High blood flow versus High Blood pressure

[rhan101277]

I have a questions about the difference between the two types of blood flow/pressure listed above.

I want to try to put them into some sentence form to see if I am understanding the physiology at a basic level behind the two.

When you have a laceration say on your forearm and you begin to bleed. Loosing blood throws your body of "balance" and it begins to try to counteract blood loss in an effort to maintain blood pressure. The first way this is done is by artery constriction, which raises blood pressure, but wouldn't that same raised blood pressure lead to worse bleeding? But maybe the bleeding would be the same because your body is just trying to keep blood pressure in normal ranges, so it should just bleed normally?

Is it also true that your body can create higher blood flow, meaning more oxygen? (e.g. running) I know your blood pressure goes up when you run, but does the body dialate the arteries and increase heart rate to provide higher blood flow without creating high blood pressure? I realize pressure goes up some.

Anyway I wanted to work these two things out in my head. See if I am thinking right of it I am way off base.

 

[jrm818]

Havent posted in a while, figure its about time I stop lurking and contribute something. For your first question:


First of all you need to realize that vasoconstriction or vasodilatation is not an all or none response. There are multiple pathways that can result in more or less constriction, and not all arteries are constricted.

In general, sympathoadrenal activation causes vasodilatation in vessels supplying skeletal muscle with peripheral and visceral vasoconstriction. The result is actually a shunt to skeletal muscle and away from visceral organs and the skin.

The question about a bleed depends on how much blood is being lost.

If the hemorrhage is very small there will be local vasoconstriction near the damaged vessel, and the blood will clot, ending the hemorrhage.

If the hemorrhage is a bit larger there will be a transient and small drop in blood pressure as a result of loss of blood volume. The lowered pressure results in a lowered hydrostatic pressure in all capillaries, reducing the amount of protein-free plasma being forced out of the circulation into interstitial fluid. The increased retention of plasma counteracts the hemorrhage, and blood pressure quickly normalizes.

If the hemorrhage is a bit larger, beyond the point where the interstitial fluid can overcome the loss of volume, the venous system collapses in on the reduced blood volume, maintaining arterial pressure.

A bit larger still and the arterial side of circulation bears the brunt of the blood loss. This is the vasoconstriction you reference, producing constriction in non-vital organs and skin. Heart rate may also increase to maintain perfusion.

The vasoconstriction is moderated by four pathways with differing potency.

A. direct sympathetic innervation. Smaller hemorrhages are sensed by venous-side baroreceptors (in the right atrium and large veins) which sense the decrease in blood VOLUME (VENOUS =VOLUME). Larger blood losses resulting in decreased blood PRESSURE (ARTERIAL=PRESSURE) are sensed by Arterial baroreceptors (pressure sensors in the carotid sinus and aortic arch). Both do the same thing, but the ARTERIAL PRESSURE sensors activate these 4 pathways to a much greater extend. Activation of either results in stimulates a neural pathway (through the nucleus of the solitary tract (NTS), if you’re interested) to stimulate sympathetic ganglion cells to release nor-epinephrine (NE) on blood vessels. Very fast response.

B. Adrenal Medulla. The NTS relays a neural signal to the adrenal medulla stimulating the release of NE and EPI into general circulation. Slower but more long lasting response than direct innervation.

C. Renin-Angiotensin system. This one is more complicated. Renin release from the kidney is stimulated by
a. NE and EPI in the circulation
b. Direct innervation via the NTS
c. Renal baroreceptors which themselves detect the loss of blood pressure

Renin secretion acts on a protein called angiotensinogen which is present in the circulation to convert it to Angiotensin I. Angiotensin I is converted by “Angiotensin converting enzyme” (ACE…ever heard of ACE inhibitors?) which is present primarily in the pulmonary circulation, to Angiotensin II. Angiotensin II is the most potent vasoconstrictor found in the body. Slow but extremely effective and very long lasting (can deal with chronic conditions).

D. Vasopressin (VP) release from the hypothalamus. VP isn’t that great of a vasoconstrictor, but it works. Moderately fast but stores become depleted in days.
NOTE: VP is also called “antidiuretic hormone” (ADH). This causes big changes in renal function resulting in decrease in urine volume. This also helps restore fluid volume.

In a HUGE hemorrhage…life threatening stage now….the body “realizes” that it is simply pumping more blood out of a hole in the body, and parasympathetic innervation of the heart is increased, slowing heart rate.

Extra gimme: In large losses there is also a mobilization of glucose from the liver (and inhibition of insulin secretion from the pancreas). This is again mediated by the NTS causing release of NE in the liver, inducing glycogenolysis. The result is an increase in BGL resulting in increased osmotic pressure forcing fluid out of cells and into interstitial fluid and the circulation.

 

[jrm818]

Overall for the first question: these compensation are all designed to allow the body time to stop the bleeding via clotting. The body doesn't necessarily move from one to the next to the next, as the rapidity with which the loss of blood volume occurs has a lot to do with the response, and all the systems may be activated at once (keeping in mind some are slower than others). The goal of all these homeostatic systems is maintained of perfusion pressure to the vial organs: the brain, heart, kidneys, liver. Without those, there is no more live body. And YES: increasing HR does increase bleeding. Until the volume loss is huge, your body is designed to trade blood loss for perfusion pressure.For the second question:

Yes (in general, in a healthy individual) increased blood flow increases available oxygen. yes the body dilates arteries supplying skeletal muscle in response to exercise, but it does constrict arteries supplying the skin and non-vital visceral organs, and yes heart rate increases. It's unlikely that BP would stay the same, as the dilation is offset by constriction, and the increase in HR is usually enough to jack up BP.

You didn't ask - but there are also systems to allow for local vasodialiation, increasing blood flow to a specific part of the body, in the case of local hypoxia (low oxygen).

 

[rhan101277]

Thanks for the post, this stuff isn't gone over in great detail in the basic class. Just that blood pressure is high or low and constriction or dialation are going on. This is why I am taking A&P I now and A&P II next semester and moving on to paramedic school next fall. They unload alot of information on us in a short amount of time. I am doing great in class but sometimes I feel overwhelmed by all of the information. I feel that I know enough to make a decision between rapid transport and stay and play. As a basic I think you make the best decision on the type of care the pt need with what his presented in front of you. Although we can't do many interventions, being a skilled basic can mean the difference between life and death.

 

[rhan101277]

Does it just take alot of experience to know all this information in detail. Some of the basics that were trying to help us in class forgot the name of one of the leg bones, the femur. But you seem highly skilled.