Cocaine intoxication

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Cocaine intoxication
Other names: Cocaine toxicity, cocaine poisoning
Cocaine
SpecialtyToxicology
SymptomsFast heart rate, high blood pressure, agitation, high body temperature, sweating[1]
ComplicationsAcute coronary syndrome, seizures, stroke, pneumothorax, rhabdomyolysis, excited delirium[1][2]
Usual onsetWithin 5 sec to 5 min[1]
CausesCocaine[3]
Diagnostic methodUrine drug test[1]
Differential diagnosisLow blood sugar, anticholinergic toxicity, delirium tremens, schizophrenia, neuroleptic malignant syndrome[2]
MedicationLorazepam, labetalol, sodium bicarbonate[1]
Frequency19 million people (2018)[4]
Deaths15,900 (2019, USA)[5]

}} Cocaine intoxication refers to the negative and potentially life threatening effects of cocaine.[3] Symptoms that occur shortly after use often include fast heart rate, high blood pressure, and agitation.[1] Other effects may include high body temperature and sweating.[1] Complications may include acute coronary syndrome, seizures, stroke, pneumothorax, and excited delirium.[1][2]

Cocaine may be smoked, injected, or snorted.[1] Onset of effects is within 5 seconds when smoked, a minute when injected, and within 5 minutes when snorted.[1] Effects last for 5 to 90 minutes.[1] Toxicity may also occur due to body packing or body stuffing.[1] Diagnosis can be supported by urine testing which remains positive for one or two days after a single us and potentially weeks with long term use.[1] False positives are uncommon.[1]

The initial treatment is typically with a benzodiazepine such as lorazepam or midazolam by injection.[1] If high blood pressure persists, it may be managed with nicardipine or labetalol.[1] High temperature may require additional cooling techniques.[1] Aspirin and nitroglycerin may be used in those with chest pain.[1] Those with a wide QRS complex or cardiac arrest may be treated with sodium bicarbonate.[1][6]

About 19 million people used cocaine globally in 2018, most commonly in North America and Western Europe.[4] In the United States about half a million episodes of cocaine use required emergency department care in 2011 and such use was involved in 15,900 deaths in 2019.[2][5] Cocaine intoxication can result in death.[2] Cocaine is frequently mixed with levamisole which may result in low white blood cells and vasculitis.[2]

Signs and symptoms

Cocaine increases alertness, feelings of well-being, euphoria, energy, sociability, and sexuality. The former are some of the desired effects of cocaine intoxication.

Mild adverse effects include anxiety, increased temperature, paranoia, restlessness, and teeth grinding. With prolonged use, the drug can cause chronic complications like insomnia, weight loss, anorexia, persistent tachycardia, heart failure, kidney failure, hallucinations, and paranoid delusions.[7]

Depression with suicidal ideation may develop in heavy users.[8] Finally, a loss of vesicular monoamine transporters, neurofilament proteins, and other morphological changes appear to indicate a long-term damage to dopamine neurons.[9] Chronic intranasal usage can degrade the cartilage separating the nostrils (the nasal septum), which can eventually lead to its complete disappearance.[10]

Studies have shown that cocaine usage during pregnancy triggers premature labor[11] and may lead to abruptio placentae.[12]

In cases of severe acute intoxication, potentially lethal adverse effects include prolonged episodes of arrhythmia (i.e., a group of abnormal heart rhythms that also include tachycardia), heavy hypoglycemia, tremors, convulsions, hyperthermia (i.e., markedly increased core temperature), untreated uremia, myocardial infarction, stroke, and sudden cardiac arrest.[1]

