An Irregular Wide Complex Tachycardia
A 66-year-old woman with a history of hypertension and persistent atrial fibrillation was referred to the Arrhythmia Clinic. Before her visit, a routine 12-lead ECG was ordered (Figure 1). The patient was asymptomatic except for minor palpitations. Her medicine regimen included apixaban, flecainide 150 mg twice daily, lisinopril, loratadine, metoprolol, and simvastatin.
What is the cardiac rhythm and what should be the initial treatment?
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Response to ECG Challenge
The ECG shows a very wide QRS complex tachycardia (QRS duration 280 ms) with variation in morphology. Following a pause of 700 ms, there are repeating sequences of 6 to 7 beats with cycle lengths of 400 to 415 ms. A second ECG demonstrated that the QRS morphology changed from a right bundle-branch block type pattern to a left bundle-branch block type pattern in lead V1 (Figure 2). On interruption of the tachycardia, atrial fibrillation with an atypical left bundle-branch block was observed followed by resumption of the wide complex tachycardia. These features are consistent with flecainide-induced, pleomorphic ventricular tachycardia.
An intravenous bolus of sodium bicarbonate was given in the clinic with return to atrial fibrillation (Figure 3). Prior medical records showed QRS duration of 84 ms before initiating flecainide with a normal echocardiogram and nuclear stress test. On admission to the hospital, the serum flecainide level measured 1.8 μg/mL.
Flecainide has a high affinity for open-state Na+ channels with slow unbinding kinetics. Flecainide also blocks the rapid component of the delayed rectifier current (IKr) and reduces spontaneous sarcoplasmic reticulum Ca2+ release by inhibiting ryanodine receptors. The mechanism of flecainide-induced ventricular tachycardia is uncertain. In canine studies, ventricular tachycardia (VT) was inducible with programmed stimulation after flecainide loading in 4 of 13 healthy dogs (31%) in comparison with 15 of 19 dogs after myocardial infarction.1 Spontaneous VT occurred in 8 of 19 dogs with prior myocardial infarction but in no healthy dogs.1 Rate-dependent conduction block transverse to fiber orientation was observed.1 In the present patient, the first and subsequent beats of each sequence of VT were similar in morphology, suggesting a focal mechanism, consistent with ECG and action potential recordings from isolated perfused guinea pig hearts treated with flecainide.2 Flecainide prolongs action potential duration significantly more in the left than in the right ventricle, thereby increasing action potential duration dispersion. In animal models, the ECG morphology of the first and subsequent beats of spontaneous VT had a consistent morphology suggesting a focal mechanism.2 In the present case, the spontaneous change from a right bundle-branch block to a left bundle-branch block QRS pattern during longer episodes of VT is consistent with either reentry or induction of a second focal mechanism.
VT induced by class 1C agents may be resistant to direct current cardioversion. Sodium bicarbonate is effective by increasing serum sodium concentration, thereby competing with the drug for negatively charged sodium channels. In addition, alkalinization shifts more of the drug to the negatively charged state, thereby reducing its entry into sodium channels.3
Our patient was treated by discontinuation of flecainide and catheter ablation of atrial fibrillation.
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- © 2017 American Heart Association, Inc.
- Ranger S,
- Nattel S
- Bou-Abboud E,
- Nattel S