Cardiac conduction system

Systema conducente cordis
Also: SA node · AV node · Bundle of His · Purkinje fibers
OrganHigh-yielddraftCardio

Specialized cardiac muscle that generates and conducts impulses (SA node → AV node → bundle of His → bundle branches → Purkinje fibers). Its blood supply explains the arrhythmias that accompany some MIs.

Core anatomy

Location

Within the walls of the heart.

Parts
  • Sinoatrial (SA) node: the pacemaker, in the wall of the right atrium near the opening of the superior vena cava, at the upper end of the crista terminalis
  • Atrioventricular (AV) node: in the interatrial septum near the opening of the coronary sinus (triangle of Koch). Delays conduction so the ventricles can fill
  • AV bundle (of His): passes through the fibrous skeleton and along the membranous interventricular septum, the only normal electrical connection between atria and ventricles
  • Right and left bundle branches: descend on each side of the muscular septum. The right branch continues in the septomarginal trabecula (moderator band)
  • Subendocardial (Purkinje) fibers: spread the impulse through the ventricular myocardium
Arterial supply

SA nodal artery: usually from the right coronary artery (about 60%), otherwise from the circumflex artery. AV nodal artery: from the dominant coronary artery, usually the RCA (about 80%). Bundle branches: septal perforators of the anterior interventricular artery (anterior two-thirds of the septum) and of the posterior interventricular artery. verify

Innervation

Sympathetic fibers increase rate and conduction velocity. Parasympathetic (vagus) fibers slow the SA node and AV conduction; the right vagus predominantly affects the SA node and the left vagus the AV node. verify

Mentioned in

Generated automatically from links in other entries.

Right atrium and right ventricle opened to show the fossa ovalis, coronary sinus opening and tricuspid valve
Interior of the right atrium: crista terminalis, SVC and coronary sinus openings, the landmarks for the SA and AV nodes.
Henry Vandyke Carter, Gray's Anatomy of the Human Body, 20th ed. (1918), Fig. 493. Source · Public domain (Public domain in the US: published before January 1, 1931 (per Wikimedia Commons))

Clinical correlations

Bradyarrhythmias and AV block in inferior MI PANCE

Mechanism / lesion

The RCA usually supplies the SA and AV nodes, so inferior MI (RCA occlusion) can cause sinus bradycardia and AV block (often transient, at the AV node).

Classic presentation

Bradycardia and hypotension with ST elevation in II, III and aVF. First-degree or Mobitz I block is typical at the AV node level.

Bundle branch block PANCE

Mechanism / lesion

Conduction delay in the right or left bundle branch (ischemia, fibrosis, hypertrophy, or after surgery).

Classic presentation

Wide QRS (120 ms or more). RBBB: rSR' in V1–V2, wide S in I and V6. LBBB: broad notched R in I, aVL, V5–V6; deep S in V1. A new LBBB with symptoms of ischemia needs evaluation for acute MI.

Pre-excitation (Wolff–Parkinson–White) PANCE

Mechanism / lesion

An accessory pathway (bundle of Kent) bypasses the AV node and connects atrium to ventricle directly.

Classic presentation

Short PR interval, delta wave, wide QRS. Predisposes to reentrant tachycardias. In atrial fibrillation with WPW, AV nodal blockers (adenosine, beta blockers, calcium channel blockers, digoxin) can be dangerous; procainamide or cardioversion is used.

Sick sinus syndrome

Mechanism / lesion

Degenerative dysfunction of the SA node, usually in older adults.

Classic presentation

Sinus bradycardia, pauses, or alternating bradycardia and tachycardia (tachy-brady syndrome), with fatigue, dizziness or syncope. Often treated with a pacemaker.

High-yield PANCE pearls

  • Conduction: SA → AV (delay) → His → bundle branches → Purkinje.
  • Inferior MI (RCA) → bradycardia / AV block (the RCA usually supplies the SA and AV nodes).
  • WPW: short PR + delta wave; avoid AV nodal blockers in pre-excited AF.
  • New LBBB with chest pain → treat as a possible acute MI.

Imaging anatomy

X-ray

The system is not visible. Pacemaker and ICD leads are seen on CXR (RA lead in the appendage, RV lead at the apex or septum).

MRI

Cardiac MRI can show infiltrative disease (sarcoidosis, amyloidosis) causing conduction disease.

Ultrasound

Echo assesses structural causes of arrhythmia (valve disease, cardiomyopathy, LA size).

Key views & landmarks
  • 12-lead ECG: the functional image of the conduction system (PR interval = AV conduction; QRS width = ventricular conduction)

Physical exam

Strength / function testing

Pulse rate and regularity. Irregularly irregular pulse = atrial fibrillation until proven otherwise. Cannon a waves in the JVP suggest AV dissociation (complete heart block). Variable intensity of S1 also occurs in complete heart block.

Self-quiz

Q1.

A 62-year-old man has ST elevation in leads II, III and aVF. His heart rate is 42/min, and the ECG shows a PR interval that lengthens progressively until a QRS is dropped. Which artery is most likely occluded?

Show answer

C

Inferior ST elevation with Mobitz I (Wenckebach) block points to the RCA, which usually supplies the AV node (right-dominant circulation).

Q2.

Where is the sinoatrial node located?

Show answer

B

The SA node lies in the right atrial wall at the junction with the SVC, at the upper end of the crista terminalis. The AV node lies near the coronary sinus opening in the interatrial septum.

Q3.

An ECG shows a short PR interval, a slurred upstroke of the QRS, and a QRS duration of 125 ms. What is the underlying abnormality?

Show answer

B

A short PR with a delta wave and wide QRS is Wolff–Parkinson–White pre-excitation: an accessory pathway (bundle of Kent) bypasses the AV node.

Q4.

Which structure carries the right bundle branch across the right ventricular cavity to the anterior papillary muscle?

Show answer

B

The septomarginal trabecula (moderator band) carries part of the right bundle branch from the septum to the base of the anterior papillary muscle, shortening conduction time.

Q5.

A 30-year-old with known Wolff–Parkinson–White syndrome presents with an irregular, wide-complex tachycardia at 210/min (pre-excited atrial fibrillation). He is hemodynamically stable. Which drug is appropriate?

Show answer

C

In pre-excited AF, AV nodal blockers (adenosine, calcium channel blockers, beta blockers, digoxin) can increase conduction down the accessory pathway and precipitate ventricular fibrillation. Procainamide (or cardioversion if unstable) is used.

Flashcards

See also