PACEMAKER/ICD PROBLEM OF THE MONTH
Ventricular safety pacing, ventricular sense response, and
ventricular tachycardia
Sern Lim, MD, CCDS
From the University Hospital Birmingham NHS Trust, Edgbaston, Birmingham, UK.
The ventricular sense response (VSR) algorithm enforces
biventricular pacing on ventricular sensing to maximize biven-
tricular pacing in patients with atrial fibrillation. This report
describes a case of recurrent ventricular tachycardia that may
be facilitated by this enforced pacing algorithm.
KEYWORDS Biventricular pacing; Pro-arrhythmia
Case summary
A 78-year-old man with a previous history of aortic valve
and root replacement (bioprosthetic valve) in 2006, parox-
ysmal atrial fibrillation (AF), severe left ventricular (LV)
impairment (estimated ejection fraction ⬍30%) and New
York Heart Association class III heart failure, paroxysmal
atrioventricular (AV) block, 1 previous documented episode
of sustained monomorphic ventricular tachycardia (VT) at a
rate of 138 beats/min and left bundle branch block (LBBB)
on electrocardiogram (ECG) underwent implantation of a
biventricular implantable cardioverter-defibrillator. His medi-
cal therapy included amiodarone and bisoprolol. The LV
lead was positioned in the lateral position and the right
ventricular (RV) lead in the RV apex.
Due to the documented paroxysmal AF and slow VT, the
biventricular implantable cardioverter-defibrillator (InSync
Maximo, Medtronic, Minneapolis) was programmed as
follows:
Pacing mode: DDD
Lower rate: 60 beats/min
Upper rate: 100 beats/min
Paced AV delay: 130 ms (minimum 100 ms)
Sensed AV delay: 90 ms (minimum 70 ms)
Rate adaptive AV on (from 90 beats/min)
Biventricular pacing, LV ⬎ RV 20 ms
Ventricular sense response on
Ventricular safety pacing on
Ventricular blanking post-ventricular pacing: 300 ms
Address reprint requests and correspondence: Dr. Sern Lim, University
Hospital Birmingham NHS Trust, Edgbaston, Birmingham B15 2TH, UK.
E-mail address: hsern@doctors.net.uk.
1547-5271/$ -see front matter © 2010 Heart Rhythm Society. All rights reserved.
ABBREVIATIONS AF ⫽ atrial fibrillation; ATP ⫽ antitachycardia
pacing; AV ⫽ atrioventricular; ECG ⫽ electrocardiogram; LBBB ⫽
left bundle branch block; LV ⫽ left ventricular; RV ⫽ right ven-
tricular; VSP ⫽ ventricular safety pacing; VSR ⫽ ventricular sense
response; VT ⫽ ventricular tachycardia
(Heart Rhythm 2010;7:567–569) © 2010 Heart Rhythm Society. All
rights reserved.
VT zone 120 to 200 beats/min: burst (8), ramp (8), ramp⫹
(8), cardioversion
VF zone ⬎200 beats/min: defibrillation
Interrogation of the device at routine 1-month follow-up
showed multiple episodes of VT terminated by antitachy-
cardia pacing (ATP). The patient re-presented 3 months
later with multiple shocks. Device interrogation revealed
over 20 episodes of VT requiring ATP therapy and over 200
episodes of nonsustained VT. He suffered multiple shocks
due to failure of ATP and acceleration of VT into the VF
zone on several occasions. Rhythm strip and ECG recorded
during the clinical assessment revealed intermittent ventric-
ular pacing in the QRS complexes (Figure 1) and frequent
nonsustained VT (Figures 2 and 3).
What is the cause of the intermittent ventricular pacing
and is this related to the frequent ventricular arrhythmias?
Discussion
The ECG and the recorded electrogram in Figure 1 show
atrial and ventricular pacing alternating with ventricular
sensed and atrial refractory events. The QRS complexes on
the surface ECG are of LBBB morphology and identical to
his intrinsic rhythm, with a rate of about 65 beats/min and
no preceding P waves. The atrial refractory events coincide
with the P waves buried in the ST segment on the surface
ECG and are probably retrograde atrial conduction. Hence,
this is likely to be a junctional rhythm. Note retrograde atrial
conduction occurs only with alternate beat (without atrial
pacing), as the atrium is refractory from atrial pacing.
Alternate-beat atrial pacing occurs as the atrial escape
interval of 870 ms (lower rate interval 1,000 ms – paced AV
delay 130 ms) expires. This is closely followed by the
intrinsic junctional beat at a rate of about 65 beats/min,
which accounts for the ventricular sensed event about 40 to
doi:10.1016/j.hrthm.2009.11.008
568 Heart Rhythm, Vol 7, No 4, April 2010

Figure 1 EGM confirming atrial pacing coinciding with intrinsic ventricular rhythm and retrograde P-wave in alternate beats without pacing stimuli. Note
ventricular safety pacing in alternate beats with atrial pacing (2 vertical lines in marker channel). EGM ⫽ electrogram.

