Microcirculation Flashcards
Microcirculation structure
Arteriole (smooth muscle) Terminal arteriole (precapillary sphincter) Capillaries Pericytic venule Venule
Blood flow rate (Q)
Volume of blood passing through a vessel per unit time
Pressure gradient equation (ΔP)
Increase pressure gradient=?
Pressure A- Pressure B
A= arterioles
B= capillaries/ other end of arteriole
Increase flow rate
Increase BP effect on
ΔP
R (Resistance)
Q (Flow rate)
Increase ΔP
Increase Q
No effect on R
Link between ΔP, R, Q (Darcy’s Law)
ΔP= Q x R
Pressure gradient= Flow rate x Resistance
Arteriolar vasoconstriction effect on
ΔP
R
Q
No direct effect on ΔP
Increase R (because decreased radius of vessel)
Decrease Q
What relates
flow into tissue
pressure gradient
resistance of organ?
Why is ΔP the same as MAP?
Without pressure difference what would happen?
F(organ)= ΔP (MAP)/ R (organ)
ΔP is basically same as MAP because pressure out of tissue is negligible
Without it blood wouldn’t reach tissue capillary beds
Effect of vasoconstriction on
radius
Resistance
flow
decrease r
increase R
decrease F
Effect of vasodilation on
radius
Resistance
flow
increase r
decrease R
increase F
Vascular tone definition
Importance?
When arteriolar smooth muscle displays a state of partial constriction
Allows for further constriction+ dilation when required
Why are radii of arterioles adjusted indpendently? (Arteriole functions) Regulated by? Stimulation? Driven by? Leads to? Name for it?
To accomplish 2 functions of arterioles:
- Match blood flow to metabolic needs of specific tissues, regulated by local intrinsic controls+ independent of nervous/ endocrine stimulation
- Help regulate systemic arterial blood pressure, regulated by extrinsic controls, travel by nerves/ blood+ usually centrally coordinated
Arteriole vasodilation
Stimulated by?
Called?
Function 1 of arterioles
Chemically driven by increased metabolites/ increased O2 usage= arteriole vasodilation
Called active hyperaemia
Arteriole vasoconstriction
Function 1 of arterioles
Decreased blood temperature/ increased stretch (distension) due to increased BP= arteriole vasoconstriction
Increased stretch effect (only) called myogenic autoregulation
Leads to decreased inflammation in injury
Myogenic autoregulation
Function 1 of arterioles
Opposite from CVS control when pressure decreases
Only happens in tissues where blood flow not required as much at the time
Increased BP→ increased flow in tissues→ sensed by stretch receptors→ causes constriction by increased resistance→ blood diverted from area
Arteriolar response to skeletal muscle arterioles in response to exercise
Active hyperaemia
Arteriolar response to small intestine arterioles in response to exercise
Myogenic vasoconstriction
Blood pressure
Cadiac output (Q)
Total peripheral resistance (TPR)
MAP= Q x TPR
Function 2 of arterioles: Neural Location? Causes? Leads to Blood loss?
Cardiovascular control centre in medulla
Vasoconstriction
Decreased TPR
Blood loss for long time= lots of tissues undergo this= very little blood flow for long time= bad
Function 2 of arterioles: Hormonal
Hormones?
Cause vasoconstriction
Vasopressin/ ADH
Angiotensin II
Adrenaline/ noradrenaline
Cause vasoconstriction
Purpose of capillaries
Delivery of metabolic substrates to cells of organism
Why is capillary density important?
Suited to enhance diffusion (Fick’s Law)
Minimise diffusion distance
Maximise SA
Maxmise time for diffusion
What has denser capillary networks?
Highly metabolically active tissues
Skeletal muscle= huge capacity but limited flow at rest
Purpose of precapillary sphincter
smooth muscle around arterioles
Allows some capillary beds to be shut down
Types of capillaries Small+ water soluble substances? Lipid soluble substances? Large+ water soluble substances? Examples?
Continuous: H20- filled gap junction= water+soluble + small can go in, lipid soluble can diffuse through membrane, large= mechanism/ protein channel required
Fenestrated: everything can enter (except very big like cells), eg. glomerulus
Discontinuous e.g. bone marrow (WBCs, large gaps for cells at points
What type of capillaries is the blood brain barrier?
Continuous but instead of H20 filled gap junctions, there are tight junctions= more control of what can enter and exit
Lipid soluble can go in
Some parts are fenestrated
Capillary fluid movement
Forces?
Increase BP= affect on forces?
Protein-free plasma filters out of capillary
Mixes with interstitial fluid
Reabsorbed
Hydrostatic force out of capillaries
Oncotic pulling force into capillaries balances by end of capillary bed because of water soluble proteins in blood
Increased BP= increase hydrostatic force but no change to oncotic pressure (because conc. of water soluble proteins doesn’t change)
Ultrafiltration pressure requirement
If pressure in capillary> Interstitial fluid
Reabsorption pressure requirement
Not as effective as ultrafiltration= consequence?
If inward driving pressures> outward pressures across capillary
Lymphatic system required for net loss of fluid from vessels
Where are lymphatic capillaries found?
Wherever there’s a blood capillary present
Difference between lymphatic capillaries+ normal capillaries
Lymphatic capillaries have a terminal point, blood capillaries are part of a circulation
Features of lymphatic capillaries
Openings for interstitial fluid to enter
Flaps= allow fluid to only travel one way down towards major lymphatic vessels
Infection effect on lymphatic system
Increased lymph node size
Site of activation of lymphocytes
Major lymphatic vessels that IF drains to
Where does lymph connect to circulation?
Right lymphatic duct
Thoracic duct
Right+ left subclavian veins
Lymph drainage: If rate of production> rate of drainage
Oedema
Elephantisis
Parasitic blockage of lymph nodes
