Exchange in, and control of, the Peripheral Circulation Flashcards
What is the difference between clefts and pores?
Clefts are the gaps between epithelial cells, pores are within the cells, allowing for exchange of gasses/substances etc.
Continuous vws Fenestrated vs Discontinuous capillaries
Continuous:
No clefts or pores (eg brain - hence blood brain barrier)
No pores, clefts only eg most capillaries/muscles
Fenestrated:
Clefts and pores eg kidneys/intestine - specialised for fluid exchange)
Discontinuous:
Clefts and MASSIVE pores - eg liver, big pores are for the proteins
How does exchange happen?
Either by diffusion or Carrier-mediated transport (mainly diffusion)
Diffusion is good because: self-regulating non-saturable non-polar substances across the phospholipid membrane polar substances through clefts/pores
carrier mediated transport eg glucose into brain
What are starlings forces and bulk flow? WHere does the extra fluid go and how much of it is there?
As the blood reaches the capilaries has approx 40mmHg pressure. The hydrostatic Pressure forces a bulk flow out of water, ions etc into interstitial space. The pressure decreases to about 20mmHg in the venules and veins heading back to the heart and so the hydrostatic force decreases. The main component left is the proteins and this therefore draws back in via oncotic pressure an increasing amount of interstitial fluid.
Overall ~20l is lost and ~17l is regained each day
Remaining 3l is returned via lymphatic system.
In other words going on in the background of all that diffusion is a mass exchange of fluid – called bulk-flow.
Hydrostatic pressure pushes fluid out through the leaky capillaries. That builds up an osmotic (oncotic) pressure which draws fluid back in.
The balance of these hydrostatic and osmotic pressures is known as Starling’s forces.
When can Oedema occur?
If there is a problem with the lymphatic drainage system back to the heart, the extra 3L interstitial fluid isn’t picked up and will lead to oedema, eg filariasis/surgery
Raised CVP (central venous pressure), causing excess fluid to be released eg due to ventricular failure
Hypoproteinemia eg due to nephrosis, liver failure, nutrition \9less proteins to draw back in the oncotic pressure )
Increased capillary permeability eg in inflammation, eg rheumatism
What is Darcy’s law?
Flow = change in pressure/resistance
What is Poiseuille’s law?
Resistance = (viscosity x length x 8) / (radius cubed x pi)
Basically increasing viscosity and/or length will increase resistance, and increasing the radius will decrease the resistance 4 fold.
Darcy and Poiseuille’s law combined =?
Flow = (Change in pressure x radius cubed x pi) / viscosity x length x 8
Basically if you increase pressure/radius, flow will be increased (radius has 4 fold effect)
If you decrease viscosity and length, flow will be increased
How can we relate: change in pressure = flow x resistance to our body?
change in pressure = flow x resistance
Therefore
MAP - CVP = CO x TPR
As CVP is v low
MAP =CO x TPR
MAP = Mean Arterial Pressure CVP = Central Venous Pressure CO = Cardiac Output TPR = Total Perhipheral Resistance
What is the most fundamental equation in relation to pressure and blood flow?
MAP = CO x TPR
In order to keep the blood flow to each vascular bed sufficient, and keep mean arterial pressure in the right range, you have to engage in some resistance juggling. How is it managed?
Via:
Local (intrinsic) mechanisms - concerned with meeting the selfish needs of each individual tissue
Central (extrinsic) mechanisms – concerned with ensuring that the total peripheral resistance (and therefore MAP) of the whole body stays in the right ball park
What does Hyperaemia mean?
High Blood Flow
Hyper = high Aemia = blood flow
What are 4 mechanisms for intrinsic control of blood flow?
Active (metabolic) herperaemia
Pressure (flow) autoregulation
Reactive Hyperaemia
The injury response
What happens in Active (metabolic) hyperaemia?
Tissue is producing more waste products (metabolites) as a result of being more active - higher metabolic rate (shock horror!). The endothelial cells pick this up and release a paracrine signal - either NO (Nitric oxide) or EDRF (Endothelium derived relaxation factor), which results in arteriolar dilation. This washes out the extra metabolites and this adaptation matches blood supply to the metabolic needs of that tissue.
What happens in Pressure/Flow autoregulation?
Trigger is a decrease in perfusion pressure:
Low MAP causes Low flow
metabolites accumulate
triggers release of paracrine signal (eg EDRF/NO)
arterioles dilate and flow is restored to normal
an adaptation to ensure that a tissue maintains its blood supply despite changes in MAP
WHat happens during reactive hyperaemia?
Trigger is occlusion of blood supply:
- this causes a subsequent increase in blood flow
- an extreme version of pressure autoregulation
eg red arm post tight bp monitor (metabolite accululation due to occlusion, mass vasodilation post area and then blood flows like crazy once released) - looks like a reaction - reaactive
WHat happens during an injury response?
Eg graze skin but not cut, injury causes redness (vasodilation) because oh histamine release from mast cells which causes arteriolar dilation (increased blood flow and increased permeability). Histamine is released as a result the C-fibre which sent a signal to the dorsal root ganglia tahat it hurt also branching off and releasing peptide P which stimulates the mast cells.
What are the central controls of blood flow and pressure?
Neural - Sympathetic and hormonal
How does the sympathetic system regulate MAP?
Sympathetic nerves release noradrenaline binds to alpha 1-receptors causes arteriolar constriction therefore reduces flow through that tissue, and tends to increase TPR
What affect does the parasympathetic system have of MAP/TPR?
usually no effect
genitalia and salivary glands are the exception
What is the key hormonal influence on MAP/TPR and how does it affect?
Adrenaline!
released from adrenal medulla
binds to Alpha 1-receptors
causes arteriolar constriction
therefore decrease flow through that tissue, and tends to Increase TPR
but in some tissues, eg skeletal and cardiac muscle, it also activates Beta 2-receptors
causes arteriolar dilation
therefore increasing flow through that tissue, and tends to decreased TPR
Significance re exercise
What does Angiotensin II do?
produced in response to low blood volume
causes arteriolar constriction
therefore increases TPR
What does Vasopressin (= antidiuretic hormone) do?
released in response to low blood volume
causes arteriolar constriction
therefore decreases TPR
What does Atrial natriuretic factor do?
released in response to high blood volume
causes arteriolar dilation
therefore decreases TPR
How is the coronary artery system different?
For some reason (either the aortic valve closing off the supply or the pressure upon heart contraction squashing arteries) the coronary arteries have their lowest pressure during systole. As the heart is v important the cells esp during exercise are v good at regulating MAP - expresses many B2 receptors. .
How is cerebral circulation different?
needs to be kept stable, whatever
shows excellent pressure autoregulation
How is pulmonary circulation different?
Opposite in that low oxygen leads to arterial constriction, ensures that blood is directed to the best ventilated parts of the lung
How is renal circulation different?
Imp to maintain the pressure so that too much fluid isn’t filtered out and you end up like a prune, but also that the MAP isn’t too low so you end up like a plump plum.
main function is filtration which depends on pressure
changes in MAP would have big effects on blood volume
shows excellent pressure autoregulation
