Massive ST Elevation After V Fib Arrest, Discordant Bedside Echo Results

A woman in her 40's was brought the ED (not by ambulance) for what is believed to be a seizure.  She was reportedly very anxious and there was a question of benzodiazepine withdrawal.  Events are uncertain (perhaps there was another seizure?), but soon thereafter, the patient was found limp and pulseless, and was found to be in ventricular fibrillation.  She underwent immediate resuscitation with chest compressions (LUCAS and ResQPod).  She was given a total of 3-4 shocks, vasopressin, bicarb x 2 and Epinephrine and, after 10 minutes on LUCAS she had ROSC and was noted to be moving on the cart.

An ECG was recorded:

Massive anterior, lateral, and inferior ST elevation, with bizarre morphology.  
What kind of STEMI is this?

The cath lab was activated.

An ED Bedside Echo was performed:

This subcostal view shows excellent LV function, at least at the apex.  However, there appears to be less than perfect contractility of the base, so this could be Reverse Takotsubo.  Also notice the profoundly hypertrophied LV walls.  This is massive concentric LVH, which in an ischemic condition can lead to very bizarre ECG abnormalities.


This is a different subcostal view,  and shows excellent ejection fraction and excellent wall motion at the cross sectional area imaged, but we do not have here a short axis video of the base, which on the above ECG appears possibly to not be contracting well.  Note again the profound concentric LVH (very thick LV walls).


In any case, these echocardiograms do not conform with coronary occlusion of any vascular territory.  An occluded wraparound LAD could result in similar ST elevation, but one would expect to see anterior, septal, apical, and inferior wall motion abnormalities, and we did not see this here.

After resuscitation, she was extremely hypertensive (230/150).  Because of severe anxiety, cardiac arrest, use of epinephrine, severe LVH, extreme BP, and the discordance between the ECG and the echocardiogram, I suspected that this syndrome was some variant of stress cardiomyopathy, and that the coronaries would probably be clean.

In daytime, with a readily available cath team, it would not be inappropriate to delay cath lab activation briefly in order to attemt to control the BP and then re-assess with a repeat the ECG.  But this was in the early morning hours with the cath team out of hospital and needing time to drive in.

She was beginning to move all extremities, so she received propofol and vecuronium.  In spite of propofol, she remained very hypertensive.  A nitroglycerine drip was started and titrated up to control BP.  

She underwent placement of an intravascular cooling catheter for targeted temperature management.

Before the BP was completely controlled, and just before transferring the the cath lab, this ECG was recorded 46 minutes after the first.:

All STE is resolved.

The angiogram showed no ACS and no significant coronary disease.


An ECG a few hours after the angiogram was recorded and nearly identical to her baseline ECG:

--Peak troponin I was 5.77 ng/mL
--Formal echo later that day showed poor global LV systolic function, more in line with standard stress cardiomyopathy, though not with typical apical ballooning
--The etiology of the arrest was unclear, but appears to be related to benzo withdrawal with seizures and high anxiety and resulting high catecholamines.
--The patient awoke and did well.

Lessons:

1. Especially when ST elevation is atypical for STEMI, use bedside echo to assess correlation of the ECG with myocardial function.  True STEMI should result in poor regional wall motion.  If it does not, suspect another etiology.
2. Correct severe physiologic dysfunction (in this case severe hypertension) before concluding that ST elevation or depression represents ACS