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.
