Pacing on the T Wave: What Is the Cause?
We present the case of a 50-year-old man who had a dual-chamber pacemaker that was implanted because of symptomatic bradycardia. The pacemaker was programmed in a DDD mode, with a lower rate of 70 beats/min; upper rate, 120 beats/min; paced atrioventricular (AV) delay, 180 ms; sensed AV delay, 150 ms; and V-blanking period, 200 ms.
How would you explain the pacing stimulus observed on the T wave in the 11th complex (Fig. 1)?
A) Ventricular undersensing with inappropriate ventricular pacing
B) Ventricular tracking of a retrograde P wave from the premature ventricular contraction
C) Ventricular event during the atrial blanking period with subsequent V-pacing
D) T-wave oversensing
E) Artifact on the electrocardiogram (ECG)—not a real pacing stimulus
Citation: Texas Heart Institute Journal 43, 1; 10.14503/THIJ-15-5351
Focus on ECGs: Answer #1
Answer
C) Ventricular event during the atrial blanking period with subsequent V-pacing
In Figure 1 (previous page), the ECG shows intermittent AV sequential electronic pacing (complexes 4–5 are sinus followed by electronic ventricular pacing), with premature ventricular contractions (PVCs) in the 3rd, 6th, 7th, and 8th complexes. In Figure 2, the short arrows designate the atrial-ventricular interval (A-V), which is a period that may elapse after an atrial activity before the ventricle must be paced. The long, horizontal arrows show the interval between atrial pacing.
Citation: Texas Heart Institute Journal 43, 1; 10.14503/THIJ-15-5351
The index PVC, the 11th beat, is a pseudo-pseudofusion beat.
If an atrial pacing output occurs in the presence of an already depolarized myocardium by an intrinsic premature beat (in this case, the PVC), the pacer output cannot contribute to the myocardial depolarization, and, therefore, the QRS is formed entirely by the intrinsic PVC beat. Furthermore, notice that the index PVC falls in the post-ventricular atrial blanking period (PVAB); therefore, the pacemaker was not inhibited.
Contributor Notes
Section Editors: Yochai Birnbaum, MD, Mohammad Saeed, MD, and James M. Wilson, MD
From: Texas Heart Institute, Baylor St. Luke's Medical Center (Drs. Birnbaum, Gahremanpour, and Saeed), Houston, Texas 77030; Section of Cardiology, Department of Medicine (Dr. Birnbaum), Baylor College of Medicine, Houston, Texas 77030; and Boston Scientific Corporation (Mr. Holt), St. Paul, Minnesota 55112
