10.2 Wide-Complex Tachycardia & VT with Pulse

What “Wide-Complex Tachycardia” Means at the Bedside

A wide-complex tachycardia (WCT) is a rapid ventricular rate with a wide QRS. In adults, “wide” is often ≥0.12 s; in children, normal QRS duration is age-dependent and shorter in infants, so “wide for age” and institutional ECG criteria matter. For PALS exam purposes, focus on the management rule more than arguing milliseconds:

Undifferentiated wide-complex tachycardia is treated as ventricular tachycardia (VT) until proven otherwise.

Why? Because VT can deteriorate to pulseless VT or VF within minutes, and therapies that are “safe” for some SVTs (certain AV nodal blockers, inappropriate adenosine use in the wrong morphology) can collapse a child who actually has VT or a pre-excited atrial arrhythmia. In the unstable child, you do not need a fellowship-level ECG differential before the first synchronized shock.

Differential (know the categories, act on the algorithm)

You will not always distinguish these on a 6-second strip in a crashing toddler. Perfusion and pulse still rule the first branch.

VT with Pulse vs Pulseless VT

This is the Chapter 8 vs Chapter 10 hinge:

Never manage pulseless VT with a leisurely “stable VT drug infusion.” Never treat a conscious child who has a pulse and monomorphic VT as if they were in arrest with stacked unsynchronized shocks as the first routine step—use synchronized cardioversion when the device can sync and the rhythm is monomorphic.

Unstable wide-complex with pulse — actions

1. Support airway, oxygen, ventilation as needed.
2. Attach monitor/defibrillator; confirm pulse present.
3. Identify cardiopulmonary compromise attributable to the rhythm.
4. Synchronized cardioversion at 0.5–1 J/kg, then 2 J/kg if needed.
5. Sedation if conscious and will not delay.
6. After conversion (or if refractory), search causes: electrolytes, toxins, congenital heart disease, myocarditis, channelopathy, ischemia (older), post-op cardiac issues.
7. Expert help (pediatric cardiology/critical care/EP) early.

Stable wide-complex — actions

“Stable” means no serious signs of cardiopulmonary compromise right now. That status can change on the next monitor update.

• Keep pads on; continuous monitoring; ABCs supported.
• Obtain a 12-lead ECG when it will not delay care if deterioration begins.
• Expert consultation is preferred before casual drug stacking.
• Consider antiarrhythmic options for perfusing VT per PALS/local protocol (Section 10.3): amiodarone infusion context, procainamide where used, lidocaine options.
• Treat reversible triggers (K⁺, Mg²⁺, toxins) while you wait for specialty input.
• If the child becomes unstable at any moment → immediate synchronized cardioversion (or defibrillation if pulseless/polymorphic pathway applies).

Polymorphic VT and torsades de pointes (exam-level)

Polymorphic VT shows beat-to-beat changes in QRS shape. Torsades de pointes is polymorphic VT associated with a prolonged QT interval, often described as QRS complexes that appear to “twist” around the baseline.

Exam-level management themes:

• If the child is pulseless or the rhythm behaves like VF, treat with high-quality CPR and unsynchronized defibrillation (shockable arrest pathway).
• Because morphology varies, synchronization may be unreliable—do not waste critical time fighting a sync button that will not lock when defibrillation is required.
• Magnesium is the classic pharmacologic adjunct taught for torsades (even when the serum magnesium is not yet known to be low in many emergency protocols)—know it as the torsades-associated drug, while still correcting other electrolytes and stopping QT-prolonging agents.
• Address causes: congenital long QT, drugs (many antiarrhythmics, antipsychotics, antibiotics, etc.), electrolyte depletion (hypokalemia, hypomagnesemia), and bradycardia-related pause-dependent torsades in specialized settings.

Adenosine caveats in wide-complex rhythms

Adenosine is a powerful tool for regular monomorphic narrow-complex SVT (Chapter 9). It is not a free “try this for every fast rhythm” drug.

Use extreme caution / generally avoid adenosine when:

• The wide-complex rhythm is irregular (risk of pre-excited atrial fibrillation or polymorphic rhythms where AV nodal blockade is harmful),
• There is known or strongly suspected pre-excitation (WPW) with an irregular wide tachycardia,
• The clinical picture is clear VT in an unstable child—electricity, not diagnostic adenosine delays.

Some advanced algorithms discuss adenosine as a diagnostic/therapeutic option only for regular monomorphic wide-complex tachycardia when the likelihood of SVT with aberrancy is reasonable and the patient is stable, under expert-informed protocols. For the PALS provider exam, the safer high-yield message is:

• Unstable WCT → cardioversion (sync if monomorphic with pulse).
• Irregular wide complex → do not adenosine like ordinary SVT.
• Expert consultation for stable WCT rather than casual drug stacking.

Putting Recognition Skills Together

Monitor clues that favor VT

• History of cardiomyopathy, repaired congenital heart disease, myocarditis, channelopathy, or prior VT
• AV dissociation, fusion/capture beats (when visible—gold-standard ECG clues, not always present)
• Very wide, bizarre QRS morphology; northwest axis in some adult criteria (less emphasized than perfusion in PALS megacodes)
• Failure of the clinical story to fit sinus tach or simple SVT

Monitor clues that raise pre-excitation / irregular wide concern

• Irregularly irregular wide tachycardia at extreme rates
• Known WPW or delta waves on prior ECG
• Beat-to-beat variation in QRS width in an irregular rhythm

If you see irregular wide tachycardia, do not reach for adenosine, digoxin, or calcium-channel blockers as if treating ordinary AF with a narrow complex. Those agents can accelerate conduction over an accessory pathway and precipitate VF. Support ABCs, expert help, and electricity when unstable.

Clinical scenarios

Scenario A — Unstable monomorphic VT with pulse: A 12-year-old with repaired tetralogy of Fallot has a regular wide tachycardia at 180/min, BP low for age, and confusion. Pulses are present. Presume VT. Synchronized cardioversion 0.5–1 J/kg, prepare for 2 J/kg, sedate only if it will not delay, seek cardiology, and evaluate electrolytes/ischemia/structural issues after conversion.

Scenario B — Pulseless VT: The same rhythm loses the pulse. This is now pVT: start CPR, defibrillate at 2 J/kg, resume CPR, escalate energy per Chapter 8—not another synchronized 0.5 J/kg attempt as the arrest strategy.

Scenario C — Stable wide complex: A school-age child is alert with normal blood pressure and strong pulses but a regular wide tachycardia. Pads on, expert consultation, consider antiarrhythmic infusion options (10.3), continuous reassessment. If mental status or BP falls, cardiovert immediately.

Scenario D — Torsades context: An adolescent on a QT-prolonging medication has polymorphic VT, brief pulses, then becomes unresponsive and pulseless. Defibrillate/CPR pathway; give magnesium for torsades context; stop the offending drug; correct K⁺/Mg²⁺.

Exam traps specific to wide complex

Bottom line for 10.2: Wide-complex tachycardia is VT until proven otherwise. Pulse and stability choose between synchronized cardioversion, defibrillation/CPR, and expert-guided stable care. Respect polymorphic/torsades and pre-excitation traps, and you will handle the hardest rhythm vignettes on the PALS written exam and megacode.