Welcome back to the 286 podcast. In this episode, I will be covering acute coronary syndrome. This is a continuation of the cardiac emergencies uh PowerPoint. So, acute coronary syndrome is an emergency situation caused by an acute onset of myioardial eskeeia. This is going to result in myioardial inffection or death. If definitive interventions are not um done promptly, this is usually caused by a buildup of plaque. As plaque continues to build up further um on anggina will progress, it can't be stable then move to unstable and then you'll see STEMI or end STEMI. If a piece of the plaque breaks off, it can cause a complete occlusion in a coronary artery and cause a STEMI as well. If it's not a complete blockage but still a large blockage then you may get the end stem or unstable angina. Other causes of MI though include vasospasm of a coronary artery. This could be caused by things like cocaine, amphetamines, extreme stress. Uh decreased oxygen supply, things like hypotension, blood loss and anemia could be the cause. Increased oxygen demand with not enough supply. Okay, so rapid heart rates again with drugs like cocaine or possible dissection of a coronary artery. Stable angina is not listed on here. Um, but some things to recognize for stable anggina. This is chest pain that does go away with rest and nitroglycerin. Usually preceded by some type of activity, uh, mowing the lawn, exercising, walking up long flights of stairs, things that are going to increase the oxygen demand for the heart. For our unstable angina, the patient has clinical manifestations of coronary eskemia, but the EKG and the cardiac biomarkers are going to show no evidence of um an MI. Chest pain with unstable angina does not go away with rest or nitroglycerin. Sometimes this is called a pre-infarction anggina because if the issue is not fixed it will progress to an MI and it can be preceded by activity but it can also occur at rest. For your N stemmies the patient has elevated cardiac biomarkers like tropponin but no definitive evidence on the EKG of an MI. Um in this type of MI there may be less damage to the myioardium. This is nontransmural uh damage. There's because there's decreased blood supply and the tissue damage or death um is there but it's not complete um and there's no occlusive blockage. The vessels are still open to an extent. However, in your STEMI, your patient um is going to have EKG evidence of an MI with characteristic changes in two leads on a 12 lead EKG. In this type of MI there is significant damage to that myioardium because there is a complete or an occlusive blockage which is an emergency. For our risk factors uh your non-modifiable include um family history. So mom, dad, brother, sister, they have any issues um with their cardiac system. it is likely that the patient will also experience this. Um risk increases with age. Men uh tend to have higher occurrences of MIS compared to women. And then our African-American patients, American Indian patients, and Hispanic patients all have a higher risk of MI as well. Then you have your modifiable risk factors like hyper lipidmia, smoking, hypertension, obesity, a sedentary lifestyle, and a stressful occupation. The most common kind of chest pain or discomfort is a pressure. Uh feels like squeezing or a heaviness on the chest like like an elephant is sitting on the patient's chest and like a crushing pain. Other signs can include a fever for up to four to five days. Uh this is like an inflammatory response from the body uh as a result of the dead cardiac cells, indigestion, anxiety, impending doom, restlessness, uh lightadedness, dizziness, cool, pale, clammy skin, elevated respiratory rate. Initially your heart rate and blood pressure pressure are going to increase as our body is trying to compensate for the decreased cardiac output but eventually the blood pressure pressure will start to decrease as more heart tissue dies and there's decreased cardiac output. This is indicative of your cardiogenic shock. You could see JVD if the MI is inducing heart failure. Uh crackles if the heart uh failure is present. And another common thing that I typically see is a really ashen skin. Women have what are called non-cardinal signs. This is usually including upper back pain, nausea, indigestion, weakness, and fatigue. For our diagnostics, uh cardiac biomarkers like troponin, uh this is going to be the most important lab to do in a patient where you are suspecting an MI because it elevates faster than the CKMBB. You have tronin uh I and T. These are specific for cardiac muscle damage. Troponent I your reference range here is 0 to 0.4 nanog per milliliter. For tronin T, you have 0 to 0.1 nanogs per milliliter. And then we also have a high sensitivity traropponin HSCTN. This is uh reference range less than 14. It's important to note though that the troponin can be elevated due to other forms of stress on the heart like sepsis, heart failure, respiratory failure, etc. Your CKMBB creatine kinase MB is cardiopecific. It elevates when there's damage to cardiac cells. And then we also have our myoglobin which is a muscle damage um enzyme that is released but it is not cardi so it may not um be drawn or ordered. We also want to get an EKG. This must be completed within 10 minutes of arrival or complaint of chest pain or other symptoms. This should really be the first intervention that is done because we need to know immediately if the patient is having ST elevation or not because that's kind of determining what we're doing next. A STEMI means that there is ST elevation in two or more leads. Since it can take traropponin three to six hours to elevate after an MI onset, the patient may or will have serial tropponins