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Physiology, Sinoatrial Node

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Last Update: October 3, 2022.


Martin Flack, a medical student, was the first to discover the sinoatrial (SA) node in the early 1900s. The SA (sinus) node represents a cluster of myocytes with pacemaker activity. Under normal circumstances, it generates electrical impulses that set the rhythm and rate of the heart. The mass of the sinus node is too small to create a substantial electrical signal that can be detected on the electrocardiogram (ECG). Instead, SA nodal pacemaker activity must be inferred indirectly from P waves generated by the atrial activity. Any dysfunction of the sinus node can affect the heart’s rate and rhythm. Noticing and understanding the various types of sinus node dysfunction can help with management decisions.[1][2][3]

Issues of Concern

The main function of the SA node is to act as the normal pacemaker of the heart. It initiates an action potential that results in an electrical impulse traveling through the heart’s electrical conduction system to cause myocardial contraction. Unlike atrial and ventricular cells, pacemaker cells in the sinus node do not have a resting phase. Instead, these cells have pacemaker potential, in which they begin to depolarize automatically after an action potential ends.[4][5]

Sinus node dysfunction can result from ischemia or necrosis of pacemaker cells due to a decrease in arterial blood secondary to worsening coronary artery disease or myocardial infarction. In such cases, the SA node will not function properly and can result in a condition known as sick sinus syndrome. Without normal sinus node function or blockage of the sinus node impulse, other myocytes with automaticity, or an ectopic focus, will become the new pacemaker.


The SA node, also known as the sinus node, represents a crescent-like shaped cluster of myocytes divided by connective tissue, spreading over a few square millimeters. It is located at the junction of the crista terminalis in the upper wall of the right atrium and the opening of the superior vena cava. These cells have the ability to spontaneous generate an electrical impulse. It is the integrated activity of these so-called pacemaker cells that form the SA node. This electrical impulse is then transmitted by perinodal cells, or transitional (T) cells, to the right atrium and then through the rest of the heart’s electrical conduction system, eventually resulting in myocardial contraction and blood distribution to the rest of the body. The sinus node continuously generates electrical impulses, thereby setting the normal rhythm and rate in a healthy heart. Hence, the SA node is referred to as the natural pacemaker of the heart.


The heart rate can vary quite remarkably depending on various environmental and physiologic factors. At rest, the SA nodal myocytes depolarize at an intrinsic rate between 60 and 100 beats per minute, which is generally considered a normal heart rate. The autonomic nervous system tightly controls input into the sinus node. The autonomic fibers regulate the firing of the sinus node to initiate the start of subsequent cardiac cycles and thus, influence the heart rate. Parasympathetic input slows down the rate of action potential production, thereby decreasing the heart rate; on the other hand, sympathetic input increases the rate of action potential production, thereby increasing the heart rate. This tight, regulated control of the sinus node allows the heart to adapt to various physiologic stressors placed on the body. For instance, the heart responds to the body’s increased oxygen demand during exercise, increasing sympathetic input, and increasing heart rate.

Because the sinus node is composed of multiple myocytes, the first myocyte to produce an electrical impulse is not always the same. This is referred to as the pacemaker shift. For example, one myocyte may produce an action potential that is faster than the myocyte that produced the previous action potential, which would increase the heart rate within normal limits. This is considered a superior shift. However, myocytes may also produce action potentials that are slower than the previous action potential produced. This would cause a decrease in heart rate still within normal limits and is considered an inferior shift. The shift in the origin of the SA nodal pacemaker activity appears to depend on predominant sympathetic or parasympathetic activation. With sympathetic predominance, the origin seems to emerge more superiorly within the sinus node, while with parasympathetic predominance, the origin seems to emerge more inferiorly within the sinus node.


Normal Sinus Rhythm

In normal sinus rhythm (NSR), the rhythm originates from the sinus node. The rhythm is often regular with constant P-P intervals. When the rhythm has some irregularity to it, it is known as sinus arrhythmia. In general, the normal heart rate in adults ranges between 60 and 100 beats per minute. However, normal variations do exist depending on the individual’s age and gender. Sinus rhythm with a rate above the normal range is called sinus tachycardia, and one below the normal range is called sinus bradycardia.

