Electrophysiology of the Heart ✨🧠

The heart isn’t just a pump — it’s a beautifully coordinated electrical organ. 
Every beat begins with ions moving across membranes in a precisely coordinated sequence.

If you understand the ions, you understand the ECG.
If you understand the ECG, you understand arrhythmias.

Let’s build it from the ground up.

1️⃣ Pacemaker Potential: Where Every Beat Begins

It all starts in the sinoatrial (SA) node, the heart’s natural pacemaker.

Unlike most cells, SA node cells do not have a stable resting membrane potential. Instead, they are electrically restless and slowly drift toward threshold all by themselves.

Phase 4 – Slow Depolarisation (Automaticity)

This gradual rise toward firing threshold happens because:

👉 Funny current (If channels)

• Open at negative membrane potentials
• Allow Na⁺ to leak in
• Slowly depolarise the cell

👉 Reduced K⁺ efflux

• Fewer K⁺ ions leaving makes the inside more positive

👉 T-type Ca²⁺ channels

• Open near threshold
• Help push the cell to firing level

The membrane potential slowly becomes less negative.
This is automaticity. No external nerve required.

Phase 0 – Depolarisation

When threshold is reached:

👉 L-type Ca²⁺ channels open

• Ca²⁺ rushes in
• This creates the upstroke of the pacemaker action potential

(Note: In pacemaker cells, depolarisation is calcium-driven — not sodium-driven like ventricular muscle.)

Phase 3 – Repolarisation

👉 K⁺ channels open

• K⁺ exits
• Membrane potential falls again

And the cycle repeats — rhythmically, automatically, intrinsically. This rhythm sets your heart rate - No external nerves required.

2️⃣ How the Electrical Wave Spreads

Once the SA node fires, the impulse spreads in a precise sequence:

👉 Atrial depolarisation

• Impulse travels through atrial myocardium via gap junctions
• Atria contract
• Seen as the P wave on ECG

👉 AV node delay

• Conduction slows significantly. Why?
• Allows time for ventricular filling - ventricles must fill before they can empty
• Delay creates the PR interval on the ECG

👉 Rapid ventricular conduction

• Bundle of His → bundle branches → Purkinje fibres
• Very fast conduction ensures near-simultaneous ventricular contraction
• Seen as the QRS complex

This coordination is essential. If conduction becomes disorganised → arrhythmias develop.

3️⃣ Ventricular Myocyte Action Potential: The Working Muscle

Ventricular myocytes are different from pacemaker cells.

They:

• Have a stable resting membrane potential (~ –90 mV)
• Fire only when stimulated
• Have a distinctive (prolonged) plateau phase

Phase 0 – Rapid Depolarisation

👉 Voltage-gated Na⁺ channels open

• Rapid Na⁺ influx
• Steep upstroke

Phase 1 – Early Repolarisation

👉 Na⁺ channels close
👉 Brief K⁺ efflux

Phase 2 – Plateau (Unique to Cardiac Muscle)

👉 L-type Ca²⁺ channels open
👉 Ca²⁺ influx balances K⁺ efflux

This plateau:

• Prolongs contraction
• Prolongs the refractory period
• Prevents tetany

The heart must relax and refill between beats — sustained contraction would be catastrophic.

Phase 3 – Repolarisation

👉 Ca²⁺ channels close
👉 K⁺ efflux restores resting potential

Phase 4 – Resting State

Maintained primarily by inward rectifier K⁺ currents.

Ready for the next beat.

4️⃣ Refractory Periods: The Built-In Safety Mechanism

Because the action potential is long, cardiac muscle has prolonged refractory periods and cannot be rapidly restimulated like skeletal muscle. 

👉 Absolute refractory period

• No new action potential possible
• Protects against premature contraction

👉 Relative refractory period

• Strong stimulus may trigger a beat
• This is where dangerous arrhythmias (e.g. R-on-T phenomenon) can occur

These refractory periods ensure:

• Coordinated contraction
• Adequate ventricular filling
• Protection against chaos

5️⃣ The ECG Connection

An ECG is simply the surface recording of all this ion movement.

👉 P wave – Atrial depolarisation
👉 QRS complex – Ventricular depolarisation
👉 T wave – Ventricular repolarisation

Every squiggle represents billions of cardiac cells moving ions in synchrony.

👉 Why Does This Matter?

