Reading the two panels
The top panel is a cell's action potential: the voltage across its membrane, in millivolts, through one heartbeat. The bottom panel is the ECG beat it belongs to, lead II. They share one time axis, so a vertical line meets the same moment in both. The colours match each phase of the action potential to the part of the ECG it draws.
One cell does not draw the ECG. The ECG records the differences between millions of cells, as a wave of activity sweeps through the heart and then fades. Keep that in mind at every step below.
The action potential, step by step
- The resting cell (phase 4). The inside of the cell is about 90 mV negative to the outside. Potassium leaks out through channels that stay open at rest, and sodium and calcium are kept out. The sodium-potassium pump moves three sodium out for every two potassium in, and keeps it that way. On the ECG: the flat line between beats.
- The upstroke (phase 0). Current from a neighbouring cell lifts this one to threshold, about −70 to −55 mV. Fast sodium channels open, sodium rushes in, and in about a millisecond the inside is 30 mV positive. Cell after cell does this as the wave passes. On the ECG: the QRS. It lasts as long as the wave takes to cross the ventricles, 80 to 100 ms, not one cell's upstroke.
- The plateau (phases 1 and 2). The sodium channels shut at once, and a brief potassium outflow makes a small notch. Then for about 200 ms the cell holds near 0 mV: calcium flows in as potassium flows out. That calcium starts the cell contracting. On the ECG: the ST segment. Every ventricular cell is on its plateau at the same time, so there are no differences to record, and the line is flat.
- Repolarisation (phase 3). The calcium channels close, and potassium carries the cell back to rest. The cells of the outer wall (the epicardium) have the shortest action potentials, so they finish first, though the wave reached them last. On the ECG: the T wave, drawn by the cells finishing at different times. It points the same way as the QRS because repolarisation runs from outside in, the opposite way to depolarisation. The T ends, and the QT with it, when the last cells, in the mid-wall, are back at rest.
- Pacemaker cells. In the SA node there is no stable rest. Phase 4 rises slowly by itself from about −60 mV until it reaches threshold, about −40 mV, and the cell fires, with a slow calcium upstroke and no plateau. The steeper that rise, the faster the heart. On the ECG: the heart rate. Choose the SA node above, then move the nerve drive.
- Refractoriness. Until phase 3 brings it back to threshold, a cell cannot fire again: the absolute refractory period, from the QRS to about the peak of the T. Near the end of phase 3 some cells have recovered and others have not. A premature beat that lands then can start a re-entrant rhythm. On the ECG: the T wave's downslope, the vulnerable period: R on T.
- Change a phase. Each control below the panels changes one phase, and the ECG changes with it. Both are drawn from the same model of the heart, so the ECG you see is the one those cells make.
The tissues
Choose "All together" above to see every tissue in the order the wave reaches it.
| Tissue | Rest | Upstroke | Fires |
|---|---|---|---|
| SA node | −60 mV, rising | Slow (calcium) | Before the P |
| Atrium | −80 mV | Fast (sodium) | During the P |
| AV node | −60 mV, rising | Slow (calcium) | In the PR |
| Purkinje | −90 mV | Fastest | Before the QRS |
| Ventricle | −90 mV | Fast | Through the QRS |
The two nodes have no plateau. The atrium's action potential is short and triangular. The Purkinje fibres have the longest plateau. In the ventricle, the mid-wall's action potential is the longest and the epicardium's the shortest.
The SA node fires fastest, 60 to 100 times a minute, so it leads. The AV junction (40 to 60) and the ventricles' own pacemakers (under 40) can fire too, but the wave from above reaches them first and resets them every beat: overdrive suppression. In the AV node's panel, its phase 4 has not reached threshold when the wave arrives. If the SA node stops, the next fastest takes over: an escape rhythm.
What each control does
- Fast sodium channels (phase 0). Fewer channels give a lower, slower upstroke, and the wave travels more slowly. On the ECG: a wider QRS.
- Calcium (phase 2). Low calcium lengthens the plateau; high calcium shortens it. On the ECG: a longer or shorter ST segment, and the QT with it.
- Potassium current in phase 3. Less of it slows phase 3 and lengthens the action potential. On the ECG: a longer QT and a flatter T.
- Potassium outside the cell (phase 4). High potassium makes the cell rest less negative, so fewer sodium channels are ready. Low potassium slows phase 3. On the ECG: high, a peaked T, then a wider QRS and a lost P; low, a longer QT.
- Nerve drive to the SA node (pacemaker phase 4). Sympathetic drive steepens the rise; vagal tone flattens it. On the ECG: a faster or slower heart rate.
Each of these is how a group of drugs acts. That comes later, in its own part.
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The currents, by name
The channels have names that drug pages use:
- I_Na, the fast sodium current: phase 0.
- I_to, the transient outward potassium current: the notch of phase 1, largest in the epicardium.
- I_Ca,L, the L-type calcium current: the plateau, and the trigger for contraction.
- I_Kr and I_Ks, the rapid and slow delayed-rectifier potassium currents: phase 3. Many drugs block I_Kr and lengthen the QT.
- I_K1, the inward-rectifier potassium current: holds the resting potential.
- I_f, the "funny" current, with the calcium clock: the slow rise of phase 4 in pacemaker cells.
Why the T is upright
Depolarisation spreads from the endocardium out to the epicardium. Repolarisation ends the other way round: the epicardium's action potential is the shortest, so it is back at rest first, while the mid-wall, whose action potential is the longest, is last. A wave of returning to rest that runs from outside in draws a deflection the same way up as a wave of activation running from inside out. That is why a normal T points the same way as its QRS.
The difference between the mid-wall and the epicardium also matters for drugs. A drug that blocks I_Kr lengthens the mid-wall's action potential most, so the cells' recovery spreads further apart: a longer QT, and a greater chance of torsades de pointes.
When a cell fires on its own
- Early afterdepolarisations: during a long plateau, calcium channels can open again and fire the cell before it has repolarised. They start torsades de pointes when the QT is long.
- Delayed afterdepolarisations: after the cell has repolarised, calcium leaking from its store drives a small inward current. If it reaches threshold, the cell fires: as in CPVT and digoxin toxicity.
Ions inside and outside
| Ion | Inside, mmol/L | Outside, mmol/L |
|---|---|---|
| Potassium | 150 | 4 |
| Sodium | 20 | 145 |
| Calcium | 0.0001 | 2.5 |
Each ion's gradient is what drives it through its channel when the channel opens. Potassium's high permeability at rest is why the resting potential sits close to potassium's own equilibrium, about −90 mV.
References
- Cardiac muscle physiology — BJA Education, 2023
- Cellular basis for the normal T wave and the electrocardiographic manifestations of the long-QT syndrome — Circulation, 1998