Hi, welcome back to Cardiovascular Nursing Essentials. Today we're going to start getting into our disease-specific modules. So we're going to start over these next couple of courses, a deeper look into some of the most common cardiology disease states so that you're familiar with the guidelines and care for these patients. So today we're going to talk about hypertension and lipid management. These are my disclosures and really just going to kind of go over pathophysiology, clinical manifestations, and the guidelines. So we'll break those down a bit. So you will notice that some of these are heavy in the reading material, and I really encourage you to take the time to do the readings and look at those optional readings as well as you can. There's a lot of components to these guidelines, so I want to make sure you're familiar with them and then also have access to them as resources while you're learning and getting more comfortable with them. So let's start with hypertension and talk about this. This is obviously one of the most common issues. It's really important because it does predict an increased risk of cardiovascular disease, so we know it can lead to so many things. And we're really going to define it because we don't want to go based off of one high blood pressure reading, obviously. We want to make sure that it is something that's maintaining high blood pressure readings over multiple times and in various settings. And it's really important because it's known as the silent killer, meaning that you're not necessarily going to get symptoms or they're not going to give you any kind of complaints until it's actually progressed. It's very silent and can really damage people without them even knowing it. And it really increases mortality risk because it's the most common risk factor for CVD and stroke. And as you can see, it causes 7.6 million premature deaths every year. So this is something we can impact. We can save lives by managing blood pressure, but we still have a challenge with that. And you can see I'm big in statistics, and that's really because it's kind of to get you to alert of how detrimental these can be and how important your work is. So it's just a reminder. So you'll see as we go through these modules, I do cover a lot of statistics. And you're going to see these maps and prevalence. And a lot of the cardiology or cardiovascular diseases are heavy in the Southeast states. So just wanted to share some geographic information with you. So as I mentioned, we call hypertension the silent killer. And why is that? Again, you're not going to really experience symptoms or even look for treatment because you often don't know it. So about 20% of our population is not aware that they actually have hypertension. So the U.S. Preventative Services Task Force recommends that we do screen for hypertension in any adult, meaning 18 years or older, with an office blood pressure. So obviously we go for our physicals. We want to check that. If there is suspicion, then we're going to move into some other monitoring scenarios and techniques that we'll talk about. But we do want to start this any time a patient is 18 or older. So there's different categories of blood pressure, and you may see variations. But we want to stick to our ACCHA categories, kind of as our source of truth. So we can see normal, obviously, is that less than 120 over 80. Elevated is that 120, kind of 130 range over 80. Where we get into what we call hypertension is really above that 130 over 80 situation. So when patients may be stage one, that's that 130, 139 over 80 to 89. And that's indications for things like lifestyle changes, which we'll talk about. Or stage two is anything over 140, over or greater than 90. So we really want to make sure that we're looking at, is it systolic or diastolic? Is it both? And as I mentioned, we don't do it based off of one reading, but it needs to be an average of more than two readings over two or more occasions. So let's talk about risk factor, because there are a lot of risk factors, some that we can impact and some that we can't. So we call those that are relatively fixed, more of our things that are embedded within us or related to our socioeconomic status. So obviously, the older we get, the higher risk we are for developing hypertension. We do know that it is higher in our black men. So that population we really want to screen for just because there is a higher prevalence there. And then a strong family history. We want to screen and make sure we're assessing that while we're working up our patients, because genes do impact not just hypertension, but cardiovascular disease in general. Lower socioeconomic status, and that's generally, you know, the things that come with it, like lower access to healthy foods, things of that nature can increase risk. And then other diseases, sleep apnea, kidney disease, and stress can definitely impact our blood pressure. Things that are modifiable are really those things that we can have control over if we make those changes and put some time and effort into it. So obviously, weight, excess weight and obesity, our lifestyle habits, like our physical activity, tobacco use, stress, are we eliminating those? Are we, things like tobacco and vaping, are we getting enough activity, trying to manage our stress? All of those can play into this. And then our diets, what we're putting into our bodies. So a lot of people are eating diets that are high in fat and salt. You know, those convenience meals or fast food, that impacts it. Alcohol intake, obviously excess alcohol can impact our bodies in multiple levels. And then stress, diabetes, and dyslipidemia, all the things that are, not to say that it's easy, but they can be addressed if there's a willingness by a patient to engage. So when we're talking about assessment, we want to remember how to accurately take the blood pressure. And we've talked about this a couple of times. So we don't want to just be haphazard in our methods. It's really important that we're getting our technique and getting the most accurate blood pressure that we can. Orthostatics are important. So again, those do take longer periods of time because of the changes and the time to wait between body changes, but we do know they are important. They can be very insightful into what's going on with a patient. And remember that we need two instances at minimum in two different settings to consider that a patient may have hypertension. On medical assessment, you know, we talked a little bit about the stages. We want to look at that and what is their level of hypertension? How elevated is it? What are some secondary causes? Is it stressful? Is it, you know, is it from diabetes or kidney disease? What could potentially be causing that hypertension? Because if we can address that, is there something we can do to lower their blood pressure? Is their target organ damaged? And that generally doesn't happen until someone's had hypertension for a prolonged period of time. What is their CVD risk? We talked about the ASCVD risk calculator by ACC that will be incorporated into this. And then what is our plan based on our findings? And we need to make sure that it's individualized for that patient. Just like everything, we want to make sure we're doing what's best for that patient. So when we suspect a patient may have hypertension, obviously there are situations where, such as white coat syndrome, where patients are anxious in the hospital or, you know, it's been stressful getting to their appointment. And so their blood pressure may be high, but is that what it is all the time? So there's some strategies and more data that's coming out around ambulatory and home blood pressure monitoring. So that we can see what their blood pressure is doing on a day-to-day basis. So both of these are really kind of self-monitoring. And our home blood pressure monitoring is generally a little bit easier and cheaper than ambulatory blood pressure monitoring. The ambulatory is more set up on specific intervals, generally a shorter period of time. And so you're not going to get quite the picture, but home blood pressure monitoring is pretty readily available and it kind of helps eliminate some of those limitations and barriers that you may see with ambulatory blood pressure. But both of them will provide estimates based on what that patient is doing. And you know, you have patients that are already checking their blood pressure at home and keeping logs. So there are actually some guidelines for home blood pressure monitoring. I believe that link is in the resources and optional readings for you. So you can look into that a little bit more. There is also some recently updated guidelines and recommendations by AHA that I would encourage you to read up on as well. It's important that we know what these patterns are doing because that's going to help us determine do they have hypertension or not. So someone obviously our goal is to be normotensive and that means we're getting good blood pressures in the office and in the home setting. So the ones that we're worried about are really those that are sustained where we're seeing high blood pressure readings, not just in the office, but at home. And then you have those scenarios like the white coat syndrome or maybe mass hypertension, which is not as common, but their blood pressure may be good in the office, but it's bad at home. So really understanding is it something that's consistent and sustained? And that's where we need to really dive in with that patient and see what options they have. So again, generally our findings are not going to be really manifesting or be obvious until it's more severe and we've got some organ damage. So obviously those elevated blood pressure readings, but there are some other clinical assessments or clinical findings that you will may be able to see such as a transient S3 or S4 when you're listening to heart sounds. Their PMI might be displaced if they've had hypertension and their left ventricle has increased in size. So it won't be in the expected place. You may see some dependent edema, you may hear a systolic murmur. Even in their eyes, sometimes they can develop what we call flame hemorrhages. So you can see, I know we don't do a lot of eye exams, but that is something that can be an indication of hypertension. These are just some really common labs and some other diagnostics you may see just in conjunction with establishing a diagnosis. So obviously they're looking if they suspect severe hypertension or it's been prolonged. Maybe they've got some PMI displacement. So they want to see is that left ventricular hypertrophy concerning enough to be potentially heart failure or not. So these are just some common labs