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ROSC from in-the-field aystole


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Hypothetical patient in a hypothetical ed in a hypothetical timeframe.  

 

Elderly pt found down at home.  EMS finds asystole and starts CPR.  3 rounds of epi before they get to ED.  Only HX att is renal failure.  Later find out advanced CA with "mets everywhere".

 

Intubated with capnography of 28. 

 

While transfering to cot the monitor confirms asystole.  2 more rounds of epi with continuous CPR, a dose of CaCL for presumed hyperK, and suddenly capnography jumps to 45.  Stop CPR for rhythm check and low and behold there is SR....with terrific perfusing pulse!  BP is 135/75.  The heart is back with a vengeance!!

 

Wha whaa  whaaa  whaaaattt????? That's not supposed to happen!!!

 

norepi drip, 2 amps D50, 10 units insulin, hang D5.  EKG shows SR with wide QRS without obvious block and various T wave depression so another dose of CaCL.  But then initial labs show a K of only 5ish

 

No neuro response at all, so Ice bags, adjust vent settings, and transfer....

 

What in the world could have been so bad that it caused asystole, but has now been fixed.  

 

Possibilities that come to my mind:

 

1:  Maybe wasn't ever really asystole.  But looked like asystole when transferred to cot, and capnography was only 28.  

 

2:  With the advanced CA, maybe it was tamponade.  But I'm not sure that pressors and fluids would resuscitate a heart that stopped pumping from tamponade. Retrospectoscopically perhaps the heart should've been sono'd, although if tamponade were found that would've meant needling the heart (yikes!)

 

3:  Maybe it was a PE that, with the CPR, got pushed out of main artery and into smaller one?  Is that even possible?  

Any other ideas on what may have been reversed??

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Only thought myself was PE, although I'm kinda reaching in that its only a gut feeling, not much to support it. If there was TPA somewhere in this equation it would probably make better sense...but you probably wouldnt have a thread going about it either.

 

Also, not to derail but tough thread over there on SDN. I haven't taken a look in over a week (I don't care for internet beef) but I was less than thrilled than the responses you two were getting. Glad you two are leading the charge.

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CA hx increases risk for PE due to coagulopathy. Tamponade -> why? Volume overload from renal failure and accumulation in sac in combination with CA? Here's the $1M question. Hypothetically, with what you described in the tx process what happened to reverse either scenario? Was asystole confirmed in a second lead? Was K+ value before insulin admin.? Hypovolemia corrected with volume? Hypothetically, this pt would've never left the residence with many current EMS protocols and would've been pronounced on scene.

 

 

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The question marks of why some have ROSC vs others is still perplexing on most patients I have worked. 

 

You have a patient that is 90 years old, multiple co-morb, a med list longer than my kids christmas list, with unknown down time and asystole and somehow cpr+epi gets them back (probably brain dead, but I send them to ICU).

 

You have a 28 year old male who collapses while at park and codes right as EMS pulls into bay, you work him for 60 min, mostly v-fib/PEA and never get ROSC. 

 

WHY does epi and electricity work for some and not others? I will never know but without a KNOWN reversible cause-- H's/T's, it's a crap shoot. 

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Thank you all for your thoughtful responses.

 

I had a guy like that with a probable big PE. similar prior hx. as we get pulses back wife comes into dept, tells us he is DNR(medics didn't know) and asks us to stop. we do. back to asystole.

 

I've gotten ROSC and then lost them again several times...and it is usually probably a "good thing".  It's often helpful for the family, who may (or may not) be the ones pushing for you to "do everything" to actually see what "everything" means.  I've had several families abruptly change their mind after watching us code their loved ones.  And then, of course, there are the family members who come in right after getting ROSC who says "My wife wouldn't have wanted all of this"......DOH!

 

This theoretical patient's pulses didn't stop.  Like normal, the pressure dropped 20-30 minutes after ROSC but a pressor drip brought back up and titrated to a MAP of 75. 

 

Only thought myself was PE, although I'm kinda reaching in that its only a gut feeling, not much to support it. If there was TPA somewhere in this equation it would probably make better sense...but you probably wouldnt have a thread going about it either.

 

Also, not to derail but tough thread over there on SDN. I haven't taken a look in over a week (I don't care for internet beef) but I was less than thrilled than the responses you two were getting. Glad you two are leading the charge.

As in the OP, with the advanced CA dx, a PE was at top of my differential, but I can't figure out why a PE would knock the heart out, and then it start pumping away so joyfully without TPA.  Without TPA, what happened to the embolism?  And this theoretical patient had no signs of right heart strain on post ROSC EKG.  

