ABIM Clinical EP key terms

The brief interval after a tissue depolarizes during which it cannot be excited again, no matter how strong the stimulus. It determines the upper limit of rate at which myocardium or conduction tissue can recover and conduct.

The distance an electrical impulse travels through tissue during one refractory period, calculated as conduction velocity multiplied by refractory period. Short wavelengths favor reentry because a wavefront can circle without colliding with its own refractory tail.

A self-sustaining arrhythmia mechanism in which an impulse circulates around an obstacle or region of slow conduction and returns to tissue that has recovered excitability. It requires an initiating trigger, a circuit, and a vulnerable substrate.

Arrhythmia arising from afterdepolarizations that reach threshold and generate new impulses. Early afterdepolarizations occur during repolarization and relate to bradycardia and long QT, while delayed afterdepolarizations occur after repolarization and relate to calcium overload.

A secondary depolarizing deflection during phase 2 or 3 of the action potential, typically from reactivation of calcium or late sodium currents. It is favored by bradycardia, hypokalemia, and QT prolongation and can initiate torsades de pointes.

A transient depolarization occurring after the action potential has fully repolarized, driven by spontaneous calcium release from the sarcoplasmic reticulum. It is classically associated with digoxin toxicity and catecholamine-sensitive arrhythmias.

The property by which conduction speed differs depending on the direction the impulse travels relative to fiber orientation. Slow transverse conduction creates the substrate for unidirectional block and reentry in ventricular and atrial tissue.

The speed at which an electrical impulse propagates along cardiac tissue, determined by the maximum rate of phase 0 depolarization, cell size, gap junction coupling, and tissue geometry. Slow velocity promotes reentry by shortening wavelength.

The length of time from depolarization to full repolarization of a cardiac cell, reflecting the balance of inward and outward currents. Prolongation is associated with early afterdepolarizations and proarrhythmia, while shortening can facilitate reentry.

Abnormal lengthening of the corrected QT interval on surface ECG, reflecting delayed ventricular repolarization. It is a marker of risk for torsades de pointes and warrants review of drugs, electrolytes, and congenital syndromes.

A heart-rate-adjusted measure of ventricular repolarization, commonly calculated with Bazett, Fridericia, or similar formulas. Correction is necessary because the raw interval shortens as rate increases, and thresholds guide decisions about drugs and monitoring.

A polymorphic ventricular tachycardia that twists around the isoelectric baseline in the setting of QT prolongation. It often terminates spontaneously but can degenerate to ventricular fibrillation and is treated by correcting causes, magnesium, and rate support.

Ventricular tachycardia with continuously varying QRS morphology, reflecting changing activation pathways. It includes torsades de pointes when QT is prolonged and can occur with ischemia or structural disease when QT is normal.

Chaotic, disorganized ventricular electrical activity with no effective mechanical contraction. It causes loss of consciousness within seconds and requires immediate defibrillation and cardiopulmonary resuscitation.

Delivery of a high-energy unsynchronized shock to terminate ventricular fibrillation or pulseless ventricular tachycardia. Energy is delivered across the myocardium to depolarize a critical mass of tissue and allow normal pacemakers to resume control.

Delivery of a shock timed to the QRS complex to terminate a tachyarrhythmia while avoiding the vulnerable repolarization period. It is used for hemodynamically unstable supraventricular or ventricular tachycardias with a detectable QRS.

An implanted device that monitors cardiac rhythm and delivers pacing, antitachycardia pacing, or shocks to terminate dangerous ventricular arrhythmias. It is used for primary or secondary prevention of sudden cardiac death in selected patients.

Delivery of rapid pacing pulses by an implanted device to interrupt a reentrant ventricular tachycardia without a shock. It is painless and effective for many organized tachycardias but may accelerate the rhythm or fail in fast or polymorphic arrhythmias.

Natural death from cardiovascular causes occurring unexpectedly and rapidly, usually within an hour of symptom onset in a person with or without known heart disease. Most cases result from ventricular tachyarrhythmias.

The fraction of left ventricular end-diastolic volume ejected with each beat, commonly measured by echocardiography. Reduced values identify patients at higher risk of arrhythmic death and guide device and medication decisions.

A supraventricular arrhythmia with disorganized atrial activation and irregular ventricular response, associated with stroke and heart failure. Management addresses rate control, rhythm control, and thromboembolic risk.

A clinical score estimating stroke risk in atrial fibrillation using age, sex, heart failure, hypertension, diabetes, stroke, and vascular disease. Higher scores support anticoagulation, while very low scores may not require it.

A tool estimating bleeding risk in patients considered for anticoagulation, incorporating hypertension, renal and liver function, stroke, bleeding history, labile INR, age, and drugs or alcohol. It flags modifiable risk factors rather than prohibiting anticoagulation.

