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Arrhythmias and Sudden Cardiac Death

A Publication of the American Heart Association

What are arrhythmias?

Normal cardiac rhythm results from electrical impulses that start in the sinoatrial (or sinus) node. They spread in a timely way through the atha to the atrioventricular (AV) node. From there each impulse travels over the many specialized fibers of the His-Purkinje system, distributing the electrical ignition signal to the ventricular muscle cells.

The transmission of impulses is delayed a fraction within the AV node. This allows time for the atrial contraction that helps fill the ventricles with blood.

The term arrhythmia refers to any change from this normal sequence of beginning and conducting impulses. Some arrhythmias are so brief (for example, a temporary pause or premature beat) that the overall heart rate isn’t significantly affected. However, if arrhythmias last for some time, they may cause the heart rate to be too slow or too fast.

The term bradycardia is used to describe a rate of less than 60 beats per minute. Tachycardia usually refers to a heart rate of more than 100 beats per minute. Tachycardia may be nonsustained (lasting only seconds) or sustained (lasting for minutes or hours).

Bundle of His

How do arrhythmias occur?

Cells in the heart’s conduction system, from the sinus node down to the outer branches of the His-Purkinje system, can fire automatically and begin electrical activity. Normally, the sinus node contains the heart’s most rapidly firing cells. (This allows this area to be a natural pace- maker.) Subsidiary pacemakers elsewhere in the heart provide a back-up rhythm when the sinus node doesn’t work properly or when the transmission of impulses is blocked somewhere in the conduction system.

Under certain conditions the automatic firing rate of secondary pacemaker tissue may become too fast. If such an abnormal locus fires faster than the sinus node, it may take over control of the heart rhythm and produce tachycardia.

Arrhythmias also may develop because of abnormalities in how impulses are conducted. Delays in the spreading of impulses can occur anywhere in the conduc- tion system. When the transmission of impulses is intermittently or completely blocked (heart block), bradycardia may result. In such cases, subsidiary pacemaker cells (located beyond the conduction block) may maintain cardiac rhythm.

In another type of abnormal conduction, impulses get caught in a merry-go-round-like sequence. This process, called reentry, is a common cause of tachycardias. Regardless of what causes them, tachycardias may be subclassified according to where they arise. Thus, ventricular tachycardias originate in the heart’s lower chambers. Supraventricular tachycardias arise higher in the heart either in the upper chambers (atria) or the middle region (AV node or the very beginning portion of the His-Purkinje system).

What are the symptoms of arrhythmias?

Arrhythmias can produce a broad range of symptoms, from barely perceptible to cardiovascular collapse and death. When they’re very brief, arrhythmias are most likely to be almost symptomless. For example, a single premature beat may be perceived as a palpitation or skipped beat. Premature beats that are frequent or occur in rapid succes- sion during a nonsustained or sustained tachycardia may cause a greater awareness of heart palpitations or a fluttering sensation in the chest or neck.

When arrhythmias last long enough to affect how well the heart works, more serious symptoms may develop. At slower rates, the heart may not be able to pump enough blood to the body. This can cause fatigue, lightheadedness, loss of consciousness or even death. Death occurs if the heart rate is zero or so slow that the heart and brain stop working.

Tachycardias can reduce the heart’s ability to pump by interfering with the ventricular chambers’ ability to properly fill with blood. They do this by reducing the time for such filling or by interfering with the booster effect normally provided by timely contraction of the atria (or both).

Loss of this atrial kick during tachycardia may be caused by a change from the usual sequence of atrial and ventricular activation. It also can be caused by rapid chaotic electrical activity in the upper chambers (cailled atrial fibrillation). The reduced pumping efficiency that can develop during tachycardia may be made worse by underlying heart muscle abnormalities or atherosclerotic blocks in the coronary arteries. It’s not surprising, then, that tachycardias can produce shortness of breath, chest pain, lightheadedness or loss of consciousness.

