Wednesday, July 14, 2010

Cardiac Arrest, Ventricular Fibrillation, Inferior and Right ventricular MI (RVMI) or "Pseudoanteroseptal MI"

A 56 yo f with h/o HTN and hypercholesterolemia called EMS from home after onset of L chest pain radiating to the left arm. Before EMS arrived, she had "seizure activity" and became unresponsive. She was defibrillated successfully from ventricular fibrillation and developed a perfusing rhythm. She was intubated. She arrived comatose and in cardiogenic shock and the following ECG was recorded.



There is a bradycardic rhythm of uncertain etiology, possibly a sinus pause with escape, and occasional PVCs. There is ST elevation in II, III, and aVF, but also ST elevation in V1, but also in V2 and V3. This is diagnostic of Right ventricular MI. RVMI that has ST elevation in V1 all the way to V3 is referred to as "pseudoanteroseptal MI," and is distinguished from LAD anterior MI by the inferior ST elevation (although a "wraparound" LAD can do this) and by the fact that there is more ST elevation in V1 than in V4.


That this is an RVMI is confirmed with the following right sided ECG:







Now it can be seen that most of the precordial ST elevation is in V4R, much more than is present on the left side of the heart (V1R, which is equivalent to V2 on the left sided ECG.



She was bradycardic and hypotensive. Normal saline bolus was given, with improvement in BP. .
Pressors were required, and the patient was transported to the cath lab with a door to balloon time of 60 minutes, where a proximal dominant RCA occlusion was opened and stented.
She underwent therapeutic hypothermia, and emerged from coma.
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She awoke and was discharged to home with no disability

3 comments:

  1. There was a comment with a couple inaccurate statements:

    1) "In RVMI, you normally see STE in lead III higher than II, and normally you'd see ST depression in V1-V3..."

    RVMI is always a result of RCA occlusion, and it is true that STE in lead III is usually higher than in lead II in RCA (as opposed to circumflex) occlusion, as seen here.

    ST depression in V1-V3 is only present if the RCA has branches to the posterior wall, which happens < 50% of the time.

    When there is concomitant RVMI and posterior MI, ST segment in V1 may be either elevated or depressed, depending on which dominates.

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  2. Doesn't the RCA give rise to the PDA and PLA in 90% of people? So if the RCA is occluded proximal enough, you;'d have a post MI as well in most cases. Right? Am I off in my assumptions?

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  3. The RCA supplies the posterior descending artery 85% of the time, but the posterior descending artery supplies the inferior wall primarily. The posterior wall is much less commonly supplied by the RCA, and (slightly) less than 50% of inferior MI involves the posterior wall also.

    The RCA always supplies the RV, through the RV marginal branch, so a proximal obstruction may result in RV MI. However, because of good collateral circulation, less wall stress on the low pressure RV (unlike the LV, it is not only perfused during diastole), and other reasons, the hemodynamic consequences of RV MI are not seen with every proximal occlusion.

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