The sinus node is the dominant pacemaker of the heart located in the right atrium. Sinus node dysfunction can cause abnormal automaticity or conduction, resulting in bradycardic rhythms like sinus bradycardia, sinus pauses, or tachycardic rhythms like inappropriate sinus tachycardia. Evaluation involves surface ECG, exercise testing, drug challenge, and invasive electrophysiological study if needed to diagnose sinus node disorders.

1. SINUS NODE DYSFUNCTION

2. ANATOMY
SA NODE:- Located laterally in the
epicardial grove of the sulcus terminalis,
near the junction of the right atrium and
the superior vena cava

4. • The sinus node is the dominant pacemaker of the heart.
• Its pacemaker function is determined by its low maximum diastolic membrane
potential and steep phase 4 spontaneous depolarization.
• It is a spindle-shaped structure with a central body and tapering ends; the
head extends toward the interatrial groove, and the tail extends toward the
orifice of IVC.
• In adults, the SA node measures 10 to 20 mm long and 2 to 3 mm wide and
thick.
• Consists of densely packed specialized myocytes of no definite orientation
within a background of extracellular connective tissue matrix.
• Commonly, prongs of nodal (P) cells and transitional (T) cells extend from the
nodal body into the atrial myocardium, but actual cell-to-cell interaction is
uncertain

5. • It is composed of nests of principal pacemaker cells which spontaneously
depolarize.
• other nests contain cells with slower intrinsic depolarization rates and
serve as backup pacemakers in response to changing physiological and
pathological conditions.
• Normal conduction velocities within the sinus node are slow (2 to 5
cm/sec), increasing the likelihood of intranodal conduction block.
• The sinus node is insulated electrically from the surrounding atrial
myocytes, except at a limited number of preferential exit sites.

6. Blood Supply
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

7. • Enhanced vagal activity can produce sinus bradycardia, sinus arrest, and
SA exit block, increased sympathetic activity can increase the SR and
reverse sinus arrest and SA exit block.
• Sinus node responses to brief vagal bursts begin after a short latency and
dissipate quickly; in contrast, responses to sympathetic stimulation begin
and dissipate slowly.
• The rapid onset and offset of responses to vagal stimulation allow dynamic
beat-to-beat vagal modulation of the heart rate, whereas the slow
temporal response to sympathetic stimulation precludes any beat-to-beat
regulation by sympathetic activity.

8. 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 transmission.

10. • Idiopathic degenerative disease is probably the most common cause of
intrinsic SND.
• IHD can be responsible for one third of cases of SND.
• Surgical trauma is responsible for most cases of SND in the pediatric
population most commonly Mustard procedure for TGA and repair of ASD,
especially of the SV type.
• Atrial tachyarrhythmias can precipitate SND, likely secondary to
remodeling of sinus node function finding supported clinically by the
observation that successful catheter ablation of AF and AFL can be
followed by significant improvements in sinus node function.
• SND has been associated with an increased propensity of atrial tachy -
arrhythmias, AF in particular.

11. • SND can sometimes result from excessive vagal tone in
individuals without intrinsic sinus node disease.
• Hypervagotonia can be seen in hypersensitive carotid sinus
syndrome and neurocardiogenic syncope.
• Well-trained athletes with increased vagal tone occasionally
may require some deconditioning to help prevent
symptomatic bradyarrhythmias.
• Surges in vagal tone also can occur during Valsalva
maneuvers, endotracheal intubation, vomiting, and
suctioning.

12. SYMPTOMS
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
FatigueHeadache
Nausea
Palpitations
Shortness of
Breath.

13. • Patients often are asymptomatic or have symptoms that are mild and
nonspecific, and the intermittent nature of these symptoms makes
documentation of the associated arrhythmia difficult.
• Symptoms, which may have been present for months or years, include
paroxysmal dizziness, presyncope, or syncope, which are predominantly
related to prolonged sinus pauses.
• Episodes of syncope are often unheralded and can manifest in older
patients as repeated falls.
• The highest incidence of syncope associated with SND occurs in
tachycardia-bradycardia syndrome, in whom syncope typically occurs
secondary to a long sinus pause following cessation of the SVT (usually
AF).
• Occasionally, a stroke can be the first manifestation of SND in patients
presenting with paroxysmal AF and thromboembolism.

