Arrhythmias and Sudden Cardiac Death

What are arrhythmias

Normal cardiac rhythm result from electrical impulses that start in the sinoatrial (SA or sinus) node. They spread in a timely way through the atria to the atrioventricular (AV) node. From there wach impulse travels over the many speacialized 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 arryhthmias are so brief (for example, a temporary pause or premature beat) that the overall heart rate isnt greatly afeccted. However, if arrhythmias last some time, they may cause the heart rate to be too slow or too fast.

The term bradycardia is used to decribe a rate of less than 60 beats per minute. Tachycardia usually refers to a heart rate or more than 100 beats per minute.

How does arrhythmias occur?

Cells in the hearts 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 hearts most rapidly firing cells. (This allows that area to be a natural pacemaker.) Subsidiary pacemaker elsewhere in the heart provide a " back-up" rhythm when the sinus node doesnt 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. It such an abnormal "focus" fires faster than the sinus node, it may take over control of the heart rhythm and produce tachycardia.

Arrythmias also 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 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 cause them, tachycardias may be subclasssified according to where they arise. Thus, ventricular tachycardias originate in the hearts 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 arrhythmias ?

Arrhythmias can produce a broad range of symptoms, from barely perceptible to cardiovascular collapse and death. When theyre very brief, arrhythmias are most likely to be almost without symptoms. For example, a single premature beat may be perceived as a "palpitation" or "skipped beat". Premature beats that are frequent or occur in rapid succession 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 fatique, lightheaded-ness, loss of consciousness or even death. Death occurs if the heart rate is zero or slow that the heart and brain stop working.

Tachycardias can reduce the hearts ability to pump by interfering with the ventricular chambers ability to properly fill with blood. They do this by reducing the time for such filing 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. It also can be caused by rapid chaotic electrical activity in the upper chambers (for example, atrial fibrillation). The reduced pumping efficiency that can develop during tachycardia may be worse by underlying heart muscle abnormalities or atherosclerotic blocks in the coronary arteries. Its not surprising, then, that tachycardias can produce shortness of breath, chest pain, lightheadedness or loss of consciousness.

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

Tachycardias sometimes can cause serious injury to other organ systems. For example, the brain, kidneys, lung 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 arrhythmias ? 

Although theres great variation in the their severity, arrhythmias occur through the population. On an everyday level, the 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 health adults are likely to have frequent or multiple types of ventricular premature beats. (This even 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 theres no overt sign of heart disease. Certain congenital conditions may make a person prone to arrhythmias. For example, an incompletely developed conduction system can cause chronic heart block and braddycardia. 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 disease 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 thats 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 arrhythmias as can various cardiac medications. Even drugs used to treat an arrhythmia may provoke another arrhythmia.