Hi, welcome to Cardiovascular Nurse Essentials. Today we're going to be talking about ischemic heart disease and peripheral artery disease. These are my disclosures. Similar format to the previous modules, here are our objectives with your readings. Again, a lot of readings, but these are really so you're comfortable with the guidelines and some additional optional resources. Ischemic heart disease is obviously one of the leading or the leading cause of death for men and women in the United States. We know the statistics with heart disease and the high prevalence of mortality and all the numbers associated with it and why our jobs are so important in trying to prevent this. You can see on our graphic, the prevalence of heart disease is southern, not quite fully east, but here in the south. I guess we could call that southeastern, but this is where we have our highest concentrations. It really all starts with atherosclerosis, which I like to think of as just hardening of the arteries and those vessels. What you'll see over time and aging and with influencing risk factors with our diet, this is that healthy endothelium. Then over time, you may get increased fat deposits underneath the endothelial lining here. That causes the lining within the arteries to become bumpy or textured. That causes platelet aggregation. You can actually have that clot formation. You can see over here where it's more progressed, where there's actually little room to go through because of those underlying lipid deposits and fibrous caps that build and can block off the artery. Just another angle or schematic for progression is it starts pretty open, obviously, when we're young. Then we go through life and we have all these risk factors and things we put in our bodies. Over time, lipid accumulates, builds up underneath, we get plaque formation that puts the roughness within the artery. That smooth endothelial lining becomes more textured and we get clot and thrombus development. We can actually have that rupture and that's what causes a lesion or an event. Myocardial ischemia is the imbalance of blood flow to the myocardial heart. With blood flow, we get oxygen and that feeds the myocardial muscle. With the myocardial ischemia, it's not getting that oxygen and can result in cell death in that myocardial muscle when it's not getting blood flow for a prolonged period of time. We see this from elevated troponins that result from the cell death or necrosis. Risk factors. There's a lot of risk factors. Our key ones are really hypertension. As we talked about earlier in this series, all the different ways we can prevent and manage hypertension. This is one of the reasons it's so important. Also, hyperlipidemia and smoking cessation. I'm sure you've seen the theme of smoking and how it wreaks havoc on our cardiovascular system. Those are our top three risk factors. Other risk factors are diabetes, obesity, that unhealthy diet that's high in saturated fats, physical inactivity, and excessive alcohol use. Nothing really new to note, but again, this just shows you the impact that lifestyle modification can have in regards to risk reduction. Most chest pain is really from musculoskeletal pain or GI pain. You can see acute chest pain that's associated with myocardial ischemia is pretty low. However, we do not want to immediately discount patients' complaints of chest pain or other symptoms because we know that it's low. We still have to work everyone up and use our clinical thinking and diagnostic skills, tools, and skills to make sure that we're ruling that out before determining it's musculoskeletal or GI pain. What is your job? Especially from a remote or ambulatory setting can be very challenging to get the full picture. You've got to differentiate. Is this chest pain cardiac related or not? These are just some tips and information to help you in your clinical decision making. We know that cardiac chest pain is the lack of oxygen to the myocardium or that heart tissue. We know that it increases the oxygen demand of the heart. We know it builds up lactic acid and we know the symptoms that it's associated with. That's generally shortness of breath, can be nausea, vomiting, can be sweating or diaphoresis, can be palpitations, or even a syncopal feeling. And sometimes patients express just this feeling of doom. They can't really explain or speak to what they're feeling other than this just terrible feeling. And I always tell people don't discount that feeling. If you feel like something's wrong, especially if they've had a cardiac event, please listen to them. They know. It's really important that we act on this because myocardial injury begins in as short of a time as two hours from when it starts. So there is a limited window that we have. Cardiac chest pain is not something like twinges in their chest. It doesn't last days to weeks. It is not typically reproducible and it does not get worse with coughing. So those are typically things that we associate with those musculoskeletal issues. Other symptoms that you may find with cardiac chest pain is dyspnea. So again, common themes of symptoms here, that general weakness, maybe that nausea and vomiting, that is more common in women. They may present just with