Have you noticed your heart skipping beats or racing? Skipped beats and extra beats often cause your chest to thump and are referred to as palpitations. Should you be concerned? Read this new article from Dr Ed to get the answer.

Your Heart's Clock Regulates Its Rhythm - Part XIV

Ed G. Lakatta, MD
December 6, 2002 (Reviewed: December 16, 2004)

To read all the articles in the series, you can go to the mini-site: "Aging of Your Heart and Blood Vessels is Risky" by clicking here.

Have you noticed your heart skipping beats or racing? Skipped beats and extra beats often cause your chest to thump and are referred to as palpitations. Should you be concerned? Situations when the heart rate is inappropriately fast (tachycardia), or slow (bradycardia), or when the heart's electrical signals travel over abnormal pathways are referred to as arrhythmias.

Consider these two scenarios. Mr. Richman is watching TV as lottery numbers are drawn. He holds a ticket in his hand. As numbers are called he realizes he has five of six winning numbers. His heart starts to beat rapidly. He gasps as the final number picked makes him a millionaire. His heart feels as if it is jumping out of his chest. He feels elated.

Meanwhile, Mr. Tachi is listening to music while relaxing in his library. Suddenly, his heart starts to beat rapidly. He feels it "racing" in his chest. He feels lightheaded, weak and becomes short of breath. He tries to get up but feels wobbly. Then, his heart rate slows down abruptly. Gradually he begins to feel normal.

Both men have just experienced a sudden rapid increase in heart rate. Mr. Tachi has probably had an arrhythmia, while Mr. Richman has had a normal response caused by the sympathetic nervous system's stimulation of the heart, which increases the heart rate in times of excitement. (See Article # 8 "Messages Transmitted From The Brain Fine Tune The Heart").

Mr. Tachi will visit his doctor and undergo numerous cardiovascular tests in the next few days, while the millionaire will probably spend his time returning the calls of new friends and lost relatives.

The Heart's Clock and Electrical Pathways

To help understand skipped beats or arrhythmias let's begin by considering where a normal heartbeat originates and how it travels through the heart.

Your heart has an internal clock that's called a "pacemaker", which initiates an electrical discharge that transmits to every part of the heart muscle along a specific path of conduction fibers. This electricity travels at varying, but controlled speeds. When the heart's pacemaker and conduction system are working correctly there is a regularly-occurring and precise spread of electricity across your heart that causes a heartbeat. Follow Figure 1 as we look at this pathway.

The heart has four chambers, two on the top, called atria (2), and two on the bottom, called ventricles (5). The stimulus for a heartbeat starts in the wall of the right atrium where the heart's pacemaker, the sinoatrial, or SA node (1), is located.

The pacemaker generates an electrical current, and this wave of electricity spreads through the right and left atria (2). In response the muscles of the atria contract and force blood from these upper chambers into the lower ones, the ventricles.

As the moving current reaches a specific area between the atria and the ventricles, called the atrioventricular, or AV node (3), it is slowed down slightly. The AV node acts as a delay switch, giving the atria time to squeeze down and contract completely so that the ventricles can fill to capacity with blood before they in turn receive the moving electrical current.

Next, the current travels down a group of fibers that divides, one bundle going into the right ventricle (5) and the other going into the left ventricle (5). This group of fibers is called the bundle of His (4), pronounced, "hiss".

When the impulse reaches the ventricles it spreads across the ventricular muscle cells and initiates the orderly contraction of these lower chambers. By this action blood is ejected from the heart.

In summary, an electrical impulse initiates in the top part of your heart, usually the SA node, producing a spread of electricity across your heart and exciting the heart muscle's cells as it travels. This ultimately results in the contraction of the lower chambers, the ventricles, from which blood is pumped throughout your body.

The Pacemaker Can Lose Control!

The spread of electricity throughout the heart muscle is possible because all heart muscle cells, not just pacemaker cells, are excitable. Usually, the heart muscle cells keep time more slowly than normal pacemaker cells. This allows the pacemaker cells within the SA node to be in control of generating and pacing the heartbeat. But, if a particular group of cells in areas remote from the SA node become extra- or hyper-excitable they can take over as the pacemaker for one or several beats, or for a longer term.

You might think of the heart's cells as a schoolyard full of young boys playing soccer. Some are inherently quick and fast and are always on top of the game, while others usually play a little slower. Now let's say that to gain the attention of a pretty cheerleader some of the slower players begin showing off, speed up and start scoring. Suddenly, they are in control of the game. Likewise, cardiac fibers anywhere in the heart muscle can become hyper-excitable. This enables them to initiate a heartbeat and overtake the normal pacemaker (the SA node), producing an arrhythmia.

