04.02 Nursing Care and Pathophysiology of Hypertension (HTN)

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Outline

Overview

  1. Diagnosed after readings fall into hypertensive category on three separate occasions.
  2. Classified in stages
    1. Visit Mayo Clinic for more information on stages: http://goo.gl/icZSxe

Pathophysiology:

Hypertension is high blood pressure. This can be caused by things like age and race or things like smoking, obesity, stress, hyperlipidemia, atherosclerosis. These causes block and harden the vessels. When the vessels become hardened and block the heart has to work harder to pump against this. When the heart pumps and works harder is becomes stressed.

Nursing Points

General

  1. Hypertension is pressure ascension
    1. High Blood Pressure
      1. BP > 130/80 (Stage 1)
      2. BP > 140/90 (Stage 2) 
  2. Physiology
    1. Peripheral Resistance
      1. Prolonged smooth muscle contraction
      2. Structural changes
    2. Renin Angiotensin Aldosterone System
      1. Angiotensin 2 and Aldosterone production = Increased BP
      2. Reference other content
    3. Atherosclerosis
      1. Plaque deposits in damaged arterial walls
  3. Silent Killer
    1. Asymptomatic until damage is done:
    2. CHF
      1. Prolonged increased cardiac work
    3. End organ damage
      1. Prolonged hypoperfusion

Assessment

  1. Assessment
    1. Risk Factors
    2. “Silent Killer” 
      1. Asymptomatic until end organ damage occurs
        1. Stroke
        2. MI
        3. Renal Failure
        4. Heart Failure
    3. Later signs
      1. Vision changes
      2. Frequent headaches
      3. Dizziness
      4. Chest Pain/Angina
  2. Monitoring
    1. Blood Pressure Cuff
      1. Too small = false high
      2. Too large = false low

Risk Factors

  1. Non-modifiable Risk Factors
    1. Familial
    2. African American
    3. Age
  2. Modifiable Risk Factors
    1. Smoking
    2. Obesity
    3. Lipids
    4. Salt

Therapeutic Management

  1. Therapeutic Management
    1. Medication therapy
      1. ACE Inhibitors
      2. Beta Blockers
      3. Calcium Channel Blockers
      4. Diuretics
    2. Diet & Lifestyle modifications
  2. Nursing Priorities
    1. Perfusion
      1. Administer BP meds
        1. Check BP/HR first
        2. Space out timing to avoid hypotension
      2. Assess for end-organ damage – renal and neuro status
      3. Strict I&O
      4. Asses for CV changes
    2. Health Promotion
      1. Diet & Lifestyle Changes
      2. BP Screening
      3. Follow-ups with HCP
    3. Patient Education
      1. See below

Patient Education

  1. Medication Instructions
    1. Continue meds even if you feel better
    2. Avoid baths / strenuous activity after meds due to vasodilation
  2. Diet – DASH
    1. Low Sodium
    2. No processed/canned foods
    3. Limit caffeine/alcohol
  3. Lifestyle changes
    1. Exercise
    2. Smoking cessation

Related Lesson

Transcript

What’s going on, guys. My name is Brad and welcome to nursing.com. And in today’s video, what we’re going to be discussing is hypertension. What I’d like to do is really dive into the pathophysiology behind hypertension. And I really feel like if you can understand that, then you’re really going to be able to grasp all of the other things that we’re going to discuss here in this lesson.  Without further ado, let’s dive in. 

So whenever we’re talking about hypertension, hypertension is pressure ascension, a nice little rhyming way to remember that, but it’s high blood pressure. That’s what hypertension is. And it’s specifically defined as a blood pressure greater than 130 over 80 in stage 1 and greater than 140 over 90 in stage 2. If that systolic blood pressure is greater than 140 or that diastolic, that bottom number is greater than 90, then the patient is considered to have hypertension. And so whenever discussing the pathophysiology of hypertension, I think it’s always important to really understand exactly what we’re talking about and what we’re dealing with here. 

