ECG Pointers: Cocaine and ST Elevation

Authors: Brannon Inman (EM Resident, Brooke Army Medical Center) and Lloyd Tannenbaum (EM Staff, Brooke Army Medical Center) // Reviewed by: Jamie Santistevan, MD (@jamie_rae_EMdoc, EM Physician, Presbyterian Hospital, Albuquerque, NM); Manpreet Singh, MD (@MPrizzleER, Assistant Professor of Emergency Medicine / Department of Emergency Medicine – Harbor-UCLA Medical Center); and Brit Long, MD (@long_brit , EM Attending Physician, San Antonio, TX)

Welcome to this edition of ECG Pointers, an emDOCs series designed to give you high yield tips about ECGs to keep your interpretation skills sharp. For a deeper dive on ECGs, we will include links to other great ECG FOAMed!

The Case:

This ECG comes from a 21-year-old male with a history of cocaine abuse.  When I say ‘history’, I mean that he just snorted some cocaine and now he has chest pain.  He looks uncomfortable and sweaty, and keeps asking you not to tell his mom that he does drugs.  He has no other medical problems.  Here is his EKG.  What do you want to do?

This ECG shows ST segment elevation in V2 and V3.  There is some slight elevations in V1 and V4 and minor ST segment depression in II, III, and aVF.

This week’s ECG pointers isn’t so much about the ECG itself, but the management of the patient in front of you.  The ECG shows ST segment elevation in V2/3.  There’s also some elevation in V1 and V4 and some ST segment depression in the inferior leads.  This is concerning for an anterior MI (LAD distribution), but the patient is 21 years old and just used cocaine!  Does this change your management?

Let’s review what cocaine does to the body:

Cocaine causes a huge catecholaminergic surge.  All those catecholamines cause vessels to clamp down (vasoconstriction).  They also make the heart pump harder (inotropy) and faster (chronotropy).  So, you have coronary vessels getting smaller and cardiac muscle working harder.  This sounds bad.  To make it even worse, the chronotropic effects of cocaine are increased when alcohol is used on top of the cocaine [1].

Statistically, who does cocaine?  Young men who smoke.  Smoking leads to early atherosclerosis [1].  That’s also bad. Cocaine also increases platelet count, aggregation and activation [1].

So, basically, the body is set up for a perfect storm.  You have a heart that likely has some early atherosclerosis that now has its blood supply cut down and its oxygen requirements increased.  So, is what we’re seeing on the ECG truly reflective of an acute MI [1]?

That’s a very tough question.  To answer it, we need to review some of the first studies looking at cocaine abuse and the associated ECG changes.

In 1994 a group of EM physicians (and cardiologists) wanted to determine which patients coming to the ED with chest pain after cocaine use were having a true MI (in this study, MI is defined as having elevated CK-MB). They enrolled 246 patients over 46 months and looked at ECGs, cardiac biomarkers, echocardiograms and catheterization reports.  This study, known as COCHPA or the Cocaine Associated Chest Pain Study, enrolled 246 patients, 14 of which had an MI based on elevated CK-MB level (5.7%; 95% confidence interval [CI], 2.7-8.7%). In this study, an ECG revealing ischemia or infarction had a 35.7% sensitivity for predicting a true MI[2]. This low sensitivity would mean that you cannot exclude acute MI just based on the absence of ischemic changes on the ECG.

But, 5.7% prevalence seems a little high, right?

COCHPA was a follow up to a study done in 1991 where 101 patients were admitted to a CCU after cocaine use to rule out an MI.  Out of all of those patients admitted 0, that’s right, ZERO, had a true MI.  The authors concluded that, “Abnormal or normal variant electrocardiographic findings are common in patients with chest pain related to cocaine use, but nevertheless the incidence of acute myocardial infarction is low.”

Hmmmm. So, what is the actual incidence of MI in these patients?

Two other studies found rates of 19% [3] and 31% [4] of ischemic appearing EKGs representing true myocardial infarctions.

Want to be a little more terrified on shift?  The average age in the COCHPA study for patients having a true MI was 36!

Now that we know that some of these patients can have a true MI, how do we treat them?

The AHA has this nice flowsheet [1]:

Unfortunately, what the AHA considers “high risk” or “low-moderate risk” is difficult to elaborate on, since those terms are not well defined in their paper. However, another paper cited in the AHA guidelines defined high risk as, “initial ECG suggested the presence of ischemia or acute MI, ST-segment elevation or depression of 1 mm or more that persisted for at least 1 minute; elevated serum levels of cardiac biomarkers; recurrent ischemic chest pain; or hemodynamic instability.”[5,6]

Let’s recap a few drugs to consider giving the cocaine-intoxicated patient:

Classical teaching is to avoid beta-blockers because they lead to unopposed alpha activity. That recommendation is reaffirmed by the AHA.  They note that giving beta-blockers without alpha blocking first led to decreased coronary blood flow, increase in rates of seizures and an increase in mortality.  The ACC/AHA guidelines specifically state: “Beta blockers should not be administered to patients with STEMI precipitated by cocaine use because of the risk of exacerbating coronary spasm”.

