01Approach to the Critical Patient/attcp50

Immediate stabilization

›Airway and breathing threats

›Airway compromise from CNS depression or seizure

›Oxygen via non-rebreather 15 L/min

›Positioning to protect airway

›Escalating oxygen requirement

›SpO2 target >94%

›Intubation if airway unprotected or respiratory failure

›Hyperthermia >40°C is immediately life-threatening

›Core temperature mandatory via rectal or esophageal probe

›Active cooling with ice packs, cold IV fluids, evaporative cooling

›Circulation priorities

›Hypertension and tachycardia management

›Benzodiazepines first-line for all sympathomimetic features

›Avoid beta-blockers due to unopposed alpha stimulation risk

›QRS widening on ECG is a cardiac emergency

›Sodium bicarbonate 1-2 mEq/kg IV bolus immediately

›Repeat until QRS narrows or pH >7.55

›Hemodynamic collapse in late-stage toxicity

›Large-bore IV access, aggressive fluid resuscitation

›Consider VA-ECMO for refractory cardiogenic shock

Monitoring and escalation targets

›Continuous monitoring bundle

›Continuous cardiac monitoring for arrhythmia detection

›QRS interval target <120 ms

›QTc monitoring for torsade risk

›Frequent vital sign reassessment

›Temperature trend every 15 minutes in hyperthermia

02History/hx75

Exposure history

›Route of administration

›Intranasal (snorting)

›Slower onset, 3-5 minute onset

›Duration 60-90 minutes

›IV injection

›Onset in seconds

›Duration approximately 30 minutes

›Inhaled (crack cocaine)

›Onset in seconds, highest peak levels

›Duration approximately 30 minutes

›Oral or rectal

›Slower onset, longer and variable duration

›Timing and quantity

›Last use and cumulative dose over the episode

›Baseline half-life 60-120 minutes

›Repeated dosing prolongs effective half-life considerably

›Binge pattern versus single use

›Binge increases hyperthermia and arrhythmia risk

›Co-ingestions

›Alcohol co-ingestion

›Produces cocaethylene via hepatic transesterification

›Cocaethylene aggravates cardiac ion channel inhibition

›Longer half-life than cocaine, prolonging toxicity

›Opioids (speedball combination)

›Respiratory depression masked by stimulant effect

›Risk of opioid toxidrome as cocaine wears off

›Other stimulants or adulterants

›Levamisole adulterant: neutropenia and vasculitis

›Fentanyl contamination: respiratory depression risk

Chief complaint and symptoms

›Cardiovascular symptoms

›Chest pain (most common ED complaint in cocaine toxicity)

›Character: pressure, burning, or atypical

›Cocaine-associated MI incidence approximately 6% in those presenting with chest pain

›Palpitations and perceived irregular heartbeat

›Dyspnea

›Neurological symptoms

›Headache: hemorrhagic stroke concern

›Thunderclap onset is particularly alarming

›Seizures: may herald severe toxicity or imminent cardiac arrest

›Focal weakness or numbness suggesting ischemic stroke

›Agitation, paranoia, or hallucinations

›Tactile hallucinations (formication, "coke bugs") characteristic

›Other symptoms

›Abdominal pain: mesenteric ischemia or body packing concern

›Hemoptysis: crack lung or pulmonary hemorrhage

›Dark urine: rhabdomyolysis

›Muscle pain or weakness: rhabdomyolysis

Body packing and stuffing

›Internal drug concealment screening

›Body packing (organized smuggling)

›Well-wrapped packets, large amounts

›Symptom onset from packet rupture; may be delayed

›Body stuffing (hasty concealment to avoid arrest)

