How is ST-segment elevation or depression treated in cocaine toxicity?

Updated: Sep 01, 2018
  • Author: Lynn Barkley Burnett, MD, EdD, LLB(c); Chief Editor: Sage W Wiener, MD  more...
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Answer

The American College of Cardiology Foundation/American Heart Association (ACCF/AHA) 2014 guidelines on unstable angina and non–ST-segment elevation myocardial infarction include the following class I recommendations for treatment of patients with ischemic chest discomfort and ST-segment elevation or depression after cocaine use [44] :

  • Administer sublingual or intravenous (IV) NTG and IV or oral calcium channel blockers (eg, diltiazem, 20 mg IV)
  • In patients whose ST segments remain elevated after NTG and calcium channel blockers, perform immediate coronary angiography, if possible; if occlusive thrombus is detected, percutaneous coronary intervention is recommended
  • Fibrinolytic therapy is useful in patients with ischemic chest discomfort after cocaine use if ST segments remain elevated despite NTG and calcium channel blockers and coronary angiography is not possible; however, fibrinolysis is often contraindicated

AHA guidelines note that patients with cocaine-induced hypertension or chest discomfort may also benefit from benzodiazepines and/or morphine, in addition to NTG. [43]

Small, incremental doses of benzodiazepines decrease norepinephrine release by the CNS, thereby counteracting the sympathomimetic effects of cocaine on the heart. Similar doses of morphine sulfate (MS) also alter hemodynamics and blood flow dramatically in patients with heightened sympathetic activity. Limiting factors for morphine and benzodiazepines include hypotension, somnolence, and respiratory depression. Kercher cautions that short-acting benzodiazepines (eg, lorazepam) should be prescribed at low doses for patients with hepatic disease, organic brain syndrome, and those taking medications inhibiting the metabolism and clearance of benzodiazepines (eg, those using nicotine or cimetidine). [54]

In patients with ST-elevation MI (STEMI) or with cocaine-associated chest pain refractory to benzodiazepines, treatment with phentolamine, an alpha antagonist, may also be considered. Phentolamine has been reported to reverse ST elevations in cocaine-associated STEMI, though it has not been studied systematically.

In patients with prolonged unexplained chest pain, perform serial ECGs and cardiac-marker measurements to rule out MI. However, in one study, Hollander reports that patients with MI were as likely to present with normal or nonspecific ECG findings as with ischemic ECG findings. The sensitivity of the ECG in predicting MI was only 35.7%; therefore, ECG appears to be less sensitive in patients with cocaine-induced myocardial ischemia than in other patients presenting with ischemic chest pain.

Interpretation of cardiac markers in patients with cocaine-induced symptoms may be difficult since levels of creatine kinase (CK) and CK MB-isoform (CK-MB) may be elevated in cocaine users who do not have an MI. However, the specificity of troponin assays is not affected by cocaine use. [30]


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