and diagnostics you may see. So and you've probably heard of primary versus secondary hypertension. So we're going to break that down a little bit. And primary hypertension is really important because it really involves things like cardiac output, SVR, systemic vascular resistance, and blood volume. And it's caused by some sort of abnormality, which causes some of these mechanisms to fail or not function properly. And one of the systems that's really important in blood pressure and fluid regulation is the RAS, or renin-angiotensin-aldosterone system, and we're going to refresh our brains about that. But this system really increases hormones to help maintain fluid balances and blood pressure. And so you can have some abnormalities in your RAS system. You can have an impaired vascular response where your ability of your vessels to dilate can be impaired. So they're actually contracting more, and that increases stress and can lead to hypertension and stiffening of those vessels. Or is it something like metabolic syndrome? And we'll talk a little bit more about that, but those are, you know, common links with things like hypertension, diabetes, and other metabolic abnormalities that are really triggering kind of an inflammatory response within the body and can put individuals at a higher risk for cardiovascular disease. When we talk about the RAS system, I want to kind of refresh us because a lot of our cardiovascular disease is impacted by this. It's a compensatory mechanism that responds to blood volumes, blood pressures, and changes internally to try to maintain homeostasis or that balance. So your liver and your kidneys are really kind of those sensors. So if they detect that you're not getting enough, if your blood pressure's lower, it responds thinking that you're losing volume. So it's going to really work to release these hormones, the renin and angiotensin, to trigger this process. So angiotensin I is converted to angiotensin II through the lungs where it picks up ACE or angiotensin converting enzyme, and that goes through the adrenals and becomes aldosterone. And aldosterone actually impacts the heart and the arteries by constricting because it wants you to hold on to fluid. If it suspects that you are losing fluid, it's reacting so that you hold sodium and water to increase the blood pressure. So it's really about maintaining that blood pressure and it will respond based on your blood pressure being low or high. Secondary hypertension, on the other hand, is caused by something. So there's some sort of condition that is causing a patient to be hypertension. So that can be things renal related or kidney related. So chronic renal disease, renovascular stenosis, where kind of having management issues in higher fluid or higher volume is causing us to have hypertension. Primary aldosteronism, obviously, if we have higher aldosterone levels, that's going to increase the fluid and hypertension and result in hypertension. Obstructive sleep apnea, we've talked briefly about this, but it can cause increased pressures in the body. Weight gain, either through obesity or pregnancy, can increase the volume and cause hypertension. And then other endocrine disorders. So thinking about Cushing's and thyroid. And I want you to notice during these series, thyroid is related to a lot of cardiovascular things. So we should be making sure we're assessing thyroid status and function in our patients. There is a little bit of a difference in how our patients may present based on if they're primary or secondary hypertension. So primary hypertension is usually more of a gradual or slower onset of that increase in blood pressure. It's generally impacted by lifestyle factors. So think about all those things, stress management, alcohol and tobacco use, diet, things like that. And then family history. So strong family history is a high indication that they will likely also develop hypertension. So you want to assess that. Secondary hypertension, on the other hand, is a reaction or a response to something. So this is generally something that comes on quicker. They may have labile or kind of volatile ups and peaks and valleys of their blood pressure. They may have other symptoms. So like if you think about obstructive sleep apnea, they may be snoring really, really loud or having just hypersomnolence during the day. Is it related to their kidneys or any sort of obstruction in their renal urinary tract? Is it related to maybe the aldosteronism? Are they having any kind of weakness or muscle cramps? Is it related to their thyroid where they may have some heat intolerance or palpitations? So based on how they're presenting, you should be able to help identify, do you want to look at things that are more primary or secondary, secondarily related to that would be causing their hypertension? This is just a good reference for some medications that can increase blood pressure because our patients are on a lot of medications. Some of these are prescribed and some are not. So as you can see, we do consider things like recreational drugs, amphetamines, alcohol. But there are some other prescribed medications that do increase or can increase somebody's blood pressure. So thinking about oral contraceptives, decongestants, so your Sudafed, things like that. There are some herbal supplements that we want to encourage our patients to double check with