nausea and vomiting, palpitations, and syncope. So with that thorough history, we want to make sure that we understand the quality of that pain. Is it positional? Is it sharp or dull? Is it stabbing, throbbing? What does it feel like? Where is it? What's the location and is it radiating or moving anywhere? So is it starting in the chest and moving down the arm or is it in the back and it's moving up the neck? Is it on the left or the right? We just need to know that information. How long has it been lasting? Is it coming or going? What started it? Does anything make it worse like exertion, rest? Is it related to high emotions and stress and anxiety, things of that nature? And does anything make it better? Does it go away when you stop doing something? Does any medications make it better? So we need to know the full picture so we can make the best decision on how to move forward for our patients. Clinical presentation, again, it's not always 100% clear. Some patients may have silent or undiagnosed heart disease until they actually have a full heart attack. I think you've heard me say it many, many times, especially with hypertension, the silent killer. If they don't know, we can't take risk reduction or measures to present it from progressing. And so it may only present at the time they've had an acute event. The chest pain or discomfort, if we hear that there's an elephant sitting on my chest, right in the middle of the chest, on the left, those are the things that we expect. However, that does not mean that every patient will have that. It could be kind of a squeezing feeling or a feeling of fullness or like an uncomfortable kind of pressure. So make sure you're listening to those cues, even if it's not the typical chest pain that you would expect. That weakness that they may feel, sometimes they have like a cold sweat associated with it. Places they may also feel pain sometimes are in the jaw, the neck line, or even the back. So we cannot discount those things. And shortness of breath. So some patients may present with chest pain and shortness of breath, but sometimes we do see shortness of breath that comes on before chest pain. So just using those full clinical assessment skills that you have and are working on. So physical assessment, it's important to know you may not have any abnormal findings on your physical assessment, but we do know there are some high-risk findings. So like a dyskinetic apex where you expect the apex to be, but it's not exactly there on auscultation. You may see some elevated JVP. You may hear that S3 or S4 or new murmur. So making sure you're in tune to those patients' heart sounds. There may be rails or crackles. They could be hypotensive. So if you're seeing those, those are what we consider high-risk findings, meaning they're at higher risk for an event. And of course we do know there are those predisposing risk factors. Some of those may include uncontrolled hypertension, thyrotoxicosis, and GI bleed. When we're diagnosing an EKG is the most valuable or important test that we can do. That initial EKG is important to get a baseline and we want to compare it to any other EKGs if they've had them. If not, this is your baseline. Now do not be surprised if on the initial EKG we do not see many changes or something that concerns us that it's an acute issue, but we will do repeat or serial EKGs every 15 and 30 minutes from the initial study just to make sure that patient does not develop. And of course if a patient kind of stabilizes and then they become symptomatic again, we would want to go ahead and obtain an EKG. Obviously our history is first, then an EKG, and then our cardiac biomarkers, which is our troponin I or troponin T or high sensitivity troponin. We do expect to see bumps in those with any kind of myocardial damage and necrosis, so you will see an elevation in those. Again, those are a series of three generally if we are concerned about an acute event. And we do classify our MIs into STEMIs versus non-STEMI. So ST elevated MI is our STEMI, and that's really pretty much as it sounds. We're going to see an elevation in their ST segment on their EKG, and it has to be greater than or equal to one millimeter and two contiguous leads. That's the primary thing we're looking for, so not necessarily one lead, but it has to be two contiguous. Sometimes a new left bundle branch block is concerning, so that can actually be a definition of a STEMI. The non-STEMI or non-ST elevated MI obviously does not have that ST elevation, but you may see things like T wave inversion specifically greater than or equal to two millimeters, or some new Q waves may be present. So those are some signs that it's still important. It just means it's not an ST segment elevated MI, so we still need to act upon it. We also further classify it to type 1 and type 2. So your type 1 is that spontaneous acute MI that results from coronary plaque rupture or erosion of a superimposed thrombus. So it's not really expected. Patients may have a history, but it is spontaneous. It's usually a STEMI or a non-STEMI. Our type 2 results from that oxygen supply and demand imbalance, and it's usually precipitated by some sort of stressor, so hypertension, tachycardia, or hypotension. So