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Unit 12 > Control of Blood Flow lecture > Flashcards

Control of Blood Flow lecture Flashcards

1
Q

What is the basis of the feedback loop affecting the rate of tissue blood flow?

A

Decreased O2 delivery or increased tissue metabolism
Results in Decreased Tissue O2
Results in relaxation of arterioles and pre-capillary sphincters.
This increases tissue blood flow

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2
Q

Define diastolic pressure

A

The lowest arterial pressure in a cardiac cycle
Pressure in arteries during ventricular relaxation aka no blood is being ejected from the left ventricle

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3
Q

Define systolic blood pressure

A

The higest arterial pressure measured during a cardiac cycle
Pressure in arteries after blood has been ejected during systole

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4
Q

What is the dicrotic notch in blood pressure?

A

A blip or temporary decrease in arterial pressure
Produced when the aortic valve closes, produces a temporary retrograde of blood from the aorta towards the valve resulting in brefily decreasing aortic pressure below the systolic value

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5
Q

Define pulse pressure?

A

The difference between systolic pressure and diastolic pressure
SP-DP
This reflected the volume of blood ejected from the left ventricle aka the stroke volume

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6
Q

Define mean arterial pulse pressure.

A

The average pressure over a complete cardiac cycle

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7
Q

What is the normal range of mean arterial pressure?

A

70-100mmHg

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8
Q

How do you calculatre mean arterial pressure?

A

DP + 1/3 pulse pressure

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9
Q

Draw a diagram to show how arterial pressure changes over one cardiac cycle.
Explain these changes.

A

Disatolic pressure - lowest pressure as heart relaxed, no blood ejected
Blood ejected as ventricles contract - eventually reach systolic pressure _ highest pressure when all blood is ejected from left ventricle
Dicrotic notch - closure of aortic valve causes temporarily back flow of blood towards the heart
Ventricles relax - return to diastolic

Mean arterial pressure is closer the diastolic than systolic as spend longer amount of cycle in diastolic than systolic.

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10
Q

Describe how blood pressure changes over age.
Why?

A

Tends to increase with age
Most rapidly from 0-20yrs, then slows down to almost stable before increasing again rapidly from 60yrs plus

Decreased elasticity in ageing arterial walls, results in decreased compliance so stroke volume ejected causes a larger increase in pressure than a young artery.

Causes an increase in pulse pressure as increase in systolic is greater than diastolic

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11
Q

Describe how baroreceptors play a role in increasing cardiac output?

A

Low blood pressure - decreasing stretch on baroreceptors (carotid sins and aortic arch) - decreased action potential generation - reduced firing rate up the glossopharyngeal and vagus afferent nerve respectively
Decreased signal detection in the nucleus tractus solitarus.
Results in increased sympathetic tone originating from the cardiac accelerator and the vasoconstrictor centre
The vasoconstrictor centre projects efferent neurons to cause vasoconstriction of arterioles and veins
The cardiac accelerator projects efferents to heart to increase firing rate of SAN and increase conduction velocity through AV node and increased contractility
Decreased activity of the cardiac decelerator centre

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12
Q

Describe how the baroreceptor reflex is activated during hypertension.

A

Increased blood pressure causes increased stretch on the baroreceptor (carotid sinus and aortic arch), resulting change in membrane potential is likely to cause an action potential
Increased afferent signals up (glossopharyngeal and vagus nerve)
Signals are interpreted in the nucleus tractus solitarus
Increased parasympathetic tone via increased activity of the cardiac decelerator centre, efferent fibres travel in vagus nerve and synpase on the SA node, resulting in decreased firing rate of the the SAN - decreased heart rate
Also reduced sympathetic tone through decreased activity of the cardiac accelerator and vasoconstrictor resulting in dilation of blood vessels, and reduced contractility and conductivity of the heart
Therefore, it has negative chronotopic, dronotropic and ionotropic effects.

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13
Q

Where is the nucleus tractus solitarus found?

A

The medulla

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14
Q

What are the antomical features of the vasoconstrictor centre?

