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FM1020 > Physiology - Regional Circulation > Flashcards

Physiology - Regional Circulation Flashcards

1
Q

How is blood flow intrinsically regulated?

A
  • metabolic regulation
  • endothelial regulation
  • myotonic regulation
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2
Q

How is blood flow to tissues extrinsically regulated?

A
  • neural stimulation
  • hormonal
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3
Q

How are the innermost layers of myocardium supplied with blood?

A

There are specialised vessels in the ventricles which supply them

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4
Q

What is resting coronary blood flow?

A

225ml/min

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5
Q

What % of total cardiac output makes up coronary blood flow?

A

5%

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6
Q

What are the basal requirements for cardiac muscle Oxygen supply

A

8-10ml/min/100g of heart tissue

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7
Q

Does haemoglobin use all 4 of the oxygens when passing through cardiac muscle?

A

Yes, nearly all O2 is extracted from blood during one passage through the coronary arteries

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8
Q

What provides the driving force of blood flow through coronary arteries?

A

Pressure in aorta

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9
Q

What determines the rate of blood flow in coronary arteries?

A

Dilation/constriction of vessels

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10
Q

What is the primary controller of resistance in coronary vessels?

A

Metabolic regulation

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11
Q

What is active hyperaemia ?

A

When blood flow to tissues is increased due to increased metabolic activity

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12
Q

What will trigger active hyperaemia ?

A

Inadequate coronary flow, inadequate O2 content of blood, increased metabolic activity

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13
Q

What are the main substances thought to be involved in active hyperaemia?

A

Adenosine and nitric oxide (NO)

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14
Q

What is the believed mechanism in active hyperaemia ?

A

A reduction in the concentration of ATP in smooth muscle causes opening of K+ ATP channels, cause it hyperpolarisation and relaxation of coronary SM.

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15
Q

How does stimulation of sympathetic nerves affect coronary blood flow?

A
  • triggers vasoconstriction by releasing NA which binds to α adrenergic receptors, triggering vasoconstriction
  • SN activity also increases HR and contractility of CM. This causes myocardial cells to work harder, causing vasodilation of blood vessels and ACTIVE HYPEREMIA
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16
Q

What effect does adrenaline have on coronary vessels?

A

Binds to β adrenergic receptors causing vasodilation

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17
Q

Does vagal stimulation have an effect on coronary vessels?

A
  • only has a slight dilatory effect of coronary resistance vessels

BUT

  • vagal stimulation of heart slows HR, which means that myocardial cells aren’t very metabolically active, meaning blood vessels are slightly constricted
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18
Q

what effect does systole have on coronary blood flow? Which side (R/L) is this more apparent on

A

CBVs are compressed -
slows, stops, temporarily reverses blood flow

More apparent on left side

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19
Q

What is ischaemia ?

A

Restriction in blood supply to a tissue

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20
Q

What are the reasons that a myocardial infarction is dangerous?

A
  • decreased cardiac output
  • fibrillation of heart
  • rupture of heart
  • pulmonary oedema since blood pools in pulmonary circulation
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21
Q

What us the rate of blood flow to skeletal muscles at rest?

A

3ml/min/100g

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22
Q

What % of cardiac output goes to skeletal muscles when resting?

A

20%

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23
Q

What us the rate of blood flow to skeletal muscles during exercise?

A

60ml/min/100g

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24
Q

What % of cardiac output goes to skeletal muscles when during exercise ?

A

80%

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25
Q

When at rest, which is more important in regulation blood flow to skeletal muscle, neural stimulation or intrinsic e stimulation ?

A

Neural regulation

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26
Q

During exercises which is more important in regulation blood flow to skeletal muscle, neural stimulation or intrinsic e stimulation ?

A

Intrinsic factors

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27
Q

Describe the state of skeletal blood vessels when the muscle is at rest.

A

SNs constantly release NA which binds to α & β1 adrenergic receptors

Vasoconstriction

90% of skeletal capillary beds not perfused

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28
Q

What modulates SN activity to skeletal muscle?

