Paeds SAQs · acute-care-resuscitation-and-toxicology
Cardiotoxic and psychotropic medication poisoning — formative SAQs
Two MedVellum formative short-answer questions on the child or adolescent with cardiotoxic and psychotropic medication poisoning: reading the ECG and the toxidrome, giving hypertonic sodium bicarbonate for tricyclic antidepressant cardiotoxicity with a widened QRS, starting high-dose insulin euglycaemic therapy for severe beta-blocker and calcium channel blocker overdose, distinguishing calcium channel blocker hyperglycaemia, managing antipsychotic QT prolongation and neuroleptic malignant syndrome, and reserving lipid emulsion and extracorporeal support for refractory cases. The marks and timing support transparent self-assessment. They are not an official board format or pass standard.
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Target exams
SAQ 1 — An adolescent with a tricyclic antidepressant overdose
Question 1 — 10 formative marks; suggested time 15 minutes [2]
A 15-year-old girl is brought to the emergency department 90 minutes after a deliberate overdose of her mother's amitriptyline. She is drowsy, opens her eyes to voice, and has dry, flushed skin with dilated pupils. Her heart rate is 130, blood pressure 78/45, and the 12-lead ECG shows a QRS of 140 milliseconds with a tall R wave in lead aVR. [2]
- What is the diagnosis, and which ECG feature predicts the dominant threat? (2 marks)
- State the antidote, the dose, and the endpoint of therapy. (3 marks)
- Name two antiarrhythmics that must NOT be given for a ventricular arrhythmia in this patient, and explain why. (2 marks)
- Describe your escalation plan if the arrhythmia or the shock does not respond to the antidote. (3 marks)
Full-credit answer — SAQ 1
Reveal full-credit answer for SAQ 1
1. Diagnosis and ECG predictor
The diagnosis is tricyclic antidepressant cardiotoxicity from sodium-channel blockade, with an anticholinergic toxidrome. The QRS duration of 140 milliseconds is the predictor of the dominant threat of ventricular arrhythmia and shock: a QRS over 100 milliseconds in the poisoned child predicts sodium-channel blockade and the risk of ventricular arrhythmia. The tall R wave in lead aVR supports the diagnosis. [2]
2. Antidote, dose and endpoint
The antidote is hypertonic sodium bicarbonate, 1 to 2 mL per kilogram of 8.4 per cent intravenously (1 to 2 mmol per kg), repeated every few minutes to narrow the QRS and raise the serum pH to 7.45 to 7.55. The endpoints are a narrowed QRS, an improved blood pressure and the target pH. Hyperventilation in the intubated child adds an alkalinising effect. [2]
3. Contraindicated antiarrhythmics
The class Ia antiarrhythmics quinidine and procainamide and the class Ic antiarrhythmic flecainide must NOT be given, and amiodarone is avoided for the same reason. Each blocks the cardiac sodium channel and worsens the conduction blockade, widening the QRS further and promoting re-entrant ventricular arrhythmia. The ventricular arrhythmia of tricyclic poisoning is treated with sodium bicarbonate first, not with a sodium-channel-blocking antiarrhythmic. [2]
4. Escalation plan
If the arrhythmia or the shock does not respond to bicarbonate, I escalate to intravenous lipid emulsion (the lipid sink for this lipophilic drug), continue prolonged cardiopulmonary resuscitation if arrest occurs, and activate a veno-arterial extracorporeal membrane oxygenation service early because the window for cannulation is narrow. I called the senior team, intensive care, retrieval and the Poisons Information Centre in parallel, and I arrange a mental-health assessment once she is safe. [2]
SAQ 2 — A toddler with a sustained-release calcium channel blocker ingestion
Question 2 — 10 formative marks; suggested time 15 minutes [4]
A 14 kg three-year-old boy is brought in four hours after being found with his grandfather's open bottle of sustained-release verapamil. He currently looks well, with a heart rate of 80 and a blood pressure of 95/60. The bedside glucose is 11 mmol per L. The formulation is confirmed as sustained-release. [4]
- What is the most likely toxidrome, and what does the raised glucose indicate? (2 marks)
- State the key definitive therapy, the dose, and the two parameters monitored hourly. (3 marks)
- Why is a well-looking phase deceptive in this child, and what is the observation plan? (3 marks)
- Describe your escalation plan if the child develops shock. (2 marks)
Full-credit answer — SAQ 2
Reveal full-credit answer for SAQ 2
1. Toxidrome and the raised glucose
The most likely toxidrome is calcium channel blocker poisoning (L-type calcium-channel blockade), with bradycardia and hypotension to come and the vasodilation of the dihydropyridine or the myocardial depression of verapamil. The raised glucose is the bedside discriminator: calcium-channel blockade blocks insulin release from the pancreatic beta cell, producing hyperglycaemia that beta-blockade does not. This points to calcium and high-dose insulin euglycaemic therapy. [4]
2. Key therapy, dose and monitoring
The key definitive therapy is high-dose insulin euglycaemic therapy plus intravenous calcium. I give insulin 1 unit per kilogram intravenous bolus then 0.5 to 1 unit per kilogram per hour, with a concurrent dextrose infusion to maintain euglycaemia. I give calcium gluconate 10 per cent, 0.6 mL per kilogram (60 mg per kg), or calcium chloride 10 per cent, 0.2 mL per kilogram (20 mg per kg), repeated. The two parameters monitored hourly are the blood glucose and the serum potassium, replacing potassium to keep it above 4 mmol per L. [3] [4]
3. The well-looking phase and the observation plan
The formulation is sustained-release, and sustained-release calcium channel blockers are the classic late-deteriorator: the child looks well for several hours and then descends into refractory shock as absorption continues. The well-looking phase is deceptive and does not exclude danger. The observation plan is admission for continuous cardiac monitoring and observation for at least 12 to 24 hours, with calcium and high-dose insulin ready and frequent reassessment of the ECG and the perfusion. [4]
4. Escalation plan for shock
If shock develops, I start the calcium and high-dose insulin euglycaemic therapy early, add vasopressors, and prepare intravenous lipid emulsion for refractory cases. I activate retrieval and an extracorporeal service early, before local support is exceeded, because veno-arterial ECMO bridges refractory calcium channel blocker overdose to recovery. I run poison-prevention counselling and safeguarding alongside the medical care. [4]
References
- [2]Chan, Brandon S; Buckley, Nicholas A Common pitfalls in the use of hypertonic sodium bicarbonate for cardiac toxic drug poisonings Clinical Toxicology (Philadelphia), 2024.PMID 38597366
- [3]Roperia, Vikrant; Kiani, Ahsan Zaheer High-Dose Insulin Euglycemic Therapy in Concomitant Beta-Blocker and Calcium Channel Blocker Overdose Journal of Investigative Medicine High Impact Case Reports, 2025.PMID 40642834
- [4]Suarez, Francis; Koyfman, Alex Pearls and Pitfalls for the Emergency Clinician: Beta Blocker and Calcium Channel Blocker Toxicity Journal of Emergency Medicine, 2026.PMID 41833262
- [7]Besag, Frank M C; Vasey, Maxine J Neurological Adverse Effects of Antipsychotic Medication in Children and Young People Paediatric Drugs, 2026.PMID 41498920