A 40-something presented after attempted prehospital resuscitation with persistent Ventricular Fibrillation

A 40-something with persistent Ventricular Fibrillation presented after attempted prehospital resuscitation

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:

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MY Comment, by KEN GRAUER, MD (7/14/2023):

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It's always rewarding to get "a Save!" — as in today's case, in which this 40-something year old patient with persistent VFib, followed by an extended complicated course — ultimately survived with intact neurologic status!

Acknowledgment:

I fully acknowledge my confused attempts at interpreting the initial ECG in today's case, that was obtained after ROSC. For this reason — I thought it worthwhile to review this initial ECG — that I've reproduced in Figure-1.

First — Some thoughts on the post-resuscitation ECG.

• As I emphasized in My Comment at the bottom of the page in the October 10, 2022 post in Dr. Smith's ECG Blog — Interpretation of a post-resuscitation ECG can be extremely challenging. This is because of how common it is to see ECG findings of diffuse subendocardial ischemia, or even false-positive ST elevation immediately after resuscitation (which is why many advise waiting a short period of time [ ~15 minutes] after ROSC — and then repeating the ECG to see if ischemic changes persist).
• For example — Baldi et al note a more than doubling in the number of false-positive ECGs for STEMI if judgments were based on post-resuscitation 12-lead tracings obtained less than 7 minutes after ROSC (Resuscitation 162:445-446, 2021).
• 
  
• Another KEY reason for the difficulty interpreting post-ROSC tracings — is the frequent lack of any history (ie, Many patients following successful resuscitation after cardiac arrest do not immediately regain consciousness — such that the presence of chest pain or other pre-arrest symptoms is all-too-often unknown).
• Finally — The ECG of patient's with cardiac arrest is often exceedingly abnormal, if not bizarre. Many of these patients have preexisting coronary and other forms of severe heart disease. The arrest itself (especially if the period of resuscitation is prolonged) — may produce profound alterations in QRS morphology, including unusual conduction defects, with difficult-to-predict repolarization changes. Little wonder that post-resuscitation tracings are so challenging to interpret.

What Confused Me about Today's Initial ECG:

Take Another LOOK in Figure-1 — at today's initial tracing.

• WHERE does the QRS complex end?
• Which deflections represent "fragmentation" of the QRS?
• Where is the J-Point in each lead? (from which we should assess for the presence of ST segment elevation or depression?).

Figure-1: The initial ECG in today's case — obtained after ROSC.

HOW to ANSWER the Above Questions:

For me — the KEY to interpreting the initial post-resuscitation tracing in today's case — is to follow the advice that Drs. Meyers & Smith routinely suggest for assessing ST segment deviations when there is Shark Fin morphology — "When the QRS is wide, the J-point will hide. So, your next step is to Trace it down, and Copy it over".

• For more on the application of this Trace-down; Copy-over technique with Shark Fin ST segment deviations — See My Comment in the May 19, 2020 post in Dr. Smith's ECG Blog.
• 
  
• With regard to Today's Tracing — Although QRS morphology in today's tracing is not "shark fin" per se — the principle for evaluation of ST segment deviations is the same (ie, "Trace-down; Copy-over"). I thought the one lead in ECG #1 that showed clear delineation between the end of the QRS complex and the beginning of the ST segment — was lead V1. I therefore "traced down" with a vertical RED line parallel to the precise point demarcating the end of the QRS complex in lead V1.
• Everything to the right of this vertical RED line marks the beginning of the ST segment. Tracing down this RED line to the simultaneously-recorded long lead II rhythm strip — marks for us the end-point of the fragmented QRS in the long lead II.
• Now that we've defined what the end-point of the QRS looks like in the long lead II rhythm strip — all that remains is for us to "copy over" this end-point to the other 3 sets of simultaneously-recorded leads — and then extend vertical lines upward (which I've done with BLUE lines) to define the end-point of the QRS in the other 9 leads.

Putting It All Together:

The QRS complex in ECG #1 shows marked fragmentation (ie, excessive "extra" notching of the QRS — seen to the left of the vertical RED and BLUE lines in Figure-2). In retrospect — it is this excessive fragmentation seen in no less than 10/12 leads that confused me in my initial attempt to assess ST-T wave deviation.

• As per Dr. Smith — there is RBBB in ECG #1 (qR complex, with predominant positivity in right-sided lead V1 — with terminal wide [albeit fragmented] S waves in lateral leads I and V6).
• I suspect there is also LAHB, given predominant negativity of the QRS in each of the inferior leads (albeit this assessment is made difficult by the excessive terminal fragmentation of the QRS in these leads).
• 
  
• ST elevation in the form of hyperacute ST-T waves is seen in leads I, aVL; and in leads V2-thru-V6 (as noted by the GREEN arrows highlighting the J-point in these leads).
• Reciprocal ST depression is seen in at least 2 of the inferior leads = leads III and aVF (this being real-but-subtle, due to small amplitude of the QRS complex in these leads).
• 
  
• BOTTOM Line: As per Dr. Smith — The finding of RBBB/LAHB + the distribution of hyperacute and elevated ST segments, beginning as early as in lead V2 — with reciprocal ST depression inferiorly — supported by persistence of these findings in the ECG repeated 8 minutes later — suggests acute proximal LAD occlusion until proven otherwise.

Figure-2: I've labeled the end point of the QRS in all 12 leads (See text).