›Poorly wrapped, small amounts

›Earlier symptom onset due to poor wrapping

›Packet rupture presentation

›Sudden onset severe toxicity after prior stability

›Massive and prolonged cocaine release

Risk factors

›High-risk features for severe toxicity

›IV or inhaled route: rapid onset and high peak levels

›Concurrent alcohol use: cocaethylene formation

›Pre-existing cardiac disease

›CAD, cardiomyopathy, LVH, channelopathies

›Brugada syndrome: cocaine unmasks latent phenotype

›Chronic cocaine use

›Accelerated atherosclerosis

›LV hypertrophy and myocardial fibrosis

›Acidosis intensifies sodium channel blockade

›Repeated dosing within episode

Past medical history

›Relevant comorbidities

›Prior cocaine-related events: MI, stroke, seizures

›Known cardiac arrhythmias or channelopathies

›Chronic kidney disease: impaired drug clearance

›Hepatic disease: cocaine metabolized by liver and plasma esterases

›HIV, hepatitis: IV drug use complications

›Psychiatric history: psychosis, bipolar disorder

03Physical Exam/exam45

Vital signs

›Hemodynamic assessment

›Tachycardia: early feature of sympathomimetic toxidrome

›Heart rate >100 bpm expected in acute toxicity

›Bradycardia: late and ominous finding

›Hypertension: early feature

›SBP >180 mmHg warrants aggressive management

›Hypotension: late-stage toxicity, circulatory failure

›Hyperthermia

›Core temperature >40°C immediately life-threatening

›Rectal or esophageal measurement required (peripheral unreliable)

›Tachypnea

Neurological exam

›Level of consciousness and agitation

›GCS score

›Agitation severity: mild to extreme (excited delirium)

›Excited delirium features

›Extreme agitation, superhuman strength, impervious to pain

›Associated with hyperthermia and sudden cardiac arrest risk

›Focal neurological findings

›Focal weakness or drift suggesting stroke

›Aphasia or neglect

›Seizure activity

›Generalized tonic-clonic versus focal

›Post-ictal state

›Pupils

›Bilateral mydriasis (characteristic of sympathomimetic toxidrome)

›Asymmetric pupils suggesting stroke or herniation

04Differential Diagnosis/ddx50

Sympathomimetic toxidromes

›Other stimulant toxicity

›Methamphetamine toxicity (T43.621 ICD-10)

›Longer duration of action (8-24 hours)

›Higher rate of hyperthermia and psychosis

›Synthetic cathinones (bath salts) (T43.69)

›Variable potency and unpredictable presentation

›MDMA toxicity (T43.641)

›Hyponatremia due to ADH release and compulsive water drinking

›Amphetamine toxicity (T43.621)

›Similar sympathomimetic profile

Hyperthermia syndromes

›Serotonin syndrome

›Clonus and hyperreflexia are prominent (distinguish from cocaine)

›Diarrhea and flushing

›Usually medication-triggered

›Neuroleptic malignant syndrome

›Lead-pipe rigidity, altered mental status, hyperthermia

›Slower onset over days

›Antipsychotic exposure history

›Anticholinergic toxidrome

›Dry skin and mucous membranes (versus diaphoresis in cocaine)

›Mydriasis and tachycardia shared features

›Urinary retention and decreased bowel sounds

›Thyroid storm (E05.5)

›Tachycardia, hyperthermia, agitation

›Precipitating event, thyroid history, goiter

05Laboratory Tests/lt43

Cardiac biomarkers

›Troponin

›Serial troponin (0h and 2-3h) for chest pain evaluation

›Cocaine-associated MI incidence approximately 6% in chest pain presentations

›Troponin elevation may reflect vasospasm, thrombosis, or direct myocardial toxicity

›High-sensitivity troponin reduces observation time requirements

Metabolic panel

›Basic metabolic panel

›Electrolytes for hyperkalemia (rhabdomyolysis) and hyponatremia

›Hyponatremia may indicate SIADH or compulsive water drinking

›Hyperkalemia with rhabdomyolysis can precipitate arrhythmia

›Renal function (creatinine, BUN)

›Acute kidney injury from rhabdomyolysis or direct renal vasoconstriction

›Glucose

›Hypoglycemia in malnourished chronic users

Rhabdomyolysis assessment

›Creatine kinase (CK)

›Rhabdomyolysis screening mandatory with agitation, hyperthermia, or seizures

›CK >5000 U/L indicates significant rhabdomyolysis

›Urine output target >2 mL/kg/h during aggressive fluid resuscitation

›Urinalysis with microscopy

›Myoglobinuria: urine dipstick positive for blood without RBCs

›Dark (tea-colored) urine is characteristic

Hematology and coagulation

›Complete blood count

›Leukocytosis in acute toxicity or infection

›Neutropenia: levamisole adulterant causing agranulocytosis

›Coagulation studies for DIC screening

06Diagnostic Tests/dt73

Scoring Systems

›ACEP clinical decision tools for cocaine-associated chest pain

›Cocaine-associated chest pain (CACP) has no validated dedicated scoring tool

›Standard ACS risk stratification applies (TIMI, GRACE) with cocaine modifications

