ABIM Clinical Cardiac Electrophysiology Certification: Decisions, Mechanisms, and Practice Study Guide

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During treatment of a regular narrow-complex tachycardia, an AV nodal blocker prolongs AV conduction without widening the QRS. Use the affected tissue’s calcium-dependent conduction to explain the response rather than assuming generalized ventricular conduction slowing.

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Compare two patients: one develops polymorphic VT after a long pause while taking a QT-prolonging drug; another develops exercise-triggered ventricular ectopy with a normal resting QT. Identify the likely afterdepolarization mechanism in each presentation.

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Assume uniform conduction at 0.5 m/s and an effective refractory period of 200 ms. The wavelength is 10 cm. A 14-cm circuit could permit recovery before return, whereas an 8-cm circuit would not under these assumptions.

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An atrial extrastimulus produces a sudden increase in AV nodal conduction time, followed by an atrial echo and regular tachycardia. Explain how differential pathway recovery and delayed conduction can create an opportunity for nodal reentry.

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During progressively faster atrial pacing, the AH interval lengthens while the HV interval remains stable. Localize the principal rate-dependent delay to the AV node and distinguish it from slowing within the His–Purkinje system.

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A patient with prior infarction has monomorphic VT and multiple late potentials within low-voltage myocardium. Use activation and entrainment evidence to distinguish a critical conducting channel from nearby abnormal tissue that merely activates late.

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A patient tolerating a QT-prolonging antiarrhythmic develops diarrhea, renal dysfunction, and pause-related ventricular ectopy. Reassess electrolytes, clearance, interacting drugs, and repolarization together before attributing the new arrhythmia to progression of structural heart disease.

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One patient develops progressive QRS widening during exercise on flecainide; another develops greater QT prolongation after slowing while taking a potassium-channel blocker. Explain why the different rate relationships point to distinct electrophysiologic drug effects.

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After starting flecainide for AF, a patient develops a regular very rapid wide-complex rhythm during exertion. Consider organized atrial flutter with 1:1 conduction alongside VT, and review both structural-heart eligibility and AV nodal protection.

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An otherwise eligible 70-year-old man weighing 72 kg with creatinine 2.0 mg/dL has clearance (70 × 72)/(72 × 2) = 35 mL/min, selecting 125 micrograms twice daily. Measure QTc/QT 2–3 hours after doses 1–5. After the first dose, an increase >15% from baseline or a value >500 ms, or >550 ms with ventricular conduction abnormalities, requires dose reduction; from 125 micrograms twice daily, reduce to once daily. After dose two or later, exceeding the applicable 500/550-ms limit requires discontinuation.

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A patient’s interacting medication remains difficult to control two weeks after amiodarone is stopped. Explain persistent tissue release and elimination rather than assuming the interaction ended with the last tablet, and continue appropriate clinical and laboratory monitoring.

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A patient with exertional syncope has a nondiagnostic panel, while a relative carries an uncertain variant. Continue phenotype-directed evaluation and expert variant interpretation rather than treating either result as a definitive answer about inherited arrhythmic risk.

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A runner receives repeated irregular-pulse notifications, but the saved tracing contains movement noise and recognizable regular QRS complexes. Obtain usable ECG documentation before assigning AF or exposing the patient to treatment based on an uncertain automated classification.

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A patient’s PR interval lengthens during atrial pacing. Intracardiac recordings show progressive AH prolongation with unchanged HV timing. Attribute the incremental delay primarily to AV nodal conduction rather than diagnosing worsening distal conduction from the surface PR alone.

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A ventricular target lies close to a coronary artery. Before increasing energy for an apparently shallow lesion, define the anatomic relationship and reassess contact and access, because greater power may increase collateral risk without solving the underlying limitation.

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An asymptomatic endurance athlete has nocturnal slowing, while another patient has presyncope coinciding with a daytime sinus pause. Use symptom–rhythm correlation and reversible-cause assessment to distinguish their pacing decisions despite superficially similar low-rate recordings.

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An otherwise stable patient has confirmed Mobitz II block on repeated ECGs without a medication or metabolic explanation. Recommend permanent pacing despite the absence of syncope, while separately assessing whether temporary support is needed during evaluation.

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A patient with 2:1 AV block has a wide QRS and exertional presyncope. Treat the findings as concerning for distal conduction disease and pursue appropriate localization and pacing assessment rather than calling the pattern benign nodal Wenckebach.

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A patient with hypertension, diabetes, and prior stroke reports only brief symptomatic AF episodes. Base anticoagulation on the substantial thromboembolic risk rather than assuming a low perceived episode burden makes aspirin or observation an adequate substitute.

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A stable patient has AF of uncertain duration and missed several anticoagulant doses. Choose a thrombus-excluding imaging strategy or a new adequate uninterrupted anticoagulation interval before elective conversion, then maintain the required anticoagulation after sinus rhythm returns.

