Microvasculature Flashcards
1
Q
Calculating mean arterial pressure (MAP)
A
- MAP = CO x TPR
- Therefore MAP will increase if CO increases and TPR is constant, or if TPR increases and CO is constant
- MAP will not increase if one increases and the other decreases as long as the product is the same
2
Q
Differences btwn arterial and venous systems
A
- Arterial: low resistance, high BP, low volume (10%), low compliance
- Venous: low resistance, low BP, high volume (70%), high compliance
3
Q
Factors affecting venous return
A
- Residual BP after capillaries (Pv)
- Venoconstriction via sympathetic output on veins
- Skeletal muscle pumps
- Respiratory pump (negative pressure from expanding thorax during inspiration drives blood back to heart)
- Cardiac suction: movement of heart during early systole sucks blood into atria
4
Q
Functions of microcirculation
A
- Regulates TPR
- Regulates distribution of blood flow
- Site of exchange of solutes btwn blood and tissue (regulated by permeability of vessels)
- Movement of fluid btwn vascular and interstitial space
5
Q
Architecture of microvasculature 1
A
- There are arterial-venous shunts (anastomoses) btwn some arterioles and venues
- There are pre-capillary sphincters (vascular smooth muscle cuffs) at the entrance of capillaries (arteriole side), largely determine Pa
6
Q
Architecture of microvasculature 2
A
- There are post-capillary resistance vessels that determine Pv
- Metarteriole connects arterioles to venules, but also sends out capillary branches to the capillary bed
- Arterioles, metarterioles and large venules/veins are innervated by sympathetics and have smooth muscles (less so in veins/venules)
7
Q
Pre-capillary resistance vessels
A
- Small arteries and arterioles have high degree of tone at rest, but this tone is the major site of TPR regulation
- Arterioles change diameter in response to more or less sympathetic stimulation, and its the diameter change in arterioles that regulates TPR
- The resistance in these vessels is also controlled by local factors
- The vessels determine the number of capillaries open and perfused at any moment, and thus control the capillary surface area exposed for solute exchange
8
Q
Physics of capillaries
A
- Due to the extremely large overall cross-sectional area, there is very slow flow thru capillaries to facilitate transport
- The blood has a greatly increased area of contact w/ surrounding tissue when it is in a small diameter vessel
- The ratio of pre-capillary resistance (resistance in arterioles, Ra) to post-capillary resistance (resistance in venules, Rv) determines the pressure in the capillary themselves (Pc)
9
Q
Vascular tone
A
- The tone in pre-capillary beds is due to physical factors (BP in vessels), chemical factors (local metabolites), and neural input
- Some pre-capillary beds have high resting tone (SKM), some have low (renal)
10
Q
Vascular smooth muscle categories
A
- Multi-unit: minimal electrical communication btwn muscle cells, depends on nerve impulses to initiate contraction
- Single-unit: capable of cell-cell propagation of APs and contains pacemaker cells (can be innervated)
- The pacemaker cells respond to stretch by increasing frequency of firing, which yields contraction of the vessel
- Single-unit vessels are very responsive to local environmental changes, while multi-unit muscles can respond to environmental changes but are mostly driven by innervation
11
Q
Distribution of different SM unit types
A
- Large arteries have mostly multi-unit, with medium sized arteries having both and arterioles having mostly single-unit
- Capillaries do not have SM
- Small venues have mostly single unit, medium veins have both, and large veins have mostly multi-unit
- Key note: The blood vessels in the brain are all exclusively single units that are not innervated, therefore blood flow to regions of the brain depend solely on local changes
12
Q
Neural control of blood flow
A
- Single units can be innervated by sympathetics, but the pre-capillary sphincters are not (local only)
- NE induces contraction of SM (alpha-adrenergic vasoconstriction)
- Inhibition of NE release leads to muscle relaxation and vasodilation
13
Q
Hormonal control of blood flow
A
- Epinephrine at low concentrations combines w/ b2 receptors and dilates blood vessels, lowering TPR
- At higher concentrations the a1 affects outweigh the b2 effects and there is vasoconstriction, increasing TPR
14
Q
Metabolic regulation of blood flow
A
- Most local metabolites will cause vasodilation, and the importance of each factor varies from bed to bed
- Increase in these factors leads to vasodilation and increase in flow
- The increase in flow decreases the amount of these factors, leading to more vasoconstriction and increased pressure
15
Q
Myogenic regulation of blood flow
A
- Only in single-unit SM, which have pacemakers that respond to stretch
- The stretch is a function of the pressure across the wall and the compliance of the wall
- Increasing the stretch increases pacemaker firing, and the smooth muscle cells respond by contracting
- Usual reason for increased stretch is increased blood pressure
16
Q
Autoregulation
A
- Only local factors impart the ability of auto regulation, where as neural and endocrine factors are extrinsic regulation
- The purpose of auto regulation is to maintain a constant blood flow, thus if there is increased pressure -> increased gradient -> increased flow then the body vasoconstricts (due to stretch-> increased pacemaker firing-> vasoconstriction) to increase resistance and restore flow to normal levels
17
Q
Solute exchange
A
- The most important mechanism for solute exchange is diffusion
- Lipid soluble substance (including CO2, O2 and H2O) can pass through the endothelial cells and thus diffuse thru any type of capillary bed (freely diffusible)
- Small molecules and ions (glc, K, Na) can pass thru pores in fenestrated and discontinuous capillaries (restricted diffusion)
- Large molecules must move through large pores/channels or via pinocytosis
- Overall, small things diffuse thru capillary walls faster than big things (smaller diffusion coefficient)
18
Q
Filtration-absorption 1
A
- The way in which fluid is moved btwn the circulatory system and interstitial fluid (ISF)
- What moves btwn the two is an ultra-filtrate of plasma not containing large proteins or cells
- This is a balance of essentially 2 factors: pressure in the capillary (Pc; pushing out) and oncotic pressure of plasma (due to plasma proteins/albumin; pulling in)
- Oncotic pressure is 25 mmHg, thus as long as Pc > 25 there is net filtration (fluid moves out of capillaries)
- If the Pc < 25 there is net absorption (fluid moves into capillaries
19
Q
Filtration-absorption 2
A
- Generally, in the upstream areas of capillaries (near arterioles) the pressure is above 25 and filtration dominates
- As the blood moves further down to the venous side Pc falls below 25 and absorption dominates
- Pc is determined by the ratio of arteriole resistance to venule resistance (Ra/Rv)
- High Ra means less flow thru arterioles and thus lower Pc
- Low Ra means more flow thru arterioles into capillaries and thus higher Pc
20
Q
Filtration-absorption 3
A
- If Ra/Rv increases (arterioles constrict), Pc decreases and absorption is more favored
- If Ra/Rv decreases (arterioles relax), Pc increases and filtration is more favored
- Since the resistance of arterioles is what most changes, Ra/Rv is largely determined by Ra (Rv is relatively static)
- It is worth noting that since Ra/Rv is generally around 5, a single unit increase in Rv has a 5x greater impact on the ratio as a single unit on Ra
21
Q
Overview of transport
A
- Bulk flow of fluid btwn ISF and capillaries: filtration-absorption
- Movement of solutes in and out of the capillaries: diffusion
- The lymphatic system picks up and recycles the excess filtrate that is not reabsorbed by the capillaries (about 2-4L/day excess filtrate)
