What EXACTLY causes GI symptoms r/t myocardial ischemia

Specialties Critical

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I'm not sure if I've been telling myself lies for the last 6 years about the pathophys behind GI symptoms (nausea, vomiting etc) as relates to an MI; I've always thought that during ACS, SVR is increased shunting blood away from the lesser vital organs (eg. the GI tract), and toward the brain and kidneys, and the lack of (or less of) perfusion is what causes the GI symptoms.

Reading my AACN CCRN book, it states that GI symptoms are caused from increased vagal tone and dosing with opiates. Ok, so increased vagal tone goes along with activation of the PARAsympathetic nervous system.

"Antiemetics may be necessary because of the high degree of acute vagal tone, and the emetic side effects of opiate analgesia"

That doesn't make sense, because the PSN = "rest and digest"

I then read another source that said the GI symptoms are caused from the flood of catecholamines, ok that makes sense because that's activation of the SNS.

Does shunting have anything to do with the GI symptoms? Is AACN's pathophys incomplete? Or is the PNS just trying to unsuccessfully compensate the SNS in the GI department?

If anyone has a good source on this topic, I'd love to read it.

Specializes in SICU.

GI symptoms and vomiting can be caused by a number of different mechanisms that can be quite complicated. I did a quick Google search to see if I could find an exact mechanism on this, and I found a whole lot of nothing.

I will say this though, I've never heard of the SNS shunting blood from the GI tract being a cause of nausea/vomiting. High levels of parasympathetic activity, however, does cause nausea/vomiting (see SLUDGE acronym for cholinergic crisis, the E standing for Emesis). I know the PNS is "rest and digest" but super high levels beyond normal of anything can really set off the vomiting reflex.

Sorry I don't have a better answer for you. I don't think there is much known on the topic actually. This is why in anesthesia, post-operative nausea and vomiting is still a problem with some people, no matter how many anti-emetics we give them.

I know from personal experience if my sympathetic or fight or flight mode kicks into high gear i can get nauseous and throw up...especially when im nervous (Getting my blood drawn) lol im a nurse that hates getting poked

Specializes in Critical Care.

I've always been under the impression that GI distress can be caused by an inferior wall MI due to vagus nerve irritation, since the inferior wall is connected to the vagus nerve.

I've always been under the impression that GI distress can be caused by an inferior wall MI due to vagus nerve irritation, since the inferior wall is connected to the vagus nerve.

Yep! That's how I've always understood it.

Just to expand, for the OP:

An inferior MI means there has been an occlusion in the RCA (right coronary artery). The RCA supplies oxygen to the right side of the heart (duh), and since the heart is tilted onto its side, that puts the right side of the heart on the bottom (inferior). This makes it closer to the stomach, which always helped me remember that the inferior wall MI is the one that causes GI symptoms.

I'm not sure what kind of patients you take care of but it's important to keep the location of the infarct in mind when you're taking care of patients post-MI, especially after one in the RCA. One of my newer coworkers once was on her way to give a patient zofran because he was feeling queasy...I saw on the report sheet that he had an inferior wall MI so I followed here in there with the EKG machine and we saw huge ST elevation. Turns out his stent had collapsed, and he had no other symptoms other than GI upset (which rapidly turned into projectile vomiting). He went back to the cath lab immediately and was ballooned in less than 15 minutes, and luckily the long term damage to his heart was minimal!

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