Heart Arrhythmias

Each heartbeat normally originates within a specialized group of cells called the sinus node. Located in the upper-right atrium, the sinus node is your heart’s natural pacemaker. It can spontaneously produce the electrical impulses that initiate heartbeats. Other cells within the heart have a similar ability, but they’re normally inactive when the sinus node is doing its job of setting your heart’s pace. Doctors refer to normal heart rhythm as normal sinus rhythm.

From the sinus node, electrical impulses travel through the heart. As an impulse travels, the heart muscle contracts. In a normal heartbeat, the impulse first spreads across the right, then the left atrium. After activating the atria from top to bottom, the impulse proceeds to the atrioventricular (AV) node, located at the center of the heart.

The AV node normally is the only electrical path between the atria and ventricles. Within it, the impulse slows for a split second to allow the atria to fill the ventricles with blood. Exiting the AV node, the impulse is conducted along two electrical pathways (right and left bundles), which spread notions throughout the right and left ventricles.

Each cell in the heart that helps to conduct the heart’s electrical impulses has two electrical states — a poised (polarized) state and a relaxed (refractory) state. In a polarized state, heart cells are ready and able to conduct the electrical impulse that will cause a heartbeat. After a heartbeat, the cells are momentarily in a refractory state before recharging to a polarized state for the next heartbeat. While it’s in the refractory state, a heart cell is unable to conduct an impulse.

In a healthy person with a normal, healthy heart, it’s unlikely for a sustained arrhythmia to develop without some outside trigger such as an electrical shock or the use of illicit drugs. That’s primarily because his or her heart is free from any abnormal elements such as a spot of scarred tissue. Scarring can result from numerous forms of the disease — most commonly, from a previous heart attack — and may disrupt the initiation or conduction of electrical impulses.

In addition, the inability of heart cells to conduct electrical impulses during the refractory period acts as a buffer, preventing the occasional offbeat electrical impulse from developing into an arrhythmia.

However, in a heart with some form of disease or deformity, the initiation or conduction of the heart’s electrical impulses may be destabilized, which makes arrhythmias more likely to develop.

If the blood supply to the heart is somehow reduced, it can alter the ability of heart tissue — including the cells that conduct electrical impulses — to function properly.

When heart tissue becomes damaged or dies, it can affect the way electrical impulses spread in the heart.

These pre-existing heart conditions may include:

Coronary Artery Disease

Although it has been linked to many arrhythmias, CAD is most closely associated with ventricular arrhythmias and sudden cardiac death. Narrowing of the arteries that occurs with CAD can progress until a portion of your heart dies from lack of blood flow (heart attack). An old heart attack leaves behind a scar. Electrical short circuits around the scar can prevent normal heart function by causing the heart to beat dangerously fast (ventricular tachycardia) or to quiver (ventricular fibrillation).

Cardiomyopathy

This occurs primarily when your ventricle walls stretch and enlarge (dilated cardiomyopathy) or when your left ventricle wall thickens and constricts (hypertrophic cardiomyopathy). In either case, cardiomyopathy decreases your heart’s blood-pumping efficiency and often leads to heart tissue damage.

Valvular Heart Diseases

Leaking or narrowing of your heart valves can lead to stretching and thickening of your muscle (myocardium). When the chambers become enlarged or weakened due to the added stress caused by the tight or leaking valve, there’s an increased risk of developing arrhythmia.

This fast and chaotic beating of the atrial chambers is the most common arrhythmia. It affects about 2 million, mainly older Americans. Your risk of developing atrial fibrillation increases past age 65 mainly due to the wear and tear that may affect your heart’s function as you age. During atrial fibrillation, the electrical activity of the atria becomes uncoordinated. The atria beat so rapidly — as fast as 300 to 400 beats a minute — that they quiver (fibrillate). The electrical waves have the same chaotic activity that you would see if you threw a handful of pebbles into a quiet pond. Fortunately, not all of these atrial impulses reach the ventricles.

The AV node between the atria and ventricles acts as a gatekeeper, usually letting only a portion of the impulses through. Still, extra impulses often get through the AV node. This may accelerate your pulse (ventricular contractions) during atrial fibrillation to 150 beats a minute or more. In addition, the atrial impulses that reach the ventricles often arrive at irregular intervals.

