Junctional Rhythm

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Background

Cardiac rhythms arising from the atrioventricular (AV) junction occur as an automatic tachycardia or as an escape mechanism during periods of significant bradycardia with rates slower than the intrinsic junctional pacemaker.

The AV node (AVN) has intrinsic automaticity that allows it to initiate and depolarize the myocardium during periods of significant sinus bradycardia or complete heart block. This escape mechanism, with a rate of 40-60 beats per minute, produces a narrow QRS complex because the ventricle is depolarized using the normal conduction pathway. An accelerated junctional rhythm (rate >60) is a narrow complex rhythm that often supersedes a clinically bradycardic sinus node rate (see images below). The QRS complexes are uniform in shape, and evidence of retrograde P wave activation may or may not be present.


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Junctional bradycardia due to profound sinus node dysfunction. No atrial activity is apparent.


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Note the retrograde P waves that precede each QRS complex.

Less commonly, the AV junction develops abnormal automaticity and exceeds the sinus node rate at a time when the sinus rate would be normal (see image below). These junctional tachycardias are most often observed in the setting of digitalis toxicity, recent cardiac surgery, acute myocardial infarction, or isoproterenol infusion.


View Image

Accelerated junctional rhythm is present in this patient. Note the inverted P waves that precede each QRS complex, with a rate of 115 bpm.

Pathophysiology

The junctional rhythm initiates within the AV nodal tissue. Accelerated junctional rhythm is a result of enhanced automaticity of the AVN that supersedes the sinus node rate. During this rhythm, the AVN is firing faster than the sinus node, resulting in a regular narrow complex rhythm. These rhythms may demonstrate retrograde P waves on ECG findings, and the rates can vary from 40-60 beats per minute.

Changes in autonomic tone or the presence of sinus node disease that is causing an inappropriate slowing of the sinus node may exacerbate this rhythm. Young healthy individuals, especially those with increased vagal tone during sleep, are often noted to have periods of junctional rhythm that is completely benign, not requiring any intervention.

Rarely, the AVN develops enhanced automaticity and overtakes a "normal" sinus node. This occasionally is observed in digitalis toxicity, following cardiac surgery (typically valve replacement), during acute myocardial infarction, or during isoproterenol infusion. Alteration in calcium metabolism in the sarcoplasmic reticulum causes accelerated junctional rhythm.[1]

Epidemiology

Frequency

United States

Junctional rhythms are common in patients with sick sinus syndrome or in patients who have significant bradycardia that allows the AV nodal region to determine the heart rate.

Mortality/Morbidity

Sex

Junctional escape rhythms, which are common in younger and/or athletic individuals during periods of increased vagal tone (eg, sleep), occur equally in males and females.

Age

History

Junctional rhythms may be accompanied by symptoms or may be entirely asymptomatic.

Physical

Causes

Laboratory Studies

Imaging Studies

Obtain a 2-dimensional echocardiograph in patients with suspected structural heart disease.

Obtain a stress echocardiograph or nuclear imaging test in patients with symptoms consistent with coronary ischemia.

Other Tests

Procedures

An EPS should reveal a His bundle depolarization preceding every QRS complex. The His-ventricular interval should be normal unless conduction system disease is present. AV and VA conductions often fluctuate.

Medical Care

The decision to treat a junctional rhythm depends on the underlying cause and the stability of the patient.[4]

Surgical Care

Consultations

Symptomatic cases may benefit from a consultation with a cardiologist and/or an electrophysiologist to better define the etiology and approach to prevention.

Medication Summary

The goals of pharmacotherapy are to reduce morbidity and prevent complications.

Atropine IV/IM

Clinical Context:  Used to increase heart rate through vagolytic effects, causing an increase in cardiac output.

Class Summary

Agents used to accelerate heart rate if symptomatic bradycardia is present.

Digoxin immune Fab (Digibind)

Clinical Context:  Immunoglobulin fragment with a specific and high affinity for both digoxin and digitoxin molecules. Removes digoxin or digitoxin molecules from tissue binding sites.

Each vial of Digibind contains 40 mg of purified digoxin-specific antibody fragments, which bind approximately 0.6 mg of digoxin or digitoxin. Dose of antibody depends on total body load (TBL) of digoxin; estimates of TBL can be made in 3 ways, as follows:

(1) Estimate quantity of digoxin ingested in acute ingestion and assume 80% bioavailability (amount ingested [mg] X 0.8 = TBL).

