SA nodal and AV nodal bradyarrhythmias can cause symptomatic sinus bradycardia requiring pacemaker implantation. The SA node regulates heart rate and its dysfunction can be caused by drugs, autonomic dysfunction, or intrinsic sick sinus syndrome. AV nodal dysfunction may involve first-degree, Mobitz type I or II, or complete heart block. Pacemakers are indicated for symptomatic bradycardia based on electrocardiography and electrophysiological study findings. Pacemaker implantation carries risks of infection, lead issues, or abnormal pacing responses.

1. SA And AV Nodal Bradyarrhythmias And
the Indication For Pacemaker
Implantation
Satyan Nanda
Junior Resident 3
Internal Medicine
KGMU

2. SA Nodal Bradyarrhthmias
Structure and Physiology Of SA node:
A cluster of small fusiform cells in the
sulcus terminalis at the right atrial-
superior vena caval junction.
SA nodal artery arises from the right
coronary artery in 55-60% and the
left circumflex artery in 40-45% of
persons.

4. Etiology of Sinus Node disease
Extrinsic:
1. Drugs(most common among the
extrinsic causes)
The drugs implicated in the causation of
SA nodal dysfunction are:
Beta blockers
Calcium Channel blockers
Digoxin
Antiarrhythmics(class I and III)
Clonidine
TCA’s like Amitriptyline
Narcotics like Methadone
Adenosine

5. Etiology(Contd…)
EXTRINSIC:
2. Autonomic Dysfunction like Carotid Sinus
hypersensitivity and Vasovagal stimulation
3. Hyperkalemia, Hypercarbia and
Hypothyroidism
4. Sleep apnea
5. Hypothermia
6. Hypoxia
7. Raised intracranial pressure
8. Endotracheal suctioning

6. Etiology(Contd…)
INTRINSIC:
Sick Sinus syndrome(SSS)
Coronary Artery Disease
Inflammatory process like Pericarditis,
Myocarditis, Rheumatic Heart Disease,
Collagen Vascular disease and Lyme disease
Senile Amyloidosis
Iatrogenic(Radiation therapy and Post
surgical)

7. Etiology(contd….)
INTRINSIC:
Chest Trauma
Familial causes
Kearns Sayre syndrome
Myotonic dystrophy
Friedrich’s Ataxia

8. Clinical Features
May be completely Asymptomatic
Sinus bradycardia may present with
symptoms such as hypotension, Syncope,
presyncope, fatigue and weakness
Patients with SSS may develop signs and
symptoms of heart failure
Patients with SSS are also at risk of
developing thromboembolism

9. Sick-Sinus Syndrome
•Syndrome encompassing a number of sinus nodal
abnormalities.
•The abnormalities can be:
1. Persistent spontaneous sinus bradycardia not
caused by drugs and inappropriate for the
physiologic circumstances.
2. Sinus arrest or exit block
3. Combinations of SA and AV node conduction
disturbances
4. Bradycardia-tachycardia syndrome
• More than one of these conditions can be
recorded in the same patient on different
occasions.

10. Electrocardiography
•Sinus bradycardia
•Sinus arrest or pause
•Sinus exit block
•Tachycardia-Bradycardia Syndrome
•Chronotropic Incompetence

11. Sinus Bradycardia: Is a rhythm driven by the SA node with a rate of <60
beats/min. It is common and typically benign. A sinus rate of <40
beats/min in the awake state in the absence of physical conditioning is
generally considered abnormal.

12. Sinus pause or arrest result from failure of the SA node to discharge,
producing a pause without P waves visible on the ECG. Sinus pauses of
upto 3 sec are common in awake athletes and elderly.

13. SA node Exit Block
Intermittent failure of conduction from the
SA node.
First degree SA block: Prolonged SA conduction
time(non-detectable on EKG; no missing P waves)
Type I second degree SA block: Progressive
prolongation of SA node conduction with intermittent
failure of the impulses originating in the Sinus node to
conduct to the surrounding atrial tissue
Type II second degree block there is no change in SA
node conduction before the pause.
Third degree SA block results in absence of P waves
on the ECG.

15. Tachycardia-Bradycardia Syndrome
Alternating sinus bradycardia and atrial
tachyarrythmias (atrial tachycardia, atrial
flutter and atrial fibrillation)

17. Chronotropic Incompetence
Inability to increase the heart rate in
response to exercise or any other stress
appropriately. This is diagnosed as:
Failure to reach 85% of maximal heart
rate at peak exercise
Failure to achieve a heart rate >100
beats/min with exercise
Maximal heart rate with exercise less
than two standard deviations below that of
an age matched control population

18. Diagnostic Testing
SA nodal dysfunction is most commonly a
clinical or electrocardiographic diagnosis. The
diagnostic modalities used are:
oResting ECG
oHolter monitors
oImplantable ECG monitors
oExercise testing
oAutonomic Nervous system testing
oElectrophysiologic testing

19. Autonomic Nervous System Testing
•This is useful in diagnosing carotid sinus
hypersensitivity.
•A low Intrinsic Heart Rate is suggestive of
SA disease
•The normal IHR is calculated after the
administration of 0.2 mg/kg propanolol and
0.04 mg/kg atropine as follows:
•IHR=117.2-(0.53*age) in beats/min

20. Electrophysiologic Testing
These are the tests to assess SA node function
invasively. The parameters used are:
SNRT: Sinus Node Recovery Time. This is defined as the
longest pause after cessation of overdrive pacing of the
right atrium near the SA node( normal: <1500 ms or
corrected for sinus cycle length, <550 ms)
SACT: SinoAtrial Conduction Time. This is defined as
one half the difference between the intrinsic sinus cycle
length and a noncompensatory pause after a premature
atrial stimulus( normal<125 ms)
The combination of an abnormal SNRT, an abnormal
SACT and a low IHR is a sensitive and specific indicator
of intrinsic SA node disease.

