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Arrhythmia Mechanisms - Reentry Arrhythmias

Reentry Arrhythmias

          The most common arrhythmia mechanism is reentry. In the simplest terms, a reentry arrhythmia occurs when the electrical wave front in the heart gets caught in a loop. When this happens, the depolarization will repeatedly cycle through the tissue utilized in the loop until something interrupts it. There are a wide variety of arrhythmias that are classified as reentrant. These include AVNRT, AVRT, atrial flutter, and some types of ventricular tachycardia. This section will examine the mechanism of reentry itself and how each of these rhythms fit the classification of reentry.

 

 

The Normal Cardiac Cycle

          Before we start to analyze reentry, it is important to look at the normal cardiac cycle keeping in mind that reentry does not occur under normal conditions. In the section on the conduction system, the path of normal conduction was outlined. In short, the first depolarization occurs in the sinus node spreading out through the atria by way of a combination of cell to cell depolarization and the intra-atrial pathways, including Bachman’s Bundle. The AV node acts as the primary conduit to the ventricles where the electrical activity passes through the right and left bundles. From there the wave front passes into the purkinje network and out into the ventricles.

          As we visualize the path of a single sinus beat, we should ask ourselves why the electrical activity dies out. Why does it stop? If cardiac cells can respond to electrical activity in nearby cells through the process of excitability, what prevents a single heart beat from repeatedly causing myocardial cells to depolarize over and over? The answer is refractoriness. Each cell becomes refractory to outside stimulus during phases 1-3 of the action potential. Under normal conditions, the cells of the heart will not respond to electrical activity until it reaches the quiescent period in phase 4. Then the cell is ready to respond. This feature of the cells of the heart prevents a single heart beat from repeatedly propagating.

          Consider how this works in each of the cardiac chambers. The right atrium begins to depolarize at the sinus node. This electrical activity passes throughout the tissue of the atrium moving towards the AV node which lies at the point that is almost diametrically opposed to the location of the sinus node. The wave front can not go backwards because the cells behind the path of depolarization have not had sufficient time to recover. They are refractory. The electrical activity exits the right atrium by way of Bachman’s Bundle and the AV node.

          The left atrium begins depolarizing at the entry of Bachman’s Bundle on the left atrial septum. This signal travels through out the atrium to ending up out on the left lateral wall. Propagation arrives on the lateral wall from both the posterior and anterior walls. As these wave fronts meet on the lateral wall, there are no excitable cells to carry the electrical activity forward. The signal stops and left atrial depolarization is complete. Note that activation through Bachman’s Bundle occurs before the AV node is activated. It is also important to note that conduction through Bachman’s Bundle is very rapid. Both right and left atrial depolarization are completed before the signal passes through the AV node.

          After the atria are depolarized, the electrical activity passes through the AV node down into the bundles by way the His bundle. It enters into the right and left bundles travelling through the protected conduction pathways until it passes into the Purkinje network. It should be noted that conduction down the bundles is protected from the ventricular myocardium. This prevents the ventricles from depolarizing at the base first. Instead, the purkinje network first activates in the papillary muscles near the apex of the ventricles. This causes the ventricular depolarization to occur from apex to base, maximizing cardiac output. The electrical signal returns to the base where it runs out of excitable tissue. The single cardiac cycle is complete.

          When we examine the path of a single depolarization, it becomes evident that the refractive property of cardiac cells is important in regulating electrical activity in the heart. Each normal cardiac cycle has a discreet beginning and a complete ending. So what is it that allows reentry loops to form? To understand this, we will start by looking at the definitions of reentry as well as some of the abnormal rhythms that occur because of reentry.

Current Definitions

          The current literature available provides similar descriptions of what reentry is with some minor differences. As with many aspects of cardiac electrophysiology, a final comprehensive definition has not yet been provided. In time, one will be presented that will address all the specific aspects of the reentry mechanism. The definitions provided below will, for now, be sufficient with regards to describing how reentry works.

