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SA And AV Nodal Bradyarrhythmias And the Indication For Pacemaker
Implantation
Satyan Nanda
Junior Resident 3
Internal Medicine
KGMU
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.
Etiology of Sinus Node diseaseExtrinsic:
1. Drugs(most common among the extrinsic causes)
The drugs implicated in the causation of SA nodal dysfunction are:
Beta blockersCalcium Channel blockers
DigoxinAntiarrhythmics(class I and III)
ClonidineTCA’s like AmitriptylineNarcotics like Methadone
Adenosine
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
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)
Etiology(contd….)
INTRINSIC:
Chest Trauma
Familial causes
Kearns Sayre syndrome
Myotonic dystrophy
Friedrich’s Ataxia
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
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 block3. Combinations of SA and AV node conduction
disturbances4. Bradycardia-tachycardia syndrome
• More than one of these conditions can be recorded in the same patient on different
occasions.
Electrocardiography
•Sinus bradycardia
•Sinus arrest or pause
•Sinus exit block
•Tachycardia-Bradycardia Syndrome
•Chronotropic Incompetence
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.
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.
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.
Tachycardia-Bradycardia Syndrome
Alternating sinus bradycardia and atrialtachyarrythmias (atrial tachycardia, atrial
flutter and atrial fibrillation)
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
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
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
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.
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
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 ostiumposteriorly, the septal tricuspid valve annulus
anteriorly and the tendon of Todarosuperiorly.
Anatomy
Etiology
Classified as either functional or structural.Functional:
Autonomic: Carotid sinus hypersensitivity and Vasovagal block
Metabolic causes like Hyperkalemia, Hypermagnesemia, Hypothyroidism and
Adrenal InsufficiencyDrugs 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
Etiology(contd….)
Structural: •Coronary Artery disease
•Congenital causes like TGA, ASD, VSD, Endocardialcushion 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
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.
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.
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.
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.
Paroxysmal AV Block
Complete Heart Block
Diagnostic Testing
Vagal Maneuvers
Carotid sinus Massage
Exercise
Administration of Drugs
Electrophysiologic Studies
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 infranodalconduction. In acquired CHB the heart rate does not increase with exercise.
Treatment
•Pacing
•Drugs like atropine or isoproterenol
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
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)
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.
Complications
Acute:
Infection
Hematoma
Pneumothorax
Cardiac perforation
Diaphagmatic/Phrenic Nerve Stimulation
Lead dislodgement
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.