Submitted by Dawn on Fri, 04/25/2014 - 14:01

This week's ECG is from a 47-year-old man who experienced a sudden onset of chest pain while mowing his lawn. He went on to suffer a cardiac arrest and was resuscitated. We do not have long-term followup on his outcome.

The experienced person will have no difficulty identifying a large acute antero-lateral wall M.I. There are massive ST segment elevations in Leads V1 through V6, reflecting acute injury from the septal side of the anterior wall (patient's right) to the anterior-lateral wall (patient's left). There are also ST elevations in Leads I and aVL, reflecting the high lateral wall. This indicates, and was confirmed in the cath lab, that the lesion is proximal - at or above the bifurcation of the left anterior descending artery and the circumflex artery. The ST depressions in the inferior wall leads (II, III, and aVF) likely represent reciprocal changes. You will note that the ST depression in Lead III has a very similar shape to the ST elevation in Lead aVL.

More bad news for this patient is the presence of pathological Q waves in Leads V1 through V4, reflecting transmural death of the myocardial tissue. This causes akinesis and poor left ventricular function. In addition, it's not only muscle tissue that dies, but also electrical structures , such as bundle branches. Papillary muscles can be infarcted, causing valve malfunction. And remember, all patients who have ST elevation due to acute injury are vulnerable to ventricular tachycardia and ventricular fibrillation, due to re-entry mechanisms in injured tissue.

This ECG will allow instructors to discuss with their students:

* which leads reflect changes from which parts of the heart

* what the ECG signs of acute M.I. are

* the pathophysiology of pathological Q waves

* the effect of damage to various parts of the heart on the patient's condition and symptoms

This "classic" M.I. pattern should be taught to all health care professionals who work in settings where ECG is used.

Related Terms:

STEMI

Anterior wall M.I.

Proximal occlusion of LAD

ST elevation

Pathological Q waves

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Comments

PEARLS in Assessment of the "Culprit Artery" with Anterior STEMI

Permalink Submitted by [email protected] on Fri, 04/25/2014 - 17:12

Dawn has mentioned the highlights regarding this obviously large acute anterolateral STEMI (ST Elevation Myocardial Infarction). I’ll add the following comments with focus on predicting the "culprit" artery.

Lead aVL is an underutilized lead for localizing the area of acute infarction. Although traditionally thought of as a “high lateral lead” - newer MRI correlations suggest lead aVL more accurately correlates to injury in the mid-anterior wall (Bayes de Luna et al - Circulation 114:1755-1760, 2006)
Whether or not there is proximal LAD (Left Anterior Descending artery) occlusion is in part suggested by whether there is ST elevation in lead aVL. The presence of anterior ST elevation in the absence of ST elevation in lead aVL suggests acute occlusion distal to takeoff of the 1st Diagonal Branch of the LAD.
Interestingly - there is not always reciprocal ST depression in the inferior leads with anterior infarction. In particular - with a more distal LAD occlusion (after takeoff of the 1st Diagonal) - in addition to lack of ST elevation in aVL - there is also often no reciprocal ST depression. Awareness of this pattern IS important - so that one does not discount the possibility of an early acute STEMI simply because there is no reciprocal ST depression.
Finally - Use of lead aVR may further contribute to localization of the likely location of acute occlusion. The remote superior and right-sided electrical viewpoint of lead aVR (looking down at the heart from the right shoulder) - provides a unique vantage point that assesses the basal part of the interventricular septum. Ischemia of the septum (as may occur with severe left main disease) produces a vector that points superiorly - resulting in ST elevation in lead aVR. This is often associated with ST elevation in lead aVL and ST depression in the inferior leads. Similar ECG findings may be seen with proximal (but NOT distal) LAD occlusion.

PEARL: Distinction between left-main disease vs proximal LAD occlusion may be suggested on ECG by the relative amount of ST elevation seen in lead aVR compared to lead V1.

Think Left-Main disease - when ST elevation in lead aVR > V1.
Think proximal LAD disease/occlusion - when ST elevation in lead V1 > aVR.

In this Case: - Findings in addition to the already noted marked anterior ST elevation with large Q waves (QS complexes) in V1-thru-V4 - are: i) marked ST elevation in aVL; ii) reciprocal inferior ST depression (at least in leads III, aVF - which manifest the ‘mirror image’ to the ST elevation in aVL); iii) NO ST elevation at all in lead aVR; and iv) marked ST elevation in lead V1. These findings ALL point toward a very proximal LAD occlusion (and not left-main disease - and not more distal LAD occlusion). Finally - It is of interest that the amount of ST elevation in lead I is at least equal to that in aVL, whereas usually aVL shows more ST elevation. We presume this is simply a reflection of the large area of acute damage from proximal LAD occlusion.

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For More Info Regarding:

ECG Signs of Acute LAD Occlusion -
Use of Lead aVR in ECG Interpretation (See beginning on page 462 re use of lead aVR in patients with coronary disease).

Ken Grauer, MD www.kg-ekgpress.com [email protected]

Off topic

Permalink Submitted by VinceD on Sat, 04/26/2014 - 23:08

Ken, on the topic of Bayes de Luna (who I'm just starting to appreciate as one of the true rock stars of electrocardiography), have you read his book "The 12 Lead ECG in ST Elevation Myocardial Infarction"? I recently got my hands on a pdf and I wish I had found it a couple of years ago. It pretty much clarifies all of the concepts regarding localizing culprit lesions that I've slowly accrued through experience and guess-and-check over the past two years in 50-some pages. I kept thinking, "I wish someone would write a book where they just describe patterns of ST-elevation and injury vectors and correlate them with coronary anatomy and pathology." Turns out he did and I just didn't know it.

Vince D
http://www.medialapproach.com

Correction

Permalink Submitted by VinceD on Sat, 04/26/2014 - 23:02

Just to clairfy, in the discussion you state, "the lesion is proximal - at or above the bifurcation of the left anterior descending artery and the circumflex artery." What you mean to say is that it is at or above the takeoff of the first-diagonal and first-septal arteries. If it was proximal to the LCx then we'd be talking about a left-main lesion.

that the lesion is proximal - at or above the bifurcation of the left anterior descending artery and the circumflex artery. - See more at: http://ecgguru.com/ecg/instructors-collection-ecg-week-april-25-2014#comment-form

Vince D
http://www.medialapproach.com