Blood Pressure (BP) Control

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Study Tools For Blood Pressure (BP) Control

Layers of a vessel (Image)
Hypertension Assessment (Picmonic)
Hypertension Intervention (Picmonic)
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Outline

Overview

  1. Blood Pressure
    1. Systolic pressure (SP)
      1. BP exerted on aorta during ventricular systole – <120 mm Hg
    2. Diastolic pressure (DP)
      1. BP exerted on aorta during ventricular diastole – <80 mm Hg
    3. Pulse pressure (PP)
      1. SP – DP = PP
      2. 120 – 80 = 40 mm Hg
      3. Wide- normal
      4. Narrow – heart not beating strong enough
    4. Mean Arterial Pressure (MAP)
      1. Average pressure in arteries during cardiac cycle
        1. Double diastolic pressure due to the pause after diastole
      2. (SP + 2*DP) ÷ 3
      3. (120 + 2*80) ÷ 3 = 93.3 mm Hg in AORTA
      4. The force that moves blood through the CV system
        1. Forces exchange in capillaries
          1. Nutrients/wastes
          2. Gases

Nursing Points

General

  1. Regulation of MAP
    1. BP = CO x PR
      1. CO = Cardiac output
      2. PR = peripheral resistance to blood flow
    2. Factors determining PR
      1. Viscosity of blood (thickness) – increases PR
        1. Too many RBC’s
        2. Severely dehydrated
      2. Smaller diameter of vessels
        1. Increased PR (pressure)
    3. Vasomotor center in medulla
      1. Constant sympathetic output to smooth muscle of arterioles → steady contraction → vasomotor tone
      2. Changes in tone
        1. Vasodilation
          1. Decreased output from vasomotor center
          2. Pressure (resistance) decreased
        2. Vasoconstriction
          1. Increased output from vasomotor center
          2. Pressure (resistance) increased
    4. Cardiac center (medulla oblongata)
      1. Cardioacceleratory center (CA)
        1. Sympathetic output
      2. Cardioinhibitory center (CI)
        1. Parasympathetic output
    5. Mechanisms controlling BP through PR
      1. Vasomotor baroreflex (sympathetic)
        1. Baroreceptors (pressoreceptors)
          1. Sense changes in pressure
            1. Aortic arch → vagus nerve
            2. Carotid sinus → glossopharyngeal nerve
          2. With ↓ BP
            1. Sympathetic impulses (norepinephrine-NE) sent to arterioles
            2. Vasoconstriction → ↑ PR → ↑ BP
          3. With ↑ BP
            1. Fewer sympathetic impulses (less NE) sent to arterioles
            2. Vasodilation → ↓ PR → ↓ BP
      2. Vasomotor chemoreflex
        1. Chemoreceptors
          1. Sense chemical changes in blood
            1. ↓O2, ↑ CO2, pH changes
            2. Most sensitive to ↓O2
          2. Aortic arch → vagus nerve
          3. Internal carotid artery → glossopharyngeal nerve
          4. ↑ sympathetic output → ↑ NE to arterioles
          5. Vasoconstriction → ↑ PR → ↑ rate of blood flow through lungs
            1. Blood becomes oxygenated
      3. Cardiac baroreflex
        1. Marey’s Law
          1. Heart rate has an inverse relationship to arterial blood pressure
          2. If BP  ↓, then sympathetic nervous system is stimulated
            1. ↑  NE = ↑  HR
        2. Baroreceptors
          1. Aorta →  vagus nerve
          2. Carotid artery → glossopharyngeal nerve
          3. With ↑ BP
            1. Impulses sent to cardiac centers
              1. CA → C sympathetic output (NE) at SA node
              2. CI → ↑ parasympathetic output (Ach) at SA node
              3. ↓ rate of depolarization at SA node → ↓ HR → ↓ CO → ↓ MAP
          4. With ↓ BP
            1. Impulses sent to cardiac centers
              1. CA → ↑ sympathetic output (NE) at SA node
              2. CI → ↓ parasympathetic output (Ach) at SA node
              3. ↑ rate of depolarization at SA node → ↑ HR → ↑ CO → ↑ MAP
      4. Cardiac chemoreflex
        1. Chemoreceptors
          1. Detect lack of O2, high CO2, and low pH
            1. Aorta → vagus nerve
            2. Internal carotid → glossopharyngeal nerve
          2. Lack of O2 in arterial blood
            1. Impulses sent to cardiac center
              1. CA → ↑ sympathetic output (NE) at SA node
              2. CI → ↓ parasympathetic output (Ach) at SA node
              3. ↑ rate of depolarization at SA node → ↑ HR → ↑ CO → ↑ MAP
              4. ↑ blood flow through body (including lungs)
                1. Blood becomes oxygenated
                2. ↑ O2 levels