When the heart’s ability to work is significantly reduced for a prolonged time, cardiac arrest and death are likely. This may result from very fast ventricular tachycardias and ventricular fibrillation (an extremely rapid, chaotic rhythm during which the heart merely quivers). If the heart can continue to pump normally, though, some ventricular tachycardias (even those that last for minutes or hours) may be well tolerated without a loss of consciousness or cardiac arrest.

Tachycardias sometimes can cause serious injury to other organ systems. For example, the brain, kidneys, lungs or liver may be damaged during prolonged cardiac arrest. Also, blood clots can form in the upper heart chambers as a result of atrial fibrillation. They may break free and cause a stroke or damage other organs.

Who is prone to arrhythias?

Although there’s great variation in their severity, arrhythmias occur throughout the population. On an everyday level, heart rate speeds up (sinus tachycardia) during physical activity, stress or excitement, and slows down (sinus bradycardia) during sleep. Even beyond these daily changes, probably everyone at one time or another develops premature atrial or ventricular beats. In fact, during a 24-hour period about one-fifth of healthy adults are likely to have frequent or multiple types of ventricular premature beats. (This includes short episodes of ventricular tachycardia in a small percentage of monitored people.)

The prevalence of atrial and ventricular arrhythmias tends to increase with age, even when there’s no overt sign of heart disease. Certain congenital conditions may predispose a person to arrhythmias. For example, an incompletely developed conduction system can cause chronic heart block and bradycardia. On the other hand, people born with extra conduction pathways, either near the AV node or bridging the atria and ventricles, are prone to reentrant supraventricular tachycardias.

Still, acquired heart disease is the most important factor predisposing a person to arrhythmias. The main causes are atherosclerosis, hypertension and inflammatory or degenerative conditions. The scarring or abnormal tissue deposits found with these diseases can cause bradycardias; they do this by interfering with the work of the sinus node or overall AV conduction. Likewise, they can cause tachycardias (originating in either the atria or ventricles) by causing cells to fire abnormally or by creating islands of electrically inert tissue. (impulses circulate in a reentrant fashion around these areas.)

A variety of other factors may predispose a person to develop arrhythmias. Prominent among them is the part of the autonomic nervous system that’s involved in cardiovascular regulation. One element of this control system slows the sinus rate and depresses AV nodal conduction. (These effects may prevail during sleep or in athletically well-trained people.) The opposing element of the autonomic nervous system tends to speed up the firing rate of the sinus node and other pacemaker tissue in the heart. Further, it may also make it easier for reentrant tachycardias to occur.

Many chemical agents may provoke arrhythmias, sometimes with serious consequences. Known factors include high or low blood and tissue concentrations of a variety of minerals, such as potassium, magnesium and calcium. These play a vital role in starting and conducting normal impulses in the heart. Addictive substances, especially alcohol, cigarettes and recreational drugs, can provoke arrhymias, as can various cardiac medications. Even drugs used to treat an arrhythmia may provoke another arrhythmia.

How are arrythmias diagnosed?

An electrocardiogram is the standard clinical tool for diagnosing arrhythmias. Such a recording shows the relative timing of atrial and ventricular electrical events. It can be used to measure how long it takes for impulses to be transmitted through the atria, AV conduction system and ventricles.

An arrhythmia is considered documented if it can be recorded on an electrocardiogram. Often, though, the electrocardiogram of a person who complains of symptoms that suggest arrhythmia doesn’t show anything (because of the fleeting nature of arrhythmias).

Suspected arrhythmias sometimes may be documented by using a small, portable recording module, called a Holter monitor. This can record 24 hours of continuous electrocardiographic signals. For suspected arrhythmias that occur less than daily, a patient can wear an event monitor. It provides for a continuously updated memory loop and can allow the heart to be monitored by telephone.

