Atrial fibrillation

Abstract

The electrophysiologic mechanism of atrial fibrillation is not certain, but many of its characteristics are compatible with reentry of multiple activation fronts. This mechanism accounts for the role of premature stimulation in initiation of fibrillation and for the existence of a vulnerable period. A reentrant mechanism is also compatible with the observed relations of atrial size and of disparate recovery times with the likelihood and persistence of fibrillation. Disordered automaticity is the other major mechanism postulated, and it cannot be definitely excluded. Pacemaker activity may be the mechanism of premature excitation which initiates fibrillation, and repeated reinitiation by this means may be involved in the persistence of fibrillation. Cardiovascular status is affected during atrial fibrillation by the loss of effective atrial systole and the rate and rhythm of ventricular responses. Provided atrial contraction was contributing to ventricular filling before atrial fibrillation, loss of this contribution acts to reduce cardiac output. The ventricular rate associated with atrial fibrillation is inappropriately rapid unless atrioventricular transmission has been impaired by disease or drugs. As in other tachycardias, if the rate is sufficiently rapid to interfere with ventricular filling, it will reduce cardiac output. Some studies have shown that the pattern of ventricular irregularity in response to atrial fibrillation is random; others have furnished evidence that cycles in a particular range of lengths cluster together. Whatever the pattern of responses, the irregularity itself has been demonstrated to have a positive inotropic effect capable of increasing cardiac output.