Cardiac Pacemakers

     The heart is bestowed with a specialized system that automatically
generates rhythmic control via the sinus node, located in the superior lateral
wall of the right atrium near the opening of the superior vena cava. The
specialized pacemaker cells dictate control of the rest of the heart through
regular electrical impulses that propagate from the right atria to the lower
ventricles. The rapid conduction of these impulses cause the muscle cells of the
atria to contract and squeeze blood into the ventricles, which contract and
force blood into the aorta and pulmonary arteries. Abnormalities of the heart
rhythm, called arrhythmias, can disrupt this normal cardiac control making it
necessary to use some artificial means to regulate the rhythm of the heart.

Today, some half a million men and women, most of them over the age of sixty,
carry implanted cardiac pacemakers that take over the duties of the natural
conduction system. Tens of thousands of these devices are implanted each year in
this country alone. Over the past thirty years cardiac pacemakers have evolved
from simple devices only capable of fixed-rate stimulation of a single chamber
of the heart to more sophisticated "implanted computers" that medical
personnel can interrogate and reprogram from outside the patient's body. These
refinements have allowed for more physiologic pacing with maintenance of
atrioventricular synchrony and cardiac output. There are various types of
cardiac pacemakers available today that can be surgically implanted to treat
specific arryhythmic disorders in the heart. Abnormal rhythms in the heart are
one of the most frequent causes of heart malfunction, and in most cases
necessitate some type of cardiac pacing unit. Cardiac arrhythmias are common in
the elderly, in whom age-related physiologic changes often alter the conduction
system of the heart. Such changes may remain asymptomatic, or they may progress
to syncope, or possibly sudden death. In the event of acute myocardial
infarction, arrhythmias are no more frequent in the elderly than in younger
subjects; in fact, ventricular premature beats are seen less commonly in
patients aged seventy years and older. Age is also not a factor in determining
the success of resuscitation from cardiac arrest, although it may be a predictor
of six-month survival. In general, there is nothing unique about arrhythmias in
the elderly. All of the commonly encountered arrhythmias may be seen in older
patients. Arrhythmias may occur in otherwise normal hearts, but with increasing
age, associated cardiac disease becomes more likely. A possible exception is
atrial flutter; in younger patients, its presence almost always indicates a
serious cardiac disorder. There are two indications for antiarrhythmic therapy:
relief of symptoms and prevention of more malignant arrhythmias. In elderly
patients, pacemakers are the preferred treatment for bradyarrhythmias. Most
arrhythmias occur in response to the aging heart. In the sinoatrial node, the
number of pacemaker cells decreases, until often less than 10% of the normal
complement remain after age 75. Beginning at age 60, there is a detectable loss
of fiber from the fascicles of the left bundle branch. Commonly, less than
one-half the original number remain, the others having been replaced by fibrous
tissue. Microcalcification is often found in this region, and can be related to
both age-associated change and pathologic processes. There is also some fibrous
tissue replacement of conduction fibers in the distal conduction system, as well
as occurrences of fibrosis and hyalinization in the media of the blood vessels
supplying the conduction tissue. Any of these age related processes can lead to
a disrupted rhythmic and conduction system of the heart. One type of arrhythmia,
bradycardia, normally necessitates the surgical implantation of a pacemaker
device. Bradycardia is a circulatory condition in which the myocardium contracts
steadily but at a rate of less than sixty contractions a minute. This condition
may be normal in some physically fit people, where their pulse may be quite
slow. This is because an athlete's heart is considerably stronger and is capable
of pumping a larger volume of blood per heart beat than someone who is less
physically active. However, in other people, cardiac output is decreased which
can cause faintness, dizziness, chest pain, and eventually syncope and
circulatory collapse. The cause of bradycardia can be an increase in the
parasympathetic nervous system. As the vagus nerve applies more acetylcholine on
the heart, the overall output of the heart decreases which means that there is
less stroke volume. In addition, severe episodic bradycardia may occur in
patients with a hypersensitive carotid sinus reflex. In these patients, their
carotid sinus region of the carotid artery becomes extremely sensitive to the
pressure receptors within the arterial wall. This creates an intense vagal
stimulation, and in some cases can even stop the heart. The possibility of an
arrhythmic etiology for symptoms of syncope or presyncope should be considered
in all patients, especially the elderly. In the absence of any other apparent
cause, this possibility should be pursued, even in the absence of abnormalities
on a standard ECG. Further investigations, including ambulatory monitoring and
intracardiac electrocardiography, should be considered in order to correlate
symptoms with any arrhythmia detected. Investigation of syncope symptoms often
fails to demonstrate any abnormality. However, patients should consider
receiving pacemaker therapy in view of the ease of permanent pacemaker
implantation and the potential dangers associated with recurrent syncope. On the
other hand, presyncope is a much less specific, less dangerous symptom. Patients
with symptoms of dizziness that appears to have a bradycardiac basis should
receive pacemakers if any conduction abnormality can be demonstrated. In the
absence of any such evidence, however, the decision can readily be deferred.