›HEART score may be applied with caution; cocaine as a risk factor

›Observation protocol for cocaine-associated chest pain

›Negative serial troponins at 0h and 2-3h with normal baseline ECG allows discharge

›6-hour observation recommended for moderate-risk presentations

›ACEP Level B recommendation for observation protocol in low-risk cocaine chest pain

Scoring Systems (toxicology)

›Poison severity score and clinical severity assessment

›Mild toxicity: tachycardia, mild hypertension, agitation resolved with benzodiazepines

›Heart rate 100-130 bpm

›SBP 140-180 mmHg

›Moderate toxicity: persistent vital sign abnormalities, seizures, ECG changes

›QRS 100-120 ms or QTc prolongation

›Severe toxicity: cardiac arrest, refractory hyperthermia, status epilepticus

›QRS >120 ms, ventricular arrhythmias

MRI

›Brain MRI indications

›Cocaine-associated stroke evaluation

›Diffusion-weighted imaging (DWI) for acute ischemic stroke

›Sensitivity for acute stroke >95% (superior to CT in posterior fossa)

›Preferred over CT when posterior circulation stroke suspected

›MRI angiography (MRA)

›Cerebral vasospasm assessment in cocaine-associated stroke

›Intracranial aneurysm screening in hemorrhagic presentation

›Cardiac MRI (CMR) for chronic users

›Myocardial fibrosis assessment

›LV function quantification in cocaine cardiomyopathy

›Not for acute ED evaluation; deferred outpatient use

CT

›CT head without contrast

›Indications in cocaine toxicity

›Sudden severe headache with cocaine use

›Focal neurological deficit

›First-time seizure in cocaine user

›Altered mental status not explained by toxidrome

›Performance for hemorrhagic stroke

›Sensitivity 98% within 6 hours of symptom onset

›Sensitivity decreases after 24-48 hours

›CT angiography of the aorta

›Indication: suspected aortic dissection

›Sensitivity and specificity approaching 100% for dissection

›ACEP Level B recommendation for CTA in aortic dissection

›CT pulmonary angiography

›If pulmonary embolism suspected in IV drug user

›Abdominal CT

›Body packing: CT abdomen and pelvis to identify and count packets

›Hyperdense packets visible on non-contrast CT

›Serial imaging until all packets confirmed passed

›Mesenteric ischemia: CT with IV contrast

›Bowel wall thickening, pneumatosis, mesenteric free air

Ultrasound

›Point-of-care cardiac ultrasound (POCUS)

›LV function assessment

›Global hypokinesis in cocaine-induced cardiomyopathy

›Regional wall motion abnormality in ACS

›Pericardial effusion screening

›IVC collapsibility for volume status

›Bedside FAST for trauma

›Cocaine-associated agitation may mask traumatic injury

›Hemopneumothorax in crack cocaine (barotrauma)

›Renal and bladder ultrasound

›Hydronephrosis if oliguria out of proportion to dehydration

›Bladder retention in anticholinergic co-ingestion

ECG

›12-lead ECG interpretation

›QRS widening

›QRS >120 ms indicates sodium channel blockade

›Right heart strain pattern (S1Q3T3) or RBBB morphology

›QTc prolongation

›QTc >500 ms: high torsade de pointes risk

›Brugada-type pattern

›Coved ST elevation in V1-V2: dose-dependent sodium channel effect

›Associated with VF predisposition; treat with sodium bicarbonate

›ST segment changes

›ST elevation: STEMI versus vasospasm versus Brugada

›Diffuse ST elevation may indicate cocaine-induced coronary vasospasm

07Disposition/dispo37

ICU admission criteria

›Indications for ICU-level care

›Hyperthermia >40°C requiring active cooling

›QRS prolongation or sustained ventricular arrhythmias

›Acute coronary syndrome with troponin elevation

›Hemodynamic instability not rapidly correcting

›Refractory seizures or status epilepticus

›Rhabdomyolysis with acute kidney injury

›Intubation for airway protection or respiratory failure

›Body packing with any symptoms of toxicity

›Aortic dissection or ischemic/hemorrhagic stroke

Monitored step-down or telemetry

›Criteria for monitored bed

›QRS or QTc abnormality on presentation ECG resolving with treatment

›Troponin elevation requiring serial monitoring

›Persistent mild hypertension or tachycardia after benzodiazepines

›Asymptomatic body packers pending packet passage confirmation

Observation (6-12 hours)

