Cardiac action potential
Cardiac muscle, conduction and action potentials
The heart beats on its own because SA node cells drift towards threshold every second. A fast sodium upstroke spreads the signal; a calcium plateau keeps each contraction long enough to pump and stops the heart from tetanising.
The core idea
Cardiac muscle sits between skeletal and smooth muscle. It is striated like skeletal muscle, but its cells are joined end to end by intercalated discs. The discs contain desmosomes, which hold the cells together mechanically, and gap junctions, which let ions pass from cell to cell. Because current flows through gap junctions, the atria contract as one unit and the ventricles contract as one unit (a functional syncytium).
Two kinds of cardiac cell behave differently:
- Pacemaker cells (SA node, AV node) have no stable resting potential. They depolarise slowly by themselves until they fire.
- Working cells (atrial and ventricular muscle, Purkinje fibres) rest at about −90 mV and fire only when a neighbour excites them.
The ventricular action potential, phase by phase
| Phase | What happens | Main current |
|---|---|---|
| 0 – upstroke | Rapid depolarisation to about +20 mV | Fast voltage-gated Na⁺ in |
| 1 – early repolarisation | Brief dip | Transient K⁺ out |
| 2 – plateau | Membrane stays depolarised for about 200 ms | L-type Ca²⁺ in balanced by K⁺ out |
| 3 – repolarisation | Back to −90 mV | K⁺ out (delayed rectifier) |
| 4 – rest | Stable at −90 mV | K⁺ leak (IK1) |
The plateau is what makes cardiac muscle different. Calcium entering during phase 2 triggers far more calcium release from the sarcoplasmic reticulum (calcium-induced calcium release through ryanodine receptors), which drives contraction. Because the plateau lasts almost as long as the contraction itself, the cell is refractory until relaxation has nearly finished. That is why the heart cannot be tetanised: a second beat cannot fuse with the first.
The SA node action potential
| Phase | What happens | Main current |
|---|---|---|
| 4 – pacemaker potential | Slow drift up from about −60 mV | Funny current (If): Na⁺ in through HCN channels, then T-type Ca²⁺ |
| 0 – upstroke | Slower upstroke than ventricle | L-type Ca²⁺ in (not Na⁺) |
| 3 – repolarisation | Back down | K⁺ out |
There is no phase 1 or phase 2. The slope of phase 4 sets the heart rate: a steeper slope reaches threshold sooner.
Autonomic control of rate and conduction
- Sympathetic (noradrenaline on β1): increases If and Ca²⁺ current, so phase 4 steepens and heart rate rises (positive chronotropy). It also speeds AV conduction (positive dromotropy) and strengthens contraction (positive inotropy).
- Parasympathetic (vagus, acetylcholine on M2): opens K⁺ channels (IK-ACh) and reduces If, so the cell starts more negative and drifts up more slowly. Heart rate falls and AV conduction slows. The vagus supplies the SA and AV nodes and atria but has little direct effect on ventricular contractility.
- Resting heart rate (~70/min) is lower than the SA node's intrinsic rate (~100/min) because vagal tone dominates at rest. A transplanted (denervated) heart rests at about 100/min.
Conduction velocity through the heart
| Tissue | Speed | Why it matters |
|---|---|---|
| Purkinje fibres | Fastest (about 4 m/s) | Whole ventricle depolarises almost together |
| Atrial and ventricular muscle | About 1 m/s | |
| AV node | Slowest (about 0.05 m/s) | Delay lets the atria finish filling the ventricles; shows as most of the PR interval |
The AV node delay also protects the ventricles in atrial fibrillation and flutter: only some atrial impulses get through.
Contractility and excitation–contraction coupling
Contractility (inotropy) is the force of contraction at a given preload. It depends on how much calcium reaches the myofilaments.
- Sympathetic stimulation (β1, then cAMP, then protein kinase A) phosphorylates L-type Ca²⁺ channels (more Ca²⁺ in) and phospholamban, which speeds SERCA uptake of Ca²⁺ into the sarcoplasmic reticulum. Result: stronger contraction and faster relaxation, so a tachycardic heart still has time to fill.
