# Chest Pain Case



## bakertaylor28 (Oct 26, 2016)

You are dispatched to a residence for a 31 year old male with chest pain.


Upon arriving, your patient, whom reports no significant past medical history, presents with with complaints of acute upper abdominal heaviness and chest pain of 2 hours’ duration. He reports he was drinking that night at a bar with friends and drank approximately 500ml of vodka. He vomited later while at home. He appears able answer questions. He quantifies his pain as 5/10 in the upper abdominal and precordial regions, dull in nature and improved on forward posture. On further questioning, he related flu-like symptoms a week ago and for the last 2 days he had a sharp chest pain limiting his exertion. A dose of ibuprofen , taken 30 minutes prior to your arival, did alleviate some of his symptoms initially, but the quickly returned.


Initial vitals revealed:

BP of 134/96mmHg, PR 79/minute, respiratory rate of 20/minute with 93% SpO2 on room air.


ECG shows low voltage waves in all leads and P-R depression in lead II. Pupils are slightly dilated but equally reactive, and the Patient is Alert and oriented, though appearing slightly intoxicated. On secondary survey, you hear muffled heart sounds and notice slightly raised veins. Pulsus paradoxus of 18mmHg is also noted.You decide to place the patient on oxygen and have established IV access.

As you begin to prepare for transport, the patient  develops 2nd Degree AVB block Type II, his pulse rate drops to 45, with respiration and SPO2 remaining relatively stable. Updated BP is 100 / 82.

What are your next steps in treating this patient?


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## VentMonkey (Oct 26, 2016)

Place pads on him "just in case", low flow O2 @ 2 lpm N/C, grab a BGL (didn't see one above?), place a second lock in this patient.

Ask the patient about his normal alcohol consumption? How often. Work into a more detailed secondary, probably some prophylactic Zofran IVP. 

Muffled heart tones and JVD along with pulsus paradoxus could be a working diagnosis of cardiac effusion--->R/O tamponade.

Any recent chest wall trauma? Perhaps an infection within this patients myocardium secondary to prolonged alcohol, and/ or drug abuse (does he use illicit drugs frequently?/ is he forth coming?)

Obviously he should be seen by a cardiologist so this is your transport destination. I am not upgrading unless he becomes an unstable and sustained high degree HB; all I got for now.


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## bakertaylor28 (Oct 26, 2016)

VentMonkey said:


> Place pads on him "just in case", low flow O2 @ 2 lpm N/C, grab a BGL (didn't see one above?), place a second lock in this patient.
> 
> Ask the patient about his normal alcohol consumption? How often. Work into a more detailed secondary, probably some prophylactic Zofran IVP.
> 
> ...



To clarify, the patient is forthcoming with answers to your questions, and reports that his Alcohol use is relatively normative (i.e. drinks but is not an alcoholic by any means), though he reports a history of the use of marijuana, though says he hasn't used it in the previous 6 months. 

There is no Hx of recent trauma, and there is no acute trauma, either. 

You get your BGL and it is normal, at 110 mg/dL.


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## VentMonkey (Oct 26, 2016)

bakertaylor28 said:


> To clarify, the patient is forthcoming with answers to your questions, and reports that his Alcohol use is relatively normative (i.e. drinks but is not an alcoholic by any means), though he reports a history of the use of marijuana, though says he hasn't used it in the previous 6 months.
> 
> There is no Hx of recent trauma, and there is no acute trauma, either.
> 
> You get your BGL and it is normal, at 110 mg/dL.


Fair enough, continue transport as stated above; not much else to do prehospital-wise.


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## bakertaylor28 (Oct 26, 2016)

VentMonkey said:


> Fair enough, continue transport as stated above; not much else to do prehospital-wise.



Interesting. Any particular reason your not considering atropine per the ACLS guidelines for symptomatic bradycardias ?


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## VentMonkey (Oct 26, 2016)

bakertaylor28 said:


> Interesting. Any particular reason your not considering atropine per the ACLS guidelines for symptomatic bradycardias ?


He's not symptomatic, ACLS guidelines don't dictate my treatment, protocols, or critical thinking skils.

Plus, last time I checked, Atropine is often ineffective in high degree HB's; some say it can even worsen them.

It sounds to me, though by no means am I a physician, as this is some form of myocardial infection be it pericarditis, myocarditis, endocarditis, or any mixture of the three. 

If this in fact the case, this patient needs antibiotics, antivirals, antifungals, or whatever treatment would reverse the _underlying cause _of his arrhythmias.

This is just my thoughts, take them for whatever you wish.


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## Tigger (Oct 26, 2016)

bakertaylor28 said:


> Interesting. Any particular reason your not considering atropine per the ACLS guidelines for symptomatic bradycardias ?


Is there any reason to? His blood pressure is fine and there is no indication of decreasing mentation or an increase/change in chest pain. There is also nothing to say that atropine will benefit a Mobitz II and may cause it to progress to a complete block though I am not sure that is proven. 

There is not enough in the initial assessment for me to say that there isn't an ischemic event going on as well.


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## Summit (Oct 26, 2016)

bakertaylor28 said:


> Interesting. Any particular reason your not considering atropine per the ACLS guidelines for symptomatic bradycardias ?


You didn't mention he was symptomatic. 

So constrictive pericarditis?


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## bakertaylor28 (Oct 26, 2016)

VentMonkey said:


> He's not symptomatic, ACLS guidelines don't dictate my treatment, protocols, or critical thinking skils.
> 
> Plus, last time I checked, Atropine is often ineffective in high degree HB's; some say it can even worsen them.
> 
> ...



Actually you are fairly well on top of it. This one actually came out of the text book, and the case turned out to be a cardiac tamponade.
Its interesting that you didn't pick up the low pulse pressure in the second set of vitals. :-D  And correct me if I'm wrong, but do we not treat AVBs to the same basic tune of the other bradys? (thinking along the terms of Atropine, Trans-cutaneous Pacing, High-dose dopamine, and Epinephrine as the basic array of standard treatment options, of a sort?)  I've never heard of Atropine having a negative effect with an AVB, and it would seem that we would want to address 2nd Degree Type II BEFORE we end up seeing 3rd degree AVB, or perhaps something more ominous.


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## bakertaylor28 (Oct 26, 2016)

Tigger said:


> Is there any reason to? His blood pressure is fine and there is no indication of decreasing mentation or an increase/change in chest pain. There is also nothing to say that atropine will benefit a Mobitz II and may cause it to progress to a complete block though I am not sure that is proven.
> 
> There is not enough in the initial assessment for me to say that there isn't an ischemic event going on as well.



100/82 doesn't ring the bell of a slightly low pulse pressure???


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## VentMonkey (Oct 26, 2016)

bakertaylor28 said:


> Actually you are fairly well on top of it. This one actually came out of the text book, and the case turned out to be a cardiac tamponade.
> Its interesting that you didn't pick up the low pulse pressure in the second set of vitals. :-D  And correct me if I'm wrong, but do we not treat AVBs to the same basic tune of the other bradys? (thinking along the terms of Atropine, Trans-cutaneous Pacing, High-dose dopamine, and Epinephrine as the basic array of standard treatment options, of a sort?)  I've never heard of Atropine having a negative effect with an AVB, and it would seem that we would want to address 2nd Degree Type II BEFORE we end up seeing 3rd degree AVB, or perhaps something more ominous.


All of the above are irrelevant IMO, again, as stated earlier this patient needs definitive care, be it pericardiocentesis, or the proper medication to reverse the underlying cause.

I'm not knocking you for throwing things out there that textbooks present as "classic s/s", just understand real-world medicine calls for a strong clinical base in order to be able to when to with hold, or continue into the next step of proper treatment modalities.

I guess to me the dropping pulse pressure (btw, you gave it away when you mentioned pulsus paradoxus; that is the "drop", so no need to get side tracked with that) isn't going to dictate much more than as previously stated, a judicious fluid bolus for me.


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## VentMonkey (Oct 26, 2016)

Again, aside from my above mentioned treatments, there's no harm in PO ASA, for me, after I have given the Zofran IVP since he's already had N/V; it's the humane thing to do.

You could try a judicious 250 ml fluid challenge, but I'd be hard pressed to go anymore than that.

Op, do you care to share your reasoning for Atropine?...aside from "ACLS guidelines" dictating such therapies?


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## Summit (Oct 26, 2016)

A blind man sees the narrow pulse pressures in the 100/82. Nobody thinks it is worth mentioning because it is so obvious.

In fact 134/96 is slightly suspicious for dehydration or other CV pathologies, except the rest of the presentation points directly towards a degree of tamponade/effusion since you so graciously give us pulsus paradoxus and low voltage.

The reason I said constrictive pericarditis is because you also gave all the other textbook crap: recent illness, now with chest pain, relieved by leaning forward, PR depression, etc etc etc... it is like reading a powerpoint slide about the classic signs of pericarditis.

OP you are asking a fair number of seasoned providers here p-school scenarios and expecting a p-school response but instead you see a bit of scenarioitis. It is to be expected.


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## Akulahawk (Oct 26, 2016)

Summit said:


> A blind man sees the narrow pulse pressures in the 100/82. Nobody thinks it is worth mentioning because it is so obvious.
> 
> In fact 134/96 is slightly suspicious for dehydration or other CV pathologies, except the rest of the presentation points directly towards a degree of tamponade/effusion since you so graciously give us pulsus paradoxus and low voltage.
> 
> ...


I was initially thinking along the same lines too until I got to the second part of the presentation but tamponade was also high on the list of what was wrong with this patient. Given that the patient developed a 2nd degree, type II AVB, I would probably have foregone anything along the lines of atropine and instead set up for immediate TCP if the patient converted into a 3rd degree or became symptomatic.

OP: I also have to echo Summit here too. While this forum does have a few knuckle dragging paramedics and EMT's, there are only a few here. Most of us are reasonably seasoned, some of us are ICU and ED nurses in addition to having prehospital experience. Then there are those experienced prehospital-only folks that think well beyond the usual p-school level.


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## bakertaylor28 (Oct 26, 2016)

My reasoning for atropine is based on the line of reasoning here: https://acls-algorithms.com/rhythms/second-degree-heart-block-type-2/


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## NomadicMedic (Oct 26, 2016)

Redacted to prevent a ban.


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## bakertaylor28 (Oct 26, 2016)

Summit said:


> A blind man sees the narrow pulse pressures in the 100/82. Nobody thinks it is worth mentioning because it is so obvious.
> 
> In fact 134/96 is slightly suspicious for dehydration or other CV pathologies, except the rest of the presentation points directly towards a degree of tamponade/effusion since you so graciously give us pulsus paradoxus and low voltage.
> 
> ...



Yes, but the thing is that it never hurts to re-enforce the basics, regardless of how seasoned one is. Especially given what seems to the tendency not to consider tamponade in the field as a realistic viable cause in non-trauma cases, from what I've been told, anyways.


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## Akulahawk (Oct 26, 2016)

bakertaylor28 said:


> My reasoning for atropine is based on the line of reasoning here: https://acls-algorithms.com/rhythms/second-degree-heart-block-type-2/


Read this very closely from that page: 





> Second-degree AV block (Type 2) should be treated with immediate transcutaneous pacing or transvenous pacing because there is risk that electrical impulses will not be able to reach the ventricles and produce ventricular contraction. Atropine may be attempted if immediate TCP is not available or time is needed to initiate TCP. Atropine should not be relied upon and in the case of myocardial ischemia it should be avoided.