 

About SDN:  I've got thick skin.  That's why I like the ED.  Seventy degrees and flourescent lighting is a much better environment than I operated in for many years.  Likewise, dealing with some super-smart kid still in medical school with a superiority complex doesn't compare to launching on missions where you know you might not make it back.  <Meh>

 

CA hx increases risk for PE due to coagulopathy. Tamponade -> why? Volume overload from renal failure and accumulation in sac in combination with CA? Here's the $1M question. Hypothetically, with what you described in the tx process what happened to reverse either scenario? Was asystole confirmed in a second lead? Was K+ value before insulin admin.? Hypovolemia corrected with volume? Hypothetically, this pt would've never left the residence with many current EMS protocols and would've been pronounced on scene. Sent from my iPad using Tapatalk

I was thinking possible pericardial effusion from the CA.  Might have built up over a week or so and just squeezed everything off.  But it's not like the tamponade suddenly reversed itself, unless CPR managed to rupture the pericardial sac.  Is that even possible? 

And for this hypothetical patient, no EKG done before ROSC.  K+ value was indeed BEFORE insulin (and even the first CaCL).  

 

our guy was vfib to pea to asystole to pea to ROCS to asystole...

 

Seen this before as well, but never seen a lengthy asystole develop ROSC, and I don't think I've ever seen an in-the-field asystole develop ROSC.  Putting these two together is what has me stumped.  

FFighter - Best prognostic indicator is "good protoplasm" versus "poor protoplasm".  This theoretical patient would be in the "extremely poor protoplasm" subsection of our patient population.  

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I usually let folks be a bit hypotensive after ROSC and don't flog them right away with pressors. they were dead 30 min ago. if they want to run a pressure of 90 for a while I give them a fluid bolus but generally am not super aggressive with fluids unless bp below 80 (unless septic of course).

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Good research out of Australia, and from Peter DeBlieux from LSU, shows much improved neuro outcomes if you try to keep MAP above 75.  Some data showing improved data with Map as high as 100 (supratherapeutic blood pressure).  For each instance of hypotension you get a much greater chance of poor neuro outcomes.  

 

 

ok, good to know. wonder if the renal outcomes are better or worse if given pressors... I'm still doing the therapeutic post arrest hypothermia.

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I dunno....I'm not the PhD type that gets into the weeds with research.  I'll let smarter folks than me do that stuff.  I mostly just listen to Mel Herbert on EMRAP, Scott Weingard on EMCRIT, or when I can stay awake the Canadian guy....along with re-reading textbooks to refresh my memory on basics.  :-)

Funny thing you mention the hypothermia.  During this hypothetical code on this hypothetical patient in this hypothetical ED during this hypothetical timeframe, a hypothetical FP physician walked into ED (let's say was attending in hospital for the day) and was resistant to the hypothermia because they didn't think it was cardiac.  Any idea where that idea would come from??

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I thought it was for all post arrest pts. I had an older family member at the mass general (and they should know being a snooty academic hospital) post arrest a few years ago after a non-cardiac related arrest and she got therapeutic hypothermia. her issue was resp. in nature. I'm also a big Mel herbert fan. also do emrap.

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I thought it was for all post arrest pts. I had an older family member at the mass general (and they should know being a snooty academic hospital) post arrest a few years ago after a non-cardiac related arrest and she got therapeutic hypothermia. her issue was resp. in nature. I'm also a big Mel herbert fan. also do emrap.

 

Agreed- doesn't matter what the nature of the arrest was, the hypothermia is more for neuro protection....

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Don't have the paper on it, but my understanding (and the current practice at my shop) was that positive outcomes were only found to come from cooling arrests with a presumed cardiac etiology. Presenting with asystole wouldn't necessarily rule it out if I remember correctly, just doesn't support cooling (as that story doesn't sound very MI-y).

 

ETA: We cooled all arrests for the longest time, however this new practice is only a couple of years old.

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About SDN:  I've got thick skin.  That's why I like the ED.  Seventy degrees and flourescent lighting is a much better environment than I operated in for many years.  Likewise, dealing with some super-smart kid still in medical school with a superiority complex doesn't compare to launching on missions where you know you might not make it back.  <Meh>

 

Understood, still a drag to see that nonsense, unsolicited.

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I'm surprised that no one has commented on an asystole being transported to begin with.  This is not a personal statement but more a change in policies noted over the years.  Last time I attended the Dallas EMS conference (Gathering of Eagles) several years back, most municipalities weren't transporting from scene with unresponsive systole.  I'd actually like to see a show of hands as to whose local EMS transports/calls (pronounces) on scene refractive asystole, and which municipality (preferably the large metro areas) if you know this to be a true protocol.