- Digoxin blocks Na⁺/K⁺-ATPase. Intracellular Na⁺ rises, so the Na⁺/Ca²⁺ exchanger removes less Ca²⁺; more Ca²⁺ is stored and released, and contraction strengthens.
- Fuel: at rest the heart burns mainly fatty acids; it switches to lactate and glucose during exercise. Myocardial oxygen extraction is already near-maximal at rest (about 70–75%), so extra demand must be met by more coronary flow, not more extraction.
Clinical links
- Class I antiarrhythmics block Na⁺ channels (phase 0); class III drugs (amiodarone, sotalol) block K⁺ channels and prolong phase 3 and the QT interval; class IV (verapamil, diltiazem) block L-type Ca²⁺ channels and slow the SA and AV nodes.
- Ivabradine blocks If and slows the heart without reducing contractility.
- Hyperkalaemia makes the resting potential less negative, inactivating Na⁺ channels and slowing conduction: peaked T waves, then wide QRS and arrest.
How FCPS asks it
Recalls test: which ion causes each phase; why cardiac muscle cannot be tetanised; what joins cardiac cells electrically; where conduction is slowest and fastest; what sets the pacemaker slope; the heart's resting fuel; and how sympathetic stimulation or digoxin increases force.
Exam trap The SA node upstroke is carried by calcium, not sodium. Ventricular phase 0 is sodium.
Exam trap "Cannot be tetanised" is explained by the long refractory period from the plateau, not by gap junctions.
Exam trap The AV node is the slowest conducting tissue; Purkinje fibres are the fastest.
Quick recall
- Gap junctions = electrical coupling; desmosomes = mechanical.
- Ventricle: Na⁺ up, Ca²⁺ plateau, K⁺ down.
- Pacemaker: If (funny current) sets the slope; Ca²⁺ upstroke.
- Vagus: more K⁺ out, flatter phase 4, slower rate and AV conduction.
- Heart at rest burns fatty acids and already extracts most of the oxygen it receives.
Test yourself on this topic
5 of the 16 questions in our bank on this topic. Choose an answer to see why every option is right or wrong.
A young man faints while having blood taken. His pulse drops to 42/min before he loses consciousness. How does the acetylcholine released onto his SA node slow the heart?
Answer: Opens K⁺ channels, less If
In a vasovagal attack a surge of vagal activity releases acetylcholine onto M2 receptors in the SA and AV nodes. M2 receptors act through Gi proteins: the βγ subunit opens acetylcholine-activated potassium channels (IK-ACh), making the maximum diastolic potential more negative, and the fall in cAMP reduces the funny current. The cell starts lower and climbs more slowly, so it takes longer to reach threshold and the rate falls. AV conduction also slows. The vagus has little direct effect on ventricular force, so the faint comes from bradycardia plus loss of sympathetic vasoconstriction. Atropine blocks M2 receptors and reverses it.
Vagus on the SA node
- M2 → Gi → K⁺ channels open
- Lower start point, flatter phase 4
- Rate ↓, AV conduction ↓
- Reversed by atropine
Remember Vagus pulls the start lower and the slope flatter.
Exam trap Muscarinic slowing is about potassium and the pacemaker slope, not sodium.
Why the other options are wrong
- Blocks fast Na⁺ channels Nodal cells do not depend on fast sodium channels for phase 0.
- Blocks L-type Ca²⁺ plateau Nodal cells have no plateau phase.
- Raises cAMP and Ca²⁺ entry That is the sympathetic β1 mechanism, which speeds the heart.
- Inhibits Na⁺/K⁺-ATPase That describes digoxin's direct action on myocytes.
A man with symptomatic sinus bradycardia of 38/min is given an isoprenaline infusion, and his sinus rate rises to 70/min. How does this drug speed up the SA node?
Answer: Steeper phase 4 depolarisation
Isoprenaline stimulates beta-1 receptors on SA node cells, raising cyclic AMP. cAMP binds HCN channels directly, increasing the funny current (If), and through protein kinase A it also increases T-type and L-type calcium currents. Phase 4 depolarisation becomes steeper, so threshold is reached sooner and the rate rises. Acetylcholine does the opposite: it opens K+ channels, makes the diastolic potential more negative and flattens phase 4.
Sympathetic effect on SA node
- Beta-1: cAMP rises
- More If (HCN) and Ca current
- Steeper phase 4
- Threshold reached sooner
Remember Sympathetic steepens the slope; vagal deepens the start.
