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Cardiorespiratory Biology > Arterial and Venous system > Flashcards

Arterial and Venous system Flashcards

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AP® Biology flashcards Biology 101 flashcards
1
Q

function of elastin fibres in aorta

A

Elastin fibres provide elasticity

– as blood is ejected the aorta expands, the rebound in diastole propels the blood onward

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2
Q

important structure in arteries

A

Arteries have a thick layer of smooth muscle

– allows them to withstand high pressures

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3
Q

collagen fibres function

A

Collagen fibres provide strength

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4
Q

how does collagen and elastin change throughout arteries

A

this and elastin decrease in abundance as arteries get smaller

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5
Q

how does collagen and elastin change WITH AGE

A

As we get old vessels get stiffer and less compliant

– one of the reasons blood pressure increases

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6
Q

Important structure of arterioles

A

Arterioles have a thick layer of smooth muscle
– as a total amount it is less than the large arteries but it is greater proportional
of the total wall

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7
Q

difference between arteries and arterioles

A

• Less elastin and collagen fibres

– less compliant compared to larger arteries

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8
Q

arterioles are site of

A

These are the site of total peripheral resistance
– think back to the Poiseuille’s Law (1 / r
4)
• Tone on these vessels determines where blood flows
– it always takes the path of least resistance

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9
Q

vascular tone

A

the level of constriction applied across vessels

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10
Q

state of arteries at rest

A

are slightly constricted meaning they can both

constrict and dilate

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11
Q

arterial tone

A

the balance of constrictors and dilators that are acting on the vascular smooth muscle

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12
Q

arterial constriction leads to..

A

decrease radius
increase resistance
decrease flow

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13
Q

arterial dilation

A

increase radius
decrease resistance
increase flow

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14
Q

what does vascular tone respond to

A

responds to both intrinsic (local) and extrinsic (systemic) factors

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15
Q

2 types of intrinsic factors

A
  1. intrinsic: mechanical stimuli E.G. stretch and shear

2. intrinsic: endothelial regulation plus other metabolites and autocoids in response to local demand

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16
Q

extrinsic

A

extrinsic: systemic regulation (nerves & hormones)

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17
Q

organs involved in primary intrinsic regulation of vascular tone

A

brain, kidney and heart
– local control regulating flow -
brain does not require external stimuli

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18
Q

primarily extrinsic regulation of vascular tone

A

skin
– think hypothalamus and temperature regulation
– also think cool peripheries following BP crash

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19
Q

interactions of regulation of vascular tone

A

skeletal muscle
– at rest systemic regulation
– during exercise local metabolites dominate

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20
Q

when do smooth muscles constrict

A

constricts when stretched
– occurs in most smooth muscles including vascular
– due to opening of Ca2+ channels

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21
Q

where does constriction occur

A

• Occurs in a number of vascular beds

– such as cerebral, renal and coronary

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22
Q

what does myogenic response of constriction of smooth muscle contribute to

A

This contributes to the basal tone of arteries and stabilises flow and prevents excessive perfusion
– it is an important feature of autoregulation

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23
Q

role of vascular endothelium

A 
– interface between blood and body tissues
– control of blood coagulation
– regulates vascular structure
– mediates inflammatory responses
– regulates vascular tone
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24
Q

endothelium performs thru the release of what factors

A

paracrine factors

acting nearby; either the smooth muscle or platelets

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25
Q

endothelial mediators. - dilators

A

nitric oxide (NO) and prostacyclin (PGI2)

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26
Q

vasoconstrictors

A

such as endothelins (ET), Ang II and thromboxane (TxA2)

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27
Q

what does nitric oxide synthase enzyme produce

A

free radical nitric oxide

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28
Q

NO function

A

a vasodilator, relaxing vascular smooth muscle
– production increased by shear stress
– also agents such as ACh, histamine and bradykinin

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29
Q

NO is an anti-//

A

anti-thrombogenic and anti-atherogenic

– a healthy endothelium provides a non-thrombogenic surface

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30
Q

drugs interacting NO pathway -nitrates

A

– e.g. glyceryl trinitrate (GTN)
– used in angina
– assumed to act as NO is released via metabolism
– also available from dietary sources

31
Q

drugs interacting NO pathway - phosphodiesterase inhibitors

A

– e.g. sildenafil (Viagra)
– erectile dysfunction and pulmonary hypertension
– prevents the breakdown of cGMP

32
Q

what promotes vasodilation

A

Increased CO2, K+ , H+ and adenosine as well as decreased O2 all promote vasodilatation
– increased tissue metabolism increases perfusion

33
Q

vasoactive substances

A

histamine, bradykinin, serotonin (5-HT) and

eicosanoids/prostanoids

34
Q

metabolic hyperaemia

A

increased metabolic rate in tissue
accumulation of metabolites CO2 H+ K+ adenosine
local vasodilation
increased blood flow
accumulated metabolites flushed out
appropriate blood flow match metabolic rate

35
Q

what nervous system is responsible for maintenance of vascular tone

A

SympatheticNS

36
Q

most arteries are innervated by what fibres

A

sympathetic fibres

37
Q

constriction is due to what hormone and what receptor

A

noradrenaline acting at α1

-adrenoceptors

38
Q

increased sympathetic activity increases

A

will increase vasoconstriction

– cold, clammy peripheries

39
Q

what receptors lead to dilation in arteries

A

β-adrenoceptors (mainly β2

-)

