Atrioventricular (AV) block is a disturbance in conduction between the normal sinus impulse and the eventual ventricular response. The block is assigned to one of three classes, depending on the severity of the conduction disturbance. First-degree AV block is a simple prolongation of the PR interval, but all P waves are conducted to the ventricle. In second-degree AV block, some atrial impulses are not conducted into the ventricle. In third-degree AV block (or complete heart block), none of the atrial impulses is conducted into the ventricle (Fig. 25-1). Holter monitoring often reveals patterns not apparent in the relatively short electrocardiogram.
First-Degree Atrioventricular Block
Description. The PR interval is prolonged beyond the upper limits of normal for the patient’s age and heart rate (see Table 3-2 and Fig. 25-1). The PR interval includes the time required for depolarization of the atrial myocardium (PA interval), the delay of conduction in the AV node (AH interval), conduction through the bundle of His, and the time of onset of ventricular depolarization (HV interval).
Causes. First-degree AV block can appear in otherwise healthy children and young adults, particularly in athletes, mediated through excessive parasympathetic tone. Other causes include congenital heart diseases (CHDs) (e.g., endocardial cushion defect, atrial septal defect [ASD], Ebstein’s anomaly), infectious disease, inflammatory conditions (rheumatic fever), cardiac surgery, and certain drugs (e.g., digitalis, calcium channel blockers).
Significance. Slow intraatrial or AV nodal conjunction is almost always the mechanism for first-degree AV block. First-degree AV block does not produce hemodynamic disturbance. Exercise, both recreational and during stress testing, induces parasympathetic withdrawal, resulting in normalization of AV conduction and the PR interval. The PR interval can be very long, but in the absence of heart disease, it usually does not progress.
Management. No treatment is indicated except when the block is caused by drugs.
Second-Degree Atrioventricular Block
Some, but not all, P waves are followed by QRS complex (dropped beats). There are three types: Mobitz type I (Wenckebach phenomenon), Mobitz type II, and high-grade (or advanced) second-degree AV block.
Mobitz Type I (Wenckebach)
Description. The PR interval becomes progressively prolonged until one QRS complex is dropped completely (see Fig. 25-1).
Causes. Mobitz type I AV block appears in otherwise healthy children. Other causes include myocarditis, cardiomyopathy, myocardial infarction, congenital heart defect, cardiac surgery, and digitalis toxicity.
FIGURE 25-1 Atrioventricular (AV) block. (From Park MK, Guntheroth WG: How to Read Pediatric ECGs, 4th ed. Philadelphia, Mosby, 2006.)
Significance. The block is at the level of the AV node (with prolonged AH interval). It usually does not progress to complete heart block. It occurs in individuals with vagal dominance.
Management. The underlying causes are treated.
Mobitz Type II
Description. The AV conduction is “all or none.” AV conduction is either normal or completely blocked (see Fig. 25-1).
Causes. Causes are the same as for Mobitz type I.
Significance. The block usually occurs below the AV node (at the level of the bundle of His). It is more serious than type I block because it may progress to complete heart block, resulting in Stokes-Adams attack.
Management. The underlying causes are treated. Prophylactic pacemaker therapy may be indicated.
Two to One (or Higher) Atrioventricular Block
Description. A QRS complex follows every second, third, or fourth P wave, resulting in 2:1, 3:1, or 4:1 AV block (see Fig. 25-1). When two or more consecutive P waves are nonconducted, the rhythm is called advanced or high-grade second-degree AV block. In contrast to third-degree complete AV block, some P waves continue to be conducted to the ventricle, and the PR interval of conducted beats is constant.
Causes. Causes are similar to those of other second-degree AV blocks.
Significance. The block is usually at the bundle of His, alone or in combination with the AV nodal block. It may progress to complete heart block. Higher grade second-degree AV block should always be regarded as abnormal. The implications of high-grade AV block appear to be similar to those of complete AV block.
Management. The underlying causes are treated. Electrophysiologic studies may be necessary to determine the level of the block. Symptomatic second-degree AV block, although uncommon, can be acutely treated with atropine, isoproterenol, and temporary pacing. Pacemaker therapy is indicated for symptomatic advanced second-degree AV block.
Third-Degree Atrioventricular Block (Complete Heart Block)
In third-degree AV block, atrial and ventricular activities are entirely independent of each other (see Fig. 25-1).
1. The P waves are regular (regular PP interval), with a rate comparable to the normal heart rate for the patient’s age. The QRS complexes also are regular (regular R-R interval), with a rate much slower than the P rate.
