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
When at rest, which is more important in regulation blood flow to skeletal muscle, neural stimulation or intrinsic e stimulation ?
Neural regulation
26
During exercises which is more important in regulation blood flow to skeletal muscle, neural stimulation or intrinsic e stimulation ?
Intrinsic factors
27
Describe the state of skeletal blood vessels when the muscle is at rest.
SNs constantly release NA which binds to α & β1 adrenergic receptors Vasoconstriction 90% of skeletal capillary beds not perfused
28
What modulates SN activity to skeletal muscle?
Baroreceptor reflex
29
Why does skeletal muscle play an important role in regulation of MAP?
Most peripheral resistance comes from skeletal muscle resistance vessels
30
What would happen to MAP if you occluded the carotid artery ?
-Baroreceptors fire less -SN activity increases -Blood flow to muscles decreased -Increase in MAP
31
What would happen to MAP if you released the carotid artery after occluding it?
- Baroreceptor firing increased - SN activity reduced - vasodilation - reduction in MAP
32
When is blood flow to muscle increased?
Within the first second after a single contraction
33
What causes an increase in blood flow to skeletal muscle during exercise?
- 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
34
What is adrenaline an agonist of?
α adrenergic receptors β1 adrenergic receptors β2 adrenergic receptors
35
At low concentrations of circulating adrenaline, what is the effect?
Binds to β1 adrenergic receptors on hear - increased HR and contractility Binds to β2 receptors on blood vessels causing vasodilation
36
At high concentrations of circulating adrenaline, what is the effect?
Adrenaline binds to α receptors which has a vasoconstrictor effect
37
What can trigger nitric oxide release?
- shear stress on blood vessels - ACh release
38
How does ACh reach blood vessels?
- some blood vessels innervated by parasympathetic nerves - some blood vessels innervated by sympathetic cholinergic nerves - diffuses over from NMJ
39
Why does ACh trigger NO release from endothelial cells?
It activated endothelial nitric oxide synthase (eNOS)
40
How does NO cause vasodilation?
- activates soluble guanyl cyclase - activates cGMP - cGMP open K+ channels - cGMP closes L type Ca++ channels causing hyperpolarisation - cGMP activates myosin light chain phophatase
41
What is functional sympatholysis ?
The ability to reduce sympathetic vasoconstriction during exercise and thus, optimize blood flow to the working muscle
42
How is functional sympatholysis carried out?
Maybe (mechanism unclear) NO inhibits NA release from varicosities And Opposes α2 mediated constriction of vascular SM
43
How can skeletal muscle fibres release NO?
They contain neuronal nitrogen oxide synthase. Contraction increases NO release
44
Overall, how does NO vasodilate smooth muscle?
1. Triggering intracellular pathway 2. Functional sympatholysis
45
How is NO produced?
1. Shear stress 2. Skeletal muscle fibres release in during contraction 3. ACh spillover from NMJ triggers its release
46
How does ACH spillover from NMJ cause vasodilation?
Diffuses to local blood vessels to promote NO production in endothelium
47
How is venous returned maintained during exercise?
The contracting muscles pump blood up the veins and valves prevent backflow
48
Why does muscle become so weak during tetany?
When muscles contract they compress skeletal blood vessels During tetany there is no relaxation so blood flow to tissues is almost completely stopped
49
What is a technique used fro measuring limb blood flow?
Venous occlusion plethysmography
50
what is venous occlusion plethysmography used for?
To study local effect of vasoactive mediations or drugs in the forearm vascular bed
51
How is venous occlusion plethysmography carried out?
- 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
52
What is responsible for the pinkish hue that skin has?
Venous plexuses which act as reservoirs for blood in the skin.
53
What part of the skin has capillaries?
The dermis
54
How does blood enter the venous plexuses in the skin?
1. Blood flows from arterioles which then flow to venous plexus 2. Blood flows directly to venous plexus via arteriovenous anastomoses
55
Where are arterioles located in the skin ?
