Semi scenario - Nitro With Inferior MI and RVI

[Handsome Robb]

I know there have been threads on it but the discussion came up in another thread so I figured I should start one.

Toned out as MVA single car vs. tree in residential neighborhood. 62 yo male, Hx of HTN, only med "ends in olol" and "2 baby aspirin a day". No family cardiac or stroke history, non-smoker, pt is average build. No signs of trauma, minimal front end damage to the car, witness said he just slowly coasted into the tree. Pt said he felt light headed prior to the accident and doesn't actually remember the accident. Only complaint is 2/10 chest pressure, non radiating and non-provokable, onset just prior to the accident. Pt A&Ox3, Pupils PERRL, RR 16 uncomplicated, SPo2 94% on RA, BP 112/78, BGL 98, HR 48 sinus brady with no ectopy on the monitor, skin is pink warm and dry. Lung sounds clear bilaterally, neuro exam is normal. Rapid trauma was unremarkable in all areas, pt self extricated out of the vehicle with help from the bystander.

12 lead shows 2 mm of ST elevation in II, III and aVF. V4R has 1-2 mm of elevation depending on who's measuring. I asked my instructor about recip changes and he stated marked depression in I and aVL. The 12 leads I was given were off a rhythm generator which unfortunately cannot generate reciprocal changes.

My brilliant self decided to go down the ACS pathway once I saw the elevation in the standard 12 lead prior to doing the right sided 12er. 2 lpm via NC, 162mg of aspirin, and SL NTG spray. Rechecked pressure after the NTG dropped to 70/p radial pulse very weak, pt becoming confused -> unresponsive, pulseless and apneic, slow PEA on the monitor started ACLS then the instructor stopped.

My question is what would you have done? I *should* have done a right sided 12 lead prior to admin of the NTG with an inferior MI but I didn't, I saw the V4r after the fact.

I've been preached to to never give a RVI NTG, what are your thoughts?

 

[usalsfyre]

Inferior MI I'll give it with V4R in hand. RVI I won't.

 

[Handsome Robb]

Inferior MI I'll give it with V4R in hand. RVI I won't.

This is how I have been taught. If you have ST elevation in V4r hold the nitro and consider fentanyl over morphine if the patient is in pain. You don't get the venous dilation with fent like you do with MS but if they are in pain and you reduce it you reduce anxiety and HR causing a decrease in myocardial o2 demand.

Unfortunately I got all excited with the elevation and went through the ACS protocol prior to getting a V4r. :unsure: h34r:

 

[Chief Complaint]

Chief you didn't have 12 leads in your program?? Didn't you just finish recently?

Wow sorry for the thread jack. /off topic.

I'm starting a new thread, standby.

Leaving me hanging with all this talk about a new thread! Couldnt wait.

Im finishing up my Paramedic degree right now, and there is not a 12 lead class in the curriculum. We have an 8 week EKG class (4 lead) as part of the Intermediate program and thats it. Mind blowing huh?

There is one other medic program in the area and they do not teach 12 leads either from what i hear. They are not a degree program.

12 leads are within the scope of practice for Intermediates/Paramedics here (I's and P's are exactly the same) but its just not taught. If you get picked up by any of the agencies in the area you will learn them at the academy. Still doesnt make sense to leave them out of the curriculum though.

Frankly, its embarrassing. I just ordered Dale Dubin's book and i will be teaching them to myself.

cut and pasted this from the other thread

 

[Handsome Robb]

*Paging Linuss* *Paging Linuss*

I understand Starling's law, but from what I have been taught, the drop in preload is so extreme that there literally is 'nothing' left for the heart to pump except for the EDV, especially with compromised function due to the infarct of the right ventricle.

 

[Handsome Robb]

Leaving me hanging with all this talk about a new thread! Couldnt wait.

Im finishing up my Paramedic degree right now, and there is not a 12 lead class in the curriculum. We have an 8 week EKG class (4 lead) as part of the Intermediate program and thats it. Mind blowing huh?

There is one other medic program in the area and they do not teach 12 leads either from what i hear. They are not a degree program.

