An explanation of how the heart works and Atrial Fibrillation

The heart pumps blood to the rest of the body. During each heart beat, the two upper chambers of the heart (atria) contract, followed by the two lower chambers (ventricles). These actions, when timed perfectly, allow for an efficient pump. The timing of the heart’s contractions is directed by the heart’s electrical system.

The electrical impulse begins in the sinoatrial (SA node), located in the right atrium (right upper heart chamber). Normally, the SA node adjusts the rate of impulses, depending on the person’s activity. For example, the SA node increases the rate of impulses during exercise and decreases the rate of impulses during sleep.

When the SA node fires an impulse, electrical activity spreads through the right and left atria, causing them to contract and force blood into the ventricles (the two lower chambers of the heart; these pump blood either to the lungs to pick up oxygen [right ventricle] or pump oxygen rich blood to the entire body [left ventricle]).

The impulse travels to the atrioventricular (AV) node, located in the septum (near the middle of the heart). The AV node is the only electrical bridge that allows the impulses to travel from the atria to the ventricles (from the top chambers of the heart to the lower chambers). The impulse travels through the walls of the ventricles, causing them to contract. They squeeze and pump blood out of the heart. The right ventricle pumps blood to the lungs, and the left ventricle pumps blood to the body.

When the SA node is directing the electrical activity of the heart, the rhythm is called “normal sinus rhythm.” The normal heart beats in this type of regular rhythm, about 60 to 100 times per minute at rest.

Atrial fibrillation (AF or AFib) is the most common irregular heart rhythm that starts in the atria. Instead of the SA node (sinus node) directing the electrical rhythm, many different impulses rapidly fire at once, causing a very fast, chaotic rhythm in the atria. Because the electrical impulses are so fast and chaotic, the atria cannot contract and/or squeeze blood effectively into the ventricle.

Instead of the impulse traveling in an orderly fashion through the heart, many impulses begin at the same time and spread through the atria, competing for a chance to travel through the AV node. The AV node limits the number of impulses that travel to the ventricles, but many impulses get through in a fast and disorganized manner. The ventricles contract irregularly, leading to a rapid and irregular heartbeat. The rate of impulses in the atria can range from 300 to 600 beats per minute.

Some people live for years with atrial fibrillation without problems. However, atrial fibrillation can lead to future problems:

• Because the atria are beating rapidly and irregularly, blood does not flow through them as quickly. This makes the blood more likely to clot. If a clot is pumped out of the heart, it can travel to the brain, resulting in a stroke. People with atrial fibrillation are 5 to 7 times more likely to have a stroke than the general population. Clots can also travel to other parts of the body (kidneys, heart, intestines), and cause other damage.
• Atrial fibrillation can decrease the heart’s pumping ability. The irregularity can make the heart work less efficiently. In addition, atrial fibrillation that occurs over a long period of time can significantly weaken the heart and lead to heart failure.
• Atrial fibrillation is associated with an increased risk of stroke, heart failure and even death.

A person can have atrial fibrillation without having any symptoms. If symptoms are present, they may include:

• Heart palpitations - Sudden pounding, fluttering or racing sensation in the chest
• Lack of energy or feeling over-tired
• Dizziness - Feeling light-headed or faint
• Chest discomfort - Pain, pressure or discomfort in the chest
• Shortness of breath - Having difficulty breathing during normal activities and even at rest

Catheter ablation may be an option for treating AF in people who cannot tolerate medications or when medications are not effective in maintaining a normal heart rhythm. Pulmonary vein ablation and ablation of the AV node are the two types of catheter ablation procedures used to treat atrial fibrillation. Both are performed by an electrophysiologist (doctor who specializes in treating heart rhythm conditions).

Fish Oil Capsules improve atrial fibrillation

Atrial fibrillation usually begins in the pulmonary veins or at their attachment to the left atrium. If you can control or prevent abnormal signals from originating in the pulmonary veins they do not affect the atrium. This allows the SA node to once again direct the heart rhythm and a normal sinus rhythm is restored; in fact this is a common form of ablation therapy for treating AF.

In this procedure the doctor inserts catheters (long, flexible tubes) into the blood vessels of the leg, and sometimes the neck, and guides the catheters into the atrium. Energy is delivered through the tip of the catheter to the tissue targeted for ablation.

Small circular scars eventually form and prevent the abnormal signals that cause atrial fibrillation from reaching the rest of the atrium. The scars block any impulses firing from within the pulmonary veins, thereby electrically “disconnecting” them or “isolating” them from the heart. This is what allows the SA node to once again direct the heart rhythm and a normal sinus rhythm is restored demonstrating how important the pulmonary veins are in AF.

In Paroxysmal Atrial Fibrillation (PAF) there is no underlying heart problem found; this accounts for up to 30% of cases of AF. In this small study 18 patients with PAF were supplemented with 6 grams of fish oil daily for an average of 40 days. 18 additional patients were not supplemented. The fish oil capsules improved the function and health of the pulmonary veins and reduced the incidence of AF spreading out the time between incidents. The atria worked better. Fish Oil capsules reduced the ability of pulmonary veins to initiate AF. The study was performed in the cardiology Department, Royal Melbourne Hospital, Victoria, Australia and is published online ahead of print in the American Journal of Cardiology.