Remarkably Widened QRS Complex Following a Lethal Dose of Propafenone—An Ominous Sign

Voltage-gated sodium channels in cardiac tissue are located in the cell membrane and open in response to the depolarization of the cell. Propafenone is a class IC antiarrhythmic drug that acts by slowing sodium influx into myocytes through voltage-gated sodium channels and is referred to as a sodium-channel blocker.¹ Propafenone binds to the transmembrane channels and decreases the number of channels available for depolarization. The effect produced on the cell is a delay in the entry of sodium ions into the cardiac myocyte, which occurs during phase 0 of depolarization.²

Multiple ECG abnormalities can be observed in the patient with blockage of cardiac sodium channels. The primary manifestation of the blockage, as mentioned previously, is the slowing of the upslope of phase 0 depolarization and thus a widening of the QRS complex (Figure, A). Propafenone blocked the sodium channel of the His-Purkinje system and ventricular muscle fibers, thereby reducing their conduction velocity, with a slightly more pronounced effect on intraventricular conduction. This led to QRS widening with relative preservation of the narrow initial portion of the QRS.³ A QRS duration of more than 200 milliseconds suggested a notable interventricular conduction delay.⁴ The initial ECG (Figure, A) demonstrated serious propafenone-associated decremental conduction, particularly affecting the intramyocardial conduction, with a QRS duration of 280 milliseconds and preservation of the narrow initial portion of the QRS. This was because the His-Purkinje conduction remained relatively unhampered by the drug. Potential differential diagnoses included the following: left bundle-branch block pattern, QRS prolongation caused by a class IC antiarrhythmic drug, accelerated idioventricular rhythm, and junctional rhythm with left bundle-branch block/intramyocardial conduction block. However, accelerated idioventricular rhythm and junctional rhythm were ruled out because of the presence of P waves preceding each ventricular complex.