# That extra 60 seconds.



## YYCmedic (Dec 14, 2008)

Recently responded to a call where bystanders state a 50 y/o was playing hockey and had a seizure on the ice, pt came to and skated to the bench under their own power at which point EMS was contacted, due to our dispatch system (the card model that some fo you may know...) the call came in as a (12A) low risk response (no flashy lights) for a postictal seizure pt.... so we got stuck at ALOT of red lights on the way. 

Upon arrival, the pt had collapsed on the bench in all of their hockey gear. They were a/o x4 with 0 complaints. Skin is ashen grey/pale and extremely diaphoretic, weak radial pulses, Bp 90/50, sitting the pt up causes them to go unconscious and 12-lead shows Massive Inferior Lateral Posterior MI with reciprocal changes. Enroute to hospital all pulses were lost heart monitor shows rate has sropped down to 30bpm and a Bp was unobtainable... BUT... the pt was still awake and talking to us, with 0/10 CP!!!!  1500cc's were pressure infused iv, adenosine was administered and 12-lead was transmitted to the recieving hospital (very short transport times) he subsequently died in the cath lab about 3 minutes after arrival. Would anyone else be wondering if that few extra minutes spent waiting at red lights would have made a difference for this person? If the dispatch had only thought to ask if this pt was diaphoretic it would have bumped up our response to lights/siren.... maybe its time to review our dispatch model but who am I to know... I just work here!!!


----------



## WuLabsWuTecH (Dec 14, 2008)

There's really no way to know and I wouldn't stress about it too much.  If the man upstairs wants him, he'll get him.  Its quite possible that yo ugetting there 60 seconds faster would have just meant that he died 4 minutes into the cath lab rather than 3.


----------



## traumateam1 (Dec 14, 2008)

WuLabsWuTecH said:


> There's really no way to know and I wouldn't stress about it too much.  If the man upstairs wants him, he'll get him.  Its quite possible that yo ugetting there 60 seconds faster would have just meant that he died 4 minutes into the cath lab rather than 3.



Amen.

Sometime, no matter what we do, if the big guy upstairs wants him to "come home" than no matter what treatment we do, it just simply wont work. Some things are just simply out of our control. Try not to stress out about it too much, it was just one of those things that happens in life.

Take care.


----------



## KEVD18 (Dec 14, 2008)

TJ_EMT said:


> Would anyone else be wondering if that few extra minutes spent waiting at red lights would have made a difference for this person?


 

nope, for two reasons.

one, its *highly* unlikely that that minimal amount of time(realistically what are we talking here, 3 minutes?) would have done him any good. sometimes, its just somebodies time(and i mean that in a completely non secular way). from what you described, that guy was throwing the big one. its not very common that you save those guy. sure, little warning mi's and even pretty decent sized ones will live to walk out the front door but when its *the big one*,  about your only chance s if you drop actually in a fully staffed cath lab.

two, you cant save everybody. you can try, but you will fail. this time, maybe it was your response time(which i doubt). or maybe it was this guy ignoring his problem for 20 years(much more likely). next time it could be faulty equipment or not enough manpower or whatever. the point im trying to make is that when your clock runs out, its game over.


----------



## remote_medic (Dec 14, 2008)

I'm going to echo what others have said.  Minutes wouldn't have mattered here.  It is up to your dispatch to have you respond in an appropriate manner to each call. Having dated a dispatcher at a major dispatch center and heard some stories...it is a job I would never want. I'm fortunate/cursed I guess that dispatch does not dictate our response coming out of the chute. They provide dispatch info and we decide for ourselves code 1 vs code 3. Does lead itself to abuse...sometimes but for the most part it works well.

(I'd have chosed a code 3 response with what you gave me).

Sounds like your dispatch follows MPDS which works well for the most part....this is an example of where if failed. Dispatch failed to ask the appropriate questions to prioritize your response (ashen grey skin, etc).



Chris


----------



## marineman (Dec 14, 2008)

Like others said I doubt that time would have changed the outcome. As far as dispatch asking extra questions yes we could staff ever dispatch center with doctors that could ask all the questions and give you a diagnosis when they finally get around to dispatching you but that's obviously impractical and asking that many questions still takes time. Dispatchers usually either go through their flip cards or have a list of questions on their computer that they have to get answered and then the computer tells them what level to dispatch the call. They ask the same questions for every call and some of them are slightly subjective causing high priority response for no reason but sometimes it works out the other way for an asymptomatic patient. I know two of the triggers in our area are breathing difficulty and spurting blood. I don't know if it's how they ask the question or what but every patient out there has breathing difficulty and of the three high priority spurting blood calls I've been on two of them were cured with a bandaid. 