12 leads are within the scope of practice for Intermediates/Paramedics here (I's and P's are exactly the same) but its just not taught. If you get picked up by any of the agencies in the area you will learn them at the academy. Still doesnt make sense to leave them out of the curriculum though.

Frankly, its embarrassing. I just ordered Dale Dubin's book and i will be teaching them to myself.

cut and pasted this from the other thread

That really surprises me that they don't include it. I definitely wish I had more instruction on it but I feel like I have a semi-decent grasp on the basics of them. I still have a ton to learn though.

 

[fast65]

Well for starters, I wouldn't have killed my patient like someone did...jk, I keed, I keed Rob.

Anyways, like usal said, I'll give it to an inferior MI if I have already done a 12-lead with V4R. I wish I had the option of giving fentanyl instead of morphine, but we only carry the latter. :/

 

[Chief Complaint]

That really surprises me that they don't include it. I definitely wish I had more instruction on it but I feel like I have a semi-decent grasp on the basics of them. I still have a ton to learn though.

You and me.....and the other 60 or so students in the program are surprised as well. Its the hand we are dealt unfortunately. As i stated above, im going to be teaching them to myself using Dale Dubin's book and some websites ive found. Really excited for the book to arrive!

On my last internship, a medic offered to show me the basics (he went through the same program i go to) of 12 leads. Sat me down and just started droppin' gems on me for about an hour and a half. I learned more about 12 leads in that short time than i have in my program all together. This guy was SMART.

Anywho, ill try not to thread jack this one. Im here to learn.

 

[firemedic0227]

My program was a 1 year program with ACLS being one quarter or about 3 months long. We did a lot of 12 lead stuff but never really covered much about Reciprocal leads or axis deviations. Anyone know of any good websites for such things? I know how to read basic 12 leads (Infarct wise) but other than that I am pretty much in the dark and I want to learn more about it. I really need to get better at this as I might be practicing real soon out in the field on my own.

 

[Handsome Robb]

Your not thread jacking at all. We used Tim Phalen's "The 12-Lead In Acute Coronary Syndromes in class. That plus Dubin's book helped me quite a bit. Phalen's book comes with a cool transparent sheet to lay over hospital sized 12-leads to help you learn which leads are looking at what part of the heart.

I second arharris' post! We touched on axis deviation but not nearly enough.

 

[Chief Complaint]

Sounds good, ill be buying Phalen's book when im done with Dubin.

Would somebody like to give me a quick lesson in reciprocal changes and their meaning? Perhaps axis deviation as well?

Ill do the leg work myself, but a brief synopsis would be awesome.

 

[Handsome Robb]

Sounds good, ill be buying Phalen's book when im done with Dubin.

Would somebody like to give me a quick lesson in reciprocal changes and their meaning? Perhaps axis deviation as well?

Ill do the leg work myself, but a brief synopsis would be awesome.

So really sparknoted it's opposite changes in the leads looking back towards the leads that are showing the ST elevation.

Check this out.

http://www.rhmedicclass.com/index.php/prehospital-12-lead-ecg-contiguous-and-reciprocal-lead-charts/

I don't feel comfortable enough with axis deviation to attempt to explain it.

 

[Shishkabob]

Like I said before... an inferior MI does not equal an RVI. The RV is involved in inferior MIs only 30-50% of the time. Yes, the RV is very preload dependent, however, as stated before, you need to do it smartly. Have an RVI pt with a 150/90 BP? Chances of a single 0.4mg dose of SL NTG bottoming them out is minimal. 100/50, even when your protocols say you can go as low as 90 systolic? That's getting too close for comfort.

Heck, we even had the lead cath lab cardiologist from Baylor speak to us a few weeks back about this issue specifically and he said the same thing: NTG is ok if done smartly. Give some fluids, let Starling do his work.

This is why I'm a huge fan of NTG IV infusions... much better control over the effect of the dilation than a big 400 mcg dump or NTG paste which isn't as consistent.



Do the fluid bolus, think it through, give the nitro.

 

[systemet]

Frankly, its embarrassing. I just ordered Dale Dubin's book and i will be teaching them to myself.

cut and pasted this from the other thread

Want some help? We can start another another thread!

