sys circulation and venous return Flashcards

1
Q

peripheral vascular beds is organized how?

A

in parallel

  • organs recieve the same oxygenated blood ejected from left ventricle
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2
Q

blood flow (flow rate) is dependent on?

A
  1. pressure gradients (change in P)
  2. veascular resistance
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3
Q

major resistance vessel is?

A

the arteriole

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4
Q

what equation associated flow with change in pressure and resistance

A

flow = change in pressure / resistance

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5
Q

what is the equation of vascular resistance

A

R=8nl/πr4

  • n = viscosity of blood
  • l = length of vessel
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6
Q

what vessel is innervated by SNS fibers

A

arteries

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7
Q

what is the major function of the artery

A
  • serve as rapid-transit conduits for blood flow form the heart
  • act as a pressure reservoir to provide a driving force for blood when heart is in diastole
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8
Q

which blood vessel has these characteristics:

  • thick smooth muscle layer
  • less collapsible
  • contains elastin allows “recoil”
  • display a state of vascular tone
A

artery

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9
Q

what does the elasticy of arteries allow for

A

distension during systole with subsequent recoil during diastole

  • systole and recoil are driving forces to move the blood
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10
Q

what produces the dicrotic notch in arterial pressure

A
  • when aortic valve closes, causing a brief period of retrograde flow, briefly decreasing aortic pressure
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11
Q

what is mean arterial pressure

A

the average pressure driving blood during a cardiac cycle

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12
Q

is the value of MAP closer to systolic or diastolic pressure? why

A

closer to diastolic pressure because 2/3 of cycle is spent in diastole

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13
Q

what is the equation for MAP

A

MAP = diastolic + 1/3(pulse pressure)

pulse pressure = systolic pressure - diastolic pressure

  • i.e. BP 120/80
    • MAP= 80 + 1/3(40) = 93 mmHg
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14
Q

Mean arterial pressure is indicative of preload or afterload

A

afterload

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15
Q

What effect does aortic stenosis have on systolic pressure, pulse pressure, and MAP

A
  • stenosis causes reduction in flow into the aorta
  • SV is reduced; less blood enters aorta
  • systolic, pulse, and MAP all decrease
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16
Q

What effect does arteriosclerosis have on systolic pressure, pulse pressure, and MAP

A
  • plaque causes stiffness and decreased compliance
  • ejection of SV causes a greater increase in pressure
  • systolic pressure, pulse pressure, and MAP all increase
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17
Q

what is pulse wave velocity

A

index of aortic stiffness and/or elasticity

  • the higher the velocity, the higher the rigidity of the wall
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18
Q

how is pulse wave velocity measured?

A
  • pulse tonometers probes are placed on carotid pulse and femoral pulse
  • PWV= change in distance / change in time
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19
Q

pulse wave velocity is a predictor of mortality from what?

A

cardiovascular mortality

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20
Q

arterioles convert pulsatile pressure swings of cardiac cycle into what?

A

non-fluctuating pressure

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21
Q

what characteristics of arteriole structure make it an ideal structure to alter resistance and hence affect blood flow within an organ?

A
  • wall contains little elastin but lots of smooth muscle cell
  • cells are innervated by SNS
  • sensitive to metabolic changes
  • displays tone at “rest”
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22
Q

tone of a vessel

A

the contractile state of the resistance vessel

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23
Q

what tone is this:

  • state of partial contraction independent of metabolic and neural mechanisms
  • dependent of the intrinsic properties of the vessel vascular smooth muscle
A

basal tone

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24
Q

what tone is this:

  • most resistance vessels are constricted somewhat more than basal due to tonic sympathetic nerve activity
A

resting tone

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25
Q

relate basal flow, maximal flow, tone, and vasodilator reserve

A
  • the lower the basal flow relative to maximal flow, the higher the tone
  • and the higher the vasodilator reserve for the organ
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26
Q

how is tone generated in a vessel

A

by smooth muscle contraction within the walls of the vessel

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27
Q

from a partially constricted state, how can a vessel reach its vasodilatory reserve?

A

a vessel can either further constrict or vasodilate to reach its vasodilatory reserve

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28
Q

what is active vasoconstriction

A

a decrease in vessel diameter due to sympathetic stimulation or constrictor hormones/metabolites

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29
Q

what is active vasodilation

A

an increase in vessel diameter due to hormones or local factors

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30
Q

what is passive vasoconstriction

A
  • return towards resting state from a dilated state due to the removal of active dilator influences
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31
Q

what is passive vasodilation

A

return towards resting state from a constricted due to the removal of active constrictor influences

32
Q

from resting tone; adding adenosine or epinephrine will have what affect?