50 ms after the atrial paced event. This ventricular sensed
event is closely followed by ventricular pacing (the second
longer vertical line on the marker channel), which is deliv-
ered within the QRS complex.
It is difficult to determine whether these ventricular
paced events represent ventricular safety pacing (VSP) or
the ventricular sense response (VSR) algorithm, as both of
these algorithms are represented in the same way on the
marker channel (labeled VS with a short and a longer
vertical line). In cases in which both VSP and VSR are
enabled, the VSP algorithm takes precedence during the
VSP interval within the paced AV delay interval (VSP is
active only after atrial paced events), whereas the VSR
operation remains active within the AV delay even after the
VSP interval expires. The ventricle is paced at the end of the
VSP interval or the programmed paced AV delay, which-
ever is shorter. The VSP interval is dependent on the current
ventricular rate: the VSP interval is 110 ms if the ventricular
rate is lower than the VSP switch rate, or 70 ms if the
ventricular rate exceeds the VSP switch rate. The VSP
switch rate is calculated as 60,000/[2 ⫻ (ventricular blank-
ing post-ventricular pacing ⫹ 110 ms)]. Hence, in this case,
ventricular pacing within the QRS complexes is likely to be
related to VSP, as the ventricular sensed events occurred
about 50 to 60 ms after the atrial paced events (within the
VSP interval). However, ventricular pacing (due to VSP) in
this case does not result in ventricular capture on ECG, thus
limiting cardiac resynchronization. Increasing the lower rate
to 70 beats/min and activation of rate-responsive pacing
resulted in consistent atrial-biventricular sequential pacing.
During the clinical assessment, the patient was noted to
have frequent nonsustained VTs, which were consistently
related to ventricular pacing on a ventricular premature beat.
Initially, this was believed to be a result of VSP. However,

Figure 2 Note initiation of VT with ventricular pacing on a ventricular premature beat. Arrow marks the onset of the QRS complex (slurred R-wave), with
ventricular sensing at least 80 ms after onset of ECG. ECG ⫽ electrocardiogram; VT ⫽ ventricular tachycardia.
Lim Pacemaker/ICD Problem
Figure 3 ECG showing initiation of VT with ventricular pacing on ventricular premature beat, but not in the absence of ventricular pacing (5th QRS
complex). This premature beat is not accompanied by VSR pacing as this would exceed the programmed VSR maximum rate. The ventricular premature beat
is consistent with left ventricular origin. ECG ⫽ electrocardiogram; VSR ⫽ ventricular sense response; VT ⫽ ventricular tachycardia.
closer examination of Figure 2 suggests that the ventricular
pacing may be enforced by VSR and not VSP. With a
post-pacing ventricular blanking period of 300 ms, the VSP
switch interval is calculated at 820 ms (2 ⫻ [300 ⫹ 110
ms]). Hence, the ventricular premature beat sensed about 80
ms after atrial pacing would not have triggered VSP, as the
VSP interval would have switched to 70 ms.
Indeed, these sequences persisted despite turning VSP
off. Crucially, the initiation of VT was associated with a
biventricular but not RV pacing configuration. In contrast,
turning VSR off led to cessation of these sequences, and the
patient remained free of VT with VSR off regardless of
whether VSP was programmed on or off, and irrespective of
pacing configuration (right or biventricular pacing), which
implicates the VSR algorithm and LV pacing in the patho-
genesis of VT in this case.
Differences between the pacing mode with VSR and
VSP may explain the pro-arrhythmic risk with the former.
Pacing enforced by VSP is delivered only to the RV if the
device is programmed to biventricular or RV pacing, but
pacing would be delivered to the LV if the device were
programmed to pace the LV only. In contrast, pacing asso-
ciated with VSR is delivered per the programmed pacing
configuration to either one or both ventricles (biventricular
in this case). When biventricular pacing is programmed,
VSR pacing uses the programmed sequence/outputs and a
2.5 ms V-V paced delay. Other operational differences
between VSR and VSP are: (1) VSR can be enabled in atrial
tracking modes or single chamber devices, and (2) VSR
cannot violate the programmed VSR maximum rate.
Biventricular pacing immediately after a ventricular
sensed event is designed to maintain some hemodynamic
benefit, particularly in patients with AF.1 However, the
potential pro-arrhythmic effects of epicardial LV pacing are
569
well described.2,3 Although the precise pro-arrhythmic
mechanism in this case cannot be determined, a re-entrant
mechanism is implied, as ATP was successful in terminat-
ing the majority of sustained VT episodes. The premature
beat (and VT) is consistent with an origin in the left ven-
tricle (Figure 3). Of note, RV sensing during the junctional
rhythm occurs early, but sensing of the LV premature beat
by the RV lead in the apex is delayed by at least 80 ms,
which may allow previously refractory tissue to recover
(Figure 2). The subsequent enforced (by VSR) delivery of
epicardial LV pacing critically timed to the LV premature
beat after the delayed sensing may enter the excitable gap as
previously refractory tissue recovers, and this pacing stimuli
may encounter unidirectional block in the re-entrant circuit
(within the left ventricle) and facilitate reentrant VT. In-
deed, ventricular premature beats of similar morphology,
which were not accompanied by ventricular pacing (Figure
3), did not result in VT. This is the first report of pro-
arrhythmia with VSR-enforced LV pacing on ventricular
premature beats. Disabling VSR in this case resulted in
cessation of VT despite frequent ventricular premature
beats.
Acknowledgment
The author thanks David Jones for his insightful comments
and discussions.
References
1. Aktas AK, Jeevanantham V, Sherazi S, et al. Effect of biventricular pacing
during a ventricular sensed event. Am J Cardiol 2009;103:1741–1745.
2. Shukla G, Chaudhry M, Orlov M, et al. Potential pro-arrhythmic effects of
biventricular pacing: fact or myth? Heart Rhythm 2005;2:951–956.
3. Medina-Ravell VA, Lankipalli RS, Yan GX, et al. Effect of epicardial or
biventricular pacing to prolong QT interval and increase transmural dispersion
of repolarization: does resynchronization therapy pose a risk for patients pre-
disposed to long QT or torsade de pointes? Circulation 2003;107:740 –746.