Cardiovascular System
Early afterdepolarisations and long QT syndrome
An early afterdepolarisation is an extra upswing in a heart cell's voltage during prolonged repolarisation (return to resting voltage), as in long QT syndrome (ventricles slow to repolarise).
Remember
A long QT interval (the ECG measure of ventricular depolarisation plus repolarisation) means a long action potential, which makes early afterdepolarisations more likely; these can trigger torsades de pointes, a fast, twisting rhythm from the ventricles.
A heart muscle cell fires an action potential: a fast upstroke, a plateau held up by calcium entering the cell, then repolarisation as potassium leaves and the voltage returns to rest. In long QT syndrome the ventricles take too long to repolarise (recover electrically). The QT interval on the ECG covers ventricular depolarisation plus repolarisation, so a longer action potential means a longer QT interval.
A prolonged action potential gives inward currents (the depolarising flow into the cell) time to re-activate before the cell has settled. The result is an early afterdepolarisation: a second bump in voltage during the plateau or late repolarisation. If the bump reaches threshold, the cell fires a premature beat. A beat set off this way, rather than by the normal pacemaker (the sinoatrial node, which produces the normal rhythm of the heart), is called triggered activity.
A premature beat that lands on slowly repolarising myocardium can start torsades de pointes. This is a polymorphic ventricular tachycardia: a fast rhythm from the ventricles in which the beats on the ECG keep changing in shape, so they seem to twist around the baseline. Episodes may stop by themselves, causing dizziness or fainting, but they can degenerate into ventricular fibrillation (chaotic quivering of the ventricles with no pumping) and cardiac arrest.
Prolongation of the action potential can be inherited, as in congenital long QT syndrome, or caused by drugs and by low potassium or magnesium. Early afterdepolarisations are favoured by slow heart rates or long pauses. A delayed afterdepolarisation is different: it comes after repolarisation is complete and is driven by calcium overload. Early means during the action potential; delayed means after it.
Key facts
- Timing
- an early afterdepolarisation occurs during repolarisation, before the cell has fully recovered.
- Setting
- it appears when the action potential is prolonged, as in long QT syndrome.
- Result
- if the bump in voltage reaches threshold, it triggers another action potential, which can lead to torsades de pointes.
- Delayed type
- delayed afterdepolarisations occur after repolarisation is complete and are driven by calcium overload.
- Usual causes of prolongation
- inherited long QT syndromes, certain medicines, and low potassium or magnesium.
- Drugs to avoid
- drugs that prolong the QT interval are avoided, because in congenital long QT syndrome early afterdepolarisations during a prolonged action potential can trigger torsades de pointes.
Exam traps
- A depolarisation that occurs after repolarisation due to excess calcium inside the cell is not an early afterdepolarisation, because it is a delayed afterdepolarisation; early afterdepolarisations occur before repolarisation is complete.
- Re-entry (a wavefront circulating around a fixed obstacle and repeatedly re-exciting recovered tissue) does not explain the trigger in long QT syndrome, because it usually needs a premature beat to start it, and in long QT syndrome that beat is the early afterdepolarisation.
- A monomorphic ventricular tachycardia from a single circuit does not explain torsades de pointes, because its beats look identical on the ECG while those of torsades keep changing.
- Enhanced automaticity is spontaneous firing by an ectopic cell (one outside the sinoatrial node) during the resting phase between beats, so it does not depend on a long action potential and does not explain the trigger of torsades de pointes.
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