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Official reprint from UpToDate www.uptodate.com ©2015 UpToDate

AuthorJordan M Prutkin, MD,MHS, FHRS

Section EditorAry L Goldberger, MD

Deputy EditorGordon M Saperia, MD,FACC

ECG tutorial: Rhythms and arrhythmias of the sinus node

All topics are updated as new evidence becomes available and our peer review process is complete.Literature review current through: Jun 2015. | This topic last updated: Aug 29, 2013.

SINUS RHYTHM — Sinus rhythm is present when the dominant pacemaker controlling impulse generationis 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".)

Consequent to this activation pattern, the normal P wave in sinus rhythm may appear slightly notched sinceactivation 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 leadIII. It is of variable polarity in lead aVL. In the precordial (chest) leads, V1 and V2, there is often a terminalnegative component of the P wave, reflecting the posterior location (with respect to the right atrium) and lateractivation of the left atrium. The P wave is typically positive in the remaining precordial leads.

In normal sinus rhythm with 1:1 atrioventricular conduction, a P wave with a uniform morphology precedeseach QRS complex. The rate is between 60 and 100 beats per minute and the cycle length is fairly uniformbetween sequential P waves and QRS complexes. In addition, the P wave morphology and PR intervalsappear identical from beat to beat.

Influence of the autonomic nervous system — Although the sinus node has an intrinsic automaticity andalways produces an impulse, the rate of impulse generation is controlled by other factors, particularly theautonomic nervous system (figure 1). (See "Manifestations and causes of the sick sinus syndrome", sectionon 'Autonomic nervous system and the SA node'.) With augmented parasympathetic (vagal) influence orreduced sympathetic stimulation, the sinus rate slows, and the PR interval prolongs due to a vagallymediated slowing of conduction through the atrioventricular node. By comparison, increased sympatheticactivity and decreased vagal effects increase the sinus nodal rate and enhance atrioventricular nodalconduction, resulting in a shortened PR interval.

SINUS ARRHYTHMIA — Sinus arrhythmia is present when there is a sinus rhythm with variability in thecycle lengths between successive P waves (waveform 3). (See "Normal sinus rhythm and sinusarrhythmia".)

The physiologic variability observed in sinus arrhythmia is the result of respiratory­related changes inautonomic tone that influence the heart rate. Inspiration and stretching of lung tissue cause a reflex inhibitionof vagal tone, which will increase the heart rate. (See "Evaluation of heart rate variability" and "Normal sinusrhythm 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 ofsinus arrhythmia. Stimulation of the carotid artery baroreceptors with cyclic application of neck suction canre­introduce sinus arrhythmia in the setting of breath holding, suggesting that the variation in venous returndue to respiration and its effect on arterial blood pressure and carotid artery baroreceptors may be theexplanation for sinus arrhythmia [1].

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

SINUS BRADYCARDIA — Sinus bradycardia is defined as a sinus rhythm with a rate less than 60 beats perminute (waveform 4). (See "Sinus bradycardia".)

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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 ofthe sinus node ("Sick sinus syndrome"), manifested as a decrease in or failure of spontaneous automaticityand impulse generation rate (waveform 5). (See "Manifestations and causes of the sick sinus syndrome".)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 nodeand the direction or vector of atrial activation is changed. Since the direction of atrial activation becomeshorizontal to limb lead I, the amplitude of the P wave is diminished in the inferior leads. When sinusbradycardia results from increased vagal tone, slowing of impulse conduction through the atrioventricularnode may also result in PR interval prolongation.

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

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

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

SINUS PAUSE OR ARREST — Sinus pause or sinus arrest is the result of intermittent failure of sinus nodeimpulse 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 ("Sick sinus syndrome") orfrom drugs that directly or indirectly (via the autonomic nervous system) depress sinus node activity. (See"Manifestations and causes of the sick sinus syndrome".)

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

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

Following the convention for atrioventricular (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 arenot seen on the surface electrocardiogram (ECG), but are inferred from the P waves of atrialactivation. The rate or cycle length of the input can be presumed from portions on the ECG wherenormal P­P cycles are observed.

