Understanding Mean Arterial Pressure Regulation

Now let's take a look at how we regulate mean arterial pressure. Now before doing so, I want to discuss the effects of some of the other concepts we have discussed, and that namely is the effect of the changing of afterload or systemic vascular resistance. So first let's define the effect of the changing of afterload. define these terms, systemic vascular resistance is the resistance that the heart is working against to try and get blood out of the ventricle. So that term can be used synonymously with afterload. this word kind of describes what it is, it's the load after the heart. So afterload and systemic vascular resistance we can use interchangeably. So what is the effect of changing afterload on stroke volume? On the bottom here, we're showing our heart, and let's imagine that this arrow that I've drawn here represents the force of contraction, the amount of blood that potentially can be ejected from the ventricle. Now that's going to be worth... working against the systemic vascular resistance. So let's call this our baseline systemic vascular resistance. So with this degree of force trying to push blood out, working against that resistance, that will result in a stroke volume. And let's just say that that arrow represents the relative amount of stroke volume. If we reduce the afterload, it would make it easier for this amount of blood to be ejected, or for this force to eject blood out. So again, we're going to depict the same arrow here being produced by the ventricle, but now we have a reduction in afterload. So notice that I've depicted that as having a larger opening because a reduced afterload or reduced systemic vessel resistance would be indicated by by a dilated lumen. So with this force, the same force we saw previously, it's going to be easier for blood to get out of the ventricle. So we'd actually expect to see an increase in stroke volume. And if we alter the systemic vascular resistance such that we increase the systemic vascular resistance, once again, we're dealing with the same amount of blood that's trying to get out with a contraction of the left ventricle. But here, we're increasing that vascular resistance. So we're depicting that by a lumen here with a smaller diameter. That's going to make it harder for the blood to be ejected. So an increase in afterload would result in a decrease in stroke volume. So this is an important concept for you to understand these relationships. Now, having just delineated how changing afterload can affect stroke volume, let's carry that forward to how that might impact our formula, which we've learned previously about mean arterial pressure. because this can sometimes be a point of confusion that I want to clarify. So we've just explained on the previous slide how an increase in systemic vascular resistance will cause a decreased stroke volume. We've also emphasized previously that by decreasing stroke volume, we said that would lead to a decrease in mean arterial pressure. So I've had to reach back into my mathematical vocabulary and remember the transitive property if we're working with equations. So using the transitive property here, it appears as though if we increase S4, SVR and that leads to a decrease in stroke volume, that that might lead to a decrease in mean arterial pressure as well. And what I want to make very clear at this point is no, that is not the case. That's not the case with a healthy heart and that's what we're learning about in this course. So an increase in SVR is going to cause an increase in mean arterial pressure. So the changes in afterload or the changes in systemic vascular resistance have a greater effect on mean arterial pressure than on stroke volume. Therefore, if we increase SVR, although yes, it does affect stroke volume, its effect on mean arterial pressure are greater. In the other direction, if we decrease systemic vascular resistance, we said that that would cause an increase in stroke volume. But we've also previously said that an increase in stroke volume would cause an increase in systemic vascular resistance. Again, we don't use the transitive property here and say that a decrease in stroke volume causes an increase in mean arterial pressure. No, a decrease in systemic vascular resistance. That's the term I should have used there previously. A decrease in systemic vascular resistance leads to a decrease in mean arterial pressure. So although changes in afterload or changes in systemic vascular resistance do indeed affect stroke volume, the changes in systemic vascular resistance have a greater impact on mean arterial pressure. So changes in systemic vascular resistance directly correlate with changes in mean arterial pressure. So whichever direction we're changing the... systemic vascular resistance, that's the direction we're going to be affecting the mean arterial pressure. That's what we mean by directly correlates with. Now let's review the different ways that we can potentially regulate our mean arterial pressure and that's going to be by our autonomic nervous system. So this is a kind of a brief overview slide of the effects of the parasympathetic and sympathetic systems on various factors that come into play with regards to mean arterial pressure. So we've said that if we activate the parasympathetic system, that works on the SA node and decreases heart rate. which in Kern can decrease cardiac output because cardiac output is heart rate times stroke volume. And if we're decreasing cardiac output, that would cause a decrease in mean arterial pressure. So that's the only significant effect that parasympathetics have on control of blood pressure, is its effect on heart rate. Sympathetics, however, work on various different organs or tissues. Sympathetics also will affect the conductive tissues of the heart, and it will cause... an increase in heart rate. That increases cardiac output, and that would increase mean arterial pressure. Sympathetics go to the ventricular muscle and cause an increase in contractility. That causes an increase in stroke volume. That would increase cardiac output, and that would increase mean arterial pressure. Sympathetics go to arterioles. They cause vasoconstriction. This increases systemic vascular resistance, and as we said on the previous slide, an increase in systemic vascular resistance causes causes an increase in mean arterial pressure. Sympathetic nerves also go to veins. They cause vasoconstriction or venoconstriction, if you will. That changes the capacitance by decreasing the compliance of the veins. That's going to increase venous return, which will increase stroke volume, which will increase mean arterial pressure. So clearly, mean arterial pressure is something that we have lots of mechanisms that we can utilize to try and make sure that it stays within a normal range. Well, with that in mind, it would make sense then that we must