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E C G E D U C AT I O N
SINUS NODE DYSFUNCTION
Part two of an educational series on ECG analysis and arrhythmia diagnosis
Dr Ronal M Jardine — Cardiologist
Linmed Hospital
First described in 1909 by Laslett, sinus node dysfunction
(SND) has increasingly been shown over the last century to
be responsible for symptoms, typically syncope or pre-syncope, but also less specific complaints such as fatigue,
dyspnoea, angina, a change in mental state (particularly in
the elderly) or palpitations if atrial tachy-arrhythmias occur.
The overall incidence is estimated to be 0.17% and it is
clearly a phenomenon of advancing age.
ELECTROCARDIOGRAPHIC MANIFESTATION
OF SINUS NODE DYSFUNCTION
• Inappropriate sinus bradycardia. Sinus bradycardia is defined as a sinus rate of less that 50 bpm, and is
sometimes appropriate, e.g. due to athletic vagotonia in
young individuals and during sleep. It is inappropriate if it
is persistent, or responsible for symptoms, or accompanied
by chronotropic incompetence (vide infra).
• Sinus arrest (or sinus pause). Pauses in sinus rhythm
of up to 3 seconds are seen in 11% of normal patients during holter monitoring, and even more commonly in athletes
(36%). In contrast pauses of > 3 seconds are rare in normal individuals and are generally regarded as pathological. They represent a failure of impulse generation within
the SA node, and as opposed to sino-atrial exit block, the
sinus pause when measured is not a multiple of the preceding sinus cycle length.
• Sino-atrial exit block. In contrast, in SA exit block,
the impulse is generated within the SA node but fails to
enter the surrounding atrial tissue. As with AV block, there
are 3 degrees of block, but only 2° SA exit block can be
diagnosed on the ECG with certainty, when a pause is
noted which is a multiple of the preceding sinus cycle
length, e.g. 2 X, 3 X, or 4 X as long. 1 degree SA block is
not evident on the surface ECG, and 3 degree SA exit
block will produce prolonged pauses not distinguishable
from sinus arrest. The distinction is not however important
as in both cases if there are symptoms, treatment is necessary.
• Tachy-brady syndrome. Typically this includes a
propensity for tachycardia, usually atrial fibrillation, but
sometimes atrial flutter or other atrial tachycardia, and
bradycardia, usually sinus bradycardia or sinus pauses.
The ECG attached demonstrates atrial fibrillation followed
by a pause before the resumption of normal sinus rhythm
208 CME April 2004 Vol.22 No.4
Fig.1
and classically this would produce a complaint of a paroxysm of palpitations followed by syncope/pre-syncope.
• Post-cardioversion asystole. If external electrical
cardioversion for atrial fibrillation is followed by a prolonged pause before the re-initiation of sinus rhythm, sinus
node dysfunction is present.
• Chronotropic incompetence. Failure of acceleration
of the sinus node in response to exercise or infusion of a
beta 1-stimulant is abnormal and termed ‘chronotropic
incompetence’. In contrast, young athletes with vagotonic
sinus bradycardia have normal acceleration, albeit with
rapid deceleration in the recovery phase after exercise.
CAUSES OF SINUS NODE DYSFUNCTION
A number of pathological mechanisms cause the aforementioned abnormalities. Failure of impulse generation and
failure of the impulse to exit the SA node have been mentioned, but there is also failure of physiological subsidiary
pacemaker activity (failed escape rhythm), and also
increased atrial vulnerability to fibrillation and other tachyarrhythmias.
The causes of sinus node dysfunction are listed in Table I.
Intrinsic causes imply organic disease of the SA node,
whereas extrinsic causes are the effects of drugs, autonomic
nervous system and other physiological changes on the
node.
INVESTIGATIONS FOR SINUS NODE
DYSFUNCTION
• ECG. Clearly a recording of a full 12-lead ECG during
symptoms is diagnostic, but often logistically difficult. For
that reason, a number of techniques for prolonged ECG
monitoring are necessary. Ambulatory 24-hour ECG
recording (Holter) is very useful, but has a relatively low
yield and may have to be repeated a number of times
before diagnostic abnormalities are recorded.
Alternatively, patients can be given an event-triggered ECG
E C G E D U C AT I O N
T ABLE I. C AUSES OF SINUS NODE DYSFUNCTION
INTRINSIC CAUSES
• Idiopathic degenerative disease
• Coronary artery disease
• Cardiomyopathy
• Hypertension
• Infiltration (amyloid, haemochromatosis, tumours)
• Collagen disease (scleroderma and SLE)
• Surgical trauma (NB cardiac transplantation)
• Congenital:familial
congenital heart disease
surgery for congenital heart disease especially the Mustard operation for transposition and ASD closure
especially sinus venosus type
• Musculo-skeletal disorders (myotonic dystrophy, Friedreich’s ataxia)
EXTRINSIC CAUSES
• Drugs: beta-blockers
calcium channel blockers
digoxin
adenosine
sympatholytic anti-hypertensives (clonidine, methyldopa and reserpine)
anti-arrhythmic drugs:
type IA
type IC
type III
others: lithium
cimetidine
amitriptyline
phenytoin
phenothiazine
• Autonomic effects: athletic vagotonia
neuro-cardiogenic syncope
other neurally-mediated syncopes
e.g. carotid sinus hypersensitivity
• Other: electrolyte abnormalities: hyperkalaemia, hypercarbia
hypothyroidism
raised intracranial pressure
hypothermia
sepsis
recorder to self-record at the time of any symptoms, and
then transmit this ECG by telephone line to a central monitoring service. Typically patients would keep this recorder
for 2 - 4 weeks. The frequency of symptoms guides the
choice of which of these 2 forms of monitoring to use in the
first instance.
