You have two hours to save this patient’s life

Written by Pendell Meyers, edits by Steve Smith

A female in her 60s with history of CAD s/p PCI and CABG, alcohol abuse, and recurrent pancreatitis presented at 14:55 complaining of sudden onset epigastric pain. Initial vital signs were heart rate 44 bpm, respiratory rate 16, BP 143/67, SpO2 96% on room air. On initial exam she was in mild distress and complaining of severe nausea.

Here is her initial ECG:

What do you think?

There is decreased ECG quality due to baseline movement. Despite this, there are clearly hyperacute T-waves in lead III with reciprocal negative hyperacute T-waves in aVL (and lead I) with likely a small amount of STD in aVL. This is diagnostic of acute transmural inferior acute MI, with the most likely etiology being acute coronary occlusion. There is clear STD in V2 indicative of posterior involvement. Sinus bradycardia despite critical illness also points toward inferior acute coronary occlusion (as the SA and AV node are generally supplied by the same vessel as the inferior wall).

Here are two immediate repeat ECGs performed in efforts to get less baseline wander and artifact:

The same findings are evident throughout, but with baseline movement obscuring various sections. There is even a very small amount of STE present in III on the third ECG.

The emergency physicians activated the cath lab. Apparently this decision was made only on perceived STE in lead III on the last of the ECGs above.

This happened to have been the 6th emergent cath lab activation called by the ED within the past 4 hours (!). The cardiologist came to bedside and deactivated the cath lab. His opinion was that the ECGs did not meet STEMI criteria, that she was probably not suffering from ACS given her pain was epigastric and he interpreted the physical exam as showing epigastric tenderness to palpation.

Initial labs returned showing a first troponin negative.

At approximately 15:30, the nurse called for a physician to bedside because the patients blood pressure dropped to 89 systolic and she became lightheaded.

Here is the repeat ECG at that time:

Massive STD V1-V5, maximal in V2-V3, diagnostic of posterior acute MI. Interestingly, the inferior hyperacute T-waves are no longer present. There is obligatory STE in aVR generated by the large amounts of STD elsewhere.  

ST Elevation in aVR in the setting of inferior MI should also tip you off to possible right ventricular MI (RV MI) and to the need for a right sided ECG. In fact, it is a good idea to do a right sided ECG in every inferior MI, as there is no finding that is 100% sensitive for RV MI on the standard 12-lead ECG.

A possible explanation is that the thrombus in the proximal segment of the vessel supplying the inferior wall may have embolized distally and occluded the portion supplying only the posterior wall. The problem with this hypothesis is that occlusion of the proximal part of the vessel should also have caused posterior ischemia at that time. It is possible that the first ECGs were too early to detect this posterior ischemia. This theory is not provable without cath, but is an anatomic possibility. We do not have records to indicate if her native RCA is patent, or what graft supplies the inferior wall if applicable.

Based on this ECG, the cath lab was reactivated with concern for posterior acute coronary occlusion.

The cardiologist came back and this time took the patient immediately to the cath lab. However, the cath lab was occupied by at least one of the prior 5 “STEMI activations” from earlier in the day, thus there was a delay in which the patient was kept in the cath holding area.

At approximately 1600, the patient acutely decompensated even further. She was rushed into the cath lab, where she lost her pulses just as she was placed on the cath lab table, suffering PEA arrest. ACLS was initiated. The notes state that a transvenous pacemaker was attempted but “never entered her heart” for unclear reasons. No left heart cath was performed. I cannot find an explanation as to why this patient was not an ECMO candidate. She was pronounced around 1700.

It is overwhelmingly likely that this patient died from acute coronary occlusion, but I do not have an angiogram to prove it. Autopsy was not performed.

Learning Points:

1) You must advocate for your patients, as “subtle” findings such as hyperacute T-waves are simply not yet recognized by a wide range of providers as an early finding of acute coronary occlusion (the event for which “STEMI” is a very poor surrogate term)

2) Repeat ECGs are important.

3) Bradycardia in the setting of any critical illness must prompt immediate consideration of hyperkalemia, acute coronary occlusion (usually inferior), and primary rhythm disturbance, among other less common and less reversible causes.

4) This patient, and many others with similar initial ECGs, is an unfortunate victim of a broken paradigm for acute MI management: STEMI vs. NSTEMI. This is a false dichotomy that inspires ignorance to anything except the ST segments. The “STEMI criteria” seem to have been one of the barriers to emergent catheterization which was not overcome in this case, ultimately leading to the patient’s death. It is very likely that this patient could have been saved in the two hours from initial ECG to cardiac arrest.

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