their pharmacist before adding any of those. This is just one of those reasons. And then NSAIDs, so our Advils, our Aleves, those do cause increase in hypertension and volume. They cause us to hold on to fluid. So we do things like Tylenol instead of those. And then our steroids, so prednisones, those can definitely increase our blood pressure. So I've got these slides in here really showing you the clinical practice guidelines, and I'm not going to go through that. We're going to break down some of these areas, but I have them in here as a reference for you so you can get used to and comfortable with these different pathways based on how a patient is presenting or diagnosed. But what you'll always notice is the first step is lifestyle habits, and we've talked about that a lot and what some of those non-medication interventions are. So when we're treating hypertension, we really got to think about the end goal. So hypertension is related to high mortality. So really you're trying to prevent death in these patients as it's related to that elevated blood pressure. So it's not about treating a number, it's about saving lives. So I want you to remember that. And we have seen where non-pharmacological therapy is, based on research, effective in preventing or lowering hypertension in adults based on what stage they are. So I'm not saying somebody who's extremely high, stage two, should not have medications, but there are ways to prevent or decrease blood pressure levels. So what are specific targets? It depends kind of on each person and what the provider feels is appropriate, but as kind of a general strategy, we really are targeting less than 130 over 80. And some of that does depend on their ASCBD score and what risk they may have for developing other cardiovascular diseases. So keep that in mind. And as we talk about some of those non-pharmacological interventions, this is just really fascinating in terms of correlating how much of a decrease in blood pressure that these interventions can have. So you can see all of these things that we keep stressing about being a healthy weight, having a healthy diet, not eating too much salt or fat, getting activity, decreasing alcohol, how that specifically detracts from those blood pressure numbers. So this is just a really interesting chart for you to reference and have at your disposal. So medications, again, it's really patient-specific, but in general, we try to target less than 130 over 80, but there are things we consider, like we said, that 10-year ASCBD risk, which is a calculator that we've talked about and you can find. So we're really trying to prevent primary hypertension and further CVD events. But if someone's had an event already, we do want to be more cautious or more aggressive in their therapy because they've already had an event putting them at higher risk. So our primary medications, generally, depending on their stage and their risk, we tend to start with diuretics, so thiazide or thiazide-like diuretics. We've talked about that, and really, again, with those, you're really wanting to make sure we're monitoring their electrolytes. ACE inhibitors or ARBs, they should be on one or the other, again, depending on if they've had any reactions or issues with ACEs. The benefits to ARBs is that patients who've had angioedema with ACE inhibitors can typically be on ARBs, pretty low risk. We do wait about six weeks between that change from an ACE to an ARB, though, but wanting to make sure that they're not on both of those. And then there's classes of calcium channel blockers that are appropriate based on whether a patient has heart failure or not. And we really do try to avoid these with concomitant use of beta blockers because there can be some severe bradycardia or heart block with those. So these are all drugs that we've talked about and you have access to, but these are most common, our first kind of line of defense for hypertension patients. Strategies and where I feel our nursing skills and connection really come in is, okay, our providers develop the strategy and the treatment plan. How can we as nurses support our patients? And again, this is a lot of things we've discussed about how do we get on our patient's level? What is their specific knowledge base? Where do they need some gaps filled in and how can you best support that with what resources do you have? What are their attitudes and beliefs? Are they willing to engage? If not, how can you try to engage them? Collaborating with other professionals, we want to make sure we're leveraging our relationships and identifying are there opportunities to engage pharmacy? Is there social support? If it's a stress and anxiety issue, do we need to engage behavioral help or therapy? Making sure that we're following through so patients have that follow-up and we're reinforcing as we can, educating about what those long-term effects are. Sometimes a little bit of tough love is required to get their attention and to try to get them to make some changes or take their medications. Individualizing the regimen, again, making it easy for that patient. So we're trying to use once a day as opposed to twice a day, minimizing the pill burden, things of that nature. And then that social support. So what does that patient have in terms of home, family, life support? Are there opportunities or gaps that we can fill by linking them