What is the pathophysiology of first-degree, second-degree (Mobitz type I and II), and third-degree (complete) atrioventricular (AV) heart block?

Pathophysiology of Atrioventricular Heart Blocks

First-Degree AV Block

First-degree AV block represents a conduction delay—not true block—where all atrial impulses reach the ventricles but with prolonged transit time (PR interval >200 ms). 1

Anatomical Location & Mechanism

• The delay typically occurs within the AV node when the QRS complex is narrow (<120 ms), indicating intact His-Purkinje conduction 1
• When the QRS is wide (≥120 ms), the delay may be either in the AV node or within the His-Purkinje system—only a His bundle electrogram can definitively localize the site 1
• The pathophysiology involves slowed conduction velocity through nodal tissue or the specialized conduction system without complete interruption of impulse transmission 2

Underlying Mechanisms

• Developmental, hereditary/genetic, metabolic, infectious, inflammatory, infiltrative, traumatic, ischemic, malignant, or degenerative processes can all impair AV conduction 2
• The process may be static or progressive in nature 2

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Second-Degree AV Block

Second-degree AV block occurs when some—but not all—atrial impulses fail to conduct to the ventricles, and is subdivided into Mobitz Type I (Wenckebach) and Mobitz Type II based on PR interval behavior and anatomical location. 2

Mobitz Type I (Wenckebach)

Pathophysiologic Mechanism

• Progressive fatigue of AV nodal conduction with each successive impulse causes incremental PR prolongation until an impulse fails to conduct entirely 3
• This creates the characteristic "group beating" pattern with a dropped QRS complex after maximal PR prolongation 3
• The PR interval immediately after the blocked beat is shorter than the PR interval before the block, reflecting recovery of nodal refractoriness 3

Anatomical Location

• The block is almost always located within the AV node itself when QRS complexes are narrow (<120 ms) 3
• This nodal location explains why the block responds to autonomic manipulation (atropine, isoproterenol, epinephrine) 3

Clinical Significance

• Mobitz type I has a benign prognosis with slow progression to complete heart block because the junctional escape mechanism is faster and more reliable 3
• The block is often reversible, particularly when caused by medications (beta-blockers, calcium channel blockers, digoxin), electrolyte abnormalities (hyperkalemia), or acute Lyme carditis 3

Mobitz Type II

Pathophysiologic Mechanism

• Mobitz type II represents an all-or-none conduction failure without visible changes in AV conduction time—PR intervals remain constant before and after the blocked P wave 4, 5
• This pattern reflects sudden failure of impulse propagation through diseased His-Purkinje tissue rather than progressive conduction fatigue 4
• The diagnosis requires a stable sinus rate because vagal surges can cause simultaneous sinus slowing and AV nodal block that superficially resembles type II block 6, 5

Anatomical Location

• The site of block is almost always infranodal (below the AV node) in the His-Purkinje system 4, 5
• Wide QRS complexes (≥120 ms) are typically present, reflecting the distal location of conduction disease 1, 4
• Narrow QRS type II block is exceedingly rare, and coexistence of type I and type II patterns with narrow QRS effectively rules out true type II block 6

Clinical Significance

• Type II block is more likely to progress rapidly and unpredictably to complete heart block and Stokes-Adams arrest 2, 4
• The block does not respond to atropine because it is infranodal 1
• Infranodal blocks require pacing regardless of symptoms 6

Important Diagnostic Pitfalls

• A 2:1 AV block cannot be classified as type I or type II based on surface ECG alone 6, 7, 5
• Concealed His bundle or ventricular extrasystoles can produce pseudo-AV block patterns that mimic both type I and type II block 4, 6, 5
• Atypical Wenckebach with constant PR intervals before the block may be misinterpreted as Mobitz type II 5

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Third-Degree (Complete) AV Block

Third-degree AV block represents complete dissociation between atrial and ventricular activity, with no atrial impulses conducting to the ventricles and the ventricles depolarized by an independent escape rhythm. 2, 1

Pathophysiologic Mechanism

• Complete interruption of electrical continuity between atria and ventricles forces the ventricles to rely on subsidiary pacemakers below the site of block 2
• The atrial rhythm (usually sinus) and ventricular escape rhythm are completely independent with no temporal relationship 7

Anatomical Location & QRS Morphology

Narrow QRS Complete Block (Intranodal/Proximal)

• Narrow QRS complexes (<120 ms) indicate the escape rhythm originates above or within the His bundle, with the block located in the AV node 1
• This produces a stable junctional escape rhythm that is relatively fast (40-60 bpm) and reliable 2
• The prognosis is better because the escape focus is more dependable 2

Wide QRS Complete Block (Infranodal/Distal)

• Wide QRS complexes (≥120 ms) indicate the escape rhythm arises from the distal His-Purkinje system or ventricular myocardium, with block below the His bundle 1
• Infra-Hisian block is the most common anatomic pattern in wide-QRS complete AV block 1
• The ventricular escape rhythm is slower (20-40 bpm), more unpredictable, and less reliable 1

Etiologies of Infra-Hisian Complete Block

• Ischemic injury from myocardial infarction damaging the His-Purkinje network 1
• Infiltrative diseases including sarcoidosis, amyloidosis, and hemochromatosis 1
• Autoimmune conditions such as rheumatoid arthritis and systemic lupus erythematosus 1
• Iatrogenic causes including cardiac valve surgery, TAVR, catheter ablation, and alcohol septal ablation 1
• Medications including beta-blockers, non-dihydropyridine calcium channel blockers, and digoxin 1
• Congenital complete heart block including familial autosomal-dominant forms 1
• Neuromuscular disorders such as myotonic dystrophy, Kearns-Sayre syndrome, and Erb's dystrophy 1
• Metabolic disturbances including hyperkalemia, hypercalcemia, hypothyroidism, and pheochromocytoma 1

Clinical Implications

• Wide-QRS complete block has significantly worse prognosis than narrow-QRS block due to the unreliable escape rhythm 1
• The wide-QRS escape rhythm does not respond to atropine, though it may improve with catecholamine infusion 1
• Progression to hemodynamic collapse is often rapid and unexpected in infra-Hisian block 1
• Electrophysiological study should be considered to definitively localize the level of block when wide QRS and AV block coexist 1