EXCITATION OF THE HEART 



299 



III! 



FIG. 17. During normal excitation 

 an electrode in the region of tlie upper 

 A-V node records nothing following 

 atrial activity. When the sinus node is 

 driven at a rapid rate, and A-V block 

 is produced, a spike-like potential 

 (indicated by arrows) appears following 

 the atrial record. Initial sequence in 

 top record is stimulus, atrial depolariza- 

 tion, ventricular depolarization. Re- 

 cords are sequential. (Scher A. M., 

 unpublished.) 



number of explanations have been offered. Among 

 these are a) the existence of an accessory conduction 

 patlivvay from atrium to \entricle, the "bundle of 

 Kent" (64); /)) ephaptic conduction from atrium to 

 ventricle across the boundary between the chambers; 

 c) mechanical coupHng of some sort between atrium 

 and ventricle; and d) ability of the A-V node to 

 "accelerate" its conduction rate under appropriate 

 conditions ( 18, 90). The experimental evidence does not 

 appear to support any of these theories; the theory of 

 accelerated A-\' conduction appears to be based on 

 experiments which invoked coupled beats and are 

 not pertinent. Of the other three theories, the existence 

 of a bundle of Kent (64) has at times been confirmed 

 but at other times vigorously denied, and it remains 

 to be proxed that such a bundle, if it exists, would 

 have a conduction \elocity of the proper magnitude 

 to advance rather than retard the instant when the 

 ventricles become activated. The best possible guess 

 regarding the origin of this syndrome seems to be a 

 coupling of beats across the interventricular septum 

 in some as yet undetermined fashion. It is possible for 

 a \entricular extrasystole to be coupled to the pre\ious 

 normal beat and it does not therefore seem unlikely 

 that a ventricular beat can in some unknown fashion 

 be coupled to pre\-ious atrial depolarization. In the 

 classical WoIff-Parkinson-^Vhite beat the \-entricular 

 complex appears to be in part extrasystole and in 

 part normal, so that a combination of normal excita- 

 tion and coupled (or conducted) abnormal excitation 

 appears to exist. 



Dual A-V Conduction System 



In studies by Moe and co-workers (77), later 

 repeated by Rosenblueth (loi), the conclusion was 



reached that there might be two processes or pathways 

 for A-\' conduction. This conclusion was reached 

 because of two apparendy distinct and separate times 

 for activation of the ventricle when the atrium was 

 stimulated at varying rates and a like phenomenon 

 for retrograde atrial activation when the ventricle 

 was similarly stimulated. The variable which was 

 altered to give these results was stimulation frequency. 

 Another piece of evidence was the existence of 

 "echoes." When the ventricle was stimulated the 

 wave of activation pas.sed to the atria and then 

 "echoed" back to the \entricle, usually with a 

 different transmission time. In the studies by Scher 

 and co-workers (116) the echo phenomenon was 

 noted and was found to occur in a very circumscribed 

 group of cells in the region of the A-V node. Further, 

 when A-\' conduction was studied with extracellular 

 electrodes, no evidence was found for a separate 

 pathway since, whatever the time required for A-V 

 conduction, the impulse was confined to the same 

 specialized tissue pathway. The echo phenomenon 

 appears to be a property of the A-V nodal region; 

 and the stepwise \ariation in A-V conduction time 

 would also appear to be a function, although an 

 unexplained one, of the ordinary A-\' conduction 

 pathway. 



In this and other aspects of its behavior, the 

 atrio\entricular conduction system behaves like a 

 network of cells with multiple interconnections. These 

 interconnections are ordinarily more than adequate 

 to allow the impulse to be transmitted from the 

 atrium to the ventricle. During normal atrioventricu- 

 lar conduction none of the network properties are 

 really apparent. If the system is put under stress by 

 disease, anoxia, mechanical damage, rapid stimula- 

 tion, or alterations of the ionic environment, these 