Common causes of such hyper-excitability of heart muscle cells include smoking, excessive alcohol consumption, stress (physical and emotional), thyroid disorders, and certain medications. Serious arrhythmias, however, are most often caused by underlying heart disease, commonly coronary heart disease, heart valve problems, and heart failure. (See Article #11 "The Inner Layer Of Your Blood Vessels Is A Battlefield", and Article #4 "Your Older Heart May Cause You To Feel Short Of Breath.")

Categorizing Arrhythmias: When and Where Does the Takeover of SA Node Pacemaking Occur?

Medical science categorizes arrhythmias in several different ways. One way is by the timing and rate of the initiating electrical discharge and the other by its location.

An initiating electrical impulse that occurs too early is called premature because it causes an early heartbeat or premature contraction to occur. A beat that occurs too late, or fails to occur, is often referred to as a blocked beat. If the rate at which initiating electrical impulses occurs is too fast it produces tachycardia (fast heart rate). If initiating electrical impulses occurs too slowly it causes bradycardia (slow heart rate).

Heart rhythms arising from excited cells outside of the SA node, in either the atria or ventricles, are referred to as ectopic. For example, premature atrial beats or contractions (PAC's), and atrial tachycardia originate in the atria. Premature ventricular beats or contractions (PVC's), and ventricular tachycardia originate in the ventricles. Premature beats can be from one focus (unifocal) or multifocal, depending on whether they always arise from the same location or from more than one location. Premature beats may be linked together, called couplets. Three in a row are called short runs of tachycardia. We all probably experience premature beats at some time or another, but they tend occur more often in persons diagnosed with heart disease, and some tend to be more serious than others.

You are almost an expert on arrhythmias at this point! You are familiar with the normal electrical pathway (called the depolarization pathway) shown in Figure 1, and you know that arrhythmias are named by when and where they originate in the heart. Imagine, that during your routine stress test your cardiologist says, "Your EKG looks great, just a couple of extra beats." You respond by asking, "Were they atrial or ventricular in origin, single beats or couplets, unifocal or multifocal, doc?"

Common Types of Arrhythmias and Their Significance

Please keep referring to Figure 1 as you follow this discussion.

1. Premature Atrial Contractions (PAC's) occur somewhere in the atria, but in a part other than the normal pacemaker, the SA node. PAC's happen before the SA node can initiate its electrical discharge (depolarization). Usually PAC's behave just like excitations from the normal SA node. They pass through the atrium, slow down when they reach the A-V node, and then continue through the ventricles.

PAC's are common. In healthy persons these beats rarely cause symptoms. Alcohol or substances that stimulate the sympathetic nervous system, such as cold or asthma medications, sometimes induce them. They have also been associated with thyroid and lung disease. While the cause of these premature beats is not fully known, an increase in their occurrence sometimes precedes the onset of a more serious arrhythmia, called atrial fibrillation. (Atrial fibrillation will be discussed below.)

2. Premature Ventricular Contractions (PVC's) are caused by electrical activation of the ventricles before the normal impulse emanating from the SA node arrives. A PVC often causes the perception of a strong beat, called a palpitation or awareness of the heartbeat. A "skip" is not sensed when the early beat occurs. But a "stopping" or "pause" follows the early beat and when the next beat occurs you may experience a "thump". This thump is the result of a super normal amount of blood being ejected which had filled the heart chamber during the pause.

Single PVC's are not dangerous. However, multiple PVC's, particularly when arising from more than a single ventricular focus, can be indicative of a serious heart problem. This scenario is sometimes associated with sudden death due to a chain reaction of abnormal excitations that could initiate ventricular tachycardia or ventricular fibrillation (discussed below). In general, PVC's don't appear to be of concern in persons without heart disease and are quite common in healthy people.

3. SA Node "Pacemaker" Rhythms That Are Too Slow or Too Fast are persistent and continuous abnormalities in the heart's excitation (rate or pattern). When the heart's clock (the SA node) continuously runs slower than normal, this is called sinus bradycardia. A heart rate of 60 to 100 beats per minute is usually considered normal. However, a rate under 60 can be normal, particularly in trained athletes. Abnormal sinus bradycardia can cause lightheadedness, fainting, chest pain and shortness of breath. Abnormal slow rates and abnormal conduction in the heart itself can be caused by medications such as those prescribed for high blood pressure or heart disease, which include beta-blockers and calcium channel blockers, (See Article # 13 "What's Your Blood Pressure and How Do Blood Pressure Medications Work?"), and also by medications for low thyroid activity.

