Branching cross-examination

This is a MedVellum formative viva. It is not an official RACP, MRCPCH, ABP, ACGME or RCPSC station, mark scheme, duration or pass standard. Release each update only after the candidate states the failing system, the immediate action and the reassessment endpoint. [2] [4]

Candidate brief

You are the senior paediatric clinician in a rural district emergency department. Speak as you would during resuscitation. Read the ECG and the toxidrome; give the antidote on its trigger; avoid the class Ia and Ic antiarrhythmic trap; prepare the rescue therapies for refractory poisoning; and escalate to retrieval and extracorporeal support before local support is exceeded. This is one continuous case. Each escalation branch leads to the next update. [4]

Question 1 — The doorway and the ECG

Stimulus update. A 16-year-old is brought by ambulance after a deliberate overdose of unknown tablets. She is drowsy, with dry flushed skin and dilated pupils. Her heart rate is 130, blood pressure 78/45, and the 12-lead ECG shows a QRS of 150 milliseconds with a tall R wave in aVR. Question: What do you say and do now? [2]

Consultant-level model answer. "I am immediately concerned. This adolescent has tricyclic antidepressant cardiotoxicity with sodium-channel blockade: the widened QRS with a tall R wave in aVR and the anticholinergic picture are diagnostic. I call the senior, resuscitation and intensive-care teams and the Poisons Information Centre now, name a leader, allocate roles, and bring weight-appropriate equipment and monitoring. I run ABCDE treating threats as they are found: protect the airway, give high-flow oxygen, ventilate if needed, attach a continuous ECG, check the bedside glucose, gain IV access, send paracetamol and salicylate levels, and give intravenous sodium bicarbonate 1 to 2 mL per kg of 8.4 per cent, repeated to narrow the QRS and raise the pH to 7.45 to 7.55." [2]

Probing follow-up. "Why bicarbonate, and why not an antiarrhythmic?" A strong answer is: "The widened QRS is sodium-channel blockade. Bicarbonate overcomes the blockade with a sodium load, alkalinises to reduce the free drug fraction, and narrows the QRS. A class Ia or Ic antiarrhythmic or amiodarone would worsen the blockade and is contraindicated." [2]

Common weak answer. "I will take a full history and order a drug screen first." This delays the targeted antidote in a child with a dangerous, ECG-visible lesion. The strip points to the action now.

Escalation branch. If the candidate gives bicarbonate and avoids the antiarrhythmic trap, release the deterioration in Question 2. If they reach for an antiarrhythmic, ask which channel it blocks and what that does to a tricyclic-poisoned heart. [2]

Question 2 — The refractory shock and the rescue therapies

Stimulus update. Despite two bicarbonate boluses the QRS narrows but the blood pressure remains low and a short run of ventricular tachycardia appears. The team asks whether to add intravenous procainamide. Question: What is your response, and what are your rescue therapies? [6]

Consultant-level model answer. "I decline the procainamide: it is a class Ia sodium-channel blocker and will worsen the conduction block and the arrhythmia. The residual ectopy is managed with further sodium bicarbonate, and I now start intravenous lipid emulsion because this is a lipophilic drug and the shock is refractory to bicarbonate. I activate a veno-arterial extracorporeal membrane oxygenation service now, because refractory tricyclic cardiac arrest is an indication for prolonged CPR and ECMO, and the retrieval window is long. I continue CPR without prematurely ceasing if she arrests, because lipid emulsion scavenges the drug and recovery is possible." [6]

Probing follow-up. "What is the mechanism of the lipid emulsion?" A strong answer is: "The lipid creates an intravascular lipid phase, the lipid sink, that sequesters the lipophilic tricyclic and lowers its free concentration at the heart and brain. A 2025 narrative review confirms its place as an adjunct for selected severe lipophilic drug toxicity." [6]

Common weak answer. "I will give procainamide to control the rhythm." This is the classic lethal trap in tricyclic poisoning.

Escalation branch. If the candidate navigates the rescue therapies, release the mixed-overdose twist in Question 3. [6]

Question 3 — The mixed overdose and the calcium channel blocker

Stimulus update. The grandmother arrives with a second bottle: the girl also took her grandfather's sustained-release verapamil. The bedside glucose is now 12 mmol per L and the heart rate has dropped to 50. Question: How does this change the plan? [3] [4]

Consultant-level model answer. "This is now a mixed tricyclic and calcium channel blocker overdose. The hyperglycaemia with a falling heart rate confirms the calcium channel blocker component, because calcium-channel blockade blocks insulin release from the beta cell. I add intravenous calcium, calcium gluconate 10 per cent 0.6 mL per kg, and start high-dose insulin euglycaemic therapy, insulin 1 unit per kg then 0.5 to 1 unit per kg per hour with dextrose, monitoring glucose and potassium hourly and keeping potassium above 4 mmol per L. Because the verapamil is sustained-release, I commit to a long observation window and keep the ECMO service activated, because sustained-release calcium channel blockers deteriorate late." [3] [4]

Probing follow-up. "Why insulin for a calcium channel blocker?" A strong answer is: "High-dose insulin euglycaemic therapy shifts the failing myocardium onto carbohydrate metabolism, restores inotropy, and corrects the toxin-induced insulin resistance of calcium channel blocker overdose. It is the key therapy for severe calcium channel blocker and beta-blocker overdose." [3]

Common weak answer. "I will just keep escalating the inotropes." Escalating inotropes alone is the failing strategy that delays the definitive therapy. [4]

Question 4 — Retrieval, disposition and safeguarding

Stimulus update. The child stabilises on insulin, calcium and vasopressors, but she is in a rural hospital with no paediatric intensive care. Question: What is your retrieval and disposition plan? [4]

Consultant-level model answer. "I called retrieval in parallel with resuscitation, before local support was exceeded. I agree the paediatric intensive-care destination, the treatment to continue en route (insulin, calcium, vasopressors, lipid emulsion ready), the escort and equipment, and the expected deterioration en route, with an ECMO contingency. I arrange a mental-health and social assessment once she is safe, because this is a deliberate overdose and the index event is a marker of ongoing risk. I run safeguarding alongside the medical care, and I give the family poison-prevention advice before any discharge." [4]

Probing follow-up. "What is the one principle you most want the team to carry forward?" A strong answer is: "Read the ECG and the toxidrome, give the targeted antidote on its trigger (bicarbonate for the tricyclic widened QRS, calcium and high-dose insulin for the calcium channel blocker), never throw a class Ia or Ic antiarrhythmic at a tricyclic rhythm, and escalate to lipid emulsion and ECMO before local support is exceeded." [2] [4]

Common weak answer. "I will wait for the retrieval team to arrive before arranging intensive care." Retrieval and intensive care must be arranged in parallel; the child needs ongoing resuscitation and a contingency for deterioration during the wait. [4]