These electrocardiographic techniques are passive; they require an arrhythmia to spontaneously occur. Other options that provoke arrhythmias and make their diagnosis (and thus their proper treatment) easier also are used. For example, treadmill testing may be considered for people whose suspected arrhythmias are clearly exercise related. In patients prone to passing out, tilt table studies may repro- duce the faint when it’s due to abnormal nervous system reflexes that cause the heart rate to slow down and the blood pressure to drop.

Electrophysiologic testing has become extremely valuable for provoking known, but infrequently occurring, arrhythmias and for unmasking suspected arrhythmias. This procedure is performed under local anesthesia. It involves placing temporary electrode catheters through peripheral veins (and sometimes through arteries) into the heart using fluoroscopic guidance. Then these catheters are positioned in the atria, ventricles or both, and at strategic locations along the conduction system. Their purpose is to record cardiac elec- trical signals and map the spread of electrical impulses during each beat.

Electrophysiologic Testing

This technique shows where the heart block is (AV node vs. His-Purkinje system). It also shows the origin of tachycardia (supraventricular vs. ventricular) far better than is usually possible using an electrocardiogram. The ability to electrically stimulate the heart at programmed rates and induce precisely timed premature beats lets a doctor assess electrical properties of the heart’s conduction system. Most significantly, it also triggers latent tachycardia or bradycardia. Induced tachycardias can usually be stopped by rapid pacing via the electrode catheters. Sometimes an externally applied shock may be required if the patient loses consciousness during the tachycardia.

Being able to turn on and turn off tachycardias during electrophysiologic studies allows antiarrhythmic drugs to be quickly tested for effectiveness. This can be done during a single study using intravenous therapy or during short follow-up studies with oral medication. Worldwide experience with electrophysiologic testing has shown it to be relatively safe; the rate of complications is very low.

When should arrythmias be treated?

Once an arrhythmia has been documented, it’s important to try to find out where it starts in the heart. It’s also necessary to find out whether it’s abnormal or merely reflects the heart’s normal physiologic processes. The arrhythmia must be abnormal and clinically significant before it justifies an antiarrhythmic intervention. In other words, it must either cause symptoms or put a person at risk for more serious arrhythmias or complications of arrhythmias in the future.

In some patients whose symptoms suggest arrhythmias, tachycardias or bradycardias may be found during diagnostic (particulady electrophysiologic) tests. In such cases, a doctor must judge whether the arrhythmia is a likely enough explanation for the patient’s original symptoms to justify therapy. The risks and benefits of the intervention also must be taken into account.

How are bradycardias treated?

Potentially life-threatening bradycardias may be treated acutely with medication. Such medication increases the automatic fidng rate of cardiac pacemaker tissue and improves the transmission of impulses through the conduction system.

Another way to maintain the cardiac rhythm is to insert a temporary pacemaker. This involves using a thin, flexible electrode wire. One end is positioned inside the heart; the other is connected to an external temporary pulse generator that can electrically stimulate the heart via the wire. If symptomatic bradycardia persists or is likely to recur, despite eliminating reversible causes, then implanting a permanent pacemaker is appropriate. This device consists of a pulse generator, which can be as small as a silver dollar. The pulse generator is hooked up to one or two pacemaker leads that are permanently affixed to a ventricular or atrial site, or to both.

Permanent pacemakers deliver electrical stimuli to the heart when the heart’s spontaneous rate falls below a set value. Physiologic sensors are being incorporated into these devices to let the pacemaker’s rate vary according to the body’s needs.

The pacemaker generator is implanted under the skin below the collarbone. Typically it works for 8-12 years before it needs to be replaced.


How are tachycardias treated?

Symptomatic tachycardias and premature beats may be treated with a variety of antiarrhythmic drugs. These may be given intravenously on an acute basis, or in oral form for long-term treatment. These drugs act by suppressing the abnormal firing of pacemaker tissue or by depressing the transmission of impulses in tissues that either conduct too rapidly or that participate in reentry. In patients with atrial fibrillation, a blood thinner (anticoagulant) is often added to reduce the risk of blood clots and stroke.

