CIEDs (such as pacemakers and ICDs) deliver an electrical impulse to the heart muscle to stimulate a contraction, correcting slow or irregular rhythms. The desired outcome is “capture,” where the heart successfully depolarizes and contracts. Failure to Capture (FTC) is a serious malfunction where the device fires its signal, but the heart tissue does not respond, leading to inadequate cardiac output.
Defining Failure to Capture in Cardiac Devices
FTC occurs when the myocardium fails to depolarize following the delivery of an electrical stimulus. The device’s attempt to stimulate the heart is visible on an electrocardiogram (ECG) as a pacing spike. Normally, this spike is followed by a P wave or QRS complex, representing a successful heart contraction.
In FTC, the pacing spike is visible, but the expected contraction waveform is absent, demonstrating dissociation between the device’s electrical output (pacing) and the heart’s biological response (capture). This lack of response often occurs because the energy delivered falls below the minimum required to excite the tissue, known as the pacing threshold.
The pacing threshold is the lowest amount of energy that reliably produces a captured beat. If the delivered energy is less than this threshold, the pacing spike becomes ineffective, resulting in FTC.
Underlying Causes and Contributing Factors
FTC causes involve device hardware issues and changes in the patient’s biological environment. A common acute cause, particularly shortly after implantation, is lead dislodgement, where the lead tip moves away from its intended contact point. This movement prevents the electrical current from effectively reaching the tissue.
Over time, mechanical stress can cause a lead fracture or a break in the insulation material. These breaks divert electrical energy away from the heart muscle, making the effective output insufficient for capture. Battery depletion is a less common cause, resulting in a weak electrical stimulus.
Physiological changes can also elevate the pacing threshold, making the device’s programmed output inadequate. Long-term causes include the formation of scar tissue or fibrosis around the electrode tip, known as an exit block. Acute changes, such as severe electrolyte imbalances (hyperkalemia) or acidosis, significantly decrease heart muscle excitability. Certain antiarrhythmic medications can similarly raise the energy requirement for successful capture.
Clinical Presentation and Diagnostic Confirmation
The clinical presentation of FTC is related to the loss of a necessary heart rhythm. Patients who rely heavily on their device may experience signs of low cardiac output, such as lightheadedness, dizziness, or syncope. Other symptoms include unusual fatigue, shortness of breath, and palpitations.
Diagnosis relies primarily on visual evidence from an ECG. The characteristic finding is a pacing spike not followed immediately by the expected P wave or QRS complex, indicating the heart did not respond. This signature differentiates FTC from “failure to pace,” where the device fails to generate the spike entirely.
A more in-depth diagnostic step is device interrogation, using a specialized external programmer to communicate with the implanted device. This procedure allows providers to check stored data, confirm programmed output settings, and directly measure the pacing threshold. A pacing threshold significantly higher than the device’s programmed output confirms the heart tissue requires more energy than it is currently receiving.
Management Strategies and Device Adjustments
Immediate management focuses on restoring successful capture and stabilizing the patient’s heart rhythm. A common initial non-invasive adjustment is to reprogram the device to temporarily increase its energy output (voltage or pulse width). This aims to deliver an electrical impulse strong enough to overcome the elevated pacing threshold and restore a stable heart rate.
Clinicians simultaneously address any reversible underlying medical conditions. If blood tests reveal an electrolyte imbalance, such as hyperkalemia, immediate medical treatment is initiated to correct the chemical abnormality. Adjusting or temporarily withholding medications that affect myocardial excitability, such as certain antiarrhythmic agents, is another common strategy.
If reprogramming or medical therapy fails, a more permanent solution, often surgical intervention, is required. When lead dislodgement or fracture is confirmed, the lead must be surgically repositioned, repaired, or completely replaced. Continuous monitoring is maintained to ensure the long-term stability and effectiveness of the pacing system.