A

Found in upper medulla and lower pons
Efferent neurons are sympathetic and synapse in the spinal cord then in the sympathetic ganglion then onto target organs
Produce vasocontrictions

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15
Q

What are the featurs of the cardiac accelerator centre?

A

Efferent are sympathetic
Synapse in spinal cord then sympathetic ganglia then finally the heart
Positive chronotropic, dromotropic (through AV noce_ and inotropic effects

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16
Q

What are the antatomical features of the cardiac decelerator centre?

A

Efferent fibres are part of the parasympathetic nervous syste,
Travel in vagus nerve and synapse in the SAN
Decrease heart rate.

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17
Q

What is the baroreceptor reflex to hemorrhage?

A

Blood loss causes a decrease in mean arterial pressure
Results in decreased stretch on carotid sinus and aortic arch baroreceptors
Decreased firing rate of glossopharyngeal and vagus nerve.
Lack of signal is interpreted in the Nucleus Tractus Solitarus
Results in increased sympathetic activity to the heart and blood vessels : inc HR, contractility, constriction of arterioles (inc TPR), constriction of veins (inc venous return and decreased unstressed volume)
Decreased parasympathetic activity to heart = decreased heart rate
Mean arterial pressure increases back to normal as HR, contractility and cardiac output increase

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18
Q

What are the three mechanisms or response aspects after a haemorrhage?

A
  1. Baroreceptor reflex
  2. RAAS system
  3. Capillaries
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19
Q

What happens in the capillary response to hemorrhage?

A

Mean hydrostatis pressure of the capillary decreased
Increased fluid absorption (due to starling forces)
Results in increased blood volume
This is self limiting - stops once starling forces are rebalanced

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20
Q

What are the different ways in which the RAAS system can be activated?

A

Decreased BP - activates SANS and dec GFR
SANS - activate Beta 1 receptors on JG cells (afferent arteriole)
Decreased GFR = dec Na+/Cl- delivery to the macula densa in DCT (osmoreceptors)
Decreased renal blood flow hence perfusion (detected by mechanoreceptors in the afferent arteriole)
All result in the conversion of pro-renin to renin and release from juxtaglomerular cells

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21
Q

What is the Frank Straling mechanism in the cardiovascular system?

A

Increased venous return
Increased pre-load
Stretch on myocytes
Increased contractility
Resutls in increased stroke volume
Hence increased cardiac output.

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22
Q

What is the molecular pathway of RAAS?

A

Renin converts angiotensinogen (produced in the liver) to angiotensin 1
ACE 1 enzyme (in lungs and kidney) converts the Angiotensin 2
Angiotensin 2 brings about physiological effects.

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23
Q

What are the physiological effects of angiotensin 2?

A
  1. Binds to adrenal cortex to zone glomerulosa to release aldosterone (inc Na+ reabsorption in DCT/CD principle cells)
  2. Binds to blood vessels to cause vasoconstriction - inc TPR
  3. Binds to hypothalamus - increase thirst and ADH secretion (V1 vasoconstriction, V2 DCT/CD principle cells aquaporins, LOH NKCC2 counter current effect)
  4. Renal blood vessels - vasoconstriction of efferent - increase GFR ( more filtering means more time to secrete and reabsorb electrolytes)
  5. Renal PCT - increase Na+ H+ exchange, inc Na+ HCO3- reabsoprtion

Binds to AT1 receptors is a GPCR.

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24
Q

By what mechanisms does RAAS result in an increase in blood pressure?

A

Increase TPR (angiotensin 2)
Increase sodium reabsoprtion - inc ECF volume leading to an increase in BP
Increased water retention - increase body fluid volume

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25
Q

What is the most important effect of the RAAS system?

A

Aldosterone increase renal Na+ reabsoprtion
Increase total Na+ content - inc ECF volume hence blood volume
Increase venous return - inc cardiac output (Frank-Starling mechanism)
Increase in cardiac output increase Pa

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26
Q

What is the average blood volume of a 70kg male?

A

5 litres

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27
Q

How is our blood volume distributed?

