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Cocaine and sympathomimetic toxicity !

Cocaine, amphetamines and ecstasy overstimulate the heart and brain, causing chest pain, high blood pressure, fever, seizures, heart attacks and strokes.

Updated 2026-11-01

Structures involved

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Why it happens

What it is

Acute toxicity from cocaine (powder, crack, «basuco») and other sympathomimetics such as amphetamines, methamphetamine and MDMA («éxtasis»). These drugs flood synapses with catecholamines, producing the sympathomimetic toxidrome and vascular, cardiac, neurological and thermal emergencies.

Who gets it

Colombia is a major cocaine-producing country, and cocaine and basuco use are significant public-health problems, along with growing synthetic drug use at parties («tusi», which often contains ketamine, MDMA and other mixtures of uncertain content). Cocaine-associated chest pain and agitation are common emergency presentations in young adults.

Causes

  • Snorted, smoked (crack, basuco) or injected cocaine
  • Amphetamines, methamphetamine and MDMA
  • Body packing or stuffing (drug swallowed in packets)
  • Mixed or adulterated party drugs

Risk factors

  • Stimulant use disorder and binge use
  • Combination with alcohol (forms cocaethylene, more cardiotoxic)
  • Hot environments, dancing and dehydration
  • Underlying coronary disease, hypertension or aneurysm
  • Packet rupture in body packers

Pathophysiology

Cocaine blocks reuptake of noradrenaline, dopamine and serotonin; amphetamines also promote their release. Excess catecholamines raise heart rate, blood pressure and myocardial oxygen demand while causing coronary vasospasm and platelet activation, leading to ischaemia and infarction, often in young people. Cocaine also blocks cardiac sodium channels (QRS widening, ventricular arrhythmias). Hypertensive surges can cause aortic dissection, intracerebral or subarachnoid haemorrhage. Increased muscle activity and agitation produce hyperthermia, rhabdomyolysis and acidosis. MDMA adds serotonin toxicity and hyponatraemia.

Symptoms and signs

  • Agitation, anxiety, paranoia, euphoria
  • Dilated pupils, sweating, tremor
  • Tachycardia and hypertension
  • Chest pain and palpitations
  • Fever and muscle rigidity in severe cases
  • Headache, nausea

Diagnosis

Clinical
Clinical diagnosis from history and the sympathomimetic toxidrome: tachycardia, hypertension, mydriasis, hyperthermia, agitation and diaphoresis (sweating separates it from anticholinergic toxicity). Ask specifically about cocaine in every young patient with chest pain or stroke.
Tests
ECG and serial troponin for chest pain; creatine kinase, electrolytes, renal function, glucose, blood gases and lactate; urine toxicology (cocaine metabolites) supports the history but does not guide acute care.
Imaging
Chest X-ray (pneumothorax, pneumomediastinum with smoked cocaine), CT angiography if aortic dissection is suspected, head CT for headache or neurological signs; abdominal imaging in body packers.

Differential diagnosis

  • Anticholinergic toxicity (dry skin, urinary retention)
  • Serotonin syndrome and neuroleptic malignant syndrome
  • Thyroid storm
  • Alcohol or sedative withdrawal
  • Primary acute coronary syndrome, sepsis or acute psychosis

Goal of treatment

Calm the sympathetic storm, cool the patient, and treat ischaemic, haemorrhagic and arrhythmic complications.

Treatment

Acute
ABC, oxygen if hypoxic, rapid cooling for hyperthermia, intravenous fluids for dehydration and rhabdomyolysis.
Medical
Benzodiazepines are first line: they control agitation, seizures, tachycardia and hypertension. Persistent hypertension is treated with vasodilators (nitrates, calcium channel blockers or phentolamine).
Medical
Cocaine chest pain: benzodiazepines, aspirin and nitrates; acute coronary syndrome treated as usual with reperfusion when indicated. Beta-blockers are traditionally avoided in the acute phase because of possible unopposed alpha stimulation.
Medical
Sodium bicarbonate for QRS widening or ventricular arrhythmias due to sodium-channel blockade.
Follow-up
Nursing priorities: continuous cardiac monitoring, temperature, blood pressure, urine output and colour, seizure precautions and a safe low-stimulus environment; observe body packers closely for signs of packet rupture.
Lifestyle
Brief intervention and referral for stimulant use disorder treatment.

Complications

  • Myocardial infarction and coronary dissection
  • Ventricular arrhythmias and sudden death
  • Aortic dissection
  • Ischaemic stroke, intracerebral and subarachnoid haemorrhage
  • Hyperthermia, rhabdomyolysis and acute kidney injury
  • Pneumothorax, pneumomediastinum and lung injury from smoking

Prognosis

Most mild intoxications resolve within hours. Prognosis worsens with hyperthermia, seizures, infarction, stroke or arrhythmias; repeated use leads to chronic cardiomyopathy and accelerated coronary disease.

Prevention

  • Prevention and treatment programmes for substance use
  • Avoid combining stimulants with alcohol and avoid overheating
  • Ask about drug use in young patients with chest pain or stroke

Test yourself

Think of the answer, then tap the question to see it.

What is the first-line drug class for cocaine-induced agitation, tachycardia and hypertension?

Benzodiazepines, which reduce central sympathetic outflow and control seizures and agitation.

Why are beta-blockers traditionally avoided in acute cocaine toxicity?

Blocking beta receptors may leave alpha stimulation unopposed, worsening vasoconstriction and coronary spasm.

How does cocaine cause myocardial infarction in a young patient?

Increased oxygen demand, coronary vasospasm and platelet activation with thrombosis.

Which ECG finding suggests cocaine sodium-channel blockade, and what treats it?

QRS widening or ventricular arrhythmias, treated with sodium bicarbonate.

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Educational information, not medical advice. For any symptom, see a health professional.

Sources: Cocaine intoxication: MedlinePlus Medical Encyclopedia (MedlinePlus (U.S. National Library of Medicine), 2026); Guía para el manejo de emergencias toxicológicas (Ministerio de Salud y Protección Social (Colombia) / OPS, 2017).

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Representative model, for educational purposes only.

Left main coronary artery highlighted on the Durgical 3D model