Editing Sinoatrial node

{{Short description|Group of cells located in the wall of the right atrium of the heart}}
{{Use dmy dates|date=April 2017}}
{{Infobox anatomy
| Name        = Sinoatrial node
| Latin       = nodus sinuatrialis
| Image       = Reizleitungssystem 1.png
| Caption     = Sinoatrial node shown at 1. The rest of [[Electrical conduction system of the heart|the conduction system of the heart]] is shown in blue.
| Width       =
| Precursor   =
| System      = [[Electrical conduction system of the heart]]
| acronym     = SA node
| Artery      = [[Sinoatrial nodal artery]]
| Vein        =
| Nerve       =
| Lymph       =
}}
The '''sinoatrial node''' (also known as the '''sinuatrial node''', '''SA node''', '''sinus node''' or '''Keith–Flack node''') is an [[ellipse|oval shaped]] region of special [[cardiac muscle]] in the upper back wall of the [[right atrium]] made up of [[Cell (biology)|cells]] known as [[pacemaker cell]]s. The sinus node is approximately 15 [[millimetre|mm]] long, 3 mm wide, and 1 mm thick, located directly below and to the side of the [[superior vena cava]].<ref name="Hall">{{cite book |last1=Hall |first1=John E. |title=Guyton and Hall textbook of medical physiology |date=2011 |location=Philadelphia, Pa. |isbn=9781416045748 |page=115 |edition=Twelfth}}</ref>

These cells produce an [[Action potential|electrical impulse]] known as a [[cardiac action potential]] that travels through the [[electrical conduction system of the heart]], causing it to [[muscle contraction|contract]]. In a healthy heart, the SA node continuously produces action potentials, setting the rhythm of the heart ([[sinus rhythm]]), and so is known as the heart's [[cardiac pacemaker|natural pacemaker]]. The rate of action potentials produced (and therefore the [[heart rate]]) is influenced by the [[nerves]] that supply it.<ref name=Monfredi>{{cite journal | last1 = Monfredi | first1 = O. | last2 = Dobrzynski | first2 = H. | last3 = Mondal | first3 = T. | last4 = Boyett | first4 = M.R. | last5 = Morris | first5 = G.M. | year = 2010 | title = The anatomy and physiology of the Sinoatrial Node-A contemporary review | journal = Pacing and Clinical Electrophysiology  | volume = 33 | issue = 11| pages = 1392–1406 | doi = 10.1111/j.1540-8159.2010.02838.x | pmid = 20946278 | s2cid = 22207608 }}</ref>

==Structure==
The sinoatrial node is an [[Ellipse|oval-shaped]] structure that is approximately 15&nbsp;[[millimetre|mm]] long, 3&nbsp;mm wide, and 1&nbsp;mm thick, located directly below and to the side of the [[superior vena cava]].<ref name="Hall">{{cite book |last1=Hall |first1=John E. |title=Guyton and Hall textbook of medical physiology |date=2011 |location=Philadelphia, Pa. |isbn=9781416045748 |page=115 |edition=Twelfth}}</ref> The size can vary but is usually between 10-30&nbsp;mm long, 5–7&nbsp;mm wide, and 1–2&nbsp;mm deep.<ref>{{Cite journal|last1=Csepe|first1=Thomas A.|last2=Zhao|first2=Jichao|last3=Hansen|first3=Brian J.|last4=Li|first4=Ning|last5=Sul|first5=Lidiya V.|last6=Lim|first6=Praise|last7=Wang|first7=Yufeng|last8=Simonetti|first8=Orlando P.|last9=Kilic|first9=Ahmet|date=2017-03-01|title=Human Sinoatrial Node Structure: 3D Microanatomy of Sinoatrial Conduction Pathways|journal=Progress in Biophysics and Molecular Biology|volume=120|issue=1–3|pages=164–178|doi=10.1016/j.pbiomolbio.2015.12.011|issn=0079-6107|pmc=4808362|pmid=26743207}}</ref><ref>{{cite journal | last1 = Chandler | first1 = N. | last2 = Aslanidi | first2 = O. | last3 = Buckley | first3 = D. | last4 = Inada | first4 = S. | last5 = Birchall | first5 = S. | last6 = Atkinson | first6 = A. | last7 = Kirk | first7 = D. | last8 = Monfredi | first8 = O. | last9 = Molenaar | first9 = P. | last10 = Anderson | first10 = R. | last11 = Sharma | first11 = V. | last12 = Sigg | first12 = D. | last13 = Zhang | first13 = H. | last14 = Boyett | first14 = M. | last15 = Dobrzynski | first15 = H. | year = 2011 | title = Computer three-dimensional anatomical recon-struction of the human sinus node and a novel paranodal area | journal = Anatomical Record | volume = 294 | issue = 6| pages = 970–9 | doi=10.1002/ar.21379| pmid = 21538926 | doi-access =  | s2cid = 45464625 }}</ref>

