Okay, so now we're going to talk about how we regulate our blood pressure. So maintaining our blood pressure requires cooperation not just from our heart, but also our blood vessels and our kidneys, which we'll talk about in a little bit. And all of this is supervised or monitored by our brain.
There's three main factors that regulate blood pressure. One of them we talked about in Chapter 18, that's our cardiac output. If you remember cardiac output, right? is equal to our heart rate times our stroke volume, peripheral resistance, and our blood volume. So our blood pressure is going to vary depending on these three variables.
So because we have these variables, we can kind of rearrange our formula. So the formula that we saw in the previous section was flow is equal to pressure divided by resistance. Well, in this case, because we're talking about the flow of blood, through our heart, we can replace flow with cardiac output. And then we have our left-foot equation, cardiac output is equal to pressure divided by resistance. And then we can rearrange it so we can put, basically solve for pressure, at which point we get pressure is equal to cardiac output times resistance.
When we're talking about pressure in our blood vessels, what we're referring to again is that mean arterial pressure. That's what we want because we don't want the fluctuating or pulsatile blood pressure that we see closest to the aorta. So we actually need to calculate our mean arterial pressure and plug it in here. When we're talking about the resistance, we're actually talking about the peripheral resistance that we have going on.
So if we change any one of these variables, that's how we are able to compensate for changes in other variables. So where we just left off was basically pressure is equal to cardiac output times resistance. We learned that the pressure in this case, we're talking or referring to the mean arterial pressure.
We learned what cardiac output was in chapter 18. So we can substitute the equation into our mean arterial pressure equation above. So if we do that, we get mean arterial pressure. is equal to stroke volume times heart rate times resistance, and this is equal to cardiac output.
So we haven't changed our equation, we've just substituted it for different variables. But this equation is really good because then we can see things that can affect our mean arterial pressure and include our stroke volume and heart rate. So because all of these are on the numerator or we don't have anything on the denominator, That means all of these variables are directly proportional to the mean arterial pressure.
So increasing any of these, whether it's stroke volume, heart rate, or resistance, would increase our mean arterial pressure. And decreasing any of these things would decrease our mean arterial pressure. So stroke volume is mostly affected by our venous return, how much blood we have coming back to the heart. Our heart rate is going to be maintained by our medullary centers.
And our resistance is mostly going to be affected by the diameter of the blood vessels themselves. So we're talking about regulating our blood pressure. We have short-term regulation and we have long-term regulation.
If we're talking about short-term regulation, we're talking about neuronal and hormonal controls. If we're talking about long-term regulation, we're talking about renal control. So we're talking about our kidneys being involved.
And again, I like these little flow charts. They kind of help you understand what's going on. So it definitely take a minute to kind of go through and make sure you understand everything and also understand what happens if you do the reverse. So for example, increasing stroke volume is going to increase cardiac output, which is going to increase mean arterial pressure. But if we decrease our stroke volume, what does that do to our mean arterial pressure or to our cardiac output?
Okay, so let's focus on our first short-term regulation, and that would be neuronal controls. So we have two main neuronal mechanisms that control our peripheral resistance. So our main arterial pressure is maintained by altering the blood vessel diameter.
If we alter the blood vessel diameter, we're able to alter the resistance. So for example, if our blood volume drops, for some reason, say we're cut, We cut ourselves severely and we're hemorrhaging blood, dropping our blood volume. It's going to cause all of our blood vessels to constrict to help increase that blood pressure to help compensate for the blood loss. We can Also, alter blood distribution to organs in response to specific demands. So my example of exercising, if we exercise, we're going to make sure that we're sending most of our blood flow to our skeletal muscle and kind of shunted away from our digestive system.
If we're talking about neural controls, these operate via reflex arcs. And we have a couple of different things like our cardiovascular center and our medulla. Baroreceptors.