A

Baroreceptor reflex

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29
Q

Why does skeletal muscle play an important role in regulation of MAP?

A

Most peripheral resistance comes from skeletal muscle resistance vessels

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30
Q

What would happen to MAP if you occluded the carotid artery ?

A

-Baroreceptors fire less
-SN activity increases
-Blood flow to muscles decreased
-Increase in MAP

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31
Q

What would happen to MAP if you released the carotid artery after occluding it?

A
  • Baroreceptor firing increased
  • SN activity reduced
  • vasodilation
  • reduction in MAP
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32
Q

When is blood flow to muscle increased?

A

Within the first second after a single contraction

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33
Q

What causes an increase in blood flow to skeletal muscle during exercise?

A
  • production of metabolites = active hyperaemia
  • blood flow to resting skeletal muscles decreased due to activation of SNs so blood is diverted to active skeletal muscle
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34
Q

What is adrenaline an agonist of?

A

α adrenergic receptors

β1 adrenergic receptors

β2 adrenergic receptors

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35
Q

At low concentrations of circulating adrenaline, what is the effect?

A

Binds to β1 adrenergic receptors on hear - increased HR and contractility

Binds to β2 receptors on blood vessels causing vasodilation

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36
Q

At high concentrations of circulating adrenaline, what is the effect?

A

Adrenaline binds to α receptors which has a vasoconstrictor effect

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37
Q

What can trigger nitric oxide release?

A
  • shear stress on blood vessels
  • ACh release
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38
Q

How does ACh reach blood vessels?

A
  • some blood vessels innervated by parasympathetic nerves
  • some blood vessels innervated by sympathetic cholinergic nerves
  • diffuses over from NMJ
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39
Q

Why does ACh trigger NO release from endothelial cells?

A

It activated endothelial nitric oxide synthase (eNOS)

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40
Q

How does NO cause vasodilation?

A
  • activates soluble guanyl cyclase
  • activates cGMP
  • cGMP open K+ channels
  • cGMP closes L type Ca++ channels causing hyperpolarisation
  • cGMP activates myosin light chain phophatase
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41
Q

What is functional sympatholysis ?

A

The ability to reduce sympathetic vasoconstriction during exercise and thus, optimize blood flow to the working muscle

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42
Q

How is functional sympatholysis carried out?

A

Maybe (mechanism unclear)

NO inhibits NA release from varicosities
And
Opposes α2 mediated constriction of vascular SM

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43
Q

How can skeletal muscle fibres release NO?

A

They contain neuronal nitrogen oxide synthase. Contraction increases NO release

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44
Q

Overall, how does NO vasodilate smooth muscle?

A
  1. Triggering intracellular pathway
  2. Functional sympatholysis
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45
Q

How is NO produced?

A
  1. Shear stress
  2. Skeletal muscle fibres release in during contraction
  3. ACh spillover from NMJ triggers its release
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46
Q

How does ACH spillover from NMJ cause vasodilation?

A

Diffuses to local blood vessels to promote NO production in endothelium

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47
Q

How is venous returned maintained during exercise?

A

The contracting muscles pump blood up the veins and valves prevent backflow

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48
Q

Why does muscle become so weak during tetany?

A

When muscles contract they compress skeletal blood vessels
During tetany there is no relaxation so blood flow to tissues is almost completely stopped

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49
Q

What is a technique used fro measuring limb blood flow?

A

Venous occlusion plethysmography

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50
Q

what is venous occlusion plethysmography used for?

A

To study local effect of vasoactive mediations or drugs in the forearm vascular bed

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51
Q

How is venous occlusion plethysmography carried out?

A
  • stop venous return from arm by inflating cuff around brachial artery to 40 mmHg
  • stop hand circulation with a wrist cuff inflated above systolic pressure
  • arterial inflow not stopped so arm circumference is increased
  • circumference, therefore volume is measured using a strain-gauge plethysmograph
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52
Q

What is responsible for the pinkish hue that skin has?

