Saturday, November 21, 2020

The resident made the diagnosis immediately. The faculty was not as certain.

This was sent by one of our G2 residents, working at a different hospital.

"A 50-something male with a history of hyperlipidemia but no known cardiac history woke up with sudden onset substernal pressure and nausea/vomiting and diaphoresis. "

EMS recorded this ECG: 

What do you think?

"The medics were concerned by the story and they saw some ST Depression in the inferior leads and so they gave ASA and nitro with some relief. On arrival to ED we got a 12-lead ECG and looked at the prehospital EKG." 

Here is that first ED ECG:

Resident: "My interpretation was STD in II, III, and aVF with hyperacute T waves in aVL and I.  I was concerned for high lateral OMI.  There is also a hyperacute T-wave in V2."

Smith: the prehospital ECG and first ED ECG are both diagnostic of a high lateral OMI.  "Inferior ST depression" is actually reciprocal to high lateral ST elevation until proven otherwise.  The inferior ST depression (rather than the ST Elevation) is often the most visually stunning feature.  The T-wave in lead III is a reciprocally inverted hyperacute T-wave.  The hyperacute T-wave in V2 makes this a mid-anterolateral OMI which is due to D1 occlusion.  There is also a bit of ischemic ST depression in V5 and V6.

Here are some old posts on inferior ST depression: 

Resident Continues: "My attending definitely thought it was a concerning EKG but not a slam dunk OMI. We started nitro drip as he was still having pain, got a CXR and a cardiac ultrasound to rule out obvious dissection and then started heparin." 

"We did get 1 repeat EKG:"

Resident: "This showed less STD and smaller T waves.  In other words, he had dynamic changes. "

Smith: T-wave in V2 is also less hyperacute.

"After about 1 hour in the department on these meds his pain was not fully resolved so we called cards. They were in agreement that he should get cathed as his pain couldn't be controlled." 

Initial troponin I was below the 99th percentile URL (not high sensitivity assay).

He went to the Cath Lab and had a 100% ostial diagonal occlusion which was stented. Troponin I peaked at 15 ng/mL. He did well and is discharging home. 

Learning Points
1. High lateral MI often has deeper reciprocal inferior ST depression than it has ST elevation in leads aVL +/- lead I.
2. The initial troponin does not help in the diagnosis of acute OMI (though it often helps if subacute OMI is supected)
3. Hyperacute T-waves are fat and/or tall.  It is the area under the curve of the T-wave, in proportion to the QRS, that distinguishes hyperacute T-waves
4. When there is a hyperacute T-wave in aVL, the T-wave in lead III is a reciprocally inverted hyperacute T-wave


MY Comment by KEN GRAUER, MD (11/21/2020):


We are told that the resident physician in today’s case correctly diagnosed OMI — but that the faculty physician was not as certain. Specifically — the faculty physician agreed there were concerning ECG findings in the first 2 tracings in today’s case — but that these findings were not diagnostic of OMI.

  • Given this difference in opinion between these 2 clinicians — I thought it worthwhile to TAKE another LOOK at these first 2 tracings (Figure-1):

Figure-1: The first 2 ECGs in today’s case (See text).


— #1) WHY is the ECG done by EMS in the field diagnostic of OMI?

  • HINT: How many leads in ECG #1 are abnormal?

— #2) Does ECG #2 (that was done on arrival in the ED) further support the diagnosis of OMI? If so — HOW?

— #3) How does assessment of the ST-T wave appearance in lead aVL help to localize the “culprit” artery?

MY Thoughts on ECG #1:

The History in today’s case is extremely concerning: This 50-something year old man with no prior cardiac history was awakened by sudden, severe chest pain, associated with diaphoresis and vomiting.

  • The rhythm in ECG #1 is sinus bradycardia and arrhythmia. All intervals and the axis are normal. There is no chamber enlargement.

