Pacemakers

Chapter 43.
Bradyarrhythmias
and Pacemakers
Pugazhendhi Vijayaraman; Kenneth A. Ellenbogen
Pacemakers
The science of cardiac pacing is only approximately 50 years old and has seen tremendous
growth and evolution. Since the introduction of transvenous pacing in 1958, 40the field of
cardiac pacing has benefited greatly from advances made in electronics, computer
technology, power sources, and miniaturization. The rapid growth in pacemaker design and
functions has made the understanding of these devices more complex and difficult. As the
potential indications for pacing had expanded, prospective, randomized trials to assess the
efficacy of these devices have become an integral part of the discipline.
Pacemaker System
A permanent pacemaker system consists of an implanted pulse generator and the leads
through which it delivers electrical stimuli in the various chambers of the heart. The
pacemaker is composed of the pulse generator, housing the complex electronic circuitry
and the battery, the power source. The pulse generator contains an output circuit, sensing
circuit, timing circuit, and telemetry coil that sends and receives programming instructions
and diagnostic information. Most current devices also have another circuit for the rateadaptive sensor. Modern pacemakers almost exclusively use lithium-iodine batteries as
their power source. The advantages of the lithium-iodine battery is that it has a high-energy
density, long shelf life, low battery life loss caused by internal self-discharge, and
predictable characteristics that allow early warning of battery depletion. Most singlechamber pacemakers have expected battery longevity of 7 to 12 years, whereas dualchamber pacemakers have an expected longevity of 6 to 10 years. Most pacemakers
generate 2.8 V at the beginning of life. When the voltage nears the end of life (2.1-2.4 V),
several elective replacement indicators in the pacemaker are activated. The common
indicators of elective replacement of the pacemaker are as follows:
Percent or fixed decrease in pacing rate on magnet application or free running rate
Increase in pulse-width duration
Change to a simpler pacing mode (DDDR to VVI; VVIR to VOO)
Reduced battery voltage
Elevated battery impedance
Restricted programmability
Once the elective replacement indicators are activated, the pacemaker is generally
replaced within weeks to months, or earlier if the patient is pacemaker dependent. When
the battery reaches the end of life (EOL, <2.1 V), the pacemaker changes to the simplest
mode (VOO), fails to communicate or reprogram, fails to pace or sense, and may function
erratically. If the pacemaker reaches end of life, it should be replaced immediately.
Pacemaker Leads
Permanent pacing leads have five major components: (1) electrodes, (2) conductors, (3)
insulation, (4) connector pin, and (5) fixation mechanism. The pacing leads may be unipolar
or bipolar. Although most of the leads used are bipolar in configuration, it is essential to
understand both lead systems. In unipolar leads, only a single electrode is present at the
lead tip (cathode) in contact with the myocardial tissue and the surface of the pacemaker
can act as the anodal terminal. Bipolar lead systems have a cathodal tip electrode and an
anodal ring electrode, 10 to 20 mm proximal to the tip electrode. Unipolar leads have a
simple structural design and excellent durability but may infrequently exhibit skeletal
myopotential oversensing, far-field sensing, crosstalk (atrial stimulus sensed by ventricular
channel), and skeletal muscle stimulation. Many newer pacemakers with bipolar leads allow
a change in configuration of the pacing/sensing function to unipolar or bipolar, as the
situation warrants. Contemporary electrodes have a small tip surface area with a porous or
roughened surface and steroid-eluting capability that reduces stimulation thresholds,
decreases current drain, and improves sensing. The electrodes are connected to the
connecter pin at the proximal end of the leads by the conductor wires that are usually made
of Elgiloy (alloy of nickel). The materials used for insulation of the pacing leads are of
silicone rubber and polyurethane varieties. Polyurethane insulation has the advantage of
having high tear strength, low friction, and smaller diameter and is relatively
nonthrombogenic compared with silicone-insulated leads.
The most commonly used transvenous endocardial leads have either a passive or an active
fixation mechanism to avoid early dislodgement. The passive fixation mechanisms include
tines, fins, or wings that are entrapped within the trabeculae of the right-sided heart
chambers and are subsequently covered by fibrous tissue. Most contemporary active
fixation leads use an extendable/retractable or exposed screw mechanism. The active
fixation leads allow precise positioning of the pacing lead in locations other than the right
atrial appendage or RV apex. They reduce the acute dislodgement rates of the right atrial
leads and are also easier to extract compared with passive fixation leads.
Pacemaker Implantation
Almost all pacemaker implantations are performed transvenously under local anesthesia
and conscious sedation using the cephalic, subclavian, or axillary veins. Axillary vein
access avoids the potential complication of compression damage to the leads inserted via
medial subclavian puncture in the tight costoclavicular angle. The pulse generator is usually
placed in the upper pectoral region subcutaneously, and occasionally the pacemaker is
implanted behind the pectoral muscle or behind the breast via an inframammary approach,
especially in young women.
Pacing Site
The atrial lead is generally placed in the right atrial appendage; however, in patients with
prior cardiac surgery, the atrial septum or the lateral wall is preferred. It is preferable to
avoid the atrial free-wall with active fixation leads, because this has the potential to cause
delayed pericardial effusion and/or cardiac tamponade. Atrial septal pacing and Bachmann
bundle pacing41 have been tested as alternate atrial pacing sites in an attempt to reduce the
frequency of episodes of atrial fibrillation. No clear benefit from pacing in the atrial
septum/Bachman bundle has been demonstrated in randomized trials. Similarly, dual-site
atrial pacing with one atrial lead placed in the atrial appendage and a second atrial lead
placed around the coronary sinus ostium has been shown to have a variable effect on the
frequency of episodes of paroxysmal atrial fibrillation.42
The ventricular lead is typically placed in the RV apex. However, attempts to maintain the
normal sequence of ventricular activation by high septal pacing near the His-bundle and the
RV outflow tract, especially in patients with cardiomyopathies, have suggested
hemodynamic benefits by improving cardiac output compared with RV apical pacing. A
randomized crossover trial of patients with congestive heart failure, LV dysfunction (ejection
fraction [EF] <42%), and chronic atrial fibrillation pacing from RV outflow tract (RVOT) or
dual-site RV pacing (RVOT + RV apex) did not consistently improve quality of life or other
clinical outcomes compared with RV apical pacing.43 Deshmukh and colleagues44 as well as
Occhetta and coworkers45 have demonstrated that direct His-bundle pacing is a viable
approach for permanent cardiac pacing in patients with dilated cardiomyopathy, and atrial
fibrillation and preserves LV function compared with RV apical pacing. Ongoing clinical
trials comparing alternate RV pacing sites are in progress.
With the advent of biventricular pacing for hemodynamic improvement in patients with
advanced heart failure and intraventricular conduction disturbances, more patients will
receive biventricular pacing systems. The LV lead is placed in the posterior or lateral vein of
the left ventricle through the coronary sinus. Epicardial pacing via thoracotomy must be
considered in occasional patients with inadequate venous access, phrenic nerve
stimulation, or mechanical prosthetic tricuspid valve; patients undergoing cardiac surgery;
patients with right to left shunting; and patients who have failed attempts at transvenous LV
lead placement.
Pacing Threshold and Sensing
Atrial and ventricular leads are placed into the appropriate chambers and sutured in place
after ensuring adequate pacing and sensing thresholds. The basic premise in obtaining
acute pacing and sensing thresholds during implant is that these thresholds may
degenerate over time, and adequate safety margins must be maintained to ensure safe
long-term pacing and sensing. It is essential to understand the strength-duration curve (Fig.
439). The strength-duration curve for stimulation is the quantity of voltage required to
stimulate the heart at a series of pulse widths. As shown in the figure, increasing the pulse
width beyond 0.6 ms usually does not decrease the voltage threshold. At implant, an atrial
pacing threshold of <1.5 V and ventricular threshold of <1 V should be obtained. The
threshold commonly increases over the next 2 to 4 weeks, reaches a peak, and then
decreases to a chronic threshold level after 6 to 8 weeks. With steroid-eluting leads, the
acute rise in threshold is ameliorated and the chronic threshold is significantly lower than in
nonsteroid-eluting leads. During initial programming, the pacing output is programmed at 3
to 5 times the threshold voltage with a pulse width of 0.4 to 0.5 ms. At the 2- to 3-month
follow-up visit, the output is decreased to no less than twice the threshold to maintain an
adequate safety margin and prevent battery drain. Some pacemakers have algorithms that
enable the device to confirm capture. These algorithms may determine pacing threshold at
programmed time intervals or on a beat-by-beat basis. Using algorithms to automatically
check pacing-capture thresholds, these pacers adjust pacing voltages to just above the
pacing threshold to reduce current drain and prolong battery longevity. Automatic capture
algorithms are or will soon be available for atrial, right ventricular, and left ventricular leads.
FIGURE 439
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Strength-duration curve. This curve is obtained by plotting the voltage threshold obtained at various pulse
widths. When programming the pacemaker output, this curve should be considered to ensure at least two
times the safety margin. Increasing the pulse width beyond 0.6 ms generally does not decrease the voltage
threshold.
Sensing is usually measured as the peak-to-peak or base-to-peak amplitude of the

