Purkinje fibers are the terminal elements of the cardiac conduction system. They rapidly distribute the electrical impulse from the bundle branches to the ventricular working myocardium, ensuring coordinated and efficient contraction.
Discovery
Named after Jan Evangelista Purkyně, who first described these cells in 1839. He initially thought they were cartilage or gelatinous tissue before their conductive function was understood.
Location and Distribution
Purkinje fibers form an extensive subendocardial network that covers the inner surfaces of both ventricles.
Right Ventricle
- Courses along the moderator band to the anterior papillary muscle
- Distributes to the right ventricular free wall
- Extends to the right ventricular apex
Left Ventricle
- Branches from the left bundle fascicles
- Forms a sheet-like network over the left ventricular septum
- Covers the papillary muscles (both anterolateral and posteromedial)
- Extends to the left ventricular apex
- Reaches the left ventricular free wall
Transmural Penetration
Most Purkinje fibers are located in the subendocardium. They do not normally penetrate the full thickness of the ventricular wall. Excitation spreads from endocardium to epicardium through working myocardium.
Exceptions:
- Deep Purkinje fibers in the septum
- Transmural Purkinje fibers in the papillary muscles
- Some penetration in the moderator band
Microscopic Anatomy
Cell Structure
Purkinje cells are highly specialized:
- Size: Largest cells in the heart (10-50 microns diameter)
- Shape: Elongated, branching cells
- Myofibrils: Sparse (fewer than working myocytes)
- Glycogen: Abundant (gives pale appearance on histology)
- Nucleus: Central, often multiple
- Mitochondria: Fewer than working myocytes
- Sarcoplasmic reticulum: Less developed
Intercellular Connections
Purkinje cells are connected end-to-end by intercalated discs:
Gap junctions:
- Abundant connexin 40 (high conductance)
- Abundant connexin 43
- Large, numerous gap junctions
- Low resistance pathways for rapid conduction
Desmosomes:
- Connect intermediate filaments
- Provide mechanical adhesion
- Less numerous than in working myocardium
Comparison with Working Myocardium
| Feature | Purkinje Cells | Working Myocytes |
|---|---|---|
| Size | 10-50 microns | 10-20 microns |
| Myofibrils | Sparse | Dense |
| Glycogen | Abundant | Moderate |
| Gap junctions | Large, numerous | Smaller, fewer |
| Conduction velocity | 2-4 m/s | 0.3-0.5 m/s |
| Resting potential | -90 to -95 mV | -80 to -90 mV |
| Action potential duration | Longest in heart | Moderate |
Electrophysiology
Action Potential
Purkinje cells have the longest action potential duration in the heart (300-500 ms).
Phases:
- Phase 0 (Upstroke): Fast sodium channel-mediated (I(Na))
- Phase 1 (Early repolarization): I(to) (transient outward current)
- Phase 2 (Plateau): I(Ca-L) and I(Ks)
- Phase 3 (Repolarization): I(Kr) and I(Ks)
- Phase 4 (Resting): Stable resting potential (normally no spontaneous depolarization)
Automaticity
Purkinje fibers can act as latent pacemakers:
- Intrinsic rate: 15-40 bpm (slower than SA and AV nodes)
- Phase 4 depolarization: Slower than nodal tissue
- Suppression: Normally overdriven by SA node
- Escape: Emerge when SA and AV nodes fail
Conduction Properties
| Property | Value |
|---|---|
| Conduction velocity | 2-4 m/s |
| Refractory period | 300-500 ms (longest in heart) |
| Safety factor | High (reliable conduction) |
| Excitability threshold | Low (easily excited) |
The Purkinje-Ventricular Junction
The interface between Purkinje fibers and working myocardium is critical for impulse transmission.
Characteristics
- Sudden increase in resistance at the junction
- Source-sink mismatch (small Purkinje fiber must depolarize large myocardial mass)
- Safety factor for transmission is relatively low
Mechanisms of Transmission
- Tapering: Purkinje fibers narrow at the junction, increasing current density
- Branching: Multiple Purkinje terminals distribute the current
- Gap junction distribution: Mixed connexin 40/43 at the junction
- Facilitation: Working myocytes near the junction have enhanced excitability
Wavefront Propagation
Endocardial to Epicardial Spread
The impulse spreads from the endocardial Purkinje network through the ventricular wall:
- Endocardium: Activated first (at the Purkinje-myocardial junction)
- Mid-myocardium: M cells (intermediate electrophysiology)
- Epicardium: Activated last
Apical Activation
The apex is activated early (via the bundle branches extending to the apex), creating a base-to-apex sequence of contraction that effectively ejects blood.
Papillary Muscle Activation
Papillary muscles are activated before the adjacent free wall, creating tension on the chordae tendineae before intraventricular pressure rises.
Clinical Significance
Ventricular Arrhythmias
Purkinje fiber-related arrhythmias:
| Arrhythmia | Mechanism | Purkinje Involvement |
|---|---|---|
| Idiopathic ventricular fibrillation | Triggered activity from Purkinje network | Purkinje source |
| Ventricular ectopy | Automaticity from distal Purkinje fibers | Common origin |
| Bundle branch reentry | Macro-reentry using bundle branches | His-Purkinje circuit |
| Post-MI arrhythmias | Abnormal automaticity from surviving Purkinje cells | Border zone Purkinje |
Purkinje fiber cardiomyopathy:
- Deleting connexin 40 in mice causes RBBB and cardiomyopathy
- Purkinje-myocardial coupling abnormalities may contribute to heart failure
Ischemia and Infarction
Purkinje fibers are relatively resistant to ischemia:
- Rich in glycogen (anaerobic metabolism)
- Less dependent on oxidative phosphorylation
- Survive longer than working myocytes in infarcted territory
Pseudo-infarct pattern:
- Loss of septal Purkinje activation can mimic infarction
- Seen in LBBB and pre-excitation syndromes
Long QT Syndrome
Purkinje fibers play a role in long QT syndrome:
- Prolonged Purkinje action potential duration contributes to QT prolongation
- Transmural dispersion of repolarization involves Purkinje-myocardial differences
- Early afterdepolarizations (EADs) arise preferentially from Purkinje fibers
- Torsades de pointes often initiated by Purkinje ectopy
Rate Adaptation
Purkinje fibers have the longest action potential duration and show prominent rate adaptation:
- At slow rates: Very long APD
- At fast rates: APD shortens significantly
- This contributes to QT interval adaptation to heart rate
Hermans-Pudlak Syndrome
- Rare condition with ceroid deposition in Purkinje fibers
- Associated with conduction abnormalities
- May cause complete heart block
- Oculocutaneous albinism and bleeding diathesis
Triggered Activity
Purkinje fibers are prone to:
- Early afterdepolarizations (EADs): Occur during phase 2-3 of APD, can trigger torsades
- Delayed afterdepolarizations (DADs): Occur after full repolarization, due to calcium overload
- Triggered activity: Underlie many ventricular arrhythmias
Aging of the Purkinje System
- Progressive loss of Purkinje cells
- Fibrosis of the conduction network
- Reduced conduction velocity
- Increased heterogeneity of repolarization
- Greater susceptibility to arrhythmias