A question asks which ion produces phase 0 of a cardiac action potential. “Sodium” may be correct—but only after you identify the cell. In a typical ventricular myocyte, the rapid upstroke depends on fast sodium channels. In a typical sinoatrial nodal cell, calcium carries the upstroke. [20]
This guide uses a consistent approach: identify the tissue, identify the electrical event, then select the relevant current. Read it alongside your MRCEM Primary revision plan and attempt the questions before looking at the answers.
RCEM describes MRCEM Primary as 180 SBAs in three hours. The updated Basic Sciences Syllabus applies from 21 April 2027; cardiac electrical excitation and excitation–contraction coupling are included. Use the official syllabus for your sitting rather than assuming an older question allocation remains unchanged. [1] [2] [3]
1. Start with the cell, not the phase number
What membrane voltage measures
Membrane potential describes voltage inside a cell relative to outside. Depolarisation makes the interior less negative; repolarisation returns it towards its preceding negative potential. Hyperpolarisation makes it more negative. These terms describe voltage changes, not contraction strength. Ion gradients, membrane permeability and electrogenic pumps jointly determine membrane potential. [4]
Channels provide pathways for ion movement. Pumps maintain gradients using energy. Avoid attributing each rapid voltage change directly to the sodium–potassium pump: changing channel conductance is central to the shape of an action potential. For a positively charged ion, inward movement tends to depolarise and outward movement tends to repolarise. [4]
Two useful teaching models
Feature | Ventricular working myocyte | Typical SA nodal cell |
|---|---|---|
Between impulses | Stable negative resting potential | Spontaneous diastolic depolarisation |
Main phase-0 current | Fast inward Na⁺ current | Inward Ca²⁺ current |
Prominent plateau | Present | Absent |
Main role in this comparison | Electrical activation of working muscle | Initiation of the rhythm |
These are teaching models, not a claim that every cardiac cell fits one of two identical shapes. Purkinje cells have fast-response action potentials but can also show latent pacemaker activity. Do not equate “capable of automaticity” with “must have a nodal calcium upstroke”. [5] [6]
2. Ventricular action potentials: phases 0–4
Follow the dominant current
Phase | Main event | Key ionic explanation |
|---|---|---|
0 | Rapid upstroke | Fast Na⁺ entry |
1 | Brief initial repolarisation | Transient outward K⁺ current; fast Na⁺ current inactivates |
2 | Plateau | Inward L-type Ca²⁺ current balanced by outward currents |
3 | Repolarisation | Outward K⁺ current predominates as Ca²⁺ current declines |
4 | Resting state | High resting K⁺ permeability supports a negative potential |
The table identifies the major teaching association, not the only open channel. A plateau does not mean that ions have stopped moving: inward and outward currents can approximately balance while substantial movement continues. [5]
Why the plateau matters
Calcium entry links electrical excitation to contraction, while the prolonged action potential helps sustain the refractory period. Electrical activation and mechanical contraction are related but are not interchangeable measurements. An action-potential trace plots voltage over time; it does not directly plot force or ventricular pressure. [20]
3. Pacemaker action potentials: phases 4, 0 and 3
Why phase 4 rises spontaneously
SA nodal cells do not sit at a stable resting potential between beats. Phase 4 moves towards threshold; phase 0 follows through L-type calcium-channel activity; phase 3 returns the membrane towards a more negative voltage through potassium efflux and declining calcium current. The simplified nodal trace lacks the distinct phases 1 and 2 of the ventricular model. [6]
What makes the funny current unusual
The funny current, If, passes through hyperpolarisation-activated cyclic nucleotide-gated (HCN) channels. It is a mixed sodium–potassium current with a net inward effect at relevant diastolic voltages. Its activation at negative potentials distinguishes it from the familiar fast sodium current of a ventricular upstroke. [7]
If contributes to diastolic depolarisation but is not the sole pacemaker mechanism. Calcium currents and changing outward potassium currents also contribute. Consequently, “sodium participates in pacemaking” does not mean “fast sodium channels produce nodal phase 0”. Keep the channel, phase and cell type together. [6] [7]
4. Refractory periods and cardiac conduction
Recovery of excitability
After activation, excitability does not immediately return. During absolute refractoriness, another action potential cannot be elicited. The effective refractory period concerns inability to generate a propagated response; relative refractoriness permits a response to a stronger stimulus. Recovery of fast sodium channels from inactivation is central in working ventricular tissue. [5] [20]
Long refractoriness helps prevent rapid repetitive activation from producing sustained tetanic contraction. The useful question is therefore “can this tissue respond and propagate now?”, rather than merely “is its voltage negative?”. Channel availability matters as well as the displayed voltage. [20]
An action potential is not an ECG
A surface ECG records voltage differences arising from the heart’s collective electrical activity. It is not a magnified recording of one ventricular cell. Avoid assigning the P wave to phase 0 or the T wave to phase 3 without specifying the tissue and level of organisation being discussed. [20]
