Lecture 4 Flashcards

1
Q

Preload/frank starling law of the heart

intrinsic reg

volume vs force relationship

A

the heart will pump whatever blood it receives
volume in = volume out

intrinsic reg bc properties related to heart and how much it fills

filled too much = stretched too much = not enough overlap of actin and myosin to contract
resting = too much overlap, no room to slide back
sweet spot = overlap is minimal but a lot of room to slide

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2
Q

afterload

A

P vents must overcome to open valves and eject blood from heart
ex. P in vent must be higher than P In aorta to push blood out

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3
Q

extrinsic influences on SV

A

change contractility w/o changing EDV

increased Ca influx
1. sympathetic stimulation = inc strength of contraction and rate of contraction + relaxation( to fill up)
2. drugs = digoxin = inc heart contractility
dec number of beats but stronger
as opp, to many but lower SV

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4
Q

how norepinephrine inc heart contractility via cyclic AMP

A

NE beings to receptor
activates G protein
G protein activates enzyme that turns ATP to cAMP
cAMP activates protein kinase
which phospohoralates Ca channels in mb + in SR
which inc release from SR + ECF
so inc Ca conc= inc Ca binding to troponin
inc cross bridge binding for contractions
= inc force of contraction

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5
Q

flow fo blood through vessels

A

arteries
arteroiles
cappilaries
venules
veins

arteries carry blood away from heart
veins carry towards heart
caps directly serve cells

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6
Q

layers of arteries

A

inner to outer

Tunica Intima =
endothelium
subendothelial layer
internal elastic mb (bc they stretch = veins don’t have bc don’t stretch)

Tunica Media
external elastic mb

Tunica externa
vasa vasorum = small network that serves the walls of the vessels to meet the needs of the cells of that vessels

***muscles are thicker in arteries

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7
Q

layers of veins

A

Tunica intima =
endothelial
sub endothelia layer
NO ELASTIC ON MUSCLE

tunica media

tunica externa *
vasa vasorum

  • thicker in veins
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8
Q

layers of caps

A

has endothelial cells
basemenent mb

don’t want thick barriers,
but pores thin enough for exchange to occur

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9
Q

3 types of arterial vessels

A

elastic/conducting arteries
musclular/distributing artereis
arterioles

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10
Q

elastic/conducting arteries

A

thick walled
large diameter near heart
biggest # of elastin
regulates P fluctuations,
recoil helps maintains pressure + flow of blood

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11
Q

musclular/distributing artereis

A

delivers blood to specific organs/tissye
controls how much goes where

more smooth muscle than elastin =
allows it to regulate diameter
dilate = more blood sent to certain location/pathway
contract = less blood sent

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12
Q

arterioles

A

smaller diameter
tunica media primarily smooth muscles
det whcih capillary beds get access, minute to minute

ex. when excercising, more to muscles

one layers, or deccccc of layers

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13
Q

3 types of capillaries

A

continuous capillaries
fenesteres capillaires
sinusoidal capillaires

least to most leaky

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14
Q

continuous

A

least leaky, not much exchange

in skin, muscle, brain
endothelial cells linked by tight ins = uninterrupted lining
are intercellular cleats that allow limited passage of fluids + small solutes, NOT IN CNS

Brain is kept separate, minimize infections

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15
Q

fenestered

A

similar to above but endothelial cells are riddled w pores (fenestrations)
inc permeability to fluids/small solutes

small int. endocrine organs, kidneys

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16
Q

sinusoidal caps

A

leakiest
fenestered, fewer tight ins, large clefts for passage of proteins, RBC,

liver, bone marrow, lymphoid tissue,

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17
Q

microcirculation

A

flow of blood from arteriole to venous via cap. bed

flow is det/reg by diameter of terminal arteriole
contract if movement not allowed

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18
Q

veins

A

blood reservoirs that return blood to heart
have 65% of blood in veins
venules
post cap venules = just endothelium
larger = couple layers of smooth muscles

veins = 3 tunics but thinner walls and larger lumens

less smooth muscle in tunica media, less elastin,

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19
Q

blood flow

A

measured ml/min
can be regulated independently for various organs + tissues
reg for what body needs

20
Q

blood pressure

A

force per unit area exerted on walls of a blood vessel by its contained blood

travels to a pressure gradient, high to low

21
Q

blood pressure drops as it travels through he body bc of

A

resistance, in vessels, against the walls

a dec in blood vessel diameter inc resistance to 4th power.

