Why is it Possible to Start and Stop Re-Entrant Tachycardias With Pacing?

In the electrophysiology lab, testing for re-entrant tachycardias is a frequently performed procedure. It is necessary to find the mechanism or the substrate that supports the tachycardia. Atrio-ventricular nodal re-entry tachycardia (AVNRT) is the most easily described tachycardia. There are several substrates that invoke re-entry. For example, bypass tracts as in Wolfe Parkinson White (WPW) syndrome, AVRT (atrio-ventricular reciprocating tachycardia) and sinoatrial (SA) node tachycardia all have conduction properties that differ within the circuit. One limb of the circuit exhibits slower conductive properties, another limb conducts faster. A re-entrant circuit requires two limbs of tissue that have different conduction velocities around a non-conductive barrier that connects with common tissue. When trying to induce a re-entrant tachycardia, progressively premature extra stimuli can be used to cause unidirectional conduction block to allow re-entry to occur. The extra stimuli will conduct down both the fast and the slow pathway. The fast pathway conducts faster, so that it reaches the common excitable tissue first. The extra stimulus brought in progressively earlier will reach a point that the fast pathway tissue is refractory. The extra stimulus conducts through the slow pathway (which takes longer), eventually reaching the common excitable tissue, and depolarizes it. The fast tissue recovers and accepts the stimulus that comes through the slow tissue, then reenters up the fast and down the slow. This initiates the tachycardia (Figure 1). AVNRT is a common re-entrant tachycardia. To initiate the arrhythmia, we bring in the extra stimulus earlier and earlier. In the electrograms below (Figures 2-5), look at the last beat in the train on the HIS signal. The A-V node is normally decremental in character. This protects our ventricles from responding too fast. The HIS channel shows the atrial deflection and the HIS deflection getting farther apart. The time between the atrial deflection and the HIS deflection suddenly elongates, causing a jump. In a extra stimulus protocol, a jump by definition is at least 50 ms longer from the atrial event to the HIS event. This is representative of the fast pathway in refractory and the slow pathway taking over. In the next electrogram, the extra stimulus goes down the slow pathway and then up the fast pathway, because it is no longer blocked and tachycardia is initiated. Characteristics of a re-entrant AVNRT tachycardia on an EKG are as follows: The initial P wave is upright and the next P wave is retrograde (inverted). There is a prolongation of the first P-R interval. There is no acceleration in the beginning of the tachycardia. A premature beat may cause the tachycardia to terminate. Terminating re-entrant tachycardia is possible by causing a simultaneous block in both limbs of the circuit. In re-entrant tachycardia, the tissue that is trailing the advancing wavefront is refractory. There is excitable tissue in front of the advancing wavefront and refractory tissue trailing the wavefront (Figure 6). The tissue between the advancing wavefront and the refractory tissue is the excitable gap. It is during this excitable gap that an extra stimulus must penetrate and propagate towards both the advancing wavefront and chase the refractory tail until it blocks in both directions. This will terminate the re-entrant arrhythmia. There are factors that affect termination: 1. Duration of the tachycardia s refractory period within the circuit. 2. Length of the tachycardia circuit. 3. Conduction velocity of the advancing wavefront. 4. The tachycardia cycle length or rate. 1. Strength of the pacing impulse. 2. Proximity of the pacing stimulus to the excitable gap. 3. Conduction velocity and refractoriness of the tissue between the re-entrant circuit and the pacing stimulus. The duration of a tachycardia s refractory period can affect how wide the excitable gap is. If the gap is wide, it will be easier to pace into the tachycardia and terminate it. The length of the tachycardia circuit is important, because if it is a micro re-entrant circuit, it probably is very fast around a small circuit. However, if it is a macro re-entrant circuit, it has farther to go, leaving more tissue in the excitable gap. Typically, if the tachycardia is slow, then it is a wide excitable gap. If the tachycardia is fast, then it is a narrow excitable gap. The speed of the circulating tachycardia also helps determine the size of the excitable gap. The strength of the pacing impulse allows capture of tissue close to the circuit. The proximity of the pacing stimulus is necessary, so that if you are not pacing directly on tissue involved in the circuit, then at least it won t take much time to propagate to the tachycardia circuit. During pacing, it is important for the tissue that is being paced to recover quickly and conduct fast. It would be difficult to get into the excitable gap if the tissue that surrounds it is weak and sick and conducts slowly the time it would take from your pacing stimulus to reach the tachycardia circuit would be too long. Sometimes changing the pacing site helps you get closer to the excitable gap, which can help terminate the tachycardia. It is usually more effective to use multiple extra stimuli to break the tachycardia. There are a number of algorithms for anti-tachycardia pacing. Try all of them if you are having difficulty terminating a tachycardia: 1. Single extrastimulus 2. Multiple extrastimulus 3. Burst or overdrive pacing 4. Fixed cycle lengths 5. Decremental burst 6. Variable cycle lengths within a burst 7. Percentage of the tachycardia cycle length 8. Ramp pacing Re-entrant tachycardias can develop around scars, valve openings, tissue conduction changes, vascular openings, PFO, or any tissue that connects proximal to distal slow and fast conduction properties. The good news is that there has been a great deal of success ablating these re-entrant rhythms, and in the end, the patients are completely cured.