Persistent Ventricular Fibrillation, ED ECMO, ED TEE, ROSC, Shark Fin ECG (also called "Giant R-wave"), Postinfarction Regional Pericarditis. What a Case!

A 40-something suffered witnessed ventricular fibrillation, had bystander CPR, but could not be defibrillated after 4 attempts.

He was transferred to the ED and put on extracorporeal life support (ECLS, ECMO).

A series of ED Transesophageal echos (TEE) was done over 23 minutes before an ECG was recorded.  

We usually do not get ROSC before angiography in these cases, and recording the ECG is not as important as usual, because we send them all to the cath lab by our ECMO protocol.

This is before another defibrillation attempt, during chest compressions:

Orientation:
The probe is in the esophagus, right next to the left atrium.  so the chamber at the top of the image is the left atrium. Directly below that is the left ventricle.

Flow on ECMO was successfully initiated.

13 minutes later, the patient was successfully defibrillated. This was the immediate TEE:

Minimal organized activity, and you can see good blood flow in the chamber due to ECMO

Another 4 minutes later:

There is organized activity, but very slow and with poor contractility

Another 6 minutes later (TEE with short axis):

Contractility and heart rate are better

An ECG was recorded:

"Shark Fin"
Diagnostic of Coronary Occlusion.
I and aVL are involved, so this is a proximal LAD.

Here are 2 more examples of Shark Fin on this blog.

The patient was taken for immediate angiogram:

Do you see the occlusion?

Here I point it out with a red arrow:

It was opened and stented:

Excellent flow

An ECG was recorded after PCI:

This appears to be a junctional rhythm (narrow) with a PVC (wide, complex 7)
The resolution of ST Elevation is a very reliable sign of reperfusion.
The narrow beats have T-wave inversion in V1-V5 and aVL, also signs of reperfusion

This was recorded the next AM:

There are QS-waves with some persistent ST Elevation
It would not be surprising if the patient ended up with an LV aneurysm (persistent STE after previous MI)

Last troponin I measured was 107 ng/mL at about 12 hours after presentation.

In the literature, this morphology has been called:

 "Shark Fin".  See here for search. 

and also:

"Giant R-wave."


This was recorded 48 hours after ECMO started:

Less persistent STE, but QS-waves persist

Formal echocardiogram at about 24 hours after the event:

Amazingly, the ejection fraction was 55%!  (there was an apical wall motion abnormality)

At 72 hours, he developed some chest pressure.  He was also hypoxic with pulmonary edema.  This ECG was recorded:

There is re-elevation of ST segments, and new upright T-waves, suggesting re-occlusion, but also consistent with postinfarction regional pericarditis.

There was thus worry for in-stent thrombosis, and the patient was taken back for repeat angiogram, but it showed open arteries.

What could account for these ECG findings?  One possibility is postinfarction regional pericarditis, described below.

This was recorded at day 6:

There is some restoration of r-waves and some persistent STE.

The patient awoke without neurologic deficit.



Postinfarction Regional Pericarditis (not to be confused with Dressler's syndrome, which happens later)

Oliva et al. (1) strongly associated myocardial rupture with postinfarction regional pericarditis (PIRP), and associated PIRP with persistent upright T-waves.  

He found 2 patterns of atypical T-wave development in PIRP:

1) persistently positive (upright) T-waves 48 hours after AMI onset, diagnostic of PIRP; and
2) premature, gradual reversal of inverted T waves to positive (upright) deflections by 48 to 72 hours after MI onset in the presence of well formed QS-waves.

The wide Q-waves suggest "transmural" MI (completed MI with infarction of the entire thickness of the ventricle).  This was common in the days before reperfusion of STEMI, but still happens in patients who present late and therefore do not get timely reperfusion therapy, or who have very severe MI.  

When there is MI extending all the way to the epicardium (transmural), that infarcted epicardium is often inflamed (postinfarction regional pericarditis, or PIRP).  In addition, when there is full thickness infarction, especially with inflammation, the myocardium is at risk of "rupture." (2)  The term "rupture" makes it sound like some sort of explosion or massive blowout, but it is usually a small, slow leak that, over time, can cause tamponade and death.  Rupture can be either free wall rupture (causing tamponade) or septal rupture, causing ventricular septal defect with left to right flow and resulting pulmonary edema and shock.  

If detected early by ultrasound, the patient can be saved.  Our own Dave Plummer of HCMC reported on survival of 2 of 6 patients with free wall myocardial rupture diagnosed by bedside ultrasound in the ED.(3)

1. Oliva PB, Hammill SC, Edwards WD. Electrocardiographic diagnosis of postinfarction regional pericarditis: ancillary observations regarding the effect of reperfusion on the rapidity and amplitude of T wave inversion after acute myocardial infarction. Circulation 1993;88(3):896-904.

2. Oliva PB, Hammill SC, Edwards WD. Cardiac rupture, a clinically predictable complication of acute myocardial infarction: report of 70 cases with clinicopathologic correlations. J Am Coll Cardiol 1993;22(3):720-6

3. Plummer D, Dick C, Ruiz E, Clinton J, Brunette D. Emergency department two-dimensional echocardiography in the diagnosis of nontraumatic cardiac rupture. Ann Emerg Med 1994;23(6):1333-42.

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MY Comment, by KEN GRAUER, MD (11/22/2019):

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Excellent case by Dr. Smith that details superb management with resultant miraculous save of this 40-something man with cardiac arrest. The Echos and cath films speak for themselves.