A

Venous plexuses which act as reservoirs for blood in the skin.

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53
Q

What part of the skin has capillaries?

A

The dermis

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54
Q

How does blood enter the venous plexuses in the skin?

A
  1. Blood flows from arterioles which then flow to venous plexus
  2. Blood flows directly to venous plexus via arteriovenous anastomoses
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55
Q

Where are arterioles located in the skin ?

A

Subcutaneous tissue

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56
Q

Where are Arteriovenous anastamoses most common in the skin?

A

Hands, feet, ears, nose, lips

57
Q

How is contraction of arteriovenous anastamoses regulated?

A

Sympathetic neural stimulation - no intrinsic regulation

58
Q

Does skin have a high requirement for blood?

A

No.

59
Q

What is the main purpose of circulation to the skin?

A

Temperature regulation

60
Q

At normal temperatures, is skin circulation dilated or constricted?

A

Skin circulation has a high degree of adrenergic tone at normal temperatures - they are quite constricted

61
Q

What happens to cutaneous circulation with increased SN activity?

A

Blood vessels and AV shunts constrict, reducing blood flow to the skin capillaries.

62
Q

What causes blushing?

A

Cerebral inhibition of smooth muscle in skin blood vessels in the face. Causes vasodilation

63
Q

Does the cutaneous circulation have any auto regulation of blood flow?

A

Only the resistance arterioles do. During reactive hyperaemia

64
Q

What is reactive hyperaemia ?

A

Increased blood flow following ischaemia

65
Q

Describe what happens in reactive hyperemia

A
  • when blood supply is cut off, tissues become hypoxic.
  • glycosidic metabolism occurs, producing vasodilatory
    metabolites
  • when blood flow resumes, there is a rapid flow of blood into arterioles
66
Q

What happens if you expose your hand to cold?

A
  1. Local axon reflexes cause vasoconstriction of the resistance and capitance vessels in the hand.
  • temperature receptors send signal to the TEMPERATURE REGULATING CENTRE of the hypothalamus
  • hypothalamus stimulates SN activity to the skin
67
Q

What part of the brain is responsible for temperature regulation?

A

Temperature regulating centre of the hypothalamus.

68
Q

What happens to the cutaneous circulation is there is extended exposure to cold?

A
  • localised cold vasodilation will occur
  • intermittent, short vasodilation which allows blood to enter tissues to prevent hypoxia.
  • if coldness persists even further, vasoconstriction and vasodilation alternate and this is done by local axon reflexes
69
Q

What happens to cutaneous circulation is the head is exposed to heat?

A
  • Causes vasodilation of blood vessels at the local region by local axon reflexes
  • heat receptors trigger hypothalamus to inhibit SN activity causing widespread vasodilation.
70
Q

What is the purpose of vasodilation of cutaneous circulation when exposed to heat?

A

Allows warm blood to be cooled by
1. External environment
2. Perspiration

71
Q

What % of cardiac output goes to the skin when it is exposed to heat?

A

30%

72
Q

What % of cardiac output normally goes to the skin?

A

1%

73
Q

How are sweat glands activated?

A

Sympathetic nerves release ACh

74
Q

How does perspiration decrease body temperature?

A

Liquid evaporates from the body and heat of evaporation is lost. This means the skin is cooler as it has less heat energy. The blood is cooled due to the decrease in heat energy

Also causes vasodilation by producing bradykinin

75
Q

How does sweat cause vasodilation ?

A
  • sweat production = incr in bradykinin
  • bradykinin causes vasodilation
  • bradykinin also stimulates NO production
76
Q

What happens when the body is warm?

A
  • SN inhibition = vasodilation
  • sweat glands = perspiration
  • sweat = bradykinin
  • unidentified vasodilatory neurotransmitter also released from cholinergic sympathetic nerves
77
Q

What happens to cutaneous circulation during exercise?

A
  1. Vasoconstriction to divert blood to skeletal muscles
  2. Vasodilation to lose excess heat
78
Q

How do local axon reflexes work?

