Axis deviation and the 12 lead

[rhan101277]

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.

 

[reaper]

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.

 

[EMTinNEPA]

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.

 

[usalsfyre]

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.

 

[usalsfyre]

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.

 

[reaper]

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.

 

[usalsfyre]

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.

 

[reaper]

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.

 

[TomB]

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

 

[82-Alpha599]

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.

 

[rhan101277]

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.

 

[TomB]

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

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.

 

[AnthonyM83]

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?

 

[TomB]

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

 

[The-Reaper]

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.

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

 

[TomB]

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

 

[MrBrown]

...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.

 

[TomB]

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

 

[MrBrown]

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.

 

[18G]

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.