SA NODE:- Located laterally in the epicardial grove of the sulcus terminalis,
near the junction of the right atrium and the superior vena cava
• The main cellular elements of the SA node are small, densely packed,
round, pale cells with sparse myofibrils and rare gap junctions.
• The pacemaker (p) cells are arranged in elongated clusters and make
contact with each other but not with the ordinary working myocardium.
• The latter communication is maintained via “transitional” cells, which
form a narrow zone at the borders of the node, most abundantly in the
Right coronary artery in 59 percent,
Left circumflex artery in 38 percent,
Dual blood supply in 3 percent.
Kyrialikdis MK, Kouraouklis CB, Papaioannou JT, et al.. Am J Cardiol 1983;51:749–750
• Both the parasympathetic and sympathetic.
• The sinus node is richly innervated with postganglionic
adrenergic and cholinergic nerve terminals.
• Vagal stimulation-- slows the sinus node discharge rate and
increases the intranodal conduction time.
• Adrenergic stimulation increases the sinus node discharge rate
SINUS NODE DYSFUNCTION
Disorders of automaticity, conduction, or both.
Abnormal automaticity, / sinus arrest--
failure of sinus impulse generation.
Abnormal conduction, or sinoatrial delay or block- failure of impulse
Stokes-Adams attacks, which is a case of fainting due to
insufficient blood to the brain. It is caused by improper
contraction of the ventricles.
Dizziness or feeling light headed.
Angina or chest pain
Shortness of Breath.
variants of sinus node dysfunction(sss)
• Sinus bradycardia (<60 beats per minute)
• Sinus arrest or pause
• Sino-atrial exit block
• Sinus tachycardia (>100 beats per minute)
• Atrial fibrillation with slow ventricular response
< 60 bpm
Atrial frequency 100-180 bpm
Ventricular frequency Same
P-wave positive in II, AVF
Sinus pause is the result of transient failure of impulse formation within the SA node or
impulse propagation from the SA node
When the postulated sinus inactivity, manifested by absent P waves, is prolonged, the
condition is called sinus arrest
SINO-ATRIAL EXIT BLOCK
• The depolarizations that occur in the sinus node cannot leave the
node towards the atria. They are blocked.
• On the ECG this is expressed as a pause.
• SA exit block can be distinguished from sinus arrest because the
pause in SA exit block is a multiple of the P-P interval that
preceded the pause.
Three subtypes can be distinguished
Type I second degree (Wenkebach) SA exit block:
the P-P interval progressively shortens prior to the pause
Type II second degree SA exit block:
the pause equals approximately 2-4 times the preceding PP interval
Third degree SA exit block:
absence of P waves (diagnosed with an sinus node electrode, during
symptoms of SA NODE dysfunction
Long Term ECG Recording
•A routine ECG may provide information in such patients.
•However, the symptoms are nonspecific and the ECG changes may not
Inability of the sinus node to achieve at least 80 percent of the age predicted
heart rate.Astrand's formula (220- age) at peak exercise.
Seen in 20 to 60 percent of patients with sinus node dysfunction.
Although the resting heart rates may be normal,
may have inability to increase their heart rate during exercise or
have unpredictable fluctuations in heart rate during activity.
-Gwynn N, R, Kratz, et al. Chronotropic incompetence. Am Heart J 1992;123:1216.
• Specific sinus node chronotropic incompetence is the
inability of the sinus node to accelerate in response to
metabolic demands secondary to intrinsic disease or
negative chronotropic drugs.
• Functional chronotropic incompetence manifests itself
either as atrial tachyarrhythmias or as retrograde
Atropine/isoproterenol — Atropine (1 or 2 mg) / isoproterenol (2 to 3 μg/min)
Abnormal response --- increase in the sinus rate of <25 %, or to a rate below 90 beats/min.
There has been no standardization of the pharmacologic testing,
No dose ranging has been reported,
The specificity and sensitivity of the tests are uncertain,
SSS may exist even if the response is normal.
Isoproterenol is risky in patients with ischemic and other types of heart disease.
Beta blockers —
Propranolol has been used to assess sinus node function on the assumption that
the chronotropic response may differ between patients with a normal and a sick sinus
This approach, however, has been disappointing
Adenosine directly inhibits sinus node activity
Due to increased potassium conductance -hyperpolarization of the resting
Adenosine should be considered as an alternative to invasive testing in patients
with suspected SSS.
Intrinsic heart rate — Atropine (0.04 mg/kg) and propranolol (0.2 mg/kg)
Heart rate at 30 minutes is called the (IHR) .