When I first started working in the field, TCP wasn't universally available. Now, unless you're working for a company that's still stuck in the stone age and can't afford a a now ancient LP-10, all ALS field providers will have TCP available along with atropine. I guarantee that I can rip out, apply, and plug-in TCP pads faster than I can start a line and administer 0.5 mg atropine and I'm no slouch at starting IV lines.


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## Handsome Robb (Oct 26, 2016)

bakertaylor28 said:


> My reasoning for atropine is based on the line of reasoning here: https://acls-algorithms.com/rhythms/second-degree-heart-block-type-2/



Can you explain the mechanism of action of atropine the the pathphysiology behind a second degree Mobitz II block outside of saying "ACLS says so."

Even if this kid was in a CHB I wouldn't pace him. His hemodynamically stable, I'd be setup to pace him if he became unstable but truly he needs an echo, labs, cultures and more than likely a pericardiocentesis. I can do the pericardiocentesis but he'd have to be peri-arrest for me to do it. I could call but no doc is going to give me that order for someone who isn't hemodynamically compromised. 


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## bakertaylor28 (Oct 26, 2016)

Akulahawk said:


> I was initially thinking along the same lines too until I got to the second part of the presentation but tamponade was also high on the list of what was wrong with this patient. Given that the patient developed a 2nd degree, type II AVB, I would probably have foregone anything along the lines of atropine and instead set up for immediate TCP if the patient converted into a 3rd degree or became symptomatic.
> 
> OP: I also have to echo Summit here too. While this forum does have a few knuckle dragging paramedics and EMT's, there are only a few here. Most of us are reasonably seasoned, some of us are ICU and ED nurses in addition to having prehospital experience. Then there are those experienced prehospital-only folks that think well beyond the usual p-school level.



By the way, HOW IS IT, pray-tell that a patient with significant chest pain and a somewhat low O2 sat with a Mobitz II NOT "symptomatic"?


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## bakertaylor28 (Oct 26, 2016)

Akulahawk said:


> Read this very closely from that page:
> When I first started working in the field, TCP wasn't universally available. Now, unless you're working for a company that's still stuck in the stone age and can't afford a a now ancient LP-10, all ALS field providers will have TCP available along with atropine. I guarantee that I can rip out, apply, and plug-in TCP pads faster than I can start a line and administer 0.5 mg atropine and I'm no slouch at starting IV lines.


But for the fact by the time it becomes necessary in the hypothetical situation, you already have your IV line in, and your fixing to load up for transport. It would seem that it would be faster to get to your drug box and draw the atropine than it would be to jack with the necessary steps on your defribrillator, etc. to set up TCP.


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## Summit (Oct 26, 2016)

bakertaylor28 said:


> By the way, HOW IS IT, pray-tell that a patient with significant chest pain and a somewhat low O2 sat with a Mobitz II NOT "symptomatic"?



CP is not new. You didnt' state that it changed. You didn't state anything changed except the rhythm and BP, 93% is not profound hypoxia and we already put O2 on them.

It is a communication disconnect for you as a student to expect us to then either assume it changed, or ask about it, when we are all thinking "if something else changed he would mention it because all other information has been handed on a silver platter." THAT is a perfect example of scenarioitis.

More to the point, once you are out in the real world more, you will see vitals and rhythms that scream "treat me aggressively" or even "this patient should be unconscious or dead." And yet they are asymptomatic chatting away even walking around. Perhaps with experience, your arrogance will subside.


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## bakertaylor28 (Oct 26, 2016)

Summit said:


> CP is not new. You didnt' state that it changed. You didn't state anything changed except the rhythm and BP, 93% is not profound hypoxia and we already put O2 on them.
> 
> It is a communication disconnect for you as a student to expect us to then either assume it changed, or ask about it, when we are all thinking "if something else changed he would mention it because all other information has been handed on a silver platter." THAT is a perfect example of scenarioitis.
> 
> More to the point, once you are out in the real world more, you will see vitals and rhythms that scream "treat me aggressively" or even "this patient should be unconscious or dead." And yet they are asymptomatic chatting away even walking around. Perhaps with experience, your arrogance will subside.



The thing is that at least within my line of thought- a Mobitz II is rarely going to remain stable- for long. Without some intervention, I would expect to see 3rd degree AVB, the question really being exactly when-  So it would seem that you would be waiting for the foot to drop, as opposed to trying to at least get to a place to where your dealing with wenkebach. (which to me would seem to be a measure of enough insurance.) Pericardiocentisis in the prehospital setting would seem to be rather extreme and a last ditch line of thought, given the fact that its best done with ultrasound guidance.


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## Akulahawk (Oct 26, 2016)

bakertaylor28 said:


> But for the fact by the time it becomes necessary in the hypothetical situation, you already have your IV line in, and your fixing to load up for transport. It would seem that it would be faster to get to your drug box and draw the atropine than it would be to jack with the necessary steps on your defribrillator, etc. to set up TCP.


I hate to tell you this but by the time I'm "fixing to load" with a patient that's got me thinking "problem", the patient is already on a monitor and has the pacer pads in place, and has an IV line in place. In less time than it takes me to ready some atropine, I've already flipped the switch over to "pace" and have set the rate... I'm a big believer in having EVERYTHING in place before transport unless something makes me move very, very quickly. My typical scene time is between 8 and 12 minutes. From the outset this patient would have me worried enough about him that I'd have already put pacer pads on him. It's rare for me to do it but it's what I'd do with him. Would I start a line? Sure. Anybody that I'm worried about enough to put on monitor is already considered sick enough to get a line. 

