7.5.

PACEMAKERS

More than a half-million people fall victim to heart attacks in the United States every year and
thousands more are critically injured in acci- dents. Taking care of these patients in special care units
of hospitals involves the use of several types of specialized equipment, among which are cardiac
pacemakers and defibrillators. Defibrillators and cardiopulmonary resuscitation equipment are also
required away from the hospital, in an ambulance or at the scene of an emergency.

In the past few years electronic pacemaker systems have become extremely important in saving and
sustaining the lives of cardiac patients whose normal pacing functions have become impaired.
Depending on the exact nature of a cardiac dysfunction, a patient may require temporary artificial
pacing during the course of treatment or permanent pacing in order to lead an active, productive life
after treatment.

This section deals with the various types of cardiac pacemakers. In addition to describing each
device, its basic purpose, the physiological conditions under which it is required, and the ways in
which it is used are also discussed. Section 7.6 covers defibrillators.196 Patient Care and Monitoring

The heart's electrical activity is described in Chapters 3 and 5, but a brief review at this point will be
helpful in understanding the need for artificial cardiac pacing. The rhythmic action of the heart is
initiated by regularly recurring action potentials (electrochemical impulses) originating at the natural
cardiac pacemaker, located at the sinoatrial (SA) node. Each pacing impulse is propagated
throughout the myocardium, spreading over the surface of the atria to the atrioventricular (AV)
node—which is located within the septum, adjacent to the atrioventricular valves—and depolarizing
the atria. After a brief delay at the AV node, the impulse is rapidly conducted to the ventricles to
depolarize the ventricular musculature.

A normal sinus rhythm (NSR) depends on the continuous, periodic performance of the pacemaker
and the integrity of the neuronal conducting pathways. Any change in the NSR is called an
arrhythmia (abnormal rhythm). Should the SA node temporarily or permanently fail because of
disease (SA node disease) or a congenital defect, the pacing function may be taken over by
pacemaker-like cells located near the AV node. However, under certain conditions, cells in the
conduction system (an idioventricular focus) may pace the ventricles instead. Similarly, an area in
the excitable ventricular musculature may try to control the heartbeat. Unfortunately, under these
conditions the heart is paced at a much slower rate than normal, ranging between 30 and 50 beats
per minute (BPM). The result is a condition called bradycardia (slow heart), in which the heart
cannot provide sufficient blood circulation to meet the body's physical demands. During the
transition period from an NSR to a slow rhythm, dizziness and loss of consciousness (syncope) may
occur because of diminished cardiac output. Heart block occurs whenever the conduction system
fails to transmit the pacing impulses from the atria to the ventricles properly. In first-degree block an
excessive impulse delay at the AV junction occurs that causes the P-R interval to exceed 0.2 second
for normal adults. Second-degree block results in the complete but intermittent inhibition of the
pacing impulse, which may also occur at the AV node. Total and continuous impulse blockage is
called third-degree block. It may occur either at the AV node or elsewhere in the conduction system.
In this case, the ventricles usually continue to contract but at a sharply reduced rate (40 BPM)
because of the establishment of an idioventricular escape rhythm or because of impulses that only
periodically originate from the atria. In all these conditions, an artificial method of pacing is generally
required to ensure that the heart beats at a rate that is sufficient to maintain proper circulation.

7.5. 1 . Pacemaker Systems

A device capable of generating artificial pacing impulses and deHvering them to the heart is known
as a pacemaker system (commonly called a (a)

Figure 7.16. (a) Implanted standby pace- maker with catheter electrodes inserted through the right
cephalic vein, (b) Pacing electrodes attached to the myocardium;

(c) Myocardial electrodes with pacemaker generator implanted in abdomen.

(b) 198 Patient Care and Monitoring pacemaker) and consists of a pulse generator and appropriate
electrodes. Pacemakers are available in a variety of forms. Internal pacemakers may be permanently
implanted in patients whose SA nodes have failed to function properly or who suffer from ermanent
heart block because of a heart attack. An internal pacemaker is defined as one in which the entire
system is inside the body. In contrast, an external pacemaker usually consists of an externally worn
pulse generator connected to electrodes located on or within the myocardium. External pacemakers
are used on patients with temporary heart irregularities, such as those encountered in the coronary
patient, including heart blocks. They are also used for temporary management of certain
arrhythmias that may occur in patients during critical postoperative periods and in patients during
cardiac surgery, especially if the surgery involves the valves or septum.