When tachycardias or premature beats occur often, the effectiveness of antiarrhythmic drug therapy may be gauged by electrocardiographic monitoring in a hospital, by using a 24-hour Holter monitor or by serial drug evaluation with electrophysiologic testing.

The relative simplicity of antiarrhythmic drug therapy must be balanced against two disadvantages. One is that the drugs must be taken daily for an indefinite period. The second is the risk of side effects. While side effects are inherent in all medication, those associated with antiarrhythmic drugs can be most difficult to manage. These side effects include proarrhythmia, which is more frequent occurrence of preexisting arrhythmias or the appearance of new arrhythmias as bad or worse than those being treated.

A host of nondrug therapies are being used to treat patients with symptomatic tachycardias. Ablative techniques refer to therapeutic methods that physically destroy the cardiac tissue that causes or contributes to a tachycardia. Until recently, such therapy was only feasible through surgery (often involving an open heart procedure). In such a surgical approach, the culprit cardiac tissue is removed or destroyed by local heating or cooling.

Newer advances now permit therapeutic ablations to be done using a transcatheter approach. In this technique, an electrode catheter inserted through a vein during electrophysiologic studies is used to perform targeted electrocautery in the heart. A patient may be cured of tachycardia through ablative therapy, so that antiarrhythmic medication is no longer needed. Transcatheter ablation is rapidly becoming the treatment of choice for many supraventricular tachycardias.

Electrical therapy is also available for treating tachycardias. On an acute basis, many pathological tachycardias can be stopped by an electric shock delivered to the heart or by rapid overdrive pacing with an electrode catheter. Implantable devices can provide automatic electrical therapy on a chronic basis for patients with recurrent tachycardias.

The greatest advance in this area is the implantable cardioverter defibrillator. It’s used in patients at risk for recurrent sustained ventricular tachycardia or fibrillation. This device consists of electrode patches, leads or both, which may be used to deliver electric shocks. It also has at least one other electrode lead to sense the cardiac rhythm and, if necessary, pace the heart.

These various leads are tunnelled from the heart to a pulse generator. (The generator is currently a little larger than a cigarette pack). It’s usually implanted in a pouch beneath the skin on the left side of the abdomen. Right now at least one of the electrode patches must be put on the heart’s surface or on its surrounding sac. This is done in an open-chest procedure. New generation devices, now being evaluated, will require an electrode patch to be put only beneath the skin in the chest wall area and electrode wires inserted into the heart via veins. This will make implanting them much simpler.

When the implantable cardioverter defibrillator detects ventricular tachycardia or fibrillation, it shocks the heart to restore the normal rhythm. New devices are becoming avail- able that can provide for overdrive pacing to electrically convert sustained ventricular tachycardia, backup pacing in the event of bradycardia, and a host of other sophisticated functions (such as storage of detected arrhythmic events and capability to perform noninvasive electrophysiologic testing).

Implantable cardioverter defibdilators have already been very useful in preventing sudden death in patients with known sustained ventricular tachycardia or fibrillation. Studies are now being done to find out whether they may have a role in preventing cardiac arrest in high-risk patients who haven’t yet had, but are at risk for, life-threatening ventricular arrhythmias.


What is sudden cardiac death (SCD)?

It’s the sudden, abrupt loss of heart function (i.e., cardiac arrest) in a person who may or may not have diagnosed heart disease, but in whom the time and mode of death occur unexpectedly. The unexpected nature of the event is the key point in the definition.

How common is the sudden cardiac death syndrome?

About half of all deaths from heart disease are sudden and unexpected, regardless of the underlying disease. Thus 50 percent of all deaths due to atherosclerosis of the coronary arteries are sudden, as are 50 percent of deaths due to degeneration of the heart muscle, or to cardiac enlargement in patients with high blood pressure.

Sudden death is a major health problem; about 250,000 sudden cardiac deaths occur each year among U.S. adults. Controlling SCD might significantly reduce death from heart diseases.

What is the impact of sudden cardiac death?