A
  • adding adenosine: active vasodilation
  • adding epinephrine: active vasoconstriction
33
Q

how do vessels return to a resting tone from a dilated and constricted tone?

A
  • removing adenosine from a dilated vessel -> resting tone
  • removing epinephrine from a constricted vessel->resting tone
34
Q

extrinsic control of vascular tone orginates from outside the tissue. What are the extrinsic factors?

A
  • neural
  • hormonal
35
Q

What are the components of the intrinsic influences that maintain vascular tone

A
  • active hyperemia
  • reactive hyperemia
  • autoregulation
36
Q

what is active hyperemia?

A
  • increase in organ blood flow that is associated with increased metabolic activity of an organ/tissue
    • local tissue metabolism: metabolites accumulate, trigger dilation by inducing relaxation which increases blood flow
37
Q

what is reactive hyperemia

A

an increase in organ blood flow that occurs following a brief period of ischemia produced by temporary arterial occlusion

  • when occlusion is removed, pressure is restored and flow is elevated. Blood flow to the deprevied area is higher than normal because the arterioles are dilated
38
Q

what is autoregulation

A

the intrinsic ability of an organ to maintain constant blood flow despite changes in blood pressure

39
Q

the myogenic mechanism states that when vascular smooth muscle is stretched from increased intravascular pressure, it responds by..?

A

contracting to restore vessel diameter, increase resistance and reduce flow

40
Q

What channels on smooth muscles mediate autoregulation

A

calcium channels

  • smooth muscle cells depolarize from stretching, leading to Ca2+ entry into cell -> contraction
41
Q

how can the metabolic mechanism explain autoregulation? scenio: increase in pressure

A
  1. increase in pressure will increase flow into organ
  2. increase in flow will increase O2 delivery and washout local metabolites
  3. washout of metabolites leads to vasoconstriction
42
Q

what endothelial factors exert a significant paracrine role in the regulation of smooth muscle tone and blood flow?

A
  1. Nitric ocxide: vasodilation
  2. EDHF: endothelium-derived hyperpolarizing factor: vasodilation
  3. PGI2 (prostacyclin): vasodilation
  4. Endothelin: vasoconstrictor
43
Q

Neural and hormonal input has extrinsic control over vascular tone. Name some players

A
  • vasopressin: vasoconstrictor
  • angiotensin II: vasoconstrictor
  • Atrial Natriuretic peptide: vasodilator
  • Neural
    • NE release from SNS fibers
44
Q

What are metarterioles

A
  • contain precapillary spincters that are not innervated, but sensitive to local metabolites
  • act as valves to control blood flow through the capillary bed
45
Q

differentiate between nutritive and non-nutritive flow

A
  • nutritive: flow through metarterioles and capillaries: exchange occurs
  • non-nutritive flow: flow through metarterioles; little exchanges occurs
46
Q

an increase in tissue metabolic activity will start what cascade? (list steps)

A
  • Low O2
  1. relaxation of precapillary spincters and ateriolar vasodilation
  2. increase delivery of O2
  3. increases exchange between blood and tissue to support increased metabolic activity
47
Q

exchange across capillaries’ walls occurs by?

A
  • diffusion (passive, down concentration gradient)
  • bulk flow: Exchange of water and solutes together due to a pressure gradient.
48
Q

What forces favor filtration (pressure in capillary is high)

A
  • interstitial fluid-colloid osmotic pressure
  • capillary hydrostatic (blood) pressure
49
Q

What forces favor reabsorption into capillary

A
  • plasma colloid osmotic pressure
  • interstitial fluid hydrostatic pressure
50
Q

What is the equation for net exchange pressure

A

= (Pc + πIF) - (πp + PIF)

  • Pc= capillary blood pressure
  • πIF= interstitial fluid osmotic pressure
  • πp = plasma osmotic pressure
  • PIF= interstitial fluid hydrostatic pressure
51
Q

what is capillary blood pressure (Pc)

