Flecainide is an antagonist of cardiac sodium channel α-subunit-5 used for the treatment of supraventricular arrhythmias in patients without structural heart disease. It slows the velocity of membrane depolarization without affecting repolarization, resulting in prolongation of the P-wave duration, PR segment, and QRS. Flecainide binds primarily to activated/open sodium channels; therefore, the block is further increased during faster rates (use dependence). Consequently, myocardial conduction is depressed, especially during higher heart rates, giving rise to a bizarre-looking WCT, mimicking VT. Flecainide slows conduction through the atrial tissue more than it prolongs refractoriness, which enables organized atrial activity and promotes atrial flutter.1 Sometimes, the atrial rate slows enough to enable 1:1 conduction through the AV node, resulting in very high heart rate, which can potentially degenerate into life-threatening arrhythmias. Therefore, patients taking flecainide also need an AV nodal-blocking agent to mitigate this risk.2 Alternatively, flecainide itself can induce VT by creation of areas of functional conduction block promoting reentry.3 This case highlights the limitations of WCT diagnostic criteria in clinical practice. The Brugada algorithm was tested in patients without antiarrhythmic drug treatment.4 The use of class I antiarrhythmic drugs results in a low specificity of the second Brugada criterion.5 Alternatively, the ventricular activation velocity ratio (vi/vt) has several advantages in this setting. To apply, measure the total vertical distance covered by the final 40 milliseconds of the QRS. If this is equal to or more than the vertical distance covered by the first 40 milliseconds of the QRS, VT is diagnosed. The concept is that with aberration, ventricular activation during the first portion of the QRS is mediated by the His-Purkinje system, whereas in VT, the His-Purkinje system is engaged later in the QRS complex.6 The use of antiarrhythmic drugs that impair conduction in the His-Purkinje system and ventricular myocardium (such as class I drugs) would be expected to decrease the vi and vt approximately to the same degree. Thus, the vi/vt ratio will not change substantially. When confronted with a WCT, it is crucial to integrate both the clinical and the ECG information and not rely exclusively on ECG algorithms. Furthermore, extended rhythm monitoring and multiple ECGs often provide critical information that can facilitate the diagnosis of challenging rhythms.