14. • Patients with sinus bradycardia or chronotropic incompetence can present
with decreased exercise capacity or fatigue.
• Chronotropic incompetence is estimated to be present in 20% to 60% of
patients with SND.
• Other symptoms include irritability, nocturnal wakefulness, memory loss,
lightheadedness, and lethargy.
• More subtle symptoms include mild digestive disturbances, periodic
oliguria or edema, and mild intermittent dyspnea.
• Additionally, symptoms caused by the worsening of conditions such as CHF
and angina pectoris can be precipitated by SND.

15. Natural History
• The natural history of SND can be variable, but slow progression (over 10 to
30 years) is expected.
• The worst prognosis is associated with the tachycardia-bradycardia
syndrome (mostly because of the risk for thromboembolic complications),
whereas sinus bradycardia is much more benign.
• The incidence of new-onset AF in patients with SND is about 5.2% per year.
• New atrial tachyarrhythmias occur with less frequency in patients who are
treated with atrial pacing (3.9%) compared with an increased incidence of
similar arrhythmias in patients with only ventricular pacing (22.3%).
• Thromboembolism occurs in 15.2% among unpaced patients with SND
versus 13% among patients treated with only ventricular pacing versus 1.6%
among those treated with atrial pacing.

16. • The incidence of advanced AV conduction system disease in patients with
SND is low (5% to 10%), and when present, its progression is slow.
• At the time of diagnosis of SND, approximately 17% of the patients have
some degree of AV conduction system disease (PR > 240 ms, BBB, HV
interval prolongation, AV Wenckebach rate < 120/min, or 2nd or 3rd-degree
AV block).
• New AV conduction abnormalities develop at a rate of approximately 2.7%
per year.
• The incidence of advanced AV block during long-term follow-up is low
(approximately 1% per year).

17. DIAGNOSTIC ALGORITHM
symptoms of SA NODE
dysfunction
Surface ECG
Excersice testing
Drugs-atropine+/-propronolol
Long Term ECG Recording
EPS (INVASIVE)

18. ECG
A routine ECG may provide information in such
patients.
However, the symptoms are nonspecific and the
ECG
changes may not be
diagnostic.

19. variants of sinus node dysfunction(sss)
Asystole
Sinustachycardia (>100 beats per
minute)
Sinusbradycardia (<60 beats per
minute)
Sinus arrest or pauseSino-atrial exit block
Atrial fibrillation with slow ventricular
response

20. SINUS BRADYCARDIA
• Sinus bradycardia (less than 60 beats/ min) is considered
abnormal when it is persistent, unexplained, and
inappropriate for physiological circumstances.
• Sinus bradycardia slower than 40 beats/min (not associated
with sleep or physical conditioning) is generally considered
abnormal.

21. INAPPROPRIATE SINUS BRADYCARDIA
Atrial frequency < 60
bpm
Ventricular frequency
same
Regularity
regular
Origin
sinus node
P-wave
normal

22. SINUS PAUSES
• Sinus arrest and sinoatrial exit block can result in sinus pauses, and they
are definite evidence of SND.
SINUS ARREST
• sinus arrest is a result of total cessation of impulse formation within the
sinus node.
• The pause is not an exact multiple of the preceding P-P interval but is
random in duration
.
• Asymptomatic pauses of 2 to 3 seconds can be seen in up to 11% of
normal individuals and in one third of trained athletes
• Pauses longer than 3 seconds are rare in normal individuals and may or
may not be associated with symptoms, but they are usually caused by
SND.

