Heart rhythm problems (arrhythmias) occur when the electrical impulses in your heart that coordinate your heartbeats don’t function properly, causing your heart to beat too fast, too slow or irregularly.
Arrhythmias are common and usually harmless. Most people have experienced these occasional, brief irregular heartbeats that feel like a skipped, fluttering or racing heartbeat. That’s not surprising when you consider that your heart beats about 100,000 times a day, or more than 2.5 billion times during the average life span.
However, some heart arrhythmias may cause bothersome — sometimes even life-threatening — signs and symptoms.
Advances in medical technology have added new treatment methods to the procedures that doctors may use to try to control or eliminate arrhythmias. In addition, because troublesome arrhythmias are often made worse — or are even caused — by a weak or damaged heart, you may be able to reduce your arrhythmia risk by adopting a heart-healthy lifestyle.
Signs and symptoms
Arrhythmias may not produce any signs or symptoms. In fact, your doctor might detect them before you do, during a routine examination. But often, abnormal heart rhythms cause noticeable signs and symptoms, which may include:
• A fluttering in your chest
• A racing heartbeat
• A slow heartbeat
• Chest pain
• Shortness of breath
• Fainting (syncope) or near fainting
Noticeable signs and symptoms don’t always indicate a serious problem. Some people who feel arrhythmias often don’t have a serious problem, while others who have life-threatening arrhythmias have no symptoms at all.
Your heart is divided into four hollow chambers. Divided top to bottom, the chambers on either half of your heart form two adjoining pumps with an upper chamber (atrium) and a lower chamber (ventricle). During a single heartbeat, the pumps operate in a two-phase cycle. First, the smaller, less muscular atria contract and fill the relaxed ventricles with blood. A split second later, the powerful ventricles contract and discharge blood as the atria relax and fill. Efficient blood circulation requires rhythmic coordination of this priming and pumping system. In addition, it requires proper heart rate control, which, in a normal heart, is 60 to 100 beats a minute when you’re at rest. Orchestration of these two factors is performed by the heart’s electrical system. Ideally, this system operates in the following three-step sequence:
• Initiation. 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 has the ability to 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.
• Propagation. 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 impulses throughout the right and left ventricles.
• Relaxation and recharging. 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 a healthy person’s heart is free from any abnormal elements such as an area of scarred tissue. Scarring can result from numerous problems — 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 evidence of disease or deformity, the initiation or conduction of the heart’s electrical impulses may be destabilized, making arrhythmias more likely to develop.
Conditions that may lead to arrhythmias
Any pre-existing structural heart condition can lead to arrhythmia development due to:
• Inadequate blood supply. If 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.
• Damage or death of heart tissue. 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 the heart’s ventricular 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.
Types of arrhythmias
Heart arrhythmias may occur when any phase in the heart’s electrical system malfunctions. Doctors classify arrhythmias not only by where they originate (atria or ventricles) but also by the speed of heart rate they cause:
• Tachycardia (tak-ih-KAHR-de-uh). This refers to a fast heartbeat — a heart rate greater than 100 beats a minute.
• Bradycardia (brad-e-KAHR-de-uh). This refers to a slow heartbeat — a resting heart rate less than 60 beats a minute.
Not all tachycardias or bradycardias indicate disease. For example, during exercise it’s normal to develop sinus tachycardia as the heart speeds up to provide your tissues with more oxygen-rich blood. Athletes at rest can have a heartbeat less than 60 beats a minute because their hearts are so efficient.
Tachycardias in the atria
Tachycardias originating in the atria include:
• Atrial fibrillation. This fast and chaotic beating of the atrial chambers is a common arrhythmia. It affects mainly older people. Your risk of developing atrial fibrillation increases past age 60 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 few the impulses through. Still, extra impulses often get through the AV node, which can greatly accelerate your pulse (ventricular contractions). 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 conditions such as stroke.
• Atrial flutter. Atrial flutter is similar to atrial fibrillation. 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.
• Supraventricular tachycardia (SVT). SVT is a broad term that includes many forms of arrhythmia originating above the ventricles (supraventricular). This type of arrhythmia may also be called paroxysmal supraventricular tachycardia (PSVT). SVTs usually cause a burst of rapid heartbeats that begin and end suddenly and can last from seconds to hours. 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 160 to 200 times a minute. Although generally not life-threatening in an otherwise normal heart, symptoms from the racing heart may feel quite strong. These arrhythmias are common in young people.
• Wolff-Parkinson-White syndrome (WPW). One type of SVT is known as Wolff-Parkinson-White syndrome (WPW). This arrhythmia 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.
Tachycardias in the ventricles
Tachycardias occurring in the ventricles include:
• Ventricular tachycardia (VT). This fast, regular beating of the heart is caused by abnormal electrical impulses originating in the ventricles. 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 problem, 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.
