NCBI Bookshelf. A service of the National Library of Medicine, National Institutes of Health.

StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2021 Jan-.

Cover of StatPearls

StatPearls [Internet].

Show details

Junctional Rhythm

; .

Author Information

Last Update: October 1, 2021.

Continuing Education Activity

The sinoatrial node is the natural cardiac pacemaker located in the upper right atrium. The atrioventricular node is a separate cardiac pacemaker located in the inferior-posterior right atrium. The His bundle is a separate cardiac pacemaker located at the inferior end of the atria and ventricle. A junctional rhythm is an abnormal heart rhythm that originates from the AV node or His bundle. This activity reviews the evaluation and management of junctional rhythm and highlights the role of the interprofessional team in educating patients about their prognosis.


  • Outline the risk factors of developing a junctional rhythm.
  • Review the pathophysiology of junctional rhythms.
  • Explain the differential diagnosis of junctional rhythm.
  • Summarize the interprofessional team's strategies for improving care coordination and communication regarding the management of patients with junctional rhythm.
Access free multiple choice questions on this topic.


The sinoatrial node (SA) is the default pacemaker and is located subepicardially and is crescent in shape. The atrioventricular node (AV) is a subendocardial structure situated in the inferior-posterior right atrium. It sits within an anatomic region bordered posteriorly by the coronary sinus ostium, superiorly by the tendon of Todaro, and anteriorly by the septal tricuspid valve annulus. This anatomic region is also commonly referred to as the triangle of Koch. The sinoatrial nodal artery supplies blood to the sinoatrial node, it branches off the right coronary artery in 60% of cases, whereas in 40% of cases, it comes from the left circumflex coronary artery. The blood supply to the AV node is from the AV nodal branch of the right coronary artery  (90%) or the left circumflex artery (10%) depending on the right or left dominant blood supply to the heart. The first septal perforator of the left anterior descending artery also supplies blood to the AV node. A junctional rhythm is where the heartbeat originates from the AV node or His bundle, which lies within the tissue at the junction of the atria and the ventricle. Generally, in sinus rhythm, a heartbeat is originated at the SA node. This electrical activity then travels through the atria to the AV node from where it reaches the Bundle of His from where the electrical signals travel to the ventricles through the Purkinje fibers.[1][2][3][4][5][6]

The terminology used to identify the type junctional rhythm depends on its rate and is as follows:

  • Junctional bradycardia: rate below 40 beats per minute 
  • Junction escape rhythm: rate 40 to 60 beats per minute 
  • Accelerated junctional rhythm: rate of 60 to 100 beats per minute
  • Junctional tachycardia: rate above 100 beats per minute


When the electrical activity of the SA node is blocked or is less than the automaticity of the AV node/His bundle, a junctional rhythm originates. Numerous conditions and medications can lead to a diseased SA node and lead to the AV node/His bundle taking over due to the higher automaticity of the ectopic pacemaker.[7][8][9]

Some of these conditions and medications are listed below.

  • Chest trauma                                                            
  • Sick sinus syndrome
  • Radiation therapy
  • Collagen vascular disease
  • Myocarditis
  • Clonidine
  • Reserpine
  • Adenosine
  • Cimetidine
  • Antiarrhythmics class I to IV
  • Lithium
  • Amitriptyline
  • Neuromuscular disorder
  • X-linked muscular dystrophy
  • Familial disorder
  • Vasovagal simulation (endotracheal suctioning)
  • Carotid sinus hypersensitivity
  • Beta-blockers
  • Calcium channel blockers
  • Digoxin
  • Ivabradine
  • Opioids
  • Cannabinoids
  • Isoproterenol infusion
  • Hypothyroidism
  • Sleep apnea
  • Hypoxia
  • Intracranial hypertension
  • Hyperkalemia
  • Anorexia nervosa
  • Amyloidosis
  • Pericarditis
  • Lyme disease
  • Rheumatic fever
  • Ischemic heart disease
  • Acute myocardial infarction
  • Acute and chronic coronary artery disease
  • Repair of congenital heart disease
  • Inherited channelopathy

Other than the above-listed causes of severe SA node disease, which can result in junctional rhythm, a high-grade second-degree heart block and a third-degree heart block can also result in a junctional rhythm. Digoxin toxicity can also lead to an accelerated junctional rhythm.


