Cardiac Arrest/ MI

Sugarcoma, RN · Nov 6, 2014

It was actually directed toward the OP who wanted to know if one (STEMI or NSTEMI) was caused by a plaque while the other is thromboembolic. I was not addressing the type of clot responsible for each, although that is very interesting and useful information, and I am glad you posted it.

I just assumed my original post wasn't clear and needed clarification. I missed that (plaque vs thromboembolic) in the OP altogether. I guess that old saying is true. When you assume you make a donkey of yourself. :sorry:

psu_213, BSN, RN · Nov 6, 2014

I just assumed my original post wasn't clear and needed clarification. I missed that (plaque vs thromboembolic) in the OP altogether. I guess that old saying is true. When you assume you make a donkey of yourself.

Eh, it happens. I really do appreciate the links though!

AnnieOaklyRN, BSN, RN, EMT-P · Nov 7, 2014

STEMI versus non-STEMI has to do with the area of injury going through the entire wall of the myocardium (Transmural) in which you with see STEMI, a non transmural or subendocardial MI can show no ST elevation, thus may be missed on a EKG and only seen when the enzymes come back.

Remember your coronary blood flow goes from the inside to the outside, not the other way around, so not all MIs involve all layers of the myocardium. So endocardium to epicardium.

Whether they come in coding or not depends on a few things, their overall health, age (the younger you are the MORE likely you are to arrest from an MI), size and location of the infarct, how long they were in denial before seeking medical care and believe it or not most patients arrest from an MI about TWO WEEKS out from the initial injury when their heart is "remodeling" or forming scar tissue. Very few MI patients actually arrest at the beginning stages!

***Remember if a patient comes in in cardiac arrest people often ASSUME they had an MI when that is not always the case, people code for all sorts of reasons, there is no proof they had an MI unless the medical examiner says so!*** or if we resuscitate they take a direct look at the vessels in a cardiac cath lab. Yes, we may get them back and do a 12 lead and lab work, but if they were defibrillated that can cause elevation temporarily and can also elevate heart enzymes. Very few patients actually code at the initial onset of an MI, except for the following.

The highest rate of cardiac arrest from MI with be in those patients having a anterior wall MI in the left ventricle( leads V3-V4 on a 12 lead), those MIs tend to be rather large, and often extend into the lateral wall (high lateral wall = leads AVL and lead I, low lateral wall = V5 and V6) , septal wall (V1-V2), and depending on the patients vasculature even into the posterior wall (leads V1-V2 , harder to find in someone having an anterior MI however, this would be EXTREMELY rare in this type of MI). There is a reason Anterior MIs involving the septal wall, anterior wall, and lateral wall are called the "widow maker", as it is the result of a proximal blockage in the LAD coronary artery. Most patients do not survive this one, it involves a very large area of injury, a large area of irritable myocytes, can cause significant problems with pump function (decreasing blood flow to the heart even more), cause significant delays in cardiac conduction, and because of this increases the chances of cardiac arrest multifold.

Inferior wall MIs (II, III, and AVF), even if they extend into the right ventricle (V3R and V4R), or into the posterior wall of the left ventricle (V1 and V2 will show and R wave with ST DEPRESSION), or into the lateral wall (see leads explanation above). Have very few instances of cardiac arrest, this involves a small portion of the heart, does not usually involve the actual electrical system directly, and the right ventricle usually fairs better with lacking oxygen since it is a) much thinner than the left ventricle and b) has a better blood supply, and effects of pump function are generally minimal. These patients often present with nausea, vomiting, diarrhea, and sometimes reflex bradycardia. The released enzymes from the inferior wall often irritate the Phrenic nerve which is part of the sympathetic nervous system, thus the irruption of this nerve can cause significant GI upset. Use caution in giving these patients nitrates at onset until they receive a right sided EKG, since in a small amount of cases those with right ventricle involvement can suffer severe hypotension if given nitrates or other medications which reduce afterload, as the right ventricle is very dependent of after load.

Other MIs including posterior, lateral, and septal are generally to small of an area to cause cardiac arrest, and they are rarely seen by themselves.

The reason you see elevation in the ST segment is because there are less cells to depolarize, since they are experiencing a lack of oxygen, thus the ventricle finishes depolarizing quicker than normal so you do not see the completed downstroke of the R wave as you would in a normal healthy heart. Now if only part of that wall is experiencing a lack of oxygen, as in an MI that is non transmural or not effecting the entire wall of the myocardium, there will still be enough cells depolarizing so you may see the entire downstroke of the R wave, or there may be minimal ST segment elevation.

You must remember too, that patients coronary blood flow can vary from person to person, which can effect which areas of the heart a blockage will effect.

The older you are the less likely you are to arrest from an MI. Older folks, overtime, adapt to coronary blockage by formation of collateral circulation, in essence there body forms its own bypass around that blockage.

The heart is releasing enzymes, the cells are "irritable" because of these enzymes and the fact that they are not getting enough oxygen. This irritability makes way for ectopic foci in the ventricle which are very dangerous in cases where you have other cells that are not functioning correctly. Scarring as well as injury to the areas of the heart which involve the conduction system can cause short circuits which enable the onset of arrhythmias set off by PVCs to include ventricular tachycardia and Ventricular fibrillation. See explanation in the anterior MI section.

During scarring, if the MI was transmural, the wall become very weak and can cause cardiac rupture causing an unfortunate death secondary to cardiac tamponade, in most cases the patent will be dead long before they are able to reach medical care.

If patients wait to long, the end result if they have a large MI and survive it is the above, heart failure, conduction abnormalities such as heart block, and valve regurgitation if a papillary muscle or muscles are infarcted.

I hope this helps you!

HPRN