›Observation indications

›Cocaine-associated chest pain with negative serial troponins and normal ECG

›Observe minimum 6 hours from last cocaine use or symptom onset

›Mild-moderate agitation resolved with benzodiazepines

›Vital signs normalized and stable for at least 1 hour off treatment

Discharge criteria

›Safe discharge requirements

›Symptom resolution with normal vital signs for at least 1 hour

›Normal or baseline ECG

›Negative serial troponins if chest pain was presenting complaint

08Treatment/t118

Benzodiazepines (first-line for all sympathomimetic features)

›Benzodiazepine dosing

›Midazolam IM

›5-10 mg IM for agitation requiring rapid control

›Onset 3-5 minutes, preferred route when IV not established

›Diazepam IV

›5-10 mg IV every 5-10 minutes

›Titrate to sedation and vital sign control

›Lorazepam IV

›2-4 mg IV every 5-10 minutes

›Repeat as needed for agitation and seizures

›High and repeated doses often required

›Cocaine toxicity may require substantially higher doses than typical anxiolysis

›Class I recommendation (AHA 2023) as primary therapy

Sodium bicarbonate for QRS widening

›Sodium bicarbonate protocol

›First-line for QRS >120 ms or Brugada-pattern ECG

›1-2 mEq/kg (approximately 2 ampoules, 100 mEq total) IV bolus

›Repeat bolus until QRS narrows to <120 ms or pH >7.55

›Mechanism

›Alkalinization reduces cocaine binding to sodium channels

›Sodium load overcomes channel blockade

›If sodium bicarbonate unavailable

›3% hypertonic saline 200 mL IV as alternative

›Refractory QRS widening

›Lidocaine 1-1.5 mg/kg IV (competitive sodium channel binding)

›Avoid class IA and IC antiarrhythmics (worsen blockade)

Lipid emulsion therapy

›20% lipid emulsion (Intralipid) indications

›Refractory cardiac arrest or severe toxicity unresponsive to standard therapy

›1.5 mL/kg IV bolus over 2-3 minutes

›Followed by 0.25 mL/kg/min infusion for 30-60 minutes

›Approximately 100 mL bolus in average adult

›Mechanism: lipid sink trapping cocaine away from cardiac tissue

›AHA 2023 guideline consideration for refractory toxicity

›Activated after sodium bicarbonate and ACLS have failed

Hyperthermia management

›Active cooling measures

›Ice packs to neck, axillae, and groin

›Cool IV fluid infusion

›Evaporative cooling: misting with fan

›Target temperature <38.5°C within 30 minutes

›Sedation and paralysis if severe agitation prevents cooling

›Benzodiazepines plus propofol or non-depolarizing neuromuscular blockade

›Succinylcholine caution: hyperkalemia risk with rhabdomyolysis

Hypertensive emergency management

›First-line: benzodiazepines (treat the underlying sympathomimetic excess)

›Second-line antihypertensives for refractory hypertension

›Phentolamine IV

›5-10 mg IV bolus (alpha-1 antagonist)

›Preferred for cocaine-induced hypertension and ischemia

›Nicardipine IV

›5 mg/h IV infusion, titrate up by 2.5 mg/h every 5-15 minutes

›Maximum 15 mg/h

›Nitroglycerin IV

›For cocaine-associated chest pain and coronary vasospasm

›5-20 mcg/min infusion, titrate to effect

›Sodium nitroprusside

›Reserved for refractory severe hypertension

›Risk of cyanide toxicity with prolonged use

Beta-blockers (contraindicated)

