Atrioventricular Dissociation 

Updated: Nov 16, 2017
Author: Chirag M Sandesara, MD, FACC, FHRS; Chief Editor: Jose M Dizon, MD 

Overview

Background

Atrioventricular (AV) dissociation is a condition whereby the atria and the ventricles activate independently of each other. The normal activation—sinus node followed by the atria, AV node, and then the His-Purkinje system causing ventricular activation—is no longer observed. AV dissociation may occur when a subsidiary pacemaker in the AV node or the ventricle overtakes the sinus node for impulse initiation due to slowing of the sinus node, or it may occur when a subsidiary site (ie, the ventricle) beats faster than the sinus node, such as in ventricular tachycardia. The causes of AV dissociation are important to understand as they impact the treatment plan.

The escape of a subsidiary (latent) pacemaker in cardiac tissue may occur if the dominant pacemaker (the sinus node) slows considerably. A subsidiary pacemaker in the AV junction or below may activate at a faster rate compared to the sinus node and thereby cause AV dissociation without retrograde atrial capture.[1, 2, 3]  For example, sinus bradycardia, with a very slow sinus rate, may allow the AV junction to become a subsidiary pacemaker and thus activate independently from the sinus node (see the image below). AV dissociation does not imply AV block, but both AV block and AV dissociation can occur concurrently.[4]

Significant slowing of the sinus node allows for a Significant slowing of the sinus node allows for a subsidiary pacemaker (atrioventricular [AV] junction) to activate, causing AV dissociation.

In general, AV block is associated with a faster atrial rate than ventricular rate. The P waves, representing atrial conduction, cannot activate the ventricles in complete heart block. In AV dissociation, a block is not necessarily present. If a P wave is properly timed, it may conduct to the ventricle in AV dissociation; this is termed a capture beat. Heart block, which may occur with AV dissociation, is discussed in detail in the Medscape Drugs & Diseases article Atrioventricular Block.

The prevalence of AV dissociation is unknown. No racial preponderance or age predilection exists, and men and women are equally affected.

Types of AV dissociation

There are two types of AV dissociation, complete and incomplete.

Complete AV dissociation

Complete AV dissociation occurs when the atria and the ventricles activate independently from one another and the atrial rate is slower or equal to the ventricular rate. The fact that none of the P waves conduct has more to do with the timing of the P waves in relation to the QRS complex rather than the presence of AV block.[5]

Incomplete AV dissociation

Incomplete AV dissociation occurs when there is either intermittent atrial capture from  the ventricles or intermittent ventricular capture from the atria. During incomplete AV dissociation, some of the P waves conduct and capture the ventricles (ie, interference AV dissociation, see the image below). 

Interference AV dissociation occurs when a well-timed P wave conducts via a nonrefractory AV conduction system. Interference AV dissociation is initiated by slowing of the sinus node due to sinus bradycardia or sinus arrest, thereby allowing an independent subsidiary pacemaker in the junction (narrow QRS complex) or the ventricle (wide QRS complex) to take over ventricular activation.[6]

This rhythm strip reveals interference atrioventri This rhythm strip reveals interference atrioventricular dissociation, as there is a P wave conducting to the ventricle in the third and seventh beats, whereas the P wave fails to conduct to the ventricle in the other beats.

In contrast, during isorhythmic AV dissociation, a synchronized dissociation occurs when the atrial and ventricular rates are similar, demonstrating an apparent association of the two cardiac chambers.[7]  Either slowing of the sinus node discharge rate or the emergence of a slightly faster subsidiary pacemaker controlling the ventricles is the common initiating event. Junctional rhythms may show isorhythmic AV dissociation as the P waves and QRS complexes appear to have a close relationship to one another; however, they are actually activating independently from one another. With close observation of the rhythm strip, the P wave may be either just prior, inscribed within, or seen in the terminal portion of the QRS complex (see the image below). 

Isorhythmic AV dissociation. There is AV dissociat Isorhythmic AV dissociation. There is AV dissociation with independent atrial and ventricular conduction at similar rates.

Ventricular tachycardia may occur without retrograde atrial activation (due to complete retrograde block) causing AV dissociation, because the atria and ventricles beat independently and the atrial rate is slower than the ventricular rate. An accelerated junctional rhythm with a slower sinus node rate may also be associated with AV dissociation and retrograde block. 

