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Atrial Fibrillation

What is Atrial Fibrillation. Who does it affect? How do we screen for it and provide a diagnosis?

Atrial fibrillation (AF) is a common arrhythmia. A heart rhythm disorder characterised by irregular and often rapid electrical impulses in the atria, resulting in an irregular heartbeat and potential complications.

Who does it affect?

Atrial fibrillation can affect people of all ages, but it becomes more common as individuals get older. Its prevalence increases with age, from about 2% in the general population, to 5% in people older than 65 years, and 10% in people older than 75 years.

Atrial fibrillation is now recognised as placing patients at a significantly increased risk for stroke. The American Heart Association estimates that 1/4, or 75,000 strokes per year in the United States are related to atrial fibrillation, with up to 23% of such patients dying and 43% suffering significant neurologic deficit. The mortality rate from other causes of stroke is only 8%.

Atrial fibrillation is a condition in which the regular pumping function of the atria is replaced by a disorganised, ineffective quivering caused by chaotic conduction of electrical signals through the upper chambers of the heart.

Atrial fibrillation is often associated with other forms of cardiovascular disease, including one or more of the following:

  • Congestive heart failure

  • Rheumatic heart disease

  • Coronary artery disease

  • Left ventricular hypertrophy

  • Cardiomyopathy

  • Hypertension.

The progression of atrial fibrillation varies among individuals. Initial episodes of atrial fibrillation are generally symptomatic, intermittent paroxysmal episodes. Some people experience recurring episodes of atrial fibrillation that progress to a chronic state of continuous fibrillation.


A broad range of physical symptoms may be associated with AF. Some people have absolutely no awareness of being in atrial fibrillation, while others know precisely the moment when their heart rhythm destabilises from normal sinus rhythm to AF.

Although not immediately life threatening, atrial fibrillation may cause up to a 30% reduction in cardiac output resulting in shortness of breath, fatigue and reduced exercise capacity and a reduction in cerebral blood flow during the fibrillation episode, resulting in fainting and fatigue.

It is difficult for those who have not experienced AF to understand the impact that it can have on one's daily life.

Battling the physical and emotional effects of AF is debilitating, yet no one knows that the battle exists because there are few outward physical symptoms. Employers, family members and yes, even treating physicians may be unaware of the decrease in functional capacity that AF causes.

As a result, patients with AF often feel that others think that they are "exaggerating" their symptoms. Ventricular rates can also rise dangerously high when the chaotic signals of the atria are conducted to these lower chambers of the heart. More seriously, since the atria provide minimal pumping function during atrial fibrillation, blood pools in the chambers, which can lead to the formation of blood clots. Blood clots in the left atrium can dislodge and travel to the brain resulting in stroke.


Screening and Diagnosis

To make a diagnosis of atrial fibrillation, your doctor may conduct cardiac tests such as the following:

Electrocardiogram (ECG)

Patches with wires (electrodes) are attached to your skin to measure electrical impulses given off by your heart. Impulses are recorded as waves displayed on a monitor or printed on paper.

Holter monitor testing

This is a portable version of an ECG. It's especially useful in diagnosing rhythm disturbances that occur at unpredictable times. The monitor is worn under your clothing. It records information about the electrical activity of your heart as you go about your normal activities for a day or two.


In this test, sound waves are used to produce a video of your heart. Sound waves are directed at your heart from a wand-like device (transducer), which is held on your chest. The sound waves that bounce off your heart are reflected back through your chest wall and processed electronically to provide video images of your heart in motion.

Blood tests

These help your doctor rule out thyroid problems or blood chemistry abnormalities that may lead to atrial fibrillation.



Sometimes, atrial fibrillation can lead to the following complications:


In atrial fibrillation, blood may pool in your heart and form clots. If a blood clot forms, it might become dislodged from your heart and travel to your brain. There it might block blood flow, causing a stroke. The risk of stroke in atrial fibrillation depends on your age (you have a higher risk as you age) and on whether you have high blood pressure, a history of heart failure, a previous stroke, and on other factors. Depending on your medical condition, your risk of stroke in atrial fibrillation may range from less than 1 percent to more than 10 percent a year. Medications such as blood thinners can greatly lower your risk.

Congestive heart failure.

Atrial fibrillation may weaken the heart, leading to heart failure — a condition in which your heart can't circulate enough blood to meet your body's needs.


How is Atrial Fibrillation treated?

There are three major goals of medical treatment of AF: the restoration of normal sinus rhythm, control of the ventricular rate during AF, and prevention of blood clot formation.

Other current treatment options include medications, electrical cardioversion, ablations, pacemakers, and surgery. The choice of therapy is quite individualised and is usually based on the degree of disability and symptoms associated with the AF.

