Evolution

We don’t often get to see evolving MIs.  Usually they go to cath lab and the ICU so serial EKGs are not available.  In this case, intervention had already been attempted but due to the nature and type of lesion no intervention was possible.  In a case such as this, surgical revascuarlization was the primary modality, but due to multiple co-morbid conditions including age, severe aortic stenosis (valve area in range of 0.55 cm²) and general deconditioning none of our surgeons would touch them.  Notice the subtle changes especially through the precordials.

20:00, Day 1

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So, what do we see? First, Q-waves in leads V1, V2 and V3.  Second, ST-elevation in V1 and V2.  Third, ST-depression in V4 (slight), V5, V6 and flipped T-waves in Leads I and aVL.  Also present is probable left atrial enlargement and  Left Axis Deviation with an axis of around -30°.  Based on this you could theorize that the LAD and Circumflex arteries have some sort of lesion.  The patient is actually hemodynamically stable at the moment.  Previous to this, they had been in atrial flutter with a rate of 110-130’s with some instability.  The cardiologist who was on the floor at the time decided to cardiovert the patient, but as we were prepping to do so they spontaneously converted back to sinus rhythm.  Teetering on the knife edge of stability they enjoyed a nice nap thanks to the Versed we had pushed while prepping for the cardioversion.  It was a reminder to follow the checklist, including ensuring that the patient is still in the rhythm you’re going to shock them out of prior to giving drugs and shocking.  The cardiologist in the last rhythm  check notices that it looks different and at that very moment the tele tech comes running in saying, “They’re in sinus!  They’re back in sinus!”

Next, 24:00 Day 1, patient c/o 5/10 substernal chest pain.

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Nothing too different, although you could say that there is a slight elevation in V3.  The other leads actually look a little better, especially the lateral leads.  No change to axis.  This was after one SL nitro though, so that dilation may have helped, one reason we try to get a 12-Lead prior to giving nitro.

06:00, Day 2

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Now there appears to be ST-elevation in V3.  The lateral leads have calmed down, with just a touch of depression in V5, V6 and I, with flipped T-waves in aVL.

14:00, Day2

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Kind of ugly now, eh?  Now we have questionable Q-waves in V1-V4 (there is a pip right before the wave drops), but fairly significant ST-elevation in the precordials.  Depression and inverted T’s in the lateral leads has returned.  Again this was during an episode of chest pain.

Later that night the patient started to decompensate fairly rapidly.  They had a drop in LOC accompanied by a drop in SPO2 to the low 80’s on 15L non-rebreather.  Lungs we very wet, obviously filling with fluid.  The nurse called the on-call cardiologist who ordered 80mg of Lasix IV, in addition to the 60mg given previously during the day that only got an output of 200ml.  Everything was starting to shut down.  We ended up calling a RRT to get a doc at the bedside, if nothing more than to see if there was anything within the patient’s advanced directive to help.

About a week prior to this, the patient had gone to the cath lab in the failed attempt mentioned above.  Angiography show a 99% occlusion of the left main and distal disease in the RCA, LAD and circumflex arteries.  The left main lesion was so bad that they interventionalist was unable to even pass a wire through, which means it was very, very tight.  They minimal blood flow the heart and absolutely no reserve.  With that in mind, the doc on the RRT realized that we could not fix the underlying problem that was causing the distress.  She spoke with the patient’s family who in the end realized that the patient didn’t have much longer, and made the patient comfort care.  They ended up expiring about an hour later.

Looking at these EKGs one could argue that the ST-elevation is actually LVH with a strain pattern. It certainly fits the criteria, especially when considering the patient had endured previous infarctions and had aortic stenosis, but I’m not completely convinced.  I’m no cardiologist, so I’m going with what I know.  But I am open to other suggestions.  It’s a sad case, especially as the family was still saying how they wanted to talk to the surgeon about open heart surgery the morning of Day 2.  Luckily, we were able to use the means available, notably medication, to give some comfort at the end for the patient, even if we couldn’t’ fix what was wrong.

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3 Comments

  1. Is this what’s referred to as a “flipped axis”? I’m a nursing student and I saw this the other day, but im really not sure what it is.

    Reply

    1. You’re looking at Q waves, ST segment elevation and ST depression. Bad things all. They were in bad shape and you’re watching the left main close down to minimally supply any blood to the heart.

      Reply

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