Again, that also goes back to the 2nd degree type 2 block and atropine. At best it's a temporary measure because something else is going on that is making the AV node drop beats. Speeding up the SA node may not help the AV node much. Thus I'll withhold it and speed up the entire heart (pacing) if the patient's condition warrants it.


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## VentMonkey (Oct 26, 2016)

Op, clearly you're not being validated, which is fine, but when you join an online forum you should really try being much more opened minded. So, do as you please, but in all fairness you got many replies, perhaps not the ones you'd hoped or wished.

The folks that have taken the time to offer up their opinions (myself not included*), are all very well versed, and seasoned professionals, as @Summit so graciously pointed out early.

Humbled is the man who falls before humility.

*I am hardly a professional.


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## VFlutter (Oct 26, 2016)

Who cares about the bradycardia? Is increasing his heart rate going to improve his hemodynamics with tamponade physiology?


Interesting....
https://www.karger.com/Article/Pdf/173266


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## VentMonkey (Oct 26, 2016)

Chase said:


> Who cares about the bradycardia? Is increasing his heart rate going to improve his hemodynamics with tamponade physiology?


This, op...THIS.


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## Tigger (Oct 26, 2016)

bakertaylor28 said:


> 100/82 doesn't ring the bell of a slightly low pulse pressure???


Well you asked what the treatment would be, not what we thought about the vitals. To me, based upon the scenario there are two top potential issues, some sort of carditis or some sort of ACS event. Or both. But really, what are we going to do with either treatment wise?


bakertaylor28 said:


> By the way, HOW IS IT, pray-tell that a patient with significant chest pain and a somewhat low O2 sat with a Mobitz II NOT "symptomatic"?


Still not sure atropine is the treatment of choice here. It may do nothing. It might work. It might also needlessly increase MVO2 demand.


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## Handsome Robb (Oct 26, 2016)

I'm still waiting for you to explain the mechanism of action of atropine and the pathphysiology of a 2* Mobitz II heart block. 

How do you figure atropine will turn a 2* Type I into a 2* Type I block? 

It's far faster to turn a knob and hit "start pacing" then increase The energy setting than it is to get the drug box, open it, get the atropine, open the atropine, assemble the prefill, push the medication, get a flush, open the flush and push the flush. 

For the record, heart blocks aren't always unstable. I have a close friend who lives with an intermittent complete heart block. He's in his mid 20s healthy as a horse and a hardcore athlete. 

I know in medic school they teach you that everyone is dying and needs intervention now but truly the most difficult part of being a good paramedic is knowing when not to intervene and to just sit back and monitor.


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## Gurby (Oct 26, 2016)

VentMonkey said:


> Obviously he should be seen by a cardiologist so this is your transport destination. I am not upgrading unless he becomes an unstable and sustained high degree HB; all I got for now.



"not upgrading" meaning you don't go lights and sirens with this patient, who just went into a heart block and whose BP just dropped 30 points in front of your eyes?  



bakertaylor28 said:


> Interesting. Any particular reason your not considering atropine per the ACLS guidelines for symptomatic bradycardias ?



Patient is symptomatic, and patient is bradycardic.... But patient does not have "symptomatic bradycardia".


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## VentMonkey (Oct 26, 2016)

Summit said:


> Perhaps with experience, your arrogance will subside.


...I think this riiiight here sums it up quite well.


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## VFlutter (Oct 26, 2016)

OP you seem to be missing the forest for the trees...

You are fixated on this hypothetical patient's bradycardia as he is approaching impending cardiac collapse for which you have no intervention. You clearly point out textbook late signs of tamponade, whether it be an effusion and/or CP, yet continue to focus on interventions that will not improve that physiology. You failed to state any intervention you can provide that would do so.

Tachycardia is an early compensation to maintain cardiac output in response to decreasing filling pressure. When you get to the point of pulsus paradoxus  and narrowing pulse pressures you have past the point of compensation, you have equalizing cardiac pressures. You can not fix extrinsic compression. You can maximize intravascular volume, these patients are extremely sensitive to hypovolemia, and assist inotropy.

You seem to have much to learn. You are picking textbook arguments with clinicians whom have treated these patients in the real world and whom have years of diverse and exceptional experience. I was guilty of this when I was a new provider, I thought I knew it all. You will get your *** handed to you and you will truly learn what it means to be humble, hopefully not at the expensive of a patients life.  

It is a great learning experience when you see a patient in true tamponade with a Swan and Art line.


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## VentMonkey (Oct 26, 2016)

Chase said:


> It is a great learning experience when you see a patient in true tamponade with a Swan and Art line.


Very well, and articulately stated, @Chase but I am afraid we're all but falling on deaf ears here.

As far as your clinical experience goes with these patients, when, or at what point would they be candidates for a pericardial window?


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## bakertaylor28 (Oct 26, 2016)

Chase said:


> OP you seem to be missing the forest for the trees...
> 
> You are fixated on this hypothetical patient's bradycardia as he is approaching impending cardiac collapse for which you have no intervention. You clearly point out textbook late signs of tamponade, whether it be an effusion and/or CP, yet continue to focus on interventions that will not improve that physiology. You failed to state any intervention you can provide that would do so.
> 
> ...



The thing is that there's not MUCH your going to do prehospital in terms of address a tamponade short of pericardiocentesis, which isn't a prehospital option 95 percent of the time or better. (i.e. absent the imediate threat of a code if you don't)  Since the tamponade is most likely CAUSING the AVB, it would seem then your best option is to address the brady and keep it on ice, since the tamponade is likely to cause the AVB to continue to progress, and it would seem to follow that you'll get stuck doing the pericardiocentesis under sub-optimal conditions (i.e. without ultrasound guidance) anyways, which is what you want to AVOID in the first place, is it not? 