Exam trap Ivabradine slows the heart by blocking If, the same current that sympathetic stimulation boosts.
Why the other options are wrong
- More negative diastolic potential This is the vagal effect, which slows the rate.
- Longer plateau phase Plateau length does not set the SA node rate.
- Higher threshold potential A higher threshold would slow the rate.
- Opening of ACh-gated K+ channels This is how acetylcholine slows the SA node.
In a ventricular myocyte, the calcium entering through L-type channels during the plateau is far too little by itself to cause a full contraction. How does it trigger contraction?
Answer: Opens ryanodine receptors on the SR
Calcium entering through L-type (dihydropyridine) channels in the T-tubules binds ryanodine receptors (RyR2) on the adjacent sarcoplasmic reticulum, opening them. A much larger burst of calcium is released from the SR, called calcium-induced calcium release. This calcium binds troponin C, shifting tropomyosin so actin and myosin interact. Relaxation follows when SERCA pumps calcium back into the SR and the Na+/Ca2+ exchanger removes it from the cell.
Calcium-induced calcium release
- L-type Ca entry in T-tubules
- Opens RyR2 on the SR
- Big SR calcium release binds troponin C
- SERCA and NCX restore it
Remember A little calcium in releases a lot of calcium inside.
Exam trap Skeletal muscle couples mechanically to RyR1; cardiac muscle needs the trigger calcium from outside.
Why the other options are wrong
- Binds troponin I directly Calcium binds troponin C, not troponin I.
- Activates myosin light chain kinase This is how smooth muscle is activated.
- Stimulates IP3 release from the SR IP3 is the main trigger in smooth muscle, not cardiac muscle.
- Reverses the Na+/Ca2+ exchanger Reverse-mode exchange is a minor calcium entry route.
During rapid pacing at 180/min, the ventricles still relax between beats rather than going into sustained contraction. Which property of cardiac muscle explains this?
Answer: Long effective refractory period
The ventricular action potential has a long plateau, sustained by L-type calcium entry, and lasts about 250–300 ms. During most of this time, sodium channels remain inactivated, so the cell cannot fire another action potential: the effective refractory period lasts almost as long as the contraction. A new beat therefore cannot start until the muscle has begun to relax, so summation and tetanus cannot occur. This lets the heart fill between beats.
No tetanus in heart
- Long plateau (L-type Ca)
- Refractory period ≈ contraction time
- No summation
- Heart can fill between beats
Remember Heart cannot be tetanised: refractory period covers the twitch.
Exam trap Do not confuse refractoriness with fatigue; the heart is protected electrically, not by tiring.
Why the other options are wrong
- Gap junction coupling Spread excitation between cells; do not stop tetanus.
- Calcium-induced calcium release Amplifies contraction; does not prevent summation.
- Abundant mitochondria Supply ATP; unrelated to tetanus.
- Small sarcoplasmic reticulum Not the reason; cardiac SR is well developed.
In which part of the heart's conduction system is conduction velocity fastest?
Answer: Purkinje fibres
Purkinje fibres are large cells with many gap junctions and conduct at about 2–4 m/s, spreading excitation almost simultaneously through the ventricles. The AV node is slowest (about 0.05 m/s), giving the delay that lets the atria empty before the ventricles contract. Atrial and ventricular muscle conduct at about 0.3–1 m/s.
Conduction speeds
- Fastest: Purkinje (2–4 m/s)
- Slowest: AV node (0.05 m/s)
- AV delay lets atria empty
- Muscle: moderate
Remember Purkinje sprint; AV node strolls.
Exam trap The AV delay appears as the PR interval.
Why the other options are wrong
- AV node Slowest.
- SA node Slow.
- Atrial muscle Moderate.
- Ventricular muscle Moderate.
Where this sits in the CPSP syllabus
- Paper 1: Cardiovascular system, Cardiac muscle, conduction system and cardiac action potentials
- Surgery & Allied, Paper 2: Cardiovascular system, Cardiac muscle, conduction system and cardiac action potentials
- Medicine & Allied, Paper 2: Cardiovascular system, Cardiac muscle, conduction system and cardiac action potentials
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