intracardiac electrogram in millivolts. The ventricular electrograms should measure at least
5 mV and frequently measure in excess of 10 to 20 mV. Ventricular sensitivity (the level in
millivolts that the intracardiac electrogram must exceed to be sensed by the device) is
generally programmed between 2 to 3 mV so that an adequate safety margin exists for
sensing intrinsic ventricular depolarization without the risk of oversensing T waves or other
artifacts. Atrial electrograms are smaller in amplitude than ventricular electrograms;
however, a minimum atrial electrogram of 1 to 2 mV should be obtained. In patients with
paroxysmal atrial fibrillation or flutter, the atrial electrogram during tachycardia might be
smaller than during sinus rhythm. The atrial sensitivity is usually programmed at 0.5 mV;
however, the sensitivity may have to be adjusted depending on the size of the far-field
ventricular electrogram and associated atrial arrhythmias. Newer pacemakers also
incorporate algorithms that automatically adjust sensitivity to the size of the atrial or
ventricular signal.
Impedance
Lead impedance is the resistance to the flow of current from the generator to the
myocardial tissue through the lead. Although there is a wide variability of normal lead
impedances (250-1200 ), chronic lead impedances should not vary widely between
outpatient follow-up visits. A fractured lead exhibits markedly elevated lead impedance.
Insulation breaks manifest by reduced lead impedances. Lead fractures or insulation
breaks often are intermittent problems. Therefore, normal lead impedances and pacing and
sensing thresholds do not rule out these problems. The leads can be stressed by having
the patient change position and do various provocative arm movements (eg, isometric
exercise) to facilitate diagnosis of lead-related problems that are not otherwise observed.
Many pacemakers intermittently monitor lead impedance and alert the physician to
measured impedances that are out of the typical range.
Pacemaker Nomenclature
The North American Society of Pacing and Electrophysiology and the British Pacing and
Electrophysiology Group have established a five-letter pacemaker code to describe the
basic pacemaker mode and function (Table 4312).46 The first letter represents the chamber
being paced: A for atrium, V for ventricle, and D for both atrium and ventricle. The second
letter refers to the chamber in which sensing occurs: Codes are similar to those for the first
position. The third position describes the response of the pacemaker to a sensed
event: I for inhibition, T for triggered, and D for both inhibition and triggering. The
pacemaker can either inhibit (I) pacing output from one or both of its leads, or it can trigger
(T) pacing after the sensed event. In a DDD pacemaker, a sensed atrial event inhibits the
atrial pacing channel and triggers ventricular pacing after a programmable AV delay. The
fourth position refers to the programmability of the device: R for rate-responsive pacing; the
letters C (communicating), P (simple programmable), and M (multi-programmable) are
obsolete because all current devices are fully programmable. The fifth position refers to
antitachycardia function; with the evolution of implantable defibrillators, this position is rarely
used. With the evolution of biventricular pacemakers, the pacemaker code currently in
practice needs to be revised.
Table 4312. The Pacemaker Code

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Pacing Modes
Vvi Mode
As the pacemaker code indicates, the ventricle is the chamber sensed and paced, with
inhibition of ventricular pacing in response to a sensed ventricular event. A sensed or paced
ventricular event initiates two timing cycles:
1.
A refractory period that is programmable (ventricular refractory period) during which

period no ventricular sensing occurs to prevent inappropriate sensing of T waves.
Any ventricular event occurring during this interval will also not reset the timing
cycle.
2.
A lower-rate interval (LRI), which corresponds to the programmed pacing rate. If

there is no sensed ventricular event after the end of the ventricular refractory period
and this interval expires, the pacemaker initiates a paced ventricular event. If a
ventricular event is sensed after the ventricular refractory period (VRP), the
pacemaker resets the timing cycle to begin a new LRI and VRP (Fig. 4310).
3.
VVI pacing is the most commonly used pacing mode. Although it is a simple pacing
mode and offers protection against bradyarrhythmias, loss of AV synchrony is not
well tolerated in many patients and may lead to pacemaker syndrome (discussed
later in the chapter). In patients with chronic atrial fibrillation, this is an ideal pacing
mode, especially if rate responsiveness is available.
FIGURE 4310

Single-chamber ventricular-inhibited pacing mode. The first two beats are ventricular-paced (Vp) events.
The third beat is a ventricular-sensed (Vs) event. A Vs or Vp event starts a lower-rate interval (LRI), at the
end of which ventricular pacing is initiated. A sensed- or paced event also initiates a ventricular refractory
period (VRP) during which no sensing will occur. The LRI after a sensed event can be separately
programmed at a longer interval to allow for native rhythm. This is called hysteresis.
Aai Mode
Similar to VVI mode, sensing and pacing occurs in the atrium, with the atrial pacing channel
inhibited in response to a sensed atrial activity. An atrial refractory period (ARP) and an LRI
are initiated in response to a sensed or paced atrial event. AAIR pacing with rateresponsiveness is an excellent pacing mode in patients with sinus node dysfunction and
normal AV conduction. Patients with sinus node dysfunction may develop AV block, which
may be a source of concern when using AAI pacing. However, with careful selection of
patients, including normal PR intervals, absence of bundle-branch block, and AV
Wenckebach phenomenon occurring at atrial pacing rates of more than 120 beats/min, the
risk of development of second- or third-degree AV block is <0.6% per year.47
Voo/Aoo Modes
In these asynchronous pacing modes, there is no sensing. The chamber is paced
asynchronously at the lower rate limit. The timing cycle consists of only an LRI and will not
be reset by any intrinsic activity. Because there is no sensing, there are no refractory
periods. This mode is rarely used except during procedures using constant electrocautery
to avoid inhibition of pacing caused by sensing of the high-frequency impulses of
electrocautery. When a magnet is applied over the pulse generator, the pacemaker
switches to an asynchronous mode (VVI to VOO, DDD to DOO). The obvious disadvantage
of this pacing mode is the possibility of asynchronous pacing during the vulnerable period
and initiation of either atrial or ventricular fibrillation (extremely rare).
Vdd Mode
In this mode the pacemaker paces only the ventricle, senses in both the atrium and the
ventricle, and responds to atrial sensing with ventricular pacing. The ventricular channel is
also inhibited by spontaneous ventricular activity. A sensed atrial event will start an
atrioventricular interval (AVI) followed by ventricular pacing. If spontaneous AV conduction
occurs before the termination of the AVI, ventricular pacing is inhibited. If there is no
spontaneous atrial activity, ventricular pacing occurs at the lower-rate limit as in a VVI
pacemaker. However, because there is no atrial pacing, this mode should not be used in
patients with sinus node dysfunction. In patients with normal sinus node function and AV
block, this is an excellent mode choice.
Ddd Mode
A DDD pacemaker senses and paces in both the atrium and the ventricle, and the
response to sensing involves both inhibition and triggered output. The DDD pacemaker
uses numerous timing cycles, and it is essential to understand the following intervals. Most
modern pacemaker timing cycles are ventricular-based (with some modifications) and are
explained as such.
The LRI starts with a sensed or paced ventricular event and ends with a paced ventricular
event and consists of two portions. The ventricular event initiates an atrial escape interval
(AEI) or VA interval at the end of which atrial pacing is initiated. The atrial paced or sensed
event initiates the AVI, at the end of which ventricular pacing is initiated. So, LRI = VA
interval + AVI. A sensed atrial event occurring before the completion of the VA interval
terminates this interval and starts the AVI. A sensed ventricular event occurring before the
completion of the AVI will terminate this interval and the LRI and reinitiate the LRI. A sensed
or paced ventricular event will also initiate the ventricular refractory period (VRP) to avoid Twave oversensing and simultaneously initiates the postventricular atrial refractory period
(PVARP). The PVARP helps prevent the sensing and tracking of any retrograde P waves.
This refractory period is programmable and is essential to the prevention of pacemakermediated, endless-loop tachycardia, which is an arrhythmia in which the dual-chamber
pacemaker serves as the antegrade limb and the patient's retrograde conduction as the
retrograde limb. The AV interval and the PVARP together constitute the total atrial refractory
period (TARP), during which period the atrial channel remains refractory and will not be
tracked. This in essence determines the upper rate interval (URI) or the maximal tracking
rate interval (MTRI) in a DDD pacemaker.
In patients with DDD pacemakers, four different rhythm scenarios are possible, and many
patients exhibit more than one scenario:
1.
Normal sinus rhythm with no atrial or ventricular pacing: Here the patient's rate is
faster than the programmed lower rate of the pacemaker, and the native PR interval
is shorter than the programmed AV interval, as a result of which both the atrial and
ventricular channels are inhibited (Fig. 4311A).
2.
Atrial sensed, ventricular pacing: The patient's atrial rate is faster than the lowerrate limit, and the AV conduction interval is longer than the programmed AV interval,
or there is no AV conduction, resulting in sensing of P waves and triggering of the
ventricular channel after the programmed AV interval. In this situation, the patient is
ventricularly paced at the patient's sinus rate until the upper rate limit (Fig. 4311B).
3.
Atrial paced and ventricular sensed: In this situation the patient's atrial rate is slower
than the programmed lower rate and the patient's AV conduction interval shorter
than the programmed AV interval. Here the patient is atrially paced at the lower-rate
limit (Fig. 4311C).
4.
Atrial and ventricular pacing: Here the sinus rate is slower than the lower-rate limit,
and AV conduction is longer or absent, resulting in atrial and ventricular pacing at
the lower-rate limit (Fig. 4311D).
FIGURE 4311
A. DDD pacing mode: atrial- and ventricular-sensed. In this example, atrial-sensed activity (As) initiates an
atrioventricular interval (AVI), and normal conduction results in a ventricular-sensed (Vs) event that
terminates the AV interval and the lower-rate interval (LRI) and initiates an LRI and the atrial escape
interval (VA). Spontaneous atrial activity (As) again terminates the VA interval and starts a new AV
interval. B. DDD pacing mode: As ventricular pacing. In this example the As event leads to Vp at the
completion of the programmed AVI, because there is no native AV conduction to the ventricle. The Vp
event starts the VA interval, the LRI, and the upper rate interval (URI). The VA and the LRIs are terminated
by the spontaneous atrial activity that starts a new AV interval. C. DDD pacing mode: atrial-paced
ventricular-sensed. In this example, Ap starts the AVI but is terminated by the ventricular event that occurs
before the completion of the AV interval. The Vs event initiates the VA and the LRI. If there is no
spontaneous atrial activity, the VA interval times out and Ap occurs. D. DDD pacing mode: atrial- and
ventricular-paced. The Ap event starts the AVI, at the completion of which the ventricle is paced because
there is no spontaneous ventricular activity. The Vp event initiates the VA interval and results in atrial
pacing, as there is no spontaneous atrial activity. Both Ap and Vp occur at the LRI.
Atrioventricular Interval
The AV interval after a sensed atrial event is usually programmed to a shorter value than
the AV interval after a paced atrial event and is termed differential AV interval. Some DDD
pacemakers also have the added capability of shortening the AV interval with increase in
heart rates; this is called dynamic, or rate adaptive, AV interval. Another available feature
increasingly incorporated into modern pacemakers is AV hysteresis or Search AV+, in
which the device periodically increases the AV interval to allow native AV conduction and
intrinsic ventricular activation.
The paced AV interval is considered as a single interval with two subportions. The initial
interval is the blanking period (12-50 ms, programmable) during which the ventricular
channel is blanked to avoid ventricular sensing of the atrial pacing artifact. If a spontaneous
ventricular event occurs in this period, it will not be sensed. The second portion of the AV
interval is the crosstalk sensing window during which a ventricular event is sensed if it
occurs and leads to ventricular safety pacing with a shorter AV interval of 100 to 110 ms.
This is to avoid cross-talk, or inhibition of the ventricular channel by sensing of the atrial
pacing artifact (Fig. 4312).
FIGURE 4312