References
Betts, J.G., et al. (2017). _Anatomy and physiology_. Houston, TX: OpenStax, Rice University. Retrieved from https://openstax.org/details/books/anatomy-and-physiology?Book%20details

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Transcript

In this lesson, we’re going to take a look at the specifics of blood pressure control

So we need to go over some basic concepts before we get into the ins-and-outs of blood pressure control.

Systolic blood pressure is the blood pressure exerted on the aorta when the ventricle contract. This is about 120 millimeters of mercury. Now when the ventricle relaxes, this is called diastole. This number is about 80 mmHg. Again this is specifically exerted on the aorta.

We also have something called pulse pressure. This measurement is the systolic pressure minus the diastolic pressure. That’s going to give your pulse pressure. A normal pulse pressure is about 40 mm of Mercury.

Pulse pressure is evaluated on two concepts it can either be narrow or wide.

A wide pulse pressure means that the number is greater than 40 mm in Mercury, and that’s a strong pulse pressure. A narrowed pulse pressure is a decreased pulse pressure so something like 20 would be a narrow pulse pressure. What that means is that they heart is weakened and can’t relax all the way.

Another measurement that we look at is something called mean arterial pressure or map. And it’s an average pressure in the arteries during the cardiac cycle. This is really important for identifying kidney perfusion.

Now the way map is calculated is that you take the diastolic pressure, and multiplied by 2 then add that to the systolic pressure, and divide that entire number by 3. Basically a map is a force is going to move to that cardiovascular system enforce the exchange of nutrients and wastes and gases in the capillaries. Now let’s take a look at the regulation of map.

When we’re calculating map this where to look at the blood pressure is going to be equal to the cardiac output and peripheral Resistance. If you haven’t taken a look at what cardiac output is, I encourage you to take a look at the cardiac physiology lesson because that explains it in pretty good detail.

So what is peripheral resistance? Well peripheral resistance is the resistance that the heart has to beat against. If you have a high level of resistance in the peripheral vascular system, that’s a lot of pressure that the heart has to beat against and it creates a bunch of work. So what are some factors that influence peripheral resistance? Well if a blood is very viscous and thick, due to an increase in red blood cells or dehydration that’s going to increase peripheral resistance. There’s also an increase in the peripheral resistance in smaller diameter Vessels. vessels

The central nervous system has a huge influence on blood pressure control. There are basically two centers that we look at and It’s the vasomotor center, and the cardiac center.

The vasomotor center is located in the medulla, and there is constant sympathetic output to the smooth muscle. This creates a steady contraction of those blood vessels and it’s going to create vasomotor tone. There are some things that influence tone.

Sometimes the blood vessels will dilate in this conveys a dilation. If there is decreased output from the vasomotor center it’s going to cause a decrease in pressure resistance.

If you have an increase in an output from the vasomotor center you will have an increase in pressure resistance and that’s called vasoconstriction because the blood vessels have constricted down.

Now in the cardiac center, there are two specific centers that we look at. One is called the cardioacceleratory center and that influences sympathetic output. Now there’s also something called cardioinhibitory Center and that influences parasympathetic output. I think about it like this. We want to accelerate and go faster and what does that? Wild norepinephrine is going to do that and that’s the response of the sympathetic output. Likewise we want to slow things down, so you can get more acetylcholine, and that’s the parasympathetic output.

We also have some receptors in our body that help to influence blood pressure. There are two that we are looking at called baroreceptors and chemoreceptors. Baroreceptors sense change in blood pressure due to actual pressure at those locations, and chemoreceptors influence chemical changes.

