Tricyclic Overdose (Sodium-Channel Blocker Toxicity)


The ECG is a vital tool in the prompt diagnosis of poisoning with sodium-channel blocking medications such as:

  • Tricyclic antidepressants (= most common)
  • Type Ia antiarrhythmics (quinidine, procainamide)
  • Type Ic antiarrhythmics (flecainide, encainide)
  • Local anaesthetics (bupivacaine, ropivacaine)
  • Antimalarials (chloroquine, hydroxychloroquine)
  • Dextropropoxyphene
  • Propranolol
  • Carbamazepine
  • Quinine

The two main adverse effects of sodium-channel blocker poisoning are seizures and ventricular dysrhythmias (due to blockade of sodium channels in the CNS and myocardium)

Handy tip: An ECG should be taken in all patients who present with a deliberate self-poisoning (or altered GCS of unknown aetiology) to screen for TCA overdose.

Typical example of TCA toxicity

Electrocardiographic Features of Sodium-Channel Blockade

Features consistent with sodium-channel blockade are:

Fast sodium channel blockade

Dominant secondary R wave (R') in aVR > 3mm

Patients with tricyclic overdose will also usually demonstrate sinus tachycardia secondary to muscarinic (M1) receptor blockade.

Clinical Features of Tricyclic Overdose

In overdose, the tricyclics produce rapid onset (within 1-2 hours) of:

  • Sedation and coma
  • Seizures
  • Hypotension
  • Tachycardia
  • Broad complex dysrhythmias
  • Anticholinergic syndrome

Tricyclics mediate their cardiotoxic effects via blockade of myocardial fast sodium channels (QRS prolongation, tall R wave in aVR), inhibition of potassium channels (QTc prolongation) and direct myocardial depression. Other toxic effects are produced by blockade at muscarinic (M1), histamine (H1) and α1-adenergic receptors.

The degree of QRS broadening on the ECG is correlated with adverse events:

  • QRS > 100 ms is predictive of seizures
  • QRS > 160 ms is predictive of ventricular arrhythmias (e.g. VT)

Management of Significant Tricyclic Overdose (> 10mg/kg) with Signs of Cardiotoxicity (ECG changes)

  • Patients need to be managed in a monitored area equipped for airway management and resuscitation.
  • Secure IV access, adminster high flow oxygen and attach monitoring equipment.
  • Administer IV sodium bicarbonate 100 mEq (1-2 mEq / kg); repeat every few minutes until BP improves and QRS complexes begin to narrow.
  • Intubate as soon as possible.
  • Hyperventilate to maintain a pH of 7.50 – 7.55.
  • Once the airway is secure, place a nasogastric tube and give 50g (1g/kg) of activated charcoal.
  • Treat seizures with IV benzodiazepines (e.g. diazepam 5-10mg).
  • Treat hypotension with a crystalloid bolus (10-20 mL/kg). If this is unsuccessful in restoring BP then consider starting vasopressors (e.g. noradrenaline infusion).
  • If arrhythmias occur, the first step is to give more sodium bicarbonate. Lidocaine (1.5mg/kg) IV is a third-line agent (after bicarbonate and hyperventilation) once pH is > 7.5.
  • Avoid Ia (procainamide) and Ic (flecainide) antiarrhythmics, beta-blockers and amiodarone as they may worsen hypotension and conduction abnormalities.
  • Admit the patient to the intensive care unit for ongoing management.

Example ECGs

Example 1a – TCA overdose

Typical ECG of TCA toxicity demonstrating:

  • Sinus tachycardia with first-degree AV block (P waves hidden in the T waves, best seen in V1-2).
  • Broad QRS complexes.
  • Positive R’ wave in aVR.


Example 1b – Worsening TCA toxicity

  • A second ECG of the same patient showing worsening TCA cardiotoxicity with marked QRS broadening producing a sine wave appearance reminiscent of hyperkalaemia.


Example 1c – Resolution of TCA toxicity with treatment (bicarbonate and hyperventilation)

  • Third ECG of the same patient after serum alkalinisation with sodium bicarbonate, intubation and hyperventilation.
  • The QRS duration has narrowed back to normal and the R’ wave in aVR has disappeared.


Example 2 – Massive TCA overdose

  • Another example of severe TCA cardiotoxicity after ingestion of 35 mg/kg doxepin.
  • There is marked QRS widening with tachycardia and a positive R’ wave in aVR.


Example 3 – Flecainide overdose

  • Similar ECG changes are seen with other sodium-channel blocking agents.
  • This ECG demonstrates QRS widening and positive R’ wave in aVR consistent with sodium-channel blockade in a patient with flecainide poisoning.


Example 4 – Flecainide overdose

  • Another example of flecainide cardiotoxicity.


Further Reading

Author Credits


  • Cameron P, Jelinek G, Kelly AM, Murray L, Brown AFT. Textbook of Adult Emergency Medicine (3rd edition), Churchill Livingstone Elsevier 2009.
  • Hutchinson MD, Traub SJ. Tricyclic Antidepressant Poisoning. Up To Date, 2008.
  • Life in the Fast Lane. Toxicology Conundrum 022 — Tricyclic antidepressant toxicity.
  • Murray L, Daly F, Little M, Cadogan M. Toxicology Handbook (second edition). Elsevier, 2011.
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  1. says

    We should get away from using mEq as they are not routinely used in teaching or prescribing. It so happens because of valence that sodium bicarb is mmol = mEq. So why not say mmol. Also 1ml = 1mmol = 1 mEq for 8.4% solution so you could say mls and stop all confusion. Don.