Before drawing the curve
Voltage is the result; current is the cause
What you should already have
About 45 minutes
Plus the time it takes to redraw this lesson’s figures from memory, which is the fastest way to find out what you have not understood.
Where this shows up
Two traces carry this whole topic, and they are not the same shape for a reason: the ventricular myocyte has a fast sodium upstroke and a calcium plateau, the nodal cell has neither. Every antiarrhythmic and every autonomic effect on rate is a change to one named current, so the trace predicts the drug rather than the other way round.
Learning outcomes
By the end of this lesson you should be able to:
- Explain why voltage is the result and current the cause, and read a trace as the sum of its currents.
- Draw the ventricular action potential with phases 0 to 4 on scaled axes, naming the current that carries each.
- Draw the nodal action potential with only phases 4, 0 and 3, and explain why it has no stable resting potential and no plateau.
- Account for automaticity from the funny current, the decline in potassium efflux and the calcium currents.
- Predict the change in the trace, and its physiological consequence, when a named drug or autonomic receptor changes a current.
Together these settle one syllabus objective: Ventricular and nodal action potentials, and automaticity. Tick it on the Physiology objective list once you can do all of the above without notes.
Depolarises
Na+ or Ca2+ entry makes the intracellular voltage less negative and moves Vm upward.
Repolarises
K+ efflux makes the intracellular voltage more negative and moves Vm downward.
Creates a plateau
During ventricular phase 2, ICa,L is approximately balanced by outward delayed-rectifier K+ current.
Abbreviations in this section
- AP
- Action potential — The voltage trace itself.
- Vm
- Membrane potential — The voltage across the cell membrane.
- RMP
- Resting membrane potential — The stable negative membrane voltage in ventricular myocytes.
- MDP
- Maximum diastolic potential — The most negative nodal voltage reached in phase 3.
- SA
- Sinoatrial — The natural pacemaker region of the heart.
- AV
- Atrioventricular — The conduction link between atria and ventricles.
Interactive physiology lab
Click the trace. Explain the current.
Start with the normal action potential, then overlay antiarrhythmic or autonomic effects. The selected segment is explained below the graph.
Fast-response tissue
Rapid depolarisation
- Voltage
- Threshold to an overshoot near +20 mV
- Dominant current
- Large inward fast Na+ current: INa
- Channel state
- Fast voltage-gated Na+ channels open briefly, then rapidly inactivate.
A regenerative Na+ influx produces the steep upstroke. The maximum rate of rise, dV/dtmax, is a major determinant of conduction velocity in atrial, ventricular and His-Purkinje tissue.
Fast-response action potential
The ventricular myocyte: phases 0 to 4
| Phase | Name | Dominant current | Channel state | Physiological meaning |
|---|---|---|---|---|
| 4 | Stable resting potential | IK1: high K+ conductance | Fast Na+ channels closed but available | Excitable; not automatic |
| 0 | Rapid depolarisation | Fast inward INa | Fast Na+ channels open, then inactivate | dV/dtmax determines fast-tissue conduction |
| 1 | Early repolarisation | Transient outward Ito | Na+ channels inactivated | Creates the notch |
| 2 | Plateau | ICa,L inward approximately balances IKr/IKs outward | L-type Ca2+ channels open | Triggers contraction; prolongs refractoriness |
| 3 | Final repolarisation | IKr/IKs, then IK1 | Ca2+ channels inactivate; Na+ channels recover as Vm falls | Sets AP duration, ERP and QT behaviour |
Phase 0 depends on available fast Na+ channels
A sufficiently negative phase-4 voltage allows recovery from inactivated to closed-but-available states. Partial depolarisation, as in hyperkalaemia or ischaemia, leaves more channels inactivated, reduces dV/dtmax and slows conduction.
The plateau keeps Na+ channels inactivated
During most of phases 0-3, too few fast Na+ channels are available to support a propagated response. The long action potential therefore makes the effective refractory period overlap almost the whole contraction.
Deep dive · Absolute, effective and relative refractory periods
Absolute refractory period: no second action potential can be initiated, however strong the stimulus.
Effective refractory period: no propagated action potential can be produced. It extends beyond the absolute period into early relative refractoriness.
Relative refractory period: a stronger-than-normal stimulus can trigger a smaller, slower response because Na+ channel recovery remains incomplete.
Do not write: ERP = ARP + the whole RRP.
Abbreviations in this section
- INa
- Fast inward Na+ current — Creates the steep ventricular phase 0 upstroke.
- Ito
- Transient outward K+ current — Produces the phase-1 notch in working myocardium.
- ICa,L
- L-type Ca2+ current — The main inward current for nodal phase 0 and the ventricular plateau.
- IKr / IKs
- Rapid / slow delayed-rectifier K+ currents — Major outward currents for ventricular repolarisation.
- IK1
- Inward-rectifier K+ current — Stabilises the ventricular resting membrane potential.
- dV/dtmax
- Maximum rate of rise of membrane potential — A major determinant of fast-tissue conduction velocity.
Abbreviations in this section
- APD
- Action-potential duration — How long repolarisation takes; often prolonged by class III drugs.
- ARP
- Absolute refractory period — No second propagated action potential can be started.
- ERP
- Effective refractory period — No propagated action potential can be generated.
- EADs
- Early afterdepolarisations — Abnormal depolarisations during prolonged phase 2 or 3; can occur with QT prolongation.
- DADs
- Delayed afterdepolarisations — Abnormal depolarisations after repolarisation; classically seen with digoxin toxicity or Ca2+ overload.
Slow-response action potential
The SA node: phases 4, 0 and 3
Hyperpolarisation starts the next beat
Current: HCN channels open and carry If, a mixed Na+/K+ current with a net inward effect at diastolic voltages.
