Friday, January 24, 2020

Ventricular Fibrillation, ROSC after perfusion restored by ECMO, then ECG. Protocols can be overridden by Physician Judgment.

A middle-aged male had sudden chest pain and called 911.  First responders arrived.  Then the patient arrested.  Chest compressions were started immediately.  Paramedics arrived a few seconds later and found the patient in ventricular fibrillation.  He could not be defibrillated after 3 attempts.  He was intubated, given epinephrine and amiodarone, and transported.

He arrived in the ED 35 minutes after arrest.  He remained pulseless and in V Fib.

Defibrillation was not successful.

Cannulation for ECMO (Extracorporeal life support -- ECLS) was begun.

He was debribrillated again and had brief (15 second) ROSC with a pulse and some function on TEE.  But it degenerated into ventricular fibrillation again.

Shortly thereafter, his lactate returned unmeasurably high at greater than 17.5.  This is an exclusion criterion for our ECMO protocol, as it is associated with prolonged and profound hypoperfusion, and thus with futility.

Cannulation was paused and we briefly discussed the situation:

Because we had achieved 15 seconds of ROSC with a pulse, we determined that exclusion criteria for the refractory ventricular fibrillation protocol should not apply to this patient. 

Cannulation was continued.

He was successfully cannulated for ECMO  and at 50 minutes after arrest was on the pump and perfusing with a good blood pressure.

While on pump, he was defibrillated again, successfully (sustained ROSC).

His ED TEE (transesophageal echo) is here:

Only the base of the heart appears to be contracting

He had a 12-lead ECG recorded before going for angiography:
What do you think?

There is sinus rhythm with RBBB and LAFB.  There is ST elevation in V1-V4, I and aVL, with reciprocal ST depression in II, III, aVF.

This is consistent with a left main or proximal LAD occlusion.

Left anterior fascicular block (LAFB) is also called left anterior hemiblock (LAH)

This combination of RBBB/LAFB and STE is almost always associated with proximal LAD or left main occlusion and with cardiac arrest or shock.  Click on this for 6 other cases.

See this paper by Widimsky et al, which shows the high association of RBBB, especially with LAFB, with LAD occlusion.  Furthermore, among 35 patients with acute left main coronary artery occlusion, 9 presented with RBBB (mostly with LAFB) on the admission ECG.

Case continued

He was taken to the cath lab and a proximal LAD occlusion was found and opened.

Here is the post cath ECG:

A balloon pump was placed, he was cooled, and perfusion maintained by ECMO circuit.

Echo after PCI:

Severe LV dysfunction, EF 20%, regional wall motion abnormalities involving the anterior circulation.

Here is the next day ECG:

Later, another echo showed EF of 10-15%.

But then his heart recovered with an EF of 58%!

The balloon pump was removed.

He later awoke, neurologically intact.

Learning Point:

Inclusion and Exclusion criteria for protocols are guidelines only.  All patients do not fit into the definitions and therefore physician discretion is necessary.  In this case, thanks to flexibility with the protocol, the patient survived.

As for the ECG: again, the combination of RBBB and LAFB with ST elevation is associated with either or both of cardiac arrest or cardiogenic shock and either proximal LAD or left main occlusion.

This is an ECG pattern you should know!!

MY Comment by KEN GRAUER, MD (1/24/2020):
FIRST and Foremost — This case details a truly amazing SAVE. It is Emergency Medicine at its finest!
  • From an ECG interpretation perspective — I found the 3 serial tracings shown in this case to be highly instructive (Figure-1).
  • MGOAL: To draw your attention to an additional important ECG finding that should be appreciated from review of these serial tracings.

Figure-1: The 3 serial tracings done in this case (See text).

