# Clinical ride cardiac arrest



## crispy91 (Sep 16, 2012)

Ok. So I was recently on a clinical ride and we ran a rather interesting call. Unfortunately, the pt died. But I have an idea as to why. 

So we were dispatched for a pt not breathing, cpr not started. We get on scene and fd was already there. They had canceled rescue, so we thought it wasn't too particularly bad . Scene was safe. The  pt was found with her daughter. She was lying recumbent in the living room next to a large basin, almost completely full of a yellow, clear, bile-like vomit. The pt spoke only swahili. Her daughter said she had been vomitting for approx 30 min. Pt had hx of controlled hypertension, and type 2 diabetes. D-stick was 223.

LOC- V, lethargic
A- patent
B- tachypneic, adequate
C- rapid, weak, regular, and equal in all extremities. Skin was pale, cool, and clammy.

We got her in the truck, started an Iv of 1000 mL NS, and took her vitals. 

Pulse- 112
BP- 100/60 (est)
Resp- 24
SaO2- 97% (2 lpm o2 via nc)
Ekg- Sinus tachy

So we started for the hospital non emergent. We gave the pt zophran for the nausea, and I started an assessment. Pupils were PERRL, and that's as far as I got. The sat straight up, made a grunting noise, and frantically pointed at her chest. She then went unresponsive.

A- occluded
B- apneic, being bagged 
C- slow, weak pulse
Pulse- 34
Bp- 70/40
SaO2- 80% (15 lpm, bvm)
EKG- Mobitz II

So I started bagging her, while my partner began pacing. We got capture at 30 Ma, and paced at 80. I asked for an OPA, but my partner said he was going to intubate. We couldn't get  her tubed because of an equipment malfunction. So, we bagged until we arrived at the hospital. We hit a bump on the way in and lost capture. A supervisor met us there and helped us get her in. She coded the first time right outside the room. We started cpr and transferred her to a bed. Nurses took over compressions while I managed her airway. Atropine was given. After about five minutes, we got rosc. The doc got her tubed, and a nurse confirmed placement. She coded once more abd we again got rosc. We later found out the pt died in ICU.

Here's my theory: I think this went on for days. I think she had either been vomitting for days , or had a cardiac problem. She probably went into shock , decompensated that day, and went irreversible in the truck. Here's my logic: the daughter, who had called, really didn't think of this as a massive issue until we got her in the truck . I think she really didn't realize how sick her mother was until it was too late.

Lemme know what you think!


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## NYMedic828 (Sep 16, 2012)

Were serial 12 leads taken?

Diabetic, heavy vomiting, classic skin presentation, progressed to a mobitz II and my guess is it went on to a complete blockage when she coded. High suspicion for inferior wall MI.

Long time diabetics sometimes do not experience the same symptoms a normal person would in the presence of an MI. Whenever I have a diabetic with abdominal pain/vomiting/nausea I record a 12 lead. The inferior wall rests on the diaphragm and during infarction irritate the diaphragm or phrenic nerve and can result in profound vomiting in some cases.


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## Martyn (Sep 16, 2012)

crispy91 said:


> Ok. So I was recently on a clinical ride and we ran a rather interesting call. Unfortunately, the pt died. But I have an idea as to why.


 
It was her time, nothing will change that, just delay it


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## Veneficus (Sep 16, 2012)

crispy91 said:


> Here's my theory: I think this went on for days. I think she had either been vomitting for days



Don't think this is the issue.



crispy91 said:


> or had a cardiac problem.



I wasn't there, you did not give enough info, but I would bet on this.



crispy91 said:


> She probably went into shock , decompensated that day, and went irreversible in the truck.



This does not sound reasonable the way I understand it. 

She was in shock for days, suddenly decompensated despite your intervention, and then went into irreversible shock post volume restoration?

It sounds to me like you don't understand shock.



crispy91 said:


> Here's my logic: the daughter, who had called, really didn't think of this as a massive issue until we got her in the truck . I think she really didn't realize how sick her mother was until it was too late.



That describes most patients who die suddenly.

