Specific electrocardiogram changes in drug toxicity

Role

Specific ECG changes support toxicological clinical assessment across several important overdose/toxicity scenarios - QRS widening in sodium channel-blocking drug overdose (tricyclic antidepressants classically), QT prolongation with numerous drug classes, and characteristic changes with digoxin toxicity and electrolyte-disturbing toxins - making a 12-lead ECG a routine, high-yield investigation in suspected significant drug toxicity
Performed routinely in any patient with suspected significant drug overdose or toxicity, given the ECG's speed, availability, and direct relevance to both diagnosis and risk stratification for several major toxicological scenarios

QRS widening reflects sodium channel blockade slowing ventricular depolarisation - classically seen in tricyclic antidepressant overdose, where QRS duration correlates with seizure and arrhythmia risk and directly guides the decision to treat with sodium bicarbonate
QT prolongation reflects delayed repolarisation from potassium channel blockade (numerous drug classes) or electrolyte disturbance, predicting torsades de pointes risk
Digoxin toxicity produces characteristic changes (any arrhythmia is possible, though bidirectional ventricular tachycardia is classically described) alongside the more common non-toxic finding of ST segment "sagging" seen at therapeutic digoxin levels (distinct from toxicity)

Serial ECG monitoring (not a single assessment) is important given that toxicity/QRS-QT changes can evolve over the following hours as drug absorption and distribution continue, particularly relevant in overdose with sustained-release preparations
ECG findings should be interpreted alongside the clinical history and other toxicological findings rather than in isolation, since several toxidromes can produce overlapping ECG changes

QRS widening in tricyclic overdose -> sodium bicarbonate, titrated to QRS narrowing, alongside standard supportive care
Significant QT prolongation -> magnesium, correction of other electrolyte disturbances, and avoidance of further QT-prolonging drug exposure
Digoxin toxicity with significant arrhythmia -> digoxin-specific antibody fragments in addition to standard arrhythmia management

Tricyclic antidepressant overdose QRS widening and sodium bicarbonate treatment (a frequently tested, specific mechanism-targeted intervention), digoxin's characteristic ECG changes at both therapeutic and toxic levels, QT prolongation risk stratification for torsades de pointes
QRS duration on ECG in tricyclic antidepressant overdose is not just a diagnostic marker but directly guides treatment - sodium bicarbonate is titrated against serial QRS measurements, narrowing the QRS as treatment succeeds in reducing the sodium channel blockade effect, making the ECG a real-time treatment-response monitoring tool in this specific toxicological scenario, not just a one-off diagnostic test

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