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Cardiac Arrest/ MI

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benmca13 has 2 years experience and specializes in MedSurg, ICU.

1,273 Profile Views; 17 Posts

So I'm new to ICU/CCU nursing. I'm completely confused by MI's and Cardiac Arrest. I've been asking my preceptors, but one tells me one thing while the other tells me something different. I go back to the cath lab and they tell me something different. All of the nurses I've precepted with have 30-40 years of experience, so I'm not sure what to believe. My question is this.

I truly don't get two things: why can someone come in with CP and another be coding? If the plaque on the walls is too thick that blood can't pass through, it's an MI, correct? If a embolus breaks off and clots a coronary, it's an MI, correct? What causes the heart to just suddenly stop, while others can go days without the heart actually stop? What's the patho I guess is what I'm asking. I just don't get what's going on in the body that some code and other just have an MI.

Secondonly, what happens in the body that differentiates between a STEMI and NSTEMI? Some told me the area of the heart it happens in, others told me it depends if it's an embolus or just plaque build up.

I just don't get heart attacks currently. I came from a medsurg floor so this is all COMPLETELY new to me. Thanks in advance!

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NICU Guy has 5 years experience as a BSN, RN and specializes in NICU.

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An MI occurs when blood stops flowing properly to a part of the heart, and the heart muscle is injured because it is not receiving enough oxygen. Usually this is because one of the coronary arteries that supplies blood to the heart develops a blockage due to an unstable buildup of white blood cells, cholesterol and fat. The event is called "acute" if it is sudden and serious.

A person having an acute MI usually has sudden chest pain that is felt behind the sternum and sometimes travels to the left arm or the left side of the neck.

ECG testing is used to differentiate between two types of myocardial infarctions based on the shape of the tracing. An ST section of the tracing higher than the baseline is called an ST elevation MI (STEMI) which usually requires more aggressive treatment. A myocardial infarction differs from cardiac arrest. STEMI is treated by restoring circulation to the heart, called reperfusion therapy, and typical methods are angioplasty, where the arteries are pushed open, and thrombolysis, where the blockage is removed using medications. Non-ST elevation myocardial infarction (NSTEMI) may be managed with medication, although angioplasty may be required if the person is considered to be at high risk.

Injured heart tissue conducts electrical impulses more slowly than normal heart tissue. The difference in conduction velocity between injured and uninjured tissue can trigger re-entry or a feedback loop that is believed to be the cause of many lethal arrhythmias. If the delay in the sequencing hits at the wrong time, it can cause the patient to go into V Fib or V tach and cardiac arrest.

Just because someone is having chest pain (MI) does not mean that their heart will go into a lethal arrhythmia, it depends on where the blockage is and how the ischemia affects the conduction of the impulse. If the ischemia is treated quickly then they have a decreased risk of cardiac arrest.

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Sugarcoma has 2 years experience as a RN and specializes in Trauma/Tele/Surgery/SICU.

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Hi benmca13. You sound very much like me. I too could not wrap my head around the differences between MI/STEMI/NSTEMI/Cardiac arrest etc. Here is what I have learned through questioning multiple docs/pa's/nurses etc.

1. MI is a circulation problem. Blood flow has either stopped (STEMI) or been reduced and is causing damage (NSTEMI)

STEMI = Think fast and acute. A clot has occluded an entire vessel and muscle has died (ST elevation =necrosis to all 3 layers of the heart muscle).

NSTEMI = Think chronic. A clot has occluded part of a vessel or vessels and muscle is ischemic (injured form lack of O2) but not yet dead.

So you would think that because they are both caused by clots they would be treated similarly with the STEMI patient being maybe a little more urgent due to the total occlusion. Or at least that is what I thought. What I have learned is that there is a difference between the clots that cause a STEMI vs. NSTEMI.

The clot in a STEMI is usually made up of fibrin (can have plaque) and is treated with a fibrinolytic medication along with PCI in order to save the muscle. If these measures fail CABG is the next step.

