eMedicine Specialties > Cardiology > Arrhythmias

Atrioventricular Dissociation

Chirag M Sandesara, MD, Fellow, Department of Internal Medicine, Division of Cardiovascular Diseases, University of Iowa Hospitals and Clinics
Brian Olshansky, MD, Professor of Medicine, Department of Internal Medicine, University of Iowa College of Medicine; Ram C Sharma, MD, MRCP, Assistant Professor of Medicine, Division of Cardiology, Department of Internal Medicine, University of Utah Health Science Center; Roger Freedman, MD, Director of Arrhythmia Service, Director of Electrophysiology Fellowship, Professor, Department of Internal Medicine, Division of Cardiology, University of Utah School of Medicine

Updated: Aug 9, 2006

Introduction

Background

Atrioventricular (AV) dissociation is a condition in which the atria and ventricles do not activate in a synchronous fashion but beat independent of each other. AV dissociation usually refers to the situation in which the ventricular rate is the same or faster than the atrial rate. 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.

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.

Frequency

International

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

Mortality/Morbidity

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

Clinical

History

AV dissociation can be asymptomatic, but if symptoms related to AV dissociation are present, they are related to bradycardia, tachycardia, AV dyssynchrony, or loss of atrial "kick" and include the following:

Exertional dyspnea
Light-headedness
Throbbing sensation in neck
Palpitations
Fatigue, malaise

Physical

Physical findings are related to bradycardia, tachycardia, AV dyssynchrony, and lack of an atrial kick at least intermittently.

General appearance - Variable pulse or blood pressure due to the changing relationship between atrial and ventricular contractions
Pulse - Pulse volume is variable, with fast or slow rates depending on the underlying cause
Blood pressure - Low in ventricular tachycardia
Jugular venous pulse - Intermittent cannon a waves are noted when atria and ventricles contract simultaneously; a waves vary as PR interval varies or if the P wave is immediately followed by a QRS
Heart sounds
- Variable intensity of first heart sound
- Cyclic increase in intensity of first heart sound as PR interval shortens, climaxed by a very loud sound (bruit de cannon); occurs when ventricular rate exceeds atrial rate and QRS occurs just after P wave
Beat-to-beat variation in systolic murmurs

Causes

Major causes of AV dissociation include ventricular tachycardia, nonparoxysmal junctional tachycardia, escape junctional rhythm, and accelerated idioventricular rhythm.

Ventricular tachycardia
Nonparoxysmal junctional tachycardia
- Junctional rhythm/tachycardia occur at a rate faster than the sinus rate, without retrograde atrial capture.
- This is observed in clinical situations such as digoxin toxicity; sinus bradycardia with escape junctional rhythm; and after cardiac surgery, particularly valve surgery or replacement.
Long postectopic cycle allowing escape junctional rhythm

Differential Diagnoses

Atrioventricular Block

Workup

Laboratory Studies

Digoxin level

Other Tests

The electrocardiogram is the most commonly used modality to diagnose this problem. Findings show the underlying rhythm and P-wave morphology. In complete AV dissociation, P waves and QRS complexes have no fixed temporal relationship to each other. P-wave morphology depends on atrial activation.
The relationship between the atrial and ventricular rates is very important to understanding AV dissociation (see Images 1-2). The ventricular rate is the same or faster than the atrial rate.
Occasionally, other methods are required to assess atrial and ventricular activation, and the diagnostic approach to AV dissociation is given in Image 3.
Determining whether a P wave conducts can be difficult. To distinguish AV conduction from AV block, having the patient perform a maneuver to change the atrial and ventricular rate may help. While attached to a monitor, the patient can sit up or can perform some form of exercise.

Treatment

Medical Care

Treatment depends on the underlying condition and its severity. The important considerations and steps in the treatment of patients with AV dissociation include the hemodynamic status of the patient and recognition of the underlying pathology.

For patients who are hemodynamically unstable, i.e., patients with ventricular tachycardia, the initial treatment of choice is direct-current cardioversion or intravenous drug therapy, depending on the stability of the patient. Treatment of digoxin toxicity should also be pursued.
Ascertaining if AV conduction is intact is important in patients with AV dissociation due to an accelerated junctional rhythm following cardiac surgery. Rarely, patients have complete AV block with an accelerated focus distal to the level of block; when the accelerated focus becomes quiescent, heart block is present.

Surgical Care

A permanent pacemaker is rarely necessary.

Consultations

Patients with unexplained or uncorrected persistent symptomatic AV dissociation due to an escape rhythm or ventricular tachycardia may require referral to an electrophysiologist or a cardiologist.

