Life-threatening adverse drug reactions causing - cardiac arrhythmias, such as, tachy and brady arrhythmias or cardiac conduction blocks

Description

Drug-induced cardiac arrhythmias and conduction block span tachyarrhythmias (QT prolongation-driven torsades de pointes being the classic mechanism), bradyarrhythmias (AV nodal blockade from beta-blockers, calcium channel blockers, digoxin), and direct conduction system toxicity - recognising a drug cause is essential since withdrawal of the causative agent is often the primary treatment

A recognised complication across numerous drug classes (antiarrhythmics themselves, antipsychotics, certain antibiotics, antidepressants, and others), given how many medications affect cardiac ion channels or autonomic tone

QT-prolonging drugs block the rapid delayed rectifier potassium current (IKr), prolonging ventricular repolarisation and creating substrate for torsades de pointes, particularly with additional risk factors (electrolyte disturbance, bradycardia, female sex, congenital long QT); AV nodal blocking agents (beta-blockers, non-dihydropyridine calcium channel blockers, digoxin) can cause excessive bradycardia/heart block, particularly when combined or with pre-existing conduction disease

ECG monitoring (QT interval, PR interval, heart rate) before and during treatment with known arrhythmogenic agents, with particular attention when starting/up-titrating or combining multiple QT-prolonging or AV nodal blocking drugs
Electrolyte correction (potassium, magnesium) reduces torsades risk and should be checked when a QT-prolonging drug is being used, particularly in unwell/hospitalised patients

Immediate causative drug withdrawal is the primary intervention for most drug-induced arrhythmias
Torsades de pointes: IV magnesium regardless of measured magnesium level, correction of other electrolytes, and temporary pacing/isoprenaline to increase heart rate if recurrent
Symptomatic bradycardia/heart block: drug withdrawal, atropine, and temporary pacing if haemodynamically significant

Combination QT-prolonging drug use (additive risk, a common prescribing error), hypokalaemia/hypomagnesaemia as risk amplifiers for torsades, digoxin toxicity and conduction block, beta-blocker/calcium channel blocker combination bradycardia risk

Torsades de pointes is treated with intravenous magnesium regardless of the measured serum magnesium level - this is a specific, frequently tested exception to the general principle of confirming a deficiency before treating it, reflecting magnesium's role in stabilising cardiac membrane excitability independent of correcting a measured deficiency

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