This may cause an irregular heart rhythm. Atrial fibrillation can be intermittent (paroxysmal), lasting a few minutes to an hour or more before returning to a regular heart rhythm. It can also be chronic, causing an ongoing problem. Atrial fibrillation is seldom a life-threatening arrhythmia, but over time it can be the cause of more serious medical conditions such as stroke.

Although atrial flutter is less common than atrial fibrillation, the arrhythmias are in some ways similar. In fact, both can coexist in your heart, coming and going in an alternating fashion. The key distinction is that more-organized and more-rhythmic electrical impulses cause atrial flutter.

These occur because atrial flutter, unlike atrial fibrillation, arises from a short circuit. In typical atrial flutter, this short circuit exists in the right atrium. This is an important distinction because typical right atrial flutter is more amenable to some forms of treatment, such as catheter ablation.

SVT is a broad term that includes many forms of arrhythmia originating above the ventricles (supraventricular). SVTs usually cause a burst of rapid heartbeats that begin and end suddenly and can last from seconds to days. These often start when the electrical impulse from a premature heartbeat begins to circle repeatedly through an extra pathway.

SVT may cause your heart to beat 140 to 200 times a minute. Although generally not life-threatening in an otherwise normal heart, symptoms from the racing heart may feel quite strong.

One type of SVT is known as Wolff-Parkinson-White syndrome (WPW). This arrhythmia may, rarely, run in families and is caused by an extra electrical pathway between the atria and the ventricles. This pathway may allow electrical current to pass between the atria and the ventricles without passing through the AV node, leading to short circuits and rapid heartbeats.

This fast, regular beating of the heart is caused by abnormal electrical impulses originating in the ventricles. Most often, these are due to a short circuit around a scar from an old heart attack and can cause the ventricles to contract more than 200 beats a minute. Most VT occurs in people with some form of heart-related problems such as scars or damage within the ventricle muscle from coronary artery disease or a heart attack.

Sometimes, VTs last for 30 seconds or less (unsustained) and are usually harmless, although they cause inefficient heartbeats. Still, an unsustained VT may be a predictor for more serious ventricular arrhythmias such as longer-lasting (sustained) VT. An episode of sustained VT is a medical emergency. It may be associated with palpitations, dizziness, fainting, or possibly death. Without prompt medical treatment, sustained VT often degenerates into ventricular fibrillation. Rarely, VT occurs in an otherwise normal heart. In this setting, it’s far less dangerous but the condition still needs the attention of a doctor.

About 90 percent of sudden cardiac deaths, which claim the lives of about 300,000 Americans each year, are caused by this arrhythmia. With ventricular fibrillation, rapid, chaotic electrical impulses cause your ventricles to quiver uselessly instead of pumping blood. Without an effective heartbeat, your blood pressure plummets, instantly cutting off the blood supply to your vital organs — including your brain.

Most people lose consciousness within seconds and require immediate medical assistance such as cardiopulmonary resuscitation (CPR). Your chances of survival may be prolonged if CPR is delivered until your heart can be shocked back into a normal rhythm with a device called a defibrillator. Without CPR or defibrillation, death results in minutes. As with VT, most cases of ventricular fibrillation are linked to some form of heart disease. Ventricular fibrillation is frequently triggered by a heart attack. However, ventricular fibrillation may also be your first indication of heart problems.

Although a heart rate below 60 beats a minute while at rest is considered bradycardia, a low resting heart rate doesn’t always signal a problem. If you’re physically fit, you may have an efficient heart capable of pumping an adequate supply of blood with fewer than 60 beats a minute at rest. However, if you have a slow heartbeat that isn’t pumping enough blood, you may have one of several bradycardias including:

Sick Sinus

If your pacemaking sinus node isn’t sending impulses properly, your heart rate may be too slow, or it may speed up and slow down intermittently. If your sinus node is functioning properly, a sick sinus can be caused by an impulse block near the sinus node that’s slowing, disrupting, or completely blocking conduction.

Conduction Block

A block of your heart’s electrical pathways can occur in or near the AV node or along the bundle branches that conduct impulses to each ventricle. Depending on the location and type of block, the impulses between your atria and ventricles may be slowed or partially, or completely blocked. If the signal is completely blocked, certain cells in the AV node or ventricles are capable of initiating a steady, although usually slower, heartbeat.