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I'm surprised that no one has commented on an asystole being transported to begin with.  This is not a personal statement but more a change in policies noted over the years.  Last time I attended the Dallas EMS conference (Gathering of Eagles) several years back, most municipalities weren't transporting from scene with unresponsive systole.  I'd actually like to see a show of hands as to whose local EMS transports/calls (pronounces) on scene refractive asystole, and which municipality (preferably the large metro areas) if you know this to be a true protocol.

 

Where I am (SE Virginia)..... in an unwitnessed arrest with asystole confirmed in 2 leads - we work the patient for 2 rounds of ACLS then call OMD and usually pronounce on scene.  There is a "Termination Protocol" we follow. 

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I didn't realize the hypothermia studies were done on just cardiac-related arrests (but then again....isn't every "arrest" a "cardiac-related arrest"?).  I would assume the neuroprotective benefit would be generalizable, but I guess we just don't know.

 

In 2012 EMRAP did a "Cardiology Corner - Post Cardiac Arrest Syndrome" with Amal Mattu and Mel Herbert where they talked about best strategies.  It included some strategies to stay ahead of the curve on the inevitable hypotension, therapeutic hypothermia, ventilator strategies, etc.  

Yes, there is certainly ethical/legal issues about resuscitating people with such poor protoplasm.  However, you never know when we will give someone one more day to say goodbye to their families.  Plus, there is the "practice" aspect of it, especially in rural settings.  When I do get patients such as this I often use the code as an exercise for my team.  

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I didn't realize the hypothermia studies were done on just cardiac-related arrests (but then again....isn't every "arrest" a "cardiac-related arrest"?).  I would assume the neuroprotective benefit would be generalizable, but I guess we just don't know.

 

I haven't actually seen the study/ies, just regurgitating what I hear being told to residents. I do some podcast listening, but I don't have time to wade through that much literature.

 

Our local EMS also has a "stay-and-play" protocol, although I'm not sure its specific to asystole alone. I do know that their medical director (in our health system) wants shorter scene times for the "witnessed clutching chest fall over" cardiac arrests, so much so that they come in without an airway or with a king etc, fairly often. Anecdotally, I do see some benefit to this as opposed to the old style down for 30 min+ cases we used to get. This may be just receiving cases with better potential for good outcomes, however, as I no longer am in EMS and only see whats brought to me.

 

OTOH, a couple of months ago we had a 40s male (slightly overweight) with no health problems suffer a torsades arrest in the turnaround (after a CP call to EMS during crossfit and a 5 min transport)  and we couldnt get jacks- back despite him getting an absolutely pristine resuscitation attempt. It was a BS case man. You win some you lose some.

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I am a student, so maybe this is a bit out of left field, but what about long-QT leading to V-Fib arrest----> Aystole (found down at home so maybe V-FIb/Tach Arrest first)? I know adriamycin, rituximab (though probably not used in his case), and others are cardiotoxici? Plus maybe family hx of long-qt? Or any other number of potential drug interactions (probably on a fair amount given his history: pain meds, anticholinergics, anti-depressants) that would have contributed to this. This would then explain why he was able to regain ROSC? I don't know just a thought, but considering the metastatic disease, drugs might have contributed to cardiovascular collapse?

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I haven't actually seen the study/ies, just regurgitating what I hear being told to residents. I do some podcast listening, but I don't have time to wade through that much literature.

 

Our local EMS also has a "stay-and-play" protocol, although I'm not sure its specific to asystole alone. I do know that their medical director (in our health system) wants shorter scene times for the "witnessed clutching chest fall over" cardiac arrests, so much so that they come in without an airway or with a king etc, fairly often. Anecdotally, I do see some benefit to this as opposed to the old style down for 30 min+ cases we used to get. This may be just receiving cases with better potential for good outcomes, however, as I no longer am in EMS and only see whats brought to me.

 

OTOH, a couple of months ago we had a 40s male (slightly overweight) with no health problems suffer a torsades arrest in the turnaround (after a CP call to EMS during crossfit and a 5 min transport)  and we couldnt get jacks- back despite him getting an absolutely pristine resuscitation attempt. It was a BS case man. You win some you lose some.

I am very hesitant to criticize EMS.  I am sitting 70 and flourescent, they are the ones at the houses, in the cars, or in the rain/sleet/snow, or the 110 degree heat.  This gives us very different perspectives.

 

40 yo...you throw the kitchen sink at those guys, and it's tough to accept the loss cause they aren't supposed to die yet.  Elderly with poor protoplasm is a different story.

