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Atrioventricular block: causes, symptoms, diagnosis, treatment

 
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Last reviewed: 07.07.2025
 
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Atrioventricular block is a partial or complete cessation of impulse conduction from the atria to the ventricles. The most common cause is idiopathic fibrosis and sclerosis of the conduction system. The pathology is diagnosed based on ECG data. Symptoms and treatment depend on the degree of blockade, but therapy, if necessary, usually includes the use of a pacemaker.

AV block is a consequence of idiopathic fibrosis and sclerosis of the conduction system in approximately 50% of patients, and in 40% - a result of coronary heart disease. The remaining cases are due to the use of drugs (for example, beta-blockers, calcium channel blockers, digoxin, amiodarone), increased vagal tone, valvulopathy, congenital pathology, genetic and other anomalies.

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Atrioventricular block 1st degree

All normal waves are accompanied by RR complexes, but PR intervals are longer than normal (> 0.2 s). First-degree AV block may be physiological in young patients with excessive vagal influence and in well-trained athletes. First-degree AV block is always asymptomatic and does not require treatment, however, if it is combined with other cardiac pathology, further examination of the patient is indicated, since it may be associated with the use of drugs.

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Atrioventricular block II degree

Some normal waves are accompanied by ventricular complexes, but some are not. There are three types of this pathology.

In Mobitz type I second-degree atrioventricular block, there is a progressive prolongation of the PR interval after each beat until atrial impulse conduction ceases altogether and the complex drops out (Wenckebach phenomenon). Conduction through the AV node is restored by the next beat, and the situation is repeated. Mobitz type I second-degree atrioventricular block may be physiological in young patients and many athletes. The block occurs in the AV junction in 75% of individuals with narrow QRS complexes and in lower-lying areas (His bundle, bundle branches, Purkinje fibers) in the remainder. If the block becomes complete, an escape junctional rhythm usually develops. There is no need for treatment until the block leads to bradycardia with clinical symptoms. It is also necessary to exclude temporary or correctable causes. Treatment involves pacemaker implantation, which may also be successful in asymptomatic patients with Mobitz type I second-degree atrioventricular block at the subnodal level detected during an electrophysiological study performed for another reason.

In Mobitz type II second-degree atrioventricular block, the PR interval is equal. Impulses are not conducted immediately, and the QRS complex drops out, usually with repeating cycles of the wave - every third cycle (1:3 block) or fourth (1:4 block). Mobitz type II second-degree atrioventricular block is always pathological. In 20% of patients, it occurs at the level of the His bundle, in the branches of this bundle - in the rest. Patients may have no clinical manifestations or experience mild dizziness, presyncope and syncope, depending on the ratio of conducted and unconducted impulses. Patients are at risk of developing high-degree clinical block or complete block, in which the escape rhythm is probably ventricular, and therefore rare and unable to provide systemic blood supply. Therefore, IVR is indicated.

High-grade second-degree block is characterized by the loss of every second or more ventricular complex. It can be difficult to distinguish between Mobitz I and Mobitz II block, since the two teeth never appear on the isoline. The risk of developing complete atrioventricular block is difficult to predict, so IVR is prescribed.

Patients with any type of second-degree atrioventricular block who have structural heart disease should be considered candidates for permanent pacing, except for transient and reversible causes.

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Atrioventricular block III degree

Atrioventricular block can be complete: there is no electrical connection between the atria and ventricles and, accordingly, no connection between the QRS waves and complexes (AV dissociation). Cardiac activity is maintained by escaping pacemaker impulses from the AV node or ventricle. The rhythm formed above the bifurcation of the His bundle produces narrow ventricular complexes of relatively high frequency (>40 per minute), a relatively significant heart rate and few symptoms (eg, weakness, postural dizziness, exercise intolerance). The rhythm formed below the bifurcation produces wide QRS complexes, a low heart rate and more severe clinical manifestations (presyncope and syncope, heart failure). Symptoms include signs of AV dissociation, such as cannon a-waves, variability of blood pressure and changes in the sonority of the first heart sound. The risk of syncope due to asystole, as well as sudden death, is higher when the pacemaker's impulse generation is insufficient.

Most patients require IVS. If the block is due to antiarrhythmic drugs, drug withdrawal may be effective, although temporary pacing is sometimes necessary. Block due to acute inferior MI usually shows signs of AV nodal dysfunction that are responsive to atropine or may resolve spontaneously within a few days. Block due to anterior MI usually indicates extensive necrosis involving the His-Purkinje system and requires immediate transvenous pacemaker placement with temporary external pacing if needed. Spontaneous resolution is possible, but AV node and downstream structures should be evaluated (eg, electrophysiology study, exercise testing, 24-hour ECG monitoring).

Most patients with congenital third-degree atrioventricular block have a nodal escape rhythm that maintains a reasonably adequate rhythm, but they require implantation of a permanent pacemaker before reaching middle age. Less commonly, patients with congenital third-degree atrioventricular block have a rare escape rhythm, which necessitates pacemaker implantation in childhood, perhaps even in early childhood.

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