrial fibrillation from other causes of wide-complex tachycardia and to review evidence based management principles in hemodynamically stable patients, including the selection of therapies that target accessory pathway conduction while avoiding atrioventricular nodal blockade.