The atrioventricular (AV) node is a specialized group of cardiac cells located in the right atrium that conducts electrical impulses from the atria to the ventricles. It provides the only normal electrical pathway between the upper and lower chambers.
Location and Gross Anatomy
The AV node is located within the triangle of Koch in the right atrium.
Triangle of Koch
Borders:
- Posterior: Coronary sinus orifice
- Anterior: Attachment of the septal leaflet of the tricuspid valve
- Superior: Tendon of Todaro (fibrous band extending from the central fibrous body to the Eustachian valve)
Contents:
- AV node (within the apex of the triangle)
- Proximal AV bundle (Bundle of His)
Position
- Subendocardial location (immediately beneath the endocardium)
- Right atrial side of the interatrial septum
- Superior to the tricuspid annulus
- Anterior to the coronary sinus ostium
Dimensions
- Length: 5-7 mm
- Width: 2-5 mm
- Thickness: 0.5-1 mm
Microscopic Anatomy
Cell Types
Nodal (N) Cells:
- Central compact AV node
- Small, pale cells with scant contractile elements
- Complex intercellular connections
- Slow conduction velocity (0.05-0.1 m/s)
- Exhibit decremental conduction
Transitional (T) Cells:
- Surround the compact node
- Intermediate between atrial myocytes and nodal cells
- Form the approaches to the AV node
- Conduction: 0.1-0.5 m/s
Lower Nodal (NH) Cells:
- Distal portion of the AV node
- Transition to the His bundle
- Larger than N cells
- Faster conduction than N cells
Inferior Extension:
- Additional nodal tissue extending toward the tricuspid annulus
- Substrate for slow AV nodal pathway
- Important for AV nodal reentrant tachycardia (AVNRT)
Stroma
The AV node contains:
- Dense connective tissue (less than SA node)
- Collagen and elastic fibers
- Fibroblasts
- Rich capillary network
Zonal Anatomy
The AV node is divided into three functional zones:
| Zone | Location | Characteristics |
|---|---|---|
| AN (Atrio-Nodal) | Proximal, atrial interface | Transitional cells, slow conduction |
| N (Nodal) | Central compact node | True nodal cells, slowest conduction |
| NH (Nodal-His) | Distal, His interface | Faster conduction, transitional to His |
Blood Supply
AV Nodal Artery
The AV nodal artery supplies the AV node.
| Origin | Frequency |
|---|---|
| Right coronary artery (at the crux) | 80-90% |
| Left circumflex artery (at the crux) | 10-20% |
Course:
- Arises at the crux of the heart (posterior atrioventricular junction)
- Courses superiority to reach the AV node
- Penetrates the central fibrous body
- Forms a capillary network within the node
Clinical Significance:
- Inferior MI (RCA occlusion) often causes AV block
- AV node ischemia is usually temporary (collateral supply)
- AV block in inferior MI typically resolves within 5-7 days
Collateral Supply
The AV node also receives blood from:
- Septal branches of the LAD
- Atrial branches of the RCA
- Collateral connections with the SA nodal artery
Innervation
Sympathetic Innervation
- Source: Left and right sympathetic chains
- Neurotransmitter: Norepinephrine
- Receptors: Beta-1 adrenergic
- Effect: Increases AV conduction velocity (positive dromotropy)
- Effect: Shortens AV nodal refractory period
Parasympathetic Innervation
- Source: Left vagus nerve
- Neurotransmitter: Acetylcholine
- Receptors: M2 muscarinic
- Effect: Decreases AV conduction velocity (negative dromotropy)
- Effect: Prolongs AV nodal refractory period
Autonomic Balance
| Stimulus | AV Conduction | Refractory Period |
|---|---|---|
| Sympathetic | Increases | Shortens |
| Parasympathetic | Decreases | Prolongs |
| Vagal maneuvers | Decreases | Prolongs |
| Exercise | Increases | Shortens |
| Sleep | Decreases | Prolongs |
Electrophysiology
Action Potential
AV nodal cells have spontaneous activity but at a slower rate than the SA node:
Phases:
- Phase 4 (Spontaneous depolarization): Slower than SA node
- Phase 0 (Upstroke): Calcium-dependent (I(Ca-L))
- Phase 3 (Repolarization): I(K) activation
Conduction Properties
| Property | Value |
|---|---|
| Conduction velocity | 0.05-0.1 m/s |
| Refractory period (anterograde) | 300-500 ms |
| Refractory period (retrograde) | 250-450 ms |
| Wenckebach block rate (typical) | 150-180 bpm |
Decremental Conduction
The AV node exhibits decremental conduction: the action potential amplitude decreases as it propagates through the node. This is due to:
- Calcium-dependent upstrokes (slow channel)
- Complex cellular coupling
- Current-to-load mismatch
Decremental conduction protects the ventricles from rapid atrial rates (e.g., atrial fibrillation).