Dispatch is not a perfect system but it in general is fairly practical looking at it from all aspects. Don't beat yourself up over it.


----------



## emtbill (Dec 14, 2008)

wait...what?



TJ_EMT said:


> Upon arrival, the pt had collapsed on the bench in all of their hockey gear. They were a/o x4 with 0 complaints. Skin is ashen grey/pale and extremely diaphoretic, weak radial pulses, Bp 90/50, sitting the pt up causes them to go unconscious and 12-lead shows Massive Inferior Lateral Posterior MI with reciprocal changes. Enroute to hospital *all pulses were lost* heart monitor shows *rate has sropped down to 30bpm and a Bp was unobtainable...* BUT... the pt was still awake and talking to us, with 0/10 CP!!!!  1500cc's were pressure infused iv, *adenosine was administered* and 12-lead was transmitted to the recieving hospital (very short transport times) he subsequently died in the cath lab about 3 minutes after arrival. Would anyone else be wondering if that few extra minutes spent waiting at red lights would have made a difference for this person? If the dispatch had only thought to ask if this pt was diaphoretic it would have bumped up our response to lights/siren.... maybe its time to review our dispatch model but who am I to know... I just work here!!!



Last time I checked adenosine is indicated for reentrant pathway SVT's, not for a profound bradycardia, and when a patient loses a pulse and BP in the presence of electrical activity on the monitor they are in PEA. Chest compressions are indicated.

I call bull:censored::censored::censored::censored: on this. It sounds like the story that floats around on some EMS boards about the asystolic cardiac arrest where the patient opens their eyes and looks at the EMT's when they are doing chest compressions.


----------



## Airwaygoddess (Dec 14, 2008)

*Some you can catch and some they will go on their own...*

* One can have every piece of equipment, and every other bell and whistle, but when it is the patient's time to leave this earth, medicine, and all who work in this profession, can't stop death, in some ways it can only be prolonged.......-_-


----------



## VentMedic (Dec 14, 2008)

TJ_EMT said:


> Recently responded to a call where bystanders state a 50 y/o was playing hockey and had a seizure on the ice, pt came to and skated to the bench under their own power at which point EMS was contacted, due to our dispatch system (the card model that some fo you may know...) the call came in as a (12A) low risk response (no flashy lights) for a postictal seizure pt.... so we got stuck at ALOT of red lights on the way.
> 
> Upon arrival, the pt had collapsed on the bench in all of their hockey gear. They were a/o x4 with 0 complaints. Skin is ashen grey/pale and extremely diaphoretic, weak radial pulses, Bp 90/50, sitting the pt up causes them to go unconscious and 12-lead shows *Massive Inferior Lateral Posterior MI with reciprocal changes*. Enroute to hospital all pulses were lost heart monitor shows rate has sropped down to *30bpm and a Bp was unobtainable... BUT... the pt was still awake and talking to us, with 0/10 CP!!!!* 1500cc's were pressure infused iv, *adenosine was administered* and 12-lead was transmitted to the recieving hospital (very short transport times) he subsequently died in the cath lab about 3 minutes after arrival. Would anyone else be wondering if that few extra minutes spent waiting at red lights would have made a difference for this person? If the dispatch had only thought to ask if this pt was diaphoretic it would have bumped up our response to lights/siren.... maybe its time to review our dispatch model but who am I to know... I just work here!!!


 
??????????????

If that was the treatment, you probably did not do the patient any favors by getting to the scene. Although that could be a matter of opinion since prolonging the inevitable is difficult also. 

Look up the probability of survival for an MI that massive. Once you understand a little more about medicine, you realize what your capabilities are and what those of nature or a higher God than EMT(P) are.


----------



## mycrofft (Dec 14, 2008)

*Seconds count in the OR and ER. Usually, minutes count in the field*

I can't address whether this is a great example of treatment in the field, and I can confirm that monitoring instruments can tell you the pt is clinically dead when he/she is still talking to you (check your leads?). I can say is that when  the old MI does the tic tac toe across your myocardium, nothing will help you after a couple minutes but a transplant.

I hate it when the dispatch includes layperson dx's like "seizure", "stroke", or "drunk".


----------



## reaper (Dec 14, 2008)

I am glad someone else caught that treatment????? Are you sure they didn't push Atropine?

