# Cardiac Muscle Electrophysiology

> Cardiac muscle electrophysiology in MBBS Physiology: ventricular and pacemaker action potential phases, conduction velocities and refractory periods.

- Canonical URL: https://prepelephant.com/topics/mbbs/physiology/cardiac-muscle-electrophysiology
- Exam / course: MBBS · Subject: Physiology
- Publisher: PrepElephant (https://prepelephant.com) — Prepared and reviewed by the PrepElephant Academic Review Team
- First published: 2026-10-02
- Last updated: 2026-10-02
- How to cite: "Cardiac Muscle Electrophysiology", PrepElephant, https://prepelephant.com/topics/mbbs/physiology/cardiac-muscle-electrophysiology

## Direct answer

Ventricular muscle action potentials have five phases: rapid upstroke (phase 0, fast sodium current), brief early repolarisation (phase 1, transient outward potassium), the long plateau (phase 2, inward L-type calcium balancing outward potassium — the feature that makes cardiac muscle twitch-like and tetany-proof), repolarisation (phase 3, potassium efflux), and a stable resting potential near −85 mV (phase 4). Pacemaker cells of the sinoatrial node instead have no stable rest: the funny current (If, sodium inflow) plus T-type calcium depolarises phase 4 towards a threshold near −40 mV, and the upstroke is carried by L-type calcium, making them slow-response fibres. Conduction is fastest in Purkinje fibres (about 4 m/s) and slowest at the atrioventricular node (about 0.05 m/s), the delay that lets the ventricles fill.

## What you must remember

- **Phase 2 is the signature:** the plateau lasts 200-300 ms (whole action potential about 250-300 ms versus 1-2 ms in nerve), from slow calcium influx — the reason systole has length and summation cannot occur.
- **Effective refractory period:** lasts nearly to phase 3's end because sodium channels stay inactivated until repolarisation; no tetanus is possible in cardiac muscle — contrast skeletal muscle, where short refractoriness permits tetanic fusion.
- **Pacemaker physiology:** maximum diastolic potential about −55 to −60 mV, threshold −40 mV; If (hyperpolarisation-activated sodium current) gives the slow diastolic depolarisation; slope determines rate — sympathetic (via noradrenaline-cAMP) steepens it, vagal acetylcholine flattens it and hyperpolarises via potassium.
- **AV node delay:** about 0.1 second in the node (conduction 0.05 m/s against Purkinje's 4 m/s), allowing atrial systole to complete ventricular filling — the PR segment's physiologic content.
- **Conduction hierarchy (rates):** Purkinje 4 m/s, ventricular muscle 0.5 m/s, atrial muscle 0.3-0.5 m/s, SA node and AV node 0.05 m/s.
- **Excitation-contraction coupling:** L-type calcium entry triggers calcium-induced calcium release from the sarcoplasmic reticulum (ryanodine receptors) — the external trigger is small, the internal release large; digoxin works by loading this system via sodium-calcium exchange.
- **Rate-dependent phenomena:** the Bowditch effect (positive staircase) — faster stimulation raises intracellular calcium and contractility; post-extrasystolic potentiation is its clinical echo.
- **ECG anchors:** QT interval approximates ventricular action potential duration (prolonged by hypocalcaemia, class III antiarrhythmics, congenital channelopathies — risk of torsades de pointes); hyperkalaemia tallens T waves and eventually abolishes P waves.

## How to work through an arrhythmia mechanism

Frame every arrhythmia as a disorder of impulse generation, conduction, or both. A patient on amiodarone (class III, potassium-channel block) develops marked QT prolongation and episodic polymorphic ventricular tachycardia with twisting axes — torsades de pointes: prolonged repolarisation allows early afterdepolarisations (phase 2-3 calcium re-entry through reopened L-type channels) that fire triggered activity. Treatment physiology: intravenous magnesium suppresses the triggered beats, and correcting bradycardia and potassium shortens the plateau.

Contrast re-entry, the mechanism of most common tachyarrhythmias: a unidirectional block plus slow conduction lets an impulse circle back and re-excite tissue that has recovered — which is why an accessory pathway (Wolff-Parkinson-White) supports atrioventricular re-entrant tachycardia, and why ischaemic scar (slow, heterogeneous conduction) hosts ventricular tachycardia. Adenosine terminates AV-nodal re-entry by transiently shutting the node's calcium-dependent conduction; ablation deletes the anatomical loop. Finally, complete heart block: the slowest reliable escape (Purkinje, 25-40 per minute versus the SA node's 60-100 and the AV junction's 40-60) is why symptomatic third-degree block gets a pacemaker — the hierarchy of automaticity written as therapeutics.

## Where students slip

Students apply nerve physiology to the heart and lose marks: there is no stable resting potential in nodal tissue, no fast sodium current there (calcium-channel blockers therefore slow the node, and they also shorten the plateau and depress contractility), and the long refractory period is functional, not an accident — it guarantees the ventricle relaxes and refills between beats. The second slip is conduction velocity ordering: candidates invert AV node and Purkinje values; anchor them with the functions — the gate must be slow (filling time), the wiring must be fast (synchronous contraction). In viva, the classic question is why skeletal muscle tetanises but cardiac muscle cannot: inactivate sodium channels for 250 ms and every stimulus during that window is wasted — the heart's protection against fuse-contracture and its own coronary perfusion, which happens in diastole.

## Frequently asked questions

### What currents create the ventricular plateau?

Phase 2 balance of inward L-type calcium against outward potassium (IKr and IKs), sustained for 200-300 ms — lengthening contraction and preventing tetanus.

### Why is the sinoatrial node the dominant pacemaker?

Its phase 4 diastolic depolarisation (If plus T-type calcium) reaches threshold fastest, about 60-100 times per minute, overdriving slower latent pacemakers which fire only when the SA node fails.

### How do sympathetic and vagal stimulation change heart rate?

Sympathetic noradrenaline raises cAMP, steepening the slope of pacemaker depolarisation (faster rate); vagal acetylcholine opens potassium channels, hyperpolarising and flattening the slope (slower rate, even brief arrest with strong stimulation).

### What is the function of slow AV nodal conduction?

The 0.1-second delay lets atrial systole finish ventricular filling before ventricular activation, and protects the ventricle from excessively rapid atrial rates as in atrial fibrillation.

### Why can torsades de pointes occur with a prolonged QT interval?

Prolonged repolarisation permits early afterdepolarisations — afterdepolarisation-triggered beats during phase 2-3 — that initiate polymorphic ventricular tachycardia, classically with potassium-channel-blocking drugs and hypokalaemia.