ECG tutorial: Rhythms and arrhythmias of the sinus node

SINUS RHYTHM — Sinus rhythm is present when the dominant pacemaker controlling impulse generation is the sinus node (waveform 1 and waveform 2). In this setting, activation of the atria is from right to left, superior to inferior, and anterior to posterior. (See "Normal sinus rhythm and sinus arrhythmia".)

Because of this activation pattern, the normal P wave in sinus rhythm may appear slightly notched since activation of the right atrium precedes that of the left atrium. The normal P wave is always positive (upright) in lead II and negative in aVR, usually positive in lead I, and it may be positive, negative, or biphasic in lead III. It is of variable polarity in lead aVL. In the precordial (chest) leads, V1 and V2, there is often a terminal negative component of the P wave, reflecting the posterior location (with respect to the right atrium) and later activation of the left atrium. The P wave is typically positive in the remaining precordial leads.

In normal sinus rhythm with 1:1 atrioventricular (AV) conduction, a P wave with a uniform morphology precedes each QRS complex. The rate is between 50 and 100 beats per minute, though some use 60 beats per minute as the lower end of normal, and the cycle length is fairly uniform between sequential P waves and QRS complexes. In addition, the P wave morphology and PR intervals appear identical from beat to beat. It is possible to have normal sinus rhythm with abnormal AV conduction also, such as with second degree or third degree AV block. In these situations, the P wave is regular with a constant morphology, but there is either a recurring pattern to the PR interval with intermittent dropped beats (second degree AV block) or no relationship at all between P waves and QRS complexes (third degree AV block).

Influence of the autonomic nervous system — Although the sinus node has an intrinsic automaticity and always produces an impulse, the rate of impulse generation is controlled by other factors, particularly the autonomic nervous system (figure 1). (See "Sinus node dysfunction: Epidemiology, etiology, and natural history", section on 'Autonomic nervous system and the SA node'.) With augmented parasympathetic (vagal) influence or reduced sympathetic stimulation, the sinus rate slows, and the PR interval prolongs due to a vagally mediated slowing of conduction through the AV node. By comparison, increased sympathetic activity and decreased vagal effects increase the sinus nodal rate and enhance AV nodal conduction, resulting in a shortened PR interval.

SINUS ARRHYTHMIA — Sinus arrhythmia is present when there is variability in the cycle length between successive P waves, most commonly associated with respiration (waveform 3). (See "Normal sinus rhythm and sinus arrhythmia".)

The physiologic variability observed in sinus arrhythmia is the result of respiratory-related changes in autonomic tone that influence the heart rate. Inspiration and stretching of lung tissue cause a reflex inhibition of vagal tone, which will increase the heart rate. (See "Evaluation of heart rate variability" and "Normal sinus rhythm and sinus arrhythmia".) The reverse occurs during expiration.

During breath holding, sinus arrhythmia is no longer present, but respiratory variation is not the only cause of sinus arrhythmia. Stimulation of the carotid artery baroreceptors with cyclic application of neck suction can reintroduce sinus arrhythmia in the setting of breath holding, suggesting that the variation in venous return due to respiration and its effect on arterial blood pressure and carotid artery baroreceptors may be the explanation for sinus arrhythmia [1].

A continuous electrocardiographic recording of sinus arrhythmia reveals a gradual increase and decrease in the heart rate since the cycle lengths between QRS complexes vary with the respiratory cycle. Although sinus arrhythmia is a normal finding, especially in young people, it may be confused with other arrhythmias if the respiratory changes in the RR intervals are prominent.

SINUS BRADYCARDIA — Sinus bradycardia is defined as a sinus rhythm with a rate less than 50 beats per minute (waveform 4). (See "Sinus bradycardia".)

Sinus bradycardia is most frequently caused by an increase in vagal tone or a reduction in sympathetic tone (and thus a physiologic change). In some cases, however, this arrhythmia is the result of intrinsic disease of the sinus node ("sinus node dysfunction"), manifested as a decrease in or failure of spontaneous automaticity and impulse generation rate (waveform 5). (See "Sinus node dysfunction: Epidemiology, etiology, and natural history".) As a result, sinus bradycardia is very common at night.

With increased vagal tone, the active pacemaker region is shifted to a more inferior portion of the sinus node and the direction or vector of atrial activation is changed. Since the direction of atrial activation becomes horizontal to limb lead I, the amplitude of the P wave is diminished in the inferior leads. When sinus bradycardia results from increased vagal tone, slowing of impulse conduction through the AV node may also result in PR interval prolongation.

