4.2 Pediatric Bradyarrhythmias, Conduction Blocks & Emergency Pacing

Pediatric Bradyarrhythmias, Conduction Blocks & Emergency Pacing: Recognition, PALS Protocols, and Pacing Mechanics

First identify whether a pulse is present and whether perfusion is compromised. Support breathing and treat reversible causes. With a pulse, start CPR when the heart rate remains below 60 beats/min with compromise despite effective ventilation with oxygen. A lost pulse changes the pathway to cardiac arrest.

A child with hypoxia, postoperative conduction injury, or medication toxicity can develop a slow rate and poor perfusion. The response depends on the cause as well as the rate.

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Pediatric Bradycardia Pathophysiology & Rate-Dependent Cardiac Output

Cardiac output equals heart rate times stroke volume ($CO = HR \times SV$). If stroke volume cannot compensate for a falling rate, cardiac output falls. Reduced perfusion can worsen acidosis and myocardial function. Compare the measured rate with age, sleep or wake state, medications, and the child's baseline. A well-perfused child with a slow resting rate and a child with the same rate plus altered consciousness need different responses.

Etiologic Categories: Secondary vs. Primary

1. Secondary (Extrinsic) Causes (Most Common):
   • Profound Hypoxia and Hypercarbia: Airway obstruction, severe pneumonia, bronchiolitis, laryngospasm, apnea, or hypoventilation.
   • Severe acidosis: Can contribute to impaired cardiac function during critical illness.
   • Hypothermia: Slows intrinsic pacemaker activity.
   • Metabolic abnormalities: Check glucose and electrolytes when indicated by the presentation.
   • Increased Intracranial Pressure (ICP): Cushing triad (bradycardia, hypertension with widened pulse pressure, and irregular respirations) caused by brainstem ischemia and reflexive vagal baroreceptor activation.
   • Excessive Vagal Tone: Vigorous pharyngeal suctioning, endotracheal intubation, nasogastric tube insertion, or severe gastroesophageal reflux.
   • Toxins / Medications: Beta-blockers, calcium channel blockers, digoxin, clonidine, and organophosphates.
2. Primary (Intrinsic) Causes:
   • Congenital complete atrioventricular block.
   • Post-surgical injury to conduction bundles (e.g., following repair of perimembranous VSD, AV canal, tetralogy of Fallot, or L-TGA).
   • Acute myocarditis or endocarditis involving the conduction septum.
   • Sinus node dysfunction (sick sinus syndrome, common late after Mustard, Senning, or Fontan operations).

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The PALS Bradycardia with Poor Perfusion Algorithm

The Pediatric Advanced Life Support (PALS) Bradycardia Algorithm establishes a strict, physiological hierarchy of intervention:

Step 1: Initial Airway, Oxygenation, and Ventilation Assessment

• Maintain a patent airway, provide oxygen, and clear secretions as needed.
• If spontaneous respiratory effort is inadequate, immediately provide bag-mask positive-pressure ventilation.
• Attach continuous cardiac monitoring, pulse oximetry, and non-invasive blood pressure.
• Reassess heart rate, pulse, mental status and perfusion as soon as ventilation is effective. Persistent compromise calls for escalation.

Step 2: The CPR Threshold Mandate & Intra-Arrest DBP Targets

• Arterial pressure during cardiac arrest: If continuous arterial pressure is available during CPR for cardiac arrest, consider targeting diastolic pressure of at least $25\text{ mmHg}$ in infants and $30\text{ mmHg}$ in children aged one year and older. Use it alongside compression quality, rhythm and the clinical context.

Step 3: Pharmacotherapy

Establish vascular access (intravenous or intraosseous) without interrupting high-quality chest compressions and ventilations:

Epinephrine (First-Line Resuscitation Vasopressor)

Give IV/IO epinephrine for bradycardia with cardiopulmonary compromise that persists after correction of factors such as hypoxia. The dose is $0.01\text{ mg/kg}$ using the $0.1\text{ mg/mL}$ concentration, up to $1\text{ mg}$.

If the child loses the pulse and has asystole or pulseless electrical activity (PEA), give the initial arrest dose as early as possible. During arrest, the algorithm uses repeat doses every 3–5 minutes. A 20 kg child receives $20 \times 0.01 = 0.2\text{ mg}$, which is $2\text{ mL}$ at $0.1\text{ mg/mL}$.

