# Axis deviation and the 12 lead



## rhan101277 (Mar 7, 2010)

We are getting into the more complicated 12 lead details.  Beyond the easy, tell where the MI is and what artery could be occluded.

Anyhow, many medics I talk to say they don't look at this.  It is extremely important though as lidocaine is contraindication in hemiblocks and LBBB or RBBB.  I am going to use all my knowledge to do the best I can in the field, regardless if others get grumpy because I don't do things the easy way.

Same goes with chest pain, when i asked one about right versus left side MI, he said I just give nitro like the protocols say.  But right MI needs fluids, if you give nitro you can make them worse off and be at their funeral.  Same goes with giving lidocaine in bradycardia or the blocks above which I previously listed or any 2nd degree or complete HB.

Seems like many medics I talk to, just blow this stuff off, like it won't happen to them.

Just wanted to blow off some steam about it.  Some medics seem to not take patient care seriously and I think it is a problem in EMS.


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## Shishkabob (Mar 7, 2010)

Just as an FYI, you can determine RBBB and LBBB without looking at axis deviation.


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## reaper (Mar 7, 2010)

If you get a chance, go to a Bob Page seminar. You will be very enlightened.


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## rmellish (Mar 7, 2010)

Right sided MIs typically respond well to fluid boluses, so they're exactly right, give nitro per protocol. Just be conservative with dosing, and be prepared to bolus. nitro can still be beneficial. This is also why it pays to have your IV access prior to dosing someone with nitro.


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## medic417 (Mar 7, 2010)

reaper said:


> If you get a chance, go to a Bob Page seminar. You will be very enlightened.



That ain't no lie.  You will find out most of what you have been taught is not very reliable.  He shows you how to raise the odds of catching items that could cost patients their lives if you miss them.  Well worth the money.


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## rhan101277 (Mar 7, 2010)

rmellish said:


> Right sided MIs typically respond well to fluid boluses, so they're exactly right, give nitro per protocol. Just be conservative with dosing, and be prepared to bolus. nitro can still be beneficial. This is also why it pays to have your IV access prior to dosing someone with nitro.



Thanks for your input.  I am being taught to just use it judiciously, but can't really use it judiciously when its .4mg SL per dose.  Maybe IV nitro is better since it is less powerful than SL.  I will do whatever is best for the patient though.  If I don't give nitro and I am wrong then I am screwed.  I will just be ready for a bolus.


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## ah2388 (Mar 7, 2010)

in right sided MI's you can also give low dose dopamine to up the patients pressure in addition to fluid boluses so that you can give NTG


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## reaper (Mar 7, 2010)

If you identify a RVI, I will bolus first, then nitro. Once you bottom the pressures, they can be very hard to bring back. It's like chasing your tail!


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## Shishkabob (Mar 8, 2010)

ah2388 said:


> in right sided MI's you can also give low dose dopamine to up the patients pressure in addition to fluid boluses so that you can give NTG



Low dose dopamine dialates renal vessels and has little/no effect on systemic circulation.  Mid-dose has B1 and B2 effects, but that's not a good thing when it comes to MI... you dont want to increase myocardial workload in a situation where it already isn't getting enough oxygen.  High-dose dopamine is where the vasoconstriction lies, but again, you're causing excess work on an injured heart.

Dopamine / Nitro ping-pong is not a good thing.  



It depends on your protocols, but usually around here, give ASA, then bolus NS up to 1l to get a decent BP before giving a vasodialator, and confer with med control.


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## reaper (Mar 8, 2010)

Bingo! We have a winner! Tell him what he wins, Wink.


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## EMTinNEPA (Mar 8, 2010)

rhan101277 said:


> Thanks for your input.  I am being taught to just use it judiciously, but can't really use it judiciously when its .4mg SL per dose.  Maybe IV nitro is better since it is less powerful than SL.  I will do whatever is best for the patient though.  If I don't give nitro and I am wrong then I am screwed.  I will just be ready for a bolus.



