Version May 2024
INTRODUCTION — Normal sinus rhythm (NSR) is the rhythm that originates from the sinus node and describes the characteristic rhythm of the healthy human heart. The rate in NSR is generally regular but will vary depending on autonomic inputs into the sinus node. When there is irregularity in the sinus rate, it is termed "sinus arrhythmia." A sinus rhythm faster than the normal range is called a sinus tachycardia, while a slower rate is called a sinus bradycardia. (See "Sinus tachycardia: Evaluation and management" and "Sinus bradycardia".)
The sinoatrial (SA) node, due to its small mass, does not have a visible manifestation on the electrocardiogram (ECG). The behavior of the SA node, therefore, must be inferred from the atrial response. The upper right atrium is depolarized first, followed by the simultaneous depolarization of the remainder of the right and some of the left atrium, and finally by depolarization of the left atrial appendage. The blood supply and anatomy of the SA node along with the ECG characteristics of NSR and sinus arrhythmia will be discussed here. Abnormalities of SA nodal function are considered elsewhere. (See "Sinus node dysfunction: Epidemiology, etiology, and natural history" and "Sinoatrial nodal pause, arrest, and exit block".)
NORMAL SINUS HEART RATE — The normal heart rate has been considered to be between 60 and 100 beats per minute, although there is some disagreement with regard to the normal rate in adults. The range (defined by 1st and 99th percentiles) is between 43 and 102 beats per minute in men and between 47 and 103 beats per minute in women (table 1) [1-3]. There is also important variability in age in young children. The normal heart rate is 110 to 150 beats per minute in infants, with gradual slowing over the first six years of life.
A variety of pharmacologic agents and physiologic conditions can result in changes to the normal sinus heart rate. These conditions are discussed in greater detail separately. (See "Sinus tachycardia: Evaluation and management", section on 'Etiology and clinical syndromes' and "Sinus bradycardia", section on 'Etiology'.)
The normal heart rate increases with exertion and decreases following the cessation of activity. The rate at which the heart rate returns to baseline following exercise can have prognostic importance, a concept which is discussed in greater detail elsewhere. (See "Prognostic features of stress testing in patients with known or suspected coronary disease", section on 'Heart rate response to exercise' and "Prognostic features of stress testing in patients with known or suspected coronary disease", section on 'Heart rate recovery after exercise'.)
ANATOMY — The sinoatrial (SA) node is located high (superiorly) in the right atrium at the junction of the crista terminalis (a thick band of atrial muscle at the border of the atrial appendage) and the superior vena cava. The SA node is located beneath the epicardial surface of the crista terminalis; there is a layer of atrial muscle between the SA node and the endocardium so that it does not occupy the entire thickness of the atrial myocardium. Human histologic studies have demonstrated that the SA node has a crescent-like shape with an average length of 13.5 mm [4].
A characteristic feature of the SA node is extensive connective tissue, mainly collagen and fibroblasts, enmeshed with specialized cells capable of pacemaking activity. All of these cells within the SA node are capable of pacemaker activity, and depending on autonomic activation, the origin of the electrical activity can shift from one area of the SA node to another (superiorly during predominant sympathetic activation and more inferiorly during predominant parasympathetic activation). Studies have described a collection of cells, known as the paranodal cells, which are electrically and histologically distinct from the SA node [5]. These cells are thought to facilitate electrical conduction from the SA node to the rest of the atrium and have been hypothesized as a source of some of the more common atrial tachycardias originating from the cristae terminalis area. (See "Focal atrial tachycardia", section on 'Sites of origin'.)
While it may appear that the electrical signals from the SA node to the atrial periphery can exit randomly, there appear to be preferential pathways of conduction from the sinus pacemaker cells to the atrium [6]. Whether these are functional or anatomical exit paths remains unclear. The conduction velocity within the SA node is very slow compared with non-nodal atrial tissue. This is a result of poor electrical coupling arising from the relative paucity of gap junctions in the center of the node compared with the periphery [7].
SA nodal dysfunction may result from abnormalities in impulse generation or in conduction across the paranodal cells. (See "Sinus node dysfunction: Epidemiology, etiology, and natural history" and "Sinoatrial nodal pause, arrest, and exit block".)
