Torsades des Pointes - goodman

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TdP (Torsades des Pointes) = polymorphic ventricular tachycardia with shifting sinusoidal waveforms. Can be differentiated from other polymorphic ventricular tachycardia because it is always associated with a prolonged QT interval.


Torsades de pointes is a dangerous rhythm because it can suddenly progress to ventricular fibrillation.

Torsades des Pointes is predisposed by:

Familial long QT syndromes—although rare, these syndromes should be considered in the differential diagnosis of previously asymptomatic young patients presenting with unprovoked syncope. There are two major congenital long QT syndromes:

Romano-Ward syndrome:
• Autosomal dominant defect in K+ channel that contributes to IK (delayed rectifier current) → prolonged QT
• Intact sensorineural hearing
Jervell and Lange-Nielsen syndrome (JLNS):
• Autosomal recessive defect in K+ channel that contributes to IK (delayed rectifier current) → prolonged QT
• Profound congenital sensorineural deafness

Electrolyte abnormalities that can predispose to torsades de pointes include:
• Hypokalemia
• Hypomagnesemia
• Hypocalcemia

Acute management of Torsades de pointes includes:
• Intravenous magnesium terminates the arrhythmia by decreasing Ca2+ influx, thereby decreasing the amplitudes of EADs (early afterdepolarizations)
• Repletion of electrolytes (e.g. Mg2+, K+) as needed

In refractory cases of Torsades de pointes, cardioversion-defibrillation may be necessary.

Patients with torsades de pointes secondary to a congenital long QT syndrome are treated with beta blockers.

Drug toxicity: Remember the mnemonic for drugs that can cause Torsades de pointes: ABCDE
• AntiArrhythmics (Class IA, III)
• AntiBiotics (e.g. macrolides)
• Anti"C"ychotics (e.g. haloperidol)
• AntiDepressants (e.g. TCAs)
• AntiEmetics (e.g. ondansetron)

Class IA antiarrhythmics (e.g. quinidine, disopyramide, procainamide) — prolong QT interval primarily by blocking Na channels. Class IA agents primarily block fast Na channels, thereby decreasing fast Na entry into cells and slowing conduction velocity; Class IA agents also block outward K channels, thereby decreasing K outflow from cells and prolonging the refractory state of cardiomyocytes.

Class III antiarrhythmics (e.g. amiodarone, bretylium, dofetilide, ibutilide, sotalol) — prolong QT interval by blocking K+ channels, thereby predisposing individuals to torsades de pointes.