Dr. Alex Jimenez Presents: How Hypertension Is Explained

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Introduction

Dr. Alex Jimenez, D.C., presents how hypertension affects the human body and some causes that can increase hypertension in many individuals in this 2-part series. We refer our patients to certified medical providers who provide multiple available treatments for many individuals suffering from hypertension associated with the cardiovascular and immune systems affecting the body. We encourage each of our patients by mentioning them to associated medical providers based on their analysis appropriately. We understand that education is a delightful way when asking our providers questions at the patient’s request and understanding. Dr. Jimenez, D.C., only makes use of this information as an educational service. Disclaimer

 

How To Look For Hypertension

Dr. Alex Jimenez, D.C., presents: Let’s go back to the decision tree so you can begin to think about how you will apply the go-to-it model in functional medicine to hypertension and how you will start better assessing somebody with hypertension rather than telling them that their blood pressure is elevated. Is the body influenced by inflammation, oxidative stress, or immune response? Is it affecting endothelial function or vascular smooth muscle from those three categories of reactions, inflammation, oxidative stress, or immune response? Do we choose a diuretic calcium channel blocker or an ACE inhibitor? And so to do that, it’s really important in our gather section. Taking the medical history and the timeline of their hypertension, you get a clue about the organ damage to the questionnaires. You’re looking at their anthropometrics.

 

This includes the following questions:

• What are the inflammatory markers?
• What are the biomarkers and clinical indicators?

 

Those are outlined through the clinical decision tree. And already just doing that, you’re going to expand and fine-tune your lens on what you might see in your hypertensive patient. Let’s add to the timeline when does hypertension begin? The timeframe of hypertension begins actually in prenatally. It’s important to ask your patient if they were early or large educational age. Was their mother stressed? Were they born early or premature? Was there nutritional stress in their pregnancy? If they know that, you can have two people with the same kidney size, but the person who didn’t have enough protein during pregnancy can have up to 40% less glomeruli. Knowing that will change how you adjust the medication decades later if you know they possibly have 40% less glomeruli.

 

The Timeline For Blood Pressure

Dr. Alex Jimenez, D.C., presents: So it’s important to take the timeline of their blood pressure. Then it’s also important to recognize what is happening when we begin to organize and collect data through the biomarkers; the basic biomarkers will give you clues about whether they have issues with insulin lipids, whether they have problems with vascular reactivity, autonomic nervous system balance, imbalance, coagulation, or immune toxin effects. So this is a reasonable thing to print off because, in your hypertensive patient, this is through just the biomarkers you can begin to get a clue as to what areas of dysfunction affect inflammation, oxidative stress, and immune response and how these biomarkers reflect that information for you. This is very reasonable to have in front of you to help change your thoughts about hypertension and also enables you to refine some of the characteristics of the person on the other side of your stethoscope in a more personalized, precise way.

 

But let’s start at the very beginning. Does your patient have high blood pressure? We know that depending on the end organ effects of their comorbidities, you may run someone a slightly higher blood pressure if you have a profusion issue in the brain and the kidneys or the heart, but some guidelines are there. Our 2017 American Heart Association guidelines for blood pressure categories are listed here. They’ve waxed and waned back and forth over the last couple of decades, but this is very clear. Having elevated blood pressure, anything above 120, really shifted how many people we start seeing or considering addressing the root causes of their blood pressure. So we will come back to this, especially in the case to help us look at how we categorize people with blood pressure issues.

 

The Criteria To Mesure Blood Pressure

Dr. Alex Jimenez, D.C., presents: What is the first step? It’s how do you have the blood pressure taken in your patient? Do they monitor it at home? Do they bring those numbers to you? How do you monitor blood pressure in your clinic? How do you get accurate readings in your clinic? Here are the criteria to accurately measure blood pressure and the questions to consider whether you’re doing all these. 