If I had to guess, which is all it is, based on the limited info, she had an MI and she was paced and atropined to death.


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## Veneficus (Sep 16, 2012)

NYMedic828 said:


> or phrenic nerve.



Step up your game 

Which branch?


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## NYMedic828 (Sep 16, 2012)

Veneficus said:


> Step up your game
> 
> Which branch?



 :wacko:


Tried to find it myself and failed. 

So is it left, right, anterior, posterior or lateral? 

I assume it isn't posterior or lateral so my vote is for anterior.



To the OP

As far as blockages in the heart

1st degree, which is benign sometimes presents with bradycardia in general and isn't a true block. It is also baseline for some people like runners.

Mobitz I, often vagal in nature. Usually occurs higher up in the AV node.

Mobitz II, start suspecting insult to the heart. This is where things start to go south. Often occurs infranodal as a result of cardiac damage.

3rd degree, total disassociation between ventricles and atria. Usually presents with a wide QRS and goes south pretty fast. 


1st and mobitz I are the only two really affected by atropine because they are presumed to be vagal induced. It may have some benefit in mobitz II depending on how many atrial impulses are really getting through but usually it's not indicated. (I've seen it once, atropine did nothing)

Blockages don't often occur as a result of hypopoxia. That's when arrthyhmias happen because hypoxia cells get irritable and unstable. Blockages are usually due to physical damage or insult to the heart and it's conduction network.


Also, always obtain a 12 lead before you begin pacing. Obviously once pacing begins, you cannot acquire a 12 without stopping. A 3 lead is not meant to be diagnostic, atleast not a substantial degree anyway. That's what a 12 is for.

I have seen people on rotations before I knew better that used Lead II as a diagnostic and looked like real morons when the ER did a 12 to discover a major inferior MI.


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## Veneficus (Sep 16, 2012)

NYMedic828 said:


> :wacko:
> 
> 
> Tried to find it myself and failed.
> ...



Not an easy answer to find online I see.

I learned that the phrenic nerve branches from both the left and the right on the thoracic diaphragm followed the same path as the arteries, so were refered to as the "superior" branches of the phrenic nerve. (supplying the diaphragm and the pericardium)

This allowed them to be functionally seperated from the abdomino-phrenic branches.

Most of the sites i found just say "no named branches."


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## NYMedic828 (Sep 16, 2012)

Never mind knowing some extra fun facts


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## TomB (Sep 16, 2012)

There's no way you had capture at 30 mA. Post the strips and if I'm wrong I'll pay you $100.00.


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## Anjel (Sep 16, 2012)

TomB said:


> There's no way you had capture at 30 mA. Post the strips and if I'm wrong I'll pay you $100.00.



I Paced my arm with 60mA lol that hurt. But 30 doesn't seem like enough.


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## the_negro_puppy (Sep 16, 2012)

Sounds like a cardiac event to me. A view of the ECG before she arrested or went unconscious would have been good


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## VFlutter (Sep 16, 2012)

NYMedic828 said:


> Long time diabetics sometimes do not experience the same symptoms a normal person would in the presence of an MI. Whenever I have a diabetic with abdominal pain/vomiting/nausea I record a 12 lead. The inferior wall rests on the diaphragm and during infarction irritate the diaphragm or phrenic nerve and can result in profound vomiting in some cases.



Or the heart block was vagally induced by emesis. However I would expect to this occur right after an episode of vomiting. 

If she truly was vomiting bile then gastroenteritis or intestinal obstruction should be on the DDX along with Lyte imbalance, sepsis, met alkolosis, etc


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## NYMedic828 (Sep 16, 2012)

Anjel1030 said:


> I Paced my arm with 60mA lol that hurt. But 30 doesn't seem like enough.



Drunk? Lost a bet? Dare?



Maybe the patient was anorexic.


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## Anjel (Sep 16, 2012)

NYMedic828 said:


> Drunk? Lost a bet? Dare?
> 
> 
> 
> Maybe the patient was anorexic.



Medic class lol

We all took turns. So we could sympathize with our patients.


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## NomadicMedic (Sep 16, 2012)

Anyone guess PE?


