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02. Cardiovascular System > Exchange in & control of the Peripheral Circulation > Flashcards

Exchange in & control of the Peripheral Circulation Flashcards

1
Q

features of capillaries

A

specialised for exchange lots of them thin walled - small diffusion barriersmall diameter (big SA:vol ratio)

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2
Q

what are the 3 types of capillaries

A
  1. continuous
  2. fenestrated
  3. discontinuous
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3
Q

continuous capillaries

A

no clefts (between cells) or pores (within cells)

e.g. brain

for the blood brain barrier, protect the brain from blood K conc

clefts only

e.g. muscleallows some exchange

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4
Q

fenestrated capillaries

A

clefts and pores e.g. intestine

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5
Q

discontinuous capillaries

A

clefts and massive pores e.g. liver

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6
Q

types of exchange

A

diffusion (majority of exchange) carrier mediated exchange bulk flow

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7
Q

where does exchange occur from capillary to cell

A

between capillary and ECF, between cell and ECF

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8
Q

how does oxygen diffuse

A

down its conc gradient is lipophilic -no barriers to diffusion

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9
Q

features of diffusion

A
  1. self regulating - if the cell starts using more oxygen there is a larger conc grad so more is supplied
  2. non-saturable - there is no point where oxygen transport is at its max
  3. non-polar substances across membrane
  4. polar substances through clefts/channels
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10
Q

describe an example of carrier mediated transport

A

glucose transportin the brain - glucose is trapped within the capillaries but is highly needed by the brain so a protein transporter is required to move the glucose across

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11
Q

features of bulk flow

A

fluid transport driven by hydrostatic and osmotic (oncotic) pressure

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12
Q

what is hydrostatic pressure

A

loss of water as you move down the capillary from arteriole to venule through cleftsbig solutes remain in the capillary

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13
Q

what is osmotic pressure

A

drawing water back in to the more concentrated plasma due to retention of large solutes in the capillary

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14
Q

what is the pressure in the arteriole end

A

~40mmHg

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15
Q

what is the pressure in the venule end

A

~20mmHg

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16
Q

what are starlings forces

A

NOT THE SAME AS STARLING’S LAW (preload on the heart) capillary hydrostatic pressure vs ISF hydrostatic pressure (determines movement of water out)

plasma osmotic pressure vs ISF osmotic pressure (determines movement of water in)net filtration pressure varies between capillary beds

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17
Q

what amount of fluid is lost and regained in the capillary network each day

A

~20L lost and ~17L regained

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18
Q

what happens to the remaining fluid that isn’t regained into the capillary network

A

drains into the lymph capillaries

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19
Q

describe the structure of lymph capillaries

A

same as blood capillaries except they are blind ended valves prevent backflow of fluid

fluid drains into the low pressure heart of the systemic circulation (vena cava)

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20
Q

define oedema

A

accumulation of XS fluid

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21
Q

what are some causes of oedema

A
  1. lymphatic obstruction e.g. due to filariasis, surgery raised CVP e.g. due to ventricular failure
  2. hypoproteinemia e.g. due to nephrosis, liver failure, malnutrition
  3. increased capillary permeability e.g. inflammation, rheumatism
22
Q

how does filariasis cause oedema

A

parasitic worm lives in lymph vessels and blocks them

23
Q

how does ventricular failure cause oedema

A

LV isnt pumpin out the blood that is coming into it

back up of pressure

increased loss of fluid from the veins

24
Q

how does rheumatoid arthritis lead to oedema

A
  1. gaps between walls of capillaries and endothelial cells to allow WBC out
  2. other contents of plasma are also drawn out so no build up of osmotic pressure
  3. fluid accumulates
25
Q

how does malnourishment lead to oedema

A
  1. lack of protein in diet
  2. less plasma protein
  3. no osmotic pressure developed
  4. water is lost and isn’t drawn back inn
26
Q

control of peripheral blood flow

A

Darcy’s law (flow = pressure difference/resistance) and Poiseuille’s law varying the radius of vessels is used to control flow and redirect blood

27
Q

how is MAP calculated

A

flow = pressure difference/resistance

MAP - CVP = CO x TPR

MAP = CO x TPR

CVP is negligible as it is so small

28
Q

what is MAP

A

mean arterial pressure ~90-95 mmHg

29
Q

what does varying the radius of resistance vessels control

A

TPR and therefore regulates MAP

MAP is the driving force pushing blood through arterioles, continuous flow out of arterioles

arteriolar radius affects flow through individual vascular beds and MAP

30
Q

what happens when the resistance of a vascular bed is reduced

A

increased flow through that vascular bed

31
Q

if TPR is reduced, what effect does that have on MAP

A

reduced MAP

smaller driving force pushing blood through all arterioles

insufficient blood flow to the other regions

32
Q

what is used to keep the blood flow to each vascular bed sufficient and keep MAP in the right range

