A man his 50s with chest pain. What happens when you treat with morphine rather than with reperfusion?

 Written by Pendell Meyers

A man in his late 50s presented to the ED with 3 days of left chest pain radiating into the jaw and neck. He described it as "heartburn." The pain radiates into his left arm and causes numbness and tingling from time to time. The history does not state what changed on day 3 that made him finally present to the ED; the history has no details as to whether the pain was off and on, or fluctuating, or whether the pain become persistent soon before arrival (these are key details and would help with many important questions we will have below!). Vitals were normal, and his triage ECG is below, at about 1pm:

What do you think?

The ECG shows sinus rhythm with a normal QRS, with STD present in leads V2-V6, I, II, and possibly aVL. There is some obligatory reciprocal ST Elevation (STE) in aVR. In the precordial leads, it is somewhat difficult to determine whether the STD is maximal in V1-V4 vs. V5-6, but in my opinion, two features favor posterior OMI: 1) the morphology of lead V2, and 2) the STD becomes less proportionally severe when going from lead V4 to V6. These two features lead me to choose STD maximal in V2-4, which is of course always the more important assumption to choose until proven otherwise!

Also, in a patient like this with clear, ongoing ACS, it doesn't actually matter whether it is pure posterior OMI, diffuse subendocardial ischemia, or both - the patient needs cath regardless. 

The patient was not on digoxin, in case you were considering that as a cause of diffuse STD especially with the morphology of lead V6.  Furthermore, the QT is not short, which would be the case in Digoxin effect.

Back to the case:

The providers did not see any reason for emergent ACS management on initial evaluation, and ordered a standard workup.

First high sensitivity troponin I returned elevated at 25 ng/L (99% URL for men is 20 ng/L).

Second troponin rose to 92 ng/L.

"The patient continued to have chest pain in the ER but his chest pain resolved after 2 nitroglycerin. Morphine was ordered "as needed," but was never needed or given. EKG shows minimal ST depression in the lateral leads but no evidence of STEMI. I discussed the case with cardiology on call, Dr. XXXXX recommended heparin bolus and admission by the hospitalist." (not at a PCI center at first)

"NSTEMI"

Meyers side note: Morphine for ongoing ACS without maximal medical therapy and without a plan to proceed to the cath lab is a recipe for an "NSTEMI" disaster.

Signed out at 6pm pending admission by the hospitalist (not the cardiologist, I'm told that at this institution cardiology doesn't even admit clear type 1 NSTEMIs usually, and the EM and IM teams are conditioned to not even call cardiology in many such cases).

While awaiting admission, the patient reported repeat chest pain. A repeat ECG was performed:

There is new inferior OMI involvement (with terminally inverted T wave also, suggesting some small reperfusion at the time of the ECG). Leads V5 and V6 have newly upright T waves suggesting lateral OMI, and leads V6 has the tiniest hint of STE (whereas previously there was STD!). Taken all together, with the first ECG, this is all diagnostic of OMI involving the inferior, posterior, and lateral walls.

He then became acutely unresponsive. He was found to be in VF and received CPR until he could be defibrillated, which was successful. Within 5 minutes of ROSC, he was awake and answering questions appropriately. 

A repeat ECG was performed with stable ROSC:

Active, ongoing OMI of at least the inferior and posterior walls. Yet no STEMI criteria are met.

"Repeat EKG shows some ST depression in V2 and posterior EKG was performed which does not show STEMI (Meyers comment: unavailable, not saved in EMR, like most posterior ECGs in my experience). I spoke with Dr. XXXXX from cardiology who recommends transfer to the PCI center."

The next troponin was 419 ng/L.

Here is his EKG on arrival to the PCI center at about 10pm:

Ongoing OMI of the inferior, posterior, and lateral walls. 

Repeat trop at the receiving PCI center was 3,491 ng/L.

2AM: 4,238 ng/L

5 AM: 6,667 ng/L (no further troponins measured after this one)

He waited all night and into the next morning for cath!

Cath showed an acute culprit lesion of the LCX 99% stenosis and TIMI 3 flow. It was stented.  Out of pure luck, the artery had spontaneously reperfused without any therapy other than antiplatelet and antithrombotic therapy.

An echocardiogram showed 60% EF and no obvious wall motion abnormalities.

Post intervention ECG:

Resolution of all ST elevation and depression, due to reperfusion

He suffered no further complications in hospital, and was discharged home. This is not due to the diligence of the caregivers, but due to pure luck.

As of 1 year after the event, he underwent cardiac rehab and has been able to return to work but seems to have some dyspnea on exertion, and has presented to the ED twice with shortness of breath without clear cause on workup (without obvious CHF findings on exam or workup). No further echocardiograms have been done since initial visit.

Learning Points:

This NSTEMI patient suffered VF cardiac arrest that was likely preventable with better ECG interpretation (and also simply following the ACC/AHA NSTEMI guidelines for ischemia refractory to medical management in this case).

Posterior OMI (or whatever you call the area of the LV myocardium directly posterior in human anatomy, directly opposite the anterior LV wall) is best identified on the standard 12-lead by STD maximal in V1-V4. As with any OMI, there can be additional, superimposed subendocardial ischemia (which causes more diffuse STD, usually maximal in V5-6 and II, with reciprocal STE in aVR).