 

I am a student, so maybe this is a bit out of left field, but what about long-QT leading to V-Fib arrest----> Aystole (found down at home so maybe V-FIb/Tach Arrest first)? I know adriamycin, rituximab (though probably not used in his case), and others are cardiotoxici? Plus maybe family hx of long-qt? Or any other number of potential drug interactions (probably on a fair amount given his history: pain meds, anticholinergics, anti-depressants) that would have contributed to this. This would then explain why he was able to regain ROSC? I don't know just a thought, but considering the metastatic disease, drugs might have contributed to cardiovascular collapse?

I had not thought of that.  I don't know if that would explain the sudden ROSC.  Maybe someone smarter than me does??

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I'm surprised that no one has commented on an asystole being transported to begin with.  This is not a personal statement but more a change in policies noted over the years.  Last time I attended the Dallas EMS conference (Gathering of Eagles) several years back, most municipalities weren't transporting from scene with unresponsive systole.  I'd actually like to see a show of hands as to whose local EMS transports/calls (pronounces) on scene refractive asystole, and which municipality (preferably the large metro areas) if you know this to be a true protocol.

our medics work asystole for maybe 5 min then call it in the field. (unless a lid or something out of the ordinary, hypothermia, etc).

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I am very hesitant to criticize EMS.  I am sitting 70 and flourescent, they are the ones at the houses, in the cars, or in the rain/sleet/snow, or the 110 degree heat.  This gives us very different perspectives.

 

40 yo...you throw the kitchen sink at those guys, and it's tough to accept the loss cause they aren't supposed to die yet.  Elderly with poor protoplasm is a different story.

 

I had not thought of that.  I don't know if that would explain the sudden ROSC.  Maybe someone smarter than me does??

 

No criticism here. I used to be out there, and indeed its a different world than my nice trauma bay. Just pointing out that in my time (limited, compared to many of you in this thread) there has been a pretty big shift in prehospital cardiac arrest care. Nothing you guys don't already know. Soon an arrest will come in with a NRB over airway, thumper going crazy, shocking without pausing compressions other than rhythm check, awaiting ECMO cannulation from the sterile doc waiting at bedside....there won't be much job left for us techs other than gofer-ing.

 

And regarding my earlier case, I second your thoughts as well. Nicer the person or more tragic the circumstances = poor prognosis indicators. Is what it is.

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I am a student, so maybe this is a bit out of left field, but what about long-QT leading to V-Fib arrest----> Aystole (found down at home so maybe V-FIb/Tach Arrest first)? I know adriamycin, rituximab (though probably not used in his case), and others are cardiotoxici? Plus maybe family hx of long-qt? Or any other number of potential drug interactions (probably on a fair amount given his history: pain meds, anticholinergics, anti-depressants) that would have contributed to this. This would then explain why he was able to regain ROSC? I don't know just a thought, but considering the metastatic disease, drugs might have contributed to cardiovascular collapse?

The question remains what did one do that would reverse these scenarios? Hyperkalmia, hypoglycemia, hypoxia were covered. Volume bolus? No mention of same. A lot of these treatments are based on PEA, but that wasn't the presenting rhythm. No mention of other drug specific therapy aside from Ca, sugar, and pushing K intracellularly. Unless you've had thrombolysis of clot it isn't going downstream since it has already "wedged". If pt were found in the freezer you could consider hypothermia. As others have said, sometimes you get "lucky", if you can call it that. Just remember asystole isn't asystole without checking two leads. A rhythm is only a rhythm unless you have perfusion.

 

 

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I'm surprised that no one has commented on an asystole being transported to begin with.  This is not a personal statement but more a change in policies noted over the years.  Last time I attended the Dallas EMS conference (Gathering of Eagles) several years back, most municipalities weren't transporting from scene with unresponsive systole.  I'd actually like to see a show of hands as to whose local EMS transports/calls (pronounces) on scene refractive asystole, and which municipality (preferably the large metro areas) if you know this to be a true protocol.

 

I've worked as a medic in multiple states; more and more agencies are changing protocols to allow a "stay and play" mentality, with the option to cease efforts on scene, especially with patients presenting initially in asystole.  All 5 agencies I have worked for have allowed termination of resuscitation on scene, however it often comes down to the medics (and FDs) comfort with the termination, and bringing all people on scene onto the same page.   Though the research has shown better ROSC outcomes with remaining on scene, many medics remain stuck in the mentality of immediately rushing to the hospital, because it is the way they have always done things, and the way they were taught.   

 

Here is a link of research review on transporting cardiac arrests; http://www.ems1.com/columnists/kenny-navarro/articles/1432503-Prove-it-Transporting-patients-in-cardiac-arrest-improves-outcome/

 

If you'd like links to more protocols/ studies send me a PM, this is one of the topics I am very passionate about.  

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