In NSR, the P wave is less than 120 milliseconds in duration and less than 0.15 mV to 0.25 mV in height in lead II. The permissible maximum varies based on the lead. If there is a biphasic P wave in lead V1, the terminal component should be less than 40 milliseconds in duration and 0.10 mV in depth. The P wave should also have a normal axis (0 degrees to more than 90 degrees) and constant morphology. The normal axis is indicated by P waves that are:

  1. upright in leads I, II, and often aVF
  2. Inverted in lead aVR
  3. Upright, inverted, or biphasic in leads III and aVL
  4. Upright or biphasic in leads V1 and V2
  5. Upright in leads V3 through V6.  

There are some cases of NSR in which the P wave duration and morphology may be abnormal. This usually reflects atrial disease and/or an atrial electrical conduction defect.

The normal PR interval ranges between 120 ms and 200 ms. It tends to be in the lower range of normal as the heart rate increases due to rate-related shortening of action potentials. Conversely, slower heart rates tend to increase the PR interval towards the upper range of normal. Nevertheless, the PR interval is independent of the presence or absence of sinus rhythm.

Sinus Node Dysfunction

Sinus node dysfunction is often due to either abnormality in impulses produced by the pacemaker cells or abnormality in conduction across the perinodal cells. It can be either acquired or inherited; the acquired form is more common. Patients may or may not be symptomatic.

There are several types and variations of sinus node dysfunction. Some of these include sinus pause, arrest, exit block, and arrhythmia as well as wandering atrial pacemaker (WAP). Because the mass of the sinus node is too small to create a significant electrical signal, it is not manifested directly on the ECG. Instead, SA nodal pacemaker activity must be inferred from the P waves of atrial depolarization. Hence, sinus node dysfunction is often noted with an inappropriate SA nodal response to the body’s metabolic demands and/or the absence of P waves.

Sinus Pause and Arrest

Sinus pause or arrest results when there is a problem with initiating electrical discharge from the SA node. As a result, the ECG will show a transient absence of sinus P waves. This can last for a few seconds or even several minutes. Because the sinus node stops firing and can start back up at any moment, there is often no relationship between previous P waves and those that follow (i.e., non-compensatory). Also, the sinus pause or arrest tends to permit enough time for escape beats or rhythms to follow. A sinus pause of a few seconds is not always pathologic and may, in fact, be seen in non-diseased hearts. However, if a sinus pause and arrest goes on for longer, patients can become symptomatic, experiencing lightheadedness, dizziness, presyncope, syncope, and possibly death.[6][7]

SA Nodal Exit Block

SA nodal exit block occurs when the sinus node fires, although the impulse cannot reach neighboring atrial tissue. It is believed to involve the perinodal (T) cells. Similar to sinus pause and arrest, the atria do not receive the proper signal to contract, and thus, the ECG shows an absence of P waves. There are three degrees of SA nodal exit block, first, second, and third-degree. They follow the conventional atrioventricular (AV) nodal blocks. To conceptualize these, there are three components to keep in mind: 1) a relatively constant input from the SA node, 2) an area across which the block occurs, and 3) output (i.e., the P waves). The type of SA nodal exit block can be determined by evaluating the P waves. 

  • First degree: With first-degree SA nodal exit block, there is impulse exit slowing with normal 1:1 conduction. A body surface EKG is not able to recognize this.
  • Second degree: Like second-degree AV nodal blocks, there are two types second-degree SA nodal exit blocks – type I (Wenckebach) and type II. With type I (Wenckebach), the P-P intervals progressively shorten in duration until a dropped P wave occurs. The dropped P wave results in a pause that is less than two P-P intervals in duration. While type II also has a pause from a dropped P wave, it is a multiple of the SA nodal pacemaker input. Therefore, the P-P intervals should remain constant and compensatory in nature.
  • Third-degree: With third-degree SA nodal exit block, the SA node impulse is unable to reach the right atrium. Thus, the atrial will not depolarize, and there will be no P wave. For this reason, it cannot be distinguished from sinus arrest.

