Pacemaker

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Pacemaker

The rhythmic, regular beating of the heart is controlled by a natural pacemaker—a small patch of cells at the top of the right atrium called the sinoatrial (SA) node that sends rhythmic electric impulses along specific conducting fibers to the heart muscles, stimulating them to contract and relax in a regular sequence. When the heart muscles fail to receive the pacemaker’s signals, the heart ceases pumping blood. Within a few minutes, the patient faints, and within a few more minutes, dies—unless the heart muscles can be stimulated to resume contracting.

An artificial pacemaker is designed to help a damaged heart beat normally; it is programmed to send an electrical impulse to stimulate the heart muscle if it does not sense a normal heart beat within a specific amount of time. Dual-chamber pacemakers, the most common type, use leads to sense and pace activity in both the atrium (upper chamber) and ventricle (lower chamber). Single-pass pacemakers use only one lead and sense only one chamber, usually the ventricle. Faster and more easily implanted than the dual lead type, this pacemaker is indicated only in certain instances.

Heart

The heart is a unique organ that must function continuously to pump blood supplying oxygen to the body. It speeds up during special times of need, as when an individual is running or doing stressful work. It slows at night or during sleep when the demand for blood decreases.

This tiny pump, about the size of a fist, squeezes approximately 2.5 fl oz (75 ml) of blood out into the body with each beat. At a normal heart rhythm, this adds up to about 10 pt (5 l) of blood each minute. The heart pumps 2,500 gal (9500 l) of blood each day, and more than 100 million gal (400 million l) of blood in an average lifetime. The SA node regulates every heartbeat in time and intensity.

The SA node may function irregularly over time or even stop functioning, which will interfere with the performance of the heart. There are other electrically active tissues that will issue regulatory signals if the SA node stops generating an electrical current. The heartbeat will slow considerably under guidance of the next layer of tissue. An abnormally slow heartbeat is called bradycardia. The heartbeat may also become irregular, developing an arrhythmia. On the other hand, the SA node may become overactive, causing the heart to race at an abnormally high speed, a condition called tachycardia.

History

English surgeon W.H. Walshe first suggested using electric impulses to restart the heart in 1862. Nearly a century later, Harvard University-educated American cardiologist Paul Maurice Zoll believed he could use the heart’s responsiveness to electrical stimulation to treat cases of blockages of the heart, what is commonly called heart block. His first attempt, passing an electrode down the esophagus, failed, but in 1952 he developed an external pacemaker, passing an electric shock to the heart through electrodes placed on a patient’s chest. In October 1952, Zoll’s pacemaker was used to maintain a heartbeat in a man suffering from congestive heart failure; after two days, the patient’s own heart took over again.

Zoll’s machine, while effective, had inherent limitations: The shocks were painful to the chest muscles, and the machine—and thus the movement of the patient—were restricted to the nearest electrical outlet. Researchers envisioned an implantable pacemaker, and American inventor Wilson Greatbatch had dreamed of building one since he first heard of heart block in

1951. The restrictive size of vacuum tubes and storage batteries, however, made it impossible. As transistors became widely available in the late 1950s, Greatbatch mentioned his idea to Dr. William Chardack of the Buffalo, New York, Veterans Administration Hospital and, with Chardack’s encouragement, put together an implantable pacemaker in three weeks, working in the barn behind his home. After two years of animal testing, in 1960, Chardack and his associates implanted the first pacemakers in the chest wall of a human patient. Also in 1960, Ake Senning and his colleague, Elmqvist, designed an implantable pacemaker with an external coil and internal receiver.

The early pacemakers were designed to regulate every single heartbeat. It took over the function of the SA node; from the time of implantation, the patient’s heartbeat was directed by the pacemaker at a preset speed (usually about 70 to 72 beats per minute). Thus the patient’s capacity for exercise was limited because no matter what conditions he was under, his heart maintained the same rate of beating. It would not speed up to provide additional oxygen needed by the tissues when the patient exercised. Since then, however, a great deal of progress has been made.

