Pediatric Third-Degree Acquired Atrioventricular Block Treatment & Management

  • Author: Charles I Berul, MD; more...
 
Updated: Sep 30, 2011
 

Approach Considerations

Treatment is focused on restoring atrioventricular (AV) sequential activation and/or maintaining a heart rate tolerated by the patient, which is assessed by the absence of symptoms.[26]

Asymptomatic patients require no immediate pacemaker treatment, although these individuals should be closely monitored. If the escape rhythm slows, they may become symptomatic and require permanent pacemaker therapy. Indications for permanent pacing are outlined in detail in the ACC/AHA/HRS expert consensus document.

Recognizing Lyme disease is important, because appropriate antibiotic therapy for 10-20 days with tetracyclines, erythromycin, intravenous penicillin, or ceftriaxone can often revert the complete AV block (in addition to preventing rheumatologic and neurologic symptoms).

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Temporary Cardiac Pacing

In symptomatic patients with atrioventricular (AV) block, perform cardiac compressions, and administer adrenergic agonists (to accelerate the escape rhythm) while preparing for temporary cardiac pacing. Temporary cardiac pacing can be transcutaneous, transesophageal, or transvenous. The ultimate goal is permanent cardiac pacing.

Acquired AV block (AVB) from myocarditis, Lyme disease, and surgically induced trauma caused by adjacent tissue edema in patients with structurally normal hearts is usually transient and may not require therapy or may require only temporary pacing. However, in 40-56% of postsurgical patients, complete AV block persists beyond 10-14 days, and pacemaker therapy is indicated.

In postoperative patients with intermittent AV block, externalized temporary cardiac pacing wires that can be attached to an external temporary pulse generator set at a predetermined rate to maintain adequate cardiac output is typically required.

In postoperative patients with persistent complete AV block lasting more than 7 days within or below the bundle of His, permanent pacemaker therapy is currently indicated.[27]

If the escape rhythm is less than 50 bpm in infants or 45 bpm in adolescents, permanent pacemaker therapy may be indicated to prevent symptoms of congestive heart failure.

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Permanent Pacing

Patients with postoperative complete atrioventricular (AV) block (AVB) and those with Kearns-Sayre syndrome require prophylactic pacemaker therapy before symptoms develop because of the high risk for sudden death from asystole (> 60% in some series).

Regardless of symptoms or underlying escape rate, patients with postoperative complete AV block should always receive a permanent pacemaker system if the AV block persists more than 8-14 days and if no contraindications to pacemaker implantation are noted.[27] However, the overall prevalence of postsurgical complete AV block has been reduced to 5%. Most patients with postoperative complete AV block recover AV conduction within the first 7-10 postoperative days. These pediatric patients do not require a permanent pacemaker if conduction has recovered.

Prophylactic pacemaker therapy is indicated for any patient with complete AV block with a wide QRS escape rhythm.[27] Pacing is also indicated in patients with complete AV block who have exercise intolerance.

Dual-chamber pacemakers are currently preferred for patients who require life-time pacing. The preferred pacemaker modalities in most centers include the single-chamber pacing and dual-chamber sensing (VDD)[28] and the dual-chamber pacing and sensing (DDD).[29] These allow totally physiologic ventricular tracking of the atrial rate.

The long-term effects of asynchronous cardiac activation induced by right ventricular (RV) apical pacing have been described in patients with congenital complete AV block and normal cardiac anatomy.[30] These effects included deleterious left ventricular (LV) remodeling, LV dilatation and asymmetric LV hypertrophy.[31] However, pacing from the RV outflow tract decreases or slows adverse cardiac remodeling[32] and improves hemodynamics.[33]

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Contributor Information and Disclosures
Author

Charles I Berul, MD  Professor of Pediatrics and Integrative Systems Biology, George Washington University School of Medicine; Chief, Division of Cardiology, Children's National Medical Center

Charles I Berul, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Cardiology, American Heart Association, Cardiac Electrophysiology Society, Heart Rhythm Society, Pediatric and Congenital Electrophysiology Society, and Society for Pediatric Research

Disclosure: Johnson & Johnson Consulting fee Consulting

Coauthor(s)

M Silvana Horenstein, MD  Assistant Professor, Department of Pediatrics, University of Texas Medical School at Houston; Medical Doctor Consultant, Legacy Department, Best Doctors, Inc

M Silvana Horenstein, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Cardiology, and American Medical Association

Disclosure: Nothing to disclose.

Peter P Karpawich, MD  Professor of Pediatric Medicine, Department of Pediatrics (Cardiology), Wayne State University School of Medicine; Director, Cardiac Electrophysiology and Pacemaker Services, Children's Hospital of Michigan

Peter P Karpawich, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Cardiology, American Heart Association, Heart Rhythm Society, Michigan State Medical Society, and Pediatric Electrophysiology Society

Disclosure: Nothing to disclose.