Sinus Arrhythmia

Sinus arrhythmia represents small variations in the sinus cycle length. More precisely, it is defined as a variation in the P-P interval of 120 milliseconds or more in the presence of normal P waves, or a change of at least 10% between the shortest and longest P-P intervals. P wave morphology remains relatively unchanged, but there can be small variations in the PR interval. Sinus arrhythmias are more commonly seen in young individuals and those exposed to morphine or digoxin. The two predominant types are a result of normal respiration and digoxin toxicity. Therefore, unless the patient has been receiving digoxin, patients are often asymptomatic and do not require treatment.

Wandering Atrial Pacemaker

WAP is not pathologic and is often seen in young, healthy individuals. It results from a change in the dominant pacemaker focus from the sinus node to ectopic atrial foci. There must be at least three dominant ectopic atrial foci to meet the diagnostic criteria for WAP. This can be seen on ECG by a variation in P wave morphology and the PR interval. Each variation in P wave morphology represents a different ectopic focus. The closer the ectopic focus is to the AV node, the shorter the PR interval will be. Because WAP is not considered pathologic and often asymptomatic, there is no indication for treatment.

Clinical Significance

While electrophysiological studies using an intracardiac electrode catheter can help delineate the underlying mechanism of sinus node dysfunction, they are rarely done because they do not tend to alter management. In general, asymptomatic patients rarely require treatment. In symptomatic patients, offending pharmacological agents should be discontinued, and a permanent pacemaker may be required.[8][9]

Review Questions


Lang D, Glukhov AV. Functional Microdomains in Heart's Pacemaker: A Step Beyond Classical Electrophysiology and Remodeling. Front Physiol. 2018;9:1686. [PMC free article: PMC6277479] [PubMed: 30538641]
Farzam K, Tivakaran VS. StatPearls [Internet]. StatPearls Publishing; Treasure Island (FL): Jul 2, 2023. QT Prolonging Drugs. [PMC free article: PMC534864] [PubMed: 30521285]
Ambesh P, Kapoor A. Biological pacemakers: Concepts and techniques. Natl Med J India. 2017 Nov-Dec;30(6):324-326. [PubMed: 30117443]
Vetulli HM, Elizari MV, Naccarelli GV, Gonzalez MD. Cardiac automaticity: basic concepts and clinical observations. J Interv Card Electrophysiol. 2018 Aug;52(3):263-270. [PubMed: 30112616]
De Ponti R, Marazzato J, Bagliani G, Leonelli FM, Padeletti L. Sick Sinus Syndrome. Card Electrophysiol Clin. 2018 Jun;10(2):183-195. [PubMed: 29784479]
Hafeez Y, Grossman SA. StatPearls [Internet]. StatPearls Publishing; Treasure Island (FL): Aug 7, 2023. Sinus Bradycardia. [PubMed: 29630253]
Hafeez Y, Quintanilla Rodriguez BS, Ahmed I, Grossman SA. StatPearls [Internet]. StatPearls Publishing; Treasure Island (FL): Feb 5, 2023. Paroxysmal Supraventricular Tachycardia. [PubMed: 29939521]
Burkhard S, van Eif V, Garric L, Christoffels VM, Bakkers J. On the Evolution of the Cardiac Pacemaker. J Cardiovasc Dev Dis. 2017 Apr 27;4(2) [PMC free article: PMC5715705] [PubMed: 29367536]
Carmona R, Ariza L, Cañete A, Muñoz-Chápuli R. Comparative developmental biology of the cardiac inflow tract. J Mol Cell Cardiol. 2018 Mar;116:155-164. [PubMed: 29452155]

Disclosure: Anthony Kashou declares no relevant financial relationships with ineligible companies.

Disclosure: Hajira Basit declares no relevant financial relationships with ineligible companies.

Disclosure: Lovely Chhabra declares no relevant financial relationships with ineligible companies.

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