Normally, excitation spreads from the SA node across the atria, through the AV node and into the His–Purkinje system. AV nodal delay allows atrial activation and contraction to precede ventricular activation. The conduction system is specialised cardiac tissue, not a chain of peripheral nerves. [10]
5. Apply the physiology to autonomic and drug effects
Change the time taken to reach threshold
Sympathetic stimulation increases the rate of SA nodal firing, including by steepening diastolic depolarisation. Vagal stimulation reduces pacemaker activity and can hyperpolarise nodal cells. Both the starting voltage and the journey towards threshold influence the interval between impulses. [8]
In an idealised comparison with unchanged threshold and starting voltage, a steeper phase-4 slope reaches threshold sooner. That shortens the cycle. Treat this as a stated model: real autonomic responses alter several currents, and rate is not controlled by one line on a diagram alone. [8]
Match the target to the tissue
Drug class | Useful mechanism association |
|---|---|
Class I | Fast sodium-channel blockade affects fast-response tissue and conduction. |
Class II | Beta blockade reduces sympathetic cardiac effects. |
Class III | Potassium-channel blockade can delay repolarisation. |
Class IV | Verapamil and diltiazem affect calcium-dependent nodal activity and conduction. |
This classification is a starting framework; individual drugs may have more than one action. A mechanism does not establish which medicine is appropriate for a particular patient. For revision, first identify the current targeted, then predict the electrical effect in the specified tissue. [9]
For the separate task of interpreting potency, efficacy and antagonism, read the pharmacodynamics guide. For clinical trace interpretation, the ECG pattern article addresses a different level of analysis.
6. Five original MRCEM Primary-style SBAs
These questions are independently written educational material, not recalled, official or RCEM-endorsed examination questions. Choose one answer for each stem.
Question 1: Identify the upstroke
In a typical central SA nodal cell, which current predominantly produces phase 0?
Fast inward sodium
Inward L-type calcium
Outward potassium
Outward chloride
Sodium–potassium pump current
Question 2: Explain a plateau
A ventricular myocyte remains depolarised during phase 2. Which explanation best accounts for the relatively flat trace?
All channels are closed
Membrane voltage is identical to calcium equilibrium potential
Inward and outward currents approximately balance
There is no ion movement
Only the sodium–potassium pump is active
Question 3: Predict the timing
In a simplified SA nodal model, the starting voltage and threshold remain unchanged while the phase-4 slope becomes steeper. What is the best prediction?
Longer time to threshold
Shorter time to threshold
A new ventricular plateau develops
The cell loses all automaticity
The upstroke must become a fast sodium current
Question 4: Recognise the definition
A ventricular cell is stimulated, but a new response cannot propagate to neighbouring tissue. Which term most directly describes this functional restriction?
Increased contractility
Enhanced automaticity
Effective refractory period
Increased preload
Greater receptor affinity
Question 5: Identify the channel
An experiment records a mixed-cation pacemaker current activated at negative membrane potentials. Which channel family best fits?
Fast voltage-gated sodium channels
L-type calcium channels
Transient outward potassium channels
HCN channels
Ligand-gated nicotinic channels
Answers and explanations
1. B — Inward L-type calcium. A belongs to the fast-response upstroke. C favours repolarisation, not the nodal upstroke. D is not the dominant current described. E maintains gradients rather than producing the rapid event asked about. [6]
2. C — Approximate current balance. A and D wrongly interpret a flat voltage as electrical inactivity. B confuses a balance of multiple currents with one ion’s equilibrium potential. E omits the channel currents central to the plateau. [5]
3. B — Shorter time to threshold. With the stated endpoints fixed, a faster rise takes less time. A reverses the relationship. C changes the cell model. D contradicts continued spontaneous depolarisation. E introduces a channel switch that the stem does not support. [8]
4. C — Effective refractory period. The defining issue is propagation of a new response. A concerns force, B impulse generation, D ventricular loading and E ligand binding. None directly describes the stated restriction. [20]
5. D — HCN channels. Hyperpolarisation activation and mixed-cation conductance identify the funny-current pathway. A confuses it with a fast upstroke; B with calcium entry; C with an outward potassium current; E with a different, ligand-gated channel mechanism. [7]
7. Consolidate your cardiac physiology revision
A three-step answering method
Before opening the answer options, write three words: tissue, event, current. Identify the named cell. Decide whether the stem concerns initiation, upstroke, plateau, recovery or propagation. Then match the current and its direction. If two options remain plausible, check whether one describes another cell type.
When you miss a question, record the exact confusion: “nodal phase 0 versus ventricular phase 0” is more useful than “revise cardiology”. Reattempt it later with the options hidden, explaining why your rejected answer belongs elsewhere. This makes the error a specific revision task.
Practise with StudyMedical
Build on this guide with the StudyMedical MRCEM Primary question bank. It offers over 7,800 questions, explanations with teaching diagrams, custom quizzes by topic, timed quizzes and the option to revisit previously incorrect answers. You can also try free sample questions without signing up. [11]