Baroreceptors are pressure-sensitive mechanoreceptors, and they're able to respond to different changes in our arterial pressure or the stretch in our arteries. We also have chemoreceptors, and chemoreceptors are going to respond to changes in chemicals. So they're going to respond to changes in blood chemical composition. So if we change the concentrations of carbon dioxide, hydrogen ion concentration, or even oxygen levels. These would be able to be sensed by those chemoreceptors.
And we also have higher brain centers that can influence our reflexes. So let's start with the cardiovascular center. What is the cardiovascular center?
It's just a cluster of sympathetic neurons in our medulla. It's going to consist of a cardiac center that has both inhibitory and acceleratory centers within it. We also have the vasomotor center. And the vasomotor center is just going to send some steady impulses via sympathetic pathways, efferent pathways. And we call these sympathetic efferents specifically vasomotor fibers to those blood vessels.
And it's going to cause continuous moderate constriction. We want a continuous moderate constriction at all times unless we need to fluctuate that base of our environment. And that continuous moderate constriction of our blood vessels is what we refer to as vasomotor tone. The degree of vasomotor tone is going to vary from organ to organ.
So for example, like I mentioned before, if we increase our sympathetic activity, we're going to increase our vasoconstriction, which is going to increase our blood pressure. So our vascular center cardiovascular center is going to receive inputs from all of the other components as well. So our baroreceptors, chemoreceptors, and higher brain centers.
So let's talk about our baroreceptors, which again, those are those pressure sensitive mechanoreceptors, and they can respond to the changes in arterial pressure and stretch. You don't need to know their location. I do have them listed here, but that's too much information.
What I want you to understand is what happens, what our body's response is if our main arterial pressure is high or our main arterial pressure is low. So if our main arterial pressure is high, that means our arteries are stretched. And remember, our baroreceptors sense that stretch.
So what's going to happen if they sense that stretch is it's going to cause it to inhibit our vascular motor and our cardioacceleratory centers. Because our cardioacceleratory centers cause vasoconstriction. So we don't want to constrict it and increase our blood pressure more.
So we want to inhibit those centers. And it's going to stimulate our cardio inhibitory center, which is going to promote vasodilation. And if we promote vasodilation, that's going to help lower our blood pressure.
So how do we actually lower the blood pressure? So I just mentioned dilation. If we enlarge the diameter of the blood vessel, that's going to lower the pressure. So we can have arteriolar vasodilation. This is going to help reduce peripheral resistance, causing our main arterial pressure to fall.
We also have venodilation, which shifts blood to our venous reservoirs, and that's going to help decrease venous return as well as cardiac output. So decreased cardiac output. Impulses to our cardiac centers are going to inhibit our sympathetic activity and help again stimulate that parasympathetic activity, which is going to cause a lower heart rate and contractility and our cardiac output is going to decrease, which is going to cause a decrease in our mean arterial pressure. So the opposite is true if our mean arterial pressure is low.
So for mean arterial pressure is low. The reflex is going to be for vasoconstriction. So we want to constrict our blood vessels so we can increase our blood pressure because it is low. And that's going to be initiated and again cause an increase in cardiac output as well as pressure.
So for example, If we stand really fast or really quickly, our blood pressure is going to fall. When our blood pressure falls, it's going to trigger a couple reflexes. Our carotid sinus reflex, so the baroreceptors there can monitor the blood pressure, as well as our aortic reflex, which helps maintain our blood pressure in our systemic circuit. So our baroreceptors are ineffective if altered blood pressure is sustained.
So for example, we would have sustained... blood pressure if we had chronic hypertension. And what happens is these baroreceptors become adapted to hypertension, and it's no longer going to be triggered by the elevated blood pressure levels. So the baroreceptors are reprogrammed and respond to changes at a higher set point.
So this is a good diagram to kind of go through. I'm not going to go through it with you right now because I know this lecture... mini lecture is already going to be long, but go through this diagram and kind of make sure you understand how we bring our body back down to some sort of homeostasis with our mean arterial pressure. If it goes too high or if it goes too low, what does our body do to counteract that? Okay, chemoreceptors.