23. SINUS ARREST
The sinus node stops firing resulting in a pause in heart
beat

24. INAPPROPRIATE SINUS TACHYCARDIA
Atrial frequency 100-180 bpm
Ventricular frequency Same
Regularity regular
Origin
sinus node
P-wave positive in II, AVF

25. SINO-ATRIAL EXIT BLOCK
The depolarizations that occur in the sinus node canno
leavethe node towards the atria. They are
blocked.
On the ECG this is expressed as a
pause.
SA exit block can be destinguished from sinusarrest
because
the pause in SA exit block is a multiple of the P-P
interval
that preceded the pause.

26. Sinus node exit block
• Exit block is classified into three types, analogous to those of AV block:
first-degree, second-degree, and third-degree exit block.
• First-degree sinoatrial exit block is caused by abnormal prolongation of the
sinoatrial conduction time (SACT).
• It occurs every time a sinus impulse reaches the atrium, but it is
conducted with a delay at a fixed interval.
• This type of sinoatrial exit block is concealed on the surface ECG and can
be diagnosed only by direct sinus node recording or indirect measurement
of SACT during an EP study.

27. 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
electrophysiological evaluation)

28. Second degree SA block
• Second-degree sinoatrial exit block is marked by intermittent failure of the
sinus impulse to exit the sinus node.
• Type I block is viewed as Wenckebach periodicity of the P wave on the
surface ECG, and it manifests as progressive delay in conduction of the
sinus-generated impulse through the sinus node to the atrium, finally
resulting in a nonconducted sinus impulse and absence of a P wave on the
surface ECG.
• As the sinus discharge is a silent event on the surface ECG, this arrhythmia
can be inferred only, because of a missing P wave and the signs of
Wenckebach periodicity seen with this type of arrhythmia.
• The increment in delay in impulse conduction through the sinus node
tissue is progressively less; thus, the P-P intervals become progressively
shorter until a P wave fails to occur. The pauses associated with this type
of sinoatrial exit block are less than twice the shortest sinus cycle.

29. Type I second degree (Wenkiebach) SA exit block

30. • Type II block manifests as an abrupt absence of one or more P waves
because of failure of the atrial impulse to exit the sinus node, without
previous progressive prolongation of SACT (and without progressive
shortening of the P-P intervals).
• Sometimes, two or more consecutive sinus impulses are blocked within
the sinus node, thus creating considerably long pauses.
• The sinus pause should be an exact multiple of the immediately preceding
P-P interval.
• Third-degree or complete sinoatrial exit block manifests as absence of P
waves, with long pauses resulting in lower pacemaker escape rhythm.
• This type of block is impossible to distinguish from sinus arrest with
certainty without invasive sinus node recordings.

31. Type 2 second degree SA exit block

32. TACHYCARDIA-BRADYCARDIA SYNDROME
• Frequently referred to as SSS, is a common manifestation of SND, and it
refers to the presence of intermittent sinus or junctional bradycardia
alternating with atrial tachyarrhythmias .
• The atrial tachyarrhythmia is most commonly paroxysmal AF, but atrial
tachycardia, atrial flutter, and occasionally AVN reentrant tachycardia or AV
reentrant tachycardia can also occur.
• Patients often experience prolonged sinus arrest and asystole on
termination of the atrial tachyarrhythmia, resulting from overdrive
suppression of the SA node and secondary pacemakers by the tachycardia.
• Long sinus pauses that occur following electrical cardioversion of AF
constitute another manifestation of SND.
• Conversely atrial tachyarrhythmias can be precipitated by prolonged sinus
pauses.

33. TACHYCARDIA-BRADYCARDIA SYNDROME
Tachycardia-bradycardia syndrome - Two surface ECG leads showing AF that
spontaneously terminates followed by a 5.9-second pause before sinus rhythm
resumes. The patient became lightheaded during this period.

34. AF WITH SLOW VENTRICULAR RESPONSE
• Persistent AF with a slow ventricular response in the absence of AVN
blocking drugs is often present in patients with SND.
• These patients can demonstrate very slow ventricular rates at rest or
during sleep and occasionally have long pauses.
• Occasionally, they can develop complete AV block with a junctional or
ventricular escape rhythm. They can also conduct rapidly and develop
symptoms caused by tachycardia during exercise.
• In some cases, cardioversion results in a long sinus pause or junctional
escape rhythm before the appearance of sinus rhythm.
• Although a combination of sinus node and AV conduction disease can be
present in many cases, examples of rapid ventricular responses during
atrial tachyarrhythmias are frequently found.

