Arrhythmias.

Normal cardiac rhythm results from electrical impulses that control the heart muscle. Any change fro the nomral sequence of impulses is termed arrhythmia. Some arrhythmias are so brief (for example, a temporary pause or premature beat) that the overall heart rate isn't affected greatly. If arrhytmias last for some time, though, they may cause the heart rate to be too slow or too fast. A rate of less than 60 beats per minute is referred to as bradycardia. Tachycardia usually describes a rate of more than 100 beats per minute.

Arrhythmia;s may develop because of abnormalities in how impulses are conducted. Delays in the spreading of impulses can occur anywhere in the conduction system. When the transmission of impulses is blocked intermittently or completely, bradycardia may result.

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.

Arrhythmias can produce a broad range of symptoms, from barely perceptible to cardiovascular collapse and death. When they are very brief, arrhythmias are most likely to be almost without symptoms. For instance, a single premature beat may be perceived as a "palpitation" or "skipped beat." Premature beats that are frequent or occur in rapid succession during 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, light-headedness, loss of consciousness, or even death. Death occur 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 fill with blood properly. 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 activity as well as rapid chaotic electrical activity in the upper chambers. 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.

When the heat's ability to work is greatly reduced for a prolonged time, cardiac arrest and death are likely. This may result from ventricular tachycardia and ventricular fibrillation (an extremely rapid, chaotic rhythm during which the heart quivers). If the heart can continue to pump normally, though, some ventricular tachycardias (even those that last for minutes or hours) may be tolerated well without a loss of consciousness or cardiac arrest. Tachycardia may be nonsustained (lasting only seconds) or sustained (lasting for munutes or hours).

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 artrial fibrillation. They may break free and cause a stroke or damage other organs.

Although there's great variation in their severity, arrhythmias occur throughout the population. On an everyday level, the heart rate speeds up during physical activity, stress, or excitement, and slows down 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 are likely to have frequent or multiple types of ventricular premature beats.

Acquired heart disease is the most important factor predisposing a person to arrhythmias. The main causes are atherosclerosis, hypertension, and inflammatory or degenerative conditions.

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

In some patients whose symptoms suggest arrhythmias, tachycardias or bradycardias may be found during diagnostic (particularly 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 intevention must be taken into account.

Potentially life-threatening bradycardias may be treated with medication that increases the automatic firing 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, implanting a permanent pacemaker is appropriate.

Symptomatic tachycardias and premature beats may be treated with a variety of antiarrhythmic drugs. These may be given intravenously on an acute basis or orally 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) often is added to reduce the risk of blood clots and stroke.

Ahost 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 only was 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 an electrode catheter inserted through a vein or artery during electrophysiologic studies to perform targeted electrocautery in the heart. A patient may be cured of tachycardia through ablative therapy, so that antiarrhythmic mediation no longer is needed. Transcatheter ablation rapidly is becoming the treatment of choice for many supraventricular tachycardias.