BLOOD SUPPLY — Historically, studies had suggested that over 90 percent of hearts have only one arterial branch to the SA node, and common wisdom was that the right coronary artery supplied the SA node in approximately 55 percent of hearts [8]. More recent data, however, suggest that the SA nodal artery may take one of six different routes, and two or more branches to the node may be present in approximately 54 percent of hearts [8]. This suggests that collateral blood supplies are common and perhaps explains the rarity of infarction involving the SA node. However, sinus node injury may be seen as a complication of left atrial ablation depending on the course of the SA nodal artery relative to the atrial tissue targeted with ablation [9,10].
ELECTROCARDIOGRAPHIC CHARACTERISTICS OF NSR
P wave duration and amplitude — The P wave is normally less than 120 milliseconds in duration and under 0.15 or 0.20 mV (or in some texts 0.25 mV) in height in standard lead II, with the permissible maximum varying according to the lead [11]. The terminal component in lead V1 should be less than 0.04 seconds long and 0.1 mV (1 mm) deep. Atrial repolarization usually is not seen on the electrocardiogram. (See "ECG tutorial: Basic principles of ECG analysis", section on 'P wave'.)
P wave axis and morphology — A normal P wave axis (0° to +90°) and morphology help define normal sinus rhythm on the ECG. The normal axis results in the following P wave characteristics on the ECG (waveform 1):
●Upright in leads I, II and usually aVF
●Inverted in aVR
●Upright, biphasic or inverted in III and aVL
●The right to left activation results in P waves that are upright or biphasic in V1 and V2, and upright in V3 through V6
The P wave duration and morphology may be abnormal during NSR, usually reflecting atrial disease or atrial electrical conduction abnormality. A brief description follows with a more comprehensive discussion presented separately. (See "ECG tutorial: Chamber enlargement and hypertrophy".)
Left atrial enlargement — The ECG pattern of "left atrial enlargement" (LAE) lacks precision since it can arise from dilatation, hypertrophy, or an electrical conduction defect. The left atrium is a leftward and posterior structure, so LAE increases the leftward and posterior vectors and, when there is an associated intraatrial conduction delay, prolongs the duration of the P wave. The ECG criteria for LAE reflect these events (waveform 2):
●The P wave is wide in lead II (≥120 milliseconds) and is usually notched in I and II.
●The P duration/PR segment duration is greater than 1.6 [12].
●The terminal P wave in lead V1 is deep and delayed with the negative deflection being greater than 40 milliseconds in duration and/or ≥0.1 mV (1 mm) in height. The Morris index of the P terminal force is the product of the amplitude and duration of the terminal portion of the P wave in V1, and a value of 40 mV-millisecond suggests left atrial enlargement [13]. A negative P duration in V1 divided by the PR segment that is ≥1.0 has also been suggested as a criterion for LAE [14].
●The axis of the late component is often to the left (40° or less).
Right atrial enlargement — Similar to LAE, the ECG pattern of right atrial enlargement (RAE) lacks precision as RAE may arise from dilatation, hypertrophy, or a conduction defect. The right atrium is a rightward and anterior structure, so RAE results in an increase in the anterior, rightward, and inferior forces of early atrial activation (which, as noted above, begins in the right atrium). This leads to the following pattern of right atrial enlargement (waveform 2):
●Prominent P waves (0.2 mV [2 mm] or greater in height) in the limb leads, particularly II and aVF, and in an anterior lead such as V1.
●The initial P force in lead V1 is often ≥60 mV-millisecond.
●The P wave duration is 110 milliseconds or less with an axis of 65° or more.
Biatrial enlargement — Biatrial enlargement has characteristics of both right atrial and left atrial abnormalities. The right atrial abnormality increases the P wave amplitude in the appropriate leads, and the left atrial abnormality will broaden and notch the P waves and may increase the terminal force of the P waves in V1 (waveform 2).
The PR interval — The normal PR interval is 120 to 200 milliseconds. The PR interval tends to shorten as the heart rate increases due to rate-related shortening of action potentials and perhaps the effects of the autonomic nervous system on the atrioventricular (AV) node. Although there is some difference between small and large adults, the maximum PR interval is:
●170 milliseconds for sinus rates over 130 beats per minute
●180 to 190 milliseconds for rates between 100 and 130 beats per minute
●200 milliseconds for rates between 70 and 100 beats per minute
●210 milliseconds for rates slower than 70 beats per minute
Children have shorter upper limits of normal for PR intervals; 0.14 seconds is a useful figure to remember under age 14, although the PR interval may be somewhat longer at slow rates and somewhat shorter at fast rates.
