ECG tutorial (Rhythms and arrhythmias of sinus node)
SINUS RHYTHM
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4.
SR is present when dominant pacemaker controlling impulse generation is SA node. In this
setting, activation of atria is from R to L, S to I, and A to P.
Consequent to this activation pattern, normal P wave in SR may appear slightly notched since
activation of RA precedes that of LA. 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 precordial (chest) leads, V1 and V2, there is
often terminal negative component of P wave, reflecting posterior location (with respect to
RA) and later activation of LA. P wave is typically positive in remaining precordial leads.
In NSR with 1:1 AV conduction, P wave with uniform morphology precedes each QRS complex.
The rate is between 60 and 100 bpm and cycle length is fairly uniform between sequential P
waves and QRS complexes. In addition, P wave morphology and PR intervals appear identical
from beat to beat.
Influence of ANS
A. Although SA node has intrinsic automaticity and always produces impulse, rate of
impulse generation is controlled by other factors, particularly ANS. With augmented
parasympathetic (vagal) influence or reduced sympathetic stimulation, SA rate slows,
and PR interval prolongs due to vagally mediated slowing of conduction through AV
node. By comparison, increased sympathetic activity and decreased vagal effects
increase sinus nodal rate and enhance AV nodal conduction, resulting in shortened PR
interval.
SINUS ARRHYTHMIA
1. Sinus arrhythmia is present when there is SR with variability in cycle lengths between
successive P waves.
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3.
The physiologic variability observed in sinus arrhythmia is result of respiratory-related
changes in autonomic tone that influence HR. Inspiration and stretching of lung tissue cause
reflex inhibition of vagal tone, which will increase HR. 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 carotid artery baroreceptors with cyclic
application of neck suction can re-introduce sinus arrhythmia in setting of breath holding,
suggesting that variation in venous return due to respiration and its effect on arterial blood
pressure and carotid artery baroreceptors may be explanation for sinus arrhythmia.
4.
A continuous ECG recording of sinus arrhythmia reveals gradual increase and decrease in HR
since cycle lengths between QRS complexes vary with respiratory cycle. Although sinus
arrhythmia is normal finding, especially in young people, it may be confused with other
arrhythmias if respiratory changes in RR intervals are prominent.
SINUS BRADYCARDIA
1. Sinus bradycardia is defined as sinus rhythm with rate < 60 bpm.
2.
SB is most frequently caused by increase in vagal tone or reduction in sympathetic tone (and
thus physiologic change). In some cases, however, this arrhythmia is result of intrinsic disease
of sinus node ("Sick sinus syndrome"), manifested as decrease in or failure of spontaneous
automaticity and impulse generation rate. As result, SB is very common at night.
3.
With increased vagal tone, active pacemaker region is shifted to more inferior portion of SA
node and direction or vector of atrial activation is changed. Since direction of atrial activation
becomes horizontal to limb lead I, amplitude of P wave is diminished in inferior leads. When
SB results from increased vagal tone, slowing of impulse conduction through AV node may
also result in PR interval prolongation.
SINUS TACHYCARDIA
1. Sinus tachycardia is defined as sinus rhythm with rate of > 100 bpm.
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ST is usually result of ANS activation and increase in circulating catecholamines, usually in
concert with decrease in cardiac vagal tone. These changes result in increase in rate of
impulse generation by SA node. In vast majority of cases, ST results from some underlying
condition, such as exercise, infection, or CHF. Volume depletion is also common cause.
Since there is also withdrawal of vagal tone, active region of SA node is shifted to its superior
portion. The vector of atrial activation is therefore directed inferiorly and amplitude of P wave
is increased in inferior leads. Since ST is usually result of sympathetic nervous system
activation and decreased vagal activity, there is usually enhanced conduction of impulse
through AV node and shortening of PR interval.
SINUS PAUSE OR ARREST
1. Sinus pause or sinus arrest is result of intermittent failure of SA node impulse generation.
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3.
Sinus pause or arrest may be due to intrinsic SA node disease and dysfunction ("Sick sinus
syndrome") or from drugs that directly or indirectly (via ANS) depress SA node activity.
On surface ECG, sinus pause or arrest is manifest as absence of P wave at expected time
interval compared to prior PP interval. This absence may simply be delay of next P wave (sinus
pause) or may be complete absence of P wave with escape beat (sinus arrest). The duration
of pause should have no relationship to prior PP interval (which suggest SA exit block).