35. PERSISTENT ATRIAL STANDSTILL
• Atrial standstill is a rare clinical syndrome in which there is no
spontaneous atrial activity and the atria cannot be electrically
stimulated.
• The surface ECG usually reveals junctional bradycardia without atrial
activity.
• The atria are generally fibrotic and without any functional myocardium.
• Lack of mechanical atrial contraction poses a high risk for
thromboembolism in these patients.

36. CHRONOTROPIC INCOMPETENCE
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
exerciseor
have unpredictable fluctuations in heart rate during
activity.-Gwynn N, R, Kratz, et al. Chronotropic incompetence.
Am Heart J
1992;123:1216.

37. CAROTID SINUS HYPERSENSITIVITY
• An abnormal response to carotid sinus massage (pause longer
than 3 seconds) can indicate SND, but this response may also
occur in asymptomatic older individuals.
Two surface ECG leads are shown during carotid sinus pressure, the PR interval is prolonged,
followed by a 7.5-second sinus pause ended by a P wave and probable junctional escape
complex. The patient was nearly syncopal during this period.

38. SINUS ARRHYTHMIA
• Respiratory sinus arrhythmia - the sinus rate increases with
inspiration and decreases with expiration, is not an abnormal
rhythm and is most commonly seen in young healthy subjects.
• P wave morphology is normal and consistent and the P-P intervals
vary by more than 120 ms.
• Non respiratory sinus arrhythmia - phasic changes in sinus rate are
not related to the respiratory cycle, can be accentuated by the use
of vagal agents such as digitalis and morphine; its mechanism is
unknown.
• Patients with nonrespiratory sinus arrhythmia are likely to be older
and to have underlying cardiac disease, although the arrhythmia is
not a marker for structural heart disease.
• None of the sinus arrhythmias indicate SND.

39. Ventriculophasic sinus arrhythmia
• It is an unusual rhythm that occurs when sinus rhythm and high-grade or
complete AV block coexist
• It is characterized by shorter P-P intervals when they enclose QRS
complexes and longer P-P intervals when no QRS complexes are enclosed.
• The mechanism is uncertain but may be related to the effects of the
mechanical ventricular systole itself: ventricular contraction increases the
blood supply to the sinus node, thereby transiently increasing its firing
rate.
• Not a pathological arrhythmia and should not be confused with PACs or
sinoatrial block

40. Ventriculophasic sinus arrhythmia. Surface ECG during sinus rhythm with second-
degree 2:1 AV block. Consecutive sinus P waves enclosing a QRS occur at shorter
intervals than that of consecutive P waves without a QRS in between (ventriculophasic
arrhythmia).

41. DRUGS
Atropine/isoproterenoll— 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.
Potential problems.
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.

42. DRUGS
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
node.This approach, however, has been
disappointing

43. DRUGS cont…
Adenosine directly inhibits sinus node
activity Due to increased potassium
conductance
-hyperpolarization of the resting membrane potential.
Adenosine should be considered as an
alternative to
invasive testing in patients with suspected SSS.

44. PHARMACOLOGICAL DENERVATION
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 = 118.1 - [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.

45. Longterm Electrocardiographic Recording
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

46. HOLTER RECORDING

47. HOLTER RECORDING
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
treating asymptomatic pauses, even if they were 3
seconds or
longer.The length of the pause correlated poorly with
symptoms
and prognosis

48. EVENT RECORDING
In many patients, the 24-hour snapshot provided by
the
Holter recording is incapable of documenting the
cause of
the patient's symptoms.
These devices are about the size of a pager and are
kept bythe patient for 30
days.

