DOI: 10.1161/circ.148.suppl_1.16250 ISSN: 0009-7322

Abstract 16250: Latent His-Purkinje Disease Unmasked by Beta Blocker Overdose

Gabriela Narowska, Joshua M Cooper, Anuj Basil
  • Physiology (medical)
  • Cardiology and Cardiovascular Medicine

Background Symptomatic bradycardia usually has a single mechanism and treatment modality. Identifying the culprit mechanism can be challenging, especially when faced with concurrent pathologies. We present a case of severe symptomatic bradycardia where appropriate management of one mechanism unmasked a second mechanism, with a need for pacemaker placement.

Case Presentation A 56-year-old patient presented with beta blocker overdose and severe bradycardia. The initial ECG showed sinus bradycardia with a sinus cycle length of 2060ms and 2:1 AV conduction, with each conducted P wave preceded by a long-coupled junctional escape beat. Atropine resulted in shortening of the junctional escape interval but had no effect on the sinus rate. There was now 1:1 AV conduction, with each P wave being preceded by a faster junctional escape beat. Glucagon resulted in acceleration of the sinus rate to a cycle length of ~820ms (73 bpm) with return of 1:1 AV conduction, a PR interval of 200ms, and no junctional beats. Conducted beats showed a right bundle branch block and left axis deviation. The dependence of AV conduction on a preceding QRS complex within a certain window of time highly suggested infranodal conduction disease manifesting as phase 4 AV block. While normal sinus rates and 1:1 AV conduction were restored with glucagon, the presence of infranodal disease warranted dual chamber pacemaker implantation. In follow-up, with atrial pacing support, there was < 1% ventricular pacing.

Discussion Two causes of bradycardia were simultaneously present - sinus bradycardia due to beta blocker overdose, and 2nd degree AV block due to His-Purkinje disease. Phase 4 AV block is a mechanism of paroxysmal AV block (PAVB) in patients with diseased His-Purkinje system. Spontaneous depolarization occurs in diseased fibers during prolonged periods of ventricular pause, such as with slowing of the sinus rate. The sodium channels are blocked during phase 4 of the action potential and therefore the conduction system is incapable of depolarizing due to low resting membrane potentials. In this case, AV 1:1 conduction can only be restored with a premature ventricular contraction. This is an overall under-recognized entity and should be managed with pacemaker implantation.

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