Understand and explain changes in mean and pulse pressure.
Mean arterial pressure (MAP) and pulse pressure (PP) are measured by baroreceptors. (Note: baroreceptors do not measure systolic or diastolic pressure- only MAP and PP.) MAP and PP can be controlled by changes in the autonomic system, or directly via changes in the cardiovascular system such as end-diastolic volume (see here).
Explain and analyse changes in mean and pulse pressure in terms of changes in underlying CVS function.
The main determinants of mean arterial pressure are cardiac output and peripheral resistance. I've explained why this is so here. Main thing to note is that MAP = CO * TPR.
The main determinants of pulse pressure are stroke volume and arterial compliance. An increased stroke volume exerts more pressure on the arterial walls, causing an increased systolic pressure and thus an increased pulse pressure. The inverse is true for decreased stroke volume. As for arterial compliance, arteries that are not compliant (i.e. they are stiff) will require more pressure for the blood to pass through, thus also causing an increased pulse pressure. (At least, that's how I think this works. I'm not sure how accurate these explanations are.)
Predict changes in stroke volume and cardiac output from the pre-load, after-load and contractility of the ventricles.
I'm going to start off by defining pre-load and after-load in the context of muscles. Pre-load is the load that stretches the muscle. If you increase the pre-load, you increase the resting muscle length. After-load, on the other hand, is the load that a muscle contracts against. Increasing the after-load also increases the velocity and amount of muscle shortening.
Now that we've got that down, I'm going to introduce you to a length-tension curve:
Don't worry, I'll link the two together in a minute. Just let me explain this curve first.
For the diastole curve, you kind of need to read it the wrong way around, i.e. figure out what muscle fibre length (x-axis) you would get for a particular tension (y-axis). This is in contrast to the systole curve, in which you read it the right way around: you find out what maximum tension (y-axis) you could get from a particular muscle fibre length (x-axis).
Things get a bit more interesting when you consider the preload and afterload on the heart. Here's the same graph above but with a few more lines and symbols thrown in for funsies:
In the above curve, let's say we have some given pre-load, represented by the green circle. The muscle can begin to generate tension at this point, but while the tension is still less than the afterload, the muscle does not actually change in length. Hence, this period is known as isometric (same length) contraction. Isometric contraction continues until the tension generated exceeds the afterload, and then the muscle fibres begin to contract.
There's an issue, however. Since maximum tension is dependent on length, contraction of the muscle fibres also decreases the amount of tension that can be generated. When the maximum amount of tension falls below the afterload, the muscle stops contracting and isometric relaxation begins. Hence, the muscle has contracted from the point at which the pink and green lines intersect to the point at which the blue and green lines intersect. (Apologies for those who are colourblind.)
So what's this got to do with stroke volume and cardiac output? Well, the more a muscle can contract, the bigger the stroke volume. As stroke volume is also related to cardiac output, a muscle that can contract more can also generate a larger cardiac output.
How do preload and afterload affect contractility? Let's consider changing each of these factors in turn.
First, we'll start with preload:
Remember, the amount of contraction depends on the distance between the intersection of pink and green lines and the intersection between blue and green lines. In the picture above, you can see that this distance is shorter for line A than it is for line B. Hence, decreasing preload also decreases contraction, and vice versa. This goes in line with what I said back in second year: increasing end-diastolic volume also increases stroke volume.
Now let's look at the effect of changing the afterload:
As you can see from the above diagram, afterload A has a shorter distance (and smaller amount of contraction) than afterload B. Hence, increasing afterload decreases contraction, and vice versa.
Interpret cardiac pressure volume curves
A pressure volume curve is, simply put, a curve showing the relationship between volume and pressure throughout the cardiac cycle. Here is a crudely drawn example of a pressure volume curve:
At point A, the mitral valve opens, allowing the ventricle to fill with blood. Hence, the volume increases, but the pressure is still low. This continues until you get to point B, when the mitral valve closes. This final volume also serves as the pre-load for the heart. Isovolumetric contraction then occurs (see here), increasing the pressure without any change in volume. This happens until the force generated by the heart is able to overcome the afterload, allowing blood to leave via the now open aortic valve (point C). At the end of systole (point D), isovolumetric relaxation then occurs: the pressure is reduced while the volume stays the same. This brings us back to point A, and the cycle starts over again.
Describe cardiac work and predict changes in work using pressure volume curves
Okay, I've searched up definitions of "work" and hopefully I've understood them well enough to explain them here. Work is whenever a force moves something, and whenever work is done, energy is transferred from one place to another. Work is usually calculated by multiplying the force and distance, but when the force varies, you need to integrate the force with respect to distance.
In fact, you can use integration to figure out how much work is done by the heart. You can integrate the pressure (which is just force divided by area) between diastolic and systolic pressures with respect to volume:
This integral is also equal to the area within the pressure volume curve.
Because integration is hard when you don't have a nice, neat mathematical equation to integrate, you can simplify this a bit further. Instead of integrating the pressure, you can take the difference between systolic and diastolic pressure and multiply this by the overall change in volume (i.e. the stroke volume). If you want the work done on a minute to minute basis, you can multiply the blood flow by the arterial venous pressure difference.
Hopefully that made sense to you! (That barely made sense to me...)
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