Atrioventricular (AV) interval and blanking periods. The AV interval after atrial pacing has two subportions.
During the initial ventricular blanking period, sensing is suspended to avoid ventricular sensing of the
leading edge of the atrial pacing artifact. During the second portion (cross talk sensing window), if
ventricular activity is sensed, ventricular pacing occurs with a shorter AV delay. The purpose of this safety
feature (ventricular safety pacing) is to avoid inhibition of the ventricular channel by sensing of the atrial
pacing artifact during this time window. Similar to the ventricular blanking period, there is an atrial blanking
period after ventricular pacing, during which sensing is suspended in the atrial channel to avoid atrial
oversensing of the far-field ventricular pacing artifact. Ap, atrial paced; Vp, ventricular paced.
Upper Rate Behavior

In VDD and DDD modes, in addition to the programmed lower rate limit, there is an upper
rate limit beyond which ventricular tracking of atrial events will not occur. When the atrial
rate exceeds the programmed upper rate limit, the pacemaker will exhibit either
Wenckebach or 2:1 AV block behavior. When the patient with complete heart block
exercises to a sinus rate beyond the upper rate limit of the pacemaker, the P wave that is
sensed is followed by ventricular pacing with prolongation of the AV interval beyond the
programmed value to avoid violating the upper rate limit for pacing. When one subsequent
P wave falls in the postventricular atrial refractory period, it will not be tracked, resulting
inpacemaker Wenckebach behavior (Fig. 4313). When the atrial rate increases further,
such that every other P wave falls in the total atrial refractory period (TARP), 2:1 pacemaker
AV block pattern occurs. The TARP should be programmed shorter than the upper rate
interval to prevent sudden development of 2:1 pacemaker AV block.
FIGURE 4313

DDD pacemaker: Wenckebach behavior at upper rate limit. The first beat shows the ventricular-paced (Vp)
event synchronized to the atrial-sensed (As) event at the programmed AV interval (AVI). The next atrial
event initiates an AVI, but when the AVI times out, the upper rate limit has not been satisfied so the AVI is
prolonged. When the upper rate limit is satisfied, ventricular pacing occurs. Because of the delayed
ventricular pacing, the next P wave falls even earlier into the next cardiac cycle and the AVI extension is
even greater. The next P wave falls within the total atrial refractory period (TARP) and is not sensed. This
atrial event (AR) is not followed by ventricular pacing. The following P wave occurs before the VA interval
expires, and tracking occurs at the programmed AV delay because the upper rate limit cannot be
exceeded. URI, upper rate interval.
In young patients with complete heart block, the upper rate of the pacemaker should be
programmed to faster rates corrected for the patient's age to prevent Wenckebach behavior
of the pacemaker during exercise. Programming dynamic AV interval and dynamic PVARP
allows the TARP to be shorter at higher pacing rates and avoid sudden slowing of
ventricular pacing rates. Another option is rate-responsive features, where a separately
programmable sensor rate allows the pacemaker to continue to pace at the sensor-driven
rate during exercise.
Mode Switch
When pacemaker patients with AV block (in DDD or VDD mode) develop atrial
tachyarrhythmias (atrial tachycardia, flutter, or fibrillation), many atrial events are sensed
and ventricular tracking occurs up to the programmed upper rate of the device. The surface
ECG typically shows an irregular ventricular paced rhythm at rates close to the upper rate
limit of the device. Occasionally in patients with slower atrial flutter, every other atrial
electrogram may fall in the PVARP, resulting in 2:1 AV block. In patients with intact
conduction, the ventricular rates are determined by the patient's intrinsic AV conduction.
In patients with persistent atrial tachyarrhythmias, reprogramming the pacemaker to DDI(R)
or VVI(R) mode avoids rapid ventricular tracking of the atrial arrhythmias. Automatic mode
switching is a programmable option in all current-generation pacemakers for patients with
paroxysmal atrial tachyarrhythmias (Fig. 4314). When the atrial rate exceeds the
programmed mode switch rate, the device automatically changes its mode to either the VVI
or DDI, in which ventricular tracking of atrial-sensed events do not occur. Current devices
can also provide a complete history of mode-switch episodes with regard to the duration
and frequency of these episodes and may also provide electrograms to confirm their nature.
During follow-up of these devices, it is important to monitor for mode-switch episodes and
confirm by reviewing the electrograms that they truly represent atrial tachyarrhythmias.
Arrhythmia logs from the device provide a very efficient way of assessing the effects of
various drug therapies in patients with atrial fibrillation.
FIGURE 4314

Mode switch behavior of DDD pacemaker during atrial flutter. Surface lead II, marker channel, and atrial
electrograms (EGMs) are shown. In the beginning of the tracing, atrial flutter is sensed and the ventricle is
paced at, but does not exceed, the upper rate limit of 110 beats/min. Once atrial tachyarrhythmia detection
criteria are met, mode switch occurs (*). Pacemaker switches mode to DDI (no atrial tracking) at 70
beats/min with rate-smoothing function to avoid an abrupt change in pacing rate.
Managed Ventricular Pacing

It is now well accepted that long-term RV pacing causes a deterioration of LV function
through complex effects on regional ventricular wall strain and loading conditions. Most
pacemakers now use a variety of different AV interval algorithms to search for intrinsic
conduction and avoid unnecessary ventricular pacing. Electrocardiograms obtained during
such pacemaker behavior may cause concern for the interpreting physicians unaware of
these pacemaker functions. Unlike traditional mode switch from DDD to VVI or DDI mode
during atrial tachyarrhythmias, newer pacemakers can switch pacing mode from AAI(R) to
DDD(R) in the Managed Ventricular Pacing (MVP) mode or the AAIsafeR2 mode. The MVP
mode provides functional AAI(R) pacing with the safety of dual-chamber ventricular support
in the presence of transient or persistent loss of conduction (Fig. 4315). The criterion to
switch to backup ventricular pacing is loss of AV conduction for two of the last four pacing
cycles (the four most recent A-A intervals). This allows fast switch to DDD(R) mode but
does not cause false switching on a single nonconducted atrial event. It is uncertain how
long the PR/AR interval should be allowed to prolong to avoid ventricular pacing.
FIGURE 4315