Regarding Q-R-S-T Changes:

  • There are no Q waves (at least no consistent Q waves). That is, of the 2 tiny QRS complexes that are seen in lead III — there is a definite initial r wave in the 1st complex, albeit a Q wave seems to be present in the 2nd complex. The clinical significance of this Q wave in the 2nd QRS complex is uncertain.
  • R wave progression is slightly delayed (ie, transition occurs between leads V4-to-V5). That said — reasonably-sized r waves are seen in leads V2, V3 and V4.
  • At least 3 T waves are hyperacute in ECG #1 — in that the T waves are taller-than-they-should-be in leads I, aVL and V2, as well as being more “voluminous” (ie, fatter-at-their-peak and broader-at-their-base than should be expected).
  • There is dramatic mirror-image ST depression in lead III (the ST-T wave in III is the mirror-image opposite of the hyperacute ST-T wave in lead aVL).
  • Reciprocal ST-T wave changes are also seen in the other 2 inferior leads — in the form of ST depression with terminal T wave positivity in leads II and aVF.
  • The T wave inversion in lead V1 is not necessarily abnormal. However, the ST segment is straightened (if not slightly depressed) in leads V3, V4, V5 and V6. This is clearly not a normal ST-T wave appearance in these 4 chest leads.

IMPRESSION: In a 50-something adult awakened from sleep by severe new-onset chest pain — the finding of acute-looking ST-T wave abnormalities in 10 of 12 leads on the EMS tracing ( = ECG #1), with definite hyperacute T waves in 3 leads and precise mirror-image opposite reciprocal changes in the inferior leads — is diagnostic of OMI.

  • It should be emphasized that the diagnosis of acute OMI can be confidently made on the basis of this EMS tracing alone.
  • NOTE: For review of the ECG findings to look for when your patient with new-onset cardiac symptoms does not manifest STEMI-criteria ST elevation on ECG — Please CHECK OUT the Figure I added to the bottom of My Comment in the November 17, 2020 post of Dr. Smith's ECG Blog.

MY Thoughts on ECG #2:

As was done in today’s case — a repeat ECG was obtained on arrival in the ED (ECG #2 in Figure-1). Repeating the ECG on arrival in the ED is important for providing insight into the progression and extent of the OMI — as well as to convey whether spontaneous reperfusion is likely to have occurred.

  • The rhythm in ECG #2 again appears to be sinus bradycardia and arrhythmia.
  • QRS morphology in both limb leads and chest leads looks similar — which tells us that lead-to-lead comparison of ST-T wave changes will be valid.

I believe there are 3 subtle-but-real changes between ECG #1 and ECG #2.

  • Although T waves in leads I and aVL of ECG #2 still look hyperacute — the shape of these T waves is different, and they are clearly less tall than they were in ECG #1 (ie, T waves were at least equal to R wave amplitude in leads I and aVL of ECG #1 — whereas T waves in these leads are less tall relative to R wave amplitude in ECG #2).
  • Relative T wave inversion in lead III of ECG #2 is less deep than it was in ECG #1 — as the shape of this inverted ST-T wave in lead III of ECG #2 has changed, so as to continue to be the precise mirror-image opposite shape of the hyperacute T wave in lead aVL.
  • There looks to be slightly more ST depression in leads V3-thru-V6 of ECG #2.

IMPRESSION: Though admittedly subtle — I think there has been some change between these first 2 tracings in today’s case.

  • This change provides further support of acute evolution in this patient with an ongoing OMI.

Optimal Use of Lead aVL:

We have emphasized on many occasions in Dr. Smith’s ECG Blog how useful mirror-image opposite ST depression in lead aVL can be in confirming the diagnosis of acute inferior OMI.

  • Whereas repolarization variants may sometimes manifest inferior lead ST elevation — there should not normally be in lead aVL the picture of mirror-image opposite ST depression, compared to the shape of the ST elevation in lead III.

The finding of ST elevation (or of a hyperacute T wave) in lead aVL may prove equally insightful in predicting the “culprit” artery in acute OMI. I still like to refer to results from an older study by Birnbaum et al (Am Heart J 131:38, 1996). For clarity — I’ve added a schematic picture of the principal branches arising from the left main coronary artery (Figure-2). Points made in the Birnbaum study are to:

  • Suspect acute LAD occlusion proximal to the 1st Diagonal IF in addition to ST elevation in aVL — there is also ST elevation in leads V2-through-V5. This is the most common situation when there is ST elevation in lead aVL. NOTE: If there is ST elevation in anterior leads but no ST elevation in lead aVL — suspect a more distal LAD occlusion (that occurs after the takeoff of the 1st Diagonal branch).
  • Suspect 1st (or 2ndDiagonal branch occlusion IF in addition to ST elevation in aVL — there is ST elevation in lead V2 (but not in leads V3, V4, V5).
  • Suspect LCx occlusion (especially of the 1st obtuse marginal branch) IF there is ST elevation in aVL, but not in lead V2 (and not in other anterior leads).


