Refractory V FIb Arrest, put on ECMO, regains an organized rhythm, and a 12-lead is recorded.

I received this case from:

Dominic Larose MD CCFP(EM) FACEP

Alain Vadeboncoeur MD CSPQ

Montreal Heart Institute

Hi Steve,

Here is a case I had a while ago. The patient was seen on the street, with sudden LOC. An off duty fireman was a bystander, so the cardiac arrest was recognised and immediate CPR was begun at 11:58. First responders arrived afterwards, and the patient was shocked twice with an AED.  ALS crew arrived 6 minutes later, and ACLS protocol was performed. The patient was in recurrent VF with wide complex PEA in between. Epinephrine and amiodarone were given. Seven shocks were given. The patient was transported from the scene 32 minutes post arrest.

The patient arrived in the ED 44 minutes post arrest in VF, was shocked and PEA followed. EtCO2 was 25 mmHg with ongoing manual CPR, and with a Combitube that was in place, with good air entry bilaterally. VBG at arrival: pH 6,95, K 4,4 mmol/L, lactate 8,2 mmol/L. First high sensitivity troponin T (hs) was 11 ng/L, the second one two hours later 723 ng/L.

[Smith translation: although all assays are different and will have slightly different results, but one can estimate that, in terms of the contemporary assays used in the U.S., this is approximately equivalent to 0.011 ng/mL and 0.723 ng/mL -- by convention, contemporary trops are stated in ng/mL and high sensitivity (hs) in ng/L. Troponin T values are far lower than cTnI, so this is (very) roughly equivalent to a hs cTnI of 10,000 ng/L (contemporary cTnI of 10.0 ng/mL. Strict troponin officionados would faint at such an attempt at equivalence, but there is literature to support this and I find it very useful, especially in EKG research.]

I decided to activate the ECMO team at 45 minutes post arrest, three minutes after arrival in the ED, for this middle aged man seemingly in previous good medical condition.

The cardiologist, perfusionist, intensivist and cardiac surgeon were on site and the cannulation procedure started 60 minutes post arrest. The procedure was somewhat difficult but 3 L/min flow was obtained 90 minutes post cardiac arrest.

Cannulation during CPR.

But here is where it gets really interesting: the patient regained a rhythm.   Here is the 12-lead ECG, recorded 5 minutes after the start of extracorporeal circulation.

The cardiologist thinks this a non-specific wide complex ECG, and tells me he will get the patient to a hospital bed after going to the head CT. I disagreed! Being a regular reader of this blog, in fact I thought the ECG show a RBBB with “shark fin” STE. There is also RAD with positive QRS in lead 1, and negative QRS in lead 2.

Smith Comment: Here is an analysis of the ECG:

There is probably atrial fibrillation (no P-waves, irregular).
It is too irregular to be ventricular tachycardia.
There is a tall R-wave in V1 indicating right bundle branch block.  There is a tall R-wave in aVL, and negative waves in II, III, aVF.  This indicates Left anterior fascicular block.
The lines indicate my determination of the end of the QRS, and thus beginning of ST segment.
As you can see, there is ST Elevation in V1, V2, (V3 missing), V4, V5, and in aVL with reciprocal ST depression in II, III, aVF.
This is diagnostic of STEMI.
It is common for this to be missed, even in such a dire situation!
I have seen many cases in which the cardiologist did not see the STEMI
This is always due to left main or proximal LAD occlusion.

Here are many posts on this topic.

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.

Dominic Larose continues:

So it is a RBBB + LAFB with STEMI. This is either a total or subtotal LM occlusion or a proximal LAD occlusion, as discussed before on the blog.

So the cardiologist agreed to take the patient to the cath lab. Here are the findings:

It was read as a 80% LM disease with a lot of vasospam, with 100% proximal occlusion of Cx artery and 80% stenosis of proximal LAD. Large doses of intracoronary nitroglycerin is given, with thrombus aspiration then a lesion is stented.

Here is the situation later:

RCA with the large venous ECMO cannula seen:

At 18h00 on the same day, the patient had cardiac standstill on echo, a transvenous pacemaker was attempted, but did not result in any contractility, so the ECMO circuit was turned off and the patient pronounced dead.

I have reviewed 14 cases of E-CPR for ED patients at our site, done in the last two years and we have had 6 survivors/14 (43%) discharged in good neurological condition. Not bad I think!

Learning Point:

1. Watch out for RBBB + LAFB STEMI, and recognise the “shark fin” pattern as STEMI!

2. Start an ECMO program (Extracorporeal Life Support).  It can save patients who have refractory ventricular fibrillation due to coronary occlusion or even pulmonary embolism.

This case illustrates similar ECG findings is great detail:

Wide Complex Tachycardia; It's really sinus, RBBB + LAFB, and massive ST elevation