Welcome to module number five, hypertension. Today, we're gonna walk through number of areas related to hypertension. It's initially though described as the silent killer. And again, from my years of doing clinical work, I will tell you hypertension, although most patients that have hypertension understand it, it's hard to get them to engage in good management around it and this will make more sense here in a little bit because it doesn't hurt. They don't necessarily have symptoms from it. It's a number. And so it's challenging sometimes to get them to take medications or different things. That's where the term the silent killer comes from. There's not a lot of symptoms until it's too late. That being said, here's a few statistics for you. So primary or contributing cause of 691,095 deaths in the US hypertension is. So it is definitely a contributing factor to our life expectancy as well as healthcare costs. Nearly half of adults have hypertension, 119.9 million at a cost of $131 billion. About one in four adults have their hypertension under control. So again, our statistics are not that good when it comes to the effectiveness of the work that we're doing. And about 34 million adults with hypertension have not been prescribed or have not started the prescribed medication. So in some cases, we're not even, haven't even gotten them started or they haven't started what we recommended for them. So this is one that's really challenging when it comes to diagnosis and adherence. So another piece is significant geographic variation. So when we look at hypertension prevalence and this is from 2018 to 2020, adults 18 and older by county across the US, the darker, but we've got counties that have a 42.3 to 58.7% prevalence. And we have others that are still living around 19 to 30% or 20 to 30%. Males are greater than females and the highest prevalence is among black male adults. So I'm gonna walk you through some five areas today. So definitions, pathophysiology, end organ damage, diagnostics and treatment. So we'll start with definitions. There's a number of different definitions out there, but I chose these to kind of get us started. So here we are, the blood pressure classification of the JNC-7 and the 2017 hypertension clinical practice guidelines suggest that a normal blood pressure is less than 120 over 80. Patients with a systolic pressure of 120 to 129 are considered to have pre hypertension. Patients with a blood pressure of 130 to 139 over 80 to 89, according to JNC-7 have pre hypertension, but according to the 2017 hypertension clinical practice guidelines, they have stage one hypertension. And then you'll see when we get into goals, our overall goals are 130 less than, keep our patients less than 130 over 80. Those with a blood pressure 140 to 159 systolic or 90 to 99 diastolic are considered to have either stage one or stage two, and then greater than 160 or greater than 100 diastolic have a stage two hypertension or considered stage two hypertension. So again, I think there's been a lot of evolution in this space over the last couple of decades. I think it's fair to say anything over 130 over 80 to 85 would be considered abnormal. So risk factors, we have a few, there's those that are relatively fixed, like increased age, it goes up the older we get. Black race, highest in non-Hispanic black men. So that's their race ethnicity that gives them risk. Family history, low socioeconomic status, obstructive sleep apnea, chronic kidney disease and psychosocial issues all lead to risk for hypertension. Those risks that are modifiable include excess weight and obesity, lifestyle habits that include lack of physical activity, stress and tobacco use, dietary factors such as diets high in fat or sodium and diets low in potassium. Excessive alcohol intake, stress, diabetes and dyslipidemia slash hypercholesterolemia are all modifiable risk factors. So let's walk through a little bit of the pathophysiology. So there's a number of things that happen that up-regulate our blood pressure that create a state of hypertension. And I'm not gonna go into major detail in all of these, but the first one is renin-angiotensin-aldosterone system, the sympathetic nervous system, endothelins, endovascular function, arginine-vasopressin and then metabolism. The ones that I wanna hit first or the one I wanna spend most of our time on are the first two, because those are the areas where we manage through our pharmacologic management as far as intervention. So I think it's important to understand the pathophysiology behind those two. So the first one is the renin-angiotensin-aldosterone pathway. So in this case, what we have here is a systemic RAAS. This starts in the liver where we have developed angiotensinogen that based on neurohormonal effects from the kidney where the kidney secretes renin that takes that angiotensinogen and turns it into angiotensin I. Angiotensin I then converts to angiotensin II and look what happens. We end up with the angiotensin II affects the cardiomyocyte, so the heart cells to create hypertrophy and disturb microvessel architecture that all lead to coronary microvascular dysfunction. In addition to that, we have the same thing happening on the cardiac side where when we start to have cardiac issues related to some potentially decreased perfusion of kidneys and other organs, we see an increase in angiotensin I conversion to angiotensin II that goes on to create microvascular damage, vasoconstriction, and impaired vasodilatation that also going on to create coronary microvascular dysfunction, as well as that angiotensin II that also affects the adrenal gland that secretes aldosterone that then has a hormonal impact on the