Cardiovascular System
Hypokalaemia: delayed repolarisation and arrhythmia risk
Hypokalaemia (low blood potassium) delays repolarisation, with a risk of arrhythmia (an abnormal heart rhythm).
Remember
With low potassium the heart is slow to reset: less potassium leaves the cell, so repolarisation is delayed and the action potential lasts longer.
A ventricular action potential (in the ventricular muscle cells) has distinct phases. Phase 0 is the rapid upstroke, carried by sodium entering the cell. Phase 2 is the plateau, when calcium enters. In phase 3, called repolarisation, potassium leaves the cell through potassium channels and the cell returns to its resting voltage.
Hypokalaemia means a low blood potassium. With less potassium outside the cell, the potassium channels work less well. Less potassium leaves the cell, so the outward potassium current falls. Repolarisation is delayed, so the action potential lasts longer.
On the ECG, repolarisation shapes the ST segment, the T wave and the U wave (parts of the trace, the U wave being a small extra wave that sometimes comes after the T wave). In hypokalaemia the typical changes are ST depression, flattened T waves, a prominent U wave and a long QT interval (the way a longer action potential shows on the ECG).
A slow reset leaves the cell electrically unstable during the plateau. Early afterdepolarisations (extra bumps in voltage before repolarisation is complete) can then set off premature beats, meaning extra beats, and ventricular arrhythmias. These include torsades de pointes, a life-threatening ventricular rhythm.
Vomiting and the use of some diuretics are causes of potassium loss. Do not mix this up with hyperkalaemia, a high potassium level. There the resting membrane potential becomes less negative and the upstroke slows.
Memory aid
low potassium makes the heart slow to reset
The cell is slow to recover, which is why the action potential lasts longer and the QT interval is long.
Key facts
- Mechanism
- low extracellular potassium (potassium outside the cell) reduces the outward potassium current in phase 3.
- Effect
- repolarisation is delayed and the action potential is prolonged.
- ECG
- the typical changes are ST depression, flattened T waves, a prominent U wave and a long QT interval.
- Risk
- extra beats and dangerous ventricular rhythms, because the slow reset makes the ventricles prone to them.
- Potassium loss
- vomiting and the use of some diuretics are among its causes.
- Hyperkalaemia
- the mirror image, with a less negative resting membrane potential and a slower upstroke.
Exam traps
- Increased sodium channel opening does not explain hypokalaemia, because sodium channels drive the upstroke and low potassium does not make them open more.
- Enhanced potassium efflux (potassium leaving the cell) gets the direction wrong, because in hypokalaemia the outward potassium current is reduced, so the action potential is longer, not shorter.
- A less negative resting membrane potential belongs to hyperkalaemia, where a high potassium level depolarises the resting membrane and slows the upstroke.
- A shortened plateau from reduced calcium channel opening is the wrong direction, because losing calcium entry would shorten the QT interval, while hypokalaemia lengthens repolarisation.
- Early afterdepolarisations are a downstream trigger of arrhythmia, not the direct effect on the action potential, which is delayed repolarisation from reduced potassium efflux.
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