===Location===
The SA node is located in the wall ([[epicardium]]) of the [[atrium (heart)|right atrium]], laterally to the entrance of the [[superior vena cava]] in a region called the [[sinus venosus|sinus venarum]] (hence ''[[wikt:sino-#Prefix|sino-]]'' + ''[[wikt:atrial#Adjective|atrial]])''.<ref name="Dorlands">{{Citation |author=Elsevier |author-link=Elsevier |title=Dorland's Illustrated Medical Dictionary |publisher=Elsevier |url=http://dorlands.com/ |postscript=.}}</ref> It is positioned roughly between a groove called the [[crista terminalis]] located on the internal surface of the [[heart]] and the corresponding [[terminal sulcus (heart)|sulcus terminalis]], on the external surface.<ref name=Monfredi/> These grooves run between the entrance of the [[superior vena cava]] and the [[inferior vena cava]].{{cn|date=May 2025}}

===Microanatomy===
[[File:Sinoatrial node 2 low mag.jpg|thumb|Figure 2: Low magnification [[H&E stain|stained]] [[histology|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 (anatomy)|lumen]]. Cardiac muscle cells of the right atrium can be seen to the left of the node, and fat tissue to the right.]]
The cells of the SA node are spread out within a mesh of [[connective tissue]], containing [[nerves]], [[blood vessels]], [[collagen]] and [[fat]]. Immediately surrounding the SA node cells are paranodal cells.<ref name=Monfredi/> These cells have structures intermediate between that of the SA node cells and the rest of the [[atrium (heart)|atrium]].<ref>{{cite journal | last1 = Chandler | first1 = NJ | last2 = Greener | first2 = ID | last3 = Tellez | first3 = JO | last4 = Inada | first4 = S | last5 = Musa | first5 = H | last6 = Molenaar | first6 = P | last7 = Difrancesco | first7 = D | display-authors = etal | year = 2009 | title = Molecular architecture of the human sinus node: Insights into the function of the cardiac pacemaker | journal = Circulation | volume = 119 | issue = 12| pages = 1562–1575 | doi=10.1161/circulationaha.108.804369| pmid = 19289639 | doi-access = free }}</ref> The connective tissue, along with the paranodal cells, insulate the SA node from the rest of the atrium, preventing the electrical activity of the atrial cells from affecting the SA node cells.<ref name=Monfredi/> The SA node cells are smaller and paler than the surrounding [[atrium (heart)|atrial cells]], with the average cell being around 8 micrometers in diameter and 20-30&nbsp;micrometers in length (1 micrometer= 0.000001 meter).<ref>{{cite journal | last1 = Honjo | first1 = H. | last2 = Boyett | first2 = M.R. | last3 = Kodama | first3 = I. | last4 = Toyama | first4 = J. | year = 1996 | title = Correlation between electrical activity and the size of rabbit sino-atrial node cells | journal = The Journal of Physiology | volume = 496 | issue = 3| pages = 795–808 | doi = 10.1113/jphysiol.1996.sp021728 | pmid = 8930845 | pmc = 1160865 }}</ref> Unlike the atrial cells, SA node cells contain fewer [[mitochondrion|mitochondria]] and [[myofibers]], as well as a smaller [[sarcoplasmic reticulum]]. This means that the SA node cells are less equipped to contract compared to the [[atrium (heart)|atrial]] and [[ventricle (heart)|ventricular]] cells.<ref name=Boyett>{{cite journal | last1 = Boyett | first1 = Honjo | last2 = Kodama | first2 = I. | year = 2000 | title = The sinoatrial node, a heterogeneous pace-maker structure | journal = Cardiovascular Research | volume = 47 | issue = 4| pages = 658–87 | doi=10.1016/s0008-6363(00)00135-8| pmid = 10974216 | doi-access = free }}</ref>