There is a reason they call that AMI the "widow maker"! It is usually a complete blockage and they don't last to make it to the cath lab. That extra 60 seconds in response time would have meant one thing. 

He would have lasted 4 minutes in the cath lab, rather then 3!


----------



## FF894 (Dec 14, 2008)

I'm thinking the adenosine probably did him in.....   Do you mean atropine?


----------



## boingo (Dec 14, 2008)

emtbill said:


> I call bull:censored::censored::censored::censored: on this. It sounds like the story that floats around on some EMS boards about the asystolic cardiac arrest where the patient opens their eyes and looks at the EMT's when they are doing chest compressions.




Why do you think this is bull?  I have personally watched a patient in VF open her eyes with chest compressions, no Urban Legend there.  I remember her well, after we converted her on our second defibrillation she awoke and stated she coudn't go to the hospital because she needed to go to work!  Was having an MI, went straight to the cath lab and discharged home 4 days later.


----------



## Outbac1 (Dec 14, 2008)

As I scrolled down this thread I was wondering if anyone would catch "adenosine". Hopefully they meant "atropine". Normally no palpable pulse would mean CPR. However if a pt is able to carry a conversation then they have a pulse and a rate of 30 and symtomatic I think pacing would be more appropriate.

 An extra 2 - 3 minutes probably would not have made a difference, but we'll never know. When your numbers up, it's up.


----------



## Sasha (Dec 14, 2008)

emtbill said:


> wait...what?
> 
> 
> 
> ...



I actually agree...


----------



## FF894 (Dec 14, 2008)

TJ- we def need confirmation on care rendered.  It seems as though pacing would have been the best choice....  Was this done?


----------



## mycrofft (Dec 14, 2008)

*We had a guy who would talk until clical asystole hit...*

Long history of witnessed V-tach to V-fib to pulselessness (still fibbing), would call us, we would get to ER, he would say "Here I go", and away he went. Did this enough timnes to be a local legend.
However, I recall reading how guillotined heads would open and roll their eyes and move their jaws from agonal cranial nerve activity.


----------



## emtbill (Dec 15, 2008)

boingo said:


> Why do you think this is bull?  I have personally watched a patient in VF open her eyes with chest compressions, no Urban Legend there.  I remember her well, after we converted her on our second defibrillation she awoke and stated she coudn't go to the hospital because she needed to go to work!  Was having an MI, went straight to the cath lab and discharged home 4 days later.



The call information just sounds sketchy at best. Like others have been saying, you treat the patient and not the monitor, but I find it hard to believe that a patient who has no palpable pulse or blood pressure, and who is suffering from a STEMI that later killed him is going to be completely asymptomatic. I have personally seen an asymptomatic STEMI patient who's ST segments were taller than the R waves, but she had so much morphine and metoprolol in her that it really didn't surprise me. With no drugs on board, no pulse and no BP this pt isn't going to be "awake and talking with 0/10 CP", and if they are alive, they won't be for long. That is just intuitive. All of that, coupled with the report of adenosine administered, just makes this story very sketchy. Either the OP was exaggerating, or someone who told him the story was mistaken, which isn't too far fetched. Stories are easily skewed as they're told from person to person.


----------



## boingo (Dec 15, 2008)

I see what your saying, my only comment was directed at a pulseless patient opening their eyes with chest compressions.  That I have seen myself.  

I also assume he meant atropine and not adenosine for the bradycardic rhythm, simple typo....I hope.


----------



## YYCmedic (Dec 15, 2008)

SORRY EVERYONE!!... thats slightly embarassing... DEFINATELY MEANT ATROPINE!!! Gave him 1.0 Mg IV, it brought his rate back up to about 56 Bpm for about 2 minutes then dropped back down to around 30... unfortunately pacing wasnt an option due to the fact that we couldnt get our pacing pads to stick at all, you'd wipe him off and he'd be dripping sweat again in seconds.

Again sorry, didnt have time to proof read, I was typing up a storm during what little down time I had on my Saturday night shift during the first blizzard of the year and the retarded drivers in this city.

...NOW! for those of you who are calling BS on this, then you obviousley have never witnessed this... fair enough. IT HAPPENED!! haha, didnt think it was possible myself! He was pulseless and completely asymptomatic (0/10 CP) but still awake and talking to us... crazy thing to see.


