There is 0.5 mm of ST elevation in inferior leads II, III, and aVF. In addition, the T-waves in II, III, and aVF are very large, significantly larger than normal in both height and width. To diagnose inferior MI, there must always be reciprocal ST depression or T-wave inversion or both in lead aVL (see abstract of our research below). This is present here.
Hyperacute T-waves can be present early, before the ST segment elevates, but they can also be present as ST elevation is resolving from spontaneous reperfusion.
In this case the diagnosis was clear due to the prehospital ECG. But suppose there had been no prehospital ECG? Or if the first ECG had looked like this? Suppose the ST segments were on the way up rather than on the way down. Would you have diagnosed this? This identical ECG could be all the evidence you might have.
If you find yourself in this diagnostic dilemma and you are uncertain of the diagnosis, remember that you can use serial ECGs, old ECGs, and immediate echocardiography to help in the diagnosis.
Also, remember the value of lead aVL: see this post. And this one
Click here for a great case of developing inferior MI with hyperacute T-waves.
Research presented at 2011 SAEM in Boston.
Published in Academic Emergency Medicine, vol. 18 (5 Suppl 1):Abstract 425, p. S164-S165.
In acute inferior STEMI, Reciprocal ST depression in aVL and T-wave inversion in aVL are both more sensitive than ST elevation criteria and appear earlier in the course of STEMI
Stephen W. Smith
Background: A previous study found that reciprocal ST depression (rSTD) is present in only 82% of inferior ST elevation (STE) acute myocardial infarction (MI). However, we believe that changes in lead aVL are far more sensitive. Objectives: To find the incidence of any rSTD or T-wave inversion (TWI) in angiographically proven inferior STEMI. Methods: We searched the catheterization laboratory database for all cases coded as acute Inferior STEMI from January 2002 through March 2008. All cases were reviewed and the presenting ECG, as well as the first ECG that was used for diagnosis of acute STEMI, were analyzed. “True STEMI” was defined as 100% occlusion or as a culprit lesion with maximum troponin I (trop) > 10 ng/ml. STE was measured in leads II, III, aVF; aVL was scrutinized for any rSTD or TWI. TWI was defined as a T-wave mostly down, or a biphasic T-wave that is first down, then up (not up then down, which is associated with lateral AMI). Reperfusion criteria were defined as STE of at least 1 mm in 2 of 3 of inferior leads II, III, aVF. Results: There were 160 unique cases. 107 had 100% occlusion, and 35 had < 100% occlusion, but had a maximum trop > 10 ng/ml, for 142 true STEMI; 18 (11%) had < 100% occlusion and a max trop < 10 ng/ml. 85% of the diagnostic ECGs of true STEMI, and 84% of all cases, met STE criteria. No true STEMI had absence of reciprocal depression in lead aVL. Of the 107 with 100% occlusion, 100 (93%) had at least 0.5 mm of rSTD; the remainder had rSTD of < 0.5 mm. Even among those without true STEMI, 94% had some rSTD in aVL. Additionally, in 44 cases (28%), there was no STE whatsoever on the presenting (first) ECG; all of them had either rSTD or TWI. See Table. Conclusion: STE criteria for inferior STEMI are insensitive, especially on the presenting ECG. Changes in aVL, both some amount of rSTD and also TWI, are more sensitive than STE criteria in the diagnosis of inferior STEMI and are nearly universally present in inferior STEMI. These changes also appear earlier than STE.