EXAM PRACTICE QUESTIONS AND CORRECT ANSWERS (VERIFIED
ANSWERS) PLUS RATIONALES Q&A INSTANT DOWNLOAD PDF
140 QUESTIONS
TABLE OF CONTENTS
# TOPIC
1 Interpret complex intracardiac electrograms and activation maps to guide ablation
2 Apply advanced knowledge of antiarrhythmic drugs and device algorithms in clinical scenarios
3 Integrate hemodynamic and electrophysiological data to manage arrhythmias in complex cases
4 Critically evaluate evidence and guidelines for sudden cardiac death risk stratification
5 Analyze complications and troubleshooting in cardiac implantable electronic devices
6 IBHRE Certified Electrophysiology Specialist
7 Adult
8 CEPS
9 Exam Practice Questions And Correct Answers
10 Verified Answers
11 Plus Rationales Q&A Instant Download Pdf
12 Foundations of Clinical Cardiac Electrophysiology
13 Applied Clinical Cardiac Electrophysiology
14 Advanced Clinical Cardiac Electrophysiology
15 Clinical Cardiac Electrophysiology Review
Page 1
,Q1 INTERPRET COMPLEX INTRACARDIAC ELECTROGRAMS AND ACTIVATION MAPS TO
GUIDE ABLATION
During an ablation procedure for a left-sided accessory pathway, a retrograde
aortic approach is used. The ablation catheter is positioned at the mitral annulus,
and the local ventricular electrogram precedes the surface delta wave by 20 ms.
However, a single radiofrequency application fails to eliminate the pathway. Which
maneuver is most likely to reveal the true mechanism?
A. Administer adenosine to expose a decremental accessory pathway
B. Map the coronary sinus and its branches for an epicardial pathway CORRECT
C. Perform a transseptal puncture to access the left atrium
D. Increase the power and duration of the radiofrequency application
RATIONALE: A left-sided accessory pathway can be epicardial, often requiring mapping within
the coronary sinus or its venous branches. The local ventricular signal preceding the delta wave
suggests a left free-wall pathway, but failure of endocardial ablation points to an epicardial
location. Adenosine would not differentiate epicardial from endocardial pathways. Transseptal
access is not needed if already retrograde. Simply increasing power is less likely to succeed if
the target is epicardial.
Q2 INTERPRET COMPLEX INTRACARDIAC ELECTROGRAMS AND ACTIVATION MAPS TO
GUIDE ABLATION
A patient with symptomatic paroxysmal atrial fibrillation and a CHA2DS2-VASc
score of 2 is undergoing pulmonary vein isolation. Which finding on the
post-ablation voltage map most strongly indicates a durable lesion set?
A. Absence of low-voltage areas within the antral region
B. Presence of electrical silence in the antral region with a clear border to healthy atrial tissue
CORRECT
C. Persistent capture of the left atrium during pacing from the ablation line
D. Reduction in atrial electrogram amplitude by 50% compared to baseline
RATIONALE: Durable lesion formation is best confirmed by complete electrical isolation,
evidenced by electrical silence (no captured potentials) within the antral region and a distinct
transition to normal voltage atrial tissue. Absence of low-voltage areas suggests incomplete
ablation. Persistent capture indicates gaps in the lesion set. A 50% amplitude reduction is not
sufficient to confirm transmurality.
Page 2
,Q3 INTERPRET COMPLEX INTRACARDIAC ELECTROGRAMS AND ACTIVATION MAPS TO
GUIDE ABLATION
A 68-year-old patient with ischemic cardiomyopathy (EF 30%) and a
single-chamber ICD presents with recurrent monomorphic VT. Device
interrogation shows ATP terminated the VT three times, but a subsequent episode
required a 30-J shock. The patient is on amiodarone. Which next step is most
appropriate to reduce the frequency of ICD shocks?