The clot in NSTEMI is made up primarily of plaque and is more platelet rich. This clot is treated with Plateletlytic medications and/or PCI This is important because fibrinolytics given to a NSTEMI patient can actually be harmful. It all has to do with the clotting cascade etc. which I will not get into here. NSTEMI can be treated with just medications or PCI if medications do not bring relief. The goal of treatment in NSTEMI is to stabilize the plaque to prevent further damage.

Cardiac arrest is an electrical problem with the heart. Something is wreaking havoc with the conduction system and impulses are either getting through poorly or not at all. There can be many causes of cardiac arrest which can be cardiac or non-cardiac. Example of non-cardiac cause are overdose, PE, acute blood loss, etc. Think H's and T's. Cardiac causes can be MI, structural damage, etc.

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spacemonkey15 has 10 years experience and specializes in Critical care.

115 Posts; 3,439 Profile Views

Think about the anatomy of your coronary arteries. Where the blockage is in the patient's artery will have an impact on how they present to you, in severity and nature of their symptoms.

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Esme12 has 40 years experience as a ASN, BSN, RN and specializes in Critical Care, ED, Cath lab, CTPAC,Trauma.

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This may help it is basic but useful....http://www.phcris.org.au/divisions/reporting/documents/ACAI_guidelines_09-10.pdf

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delphine22 has 5 years experience and specializes in Quality, Cardiac Stepdown, MICU.

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You're asking, why are some MIs instantly fatal and some last for days? It's about collaterals and compensation. It's also why you hear of the energetic 42-year-old man having a heart attack and being dead before his body hit the floor, and the 72-year-old sedentary gent who's had 6 MIs in his lifetime, and is still alive. When you've had coronary artery disease for a long time, your body compensates by growing collaterals, or detours around areas with decreased blood flow. This is how a pt can have a total occlusion but still be alive. A young person hasn't had time to develop those compensatory vessels, which is why MIs are usually more fatal in the under-50 set.

As to the MI vs cardiac arrest question, someone else mentioned electrical. I like to tell my pts to think of the heart as a house: it has an electrical system, which controls your rate and rhythm. It has a plumbing system -- your coronary arteries, and when a pipe gets clogged, you are in trouble. It also has walls and doors: if the doors are drafty or stuck, those are your valve problems (regurg and stenosis, respectively). If your walls are too thick or too thin or too weak: cardiomyopathy.

Obviously if your plumbing is backed up and your heart muscle starts to die, dead tissue won't conduct electricity, so there's your MI. Or I may be super oversimplifying things bc I'm tired. :unsure:

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The difference between just chest pain and full code depends on amount of damage done and also which vessels.

first if its the lad or left main, that vessel goes to the main muscle of the heart for squeezing the left ventrical. so as muscle dies, the ventrical squeezes less.

second, also depends on if pt has collatoral blood flow, if pt has collatoral blood flow it means blood from one of the other main vessels is supplying blood to that area as a secondary filler. the dr will refer in his report filling left to right or filling right to left, means which way blood is flowing to the area that is blocked.

third, a pt may have cp and still have blood flow to that area in which it supplies, the pain is a lack of or insufficient amount of oxygen to the muscle. a muscle spasm with some blockage will cause cp. people with angina which is a chronic cp that is related to coronary vessels that are to small to bypass or stent, causing on and off cp for that pt. everytime pt has cp it causes more and more muscle to die.

Basically mi's dont present the same in every person, a womans mi presents with symptoms of chest pressure, gas, indigestion with sob, diabetics present totally different as well. Not all americans have the cardinal signs of mi. left sided cp or sternal pain radiating into neck and down left arm, with sob, n/v, so many may have symptoms of not feeling well for couple days to couple weeks. and by the time they do come into the er the mi is over or pt has signifigant damage for life.

muscle damage also relates to ejection fraction. normal is 60-65%, after a mi it is always reduced. The amount reduced is equal to amount of damage to the myocardium and the lateral wall that contracts the left ventrical. Hope this helps some.

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Here.I.Stand has 16 years experience as a BSN, RN and specializes in SICU, trauma, neuro.

