Opioid, sedative and recreational-drug toxicity

Overview & Definition

Opioid, sedative and recreational-drug toxicity is the harmful effect of a substance on the brainstem, the cardiovascular system or the body's temperature and metabolic balance, recognised first by the clinical pattern it produces and treated by supportive care plus a small number of antidotes. The child or adolescent arrives sedated, agitated, breathing slowly or racing, hot or cold, and your job in the first minute is to protect the airway, oxygenate, ventilate and find the pattern — not to identify the exact drug. [1] [2]

A toxidrome is a recognisable cluster of signs produced by a class of drug acting through a shared mechanism. Recognising the pattern is faster and more useful than waiting for a drug screen, and it points directly to the immediate treatment. The opioid pattern combines pinpoint pupils, slow shallow breathing and sedation. The sedative-hypnotic pattern combines sedation and ataxia with normal or near-normal pupils. The sympathomimetic pattern combines agitation, dilated pupils, a racing heart, high blood pressure and a hot sweaty body. The anticholinergic pattern adds dry, flushed skin and delirium to dilated pupils. [1]

[1] [2]

Management is built around supportive care, because most poisoned children recover once the airway, breathing and circulation are held safe and the drug is metabolised. Naloxone reverses opioid respiratory depression but must be titrated to effective ventilation rather than full consciousness, both to avoid precipitating acute withdrawal and because the goal is to keep the child breathing safely. Flumazenil reverses benzodiazepines but is not routine, because it can precipitate seizures in exactly the patients who present with mixed or chronic use. Sympathomimetic and serotonergic toxicity is treated with benzodiazepines, cooling and fluids, with cyproheptadine considered for severe serotonin syndrome. [2] [8]

Classification

The single most useful classification is by toxidrome, because it converts a guessing game about the drug into a decision about the next action. Look at the pupils, the mental state, the vital signs and the skin, and the pattern emerges within a minute. [1]

[1]

Classification by intention and age frames the two peaks of paediatric toxicity. The toddler peak is exploratory ingestion of a caregiver's medication — an opioid, a benzodiazepine, an antihypertensive — found with a medicine bottle on the floor. The adolescent peak is intentional or recreational use of ethanol, MDMA, cocaine, benzodiazepines, ketamine, GHB or a novel psychoactive substance, often with co-ingestion and uncertainty about the dose. Both need the same ABCDE structure, but the differential, the doses, the safeguarding assessment and the disposition differ. [1] [3]

Epidemiology & Risk Factors

Poisoning is among the most common reasons a previously well child or adolescent presents acutely unwell. In young children the driver is access to medications and household substances in the home. In adolescents the driver is experimentation, intentional self-harm, and the recreational use of ethanol and a widening range of substances including opioids, benzodiazepines, MDMA, cocaine, ketamine, GHB and novel psychoactive substances. [1] [3]

[1] [10]

Risk is magnified by opioid tolerance and its absence. An opioid-tolerant adolescent may carry a large dose without respiratory depression, while an opioid-naive toddler taking a single sustained-release tablet of a caregiver's opioid can arrest within the hour. The arrival of fentanyl and its analogues has raised the stakes, because these agents are potent, may require higher or repeated naloxone doses, and can recur as the opioid outlasts the antidote. Novel psychoactive substances complicate recognition, because they mimic and blur the classic toxidromes and escape standard drug screens. [2] [11]

Pathophysiology

Toxicity follows from the receptor the drug binds. Three mechanisms dominate the recreational and sedative picture, and each maps onto a toxidrome and its signature threat. [1] [2]

Opioids bind mu-receptors in the medullary respiratory centre, slowing the respiratory rate and the tidal volume until ventilation is inadequate. Pupillary constriction is the tell-tale sign, driven by mu-receptors in the Edinger-Westphal nucleus. The dominant threat is hypoxia from respiratory depression, and the antidote naloxone competes at the receptor to restore the drive to breathe. Sedative-hypnotics enhance GABA-A signalling, the brain's main inhibitory pathway, producing sedation, ataxia and at higher doses respiratory depression. Benzodiazepines act here, which is why flumazenil can reverse them, but also why removing GABA-mediated inhibition in a dependent or co-ingested brain can release seizures. [2] [8]

