Reentry
The architecture of a short circuit. Why the vast majority of clinical tachycardias are not caused by cells firing too fast, but by a wavefront that forgets how to stop.
When we see a heart racing at 200 beats per minute, our instinct is to assume a group of cells has gone rogue, firing like a machine gun. Sometimes that is true. But usually, it is completely wrong.
The most common mechanism for sustained tachycardia is not a rogue firing squad. It is a single, solitary spark that gets caught in a revolving door. The wavefront chases its own tail endlessly, returning to the same tissue over and over, driving the heart rate at the speed of its loop. This is reentry.
Reentry is the mechanism behind AVNRT, AVRT, Atrial Flutter, Atrial Fibrillation, and the vast majority of Ventricular Tachycardia. If you understand the three requirements for reentry, you understand the target of almost every ablation we perform.
The Recipe for a Loop
A normal electrical wave starts at the SA node, sweeps across the heart, and eventually runs out of excitable tissue. It crashes into the "shore" of the fibrous valves or the apex of the ventricles and dies. To get a wave to spin continuously, you must carefully arrange three elements.
The Circuit
There must be two distinct parallel pathways that connect at the top and the bottom, creating a circle. This can be anatomical (scar tissue) or functional.
Unidirectional Block
If an impulse travels down both pathways simultaneously, they collide at the bottom and die. One pathway must temporarily block the incoming wave so it only goes down one side.
Slow Conduction
The wavefront must travel slowly enough down the open pathway that by the time it reaches the bottom and turns around, the previously blocked pathway has had time to recover its excitability.
Let's watch this play out.
Anatomy of a Short Circuit
- A premature beat (the spark) arrives at the top of the circuit.
- Unidirectional Block: The left pathway is still refractory from the previous beat. The wavefront hits it and dies (the red X).
- Slow Conduction: The right pathway has recovered. The wavefront creeps down the right side.
- Because the right side was so slow, by the time the wavefront reaches the bottom, the left pathway has finally recovered.
- The wave turns around, travels retrograde up the left pathway, and re-enters the top of the circuit. The loop is closed.
The Excitable Gap
For a reentry circuit to spin endlessly, the "head" of the wavefront can never catch up to its own "tail."
The tail is the refractory period of the tissue it just fired. If the wavefront travels too fast, or if the circuit is too small, the head will crash into the refractory tail of the previous lap and extinguish itself.
The distance between the refractory tail and the oncoming head is called the excitable gap. It is a window of fully recovered, excitable tissue that the wavefront is constantly chasing but never quite catching.
The excitable gap is critical for two reasons:
- It is why antiarrhythmics work. If we give a Class III drug (potassium channel blocker) that prolongs the action potential, we are physically making the "tail" longer. If we make the tail long enough, it swallows the excitable gap. The head crashes into the tail, and the circuit breaks.
- It is how we map and pace. Because there is a gap of excitable tissue in the loop, we can insert a pacing stimulus into that gap from a catheter. This allows us to interact with the circuit without breaking it — a concept we will explore deeply in Volume V.
Clinical Takeaway: Anatomy vs Physiology
Reentry circuits come in two main flavors:
Anatomical Reentry: The circuit is defined by fixed physical structures. In Atrial Flutter, the wave circles around the tricuspid valve. In Scar VT, it weaves around patches of dense collagen left by a heart attack. Because the path is physically fixed, the morphology of the tachycardia is identical on every single beat. We can cure these by drawing a line of ablation (a burn) across the critical isthmus, physically cutting the wire.
Functional Reentry: The circuit is not defined by scar, but by transient differences in electrical properties. Atrial Fibrillation and Ventricular Fibrillation are driven by multiple, small, unstable "rotors" that drift around the tissue. The core of the rotor isn't a scar; it's a zone of refractory tissue created by the spinning wave itself. Because the paths are not physically fixed, the ECG looks chaotic and constantly changing. These are much harder to ablate because there is no single "wire" to cut.
When we ablate an anatomical reentrant circuit (like typical Atrial Flutter or Scar VT), we do not burn the entire loop. We look for the critical isthmus.
The isthmus is a narrow corridor of surviving tissue bounded by two uncrossable barriers (like a valve annulus on one side and a dense scar on the other). The entire electrical tornado is forced to squeeze through this tiny chokepoint on every lap.
If we can map the circuit and find that isthmus, we only need to deliver a few millimeters of RF energy to create a line of block from one barrier to the other. By severing the isthmus, we break the loop forever. Finding that isthmus is the art of electrophysiology.
Key Takeaways
- Reentry is a continuous loop of electrical activation and is the mechanism behind most sustained tachycardias.
- It requires three things: a circuit, unidirectional block (usually due to a premature beat hitting refractory tissue), and slow conduction (to allow the blocked pathway time to recover).
- The excitable gap is the fully recovered tissue between the tail of the previous wave and the head of the next wave. Prolonging refractoriness (with drugs) closes this gap and breaks the circuit.
- Anatomical reentry (Flutter, Scar VT) relies on fixed physical structures and is highly amenable to ablation by targeting the critical isthmus.
- Functional reentry (AFib, VFib) relies on dynamic electrical properties, making it chaotic and harder to target structurally.