When the SA node clock is set too fast it stimulates the heart at a more rapid rate than appropriate for a given circumstance. This is referred to as sinus tachycardia. A normal reaction to exercise or stress can cause the heart's clock to generate a heart rate that exceeds 150 beats per minute. Causes of abnormal sinus tachycardia include fever, infections, hyperthyroid, dehydration, anemia, heart failure, poor physical conditioning, and certain medications such as caffeine, nicotine, and decongestants.

4. Atrial Tachycardia is a regular, fast heart rate that occurs suddenly and is triggered in a part of the atria other than the SA node. The rate can be from 160 to 200 beats per minute. It can be triggered by premature atrial beats (PAC's) that initiate an impulse and send it on an abnormal path to the ventricles. It can last from a few minutes to hours and tends to start and stop suddenly. The episodes are unpleasant because uncomfortable palpitations and weakness occur, but the condition is usually not dangerous.

5. Ventricular Tachycardia is a heart rate over 120 beats per minutes, which is triggered from within the ventricular wall. Most commonly this occurs when there is damage to the ventricle's muscular tissue, such as following a heart attack. An early symptom is palpitations. If the tachycardia is sustained the ventricles can't fill and they can't pump blood adequately. Heart failure occurs. Sustained ventricular tachycardia can degenerate into ventricular fibrillation, which leads to cardiac arrest and sudden death.

6. Heart Flutter and Fibrillation
Heart Flutter and Fibrillation are uncoordinated series of very rapid electrical discharges that result in ineffective contractions throughout either the upper (atria) or lower chambers (ventricles) of the heart caused by multiple chaotic electrical impulses.

Atrial Fibrillation is a rapid electrical discharge pattern in which the atria fail to maintain a regular pattern of depolarization. Electrical impulses occur randomly and the mechanical contraction of the atria is lost. This transmission of rapid fibrillatory excitations to the ventricles causes them to contract faster and less efficiently than normal. This is serious because when impulses are conducted to the ventricles in rapid succession there is not enough time for them to fill with blood and therefore enough blood cannot be pumped from the heart, even though the rate is fast. The AV node between the atria and ventricles helps the situation somewhat by slowing down and diminishing the number of impulses passing through it to the ventricles. Symptoms vary from palpitations, chest pains, lightheadedness, and shortness of breath, which is a possible indication of impending heart failure.

Atrial Flutter is a more organized pattern of rapid atrial excitation than atrial fibrillation. The atria beat regularly, but at an extremely high rate, sometimes over 300 beats per minute. This rapid pace is tolerated fairly well by the atria, but not by the ventricles.

Ventricular Fibrillation is an uncoordinated series of rapid ineffective contractions throughout the ventricles. It is life threatening and can cause death within a few minutes, because there are no coordinated ventricular excitations or contractions and therefore no blood can be pumped from the heart. The cause is usually inadequate blood flow to the heart due to coronary artery disease or a heart attack. Other causes include low potassium levels and shock. Treatment must be immediate or death occurs.

How To Fix Broken Heart Clocks and Heart Cells That Misbehave

1. Suppress or Remove Hyper-Excited Heart Muscle Cells

Because all heart muscle cells are capable of become excited and can take over the role of the pacemaker, the suppression of hyper-excited cells can stop some arrhythmias. Suppression includes: avoidance of causes, antiarrhythmic drugs, and in some cases destruction of the hyper-excited cells. Things to avoid include stimulants such as alcohol, caffeine, and even cold remedies, which contain substances such as ephedrine or pseudoephedrine that stimulate the sympathetic nervous system. Reducing stress can also eliminate or decrease the frequency of PVC's.

Drugs called antiarrhythmics can make the heart muscle's cell membrane more difficult to depolarize and thus can decrease the incidence of arrhythmia. Hyper-excited cells can be permanently destroyed by methods such as surgical removal of the areas of heart muscle that contain them, in a procedure called catheter ablation. Catheter ablation can destroy the AV node by delivery of radio-frequency energy through a catheter, or wire, placed in the heart. This interrupts conduction of rapid electrical impulses from the atria to the ventricles. Treatment options depend on the severity of the arrhythmia and co-existing medical conditions.