[1] [2]

Sympathomimetics drive a catecholamine and serotonin surge. MDMA, cocaine and amphetamine release noradrenaline, dopamine and serotonin, producing agitation, tachycardia, hypertension, mydriasis and hyperthermia. MDMA is distinctive because it can also cause profound hyponatraemia through a combination of excess water intake and inappropriate antidiuretic hormone release, and because its serotonergic effect can tip the child into serotonin syndrome with rigidity, clonus and hyperthermia. Cocaine adds direct cardiovascular toxicity through coronary vasospasm and sodium-channel effects, which is why chest pain and arrhythmia are part of its presentation. [10] [12]

Ethanol causes the specific danger of hypoglycaemia in young children by suppressing hepatic gluconeogenesis while glycogen stores are small. A toddler who has ingested ethanol can become profoundly hypoglycaemic, and the low glucose worsens the cerebral depression. GHB produces a distinctive pattern of rapid deep coma with rapid spontaneous recovery as it is cleared, while ketamine produces a dissociative state with nystagmus, hypersalivation and a sympathomimetic tinge. Novel psychoactive substances, including synthetic cannabinoids, blur these patterns and can produce severe agitation, seizures and even acute kidney injury. [10] [11]

Clinical Presentation

Begin with the first impression and a hands-on primary survey, then convert what you see into a toxidrome rather than a drug name. State what you see objectively: "This adolescent is agitated, hot and sweaty with dilated pupils and a heart rate of 140 — that is a sympathomimetic picture." [1]

The opioid toxidrome combines pinpoint pupils, a slow respiratory rate with shallow breaths, and reduced conscious level. The child is cool and sedated, and the threat is hypoxic respiratory arrest. The sedative-hypnotic toxidrome combines sedation, slurred speech and ataxia with pupils that are normal or only slightly small; respiratory depression may be present but is usually milder than in opioid toxicity. The sympathomimetic toxidrome is the mirror image: agitation, dilated pupils, tachycardia, hypertension, diaphoresis and hyperthermia. The anticholinergic toxidrome adds dry, flushed skin, urinary retention and a confused, delirious mental state. [1] [10]

[1]

Specific agents colour the pattern. MDMA presents with agitation, tachycardia and hyperthermia, and can progress to muscle rigidity, clonus and confusion signalling serotonin syndrome, or to collapse from hyponatraemia or a cardiac arrhythmia. Cocaine and amphetamine present with hypertension, tachycardia and chest pain, and can produce seizures and stroke. Ethanol in a young child presents with ataxia, sedation and the danger of hypoglycaemia; the child may be cold and clammy rather than warm. GHB presents as rapid deep coma, often with bradycardia and hypothermia, then rapid recovery over hours. Ketamine presents with a dissociative state, nystagmus and hypersalivation. Synthetic cannabinoids can produce severe agitation, seizures and vomiting. [10] [11]

Differential Diagnosis

A toxic cause is one explanation for an altered or collapsed 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] [10]

The decisive point is that hypoglycaemia, hypoxia and a structural brain problem are missed only if you do not look for them. Check bedside glucose at the bedside in every suspected intoxication, because ethanol and beta-blocker overdose drop it fast and the low glucose is corrected in seconds with intravenous dextrose. Examine the pupils for asymmetry and the head for signs of injury. Keep sepsis and meningoencephalitis open when the child is febrile and drowsy, because fever can coexist with or mimic a sympathomimetic toxidrome. [1]

Clinical & Bedside Assessment

Run the ABCDE primary survey adapted to the poisoned child, then reassess after each intervention. The airway and breathing are the foreground, because respiratory depression is the common pathway to death in opioid and sedative toxicity. [1] [2]

Open and protect the airway, give high-flow oxygen to any child with respiratory depression or hypoxia, and ventilate with a bag and mask if breathing is inadequate. Check the bedside glucose at the bedside: a low reading is treated immediately with intravenous dextrose before any further assessment. Establish intravenous or intraosseous access. Assess the circulation for heart rate, blood pressure, capillary refill and temperature. Measure the temperature, because hyperthermia in MDMA or cocaine toxicity is an emergency that demands active cooling. Only then perform the focused toxicological examination. [1]