Dual AV Nodal Pathways
Approximately 25% of individuals have dual AV nodal pathways:
Fast Pathway (FP):
- Anterior approach to the AV node
- Shorter refractory period
- Faster conduction
- Located near the atrial septum
Slow Pathway (SP):
- Posterior approach to the AV node
- Longer refractory period
- Slower conduction
- Located near the coronary sinus
Clinical significance: Dual pathways are the substrate for AV nodal reentrant tachycardia (AVNRT).
Function
Primary Functions
- Conduction delay: The AV node delays the impulse by approximately 120-200 ms, allowing time for atrial contraction to complete before ventricular systole
- Protective filtering: Prevents rapid atrial rates from reaching the ventricles (e.g., atrial fibrillation with controlled ventricular response)
- Backup pacemaker: If the SA node fails, the AV node can generate escape rhythms at 40-60 bpm
- Modulation: Autonomic input adjusts conduction velocity
Wenckebach Phenomenon
The AV node demonstrates Wenckebach (Mobitz I) block:
- Progressive PR prolongation
- Then a dropped QRS
- The cycle repeats
- Physiologic response to rapid atrial pacing
Clinical Significance
AV Block
First-Degree AV Block:
- PR interval > 200 ms
- All impulses conducted
- Usually benign
Second-Degree AV Block:
| Type | Feature | Location |
|---|---|---|
| Mobitz I (Wenckebach) | Progressive PR prolongation, then dropped QRS | AV node (usually) |
| Mobitz II | Fixed PR, then dropped QRS | Infranodal (His-Purkinje) |
Third-Degree AV Block (Complete Heart Block):
- No atrial impulses conducted to ventricles
- Escape rhythm: AV nodal (40-60 bpm) or ventricular (< 40 bpm)
- Atria and ventricles beat independently (AV dissociation)
AV Nodal Reentrant Tachycardia (AVNRT)
The most common paroxysmal supraventricular tachycardia (PSVT).
Mechanism: Reentry using dual AV nodal pathways
- Typical (slow-fast): Antegrade via slow pathway, retrograde via fast pathway
- Atypical (fast-slow): Antegrade via fast pathway, retrograde via slow pathway
Treatment:
- Vagal maneuvers (Valsalva, carotid sinus massage)
- Adenosine (blocks AV nodal conduction)
- Catheter ablation of the slow pathway (curative)
AV Nodal Ablation
Purposeful destruction of the AV node for rate control in atrial fibrillation:
- Target: Compact AV node or slow pathway region
- Approach: Radiofrequency or cryoablation
- Result: Complete heart block, pacemaker-dependent
AV Node in Inferior MI
- RCA occlusion causes AV nodal ischemia
- AV block develops in 12-20% of inferior MI
- Usually transient (resolves in 5-7 days)
- May require temporary pacing
Pharmacologic Effects
| Drug | Effect on AV Node |
|---|---|
| Adenosine | Transient complete AV block |
| Verapamil/Diltiazem | Prolongs refractoriness, slows conduction |
| Beta-blockers | Prolongs refractoriness |
| Digoxin | Prolongs refractoriness |
| Amiodarone | Prolongs refractoriness |
| Atropine | Increases conduction (vagolytic) |
| Isoproterenol | Increases conduction (beta-agonist) |
Age-Related Changes
- Fibrosis of the AV node and surrounding tissues
- PR interval prolongation with age
- Increased incidence of first-degree AV block
- Decreased AV nodal conduction velocity
- Increased AV nodal refractory period