TCA toxicity

Learning objectives

Tricyclic antidepressants (TCAs) are used to treat depression, chronic pain, and some forms of acute pain
The mode of action is by the prevention of presynaptic re-uptake of norepinephrine and serotonin
- Also anti-muscarinic, antihistaminergic, and anti-a1-adrenergic effects
TCA toxicity is caused by excessive medication of:
- Amitriptyline
- Imipramine
- Nortriptyline
- Doxepin
- Dothiepin
- Clomipramine
TCAs have a narrow therapeutic index which carries a high risk of toxicity
Most poisoning presentations are from acute ingestion; however chronic poisoning can also present acutely
A dose >10mg/kg can be potentially life-threatening
Severe toxicity usually manifests itself within 2 and no later than 6 hours after ingestion
Exclude co-ingestion of other toxic agents (eg. paracetamol)
Excess sodium bicarbonate can be lethal due to severe hypernatremia, hypokalemia, and alkalemia, don’t give more than 6 mmol/kg
The goals of sodium bicarbonate treatment are:
- pH 7.5-7.55
- Max. Na 155 mmol/L
- QRS <140 ms

Anticholinergic effects	Fever Inability to sweat Dry mouth Mydriasis Blurred vision Constipation Urinary retention
Cardiovascular effects	Sinus tachycardia Hypotension ABG: mixed acidosis with both respiratory depression and ↑ lactate ECG: QRS and PR/QT prolongation Large terminal R wave in aVR, Predisposing to broad complex tachyarrhythmia (VT)
Central nervous system	Change in mental status Agitation Seizures Coma

TCA toxicity, ECG, sodium bicarbonate, benzodiazepines, crystalloids, activated charcoal, VA-ECMO, vasopressords cardioversion