[1]

The focused examination targets the toxidrome. Look at the pupils for size and reactivity, the mental state, the muscle tone and reflexes for rigidity or clonus, the mucous membranes and skin for dryness, sweating and temperature, the bowel sounds, and the bladder for retention. Take a collateral history from caregivers, friends or the ambulance crew: what was found at the scene, what bottles or paraphernalia were present, the timing, any access to medications in the home, and any recreational or intentional use. In the adolescent, take a brief, non-judgemental history that respects confidentiality while securing safety. Use a professional interpreter whenever needed. [1] [3]

The reassessment after each intervention is the examination that matters most. After naloxone, ask whether the respiratory rate and depth have improved and the child is breathing effectively, not whether they are fully awake. After benzodiazepines for a sympathomimetic picture, ask whether the agitation and the heart rate are settling and the temperature is falling. State the change you expected, and compare it with what actually happened. [2] [5]

Investigations

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

[1]

Interpret the tests as physiology and threat, not as a drug label. A low glucose is acted on in seconds. A metabolic acidosis with a large anion gap raises toxic alcohol or salicylate poisoning. A raised creatine kinase in MDMA toxicity signals rhabdomyolysis and drives fluid management to protect the kidney. A low sodium in an MDMA user points to water intoxication or inappropriate antidiuretic hormone and constrains fluid choice. The electrocardiogram in the unknown overdose screens for the widened QRS of sodium-channel blockade, which would redirect management toward sodium bicarbonate. [1] [10]

[1]

Management — Resuscitation

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

[1] [1] [2]

Airway and breathing

The airway and breathing are the priority because respiratory depression is the common pathway to death in opioid and sedative toxicity. Open and protect the airway, give high-flow oxygen, and ventilate with bag and mask if breathing is inadequate. In the deeply comatose child or the one with an unprotected airway, prepare for a definitive airway and call for senior or intensive-care help early. Do not wait for an antidote to protect the airway; ventilation comes first. [1] [2]

Naloxone for opioid toxicity

Naloxone reverses opioid respiratory depression by competing at the mu-receptor. The principle that protects the child is to titrate naloxone to effective ventilation, not to full wakefulness. Reversing too far precipitates acute opioid withdrawal, agitation, vomiting and aspiration, and in rare cases pulmonary oedema, while the goal is simply to restore adequate breathing. [2] [5]

[2] [5]

An initial naloxone dose of 10 micrograms per kilogram by the intravenous, intraosseous or intramuscular route is reasonable, repeated every two to three minutes until ventilation is effective. In the apnoeic or severely depressed child, where the priority is rapid reversal, a larger dose of up to 100 micrograms per kilogram per dose is used, to a maximum of 2 mg per dose. Intranasal naloxone is an alternative route with rapid systemic uptake in children, and a pilot randomised trial found intranasal administration feasible in paediatric opioid poisoning, though intravenous remains the fastest route when access is established. [4] [6]

[4] [6]

Naloxone has a short half-life of roughly 60 to 90 minutes, shorter than most opioids. A child who responds to a bolus can slip back into respiratory depression as the naloxone wears off, and this recurrence is the rule rather than the exception with long-acting agents such as methadone, sustained-release morphine or oxycodone, and fentanyl and its analogues. After the effective bolus dose is found, start a naloxone infusion at about two-thirds of that effective dose per hour, titrated to keep ventilation adequate, and observe the child for long enough to cover the duration of action of the opioid. [2] [5]

Flumazenil: the caution

Flumazenil reverses benzodiazepines at the GABA-A receptor, but it is not a routine reversal agent in the poisoned child. Removing GABA-mediated inhibition in a benzodiazepine-dependent patient, in a mixed overdose, or where a proconvulsant such as a tricyclic antidepressant has been co-ingested can precipitate seizures that are difficult to control. Paediatric case reports document seizure after flumazenil administration, and the standard teaching is to prefer supportive airway and ventilatory care over reversal. [7] [8]

