A 59-year-old male was referred to the emergency room with palpitations. He underwent radiofrequency ablation of persistent atrial fibrillation 2 years before and was taking flecainide 75 mg twice per day, bisoprolol 2.5 mg per day, and warfarin sodium 3.75 mg per day. His blood pressure was 120/80 mm Hg, heart rate 202 bpm, and oxygen saturation 99% on room air. His serum sodium level was 129 mEq/L (normal range, 135–145 mEq/L), serum potassium level 5.1 mEq/L (normal range, 3.5–5.5 mEq/L), and serum creatinine 1.06 mg/dL (normal range, 0.7–1.2 mg/dL). A 12-lead ECG (Figure 1) was obtained on admission. What are the notable ECG findings? What is the diagnosis?

Figure 1. A 12-lead ECG obtained upon admission.

Please turn the page to read the diagnosis.

The ECG (Figure 1) exhibits a relatively regular wide QRS complex tachycardia at a rate of about 200 bpm. The QRS morphology exhibits a right bundle branch block pattern with right axis deviation. The predominant positive force in lead aVR is more suggestive of ventricular tachycardia. However, note that there was 1 dropped QRS complex (Figure 2A). A careful inspection revealed subtle morphologic changes in the QRS waves unveiling P waves before the dropped QRS complex, as well as a P wave between QRS complexes at the same PP interval. The cycle length of the P wave is constant at 300 ms. The PR interval gets longer and the RR interval also gets longer before the dropped complex. That is compatible with atypical atrioventricular Wenckebach block (5:4 conduction pattern) (Figure 2B). In typical atrioventricular Wenckebach conduction, the PR interval increases and the RR interval decreases before the atrioventricular block.¹ The rhythm changed to a narrow QRS complex tachycardia at a rate of about 100 bpm (Figure 3). Of note, the PP interval was identical (300 ms) to that seen in Figure 2, which was compatible with the same rhythm as the atrial tachycardia that changed from 1:1 to 2:1 atrioventricular conduction. He underwent a successful radiofrequency ablation of an atrial focus on the ridge between the mitral annulus and left lower pulmonary vein.

Figure 2. A 12-lead ECG obtained upon admission. A, Note that there was 1 dropped QRS complex (box with broken line). The arrowheads indicate P waves. B, Magnified strip from the box. A careful inspection revealed subtle morphologic changes in the QRS waves unveiling P waves before the dropped QRS complex, as well as a P wave between QRS complexes at the same PP interval. The cycle length of the P waves is constant at 300 ms. The PR interval gets longer and the RR interval also gets longer before the dropped complex. That is compatible with atypical atrioventricular Wenckebach block (5:4 conduction pattern, red circles).

Figure 3. Follow-up ECG. The rhythm changed to a narrow QRS complex tachycardia at a rate of about 100 bpm. Of note, the PP interval is identical (300 ms) to that seen in Figure 2, which is compatible the same rhythm of the atrial tachycardia that changed from 1:1 to 2:1 atrioventricular conduction. The red circles indicate P waves.

Flecainide blocks the cardiac sodium channels and slows the velocity of the membrane depolarization without affecting the repolarization, which results in a prolongation of the P-wave duration, PR interval, and QRS width. Flecainide binds primarily to activated sodium channels, and the blocking effect increases with faster heart rates, a so-called “use dependency.” Flecainide slows the conduction in the atrial tissue more than it prolongs the refractoriness, which promotes an organized atrial activity, especially atrial flutter. It prolongs the flutter cycle length and may paradoxically increase the ventricular rate by promoting 1:1 atrioventricular conduction, which can degenerate into lethal ventricular arrhythmias. Therefore, atrioventricular nodal blocking agents should be coadministered with flecainide to mitigate these risks. In the current case, slowing of the heart rate during 2:1 conduction was accompanied by QRS narrowing. Those changes reflected flecainide’s use-dependent properties.

Excess QRS widening is a reflection of flecainide toxicity. Flecainide has a narrow therapeutic window (0.2–1.0 μg/mL), which enhances the possibility of drug-related toxic effects. In flecainide overdosing, the adverse effects are mainly a result of an excessive cardiac sodium channel blockade causing delayed conduction, negative inotropy,² and cardiac arrhythmias, including bradyarrhythmias, atrioventricular nodal block, and ventricular tachycardia/fibrillation.³ It is important to emphasize that flecainide toxicity may result in a QRS widening that mimics the features of ventricular tachycardia. A mortality rate of 22% associated with class Ic drug overdosing has previously been reported.⁴ The discontinuation of flecainide and sodium bicarbonate therapy has been proposed as a treatment for sodium channel blocker toxicity.⁵ In this patient, ablation of the atrial tachycardia focus was chosen to preclude its acting as a possible trigger of atrial fibrillation.