2. Restore Normal Electric Impulse Generation

When a broken SA node causes an arrhythmia, or normal impulses are blocked either at the AV node or elsewhere in the conduction system, treatment is necessary to restore normal electric impulse generation. This can be done with the implantation of a permanent artificial pacemaker. Pacemakers are, most often, designed to assist when the heart is going too slow, such as in bradycardia, or for chronic heart block, in which SA nodal impulses are blocked below the AV node. The device is implanted under the skin and permanently attached to the heart. The battery-operated device delivers an electrical impulse when a slowing or irregularity of the heart rhythm is detected.

3. Stop Ventricular Fibrillation and Prevent Sudden Death

To prevent sustained bouts of ventricular tachycardia and prevent sudden death due to degeneration into ventricular fibrillation an automatic implantable cardioverter-defribrillator (AICD) can be used. Wires are implanted on the heart's surface and are connected to a pulse generator, which is implanted under the skin near the chest. When the device senses ventricular tachycardia or fibrillation, it gives a shock, or electrical discharge, to the heart to restore a normal rhythm. Similar to pacemakers, AICD's have a sensory system that records the heart rate and adjusts electrical pulses based on the heart's activity.

Does Aging Cause Your Heart's Clock to Wear Out?

Age-related changes in your heart's ability to initiate and conduct electric messages to other parts of the heart muscle are common. In older persons, changes in cardiac structure and the increased incidence of cardiovascular disease contribute to the striking increase in the incidence of arrhythmias. For example, it has been shown that the number of pacemaker cells in the SA node begins to decline progressively by age 60 and only about 10% of the cells are still present at age 75.

Atrial tachycardia increases with age. Nonsustained atrial tachycadia has been detected by exercise EKG in 10% of apparently healthy persons aged 80 to 89. Tachycardia in this group is not associated with an increased risk of heart attacks. However, the prevalence of atrial fibrillation also increases with age and this is associated with a higher risk of cardiovascular death, congestive heart failure and stroke in older patients.

Treatment with antiarrhythmic drugs is more likely to cause adverse effects in the elderly than in younger patients. One reason is that blood flow to the liver, which breaks down drugs to prevent higher than desired levels in the body, decreases with age. We need a better understanding of how aging affects the ways drugs are broken down (metabolized), as well as research into better pharmaceuticals for older people.

Ventricular ectopic beats increase with age. Isolated ventricular ectopic beats have been detected in 80% of healthy persons aged 60 to 85 who had no evidence of heart disease. Frequent ectopic beats, meaning more than 100 in 24 hours, have been detected in 17%. These may be due to pathologic and age-related changes, and more frequent use of drugs such as digoxin, beta-blockers, and the overuse of diuretics (water pills) in the elderly. The good news here is that the presence of ventricular ectopic beats, isolated or frequent, does not appear to increase the long-term risk of cardiac death in elderly persons without heart disease. But the risk is increased in persons with coronary artery disease, even if they are isolated ventricular ectopic beats.

The most common arrhythmia of clinical significance to older persons is sustained ventricular tachycardia. Asymptomatic runs of exercise-induced ventricular tachycardia have been reported in nearly 4% of apparently healthy persons 65 and older. Regardless of age, patients with ventricular tachycardia that is sustained or that produces symptoms such as low blood pressure or weakness must be treated immediately. This arrhythmia is sometimes treated with the AICD device previously discussed. Almost two-thirds of the patients who receive an AICD are over sixty-five. However, the benefit of this device compared with drugs is unclear for patients over seventy-five years of age. More research needs to be conducted in this older age group.

Heart Block is also common in the elderly because of inherent conduction disease, diminished blood supply to areas of the heart muscle due to disease, and digitalis or other drug toxicity. Pacemakers are often the treatment of choice. However, even with today's technology, most pacemakers implanted today only keep the heart from beating too slowly; they do not correct irregular beating or prevent the heartbeat from going too fast. Research is required to produce more sophisticated pacing devices to handle these other arrhythmias.

At present there is much scientific research being done into the mechanisms and therapies for arrhythmias, but there are more questions than answers with older people. Additional research is needed to help identify persons at high risk for ventricular arrhythmias in order to prevent sudden death. Investigation into gene-based therapies also needs to be encouraged and supported. When we understand how genetic makeup predisposes a person to arrhythmia, we may be able to treat those at risk with preventive therapies while young, and avoid the problems encountered due to co-existing medical conditions and frailty in the elderly.

Dr. Ed is a physician/scientist, who is internationally recognized for studies that range from humans to molecules on how the heart and blood vessels work in health and disease as the body ages.

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