What is the diagnosis for a condition with a progressively prolonged PR (P-R) interval involved with a non-conducted P wave and subsequent dropping of a QRS (quadrature amplitude modulation) complex?

Second-Degree Atrioventricular Block, Mobitz Type I (Wenckebach)

The clinical presentation of progressively prolonged PR intervals culminating in a non-conducted P wave with a dropped QRS complex is diagnostic of second-degree atrioventricular block, Mobitz type I (Wenckebach phenomenon). 1

Electrocardiographic Characteristics

The hallmark features that define this diagnosis include:

• Progressive PR interval prolongation before the blocked beat, with the PR interval gradually lengthening with each successive cardiac cycle 1
• A single non-conducted P wave that fails to generate a QRS complex after the progressive prolongation 1
• "Group beating" pattern on ECG due to the repetitive cycles of progressive PR prolongation followed by dropped QRS complexes 1
• Shorter PR interval after the blocked beat compared to the PR interval immediately before the block 1
• Inconstant PR intervals throughout the cycle, which distinguishes this from Mobitz type II 1

Anatomical Location and QRS Morphology

The QRS width provides critical information about the anatomical site of block:

• Narrow QRS complexes (typically <120 ms) indicate the block is almost always located within the AV node, which carries a more benign prognosis 2, 3, 4
• Wide QRS complexes with Mobitz type I pattern suggest the block may be infranodal (below the AV node in the His-Purkinje system) in 60-70% of cases, which carries worse prognosis 4, 5
• Only His bundle electrography can definitively localize the site of delay when QRS is wide 2

Clinical Significance and Prognosis

Mobitz type I block has distinctly different clinical implications compared to Mobitz type II:

• Generally benign prognosis with slower progression to complete heart block 6, 4
• Associated with a faster and more reliable junctional escape mechanism 1
• Responds to autonomic manipulation including atropine, isoproterenol, and epinephrine administration 1
• Often reversible and may be related to increased vagal tone, medications, or metabolic disturbances 6, 5

Critical Diagnostic Pitfalls to Avoid

Several conditions can mimic Mobitz type I block and must be excluded:

• Vagal surge causing simultaneous sinus slowing and AV nodal block can superficially resemble type II block but is actually benign type I 4, 5, 7
• Non-conducted premature atrial contractions may be mistaken for second-degree AV block 3
• Atrial bigeminy with blocked premature beats can create a pattern resembling AV block 1
• Concealed His bundle or ventricular extrasystoles confined to the conduction system can produce pseudo-AV block patterns 4, 5, 7
• Isorhythmic dissociation where atrial and ventricular rates are similar but independent may be misinterpreted as AV block 1

Reversible Causes Requiring Evaluation

Before attributing the block to permanent conduction disease, exclude:

• Medication effects: beta-blockers, calcium channel blockers (verapamil, diltiazem), digoxin, and antiarrhythmic drugs 1, 6
• Electrolyte abnormalities, particularly hyperkalemia 6
• Acute Lyme carditis, which may resolve spontaneously 1, 6
• Acute myocardial infarction, especially inferior MI 1
• Increased vagal tone from sleep, obstructive sleep apnea, or high-level athletic conditioning 1

Distinguishing from Mobitz Type II Block

This distinction is clinically critical as Mobitz type II requires pacemaker implantation:

• Mobitz type II has constant PR intervals before and after blocked beats, not progressive prolongation 1, 7
• Mobitz type II is almost always infranodal with wide QRS complexes 3, 4, 5
• Mobitz type II has higher risk of progression to complete heart block and sudden cardiac death 1, 3
• 2:1 AV block cannot be classified as type I or type II based on ECG alone, though QRS width provides clues 1, 4, 5

Management Implications

For correctly diagnosed Mobitz type I with narrow QRS:

• Permanent pacemaker generally not indicated if asymptomatic and no structural heart disease 1
• Observation and reversible cause correction is appropriate for most cases 6
• Pacemaker consideration only if symptomatic with documented bradycardia causing symptoms 1
• If wide QRS or infranodal location confirmed, pacing may be required regardless of symptoms 4, 5