Physiology, Sinoatrial Node

Issues of Concern

The main function of the SA node is to act as the heart's normal pacemaker. 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, which begins 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 does 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 become the new pacemaker.

Function

The SA node, or the sinus node, represents a crescent-like 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 can spontaneously generate an electrical impulse. The integrated activity of these so-called pacemaker cells forms 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, setting a healthy heart's normal rhythm and rate. Hence, the SA node is referred to as the heart's natural pacemaker.

Mechanism

The heart rate can vary 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, 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, sympathetic input, and heart rate.

Because the sinus node comprises 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, 1 myocyte may produce an action potential faster than the 1 that produced the previous one, increasing 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 decreased heart rate that is 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.

Pathophysiology

Normal Sinus Rhythm

The rhythm originates from the sinus node in normal sinus rhythm (NSR). The rhythm is often regular with constant P-P intervals. When the rhythm has some irregularity, it is known as sinus arrhythmia. Generally, adults' normal heart rate ranges between 60 and 100 beats per minute. However, normal variations exist depending on the individual’s age and gender. A sinus rhythm with a rate above the normal range is called sinus tachycardia, and 1 below the normal range is called sinus bradycardia.

In NSR, the P wave is less than 120 milliseconds long and less than 0.15 mV to 0.25 mV in height in lead II. The permissible maximum varies based on the lead. If a biphasic P wave exists 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 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. Nevertheless, the PR interval is independent of the presence or absence of sinus rhythm.

Sinus Node Dysfunction

Sinus node dysfunction is often due to abnormal impulses produced by the pacemaker cells or abnormal conduction across the perinodal cells. It can be 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, arrhythmia, and 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 shows 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 (ie, 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 be seen in non-diseased hearts. However, if a sinus pause and arrest go 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 3 degrees of SA nodal exit block: first, second, and third degree. They follow the conventional atrioventricular (AV) nodal blocks. To conceptualize these, there are 3 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 (ie, the P waves). The SA nodal exit block type can be determined by evaluating the P waves. 

• First degree: With first-degree SA nodal exit block, impulse exit slows 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 2 types of 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 of less than 2 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.
• Third-degree: The SA node impulse cannot reach the right atrium with a third-degree SA nodal exit block. Thus, the atrial does not depolarize, and there won't be a 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 2 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. At least 3 dominant ectopic atrial foci must 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. Because WAP is not considered pathologic and is 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]