drawn. So let's say the first one comes back negative and the EKG looks okay, but they have signs and symptoms of eskeeia. They'll probably be admitted for observation. We'll continue to do those traropponin um levels uh and repeat an EKG every 6 hours times three. By the time that we draw the third tropponin and get the third EKG, it will have been 18 hours since the patient presented with the signs and symptoms of eskeeia. So we'll know at that point if they're having an N STEMI or STEMI uh since the tropponin is going to be elevated and the EKG may or may not show those signs of ST elevation. Our CKMBB is going to elevate when there's signs or when there is damage to cardiac cells again as well as our myoglobin which may or may not be um as accurate because it's not cardiopecific. Myoglobin is going to increase within 1 to 3 hours after um an infar peaking within 12 decreasing within 24 to 36 hours. So it's it's pretty rapid con um in comparison to your troponin and your CKMB. For unstable anggina and NT STEMI, we may do an echo cardiogram uh to measure rejection fraction and look for signs of eskeemia. Uh but we're also probably going to get an echo once our STEMI patient becomes more stable. uh for your unstable patient or the unstable um anggina and stemmies, we're also going to schedule this patient for cardiac cath or sorry, excuse me, cardiac stress test, not cardiac cath. For our uh EKG findings, um your expected EKG changes include T-wave inversion, ST segment elevation, and an abnormal Qwave. Uh usually earlier signs of eskemia are going to include your ST depression and your eventual T-wave inversion. If these aren't addressed and treated appropriately, it can progress to a full-blown MI with ST elevation. So ST elevation is where your J point is elevated. I think I have this on the next slide for you. Right, there's your J point elevated there. it's elevated 1 millm or more, which is one small box on the EKG uh from the iso electric line. The different signs or changes we're seeing on an EKG is just showing us the damage to the heart and the alterations in the depolarization and repolarization of cardiac cells. Remember, depolarization is contraction, depolarization doing stuff, and repolarization is resting or relaxation. Abnormal Q waves are going to develop within 1 to three days after the MI and is a sign of no depolarization in certain parts of cardiac tissue that were affected by the MI. So the eskeeia is pretty advanced at this point. If an abnormal Qwave with no ST or T-wave changes um is present on the EKG, this is going to be a sign of uh an old MI, a previous invar. If the abnormal uh Q wave with ST elevation or T-wave changes um is present currently uh this is where you will see the acute MI or eskeeia. As your patient recovers and the cardiac biomarkers return to baseline, the ST elevation will also resolve. The changes in the Qwave are usually permanent. Like I said, um with that abnormal Qwave with no ST or T-wave changes, this is where you'll have that old infar. This is how we notice that old infar is with the Q waves. And then T-wave changes may or may not stay permanent. It's it's kind of up for debate on that one. So here's your J point for the ST elevation. uh measuring um 0.6 to 0.8 seconds after the start of a J point and the J point is the end of your RS segment. So we see this uh elevation at least 1 millm from the PR segment and elevation in at least two leads on that 12 lead EKG. The location of the ST elevation is going to tell you which part of the heart is experiencing the ES eskemia. really important for your cardiologist to diagnose um where the infarct is occurring. For us, it's just kind of fun to know. So, I wouldn't spend too much time um with your 12 lead EKG interpretations, just your regular rhythm strip interpretations. So, for our initial management, um don't forget Roman. Roman is your new best friend. I know it was Mona, but we added some rest in there. So, rest, oxygen, morphine, aspirin, and nitro. We're going to get this patient on continuous EKG monitoring. We're going to give them oxygen via a nasal canula. Ideally, we'd like to keep the oxygen saturation greater than 93% uh more if possible. We want to get some IVs. Two large bore IVs would be ideal. We want our patient to rest, right? decrease that workload, decrease the oxygen demand on the heart, try to keep them calm, have them on bed rest and no getting up and moving around. Uh realistically, uh the Roman pneumonic is nice to remember, but it is not always the um order that we do things in. Uh but just to give you an idea uh nitroglycerin uh we want to give this to decrease the afterload um which decreases the work on the heart but also increases blood flow to the coronary arteries as a vasoddilator. We're only going to give morphine um not only we usually give morphine if nitro does not relieve the pain but we can also give morphine if um the patient is anxious because morphine at this um for this reason is not necessarily for pain. It is to decrease the preload and afterload of the heart which is going to decrease the workload. So, it makes it easier for the heart to pump and now the heart is not requiring as much oxygen. So, we'll probably still give the morphine, but it's really if your um nitro is not working as well as it should. So, it's it's really not to give um for pain at this point. We will be checking though pain scales before and after administration of your nitro and your morphine because that's the whole point, right? We want to basilate so that we don't have pain. Uh because morphine can uh lower blood pressure. We do want to watch out for hypotension and decrease respiratory rate. We don't want um to