4.2 Conduction System Defects

4.2 Conduction System Defects

Conduction system defects may be inherited, acquired from metabolic or drug effects, or created by surgical trauma near the AV node and His-Purkinje system. In the PICU, these problems matter because they convert a monitored child into a sudden arrest risk—often without the dramatic “SVT storm” appearance that teams expect. Mastery for the CCRN Pediatric exam means linking ECG clues (QT interval, delta wave, progressive AV block) to concrete nursing actions: medication review, electrolyte repletion, defibrillator readiness, and temporary pacing competence.

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Prolonged QT Interval

The QT interval reflects ventricular depolarization and repolarization. Because QT shortens at faster heart rates, clinicians use a rate-corrected QT (QTc) for comparison. Exact numeric cutoffs vary slightly by age and sex, but a substantially prolonged QTc—especially with concerning morphology, syncope history, or family sudden-death history—demands action.

Congenital long QT syndrome (LQTS)

Congenital LQTS involves ion-channel or structural protein defects that prolong myocardial repolarization. Children may present with syncope during swimming, startling auditory stimuli, or exertion, depending on genotype patterns taught in cardiology practice. In the PICU, congenital LQTS may be newly diagnosed after a near-arrest, or may already be known in a child admitted for another reason. Nursing priorities include:

• Continuous ECG monitoring with QT/QTc trending when available
• Strict avoidance of QT-prolonging drugs unless no alternative exists and cardiology agrees
• Maintaining potassium and magnesium in robust, often high-normal ranges per cardiology targets
• Rapid recognition of polymorphic VT / torsades de pointes
• Ready access to defibrillation and magnesium therapy for torsades per resuscitation guidance and orders

Acquired QT prolongation

Acquired prolongation is extremely common in critical care. Typical contributors include hypokalemia, hypomagnesemia, hypocalcemia, hypothermia, myocardial ischemia, and medications (many antiarrhythmics, antipsychotics, macrolide or fluoroquinolone antibiotics, antiemetics such as ondansetron in susceptible patients, and methadone, among others). Polypharmacy in the postoperative cardiac child creates cumulative risk.

Torsades de pointes is a polymorphic VT associated with prolonged QT. It may be pause-dependent and can self-terminate or degenerate to VF. Nursing recognition of the twisting QRS morphology around the baseline, plus immediate team activation, is critical. Do not treat torsades as monomorphic VT with drugs that further prolong QT.

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Wolff-Parkinson-White (WPW)

WPW involves an accessory atrioventricular pathway that bypasses the AV node. In sinus rhythm, ventricular pre-excitation produces the classic ECG triad:

1. Short PR interval
2. Delta wave (slurred QRS upstroke)
3. Widened QRS reflecting fusion of pathway and normal conduction

Not every child with a delta wave is continuously symptomatic. Some have intermittent pre-excitation. Problems arise when the accessory pathway participates in reentrant SVT (orthodromic or antidromic AVRT) or—most dangerously—when atrial fibrillation conducts rapidly over the pathway to the ventricles.

Why AV-nodal blockers are dangerous in WPW with AF

Drugs that block the AV node (examples commonly cited in teaching: digoxin, verapamil, diltiazem, and sometimes adenosine in the wrong clinical context) can favor conduction over the accessory pathway. If atrial fibrillation is present, that can produce an extremely rapid, irregular, wide-complex ventricular response and degenerate to VF. Therefore, when an irregular wide-complex tachycardia raises concern for pre-excited AF, avoid empiric AV-nodal blockade and escalate emergently—unstable patients need synchronized cardioversion/defibrillation readiness per pulse status, and expert consultation.

PICU nursing focus in known or suspected WPW

• Document baseline pre-excitation so new bundle-branch block is not confused with delta-wave morphology changes
• For SVT in a known WPW patient, follow hemodynamic priorities identical to other SVT care: unstable → synchronized cardioversion
• Keep defibrillator pads nearby during adenosine administration if pathway-mediated SVT is suspected, because rare degeneration can occur
• Educate that “rate control with a calcium-channel blocker” adult habits do not transfer safely to pre-excited AF

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Acquired Conduction Injury After Congenital Heart Surgery

Surgical trauma, edema, hemorrhage, or suture injury near the conduction system can produce transient or permanent AV block. Risk is highest when the repair is anatomically adjacent to the AV node or penetrating bundle.

Lesions and operations with elevated block risk

Clinical progression the bedside nurse must catch

Acquired injury may appear immediately in the operating room or evolve over the first postoperative hours to days as edema peaks. Watch for:

• Lengthening PR interval (first-degree AV block)
• Mobitz I or II second-degree patterns
• Sudden complete (third-degree) AV block with AV dissociation
• Slow junctional or ventricular escape rates that cannot support cardiac output
• Intermittent capture if temporary pacing is inconsistently sensing or outputting

Temporary epicardial pacing: nursing essentials

Many postoperative congenital heart patients return with atrial, ventricular, or atrioventricular temporary wires. Core competencies include:

1. Know the wire labeling (atrial vs ventricular) and secure connections to the external pacemaker.
2. Verify output and sensing settings ordered by the surgical/cardiology team; understand demand versus asynchronous modes at a conceptual level.
3. Confirm electrical capture (pacing spike followed by QRS for ventricular pacing) and mechanical capture (pulse/arterial waveform with paced beats).
4. Recognize failure to capture or sense—loose cables, depleted batteries, rising thresholds from edema, or wire fracture/dislodgement.
5. Protect wires during cares; accidental traction can remove the only bridge to an adequate rate.
6. Keep isoproterenol or epinephrine rescue plans per order set if pacing suddenly fails while waiting for intervention.

Transient block often improves over several days as inflammation subsides. Persistent complete heart block—commonly discussed in surgical literature as lasting beyond approximately 7–14 days, depending on institutional and guideline practice—typically prompts permanent pacemaker implantation. Do not be falsely reassured by a “tolerated” escape rate in a sedated, ventilated child; demand may rise with weaning, fever, or mobilization.

Medical adjuncts and team communication

Some centers use anti-inflammatory strategies (for example, steroids) in selected early postoperative block cases, aiming to reduce edema around the conduction tissue. This is a physician-directed decision and not a substitute for pacing readiness. Nursing contribution is precise documentation of when block began, escape rates, pacing dependence percentage, and hemodynamic correlates—data that guide whether injury is recovering.

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Integrating Conduction Defects With Rhythm Emergencies

Conduction defects intersect with Chapter 4.1 dysrhythmia care. Prolonged QT predisposes to torsades that may require defibrillation if pulseless. WPW predisposes to SVT and hazardous pre-excited AF. Postoperative AV block predisposes to profound bradycardia that needs pacing rather than blind reliance on atropine. In each pathway, the PICU nurse’s value is early ECG pattern recognition, prevention (electrolytes, drug safety, wire security), and immediate execution of electrical therapies when perfusion fails.

For exam items, translate stems into one of three buckets: repollarization risk (QT), accessory pathway risk (WPW), or surgical AV node injury (post-op block)—then choose the intervention that protects the ventricle from either a malignant tachyarrhythmia or a nonperfusing bradycardia.