The shock of sudden cardiac death lies in its unexpectedness. Although the direct medical costs are much less than for lingering illnesses, its economic and social impacts are huge. Sudden cardiac death occurs at an average age of about 60 years, claims many people during their most productive years and devastates unprepared families.

What causes sudden cardiac death?

SCD is the result of an unresuscitated cardiac arrest, which may be caused by almost all known heart diseases. Most cardiac arrests are due to rapid and/or chaotic activity of the heart (ventricular tachycardia or fibrillation); some are due to extreme slowing of the heart. These events are called life-threatening arrhythmias and are responsible for sudden death.

The term massive heart attack, commonly used in the media to describe sudden death, only infrequently is responsible. Heart attack more properly refers to death of heart muscle tissue due to the loss of blood supply. While a heart attack may cause cardiac arrest and sudden cardiac death, the terms aren’t synonymous.

Can the cardiac arrest that causes sudden cardiac death be reversed?

Cardiac arrest is reversible in most victims if it’s treated within a few minutes. This first became clear in the early 1960s with the development of coronary care units and electrical devices that shocked the heart to turn an abnormally rapid rhythm into a normal one. Before then, heart attack victims had a 30 percent chance of dying if they got to the hospital alive; 50 percent of these deaths were a consequence of cardiac arrest.

In-hospital survival after cardiac arrest in heart attack patients improved dramatically when the DC defibrillator and bedside monitoring were developed. Later, it also became clear that cardiac arrest could be reversed outside a hospital by appropriately staffed emergency rescue teams trained to perform CPR and to defibrillate. Thus, the problem isn’t the ability to reverse cardiac arrest, but reaching the victim in time to do so. The American Heart Association supports the concept of the need for a chain of survival to rescue the person who suffers cardiac arrest in the community.

Chain of Survival

Who’s at risk for sudden cardiac death?

Underlying heart disease is nearly always found in victims of sudden cardiac death. Typically in adults this takes the form of atherosclerotic heart disease. Two or more major coronary arteries are narrowed in 90 percent of cases; scarring from a prior heart attack is found in two-thirds of victims. It’s not surprising, then, that predisposing factors for sudden cardiac death are similar to risk factors for atherosclerotic heart disease and include cigarette smoke and high blood pressure.

A heart that’s scarred or enlarged from any cause is prone to develop life-threatening ventricular arrhythmias. The first six months after a heart attack is a particularly high-risk period for sudden cardiac death in patients who have atherosclerotic heart disease. A thickened heart muscle from any cause (typically high blood pressure or valvular heart disease) - especially when there’s congestive heart failure, too - is an important predisposing factor for sudden cardiac death.

Under certain conditions, various heart medications can set the stage for arrhythmias that cause sudden cardiac death. In particular, so-called antiarrhythmic drugs, even at normally prescribed doses, sometimes may produce lethal ventricular arrhythmias (proarrhythmic effect). Regardless of whether there’s organic heart disease, significant changes in blood levels of potassium and magnesium (from using diuretics, for example) also can cause life-threatening arrhythmias and cardiac arrest.

When sudden cardiac death occurs in young adults, atherosclerotic heart disease usually isn’t the cause. More often these young victims have a thickened heart muscle (hypertrophic cardiomyopathy) without accompanying high blood pressure.

Certain electrical abnormalities within the heart may be responsible for sudden cardiac death in the young. These include a short circuit between the upper and lower chambers (Wolff-Parkinson-White syndrome). This sometimes can allow dangerously rapid rates to develop in the lower chamber when there’s a rapid rhythm disturbance in the upper chamber and a congenitally prolonged electrical recovery after each heartbeat (long-QT syndrome) that may set the stage for fatal ventricular arrhythmias.

Less often, inborn abnormalities of the blood vessels, particularly the coronary arteries and aorta, may be present in young sudden death victims.

Adrenalin released during intense physical or athletic activity often acts as a trigger for sudden cardiac death when these predisposing conditions are present.

