To understand ventricular fibrillation, consider a normal heartbeat.

What's a normal heartbeat?

When your heart beats, the electrical impulses that cause it to contract follow a precise pathway through your heart. Interruption in these impulses can cause an irregular heartbeat (arrhythmia).

Your heart is divided into four chambers. The chambers on each half of your heart form two adjoining pumps, with an upper chamber (atrium) and a lower chamber (ventricle).

During a heartbeat, the smaller, less muscular atria contract and fill the relaxed ventricles with blood. This contraction starts after the sinus node — a small group of cells in your right atrium — sends an electrical impulse causing your right and left atria to contract.

The impulse then travels to the center of your heart, to the atrioventricular node, which lies on the pathway between your atria and your ventricles. From here, the impulse exits the atrioventricular node and travels through your ventricles, causing them to contract and pump blood throughout your body.

What causes ventricular fibrillation?

The cause of ventricular fibrillation isn't always known. The most common cause is a problem in the electrical impulses traveling through your heart after a first heart attack or problems resulting from a scar in your heart's muscle tissue from a previous heart attack.

Some cases of ventricular fibrillation begin as a rapid heartbeat called ventricular tachycardia (VT). This fast, regular beating of the heart is caused by abnormal electrical impulses that start in the ventricles.

Most VT occurs in people with a heart-related problem, such as scars or damage from a heart attack. Sometimes VT can last less than 30 seconds (nonsustained) and may not cause symptoms. But VT may be a sign of more-serious heart problems. If VT lasts more than 30 seconds, it will usually lead to palpitations, dizziness or fainting. Untreated VT will often lead to ventricular fibrillation.

Most cases of ventricular fibrillation are linked to some form of heart disease.

Nov. 01, 2014

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