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Atrioventricular Dissociation

  • Author: Chirag M Sandesara, MD; Chief Editor: Jeffrey N Rottman, MD  more...
 
Updated: Dec 18, 2014
 

Background

Atrioventricular (AV) dissociation is a condition in which the atria and ventricles do not activate in a synchronous fashion but beat independently of each other. AV dissociation usually refers to the situation in which the ventricular rate is the same or faster than the atrial rate.[1, 2] When the atrial rate is faster and the atria and ventricles are beating independently, complete heart block is present; this is distinct from AV dissociation. While complete heart block can be properly considered a form of AV dissociation, it is discussed in detail in Atrioventricular Block and is not considered further in this article. Also, in AV dissociation, no retrograde ventriculoatrial conduction occurs.

When the atrial rate is the same as the ventricular rate but the P wave is not conducting, the rhythm disturbance is known as isorhythmic AV dissociation. When the rates are similar but occasionally the atria conduct to the ventricles, the rhythm is known as interference AV dissociation.

AV dissociation can be a benign phenomenon and can be complete or incomplete. When incomplete, some of the P waves conduct and capture the ventricles (ie, interference AV dissociation), but if they do not, it is complete AV dissociation. Complete AV dissociation can mimic AV block, but the fact that none of the P waves conduct has more to do with timing of the P waves in relation to the QRS complex rather than the presence of AV block.

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Pathophysiology

A normal cardiac impulse arises from the sinus node and is conducted through the AV junction, the bundle of His, and the bundle branches to the ventricles. The sinus node is the dominant pacemaker because its intrinsic rate is faster than subsidiary pacemakers in the AV junction or in the ventricle. AV dissociation can result from (1) slowing of the dominant pacemaker (sinus node), which allows an escape junctional or ventricular rhythm, or (2) acceleration of a normally slower (subsidiary) pacemaker, such as a junctional site or a ventricular site that activates the ventricles without retrograde atrial capture.

Conditions that can initiate AV dissociation include surgical and anesthesia interventions (including intubation), conditions that increase catecholamine levels (including infusions of inotropes) and drugs that block catecholamines, sinus node disease, digoxin toxicity, myocardial infarction and other structural heart disease, hyperkalemia, vagal activation (eg, neurocardiogenic syncope, vomiting), ventricular tachycardia, or ventricular pacing. AV dissociation can be seen after radiofrequency ablation of the slow pathway responsible for AV nodal reentry if some of the vagal fibers are damaged. After exertion, if AV dissociation is present from an escape pacer, it can be a normal phenomenon. Whatever the cause, AV dissociation usually is secondary to some other cause.

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Epidemiology

Frequency

International

Little epidemiologic information is available regarding the frequency of AV dissociation.

Mortality/Morbidity

The prognosis of AV dissociation depends on the underlying cardiac condition and effects of drug toxicities.

AV dissociation by itself can be benign. Any adverse effects are related to ensuing bradycardia, AV dyssynchrony, or underlying conditions.

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Contributor Information and Disclosures
Author

Chirag M Sandesara, MD Virginia Cardiovascular Associates, Cardiac Rhythm Care

Chirag M Sandesara, MD is a member of the following medical societies: American College of Cardiology, American College of Physicians-American Society of Internal Medicine, American Heart Association, American Medical Association, Heart Rhythm Society

Disclosure: Nothing to disclose.

Coauthor(s)

Brian Olshansky, MD Professor Emeritus of Medicine, Department of Internal Medicine, University of Iowa College of Medicine

Brian Olshansky, MD is a member of the following medical societies: American College of Cardiology, Heart Rhythm Society, Cardiac Electrophysiology Society, American Heart Association

Disclosure: Received honoraria from Guidant/Boston Scientific for speaking and teaching; Received honoraria from Medtronic for speaking and teaching; Received consulting fee from Guidant/Boston Scientific for consulting; Received consulting fee from BioControl for consulting; Received consulting fee from Boehringer Ingelheim for consulting; Received consulting fee from Amarin for review panel membership; Received consulting fee from sanofi aventis for review panel membership.