Overdose

Cocaine can be snorted, swallowed, injected, or smoked. Most deaths due to cocaine are accidental but may also be the result of body packing or stuffing with rupture in the gastrointestinal tract. Use of cocaine causes abnormally fast heart rhythms and a marked elevation of blood pressure (hypertension), which can be life-threatening. This can lead to death from acute myocardial infarction, acute respiratory failure (i.e., hypoxemia, with or without hypercapnia), stroke, cerebral hemorrhage, and sudden cardiac arrest.[13] Cocaine overdose may result in hyperthermia as stimulation and increased muscular activity cause greater heat production. Heat loss is also inhibited by the cocaine-induced vasoconstriction. Cocaine and/or associated hyperthermia may cause muscle cell destruction (rhabdomyolysis) and myoglobinuria resulting in kidney failure. Individuals with cocaine overdose should be transported immediately to the nearest emergency department, preferably by ambulance in case cardiac arrest occurs en route. According to the National Institute on Drug Abuse, approximately 14,600 deaths occurred in the US in 2017 due to cocaine overdose.[14] Because of the increase in heart rate, cocaine users can be prone to elevated body temperatures, tremors, chest pains, and subject to nausea and vomiting. Some psychological symptoms due to an overdose include paranoia, delirium, anxiety as well as panicked feelings.[15] Some signs of an overdose of cocaine are difficulty breathing, loss of urine control, bluish color of the skin, loss of awareness or surroundings, and high blood pressure. Although not as common, death can be caused from an over intoxication of cocaine.[16] Most severe overdoses occur when users combine cocaine with other substances like alcohol or heroin, which increase the effects and heighten the chances of having a dangerous overdose. Treating an overdose can be done by bringing back blood flow to the heart, and restoring the body with oxygen rich blood, especially for the brain to reduce the risk of stroke.[17] Cocaine overdoses have fluctuated over the years. From 2006 to 2010 there has been a decline in the number of reported cases. Though, from 2010 to 2015 there has been an increase in the reported cases involving over cocaine Intoxication. As far as biological sex is concerned, it's found that males have a much higher chance of overdosing than females. The ratio of male to female cocaine overdoses is 3:1.[18]

  • US yearly overdose deaths involving cocaine.[14]

    US yearly overdose deaths involving cocaine.[14]

  • US opioid involvement in cocaine overdose deaths. Green line is cocaine and any opioid. Gray line is cocaine without any opioids. Yellow line is cocaine and other synthetic opioids.[14]

    US opioid involvement in cocaine overdose deaths. Green line is cocaine and any opioid. Gray line is cocaine without any opioids. Yellow line is cocaine and other synthetic opioids.[14]

Withdrawal

Cocaine withdrawal isn't as severe as the withdrawal from other substances. For example, substances like alcohol and benzodiazepines can involve severe physical withdrawal symptoms while cocaine results in mostly psychological symptoms. Physiological changes caused by cocaine withdrawal include vivid and unpleasant dreams, insomnia, hypersomnia, anger, increased appetite, weight gain, psychomotor retardation, agitation, depression, and anxiety. According to a study done by Gawin and Kleber in 1986, there are three phases in the withdrawal process. They observed the behavior of 30 cocaine-dependent individuals. Phase one, the crash, is characterized by acute dysphoria, irritability and anxiety, increased desire for sleep, exhaustion, increased appetite, decreased craving to use. Phase two, withdrawal, is characterized by increasing craving to use, poor concentration, some irritability and some lethargy, which persisted for up to 10 weeks. Lastly, phase three is characterized by the intermittent craving to use in the context of external cues.[19] Cocaine and its metabolites are completely eliminated from the body by 3 days.[20] There are not any FDA-approved medications that specifically help treat cocaine withdrawal, however, there are some useful medications that could possibly help individuals overcome their addiction.

Pathophysiology

Cocaine pharmacodynamics involve multiple complex mechanisms. Although it has a short half-life (~ 1 hour),[20] cocaine metabolites, which rise in concentrations several hours after cocaine ingestion, persist in circulation for up to 24 hours, and may cause delayed or recurrent coronary vasoconstriction.[21] This drug binds and blocks monoamine (dopamine, epinephrine, norepinephrine, and serotonin) re-uptake transporters with equal affinity. Monoamines accumulate in the synaptic cleft resulting in enhanced and prolonged sympathetic effects. Cocaine's acute effect in the central nervous system is to raise the amount of dopamine and serotonin in the nucleus accumbens (the pleasure center in the brain). When this effect ceases due to metabolism of cocaine, depletion of associated neurotransmitters, and receptor down-regulation (tachyphylaxis), the cocaine user may experience dysphoria, or a "crash" after the initial high. The principal actions of cocaine on the cardiovascular system are from alpha- and beta-1-adrenoceptor stimulation resulting in increased heart rate, systemic arterial pressure, and myocardial contractility, which are major determinants of myocardial oxygen demand. Cocaine and its metabolites may cause arterial vasoconstriction hours after use. Epicardial coronary arteries are especially vulnerable to these effects, leading to decreased myocardial oxygen supply. Cocaine-induced platelet activation and thrombus formation is another deleterious effect, caused by alpha-adrenergic- and adenosine diphosphate-mediated increase in platelet aggregation.[22] Plasminogen activator inhibitor is also increased following cocaine use, thereby promoting thrombosis. Cocaine acts like a class I antiarrhythmic agent by blocking sodium and potassium channels, in a similar way of local anesthetics such as lidocaine, and interferes with action potential propagation.[23][24] This Vaughn-Williams class IC effect increases the risk of conduction disturbance and tachyarrhythmias. Adding to its complex toxicity, cocaine targets muscarinic acetylcholine, N-methyl-D-aspartate (NMDA), sigma, and kappa-opioid receptors.[25][26][27][28]

