Sinoatrial node

From Wikipedia, the free encyclopedia
Jump to: navigation, search
Sinoatrial node
Reizleitungssystem 1.png
Image showing the conduction system of the heart. The SA node is labelled 1.
System Electrical conduction system of the heart
Artery Sinoatrial nodal artery
Latin nodus sinuatrialis
Acronym(s) SAN; SA node
MeSH A07.541.409.819
TA A12.1.06.003
FMA 9477
Anatomical terminology

The sinoatrial node (often abbreviated SAN; also commonly called the sinus node and less commonly the sinuatrial node) is the normal natural pacemaker of the heart and is responsible for the initiation of the cardiac cycle (heartbeat). It spontaneously generates an electrical impulse, which after conducting throughout the heart, causes the heart muscle to contract.

The sinoatrial node is located in the myocardial wall near where the sinus venarum joins the right atrium; hence sino- + atrial.[1]

The heart rate, usually generated from the electrical impulses generated in the sinoatrial node, is influenced by nerves affecting the node.



The SA node is in the wall of the right atrium just lateral to the sinus venosus at the junction where the superior vena cava enters the right atrium.[1] The SA node is located in the myocardium just internally to the epicardium. Its inner aspect abuts heart muscle cells belonging to the right atrium, while its outer aspect is covered by fat tissue. It is an elongated structure extending between 1 and 2 cm on the right from the crista terminalis the crest of the right atrial appendage, and runs posteroinferiorly into the upper part of the terminal groove.


Low magnification stained image of the SA node (center-right on image) and its surrounding tissue. The SA node surrounds the sinoatrial nodal artery, seen as the open lumen. Cardiac muscle cells of the right atrium can be seen to the left of the node, and fat tissue to the right.

SA node fibres are specialized heart muscle cells that vaguely resemble normal, contractile heart muscle cells; however, although they possess some contractile filaments they do not contract as strongly. Additionally, SA node fibers are thinner, more tortuous and stain less intensely.

Nerve supply[edit]

The SA node has a rich nerve supply, receiving parasympathetic supply from the vagus nerve and sympathetic supply from the T1-4 spinal nerves. Nerve signals sent through the nerves have opposing effects.

Stimulation of the vagus nerves cause a decrease in the SA node rate, decreasing the heart rate. The parasympathetic nervous system, through the action of vagus nerve, exerts a negative inotropic effect upon the heart.[2] Stimulation sympathetic fibers of the spinal nerves causes an increase in the SA node rate, increasing the heart rate and force of contraction. Sympathetic fibers can increase the force of contraction because in addition to innervating the SA and AV nodes, they innervate the atria and ventricles themselves.[citation needed]

Blood supply[edit]

The SA node receives blood supply from the SA node artery. Anatomical dissection studies have shown that this supply may be a branch of the right coronary artery in the majority (about 60-70%) of hearts, and a branch of the left coronary artery (usually the left circumflex artery) in about 20-30% of hearts.[3] Rarer variants may include blood supply from both right and left coronary arteries or two branches of the right coronary artery.[4]


Conduction system of the heart, showing the sinoatrial node at the top left


Although some of the heart's cells have the ability to generate the electrical impulses (or action potentials) that trigger cardiac contraction, the sinoatrial node normally initiates it, simply because it generates impulses slightly faster than the other areas with pacemaker potential. Heart muscle cells, like all muscle cells, have refractory periods following contraction during which additional contractions cannot be triggered. Hence, although they may be capable of generating a rhythm, their pacemaker potential is overridden by the faster sinoatrial or atrioventricular nodes.

In the absence of nerve or hormonal influences, cells in the SA node will naturally generate a heartrate of more than 100 beats/minute.[5] Under the influence of the parasympathetic nervous system, that rate is slowed down to about 70 - 75 beats per minute [5] Because the sinoatrial node is responsible for the rest of the heart's electrical activity, it is sometimes called the primary pacemaker of the heart.

Impulses generated from the node are transmitted through the electrical conduction system of the heart to heart muscle cells.

Clinical significance[edit]

Sinus node dysfunction describes an irregular heartbeat caused by faulty electrical signals of the heart. When the heart's sinoatrial node is defective, the heart’s rhythms become abnormal – typically too slow or exhibiting pauses in its function or a combination, and very rarely faster than normal.[6]

Blockage of the arterial blood supply to the SA node (most commonly due to a myocardial infarction or progressive coronary artery disease) can therefore cause ischaemia and cell death in the SA node. This can disrupt the electrical pacemaker function of the SA node, and can result in sick sinus syndrome.

If the SA node does not function, or the impulse generated in the SA node is blocked before it travels down the electrical conduction system, a group of cells further down the heart will become its pacemaker.[7]


The sinoatrial node was first discovered by a young medical student, Martin Flack, in the heart of a mole, whilst his mentor, Sir Arthur Keith, was on a bicycle ride with his wife. They made the discovery in a makeshift laboratory set up in a picturesque farmhouse in Kent, England, called Mann's Place. Their discovery was published in 1907.[8][9]

Additional images[edit]

See also[edit]

This article uses anatomical terminology; for an overview, see Anatomical terminology.


  1. ^ a b Elsevier, Dorland's Illustrated Medical Dictionary, Elsevier. 
  2. ^ Lewis, M. E.; Al-Khalidi, A. H.; Bonser, R. S.; Clutton-Brock, T.; Morton, D.; Paterson, D.; Townend, J. N.; Coote, J. H. (2001). "Vagus nerve stimulation decreases left ventricular contractilityin vivoin the human and pig heart". The Journal of Physiology. 534 (2): 547–52. doi:10.1111/j.1469-7793.2001.00547.x. PMC 2278718Freely accessible. PMID 11454971. 
  3. ^ Pejković, B.; Krajnc, I.; Anderhuber, F.; Kosutić, D. (2008). "Anatomical aspects of the arterial blood supply to the sinoatrial and atrioventricular nodes of the human heart". The Journal of international medical research. 36 (4): 691–698. doi:10.1177/147323000803600410. PMID 18652764. 
  4. ^ Onciu, M.; Tuţă, L. A.; Baz, R.; Leonte, T. (2006). "Specifics of the blood supply of the sinoatrial node". Revista medico-chirurgicala a Societatii de Medici si Naturalisti din Iasi. 110 (3): 667–673. PMID 17571564. 
  5. ^ a b [ AnatomySAnode
  6. ^ Sinus node dysfunction Mount Sinai Hospital, New York
  7. ^ Junctional Rhythm at eMedicine
  8. ^ Silverman, M.E.; Hollman, A. (1 October 2007). "Discovery of the sinus node by Keith and Flack: on the centennial of their 1907 publication". Heart (journal). 93 (10): 1184–1187. doi:10.1136/hrt.2006.105049. PMC 2000948Freely accessible. PMID 17890694. 
  9. ^ Boyett MR, Dobrzynski H (June 2007). "The sinoatrial node is still setting the pace 100 years after its discovery". Circ. Res. 100 (11): 1543–5. doi:10.1161/CIRCRESAHA.107.101101. PMID 17556667. 

External links[edit]