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Nitro question


swn919

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Hey guys and gals,

Another medic and I have a question. Why is it that when you give nitro in a true AMI event chest pain is not generally relieved but in situations like angina it releves pain?

Thanks for you help,

Scott

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Hey guys and gals,

Another medic and I have a question. Why is it that when you give nitro in a true AMI event chest pain is not generally relieved but in situations like angina it releves pain?

Thanks for you help,

Scott

What do you mean by true MI? Are we talking STEMI, NSTEMI? Nitro works in both to relieve pain. It works better for pain in angina becaue the tissue to ischemic. It's still living, but on its way out. If you improve the blood flow and take it out of an ischemic state the pain goes away. With an MI, the tissue has actually infarcted. There is no saving it, so the pain is not as easy to relieve. I have no evidence to support this, but it intuitively makes sense to me.

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What do you mean by true MI? Are we talking STEMI, NSTEMI? Nitro works in both to relieve pain. It works better for pain in angina becaue the tissue to ischemic. It's still living, but on its way out. If you improve the blood flow and take it out of an ischemic state the pain goes away. With an MI, the tissue has actually infarcted. There is no saving it, so the pain is not as easy to relieve. I have no evidence to support this, but it intuitively makes sense to me.

When I say true MI I am talking STEMI.

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What do you mean by true MI? Are we talking STEMI, NSTEMI? Nitro works in both to relieve pain. It works better for pain in angina becaue the tissue to ischemic. It's still living, but on its way out. If you improve the blood flow and take it out of an ischemic state the pain goes away. With an MI, the tissue has actually infarcted. There is no saving it, so the pain is not as easy to relieve. I have no evidence to support this, but it intuitively makes sense to me.

I agree with Doc, that is also why the CP in a STEMI is also a more pronounced "crushing" chest pain than a stabbing kind of pain. Think of it as the difference between leg muscles that hurt because you just ran 10 miles, and muscles that hurt because you just got severe degree burns to them. The first kind of pain can be relieved relatively easy, especially compared to how hard it would be to relieve the pain from the second. Same kind of muscle dying (ischemic) pain vs. the dead (infarcted) kind of pain.

At least that is a (semi-loose) kind of analogy.

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Angina results from a reduction in blood flow, STEMI occurs following an elimination (or near elimination) of blood flow. When you use NTG, you are hoping that there are collateral vessels around an occlusion that you can dilate to improve the blood supply. For the anginal patient, this is relatively easy. For the occluded vessel, not so much.

Ischemic tissue is at risk, but still has nerve endings that work. Improve the blood supply, and the nerves don't pick up quite as much pain. Infarcted tissue is dead. No perception of pain. The penumbra around the dead tissue tends to be larger, increasing the sensation of pain.

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Three more things:

(1) Burn yourself. Take away the burning object. You still hurt don't you? More to the point. Lift weights. When you stop lifting, you still are sore. You are sore the next day too. When muscle is fatigued or damage, the pain will continue even after the insult is removed.

(2) Nitroglycerin is a relatively mild coronary vasodilator. Its primary action is venous dilation leading to a reduced venous return, reducing frank-starling forces reducing how hard the heart has to work. As more blood fills the chamber the harder and more forcefully the muscle contracts (and therefore uses more oxygen of which it is already starved). So with advanced stages of ACS, the heart muscle has already suffered the insult and reducing the venous return cannot eliminate the damage nor the pain. At early stages (NSTEMI and angina) the minor coronary dilation and major reduction in venous return spares the tissue greater insult. This is the equivalent of lifting light weights for a little soreness. Nitro acts as a spotter.

(3) Coronary Steal. While the main effect of nitroglycerin (and NOT all nitrates) is to reduce venou return, it does have some effect on coronary vasodilation. This also contributes to alleviating pain from angina or NSTEMI. As venous return is reduced and coronary arteries expand, both collateral circulation and direct flow through the occluded artery are increased. So, by reducing the work load on the heart and improving coronary flow the pain is relieved. In advanced stages of ACS coronary dilation has already occurred, most likely to the max. As a vessel becomes occluded and the tissue distal to the occlusion becomes starved for oxygen chemical signals (primarily C02) induce vasodilation of the vessels supplying the tissue. Arteries can dilate, but they are limited in dilation. If a vessel is totally occluded or has been for some time, the maximum dilation can already be reached. This patient is most definitely STEMI, probably Q wave. As you give nitro to this patient you reduce venous return which helps them (yay!). However, the minor coronary dilation that occurs occurs NOT in the occluded vessel (which is dilated already as a result of hypercabnia [high c02] or hypoxia) but in coronary vessels near to it. Those vessels WERE constricted to provide increased flow to deficient tissues and are now dilated, so blood flow that could potentially go to the starved tissue is "stolen" (thus the term cardiac steal) to healthy perfused tissue. Again, not really a problem with Nitroglycerin, but is the purpose of some nitrates. Also, obviously, if there is 100% occlusion they are screwed anyway. Keeping with the lame analogy, this is like lifting more than you can, calling a spotter to help, and having him push down against you.

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I think that if I had the gift of eloquence, I would have said it like Overactive did.

Overactive: you hit the nail on the head. Thank you for saying it better than I could. Man, I gotta work on my communication skills....

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