Atrioventricular (AV) block is partial or complete interruption of impulse transmission from the atria to the ventricles. The most common cause is idiopathic fibrosis and sclerosis of the conduction system. Diagnosis is by ECG; symptoms and treatment depend on degree of block, but treatment, when necessary, usually involves pacing.
AV block is caused by idiopathic fibrosis and sclerosis of the conduction system in about 50% of patients and by ischemic heart disease in 40%; the rest are due to drugs (eg, β-blockers, Ca channel blockers, digoxin, amiodarone); increased vagal tone; valvulopathy; or congenital heart, genetic, or other disorders.
First-degree AV block:
All normal P waves are followed by QRS complexes, but the PR interval is longer than normal (> 0.20 sec—see Fig. 6: Atrioventricular block.).
First-degree AV block may be physiologic in younger patients with high vagal tone and in well-trained athletes. First-degree AV block is rarely symptomatic and no treatment is required, but further investigation may be indicated when it accompanies another heart disorder or appears to be caused by drugs.
Second-degree AV block:
Some normal P waves are followed by QRS complexes, but some are not. Three types exist:
In Mobitz type I 2nd-degree AV block, the PR interval progressively lengthens with each beat until the atrial impulse is not conducted and the QRS complex is dropped (Wenckebach phenomenon); AV nodal conduction resumes with the next beat, and the sequence is repeated (see Fig. 7: Mobitz type I 2nd-degree atrioventricular block.).
Mobitz type I 2nd-degree AV block may be physiologic in younger and more athletic patients. The block occurs at the AV node in about 75% of patients with a narrow QRS complex and at infranodal sites (His bundle, bundle branches, or fascicles) in the rest. If the block becomes complete, a reliable junctional escape rhythm typically develops. Treatment is therefore unnecessary unless the block causes symptomatic bradycardia and transient or reversible causes have been excluded. Treatment is pacemaker insertion, which may also benefit asymptomatic patients with Mobitz type I 2nd-degree AV block at infranodal sites detected by electrophysiologic studies done for other reasons.
In Mobitz type II 2nd-degree AV block, the PR interval remains constant. Beats are intermittently nonconducted and QRS complexes dropped, usually in a repeating cycle of every 3rd (3:1 block) or 4th (4:1 block) P wave (see Fig. 8: Mobitz type II 2nd-degree atrioventricular block.).
Mobitz type II 2nd-degree AV block is always pathologic; the block occurs at the His bundle in 20% of patients and in the bundle branches in the rest. Patients may be asymptomatic or experience light-headedness, presyncope, and syncope, depending on the ratio of conducted to blocked beats. Patients are at risk of developing symptomatic high-grade or complete AV block, in which the escape rhythm is likely to be ventricular and thus too slow and unreliable to maintain systemic perfusion; therefore, a pacemaker is indicated.
In high-grade 2nd-degree AV block, every 2nd (or more) P wave is blocked (see Fig. 9: Second-degree atrioventricular block (high grade).).
The distinction between Mobitz type I and Mobitz type II block is difficult to make because 2 P waves are never conducted in a row. Risk of complete AV block is difficult to predict, and a pacemaker is indicated.
Patients with any form of 2nd-degree AV block and a structural heart disorder should be considered candidates for permanent pacing unless there is a transient or reversible cause.
Third-degree AV block:
Heart block is complete (see Fig. 10: Third-degree atrioventricular block.):
There is no electrical communication between the atria and ventricles and no relationship between P waves and QRS complexes (AV dissociation). Cardiac function is maintained by an escape junctional or ventricular pacemaker. Escape rhythms originating above the bifurcation of the His bundle produce narrow QRS complexes, relatively rapid (> 40 beats/min) and reliable heart rates, and mild symptoms (eg, fatigue, postural light-headedness, effort intolerance). Escape rhythms originating below the bifurcation produce wider QRS complexes, slower and unreliable heart rates, and more severe symptoms (eg, presyncope, syncope, heart failure). Signs include those of AV dissociation, such as cannon a waves, BP fluctuations, and changes in loudness of the 1st heart sound (S1). Risk of asystole-related syncope and sudden death is greater if low escape rhythms are present.
Most patients require a pacemaker (see Table 3: Pacemaker Codes). If the block is caused by antiarrhythmic drugs, stopping the drug may be effective, although temporary pacing may be needed. A block caused by acute inferior MI usually reflects AV nodal dysfunction and may respond to atropine or resolve spontaneously over several days. A block caused by anterior MI usually reflects extensive myocardial necrosis involving the His-Purkinje system and requires immediate transvenous pacemaker insertion with interim external pacing as necessary. Spontaneous resolution may occur but warrants evaluation of AV nodal and infranodal conduction (eg, electrophysiologic study, exercise testing, 24-h ECG).
Most patients with congenital 3rd-degree AV block have a junctional escape rhythm that maintains a reasonable rate, but they require a permanent pacemaker before they reach middle age. Less commonly, patients with congenital AV block have a slow escape rhythm and require a permanent pacemaker at a young age, perhaps even during infancy.
Last full review/revision July 2012 by L. Brent Mitchell, MD
Content last modified September 2013