with others? So looking for those things. As we move into hyperlipidemia, you're going to see kind of the same structure and a lot of commonalities between hypertension and hyperlipidemia and just the prevalence. So we have many, many, many millions of Americans that have total cholesterol levels greater than 200. This is also a silent killer because it's no symptoms, but it leads to high risk of cardiovascular disease and stroke. So we want to make sure we're also doing our due diligence here. And again, when you look at prevalence, very heavy in the Southeast states, it tells us where our hotspots are so we can direct our therapies. So let's talk a little bit more about the structure of our lipid particles because there's three main components, cholesterol, triglycerides, and lipid proteins. All of these are important and they do have functions, but we obviously want to make sure that they're not too high. So cholesterol is really an essential part to help build our cell membranes as part of our nervous system. So we need them. It's produced in the liver and then obviously we also get it from our diet. So how much high fat, high lipid foods we intake obviously is going to increase, but they're needed to help produce our hormones. So they are critical to our balance internally. Triglycerides are really the most common type of fat and it's really our big primary source for energy. It too is made in the liver and the intestines. So it's increased with higher fat and caloric diets as well. So we do produce some, but then we tend to add excess by our diets. The lipid proteins are what actually carries that cholesterol through the blood and we're going to break these down a little bit more because you've got your good, your bad, and then there's some new ones that we're also learning about. So your HDL or your high density lipid protein, these are what we call your good cholesterol. And really what happens is your HDL takes your cholesterol to your liver to excrete it or get out of your body. So that's how it helps maintain a balance. It is associated with a reduced risk of CBD because it's helping get rid of that cholesterol. Very low or VLDL and your LDLs are the ones that put you at increased risk for CBD. So again, they mainly carry triglycerides throughout the body and deposit to the tissues. But we want to make sure this is the one that really we're monitoring for those high levels because they are quote unquote bad cholesterol and both associated with higher cardiovascular events. Now lipoprotein A is kind of one of the newer ones that we're studying and it's just a modified form of LDL. And what happens is it builds up in those blood vessels. So it increases the atherosclerosis or hardening of those vessels, which again promotes plaque formation and rupture because we're increasing inflammation. So the higher the lipoprotein A is the higher risk we have for ASCVD. We don't necessarily run this on everyone. We do see it more commonly, but we really should consider it in women who have hypercholesterolemia and trying to understand their risk associated with higher LPAs. A good population to focus on is those patients that have had ASCVD, but there's no real obvious reason or risk factors. This might have some insight into if there's a hyperlipidemia factor that's not obvious. Our APOB is also kind of in the same vein. It's embedded within those lower density lipoproteins and again, fairly new. We do not run it on everyone because it is expensive and there's some question of reliability in terms of the lab results. We do sometimes consider it if we have really high triglycerides, like greater than 200, because it does correspond to a higher LDL level and we all know that that increases our risk factor. This is something you may hear more about. Our risk factor is very similar to our hypertension, what's modifiable versus relatively fixed. Family history of a premature event, cardiovascular event, that metabolic syndrome, chronic kidney disease or inflammatory conditions. Our highest risk population for hyperlipidemia is actually South Asian ancestry, so something to be aware of. So those modifiable risks, again, are what are we putting into our body? High in fat and cholesterol, are we getting enough activity? Are they smoking or exposed to secondhand smoke? And then what is their weight status, their body habitus? So some other lipid biomarkers you may see, we talked a little bit about the standard cholesterol panel, but we may run some CRPs. These are those LPAs and APOBs. Sometimes we do some ABIs as well, just for concern of claudification from increased viscosity of blood. So those are some additional labs. The standard is really looking at that total cholesterol, triglycerides and HDL, and then that LDL, looking at those different levels to paint the big picture. The main thing for your patients in terms of preparation is they should be fasted for 12 hours before the blood work is drawn. Do you want to call out some of our newest ACS guidelines? So while you're in the clinic, you may have a follow-up for a patient that was admitted with acute coronary syndrome, and we're really trying to target lipid management in this population to prevent further secondary events. So we generally collect lipid profiles within 24 hours of admission for an ACS event. But at discharge, we're really wanting to discharge