49. IMPLANTABLE LOOP RECORDER
For patients with infrequent and transient symptoms,
neitherHolter 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
insertedunder the skin at about the second rib on the left front of t
chest
and is activated by passing a special magnet over the dev

50. LOOP RECORDERS

51. EPS

52. Indications
The symptomatic patient who has no ECG
findingssuggestive of
SSS.
The symptomatic patient in whom ECG fail to correlate
with
symptoms.
The patient who develops dysfunction of the SA node on
usual
doses of drugs.
ELECTROPHYSIOLOGICAL TESTING

53. EPS indications cont…
The patient with syncope or near syncope who has bund
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 dysfunctio
allows the selection of appropriate therapy in up to 50
percent
of these patients.

54. TECHNIQUE
PACING SITE - Pacing is performed in the high RA at a site near the sinus
node, to decrease the conduction time to and from the sinus node.
PACING CYCLE LENGTH.
- SNRT is preferably measured after pacing at multiple CLs.
- Pacing is started at a CL just shorter than the sinus CL.
- After a 1-minute rest, pacing is repeated at progressively shorter CLs
(with 50- to 100-ms decrements) down to a pacing CL of 300 ms.
PACING DURATION.
• Pacing is continued for 30 or 60 seconds at a time.
• durations >15 usually have little effect on the SNRT in healthy subjects,
patients with SND can have marked suppression after longer pacing
durations.
• It is also preferable to perform pacing at each CL for different durations
(30, 60, or 120 seconds), to ensure that sinus entrance block has not
obscured the true SNRT.

55. CONTRAINDICATIONS
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.

57. Sinus node recovery time (SNRT). Surface ECG leads and high right atrial (HRA) recordings are
shown at the end of a burst of atrial pacing, suppressing sinus node automaticity. The interval at
which the first sinus complex returns (SNRT) is abnormally long at 1625 milliseconds. With a
baseline sinus cycle (CL) of 720 ms, the corrected SNRT (1625 − 720 = 905 ms) is also prolonged.
In addition, there is a secondary pause after the first two sinus complexes
SNRT

58. SINOATRIAL NODE RECOVERY TIME
The SNRT is perhaps the most useful test of overa
sinus nodal
automaticity.
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
sinusnode.

59. SNRT cont….
It is performed by placing a catheter near the
SN.
Overdrive stimulation is performed at a rate higher than tha
of
the SA node for about one minute (the range in most
published
reports is 30 to 180 sec).
Pacing is then stopped, and the time from the last paced at
beat
to the first spontaneous electrical beat with a sinus
morphology is
measured. Pacing is increased 10 to 20 beats/min up to 20
beats/min, if tolerated.

60. SNRT cont….
SNRTc
corrected by subtracting the sinus cycle length from
the
SNRT
SNRTn
a function of the cycle length-
,SNRT/sinus cycle
length.
Total recovery time (TRT)
which is the time required to return to thebasal sinus
rate..

61. SNRT

62. Normal values have generally been estimated as
follows:
SNRT/SCL <150 percent
CSNRT < 550
millisecondsTRT less than five
seconds.
Josephson, ME. Sinus Node Dysfunction. In: Josephson ME, ed. Clinical Cardiac
Electrophysiology. Techniques and
Interpretations. Third ed. Philadelphia: Lippincott; 2002:68.

63. The SNRT or SNRTc is abnormal in more than 50 perc
of
patients with suspected SSS.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

64. SECONDARY PAUSES
• Normally, following cessation of overdrive pacing, a gradual shortening of
the sinus CL is observed until the baseline sinus CL is reached, typically
within a few beats.
• Secondary pauses are identified when there is an initial shortening of the
sinus CL after the SNRT, followed by an unexpected lengthening of the CL.
• Sudden and marked secondary pauses occurring during sinus recovery are
abnormal. SA exit block of variable duration is the primary mechanism of
prolonged pauses, with a lesser component of depression of automaticity.
• secondary pauses can be a normal reflex following hypotension induced
by pacing at rapid rates or in response to pressure overshoot in the first
recovery beat resulting from the prolonged filling time.
• Because these secondary pauses represent SND and because they occur
more frequently following rapid atrial pacing, pacing should be performed
at rates up to 200 beats/min

65. 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
Secondary pauses.
In fact, direct SN recordings have demonstrated that the majority of
thesepauses are due to sinoatrial exit block rather than impaired
automaticity.
- Tracy, CM, Akhtar, M, DiMarco, JP, et
al

66. 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.

