Accessory AV pathways are present in some individuals. These pathways, which are often part of a reentry loop, can lead to serious cardiac rhythm disturbances. The most common clinical disorder associated with these pathways is Wolff-Parkinson-White syndrome, a congenital disturbance. In most cases, this syndrome does not cause any functional abnormalities. However, it can be easily detected on an ECG due to the abnormal configuration of the ventricular complex. Occasionally, a reentry loop develops where the atrial impulse travels to the ventricles through one of the AV pathways and then back to the atria through the other pathway. This continuous circling around the loop results in a very rapid rhythm called supraventricular tachycardia. This rapid rhythm can be debilitating as it may not allow sufficient time for ventricular filling. Temporary blockage of the AV node by administering adenosine intravenously or by increasing vagal activity can usually abolish the tachycardia and restore a normal sinus rhythm.

In atrial myocytes, the atrial plateau is shorter and less developed, and repolarization is slower compared to typical ventricular fibers. This is because efflux of potassium (K+) is greater during the plateau phase in atrial myocytes. The shorter action potential duration in atrial myocytes is also attributed to the presence of an ultrarapid K+ current (IKur) which facilitates greater K+ efflux. This current is not present in ventricular myocytes.

The AV node, through which the atrial excitation wave reaches the ventricles, is located posteriorly on the right side of the interatrial septum near the ostium of the coronary sinus. It is approximately 15 mm long, 10 mm wide, and 3 mm thick in adult humans. The AV node consists of two cell types, similar to the SA node, but the round cells are less abundant and the elongated cells predominate. The AV node is divided into three functional regions: the atrionodal (AN) region, which acts as a transitional zone between the atrium and the rest of the node; the nodal (N) region, located in the midportion of the AV node; and the nodal-His (NH) region, where nodal fibers gradually merge with the bundle of His. The AV node and the bundle of His are the only pathways responsible for transmitting the cardiac impulse from the atria to the ventricles.
SomepeoplehaveaccessoryAVpathways.Becausethesepathwaysoftenserveasapartofareentryloop(seethesection“ ”),theycanbeassociatedwithseriouscardiacrhythmdisturbances.Wolff-Parkinson-Whitesyndrome,acongenitaldisturbance,isthemostcommonclinicaldisorderinwhichabypasstractofmyocardialfibersbecomesanaccessorypathwaybetweentheatriaandventricles.Ordinarily,thesyndromecausesnofunctionalabnormality.ThedisturbanceiseasilydetectedonanECGbecauseaportionoftheventricleisexcitedviathebypasstractbeforetheremainderoftheventricleisexcitedviatheAVnodeandtheHis-Purkinjesystem.Thispreexcitationappearsasabizarreconfigurationintheventricular(QRS)complexoftheECG.Onoccasion,however,areentryloopdevelopsinwhichtheatrialimpulsetravelstotheventriclesviaoneofthetwoAVpathways(AVnodeorbypasstract)andthenbacktotheatriathroughtheotherofthesetwopathways.Continuouscirclingaroundtheloopleadstoaveryrapidrhythm(supraventriculartachycardia).Thisrapidrhythmmaybeincapacitatingbecauseitmightnotallowsufficienttimeforventricularfilling.TransientblockoftheAVnodebyaninjectionofadenosineintravenouslyorbyareflexiveincreaseinvagalactivity(bypressingontheneckoverthecarotidsinusregion)usuallyabolishesthetachycardiaandrestoresanormalsinusrhythm.
The atrial plateau (phase 2) is briefer and less developed, and repolarization (phase 3) is slower (see
Fig. 16.10 ) than in a typical ventricular fiber. The action potential duration in atrial myocytes is briefer than that in ventricular myocytes because efflux of K+ is greater during the plateau in atrial myocytes than in ventricular myocytes. The presence of an ultrarapid K+ current (IKur) in atrial myocytes, but not in ventricular myocytes, contributes to greater K+ efflux and shorter action potentials in atrial myocytes.
The atrial excitation wave reaches the ventricles via the AV node. In adult humans, this node is approximately 15 mm long, 10 mm wide, and 3 mm thick. The node is situated posteriorly on the right side of the interatrial septum near the ostium of the coronary sinus. The AV node contains the same two cell types as the SA node, but the round cells •Fig. 16.21 Membranepotentialsrecordedfromanatrioventricularnodecellundercontrolconditions(C)andinthepresenceofthecalciumchannelantagonistdiltiazematconcentrationsof0.1,0.3,and1µmol/L.(RedrawnfromHirthC,etal.J Mol Cell Cardiol. 1983;15:799.)–25 0 25 msec C 0.1 0.3 1 mV in the AV node are less abundant and the elongated cells predominate. The AV node is made up of three functional regions: the atrionodal (AN) region, or the transitional zone between the atrium and the remainder of the node; (2) the nodal (N) region, or the midportion of the AV node; and the nodal-His (NH) region, or the zone in which nodal fibers gradually merge with the bundle of His, which is the upper portion of the specialized conducting system for the ventricles (see
Fig. 16.17). Normally, the AV node and the bundle of His are the only pathways along which the cardiac impulse travels from atria to ventricles.