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Also, keep in mind that a cardiac arrest is not necessarily due to ischemia. Someone with perfect coronary arteries could go into a VT, VF, PEA arrest--think H's and T's. https://acls-algorithms.com/hsandts

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psu_213 has 6 years experience as a BSN, RN and specializes in Emergency, Telemetry, Transplant.

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MI = myocardial infarction. By definition this means that heart muscle is dying. This occurs, usually, by occlusion of a coronary artery either by plague, embolism/thrombus, or a combination of both.

STEMI = ST elevation MI. Again, by definition this means that cardiac muscle death is occurring and the ST segment is elevated on an EKG. NSTEMI = non-ST elevation MI. Cardiac muscle has died, but there are no EKG changes to suggest that. Generally, NSTEMIs generally have less muscles death than STEMIs, but they are serious none-the-less (and STEMI vs. NSTEMI has nothing do to with blood clot vs. plaque). Most of the time, STEMIs will go right to the cath lab. Most NSTEMIs will not go to the cath lab, and a heparin gtt will be started in the ED (assuming they present there) and the pt will be admitted, often just to telemetry, though occasionally to the ICU. NSTEMI, obviously, is not diagnosed by the EKG, but rather through a positive troponin.

The thing about chest pain indicating an MI, it does not always happen. Women, especially elderly women, and diabetics often do not have chest pain as their main symptom, even if they are having an MI. I remember an ED doctor telling a resident that in elderly woman, the most common presenting symptom of MI is SOB.

Finally, I remember an NCLEX practice question: "What is the most common side effect from an MI?" Answer: dysrhythmias. Needless to say, that can cause an arrest. Some get to the ER with chest pain before a dysrhythmia occurs…others are not so fortunate. Also, as more of the heart is deprived of blood, more of the conduction tissue dies. Which means? Dysrhythmias. Which is even more of a problem if a patient dismisses chest pain…for instance, just writing it up to GERD, or if they are having the atypical symptoms of an MI, and they don't seek medical care as quickly.

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Sugarcoma has 2 years experience as a RN and specializes in Trauma/Tele/Surgery/SICU.

410 Posts; 11,653 Profile Views

(and STEMI vs. NSTEMI has nothing do to with blood clot vs. plaque).

I am assuming that this is directed at my original response. I actually didn't say anything about blood clot vs. plaque, only that there is a difference in the makeup of the clots that lead to either a NSTEMI or STEMI.

Studies have shown that there is a statistically relevant difference in the types of lesions that result in either a STEMI or NSTEMI. STEMIs are most often caused by what is considered a "red clot" while NSTEMIS are most often caused by what is considered a "white clot." This is why fibrinolytics are not useful in the treatment of NSTEMI.

Please see the following studies.

Red versus white thrombi in patients with ST-elevation myocardial i... - PubMed - NCBI

Red versus white thrombi in patients with ST-elevation myocardial infarction undergoing primary percutaneous coronary intervention: clinical and angiographic outcomes.

New Morphological Insights on Coronary Plaque Rupture: Bridging the Gap From Anatomy to Clinical Presentation???Editorials published in JACC: Cardiovascular Interventions reflect the views of the authors and do not necessarily represent the views of

New Morphological Insights on Coronary Plaque Rupture : Bridging the Gap From Anatomy to Clinical Presentation?

http://www.ncbi.nlm.nih.gov/pubmed/21251632

[h=1]Difference of culprit lesion morphologies between ST-segment elevation myocardial infarction and non-ST-segment elevation acute coronary syndrome: an optical coherence tomography study.[/h]This is also discussed on page 16 of the following text: Evidence based Cardiology Consult, Kathleen Stergiopoulus and David Brown.

While not a scientifically acceptable source, the following blog also discusses this: https://drsvenkatesan.wordpress.com/2008/09/10/why-thrombolysis-is-contraindicated-in-unstable-angina/

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psu_213 has 6 years experience as a BSN, RN and specializes in Emergency, Telemetry, Transplant.

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I am assuming that this is directed at my original response. I actually didn't say anything about blood clot vs. plaque, only that there is a difference in the makeup of the clots that lead to either a NSTEMI or STEMI.

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. :up:

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