Modern technology

Modern pacemakers are much improved over these designs. They are lightweight and relatively easy to install, and their lithium batteries last up to ten years as opposed to the mercury-zinc battery’s life of twenty months. The first generation of pacemakers sent signals at a preset rate; researchers Ken Anderson and Dennis Brumwell of Medtronic, Inc., in Minneapolis, Minnesota, advanced pacemaker technology immensely when they invented activity-responsive pacing in 1981 by using piezoelectric crystals that reacted to differing levels of body exertion. Medtronic’s Activitrax^®, introduced in 1985, was the first pacemaker to adjust pacing rate to exercise level. Several even more advanced pacemakers became available in the late 1980s, among them Medtronic’s Legend^®. These devices can be reprogrammed while they are still implanted, using radio-frequency signals to reset the pacemaker’s microprocessor. They also store information about cardiac events, and some models can even transmit that information over the telephone, directly from the patient’s chest to the doctor’s office.

Implantable cardioverter defibrillators (ICDs) designed by Guidant Corporation and other manufacturers primarily for other purposes, including the treatment of heart rhythms that are abnormally fast and life threatening (e.g., atrial fibrillation), can function as pacemakers for patients affected by these arrhythmias.

In a long-term study of malfunction rates of pacemakers and ICDs, researchers from the U.S. Food and Drug Administration (FDA), Beth Israel Deaconess Medical Center (Boston, Massachusetts), and Harvard Medical School (Boston, Massachusetts), found that from 1990 to 2002, 2.25 million pacemakers and 415,780 ICDs were implanted in the United States. The FDA estimates that the number of pacemakers implanted annually increased from about 95,000 in 1990 to more than 267,000 in 2002.

Current models of pacemakers monitor the heart to determine the heart rate and do not interfere with the heart function unless the heart rate drops below a predetermined speed (usually 66 to 68 beats per minute). Only then will the pacemaker deliver an electrical signal to drive the heart until the pacemaker determines that the SA node is again on track. The mechanical device then ceases its signals and returns to monitoring the heart rate. This is called demand pacing.

Current pacemakers weigh less than one ounce (25 g), are about the size of a quarter, and pace the upper and lower chamber as needed.

Some patients are at risk of a form of arrhythmia called fibrillation, which is a completely uncoordinated, quivering, nonfunctional heartbeat. If not corrected quickly, fibrillation can cause death. Since 1985, pacemakers have been available to monitor the speed of the

KEY TERMS

Arrhthymia —Any abnormal rhythm of the heart, which can be too rapid, too slow, or irregular in pace.

Atria —The two upper chambers of the heart.

Demand pacing —A type of pacemaker that responds to the needs of the body rather than uniformly pacing heartbeats at a single rate.

Ventricles —The two lower chambers of the heart; also the main pumping chambers.

heart and deliver an appropriate electrical shock to the heart muscle if it begins to fibrillate. The device can deliver a low-level pacing shock, an intermediate shock, or a jolting, defibrillating shock if necessary.

Surgeons prefer to implant pacemakers in the shoulder because the procedure can be carried out under local anesthetic. The wire from the pacemaker is inserted into one of the large veins in the shoulder and fed down into the heart, through the right atrium and into the ventricle where it is attached to the heart muscle. If the wire cannot be fed through veins that are too small or diseased, the pacemaker can be implanted in the abdomen.

Doctors must see patients with pacemakers frequently to check the battery power and make sure the circuitry is intact. Leads may become disconnected, the wire may break, or scarring may form around the electrode, all of which can render the pacemaker useless. Patients should avoid sources of electromagnetic radiation, including security scanning devices at airports and diagnostic tests using magnetic resonance imaging (MRI), both of which can turn off the pacemaker. Some states prohibit a person from driving an automobile for a period of time after he/she has received a pacemaker if he/she has previously experienced unconsciousness as a result of arrhythmia.

See also Circulatory system.