vascular system Flashcards
poiseuilles law
flow=change in pressure/resistance
flow=(change in pressure)(radius)^4pi/(length)(viscosity)8
-increasing vessel length increases resistance and decreases flow
-increasing blood viscosity increases resistance and decreases flow
-increasing blood vessel radius decreases resistance and increases flow
a change in blood vessel radius is known as what
constriction or dilation
-accomplished by adjusting the tension of vascular smooth muscle cells
continuous flow system, location of highest resistance?
- location of highest resistance is where the greatest pressure drop is observed
- pressure will be high upstream of this section and low downstream
importance of high resistance section
where the overall flow can be controlled
where is the high resistance section located
small arterioles
-where vasocontriction or vasodilation are effective at controlling blood flow and the upstream and downstream pressures
flow velocity
flow velocity=flow rate(cm^3/min)/cross sectional area(cm^2)
-faster through arteries and slower in capillaries and veins because the capillaries and veins are numerous and so have a large combined cross-sectional area
poiseuille’s law for the systemic circulation
CO=(MAP-CVP)/TPR
MAP
mean arterial pressure
- systolic pressure-diastolic pressure=pulse pressure
- diastolic pressure + 1/3 pulse pressure=MAP
CVP
central venous pressure
- pressure in the right atrium
- CVP is usually very close to zero
TPR
total peripheral resistance
- resistance to blood flow throughout the whole system, and it depends on the resistance through each of the routes blood could take
(e. g. the route supplying blood to the brain, to the muscles, to the gut, etc.) - TPR controlled by the arteries, which are known as resistance vessels
- most of the blood at any given time is in the veins.
what are the veins also called
capacitance vessels
-because they contain most of the blood
blood flow to the tissues
each tissue has a set of arterioles delivering blood to it
blood flow to and individual tissue
depends on the resistance of its arterioles and on the perfusion pressure
-each set of arteriole can be independently controlled to adjust blood flow to tissues based on their individual demands
perfusion pressure
mean arterial pressure-venous pressure
PP=MAP-VP
-perfusion pressure (how much pressure pushes flow through tissue)
venous pressure
- NOT central venous pressure, which is near zero
- has a value of about 15mmhg
TPR determined by..
all the individual resistances of the tissue arterioles
autoregulation
local control of blood flow to a tissue by control of tissue arteriole resistance
- tissue arteriole smooth muscles respond to local conditions
- conditions caused by tissue activity will cause vasodilation
how to change flow of blood
MAP=COxTPR
-MAP remains somewhat constant, change resistance to change flow
tissue blood flow (flow equation)
PP/R
list of factors that will cause vasodilation
- decreased [O2}
- increased [CO2]
- decreased pH
- increased temperature
- increased [K+]
- adenosine
- nitric oxide
- histamine
- activity is indicated when these change
- cause arterial smooth muscle to relax
- this is a local negative feedback system to maintain these concentrations at their set points within the tissues
MAP remains constant no matter what, examples of changes
if TPR drops, MAP drops
-CO increases to increase MAP
hyperemia
an increase in blood flow due to the local conditions and paracrines
active hyperemia
tissue responds to its own increased metabolism
reactive hyperemia
tissue responds to period of reduced blood flow
sensors for negative feedback loop to keep MAP constant
aortic and carotid baroreceptors
- these are stretch receptors in the walls of the carotid sinus and aortic sinus
- their action potential frequency increases as the blood pressure increases
afferent pathway of stretch receptors for pressure
visceral sensory nerves
integrator
nuclei in the medulla oblongata, including the solitary nucleus
efferent pathways
- autonomic nerves
- epinephrine
- angiotensin
effectors
- heart controls cardiac output by adjusting rate and contractility
- veins control cardiac output by influencing venous return and EDV
- arterioles control TPR by vasocontriction and vasodilation
venous return equation
=(VP-CVP)/R
-VP=15
CVP=0
R=constant in veins
-VP changes due to skeletal muscle pumps (constrict veins, increasing pressure)
-change in VP to CVP drives blood back to the heart (gradient)
how does expiration and inspiration effect pressure
expiration=increases pressure in thoracic cavity
- inspiration=decrease in pressure in thoracic cavity (leads to decreased (CVP and increased venous return)
- affects CVP +/- 1
what effect does VR have on cardiovascular system
change VR, changes CO (more VR=more CO)
-while arteries changing changes TPR
what effect does norepinephrine have on veins
vasoconstricts veins, which increases venous pressure, increasing venous return, increasing CO
why is central venous pressure lower than venous pressure and what does this do
because of the low pressure inside the thoracic cavity
(CVP is measured inside the atrium)
-causes blood to flow towards heart (lowest pressure)
-increased venous return (during inspiration) stretches the right atrium, which causes a reflex increase in HR during inspiration
what do sympathetic nerves do in relation to venous dilation
=alpha adrenergic receptors
-cause venous vasocontriction
how does Frank-starlings law of the heart apply to venous return
increased venous return increases cardiac output
- increased EDV leads to increased SV (F-S law)
- stretch of right atrium leads to increased HR
orthostatis hypotension
the response to it is a baroreceptor reflex that involves the hear, veins, and arteries
difference of diastole and diastolic pressure
diastolic pressure (and systolic pressure) occurs in systole
velocity in capillaries
slow because of large combined cross-sectional area
exchange of nutrients and wastes between blood and tissue fluid happens by..
- diffusion: through endothelial cells and between cells
- filtration/absorption: bulk flow of water and solutes between cells and through fenestrations
- transcytosis: pinocytosis from blood, exocytosis into tissue (transport of proteins, antibodies, etc through mysiums)
filtration
water and solutes leaving the capillaries by bulk flow
absorption
water and solutes entering capillaries by bulk flow
balance btwn absorption/filtration maintained by?
by the balance between hydrostatic and osmotic pressures
hydrostatic pressure in arteriole vs venule end of capillary
its 35mmhg at arteriole end of capillary and 15mmhg at the venule end of capillary
-this force is favoring filtration
osmotic pressure in capillaries
- always greater inside the capillary because plasma proteins contribute to oncotic pressure
- favors absorption
oncotic pressure
relatively constant down the length of the capillary at about 25mmhg
- relatively constant down the length of the capillary at about 25mmhg
- pressure difference between capillaries and tissue fluid due to plasma protein=albumin
net filtration occurs where
in the arteriole end of the capillary where the outward hydrostatic force exceeds the inward osmotic force
where are the two forces balanced
towards the middle of the capillary, no net filtration or absorption occurs
net absorption occurs where
at the venule end of the capillary where the osmotic force exceeds the hydrostatic force
net filtration occuring?
yes, even though filtration/absorption mostly balance each other out thoughout the capillary
-extra fluid that leaves the blood and accummulates in the tissue fluid is taken up into the lymph capillaries, and brought back into circulation by the lymphatic system
edema
an imbalance in forces across the capillary
- an accumulation of excess tissue fluid
- excess hydrostatic pressure (high blood pressure)
- decreased plasma oncotic pressure
- increased tissue oncotic pressure
- blockage of lymph vessels
oncotic edema
not enough protein, therefore not enough plasma protein
-oncotic pressure decreases