I'm not sure how far along you are in school, so if I seem preachy and I'm telling you something you already know, forgive me.

It's not that the IV nitro is less powerful, it's just a much smaller dose.  MUCH smaller dose as in MICROgrams.  Nitro drips are good for maintenance, but in the setting of pre-hospital treatment for Acute Coronary Syndromes, you might as well have brought a toothpick to a gunfight.

What happens with giving nitro to right-sided MIs is nitro causes vasodilation, which decreases peripheral vascular resistance and in turn cardiac workload... however, it also decreases blood pressure and venous return, which in turn decreases preload, which decreases cardiac output.  This is why you always want to have a patent IV line before you administer nitro to an inferior wall MI, because if their pressure craps out, you might not be able to get an IV.  This is also why you always check a blood pressure before repeat doses.


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## zmedic (Mar 9, 2010)

Also keep in in mind that there isn't good evidence that nitro decreases mortality. Aspirin and Beta blockers are the only two pre hospital meds that have been shown to do that. So the real question is why are you playing with fire, trying to give nitro to a right sided MI? I think that for CYA that is a good time to call online medical control and say "we have big elevations in II, III, AvF, did a V4R and think it's a right sided MI. Pressure is 110/70, should I give nitro because I'm worried about bottoming out the patient's pressure."


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## usalsfyre (Mar 11, 2010)

I can't find the citation right now, but I believe the American College of Cardiology is reccomending against using *ANY* NTG in the setting of RVI. 

IV NTG is not bringing a toothpick to a gun fight, it's just usually underdosed in the prehospital setting. 400  mcgs SL every 5 minutes with a 75% absporption rate (the usual figure for SL) is roughly 60mcgs/min. How many folks are scared to take their IV NTG doses that high?


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## TomB (Mar 11, 2010)

usalsfyre -

If you can find the citation, I'd love to see it. I think of RVI as a relative contraindication rather than an absolute.

If anyone is interested there is a comprehensive tutorial on axis determination that you can find HERE.

Tom


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## usalsfyre (Mar 12, 2010)

It's here in the "ACC/AHA Guidelines for the Management of Patients With
ST-Elevation Myocardial Infarction" located at http://www.acc.org/qualityandscience/clinical/guidelines/stemi/STEMI Full Text.pdf

Check page E35, it places NTG as a class III(Conditions for which there is evidence and/or general agreement that a procedure/treatment is not useful/effective and in some cases may be harmful)for suspected right ventricular infarction.


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## reaper (Mar 12, 2010)

Funny, I was at a cardiac seminar and all 5 cardiologists there said "Do not withhold NTG", But also stated that Fluid boluses are a must. We are not talking 500-1000cc's, they are talking 2-3 liters. 

They talked about RVI Pt's going to Cath lab. Some are getting up to 15-20 liters, prior to procedure!


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## AnthonyM83 (Mar 12, 2010)

Linuss said:


> Low dose dopamine dialates renal vessels and has little/no effect on systemic circulation.  Mid-dose has B1 and B2 effects, but that's not a good thing when it comes to MI... you dont want to increase myocardial workload in a situation where it already isn't getting enough oxygen.  High-dose dopamine is where the vasoconstriction lies, but again, you're causing excess work on an injured heart.
> 
> Dopamine / Nitro ping-pong is not a good thing.
> 
> ...



Would you say the same for CHF'ers? With pulmonary edema, you're having left-side failure, but one would assume right-side would go along with it (especially if Pedal edema and JVD). Being limited in amount of fluids you'd give in this case (and not a STEMI) would you give the dopamine even with its effects effects on the failing heart?

Just looking for opinions on this. Heard some differing ones....


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## usalsfyre (Mar 12, 2010)

reaper said:


> Funny, I was at a cardiac seminar and all 5 cardiologists there said "Do not withhold NTG", But also stated that Fluid boluses are a must. We are not talking 500-1000cc's, they are talking 2-3 liters.
> 
> They talked about RVI Pt's going to Cath lab. Some are getting up to 15-20 liters, prior to procedure!