Figure-2: Schematic depiction of normal coronary anatomy of the left coronary artery and its major branches. The LCA (Left Coronary Artery) begins as a short LMain (Left Main Coronary Artery) branch — which then bifurcates into the LAD (Left Anterior Descending Arteryand the LCx (Left Circumflex Artery).

Panel A — Anterior view. Panel B — RAO (Right Anterior Oblique) view.

Abbreviations: S-1, S-2 (Septal Perforator branches); D-1, D-2 (Diagonal branches); M-1, M-2 (Obtuse Marginal branches from the LCx). (Figure reproduced from Grauer K, ECG-2014 ePub Pocket Brain).

PEARL #1: We can predict acute occlusion of the 1st (or 2nd) Diagonal branch of the LAD as the “culprit” artery in the ECGs shown in Figure-1 on the basis of findings I cited above from the Birnbaum study:

  • The T wave in lead aVL is obviously hyperacute. This is especially marked in ECG #1 — in which T wave amplitude surpasses R wave amplitude in this lead, with a “fat” T wave peak and marked widening of the T wave base. (Similar hyperacute changes are seen in the other high-lateral lead = lead I).
  • There are equally obvious hyperacute changes in lead V2.
  • None of the other chest leads show ST elevation. Instead — leads V3-thru-V6 show ST segment flattening and slight depression.

PEARL #2: As we have seen in today’s case — there is ongoing ST-T wave evolution over the course of the 3 tracings presented above as OMI is ongoing.

  • In my experience — initial ECGs from acute LAD occlusion may at times only show ST elevation in leads aVL and V2. In such cases, I’ve initially suspected OMI of the 1st or 2nd Diagonal branch — only to change my prediction later on as chest lead ST elevation became more generalized.
  • This did not occur in today’s case — as hyperacute changes remained localized to high-lateral leads I and aVL and to chest lead V2 — but without ever developing ST elevation in other chest leads.
  • Recognition of this finding of ST elevation that remains localized to lead aVL (with or without similar findings in lead I) and to lead V2, but without ST elevation in other chest leads — can be important clinically! I am aware of more than 1 case in which initial review of cath films did not detect OMI of a 1st or 2nd Diagonal branch. In these cases — it was the ECG finding of ST elevation limited to leads aVL and V2 that prompted a 2nd look at the cath films, that then detected the Diagonal branch occlusion.


  1. Dr. Smith, Once again great post on culprit artery localisation ( Saturday, Nov 21 2020 ). These
    days cardiologists believe that culprit artery localisation is purely academic in the era of emergent PCI. So the discussion on this beautifull ECG cannot be complete without highlighting the
    excellent academic points which you have already touched upon but needs little highlighting as follows.
    First of all, D1 block is unique in that it is a STEMI involving non-consecutive Leads, I, aVL & V2.
    Secondly, it shows morphologically two different types of ST depression - in III & aVF there is
    STD with INVERTED T reciprocal to STE in aVL. There is also STD with POSITIVE T in V3 to V6 due
    to subendocardial ischemia. Together, these findings in this ECG is spread over I, aVL, V2 and V3
    through V6. This distribution has been aptly likened to the South African Flag sign.
    Sclarovsky et al in their paper ( International Journal of cardiology 1994:Aug 46 (1) 37-47) have
    highlighted these points and add that D1 block STEMI is rare ( 1.7% of ant wall infarction in their
    study). So, I congratulate the Resident who picked up this rare diagnosis.
    with regards,

    1. Thank you Dr. Balaubramanian. I do not agree that this ECG shows subendocardial ischemia. The STD and inverted T-wave in III is simply reciprocal to the hyperacute T-wave in aVL, not subendo (as you said). In precordial leads, posterior transmural ischemia (posterior OMI) may have either downsloping STD with TW inversion, or upsloping STD with upright T-waves in the acute phase, for complex reasons. Later, or after reperfusion, the precordial T-waves in posterior MI are always upright.

      Thanks again,

      Steve Smith

  2. A similar case:

  3. As per DR. KEN GRAUER "The T wave inversion in lead V1 is not necessarily abnormal. However, the ST segment is straightened (if not slightly depressed) in leads V3, V4, V5 and V6. This is clearly not a normal ST-T wave appearance in these 4 chest leads." This Q-R-S-T changes could be made by posterolateral AMI?
    Anderson Santos, Thanks a lot, one day=one learn.


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