05. Sinoatrial and Atrioventricular Conduction Blocks

Atrioventricular (AV) and sinoatrial conduction delays in pediatric patients range from benign, vagally-mediated nocturnal findings to autoimmune congenital complete heart block requiring urgent pacing.

Complete Heart Block ECG Figure 5.1: 12-lead ECG of Complete Third-Degree AV Block in an infant displaying complete dissociation between P waves and slow, regular QRS complexes. Rendered with solid white background.


1. Clinical Presentation & Bedside Evaluation

  • Congenital Complete Heart Block (CCHB): In utero presentation with fetal bradycardia ($HR < 100\text{ bpm}$) or non-immune hydrops fetalis. Postnatally: poor feeding, lethargy, pallor, cannon 'a' waves in the jugular venous pulse, and variable intensity first heart sound ($S_1$).
  • Acquired Heart Block: History of tick bite (Lyme carditis), fever/chorea (Rheumatic carditis), recent cardiac surgery (VSD/AV canal patch repair), or myocarditis.

2. Electrocardiographic Classification & Criteria

AV Block ClassificationPR Interval BehaviorConduction RatioAnatomical Site of BlockClinical Significance
First-Degree AV BlockConstant prolongation $>98\text{th}$ percentile for age and rate (e.g. $>0.16\text{ s}$ in young child, $>0.18\text{ s}$ in adolescent).$1:1$AV NodeMinor Jones criterion in Acute Rheumatic Fever; Lyme carditis; Endocardial cushion defects.
Second-Degree Mobitz I (Wenckebach)Progressive PR lengthening until a P wave is non-conducted (dropped QRS). Grouped beating.Variable ($3:2, 4:3$)AV NodeHigh vagal tone in athletic children, nocturnal; usually benign.
Second-Degree Mobitz IIConstant PR interval with intermittent, unheralded non-conducted P waves.Variable ($2:1, 3:1$)Infranodal (His-Purkinje)Pathological; high risk of progression to Complete Heart Block.
Third-Degree Complete AV BlockComplete AV dissociation; P-P intervals regular (atrial rate normal) and R-R intervals regular (ventricular escape rate slow); PR intervals completely variable.$0:1$ (No conduction)AV Node / InfranodalCongenital autoimmune (Anti-Ro/La) or surgical/infective injury.

First Degree AV Block Figure 5.2: First-degree AV block demonstrating constant, prolonged PR interval across all leads.

Second Degree Mobitz I Wenckebach Figure 5.3: Mobitz Type I (Wenckebach) showing progressive PR prolongation culminating in a dropped QRS.


3. Pathophysiology of Congenital Complete Heart Block (CCHB)

  • Autoimmune Transplacental Transmission: Maternal autoantibodies (anti-Ro/SSA and anti-La/SSB) cross the placenta between $16-24$ weeks gestation, binding to fetal L-type calcium channels and triggering immune-mediated myocarditis, calcification, and irreversible fibrous replacement of the fetal AV node.
  • Structural CCHB: Corrected Transposition of the Great Arteries (L-TGA) and Left Isomerism (Polysplenia syndrome).

4. Multimodality Diagnostic Investigations

  • Fetal Echocardiography: Measures mechanical PR interval using pulsed-wave Doppler (mitral inflow / aortic outflow sampling).
  • Maternal Serologies: Anti-Ro/SSA and Anti-La/SSB antibody titers.
  • 24-Hour Ambulatory Holter Monitoring: Quantifies mean hourly heart rate, pauses, and ventricular escape ectopy.

5. Evidence-Based Management Protocols

  • In Utero Therapy (Second-Degree / Early Third-Degree Block): Maternal Dexamethasone ($4\text{ mg/day}$ orally, crosses placenta) $\pm$ IVIG to arrest inflammatory progression.
  • Emergency Neonatal Management:
    • IV Isoproterenol infusion ($0.05-0.5\ \mu\text{g/kg/min}$) or Epinephrine for symptomatic bradycardia.
    • Temporary transcutaneous or transvenous pacing.
  • Indications for Permanent Epicardial/Endocardial Pacemaker Implantation in CCHB:
    1. Symptomatic bradycardia, syncope, or congestive heart failure.
    2. Infant resting ventricular rate $<50-55\text{ bpm}$ ($<70\text{ bpm}$ with structural CHD).
    3. Ventricular pauses $>3\times$ basic cycle length.
    4. Wide QRS escape rhythm, complex ventricular ectopy, or prolonged $QTc$.

6. Clinical Pearls & Diagnostic Traps

Clinical Pearl: Maternal asymptomatic status does not exclude anti-Ro antibodies. More than $80\%$ of mothers whose infants are born with CCHB are completely asymptomatic at the time of delivery.