Beta-Blocker & Calcium-Channel Blocker Overdose

[1]

Meet the patient

A 54-year-old woman is brought in two hours after swallowing two boxes of her mother's sustained-release verapamil. She is awake, chatty, normotensive, and annoyed to be in the emergency department. Her heart rate is 64, her glucose is 11 mmol/L, her venous pH is 7.28 with a base excess of minus 7.[1]

The team is already discussing discharge. Resist it. This is the lethal subtype playing its favourite trick — the deceptive latent phase. By hour twelve she will be in refractory cardiogenic shock, and everything you do in the next six hours decides whether she survives. Two questions run this resus bay: which channel or receptor is blocked? and is this a sustained-release formulation? Everything below answers them.[1][2]

One toxidrome, two drugs, one discriminator

Beta-blockers and calcium-channel blockers are taught together because they are the same resuscitation problem wearing two biochemistry coats. Both slow the heart, drop the pressure, and block AV conduction, and both produce a cardiogenic shock that standard ACLS cannot reverse — because atropine withdraws vagal tone and adrenaline stimulates beta-receptors, and in severe toxicity the receptor (beta-blocker) or the channel (calcium-channel blocker) is directly blocked, downstream of both.[1]

They share an antidote ladder for the same reason: intravenous calcium, high-dose insulin euglycaemia therapy, vasopressors, lipid emulsion, pacing, and VA-ECMO all work by routes that bypass the blocked target. Glucagon is the one beta-blocker-specific rung. Co-ingestion is common — many hypertensive patients take both — and the combination is dramatically more lethal than either alone.[2]

The discriminator that ends the viva lives on a glucose strip. Calcium-channel blockade stops calcium entry into pancreatic beta cells, so insulin release fails and the patient becomes hyperglycaemic with a lactic acidosis. Beta-blockade does the opposite — it can cause and then mask hypoglycaemia, especially in children. Hyperglycaemia plus acidosis in a bradycardic overdose is essentially pathognomonic for a calcium-channel blocker.[1]

[1]

The two drug classes, face to face

Classify each class on the axis that predicts the danger, then bolt on the discriminator. For beta-blockers the dangerous axis is lipophilicity and membrane-stabilising activity; for calcium-channel blockers it is the dihydropyridine split. The discriminator row is the glucose.[2]

[1]

The discriminator line: check a finger-prick glucose at first contact — high means calcium-channel blocker, low or normal points to beta-blocker. One strip, one answer, before any level comes back.[1]

Three beta-blocker axes that decide severity

Know the beta-blocker by the three axes that change management. Lipophilicity decides whether the brain and the lipid sink matter; cardioselectivity decides whether bronchospasm is a risk; membrane-stabilising activity decides whether the QRS will widen.[2]

[2]

The lethal subtype — read the clock, not the patient

Sustained-release verapamil and diltiazem carry the highest mortality of any prescription overdose. The tablet absorbs slowly, so the patient looks entirely well for 6 to 12 hours — sometimes 24 — while the drug keeps loading, then collapses into refractory cardiogenic shock. Up to 20 to 30 per cent of severe ingestions die even in young, previously well patients.[1]

The classic trap is the well-looking patient at hour four who is sent home or under-treated and arrests at hour twelve. The defence is operational, not intellectual: every suspected sustained-release calcium-channel-blocker ingestion is admitted to a high-dependency or ICU bed for at least 24 hours of continuous cardiac monitoring, receives whole-bowel irrigation, and starts therapy early. Immediate-release preparations declare themselves within 1 to 6 hours and can be discharged after a 6-hour observation if asymptomatic with a normal ECG.[1]

[1]

How common, how lethal, who dies

These are deliberate self-harm drugs in adults, accidental grandparent-pill ingestions in toddlers, and dose errors in the elderly. A few verapamil or propranolol tablets can kill a child, so any paediatric ingestion gets a finger-prick glucose, a pill count, and a safeguarding review.[2]