The Fogoros’ definition, as provided in the book Electrophysiology Testing, describes reentry as having three required criteria;

1. Two roughly parallel conductive pathways must be connected proximally and distally by conducting tissue, thus forming a potential electrical circuit.
2. One of the pathways must have a refractory period that is substantially longer than the refractory period of the other pathway. This will be referred to as pathway A.
3. The pathway with the shorter refractory period must conduct electrical impulses more slowly than the other pathway. This will be referred to as pathway B.

          Once these three conditions are met, reentry becomes possible. If an extra impulse such as a premature contraction or extra stimulus is introduced into the circuit when pathway A is unable to accept a signal but pathway B is capable of depolarization, the signal will traverse pathway B until it reconnects with pathway A. If that pathway is now ready to receive a signal, the wave front will enter into that portion of the circuit and travel back to the point where it connects with pathway B. Because this pathway has a shorter refractory period and recovers faster, it will be ready to receive the incoming activation. The wave front will travel into pathway B where it will reenter that portion of the circuit, completing the loop.

Natalie’s Definition

1. At least two pathways or the presence of barrier: The barrier may be anatomic, pathologic or functional.
2. Unidirectional Block: The block can be physiologic (premature depolarization or increased heart rate) or pathologic (changes in repolarization).
3. Slow conduction must be present to prevent the collision of the leading edge of the wave front into the trailing edge.

Josephson Definition

1. At least two functionally or anatomically distinct potential pathways that join proximally and distally to form a closed circuit of conduction.
2. Unidirectional block in one of the potential pathways.
3. Slow conduction down the unblocked pathway allowing the previously blocked pathway time to recover excitability; that is, the conduction time along the alternative pathway must exceed the refractory period of the pathway initially blocked.

Zipes / Jallife

          In the book Cell to Bedside, Zipes and Jallife expand upon the traditional model of reentry by describing Classic Reentry as being anatomical in nature or pinned to an obstacle. Functional Reentry is described as being unpinned from an anomic structure or obstacle. The specifics of the information presented in this text should be reviewed by advanced readers and will not be covered in this location.

An Analogy of Fast and Slow Conduction Zones

          One of the tenants of reentry is the presence of two zones that each have different conduction properties. When I was learning EP, I remember those with more knowledge describing these two regions, or pathways. One was supposed to conduct faster yet recover slower. The pathway that conducted more slowly was described as recovering faster. For those who are new to EP, I have come up with an analogy that will help you understand how these different pathways function.

          Think back to your high school days when you were taking Physical Ed. Invariably, there was a period of time where running was the focus of PE.  It is here that we find the examples that help us understand fow reentry can occur. Picture yourself on the quarter mile oval track. To warm up, the coach instructs you to jog once around the track at an easy pace and stop when you reach the point where you started. This is analgous to conduction through a slow pathway. When you complete your circuit and come to a stop you are told to repeat the trip around the track once you feel that you have rested long enough to complete a second trip without stopping. For most of us, the rest interval will not be very long. The amount of energy exerted was not substantial so it does not take long to recover.

          After the warm up exercises have been completed the coach now instructs you to take another lap. This time he tells you to sprint all the way around the lap. He states that you are to go "all out" for the complete circuit. Once you get back to the starting point, the coach indicates that you are to rest until you are ready to complete another circuit at the all out pace. The recovery time after doing the fast trip around the track is longer than it was when we did an easy jog along the same circuit. We have expended significantly more energy and thus need to rest longer.

          Now consider the two pathways specific to a reentry circuit. The slower conduction is analagous to the easy jog around the track, slower transit and faster recovery. The faster portion of the circuit corresponds with the sprint around the track. The faster transition requires a longer recovery period. If you apply this example to a reentry rhythm like AV Nodal Reentry Tachycardia, it becomes much easier to understand.

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