FREE ESSAY ON CARDIAC PACEMAKERS

CARDIAC PACEMAKERS

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 arrhythmic 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 who 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
Brady arrhythmias. 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 remains 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. Micro
calcification 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 heartbeat 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, and 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 sub mammary 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 venous
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 heartbeats
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.
BIBLIOGRAPGHY 
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