Device Troubleshooting

Failure to capture means the device delivers a pacing stimulus, but no myocardial depolarization follows. On ECG, pacing spikes appear at the programmed rate with no QRS complex after each spike.

In the first weeks after implant, the most common cause is lead dislodgement. The lead tip has shifted away from excitable myocardium. A chest X-ray confirms the position change, and threshold testing shows a markedly elevated capture threshold or no capture at any output.

Later, threshold rise from inflammation or fibrosis at the lead tip can exceed the programmed output. This is sometimes called exit block. Steroid-eluting leads were designed to minimize this problem, and they have largely succeeded.

Battery depletion reduces the available voltage. As the generator approaches end of life, output may fall below the capture threshold. This is detectable during routine interrogation well before it becomes a clinical problem.

Lead fracture disrupts the electrical circuit entirely. A fractured conductor cannot deliver the pacing stimulus to the myocardium. Lead impedance rises sharply, often above 2000 ohms. The diagnosis is confirmed by impedance trends and fluoroscopic inspection of the lead.

Undersensing occurs when the device fails to detect native cardiac activity and delivers pacing stimuli despite the presence of intrinsic beats. On ECG, pacing spikes appear where they should not, landing on or near native QRS complexes without regard for the underlying rhythm.

The fundamental issue is that the intrinsic electrical signal at the lead tip is too small for the device to recognize. Low signal amplitude occurs with lead dislodgement, progression of myocardial disease, or unfavorable lead position relative to the local electrical vector.

Sensitivity is programmed as a voltage threshold. A lower number (for example, 0.5 mV) means higher sensitivity: the device will detect smaller signals. A higher number (for example, 5.0 mV) means lower sensitivity: only large signals are counted. If the programmed value is set too high, the device misses genuine depolarizations.

The fix depends on the cause. If the intrinsic electrogram amplitude is adequate, reprogramming the sensitivity threshold resolves the problem. If the amplitude is genuinely too low because of lead malfunction or progressive disease, the lead may need revision.

Oversensing means the device detects electrical signals that are not true cardiac depolarizations and counts them as heartbeats. The consequences depend on the device type.

In a pacemaker, oversensing causes inappropriate inhibition. The device mistakenly believes the heart is beating on its own and withholds pacing. A pacemaker-dependent patient can develop symptomatic pauses or asystole.

In an ICD, oversensing can trigger inappropriate shocks. If the device counts artifact as rapid ventricular activity, it may diagnose VF and deliver a shock to a patient in normal sinus rhythm.

T-wave oversensing occurs when the device counts the T wave as a separate R wave, effectively doubling the detected ventricular rate. The real rate may be 80 bpm, but the device counts 160 bpm and enters the VT zone. This is more common with integrated bipolar leads and in patients with prominent T waves.

Lead fracture noise generates high-frequency electrical artifacts. The device interprets these short, irregular signals as VF. The intervals are characteristically extremely short (below 110ms), faster than any physiological tachycardia. Lead impedance is typically elevated.

Diaphragmatic myopotentials can be sensed in unipolar configurations. The electrical activity from the diaphragm is picked up by the lead and counted as cardiac signal. Switching to bipolar sensing usually eliminates this.

Pacemaker-mediated tachycardia (PMT) is a reentrant loop unique to dual-chamber pacemakers. The device itself becomes one limb of the circuit.

The sequence begins when a ventricular event (paced or premature) conducts retrograde through the AV node to the atrium. The atrial channel senses this retrograde P wave and interprets it as a native atrial beat. Following its programmed AV delay, the device paces the ventricle. That ventricular paced beat again conducts retrogradely to the atrium, and the cycle repeats.

The resulting tachycardia runs at a regular rate determined by the programmed upper tracking rate. On ECG, it appears as a paced tachycardia: regular, at a rate that matches the device's programmed maximum, with retrograde P waves visible after each paced QRS.

The device can prevent PMT through the PVARP (post-ventricular atrial refractory period). During this interval after a ventricular paced or sensed event, the atrial channel ignores any sensed signals. If the PVARP is long enough to cover the retrograde conduction time, the retrograde P wave falls within the refractory period and is not tracked.

Most modern devices include automatic PMT termination algorithms. When the device recognizes a sustained sequence of ventricular pacing followed by atrial sensing at the upper tracking rate, it extends the PVARP for one cycle, breaks the chain, and restores normal tracking.

Lead failure produces distinct electrical signatures, each pointing to a specific mechanism.

A fractured conductor shows high impedance, because the break in the wire increases resistance. Pacing may fail intermittently or completely. On the intracardiac electrogram, noise artifacts from the fracture site appear as high-frequency signals. Fluoroscopy can sometimes visualize the fracture directly, though many breaks are subtle and visible only under magnification.

An insulation breach shows the opposite impedance pattern: low impedance. Current leaks through the damaged insulation into the surrounding tissue, creating an alternate electrical path. Oversensing is common, as the exposed conductor picks up extraneous signals. Capture may remain intact initially but deteriorates as the breach widens.

Lead perforation occurs when the lead tip migrates through the myocardial wall. Capture thresholds may change abruptly. Diaphragmatic stimulation (phrenic nerve capture) can occur if the lead perforates the thin RV free wall. Pericardial effusion is the most serious complication and should be evaluated promptly with echocardiography.

When a lead fails irreparably or becomes infected, extraction is necessary. Modern extraction techniques use laser or mechanical sheaths to free the lead from fibrous adhesions that develop over months to years of implantation.

Device generators have a finite battery life. The lithium-iodide cells in pacemakers typically last 8 to 12 years. ICD generators last 5 to 8 years because capacitor charging for defibrillation draws significantly more current.

As the battery depletes, the voltage drops in a predictable curve. The device monitors this internally and flags two critical milestones.

The elective replacement indicator (ERI) signals that the battery is approaching depletion but still has enough reserve for safe operation over weeks to months. At ERI, many devices switch to a backup pacing mode, typically VVI at a fixed lower rate. This ensures basic pacing while alerting the clinical team that generator replacement is needed.

End of life (EOL) follows ERI if the generator is not replaced. Pacing output becomes unreliable, and the device can no longer guarantee therapy delivery. Reaching EOL should be prevented through routine monitoring and timely replacement.