The PR interval is independent of whether or not sinus rhythm is present. Normal sinus rhythm can be present even in the presence of complete heart block. (See "Third-degree (complete) atrioventricular block".)
SINUS ARRHYTHMIA — Sinus arrhythmia is defined as an irregularity in the rate of normal sinus rhythm. Sinus arrhythmia is considered present when there is a variation in the P-P interval by 0.12 seconds (120 milliseconds) or more but atrial activation appears to be occurring via the sinus node. Occasionally, there can be irregularity in the sinus rate, but the P-wave morphology varies and this can be consistent with "wandering atrial pacemaker" discussed elsewhere.
There are three types of sinus arrhythmia:
●Respiratory, or phasic
●Nonrespiratory, or nonphasic
●Nonrespiratory, ventriculophasic sinus arrhythmia
Respiratory type — Respiratory sinus arrhythmia is a common, benign, and usually normal phenomenon that is related mechanistically to alternations in autonomic input directly and due to changes in cardiac filling during respiration. Respiratory sinus arrhythmia has been associated with obesity, diabetes mellitus, and hypertension. Some studies suggest that respiratory sinus arrhythmia is the result of these conditions, while others have documented a reduced respiratory sinus arrhythmia among individuals prior to the onset of disease. While severe respiratory sinus arrhythmia has been associated with several systemic conditions, for the most part, respiratory sinus arrhythmia is benign and does not require additional cardiac evaluation.
During the respiratory cycle, inspiration reflexively inhibits vagal tone, thereby increasing the sinus rate, while with expiration vagal tone rises to its previous state, and the rate declines (waveform 3) [15]. This type of sinus arrhythmia disappears with breath holding. However, stimulation of the carotid baroreceptors by neck suction during breath holding will restore sinus arrhythmia, suggesting that the autonomic changes responsible for sinus arrhythmia can also be due to baroreflex stimulation. Baroreceptor stimulation may result from cyclic alterations in arterial blood pressure induced by the respiratory effect on venous return [16].
Respiratory sinus arrhythmia also appears to be less prominent as people age. As an example, in a study of 24 healthy volunteers without evidence of cardiovascular disease or risk factors for cardiovascular disease, respiratory sinus arrhythmia in older subjects (age 59 to 71 years, n = 15) was less than 20 percent of that in younger subjects (<31 years of age, n = 9) [17]. A possible reason for this observation is an age-related decrease in carotid distensibility and baroreflex sensitivity, without a change in resting vagal tone.
Other factors may contribute to respiratory sinus arrhythmia. These include sympathetic mechanisms, elevations in arterial PCO2 that increase the magnitude of respiratory sinus arrhythmia, probably via a direct effect on the medulla, and drugs that increase vagal tone, such as morphine or digitalis [18-21]. By contrast, hypocapnia caused by voluntary hyperventilation reduces sinus arrhythmia [19]. Sinus arrhythmia is also reduced in diabetes mellitus, perhaps reflecting autonomic dysfunction [22].
In some subjects, autonomic changes during respiration cause the activation within the SA node to change, leading to subtle changes in P wave morphology and the PR interval. If depression of the SA node is sufficient, ectopic atrial pacemakers may occur; in this setting, prominently different P waves may be seen. (See "ECG tutorial: Atrial and atrioventricular nodal (supraventricular) arrhythmias", section on 'Wandering atrial pacemaker' and "Multifocal atrial tachycardia", section on 'Definition, pathogenesis, and prevalence'.)
Nonrespiratory type — Nonrespiratory sinus arrhythmia differs in that the acceleration and deceleration of the SA node is not related to the respiratory cycle. This form of sinus arrhythmia can occur in the normal heart, in the diseased heart, or after digitalis intoxication.
Ventriculophasic type — A ventriculophasic sinus arrhythmia occurs most often in patients with third-degree AV block, but it can also be seen after a compensatory pause induced by a premature ventricular complex/contraction (PVC; also referred to a premature ventricular beats or premature ventricular depolarizations). This arrhythmia is characterized by intermittent differences in the PP intervals based upon their relationship to the QRS complex. The two P waves surrounding a QRS complex have a shortened interval (ie, they occur at a faster rate) when compared with two P waves that occur sequentially without an intervening QRS complex (waveform 4). The cause is not fully understood but seems to be related to increased filling during the long cycle; this is followed by a forceful systole and increased stroke volume which, in turn, trigger a baroreceptor response. In orthotopic cardiac transplantation, ventriculophasic arrhythmia is absent despite intact vagal innervation to the atrial remnant, which suggests that the lack of pulsatile blood flow in the SA node may contribute to the absence of the ventriculophasic arrhythmias [23].