have some sort of way to monitor blood pressure. And indeed we do, and that's through what we call baroreceptors. Now, there are different baroreceptors throughout our body. The ones that we're going to be focusing on here that play a major role in helping to immediately regulate blood pressure are the... those that are located in the arch of the aorta and at the carotid bifurcation. So these baroreceptors, they actually don't directly measure pressure, rather they are stretch receptors. So as we increase the pressure in these large vessels, you can imagine those vessels have some degree of stretch in their walls. So an increase in pressure causes an increase in stretch, and that's what these baroreceptors are. able to measure, and a decrease in pressure would cause a decrease in stretch. So either way, these baroreceptors can pick up on those changes, and they then in turn are going to send information to the cardiovascular control center, which is located in the medulla. The cardiovascular control center then gets this information and is going to respond appropriately to try and get our blood pressure back to where it belongs. So the way that it can do this is by utilizing the blood pressure. utilizing the sympathetic and parasympathetic systems. So think of the cardiovascular control center as having two dials. One dials for the parasympathetic, one dials for the sympathetic. It can adjust both to bring about the appropriate changes. With regards to the SA node, the sympathetics go there and they are going to act on beta-1 receptors. Parasympathetics go to the same location. They will be acting on muscarinic receptors. The sympathetics go to the ventricular muscle, acting on beta-1 receptors. They go to the systemic arterioles, acting on alpha receptors, and to the veins, also utilizing alpha receptors. So if we have a drop or an increase in mean arterial pressure, these changes are immediately sensed by the baroreceptors. Signals are then sent to the cardiovascular control center. If we have a drop in blood pressure, that's going to cause us to have an increase in sympathetic output and a decrease in parasympathetic output. If we have an increase in menopausal pressure, the opposite will hold true. So let's look now at more specifics of what kind of changes are brought about. So let's imagine that we have a drop in blood pressure. So if we have a drop in blood pressure, what we're going to be describing is the response to that. So we're not getting into why did the blood pressure drop? We're simply saying we've had a drop in blood pressure. What kind of homeostatic mechanisms are going to kick in to try and bring our blood pressure back to normal? So if we have a drop in blood pressure as seen in this equation on the bottom, a drop in blood pressure, what we're going to want to do is we're going to want to do things that would increase these three variables. So let's see how that's done. So we monitor or we detect this drop in blood pressure by our baroreceptors. Our cardiovascular control center then is going to activate or turn up sympathetic output. As a result of turning up the sympathetic output, we're going to be acting through beta-1 receptors. So we're increasing the activity of beta-1 receptors on the SA node, and this is going to cause increased opening of the sodium funny channels, increased opening of the T-type calcium channels, Recall that these are what are responsible for the pacemaker potential. The pacemaker potential is what's going to get us to threshold. So the combined effects here is going to increase our pacemaker potential, meaning that we're getting to threshold more rapidly, and that will increase our heart rate. At the ventricle, we're increasing stimulation of beta-1 receptors, and here we see that that results in an increase in contractility, a more forceful contraction resulting in a greater ejection fraction. As a result, we have an increase in stroke volume. The arterioles are going to be stimulated by sympathetics via alpha receptors. This causes vasoconstriction of the systemic arterioles. This results in an increase in systemic vascular resistance or an increase in afterload. On the veins, alpha receptors again cause vasoconstriction or venoconstriction. This decreases the compliance of the veins, thereby decreasing the capacitance of the veins. These effects will cause an increase in venous return, which will increase stroke volume by the Frank-Starling mechanism. Now recall that the cardiovascular control center not only can utilize the sympathetics by increasing its activity, it can also decrease parasympathetic activity. So by decreasing parasympathetic activity, we are going to be increasing heart rate. Let's look at the other thing that may occur. What if we have an increase in blood pressure? In this case, if we have an increase in blood pressure, our response is going to be to want to try and decrease these variables. Once again, that increase in blood pressure is going to be detected by our baroreceptors. The cardiovascular control center in this case is going to decrease sympathetic output. So by decreasing sympathetic output to the SA node, we're decreasing beta-1-steroid stimulation, so that's going to result in a decreased heart rate. We're going to decrease the normal stimulation of our beta-1 receptors. So realize that all of these receptors we're mentioning always have some degree of activity. So when we say we're decreasing sympathetic output, we're turning down that normal level of activity. So when we decrease the normal activity of the beta-1 receptors, we will be decreasing contractility. the ejection fraction, which will decrease stroke volume. On our arterioles, we're also decreasing sympathetic activity. So if we decrease the normal stimulation of alpha receptors, that's going to result in vasodilation. That will result in a decrease in systemic vascular resistance or afterload, and that will result in a decrease in blood pressure. We decrease the sympathetic stimulation of our alpha receptors on veins. That leads to vasodilation. That increases the compliance of the vasodilator. of the veins that increases their capacitance, which means they're holding onto more blood, so the venous return decreases. That results in a decreased stroke volume via the Frank-Starling mechanism. Now in this case, our parasympathetic system is going to increase. So we're going to increase stimulation of muscarinic receptors on the SA node, and that's going to result in the opening of potassium channels that will drive our resting membrane potential. more negative, so it pushes us further away from threshold. We're also going to decrease our sodium funny channel activity as well as the T-type calcium channel activity, so the combined effects of all this is to decrease our pacemaker potential, which means it takes us longer to get to threshold, which means our heart rate will decrease.