A
  • no CNS involved
  • local sensory nerves stimulated by pain and termperature receptors release neurotransmitters
  • causes an effect e.g redness if you get hit (pain receptor)
79
Q

What is countercurrent heat exchange?

A

Major arteries and veins in close proximity
Protects core body temp from extremes of heat

Example : cold venous blood returning to core is warmed by arterial blood in adjacent artry

80
Q

How does blood get to the cerebral circulation?

A

Internal carotid arteries & vertebral arteries -> basilar artery -> circle of Willis -> cerebral arteries -> brain tissue

81
Q

What is the importance of the circle of Willis?

A

Acts as an anastamoses so blood can reach all parts of the brain

82
Q

What is intercranial pressure?

A

Pressure within cranium

83
Q

What is the normal value of intercranial pressure?

A

0-10mmHg

84
Q

How is blood flow out of the brain maintained?

A

ICP > central venous pressure

85
Q

Changes in intercranial pressure affect what?

A

Cerebral perfusion

86
Q

How do you calculate cerebral perfusion pressure?

A

CPP = MAP - ICP

87
Q

What is the normal rate of blood supply to brain tissue?

A

55ml/min/100g

88
Q

What % of cardiac output is received by the brain?

A

14%

89
Q

Is brain tissue sensitive to ischaemic ? Why/why not?

A
  • yes
  • Hugh requirement for O2 and glucose
90
Q

What can happen after.5 seconds of ischaemia in the Brain?

A

Unconsciousness

91
Q

How long must the Brian be ischaemic for before irreversible Brian damage occurs?

A

4 mins

92
Q

What is the main driving force for brain perfusion?

A

MAP

93
Q

How does the cerebral circulation maintain a Normal CPP ?

A

Cerebral circulation exhibits autoregulation of blood flow.
Vascular tone can be altered to make sure blood flow stays constant

94
Q

Over what range of MAP can the cerebral circulation auto regulate blood flow?

A

60-160mmHg

95
Q

What happens to cerebral circulation if MAP is below 60mmHg

A
  • CPP falls, blood flow reduced, syncope
96
Q

What happens to cerebral circulation if MAP is above 160mmHg?

A

Blood brain barrier can be damaged leading to cerebral oedema

97
Q

How is the Brain protected in somebody with chronic hypertension?

A

Autoregulation of cerebral circulation accommodated the higher blood pressure, so it will take even higher values of b.p to damage the blood brain barrier

98
Q

Is blood flow constant to all parts of the brain all the time?

A

No. When the brain is active, regional neural activity can increase blood flow to the active regions.

99
Q

Which is more important in cerebral blood flow, intrinsic or extreinsic regulation?

A

Intrinsic

100
Q

The cerebral circulation can use functional sympatholysis t/f?

A

True. Metabolic regulation causes it

101
Q

Does the baroreceptor reflex affect cerebral blood flow?

A

No. Very little effect

102
Q

Maximum SN activity increases cerebral resistance by __ %

A

20%

103
Q

What is the most important vasodilatory factor in the cerebral circulation?

A

CO2

104
Q

Why is CO2 so important in the cerebral circulation?

A

CO2 reduces pH of CSF. This triggers vasodilation of cerebral arterioles

105
Q

How can a reduction in CPP cause CO2 to vasodilate cerebral blood vessels?

A

The reduces CPP means that the flow of CO2 out of brain is reduced. Increased CO2 conc in CSF causes vasodilation

106
Q

What is hypercapnia?

A

Increased PCO2 ( partial pressure of CO2 )

107
Q

What is hypocapnia ?

A

Decreased PCO2

108
Q

Does hypercapnia vasodilate or vasoconstriction cerebral blood vessels?

A

Dilate

109
Q

Does hypocapnia vasodilate or vasoconstriction cerebral blood vessels?

A

Constrict

110
Q

Why does hyperventilation cause dizziness?

