Initiation and Termination of Ventricular Tachycardia — Reentrant Circuits
It is said that there are three main causes of ventricular tachycardias: automaticity, reentrant circuits, and triggered activity. Automaticity and triggered activity are important to keep in mind while assessing a patient because once they are diagnosed they can be effectively treated. However, we will only be talking about reentrant tachycardia here.
Reentrant tachycardia is different from both automatic tachycardia and triggered activity in that it is not associated with the leakage of ions across the cardiac cell membrane nor is it associated with underlying metabolic issues. Reentrant tachycardias only arise in the presence of surrounding scar tissue. Scar tissue is created by myocardial diseases such as myocardial infarction — a.k.a heart attacks. Because scar tissue cannot conduct electrical impulses like healthy myocardium can, scar tissue creates the anatomic channels necessary for creating a reentrant circuit.
It is the reentrant circuit that causes accelerated heart rates. Below is a diagram of a reentrant circuit during normal sinus rhythm (NSR):
Several conditions must be present in order for a reentrant circuit to cause ventricular tachycardia. Firstly, the circuit must contain two roughly parallel channels of conducting tissue, and they must be connected at two different points by more conducting tissue. In the figure above, the tip of the triangle is one connection and the base of the triangle is the other connection.
Secondly, one of the channels must have a slower conduction velocity AND a shorter refractory period than the other channel. Lastly, a premature impulse must enter the circuit in order for tachycardia to be initiated. In the above diagram, pathway A is the slower channel and pathway B is the faster channel. A normally-timed impulse enters the circuit and conducts down pathway B. Pathway B conducts quickly enough to terminate the impulse coming down pathway A. The only impulse to exit the circuit and reach the rest of the heart is the one that conducted down B.
What does the reentrant circuit look like during tachycardia? A premature impulse reaches the circuit early enough to where pathway B has not recovered from its refractory period just yet. The impulse conducts down pathway A only and exits the circuit, depolarizing the rest of the heart. Now the impulse also reaches B from the opposite direction — and now B is ready to conduct again. The impulse travels retrogradely up B, back down A, and the cycle continues, usurping the intrinsic heart rate in the process. The cycle length of the tachycardia becomes the time it takes to conduct down A + the time it takes to conduct up B. A visualization is below:
Reentrant tachycardia is special in one defining way — just as a premature impulse can initiate it, a premature impulse can also terminate it. Termination is not as easy as initiation, however. In fact, there are three possible outcomes of a premature impulse reaching an accelerated circuit*: block, reset, or termination.
Premature Impulse Block
If a premature impulse blocks in an accelerated circuit, that means it reaches the circuit while both channels are refractory. The premature impulse terminates immediately and the tachycardia continues as if nothing ever happened to it. A visualization is below:
If a premature impulse resets an accelerated circuit, that means it is able to penetrate the circuit but is unable to terminate the tachycardia. In other words, it briefly terminates the tachycardia yet also restarts it. If one were to to graph the time at which every accelerated impulse exits the circuit, one would see a slight shift in the overall tachycardia pattern during reset, but would not see a return to normal sinus rhythm.
Tachycardia reset can happen in one of two cases. The first case is when a premature impulse reaches an accelerated circuit while both channels are not refractory. The impulse will conduct down both channels, as in the figure below. The premature impulse terminates the incoming accelerated impulse in B but creates a new accelerated impulse in A.
The second case for tachycardia reset is when a premature impulse reaches an accelerated circuit while only the faster channel is refractory. The premature impulse will conduct down the slower channel only, and create a new accelerated impulse. The old accelerated impulse will terminate when it encounters refractory tissue freshly left behind by the new impulse.
Lastly, if a premature impulse terminates an accelerated circuit, that means it crashes with and abolishes the accelerated impulse. Once the accelerated impulse is destroyed, normal sinus rhythm can take over again.
A premature impulse will terminate reentrant tachycardia if it reaches the circuit while the slower channel is refractory but the faster channel isn’t. This is very similar to our first case of reset, but this time the premature impulse is unable to create a new accelerated impulse and the tachycardia is terminated for good.
*accelerated refers to the context of tachycardia, as opposed to normal sinus rhythm
How are the concepts of tachycardia initiation and termination applicable to the clinical setting?
Reentrant ventricular tachycardia is thought to be one of the primary causes of sudden death in America, along with ventricular fibrillation. In the electrophysiology study, devices called implantable cardioverter defibrillators (ICDs) are used to send pacing impulses toward reentrant circuits in an effort to terminate life-threatening tachycardias. Sophisticated techniques have been developed for both mapping out the location and characteristics of reentrant circuits and for determining the most efficacious pacing techniques. These pacing techniques are formally known as antitachycardia pacing (ATP). ATP is based on the basic principles that are outlined above and is heavily studied because of its ability to terminate tachycardia without the deployment of a painful shock.