Table 7.

Potential ECG changes after AAD administration for monomorphic VT termination

ECG parameter	Electrophysiologic mechanism	VM class of AAD
VT cycle length prolongation	AAD-induced slowing of conduction due to reduced Na+ channel activation or Prolongation of refractoriness impinging on the excitable gap and widening the re-entrant VT circuit	More marked with Class Ic than with Class III AADs Also seen with Class Ia procainamide More marked with higher dosed and the higher the VT rate (use dependency)
QRS complex morphology change	Multiple exits, which result from stopping one circuit and initiating another	May occur especially with Class Ic AAD
QRS complex widening during VT	Reduction of conduction velocity of the ventricular activation through the myocardium independent from the AAD effect in the re-entrant circuit; comes with the risk of acute heart failure, AV block, and sinusoidal VT	Mainly with Class Ic AADs and more marked with faster VTs (use dependency)
QT interval lengthening during VT	Prolongation of the action potential may associate TdP due to combination of relative bradycardia and bradycardia-dependent AAD-induced long QT after tachycardia termination	Mainly with Class III drugs. Not expected with Class Ia drugs Post-termination long QT may relate to reverse use dependency of Class III AAD

Abbreviations: AAD, anti-arrhythmic drug; ECG, electrocardiogram; VM, Vaughan Williams; VT, ventricular tachycardia.