Intermittent failure to capture: What is the mechanism?

Case report An 82-year-old Caucasian female patient, who had a history of hypertension, dual-chamber pacer implantation for paroxysmal atrial fibrillation, and sick sinus syndrome 3 years ago, was transferred from an outside hospital for evaluation and management of a wide complex tachycardia at 115 beats per minute (bpm). Her home medications included candesartan-hydrochlorothiazide (32/12.5 mg daily), flecainide (100 mg twice daily), metoprolol tartrate (25 mg twice daily), and amiodarone (200 mg daily). She was started on doxycycline for left foot infection 4 days prior to the admission, which resulted in nausea and multiple episodes of vomiting. She was hemodynamically stable. Initial laboratory test results were pertinent to acute kidney injury, with serum bicarbonate level of 12 mmol/L (normal range 17–29 mmol/L), blood urea nitrogen level of 63 mg/dL (normal range 8–23 mg/dL), and serum creatinine concentration of 2.5 mg/dL (normal 0.5–1.0 mg/dL). Her presenting electrocardiogram (ECG) showed a wide complex rhythm with intermittent loss of ventricular capture (Figure 1A). What is the mechanism of this intermittent failure to capture? The initial ECG (Figure 1A) showed a very wide complex tachycardia (QRS duration of 240 ms) at 115 bpm with group beating due to intermittent failure to capture. An examination of the lead V1 results demonstrated P waves preceding every QRS complex, which was consistent with P