Sinoatrial node

Nodus sinuatrialis

Also known as: SA node, sinus node, pacemaker, node of Keith and Flack

The sinoatrial (SA) node is the heart's natural pacemaker. It is a crescent of specialised muscle cells where the superior vena cava meets the right atrium, and it depolarises spontaneously 60–100 times a minute at rest.

Overview

Resting rate60–100/min (intrinsic ≈100–110/min)

Maximum diastolic potential≈−60 mV

Threshold≈−40 mV

Length≈1–2 cm

Location and structure. The SA node lies just beneath the epicardium at the upper end of the crista terminalis, along the sulcus terminalis, close to where the SVC enters the right atrium. It is about 1–2 cm long. It consists of small, pale nodal (P) cells with few myofibrils, embedded in dense connective tissue around a central nodal artery, and it is richly supplied with autonomic nerves.

Why it leads. Its cells have the fastest intrinsic rate of spontaneous depolarisation in the heart. Each impulse it fires resets the slower pacemakers further down the conduction system before they can fire on their own (overdrive suppression).

Rate. A denervated SA node, as in a transplanted heart, fires at about 100–110/min. At rest, continuous vagal tone slows it to the familiar 60–80/min.

Location

Under the epicardium where the SVC joins the right atrium, at the upper end of the crista terminalis.

Function

Initiates each heartbeat and sets the sinus rhythm.

Integrates autonomic and hormonal inputs to adjust heart rate.

Physiology

Pacemaker potential (phase 4). After each beat the membrane potential is at its most negative, about −60 mV (the maximum diastolic potential). It then drifts upward. This drift is driven by the funny current (If) through HCN4 channels, which open when the cell repolarises, together with T-type Ca²⁺ current and a falling K⁺ conductance. Rhythmic Ca²⁺ release from the sarcoplasmic reticulum, which drives inward Na⁺/Ca²⁺ exchange current (the "calcium clock"), also contributes.

Upstroke (phase 0). At threshold, about −40 mV, L-type Ca²⁺ channels open and produce a relatively slow upstroke.

Repolarisation (phase 3). K⁺ channels open and return the membrane to about −60 mV.

Regulation

Sympathetic. Noradrenaline acts on β1 receptors and raises cAMP. This increases If and L-type Ca²⁺ current, steepens phase 4 and raises the heart rate (positive chronotropy).

Parasympathetic. Acetylcholine, released mainly by the right vagus, acts on M2 receptors. It opens K⁺ channels (IK,ACh), which hyperpolarise the cell, and lowers cAMP. Both effects flatten phase 4 and slow the rate.

Drugs. Ivabradine blocks If and slows the sinus rate without reducing contractility.

Clinical significance

Sick sinus syndrome

Sick sinus syndrome is dysfunction of the SA node, usually from age-related fibrosis. It causes sinus bradycardia, pauses or arrest, often alternating with atrial tachyarrhythmias (tachy–brady syndrome). Symptoms include dizziness and syncope, and treatment is a permanent pacemaker.

Sinus arrhythmia

In sinus arrhythmia, heart rate rises on inspiration and falls on expiration through respiratory changes in vagal tone. It is normal, and most marked in children and young adults.

Test yourself

The upstroke (phase 0) of the sinoatrial node action potential is carried mainly by:

Fast voltage-gated Na⁺ channels
L-type Ca²⁺ channels
Delayed-rectifier K⁺ channels
HCN ("funny") channels

Answer: L-type Ca²⁺ channels

In nodal cells the fast Na⁺ channels are inactivated at the low resting potential, so the upstroke depends on L-type Ca²⁺ current and is slow. HCN channels (If) carry the slow diastolic depolarisation of phase 4, not the upstroke.