The severity accelerators are the ones examiners love: co-ingestion of a second cardiovascular drug (beta-blocker plus calcium-channel blocker, or with digoxin or a tricyclic), advanced age and pre-existing cardiac disease, hepatic or renal impairment, and a new CYP3A4 inhibitor — clarithromycin, erythromycin, itraconazole, grapefruit juice, or a protease inhibitor — raising a previously tolerated verapamil or diltiazem level into chronic toxicity.[3]

The named agent risks are worth memorising verbatim. Propranolol is the most neurotoxic beta-blocker — highly lipophilic with potent membrane-stabilising activity, it causes seizures, coma and QRS widening. Sotalol has a 12 to 16 hour half-life and blocks the delayed-rectifier potassium channel, producing a long QT with torsades de pointes that needs quite different management. Verapamil is the most cardiotoxic calcium-channel blocker — profound negative inotropy and AV nodal block.[2]

[3]

Why the myocardium fails — two routes to the same dead channel

Trace both cascades to the L-type calcium channel and the management writes itself. A beta-blocker closes the channel indirectly, by starving the receptor of cAMP; a calcium-channel blocker closes it directly. Either way the myocyte cannot bring calcium in, and contraction, conduction and rate all fail.[2]

The beta-blocker cascade — receptor to cAMP to calcium

A beta-blocker is a competitive antagonist of the beta-adrenergic Gs-coupled receptor. Normally receptor stimulation activates adenylyl cyclase, raises cAMP, activates protein kinase A, and PKA phosphorylates the L-type calcium channel and phospholamban — so more calcium enters during the plateau and more is released from the sarcoplasmic reticulum. Beta-blockade reverses every step: cAMP falls, PKA activity falls, the channel opens less, and the reticulum releases less.[2]

The haemodynamic consequence is the three cardinal effects: negative chronotropy (the SA node funny-current is cAMP-dependent), negative dromotropy (AV nodal cells are slow-response tissue that rely on the calcium upstroke), and negative inotropy. The net picture is bradycardia, hypotension, AV block and a falling cardiac output. Non-selective agents add bronchospasm, unopposed alpha vasoconstriction, and the masking of hypoglycaemia — the adrenergic warning signs are beta-mediated, so the patient sweats and tremors less while the glucose collapses.[2]

The calcium-channel-blocker cascade — direct channel closure

A calcium-channel blocker directly blocks the L-type channel that carries the slow inward calcium current. In nodal tissue that current is the phase-0 upstroke, so the SA node slows and AV conduction blocks; in working myocardium it is the plateau influx that drives excitation-contraction coupling, so contractility falls. Dihydropyridines preferentially hit arteriolar smooth muscle, causing vasodilation and an early reflex tachycardia — the clue to an amlodipine ingestion — before severe overdose depresses the myocardium too.[2]

The pancreatic discriminator — the exam fact

L-type calcium channels on pancreatic beta cells trigger insulin granule exocytosis, so calcium-channel blockade stops insulin release and the glucose climbs. Add the impaired cardiac carbohydrate metabolism and shock-driven hypoperfusion and you get a metabolic acidosis. The combination — hyperglycaemia plus acidosis in a bradycardic overdose — is pathognomonic for a calcium-channel blocker and is the single fastest discriminator from a beta-blocker, which never does this.[2]

Etymology for viva gold: the word calcium traces to the Latin calx, lime — the channel it names was characterised long after the mineral. Verapamil, the prototype, was synthesised as a vasodilator and only later recognised as the first calcium-channel blocker; its name is pharmaceutical, not classical, but it sits at the birth of an entire drug class.[2]

Why standard ACLS fails — and the logic of the ladder

Standard bradycardia and shock resuscitation relies on atropine and adrenaline, and both miss the blocked target. Atropine withdraws vagal tone; the channel or receptor is already blocked downstream, so the heart does not speed up. Adrenaline stimulates beta-receptors that a beta-blocker has occupied. This is why the ladder does not stop there — it adds therapies that bypass the blockade entirely.[1]

Calcium floods a supraphysiological gradient that pushes through the blocked channel. High-dose insulin euglycaemia therapy restores inotropy through a receptor-independent metabolic switch. Glucagon (for beta-blockers) activates adenylyl cyclase through its own receptor, sidestepping the blocked beta-receptor. Lipid emulsion sequesters lipophilic drug in an intravascular lipid sink. VA-ECMO replaces the circulation while the drug clears. The mantra is: do not wait for each rung to fail before adding the next — they are complementary, run them forward together.[1][2]