Pathophysiology

The cause of atrioventricular (AV) dissociation is due to an increased rate of a subsidiary (escape) pacemaker and/or a decreased rate of the sinus node. The use of certain medications including beta-blockers, digitalis, and calcium channel blockers may lead to slowing of the sinus node and cause a subsidiary pacemaker to activate in the ventricle or AV junction.[8] Vagal activation (eg, neurocardiogenic syncope, vomiting) may cause this as well. AV dissociation can also be seen after radiofrequency ablation of the slow pathway responsible for AV nodal reentry tachycardia, leading to acceleration of an AV junctional activation that is faster than the sinus node activation. After exertion, if AV dissociation is present from an escape pacemaker, it can be a normal phenomenon.  

Accelerated activation of the subsidiary pacemaker can occur during surgical and anesthesia interventions (including intubation), conditions that increase catecholamine levels (including vasoconstrictor infusions of inotropes), myocardial infarction, structural heart disease, hyperkalemia, ventricular tachycardia, or ventricular pacing.

Etiology

Major causes of atrioventricular (AV) dissociation include high vagal tone, sinus bradycardia, ventricular tachycardia, nonparoxysmal junctional tachycardia, junctional escape rhythm, and an accelerated idioventricular rhythm.[9, 10, 11, 12, 13]

In nonparoxysmal junctional tachycardia, junctional rhythm/tachycardia occurs 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 aortic valve surgery or replacement due to its close anatomic approximation to the AV node and His-Purkinje system.[14]

Long postectopic cycles allow an escape junctional rhythm as well. A normal sinus beat followed by a premature ventricular beat resets the sinus node timing cycle. Occasionally, especially in sinus node disease, the sinus impulse takes longer to activate than usual and a junctional escape beat or rhythm may follow, and this may lead to AV dissociation as the sinus node activates much slower than the junctional escape rhythm.

Prognosis

The prognosis is generally good, but it may depend on the severity of the underlying problem causing the AV dissociation. Although benign, it may indicate serious underlying cardiovascular issues (eg, ischemia, digoxin toxicity). For conditions in which AV dissociation may be iatrogenic (ie, high doses of beta-blockers, calcium channel blockers, or digitalis in the setting of renal failure), the prognosis is excellent, as removal of the cause eliminates the problem. Occasionally, AV dissociation can affect hemodynamics and cause a reduction in cardiac output or blood pressure, but once treated the prognosis is excellent.

Mobidity/mortality

AV dissociation is generally benign. Any adverse effects are related to the ensuing bradycardia, AV dyssynchrony, or underlying conditions.

Complications

Complications of AV dissociation are generally due to hemodynamic compromise due to the processes that cause AV dissociation (eg, ventricular tachycardia, severe sinus bradycardia). The low blood pressure and very fast or very slow heart rate may lead to traumatic syncope. Hypoperfusion of end organs due to brady or tachyarrhythmias is possible. Acute renal failure from a reduction in renal blood flow due to a low cardiac output is commonly seen in severe bradycardia and AV dissociation. Ischemia or myocardial infarction could occur in cases in which the tachyarrhythmia or bradyarrhythmia coupled with AV dissociation may lead to reduced coronary artery perfusion. These clinical situations may require immediate resuscitative efforts to establish both normal a blood pressure and heart rate to allow adequate end-organ perfusion.

Patient Education

AV dissociation should be discussed with a patient who is symptomatic to identify the underlying cause(s) and discuss methods to prevent the problem. Patients with marked sinus bradycardia and AV dissociation may need a pacemaker. Patients with a history of AV dissociation requiring treatment or withdrawal of an offending drug (ie, medication induced) must be informed of the condition that led to AV dissociation (ie, digitalis use in renal failure or high dose beta blocker use to treat hypertension), be aware of the consequences if no changes in medications are made (recurrent dizziness, syncope, trauma) and must inform their health care providers to avoid such medications to prevent it from recurring. Patients must be also be counselled on the effects of deleterious drug-drug interactions (ie, taking clonidine for hypertension and a concomitant beta blocker for atrial fibrillation) to avoid initiation of AV dissociation.

 

Presentation

History

Symptoms related to atrioventricular (AV) dissociation depend on the patient's underlying heart rate, the presence of structural heart disease and/or comorbidities, and the frequency and persistence of AV dissociation. Patients may present with fatigue, palpitations, or syncope. For example, persistent AV junctional rhythm, after a slow pathway ablation for AV node reentry is often highly symptomatic.