So these have a larger role in influencing our respiratory rate really than rather than our blood pressure. but we're still going to kind of talk about them. So basically, we have chemoreceptors that can detect high levels of carbon dioxide or a drop in pH or oxygen.
So if we're talking about an increase in carbon dioxide, that means we're not getting enough blood to our lungs to expel the carbon dioxide. So carbon dioxide is also an acid. Because carbon dioxide is an acid, a low pH would correlate that.
with that. So if we have high levels of carbon dioxide, we've increased the acidity or lowered the pH of our blood. So those kind of go hand in hand.
Also, if we have too much carbon dioxide built up, that means we don't have enough oxygen. So low levels of oxygen. So all of these kind of mean the same thing. High levels of carbon dioxide means that we don't have a lot of oxygen. So it's low levels of oxygen.
High levels of carbon dioxide means that we have high acidity. which means that we have a low pH. So all of these things can cause increased blood pressure by signaling the cardioacceleratory center to increase cardiac output. We want to increase cardiac output because if we have high levels of carbon dioxide and low oxygen, we really want to expel that carbon dioxide from our lungs.
Also signaling our vasomotor center to help increase vasoconstriction. Again, to increase their blood pressure, to speed the return of blood to our heart and to the lungs. Okay, higher brain centers. If we're talking about higher brain centers and the reflexes that actually regulate blood pressure, these are going to be found in the medulla in the brainstem. So the hypothalamus and the cerebral cortex can help modify the arterial pressure by relays to the medulla.
So hypothalamus increases the blood pressure during times of stress. So even if we're not exercising, if we feel stressed out, we're going to have an increase in blood pressure. The hypothalamus also mediates redistribution of blood flow if we are exercising. Again, taking our blood to our skeletal muscle and kind of preventing it from going or as much going to our digestive system, as well as changes in our body temperature. The second component of the short-term regulation was hormonal controls.
So hormones can regulate our blood pressure in the short-term. Again, it's a short-term control by changing the peripheral resistance. Or they can also change it long-term by changing the amount of volume of blood that we have in our body. So a couple important hormones.
are the adrenal medulla hormones, so epinephrine and norepinephrine. From the adrenal gland, these are going to cause an increase in cardiac output as well as vasoconstriction. They also initiate the reflexes that regulate the blood pressures that we were talking about before. Angiotensin 2, this is going to stimulate vasoconstriction. What happens is that low blood pressure is going to cause our kidneys to release renin.
Renin is needed to convert angiotensin 1 into angiotensin 2. When we hit the urinary system, we'll talk more about these hormones as well as the endocrine system. ADH is another one. So high levels of ADH or the antidiuretic hormone can also cause vasoconstriction because they're going to stimulate the kidneys to conserve water.
If they stimulate the kidneys to conserve water, that's going to increase our blood volume. If we increase our blood volume, that's going to increase our blood pressure. So these three right here are going to cause an increase in blood pressure. Oops. The fourth hormone is our atrial natriuretic peptide.
This one's going to do the opposite. It's actually going to decrease our blood pressure. And it does this by antagonizing aldosterone, which causes a decreased blood volume and therefore a decreased blood pressure.
What it actually does is it causes our kidneys to excrete more sodium. If we excrete more sodium, water always follows salt. So what happens is we end up lowering our blood volume because we're losing water and therefore going to lower our blood pressure. So you don't need to know the side of action for these hormones.
You will when we hit the endocrine system, that chapter. For now, just understand the four hormones that play a role in blood pressure and whether or not they help increase our blood pressure or decrease our blood pressure. So long-term regulation, again, if we're talking about long-term regulation, we're talking about renal regulation, meaning that we need our kidneys to be involved.
Because those baroreceptors quickly adapt to hypertension or to hypotension. And so they're not really effective for long-term regulation. So long-term mechanisms are actually going to control our blood pressure by altering the blood volume via our kidneys.