Medication

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

Anticholinergic agents

Competitive inhibitor at autonomic, postganglionic, and cholinergic receptors.

Atropine Sulfate

Increases heart rate through vagolytic effects, causing increase in cardiac output.

Dosing

Adult

0.5-1.0 mg IV or ET q3-5min; not to exceed 3 mg total (0.04 mg/kg)

Pediatric

0.02 mg/kg/dose IV; minimum of 0.1 mg

Interactions

Other anticholinergics have additive effects; may increase pharmacologic effects of atenolol and digoxin; may decrease antipsychotic effects of phenothiazines; tricyclic antidepressants with anticholinergic activity may increase effects

Contraindications

Documented hypersensitivity; thyrotoxicosis; narrow-angle glaucoma; tachycardia

Precautions

Pregnancy

C - Safety for use during pregnancy has not been established.

Precautions

Avoid in Down syndrome and/or children with brain damage to prevent hyperreactive response; avoid in coronary heart disease, tachycardia, congestive heart failure, cardiac arrhythmias, and hypertension; caution in peritonitis, ulcerative colitis, hepatic disease, and hiatal hernia with reflux esophagitis; in patients with prostatic hypertrophy, prostatism is associated with dysuria and may require catheterization

Adrenergic agonist agents

Stimulate myocardial performance and improve coronary artery blood flow.

Isoproterenol (Isuprel, Isopro)

Has beta1- and beta2-adrenergic receptor activity. Binds beta-receptors of heart, smooth muscle of bronchi, skeletal muscle, vasculature, and alimentary tract. Has positive inotropic and chronotropic actions.

Dosing

Adult

Dilute 1 mL of 1:5000 solution (0.2 mg) with 10 mL saline solution or D5W for injection
Dose: 2-6 mcg/min IV (1-3 mL of diluted solution)
Alternatively, dilute 10 mL of 1:5000 solution (2 mg) in 500 mL of D5W or dilute 5 mL of 1:5000 solution (1 mg) in 250 mL of D5W and administer 5 mcg/min (1.25 mL/min of diluted solution) to achieve heart rate of 90-100 bpm

Pediatric

Not established

Interactions

Tricyclic antidepressants may potentiate pressor response of direct-acting vasopressors

Contraindications

Documented hypersensitivity; tachyarrhythmias, tachycardia, or heart block caused by digitalis intoxication; ventricular arrhythmias that require inotropic therapy; angina pectoris

Precautions

Pregnancy

C - Safety for use during pregnancy has not been established.

Precautions

May have a deleterious effect on ischemic or failing heart by increasing myocardial oxygen requirements while decreasing effective coronary perfusion; in some patients, presumably with organic disease of AV node and its branches, may paradoxically worsen heart block or precipitate Adams-Stokes attacks; caution in coronary disease, coronary insufficiency, diabetes, hyperthyroidism, and sensitivity to sympathomimetic amines; if heart rate exceeds 110 bpm, may be advisable to decrease infusion rate or temporarily discontinue infusion

Antidotes

Used to treat digitalis intoxication.

Digoxin immune Fab (Digibind)

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 that bind approximately 0.6 mg of digoxin or digitoxin. The dose of antibody depends on total body load (TBL) of digoxin; estimates of TBL can be calculated in 3 ways, (1) estimate of the quantity of digoxin ingested in the acute ingestion and assume 80% bioavailability (mg ingested X 0.8 = TBL); (2) obtain a serum digoxin concentration and, using a pharmacokinetics formula, incorporate the volume of distribution (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); and (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. Please see PDR for more complete information.

Dosing

Adult

Suggested: 10 and 5 vials IV for acute and chronic toxicity, respectively

Pediatric

Not established

Interactions

None reported

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

C - Safety for use during pregnancy has not been established.

Precautions

Caution in cardiac and renal failure; hypokalemia may occur following reversal of digoxin intoxication

Follow-up

Deterrence/Prevention

Close monitoring for medications that can cause AV dissociation
Correction of electrolyte imbalances

Prognosis

Depends on the underlying cardiac condition and effects of drug toxicities

Miscellaneous

Medicolegal Pitfalls

Failure to ensure that AV conduction is intact, particularly in patients with accelerated junctional rhythm following cardiac surgery
Failure to diagnose and correct digoxin toxicity if present

Multimedia

Media file 1: Atrioventricular (AV) dissociation. Ventricular tachycardia and complete AV dissociation. P waves are marked.

Media file 2: Atrioventricular (AV) dissociation. Complete AV block and no fixed relationship between P waves and QRS complexes.

Media file 3: Diagnostic algorithm for atrioventricular dissociation.