this word kind of describes what it is, it's the load after the heart. So afterload and systemic vascular resistance we can use interchangeably. So what is the effect of changing afterload on stroke volume?

On the bottom here, we're showing our heart, and let's imagine that this arrow that I've drawn here represents the force of contraction, the amount of blood that potentially can be ejected from the ventricle. Now that's going to be worth... working against the systemic vascular resistance. So let's call this our baseline systemic vascular resistance. So with this degree of force trying to push blood out, working against that resistance, that will result in a stroke volume.

And let's just say that that arrow represents the relative amount of stroke volume. If we reduce the afterload, it would make it easier for this amount of blood to be ejected, or for this force to eject blood out. So again, we're going to depict the same arrow here being produced by the ventricle, but now we have a reduction in afterload.

So notice that I've depicted that as having a larger opening because a reduced afterload or reduced systemic vessel resistance would be indicated by by a dilated lumen. So with this force, the same force we saw previously, it's going to be easier for blood to get out of the ventricle. So we'd actually expect to see an increase in stroke volume.

And if we alter the systemic vascular resistance such that we increase the systemic vascular resistance, once again, we're dealing with the same amount of blood that's trying to get out with a contraction of the left ventricle. But here, we're increasing that vascular resistance. So we're depicting that by a lumen here with a smaller diameter. That's going to make it harder for the blood to be ejected. So an increase in afterload would result in a decrease in stroke volume.

So this is an important concept for you to understand these relationships. Now, having just delineated how changing afterload can affect stroke volume, let's carry that forward to how that might impact our formula, which we've learned previously about mean arterial pressure. because this can sometimes be a point of confusion that I want to clarify. So we've just explained on the previous slide how an increase in systemic vascular resistance will cause a decreased stroke volume. We've also emphasized previously that by decreasing stroke volume, we said that would lead to a decrease in mean arterial pressure.

So I've had to reach back into my mathematical vocabulary and remember the transitive property if we're working with equations. So using the transitive property here, it appears as though if we increase S4, SVR and that leads to a decrease in stroke volume, that that might lead to a decrease in mean arterial pressure as well. And what I want to make very clear at this point is no, that is not the case.

