Atrioventricular Dissociation

Etiology

The rate of discharge from the SA node may slowdown, giving subsidiary pacemakers along with the conduction system preference, leading to non-sinus rhythms and dissociation in the atria and ventricle. Causes of this may include:

• Sinus bradycardia
• High vagal tone
• Heart rate control medications, such as beta-adrenergic blockers and calcium channel blockers

Conversely, some insults lead to an accelerated rate of the subsidiary pacemakers, causing them to conduct preferentially. For instance:

• Myocardial ischemia
• High catecholamine state
• Digitalis toxicity

Various arrhythmias with disorganized conduction can lead to AV dissociation. Examples of which are:

• Wide complex ventricular tachycardia[1]
  • AV dissociation with capture and fusion beats are diagnostic characteristics of ventricular tachycardia. 
  • It stands as a prevalent cause of AV dissociation.
• Bundle branch reentrant ventricular tachycardia (BBRVT)[2]
  • It is a form of ventricular tachycardia that uses both bundle branches in its reentrant circuit. These circular circuits do not involve the atria, thus leading to an AV dissociation
• Junctional tachycardia
  • The AV node can become autonomous and exceed the sinus rate. Often in the setting of digoxin toxicity, cardiac surgery, or myocardial infarction.[3]

There is debate regarding the inclusion of a complete heart block in the definition of AV dissociation. Nevertheless, complete heart block causes significant AV dissociation as the impulses from the SA node do not conduct to the ventricles. A distinction has to be made, as very often, any case of AV dissociation is assumed as a complete heart block. However, though all cases of complete heart block include AV dissociation, not all cases of AV dissociation are complete heart block.

Epidemiology

AV dissociation occurs in 0.48% to 0.68% in all electrocardiogram (ECG) tracings. It is seen more often in elderly patients with comorbid degenerative cardiovascular disease. If included with the incidence of complete heart block, the incidence is higher.[4][5]

Pathophysiology

Three basic pathologic occurrences lead to atrioventricular dissociation in a patient. These include:

1. AV Dissociation by Default: This occurs due to the slowing of the dominant pacemaker, such as the SA node, leading to the dominance of an independent ventricular pacemaker. Demonstrated by junctional and escape rhythms. Often seen due to normal causality.
2. AV Dissociation by Usurpation: Acceleration of latent pacemakers in the ventricles, whose rates exceed the intrinsic atrial rates. Retrograde atrial capture will not be witnessed here. Often pathological as opposed to AV dissociation by default.[5]
3. Complete Heart Block: Conduction between the SA node and the ventricles is prevented due to a pathological blockade, leading to independent rhythms.[6]

Toxicokinetics

Digoxin, a negative chronotropic agent, slows the conduction in the atrioventricular node, which is used as an advantage in diseases such as atrial fibrillation. It also increases the automatically in cardiac tissue, creating the potential complication of AV dissociation if toxic dose levels occur. Normal digoxin levels are (0.8-2 ng/ml) with signs of toxicity arriving with levels of more than 2ng/ml. Digoxin is excreted mainly from the kidneys, thus associated renal failure can lead to a dangerous rise in digoxin levels.[7] Acute toxicity presents predominantly with nausea, vomiting along with cardiotoxicity.ECG findings of digoxin toxicity are as follows:

1. Downsloping ST depression with a characteristic “Salvador Dali sagging” appearance
2. Junctional AV nodal tachycardia
3. Ventricular tachycardia
4. Conduction block
5. Ventricualr bigeminy rhythm
6. AV dissociation[8]

Treatment of digitalis toxicity is via digoxin immune Fab.

Toxicities from rate control anti-hypertensives can also contribute to atrioventricular dissociation. Calcium channel blockers and beta-blockers can cause myocardial conduction deficits leading to AV dissociation. Clinical presentation is differentiated as patients overdose on calcium channel blockers as the patients are more alert despite severe bradycardia and hypotension, while beta-blocker overdose patients have altered mental status with respiratory depression. Treatment of either overdose is similar, with intravenous fluids, calcium chloride, glucagon, and atropine. Calcium chloride helps facilitate calcium back into myocardial tissue, competitively in cases of calcium channel blocker toxicity. Glucagon has an established role in the treatment of beta-blocker overdose.[9]

History and Physical

Clinical presentation of the patient may include dizziness, syncope, dyspnea, and chest pain; due to inadequate perfusion. The general physical examination can show abnormalities in vitals due to tachy- or bradyarrhythmias. Cardiovascular specific findings on physical examination may reveal variability in first heart sound intensity, large cannon 'a' waves, and paradoxical splitting of the second heart sound.[5][10]

Evaluation

 A thorough history needs to be ascertained, including:

• History of heart disease
• Symptoms of heart block
• Recent cardiac procedures
• Review of medications and dosing. Especially cardiogenic drugs such as,
  • Beta-blockers, calcium channel blockers, and other rate-limiting drugs
  • Amiodarone and other anti-arrhythmic drugs

A 12-lead ECG is required for diagnosis. The characteristic features of AV dissociation are:

• Dissociated P Waves: These appear as "P waves marching through the QRS complex." PR intervals might appear getting progressively shorter.
• Capture and Fusion Beats: Capture beats occur when an occasional atrial impulse reaches the ventricle when it is not refractory, leading to the capture of sinus rhythm. Fusion beats occur when a ventricular and supraventricular impulse simultaneously activates the ventricles. They fuse into a morphed ECG wave.

