Failure to capture12/17/2023 ![]() Furthermore, it has a known negative inotropic effect ( 6). In addition, flecainide can increase the capture threshold of pacemakers by up to 200% ( 4), which leads to loss of capture with a correlation between the degree of QRS widening and the increase in pacing thresholds.įlecainide has also been associated with increased dyssynchrony with decreased cardiac output in an animal model with baseline left bundle branch block ( 5). With standard programming, the timing of the pacing spike fell in a refractory period after the wide preceding ventricular paced complex. These decreased conduction times, with corresponding widening of the paced QRS morphology and increased refractoriness, resulted in intermittent capture. Therefore, toxic levels can lead to an extremely wide QRS and QTc, as seen in our patient. Furthermore, it inhibits the rapid phase of the delayed rectifier potassium current (IKr), which leads to prolongation of ventricular action potentials ( 3). Specifically, its high affinity for open-state sodium channels with slow unbinding from these channels in diastole leads to prolonged ventricular refractoriness ( 3). The acute changes of the QRS and QTc width associated with pacemaker loss of capture were consistent with the acute flecainide toxicity confirmed by serum levels.įlecainide is a Class IC antiarrhythmic that slows phase 0 of the fast sodium channel, which leads to decreased conduction velocity of the conduction system and myocardial electrical propagation ( 2). Instead, flecainide toxicity had produced a dose-dependent decrease in intracardiac conduction, increased ventricular refractoriness, and had consequently affected the ability of the pacemaker to capture both the atrial and ventricular channels ( 1). However, there were no issues with the pacemaker’s placement or programming. When the patient first presented with loss of capture, the initial reflex was to search for an intrinsic malfunction of his pacemaker. This case report illustrated the multiple cardiovascular effects of flecainide toxicity that could affect device therapy. Coronary angiography showed no evidence of obstructive coronary artery disease. Marked mechanical ventricular dyssynchrony was present ( Video 1). Echocardiography after resuscitation showed an ejection fraction of 20% to 25% with marked asymmetric LVH, with a measured interventricular septum of 1.8 cm ( Figure 3). His initial flecainide level was elevated to 2.44 μg/ml, which was more than twice the upper limit of normal (0.99 μg/ml). The initial lactic acid on admission was 6.4 with a pH of 7.05 and bicarbonate of 20 mmol/l he subsequently developed acute renal failure. No ventricular arrhythmias were detected. Thus, we did not know the nadir ventricular rate during arrest. These events were incidentally captured as automatic mode switching events because of lack of capture and oversensing in the atrial channel. There were clear episodes of loss of reliable ventricular and atrial capture that seemed to correlate temporally to the presumed time of the patient’s arrest ( Figure 2). Ventricular outputs were 2.5 V at 0.4 ms but increased at the time of interrogation to 4 V to provide a 2:1 safety margin. This threshold was performed several hours after initial resuscitation. The patient’s pacemaker interrogation revealed programming of DDDR 70 with increased ventricular thresholds from a baseline of 1 V at 0.4 ms to 1.75 V at 0.4 ms. The ventricular rate by ECG was approximately 40 beats/min ( Figure 1A). Electrocardiography (ECG) revealed a wide complex rhythm (QRS duration ∼320 ms) with intermittent capture of his pacemaker spikes (2:1 ventricular capture). ![]() Cardiac auscultation revealed a slow but regular rhythm with normal S1 and S2 without significant murmurs or gallops. As per emergency room documentation, initial heart rate after resuscitation was approximately 30 beats/min, with a mean arterial pressure of 60 mm Hg. The initial physical examination was significant for an unresponsive man on mechanical ventilation.
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