What you will find at the bedside

The cardiovascular picture is shared; the extras point to the agent. Run the focused assessment in this order and the agent usually declares itself.[2]

The shared cardiovascular findings are bradycardia (sinus, junctional escape, or idioventricular), hypotension from reduced output and — in calcium-channel-blocker overdose — vasodilation, AV conduction block progressing from first to third degree, and cardiogenic shock with cool peripheries, weak pulse, prolonged capillary refill, oliguria and a rising lactate. Severe poisoning ends in cardiovascular collapse and PEA arrest.[2]

The beta-blocker extras are CNS depression, seizures and coma (lipophilic agents), QRS widening from membrane-stabilising activity, bronchospasm in asthmatics, hypoglycaemia — especially in children, with its warning signs masked — and, with sotalol, a long QT and torsades. The calcium-channel-blocker extras are hyperglycaemia, a metabolic acidosis, warm vasodilated peripheries early (dihydropyridines), nausea and vomiting with verapamil, and bowel ischaemia from mesenteric vasospasm.[2]

The time course is itself diagnostic. Immediate-release preparations produce toxicity within 1 to 6 hours. Sustained-release verapamil or diltiazem can carry a 6 to 12 hour latent phase — sometimes 24 — before sudden collapse. The patient who looks well at four hours can arrest at twelve; admit for 24 hours of observation.[2]

The bradycardic-shock mimics — exclude the others

Every unexplained bradycardic overdose is a toxin hunt until the agent is named. The ECG and a few bedside tests separate the cardiovascular toxins from the sodium-channel toxins and the non-toxic causes.[2]

[1]

The decisive bedside question: is this a beta-blocker, a calcium-channel blocker, both, or another bradycardic toxin? The finger-prick glucose is the fastest discriminator (hyperglycaemia means calcium-channel blocker). The ECG adds the rest — long QT means sotalol or a tricyclic, a wide QRS means propranolol or a tricyclic, peaked T waves mean hyperkalaemia. The family pill-bottle count usually names the agent.[1]

The history is the investigation

Pin down six facts and the management pathway is set. First, the drug name and formulation — immediate or sustained release — because that single fact decides whole-bowel irrigation and 24-hour ICU. Second, the number of tablets and time of ingestion. Third, co-ingestants — always ask and always screen paracetamol, salicylate and ethanol. Fourth, the reason, deliberate or accidental, with a household-pill inventory and safeguarding review in a child. Fifth, the usual medications and cardiac history. Sixth, renal and hepatic function for clearance.[2]

The focused examination runs ABCDE: vital signs with a finger-prick glucose, respiratory effort and wheeze, cardiovascular signs of cardiogenic versus distributive shock, the abdomen for distension and bowel sounds, and a neurological GCS with pupils. Obtain a 12-lead ECG and a continuous rhythm strip and read it for sinus or junctional bradycardia, PR prolongation and AV block, QRS widening, and a long QT. Establish continuous monitoring, two large-bore cannulae, and a urinary catheter for output in shock.[2][2]

Investigations — driven by haemodynamics, not levels

The first-line panel is the resus panel, and treatment is driven by haemodynamics and the ECG, never by a drug level. Draw a venous gas for pH, lactate and base excess, finger-prick and laboratory glucose, electrolytes including magnesium and calcium, urea and creatinine, LFTs, troponin if ischaemia is suspected, FBC, a beta-hCG in women of childbearing potential, and a paracetamol and salicylate level in any deliberate overdose.[2]

Serum drug levels are not routinely useful in beta-blocker or calcium-channel-blocker overdose — they correlate poorly with severity, the turnaround is slow, and management is decided entirely by the blood pressure, the ECG and the lactate. A rising lactate and worsening base excess are the triggers to escalate up the ladder.[2]

[2]

Bedside echocardiography shows the severe global myocardial depression — a small, collapsing LV with a low ejection fraction — that distinguishes toxin-induced cardiogenic shock from the normal or high ejection fraction of distributive vasoplegia and from obstructive shock. Repeat the 12-lead ECG with any haemodynamic change and before and after each calcium or insulin bolus.[2]