there's usually a reason that the blood flow and oxygen supply is not meeting the demands of the heart. Some patients have stable disease, and these are not emergent situations, and you'll probably get to know these patients. They may be kind of higher anxiety, but this is that stable chronic kind of chest pain syndrome. It's considered lower risk, but it really presents as a ischemic equivalent. So it can show up like it is an acute or ischemic event, but they're well-known and established. They've been ruled out to have anything really going on, so we do rule them out before labeling them stable or chronic, if you will. There are guidelines now that help with symptomatology, symptom management, and the appropriate guideline-directed medical therapy, and potential interventions that can help with revascularization for these patients. So treatment, first line is medical management. Generally, we're looking at antiplatelets and anticoagulation to prevent that thrombus formation, especially in an injured area. We do not want there to be a re-embolization or clot formation there. If a patient needs PCI, we do have options in terms of stents. We can do just angioplasty, which is basically ballooning open that vessel. We do not leave a stent, but for the most part, we use bare metal stents or drug-eluting stents these days to help keep that vessel open. They do need that antiplatelet therapy to prevent clot formation on the stent for the first period after that stent is placed. Patients who are not eligible for the PCI intervention may need CABG. Then, of course, we love to talk about our lifestyle changes and modification and how you can impact those. So that's nutrition, that stress management is really important in this population, and it's really important that we engage them in cardiac rehab, as we've discussed. Let's talk about these scenarios, and I'm sure if you've not experienced one like this, you will soon enough in your practice. So I want you to meet Jerry, who is a 48-year-old white male, and he's come to the ED with two hours of substernal chest pain that's radiating to his left arm, and he's complaining of nausea, and he's very diaphoretic. So we take an EKG, and he's got ST elevation in V1 through V4, and we know that that ST elevation is greater than one millimeter, and we know this is in four leads, so it meets the minimum criteria of two contiguous leads. So he goes immediately to the cath lab, and we find a 95 percent occlusion in his LAD, and we stent him. The stent was placed successfully, no issues. Post-PCI echo shows his ejection fraction is 40 percent, and he has some hypokinesis in his interior wall. He was in the hospital with troponin elevation up to 60, and was discharged two days later. Okay, so that's a pretty common occurrence, and when Jerry's discharged, you can see his medication. So he's on aspirin, he's on a beta blocker, an ACE, he's got his Prolenta and his Lipitor for his cholesterol management. He's got an appointment to follow up with the cardiology clinic in three to five days, and they enrolled him in cardiac rehab, so he's going to start that two weeks after his discharge. So he goes to his follow-up appointment, and all seemed well. Jerry's excited, he's thinking he's going to get back on track, and he's pumped about his first cardiac rehab visit. So he shows up, but he had to take off work, and he doesn't know that he can take off work that much, because he's got a full-time job. Then he got his insurance bill, or his bill from the cardiac rehab, and his insurance didn't pay for it. So Jerry did not return. He couldn't afford it, he couldn't afford the payments, and he couldn't afford to take off work. So he's stuck with his medications, but after a while, he stopped filling his prescriptions, because they were so expensive. So he had to spend $375 for a month's worth of prescriptions, and he got all this information and education materials, and he started reading through it, and quickly put it away, because he was intimidated by the information. So Jerry quit his meds, he didn't take his medications, he stopped going to rehab, and here we are five years later, and Jerry is now 53. He's unable to keep up with his physical activities, his pants are getting tight, his socks are leaving marks. He's young, so what's happening to him? He goes to his doctor, and they prescribe him some antibiotics for bronchitis. They do a chest x-ray, and he's got some vascular congestion, and his BMP is 1400. So knowing his history, they do an echo, and his EF is now 30% with global hypokinesis. So now, five years after his PCI, Jerry has dilated cardiomyopathy, because he stopped his medications after six months of that event, and has not followed up since then. Patients have a lot of responsibility, they don't have the finances or the time, so we kind of have this fix it and forget it attitude, and then things reveal themselves, and in Jerry's case and many others, it's much worse. So what are these barriers? Patients' beliefs and behaviors do play a part in their care. So there's lots of research that shows forgetfulness, the issues and concern about potential side effects, the cost issues, that they don't need the medication, those