URICULAR paroxysmal tachycardia was long ago described and recognized as a clinical entity, but the fundamental mechanism or mechanisms responsible for this disorder have not yet been finally ascertained.', 2 Unlike auricular flutter and auricular fibrillation, it cannot be readily induced in experimental animals, and cannot, therefore, be easily studied by this met,hod. Speculations as to its nature must, therefore, be based on pertinent observations on man. We propose to discuss from this standpoint the following features of this disturbance : (1) the form of the anricular deflect.ions; (2) the effects of exertion, vagal stimulation, digitalis, quinidine, and other drugs upon the auricular rate and the duration of the paroxysms; (3) similarities, differences, and relations between it and auricular flutter and fibrillation; (4) the spontaneous occurrence of auriculoventricular block in a small number of cases and the difficulty or impossibility of producing it in most of the others; and (5) the occurrence of alternation in the auricular cycle length. We wish particularly to examine the su ggestion3 that auricular paroxysmal tachycardia is caused by circus rhythm involving one of the specialized auricular nodes. When Mines4 described circus rhythm he suggested that it might be responsible for some cases of paroxysmal. tachycardia in man. Iliescu and Sebastian? were among the first to su ggest that auricular paroxysmal tachycardia is due to circus contraction. Their reasoning was based chiefly on the a,ction of quinidine in this disorder. Lewis2 pointed out that the tot.al amount of auricular muscle is not sufficiently large to accommodate a circus mechanism at known rates of conduction in aurieular
