AV Block — Atrioventricular Conduction Disease

Atrioventricular (AV) block refers to impaired or failed conduction of atrial impulses to the ventricles through the AV conduction system. The conduction axis comprises four anatomically and functionally distinct regions: the AV node (compact node within Koch's triangle), the His bundle (penetrating and branching portions traversing the central fibrous body), the right and left bundle branches, and the Purkinje network. Block can occur at any level, and precise localization is essential because it determines prognosis and the need for permanent pacing.

The AV node is a compact cluster of specialized cells located at the apex of Koch's triangle, anterior to the coronary sinus ostium. It receives dual inputs — a posterior extension near the CS os and an anterior extension along the tendon of Todaro. The AV node exhibits decremental conduction (slower conduction with faster rates), which is the physiologic basis of first-degree AV block and Mobitz Type I (Wenckebach) block. AV nodal block carries a favorable prognosis because the junctional escape rhythm is typically narrow-complex and reliable at 40–60 bpm.

The His bundle emerges from the AV node as a compact cable of longitudinal fibers that penetrates the central fibrous body. It bifurcates at the crest of the muscular interventricular septum into the right bundle branch (a discrete cord traversing the right side of the septum toward the moderator band) and the left bundle branch (a broad sheet of fibers fanning over the left septal surface). Infra-Hisian block — within or below the His bundle — is pathological, produces unreliable wide-complex escape rhythms at 20–40 bpm, and carries a high risk of syncope and sudden cardiac death.

Classification of AV Block

First-degree AV block is defined as prolongation of the PR interval beyond 200 ms with 1:1 AV conduction preserved. It most commonly reflects conduction delay within the AV node, though marked PR prolongation (>300 ms) can arise from infra-nodal disease. Although traditionally considered benign, a markedly prolonged PR (>300 ms) can produce hemodynamic compromise through loss of AV synchrony (so-called “pacemaker syndrome” physiology).

Second-degree Mobitz Type I (Wenckebach) features progressive PR prolongation with a shortening of the RR increment until a non-conducted P wave occurs. The block is almost always within the AV node. Its physiology reflects decremental conduction: each successive impulse arrives during a progressively more refractory AV node. Wenckebach periodicity in isolation is common during sleep and in trained athletes, reflecting heightened vagal tone rather than structural disease.

Second-degree Mobitz Type II is characterized by a constant PR interval preceding the dropped beat. The block is almost always infra-Hisian (within or below the His bundle) and carries a significant risk of progression to complete heart block. It typically occurs in the setting of organic conduction system disease — fibrosis, ischemia, or infiltration of the His-Purkinje system. The QRS during conducted beats is usually wide (bundle branch block morphology), reflecting diffuse conduction system disease.

2:1 AV block is a unique pattern where every other P wave is blocked. It cannot be classified as Mobitz I or II from a single rhythm strip because consecutive conducted beats are needed to assess PR interval behavior. Distinguishing nodal from infra-nodal 2:1 block relies on QRS width, response to autonomic maneuvers, and EP study findings.

Third-degree (complete) AV block involves complete failure of AV conduction with AV dissociation. The atrial rate exceeds the ventricular rate, and no relationship exists between P waves and QRS complexes. The escape rhythm morphology is the critical clue to the level of block: a narrow QRS escape at 40–60 bpm suggests a junctional (AV nodal or proximal His) focus, while a wide QRS escape at 20–40 bpm indicates an infra-Hisian or ventricular origin with far higher risk of hemodynamic collapse.

Congenital complete AV block is most commonly associated with maternal anti-Ro/SSA and anti-La/SSB antibodies (neonatal lupus syndrome). The block is usually at the AV node with a reliable narrow-complex escape, and many patients survive into adulthood without pacing, though late decompensation and exercise intolerance can develop. Acquired AV block in adults is most often caused by idiopathic progressive fibrosis (Lev and Lenegre disease), ischemia (inferior MI for nodal block, anterior MI for infra-nodal block), infiltrative diseases (sarcoidosis, amyloidosis), medications (beta-blockers, calcium channel blockers, digoxin, amiodarone), and post-surgical/procedural injury (TAVR, septal myectomy, VSD repair).

Distinguishing vagally mediated AV block from pathological block is essential. Vagal AV block is characterized by simultaneous sinus slowing, occurs predominantly during sleep or rest, resolves with sympathetic activation, and localizes to the AV node. Pathological infra-nodal block, in contrast, may worsen with exercise as faster rates stress the diseased His-Purkinje system.

The surface ECG remains the primary tool for identifying and localizing AV block. Careful analysis of the PR interval, QRS morphology, and the relationship between P waves and QRS complexes provides critical diagnostic information.