The IHR is a function of age
IHR, in beats/min = 117.2 - [0.53 x age]
IHR separates intrinsic SSS from extrinsic SSS
Intrinsic SSS is presumed to be present if the sinus rate does not exceed
the predicted IHR after atropine.
In patients engaged in normal daily activities
• document and quantitate the frequency and complexity of an arrhythmia
• correlate the arrhythmia with the patient's symptoms, and
• evaluate the effect of antiarrhythmic therapy on spontaneous arrhythmia.
• For example, recording normal sinus rhythm during the patient's typical
symptomatic episode effectively excludes cardiac arrhythmia as a cause
• If symptoms are frequent, 24- or 48-hour ambulatory Holter monitoring
can be useful.
• Documentation of symptoms in a diary by the patient.
• Often the sinus pauses recorded are not associated with symptoms.
• Several Holter monitor studies demonstrated the futility of treating
asymptomatic pauses, even if they were 3 seconds or longer.
• The length of the pause correlated poorly with symptoms and prognosis
• In many patients, the 24-hour snapshot provided by the Holter
recording is incapable of documenting the cause of the patient's
• These devices are about the size of a pager and are kept by the
patient for 30 days.
IMPLANTABLE LOOP RECORDER
• For patients with infrequent and transient symptoms, neither Holter
recorders nor 30-day event recorders may yield diagnostic information.
• In such patients, implantable loop recorders may be used.
• This device (about the size of a pack of
chewing gum) is inserted under the skin
at about the second rib on the left front
of the chest and is activated by passing
a special magnet over the device.
Signal-averaged P wave
fractionated endocardial electrograms in the SSS:-
• Long, low amplitude signals early during the signal averaged P wave
were found to be characteristic of SSS.
• In paroxysmal atrial fibrillation the incidence of SSS was higher in
those with low amplitude atrial early potentials on a signal-averaged
- Yamada, et al. J Am Coll Cardiol 1996; 28:738.
•The symptomatic patient who has no ECG findings suggestive of SSS.
•The symptomatic patient in whom ECG fail to correlate with
•The patient who develops dysfunction of the SA node on usual doses
EPS indications cont…
•The patient with syncope or near syncope who has bundle branch or
multifascicular block may require electrophysiologic evaluation of the SA
node, the AV node, and the infranodal His-bundle branch-Purkinje system.
•Electrophysiologic testing that shows SA nodal dysfunction allows the
selection of appropriate therapy in up to 50 percent of these patients.
• Unstable angina
• Bacteremia or septicemia
• Acute decompensated congestive heart failure not
caused by the arrhythmia
• Major bleeding diathesis
• Acute lower extremity venous thrombosis if femoral
vein cannulation is desired.
SINOATRIAL NODE RECOVERY TIME
• — The SNRT is perhaps the most useful test of overall sinus nodal
• The atria are driven rapidly:
a normal SA node will have a recovery time within certain limits,
• while recovery will be delayed in a depressed or sick sinus node.
It is performed by placing a catheter near the SN.
Overdrive stimulation is performed at a rate higher than that of the SA
node for about one minute (the range in most published reports is 30 to
Pacing is then stopped, and the time from the last paced atrial beat to the
first spontaneous electrical beat with a sinus morphology is measured.
Pacing is increased 10 to 20 beats/min up to 200 beats/min, if tolerated.
corrected by subtracting the sinus cycle length from the SNRT
defined as the recovery interval in excess of the sinus cycle
Total recovery time (TRT)
which is the time required to return to the basal sinus rate.
Normal values have generally been estimated as follows :
•SNRT < 1500 milliseconds
•CSNRT < 550 milliseconds
•TRT less than five seconds.
Josephson, ME. Sinus Node Dysfunction. In: Josephson ME, ed. Clinical Cardiac Electrophysiology. Techniques and Interpretations. Third ed. Philadelphia:
• The SNRT or SNRTc is abnormal in more than 50 percent of patients with
J Am Coll Cardiol 1995; 26:555
• Overdrive suppression, used in conjunction with intravenous disopyramide ,
may increase the sensitivity of the test and its potential to diagnose a SSS .
Ishikawa, et al.. Sinus node recovery. Europace 2000; 2:54
• The noninvasive determination of the sinus cycle length, corrected to the basic
cycle length, after a bolus of adenosine is also an indicator of SSS.