Action potentials pass from one [[heart|cardiac cell]] to the next through pores known as gap junctions. These gap junctions are made of proteins called [[connexin]]s. There are fewer gap junctions within the SA node and they are smaller in size. This is again important in insulating the SA node from the surrounding atrial cells.<ref name=Monfredi/><ref name=Boyett/>

===Blood supply===
The sinoatrial node receives its blood supply from the [[sinoatrial nodal artery]]. This blood supply, however, can differ hugely between individuals. For example, in most humans, this is a single [[artery]], although in some cases there have been either 2 or 3 sinoatrial node arteries supplying the SA node. Also, the SA node artery mainly originates as a branch of the [[right coronary artery]]; however in some individuals it has arisen from the [[Circumflex branch of left coronary artery|circumflex artery]], which is a branch of the [[left coronary artery]]. Finally, the SA node artery commonly passes behind the [[superior vena cava]], before reaching the SA node; however in some instances it passes in front. Despite these many differences, there doesn't appear to be any advantage to how many sinoatrial nodal arteries an individual has, or where they originate.<ref>{{cite journal | last1 = Vikse | first1 = J. | last2 = Henry | first2 = B.M. | last3 = Roy | first3 = J. | last4 = Ramakrishnan | first4 = P.K. | last5 = Hsieh | first5 = W.C. | last6 = Walocha | first6 = J.A. | last7 = Tomaszewski | first7 = K.A. | year = 2016b | title = Anatomical variations in the Sinoatrial Nodal artery: A Meta-Analysis and clinical considerations | journal = PLOS ONE | volume = 11 | issue = 2| page = e0148331 | doi = 10.1371/journal.pone.0148331 | pmid = 26849441 | pmc = 4743947 | bibcode = 2016PLoSO..1148331V | doi-access = free }}</ref>

===Venous drainage===
There are no large [[veins]] that drain blood away from the SA node.  Instead, smaller [[venule]]s drain the blood directly into the [[atrium (heart)|right atrium]].<ref>{{cite journal | last1 = Anderson | first1 = K.R. | last2 = Ho | first2 = S.Y. | last3 = Anderson | first3 = R.H. | year = 1979 | title = Location and vascular supply of sinus node in human heart | journal = Heart | volume = 41 | issue = 1| pages = 28–32 | doi = 10.1136/hrt.41.1.28 | pmid = 426954 | pmc = 514694 }}</ref>

==Function==
===Pacemaking===
{{See also|Cardiac pacemaker}}
The main role of a sinoatrial node cell is to initiate action potentials of the heart that can pass through [[cardiac muscle cell]]s and cause contraction. An action potential is a rapid  change in [[membrane potential]], produced by the movement of charged atoms ([[ions]]). In the absence of stimulation, non-pacemaker cells (including the [[Ventricle (heart)|ventricular]] and [[Atrium (heart)|atrial cells]]) have a relatively constant membrane potential; this is known as a [[resting potential]]. This resting phase (see [[cardiac action potential|cardiac action potential, phase 4]]) ends when an action potential reaches the cell. This produces a positive change in membrane potential, known as [[depolarization]], which is propagated throughout the heart and initiates [[muscle contraction]]. Pacemaker cells, however, do not have a resting potential. Instead, immediately after [[repolarization]], the membrane potential of these cells begins to depolarise again automatically, a phenomenon known as the [[pacemaker potential]]. Once the pacemaker potential reaches a set value, the [[threshold potential]], it produces an action potential.<ref name=Monfredi/> Other cells within the heart (including the [[Purkinje fibers]]<ref>{{Cite journal|last1=Tsien|first1=R. W.|last2=Carpenter|first2=D. O.|date=1978-06-01|title=Ionic mechanisms of pacemaker activity in cardiac Purkinje fibers|journal=Federation Proceedings|volume=37|issue=8|pages=2127–2131|issn=0014-9446|pmid=350631}}</ref> and [[atrioventricular node]]) can also initiate action potentials; however, they do so at a slower rate and therefore, if the SA node is functioning properly, its action potentials usually override those that would be produced by other tissues.<ref name="Vassalle1977">{{cite journal|last=Vassalle|first=M.|year=1977|title=The relationship among cardiac pacemakers: Overdrive suppression|journal=[[Circulation Research]]|volume=41|issue=3|pages=269–77|doi=10.1161/01.res.41.3.269|pmid=330018|doi-access=free}}</ref>

