How to recognize TCA toxicity

We learnt how to recognize TCA toxicity via discussion of a case of a 54 yo F who was brought in unresponsive by EMS after her son called 911. She had a PMH of HCV, prior opioid abuse, depression who was on several medications including toprol, lisinopril, ASA, chlorthalidone, celexa, buspirone, mirtazipine, amitryptiline, MS Contin, klonipin and oxycodone.

On exam she was found to be hypertensive at 205/110 with sinus tachycardia at 130s breathing at 15. She was noted to be very flushed, warm/dry skin, pupils 4mm minimally reactive with no focal neurological findings.

Her EKG was noted to be have a triad which should raise suspicion of TCA toxicity consisting of the following:

  1. prolonged QTc
  2. prolonged QRS (interventricular conduction delay) (due to blockade of fast Na channels in conduction system)
  3. sinus tachycardia (due to vagolytic effect) This triad should raise suspicion of TCA cardiac toxicity

A specific finding also seen in TCA toxicity is a large (>3mm) R wave in avR (which this patient did not have).

Treatment: If QRS is prolonged (>120) then patient should receive IV pushed of hypertonic NaHC03 followed by bicarb gtt (3 amps in 1L D5W @250cc/hr) and QRS is to be monitored alongwith a goal pH of 7.5-7.55. This molecule is lipophilic and thus non-dialyzable. To also contact poison control for assisstance.

Reference articles: Guidelines for management of TCA toxicity; EKG manifestations of TCA cardiac toxicity; aVR in TCA toxicity;