all actually contribute to a patient not maintaining their therapy plan. And then kind of what happens is they get through that initial hump, and they're feeling maybe better, they don't have any symptoms, and so they don't feel a need to continue to take those medications, or do cardiac rehab, or follow up with their physician. So it's up to us, and as we know, as nurses, we're well positioned to help give that information. You know, our providers are short on time, they don't have the time to go through it, so please take the time to talk through the education, answer questions for those patients. And we do want to keep that regimen simple, so it's always better to do a once daily as opposed to two, three, four times a day medications for compliance. So keeping it simple, trying to use combination therapies when able, there are some things, we obviously can't control everything, but there are some things we can do to try to decrease those barriers and improve compliance within the patients. All right, and now we're going to talk a little bit about peripheral artery disease, closely related to cardiovascular disease. PAD does not really differentiate between men and women, so it does impact both sexes, and in this instance, African Americans are at an increased risk. You can see it's a high volume of Americans starting at a relatively young age that have PAD, and really it's important because PAD increases the risk of developing CAD or a stroke. So we want to make sure that we're detecting and intervening as soon as possible, and you can see that 40% of the population do not complain of leg pain as we would expect. The most significant risk factor is smoking, so we know a lot of risk factors, but number one is smoking, and that's important because if we can quit smoking, we can quickly reduce the risk of developing PAD and further disease. So pretty typical as we would expect, that hypertension, diabetes, hyperlipidemia, other things like atherosclerosis, so it's kind of intuitive that if a patient has atherosclerosis, you know, it's not going to just stick to the heart, it will stick, you know, it will be within the other vessels. Renal disease, advancing age, and genetics can all play a part in risk factors for PAD. So our clinical presentation, the classic symptom is that pain in the legs with activity that will improve with rest. This is known as claudication, so this is that classic symptom that we're looking for. So when you're doing your assessment, I want you to think of the five P's. Is there pulselessness, paralysis, paresthesias, pain, and pallor? Those are five key indications that we need to dive into this further and see if this patient has PAD. They can complain of cramping in their lower extremities, like their legs, thighs, calves, even their feet. There can be tissue loss, so you may see some ulcers or wounds that will not heal. They may have poor nail growth because they're not getting that blood flow and circulation. Associated with that could be kind of hair loss and kind of that shiny smooth skin. Those are some pretty good indications. You may have temperature variation, so you may go from warm to cold. And worst case, they can have gangrene. So diagnosis is generally by the AABI or ankle brachial index. This is the cornerstone evaluation. It's pretty low cost and it's non-invasive. So what we do is take some measures in the ankles and compare it to the blood pressure in the arms at rest and after exercise. We calculate this index. The score given will tell you if there's normal, mild, moderate, or severe obstruction that is likely within the patient. Further classification is this Rutherford classification going from stage 0 to stage 6. Really remembering it's based on claudication, which is that kind of cramping pain in the legs with ambulation, and it is relieved by rest. So that's kind of your point, your northern star, if you will. So stage 0 means they have none of that, no claudication, and stage 6 is all the way up to gangrene and that oral ulceration because of that lack of blood flow where it's not mobilized, that it's staying and pooling and not getting oxygen to the vessels. So management, again, we said the number one risk factor is smoking. So if they're smoking, they should stop immediately, and it's really about treating their other comorbidities. So hypertension, diabetes, dyslipidemia, we want to get all of those under control. They may be on antiplatelet therapy with aspirin or Plavix, and then exercise rehab is really good for these patients as well. We can do some interventions, but this is really for severe vascular disease. So we can do a percutaneous angioplasty or bypass surgery, and really the indications are claudication that is incapacitating with a person's ability to work or live a life, basically, or if a patient is at risk of losing that limb, we would definitely consider this. So it's really more in extreme cases. We want to try to do everything we can to prevent that, but there is the option. With that, I hope you found this module helpful. Please email academyatmedaxiom.com with any questions.

ischemic heart disease

peripheral artery disease

atherosclerosis

plaque formation

risk factors

treatment options