A

85% in systemic circulation - 3/4 in the veins and remaining in arteires and capillaries
10% in pulmonary circulation
5% remains in cardiac chambers at end of diastole

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28
Q

What different histological features regulate the properties of blood vessels?

A

Endothelial cells
Elastic fibres
Collagen fibres
Smooth muscle

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29
Q

What is the role of endothelial cells in blood vessels?

A

Single layer throughout vascular tree
Connected by junctional complexes in arteries (less so in veins)
Capillaries have varying leakiness of junctional complexes - key features between sinusoidal, continuous and fenestrated capillaries

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30
Q

What is the role of elastic fibres in blood vessels?

A

Made of an elastin core covered by microfibrils
Elastic properties of arteries, arterioles and veins (not present in capillaries)
Allow to stretch under high blood pressure and return to normal state during diastole - responsible for passive tension of the blood vessel wall

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31
Q

What is the role of collagen fibres in blood vessels?

A

Stiffer than elastic fibres
In all vessels except capillaries
Responsible for passive tension of blood vessel walls

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32
Q

What is the role of smooth muscle cells in blood vessels?

A

All but not capillaries
Contraction is responsible for active tension in blood vessels.

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33
Q

What is the function of veins?

A

Carry blood at very low pressures
Walls very thin muscle controlled by ANS
Wide lumen for large blood volume
Blood reservoirs to adjust preload

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34
Q

What are the properties of venules?

A

Carry blood at low pressures
Walls resemble capillaries but have some extra minimal smooth muscle and connective tissue
Low pressure conduits.

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35
Q

What are the properties of capillaries?

A

Carry blood at low pressure
walls are as thick as a single endothelial cell (+/- basement membrane)
Very low flow rate
Maximise exchange between blood and cells

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36
Q

What are the features of small arteries/arterioles?

A

Carry blood at modest pressure
Thick muscular waslls
Muscle under ANS and local factor control
Faucet to control flow to tissues

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37
Q

What are the features of arteries?

A

Carry blood at high pressure
Thick muscular walls for strength
Elastic allows minimal expansion
Relativly narrow lumen
High pressure conduits.

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38
Q

Why are arterioles the most important structures at regulating blood flow to the tissues?

A

Have an extensive smooth muscle wall - can provide the highest resistance to blood flow
Is tonically activate (always contracted)
SANS can act on alpha 1 adrenergic receptors in periphery to cause constriction to further increase resistance
SANS can act on beta 2 adrenergic receptors in arterioles in skeletal muscle to cause dilation to decrease resistance (this is rarer)

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39
Q

How do you calculate the velocity of blood flow?

A

Velocity (cm/s) = flow (think of as volume displaced) (ml/s) divided by cross sectional area (cm2)

40
Q

How does velocity of blood flow vary by different blood vessels suggest why this might be?

A

Velocity decreases from aorta to capillaries

Area increases (consider combined area of capillaries) but the flow of blood remains the same (as determined by cardiac output)
Therefore the same flow divided by a larger area gives a smaller velocity.

Think of water hose - put finger over end to decrease diameter and water flows out faster.

41
Q

How do you calculate the flow of blood through a vessel?

A

Flow (ml/min) =
Pressure difference between vessels (mmHg)
Divided by
Resistance (hg/ml/min)

42
Q

What factors influence the rate of blood flow through a vessels?

A

Pressure difference between vessels
The resistance of a vessel to blood flow

43
Q

What is total peripheral resistance and how would you calculate it?

A

The ressistance of the entire systemic vasculature
Flow = pressure dif/resistance
Flow = cardiac output
Pressure dif = between aorta and IVC
Resistance = Pressure diff/flow

44
Q

Considering the properties of pressure and resistance in the vascular system how can we increase blood flow to an organ system

A

Arterial pressure is usually held constant by baroreflex (fluctuates), this fluctuation has normally stopped once reached arterioles as further away from heart.
Pressure is normally held constant by baroreflex
Therefore must change resistance

45
Q

What is perfusion pressure?