References

Braunwald E. Atrioventricular dissociation. In: Braunwald E, Zipes DP, Libby P, eds. Heart Diseases: A Textbook Of Cardiovascular Medicine. 6th ed. Philadelphia, Pa: WB Saunders Co;. 2001.
Duffield JS, Jacob AJ, Miller HC. Recurrent, life-threatening atrioventricular dissociation associated with toxoplasma myocarditis. Heart. Nov 1996;76(5):453-4. [Medline].
Luzza F, Oreto G. Pseudo-atrioventricular dissociation caused by interpolated ventricular extrasystoles in the presence of dual atrioventricular nodal pathway. Chest. May 1994;105(5):1587-9. [Medline].
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. Dec 1996;76(6):541-7. [Medline].
Pick A. A-V dissociation. A proposal for a comprehensive classification and consistent terminology. Am Heart J. Aug 1963;66:147-50. [Medline].
Wagner GS. Atrioventricular dissociation. In: Wagner GSS, Marriott HJ, eds. Marriott's Practical Electrocardiography. 9th ed. Baltimore, Md: Williams & Wilkins;. 1994.

Keywords

atrioventricular dissociation, AV dissociation, A-V dissociation, AV block, A-V block, heart block, complete heart block, bradycardia, tachycardia, AV dyssynchrony, ventricular tachycardia, nonparoxysmal junctional tachycardia, junctional tachycardia, escape junctional rhythm, accelerated idioventricular rhythm

Contributor Information and Disclosures

Author

Chirag M Sandesara, MD, Fellow, Department of Internal Medicine, Division of Cardiovascular Diseases, University of Iowa Hospitals and Clinics
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, and American Medical Association
Disclosure: Nothing to disclose.

Coauthor(s)

Brian Olshansky, MD, Professor of Medicine, Department of Internal Medicine, University of Iowa College of Medicine
Brian Olshansky, MD is a member of the following medical societies: American Autonomic Society, American College of Cardiology, American College of Chest Physicians, American College of Physicians, American College of Sports Medicine, American Federation for Clinical Research, American Heart Association, Cardiac Electrophysiology Society, Heart Rhythm Society, and New York Academy of Sciences
Disclosure: Guidant/Boston Scientific Honoraria Speaking and teaching; Medtronic Honoraria Speaking and teaching; Guidant/Boston Scientific Consulting fee Consulting; Reliant Grant/research funds Other; Novartis Honoraria Speaking and teaching; Novartis Consulting fee Consulting

Ram C Sharma, MD, MRCP, Assistant Professor of Medicine, Division of Cardiology, Department of Internal Medicine, University of Utah Health Science Center
Ram C Sharma, MD, MRCP is a member of the following medical societies: American College of Physicians and American Heart Association
Disclosure: Nothing to disclose.

Roger Freedman, MD, Director of Arrhythmia Service, Director of Electrophysiology Fellowship, 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, American College of Physicians, American Heart Association, Heart Rhythm Society, Phi Beta Kappa, and Sigma Xi
Disclosure: St. Jude Medical Grant/research funds Other; St. Jude Medical Consulting fee Consulting; St. Jude Medical Ownership interest Other; Boston Scientific Grant/research funds Other; Boston Scientific Consulting fee Consulting; Medtronic Grant/research funds Other; Medtronic Consulting; Sorin Consulting fee Consulting

Medical Editor

Alan D Forker, MD, Professor of Medicine, Program Director of Cardiovascular Fellowship, MidAmerica Heart Institute, University of Missouri at Kansas City School of Medicine; Director, Outpatient Lipid Diabetes Research Center, MidAmerica Heart Institute of Saint 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

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

Marschall S Runge, MD, PhD, Marion Covington Distinguished Professor of Medicine, Vice Dean for Clinical Affairs, Chairman, Department of Medicine, University of North Carolina at Chapel Hill School of Medicine
Marschall S Runge, MD, PhD is a member of the following medical societies: American Association for the Advancement of Science, American College of Cardiology, American College of Physicians-American Society of Internal Medicine, American Federation for Clinical Research, American Federation for Medical Research, American Heart Association, American Physiological Society, American Society for Clinical Investigation, American Society for Investigative Pathology, Association of American Physicians, Association of Professors of Cardiology, Association of Professors of Medicine, Southern Society for Clinical Investigation, and Texas Medical Association
Disclosure: Nothing to disclose.

CME Editor

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

Leonard Ganz, MD, Associate Professor of Medicine, Temple University School of Medicine; Cardiac Electrophysiologist, Children's Hospital of Pittsburgh, University of Pittsburgh Medical Cent, West Penn Hospital
Disclosure: Nothing to disclose.

Further Reading