Bradyarrythmias sa node

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Bradyarrhythmias - SA Node (Sinus Node Dysfunction)

Overview

Bradyarrhythmias originating from the SA node are collectively grouped under sinus node dysfunction (SND). This encompasses a spectrum of disorders where the SA node fails to generate or conduct impulses at an appropriate rate.

Goldman-Cecil Medicine, Chapter 51

Classification of SA Node Bradyarrhythmias

Disorder	Key Feature
Sinus bradycardia	Rate < 60 bpm (pathologic < 45-50 bpm)
Sinoatrial exit block (1°, 2°, 3°)	Sinus fires, but impulse blocked before reaching atria
Sinus arrest/pause	Pause > 2-3 seconds during sinus rhythm
Chronotropic incompetence	Max HR < 100 bpm on exertion
Tachy-brady (sick sinus) syndrome	Alternating tachycardia and bradycardia

1. Sinus Bradycardia

Definition: Sinus rate < 60 bpm. Rates of 45-50 bpm at rest can be physiologically normal (e.g., well-trained athletes or during sleep with high vagal tone).

ECG: Regular P waves with normal morphology and PR interval; rate < 60 bpm.

Sinus bradycardia - progressive slowing related to heightened vagal tone during sleep

Figure: Sinus bradycardia - progressive sinus slowing related to heightened vagal tone while sleeping. (Goldman-Cecil Medicine)

Common causes:

Physiologic (athletes, sleep, vagal stimulation)
Drugs: beta-blockers, calcium channel blockers, digoxin, amiodarone, ivabradine
Hypothyroidism, hypothermia
Inferior MI (RCA supplies the SA node in ~60% of people)
Increased intracranial pressure (Cushing reflex)
Infiltrative disease (amyloidosis, sarcoidosis)

2. Sick Sinus Syndrome (SSS)

Sinus node dysfunction plus symptoms (fatigue, dizziness, near-syncope, syncope, worsening heart failure) = Sick Sinus Syndrome. It is the most common indication for permanent pacemaker implantation in the US.

Manifestations include:

Sinus bradycardia (< 40 bpm)
Sinus pauses > 2 seconds
Sinus arrest with escape junctional rhythm
Sinoatrial exit block
Tachy-brady syndrome (most characteristic)

3. Tachy-Brady Syndrome

The most recognizable pattern of SSS. Characterized by:

Episodes of atrial tachyarrhythmia (most commonly atrial fibrillation) alternating with significant bradycardia or prolonged pauses
The pauses are classically seen at the termination of AF due to prolonged sinus node recovery time

Tachy-Brady syndrome ECG: atrial fibrillation with tachycardic response followed by conversion to sinus bradycardia with long pause

Figure: ECG showing tachy-brady syndrome - AF with tachycardic ventricular response followed by conversion to sinus bradycardia. (Goldman-Cecil Medicine)

4. Sinoatrial Exit Block

The SA node fires but the impulse is blocked (or delayed) before reaching atrial tissue. Diagnosed on the surface ECG by analyzing PP intervals.

Type	ECG Pattern
1st degree	Prolonged SA conduction time - NOT visible on surface ECG
2nd degree Type 1 (Wenckebach)	Progressive PP shortening before a pause; pause PP > 2x preceding PP
2nd degree Type 2	Pause = exact multiple of PP interval (constant PP before and after)
3rd degree (complete)	No sinus P waves; atrial standstill

5. Chronotropic Incompetence

Inability to appropriately increase sinus rate in response to exercise or physiologic demand. Defined as a maximal HR < 100 bpm on exercise testing. Represents a form of SND and can cause exercise intolerance.

Causes of Sinus Node Dysfunction

Intrinsic:

Idiopathic fibrocalcific degeneration (most common - age-related)
Ischemic heart disease (especially inferior MI)
Infiltrative disease: amyloidosis, sarcoidosis, hemochromatosis
Inflammatory: myocarditis, rheumatic heart disease, Lyme disease (reversible complete heart block)
Congenital heart disease, post-surgical (e.g., Fontan)

Extrinsic (reversible):

Drugs: beta-blockers, CCBs, digoxin, amiodarone, lithium, quinidine, donepezil
Autonomic: high vagal tone, vasovagal episodes
Metabolic: hypothyroidism, hypothermia, hyperkalemia, hypoxia
Increased ICP

Symptoms

Symptoms arise from reduced cardiac output during bradycardic episodes:

Fatigue, exercise intolerance, dyspnea
Dizziness, presyncope, syncope (Stokes-Adams attacks)
Worsening heart failure
Palpitations (during tachycardic phase of tachy-brady)

Diagnostic Evaluation

Test	Purpose
12-lead ECG	Baseline rhythm, AV conduction, QRS
24-48h Holter monitor	Very frequent episodes
External event monitor	Moderately frequent episodes
Implantable loop recorder	Infrequent/unexplained syncope
Exercise stress test	Chronotropic incompetence
Electrophysiology study	SNRT (sinus node recovery time), sinoatrial conduction time
Echocardiogram	Structural heart disease
Labs	TSH, electrolytes, drug levels

Electrophysiology: Corrected sinus node recovery time (CSNRT) > 550 ms is abnormal and suggests SND.

Treatment

Step 1 - Remove offending agents

Always stop or reduce medications that may precipitate SND (beta-blockers, CCBs, digoxin, amiodarone, lithium).

Acute symptomatic bradycardia

IV Atropine 1 mg (first-line)
Isoproterenol 1-2 mcg/min infusion (if atropine fails)
Temporary transcutaneous or transvenous pacing if medications ineffective

Chronic management

Situation	Treatment
Asymptomatic sinus bradycardia	No therapy required
Symptomatic SND (persistent)	Permanent pacemaker (therapy of choice)
Tachy-brady syndrome requiring antiarrhythmics	Pacemaker first, then antiarrhythmic drugs
SND + systolic dysfunction + AV block	Biventricular pacemaker preferred
Lyme disease heart block	Antibiotics (resolves within ~1 week)

Pacemaker mode

AAI or AAIR (rate-responsive atrial pacing): for isolated SND with intact AV conduction
DDD or DDDR: if concurrent AV conduction disease
Newer: His bundle pacing or left bundle branch area pacing for more physiologic conduction

Class I Indications for Permanent Pacemaker (SND)

Symptomatic sinus bradycardia due to required drug therapy
Symptomatic chronotropic incompetence
Symptomatic sinus pauses

Class IIa Indications (Reasonable)

HR < 40 bpm without clear symptom-rhythm correlation
Syncope of unclear etiology when SND demonstrated on EP testing

Important Pearls

Asymptomatic sinus bradycardia in middle-aged or older adults is not associated with increased cardiovascular mortality unless the patient is on rate-modifying drugs
Recurrent syncope occurs despite pacemaker in ~20% of patients over 5 years
Lyme disease is the major reversible cause of complete heart block
The susceptibility of SND to medications suggests an underlying conduction abnormality that may worsen over time even after drugs are stopped
Cardiac neural ablation (parasympathetic ganglia ablation) is an emerging therapy for refractory SND

Sources: Goldman-Cecil Medicine (International Ed.), Chapter 51; The Washington Manual of Medical Therapeutics; Roberts and Hedges' Clinical Procedures in Emergency Medicine

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