Management

A "cocaine alert" sign posted by GGD Amsterdam: the sign reminds people to "Call 112 for an ambulance."

Emergency treatment of cocaine-associated high body temperature consists of giving a benzodiazepine and physical cooling. Cooling is best accomplished with tepid water misting and cooling with a fan.[29][30] There is no specific antidote for cocaine. The chest pain, high blood pressure, and increased heart rate caused by cocaine may be also treated with benzodiazepines.[31] Multiple and escalating dose of benzodiazepines may be necessary to achieve effect, which increases risk of over-sedation and respiratory depression. A review of cocaine cardiovascular toxicity found benzodiazepines may not always reliably lower heart rate and blood pressure.[32]

Aspirin is often recommended for cocaine-associated chest pain.[24][33][34]

Nitric-oxide mediated vasodilators, such as nitroglycerin and nitroprusside, are effective at lowering blood pressure and reversing coronary arterial vasoconstriction, but not heart rate.[32] Nitroglycerin is useful for cocaine-induced chest pain, but the possibility of reflex tachycardia must be considered.[35]

Alpha-blockers such as phentolamine have been recommended[31] and may be used to treat cocaine-induced hypertension and coronary arterial vasoconstriction, but these agents do not reduce heart rate.[32][36] Furthermore, phentolamine is rarely used, not readily available in many emergency departments, and many present-day clinicians are unfamiliar with its use.

People who are agitated are best treated with benzodiazepines, though antipsychotics such as haloperidol and olanzapine may also be useful.[32] The alpha-2 agonist dexmedetomidine may also be useful for agitation, but effects on heart rate and blood pressure are variable based on several studies and case reports.[32] Lidocaine and intravenous lipid emulsion have been successfully used for serious ventricular tachyarrhythmias in several case reports.

Beta blockers

The use of labetolol is supported by the AHA/ACC for people who have cocaine associated high blood pressure or sinus tachycardia.[34] Labetalol is a non-selective β blocker and selective α1 blocker.[32][37][38] No negative effects have been see with the use of labetalol and carvedilol in cocaine induced high blood pressure as of 2016.[32]

The use of beta blockers has been controversial being relative contraindication in some guidelines for the treatment of cocaine toxicity despite limited evidence of harm.[6][39] The phenomenon of “unopposed alpha-stimulation,” in which blood pressure increases or coronary artery vasoconstriction worsens after blockade of beta-2 vasodilation in people using cocaine, is controversial.[40][41] Many clinicians have disregarded this dogma and administer beta-blockers for cocaine-related chest pain and acute coronary syndrome, especially when there is demand ischemia from uncontrolled tachycardia.[42][43][44] Of 1,744 people in a systematic review, 7 adverse events from positible “unopposed alpha-stimulation” occurred and these were associated with propranolol (n=3), esmolol (n=3), and metoprolol (n=1).[32]

Calcium channel blockers

Calcium channel blockers may also be used to treat hypertension and coronary arterial vasoconstriction,[45] but fail to lower tachycardia based on all cocaine-related studies.[32] Non-dihydropyridine calcium channels blockers such as diltiazem and verapamil are preferable, as dihydropyridine agents such as nifedipine have much higher risk of reflex tachycardia (however, clinicians can prevent reflex tachycardia by administering beta-blockers some minutes before using the latter class of CCBs).