In young people without organic heart disease, recreational drug abuse is an important cause of sudden cardiac death.

How can survivors of unexpected cardiac arrest be protected from fatal recurrences?

Survivors of unexpected cardiac arrest (aborted sudden cardiac death) due to ventricular tachycardia or fibrillation are at risk for recurrent arrest. This is especially true if they have underlying heart disease. Patients with atherosclerotic heart disease are at risk of recurrent cardiac arrests when the first, aborted sudden death episode occurs in the absence of a new heart attack, because this implies a persistent underlying tendency toward electrical instability.

To find the treatment program most likely to prevent recurrent cardiac arrest in a patient, it’s critical to identify any predisposing anatomic or electrophysiologic abnormalities. This often requires cardiac catheterization (to show the heart and coronary blood vessels) and electrophysiologic testing. It’s also necessary to determine the possible contribution of reversible causes; if they’re identified and removed or corrected, the risk of recurrent cardiac arrest can be markedly reduced or eliminated. Such factors may include excessive doses of various cardiac drugs, the presence of antiarrhythmic agents and abnormal blood levels of various minerals, especially potassium.

The treatment program used to prevent fatal recurrences in survivors of cardiac arrest due to ventricular tachycardia or fibrillation must be chosen based upon several factors that depend on the individual. These include the underlying cardiac condition, how well the heart can pump and the demonstration of ventricular tachycardia or fibrillation during electrophysiologic testing.

For example, cardiac arrest survivors with the Wolff-Parkinson-White syndrome (who otherwise have normal hearts) may be satisfactorily treated simply with a catheter procedure that destroys the short circuit between the upper and lower heart chambers. At the other extreme, a heart transplant may be recommended for patients who’ve had a cardiac arrest as a result of very severe heart failure.

In cardiac arrest survivors with atherosclerotic heart disease but without a new heart attack, attention must be paid to both the degree of narrowing in the coronary arteries and the presence of ventricular tachycardia and fibrillation that can occur during electrophysiologic testing. Therapy limited to reversing or blunting the effects of reduced blood supply to the heart (through bypass surgery, angioplasty or medication) is likely to protect only a minority of these aborted sudden death patients from recurrent cardiac arrest. The reason is that such treatments alone don’t stabilize the electrical abnormalities in scarred heart muscle that can lead to recurrent cardiac arrest.

A number of therapies exist for controlling potentially life-threatening ventricular tachyarrhythmias that result from diseased or scarred heart muscle. Antiarrhythmic medication may protect against subsequent sudden death in certain subsets of cardiac arrest survivors (for example, in persons whose hearts pump well who are given a drug that suppresses ventricular tachycardia induced during electrophysiologic testing). However, antiarrhythmic medication is limited by the need for life-long dosing and the potential for intolerable or lethal side effects. Consequently, there’s been increasing reliance on the use of implantable cardioverterdefibrillators. They can automatically detect ventricular tachycardia or fibrillation when it occurs and, within seconds, deliver a lifesaving electrical shock to restore the normal rhythm.

Rapid heart rhythms account for the great majority of sudden cardiac deaths. Still, very slow rhythms due to conduction system failure are sometimes responsible for cardiac arrest. Persons resuscitated from this uncommon type of cardiac arrest are treated with a permanent pacemaker after acute reversible causes, such as drug toxicity, have been ruled out.

What are the hopes for the future?

If the past is any indication, there’s great hope for the future. The dramatic progress during the past 30 years, focused largely on very high-risk groups (such as cardiac arrest survivors), has shown what can be achieved. At the same time, recent advances in treating heart attack victims appear to be reducing the significant risk of sudden death during the first year after a heart attack.

In the future, we need to develop ways to identify potential victims. People whose risk may not be very high account for the vast majority of sudden death victims in absolute numbers - perhaps 80 percent of the deaths per year. Once identified, it will be possible to devise broader strategies to prevent sudden cardiac arrest.
Last Updated: August 9, 1995

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