[8] [9]

The narrow circumstance in which flumazenil is considered is the isolated, known benzodiazepine ingestion in a benzodiazepine-naive patient with significant respiratory depression where airway and ventilation cannot be maintained, or the reversal of iatrogenic oversedation during procedural sedation. Even then, give it in small titrated increments of 10 micrograms per kilogram intravenously to a maximum of 500 micrograms per dose, with resuscitation equipment and a plan for seizure management to hand. The default for the poisoned child with benzodiazepine toxicity remains supportive: protect the airway, oxygenate and ventilate. [7] [9]

Sympathomimetic and serotonergic toxicity

Sympathomimetic toxicity from MDMA, cocaine or amphetamine is treated with benzodiazepines as first-line therapy, active cooling and intravenous fluids. Benzodiazepines calm the agitation, reduce the muscle activity that generates heat, lower the heart rate and blood pressure, and treat the serotonergic component. Use adequate titrated doses of a benzodiazepine such as diazepam or lorazepam. Cool the hyperthermic child actively with evaporative cooling, ice packs or cooled intravenous fluids, and treat the rhabdomyolysis with intravenous fluids to protect the kidney. [10] [12]

[10] [12]

Where MDMA or another serotonergic agent has produced serotonin syndrome with the triad of neuromuscular hyperexcitability (clonus, rigidity, hyperreflexia), autonomic instability and altered mental state, escalate the benzodiazepine dose, cool actively, and consider cyproheptadine in consultation with a toxicologist. Avoid beta-blocker monotherapy in cocaine and amphetamine toxicity, because blocking beta-2 vasodilation leaves unopposed alpha vasoconstriction and can paradoxically worsen hypertension. Severe refractory hypertension is treated with a direct vasodilator such as phentolamine, and chest pain from cocaine is managed as an acute coronary syndrome with aspirin, nitrates and benzodiazepines. [12]

Ethanol, GHB, ketamine and unknown agents

Ethanol intoxication in the young child carries the specific threat of hypoglycaemia. Check glucose at the bedside and treat a low reading immediately with intravenous dextrose, then sustain with a glucose-containing fluid and recheck, because the hypoglycaemia can recur. GHB and its precursors produce a rapid deep coma, often with bradycardia and hypothermia, and typically recover spontaneously over a few hours; management is supportive, protecting the airway and watching for the recovery. Ketamine produces a dissociative state with nystagmus and hypersalivation that settles with supportive care, benzodiazepines for distress, and attention to the airway. For the unknown or novel psychoactive substance, manage the toxidrome in front of you, secure the airway and circulation, and call the Poisons Information Centre and a toxicologist for specific guidance. [10] [11]

Management — Definitive & Stepwise

Once the first minutes are safe, definitive care moves to ongoing monitoring, sustained antidote therapy where needed, correction of metabolic and electrolyte disturbance, temperature control, and the clarification of the agent and the intent. This phase runs hour by hour with the trend, and the disposition follows the response. [1] [3]

Ongoing monitoring and sustained antidote therapy

Continue monitoring the airway, breathing, circulation, oxygen saturation, conscious level and temperature. For opioid toxicity from a long-acting agent, run a naloxone infusion and observe long enough to cover the duration of action of the opioid; for sustained-release preparations and methadone this is many hours. Reassess the adequacy of ventilation repeatedly, and titrate the infusion to keep the child breathing safely rather than fully awake. [2] [5]

Metabolic, electrolyte and temperature control

Correct the metabolic and electrolyte consequences. Treat MDMA hyponatraemia with fluid restriction and, in severe cases with seizures, hypertonic saline per local protocol. Treat rhabdomyolysis with adequate intravenous fluids to maintain urine output and protect the kidney. Drive the temperature down actively in severe hyperthermia, because sustained high temperature causes harm rapidly. Correct ethanol hypoglycaemia with dextrose and recheck. [10] [12]