67. SACT
Sino Atrial Conduction Time
Can be measured in two
ways
Indirect
Direct

68. SACT cont…
Indirect method;
The usual method
This approach involves the placement of a catheter
near the
sinus node.
Strauss methodprogressively premature atrial extrastimuli (A2) are
introduced after every eighth to tenth beat of stable
sinus
rhythm.Narula method
Brief periods of atrial pacing at rates above
sinus.
.

69. SACT
A1-A1
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
aftertermination of the
pacing.A2-A3
The interval between the final paced impulse (A2) and th
first
spontaneous beat (A3) is referred toas the return
interval
Four zones after APD

70. No reset/collision/Interferance
APD IN LAST 20-30% OF
SCL

71. RESET(MAJOR PART)
ie, less than compensatory-impulse in
earliestthird of zone 2(40-50% OF
SCL)

72. INTERPOLATION

73. ZONE III: ZONE OF INTERPOLATION.
• This zone is defined as the range of A1-A2 intervals at which the A2-A3
interval < A1-A1 interval and the A1-A3 interval is < 2 x A1-A1 interval.
• The A1-A2 coupling intervals at which incomplete interpolation is first
observed define the relative refractory period of the perinodal tissue.
• Some investigators refer to this as the sinus node refractory period. In this
case, A3 represents delay of A1 exiting the sinus node, which has not been
affected.
• The A1-A2 coupling interval at which complete interpolation is observed
probably defines the effective refractory period of the most peripheral of
the perinodal tissue because the sinus impulse does not encounter
refractory tissue on its exit from the sinus node.
• In this case, (A1-A2) + (A2-A3) = A1-A1, and sinus node entrance block is
said to exist.

74. SA ECHO’S/RE-ENTRY

75. Strauss Method
Strauss sinoatrial conduction time zones. Leads 2 and recording from the high right atrium (HRA) are shown, with a single
extrastimulus (S) delivered during sinus rhythm (cycle length, 660 ms) at progressively shorter coupling intervals as indicated
relative to the preceding sinus complex. The timing of the subsequent sinus P wave relative to when it would be expected if
there were no extrastimulus determines the zone of effect: A, collision; B, reset; C, interpolation; and D, reentry.

76. Response of the sinus node to atrial premature depolarizations (APDs). Four zones of response are seen. A1-
A1 is the spontaneous sinus cycle length. In zone 1 an APD (A2) delivered late in the cardiac cycle does not
affect the sinus node, as manifested by the next sinus beats (A3) occurring on time. In zone II, a more
premature A2 results in resetting of the sinus node so that A3 occurs early although A2-A3 is greater than A1-
A1 owing to conduction time between the atrium and sinus node. In zone III, A2 results in a return cycle (A3)
that is early. Since A2-A3 is less than A1-A1, that is, A2 is interpolated. In zone IV, A2 results in an even earlier
return cycle, so that A1-A2 + A2-A3 < A1-A1 is consistent with sinus node reentry.

78. SACT
The A1-A1 interval
Time required to generate a sinus impulse., conductio
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)] / 2Normal SACT times generally range from 40 to 150
milliseconds

79. SACT
Calculation of sinoatrial conduction time (SACT) using the Strauss method. The baseline sinus cycle
length (A1-A2) equals X. The third P wave represents an atrial extrastimulus (A2) that reaches and
discharges the sinoatrial (SA) node, which causes the next sinus cycle to begin at that time. Therefore,
the A2-A3 interval = X + 2Y milliseconds, assuming no depression of sinus node automaticity.
Consequently, SACT = Y = ([A2-A3] − [X])/2.

