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Cardiovascular physiology > Control of blood flow > Flashcards

Control of blood flow Flashcards

1
Q

What is perfusion pressure?

A

Arterial bp - venous bp

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2
Q

What is equation for tissue blood flow?

A

Perfusion pressure/resistance

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3
Q

What is equation for resistance?

A

Poiseuille’s law

8 x viscosity x l / pi x r^4

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4
Q

What are the two ways that blood flow can be controlled?

A

Change blood pressure

Change resistance

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5
Q

3 ways of changing pressure?

A

Cardiac contraction (i.e. hormones, nerve, Starling)

Water/salt balance (i.e. blood volume through kidney, sweating)

Vessel compliance and tension

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6
Q

Why does increasing volume increase pressure?

A

Blood virtually incompressible unlike air

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7
Q

Normally increasing blood volume increases pressure, Why is increase in blood volume dampened in circulatory system?

A

Arteries are compliant and stretch to accommodate more fluid without proportional increase in pressure

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8
Q

Why does bp increase with age (how do arteries change)?

A

Vessels more stiff and less compliant e.g. atherosclerosis

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9
Q

What is problem with controlling blood flow by changing blood pressure?

A

Changes in bp often associated with pathology, and doesn’t allow local regulation to be achieved.

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10
Q

What is after-load?

A

The resistance against which heart has to work to pump blood into arteries

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11
Q

What is resistance to blood flow determined by (i.e. afterload)?

A

Diameter, total cross sectional area and blood viscosity

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12
Q

Why are arterioles resistance vessels?

A

Greatest drop in blood pressure as blood flows through arterioles.

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13
Q

Which vessel is mainly responsible for resistance to flow?

A

Arterioles

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14
Q

How does blood flow change going from arteries through to veins?

A

Stays the same, from artery, arterioles, capillary etc

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15
Q

How do pressure and resistance change as you go from artery to venules?

A

In arterioles, large rise in resistance and thus drop in pressure (to maintain constant flow)

Resistance then drops by the time you’ve reached capillaries and remains low, as does pressure.

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16
Q

How can large arteries change to increase bp?

A

Large artery contraction reduces their compliance and increases bp

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17
Q

Describe the state of the muscles of arterioles?

A

Most in tonic constriction due to symp stimulation

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18
Q

How does increase in diameter by factor 2 change bp?

A

By factor 16

2^4

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19
Q

Same flow throughout given vascular bed so greatest fall in pressure in region…

A

Of greatest resistance

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20
Q

How can arteriole resistance be altered?

A

Modulate vascular tone

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21
Q

Describe how control of vascular tone of arteries and arterioles differ

A

Artery under extrinsic control only, arterioles both intrinsic and extrinsic

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22
Q

High basal tone of arterioles in areas where….

A

Blood flow needs to be changed to greater degree e.g. skeletal muscle

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23
Q

What happens when you vasoconstrict arterioles (to larger vessels and capillaries)?

A

Pressure upstream increases (hence hypertension in large vessels)

Also decrease capillary perfusion downstream

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24
Q

What happens to capillaries as you vasodilate?

A

Increased capillary recruitment and increase capillary perfusion

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25
Q

How do arterial and capillary bp change with vasoconstriction of arterioles?

A

Arterial bp increases

Capillary pressure decreases

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26
Q

How does capillary recruitment occur, which tissue is it important for?

A

Some capillaries only recruited at higher perfusion pressures
important in skeletal muscle

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27
Q

Describe relationship between arterial bp and blood flow

A

Directly proportional

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28
Q

Where is high basal flow needed (which organs), what’s the consequence?

A

Vascular beds of kidneys and brain (otherwise renal failure, coma)

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29
Q

What does perfusion normally match?

A

Metabolic rate

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30
Q

Which organs are overperfused (greater than metabolic need, why?

A

Other/non-metabolic need for high blood flow

Kidney: blood needed to be filtered

Skin: blood to lose heat

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31
Q

Which organs are usually underperfused?

A

Brain and heart

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32
Q

What are some extrinsically triggered factors that can affect local flow?

A

Sympathetic: Adrenaline, noradrenaline

Parasympathetic: Acetylcholine

Angiotensin

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33
Q

What are some local autocoids that control blood flow locally?

A 
Histamine
Bradykinin
Prostaglandis
Leukotrienes
Endothelins
NO
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34
Q

What are metabolic factors that control blood flow locally?

A 
High extracellular K+
Acidity
Adenosine
Temp
Hypoxia
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35
Q

Where do we not see autoregulation?

A

Pulmonary, cutaneous

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36
Q

What does autoregulation allow?

A

Tissues to control/stabilise perfusion independent of arterial bp

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37
Q

What is the Bayliss effect?

A

Myogenic autoregulation keeps blood flow constant. as blood pressure distends vessels, they undergo sustained contraction (maintains basal tone)

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38
Q

What is the mechanism behind the Bayliss effect?