A

Determins how much blood an organ recivies
The difference between the arterial and venous pressure in that organ.

46
Q

What drives blood flow to tissues?
How is this controled

A

Difference in pressure between arterial and venous circulation.
May consider MAP as the driving force for whole body
Can alter MAP by changing the cardiac output or the systemic vascular resistance

47
Q

How do you calculate MAP from cardiac output?

A

MAP = CO x SVR

48
Q

How does the cardiovascular system show series resistance and what does this mean?

A

Arrangement of blood vessels within a given organ
(artery, arteriole, capillary, venule etc - all in one long line)
Total resistance is the sum of resistance of each vessel
(imagine trying to push through a single file queue, must get past everyone to get to the front)

49
Q

How does the cardiovascular system show parallel resistance?
What does this mean?

A

Shown by brnaches off a main blood vessel (for example the major arteries from the aorta)
The total resistance is less than the sum of the resistance of all the branches.

1/Rt = 1/R1 + 1/R2 etc

50
Q

What affects the level of resistance to blood flow?

A

Blood vessels diameter
Blood viscosity
Arrangement of blood vessels in series or parallel.

51
Q

What is posieuilles Law?

A

Shows all the factors affecting the resistance of a single blood vessel

R = 8xnxL /Pie x r^4
n = fluid viscosity
L = vessel length
r = vessel radius

51
Q

How is poiseuilles law simplified?
What does this mean for the relationship between resistance and blood vessel radius?

A

Resistance is directly proportional to 1/r^4.

Halve radius, resistance increases by 16 fold.
Small change in radius has a great effect on resistance of vessels

52
Q

What version of Poiseuilles law do we need to remember?

A

R = 1 / r^4

53
Q

What does it mean when the blood flow in the cardiovascular system is described as laminar?

A

Is smooth parabolic
Velocity is highest in the centre of the vessel and lowest towards to vessel walls
This is because the outer later adheres to the wall, as walls become more inner less adhrence to previously layer so faster flow.
Is unidirectional

54
Q

What is meant by turubulent blood flow in the cardiovascular system?
What causes this?

A

A irregulatiry in the blood vessels disrupts the laminar stream and blood lfo becomes turbulent
This is audible
Streams mix radially and axially, this wastes kinetic energy so more pressure is required to drive turbulent blood flow compared to laminar blood flow

Creates korotkoff sounds and murmurs.

55
Q

What is Reynolds number?

A

A dimensionless number used to predict whether blood flow will be laminar or turbulent
Considers the diameter of the vessel, velocity of flow and viscosity of blood.
A value less than 2000 indicates laminar flow
A value greater than 3000 indicates turbulent flow

56
Q

How do you calculate Reynolds number?

A

pdv/n

Density of blood * diameter of vessel * velocity of blood

Divided
by
Viscosity of blood

57
Q

What are the major influences on Reynolds number?

A

Changes in blood viscosity
Changes in blood velocity of blood flow

58
Q

How does velocity and vessels diameter relationship present and influence Reynolds number?

A

A decrease in vessel diameter should decrease Reynolds number
However also changes velocity of blood flow
V= Q/A = Q/pie*r^2
Therefore as diameter decreases velocity increases by a second power
Therefore change in velocity has a greater effect over the Reynolds number than change in vessel diameter.

59
Q

How does reynolds number apply to anaemia?

A
  1. Decreased haemotocrit
    Leads to decreased viscotity and increased velocity, this increases Reynolds number.
  2. Increased CO increased velocity increasing reynaulds number

Causes turbulent flow

60
Q

How does cardiac valvular disease apply to Reynolds number?

A

Valve narrowing or not opening properly = stenosis
This increases the velocity - increases reynolds number leading to a murmur.

61
Q

How does atherosclerosis relate to reynolds number?

A

Narrowing of arteries leads to increased velocity, increasing reynolds number causing bruits

62
Q

How doe thrombi relate to reynolds number?

A

Decreased blood vessel diameter
Leads to increased velocity of blood flow
Increased Reynolds number
Causes turbulence.

