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.