In this post I link to and excerpt from Emergency Medicine Cases’ ECG Cases 17 – ST ELEVATIONS mnemonic and Occlusion MI. January, 2021, by Dr. Jesse McClaren; Peer Reviewed and edited by Anton Helman. January 2021
Note to myself when reviewing: First review the notes below from Dr. McClaren’s post and then go to the post itself to test myself by reviewing the ten ECGs he has provided for us.
All that follows is from the above post:
In this ECG Cases blog we look at 10 patients who presented with ST elevation, and review the differential diagnosis of ST elevation using the ELEVATIONS mnemonic. Which had occlusion MI?
ST ELEVATIONS mnemonic and Occlusion MI
Most patients presenting to the ED with chest pain and ST elevation don’t have acute thrombotic occlusion [1]. The differential of ST elevation includes hyperkalemia, baseline conduction (LBBB, early repolarization), structural changes (LVH, LV aneurysm), acute ischemia or inflammation (including occlusion mimics discovered on angiography, like coronary vasospasm, myocarditis or takotsubo), and miscellaneous rarer causes. These can be remembered by the mnemonic “ELEVATIONS”:
- Electrolyte (hyperkalemia)
- LBBB/ventricular paced
- Early repolarization
- Ventricular hypertrophy
- Aneurysmal LV
- Thrombotic occlusion (OMI)
- Inflammation (pericarditis)
- Osborn wave (hypothermia)
- Neurogenic (eg SAH, ICP)
- Sudden death (Brugada)
These all have ST elevation and are not mutually exclusive (eg, hyperkalemia or ischemia can induce the Brugada phenocopy, or patients with LBBB or LVH can develop thrombotic occlusion). As a result, only looking at the ST segment and dichotomizing it by millimeter criteria doesn’t differentiate between different causes of ST elevation (eg early repolarization, pericarditis, thrombotic occlusion), and doesn’t identify acute occlusion in the presence of chronic ST elevation (eg from LBBB, LVH or LV aneurysm). These limits of the STEMI paradigm were identified early on, as the National Heart Attack Alert Program Coordinating Committee explained in 1994: “ECG abnormalities may be subtle or open to different interpretation, such as early repolarization or pericarditis. Only borderline or minimal ST-segment elevation may be present, and the emergency physician may be uncertain of its significance. The presence of left bundle branch block or left ventricular hypertrophy may complicate ECG diagnosis. The emergency physician may suspect that the ST elevation is old, but a previous ECG may be unavailable for comparison. The computer interpretation of the ECG on which some physicians rely may be incorrect.” [2] At the time little could be done to address these limitations, beyond other false dichotomies—for example that concave ST elevation differentiates benign causes (eg pericarditis or early repolarization) from occlusion, or that Q waves distinguish old from new MI. The STEMI paradigm was further reinforced by a definition that excludes LBBB and LVH and that excludes minimal ST elevation as “Non-STEMI”. As a consequence, the STEMI paradigm misses 25% of acute coronary occlusions that don’t meet criteria[3], and can result in unnecessary cath lab activation for ST elevation not caused by acute occlusion.
But over the past 25 years later, there have been major advances in ECG interpretation that have addressed many of the earlier limitations. While computer interpretation is still notoriously inaccurate, there are many useful decision rules that can help[4]. While 40% of LAD occlusion present with concave and borderline ST elevation, there is a rule for differentiating early repolarization from LAD occlusion—not just based on magnitude and morphology of ST elevation, but also Q waves, terminal QRS distortion, ST depression, T wave inversion, reciprocal changes, and a formula for subtle cases[5]. While STEMI criteria has poor sensitivity for inferior MI, reciprocal ST depression in aVL is much better at identifying subtle inferior MI and differentiating MI from pericarditis. [6]. While Q waves can develop within an hour of occlusion, the ratio of T waves to QRS complex can distinguish anterior STEMI from old LV aneurysm morphology. [7] While LVH continues to complicate the diagnosis of acute coronary occlusion, the modified Sgarbossa criteria can identify occlusion in the presence of LBBB.[8].
A paradigm shift from STEMI to Occlusion MI (OMI) would benefit both those currently diagnosed as “STEMI” and those currently diagnosed as “NSTEMI”. A quarter of Code STEMI patients with culprit lesions have STEMI-equivalents or subtle occlusion on their first ECG that don’t meet STEMI criteria and that are associated with prolonged ECG-to-Activation time, which would benefit from earlier recognition[9]. And a quarter of patients admitted as “NSTEMI” can be reclassified as Occlusion MI based on advanced ECG interpretation (eg minor STE with reciprocal STD, or hyperacute T waves), and this STEMI(-)OMI(+) subgroup has a higher mortality rate that would benefit from earlier reperfusion. [10]
Now go to Dr. McClaren’s post and test yourself against his ten ECGs.
And when you analyze the ECG, use the H E A R T S mneumonic to analyze the ECG.
So, the first time through, I’m going to go thru the H E A R T S mneumonic answer for each of the ten ECGs.
So go to the post and to the second ten ECGs after Dr. McClaren’s review notes. I’ll list the ten H E A R T S template answers for my review.
Returning to Dr. McClaren’s post:
Ten patients presented with potentially ischemic symptoms and ST elevation. Which had Occlusion MI (OMI)?
Case 1: 40yo ESRD with weakness, nausea/vomiting. AVSS
Case 1: hyperkalemia
- Heart rate/rhythm: NSR
- Electrical conduction: prolonged PR/QRS, LAFB
- Axis: left
- R-wave: delayed R wave progression
- Tension: no hypertrophy
- St/T: mild anterior concave STE and diffuse narrow/peaked T waves
Impression: multiple findings of hyperkalemia. Treated empirically with calcium, insulin/dextrose, and dialysis. Potassium level 9.0. Post-dialysis ECG had resolution of conduction delays, ST elevation and peaked T waves:
