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HANDBOOK OF PHYSIOLOGY 



CIRCULATION I 



Cranefield and co-vvorkers (33). The latter group 

 found that acetylchohne acts on the same atrionodal 

 junction when it slows conduction (fig. 15). In the 

 studies of Scher et al. (116) there was rarely, if ever, 

 block between the A-V node and the bundle of His. 

 The sensitive junction during forward and retrograde 

 conduction was between atrial and nodal fibers. 

 Rosenblueth & Rubio (103) have presented indirect 

 evidence for other conclusions. In a study by Sano 

 et al. (108) evidence was presented that complete 

 retrograde A-V block can occur in the ventricular 

 portion of the A-V conduction system. There is no 

 necessary conflict between this study and that of 

 Scher et al., since the latter group only studied hearts 

 in which retrograde conduction occurred. 



In several studies, hypotheses based on the ge- 

 ometry of the A-V region have been advanced to 

 account for the .slow conduction. It appears likely 

 that the small size of the fibers in the boundary be- 

 tween the A-V node and the atrium, as well as of 

 those within the node, accounts in part for the slow 

 conduction velocity, and that there may be a region 

 where small fibers, or a small bundle of fibers, has 

 difficulty in exciting either large fibers or a large 

 bundle of fibers. It is further probable, as stated by 

 Pruitt & Essex (91), that the random orientation of 

 the nodal fibers with respect to one another leads to 

 cancellation of some potentials even though a wave- 

 front is moving from the atrionodal to the nodobundle 

 junction. It is also possible that the cell-to-cell con- 

 nections influence conduction velocity. It was esti- 

 mated by Scher and co-workers that the velocity in 

 the atrionodal junction is about .05 m per sec and in 

 the node o. i m per sec. 



Potentials from the A-V Region in the Frog Heart 



As indicated previously, the region of the A-V 

 ring in a number of cold-blooded animals contains 

 cells which link the atrium and ventricle. Inoue (59) 

 has placed intracellular electrodes into this region in 

 the frog heart. The potentials which he recorded 

 appear to be similar to those reported by Sano and 

 Matsuda and their co-workers (see above). 



Summary 



Some ciuestions may be raised concerning the 

 shapes of potentials recorded extracellularly. As 

 stated above, .several hypotheses have been advanced 

 to account for the peculiarities of these records. The 



FIG. 16. Electrocardiogram of the Wolff- Parkinson-Wliite 

 syndrome; leads I, II, and III from above down. Note that the 

 P wave is continuous with the QRS complex, and that the 

 QRS complex shows an initial slow deflection (heasy line in 

 lead I) which is generally referred to as a delta wave. The 

 latter portion of the complex is quite similar to late portion of 

 a normal electrocardiogram. [From Wolff c/ al. (147).] 



reason for the lack of rapid negati\e-going spikes as 

 the atrionodal and nodal cells fire is a matter for 

 speculation, as is the fact that in some studies there 

 does seem to be a period when virtually no potential 

 changes are recorded. 



From all the studies cited, it appears that conduc- 

 tion from the atrium to the common bundle involves 

 no basic mechanisms differing from those which 

 generally obtain in cardiac muscle. Conduction is 

 continuous, although velocity is not constant in all 

 portions of the system. Conduction is not one-way (as 

 is synaptic transmission), since an impulse can be 

 conducted from ventricle to atrium. Conduction does 

 not involve chemical transmission from cell to cell as 

 does synaptic transmission. 



Wolff-Parkinson-White Syndrome.- Alternate 

 A-V Conduction Pathways 



A clinical condition known as the \Volff-Parkinson- 

 White syndrome (100, 1-24, 147) has led to much 

 speculation concerning A-V conduction. In this 

 syndrome, the interval between atrial firing and 

 \entricular firing is markedly reduced (fig. 16). A 



