Cardiac Muscle Electrophysiology
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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.