Sometimes, patients may present for a routine evaluation and incidentally have an electrocardiogram demonstrate isorhythmic AV dissociation; this is more commonly noted in a younger patient population and may be due to a high resting vagal tone. An acute clinical acumen is needed to recognize the possibility of AV dissociation being caused by another underlying problem if the clinical context fits.

AV dissociation may be asymptomatic if it is short lived, but if symptoms related to AV dissociation are present, they are related to bradycardia, tachycardia, AV dyssynchrony, and/or loss of atrial "kick" (ie, loss of increased ventricular filling from active atrial contraction) and include the following:

  • Exertional dyspnea
  • Lightheadedness
  • Throbbing sensation in neck
  • Palpitations
  • Fatigue, malaise

Physical Examination

Evaluation of the patient's vital signs to assess for hemodynamic stability is the first step in the physical examination. It is important to note the heart rate and the blood pressure as significantly high, or low readings may lead to hemodynamic compromise and urgent attention to treatment may be necessary. However, the vital sign findings will not diagnose the cause of the atrioventricular (AV) dissociation.

Careful assessment of the pulse pressure, which can be variable due to the relationship of the atria and ventricles, carotid upstroke, and identifying cannon “A” waves (simultaneous and/or variable contraction of the atrium and ventricle) are useful in trying to identify the etiology of the arrhythmia. There may be variability in the intensity of the first heart sound, paradoxical splitting of the second heart sound, irregularity of the pulse due to ventricular or junctional escape complexes, and beat-to-beat variation in systolic murmur.

 

DDx

Diagnostic Considerations

It is important to determine if atrioventricular (AV) conduction is intact, particularly in patients with an accelerated junctional rhythm following cardiac surgery—this may indicate significant AV  conduction disease. 

Proper review of the patient's medication list is essential in determining the cause as well. High digoxin levels can be associated with AV dissociation. It is equally as important to treat other medical causes that may have led to AV dissociation, such as correction of potassium levels (if too high or low) or urgent treatment of renal failure for the same reasons.

If isorhythmic AV dissociation is difficult to differentiate from sinus rhythm, increasing the sinus rate with apre position change or walking may help make the diagnosis.

Important considerations in the differential diagnosis

It is important to differentiate AV dissociation from AV block and from blocked premature atrial complexes. Blocked premature atrial contractions may appear to resemble AV dissociation but in AV block and in AV dissociation the atrial rate is constant (except if AV dissociation is due to ventricular tachycardia and there is intermittent retrograde conduction). 

Conditions to consider in the differential diagnosis of AV dissociation are ventricular tachycardia and any supraventricular tachycardia that includes nonparoxysmal or paroxysmal junctional tachycardia with complete or intermittent retrograde block.[15, 16, 17]  

Bundle branch reentry ventricular tachycardia is associated with AV dissociation, as the reentrant circuit usually requires antegrade conduction via the right bundle branch and retrograde conduction via the left bundle branch. The atria are not part of the reentry circuit. 

AV dissociation is rare in supraventricular tachycardias. AV nodal reentry tachycardia or even orthodromic tachycardia associated with a nodofasicular or nodoventricular bypass tract may demonstrate AV dissociation. If AV dissociation occurs, it is transient because the atria may not necessarily be part of the reentry circuit.

Differential Diagnoses

 

Workup

Approach Considerations

The standard workup of the patient presenting with atrioventricular (AV) dissociation includes taking a thorough history and performing a physical examination in addition to reviewing pertinent laboratory data, reviewing electrocardiograms/rhythm strips, and longer term monitoring. To help determine if AV dissociation or AV block is present when there is isorhythmic activation, changing patient positions and physical activity can help.

No specific radiologic imaging studies are needed for AV dissociation.

 

Laboratory Studies

There is no specific laboratory evaluation for atrioventricular dissociation, but in select cases, obtaining the following studies may be useful to consider if clinically indicated:

  • Serum potassium levels
  • Serum creatinine levels
  • Digoxin levels
  • Troponin levels, if recent or current ischemia
  • Thyroid stimulating hormone level [18]

Electrocardiography

An electrocardiogram (ECG), prolonged rhythm strips, and Holter or event recorder monitoring are the most commonly used modalities to diagnose atrioventricular (AV) dissociation.

Please refer to the following ECG images of interference and isorhythmic AV dissociation along with sinus bradycardia with junctional escape rhythm. See Background for more details.

