Venous Pressure and Vascular Function Curves

This lecture was more complicated than it looked at first, which isn't all too helpful given that I can feel a headache coming on :P Oh well. This will be our last lecture on cardiovascular physiology for this unit for a little while.

Explain how central venous pressure determines cardiac pre-load and output.

As you should hopefully know by now, blood flows from a place of higher pressure to a place of lower pressure until the pressures are equal. Hence, blood will flow from the veins into the ventricles of the heart during diastole until the pressures are equal. The central venous pressure thus determines the amount of filling, which determines cardiac pre-load. As covered here and here, increased end-diastolic volume/increased pre-load increases stroke volume and, by extension, cardiac output.

Understand how central venous pressure is regulated through the vascular function curve, including the actions of blood volume, vasotone and veno-tone.

Blood volume alters venous pressure pretty much the same way it alters arterial pressure: increasing blood volume increases pressure and decreasing blood volume decreases pressure. So far, so good.

The effects of vasotone (arterial contraction) on central venous pressure are less intuitive. If vasotone increases, less blood can get through to the venous side. (Remember, flow is inversely proportional to resistance, and resistance increases as you constrict the blood vessels). Hence, increased vasotone will actually decrease venous pressure.

The effects of venotone (venous contraction) are a bit easier to grasp. Increased venous constriction will increase the pressure, and vice versa.

The relationship between cardiac output and central venous pressure can be plotted on the vascular function curve:

This graph can be a bit tricky to interpret. For starters, you actually have to read it the "wrong way around": you have to find a venous pressure from a given cardiac output, not the other way around. It's done this way so that both the vascular function curve and the cardiac function curve can be plotted on the same axes, as you shall soon see.

Another thing you'll notice about this graph is that the graph levels out below a certain venous pressure. This is because ventricular filling depends on a pressure gradient between the veins and the ventricles, and if venous pressure drops to the same pressure or lower than ventricular pressure, then the ventricles cannot fill any more and cardiac output cannot be increased. One more thing to point out is the x-intercept at the graph: this point represents the venous pressure if there was no cardiac output (i.e. if the heart had stopped and the blood pressure was allowed to simply equilibrate throughout the entire system of blood vessels). This pressure is also known as the mean circulatory (MC) pressure, and is usually around 7mmHg.

When blood volume is increased, such as during a blood transfusion, the entire graph shifts up and right. A greater cardiac output can be produced, and the MC pressure is higher. (Remember, if you have more "stuff" in what is essentially the same amount of space, you're going to have a higher pressure.) The reverse is true for when blood volume is decreased.

Now, blood vessels are not just passive: they can constrict and relax. How does that affect the vascular function curve?

Venoconstriction has a similar effect to increasing the blood volume: it raises the curve up and right. It also changes the slope of the curve slightly (the above picture is possibly exaggerated), leading to a higher possible venous pressure at zero cardiac output. This makes sense: pressure is inversely proportional to volume, so if you constrict the veins, thereby reducing the space inside, you'll increase the pressure. Vasoconstriction, on the other hand, does not change venous pressure when cardiac output is zero. (I'm not sure why- I'm thinking it's because arteries are smaller than veins and thus vasoconstriction has less of an overall effect on volume than venoconstriction? That's something I'll have to check.) Maximum cardiac output is greatly reduced- as mentioned here, MAP = CO*TPR. Rearranging this equation gives CO = MAP/TPR, so it follows that an increased peripheral resistance, as occurs during vasoconstriction, will decrease cardiac output.

Understand how cardiac output is set by the interaction between the vascular and cardiac function curves.

Some of the stuff in this post might seem a bit unintuitive, especially given the relationship between diastolic volume (and venous pressure) and cardiac output. In previous posts, I've said that stroke volume, and therefore cardiac output, is dependent on ventricular filling, which in turn is dependent on venous pressure. However, venous pressure is also dependent on cardiac output! Increasing cardiac output increases the amount of blood taken out of the veins and put into the arteries, and thus decreases venous pressure. So how can we put all of this together into a coherent picture?

The answer is simply to use two graphs: the vascular function curve, which I mentioned above, as well as the cardiac function curve (the one I showed you when talking about the Frank-Starling Law). These two graphs can be plotted on the same axes. The place at which they overlap gives the cardiac output and central venous pressure at steady state.

When there is a deviation from steady state, the cardiac output and venous pressure will gradually adjust until steady state is reached. As an example, let's say that we have some venoconstriction, raising the venous pressure:

Venoconstriction raises the venous pressure to point A. From the cardiac function curve, that venous pressure will cause the cardiac output to increase to point B. However, from the vascular function curve, that cardiac output should cause the venous pressure to decrease to C'. Because of the conflicting results from these curves, the venous pressure decreases a bit, causing cardiac output to decrease, and then venous pressure decreases a bit more, and so on until steady state is reached again.

Any stimulus that causes one or both of these curves to change can change the steady state. For example, as mentioned here, increased inotropy will raise the cardiac function curve:

As can be seen in the graph above, changing the cardiac function curve will also change the intercept between the vascular and cardiac function curves.

Of course, there are many different stimuli that can affect the curves, but I feel like I've already drawn more than my fair share of crappy Paint diagrams for this post. If you want to see how a particular stimulus will affect steady state, why not draw a diagram for yourself and find out?