Goals and disposition

Set explicit recovery endpoints and watch the trend toward them: a safe airway, effective ventilation, a normalising temperature, settling agitation, a normal glucose and electrolyte profile, and a protected kidney. A child who has required naloxone for a long-acting opioid is observed for many hours because of the risk of recurrence. A child with MDMA toxicity and rhabdomyolysis is observed until the creatine kinase trend is reassuring and the kidney function is stable. Asymptomatic children with accidental ingestions are observed for the relevant window — around four to six hours for most agents, longer for sustained-release preparations — before discharge with safety-netting. [1] [3]

Specific Subtypes & Scenarios

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

[1] [11]

In the toddler with exploratory ingestion, the dose per kilogram is magnified by the small body mass, and a single sustained-release opioid tablet can be lethal. The adolescent with intentional or recreational use often presents with co-ingestion and uncertainty about the dose; screen for paracetamol and salicylate regardless of the stated history, because these co-ingestions change the management and the prognosis. Fentanyl and its analogues may require higher or repeated naloxone doses, and the recurrence after a bolus is common enough that an infusion and prolonged observation are the safer default. [2] [11]

Complications & Pitfalls

Most preventable harm in paediatric drug toxicity comes from a small number of errors: giving flumazenil routinely, reversing naloxone to full wakefulness, missing hypoglycaemia, using a beta-blocker alone for cocaine, or neglecting the recurrence of a long-acting opioid. Each is a failure of the principle rather than a failure of knowledge. [1] [8]

[1] [8]

After resuscitation, watch actively for harm from the toxicity itself and from its treatment: aspiration from reduced conscious level, pulmonary oedema from opioid over-reversal, rhabdomyolysis-induced kidney injury in MDMA toxicity, hyponatraemic seizures, serotonin syndrome, and the seizure that follows an ill-judged dose of flumazenil. The child who survives the first hour still needs meticulous ongoing care, and a new sign can mark a complication as readily as a relapse. [9] [10]

[1] [8]

Prognosis & Disposition

Disposition follows the agent, the trend and the observation window, not a single reassuring reading. Consider the duration of action of the substance, the co-ingestants, the response to treatment, the local resources, the transport risk, and the social and mental-health context. [1] [3]

[1]

Outcome is generally good for children who receive prompt supportive care, because most agents are metabolised once the airway, breathing and circulation are held safe. The children who do worst are those with delayed airway protection, missed hypoglycaemia, severe hyperthermia from MDMA, cardiovascular instability from cocaine, or the rare but severe presentations of novel psychoactive substances. Survivors of an intentional or recreational presentation need a mental-health and social assessment before discharge, with a safety plan, harm-reduction advice, and clear follow-up, because the index event is a marker of ongoing risk. [1] [3]

Special Populations

Adapt how you assess, dose and escalate, but never lower the standard for recognising a toxidrome. The principles apply across ages and abilities; the differences are in tolerance, communication, drug handling and the social context. [1]

[1] [3]

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 in rare cases an unsafe home environment, while an adolescent presentation may signal self-harm, exploitation 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, bedside glucose, access, the call to the Poisons Information Centre, and the targeted antidote — is consensus across the major paediatric and toxicology sources. The two areas of active evidence are the route and dose of naloxone and the role of flumazenil, and both refine rather than replace the supportive-care backbone. [1] [2]

[5] [6]

On flumazenil, the evidence and the consensus are clear: it is not a routine reversal agent in the poisoned patient. Case reports and clinical experience show that seizures after flumazenil occur in exactly the children most often brought to the emergency department — chronic benzodiazepine users, mixed overdoses and co-ingestions with proconvulsants. The standard teaching is supportive airway and ventilatory care, with flumazenil reserved for the narrow case of an isolated, known benzodiazepine ingestion in a benzodiazepine-naive patient or for iatrogenic reversal. [7] [9]

On novel psychoactive substances, the evidence is sobering: synthetic cannabinoids and other novel agents produce severe toxicity that blurs the classic toxidromes and escapes standard drug screens, and management is predominantly supportive, with escalation to a toxicologist. The recreational landscape shifts faster than the testing does, which is why the toxidrome and the physiology, rather than the drug name, drive the first hour. [10] [11]

Jurisdictional implementation

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

Exam Pearls

[1] [2]

Viva: why titrate naloxone to ventilation, not wakefulness?