Understanding electrophysiology allows you to:

• Diagnose arrhythmias
• Interpret ECGs
• Understand drug actions (beta blockers, calcium channel blockers, antiarrhythmics)
• Recognise ischaemia-related electrical instability

It’s not about memorising waveforms.
It’s about understanding what the ions are doing — and why.

If this feels like a lot, that’s normal.

Electrophysiology can seem abstract at first because you can’t see ions moving. But everything you’ve learned here connects directly to what you’ll study next:

• ECG interpretation
• Arrhythmias
• Electrolyte disturbances
• Pharmacology

Right now, you’re laying the wiring diagram.

Later, when you see a rhythm strip or hear about a conduction block, it won’t feel like pattern recognition — it will feel like physiology.

And that shift — from memorising to reasoning — is when medicine starts to make sense.

 🧠Questions to consider

1. During a physiology practical, students stimulate skeletal muscle repeatedly and observe sustained contraction (tetany).
They then discuss why the same phenomenon cannot occur in normal cardiac muscle.

Why is tetany impossible in normal cardiac muscle?

A. Cardiac muscle lacks sodium channels
B. The refractory period overlaps with contraction
C. Calcium is not required for contraction
D. Action potentials are shorter than skeletal muscle
E. Gap junctions prevent summation

2. In a lecture comparing pacemaker cells and ventricular myocytes, a student asks why the SA node does not behave like ordinary cardiac muscle.

Which feature distinguishes SA node cells from ventricular myocytes?

A. Presence of voltage-gated sodium channels
B. Stable resting membrane potential
C. Calcium-mediated Phase 0 depolarisation
D. Plateau phase
E. Inward rectifier potassium current

3. During late Phase 3 of the ventricular action potential, the membrane potential is returning toward its resting level. A sufficiently strong stimulus at this point can sometimes trigger another action potential.

Which cellular change allows this to occur?

A. All sodium channels are fully closed and inactive
B. All potassium channels are closed
C. Some sodium channels have recovered from inactivation
D. Calcium channels are maximally open
E. Resting membrane potential is fully restored

4. In an experimental model, the duration of the ventricular plateau phase (Phase 2) is artificially shortened.

Which consequence would most directly result from this change?

A. Faster Phase 0 depolarisation
B. Reduced duration of the refractory period
C. Increased slope of Phase 4 depolarisation
D. More negative resting membrane potential
E. Elimination of potassium efflux

5. A researcher increases potassium permeability during Phase 3 of the ventricular action potential.

What would be the most immediate effect?

A. Faster repolarisation
B. Prolonged plateau phase
C. Slower sodium influx
D. Increased automaticity
E. More positive resting membrane potential

Answers

1. Correct answer: B

Explanation:
In ventricular myocytes, the plateau phase prolongs the action potential and therefore prolongs the refractory period. Because contraction occurs during this refractory period, the muscle cannot be re-stimulated before relaxation occurs. This prevents summation and makes tetany physiologically impossible in normal cardiac muscle.

2. Correct answer: C

Explanation:
SA node cells depolarise during Phase 0 via L-type calcium channels, whereas ventricular myocytes use fast voltage-gated sodium channels for rapid depolarisation. Ventricular cells also have a stable resting membrane potential and a prominent plateau phase, which pacemaker cells lack.

3. Correct answer: C

Explanation:
During the relative refractory period (late Phase 3), some fast sodium channels begin to recover from inactivation. Because not all channels have reset, a stronger-than-normal stimulus is required to reach threshold. This partial recovery explains why re-excitation is possible but more difficult.

4. Correct answer: B

Explanation:
The plateau phase prolongs the action potential, which in turn prolongs the refractory period. If Phase 2 is shortened, the overall action potential duration decreases, and the refractory period shortens accordingly. Because the refractory period normally prevents premature re-excitation, shortening it increases the possibility of re-stimulation before full relaxation.

5. Correct answer: A

Explanation:
Phase 3 repolarisation is driven by potassium efflux. Increasing potassium permeability increases outward current, accelerating repolarisation and shortening action potential duration.

🧠 Test Yourself (Before You Move On)

Pause for a moment. No notes.

See if you can answer these in your head:

• Why does the heart not undergo tetany?
• Why is Phase 0 calcium-driven in the SA node but sodium-driven in ventricular muscle?
• What determines how quickly the SA node fires?
• Why does shortening the plateau phase increase the risk of premature re-excitation?
• What is happening at the ion channel level during the relative refractory period?

If you can explain these out loud — even imperfectly — you understand the foundations.

Not memorised, understood.
Build the physiology carefully — the clinical reasoning will follow.