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Six months after apparently successful pulmonary vein isolation, a patient with previous embolic stroke asks to stop anticoagulation because palpitations have disappeared. Explain why baseline risk supports continued treatment despite a favorable rhythm-control result.

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Flutter terminates during an isthmus lesion, but pacing still demonstrates conduction across the line. Continue evaluating and completing the line rather than declaring success solely because the presenting tachycardia has stopped and sinus rhythm is present.

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A patient develops organized atrial tachycardia after left atrial ablation. Map activation around prior lesions and test a suspected channel before choosing a new line, rather than assuming every flutter-like ECG requires right atrial isthmus ablation.

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Record atrial, His, and ventricular signals during blocked cycles. A His electrogram without a subsequent ventricular electrogram localizes block distal to the recorded His; absence of His activation can reflect block above the His but below an AVNRT circuit. When ventricular overdrive pacing demonstrably entrains the atrium, a true V-A-A-V return sequence supports atrial tachycardia, whereas V-A-V favors AVNRT or AVRT. Identify the last paced atrial activation carefully because apparent extra atrial responses can mislead.

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A patient with symptomatic persistent AF, reduced ejection fraction, and uncontrolled rates has failed suitable drug and rhythm-control strategies. Discuss AV junction ablation together with a pacing plan that accounts for ventricular dysfunction and near-continuous ventricular pacing.

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A patient has recurrent regular narrow-complex tachycardia but no resting preexcitation. During testing, a left-sided retrograde connection is identified. Keep orthodromic AVRT in the differential despite the normal baseline QRS and assess whether that connection sustains the rhythm.

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A patient with known ventricular preexcitation presents with regular wide-complex tachycardia. Consider antidromic AVRT, but evaluate VT and other preexcited rhythms before selecting therapy based solely on the previously documented accessory pathway.

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During regular SVT, a confirmed His-refractory ventricular extrastimulus advances the next atrium and subsequent tachycardia timing. Use this response to support an accessory connection and assess circuit participation rather than interpreting short VA timing alone.

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An alert patient has an irregular wide-complex tachycardia with varying degrees of preexcitation and preserved blood pressure. Recognize preexcited AF and choose a pathway-appropriate treatment rather than applying the usual AV nodal rate-control approach for ordinary AF.

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During an electrophysiologic study, induced AF conducts over an accessory pathway with a shortest preexcited RR interval of 220 ms. Explain why this demonstrates potentially dangerous antegrade conduction and supports discussing definitive pathway ablation.

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A regular narrow-complex tachycardia begins after an atrial premature beat causes marked AH prolongation. Nearly simultaneous septal atrial and ventricular activation supports typical AVNRT, provided additional testing excludes a septal accessory pathway and atrial tachycardia.

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A patient’s incessant narrow-complex tachycardia has retrograde-appearing P waves well after each QRS. Build a differential including atypical AVNRT, slowly conducting AVRT, and atrial tachycardia, then select pacing maneuvers that test ventricular and atrial participation.

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After slow-pathway modification, tachycardia is no longer inducible although a residual AH jump remains. Evaluate the accepted procedural endpoint and conduction safety rather than delivering extra lesions solely to erase every sign of dual nodal physiology.

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Following cardiac surgery, a patient develops a junctional rhythm that gradually accelerates and continues independently of atrial activation. Review postoperative drivers and an automatic mechanism rather than assuming a conventional AVNRT circuit requiring routine slow-pathway ablation.

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A patient with prior infarction remains awake during regular wide-complex tachycardia. Independent P waves and an occasional narrower capture beat support VT despite preserved blood pressure, directing management toward a ventricular rather than assumed supraventricular mechanism.

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A patient without evident structural disease has frequent monomorphic PVCs with a left bundle branch block pattern and inferior axis. Begin with an outflow-tract localization hypothesis, then compare activation at adjacent right- and left-sided structures before choosing the safest target.

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A patient with an old infarction has recurrent identical VT that causes hypotension during induction. Use scar imaging, voltage mapping, and abnormal electrograms to plan a substrate strategy rather than repeatedly sustaining an intolerable rhythm solely to obtain a complete activation map.

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During stable VT with a 360-ms cycle length, pacing produces concealed fusion and a 380-ms postpacing interval. The 20-ms difference supports circuit proximity under appropriate assumptions; compare additional timing evidence before identifying the site as a critical isthmus.

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Two neighboring sites produce similar pace maps, but only one consistently records substantially earlier activation during the clinical PVC. Favor the timing-supported site after confirming contact and anatomy rather than selecting solely by visual QRS resemblance.

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A patient develops reduced ejection fraction with a high burden of one PVC morphology and no clear ischemic explanation. Assess for other myocardial disease, then discuss suppression and follow-up imaging to determine whether ventricular function recovers.