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## NYMedic828 (Sep 16, 2012)

n7lxi said:


> Anyone guess PE?



With a mobitz II? I'd say cardiac?


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## NomadicMedic (Sep 16, 2012)

NYMedic828 said:


> With a mobitz II? I'd say cardiac?



Sure, the electrolyte imbalance or a big old MI might have been the cause...

But I'm still not convinced of the validity of the details. The capture at 30mA is telling. The OP is a basic. How much of this is valid info? Was it really a Type II? 
Eval consists of PERL and that's it?

Really?

Too much guess work. Sepsis, electrolyte imbalance, PE, an MI... Demonic possession? Could be anything. 

No way to hazard a guess without being there.


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## Anjel (Sep 16, 2012)

And zophran! Don't forget the zophran!


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## NYMedic828 (Sep 16, 2012)

ChaseZ33 said:


> Or the heart block was vagally induced by emesis. However I would expect to this occur right after an episode of vomiting.
> 
> If she truly was vomiting bile then gastroenteritis or intestinal obstruction should be on the DDX along with Lyte imbalance, sepsis, met alkolosis, etc



Mobitz I is usually presumed to be vagal induced.

Mobitz II is usually infranodal and not affected by vagal tone.




Also I think OP is a medic student, but just a guess.


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## Veneficus (Sep 16, 2012)

n7lxi said:


> Sure, the electrolyte imbalance or a big old MI might have been the cause...
> 
> But I'm still not convinced of the validity of the details. The capture at 30mA is telling. The OP is a basic. How much of this is valid info? Was it really a Type II?
> Eval consists of PERL and that's it?
> ...


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## VFlutter (Sep 16, 2012)

NYMedic828 said:


> Mobitz I is usually presumed to be vagal induced.
> 
> Mobitz II is usually infranodal and not affected by vagal tone.



Anecdotally, I rarely see Mobitz I after vagal stimulation. Mobitz II is more common followed by 3rd degree/AV diss and then some people have sinus arrest and just go into Junctional/Ventricular escape. That is just personal experience but I see it quite frequently. Very common to see with out patients on Chemo.


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## NYMedic828 (Sep 16, 2012)

ChaseZ33 said:


> Anecdotally, I rarely see Mobitz I after vagal stimulation. Mobitz II is more common followed by 3rd degree/AV diss and then some people have sinus arrest and just go into Junctional/Ventricular escape. That is just personal experience but I see it quite frequently. Very common to see with out patients on Chemo.



Point taken. I am going off of textbook knowledge. I have literally seen Mobitz II once and it was on a rotation. The crew gave atropine and didn't pace...

Wish I knew better at the time. Patient might of had a chance... (they never did a 12 lead, gave 0.5mg of atropine, no effect. Got to ER, they discover major II/III/AVF elevation. Begin pacing, pretty sure she didn't make it.


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## Doczilla (Sep 17, 2012)

Anjel1030 said:


> I Paced my arm with 60mA lol that hurt. But 30 doesn't seem like enough.



There's easier ways to work out your arms


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## NYMedic828 (Sep 17, 2012)

Where'd the OP go?

I still wanna see a 12 lead.

Assuming the story is factual, people should save strips from these kinds of things for self education and education of others who may never have/will see one.


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## Veneficus (Sep 17, 2012)

*Don't try this at home...*

In my medic class, one of our classmates, a marine, volunteered to be paced without sedation. 

So we hooked him up to the LP 10 at 70ma and 70 beats. 

He was able to tough out the first shock. By the second he had tears in his eyes and after the third he tore the pads off. 

We also tried holding a nitro in our ungloved hand and taking one to see how bad and how long the headache lasts.

Just some of the many exploits that make it amazing we are still alive.


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## Anjel (Sep 17, 2012)

Doczilla said:


> There's easier ways to work out your arms



I did feel the burn. Lol

On kid took his to the max at 175 on his leg. Hilarious.