kidney and that goes on to increase hypertension or increase that blood pressure as well. So there's a couple of things that are happening in here. One, we see the cardiomyocyte dysfunction and hypertrophy. We also see when we get into the kidney issue over here, we start to see some sodium retention, which increases volume that then therefore increases blood pressure. And we also see vasoconstriction that happens right here. And when we see vasoconstriction, that also increases blood pressure. And all of this is under the guise of increased inflammation that further creates another environment to, it's kind of, it's very cyclical. So it begins to create or really move that RAAS cycle even further. And although this may be a fairly elementary way to think about blood pressure, there's really three things that drive your blood pressure or create a state of hypertension. Your pump, your pipes, and the volume in your pipes. So the harder is your pump, the harder the heart contracts, the increased pressure that's being put out into the vessels or the pipes. The smaller the pipes are, the more pressure that's in the pipe. So if you vasoconstrict down, you're going to have, take that same volume in a smaller pipe, it's going to increase the pressure in the pipe. And then if you add more volume to the pipe, it's going to increase the pressure in the pipe because we're moving more volume or more fluid through those pipes. So translate that to what we're seeing right here, and we're seeing increase in volume or fluid retention. So that's increasing the volume. We're seeing vasoconstriction. So that's decreasing the size of the pipes. And then we're seeing cardiomyocyte hypertrophy that is potentially going on to increase cardiac function. Now, the next area, and I said, we're going to talk about two, the next one is a sympathetic nervous system. So these afferent sympathetic nerves create an environment where they also increase cardiac output, increase contractility, that also increases pressure. But the same sympathetic nervous system also increases vascular resistance. So they also create vasoconstriction that goes on to have challenges related to vascular remodeling and smooth muscle hypertrophy. And then on the kidney side, it increases renin release, which activates the renin-angiotensin-aldosterone system, increase sodium retention, and decrease renal blood flow that again, turns into another kind of cyclical pathway for increasing vascular dysfunction and hypertension. So there's a couple of different types of hypertension. There's primary and secondary. Primary is complex. It involves mechanisms that influence cardiac output, systemic vascular resistance, and blood volume, all those things I just talked about. It's caused by one or several abnormalities in the function of these mechanisms or the failure of other factors to compensate for these malfunctioning mechanisms. And I mentioned the renin-angiotensin-aldosterone system. There's an increase in renin-angiotensin-aldosterone activity, there's extracellular fluid volume expansion, and an increase in systemic vascular resistance. We also see an impaired vascular response that includes impaired dilatation and increases in contraction, and then increase oxidative stress that equals hypertension and atherogenesis. And then finally, metabolic syndrome. There's a common link here to hypertension, diabetes, and other metabolic abnormalities that include abdominal obesity, with or without impaired glucose tolerance, plus a pro-thrombotic and pro-inflammatory state, and place individuals at a higher cardiovascular risk. So primary hypertension. Secondary hypertension is hypertension caused by another condition, and I've laid them out here. So there's a number of them. Diabetic nephropathy, polycystic kidney disease, glomerular disease, renal vascular hypertension. Those all kind of live in the kidney. Then there's Cushing syndrome, aldosteronism, pheochromocytoma, thyroid disease, hyperparathyroidism. Those all live within our neurohormonal system, our hormones in the different axes that manage all of that. And then there's the coarctation of the aorta, sleep apnea, obesity, pregnancy, and then finally medications and supplements. So I think the key take home here is that when you have a patient that is a new diagnosis of hypertension, and we'll walk through this, but there's a number of things that you need to do as far as working that patient up to really look for any secondary causes that should be managed. So one of the key things when we get into treatment is, and I'm kind of the end before the means, is end organ damage. So these are the things we're seeking to prevent. And there's really four areas that untreated hypertension, there's more than this, but the big four are cerebrovascular disease, so stroke, peripheral vascular disease, left ventricular hypertrophy that can go on to lead to heart failure, and then renal vascular disease that can lead to chronic kidney disease. So our goal by managing our hypertension is to really minimize the effect from a vascular perspective on these different end organs. So let's talk about diagnostics. So as a medical provider, your medical assessment should include these key pieces. So hypertension diagnosis and stage, any secondary causes of hypertension, the presence of target organ damage, the level of global cardiovascular disease risk, and the plan for individualized monitoring and therapy. So how do we go about that? Well, first of all, let's start with those blood pressure measurement definitions and corresponding values. What you're gonna find when you get into the literature is that you've got your office-based blood pressure, that's