›Beta-blocker contraindication

›Beta-blockade causes unopposed alpha-1 receptor stimulation

›Worsened coronary vasoconstriction

›Potential paradoxical hypertension and bradycardia

›Propranolol demonstrated worsened coronary vasoconstriction in human studies

›Metoprolol associated with PEA arrest and death in case reports

›If beta-blockade absolutely required

›Labetalol or carvedilol (combined alpha/beta blockade) less harmful

›Remains controversial; consult toxicology

Cocaine-associated chest pain and ACS

›Initial management of cocaine-associated chest pain

›Aspirin 162-325 mg chewed if ACS suspected

›Nitroglycerin for vasospastic or ischemic chest pain

›Benzodiazepines for associated agitation and hypertension

›Avoid beta-blockers as initial therapy

›STEMI management

›PCI preferred over fibrinolytics

›Fibrinolytics associated with higher hemorrhagic complications in cocaine users

›Proceed to cath lab if STEMI confirmed and PCI available

›Antiplatelet therapy per standard ACS protocol

›Heparin anticoagulation per standard protocol

Seizure management

›Cocaine-induced seizure protocol

›Benzodiazepines first-line

›Lorazepam 2-4 mg IV or diazepam 5-10 mg IV

›Repeat every 5 minutes if seizure continues

›Second-line for refractory seizures

›Phenobarbital 15-20 mg/kg IV at 50-100 mg/min

›Propofol infusion with airway secured

›Phenytoin is contraindicated

›Sodium channel blocking properties worsen cocaine cardiotoxicity

›Post-seizure evaluation

›CT head to exclude hemorrhagic stroke

›Metabolic workup including glucose, electrolytes

Rhabdomyolysis treatment

›Rhabdomyolysis management

›Aggressive IV hydration

›Normal saline 1-2 L/h initially

›Target urine output >2 mL/kg/h

›Urinary alkalinization not routinely recommended

›May inhibit elimination of co-ingested amphetamines

›Electrolyte monitoring

›Serial potassium for hyperkalemia

›Calcium for hypocalcemia (sequestered in damaged muscle)

›Renal replacement therapy if AKI progresses and diuresis inadequate

Agitation management adjuncts

›Second-line agitation agents

›Droperidol IM or IV

›5-10 mg IM; faster onset than lorazepam for severe agitation

›Monitor QTc after administration

›Dexmedetomidine IV

›0.5-1 mcg/kg/h infusion

›Alpha-2 agonist reduces agitation, hypertension, and tachycardia

›Ketamine IM for excited delirium

›4-5 mg/kg IM for chemical restraint when immediate control needed

›Provides dissociative sedation while maintaining airway reflexes

Body packer management

›Asymptomatic body packers

›Whole bowel irrigation with polyethylene glycol solution

›1-2 L/h orally or via NG tube until rectal effluent clear

›Serial abdominal imaging until all packets confirmed passed

›Activated charcoal only if packet rupture suspected and airway protected

›Strict NPO and continuous cardiac monitoring

›Symptomatic body packers (packet rupture)

›Immediate surgical consultation for laparotomy

›No antidotal therapy reverses lethal cocaine release from ruptured packets

›Aggressive supportive care pending surgery

›Benzodiazepines and sodium bicarbonate as toxidrome-directed therapy

09Special Populations/sp44

Pregnancy

›Cocaine toxicity in pregnancy

›Maternal cardiovascular effects

›Severe hypertension increases risk of placental abruption

›Preeclampsia mimicry: differentiate from true preeclampsia

›Hypertensive urgency managed with labetalol or hydralazine

›Fetal effects

›Uteroplacental vasoconstriction leading to fetal distress

›Fetal heart rate monitoring mandatory

›Preterm labor precipitation

›Medication considerations in pregnancy

›Benzodiazepines: use at lowest effective dose (pregnancy category D in third trimester)

›Sodium bicarbonate: safe for QRS widening

›Avoid phentolamine: limited safety data

›Obstetric consultation mandatory for any pregnant patient with cocaine toxicity

›Fetal viability assessment

›Emergency C-section if fetal compromise

Geriatric

›Cocaine toxicity in older adults

›Higher baseline cardiovascular risk

›Pre-existing CAD, LVH, heart failure increase complication rates

›Lower threshold for troponin elevation and ACS diagnosis

›ECG baseline abnormalities complicate QRS/QTc interpretation

›Pharmacokinetic considerations

›Reduced hepatic and renal clearance prolongs toxicity duration

›Decreased volume of distribution increases peak concentrations

›Medication adjustments

›Benzodiazepines: start low, titrate carefully due to respiratory depression risk