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## VFlutter (Sep 17, 2012)

NYMedic828 said:


> Point taken. I am going off of textbook knowledge. I have literally seen Mobitz II once and it was on a rotation. The crew gave atropine and didn't pace...
> 
> Wish I knew better at the time. Patient might of had a chance... (they never did a 12 lead, gave 0.5mg of atropine, no effect. Got to ER, they discover major II/III/AVF elevation. Begin pacing, pretty sure she didn't make it.



Like I said its just anecdotal. I rarely see sustained Mobitz II, usually just isolated runs. 

I remember a guy who came into the ER in Type II in the 20s. Initially he was somewhat stable so they transQ paced him but then lost capture and did a transvenous at the bedside. It was pretty hectic, he got a PPM in the morning.


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## TomB (Sep 17, 2012)

Having paced myself on several occasions it's just plain mean to dial up the mA too quickly. It makes the muscle contractions more violent. They are far more tolerable when you increase the energy gradually. I capture at 110-120 mA with AP pad placement. Interestingly, the energy has to drop below 90 mA for me to lose capture (then all the way back up to 110-120 mA to achieve capture again). I would consider being paced uncomfortable -- a painful "prickly" feeling,  but not intolerable. Having said that, I was choosing to do it and knew I could stop at any time. I think the loss of control and anxiety aspect contributes to a patient's suffering.


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## Brandon O (Sep 19, 2012)

TomB said:


> Having paced myself on several occasions



One of these days I'll learn to do this...


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## firetender (Sep 20, 2012)

I believe the movie was named *Flatliners! *

Kiefer Sutherland was in it.

Be careful out there!


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## Eli (Sep 25, 2012)

This was an interesting case to review. I noticed that the OP hasn't chimed in so I'm guessing all the responses are academic. 

I agree that the issue here was likely a primary cardiac event. I don't agree that a 12 lead "always" (NYCMedic828) needs to done before pacing. It certainly is preferable and should be very high on the priority list. I try to obtain a 12 lead along with the first V/S. Depending on the capabilites of my partner and 1st responders, that is easier said than done sometimes. 

I didn't like seeing the first set of vitals until after the patient had been moved to the truck. Specifically the BP. I'm confident that isn't exactly the way it was. Hopefully they had V/S from the FD but it simply wasn't listed. That being said, the shock and failure to recognize it and treat it early on might have been that only thing to be done that could have prevented this catastrophic collapse of the patient's condition. Was sufficient supplemental oxygen was provided? Was the patient kept in as much of a Trendelenburg position as possible? Fluid resuscitation might have been helpful prior to moving that patient but I don't believe it's presence or absence likely made a difference in this case. For the sake of argument, I will assume basis O2 and pateint positioning was done. If all that is true then I'd guess the EMS team did everything they could to help this patient. 

I didn't really follow the comments about pacing and Atropine. I think there was some sarcasm there. But I beleive pacing was the most appopaite course of action at the time when the patient's condition detiorated.

It always good to see how these scanarios develop for others.


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## Aidey (Sep 25, 2012)

Since when was trendelenburg shown to be beneficial for anything in the pre hospital setting?


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## NomadicMedic (Sep 25, 2012)

We always called trendelenburg "the king county fluid bolus".


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## NYMedic828 (Sep 25, 2012)

http://www.cjem-online.ca/v6/n1/p48

Trendelenburg has never been proven to have any positive effects. Blood return from the legs is not assisted much by gravity so much as it is by the skeletal muscle pump in the legs which the body will use to compensate on its own.

Other studies I've read also state it is has negative effects on the inferior vena cava because the raising of the legs pushed the abdominal organs towards the heart potentially further limiting venous return.


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## Eli (Sep 28, 2012)

NYMedic828 said:


> http://www.cjem-online.ca/v6/n1/p48
> 
> Trendelenburg has never been proven to have any positive effects. Blood return from the legs is not assisted much by gravity so much as it is by the skeletal muscle pump in the legs which the body will use to compensate on its own.
> 
> Other studies I've read also state it is has negative effects on the inferior vena cava because the raising of the legs pushed the abdominal organs towards the heart potentially further limiting venous return.



Thanks for the link. I'm a "just the facts, ma'am" kinda of guy. 

