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.