Outlined below are the 3 phases of a sinoatrial node action potential. In the [[cardiac action potential]], there are 5 phases (labelled 0-4), however pacemaker action potentials do not have an obvious phase 1 or 2.

'''Phase 4'''
[[File:Sinoatrial action potential.jpg|thumb|Figure 3: Sinoatrial node action potential waveform, outlining major ion currents involved (downward deflection indicates ions moving into the cell, upwards deflection indicates ions flowing out of the cell).]]
This phase is also known as the [[pacemaker potential]]. Immediately following repolarization, when the membrane potential is very negative (it is hyperpolarised), the voltage slowly begins to increase. This is initially due to the closing of [[potassium channel]]s, which reduces the flow of [[potassium]] ions (I<sub>k</sub>) out of the cell (see phase 2, below).<ref>{{cite journal | last1 = Irisawa | first1 = H | last2 = Brown | first2 = HF | last3 = Giles | first3 = W | year = 1993 | title = Cardiac pacemaking in the sinoatrial node | journal = Physiol Rev | volume = 73 | issue = 1| pages = 197–227 | doi=10.1152/physrev.1993.73.1.197| pmid = 8380502 }}</ref> Hyperpolarization also causes activation of [[HCN channel|hyperpolarisation-activated cyclic nucleotide–gated (HCN) channels]]. The activation of ion channels at very negative membrane potentials is unusual, therefore the flow of [[sodium|sodium (Na<sup>+</sup>)]] and some K<sup>+</sup> through the activated HCN channel is referred to as a ''[[funny current]]'' (I<sub>f</sub>).<ref>{{cite journal | last1 = DiFrancesco | first1 = D | year = 2010 | title = The role of the funny current in pacemaker activity | journal = Circulation Research | volume = 106 | issue = 3| pages = 434–46 | doi=10.1161/circresaha.109.208041| pmid = 20167941 | doi-access = free }}</ref> This funny current causes the membrane potential of the cell to gradually increase, as the positive charge (Na<sup>+</sup> and K<sup>+</sup>) is flowing into the cell.  Another mechanism involved in pacemaker potential is known as the [[calcium]] clock. This refers to the spontaneous release of calcium from the [[sarcoplasmic reticulum]] (a calcium store) into the cytoplasm, also known as [[calcium sparks]]. This increase in calcium within the cell then activates a [[sodium-calcium exchanger]] (NCX), which removes one Ca<sup>2+</sup> from the cell, and exchanges it for 3 Na<sup>+</sup> into the cell (therefore removing a charge of +2 from the cell, but allowing a charge of +3 to enter the cell) further increasing the membrane potential. Calcium later reenters the cell via [[SERCA]] and [[calcium channel]]s located on the cell membrane.<ref>{{cite journal | last1 = Joung | first1 = B. | last2 = Chen | first2 = P. | last3 = Lin | first3 = S. | year = 2011 | title = The role of the calcium and the voltage clocks in sinoatrial node dysfunction | journal = Yonsei Medical Journal | volume = 52 | issue = 2| pages = 211–9 | doi=10.3349/ymj.2011.52.2.211| pmid = 21319337 | pmc = 3051220 }}</ref> The increase in membrane potential produced by these mechanisms, activates [[T-type calcium channel]]s and then [[L-type calcium channels]] (which open very slowly). These channels allow a flow of Ca<sup>2+</sup> into the cell, making the membrane potential even more positive.