21. Treatment
Exclusion of the Extrinsic causes of SA node
dysfunction.
Pacemaker Implantation: This is the primary
therapeutic intervention in patients with
symptomatic SA nodal dysfunction.
Pharmacotherapy:
• IV Isoproterenol
• IV Atropine
• Theophylline

22. AV Nodal Bradyarrythmias
Anatomy: The compact AV node is situated at
the apex of the triangle of Koch, which is
defined by the coronary sinus ostium
posteriorly, the septal tricuspid valve annulus
anteriorly and the tendon of Todaro
superiorly.

23. Anatomy

24. Etiology
Classified as either functional or structural.
Functional:
Autonomic: Carotid sinus hypersensitivity and
Vasovagal block
Metabolic causes like Hyperkalemia,
Hypermagnesemia, Hypothyroidism and
Adrenal Insufficiency
Drugs like Beta blockers, Calcium channel
blockers, Antiarrythmics(Class I and III),
Adenosine, Digitalis and Lithium
Infectious: Endocarditis, Lyme disease,
Chagas disease, Syphilis, Tuberculosis,
diphtheria and toxoplasmosis

25. Etiology(contd….)
Structural:
•Coronary Artery disease
•Congenital causes like TGA, ASD, VSD, Endocardial
cushion defects and single ventricle defects; Kearns
Sayre syndrome, dystrophies and maternal SLE
•Inflammatory causes like SLE, Rheumatoid Arthritis,
MCTD and Scleroderma
•Infiltrative diseases like Amyloidosis, Sarcoidosis and
Hemochromatosis
•Neoplastic lesions like Lymphoma, Melanoma and
radiation
•Degenerative diseses like Lev disease and Lenegre
Disease
•Idiopathic Progressive fibrosis

26. AV blocks in CAD
CAD may produce transient or persistent AV block.
In acute MI AV block develops transiently in 10-
25% patients.
Most commonly the AV block is first or second
degree block.
Second degree and higher grade AV blocks occur
more often in inferior than anterior acute MI.
Acute anterior MI is associated with block in the
distal AV nodal complex, His bundle or bundle
branches and results in wide complex, unstable
escape rhythms and a worse prognosis with high
mortality rates.

27. Electrocardiography and
electrophysiology of AV block
•First degree AV block : This is due to
slowing of conduction through the AV
junction. The site of delay is typically in
the AV node but may be in the atria,
bundle of His or His purkinje system. A
wide QRS is suggestive of delay in the AV
node proper or less commonly in the
Bundle of His.

29. Second Degree Block
Type I Mobitz(Wenckebach):
Progressively lengthening of PR interval,
Shortening of the RR interval and a pause
that is less than two times the
immediately preceding RR interval on the
ECG. The ECG complex after the pause
exhibits a shorter PR interval than that
immediately preceding the pause.

31. Mobitz Type II Second Degree AV
Block
Characterised by intermittent failure of
conduction of the P-wave without
changes in the preceding PR or RR
intervals.
Typically occurs in the distal or infra-His
conduction system.
More likely to proceed to higher grades
of AV block.
May be associated with a series of
nonconducted P waves referred to as
Paroxysmal AV Block.

33. Paroxysmal AV Block

34. Complete Heart Block

35. Diagnostic Testing
Vagal Maneuvers
Carotid sinus Massage
Exercise
Administration of Drugs
Electrophysiologic Studies

36. Diagnostic Testing
Vagal stimulation and carotid sinus
massage slow conduction in the AV node
but have less of an effect on infranodal
tissue.
Likewise atropine, isoproterenol and
exercise improve conduction through the
AV node and impair infranodal
conduction. In acquired CHB the heart
rate does not increase with exercise.

37. Treatment
•Pacing
•Drugs like atropine or isoproterenol

38. Permanent Pacemakers
Nomenclature: Pacemaker modes and function
are named using a five letter
code(NASPE/BPEG).
• The first letter indicates the chamber that is
paced.(O:none; A:Atrium; V: Ventricle; D: Dual;
S: Single)
•The second letter indicates the chamber in
which sensing occurs.(O: none; A: Atrium; V:
Ventricle; D:Dual; S: Single)
•The third is the response to a sensed event(O:
none; I: Inhibition; T: Triggered; D:
Inhibition+Triggered

39. Nomenclature
(contd…)
•The fourth refers to programmability or rate
response(O: None; R: Rate Responsive)
•The fifth refers to multisite pacing(O: None;
A:Atrium; V: Ventricle; D: Dual)

40. Indications
•Class I: are those conditions for which there is
evidence or consensus of opinion that therapy
is useful and effective.
•Class II: those for which there is conflicting
evidence or a divergence of opinion about the
efficacy. IIa refers to conditions for which the
evidence favors treatment. IIb are those
conditions for which the efficacy is less well
established.
•Class III: The weight of opinion indicates that
the therapy is not efficacious and may be
harmful.

45. Complications
Acute:
Infection
Hematoma
Pneumothorax
Cardiac perforation
Diaphagmatic/Phrenic Nerve
Stimulation
Lead dislodgement

46. Complications(contd…)
Chronic:
•Infection
•Erosion
•Lead failure
•Abnormalities resulting from
programming
•Twiddler’s Syndrome: Rotation of the
pacemaker pulse generator in its
subcutaneous pocket leading to failure to
sense or pace the heart.