Crushing Chest Pain and Can't see OMI on the ECG? Just give morphine, right?

Submitted anonymously, written by Willy Frick

A man in his late 30s with a 10 pack-year smoking history presented with acute substernal chest pressure radiating into his left shoulder with associated nausea, vomiting, and diaphoresis which began suddenly while he was getting ready for work. He described it as feeling like "a bulldozer on [his] chest." He rated it 10/10 intensity.

With no additional information, the HPI puts this patient at very high pre-test probability of OMI.

ECG 1

What do you think of his presenting ECG?

Queen of Hearts interpretation with explainability:

Although it is not apparent from this ECG by itself, there is actually LA-LL reversal here. LA-LL reversal is usually identified by P wave in lead I which is larger than in lead II. In this case, it is clear only from comparison to subsequent ECGs. LA-LL reversal causes the following:

• I and II switch places
• aVL and aVF switch places
• III is inverted

Below is what it looks like after correction.

ECG 1 (corrected)

Remember that for patients at very high pre-test probability of OMI, you have to rule it out regardless of the ECG. Remember that the European guidelines recommend immediate angiography for refractory chest pain. Remember that such patients ACTUALLY get such guideline appropriate therapy only 6.4% of the time.

Knowing that the patient is probably having an OMI, we see what might be hyperacute T waves inferiorly. An even stronger clue is the extremely subtle downsloping depression in aVL. I do not think anyone could call this ECG diagnostic for OMI. But it is very suspicious.  The patient was still in the waiting room at this time. No labs were drawn, but he had the following repeat ECG 25 minutes after the first.

ECG 2, t + 25 minutes

What do you think?

Here are some of the key leads shown side-by-side for serial comparison, ECG 1 (corrected) on the left, ECG 2 on the right.

We appreciate the following changes:

• Correction of the LA-LL reversal (although it would be within reason to wonder if this is actually the reversed tracing, since P in lead I is larger than in lead II).

• There is slightly more STE in III.

• The subtle STD in aVL is slightly more pronounced. Even more worrisome, it has the (inverted) coved appearance which is highly concerning for ischemia.

• Lead I is also beginning to show reciprocal depression.

• The J point in V3 which was previously about 1.5 mm elevated (which is normal) is now abnormally isoelectric. Stated differently, it is now relatively depressed, suggestive of posterior extension.

Case Continued

Unfortunately, these changes were not appreciated, and the patient remained in the waiting room for the next several hours. High sensitivity troponin I drawn around the time of ECG 2 was 13 ng/L (ref. ≤ 35). Repeat troponin about two hours later was 44 ng/L. This confirms the diagnosis of MI which requires 1. dynamic troponin elevation, and 2. signs or symptoms of ischemia.

I sent this 2nd ECG to our "ECG Nerdz" group without any clinical information and the response was immediately "Inferior OMI"

Unfortunately, although it is diagnostic, in this case the Queen of Hearts stated "Not OMI with High Confidence"

The patient was roomed at t + 4 hours. The ED physician documented that the patient was complaining of 8/10 chest pain. The ED physician's note included a differential diagnosis with ACS listed as the first possibility. He was given famotidine 20 mg IV, morphine 4 mg IV, and SL NTG. Giving morphine to suspected ACS without activating lab is like removing the batteries from the alarming carbon monoxide detector and staying in the house.

The patient went for CT angiogram to rule out aortic dissection. Eagle-eyed readers may notice something the radiologist overlooked. (Answer at the end of the case.)

Repeat hsTnI at t + 5 hours was 244 ng/L, at which time cardiology was consulted. After evaluating the patient who had ongoing pain, cardiology recommended admission and planned catheterization after the weekend. (This was Friday afternoon.) A fourth troponin at t + 6 hours was 608 ng/L.

Around this time, the patient was redistributed from the cardiology consult service to the admitting service. 

The cardiologist on the admitting service is a reader of Dr. Smith's ECG Blog. When he heard about the case, he immediately evaluated the patient who told him he had severe, persistent chest pain. At that point, the cardiologist activated the cath lab. His angiogram is shown below:

Here is a representative still. The red arrow head points to the LAD, green to a very high OM (or Ramus Intermedius if you prefer), and orange to LCx.

The cardiologist noted that, aside from a mid left circumflex occlusion with TIMI 0 flow (meaning absolutely no flow beyond the occlusion), the remaining coronary arteries appeared normal. After aspiration thrombectomy, he confirmed absence of coronary plaque using intravascular ultrasound. He therefore did not place a stent.

After PCI, troponin rose from 608 to 37,186 ng/L, a huge infarct. Echocardiogram showed LVEF 42%, akinetic inferior wall, hypokinetic inferolateral wall leaving this patient with heart failure while in his 30s.

Door-to-balloon time was 10 hours and 50 minutes. The patient infarcted his inferior and inferolateral walls in the ED of a hospital with a cath lab.

He was worked up for sources of embolism.

Shown below is TEE, mid-esophageal 2-chamber view zoomed in on the mitral valve.

Here is a still shot with a red circle showing a mass concerning for vegetation.

Dental x-rays showed caries and missing teeth. All blood cultures and serologies were negative, and he was treated for 6 weeks with broad spectrum antibiotics for culture-negative endocarditis.

ECG 3 was obtained 2 days after PCI

We see the following:

• New inferior Q waves

• Terminal TWI in III and aVF due to reperfusion

• Very tall T waves most pronounced in V1-V4, reciprocal to posterior TWI (i.e., posterior reperfusion T-waves)

Learning Points:

• OMI is a clinical diagnosis.

• A "negative" ECG does not rule out OMI.

• A normal troponin does not rule out OMI.

• Troponin may rise very slowly in OMI. Troponin becomes "trapped" in the ischemic myocardium. You may first see dramatic rise after reperfusion.

• The CTA in this case actually showed OMI. Note that the inferoposterior wall does not take up contrast.

• Medically refractory chest pain needs immediate angiography.

• In this patient's case, the diagnosis was immediately obvious from presentation, but the physicians who saw him were falsely reassured by ECG and troponin.