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Cardiac pacemakers

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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 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 ...

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