  1. Restoration of Sinus Rhythm Sinus rhythm is often restored with medications by slowing the conduction of electrical impulses, decreasing the excitability and automaticity of cardiac cells, or prolonging the refractory period (rest period) of cardiac tissue. Several medications may be used to terminate atrial fibrillation including amiodarone (Cordarone), flecainide (tambocor), procainimide (Pronestyl), disopyramide (Rhythmodan). The effectiveness of pharmacological cardioversion and one's tolerance of drug therapy is quite individualised. The drugs effectively maintain sinus rhythm for at least one year in 50%to 65% of people. However, they can cause side effects such as nausea and fatigue as well as some long-term risks. Some of these drugs can have proarrhythmic effects, causing the heart to become even more irritable and setting the stage for new arrhythmias to occur.

  2. Control of Ventricular Rate When atrial fibrillation can't be converted, the goal is to slow the heart rate (rate control). Traditionally, doctors have prescribed the medication digoxin (Lanoxin). It can control heart rate at rest but not as well during activity. A newer approach is to use calcium channel blockers or beta blockers. These more consistently control heart rate both at rest and during activity. In general, your heart rate should be under 80 beats a minute when you're at rest, and shouldn't exceed 110 to 120 beats a minute when you're moving moderately, such as with a hallway walk. It is important that the ventricular rate be controlled, to effectively reduce the symptoms associated with AF. The irregular, flopping sensation in the chest that is so uncomfortable and worrisome to patients with AF is not from the irregular atrial beat, but rather is from the irregular ventricular beat in response to the AF. In fact, patients are not capable of feeling their atria beating, only the ventricles. So, the faster the ventricles go, the more symptomatic patients usually become. The goal of medications such as beta blockers, calcium channel blockers, and digoxin is to slow down the heart rate by decreasing the excitability of the cardiac cells and by slowing the conduction of the electrical impulses through the AV node. Control of the ventricular rate in AF is also important in that a prolonged rapid heart rate can actually cause permanent physiologic changes to take place in the cardiac cells. These cells can undergo a form of "remodelling" that may in turn, reduce the contractility of the heart muscle and cause a tachycardia-induced cardiomyopathy to develop. It can be very challenging for the cardiologist to achieve adequate ventricular rate control in some patients. In such cases, the patient's heart rate is well-controlled with medication while at rest, but quickly exceeds the desired range as soon as the patient becomes moderately active. Conversely, medication that may be prescribed to control the patient's heart rate during activity can cause the heart to slow excessively when the patient is at rest. Finetuning one's medication regimen becomes necessary in order to achieve a balance between reducing the discomfort and minimising adverse physiologic changes that can occur with poorly-controlled ventricular rates in AF.

  3. Prevention of Blood Clot Formation During atrial fibrillation, the atria lose their organised pumping action and fibrillate (quiver) in response to the continuous electrical stimulation. In normal sinus rhythm, the atria contract, the valves open and blood fills the ventricles (the lower chambers). The ventricles then contract to complete the organised cycle of contraction that occurs with each heartbeat. Since the atria don't contract during AF, the blood is not able to empty efficiently from the atria into the ventricles with each heartbeat. Blood can then pool and become stagnant in the atria, creating a site for blood clot formation. Since the left side of the heart pumps the oxygenated blood to all parts of the body, clot formation in the left atrium can become a primary source of stroke in patients with AF. One type of stroke (thromboembolic cerebral vascular accident, or CVA) occurs when a blood clot travels to the brain and lodges in a vessel causing the normal blood flow to stop and the brain tissue to die from lack of oxygen. This serious complication of AF occurs approximately six times more often in the elderly. Since atrial fibrillation is the most common arrhythmia in this group, it poses a substantial and potentially devastating risk. Research has demonstrated that anticoagulation with warfarin (marevan) is effective in reducing the risk of blood clot formation and stroke but it does not totally eliminate the risk. An anticoagulant or blood thinner such as warfarin interferes with the body's normal clotting mechanism. The dose of warfarin is highly individualised and must be carefully monitored with blood tests to ensure safety. The blood test used to determine the level of anticoagulation is called the INR (International Normalised Ratio). The therapeutic range is usually between 2.0 and 3.0 for the prevention of stroke. Aspirin is an antiplatelet drug that is also used for stroke prevention. Aspirin decreases the stickiness of circulating platelets (small blood cells that initiate the normal clotting process), so they will not adhere to one another and thus reduces the likelihood of forming blood clots. Aspirin is much safer than Warfarin because it is less likely to cause abnormal bleeding, including even strokes from bleeding due to the Warfarin itself. However, current research indicates that aspirin is not as effective in preventing blood clots (and therefore, strokes) as Warfarin. Patients who are otherwise considered to be at low risk may be advised by their physician to take aspirin for stroke prevention. Patients with atrial fibrillation should discuss the risk of stroke with their physician in order to make appropriate decisions regarding the choice of therapy


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