them with high-intensity statins and schedule a follow-up, so an appointment, but also another lipid panel within 75 days post-discharge so that we can ensure we're addressing their lipid therapies if we need to increase to continue to drive their LDL down. Not going to really read this, but this is just kind of for your reference in terms of what our target goals are for lipid panels for all the different values, so you know what the desirable versus the very high are. When we talk about our clinical assessment, you can't look at a patient necessarily and just tell they have hyperlipidemia. We do want to consider lipid profiles with any kind of initial concerns, especially with endocrine disorders, family history. There are some genetic forms that we'll talk about. We're learning a lot more about those and seeing those more frequently now. I will say there are some things called xanthomas, which are actually lipid deposits that we can get on our tendons, and it's a severe lipid imbalance, so not common, but they can occur. Some words of advice about abdomens. So they're at higher risk for pancreatitis if we have higher levels of triglycerides, so that's something to consider if they're having abdominal issues. And then abdominal pain with unknown origin can also actually be associated as a physical finding with hyperlipidemia. Lipids can actually increase the thickness of the blood and cause blockages and particles that are impeding blood flow and can impact tissue or cause tissue death. So not common, but just something to be aware of. So our different lipid abnormalities, the main two are hypercholesterolemia or hypertriglyceridemia. So obviously hypercholesterolemia is our most common one, and that's generally related to our diets that are high in cholesterol, high in saturated fats. And really what happens is our body does not get cleared of our LDL, so we know that's what helps get rid of our triglycerides and our cholesterol. So that's why that is so common as a lot of it is what we're ingesting into our bodies. There is still not a real clear relationship between triglycerides and CVD. It makes sense, of course, that higher triglycerides do impact a higher risk for CVD. Elevated triglycerides are usually observed in patients that have lower levels of our good cholesterol or HDL. So there is an inverse relationship there. It's also been linked to high carbohydrate or alcohol intake. So again, a lot of how we feed our bodies are related to what's going on inside. And again, this metabolic syndrome is really a name we have for a group of health conditions that will increase risk of heart disease. And that's really high blood sugar, low HDL or that good cholesterol, high levels of LDL or the bad cholesterol, large waist circumference or that kind of apple body shape and high blood pressure. So it's just kind of the perfect storm for increasing and putting somebody at risk for cardiovascular event. There is something called familial hypercholesterolemia or FH, and there are two different types. And this is different from just traditional where it's what we put into our bodies. This is actually a genetic disorder. So don't think of it as, oh, they have this because it runs in their family history. It's actually a genetic disorder. And the reason it's so dangerous is because that person is exposed to LDL levels that are higher elevated over their whole lifetime. So obviously they're at a really high risk of cardiovascular disease. So there's really an urgency to identify this. So we're still learning a little bit about that, but there's heterozygous FH and homozygous FH. Heterozygous FH is really important because again, we want to really treat it before anything develops. And it typically can present with those cardiovascular disease at 55 or 60. So fairly young, if it's not treated. Typically there's one normal gene on the LDL receptor and one abnormal gene. So what happens is you're not excreting LDL at the full rate. So it's really about two thirds of the normal rate. So you have that two to three times increase in LDL levels. Homozygous is people who develop it before they're 20. So obviously that's related or linked to early mortality and they have two abnormal genes. So their levels can get up to six times what the normal level would be. So we really want to make sure that people who are at risk of FH are assessed early. So we can try to prevent that and get them on therapy as soon as possible. And it's interesting because the heterozygous prevalence is about one in every two to 300 people. So it's more common than we probably think. Now, homozygous is not quite as common. It's usually one in 160,000 to 300,000. But still, if it's that one patient or that was your family member, we would want to make sure we're aware of it. And remember, we talked about those xanthomas. So if you're hanging on to LDL, the body only has so many places that can keep it. So it starts actually depositing in tendons and joints can lead to some eye issues too. So those are some kind of later symptoms, but important to note. So diagnosis is based on genetic testing or clinical criteria. So it's really important if it's identified, we do some cascading family histories and screening because others will probably need to be screened and tested. The genetic testing may not be absolutely definitive, but we do want to make sure