(2) Obtain a serum digoxin concentration and, using a pharmacokinetics formula, incorporate the Vd of digoxin and the patient's body weight in kg (TBL = digoxin serum level [ng/mL] X 6 L/kg X body weight in kg).

(3) Use an empiric dose based on average requirements for an acute or chronic overdose in an adult or child.

If the quantity of ingestion cannot be estimated reliably, administer empirically (safest to use the largest calculated estimate); alternatively, be prepared to increase dosing if resolution is incomplete.

Class Summary

Used to treat digitalis toxicity.

Phenytoin (Dilantin)

Clinical Context:  Depresses spontaneous depolarization in ventricular tissues.

Class Summary

These agents alter the electrophysiologic mechanisms responsible for arrhythmia.

Further Inpatient Care

Further Outpatient Care

Most of the workup on an otherwise healthy patient can be completed in an outpatient setting. Documentation of the arrhythmia on a rhythm strip is essential to properly diagnose the rhythm and to help exclude other causes.

Complications

Prognosis

Author

Sean C Beinart, MD, FACC, FHRS, Electrophysiologist, Cardiac Associates, PC

Disclosure: Nothing to disclose.

Specialty Editors

Alan D Forker, MD, Professor of Medicine, University of Missouri at Kansas City School of Medicine; Director, Outpatient Lipid Diabetes Research, MidAmerica Heart Institute of St Luke's Hospital

Disclosure: Research Grant Grant/research funds Hospital contracts to do research; I am a hospital employee with no personal profit; Speakers Bureau Honoraria Speaking and teaching

Francisco Talavera, PharmD, PhD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Steven J Compton, MD, FACC, FACP, FHRS, Director of Cardiac Electrophysiology, Alaska Heart Institute, Providence and Alaska Regional Hospitals

Disclosure: Nothing to disclose.

Amer Suleman, MD, Private Practice

Disclosure: Nothing to disclose.

Chief Editor

Jeffrey N Rottman, MD, Professor of Medicine and Pharmacology, Vanderbilt University School of Medicine; Chief, Department of Cardiology, Nashville Veterans Affairs Medical Center

Disclosure: Nothing to disclose.

Additional Contributors

The authors and editors of Medscape Reference gratefully acknowledge the contributions of previous authors Jonathan Langberg, MD; Spencer Rosero, MD; Wojciech Zareba, MD, PhD, FACC; and David Huang, MD to the development and writing of this article.

References

  1. Kim D, Shinohara T, Joung B, Maruyama M, Choi EK, On YK. Calcium dynamics and the mechanisms of atrioventricular junctional rhythm. J Am Coll Cardiol. Aug 31 2010;56(10):805-12. [View Abstract]
  2. Deal BJ, Wolff GS, Gelband H. Current Concepts in Diagnosis and Management of Arrhythmias in Infants and Children. New York, NY: Futura Publishing; 1998:73-5.
  3. Josephson ME. Clinical Cardiac Electrophysiology. 4th ed. Baltimore, Md: Williams & Wilkins; 2008.
  4. Libby P, Bonow RO, Mann DL, Zipes, DP. Specific arrhythmias: diagnosis and treatment. In: Braunwald E, ed. Heart Disease: A Textbook of Cardiovascular Medicine. 8th ed. Philadelphia, Pa: WB Saunders; 2007:640-5.
  5. Daubert JP, Rosero SZ, Corsello A. Tachycardias. In: Rakel RE, Bope ET, eds. Conn's Current Therapy. New York, NY: WB Saunders; 2001:286-95.

Junctional bradycardia due to profound sinus node dysfunction. No atrial activity is apparent.

Note the retrograde P waves that precede each QRS complex.

Accelerated junctional rhythm is present in this patient. Note the inverted P waves that precede each QRS complex, with a rate of 115 bpm.

Junctional bradycardia due to profound sinus node dysfunction. No atrial activity is apparent.

Note the retrograde P waves that precede each QRS complex.

Accelerated junctional rhythm is present in this patient. Note the inverted P waves that precede each QRS complex, with a rate of 115 bpm.

Junctional bradycardia due to profound sinus node dysfunction. No atrial activity is apparent.

Note the retrograde P waves that precede each QRS complex.

Accelerated junctional rhythm is present in this patient. Note the inverted P waves that precede each QRS complex, with a rate of 115 bpm.