So, can we use blood pressure as a measure of vascular resistance to get a sense of the biggest factor that determines blood flow? At one point, I believed that diastolic blood pressure was a good indicator of "afterload", which I interpreted as systemic vascular resistance.
Let's look at the factors that affect resistance; in a single blood vessel with non-turbulent flow we can use Poiseuille's equation:
There are three main things that effect resistance (R); length of the blood vessel (L), the viscosity of blood ("n" is the closest I can get to the symbol you see), and the diameter or radius of the vessel (r). The viscosity of blood stays within such a small range except in extreme cases that it's typically considered to be a constant. As you can see, vessel radius has a huge impact on resistance; small decreases in resistance can cause dramatic increases in resistance and decreases in flow.
We typically assume that all portions of the arterial vasculature have equal responsibilities of blood distribution and resistance, but that's not the case. Large arteries play a much larger role in distribution than in resistance; the arterioles have the biggest impact on resistance because of their size (less than 200 micrometers). Where do we typically measure blood pressure? A large artery.
Blood pressure isn't a good measurement of vascular resistance.
Now, Poiseuille's equation might lead us to believe that since the radius of a blood vessel is so important at determining resistance, small changes to the size of a large artery (say, the brachial one) during hypotension can significantly decrease distal blood flow to the capillary beds and cause hypoperfusion. However, there's another factor to consider; arterioles, capillaries and venules exist in parallel networks to bathe the individual cells with opportunities for microcirculation.
Even this image can't accurately describe the sheer number of tiny blood vessels in the tissue bed of an organ; there are thousands, probably tens of thousands of them. This is hugely important, because parallel vessels decrease the overall vascular resistance of the tissue bed or organ. We also have to consider that the total resistance in this vascular bed is the sum of the individual vessel resistances;
Total resistance (Rt)=RA + Ra + Rc + Rv + RV
(A=artery, a=arteriole, c=capillary, v=venule, V=vein)
The take-home point to this is that decreasing the diameter of a large or small artery will have very minor effects on the total vascular resistance of the tissues in question because it's such a small percentage of blood vessels involved in perfusing that area. As a matter of fact, a large or small artery has to have it's diameter increased by more than 60-70% before it starts to have a significant effect on tissue perfusion!
The reason our tissues can get away with this goes back to the relationship between resistance and flow; even at low perfusion pressures you can increase flow to the tissues by decreasing resistance in the arterioles (known as "autoregulation"). And it just happens that I have some research to support this :)
http://www.jccjournal.org/article/S0883-9441(12)00060-3/abstract
In this study, researchers measured mean arterial pressure and microcirculatory flow in hemodynamically unstable patients; they found that microcirculatory flow changed significantly despite a relatively unchanged MAP.
Hypotension does not always mean hypoperfusion.
So, at this point we've determined that:
1) Blood pressure doesn't measure perfusion, or even perfusion pressure.
2) Blood pressure doesn't measure vascular resistance.
3) Because of the concepts of total vascular resistance, hypotension in an artery doesn't always equate to hypoperfusion in the tissue bed.
In the next post, we'll wrap it all up by looking at traditional blood pressure measurement versus mean arterial pressure, and figure out how to use blood pressure measurement in the clinical environment. Stay tuned!
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