10Background/b79

Epidemiology

›Cocaine use statistics

›Prevalence in the United States

›Approximately 5 million current cocaine users in the US

›Second most common illicit drug-related ED visit after cannabis

›Demographics

›Most common age group: 18-45 years

›Male predominance in ED presentations

›ED visit burden

›Cocaine associated with approximately 500,000 ED visits annually in the US

›Chest pain is the most common presenting complaint

›Mortality

›Cocaine implicated in approximately 24% of drug-related cardiovascular deaths

›Most fatalities from cardiac arrhythmia, MI, or stroke

›Body packing epidemiology

›3-5% mortality if packets rupture and are not surgically removed

›French poison center data: 2020-2024 body packer rupture mortality significant

Pathophysiology

›Cocaine mechanism of action

›Catecholamine reuptake blockade (primary mechanism)

›Blocks dopamine, norepinephrine, and serotonin reuptake transporters

›Net effect: sympathomimetic excess

›Clinical: tachycardia, hypertension, mydriasis, diaphoresis, hyperthermia

›Sodium channel blockade (local anesthetic effect)

›Blocks fast voltage-gated sodium channels (class I antiarrhythmic property)

›QRS prolongation and ventricular arrhythmia risk

›Brugada phenotype unmasking in genetically susceptible individuals

›Effect worsened by acidosis and hyponatremia

›Potassium channel blockade

›QTc prolongation and torsade de pointes risk

›Cardiovascular pathophysiology

›Coronary vasospasm

›Alpha-1 receptor activation in coronary vessels

›Endothelin-1 upregulation

›Persists up to 90 minutes after cocaine use

›Coronary thrombosis

›Platelet activation and aggregation

›Catecholamine-induced prothrombotic state

›Aortic dissection mechanism

›Acute hypertensive surge tears aortic intima

›Underlying medial degeneration from chronic cocaine use

›Cardiomyopathy with chronic use

›LV hypertrophy, myocardial fibrosis, dilated cardiomyopathy

›Cocaethylene formation

›Hepatic transesterification of cocaine and ethanol

›Produces cocaethylene with similar potency to cocaine

›Half-life longer than cocaine, prolonging and intensifying toxicity

›Higher cardiotoxicity than cocaine alone

›Pharmacokinetics

›Elimination

›Plasma half-life 60-120 minutes

›Metabolized by plasma cholinesterases and liver esterases

›Major urinary metabolite: benzoylecgonine (detectable 2-4 days)

›Norcocaine metabolite

›Hepatotoxic metabolite from hepatic N-demethylation

›Responsible for liver injury in cocaine users

Therapeutic Considerations

›Evidence base for benzodiazepines

›First-line for agitation, hypertension, tachycardia, seizures, and hyperthermia

›AHA 2023 Focused Update: Class I recommendation

›Treat underlying sympathomimetic excess before specific antihypertensives

›High doses often required in severe toxicity

›No ceiling effect in emergency setting when airway managed

›Sodium channel blockade treatment evidence

›Sodium bicarbonate for QRS widening

›Expert consensus and case series support (Class IIa)

›Alkalinization reduces cocaine-sodium channel affinity

›Hypertonic saline as alternative for isolated sodium loading

›Lipid emulsion evidence

›Case reports and animal studies show benefit in refractory toxicity

›AHA 2023 guideline: consider for refractory cardiac arrest from local anesthetic toxicity

›Beta-blocker controversy

›Traditionally contraindicated due to unopposed alpha stimulation

›Human studies confirm worsened coronary vasoconstriction with propranolol

›Labetalol has combined alpha/beta blockade and is less harmful

›Esmolol and metoprolol generally avoided

›AHA 2023 guideline: beta-blockers generally contraindicated in cocaine toxicity

›Cocaine-associated ACS treatment differences from standard ACS

›Vasospasm is primary mechanism; thrombosis is secondary

›Nitroglycerin and benzodiazepines preferred over beta-blockers

›PCI preferred over fibrinolytics due to hemorrhagic complication risk

›2021 AHA/ACC Chest Pain Guideline: specialized protocol for cocaine-associated chest pain