"...Recognizing that the quality of the research is poor,..."1 I was a little worried until I got to that sentence. I have never researched this particular treatment. I have recognized that the one position available for this position on cots is pretty extreme for many patients. Goodness, the discomfort from the position alone can cause enough anxiety to defeat any benifits. I've used pillows and such to fabricate more reasonable angles in the past. All that being said, in the first moments positioning and supplemental oxygen are helpful (in my experience). They are also sometimes overlooked.

1: http://www.cjem-online.ca/v6/n1/p48


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## Veneficus (Sep 28, 2012)

Eli said:


> Thanks for the link. I'm a "just the facts, ma'am" kinda of guy.
> 
> "...Recognizing that the quality of the research is poor,..."1 I was a little worried until I got to that sentence. I have never researched this particular treatment. I have recognized that the one position available for this position on cots is pretty extreme for many patients. Goodness, the discomfort from the position alone can cause enough anxiety to defeat any benifits. I've used pillows and such to fabricate more reasonable angles in the past. All that being said, in the first moments positioning and supplemental oxygen are helpful (in my experience). They are also sometimes overlooked.
> 
> 1: http://www.cjem-online.ca/v6/n1/p48



The full conclusion is a lot more damning.

*"The Trendelenburg position is taught in schools and on the wards as an initial treatment for hypotension. Its use has been linked to adverse effects on pulmonary function and intracranial pressure. Recognizing that the quality of the research is poor, that failure to prove benefit does not prove absence of benefit, and that the definitive study examining the role of the Trendelenburg position has yet to be done, evidence to date does not support the use of this time-honoured technique in cases of clinical shock, and limited data suggest it may be harmful. Despite this, the ritual use of the Trendelenburg position by prehospital and hospital staff is difficult to reverse, qualifying this as one of the many literature resistant myths in medicine."*

I think you will find that most emergency treatments in critical patients do not have strong research studies.

The reason isn't because of lack of interest, the reason is because of the ethical and legal ramifications.

You will never see studies like: CPR vs. no CPR or The Latest Thing We Could Think of Compared to Time Recognized Standards...

In order to do shock research, I had to resort to neonates because ethics bodies will not approve new or control treatments in adults.

With neonates, the mantra is: "we don't know if the same treatments will work" and it is actually easier to get ethical approval despite the pathophysiology being exactly the same.


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## usalsfyre (Sep 28, 2012)

Eli said:


> Thanks for the link. I'm a "just the facts, ma'am" kinda of guy.
> 
> "...Recognizing that the quality of the research is poor,..."1 I was a little worried until I got to that sentence. I have never researched this particular treatment. I have recognized that the one position available for this position on cots is pretty extreme for many patients. Goodness, the discomfort from the position alone can cause enough anxiety to defeat any benifits. I've used pillows and such to fabricate more reasonable angles in the past. All that being said, in the first moments positioning and supplemental oxygen are helpful (in my experience). They are also sometimes overlooked.
> 
> 1: http://www.cjem-online.ca/v6/n1/p48



The position on stretchers is actually like "Trendelenburg lite". The actual surgical position is much more extreme.

Supplemental O2 (for a patient that probably has an ungodly high PaO2 anyway) and positioning are unlikely to do anything. How much experience are you basing this off of?


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## Brandon O (Sep 28, 2012)

Veneficus said:


> *the ritual use of the Trendelenburg position by prehospital and hospital staff is difficult to reverse*



It may be more accurate to say that the TEACHING of Trendelenburg is inextricably woven into prehospital medicine. Its actual PRACTICE, in my experience, is not particularly embraced.


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## Eli (Sep 30, 2012)

usalsfyre said:


> Supplemental O2 (for a patient that probably has an ungodly high PaO2 anyway) and positioning are unlikely to do anything.



Define unlikely. Then define whether the potential benefit might be outweighed by the potential risk. Many cardiac arrests we work have less than 1% chance of survival. Should we not treat them? Is that the philosophy that I'm hearing in these threads?



usalsfyre said:


> How much experience are you basing this off of?