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For Sources of Funding and Disclosures, see page 966.

Circulation is available at www.ahajournals.org/journal/circ .

一名 59 岁男性因心悸被送往急诊室。2年前，他接受了持续性心房颤动的射频消融术，并服用氟卡尼75毫克每天两次，比索洛尔每天2.5毫克，华法林钠3.75毫克每天。他的血压为 120/80 mm Hg，心率为 202 bpm，室内空气中的氧饱和度为 99%。他的血清钠水平为129 mEq/L（正常范围，135-145 mEq/L），血清钾水平为5.1 mEq/L（正常范围，3.5-5.5 mEq/L），血清肌酐1.06 mg/dL（正常范围） ，0.7–1.2 毫克/分升）。入院时进行了 12 导联心电图（图 1）。心电图有哪些值得注意的发现？诊断是什么？

图 1. 入院时获得的 12 导联心电图。

请翻页阅读诊断书。

心电图（图 1）显示相对规则的宽 QRS 波心动过速，速率约为 200 bpm。QRS 形态呈现右束支传导阻滞模式，电轴右偏。aVR 导联的主要正向力更提示室性心动过速。然而，请注意，有 1 个 QRS 复合波下降（图 2A）。仔细检查发现 QRS 波存在细微的形态变化，揭示了 QRS 波群下降之前的 P 波，以及相同 PP 间期的 QRS 波群之间的 P 波。P 波的周期长度恒定为 300 ms。在复合体下降之前，PR 间期变长，RR 间期也变长。这与非典型房室温克巴赫传导阻滞（5:4 传导模式）兼容（图 2B）。在典型的房室文克巴赫传导中，房室传导阻滞之前PR间期增加，RR间期减少。¹心律变为窄 QRS 波心动过速，频率约为 100 bpm（图 3）。值得注意的是，PP 间期与图 2 中所示的相同（300 ms），这与房室传导从 1:1 变为 2:1 的房性心动过速具有相同的节律。他成功地对二尖瓣环和左下肺静脉之间的心房病灶进行了射频消融。

图 2. 入院时获得的 12 导联心电图。A，请注意，有 1 个 QRS 波群下降（带虚线的方框）。箭头表示 P 波。B，盒子上的放大条。仔细检查发现 QRS 波存在细微的形态变化，揭示了 QRS 波群下降之前的 P 波，以及相同 PP 间期的 QRS 波群之间的 P 波。P 波的周期长度恒定为 300 ms。在复合体下降之前，PR 间期变长，RR 间期也变长。这与非典型房室文克巴赫传导阻滞（5:4 传导模式，红色圆圈）相一致。

图 3. 后续心电图。心律变为窄 QRS 波心动过速，频率约为 100 bpm。值得注意的是，PP 间期与图 2 中所示的相同（300 ms），这与房室传导从 1:1 变为 2:1 的房性心动过速的相同节律兼容。红色圆圈表示 P 波。

氟卡尼阻断心脏钠通道并减慢膜去极化速度而不影响复极化，从而导致 P 波持续时间、PR 间期和 QRS 宽度延长。氟卡尼主要与激活的钠通道结合，阻断作用随着心率加快而增强，即所谓的“使用依赖性”。氟卡尼减缓心房组织传导的作用大于延长不应期，从而促进有组织的心房活动，尤其是心房扑动。它延长了扑动周期长度，并且可能通过促进 1:1 房室传导而反而增加心室率，这可能会退化为致命的室性心律失常。因此，房室结阻滞剂应与氟卡尼联合使用以减轻这些风险。在当前病例中，2:1 传导期间心率减慢伴随着 QRS 变窄。这些变化反映了氟卡尼的依赖于使用的特性。

QRS 过度增宽是氟卡尼毒性的反映。氟卡尼的治疗窗较窄（0.2–1.0 μg/mL），这增加了药物相关毒性作用的可能性。氟卡尼过量服用时，不良反应主要是由于过度的心脏钠通道阻断导致传导延迟、负性肌力变性²和心律失常，包括缓慢性心律失常、房室结传导阻滞和室性心动过速/颤动。³需要强调的是，氟卡尼毒性可能导致 QRS 增宽，类似于室性心动过速的特征。此前曾报道与 Ic 类药物过量相关的死亡率为 22%。⁴已建议停止氟卡尼和碳酸氢钠治疗作为钠通道阻滞剂毒性的治疗方法。⁵在该患者中，选择消融房性心动过速病灶以防止其成为心房颤动的可能触发因素。

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没有任何。

有关资金来源和披露信息，请参阅第 966 页。

流通量可在 www.ahajournals.org/journal/circ 上获取。