Junctional Rhythm 

  • Author: Sean C Beinart, MD, FACC, FHRS; Chief Editor: Jeffrey N Rottman, MD   more...
 
Updated: Dec 15, 2010
 

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.

Junctional bradycardia due to profound sinus node Junctional bradycardia due to profound sinus node dysfunction. No atrial activity is apparent. Note the retrograde P waves that precede each QRS 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.

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

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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

  • The heart rate during a junctional rhythm often determines whether the patient has symptoms.
  • Presence of AV disassociation can lead to symptoms in patients because of atrial conduction and subsequent contraction when the tricuspid valve is closed (ie, canon a waves).
  • Periods of junctional rhythm are not necessarily associated with an increase in mortality. If an obvious cause is present, such as complete heart block or sick sinus syndrome, then the morbidity or mortality is directly related to that and not to the junctional rhythm mechanism, which is serving as a "backup rhythm" during the periods of bradycardia. Accelerated junctional rhythms may be a sign of digitalis toxicity.

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

  • This rhythm may occur in persons of any age.
  • Junctional rhythms during sleep are common in children and in athletic adults.
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Contributor Information and Disclosures
Author

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

Sean C Beinart, MD, FACC, FHRS is a member of the following medical societies: Alpha Omega Alpha, American College of Cardiology, American College of Physicians, American Medical Association, and Heart Rhythm Society

Disclosure: Nothing to disclose.

Specialty Editor Board

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

Alan D Forker, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Cardiology, American College of Physicians, American Heart Association, American Medical Association, American Society of Hypertension, and Phi Beta Kappa

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  Senior Pharmacy Editor, eMedicine

Disclosure: eMedicine Salary Employment

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

Steven J Compton, MD, FACC, FACP is a member of the following medical societies: Alaska State Medical Association, American College of Cardiology, American College of Physicians, American Heart Association, American Medical Association, and Heart Rhythm Society

Disclosure: Nothing to disclose.

Amer Suleman, MD  Consultant in Electrophysiology and Cardiovascular Medicine, Department of Internal Medicine, Division of Cardiology, Medical City Dallas Hospital

Amer Suleman, MD is a member of the following medical societies: American College of Physicians, American Heart Association, American Institute of Stress, American Society of Hypertension, Federation of American Societies for Experimental Biology, Royal Society of Medicine, and Society of Cardiac Angiography and Interventions

Disclosure: Nothing to disclose.

Chief Editor

Jeffrey N Rottman, MD  Professor of Medicine and Pharmacology, Director, Clinical Cardiac Electrophysiology Fellowship Program, Vanderbilt University School of Medicine; Chief, Department of Cardiology, Nashville Veterans Affairs Medical Center

Jeffrey N Rottman, MD is a member of the following medical societies: American Heart Association and North American Society of Pacing and Electrophysiology (NASPE)

Disclosure: Nothing to disclose.

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. [Medline].

  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.

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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.
 
 
 
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