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.



View Image

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



View Image

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.



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

See Can't-Miss ECG Findings, Life-Threatening Conditions: Slideshow, a Critical Images slideshow, to help recognize the conditions shown in various tracings.

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

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.

History

Junctional rhythms may be accompanied by symptoms or may be entirely asymptomatic. Note the following:

Physical

A predominant junctional rhythm may be associated with structural heart disease, sick sinus syndrome, or both, during which the junctional escape rhythm supersedes the sinus rate and provides a safety mechanism.

During a predominant junctional rhythm, the pulse usually is regular and the heart rate may be within reference range. Frequently, the junctional rhythm is 40-60 beats per minute.

Prominent jugular venous pulsations (ie, cannon a waves) may be present due to the right atrium contracting with a closed tricuspid valve.

Causes

Causes of junctional rhythm include the following:

Laboratory Studies

Evaluation of serum electrolyte levels is generally indicated for patients with comorbidities that may predispose them to accelerated junctional rhythms because of intrinsic bradycardia or AV block. Suggested evaluations include the following:

Junctional rhythms are common during sleep in younger patients.

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

The 12-lead ECG is essential to making the correct diagnosis of any junctional rhythm (see images below). Telemetry strips demonstrating the onset and termination pattern of the unknown narrow complex rhythm often provide clues regarding the diagnosis. The 12-lead ECG findings also help identify patients with underlying structural heart disease or conduction abnormalities.[3]



View Image

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



View Image

Note the retrograde P waves that precede each QRS complex.



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.

Note the following:

A cardiac event monitor is indispensable for patients who are difficult to diagnose, such as those with transient symptoms of palpitations or minimal documentation of an abnormal rhythm. Patients may carry the event monitor for an indefinite period (usually 30 d) and press a button to record a rhythm strip during symptoms. The onset and termination of the rhythm is documented and may help guide therapy and may help exclude more potentially lethal arrhythmias, such as ventricular tachycardia, as a cause of the symptoms.

An implantable loop recorder may help diagnose junctional rhythm in patients with very infrequent symptoms.

In patients with an accelerated junctional rhythm after cardiac surgery, documentation of AV conduction is imperative. The accelerated junctional rhythm may be a manifestation of inflammation and/or damage to the AV junction; once the accelerated rhythm resolves, AV block may be present. If atrial epicardial wires are present, pacing the atrium at a more rapid rate allows verification of AV conduction.

If the diagnosis is still not certain, an electrophysiologic study (EPS) or invasive electrophysiologic evaluation can be performed.[4]

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.[5]  Note the following:

Surgical Care

If junctional rhythm is due to symptomatic sick sinus syndrome, permanent pacemaker implantation is indicated.

If ectopic junctional tachycardia, which usually occurs in the pediatric population, is incessant and symptomatic, then radiofrequency ablation via a percutaneous approach is indicated.

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 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.

Further Inpatient Care

AV nodal junctional rhythms generally are well tolerated; however, bradycardia for prolonged periods often causes symptoms such as dizziness and presyncope or, rarely, frank syncope in younger patients. Patients with coronary artery disease, those with significant comorbidities, or elderly patients may not tolerate a secondary junctional rhythm well and, in the acute setting, may require intervention such as a pacemaker.

Currently, the choices of treatment strategy include determination of the underlying cause and whether it is a normal physiologic response (ie, that observed in a young athlete) or due to a primary cardiac abnormality such as heart block.

Complications

Complications are usually limited to symptoms such as dizziness, dyspnea, or presyncope.

Accidental injury may result from syncope if the arrhythmia is not tolerated well.

Exacerbation of cardiac comorbidities, such as congestive heart failure and rate-related cardiac ischemia, may occur.

Prognosis

No evidence suggests increased mortality.

Prognosis is good.

Author

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

Disclosure: Nothing to disclose.

Specialty Editors

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

Disclosure: Received salary from Medscape for employment. for: Medscape.

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

Disclosure: Nothing to disclose.

Chief Editor

Jeffrey N Rottman, MD, Professor of Medicine, Department of Medicine, Division of Cardiovascular Medicine, University of Maryland School of Medicine; Cardiologist/Electrophysiologist, University of Maryland Medical System and VA Maryland Health Care System

Disclosure: Nothing to disclose.

Acknowledgements

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, et al. Calcium dynamics and the mechanisms of atrioventricular junctional rhythm. J Am Coll Cardiol. 2010 Aug 31. 56(10):805-12. [View Abstract]
  2. Cools E, Missant C. Junctional ectopic tachycardia after congenital heart surgery. Acta Anaesthesiol Belg. 2014. 65(1):1-8. [View Abstract]
  3. 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.
  4. Josephson ME. Clinical Cardiac Electrophysiology. 4th ed. Baltimore, Md: Williams & Wilkins; 2008.
  5. Libby P, Bonow RO, Mann DL, Zipes, DP. Specific arrhythmias: diagnosis and treatment. Braunwald E, ed. Heart Disease: A Textbook of Cardiovascular Medicine. 8th ed. Philadelphia, Pa: WB Saunders; 2007. 640-5.
  6. Daubert JP, Rosero SZ, Corsello A. Tachycardias. 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.