A

PCO2 is recused. This causes vasoconstriction.

111
Q

What must PO2 drop below to cause vasodilation in cerebral circulation? Why?

A

50mmHg
Haemoglobin still has O2 bound to it despite PO2 in arteries decreasing

112
Q

What can cause increased ICP ?

A

Brain trauma
Cerebral oedema

113
Q

What can happen if ICP>MAP ?

A

Severe cerebral ischaemia

114
Q

What is the Cushing reflex?

A
  • activates symp NS, causing peripheral vasoconstriction which increases MAP
  • This stimulated Baroreceptors which slow HR -> BRADYCARDIA
115
Q

What is Cushings Triad?

A
  • hypertension
  • bradycardia
  • irregular respiration
116
Q

Who can cushings triad be seen in?

A

Patients with brain trauma and increased ICP

117
Q

Splanchnic circulation makes up ___% of total CO

A

20-25 %

118
Q

Why is necrosis of villi common?

A

Blood is shunted from arterioles directly to venues at base of microvilli

119
Q

What is countercurrent exchange in villi?

A

When blood flows directly from arterioles to venules

120
Q

Why is necrosis of villi not usually a huge problem?

A

Stem cells are found in clefts between villi and they can replace the endothelial cells

121
Q

When is blood flow to intestines reduced?

A

During exercise as blood is diverted to the active muscles and th e heart

122
Q

How is blood flow to intestinal blood vessels reduced?

A

SN nerves release NA and this vasoconstriction mesenteric arterioles and capitance vessels

123
Q

What is functional hyperaemia ?

A

Increased blood supply to tissues due to an increase in functional activity of the tissues

124
Q

What happens to intestinal blood supply when food is ingested?

A

Functional hyperaemia caused by vasodilation due to
- gastrin (digestive hormone)
- metabolites due to incr metabolic activity of tissue (ADENOSINE)
- NO is produced locally

Gastrin and Adenosine have vasodilatory properties

125
Q

Does the parasympathetic NS innervate blood vessels in the Gi tract?

A

No. Only supplies interstitial smooth muscle and glands

126
Q

Does parasympathetic NS increase blood flow to intestines?

A

Maybe indirectly by producing bradykinin and NO

127
Q

The liver receives __% of CO

A

25%

128
Q

Where does blood flow to the liver come from?

A

75% from hepatic portal vein
25% from hepatic artery

129
Q

Describe the hepatic circulation

A

Portal venue ar and hepatic arterioles enter the centre of an ACINUS and deliver blood to sinusoids

The sinusoids bring blood to periphery of acinus and deliver it to hepatic venules -> hep vein -> IVC

130
Q

What is the name of the structure in the liver that hepatic portal vein and hepatic artery conjoin at?

A

Acinus

131
Q

Why is so much my phone produced in the liver?

A

Oncotic pressure of plasma is very low in the liver

132
Q

What % of lymph in the body is made in the liver?

A

50%

133
Q

Why must hydrostatic pressure of liver capillaries be controlled?

A

If hydrostatic presssure increases, too much fluid will leave capillaries and too much lymph will be produced

134
Q

Why is blood flow to liver reciprocally regulated?

A

Incr blood flow through hepatic portal vein = decrease in blood flow through hepatic artery and vice verse.

Prevents increase in hydrostatic pressure in liver capillaries

135
Q

What % of blood volume of ht e body is stored in the liver?

A

15%

136
Q

When is sympathetic NS stimulation increased in the liver and why?

A

During exercise or severe blood loss

Constricts liver vessels to return blood to heart and circulation

137
Q

What is ascites

A

Accumulation of fluid in abdominal cavity

138
Q

What can cause ascites?

A

HEART FAILURE.
Causes incr in central venous pressure
Incr in hepatic venous and sinusoidal pressures
Incr in hydrostatic pressure
Hepatic oedema

LIVER CIRRHOSIS
- causes portal hypertension which incr hydrostatic pressure -> hepatic oedema

FM1020 (11 decks)

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