Clinical Points Regarding ECG #1:
As per Dr. Smith — ECG #1 shows sinus rhythm with bifascicular block (RBBB/LAHB). There is marked anterior ST elevation with equally marked inferior ST segment depression. I’d add the following points:
  • The long lead rhythm strip shows a PAC (ie, beat #9 occurs early, with a different-looking P wave and a shorter PR interval) + a PVC in the following beat (ie, beat #10 which is wide, of different morphology, and not preceded by any P wave).
  • There is a Shark Fin” morphology to the ST segment elevation! This ECG pattern has been previously discussed on several prior Dr. Smith ECG Blog posts (Please See My Comment on the 11/22/2019 post).
  • Because the last portion of the QRS complex blends in almost imperceptibly with the beginning of the ST segment — assessment of both QRS width and the amount of ST segment deviation becomes challenging with “Shark Fin” morphology. To recite Dr. Meyers’ eloquent quote — “When the QRS is wide, the J-point will hide. So, your next move is to Trace it down, and Copy it over”. I have done this in ECG #1 — in which the vertical BLUE lines indicate the J-point in each of the 12-leads. This reveals no less than 10 mm of ST elevation in lead V2, and ~5 mm of reciprocal ST depression in each of the inferior leads.
  • Note there is also considerable ST elevation in lead aVL. I always hone in on lead aVL — as the combination of marked anterior ST elevation + marked inferior lead reciprocal ST depression + significant ST elevation in lead aVL — is a reliable indicator of proximal LAD (if not LMain) occlusion.
  • Small, but fairly wide Q waves have already formed in leads V1, V2 and V3.
  • R wave amplitude looks small in virtually all of the lateral leads (which I initially attributed to loss of anterolateral forces from the large ongoing STEMI ).

What Has Happened After Cardiac Cath? (ie, in ECG #2):
  • HINT: Did YOU look at the RED arrow in ECG #2?

ANSWER: The post-cath ECG ( = ECG #2) shows sinus rhythm at a somewhat slower rate than was seen in ECG #1.
  • The RBBB persists in association with relatively large Q waves in leads V1, V2.
  • LAHB has resolved.
  • Although there remains some residual ST elevation in leads V1 and V2 — the amount of ST segment deviation (elevation and depression) has dramatically decreased since the “Shark Fin” pattern that we saw in ECG #1.
  • The RED arrow in ECG #2 points to the standardization mark — which remains at 10 mm (0.1 mV/mm). But despite NO change in the standardization mark setting — QRS amplitude is dramatically reduced in virtually all 12 leads!

What DYou See in ECG #3?
  • HINT: Did YOU look at the RED arrow in ECG #3?

ANSWER: The “good news” in ECG #3, is that the RBBB has now resolved. ST segment deviation is now no more than barely present.
  • That said, despite no change in the standardization mark setting — QRS amplitude has further decreased !!!

COMMENT: As I emphasized at the outset — this case constitutes a truly amazing SAVE! I’d add the following to the Learning Points in this case:
  • True Low Voltage is not a common ECG finding. I’ve adapted from the section in Life-In-The-Fast-Lane on this subject, adding from my personal experience — in which I list Causes tConsider when you see true Low Voltage on an ECG (Figure-2).
  • Going through this list — we arrive at that last cause that I’ve listed = a large acute MI. Considering ongoing clinical events in this case — everything points to myocardial stunning” as the cause of progressive reduction in QRS amplitude over the 3 serial ECGs that appear in Figure-1. Follow-up Echo the day following resuscitation revealed an estimated EF ~10-15% (presumably corresponding to about the time ECG #3 was obtained). But then — there was spontaneous recovery of contractility, with an EF that rapidly recovers to a normal value = 58%!
  • MyocardialStunning — has been described as a transient marked reduction in cardiac contractility, that occurs in response to a major acute insult. This phenomenon has been associated with cardiac arrest; after cardiac surgery; post-cardioversion following a sustained tachyarrhythmia; with certain types of acute cerebrovascular events (such as subarachnoid hemorrhage) — and, in association with large acute MI, which is clearly the clinical scenario in this case! 
  • P.S. I would have LOVED to see one more follow-up ECG (done ~12-36 hours after recovery of normal contractility) — to see if QRS amplitude substantially increased!

Our THANKS to Dr. Smith for presenting this case!
Figure-2: Causes of Low Voltage on ECG (See text).


  1. love the tee gif

  2. Such a good, thorough list of the causes of low QRS voltage by Dr. Ken Grauer!!! You can see why this "Dr. Smith's ECG blog" is so popular and clinically useful, helping clinicians to provide quality patient care!!!
    K. Wang.

    1. THANK YOU so much K for the kind words! — :)

    2. In my opinion this blog is the best the world,i love it.It's very useful for me.I learned and learn and will learn much here,i hope kkk.I only can tell: THANKS A LOT!!!
      Greetings from Brazil.

    3. @ Unknown (from Brazil) — Muito obrigado pelo seu comentário! Estamos felizes que este ECG blog seja tão útil para você! (Thanks so much for your comment. We're happy that this ECG blog is so useful for you) — :)

  3. This has been a great blog, but has grown more valuable since Dr Grauer´s section was incorporated.
    A must read. THANKS FROM Venezuela
    Hecmunozob, MD

    1. Muchisimas gracias Hector! (Thanks so much Hector) — :)


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