The only thing I would say is, why are we fluid loading (i.e. increasing preload) patients to give an agent that is primarily used to reduce preload? 

I'm not saying don't go withwhat your local standard is, just that the largest group of cardiologist in the country has come to a consensus that it probably won't help and may hurt.


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## usalsfyre (Mar 12, 2010)

AnthonyM83 said:


> Would you say the same for CHF'ers? With pulmonary edema, you're having left-side failure, but one would assume right-side would go along with it (especially if Pedal edema and JVD). Being limited in amount of fluids you'd give in this case (and not a STEMI) would you give the dopamine even with its effects effects on the failing heart?
> 
> Just looking for opinions on this. Heard some differing ones....



Cardiogenic shock is often not caused by fluid overload but rather not being able to move fluid. I wouls still try a *VERY CONSERVATIVE* fluid bolus before jumping to vasoactives. 

Dopamine in the setting of CHF/cardiogenic shock is one of those treatments that might help short term but may kill the patient down the road. Sometimes we've got to do what we can to keep people kicking to the ED and hope any damage we did can be undone.


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## reaper (Mar 12, 2010)

usalsfyre said:


> It's here in the "ACC/AHA Guidelines for the Management of Patients With
> ST-Elevation Myocardial Infarction" located at http://www.acc.org/qualityandscience/clinical/guidelines/stemi/STEMI Full Text.pdf
> 
> Check page E35, it places NTG as a class III(Conditions for which there is evidence and/or general agreement that a procedure/treatment is not useful/effective and in some cases may be harmful)for suspected right ventricular infarction.



I have not had time to read the entire study, but did read E35 and E100. In neither place did it mention that NTG was harmful or not effective in RVI.

It stated the same as any other literature. That NTG may cause hypotension, which is treatable by fluid bolus of NS.

It also states that agressive fluids may be needed and that NTG does help dilate the RCA. That is the main reason why you are giving it in the first place.


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## rhan101277 (Mar 12, 2010)

reaper said:


> Funny, I was at a cardiac seminar and all 5 cardiologists there said "Do not withhold NTG", But also stated that Fluid boluses are a must. We are not talking 500-1000cc's, they are talking 2-3 liters.
> 
> They talked about RVI Pt's going to Cath lab. Some are getting up to 15-20 liters, prior to procedure!



Did you type this in wrong?  15-20 liters prior to procedure?  We only have 6 liters of blood.  As far as surgery goes with bolusing really high, aren't they worried about clotting factors getting to diluted.

Has anyone ever administered some nitro, whatever the case, and seen ischemia go away during a long run to the ER?  Like seeing ST depression clear up.  I know checking patient is best but I'm just asking.


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## reaper (Mar 13, 2010)

No not a typo! They will give upwards of that amount.

I have seen many pt's clear up a STEMI from NTG and ASA. That is why it is important to obtain a 12 lead, prior to any treatments. This way you have the proof it did exist.

Most Cardiologist will take the before and after and base treatment plan off of that.


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## EMTinNEPA (Mar 13, 2010)

It's true.  At school they hammered into us that a 12-lead must be obtained prior to treatment because your initial 12-lead may be the only proof that an infarction is/was occurring, and as such may be the only thing that determines whether the patient goes straight to the cath lab or sits in the ER for a few hours.


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## usalsfyre (Mar 13, 2010)

As far as medications terminating ACS, NSTEMI maybe, UA for sure, but I'm not convinced that many of the "cleared up" STEMIs aren't mimicks. STEMI usually indicates a very high degree of blockage, hence why we bypass the ED and head straight to the cath lab with these folks. Pharmocological agents are not the treatment for STEMIs, PCI is.


