Chest Pain Case

[bakertaylor28]

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.

 

[Summit]

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.

 

[bakertaylor28]

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.

 

[Akulahawk]

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.

 

[VentMonkey]

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.

 

[VFlutter]

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

 

[VentMonkey]

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

This, op...THIS.

 

[Tigger]

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?

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.

 

[Handsome Robb]

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]

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?

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".

 

[VentMonkey]

Perhaps with experience, your arrogance will subside.

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

 

[VFlutter]

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.

 

[VentMonkey]

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?

 

[bakertaylor28]

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.

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?

 

[VFlutter]

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.

 

[Gurby]

 

[Handsome Robb]

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]

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?

 

[FLdoc2011]

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.

 

[TXpeds16]

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.