Additional Contributors

Alvin J Chin, MD Professor of Pediatrics, University of Pennsylvania School of Medicine; Attending Physician, Cardiology Division, Children's Hospital of Philadelphia

Alvin J Chin, MD, is a member of the following medical societies: American Association for the Advancement of Science, American Heart Association, and Society for Developmental Biology

Disclosure: Nothing to disclose.

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

References

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This is an example of a normal finding on intracardiac electrophysiologic (EP) study. The surface electrocardiogram (ECG) is represented in different colors, with its corresponding intervals (ie, PR, QT) on top. A catheter with several electrodes is placed inside the heart, close to the superior vena cava–right atrial junction. This catheter records the sinoatrial node (SN) activity and is depicted here as the high-right atrial (HRA) deflection. Beneath the HRA intracardiac electrogram is the His-bundle intracardiac electrogram, which is recorded by the electrodes of a second catheter placed across the posterior aspect of the tricuspid valve. The His-bundle electrogram provides the most information about atrioventricular (AV) conduction. Three main deflections are present, with 2 intervals: (1) the A deflection corresponds to the activation of the low-right atrium, (2) the H deflection corresponds to the activation of the His-bundle before its branching into the Purkinje system, and (3) the V deflection corresponds to the activation of the proximal portion of the right ventricle. The atrium-His (A-H) interval represents the conduction time through the AV node. It shows the time elapsed between the activation of the low-right atrium (A) and the activation of the His-bundle (H), ranging normally from 50-120 milliseconds. The His-ventricle (H-V) interval is measured from the beginning of the H deflection to the beginning of the V deflection and represents the conduction time through the His-Purkinje system (normally 35-55 ms). Disease in the AV node prolongs the A-H interval, whereas disease in the distal conducting system prolongs the H-V interval.
This is a Mobitz type II second-degree atrioventricular (AV) block. The surface electrocardiograph (ECG) shows normal PR intervals and a P wave that is not followed by a QRS (in this graphic, the first P wave does not conduct through the AV node). The intracardiac electrogram shows no His deflection (H) after the blocked A deflection. In this case, the escape rhythm originates higher in the AV node at a rate of 40-50 beats per minute and is fairly reliable. However, patients may report symptoms of bradycardia such as dizziness, fatigue, and syncope. Because this type of AV block may progress to complete or third-degree AV block, patients should be monitored regularly even in the absence of symptoms.
This is a Mobitz type II second-degree atrioventricular (AV) block that may likely progress to a third-degree, or complete, AV block. The difference from the previous image is that, in this case, a His (H) deflection is present after the A deflection (the atrium-His [A-H] interval is maintained); however, no ventricle (V) deflection is present after the first H deflection. Therefore, in this case, the escape rhythm is slower than in the intracardiac electrophysiologic study of the patient in the previous image (< 40/min) and less reliable. This patient is more likely to receive a pacemaker because of the higher incidence of sudden death secondary to prolonged asystole.
This is a 12-lead electrocardiograph (ECG) of a 2-year-old girl with first-degree atrioventricular (AV) block that progressed to a complete, or third-degree, AV block (which is shown here). Her mother brought her to the clinic with described symptoms of easy tiredness and refusal to walk more than 1 block, which was a dramatic change for this girl. A normal sinus rhythm is present (shown by upward P waves in leads I, II, and aVF) at a rate of 135 per minute, which is completely dissociated from the QRS at a rate of 67 per minute. The QRS is narrow at 100 milliseconds with a frontal axis of 62°. No ventricular hypertrophy is present by voltage criteria. Because of the narrow QRS and its escape rate, this ECG is interpreted as complete AV block with junctional escape rhythm.
This is a 12-lead electrocardiograph (ECG) of a 2-year-old girl with first-degree atrioventricular (AV) block that progressed to a complete, or third-degree, AV block (see the previous image). This ECG was taken after dual chamber (DDD-R) pacemaker placement. Sinus P waves are present at a rate of 90 per minute, followed by a pacemaker spike that produces a wide QRS of 128 milliseconds. No spike occurs before each P wave, because this type of pacemaker senses the patient's own P waves and stimulates the ventricle afterward. Therefore, the patient's ventricular rate follows her physiologic needs by tracking the patient's own atrial rate. With a DDD-R pacemaker, if the patient develops sinus bradycardia, the pacemaker takes over and paces the right atrium at the programmed rate, which is followed by the ventricular stimulation, maintaining AV synchrony.
 
 
 
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