Though, The point of maximizing volume as a strategy also seems to make sense- an alternate ends to the same means, though it would follow that by increasing volume as opposed to rate your going to end up with the effusion getting larger in response to the volume increase (given the intracellular fluid dynamics- the effusion is getting its volume from somewhere in Short order), and thus my first instinct would be to avoid increasing volume, but rather increase rate- since in reality there cannot be a true hypovolemic state, since there's no fluid loss, If I remember correctly. 

And FYI, I am not arrogant- I am just of the sort that does not believe in departing from the ACLS guidelines without a clear line of thought for doing so, that is going to be 100 per cent justifiable in the event it hits the fan, and I find myself holding the cookie bag and explaining. It just seems much more difficult for someone to sue when your backed up with following standard protocol, as opposed to a line of thought that makes sense but still leaves you holding the cookie bag at the end of the day. I mean, really, do you want some attorney reading in your report that you DIDN'T follow an applicable standard protocol?


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## VFlutter (Oct 26, 2016)

VentMonkey said:


> As far as your clinical experience goes with these patients, when, or at what point would they be candidates for a pericardial window?



It really depends on the underlying cause of the effusion. Pericardiocentesis is the treatment for an effusion with acute hemodynamic compromise. Pericardial windows are more for recurrent or complex effusions. For instance patients with malignant effusions may initially get drained and then get a window when stable to prevent future issues. Constrictive pericarditis may end up with a pericardiectomy. The decision on when to perform a pericardiocentesis is really dependent on the physician but usually hypotension with RA/RV collapse on echo gets drained.


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## Gurby (Oct 26, 2016)




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## Handsome Robb (Oct 26, 2016)

bakertaylor28 said:


> The thing is that there's not MUCH your going to do prehospital in terms of address a tamponade short of pericardiocentesis, which isn't a prehospital option 95 percent of the time or better. (i.e. absent the imediate threat of a code if you don't)  Since the tamponade is most likely CAUSING the AVB, it would seem then your best option is to address the brady and keep it on ice, since the tamponade is likely to cause the AVB to continue to progress, and it would seem to follow that you'll get stuck doing the pericardiocentesis under sub-optimal conditions (i.e. without ultrasound guidance) anyways, which is what you want to AVOID in the first place, is it not?
> 
> Though, The point of maximizing volume as a strategy also seems to make sense- an alternate ends to the same means, though it would follow that by increasing volume as opposed to rate your going to end up with the effusion getting larger in response to the volume increase (given the intracellular fluid dynamics- the effusion is getting its volume from somewhere in Short order), and thus my first instinct would be to avoid increasing volume, but rather increase rate- since in reality there cannot be a true hypovolemic state, since there's no fluid loss, If I remember correctly.
> 
> And FYI, I am not arrogant- I am just of the sort that does not believe in departing from the ACLS guidelines without a clear line of thought for doing so, that is going to be 100 per cent justifiable in the event it hits the fan, and I find myself holding the cookie bag and explaining. It just seems much more difficult for someone to sue when your backed up with following standard protocol, as opposed to a line of thought that makes sense but still leaves you holding the cookie bag at the end of the day. I mean, really, do you want some attorney reading in your report that you DIDN'T follow an applicable standard protocol?



Following my MDs SOCs we wouldn't treat this guy with atropine. We wouldn't pave him either and if I did pace him he'd get a bunch of ketamine first. Because of the tamponade your ventricular filling sucks, speeding the rate can further impair your ventricular filling which can potentially worsen his hemodynamically status. I'll go back to what I said before, knowing when to not do something is the marker of a good provider. 

I'm still interested to hear how atropine is going to change a Mobitz II to a Mobitz I block. 

ACLS isn't the end-all-be-all. Just like for SVT we do adenosine 12mg repeated once then no more which is different than ACLS recommendations as well. Increase or decrease our dose 50% if they take certain home medications. 




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## VentMonkey (Oct 26, 2016)

Op, you are coming across as _very _arrogant, but before this becomes some over heated "debate" or goes somewhere it really shouldn't, you should, again try actually listening to A) yourself, and B) others on here.

Would you care to share your clinical background? You seem very hung up on ACLS guidelines, and now attorneys, and lawsuits being tied to them? 

What if my protocols don't parallel ACLS guidelines? How does that make for a lawsuit waiting to happen? I am also not a lawyer, but I would like to think I have enough common sense, and confidence in how I perform my tasks to work through a PCR that would potentially be plastered on a giant projector screen for an entire court room to see.

@Handsome Robb has asked at least twice that I can see, a valid question...with no reply. 

Others have fed you clinical pathologies, treatments, and reasoning quite well I might add. I don't see what point you are trying to prove here.

No one else agrees with giving Atropine and has given their logical explanations, get over it; you're not convincing anyone otherwise. 

Perhaps you will have better luck with another scenario. What else is it you think a paramedic should be doing aside from what's already been mentioned in this settting?


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## FLdoc2011 (Oct 26, 2016)

I wouldn't give this atropine or be too worried about a HR in mid 40's at this point.   Based on the description he's in tamponade or about to be and about the only you can do at this point is give fluid.  So open up the fluid and get him in.   Don't limit the fluids thinking it's just going to go into the pericardial space, he's pre-load dependent at this point.


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## TXpeds16 (Oct 27, 2016)

I read through some of the responses OP, and one piece of advice I can give you; symptomatic does not always = unstable.

With the given scenario my first thought would be peri/myo/endocarditis.  At my service we would have been 25-35 minutes to a tertiary center with full cardiac support, and thats what he needs.  There is not much to do in the field for treatment of this.  Atropine isn't likely to do anything for the 2* block, and unless he becomes lethargic with an increasing AMS, I am not pacing him either.

