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

# The SA node pacemaker potential

- Mechanism
- Exam priority: high

Cells in the sinus node slowly charge themselves up until they fire, which sets the heart rate without any nerve signal.

Updated 2026-11-01

Also called: Slow-response action potential, Funny current (If)

**See it in 3D:** [Sinoatrial (SA) node](https://durgical.com/en/anatomy/sinuatrial-node/) · [Right atrium](https://durgical.com/en/anatomy/right-atrium/) · [Vagus nerve](https://durgical.com/en/anatomy/vagus-nerve/)

## Key points

- Phase 4 slope comes from the funny current (If, HCN channels, Na⁺ in), T-type Ca²⁺ current and falling K⁺ outflow.
- The upstroke (phase 0) is carried by L-type Ca²⁺, not Na⁺: it is slow, so nodal conduction is slow.
- Sympathetic (β1, cAMP) steepens phase 4 → faster rate; vagal ACh opens K⁺ channels (IK-ACh), hyperpolarizes and flattens phase 4 → slower rate.
- Hierarchy of pacemakers: SA node ≈ 60–100/min, AV junction ≈ 40–60/min, ventricular Purkinje ≈ 20–40/min.
- Intrinsic SA rate with no autonomic input is ≈ 100/min; at rest vagal tone dominates and brings it down to 60–80/min.

## What it is

Sinoatrial (SA) node cells have no stable resting potential. During diastole they depolarize slowly (phase 4) until they reach threshold and fire a Ca²⁺-driven action potential. Because they reach threshold first, they set the rate of the whole heart; autonomic nerves change the rate by changing the slope of phase 4.

## How it works, step by step

- After repolarization the cell reaches its most negative value, about −60 mV.
- Hyperpolarization opens HCN channels; Na⁺ leaks in (funny current) and the membrane drifts upward.
- Near −50 mV T-type Ca²⁺ channels add inward current and K⁺ outflow keeps falling.
- At ≈ −40 mV L-type Ca²⁺ channels open and the cell fires a slow upstroke.
- K⁺ channels then repolarize the cell and the cycle begins again.
- Noradrenaline on β1 receptors raises cAMP, which increases If and Ca²⁺ currents: phase 4 is steeper and threshold is reached sooner.
- Acetylcholine on M2 receptors lowers cAMP and opens K⁺ channels: the cell starts more negative, the slope flattens and rate falls.

### Action potential

**Maximum diastolic potential** −60 mV **Threshold** −40 mV **Peak** +10 mV **Cycle** ≈ 700 ms (≈ 85 bpm)

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⁺
- Maximum diastolic potential
- Threshold
- ARP: absolute refractory period
- RRP: relative refractory period

Tap phase 4 to see the funny current; compare with the ventricular variant.

## Reference values

| Parameter | Value |
| --- | --- |
| Maximum diastolic potential (SA node) | ≈ −55 to −60 mV |
| Threshold (SA node) | ≈ −40 mV |
| Intrinsic SA rate (denervated heart) | ≈ 100/min |
| Resting adult heart rate | 60–100/min |

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

## Regulation

- *+* **Sympathetic nerves and adrenaline (β1)**: Steeper phase 4, faster heart rate (positive chronotropy).
- *−* **Vagus nerve (ACh on M2)**: Hyperpolarizes the cell and flattens phase 4: slower heart rate.
- *+* **Fever, hyperthyroidism**: Faster spontaneous depolarization and higher rate.
- *−* **Beta blockers, hypothermia**: Less steep phase 4 and slower rate.

## Clinical notes

- Sick sinus syndrome (and Chagas cardiomyopathy, common in Colombia) can damage the SA node, giving bradycardia and escape rhythms from lower pacemakers.
- A well-trained athlete has high vagal tone and may have a resting rate below 50/min without disease.

## Memory aid

The SA node is a leaky bucket that fills itself: sympathetic opens the tap, the vagus tilts the bucket so it takes longer to overflow.

## Test yourself

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

## Why is the upstroke of an SA node action potential slow compared with a ventricular myocyte?

It is carried by L-type Ca²⁺ channels, which open and pass current more slowly than the fast Na⁺ channels; at nodal potentials most Na⁺ channels are inactivated.

## How does vagal stimulation lower heart rate at the level of the SA node cell?

ACh on M2 receptors opens K⁺ channels (hyperpolarizing the cell) and lowers cAMP (less funny current), so phase 4 starts lower and rises more slowly.

## If the SA node fails, what rhythm and rate would you expect next?

An escape rhythm from the AV junction at about 40–60/min; if that also fails, a ventricular escape at about 20–40/min with wide QRS complexes.

## A heart transplant recipient has a resting rate near 100/min. Why?

The transplanted heart is denervated, so there is no vagal tone; the SA node beats at its intrinsic rate, which is faster than the usual resting rate.

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

## See it in 3D

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

- [Sinoatrial (SA) node](https://durgical.com/en/anatomy/sinuatrial-node/)
- [Right atrium](https://durgical.com/en/anatomy/right-atrium/)
- [Vagus nerve](https://durgical.com/en/anatomy/vagus-nerve/)

## Related topics

- [The ventricular action potential](https://durgical.com/en/physiology/the-ventricular-action-potential/)
- [The cardiac conduction system](https://durgical.com/en/physiology/the-cardiac-conduction-system/)
- [How arrhythmias arise](https://durgical.com/en/physiology/how-arrhythmias-arise/)
- [Nervous control of the circulation and the CNS ischemic response](https://durgical.com/en/physiology/nervous-control-of-the-circulation-and-the-cns-ischemic-response/)

## Related conditions

- [Atrioventricular (heart) block](https://durgical.com/en/conditions/atrioventricular-block/)
- [Chagas cardiomyopathy](https://durgical.com/en/conditions/chagas-cardiomyopathy/)

## In Pharmacology

- [Beta blockers](https://durgical.com/en/pharmacology/classes/beta-blockers/)
- [Propranolol](https://durgical.com/en/pharmacology/propranolol/)
- [Digoxin](https://durgical.com/en/pharmacology/digoxin/)

[← 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); [19.4 Cardiac Physiology](https://openstax.org/books/anatomy-and-physiology-2e/pages/19-4-cardiac-physiology) (OpenStax (Rice University), 2022); 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.

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