Samuel J. Asirvatham, MD

CASE

12.1

Patient History

A 43-year-old male with mild global left ventricular systolic dysfunction and sinus node dysfunction underwent dual-chamber pacemaker implantation. An ECG (Figure 12.1.1) was obtained at the time of pacemaker interrogation next day. ECG prior to pacemaker implantation is shown in Figure 12.1.2.

Figure 12.1.1

Figure 12.1.2

Questions

1. What is the rhythm shown in Figure 12.1.1?

2. What can you say about the pacemaker based on the QRS morphology?

Discussion, Interpretation, and Answers

This is a ventricular paced rhythm at 90 bpm. The dissociated sinus rhythm at 60 bpm can be seen marching through the tracing (Figure 12.1.3, black arrows). No obvious pacing artifact is noticeable.

Figure 12.1.3

The QRS morphology is similar to ventricular preexcitation during sinus rhythm in patients with an anteroseptal accessory pathway.¹ The red arrow (Figure 12.1.3) points to the onset of the QRS complex (“delta wave”) followed by the blue arrow showing a change to a sharper component. This suggests activation of the ventricular myocardium (red arrow) preceding and subsequently fusing with ventricular excitation through the His-Purkinje system (blue arrow). The pacing stimulus, in this case at the site of proximal right bundle branch, recruits the local ventricular myocardium immediately and inscribes the delta wave. It also stimulates the proximal right bundle from where there is a finite delay for excitation to propagate through the insulated conduction system before exiting from the distal Purkinje network.

The delta wave is negative in lead V₁ (left bundle branch block morphology) suggesting right ventricular or septal site of initial activation. Positive initial activation in leads V₄−V₆ suggests basal rather than an apical site. The overall QRS is relatively narrow with the frontal plane axis horizontally to the left (positive aVL, negative aVR). This localizes to the septal tricuspid valve region in anatomic proximity to the His-bundle/proximal right bundle branch. Preexcitation over an accessory pathway inserting to the ventricle at the septal atrioventricular annulus results in quick transition of delta wave from negative to positive from lead V₁ to V₂. In this case, the delta wave is negative in lead V₂ (red arrow) and becomes positive only by lead V₄, due to stimulation further away from the annulus and approaching the septal right ventricular outflow tract myocardium. Chest radiographs showing the right bundle pacing electrode (arrows) are shown in Figure 12.1.4 (asterisk—electrode in the right atrial appendage).

Figure 12.1.4

A differential diagnosis for Figures 12.1.1 and 12.1.3 is an accelerated idioventricular rhythm from the interventricular septum. Activation from a septal site in a structurally normal heart also results in a relatively narrow QRS due to centrifugal simultaneous depolarization of both ventricles; however, the QRS should not be notched (leads V₁ and V₂). Notching of QRS (Figure 12.1.3, blue arrows) reflects an abrupt change in the direction of the depolarizing wavefront on account of the activation from the conduction system catching up and fusing with the delta wave. A similar phenomenon resulting in abrupt changes in direction of the wavefront and notching in QRS could also occur on account of regions of conduction block (e.g., myocardial infarcts or surgical suture lines). Also notable in this ECG is the slight variation in the degree of contribution of the delta wave (leads aVL and V₄). This is probably due to small changes in the timing and field of capture of the insulated conduction system relative to the local myocardium with respirophasic movement of the pacing electrode.

There has been a resurgence of interest in pacing the proximal conduction system to preserve left ventricular electrical synchrony as opposed to the adverse hemodynamic effects from dyssynchrony related to right ventricular apical pacing.² Figure 12.1.5 is an anatomic section through the membranous septum with illustration of the course of the proximal ventricular conduction system. Though referred to as “His-bundle pacing,” placement of an active fixation electrode at the bundle of His is technically difficult due to its short course through the thin membranous septum before splitting into the bundle branches. Further, the fixation screw of a pacing electrode deployed at the true anatomic bundle of His could perforate into the left ventricle, get dislodged, or have problems with oversensing/pacing the atrium. Often the proximal right bundle branch is the actual site of pacing. Pacing the conduction system from this site with adequate output can result in a narrow QRS complex even in cases with underlying left bundle branch block.³

Figure 12.1.5

References

1. Arruda MS, McClelland JH, Wang X, et al. Development and validation of an ECG algorithm for identifying accessory pathway ablation site in Wolff-Parkinson-White syndrome. J. Cardiovasc. Electrophysiol. 1998;9(1):2–12.

2. Sharma PS, Dandamudi G, Naperkowski A, et al. Permanent His-bundle pacing is feasible, safe, and superior to right ventricular pacing in routine clinical practice. Heart Rhythm. 2015;12(2):305–312.

3. Lustgarten DL, Crespo EM, Arkhipova-Jenkins I, et al. His-bundle pacing versus biventricular pacing in cardiac resynchronization therapy patients: A crossover design comparison. Heart Rhythm. 2015;12(7):1548–1557.

Patient History

An 82-year-old female implanted with a pacemaker 8 years prior for AV block presented to the emergency department due to dizziness and dyspnea. The ECG recorded upon her admission (Figure 12.2.1) is shown.

Figure 12.2.1 ECG recorded upon the patient’s admission.

Question

What is the rhythm?

