Right Side MI and Nitro

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I'd like to get a bit more understanding about right side MI's. I was working with two medics last night (I'm a basic) and they know I like to ask questions and they are great at trying to make me understand... but there's a part of this I'm not getting.

He asked me "what cardiac patients do we NOT give Nitro to?" (later he explained that you can, CAREFULLY and he was trying to give an example where you don't just say if-chest-pain-then-nitro). So we had quite a bit of discussion about this. I certainly "get" the idea of an inferior MI, and apparently something like 40% or more have right side involvement. I get the concept of cardiac preload, I suppose and I get that the RV is physiologically a lot different than the LV. Of course I learned well that nitro is a dialator and can cause a significant/severe drop in BP. And obviously I get that there is a risk of a RVMI patient with a bp of 150+/90 crashing to 60 over nothing because I've now heard several first and second hand stories about it happening.

But honestly what I don't really get is what is going on here physiologically? To me, dialation is the container, the vasculature, getting bigger. Why is the EF plummeting? Presumably the RV was already injured in this case and was pumping what it could and was able to maintain a BP (150/90 for example). Does the RV itself also dialate from the nitro? There's something I'm not getting.
 
The right myocardial infarction is often accompanied with the symptom of right heart failure. The preload reduce with Nitro here can may be wrong. There is a risk of hypotension and cardiogenic shock.
 
What it all boils down to is a problem of a reduction of preload of the left side of the heart. . This results in a reduction of cardiac output, and the body compensates for it. Ultimately, this is why you see good blood pressure in the setting of right ventricular infarct. What's really going on is cardiac output has been reduced substantially from normal and of the body is dependent, more so, on the left side of the heart, then it is used to. With the right side of the heart in failure because of infarct, the left side has to work a lot harder and the peripheral vascular system has to clamp down more to maintain blood pressure and as good an output as it possibly can. This is so that you can have good blood flow through the pulmonary circuit and the heart. When you add in a vasodilator, like nitroglycerin, a big portion of the body's ability to compensate for right failure is removed. Preload of the right side basically drops to zero. This reduces blood flow through that side of the heart through the pulmonary circuit and also, by extension, through the left side too. This has the result of plummeting blood pressure because now there's no flow through the heart.

This is why in emergency care if were looking at a right ventricular infarct, we want to have an IV line established prior to giving nitroglycerin. This is so that we can provide some fluid so that we can fill that container up and maintain preload and therefore maintain flow through the heart and not plummet that blood pressure.

When we have a typical left-sided infarct, there's more muscle mass available to compensate for the loss of function of the infarcted tissue. The body doesn't have to compensate as much for that loss of tissue so when we give a vasodilator to a left intraventricular infarct patient,we don't have to have as much concerned about giving the vasodilator because were not going to plummet cardiac output enough that it's going to be a problem. And to a degree we actually want to reduce the workload of the heart and therefore reduce oxygen demand, and thus limit the size of the infarct on that left side. It is just in that in the setting of right ventricular infarct patients are just a lot more sensitive to the effects of a vasodilator, so we have to be much more careful about giving those vasodilators to those patients.

I'm sure I've left out quite a bit, but hopefully I've given you enough to wrap your mind around it.
 
And that is an argument for taking a good EKG and not just "horseback" one, correct? This is an instance where vital signs including pulse and BP would not be fooled. What signs and symptoms observable by a Basic or first aid person might be seen and noted to pass up the line?

Oh, and also a big reminder never to use another person's meds.
 
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mycrofft said:
And that is an argument for taking a good EKG and not just "horseback" one, correct? This is an instance where vital signs including pulse and BP would not be fooled. What signs and symptoms observable by a Basic or first aid person might be seen and noted to pass up the line?

Oh, and also a big reminder never to use another person's meds.
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And now I'm feeling especially stupid, like that dream where you're in your underwear at the final exam. The only thing relevant I can think of right now are what I think are longer term signs, like pedal edema, and JVD. They would also might be tachy and short of breath.
 