80. Limitations of SACT
The assumption that entrance into and exit out of the SN takes the same
amount of time is not necessarily valid
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
sinus arrhythmia
shift in intrinsic pacemaker site
Depression of automaticity, and
sinus entrance block

81. Endocardial recordings demonstrate diastolic phase 4
activity
followed by a slow upstroke culminating in a rapid atria
EGM.
The directly measured SACT was defined as the
intervalbetween the local EGM and the rapid atrial
deflection.
Sinoatrial block occurs when the local EGM was seen i
theabsence of an atrial
deflection
Direct recording of the sinoatrial conduction
time (sinus node electrogram)

83. SACT-DIRECT METHOD

86. SENSITIVITY OF SNRT AND
SACT
70%
SPECIFICITY OF SNRT AND
SACT
90%

87. CORRELATION OF SNRT AND
SACT WITH ECG ABNORMALITIES
Patients with Symptomatic sinus bradycardia
–
longer SNRT and SACT
Patients with SA block -longer SACT;
and
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 1977; 56:43.

88. SA NODE AND ATRIAL REFRACTORY PERIOD
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 refractorines
inman. Circulation
1983; 68:1231.
.
.

89. SACT IN PATIENTS WITH SND
• The normal SACT is 45 to 125 milliseconds.
• There is a good correlation between direct and indirect measurements of
SACT in a patient with or without SND.
• However, SACT is an insensitive indicator of SND, especially in patients
with isolated sinus bradycardia.
• SACT is prolonged in only 40% of patients with SND, and more frequently
(78%) in patients with sinoatrial exit block or bradycardia tachycardia
syndrome, or both.
• In patients with sinus pauses, corrected SNRT is more commonly
abnormal than SACT (80% versus 53%).
• SACT appears to be directly related to the baseline sinus CL, and the sinus
node refractory period is directly related to the drive CL

90. COMPLICATIONS DURING EP STUDY
Hematoma at the puncture site in the groin and or neck
Hemorrhage
Infection caused by manipulation of catheters (theoretical
risk)
Perforation upon catheter manipulation inside the heart
ofsmall patients (most commonly involving the right
atrial
appendage and the right ventricular outflow tract)

92. 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.
sensitivity-76%
specificity-91%
In paroxysmal atrial fibrillation the incidence of SSS was
higher
in those with low amplitude atrial early potentials on a
signal-
averaged P wave - Yamada, et al. J Am Coll Cardiol
1996;28:738.

93. TREATMENT OF SSS
Mainly directed at
symptoms
Search for remidial
causes
Drugs
-
-Ischemia
-Autonomic
imbalance
Mostly by pace
makers.
Drugs-Theopylline
Ablation for AF

95. A number of additional pacemaker features may be useful in
selected patients:
Rate responsive programming
SSS and chronotropic insufficiency and exertional
symptoms.
Mode switching
SSS who have paroxysmal atrial tachycardia.

98. DRUG-INDUCED SINUS NODE DYSFUNCTION
Some patients will meet the above indications
for
pacemaker implantation due to the effects of
medications that are necessary for the treatme
of arrhythmias or other medical conditions.
In such cases, patients should be considered to
have the
same indication for pacemaker implantation as tho
with intrinsic sinus node dysfunction

99. • For those patients with SND who have normal AV conduction, a single-
chamber atrial pacemaker is a reasonable consideration, although a dual-
chamber pacemaker is usually implanted, largely because of the 1% to 3%
annual risk of developing AV block.
• The use of rate-adaptive pacing is important for patients with
chronotropic incompetence.
• For patients with intermittent atrial tachyarrhythmias, atrial pacing has
been shown to decrease the incidence of AF and thromboembolism
greatly, whereas patients who have only ventricular pacing have not seen
a similar benefit.
• Current pacemakers used to treat the tachycardia-bradycardia syndrome
follow a special algorithm to switch from a DDD or DDDR mode of
operation to a VVI, VVIR, DDI, or DDIR mode on sensing an atrial
tachyarrhythmia, and back again to DDD or DDDR mode when a normal
atrial rate is sensed.
• For patients with permanent AF, implantation of a single-chamber
ventricular pacemaker is appropriate.

100. FOLLOW-UP
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.

101. THANK YOU