First-degree AV block is recognized by a PR interval >200 ms with preserved 1:1 conduction. When the PR interval exceeds 300 ms, the P wave may fall on or near the preceding T wave, potentially producing pseudo-pacemaker syndrome with symptoms of fatigue and dyspnea due to atrial contraction against a closed mitral valve.

Mobitz Type I (Wenckebach) demonstrates progressive PR prolongation with the greatest increment occurring between the first and second conducted beats. The RR intervals progressively shorten before the dropped beat, creating a characteristic “group beating” pattern. The pause containing the dropped beat is less than twice the preceding RR interval. The QRS is typically narrow. Atypical Wenckebach patterns are common and may show variable PR increments, but the essential feature remains progressive PR lengthening before a non-conducted P wave.

Mobitz Type II is identified by a constant PR interval in conducted beats with an abrupt failure of conduction — a P wave followed by no QRS without any preceding PR change. The conducted QRS is usually wide, showing a bundle branch block pattern (RBBB or LBBB), which indicates underlying His-Purkinje disease. Mobitz II with a narrow QRS is rare and should prompt consideration of intra-Hisian block.

2:1 AV block is a diagnostic challenge because only one conducted beat separates each dropped beat, preventing assessment of PR interval trends. Several ECG clues help localize the block:

Complete AV block on ECG shows P waves marching through at a constant rate, QRS complexes occurring at a slower constant rate, and no fixed PR relationship. The P waves “walk through” the QRS complexes. Importantly, AV dissociation is not synonymous with AV block — AV dissociation can also occur from accelerated junctional or ventricular rhythms (isorhythmic dissociation) where the subsidiary pacemaker is faster than the sinus rate, but AV conduction capability is preserved.

For 2:1 block differentiation: a narrow QRS with a prolonged PR on conducted beats favors AV nodal block; a wide QRS with a normal PR on conducted beats favors infra-nodal block. Administration of atropine improves AV nodal block (increases the conduction ratio from 2:1 to 3:2 or 1:1) but may worsen infra-nodal block by increasing the sinus rate without improving His-Purkinje conduction. Exercise has the same differential effect: sympathetic stimulation improves nodal conduction but stresses a diseased His-Purkinje system.

The electrophysiology study provides definitive localization of AV block and is indicated when non-invasive assessment is inconclusive, particularly in patients with 2:1 AV block of uncertain level, syncope with bundle branch block, or when the need for permanent pacing is equivocal. The key measurements are the AH interval (atrium-to-His, reflecting AV nodal conduction) and the HV interval (His-to-ventricle, reflecting infra-nodal conduction through the His-Purkinje system).

HV Interval

The HV interval is the single most important measurement for risk stratification of infra-nodal conduction disease. The normal HV interval is 35–55 ms. An HV of 55–70 ms represents borderline prolongation. An HV >70 ms is clearly abnormal and indicates significant His-Purkinje disease with a meaningful risk of progression to complete heart block. An HV >100 ms is associated with a high rate of progression to symptomatic AV block and is considered a pacing indication even in asymptomatic patients. A split His potential (two distinct His deflections separated by ≥20 ms) signifies intra-Hisian conduction delay or block.

AH Interval

The normal AH interval is 60–125 ms and reflects conduction through the AV node. A prolonged AH interval indicates AV nodal conduction delay and is the electrophysiologic correlate of first-degree AV block when the PR prolongation is nodal in origin. During Mobitz Type I block, the EP study shows progressive AH prolongation followed by a blocked atrial impulse with no His deflection — confirming the block is supra-Hisian (within the AV node). In contrast, Mobitz Type II block shows a constant AH interval with intermittent failure of the His-to-ventricle conduction: the His potential is recorded but no ventricular electrogram follows.

Intra-Hisian Block

Intra-Hisian block is an uncommon but clinically important entity where conduction fails within the His bundle itself. The EP study shows a split His potential: two discrete His deflections (H and H′) separated by a prolonged interval, with block occurring between them. During complete intra-Hisian block, the proximal His (H) is recorded without a distal His (H′) or ventricular electrogram. This is a critical finding because intra-Hisian block carries the same prognostic implications as infra-Hisian block and mandates permanent pacing.

Atrial Pacing and Wenckebach Point

Incremental atrial pacing is performed to determine the AV nodal Wenckebach cycle length — the pacing rate at which AV nodal Wenckebach occurs. A normal AV nodal Wenckebach point is ≥130 bpm (CL ≤460 ms). A Wenckebach point below 100–120 bpm may indicate AV nodal disease, though it must be interpreted in the context of medications (beta-blockers, calcium channel blockers) and autonomic tone. During incremental pacing, if block occurs below the His bundle (His deflection recorded without subsequent ventricular activation), this constitutes infra-Hisian block and is pathological at any pacing rate — a definitive indication for permanent pacing.

