Collapse, pulse present, ECG shows inferior OMI. Then there is loss of pulses with continued narrow complex on the monitor ("PEA arrest")

An elderly woman was witnessed to collapse.  911 was called and when EMS arrived, she was unresponsive with shallow respirations, a GCS of 3, pulse of 70 and BP of 78/67 by cuff pressure.

3 prehospital ECGs were recorded:

There is an obvious inferior OMI/STEMI, right?

The patient then had a PEA arrest while on the cardiac monitor, and CPR was started.

On arrival, all the usual things were done for cardiac arrest.

Transthoracic cardiac POCUS was of low quality, and so after intubation a TEE probe was inserted.

Aside: here is a recent report of our experience with over 550 TEE exams in the Hennpin ED: Feasibility, utility, and safety of fully incorporatingtransesophageal echocardiography into emergency medicinepractice

Here is the video:

You can see on the left the RV, which is very large, and on the right is the LV, which has a tiny chamber with excellent function.  This is all but diagnostic of severe acute RV failure.  

Sudden severe RV failure can be due to either: 

Inferior AND right ventricular infarction. 

But there will usually be some STE in V1 when V2 is isoelectric.

Or:

 Acute pulmonary embolism.

Assessment:

This patient is in extremis and is going to die unless something is done immediately, and probably even if the correct steps are taken.   

"PEA" arrest only means that the providers cannot feel a pulse, not that there is no cardiac activity.

As you can see from the ultrasound, there is cardiac activity, but extreme hypotension.  This is the situation in the vast majority of PEA arrest.  There is a pulse; you just cannot feel it.  But you can see activity on a high quality ultrasound.

ECG: 

Acute PE may present with ST Elevation mimicking type I OMI if coronary perfusion is extremely poor.

Acute OMI may present as PEA arrest on the monitor if there is additional severe RV infarct.  This would usually manifest as STE in V1 as long as there is no STD in V2 (and there is not).  Most OMI cardiac arrest are ventricular fibrillation; when they develop witnessed PEA arrest (on the monitor!), they usually manifest LV dysfunction, not RV dysfunction (unless, of course, they are huge RV MI also).

There is one other complicating factor: GCS of 3 when the patient still has a pulse and blood pressure.  This must bring the possibility of sudden intracranial hemorrhage into the differential.

However:

1. Patients who have cardiac arrest, or near arrest, due to intracranial hemorrhage do not survive. 

     a.  Intracranial hemorrhage that causes arrest is massive

     b. The combination of high intracranial pressure from the bleed and the low blood pressure from the arrest results in a cerebral perfusion pressure of zero, and brain death.

So the differential is: 

1. OMI with RV MI

2. Pulmonary embolism with type 2 OMI (severe supply demand mismatch); this is strongly supported by PEA and the cardiac ultrasound.

3. Intracranial hemorrhage.

The first 2 can be treated with thrombolytics.  

The latter will die with or without thrombolytics.  

So the benefit/risk ratio is to give thrombolytics.  The faster the better.

Outcome:

100 mg of tPA was given in a bolus but the patient did not survive.