[2]

The first hour — resuscitate, then calcium

Begin with ABCDE and secure the airway early. Intubate if the GCS is depressed — sustained-release verapamil patients deteriorate suddenly and an unprotected airway is the first thing to lose. Give high-flow oxygen if hypoxic, establish two large-bore cannulae, attach continuous monitoring, and treat the immediately life-threatening bradyarrhythmia or shock first.[3]

Cautious fluids and glucose first. Give 250 to 500 mL aliquots of balanced crystalloid titrated to blood pressure — the myocardium is failing and over-resuscitation worsens pulmonary oedema. Check and treat hypoglycaemia with IV dextrose, especially in children with beta-blocker overdose where hypoglycaemia is a major cause of morbidity and its warning signs are masked.[3]

Atropine for symptomatic bradycardia — but expect it to fail. Give atropine 0.5 to 1 mg IV every 3 to 5 minutes up to 3 mg (30 microgram/kg in children), and know that it is often ineffective in severe toxicity because the channel or receptor is blocked downstream of vagal tone. Do not waste time escalating atropine in a deteriorating patient — move straight to calcium and high-dose insulin.[3]

IV calcium is the first specific antidote. Give calcium chloride 10 per cent, 10 to 20 mL (1 g) over 5 to 10 minutes via a central line (it is caustic to peripheral veins), or calcium gluconate 10 per cent, 30 to 60 mL (3 to 6 g) via a peripheral line — each 10 mL of gluconate carries about a third of the elemental calcium of 10 mL of chloride. Repeat every 10 to 20 minutes to effect, up to three or four doses, then start an infusion. The rationale is a supraphysiological extracellular gradient that overcomes the channel blockade; the effect can be dramatic in calcium-channel-blocker overdose. Monitor the ionised calcium and watch the ECG for QT shortening.[3]

Pace when bradycardia is refractory — transcutaneous then transvenous — but expect poor mechanical capture, because the myocardium is failing, and treat the inotropic failure with high-dose insulin and vasopressors alongside the pacing. In severe toxicity escalate rapidly through calcium, high-dose insulin, vasopressors, lipid and ECMO; do not wait for each therapy to fail before adding the next.[3][2]

The antidote ladder — CALCIUM

The ladder is the most examined part of the topic, and the doses must come verbatim. Run it as the mnemonic CALCIUM, escalate forward together in a deteriorating patient, and never treat a sustained-release ingestion with patience.[3]

[3] [3]

High-dose insulin euglycaemia therapy — the most effective inotrope

High-dose insulin euglycaemia therapy is the single most effective inotropic therapy and must not be delayed. The poisoned myocardium is in carbohydrate-metabolism failure, shifting to inefficient fatty-acid oxidation; insulin shifts it back toward efficient glucose oxidation, yielding more ATP per unit of oxygen and delivering positive inotropy that is independent of the blocked receptor or channel. That is why it works when receptor agonists fail.[3]

[3] [3]

Give regular insulin 1 unit/kg IV as a bolus, then an infusion of 0.5 to 1 unit/kg/h titrated up to 10 units/kg/h in severe poisoning. Give 25 g of dextrose as a bolus (50 mL of 50 per cent dextrose) then an infusion of 0.5 to 1 g/kg/h, titrated to keep glucose 5 to 10 mmol/L. Supplement potassium to keep it at least 2.5 to 2.8 mmol/L initially — insulin drives potassium into cells and hypokalaemia is a major complication. Check glucose every 30 to 60 minutes and potassium every 1 to 2 hours; this needs an ICU bed. Onset is 15 to 45 minutes; continue for 12 to 24 hours after haemodynamic stability, then wean gradually, because abrupt cessation causes rebound hypoglycaemia or recrudescence of toxicity.[3]

