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PHSL 232 > L8 > Flashcards

L8 Flashcards

1
Q

what is a very broad way of describing the arterial network structure

A

a multilayered system of tubes

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2
Q

compare and contrast arteries and arterioles

A

the most inner layer is the endothelial layer

arteries have lots of elastic tissue which is important for their function

arterioles have finger like smooth muscle that wraps around the lumen which gives it its function

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3
Q

what is the function of aorta and large arteries

A

Distribute blood

Pressure reservoir
- Reduce fluctuations in pressure and flow = maintain flow throughout cardiac cycle

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4
Q

what makes the arteries act as a pressure reservoir

A

The arteries and the aorta have lots of elastic tissue therefore it has the ability to change shape which is what helps it be a pressure reservoir

Some blood goes towards the periphery but some goes out which causes the arterial balloon (stretch)

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5
Q

what is recoil

A

Recoil happens during diastole. it is when the arterial walls snap back which causes the elastic potential energy to be released causing blood flow away from heart as aortic valve shut!

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6
Q

what happens in the aorta and large arteries during systole

A

Systole = stretching =

stores potential energy

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7
Q

what happens in the aorta and large arteries during diastole

A

Diastole = recoil =

release stored energy

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8
Q

what is compliance

A

the stretchiness

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9
Q

what does compliance =

A

dV / dP

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10
Q

what does stiffness =

A

1 / compliance

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11
Q

what happens to our arteries as we age

A

Young arteries are compliant

When you age you get increased smooth muscle layers, collagen and fibrous which makes it less complaint

this is also what you see in cardiovascular disease

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12
Q

what is the roles of the small arterioles

A

Main determinant of resistance (local and total peripheral resistance)

Important in controlling local flow

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13
Q

what is vasoconstriction and vasodilation

A

vasoconstriction = contraction of smooth muscle

vasodilation = relaxation of smooth muscle

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14
Q

how does vasoconstriction and vasodilation control the resistance of the arterioles

A

Smooth muscle cells wrap around the lumen.

Contraction squeezes lumen to reduce diameter

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15
Q

what is the min pressure just before ventricular contraction

A

diastolic pressure (DP)

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16
Q

what is the maximum arterial pressure reached during peak ventricular ejection

A

systolic pressure (SP)

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17
Q

what is the normal blood pressure

A

120 / 80 mmHg

systolic / diastolic

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18
Q

if you had hypertension what would you expect the blood pressure to be

A

> 140 / 90 mmHg

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19
Q

if you had hypotension what would you expect the blood pressure to be

A

< 90 / 60 mmHg

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20
Q

what is pulse pressure

A

systolic pressure - diastolic pressure

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21
Q

what is the calculation of mean arterial blood pressure

A

mean ABP = DP + 1/3(SP-DP)

diastolic pressure + 1/3 of the pulse pressure

we calc like this because the heart spends longer in diastole

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22
Q

what is the value for mean arterial blood pressure

A

90mmHg

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23
Q

what is the dicrotic notch

A

when the aortic valve closes at the end of systole. This causes a slight transient increase in pressure

24
Q

why do we need to keep BP constant

A

for pufusion

25
Q

what is mean arterial blood pressure dependent on

A

CO and TPR

MABP = CO x TPR

26
Q

how is TPR determined

A

it is the sum of global resistance from all the vascular beds

27
Q

how is blood pressure increase via TPR

A

when you had a drop in blood pressure you get vasoconstriction from SM in the arterioles

28
Q

how does CO increase blood pressure

A

the heart increases HR which increases CO which increases BP

29
Q

why is it important the BP is maintained at a homeostatic level

A

to maintain perfusion

30
Q

describe how arterioles determine how blood flow is distributed

A

when specific organs need more blood then you get vasodilation of arterioles at that organ and vasoconstriction to the organs that don’t need as much blood at that time

the increase in blood flow comes from decrease in blood flow from another vascular bed

This is all designed to keep MAP at a stable level

31
Q

what is important to note from changing blood flow distributions

A

there is no change in pressure as resistance and flow change

it is also important to know that the total volume of blood does NOT change as the increased volume of blood to one vascular bed has come from another

therefore volume to that organ changes but total volume does not

32
Q

what are the control mechanisms for vascular resistance

A

neural controls, hormonal controls and local controls

33
Q

what are the 2 ways of neural control on vascular resistance

A

sympathetic nervous system (noradrenalin)

postganglionic autonomic nerves

34
Q

how does the sympathetic nervous system have extrinsic control over vascular resistance