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## usalsfyre (Mar 13, 2010)

reaper said:


> I have not had time to read the entire study, but did read E35 and E100. In neither place did it mention that NTG was harmful or not effective in RVI.
> 
> It stated the same as any other literature. That NTG may cause hypotension, which is treatable by fluid bolus of NS.
> 
> It also states that agressive fluids may be needed and that NTG does help dilate the RCA. That is the main reason why you are giving it in the first place.



In the introduction (page e5) it defines a Class III intervention as "Conditions for which there is evidence and/or general agreement that a procedure/treatment is not useful/effective and in some cases may be harmful"

Right off of e35 is 
Class III 
1. Nitrates should not be administered to patients with
systolic blood pressure less than 90 mm Hg or greater
than or equal to 30 mm Hg below baseline, severe
bradycardia (less than 50 beats per minute [bpm]),
tachycardia (more than 100 bpm), or suspected RV
infarction. (Level of Evidence: C)

NTG is no longer thought to have much effect on the coronary vessels, it is primarily a venodilator used to reduce preload. Again I ask, why are we giving an agent used primarily to treat preload if we have to drasticly increase preload to administer it.


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## reaper (Mar 13, 2010)

But, the very article you posted, written by Cardiologists, states that NTG is found to be very affective in Coronary Artery dilation. Which in turns allows more flow?

Research affects of preload increase on RVI.


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## usalsfyre (Mar 14, 2010)

I'm familiar with the effects of increasing preload in RVI. I'm not implying these patients don't need fluid. Many severe RVIs benefit from inotropic support as well. A few (the minority) could benefit from NTG.

I would be VERY hesitant to go around dropping nitrostat under these folks tounges however. At most a conservitave trial of IV NTG might be waranted, as it's much more precise and easier to titrate. I would be hesitant to do this however unless they were boderline hypertensive. You risk taking someone with stable hemodynamics and putting them in cardiogenic shock.

RVIs still benefit from early cathlab activation, O2, ASA, heparin, opiate pain control and immediate treatment of lethal dysrhythmias. I'm just not sure routine use of nitrates is appropriate.


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## reaper (Mar 14, 2010)

A lot of times with RVI, they will wait 2-4 weeks before taking them to the Cath lab. Sometimes it needs to be preformed right away, but a lot of times, they wait.

I used to have the same thinking as you, with NTG in RVI's. Then I started talking to a lot of Cardiologist. Everyone of them pushed for NTG use in RVI. They stated that as long as you are preloading the bolus, the benefits outweigh the risks.


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## TomB (Mar 14, 2010)

usalsfyre said:


> As far as medications terminating ACS, NSTEMI maybe, UA for sure, but I'm not convinced that many of the "cleared up" STEMIs aren't mimicks. STEMI usually indicates a very high degree of blockage, hence why we bypass the ED and head straight to the cath lab with these folks. Pharmocological agents are not the treatment for STEMIs, PCI is.



Just a quick point. You can't "clean up" a mimic with MONA. If it's BER, LVH, LBBB, paced rhythm, and so on, it will remain exactly the same after MONA. So if you "clean up" a ST/T wave abnormality, it almost certainly suggests the dynamic supply vs. demand characteristics of ACS. It's not worth nitpicking whether or not it's NSTEMI or STEMI at that point. It's an acute thrombotic event in an epicardial artery. In my jurisdiction they go to the cath lab emergently, and so far they've always had a culprit artery.

Tom


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## 82-Alpha599 (Mar 14, 2010)

Regarding hemiblocks, other than MONA, how do you treat them. If you call your local hospitals and say what you have do then even know what your talking about. Is a hemiblock considered a STEMI like a new onset LBBB or NSTEMI.


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## rhan101277 (Mar 14, 2010)

82-Alpha599 said:


> Regarding hemiblocks, other than MONA, how do you treat them. If you call your local hospitals and say what you have do then even know what your talking about. Is a hemiblock considered a STEMI like a new onset LBBB or NSTEMI.