Managed ventricular pacing (MVP). A. Primarily, MVP mode looks like AAI(R) mode, except that it allows
for prolonged AV interval. It is an atrial-based pacing (Ap) mode that looks for any consecutive A-A
intervals without associated ventricular events. For occasional, single, nonconducted normal atrial
contractions, the device provides backup ventricular pacing to ensure ventricular support. The backup
ventricular pace (Vp) is scheduled to occur after any A-A interval in which there is no Vp event (*). The Vp
occurs 80 ms after the scheduled Ap (if pacing is occurring in the chamber), or after the inhibited atrial
pace (ie, 80 ms after the escape A-A interval). B. MVP switches from AAI(R) operation to DDD(R)
operation when there is evidence of persistent loss of AV conduction. The criterion to switch is loss of AV
conduction for two of the last four pacing cycles (the four most recent A-A intervals). The strip illustration
shows that immediately after the first A-A interval with no conducted ventricular sensed event (Vs), a
backup Vp is delivered 80 ms after the scheduled Ap. Then a second A-A interval occurs with no
conducted Vs event. Again, the backup Vp is delivered followed by a permanent switch to DDD(R)
operation, wherein the AV delay is the programmed paced (or sensed) AV delay of 150 ms. AV,
atrioventricular.
Rate-Responsive Pacing
Rate-responsive pacing refers to the ability of the pacemaker to increase its lower rate in
response to physiologic stimuli. Simple VVI and AAI pacemakers do not have the ability to
increase their pacing rates in response to exercise. In patients with normal sinus node
function and DDD pacemakers, the ventricular pacing rate increases in response to an
increase in sinus rate and is physiologic. However, in the presence of sinus node
dysfunction, the pacing rate does not increase commensurate with the increase in
physiologic need. Rate-responsive pacemakers provide the ability to increase pacing rates
through special sensors incorporated in the pacing system that monitor various physiologic
processes. Based on information from the sensors, the lower rate of the pacemakers
constantly varies up to the upper sensor rate. At any point in time, the sensor rate overrides
the programmed lower rate of the pacemaker. Rate-responsive pacing is available in almost
all current pacemakers in VVIR, AAIR, DDIR, and DDDR modes. In patients with sinus
node dysfunction, rate-responsive pacing in AAIR, DDIR, or DDDR mode is preferable to
nonsensor-driven pacing. Also, in patients with chronic atrial fibrillation and heart block,
VVIR pacing is preferable to VVI pacing. In patients with severe coronary artery disease, it
may be necessary to limit the programmed upper rate limit. The ideal mode for pacing is
decided based on information regarding sinus node function, AV nodal function, atrial
arrhythmias, heart rate response to exercise, and patient-specific clinical factors (Fig. 43
16).
FIGURE 4316

Pacemaker mode selection. AF, atrial fibrillation; AV, atrioventricular.
Rate-Responsive Sensors
An ideal rate-responsive pacing system should provide rate response appropriate for the
metabolic demand during a wide range of activities. The optimal sensor should provide the
following:
Proportionate increase in heart rate to match increase in metabolic demand
Appropriate rapid change in heart rate with exercise onset
High sensitivity and specificity
Appropriate slowing of heart rate after exercise
Sensors available or under development can be classified using a physiologic or technical

classification system. In physiologic classification, the sensors are classified according to
the physiologic level at which they sense (Table 4313).
Table 4313. Physiologic Classification of Sensors

Activity Sensors
Activity-based sensors using piezoelectric crystals or accelerometers to detect vibration are

the most widely used sensors. Although the piezoelectric crystal senses vibration
associated with up-and-down motion, the accelerometer detects anteroposterior motion of
the body. Accelerometer-based sensors provide adequate and quick increases in heart rate
during treadmill exercise as compared with that of piezoelectric crystals. Although both
sensors have been shown to provide excellent rate-responsiveness, direct manual
pressure, walking down stairs, horseback riding, or riding on a bumpy street can cause an
inappropriate increase in heart rate with the piezoelectric crystal-based sensor. These
activity-based sensors do not provide adequate heart rate response with emotional stress
or isometric exercises. Currently, the accelerometer is the most widely used rate response
sensor.
Minute-Ventilation Sensor
The specificity and sensitivity of minute-ventilation sensing pacemakers for changes in

metabolic workload are excellent. Current pulses are emitted from the pacemaker can, and
the proximal ring electrode of the RV lead (or right atrial lead) and transthoracic
impedances are measured. Measurement of phasic impedance changes provides
respiratory rate and tidal volume information, thus determining the minute ventilation. The
minute ventilation changes are used to calculate the pacing rate and have excellent
correlation with exercise. Minute-ventilation sensing pacemakers can inappropriately
increase pacing rates with hyperventilation, coughing, and mechanical ventilation and in
patients with chronic obstructive pulmonary disease exacerbations.
Dual Sensors
Most of the currently available sensors have an excellent track record, but they may
occasionally respond to nonphysiologic stimuli. A multisensor rate-responsive pacemaker
can improve specificity by having one sensor verify the other sensor (eg, sensor crosschecking). A combination of two sensors can better simulate the normal sinus node
response. Both sensors must indicate a need for rate response to allow an increase in
sensor-driven heart rate. Some sensor systems provide the advantage of more physiologic
pacing during steady state, but have a slow response time during initiation of exercise.
Other sensors, particularly activity sensors, have faster response times at initiation of
activity but may not produce physiologic responses during peak or steady-state activity.
Pacemakers with dual sensors can provide patients with rapid responses during the start of
exercise and then use a more physiologic sensor (minute ventilation) to provide more
proportional heart rate responses during steady state (eg, sensor blending).
Indications for Pacing

The guidelines of the American College of Cardiology, the American Heart Association, and
the Heart Rhythm Society for the implantation of pacemakers were revised and updated in
2008. The indications for permanent pacing can be considered in categories of
bradyarrhythmia and nonbradyarrhythmia. The bradyarrhythmic indications were discussed
in the earlier part of this chapter.
Pacing to Prevent or Terminate Tachyarrhythmias
Pacing can help prevent and terminate tachyarrhythmias. The long QT syndrome is
characterized by abnormally prolonged ventricular repolarization with the tendency to
develop pause-dependent ventricular arrhythmias (torsade de pointes), syncope, and
sudden death. In patients with long QT syndrome, recurrent pause-dependent VT may be
prevented by continuous pacing, and pacing, in addition to - blockade, has been shown to
shorten QT interval and prevent sudden death in high-risk patients.48
Reentrant supraventricular arrhythmias such as AV node reentrant tachycardia, AV
reentrant tachycardia, and atrial flutter may be terminated by a variety of pacing methods
that include programmed stimulation and short bursts of rapid overdrive pacing. These
antitachycardia pacemakers must detect a tachyarrhythmia and then spontaneously initiate
an antitachycardia pacing algorithm, or they can be programmed to respond to external
magnet application. With significant advances with catheter ablation, the need for
pacemakers to treat supraventricular arrhythmias has virtually vanished.
Further trials are ongoing to determine the best pacing algorithms and atrial lead locations
to prevent or terminate atrial fibrillation. A large number of studies have been performed to
measure the benefit of algorithms that pace the atrium at more rapid rates than the intrinsic
sinus rate (eg, DAO-dynamic atrial overdrive) for periods of time. The majority of studies
have been unable to confirm any clinically important benefit of pacing algorithms to
decrease the frequency, duration, or burden of atrial fibrillation in patients with preexisting
bradycardia indications for pacing or patients without bradycardia. The indications for
pacemaker therapy to prevent or treat tachyarrhythmias are shown in Table 4314.
Table 4314. Indications for Pacing to Prevent or Terminate Tachycardias

Pacing in Dilated Cardiomyopathy
Permanent dual-chamber pacing with a short AV delay and a conventional pacemaker
(ventricular lead in the RV apex) was initially proposed 2 decades ago as adjuvant
treatment of advanced heart failure.49 However, initially encouraging results were not
confirmed in several subsequent, small randomized, prospective studies. Bakker and
colleagues first suggested a clinical benefit from biventricular pacing in heart failure patients
with intraventricular conduction disorder.50 Thereafter, biventricular pacing has been studied
in a number of acute and short-term studies followed by many prospective, randomized
trials, the results of which are summarized in Table 4315. Approximately 30% of the
patients with chronic heart failure manifest intraventricular conduction disorder with QRS
intervals longer than 130 ms.51 Intraventricular conduction disturbances of the left bundlebranch blocktype lead to delay in the activation of the LV free wall as compared with the
septum and right ventricle, resulting in intra- and interventricular mechanical dyssynchrony.
Ventricular dyssynchrony is associated with paradoxical septal motion, decreased diastolic
filling times, prolonged mitral regurgitation, and reduced LV stroke volume. Biventricular
pacing by simultaneous pacing of the right and left ventricle has been shown to coordinate
the septal and the LV free-wall contraction and decrease right and left atrial filling pressures
and mitral regurgitation, as well as improve diastolic filling, cardiac output, and left
ventricular ejection fraction (LVEF) in patients with severe LV systolic dysfunction and
prolonged IVCD.52 Biventricular pacing also has been shown to reduce myocardial oxygen
consumption, with improvement in ventricular contraction.53
Table 4315. Trials of Biventricular Pacing for Heart Failure

