phys 4

endothelial layer

all vessels have endothelium (1 cell layer thick)

innermost

elastin layer

• allows more constriction or dilation

• on vein and arteries

smooth mm layer

contracts to shunt blood to correct location under medium pressure

• highest in artery, then a little less in arterioles and veins for shunting a ton of blood

fibrous layer

reinforces wall w/ high pressure (artery)

• highest in veins and arteries, a little in venules

• outermost layer

blood flow

• parallel (brain, heart, liver, …)

• recondition to keep contents the same in blood

  • reconditioning organ receive more blood than needed for metab

  • kidneys, liver, heart

• organs vary is tolerability of lowered blood flow (brain has almost no tolerabililty

flow rate

F = Delta P / R

• delta P = pressure gradient from heart

  • pressure diff between beginning and end of vessel

  • decreases when resistance R increases

• R = resistance from friction

  • blood viscosity

  • vessel length (longer = more res, does not change)

  • vessel radius (smaller = more res, changes often dila or constri)

R

radius is biggest determinant of flow rate

increases by factor of 4 each time radius is increased by 1

• R = 1/ r^4

• r + 1 = F x4

poiseuiles law

F = (3.14 x delta P x r^4) / (8 x n x l)

n = viscosity (# of RBCs)

l = length

Surface area

• vessel length and radius

• RBCs bumping against the cell wall

• extrinsic factors = symp release nor on a1 = constriction

• intrinsic = signals from tissue

MAP

avg arterial pressure driving blood forward

• diastolic + 1/3 pulse pressure

determined by

• CO

• TPR

• volume

formula

• CO x TPR (total peripheral resistance)

  • TPR increases → MAP increases → increased blood flow to specific organ

  • closer to diastolic pressure

mean systemic pressure

slowly decreases from 95 in aorta to almost 0 in vena cava

pressure on arteriolar side (high)

determined by

• CO

• SV

• total peripheral res / systemic vascular res

less venous compliance = less venous return

central venous pressure

• low pressure

systole

peak pressure against walls

1/3 of blood from artery enters arterioles

diastole

minimum pressure on walls

blood draining down vessels (not arteries)

elastic recoil and pressure pushes blood into arterioles

smooth mm

• receptor a1

• neurotran = epi = speeds up reaching threshold

• gap jxns

• more actin, no troponin, less SR

• actin/myosin arranged in diagonal bundles

• unstable resting mem potential → threshold = multiple AP

arteries

large r = little res

aorta has highest pulsing pressure and slowly decreases as it flows outward

elastic recoil sends blood further

• pressure reservoir b/c when heart is relaxed and no blood is pumped, blood still flows from driving force from elastin

MAP is 93

arterioles

• MAP is 40, largest drop in pressure

• converts the pulsing pressure into stable pressure in capillaries

• dictates blood flow w/ cons or dil or smooth mm

• inn by symp postganglions → inc blood pressure

• controlled by

  • local factors

  • hormones (nitric oxide = dilation)

  • mechanical stretch (intrinsic)

vascular tone

• constant partial contraction = baseline res

• increase/dec pressure as needed

• determined by

  • Ca channels

  • continuous release of Nor from sym

adrenoreceptors

a1: vasocon

a2: inhibition of nor/Ach in CNS

B1: tachycardia

B2: vasodilation

a1 receptor

• increased peripherial res, increased BP

• on all tissue except the brain

• vasoconstriction

B2 receptor

vasodilation, decreased peripheral res, bronchodilation

• activated by epi

• mostly in arteriolar smooth mm in coronary arteries, lungs, smooth skeletal mm

vasoconstriction

• increased myogenic activity/tonic for ongoing contraction

• increased O2

• decreased CO2, metabolites

• increased endothelin

• increased symp vasopressin/angiotensin II

vaso dilation

• decreased myogenic activity/tonic for ongoing contraction

• decreased O2

• increased CO2, metabolites

• increased nitric oxide

• decreased symp histamine/ heat

capillaries

single layer of endothelial

sphincter = stopcock, since no smooth mm

• contraction = reduced flow to organ

• relax = increased flow

2 types of passive exchange

• diffusion: CO2 and O2

• bulk flow: plasmid fluid

diffusion

cap only regulate plasma protein movement = extent of diffusion is determined by conc gradient

bulk flow

difference of hydrostatic pressure and colloid osmotic pressure

protein free plasma leaks from cap → mixes in ECF → reabsorbed in cap

• pressure inside > outside = ultrafiltration/hydrostatic/pushing pressure

• proteins are contained in the cap = inward pressure = osmotic/absorbing pressure

capillary flow

total cross sectional area is 750x greater than the aorta

blood slows considerably down to allow for diffusion and transport of glucose through channels

endothelial cells in cap

joined together w/ water filled pores = passage of water soluble substances

• Na, K, glucose

lipid soluble pass thorugh lipid bilayer

• O2, CO2

plasma proteins

transport things to organs (hormones)

