All ECG cases are subject to patient consent, full confidentiality, and anonymised data. I am nowhere near an expert on ECGs, just interested in learning more. This ECG analysis is intended to stimulate discussion only.
From the printed information, this is a 57-year-old male however there was no information with this ECG so we’ll assume a cardiac presentation.
The rate is normal at 62 bpm.
Although there is no rhythm strip it appears to be a regular rhythm, making AF unlikely (although not impossible.
The axis is approximately 45 degrees, which is normal.
Atria (P, PR)
P waves are clearly visible in lead II, the PR interval is normal at 0.17 (Normal = 0.12-0.20), and there is no evidence of gradual prolongation or disassociation from the QRS, ruling out AV blocks.
Ventricles (QRS, QTc)
Given there are no AV blocks and each QRS follows a P wave, it is clear that the QRS complexes are conducted from the atria (rather than being ventricular in origin). They are normal at a rate of approx. 0.80 (Normal = <0.11). This is best seen in V3.
Nb. The computer has calculated the QRS to be very broad at 0.152 however this is due to it ‘mistaking’ the ST abnormalities as part of the QRS complex (never trust the computer!)
The QTc is normal at 0.365 (Normal for men = <0.440, Normal for women = <0.460).
Nb QTc means the ‘corrected QT interval’ which the computer calculates by expressing the actual QT as it would be for a heart rate of 60 (as this patient has a HR of 62 there is very little difference between the QT and the QTc).
Ischaemia (ST, T, Q, R)
From the first glance at this ECG, it is fairly clear that ischaemia is the primary concern. However it is important to rule out the above as certain rhythms (i.e. ventricular escape rhythms) and blocks (i.e. bundle branch blocks) can mimic ST elevation and lead people to incorrect conclusions.
The ST elevation in the inferior leads (1mm in lead II, 2mm in leads III and aVF), indicates an infarct of the inferior part of the heart, which is normally supplied by the right coronary artery.
In some patients however (approx. 18%), the inferior part of the heart is supplied by a dominant left circumflex (LCx) coronary artery (see ‘Left’ image here). This appears to be the case here as the elevation is greater in III than II, and there is lateral elevation (V5, V6), suggesting the left side of the heart is also involved.
The ST depression in the septal leads could be due to ischaemia, however ischaemia in a completely different part of the heart is unlikely with an inferior infarct. Furthermore, the shape of the ST depression looks like an upside down version of the inferior ST elevation, and is therefore more likely to be a reciprocal change to the inferior/posterior infarct.
Nb If you follow the orange LCx artery in the ‘Left’ picture here, you can see it goes laterally (where there is elevation), then posteriorly (where there are anterior reciprocal changes), and then finally terminates inferiorly (where there is more ST elevation).
ST abnormalities aside, there are no abnormally inverted T waves (a sign of subendocardial ischaemia), no pathological Q waves (an irreversible sign of full thickness MI), and there is good R-wave progression in the anterior leads (R-wave progression is often poor in antero-septal MIs).
To conclude, this is an inferior STEMI likely caused by a complete, proximal occlusion of a dominant LCx artery. With elevation greater than 2mm in 2 consecutive leads, this patient is a candidate for pPCi.
Treatment should follow the modified MONA algorithm:
Clopidogrel/Ticagrelor is also indicated in patients undergoing pPCi, and O2 is only required to maintain SpO2 >94%. Excessive oxygen administration has been shown to increase mortality in adults suffering acute STEMI.
It is worth considering that up to 40% of patients with an inferior STEMI will have a concomitant right ventricular infarction (RVI). This poorly functioning RV can affect preload and these patients are often very reliant on fluids to combat this. They are also at risk of severe hypotension if administered nitrates.
Although a concomitant RVI is all but ruled out given the likelihood of a LCx occlusion, repeating an ECG with V4 on the right chest (V4R) may be worthwhile. Elevation of greater than 1mm in V4R is considered prognostic for RVI.
Because MIs are an on-going process involving the clotting cascade, they can evolve quickly. As such, repeat ECGs should always be taken and compared to the previous to look for dynamic changes.