Chest Pain Case

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.

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

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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Have you heard of the Dunning-Kruger effect?
 
Summit said:
OK... now I have to ask... have you ever actually given atropine?
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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.
 
Gurby said:
Have you heard of the Dunning-Kruger effect?
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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.
 
bakertaylor28 said:
"In simplistic terms"
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:confused: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
 
VentMonkey said:
:confused: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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Mind you you should bear in mind that I'm in a MD program NOT a paramedic program.
 
@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.

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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bakertaylor28 said:
Mind you you should bear in mind.
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IMG_2215.JPG
 
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.
 
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.
 
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?
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:
Click to expand...

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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