Cardiovascular mechanisms Flashcards

1
Q

what are capillaries the site of

A

Exchange of gas, nutrients and water between blood and tissues

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2
Q

what blood vessels contain majority of blood volume during rest

A

veins

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3
Q

what is afterload

A

the stress in the wall of the left ventricle during ejection or the end load against which the heart contracts to eject blood

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4
Q

how is MAP calculated using CO

A

CO x SVR

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5
Q

how is SVR regulated

A

by vascular smooth muscles in blood vessels

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6
Q

vasocontriction of vascular smooth muscle causes what

A

increases MAP and SVR

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7
Q

vasodilation of vascular smooth muscle causes what

A

decreases SVR and MAP

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8
Q

what are vascular smooth muscles controlled by

A

extrinsic and intrinsic mechanisms

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9
Q

where through pathway of blood through circulation is the biggest drop in pressure

A

when blood travels from arterioles to capillaries

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10
Q

what is resistance to blood flow directly proportional to

A

blood viscosity and length of blood vessel

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11
Q

what is resistance to blood flow indirectly proportional to

A

the radius of blood vessel to the power 4

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12
Q

what is the resistance to blood flow mainly controlled by

A

via vascular smooth muscle through changes in the radius of arterioles

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13
Q

what nerves supply vascular smooth muscles

A

sympathetic nerve fibres

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14
Q

what is the neurotransmitter for sympathetic nerve fibres and what receptors do they act on

A

noradrenaline, alpha receptors

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15
Q

what is the vasomotor tone

A

due to continuous release of noradrenaline vascular smooth muscles are partially constricted at rest

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16
Q

what does increased sympathetic discharge cause

A

increases the vasomotor tone

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17
Q

where is vasculature innervated with parasympathetic nerve fibres

A

penis and clitoris only

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18
Q

what does adrenaline acting on alpha receptors do

A

causes vasoconstriction

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19
Q

what does adrenaline acting on beta 2 receptors do

A

causes vasodilatation

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20
Q

when are alpha receptors predominant

A

skin, gut and kidney arterioles

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21
Q

where are B2 receptors predominant

A

cardiac and skeletal muscle arterioles

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22
Q

what do B2 receptors in muscle arterioles help to achieve

A

strategic redistribution of blood e.g. during exercise

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23
Q

what are two other hormones that affect vascular smooth muscle (and what do they do)

A

Angiotensin II: causes vasoconstriction

Antidiuretic hormone (vasopressin): causes vasoconstriction

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24
Q

what are Angiotensin II and Antidiuretic hormone (vasopressin) important in controlling

A

the intermediate control of blood pressure

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25
Q

what do the intrinsic control mechanisms of VSM match to what

A

the blood flow of their tissue to their metabolic needs

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26
Q

what can the extrinsic control mechanisms over-ride

A

extrinsic control mechanisms

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27
Q

what do intrinsic control mechanisms include

A

LOCAL chemical and physical factors

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28
Q

what is the main way local blood flow is controlled

A

local intrinsic control mechanisms

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29
Q

what can local metabolic changes within an organ influence

A

the contraction of arteriolar smooth muscles

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30
Q

name the local metabolic factors causing relaxation of arteriolar smooth muscles (6)

A

Decreased local PO2

Increased local PCO2

Increased local [H+] (decreased pH)

Increased extra-cellular [K+]

Increased osmolality of ECF

Adenosine release (from ATP)

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31
Q

what does relaxation of arteriolar smooth muscles result in

A

vasodilatation and metabolic hyperaemia

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32
Q

what us hyperaemia

A

excess of blood in a vessel

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33
Q

In addition to metabolites what other local chemicals released within an organ influence the contraction of arterial and arteriolar smooth muscles

A

local humoral agents

34
Q

what can the release of local humoral agents be caused by

A

tissue injury or inflammation

35
Q

give three examples of local humoral agents that cause relaxation of ASM

A

Histamine

Bradykinin

Nitric Oxide (NO)

36
Q

describe the release if NO

A

continuously released by endothelial cells of arteries and arterioles

37
Q

what are local humoral agents classed as as a mechanisms

A

intrinsic control mechanisms of VSM (chemical)

38
Q

how is NO produced

A

by the vascular endothelium from the amino acid L-arginine through enzymatic action of Nitric Oxide Synthase (NOS)

39
Q

what is the role of NO

A

is a potent vasodilator which is important in the regulation of blood flow and maintenance of vascular health

40
Q

what is the duration of life of NO

A

few seconds

41
Q

what causes the release of calcium in vascular endothelial cells and what does this cause (WHAT IS THIS CALLED)

A

FLOW DEPENDANT NO FORMATION
Shear stress on vascular endothelium, as a result of increased flow- subsequent activation of NOS (which will produce NO from L-arginine )

