Key Facts

Torsades de Pointes (TdP) is a specific form of polymorphic ventricular tachycardia that occurs in the setting of QT interval prolongation. The name ('twisting of the points') describes the characteristic ECG pattern where the QRS complexes appear to rotate around the isoelectric baseline.

Epidemiology

• Exact incidence is difficult to determine; many episodes are self-terminating
• Drug-induced QT prolongation is the most common cause in clinical practice
• Women have a longer baseline QTc and are at higher risk of drug-induced TdP
• Congenital long QT syndrome prevalence: ~1 in 2,000

Aetiology

Acquired (most common):

• Drugs: class Ia/III antiarrhythmics (sotalol, amiodarone, quinidine), macrolide antibiotics, fluoroquinolones, antipsychotics (haloperidol, droperidol), methadone, tricyclic antidepressants
• Electrolyte disturbances: hypokalaemia, hypomagnesaemia, hypocalcaemia
• Bradycardia (pause-dependent TdP)
• Myocardial ischaemia, hypothermia, starvation

Congenital:

• Romano-Ward syndrome (autosomal dominant, isolated long QT)
• Jervell and Lange-Nielsen syndrome (autosomal recessive, long QT + sensorineural deafness)
• Multiple genetic subtypes: LQT1 (KCNQ1), LQT2 (KCNH2/HERG), LQT3 (SCN5A)

Pathophysiology

• QT prolongation reflects delayed ventricular repolarisation
• This creates a vulnerable period during which early afterdepolarisations (EADs) may trigger re-entrant circuits
• EADs are more likely at slow heart rates ('pause-dependent' TdP)
• The polymorphic QRS morphology arises from shifting re-entrant circuits or triggered activity from multiple foci

Typical Presentation

• Palpitations, dizziness, presyncope, or syncope
• May be self-terminating (brief episodes) or sustained
• Sustained TdP may degenerate into ventricular fibrillation and cause cardiac arrest

ECG Features

• Preceding prolonged QT interval (QTc >500 ms is high risk)
• Polymorphic wide-complex tachycardia with progressive change in QRS amplitude and axis
• 'Twisting' of QRS complexes around the baseline
• Often initiated by a 'short-long-short' sequence (premature beat, compensatory pause, then TdP onset)
• Rate typically 150-300 bpm

Red Flags

• Haemodynamic compromise: hypotension, reduced consciousness
• Pulseless VT/VF requiring immediate defibrillation
• Recurrent syncope in a patient with known QT prolongation
• Family history of sudden cardiac death (consider congenital long QT)
• Multiple QT-prolonging drugs in combination

Bedside

• 12-lead ECG: QT interval measurement (correct for heart rate using Bazett formula: QTc = QT/√RR), rhythm strip
• Continuous cardiac monitoring: capture transient arrhythmias
• Observations: BP, HR, SpO₂

Bloods

• U&Es: potassium, magnesium, calcium levels (critical)
• Magnesium level: often low even when serum appears normal
• Calcium (corrected): hypocalcaemia prolongs QT
• TFTs: hypothyroidism can prolong QT
• Drug levels: if on medications known to prolong QT

Imaging

• Echocardiography: structural heart disease assessment
• Cardiac MRI: if structural cause suspected

Special Tests

• Genetic testing: if congenital long QT syndrome suspected (KCNQ1, KCNH2, SCN5A)
• Pharmacogenomic assessment: in families with drug-induced TdP
• Signal-averaged ECG: late potentials

Non-pharmacological

• Remove causative agents: stop all QT-prolonging drugs immediately
• Correct electrolyte abnormalities: target K⁺ >4.5 mmol/L, Mg²⁺ >1.0 mmol/L
• Continuous cardiac monitoring in a high-dependency setting
• DC cardioversion (synchronised if organised rhythm, unsynchronised if VF/pulseless) if haemodynamically unstable

Pharmacological

• IV magnesium sulphate 2g (8 mmol) over 10-15 minutes as first-line, even if serum Mg²⁺ is normal
• Repeat magnesium 2g if TdP recurs
• IV potassium replacement: aim K⁺ >4.5 mmol/L (40 mmol KCl in 1L NaCl over 4 hours, or faster via central line if critical)
• Isoprenaline infusion (1-10 mcg/min): increases heart rate, shortens QT interval; useful for pause-dependent TdP
• IV calcium gluconate: if hypocalcaemia contributing
• AVOID: amiodarone, sotalol, procainamide, and all other QT-prolonging agents
• For congenital long QT: beta-blockers (nadolol, propranolol) for long-term prevention

Surgical/Interventional

• Temporary transvenous overdrive pacing: rate 90-110 bpm to suppress pause-dependent TdP when pharmacological measures fail
• ICD implantation: for survivors of cardiac arrest due to congenital long QT, or recurrent TdP despite medical therapy
• Left cardiac sympathetic denervation: for refractory congenital long QT syndrome

Referral Criteria

• All patients with TdP should be managed in a monitored setting
• Referral to electrophysiology for recurrent TdP or suspected congenital long QT
• Genetic counselling and family screening for congenital long QT syndrome

• Untreated sustained TdP: high mortality due to degeneration into VF
• With prompt treatment (magnesium, pacing), prognosis is excellent for acquired TdP
• Congenital long QT with beta-blocker therapy: annual event rate ~1-2%
• ICD reduces sudden death risk in high-risk congenital long QT to <2% per year
• Drug-induced TdP: recurrence unlikely if offending drug avoided
• LQT3 (SCN5A) carries the highest risk of fatal arrhythmia per event

Common QT-Prolonging Drugs (Exam Favourites)

QTc Risk Thresholds