Blood Flow, Blood Pressure And Blood Vessels

Front 1

Mean Arterial Pressure (MAP)

Back 1

of the aorta is approximately 85mmHg.

Front 2

Central Venous Pressure (CVP)

Back 2

of the large veins emptying into the R. Atrium isabout 2-8mmHg. Since the CVP is sosmall, it is usually ignored and the ΔP is 85mmHg.

Front 3

Resistance– determined by 3 factors:

Back 3

Vessel radius

Vessel length

Blood viscosity

Front 4

Vessel radius

Back 4

as radius decreases (vasoconstriction), resistance increases and as radius increases (vasodilation) the resistance decreases

Front 5

Vessel length

Back 5

as the vessel length increases, resistanceincreases (and vice versa.

Front 6

Blood viscosity

Back 6

as viscosity (thickness) increases, resistanceincreases

Front 7

What is the flow of the blood vessels

Back 7

BloodVessels = Vasculature: heart - arterioles - capillaries - venules - veins - heart

Front 8

Arteries

Back 8

conduct blood away from the heart

Front 9

Large Arteries

Back 9

In large arteries, the wall contains smooth muscle and lots of elastinfibers. The large arteries actas pressure reservoirs(storage sites for pressure to ensure continual, smooth flow ofblood).

a.Asthe arterial walls are expanding due to increased volume duringsystole, the elastin fibers are like a spring being stretched. b.Theelastic force is stored such thatduring diastole, when no moreblood is entering the arteries, the walls passively recoil inward, propelling blood forward.

Front 10

Arterioles

Back 10

we go from large arteries to arterioles

Front 11

What happens once the large arteries go to arterioles

Back 11

(1) the amount of elastinfibers decrease;

(2) the smooth muscle of the wall becomes thepredominant feature; and

(3) the pressure drops.

Front 12

What happens to the arterioles

Back 12

The arterioles provide the greatest resistance to blood flow (~60%)– 2 reasons: i. thevessel radius decreases ii. vasoconstriction and vasodilation(contract or relaxmuscle)

* This resistance determines (1) amount ofblood flow to capillaries and (2) blood pressure.

Front 13

The vasoconstriction and vasodilation iscontrolled by

Back 13

Intrinsic and extrinsic control mechanisms

Front 14

Intrinsic control mechanisms

Back 14

these are controls occurring in the organitself. 4 examples:

Front 15

What are the 4 examples of Intrinsic control mechanism

Back 15

Active Hyperemia

Reactive Hyperemia

Myogenic Response

Chemical Messengers

Front 16

Active Hyperemia

Back 16

a vasodilation or vasoconstriction based onmetabolic activity

Front 17

Reactive Hyperemia

Back 17

a vasodilation based on a decrease in blood flow.

Front 18

Myogenic Response

Back 18

arteriole smooth muscle contains stretch-sensitivefibers. Thus, as the MAP increases, the arteriolar wall isstretched. The response is vasoconstrictionand vice versa!

Front 19

Chemical Messengers

Back 19

the cells lining the blood vessel (in theendothelium) can release chemicals, which relax or contract arteriolar muscle:Exs

-nitricoxide = vasodilator

-endothelin-1= vasoconstrictor

Front 20

There are 3 types of Extrinsic Control Mechanisms, what are they

Back 20

Sympathetic Nervous System

Vasopressin

Angiotensin II

Front 21

Sympathetic Nervous System

Back 21

under stress the neurons of this system areactivated.norepinephrine is released, which binds to the alpha adrenergicreceptors on the smooth muscle cells causing vasoconstriction,increased R, and increased MAP.

Front 22

Where is Epinephrine released from

Back 22

adrenal gland

Front 23

what binds to epinephrine

Back 23

Like norepinephrine it will bind to the alphaadrenergic receptors and cause vasoconstriction

It can also bind to beta 2 adrenergicreceptors. At low levels it has ahigher affinity for beta 2 adrenergic receptors (= vasodilation), butat high levels it can bind to either. Since most arteriolar muscle contains alphas the effect is primarily vasoconstriction,but in the arteriolar muscle of heart and skeletal muscle, betas predominate = vasodilation.

