Triggered Activity
When the electrical baseline wobbles. The subtle cellular leaks that accidentally spark an extra beat.
Reentry is a traffic problem — a wavefront caught in a loop. But what happens when the problem isn't the road, but a single car that hits the gas when it's supposed to be parked?
Sometimes, a working myocyte gets "itchy." This is not automaticity. True automaticity (like the SA node) is a reliable, rhythmic, built-in clock. This is something much more erratic: an abnormal leakage of ions in a stressed cell that causes the resting voltage to physically wobble.
If that wobble is large enough to hit the sodium channel threshold, the cell abruptly fires a completely new, unplanned action potential. We call this triggered activity, because it is an extra beat directly triggered by the preceding beat.
These wobbles happen at two distinct times: while the cell is still trying to repolarize (Early), or after it has completely finished and is resting (Delayed).
The Two Types of Afterdepolarizations
Early Afterdepolarizations (EADs)
The Setup: The action potential is taking too long to finish (a prolonged QT interval). The cell is lingering at mid-level voltages.
The Spark: Because the cell sits in this intermediate voltage state for so long, channels that should be closed (like L-type Calcium channels) actually have time to recover from inactivation and reopen. Positive charge floods back in while the cell is still trying to repolarize, causing an upward swing.
Delayed Afterdepolarizations (DADs)
The Setup: The cell has finished repolarizing and is resting. But the interior of the cell is severely overloaded with calcium.
The Spark: The sarcoplasmic reticulum (SR) is too full and spontaneously "burps" calcium into the cytoplasm during diastole. The Na⁺/Ca²⁺ exchanger (NCX) panics and pumps the calcium out, but it exchanges 1 Ca²⁺ out for 3 Na⁺ in. This net inward positive charge pushes the resting voltage up toward threshold.
Rate Dependency: Fast vs Slow
The most elegant part of understanding triggered activity is how it responds to heart rate. EADs and DADs are perfect opposites in the clinic.
EADs love bradycardia.
A slow heart rate inherently prolongs the action potential duration (the QT interval). The longer the cell sits in Phase 2 or 3, the more time channels have to recover and cause an EAD. This is why patients with Long QT Syndrome are at highest risk of Torsades de Pointes when their heart rate drops (or during a post-PVC pause). The treatment? Pace them faster. Increasing the heart rate shortens the action potential, giving the EAD no time to form.
DADs love tachycardia.
A fast heart rate floods the cell with calcium (because the cell is firing constantly, opening L-type calcium channels over and over). Catecholamines (adrenaline) make it even worse by hyper-activating the SR. This calcium overload leads to the spontaneous diastolic "burps" that cause DADs. This is why conditions like CPVT (Catecholaminergic Polymorphic Ventricular Tachycardia) and Digoxin toxicity cause arrhythmias primarily during exercise or stress. The treatment? Slow them down. Beta-blockers or calcium channel blockers reduce the calcium load and suppress the DADs.
How do we differentiate triggered activity from reentry in the EP lab? We use pacing, but in the exact opposite way we do for reentry.
Reentry is initiated by a single, carefully timed premature extra-stimulus that causes block in one pathway.
Triggered DADs are initiated by burst pacing. We pace the heart rapidly for several seconds (to aggressively load the cell with calcium), and then suddenly stop. The calcium-overloaded cells will generate a massive DAD, and an extra beat (or run of VT) will spontaneously emerge immediately after the pacing stops. If we can reliably turn the arrhythmia on by fast burst pacing and Isuprel, and we cannot map a reentrant circuit, we are dealing with a triggered rhythm.
Key Takeaways
- Triggered activity occurs when an abnormal voltage wobble (afterdepolarization) reaches threshold and fires a new beat.
- EADs occur during Phase 2 or 3. They are driven by prolonged action potentials (Long QT) and are worsened by slow heart rates (bradycardia). They are the mechanism of Torsades de Pointes.
- DADs occur during resting Phase 4. They are driven by intracellular calcium overload (Digoxin toxicity, CPVT) and are worsened by fast heart rates (tachycardia) and catecholamines.
- The NCX (Na⁺/Ca²⁺ exchanger) is the primary culprit in generating the positive inward current that causes a DAD.