A. Increase the number of ATP bursts per episode
B. Add mexiletine to the amiodarone regimen
C. Perform catheter ablation of the VT substrate CORRECT
D. Change the ICD to a dual-chamber device
RATIONALE: Recurrent VT despite amiodarone, with shocks, warrants catheter ablation to
reduce arrhythmia burden and shocks. The VANISH trial demonstrated that catheter ablation is
superior to escalation of antiarrhythmic therapy (adding mexiletine) in reducing the composite of
death, VT storm, and appropriate ICD shocks. Increasing ATP bursts may help but does not
address the arrhythmia substrate. Dual-chamber ICD does not prevent VT.
Q4 INTERPRET COMPLEX INTRACARDIAC ELECTROGRAMS AND ACTIVATION MAPS TO
GUIDE ABLATION
A patient with a dual-chamber pacemaker programmed to DDD mode at a lower
rate of 60 ppm develops pacemaker-mediated tachycardia (PMT) after a premature
ventricular contraction. Which programmed setting is most likely to prevent
recurrence without compromising hemodynamics?
A. Increase the post-ventricular atrial refractory period (PVARP) to 350 ms CORRECT
B. Enable a PMT detection algorithm that triggers a 400-ms post-ventricular atrial blanking
C. Shorten the atrioventricular delay to 100 ms
D. Switch the pacing mode to VVI at 70 ppm
RATIONALE: PMT occurs when a retrograde P wave falls outside the PVARP and is sensed,
triggering ventricular pacing. Prolonging PVARP to 350 ms typically exceeds the retrograde
conduction time, preventing sensing of the retrograde P wave. PMT algorithms detect and
terminate PMT but do not prevent initiation. Shortening AV delay does not prevent PMT. VVI
mode avoids atrial sensing but is not hemodynamically optimal for most patients.
Page 3
, Q5 INTERPRET COMPLEX INTRACARDIAC ELECTROGRAMS AND ACTIVATION MAPS TO
GUIDE ABLATION
During an electrophysiology study for syncope, a 45-year-old patient with a
structurally normal heart has a normal baseline ECG. During programmed
ventricular stimulation with up to three extrastimuli, a polymorphic VT is induced
that degenerates into ventricular fibrillation requiring defibrillation. Which is the
most appropriate interpretation?
A. The patient has a high risk of sudden cardiac death and should receive an ICD
B. The induction is a non-specific response and does not necessarily indicate a poor prognosis
CORRECT
C. The patient likely has Brugada syndrome and should undergo ajmaline testing
D. The patient should be treated with beta-blockers to prevent recurrent VT
RATIONALE: In patients with a structurally normal heart and no history of ventricular arrhythmias,
induction of polymorphic VT/VF with aggressive stimulation (three extrastimuli) is a non-specific
finding. It does not warrant an ICD. Brugada syndrome would require characteristic ECG
changes. Beta-blockers are not indicated without a specific diagnosis.
Q6 INTERPRET COMPLEX INTRACARDIAC ELECTROGRAMS AND ACTIVATION MAPS TO
GUIDE ABLATION
A 72-year-old patient with persistent atrial fibrillation and a CHA2DS2-VASc score
of 4 is undergoing elective cardioversion. A transesophageal echocardiogram
(TEE) shows a thrombus in the left atrial appendage (LAA). Which is the most
appropriate management strategy?
A. Proceed with cardioversion after increasing the INR to 3.0
B. Cancel cardioversion, continue anticoagulation for at least 3 weeks, and repeat TEE
CORRECT
C. Proceed with cardioversion immediately and add a glycoprotein IIb/IIIa inhibitor
D. Perform a left atrial appendage occlusion device implantation and then cardiovert
RATIONALE: Presence of a thrombus on TEE is a contraindication to cardioversion. The patient
should be anticoagulated with a vitamin K antagonist (INR 2-3) or a direct oral anticoagulant for
at least 3 weeks, then a repeat TEE should be performed to document thrombus resolution.
Increasing INR to 3.0 is not sufficient. Antiplatelet therapy does not prevent embolization. LAA
occlusion is not indicated in this acute setting.
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