Case No. 14: Rear View Mirror

A 59 year-old white female presents to EMS with two hours of 9/10 substernal chest pressure radiating into her left arm. Her history is significant for HTN, hyperlipidemia, and 30 pack-years smoking. The blood pressure is 90/50; she is diaphoretic and pale.

1st degree AV block can be seen complicating this inferolateral MI. Note that the STE in lead III is greater than that in II and caution should therefore be observed regarding right ventricular involvement. Of additional note is the unexpectedly tall R-wave in V2, a remarkable finding when met with right sided ST-depression.

In light of the ST elevations in V5 and 6, II, III, avF, and right precordial depressions suggestive of posterior wall infarction, it might seem reasonable to assume that a proximal culprit lesion is placing a large territory of myocardium at risk. In the past, however, there has been a lack of consensus among investigators with regard to whether either the number of leads demonstrating STE or the net magnitude of STE can be reliably correlated with the extent of myocardial injury. (Birnbaum and Drew, 2003, 492-493)

Without engaging the question of how myocardial injury can or should be quantified, it is clear that the 12-lead EKG does not equitably represent all myocardial territories. Not only are some regions better visualized than others, but electrical vectors can augment and dampen one another. This phenomenon is of particular interest when we consider that ST elevation in V4R, V1, and V2 due to right ventricular involvement may be canceled from view by the opposing vectors of a concomitant posterior wall infarction. Posterior forces may be likewise mitigated, even as they already demonstrate proportionally lower voltage due to the greater distance of the surface electrodes from the depolarizing myocardium.

Case reports of “normalization” resulting from the opposition of two independent currents of injury have been described. Wang and colleagues present a case in which the electrocardiographic evidence of acute anteroseptal infarction suddenly disappeared from view, they contend, as a direct result of a new, electrically oppositional, infarction of the posterior wall. Their abstract is as follows:

In a 76-year-old man an electrocardiographic pattern of acute anteroseptal myocardial infarction disappeared suddenly. At necropsy, a more recent posterior myocardial infarct was found, in addition to an acute anteroseptal infarct. “Normalization” of the electrocardiogram from the pattern of anteroseptal myocardial infarction in this case resulted from the loss of opposing electromotive forces in the posterior wall because of posterior infarction. (Wang, K., et al., 1976)

Thus, when considering the “rear view” leads, there is a real sense in which things “may be larger than they appear.” Therefore, regardless of ones skepticism as to the proportionality between ST elevation and actual myocardial tissue necrosis (Birnbaum), a high index of suspicion should be maintained when a pattern of acute changes implicates an arterial lesion likely placing two ischemic myocardial territories opposite one another (Wang).

Although this 15-lead EKG shows only non-specific T-wave inversion in V4R, the posterior leads V7 and V8 demonstrate subtle ST elevation, thus confirming what can be suspected from the initial tracing. The 1st degree block has resolved, and the magnitude of ST elevation has diminished.

Despite what appeared to be an initially positive response to medical management, the final pre-hospital tracing recorded from this patient shows unifocal PVCs in the pattern of bigeminy.

This was to prove an ominous sign in this case, as shortly after arrival in the ED the patient became unconscious and was noted to be in ventricular tachycardia. Pulses were initially present and cardioversion was performed. Sinus rhythm resumed briefly but again gave way to VT, this time without pulses. Despite aggressive efforts, refractory VF persisted for over 30 minutes and the patient could not be resuscitated.

Dr. Stephen Smith has discussed the issue of posterior wall STEMI through a series of case presentations and his insights on this topic can be found here.

Tom Bouthillet also has a superior set of case studies addressing the issue of posterior STEMI; the category “Acute Posterior STEMI” can be found here, in his site index.

Of additional note, AV block is a frequent finding in inferior wall MI and further case studies illustrating this and discussing the mechanism involved can be found on this site in the case series of September, 2010.

References

Birnbaum, Y. and Drew, B. 2003. The electrocardiogram in ST elevation acute myocardial infarction: correlation with coronary anatomy and prognosis. Postgrad. Med. J. 2003;79;490-504. doi:10.1136/pmj.79.935.490

Wang, K., et al. 1976. Sudden disappearance of electrocardiographic pattern of anteroseptal myocardial infarction. Result of superimposed acute posterior myocardial infarction. Chest. 1976;70;402-404. doi: 10.1378/chest.70.3.402 

Advertisements

2 responses

  1. Certainly looks like a proximal RCA occlusion, given the posterior changes and AV nodal changes.

    Great case!

    August 25, 2011 at 9:06 pm

    • Thanks for the support Christopher! I absolutely agree– the AV nodal features and STE distribution localize the lesion, however the severity of the infarction (i.e. magnitude of damage done) is not clearly something that can be gauged via 12-lead alone.

      August 27, 2011 at 7:39 pm

Leave a Reply

Fill in your details below or click an icon to log in:

WordPress.com Logo

You are commenting using your WordPress.com account. Log Out / Change )

Twitter picture

You are commenting using your Twitter account. Log Out / Change )

Facebook photo

You are commenting using your Facebook account. Log Out / Change )

Google+ photo

You are commenting using your Google+ account. Log Out / Change )

Connecting to %s