Sinoatrial  Block 

What is Sinoatrial (SA) Block?

The SA node generates the impulse normally, but transmission to surrounding atrial tissue is delayed or blocked.

This differentiates it from:

• Sinus bradycardia → slow impulse generation
• Sinus arrest → failure of impulse generation

Anatomy of the SA Node

Location

• Junction of SVC and right atrium
• Subepicardial

Blood Supply

• Right coronary artery (RCA) in ~60%
• Left circumflex artery (LCX) in ~40%

This is clinically important in inferior wall MI, especially right coronary artery infarcts.

 Pathophysiology

Impulse generation → SA node
Impulse conduction → Atrial myocardium

In SA block:

• SA node fires normally
• Impulse fails to reach atria
• Result → Dropped P wave + dropped QRS

Mechanism:

• Increased vagal tone
• Ischemia of SA node
• Fibrosis (degenerative disease)
• Drugs
• Electrolyte imbalance

Classification of SA Block

1️⃣ First Degree SA Block

• Delay in conduction from SA node to atrium
• Cannot be diagnosed on surface ECG
• Only detectable via intracardiac recording

Clinically silent.

2️⃣ Second Degree SA Block

Two types:

🔹 Type I (Wenckebach SA Block)

Mechanism

Progressive prolongation of SA conduction until impulse fails.

ECG Features

• Progressive shortening of PP intervals
• Followed by dropped P wave
• Pause less than 2× basic PP interval

Clinical Scenario

• High vagal tone
• Athletes
• Sleep

🔹 Type II SA Block

Mechanism

Sudden failure of conduction without prior PP change.

ECG Features

• Constant PP intervals
• Sudden dropped P wave
• Pause = multiple of basic PP interval (e.g., 2×, 3×)

 More dangerous than Type I

Associated with:

• SA node ischemia
• Fibrosis
• Sick sinus syndrome

3️⃣ Third Degree SA Block (Complete SA Block)

• No impulses conducted to atria
• Atrial standstill
• Escape rhythm appears (junctional or ventricular)

ECG:

• No P waves
• Escape rhythm present

This resembles sinus arrest but differs mechanistically.

ECG Patterns

Etiology of SA Block

1️⃣ Increased Vagal Tone

• Athletes
• Sleep
• Carotid sinus stimulation

2️⃣ Ischemia

• Inferior wall MI (RCA)
• Right ventricular infarction

3️⃣ Degenerative Fibrosis

• Elderly
• Sick sinus syndrome

4️⃣ Drugs

• Beta blockers
• Calcium channel blockers
• Digoxin
• Amiodarone

5️⃣ Electrolyte Disturbances

• Hyperkalemia

6️⃣ Infiltrative Disease

• Amyloidosis
• Sarcoidosis

Clinical Presentation

Asymptomatic (most common)

Symptomatic

• Dizziness
• Presyncope
• Syncope
• Fatigue
• Exercise intolerance

Severe cases → Stokes–Adams attacks

Hemodynamic Consequences

• Reduced cardiac output
• Loss of atrial kick
• Hypotension
• Worsened in elderly / LV dysfunction

Diagnosis

1️⃣ ECG

Primary tool.

2️⃣ Holter Monitoring

Useful for intermittent episodes.

3️⃣ Electrophysiology Study

Rarely needed.

Permanent Pacemaker

Indications:

• Symptomatic bradycardia
• Documented pauses >3 seconds with symptoms
• Sick sinus syndrome

Preferred mode:

• Dual chamber pacing (DDD)