taken in the clinic setting using a osculometric or aneuroid device. You've got your ambulatory outpatient blood pressure that's taken in the clinic setting using a commercially available device. You've got the home blood pressure monitoring taken by the patient at home, and you've got the ambulatory, which is a device worn that takes regular interval blood pressure measurements. And depending on the time of day, depending on the setting, what's considered abnormal versus normal may be different. So I laid those out for you here. As far as measurements, you've got two options. There's the auscultative, which is really the manual, and then the oxalimetric, which is the automated using a software within the device that detects the waveforms and creates your measurement. The key to both of those is properly preparing your patients and following the steps. And I think this is really important because using proper technique, taking proper measurements, properly documenting the blood pressure, averaging the readings and providing the blood pressure to the patient are all key tasks in order to manage through or develop. So the idea of rushing a patient from the waiting room who just got out of bad traffic into an exam room and quickly slapping on the blood pressure cuff while they're sitting and quickly taking a blood pressure may not provide you the most accurate number. And so oftentimes, especially when I do clinical work and I have a blood pressure documented from the medical assistant or whoever roomed the patient, I will oftentimes, especially if it's elevated, I will repeat that because they've had a chance to sit. They've had a chance to kind of relax and it gives me, I believe, a more accurate reading than one that was taken after they rushed back to the exam room. There's a number of ways we can do out-of-office monitoring. And this is important because a number of our patients, when we do this in our exam rooms, can have what's called white coat hypertension, meaning that they're nervous, they just rushed in. And so their typical activities at home and throughout the day, then when they're not sitting in your clinic, patient's blood pressures don't tend to be as high. So if you're at all concerned that the patient might have white coat hypertension, we have opportunities for out of office monitoring. The first one I mentioned, actually walked through these already for you, but there's the ambulatory blood pressure monitoring. This is used to tame blood pressure readings at set intervals, usually over a 24 hour period. There's home blood pressure monitoring. That's where they manage or assess self-monitoring. So they're taking their own readings. Both provide blood pressure estimates that are based on multiple measurements and increasing number of individuals are using them regularly to check their blood pressure at home. This is a great way to promote patient engagement and get you good information in which to better manage your patients. Both of these are recommended as far as for surveillance. And in some cases, even for diagnosis, again, if you're worried about the white coat syndrome. Few things related to home blood pressure measurement considerations. The patient should measure two sets of two to three readings each day. One set in the AM, one set in the PM. AM and PM sets from at least three days over the course of one week should be collected. The first set should start after five minutes of rest with additional readings at one minute intervals and average the lowest readings each day, both the AM and the PM set. Encourage patients to validate their device with an office device annually. So when they come in for their visits, having them bring their home cup so that you can calibrate it or at least validate to understand how close it is to the ones that you're using in the office. From a clinical finding, what you might see in patients that have hypertension, hyperpensions will typically not manifest until it becomes severe or you start to see some end organ damage or target organ damage. But elevated blood pressure readings, dependent edema in chronic disease, transient S3 or S4 heart sounds may occur. You could have a systolic murmur, especially if the patients have aortic stenosis. Displaced point of maximal impulse from left ventricular hypertrophy or flame hemorrhages on retinal exam. So again, when you're examining your patient or working your patient up, these are the sorts of things that you might see if they have undiagnosed hypertension. So your workup objectives are twofold, identify precipitating factors as well as identify target organ damage. So those precipitating factors start with a good history. So previous diagnosis, previous blood pressure readings, any risk factors, family history, tobacco, alcohol use, activity, weight gain, sleep, stress, other comorbidities, and then target organ damage such as neurovascular, any history of stroke, any history of cardiac or peripheral disease, and any previous therapies if they've been on medications in the past or other therapies. So for a physical exam, a BMI, waist circumference, really looking for any evidence of obesity, fundoscopic exam, looking for any vascular damage, neurologic exam, cardiac exam, pulmonary and peripheral arterial exam, again, looking for any vascular disease evidence. From a lab or diagnostic tests, a hemoglobin hematocrit, fasting blood sugar, a hemoglobin A1C, looking for underlying diabetes, lipid panel, serum electrolytes, uric acid, renal function such as a creatinine BUN, and then a urinalysis are all good, easy routine diagnostics tests that provide some insights as far as some of the comorbidities or drivers of