That's not the case with a healthy heart and that's what we're learning about in this course. So an increase in SVR is going to cause an increase in mean arterial pressure. So the changes in afterload or the changes in systemic vascular resistance have a greater effect on mean arterial pressure than on stroke volume.

Therefore, if we increase SVR, although yes, it does affect stroke volume, its effect on mean arterial pressure are greater. In the other direction, if we decrease systemic vascular resistance, we said that that would cause an increase in stroke volume. But we've also previously said that an increase in stroke volume would cause an increase in systemic vascular resistance. Again, we don't use the transitive property here and say that a decrease in stroke volume causes an increase in mean arterial pressure. No, a decrease in systemic vascular resistance.

That's the term I should have used there previously. A decrease in systemic vascular resistance leads to a decrease in mean arterial pressure. So although changes in afterload or changes in systemic vascular resistance do indeed affect stroke volume, the changes in systemic vascular resistance have a greater impact on mean arterial pressure.

So changes in systemic vascular resistance directly correlate with changes in mean arterial pressure. So whichever direction we're changing the... systemic vascular resistance, that's the direction we're going to be affecting the mean arterial pressure.

That's what we mean by directly correlates with. Now let's review the different ways that we can potentially regulate our mean arterial pressure and that's going to be by our autonomic nervous system. So this is a kind of a brief overview slide of the effects of the parasympathetic and sympathetic systems on various factors that come into play with regards to mean arterial pressure.

So we've said that if we activate the parasympathetic system, that works on the SA node and decreases heart rate. which in Kern can decrease cardiac output because cardiac output is heart rate times stroke volume. And if we're decreasing cardiac output, that would cause a decrease in mean arterial pressure.

So that's the only significant effect that parasympathetics have on control of blood pressure, is its effect on heart rate. Sympathetics, however, work on various different organs or tissues. Sympathetics also will affect the conductive tissues of the heart, and it will cause... an increase in heart rate.

That increases cardiac output, and that would increase mean arterial pressure. Sympathetics go to the ventricular muscle and cause an increase in contractility. That causes an increase in stroke volume. That would increase cardiac output, and that would increase mean arterial pressure. Sympathetics go to arterioles.

They cause vasoconstriction. This increases systemic vascular resistance, and as we said on the previous slide, an increase in systemic vascular resistance causes causes an increase in mean arterial pressure. Sympathetic nerves also go to veins. They cause vasoconstriction or venoconstriction, if you will.

That changes the capacitance by decreasing the compliance of the veins. That's going to increase venous return, which will increase stroke volume, which will increase mean arterial pressure. So clearly, mean arterial pressure is something that we have lots of mechanisms that we can utilize to try and make sure that it stays within a normal range. Well, with that in mind, it would make sense then that we must have some sort of way to monitor blood pressure. And indeed we do, and that's through what we call baroreceptors.

Now, there are different baroreceptors throughout our body. The ones that we're going to be focusing on here that play a major role in helping to immediately regulate blood pressure are the... those that are located in the arch of the aorta and at the carotid bifurcation. So these baroreceptors, they actually don't directly measure pressure, rather they are stretch receptors.

So as we increase the pressure in these large vessels, you can imagine those vessels have some degree of stretch in their walls. So an increase in pressure causes an increase in stretch, and that's what these baroreceptors are. able to measure, and a decrease in pressure would cause a decrease in stretch.

So either way, these baroreceptors can pick up on those changes, and they then in turn are going to send information to the cardiovascular control center, which is located in the medulla. The cardiovascular control center then gets this information and is going to respond appropriately to try and get our blood pressure back to where it belongs. So the way that it can do this is by utilizing the blood pressure. utilizing the sympathetic and parasympathetic systems.

So think of the cardiovascular control center as having two dials. One dials for the parasympathetic, one dials for the sympathetic. It can adjust both to bring about the appropriate changes. With regards to the SA node, the sympathetics go there and they are going to act on beta-1 receptors. Parasympathetics go to the same location.

They will be acting on muscarinic receptors. The sympathetics go to the ventricular muscle, acting on beta-1 receptors. They go to the systemic arterioles, acting on alpha receptors, and to the veins, also utilizing alpha receptors.

