specialised circulations Flashcards
Cutaneous circulation - special requirements
3 key features?
temp skin can range from?
Defence against the environment
Temperature regulation – blood flow delivers heat from body core
Skin is a poikilo-thermic (not homeo-) organ
Its temperature can range from 0oC to 40oC (briefly)
without damage for short periods of time
How does body transfer heat?
4 ways (how?)
Radiation (skin vs. ambient temperature)
Conduction - skin onto other object
Convection - removal by air/water
Sweating (latent heat of evaporation)
what does skin temperature depend on? (2)
skin blood flow
ambient temperature
Cutaneous circulation - special structural features
what are AVAs? what do they have and do? why?
Arterio-Venous Anastomoses (AVAs) - Direct connections of arterioles and venules –> expose blood to regions of high surface area
AVAs where blood flow is directed from the arterioles into the venous system which is more compliant therfore can hold more blood and acts as a blood reservoir -> more blood will be at skin so we can lose heat
How is blood directed from arterioles to AVAs?
what innervations are needed?
what two fibres work together? and how?
sympathetic vasoconstrictor will vascoconstrict at aterioles and decrease blood flow there
sudomotor vasodilator fibres will dilate and increase blood flow into AVAs
Both are sympathetic innervations to increase blood flow to veins so it holds more blood and more blood is lost
What controls blood flow to AVAs?
how does it act?
Driven by temperature regulation nerves in hypothalmus
Core temperature receptors in hypothalamus control sympathetic activity to skin & hence skin blood flow
Cutaneous circulation - special functional features
what does it respond to?
how does it change?
what is the paradox?
Responsive to ambient & core temperatures
Increased ambient temperature causes vaso- and venodilatation -> helps heat loss
Decreased ambient temperature causes vaso- and venoconstriction -> helps to conserve heat
Severe cold causes ‘paradoxical cold vasodilatation’
20 mins period of local cooling by ice - first 10 mins
what happens?
why?
how does it do this?
significance of the receptors?
Cold-induced vasoconstriction
To conserve heat
Caused by abundance of
a2 receptors (decreased AC/cAMP/PKA – switch off vasorelaxation processes) on VSMCs in skin
Bind NA at lower temperatures than α1 receptors
a2 receptors work well in cold
NA released by sympathetic nerves act better on a2 than a1 receptors hence why hand will go pale
20 mins period of local cooling by ice - last 10 mins
what happens?
why?
how?
what happens during long term exposure?
Paradoxical cold vasodilatation
To protect skin damage
Caused by paralysis of sympathetic transmission
(less NA released) hence a2 receptors not stimukated as much and there is more vaso-dilation
Long-term exposure leads to oscillations of contract/relax
Increased cutaneous perfusion with increased cored temperature (e.g. exercise)
what detects this?
what two key effect take place to reduce temp?
Increased Core temp
Stimulate warmth receptors in anterior hypothalamus
causes:
Sweating
Increased sympathetic activity (Ach) to sweat glands
Vasodilatation
Increased sympathetic sudomotor activity (Ach act on endothelium to produce NO) to arterioles in extremities
Cutaneous circulation - special feature
Baroreflex/RAAS/ADH-stimulated vasoconstriction of skin blood vessels
importance of this?
mediated by? what does it cause?
what does this look like on the person?
If drop in BP following haemorrhage, sepsis, acute cardiac failure need more blood flow to the organs which potentially could get under perfused hence shift blood flow to these organs via switching off blood flow to our skin
Mediated by sympathetic vasoconstrictor fibres
+ adrenaline + vasopressin + angiotensin II which all cause vasoconstriction of blood vessels of skin
it causes - pale/cold skin of patient in shock
why heating up body after haemorrhage is bad?
what happens to body when you heat it up? why is this bad?
During haemorrhage – warm up body too quickly – reduce cutaneous vasoconstriction – blood flow to skin not vital organs/tissues - potentially dangerous
emotional communication - what happens and how?
e.g. blushing (sympathetic sudomotor nerves)
Lewis triple response of skin to trauma
what is the triple response?
how does it work?
what will the trauma stimulate and where do these fibres go? where do some collateral fibres go? what do these release? what do they act as and cause?
Local redness: Site of trauma
Local swelling: Inflammatory oedema (wheal)
Spreading flare: Vasodilatation spreading out from site of trauma
trauama will stimulate c fibres which go to the spinal cord and help us recognise pain and collateral come off c fibres which cause the release of neuromodulators such as substance P + substances that stiumukate mast cells which release histamine
BOTH act as vasodilators which cause a flare response therfore more vasodilation, more blood flow to trauma and more immune cells to area.
inflammatory oedema due to increased blood flow therefore more fluid moving out of blood and into local interinterstitial fluid
Cutaneous circulation - special problems
prolonged obstruction of flow by compression
why does laying in bed for lomg periods of time cause ischemia? what can it lead to?
how can this be avoided? (2)
Laying in bed for a long period of times, you compress blood flow to the skin can lead to ischemia
Severe tissue necrosis
‘bed sores’; heals, buttocks, weight bearing areas
Avoided by:
Shifting position / turning causing reactive hyperaemia hence will get blood flow back to area (on removal of compression)
High skin tolerance to ischemia