See also

References

  1. ↑ 1.00 1.01 1.02 1.03 1.04 1.05 1.06 1.07 1.08 1.09 1.10 1.11 1.12 1.13 1.14 1.15 1.16 1.17 1.18 1.19 Zimmerman, Janice L. (2012-10-01). "Cocaine intoxication". Critical Care Clinics. 28 (4): 517–526. doi:10.1016/j.ccc.2012.07.003. ISSN 1557-8232. PMID 22998988.
  2. ↑ 2.0 2.1 2.2 2.3 2.4 2.5 Richards, JR; Le, JK (January 2021). "Cocaine Toxicity". PMID 28613695. {{cite journal}}: Cite journal requires |journal= (help)
  3. ↑ 3.0 3.1 "Cocaine Toxicity • LITFL • CCC Toxicology". Life in the Fast Lane • LITFL. 13 January 2019. Archived from the original on 10 April 2021. Retrieved 12 April 2021.
  4. ↑ 4.0 4.1 WORLD DRUG REPORT 2020 (SET OF 6 BOOKLETS) (PDF). [S.l.]: UNITED NATIONS. 2020. pp. 17–18. ISBN 978-92-1-148345-1. Archived (PDF) from the original on 15 April 2021. Retrieved 12 April 2021.
  5. ↑ 5.0 5.1 Abuse, National Institute on Drug (29 January 2021). "Overdose Death Rates". National Institute on Drug Abuse. Archived from the original on 25 January 2018. Retrieved 12 April 2021.
  6. ↑ 6.0 6.1 Lavonas, EJ; Akpunonu, PD; Arens, AM; Babu, KM; Cao, D; Hoffman, RS; Hoyte, CO; Mazer-Amirshahi, ME; Stolbach, A; St-Onge, M; Thompson, TM; Wang, GS; Hoover, AV; Drennan, IR; American Heart, Association (17 October 2023). "2023 American Heart Association Focused Update on the Management of Patients With Cardiac Arrest or Life-Threatening Toxicity Due to Poisoning: An Update to the American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care". Circulation. 148 (16): e149–e184. doi:10.1161/CIR.0000000000001161. PMID 37721023.
  7. ↑ Glauser, Jonathan; Queen, John R. (2007-02-01). "An overview of non-cardiac cocaine toxicity". The Journal of Emergency Medicine. 32 (2): 181–186. doi:10.1016/j.jemermed.2006.05.044. ISSN 0736-4679. PMID 17307630.
  8. ↑ Narvaez, Joana C. M.; Jansen, Karen; Pinheiro, Ricardo T.; Kapczinski, Flávio; Silva, Ricardo A.; Pechansky, Flávio; Magalhães, Pedro V. (2014-08-01). "Psychiatric and substance-use comorbidities associated with lifetime crack cocaine use in young adults in the general population". Comprehensive Psychiatry. 55 (6): 1369–1376. doi:10.1016/j.comppsych.2014.04.021. ISSN 1532-8384. PMID 24933652.
  9. ↑ Little, Karley Y.; Ramssen, Eric; Welchko, Ryan; Volberg, Vitaly; Roland, Courtney J.; Cassin, Bader (2009-08-15). "Decreased brain dopamine cell numbers in human cocaine users". Psychiatry Research. 168 (3): 173–180. doi:10.1016/j.psychres.2008.10.034. ISSN 0165-1781. PMID 19233481. S2CID 27618292.
  10. ↑ Trimarchi, M.; Bussi, M.; Sinico, R. A.; Meroni, Pierluigi; Specks, U. (2013-02-01). "Cocaine-induced midline destructive lesions - an autoimmune disease?". Autoimmunity Reviews. 12 (4): 496–500. doi:10.1016/j.autrev.2012.08.009. ISSN 1873-0183. PMID 22940554.
  11. ↑ Cain, Mary A.; Bornick, Patricia; Whiteman, Valerie (2013-03-01). "The maternal, fetal, and neonatal effects of cocaine exposure in pregnancy". Clinical Obstetrics and Gynecology. 56 (1): 124–132. doi:10.1097/GRF.0b013e31827ae167. ISSN 1532-5520. PMID 23314714.
  12. ↑ Flowers, D.; Clark, J. F.; Westney, L. S. (1991-03-01). "Cocaine intoxication associated with abruptio placentae". Journal of the National Medical Association. 83 (3): 230–232. ISSN 0027-9684. PMC 2627035. PMID 2038082.
