Cardiotoxic and psychotropic medication poisoning

Overview & Definition

Cardiotoxic and psychotropic medication poisoning is the harmful effect of a prescribed drug on the heart's electrical system or its pumping, recognised first by the ECG and the bedside pattern and treated by supportive care plus a small number of targeted antidotes. The child or adolescent arrives bradycardic or hypotensive, with a widened QRS or a long QT, and your job in the first minute is to protect the airway, attach a continuous ECG, check a bedside glucose, and read the strip — because the QRS width and the QT length decide the antidote. [1] [9]

A toxidrome is a recognisable cluster of signs produced by a class of drug acting through a shared mechanism, and the cardiotoxic toxidromes are read from the heart. The tricyclic antidepressant pattern combines a widened QRS with an anticholinergic picture and hypotension. The beta-blocker and calcium channel blocker patterns combine bradycardia and hypotension with poor perfusion. The antipsychotic pattern combines sedation and QT prolongation. Recognising the pattern is faster and more useful than waiting for a drug level, and it points directly to the immediate treatment. [1] [4]

[1] [2]

Management is built around supportive care, because most cardiotoxic drugs are metabolised once the airway, the breathing, the circulation and the perfusion are held safe. Sodium bicarbonate is the specific antidote for sodium-channel-blockade cardiotoxicity and is given to a defined trigger and a defined endpoint. High-dose insulin euglycaemic therapy is the key therapy for severe beta-blocker and calcium channel blocker overdose, shifting the failing myocardium onto a more efficient fuel. Intravenous lipid emulsion and extracorporeal support are rescue options for the child who does not respond to standard care. [2] [3]

Classification

The single most useful classification is by the ECG and the ion channel the drug blocks, because it converts a guessing game about the bottle into a decision about the next action. Look at the QRS width and the QT length, add the rate and the blood pressure, and the cardiotoxic class emerges within a minute. [1] [4]

[1] [4]

Classification by intention and age frames the two peaks of paediatric cardiotoxic poisoning. The toddler peak is exploratory ingestion of a grandparent's verapamil or nifedipine — a single sustained-release tablet can be lethal in a small body. The adolescent peak is deliberate overdose of a tricyclic antidepressant, quetiapine or a beta-blocker, often with ethanol and uncertainty about the dose. Both need the same ABCDE structure and the same ECG-led approach, but the doses, the observation window and the safeguarding assessment differ. [8] [9]

Epidemiology & Risk Factors

Cardiotoxic prescription medications are among the most dangerous paediatric ingestions because a single adult dose can kill a child. Calcium channel blockers and tricyclic antidepressants consistently lead mortality series of paediatric poisoning, and the risk is magnified by the small body mass of the toddler and by sustained-release formulations that absorb slowly and then poison late. [1] [9]

[1] [9]

Risk is magnified by formulation and co-ingestion. A sustained-release verapamil preparation is the classic late-deteriorator: the child looks well for several hours and then descends into refractory shock, which is why the observation window must be long. Co-ingestion of ethanol deepens the sedation and drops the blood pressure; co-ingestion of two cardiotoxins blurs the ECG and demands combined antidotes. Underlying cardiac disease, long-QT medication and electrolyte disturbance all lower the threshold for arrhythmia. [4] [8]

Pathophysiology

Toxicity follows from the ion channel or receptor the drug blocks, and four mechanisms dominate the cardiotoxic picture. Each maps onto a toxidrome and its signature ECG threat, and each points to a different antidote. [1] [4]

Tricyclic antidepressants bind the fast cardiac sodium channel and slow the phase 0 upstroke of the ventricular action potential. Slowed depolarisation slows conduction through the His-Purkinje system and the myocardium, which widens the QRS, and the slow conduction is what allows re-entry and ventricular arrhythmia. A tall R wave in lead aVR reflects the rightward conduction shift. TCAs also block alpha-1 receptors (causing hypotension), muscarinic receptors (the anticholinergic picture) and potassium channels (adding QT prolongation), and they antagonise GABA, which is why seizures complicate severe poisoning. [2] [9]

[1] [4]