----------



## VentMedic (Dec 15, 2008)

TJ_EMT said:


> ...NOW! for those of you who are calling BS on this, then you obviousley have never witnessed this... fair enough. IT HAPPENED!! haha, didnt think it was possible myself! He was pulseless and completely asymptomatic (0/10 CP) but still awake and talking to us... crazy thing to see.


 
There are reasons doppler ultrasound is used in the ED.

One could also check for an LVAD but hopefully that is noticed quickly.


----------



## mycrofft (Dec 16, 2008)

*As I treid to spell before, "CLINICALLY pulseless"*

Sort of the opposite of EMD.


----------



## emtbill (Dec 16, 2008)

TJ_EMT said:


> SORRY EVERYONE!!... thats slightly embarassing... DEFINATELY MEANT ATROPINE!!! Gave him *1.0 Mg IV* it brought his rate back up to about 56 Bpm for about 2 minutes then dropped back down to around 30... unfortunately pacing wasnt an option due to the fact that we couldnt get our pacing pads to stick at all, you'd wipe him off and he'd be dripping sweat again in seconds.



wait...what?

The dosage of atropine for symptomatic bradycardia in an alive adult patient 0.5 mg. That's what I was taught and is the dosage I give to my patients. One milligram is for an asystolic/slow PEA cardiac arrest. Can you have that much leeway when giving cardiac drugs (I'm a new ALS provider)?


----------



## FF894 (Dec 16, 2008)

VentMedic said:


> There are reasons doppler ultrasound is used in the ED.
> 
> One could also check for an LVAD but hopefully that is noticed quickly.



If he was CAO I would hope he would mention that part....


----------



## FF894 (Dec 16, 2008)

emtbill said:


> wait...what?
> 
> The dosage of atropine for symptomatic bradycardia in an alive adult patient 0.5 mg. That's what I was taught and is the dosage I give to my patients. One milligram is for an asystolic/slow PEA cardiac arrest. Can you have that much leeway when giving cardiac drugs (I'm a new ALS provider)?



No, its ok - it was 2am.  If 0.5mg will work then 1mg will work better.


----------



## VentMedic (Dec 16, 2008)

FF894 said:


> If he was *CAO* I would hope he would mention that part....


 
*TJ_EMT quote*


> He was *pulseless* and completely *asymptomatic* (0/10 CP) but still *awake* and *talking* to us


 
Doppler ultrasound is used on patients when pulses can not be readily palpated. On some people you just can't feel a pulse easily and that is why the AHA changes some of its quidelines for lay person CPR. 

Unltrasound is also used to determine any cardiac activity during a code. Btween that and the ETCO2, we have a good prediction for resuscitation success. 

At least cardiac monitors today are usually sophisticated enough to identify a problem with the electrodes...but not always.

It is not that uncommon to see a patient awake during VT and the doppler may be used to assess the pulses or BP but often it is not required. VT may perfuse very well for extended periods of time. A person can be shocked from V-fib and awaken. That usually happens best when the healthcare provider is at beside. The precordial thump can work well in the ICU. 

Pt's with Sick Sinus Syndrome with have up to 20 second pauses regularly which looks frightening on a monitor screen of a just a few seconds. Some may feel asymptomatic while laying in bed.    These patients usually frustrate me if I'm trying to draw arterial blood.


----------



## YYCmedic (Dec 16, 2008)

emtbill said:


> wait...what?
> 
> The dosage of atropine for symptomatic bradycardia in an alive adult patient 0.5 mg. That's what I was taught and is the dosage I give to my patients. One milligram is for an asystolic/slow PEA cardiac arrest. Can you have that much leeway when giving cardiac drugs (I'm a new ALS provider)?



Our protocol for bradycardia is Atropine 1.0Mg IV q 3-5 mins to max of 3.0Mg or 0.04Mg/Kg. Our Asystole/PEA protocol is the same.


----------



## sharpenu (Dec 17, 2008)

One way I look at it is like this:

If the Pt is pulseless, consider that it takes a systolic BP of 40 to produce a palpable carotid pulse. With that fact in mind, a patient that has no palpable carotid pulse cannot be perfusing the brain with the required oxygen. Doppler is a waste of time. The goal here is to deliver O2 to the brain, and while a systolic of 30 may be detectable with a doppler, who cares? The brain is still starving for oxygen.

A cardiac patient who is having an inferior MI will frequently present atypically- they will most often complain of nausea and vertigo. Such a patient who has a seizure is likely experiencing runs of VT or VF. In such a case, time is critical and preventing the patient from going over the edge is a challenge. 