Discussion

The issue with this ECG recording is its scale, which was accidentally set to 4 cm/mV (see the calibration mark on the bottom left of the tracing). The same ECG is shown reduced to 25% in the vertical axis (corresponding to a scale of 1 cm/mV, see Figure 12.2.2), showing sinus rhythm with complete AV block, and a ventricular paced rhythm alternating with a junctional rhythm. The patient had not been seen for a pacemaker follow-up for a year, and the battery had reached end of life, with delivery of erratic pacing spikes by the device. This example shows the importance of systematic ECG interpretation, which includes analyzing calibration.

Figure 12.2.2 ECG reduced to 25% in the vertical axis and corresponding to a usual scale of 1 cm/mV, with recognizable P waves (asterisks), complete AV block, paced QRS complexes (blue arrows), and junctional beats (green arrows).

Patient History

A 68-year-old male with history of coronary artery disease and ventricular tachycardia underwent implantation of dual-chamber implantable-cardioverter defibrillator (Guidant, Ventak Prizm 2DR) 5 years ago. He was admitted to the hospital with symptoms of nausea, palpitations, presyncope, and low blood pressure. The rhythm strip while on telemetry is shown in the Figure 12.3.1. Device interrogation was done which showed the following parameters:

Figure 12.3.1 Rhythm strip.

Questions

A.What is the diagnosis based on the rhythm strip (Figure 12.3.1)?

1. Pacemaker-mediated tachycardia (PMT)

2. Atrial lead malfunction resulting in loss of capture

3. Repetitive nonreentrant ventriculo-atrial synchrony

4. AV search hysteresis

5. Both 3 and 4

B. How do you treat this condition?

1. Increase the post-ventricular atrial refractory period (PVARP)

2. Atrial lead revision

3. Shorten the AV delay

4. Shorten the PVARP

5. Both 3 and 4

Answers

A. 5

B. 5

Discussion

The rhythm strip demonstrates both repetitive nonreentrant ventriculo-atrial synchrony (RNRVAS) and AV search hysteresis (Figure 12.3.2). The first seven beats show atrial-paced, ventricular-sensed (AP-VS) complexes. This is followed by a PVC with retrograde atrial conduction. Note the inverted P waves in lead II (dashed arrows). The device does not sense the retrograde P as it falls in the PVARP that has extended to 400 ms following a PVC. This is followed by an atrial pacing spike that does not capture the atrium because the pacing spike falls into the absolute refractory period of the atrium. The paced AV interval expires resulting in a VP with subsequent retrograde atrial activation and the process repeats. This repetitive process of functional atrial undersensing due to retrograde atrial activation falling within the PVARP along with functional atrial noncapture due to the pacing stimulus falling in the absolute refractory period of the atrium is termed as RNRVAS. It may also be called AV desynchronization arrhythmia or pseudo atrial exit block. RNRVAS is a less common form of endless loop tachycardia resulting from ventriculo-atrial conduction; the more common form being PMT.

Figure 12.3.2 Annotated rhythm strip demonstrating repetitive nonreentrant ventriculo-atrial synchrony (RNRVAS) and AV search hysteresis.

Although the upper pacing rate is not seen with RNRVAS, the hemodynamics are similar to PMT. Patients typically present with symptoms suggestive of loss of AV synchrony; fatigue, palpitations, dizziness, hypotension, dyspnea, and syncope. RNRVAS can be stored as automatic mode-switching events because two atrial events [retrograde atrial activation and AP] are recorded by the device for each VP signal. RNRVAS can be prevented by shortening the PVARP (although this increases the risk of PMT), shortening the AV delay, reducing the lower rate limit or sensor-driven rate, using noncompetitive atrial pacing algorithm (manufacturer specific, NCAP delays AP by 300 ms when retrograde atrial activation falls in the PVARP) or by synchronous AP on PVC detection (functional noncapture of retrograde atrial impulse).

The other finding demonstrated on this rhythm strip is AV search hysteresis. Dynamic AV delay and AV search hysteresis were turned on in this patient’s device. In the beats prior to the PVC, the paced AV delay is approximately 190 ms. Post PVC, the paced AV delay extends out to 300 ms despite the maximum dynamic AV delay set at 270 ms. This is due to AV search hysteresis algorithm designed to promote intrinsic AV conduction and reduce deleterious effects of chronic right ventricular pacing. As there was no intrinsic R wave sensed by the end of the extended AV delay (300 ms in this case), VP occurred. In the present case, turning off the AV search hysteresis will shorten the AV delay, and may potentially prevent RNRVAS.

Patient History

A 91-year-old female with a history of hypertension, end-stage renal disease on hemodialysis, and sick sinus syndrome for which she underwent a dual-chamber permanent pacemaker (St. Jude Medical, Accent DR RF 2210 Pacemaker) implant 1 year ago, was admitted to the hospital with sepsis. The device was programmed to DDD mode with a base rate of 70 bpm, sensed AV delay of 170 ms, and paced AV delay of 200 ms. She was atrially paced 60% and ventricular paced 66%. Sensing, pacing threshold, and impedance on right atrial and ventricular leads were within normal limits. ECG during hospitalization is shown in Figure 12.4.1.

Figure 12.4.1 Baseline ECG.

Question 1

What does the ECG show?

1. Undersensing

2. Intermittent failure to pace

3. Fusion beat

4. Pseudo-fusion beat

5. Pseudo-pseudo fusion beat

Answer 1

The correct answer is 5.

Question 2

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