A

2 levels of control over the smooth muscle surrounding arterioles

intrinsic and extrinsic mechanisms

33
Q

what are intrinsic mechanisms

A

concerned with meeting the selfish needs of each individual tissue

34
Q

what are extrinsic mechanisms

A

tend to affect the whole body concerned with ensuring that the TPR (and therefore MAP) of the whole body stays in the right range

35
Q

extrinsic control (neural)

A

sympathetic nerves :

  1. release noradrenaline
  2. binds to alpha 1 receptors
  3. arteriolar constriction
  4. reduced flow through that body region
  5. increased TPR

parasympathetic nerves :

  1. usually no effect
36
Q

what is the smooth muscle around vessels innervated by

A

heavily innervated by sympathetic post-ganglionic fibres

37
Q

extrinsic control (hormonal - adrenaline )

A

adrenaline :

  • released from adrenal medulla when sympathetic nerves are activated
  • binds to alpha 1 receptors
  • arteriolar constriction
  • reduced flow through that tissue
  • increased TPR
  • in some tissues (skeletal and cardiac muscle) it also activates beta 2 receptors, arteriolar dilation (2y messengers coupled to receptors), increased flow through that tissue and reduced TPR redirects blood to these muscles where it is needed
38
Q

extrinsic control (other hormonal controls)

A

angiotensin II :

  • produced in response to low blood vol
  • arteriolar constriction
  • increased TPR vasopressin (antidiuretic hormone) - released in response to low blood vol
  • arteriolar constriction
  • increased TPR

atrial natriuretic factor :

  • released in response to high blood vol
  • arteriolar dilation
  • reduced TPR
39
Q

what are the 4 types of intrinsic control

A
  1. active (metabolic) hyperaemia
  2. pressure (flow) auto-regulation
  3. reactive hyperaemia
  4. the injury response
40
Q

active (metabolic) hyperaemia

A
  • increased blood flow in response to increased metabolism
  • increased conc of metabolites triggers the release of EDRF/NO by endothelium causes arteriolar dilation
  • increased flow to wash out metabolites
  • an adaptation to match blood supply to the metabolic needs of that tissue
41
Q

what are paracrines

A

local signalling molecules e.g. EDRF

42
Q

what does EDRF stand for

A

endothelium derived relaxing factor

43
Q

give 3 examples of metabolites

A

CO2

H+

K+

44
Q

pressure (flow) autoregulation

A

sudden event which leads to sudden decreased MAP, reduced flow and accumulation of metabolites

triggers release of EDRF/NO

arterioles dilate and flow is restored to normal (or it could be myogenic - when smooth muscle is stretched it tends to contract which can contribute to the same effect)

an adaptation to ensure that a tissue maintains its blood supply despite changes in MAP

45
Q

reactive hyperaemia

A
  • occlusion of blood supply causes a subsequent increase in blood flow
  • an extreme version of pressure auto-regulation
  • accumulation of metabolites when flow is cut off, local arteriolar dilation
  • when pressure is released there is a sudden flow of blood through dilated arterioles
46
Q

the injury response

A
  • aids delivery of blood born leucocytes etc to injured area
  • increased C fibre
  • substance P acts on mast cells
  • histamine released by mast cells
  • arteriolar dilation, increased blood flow + increased permeability
47
Q

special areas of circulation

A

coronary circulation

cerebral circulation

pulmonary circulation

renal circulation

48
Q

coronary circulation

A
  • majority of blood flow to coronary arteries is during diastole
  • blood supply is interrupted by systole
  • still has to cope with increased demand during exercise
  • shows excellent active hyperaemia
  • expresses many beta 2 receptors
  • these swamp any sympathetic arteriolar constriction
49
Q

cerebral circulation

A
  • always needs to be kept stable
  • shows excellent pressure auto-regulation
  • if MAP decreases, the arterioles in the brain dilate enough to maintain enough blood flow to the brain
50
Q

pulmonary circulation

A
  • reduced oxygen causes arteriolar constriction (the opposite response to most tissues)
  • ensures that the blood is directed to the best ventilated parts of the lung
  • prevents V/Q mismatch
51
Q

renal circulation

A
  • main function is filtration which depends on pressure
  • changes in MAP would have big effects on blood volume
  • shows excellent pressure auto-regulation
  • if MAP falls, arterioles dilate and vice versa to maintain filtration at a constant level

02. Cardiovascular System (72 decks)

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