Roger Freedman, MD Director of Clinical Cardiology, Professor, Department of Internal Medicine, Division of Cardiology, University of Utah School of Medicine

Roger Freedman, MD is a member of the following medical societies: American College of Cardiology, Heart Rhythm Society, American College of Physicians, American Heart Association, Phi Beta Kappa, Sigma Xi

Disclosure: Received grant/research funds from St. Jude Medical for other; Received consulting fee from St. Jude Medical for consulting; Received ownership interest from St. Jude Medical for other; Received grant/research funds from Boston Scientific for other; Received consulting fee from Boston Scientific for consulting; Received grant/research funds from Medtronic for other; Received consulting fee from Medtronic for consulting; Received consulting fee from Sorin for consulting.

Specialty Editor Board

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.

Marschall S Runge, MD, PhD Charles and Anne Sanders Distinguished Professor of Medicine, Chairman, Department of Medicine, Vice Dean for Clinical Affairs, University of North Carolina at Chapel Hill School of Medicine

Marschall S Runge, MD, PhD is a member of the following medical societies: American Physiological Society, American Society for Clinical Investigation, American Society for Investigative Pathology, Association of American Physicians, Texas Medical Association, Southern Society for Clinical Investigation, American Federation for Clinical Research, Association of Professors of Medicine, Association of Professors of Cardiology, American Association for the Advancement of Science, American College of Cardiology, American College of Physicians-American Society of Internal Medicine, American Federation for Medical Research, American Heart Association

Disclosure: Received honoraria from Pfizer for speaking and teaching; Received honoraria from Merck for speaking and teaching; Received consulting fee from Orthoclinica Diagnostica for consulting.

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

Jeffrey N Rottman, MD is a member of the following medical societies: American Heart Association, Heart Rhythm Society

Disclosure: Nothing to disclose.

Acknowledgements

Ram C Sharma, MD, MRCP Assistant Professor of Medicine, Division of Cardiovascular Medicine, Department of Internal Medicine, University of Louisville

Ram C Sharma, MD, MRCP is a member of the following medical societies: American Academy of Sleep Medicine, American College of Cardiology, and Royal College of Physicians of the United Kingdom

Disclosure: Nothing to disclose.

References
  1. Braunwald E. Atrioventricular dissociation. Braunwald E, Zipes DP, Libby P, eds. Heart Diseases: A Textbook Of Cardiovascular Medicine. 6th ed. WB Saunders Co: Philadelphia, Pa; 2001.

  2. Wagner GS. Atrioventricular dissociation. Wagner GSS, Marriott HJ, eds. Marriott's Practical Electrocardiography. Baltimore, Md: Williams & Wilkins; 1994. 9th ed:

  3. Oreto G, Smeets JL, Rodriguez LM, et al. Wide complex tachycardia with atrioventricular dissociation and QRS morphology identical to that of sinus rhythm: a manifestation of bundle branch reentry. Heart. 1996 Dec. 76(6):541-7. [Medline].

  4. Ho RT, Pietrasik G, Greenspon AJ. A narrow complex tachycardia with intermittent atrioventricular dissociation: What is the mechanism?. Heart Rhythm. 2014 Nov. 11(11):2116-9. [Medline].

  5. Duffield JS, Jacob AJ, Miller HC. Recurrent, life-threatening atrioventricular dissociation associated with toxoplasma myocarditis. Heart. 1996 Nov. 76(5):453-4. [Medline].

  6. Luzza F, Oreto G. Pseudo-atrioventricular dissociation caused by interpolated ventricular extrasystoles in the presence of dual atrioventricular nodal pathway. Chest. 1994 May. 105(5):1587-9. [Medline].

  7. Ogunlade O, Akintomide AO, Ajayi OE, Eluwole OA. Marked first degree atrioventricular block: an extremely prolonged PR interval associated with atrioventricular dissociation in a young Nigerian man with pseudo-pacemaker syndrome: a case report. BMC Res Notes. 2014 Nov 4. 7:781. [Medline]. [Full Text].

  8. Pick A. A-V dissociation. A proposal for a comprehensive classification and consistent terminology. Am Heart J. 1963 Aug. 66:147-50. [Medline].

 
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Atrioventricular (AV) dissociation. Ventricular tachycardia and complete AV dissociation. P waves are marked.
Atrioventricular (AV) dissociation. Complete AV block and no fixed relationship between P waves and QRS complexes.
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