You did not mention what rhythm was producing the HR of 30. Was this a wide complex brady? Possibly a ventricular escape rhythm? Or was it a high degree AV block? Since this was an inferior wall, did you perform a 12 lead containing a right sided lead, such as V4R? If there was right sided involvement, that further complicates things.

Atropine given in such cases has been known to precipitate VF. Atropine increases myocardial oxygen demand, and if it fails to increase cardiac output in the process, you have just made the problem worse.

A better choice in such a case could be dopamine at 2-10 mcg/kg/min, assuming that pacing is not possible. Remember that this is a cardiogenic shock you are dealing with here.


----------



## VentMedic (Dec 17, 2008)

sharpenu said:


> If the Pt is pulseless, consider that it takes a systolic BP of 40 to produce a palpable carotid pulse. With that fact in mind, a patient that has no palpable carotid pulse cannot be perfusing the brain with the required oxygen. Doppler is a waste of time. The goal here is to deliver O2 to the brain, and while a systolic of 30 may be detectable with a doppler, who cares? The brain is still starving for oxygen.


 
The Doppler ultrasound is probably one of the most useful tools one could have access to. Not all of what you think to be the truth is actual reality. You can not treat PEA if one still has a pulse. There are many other effective treatments for low BP that doesn't involve running a code algorithm.

Textbook numbers are great but not always appropriate for every patient.  There are, again, reasons why the AHA changed some of its guidelines.


----------



## sharpenu (Dec 17, 2008)

That would be why it is now called PEA and not EMD. PEA means PULSELESS. If it is not pulse producing, explain to me why I care? Where in any ACLS situation does it say use a doppler? Why do you think that is?

If you are not perfusing the brain with oxygen, it does not matter if you have some small amount of cardiac output. I see so many in the ER wasting time looking for a doppler pulse, when there is no blood pressure perfusing the brain.


----------



## WuLabsWuTecH (Dec 17, 2008)

sharpenu said:


> One way I look at it is like this:
> 
> If the Pt is pulseless, consider that *it takes a systolic BP of 40 to produce a palpable carotid pulse*. With that fact in mind, a patient that has no palpable carotid pulse cannot be perfusing the brain with the required oxygen. Doppler is a waste of time. The goal here is to deliver O2 to the brain, and while a systolic of 30 may be detectable with a doppler, who cares? The brain is still starving for oxygen.
> 
> ...



Sorry, a bit of a sidetrack...

Really?  We were taught 60 mmHg for perfusion of the brain (palpable carotid pulse).  70 mmHg for femoral, and 80mmHg for radial.  Is this not right?


----------



## WuLabsWuTecH (Dec 17, 2008)

VentMedic said:


> The Doppler ultrasound is probably one of the most useful tools one could have access to. Not all of what you think to be the truth is actual reality. *You can not treat PEA if one still has a pulse.* There are many other effective treatments for low BP that doesn't involve running a code algorithm.
> 
> Textbook numbers are great but not always appropriate for every patient.  There are, again, reasons why the AHA changed some of its guidelines.



I think i'm confused a bit, or just really tired today.

If you're in PEA -- Pulseless Electrical Activity -- how can you still have a pulse?


----------



## VentMedic (Dec 17, 2008)

WuLabsWuTecH said:


> I think i'm confused a bit, or just really tired today.
> 
> If you're in PEA -- Pulseless Electrical Activity -- how can you still have a pulse?


 
If people don't immediately feel a pulse they assume it is PEA. If the doppler picks up blood flow or a pulse, it is NOT PEA and should not be treated as such.


----------



## Arkymedic (Dec 17, 2008)

We carried them at one service I worked for and used them frequently.



sharpenu said:


> That would be why it is now called PEA and not EMD. PEA means PULSELESS. If it is not pulse producing, explain to me why I care? Where in any ACLS situation does it say use a doppler? Why do you think that is?
> 
> If you are not perfusing the brain with oxygen, it does not matter if you have some small amount of cardiac output. I see so many in the ER wasting time looking for a doppler pulse, when there is no blood pressure perfusing the brain.


----------



## sharpenu (Dec 17, 2008)

VentMedic said:


> If people don't immediately feel a pulse they assume it is PEA. If the doppler picks up blood flow or a pulse, it is NOT PEA and should not be treated as such.



People assume that because that is correct. PEA is defined as:

A form of cardiac arrest in which the continuation of organized electrical activity in the heart is not accompanied by a palpable pulse or effective circulation.