Internal pacemaker systems are implanted with the pulse generator placed in a surgically formed
pocket below the right or left clavicle, in the left subcostal area, or, in women, beneath the left or
right major pectoraHs muscle. Internal leads connect to electrodes that directly contact the inside of
the right ventricle or the surface of the myocardium (see Figure 7.16). The exact location of the pulse
generator depends primarily on the type of electrode used, the nature of the cardiac dysfunction,
and the method (mode) Figure 7.17. Portable external pacemaker. Patient is being temporarily
paced with an external demand pacemaker and trans- venous pacing catheter. (Courtesy of
Medtronic, Inc., Minneapolis, MN.)

Figure 7.18. Portable external pacemaker, strapped on arm. (Courtesy of Medtronic, Inc.,
Minneapolis, MN.)

Figure 7.19. Detail view of external demand pacemaker showing adjustment controls. (Courtesy of
Medtronic, Inc., Minneapolis, MN.) of pacing that may be prescribed. Pacing electrodes and modes
are described later in this chapter. Since there are no external connections for applying power, the
pulse generator must be completely self-contained, with a power source capable of continuously
operating the unit for a period of years. External pacemakers, which include all types of pulse
generators located outside the body, are normally connected through wires introduced into the
right ventricle via a cardiac catheter, as shown in Figure 7.17. The pulse generator may be strapped
to the lower arm of a patient who is confined to bed, or worn at the midsection of an ambulatory
patient, as shown in Figures 7.17 and 7.18. A detailed view of the external pulse generator appears
in Figure 7.19. Figure 7.17 depicts an older model replaced by that in Figures 7.18 and 7.19, but the
idea remains the same.

199

200 Patient Care and Monitoring

7.5.2. Pacing Modes and Pulse Generators

Several pacing techniques are possible with both internal and external pacemakers. They can be
classed as either competitive and noncompetitive
pacing modes as shown in Figure 7.20. The noncompetitive method, which

uses pulse generators that are either ventricular programmed or progranmied

by the atria, is more popular. Ventricular-programmed pacemakers are designed to operate either in
a demand (R-wave-inhibited) or standby

(R-wave-triggered) mode, whereas atrial-programmed pacers are always

synchronized with the P wave of the ECG.

The first (and simplest) pulse generators v/qtq fixed-rate or asynchronous

(not synchronized) devices that produced pulses at a fixed rate (set by the

physician or nurse) and were independent of any natural cardiac activity.

Asynchronous pacing is called competitive pacing because the fixed-rate

impulses may occur along with natural pacing impulses generated by the

heart and would therefore be in competition with them in controlling the

heartbeat. This competition is largely eliminated through use of ventricular- or atrial-programmed

pulse generators.

Fixed-rate pacers are sometimes installed in elderly patients whose SA

nodes cannot provide proper stimuli. They are also used temporarily to determine the amplitude of
impulses needed to pace or capture the heartbeat

of a patient prior to or during the implantation of a more permanent unit. The amplitude at which
capture occurs is referred to as the pacing threshold. While the implantable fixed-rate units tend to
fail less frequently than the more sophisticated demand or standby pacers, their battery life (if the

Figure 7.20. Types of pacing modes.

Pacing modes

Competitive Non-competitive

Ventricular programmed

Atrial programmed

Fixed rate (asynchronous) R-wave inhibited (demand) R-wave triggered (standby) P-wave

synchronized

7.5. Pacemakers 201

batteries are not rechargeable) is generally shorter because they are in constant operation.

The problems of shorter battery life and competition for control of the

heart led, in part, to the development of ventricular-programmed (demand

or standby) pulse generators. The models shown in Figures 7.19 and 7.21 are of the demand type.
Either type of ventricular-programmed pulse
generator, when connected to the ventricles via electrodes, is able to sense

the presence (or absence) of a naturally occurring R wave. The output of an R-wave-inhibited
(demand) unit is suppressed (no output pulses are produced) as long as natural (intrinsic) R waves
are present. Thus, its output is held back or inhibited when the heart is able to pace itself. However,
should

standstill occur, or should the intrinsic rate fall below the preset rate of the

pacer (around 70 BPM), the unit will automatically provide an output to pace the heart after an
escape interval at the designated rate. In this way,

ventricular-inhibited pacers are able to pace on demand. Some external

demand-mode pacers may be adjusted to operate in a fixed-rate mode by means of an accessible

mode control of the type shown on the unit in Figure 7.19. Other controls allow the setting of the
pacer's rate anywhere

between 30 and 180 BPM, as well as the amplitude of output pacing pulses

between 0.1 and 20 mA. Some external demand pacers have a sense-pace

indicator that deflects for each detected R wave or pacer-initiated impulse.

