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Flashcards in Microvasculature Deck (21)
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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)