SINUS TACHYCARDIA — Sinus tachycardia is defined as a sinus rhythm with a rate of greater than 100 beats per minute (waveform 6). (See "Sinus tachycardia: Evaluation and management".)

Sinus tachycardia is usually the result of sympathetic nervous system activation and an increase in circulating catecholamines, usually in concert with a decrease in cardiac vagal tone. These changes result in an increase in the rate of impulse generation by the sinus node. In the vast majority of cases, sinus tachycardia results from some underlying condition, such as exercise, infection, volume depletion, or heart failure, which alters the autonomic nervous system.

Since there is also withdrawal of vagal tone, the active region of the sinus node is shifted to its superior portion. The vector of atrial activation is therefore directed inferiorly and the amplitude of the P wave is increased in the inferior leads. Since sinus tachycardia is usually the result of sympathetic nervous system activation and decreased vagal activity, there is usually enhanced conduction of the impulse through the AV node and a shortening of the PR interval.

SINUS NODE DYSFUNCTION — Sinus node dysfunction results from intrinsic disease of the sinus node. (See "Sinus node dysfunction: Epidemiology, etiology, and natural history" and "Sinus node dysfunction: Clinical manifestations, diagnosis, and evaluation".) Some individuals with this syndrome also have underlying disease of other portions of the conduction system, particularly the AV node.

Types — Sinus node dysfunction includes a variety of different arrhythmias, all of which result in bradyarrhythmia.

●Tachycardia-bradycardia ("tachy-brady") syndrome: In this form of sinus node dysfunction, there is sinus or atrial bradycardia alternating with a tachyarrhythmia, most commonly rapid atrial fibrillation or flutter (waveform 5). Sometimes, there are sinus pauses when the tachyarrhythmia terminates, and there may be no junctional escape rhythm because of associated AV node disease.

The tachycardia-bradycardia syndrome is the result of overdrive suppression of the sinus node by the atrial arrhythmia. After arrhythmia termination, there is a variable delay before the sinus node recovers and again generates an impulse because of sinus node dysfunction. For example, profound sinus pauses and even sinus arrest with syncope can occur after spontaneous conversion of paroxysmal atrial fibrillation to sinus.

●Chronotropic incompetence: An abnormal heart rate response to exercise, defined as inability to achieve 80 percent of the age-predicted maximum heart rate, is one manifestation of a diseased sinus node. However, there is debate regarding this 80 percent threshold, and a better definition may simply be the physiologic inability to raise the heart rate to meet the metabolic demand. The resting electrocardiogram (ECG) may be normal or abnormal. (See "Prognostic features of stress testing in patients with known or suspected coronary disease", section on 'Heart rate response to exercise'.)

●Other forms: Additional variations of sinus node dysfunction are sinus bradycardia (see 'Sinus bradycardia' above), sinus pauses (see 'Sinus pause or arrest' below), sinoatrial exit block (see 'Sinoatrial exit block' below), ectopic atrial bradycardia, and isorhythmic dissociation, where the atrial rate is slower than the ventricular rate from a junctional or ventricular rhythm.

SINUS PAUSE OR ARREST — Sinus pause or sinus arrest is the result of intermittent failure of sinus node impulse generation (waveform 7). (See "Sinoatrial nodal pause, arrest, and exit block".)

Sinus pause or arrest may be due to intrinsic sinus node disease and dysfunction ("sinus node dysfunction") or from drugs that directly or indirectly (via the autonomic nervous system) depress sinus node activity. (See "Sinus node dysfunction: Epidemiology, etiology, and natural history".)

On the surface electrocardiogram, a sinus pause or arrest is manifest as the absence of a P wave at the expected time interval compared to the prior PP interval. This absence may simply be a delay of the next P wave (sinus pause) or may be the complete absence of a P wave with an escape beat (sinus arrest). The duration of the pause should have no relationship to the prior PP interval (which would suggest sinoatrial exit block).

SINOATRIAL EXIT BLOCK — Sinoatrial (SA) exit block most commonly arises from a change in the electrophysiologic characteristics of the tissue surrounding the sinus node, which results in an inability to respond to or conduct an impulse from the sinus node into the atrium. This can be due to drugs, disease, or increased vagus nerve activity. (See "Sinoatrial nodal pause, arrest, and exit block".)

Following the convention for AV nodal block, SA nodal exit block can be first degree, second degree, or third degree. This problem is most easily conceptualized as having three components:

●A relatively constant input: The input is from the pacemaker cells within the sinus node, which are not seen on the surface electrocardiogram (ECG), but are inferred from the P waves of atrial activation. The rate or cycle length of the input can be presumed from portions on the ECG where normal P-P cycles are observed.

