SSmith-DRAFT-40s-VFib (5-30.1-2023)-ME_TO_DO

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My Comment by KEN GRAUER, MD (5/30/2023):

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I was initially confused by the bizarre QRST — but a Learning Point is that in a large MI s/p cardiac arrest — this is NOT unusual !!!!

Once you figure out where the QRS ends (dark BLUE line) — you can transfer to other leads (light BLUE line) — and then the ST elevation is obvious (ST elev. also seen in lead aVL, as well as in other limb leads!

Interesting how there is so much fragmentation (but there IS a wide terminal S in leads I, V6 — consistent with RBBB !!!!)

The ST-T wave in lead V2 looks like a Wellens' T wave !!!!

Note artifact from Left Foot! 

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Figure-1: XXX

ADDENDUM by Ken Grauer, MD (5/27/2023):

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Figure-1: The initial ECG in today's case. (To improve visualization — I've digitized the original ECG using PMcardio).

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SSmith DRAFT as of 5/30/2023:

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A 40-something with no previous cardiac history presented to the ED in persistent Ventricular Fibrillation after attempted prehospital resuscitation.  He underwent further standard resuscitation EXCEPT that we applied the Inspiratory Threshold Device (ResQPod) AND applied Dual Sequential Defibrillation (this simply means we applied 2 sets of pads, had 2 defib machines, and defibrillated with both with only a fraction of one second separating each defibrillation.

Two recent interventions have proven in randomized trials to improve neurologic survival in cardiac arrest: 1) the combination of the ResQPod and the ResQPump (suction device for compression-decompression CPR -- Lancet 2011) and 2) Dual Sequential defibrillation. 

Finally, head-up CPR (which was not used here), makes for better resuscitation.  In fact, it is best when the head is gradually raised during resuscitation and this can be done using the Elegard.  Non-randomized trials show better outcomes (neurologic survival) using this device; see this article in Resuscitation: Head and Thorax Elevation during cardiopulmonary resuscitation using circulatory adjuncts is associated with improved survival.

The patient had ROSC and maintained it.

A 12-lead ECG was obtained:

What do you think?

My interpretation was: RBBB with hyperacute T-waves in V4-V6 that are all but diagnostic of LAD occlusion vs. post ROSC ischemia.

I sent this ECG to the Queen of Hearts (PMcardio OMI), and here is the verdict: 

(The Queen is not given any clinical data; she does not know if there is chest pain or not and does not know that there was a cardiac arrest; all verdicts are based on a pretest probability of chest pain):

We recorded another 8 minutes later to see if there was any resolution:

The T-waves are even more hyperacute.

So we activated the Cath Lab

Angiogram:

Impression and Recommendations:

Culprit for the patient's anterior ST segment myocardial infarction and out of hospital V-fib cardiac arrest is a thrombotic occlusion of the mid LAD

The first troponin returned barely elevated at 36 ng/L (URL = 35)

In our study of initial troponin in STEMI, 26.8% had an initial hs-cTnI less than 52 ng/L (a level with a high PPV for Type 1 MI -- OMI or NOMI)

Trops peaked at greater than 36,000 ng/L  (very large MI of course)

Post PCI ECG the next day:

Looks like a nearly completed anterior MI, in spite of rapid reperfusion.

Formal Echocardiogram:

Normal left ventricular size and wall thickness.

Moderately decreased left ventricular systolic function with an estimated EF of 36%.

Regional wall motion abnormality--apical anterior, mid anteroseptal, apical septal, and apical inferior akinesis.

The patient had a volatile clinical course but awoke neuro intact.

That volatile course included Atrial flutter with RVR: