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Blood pressure Cross sectional area Velocity of flow and Blood volume for the vessel types. All vessels act as conduits to move blood from the heart out to the peripheral organs . Especially, the large arteries and veins .
for the vessel types
All vessels act as conduits to move blood from the heart out to the peripheral organs.
Especially, the large arteries and veins
Blood pressure is highest in the aorta, and monotonically falls to near zero in the vena cava.
Pressure is pulsatile in the arteries but becomes damped in the microcirculation and veins
R = ΔP/F
The biggest pressure drop is across the arterioles.
IFΔP is large then the resistance must be large
R = ΔP/F
Because arterioles have a large resistance and can change their resistance, they act as control valves to control flow
Surface area is highest in capillaries which promotes exchange of nutrients and waste products with tissue.
That allows blood to stay in the capillary long enough to equilibrate with the tissues by diffusion.
Smooth muscle in the small veins and venules can contract and squeeze blood out of the venous reservoir raising the venous filling pressure in the heart and thus the cardiac output
The properties of the various vessel types in the cardiovascular system.
A. distribution of pressure (highest in the aorta and lowest in the veins)
B. distribution of velocity (highest in the root of the aorta lowest in capillaries)
C. distribution of surface area (highest in capillaries which aids exchange)
D. distribution of resistance (highest in arteriole which is important for blood flow control)
E. distribution of blood volume highest: in veins (making them act as reservoirs).
The aorta is compliant and its pressure is a function of its volume.
Compliance = volume / pressure
The heart pumps in short spurts. The compliant aorta stores this energy during ejection and releases it during diastole so that flow into the periphery continues throughout the cardiac cycle
The bagpipe player blows into the bag in short spurts. That energy is stored in the bag and the air escapes through the pipes in a continuous stream thanks to the bag's compliance.
If the vessels were rigid pipes then all forward flow would have to occur during the ejection period which is only about 1/3 of the cardiac cycle.
Blood pressure would have to be 3 times higher during that period to maintain the cardiac output.
With each ejection the aortic volume increases by one stroke volume.
To maintain a steady state one stroke volume of blood must leave the aorta before the next beat.
Blood pressure is measured by listening for sounds made when the cuff pressure is between systolic and diastolic pressure.
The opening and closing causes turbulence when the artery’s lumen is very narrow (just as it opens or as it closes).
The mean aortic pressure is determined only by the cardiac output and the peripheral resistance.
aortic pressure = CO x peripheral resistance
Peripheral resistance does not affect the pulse pressure
pulse pressure = SV/compliance
Autoregulation: matches flow to requirements
Heart, brain, kidney, muscle, intestine autoregulate
Skin does not
Other aspects of intrinsic regulation
1. Active hyperemia
2. Reactive hyperemia
Sympathetic nerves constrict blood vessels (epinephrine and norepinephrine)
Receptors on the blood vessel that are coupled with Gs stimulate adenylyl cyclase, increase cAMP, and relax the vessel.
cAMP increases Ca++ but also inhibits myosin light chain kinase which controls smooth muscle contraction.
Receptors coupled with Gq activate phospholipase C (PL-C) causing the formation of inositol triphosphate (IP3) from phosphatidylinositol (PIP2). The IP3 then stimulates the sarcoplasmic reticulum (SR) to release calcium. The formation of diacylglycerol (DAG) activates protein kinase C (PK-C) further contributes to vascular smooth muscle contraction via protein phosphorylation.
Nitric Oxide is a locally produced dilator. Acetylcholine is a direct constrictor of VSM but in the body it is actually a dilator because it stimulates NO production by eNOS in the endothelium. NO overrides the constrictor activity of the acetylcholine and dilates the vessel.
Before NO was identified it was referred to as Endothelial Derived Relaxing Factor or EDRF
Circulating vasconconstrictors include angiotensin, endothelin, vasopressen and catecholamines.
Targets for anti-hypertensive drugs
There are no widespread neuro dilators. In many cases an active hyperemia follows neuronal activation of an organ by a substance that also happens to be a dilator e.g. acetylcholine in the gut or bradykinin in salivary glands. The primary effect was to stimulate the organ and the dilation that occurred was an active hyperemia.
Hydrostatic pressure (Pc) forces water out of the capillary and that is balanced by osmotic pull of plasma proteins (albumin) that pulls water back in. The osmotic pressure (πc) of plasma in the capillaries is ~25 mmHg and that of interstitial fluid (πt) is near zero.
Fluid is filtered at the arterial end and reabsorbed at the venous end
The four forces controlling fluid balance at the capillary are called the Starling Forces after Ernest Starling
Jv = Kfc ( Pc + πt– Pt – πc)
Kfc = fluid filtration coefficient (tells how fast fluid flows for any pressure gradient)
Raising capillary pressure causes edema (swelling).
Loss of plasma proteins due to starvation causes edema (swelling).