Entrainment is a powerful tool in the armoury of the electrophysiologist. It can be used to probe the mechanism of arrhythmias, as a method for differential diagnosis and to locate targets for ablation. Entrainment mapping is employed in determining sites that are part of a re-entry circuit and those that are not. Moreover it allows localisation of the critical isthmus that is the target of ablative therapy for re-entrant rhythms.
The principles of reset and entrainment are not obvious and are often not explained. This article introduces some of these principles.
Resetting and Entrainment
Resetting involves the use of a single extrastimulus. Timed premature stimuli delivered during a sustained rhythm may interact with it, causing a pause that is not fully compensatory before resumption of the original rhythm; this phenomenon is referred to as resetting. To reset a tachycardia, the impulse must be able to reach the tachycardia site of origin and find it excitable. The phenomenon of resetting was originally described for the sinus node and automatic focal rhythms.
Continuous resetting with multiple stimuli is called entrainment and is a specific response to overdrive pacing: Following the first beat of a train of stimuli that penetrates and resets the tachycardia, subsequent stimuli interact with the reset circuit. Although resetting was itself first described in focal rhythms, entrainment has been exhaustively studied in re-entrant rhythms and the term in usually applied in the context of a re-entrant tachycardia. Continual resetting is seen in focal rhythms but has different characteristics to the classical description of entrainment. The term overdrive suppression is sometimes used for continual resetting of a focal tachycardia. Analysis of responses to resetting and entrainment by extrastimuli can confirm the diagnosis of a re-entrant mechanism.
Resetting responses can be explained on the basis of the excitable gap and recovery properties of the tissue encountered by the pacing stimuli.
Excitable Gap
In the case of a re-entrant arrhythmia, an excitable gap must exist between the leading edge of the tachycardia impulse and the wave of refractoriness following the impulse - otherwise the tachycardia would terminate as the leading edge would be extinguished by encountering refractory tissue. The excitable gap is the interval of excitability between the head of activation of one impulse and the tail of refractoriness of the prior impulse.
The size of the excitable gap can vary greatly from one arrhythmia to another determined by the conduction velocity and refractory properties of the circuit. The coupling intervals over which resetting occurs gives a measure of the duration of the excitable gap.
For a stimulated impulse to interact with a tachycardia – to reset, entrain or terminate it the impulse must be introduced at a time when it can penetrate the excitable gap. This may be possible with a single stimulus, or multiple stimuli may be required in order to align the refractory periods of tissue between the pacing site and the circuit (“peeling back refractoriness”). This may be thought of as the first impulses clearing a path for later ones and is one reason that ATP delivered by ICDs usually consist of several consecutive stimuli.
A stimulated impulse can interact with a re-entrant circuit if it enters the excitable gap. The stimulated impulse may then propagate in both directions around the circuit. The wave travelling in the opposite direction to the spontaneous tachycardia (antidromically) will inevitably collide with the already circulating tachycardia wavefront and both are extinguished. The stimulated impulse also conducts orthodromically (in the same direction as the tachycardia wavefront) if the tissue is not refractory. The stimulated impulse then continues to traverse the reentrant circuit to reset the tachycardia - arriving at the exit at an earlier than expected time advancing the timing of activation in the circuit and the tissue activated by it.
Termination occurs when the stimulated impulse collides retrogradely with the preceding tachycardia impulse (as it must) but also blocks antegradely owing to encroachment on the refractory period of the preceding wavefront.
Return cycle and post pacing interval and entrainment mapping
During entrainment each impulse following the first to reset the tachycardia propagates in both an antidromic and orthodromic direction around the circuit. The antidromic impulse of the last introduced stimulus collides with the orthodromic impulse of the preceding stimulus. The orthodromic impulse of the last introduced stimulus propagates around the circuit to become the first complex of the resumed tachycardia.
Entrainment mapping involves pacing at cycle lengths shorter than that of the tachycardia cycle length from a variety of sites within the chamber of interest and analyzing the return cycles. The return cycle is subtracted from the tachycardia cycle length to give the post pacing interval (PPI). Sites that are within the circuit demonstrate a return cycle equal to the tachycardia cycle length (PPI approaches zero). When stimulation is carried out at sites distant from the circuit, the return cycle exceeds the tachycardia cycle length because the pacing impulse must first travel to the site of the circuit travel around the circuit and then return to the pacing site (long PPI). The return cycle is typically and ideally measured at the pacing site and is the time from the last introduced stimulus to the the electrogram resulting from the resumed tachycardia (see fig 4).
Entrainment mapping can be used to determine the distance of a pacing site to a re-entrant circuit, sites that are within the circuit and the location of the critical isthmus. It is often employed during the mapping of atrial and ventricular tachycardias because the location of the culprit circuit is highly variable and must be established to identify targets for successful ablation.
For entrainment mapping pacing is carried out at a rate just fast enough to observe that the tachycardia has been accelerated to the pacing rate and no faster. Entraining at too fast a rate can result in slowing of conduction secondary to interval-dependent conduction delay through tissue that has only partially recovered excitability when the stimulus reached the circuit. Conduction slowing will interfere with assessment of the PPI. Entrainment is typically performed by pacing at 10-40ms faster than the tachycardia rate.
During entrainment different degrees of ECG fusion can be seen resulting from the interaction between paced activation and orthodromic and antidromic activation of the circuit. The terms entrainment with manifest and concealed fusion will be dealt with in the next article and the concept is important in establishing the tachycardia mechanism and for identifying the critical isthmus of re-entrant circuits.
References
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Almendral JM, Stamato NJ, Rosenthal ME, Marchlinski FE, Miller JM, Josephson ME. Resetting response patterns during sustained ventricular tachycardia: relationship to the excitable gap. Circulation 1986;74;722-730
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Josephson ME. Clinical Cardiac Electrophysiology: Techniques and Interpretations 3rd edition. Lippincott Williams & Wilkins Publishers 2001
