Ventricular Fibrillation, ICD, LBBB, QRS of 210 ms, Positive Smith Modified Sgarbossa Criteria, and Pacemaker-Mediated Tachycardia

An elderly man collapsed. There was no bystander CPR.  Medics found him in ventricular fibrillation.  He was defibrillated, but they also noticed that he was being internally defibrillated and then found that he had an implantable ICD.

He was unidentified and there were no records available

After 7 shocks, he was successfully defibrillated and brought to the ED.

Bedside ED ultrasound showed exceedingly poor global LV function, and no B lines.

Here is the initial ED ECG.  

What do you think?

Rhythm:  Residents asked me why it is not VT.  If you use calipers (or equvalent), it is clear that the rhythm is irregularly irregular.  So it must be atrial fibrillation.  Then I always look to see if the initial deflection of the QRS has a lot of voltage change per change in time (seen in tachycardias that are initiated from above the ventricle because the propagate through fast conducting purkinje fiber.  In other words, is the initial deflection "steep" [fast depolarization (supraventricular)] or is it not very steep [slow (VT)]?

Answer: it is irregularly irregular and the initial part of the QRS is fast, so this is atrial fibrillation with Left Bundle Branch Block (LBBB).

QRS: very wide (213 ms)

ST-T: The ST-T has a lot of proportionally discordant ST Elevation.  In lead III, the ST/S ratio is 25% (ST measured at the J-point, relative to the PQ junction, is 4.5 mm; the S-wave is 18 mm.  This meets the Smith Modified Sgarbossa criteria for acute OMI in LBBB and Paced Rhythm.

So we should activate the cath lab, right?

I was there and said, "No, I think this is all due to severe chronic cardiomyopathy and cardiac arrest due to primary ventricular fibrillation, not due to ACS."

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Why did I say that?

1. Patient has an ICD, which is primarily placed in patients with cardiomyopathy.

2. The QRS is extremely wide.  (Other thought this was due to hyperkalemia, but the ECG does not have the appearance of hyperkalemia but does have the appearance of severe cardiomyopathy -- LBBB with very wide QRS)

3. The bedside echo showed dilated cardiomyopathy with relatively thin walls.

4. Tachycardia exaggerates ST Elevation in LBBB and Paced rhythm

5. Post cardiac arrest with low flow states can also distort ST and T-wave

See these 3 posts:

--Massive Excessively Discordant Anterior ST Elevation in a Paced Rhythm due to cardiomyopathy

--Wide Complex Tachycardia with Huge ST Elevation. ST segments distorted by tachycardia

--Patient with Paced Rhythm in Severe Cardiomyopathy Presents with SOB due to Acute Decompensated Heart Failure

My suspicion was that the Queen of Hearts would say this was OMI, and I am glad that she did because it is too nuanced to say Not:

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__________________________

Case continued

He was intubated.  There was hypotension, initially controlled with an epinephrine infusion.  We considered attempting electrical cardioversion to improve blood pressure, but I suspected that he is in chronic atrial fibrillation that would be resistant to cardioversion, either electrical or chemical.

Strangely, the monitor began to show a ventricular paced rhythm at tachycardic rates up to 130.  Why?   Pacemaker mediated tachycardia!  Atrial sensing lead senses, which leads to firing of the ventricle, which creates an impulse going back to atrium and around and around in an endless loop.

Pacemaker mediated tachycardia, also called "Endless Loop Tachycardia," cannot happen during atrial fibrillation, so the A fib must have converted.  The way to terminate PMT is with a magnet, which eliminates sensing so that the infinite loop is terminated.

At this point, the patient was hemodynamically stable.  Moreover, it was not until later that I recognized we were dealing with PMT, so we did not apply a magnet.

Calcium was given for possible hyperkalemia, but K returned at 3.4 mEq/L.

Another ECG was recorded 12 minutes later:

Paced rhythm, probable Pacemaker-Mediated Tachycardia?

Now there is increased ST Elevation and increased ST/T ratio.

This gave me pause, but I still thought this was a false positive due to severe cardiomyopathy.

At 51 minutes, another was recorded:

Still higher ST/S ratio

Ken Grauer notes possible P-waves preceding the 2nd complex, and in 2 of the last 3 complexes in the long lead rhythm strip.

First high sensitivity troponin I returned at 200 ng/L.

Then the patient's electronic record from an outside hospital appeared.

It stated that he had a non-ischemic cardiomyopathy, with EF of 15% and atrial fibrillation, and a normal angiogram 3 years prior.

I wrote the following note in the chart:

"V Fib arrest, has ICD.  Bedside US shows extremely poor EF with dilated cardiomyopathy.  In A fib with RVR, sometimes being paced.

"ECG with LBBB and QRS of > 210 ms.  The ECG meets Smith modified sgarbossa criteria but this often is the case with severe cardiomyopathy.  Presence of ICD and dilation on bedside US is c/w chronic severe cardiomyopathy, with large end diastolic diameter and thin walls.

"For this reason we did not believe this was an acute coronary event and did not activate the cath lab.

"Cardiology agreed.

"Subsequent ECGs showed even more ST elevation, but I still thought this was chronic.

"Old records still had not appeared.

"Around 1015 we were able to access Care everywhere and this showed that he has a non-ischemic cardiomyopathy with EF of 15%.  Angiogram in 2021 was normal.  Could not obtain a previous 12-lead ECG even by calling the U. They stated there were none in the record (hard to believe).  Initial trop ~200.  

"This confirmed my suspicions.

"The patient was admitted without angiogram."

Here is the troponin profile overnight:

This is consistent with cardiac arrest without acute coronary occlusion.

An ECG was recorded the next AM:

Pacemaker-mediated tachycardia is resolved

Ken Grauer noted that there appear to be P-waves preceding pacer spikes (I don't think this changes anything significantly).

Now with a lower heart rate and less proximity to cardiac arrest, the ST segments are proportional.

A few hours later, a formal echo was recorded:

The estimated left ventricular ejection fraction is 11 %.

The estimated pulmonary artery systolic pressure is 23 mmHg + RA pressure.

No wall motion abnormality

Decreased left ventricular systolic performance, severe

Left ventricular enlargement, marked

Dilated cardiomyopathy severe

Est. stroke volume 52 cc at HR 70 = 3.64 l/min cardiac output.

Est. Cardiac index: 1.39 l/min/m2

 

Decreased right ventricular systolic performance .

Asynchronous interventricular septal motion IVCD

Asynchronous interventricular septal motion left bundle branch block.

Device lead(s) visualized in right heart chambers.

Asynchronous interventricular septal motion right ventricular pacing. 

Follow Up:

Later history: a witness who was present with the patient when it all started stated that he became short of breath before collapsing.  

ICD Interrogation:  ICD interrogation the next day showed that the patient had developed an irregular supraventricular tachyarrhythmia (probably atrial fibrillation with RVR, which was the probable etiology of shortness of breath) that incited internal defibrillation into ventricular fibrillation (whereupon he collapsed). Patient received 11 shocks by ICD and was in V-fib when EMS arrived. 

Finally, the pacer is a biventricular pacer for "CRT = cardiac resynchronization therapy."  Most patients with heart failure with reduced ejection fraction and left bundle branch block with a QRS over 130 ms should get one.  Briefly, LBBB causes "dyssynchrony" between the ventricles.  In other words, the RV contracts before the LV and this results in diminished LV EF.  So a dual chamber pacer is placed with one lead through the coronary sinus to the LV.  Then, during placement, the electrophysiologist varies the interval between the stimuli of the 2 ventricles until EF is optimal.

The patient awoke and had a good outcome!