An hypothesis of the mechanism by which normal rhythm is restored in atrial fibrillation

Abstract

The abrupt change from atrial fibrillation or flutter to normal sinus rhythm has become rather familiar to us since the use of quinidin. In spite of our greatly improved knowledge of the mechanism of fibrillation and flutter the exact way in which normal rhythm supersedes these arrhythmias is still a matter of speculation. The most prominent explanation, offered by Lewis, 1 has recently been considerably modified 2 and is still rather unsatisfactory because it fails to take into consideration events that may be taking place in the region of the sinuatrial node.

It is the opinion of the writer that an adequate and satisfactory explanation of the change to regular rhythm will include a consideration not only of changes in the condition of circus contraction, but also of events in the immediate neighborhood of the normal pacemaker. This becomes more evident when we remember that the change in rhythm takes place quite suddenly at a time when the rate of flutter or fibrillation has been slowed to approximately twice the normal sinus rate.

Furthermore, the experimental evidence that we now have confirms our view, suggested by the experiments of Lillie on conduction and our own records of the effect of quinidin on the human heart, that quinidin not only increases the refractory interval but also slows the conduction rate. In fact the conduction rate seems, at least in some cases, 2 to be much more markedly affected than does the refractory interval. This is quite at variance with previous explanations of the effect of quinidin.

It is more in accord with known facts to believe that quinidin restores normal rhythm in the fibrillating or fluttering atrium, not by prolonging the refractory period to such an extent that circus movement is no longer possible, but by decreasing the conduction rate and so slowing up the circus movement to such an extent that the rhythmic function of the atrial muscle can reassert itself.