He would have gotten a line or two and a 250ml challenge to try and increase preload.  I also would have considered trendellenburg, I know its fallen out of favor, but i've had great success with it in many applications.  My thoughts behind it would be to increase preload further without increasing afterload. Other than that, I would have put pads on him, so if further deterioration occurred, pacing is ready to go.


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## bakertaylor28 (Oct 27, 2016)

Handsome Robb said:


> Following my MDs SOCs we wouldn't treat this guy with atropine. We wouldn't pave him either and if I did pace him he'd get a bunch of ketamine first. Because of the tamponade your ventricular filling sucks, speeding the rate can further impair your ventricular filling which can potentially worsen his hemodynamically status. I'll go back to what I said before, knowing when to not do something is the marker of a good provider.
> 
> I'm still interested to hear how atropine is going to change a Mobitz II to a Mobitz I block.
> 
> ...


To Clarify as to how Atropine might deal with a Mobitz II-  First think- what is a mobitz II? Nothing more than a multiple dropped QRS complexes in basic essence- Where wenkebach is nothing more than a prolonged P-R that is progressive in nature until it finally drops a QRS, and then immediately reverts for the moment to sinus rhthymn to continually repeat the process. We also know that Atropine increases ventricular rate- and CAN tend to do so quite fast- with vassoconstriction being the main intermediary, hence Atropine predisposes one to tachyarrythmias if anything. Since 3rd Degree AVB is a brady, It would be parodoxical for Atropine to cause things to go in that direction.The idea is that by increasing ventricular rate- we will covert the Mobitz II toward something in the direction of NSR.

In simplistic terms- Half of the problem with AVBs is that they are bradyarrthymias. (I've YET to see a Mobitz II with a rate that doesn't qualify it as a brady- depending upon how you really want to define it.) Therefore, Atropine solves at leas HALF of the problem. (the other half of the problem being the dropped QRS complexes)

Also, I'm bearing in mind that If we want to increase the output of a pump in a closed system- we do so by two means- either increasing the pressure inside the closed system by making the total volume of that system smaller (vassoconstriction- Atropine) OR by increasing the volume contained in the system. (Normal Saline at a ridiculous rate.) I'm NOT so keen on the later technique because of the fact that over time, its going to jack with the potassium levels- which is NOT GOOD if we don't want the potential for arrest.

On the other hand- if we increase the rate too much we further compromise ventricular filling which we don't want to do if we even THINK we might be dealing with tamponade. Therefore, the idea is to go with just enough atropine to increase the rate to where we want it. The problem is that due to the issues inherent with pharmacology- its going to be extermely difficut to do this- because of the fact that there's no way we consistently predict the patient's sensitivity to the drug, as to be able to determine an absolute linear equation which is what we need, as opposed to an equation that presents itself with a raised variable.


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## Summit (Oct 27, 2016)

OK... now I have to ask... have you ever actually given atropine?


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## bakertaylor28 (Oct 27, 2016)

TXpeds16 said:


> I read through some of the responses OP, and one piece of advice I can give you; symptomatic does not always = unstable.
> 
> With the given scenario my first thought would be peri/myo/endocarditis.  At my service we would have been 25-35 minutes to a tertiary center with full cardiac support, and thats what he needs.  There is not much to do in the field for treatment of this.  Atropine isn't likely to do anything for the 2* block, and unless he becomes lethargic with an increasing AMS, I am not pacing him either.
> 
> He would have gotten a line or two and a 250ml challenge to try and increase preload.  I also would have considered trendellenburg, I know its fallen out of favor, but i've had great success with it in many applications.  My thoughts behind it would be to increase preload further without increasing afterload. Other than that, I would have put pads on him, so if further deterioration occurred, pacing is ready to go.


 
OK now your speaking my language- The thing is that having re-read some posts- some people have taken symptomatic bradycardia to mean unstable bradyardia- in Which case, the philosophy which with I was taught makes the keen distinction between the adjectives- kind of like that irritating group of people that likes to say that cardioversion and defirbrillation are separate things- yet when they say 
"cardioversion" their not telling you that they had impiled the word "synchronized" in front of the term- which then makes the term more "correct" for the process we would be talking about.


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## Gurby (Oct 27, 2016)

bakertaylor28 said:


> To Clarify as to how Atropine might deal with a Mobitz II-  First think- what is a mobitz II? Nothing more than a multiple dropped QRS complexes in basic essence- Where wenkebach is nothing more than a prolonged P-R that is progressive in nature until it finally drops a QRS, and then immediately reverts for the moment to sinus rhthymn to continually repeat the process. We also know that Atropine increases ventricular rate- and CAN tend to do so quite fast- with vassoconstriction being the main intermediary, hence Atropine predisposes one to tachyarrythmias if anything. Since 3rd Degree AVB is a brady, It would be parodoxical for Atropine to cause things to go in that direction.The idea is that by increasing ventricular rate- we will covert the Mobitz II toward something in the direction of NSR.
> 
> In simplistic terms- Half of the problem with AVBs is that they are bradyarrthymias. (I've YET to see a Mobitz II with a rate that doesn't qualify it as a brady- depending upon how you really want to define it.) Therefore, Atropine solves at leas HALF of the problem. (the other half of the problem being the dropped QRS complexes)
> 
> ...



Have you heard of the Dunning-Kruger effect?


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## bakertaylor28 (Oct 27, 2016)

Summit said:


> OK... now I have to ask... have you ever actually given atropine?


A couple of times, actually- and we combined it with TCP practically simultaneously. If I recall correctly, both cases were Mobitz II. Mind you our cart allows much quicker access to the drugs than does having to cope with a drug box. (the nice thing about having a cart- really-  Problem is that in the field you have nowhere to put it.


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## bakertaylor28 (Oct 27, 2016)

Gurby said:


> Have you heard of the Dunning-Kruger effect?



