Atrial fibrillation

Atrial fibrillation

Atrial fibrillation


Atrial fibrillation is the most common heart rhythm disorder, accounted for relatively one-third of all hospital visits due to arrhythmia. The prevalence of this problem is 0,6 – 1% globally, more expressed in the western world (2 – 3% in Europe and America) than in the developing world (0,5%). Atrial fibrillation occurs approximately 1,5 more times in men as to women, and the risk is higher for people of American or European descent opposed to people of African origin. The prevalence is also increasing with aging, meaning that the people younger than 65 years have prevalence <1% while the people older than 85 years have prevalence > 10%.


Atrial fibrillation is a condition where the atria of the heart generate fast and irregular electrical impulses, losing their primary function. They beat at a very fast rate between 350 – 600  beats per minute, but the Atrioventricular node protects the ventricles from depolarization with its electrophysiological characteristics, so the rhythm of the ventricles is rarely passing 180 bpm. Atrial fibrillation often doesn’t present any symptoms, although it increases the risk for thromboembolism and stroke occurrence. Since the beats are produced in enormous amount, atria can’t contract, and the retention of blood is making it easier to coagulate. Ventricles can perform their function since the 70% of the blood is passing to it passively, and 30% are pushed by the atria.


Usually, the cause for atrial fibrillation is a reentry mechanism. Since the electrical activity of the heart is following a certain pattern where it’s being made in the Sinoatrial node (the natural pacemaker), passing over the atria then going through the Atrioventricular node, and over across the ventricles, traveling along the Bundle of His to left and right branch finally to Purkinje fibers which transmit the electrical charge to heart muscle. If the fibrous tissue is gained after the heart attack, an inflammation damages it or the heart muscle tissue is changed in another way, an irregular electrical conductivity, known as a reentry mechanism might occur blocking the conductivity in one way completely or slowing it down after the certain spot. This can happen in atria or the ventricles.

When the signal activates muscle cells it normally blocks itself on the way back. If the tissue is changed, the signal is not passing equivalently meaning that one part of the signal is propagating fast, and the other one slowly. The slower one can reactivate cells that were activated previously by a faster one, circulating and re-entering again.


Paroxysmal atrial fibrillation

Paroxysmal atrial fibrillation is often idiopathic (with an unclear cause), lasting from several seconds up to a week, mainly 24 – 48h. It stops in itself, and the heart rhythm restores to normal, sometimes without any symptoms.

Persistent atrial fibrillation

Persistent atrial fibrillation lasts at least for 7 days, and it doesn’t end on its own. Cardioversion or medications are used to help a heart to restore rhythm to a normal level.

Long-standing persistent atrial fibrillation

Long-standing persistent atrial fibrillation is a type that lasts longer than 1 year. Medications are often ineffective so other invasive methods and preventive measures are needed.

Permanent atrial fibrillation

Permanent atrial fibrillation is a state where a heart is non stop in atrial fibrillation which can’t be cured. It lowers the quality of life and increases the chance for major cardiac events. Heart rhythm can’t be restored, but it can be controlled with medications.


Although atrial fibrillation can be without any symptoms typical ones include:

The hemodynamic (dynamics of blood flow) changes are creating the symptoms of atrial fibrillation because lack of atrial contraction is decreasing the filling of left ventricle along with irregular and fast heart rate which may weaken the blood flow through coronary arteries and the brain. Atrial fibrillation may induce or embrace existing heart failure. A significant number of elderly people are asymptomatic, showing no symptoms until the atrial fibrillation worsens.

Risk factors


The most severe complications of atrial fibrillation include stroke and heart failure.

Stroke – In atrial fibrillation, blood inside the atria is flowing slowly or stagnating making it easier for thromboembolism to occur. The thrombus made in the heart that is torn out, and can flow through the circulation is called an embolus. That embolus can obstruct one of the arteries in the brain leading to ischemic stroke. About 20 – 30% of all ischemic strokes are due to atrial fibrillation.

Dementia – A lot of mini-strokes can go without any symptoms, altering the blood flow, causing inflammation, and damaging the brain step by step until it causes dementia.

Heart failure – An atrial fibrillation is interfering with heart’s pump function, not allowing it to achieve its full effect. This can weaken the heart, and cause it to fail in fulfilling the organism’s blood supply demand.

Diagnosis of atrial fibrillation

Diagnosis of atrial fibrillation is set on behalf of the clinical picture, ECG, Holter monitor with or without additional echocardiography or coronary catheterization.