40
Q

arteries are a target for circulating what hormone and what do they prevent

A

mainly a target for circulating adrenaline (adrenal medulla)

– prevalent in the skeletal muscle vascular beds and heart

41
Q

vasodilator innervated by

A

parasympathetic innervation

42
Q

organs innervated by PNS

A

face
gut
penis

43
Q

PNS innervated vessels mediated by what hormone

A

ACh & nonadrenergic non-cholinergic (NANC)

– NANC transmitters include NO, substance P, VIP

44
Q

mechanism of action of vasoactive hormones

A

Adrenaline from adrenal medulla.
– tends to act via β adrenoceptor
– constriction or dilation is vascular bed dependent
• Angiotensin II
– acts on AT receptors potent vasoconstrictor
• Vasopressin (anti-diuretic hormone, ADH)
– vasoconstrictor
• Insulin and oestrogens
– dilators by various mechanisms

45
Q

function of venules and veins

A

carry blood from capillaries back to the heart

right atrium

46
Q

structural difference between veins and arteries

A

Structurally veins are similar to arteries but have much thinner walls
– very little smooth muscle, small amounts of collagen/elastin

47
Q

what gives veins their capacitance function

A

distensibility gives then a capacitance function
– two thirds of the blood volume is held in the venous system
– x20 compliance of arteries

48
Q

what are the veins innervated by and what hormones and receptors mediate them

A

• Like arteries, veins are innervated by SNS fibres
– noradrenaline acts at ɑ1
-adrenoceptors to constricts veins

49
Q

are veins capable of constricting

A

yes

50
Q

affect of SNS fibres and noradrenaline

A

The effect of this is to raise pressure and decrease venous
capacitance
– redistributing the blood

51
Q

function of valve

A

prevent backflow, blood is moved towards the heart

– increasing cardiac output via Starling’s Law

52
Q

venous return is altered by

A

Skeletal muscle and thoracic pumps
– vary the pressure gradient during their activity
• Venous pressure/venoconstriction
gravity

53
Q

how does gravity influence pressure

A

Hydrostatic pressure increases 0.74 mmHg for every 1 cm beneath the heart
– venous pressure the foot 100 mmHg, yet -10 mmHg in brain

54
Q

how does gravity influence venous return and veins

A

• This increased transmural pressure distends the veins and venous return temporarily decreases
– this is venous pooling

55
Q

how does gravity influence muscle, valves and thoracic pump

A

The valves and muscle and thoracic pump break up the column into smaller sections aiding return
– lack of movement (and muscle pump) increases ankle oedema

56
Q

impact of failure of of valves

A

• Failure of valves also decrease return and increase venous pooling/oedema
– varicose veins

57
Q

what is triggered when pressure falls

A

Baroreceptor reflex is triggered as cardiac output and pressure fall
– increased vaso/venoconstriction, heart rate and contractility
– this should be imperceptible

58
Q

what happends when baroreceptors cannot respond

A

In states where the baroreceptors cannot respond then there is
postural drop and possibly syncope
– dehydration, already low pressure, old age (stiffer vessels)

59
Q

affect of positive g force - pilot in a steep climb

A

– black out as venous pooling increases
– venous return drops as does cerebral perfusion
– in a suit pilots can tolerate ~9 G

60
Q

affect of negative g force - pilot in a steep dive

A

“red out” and blood rushes to head (red eyes)

– even in suit can only tolerate about 3 G

61
Q

what does central venous pressure measure -CVP

A

measures right atrial pressure via

catheter in central vein

62
Q

what does CVP reflect and what is used to assess

A

it reflects the venous return and cardiac function

– can be used to assess fluid volume in fluid replacement

63
Q

how does CVP change in heart failure

A

CVP increases in heart failure due to volume expansion

64
Q

where is jugular venous pressure - JVP

A

seen in the internal jugular vein

of a person sitting

65
Q

A,C,V waves of the jugular venous pulse in the ..

A

right atrium

66
Q

how to measure jugular venous pressure

A

• Sit patient at 45 degrees
• The internal jugular veins fills from above
– where can you visualise is the filling point?
• The sternal angle is the zero point, more than 3 cm above is abnorma

67
Q

what does increased jugular venous pressure suggest

A

A raised JVP suggest increased right atrial pressure
– fluid overload
– RV failure
– tricuspid valve stenosis/regurgitation

68
Q

hepatic portal vein function

A

carries blood from the gastro-intestinal tract to the liver
– from intestinal capillaries to liver capillaries via portal vein
– two capillary beds in series

69
Q

what type of capillaries are the capillaries in the liver

A

sinusoidal type

– large gaps allows large substances to be absorbed

70
Q

how do diseases like cirrhosis impact hepatic portal circulation and how is it corrected

A

, resistance in the hepatic portal system increases
– to maintain flow pressure must increase (Q = ΔP ÷ R)
– pressure increases giving portal hypertension

71
Q

how are nutrients absorbed in the hepatic portal circulation

A

All substances absorbed from the intestines pass through the liver
– this includes orally taken drugs – first pass metabolism

72
Q

high portal pressure leads to

A 
shunt vessels (varices) that bypass the
liver back into systemic venous system
73
Q

what can shunt vessels lead to

A

this leads to morbidity
– bleeding abnormalities and toxins damaging other organs
– (hepatorenal syndrome and hepatopulmonary syndrome)

Cardiorespiratory Biology (25 decks)

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