A

fluid pressure exerted on the inside of the capillary wall by the blood

  • forces fluid out: favors filtration
52
Q

what is the capillary blood pressure at the ateriolar end and venular end

A
  • ateriolar end: 37 mmHg
  • venular end: 17 mm Hg
53
Q

what is plasma-colloid osmotic pressure (πp)

A
  • force caused by plasma proteins
  • encourages reabsorption
54
Q

What is interstitial fluid hydrostatic pressure (PIF)

A
  • fluid pressure exerted on the outside of the capillary wall by the interstitial fluid
  • tends to force fluid into the capillaries: f_avors reabsorption_
55
Q

What is interstitial fluid-colloid osmotic pressure (πIF)

A
  • force exerted by the small fraction of proteins that have leaked from the capillaries into the interstitium
  • Favors filtration
  • **becomes critical when proteins leak out in the presence of histamine
56
Q

what are net outward pressure at arteriolar end and inward reabsorption pressure at the venular end

A
  • net outward pressure at arteriolar end: 11 mmHg
  • inward reabsorption pressure at the venular end: 9 mm Hg
57
Q

what happens to filtered fluid that is “left behind”

A

forced into lympathic system

58
Q

what is the network of one-way vessels that return fluid back into the blood? What facilitates it?

A
  • lymphatics
  • facilitated by the muscle pump
59
Q

what characteristics of veins make them capable of being highly distended

A
  • thin inner walls
  • less smooth muscle
  • less elasticity and tone
  • more collagen
60
Q

compaure the compliance between veins and arteries at low and high pressure

A
  • low pressure: venous compliance is up to 20x higher than arterial compliance
  • high pressure: compliance is similar
61
Q

blood spends the majority of its time in what vessels?

A

veins

  • at rest, many capillary beds are closed, increases the venous reservoir
62
Q

relate cardiac output and venous blood

A

CO is the determinant of how much blood arrives from the venous side

63
Q

what is venous return

A

all the blood arriving at the right atrium to be pumped into the systemic circulation

64
Q

Since Cardiac output and venous return are balanced; factors that alter one will ?

A

affect the other

65
Q

what is the major factor determining cardiac output

A

left ventiruclar end diastolic volume

  • LVEDV depends on venous return
66
Q

as venous return increases, what affect does this have on the right atrial pressure and EDV?

A

right atrial pressure increases -> increased EDV -> increases CO

67
Q

When Right atrium pressure reaches 4-5 mmHs, what happens to cardiac output

A
  • matching levels off and CO can no longer keep up with venous return
  • CO reaches a maximum of 9 L/min
68
Q

explain the relationship between venous return and right atrial pressure

A
  • VR is driven by pressure gradient
  • the lower the pressure in the RA, the higher the pressure gradient between the systemic arteries and the RA and the greater the venous return

*** as RAP increases, pressure gradient decreases, and VR decreases

69
Q

what is mean systemic pressure?

A

venous return = zero and RAP is maximal

*where the curve intersects the x-axis

  • pressure measured in the CV system if the heart stopped pumping
70
Q

what influences mean systemic pressure

A
  • blood volume
  • distribution of blood between the unstressed and stressed volume
71
Q

what volume volume will be in the unstressed volume, at which the MSP is zero

A

volume that is < 4 L

  • if total total volume is 5L, 4L is unstressed and 1L is stressed volume which produces a MSP of 7 mmHG
72
Q

increased blood volume and decreased compliance have what effect in MSP

A

produce an increase in MSP

  • if compliance of veins decreases (venoconstriction), veins hold less blood and the blood shifts to the stressed volume
73
Q

a positive inotropic (agent that alters the force or energy of muscular contractions) has what effect on contractility, SV, and CO

A
  • increases contractility, SV and CO for any level of RAP
74
Q

what effects does a positive and negative inotropic effect have on CO and RAP

A
  • in either situtation, vascular curve remains the same
  • positive: CO increases, RAP decreases and curve shifts upward
  • negative: CO decreases, RAP increases and curve shifts downward
75
Q

an increase in blood volume has what effect on MSP

A

increase in blood volume increases the amount of blood in the stressed volume and therefore increased MSP

  • CO and RAP are increased
76
Q

an increase in total peripheral resistance has what affect on arterial pressure

A

increases arterial pressure by holding blood in the arteries

  • increases afterload
  • decreases CO
77
Q

an increase in total peripheral resistance has what affect on the vascular function curve

A

produces a counterclockwise rotation of the curve, which means less blood returns to the heart for a given RAP and VR is decreased