Some blocks may cause no signs or symptoms, and others may cause skipped beats or bradycardia. Even without signs or symptoms, a conduction block is usually detectable on an electrocardiogram (ECG). Since some blocks are caused by heart disease, an ECG showing a block may be an early sign of heart problems.

With age, your heart muscle naturally weakens and loses some of its suppleness. This may affect how electrical impulses are conducted.

Being born with a heart abnormality such as the extra electrical pathway that occurs with Wolff-Parkinson-White syndrome may affect your heart’s electrical function.

Narrowed heart arteries, heart attack, or other heart damage are risk factors for almost any kind of arrhythmia.

Your metabolism speeds up when your thyroid gland releases excess hormones. This may cause fast or irregular heartbeats and is most commonly associated with atrial fibrillation. Your metabolism slows when your thyroid gland releases too few hormones, which may cause bradycardia.

Over-the-counter cough and cold medicines containing the herbal supplement ephedra (ma-huang) and certain prescription drugs may contribute to arrhythmia development. In late December 2003, the Food and Drug Administration announced the ban of ephedra from the marketplace because of health concerns.

This increases your risk of developing coronary artery disease. It may also cause the walls of your left ventricle to thicken, possibly altering how your heart’s electrical impulses are conducted.

Your risk of developing coronary artery disease and hypertension greatly increases with uncontrolled diabetes. In addition, episodes of low blood sugar (hypoglycemia) can trigger an arrhythmia.

This disorder can cause bradycardia and bursts of atrial fibrillation.

Electrolyte minerals such as potassium, sodium, calcium, and magnesium help trigger and conduct the electrical impulses in your heart.

Electrolyte levels that are too high or too low can affect your heart’s electrical impulses and contribute to arrhythmia development.

Drinking too much alcohol can affect factors that alter the conduction of electrical impulses in your heart or increase the chance of developing atrial fibrillation. In fact, the development of atrial fibrillation after an episode of heavy alcohol intake is sometimes called a holiday heart. Chronic alcohol abuse may depress the function of your heart and can lead to cardiomyopathy. Both are factors in arrhythmia development.

Stimulants such as caffeine and nicotine can cause premature heartbeats and may contribute to the development of more serious arrhythmias. Illicit drugs such as amphetamines and cocaine may profoundly affect the heart and lead to many types of arrhythmias or to sudden death due to ventricular fibrillation.

During an ECG, sensors (electrodes) that can detect the electrical activity of your heart are attached to your chest and sometimes to your limbs. An ECG measures the timing and duration of each electrical phase in your heartbeat.

This portable ECG device can be worn for a day or more to record your heart’s activity as you go about your routine.

For sporadic arrhythmias, you keep this portable ECG device at home, attaching it to your body and activating it only when you experience symptoms of an arrhythmia. The device is small, about the size of a portable compact disc player, and you can clip it to your belt. It has wires and sticky pads that you can apply to your chest or take off, as when you shower.

When you feel symptoms, you push a button, and an ECG strip of the preceding few minutes and the following few minutes is recorded. This permits your doctor to determine your heart rhythm at the time of your symptoms, to see if there’s an association.

A hand-held device (transducer) placed on your chest uses sound waves to produce images of your heart’s size, structure, and motion.

Heart monitoring tests that your doctor may use to induce an arrhythmia include:

Stress Test

Some arrhythmias are triggered or worsened by exercise. During a stress test, you’ll be asked to exercise on a treadmill or stationary bicycle while your heart activity is monitored by an ECG. Your doctor may use a drug to stimulate your heart in a way that’s similar to exercise. This may be particularly helpful if you have difficulty doing exercises and can also be used to detect coronary artery disease.

Tilt Table Test

Your doctor may recommend this test if you’ve had recurrent fainting spells. Your heart rate and blood pressure are monitored as you lie flat on a table. The table is then tilted as if you were standing up. Your doctor observes how your heart — and the nervous system that controls your heart — respond to the change in angle.

Electrophysiologic Testing and Mapping

In this test, thin, flexible tubes (catheters) tipped with electrodes are threaded through your blood vessels to a variety of spots within your heart. Once in place, the electrodes can precisely map the spread of electrical impulses through your heart. In addition, your cardiologist can use the electrodes to stimulate the heart to beat at rates that may trigger — or halt — an arrhythmia.

