Atrioventricular Dissociation: Types, Causes, Symptoms and Treatment

What is the Atrioventricular Dissociation?

It is a condition in which the atria and ventricles are activated independently.

It can occur when a secondary pacemaker in the AV node or ventricle reaches the sinus node (natural “pacemaker” of the heart) to start the impulse due to the deceleration of the sinus node.

It can also occur when the ventricle beats faster than the sinus node, as in ventricular tachycardia.


  • Complete atrioventricular dissociation: Complete atrioventricular dissociation occurs when the atria and ventricles are activated independently, and the atrial rate is slower or equal to the ventricular rate.
  • Incomplete atrioventricular dissociation: Incomplete atrioventricular dissociation occurs when there is intermittent atrial capture of the ventricles or intermittent ventricular capture of the atria.

During incomplete atrioventricular dissociation, some of the P waves conduct and capture the ventricles (i.e., atrioventricular dissociation of interference).

The atrioventricular dissociation of interference occurs when a well-synchronized P wave is conducted through a non-refractory AV conduction system.

The atrioventricular dissociation of interference is initiated by slowing down the sinus node due to sinus bradycardia or sinus arrest, which allows an independent secondary pacemaker at the junction (narrow QRS complex) or the ventricle (expansive QRS complex) to take over the ventricular activation.


In contrast, during isorhythmic atrioventricular dissociation, synchronized dissociation occurs when the atrial and ventricular frequencies are similar, demonstrating an apparent association between the two cardiac chambers.

Alternatively, the joint initiating event is the deceleration of the discharge velocity of the sinus node or the appearance of a slightly faster secondary pacemaker that controls the ventricles.

The rhythms of the joints can show an AV isorhythmic dissociation since P waves and QRS complexes seem to have a close relationship to each other; however, they are activated independently of each other.

With close observation of the rhythm, the P wave may be just before, inscribed within, or seen in the terminal portion of the QRS complex.

Ventricular tachycardia can occur without retrograde atrial activation (due to complete retrograde block) that causes atrioventricular dissociation because the atria and ventricles beat independently, and the atrial rate is slower than the ventricular rate.

An accelerated binding rate with a slower sinus node frequency may also be associated with atrioventricular dissociation and retrograde block.


The causes of atrioventricular dissociation are essential since they affect the treatment plan.

The escape of a secondary (latent) pacemaker into cardiac tissue can occur if the dominant pacemaker (the sinus node) decelerates considerably.

A secondary pacemaker at the AV junction or lower can be activated at a faster rate compared to the sinus node and, therefore, causes atrioventricular dissociation without retrograde atrial capture.

For example, sinus bradycardia, with a very slow sinus frequency, may allow the AV junction to become a secondary pacemaker and, therefore, be activated independently of the sinus node.

The atrioventricular dissociation does not involve AV block, but both AV block and atrioventricular dissociation can co-occur.

AV block is generally associated with a faster atrial rate than the ventricular rate. P waves, which represent atrial conduction, can not activate the ventricles in complete heart block.

In atrioventricular dissociation, a block is not necessarily present. If a P wave is correctly timed, it can lead to the ventricle in atrioventricular dissociation; This is called the capture rate.

The prevalence of atrioventricular dissociation is unknown. There is no racial preponderance or predilection for age, and men and women are equally affected.


Symptoms related to atrioventricular dissociation depend on the underlying heart rate of the patient, the presence of structural heart disease and comorbidities, and the frequency and persistence of atrioventricular dissociation.

Patients may experience fatigue, palpitations, or syncope. For example, the persistent rhythm of the AV junction after a slow-pathway ablation for the reentry of the AV node is often very symptomatic.

Sometimes, patients may present for a routine evaluation and, by the way, have an electrocardiogram that demonstrates an isorhythmic atrioventricular dissociation; this is most commonly seen in a population of younger patients and may be due to a high vagal tone at rest.

If the clinical context is adjusted, acute clinical insight is needed to recognize the possibility that another underlying problem causes atrioventricular dissociation.

Atrioventricular dissociation may be asymptomatic if it is of short duration. However, if there are symptoms related to atrioventricular dissociation, they are associated with bradycardia, tachycardia, dyssynchrony, and loss of atrial “kick” (i.e., loss of ventricular filling, atrial contraction). active) Moreover, include the following:

  • Dyspnea of ​​effort.
  • Daze.
  • Feeling of heartbeat in the neck.
  • Palpitations
  • Fatigue, general malaise.


Patients with atrioventricular dissociation treatment depend on their symptoms, the underlying condition, and the presence of hemodynamic instability.

For hemodynamically unstable patients with sinus bradycardia, atrial pacing may be necessary.

If the atrioventricular dissociation is due to a supraventricular or ventricular tachycardia, the completion of the tachycardia is required.

The treatment of digoxin toxicity should also be sought if indicated. The treatment of the underlying cause usually resolves the dissociation.

Medical care

The increase in atrial frequency with medications such as isoproterenol or atropine can be considered acutely. Occasionally, theophylline may be considered.

The goal is to increase sinus frequency and slow the AV binding rate for those with atrioventricular dissociation due to sinus node disease.

If there is an accelerated binding rate, the goal is to decrease the binding speed. Medications that can do this can also decrease sinus frequency (calcium channel blockers, beta-blockers, etc.).

Surgical intervention

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


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

Prevention and long-term monitoring

The prevention of atrioventricular dissociation is generally impossible except to eliminate any known trigger.

Routine monitoring of the outpatient clinic is required to prevent the recurrence of atrioventricular dissociation, mainly if an inciting cause was found and treated.

It is reasonable to consider a Holter or monitor of events in patients treated for atrioventricular dissociation and who may have ambulatory symptoms of stunning or presyncope.

Monitoring can reveal the recurrence of atrioventricular dissociation, affecting treatment decisions.