63
Q

What are the different factors that contribute to vascular control?

A

Local - may be metabolic or myogenic
Central (neural)
Hormonal
Endothelial

64
Q

How do local metabolic factors affect the control of blood flow volume?

A

As metabolic activity increases metabolic byproducts accumulate in the ECF and oxygen levels in the ECF fall
These metabolites can act directly on the smooth muscle cells or indirectly via the endothelium in vessels.
Causes vascular smooth muscle cells to relax causing vasodilation of vessels
Increases blood flow to remove waste and supply more nutrients
When metabolic activity decreases metabolites return to norm and reflex vasoconstriction gainst matches flow need.

65
Q

How do local myogenic factors affect the volume of blood flow?

A

Vessels constrict reflexively when intraluminal pressure increases
Is mediated by stretch-activated Ca2+ channels in the smooth muscle
This increases resistance to blood flow, helps maintain blood flow within the autoregulatory range.
This protects capillaries from surges in arterial pressure such as when postural changes can sudden gravity-induced pressure spikes of >200mm Hg in the pedal vasculature.

66
Q

What are the two different consequences of local control of blood flow?

A
  1. Autoregulation
  2. Hyperemia
67
Q

What is autoregulation as a consequence of local control over blood flow?

A

Autoregulation - intrisinc ability of organ to maintain stable blood flow in changing perfusion pressures.

Pressure extremes can overwhelm this by blood flow is able to remain constant over a broad range of blood pressures

68
Q

What is the autoregulatory response to a drop in arterial pressure?

A

Blood flow also decreases
1. metabolic byproducts accumulate in the ECF and oxygen levels in the ECF fall
These metabolites can act directly on the smooth muscle cells or indirectly via the endothelium in resistance vessels.
Causes vascular smooth muscle cells to relax causing vasodilation of vessels
Increases blood flow to remove waste and supply more nutrients.
2. myogenic response - no smooth muscle contraction as lack of stretch of stretch activated calcium ion channels

Allos vasodilation until conditions change and reflex vasoconstriction return to normal range.

69
Q

What is the autroregulatory response to a sudden increase in arterial pressure?

A

Blood flow also increases, metabolites are washed away faster than predicted
Results in reflexive constriction by metabolic pathway
Myogenic response also potentiates this effect
Conscrition return blood flow back to normal.

70
Q

What is hyperaemia?
What are the three different types?

A

An excess of blood supplying organs
Active hyperaemia
Postexercise hyperaemia
Reactive hyperaemia

71
Q

What is active hyperaemia?

A

A normal vasodilatory response to increased tissue activity and rising metabolite levels.
Results in decreased resistance and increased blood flow, to increase/restore O2 and nutrients for increased metabolism

The same as metabolic hyperaemia and functional hyperaemia

72
Q

What is post-exercise hyperaemia?

A

A period of increased blood flow that persists even after activity has ceased

73
Q

What is reactive hyperaemia?

A

A period of increased blood flow that follows transient ischemia often caused by occlusion.
Metabolic vasodilators accumulate in ECF, dilate arteries but occlusion prevents blood flow
Occlusoin is removed - resistance decreased increased blood flow

Therefore hyperaemia is a response to previous ischemia (is delayed until blockage removed)

As vasodilator washes away return to normal diameter/xontraction/ flow state.

74
Q

What is the central role in controlling blood flow?

A

Smooth muscle walls are tonically active.
Innervated by sympathetic adrenergic nerve fibres.

Alpha 1 adrenergic receptors on arterioles of vascular beds (skin and splanchnic) cause contraction/constriction of vascular smooth muscle - noradrenaline dependent

Beta 2 adrenergic receptors - arterioles of skeletal muscle - relaxation or dilation of vascular smooth muscle - adrenaline dependent

Both only effects arterioles.

75
Q

What are the different hormonal controls over blood flow?

A

ADH
Ang. 2
ANp
Adrenaline (epinephrine0

76
Q

How does ADH affect volume of blood flow?

A

Released from post. pituitary gland
Acts on V1alpha receptors on arterioles
Cause vasoconstriction

77
Q

How does Angiotensin 2 regulate the volume of blood flow?

