Special Circulations Flashcards

(49 cards)

1
Q

perfusion is determined by

A

pressure gradient/resistance

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2
Q

what drives local perfusion

A

alterations in vascular tone

1/r^4

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3
Q

vascular tone reacts to

A

intrinsic - local

extrinsic - systemic factors

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4
Q

examples of intrinsic mechanical stimuli

A

stretch
shear
endothelial regulation
metabolites

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5
Q

examples of extrinsic systemic regulation

A

nerves

hormones

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6
Q

primarily intrinsic organs

A

brain
kidney
heart - local control regulating flow
benefit: local autonomy

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7
Q

primarily extrinsic organs

A

skin

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8
Q

coronary artery supply what tissue and drain where

A

myocardium and drain in the right atrium

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9
Q

most of the coronary arteries are ..

A

end arteries and some collaterals between arterioles
- high O2 demand
no alternative routes
blockage means no oxygen

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10
Q

how does coronary artery type be a risk

A

increased risk of ischaemia

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11
Q

heart receives what %age of cardiac output

A

5%

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12
Q

how does perfusion across the heart and its arteries occur in conjunction with diastole and systole

A

perfusion occurs in diastole - arteries compressed in systole
increased activity - increased perfusion
typical O2 extraction more than 65% compared to 25% of rest of body

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13
Q

why the difference between left and right circulations

A

right ventricle is so small on the left we dont get same compression

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14
Q

how is high capillary to myocyte density seen as a coronary adaptation coronary adaptation

A

high capillary to myocyte density - low diffusion distance high myoglobin
very efficient oxygen exchange
control mostly intrinsic via metabolite induced vasodilation

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15
Q

how does intrinsic metabolite induced vasodilation help adapt the coronary arteries

A

work by myocytes - K+ and H+ made, muscles use ATP - more adenosine - dilators
increases flow - more NO via shear stress
interact smooth muscle cells decrease resistance
increased perfusion

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16
Q

how is extrinsic effect via SNS adapt to coronary arteries

A

beta adrenoreceptors SNS action can constrict - alpha AR and dilate beta AR
SNS action increase heartwork - increase metabolites and dilation

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17
Q

coronary adaptation

A

High capillary to myocyte density
Control mostly intrinsic via metabolite-induced vasodilatation
Extrinsic effects via the SNS

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18
Q

O2 extraction of cerebral circulation

A

35%

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19
Q

if one artery of cerebral circulation is blocked what allows perfusion

A

circle of willis

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20
Q

Mean cerebral O2 consumption

A

7 ml/min/100 g

21
Q

when will irreversible damage occur in cerebral circulation

A

by around 4 mins of ischaemia

22
Q

• Basal grey matter flow ≈

A

100 ml/min/100 g

23
Q

how is basal grey matter flow maintained

A

across physiological range of arterial pressure

24
Q

calculate cerebral perfusion pressure

A

mean arterial pressure minus the
intracranial pressure
– CPP = MAP – ICP

25
how will increased intracranial pressure affect cerebral perfusion
decrease cerebral perfusion | tumour/oedema
26
Cerebral blood flow calculation
cerebral perfusion pressure divided by the cerebral vascular resistance – CBF = CPP / CVR (which is the same as Q = ΔP/R or I = V/R)
27
how is blood flow is cerebral tissue maintained
by constriction and dilatation in response to challenge | – can better deal with high pressure than with low pressures
28
nerve firing in cerebral tissue is linked to what substances and in what practice is this beneficial
nerve firing linked to vasoactive K+, adenosine and NO | – this is the basis of functional MRI
29
cerebral structural adaptations benefits
connected to circle of willis and high capillary density neurovascular coupling SNS fibres present lack alpha 1 at LIMIT response
30
how is SNS fibres present but lack of α1 | -AR limit response beneificial for cerebral tissue
– thus brain spared from baroreceptor activation | – PNS releasing ACh and VIP may contribute to vasodilatation
31
cerebral autoregulation via..
via myogenic activity and those of local mediators
32
when will cerebral arteries contract and for what purpose
will contract when stretched | – constricting to increased pressure, limits blood flow
33
what happens to cerebral arteries when low PaO2
an increase in cerebral blood flow involving NO and local | adenosine release leading to dilatation
34
how is systemic hypoxia complicated and explain how
by changes in ventilation and CO2 | • CO2 is potent cerebrovascular dilator (get more perfusion) and hypoxic-induced hyperventilation will decrease PaCO2
35
difference of local hypoxia and systemic hypoxia
local hypoxia - increase dilation and increase perfusion | systemic hypoxia - decrease CO2 and cerebral perfusion
36
cerebral challenges
• Vascular dilatation (headaches/migraine) Postural hypotension/syncope Cerebrovascular accidents (strokes) Changes to intracranial pressure
37
how can change to intracranial pressure negatively impact cerebral perfusion
increased pressure from space occupying lesion can decrease perfusion
38
how can Postural hypotension/syncope negatively impact cerebral perfusion
transient fall in cerebral perfusion on standing | – usually prevented by baroreflex – indicative of dehydration
39
Cerebral Ischaemic Response
redistributes blood to the brain away from periphery to brain drop in arterial pressure -> sympathetic vasoconstriction from baroreceptor reflex resistance increases -> few cerebral resistance brain has few SNS receptors
40
cushing reflex occurs when
brain volume increases and ICP increases - decreases perfusion and constrict cerebral vessels
41
for cushing reflex what does increased ICP lead to
increased SNS constriction and MAP
42
2 problems with cushing reflex
more blood in the cerebral circulation raises the ICP and risk of oedema systemic pressure control perceives MAP too high and triggers baroreceptor medicated bradycardia
43
splanchnic circulation supplies blood to
liver and GI tract
44
splachnic circulation receives what percentage of cardiac output
25%
45
when does blood flow increase in splanchnic circulation
with food digestion under extrinsic hormonal control
46
what dilates splachnic arterioles and what affect will that have on blood flow
``` gastric hormones (gastrin & CCK) dilate splanchnic arterioles can double the GI blood flow – functional hyperaemia ```
47
splanchnic circulation is innervation with what nerves
sympathetic innervation
48
how is blood redistributed during sympathetic activation
During sympathetic activation (exercise, fight/flight) vasoconstriction redistributes blood away from GI tract to the heart and skeletal muscle
49
how can prolonged redistribution of splanchnic circulation affect the liver and GI tract give an example of when this scene would be happen
necrosis of microvilli | in haemorrhage