'''Phase 0'''

This is the depolarization phase. When the membrane potential reaches the threshold potential (around -20 to -50 mV), the cell begins to rapidly depolarise (become more positive).<ref>Verkerk, A., Borren, van, Peters, R., Broekhuis, E., Lam, K., Coronel, R., Bakker, de, Tan, H. and Wilders, R. (2007) 'Single cells isolated from human sinoatrial node: Action potentials and numerical reconstruction of pacemaker current', Conference proceedings : ... Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE Engineering in Medicine and Biology Society. Annual Conference., 2007, pp. 904–7.</ref> This is mainly due to the flow of Ca<sup>2+</sup> through L-type calcium channels, which are now fully open. During this stage, T-type calcium channels and HCN channels deactivate.

'''Phase 3'''

This phase is the repolarization phase. This occurs due to the inactivation of L-type calcium channels (preventing the movement of Ca<sup>2+</sup> into the cell) and the activation of potassium channels, which allows the flow of K<sup>+</sup> out of the cell, making the membrane potential more negative.<ref>{{cite journal | last1 = Clark | first1 = R.B. | last2 = Mangoni | first2 = M.E. | last3 = Lueger | first3 = A. | last4 = Couette | first4 = B. | last5 = Nargeot | first5 = J. | last6 = Giles | first6 = W.R. | year = 2004 | title = A rapidly activating delayed rectifier K+ current reg-ulates pacemaker activity in adult mouse sinoatrial node cells | journal = American Journal of Physiology. Heart and Circulatory Physiology| volume = 286 | issue = 5| pages = 1757–1766 | doi = 10.1152/ajpheart.00753.2003 | pmid = 14693686 | s2cid = 476037 }}</ref>

==Nerve supply==
[[Heart rate]] depends on the rate at which the sinoatrial node produces [[Cardiac action potential|action potentials]]. At rest, heart rate is between 60 and 100 beats per minute. This is a result of the activity of two sets of nerves, one acting to slow down action potential production (these are [[parasympathetic nervous system|parasympathetic nerves]]) and the other acting to speed up action potential production ([[sympathetic nervous system|sympathetic nerves]]).<ref>{{cite journal | last1 = Gordan | first1 = R. | last2 = Gwathmey | first2 = J.K. | last3 = Xie | first3 = L.-H. | year = 2015 | title = Autonomic and endocrine control of cardiovascular function | journal = World Journal of Cardiology | volume = 7 | issue = 4| pages = 204–14 | doi = 10.4330/wjc.v7.i4.204 | pmid = 25914789 | pmc = 4404375 | doi-access = free }}</ref>

Modulation of heart rate by ANS is carried by two types of channel: [[Inward-rectifier potassium channel|Kir]] and [[HCN channel|HCN]] (members of the [[Cyclic nucleotide–gated ion channel|CNG gated channels]]).

The sympathetic nerves begin in the [[Thoracic nerves|thoracic]] region of the spinal cord (in particular T1-T4). These nerves release a neurotransmitter called [[norepinephrine|noradrenaline (NA)]]. This binds to a receptor on the SA node membrane, called a [[Beta-1 adrenergic receptor|beta-1adrenoceptor]]. Binding of NA to this receptor activates a G-protein (in particular a [[Gs alpha subunit|G<sub>s</sub>-Protein]], S for stimulatory) which initiates a series of reactions (known as the [[CAMP-dependent pathway|cAMP pathway]]) that results in the production of a molecule called [[Cyclic adenosine monophosphate|cyclic adenosinemonophosphate (cAMP)]]. This cAMP binds to the HCN channel (see above). Binding of cAMP to the HCN increases the flow of Na<sup>+</sup> and K<sup>+</sup> into the cell, speeding up the pacemaker potential, so producing action potentials at a quicker rate and increasing heart rate.<ref>Larsson, P.H. (2010) 'How is the heart rate regulated in the sinoatrial node? Another piece to the puzzle', 136(3).</ref> An increase in heart rate is known as positive [[Chronotropic|chronotropy]].

