IBHRE CEPS key terms

The longest coupling interval of a premature extrastimulus that fails to conduct, marking the tissue's recovery limit. Measured during pacing protocols, it defines the window in which reentry can initiate and guides programmed stimulation testing.

A pacing protocol using drive trains plus premature extrastimuli at decrementing coupling intervals to test refractoriness and inducibility. Findings such as inducible ventricular tachycardia help risk-stratify patients and plan ablation or device therapy.

Pacing slightly faster than a reentrant tachycardia so that the circuit is captured without terminating it. On stopping, the post-pacing interval minus tachycardia cycle length reveals how close the pacing site sits to the circuit.

The interval from the last paced beat to the first returned electrogram after overdrive pacing stops. Subtracting the tachycardia cycle length gives the return cycle; small differences indicate pacing near the reentrant circuit.

Capture of a reentrant circuit during pacing without changing the surface P-wave or QRS morphology, because the paced wavefront collides with the activation already traveling the opposite direction. It confirms a protected circuit rather than a bystander pathway.

The interval between consecutive atrial or ventricular activations during a tachycardia. Comparing it with pacing intervals and with PPI values localizes circuits and distinguishes mechanisms such as reentry, automaticity, and triggered activity.

The brief refractory period during which a single stimulus can induce ventricular fibrillation without prior arrhythmia. Its presence during defibrillation threshold testing reflects the heart's electrical instability and the need for reliable shock delivery.

Progressive PR prolongation before a dropped beat, caused by decremental conduction in the AV node. Typical AV nodal Wenckebach is benign; the pattern in His-Purkinje tissue signals more advanced conduction disease and often prompts pacing.

The conduction time from the His bundle electrogram to the earliest ventricular activation, normally 35 to 55 ms. Prolongation suggests His-Purkinje disease and predicts risk of progression to complete heart block.

A narrow-complex tachycardia using fast and slow pathways within the AV node. Typical slow-fast conduction produces a short RP interval; slow pathway modification is the definitive treatment and is highly effective.

The anatomic triangle bounded by the tricuspid annulus, tendon of Todaro, and coronary sinus ostium. It contains the AV node and slow pathway, making it the target region for slow pathway ablation.

Radiofrequency ablation in the inferior triangle of Koch that eliminates slow pathway conduction while preserving AV conduction. Success is judged by loss of dual pathway physiology and non-inducibility of AVNRT.

An anomalous muscular connection between atrium and ventricle that bypasses the AV node. It causes pre-excitation on ECG and can support orthodromic or antidromic tachycardia; ablation targets the pathway along the annulus.

Pre-excitation on ECG combined with symptomatic tachyarrhythmias. Risk of rapid conduction over the pathway during atrial fibrillation makes risk stratification and ablation important, especially in younger patients.

A narrow-complex tachycardia that travels antegrade down the AV node and retrograde up an accessory pathway. It produces a regular rhythm with retrograde P waves and is cured by ablating the pathway.

A macroreentrant atrial tachycardia, typically using the cavotricuspid isthmus, with sawtooth flutter waves. Typical counterclockwise flutter is treated by isthmus ablation, which interrupts the circuit.

Creation of a continuous line of radiofrequency lesions between the tricuspid annulus and inferior vena cava to interrupt typical atrial flutter. Bidirectional isthmus block confirms durable conduction block across the line.

The cornerstone ablation strategy for atrial fibrillation, electrically isolating pulmonary vein ostia from the left atrium. Durable isolation, confirmed by entrance and exit block, correlates with freedom from recurrent arrhythmia.

The extent to which a radiofrequency lesion extends through the full thickness of myocardium, producing durable conduction block. Contact force, power, duration, and catheter stability determine transmurality and long-term success.

A complication of ablation near the right or left phrenic nerve, especially during pulmonary vein isolation or superior vena cava procedures. Continuous diaphragmatic pacing and monitoring help detect and limit this injury.

A rare but often fatal complication of atrial fibrillation ablation in which thermal injury creates a connection between the left atrium and esophagus. Presenting days to weeks later with fever, dysphagia, or neurological signs, it requires urgent evaluation.

Biventricular pacing used in heart failure with reduced ejection fraction and electrical dyssynchrony, typically a wide QRS with left bundle branch block. It improves symptoms and survival in appropriately selected patients.

Pacing that captures the native His-Purkinje system to produce physiologic ventricular activation. It avoids pacing-induced dyssynchrony and is an alternative to biventricular pacing in selected patients with conduction disease.

A QRS pattern with broad, notched complexes in lateral leads and absent septal Q waves, reflecting delayed left ventricular activation. It identifies dyssynchrony responsive to cardiac resynchronization and predicts benefit from biventricular pacing.

Sinus node dysfunction in which paroxysmal atrial tachyarrhythmias are followed by prolonged pauses on termination. Pacing prevents symptomatic bradycardia while rate control or ablation manages the tachyarrhythmia.

Impaired sinoatrial impulse generation or exit, causing bradycardia, pauses, or chronotropic incompetence. Symptomatic cases are treated with atrial pacing, with rate response added when exercise capacity is limited.

A pacemaker feature that changes from a tracking mode to a non-tracking mode during paroxysmal atrial tachyarrhythmias. It prevents rapid ventricular pacing from tracking atrial rates that exceed programmed limits.

Intraoperative induction of ventricular fibrillation to confirm that the implanted device terminates it with a safety margin. It verifies lead position and shock efficacy but is now used selectively based on patient risk.

Shocks or antitachycardia pacing delivered for rhythms other than ventricular tachycardia or fibrillation, such as atrial fibrillation, sinus tachycardia, or lead artifact. Reprogramming, medical therapy, or lead revision reduces recurrence.

A broad-spectrum antiarrhythmic with class III, sodium-channel, and calcium-channel effects. It treats ventricular and atrial arrhythmias but requires monitoring for thyroid, hepatic, pulmonary, and ocular toxicity.

A class III antiarrhythmic that blocks the rapid delayed rectifier potassium current and prolongs repolarization. Initiation requires inpatient monitoring for QT prolongation and torsades de pointes, with dose adjusted for renal function.

Abnormal lengthening of ventricular repolarization that predisposes to torsades de pointes. Drugs, bradycardia, and electrolyte abnormalities are common causes, and the risk guides monitoring during antiarrhythmic initiation.

Use of oral anticoagulants to prevent cardioembolic stroke, guided by validated risk scores such as CHA2DS2-VASc. Direct oral anticoagulants are preferred for most patients, with warfarin reserved for specific indications.

The ability to maintain consistent electrode-tissue contact during mapping and ablation. Poor stability reduces lesion quality and mapping accuracy, so contact-force sensing and respiratory compensation are used to improve it.

Technology that measures the force and direction between an ablation catheter tip and myocardium. Adequate contact force improves lesion depth and reduces steam pops, while excessive force risks perforation.

Three-dimensional reconstruction of cardiac chambers using catheter position and electrical signals. It guides ablation by displaying activation timing, voltage, and anatomic landmarks, reducing fluoroscopy and improving procedural precision.

Three or more episodes of sustained ventricular tachycardia within 24 hours requiring intervention. Management includes antiarrhythmics, beta-blockade, sedation, and catheter ablation, often with device reprogramming.