irregular rhythm of contraction of the muscles of the atrium, the upper chamber of the heart. In some cases the fibrillations are not noticed by the patient, but frequently the chaotic, rapid, and shallow beats are felt as significant palpitations of the heart, often accompanied by shortness of breath, dizziness, and fatigue. Atrial fibrillation is the most common type of cardiac arrhythmia, or disturbance in normal rhythm. It is not necessarily a serious condition in itself and need not result in significant restriction of activity; nevertheless, its presence may create problems for other cardiac functions, particularly in the ventricles, or lower chambers of the heart.

Atrial fibrillation arises when muscle cells in the wall of the atrium go through changes that interfere with the proper propagation of electrical nerve impulses. It is known to occur more frequently as the amount of fibrous tissue increases in the aging heart; there is also a significant familial propensity to the condition. Atrial fibrillation can also be brought on by other cardiac conditions that increase the load on the atrium, such as mitral valve disease and chronic congestive heart failure. Finally, atrial fibrillation may occur transiently as a result of overstimulation (as in hyperthyroidism) or irritation (as in pericarditis).

Atrial fibrillation interrupts the normal functioning of the sinoatrial node, a mass of specialized muscle tissue in the right atrium that is the primary source of the impulses which serve as the natural pacemaker of the heart. Thus, not only is atrial rhythm disturbed but also the impulses activating the ventricles, which pump blood to the lungs and body. The ventricles are protected by another node, known as the atrioventricular node, from the extraordinary bombardment of impulses originating in the fibrillating atrium; however, people with atrial fibrillation, upon exercise or stress, frequently experience excessive increases in heart rate that must be treated with beta-adrenergic blocking agents ( beta-blockers), calcium channel blockers, or digitalis. In addition, atrial fibrillation can worsen the condition of cardiac patients whose ventricular functions are already impaired by heart failure or thickening of the ventricular walls (ventricular hypertrophy) by eliminating the secondary ventricular filling energy provided by a normally contracting left atrium. The most prevalent complication of atrial fibrillation results from the formation of blood clots in the wall of the fibrillating left atrium. These clots frequently break off into the circulation, where they may form emboli that can block arterial beds, thus causing substantial tissue damage. It is estimated that 25 percent of people with chronic atrial fibrillation ultimately will suffer a major embolism and stroke if they are not treated with anticoagulants such as warfarin (Coumadin©).

The primary strategy for treating atrial fibrillation is to address the underlying abnormality. Fibrillations can be interrupted by administering electric shocks to the ventricles, though in most cases this treatment must be followed by drug therapy to maintain a normal rhythm. Recent progress in clinical electrophysiology has offered the promise of a technique in which aberrant pacemakers can be ablated by ultrasound delivered through a catheter in order to provide stable defibrillation in some patients. However, in many cases, atrial fibrillation persists or recurs, and patients with chronic atrial fibrillation require treatment with the anticoagulant and antiarrhythmic drugs mentioned above. See also ventricular fibrillation.