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The poisoned patient: toxidromes and antidotes

Critical care, resuscitation and trauma·~5 min read· Physician-reviewed✓ Sourced · 5

Stem

A 26-year-old woman, 60 kg, is brought to the emergency department an hour after swallowing her mother's amitriptyline. Her Glasgow Coma Scale is 8, heart rate 128, blood pressure 82/48 mmHg, temperature 38.2 °C. Her pupils are 7 mm, her skin is hot, flushed and dry, and bowel sounds are absent. The ECG shows sinus tachycardia with a QRS of 150 ms and a 4-mm R wave in aVR. You are called to secure her airway.

Question

What toxidrome is this, and how will you manage her?

Ideal answer

HeadlineAn anticholinergic toxidrome with sodium-channel blockade: tricyclic overdose. The wide QRS is the killer, so bicarbonate starts before I touch the airway.

  1. Sodium bicarbonate 2 mEq/kg, about 120 mEq, now, repeated every few minutes against the QRS, aiming for pH 7.50–7.55.1
  2. After a bicarbonate bolus, rapid sequence intubation, reduced-dose induction; then I match her pre-intubation minute ventilation so CO2 never rises, with bicarbonate still the primary therapy.1
  3. Fluids, norepinephrine, benzodiazepines. Crystalloid 10–20 mL/kg, norepinephrine for alpha-blockade hypotension, benzodiazepines for seizures.1
  4. Avoid what worsens it: no physostigmine, no class Ia, Ic or III antiarrhythmics.2
  5. Rescue if refractory: lipid emulsion, hypertonic saline, ECMO, and the poison center early.1

Watch for: QRS back to her baseline or below 140 ms; gases every 30 minutes, pH 7.50–7.55, never higher; sodium ≤155; falling potassium.1

Breaking down the answer

  • Reading the toxidrome — hyperthermia, flushed dry skin, dilated pupils, delirium, ileus and urinary retention are anticholinergic; hypotension adds alpha blockade; QRS widening is sodium-channel block.2 Changes if: miosis, secretions and bradycardia; that is cholinergic poisoning.
  • The ECG grades the risk — QRS over 100 ms predicts seizures, over 160 ms ventricular arrhythmias; an aVR R wave over 3 mm adds weight.1 Changes if: the QRS is normal; I still monitor for hours.
  • Why bicarbonate works — the sodium load and alkalosis narrow the QRS, treat arrhythmias and raise pressure, even without acidosis.2 Changes if: I reach 6 mmol/kg; I call a toxicologist first.1
  • The arrhythmia drug — lidocaine 1–1.5 mg/kg then an infusion, because amiodarone and procainamide deepen the block.1 Changes if: the rhythm is pulseless; ACLS with continued bicarbonate.
  • The cholinergic contrast — atropine 2–5 mg, doubled every 3–5 minutes until secretions dry and bronchoconstriction resolves; pralidoxime 30 mg/kg over 30 minutes, then at least 8 mg/kg/h.3 Changes if: staff exposure; protective equipment and decontamination come first.3

Follow-up question

Her partner arrives with an empty bottle of amlodipine as well. An hour later, intubated and alkalinized with a QRS of 112 ms, her blood pressure is 70/40 and heart rate 52 despite norepinephrine 0.3 mcg/kg/min. What now?

Follow-up answer

HeadlineCalcium-channel blocker poisoning on top of the tricyclic: vasoplegic, bradycardic shock. I say so and change the drugs.

Calcium chloride 1–2 g every 10–20 minutes, then high-dose insulin: 1 unit/kg bolus and 1 unit/kg/h, with dextrose for euglycemia and close potassium checks, because bicarbonate has already lowered it.4 Norepinephrine or epinephrine continue; atropine or pacing for symptomatic bradycardia. If echo shows poor contractility, I titrate insulin up to 10 units/kg/h; refractory shock gets lipid emulsion, and refractory cardiogenic shock VA-ECMO.4

Pitfalls that cost points

  • Stacking aggressive hyperventilation on bicarbonate: severe alkalosis.2
  • Succinylcholine in organophosphate poisoning: plasma cholinesterase is inhibited, so its metabolism, and the paralysis, is markedly prolonged.3
  • Trusting a normal SpO2 after smoke or carbon monoxide exposure.

Rapid-fire

Q: Smoke inhalation with lactic acidosis: the antidote? A: Hydroxocobalamin 5 g IV over 15 minutes, a second 5 g if needed; not in the same line as sodium thiosulfate.5

Q: What will hydroxocobalamin do to the labs? A: Red skin and urine, colorimetric assay interference and false blood-leak alarms on dialysis machines.5

Q: The atropine endpoint in organophosphate poisoning? A: Dry respiratory secretions and no bronchoconstriction; dry skin, mydriasis and tachycardia are only supporting signs.3

Q: Which first-line drugs for calcium-channel blocker shock? A: IV calcium, high-dose insulin and norepinephrine or epinephrine.4

Q: Benzocaine spray and gray skin, SpO2 85%? A: Methemoglobinemia: co-oximetry, then methylene blue unless G6PD-deficient; see methemoglobinemia-carboxyhemoglobin.

Numbers to know

Item Value
Sodium bicarbonate 2 mEq/kg boluses; toxicologist at 6 mEq/kg1
Targets pH 7.50–7.55, sodium ≤1551
QRS risk >100 ms seizures; >160 ms arrhythmias1
High-dose insulin 1 U/kg, then 1 U/kg/h, up to 104
Calcium chloride 10% 1–2 g every 10–20 min4
Hydroxocobalamin 5 g over 15 min; total 10 g5
Pralidoxime 30 mg/kg, then ≥8 mg/kg/h3

Sources

  1. 1.Tricyclic antidepressant toxicity · Life in the Fast Lane (LITFL) Critical Care Compendium · litfl.comBicarbonate 2 mmol/kg (100 mmol) boluses; call a toxicologist at 6 mmol/kg; target pH 7.50-7.55, sodium <=155.
  2. 2.Tricyclic antidepressant overdose · OpenAnesthesia (IARS) · openanesthesia.org
  3. 3.Organophosphate poisoning · OpenAnesthesia (IARS) · openanesthesia.org
  4. 4.Experts Consensus Recommendations for the Management of Calcium Channel Blocker Poisoning in Adults · Critical Care Medicine (St-Onge et al.), 2017 · ebi.ac.ukFull text via Europe PMC (PMC5312725, PMID 27749343).
  5. 5.Cyanokit (hydroxocobalamin) Prescribing Information · Drugs.com (FDA label) · drugs.com

Facts on this page were checked against these sources on Oct 22, 2026. Guidelines change; confirm doses against current institutional protocols.

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