Glucagon, vasopressors, lipid, ECMO

Glucagon is the beta-blocker-specific rung. Give 5 to 10 mg IV over 1 to 2 minutes (50 to 150 microgram/kg in children) then an infusion of 1 to 5 mg/h. It bypasses the blocked beta-receptor by directly activating adenylyl cyclase through its own Gs-coupled receptor. It causes vomiting — give an antiemetic first — and hyperglycaemia, and the volumes are enormous: a 10 mg dose reconstituted from powder needs many vials. Historically first-line for beta-blocker overdose, it has been superseded by high-dose insulin in many centres but remains a useful adjunct.[3]

Vasopressors and inotropes are frequently required in high doses and in combination. Use noradrenaline 0.05 to 1 microgram/kg/min for vasoplegia, especially in dihydropyridine overdose, and adrenaline for combined inotropy and chronotropy. Do not be afraid of high doses in refractory toxin-induced shock — multiple agents at high doses alongside calcium and insulin is expected, not a failure.[3]

Intravenous lipid emulsion creates a lipid sink for lipophilic drugs. Give 20 per cent lipid emulsion 1.5 mL/kg as a bolus, then 0.25 mL/kg/min for 30 to 60 minutes, repeating the bolus for refractory collapse, to a maximum of about 10 mL/kg in the first 30 minutes. It sequesters lipophilic drug away from receptors and provides fatty-acid substrate to the myocardium. Reserve it for refractory collapse — concerns are fat embolism, pancreatitis, assay interference and ARDS — and reach for it early with propranolol and verapamil.[3]

VA-ECMO is the bridge to drug clearance. For refractory cardiogenic shock unresponsive to calcium, insulin, vasopressors and lipid, refer early to an ECMO centre — survival is good even in profoundly toxic patients whose circulation is supported by the circuit while the drug clears over 24 to 72 hours. Late referral costs lives.[3]

Decontamination — formulation decides the method

Activated charcoal and whole-bowel irrigation are decided by the formulation and the airway. Give activated charcoal 50 g (1 g/kg in children) within 1 to 2 hours of ingestion if the airway is protected or will be imminently — beyond that window it is of limited benefit for immediate-release but may still help sustained-release preparations. Give whole-bowel irrigation with polyethylene glycol 1 to 2 L/h in adults (20 to 40 mL/kg/h in children) via nasogastric tube for sustained-release preparations or large ingestions, continuing until the rectal effluent is clear, typically 4 to 6 hours. It is essential for sustained-release verapamil and diltiazem.[3]

Subtypes and scenarios that change the plan

Sotalol, propranolol, sustained-release verapamil and the paediatric ingestion each rewrite the algorithm. Name the subtype and the management pivots.[2]

The sustained-release verapamil or diltiazem overdose is the lethal subtype — delayed and prolonged, biphasic, high-mortality. Admit for 24-hour ICU observation, give whole-bowel irrigation, start early and prolonged high-dose insulin, and keep a low threshold for ECMO. The most important single decision is to not be reassured by the initially well patient.[3]

The dihydropyridine overdose (amlodipine, nifedipine) is predominantly vasodilatory — warm vasoplegic shock with an early reflex tachycardia, then bradycardia and collapse in severe poisoning. It needs high fluids and vasopressors; calcium and high-dose insulin are effective.[3]

The sotalol overdose is a long-QT disease — torsades de pointes. Give IV magnesium sulphate 2 g, correct potassium and magnesium, and use an isoprenaline infusion or overdrive pacing to shorten the QT by raising the heart rate, while avoiding other QT-prolonging drugs. The 12 to 16 hour half-life means prolonged monitoring.[3]

The propranolol overdose is the neurotoxic beta-blocker — seizures and coma from membrane-stabilising fast sodium-channel activity, with QRS widening. Treat seizures with benzodiazepines, consider sodium bicarbonate for QRS widening as in tricyclic toxicity, and reach for lipid emulsion in refractory collapse because propranolol is highly lipophilic.[3]

The paediatric ingestion needs weight-based dosing for every antidote and a particular watch for beta-blocker hypoglycaemia — check glucose frequently and give dextrose. A few tablets are lethal; involve child safeguarding. Co-ingestion with digoxin or a tricyclic dramatically raises mortality — treat both toxidromes, calcium for the channel and Fab fragments for the digoxin, sodium bicarbonate for the tricyclic QRS. Note the digoxin caveat: the contested stone-heart teaching cautions against IV calcium when digoxin co-toxicity is plausible; in pure beta-blocker or calcium-channel-blocker toxicity calcium is safe and indicated.[2]

