ADVANCED DYSRHYTHMIAS EXAM:
(LATEST 2026/2027 UPDATE) QUESTIONS
WITH ANSWERS | GRADE A | 100%
CORRECT, ADVANCED CARDIAC
DYSRHYTHMIAS COMPREHENSIVE
EXAMINATION
ADVANCED CARDIAC DYSRHYTHMIAS
COMPREHENSIVE EXAMINATION
Advanced Dysrhythmias Exam 2026/2027 – Full MCQs | Advanced
Cardiac Dysrhythmias Comprehensive Examination
1. ECG shows regular saw-tooth flutter waves at 300/min, 2:1 conduction,
narrow QRS. Diagnosis?
A. Atrial fibrillation
B. Atrial flutter
C. SVT
D. VT
Rationale: Classic “saw-tooth” F waves, atrial rate 250–350/min, fixed 2:1 AV
conduction, and narrow QRS indicate typical atrial flutter. This arrhythmia originates in
the right atrium with a reentry circuit. Clinical management focuses on rate control,
anticoagulation, and consideration for catheter ablation if recurrent or symptomatic.
2. Rhythm strip: ventricular rate 38, P independent of QRS, PR varies, QRS
0.08 s. Block?
A. 1° AVB
B. 2° type I
C. 2° type II
D. 3° AVB
Rationale: AV dissociation with an atrial rate faster than the ventricular rate and a
narrow escape rhythm indicates complete heart block (3° AV block). The atria and
,ventricles beat independently. Management depends on hemodynamic stability;
permanent pacemaker placement is often required for symptomatic patients.
3. Ventricular rhythm 180, wide bizarre QRS, no P waves, concordant upward
V1–V6. Rhythm?
A. SVT with aberrancy
B. VT
C. Antidromic AVRT
D. Hyperkalemia
Rationale: Wide-complex tachycardia >150 bpm with concordant QRS in precordial
leads suggests ventricular tachycardia (VT), supported by the Brugada sign. VT
originates from a ventricular focus and is potentially life-threatening. Immediate
assessment for hemodynamic stability is required, with synchronized cardioversion if
unstable.
4. ECG: irregularly irregular narrow QRS, no discrete P waves, ventricular
response 130. Management?
A. Adenosine 12 mg
B. Diltiazem bolus
C. Synchronized cardioversion
D. Amiodarone 150 mg
Rationale: This pattern represents atrial fibrillation with rapid ventricular response.
Hemodynamically stable patients benefit from rate control using calcium channel
blockers (e.g., diltiazem) or beta-blockers. Anticoagulation may be indicated
depending on stroke risk.
5. Polymorphic wide QRS alternating axis, QT 560 ms, rate 220. Immediate
action?
A. Magnesium 2 g IV
B. Adenosine
C. Lidocaine
D. Procainamide
Rationale: Polymorphic VT with prolonged QT interval indicates torsades de pointes.
Magnesium sulfate is first-line therapy even if serum magnesium is normal, as it
stabilizes myocardial membranes and terminates the arrhythmia. Correction of
underlying causes (electrolytes, drugs) is essential.
,6. Pacemaker spikes precede each narrow QRS at 60/min; no native P waves.
Interpretation?
A. AAI pacing
B. VVI pacing
C. DDD pacing
D. Epicardial VT
Rationale: Single-chamber ventricular pacing produces a ventricular spike followed
by a QRS complex without atrial activity. VVI pacing ensures a minimum heart rate
and is indicated when atrial activity is absent or ineffective. Patient symptoms and
underlying rhythm guide further device programming.
7. ECG: grouped beating, PR lengthens then dropped QRS, cycle repeats.
Diagnosis?
A. 2° type I AVB
B. 2° type II AVB
C. Non-conducted PACs
D. 3° AVB
Rationale: Progressive PR prolongation until a QRS drop identifies Mobitz type I
(Wenckebach) AV block. Usually benign, especially if asymptomatic. Observation is
often sufficient unless symptomatic bradycardia develops.
8. Narrow-complex tachycardia 190, regular, P visible after QRS (RP < PR).
Likely mechanism?
