The term atrioventricular (AV) dissociation describes a family of arrhythmias where independent pacemakers control the atria and ventricles. The standard activation of the cardiac circuits works in the order of impulse transmission from the sinoatrial (SA) node to the atria, the AV node, and ventricular activation via the His-Purkinje system.
Disruption in this pathway leads to a dissociation between the conduction rates of the atria and ventricle. The severity of this event varies, from benign in cases of isorhythmic AV dissociation to complete heart block, which in cases might be fatal if not treated with a permanent pacemaker. Another important cause of this condition is ventricular tachycardia, which is lethal if not recognized or treated appropriately.
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:
Conversely, some insults lead to an accelerated rate of the subsidiary pacemakers, causing them to conduct preferentially. For instance:
Various arrhythmias with disorganized conduction can lead to AV dissociation. Examples of which are:
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.
Three basic pathologic occurrences lead to atrioventricular dissociation in a patient. These include:
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. Acute toxicity presents predominantly with nausea, vomiting along with cardiotoxicity.
ECG findings of digoxin toxicity are as follows:
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.
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.
A thorough history needs to be ascertained, including:
A 12-lead ECG is required for diagnosis. The characteristic features of AV dissociation are:
Based upon the presence or lack of capture beats, AV dissociation can be classified as incomplete or complete AV dissociation.
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.
Moreover, the diagnosis of a complete heart block should not be made unless the ventricular rate is less than 40 beats per minute. 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. 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. 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 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.
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. There are three choices of permanent pacemakers:
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.
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:
Atrioventricular dissociation is usually transient unless it includes a complete heart block in its definition. 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.
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.
Symptomatic patients need to be educated about the details of AV dissociation, inclusive of its etiology and impact on everyday life. Offending agents should be discontinued, and medications reviewed. The review should include warnings on dosages, for example, digoxin dosages in patients with renal failure. Drug interactions should also be counseled.
Patients with pronounced bradycardia and AV dissociation will benefit form pacemakers.
The patient should receive education upon the risk of the procedure. Furthermore, they should be informed about regular checkups for lead function and threshold and battery evaluations. They should be warned about electromagnetic interference and imaging abnormalities and caution during future evaluations.
Atrioventricular dissociation poses a diagnostic dilemma. Patients may present with non-specific signs and symptoms or, at times, even be asymptomatic. Moreover, the ECG diagnosis of AV dissociation is easy to be misread and challenging to differentiate from other confounders. The initial diagnosis and management of the patient often begin with an emergency department physician, hospitalist, or intensivist. Stabilization of a patient with hemodynamic collapse or severe sinus bradycardia requires close coordination between the nursing staff and ancillary health care workers for executing the algorithms of advanced cardiac life support. They are also necessary for the possible transport of the patient to a critical care facility if they are not in one already. The crucial nursing staff will monitor the patient’s vital signs and telemetry while also coordinating with the patient and the family with the education of the disease.
The pharmacist who will be in close communication with the nurses will ensure the patient is on the right medication, check for drug-drug interaction [Level 5] and recommend dosage adjustments based on changing the clinical setting and comorbid conditions of the patient.
The primary care team will coordinate with consulting physicians, as a cardiologist is required for an advanced ECG reading and care of the patient. An electro-physicist may be needed for the placement of a temporary pacemaker in cases of complete heart block. An interventional cardiologist might be necessary as myocardial ischemia can present with dissociation. He might be required for the placement of a permeant pacemaker as well.
Although the outcomes of AV dissociation is dependent on the cause, an interprofessional team approach, including physicians, consulting physicians, specialty-trained nurses, and pharmacists are required for optimal patient outcomes.
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