Burnett, D, Abi-Samra, F, Vacek, JL. Use of intravenous adenosine
asnoninvasive diagnostic test for sick sinus syndrome. Am Heart J
Limitations of SNRT
Changes in autonomic tone due to the effects of pacing
Changes in P-wave morphology suggesting a pacemaker shift
Sinoatrial entrance block
The hemodynamic effects of atrial pacing
In fact, direct SN recordings have demonstrated that the majority of
these pauses are due to sinoatrial exit block rather than impaired
- Tracy, CM, Akhtar, M, DiMarco, JP, et al
THE USE OF TRANSESOPHAGEAL ATRIAL PACING
Transesophageal pacing has been used to assess sinus node dysfunction,
primarily by assessing SNRT, and has been recommended in the
evaluation of patients with syncope.
• Brembilla-Perrot, B, Beurrier, D, Houriez, P, et al. Utility oftransesophageal atrial pacing in the
diagnostic evaluation of patientswith unexplained syncope associated or not with
palpitations. Int JCardiol 2004; 96:347.
• Sino Atrial Conduction Time
• Can be measured in two ways
The usual method
This approach involves the placement of a catheter near the sinus
progressively premature atrial extrastimuli (A2) are introduced after
every eighth to tenth beat of stable sinus rhythm.
Brief periods of atrial pacing at rates above sinus.
The interval between each of the normal sinus beat or the stable
sequence of paced beats.
• A2-paced impulse
• A3-The first spontaneous sinus beat that occurs after
termination of the pacing.
The interval between the final paced impulse (A2) and the first
spontaneous beat (A3) is referred to as the return interval
• Four zones after APD
APD IN LAST 20-30% OF SCL
ie, less than compensatory-impulse in earliest
third of zone 2(40-50% OF SCL)
The A1-A1 interval
Time required to generate a sinus impulse., conduction time does
not contribute to A1-A1.
A2-A3 (Because A2 resets the SN, the return cycle length) =
generation of the next sinus beat (reflecting SNautomaticity)
conduction of the impulse into and out of SN tissue.
(A2-A3) –(A1-A1) =
Total time it takes to enter and exit the SN tissue.
This number represents twice the SACT
SACT = [(A2-A3) – (A1-A1)] / 2
Normal SACT times generally range from 40 to 150 milliseconds
Limitations of SACT
The assumption that entrance into and exit out of the SN takes the same amount of time is not
Distance of the stimulation site from the SN is another source of error. The farther the site is from the
SN, the greater the potential for overestimation of the SACT due to conduction delays in both atrial
and perinodal tissues.
Reproducibility of results
shift in intrinsic pacemaker site
Depression of automaticity, and
sinus entrance block
Direct recording of the sinoatrial
conduction time (sinus node electrogram)
• Endocardial recordings demonstrate diastolic phase 4 activity followed by
a slow upstroke culminating in a rapid atrial EGM.
• The directly measured SACT was defined as the interval between the local
EGM and the rapid atrial deflection.
• Sinoatrial block occurs when the local EGM was seen in the absence of an
• SENSITIVITY OF SNRT AND SACT
• SPECIFICITY OF SNRT AND SACT
CORRELATION OF SNRT AND SACT WITH ECG
Patients with Symptomatic sinus bradycardia – longer SNRT and SACT
Patients with SA block - longer SACT
Patients with the tachycardia-bradycardia syndrome had a longer SNRT
Breithardt, G, Seipel, L, Loogen, F. Sinus node recovery time and calculated
sinoatrialconduction time in normal subjects and patients with sinus node dysfunction. Circulation
SINUS NODE AND ATRIAL REFRACTORY
SA nodal refractoriness has been determined using both the extrastimulus
and pacing train techniques.
Normal subjects having a SNERP of 250 to 350 msec as compared to a value
of 500 to 550 msec in patients with the SSS
Kerr, CR, Strauss, HC. The measurement of sinus node refractoriness inman. Circulation 1983;
COMPLICATIONS DURING EP STUDY
• Hematoma at the puncture site in the groin and or neck
• Infection caused by manipulation of catheters (theoretical risk)
• Perforation upon catheter manipulation inside the heart of small patients
(most commonly involving the right atrial appendage and the right ventricular
TREATMENT OF SSS
Mainly directed at symptoms
Search for remidial causes - Drugs
Mostly by pace makers.
Ablation for AF
A number of additional pacemaker features may be useful in selected patients:
Rate responsive programming
SSS and chronotropic insufficiency and exertional symptoms.
SSS who have paroxysmal atrial tachycardia.
Three major issues that need to be considered;
1. Ventricular pacing can induce dyssynchrony observe for evidence of heart failure.
2. In patients with an AAI pacemaker, monitoring for progression to high degrees of AV block is essential
as the reported rate varies from 0.6 to as high as 3 percent.
3. Due to the thromboembolic risks associated with unrecognized AF, patients should be observed for the
development of atrial arrhythmias.