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A patient with nonischemic cardiomyopathy has recurrent VT despite limited endocardial abnormalities. Imaging shows subepicardial inferolateral fibrosis. Reassess substrate depth and access strategy rather than interpreting the endocardial map as proof that scar-related VT is absent.

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A patient taking a QT-prolonging drug develops a long pause followed by polymorphic VT and marked baseline QT prolongation. Address acquired long-QT triggers and pause dependence rather than reflexively adding another repolarization-prolonging antiarrhythmic.

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An ICD recipient with an old infarction has repeated appropriate therapies for monomorphic VT despite amiodarone. After reviewing reversible triggers and programming, discuss scar-based catheter ablation rather than simply adding successive drug escalation without reassessing the substrate.

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Compare a patient in sinus rhythm with complete AV block and another with permanent AF and slow ventricular response. Explain why their atrial sensing and tracking requirements differ before choosing a pacing mode and assessing ventricular pacing strategy.

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A pacing-dependent patient has visible ventricular pacing spikes without subsequent QRS complexes. Prioritize confirmation of capture failure and urgent support, then examine thresholds, lead position, and reversible physiologic causes rather than treating the tracing as simple oversensing.

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An ICD delivers shocks during arm movement, and stored electrograms show brief high-frequency signals inconsistent with the surface pulse. Investigate noise and lead integrity rather than escalating antiarrhythmic medication for a presumed increase in true VT burden.

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A dual-chamber device records a regular paced tachycardia after a ventricular premature beat, with each ventricular pace followed by a sensed retrograde atrial event. Review the refractory timing and pacemaker-mediated tachycardia intervention settings to interrupt the tracking loop.

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A patient with a remote infarction, LVEF 45%, and sustained monomorphic VT requiring cardioversion has no acute ischemia, drug toxicity, or explanatory electrolyte disturbance. If meaningful survival exceeds one year, the patient meets the stated secondary-prevention indication despite an LVEF above 35%.

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An ICD recipient receives therapy for several brief ventricular runs that were already slowing. Reassess detection duration and classification settings to reduce avoidable intervention while preserving coverage of the patient’s documented sustained VT and hemodynamic tolerance.

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A patient’s recurrent monomorphic VT repeatedly terminates with the first ATP sequence and no symptoms. Preserve an effective ATP-first strategy in the relevant zone while maintaining appropriate backup shock therapy and reviewing the underlying recurrence burden.

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A young patient needs defibrillator protection but has no bradycardia, resynchronization requirement, or recurrent ATP-responsive VT. Discuss a subcutaneous system after appropriate screening, while explaining how future pacing needs could change the device strategy.

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A patient remains NYHA class III despite appropriate therapy, with LVEF 28%, sinus rhythm, and LBBB measuring 168 ms. Recognize the strong CRT phenotype and evaluate device planning rather than continuing to assess ejection fraction in isolation.

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For a patient without baseline LBBB, a stimulus-to-V6 R-wave peak time of 70 ms meets Table 7's <74-ms criterion. Measure from the pacing stimulus, not QRS onset. Compare outputs using the same measurement origin and exclude intrinsic fusion.

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A patient has persistent bloodstream infection and a device lead mass. Integrate organism, repeated cultures, pocket examination, and imaging to assess infection and removal needs; do not dismiss the finding as incidental solely because the pocket appears normal.

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A patient has unexplained episodes separated by several months and an unrevealing short monitor. Consider prolonged implantable recording when appropriate to the risk assessment, explaining that the goal is diagnostic correlation rather than immediate pacing or defibrillation treatment.

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A patient with unexplained syncope has repeated QTc measurements above 500 ms after electrolyte normalization and withdrawal of QT-prolonging drugs. Evaluate an inherited long-QT phenotype and family implications rather than attributing persistent prolongation to the resolved illness.

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A patient with known Brugada syndrome develops a febrile infection. Treat fever promptly, review medications for syndrome-related hazards, and assess symptoms and ECG changes rather than assuming an unchanged everyday activity level means the temperature is irrelevant.

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An adolescent with exertional syncope, normal echocardiography, and a normal resting QT develops bidirectional VT during supervised exercise testing. This pattern strongly suggests CPVT. After starting nadolol, confirm adherence and reassess with exercise testing. Persistent ventricular arrhythmias despite maximally tolerated treatment support adding flecainide and repeating assessment of treatment response. Arrange family evaluation.

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A competitive athlete collapses mid-exercise and has ventricular ectopy plus a first-degree relative who died suddenly. Investigate structural and inherited substrates with targeted cardiac assessment rather than attributing the event to dehydration simply because recovery was rapid.

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A relatively young adult presents with unexplained high-grade AV block and later monomorphic VT. Investigate inflammatory and infiltrative myocardial disease, including sarcoidosis, while addressing pacing and defibrillation needs according to the complete clinical risk profile.