PEA is composed of a group of rhythms that include:

EMD
pseudo-EMD
idioventricular rhythms
ventricular escape rhythms
post-defibrillation idioventricular rhythms
bradyasystolic rhythms

The only thing a doppler tells you is that you are not dealing with EMD. The rhythm is still PEA. In this case, we KNOW that this is not hypovolemia or EMD. This is obviously a cardiogenic shock. What good does a doppler do here?


----------



## VentMedic (Dec 17, 2008)

sharpenu said:


> People assume that because that is correct. PEA is defined as:
> 
> A form of cardiac arrest in which the continuation of organized electrical activity in the heart is not accompanied by a palpable pulse or effective circulation.
> 
> ...


 
Have you seen a doppler ultrasound in action? 

True PEA is a condition in which cardiac contractions are absent in the presence of coordinated electrical activity.

Pseudo-PEA is what you have described. The doppler ultrasound may assist with identifying the presence of cardiac contractions. Patients with pseudo-PEA may have a rapidly reversible cause such as auto-PEEP and hypovolemia. Auto-PEEP is a condition of over ventilation either mechanically by a ventilator or manually with a BVM. It can be easily remedied. 

Compressions and initiating the PEA protocol maybe needed but a different plan of care may be taken according to the heart's contraction quality and tamponades as well as other cardiac structure problems can also be readily identified. 

You may be limited to only the capabilities within your service but don't knock those that are in progressive EMS systems or the EDs that routinely utilize this technology. It is another tool to provide a more patient defined treatment. The doppler ultrasound is also now listed in almost every service capable of doing doppler ultrasound or ED ACLS protocols. Combine that with the ETCO2 and one can see if their resuscitation efforts are going in the right direction. 

Granted, the ultrasound is not cost effective for every EMS service and the training might be even more farfetched to consider for some services where Paramedic insist on just getting trained by the slim contents of the new ACLS book of guidelines. In many EMS systems the doppler ultrasound would probably not change the care given because of limitations in their practice. But, that doesn't make the use of the doppler ultrasound wrong in the hands of trained and educated providers.


----------



## sharpenu (Dec 17, 2008)

EMD, Electrical Mechanical Dissassociation is coordinated electrical activity with an absence of myocardial contractions. That is exactly what the name means, the electrical system is active, but is disassociated from the myocardium. If you were to open the chest, you would see that the heart is not contracting at all.

Pseudo EMD is electrical activity with coordinated muscle contractions that produce cardiac output that is not palpable- this is what a doppler detects. That is, you are moving blood, but not at a palpable pressure. The most common cause for this is hypovolemia.

There is no such thing as pseudo PEA. You are confusing PEA and EMD.

Don't take my word for it, read a cardiology journal:
http://www.chestjournal.org/cgi/reprint/101/1/123.pdf

_We measured aortic pressure during clinically apparent
cardiac electromechanical dissociation (EMD). Patients
with pulse pressures were designated as having pseudo-
EMD; those without, as having true EMD. _

Don't patronize me about being progressive or about experience. This is not about who is the biggest kid on the block. Simply put, in a code situation it is in appropriate to play with toys when your patient is not perfusing. I know it isn't sexy, but the fact is, we treat patients, not technology.


----------



## VentMedic (Dec 17, 2008)

sharpenu said:


> EMD, Electrical Mechanical Dissassociation is coordinated electrical activity with an absence of myocardial contractions. That is exactly what the name means, the electrical system is active, but is disassociated from the myocardium. *If you were to open the chest, you would see that the heart is not contracting at all.*
> 
> Pseudo EMD is electrical activity with coordinated muscle contractions that produce cardiac output that is not palpable- this is what a doppler detects. That is, you are moving blood, but not at a palpable pressure. The most common cause for this is hypovolemia.
> 
> ...


 
When did you last take an ACLS class?

That article is from 1992.

You no longer have to crack the chest to see heart movement. We now have ultrasound in the year 2008.

Please refer to page 52 of the current ACLS book.


----------



## VentMedic (Dec 17, 2008)

sharpenu said:


> Simply put, in a code situation it is in appropriate to play with toys when your patient is not perfusing. I know it isn't sexy, but the fact is, we treat patients, not technology.


 
PEA is one of those different situations where you may have to search for a cause. If you don't find a cause quickly that can be corrected, the code will probably be futile and the patient will be dead. 

If I have access to ultrasound or a Point-of-Care machine to assist me in finding one of the Hs and Ts, I will use it. 

