The 12-lead ECG demonstrates atrial fibrillation with a narrow QRS complex rhythm at a rate of 55 beats/minute with intermittent irregularity. More importantly, there are small pacer spikes seen throughout the 12-lead ECG that have no clear or consistent association with the QRS complexes. (Fig. 2: circles.) This finding, along with the fact that her rate is bradycardic and below most programmed pacing thresholds is consistent with pacemaker failure to capture.
Implantable cardiac pacemakers were first used to prevent Adams-Stokes attacks. Since then, indications for pacemakers have grown remarkably and now include atrioventricular (AV) node and sinus node dysfunction, hypersensitive carotid sinus syndrome and neurally-mediated syncope (vasovagal syncope), prevention of tachycardia with long QT syndrome, hypertrophic cardiomyopathy, certain cases of congestive heart failure, and prevention of atrial fibrillation. (Circulation 1998;97:1325.) Advances in technology, expanding indications, and the aging population ensure that EPs will encounter more patients with cardiac pacemakers on a regular basis.
A five-position code has been developed to describe pacemakers. (Pacing Clin Electrophysiol 1993;16:1776.) Position I indicates the chambers being paced, atrium (A), ventricle (V), both (D, dual), or none (0). Position II gives the location where the pacemaker senses native cardiac electrical activity (A, V, D, or O). Position III indicates the pacemaker's response to sensing: triggering (T), inhibition (I), both (D), or none (O). Position IV indicates the programmability of the pacemaker and the capability to adaptively control rate; position V identifies the presence of antitachydysrhythmia functions. Pacemakers are commonly classified to the first three position codes. Most patients will have a card in their wallet identifying the make and model of pacemaker. Manufacturers also place an identification number in the generator that is sometimes visible on chest x-ray.
The most commonly encountered pacer is the DDD pacemaker, where both the atria and the ventricles are sensed and either paced or inhibited depending on the native cardiac activity sensed. VVI pacing is useful in those with chronically ineffective atria, such as chronic atrial fibrillation or atrial flutter. In this mode, the ventricle is sensed and paced. If the native ventricular activity is sensed, then pacing is inhibited.
Because the ventricular pacing lead is placed in the right ventricle, the ventricles depolarize from right to left rather than by the regular conduction system, producing an overall QRS morphology similar to a left bundle branch block with QRS interval prolongation (occasionally, intracardiac pacemaker leads may be placed over the left ventricle, resulting in a right bundle branch block pattern). (Emerg Med Clinics NA 2006;24:179.) Because of the abnormal ventricular depolarization seen in paced rhythms, repolarization also occurs abnormally, and ST segments and T waves should typically be discordant with the QRS complex. (Acad Emerg Med 1998;5:52.)
Pacemaker malfunction includes failure to pace, failure to capture, undersensing, and pacemaker-mediated dysrhythmias. Failure to pace occurs when the pacemaker does not fire when pacing should occur. On the ECG, there are no visible pacing spikes where they should have occurred. Causes include oversensing, pacing lead problems (dislodgement or fracture), battery or component failure, and electromagnetic interference.
Failure to capture occurs when a pacing stimulus is generated, but fails to trigger myocardial depolarization. On the ECG, failure to capture is identified by the presence of pacing spikes without associated myocardial depolarization. Causes include pacing lead problems, battery or component failure, low pacing voltage or elevated myocardial pacing thresholds, and exit block. Undersensing occurs when a pacemaker fails to sense or detect native cardiac activity. Pacing spikes will be seen when none should occur.
Patients with pacemaker malfunction often have vague and nonspecific symptoms. Beyond the 12-lead ECG, cautious use of a magnet can assist in evaluating pacer function. For example, if there is no pacemaker activity on the ECG, placing a magnet over the pacer will switch the pacemaker to asynchronous pacing and allow for assessment of capture. Appropriate experience with this diagnostic approach is urged prior to its use, however. Similarly, if the patient's native cardiac rhythm is above the lower rate threshold for pacing, cautious attempts to slow the rate with carotid massage or adenosine can be helpful, but should be performed with extreme caution in the pacemaker patient. Finally, if routine evaluation yields no abnormalities, the pacemaker should be interrogated.
The cause of this patient's pacemaker malfunction and failure to capture were seen on the chest radiograph, which demonstrated a fracture in the pacing wire. (Fig. 3: circle.) This wire fracture not only caused the failure to capture, but also failure to sense native ventricular activity as well as some aspect of failure to pace with low amplitude pacer spikes. The patient was admitted to the electrophysiology service, at which time the fractured right ventricular pacing lead as well as pacemaker generator were replaced. After the procedure, the patient's symptoms resolved. A follow-up12-lead ECG demonstrates normal ventricular pacing. (Fig. 4.)
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