[Durgical](https://durgical.com/en/) › [DurgiPedia](https://durgical.com/en/durgipedia/) › [Physiology](https://durgical.com/en/physiology/) › [Cardiovascular](https://durgical.com/en/physiology/#s-cardio) › The ventricular action potential

[Physiology](https://durgical.com/en/physiology/) · [Cardiovascular](https://durgical.com/en/physiology/#s-cardio)

# 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](https://durgical.com/en/anatomy/left-ventricle/) · [Right ventricle](https://durgical.com/en/anatomy/right-ventricle/)

## Key points

- Phase 0 = fast Na⁺ influx; phase 1 = transient K⁺ outflow (Ito); phase 2 plateau = L-type Ca²⁺ in balanced by K⁺ out; phase 3 = delayed rectifier K⁺ out; phase 4 = stable rest near −90 mV (IK1).
- The long effective refractory period lasts almost as long as the contraction, so cardiac muscle cannot summate into tetanus.
- Class I antiarrhythmics block phase 0 Na⁺ channels; class III prolong phase 3 (longer QT); class IV act on L-type Ca²⁺ mainly in nodal tissue.
- Hyperkalemia makes the resting potential less negative, inactivating Na⁺ channels: slower upstroke, wide QRS, and risk of arrest.
- On the ECG, QRS ≈ phase 0 across the ventricles and the T wave ≈ phase 3; the QT interval tracks action potential duration.

## 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 mV **Threshold** −70 mV **Peak** +25 mV **Duration** ≈ 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.

## Memory aid

Think of the beat as a sprint, a long hold and a walk home: sodium sprints in, calcium holds the plateau, potassium walks the cell back to rest.

## 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.

[Add to my cards (4)](https://durgical.app/estudiar/?add=/en/physiology/the-ventricular-action-potential/)

## See it in 3D

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

- [Left ventricle](https://durgical.com/en/anatomy/left-ventricle/)
- [Right ventricle](https://durgical.com/en/anatomy/right-ventricle/)

## Related topics

- [The SA node pacemaker potential](https://durgical.com/en/physiology/the-sa-node-pacemaker-potential/)
- [Cardiac excitation–contraction coupling](https://durgical.com/en/physiology/cardiac-excitation-contraction-coupling/)
- [ECG basics: waves, intervals and leads](https://durgical.com/en/physiology/ecg-basics-waves-intervals-and-leads/)
- [How arrhythmias arise](https://durgical.com/en/physiology/how-arrhythmias-arise/)
- [The ECG in potassium and calcium disorders](https://durgical.com/en/physiology/the-ecg-in-potassium-and-calcium-disorders/)

## Related conditions

- [Atrioventricular (heart) block](https://durgical.com/en/conditions/atrioventricular-block/)
- [Hyperkalaemia](https://durgical.com/en/conditions/hyperkalaemia/)

## In Pharmacology

- [Lidocaine](https://durgical.com/en/pharmacology/lidocaine/)
- [Beta blockers](https://durgical.com/en/pharmacology/classes/beta-blockers/)

[← All of physiology](https://durgical.com/en/physiology/)

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](https://openstax.org/books/anatomy-and-physiology-2e/pages/19-2-cardiac-muscle-and-electrical-activity) (OpenStax (Rice University), 2022); [Atrioventricular Block](https://www.ncbi.nlm.nih.gov/books/NBK459147/) (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).

## **Spotted a mistake?** We are always improving for the community. Tell us what is wrong and our team will review it. Report a mistake

Representative model, for educational purposes only.

---
Source: https://durgical.com/en/physiology/the-ventricular-action-potential/
License: CC BY 4.0 (https://creativecommons.org/licenses/by/4.0/). Cite as: DurgiPedia (durgical.com), https://durgical.com/en/physiology/the-ventricular-action-potential/