So our kidneys can regulate our arterial blood pressure by two different ways. We have the direct renal mechanism and the indirect renal mechanism, which is going to involve that renin, angiotensin, aldosterone. I mentioned it above as one of the hormones. So the direct renal mechanism, this alters blood volume independently of hormones.
So increased blood pressure or blood volume causes elimination of more urine. The more urine we're eliminating, we're... helping lower the blood volume and reducing the blood pressure.
If we have a decreased blood pressure, blood volume is going to cause the kidneys to conserve more water to increase our blood volume and therefore our blood pressure. So again, the direct mechanism we're just talking about, we're just affecting the blood volume by affecting how much water we eliminate in our urine. Indirect mechanism is going to involve the hormones. So indirect mechanism is our renin, angiotensin, aldosterone mechanism.
So decreased arterial blood pressure causes the release of renin from our kidneys. So if we have low blood pressure, because remember, aldosterone and angiotensin increase our blood pressure. If we have low arterial blood pressure, that's going to cause an enzyme called renin to be released from our kidneys. Renin is going to enter the bloodstream.
blood and it's really crucial because it's going to convert angiotensinogen into angiotensin 1. We have another enzyme that comes in called the angiotensin converting enzyme or also called ACE that converts angiotensin 1 into angiotensin 2. We need renin to be released from the kidney essentially in order to get angiotensin 2. Angiotensin 2 is really, really important because it can do four different things to help stabilize our arterial blood pressure and our extracellular fluid. So one of the things angiotensin 2 can do is stimulate the release of aldosterone. And if you remember, aldosterone was the hormone that's responsible for increasing sodium reabsorption. It's also going to cause ADH, so our antidiuretic hormone, to be released from our posterior pituitary. hearing.
ADH's role is to increase water reabsorption. It's also going to trigger the hypothalamic thirst center, causing us to say, hey, we're thirsty and signaling us to drink some water or some fluid. It also acts as a potent vasoconstrictor and directly increases our blood pressure because it's constricting our blood vessels. So just to kind of walk you through the renin, angiotensin, aldosterone system.
So. So we have angiotensinogen. This is produced by our liver, which isn't important right now.
That's converted into angiotensin 1. We need renin in order to convert angiotensinogen, this is released from our kidney, into angiotensin 1. And then we need another enzyme called the angiotensin converting enzyme or ACE to convert angiotensin 1 into angiotensin 2. And then angiotensin 2 is what goes on to do all of these four things that help increase our blood pressure. So it's multifaceted in its way. So angiotensin 2 is really, really important in the event that we have low blood pressure.
So the direct renal mechanism, like we talked about, if we have low arterial pressure, we're going to have a low filtration by the kidneys, low urine formation, and a high blood volume. If we have a high blood volume, we're going to have a high blood volume. have a high mean arterial pressure.
Same thing for the indirect renal mechanism, which has to do with renin, angiotensin, aldosterone system. If we have low arterial pressure, that's going to inhibit the baroreceptors. And increase our sympathetic nervous system activity.
Increased sympathetic nervous system activity causes renin to be released from the kidneys. So we need renin released from the kidneys to ultimately get the angiotensin 2, which is what we want. So renin... comes in, it's going to convert angiotensinogen into angiotensin 1. Then we have ACE, an enzyme that's readily available to convert angiotensin 1 into angiotensin 2. And we need both renin and the ACE. enzyme to get angiotensin 2, but angiotensin 2 is super important because it does so much things.
It causes aldosterone to be secreted from the adrenal cortex, an increase of ADH release, an increase in us feeling like we're thirsty, and vasoconstriction. All four of these contribute to increasing our mean arterial pressure. So just to summary, the goal of blood pressure regulation is to keep our blood pressure high enough to provide adequate tissue perfusion, meaning we can get enough blood from our capillaries into our tissue, but not so high that we're damaging the blood vessels that are feeding our tissues themselves. So if our blood pressure to our brain is too low, that means the perfusion is inadequate.
