A 32-year-old man is brought to the emergency department following the sudden onset of excruciating left-sided chest pain. Temperature is 37.2 C (99 F), blood pressure is 160/90 mm Hg, pulse is 125/min and regular, and respirations are 20/min. The patient is anxious and agitated and is sweating profusely. Both pupils are dilated, and the nasal mucosa is atrophic. Heart sounds are regular with no murmurs or rubs. The lungs are clear on auscultation. An initial ECG shows ST-segment depression and T-wave inversion in leads V4-V6. The first set of cardiac enzymes, including CK-MB and troponin T, is normal. Chest x-ray reveals no acute abnormality. Which of the following is the most appropriate next step in management of this patient?

Question

A 32-year-old man is brought to the emergency department following the sudden onset of excruciating left-sided chest pain.  Temperature is 37.2 C (99 F), blood pressure is 160/90 mm Hg, pulse is 125/min and regular, and respirations are 20/min.  The patient is anxious and agitated and is sweating profusely.  Both pupils are dilated, and the nasal mucosa is atrophic.  Heart sounds are regular with no murmurs or rubs.  The lungs are clear on auscultation.  An initial ECG shows ST-segment depression and T-wave inversion in leads V4-V6.  The first set of cardiac enzymes, including CK-MB and troponin T, is normal.  Chest x-ray reveals no acute abnormality.  Which of the following is the most appropriate next step in management of this patient?

Quizplus · Accepted Answer

11ec25c8_d17f_9945_bc81_dda2704136fb_MD0003_00 This patient has psychomotor agitation, dilated pupils, atrophic nasal mucosa, hypertension, and acute myocardial ischemia (chest pain, ECG with ST-segment depressions and T-wave inversions), findings highly suggestive of acute cocaine intoxication. Cocaine potentiates sympathomimetic actions by inhibiting norepinephrine reuptake into the sympathetic neuron. This stimulates alpha- and beta-adrenergic receptors and can result in coronary vasoconstriction and increases in heart rate, systemic blood pressure, and myocardial oxygen demand. It also enhances thrombus formation by promoting platelet activation and aggregation. All patients with acute cocaine toxicity and myocardial ischemia should be treated initially with supplemental oxygen and intravenous benzodiazepines. By reducing sympathetic outflow, benzodiazepines (eg, diazepam) reduce anxiety and agitation, lower blood pressure and heart rate, and alleviate cardiovascular symptoms. Aspirin slows thrombus formation; nitrates and calcium channel blockers (vasodilators) are beneficial for cocaine-induced coronary artery vasoconstriction. Beta blockers, including cardioselective agents (eg, metoprolol, atenolol, bisoprolol), generally should not be used to treat cocaine-induced myocardial ischemia or infarction until the cocaine has been eliminated from the patient's body. Their use can theoretically cause unopposed alpha-adrenergic stimulation and worsen coronary vasoconstriction (Choice D). Although some retrospective studies and case reports suggest beta blocker administration is safe in patients with cocaine intoxication, methodological limitations and bias may limit the validity of their results. Mixed alpha and beta blockers may be safe, but the overall evidence is limited. (Choice A) Cardiac catheterization should be performed in patients with STEMI and in those with persistent chest pain despite aggressive optimal medical therapy. (Choice B) This patient has signs of acute cocaine toxicity and ongoing myocardial ischemia. Observation is not appropriate. (Choice E) Thrombolytic agents are indicated only in patients with ST-segment elevation myocardial infarction (STEMI) when timely access to coronary angiography is not available. Their use has been associated with increased rates of intracranial hemorrhage in patients with cocaine use. A small number of patients with cocaine-associated chest pain can also have aortic dissection, which was not ruled out in this patient. Administering a thrombolytic agent in that setting could be catastrophic and is absolutely contraindicated. Educational objective: Patients with cocaine-associated chest pain should be treated initially with intravenous benzodiazepines. These improve the symptoms of psychomotor agitation, reduce myocardial oxygen demand, and alleviate cardiovascular symptoms. Aspirin, nitroglycerin, and calcium channel blockers are also effective in the initial management of cocaine-associated chest pain. Beta blockers are generally not recommended. References: 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. (http://www.ncbi.nlm.nih.gov/pubmed/18347214)

A 32-Year-Old Man Is Brought to the Emergency Department Following