9.1 Bradyarrhythmias, AV Block Classification & Conduction System Disease

Key Takeaways

  • Mobitz I shows progressive PR prolongation before a dropped beat and is usually AV nodal, benign, and atropine-responsive; Mobitz II shows a fixed PR before an abrupt dropped beat and is infranodal and unstable.
  • In 2:1 AV block the Wenckebach pattern is invisible, so the site is inferred from QRS width, the response to atropine or exercise, and ultimately from the His electrogram.
  • Carotid sinus hypersensitivity is defined by a pause of 3 seconds or longer, a systolic blood pressure fall of 50 mmHg or more, or both.
  • Sinus node dysfunction is diagnosed by symptom-rhythm correlation, not by an isolated heart rate value; a corrected sinus node recovery time above 550 ms is abnormal.
  • Escape rates fall down the hierarchy: junctional escape at 40-60 beats per minute with a narrow QRS, ventricular escape at 20-40 with a wide QRS.
Last updated: September 2026

9.1 Bradyarrhythmias, AV Block Classification & Conduction System Disease

CCI's knowledge list includes ECG/EGM rhythm analysis and interpretation, cardiac pathophysiology, and indications for CIED procedures. Bradyarrhythmia classification is where these meet: the surface ECG pattern predicts the site of block, the site of block predicts prognosis, and prognosis determines whether a pacemaker is implanted.


1. Sinus Node Dysfunction

EntityDefinition
Sinus bradycardiaSinus rhythm below 60 bpm; pathologic only when symptomatic and inappropriate to demand
Sinus pause / arrestFailure of the sinus node to depolarize; pauses > 3 s while awake are generally significant
Sinoatrial exit blockImpulse formed but not conducted out of the node; the pause is a multiple of the basic P-P interval
Chronotropic incompetenceFailure to reach ~80% of age-predicted maximum heart rate (220 − age) with exertion
Tachy-brady syndromeAlternating atrial tachyarrhythmia and post-conversion pauses

The distinction between sinus arrest (pause of random duration) and SA exit block (pause that is an exact multiple of the P-P interval) is a favorite ECG question, because the arithmetic relationship is the only way to tell them apart on the surface tracing.

Diagnosis rests on symptom-rhythm correlation. A resting rate of 44 bpm in a trained athlete is normal; the same rate in a symptomatic 78-year-old with dizziness is sinus node dysfunction. Ambulatory monitoring, event recorders, and implantable loop recorders exist precisely to establish this correlation. In the EP lab, the corrected sinus node recovery time (cSNRT = SNRT − sinus cycle length) is abnormal above about 550 ms, and sinoatrial conduction time is measured by the Strauss or Narula method.

Sinus node dysfunction causes symptoms but does not itself shorten life; pacing relieves symptoms without a demonstrated mortality benefit. This contrasts sharply with high-grade AV block, where pacing is life-saving — a distinction that explains the different urgency in the two indications.


2. Atrioventricular Block

First-degree AV block

PR interval > 200 ms with every P wave conducted. Usually AV nodal delay. Marked prolongation (> 300 ms) can produce a pacemaker-syndrome-like picture because atrial contraction falls against a closed mitral valve.

Second-degree AV block

Mobitz type I (Wenckebach)Mobitz type II
PR before the dropped beatProgressively lengthensConstant
R-R intervalsProgressively shorten before the pauseConstant, then an abrupt pause
PauseLess than twice the shortest R-RUsually exactly twice the P-P
SiteAV node (~72%)Infranodal — His or below (~80%)
QRSUsually narrowUsually wide
Response to atropine / exerciseImprovesWorsens or unchanged
Response to vagal maneuversWorsensImproves (fewer impulses reach the diseased tissue)
Progression to complete blockUncommonCommon and unpredictable
PacingOnly if symptomaticIndicated regardless of symptoms

The paradoxical responses to atropine and to vagal maneuvers are the highest-yield discriminator on this table, and the physiology explains them: atropine speeds the sinus rate, which helps a decrementally conducting AV node recover but floods a diseased His-Purkinje system with more impulses than it can handle.

2:1 AV block

With alternate beats blocked there is never a second consecutive conducted PR interval to compare, so 2:1 block cannot be classified as Mobitz I or II from the surface ECG alone. Inference relies on indirect evidence:

Suggests AV nodalSuggests infranodal
Narrow QRSWide QRS
Long PR on conducted beatsNormal PR on conducted beats
Improves with atropine or exerciseWorsens with atropine or exercise
Improves with sympathetic stimulationImproves with carotid sinus massage

The definitive answer comes from the His bundle electrogram: if the blocked atrial electrogram is followed by a His deflection with no ventricular electrogram, the block is infra-Hisian; if there is no His deflection after the blocked A, the block is within the AV node.