Based upon the presence or lack of capture beats, AV dissociation can be classified as incomplete or complete AV dissociation.

• Incomplete: An occasional capture of an atrial beat occurs. Irregular periods of RR intervals will be witnessed, interrupted by "capture beats." Two specific variants of incomplete AV dissociation are:
  • Interference AV Dissociation: This occurs when impulses from the slowing SA node or independent ventricular impulses collide due to retrograde conduction. Often seem in second-degree heart block.[10] Typically there will be evidence of progressively shortening PR intervals until the P wave "crosses over" the QRS. In a niche example, a dual AV nodal physiology presents with alternating shortening and lengthening of PR intervals (PR alternans). This indicates fast and slow conduction pathways for the ventricles which occur together.[11]
  • Isorhythmic AV Dissociation: A synchronized dissociation, while the atria and ventricles are beating independently of each other, they beat at the same rate. Thus, appearing as an association between the two chambers. This is often seen in junctional rhythms and might require a longer ECG strip for measurement.[12]
• Complete: The atria and ventricles are entirely independent of each other, giving no opportunity to capture beats. The atrial rate is often slower or equal to the ventricular rate. The PP and the RR intervals remain constant, but the PR interval varies.

Importantly, the lack of conduction of the P waves is mainly due to the timing of the P waves in relation to the QRS complex, as P waves arriving during the refractory phase of the ventricles will not be conducted. Rather than an affirmative presence of complete AV block. Current revisions of the nomenclature now recommend the classification to change to AV dissociation with or without capture beats. After confirming the presence of AV dissociation, the next step is to compare the atrial and ventricular rates to identify the presence of a complete heart block.[13]

• Atrial rate more than ventricular rate: Diagnostic of complete heart block
• Ventricular rate more than atrial rate: rules out complete heart block

Moreover, the diagnosis of a complete heart block should not be made unless the ventricular rate is less than 40 beats per minute.[14] Further evaluation of reversible causes of heart block should be enacted. Lyme carditis, especially for patients in endemic areas. 49% of patients with Lyme carditis are prone to develop third-degree heart block, especially those with a P-R interval of ≥300 ms.[15] These patients should be evaluated by a skin examination for an erythematous macular rash with central clearing, along with serological testing. Hyperkalemia is also a potential cause. Potassium levels of more than 7mmol/L can lead to AV conduction disturbances. Electrolytes should be drawn, and ECG should be observed for hyperkalemic changes, though the correlation between ECG changes and potassium levels is poor.[16] Other causes may include hypothyroidism and viral myocarditis. Investigations into reversible causes of heart block are crucial for treatment as a pacemaker cannot be placed until such causes have been ruled out.

Treatment / Management

Treatment of the underlying cause often resolves the atrioventricular dissociation. If the AV dissociation is a consequence of supraventricular or ventricular tachycardias, termination of the arrhythmia is warranted. Careful consideration should be taken in junctional arrhythmias as terminating it would also eliminate the sole source of conduction. Digitalis toxicity can be treated with a combination of digoxin immune Fab. Medications such as isoproterenol and atropine can be considered to increase the SA nodal rate. In the case of a complete heart block, atropine will be ineffective in increasing the heart rate, as it works on the AV node. Reversible causes of heart block should be treated. Lyme carditis is self-limiting; however, antibiotics can shorten the disease course.[17] (B3)

Potassium replacement therapy, including the use of beta 2 agonist agents and insulin, along with calcium gluconate for cardiac protection, should be undertaken if there are ECG and laboratory evidence of hyperkalemia induced complete heart block. Once reversible causes are ruled out, complete heart block patients require pacemaker placement. A transcutaneous pacemaker is the fastest way to ensure cardiac pacing. If this is not successful in achieving electric and mechanical capture, a transvenous pacemaker should be considered.[18] There are three choices of permanent pacemakers:

1. Single chamber pacemakers, a single lead in either the right atrium or ventricle.
2. Dual chambered pacemaker, with two leads implanted in right atrium and ventricle.
3. Biventricular pacemaker, similar to the dual chamber but with an additional lead advancing into the coronary sinus for left ventricular epicardial pacing.

Among these three, the dual-chambered pacemaker is the most common and effective in cases of AV block. Though recent studies now indicate the superiority of biventricular pacemakers to reduce future incidence of heart failure from pacing.[19]

Differential Diagnosis

Atrioventricular dissociation could mimic a few other disorders leading to tachycardia, so it is crucial for health care providers to know the other disorders which could present in a similar fashion. The following are some important differential diagnoses of AV dissociation:

1. High-grade Atrio-ventricular block 
2. Atrioventricular nodal re-entrant tachycardia
3. Supraventricular tachycardia with aberrancy 
4. Orthodromic tachycardia

Prognosis

Atrioventricular dissociation is usually transient unless it includes a complete heart block in its definition.[5] The prognosis of AV dissociation is dependent on the cause of the insult, rather than the effect of the AV dissociation itself. Often with the elimination of the causative insult, there is a complete recovery in patients.

Complications

Atrioventricular dissociation related complications arise from the associated hemodynamic compromise. Often from its causative insult, namely severe sinus bradycardia and ventricular tachycardia. Syncope is by far the most common complication. Further untreated effects of hypoperfusion can lead to severe complications such as acute renal failure (due to renal artery hypoperfusion) or myocardial ischemia.