Beta-blockers occupy the beta-1 adrenergic receptor, reducing the Gs-to-adenylyl-cyclase-to-cAMP cascade that normally drives heart rate, contractility and AV conduction. The result is bradycardia, AV block and negative inotropy. Some beta-blockers add direct sodium-channel blockade (the membrane-stabilising effect), most notably propranolol, which is why propranolol overdose can widen the QRS and cause seizures on top of the bradycardia. Calcium channel blockers block the L-type calcium channel in cardiac myocytes, in the SA and AV nodes, and in vascular smooth muscle. The non-dihydropyridines verapamil and diltiazem cause profound bradycardia, AV block and myocardial depression, while the dihydropyridines (such as nifedipine and amlodipine) cause predominant vasodilation. Calcium channel blockade also blocks insulin release from the pancreatic beta cell, which is why calcium channel blocker overdose produces hyperglycaemia while beta-blocker overdose does not. [4] [5]

Antipsychotics block the delayed-rectifier potassium channel (the hERG channel) and lengthen the action potential, which prolongs the QT interval and sets up early after-depolarisations and torsades de pointes. They also block alpha-1 receptors (hypotension), histamine and muscarinic receptors (sedation and anticholinergic effects) and dopamine receptors (extrapyramidal effects). The neuroleptic malignant syndrome is a separate, idiosyncratic consequence of central dopamine blockade, producing hyperthermia, lead-pipe rigidity, altered consciousness and autonomic instability with a rising creatine kinase. [7] [8]

Two adjunct mechanisms deserve a place in the fellowship answer. High-dose insulin euglycaemic therapy works by shifting the failing, toxin-depressed myocardium onto carbohydrate metabolism, restoring inotropy while glucose is co-administered to keep the patient euglycaemic; it also corrects the toxin-induced insulin resistance seen in calcium channel blocker overdose. Intravenous lipid emulsion creates an intravascular lipid phase (the lipid sink) that sequesters lipophilic drug and lowers its free concentration at the tissues, a mechanism now applied to several lipophilic cardiotoxins beyond its original local-anaesthetic role. [3] [6]

Clinical Presentation

Begin with the first impression, a continuous ECG and a hands-on primary survey, then convert what you see into a cardiotoxic class rather than a drug name. State what you see objectively: "This adolescent is drowsy and hypotensive with a QRS of 140 milliseconds and dry flushed skin — that is tricyclic antidepressant toxicity with sodium-channel blockade." [1]

The tricyclic antidepressant picture combines an anticholinergic toxidrome (dry, flushed skin, dilated pupils, urinary retention, reduced bowel sounds) with the cardiac signature: a widened, notched QRS, a tall R wave in aVR, hypotension and tachycardia that can degenerate into bradycardia and ventricular arrhythmia. Severe poisoning adds seizures, respiratory depression and a rapid descent into shock. The beta-blocker picture is bradycardia with hypotension and AV block, with propranolol adding seizures and a widened QRS. The calcium channel blocker picture is bradycardia with hypotension and vasodilation (dihydropyridines) or profound myocardial depression (verapamil, diltiazem), and the bedside glucose is often high. [2] [4]

[1] [2]

The antipsychotic picture combines sedation with QT prolongation, anticholinergic effects, extrapyramidal signs and postural hypotension; torsades de pointes is the feared arrhythmia, and the neuroleptic malignant syndrome presents hours to days after exposure with hyperthermia, rigidity, confusion and autonomic instability. A mixed or sustained-release ingestion is the trap: the child can look well for hours and then deteriorate, which is why the observation window must be long and the reassessment frequent. [7] [8]

Differential Diagnosis

A toxic cause is one explanation for a bradycardic, hypotensive or widened-QRS child, and the resuscitation does not wait for certainty. Build the differential in a fixed order: what can kill now, what is most likely, what is reversible, and what is most harmful to miss. [1]

[1] [9]

The decisive point is that hyperkalaemia, hypoglycaemia and a primary cardiac cause are missed only if you do not look for them. Check a bedside glucose and a venous gas in every suspected cardiotoxic ingestion, because a low glucose is corrected in seconds and a high potassium is corrected with calcium. The hyperglycaemia of a calcium channel blocker overdose is a useful discriminator: a bradycardic, hypotensive child with a high glucose points to a calcium channel blocker rather than a beta-blocker. The response to a targeted antidote also confirms the diagnosis — a QRS that narrows after sodium bicarbonate is tricyclic cardiotoxicity. [4] [9]

Clinical & Bedside Assessment

Run the ABCDE primary survey adapted to the cardiotoxic-poisoned child, then reassess after each intervention. The continuous ECG and the circulation are the foreground, because cardiotoxic drugs kill through arrhythmia and shock. [1] [4]

