We are now going to apply some of the information that we've learned with regards to the regulation of mean arterial pressure. Now before we do we need to also introduce or more thoroughly cover this concept of called venous return. So as you recall our heart is pumping blood out to the systemic circulation we call that total amount of blood, our cardiac output, and then this is going to return to the heart from the veins.
So the term that we call that is called venous return. And venous return is significant because it's the venous return that is going to determine our end diastolic volume, which in turn will determine our stroke volume through the Frank Starling mechanism. So recall that veins are capacitance vessels.
They are our volume reservoirs. They hold the majority of blood in our cardiovascular system within any given time. The veins are surrounded by smooth muscle, just like we saw with the arterioles. So if we contract this smooth muscle, or what we call vasoconstriction, that stiffens the veins.
By stiffening the veins, that reduces their compliance and therefore reduces their capacitance or their ability to hold blood. Veins are innervated by sympathetic nerves, and these act on alpha receptors. So if we sympathetically stimulate a vein, the alpha receptor causes the smooth muscle to contract, thus stiffening the vein, reducing their compliance, reducing their capacitance, and therefore blood must go somewhere.
We have valves in our veins, and so the blood cannot go backwards, so the blood is going to be pushed back to the heart. So by sympathetically stimulating veins, we are going to increase venous return. And again, increasing... Increasing venous return increases end diastolic volume, which in turn increases stroke volume.
Now there's some other factors that can also play a role in venous return, and one of those things is called the skeletal muscle pump. So imagine this picture represents a very simplified diagram of a lower extremity with a large vein running up the middle, surrounded by skeletal muscle. We have drawn in the vein that we have valves. So what happens is, as we exercise, these muscles are going to compress. the veins.
So notice that as they compress the veins they're going to be reducing the volume. that the veins can hold and therefore blood is going to have to move. Once again we have valves that are going to prevent blood from moving backwards so they're going to cause the blood to return to the heart. So the skeletal muscle pump is a mechanism by which we can increase venous return. This is particularly important during exercise when we have extensive contraction of our skeletal muscles.
Another mechanism has to do with our normal respiratory pattern. Now, we'll be talking about ventilation during pulmonary physiology, but just to give a brief introduction to this, that our heart is located in our thoracic cavity. We have our venous return coming back to the heart because the pressure in the heart is less than the pressure in the veins.
Therefore blood will return to the heart. Well, when we take a breath in, what's going to happen is that our thoracic cavity, the volume increases. And per Boyle's Law, if we increase volume, we decrease pressure. So with inspiration, the pressure decreases, and that then will cause a greater pressure gradient, and that will increase venous return.
Another term that we need to discuss is one called systemic vascular resistance. Systemic vascular resistance is the resistance the left ventricle must overcome to pump blood to the body. The primary side of resistance is going to be at the arterioles. Our arterioles are our resistance vessels.
In addition to the arterioles, we may also see changes in systemic vascular resistance affected by our outflow tract valves. This would, on the left side of the heart, be the aortic valve. So under normal conditions, this is not a problem.
But if we had problems with the aortic valve, such as aortic stenosis, so this represents the aortic valve open, a healthy aortic valve, and notice that the leaflets all basically push right up against the wall of the aorta, so it causes very little resistance to flow. In some situations, though, we can have narrowing of that aortic valve where it doesn't open widely. This then would cause an increase in resistance to flow.
Now looking at our way of calculating or discussing mean arterial pressure, we can refer back to a property of electric flow. This would be Ohm's Law. So Ohm's Law says that voltage equals flow times resistance.
If we modify this for blood pressure, we would say that pressure, or mean arterial pressure, equals flow times resistance. In modifying these terms, we can say flow represents cardiac output, and resistance would represent our systemic vascular resistance. And recall that cardiac output is stroke volume times heart rate.
So this is our formula to show us the relationship between stroke volume, heart rate, and SVR and how they relate to mean arterial pressure. So mean arterial pressure can be regulated by adjusting any three of those variables. This diagram is meant to depict our arterial side of our circulatory system, our resistance, this would be representing our arterioles, and then the venous side of our circulatory system.
We have a pressure monitor plugged into the artery, and this will help us read what our main arterial pressure is. So realize that initially with blood just sitting in our cardiovascular system, system, if we were to measure the pressure, we would have zero blood pressure. If however, we now begin to pump the blood. When we pump the blood, this heart now is going to be pulling the blood out of the venous system and it's going to be putting it into the arterial system. So notice now that we now have blood pumping into the system, and it's going to run up against some resistance.
So now if we measured our arterial pressure, we would actually be able to measure a pressure. Now for our purposes, I want you to be able to relate how would changing any of these three variables directly affect mean arterial pressure. So for example, if we said we were going to increase the heart rate, Well, increasing the heart rate would cause an increase of flow. We'd be pulling more blood out of the venous system, putting more into the arterial system, and you'll notice that we saw an increase in blood pressure. So an increase in heart rate would lead to an increase in blood pressure.
Now, what if we were to change our systemic vascular resistance? When we change our systemic vascular resistance, let's imagine that we are going to vasoconstrict some arterioles. This is going to cause an increased resistance to flow, which means there's...
going to be a backup of blood in the arterial system, and that would be reflected as an increase in pressure. Likewise, if we caused a greater increase in systemic vascular resistance, we would expect to see an additional increase in mean arterial pressure. A few terms that I want you to be familiar with. One is called preload.
So preload is basically referring to the amount of blood that fills the ventricle prior to contraction. So this is related to our venous return. This is going to be setting the length of the sarcomeres prior to contraction and that will then in turn affect stroke volume. Our systemic vascular resistance, we've already utilized this term.
We refer to that as our afterload.