decrease too much. And then lastly, we have aspirin. Chewable aspirin 164 to 324 milligrams. If we're going to Kath lab, the cardiologist may also order um another antiplatlet on top of the aspirin. Hepin bransa is another one. And then we pretty much prepare them for the calathlab. Uh other management, we're going to get them a beta blocker uh if an arhythmia occurs. Um, regardless though, it's going to be initiated within 24 hours of admission to decrease the workload on the heart and prevent a recurrence of an MI. Remember to take the apical pulse for one full minute. Um, and then hold the heart uh hold the medication if it's less than 60. Uh, we can give anti-coagulants, usually hepin or large doses of Plavix, to help prevent any further clot formation. For statins, a large dose may be administered, but we're also going to start our patient on a daily regimen. This is like your tova statin, ruba statatin, simbaatin. There's tons out there. Uh this is to help um initiate that lipid lowering regimen. If they're not on a statin, we want to start them on one to start lowering lipids and prevent their reoccurrences. But it can also decrease some inflammation associated with an MI. Statins decrease triglycerides, your bad cholesterol. Um, but some things that our patients may need to look out for, it can cause liver damage. Um, so looking for any yellowing of the skin, dark urine. We will be checking liver function tests. Uh, they may have changes in appetite, nausea, abdominal discomfort, decreased libido, and pancreatitis can also occur. ACE inhibitors help decrease blood pressure, but they do also cause some mild diuresis. These decrease workload and oxygen demand of the heart. Uh big things to watch for here a chronic dry cough, angioadema, hypercalemia. Uh if our patient is not able to tolerate uh an ACE inhibitor, they may be prescribed an angotensin renin blocker or ARBs receptor blockers. Uh then we get them ready for PCI. Right. Perccutaneous coronary intervention. Uh doorto balloon time. Really important to remember this 60 minutes. Remember time is tissue, time is muscle, time is heart, however you want to remember that. Uh this is a procedure that goes in opens up the accluded artery to restore profusion to the area of the heart that's not been receiving oxygen. Um preferred treatment if if a calf lab is available. Um if the patient does not um present to an ER that has a cath lab then we can administer thrombolytic therapy like ultipplace the same kind of drugs that we use for strokes uh to help dissolve the clot that's oluding the artery and restore profusion and blood flow um while we get the patient to a place that has a kath lab. This is going to be contraindicated though um for people who have bleeding disorders, have current bleeding, any recent traumas or uncontrolled hypertension. Uh some of the same parameters that we talked about with our stroke and tpa. Uh if your facility does not have a kath lab and your patient presents with an MI, we need to give thrombolytics within 30 minutes of symptoms start or consider remember that door to needle time as well. uh we can't give thrombolytics um if it's been greater than 30 minutes uh sorry 12 hours after symptom onset um but some sources will say 6 hours it just depends on facility policy if we give thrombolytics we need to watch for bleeding anaphilaxis angioadeema afterwards we can't give any IM injections we need to do direct pressure and pressure dressings uh if your patient starts to bleed a lot and then remember your reversal agent is your aminoaproic acid. Once the clot is dissolved and blood rushes back into the heart that was not getting oxygen before, it can kind of irritate the cardiac tissue. So your patient may experience cardiac arhythmias, palpitations. So we have them on continuous cardiac monitoring and um we have them uh an anti-arithmic available for them for your further management. It's really about lifestyle changes and management here. So your patient may uh meet with a nutritionist. They're going to learn about the DASH diet, dietary approaches to stop hypertension, or realistically a cardiac diet, which is going to help lower blood pressure and get rid of the LDL, which is your bad cholesterol. DASH diet is high um in foods high in potassium and magnesium, which help prevent hypertension, while also being low in high sodium foods. We're limiting saturated fats and also added sugars. Other things that your patient should um consider smoking sessation, decreasing or alcohol sessation, as well as exercise. Uh we may put our patient into cardiac rehab. We want our patient to be able to return to work and their pre-illness lifestyle if available or possible for them while preventing a future cardiac event. This is achieved gradually over time. So remind the patient not to overdo it. We need to tell them to not exercise if their symptoms are reoccurring. So no chest pain, dispna, weakness, fatigue, palpitations, anything like that. Uh we can get our patients to work with a physical therapist or again cardiac rehab. They could attend sessions multiple times a week for a few months just to make sure that they're safe to return to normal. For medications, compliance is key here. So we need to make sure our patients understand how, when, and why those medications are necessary as well as making sure that we can um help them afford their medications. So case management can help with that. Um reducing anxiety and fear. This is a lifelong disease. Um but it is possible to res resume a normal life after an MI. So those lifestyle modifications and compliance with medications can help prevent another MI from occurring. And that will be it. Stay tuned for part three.