Open and protect the airway, give high-flow oxygen, and ventilate with a bag and mask if breathing is inadequate or the conscious level is depressed. Attach a continuous cardiac monitor and obtain a 12-lead ECG at the bedside, measuring the QRS width and the corrected QT. Check the bedside glucose immediately, because calcium channel blocker overdose raises it and beta-blocker overdose can occasionally drop it. Establish intravenous or intraosseous access. Assess the circulation for heart rate, blood pressure, capillary refill, skin temperature and perfusion, and measure the temperature. [1] [2]

[1] [2]

The focused examination targets the cardiotoxic class. Look at the pupils (dilated and dry in anticholinergic or antipsychotic toxicity), the skin (flushed and dry in anticholinergic, poorly perfused in shock), the muscle tone (lead-pipe rigidity in neuroleptic malignant syndrome), the glucose (high in calcium channel blocker overdose) and the perfusion. Take a collateral history from caregivers or the ambulance crew: what bottles or blister packs were found, how many are missing, the timing, whether the formulation is sustained-release, and any access to multiple prescriptions. Preserve the bottles. [4] [9]

The reassessment after each intervention is the examination that matters most. After sodium bicarbonate, ask whether the QRS has narrowed and the blood pressure improved. After high-dose insulin, ask whether the heart rate, the perfusion and the lactate are improving, while watching the glucose and potassium. State the change you expected, and compare it with what actually happened. [2] [3]

Investigations

Stabilise first, then order each test for a named question. In suspected cardiotoxic poisoning the immediate tests identify the reversible threats and the co-ingestants that change management, rather than naming the drug. [1]

[1] [9]

Interpret the tests as physiology and threat, not as a drug label. A low glucose is acted on in seconds; a high glucose in a bradycardic child points to a calcium channel blocker. A metabolic acidosis with a rising lactate signals worsening shock and the need to escalate. A low potassium or magnesium during high-dose insulin therapy must be corrected because hypokalaemia and hypomagnesaemia prolong the QT and invite torsades. The serial ECG is more useful than a single tracing, because the QRS and QT trends track both deterioration and response. [3] [7]

[1] [9]

Management — Resuscitation

Resuscitation follows a fixed order: ABCDE primary survey, high-flow oxygen, bag-mask ventilation for apnoea or a depressed airway, bedside glucose, intravenous access, continuous ECG, a call for senior, intensive-care and Poisons Information Centre help, and the targeted antidote. Each element runs in parallel, and each action is followed by reassessment of the strip and the circulation. [1] [2]

[1] [1] [2]

Tricyclic antidepressant cardiotoxicity and sodium bicarbonate

The widened QRS of a tricyclic antidepressant is sodium-channel blockade, and the antidote is hypertonic sodium bicarbonate. Sodium bicarbonate works by three mechanisms: the sodium load overcomes the channel blockade and speeds conduction, the alkalinisation raises the pH and reduces the free fraction of the drug, and the extracellular sodium narrows the QRS. The trigger is a widened QRS (over 100 milliseconds), a ventricular arrhythmia or hypotension, and the endpoint is a narrowed QRS and a serum pH of 7.45 to 7.55. [2] [9]

[2]

The common pitfalls with bicarbonate are well described: giving it without a clear trigger or endpoint, failing to repeat the bolus to narrow the QRS, and forgetting that hyperventilation adds an alkalinising effect in the intubated child. A ventricular arrhythmia in tricyclic poisoning is treated with sodium bicarbonate first, not with a class Ia or Ic antiarrhythmic — quinidine, procainamide and flecainide each worsen sodium-channel blockade, and amiodarone is avoided for the same reason. If the arrhythmia persists, expert consensus supports intravenous lipid emulsion, and refractory cardiac arrest is an indication for prolonged cardiopulmonary resuscitation and extracorporeal support. [2] [6]

Beta-blocker and calcium channel blocker overdose

Severe beta-blocker and calcium channel blocker overdose cause bradycardia, hypotension and myocardial depression that is poorly responsive to atropine and escalating inotropes alone. The modern approach layers intravenous calcium, high-dose insulin euglycaemic therapy, vasopressors and, for refractory cases, lipid emulsion and extracorporeal support. [3] [4]

