Wide Complex Tachycardias & Channelopathies

Rapid Review·Cardiovascular

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PATHOLOGY

T1Must know

P311

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Rhythms from below the AV node, the twisting one, and the inherited channel defects that kill young people.

Key takeaways

Why wide means ventricular

Wide QRS of 120 msec or more

the ventricles were activated slowly and outside the normal conduction system, so the tachycardia originates below the AV node.

The three ventricular rhythms

Ventricular tachycardia

typically regular, rate above 100, with uniform wide complexes, as on the ventricular tachycardia tracing. Usually an abnormal reentry circuit in structural heart disease, especially scarring after an MI. High risk of sudden cardiac death.

Torsades de pointes

polymorphic VT whose amplitude waxes and wanes, so the complexes appear to twist around the baseline, as on the torsades tracing. Torsades = "twisting of the points."

May degenerate into ventricular fibrillation.
A long QT predisposes, i.e. delayed repolarization. Caused by drugs, low K+, low Mg2+, low Ca2+.
Treatment: defibrillation if unstable, magnesium sulfate if stable.

Ventricular fibrillation

disorganized rhythm with no identifiable waves, from reentrant circuits in damaged myocardium, as on the ventricular fibrillation tracing. Fatal without immediate CPR and defibrillation.

Drug-induced long QT, by "ABCDEF + NO"

anti-Arrhythmics (class Ia and III) and Arsenic
anti-Biotics (macrolides, fluoroquinolones)
anti-Cychotics (haloperidol) and Chloroquine
anti-Depressants (TCAs) and Diuretics (thiazides)
anti-Emetics (ondansetron)
anti-Fungals (fluconazole)
Navir drugs (protease inhibitors)
Opioids (methadone)

The wide complex tachycardias
Arrhythmia	Rhythm	Cause	Treatment
Ventricular tachycardia	Regular, rate above 100	Structural heart disease, post-MI scar	Antiarrhythmics, ICD
Torsades de pointes	Polymorphic, twisting	Long QT: drugs, low K+, Mg2+, Ca2+	Magnesium sulfate if stable, defibrillation if unstable
Ventricular fibrillation	No identifiable waves	Usually degeneration from VT	CPR and defibrillation, fatal otherwise

The inherited channelopathies

What they are

inherited mutations of cardiac ion channels that distort the action potential and raise the risk of ventricular tachyarrhythmia and sudden cardiac death.

Brugada syndrome

autosomal dominant loss-of-function mutation of Na+ channels. Increased prevalence in Asian males. ECG shows pseudo-right bundle branch block with ST elevation in V1 to V3. Prevent sudden cardiac death with an ICD.

Congenital long QT syndrome

most commonly a loss-of-function mutation of K+ channels (KCNQ1), impairing repolarization.

Romano-Ward: autosomal dominant, pure cardiac phenotype with no deafness.
Jervell and Lange-Nielsen: autosomal recessive, with sensorineural deafness.

The two congenital long QT syndromes
Feature	Romano-Ward	Jervell and Lange-Nielsen
Inheritance	Autosomal dominant	Autosomal recessive
Deafness	NO, pure cardiac	YES, sensorineural
Channel	K+, loss of function	K+, loss of function

Brugada vs Congenital long QT
Feature	Brugada syndrome	Congenital long QT
Channel	Na+, loss of function	K+, loss of function
Inheritance	Autosomal dominant	AD (Romano-Ward) or AR (Jervell)
Demographics	Asian males	Any
ECG	Pseudo-RBBB with ST elevation V1 to V3	Prolonged QT
Prevention	ICD	ICD, beta-blockers

The slow side

Sick sinus syndrome

age-related (over 65) degeneration of the SA node, giving bradycardia, sinus pauses (delayed P waves), sinus arrests (dropped P waves), and junctional escape beats, as on the sick sinus tracing.

A stable patient has twisting polymorphic VT and a normal magnesium level. What do you give?

Magnesium sulfate anyway. It treats torsades regardless of the level; defibrillate only if the patient becomes unstable.

How it's tested

Torsades de pointes in a stable patient is treated with magnesium regardless of whether the magnesium level is low, which is the detail that surprises students and the reason the question exists. The channelopathy pair is a clean contrast worth holding as one unit: Brugada is a sodium channel problem in Asian males with ST elevation in V1 to V3, while congenital long QT is a potassium channel problem, and the recessive version is the one that comes with deafness.

Go deeper

First Aid 2026 — CV/Pathology (p.311) · B&B — Ventricular arrhythmias · Mehlman — HY Cardio (torsades, long QT drugs, Brugada)

High-yield images5

ACLS algorithm for adult tachycardia with a pulse. Sinus tachycardia is treated by finding the cause; hemodynamic instability goes straight to synchronized cardioversion. Otherwise QRS width sorts the rhythm: narrow irregular is likely AF or flutter (rate control), narrow regular is non-AF SVT such as AVNRT (vagal maneuvers then adenosine), wide irregular is AF with aberrancy, pre-excited AF or polymorphic VT (procainamide for pre-excited AF, magnesium for PMVT), and wide regular is likely monomorphic VT (pharmacologic cardioversion with amiodarone, procainamide, lidocaine or sotalol).

Monomorphic ventricular tachycardia on ECG: a regular run of wide, uniform QRS complexes at a rate above 100, with no preceding P waves and every complex the same shape.

Torsades de pointes on ECG: polymorphic ventricular tachycardia whose QRS amplitude waxes and wanes so the complexes appear to twist around the baseline, traced here by the sinusoidal envelope.

Ventricular fibrillation on ECG: completely disorganized, chaotic deflections with no discernible P waves, QRS complexes or T waves, and therefore no effective cardiac output.

Sick sinus syndrome on ECG: sinus bradycardia interrupted by a long pause where the expected P wave never appears (sinus arrest), before conduction resumes.

Flashcards for this page

Card 1 of 5 · try-out only, nothing is saved

What is the genetic mutation associated with Brugada syndrome?

(...) of function mutation affecting (...) channels

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