That is a good question.  A hemiblock does mean that the current travel is not taking normal pathways and is blocked.  It could lead to dysrhythmias I suppose.  Especially if you had some irritability.


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## TomB (Mar 14, 2010)

Recent evidence suggests that patients with new (previously undetected) LBBB do not rule in for MI at any higher rate than other patients, unless they also meet Sgarbossa's criteria for AMI in the presence of LBBB. Generally speaking LAFB and LPFB (a diagnosis of exclusion that is extremely rare as an isolated finding) do not distort the ST-segment the way LBBB does. If it's a "new" hemiblock secondary to acute STEMI, ST-elevation will also be present.

Tom



82-Alpha599 said:


> Regarding hemiblocks, other than MONA, how do you treat them. If you call your local hospitals and say what you have do then even know what your talking about. Is a hemiblock considered a STEMI like a new onset LBBB or NSTEMI.


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## AnthonyM83 (Mar 15, 2010)

reaper said:


> But, the very article you posted, written by Cardiologists, states that NTG is found to be very affective in Coronary Artery dilation. Which in turns allows more flow?
> 
> Research affects of preload increase on RVI.



As a reminder, the primary reason we give NTG is for the decrease in preload effect. Coronary dilation is a secondary effect.

So, if preload is already low in RVI, you'd be giving it merely for its secondary effects, while putting the patient at risk for decreasing his preload / BP....just for secondary effects. So, the question should be, how "helpful" are those secondary effects?


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## TomB (Mar 15, 2010)

I would say "if preload is already low" in the setting of possible RVI. You have to look at the clinical picture. Not all patients with inferior STEMI have concurrent RVI and not all patients with RVI develop the hypotensive syndrome. Often hypotension and bradycardia in the setting of inferior STEMI is a manifestation of the Bezold-Jarisch reflex (hypervagotonia). So obviously NTG should be used sparingly or not at all if the patient starts out bradycardic and hypotensive. On the other hand, if the patient has an adequate blood pressure, I see no harm in a trial of NTG, expecially if you start and IV first. Like another poster mentioned before, for all you know it's a vasospastic STEMI. Incidentally, I was never taught the primary reason we give NTG for AMI is to reduce preload. Now CHF on the other hand...

Tom


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## The-Reaper (Mar 20, 2010)

Linuss said:


> Low dose dopamine dialates renal vessels and has little/no effect on systemic circulation.  Mid-dose has B1 and B2 effects, but that's not a good thing when it comes to MI... you dont want to increase myocardial workload in a situation where it already isn't getting enough oxygen.  High-dose dopamine is where the vasoconstriction lies, but again, you're causing excess work on an injured heart.
> 
> Dopamine / Nitro ping-pong is not a good thing.
> 
> ...



I fully agree and cant believe anyone would consider dopamine in an MI, that is just like giving some one atropine that is having bradycardia with an MI. Just not a good practice to do


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## TomB (Mar 21, 2010)

The-Reaper said:


> I fully agree and cant believe anyone would consider dopamine in an MI, that is just like giving some one atropine that is having bradycardia with an MI. Just not a good practice to do



I agree with this sentiment. However, there is a tipping point. Finding that tipping point is the mark of a true clinician. If the bradycardia is causing significant hemodynamic instability, the use of atropine may be warranted. Since the hypotension and bradycardia associated with acute inferior STEMI is often a manifestation of the Bezold-Jarisch reflex (hyervagotonia), there's an excellent chance that atropine will improve the patient's circulatory status. The flip-side (as you obviously know) is that the number one determinate of myocardial oxygen demand is heart rate. I'm aware of at least one case report (in Braunwald's Heart Disease) where the administration of atropine led to a reduction in the amount of ST-elevation with acute inferior STEMI. So if the patient is bradycardic and in shock, and a fluid bolus doesn't help, I would consider 0.5 mg atropine, but it certainly wouldn't be a cavalier decision on my part. It's a balance between supply-side ischemia and demand-side ischemia. On the other hand, the "tie" usually goes to doing nothing (first do no harm). Antiarrhythmics are dangerous drugs, and it's a wonder we're allowed to use them at all (for conscious, breathing patients) in light of the relatively shallow educational requirements for paramedics in the United States.