Clinical Trials
The Multisite Stimulation in Cardiomyopathy (MUSTIC) trial was the first randomized,
prospective study of biventricular pacing (see Table 4315).56 There was a significant
improvement in the 6-minute walk distance, quality of life, and reduction in hospitalizations
in the pacing group as compared with the nonpacing group. Biventricular pacing was the
preferred pacing mode in >80% of patients. In long-term open-label follow-up of these
patients, significant clinical benefits were maintained at 24 months. The Multicenter InSync
Randomized Clinical Evaluation (MIRACLE) study was a prospective, randomized, placebocontrolled, double-blind trial of patients with class III to IV heart failure, LVEF of ≤35%,
and QRS duration of 130 ms.58 Patients who received biventricular pacing experienced
significant improvement in the 6-minute distance walked (+39 min vs +10 min; P = .005),
functional class, quality of life, and EF (+4.6% vs 0.2%; P<.001). Both trials showed
significant clinical improvement in patients with biventricular pacing despite maximal
medical therapy for congestive heart failure with -blockers, diuretics, digoxin, and
angiotensin-converting enzyme inhibitors.
Meta-analysis pooling data from four randomized studies showed that cardiac
resynchronization therapy (CRT) reduced death from progressive heart failure by 51%
compared with control (odds ratio, 0.49; 95% CI, 0.25-0.93), and reduced heart failure
hospitalization by 29% (odds ratio, 0.71; 95% CI, 0.53-0.96). CRT was not associated with
a statistically significant effect on nonheart failure mortality or a reduction in the number of
patients experiencing VT or ventricular fibrillation.67 Experience with a biventricular
pacemaker in combination with an implantable cardioverter defibrillator (ICD) has been
published.61 The early termination of the COMPANION (Comparison of Medical,
Resynchronization, and Defibrillation Therapies in Heart Failure) trial has answered the
question regarding the mortality benefit of ICD therapy combined with biventricular pacing
in this patient group.62 The trial was terminated prematurely after enrolling almost 1600
patients because initial results demonstrated that combined biventricular pacemakerICDs
reduced mortality by 42% compared with optimal medical therapy, whereas biventricular
pacemakers alone showed only a 15% reduction in mortality. The CARE-HF (Cardiac
Resynchronization Heart Failure) trial63 enrolled 813 patients with severe New York Heart
Association (NYHA) class III to IV heart failure, reduced LVEF of <35%, and cardiac
dyssynchrony with QRS duration >120 ms, and randomized patients to optimal medical
therapy versus biventricular pacing, with follow-up for a mean of 29.4 months. The primary
end point of composite of death from any cause and unplanned hospitalization for a major
cardiac event was reached in 55% of patients in the medical therapy group compared with
39% in the biventricular pacing group. All-cause mortality was 30% in the medical therapy
group compared with 20% in the biventricular pacing group. This is the first study to
demonstrate a mortality benefit from the biventricular pacemaker alone.
The Post AV node ablation Evaluation (PAVE) study64 was a prospective, randomized trial
comparing BiV pacing with RV pacing in 184 patients with chronic atrial fibrillation
undergoing AV node ablation. At 6 months' post ablation, the patients in the biventricularly
paced group had significant improvement in 6-minute walk distance. The LV ejection
fraction remained stable in the BiV pacing group compared with a decrease in ejection
fraction in the RV pacing group.
Although the clinical benefits of CRT therapy in patients with advanced heart failure had
been well proven, recently completed studies promise possible benefits even in patients
with mild heart failure. In the REVERSE trial,67 610 patients with NYHA functional class I or
II heart failure with a QRS 120 ms and a LV ejection fraction ≤40% received a CRT
device (biventricular defibrillator) and were randomly assigned to active CRT (CRT-ON; n =
419) or control (CRT-OFF; n = 191) for 12 months. The primary end point of heart failure
clinical composite response worsened in 16% in CRT-ON compared with 21% in CRT-OFF
(P = not significant), whereas the prespecified secondary end point of LV end-systolic
volume index was significantly improved, along with a significant delay in the time to first
hospitalization for heart failure. In the European arm of this trial, the follow-up was
continued for 24 months in 262 patients. The heart failure clinical composite response
worsened in 34% compared with 19% in the CRT-ON group (P = .01), and the LV endsystolic volume index and LVEF improved significantly.
Moss et al66 randomly assigned 1820 patients with LVEF ≤30%, QRS duration 130 ms,
and NYHA class I or II symptoms in a 3:2 fashion to CRT plus an ICD versus an ICD alone
and followed them for an average of 2.4 years. The primary end point of death from any
cause or a nonfatal heart failure event occurred in 17.2% of patients in the CRT-ICD group
compared with 25.3% in the ICD-alone group (HR 0.66; P < .001). The superiority of CRT
was driven by a 41% reduction in the risk of heart-failure events, a finding that was evident
primarily in a prespecified subgroup of patients with a QRS duration 150 ms. CRT was
associated with a significant reduction in LV volumes and improvement in the ejection
fraction. There was no significant difference between the two groups in the overall risk of
death, with a 3% annual mortality rate in each treatment group. Thus CRT therapy in
patients with mild heart failure may modify disease progression and improve clinical
outcomes.
Biventricular Pacemaker System
In addition to the usual right atrial and RV lead, the biventricular pacing system uses an
additional lead to pace the left ventricle. Most leads have been specifically designed with a
lumen to allow for passage of the lead over a guidewire into the coronary venous system
and further manipulation through the vein branches until an adequate site with acceptable
pacing and sensing thresholds is located on the LV epicardium. Acute data indicate that
optimal hemodynamic response in most patients is obtained if the LV lead is placed in a
posterolateral, lateral, or anterolateral vein to provide resynchronization therapy.54Figure 43
17 demonstrates an occlusive venogram of the coronary sinus, showing great cardiac vein
and branch vein anatomy. Chest radiographs in posteroanterior and lateral views of a
patient with a biventricular pacemaker are shown in Fig. 4318. Figure 4319demonstrates
the ECGs of this patient in sinus rhythm with left bundle-branch block and with biventricular
stimulation, respectively. The hallmark of LV capture is an R/S ratio 1 in lead V1 or R/S
ratio ≤1 in lead I. The sensitivity of these findings to correctly identify loss of LV capture is
94%. The preferred pacing mode is VDD, in which both ventricles are paced simultaneously
after sensed atrial activity with a short AV interval. The InSync III trial suggested a possible
increased hemodynamic benefit with sequential biventricular pacing by varying the interventricular activation sequence compared with simultaneous biventricular pacing. 59 For this
therapy to be effective, the patients must maintain ventricular pacing (>90% ventricular
pacing). Biventricular pacing has also been shown to improve functional status and heart
failure symptoms in patients with chronic atrial fibrillation and AV-node ablation. 57,68 The
current indications for biventricular pacing in patients with severe systolic heart failure are
shown in Table 4316.
Table 4316. Indications for Biventricular Pacing in Patients with Severe Systolic
Heart Failure
FIGURE 4317

Right anterior oblique view of an occlusive venogram of the great cardiac vein and the other branch veins
of the coronary sinus (left marginal vein, left posterior vein, and the middle cardiac vein).
FIGURE 4318

Posteroanterior and lateral chest radiographs demonstrating the right atrial, right ventricular, and the left
ventricular (LV) leads in a patient with a biventricular pacemaker. The LV lead (arrow) is placed in the
posterolateral vein branch of the coronary sinus, allowing for simultaneous activation of the septum and the
LV free wall.
FIGURE 4319
Electrocardiogram of biventricular pacing. Normal sinus rhythm with left bundle-branch block and QRS
width of 200 ms (top). Atrial-sensed biventricular stimulation; note how the paced QRS complex has
narrowed significantly from the baseline (bottom).
Pacing in Hypertrophic Cardiomyopathy

Dynamic LV outflow tract obstruction is present in approximately 25% of patients with
hypertrophic cardiomyopathy. Symptoms such as dyspnea, angina, palpitations, and
syncope may coexist in patients with LV outflow obstruction. Although the severity of
symptoms does not correlate well with the severity of obstruction, reduction or elimination of
the outflow gradient seems to correlate with clinical improvement. RV apical pacing results
in preexcitation of the interventricular septum and reverses the ventricular activation
sequence, leading to an increase in the outflow tract diameter and reduction of the outflow
gradient. Although gradient reduction may reduce effective cardiac workload, abnormal
ventricular activation from pacing may cause impaired relaxation and may be more
detrimental in patients with preexisting diastolic abnormalities.
Hassenstein and Wolter reported in 1967 that RV pacing resulted in significant reduction of
the LV outflow gradient in patients with hypertrophic cardiomyopathy. 69 Subsequent to this
and a few other reports, many small and large observational studies suggested reduction of
the outflow tract gradient, modest improvement in exercise tolerance, and favorable
changes in the degree of angina, syncope, and functional class after dual-chamber
pacemaker implantation.70 Subsequent placebo-controlled, blinded, randomized studies
have shown only modest benefit with pacemaker therapy. For example, the Pacing in
Hypertrophic Cardiomyopathy (PIC) trial examined 83 patients with hypertrophic
cardiomyopathy and randomized to DDD pacing or AAI pacing for 12 weeks and then
crossed over. DDD pacing was associated with 51% reduction in the LV outflow gradient
and 63% improvement in functional class. DDD pacing, however, did not improve exercise
tolerance. At the end of 6 months, 76 patients preferred the active DDD pacing
mode.71Dual-chamber pacing is considered only for patients who are not surgical
candidates or who cannot tolerate or fail medical therapy (Table 4317).
Table 4317. Indications for Pacing in Hypertrophic Obstructive Cardiomyopathy