• dont want leaking into endo cells

• losing = losing osmolarity

metarteriole

cluster of constricting mm between arteriole and venule

many caps are not open

precap sphincter

not inn

sensitive to local and metab changes

high metabolic activity on cap

decrease in O2 = decrease in pH (acidic)

increase in O2 = increased conc gradient

extracellular fluid

20% = plasma

80% = bathes cells

fluid exchange

4 factors that influence movement

• cap blood pressure (plasma) push out

• plasma colloid osmotic pressure (plasma) push in

• interstitial fluid hydrostatic pressure, push in

• interstitial fluid colloid osmotic pressure, push out

cap blood pressure (plasma) Pcap

• hydrostatic pressure pushing towards the interstitial fluid on cap walls

• pushes fluid from cap into interstitial fluid

• 32 mmHg: higher in arterioles = net filtration

• 15 mmHg: decreases below colloid osmotic pressure in venules = net absorption

plasma colloid osmotic pressure (plasma) PI p

• determined by protein conc in cap

• pushes to move fluid into cap

• -25 mmHg: remains the same in both arteries and venules (protein conc remain the same)

plasma fluid exchange

decreased plasma vol = decreased capillary BP

• decrease in outward pressure = decrease ultrafiltration, increase reabsorption → fluid entering plasma

interstitial fluid hydrostatic pressure P if

pressure of interstitial fluid pushing on outside of vessel

interstitial fluid colloid osmotic pressure PI if

pressure of ISF pushing to leave vessel

• very little to no leakage (plasma proteins)

• negligible

complete calculation of fluid exchange

net exchange = (Pc + PI if) - (Pif + PI c)

lymphatic sys

• picks up excess fluid that was not reabsorbed by 1 way valve

• immune fxn : passes lymph nodes on their way to the heart

• transport of absorbed fat

• return of filtered protein

blind end lymph cap

remove fluid and filtered proteins at dead ends on caps

edema causes

• reduced conc of plasma proteins (low osmotic pressure)

• increased permeability of capillary wall (plasma pro/fluids escaping)

• incresaed venous pressure

• lymph vessel blockage

edema solution

easiest = increase ECF hydrostatic pressure or

increase plasmid colloid osmotic pressure → fluid back into cap

veins

• blood reservoir

  • low myogenic tone, low. elasticity, low recoil ability

  • easily distend w/ small increase in pressure

• larger radius = smaller resistance

• when reservoir is needed

1. constrict smooth mm

2. increased venous return

3. increased CO to heart (starlings law)

venous capacity

depends on

• compliance/stretchability of vein walls

• influence of external pressure (smooth mm, skeletal mm pump, cardiac pump)

increased symp activity on venous return

• decreased venous capacity

• more blood pumped out of heart and more pumped back = increased end diastolic volume = increased CO

difference in vasocon flow in A and V

in arteries = restricted flow from higher resistance

in veins = increased flow from decrease in capacity

factors enhancing venous return

1. cardiac contraction driving pressure

2. symp induced venous vasoconstriction

3. skeletal mm activity

4. venous valves

5. resp activity

6. cardiac suction

7. blood volume : bulk flow return to cap, no edema

cardiac contraction driving pressure

very very small almost negligable

symp induced venous vasoconstriction

nor binds a1 receptors on smooth mm

skeletal mm activity

mm squeezing on skin in intervals along the veins

veins under increased pressure (below heart) = increased capacity = increased blood pooling = decreased CO

venous valves

one way valves to keep blod from falling back

resp activity

pressure in chest is 5 mmHg lower than atmosphere

normal pressure in lower extremities = driving force for movement up

cardiac suction

ventricular contraction pulls on atria = small vacuum = artrial pressure below 0 = driving force for movement into atria

baroreflex

negative feedback that detects arterial stretch

synapses on NTS → CVLM + nAmb → RVLM

if blood pressure drops = no stretch on baroreceptors = no NTS and nAmb stimulus → foot off the break (parasym)

RVLM

rosteroventral lateral medulla

increases symp activity

CVLM

gabaergic → inhibits RVLM → decreases symp activity

nAmb

stims vagus → slows HR