atrioventricular node

**Anatomy/location:** Lies in Koch's triangle (bounded by the tendon of Todaro, septal leaflet of the tricuspid valve, and coronary sinus ostium) in the right atrial wall of the interatrial septum. It continues as the bundle of His, which penetrates the fibrous skeleton, then divides into right and left bundle branches and Purkinje fibers.

**Blood supply:** AV nodal artery, usually from the RCA (~85-90% of people, right-dominant); from the LCx in left-dominant hearts. Inferior MI (RCA occlusion) therefore commonly causes AV block (first-degree, Wenckebach/Mobitz I, or complete heart block), which is often transient and responds to atropine.

**Physiology:** - The cells have a slow conduction velocity (the slowest in the heart), because they have small-diameter fibers with few gap junctions and depend on slow L-type Ca2+ channel-mediated upstroke (phase 0), not fast Na+ channels. - This causes the AV delay (~100 ms; corresponds to the PR segment), which allows ventricular filling (atrial kick) before systole. - Intrinsic pacemaker rate is ~40-60 bpm. It is the backup pacemaker if the SA node fails (junctional escape rhythm). The SA node dominates normally (60-100 bpm) through overdrive suppression. - Decremental conduction: the AV node conducts progressively more slowly with faster rates. This protects the ventricles in atrial flutter/fibrillation and allows Wenckebach-type block. - Autonomic control: Parasympathetic (vagus, M2) slows conduction (↑ PR interval), while sympathetic (β1) speeds conduction (↓ PR interval).

**Clinical correlations:** - *First-degree AV block:* PR >200 ms, all P waves conducted. It is benign and often caused by increased vagal tone, drugs, or Lyme disease. - *Second-degree Mobitz I (Wenckebach):* progressive PR lengthening until a dropped QRS. Block is within the AV node; usually benign. - *Second-degree Mobitz II:* fixed PR with intermittent dropped beats. Block is infranodal (His-Purkinje), and it can progress to complete heart block, so it often needs a pacemaker. - *Third-degree (complete) block:* AV dissociation, with P waves and QRS complexes independent. Causes include Lyme disease, ischemia, congenital (maternal SLE/anti-Ro), and degenerative disease. - *AVNRT:* the most common paroxysmal SVT, caused by a reentrant circuit with slow and fast pathways in the AV node. Treat with vagal maneuvers, then adenosine (transient AV block via ↑ K+ efflux/hyperpolarization). Second-line options are verapamil/diltiazem and β-blockers. - *AVRT/WPW:* an accessory pathway (bundle of Kent) bypasses the AV node, so the delta wave and short PR appear. In WPW with AF, avoid AV nodal blockers (e.g., verapamil, digoxin, β-blockers, adenosine) because they may promote conduction down the accessory pathway and cause VF. Use procainamide or cardioversion. - *Rate control in AF:* β-blockers, non-dihydropyridine CCBs (verapamil, diltiazem), and digoxin (↑ vagal tone) slow AV nodal conduction. - *Embryology:* the AV node derives from the AV canal region. Congenital heart block is associated with neonatal lupus (anti-Ro/SSA, anti-La/SSB antibodies crossing the placenta). - *Other causes of AV block:* ↑ vagal tone (athletes), drugs (β-blockers, CCBs, digoxin, amiodarone), hyperkalemia, myocarditis, infective endocarditis with aortic root abscess (prolonging PR), Lyme carditis, and sarcoidosis.

**High-yield pearls:** The SA node is the primary pacemaker (fastest phase 4 depolarization). The AV node is the only normal electrical connection between atria and ventricles because the fibrous skeleton insulates the rest. Adenosine has a half-life <10 s; warn patients about chest tightness/flushing. Methylxanthines such as caffeine and theophylline antagonize adenosine.