Europace Advance Access originally published online on January 28, 2008
Europace 2008 10(5):591-592; doi:10.1093/europace/eun003
Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2008. For permissions please email: journals.permissions@oxfordjournals.org
ALTERNATIVE VENTRICULAR PACING SITES
Pseudomalfunction of a dual chamber pacemaker caused by accelerated junctional rhythm and alternating ventricular safety pacing
Shih-Tsung Cheng and
Kuan-Hung Yeh*
Division of Cardiology, Buddhist Tzu Chi General Hospital, Taipei Branch, 289, Jianguo Road, Xindian City, Taipei, Taiwan, Republic of China
Manuscript submitted 7 October 2007. Accepted after revision 28 December 2007.
* Corresponding author. Tel: +886 2 6628 9779, ext 5709; fax: +886 2 2705 9021. E-mail address: ufddsykh{at}ms15.hinet.net
Key Words: Pseudomalfunction, Ventricular safety pacing, Pacemaker, Electrocardiography
A 78-year-old woman presented at the emergency department (ED) with palpitation, cold sweating, and dizziness. A dual chamber pacemaker (PM) (Medtronic Kappa KDR903) had been implanted due to brady-tachycardia syndrome 2 years before and she had a history of hypertension and diabetes. Twelve-lead ECG at the ED showed a regular narrow QRS rhythm with a rate of 
70 bpm and alternating atrial–ventricular sequential pacing spikes leading to suspicion of PM malfunction (Figure 1). The patient, however, had no abnormalities on a PM check-up 2 weeks prior to the ED visit. After amiodarone therapy for 2 years, the patient became PM-dependent. Histogram from the PM showed 100% atrial–ventricular sequential pacing with no evidence of atrial tachyarrhythmia. The functions of the PM were all normal, and it was set in the DDDR mode with a lower rate 60 bpm and atrioventricular interval (AVI) 150 ms. Physical examination and biochemistry at the ED were unremarkable except for hypoglycaemia and hypokalaemia (sugar 53 mg/dL and potassium 2.7 mmol/L). Tracing the history, the patient reported having accidentally taken two additional tablets of glimepiride in the morning before the episode. Her symptoms subsided completely after glucose water intravenous injection and the ECG resumed atrial–ventricular sequential pacing at a rate of 60 bpm, AVI 150 ms, and good capture. Chest X-ray showed no atrial or ventricular lead dislodgement and follow-up PM check revealed no abnormalities. The findings support the hypothesis that the junctional rhythm occurred secondary to hypoglycaemia. A coincidence between the lower rate interval (LRI), AVI, the rate of the junctional rhythm, and the features of ventricular safety pacing (VSP) led to misinterpretation of the ECG as PM malfunction. As shown in Figure 2, when the PM sensed a junctional beat (ventricular sensing* and VS*), the LRI was truncated (shaded bar) and initiated a new LRI. At the end of the atrial escape interval (AEI, AEI = LRI–AVI), an atrial stimulus was delivered and a VSP window was initiated. VSP was designed to prevent the consequences of atrioventricular crosstalk. The VSP window starts at the time of atrial pacing (AP) and its duration is 110 ms. The VSP window can be divided into two portions (Figure 3). The initial 28 ms of the VSP window is the post-atrial ventricular blanking (PAVB) period. Ventricular sensing cannot occur during this period. Ventricular activity sensed in the second portion of the VSP window will trigger ventricular pacing at the end of the VSP window. If the junctional beat (VS# in Figure 2) falls in the PAVB period, or in the second portion of the VSP window but the PM fails to sense it, the PM will be unaware of the ventricular activity and will deliver a ventricular stimulus at the end of AVI (150 ms). In this case, the junctional beat (VS#) fell in the second portion of the VSP window and was sensed properly. Therefore, the AVI was truncated (dotted bar) and a ventricular pacing spike occurred 110 ms after an AP spike. A short, non-physiological, truncated AVI at 110 ms was the key to proper interpretation of this pseudomalfunction.
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