A

Stretch creates tension, opens non-specific cation channels, opens voltage gated Ca2+ channels, raised concentration of Ca2+ leads to contraction of the vessel.

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39
Q

What can override autoregulation?

A

Local metabolic control

40
Q

How can high perfusion pressure contribute to autoregulation?

A

Increased perfusion pressure increases blood flow, flushing away vasodilators so vascular tone increases

41
Q

How can local metabolic control allow flow to a individual vascular bed to be controlled?

A

Flow altered based on tissue’s metabolic demand. Arterioles sensitive to metabolic demands of tissue

42
Q

What can trigger increase in local factors?

A

Increased metabolites, ischaemia, increased sheer stress to elevated blood flow

43
Q

What do metabolic byproducts cause, why is this important?

A

Vasodilation, increased blood flow through vascular bed for increased oxygen supply and waste removal

44
Q

What is metabolic hyperaemia?

A

Increase in blood flow to a more metabolically active tissue

45
Q

Where is adenosine release important?

A

Coronary circulation, less so skeletal

46
Q

How does adenosine cause vasodilation?

A

Increased ATP demand in coronary vessels as oxygen consumption increases

Less ATP available as it’s used up, AMP builds up released from cells

Forms adenosine (primary product of ATP breakdown)

Stimulates A2A receptors on smooth muscle

Increases cAMP

Decreased MLCK activity (PKA phosphorylates) vasodilation

47
Q

What does adenosine do to kidney circulation?

A

Vasoconstriction (A1 adenosine receptor)

48
Q

Where is acidity an important local factor?

A

The brain

49
Q

How does acidity lead to increased cerebral circulation?

A

Increased rate of metabolism/respiration/oxidative phosphorylation

Increased pCO2

Increased carbonic acid concentration

Increased acidity decreases open probability of ion channels in membrane and inhibits MLCK

Vasodilation

50
Q

What does low pCO2 cause to vessels in brain, what are the symptoms?

A

Vasoconstrict, so dizziness

51
Q

Where is accumulation of K+ important metabolic factor?

A

Skeletal muscle and brain

52
Q

What is the mechanism for increased K+ extracellularly and blood flow?

A

K+ release by action potentials in active muscle fibres

In intense exercise, high frequency of AP fired, not all of K+ can go back into cell

Small increase in extracellular potassium conc

Leads to Increased potassium permeability

Hyperpolarisation as Ek is neared

Vasodilation

53
Q

Where does reactive hyperaemia occur?

A

Skeletal muscle

54
Q

What is reactive hyperaemia?

A

If you contract muscle, muscle compresses arterioles and capillaries, TPR increases, leading to ischaemic tissue then you accumulate metabolites,

When you release compression, leads to massive increase in blood flow as these vasodilator metabolites cause vasodilation

55
Q

How can metabolic demand be coupled to blood flow given arterioles are upstream of capillary beds?

A

Arteriole can affect capillary perfusion

Intracellular signal in response to vasoactive substance propagating through gap junctions.

Paracrine signalling, e.g. in nephron, cells of macula densa which sense metabolic demand and are stuck on top of afferent arteriole.

56
Q

Why is local control systems better than sympathetic stimulation to control vascular tone?

A

Sympathetic system can’t be used as well to respond to needs of a particular tissue/organ

57
Q

How is endothelium important in control of blood flow, what does it respond to?

A

Produce modulators of local vessel tone in response to changes in local environment

58
Q

What does endothelium produce (gas) and when?

A

NO produced in response to hypoxia, shear stress, circulating neuroendocrine factors (e.g. Ach, bradykinin)

59
Q

How is NO made?

A

Stimuli increases intracellular calcium, binds calmodulin and activates eNOS (produces NO)

60
Q

What happens to NO after it’s made?

A

Diffuses into vessel wall, activation of guanylyl cyclase, cGMP made, activates PKG

61
Q

What does PKG phosphorylate?

A

MLCP which is activated to inhibit MLCK

K+ channels (which open) so reduced Ca2+ influx through VGCC

SERCA - so Ca2+ removal from cytosol

Ca2+ channels so they open less

62
Q

What else apart from NO does endothelium produce?

A

Prostacyclin 2
PGE2
Endothelium derived hyperpolarising factor

63
Q

What are some vasoconstrictors?

A

Thromboxane AE, endothelins

64
Q

What are some autacoids that are vasodilators?

A 
Prostaglandis
Leukotreienes
Histamine
Bradykinin
NO
65
Q

What produces Thromboxane A2?

A

Platelets

66
Q

Why is extrinsic control of blood flow important?

A

Fulfil wider CV functions and anticipate future demand (e.g. coordinated response to exercise)

67
Q

How does SNS lead to vasoconstrition?

A

NA acts on alpha 1 on vascular smooth muscle.

