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Atrioventricular node
Isolated Heart conduction system showing AV node
Latin nodus atrioventricularis
Gray's subject #
System
MeSH [1]
Heart; conduction system

The atrioventricular node (abbreviated AV node) is a part of the electrical control system of the heart that coordinates heart rate. It electrically connects atrial and ventricular chambers.[1] The AV node is an area of specialized tissue between the atria and the ventricles of the heart, specifically in the posteroinferior region of the interatrial septum near the opening of the coronary sinus, which conducts the normal electrical impulse from the atria to the ventricles. The AV node is quite compact (~1 x 3 x 5 mm).[2] It is located at the center of Koch's Triangle—a triangle enclosed by the septal leaflet of the tricuspid valve, the coronary sinus, and the membraneous part of the interatrial septum.[3]

The AV node may also be (rarely) referred to as the Aschoff-Tawara node named so after Ludwig Aschoff and Sunao Tawara.[4]

FunctionEdit

Contraction of myocytes (heart muscle cells) requires depolarization and repolarization of their cell membranes. Movement of ions across cell membranes causes these events. The cardiac conduction system (and AV node part of it) coordinates myocyte mechanical activity. A wave of excitation spreads out from the sinoatrial node through the atria along specialized conduction channels. This activates the AV node.[1] The atrioventricular node delays impulses by approximately 0.12s. This delay in the cardiac pulse is extremely important: It ensures that the atria have ejected their blood into the ventricles first before the ventricles contract.[5] This also protects the ventricles from excessively fast rate response to atrial arrhythmias (see below).[6]

The AV node receives two inputs from the atria: posteriorly, via the crista terminalis, and anteriorly, via the interatrial septum.[7]

AV conduction during normal cardiac rhythm occurs through two different pathways:

  • the first “pathway” has a slow conduction velocity but shorter refractory period
  • the second “pathway” has a faster conduction velocity but longer refractory period.[8]

An important property that is unique to the AV node is decremental conduction,[9] in which the more frequently the node is stimulated the slower it conducts. This is the property of the AV node that prevents rapid conduction to the ventricle in cases of rapid atrial rhythms, such as atrial fibrillation or atrial flutter.

The AV node's normal intrinsic firing rate without stimulation (like from the SA node) is 40-60 times/minute.[10]

Blood supplyEdit

The blood supply can vary.[11]

  • In the remainder of individuals, the AV node is still supplied by the posterior interventricular artery, but that artery is a branch of the left circumflex artery; the coronary circulation of these individuals is considered left-dominant.

DisordersEdit

DevelopmentEdit

BMP (Bone morphogenetic protein) cell signaling plays a key role in diverse aspects of cardiac differentiation and morphogenesis. (BMPs) are multifunctional signaling molecules critical for the development of AV node. BMP influences AV node development through Alk3 receptor (Activin receptor-like kinase 3). Abnormalities seen in BMP and Alk3 are associated with some cardiovascular diseases like Ebstein’s anomaly and AV conduction disease.[14]

See alsoEdit

ReferencesEdit

  1. 1.0 1.1 Gray, Huon H.; Keith D. Dawkins, Iain A. Simpson and John M. Morgan (2002). Lecture Notes on Cardiology, Boston: Blackwell Science.
  2. Full Size Picture triangle of-Koch.jpg. Retrieved on 2008-12-22
  3. Harrison's Principles of Internal Medicine, 17e” Section 3: Disorders of Rhythm
  4. Who Named It synd/454
  5. Campbell, N., & Reece, J. (2002). Biology. 6th ed. San Francisco: Benjamin CummingsTemplate:Page needed
  6. Gray, Huon H.; Keith D. Dawkins, Iain A. Simpson and John M. Morgan (2002). Lecture Notes on Cardiology, Boston: Blackwell Science.
  7. Fuster V, Rydén LE, Asinger RW, et al. (October 2001). ACC/AHA/ESC guidelines for the management of patients with atrial fibrillation. Journal of the American College of Cardiology 38 (4): 1231–66.
  8. 8.0 8.1 Gray, Huon H.; Keith D. Dawkins, Iain A. Simpson and John M. Morgan (2002). Lecture Notes on Cardiology, Boston: Blackwell Science.
  9. Patterson E, Scherlag BJ (October 2002). Decremental conduction in the posterior and anterior AV nodal inputs. Journal of Interventional Cardiac Electrophysiology 7 (2): 137–48.
  10. Guyton, Arthur C.; John E. Hall (2006). Textbook of Medical Physiology, 11, Philadelphia: Elsevier Saunders.
  11. Van der Hauwaert LG, Stroobandt R, Verhaeghe L (October 1972). Arterial blood supply of the atrioventricular node and main bundle. British Heart Journal 34 (10): 1045–51.
  12. Benson DW (October 2004). Genetics of atrioventricular conduction disease in humans. The Anatomical Record. Part A: Discoveries in Molecular, Cellular, and Evolutionary Biology 280 (2): 934–9.
  13. Sharma G, Linden MD, Schultz DS, Inamdar KV (January 2009). Cystic tumor of the atrioventricular node: an unexpected finding in an explanted heart. Cardiovascular Pathology : the Official Journal of the Society for Cardiovascular Pathology 19 (3): e75–8.
  14. Stroud DM, Gaussin V, Burch JB, et al. (November 2007). Abnormal conduction and morphology in the atrioventricular node of mice with atrioventricular canal targeted deletion of Alk3/Bmpr1a receptor. Circulation 116 (22): 2535–43.

External linksEdit



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