386 



Scientific Proceedings (124). 



circus movement below the normal sinus rate in order to obtain 

 proper conditions for the restoration of normal sinus rhythm. 

 Let us take for example a heart in which the normal sinus rate is 

 100 per minute, and in which the rate of circus movement has 

 been slowed by quinidin to about 190 per minute. Let us follow 

 our circus contraction and observe the events that take place. 

 At first we notice that the circus movement stimulates the atrial 

 muscle in the region of the sinu-atrial node and stimulates the 

 node itself. But the node probably has a much greater nerve 

 supply than the ordinary atrial musculature and therefore can be 

 more sensitive to nervous influence and more subject to changes 

 in the refractory period. As we watch we see that the region of 

 the node, being for an instant slightly more refractory than usual, 

 has failed to respond to one circus stimulus. But the rhythm of 

 the node itself is sufficiently fast so that before the next stimulus 

 arrives the node itself inaugurates a contraction. Whether or not 

 this stimulus inaugurated by the node has time to spread very far 

 before the next circus stimulus arrives depends on the exact time 

 relations of the circus movement and the normal pacemaker, but 

 if the stimulus inaugurated by the pacemaker has progressed as 

 far as the central path of the circus movement it is evident that 

 the circus movement will be blocked and will therefore cease, 

 giving way suddenly to normal sinus rhythm. 



In addition to the possibility of interruption of the circus move- 

 ment by the normal pacemaker we must consider also the possi- 

 bility of interruption by atrial premature contractions of extra- 

 nodal origin. Such atrial premature contractions or extrasystoles 

 are frequently encountered in patients with irritable nervous sys- 

 tems, and especially in patients who are being treated with quini- 

 din. The manner in which the circus movement might be inter- 

 rupted by an extranodal center is similar to that just described. 

 The very frequent occurrence of atrial extrasystoles in patients 

 who respond to quinidin therapy impels us to allot considerable 

 importance to the role of such extrasystoles in the restoration of 

 normal rhythm. 



To summarize we propose for consideration the view that the 

 way in which quinidin restores normal rhythm in the fibrillating 

 atrium is by slowing up the conduction rate to such an extent 



