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Cardiorespiratory Biology > Special Circulations > Flashcards

Special Circulations Flashcards

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AP® Biology flashcards Biology 101 flashcards
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
Q

how will increased intracranial pressure affect cerebral perfusion

A

decrease cerebral perfusion

tumour/oedema

26
Q

Cerebral blood flow calculation

A

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
Q

how is blood flow is cerebral tissue maintained

A

by constriction and dilatation in response to challenge

– can better deal with high pressure than with low pressures

28
Q

nerve firing in cerebral tissue is linked to what substances and in what practice is this beneficial

A

nerve firing linked to vasoactive K+, adenosine and NO

– this is the basis of functional MRI

29
Q

cerebral structural adaptations benefits

A

connected to circle of willis and high capillary density
neurovascular coupling
SNS fibres present lack alpha 1 at LIMIT response

30
Q

how is SNS fibres present but lack of α1

-AR limit response beneificial for cerebral tissue

A

– thus brain spared from baroreceptor activation

– PNS releasing ACh and VIP may contribute to vasodilatation

31
Q

cerebral autoregulation via..

A

via myogenic activity and those of local mediators

32
Q

when will cerebral arteries contract and for what purpose

A

will contract when stretched

– constricting to increased pressure, limits blood flow

33
Q

what happens to cerebral arteries when low PaO2

A

an increase in cerebral blood flow involving NO and local

adenosine release leading to dilatation

34
Q

how is systemic hypoxia complicated and explain how

A

by changes in ventilation and CO2

• CO2 is potent cerebrovascular dilator (get more perfusion) and hypoxic-induced hyperventilation will decrease PaCO2

35
Q

difference of local hypoxia and systemic hypoxia

A

local hypoxia - increase dilation and increase perfusion

systemic hypoxia - decrease CO2 and cerebral perfusion

36
Q

cerebral challenges

A

• Vascular dilatation (headaches/migraine)
Postural hypotension/syncope
Cerebrovascular accidents (strokes)
Changes to intracranial pressure

37
Q

how can change to intracranial pressure negatively impact cerebral perfusion

A

increased pressure from space occupying lesion can decrease perfusion

38
Q

how can Postural hypotension/syncope negatively impact cerebral perfusion

A

transient fall in cerebral perfusion on standing

– usually prevented by baroreflex – indicative of dehydration

39
Q

Cerebral Ischaemic Response

A

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
Q

cushing reflex occurs when

A

brain volume increases and ICP increases - decreases perfusion and constrict cerebral vessels

41
Q

for cushing reflex what does increased ICP lead to

A

increased SNS constriction and MAP

42
Q

2 problems with cushing reflex

A

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
Q

splanchnic circulation supplies blood to

A

liver and GI tract

44
Q

splachnic circulation receives what percentage of cardiac output

A

25%

45
Q

when does blood flow increase in splanchnic circulation

A

with food digestion under extrinsic hormonal control

46
Q

what dilates splachnic arterioles and what affect will that have on blood flow

A 
gastric hormones (gastrin & CCK) dilate splanchnic arterioles
can double the GI blood flow – functional hyperaemia
47
Q

splanchnic circulation is innervation with what nerves

A

sympathetic innervation

48
Q

how is blood redistributed during sympathetic activation

A

During sympathetic activation (exercise, fight/flight) vasoconstriction
redistributes blood away from GI tract to the heart and skeletal muscle

49
Q

how can prolonged redistribution of splanchnic circulation affect the liver and GI tract
give an example of when this scene would be happen

A

necrosis of microvilli

in haemorrhage

Cardiorespiratory Biology (25 decks)

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