Marathon-related ECG Exasperation

aka ECG Exigency 005

The following two ECGs were taken from a 36-year old marathon runner presenting to the ED with acute gastroenteritis. He was completely asymptomatic at the time the ECGs were taken, with normal blood pressure and no chest pain, palpitations or dizziness. Electrolytes were normal.

ECG 1

ECG exigency 005 a

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ECG 2

ECG exigency 005 b

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Questions

Q1. What are the ECG findings ?

The ECGs findings include:

  • Accelerated idioventricular rhythm (AIVR) at around 60 bpm
  • Multiple sinus capture beats
  • Isorhythmic AV dissociation:
    Sinus P waves are buried in the QRS complexes and T waves at a similar rate to the ventricular rhythm – best seen in the rhythm strip in ECG # 2
  • Sinus arrhythmia, with variation in the PP interval of up to 0.2 s

Summary

Competing sinus and idioventricular pacemakers are present. There is underlying sinus arrhythmia, with sinus capture occurring when the sinus rate exceeds the idioventricular rate.

Definitions

  • Accelerated idioventricular rhythm:
    An ectopic ventricular rhythm consisting of three or more ventricular complexes occurring at a rate of 50-110 bpm. The rate differentiates AIVR from ventricular escape rhythms (rate < 50 bpm) and VT (> 110bpm).
  • Isorhythmic AV dissociation:
    AV dissociation with sinus and ventricular complexes occurring at similar rates, unlike 3rd degree heart block where the atrial rate is usually faster than the ventricular rate.  Isorhythmic AV dissociation is usually due to functional block at the AV node from retrogradely conducted ventricular impulses (“interference-dissociation”), which leaves the AV node refractory to the anterograde sinus impulses.
  • Sinus arrhythmia:
    Sinus rhythm in which the PP interval varies by 0.16 s or more.

Q2. What is the mechanism of this arrhythmia?

The likely mechanism of the AIVR in this patient is enhanced automaticity of an ectopic pacemaker in the ventricles coupled with sinus bradycardia and sinus arrhythmia due to athletic training.

There are pacemaker cells at various sites throughout the conducting system, with each site capable of independently sustaining the heart rhythm. The rate of spontaneous depolarisation of pacemaker cells decreases down the conducting system:

  • SA node (60-100 bpm)
  • Atria (< 60 bpm)
  • AV node (40-60 bpm)
  • Ventricles (20-40 bpm)

Under normal conditions, subsidiary pacemakers are suppressed by the more rapid impulses from the sinus node. AIVR occurs when the rate of an ectopic ventricular pacemaker exceeds that of the sinus node.

Athletic training leads to changes in the autonomic nervous system, with increased resting vagal tone and decreased sympathetic tone. This hypervagotonic state causes suppression of impulse generation by the SA node and propagation by the AV node. As a result, athletic individuals will commonly exhibit sinus bradycardia and low-grade AV blocks (e.g. 1st degree heart block, Mobitz I).

Q3. What are the other causes of this arrhythmia?

AIVR is most commonly seen during the reperfusion phase of an acute myocardial infarction.

It is also seen with:

  • Drug toxicity, especially digoxin, cocaine and volatile anaesthetics such as desflurane
  • Electrolyte abnormalities
  • Cardiomyopathy
  • Congenital heart disease
  • Myocarditis
  • Following return of spontaneous circulation in the post-cardiac-arrest period

Q4. What other ECG abnormalities are common in athletes?

The following abnormalities may be present, due to autonomic conditioning (enhanced vagal tone, decreased sympathetic tone) and ventricular hypertrophy:

  • Sinus arrhythmia
  • Sinus bradycardia
  • Junctional or ventricular escape rhythms
  • 1st degree heart block
  • Wenckebach phenomenon
  • Left ventricular hypertrophy
  • Axis deviation
  • Incomplete RBBB

Q5. How should this rhythm be managed?

Management

  • AIVR is a benign rhythm in most settings and does not usually require treatment.
  • Administration of anti-arrhythmics may cause precipitous haemodynamic deterioration and should be avoided.
  • Treat the underlying cause:
    — correct electrolytes
    — restore myocardial perfusion
    — give Digibind in the case of digoxin toxicity.
  • Patients with low-cardiac-output states (e.g. dilated cardiomyopathy) may benefit from restoration of AV synchrony to restore atrial ’kick’ – in this case atropine may be used to increase sinus rate and AV conduction

For more great ECG cases see the ECG library or ECG clinical case library

References

  • Davis M, Davis P, Ross D. Expert Guide to Sports Medicine, American College of Physicians 2003.
  • Mattu A, Brady W. ECGs for the Emergency Physician 2, BMJ Books 2008.
  • Phibbs, BP. Advanced ECG: Boards and Beyond (2nd Edition), Saunders Elsevier 2006.
  • Riera ARP, Barros RB, de Sousa FD, Baranchuk A. Accelerated Idioventricular Rhythm: History and Chronology of the Main Discoveries. Indian Pacing and Electrophysiology Journal; 2010; 10(1):40-48
  • Wagner, GS. Marriott’s Practical Electrocardiography (11th edition), Lippincott Williams & Wilkins 2007.
  • Zimmerman FH. Clinical Electrocardiography: PreTest Self-Assessment and Review, McGraw-Hill 1994.
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Comments

  1. says

    Thank you for this excellent case study and contribution to the EKG community. I am curious as to statistically how long these episodes last and in which clinical contexts; likewise, if there is any increased morbidity or mortality associated with length of episode. The one case of this that I have seen was relatively idiopathic, but I am open to all suggestions. The case is presented here:

    http://thejarvik7.wordpress.com/

    Thanks again!

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