hypertension. So identifying target organ damage outside of the physical exam. There's a few things here. So 12 lead EKG that may give you evidence or give you signs of evidence of left ventricular hypertrophy or any other structural changes. I say that it's not sensitive or incredibly specific, but when it's abnormal, it just gives you a sign, if you will, that you need to look for something more. So probably need an echocardiogram. Urinalbumin that looks at the urinalbumin creatinine ratio, kind of help understand if there's any level of chronic kidney disease, that serum creatinine, their estimated glomerular filtration rate. Again, any evidence of chronic kidney disease. I mentioned the echocardiography or echocardiogram. Carotid artery ultrasound to look for any vascular disease or thickening or stenosis. Coronary artery calcium score that again, looks for any calcium that it just looks for any vascular disease. Abdominal aortic ultrasound, kidney ultrasound, ankle brachial index that again, easy way to measure our concerns around peripheral vascular disease. A retinal exam, brain imaging, if you're concerned that there's been a stroke and then cognitive function testing. Again, these in totality are not required on every patient. These would be related that if you find something on physical exam, that you're concerned about target organ damage. These are the sorts of studies that you would look to confirm that. All right, let's talk about treatment. So from a treatment perspective, you really have three objectives. Number one, to identify, remove medications that increase their blood pressure, lifestyle interventions and pharmacologic therapies. So I'm gonna provide a list of frequently used medications and substances that may increase blood pressure. Again, your goal is to look for those precipitating events. So on here, you'll see alcohol, amphetamines, atypical antipsychotics, caffeine, decongestants, herbal supplements, oral contraceptives, anti-inflammatories, recreation drugs, steroids, all of these can increase blood pressure. So you need to start with, what are the things we can change that may, maybe some of these are related to medication use for other reasons. And then we start to think about the actual intervention. So our goal would be to prevent morbidity mortality related to elevated blood pressure. Non-pharmacologic therapy alone is effective for prevention of hypertension in adults with elevated blood pressure and the management of uncomplicated and milder forms of hypertension. So those lifestyle pieces related to activity, weight loss, and I'm gonna talk about that in a minute. From a target blood pressure, so for adults with confirmed hypertension and known cardiovascular disease or a 10-year atherosclerotic cardiovascular disease event risk of greater than 10%, your goal is 130 over 80 millimeters of mercury. For adults with confirmed hypertension and no additional markers of cardiovascular disease, the goal of 130 over 80 may still be reasonable. So I'm gonna make this simple for you. I think 130 over 80 is the number that we need to shoot for when it comes to management of our patients. So here's kind of a long list of non-pharmacologic interventions that include weight loss. And I mentioned earlier that an aim for a one kilogram reduction at least decreases your blood pressure one millimeter of mercury or for every one kilogram lost. So you can have, even with just a little bit of weight loss, you can have a fair amount of impact on blood pressure reduction. Healthy diet, you can see a decrease in 11 millimeters of mercury. So you can take a patient with a blood pressure of 140, have them change their diet and they can drop it down to 130. Reduce sodium intake. Again, especially if they're a high salt user, reducing their goal. And in this case, recommending a 1500 milligram a day goal can have, again, significant. Enhanced potassium intake and then physical activity. So, and alcohol in moderation. So when you start to look at the potential reduction, these things can add up. So if you have a patient with a pre hypertension or a stage one hypertension with no target organ damage, you may get fairly good results from lifestyle. However, engagement can be tough. So when you think about the difference between the physical activity, the diet, the weight loss, although I would argue physical activity and diet will create weight loss, and probably the biggest challenge is just patient engagement and adherence to getting the effect that you and they are seeking. So most patients end up on medications. Adults, again, how do we think about this? Adults with an estimated 10 year atherosclerotic CVD risk of less than 10% and no history of CVD and a blood pressure of greater than 140 or over 90 for primary prevention of cardiovascular events. You can kind of read through here. Estimated 10 year atherosclerotic cardiovascular risk of greater than 10% with a blood pressure greater than 130 over 80 for primary prevention of cardiovascular events, secondary prevention. So if they'd had no cardiovascular events that we wanna treat these patients. And in all of these cases, we're looking for a blood pressure target of less than 130 over 80. So our primary agents include thiazides or thiazide like diuretics. And I gave you a small list. ACE inhibitors, angiotensin receptor blocking agents, calcium channel blockers. And there's two different kinds. There's the dihydropyridines and the non-dihydropyridines. We've listed out a few. So as you think about these different classes, they each have a different mechanism of action that target blood pressure reduction in one of those three different areas. So the first