• Exercise ECG testing is helpful in the diagnosis only in
terms of establishing that there is chronotropic incompetence, i.e. that this is not athletic vagotonia, and this will
also guide in the choice of pacemaker, i.e. some form of
rate-responsive pacemaker will be necessary for chronotropic incompetence.
• Autonomic testing. Two groups of autonomic test can
yield some information, specifically as to whether this is an
intrinsic or extrinsic form of sinus node dysfunction. Testing
of autonomic reflexes with e.g. carotid sinus massage, the
Valsalva manoeuvre, and tilt testing is possible. Of these,
only carotid sinus massage is mandatory is all cases,
because the presence of carotid sinus hypersensitivity indicates the need for a dual-chambered pacemaker as
opposed to a single-chambered atrial pacemaker which is
applicable to most forms of sinus node dysfunction.
Pharmacological tests of autonomic function by injections of
isoprenaline, atropine, propranolol, or the combination of
atropine and propranolol have been studied. The atropine
plus propranolol combination effectively results in total autonomic blockade, and allows the measurement of a parameter called the ‘Intrinsic Heart Rate’ for which there are
defined normal values, and if lower than this, supports the
diagnosis of sinus node dysfunction if it is in question.
• Electro-physiological testing. Measurement of the
intrinsic heart rate can be done at the time of electrophysiological testing also. A number of electrophysiological
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E C G E D U C AT I O N
parameters have been devised over the past 30 years to
enable a diagnosis of sinus node dysfunction, but they all
suffer from a relatively low sensitivity of 70%, albeit with an
acceptable level of specificity of about 90% overall. These
tests are also tedious and suffer from a wide range of
reported normal values. Consequently they are not widely
applied at present. They include sinus node recovery time
(SNRT) after a period of atrial pacing, to test overdrive suppression of sinus node automaticity, and the corrected SNRT
(CSNRT) taking into account the underlying sinus rate.
Sino-atrial conduction time (SACT) through timed extra-stimuli during sinus rhythm or an atrial paced rhythm, measures
conduction in and out of the node. At the same time, sinus
node effective refractory period (SNERP) is measurable.
thrombo-embolism, certainly in patients aged 65 years or
more, with the target INR of 2.0 - 3.0.
Drug therapy for the brady-arrhythmias of sinus node dysfunction is generally not recommended (vagolytic and sympathomimetic drugs and hydrallazine have not been found
to be useful in the past). There is a small group of young
patients with sinus node dysfunction, which is probably
vagotonic, who respond to long-acting theophylline as
symptomatic treatment until the sinus node dysfunction has
self-resolved. This small niche for drug therapy does obviate the need for permanent pacemaker implantation in
young persons, which is highly desirable.
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Treatment
•Asymptomatic patients. It is clear from natural history
studies that the long-term prognosis for patients with sinus
node dysfunction is no different from the general population
provided that there is no associated structural heart disease
and that atrial fibrillation is not part of the presentation.
This means there is no mortality benefit from permanent
pacemaker implantation in this group. They must merely
avoid the drugs known to suppress the SA node
(see Table I), and if atrial fibrillation is known to be present,
must receive chronic anti-coagulation with warfarin to keep
the INR between 2.0 and 3.0.
•Symptomatic patients. Permanent pacemaker implantation is a very effective form of symptom relief. It abolishes brady-arrhythmic symptoms, and if an appropriate A-V
sequential mode is used, also diminishes the frequency of
atrial fibrillation.
Numerous studies have shown the detrimental effects of single chambered ventricular pacing (VVI/VVI-R) in patients
with sinus node dysfunction, because of the increased incidence of atrial fibrillation due to intact retrograde VA conduction. This has swayed most cardiologists towards
implantation of a dual-chambered pacing system (DD/DDDR), and this has been driven on by unfounded fears about
the possibility of future AV block in these patients. If at the
time of presentation/implantation there is no evidence of
AV conduction delay (e.g. prolongation of the PR interval,
bundle branch block, an AV Wenckebach rate of
<120 bpm, prolongation of the HV interval at EP study, or
documented 2° or 3° AV block), the subsequent risk of AV
block is 2.7% per annum and this figure includes 1° and
Wenckebach type 2° AV clock. Therefore, a simpler,
cheaper, and equally effective form of pacing is singlechambered atrial pacing
(AAI/AAI-R).
In cases of the tachy-brady syndrome, atrial pacing alone
will diminish the risk for atrial tachy-arrhythmias, but if they
recur, anti-arrhythmic drugs can be used, bearing in mind
their possibility for influencing AV nodal conduction. Anticoagulation with warfarin is mandatory for prevention of
210 CME April 2004 Vol.22 No.4
• Asymptomatic sinus pauses > 2 seconds occur in 11%
of normal individuals and even more commonly in athletes (36%).
• Tests for sinus node dysfunction at electro-physiological
study are only 70% sensitive and 90% specific.
• The key to successful treatment of sinus node dysfunction is to establish a link between ECG abnormalities
and symptoms – a difficult task.
• Single-chamber ventricular pacing is a poor form of
treatment for sinus node dysfunction because it promotes the development of atrial fibrillation.
• Provided that there is no evidence of AV conduction
delay at the time of implantation/presentation, singlechamber atrial pacing is a good treatment for sinus
node dysfunction because the subsequent development
of AV block is only 2.7% per annum.
A SPECIAL INTEREST GROUP OF SA HEART ASSOCIATION
P.O. Box 2826, Benoni, 1500
E-mail: [email protected]
Fax: 021-448 7062
This article is sponsored by Johnson & Johnson Medical,
in the interest of continued medical education
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