SINOATRIAL EXIT BLOCK
1. SA exit block most commonly arises from change in electrophysiologic characteristics of
tissue surrounding SA node, which results in inability to respond to or conduct impulse from
SA node into atrium. This can be due to drugs, disease, or increased vagus nerve activity.
2. Following 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 3 components.
A. A relatively constant input – The input is from pacemaker cells within SA node, which
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are not seen on surface ECG, but are inferred from P waves of atrial activation. The rate
or cycle length of input can be presumed from portions on ECG where normal P-P cycles
are observed.
B. An area across which block occurs – Exit block is thought to involve perinodal T cells.
The type of exit block in perinodal tissues must be inferred from output or response
(from P waves).
C. An output –P wave abnormalities reflect type of exit block that is present.
First degree SA nodal exit block reflects slowing of impulse exit but there is still 1:1
conduction. 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 pause caused by dropped P wave; pause has
duration that is < 2 P-P cycles. The mechanisms of Wenckebach conduction are discussed
elsewhere but are similar to AV Wenckebach block.
5.
In type II exit block, P-P output is arithmetic multiple of presumed sinus pacemaker input (2:1,
3:1, 4:1). Therefore P-P cycle length surrounding pause is multiple of normal P-P interval.
6.
Third degree SA nodal exit block prevents pacemaker impulses from reaching RA, giving
appearance of sinus arrest (no P waves).
7. For first and second degree SA nodal exit block, P wave is originating in SA node and had
normal P wave morphology. For third degree SA nodal exit block, there will either be escape
atrial, junctional, or ventricular rhythm, and P waves will either be different morphology or
absent.
SICK SINUS SYNDROME
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2.
SSS results from intrinsic disease of SA node. Some individuals with this syndrome also have
underlying disease of other portions of conduction system, particularly AV node.
Types
A. Tachycardia-bradycardia syndrome
i.
This form of syndrome is most often characterized by bursts of atrial
tachyarrhythmia (usually Af), which terminate spontaneously and are followed by
long offset pauses and symptomatic bradycardia (waveform 5). The pause is often
long and there may be no junctional escape rhythm because of associated AV
node disease.
ii.
The tachycardia-bradycardia syndrome is result of overdrive suppression of sinus
node by atrial arrhythmia. After arrhythmia termination, there is a variable delay
before SA node recovers and again generates impulse because of SA node
dysfunction. For example, profound sinus pauses and even sinus arrest with
syncope can occur after spontaneous conversion of PAf to sinus.
B. Bradycardia-tachycardia syndrome
i.
In this form of sick sinus syndrome, escape tachyarrhythmia, such as Af, results
from initial significant SB.
C. Chronotropic incompetence
i.
An abnormal HR response to exercise, defined as inability to achieve 85% of
age-predicted maximum HR, is one manifestation of diseased sinus node. The
resting ECG may be normal or abnormal.
D. Other forms
i.
Additional variations of SSS are fixed and symptomatic SB, long sinus pauses, or
sinus node arrest.
SINUS NODE REENTRY
1. Sinus node reentry or sinoatrial nodal reentry is infrequently seen SVT.
2.
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4.
Electrophysiologically, sinus node re-entry is due to continuous activity or circus movement
within SA node alone or in combination with perinodal tissue. This disturbance may result
from altered autonomic tone, which affects SA node and sinoatrial junction, and vagal
maneuvers such as carotid sinus massage may abruptly terminate rhythm.
This arrhythmia has sudden onset and offset with rate that is usually 100 to 160 bpm. P wave
precedes each QRS complex, unless there is simultaneous AVB with variable conduction, and
has morphology identical to sinus P wave.
PR interval is also similar to that of SR. However, this interval may be slightly longer than that
observed during sinus rhythm due to decremental conduction through AV node. Sinus node
re-entry is usually classified as long RP tachycardia.
5. Sinus node re-entry may be confused with atrial tachycardia, but P wave morphology and
response to vagal maneuvers helps differentiate. It may also be confused with conventional
ST but sudden onset of tachycardia and its abrupt termination suggest sinus node reentry.
SUMMARY
1. In normal sinus rhythm (including normal 1:1 AV conduction), an upright P wave in lead II with
a uniform morphology precedes each QRS complex. The rate is between 60 and 100 bpm 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.
2.
3.
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Sinus arrhythmia is present when there is a sinus rhythm with variability in the cycle lengths
between successive P waves. 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 < 60 bpm.
Sinus tachycardia is defined as a sinus rhythm with a rate of > 100 bpm.
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.
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 ECG.