The ventricular action potential !

Mechanism
Exam priority: high

Each ventricular muscle cell fires a long electrical signal with a plateau, so the heart squeezes fully and cannot be tetanized.

Updated 2026-11-01

Also called: Fast-response action potential, Phases 0–4

See it in 3D: Left ventricle · Right ventricle

What it is

Ventricular (and atrial and Purkinje) myocytes produce a fast-response action potential lasting about 200–300 ms. A rapid sodium upstroke is followed by a long calcium plateau, then potassium repolarization. The plateau links each beat to contraction and keeps the cell refractory until the muscle has relaxed.

How it works, step by step

At rest (phase 4) inward-rectifier K⁺ channels hold the membrane near the K⁺ equilibrium potential, about −90 mV.
Current spreading through gap junctions brings the cell to threshold (≈ −70 mV), and voltage-gated Na⁺ channels open: a steep upstroke to ≈ +20 mV (phase 0).
Na⁺ channels inactivate within milliseconds; a transient outward K⁺ current makes a small notch (phase 1).
L-type Ca²⁺ channels open; Ca²⁺ entering roughly balances K⁺ leaving, so voltage stays near 0 mV for ~200 ms (phase 2, the plateau).
The Ca²⁺ that enters triggers more Ca²⁺ release from the sarcoplasmic reticulum, which drives contraction.
Ca²⁺ channels close and delayed-rectifier K⁺ currents grow, returning the membrane to rest (phase 3).
Until about mid-phase 3 no new action potential can start (effective refractory period); a strong stimulus late in phase 3 can (relative refractory period).

Action potential

Rest −90 mVThreshold −70 mVPeak +25 mVDuration ≈ 280 ms

Tap a phase (the pills above or its band) or a refractory period (ARP, RRP) at the base of the plot.

Mainly Na⁺
Mainly K⁺
Mainly Ca²⁺
Rest
Threshold
ARP: absolute refractory period
RRP: relative refractory period

Tap each phase to see which channel is open; switch to high K⁺ to see the upstroke slow.

Reference values (adult)

Parameter	Value	Note
Resting membrane potential	≈ −85 to −90 mV
Action potential duration	≈ 200–300 ms	shorter at fast heart rates
Peak of upstroke	≈ +20 to +30 mV

Approximate values for a healthy adult at rest; each laboratory sets its own ranges.

Ventricular versus SA node action potential

Feature	Ventricular myocyte	SA node cell
Resting / diastolic potential	Stable, ≈ −90 mV	Drifts up from ≈ −60 mV (no true rest)
Upstroke current	Fast Na⁺	Slower L-type Ca²⁺
Plateau	Long (Ca²⁺ vs K⁺)	None
Conduction speed it supports	Fast	Slow
Automaticity	None normally	Yes (funny current, If)

Clinical notes

Hyperkalemia: peaked T waves first, then wide QRS and a sine-wave pattern as Na⁺ channels inactivate.
Drugs or genes that slow phase 3 lengthen the QT and allow early afterdepolarizations and torsades de pointes.

Test yourself

Think of the answer, then tap the question to see it.

Why can cardiac muscle not be tetanized like skeletal muscle?

Its effective refractory period, set by the long Ca²⁺ plateau, lasts almost until the muscle relaxes, so a second action potential cannot add onto an ongoing contraction.

Which ion current mainly creates the plateau of the ventricular action potential?

Inward Ca²⁺ through L-type channels, balanced by outward K⁺ currents; the Ca²⁺ also triggers Ca²⁺ release from the sarcoplasmic reticulum.

How does severe hyperkalemia slow conduction in the ventricles?

A less negative resting potential leaves many fast Na⁺ channels inactivated, so phase 0 is slower and smaller, conduction slows and the QRS widens.

A drug blocks delayed-rectifier K⁺ channels. What happens to the QT interval and why?

It lengthens: phase 3 repolarization is slowed, so the action potential lasts longer, which raises the risk of early afterdepolarizations and torsades.

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See it in 3D

The structures of Durgical's 3D anatomy where it happens.

In Pharmacology

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Educational physiology content; not a diagnostic or treatment guide and no substitute for a health professional's advice. Values are approximate references. No doses are given.

Sources: 19.2 Cardiac Muscle and Electrical Activity (OpenStax (Rice University), 2022); Atrioventricular Block (StatPearls (NCBI Bookshelf), 2025); Hall JE. Guyton and Hall Textbook of Medical Physiology, 13th ed. (ch. 10). Reference book used to check facts; its text and figures are not reproduced (Elsevier, 2016).

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Representative model, for educational purposes only.