Gap Junctions & Wavefront Travel

The Physical Bridge

Cardiac cells are joined end-to-end at specialized structures called intercalated discs. Within these discs lie gap junctions. A gap junction is an actual physical pore connecting the cytosol of one cell directly to the cytosol of its neighbor.

These pores are made of proteins called connexins. Because the cytosols are physically connected, the electrical resistance between the two cells is extremely low. Ions can diffuse freely from one cell to the next.

Local Circuit Current

Imagine two adjacent cells: Cell A and Cell B. Both are sitting peacefully at a resting membrane potential of −90 mV.

Suddenly, Cell A is stimulated. Its fast sodium channels snap open (Phase 0). Sodium ions rush into Cell A from the extracellular space. The inside of Cell A rapidly becomes positive (+20 mV).

Now, look at the boundary. The inside of Cell A is +20 mV. The inside of Cell B is still −90 mV. Because there is a voltage difference, and because the gap junctions provide a low-resistance pathway, positive ions (mostly potassium, but effectively conveying the charge) flow from Cell A directly into Cell B.

This flow of ions is called local circuit current. As positive charge pours into Cell B, Cell B's membrane voltage is pushed upward from −90 mV. Once Cell B reaches its threshold (around −70 mV), its own sodium channels snap open. Cell B fires its own Phase 0. It is now positive, and it will push current into Cell C. The wave propagates.

How fast does this wave travel? Conduction velocity depends on three main variables. If you understand these three, you can predict almost any conduction abnormality on an ECG.

1. The Push (Vmax of Phase 0)

The faster and higher Cell A depolarizes, the larger the voltage gradient it creates between itself and Cell B. A massive, steep Phase 0 (high Vmax) injects a huge amount of local circuit current very quickly. Cell B hits threshold almost instantly. The wave moves fast.

If Cell A's sodium channels are partially blocked by a drug, or partially inactivated because the cell is resting at a less negative voltage (like in ischemia), Phase 0 becomes sluggish. It injects current slowly. Cell B takes longer to reach threshold. The wave slows down.

2. The Resistance (Gap Junctions)

Even with a massive push, the current must cross the bridge. In healthy tissue, gap junctions are open and abundant. Resistance is low.

However, gap junctions are dynamic. If a cell becomes ischemic, its internal pH drops (acidosis) and intracellular calcium rises. The gap junctions sense this distress and close. This is a brilliant evolutionary defense mechanism — it seals off the dying cell so it doesn't drag its healthy neighbors down with it. But electrically, it is disastrous. The resistance between cells skyrockets, and conduction grinds to a halt.

3. The Architecture (Anisotropy)

Cardiac cells are not spheres; they are long cylinders. Gap junctions are heavily concentrated at the ends of the cylinders (the intercalated discs) and are much sparser along the sides.

Because of this architecture, electrical current flows much faster down the length of a fiber than it does across the fibers. This directional dependence of speed is called anisotropy. In the EP lab, pacing pacing parallel to fiber orientation produces a fast, sharp signal; pacing perpendicular to it produces a slower, wider signal.

When a patient has a myocardial infarction, the dead myocardium is eventually replaced by collagen — an electrically inert scar. But the scar is rarely a solid brick. It is often a patchy, heterogeneous mix of dense collagen interwoven with surviving strands of struggling myocytes.

In these border zones, the architecture is destroyed. Fibrous tissue physically separates the surviving cells, drastically reducing the number of gap junctions between them. The wavefront can no longer sweep forward in a broad, fast line.

Instead, the electrical impulse must navigate a microscopic maze. It creeps down a surviving strand of cells, hits a dead end of collagen, and has to turn 90 degrees to find a lateral gap junction to the next surviving strand. This zig-zagging dramatically slows the macroscopic conduction velocity.

This slow conduction is the essential ingredient for reentry. While the wavefront is crawling through the maze of the scar border zone, the rest of the healthy ventricle has time to recover from its refractory period. When the creeping wave finally emerges from the scar, it finds recovered, excitable tissue waiting for it. The loop closes, and Ventricular Tachycardia (VT) begins.