WIkipedia:
"Right-sided failure
Physical examination can reveal pitting peripheral edema, ascites, and hepatomegaly. Jugular venous pressure is frequently assessed as a marker of fluid status, which can be accentuated by eliciting hepatojugular reflux. If the right ventricular pressure is increased, a parasternal heave may be present, signifying the compensatory increase in contraction strength."

Parasternal heave, ibid.: "A parasternal impulse may be felt when the heel of the hand is rested just to the left of the sternum with the fingers lifted slightly off the chest. Normally no impulse or a slight inward impulse is felt. The heel of the hand is lifted off the chest wall with each systole. Palpation with the fingers over the pulmonary area may reveal the palpable tap of pulmonary valve closure (palpable P2) in cases of pulmonary hypertension".
 
mycrofft said:
And that is an argument for taking a good EKG and not just "horseback" one, correct? This is an instance where vital signs including pulse and BP would not be fooled. What signs and symptoms observable by a Basic or first aid person might be seen and noted to pass up the line?

Oh, and also a big reminder never to use another person's meds.
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in 12-lead ECG I can see the right myocardial infarction if I'm lucky in II, III, aVF.

suspected myocardial infarction at the right you should also write a right ventricular ECG leads. You could see the infarction in the ECG leads V1, V3r-V6R.

I hope that's correct.
 
Rettsani said:
in 12-lead ECG I can see the right myocardial infarction if I'm lucky in II, III, aVF.

suspected myocardial infarction at the right you should also write a right ventricular ECG leads. You could see the infarction in the ECG leads V1, V3r-V6R.

I hope that's correct.
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You wouldn't see it in leads II, III, aVF, those would only show an inferior infarction, and as you know it gives you a higher index of suspicion for a right-sided infarct, thus you would run V4R.
 
fast65 said:
You wouldn't see it in leads II, III, aVF, those would only show an inferior infarction, and as you know it gives you a higher index of suspicion for a right-sided infarct, thus you would run V4R.
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Thank you
My books were a bit misleading, so I've thrown it so in the room. I will correct it immediately. In a German rescue-forum they would therefore my head tear off now . :)
 
Rettsani said:
Thank you
My books were a bit misleading, so I've thrown it so in the room. I will correct it immediately. In a German rescue-forum they would therefore my head tear off now . :)
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Eh, 12-leads can be confusing, no worries lol
 
fast65 said:
Eh, 12-leads can be confusing, no worries lol
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I think it's important that I have a 12-lead ECG can write and i understand it. However I do think, i must not to be Perfect. A right myocardial infarction is very rare. Out from my own understanding, I often write in a NON STEMI with right heart failure symptoms a Rechtstorakale ECG lead. I think it does not harm.
 
To add to what's already been said.... with right sided MI there is myocardial stunning of the right ventricle which essentially turns it into a conduit.... which is where there is no to very limited pumping action by the right ventricle and blood just passively flows though it. This was pretty much already explained but sometimes a little variation of the same thing helps understanding.

Anytime you have an inferior wall MI there is increased probability of right sided involvement which should get a V4R. Also important to note with inferior wall MI's is the increased incidence and severity of nausea and vomiting due to what's believed to be the way innervation is at the inferior portion of the heart.

Bradycardia is also frequently seen with inferior wall and right sided involvement. This is often due to ischemia of the SA node.

As far as NTG for right-sided MI. There are differing opinions although all state if it is administered to do so cautiously due to often dramatic reduction in preload which the heart is depending on for its stretch and contractility which ultimately provides the cardiac output. Some protocols absolutely contradict NTG while others just state to ensure IV access and be alert for precipitous drop in B/P.

It's been my teaching that these patients need fluid to maintain cardiac output and a pre-emptive fluid bolus can be given prior to the NTG. Obviously if the pressure dumps on ya your gonna open the fluid and if refractory to that consider dopamine.
 
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Starling's law comes to mind. I'll expand on my thought when I finish this movie and get on my computer rather than my phone.

Someone may have already said it but I'll simplify it. Right side is "low pressure" whereas the left side is "high pressure" and is fed by the "low pressure" system of the heart. By dilating the venous system and reducing preload the the right side of the heart you also reduce preload to the left side which is why you see the profound drop in pressure.

Again this is my understanding of it and I may be wrong about it.