At the same time, K+ channels responsible for the previous phase 3 progressively close, so outward K+ current falls.
The membrane drifts toward threshold
Current: If plus declining K+ efflux create the pacemaker potential. Transient T-type Ca2+ entry assists the late approach to threshold.
The slope of this phase, the maximum diastolic potential and the threshold voltage determine the interval to the next discharge.
L-type Ca2+ channels generate the upstroke
Current: At approximately -40 mV, ICa,L becomes the dominant inward current.
Because the nodal upstroke is Ca2+-dependent rather than fast-Na+-dependent, it is slower and supports slower conduction than a ventricular phase 0.
K+ current repolarises the cell
Current: L-type Ca2+ channels inactivate while outward voltage-gated K+ current increases.
The cell returns toward a maximum diastolic potential around -60 mV; HCN channels then reactivate and the cycle repeats.
Fast response versus slow response
| Feature | Fast response | Slow response |
|---|---|---|
| Principal tissues | Atrial and ventricular myocytes; His-Purkinje fibres | SA and AV nodal cells |
| Resting behaviour | Stable phase 4 near -90 mV | No true resting potential; maximum diastolic potential roughly -60 mV |
| Phases | 0, 1, 2, 3 and 4 | 4, 0 and 3; no distinct phases 1 or 2 |
| Phase-0 ion | Fast Na+ influx | L-type Ca2+ influx |
| Plateau | Present: ICa,L approximately balances K+ efflux | Absent |
| Automaticity | Normally absent in working myocytes | Intrinsic because phase 4 reaches threshold spontaneously |
| Key drug sensitivity | Class I Na+ block; class III K+ block | Class II beta block; class IV Ca2+ block; adenosine |
Abbreviations in this section
- If
- Funny current — A mixed Na+/K+ current that helps start the pacemaker potential.
- HCN
- Hyperpolarisation-activated cyclic nucleotide-gated channel — The channel family that carries If in pacemaker tissue.
- ICa,T
- T-type Ca2+ current — A transient Ca2+ current that helps late phase 4 in nodal tissue.
Predictive pharmacology
Change the target; predict the trace
| Class | Primary target | Examples | Action-potential effect | Surface clue |
|---|---|---|---|---|
| IA | Na+ block plus K+ block | Quinidine, procainamide, disopyramide | Phase 0 slope down; APD/ERP usually up | QRS and QT may increase |
| IB | Weak/rapid Na+ block; favours inactivated channels | Lidocaine, mexiletine | Phase 0 modestly reduced in diseased tissue; APD/ERP down | Little change in normal QRS |
| IC | Marked/slow Na+ block | Flecainide, propafenone | Phase 0 slope markedly down; little APD change | QRS increases |
| II | Beta1 blockade | Propranolol, metoprolol, esmolol | Nodal phase 4 flattens; nodal phase 0 and AV conduction slow | Heart rate down; PR may increase |
| III | Repolarising K+ block | Amiodarone, sotalol | Phase 3, APD and ERP increase | QT increases |
| IV | L-type Ca2+ block | Verapamil, diltiazem | Nodal phase 0 becomes smaller/slower; AV nodal ERP increases | PR may increase |
| Other | Adenosine A1; digoxin vagal plus Na+/K+-ATPase effects | Adenosine, digoxin | Nodal hyperpolarisation/AV block; digoxin toxicity may cause DADs | Not a single Vaughan-Williams class |
Steeper nodal phase 4
Gs-cAMP increases If and Ca2+ current: faster SA firing and AV conduction. In working myocytes, Ca2+ handling increases inotropy and lusitropy.
Reflex slowing may dominate
Phenylephrine raises SVR and arterial pressure. Baroreceptor-mediated vagal activation may flatten nodal phase 4 and slow the heart; this is indirect, not a canonical alpha1 nodal current.
Hyperpolarised and flatter
Gi lowers cAMP while GIRK increases K+ efflux: the maximum diastolic potential becomes more negative and threshold is reached later.
Abbreviations in this section
- Gs / Gi
- Stimulatory / inhibitory G proteins — Gs raises cAMP; Gi lowers cAMP.
- GIRK
- G protein-activated inward rectifier K+ channel — Opened by vagal M2 signalling to increase K+ efflux.
Abbreviations in this section
- RyR2
- Ryanodine receptor type 2 — Releases Ca2+ from the sarcoplasmic reticulum during excitation-contraction coupling.
- SERCA
- Sarcoplasmic reticulum Ca2+-ATPase — Pumps Ca2+ back into the sarcoplasmic reticulum during relaxation.
- Na+/K+-ATPase
- Sodium-potassium pump — Maintains transmembrane gradients; it does not generate the action-potential phases directly.
Abbreviations in this section
- ECG
- Electrocardiogram — Surface recording that reflects conduction and repolarisation timings.
- PR
- Atrial depolarisation to ventricular depolarisation interval — Reflects AV nodal conduction time.
- QRS
- Ventricular depolarisation on ECG — Widens when ventricular conduction slows.
- QT
- Ventricular depolarisation and repolarisation on ECG — Lengthens when ventricular repolarisation is delayed.
Reading the trace
Drawing the traces, and narrating the ions
- Voltage axis from about -100 to +30 mV
- Time axis to about 400 ms
- Phases 0-4 in the correct positions
- INa, Ito, ICa,L, IKr/IKs and IK1
- Plateau and refractory interval
- Maximum diastolic potential and threshold
- Only phases 4, 0 and 3
- Upward phase 4—not a downslope
- If, declining K+, ICa,T, ICa,L and outward K+
- No true resting potential and no plateau