The ON-OFF switch of some external pacers is provided with an interlock

mechanism to prevent the unit from being accidentally turned off. A demand pacer, in the absence
of R waves, automatically reverts to a

fixed-rate mode of operation. For testing purposes at the time of implantation and for evaluation
later, implanted demand pacers are purposely placed

in a fixed-rate mode, usually by means of a magnet provided by the manufacturer. When placed
over the skin layer covering the pacer, the magnet

activates a magnetically operated switch that prevents the pacer from sensing

R-wave activity. This process causes the pacer to operate in a fixed-rate mode at a slightly higher
rate (about 10 BPM higher than the demand-mode

pacing rate that had been preset). For a patient with a normal sinus rhythm,

this procedure is used to ensure that an implanted demand pacer whose

output is normally inhibited is capable of providing pacing pulses when

needed. Evidence of the presence of pacing impulses is obtained from the

electrocardiogram. Pacing impulses appear as pacing artifacts or spikes.

Occasionally, they may seriously distort the recorded QRS complex.

When required, the basic pacing rate of some of the earlier implanted

pacers (both fixed-rate and demand types) may be changed with the use of

a needle-like screwdriver (a Keith surgical skin needle) that is inserted

transcutaneously to alter the rate control in the pulse generator. The

amplitude of the impulses may also be adjusted in some earlier pacers by

using the same type of needle in the appropriate control. In a newer type of

202 Patient Care and Monitoring

pacer, these adjustments are accomplished by means of coded impulses that are magnetically
coupled to the implanted pulse generator from the skin

surface, thus eliminating the need to puncture the skin. To adjust this pacemaker, a special
programming device with an attached coil is placed over

the implanted pulse generator. Appropriate controls on the programmer

allow the unit to transmit coded signals that cause the pacer to change its basic rate and vary the
amplitude of its impulses. The basic rate and impulse

amplitude of other recent implantable pulse generators are fixed by the

manufacturer and cannot be changed, however.

As explained earlier, R-wave-triggered pulse generators, like the Rwave-inhibited units, sense each
intrinsic R wave. However, this pacer emits an impulse with the occurrence of each sensed R wave.
Thus, the unit is triggered rather than inhibited by each R wave. The pacing impulses are transmitted
to the myocardium during its absolute refractory period, however, so they will have no effect on
normal heart activity. Should the intrinsic heart rate fall below the preset rate of the pacer, the
pacer will automatically

operate synchronously at its preset rate to pace the heart. Thus, this pacemaker stands by to pace
when needed. Ventricular-triggered pacing is used

less frequently than inhibited-mode pacing. Evidence of pacing impulses

from this type of pacer is present on the patient's ECG, although some

monitoring modes that utilize greater filtering may distort and even block

the pacer artifact. In this case, one should document the ventricular complex

following a pacer spike and compare it to the complex in question. In cases of complete heart block
where the atria are able to depolarize

but the impulse fails to depolarize the ventricles, atrial synchronous pacing

may be used. Here the pulse generator is connected through wires and elec- trodes to both the atria
and the ventricles. The atrial electrode couples atrial impulses to the pulse generator, which then
emits impulses to stimulate the

ventricles via the ventricular electrode. In this way, the heart is paced at the same rate as the natural
pacemaker. When the SA node rate changes because

of vagus or sympathetic neuronal control, the ventricle will change its rate accordingly but not above
some maximum rate (about 125 per minute).

Pulses applied directly to the heart are usually rectangular in shape

with a duration of from 0.15 to 3 msec, depending on the type of pulse

generator used and the needs of the patient. Depending on the value of

impulse current required to capture, pulse amplitudes may range from 5 to

15 mA for adults, while infants and children require less. If, in an emergency,

pacing must be done through the intact chest wall, amplitudes 10 times as

great are required. These higher values of current are often painful and may

cause burns and contractions of the chest muscles and diaphragm. The

amplitude of impulse required to capture the heartbeat of a patient is affected

by the duration of the pulse. For example, an impulse of 2-msec duration

7.5. Pacemakers 203

may capture when its amplitude is only 3 mA. On the other hand, a 0.8-msec

pulse may reach 6 mA before capture occurs. The ability to capture and hence the threshold value of
a pacer impulse

that has a given amplitude and duration also depend on the electrical quality

of the contact between the electrode and the heart. Capture will occur at a

higher threshold value for a poor contact than for a good electrical contact

at the electrode-heart muscle interface.

The quality of the electrode-heart muscle contact also affects a demand

pacer's inhibition capability or sensitivity. A good contact will permit

the pacer's output to remain inhibited for smaller values of sensed R waves. The performance of the
pulse generators can be checked with the use of a special tester. In one type of tester, pacing
impulses are indicated by a lamp that blinks at the pacing rate. In another type, the pacer's pulse
rate,

amplitude, width, and interval are displayed in digital form. This type of

tester is also able to generate impulses used to check the inhibition capability

of a demand pacer.