Pacemaker Complications
Patients undergoing a new pacemaker system implantation are generally monitored in the
hospital for a day in anticipation of any untoward complications. The various complications
associated with pacemakers are outlined in Table 4318.
Table 4318. Pacemaker Complications

Pneumothorax
At the time of implantation, subclavian or axillary venous access can rarely result in
pneumothorax, hemothorax, or hemopneumothorax. This can occur from inadvertent
puncture and laceration of the subclavian vein or the subclavian artery or the lung. The use
of venograms to locate the venous system in difficult cases and the routine use of axillary
venous access have reduced these complications significantly. Occasionally, air embolism
may occur during cephalic vein or subclavian vein cannulation. The use of safe
sheaths with one-way valve mechanism minimizes this risk.
Cardiac Perforation
Cardiac perforation resulting in pericardial effusion and occasionally cardiac tamponade is
a rare but potentially life-threatening complication of pacemaker lead insertion. This may be
recognized at the time of lead insertion by fluoroscopic position of the lead, right bundlebranch block morphology of the paced QRS complex, diaphragmatic stimulation, or
hypotension resulting from cardiac tamponade. If identified at the time of implantation, lead
withdrawal and repositioning is usually not associated with tamponade. In patients with
chest pain, friction rub, and a small pericardial effusion, serial echocardiograms may be
performed to assess for hemodynamic deterioration. Cardiac perforation and pericarditis
may also develop as a late complication and occasionally lead to tamponade weeks to
months after the pacemaker implantation, especially with active fixation leads.
Hematomas
Hematomas occurring at the pacemaker pocket site can vary from a small ecchymosis to
large and tense swelling. Most small hematomas can be managed conservatively with cold
compresses and withdrawal of antiplatelet or antithrombotic agents. Occasionally, large
hematomas that compromise the suture line or skin integrity may have to be surgically
evacuated. In patients who require therapeutic anticoagulation, heparin should be delayed
for at least 24 to 48 hours after implantation to avoid bleeding complications. Several recent
studies indicate that the risk of hematomas is lower if the procedure is performed
while warfarin is continued at therapeutic levels.
Venous Occlusion
Venous occlusion may result from acute subclavian or axillary vein thrombosis and lead to
ipsilateral arm edema and thrombosis. Venous thrombosis is generally treated
with heparinand 3 to 6 months of warfarin. Rarely invasive surgical interventions may be
required. Up to 30% to 42% of patients undergoing pacemaker implantation may develop
partial to complete venous occlusion over time and may remain asymptomatic because of
the development of venous collaterals. Occasionally, superior vena caval occlusion leading
to superior vena cava syndrome may result from pacemaker lead implantation.
Infection
The use of prophylactic antibiotics and pocket irrigation with antibiotic solutions has
decreased the rate of acute infections after pacemaker implantations to <1% to 2% in most
series. Although early infections are generally caused by Staphylococcus aureus and may
be aggressive, late infections associated with pacemakers are usually caused by S.
epidermidis, and their course tends to be indolent. The signs of infection include local
inflammation and abscess formation, erosion of the pacer, and fever with positive blood
cultures without an identifiable focus of infection. Occasionally the infected pacemaker

tends to erode through the skin. Transesophageal echocardiography helps determine
whether vegetations are present on the pacemaker leads. Removal of the pacemaker leads
and generator is usually required to completely eliminate pacemaker infections. 72
Lead Dislodgement
Leads may dislodge from the initial implant site in the first few days to few weeks after
implantation. Active and passive fixation mechanisms of leads help prevent this
complication. Atrial lead dislodgement is slightly more common than it is for ventricular
leads. Although passive fixation leads are stable in the atrial appendage, active fixation
leads are necessary to prevent dislodgment in patients with prior cardiac surgery. Lead
dislodgment may result in an increase in pacing thresholds, failure to capture, or failure to
sense. Lead dislodgment may be radiographically visible or it may be
amicrodislodgement, where there is no radiographic change in position, but there is
significant increase in pacing threshold and/or decline in the electrogram amplitude.
Diaphragmatic/Phrenic Nerve Stimulation
Diaphragmatic/phrenic nerve stimulation may lead to significant discomfort. This
phenomenon is most commonly observed in patients with LV coronary vein branch lead
placement for biventricular stimulation. During implant, high-output pacing at maximal
voltage and pulse width should be tested routinely to avoid diaphragmatic stimulation. With
the advent of bipolar LV leads, multiple pacing vectors are possible and allow the physician
to avoid repeat surgery by reprogramming the stimulation vector.
Twiddler Syndrome
Twiddler syndrome is a term applied to patients who intentionally or unintentionally
manipulate their pulse generator, causing twisting of the entire pacemaker system. This
leads to lead dislodgment or lead fracture.
Pacemaker Syndrome
The constellation of neurologic and cardiovascular signs and symptoms resulting from
deleterious hemodynamics induced by ventricular pacing has been termed pacemaker
syndrome. The variety of symptoms and signs associated with pacemaker syndrome are
listed in Table 4319. They are attributable to a decrease in cardiac output and arterial
pressure caused by loss of AV synchrony or to cardiovascular or humoral reflexes elicited
by increases in pulmonary venous or right atrial pressures. The basis for pacemaker
syndrome is not only loss of AV synchrony but also the presence of ventriculoatrial (VA)
conduction. Atrial contraction against closed AV valves leads to increases in jugular and
pulmonary venous pressure, causing cough and malaise in patients with intact cardiac
function and congestive heart failure in other patients with structural heart disease. The
symptoms may vary from mild to severe and the onset of symptoms range from acute to
chronic.
Table 4319. Symptoms and Signs of Pacemaker Syndrome

The exact incidence of pacemaker syndrome is unknown, but severe manifestations are
expected to occur in 5% to 7% of ventricularly paced patients. Milder symptoms or
significant drops in systolic blood pressure and cardiac output during ventricular pacing
occur in >20% of patients. In the Pacemaker Selection in the Elderly trial, 26% of patients in
the ventricular pacing arm crossed over to the DDD pacing mode because of symptoms
caused by pacemaker syndrome.25
The management of pacemaker syndrome usually requires restoration of AV synchrony. In
many patients, an upgrade to a dual-chamber pacer is indicated. In some patients with
intact sinus and AV conduction, lowering the pacing rate in VVI mode and using the
hysteresis mode may promote sinus rhythm, lessening the symptoms associated with
pacemaker syndrome.
Pacemaker-Mediated Arrhythmias
Pacemaker-Mediated Tachycardia
Pacemaker-mediated tachycardia (PMT), or endless-loop tachycardia, is a well-recognized
arrhythmia mediated by the pacemaker in patients with atrial-sensed ventricular pacing
systems. In patients with intact VA conduction, a premature ventricular contraction may
result in retrograde conduction to the atria, which, if outside the PVARP, is sensed and
followed by ventricular pacing after the programmed AV interval. The paced ventricular
event will again be followed by VA conduction, resulting in endless-loop tachycardia. PMT
can be prevented by programming the PVARP to be longer than the native VA conduction
time. However, if the VA interval is very long, the PVARP cannot be lengthened, as this will
limit the upper rate. Modern pacemakers have several options to prevent or terminate PMT.
One such feature is automatic extension of PVARP after a sensed premature ventricular
beat to prevent tracking of retrogradely conducted P waves. If PMT is established (atrialsensed ventricular pacing close to the upper rate limit with stable VA intervals), the PVARP
is automatically extended to a longer interval of 500 ms for one cycle, usually terminating
the tachycardia (Fig. 4320).
FIGURE 4320

Pacemaker-mediated tachycardia. Surface electrocardiogram; marker channel with AV, VA, and VV
intervals; and intracardiac atrial electrograms are displayed. The atrium is paced (A) at subthreshold
output, leading to noncapture after the second ventricular paced beat, resulting in atrioventricular
dissociation. The second-paced ventricular event is followed by a native P wave with a VA interval of 320
ms (PVARP 275 ms) and is sensed, leading to ventricular pacing. This is followed by a retrogradely
conducted P wave (open arrow), with a VA interval of 420 ms, and sets up the endless-loop tachycardia.
Because the ventricular pacing rate is above the programmed pacemaker-mediated tachycardia rate of 100
beats/min, the device automatically extends the PVARP on the second-to-last ventricular paced beat to 500
ms (arrow), resulting in nonsensing of the retrograde P wave, terminating the tachycardia. PVARP,
postventricular atrial refractory period.
Lead Failure
The pacemaker leads are subject to long-term complications. The insulation of the leads
may break, leading to problems with over-sensing (caused by electrical noise),
undersensing, and failure to capture (caused by current leak). This problem often manifests
intermittently and may be difficult to detect during a routine pacer check. The patient may
complain of pectoral muscle stimulation caused by current leakage around an insulation
break. An abnormally low impedance with demonstrable lead malfunction is diagnostic for
insulation break. Leads may also fracture over time. Early lead fractures lead to increased
impedances associated with failure to capture, oversensing, and undersensing. Lead
damage can occur at the site of venous access (subclavian vein) in the costoclavicular
space, causing the crush syndrome.
Pacemaker System Malfunction: Troubleshooting