I might have it totally back asswards though.
 
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Alright I'm on a computer.

So I basically covered what I thought I was too lazy to cover on my phone.

Starling's law states increased ventricular stretching causes an increase in contractile force along with cardiac output.

So common sense would say decreased filling would reduce contractile force along with cardiac output but I feel like I may be understanding it incorrectly.

From what my partners have told me the RVI/NTG gremlin isn't as scary as school makes it seem but you need to use common sense. If they are borderline on the systolic pressure withhold the NTG and give a fluid bolus to bring it up then give the nitro. On the other hand you aren't going to bottom someone out with NTG who is hypertensive along with an RVI*. Furthermore from discussions I have had with people on here along with others a true RVI will usually present with hypotension and rule the NTG out by itself but there are always those cases that present irregularly .

*follow your protocols and take what I say with a grain of salt. I presented my opinion and will not be held accountable if something goes wrong :P
 
NVRob said:
Alright I'm on a computer.

So I basically covered what I thought I was too lazy to cover on my phone.

Starling's law states increased ventricular stretching causes an increase in contractile force along with cardiac output.

So common sense would say decreased filling would reduce contractile force along with cardiac output but I feel like I may be understanding it incorrectly.

From what my partners have told me the RVI/NTG gremlin isn't as scary as school makes it seem but you need to use common sense. If they are borderline on the systolic pressure withhold the NTG and give a fluid bolus to bring it up then give the nitro. On the other hand you aren't going to bottom someone out with NTG who is hypertensive along with an RVI*. Furthermore from discussions I have had with people on here along with others a true RVI will usually present with hypotension and rule the NTG out by itself but there are always those cases that present irregularly .

*follow your protocols and take what I say with a grain of salt. I presented my opinion and will not be held accountable if something goes wrong :P
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That is mostly correct, Starlings law does play a part in it. The big thing is that by reducing the preload, you are reducing the amount of blood entering the RV, which is already impaired by infarct, reducing supply to the lungs and by extension the LV. This reduced EF, coupled with the now larger container = the gremlin we all fear, bottoming out the BP and killing the patient. But you are absolutely correct, we shouldn't fear the RVI, but rather respect it and keep an eye out for it. Fluid replacement and common sense on when to give the NTG, with those, you can never (generally lol) go wrong. I almost always run a V4R before I give NTG, doesnt really take much effort on my part to move the lead over and hit print.
 
Nervegas said:
That is mostly correct, Starlings law does play a part in it. The big thing is that by reducing the preload, you are reducing the amount of blood entering the RV, which is already impaired by infarct, reducing supply to the lungs and by extension the LV. This reduced EF, coupled with the now larger container = the gremlin we all fear, bottoming out the BP and killing the patient. But you are absolutely correct, we shouldn't fear the RVI, but rather respect it and keep an eye out for it. Fluid replacement and common sense on when to give the NTG, with those, you can never (generally lol) go wrong. I almost always run a V4R before I give NTG, doesnt really take much effort on my part to move the lead over and hit print.
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You did a better explaining it than I did. Thanks.

Edited because I basically repeated the OP's question.
 
Soooo, if I were to tell everyone that the American College of Cardiology listed NTG in RVI as a class III intervention (not helpful and possibly harmful) as a a consensus opinion would everyone still think it was important in managing RVI?
 
Rettsani said:
in 12-lead ECG I can see the right myocardial infarction if I'm lucky in II, III, aVF.

suspected myocardial infarction at the right you should also write a right ventricular ECG leads. You could see the infarction in the ECG leads V1, V3r-V6R.

I hope that's correct.
Click to expand...

You could do a right side ECG. But what would really give you an initial idea of where the infarction might be would be seeing what leads showed reciprocal ST depression and Which ones would not. On a RVMI you'd see these depressions in Leads I, aVl, V5, and V6. You might also note a slower heart rate and a lower than expected BP.

Remember MI's aren't just about elevation. It's more than that. There is a bigger picture. We need to look at the whole thing.
 
...and a major cause of right failure is left failure. ("Failure" may be too general a term when getting into the finely parsed mechanics, but it seems ok when considering the general presentation and syndrome).
 
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