You have to know what the advantages and capabilities are for each piece of technology. Don't be afraid of technology but do understand it. 

That being said, am I going to trust an SpO2 reading on a patient we are doing chest compressions on? No.

However, when it comes to the ETCO2 monitor, many just use it to "see a wave if the tube is in" with little or no idea of all the information the machine can provide if correlated to the patient.


----------



## sharpenu (Dec 17, 2008)

VentMedic said:


> When did you last take an ACLS class?
> 
> That article is from 1992.
> 
> ...



I was making a point. I *TEACH* ACLS as an EP instructor, and have for quite a few years. I understand and use doppler. I also stand by my statements. Go play with your toys, I will continue to save actual patients.

I repeat my original question:

What would a doppler have done to help this patient? Nothing. This was a cardiogenic event. Doppler will solve nothing here.

I am out of this pointless conversation.


----------



## VentMedic (Dec 17, 2008)

sharpenu said:


> I was making a point. I *TEACH* ACLS as an EP instructor, and have for quite a few years. I understand and use doppler. I also stand by my statements. Go play with your toys, I will continue to save actual patients.
> 
> I repeat my original question:
> 
> ...


 

This conversation started with my reply to this post:



TJ_EMT said:


> ...NOW! for those of you who are calling BS on this, then you obviousley have never witnessed this... fair enough. IT HAPPENED!! haha, didnt think it was possible myself! He was pulseless and completely asymptomatic (0/10 CP) but still awake and talking to us... crazy thing to see.


 
As an ACLS, maybe you should get the new book and update your literature sources to at least 2005.


----------



## mycrofft (Dec 17, 2008)

*So, how long does Uncle Morty last...*

...from this condition's inception before he first starts shedding brain and kidney cells, then winds up with his liver temperature being taken?
What can be done by laypersons on scene if these conditons ensue?
How long will one spend figuring what to definitvely do versus the first question?

I am appalled by the price of medical devices and their persnickety construction. If NASA can contract and get machines that withstand rocket launchings, zero gravity, Van Allen belt radiation, banging down on Mars in an airbag then rove the surface years longer than planned, I do not understand why they can't come out with an ultrasound (or any other device) with similar characteristics and a low price after amortization and before malpractice insurance.


----------



## boingo (Dec 18, 2008)

B]





sharpenu said:


> One way I look at it is like this:
> 
> If the Pt is pulseless, consider that it takes a systolic BP of 40 to produce a palpable carotid pulse. With that fact in mind, a patient that has no palpable carotid pulse cannot be perfusing the brain with the required oxygen. Doppler is a waste of time. The goal here is to deliver O2 to the brain, and while a systolic of 30 may be detectable with a doppler, who cares? The brain is still starving for oxygen.
> 
> ...



*TCP may be better than adding another drug to the mix.  Dopamine may end up being used, but a rate of 30 needs to be addressed, and TCP would be the way to do it.*


----------



## traumateam1 (Dec 18, 2008)

WuLabsWuTecH said:


> Sorry, a bit of a sidetrack...
> 
> Really?  We were taught 60 mmHg for perfusion of the brain (palpable carotid pulse).  70 mmHg for femoral, and 80mmHg for radial.  Is this not right?



Yeah thats what I was taught too.. well a little different.

60 mmHg for Carotid.
70-80 mmHg for Femoral
and 90 mmHg for Radial


----------



## JPINFV (Dec 18, 2008)

This is a small study with some glaring short comings, but it does give something to talk about.

"Accuracy of the advanced trauma life support guidelines for predicting systolic blood pressure using carotid, femoral, and radial pulses: observational study"



> After obtaining approval of the study by the ethics committee, we studied sequential patients with hypotension secondary to hypovolaemic shock and in whom invasive arterial blood pressure monitoring had been established. *An observer blinded to the blood pressure palpated the radial, femoral, and carotid pulses, and the invasive systolic blood pressure was recorded.*





> The advanced trauma life support guidelines for assessing systolic blood pressure are inaccurate and generally overestimate the patient's systolic blood pressure and therefore underestimate the degree of hypovolaemia. *The minimum blood pressure predicted by the guidelines was exceeded in only four of 20 patients.* The mean blood pressure and reference range obtained for each group indicate that the guidelines overestimate the systolic blood pressure associated with the number of pulses present. This study therefore does not support the teaching of the advanced trauma life support course on the relation between palpable pulses and systolic blood pressure.