22
Q

resistance = R

influences by

A

total of frictional forces that slow flow
flow and R are inversely related

influenced by
viscosity
vessel length
vessel diameter

23
Q

how does viscosity affect R

A

inc viscosity bc of formed elements
dehydrated, blood doping
not a natural change

24
Q

vessel L

A

more cumulative resistance
for ex if put on weight = inc # of tissue that has to be vascularize
more length = more workload = big enough push to go through entire length

25
vessel Diam
can be reg, if more fluid not touching walls moves faster since less R
26
pulse pressure
vigrot of contraction of ventricles provides information on elasticity of aorta and major arteries- how? bc aorta + large vessels branch out won't stretch, so sys bp inc won't recoil as much so won't move fwd as much so diastole bp Inc
27
mean arterial pressure = MAP
pressure that propels blood to tissue during cardiac cycle dec w distance from heart by end of arterial tree, blood flow is steady and pulse pressure has disappeared
28
capillary blood pressure
low P, bc are fragile, High P would rupture them most caps are extremely permeable, so lots of exchange at low bp
29
venous bp
steady and changes slightly during cardiac cycle is a gradient, and veins will provide more open paths so blood will keep moving fwds
30
factors aiding venous return
venous valves + muscular pumps respiratory pump sympathetic venoconstriction
31
venous valves + muscular pumps
muscles in legs, contract + push on outside of veins, push upwards, when sitting/stadnig, is harder bc of gravity could get fluid+ blood pooling/buildup so moving helps blood move
32
resp pump
as it travels from Lower limbs to heart passes though visceral organs, past lungs as we breath = P changes occur inc P = squeeze on vessels going up/fwds dec P = pulls blood up on last part twas R atrium
33
sympathetic venoconstriction
bc 60% in venous sys SNS = stim contraction fo smooth vessels in veins to push on blood pushing it fwds push makes 60% move more quickly to start circulating
34
pulse
P wave bc of expansion and recoil of arteries to find pulse, push surface artery against firm tissue
35
pressure points
if lots of blood loss, press on pressure points to reduce blood loss,
36
blood pressure usually measured in + numbers
usually measured in brachial artery Systolic P = 120 pressure ejecting blood Dyastoic P = 80 filling in
37
short tem vs long term reg of BP
works w total peripheral R (blood vessel d) and CO vs works w blood volume = level of kidney
38
main goal of ST reg
alter blood distribution to specific demands maintain adequate MAP by altering bed reflex arcs involving = baroreceptors, vasomoto centre, vascular smooth muscles b= measures amount of stretch, thrfr measures bp vsm = smooth muscles of vessel reg d of vessels more contracted vs relaxed
39
vasomotor tone + vasomotor centre
vasomotor centre = cluster of sympathetic neurons in medulla part of cardiovascular centre = responds to baroreceptor, chemoreceptors, higher brain centres vasomotor tone = constant output = low levels of SNS output, can be opened/closed as needed inc in sympNS = vasoconstriction, inc in bp, dec = reverse, esp in GI system, can fn w less blood flow
40
baroreceptors
in carotid sinuses, aortic arch, and other large arteries of neck and thoracic, = monitor bp when MAP inc, it stretch receptors, so response is 1. dilate arteriles = keep bp under control so won't get too high 2. venodilation to shift blood to venous reserves 3. stimulate paraNS and inhibit symp N, dec HR + froce. communicate w heart to slow it down, push less forcefully, to bring bp closer to what it should be when MAP dec. = opp reponses
41
goal of baroreceptors
protect against ST changes in bp bc of changing positions ineffective in chronically, so if chronically have high bp, body will stop trying to Lowe it and body will be used to having high bp vales
42
chemoreceptor initiated refelces
causes = drop in O2, rise of Co2, drop of pH chemoreceptors in aortic arch + large arteries of neck to vasomotor centres = vasoconstriction result = inc in bp, speeds return of blood to heart and lungs
43
influences of higher brain centres
Fight of flight, stress, excretes, cerebral cortex and hypothalamus get involved bc you are aware
44
Hormones of ST reg of bp
Adrenal medulla hormones = E/NE, Fi/Fl increase cardiac output vasocontriciton *same as activating sympNS angiotensin II intense generalized vasocontriciton ANP made by atria of heart when bp is too high dec bp by vasodilation ADH = mostly for LT, but if insanely low bp, more ADH is released, high levels cause vasoconstriction
45
kidneys and LT regulation of Bp
adjust blood volume, a more complete response, but longer
46
direct action
inc blood volume = inc bp = in rate of filtrate formation = not enough time to reclaim water = inc volume of urine
47
indirect action
renin-angiotensin system is MAP dec = kidney cells release renin = eventually leads to producing angiotensin II a vasoconstrictor angiotensin II stimulates release of aldosterone aldosterone = inc renal absorption of Na so inc water absorption also sit release of ADH = inc water absorption inc thirst via hypothalamus constricts vessels