sys circulation and venous return Flashcards
peripheral vascular beds is organized how?
in parallel
- organs recieve the same oxygenated blood ejected from left ventricle
blood flow (flow rate) is dependent on?
- pressure gradients (change in P)
- veascular resistance
major resistance vessel is?
the arteriole
what equation associated flow with change in pressure and resistance
flow = change in pressure / resistance
what is the equation of vascular resistance
R=8nl/πr4
- n = viscosity of blood
- l = length of vessel
what vessel is innervated by SNS fibers
arteries
what is the major function of the artery
- serve as rapid-transit conduits for blood flow form the heart
- act as a pressure reservoir to provide a driving force for blood when heart is in diastole
which blood vessel has these characteristics:
- thick smooth muscle layer
- less collapsible
- contains elastin allows “recoil”
- display a state of vascular tone
artery
what does the elasticy of arteries allow for
distension during systole with subsequent recoil during diastole
- systole and recoil are driving forces to move the blood
what produces the dicrotic notch in arterial pressure
- when aortic valve closes, causing a brief period of retrograde flow, briefly decreasing aortic pressure
what is mean arterial pressure
the average pressure driving blood during a cardiac cycle
is the value of MAP closer to systolic or diastolic pressure? why
closer to diastolic pressure because 2/3 of cycle is spent in diastole
what is the equation for MAP
MAP = diastolic + 1/3(pulse pressure)
pulse pressure = systolic pressure - diastolic pressure
- i.e. BP 120/80
- MAP= 80 + 1/3(40) = 93 mmHg
Mean arterial pressure is indicative of preload or afterload
afterload
What effect does aortic stenosis have on systolic pressure, pulse pressure, and MAP
- stenosis causes reduction in flow into the aorta
- SV is reduced; less blood enters aorta
- systolic, pulse, and MAP all decrease
What effect does arteriosclerosis have on systolic pressure, pulse pressure, and MAP
- plaque causes stiffness and decreased compliance
- ejection of SV causes a greater increase in pressure
- systolic pressure, pulse pressure, and MAP all increase
what is pulse wave velocity
index of aortic stiffness and/or elasticity
- the higher the velocity, the higher the rigidity of the wall
how is pulse wave velocity measured?
- pulse tonometers probes are placed on carotid pulse and femoral pulse
- PWV= change in distance / change in time
pulse wave velocity is a predictor of mortality from what?
cardiovascular mortality
arterioles convert pulsatile pressure swings of cardiac cycle into what?
non-fluctuating pressure
what characteristics of arteriole structure make it an ideal structure to alter resistance and hence affect blood flow within an organ?
- wall contains little elastin but lots of smooth muscle cell
- cells are innervated by SNS
- sensitive to metabolic changes
- displays tone at “rest”
tone of a vessel
the contractile state of the resistance vessel
what tone is this:
- state of partial contraction independent of metabolic and neural mechanisms
- dependent of the intrinsic properties of the vessel vascular smooth muscle
basal tone
what tone is this:
- most resistance vessels are constricted somewhat more than basal due to tonic sympathetic nerve activity
resting tone
relate basal flow, maximal flow, tone, and vasodilator reserve
- the lower the basal flow relative to maximal flow, the higher the tone
- and the higher the vasodilator reserve for the organ
how is tone generated in a vessel
by smooth muscle contraction within the walls of the vessel
from a partially constricted state, how can a vessel reach its vasodilatory reserve?
a vessel can either further constrict or vasodilate to reach its vasodilatory reserve
what is active vasoconstriction
a decrease in vessel diameter due to sympathetic stimulation or constrictor hormones/metabolites
what is active vasodilation
an increase in vessel diameter due to hormones or local factors
what is passive vasoconstriction
- return towards resting state from a dilated state due to the removal of active dilator influences
what is passive vasodilation
return towards resting state from a constricted due to the removal of active constrictor influences
from resting tone; adding adenosine or epinephrine will have what affect?
- adding adenosine: active vasodilation
- adding epinephrine: active vasoconstriction
how do vessels return to a resting tone from a dilated and constricted tone?
- removing adenosine from a dilated vessel -> resting tone
- removing epinephrine from a constricted vessel->resting tone
extrinsic control of vascular tone orginates from outside the tissue. What are the extrinsic factors?
- neural
- hormonal
What are the components of the intrinsic influences that maintain vascular tone
- active hyperemia
- reactive hyperemia
- autoregulation
what is active hyperemia?
- increase in organ blood flow that is associated with increased metabolic activity of an organ/tissue
- local tissue metabolism: metabolites accumulate, trigger dilation by inducing relaxation which increases blood flow
what is reactive hyperemia
an increase in organ blood flow that occurs following a brief period of ischemia produced by temporary arterial occlusion
- when occlusion is removed, pressure is restored and flow is elevated. Blood flow to the deprevied area is higher than normal because the arterioles are dilated
what is autoregulation
the intrinsic ability of an organ to maintain constant blood flow despite changes in blood pressure
the myogenic mechanism states that when vascular smooth muscle is stretched from increased intravascular pressure, it responds by..?
contracting to restore vessel diameter, increase resistance and reduce flow
What channels on smooth muscles mediate autoregulation
calcium channels
- smooth muscle cells depolarize from stretching, leading to Ca2+ entry into cell -> contraction
how can the metabolic mechanism explain autoregulation? scenio: increase in pressure
- increase in pressure will increase flow into organ
- increase in flow will increase O2 delivery and washout local metabolites
- washout of metabolites leads to vasoconstriction
what endothelial factors exert a significant paracrine role in the regulation of smooth muscle tone and blood flow?