Yeah. Its a syndrome that results in ***some people*** using a defibrillator without having first read the manual. Not naming any names, but we all KNOW who I'm talking about.


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## VentMonkey (Oct 27, 2016)

bakertaylor28 said:


> "In simplistic terms"


Op who do you think you are talking to? 

This forum is for advice, debate, and reason. At this point you're merely talking to hear yourself talk.

I wish you the best of luck once you are actually a _functioning paramedic. _Again, we get it, you would have used Atropine for reasons stated, cool deal. 

Your online peers disagree, many of whom are full fledged seasoned paramedics, and/ OR ED and ICU nurses.

Again, best of luck, but allow me to leave one last bit of food for thought...

http://www.mayoclinic.org/diseases-...ality-disorder/basics/definition/con-20025568


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## bakertaylor28 (Oct 27, 2016)

VentMonkey said:


> Op who do you think you are talking to?
> 
> This forum is for advice, debate, and reason. At this point you're merely talking to hear yourself talk.
> 
> ...


Mind you you should bear in mind that I'm in a MD program NOT a paramedic program.


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## Summit (Oct 27, 2016)

@bakertaylor28

1. Why would you simultaneously pace and give atropine?
2. Have you ever given atropine by itself? How long does it last?
3. You state you want more precise control over effect, what is most likely to provide that in this or any situation, TCP or atropine?
4. You keep beating this atropine drum... can you please provide the literature recommending atropine in Mobitz II? I can find plenty of recommendations against it if TCP is available...
5. This scenario came out of your book. What book is it?
6. What does the book suggest?
7. Please read and respond to one of the best posts in this whole thread:


Chase said:


> OP you seem to be missing the forest for the trees...
> 
> You are fixated on this hypothetical patient's bradycardia as he is approaching impending cardiac collapse for which you have no intervention. You clearly point out textbook late signs of tamponade, whether it be an effusion and/or CP, yet continue to focus on interventions that will not improve that physiology. You failed to state any intervention you can provide that would do so.
> 
> ...


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## VentMonkey (Oct 27, 2016)

bakertaylor28 said:


> Mind you you should bear in mind that I'm in a MD program NOT a paramedic program.


Eh, even scarier IMO cheers.

Perhaps @ERDoc , or @Nova1300 would care to chime in, since we know nothing of the sort.

We are all beneath you, forgive us.


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## VFlutter (Oct 27, 2016)

bakertaylor28 said:


> Mind you you should bear in mind that I'm in a MD program NOT a paramedic program.



Then we should hold you to a higher standard


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## MonkeyArrow (Oct 27, 2016)

bakertaylor28 said:


> Mind you you should bear in mind that I'm in a MD program NOT a paramedic program.


Then why are you on this forum?


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## VentMonkey (Oct 27, 2016)

bakertaylor28 said:


> Mind you you should bear in mind.


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## Summit (Oct 27, 2016)

MonkeyArrow said:


> Then why are you on this forum?


apparently


bakertaylor28 said:


> to re-enforce the basics


Because prehospital folks just don't understand atropine for Mobitz II secondary to tamponade and need remediation by a MS2.


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## NomadicMedic (Oct 27, 2016)

This HD been troll bait since the beginning.
As I said before (and then redacted to avoid a ban) this is the stuff that SDN is famous for.


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## VentMonkey (Oct 27, 2016)




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## FLdoc2011 (Oct 27, 2016)

I'm not really sure what all the above means and not sure if really trolling or just thinking too much into things.

Anyway,  I would say get this guy to a hospital that has cardiac services, start on aggressive IV fluids and bolus if need be and just monitor his heart rate for now.  If you want to place pads in case things go south that's fine to though I would just watch his HR and rhythm for now.    Being that young the statistics point away from significant infra-Nodal conduction disease so this could just be vagally induced at the AV node level.


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## VentMonkey (Oct 27, 2016)

FLdoc2011 said:


> start on aggressive IV fluids and bolus if need be


Fair enough, but may I ask what your reasoning for _aggressive IV fluids _continues to be? I understand them being heavily preload dependent, bur by no means will this be a life-saving measure...

http://ether.stanford.edu/library/cardiac_anesthesia/Cardiology/Acute Cardiac Tamponade.pdf


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## bakertaylor28 (Oct 27, 2016)

Summit said:


> @bakertaylor28
> 
> 1. Why would you simultaneously pace and give atropine?
> 2. Have you ever given atropine by itself? How long does it last?
> ...



Support for atropine to convert Mobitz II can be found here: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2884443/  Supression of the SA node is usually the most direct origin of AVBs, within the sense of electro-physiology.  In the case of a tamponade, the SA node becomes supressed due to homostasis as the heat wants to drop its rate, because the nervous system percieves that pressure has increased when it hasn't- which is one of the direct effects of the tamponade itself. 

As for simutenously pacing and giving atropine- the reason I was given by the attending (considering that I was asking the same question at the time.) is because it MAY allow for a lesser need for pacing in the long-run. 

The scenario came out of Cardiology for the Paramedic, 2nd Ed. by Michelle Kuntz, (1987) which is now out of publication. 
The book's solution is to continue to monitor, to consider appropriate interventions for symptomatic bradycardia, and to consider 
pericardiocentesis if the patient deteriorates into 3rd degree AVB. 

As for a response to the post, I will reiterate that converting a Mobitz-II in and of itself will improve cardiac output, because of the fact your increasing the frequency of QRS complexes. This is a short term goal in any case where Mobitz-II presents as such.


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## VentMonkey (Oct 27, 2016)

bakertaylor28 said:


> *The scenario came out of Cardiology for the Paramedic, 2nd Ed. by Michelle Kuntz, (1987) which is now out of publication.*


Op, I think we found our disconnect.


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## VFlutter (Oct 27, 2016)

VentMonkey said:


> Op, I think we found our disconnect.