Subcutaneous tissue
56
Where are Arteriovenous anastamoses most common in the skin?
Hands, feet, ears, nose, lips
57
How is contraction of arteriovenous anastamoses regulated?
Sympathetic neural stimulation - no intrinsic regulation
58
Does skin have a high requirement for blood?
No.
59
What is the main purpose of circulation to the skin?
Temperature regulation
60
At normal temperatures, is skin circulation dilated or constricted?
Skin circulation has a high degree of adrenergic tone at normal temperatures - they are quite constricted
61
What happens to cutaneous circulation with increased SN activity?
Blood vessels and AV shunts constrict, reducing blood flow to the skin capillaries.
62
What causes blushing?
Cerebral inhibition of smooth muscle in skin blood vessels in the face. Causes vasodilation
63
Does the cutaneous circulation have any auto regulation of blood flow?
Only the resistance arterioles do. During reactive hyperaemia
64
What is reactive hyperaemia ?
Increased blood flow following ischaemia
65
Describe what happens in reactive hyperemia
- 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
What happens if you expose your hand to cold?
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
What part of the brain is responsible for temperature regulation?
Temperature regulating centre of the hypothalamus.
68
What happens to the cutaneous circulation is there is extended exposure to cold?
- 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
What happens to cutaneous circulation is the head is exposed to heat?
- 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
What is the purpose of vasodilation of cutaneous circulation when exposed to heat?
Allows warm blood to be cooled by 1. External environment 2. Perspiration
71
What % of cardiac output goes to the skin when it is exposed to heat?
30%
72
What % of cardiac output normally goes to the skin?
1%
73
How are sweat glands activated?
Sympathetic nerves release ACh
74
How does perspiration decrease body temperature?
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
How does sweat cause vasodilation ?
- sweat production = incr in bradykinin - bradykinin causes vasodilation - bradykinin also stimulates NO production
76
What happens when the body is warm?
- SN inhibition = vasodilation - sweat glands = perspiration - sweat = bradykinin - unidentified vasodilatory neurotransmitter also released from cholinergic sympathetic nerves
77
What happens to cutaneous circulation during exercise?
1. Vasoconstriction to divert blood to skeletal muscles 2. Vasodilation to lose excess heat
78
How do local axon reflexes work?
- 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
What is countercurrent heat exchange?
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
How does blood get to the cerebral circulation?
Internal carotid arteries & vertebral arteries -> basilar artery -> circle of Willis -> cerebral arteries -> brain tissue
81
What is the importance of the circle of Willis?
Acts as an anastamoses so blood can reach all parts of the brain
82
What is intercranial pressure?
Pressure within cranium
83
What is the normal value of intercranial pressure?
0-10mmHg
84
How is blood flow out of the brain maintained?
ICP > central venous pressure
85
Changes in intercranial pressure affect what?
Cerebral perfusion
86
How do you calculate cerebral perfusion pressure?
CPP = MAP - ICP
87
What is the normal rate of blood supply to brain tissue?
55ml/min/100g
88
What % of cardiac output is received by the brain?
14%
89
Is brain tissue sensitive to ischaemic ? Why/why not?
- yes - Hugh requirement for O2 and glucose
90
What can happen after.5 seconds of ischaemia in the Brain?
Unconsciousness
91
How long must the Brian be ischaemic for before irreversible Brian damage occurs?
4 mins
92
What is the main driving force for brain perfusion?
MAP
93
How does the cerebral circulation maintain a Normal CPP ?
Cerebral circulation exhibits autoregulation of blood flow. Vascular tone can be altered to make sure blood flow stays constant
94
Over what range of MAP can the cerebral circulation auto regulate blood flow?
60-160mmHg
95
What happens to cerebral circulation if MAP is below 60mmHg
- CPP falls, blood flow reduced, syncope
96
What happens to cerebral circulation if MAP is above 160mmHg?
Blood brain barrier can be damaged leading to cerebral oedema
97
How is the Brain protected in somebody with chronic hypertension?