The preventable deaths — pitfalls that kill

Most deaths in this overdose are preventable and traceable to a short list of recurring errors. Run the list in your head for every patient.[3]

The recurring errors are being reassured by the well-appearing sustained-release verapamil patient who later collapses; relying on atropine alone and delaying calcium or insulin; under-dosing calcium, insulin and vasopressors when severe toxicity demands supraphysiological doses; omitting whole-bowel irrigation for sustained-release preparations; failing to check and treat glucose and potassium — beta-blocker hypoglycaemia and insulin-driven hypokalaemia; referring late for ECMO; missing co-ingestants such as digoxin, a tricyclic or paracetamol that change the antidote plan; and giving IV calcium in suspected digoxin co-toxicity under the stone-heart caveat. Rebound after apparent stabilisation is real — the sustained-release drug keeps absorbing — so wean insulin and vasopressors slowly and observe at least 12 to 24 hours after the last vasopressor dose.[3]

Prognosis and disposition

Sustained-release verapamil and diltiazem overdose carry the highest mortality of any prescription overdose — up to 20 to 30 per cent in severe series — but early aggressive therapy including ECMO gives good survival even in profoundly toxic patients. The poor-outcome predictors are the sustained-release formulation, a large ingested dose, delayed presentation, co-ingestants, advanced age, pre-existing cardiac disease, severe acidosis or hyperlactataemia, and the need for multiple vasopressors.[3]

The disposition rule is simple and non-negotiable. Admit every sustained-release ingestion to a high-dependency or ICU bed for at least 24 hours of observation even if initially well, because of the delayed peak and biphasic course. Observe immediate-release ingestions for 6 hours; discharge only if asymptomatic with a normal ECG and haemodynamics, and after psychiatric assessment if deliberate. Every deliberate overdose gets psychiatric assessment after medical stabilisation, with the medication supply secured and child safeguarding involved for paediatric accidental ingestion.[2]

Special populations

In pregnancy the management is unchanged — calcium, high-dose insulin, vasopressors, lipid and ECMO are all used, and the fetus is at risk from maternal hypotension and acidosis. Urgent perimortem Caesarean may be needed in refractory maternal arrest after 20 weeks. The elderly do worse — polypharmacy and CYP3A4 inhibitors raise verapamil and diltiazem levels, sarcopenia reduces the buffer for hypotension, and the threshold for ICU and high-dose insulin is lower. Pre-existing cardiac disease lowers baseline contractility and worsens pacing capture. Renal or hepatic impairment affects clearance — high-dose insulin dosing is unchanged but glucose and potassium monitoring tighten — and dialysis does not remove these drugs, though it may be needed for the resulting acute kidney injury.[2]

Evidence, guidelines, and regional practice

The two anchoring references shape modern practice. The St-Onge 2017 expert consensus (Critical Care Medicine) is the international graded recommendation set for calcium-channel-blocker poisoning — it establishes high-dose insulin as the most effective single inotropic therapy and supports early multimodal therapy across calcium, insulin, vasopressors, lipid, ECMO and decontamination. The Graudins 2016 review (British Journal of Clinical Pharmacology) sets out the rationale for each antidote and documents the shift from glucagon toward high-dose insulin.[1][2]

The live controversies are glucagon (modest efficacy, vomiting-inducing enormous doses, superseded by insulin), lipid emulsion (animal and case-report evidence, reserved for refractory collapse versus used earlier for lipophilic agents), and ECMO timing (early bridge versus last resort, with observational data favouring early referral). Regionally, AACT and ACMT guide whole-bowel irrigation, Toxbase and NPIS guide UK practice, and in resource-limited settings without ECMO the practical mainstay is calcium, insulin and vasopressors. In South Asia the easy availability of verapamil, diltiazem, propranolol and amlodipine makes deliberate self-harm with these agents common, and cross-toxicity with oleander — a cardiac glycoside — is a regional consideration that mandates checking for co-ingestion.[2]