one being, remember that volume increase. So the thiazides, the diuretics decrease the volume. The ACE inhibitors and ARBs manage the renin-angiotensin-aldosterone system that decreases the vasoconstriction or actually creates vasodilatation. So it increases the size of pipes. And calcium channel blockers, although mechanism of how we do it's a little bit different, also have some vasodilatory properties as well as in some cases like the verapamil, diltiazem or the non-dihydropyridines actually increase some heart rate that increases again, cardiac output. So decreases some of that pump. In addition, we have some other things to think about. So in here, I wanted to provide you the mechanism of actions. As I mentioned already for each of these, there's some significant contraindications. So ACE inhibitors would be very careful with hyperkalemia. Patients that are pregnant can not have ACE inhibitors or ARBs. Mentioned, did not mention beta blockers yet. So beta blockers decrease heart rate and contractility through blocking that sympathetic nervous system. So they're gonna increase that pump contraction that then decreases blood pressure. However, also decreases heart rate. And so we have to be careful related to bradycardia. And we also have some issues for those patients with reactive airway disease that can develop some additional wheezing or active wheezing. So they have to be used with caution in those patients. And then I mentioned the diuretics already. So a few strategies to promote blood pressure control. Number one, identify knowledge, attitudes, and beliefs with your patients. So I remember I mentioned is the silent killer. It doesn't have a lot of symptoms until people hit target organ damage. And so it's really, and yet, that's not where we wanna make the diagnosis. So it takes time and it takes helping your patients understand what the risks are and why. We need to educate them about conditions and treatment experience. We need to collaborate with other professionals. So again, we live in the cardiovascular space, but we need to collaborate, communicate with primary care and some of the other specialties. We need to individualize the regimen. If I go back to this, there's a number of side effects and things that need to happen and contraindications. So we need to help our patients understand kind of what to expect and create the best regimen for them. We need to provide follow-up and reinforcement. None of these are a one and done. Most of these medications require titration to maximal effect. And then we need to promote social support. Again, if you go back to those initial prevalence, one third of Americans probably have hypertension, whether diagnosed or undiagnosed. So again, I think we have a long way to go, but here's a few things to kind of help you think about how best to work with your patients and develop that adherence. And then the last thing that I wanted to provide for you is just the most recent guideline considerations from the ACC AHA. So there's a few things in here that I think are important. An adult with untreated systolic blood pressure greater than 130, but less than 160, it is reasonable to screen for the presence of white coat hypertension with ambulatory blood pressure monitoring or home blood pressure monitoring. So if a patient walks in, the first time they've had a blood pressure of 140 or 150, you won't see any evidence of target organ damage on exam. It's okay to send them home to monitor some blood pressures or send them home on an ambulatory blood pressure monitor and see what their blood pressure is when they're not in your office. Number two, screening for primary aldosteronism is recommended in the presence of any of the following, resistant hypertension. So those patients that you're on three, four drugs and you're still not getting them under good control, patients with underlying hypokalemia, any evidence of adrenal mass or a family history or early onset hypertension, stroke at a young age. And I can tell you stories of patients that I managed that fell in this category. And once we tested them for aldosteronism and realized that they actually had hyperaldosteronism and treated it, their blood pressure came down nicely. But before that, it was very challenging. So primary aldosteronism is real. And when your patients fit this criteria, it's important to do some additional diagnostics. Alcohol consumption should be limited to two or less drinks per day for men and one drink for women. This also contributes significantly to hypertension. And I tell my patients, you can't save it all up for one day. So you can't binge drink on the weekends, that doesn't count. You really want to manage this, you know, no more than that in one day. Two or more antihypertensive medications are recommended to achieve a blood pressure target of less than 130. It typically takes more than one class to do that. ACEs and ARBs, as I mentioned, should not be used in pregnant women. And then finally, patients with a systolic pressure greater than 180 or diastolic blood pressure greater than 110 should be treated promptly. So you need to treat them that day. And if there's any concerns over target organ damage or that they actually have pressures higher than this, they may need to be hospitalized for better blood pressure and urgent blood pressure management. So that ends the hypertension module. We appreciate your engagement. And as always, any questions or feedback, please reach out. We're always looking for ways that we can improve, but so much appreciate your engagement. So thank you.

hypertension

silent killer

blood pressure

diagnosis

treatment adherence

risk factors

pharmacologic therapies