Over at EDECMO we talk about the huge benefits of ECPR demonstrated by the fact that there are neurologically intact survivors when ECMO is initiated at the point of cessation of standard ACLS. But what if standard ACLS had not stopped... What if you just kept going?

Mirroring Cliff Reid's amazing talk: When Should We Stop Resuscitation?, I present Sam Ghali's (@EM_ResUS) case.

From Sam Ghali:

I just experienced probably the most amazing case I’ve ever been a part of this past Monday.     This case has become the talk of the place, as it was very controversial within the world emergency medicine, critical care and cardiology here @ Janus General.  It was discussed in M&M and there is gonna be a joint multidisciplinary thing, etc.  But otherwise there is no one else’s opinion I would be more interested to hear than yours, so I wanna share it with you:

I was working shift in Major Treatment Area here at Janus General, and we hear we’re getting a med resusc… rolls in a guy looks to be in about his 60’s (turns out he was 59).  Story was :

Witnessed Arrest with bystander CPR… shockable for EMS, but shocked 6-7 times… meds given were for some reason only bicarb and Lidocaine (not sure why?)

I will share with you my documentation, only b/c it will save me tons of typing and I trust sending it to you..

This patient was seen in the resuscitation bay along side Dr. XXXXX concurrently.  This patient presents status-post witnessed cardiac arrest after return of spontaneous circulation.  His rhythm was always shockable per EMS.  He arrived with a King airway in place.  There was a large air leak noted.  CPR was in progress shortly after arrival as he was noted to not have pulses.  Chest compressions were resumed immediately and multiple rounds of CPR with multiple rounds of epinephrine, and medications including amiodarone, bicarbonate, calcium, magnesium were administered.  Please see nursing medications charting.

Multiple echocardiographic images were obtained by myself.  Please see computer for images.  The patient was noted to be in and out of ventricular fib.  CPR was continued in line with ACLS protocol.  The King Airway was removed and endotracheal intubation was performed by myself using a MAC 4 blade and an 8.0 endotracheal tube without difficulty.  There was good condensation on the tube, good chest rise, and end tidal CO2 was detected immediately with excellent wave-form.  Intra-code bedside echo was performed and revealed no evidence of right ventricular enlargement or strain on echo, or any other signs of massive pulmonary embolism.  There was also no pericardial effusion.  Echo did show akinesis/hypokinesis inferiorly and somewhat laterally as well.  The inferior wall was essentially akinetic.   Anterior wall motion was clearly preserved.  This was best seen on the parasternal long and short axes.

There was very high suspicion for acute coronary event.  Furthermore there was no evidence of hypoglycemia, hyperglycemia, hypokalemia, hyperkalemia.  The patient’s pH was noted to be significantly acidotic, and 2 additional ampules of sodium bicarbonate were administered at that time.  There was good sliding bilaterally on ultrasound.  There was no evidence of massive pulmonary embolism on echo, and there was no evidence of pneumothorax.  Intravenous fluids were pressure bagged in.  There was no significant hypothermia.   End tidal was difficult to interpret due to multiple ampules of sodium bicarbonate.  After nearly 45 minutes of aggressive CPR the decision was made to use thrombolytics because we felt strongly that this was an acute myocardial event, it was also strongly felt that without thrombolytics stabilization and termination of electrical storm could otherwise not be accomplished,