  13. ↑ O'Leary, Michael E; Hancox, Jules C (2010). "Role of voltage-gated sodium, potassium and calcium channels in the development of cocaine-associated cardiac arrhythmias". British Journal of Clinical Pharmacology. 69 (5): 427–442. doi:10.1111/j.1365-2125.2010.03629.x. ISSN 0306-5251. PMC 2856043. PMID 20573078.
  14. ↑ 14.0 14.1 14.2 Overdose Death Rates Archived 2015-11-28 at the Wayback Machine. By National Institute on Drug Abuse (NIDA).
  15. ↑ Editorial Staff. "Cocaine Overdose: Symptoms and Dangers". American Addiction Centers. Archived from the original on 2020-12-03. Retrieved 2019-10-21.
  16. ↑ "Cocaine intoxication: MedlinePlus Medical Encyclopedia". medlineplus.gov. Archived from the original on 2020-12-03. Retrieved 2019-10-21.
  17. ↑ Abuse, National Institute on Drug. "Cocaine". www.drugabuse.gov. Archived from the original on 2015-07-11. Retrieved 2019-10-21.
  18. ↑ Editorial Staff. "Cocaine Overdose: Symptoms and Dangers". American Addiction Centers. Archived from the original on 2020-12-03. Retrieved 2019-10-29.
  19. ↑ "Department of Health | The cocaine withdrawal syndrome". www1.health.gov.au. Archived from the original on 2020-12-03. Retrieved 2019-10-29.
  20. ↑ 20.0 20.1 Jufer, R. A.; Wstadik, A.; Walsh, S. L.; Levine, B. S.; Cone, E. J. (2000-10-01). "Elimination of cocaine and metabolites in plasma, saliva, and urine following repeated oral administration to human volunteers". Journal of Analytical Toxicology. 24 (7): 467–477. doi:10.1093/jat/24.7.467. ISSN 0146-4760. PMID 11043648.
  21. ↑ Brogan, Walter C.; Lange, Richard A.; Kim, Anatole S.; Moliterno, David J.; Hillis, L. David (1991-08-01). "Alleviation of cocaine-induced coronary vasoconstriction by nitroglycerin". Journal of the American College of Cardiology. 22nd Bethesda Conference: Congenital heart disease after childhood: An edpanding patient population. 18 (2): 581–586. doi:10.1016/0735-1097(91)90617-I. ISSN 0735-1097. PMID 1906905. Archived from the original on 2021-08-28. Retrieved 2020-12-31.
  22. ↑ Heesch, C. M.; Wilhelm, C. R.; Ristich, J.; Adnane, J.; Bontempo, F. A.; Wagner, W. R. (2000-06-01). "Cocaine activates platelets and increases the formation of circulating platelet containing microaggregates in humans". Heart. 83 (6): 688–695. doi:10.1136/heart.83.6.688. ISSN 1468-201X. PMC 1760877. PMID 10814631.
  23. ↑ Hariman, Robert J.; Liu, Dong; Loeb, Henry S.; McKieman, Thomas L.; Scanlon, Patrick J.; Bauman, Jerry L. (1996-02-01). "Competitive binding between cocaine and lidocaine". Journal of the American College of Cardiology. 27 (2): 80. doi:10.1016/S0735-1097(96)80520-1.
  24. ↑ 24.0 24.1 Schwartz Bryan G.; Rezkalla Shereif; Kloner Robert A. (2010-12-14). "Cardiovascular Effects of Cocaine". Circulation. 122 (24): 2558–2569. doi:10.1161/CIRCULATIONAHA.110.940569. Archived from the original on 2021-04-28. Retrieved 2021-02-28.
  25. ↑ Williams, Mark J.; Adinoff, Bryon (2008-07-01). "The role of acetylcholine in cocaine addiction". Neuropsychopharmacology. 33 (8): 1779–1797. doi:10.1038/sj.npp.1301585. ISSN 0893-133X. PMC 2667818. PMID 17928814.
  26. ↑ Haile, Colin N.; Mahoney, James J.; Newton, Thomas F.; De La Garza, Richard (2012-05-01). "Pharmacotherapeutics directed at deficiencies associated with cocaine dependence: focus on dopamine, norepinephrine and glutamate". Pharmacology & Therapeutics. 134 (2): 260–277. doi:10.1016/j.pharmthera.2012.01.010. ISSN 1879-016X. PMC 3341931. PMID 22327234.