Now, the first thing that I’d like to do, I’d like to discuss here with hypertension is peripheral resistance. So, what we have here is basically a little cross section of a vessel. Imagine that the inside of this, this is the inside of the vessel wall, where your little red blood cells are going. And so it’s important to understand that the lining of your arteries, the lining of your vessel, are actually lined with smooth muscle. Now, why is this important?  With hypertension, what you are looking at is prolonged contraction of that smooth muscle. Prolonged contraction of that smooth muscle ends up leading to hypertrophy of that smooth muscle, right? The inside lining of that vessel becomes much more narrow. There are actual structural changes that occur.  Just like if you went to the gym, right? And you did biceps.  And you did biceps every day for five years, that muscle is going to grow. Same thing here, you have prolonged contraction of that smooth muscle, which ends up leading to hypertrophy or enlargement of that muscle. And as a result that inside lumen becomes much more narrow. That causes hypertension. 

Now, the second thing to look at is the renin angiotensin aldosterone system. Also known as the RAAS system. I’m not going to dive into that in a lot of depth because it’s a very in-depth cascade of reactions that produces hypertension. We have some material here on nursing.com. I highly encourage you to check that out regarding the renin angiotensin aldosterone system. And the reason why it’s so important is a lot of the medications that we’re going to give such as ACE inhibitors, angiotensin converting enzyme inhibitors, or ARBs angiotensin receptor blockers, these antihypertensives, they’re going to directly work on that renin angiotensin aldosterone system. Very in-depth, very intricate. I highly, highly recommend you do more research on that. 

And then atherosclerosis, of course, is also a contributing factor to hypertension. The deposition of fat on the inside of these vessels,  You can imagine as fat gets deposited on the inside of that vessel, imagine this is fat, well that has now narrowed that intra-arterial lumen.  It’s  become more narrow, therefore causing more hypertension. And actually an interesting thing, an interesting by-product of this prolonged smooth muscle contraction, it actually causes little micro tears in that smooth muscle.  And those micro tears, those micro lacerations of the inside lining of that smooth muscle, actually causes fat to be deposited directly into those little crevices. 

So now that we’ve discussed some of the pathophysiology surrounding hypertension, I think it’s really important to understand that whenever hypertension is discussed, you’ll often hear it called the silent killer. And it’s very true. Now, why is it considered the silent killer? Well, hypertension, high blood pressure, in and of itself often has no symptoms. There’s no signs or symptoms that you would be aware that you have high blood pressure. And again, this is something that usually occurs over a prolonged period of time. If a patient goes and remains undiagnosed with a high blood pressure, this is going to cause some often permanent and  irreversible damage, often end organ damage. 

So one of the things that we’ll definitely see is congestive heart failure. I recommend you check out our hemodynamic lecture regarding cardiac output preload and afterload and things of that nature, but hypertension essentially increases afterload. I’m not going to dive into that a lot, but the more narrow that lumen, that inside lumen of that vessel, the more resistance that heart has to pump against in order to get blood out of the heart. Again, with this high blood pressure, we’re basically looking at poorly perfused end organs, so we can see eyes be affected, kidneys be affected, a lot of other things that we’re actually going to touch on again here momentarily. 

So whenever discussing some of the hypertension risk factors, we usually break it down between modifiable and non-modifiable risk factors. And these are pretty straightforward. A lot of the non-modifiable risk factors include things like genetics. Hypertension is actually familial, it can be genetic, a component related to that. If your parents had hypertension, you very well may be predisposed to having it as well. African-Americans are more predisposed to having hypertension.  And age can also play a component. 

Now a lot of the modifiable risk factors, a lot of the things that we’re going to be educating our patient on as we’ll see here shortly, these are modifiable, right? So, smoking. Smoking, as we previously mentioned in other lessons, can directly cause coronary and systemic vasoconstriction. So it causes your blood vessels to constrict, causes that smooth muscle to constrict, and results in hypertension. 

Obesity, lipids, poor diet, right? If you consume a lot of fatty or fried foods, you’re going to increase the deposition of fat of atherosclerotic plaque on the inside lining of those vessels. And also salt. Salt intake is something that’s going to also directly affect your blood pressure. You will recall from diffusion, our lesson on diffusion, that water’s going to follow more highly concentrated solute. So if you’re consuming a lot of salt through your diet, it’s going to basically cause more fluid to go follow that salt inside of the vessels. More fluid inside of the vessels increases blood pressure. 