Atropine (Parasympatholytic Antimuscarinic)

Atropine is a competitive antagonist of acetylcholine at post-ganglionic muscarinic ($M_2$) receptors, blunting vagal tone on the SA and AV nodes. Use atropine for bradycardia with cardiopulmonary compromise due to increased vagal tone or primary AV block. The 2025 bradycardia-with-a-pulse algorithm specifies $0.02\text{ mg/kg}$ IV/IO, with a $0.1\text{ mg}$ minimum and $0.5\text{ mg}$ maximum per dose. It may be repeated once. The algorithm's dosing applies to this treatment indication. If atropine is selected as premedication for emergency intubation, the guideline permits $0.02\text{ mg/kg}$ without a minimum dose. Cholinergic poisoning has a separate atropine protocol directed by toxicology.

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Atrioventricular Conduction Blocks

Conduction blocks reflect impaired or absent electrical propagation from the atria to the ventricles.

1. First-Degree AV Block

• ECG criteria: Every P wave conducts, but the PR interval is prolonged for the child’s age and heart rate. Compare with pediatric reference values.
• Clinical significance: Isolated first-degree AV delay often requires observation. Review medications and the clinical context, especially if the finding is new or symptoms are present.

2. Second-Degree AV Block: Mobitz Type I (Wenckebach)

• ECG Criteria: Progressive prolongation of the PR interval until a P wave fails to conduct (dropped QRS complex). Grouped beating occurs; the R-R interval progressively shortens prior to the dropped beat.
• Clinical significance: Wenckebach often reflects AV nodal delay and can occur during sleep. Evaluate the clinical context and perfusion before attributing it to benign vagal tone.

3. Second-Degree AV Block: Mobitz Type II

• ECG criteria: With a regular atrial rhythm, PR intervals stay constant before and after an isolated nonconducted P wave. A 2:1 conduction pattern alone does not establish Mobitz type because there are too few consecutive conducted beats to evaluate PR behavior.
• Clinical significance: Mobitz type II usually reflects His–Purkinje disease and can progress to complete block. Monitor and seek urgent cardiology guidance, especially when perfusion is impaired.

4. Third-Degree (Complete) AV Block

• ECG criteria: Atrial and ventricular activity are independent. P waves and escape QRS complexes have no consistent PR relationship.
• Congenital complete AV block: Maternal anti-Ro/SSA and anti-La/SSB antibodies can cross the placenta and injure the fetal conduction system. Assess newborn perfusion, ventricular function and the escape rhythm. In isolated congenital complete AV block, PACES supports permanent pacing for symptomatic bradycardia, wide QRS escape, complex ventricular ectopy or ventricular dysfunction, and in asymptomatic neonates or infants with a mean ventricular rate of $50\text{ bpm}$ or less. Complex congenital heart disease has separate criteria.
• Acquired complete AV block: Injury to the conduction system can follow congenital heart surgery. Use temporary pacing as needed for perfusion. PACES recommends permanent pacing for advanced second- or third-degree postoperative AV block persisting at least 7–10 days. Earlier implantation may be considered if recovery is unlikely.

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Emergency Temporary Cardiac Pacing

For bradycardia with a pulse and poor perfusion due to complete heart block or sinus node dysfunction that persists despite resuscitative measures, consider emergency transcutaneous pacing. In a postoperative child with functioning temporary epicardial wires, the cardiac team can use those wires for temporary pacing. With pulseless asystole, follow the arrest algorithm.

Transcutaneous Pacing (TCP)

Transcutaneous pacing delivers electrical impulses across the chest wall via large external pacing pads to depolarize the myocardium non-invasively.

1. Follow the device's pediatric instructions for pad placement, mode and current. Titrate the output until a paced ventricular complex follows the pacing stimulus.
2. Verify mechanical capture. Look for a corresponding arterial pressure waveform or pulse and improving perfusion. Chest-wall muscle contractions can mimic a pulse.
3. Reassess capture and blood pressure continuously. If the pulse is lost, resume or continue CPR and use the arrest algorithm. Assess the need for analgesia and sedation with the resuscitation team without delaying urgent support.

Transvenous and Temporary Epicardial Pacing

• Temporary epicardial wires: If present, identify the wire labels and confirm connections, sensing, and capture. The cardiac team selects the pacing mode based on the rhythm and available wires.
• Transvenous pacing: The cardiac team may consider a temporary intracardiac lead when external pacing is ineffective or longer support is needed.

AHA/AAP 2025 pediatric advanced life support · Bradycardia with a pulse algorithm · Cardiac arrest algorithm · PACES pediatric pacing consensus · Pediatric ECG reference study · ACC/AHA/HRS AV block definitions