A physician-validated, board-style question from the Active Transport QBank. Try it, then check the reasoning for every option.
A 17-year-old woman is rushed into the emergency department by her father who found her collapsed in her bedroom 15 minutes before the ambulance's arrival. There was an empty bottle of clomipramine in her bedroom which her mother takes for her depression. Vital signs include the following: respiratory rate 8/min, pulse 130/min, and blood pressure 100/60 mm Hg. On physical examination, the patient is unresponsive to vocal and tactile stimuli. Oral mucosa and tongue are dry, and the bladder is palpable. A bedside electrocardiogram (ECG) shows widening of the QRS complexes. Which of the following would be the best course of treatment in this patient?
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A
Sodium bicarbonateCorrect. IV sodium bicarbonate is the priority intervention for TCA-induced QRS widening - it loads sodium to overcome TCA-induced sodium channel blockade and alkalinization increases protein binding.
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B
Induced vomitingIncorrect. Induced vomiting is contraindicated in this obtunded patient (aspiration risk) and is not recommended in modern toxicology protocols.
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C
NorepinephrineIncorrect. Norepinephrine is the preferred vasopressor for TCA-induced hypotension that is refractory to fluids and bicarbonate, but is not the FIRST step - sodium bicarbonate addresses the cardiotoxicity directly.
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D
DiazepamIncorrect. Diazepam treats TCA-induced seizures but is not the first step for QRS widening; sodium bicarbonate addresses the immediate cardiotoxicity.
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E
PhysostigmineIncorrect. Physostigmine reverses anticholinergic toxicity but is contraindicated in TCA overdose because it can precipitate seizures, asystole, and worsen cardiotoxicity; sodium bicarbonate is the priority intervention.
↑ Tap an answer to reveal the reasoning
Answer: A. An unresponsive young woman with an empty bottle of clomipramine (tricyclic antidepressant) and findings of anticholinergic toxidrome (dry mucous membranes, urinary retention with palpable bladder), tachycardia, hypotension, respiratory depression, and a WIDENED QRS on ECG has acute tricyclic antidepressant overdose. TCAs are among the most lethal common overdoses because of three concurrent toxicities: (1) sodium channel blockade in cardiac myocytes causing QRS widening, ventricular arrhythmia, and conduction block; (2) muscarinic anticholinergic effects causing the toxidrome; (3) alpha-adrenergic blockade causing hypotension.
The priority intervention for QRS >100 ms or ventricular arrhythmia is IV sodium bicarbonate. Two mechanisms: (1) the sodium load competes with TCA for fast sodium channels, narrowing QRS and preventing arrhythmia; (2) alkalinization (target pH 7.45-7.55) increases protein-bound TCA fraction, reducing free drug. Sodium bicarbonate is the SINGLE most important intervention and should be given empirically when QRS widening is seen, even before serum levels return.
Induced vomiting is contraindicated in obtunded patients (aspiration risk) and is no longer routinely recommended in any overdose; activated charcoal can be considered if airway is protected and ingestion was recent. Norepinephrine is the preferred pressor for TCA-induced hypotension refractory to fluids and bicarbonate, but is not the FIRST step. Diazepam treats TCA-induced seizures but is not the initial step for the wide QRS finding.
**Why each option:**
**A.** Correct. IV sodium bicarbonate is the priority intervention for TCA-induced QRS widening - it loads sodium to overcome TCA-induced sodium channel blockade and alkalinization increases protein binding.
**B.** Induced vomiting is contraindicated in this obtunded patient (aspiration risk) and is not recommended in modern toxicology protocols.
**C.** Norepinephrine is the preferred vasopressor for TCA-induced hypotension that is refractory to fluids and bicarbonate, but is not the FIRST step - sodium bicarbonate addresses the cardiotoxicity directly.
**D.** Diazepam treats TCA-induced seizures but is not the first step for QRS widening; sodium bicarbonate addresses the immediate cardiotoxicity.