 

[systemet]

L
Heck, we even had the lead cath lab cardiologist from Baylor speak to us a few weeks back about this issue specifically and he said the same thing: NTG is ok if done smartly. Give some fluids, let Starling do his work.

This is why I'm a huge fan of NTG IV infusions... much better control over the effect of the dilation than a big 400 mcg dump or NTG paste which isn't as consistent.

Do the fluid bolus, think it through, give the nitro.

I agree that if we're going to give a vasodilator, IV NTG is the way to go. I just question whether it's necessary to give a vasodilator at all in RVMI.

In the LV MI setting, we're decreasing CVP / preload, so that we can decrease wall tension in the left ventricle and decrease oxygen demand.

In the RV MI, we're not getting enough CVP / preload, so we're giving fluid to get the right ventricle to a point where it's getting adequate preload to fill the LV, produce a diastolic pressure, and get better coronary perfusion pressures.

Why give NTG here? What are we hoping to accomplish? It's going to decrease our preload and CVP, for what potential benefit?

How's about, ASA, fluids +/- dopamine +/- atropine +/- fentanyl for pain +/- gravol for n/v, initiate reperfusion therapy (whether ER bypass to PCI, ER alerts, or field thrombolysis), and adjunctive therapy (plavix / enoxaparin)?

 

[Nervegas]

Sounds good, ill be buying Phalen's book when im done with Dubin.

Would somebody like to give me a quick lesson in reciprocal changes and their meaning? Perhaps axis deviation as well?

Ill do the leg work myself, but a brief synopsis would be awesome.

Reciprocal change is in its simplest form, an inverted change in the ST segment in a boundary lead. Lets say we have an acute STEMI in II,III and aVF, with 1-2 MM of elevation, no RVI, a classic Inferior MI. We might see a reciprocal change in I and aVL, or ST depression as these tissues are on the boundary of the Inferior MI in the lateral leads, representing injury or ischemia but not infarct to these tissues. One might also see ST depression due to looking through the heart at an infarct, such as a Posterior MI, in which there is no elevation in any lead, but V1-4 show ST depression as we are seeing the infarct from the opposite side of the heart.

The link NVRob sent is a decent down and dirty version of reciprocal change.

Axis deviation is a deviation to the right or left from normal of the electrical pathway of the heart. It can be caused by hypertrophy of the muscle, causing a physical shift, a L or R BBB causing electrical shift, or an MI causing a shift due to myocardium dying and other causes.

Down and dirty version: http://www.fammed.wisc.edu/medstudent/pcc/ecg/axis.html

I agree that if we're going to give a vasodilator, IV NTG is the way to go. I just question whether it's necessary to give a vasodilator at all in RVMI.

In the LV MI setting, we're decreasing CVP / preload, so that we can decrease wall tension in the left ventricle and decrease oxygen demand.

In the RV MI, we're not getting enough CVP / preload, so we're giving fluid to get the right ventricle to a point where it's getting adequate preload to fill the LV, produce a diastolic pressure, and get better coronary perfusion pressures.

Why give NTG here? What are we hoping to accomplish? It's going to decrease our preload and CVP, for what potential benefit?

How's about, ASA, fluids +/- dopamine +/- atropine +/- fentanyl for pain +/- gravol for n/v, initiate reperfusion therapy (whether ER bypass to PCI, ER alerts, or field thrombolysis), and adjunctive therapy (plavix / enoxaparin)?

Doesn't NTG also dilate the small blood vessels of the heart leading to more oxygenated blood being allowed to pass through the smaller capillary networks to the Infarcted tissue? The possibility of a RVI is why I think it is quite scary to allow EMT's to administer NTG solely on BP only, especially when they teach 100SBP as being the threshold.

 

[Chief Complaint]

Awesome post, thank you.

 

[systemet]

Doesn't NTG also dilate the small blood vessels of the heart leading to more oxygenated blood being allowed to pass through the smaller capillary networks to the Infarcted tissue?

I haven't read as much of the research on this as I should have. But, from what I understand, the primary and most beneficial action of NTG in myocardial infarction is to reduce myocardial oxygen demand by decreasing preload. A lot of the texts out there talk about how this is especially useful in LV MI complicated by pulmonary HTN / CHF.