[1]

Ward-round test — four stems

Stem 1 — the chatty woman two hours after sustained-release verapamil (answer)

A 54-year-old woman is brought in two hours after swallowing two boxes of sustained-release verapamil. She is awake, normotensive, heart rate 64, glucose 11 mmol/L, venous pH 7.28. The team wants to discharge her. What is the right call, and why? Model: Do not discharge — this is the lethal subtype in its deceptive latent phase. The sustained-release tablet will keep absorbing for hours and she can collapse into refractory cardiogenic shock at hour twelve. Admit to ICU for at least 24 hours of continuous cardiac monitoring, start whole-bowel irrigation with polyethylene glycol via a nasogastric tube, give activated charcoal if the airway is protected, draw a venous gas, electrolytes, lactate and a paracetamol-salicylate screen, and start IV calcium and high-dose insulin early. The hyperglycaemia with acidosis confirms a calcium-channel blocker. Reassure nobody with a normal blood pressure at four hours.[1]

Stem 2 — bradycardic shock with a glucose of 2 mmol/L (answer)

A 30-year-old is brought in obtunded after an unknown overdose, heart rate 34, blood pressure 72/40, QRS 140 ms, glucose 2 mmol/L. The team reaches for atropine. What is the agent, and what is the first specific therapy? Model: The hypoglycaemia with QRS widening points to a beta-blocker with membrane-stabilising activity — propranolol. Give IV dextrose for the hypoglycaemia first, then IV calcium (calcium chloride 10 per cent 10 to 20 mL central, or gluconate 30 to 60 mL peripheral) and start high-dose insulin euglycaemia therapy — insulin 1 U/kg then 0.5 to 1 U/kg/h with dextrose and potassium supplementation. Atropine will likely fail because the receptor is blocked downstream of vagal tone. For the QRS widening add sodium bicarbonate as in tricyclic toxicity, treat seizures with benzodiazepines, and have lipid emulsion ready because propranolol is highly lipophilic.[1][2]

Stem 3 — sotalol overdose with a polymorphic VT (answer)

A patient on sotalol for atrial fibrillation presents after a large overdose with a long QT and a run of polymorphic ventricular tachycardia. What is the rhythm, and how do you treat it? Model: This is torsades de pointes from sotalol's class III potassium-channel blockade. Give IV magnesium sulphate 2 g, correct potassium and magnesium, and start an isoprenaline infusion or overdrive pacing to shorten the QT by raising the heart rate, while stopping all other QT-prolonging drugs. Alongside the torsades-specific therapy give IV calcium and high-dose insulin for the beta-blockade, and observe for a prolonged period — the sotalol half-life is 12 to 16 hours.[1]

Stem 4 — refractory shock on three pressors (answer)

A patient with massive verapamil overdose remains in cardiogenic shock despite calcium, high-dose insulin, noradrenaline and adrenaline at high doses. What is the next move, and what is the trap? Model: Add intravenous lipid emulsion — 1.5 mL/kg of 20 per cent lipid bolus then 0.25 mL/kg/min — for the refractory collapse, and refer urgently to an ECMO centre for VA-ECMO as a bridge to drug clearance; survival is good even in profoundly toxic patients once the circuit supports the circulation. The trap is treating the ladder as sequential — in a deteriorating patient these therapies are complementary and run forward together, and the other trap is referring late for ECMO. Continue everything for at least 12 to 24 hours after stability and wean slowly, because the sustained-release drug keeps absorbing and toxicity can recrudesce.[1]

References

1. [1]St-Onge M, Anseeuw K, Cantrell FL, et al. Experts Consensus Recommendations for the Management of Calcium Channel Blocker Poisoning in Adults Crit Care Med, 2017.PMID 27749343
2. [2]Graudins A, Lee HM, Druda D Calcium channel antagonist and beta-blocker overdose: antidotes and adjunct therapies Br J Clin Pharmacol, 2016.PMID 26344579
3. [3]Rotella JA, Greene SL, Koutsogiannis Z, et al. Treatment for beta-blocker poisoning: a systematic review. Clin Toxicol (Phila), 2020.PMID 32310006