eMedicine Specialties > Cardiology > Arrhythmias

Atrioventricular Dissociation

Author: Chirag M Sandesara, MD, Fellow, Department of Internal Medicine, Division of Cardiovascular Diseases, University of Iowa Hospitals and Clinics
Coauthor(s): 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
Contributor Information and Disclosures

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

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