Intravenous calcium provides a bolus of extracellular calcium that overcomes the channel blockade and transiently improves contractility and blood pressure. Calcium gluconate 10 per cent (0.6 mL per kg, 60 mg per kg) or calcium chloride 10 per cent (0.2 mL per kg, 20 mg per kg) is given intravenously and can be repeated, with attention to the IV access — calcium chloride needs a central line or a large, reliable cannula because it is irritant in extravasation. [4]

[3] [4]

High-dose insulin euglycaemic therapy is the key therapy for severe overdose of either class. It shifts the failing myocardium onto carbohydrate metabolism and restores inotropy, and it corrects the toxin-induced insulin resistance of calcium channel blocker overdose. The dose is an insulin bolus of 1 unit per kilogram followed by an infusion of 0.5 to 1 unit per kilogram per hour, with a dextrose infusion to keep the patient euglycaemic; the response builds over 15 to 45 minutes, and the glucose and potassium must be checked hourly because insulin drives both down. Atropine, glucagon, vasopressors and cardiac pacing are adjuncts rather than replacements for insulin. A systematic review of propranolol toxicity confirms that high-dose insulin and lipid emulsion are the interventions most consistently associated with improvement. [3] [5]

[5] [6]

Antipsychotic poisoning and the QT

Antipsychotic overdose prolongs the QT and risks torsades de pointes. The management is electrolyte correction first (potassium above 4 mmol per L and magnesium above 0.8 mmol per L, because hypokalaemia and hypomagnesaemia lengthen the QT), intravenous magnesium for QT prolongation or torsades, and the strict avoidance of every other QT-prolonging drug, including many antiemetics, antibiotics and methadone. [7] [8]

[7]

Torsades de pointes that is sustained or recurrent is treated with intravenous magnesium, the correction of potassium and magnesium, and electrical cardioversion or overdrive pacing if the child is unstable. The neuroleptic malignant syndrome is managed supportively — cessation of the antipsychotic, active cooling, benzodiazepines, and correction of the fluid, electrolyte and renal consequences of the rhabdomyolysis — with dantrolene and bromocriptine considered in specialist consultation for severe cases. Sedation, hypotension and the anticholinergic effects are managed supportively, with the airway protected if the conscious level is depressed. [7] [8]

Refractory poisoning: lipid emulsion and extracorporeal support

When a lipophilic cardiotoxic drug (a tricyclic antidepressant, a beta-blocker or a calcium channel blocker) does not respond to the targeted antidote, intravenous lipid emulsion is the next rescue therapy. The mechanism is the lipid sink: the lipid phase sequesters the lipophilic drug 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, guided by a toxicologist. [6]

Refractory cardiotoxic shock or cardiac arrest unresponsive to bicarbonate, calcium, insulin, vasopressors and lipid emulsion is an indication for veno-arterial extracorporeal membrane oxygenation, which bridges the child while the drug is metabolised. Early activation of an extracorporeal service is essential, because the window for cannulation is narrow and the retrieval time is long. [10]

Management — Definitive & Stepwise

Once the first minutes are safe, definitive care moves to continuous haemodynamic and ECG monitoring, sustained antidote therapy, electrolyte and glucose control, and the clarification of the agent and the formulation. This phase runs hour by hour with the trend, and the disposition follows the response. [1] [4]

Ongoing monitoring and sustained antidote therapy

Continue continuous ECG, blood pressure and perfusion monitoring, with serial QRS and corrected QT measurement. For tricyclic poisoning, repeat sodium bicarbonate to keep the QRS narrow and the pH in the target range, then watch for recurrence as the bicarbonate is metabolised. For beta-blocker and calcium channel blocker overdose, titrate the high-dose insulin infusion to the perfusion and the lactate, and replace potassium and glucose as needed. For antipsychotic overdose, keep the potassium and magnesium corrected and the QT monitored until it normalises. [2] [3]

Electrolyte, glucose and perfusion control

Correct the metabolic consequences actively. Replace potassium during high-dose insulin therapy to keep it above 4 mmol per L, and give dextrose to maintain euglycaemia. Treat the hyperglycaemia of calcium channel blocker overdose with the insulin infusion rather than separate hypoglycaemics, because the insulin serves both the glucose and the inotropy. Drive the perfusion with fluids, vasopressors and the antidotes, watching the lactate fall and the capillary refill improve as the endpoints. [3] [4]

