ABSTRACT
Cocaine abuse remains a significant worldwide health problem. Patients with cardiovascular toxicity from cocaine abuse frequently present to the emergency department for treatment. These patients may be tachycardic, hypertensive, agitated, and have chest pain. Several pharmacological options exist for treatment of cocaine-induced cardiovascular toxicity. For the past 3 decades, the phenomenon of unopposed α-stimulation after ß-blocker use in cocaine-positive patients has been cited as an absolute contraindication, despite limited and inconsistent clinical evidence. In this review, the authors of the original studies, case reports, and systematic review in which unopposed α-stimulation was believed to be a factor investigate the pathophysiology, pharmacology, and published evidence behind the unopposed α-stimulation phenomenon. We also investigate other potential explanations for unopposed α-stimulation, including the unique and deleterious pharmacologic properties of cocaine in the absence of ß-blockers. The safety and efficacy of the mixed ß-/α-blockers labetalol and carvedilol are also discussed in relation to unopposed α-stimulation.
Subject(s)
Adrenergic beta-Antagonists/therapeutic use , Cardiovascular Diseases/drug therapy , Cardiovascular System/drug effects , Central Nervous System Stimulants/adverse effects , Cocaine-Related Disorders/complications , Cocaine/adverse effects , Hemodynamics/drug effects , Receptors, Adrenergic, alpha/drug effects , Sympathetic Nervous System/drug effects , Adrenergic beta-Antagonists/adverse effects , Animals , Cardiovascular Diseases/etiology , Cardiovascular Diseases/metabolism , Cardiovascular Diseases/physiopathology , Cardiovascular System/innervation , Cardiovascular System/metabolism , Cocaine-Related Disorders/metabolism , Cocaine-Related Disorders/physiopathology , Humans , Receptors, Adrenergic, alpha/metabolism , Sympathetic Nervous System/metabolism , Sympathetic Nervous System/physiopathology , Treatment OutcomeABSTRACT
INTRODUCTION: Although it is commonly stated that the use of beta adrenergic receptor antagonists is contraindicated in patients with cocaine toxicity, actual clinical evidence of harm is lacking. This case helps to highlight the risks of beta adrenergic receptor antagonists in patients with chest pain associated with cocaine use. CASE REPORT: A 54-year-old man was brought to the emergency department (ED) complaining of chest pain after using approximately 1 gram of intranasal cocaine. Aspirin and nitroglycerin spray relieved his pain. Although he remained pain free, tachycardia persisted despite 15 mg of diazepam intravenously. Nearly two hours after presentation, a total of 5 mg of metoprolol was given for persistent tachycardia (115/minute) and an elevated troponin. Shortly thereafter, the patient complained of crushing substernal chest pain, developed pulseless electrical activity, and could not be resuscitated. DISCUSSION: The administration of beta adrenergic receptor antagonists exacerbates cocaine-induced lethality in animals. In humans given smaller doses of cocaine, beta adrenergic receptor antagonists exacerbate coronary vasoconstriction. Both effects are presumed to occur through unopposed alpha adrenergic receptor agonism. Despite these data, actual cases describing adverse effects in cocaine users given beta adrenergic receptor antagonists are uncommon. This case supports the potential lethality of a cocaine-beta adrenergic receptor antagonist interaction.