So if we have a drop or an increase in mean arterial pressure, these changes are immediately sensed by the baroreceptors. Signals are then sent to the cardiovascular control center. If we have a drop in blood pressure, that's going to cause us to have an increase in sympathetic output and a decrease in parasympathetic output. If we have an increase in menopausal pressure, the opposite will hold true.

So let's look now at more specifics of what kind of changes are brought about. So let's imagine that we have a drop in blood pressure. So if we have a drop in blood pressure, what we're going to be describing is the response to that.

So we're not getting into why did the blood pressure drop? We're simply saying we've had a drop in blood pressure. What kind of homeostatic mechanisms are going to kick in to try and bring our blood pressure back to normal?

So if we have a drop in blood pressure as seen in this equation on the bottom, a drop in blood pressure, what we're going to want to do is we're going to want to do things that would increase these three variables. So let's see how that's done. So we monitor or we detect this drop in blood pressure by our baroreceptors.

Our cardiovascular control center then is going to activate or turn up sympathetic output. As a result of turning up the sympathetic output, we're going to be acting through beta-1 receptors. So we're increasing the activity of beta-1 receptors on the SA node, and this is going to cause increased opening of the sodium funny channels, increased opening of the T-type calcium channels, Recall that these are what are responsible for the pacemaker potential.

The pacemaker potential is what's going to get us to threshold. So the combined effects here is going to increase our pacemaker potential, meaning that we're getting to threshold more rapidly, and that will increase our heart rate. At the ventricle, we're increasing stimulation of beta-1 receptors, and here we see that that results in an increase in contractility, a more forceful contraction resulting in a greater ejection fraction.

As a result, we have an increase in stroke volume. The arterioles are going to be stimulated by sympathetics via alpha receptors. This causes vasoconstriction of the systemic arterioles.

This results in an increase in systemic vascular resistance or an increase in afterload. On the veins, alpha receptors again cause vasoconstriction or venoconstriction. This decreases the compliance of the veins, thereby decreasing the capacitance of the veins. These effects will cause an increase in venous return, which will increase stroke volume by the Frank-Starling mechanism. Now recall that the cardiovascular control center not only can utilize the sympathetics by increasing its activity, it can also decrease parasympathetic activity.

So by decreasing parasympathetic activity, we are going to be increasing heart rate. Let's look at the other thing that may occur. What if we have an increase in blood pressure? In this case, if we have an increase in blood pressure, our response is going to be to want to try and decrease these variables.

Once again, that increase in blood pressure is going to be detected by our baroreceptors. The cardiovascular control center in this case is going to decrease sympathetic output. So by decreasing sympathetic output to the SA node, we're decreasing beta-1-steroid stimulation, so that's going to result in a decreased heart rate. We're going to decrease the normal stimulation of our beta-1 receptors. So realize that all of these receptors we're mentioning always have some degree of activity.

So when we say we're decreasing sympathetic output, we're turning down that normal level of activity. So when we decrease the normal activity of the beta-1 receptors, we will be decreasing contractility. the ejection fraction, which will decrease stroke volume. On our arterioles, we're also decreasing sympathetic activity. So if we decrease the normal stimulation of alpha receptors, that's going to result in vasodilation.

That will result in a decrease in systemic vascular resistance or afterload, and that will result in a decrease in blood pressure. We decrease the sympathetic stimulation of our alpha receptors on veins. That leads to vasodilation.

That increases the compliance of the vasodilator. of the veins that increases their capacitance, which means they're holding onto more blood, so the venous return decreases. That results in a decreased stroke volume via the Frank-Starling mechanism. Now in this case, our parasympathetic system is going to increase. So we're going to increase stimulation of muscarinic receptors on the SA node, and that's going to result in the opening of potassium channels that will drive our resting membrane potential.

more negative, so it pushes us further away from threshold. We're also going to decrease our sodium funny channel activity as well as the T-type calcium channel activity, so the combined effects of all this is to decrease our pacemaker potential, which means it takes us longer to get to threshold, which means our heart rate will decrease.

Transcript for:Understanding Mean Arterial Pressure Regulation

Transcript for:
Understanding Mean Arterial Pressure Regulation