EXCITATION OF THE HEART 



293 



35-40 



FIG. 8. Pathway and mode of atrial activation. Lejt: right 

 atrium and right atrial appendage viewed from right. Activity 

 begins in sinus node (black) and progresses toward borders of 

 atrium. Center: activation of atria viewed from anterior aspect. 

 Right: activation of left atrium and appendage. Shading shows 

 areas activated within each 5-msec period. Duration of P 

 wave was 50 msec, [.'\fter Puech (92).] 



FIG. 9. A view from the interior of the rabbit's right atrium. 

 Trabeculated area is at the left as indicated. Numbers indicate 

 the instant of activity in milliseconds after depolarization of 

 the sinus node. Note that activity spreads approximately 

 radially from the sinus node, which is in the upper central 

 region of the figure. The shapes of action potentials recorded 

 are indicated by the various symbols in the figure. Note along 

 the atrioventricular margin on the right (circle with vertical 

 line) the region of the common bundle. Immediately upstream 

 from this (circle with cross) are cells from an intermediate 

 region along the A-V conduction pathway, which the experi- 

 menters termed nodobundle cells. Above these (black circle 

 with horizontal white line) are cells which the researchers 

 considered to be the first link in the A-V transmission system 

 and which they termed atrial-nodal cells. Note further that these 

 atrial-nodal cells extend from the trabecular region into the 

 A-V nodal region. (From Paes de Carvalho et al. (82).] 



diastolic depolarization to threshold (7, 20, 134, 140- 

 142). Prior to study with the intracellular electrode 

 Lewis (71) had shown that the S-A node is the site of 

 earliest negativity, and other workers (11, 19, 95) had 

 demonstrated that an electrode in this region shows a 



potential .slightly earlier than the firing of ordinary 

 atrial muscle. The process by which the S-A and A-V 

 nodes generate impulses is not known. It is possible 

 that these cells differ from others in being more 

 permeable to sodium when at rest and consequently 

 gradually depolarize at the end of each cycle to the 

 level at which rapid depolarization takes place. 



Activity in the atrium commences in the S-A node 

 and spreads outward like the wave produced when a 

 stone is dropped into still water (21, 71, 82, 92). The 

 plots of atrial excitation by Lewis (71) and more 

 recently by Brendel and co-workers (21), Puech (92), 

 and Paes de Carvalho and co-workers (82) agree 

 closely (figs. 8, 9). From the region of the S-A node, 

 the wave of atrial depolarization proceeds at a 

 velocity of slightly less than i m per sec toward the 

 borders of the two atria and of the interatrial septum. 



Among the theories which constantly recur in the 

 anatomical literature are those concerning the 

 existence or absence of a specialized conduction 

 system in the atrium (see above). The belief that such 

 a conduction system is present in birds has led 

 individuals with a strong interest in comparative 

 physiology to feel that there must be such a system 

 in other species. There seems to be no compelling 

 evidence for such a system in "gross" plots of atrial 

 excitation in mammals. However, Paes de Carvalho 

 and his co-workers (82) believe that potential shapes 

 similar to those recorded from the A-V nodal and 

 other specialized cells (i.e., potentials showing dias- 

 tolic depolarization, etc.) can be found throughout 

 the atria. These investigators also report evidence for 

 rapid conduction between the S-A and A-V nodes in 

 tissue which they refer to as the S-A ring bundle in 

 the rabbit (fig. 9). It is possible that this rapid con- 

 duction occurs along the long axes of the fibers 

 rather than in specialized tissue. In other disputed 

 studies it has been claimed that certain small 

 strategically placed cuts in the interatrial septum will 

 disrupt A-V conduction. Since the potentials found 

 by Paes de Carvalho et al. (82) are reminiscent of 

 pacemaker (S-A and A-V) cells it seems pertinent to 

 ask whether pacemaker activity occurs in the atria 

 when neither the S-A node nor the A-V node is 

 present. In certain animal experiments and in certain 

 human lesions complete atrial standstill ma)' occur if 

 both nodes are removed or inactive (despite the fact 

 that isolated ventricular Purkinje fibers may act as 

 pacemakers). Also, the human heart with complete 

 A-V block and without a sinus pacemaker may show 

 no clear atrial potentials. On the other hand, atrial 



