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.