Differentiation of "A-V Junctional Rhythms"

Abstract

Considerable controversy exists regarding the site(s) of origin of so-called junctional rhythms. However, experimental and clinical evidence indicates that a more precise identification of the origin of these rhythms is now possible. Microelectrode recordings from the atrioventricular (A-V) junction have clearly demonstrated that all three zones of the A-V node (upper nodal [AN], midnodal [N], and lower nodal [NH] regions) exhibit action potentials which are functionally different from those recorded in contiguous atrial and His bundle cells. In addition, the amplitude and rate of rise of A-V nodal action potentials are markedly depressed by acetylcholine, a relative sensitivity not shared by atrial and His bundle cells. Cells of the AN and NH regions of the A-V node do show pacemaker activity as do His bundle cells. Experimental studies using His bundle recording techniques indicate significant differences in heart rate between nodal rhythms produced by sinus node isolation or suppression (average: 94 ± 22 beats/min) and His bundle rhythms caused by A-V nodal destruction (average: 39 ± 9 beats/min). Nontoxic doses of ouabain significantly reduced the average A-V nodal rate to 55 beats/min whereas the same dose regimen did not change the average rate of His bundle rhythms. Several clinical studies have claimed that the absence of "A-V nodal" potentials during so-called middle and lower A-V nodal rhythms indicate a site of origin in the His bundle and not the A-V node. However, the nondescript, sometimes spurious nature of A-V nodal recordings severely limits this approach to differentiation of junctional rhythms. Recent clinical studies using His bundle recordings showed that patients with complete heart block and narrow QRS complexes could be clearly divided into two groups. In one group the heart rates ranged from 45-60 beats/min and invariably increased significantly following atropine administration (A-V nodal pacemakers). In the other group heart rates ranged from 35-45 beats/min and there was no significant response to atropine (His bundle pacemakers). Intra-His bundle block could be documented in several patients in the latter group, confirming the His bundle location of the ventricular pacemaker. In conclusion, evidence gained from experimental in vivo and in vitro animal studies and from clinical investigations clearly suggests the existence of at least two pacemakers in the A-V junction. The two A-V junctional pacemakers are distinctly different in both heart rate and chronotropic response to cholinergic or cholinergic-blocking agents.