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
Is blood flow constant to all parts of the brain all the time?
No. When the brain is active, regional neural activity can increase blood flow to the active regions.
99
Which is more important in cerebral blood flow, intrinsic or extreinsic regulation?
Intrinsic
100
The cerebral circulation can use functional sympatholysis t/f?
True. Metabolic regulation causes it
101
Does the baroreceptor reflex affect cerebral blood flow?
No. Very little effect
102
Maximum SN activity increases cerebral resistance by __ %
20%
103
What is the most important vasodilatory factor in the cerebral circulation?
CO2
104
Why is CO2 so important in the cerebral circulation?
CO2 reduces pH of CSF. This triggers vasodilation of cerebral arterioles
105
How can a reduction in CPP cause CO2 to vasodilate cerebral blood vessels?
The reduces CPP means that the flow of CO2 out of brain is reduced. Increased CO2 conc in CSF causes vasodilation
106
What is hypercapnia?
Increased PCO2 ( partial pressure of CO2 )
107
What is hypocapnia ?
Decreased PCO2
108
Does hypercapnia vasodilate or vasoconstriction cerebral blood vessels?
Dilate
109
Does hypocapnia vasodilate or vasoconstriction cerebral blood vessels?
Constrict
110
Why does hyperventilation cause dizziness?
PCO2 is recused. This causes vasoconstriction.
111
What must PO2 drop below to cause vasodilation in cerebral circulation? Why?
50mmHg Haemoglobin still has O2 bound to it despite PO2 in arteries decreasing
112
What can cause increased ICP ?
Brain trauma Cerebral oedema
113
What can happen if ICP>MAP ?
Severe cerebral ischaemia
114
What is the Cushing reflex?
- activates symp NS, causing peripheral vasoconstriction which increases MAP - This stimulated Baroreceptors which slow HR -> BRADYCARDIA
115
What is Cushings Triad?
- hypertension - bradycardia - irregular respiration
116
Who can cushings triad be seen in?
Patients with brain trauma and increased ICP
117
Splanchnic circulation makes up ___% of total CO
20-25 %
118
Why is necrosis of villi common?
Blood is shunted from arterioles directly to venues at base of microvilli
119
What is countercurrent exchange in villi?
When blood flows directly from arterioles to venules
120
Why is necrosis of villi not usually a huge problem?
Stem cells are found in clefts between villi and they can replace the endothelial cells
121
When is blood flow to intestines reduced?
During exercise as blood is diverted to the active muscles and th e heart
122
How is blood flow to intestinal blood vessels reduced?
SN nerves release NA and this vasoconstriction mesenteric arterioles and capitance vessels
123
What is functional hyperaemia ?
Increased blood supply to tissues due to an increase in functional activity of the tissues
124
What happens to intestinal blood supply when food is ingested?
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
Does the parasympathetic NS innervate blood vessels in the Gi tract?
No. Only supplies interstitial smooth muscle and glands
126
Does parasympathetic NS increase blood flow to intestines?
Maybe indirectly by producing bradykinin and NO
127
The liver receives __% of CO
25%
128
Where does blood flow to the liver come from?
75% from hepatic portal vein 25% from hepatic artery
129
Describe the hepatic circulation
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
What is the name of the structure in the liver that hepatic portal vein and hepatic artery conjoin at?
Acinus
131
Why is so much my phone produced in the liver?
Oncotic pressure of plasma is very low in the liver
132
What % of lymph in the body is made in the liver?
50%
133
Why must hydrostatic pressure of liver capillaries be controlled?
If hydrostatic presssure increases, too much fluid will leave capillaries and too much lymph will be produced
134
Why is blood flow to liver reciprocally regulated?
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
What % of blood volume of ht e body is stored in the liver?
15%
136
When is sympathetic NS stimulation increased in the liver and why?
During exercise or severe blood loss Constricts liver vessels to return blood to heart and circulation
137
What is ascites
Accumulation of fluid in abdominal cavity
138
What can cause ascites?
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