Electrocardiogram (ECG) – An electrocardiogram is crucial in diagnosing the atrial fibrillation. It detects electrical signals traveling through the heart which are seen as waves showing up a depolarization and repolarization of the heart muscle. Unclear or unequal P waves, unequal PR interval or irregular QRS complex are signs of atrial fibrillation.

Holter – Holter monitor is worn for 24 hours by a patient. It gives a larger picture in the heart’s electrical activity.

Echocardiography – The heart ultrasound is used to see if there are structural changes in the heart sending the sound waves which then create a visual image.

Coronary catheterization – An invasive method used to detect structural changes in coronary arteries using a catheter, contrast agent and X-ray imaging.


Prevention of atrial fibrillation episodes relies on a healthy lifestyle. Lower your high blood pressure with a healthy diet, regular physical activity, and other measures (see hypertension). Weight loss is recommended as obesity is linked to atrial fibrillation. Alcohol can induce atrial fibrillation episode. Its intake should be decreased to a minimum. Avoid stressful situations as they can induce an episode, so try to relax. Caffeine can also affect a heart rate so it should be used with caution.


In hemodynamically unstable patients with: heart rate > 150 bpm, prolonged chest pain, systolic blood pressure value <90 mm HG or loss of consciousness, immediate cardioversion (Direct current – DC shock) is needed.

In hemodynamically stable patients the main goal is to reset and maintain the heart rhythm or to control the heart rate, always preventing thromboembolic events.

Resetting and maintaining the heart rhythm

Heart rhythm may be restored by electrical cardioversion or by drugs. Electrical cardioversion is a brief procedure done under the sedation where the electrical shock stops heart’s electrical activity resetting it to normal sinus rhythm which can later be maintained by medicines. Drugs called the antiarrhythmics can reset and maintain the heart rhythm also.

Class I of antiarrhythmic agents

These antiarrhythmic drugs block the sodium channels slowing down the sodium crossing into the cell. The central effect is done on blocking the use-dependent sodium channels, stopping a high-frequency myocardial excitation not affecting the areas with normal heart rate. They bind stronger to receptors that are activated or inactivated rather than to receptors that are in relaxing state so the blocking rate is higher in receptors that are activated frequently.

Class Ia antiarrhythmic agents -Class Ia agents (quinidine, disopyramide) are the fast channel blockers which block voltage-gated Nachannels affecting the QRS complex.

Class Ic antiarrhythmic agents -Class Ic agents (propafenone, flecainide) are the first line of drugs used in the heart without structural changes. They are binding to sodium channels with slow association and dissociation.

Class III antiarrhythmic agents

Class III antiarrhythmic agents (amiodarone) are predominantly blocking the potassium Kchannels prolonging the action potential duration and the refractory period (recovery time in which it can’t be activated) of myocardial tissue preventing the re-entry arrhythmia. Sodium channels aren’t affected so the conductivity is not decreased. Amiodarone is commonly used in people with structural changes in the heart.

Heart rate control

Controlling the heart rate can be achieved with beta blockers, calcium (Ca2+) channel blockers, and digoxin.

Ca2+ channel blockers  (verapamil, diltiazem) are decreasing the ventricle heart rate slowing down the electrical conductivity in Atrioventricular node which is in particular effective in a heart with preserved functionality.

Beta blockers (metoprolol, propranolol) are blocking the effect of epinephrine also decreasing the electrical conductivity in Atrioventricular node. These medicines should be taken with care because they can significantly lower the blood pressure causing hypotension or bradycardia (heart rate < 60 bpm).

Digoxin is used in older people or patients with heart failure. Digoxin is slowing down the conductivity in Atrioventricular node similarly to Ca2+ channel blockers as well as beta blockers, and it could be combined with these two types of medicines.

Ca2+ channel blockers and beta blockers shouldn’t be used simultaneously because their combination can lead to AV block, severe hypotension, and heart failure.

Prevention of thromboembolic events

People with atrial fibrillation are in increased risk of blood clotting which can cause a stroke. The most commonly used drugs are vitamin K antagonists (warfarin, acenocoumarol less often). These drugs are inhibiting the reactivation of inactive vitamin K thus reducing the blood clotting. Vitamin K is one of the main components required for the production of proteins important for blood clotting.  Its anticoagulant effect is measured via INR (International Normalised Ratio) which is determining the blood clotting tendency. INR should be kept between 2 – 3 in atrial fibrillation, while in people with heart valve problem between 3 – 4. Warfarin may cause dangerous bleeding, and its effects should be monitored regularly. Newer oral anticoagulants include dabigatran, rivaroxaban, apixaban as well as edoxaban. They are equally or even more efficient than warfarin. They have less food and drug interactions so monitoring is not needed, but the price of these drugs is very high.