A sudden change from 1:1 AV conduction to complete block of consecutive P waves without an escape rhythm or with unreliable escape rhythm.

abrupt and unexpected long pause and the resultant ventricular asystole may lead to syncope and potential sudden cardiac death.

Types of paroxysmal AV block

1. Idiopathic paroxysmal AV block

Intrinsic AV block due to AV conduction disease

Extrinsic (vagal) AV block

Idiopathic paroxysmal AV block

  A paroxysmal third-degree AV block that displays an abrupt onset and no other rhythm disturbances before or during the block and that occurs in patients with a normal heart and normal ECG.

  These patients have low baseline adenosine plasma level (APL) values and show an increased susceptibility to exogenous adenosine.

  Most patients with idiopathic AV block show a high susceptibility to the rapid IV injection of 18 mg adenosine or 20 mg adenosine triphosphate (ATP) test. The adenosine/ATP test fairly reproduces spontaneous AV block. The adenosine response is abolished by theophylline, an adenosine antagonist, but not by atropine, a vagal antagonist.

  Tilt table test may be positive, but positivity rate is lower than in patients with vasovagal syncope and is never able to reproduce an AV block.

  Carotid sinus massage is almost invariably negative.

  If an electrophysiological study is performed, usually normal results are observed.

Common clinical features of idiopathic paroxysmal AV block

  A long history of recurrent syncope due to idiopathic paroxysmal AV block with long pauses.

  Absence of progression to persistent forms of AV block.

  Absence of cardiac and ECG abnormalities.

  Benefits from cardiac pacing therapy.

Intrinsic paroxysmal AV block

  is regarded as a manifestation of an intrinsic disease of the AV conduction system (Stokes-Adams attack), which is confirmed by abnormal electrophysiologic findings.

  usually occurs in patients with underlying heart disease and/or abnormal standard ECG.

  The AV block is usually initiated by
atrial, His, or ventricular premature extrasystole,

      increased heart rate (
tachy-dependent AV block or phase 3 paroxysmal AV block) or

      decreased heart rate (
brady-dependent AV block or phase 4 paroxysmal AV block).

Findings highly suggestive of Extrinsic (vagal) AV block

  Gradual slowing of the sinus rate (P-P lengthening).

  Significant PR prolongation or Wenckebach before initiation of AV block.

  Prolonging P-P interval during ventricular asystole.

  Resumption of AV conduction on sinus acceleration (shortening of P-P interval).

  Significant PR prolongation on resumption of AV conduction.

  Clinical history highly suggestive of heightened vagal tone (i.e., during micturition, phlebotomy, etc.).

  No retrograde activation of the His bundle with a ventricular or His extrasystole to reset and abolish AV block.


  J Atr Fibrillation 2016;9(3):1449.

  Cardiol Clin 2015;33(3):441-447.

  J Am Coll Cardiol 2011;58(2):167-173.

  Heart Rhythm 2009;6(8):1229-1234.

ECG 1a. The ECG tracing above is from the Holter recording of a 77 years-old woman complaining of dizziness. She was
referred to a Cardiologist by the Neurologist. This Holter tracing has 3 channels and the tracing below is the continuation of
the above rhythm. The tracing shows intrinsic paroxysmal AV block. On the left side of the upper tracing, there is
a normally
conducted P wave
. Then an ectopic atrial focus fires but fails to depolarize the ventricles . After this premature atrial beat
with a negative P wave configuration,
sinus P waves follow but they also fail to depolarize the ventricles resulting in
a pause of 6.5 seconds. At the end of this pause
P waves again start to be conducted to the ventricles.

Click here for a more detailed ECG

ECG 1b. Another tracing from the same patient's Holter recording: intrinsic paroxysmal AV block.
At the left side of the upper tracing
a normally conducted
P wave
is seen. Then an ectopic atrial focus fires but cannot succeed to depolarize the ventricles .
sinus P waves follow
but they fail to depolarize the ventricles
resulting in a pause of 6.2 seconds. At the end, a nodal escape beat comes .
P wave coming at the same time coincides with the ST segment of the nodal escape beat.
Normal conduction of
P waves to the ventricles resumes with the nodal escape beat.

Click here for a more detailed ECG

ECG 1c. Another tracing from the same patient's Holter recording: At the left side of the upper tracing
a normally conducted
P wave
is seen. Later on a pause of 8.3 seconds follows throughout which no P wave can be conducted to the ventricles . Then
a junctional escape beat comes . But the following 5 P waves still cannot be conducted to the ventricles . There is another
nodal escape beat
at the right lower corner of the tracing. The P wave preceeding the second nodal beat is not related to it,
the interval between them is longer than a normal PR interval (compare it to the PR interval following the P wave at the
left upper corner