Also ATP and neuropeptide Y often cotransmitters with NA which cause rapid and long lasting vasoconstriction respectively

68
Q

What underpins resting tone of most arteries and arterioles?

A

Tonic activity of sympathetic vasoconstrictor fibres

69
Q

How does stimulation of beta receptors in kidney lead to vasoconstriction?

A

Activate renin angiotestin aldosterone system (RAAS)

Angiotensin 2 production and vasoconstriction through stimulation of AT1 receptors on smooth muscle

70
Q

How can sympathetic stimulation cause vasodilation?

A

Beta 2 receptors in arterioles (and some veins) supplying skeletal muscle. activated by NA

71
Q

How can parasympathetic fibres cause vasodilation?

A

In cerebral and coronary arteries, ACh released acting on M2 receptors on VSM. Hyperpolarisation and vasodilation

72
Q

What does ADH get produced in response to?

A

Fall in blood volume

73
Q

What releases ADH?

A

Posterior pituitary

74
Q

What does vasopressin do to blood vessels?

A

Vasoconstriction in most tissues but vasodilation in cerebral and coronary tissue (redistribute blood)

75
Q

When is renin secreted?

A

Fall in blood pressure and fall in Na+ in distal tubule

76
Q

What does renin do help to maintain bp and thus blood flow?

A

Converts angiotensinogen to angiotensin 1, which is converted to angiogensin 2 in lungs (by ACE). Angiotensin 2 causes vasoconstriction.

Also causes increased aldosterone secretion leading to greater salt and water reabsorption from distal tubule so increased blood volume

77
Q

What is ANP, where is it made?

A

Atrial natriueretic peptide made by atrial myocytes

78
Q

When is ANP made?

A

In response to high cardiac filling pressures. Triggers excretion of salt and water by renal tubules and weakly vasodilates resistance vessels

79
Q

How is coronary circulation mainly controlled?

A

Metabolic hyperaemia (adenosine)

Sympathetic stimulation
and circulating adrenaline (beta 2 receptors on VSM causes vasodilation)

80
Q

Why does oxygen extraction for heart need to be very high?

A

During periods of high cardiac work as contraction more forceful and frequent.

High pressure in ventricular wall in systole shuts off coronary circulation

81
Q

What are the 2 resistance vessels in cutaneous circulation, what controls them?

A

Arterioles (sympathetic and local metabolic control)

Arteriovenous anastomoses AVAs (sympathetic vasoconstrictors control only)

82
Q

How does fall in temp affect cutaneous circulation?

A

Receptors in hypothalamus detect it.
Sympathetic signalling increases so AVA constrict so high resistance shunt created and reduced cutaneous flow.

Directs blood away from surface of skin

83
Q

What is the effect of dilating AVAs?

A

Increased heat loss

84
Q

What are the different ways skeletal muscle circulation can be altered?

A

Metabolic hyperaemia (esp K+, some adenosine)
Capillary recruitment
Reactive hyperaemia
(autoregulation affects flow too)

85
Q

How does TPR fall in exercise, what stops it completely falling in exercise?

A

Metabolic hyperaemia (e.g. K+) causes vasodilation, TPR decreases.

Fall in bp detected by baroreceptors which trigger sympathetic activation to further increase perfusion of active muscle and prevent excessive fall in TPR.

86
Q

How is renal circulation controlled?

A

Autoregulation keeps flow constant

Angiotensin 2 and ADH (vasoconstrictors regulate renal blood flow)

Sympathetic stimulation: vasoconstriction

87
Q

What alters pulmonary circulation?

A

Hypoxia/hypercapnia arterioles constrict, diverting blood to well oxygenated areas (better V/Q mismatch). Pulmonary hypoxic vasoconstriction

88
Q

Why is there no autoregulation in pulmonary circulation?

A

If excessive vasoconstriction occurred in pulmonary regulation, blood from RHS of heart would not be able to bypass lungs to reach LHS and also lungs vulnerable to hypertension (oedema)

89
Q

What does 5HT do?

A

Vasodilator via NO production

90
Q

What does vagus stimulation to coronary resistance vessels do?

A

Dilates them

91
Q

True of false, lowered pH, and hypoxia causes relaxation of coronary vessels?

A

False, adenosine is the only real coronary vasodilator

92
Q

How do you calculate mean arterial blood pressure?

A

Estimated using a formula in which the lower (diastolic) blood pressure is doubled and added to the higher (systolic) blood pressure and that composite sum then is divided by 3

93
Q

Is MAP calculated by arithmetic average of diastolic and systolic pressure?

A

No

94
Q

When do the heart sounds come relative to the ECG?

A

1st: After QRS
2nd: After T wave

95
Q

Describe ECG for 3rd degree heart block

A

Third-degree AV block exists when more P waves than QRS complexes exist and no relationship (no conduction) exists between them.

96
Q

What vessels have the greatest compliance?

A

Veins

Cardiovascular physiology (11 decks)

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