  27. ↑ Narayanan, Sanju; Mesangeau, Christophe; Poupaert, Jacques H.; McCurdy, Christopher R. (2011-01-01). "Sigma receptors and cocaine abuse". Current Topics in Medicinal Chemistry. 11 (9): 1128–1150. doi:10.2174/156802611795371323. ISSN 1873-4294. PMID 21050176.
  28. ↑ Kivell, Bronwyn M.; Ewald, Amy W. M.; Prisinzano, Thomas E. (2014-01-01). Salvinorin A analogs and other κ-opioid receptor compounds as treatments for cocaine abuse. Advances in Pharmacology. Vol. 69. pp. 481–511. doi:10.1016/B978-0-12-420118-7.00012-3. ISBN 9780124201187. ISSN 1557-8925. PMC 4128345. PMID 24484985.
  29. ↑ Smith, Caroline J.; Johnson, John M. (2016-04-01). to hyperthermia.pdf "Responses to hyperthermia. Optimizing heat dissipation by convection and evaporation: Neural control of skin blood flow and sweating in humans" (PDF). Autonomic Neuroscience: Basic & Clinical. 196: 25–36. doi:10.1016/j.autneu.2016.01.002. ISSN 1872-7484. PMID 26830064. S2CID 3790152. Archived from the original on 2019-04-26. Retrieved 2019-07-26. {{cite journal}}: Check |url= value (help)
  30. ↑ Richards, John R.; Colby, Daniel K. (2016-01-01). "Stimulant-induced hyperthermia and ice-water submersion: Practical considerations". Clinical Toxicology. 54 (1): 69–70. doi:10.3109/15563650.2015.1104536. ISSN 1556-9519. PMID 26515112. S2CID 207553540.
  31. ↑ 31.0 31.1 McCord, J; Jneid, H; Hollander, JE; de Lemos, JA; Cercek, B; Hsue, P; Gibler, WB; Ohman, EM; Drew, B; Philippides, G; Newby, LK; American Heart Association Acute Cardiac Care Committee of the Council on Clinical, Cardiology (Apr 8, 2008). "Management of cocaine-associated chest pain and myocardial infarction: a scientific statement from the American Heart Association Acute Cardiac Care Committee of the Council on Clinical Cardiology". Circulation. 117 (14): 1897–907. doi:10.1161/CIRCULATIONAHA.107.188950. PMID 18347214.
  32. ↑ 32.0 32.1 32.2 32.3 32.4 32.5 32.6 32.7 32.8 Richards, John R.; Garber, Dariush; Laurin, Erik G.; Albertson, Timothy E.; Derlet, Robert W.; Amsterdam, Ezra A.; Olson, Kent R.; Ramoska, Edward A.; Lange, Richard A. (2016-06-01). "Treatment of cocaine cardiovascular toxicity: a systematic review". Clinical Toxicology. 54 (5): 345–364. doi:10.3109/15563650.2016.1142090. ISSN 1556-9519. PMID 26919414. S2CID 5165666.
  33. ↑ "The current practice for cocaine-associated chest pain in the Netherlands". Toxicology Reports. 8: 23–27. 2021-01-01. doi:10.1016/j.toxrep.2020.12.011. ISSN 2214-7500. PMC 7770504. PMID 33384944. Archived from the original on 2020-12-21. Retrieved 2021-02-28.
  34. ↑ 34.0 34.1 Anderson, Jeffrey L.; Adams, Cynthia D.; Antman, Elliott M.; Bridges, Charles R.; Califf, Robert M.; Casey, Donald E.; Chavey, William E.; Fesmire, Francis M.; Hochman, Judith S. (2013-06-11). "2012 ACCF/AHA focused update incorporated into the ACCF/AHA 2007 guidelines for the management of patients with unstable angina/non-ST-elevation myocardial infarction: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines". Journal of the American College of Cardiology. 61 (23): e179–347. doi:10.1016/j.jacc.2013.01.014. ISSN 1558-3597. PMID 23639841.
