February 26th Question
A 71-year-old male with history of persistent atrial fibrillation, who underwent a prior ablation procedure, presents with recurrent drug-refractory atrial tachycardia. The tracing in the Figure is recorded in the electrophysiology laboratory, with pacing performed from the cavotricuspid isthmus. What is the mechanism of the arrhythmia?
A. Dual loop macroreentrant atrial tachycardia
B. Macroreentrant atrial tachycardia
C. Microreentrant atrial tachycardia
D. Focal automatic atrial tachycardia
E. Need more data
ANSWER TO FEBRUARY 19th QUESTION
D. Sinus rhythm with second-degree type I AV block, bifascicular (right and left superior fascicle) block, and rate-related pseudonormalization of QRS
The Figure shows a part of lead II rhythm strip overlaid with ladder diagrams to explain the cardiac rhythm. There are regular P waves marching through the tracing (sinus rhythm). There is a repetitive pattern of 3 P waves associated with 2 QRS complexes. The top shows a P wave conducted with a long PR interval. There is no QRS complex following the next P wave. This suggests second-degree atrioventricular (AV) block. The third P wave is followed after a shorter PR interval by a wider QRS complex, potentially an escape ventricular complex (asterisk). However, this explanation is not provided among the available answer options.
The bottom is an alternative explanation for the ECG rhythm (Option D). There is prolongation of PR interval from first to second P wave, with block of third P wave, consistent with second-degree type I (Wenckebach) 3:2 AV block. The first QRS complex is aberrant as the right bundle branch conduction is delayed compared with the left posterior fascicle. The second QRS complex occurs with a shorter preceding RR interval that can lead to rate-related delay in conduction through the left posterior fascicle, which now coincides with the conduction through the right bundle branch (pseudonormalization of QRS).
Option A is incorrect because first-degree AV block fails to explain the prolongation of PR interval and block of the third P wave that fails to generate a QRS complex. Further, it is less likely for premature junctional complexes to have normal narrow QRS in presence of underlying bifascicular block, although as described above, pseudonormalization could occur due to rate related delay in left posterior fascicle. Option B again fails to explain the PR prolongation and block of the third P wave. Further, the aberrant QRS complexes are not premature. Second-degree type I AV block can explain the block of the third P wave in the AV node; however, option C is incorrect because the aberrant QRS complex occurs after a longer, not a shorter (rate related), preceding RR interval. As there is a consistent temporal relationship between the P waves and the QRS complexes, complete AV block invoked by option 5 is incorrect.
Circ Arrhythm Electrophysiol is available at http://circep.ahajournals.org.
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