So some of the assessment findings that we’re going to come across in patients who are experiencing hypertension, as we’ve already mentioned, right? The big one, we’re going to see a blood pressure greater than 140 over 90 (stage 2). Now what we also need to recall, we need to remember now this is very important, Okay. Forgive my drawing, what we’re looking at here, whenever we’re dealing with a patient who has hypertension, we’ve called it the silent killer, right? What we’re really looking at is a prolonged hypoperfusion. Okay. As we have prolonged hypoperfusion of our end organs, we’re going to begin to see end organ failure, as we’ve already mentioned.  Imagine all of these tiny, tiny, intricate vessels that feed into these delicate eye tissues as those vessels are narrowed over a longer period of time, and those eyes are chronically hypoperfused, we’re going to begin to see vision changes, vision loss, headaches, angina. If you recall our lesson on angina, you will know prolonged hypertension or prolonged vasoconstriction of those coronary arteries can end up causing chest pain and maybe eventually a myocardial infarction. And then also let’s take a look at this kidney over here. We’re specifically looking at this artery here. Imagine over a prolonged period of time, this vessel gets more and more and more narrow. And as a result, the blood that’s being fed to that kidney over years and years, gets reduced. So that again, prolonged hypoperfusion of the kidneys, we’re going to start to see end organ damage, possible renal failure. We’re going to see that glomerular filtration rate, that GFR, begin to drop. And also as a result, urine output is going to drop as well. 

So what kind of medications might we see prescribed for patients with hypertension? Well, you’re going to have, certainly, ACE inhibitors, such as lisinopril. They end in pril. They’ll also have angiotensin receptor blockers, these end in sartan, medications like Losartan. And again, you’ll recall these two medications work directly on that renin angiotensin aldosterone system. So again, I can’t more highly recommend enough you go check out some material on that. We also have beta blockers like Metoprolol. They end in olol.  And calcium channel blockers like amlodipine, end in pine. And you can also see diuretics be given as well. So all of these antihypertensives, used in conjunction with one another, to reduce that smooth muscle contraction to reduce blood pressure. And then diuretics are given to try and, you know, deplete that extra volume of fluid inside of these vessels. Medications such as furosemide are given.  Diuretics, used to decrease intravascular volume and therefore decrease hypertension. 

And so what are we going to educate our patients on who have hypertension.  Now, again, a lot of these have to deal with those modifiable risk factors. So lifestyle changes, right? Patients with obesity, patients who are smoking, we want to encourage exercise to reduce the risk of atherosclerotic plaque development. We want to make sure we’re educating on smoking cessation, reducing the likelihood of vasoconstriction, prolonged smooth muscle contraction.  Dietary as well. Reducing fatty foods, reducing fried foods, also limiting salt intake, as we’ve already mentioned. 

And of course, a lot of these patients who have hypertension are going to be prescribed one or a combination of those antihypertensives and possible diuretics. So it’s going to be of the utmost importance that we educate our patient on the importance of adhering to the medications they’re prescribed. 

And so to summarize some of our key points, remember hypertension is pressure ascension.  Purely, it means high blood pressure. And usually it’s reflective of a blood pressure greater than 140 over 90 (stage 2). Remember the pathophysiology, that peripheral resistance, that prolonged smooth muscle contraction of our vessels. Also the renin angiotensin aldosterone system and the atherosclerotic plaque that can be deposited in those micro tears from that prolong smooth muscle contraction, as well as from poor dietary intake. And, also recall those non-modifiable versus the modifiable risk factors, as well as some of those assessment components that you’re going to see in patients with hypertension, remembering that it all basically comes back to the fact that we have prolonged hypoperfusion of these end organs and the medications that we just discussed regarding the antihypertensives and diuretics. 

I hope that you guys really enjoyed this video. Make sure that you check out a lot of the other supplemental references that I referenced in this video. I hope you have a great day and make sure you go out there and be your best selves and as always happy nursing.