|Cardiac Pacemakers Essay, Research Paper
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.
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