A. Typical AVNRT
B. Orthodromic AVRT
C. Atypical AVNRT
D. Sinus tach
Rationale: Short RP tachycardia (RP < PR) suggests slow–fast AV nodal reentrant
tachycardia (AVNRT). Vagal maneuvers or adenosine can terminate the arrhythmia in
stable patients. Identification of the P-wave position helps distinguish from other
supraventricular tachycardias.
9. ECG shows regular wide QRS 140, RBBB pattern, capture/fusion beats
visible. Rhythm?
A. SVT with RBBB
B. VT
C. Antidromic AVRT
D. Aberrancy
, Rationale: Presence of capture and fusion beats is pathognomonic for ventricular
tachycardia. Wide QRS with an abnormal morphology confirms a ventricular origin.
Management depends on hemodynamic stability, with synchronized cardioversion for
unstable patients.
10. ICD interrogation: 5 episodes VF 250–260 J successfully delivered.
Patient asymptomatic. Action?
A. Replace ICD generator
B. Start amiodarone
C. Check electrolytes & meds
D. Program VT zone higher
Rationale: Recurrent ICD shocks in asymptomatic patients may reflect reversible
triggers, including hypokalemia, ischemia, or proarrhythmic drugs. Correcting
underlying causes is critical before considering device or antiarrhythmic therapy
adjustments.
11. Sinus rhythm 70, PR 0.36 s, QRS 0.08 s. No symptoms. Management?
A. Permanent pacemaker
B. Atropine
C. Observation
D. Isoproterenol
Rationale: First-degree AV block with prolonged PR but narrow QRS is often benign in
asymptomatic patients. No therapy is required unless symptoms develop or there is
progression to higher-degree block. Regular follow-up ECGs are recommended.
12. ECG: irregular wide QRS 120–180, Ashman beats, underlying AF. Caus
A. Torsades
B. VT
C. Aberrant conduction / Ashman phenomenon
D. WPW
Rationale: Ashman phenomenon is a rate-dependent aberrancy often seen during
atrial fibrillation when a long R-R interval is followed by a short cycle. Recognizing this
prevents misdiagnosis of VT. Management focuses on treating underlying AF rather
than the occasional aberrant beat.
(LATEST 2026/2027 UPDATE) QUESTIONS
WITH ANSWERS | GRADE A | 100%
CORRECT, ADVANCED CARDIAC
DYSRHYTHMIAS COMPREHENSIVE
EXAMINATION
ADVANCED CARDIAC DYSRHYTHMIAS
COMPREHENSIVE EXAMINATION
Advanced Dysrhythmias Exam 2026/2027 – Full MCQs | Advanced
Cardiac Dysrhythmias Comprehensive Examination
1. ECG shows regular saw-tooth flutter waves at 300/min, 2:1 conduction,
narrow QRS. Diagnosis?
A. Atrial fibrillation
B. Atrial flutter
C. SVT
D. VT
Rationale: Classic “saw-tooth” F waves, atrial rate 250–350/min, fixed 2:1 AV
conduction, and narrow QRS indicate typical atrial flutter. This arrhythmia originates in
the right atrium with a reentry circuit. Clinical management focuses on rate control,
anticoagulation, and consideration for catheter ablation if recurrent or symptomatic.
2. Rhythm strip: ventricular rate 38, P independent of QRS, PR varies, QRS
0.08 s. Block?
A. 1° AVB
B. 2° type I
C. 2° type II
D. 3° AVB
Rationale: AV dissociation with an atrial rate faster than the ventricular rate and a
narrow escape rhythm indicates complete heart block (3° AV block). The atria and
,ventricles beat independently. Management depends on hemodynamic stability;
permanent pacemaker placement is often required for symptomatic patients.
3. Ventricular rhythm 180, wide bizarre QRS, no P waves, concordant upward
V1–V6. Rhythm?
A. SVT with aberrancy
B. VT
C. Antidromic AVRT
D. Hyperkalemia
Rationale: Wide-complex tachycardia >150 bpm with concordant QRS in precordial
leads suggests ventricular tachycardia (VT), supported by the Brugada sign. VT
originates from a ventricular focus and is potentially life-threatening. Immediate
assessment for hemodynamic stability is required, with synchronized cardioversion if
unstable.
