ECG criteria
- Progressive (cyclic) lengthening of the PR interval from cycle to cycle over 3–5 or more beats
- The PR interval lengthens most significantly right before the pause (block) — this is the main criterion
- Periodic dropout of the QRS complex: only the P wave is visible in place of the expected complex (blocked impulse)
- Following the QRS dropout, a pause occurs (RR interval is longer than usual), after which the cycle repeats
- The first PR after the pause returns to its baseline (shortest) value, as the AV node fully recovers during the pause — the cycle starts anew
- The width of the dropped QRS complex is normal (narrow), if a fragment of it is present (P-wave deformation before the block is rarely seen)
- Sinus rhythm is preserved; P waves are visible regularly, including the blocked impulse within the pause
What it looks like on ECG
The ECG shows a characteristic 'ladder' pattern: the PR interval progressively increases (by approximately 0.02–0.06 s each cycle) until it reaches a critical value, and the next impulse is completely blocked. In place of the dropped QRS complex, only a P wave remains—this is a blocked impulse that fails to conduct through the AV node and does not reach the ventricles.
The pause between the last normal complex and the next beat is longer than a normal RR interval. Important: the pause is typically less than two normal RR intervals, which helps differentiate Wenckebach from complete block or sinoatrial block, where the pause is often a multiple of several cycles.
After the pause, the cycle repeats: the new PR interval starts relatively short again and progresses once more. QRS complexes retain their normal morphology (narrow) because the block is located in the AV node rather than the His-Purkinje system.
Mechanism
The mechanism is based on decremental conduction of the impulse through the AV node. Each sinus impulse encounters nodal tissue with incompletely recovered excitability and is conducted with a delay (PR lengthening). As the rhythm continues, the delay accumulates until the incoming impulse finds the node in a state of absolute refractoriness and is completely blocked. The pause allows full recovery of the node, and the cycle starts over. This is a physiological property of the AV node, frequently seen with high vagal tone or under ischemic conditions.
Causes and associations
- High vagal tone (athletes, young individuals at night)
- Inferior wall myocardial infarction (nodal ischemia)
- Rheumatic heart disease
- Myocarditis
- Degenerative disease of the conduction system (Lenègre's disease)
- Hypothyroidism
- Medications: digoxin, beta-blockers, calcium channel blockers, adenosine
- Hyperkalemia
- Lyme disease (in endemic areas)
Differential diagnosis
Mobitz II: block in the bundle of His; the PR interval does NOT lengthen before the drop—impulses are conducted with a constant PR, and then one suddenly drops without warning. Mobitz II is more dangerous and frequently requires pacing.
2:1 AV block: every second complex drops out (1:1 conduction is impossible). The ECG shows complexes only every other beat, with no cyclic PR lengthening.
Complete AV block (third-degree): no relationship between P waves and QRS complexes; P waves march at their own rate, and QRS complexes at theirs, independently.
Sinoatrial block: the P wave drops out (fails to initiate the pause); in Wenckebach, the P wave is always visible, even when blocked.
Clinical significance and management
Mobitz I generally has a favorable prognosis, particularly in young patients and athletes without structural heart disease. Cardiac output reduction is rarely significant because pauses are brief (usually 1–2 seconds).
Management:
- If the patient is asymptomatic and the cause is benign (vagal tone), observation and repeat ECG.
- If dizziness, presyncope, or syncope are present, rule out Mobitz II and perform 24-hour Holter monitoring.
- Discontinue drugs that slow AV conduction (digoxin, beta-blockers, verapamil) if possible.
- In inferior wall MI, observation; the block is usually transient, and pacing is rarely needed.
- Intravenous atropine or isoproterenol if hemodynamic instability develops.
- Temporary pacing is indicated for symptomatic bradycardia; permanent pacing is generally not required except in rare progressive cases.
Common interpretation errors
- Confusion with Mobitz II: failing to verify whether the PR interval actually lengthens prior to the block. Mobitz I necessarily involves cyclic lengthening; if absent, it is not Wenckebach.
