Wednesday, April 2, 2014

A Non STEMI that needs the cath lab now.

A male in his 60's called 911 for chest pain.  He had some cardiac risk factors including hypertension, on meds, but no previous coronary disease.   His pain was intermittent and he was vague about when it was present and when it was resolved.  Here is his prehospital ECG:

Diagnosis? 

He had an immediate ED ECG:
There is artifact, but the findings appear to be largely gone now





















The diagnosis is acute MI, but not STEMI.  There is slight ST elevation in lead III with reciprocal ST depression in aVL.  The T-wave is inverted in III, indicating reperfusion (what I like to call "inferior Wellens' syndrome).  There is no Q-wave, so this is unlikely to be old MI, and more likely to be acute NonSTEMI of the inferior wall.

I saw these ECGs, and since there was no immediate urgency, allowed the resident to manage it without any comment.  However, he did not see the abnormality on the prehospital ECG, so I finally said something like: "What are you going to do about the MI patient?".    When I pointed out the findings, we recorded another ECG:
Now there is increased ischemia, but where is it? My interpretation was that this is an inferior MI with posterior extension, as the ST depression in the precordial leads was maximal in V3 (opposite the posterior wall). There is about  1 mm of STE in aVR  I considered but rejected subendocardial ischemia.  

The ST elevation vector is posterior, inferior, and right, to the right of lead III and also posterior.  Is it subendocardial ischemia, or inferior MI?  See this post on the (Five primary patterns of ischemic ST depression, without ST elevation)

Because of the dynamic ACS, we activated the cath lab in the middle of the night.  Aspririn, Plavix (in spite of STE in aVR, because I thought this was inferior MI), Heparin were given.  The BP was elevated, so we gave metoprolol 5 mg IV x3 + 50 mg po.

His pain resolved and another ECG (but with precordial leads on the right) was recorded:
ST Depression is Resolved in V2 (=V1 R).  No evidence of RV MI.


Then the patient complained of increasing pain again:
There is now profound ST depression and STE in aVR, and the ST depression extends deeply in V5 and V6.  There is little ST elevation in inferior leads.

This time, the ST vector is more rightward, toward aVR and also posterior.

Now I regretted giving Plavix, as the probability of 3 vessel disease or left main insufficiency (not occlusion!) was much higher.  Thus, the chance of needing CABG was higher and Plavix can cause much operative bleeding.

Amazingly, the bedside echo showed very good LV function.

A nitro drip and sublingual nitro was given, the drip rapidly titrated to 80 mcg/min.  The BP came under better control and the patient was moved to the cath lab.

Outcome:

Was it RCA or LCX with inferior MI?  Or was it 3 vessel disease/left main insufficiency?

Both!

The active culprit was an RCA thrombus with 99% occlusion, but there was severe LAD and circumflex disease as well (severe 3 vessel disease).

The RCA was opened with POBA ("plain old balloon angioplasty") and eptifibatide was started.  The patient was referred for CABG and did well.


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