A

Acts on AT1 receptors
Cause vasoconstriction

78
Q

How does ANP control volume of blood flow?

A

Released from atrial myocytes in times of increased BP or BV
Acts on NPR1 receptors
Causes vasodilation

79
Q

How does adrenaline control the volume of blood flow?

A

Released from adrenal medulla
Acts on alpha 1 adrenergic receptors to cause vasoconstriction
Acts on Beta 2 adrenergic receptors to cause vasodilation.

80
Q

What is the process of epinephrine synthesis?

A

Tyrosine converted to L-Dopa by tyrosine hydroxylase
Converted to Dopamine released from dopaminergic neurons by dopa decarboxylase
Convertes to Norephinephrine released by adrenergic neurons by dopmaine beta-hydroxylase
Converted to epinephrine released in adrenal medulla by phenylethaonolamine-N-methyltrasnferase.

81
Q

What are the three main molecules in the process of norepinephrine synthesis?

A

Tyrosine
Dopamine
Norephineprhine
Epinephrine

82
Q

How can dopamine be broken down?

A

By MOA to dihydroxyphrenylacetic acid
By COMT to 3-Methyltyramine
By COMT and MOA to homovanillic acid

83
Q

How is norepinephrine borken down?

A

By MAO to dihydroxymandelic acid
By COMT to normetanephrine
By MAO and COMT to VMA

84
Q

How is epinephrine borken down?

A

By MAO to dihydroxymandelic acid
By COMT to metanephrine
By MAO and COMt to VMA

85
Q

How can endothelial cells cause contraction of blood vessels?

A

Secrete PGF and thromboxane
Trauma and Ang-2 case endothelin secretion
All increase Calcium ion conc in smooth muscle causing contraction

86
Q

How do endothelial cells cause vasodilation of blood vessels?

A

Release PGE, PGI2, EDHF
Sheer stress, bacterial endotoxins, bradykinins, ATp, ACh and substance P can cause NO release
These decrease smooth muscle intracellular calcium ion concentration, results in vasodilation as contraction is inhibited.

87
Q

What are the consequences of having parallel resistance blood flow? aka main branches from the abdominal aorta

A

Parallel arrangement of arteries off aorta means all pressure is equal (MAP)
Resistance of each branch can be modulated independently through local control mechanisms of the arterioles.
This allows different volume of blood to go to different regions of the body.

88
Q

How does series resistance in the cardiovascular system affect the blood flow to each organ?

A

Blood flow decreases along the line, as used up by previous or first organ before reaches end of line.

89
Q

According to Poiseuilles law what factors increase resistance to blood flow?

A

Decreased radius
Increased viscosity
Increased vessel length

90
Q

According to Poiseuilles law what factors decrease reistance to blood flow?

A

Increased radius of vessel
Decrease viscosity of blood flow
Decreased blood vessel length

91
Q

What are the important values relating to Reynolds number?

A

Above 3000 indicates turbulent flow
Below 2000 indicates laminar flow

92
Q

According to reynolds number what factors increase the risk of turbulent blood flow.

A

Increased diameter, increased density of blood, increase velocity of blood
Decreased viscosity of blood

93
Q

According to Reynaolds number what factors decrease the risk of turbulent blood flow?

A

Increased viscotiy of blood flow
Decreased density of blood, diamter of blood vessl and velocity of blood flow

94
Q

What is the simplified version of Reynalds number equation?

A

Velocity divided by viscotity

Therefore: high velocoty and low viscotiy increase turbulent flow.

95
Q

What are some of the intrinsic factors in the metabolic reflex that promotes vasodilation of blood vessels?

A

Adenosine
K+
Lactate
CO2
H2

96
Q

What is the myogenic response in decreased blood pressure?

A

Decreased pressure/stretch on arteriole walls
Smooth muscle relaxes causing vasodilation, mediates increased blood flow into the area.
Helps maintain blood flow within the autoregulatory range.

Unit 12 (23 decks)

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