Pacemaker system malfunction can be secondary to pacemaker circuitry failure or to lead
dysfunction. Not uncommonly, what appears to be pacemaker malfunction may actually
represent normal functioning of the pacemaker: A pacing artifact may be delivered in the
middle of the normal QRS and may represent pseudofusion (caused by late sensing) and
not undersensing. Unexplained longer pauses after sensed, but not paced, complexes
might suggest oversensing, but it may represent normal function caused by hysteresis.
Major electrocardiographic abnormalities of pacemaker system malfunction are broadly
categorized into the following: failure to capture, failure to output, undersensing, and
oversensing.
Failure to Capture
The loss of pacemaker capture occurs when there is a visible pacing stimulus and no atrial
or ventricular depolarization. The differential diagnosis of failure to capture is outlined
inTable 4320. Failure to capture may be intermittent or persistent. Lead dislodgment can
cause obvious failure to capture. An increase in the pacing threshold above the
programmed pacing output can occur as a result of the rise of the threshold within a few
weeks after lead placement because of drug therapy, electrolytes, MI, or ischemia. Fracture
of the lead, insulation breaks, and loose setscrews are mechanical problems that can
cause failure to capture (Fig. 4321). Last, battery depletion may cause the pacing output
to decline sufficiently such that pacing failure occurs. Loss of capture requires a check of
the pacing threshold and of pacing lead impedance and a chest radiograph. For instance, if
the problem is an elevated pacing threshold, pacing outputs must be increased. Abnormal
lead impedances may confirm a lead failure and the need for lead replacement. Functional
noncapture occurs when a stimulus falls during the physiologic refractory period of a native
depolarization. It may be secondary to undersensing or as a function of the pacing mode
(AOO, VOO).
Table 4320. Differential Diagnosis of Failure to Capture

FIGURE 4321
Failure to capture. Surface electrocardiogram of a patient with VVI pacemaker at a lower-rate limit of 60
ppm is shown at the bottom. The pacemaker spikes (*) are not followed by ventricular depolarization (no
capture). Patient has spontaneous ventricular activity at 35 beats/min. The device clearly senses the
ventricular event because the pacemaker spike appears 1000 ms (60 ppm) after the sensed event. On
interrogation of the device, His lead impedance was significantly lower (300 ) than the implant values,
and the pacing threshold had increased significantly. These findings are consistent with lead failure
secondary to insulation break. Chest radiograph revealed evidence of insulation break at the subclavian
venous access site. VVI, ventricular demand pacing.
Failure to Output
Another pacing system malfunction is the absence of pacing stimuli and hence no capture.
In bipolar systems the pacing artifact is diminutive, especially if isoelectric in some surface
leads. It is important to record multiple leads simultaneously. Failure to output is often
caused by oversensing and inhibition of pacing output and is less commonly caused by
circuitry failure (Table 4321). Oversensing may be caused by T waves, P waves, or farfield R waves and may cause inhibition of pacing output. In unipolar systems, oversensing
of myopotentials is common. A loose setscrew may cause noise and oversensing, leading
to inhibition of pacing output (Fig. 4322). Electromagnetic signals from arc welding and
electrocautery may be sensed by the pacemaker. Occasionally, the ventricular channel may
be inhibited by oversensing the atrial channel output (crosstalk). If the absence of pacing
output is caused by oversensing, a magnet application changes the pacemaker to an
asynchronous mode to eliminate the pauses. In generator component malfunction, there is
no delivery of pacing output by the device and magnet application does not restore pacing
output. Systematic analysis of the pacing parameters, evaluation of lead impedances at
rest, and provocative isometric exercises and chest radiograph may help identify the cause.
Table 4321. Differential Diagnosis of Failure to Output

FIGURE 4322

Failure to output. Surface electrocardiogram and atrial and ventricular electrograms with pacemaker event
markers are shown. In this patient with dual-chamber pacemaker, a loose setscrew resulted in noise on the
ventricular channel, leading to oversensing and inhibition of the ventricular output. Ap, atrial paced; As,
atrial sensed; Vp, ventricular paced; Vs, ventricular sensed.
Oversensing
In a single-chamber pacemaker, oversensing leads to inhibition of the pacing channel and
causes inappropriate pauses. However, in dual-chamber pacemakers, oversensing elicits
either inappropriate inhibition or triggering, depending on the channel in which oversensing
occurs and the programmed pacing mode. Oversensing in the ventricular channel in the
DDD or DDI mode results in inhibition of both atrial and ventricular outputs and resetting of
timing cycles. In patients with complete heart block, this may result in ventricular asystole
(Fig. 4323). Oversensing in the atrial channel can lead to inappropriate triggering of
ventricular output. The various etiologies of oversensing were discussed in the previous
section. One example of oversensing peculiar to dual-chamber pacemakers is crosstalk.

The atrial channel output can be sensed in the ventricular channel as a far-field signal and
inhibits the ventricular pacing output. In patients with complete heart block, this can result in
ventricular asystole. Although far more common with unipolar systems, crosstalk can also
occur in bipolar pacing systems. To prevent this phenomenon, there is a programmable
ventricular blanking period (51-150 ms) after atrial pacing, during which the ventricular
channel is refractory. Additionally, there is a crosstalk-sensing window after the blanking
period, during which a ventricular event, if sensed, will lead to ventricular pacing with a
shorter AV interval. Oversensing due to lead fracture, insulation break, or other electrode
problems will usually be random and erratic. With early lead problems, the malfunction is
typically intermittent and may be exacerbated by certain body positions or motions. In later
stages, the combination of oversensing, undersensing, and failure to capture is almost
always diagnostic of a lead-related problem. Programming to an asynchronous mode may
temporarily control this problem while awaiting lead replacement, which should be carried
out as promptly as possible.
FIGURE 4323

Oversensing of diaphragmatic myopotentials. Surface electrocardiogram and atrial and ventricular
electrograms with event markers are shown. In this patient with a dual-chamber defibrillator, deep
respiration reproduced the diaphragmatic myopotentials, resulting in inhibition of ventricular output. The
patient developed dizzy spells caused by underlying complete heart block and inhibition of pacing due to
oversensing. The ventricular lead was repositioned in the RV outflow tract eliminating the diaphragmatic
oversensing. As, atrial sensed; VF, ventricular fibrillation; Vp, ventricular paced; Vs, ventricular sensed.
Undersensing
An inadequate intracardiac signal can lead to undersensing. The intracardiac electrograms
can deteriorate because of inflammation or scar formation at the tissue lead interface.
Additionally, some drugs, electrolyte abnormalities, infarction, ischemia, lead fracture, or
insulation breaks can all lead to undersensing. Cardioversion or defibrillation can also
cause attenuation of intracardiac electrograms. Usually, undersensing is a greater problem
in the atrium than the ventricle. The atrial electrograms are typically significantly lower in
amplitude during atrial fibrillation than they are during sinus rhythm. The optimal solution is
to program an enhanced sensitivity (decreased sensing level, eg, from 1.5-0.55 mV). With
bipolar systems, the programmed sensitivity can usually be reduced to as low as 0.18 mV
in the atrium in some devices, without oversensing of myopotentials or other extraneous
signals. Other etiologies for undersensing occur when intrinsic atrial or ventricular
complexes fall within one of the programmed refractory periods. Undersensing can also
result when a pacemaker is inadvertently programmed to an asynchronous mode
(occasionally occurring with battery depletion or pacemaker generator reset).
Electromagnetic Interference
Electromagnetic interference (EMI) is defined as any nonphysiologic electrical signal that
interferes with pacemaker function. EMI can originate from a variety of sources both within
the hospital environment and outside. EMI can result in the inhibition of the pacemaker,
inappropriate triggering, noise reversion, resetting of the pacemaker parameters, and

occasionally damage to the circuitry or electrodemyocardial interface; unipolar
pacemakers are more susceptible to EMI than bipolar pacemakers. EMI has become an
increasingly important problem because sources of interference are ubiquitous in the
hospital and workplace.
In the hospital environment, the most common sources of EMI include electrocautery and
defibrillation. Electrocautery can cause inhibition of the pacemaker, and in a pacemakerdependent patient, this may result in severe bradycardia or asystole. Specific perioperative
management of a device includes the following73:
Identify the type of the device and its manufacturer; identifying the manufacturer is
essential.
Identify whether the patient is dependent on the device for antibradycardia pacing;
this may be obtained from the history of syncope, complete heart block, or AV node
ablation requiring pacemaker placement. Interrogating the device may help identify
whether the patient has a stable underlying escape rhythm.
Determine whether EMI is likely to occur during the procedure. The device should
be reprogrammed to asynchronous mode (VOO or DOO) or triggered mode (VVT),
especially if the patient is dependent. Rate-adaptive pacing function should be
turned off. Antitachyarrhythmia functions should be suspended (if an ICD). The
surgeon should be advised to use a bipolar electrocautery (if possible) to minimize
EMI.
Place a magnet over the pacemaker to convert this device to function in an

asynchronous mode (VVI to VOO or DDD to DOO) for as long as the magnet
remains over the device. Removing the magnet returns the device to its original
mode. In patients with ICDs, placing a magnet disables its antitachycardia therapies.
However, this will not alter its pacemaker function. Magnets should be used when
reprogramming options are not immediately available. All operating room personnel,
including the surgeon, anesthesiologist, and nursing staff, must be aware of the
presence of the device, the potential for electromagnetic interference encountered in
the operating room, and corrective techniques. An external defibrillator with
transcutaneous pacing capabilities should be readily available.
Intraoperatively, electrocardiographically monitor all patients to assess for device