42
Q

what is receptor stimulated NO formation

A

when chemical stimuli induce NO formation

43
Q

describe the path of NO

A

diffuses from endothelium into the adjacent smooth muscle cells

44
Q

what does NO do when in smooth muscle cells

A

activates the formation of cGMP that serves as a second messenger for signalling smooth muscle relaxation

45
Q

give four examples of humoral agents which cause contraction of arteriolar smooth muscles resulting in VASOCONSTRICTION

A

Serotonin

Thromboxane A2

Leukotrienes

Endothelin

46
Q

describe endothelin

A

is a potent vasoconstrictor released from endothelial cells

47
Q

what is the production of endothelin caused by

A

various agents which cause vasoconstriction

48
Q

what can damage endothelium

A

high blood pressure, high cholesterol, diabetes and smoking

49
Q

describe endothelial produced vasodilators

A

anti-thrombotic, anti-inflammatory, anti-oxidants

50
Q

describe endothelial produced vasoconstrictors

A

are pro-thrombotic, pro-inflammatory, pro-oxidants

51
Q

what are the three physical control mechanisms of VSM

A

temperature, myogenic response, sheer stress

52
Q

what does myogenic response stop

A

changes in blood affecting the brain and the kidneys

53
Q

describe the action of myogenic response if MAP increases

A

resistance vessels automatically constrict to limit flow

54
Q

describe the action of myogenic response if MAP falls

A

resistance vessels automatically dilate to increase flow

55
Q

what creates sheer stress and what does it cause

A

Dilatation of arterioles causes sheer stress in the arteries upstream to make them dilate. This increases blood flow to metabolically active tissues

56
Q

what is the autoregulation of cerebral blood flow

A

myogenic response

57
Q

what else is cerebral blood flow controlled by

A

Sympathetic nerve stimulation

58
Q

what four factors increase venous return

A

increased;
venomotor tone, skeletal muscle pump,
blood volume, respiratory pump

59
Q

what pressure does increased venous return increase

A

atrial pressure

60
Q

how does increased venous return affect EDV

A

increases it

61
Q

how does increased venous return affect SV

A

increases it (starling curve)

62
Q

describe the respiratory pump

A

Descend of diaphragm when breathing increases abdominal pressure and decreases intrathoracic pressure which decreases pressure in RA which creates a bigger pressure gradient therefore increasing venous return

63
Q

what type of vessels are veins

A

capacitance vessels

64
Q

what nerve fibres are venous smooth muscles supplied with

A

sympathetic

65
Q

what does increased venomotor tone lead to (3)

A

increased;

venous return, SV and MAP

66
Q

what does invrease vasomotor tone do (2)

A

increased;

SVR and MAP

67
Q

how does skeletal muscle activity affect venous return and how

A

increased activity increases venous return as large veins in limbs lie between muscle which pump blood when they constrict

68
Q

what affects blood volume (2)

A

fluid shifts across capillaries and salt & water balance

69
Q

what happens to sympathetic nerve activity during exercise

A

increases

70
Q

what happens to HR and SV during exercise

A

increases

71
Q

what is the action of sympathetic vasomotor nerves during exercise

A

reduce flow to kidneys & gut - vasoconstriction

72
Q

what overcomes vasomotor drive in skeletal and cardiac muscle during exercise and casuing what

A

metabolic hyperaemia, vasodilation

73
Q

in proportion to what during exercise does blood flow increase

A

metabolic activity

74
Q

what do the increases in CO during exercise do to systolic BP

A

increase it

75
Q

what does the metabolic hyperaemia do to SVR and DBP

A

decreases them

76
Q

why does DBP decrease during exercie

A

as muscle bed big tissue so has lot of vasodilatation

77
Q

what is the effect of sympathetic stimulation on the heart

A

increases HR by increasing SA node firing and decreasing nodal delay and increases force of contraction

78
Q

what does sympathetic stimulation do to the slope of pacemaker potential

A

decreases it, positive chronotropic effect

79
Q

what is the effect of sympathetic nerve stimulation on ventricular contraction

A

Peak ventricular pressure rises - contractility of heart at a given EDV rises

80
Q

what is the effect of sympathetic nerve stimulation on the frank starling curve

A

shifted to the left

81
Q

what does regular aerobic exercise help to reduce

A

BP

82
Q

what might chronic cardiovascular responses to regular exercise include (6)

A

Reduction in sympathetic tone and noradrenalile levels

Increased parasympathetic tone to the heart

Cardiac remodeling

Reduction in plasma renin levels, reduces BP

Improved endothelial function: more vasodilators less vasoconstrictors

less arterial stiffening- therefore decrease BP