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In Chapter 16 of the textbook, Fig. 16.23D demonstrates a scenario where the impulse is able to travel down the left branch normally but is blocked in the right branch in the forward direction due to some pathological change in the myocardial cells in that branch. However, the impulse that was conducted down the left branch and through the connecting bundle may still be able to penetrate the depressed region in the right branch from the opposite direction, known as the retrograde direction. This happens even though the forward impulse had been blocked previously at the same site. The reason for this is that the forward impulse arrives at the depressed region in the right branch earlier than the retrograde impulse due to the shorter path length of the forward impulse. As a result, the forward impulse may be blocked simply because it arrives at the depressed region during its effective refractory period. On the other hand, if the retrograde impulse is delayed enough, the refractory period may have ended in the affected region, allowing the impulse to be conducted back through this region and return to the single bundle.

While unidirectional block is necessary for reentry to occur, it alone cannot cause reentry. For reentry to take place, the effective refractory period of the reentered region must be shorter than the conduction time around the loop. In Fig. 16.23D, if the tissue just beyond the depressed zone in the right branch is still refractory from the forward depolarization, the retrograde impulse will not be conducted into the single bundle branch. Therefore, conditions that promote reentry are those that prolong the conduction time or shorten the effective refractory period.

The functional characteristics of the different components of the reentry loops responsible for specific cardiac arrhythmias vary. Some loops are large and involve entire specialized conduction bundles, while others are microscopic. The loop may consist of myocardial fibers, specialized conducting fibers, nodal cells, and junctional tissues arranged in various ways. Furthermore, the various cardiac cells in the loop may be normal or abnormal.

Normally, the propagation velocity along a multicellular cardiac conduction fiber is facilitated by gap junctions between consecutive conducting fibers. Variations in the protein structure of these gap junctions, known as connexins, can affect the propagation velocity along these fibers. The specific connexins can vary locally in cardiac tissues, leading to local variations in propagation velocity. These variations in velocity can include regions of unidirectional block that induce reentrant rhythm disturbances.

Triggered activity is named so because it is always coupled to a preceding action potential. Since reentrant activity is also coupled to a preceding action potential, it can be difficult to distinguish between arrhythmias induced by triggered activity and those induced by reentry. Triggered activity is caused by afterdepolarizations, which can be categorized into two types: early afterdepolarizations (EADs) and delayed afterdepolarizations (DADs). EADs may occur either at the end of the action potential plateau (phase 2) or approximately halfway through repolarization (phase 3), while DADs occur near the very end of repolarization or just after complete repolarization (phase 4).

EADs are more likely to occur when the heart rate is slow, while a rapid heart rate suppresses EADs.

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Fig. 16.23D , the impulse may travel down
CHAPTER 16 Elements of Cardiac Function the left branch normally but is blocked in the antegrade direction in the right branch because of some pathological change in the myocardial cells in that branch. The impulse that was conducted down the left branch and through the connecting branch of the connecting bundle may then be able to penetrate the depressed region in the right branch from the retrograde direction, even though the antegrade impulse had been blocked previously at this same site. Why is the antegrade impulse blocked but not the retrograde impulse? The reason is that the antegrade impulse arrives at the depressed region in the right branch earlier than the retrograde impulse because the path length of the ante-grade impulse is very short, whereas the retrograde impulse traverses a much longer path. Therefore, the antegrade impulse may be blocked simply because it arrives at the depressed region during its effective refractory period. If the retrograde impulse is delayed sufficiently, the refractory period may have ended in the affected region, and the impulse can then be conducted back through this region and return to the single bundle.
Although unidirectional block is a necessary condition for reentry, it alone cannot cause reentry. For reentry to occur, the effective refractory period of the reentered region must be shorter than the conduction time around the loop. In
Fig. 16.23D , if the tissue just beyond the depressed zone in the right branch is still refractory from the ante-grade depolarization, the retrograde impulse will not be conducted into the single bundle branch. Therefore, the conditions that promote reentry are those that prolong the conduction time or shorten the effective refractory period.
The functional characteristics of the various components of the reentry loops responsible for specific cardiac arrhythmias are diverse. Some loops are large and involve entire specialized conduction bundles, whereas others are microscopic. The loop may include myocardial fibers, specialized conducting fibers, nodal cells, and junctional tissues in almost any conceivable arrangement. In addition, the various cardiac cells in the loop may be normal or abnormal.
The propagation velocity along a multicellular cardiac conduction fiber is normally facilitated by gap junctions that lie between consecutive conducting fibers. Variations in the protein structure of the connexins in the gap junctions can affect the propagation velocity along these fibers. The chemical structure of the specific connexins can vary locally in cardiac tissues and, as a result, can establish local variations in propagation velocity. Such topical variations in velocity might include regions of unidirectional block that induce reentrant rhythm disturbances.
Triggered activity is so named because it is always coupled to a preceding action potential. Because reentrant activity is also coupled to a preceding action potential, the arrhythmias induced by triggered activity are usually difficult to distinguish from those induced by reentry. Triggered activity is caused by afterdepolarizations, of which two types •Fig. 16.24 Effect of Pacing at Different Cycle Lengths (CL) on Cesium-Induced Early Afterdepolarizations (EADs) in a Purkinje Fiber. A, EADsarenotevident.B, EADsfirstappear(arrows). ThethirdEADreachesthresholdandtriggersanactionpotential(third arrow). C, EADsthatappearaftereachdrivendepolarizationtriggeranactionpotential.D, Triggeredactionpotentialsoccurinsalvos.(ModifiedfromDamianoBP,RosenM.Circulation. 1984;69:1013.) are recognized: early afterdepolarizations (EADs) and delayed afterdepolarizations (DADs). EADs may appear either at the end of the action potential plateau (phase 2) or approximately midway through repolarization (phase 3), whereas DADs occur near the very end of repolarization or just after full repolarization (phase 4).
EADs are more likely to occur when the prevailing heart rate is slow; a rapid heart rate suppresses EADs (