25+ patients/week through the 80's and 90's in an urban system where physicians and EMS workers drove the practice based on balancing quality/value vs. profit.


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## Veneficus (Sep 30, 2012)

*I hate when the reply I am typing disappears.*

Firetender is a much better writer than I am. 

I humbly encourage you to read this.

http://emsoutsideagitator.com/



Eli said:


> Define unlikely. Then define whether the potential benefit might be outweighed by the potential risk. Many cardiac arrests we work have less than 1% chance of survival. Should we not treat them? Is that the philosophy that I'm hearing in these threads?



A shorter version:

Blunt traumatic arrest is not worth trying to resuscitate at all. We should not be doing it. 

Penetrating is better but still comes in <10% most places. (usually around 6%)

VF/VT from medical cause have a much higher rate, the worst reported numbers in the US I have seen is 9%. 

asystole/pea arrests are no longer counted. With the exception of a few immediately identifyable and reversible causes or already in a healthcare facility with a known cause, these people are for all intents and purposes, dead. We should not waste resources trying to resuscitate them.

I have written extensively about supplemental O2, bottom line: Unless the specific pathology requires it, it is a waste and we should not be doing it. That is especially true in trauma.

Positioning in trauma was covered above, but I will just reiterate, it is a waste of time and there is no reason to bother.




Eli said:


> 25+ patients/week through the 80's and 90's in an urban system where physicians and EMS workers drove the practice based on balancing quality/value vs. profit.



The game has changed considerably. Value for the patient (or relatives) is no longer even part of the equation in the US. Now it is all about profit.

We also realize we are no longer in combat with death. Survival is measured to neuro intact discharge, not by a pulse in the ED. 

Welcome to the forum.


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## Aidey (Sep 30, 2012)

Eli said:


> Define unlikely. Then define whether the potential benefit might be outweighed by the potential risk. Many cardiac arrests we work have less than 1% chance of survival. Should we not treat them? Is that the philosophy that I'm hearing in these threads?



Yes, it is. If the cardiac arrests you are working have a collective 1% survival rate you are picking the wrong codes to work.


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## VFlutter (Oct 1, 2012)

Veneficus said:


> VF/VT from medical cause have a much higher rate, the worst reported numbers in the US I have seen is 9%.
> 
> asystole/pea arrests are no longer counted. With the exception of a few immediately identifyable and reversible causes or already in a healthcare facility with a known cause, these people are for all intents and purposes, dead. We should not waste resources trying to resuscitate them.



In the hospital it is extremely rare to see a true asystole/PEA arrest. I can remember 3 in the past year compared to ~30 V tach/Fib arrests.

1. Asystole arrest was s/p ablation....didn't make it.
2. PEA was s/p CABG and tamponded, opened the chest @ bedside with internal cardiac massage... Didn't make it. 
3. PEA was a Saddle PE that was lsyed and resuscitated 

In hospital cardiac arrest data 
http://www.ncbi.nlm.nih.gov/pubmed/19770741


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## TomB (Oct 1, 2012)

Asystole/PEA arrest is very common in the in-hospital setting compared to primary VF/VT arrest. I saw it many times when I worked in the hospital on a stepdown unit and the link you provided indicates that asystole/PEA is the first pulseless rhythm 76% of the time.

Tom



ChaseZ33 said:


> In the hospital it is extremely rare to see a true asystole/PEA arrest. I can remember 3 in the past year compared to ~30 V tach/Fib arrests.
> 
> 1. Asystole arrest was s/p ablation....didn't make it.
> 2. PEA was s/p CABG and tamponded, opened the chest @ bedside with internal cardiac massage... Didn't make it.
> ...


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## VFlutter (Oct 1, 2012)

TomB said:


> Asystole/PEA arrest is very common in the in-hospital setting compared to primary VF/VT arrest. I saw it many times when I worked in the hospital on a stepdown unit and the link you provided indicates that asystole/PEA is the first pulseless rhythm 76% of the time.
> 
> Tom



Thanks for pointing that out. I guess I just assumed based off my own personal experience. I stand corrected


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