Significant slowing of the sinus node allows for a Significant slowing of the sinus node allows for a subsidiary pacemaker (atrioventricular [AV] junction) to activate, causing AV dissociation.
This rhythm strip reveals interference atrioventri This rhythm strip reveals interference atrioventricular dissociation, as there is a P wave conducting to the ventricle in the third and seventh beats, whereas the P wave fails to conduct to the ventricle in the other beats.
Isorhythmic AV dissociation. There is AV dissociat Isorhythmic AV dissociation. There is AV dissociation with independent atrial and ventricular conduction at similar rates.
 

Treatment

Approach Considerations

Treatment of patients with atrioventricular (AV) dissociation depends on their symptoms, the underlying condition, and the presence of hemodynamic instability.  For patients who are hemodynamically unstable with sinus bradycardia, atrial pacing may be needed. If AV dissociation is due to supraventricular or ventricular tachycardia, termination of the tachycardia is required. Treatment of digoxin toxicity should also be pursued if indicated. Treatment of the underlying cause generally resolves the dissociation.

Medical care

Increasing the atrial rate with medications such as isoproterenol or atropine may be considered acutely. Occasionally, theophylline can be considered. The goal is to increase the sinus rate and slow the AV junctional rate for those who have AV dissociation due to sinus node disease. If there is an accelerated junctional rhythm, the goal is to slow the junctional rate. Drugs that can do this can also slow the sinus rate (calcium channel blockers, beta blockers, etc). 

Surgical intervention

A permanent pacemaker is necessary for severe symptomatic sinus bradycardia. Ablation of a junctional or ventricular tachycardia is required if this is the cause of the problem.

Consultations

Patients with unexplained or uncorrected persistent symptomatic AV dissociation due to an escape rhythm or ventricular tachycardia should be referred to an electrophysiologist or a cardiologist.

Prevention and long-term monitoring

Preventing AV dissociation is generally not possible except to eliminate any known triggers.

Routine outpatient clinic follow-up is required to prevent recurrence of AV dissociation, especially if an inciting cause was found and treated. It is reasonable to consider a Holter or event monitor in patients who were treated for AV dissociation and who may have ambulatory symptoms of lightheadedness or presyncope. Monitoring may uncover recurrence of AV dissociation, and this may affect treatment decisions.

 

Medication

Medication Summary

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

Anticholinergic agents

Class Summary

Competitive inhibitor at autonomic, postganglionic, and cholinergic receptors.

Atropine IV/IM

Atropine is a competitive inhibitor at autonomic, postganglionic, and cholinergic receptors. It may be administered in patients in whom a very slow sinus node activation is seen with a junctional escape rhythm.

Inotropic Agents

Class Summary

Inotropic agents are used to increase the force of cardiac contractions. Intravenous positive inotropic agents should only be used in inpatient settings—and then only in patients who manifest signs and symptoms of low cardiac output syndrome (volume overload with evidence of organ hypoperfusion).

Dopamine (Intropin)

Dopamine is an inotrope and may increase renal blood flow, cardiac output, and heart rate. At a low dose (2-10 mcg/kg/min) it has primarily beta1 properties and increases the heart rate, but at doses above 10 mcg/kg/min, it has inotropic properties.

This agent may be used when severe sinus bradycardia leads to a junctional escape rhythm causing AV dissociation and thereby help restore 1:1 AV conduction by increasing the sinus rate. Dopamine should be used with caution, as it may cause an increased risk for the development of junctional or ventricular tachycardia in certain situations. 

Adrenergic agonist agents

Class Summary

Stimulate myocardial performance and improve coronary artery blood flow.

Isoproterenol (Isuprel, Isopro)

Isoproterenol is a beta1/beta2 agonist; it may increase the sinus node rate in cases of severe bradycardia to treat AV dissociation caused by the initiation of a subsidiary pacemaker in the AV junction. The sinus node rate increases and would prevent the junctional pacemaker from initiating. However, similar to dopamine, isoproterenol must be used with caution, as junctional or ventricular tachycardia may occur. 

Antidotes

Class Summary

Used to treat digitalis intoxication.

Digoxin immune Fab (Digibind)

Digoxin immune Fab is an 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 the total body load (TBL) of digoxin; estimates of TBL can be calculated in three ways: (1) estimating the quantity of digoxin ingested in the acute ingestion and assume 80% bioavailability (mg ingested × 0.8 = TBL); (2) obtaining 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] × 6 L/kg × body weight in kg); and (3) using an empiric dose based on average requirements for an acute or chronic overdose in an adult or child.