Tom


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## MrBrown (Mar 21, 2010)

TomB said:


> ...Antiarrhythmics are dangerous drugs, and it's a wonder we're allowed to use them at all (for conscious, breathing patients) in light of the relatively shallow educational requirements for paramedics in the United States.



So when can you use amiodarone? We can use it at Paramedic level for cardiac arrest and at Intensive Care level for significantly compromising arrythmia (fast AF or VT)..

That said let's say we pick up nana who is grey, nauseous, screaming chest pain, having reciprocal ST elevation and throwing serious PVCs.  Because we have no online direction here I'd be inclined to hang up some amiodarone but I don't generally have anybody to ask if that's a good idea or not.


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## TomB (Mar 23, 2010)

MrBrown said:


> So when can you use amiodarone? We can use it at Paramedic level for cardiac arrest and at Intensive Care level for significantly compromising arrythmia (fast AF or VT)..
> 
> That said let's say we pick up nana who is grey, nauseous, screaming chest pain, having reciprocal ST elevation and throwing serious PVCs.  Because we have no online direction here I'd be inclined to hang up some amiodarone but I don't generally have anybody to ask if that's a good idea or not.



I guess it's pretty obvious that I'm not a huge fan of prehospital antiarrhythmics. It seems to me that if a tachydysrhythmia is "significantly compromising" then it should be cardioverted. If it's hemodynamically stable, why are we messing with it? We don't know what we're going to get when we push amiodarone. Maybe the patient will get better. Maybe the patient will get worse. The nana who's having a STEMI needs reperfusion, not amiodarone, IMO.

Tom


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## MrBrown (Mar 23, 2010)

TomB said:


> I guess it's pretty obvious that I'm not a huge fan of prehospital antiarrhythmics. It seems to me that if a tachydysrhythmia is "significantly compromising" then it should be cardioverted. If it's hemodynamically stable, why are we messing with it? We don't know what we're going to get when we push amiodarone. Maybe the patient will get better. Maybe the patient will get worse. The nana who's having a STEMI needs reperfusion, not amiodarone, IMO.
> 
> Tom



Here in Kiwi we can give amiodarone for an arrythmia that is "significantly compromising" and our Medical Director has said that the decision to use amiodarone vs cardiovert is left up to the individiual Officer.

That said, if I pick up somebody who is in fast AF and having screaming chest pain I'm more inclined to go down the hang up some amiodarone and give him a bit of morph track than slap the pads on him and cardiovert.

Somebody who is in VT on the other hand, I'm gonna cardiovert rather than pee around mixing up an amiodarone drip and waiting for it to work coz aw shucks they might be dead by then!

We can also hang amiodarone for post-cardioversion and post-cardiac arrest maintenance (if that is the right term) but I hear that's gonna be going by the wayside at least in post cardiac arrest in 2012 when our new Guidelines come out.

I think amiodarone has its place but it should be treated with caution, like all drugs.  Dishing out amio to somebody who has had a few too many soda's and is throwing the ocassional PVC might not be a good idea.


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## 18G (Mar 23, 2010)

I had a Paramedic tell me about a patient he had that was in V-Tach. Pt. was borderline so he opted to cardiovert. Pt. went into arrest immediately upon cardioversion. He questions now whether or not lidocaine first would have suppressed the rhythm and had the patient fair out better. We will never know.

I am not against antidysrhymics.