Role in Syncope Workup

An EP study is valuable in patients with syncope and bifascicular block (RBBB + LAHB or RBBB + LPHB) on the surface ECG. In this population, an HV >70 ms or inducible infra-Hisian block with atrial pacing supports permanent pacing even in the absence of documented spontaneous AV block. Pharmacologic provocation with procainamide (10 mg/kg IV) can unmask latent His-Purkinje disease: a post-procainamide HV >100 ms or infra-Hisian block is highly specific for impending spontaneous AV block.

Permanent pacing is the definitive treatment for symptomatic AV block and is lifesaving in patients with infra-nodal disease. The 2018 ACC/AHA/HRS Bradycardia and Conduction Delay guidelines provide a systematic framework for indications based on the level of block, symptom correlation, and clinical context.

Class I Indications (Permanent Pacing Recommended)

Class IIa Indications (Pacing Reasonable)

Pacing Mode Selection

Dual-chamber pacing (DDD/R) is the preferred mode for AV block to preserve AV synchrony. The DAVID trial and subsequent studies demonstrated that unnecessary right ventricular pacing can cause left ventricular dyssynchrony and increase heart failure risk. Therefore, minimizing ventricular pacing percentage is desirable in patients with intact AV conduction, but in patients with complete AV block who require near-100% ventricular pacing, the pacing site and modality become critical.

Single-chamber ventricular pacing (VVI/R) may be considered in patients with permanent atrial fibrillation and AV block, where atrial pacing provides no benefit. Single-chamber atrial pacing (AAI/R) is inappropriate in AV block, as it does not address the conduction disorder.

Physiologic Pacing: His Bundle Pacing and LBBAP

His bundle pacing (HBP) delivers pacing stimuli directly to the His bundle, producing native conduction through the His-Purkinje system and resulting in a physiologic, narrow QRS activation pattern. HBP avoids the ventricular dyssynchrony associated with RV apical pacing and has shown improvements in echocardiographic parameters and heart failure outcomes in observational studies. However, HBP has practical limitations: higher capture thresholds requiring larger output, reduced battery longevity, sensing difficulties (far-field signals from the atrium and ventricle), and difficulty achieving stable fixation in some patients. HBP success rates for AV block are lower than for CRT indications because complete AV block may involve disease at or below the His bundle recording site.

Left bundle branch area pacing (LBBAP) has emerged as a practical alternative to HBP that overcomes many of its limitations. LBBAP involves advancing the pacing lead from the right ventricular septum through the interventricular septum to capture the left bundle branch or its fascicles. LBBAP achieves stable, low capture thresholds with reliable sensing and has demonstrated narrower paced QRS complexes than RV pacing. For AV block, LBBAP can bypass the level of block when the disease is at the AV node or proximal His, producing a physiologic left bundle activation pattern. The LEFT-BUNDLE-AV-BLOCK trial and other registries have shown high implant success rates (>90%) with favorable pacing parameters at follow-up.

Temporary Pacing Indications

Temporary transvenous pacing is indicated for hemodynamically unstable AV block as a bridge to permanent pacing or until a reversible cause resolves. Common scenarios include acute anterior MI with new Mobitz II or complete AV block, symptomatic drug-induced AV block (pending drug clearance), post-cardiac surgery transient AV block, and as a bridge during device infection requiring lead extraction. Transcutaneous pacing serves as an immediate temporizing measure but is poorly tolerated and unreliable for prolonged use.

Post-TAVR AV Block

New-onset conduction disturbances are among the most common complications of transcatheter aortic valve replacement (TAVR), occurring in 5–30% of cases depending on valve type and implant depth. The risk is highest with self-expanding valves (CoreValve/Evolut) and with deep implantation below the annular plane. New LBBB occurs in 10–25% of patients, and high-grade or complete AV block requiring permanent pacing occurs in 5–15%. The 2023 ACC expert consensus recommends a period of monitoring (typically 24–48 hours) with ambulatory monitoring prior to discharge for new conduction abnormalities. Patients with persistent high-grade AV block ≥24–48 hours post-TAVR should receive permanent pacing. New LBBB with prolonged HV interval (>65 ms) on EP study warrants closer surveillance or prophylactic pacing. Given the high ventricular pacing burden expected, conduction system pacing (LBBAP or HBP) should be strongly considered over conventional RV pacing in TAVR patients who need a permanent pacemaker.