In normal hearts, the top two chambers (‘atria’) pump blood in a coordinated fashion into the two bottom chambers (‘ventricles’), which then pump this blood to the rest of the body. This normal relationship is maintained by a well-defined electrical impulse (normal sinus rhythm) occurring at the rate of between 60 and 100 beats per minute.
In AF, the normal electrical impulse in the 2 atria is disrupted and is replaced by totally chaotic electrical activity, consequently there is a deterioration of atrial mechanical function. The Atria now ‘fibrillate’ at a rate of 300-400 times a minute and the ventricles follow in a fast irregular fashion at rates up to 200 beats per minute. Blood will still flow from the atria to the ventricles but some of the hearts efficiency is lost.
For years, AF was a poorly understood arrhythmia. Now we know that AF in most cases is caused by rapid firing of electrical impulses from one or more of the 4 pulmonary veins, the tubes that drain blood from the lungs into the heart. This is then sustained by multiple waves of activity within the atria. Sometimes this will stop spontaneously but in some patients it will become persistent.
AF may be triggered by acute, temporary causes including alcohol intake, surgery, pulmonary embolism (blood clot in the lung), hyperthyroidism (overactive thyroid). There are well known chronic causes like high blood pressure, ischemic heart disease (‘heart attack’), heart failure, sleep apnoea and diseases of heart valves. It is also notable that AF affects athletes and ‘large people’ (who are not necessarily obese) disproportionately. The exact reasons for this are unclear. These do not account for all cases of AF however, and there is a large minority of cases of unknown origin that fall into the category of ‘Lone AF’.