Tricyclic Antidepressant Poisoning
On this page
Direct answer
Tricyclic antidepressant poisoning is toxicity from sodium channel blockade in the heart and brain, combined with anticholinergic effects. A QRS width above 100 milliseconds predicts seizures, and above 160 milliseconds ventricular arrhythmias, making the ECG the most useful bedside marker. Sodium bicarbonate is the mainstay of treatment, aiming to narrow the QRS and correct acidosis, while physostigmine is generally avoided.
What you must remember
- Anticholinergic toxidrome: dry skin, mydriasis, urinary retention, hyperthermia, tachycardia, ileus and agitation or delirium, caused by muscarinic blockade.
- QRS width: above 100 milliseconds predicts seizures and above 160 milliseconds ventricular arrhythmias, and a terminal R wave in lead aVR above 3 mm is another strong marker of toxicity.
- Sodium bicarbonate: an intravenous bolus of about 1 to 2 mEq/kg, aiming for an arterial pH near 7.5 and a narrower QRS.
- Seizures: benzodiazepines are the first-line treatment, and physostigmine can precipitate asystole and should be avoided.
- Hypotension: intravenous fluids first, with norepinephrine if the hypotension persists despite fluids.
- Antiarrhythmics: class IA agents such as quinidine and procainamide add to sodium channel blockade, and class III agents are generally avoided.
- Common agents: amitriptyline is the agent most often implicated in many series, and it is among the most toxic of the commonly used tricyclics.
- Rescue therapy: lipid emulsion is used for refractory cardiovascular collapse, under specialist guidance.
A stepwise approach to a tricyclic overdose
Tricyclic toxicity unfolds in a predictable sequence, and the ECG gives the earliest warning of what is coming.
- Recognise the toxidrome: check pupils, skin, bowel sounds, urinary retention and temperature to confirm an anticholinergic picture.
- Read the ECG: measure the QRS width and look for a terminal R wave in aVR, since a QRS above 100 milliseconds defines high risk.
- Give bicarbonate: a bolus of sodium bicarbonate, repeated or followed by an infusion as the ECG and blood gas direct, aiming for a pH near 7.5 and a narrower QRS.
- Control seizures: benzodiazepines come first, and physostigmine is avoided because it can precipitate asystole.
- Support blood pressure: intravenous fluids come first, with norepinephrine if hypotension persists, while class IA and III antiarrhythmics are avoided.
- Consider lipid emulsion: reserve it for refractory cardiac toxicity, under specialist guidance.
- Monitor until stable: continue cardiac monitoring until the QRS has normalised and the patient is clinically stable, since the QRS can re-widen.
Where the exam tries to catch you
Most errors come from treating tricyclic toxicity as a simple psychiatric or anticholinergic problem.
- Trap: giving physostigmine for an agitated, tachycardic patient after a tricyclic overdose Correct: physostigmine can cause asystole and seizures, so it is generally avoided in tricyclic toxicity.
- Trap: treating a wide QRS with a class IA antiarrhythmic Correct: these worsen sodium channel blockade; sodium bicarbonate is the drug of choice.
- Trap: judging severity by consciousness or pupil size alone Correct: QRS width and the aVR terminal R wave predict arrhythmia better, so the ECG is the key prognostic tool.
- Trap: calling the patient safe once the QRS narrows, without observation Correct: the QRS can re-widen, so monitoring continues until the patient is stable.
Frequently asked questions
Why is QRS width important in tricyclic antidepressant poisoning?
QRS width is important in tricyclic antidepressant poisoning because a QRS above 100 milliseconds predicts seizures and above 160 milliseconds ventricular arrhythmias. It also guides sodium bicarbonate therapy, so it serves as both a severity marker and a treatment target.
Why is physostigmine avoided in tricyclic antidepressant poisoning?
Physostigmine is generally avoided in tricyclic antidepressant poisoning because it can precipitate asystole, seizures and bradyarrhythmias. It is reserved for pure anticholinergic syndromes without cardiac or seizure features, and only under specialist supervision.
What dose of sodium bicarbonate is used for tricyclic toxicity?
Sodium bicarbonate is given as an intravenous bolus of about 1 to 2 mEq/kg in tricyclic antidepressant poisoning, aiming for an arterial pH near 7.5 and a narrower QRS. Repeated boluses or an infusion are used as the ECG and blood gas direct.
Which antiarrhythmics should be avoided in tricyclic antidepressant poisoning?
Class IA antiarrhythmics such as quinidine and procainamide should be avoided in tricyclic antidepressant poisoning, because they add to sodium channel blockade. Class III agents such as amiodarone are also generally avoided, and sodium bicarbonate is preferred for a wide QRS.
What is the anticholinergic toxidrome of a tricyclic overdose?
The anticholinergic toxidrome of a tricyclic overdose causes dry skin, mydriasis, urinary retention, hyperthermia, tachycardia, ileus and agitation or delirium. It results from muscarinic receptor blockade and often occurs alongside the sodium channel effects on the heart.