Baroreceptors are found in the vagus nerve at the aortic arch, and the glossopharyngeal nerve at the carotid sinus. If there is a decrease in blood pressure since by the baroreceptors, there’s going to be a sympathetic impulses sent to the arterioles with norepinephrine. This is going to create a vision construction and that’s going to increase the peripheral resistance and therefore increase the blood pressure. If there is an increase in blood pressure, there’s what you mean fewer sympathetic impulses sent you those arterioles, so it’s going to be less norepinephrine. What ends up happening is you get a vasodilation and that decreases the peripheral resistance and it’s going to decrease blood pressure.

With chemoreceptors, chemoreceptors sent decreases or changes in oxygenation, increases or changes in carbon dioxide, and also pH changes. Chemoreceptors are located in the aortic arch for the vagus nerve, and then in the internal carotid artery for the glossopharyngeal nerve.

If these chemoreceptors sent a decrease in oxygen, or increase in carbon dioxide and the body’s responses to get more oxygen to the tissue, it will increase the sympathetic output. Is it going to be an increase in the norepinephrine in the arterioles, and that’s going to create phase of construction and increased blood pressure because of the increased resistance. What’s going to happen if it is going to be increased blood going through the lungs and it’s going to result in an increase in oxygenation

So how does this look in sequence? This is called Marey’s law.

So we’re basically looking at the body’s response to an increase in blood pressure. Basically there is an Impulse sense at the aorta or the glossopharyngeal nerve that says that there is a problem with the peripheral resistance and we need to make a change. What happens if their impulses are sent to those cardiac centers

Specifically with the barrel reflex, the Cardioacceleratory Center decreases the amount of sympathetic output from the SA node decreasing the norepinephrine.

The cardioinhibitory center increases parasympathetic output at the SA node which is an increase of acetylcholine.
And because of this, you’re going to get a decreased rate of depolarization at that SA node and it’s going to result in a slowing of the heart rate and you’re going to have a decreased cardiac output and a decreased mean arterial pressure. As you see here this is what’s happening you have an increased heart rate and it’s going to slow down.
So what happens if the opposite occurred? What’s a the blood pressure drops. well there’s going to be that impulse from those baroreceptors to the cardiac centers that are set
Because the blood pressure is low, there needs to be increased from the cardioacceleratory center in the brain. So you’re going to get an increase in sympathetic output at the SI no due to norepinephrine
Similarly and the cardioinhibitory center, that impulses and a decrease in you’re going to get less parasympathetic output at the SA node. So there will be less acetylcholine to slow the heart rate down
Increased rate of depolarization at the SA node and that’s going to increase the heart rate and cardiac output and subsequently is mean arterial pressure

So what about the cardiac chemoreflex?

Those chemoreceptors are there to help detect these changes. If there’s a detection in less oxygen, an increase in that carbon dioxide, or you get this pH changes these chemoreceptors are going to fire.

Now a signals going to be sent to the cardioacceleratory centers, increasing that sympathetic output of norepinephrine at the SA node, and the cardioinhibitory centers are they going to decrease the acetylcholine outfit of the parasympathetic nervous at the SA node. This is going to increase the rate of depolarization because we want to get more increase the blood flow through the body. This is going to result in higher oxygenation level because the blood is traveling to the lungs at a faster rate

The thing I really want you to realize is that blood pressure has a lot that influences it. Sometimes these systems can work by themselves, they can work in unison, they can work synergistically, or they can work at different times. What you also need to realize that there are two centers which of the base of made of Center and a cardiac center. Vasomotor Center is responsible for sympathetic only input, and a cardiac centers are responsible for both sympathetic and parasympathetic. Just realized that there’s more than one input when it comes to blood pressure that helps influence how our body responds.
Okay so let’s recap.

Baroreceptors are responsible for detecting pressure changes in the blood, and chemoreceptors are responsible for sensing the chemical changes in the blood.

The vasomotor center in the brain is responsible for the sympathetic response only, where the cardiac center is responsible for both the sympathetic and parasympathetic responses.

Norepinephrine and acetylcholine are imperative in understanding blood pressure control. Norepinephrine help speed up the heart rate increase peripheral resistance, and acetylcholine slows down heart rate, and creates vasodilation as a response to parasympathetic input
And that’s it for a lesson on blood pressure control. Make sure you check out all the resources attached to this lesson. Now go out and be your best selves today, and is always happy nursing

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