Use of medications such as warfarin or direct oral anticoagulants to prevent clot formation and stroke, particularly in atrial fibrillation and after mechanical valve replacement. Choice depends on renal function, bleeding risk, and valve status.

A pouch-like extension of the left atrium where thrombi commonly form during atrial fibrillation. It can be excluded surgically or with a percutaneous occluder to reduce stroke risk when long-term anticoagulation is unsuitable.

A procedure using radiofrequency, cryothermal, or pulsed-field energy delivered through catheters to destroy or isolate arrhythmogenic tissue. It is used for atrial fibrillation, supraventricular tachycardias, and selected ventricular arrhythmias.

The cornerstone ablation strategy for atrial fibrillation, in which tissue around the pulmonary vein ostia is ablated to electrically disconnect the veins from the left atrium. Veins are common triggers for atrial fibrillation initiation.

An anomalous muscular connection between atrium and ventricle that bypasses the atrioventricular node. It can cause preexcitation and reciprocating tachycardias, and its presence may limit the use of AV nodal blocking drugs.

A syndrome of preexcitation on ECG combined with tachyarrhythmias, caused by an accessory pathway. Atrial fibrillation can conduct rapidly down the pathway and degenerate into ventricular fibrillation, so pathway ablation is often curative.

Early ventricular activation by an accessory pathway before the impulse travels through the normal atrioventricular node, producing a short PR interval and delta wave. The pattern may be asymptomatic or associated with reentrant tachycardia.

A common paroxysmal supraventricular tachycardia using two functionally distinct pathways within the atrioventricular node. It typically produces a regular narrow-complex rhythm and responds to vagal maneuvers, adenosine, or slow-pathway ablation.

An ultra-short-acting intravenous agent that transiently blocks the atrioventricular node and can terminate reentrant supraventricular tachycardias. It also unmasks atrial flutter or fibrillation by slowing the ventricular response.

A broad category of rapid rhythms originating above the ventricles, including AV nodal reentry, accessory pathway tachycardias, and atrial tachycardias. Most are narrow-complex and regular, though atrial fibrillation is an irregular exception.

A clinical syndrome of impaired cardiac output or elevated filling pressures causing dyspnea, fatigue, and fluid retention. It is a major substrate for ventricular arrhythmia and sudden death and influences device and medication decisions.

Biventricular pacing designed to restore coordinated ventricular contraction in patients with heart failure, reduced ejection fraction, and a wide QRS complex. It can improve symptoms and reduce hospitalization.

A transient loss of consciousness due to cerebral hypoperfusion, characterized by rapid onset, short duration, and complete spontaneous recovery. Evaluation distinguishes reflex, orthostatic, and cardiac causes, with cardiac causes carrying the highest risk.

A provocative test in which a patient is positioned upright on a table while heart rate and blood pressure are monitored to reproduce reflex syncope. It is most useful when the history is atypical and cardiac causes have been excluded.

A small subcutaneous device that continuously monitors the heart rhythm for months to years. It is used to diagnose infrequent syncope or palpitations when other monitoring has been nondiagnostic.

An invasive procedure using catheters to record intracardiac electrical signals and to test inducibility, refractory periods, and conduction properties. It guides diagnosis and ablation of arrhythmias and risk assessment in selected conditions.

A collaborative process in which clinicians and patients discuss options, benefits, harms, and patient values before choosing a plan. It is central to decisions such as anticoagulation, device implantation, and ablation.

The process of explaining a procedure's purpose, risks, benefits, and alternatives in understandable terms and confirming the patient's voluntary agreement. It must occur before invasive electrophysiology procedures and device implantation.

A structured database that collects standardized data on procedures and outcomes across sites to compare performance and identify improvement targets. Participation supports practice-based learning and systems-level quality improvement.

Systematically developed recommendations that synthesize evidence to guide decisions for specific clinical circumstances. Guidelines inform but do not replace individualized judgment, and clinicians should appraise their currency and applicability.

The integration of the best available research evidence with clinical expertise and patient values to make care decisions. It involves formulating questions, appraising studies, and applying findings to the individual patient.

A structured method for investigating an adverse event to identify underlying system failures rather than blaming individuals. Findings inform changes in processes, communication, and safeguards to prevent recurrence.

A team communication technique in which a message is sent, acknowledged, and confirmed by the receiver to ensure shared understanding. It reduces errors during resuscitation and high-stakes electrophysiology procedures.

The transfer of patient information and responsibility between clinicians or teams, ideally using a standardized format. Poor handoffs are a common source of preventable harm and should include current issues, pending results, and contingency plans.