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## rhan101277 (Mar 24, 2010)

TomB said:


> I guess it's pretty obvious that I'm not a huge fan of prehospital antiarrhythmics. It seems to me that if a tachydysrhythmia is "significantly compromising" then it should be cardioverted. If it's hemodynamically stable, why are we messing with it? We don't know what we're going to get when we push amiodarone. Maybe the patient will get better. Maybe the patient will get worse. The nana who's having a STEMI needs reperfusion, not amiodarone, IMO.
> 
> Tom



Deleted post, its to late tonight and I confused myself.


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## MrBrown (Mar 24, 2010)

18G said:


> I had a Paramedic tell me about a patient he had that was in V-Tach. Pt. was borderline so he opted to cardiovert. Pt. went into arrest immediately upon cardioversion. He questions now whether or not lidocaine first would have suppressed the rhythm and had the patient fair out better. We will never know.
> .



That is a rare complication of cardioversion.

For a borderline patient who is still tolerating the rhythm I might hang some amiodarone first, slap on the pads and see how we go; if the amiodarone doesn't work I'd cardiovert


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## 82-Alpha599 (Apr 3, 2010)

TomB said:


> Recent evidence suggests that patients with new (previously undetected) LBBB do not rule in for MI at any higher rate than other patients, unless they also meet Sgarbossa's criteria for AMI in the presence of LBBB. Generally speaking LAFB and LPFB (a diagnosis of exclusion that is extremely rare as an isolated finding) do not distort the ST-segment the way LBBB does. If it's a "new" hemiblock secondary to acute STEMI, ST-elevation will also be present.
> 
> Tom



Well I guess my question really is what does a new onset hemiblock (with chest pain)  without the presence of ST changes  signify?
NSTEMI?
Or is it more often then not nothing other than insignificant conduction ectopy?


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## TomB (Apr 7, 2010)

82-Alpha599 said:


> Well I guess my question really is what does a new onset hemiblock (with chest pain)  without the presence of ST changes  signify?
> NSTEMI?
> Or is it more often then not nothing other than insignificant conduction ectopy?



The point seems to be that if a previously undetected conduction abnormality is secondary to acute ischemia it will also be accompanied by an ST-segment abnormality.

So no, I don't think it implies NSTEMI, since patients with "new" LBBB do not "rule in" for AMI at any greater frequency than other patients worked up for chest pain (STEMI or NSTEMI).

Tom


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## sdadam (Apr 13, 2010)

Just a thought to the OP.

There was a day when I said things like this, but I think you should take a little time and check your attitude, you don't have the knowledge or experience yet to tell a good medic from a bad. Being in school and being inundated with new information can make you feel like you know all about paramedicine when in fact, you know just enough to look stupid in front of everyone.

Now, I'm not saying there aren't medics out there who suck, there are plenty, but I'm very wary of paramedic interns who talk about how they are going to be so much better than everyone out there once they get done, and how they know so much more than all these crappy medics, an ounce of experience is often worth a ton of knowledge.

I understand you are blowing off steam because people in the field told you that all the cool things you are learning don't play out in a clinical setting just the way you wanted them to, but the answer is often to learn from experience, and be patient and quiet, rather than deciding you are going to re-invent the wheel of paramedicine as an intern.

Check the attitude, or you are in for a rough ride in clinical and internship.


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## dmiracco (Apr 13, 2010)

For the love, give nitro.


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## rhan101277 (Apr 13, 2010)

sdadam said:


> Just a thought to the OP.
> 
> There was a day when I said things like this, but I think you should take a little time and check your attitude, you don't have the knowledge or experience yet to tell a good medic from a bad. Being in school and being inundated with new information can make you feel like you know all about paramedicine when in fact, you know just enough to look stupid in front of everyone.
> 
> ...



My attitude is fine, I didn't mean it to seem like I had an attitude.  I have had some great field experiences since this post as well.  Some of my preceptors really drill me for info and let me team lead, which is tough but I do my best and then they tell me how I could have done better etc.

Also I never talk to medics like I know everything because I don't.  If I think something needs to be done or I wonder why it was not, I use tact to do that.


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## dmiracco (Apr 13, 2010)

Give the nitro


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