  35. ↑ Ma, Sheng-xing; Schmid, Phillip G.; Long, John P. (1994-01-01). "Noradrenergic mechanisms and the cardiovascular actions of nitroglycerin". Life Sciences. 55 (21): 1595–1603. doi:10.1016/0024-3205(94)00325-4. PMID 7968233.
  36. ↑ Lange, Richard A.; Cigarroa, Ricardo G.; Yancy, Clyde W. Jr.; Willard, John E.; Popma, Jeffrey J.; Sills, Michael N.; McBride, Wade; Kim, Anatole S.; Hillis, L. David (1989-12-07). "Cocaine-Induced Coronary-Artery Vasoconstriction". New England Journal of Medicine. 321 (23): 1557–1562. doi:10.1056/NEJM198912073212301. ISSN 0028-4793. PMID 2573838.
  37. ↑ Boehrer, James D.; Moliterno, David J.; Willard, John E.; Hillis, L.David; Lange, Richard A. (1993-06-01). "Influence of labetalol on cocaine-induced coronary vasoconstriction in humans". The American Journal of Medicine. 94 (6): 608–610. doi:10.1016/0002-9343(93)90212-8. ISSN 0002-9343. PMID 8506886.
  38. ↑ Richards, John R.; Lange, Richard A. (2016-02-01). "Labetalol and cardiovascular consequences of cocaine use". Trends in Cardiovascular Medicine. 26 (2): 202–203. doi:10.1016/j.tcm.2015.05.002. ISSN 1873-2615. PMID 26116092.
  39. ↑ Shin, Doosup; Lee, Eun Sun; Bohra, Chandrashekar; Kongpakpaisarn, Kullatham (2019). "In-Hospital and Long-Term Outcomes of Beta-Blocker Treatment in Cocaine Users: A Systematic Review and Meta-analysis". Cardiology Research. 10 (1): 40–47. doi:10.14740/cr831. ISSN 1923-2829. PMC 6396807. PMID 30834058.
  40. ↑ Schurr, James W.; Gitman, Brenda; Belchikov, Yuly (2014-12-01). "Controversial therapeutics: the β-adrenergic antagonist and cocaine-associated cardiovascular complications dilemma". Pharmacotherapy. 34 (12): 1269–1281. doi:10.1002/phar.1486. ISSN 1875-9114. PMID 25224512. S2CID 5282953.
  41. ↑ Freeman, Kalev; Feldman, James A. (2008-02-01). "Cocaine, myocardial infarction, and beta-blockers: time to rethink the equation?". Annals of Emergency Medicine. 51 (2): 130–134. doi:10.1016/j.annemergmed.2007.08.020. ISSN 1097-6760. PMID 17933425.
  42. ↑ Dattilo, Philip B.; Hailpern, Susan M.; Fearon, Kerrie; Sohal, Davendra; Nordin, Charles (2008-02-01). "Beta-blockers are associated with reduced risk of myocardial infarction after cocaine use". Annals of Emergency Medicine. 51 (2): 117–125. doi:10.1016/j.annemergmed.2007.04.015. ISSN 1097-6760. PMID 17583376.
  43. ↑ Rangel, Carlos; Shu, Richard G.; Lazar, Lawrence D.; Vittinghoff, Eric; Hsue, Priscilla Y.; Marcus, Gregory M. (2010-05-24). "Beta-blockers for chest pain associated with recent cocaine use". Archives of Internal Medicine. 170 (10): 874–879. doi:10.1001/archinternmed.2010.115. ISSN 1538-3679. PMID 20498415.
  44. ↑ Ibrahim, Morhaf; Maselli, Diego Jose; Hasan, Reham; Hamilton, Andrew (2013-03-01). "Safety of β-blockers in the acute management of cocaine-associated chest pain". The American Journal of Emergency Medicine. 31 (3): 613–616. doi:10.1016/j.ajem.2012.09.027. ISSN 1532-8171. PMID 23122421.
  45. ↑ Negus, Brian H.; Willard, John E.; Hillis, L.David; Glamann, D.Brent; Landau, Charles; Snyder, Richard W.; Lange, Richard A. (1994-03-01). "Alleviation of cocaine-induced coronary vasoconstriction with intravenous verapamil". The American Journal of Cardiology. 73 (7): 510–513. doi:10.1016/0002-9149(94)90684-x. ISSN 0002-9149. PMID 8141094.

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