An area across which block occurs – Exit block is thought to involve the perinodal T cells. The type ofexit 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

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looks normal with this abnormality.

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

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

Third degree SA nodal exit block prevents pacemaker impulses from reaching the right atrium, giving theappearance 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 had thenormal 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.

SICK SINUS SYNDROME — Sick sinus syndrome results from intrinsic disease of the sinus node. (See"Manifestations and causes of the sick sinus syndrome" and "Diagnosis and evaluation of the sick sinussyndrome".) Some individuals with this syndrome also have underlying disease of other portions of theconduction system, particularly the atrioventricular node.

Types — Sick sinus syndrome includes a variety of different arrhythmias, all of which result inbradyarrhythmia.

Tachycardia­bradycardia syndrome – This form of the syndrome is most often characterized by burstsof an atrial tachyarrhythmia (usually atrial fibrillation), which terminate spontaneously and are followedby long offset pauses and symptomatic bradycardia (waveform 5). The pause is often long and theremay be no junctional escape rhythm because of associated atrioventricular node disease.

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

Bradycardia­tachycardia syndrome – In this form of sick sinus syndrome, an escape tachyarrhythmia,such as atrial fibrillation, results from an initial significant sinus bradycardia.

Chronotropic incompetence – An abnormal heart rate response to exercise, defined as inability toachieve 85 percent of the age­predicted maximum heart rate, is one manifestation of a diseased sinusnode. The resting electrocardiogram (ECG) may be normal or abnormal. (See "Exercise ECG testingto determine prognosis of coronary heart disease", section on 'Heart rate response to exercise'.)

Other forms – Additional variations of the sick sinus syndrome are a fixed and symptomatic sinusbradycardia, long sinus pauses, or sinus node arrest.

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

Electrophysiologically, sinus node re­entry is due to continuous activity or circus movement within the sinusnode 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 sinusmassage 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. A Pwave precedes each QRS complex, unless there is simultaneous atrioventricular (AV) block with variableconduction, and has a morphology identical to the sinus P wave.

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The PR interval is also similar to that of sinus rhythm. However, this interval may be slightly longer than thatobserved during sinus rhythm due to decremental conduction through the atrioventricular node. Sinus nodere­entry is usually classified as a long RP tachycardia. (See "Clinical manifestations, diagnosis, andevaluation of narrow QRS complex tachycardias", section on 'RP relationship'.)

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

SUMMARY

In normal sinus rhythm (including normal 1:1 AV conduction), an upright P wave in lead II with auniform morphology precedes each QRS complex. The rate is between 60 and 100 beats per minuteand the cycle length is fairly uniform between sequential P waves and QRS complexes, or respiratorysinus arrhythmia may be seen. In addition, the P wave morphology and PR intervals appear identicalfrom 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 betweensuccessive P waves (waveform 3). (See 'Sinus arrhythmia' above.) Respiratory sinus arrhythmia is aphysiologic variant and is especially notable in young, healthy subjects.

Sinus bradycardia is defined as a sinus rhythm with a rate less than 60 beats per minute (waveform4). (See 'Sinus bradycardia' above.)

Sinus tachycardia is defined as a sinus rhythm with a rate of greater than 100 beats per minute(waveform 6). (See 'Sinus tachycardia' above.)

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

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

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REFERENCES

1. Piepoli M, Sleight P, Leuzzi S, et al. Origin of respiratory sinus arrhythmia in conscious humans. Animportant role for arterial carotid baroreceptors. Circulation 1997; 95:1813.

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GRAPHICS

Sinus rhythm

The normal P wave in sinus rhythm is slightly notched since activation ofthe right atrium precedes that of the left atrium. The P wave is upright ina positive direction in leads I and II. A P wave with a uniformmorphology precedes each QRS complex. The rate is between 60 and100 beats per minute and the cycle length is uniform between sequentialP waves and QRS complexes. In addition, the P wave morphology and PRintervals are identical from beat to beat.