Front 24

Vasopressin

Back 24

(AntidiureticHormone, ADH) – increases MAP; vasoconstricts,

Front 25

Angiotensin II

Back 25

increases MAP; vasoconstricts

Front 26

Capillaries

Back 26

smallest blood vessels (10-40 billion in thebody); exchanges between the blood and the tissue cells occur through theirthin walls by diffusion

Front 27

What are the two types of capillaries

Back 27

Continuous

Fenestrated

Front 28

Continuous (Capillaries)

Back 28

most common,they have small gaps between the cells which allows for permeability of smallsized molecules and/or lipid soluble molecules (oxygen, carbon dioxide, steroidhormones, etc.). Permeability of largemolecules (proteins) is low.

Front 29

Fenestrated

Back 29

the cells havepores (= fenestrations). The pores allow for rapid movement of water-soluble molecules (sodium,potassium, glucose, etc), large proteins and even cells. Found in organs (kidneys, liver, and bonemarrow) which depend on rapid movement of materials.

Front 30

how is the flow into capillary beds (networks)

Back 30

regulated by themetarterioles and precapillary sphincters.

Front 31

how does the bulk flow across capillary wall

Back 31

from blood tointerstitial fluid = filtration; from interstitialfluid to blood = absorption. The forces driving the movement into andout of the capillaries = Starling’sforces (4 of them).

Front 32

What are the 4 Starling forces

Back 32

1. Capillary hydrostatic pressure

2. Interstitial fluid pressure

3. Capillary osmotic pressure

4. Interstitial fluid osmotic pressure

Front 33

Capillary hydrostatic pressure

Back 33

the pressureexerted by the fluid in the capillary = blood pressure. This favors filtration. This pressure decreases as you move down thecapillary (from arteriolar end to venule end).

Front 34

Interstitial fluid pressure

Back 34

this forceopposes Capillary hydrostatic pressure At the venule end, when CHP. decreases, the interstitial fluid pressure is greater and absorptionis favored.

Front 35

capillary osmotic pressure

Back 35

NOTE: thepresence of a nonpermeating solute exerts an osmotic pressure that tends todraw water to the side where it is present in greater concentration. The most prevalent of these solutes in theblood are large proteins. These generatethe capillary osmotic pressure. Thisfavors absorption.

Front 36

interstitial fluid osmotic pressure

Back 36

interstitial fluid osmotic pressure

Front 37

Net Filtration Pressure (NFP)

Back 37

filtration pressure– absorption pressure NFP= (Capillary hydrostatic pressure + interstitial fluid osmotic pressure) – (interstitial fluid pressure + capillary osmotic pressure)

Front 38

Arteriolar end

Back 38

NFP = (38 + 0) – (25 + 1) NFP = 12mm Hg (filtration)

Front 39

· Venuleend:

Back 39

NFP = (16 + 0) – (25 + 1)NFP = - 10mm Hg (absorption)

Front 40

Venules

Back 40

vessels slightlylarger than the capillaries. They fusetogether to form veins.

Front 41

Veins

Back 41

these have thinwalls compared to arteries (considerably less pressure here) and have muchlarger lumens. The larger veins have one-way valves. They are high compliance vessels (thatis, a relatively small increase in the pressure within veins causes a relativelylarge degree of expansion [increase in volume]). Thus, at any givenpressure, veins can hold more blood than arteries = volume reservoir. At anygiven time ~ 60% of the blood is in the veins. 4 factors affect the flow of blood through the veins:

Front 42

skeletal muscle pump

Back 42

when musclescontract venous pressure increases and return increases

Front 43

respiratory pump

Back 43

when we take abreath the chest pressure drops (no valves in chest veins), the diaphragmflattens, and abdominal pressure increases (abdominal veins have valves); bloodis pushed upward into chest.

Front 44

blood volume

Back 44

as blood volumedecreases, venous pressure falls, venous return to heart falls, end-systolicvolume drops, cardiac output falls and thus MAP drops and vice versa.

Front 45

vasomotor tone

Back 45

when thesympathetic nervous sys. is activated, the veins constrict, venous pressurerises, venous return increases, CO increases, and MAP increases.