Sunday, January 15, 2012

Serial ECGs confirm initial suspicion of anterior STEMI (LAD occlusion)

A 52 yo man began having substernal chest discomfort and presented 2 hours later.  His prehospital ECG, which I cannot find, reportedly had some ST depression in precordial leads.  He had this ECG recorded at 0658:

There are hyperacute T-waves in V1-V4.  There is minimal ST elevation, almost 1 mm in V2 and less than 0.5 mm in V3, but this is diagnostic of anterior STEMI even without ST elevation.  Using the equation (which may not be applicable because there is not enough ST elevation to even qualify for early repol), and the computerized QTc of 424, the value is 25.995 (greater than 23.4 is LAD occlusion).
The clinicians who saw this patient do not, like me, spend their lives analyzing the minutiae of ECGs, so they were not certain of the diagnosis, but they did suspect it, so they did the entirely appropriate management of obtaining serial ECGs, and a repeat ECG was done at0713:

Still suspicious for hyperacute T's but no ST elevation or significant evolution.  The T-wave in V2 is less prominent, suggesting some reperfusion.  QTc is 436 and equation remains greater than 23.4

So another was recorded at 0720:
Now there is ST elevation in V2 and V3, diagnostic of LAD occlusion
 Another at 0726:
Not much changed
 Another at 0744:
Now it is unequivocal
 At this point, the cath lab was activated. 

This is the post cath ECG:

Cath showed a complete mid-LAD occlusion.  Peak troponin I was 120, even with a short door to balloon time, and even though the initial ECG was not striking.  The echo showed a large anteroapical wall motion abnormality.

I suspect the prehospital ECG had de Winter's ST depression and T-waves

12 comments:

  1. hi Dr. Smith. I am curious about the st-dep in in the inferior and lateral leads, is that reciprocal to the anterior stemi/occlusion? No STE in aVL thus not reciprocal to lateral ste. Could the inferior and lateral ST-dep be due to some collateral flow, and thus ischemia or do you think it represents reciprocal changes?

    Is inferior st- dep more common in anteroseptal MI V1-V3 vs more diffuse STE in precordial leads? Also, and it might be a strecth.. could the St-dep localize in case of a lesion of a wrap-around LAD with occlusion, with post occlusion collaterals to the inferior wall?

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  2. Hi Dr. Smith...
    Great post as usual...

    In comparing the second ECG to the first, i noticed a subtle flattening of the ST segment in V1-V3, and a notable loss of the S wave, most noticeable in V2 (it seems sometimes evolving ST elevation "drags up" the S wave)...

    i was wondering what your thoughts are of those observations, and if they impact your risk stratification of an ECG..

    thanks,
    Dave B

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  3. It also appears that the first ECG (0658) has ~1mm ST-depression in II and aVF. Great case for serial 12-leads!

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  4. good question, which I cannot answer definitively. ST depression in II and aVF are opposite ST elevation in aVR. They also correspond to ST depression in left precordial leads (I prefer not to call them "lateral" leads because the ST depression is not localizing to lateral walls). There is also ST elevation in V1, highly suggestive of subepicardial ischemia of the high septum, or even of the right ventricle, as the LAD does sometimes supply part of the RV. All of this points to high subepicardial ischemia, causing ST elevation, with all of the ST depression being reciprocal. However, this is not all consistent with a mid-LAD occlusion, which we know was the underlying pathology. Unless, of course, the cath report was incomplete.

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  5. I don't understand the second question all that well. Suffice it to say that when there is subendocardial ischemia, you can't tell by the ECG where it is. And when there is subendocardial ischemia, there is usually ST depression in I, II, III, aVF, V4-V6 with ST elevation in aVL. Or there may be ST depression in just V4-V6.

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  6. I think that is exactly what happens, and one of the reasons why the T-wave looks big in STEMI: it looks large relative to a diminishing R and S wave

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  7. if the early ECG at 0658 was nearly diagnostic of anterior STEMI, why was the cath lab only activated at 0744? is this a difference in approach between the ED and the cath lab? or do they require something more concrete to call in the cath team?

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  8. My partner who took care of the patient is not as certain when he sees these ECGs as I am, and most people will not be. Most do not spend their lives, like you and I do, studying this, and just can't immediately recognize these cases. And if they tried, they would have too many false positives. So he appropriately did serial ECGs and then made the diagnosis. If you're not obsessed with ECGs like you and I are, and can't be certain of subtle findings, then this is the way to go.

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  9. Hi Dr Smith,
    Regarding LAD feeding RV on occasion. Is it advised to do RV3 RV4 in what would be otherwise called an Anterioseptal AMI ECG? Or, is there another clue on the standard 12 lead to go looking for an RV infarct?

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  10. These do not extend to the right side, but primarily affect the anterior part of the RV free wall, so the best leads are V1 (V2R) and V2 (V1R). These RV infarctions are clinically insignificant. Most RV infarctions, even due to occlusion of the proximal RCA, do not cause hypotension because of some collateral flow from the LAD.

    1. Andersen HR, Falk E, Nielsen D. Right ventricular infarction: frequency, size and topography in coronary heart disease: a prospective study comprising 107 consecutive autopsies from a coronary care unit. Journal of the American College of Cardiology 1987;10(6):1223-32.
    2. Andersen HR, Falk E, Nielsen D. Right ventricular infarction: diagnostic accuracy of electrocardiographic right chest leads V3R to V7R investigated prospectively in 43 consecutive fatal cases from a coronary care unit. British heart journal 1989;61(6):514-20.

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  11. Dr. Smith,
    regarding your comment above, regarding most RV infarctions not causing hypotension...
    what is your position regarding giving NTG to patients with possible RVI?

    It is always a debated topic, and unless an arbitrary systolic number is used, there seems to be much uncertainty... after all, one person's normotension is another's hypotension.

    thoughts?

    Dave B

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  12. I would avoid in inferior MI only if there is ST elevation in right-sided leads or hypotension. If no R side STE and no hypotension, a single nitro is safe. And you can always give fluids if it precipitates hypotension.

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