This allows your doctor to observe the location of the arrhythmia and the mechanisms that may be causing it. The ability to start and stop your arrhythmia also may be used to test various treatment methods for effectiveness. If your cardiologist determines that radiofrequency catheter ablation — a catheter-based treatment option for many arrhythmias — is appropriate, he or she can perform this procedure during an electrophysiologic test.

If you’ve received a diagnosis of arrhythmia, treatment may or may not be necessary. Usually, it’s required only if the arrhythmia is causing significant symptoms or if it’s putting you at risk of more serious arrhythmia or arrhythmia complications.

If symptom-producing bradycardias don’t have a cause that can be corrected — such as hypothyroidism or a drug side effect — doctors often treat them with a pacemaker. A pacemaker is a small, battery-powered device that’s usually implanted near your collarbone. One or more electrode-tipped wires run from the pacemaker through your blood vessels to your inner heart.

If your heart rate is too slow or if it stops, the pacemaker sends out electrical impulses that stimulate your heart to beat at a steady, proper rate. The newest pacemakers can monitor and pace your atria or ventricles — or both — in the proper sequence to maximize the output of blood from your heart. In addition, your doctor can program your pacemaker to meet your pacing needs. For tachycardias originating in the atria or ventricles, treatments may include one or more of the following:

Vagal Maneuvers

You may be able to stop a supraventricular tachycardia (SVT) by using particular maneuvers, which include holding your breath and straining, dunking your face in ice water, or coughing. Your doctor may be able to recommend other maneuvers to halt a fast heartbeat.

These maneuvers affect the nervous system that controls your heartbeat (vagal nerves), often causing your heart rate to slow.

Medications

Doctors use many different antiarrhythmic drugs for emergency or long-term treatment of arrhythmias or potential arrhythmia complications. Most antiarrhythmic medications work to slow your heart rate in one of two ways. One way suppresses the activity of pacemaking tissue that’s initiating impulses too quickly.

The other slows the transmission of fast impulses inside the heart. Antiarrhythmic drugs may have certain potential side effects. One such side effect is when an antiarrhythmic drug causes your particular arrhythmia to occur more frequently — or even causes a new arrhythmia to appear that’s as bad as or worse than your pre-existing condition. Side effects not related to the heart also may occur.

 

 

I-A

Sodium channel blockers. Examples include disopyramide, procainamide, and quinidine.

Historically used for ventricular arrhythmias, now rarely used, or only in combination with other treatments such as a defibrillator.

Occasionally used for atrial arrhythmias. Intermediate potency for class I drugs.

I-B

Sodium channel blockers. Examples include lidocaine, mexiletine, and tocainide.</

Treats ventricular tachycardias. Fastest-acting but least potent class I drugs.

I-C

Sodium channel blockers. Examples include flecainide and propafenone.

Often used to treat atrial fibrillation in people with an otherwise normal heart. Occasionally used for other arrhythmias. Slowest-acting and most potent class I drugs.

II

Beta-blockers. Examples include atenolol, carvedilol, and metoprolol.

Treats supraventricular tachycardias. Also lowers the risk of death after a heart attack or in congestive heart failure.

III

Potassium channel blockers. Examples include amiodarone, dofetilide, ibutilide and sotalol.

Suppresses a variety of supraventricular and ventricular tachycardias.

IV

Certain calcium channel blockers. Examples include diltiazem and verapamil.

Decreases the frequency and force of your heartbeats. Can be used to treat most supraventricular tachycardias. Also slows heart rate in atrial fibrillation.

N/A

Digitalis. Examples include digoxin.

Slows a fast heart rate, but often with only modest effectiveness, so other medications are needed. Can treat some supraventricular arrhythmias. Improves heart pump function in heart failure.

Except for digitalis, antiarrhythmic drugs are often classified by the effect they have on your heart’s electrical conduction.

ACE inhibitors: A cause of abnormal heart rhythms?

If you have atrial tachycardia, including atrial fibrillation, your doctor may use drugs or an electrical shock to reset your heart to its regular rhythm. In some cases, a blood thinner may be prescribed before cardioversion is attempted, to prevent clots from developing in your heart. Cardioversion with drugs uses certain antiarrhythmics and is usually done in a hospital so that your heart can be monitored.