That is the classic teaching, and from a physiological standpoint, this seems like sound reasoning. In fact, there have even been randomized controlled trials in which healthy volunteers were given cocaine and a beta-blocker. Let’s table the discussion on how you get your IRB to approve that.  Did these studies back up the dogma of avoiding beta-blockers in cocaine-intoxicated patients?

Interestingly, yes and no.  Initially, one study showed that the combination of cocaine and propranolol potentiated coronary vasoconstriction and causes flow limitation [7]. However, in a similar RCT published 3 years later using labetalol, no change in coronary flow rate was found and labetalol actually lowered the sympathomimetic driven MAP increase [8].  What about the patient centered outcomes? Unopposed alpha stimulation in the setting of a heart already predisposed to supply demand mismatch must surely be a set up for a poor patient outcome, right? Well maybe, maybe not. One 2014 observational study in patient hospitalized for cocaine associated chest pain found no statistically significant difference in MI, stroke, arrhythmia or all-cause mortality in patients using cocaine and treated with beta-blockers [9].  Another prospective study published in 2018 examined 1002 patients with ACS and associated cocaine use. In this study beta-blockers were associated with improved clinical outcomes (reduced rates of death, MI) [10]. Certainly, all of the studies mentioned have their limitations. The RCT’s were small involving 30 and 15 patients, respectively.While the latter two trials mentioned have more patients, they were observational in nature and thus do not control well for confounders.

It’s true that there is not enough evidence for using beta-blockers in cocaine toxicity to make this practice legally defensible. Nor is anyone here recommending this. There is, however, sufficient evidence to question the dogmatic teaching that one should never give a beta-blocker to a patient who uses cocaine.  Perhaps we need more IRBs willing to approve studies involving cocaine in the future.

What about benzodiazepines or phentolamine?  

The AHA notes that benzos can resolve chest pain and have beneficial cardiovascular hemodynamic effects.  Benzos can decrease the patient’s anxiety and assist in reducing the sympathomimetic overdrive in cocaine toxicity, which will often resolve tachycardia and hypertension.  If the patient is still hypertensive, consider phentolamine [1].

Phentolamine is an alpha-blocker that has been shown to return coronary blood vessel diameter to normal, lower heart rates, and blood pressure.  Can we take 30 seconds and talk about how this was discovered?  They took volunteers, brought them to the cath lab, gave them low dose cocaine up the nose, and watched their vitals.  Patients became tachycardic and hypertensive.  They cath’d them and found the average coronary vessel to be narrowed by approximately 13%.  The patients were then given phentolamine, their vitals normalized, and the cath was repeated.  This showed the vessels were now back to normal size[1].   Apparently the 1980s were a crazy time!

Case Conclusions:

Back to our patient—His ECG showed ST elevation with reciprocal depressions and CODE STEMI was called.  Cardiology came to the bedside, evaluated him, and decided to take him to the cath lab.  The patient was found to have atherosclerosis, but no interventions were required in the cath lab.  He made an uneventful recovery in the ICU and was discharged two days later.


  1. McCord J, Jneid H, Hollander JE, et al. Management of Cocaine-Associated Chest Pain and Myocardial Infarction. Circulation. 2008;117:1897-1907.
  2. Hollander JE, Hoffman RS, Gennis P, Fairweather P, DiSano MJ, Schumb DA, Feldman JA, Fish SS, Dyer S, Wax P, et al. Prospective multicenter evaluation of cocaine-associated chest pain. Cocaine Associated Chest Pain (COCHPA) Study Group. Acad Emerg Med. 1994 Jul-Aug;1(4):330-9.
  3. Tokarski GN, Paganussi P, Urbanski  R, et  An evaluation  of cocaine induced chest pain. Ann Emerg Med. 1990; 19:1088-92.
  4. Amin M, Gableman  G,  Karpel J, Buttrick P. Acute  myocardial infarction and chest pain syndromes after cocaine use. Am J Cardiol. 1990; 66:1434-7.
  5. Weber JE, Shofer FS, Larkin GL, Kalaria AS, Hollander JE. Validation of a brief observation period for patients with cocaine-associated chest pain. N Engl J Med. 2003 Feb 6;348(6):510-7.
  6. Schwartz BG, Rezkalla S, Kloner RA. Cardiovascular effects of cocaine. Circulation. 2010 Dec 14;122(24):2558-69.
  7. Lange RA, Cigarroa RG, Flores ED, et al. Potentiation of cocaine-induced coronary vasoconstriction by beta-adrenergic blockade. Ann Intern Med. 1990 Jun 15;112(12):897-903.
  8. Boehrer JD, Moliterno DJ, Willard JE, et al. Influence of labetalol on cocaine-induced coronary vasoconstriction in humans. Am J Med. 1993 Jun;94(6):608-10.
  9. Fanari Z, Kennedy KK, Lim MJ, et al. Comparison of in-hospital outcomes for beta-blocker use versus non-beta blocker use in patients presenting with cocaine-associated chest pain. Am J Cardiol. 2014 Jun 1;113(11):1802-6.
  10. Cediel G, Carrillo X, García-García C, et al. β-Blocker treatment and prognosis in acute coronary syndrome associated with cocaine consumption: The RUTI-Cocaine Study. Int J Cardiol. 2018 Jun 1;260:7-10.


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