4. ECG: irregularly irregular narrow QRS, no discrete P waves, ventricular
response 130. Management?
A. Adenosine 12 mg
B. Diltiazem bolus
C. Synchronized cardioversion
D. Amiodarone 150 mg
Rationale: This pattern represents atrial fibrillation with rapid ventricular response.
Hemodynamically stable patients benefit from rate control using calcium channel
blockers (e.g., diltiazem) or beta-blockers. Anticoagulation may be indicated
depending on stroke risk.
5. Polymorphic wide QRS alternating axis, QT 560 ms, rate 220. Immediate
action?
A. Magnesium 2 g IV
B. Adenosine
C. Lidocaine
D. Procainamide
Rationale: Polymorphic VT with prolonged QT interval indicates torsades de pointes.
Magnesium sulfate is first-line therapy even if serum magnesium is normal, as it
stabilizes myocardial membranes and terminates the arrhythmia. Correction of
underlying causes (electrolytes, drugs) is essential.
,6. Pacemaker spikes precede each narrow QRS at 60/min; no native P waves.
Interpretation?
A. AAI pacing
B. VVI pacing
C. DDD pacing
D. Epicardial VT
Rationale: Single-chamber ventricular pacing produces a ventricular spike followed
by a QRS complex without atrial activity. VVI pacing ensures a minimum heart rate
and is indicated when atrial activity is absent or ineffective. Patient symptoms and
underlying rhythm guide further device programming.
7. ECG: grouped beating, PR lengthens then dropped QRS, cycle repeats.
Diagnosis?
A. 2° type I AVB
B. 2° type II AVB
C. Non-conducted PACs
D. 3° AVB
Rationale: Progressive PR prolongation until a QRS drop identifies Mobitz type I
(Wenckebach) AV block. Usually benign, especially if asymptomatic. Observation is
often sufficient unless symptomatic bradycardia develops.
8. Narrow-complex tachycardia 190, regular, P visible after QRS (RP < PR).
Likely mechanism?
A. Typical AVNRT
B. Orthodromic AVRT
C. Atypical AVNRT
D. Sinus tach
Rationale: Short RP tachycardia (RP < PR) suggests slow–fast AV nodal reentrant
tachycardia (AVNRT). Vagal maneuvers or adenosine can terminate the arrhythmia in
stable patients. Identification of the P-wave position helps distinguish from other
supraventricular tachycardias.
9. ECG shows regular wide QRS 140, RBBB pattern, capture/fusion beats
visible. Rhythm?
A. SVT with RBBB
B. VT
C. Antidromic AVRT
D. Aberrancy
, Rationale: Presence of capture and fusion beats is pathognomonic for ventricular
tachycardia. Wide QRS with an abnormal morphology confirms a ventricular origin.
Management depends on hemodynamic stability, with synchronized cardioversion for
unstable patients.
10. ICD interrogation: 5 episodes VF 250–260 J successfully delivered.
Patient asymptomatic. Action?
A. Replace ICD generator
B. Start amiodarone
C. Check electrolytes & meds
D. Program VT zone higher
Rationale: Recurrent ICD shocks in asymptomatic patients may reflect reversible
triggers, including hypokalemia, ischemia, or proarrhythmic drugs. Correcting
underlying causes is critical before considering device or antiarrhythmic therapy
adjustments.
11. Sinus rhythm 70, PR 0.36 s, QRS 0.08 s. No symptoms. Management?
A. Permanent pacemaker
B. Atropine
C. Observation
D. Isoproterenol
Rationale: First-degree AV block with prolonged PR but narrow QRS is often benign in
asymptomatic patients. No therapy is required unless symptoms develop or there is
progression to higher-degree block. Regular follow-up ECGs are recommended.
12. ECG: irregular wide QRS 120–180, Ashman beats, underlying AF. Caus
A. Torsades
B. VT
C. Aberrant conduction / Ashman phenomenon
D. WPW
Rationale: Ashman phenomenon is a rate-dependent aberrancy often seen during
atrial fibrillation when a long R-R interval is followed by a short cycle. Recognizing this
prevents misdiagnosis of VT. Management focuses on treating underlying AF rather
than the occasional aberrant beat.
