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|Low magnification micrograph of a sinoatrial node (center-right on image) and its surrounding tissue. The SA node surrounds the (sinuatrial) nodal artery (on lumen in the image), a branch of the right coronary artery, abuts cardiac myocytes (of the right atrium) on its deep aspect (left of image) and adipose tissue on its superficial (epicardial) aspect (right of image). H&E stain.|
|Isolated Heart conduction system, showing SA node|
The sinoatrial node (also commonly spelled sinuatrial node, abbreviated SA node or SAN, also called the sinus node) is the impulse-generating (pacemaker) tissue located in the right atrium of the heart, and thus the generator of normal sinus rhythm. It is a group of cells positioned on the wall of the right atrium, near the entrance of the superior vena cava. These cells are modified cardiac myocytes. Though they possess some contractile filaments, they do not contract.
It was first described in 1907 by Arthur Keith and Martin Flack.
Role as a pacemaker
Although all 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. Cardiac myocytes, like all muscle cells, have refractory periods following contraction during which additional contractions cannot be triggered; their pacemaker potential is overridden by the sinoatrial or atrioventricular nodes.
In the absence of extrinsic neural and hormonal control, cells in the SA node, situated in the upper right corner of the heart, will naturally discharge (create action potentials) at about 60-100 beats/minute. Because the sinoatrial node is responsible for the rest of the heart's electrical activity, it is sometimes called the primary pacemaker.
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 the heart's pacemaker. These cells form the atrioventricular node (AV node), which is an area between the atria and ventricles, within the atrial septum. If the AV node also fails, Purkinje fibers(or known by some as the bundle of his) are capable of acting as the pacemaker. The reason Purkinje cells do not normally control the heart rate is that they generate action potentials at a lower frequency than the AV or SA nodes.
The sinoatrial node is submyocardial at the lateral aspect of the junction of the superior vena cava and right atrium. Its deep aspect abuts cardiac myocytes belonging to the right atrium. Its superficial aspect is covered by adipose tissue. The SA node fibres vaguely resemble cardiac myocytes; however, they are measurably thinner, more tortuous and stain less intensely (on H&E) than cardiac myocytes.
The SA node is richly innervated by parasympathetic nervous system fibers (CN X: Vagus Nerve) and by sympathetic nervous system fibers (T1-4, Spinal Nerves). This unique anatomical arrangement makes the SA node susceptible to distinctly paired and opposed autonomic influences.
- Stimulation of the vagus nerves (the parasympathetic fibers) causes a decrease in the SA node rate (thereby decreasing the heart rate). Parasympathetic fibers cannot change the force of contraction, however,because they only innervate the SA node and AV node (which control heart rate only)***(NOTE: This statement is not entirely accurate. The following study: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2278718/ demonstrates how the parasympathetic nervous system, through the action of vagus nerve, exerts a negative inotropic effect upon the heart)
- Stimulation via sympathetic fibers causes an increase in the SA node rate (thereby 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.
In the majority of individuals, the SA node receives blood from the right coronary artery, meaning that a myocardial infarction occluding it will cause ischaemia in the SA node unless there is a sufficiently good anastomosis from the left coronary artery. If not, death of the affected cells will stop the SA node from triggering the heartbeat, and pacemaker function will be manifest more distal in the cardiac system (eg. AV node).
Sinus node dysfunction
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 – either too fast, too slow, or a combination.
- Cardiac pacemaker
- Electrical conduction system of the heart
- Heart block
- Sinus bradycardia
- Sinus tachycardia
- 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.
- Sinus node dysfunction Mount Sinai Hospital, New York
- Dictionary at eMedicine sinuatrial+node
- SUNY Figs 20:06-01 - "The conduction system of the heart."
- Diagram at gru.net
- Norman/Georgetown thoraxlesson4 (thoraxheartinternalner)
Anatomy of torso, cardiovascular system: heart
base • apex • grooves (coronary/atrioventricular, interatrial, anterior interventricula, posterior interventricular) • surfaces (sternocostal, diaphragmatic) • borders (right, left)
(vena cavae, coronary sinus) → right atrium (auricle, fossa ovalis, limbus of fossa ovalis, crista terminalis, valve of the inferior vena cava, valve of the coronary sinus) → tricuspid valve → right ventricle (conus arteriosus, moderator band/septomarginal trabecula) → pulmonary valve → (pulmonary artery and pulmonary circulation)
pericardium: fibrous pericardium • serous pericardium (pericardial cavity, epicardium/visceral layer) • pericardial sinus
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