• Do you ask your patient whether they’ve had caffeine in the last hour?
• Whether they’ve smoked in the previous hour?
• Were they exposed to smoke in the last hour? 
• Is the place where you’re taking blood pressure warm and quiet?
• Are they sitting with their back supported in a chair with their feet on the ground?
• Do you use the roll-around side table to rest your arm at the heart level?
• Are they sitting at the exam table with their feet dangling, and a nurse aide elevates their arm and puts in their axillary fold to hold their arm there?
• Are their feet on the ground? 
• Have they sat there for five minutes? 
• Have they exercised in the previous 30 minutes? 

 

You may have systolic blood pressure if everything is in the criteria. Here’s the challenge. There are 10 to 15 millimeters of mercury higher when it comes to sitting and taking blood pressure. What about the cuff size? We know last century; most adults had an upper arm circumference of fewer than 33 centimeters. Over 61% of people now have an upper arm circumference greater than 33 centimeters. So the size of the cuff is different for around 60% of your adult patients, depending on your population. So you have to use a large cuff. So take a look at how blood pressure is collected in your office. Let’s say the blood pressure is elevated in your patients; then we have to ask, is it normal? Great.

 

The Different Types Of Hypertension

Dr. Alex Jimenez, D.C., presents: Is it elevated because of white-coat hypertension? Do they have normal blood pressure, elevated outside the clinic, or masked hypertension? Or do they just have sustained hypertension which is a challenge? We’ll talk about that. So when you interpret, it is also important to consider ambulatory blood pressure monitoring. So if you have somebody who’s hypertensive and don’t know whether the blood pressure goes down and you’re trying to figure out whether they have sustained hypertension, you can use 24-hour blood pressure monitoring. The mean daytime blood pressure above 130 over 80 is hypertensive the mean nighttime blood pressure above 110 over 65 is hypertensive. So why is this important? The average blood pressure dips to around 15% at night because of the issue with blood pressure dipping. Failure to have blood pressure drop while you sleep at night could develop problems that can affect a person throughout the day. 

 

If your patient sleeps at night, it should drop about 15% when they sleep. If they have non-dipping blood pressure, it is associated with comorbidities. What are some of those comorbidities in non-dipping blood pressure? Some of the conditions correlated with non-dipping blood pressure include:

• Congestive Heart Disease
• Cardiovascular Disease
• Cerebrovascular Disease
• Congestive Heart Failure
• Chronic Renal Failure
• Silent Cerebral Infractions

Co-morbidities Associated With Non-Blood Pressure

Dr. Alex Jimenez, D.C., presents: These are the comorbidities associated with non-blood pressure. All of us agree that elevated blood pressure is not necessarily good in all those conditions. So when you look at different people groups or other comorbidities, non-dipping blood pressure is most commonly associated with sodium-sensitive folks, people who have renal insufficiency, people who have diabetes, people who have left ventricular hypertrophy, people who have refractory hypertension or autonomic nervous system dysfunction and finally, sleep apnea. So, non-dipping blood pressure increases your association with subclinical cardiac damage. Okay, Reverse dipping means you are more hypertensive at night and is more ascent associated than during the day is more related to hemorrhagic stroke. And if you have somebody with nocturnal hypertension, you have to start thinking about things like the carotid arteries and increased carotid, internal medial thickness. You start thinking about left ventricular hypertrophy and may see it on EKG. Here’s what we know about nocturnal hypertension. Nocturnal hypertension is a nighttime blood pressure greater than 120 over 70. It is associated with greater predictability of cardiovascular morbidity and mortality.

 

If you have nocturnal hypertension, it increases your risk of mortality from cardiovascular disease by 29 to 38%. We must know what’s happening at night when we sleep, right? Well, what’s another refinement? Another refinement is recognizing that resting blood pressure is controlled by your renin-angiotensin system. Waking blood pressure is controlled by your sympathetic nervous system. So let’s talk about how their renal angiotensin system drives their nighttime hypertension, and you think about what medication they’re taking. You might change the medication dosing to nighttime. Well, studies have shown that if you have nighttime hypertension and are a non-dipper, it’s best to take your ACE inhibitors, ARBs, calcium channel blockers, and certain beta blockers at night before bed. But it makes sense that you wouldn’t move your diuretics to nighttime, or you will have a disruptive sleep.