I wasn't even born yet


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## gotbeerz001 (Oct 27, 2016)

bakertaylor28 said:


> Yeah. Its a syndrome that results in ***some people*** using a defibrillator without having first read the manual. Not naming any names, but we all KNOW who I'm talking about.



Do we? I made a comment about reading the manual... Are you talking about me?


Sent from my iPhone using Tapatalk


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## FLdoc2011 (Oct 27, 2016)

VentMonkey said:


> Fair enough, but may I ask what your reasoning for _aggressive IV fluids _continues to be? I understand them being heavily preload dependent, bur by no means will this be a life-saving measure...
> 
> http://ether.stanford.edu/library/cardiac_anesthesia/Cardiology/Acute Cardiac Tamponade.pdf



Well no,  never said it's a definitive treatment but aside from an emergent pericardiocentesis (whether pre-hospital or in the hospital) it's one of the only few things y'all can do in the field.   I'm not talking about flooding them with 2L but give them a 500ml bolus or something to see if hemodynamics improve a bit while they're waiting for definitive treatment.    Not much good data either way on it and yea, I'm sure you'll read all sorts of opinions in the literature about it but practically I'd say that's how a lot of us approach it while we're waiting for either the tap or a surgical window.


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## Handsome Robb (Oct 27, 2016)

gotshirtz001 said:


> Do we? I made a comment about reading the manual... Are you talking about me?
> 
> 
> Sent from my iPhone using Tapatalk



You and me both. 




Sent from my iPhone using Tapatalk


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## ERDoc (Oct 27, 2016)

Sometimes the best thing to do is to do nothing.  People can remain in Mobitz II for long periods without being unstable.  The dude needs a pericardiocentesis so the best thing to do is get him to the ER quickly and safely.


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## VentMonkey (Oct 27, 2016)

FLdoc2011 said:


> Based on the description he's in tamponade or about to be and about the only you can do at this point is give fluid.  So open up the fluid and get him in.   Don't limit the fluids thinking it's just going to go into the pericardial space, he's pre-load dependent at this point.


I think given that you had initially mentioned this, I was under the impression that you were willing to dump fluids in liberally without regard.


FLdoc2011 said:


> Well no,  never said it's a definitive treatment but aside from an emergent pericardiocentesis (whether pre-hospital or in the hospital) it's one of the only few things y'all can do in the field.   I'm not talking about flooding them with 2L but give them a 500ml bolus or something to see if hemodynamics improve a bit


But ultimately it would appear that our thought processes are along the same vein. I jwas simply curious, cheers.


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## VentMonkey (Oct 27, 2016)

ERDoc said:


> Sometimes the best thing to do is to do nothing.


...in the words of a practicing EM physician, thanks doc!


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## FLdoc2011 (Oct 27, 2016)

VentMonkey said:


> I think given that you had initially mentioned this, I was under the impression that you were willing to dump fluids in liberally without regard.
> 
> But ultimately it would appear that our thought processes are along the same vein. I jwas simply curious, cheers.



No problem.  I was mainly trying to to bring it back to some sort of practical discussion given some of the earlier posts, lol.     Don't always have something to add but this happened to be in my field and deal with it not infrequently.


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## bakertaylor28 (Oct 29, 2016)

gotshirtz001 said:


> Do we? I made a comment about reading the manual... Are you talking about me?
> 
> 
> Sent from my iPhone using Tapatalk


 
You really have to ask? I was referencing members of the male sex in general- whom rarely read an instruction manual and then WONDER how it is that they end up on an episode of home improvement opposite Al. (a dated reference I know- but for lack of a better one.)


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## bakertaylor28 (Oct 29, 2016)

FLdoc2011 said:


> No problem.  I was mainly trying to to bring it back to some sort of practical discussion given some of the earlier posts, lol.     Don't always have something to add but this happened to be in my field and deal with it not infrequently.


Interesting... Maybe you should consider proctology as a secondary sub? You seem to have the personality for it. just a thought....lol ;-)


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## Nova1300 (Nov 1, 2016)

VentMonkey said:


> Eh, even scarier IMO cheers.
> 
> Perhaps @ERDoc , or @Nova1300 would care to chime in, since we know nothing of the sort.
> 
> We are all beneath you, forgive us.



Thus far, this thread has only left my head spinning.


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## bakertaylor28 (Nov 4, 2016)

Chase said:


> I wasn't even born yet



Yeah and whats more is that the older materials didn't even THINK about going into the territory of subjective decision making- i.e. where they present an technically O.K. answer and then a "regarded to be correct" answer on the tests, because in the 70's and 80's a medic relied on medical direction for EVERYTHING.  We started migrating to our present form of things in the late 80s and early 90s. Back in the 70s Paramedic training had more of the emphasis of HOW to do things Vs. Subjective Reasoning of WHEN to do things. Hence, there was a medical order for every time you pushed a drug, defibrillation actually required that the ecg be transmitted first, ect. in the Early 80s the current notion of things were being developed as cohesive training methods, and were beginning to be implemented in the field with resistance from some (whom probably saw the paramedic as mounting a status challenge to the M.D. at the time given that the separation of the two were in a bit of a flux at the time) starting around 1985 or so. The early 90s saw a steep learning curve for out of hospital treatment providers- as the transition to our current state of things was full throttle at that point.


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## MonkeyArrow (Nov 4, 2016)

bakertaylor28 said:


> defibrillation actually required that the ecg be transmitted first,


Source?


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## NomadicMedic (Nov 4, 2016)

MonkeyArrow said:


> Source?


 
Any retelling of paramedic history.  The development of telemetry for space missions is what led to telemetry transmission to allow defibrillation in the field by paramedics.

 That's actual and factual. I'll be happy to pull up some sources for you later on, but that's all truth


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