CONGRESS ABSTRACT

The differential diagnosis of wide-QRS tachycardia is among the most complex challenges in cardiology, particularly in emergency settings. The diagnostic difficulty is magnified in critical situations where immediate stabilization of hemodynamically unstable patients is paramount, often precluding comprehensive diagnostic evaluation. A 21-year-old male with no prior medical history was found unresponsive on the street following a generalized tonic-clonic seizure that required intubation. On admission to the Emergency Department, the patient presented with extreme hypotension (70/30 mmHg) and tachycardia (150 bpm), despite receiving high doses of vasopressors. Arterial blood gas analysis revealed profound metabolic acidosis (pH 6.8), severe hyperlactatemia (>17 mmol/L), and a wide-QRS tachycardia with a left bundle branch block morphology on ECG. Neurological imaging showed no abnormalities. Given the hemodynamic instability, electrical cardioversion was attempted but proved ineffective. Subsequently, the ECG demonstrated a shift from an LBBB to a right bundle branch block pattern with coved ST-segment elevation in leads V1 and V2, mimicking Brugada syndrome. Toxicology testing confirmed cocaine and alcohol use, and transthoracic echocardiography revealed preserved biventricular function.To further clarify the rhythm, adenosine was administered, revealing a transient accelerated junctional escape rhythm with sporadic dissociated P waves. The wide-QRS arrhythmia quickly recurred, likely due to aberrant conduction over the left bundle branch. This findings suggested the hypothesis that QRS widening was driven by toxic and metabolic factors. Sodium bicarbonate was then administered to address both the metabolic acidosis and the sodium channel blockade effects of cocaine. As the acidosis resolved, the ECG abnormalities normalized. A focal preexisting RBBB was identified on the final ECG recorded the next day. This case underscores the critical impact of metabolic and toxicological factors on cardiac conduction. The dynamic alternation between LBBB and RBBB patterns highlights the reversibility of conduction abnormalities in the context of toxic-metabolic derangements. Before initiating antiarrhythmic therapy, clinicians should carefully assess these underlying factors. The use of adenosine to elucidate the rhythm and sodium bicarbonate to correct metabolic disturbances proved instrumental in this case, avoiding unnecessary and potentially harmful interventions