Heart rate turbulence (HRT) is based on the evaluation of ventriculophasic arrhythmia following a PVC and describes the short-term fluctuation in sinus cycle length that follows such a beat. This is discussed in greater detail separately. (See "Evaluation of heart rate variability", section on 'Heart rate turbulence'.)
SUMMARY AND RECOMMENDATIONS
●Normal sinus rhythm (NSR) is the characteristic rhythm of the healthy human heart. NSR is considered to be present if the heart rate is in the normal range, the P waves are normal on the ECG, and the rate does not vary significantly. (See 'Introduction' above.)
●The sinus node is located high (superiorly) in the right atrium at the junction of the crista terminalis, a thick band of atrial muscle at the border of the atrial appendage, and the superior vena cava. Human histologic studies have demonstrated that the sinus node has a crescent-like shape with an average length of 13.5 mm. A collection of cells known as the paranodal cells, which are electrically and histologically distinct from the sinus node, are thought to facilitate electrical conduction from the sinus node to the rest of the atrium. (See 'Anatomy' above.)
●The blood supply to the sinoatrial (SA) node is complex as the SA nodal artery may take one of six different routes, and two or more branches to the node may be present in more than 50 percent of the population. This suggests that collateral blood supplies are common and perhaps explains the rarity of infarction of the SA node. (See 'Blood supply' above.)
●The P wave is normally less than 0.12 seconds in duration and under 0.15 or 0.20 mV (or in some texts 0.25 mV) in standard lead II, with the permissible maximum varying according to the lead. The terminal component in lead V1 should be less than 0.04 seconds long and 1 mm deep. (See 'P wave duration and amplitude' above.)
●A normal P wave axis (0º to +90º) and morphology help define the normal sinus mechanism on the ECG. (See 'P wave axis and morphology' above.)
●The normal PR interval is 120 to 200 milliseconds. The PR interval tends to shorten as the heart rate increases due to rate-related shortening of action potentials and perhaps the effects of the autonomic nervous system on the AV node. (See 'The PR interval' above.)
●If the heart rate is in the normal range and the P waves are normal on the ECG but the R-R interval is variable, the rhythm is called sinus arrhythmia. The formal definition of sinus arrhythmia is a variation in the P-P interval by 0.12 seconds (120 milliseconds) or more in the presence of normal P waves and the usual PR interval. (See 'Sinus arrhythmia' above.)
●There are three types of sinus arrhythmia: respiratory, or phasic; and nonrespiratory, or nonphasic.
•Respiratory sinus arrhythmia is common, usually normal, and decreases with age. Respiratory sinus arrhythmia results from changes in autonomic tone during the respiratory cycle. Inspiration reflexively inhibits vagal tone, thereby increasing the sinus rate. With expiration, vagal tone rises to its previous state, and the rate declines (waveform 3). In some subjects, autonomic change during respiration causes the pacemaker to change location within the SA node, leading to subtle changes in P wave morphology and the PR interval. If depression of the SA node is sufficient, ectopic atrial pacemakers may occur. (See 'Respiratory type' above.)
•Nonrespiratory sinus arrhythmia differs in that the acceleration and deceleration of the SA node is not related to the respiratory cycle. This form of sinus arrhythmia can occur in the normal heart, in the diseased heart, or after digitalis intoxication.
•Ventriculophasic sinus arrhythmia occurs in patients with third-degree atrioventricular (AV) block but can also be seen after a compensatory pause induced by a PVC. This arrhythmia is characterized by intermittent differences in the PP intervals based upon their relationship to the QRS complex. The two P waves surrounding a QRS complex have a shortened interval (ie, they occur at a faster rate) when compared with two P waves that occur sequentially without an intervening QRS complex (waveform 4). (See 'Nonrespiratory type' above.)
●Respiratory sinus arrhythmia by itself does not require any specific cardiac evaluation. (See 'Sinus arrhythmia' above.)
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