Junctional rhythm is typical among individuals who have a sinus node dysfunction (SND), and 1 in every 600 cardiac patients above the age of 65 within the United States has SND. Patients with sick sinus syndrome, young children, and athletes who have increased vagal tone may also intermittently exhibit junctional rhythm, especially during sleep. Junctional rhythm is reported equally among males and females.[10]


A heart has numerous pacemaker sites within its conduction system, which are independently able to keep the heart beating. And the rate of a heartbeat depends upon the pacemaker site, and as we go down its conduction system, the rate of spontaneous depolarization at pacemaker sites decreases. [1][2][3]

Pacemaker sites and their depolarization rates are listed below:

  • Sinoatrial node: 60 to 100 beats per minute 
  • Atria: less than 60 beats per minute 
  • Atrioventricular node: 40 to 60 beats per minute 
  • Ventricles: 20 to 40 beats per minute


Histopathology of a disease SA node that can contribute to the AV node/His bundle taking over as a pacemaker secondary to their intrinsic automaticity includes SA node fibrosis, atrophy, hypoplasia, or amyloidosis. A normal SA node histopathology does not rule out reduced SA node automaticity contributing to a junctional rhythm.[11][12]

History and Physical

Patients with junctional rhythm may present with a varied array of symptoms or may be asymptomatic. Symptoms mostly depend on the underlying cause of the junctional rhythm, for instance, a patient presenting with heart failure exacerbation may present with shortness of breath, wheezing, and lower extremity edema. Patients with rheumatic fever may present with a heart murmur secondary to the damage to the heart valves, fever, joint pain, and a rash with an electrocardiogram showing a junctional rhythm. Some patients might present with generalized complaints such as dizziness, fatigue, syncope/presyncope, and intermittent palpitations. Non-specific physical exam findings include pulsating veins and regular heart rate with the heart rate varying from 20 to over 100 beats per minute.[13][14][15]


A significant component of an assessment for a patient who presents with signs and symptoms of junctional rhythm is history and physical exam. These should include vital signs (respiratory rate, blood pressure, temperature, and heart rate), a review of the patient's medication list, and an electrocardiogram. See the image below. During their evaluation, it should be established if the patient is hemodynamically stable. The patient should be assessed for any underlying ischemic heart disease or heart failure. A healthcare provider should consider thyroid function testing, pulmonary function testing, including routine blood work, and echocardiography as part of their initial evaluation.[13][14][15]

Treatment / Management

Treatment of a junctional rhythm primarily depends on the underlying cause of the rhythm. In circumstances where the junctional rhythm is a result of underlying sinus node dysfunction that is leading to asystole or bradycardia, it should not be terminated, for it is maintaining the heart rate. Therefore, before establishing a management plan for patients presenting with a junctional rhythm, an underlying etiology must be determined first. Otherwise, healthy individuals who have junctional rhythm and are asymptomatic need no medical management as the rhythm is usually a result of their increased vagal tone suppressing the SA node intrinsic automaticity. In the setting of digoxin toxicity, a patient must be treated with atropine and digoxin-specific antibody. If a patient is refractory to these pharmacologic treatments and goes into junctional tachycardia, intravenous phenytoin can be administered in a monitored setting as these patients can develop hypotension. In the pediatric population, persistent symptomatic junctional tachycardia is an indication for percutaneous radiofrequency ablation. In patients with sick sinus syndrome, or complete or high-grade AV block, a permanent pacemaker is indicated.[16][17][18][19][20]

Differential Diagnosis

  • Digoxin toxicity
  • Atrioventricular nodal reentrant tachycardia
  • Atrioventricular reentrant tachycardia
  • Sinus node dysfunction
  • High-grade second-degree heart block
  • Third-degree heart block


Prognosis is good when the rhythm is promptly identified by a healthcare provider. 


If not identified promptly symptomatic complications such as syncope, fatigue, or dizziness can occur. 

Deterrence and Patient Education

If available patient education should be provided using resources familiar to the patient including online resources and pamphlets. 

Pearls and Other Issues

Always check serum digoxin levels in patients who are on it for comorbidities. Also, check Lyme titers and empirically treat those patients who present with junctional rhythm and have possible exposure to ticks with antibiotics.

Enhancing Healthcare Team Outcomes

Educating patients at risk for this rhythm and making a closed-loop communication between them and their providers can help further improve the management of these rhythms. An interprofessional team best manages this condition. Initial diagnosis is by primary care or emergency providers. Referral to a cardiologist may be indicated. Cardiology and emergency department nurses administer treatment, monitor responses, and report back to the physician or nurse practitioner. Pharmacists should review prescribed medications, check for drug-drug interactions, and educate patients about dosing and side effects. [Level 5]

