Drug-induced prolonged QT and arrhythmias

Overview

Drug-induced QT prolongation occurs when drugs block the hERG (IKr) potassium channel, slowing phase 3 repolarisation. This prolongs the action potential, predisposes to early afterdepolarisations (EADs), and can trigger torsades de pointes (TdP) - a polymorphic VT that may degenerate into VF.

QTc calculated using Bazett formula: QTc = QT / √RR
Prolonged QTc: >440 ms (males), >460 ms (females); QTc >500 ms = high-risk threshold

Risk factors

Risk factors for drug-induced QT prolongation
Female sex
Advanced age
Pre-existing cardiac disease / heart failure
Congenital long QT syndrome (even subclinical)
Hypokalaemia
Hypomagnesaemia
Hypocalcaemia
Bradycardia
Polypharmacy with multiple QT-prolonging drugs
CYP3A4 inhibitors raising drug plasma levels
IV route of administration
High doses

Presentation

Palpitations - often first symptom; self-terminating TdP episode
Pre-syncope / syncope - sudden onset, rapid recovery if TdP self-terminates
Cardiac arrest - TdP degenerating to VF; may be first presentation
Incidental ECG finding - QTc prolongation on routine monitoring
🎯
Syncope in a patient recently started on a new antibiotic, antipsychotic, or antiemetic - always do an ECG. TdP on ECG appears as polymorphic VT with QRS complexes twisting around the isoelectric baseline.

Investigations

🥇 First-line

12-lead ECG - measure QTc in leads II, V5, or V6; identify TdP if present
Serum electrolytes (U&Es, magnesium, calcium) - correct hypokalaemia, hypomagnesaemia, hypocalcaemia
Full drug history - identify all QT-prolonging agents and CYP3A4 interactions
Continuous cardiac monitoring / telemetry - if QTc >500 ms or symptomatic

🥈 Second-line

Holter monitoring - paroxysmal TdP in unexplained syncope on QT-prolonging drugs
Genetic testing for congenital long QT syndrome - if strong family history, recurrent TdP, or disproportionate QT prolongation

Management

Step 1 · Acute TdP
  1. 1Withdraw causative drug immediately
  2. 2IV magnesium sulphate 2 g over 10-15 min - first-line for TdP even if magnesium is normal
  3. 3Correct hypokalaemia - target K⁺ >4.0 mmol/L with IV potassium
  4. 4Continuous cardiac monitoring
  5. 5Cardiology review
TdP self-terminates
Continue monitoring; correct electrolytes; identify and remove all QT-prolonging drugs; QTc typically normalises within 24-72 hours
TdP degenerates to VF / haemodynamic compromise
Immediate DC cardioversion / defibrillation per ALS protocol; consider overdrive pacing to shorten QT
Step 2 · QTc prolongation found incidentally (no TdP)
  1. 1Withdraw or reduce dose of causative drug
  2. 2Correct electrolyte disturbances
  3. 3Review all co-prescribed QT-prolonging agents
  4. 4Repeat ECG after correction
Step 3 · Long-term follow-up
  1. 1Cardiac follow-up to exclude congenital long QT syndrome
  2. 2Add clear medication alert to patient records
  3. 3Inform future prescribers

Causative drug classes

Macrolide antibiotics - erythromycin, clarithromycin
Antiemetics - domperidone, ondansetron (dose-dependent; avoid IV where oral suffices)
Antipsychotics - haloperidol, amisulpride, pimozide
Antiarrhythmics - class Ia (quinidine, procainamide), class III (amiodarone, sotalol)
Antihistamines - mizolastine
Antimalarials - chloroquine, quinine
Other - ivabradine, tolterodine, some antifungals and antivirals

Prevention and contraindicated combinations

Check full drug history before prescribing - avoid two or more QT-prolonging drugs concurrently
Check and correct electrolytes before starting high-risk agents
Baseline ECG in high-risk patients (cardiac disease, known electrolyte disturbances, IV QT-prolonging drugs)
Use lowest effective dose and shortest course; prefer oral over IV where possible
Do not prescribe macrolides to patients with prior QT prolongation, prior TdP, or significant electrolyte disturbances
⚠️

Contraindicated combinations:

  • Erythromycin or clarithromycin + domperidone
  • Erythromycin or clarithromycin + pimozide
  • Erythromycin + mizolastine, tolterodine, or amisulpride
  • Clarithromycin + ivabradine (CYP3A4 inhibition raises ivabradine levels AND additive QT risk)

If a macrolide is essential and a contraindicated combination exists, seek microbiologist advice for an alternative antibiotic (e.g. doxycycline).

💡
Macrolides inhibit CYP3A4 and raise plasma levels of co-prescribed QT-prolonging drugs metabolised by this enzyme, compounding electrophysiological risk beyond the direct QT effect.