This is only relevant in rate responsive pacemakers. Failure to rate adjust, which means that the pacemaker fails to adjust its rate according to haemodynamic needs.Failure to sense (undersensing), which means that it fails to sense true P-waves or R-waves.Sensing of such signals normally inhibits the pacemaker.
Oversensing, which means that the pacemaker senses signals that are not true P-waves or R-waves.Failure to pace (FTP), which means that the pacemaker does not stimulate as expected.
Failure to capture (FTC), which means that the pacemaker stimulations do not result in myocardial activation.The nonpaced ECG before and after treatment demonstrated remarkable narrowing of QRS complexes ( Figures 2A and 2B).Pacemaker malfunction, troubleshooting and ECGĬonventional surface ECG can reveal the following types of pacemaker dysfunction: After 48 hours of conservative management, her acidosis and acute kidney injury resolved. Flecainide levels obtained at the time of admission were elevated, at 1400 ng/mL (normal 200–1000 ng/mL). Anion gap metabolic acidosis, in the setting of a very wide QRS, was acutely treated with 100 milliequivalents of intravenous sodium bicarbonate. The patient was aggressively hydrated with intravenous fluids. The pacing device was reprogrammed from DDD mode to DDI mode at 70 bpm to avoid tracking and to decrease the ventricular rate. Flecainide and amiodarone therapies were discontinued. These ECG findings in our patient in the setting of acute kidney injury from intravascular volume depletion (multiple episodes of vomiting, use of diuretic) and concurrent use of amiodarone strongly raised the suspicion for flecainide toxicity. This phenomenon is referred to as functional noncapture. The intermittent failure to capture during ventricular pacing is the result of the pacing stimulus occurring during the refractory period of the previous beat, with a very delayed depolarization ( Figures 1A and 1B). This phenomenon of rate-dependent or use-dependent widening of QRS complexes is classically seen with flecainide (class IC antiarrhythmic agent). Interestingly, the width of the QRS complex gradually increased such that the last QRS complex before the pause was much wider than the first QRS after the pause. Differential diagnoses included sinus tachycardia or atrial tachycardia with ventricular tracking. This finding was also demonstrated on the intracardiac electrogram from the pacing device ( Figure 1B).
An examination of the lead V1 results demonstrated P waves preceding every QRS complex, which was consistent with P synchronous ventricular pacing. 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. What is the mechanism of this intermittent failure to capture? Her presenting electrocardiogram (ECG) showed a wide complex rhythm with intermittent loss of ventricular capture ( Figure 1A). 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). She was started on doxycycline for left foot infection 4 days prior to the admission, which resulted in nausea and multiple episodes of vomiting. 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). 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).
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