A 68 y/o male c/o light-headedness and near syncope.
Q1. What does the EKG demonstrate?
A1. Pacemaker malfunction – failure to capture and failure to sense
Pacemaker malfunction can be separated into three broad categories: (1) failure to capture (pacemaker spikes not followed by an atrial or ventricular complex), (2) inappropriate sensing (oversensing or undersensing spikes occur prematurely or do not occur even though the programmed interval is exceeded), or (3) inappropriate pacemaker rate. Malfunction is most commonly due to inappropriate sensing, followed by failure to capture.
Failure to capture is most commonly a lead problem (lead displacement or lead fracture). In lead displacement, the chest radiograph may demonstrate the tip of the pacing catheter displaced from the right ventricular apex. The catheter tip is commonly found in the pulmonary outflow tract, where it may have intermittent contact with endocardium, resulting in intermittent failure to pace and sense. The atrial leads of dual-chamber devices are commonly displaced into the body of the right atrium, resulting in loss of contact between the pacing lead and the atrial endocardium. Lead fractures occur at the site of attachment to the pulse generator or at abrupt angulations that serve as stress points. Inadequate contact of the lead with the pulse generator can mimic a lead fracture. Occasionally, when a lead fracture is complete or nearly complete, a break in the catheter or its insulation can be detected on an overpenetrated posteroanterior chest radiograph. Loss of lead–pulse generator contact can be detected on the chest radiograph with close inspection of the pulse generator. Exit block (the failure of an adequate stimulus to depolarize the paced chamber) can also result in failure to pace. Exit block should be considered when failure to capture occurs in the presence of a normally functioning pulse generator and an intact lead system. This problem is most commonly due to changes in the endocardium in contact with the pacing system. Etiologies include ischemia or infarction of the endocardium in contact with the electrodes; systemic hyperkalemia; and the use of class III antiarrhythmic drugs, such as amiodarone, which affect ventricular depolarization.
Failure to sense may result after acute right ventricular infarction or during the progressive fibrosis that accompanies many cardiomyopathies, causing intracardiac signals to decrease in amplitude. Lead displacement, fracture, and poor contact with the endocardium may also cause undersensing. Undersensing is typically recognized electrocardiographically as the appearance of pacemaker spikes occurring earlier than the programmed rate. The spike may or may not be followed by a paced complex, depending on when it occurs during the cardiac refractory period. Failure of a stimulus spike to produce a complex when it occurs during the atrial or ventricular refractory period should not be interpreted as failure to pace.