 

Addressing Daytime & Nighttime Blood Pressure

Dr. Alex Jimenez, D.C., presents: So if we don’t address daytime and nighttime blood pressure, we have to consider the effect of blood pressure load. What is your average daytime blood pressure and your moderate sleeping blood pressure is. We know that blood pressure load in young adults is hypertensive only about 9% of the time. So meaning the systolic load is about 9% versus in the elderly, about 80% of the blood pressure load is systolic. And so when you have a higher systolic load, you have more complications and end-organ damage. So what we’re talking about is helping identify your patient with hypertension; what is their timeline? What is their phenotype? Are they only hypertensive during the day, or they’re hypertensive at night also? We have to look at what helps balance that.

 

Here’s the other point, only about 3.5% of people with hypertension do it have a genetic cause. Only 3.5% of people their genes cause hypertension. The power is at the bottom of the matrix and recognizing these patterns, right? So you look at exercise, sleep, diet, stress, and relationships. So we know that these four autonomic balances help determine blood pressure. We will examine the renal angiotensin system, plasma volume where they hold onto too much fluid, secondary salt load, and endothelial dysfunction. Abnormalities in any of these can lead to hypertension. We’ve been talking about another one that can lead to hypertension: the link between insulin resistance and hypertension.

 

This diagrammatically gives you an idea of the physiologic interactions between insulin resistance and hypertension. It affects increasing sympathetic tone and increasing renal-angiotensin system balance. So let’s spend a few minutes on the renin-angiotensin system pathway angiotensinogen down to angiotensin two. We take advantage of these enzymes by giving inhibitors to angiotensin-converting enzymes in our hypertensives patients. Elevated angiotensin two leads to cardiovascular hypertrophy, leads to sympathetic phase constriction, increased blood volume, sodium fluid, retention, and aldosterone release. Can you inquire about your patient biomarkers? Can you ask whether they have elevated renin levels?

 

Look For The Signs

Dr. Alex Jimenez, D.C., presents: Well, you can. You can check plasma renin activity and aldosterone levels. It’s important to do this if your patient is hypertensive and has never been on medication because this is where nitrous oxide is so important. This is where your endothelial nitric oxide synthase is present. This is where you have sheer and hemodynamic stress. This is where dietary intake of arginine or the environment that affects nitric oxide plays such a role in the health of this layer of endothelia. If you lay it all together somehow, miraculously, or at least in your mind’s eye, it’ll cover six tennis courts in the average adult. It’s a huge surface area. And the things that cause endothelial dysfunction are not new news to people in functional medicine. Increased oxidative stress and inflammation are two things we mentioned that play an effect.

 

And then, look at some of these other components, your ADMA being elevated and correlated with insulin resistance. It all begins to form together in a matrix that interacts. So you look at one comorbidity in cardiometabolic syndrome, and it affects another comorbidity. You suddenly see the interrelation between them or hyperhomocysteinemia, which is a one-carbon metabolism marker, meaning you’re looking at the adequacy of folate, b12, b6, riboflavin, and that activity of your one-carbon metabolism. So let’s look at some of these emerging risk markers to improve and track in patients with hypertension. Let’s reanalyze ADMA again. ADMA stands for asymmetric dimethyl arginine. Asymmetric, dimethyl arginine is a biomarker of endothelial dysfunction. That molecule inhibits nitric oxide synthase while impairing endothelial function, and in all of the comorbidities associated with cardiometabolic syndrome, ADMA can be elevated.

Conclusion

So, as a quick review, L-arginine is converted to nitric oxide via nitric oxide synthase, and nitric oxide adequacy leads to vasodilation. ADMA blocks this conversion. And if your ADMA levels are elevated and your nitric oxide levels are low, then you have decreased nitric oxide platelet aggregation increases in LDL oxidation. So many things reduce nitric oxide or are associated with lower nitric oxide levels, sleep apnea, low dietary arginine, protein, zinc insufficiency, and smoking.

 

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