Review Questions

Junctional Rhythm


Junctional Rhythm. Contributed by Dhaval Desai, MD, MPH


Spodick DH. Normal sinus heart rate: sinus tachycardia and sinus bradycardia redefined. Am Heart J. 1992 Oct;124(4):1119-21. [PubMed: 1529897]
Thery C, Gosselin B, Lekieffre J, Warembourg H. Pathology of sinoatrial node. Correlations with electrocardiographic findings in 111 patients. Am Heart J. 1977 Jun;93(6):735-40. [PubMed: 871100]
Dobrzynski H, Anderson RH, Atkinson A, Borbas Z, D'Souza A, Fraser JF, Inada S, Logantha SJ, Monfredi O, Morris GM, Moorman AF, Nikolaidou T, Schneider H, Szuts V, Temple IP, Yanni J, Boyett MR. Structure, function and clinical relevance of the cardiac conduction system, including the atrioventricular ring and outflow tract tissues. Pharmacol Ther. 2013 Aug;139(2):260-88. [PubMed: 23612425]
Van der Hauwaert LG, Stroobandt R, Verhaeghe L. Arterial blood supply of the atrioventricular node and main bundle. Br Heart J. 1972 Oct;34(10):1045-51. [PMC free article: PMC458545] [PubMed: 5086972]
Pejković B, Krajnc I, Anderhuber F, Kosutić D. Anatomical aspects of the arterial blood supply to the sinoatrial and atrioventricular nodes of the human heart. J Int Med Res. 2008 Jul-Aug;36(4):691-8. [PubMed: 18652764]
Chua K, Upadhyay GA, Lee E, Aziz Z, Beaser AD, Ozcan C, Broman M, Nayak HM, Tung R. High-resolution mapping of the triangle of Koch: Spatial heterogeneity of fast pathway atrionodal connections. Heart Rhythm. 2018 Mar;15(3):421-429. [PubMed: 29081398]
Semelka M, Gera J, Usman S. Sick sinus syndrome: a review. Am Fam Physician. 2013 May 15;87(10):691-6. [PubMed: 23939447]
Trappe HJ. Tachyarrhythmias, bradyarrhythmias and acute coronary syndromes. J Emerg Trauma Shock. 2010 Apr;3(2):137-42. [PMC free article: PMC2884444] [PubMed: 20606790]
Silvestri NJ, Ismail H, Zimetbaum P, Raynor EM. Cardiac involvement in the muscular dystrophies. Muscle Nerve. 2018 May;57(5):707-715. [PubMed: 29130502]
Romhilt DW, Doyle M, Sagar KB, Hastillo A, Wolfgang TC, Lower RR, Hess ML. Prevalence and significance of arrhythmias in long-term survivors of cardiac transplantation. Circulation. 1982 Aug;66(2 Pt 2):I219-22. [PubMed: 6177443]
Rodriguez RD, Schocken DD. Update on sick sinus syndrome, a cardiac disorder of aging. Geriatrics. 1990 Jan;45(1):26-30, 33-6. [PubMed: 2403955]
Sanders P, Kistler PM, Morton JB, Spence SJ, Kalman JM. Remodeling of sinus node function in patients with congestive heart failure: reduction in sinus node reserve. Circulation. 2004 Aug 24;110(8):897-903. [PubMed: 15302799]
Kim D, Shinohara T, Joung B, Maruyama M, Choi EK, On YK, Han S, Fishbein MC, Lin SF, Chen PS. Calcium dynamics and the mechanisms of atrioventricular junctional rhythm. J Am Coll Cardiol. 2010 Aug 31;56(10):805-12. [PMC free article: PMC3050609] [PubMed: 20797495]
Cools E, Missant C. Junctional ectopic tachycardia after congenital heart surgery. Acta Anaesthesiol Belg. 2014;65(1):1-8. [PubMed: 24988822]
Di Biase L, Gianni C, Bagliani G, Padeletti L. Arrhythmias Involving the Atrioventricular Junction. Card Electrophysiol Clin. 2017 Sep;9(3):435-452. [PubMed: 28838549]
Tuohy S, Saliba W, Pai M, Tchou P. Catheter ablation as a treatment of atrioventricular block. Heart Rhythm. 2018 Jan;15(1):90-96. [PubMed: 28823599]
Antman EM, Wenger TL, Butler VP, Haber E, Smith TW. Treatment of 150 cases of life-threatening digitalis intoxication with digoxin-specific Fab antibody fragments. Final report of a multicenter study. Circulation. 1990 Jun;81(6):1744-52. [PubMed: 2188752]
Hauptman PJ, Kelly RA. Digitalis. Circulation. 1999 Mar 09;99(9):1265-70. [PubMed: 10069797]
Kelly RA, Smith TW. Recognition and management of digitalis toxicity. Am J Cardiol. 1992 Jun 04;69(18):108G-118G; disc. 118G-119G. [PubMed: 1626485]
Dobrzynski H, Boyett MR, Anderson RH. New insights into pacemaker activity: promoting understanding of sick sinus syndrome. Circulation. 2007 Apr 10;115(14):1921-32. [PubMed: 17420362]
Copyright © 2021, StatPearls Publishing LLC.

This book is distributed under the terms of the Creative Commons Attribution 4.0 International License (, which permits use, duplication, adaptation, distribution, and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, a link is provided to the Creative Commons license, and any changes made are indicated.

Bookshelf ID: NBK507715PMID: 29939537


  • PubReader
  • Print View
  • Cite this Page

Related information

  • PMC
    PubMed Central citations
  • PubMed
    Links to PubMed

Similar articles in PubMed

See reviews...See all...

Recent Activity

Your browsing activity is empty.

Activity recording is turned off.

Turn recording back on

See more...