As described elsewhere, conduction blocks can cause bradycardia; however, they can also cause tachycardia. This occurs when impaired conduction leads to a phenomenon termed "reentry." In fact, this mechanism may account for most tachyarrhythmias found in patients.
Reentry can take place within a small local region within the heart or it can occur, for example, between the atria and ventricles (global reentry). For reentry to occur, certain conditions must be met that are related to the following:
- the presence of a unidirectional block within a conducting pathway
- critical timing
- the length of the effective refractory period of the normal tissue
A model for reentry is shown to the right. In normal tissue (top panel of figure), if a single Purkinje fiber forms two branches (1 & 2), the action potential will travel down each branch. An electrode (*) in a side branch off of branch 1 would record single, normal action potentials as they are conducted down branch 1 and into the side branch. If branches 1 & 2 are connected together by a common, connecting pathway (branch 3), the action potentials that travel into branch 3 will cancel each other out.
Reentry (bottom panel) can occur if branch 2, for example, has a unidirectional block. In such a block, impulses can travel retrograde (from branch 3 into branch 2) but not orthograde. When this condition exists, an action potential will travel down the branch 1, into the common distal path (branch 3), and then travel retrograde through the unidirectional block in branch 2 (blue line). Within the block (gray area), the conduction velocity is reduced because of depolarization. When the action potential exits the block, if it finds the tissue excitable, then the action potential will continue by traveling down (i.e., reenter) the branch 1. If the action potential exits the block in branch 2 and finds the tissue unexcitable (i.e., within its effective refractory period), then the action potential will die. Therefore, timing is critical in that the action potential exiting the block must find excitable tissue in order for that action potential to continue to propagate. If it can re-excite the tissue, a circular (counterclockwise in this case) pathway of high frequency impulses (i.e., a tachyarrhythmia) will become the source of action potentials that spread throughout a region of the heart (e.g., ventricle) or the entire heart. Local sites of reentry may involve only a small region within the ventricle or atrium and can precipitate ventricular or atrial tachyarrhythmias, respectively. Because both timing and refractory state of the tissue are important for reentry to occur, alterations in timing (related to conduction velocity) and refractoriness (related to effective refractory period) can either precipitate reentry or abolish reentry. For this reason, changes in autonomic nerve function can significantly affect reentry mechanisms, either precipitating or terminating reentry. Many antiarrhythmic drugs alter effective refractory period or conduction velocity, and thereby affect reentry mechanisms (hopefully abolish).
The model used above is not only useful for explaining local reentry (e.g., within a small region of the ventricle or atrium), but it can also be used to explain global reentry (e.g., between the atria and ventricles) as shown to the right. Global reentry between the atria and ventricles may involve accessory conduction pathways ("bypass tracts") such as the bundle of Kent. The AV node is normally the only electrical pathway connecting the atria and ventricles. When accessory pathways exist, impulses can travel between the atria and ventricles by multiple pathways. In the example shown to the right, the impulse is traveling through the accessory pathway (bundle of Kent), depolarizing ventricular tissue, then traveling backwards (retrograde) through the AV node to re-excite the atrial tissue and establishing a counter-clockwise global reentry. This type of reentry results in supraventricular tachyarrhythmias (e.g., Wolff-Parkinson-White syndrome, or WPW, found in 0.1% of the population). As described above, timing and refractory lengths determine if this reentry can occur.
There is also an AV nodal reentry tachycardia that occurs within the AV nodal tissue, which is normally comprised of a bundle of conducting fibers. Some people have different conduction velocities and refractory periods in these multiple pathways within the AV node, which can cause reentry within the AV node. AV nodal reentry is a common cause of paroxysmal supraventricular tachycardias, with impulses traveling from the atria to the ventricles and then from the ventricles back to the atria through the AV node. The atrial rate, stimulated by reentrant impulses, drives the ventricular rate so there is still a one-to-one correspondence between the atrial and ventricular rates, and therefore the rhythm is termed "supraventricular." These types of tachyarrhythmias are often paroxysmal in nature (sudden onset and disappearance) because the conditions necessary to establish and maintain reentry are altered by normal variations in conduction velocity and refractoriness. Drugs that depress AV nodal conduction, such as adenosine, beta-blockers and calcium channel blockers, are very effective in terminating these these reentry supraventricular tachycardias.