11Patient Discharge Instructions/pdi31

copy discharge instructions

›Cocaine toxicity discharge instructions

›What happened to you today

›You came to the emergency department because of harmful effects of cocaine

›Your heart, blood pressure, and nervous system were affected

›You have been treated and your condition has stabilized

›Return to the emergency department immediately if you experience

›Chest pain, pressure, or tightness

›Palpitations or feeling your heart racing or skipping beats

›Shortness of breath or difficulty breathing

›Severe headache, especially if sudden and worst of your life

›Weakness, numbness, or paralysis of face, arm, or leg

›Difficulty speaking or understanding speech

›Seizures or convulsions

›Fever or feeling extremely hot

›Dark or tea-colored urine

›Severe abdominal pain

›Feeling faint or loss of consciousness

›Important information about cocaine and your health

›Cocaine use causes serious and life-threatening heart and brain problems

›Effects can be worsened and prolonged by alcohol consumed with cocaine

›Fentanyl is commonly mixed into cocaine without your knowledge and is fatal

›Each episode of cocaine use increases your risk of heart attack and stroke

›Medications and follow-up

›Take all medications prescribed exactly as directed

›Follow up with your family doctor or specialist as scheduled

›Contact your doctor if new or worsening symptoms develop before your appointment

›Resources and support

12References/r29

Guidelines and key sources

›American Heart Association guidelines

›Lavonas EJ, et al. 2023 AHA Focused Update on Management of Cardiac Arrest or Life-Threatening Toxicity Due to Poisoning. Circulation. 2023

›Primary guideline for cocaine toxicity management including benzodiazepines, sodium bicarbonate, lipid emulsion

›Cao D, et al. Part 10: Adult and Pediatric Special Circumstances of Resuscitation. 2025 AHA Guidelines for CPR and ECC. Circulation. 2025

›Updated resuscitation protocols for toxicological cardiac arrest

›Gulati M, et al. 2021 AHA/ACC Guideline for Evaluation and Diagnosis of Chest Pain. J Am Coll Cardiol. 2021

›Evidence-based approach to cocaine-associated chest pain evaluation

›Cardiovascular toxicity references

›Havakuk O, Rezkalla SH, Kloner RA. The Cardiovascular Effects of Cocaine. JACC. 2017

›Comprehensive review of cocaine cardiovascular mechanisms and management

›Lucyk SN. Acute Cardiovascular Toxicity of Cocaine. Can J Cardiol. 2022

›Canadian perspective on acute cocaine cardiovascular management

›Lange RA, Hillis LD. Cardiovascular Complications of Cocaine Use. NEJM. 2001

›Landmark review of cocaine cardiovascular pathophysiology

›Pharmacology and toxicology

›Roque Bravo R, et al. Cocaine: An Updated Overview on Chemistry, Detection, Biokinetics, and Pharmacotoxicological Aspects. Toxins. 2022

›Pharmacokinetics, metabolism, and pharmacodynamics

›Riezzo I, et al. Side Effects of Cocaine Abuse: Multiorgan Toxicity and Pathological Consequences. Curr Med Chem. 2012

›Systemic toxicity mechanisms across organ systems

›Zimmerman JL. Cocaine Intoxication. Crit Care Clin. 2012

›Critical care management of severe cocaine toxicity

›Body packing references

›von Fabeck K, et al. Body Packers and Body Stuffers: Cocaine Intoxications Reported to French Poison Centers (2020-2024). Clin Toxicol. 2025

›Traub SJ, Hoffman RS, Nelson LS. Body Packing: The Internal Concealment of Illicit Drugs. NEJM. 2003

›Heymann-Maier L, et al. Emergency Department Management of Body Packers and Body Stuffers. Swiss Med Wkly. 2017

›Addiction medicine guidelines

›The ASAM/AAAP Clinical Practice Guideline on the Management of Stimulant Use Disorder. J Addict Med. 2024

Evidence & Review

Evidence & Review