If successful, the same or similar drugs may be used to help maintain rhythm. In electrical cardioversion, a shock is delivered to your heart through paddles or patches on your chest. Done under light anesthesia, the shock stops your heart for a split second. When it beats again, it often resumes a normal rhythm. Electrical cardioversion alone can sometimes permanently restore your heart’s normal rhythm. But, more often, antiarrhythmic drugs are required to maintain a normal rhythm over the long term. However, long-established atrial fibrillation isn’t likely to respond.

In this procedure, one or more catheters are threaded through your blood vessels to your inner heart. They’re positioned along electrical pathways identified by your doctor as causing your arrhythmia. Electrodes at the catheter tips are heated with radiofrequency energy. This destroys (ablates) a small spot of heart tissue and creates an electrical block along the pathway that’s causing your arrhythmia. Usually, this stops your arrhythmia.

Catheter ablation works best to block a single abnormal electrical pathway, which is the cause of arrhythmias such as atrial flutter and Wolff-Parkinson-White syndrome. However, catheter ablation may also be used to treat some arrhythmias with multiple electrical pathways such as atrial fibrillation. Complications — which can include heart injury or infection, or blood clot development — are few. In addition, catheter ablation causes little or no discomfort and can be done under mild sedation with local anesthesia. For these reasons, catheter ablation has generally become the preferred first-treatment method over open heart surgery for many types of arrhythmias that are difficult to treat with medications.

Pacemaker

A pacemaker is an implantable device that helps regulate slow heartbeats (bradycardia). The battery-driven device, which is smaller than a matchbox, is placed under the skin near the collarbone in a minor surgical procedure. An insulated wire extends from the device to the right side of the heart, where it’s permanently anchored. If a pacemaker detects a heart rate that’s too slow or has no heartbeat at all, it emits electrical impulses that stimulate your heart to speed up or begin beating again. Most pacemakers have a sensing device that turns them off when your heartbeat is above a certain level.

It turns back on when your heartbeat is too slow. Most people can be discharged from the hospital one to two days after a pacemaker is implanted. Sometimes, same-day discharge is possible. If you have a pacemaker, be aware of your surroundings and the devices that may interfere with its performance, such as antitheft systems in stores and metal detectors. These devices may not cause a problem, but it’s best just to walk through them and not linger by them. Microwave ovens and other common appliances don’t interfere with pacemakers. In addition, be sure to carry identification with you that indicates you have a pacemaker. And always tell your doctor or dentist before they administer any testing that uses medical or electronic devices.

Implantable Cardioverter Defibrillator (Icd)

Your doctor may recommend this effective, high-tech device — first introduced in the mid-1980s — if you’re at high risk of developing dangerous ventricular tachycardia (VT) or ventricle fibrillation (VF). Implantable defibrillator units designed to treat atrial fibrillation also are available. An ICD is a battery-powered unit that’s implanted near the left collarbone. One or more electrode-tipped wires from the ICD run through veins to the heart.

The ICD constantly monitors your heart rhythm. If it detects a rhythm that’s too slow, it paces the heart as a pacemaker would. If it detects VT or VF, it sends out low- or high-energy shocks to reset the heart to a normal rhythm. An ICD may lessen your chance of having a fatal arrhythmia by about 50 percent over preventive drug treatment.

Coronary Bypass Surgery

If you have severe coronary artery disease in addition to frequent ventricular tachycardia, your doctor may recommend coronary bypass surgery. This may improve the blood supply to your heart and reduce the frequency of your ventricular tachycardia, similar to angioplasty.

Gradual weight loss will lessen the load on affected weight-bearing joints. Losing weight may also decrease uric acid levels. Avoid fasting or rapid weight loss because doing so may temporarily raise uric acid levels.

Although medications have decreased the need for severe dietary restrictions in people with gout, some dietary changes can help lessen the severity of gout attacks. They may also serve as an alternative treatment for those who have problems with gout medications.

Most experts advise eating no more than 6 ounces of lean meat, poultry, or fish a day for nearly everyone — especially people who have gout because high-protein foods increase the blood level of uric acid. Organ meats (liver, brain, kidney, and sweetbreads), anchovies, herring, and mackerel are exceptionally high in purines.

Consuming too much alcohol can inhibit the excretion of uric acid, which in turn can lead to gout. Limit alcohol to no more than two drinks a day if you’re a man and one drink a day if you’re a woman or over age 65. If you’re having a gout attack, it’s best to avoid alcohol completely.

Fluids help dilute uric acid in your blood and urine.