High-grade and third-degree AV block

High-grade (advanced) AV block: two or more consecutive P waves blocked with evidence of some conduction. Third-degree (complete) block: no atrial impulse conducts, and atria and ventricles beat independently — AV dissociation with the atrial rate faster than and unrelated to the ventricular rate.

The escape rhythm localizes the block and predicts stability:

Escape originRateQRSReliability
Junctional40-60 bpmNarrowRelatively stable; block is at or above the His
Ventricular20-40 bpmWideUnreliable, prone to asystole; block is infranodal

A wide, slow escape is an emergency; a narrow escape at 50 buys time.

Distinguish complete AV block from AV dissociation by interference. In complete block the atrial rate exceeds the ventricular rate and no P conducts. In isorhythmic dissociation with an accelerated junctional rhythm, the ventricular rate exceeds the atrial rate, and capture beats prove that conduction is intact — the block is functional, not anatomic.


3. Intraventricular Conduction Disease

Bifascicular block — right bundle branch block with left anterior or left posterior fascicular block — leaves conduction dependent on the remaining fascicle. Trifascicular disease implies additional delay in the surviving fascicle (often expressed as bifascicular block plus first-degree AV block, though the term is imprecise because first-degree block may be nodal).

Bifascicular block progresses to complete heart block at only about 1-2% per year, so it is not by itself a pacing indication. The decision hinges on symptoms: syncope with bifascicular block prompts an EP study, and HV prolongation ≥ 70 ms, or infra-Hisian block provoked by atrial pacing or by procainamide challenge, establishes the indication for pacing.

Alternating bundle branch block — RBBB on some beats and LBBB on others — indicates disease in both bundles and is a pacing indication on its own.


4. Reflex and Situational Bradycardia

SyndromeMechanismDiagnostic criterion
Carotid sinus hypersensitivityExaggerated baroreceptor reflexAsystole ≥ 3 s (cardioinhibitory), systolic BP fall ≥ 50 mmHg (vasodepressor), or both (mixed) during carotid sinus massage
Vasovagal syncopeNeurally mediated withdrawal of sympathetic tone with vagal surgeReproduction on head-up tilt table testing; typical prodrome
Situational syncopeCough, micturition, defecation, swallowHistory

Carotid sinus massage is contraindicated in the presence of a carotid bruit, or with a stroke, transient ischemic attack, or myocardial infarction in the preceding three months. It is performed one side at a time, never both, with continuous ECG and blood pressure monitoring and resuscitation equipment at hand.

Head-up tilt table testing places the patient at 60-80 degrees for 20-45 minutes, sometimes with nitroglycerin or isoproterenol provocation, and is positive when symptoms are reproduced with hypotension, bradycardia, or both. Because the vasodepressor component usually dominates, most vasovagal syncope is not treated with a pacemaker.


5. Reversible Causes First

Before any pacing decision, reversible contributors are excluded:

CategoryExamples
DrugsBeta blockers, non-dihydropyridine calcium blockers, digoxin, amiodarone, sotalol, ivabradine, clonidine, lithium, dexmedetomidine
MetabolicHyperkalemia, hypothyroidism, hypothermia, hypoxia
IschemiaInferior infarction (AV nodal, usually transient); anterior infarction (infranodal, usually permanent)
InfectionLyme carditis (often fully reversible), infective endocarditis with septal abscess
Inflammatory / infiltrativeCardiac sarcoidosis, amyloidosis, giant cell myocarditis
Neurally mediatedVagal surge during sedation, sheath insertion, or transseptal puncture
Post-proceduralSlow-pathway ablation, transcatheter aortic valve replacement, surgical valve replacement

Lyme carditis and drug effect are the two most commonly tested reversible causes, because implanting a permanent device in either case is a preventable error.

Test Your Knowledge

A patient has 2:1 atrioventricular block with a QRS duration of 145 ms and a right bundle branch block pattern. During exercise the ventricular rate falls and the block worsens to 3:1. What does this establish about the site of block?

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Test Your Knowledge

A rhythm strip shows P waves at a constant rate of 84 beats per minute, wide QRS complexes at a regular rate of 32 beats per minute, and no fixed relationship between them. Which conclusion is correct?

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D
Test Your Knowledge

A 68-year-old presents with syncope, is found to have complete heart block, and is on no cardiac medications. Serum potassium is 6.9 mEq/L with peaked T waves. What is the correct initial management priority?

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D