A

the SNS releases noradrenaline which binds to the a1 adrenergic receptor

when NA is bound it causes venoconstriction

when there is less NA bound there is vasodilation

therefore there is a tonal activation of the SNS

35
Q

how do we regulate how much of an effect noradrenaline has

A

Innervation density varies depending on vascular bed

this is because different vascular beds have different amount of the a1 adrenergic receptors

eg the brain has low numbers of α1- adrenergic receptors = limited vasoconstriction which is important because
brain needs constant flow

where as skin and GI have lots of receptors because flow needs to be flexible

36
Q

how does parasympathetic have control over venous resistance

A

it doesn’t

37
Q

how do postganglionic autonomic nerves have extrinsic control over vascular resistance

A

PGAN release nitric oxide which causes the relaxation of smooth muscle

this is a specialised system which is only found in specific areas of the body (GI and penis)

38
Q

where does NO effect vascular resistance in the body

A

GI tract and penis

39
Q

how does viagra work

A

Viagra works because it is used in the postganglionic autonomic nerve pathway, it releases NO which causes dilation to get more blood flow to the penis

40
Q

what hormones cause vasoconstriction

A

adrenaline, angiotensin 2 and vasopressin

41
Q

what hormones cause vasodilation

A

adrenaline, atrial natriuretic peptide

42
Q

how does adrenaline cause both vasoconstriction and vasodilation

A

because there are 2 adrenaline receptors

a 1 adrenergic receptors = constriction

B2 = dilation

this is controlled by how many receptors are expressed

Eg skeletal muscle B2 > a1

whereas skin a1 > B2

43
Q

what do ADH and angiotensin 2 do

what they usually do that effects blood

and their effect in the vasculature

A

they increase blood volume

ADH increases water reabsorption in the kidney which increases blood volume

angiotensin 2 causes Na+ reabsorption in the kidneys. water follows salt therefore increasing blood volume

when it acts on the vasculature it causes vasoconstriction

44
Q

what does atrial natriuretic peptide do

A

it decreases blood volume by decreasing water reabsorption in the kidney

when it acts on the vasculature it causes vasodilation

45
Q

what are the local control mechanisms

A

active hyperemia (metabolic autoregulation)

flow autoregulation (myogenic autoregulation)

these are the intrinsic control factors

46
Q

describe what happens in active hyperemia

A

this happens when you are using that organ alot (eg skeletal muscles when exercising). you need more blood flow to take more O2 to make energy

the products of metabolism cause vasodilation in the vascular bed

this is a tissue specific response

47
Q

where is active hyperemia highly developed

A

skeletal and cardiac muscle because of their high metabolic demands

48
Q

what is flow autoregulation

A

it is the control of blood flow to maintain flow despite changes in perfusion pressure

49
Q

how does flow autoregulation work

A

When the pressure goes up then the smooth muscle cells stretch which stimulates them to contract

Reduction in blood flow decreases the pressure reduction is stretch on the vessel stimulates them to contract

50
Q

Direct sympathetic stimulation of the systemic arterioles can
cause:

A: vasoconstriction mediated by α1 adrenergic receptors

B: vasodilation mediated by α1 adrenergic receptors

C: vasoconstriction mediated by β2 adrenergic receptors

D: vasoconstriction mediated by β1 adrenergic receptors

A

A

51
Q

The aorta and large arteries maintain the flow of blood during diastole

BECAUSE

the strong elastic recoil of the arterial walls forces blood away from the heart as
the aortic valve is shut.

A

Both statements are true and causal

52
Q

Mean arterial blood pressure is calculated by:

A: adding diastolic and systolic pressure

B: subtracting diastolic from systolic pressure

C: adding the diastolic and systolic pressure and dividing by 2

D: adding one-third of the difference between the diastolic and systolic pressure to the diastolic pressure

A

D

53
Q

Which of these statements is INCORRECT?

Vasopressin increases mean arterial blood pressure by:

A: increasing water absorption in the kidneys

B: decreasing stroke volume

C: causing vasoconstriction

D: increasing cardiac output

A

…

54
Q

The flow of blood away from the heart is maintained during diastole

BECAUSE

smooth muscle cells within the
walls of the aorta constrict during diastole.

A

the first statement is true and the second is false

55
Q

Adrenaline will increase blood flow to skeletal muscles (assuming no change in perfusion pressure)

BECAUSE

adrenaline stimulates alpha-1 adrenergic receptors in the vascular smooth muscle of skeletal arterioles to provoke
vasodilation.

A

a1 is constriction

therefore first is true and second is false

PHSL 232 (30 decks)

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