Cardiac conduction cells are specialised modified cardiomyocytes with reduced contractile capacity and enhanced electrical automaticity and conduction velocity. The SAN pacemaker cells have the fastest spontaneous depolarisation rate (60-100 bpm), suppressing subsidiary pacemakers. The His-Purkinje system conducts at 2-4 m/s compared to 0.5 m/s for working myocardium, ensuring rapid synchronous ventricular activation.
| Origin | Modified cardiomyocytes in the sinoatrial node (right atrium), atrioventricular node (interatrial septum), His bundle (membranous interventricular septum), bundle branches (right and left ventricular subendocardium), and Purkinje fibre network (ventricular endocardium) |
|---|---|
| Insertion | Subendocardial distribution throughout the ventricular walls, with the Purkinje network penetrating to the papillary muscles and trabecular myocardium |
| Nerve Supply | Sympathetic (beta-1 receptors): increases automaticity, conduction velocity, and contractility; Parasympathetic via vagus (M2 receptors): slows SA node rate and AV node conduction; Intrinsic automaticity of conduction cells is independent of innervation |
| Blood Supply | Sinoatrial nodal artery (from RCA 60%, LCx 40%); atrioventricular nodal artery (from RCA in 85%); septal perforating arteries (His bundle and bundle branches) |
| Actions | The sinoatrial node spontaneously depolarises at 60-100 bpm setting the cardiac rhythm; the AV node delays impulse transmission allowing atrial contraction to complete before ventricular systole; the His-Purkinje system rapidly transmits the impulse throughout the ventricular myocardium to produce coordinated ventricular contraction |
|---|
SAN dysfunction (sick sinus syndrome) produces bradycardia, sinus pauses, and tachy-brady syndrome from fibrosis of the SAN and surrounding atrial conduction tissue, requiring pacemaker implantation. AV nodal block (first, second Mobitz I/II, and complete) interrupts conduction at the AV node, requiring pacing for complete block. Bundle branch block (right BBB, left BBB) delays ventricular activation in the affected ventricle, producing QRS widening on ECG. Left bundle branch block is pathological in 98% of cases. Catheter ablation of arrhythmia substrates targets specific areas of the conduction system.
Fibrosis, ischaemia, or iatrogenic injury (cardiac surgery, catheter ablation, valve replacement) of the AV node produces complete heart block with independent atrial and ventricular rhythms; the escape rhythm from the His-Purkinje system is typically 20-40 bpm insufficient to maintain cardiac output; emergency temporary pacing and permanent pacemaker implantation are the standard treatments.