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Normal rhythm strip

Normal rhythm strip in lead II. The PR interval is 0.15 sec and the QRSduration is 0.08 sec. Both the P and T waves are upright.

Courtesy of Morton F Arnsdorf, MD.

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Autonomic innervation of the heart

The heart, especially the pacemaker tissue, is innervated by fibers fromboth the parasympathetic and sympathetic nervous systems.

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Sinus arrhythmia

Sinus arrhythmia is present when there is a sinus rhythm with variability in thecycle lengths between successive P waves. This rhythm strip reveals a gradualincrease and decrease in the heart rate with the respiratory cycle; the heart rateincreases with inspiration and decreases with expiration.

Graphic 73688 Version 2.0

Sinus rhythm

The normal P wave in sinus rhythm is slightly notched since activationof the right atrium precedes that of the left atrium. The P wave isupright in a positive direction in leads I and II. A P wave with auniform morphology precedes each QRS complex. The rate is between60 and 100 beats per minute and the cycle length is uniform betweensequential P waves and QRS complexes. In addition, the P wavemorphology and PR intervals are identical from beat to beat.

Graphic 69872 Version 2.0

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Sinus bradycardia

Sinus bradycardia is defined as a sinus rhythm with a rate less than 60beats per minute. This rhythm strip shows a sinus rate of 50 beats perminute.

Graphic 64425 Version 2.0

Sinus rhythm

The normal P wave in sinus rhythm is slightly notched since activationof the right atrium precedes that of the left atrium. The P wave isupright in a positive direction in leads I and II. A P wave with auniform morphology precedes each QRS complex. The rate is between60 and 100 beats per minute and the cycle length is uniform betweensequential P waves and QRS complexes. In addition, the P wavemorphology and PR intervals are identical from beat to beat.

Graphic 69872 Version 2.0

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Sick sinus syndrome

Tracing of sick sinus syndrome (tachycardia­bradycardia syndrome). Theinitial three beats show atrial fibrillation (AF) which terminates abruptlyand is followed after a long offset pause by a junctional escape beat (J)and then a sinus beat (S).

Graphic 62975 Version 2.0

Sinus rhythm

The normal P wave in sinus rhythm is slightly notched since activationof the right atrium precedes that of the left atrium. The P wave isupright in a positive direction in leads I and II. A P wave with auniform morphology precedes each QRS complex. The rate is between60 and 100 beats per minute and the cycle length is uniform betweensequential P waves and QRS complexes. In addition, the P wavemorphology and PR intervals are identical from beat to beat.

Graphic 69872 Version 2.0

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Sinus tachycardia

Sinus tachycardia is defined as a sinus rhythm with a rate of greaterthan 100 beats per minute and less than approximately 160 to 180beats per minute. In this tracing, the rate is about 130 beats perminute.

Graphic 56631 Version 2.0

Sinus rhythm

The normal P wave in sinus rhythm is slightly notched since activationof the right atrium precedes that of the left atrium. The P wave isupright in a positive direction in leads I and II. A P wave with auniform morphology precedes each QRS complex. The rate is between60 and 100 beats per minute and the cycle length is uniform betweensequential P waves and QRS complexes. In addition, the P wavemorphology and PR intervals are identical from beat to beat.

Graphic 69872 Version 2.0

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Sinus pause

Sinus pause is the result of intermittent failure of sinus node impulsegeneration. This is manifest as a long RR cycle length (in this tracing P toP interval) which is longer than the RR interval of the underlying sinusrhythm. There is no relationship between the cycle length of the pauseand that of the intrinsic sinus rhythm. The P­P interval for the beatsbefore and after the pause are less than two times the underlying sinusP­P interval.

Graphic 75018 Version 2.0

Sinus rhythm

The normal P wave in sinus rhythm is slightly notched since activationof the right atrium precedes that of the left atrium. The P wave isupright in a positive direction in leads I and II. A P wave with auniform morphology precedes each QRS complex. The rate is between60 and 100 beats per minute and the cycle length is uniform betweensequential P waves and QRS complexes. In addition, the P wavemorphology and PR intervals are identical from beat to beat.