we're assessing for FH. The main thing is we're started as soon as possible. So we want to target lower LDL levels. So those without any kind of cardiovascular disease target less than 100. For those that do have CVD, less than 70. So we're really want to be aggressive in our therapeutics. And we just start with those traditional lipid lowering medications and intensify as needed. There are some additional therapies that may be available to those with FH, including apheresis, where it's actually moving those LDL components from the plasma. And then there are some medications that work within the intestine and liver and an mRNA level to help eliminate or reduce the production of LDL. So there are some therapies out there. Again, as we get into our guidelines, again, just making sure you're aware of what these are and how we can treat them. And again, mainly our therapies are targeted at what's associated with their ASCVD risk and how high that is. But again, note the number one thing is that healthy lifestyle. So lifestyle modification. And then this breaks it down a little bit more in detail for you in terms of what their actual ASCVD risk score is. So just for your reference. The most recent guidelines are from 2018. And I just wanted to provide you with some of the main points or the 10 key points. And it's really important just in general that we're promoting heart healthy lifestyles. You and I all know how important that is. So no matter who your patient is, that's an important part. And then just how we treat based on what their ASCVD risk is. How do we decrease their LDL? Is that through high intensity statins? How do we get them on that highest dose and max tolerated dose? When do we add things in addition to our statins like our Zadia, our PCSK9 inhibitors, some of those other medications we talked about when that's appropriate. So get yourself familiar with these guidelines because that will help you in your assessment your patient care to anticipate the therapies. I will say I think it's important that you have these readily available because the majority of our patients we see are at risk for ASCVD. So be familiar. Know what your primary prevention strategies are. Know those who are at highest risk, meaning they've got high cholesterol, LDL levels, triglycerides maybe. And know that there's different pathways for them and it's going to be shared decision making between that patient and their provider. And you have a big part in that in educating your patients. As we've talked about statin therapies, we do have different kind of ranges. So you've got high intensity, moderate intensity, and low intensity. So this just kind of breaks it down a little bit easier for you and the associated decreases. So high intensity statins are the most aggressive because they're trying to cut that LDL by about half. So sometimes we have to be very aggressive. Like our ASC patients who've had an active event and they've just been discharged. We don't want to start low and go up. We want to start high and then eventually come down. So this is just for your reference. Some more guidance on primary and secondary prevention. The main things I wanted to talk about with this is when to refer to a lipid specialist because we do have some lipid clinics that are popping up. You may or may not have had one, worked with one. Maybe you're discussing one. And obviously this is not going to be every single patient, but those patients that are really difficult to manage and maybe have LDLs that are intolerant to some statin therapies, maybe they need a specialist. So knowing when, if you have access to a lipid specialist is really important because these patients need to be treated to prevent the risk of CVD and even death. So ask if you're not familiar with that within your organization. So to conclude, I think nurses that we're in the best position to really promote adherence. We tend to have that relationship with the patients. We tend to have higher touch points with them. So we really are well positioned to help them understand, just educate them so they have better knowledge, help clarify any misconceptions, talk to them about their beliefs and attitudes. Some things you can impact, some things you can't. But if you don't know, you won't even have the chance to attempt. So make sure that you're speaking to what that patient needs. Try to be clear and specific, explore opportunities within their belief system and their environments. Is there social support you can tap into? Be honest with them about potential side effects. Obviously they need to be aware, not to be scared, but to be educated on that. And really just trying to make things part of their routine and following up with them in terms of when you have touch points with them, providing feedback and reinforcement. Your relationships matter. A lot of patients really value you and trust you. So use that relationship to try to get through to them and help better their lives and decrease their risk so they can live longer, healthier lives. With that, we are going to finish up this module. Please take the time to do your readings. If you have any questions, don't hesitate to reach out to academy at medaxium.com.

hypertension

lipid management

cardiovascular nursing

silent killer

cardiovascular disease

blood pressure assessment

lifestyle modifications

medication therapies