Hyperkalaemia and slowed ventricular conduction
Hyperkalaemia (a raised potassium concentration outside the cell) leaves some sodium channels (pores) inactivated, shut and unavailable to open, so impulses spread more slowly through the ventricles as potassium rises.
Remember
A high potassium concentration outside the cell makes the resting membrane potential less negative, so some sodium channels inactivate, the upstroke (the rapid depolarisation of the action potential) slows and, as the concentration rises, conduction (the speed at which an impulse spreads) slows.
Memory aid
Too much potassium outside holds the cell part-way to firing, so the sodium channels cannot reset.
Picture a cell held part-way to firing, with its sodium channels unable to reset, so the response is slow.
Heart muscle cells (myocytes) normally sit at a strongly negative resting membrane potential, the voltage across the membrane at rest. Potassium normally leaves the cell down its concentration gradient and sets that voltage. When the potassium concentration outside the cell rises, the gradient is smaller, so the resting voltage becomes less negative and the cell sits slightly depolarised, closer to zero.
Fast voltage-gated sodium channels (pores that open when the membrane voltage changes) drive phase 0, the rapid upstroke of the ventricular action potential. They need a negative resting voltage to reset. Held at the less negative voltage, some become inactivated, which means shut and unavailable to open. Fewer channels respond when the next impulse arrives, so the upstroke is slower.
Conduction through the ventricles depends on how quickly each cell depolarises. A slower upstroke therefore means slower spread, and once the potassium concentration is high the QRS complex, the ECG trace of ventricular depolarisation, widens.
For the slowed conduction, the other ion movements are secondary. Calcium entry sustains the plateau that follows the upstroke, potassium leaving the cell drives repolarisation, and the sodium-potassium pump works in the background to restore the gradients. Severe hyperkalaemia can progress to asystole, which means no electrical activity, so it is treated urgently.
Key facts
- Resting potential
- a high potassium concentration outside the cell makes it less negative.
- Sodium channels
- some become inactivated, so fewer are available.
- Upstroke
- it becomes slower as the potassium concentration rises, so conduction slows.
- QRS complex
- at higher potassium concentrations it widens because the impulse spreads slowly through the ventricular muscle.
- Danger
- severe hyperkalaemia can progress to asystole, so it is treated urgently.
- Heart protection
- a wide QRS complex in hyperkalaemia needs urgent treatment with intravenous calcium, which protects the heart muscle.
Exam traps
- Calcium entry does produce the plateau (phase 2), but the plateau follows the upstroke, so it does not explain a change in the sodium-driven phase 0.
- A higher potassium concentration outside the cell does not make the resting potential more negative: it reduces the gradient for potassium to leave, so the resting potential becomes less negative.
- Faster repolarisation does occur in hyperkalaemia, but it does not explain broad QRS complexes, because conduction speed depends on how quickly phase 0 rises.
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