- Nitric ocxide: vasodilation
- EDHF: endothelium-derived hyperpolarizing factor: vasodilation
- PGI2 (prostacyclin): vasodilation
- Endothelin: vasoconstrictor
Neural and hormonal input has extrinsic control over vascular tone. Name some players
- vasopressin: vasoconstrictor
- angiotensin II: vasoconstrictor
- Atrial Natriuretic peptide: vasodilator
- Neural
- NE release from SNS fibers
What are metarterioles
- contain precapillary spincters that are not innervated, but sensitive to local metabolites
- act as valves to control blood flow through the capillary bed
differentiate between nutritive and non-nutritive flow
- nutritive: flow through metarterioles and capillaries: exchange occurs
- non-nutritive flow: flow through metarterioles; little exchanges occurs
an increase in tissue metabolic activity will start what cascade? (list steps)
- Low O2
- relaxation of precapillary spincters and ateriolar vasodilation
- increase delivery of O2
- increases exchange between blood and tissue to support increased metabolic activity
exchange across capillaries’ walls occurs by?
- diffusion (passive, down concentration gradient)
- bulk flow: Exchange of water and solutes together due to a pressure gradient.
What forces favor filtration (pressure in capillary is high)
- interstitial fluid-colloid osmotic pressure
- capillary hydrostatic (blood) pressure
What forces favor reabsorption into capillary
- plasma colloid osmotic pressure
- interstitial fluid hydrostatic pressure
What is the equation for net exchange pressure
= (Pc + πIF) - (πp + PIF)
- Pc= capillary blood pressure
- πIF= interstitial fluid osmotic pressure
- πp = plasma osmotic pressure
- PIF= interstitial fluid hydrostatic pressure
what is capillary blood pressure (Pc)
fluid pressure exerted on the inside of the capillary wall by the blood
- forces fluid out: favors filtration
what is the capillary blood pressure at the ateriolar end and venular end
- ateriolar end: 37 mmHg
- venular end: 17 mm Hg
what is plasma-colloid osmotic pressure (πp)
- force caused by plasma proteins
- encourages reabsorption
What is interstitial fluid hydrostatic pressure (PIF)
- fluid pressure exerted on the outside of the capillary wall by the interstitial fluid
- tends to force fluid into the capillaries: f_avors reabsorption_
What is interstitial fluid-colloid osmotic pressure (πIF)
- force exerted by the small fraction of proteins that have leaked from the capillaries into the interstitium
- Favors filtration
- **becomes critical when proteins leak out in the presence of histamine
what are net outward pressure at arteriolar end and inward reabsorption pressure at the venular end
- net outward pressure at arteriolar end: 11 mmHg
- inward reabsorption pressure at the venular end: 9 mm Hg
what happens to filtered fluid that is “left behind”
forced into lympathic system
what is the network of one-way vessels that return fluid back into the blood? What facilitates it?
- lymphatics
- facilitated by the muscle pump
what characteristics of veins make them capable of being highly distended
- thin inner walls
- less smooth muscle
- less elasticity and tone
- more collagen
compaure the compliance between veins and arteries at low and high pressure
- low pressure: venous compliance is up to 20x higher than arterial compliance
- high pressure: compliance is similar
blood spends the majority of its time in what vessels?
veins
- at rest, many capillary beds are closed, increases the venous reservoir
relate cardiac output and venous blood
CO is the determinant of how much blood arrives from the venous side
what is venous return
all the blood arriving at the right atrium to be pumped into the systemic circulation
Since Cardiac output and venous return are balanced; factors that alter one will ?
affect the other
what is the major factor determining cardiac output
left ventiruclar end diastolic volume
- LVEDV depends on venous return
as venous return increases, what affect does this have on the right atrial pressure and EDV?
right atrial pressure increases -> increased EDV -> increases CO
When Right atrium pressure reaches 4-5 mmHs, what happens to cardiac output
- matching levels off and CO can no longer keep up with venous return
- CO reaches a maximum of 9 L/min
explain the relationship between venous return and right atrial pressure
- VR is driven by pressure gradient
- the lower the pressure in the RA, the higher the pressure gradient between the systemic arteries and the RA and the greater the venous return
*** as RAP increases, pressure gradient decreases, and VR decreases
what is mean systemic pressure?
venous return = zero and RAP is maximal
*where the curve intersects the x-axis
- pressure measured in the CV system if the heart stopped pumping
what influences mean systemic pressure
- blood volume
- distribution of blood between the unstressed and stressed volume
what volume volume will be in the unstressed volume, at which the MSP is zero
volume that is < 4 L
- if total total volume is 5L, 4L is unstressed and 1L is stressed volume which produces a MSP of 7 mmHG
increased blood volume and decreased compliance have what effect in MSP
produce an increase in MSP
- if compliance of veins decreases (venoconstriction), veins hold less blood and the blood shifts to the stressed volume
a positive inotropic (agent that alters the force or energy of muscular contractions) has what effect on contractility, SV, and CO
- increases contractility, SV and CO for any level of RAP
what effects does a positive and negative inotropic effect have on CO and RAP
- in either situtation, vascular curve remains the same
- positive: CO increases, RAP decreases and curve shifts upward
- negative: CO decreases, RAP increases and curve shifts downward
an increase in blood volume has what effect on MSP
increase in blood volume increases the amount of blood in the stressed volume and therefore increased MSP
- CO and RAP are increased
an increase in total peripheral resistance has what affect on arterial pressure
increases arterial pressure by holding blood in the arteries
- increases afterload
- decreases CO
an increase in total peripheral resistance has what affect on the vascular function curve
produces a counterclockwise rotation of the curve, which means less blood returns to the heart for a given RAP and VR is decreased
