EKG of the Week – Week 16 ANSWERS
This week’s EKG isn’t so much about the EKG itself, but the management of the patient afterwards. The EKG shows ST segment elevation in V2/3. There’s also some maybe elevation in V1 and V4 and some ST segment depression in the inferior leads. I’d argue that this is concerning for an anterior MI. However, the patient is 21 years old and just used cocaine. Does this change our management? Let’s review cocaine quickly:
(Most of this info is taken from the AHA’s Scientific Statement on the Management of Cocaine Associated Chest Pain and Myocardial Infarction)
Cocaine causes a huge catecholaminergic surge. All those catecholamines cause vessels to clamp down. They also make the heart work harder. So you have vessels getting smaller and needing to work 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.
Statistically, who does cocaine? Young men who smoke. Smoking leads to early atherosclerosis. That’s also bad
Cocaine also increases platelet count, aggregation and activation. More badness.
So, basically, we’re setting up for the 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 EKG truly reflective of an MI?
Brief history lesson: In 1994 a group of ER doctors (and cardiologists) wanted to determine which patients coming to the ER with chest pain after cocaine use were having a true MI. They enrolled 246 patients over 46 months and looked at EKGs, Cardiac biomarkers, Echos and cath reports. This study, known as COCHPA or the Cocaine Associated Chest Pain Study, found that an EKG revealing ischemia or infarction only had a 35.7% sensitivity for predicting a true MI. Only 5.7% of all of the patients in their study had a true MI, diagnosed as EKG changes with a positive CKMB.
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.”
Hmmm.
The truth is likely somewhere in between. Two other studies found sensitivities of 19% and 31% for ischemic EKG changes being predictive of true MIs.
Want to be a little more terrified? The average age in the COCHPA study for patients having a true MI was 36!
Ok, history lesson over. So now that we know that these patients probably can have a true MI, how do we treat them?
The AHA has this cool flowsheet in their paper:
I’m having some trouble picking out what the AHA considers “high risk” or “low-moderate risk” since those terms don’t seem well defined in their paper.
Let’s just recap a few drugs to give with the cocaine intoxicated patient really quickly:
Classical teaching is to avoid beta blockers because they lead to unopposed alpha activity. That 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”
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, which will often resolve tachycardia and hypertension. If the patient is still hypertensive, consider phentolamine.
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 tachy and hypertensive. They cathed them and found the average coronary vessel to be narrowed by approx 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. Apparently the 1980s were a crazy time.
Lots of words, what do we do with these patients?
For me, I’d call a CODE STEMI on that EKG. With rates as high as 36% of these patients having a true MI, with those EKG changes, I’d want a cardiologist next to me, discussing the patient before I’d call it off. If I were deployed in the middle of nowhere, would I push lytics? tough question. I think it would be a risk/benefit discussion with the patient.