-Deakin, C. D., Low, J. L. "Accuracy of the advanced trauma life support guidelines for predicting systolic blood pressure using carotid, femoral, and radial pulses: observational study." BMJ 2000;321:673-674 

http://www.bmj.com/cgi/content/full/321/7262/673


----------



## ChristinaM (Dec 31, 2008)

We have the same type dispatch system here... called EMD certified dispatching... just coming online to us. Our dispatchers also leave it up to us as to how we respond - responding (lights and sirens) or en route (no lights and sirens). They will even say "your discretion" when asked. All of us have gotten burned one way or the other. Dispatching is a job I would never want to have and they go on what information they have. 

Recently we were dispatched to a "fall" at a local ALF only to arrive and find that the patient fell down dead... just so happens he was coming down a flight of concrete steps at the time he had a significant cardiac event, stroke, etc., and smacked the back of his head to boot. We were informed that CPR was in progress as we  casually strolled up to the patient's location. Thankfully, we have everything we need to work a code, except suction, right on our stretcher.

You can only do what you can do and no more. No need to beat yourself up. Though there are those out there that may think so... we are not Gods.


----------



## daedalus (Dec 31, 2008)

VentMedic said:


> ??????????????
> 
> If that was the treatment, you probably did not do the patient any favors by getting to the scene. Although that could be a matter of opinion since prolonging the inevitable is difficult also.
> 
> Look up the probability of survival for an MI that massive. Once you understand a little more about medicine, you realize what your capabilities are and what those of nature or a higher God than EMT(P) are.



I agree!!!

The 60 seconds would not have saved the pt, but the ADENOSINE you gave killed him! Look up the studies on adenosine for MI! What were you thinking!!??


----------



## daedalus (Dec 31, 2008)

emtbill said:


> The call information just sounds sketchy at best. Like others have been saying, you treat the patient and not the monitor, but I find it hard to believe that a patient who has no palpable pulse or blood pressure, and who is suffering from a STEMI that later killed him is going to be completely asymptomatic. I have personally seen an asymptomatic STEMI patient who's ST segments were taller than the R waves, but she had so much morphine and metoprolol in her that it really didn't surprise me. With no drugs on board, no pulse and no BP this pt isn't going to be "awake and talking with 0/10 CP", and if they are alive, they won't be for long. That is just intuitive. All of that, coupled with the report of adenosine administered, just makes this story very sketchy. Either the OP was exaggerating, or someone who told him the story was mistaken, which isn't too far fetched. Stories are easily skewed as they're told from person to person.



I just got back from an emergency CCT call. We picked up a pt from a rinky dink ER and brought him to County USC med center. He had massive elevation on the monitor and no pain. His only complaint was anxiety and not feeling right.


----------



## YYCmedic (Jan 11, 2009)

daedalus said:


> I agree!!!
> 
> The 60 seconds would not have saved the pt, but the ADENOSINE you gave killed him! Look up the studies on adenosine for MI! What were you thinking!!??



I already fixed my post about the Adenosine, haha I'm really not retarded just a symple typo at 3am during a loooong shift hahaha.


----------



## ErinCooley (Jan 11, 2009)

This is yet another area where I really show the newbie...

are there seriously areas where dispatch decides whether lights and sirens are warranted?  Is that not a HUGE liability???

In my county, if you call 911, youre getting a truck w/ lights and sirens, even if you request no l/s due to liablity.


----------



## reaper (Jan 11, 2009)

Yes, it is called EMD (Emergency Medical Dispatch) Almost every large city uses it now. It was designed to cut down on the amount of calls ran L/S. Not every call needs a L/S response and it puts your crews in unnecessary danger.

If a caller calls 911 and states that they were jogging and twisted their ankle, would you want to run L/S to this call?


----------



## rescuepoppy (Jan 12, 2009)

reaper said:


> Yes, it is called EMD (Emergency Medical Dispatch) Almost every large city uses it now. It was designed to cut down on the amount of calls ran L/S. Not every call needs a L/S response and it puts your crews in unnecessary danger.
> 
> If a caller calls 911 and states that they were jogging and twisted their ankle, would you want to run L/S to this call?



Just to keep in line with the post those extra sixty seconds probably would not have mattered. To address the matter of dispatch areas that use the EMD systems also use EMDPRS cards that are guidlines as to how to dispatch the call. These are set up to help reduce the unneeded lights and siren response to every call and when properly used can be a tool to help reduce your systems liability. They also can be overridden by local protocol for incidents which involve enviromental conditions or other factors which could change response. We have been using it in our area for several years it works great.


----------