The goal of naloxone is to restore effective ventilation and prevent hypoxic death, not to make the child fully alert. Naloxone has a half-life of roughly 60 to 90 minutes, shorter than most opioids, and over-reversal precipitates acute opioid withdrawal with agitation, vomiting and aspiration, and in rare cases pulmonary oedema. A child reversed to wakefulness may also refuse further observation and slip back into respiratory depression as the naloxone wears off. Titrate in small increments until ventilation is adequate, then observe and, for a long-acting opioid, start an infusion.

[2] [5]

Viva: when is flumazenil appropriate, and when is it dangerous?

Flumazenil reverses benzodiazepines at the GABA-A receptor, but removing GABA-mediated inhibition can release seizures. It is dangerous in chronic benzodiazepine users, in mixed or unknown overdoses, where a proconvulsant such as a tricyclic antidepressant has been co-ingested, and in a patient with a known seizure disorder. It is appropriate only in the narrow case of an isolated, known benzodiazepine ingestion in a benzodiazepine-naive patient with significant respiratory depression that cannot be managed supportively, or for iatrogenic reversal of procedural sedation. The default for the poisoned child is supportive airway and ventilation.

[8] [9]

Structured oral: an adolescent with MDMA toxicity and hyperthermia

Recognise the sympathomimetic or serotonergic pattern: agitation, tachycardia, hypertension, mydriasis and hyperthermia, with rigidity and clonus pointing to serotonin syndrome. Run the ABCDE survey, secure the airway and give oxygen, check bedside glucose, establish access, and call the senior team, a toxicologist and the Poisons Information Centre. Give titrated benzodiazepines first line to control agitation and reduce heat generation, cool actively with evaporative cooling and cooled fluids, give intravenous fluids to protect the kidney from rhabdomyolysis, correct a low sodium carefully, and consider cyproheptadine for severe serotonin syndrome. Avoid beta-blocker monotherapy. Escalate to intensive care if hyperthermia is uncontrolled, seizures occur or the circulation is unstable, and arrange a mental-health and social assessment once the child is safe.

[10] [12] [1] [2] [8] [1] [8] [10]

References

1. [1]Hoffman, Robert J Toxidromes and a general approach to poisoning Archives of disease in childhood, 2025.PMID 39978865
2. [2]Boyer, Edward W Management of opioid analgesic overdose The New England journal of medicine, 2012.PMID 22784117
3. [3]Ball, Allison Naloxone and Buprenorphine Treatment for Adolescent Opioid Overdose and Opioid Use Disorder: A Review JAMA pediatrics, 2026.PMID 41661628
4. [4]Gholami, N A pilot randomized feasibility clinical trial of intranasal vs. intravenous naloxone in pediatric opioid poisoning Drug and alcohol dependence, 2026.PMID 42413284
5. [5]Aziz, R The Optimal Initial Dose and Route of Naloxone Administration for Successful Opioid Reversal: A Systematic Literature Review Cureus, 2024.PMID 38380203
6. [6]Malmros Olsson, E Rapid systemic uptake of naloxone after intranasal administration in children Paediatric anaesthesia, 2021.PMID 33687794
7. [7]Segev, O Flumazenil in the Treatment of Benzodiazepine Toxicity: The Experience of a Large Urban Tertiary Care Hospital The Israel Medical Association journal : IMAJ, 2026.PMID 42298935
8. [8]Kreshak, Angela A Flumazenil administration in poisoned pediatric patients Pediatric emergency care, 2012.PMID 22531190
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10. [10]Levine, Mark New Designer Drugs Emergency medicine clinics of North America, 2021.PMID 34215409
11. [11]Assi, Salem Profile, effects, and toxicity of novel psychoactive substances: A systematic review of quantitative studies Human psychopharmacology, 2017.PMID 28631432
12. [12]Lucyk, Sarah N Acute Cardiovascular Toxicity of Cocaine The Canadian journal of cardiology, 2022.PMID 35697321