• I limit my comments to several advanced ECG interpretation concepts that I found fascinating. None of these ECG findings altered clinical results in this case — but they are worthy of mention, since awareness of these intriguing ECG findings may indeed be helpful in other cases.
• For clarity and illustrative purposes — I’ve reproduced and labeled 3 of the 6 tracings shown in this case in Figure-1.

Figure-1: Three of the 6 ECGs that were done in this case (See text).

Comment on ECG #1 — As per Dr. Smith, the initial ECG in this case (ECG #1) — manifested a dramatic “Shark Fin” morphology that was diagnostic of acute proximal LAD occlusion.

• Shark Fin morphology has been discussed a number of times on Dr. Smith’s ECG Blog. As per Dr. Meyers (ECG post from Oct. 4, 2019) — “When the QRS is wide, the J-point will hide. So, your next move is to Trace it down, and Copy it over”.
• Following Dr. Meyers’ directive reveals how narrow the QRS complex actually is in ECG #1. I started by looking at leads V1,V2,V3 in this tracing — since I thought the R’ in lead V1, and the change in slope in the dramatic Shark Fin seen in leads V2 and V3, provided a good landmark for defining the end of the QRS complex (vertical DARK BLUE line in ECG #1). Tracing this DARK BLUE line down to the lead II rhythm strip complex suggested to me that the extra “hump” to the right of this BLUE line (RED arrow) was an Osborn wave!
• “Copying over” this point where the DARK BLUE line under the 2nd complex in leads V1,V2,V3 intersected at the end of the QRS in the other 3 sets of simultaneously-recorded leads — yielded the LIGHT BLUE vertical lines in ECG #1. To me, this suggested the presence of prominent Osborn waves in multiple leads! (RED arrows).

OSBORN Waves: The Osborn wave has been described as a deflection with a dome or hump that occurs at the point where the end of the QRS complex joins with the beginning of the ST segment. This is the J-Point (ie, it Joins the end of the QRS with the beginning of the ST segment) — so Osborn waves are exaggerated J-point waves. They’ve also been called the “camel-hump” sign.

• Osborn waves are most commonly associated with significant hypothermia (usually not seen until core temperature is below 90°F).
• PEARL #1 — It is important to appreciate that other conditions may also be associated with this prominent J-point deflection. Osborn waves have been reported with hypercalcemia, brain injury, subarachnoid hemorrhage, Brugada syndrome, cardiac arrest from VFib — and — severe, acute ischemia resulting in acute MI (as in this case! ). The development of Osborn waves in association with acute ischemia/infarction may be a marker of impending VFib.

Comment on ECG #2 — There are several advanced ECG concepts associated with ECG #2.

• The rhythm is not sinus! That’s because there is no upright P wave in lead II. In fact, there is no more than perhaps the tiniest negative “dip” of a P wave in lead II (GRAY arrow).
• Note that P waves are more noticeable in the other 2 inferior leads (GRAY arrows highlighting negative P wave deflections in leads III and aVF).
• Definite positive P waves are seen in leads I and aVL (BLUE arrows in these leads).
• All of the above noted P waves are conducting — because the PR interval remains constant. This is a normal PR interval (~0.16 second).
• PEARL #2 — The combination of P waves conducting with a normal PR interval — with a null or negative P wave deflection in the inferior leads — and positive P waves in leads I and aVL — suggests that rather than a junctional rhythm, there is a low atrial (or coronary sinus) rhythm in ECG #2.

Recognition of definite P waves in ECG #2 is important in helping to define what the wide beat ( = beat #7) in leads V1, V2 and V3 is.

• I’ve labeled with the letters a, b, c — the 3 P waves that we see in lead V1 of ECG #2 (BLUE arrows in this lead). Note that this low atrial rhythm remains regular throughout (P waves a, b, c are all right on time) — which tells us that the initial tiny positive deflection in front of the wide beat (beat #7) is the initial part of an on-time P wave!
• Beat #7 is clearly of ventricular etiology. But given that an on-time P wave precedes it with a shorter-than-expected PR interval — beat #7 is almost certainly a Fusion beat (ie, with delayed and partial conduction of the P wave labeled “b” — that “fuses” with the ventricular beat).
• I like to distinguish further the type of “PVC” that beat #7 is. Yes, it is “premature” — because it occurs slightly before where the next normally conducted sinus beat would be seen. But this is a “late-cycle” (ie, end-diastolic) PVC — which is important, because it carries the same clinical significance as the rhythm AIVR (Accelerated IdioVentricular Rhythm) does in a patient with acute MI — namely, that it is a marker for reperfusion! As per Dr. Smith — the resolution of ST elevation + T wave inversion in ECG #2 are other markers of reperfusion in this case. That said = PEARL #3 — Sometimes the onset of either AIVR and/or late-cycle PVCs may suggest there has been acute reperfusion before you see resolution of ST elevation and T wave inversion!
• Finally — Note that prominent Osborn waves are still present in many leads in ECG #2 (RED arrows).

Comment on ECG #4 — I believe ECG #4 supports my previous comments regarding how narrow the QRS complex actually was in ECG #1 — as well as that RED arrows in the prior tracings did in fact represent prominent Osborn waves.

• Using the vertical lighter and darker BLUE lines in ECGs #1 and 2 as the end point of the QRS complex — it appears that this very narrow QRS morphology remains consistent through all tracings! This supports that the “extra hump” (RED arrows) were indeed prominent Osborn waves — which finally resolve (light GREEN arrows) in ECG #4 as the patient improves.

Our THANKS again to Dr. Smith for this fascinating case with positive clinical result!