• Ventricular fibrillation. As many as 340,000 Americans die every year from sudden cardiac death believed to be caused by ventricular fibrillation. 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 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.
• Long QT syndrome. This syndrome may be either an acquired or an inherited condition. In older adults, this rare arrhythmia may be triggered by one — or a combination — of more than 50 drugs, many of them commonly used. These drugs affect the heart’s electrical function. On an electrocardiogram, the letter Q marks the point where an electrical impulse signals the ventricles to contract. The letter T marks the point where the cells of your ventricles have electrically recharged for the next heartbeat. When the QT interval is prolonged, ventricle cells may not have recovered in time to properly conduct the next heartbeat. People with long QT syndrome are prone to palpitations and fainting spells, and may have an increased risk of sudden death.
Although a heart rate below 60 beats a minute while at rest is considered a 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, 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.
Premature heartbeats can originate in either the atria or the ventricles. Although it often feels like a skipped heartbeat, a premature heartbeat is actually an extra beat between two normal heartbeats. Premature heartbeats occurring in the ventricles come before the ventricles have had time to fill with blood following a regular heartbeat.
Thus, the beat feels weak if it’s felt at all. This premature beat is usually followed by a pause, during which time the ventricles fill with more than the usual amount of blood. The ejection of more blood from the ventricle causes the next regular heartbeat to feel stronger than normal.
Although you may feel an occasional premature beat, they seldom indicate a more serious problem. Still, a premature beat can trigger a longer lasting arrhythmia — especially in people with heart disease. These types of arrhythmias are commonly caused by stimulants, such as caffeine from coffee, tea and soft drinks, over-the-counter cold remedies containing pseudoepedrine, and some asthma medications.
Certain factors may increase your risk of developing an arrhythmia. These include:
• Age. With age, your heart muscle naturally weakens and loses some of its suppleness. This may affect how electrical impulses are conducted.
• Genetics. 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.
• Coronary artery disease. Narrowed heart arteries, heart attack or other heart damage are risk factors for almost any kind of arrhythmia.
• Thyroid problems. 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 a bradycardia.
• Drugs and supplements. Over-the-counter cough and cold medicines containing pseudoephedrine and certain prescription drugs may contribute to arrhythmia development. The herbal supplement ephedra also increased the risk of arrhythmia, but in early 2004, the Food and Drug Administration banned ephedra from the marketplace because of such health concerns.
• High blood pressure. 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.
• Obesity. Along with being a risk factor for coronary artery disease, obesity may increase your risk of developing an arrhythmia.
• Diabetes. Your risk of developing coronary artery disease and hypertension greatly increase with uncontrolled diabetes. In addition, episodes of low blood sugar (hypoglycemia) can trigger an arrhythmia.
• Obstructive sleep apnea. This disorder can cause bradycardia and bursts of atrial fibrillation.
• Electrolyte imbalance. Electrolytes, 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.
• Alcohol consumption. 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, development of atrial fibrillation after an episode of heavy alcohol intake is sometimes called “holiday heart syndrome.” Chronic alcohol abuse may depress the function of your heart and can lead to cardiomyopathy. Both are factors in arrhythmia development.
• Stimulant use. 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.
When to seek medical advice
Arrhythmias may cause you to feel premature beats, or you may feel that your heart is racing or beating too slowly. Other signs and symptoms may be related to diminished blood output from your heart. These include shortness of breath or wheezing, weakness, dizziness, lightheadedness, fainting or near fainting and chest pain or discomfort. Seek urgent medical care if you suddenly or frequently experience any of these signs and symptoms at a time when you wouldn’t expect to feel them.
With little or no blood being pumped through the body, a person with ventricular fibrillation will collapse within seconds and soon won’t be breathing or have a pulse. If this occurs, follow these steps:
• Call 911 or the emergency number in your area.
• If you or someone nearby knows cardiopulmonary resuscitation (CPR), administer it if it’s needed. CPR can help maintain blood flow to the organs until an electrical shock (defibrillation) can be given.
• Portable defibrillators are available in an increasing number of places, such as airplanes, police cars and shopping malls and can even be purchased for your home. These automated external defibrillators come with built-in instructions for their use. They’re programmed to allow a shock only when appropriate.
Screening and diagnosis
To diagnose a heart arrhythmia, your doctor may ask about — or test for — conditions that may trigger your arrhythmia, such as heart disease or a problem with your thyroid gland. Your doctor may also perform heart monitoring tests specific to arrhythmias. These tests either passively monitor your heart or try to actively induce an arrhythmia while closely monitoring your heart.
Passive heart monitoring tests may include:
• Electrocardiogram (ECG). 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.
• Holter monitor. This portable ECG device can be worn for a day or more to record your heart’s activity as you go about your routine.
• Event monitor. 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 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.
• Echocardiogram. 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 it 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 your 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.