Physiology chapters
Cardiac action potentials
The five phases of the ventricular muscle action potential and the channels behind each, the pacemaker action potential of the SA node and how it differs, refractory periods, and how autonomic nerves and drugs change them.
- The ventricular action potential has phases 0–4: fast Na+ upstroke, brief notch, long Ca2+ plateau, K+ repolarisation and a stable resting potential of about −90 mV.
- The SA nodal action potential has no stable resting potential: a slow pacemaker potential (funny current, then Ca2+) is followed by a slow Ca2+-driven upstroke.
- The plateau makes the refractory period long, so the heart cannot be tetanised.
On this page
Overview
Heart cells have two main kinds of action potential:
- Fast-response action potentials in atrial and ventricular muscle and Purkinje fibres.
- Slow-response (pacemaker) action potentials in the SA and AV nodes.
Knowing which ion moves in each phase explains the ECG, the action of many heart drugs, and the effects of electrolyte changes.
The ventricular muscle action potential
| Phase | Name | Main ion movement | Channels |
|---|---|---|---|
| 0 | Rapid depolarisation | Na+ in | Fast voltage-gated Na+ channels |
| 1 | Initial brief repolarisation | Na+ channels close; K+ out (transient outward current) | Transient K+ channels |
| 2 | Plateau | Ca2+ in balanced by K+ out | L-type (long-lasting) Ca2+ channels |
| 3 | Rapid repolarisation | K+ out; Ca2+ channels close | Delayed rectifier K+ channels |
| 4 | Resting potential (about −90 mV) | K+ leak keeps it stable | Inward rectifier K+ channels |
The ventricular action potential lasts about 0.2–0.3 seconds, compared with about 1 ms in a nerve.
The plateau (phase 2) is due to Ca2+ entry through L-type channels. This Ca2+ also triggers release of more Ca2+ from the sarcoplasmic reticulum (calcium-induced calcium release), which causes contraction.
The upstroke of ventricular muscle is Na+; the upstroke of the SA node is Ca2+.
Why the plateau matters
- It keeps the muscle depolarised long enough for a strong, sustained contraction.
- It makes the refractory period long, preventing tetanus and allowing the heart to fill.
- K+ permeability falls during the plateau, which helps keep it going.
Refractory periods
- Effective (absolute) refractory period: from phase 0 to the middle of phase 3. No new action potential can be produced because the Na+ channels are inactivated. It lasts about 0.25–0.30 seconds in the ventricles.
- Relative refractory period: late phase 3; a stronger stimulus can produce an action potential.
- The atrial refractory period is shorter, so atria can beat faster than ventricles.
The effective refractory period covers almost all of the contraction. That is why heart muscle cannot be tetanised.
The SA nodal (pacemaker) action potential
| Phase | What happens | Main current |
|---|---|---|
| 4: pacemaker potential | Slow, steady depolarisation from about −60 mV to threshold (about −40 mV) | Funny current (If): Na+ in through HCN channels, opened by hyperpolarisation; then T-type Ca2+ channels; falling K+ outflow |
| 0: upstroke | Slow depolarisation to about 0 or slightly positive | L-type Ca2+ in |
| 3: repolarisation | Back to about −60 mV | K+ out |
Differences from ventricular muscle
| Feature | Ventricular muscle | SA node |
|---|---|---|
| Resting potential | Stable, about −90 mV | No stable rest; most negative about −55 to −60 mV |
| Phase 4 | Flat | Slow depolarisation (pacemaker potential) |
| Upstroke | Fast, Na+ | Slow, Ca2+ |
| Phases 1 and 2 | Present | Absent |
| Conduction speed | Fast | Slow |
Why is the nodal resting level less negative? Nodal cells have few inward rectifier K+ channels and leak Na+ inwards. At this voltage, the fast Na+ channels stay inactivated, so only Ca2+ channels can produce the upstroke.
The funny current (If) is unusual: it is an inward Na+ current switched on by hyperpolarisation. It drives the pacemaker potential. Ivabradine blocks it to slow the heart.
Effect of the autonomic nerves
- Sympathetic (β1): increases If and Ca2+ currents. The pacemaker potential rises faster, so heart rate increases. More Ca2+ enters muscle cells, so force increases.
- Parasympathetic (ACh, M2): opens extra K+ channels and reduces If and Ca2+ currents. The cell starts from a more negative level and depolarises more slowly, so heart rate falls.
Effect of electrolytes
- Hyperkalaemia: resting potential less negative; Na+ channels partly inactivated; slower conduction; tall T waves, then wide QRS, then arrest.
- Hypokalaemia: slower repolarisation; prolonged action potential; U waves; arrhythmias.
- Hypercalcaemia: shorter plateau and QT interval. Hypocalcaemia: longer plateau and QT interval.
Drugs that act on these channels
| Drug class | Target | Main effect |
|---|---|---|
| Class I antiarrhythmics (e.g. lidocaine) | Fast Na+ channels | Slower phase 0 and conduction |
| Class II (beta-blockers) | β1 receptors | Slower SA rate and AV conduction |
| Class III (e.g. amiodarone) | K+ channels | Longer phase 3 and refractory period |
| Class IV (verapamil, diltiazem) | L-type Ca2+ channels | Slower SA and AV nodes; less force |
| Ivabradine | If (funny current) | Slower SA rate only |
Clinical relevance
Long QT syndrome
How it happens: inherited K+ or Na+ channel defects, or drugs that block K+ channels, delay repolarisation.
What you see: a long QT interval and risk of a dangerous ventricular arrhythmia (torsades de pointes).
Calcium channel blockers
How it happens: verapamil blocks L-type channels in the SA and AV nodes.
What you see: slower heart rate and AV conduction; used to control fast atrial rhythms.
Expect: which ion causes each phase of the ventricular action potential, the cause of the plateau, the upstroke of the SA node, the funny current and ivabradine, differences between nodal and non-nodal action potentials, the effective refractory period, and how autonomic nerves alter the pacemaker potential.
Quick revision
- Ventricle: 0 Na+ in; 1 transient K+ out; 2 Ca2+ in (plateau); 3 K+ out; 4 rest at −90 mV.
- SA node: phase 4 pacemaker (If, then T-type Ca2+); phase 0 L-type Ca2+; no phases 1 and 2.
- Plateau → long refractory period → no tetanus.
- Sympathetic: steeper pacemaker potential. Vagus: more negative start and slower rise.
- Class I Na+; II beta; III K+; IV Ca2+; ivabradine If.
Written by The House Job from standard physiology references (Guyton and Hall Textbook of Medical Physiology; BRS Physiology).
FAQ
What causes the plateau of the cardiac action potential?
The slow entry of calcium through L-type calcium channels, balanced by potassium leaving the cell.
What causes the upstroke in the SA node?
Calcium entry through L-type calcium channels, not sodium.
What is the funny current?
An inward sodium current through HCN channels that is activated by hyperpolarisation and drives the pacemaker potential.
Why does the SA node have no stable resting potential?
Its cells leak sodium inward and have few inward rectifier potassium channels, so they depolarise slowly and continuously between beats.