Another type of rhythmic disorder of the heart that should be carefully
considered as an indication for pacemaker therapy is sick sinus syndrome. The
incidence of sick sinus syndrome increases with age, and includes a variety of
disorders thought to originate in abnormalities of the sinoatrial node, its
neurogenic control, or in the perisinus tissue. Presentation varies from sinus
bradycardia to a bradycardia-tachycardia syndrome. Pacemaker therapy of sick
sinus syndrome should be reserved for symptomatic patients, as even moderated
bradycardia may be associated with normal rest and exercise hemodynamics in the
elderly. In the bradycardia-tachycardia syndrome, anti-tachycardia drug therapy
may also be required, but often pacing alone controls both aspects of the
arrhythmia. Pacemaker therapy may also be indicated in some patients to permit
therapy with channel blocking agents, which could otherwise cause an excessive
bradycardia. Patients with congestive heart failure in a setting of bradycardia
may be improved if their heart rate is increased with pacing, although, often,
the attendant loss of atrial synchrony offsets the benefit of increasing the
rate. There are various types of pacemakers available today, each of which
functions differently from the next. Yet, at the bottom level, all pacemakers
consist of two components: a pulse generator, which includes electronic
circuitry and a power source, and a lead - one or more insulated wires connected
to the pulse generator that terminate in an electrode, through which electrical
current enters or leaves the heart. The pulse generator corrects for a defective
sinus node or conduction pathway by emitting rhythmic electrical impulses
similar to those of the sinus node. In the mid-1950's cardiac pacemakers
referred to a large piece of electrical equipment that resuscitated patients at
the hospital. Since the transistor technology had not yet surfaced, the pulse
generator was simply a plug-in device the size of an old tabletop radio. The
leads were thick wires, and the electrodes were strapped to the patient's chest.

These cardiac units were restricted to mobility, as they had to be plugged into
an electrical outlet. During the late 1950's and 60's when transistors found its
niche in the electrical industry, the pulse generator shrunk to the size of a
pocket watch. A battery replaced the old power source, the circuitry was
encapsulated in rubber, and the unit was implanted inside of the body with the
electrodes attached to the outer wall of the heart. There have been several
different types of pacemaker units that have surfaced over the past twenty to
thirty years. The ventricular demand pacemaker (VVI) was one of the most
commonly employed pacing systems implemented in the 1960's. It is a
single-chambered unit that paces in the ventricle, senses electrical activity in
the ventricle, and is inhibited by ventricular events. This early device has
only one wire and paces the ventricles at regular intervals. The pacing rate,
usually around seventy beats a minute, is determined by a physician. The ECG in
a patient with a VVI pacemaker shows a sharp spike of the pacemaker artifact
before each paced beat, followed by a wide QRS wave. No pacemaker spike is
present on sensed beats. Retrograde conduction of the paced impulse from the
ventricles to the atria, VA conduction, may not be present. If it is present,
retrograde P waves follow the paced QRS complex. When VA conduction is absent,
dissociated atrial activity is seen. Ventricular demand pacemakers are found in
patients who: are physically inactive, regardless of age, and therefore do not
require rate variability; have chronic atrial fibrillation or flutter, or giant,
silent atria; or have mental incapacity or terminal illnesses that make
dual-chambered pacing impractical. Another type of unit, atrioventricular
sequential pacemakers (DVI), is capable of pacing in both the atrium and
ventricle, senses only in the ventricle, and is inhibited by ventricular events.

Most AV sequential pacemakers are noncommitted. After a brief blanking period of

30 to 50 milliseconds following an atrial stimulus, sensing is continuous during
the AV interval. Therefore, noncommitted DVI pacing systems may pace atrium and
ventricle both, or atrium only, or be totally inhibited, depending on where the

R wave is detected with respect to the pulse generator's timing cycle. The ECG
in a DVI pacemaker shows a sharp spike before each P wave on paced atrial beats
and before each QRS on paced ventricular beats. The atrial and ventricular
spikes are separated by a present or programmable AV interval. Patients who have
a sick sinus syndrome accompanied by AV nodal or His-Purkinje disease or an AV
block with abnormal sinus node function and lack of ability to increase atrial
rate with exercise typically benefit from these pacemakers. They are also useful
in patients who have developed pacemaker syndrome with single-chambered
ventricular demand units, since the normal atrioventricular relationship is then
restored. A third, more commonly used type of pacemaker is the DDD pacemaker. A