Typical internal pulse generators are shown in Figure 7.21(a). The

Xyrel Models 5972 and 5973 pulse generators are of the ventricular-inhibited

(demand) type. Programmed from the QRS complex, they deliver their

impulses only when the patient's ventricular rate falls below the basic

pacing rate of the pulse generator. Rate is preset during manufacture at a

typical 72 pulses per minute (ppm). The Model 5972 is a bipolar pulse
generator. The 5973 is a unipolar pulse generator. Unipolar electrodes have one electrode placed on
or in the heart and the other (reference) electrode

located somewhere away from the heart, whereas bipolar electrodes have

both electrodes on or in the heart.

The pulse generators are powered by a hermetically sealed lithiumiodine power source and utilize
hermetically sealed hybrid electronic cir- cuitry. To further protect the components of the pulse
generator from intrusion of body fluids the electronics assembly and power source are encapsulated
and hermetically sealed within a titanium shield. Nominal dimensions of the circular-shaped pulse
generators are 56 mm

(2.2 in.) in diameter by 18 mm (0.71 in.) in thickness. Weight is a nominal

95 grams.

Both pulse generators have a self-sealing connector assembly with a

corrosion-resistant titanium-alloy body and socket setscrew(s). To help

prevent potential migration or rotational complications, the pulse generators

have a suture pad which enables the physician to secure the pulse generator

within the pocket.

The power source is rated at 5.6 V with 1.1-Ahour capacity and is expected to last for 7 to 10 years
with continuous pacing at 72 pulses per

minute. Two power-source-depletion indicators are programmed into the

204 Patient Care and Monitoring

circuitry of the pulse generators—a rate decrease and a pulse duration

increase. The decrease in rate occurs when voltage has been depleted to about 4.0 V. At this point,
replacement of the pulse generator is indicated.

The increase in pulse duration, which serves as a secondary power-sourcedepletion indicator, is

gradual and occurs simultaneously with the depletion

of the Hthium-iodine power source.

Figure 7.21. Internal pacemaker, (a) Photograph of two units, (b) Block diagram. (Courtesy of
Medtronic, Inc., Minneapolis, MN.)

REVERSION

CIRCUIT ^ SENSING

CIRCUIT REFRACTORY

CIRCUIT ^^

1r

TIMING
CIRCUIT PULSE WIDTH

CIRCUIT

RATE

LIMIT CIRCUIT OUTPUT

CIRCUIT t t

RATE 4— VOLTAGE

MONITOR

ENERGY COMPEN

SATION

CIRCUIT

CIR(:uiT (b)

7.5. Pacemakers 206

Models 5972 and 5973 have a rate-limit circuit which prevents the rate from going above 120 ppm
for most single-component failures. In the pres- ence of strong continuous interference, the pulse
generators are designed

to revert to asynchronous operation. The reversion rate is approximately

the same as the basic pacing rate. The pacing function of the pulse generators can be verified during

periods of sinus rhythm (when the pulse generator's output is suppressed)

by means of a magnet held against the skin over the implanted pulse generator.

The rate with the application of the magnet can be slightly higher than

the basic pacing rate. Radiopaque identification permits positive determination of model

and series number at all times. With standard X-ray procedures, the five- character code inside the
titanium shield appears as black letters and

numerals on a white background.

Figure 7.21(b) is a block diagram showing components of the circuitry.

The timing circuit which consists of an RC network, a reference voltage

source, and a comparator determines the basic pacing rate of the pulse

generator. Its output signal feeds into a second /?C network, the pulse width

circuit, which determines the stimulating pulse duration. A third RC net- work, the rate-limiting
circuit, disables the comparator for a preset interval

and thus limits the pacing rate to a maximum of 120 pulses per minute for

most single-component failures. The output circuit provides a voltage pulse

to stimulate the heart. The voltage monitor circuit senses cell depletion and

signals the rate slowdown circuit and energy compensation circuit of this event. The rate slowdown
circuit shuts off some of the current to the basic

timing network to cause the rate to slow down 8 ± 3 beats per minute when

cell depletion has occurred. The energy-compensation circuit causes the

pulse duration to increase as the battery voltage decreases, to maintain

nearly constant stimulation energy to the heart.

There is also a feedback loop from the output circuit to the refractory

circuit, which provides a period of time following an output pulse or a

sensed R-wave during which the amplifier will not respond to outside signals.

The sensing circuit detects a spontaneous R wave and resets the oscillator
timing capacitor. The reversion circuit allows the amplifier to detect a spontaneous R wave in the
presence of low-level continuous wave inter- ference. In the absence of an R wave, this circuit allows
the oscillator to pace at its preset rate ± 1 beat per minute.