The [[parasympathetic nervous system|parasympathetic nerves]] supplying the SA node (in particular the [[Vagus nerves]]) originate in the [[brain]]. These nerves release a neurotransmitter called [[Acetylcholine|acetylcholine (ACh)]]. ACh binds to a receptor called an [[muscarinic acetylcholine receptor M2|M2 muscarinic receptor]], located on the SA node membrane. Activation of this M2 receptor then activates a protein called a G-protein (in particular [[Gi alpha subunit|G<sub>i</sub> protein]], i for inhibitory). Activation of this G-protein blocks the cAMP pathway, reducing its effects, therefore inhibiting sympathetic activity and slowing action potential production. The G-protein also activates a potassium channel [[KCNJ3|GIRK-1]] and [[KCNJ5|GIRK-4]], which allows K<sup>+</sup> to flow out of the cell, making the membrane potential more negative and slowing the pacemaker potential, therefore decreasing the rate of action potential production and therefore decreasing heart rate.<ref>Osterrieder W., Noma A., Trautwein W. (1980) On the kinetics of the potassium current activated by acetylcholine in the SA node of the rabbit heart. Pflügers Arch. 386:101–109.</ref> A decrease in heart rate is known as negative [[Chronotropic|chronotropy]].

The first cell to produce the action potential in the SA node isn't always the same; this is known as pacemaker shift. In certain species of animals—for example, in dogs—a superior shift (i.e., the cell that produces the fastest action potential in the SA node is higher than previously) usually produces an increased heart rate whereas an inferior shift (i.e. the cell producing the fastest action potential within the SA node is further down than previously) produces a decreased heart rate.<ref name=Monfredi/>

==Clinical significance==
[[Sinus node dysfunction]] also known as ''sick sinus syndrome'' is a group of [[Arrhythmia|irregular heartbeat]] conditions 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.<ref>[http://www.mountsinai.org/patient-care/health-library/diseases-and-conditions/sick-sinus-syndrome Sinus node dysfunction] [[Mount Sinai Hospital, New York]]</ref>

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 [[ischemia]] and cell death in the SA node. This can disrupt the electrical pacemaker function of the SA node, and can result in sinus node dysfunction.

If the SA node does not function or the impulse generated in the [[Sinoatrial block|SA node is blocked]] before it travels down the electrical conduction system, a group of cells further down the heart will become its pacemaker.<ref>{{EMedicine|article|155146|Junctional Rhythm}}</ref>

==History==
The sinoatrial node was first discovered by a young medical student, [[Martin Flack]], in the heart of a [[Mole (animal)|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 farmhouse in [[Kent]], [[England]], called Mann's Place. Their discovery was published in 1907.<ref name=heart>{{cite journal |last1=Silverman |first1=M.E. |last2=Hollman |first2=A. |title=Discovery of the sinus node by Keith and Flack: on the centennial of their 1907 publication |journal=[[Heart (journal)|Heart]] |date=1 October 2007 |volume=93 |issue=10 |pages=1184–1187 |doi=10.1136/hrt.2006.105049 |pmc=2000948|pmid=17890694}}</ref><ref name="pmid17556667">{{cite journal |author=Boyett MR, Dobrzynski H |title=The sinoatrial node is still setting the pace 100 years after its discovery |journal=Circ. Res. |volume=100 |issue=11 |pages=1543–5 |date=June 2007 |pmid=17556667 |doi=10.1161/CIRCRESAHA.107.101101 |doi-access= |s2cid=17882001 }}</ref>

==Additional images==
<gallery>
 Image:Reizleitungssystem 1.png|Heart; conduction system (SA node labeled 1)
 Image:Gray501.png |Schematic representation of the atrioventricular bundle
</gallery>

==See also==
{{Anatomy-terms}}
* [[Cardiac pacemaker]]
* [[Cardiology]]
* [[Heart block]]
* [[Sinus bradycardia]]
* [[Sinus tachycardia]]
* [[Cardiothoracic Surgery]]

==References==
{{Reflist}}

==External links==
* {{SUNYAnatomyFigs|20|06|01}} - "The conduction system of the heart."
* [https://web.archive.org/web/20070313214609/http://user.gru.net/clawrence/vccl/chpt2/adlt46.gif Diagram at gru.net]
* {{NormanAnatomy|thoraxlesson4}} ({{NormanAnatomyFig|thoraxheartinternalner}})
* https://web.archive.org/web/20070929080346/http://www.healthyheart.nhs.uk/heart_works/heart03.shtml

{{Heart anatomy}}
{{Authority control}}

{{DEFAULTSORT:Sinoatrial Node}}
[[Category:Cardiac anatomy]]