- Ignoring the blocked impulse: mistaking the P wave within the pause for noise or an artifact, even though it is a key diagnostic criterion.
- Incorrect cycle counting: failing to determine the ratio at which the cycle repeats (3:2, 4:3, 5:4, etc.). This is important for assessing the degree of block.
- Overestimating risk: ordering pacemakers for asymptomatic patients, although Mobitz I rarely requires intervention.
- Missing sinoatrial block: if pauses occur without a visible P wave (the sinus node impulse itself drops out), this is SA block, not Wenckebach.
'Ladder and pause' — the PR interval increases like a ladder until a complex drops; the P wave in the pause is a blocked impulse.
1. The ECG shows cyclic PR interval lengthening with periodic QRS complex dropout. A P wave is visible in the pause. What type of AV block is this?
Cyclic PR lengthening before complex dropout and a visible P wave in the pause (blocked impulse) are typical features of Mobitz I (Wenckebach). Other variants do not show these signs.
2. A 28-year-old athlete. ECG shows Wenckebach periodicity, 4:3 ratio. Asymptomatic, heart rate 55 bpm. What is the primary management strategy?
In a young, asymptomatic athlete, Wenckebach is frequently caused by high vagal tone and carries a favorable prognosis. Pacing is not indicated. Confirm the diagnosis (Holter), rule out other causes, and observe.
3. What is the main difference between Mobitz I and Mobitz II?
The key criterion for Mobitz I is progressive PQ prolongation before a dropped beat (decremental conduction). In Mobitz II, PQ remains constant and the impulse is blocked without warning, which indicates a block below the node and requires pacing.
Frequently asked questions
Is second-degree AV block, Mobitz type I dangerous?
Wenckebach rarely causes serious complications in a stable setting, especially if the pauses are short (under 2 sec). However, it requires monitoring as it may indicate an inferior myocardial infarction or progress to a high-grade block. An asymptomatic patient generally does not require pacing.
How to distinguish Mobitz I from Mobitz II on ECG?
In Mobitz I, the PQ interval prolongs BEFORE the QRS complex is dropped — this is the main criterion. In Mobitz II, the PQ interval remains constant, and the complex drops without warning. Mobitz II is more dangerous and frequently requires pacing.
Which specialist should follow a patient with Wenckebach periodicity?
Cardiologist. Organic heart disease (MI, myocarditis, valvular disease) must be ruled out, a Holter monitor performed to clarify the nature of the block, AV nodal function assessed, and treatment indications determined.
Is pacing necessary for Mobitz I AV block?
No, if the patient is asymptomatic and the cause is functional (vagal tone, athletic heart). Pacing is indicated for symptomatic bradycardia with hemodynamic instability or progression to high-grade block.
Can Wenckebach block resolve on its own?
Yes, especially if the cause is transient: drug discontinuation, recovery from an inferior MI, or restoration of autonomic nervous system balance. In case of organic nodal damage, the block may persist or progress.
ECG Course
Interpretation from basics to myocardial infarction — learn to read any ECG using a systematic algorithm.
- Video lessons and theory for every topic
- Simulator case studies under every lesson
- Unlimited ECG simulator practice
- Study guide: "All ECGs in 25 minutes"
ECG Strip Simulator
ECG, radiology, histology, pathomorphology, pharmacology — thousands of flashcards with detailed explanations.
- Real ECG strips, not textbook drawings
- Instant answers and explanations
- Streaks and progress tracking in your dashboard
Related terms
More in the «AV Blocks» section
Sources
- Goldberger A.L., Goldberger Z.D., Shvilkin A. Goldberger's Clinical Electrocardiography. — 9th ed., 2018
- Hampton J.R. The ECG Made Easy. — 9th ed., 2013
- Orlov V.V. Rukovodstvo po elektrokardiografii. — 10th ed., 2019 (Orlov V.V. Electrocardiography Guide)
- Recommendations for the standardization and interpretation of the electrocardiogram (AHA/ACCF/HRS, 2009)
Educational material for medical students and physicians. Does not replace clinical guidelines and physical examination; the ECG must always be interpreted in conjunction with the clinical picture.