inhibition and with peripheral pulse evaluation (plethysmography or arterial pressure,
etc) in case of electrocautery-induced artifact on telemetry. Individuals performing
the procedure should be advised to avoid electrocautery in the immediate field of the
device generator and leads. Electrocautery should be used in short, intermittent,

and irregular bursts.
If the patient requires electrical cardioversion, deliver the shock as far as possible
from the pulse generator and place the defibrillation pads on an axis perpendicular
to that of the leads and pulse generator (to avoid transient undersensing or pacing
inhibition).
Interrogate devices postprocedure to assess for threshold changes and to

reprogram the device to its original function if necessary.
Other potential sources of EMI in the hospital include extracorporeal lithotripsy, radiation
therapy, and MRI. MRI scan volume is growing at 10% per year, and it is estimated that at
least 50% of patients who receive an implantable pacemaker or defibrillator will need an
MRI study at some point in their life. Generally, MRI should be avoided in patients with
pacemakers because it is potentially hazardous, most commonly when it causes rapid
pacing triggered by the pulsing of the magnetic field. Other potential complications related
to MRI include device reprogramming, reed switch closure, heating at the myocardial-lead
interface, and mechanical movement of the device, as well as the device causing distortion
of the MRI image. Approaches to minimize the risk of MRI to patients consist of
programming the device to asynchronous mode, reducing the pacemaker output, limiting
the MRI to areas remote from the device, and monitoring blood pressure and ECG during
the MRI scanning. However, at present, MRI should be considered strongly contraindicated
or performed under a strict protocol that includes physician monitoring of the patient. It is
likely that pacemaker systems approved by the US Food and Drug Administration (FDA) will
be available in the near future that are either MRI safe or compatible in patients with
implantable devices. Recently, a pacemaker has been approved by the European
authorities and is pending approval in the United States as MRI safe.
Lithotripsy can also result in inappropriate inhibition or oversensing, especially in rateresponsive pacemakers with piezoelectric crystals. The pacemaker should generally be
programmed to VVI or VOO mode with the rate-responsive feature turned off before
lithotripsy. Radiation therapy should be avoided directly over the field of the pacemaker. If
shielding the pacemaker and limiting the field of radiation cannot be performed with safety,
repositioning of the pacemaker before radiotherapy should be considered. Other possible
EMI sources in the hospital include therapeutic diathermy, radiofrequency catheter ablation,
transcutaneous electric nerve stimulation (TENS) units, and spinal cord stimulators.
Daily sources of EMI include digital cellular phones, electronic article surveillance devices,
metal detectors, and electric razors, and work or industrial environment sources include
high-voltage power lines, transformers, welding, and electric motors. Activated digital cell
phones should not be placed in the breast pocket ipsilateral to the pacemaker, and the
phone should be held to the ear contralateral to the pacemaker. Electronic surveillance
devices or antitheft devices present in most stores and libraries can cause transient
asynchronous pacing, atrial oversensing with tracking, and ventricular oversensing and
inhibition. Patients with pacemakers should quickly walk through these devices and avoid
lingering near them. Common household appliances such as electric can openers, stereos,
televisions, video recorders, power tools, electric blankets, electric shavers, microwave
ovens, and electric lawnmowers do not cause any pacemaker interference.
Device Recall, Advisory, and Alerts

Currently, there are approximately two million patients with implantable pacemakers or
defibrillators worldwide. In the year 2005, >420,000 patients received a new pacemaker or
defibrillator implant in the United States alone. As the number of implantable cardiac
devices has increased, device alerts and advisories have become a part of routine clinical
practice. When a physician is faced with the management of a patient with an implanted
device that has been the subject of a recall or advisory, the major concern facing the
clinician is how to manage the patient and whether the device must be replaced. Compared
with other medical devices, these devices are unique because they are often implanted for
life-threatening problems for which device failure may be causally linked to death or poor
outcome. A recent review by Maisel and colleagues of device manufacturer performance
reports issued between 1990 and 2002 found that >17,000 devices were explanted during
this timeframe for confirmed malfunction.74 The explanted devices were evenly split among
pacemakers and ICDs, but when comparing the number of implants in each category, ICDs
appeared to be four times more likely to malfunction and require explantation. A metaanalysis of device registries found that pacemaker reliability has improved markedly and
consistently over the past 20 years.75
There are a wide variety of malfunctions that have been reported with pacemakers and
ICDs. These include both hardware component malfunction and software problems. In
general, hardware malfunction tends to be far more common than software malfunction and
is also more problematic for physicians and patients. Among hardware problems,
battery/capacitor and electrical issues account for more than half of the reported
malfunctions. Gould and Krahn76 reported the results from a multicenter Canadian study of
the consequences of various ICD advisories. From approximately 18% (533 of 2915
patients) of devices electively replaced because of advisories, complications were observed
in 8.1% of cases within 2.7 months after ICD generator replacement (5.8% were major
complications requiring reoperation, including two deaths). In contrast, there were only
three (0.1%) device malfunctions from the devices that were included in advisories but no
clinical complications from these malfunctions. In some centers, very low rates of
complications have been observed, emphasizing the importance of individualizing patient
management and knowing an individual center's risk of complications.77
Currently, several groups have recently provided specific recommendations or guidelines
for managing patients with devices affected by recalls or advisories. 78-80 The Heart Rhythm
Society has proposed a series of recommendations for physicians and industry. Device
manufacturers and the FDA notify physicians and patients after determining a device
problem by an advisory; however, decisions about management are left to physicians. All
patients with devices affected by recall, advisories, or alerts should be seen in the office for
immediate device interrogation and discussion of the implications of the notification to the
patient and their immediate and long-term device management and clinical status. The
patient's indication for device implantation and relative device dependence should be
discussed, and well as potential consequences of device failure. The decision regarding
which patients affected by the advisory/recall should undergo device replacement may be
difficult for both the patient and the physician. Pacemaker dependence, ICDs implanted for
secondary prevention, and high likelihood of device failure are some of the factors that lead
to consideration for device replacement. Several quantitative decision analysis models have
examined the question of whether to replace a device that has been the subject of an FDA
advisory or recall. In one model, for patients who are pacemaker-dependent, replacement
should be considered when the reported device failure rate exceeds 0.3%. 77 Alternately,
patients may be scheduled for more frequent in-clinic follow-up or by transtelephonic or
computer-based remote monitoring based on a careful review of the company, FDA, and
any outside physician panel recommendations. Patients should be instructed to present to
device clinic or use remote follow-up whenever any symptoms (ie, syncope, presyncope,
palpitations, angina, etc) or other symptoms that suggest possible device malfunction are
experienced. Device self-monitoring capabilities and the ability to do intensive remote
follow-up allows for more reliable device follow-up in the future. Remote automatic checks
with wireless or Internet-based physician notification schemes may improve monitoring of
device performance, but currently office interrogations remain the most commonly used
modality for follow-up. Diagnostic tools are being developed to help detect potential
hardware problems that could lead to malfunction.81

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Chapter 43.

Increase in pulse-width duration

Change to a simpler pacing mode (DDDR to VVI; VVIR to VOO)

Reduced battery voltage

Elevated battery impedance

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Sensing is usually measured as the peak-to-peak or base-to-peak amplitude of the

Table 4312. The Pacemaker Code

A refractory period that is programmable (ventricular refractory period) during which

A lower-rate interval (LRI), which corresponds to the programmed pacing rate. If

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Upper Rate Behavior

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Managed Ventricular Pacing

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Proportionate increase in heart rate to match increase in metabolic demand

Appropriate rapid change in heart rate with exercise onset

High sensitivity and specificity

Appropriate slowing of heart rate after exercise

Sensors available or under development can be classified using a physiologic or technical

Table 4313. Physiologic Classification of Sensors

Activity-based sensors using piezoelectric crystals or accelerometers to detect vibration are

The specificity and sensitivity of minute-ventilation sensing pacemakers for changes in

Indications for Pacing

Table 4314. Indications for Pacing to Prevent or Terminate Tachycardias

Table 4315. Trials of Biventricular Pacing for Heart Failure

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Pacing in Hypertrophic Cardiomyopathy

Table 4317. Indications for Pacing in Hypertrophic Obstructive Cardiomyopathy

Table 4318. Pacemaker Complications

cultures without an identifiable focus of infection. Occasionally the infected pacemaker

Table 4319. Symptoms and Signs of Pacemaker Syndrome

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Pacemaker System Malfunction: Troubleshooting

Table 4320. Differential Diagnosis of Failure to Capture

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Table 4321. Differential Diagnosis of Failure to Output

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section. One example of oversensing peculiar to dual-chamber pacemakers is crosstalk.

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inappropriate triggering, noise reversion, resetting of the pacemaker parameters, and

Place a magnet over the pacemaker to convert this device to function in an

Intraoperatively, electrocardiographically monitor all patients to assess for device

device generator and leads. Electrocautery should be used in short, intermittent,

Interrogate devices postprocedure to assess for threshold changes and to

Device Recall, Advisory, and Alerts

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