DDD pacemaker can sense intrinsic activity in the atrium and ventricle, pace
either or both chambers when not inhibited by native activity, and thereby
maintain atrioventricular synchrony over a wide range of heart rates. DDD units
are noncommitted employing an atrial "blanking period following atrial
stimuli to avoid sensing of such events on the ventricular channel. All such
pacemakers have upper rate characteristics and blocking modes to prevent 1:1
conduction during atrial arrhythmias such as flutter and fibrillation. Virtually
all such devices are extensively programmable, and most have the ability to
telemeter both programmed and real-time parameters. One of the major initial
problems encountered with DDD pacing is pacemaker-mediated tachycardia, which is
where the pacemaker acts as one limb of a re-entrant circuit. However, this has
been solved by the ability to program the interval at which atrial sensing
resumes after a ventricular sensed or paced event. Normally, this device
sequentially paces both the atrium and ventricle when atrial activity falls
below the preset base rate and atrial pacing is not followed by a ventricular
event. When the patient's intrinsic atrial activity exceeds the base rate, and
if a spontaneous QRS does not occur within the programmed AV interval, the
pacemaker switches to an atrial sensing-ventricular pacing mode. In this case,
the ECG shows a P wave that is followed by a sharp spike and a paced QRS. Sensed
ventricular events inhibit both atrial and ventricular output and reset the
atrial escape interval. The DDD pacemakers are found in patients who possess: AV
block with or without sinus node dysfunction; or moderate sick sinus syndrome
and AV nodal or His-Purkinje disease, with at least some ability to increase
atrial rate with exercise. Surgical implantation of cardiac pacemakers has
dramatically improved over the years. During the late 1950's and early 1960's
when artificial pacing was first being implemented, patients with severe

Stokes-Adams attacks received some of the first battery operated pacemakers
developed by William M. Chardack, chief of thoracic surgery at the Veterans

Administration hospital and his colleague Wilson Greatbatch. Physicians who
implanted pacemakers in these patients reported numerous serious failures that
required new operation: broken or dislodged leads, premature battery depletion,
leakage of body fluids into the pulse generator. Yet despite the problems,
pacemakers proved effective at giving people months or years of life that they
would not otherwise have enjoyed. The operative procedure during this particular
era was carried out under general anesthesia with an endotracheal tube in place.

Patients undergoing surgery were under the control of an external pacemaker with
a cardiac electrode catheter passing through the right saphenous vein.

Electrocardiographic leads were attached to the arms and legs, and a continuous

ECG was displayed on an oscilloscope. Two incisions were made: a six inch
incision near the umbilicus (naval) and a left submammary incision. A twin lead
was passed up a subcutaneous tunnel, which connects the chest and abdominal
incisions to the pericardium. The two electrodes were separated and implanted in
the myocardium. The bared wire was passed back through to the entry point of the
insulated portion of the electrode. The second electrode was implanted in the
same fashion one centimeter from the first. The pacemaker was placed in the
subcutaneous pocket and attached to the anterior rectus sheath. The external
unit was taped to the abdomen and set between 80 and 90 pulses/min. Today
doctors who implant pacemakers almost never expose the patient's heart. Instead,
using local anesthesia, they make a two to three inch incision just below the
left or right collarbone. Then, they cut into one of the prominent veins running
across the upper chest toward the heart, either the cephalic or the subclavian
vein. The pacing wire is contained within a veous catheter. While observing the
process on a fluoroscope screen, the doctor advances and guides the catheter
down the venous system, through the right atrium of the heart, and into the
right ventricle. Once the lead is positioned securely against the wall of the
ventricle and tested for its electrical characteristics, the physician plugs it
into the pulse generator and buries the generator beneath the chest muscle at
the site of the incision. An experienced implanter can carry out this procedure
in forty-five minutes or less, though complex cases take longer depending on the
complexity. Tines at the tip of the lead hold it securely in position against
the endocardium, the inner lining of the heart. Over a period of a week or two,
fibrous tissue grows around the electrode and binds it tightly to the
endocardium. About six weeks after the operation, the recipient goes back to the
doctor's office to have the pacemaker's initial settings adjusted so that its
batteries will last as long as possible. After that, a transmitter connected by
telephone to a monitoring service can check the device. This is done every two
months for the first three years and then once a month until the battery runs
out. Batteries need to be replaced about every seven to nine years for
dual-chamber devices and every ten to twelve years for single-chamber units.

Battery replacement surgery is an outpatient procedure. Artificial pacemakers
have been around a long time and have improved dramatically with technology.

Though there are several different types of pacemakers available on the market,
they are all designed with the same intentions, to treat conditions such as
bradycardia, sick-sinus syndrome, heart blockage, and various other irregular
heart beats by artificially controlling cardiac rhythm and output with
electrical waves that propagate through the myocardium. Cardiac pacing units
have prolonged the lives of millions of Americans suffering from heart
arrhythmias and other heart related diseases. Through technological advances in
the health/sciences and engineering industries, patients are now able to resume
their daily activities without having to worry about moderate physical exertion.


Glenn W. L., William.

Cardiac Pacemakers. Annals of the New York Academy of Sciences v. 111 art. 2-3,

1964. Furman, Seymour. Advances in Cardiac Pacemakers. Annals of the New York

Academy of Sciences v. 167, art. 2, 1969. Spielman R. Scott. Pacemakers in the
elderly: New knowledge, new choices. Geriatrics v. 41, no. 2, Feb. 1986.

Tordjman, Therese. Recent Developments in Cardiac Pacemakers. The Physician and

Sportsmedicine v. 15, no. 1, Jan. 1997. Morse, Dryden. A Guide to Cardiac

Pacemakers. New England Journal of Medicine v. 315, p. 1557+, Dec. 11, 1986.