This patient presented for routine clinic evaluation of a dual chamber pacemaker. Please refer to Figure 1 for initial programming. The patient was in sinus rhythm, had a rate 83 BPM, and was asymptomatic.

Measured p-wave signals were 3-4 mv in amplitude. Atrial sensing was programmed to Auto, thus, the pacemaker sensing level would self-adjust to measure intrinsic atrial activity. This particular device uses a weighted average of the measured p-wave amplitudes to determine the average p-wave amplitude. The sensing level is also programmed to set itself at twice the estimated noise level. This feature provides protection from oversensing potentially resulting from electrical noise on a lead which may result in inappropriate inhibition of pacing. In this case, the three impulses preceeding the non-sensed beat were significantly larger, therefore setting the sensing window too big to see the circled p. The sensing window then became smaller and was able to sense the following impulse. Was this significant in terms of a negative outcome related to the pacemaker response? No, because the patient was in sinus rhythm and maintaining his own rhythm. However, to correct this problem, we took off the Auto sensing, and reprogrammed atrial sensitivity to a fixed 0.5 mv. Previously non-sensed p-waves were all sensed.

There are several timing schemes used by pacemaker devices, depending on the manufacturer. Alternatives are atrial- or ventricular-based and modified atrial or ventricular. The commonality is that after every sensed or paced ventricular impulse, an atrial escape interval (AEI) is initiated. By the end of this interval, if no atrial or ventricular impulses are seen, an atrial pacing stimulus will be delivered. The goal of the timing schemes is to keep the paced ventricular rate as smooth as possible. In this device which uses a form of modified atrial based timing, the AEI consists of the lower rate limit interval minus the programmed AV interval or the intrinsic PR interval (In this case, 1000 ms - 160 ms = AEI of 840 ms.). If no atrial activity is sensed at the end of the AEI timed from the last ventricular impulse, an atrial pacing output will occur. In Figure 2, the R-R interval around the non-sensed p is 720 ms, thus, atrial pacing did not occur because a sensed ventricular impulse occurred before the AEI timed out resetting the AEI timer.

A 55-year-old male received an implantable cardioverter-defibrillator (ICD) 6 months earlier for MADIT II criteria (coronary artery disease, ejection fraction < 30%, no documented arrhythmias). Four months after the implant, he had a shock preceeded by lightheadedness and near syncope. Figure 3 shows the electrograms retrieved from the device. Post-shock, the patient immediately felt fine.

Two months later, the patient was involved in a minor auto accident. While sitting on his car talking to the police, he received four shocks. He was asymptomatic from an arrhythmia standpoint. By the time the paramedics came and obtained a surface ECG recording, the patient was in sinus rhythm. The following electrogram for this event was later retrieved from the device (Figure 4).

In Figure 3, the pre-arrhythmia rhythm is sinus rhythm, and P-R association exists. Heart rate is about 80 BPM. Note that the tachycardia starts with a PVC, R is early and the PR interval is too short to be conducted. Of importance to note is that there is A-V dissociation during the tachycardia with the atrial rate being significantly slower than the ventricular rate. The tachycardia rate is very fast, approximately 270 to > 300 BPM. The rhythm is a ventricular fibrillation, which is terminated by a 675 Volt shock leading to A-V pacing at about 50 BPM. After the shock, the patient felt fine.

The PR interval in Figure 3, sinus rhythm at a heart rate of 80 BPM, was 160 ms; therefore, it is unlikely that at this faster heart rate of 166 BPM, the PR interval would be 320 ms. Normal physiologic response is that as the heart rate increases, the PR interval shortens.

P s seem to follow R s at approximately a 40 ms R-P interval. The tachycardia appeared to be AV nodal re-entry tachycardia (AVNRT). In typical AVNRT, the R-P interval is less than 90 ms.

An EP study was performed the next day, confirming the diagnosis of typical AVNRT. The electrical impulse was going from the atrium down a slow pathway to the His (activating the ventricle) and re-entering to the atrium via a fast pathway and then repeating the circuit continuously. Each time the impulse passes by the His, it activates the ventricles antegrade and the atrium retrograde. In the clinical episode, a shock to the ventricles did not terminate the arrhythmia as the ventricles are not a critical or necessary part of the re-entrant circuit.

Upon further questioning of the patient, he admitted to having had occasional periods of palpitations for many years. The auto accident scenario was a catecholamine-producing situation, creating a favorable setting for the initiation of AVNRT. During his visit to the EP lab, a radiofrequency ablation of the slow pathway was performed. Since the slow-pathway ablation, the patient has had no further palpitations or tachycardia episodes.

With a dual chamber ICD system, supraventricular tachycardia (SVT) discriminators may be programmed on, which could help prevent inappropriate shocks for SVT. Algorithms vary from device to device; however, some common discriminators are morphology, onset, stability of rhythm, and the number of A s compared to V s.

This patient (Mr. N) is an 82-year-old male who participates regularly in a monitored exercise program. He had received a single chamber pacing/ICD system for criteria as follows: history of coronary artery disease, S/P CABG, ischemic cardiomyopathy and non-sustained VT (MADIT criteria).

He was doing well post implant, other than occasionally during rehab, he would get sudden bradycardia producing symptoms of not feeling well at all (Figure 5). It was difficult to determine what his underlying rhythm was per the monitor strips from rehab (Figure 6).

We brought Mr. N in for an exercise stress test. First, we turned the pacer rate response off and set the lower rate limit to 40 BPM. The patient exercised 12 minutes at a standard Bruce protocol and achieved a maximum heart rate of 112 BPM. He was asymptomatic. During cool down, his heart rate remained about 95 BPM, and we questioned whether he might have AV nodal reentry tachycardia. To rule this out, we administered adenosine 12 mg IV and got normal expected AV block (Figure 7). We were also able to determine the underlying rhythm was sinus rhythm with a prolonged 1st degree AV block, and a PR interval of 340 ms.

During recovery, we also noted that in sinus rhythm when the patient had a PVC (Figure 8) retrograde conduction occurred making the AV node refractory and blocking antegrade conduction of the atrial impulse. Ventricular pacing started at a slower rate. With each paced beat, the same refractoriness was produced continuing AV block. To treat this situation, the patient s ICD/pacemaker system will be upgraded to a dual chamber system to hopefully abolish symptoms associated with sudden rate drop and possible pacemaker syndrome symptoms.