What does it mean when a pacemaker fails to capture in an adult patient with a history of bradyarrhythmia (e.g., sinus node dysfunction or atrioventricular block)?

Pacemaker Failure to Capture

Loss of capture means the pacemaker delivers an electrical impulse (visible as a pacing spike on ECG) but fails to depolarize the myocardium, resulting in no subsequent P wave or QRS complex—this represents a potentially life-threatening malfunction that requires immediate evaluation and intervention. 1

Definition and Clinical Significance

Failure to capture occurs when the pacemaker's electrical stimulus is insufficient to depolarize cardiac tissue, leaving the patient without the intended pacing support. 2 This malfunction can occur anywhere within the pacing system—from the pulse generator through the leads to the electrode-myocardium interface. 1

The clinical consequences depend entirely on the patient's underlying rhythm:

• Pacemaker-dependent patients (those with complete heart block or no escape rhythm) face immediate hemodynamic collapse and potential cardiac arrest when capture fails. 2
• Non-dependent patients may tolerate intermittent loss of capture if their intrinsic rhythm provides adequate cardiac output. 2

Causes of Loss of Capture

Acute Causes (Within Days to Weeks of Implantation)

The most common acute cause immediately after implantation is lead dislodgement or malposition. 2 This typically occurs within the first few weeks as the lead has not yet fibrosed into place. 2

Other acute causes include:

• Myocardial perforation with the lead tip no longer in contact with viable myocardium. 2
• Inadequate initial lead positioning during the implantation procedure. 2

Chronic Causes (Months to Years After Implantation)

An increase in capture threshold over time is the predominant chronic mechanism, requiring higher energy output than the pacemaker is programmed to deliver. 2 This threshold elevation results from:

• Fibrosis at the electrode-myocardium interface, which increases impedance and reduces effective current delivery. 2
• Lead fracture or insulation break, preventing adequate current transmission to the myocardium. 2
• Exit block, where local tissue changes prevent electrical propagation despite adequate lead function. 2
• Progressive cardiomyopathy with reduced myocardial excitability. 2

Metabolic and Pharmacologic Causes

Several reversible factors can acutely elevate capture thresholds: 2

• Severe hyperkalemia (>6.5-7.0 mEq/L) increases threshold dramatically. 2
• Severe acidemia impairs myocardial responsiveness. 2
• Class I antiarrhythmic drugs (flecainide, propafenone) increase capture thresholds. 2
• Severe hypothyroidism can elevate thresholds. 2

Technical and Programming Issues

• Inappropriately low output settings programmed below the patient's actual capture threshold. 2
• Battery depletion resulting in insufficient voltage delivery (though modern devices typically alert before complete failure). 2
• External electromagnetic interference from sources like MRI or electrocautery. 2

Diagnostic Approach on ECG

On ECG, loss of capture appears as pacing spikes without subsequent atrial (P wave) or ventricular (QRS complex) depolarization. 1 The key is distinguishing this from normal function:

• Pacing spike present + no P wave or QRS = loss of capture. 1
• No pacing spike + no P wave or QRS = failure to pace (undersensing or failure to output). 1
• Pacing spike + appropriate P wave or QRS = normal capture. 1

Immediate Management Priorities

For pacemaker-dependent patients with symptomatic bradycardia or hemodynamic instability, immediate transcutaneous pacing or temporary transvenous pacing is required while the underlying cause is identified. 2 This is a medical emergency requiring urgent intervention. 1

For stable patients:

• Interrogate the device immediately to assess programmed output, measured impedance, and capture thresholds. 2
• Obtain chest X-ray to evaluate for lead dislodgement, fracture, or perforation. 2
• Check electrolytes (potassium, magnesium, calcium) and correct abnormalities. 2
• Review medications for drugs that increase capture threshold. 2
• Assess metabolic status including thyroid function and acid-base balance. 2

Definitive Management

If capture threshold has increased but the lead is intact and well-positioned, reprogram the pacemaker to higher output (typically 2-3 times the measured threshold as a safety margin). 2 The ACC/AHA guidelines reference capture thresholds as a critical parameter requiring monitoring. 3

Lead revision or replacement is required for: 2

• Confirmed lead dislodgement or fracture on imaging. 2
• Persistently elevated thresholds that cannot be managed with programming adjustments (typically >5V at 0.5ms). 2
• Myocardial perforation requiring lead repositioning. 2

Critical Pitfalls

• Never assume loss of capture is benign—always assess the patient's pacemaker dependency and hemodynamic status first. 1, 2
• Reversible causes must be excluded before attributing loss of capture to device malfunction requiring invasive intervention. 2
• In patients with neuromuscular diseases (myotonic dystrophy, Kearns-Sayre syndrome), even minor pacing abnormalities warrant aggressive evaluation given unpredictable progression of conduction disease. 4
• Battery depletion typically provides warning through elective replacement indicators; sudden complete loss of capture from battery failure is rare with modern devices. 2