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Single­lead electrocardiogram (ECG) showing leadV1 in type I (Wenckebach type) sinoatrial block

There is a 3:2 SA block, resulting in group beating of pairs of sinus beats.The P­P interval during the pause has a duration (1040 msec) that is lessthan two P­P cycles (1360 msec); this finding distinguishes this arrhythmiafrom type II SA block in which the pause duration is the same as that oftwo P­P cycles.

Courtesy of Morton Arnsdorf, MD.

Graphic 68081 Version 3.0

Normal rhythm strip

Normal rhythm strip in lead II. The PR interval is 0.15 sec and theQRS duration is 0.08 sec. Both the P and T waves are upright.

Courtesy of Morton F Arnsdorf, MD.

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Single­lead electrocardiogram (ECG) showing leadV5 in type II sinoatrial block

There is a 3:2 SA block, resulting in group beating of pairs of sinus beats.The P­P interval during the pause has a duration (1840 msec) that isapproximately equal to two P­P cycles (920 msec); this findingdistinguishes this arrhythmia from type I SA block in which the pauseduration is less than that of two P­P cycles. There may be some sinusvariability, as in this case, due to sinus arrhythmia and possibly tobaroreceptor responses to varying diastolic filling intervals.

Courtesy of Morton Arnsdorf, MD.

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Normal rhythm strip

Normal rhythm strip in lead II. The PR interval is 0.15 sec and theQRS duration is 0.08 sec. Both the P and T waves are upright.

Courtesy of Morton F Arnsdorf, MD.

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Sinoatrial exit block

Failure of impulse conduction from the sinus node into the atrium results insinoatrial block. This arrhythmia is characterized by an absent P wave and aprolongation of the RR cycle length (measured as P to P length in this tracing),usually twice the underlying sinus P­P interval. This is a distinguishing featurefrom sinus pause in which the beat after the pause has a P­P interval less thantwo times the underlying sinus P­P interval.

Graphic 50086 Version 2.0

Sinus rhythm

The normal P wave in sinus rhythm is slightly notched since activationof the right atrium precedes that of the left atrium. The P wave isupright in a positive direction in leads I and II. A P wave with auniform morphology precedes each QRS complex. The rate is between60 and 100 beats per minute and the cycle length is uniform betweensequential P waves and QRS complexes. In addition, the P wavemorphology and PR intervals are identical from beat to beat.

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Sinus node reentry

Sinus node re­entry is due to continuous activity or re­entry within thesinus node or the sinoatrial junction. This arrhythmia has a sudden onsetand offset with a rate that is usually 100 to 160 beats per minute. A Pwave proceeds each QRS complex and has a morphology identical to thesinus P wave. The PR interval is also similar to that of sinus rhythm. Thus,it is only the abrupt onset and offset that distinguishes this arrhythmiafrom sinus tachycardia.

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Sinus rhythm

The normal P wave in sinus rhythm is slightly notched since activationof the right atrium precedes that of the left atrium. The P wave isupright in a positive direction in leads I and II. A P wave with auniform morphology precedes each QRS complex. The rate is between60 and 100 beats per minute and the cycle length is uniform betweensequential P waves and QRS complexes. In addition, the P wavemorphology and PR intervals are identical from beat to beat.

Graphic 69872 Version 2.0

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Disclosures: Jordan M Prutkin, MD, MHS, FHRS Grant/Research/Clinical Trial Support: BostonScientific [Heart block (Pacemakers and ICDs)]; St. Jude Medical [Sudden death (Pacemakers andICDs)]. Ary L Goldberger, MD Nothing to disclose. Gordon M Saperia, MD, FACC Nothing to disclose.Contributor disclosures are reviewed for conflicts of interest by the editorial group. When found, these areaddressed by vetting through a multi­level review process, and through requirements for references to beprovided to support the content. Appropriately referenced content is required of all authors and mustconform to UpToDate standards of evidence.Conflict of interest policy

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