A man in his 50s with schizophrenia, hypoglycemia, and vague chest pain and shortness of breath for a few days

Written by Pendell Meyers with edits by Steve Smith

Bystanders called EMS for a man in his 50s "not acting right." Medics found a man with altered mental status, immediately measured a blood glucose of 42 ng/mL, and administered glucose.  There was immediate improvement in his mentation, but it was "not back to normal." Now that the patient was able to give some history, he was able to complain of chest pain and shortness of breath off an on for "a few days." 

The impression that I get from the documentation is that the patient was still felt to be somewhat altered, and the history was felt to be somewhat unreliable and vague. The notes report that the patient has a history of schizophrenia, HTN, diabetes, and atrial fibrillation not on anticoagulation due to noncompliance. At triage, the patient was again able to independently report "shortness of breath" as the chief complaint. His vitals were within normal limits.

His triage ECG at 1741 is shown here:

What do you think?

A baseline ECG was available:

I see atrial fibrillation without any clear signs of ischemia. Borderline low voltage. Even with the baseline ECG available, I don't see a meaningful change.

A broad workup was ordered, including troponin and head CT. 

The head CT showed no acute intracranial abnormality. The patient was given food, and serial fingersticks did not show any further hypoglycemia. All reports continue to describe the patient as "encephalopathic" and a "poor historian," but all reports also agree that the patient would complain of vague chest pain and shortness of breath when asked.

The initial high sensitivity troponin I returned elevated at 62 ng/L (URL 14 ng/L). Due to the elevated troponin, another ECG was ordered at 2036 (unclear whether the patient had ongoing symptoms at this time):

This ECG is importantly and diagnostic different than the first! 

There is new STE in V3 through V5, and perhaps a hint inferiorly (but the baseline is not perfectly clear). More importantly the T waves in V3-V6, and also in inferior leads, are newly hyperacute compared to the first ECG.

These changes were not appreciated, and no more troponins were ordered in the ED. The patient was admitted to medicine.

The medicine team decided to trend troponins overnight, which showed a steady rise of 1260, 2749, and 6210 ng/L. 

At 0630 that morning, another ECG was ordered (unclear if due to change in pain, or because of the consistently rising troponin):

Evolution to obvious STEMI(+) OMI. Interestingly, the inferior hyperacute T waves are no longer hyperacute.

For unclear reasons, nothing seems to happen immediately based on this ECG.

At 0750, anther ECG is performed:

Still obvious STEMI(+) OMI.

Angiogram was finally done at around 0930 which showed a proximal LAD dissection with distal LAD thrombotic occlusion (TIMI 0 flow). They elected to treat the dissection medically. The report does not mention any intervention or aspiration of the distal LAD thrombus, and does not mention the state of the distal artery flow at the end of the case, but the post-cath note describes resolution of chest pain (and the post-cath ECGs below show reperfusion).

Here is the ECG after cath:

Beginning of reperfusion.

The next troponin resulted at greater than 25,000 ng/L (our lab does not report higher), and no further measurements were done.

Day 3 ECG 0900:

Day 3 1300:

Here is the whole sequence of ECGs, from baseline through reperfusion, showing just leads V3-6 side by side, with the relevant portions of the OMI progression for reference underneath:

Learning Points:

Serial ECGs with careful side by side inspection could have helped identify this OMI sooner.

Hyperacute T waves are not yet defined, but trained electrocardiographers know them when they see them. Serial ECGs can prove that otherwise reasonable T waves are actually hyperacute compared to prior. 

Ongoing ischemic symptoms, ongoing ECG ischemia, or ongoing troponin rise in ACS are reasons to pursue immediate reperfusion, and NOT to wait until clear STEMI criteria are manifest. These are indications for emergent angiogram in all guidelines around the world, but are simply not followed in many settings for unclear reasons. The STEMI paradigm makes most providers believe that they are not missing OMI, makes them believe there is no need to ever treat an NSTEMI emergently.

Remember, the myocytes do not "know" the etiology of their focal full thickness complete ischemia - the ECG findings are the same regardless of the etiology of OMI. Angiogram is the only way to tell whether it will be one of the majority of cases that benefit from an intervention. Lack of a discrete intervention does not mean that the patient and patients like him do not need to be taken to the cath lab.

Maintaining a high level of suspicion, particularly in those who may not be able to advocate for themselves (e.g., hx of psychiatric disorders) when faced with abnormal findings, such as a rising troponin, and learning to recognize electrocardiographic findings for OMI beyond STEMI can help to deliver the highest quality, most expedient care for our patients.