Goals and disposition

Set explicit recovery endpoints and watch the trend toward them: a safe airway, a narrowed QRS, a normalising QT, an adequate blood pressure and perfusion, a falling lactate, and a stable glucose and electrolyte profile. A child who has received sodium bicarbonate for tricyclic cardiotoxicity is observed until the ECG has normalised and stayed normal, because the QRS can re-widen. A child with a sustained-release calcium channel blocker ingestion is observed for at least 12 to 24 hours because of the risk of late deterioration. Asymptomatic children with immediate-release ingestions are observed for the relevant window before discharge with safety-netting. [1] [4]

Specific Subtypes & Scenarios

The structure stays the same, but age, agent, formulation and setting change what you watch for, which antidote you reach for, and how early you escalate. [1]

[1] [4]

In the toddler with exploratory ingestion of a grandparent's verapamil, the dose per kilogram is magnified by the small body mass, and a sustained-release preparation can deteriorate hours after a well-looking presentation; calcium and high-dose insulin euglycaemic therapy are started early and the child is observed for at least 12 to 24 hours. The adolescent with a deliberate tricyclic overdose and a widened QRS receives sodium bicarbonate to narrow the QRS, while flumazenil is withheld because it can precipitate seizures when a proconvulsant such as a tricyclic has been co-ingested. A mixed beta-blocker and calcium channel blocker overdose is the scenario where combined high-dose insulin euglycaemic therapy is most clearly indicated, layering calcium, insulin and vasopressors. [3] [9]

Complications & Pitfalls

Most preventable harm in paediatric cardiotoxic poisoning comes from a small number of errors: throwing a class Ia or Ic antiarrhythmic at a tricyclic-induced rhythm, forgetting glucose and potassium during high-dose insulin, missing sustained-release delayed toxicity, withholding bicarbonate for a borderline QRS, or escalating inotropes alone in a beta-blocker or calcium channel blocker overdose. Each is a failure of the principle rather than a failure of knowledge. [1] [2]

[1] [2]

After resuscitation, watch actively for harm from the toxicity itself and from its treatment: ventricular arrhythmia and hypoxic brain injury from delayed sodium bicarbonate, hypoglycaemia and hypokalaemia from high-dose insulin, hypercalcaemia and pancreatitis from repeated calcium doses, pancreatitis and acute respiratory distress syndrome from lipid emulsion, and aspiration from a depressed airway. The child who survives the first hour still needs meticulous ongoing care, and a new ECG change or a falling blood pressure can mark a complication as readily as a relapse. [6] [9]

[1] [2]

Prognosis & Disposition

Disposition follows the agent, the formulation, the trend and the observation window, not a single reassuring reading. Consider the duration of action of the substance, the sustained-release nature, the co-ingestants, the response to treatment, the local resources, the transport risk, and the social and mental-health context. [1] [4]

[1]

Outcome depends on the speed of airway protection, the early reading of the ECG, and the prompt use of the targeted antidote. The children who do worst are those with delayed bicarbonate for a tricyclic arrest, sustained-release verapamil ingestion with late shock, and large co-ingestions. Outcome is generally good when the airway, breathing, circulation and the ECG are held safe and the targeted antidote is given early. Survivors of a deliberate overdose need a mental-health and social assessment before discharge, with a safety plan and clear follow-up, because the index event is a marker of ongoing risk. [1] [8]

Special Populations

Adapt how you assess, dose and escalate, but never lower the standard for reading the ECG and the toxidrome. The principles apply across ages and abilities; the differences are in weight-based dosing, drug handling, communication and the social context. [1]

[1] [9]

Safeguarding runs in parallel with medical care, and immediate stabilisation comes first. An ingestion in a young child may reflect unsafe medication storage, neglect, or an unsafe home environment, while an adolescent presentation may signal self-harm or risk that needs a careful psychosocial assessment. Ask only necessary open, non-leading questions, document objective findings and spontaneous words, and use the local safeguarding and mental-health pathway. Reporting thresholds, consent rules and confidentiality provisions differ by Australian state or territory, UK nation, US state and Canadian province or territory. [1]

Evidence, Guidelines & Regional Differences

What the evidence can and cannot support

The structure of management — ABCDE primary survey, oxygen and ventilation, continuous ECG, bedside glucose, access, the call to the Poisons Information Centre, and the targeted antidote — is consensus across the major paediatric and toxicology sources. The four areas of active evidence are sodium bicarbonate for tricyclic cardiotoxicity, high-dose insulin euglycaemic therapy for beta-blocker and calcium channel blocker overdose, intravenous lipid emulsion, and extracorporeal support; each refines rather than replaces the supportive-care backbone. [1] [2]

