Torsades de pointes

Overview

Torsades de pointes (TdP) is a polymorphic ventricular tachycardia characterised by QRS complexes of varying amplitude twisting around the isoelectric baseline - obligately associated with a prolonged QT interval.

Presentation

•Recurrent self-terminating episodes of palpitations, dizziness, presyncope

•Syncope - most clinically significant symptom

•Sudden cardiac death - in up to 10% as first presentation; TdP degenerates into VF

Investigations

•12-lead ECG - polymorphic VT with twisting QRS morphology; QTc >440 ms (men) or >460 ms (women) between episodes; QTc >500 ms = high risk

•Serum electrolytes (U&Es, Mg²⁺, Ca²⁺) - identify hypokalaemia, hypomagnesaemia, hypocalcaemia

•Drug history review - identify all QT-prolonging agents

•TFTs - hypothyroidism is a reversible cause

Differential diagnosis

TdP vs monomorphic VT vs VF

Feature	TdP	Monomorphic VT	VF
QRS morphology	Polymorphic - twisting amplitude	Regular, uniform	Chaotic - no QRS
QT interval	Prolonged	May be normal	Not assessable
Stable treatment	IV magnesium sulphate	IV amiodarone	N/A - pulseless
Unstable treatment	Synchronised DC cardioversion	Synchronised DC cardioversion	Defibrillation (unsynchronised)

🎯

IV magnesium sulphate = first-line for TdP regardless of serum magnesium level. IV amiodarone = first-line for stable monomorphic VT. DC cardioversion = any haemodynamically unstable tachyarrhythmia.

Management

Assess haemodynamic stability first. Markers of instability: systolic BP <90 mmHg, syncope, ongoing ischaemia, or heart failure. Identify and correct all reversible causes in parallel.

⚠️

Amiodarone must NOT be given for TdP - it blocks IKr potassium channels, further prolonging the QT interval and worsening the arrhythmia. It is correct for monomorphic VT but dangerous in TdP.

Causes of QT prolongation

It is the HYPO states that cause QT prolongation - hypercalcaemia and hypermagnesaemia do NOT cause TdP.

🧠

TIMES mnemonic for acquired QT prolongation: Toxins (heavy metals, hypothermia) · Ischaemia (acute MI) · Medications · Electrolytes (↓K⁺, ↓Mg²⁺, ↓Ca²⁺) · Subarachnoid haemorrhage

•Hypothermia - slows ion channel kinetics; repolarising K⁺ currents disproportionately affected; classic vignette = homeless patient found collapsed

•Electrolytes - hypokalaemia, hypomagnesaemia, hypocalcaemia

•QT-prolonging drugs - class Ia antiarrhythmics (quinidine, procainamide), class III (sotalol, amiodarone), macrolides (erythromycin, clarithromycin), antifungals (fluconazole), antipsychotics (haloperidol, quetiapine), tricyclic antidepressants, methadone