Cardiac conduction system
17 named structures.
Draft — not yet clinically reviewed. The structure of this map is checked automatically, but its wording has not been fact-checked against a textbook. Do not rely on it for an exam answer yet.
Hover or tab a structure to trace what it connects to. Some structures reveal further branches.
Clinical detail
- Sinoatrial node60–100/min RCA ~60% LCx ~40%Fibrosis or ischaemia of the node and its surroundings (sick sinus syndrome, usually elderly)1 question
- Internodal pathways (anterior, middle, posterior)Ectopic focus or micro-re-entry along the crista terminalis2 questions
- Bachmann's bundle (interatrial band)Fibrosis of the bundle from age, hypertension, ischaemia or left atrial dilatation2 questions
- Right atrial myocardiumMacro-re-entry around the tricuspid annulus through the cavotricuspid isthmus (typical anticlockwise flutter)2 questions
- Left atrial myocardiumRapid pulmonary-vein ectopic firing on a dilated, fibrotic left atrial substrate2 questions
- Atrioventricular node40–60/min RCA ~90% ~100 ms delaySlowed nodal conduction from vagal tone, athletic training, beta-blockers, digoxin, verapamil, inferior MI or myocarditis1 question
- Accessory pathway (bundle of Kent)Orthodromic AVRT — antegrade down the AV node, retrograde up the pathway (over 90% of AVRT)2 questions
- Bundle of His (atrioventricular bundle)40–60/min AVN artery + LAD septalIntermittent conduction failure within or below the bundle — Lenègre's idiopathic fibrosis, Lev's calcification of the fibrous skeleton in the elderly, anteroseptal MI, sarcoidosis, cardiac surgery2 questions
- Right bundle branchLAD septals (proximal)Block of the right bundle — normal variant; RV strain from PE, ASD or pulmonary hypertension; anteroseptal MI; myocarditis; Chagas disease; degenerative fibrosis2 questions
- Left bundle branchLAD septals + AVN arteryInterruption of the broad left bundle — almost always structural: ischaemic heart disease, anterior MI, dilated cardiomyopathy, hypertensive LVH, aortic stenosis, Lev/Lenègre fibrosis, post-TAVI2 questions
- Left anterior (superior) fascicleLAD septals onlyBlock of the anterior fascicle from anterior MI, hypertension, aortic valve disease, cardiomyopathy or degenerative fibrosis (also common in the healthy elderly)2 questions
- Left posterior (inferior) fascicleLAD + PDA (dual)Block of the posterior fascicle (extensive ischaemia, almost always with RBBB)2 questions
- Purkinje fibre network20–40/min 2–4 m/sComplete heart block below the His bundle2 questions
- Interventricular septumSeptal infarction from proximal LAD occlusion1 question
- Right ventricular myocardiumLoss-of-function SCN5A sodium-channel mutation reducing RVOT epicardial depolarisation (Brugada syndrome)1 question
- Left ventricular myocardiumRe-entry around surviving muscle strands in an old infarct scar1 question
- Moderator band (septomarginal trabecula)Injury during endomyocardial biopsy, catheter manipulation or surgery; sarcoid or infarct involving the band
Common questions
How do I tell nodal from infranodal block, and why does it matter?
Nodal block (AV node) gives Mobitz I with a lengthening PR, a narrow-QRS junctional escape at 40–60/min, follows inferior MI or AV-blocking drugs, and responds to atropine. Infranodal block (His bundle, bundle branches) gives Mobitz II with a fixed PR and sudden dropped beats, a wide-QRS ventricular escape at 20–40/min, follows anterior MI or degenerative fibrosis, does not respond to atropine and can progress abruptly to asystole — it needs pacing.
Why do inferior and anterior infarcts cause different types of heart block?
The RCA supplies the AV nodal artery in ~90% of hearts, so inferior MI blocks the node itself, often through vagal reflexes, producing transient nodal block with a narrow escape. The LAD septal perforators supply the His bundle and both bundle branches, so anterior MI destroys infranodal tissue, producing Mobitz II or complete block with a wide, unreliable escape and a poor prognosis.
Which drugs are dangerous in atrial fibrillation with WPW?
Adenosine, verapamil, diltiazem, beta-blockers and digoxin all slow or block the AV node, which forces every fibrillatory impulse down the accessory pathway (which has no decremental conduction) and can precipitate VF. Use DC cardioversion, or, if stable, procainamide, ibutilide or flecainide.
Why is left anterior fascicular block so much commoner than left posterior?
The anterior fascicle is a long, thin single trunk in the high-pressure outflow tract, supplied only by LAD septal perforators. The posterior fascicle is short, broad and fan-shaped, lies in the low-pressure inflow tract and has a dual supply from the LAD and the posterior descending artery, so it survives most insults.
What are the intrinsic rates down the conduction system, and why does the SA node normally win?
SA node 60–100/min, AV junction (node and proximal His) 40–60/min, distal His–Purkinje 20–40/min. Each lower pacemaker reaches threshold more slowly because its phase 4 slope is shallower; the SA node fires first every cycle and overdrive-suppresses the rest, which only emerge as escape rhythms when the impulse above them fails.
Which coronary artery supplies the SA node and the AV node?
The SA nodal artery comes from the proximal RCA in about 60% of people and from the LCx in the rest. The AV nodal artery arises at the crux from the dominant artery — the RCA in ~85–90%, the LCx in ~10–15% — with additional supply from LAD septal perforators.