2. In congenital complete heart block (and some acquired types), the duration of the QRS complex is normal because the pacemaker for the ventricular complex is at a level higher than the bifurcation of the bundle of His. The ventricular rate is faster (50–80 beats/min) than that in the acquired type, and the ventricular rate is somewhat variable in response to varying physiologic conditions.
3. In surgically induced (and in some acquired) complete heart block, the QRS duration is prolonged because the pacemaker for the ventricular complex is at a level below the bifurcation of the bundle of His. The ventricular rate is in the range of 40 to 50 beats/min (idioventricular rhythm), and the ventricular rate is relatively fixed.
Congenital type. In the absence of CHD, 60% to 90% of cases of congenital heart block are caused by neonatal lupus erythematosus. Maternal antibodies for autoimmune connective diseases cross the placenta to the fetus, causing the heart block. In 25% to 33%, it is associated with CHDs, most commonly with L-transposition of the great arteries, single ventricle, or polysplenia syndrome. Neonatal myocarditis and several genetic disorders such as familial ASD and Kearns-Sayre syndrome have been identified.
Acquired type. Cardiac surgery is the most common cause of acquired complete heart block in children. Other rare causes include severe myocarditis, Lyme carditis, acute rheumatic fever, mumps, diphtheria, cardiomyopathies, tumors in the conduction system, myocardial infarction, and overdoses of certain drugs. These causes produce either temporary or permanent heart block.
1. Complete heart block can be diagnosed by fetal bradycardia during fetal echocardiographic study between 18 and 28 weeks of gestation. Complications in utero may include hydrops fetalis, myocarditis, and fetal death.
2. Congestive heart failure (CHF) may develop in infancy, particularly when there are associated congenital heart defects.
3. About 40% of congenital heart blocks do not present until childhood (mean age, 5–6 years). Those who survive infancy are usually asymptomatic and achieve normal growth and development for 5 to 10 years. Presenting symptoms may include reduced exercise tolerance, presyncope, syncope, or slow pulse detected during routine examination. Chest radiography may show cardiomegaly (from large stroke volume needed to compensate for the slow heart rate).
4. Syncopal attacks (Stokes-Adams attacks) may occur with a heart rate below 40 to 45 beats/min. A sudden onset of acquired heart block may result in death unless treatment maintains the heart rate in the acceptable range.
1. When detected in utero, steroid therapy may be applied if associated with anti-Ro/SSA and anti-La/SSB.
2. Atropine or isoproterenol is indicated in symptomatic children and adults until temporary ventricular pacing is secured.
3. A temporary transvenous ventricular pacemaker is indicated in patients with heart block, or it may be given prophylactically in patients who might develop heart block.
FIGURE 25-2 Diagram of atrioventricular (AV) dissociation owing to either marked slowing of the sinus node or acceleration of the AV node. The fourth complex is conducted, changing the rhythm (called “interference”). All of the other complexes originate in the AV node, where there is higher automaticity than usual.
4. No treatment is required for children with asymptomatic congenital complete heart block with an acceptable rate, a narrow QRS complex, and normal ventricular function. Most of these patients ultimately require pacemaker placement.
5. Pacemaker therapy is indicated under the following situations:
a. If the patient is symptomatic or develops CHF. Dizziness or lightheadedness may be an early warning sign of the need for a pacemaker
b. If an infant has a ventricular rate below 50 to 55 beats/min or if the infant has a CHD with a ventricular rate below 70 beats/min
c. If the patient has a wide QRS escape rhythm, complex ventricular ectopy or ventricular dysfunction
6. A permanent artificial ventricular pacemaker is indicated in patients with surgically induced heart block that is not expected to resolve or persists at least 7 days after cardiac surgery.
7. A variety of problems may arise after a pacemaker is placed in children. Stress placed on the lead system by the linear growth of the child, fracture of the lead system in a physically active child, electrode malfunction (scarring of the myocardium around the electrode, especially in infants), and the limited life span of the pulse generator require follow-up of children with an artificial pacemaker.
Atrioventricular dissociation should not be confused with third-degree AV block. AV dissociation results from a marked slowing of the sinus node or atrial bradycardia or acceleration of the AV node. Whereas in AV dissociation, the atrial rate is slower than the ventricular rate, in complete heart block, the ventricular rate is usually slower than the atrial rate. In AV dissociation, an atrial impulse may conduct to the AV node if it comes at the right time (Fig. 25-2). The conducted beat can be recognized by its relative prematurity.