●An area across which block occurs: Exit block is thought to involve the perinodal T cells. The type of exit block in the perinodal tissues must be inferred from the output or response (ie, from the P waves).

●An output: The P wave abnormalities reflect the type of exit block that is present.

First degree SA nodal exit block reflects a slowing of impulse exit but there is still 1:1 conduction. The ECG looks normal with this abnormality.

Second degree SA nodal exit block has two types. Type I (Wenckebach type) is characterized by progressively decreasing P-P intervals prior to a pause caused by a dropped P wave; the pause has a duration that is less than two P-P cycles (waveform 8). The mechanisms of Wenckebach conduction are discussed elsewhere but are similar to AV Wenckebach block. (See "Second-degree atrioventricular block: Mobitz type I (Wenckebach block)".)

In type II exit block, the P-P output is an arithmetic multiple of the presumed sinus pacemaker input (eg, 2:1, 3:1, 4:1). Therefore the P-P cycle length surrounding the pause is a multiple of the normal P-P interval (waveform 9 and waveform 10).

Third degree SA nodal exit block prevents pacemaker impulses from reaching the right atrium, giving the appearance of sinus arrest (ie, no P waves).

For first and second degree SA nodal exit block, the P wave is originating in the sinus node and has a normal P wave morphology. For third degree SA nodal exit block, there will either be an escape atrial, junctional, or ventricular rhythm, and the P waves will either be different morphology or absent.

SINUS NODE REENTRY — Sinus node reentry or sinoatrial nodal reentry is an infrequently seen supraventricular tachyarrhythmia (waveform 11). (See "Sinoatrial nodal reentrant tachycardia (SANRT)".)

Electrophysiologically, sinus node reentry is due to continuous activity or circus movement within the sinus node alone or in combination with perinodal tissue. This disturbance may result from altered autonomic tone, which affects the sinus node and the sinoatrial junction, and vagal maneuvers such as carotid sinus massage may abruptly terminate the rhythm.

This arrhythmia has a sudden onset and offset with a rate that is usually 100 to 160 beats per minute. The P wave has a morphology identical to the sinus P wave, and a P wave precedes each QRS complex, unless there is simultaneous AV block with variable conduction.

The PR interval is also generally similar to that during sinus rhythm. However, this interval may be slightly longer than that observed during sinus rhythm due to decremental conduction through the AV node. Sinus node reentry is usually classified as a long RP tachycardia. (See "Narrow QRS complex tachycardias: Clinical manifestations, diagnosis, and evaluation", section on 'RP relationship'.)  

Sinus node reentry may be confused with atrial tachycardia, but P wave morphology and response to vagal maneuvers helps differentiate. It may also be confused with conventional sinus tachycardia but the sudden onset of the tachycardia and its abrupt termination suggest sinus node reentry.

SUMMARY

●In normal sinus rhythm (including normal 1:1 atrioventricular [AV] conduction), an upright P wave in lead II with a uniform morphology precedes each QRS complex. The rate is between 50 and 100 beats per minute and the cycle length is fairly uniform between sequential P waves and QRS complexes, or respiratory sinus arrhythmia may be seen. In addition, the P wave morphology and PR intervals appear identical from beat to beat (waveform 1 and waveform 2). (See 'Sinus rhythm' above.)

●Sinus arrhythmia is present when there is a sinus rhythm with variability in the cycle lengths between successive P waves (waveform 3). (See 'Sinus arrhythmia' above.) Respiratory sinus arrhythmia is a physiologic variant and is especially notable in young, healthy subjects.

●Sinus bradycardia is defined as a sinus rhythm with a rate less than 50 beats per minute (waveform 4). (See 'Sinus bradycardia' above.)

●Sinus node dysfunction includes sinus bradycardia, ectopic atrial bradycardia, sinoatrial exit block, sinus pause, sinus node arrest, tachycardia-bradycardia syndrome, chronotropic incompetence, and isorhythmic dissociation.

●Sinus pause or arrest is manifest as a long PP cycle length that is longer than the PP interval of the underlying sinus rhythm. There is no relationship between the cycle length of the pause and that of the intrinsic sinus rhythm (waveform 7). (See 'Sinus pause or arrest' above.)

●Sinoatrial exit block exists in three forms, similar to AV block. In contrast to AV block, not all forms of sinoatrial exit block are manifest on the electrocardiogram (ECG). (See 'Sinoatrial exit block' above.)