Nitroglycerin in MI

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I read somewhere that sublingual nitro (or morphine for that matter) is contraindicated for someone you suspect is having an inferior MI since the right ventricle relies on a high preload to contract enough fluids to push into the lungs. However, can we not say the same for the left ventricle in someone presenting with an anterior MI? Also, the point of administering nitro is to aid in coronary perfusion, correct? So...?

Is subl nitro contraindicated 100% of the time in inferior MI or is this dependent on a case by case basis? Thanks for any clarification!

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This is one of those "rules" that get repeated for so long that people stop thinking about the "why?" part. The concern is about blood distribution of the right coronary artery which includes the inferoseptal and inferior wall segments of the left ventricle.

It's the RCA, but it's distribution includes the left ventricle.

The while the left coronary artery blood flow occurs only during diastole, the RCA flow occurs during systole and diastole. If you're seeing signs of inferior wall segment ischemia, you're concerned with maintaining a good pressure head down that artery so that the LV isn't further deprived of blood.

NTG can drop the systolic blood pressure and make RCA mediated ischemia worse. Systolic pressure is less of an issue with the LCA.

If the pressure is in the tank, not giving it is a good idea, but careful IV administration in patients whose BP is high or normal can be done safely. SL is harder to titrate.

If there is RV involvement as well, as you say, worsened ischemia can reduce blood arriving to the LV from the RV/lungs...

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Specializes in Emergency Department.

SL nitro isn't contraindicated in inferior MI... nor is it actually contraindicated in RV MI situations either. That being said, there are times you do NOT want to give SL nitro. The right heart output is very sensitive to preload. If preload drops off, then right heart output drops, LA preload drops and so then does LV output. The idea behind giving nitro, of course, is that you want to dilate the coronary arteries as well as reduce afterload (and therefore workload on the heart). Since RCA blood flow depends upon systolic and diastolic pressure to flow well, when you drop cardiac output (and therefore pressure) too much, the RCA flow can also drop, thus increasing the size of the infarct area. If you don't have any means to increase preload in the RVMI or IWMI situations, you don't give the nitro unless blood pressure is VERY good.

The other issue is that SL nitro is very difficult to titrate (read that as nearly impossible). You could end up spending a significant bit of time giving fluid boluses, checking BP, and giving nitro.

Basically because I don't want to cause further problems, if I see RVMI, IWMI, or PWMI hints... line goes in before the NTG goes under the tongue.

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The while the left coronary artery blood flow occurs only during diastole, the RCA flow occurs during systole and diastole. If you're seeing signs of inferior wall segment ischemia, you're concerned with maintaining a good pressure head down that artery so that the LV isn't further deprived of blood.

By chance, do you happen to know the percentage of blood flow in RCA during systole vs diastole? I'm assuming there's greater flow during diastole. Just curious. Thank you both for your in depth infos!

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That's a good question and I don't know the answer. It has to be substantial because, for example, maintaining a high normal systolic pressure in a patient with severe to critical aortic valve stenosis is a primary element of care in those patients. And the reason is RCA perfusion.

If you know a friendly cardiologist that likes to teach, ask him/her that question.

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Specializes in ICU, CVICU, E.R..

On top of what was already explained, the RV is preload dependent. NTG causes vasodilation of the peripheral vascular bed causing pooling of blood volume, thus decreasing your blood pressure and RV preload. As long as the patient is not volume depleted and has a stable blood pressure, I don't see a problem.

It's similiar to the "don't give more than 2L/min O2 to a COPD patient" kinda rule LOL!

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It's also worth noting that for patients with a typical atherosclerostic/thrombotic MI, NTG has minimal effect on the involved coronary vessels. A coronary vessel will typically autoregulate and dilate to meet the needs of the myocardium it is perfusing. As a person develops CAD the vessel walls become increasingly thick, stiff, and unable to dilate any further; by themselves, or with NTG. The beneficial effect of NTG is based on its preload and afterload reduction which reduce myocardial O2 consumption, but NTG does not meaningfully increase coronary blood flow to the ischemic area. In fact, coronary vasodilation is potentially harmful to myocardium perfused by an occluded vessel.

Don't believe me? Many pharmacological cardiac stress tests work on this principle. The drugs given cause coronary vasodilation, which works to vasodilate healthy coronary arteries. Atherosclerotic vessels cannot dilate any further, so blood preferentially flows down the path of least resistance created by these newly dilated healthy vessels. This shunting, or "coronary steal" is what accounts for the ischemic changes in the territory of the occluded vessels, as even less blood flows down the tight vessels.

Exception: for patient's with Printzmetal's/vasospastic angina NTG works both as a coronary vasodilator, and a preload/afterload reducer to treat ischemic symptoms. Similarly, intracoronary NTG during cath lab procedures works against vasospasm induced by manipulation of the vessel.

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Specializes in ER/Critical Care/Accrediation/PI/Quality.

Good question. I have given SL Ntg many times for chest pain and do not recall a particular type of MI as a contra-indication. As a general rule, we withheld it for a systolic BP less than 90.

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Specializes in MICU.

I read about this in one article that it is contraindicated in inferior MI, and obstructive cardiomyopathy due to reflex tachycardia. I cant remember the rationale but I do know is because of the decrease in preload

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