We're not getting enough nutrients from our blood into the brain tissue, and our person can lose consciousness. If the blood pressure in our brain is too high, the person could actually have a stroke. So again, I'm not going to go through this with you.
This flow chart is really, really good because it ties in everything that we've talked about so far. So go in and make sure you can follow this and understand what's going on. Okay, so we talked about hypertension before, but let's talk more about what is exactly hypertension defined as.
Well, if you have a blood pressure of about 140 over 90 or higher, you're considered to have hypertension. If you're close... to that value, so say somewhere between 120 and 140 or between 80 and 90, but not quite at those levels, then you're said to have pre-hypertension. Prolonged hypertension is a major cause of heart failure.
failure, vascular disease, renal failure. Now you can see why it can cause damage to the kidneys, as well as a stroke. So like before I mentioned, hypertension is referred to as a silent killer, because you might not physically see any of the effects until it's already too late. Some of the effects are your heart has to work a lot harder.
Your myocardium is going to enlarge. So people with chronic hypertension have really, really, really thick muscle layer, which is not a good thing. thing, which means it's actually weaker and it can also become flabby.
So we can kind of classify hypertension even further. So if we have primary hypertension, this is 90% or the bulk of the hypertensive conditions. No underlying cause has been identified. But if you could be based off of genetics, have bad genetics, based off your diet, if you're obese, the age, if you have diabetes, if you... smoke, or if you're under a lot of stress, this could lead to primary hypertension.
Again, not really sure what the exact cause is. Just know that you have hypertension, which is likely the result of one of these things. No cure, but it can be controlled.
Diet regulation is huge, so restricting your salt intake. If you have a lot of salt, remember I said water follows. So if you have a lot of salt in your body, you're retaining a lot of water. If you're retaining a lot of water, you're increasing your blood volume and therefore your blood pressure.
So if you already have high blood pressure, you don't want to retain as much water. So you want to lower the amount of salt you have in your diet. Fat and cholesterol also. So recommendations are to always increase exercise, lose weight, and if you smoke, to stop smoking. And then you can also use some sort of therapeutics like antihypertensive drugs.
which are actually ACE inhibitors. So that enzyme that I spoke about before that converts angiotensin 1 into angiotensin 2, you could inhibit that enzyme and no longer get angiotensin 2 if you have high blood pressure, which is a good thing because everything that angiotensin 2 does causes an increase in blood pressure. So you wouldn't necessarily want that hormone to be working.
Secondary hypertension is less common. So about 10% of the cases, but we know why this hypertension is being caused. So for example, if you have an obstructed renal artery, some sort of kidney disease, and an endocrine disorder such as hypothyroidism or Cushing syndrome.
So really, if you have secondary hypertension and you know what's causing the high blood pressure, your treatment is going to focus on fixing the underlying condition itself. So we also have hypotension, where you actually have low blood pressure. And hypotension is defined as having a 90 over 60 or lower blood pressure. Usually not really concerned if you have hypotension, unless it is preventing blood flow to some of your tissues. We have a couple different types of hypotension.
We have orthostatic hypertension. This is just a temporary low blood pressure or dizziness. So if you stand, like I said, really quickly, your blood pressure drops. That would be considered orthostatic hypertension.
You can also have chronic hypotension, but typically this is the result of poor nutrition. We'll talk about hypothyroidism and Addison's disease when we hit the endocrine system. We also have acute hypotension, and this is an important sign of circulatory shock. So what is circulatory shock? It's a condition where your blood vessels are inadequately filled and cannot circulate the blood normally.
So we have inadequate blood flow and we cannot meet the tissue's demands with the nutrients and gases that they need. And because of that, the cells die and you end up with organ damage. So we have hyperboleic shock that can result from large scale blood loss, such as a hemorrhage.
We can also have vascular shock. which results from extreme vasodilation and decreased peripheral resistance. And we also have cardiogenic shock, which results when an inefficient heart cannot sustain adequate circulation.
So basically, your pump has failed. Maybe you have had multiple myocardial infarctions or heart attacks.