Torsades de pointes (polymorphic ventricular tachycardia)

What it is

Ventricular tachycardia is 3 or more consecutive ventricular complexes, wide QRS complex, at a frequency of 100 per minute or more. It is classified twice over. By duration: VT that is not sustained lasts under 30 seconds, while sustained VT lasts 30 seconds or more. By morphology: monomorphic VT, where every QRS looks the same, and polymorphic VT, where they do not.

Torsades de pointes is the polymorphic form, and naming it correctly is what changes the drug: polymorphic VT, that is torsades de pointes, is treated by magnesium sulfate, while monomorphic VT is not. Where sinus rhythm runs at 60-100 BPM from the sinus node, ventricular tachycardia runs at 100-320 BPM from the ventricle, and in the polymorphic form the signal comes from different nodes rather than one.

Causes and risk

• Cardiac scars secondary to myocardial infarction.
• Electrolyte imbalances: hypokalemia, hypomagnesemia, hypocalcemia.
• Digoxin toxicity.

Low magnesium earns its own line, because it gives tetany, torsades de pointes and hypokalemia together. Low Mg leads to low PTH and so to low Ca, and it causes renal K wasting and so to low K. This is why Mg is checked in cases of hypocalcemia or hypokalemia, and why Mg is always corrected in refractory hypokalemia or hypocalcemia.

Amiodarone belongs on the other side: among its major side effects is a risk of proarrhythmias, with QT prolongation and a risk of torsades de pointes, alongside sinus bradycardia and heart block.