On sodium bicarbonate, the mechanism and the expert consensus are clear, but the evidence base is largely mechanistic and observational, and recent review highlights the common pitfalls of giving it without a trigger or an endpoint. On high-dose insulin euglycaemic therapy, observational data and a systematic review of propranolol toxicity support its early use in severe beta-blocker and calcium channel blocker overdose, with glucose and potassium monitoring. On lipid emulsion, a 2025 narrative review confirms its place as an adjunct for selected severe lipophilic drug toxicity. On extracorporeal support, case series and reports describe veno-arterial ECMO bridging refractory calcium channel blocker overdose to recovery. [2] [5]

Jurisdictional implementation

[1] [1] [1] [1]

Exam Pearls

[1] [2]

Viva: why sodium bicarbonate for the tricyclic widened QRS?

The widened QRS of tricyclic antidepressant poisoning is sodium-channel blockade, and sodium bicarbonate is the antidote by three mechanisms. The sodium load overcomes the channel blockade and speeds conduction, narrowing the QRS. The alkalinisation raises the pH and reduces the free fraction of the drug by increasing its protein binding and shifting it off the receptor. The extracellular sodium raises the gradient that the channel needs. Give 1 to 2 mL per kilogram of 8.4 per cent intravenously, repeated to narrow the QRS and raise the serum pH to 7.45 to 7.55, and never substitute a class Ia or Ic antiarrhythmic, which worsens the blockade.

[2] [9]

Viva: what is high-dose insulin euglycaemic therapy and when is it used?

High-dose insulin euglycaemic therapy is the key therapy for severe beta-blocker and calcium channel blocker overdose with shock or myocardial depression. It shifts the failing, toxin-depressed myocardium onto carbohydrate metabolism and restores inotropy, and it corrects the toxin-induced insulin resistance of calcium channel blocker overdose. The dose is insulin 1 unit per kilogram intravenous bolus then 0.5 to 1 unit per kilogram per hour, with a dextrose infusion to maintain euglycaemia and hourly glucose and potassium monitoring. Calcium and vasopressors are given in parallel, and lipid emulsion and ECMO are prepared for refractory cases.

[3] [4]

Structured oral: a toddler who has taken a grandparent's sustained-release verapamil

Recognise the calcium channel blocker picture: bradycardia with hypotension and, typically, hyperglycaemia. Run the ABCDE survey, secure the airway and give oxygen, attach a continuous ECG, check the bedside glucose, establish access, and call the senior team, intensive care, retrieval and the Poisons Information Centre. Start intravenous calcium and high-dose insulin euglycaemic therapy early, add vasopressors, and prepare intravenous lipid emulsion and veno-arterial ECMO for refractory shock. Because the formulation is sustained-release, observe for at least 12 to 24 hours for late deterioration, and run poison-prevention counselling and safeguarding alongside the medical care.

[3] [10] [1] [2] [3] [1] [2] [7]

References

1. [1]Hoffman, Robert J; Nillas, Anthony Toxidromes and a general approach to poisoning Archives of Disease in Childhood, 2025.PMID 39978865
2. [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. [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. [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
5. [5]Hu, Yi; Mujahid, Kaleem Effectiveness of treatments for propranolol toxicity: a systematic review of current approaches and evidence European Journal of Clinical Pharmacology, 2026.PMID 41546730
6. [6]Nendumba, Gosberthan; Blackman, Stephen Use of intravenous lipid emulsions in drug-induced toxicities: a 2025 narrative review Annals of Intensive Care, 2025.PMID 41247632
7. [7]Besag, Frank M C; Vasey, Maxine J Neurological Adverse Effects of Antipsychotic Medication in Children and Young People Paediatric Drugs, 2026.PMID 41498920
8. [8]Darke, Shane; Duflou, Joanne Characteristics and toxicology of adult deaths due to quetiapine toxicity in Australia, 2000-2024 Journal of Forensic Sciences, 2025.PMID 40588799
9. [9]Frithsen, Iliana L; Simpson, William M Jr Recognition and management of acute medication poisoning American Family Physician, 2010.PMID 20112890
10. [10]Cheon, Jae Hee; Miller, Matthew Beyond vasopressor support: VA-ECMO for refractory calcium channel blocker overdose South African Medical Journal, 2025.PMID 41378535