The collateral flow is probably a very much secondary effect. The coronary vessels are already very responsive to local conditions, so in ischemic regions they tend to be dilated already. With nitroprusside (another arterial dilator), there's a tendency to dilate vessels that are serving healthy myocardium, and a relatively constricted, diverting blood away from the ischemic region. This is called "coronary steal". It seems like NTG has less of a tendency to do this.

From what little I've read, it sounds like there's little-to-no evidence that NTG use actually improves outcomes in MI. Things like time-to-cathlab, time-to-PCI, and other adjunctive therapies like heparin / LMWH, glycoprotein inhibitors, beta-blockers, etc. have more evidence to support their use. A few of the EM / cardiology texts suggest that there's little reason to continue administering NTG even in LVMI if there's an absence of pain reduction and no pulmonary edema.


Nitroglycerin is commonly administered to relieve ischemic pain in patients presenting with MI, but evidence that nitrates improve mortality in MI is sparse. Because they reduce ventricular preload through vasodilation, nitrates are effective in relief of pulmonary congestion. A decreased ventricular preload should be avoided in patients with right ventricular infarction because higher right-sided heart filling pressures are needed in this clinical context. Nitrates are relatively contraindicated in patients with systemic hypotension. According to the American Heart Association/American College of Cardiology (AHA/ACC) guidelines, "nitrates should not be used if hypotension limits the administration of blockers, which have more powerful salutary effects" (Antman et al., 2004).
Because the proximate cause of MI is intracoronary thrombosis, reperfusion therapies are critically important, employing, when possible, direct percutaneous coronary interventions (PCIs) for acute MI, usually using drug-eluting intracoronary stents (Antman et al., 2004). Thrombolytic agents are administered at hospitals where emergency PCI is not performed, but outcomes are better with direct PCI than with thrombolytic therapy (Antman et al., 2004) (see discussion of thrombolytic and antiplatelet therapies in Chapter 30).

[From Goodman & Gilman's The Pharmacological Basis of Therapeutics, 12e > Section III. Modulation of Cardiovascular Function > Chapter 27. Treatment of Myocardial Ischemia and Hypertension]

The possibility of a RVI is why I think it is quite scary to allow EMT's to administer NTG solely on BP only, especially when they teach 100SBP as being the threshold.

I agree. It seems like there's a very cavalier attitude towards NTG use in EMS sometimes. There seems to be this idea that:

* NTG-induced hypotension is not dangerous (not true. Take your patient's BP from 110/70 to 60/30, see what happens to their coronary perfusion, consider the myocardium is already ischemic, and imagine how many patient's first warning sign might be VF arrest).

* We can just treat it with fluids if it happens (maybe, if they don't arrest / have a lethal arrhythmia. Is this likely to be good for infarct extension? Therapeutic ischemia to allow delivery of a drug with undetermined to negligible benefit?)

* If the patient has been previously prescribed NTG, it's going to be fine this time (Maybe. But maybe they just plugged their RCA)

* People give themselves NTG all the time (Yes. If they have angina, or a condition similar to angina, they've been evaluated by a physician, and if they're giving it for exertional angina! Not for MI).

On the other hand:

* Most of our patients will probably have angina / non-preload sensitive MI, and be just fine.

* NTG may relieve the symptoms of ischemia, may improve the hemodynamics in some MI patients, and should reasonably limit infarct extension (even if the outcome data isn't there to support this).

* It will relieve many non-cardiac causes of chest pain.

* It's safe in the vast majority of patients.


For me, I just don't see the concern with getting this drug administered ASAP to every patient. The 12-lead and the ASA are the important parts of prehospital treatment. They're proven to work.

I would just get the ECG, get the line, then give the NTG if it's not suspicious for RVMI. We're talking about a 5-10 minute delay giving a drug that has minimal evidence to support its use and is potentially dangerous, on patients who on average have waited at least 90 minutes from symptom onset before calling 911.

[And this isn't delaying anything time-sensitive, if anything, we're getting the ECG quicker.]