1) SV gets split up and goes to different organs.  The organs all get homogenous blood.

2) P_a (input pressure) is the same for each organ

3) Since, different organs require different amounts of blood flow each organ blood flow is regulated separately.  Relaxing/contracting smooth muscle vasculature controls blood flow through the organs.

4)  TPR is collective

Q= ΔP/R

Discuss the pieces of this equation

1) pressure: measured above atmospheric pressure (760mmHg)- average 100mmHg- force pushing on blood to propel it.  Venous pressure is basically equal to atm pressure

2) Flow=Q=νA (velocity)(cross-sectional area)

Q=volume/time

v=distance/time

3) P₁ (pressure applied) must be greater than P₂ (pressure that must be overcome) in order for blood to flow

In series: side by side connections- resistance is the sum of the resistances of the individual vessels- more vessels means more resistance

In parallel: vessels branch off so the blood is dispersed in more vessels,so the total resistence is less than the individual resistances

R_parallel=R_single/#vessels

-Vascular smooth muscle controls diameter

-Blood flow is very sensitive to the radius of the vessel; if you double radius you increase flow 16 times

Q=ΔP/R

R=8ηl/πr⁴

Velocity of blood is not uniform through out the vessel: flow has a parabolic curve with maximum flow in the center (RBCs flatten and undergo axial migration)

Pressure is largest in the ateries and decreases as it goes through the vascular system.  The largest drop occurs at the arterioles, where the majority of the resistance is located.

From arteries to cappilaries, vessel diameter decreases, total number of vessels increases, and pressure decreases.

From capilaries to veins, vessel diameter increases, total number of vessels decreases, and pressure decreases.

Newtonian fluid: viscosity is independent of flow, example plasma

Non-newtonian fluid: viscosity depends on flow, example whole blood

This is important because R is proportional to viscosity

1)Temperature: changes in the opposite direction, increased temp (exercise) decrease viscosity, decrease (hypothermia) increases viscosity

2)Hematocrit: RBC %volume, changes in the same direction, increased RBC (polycythemia) increased viscosity, decreased RBC (anemia) decreased viscosity

3)Tube/Vessel diameter: viscosity depends on size of vessel when the size is less than 300microns (Hct is lower in very small vessels, so the viscosity is lower)

RBCs are flexible and undergo axial migration, so they don't fill the entire vessel, only plasma is against the walls.  Due to the parabolic nature of velocity, average RBC velocity is higher than average plasma velocity

80% of TPR is in the arteriole system

Volume has a direct relationship with pressure, due to elastic recoil of vessels

Capacitance (C_a)- the distinsability of the vessel, higher in young people, lower in older people.  So, older people will have higher P_P at the same SV.

C_a=SV/P_p

P_P=P_S-P_D

P_a= 1/3P_S+2/3P_D (because the LV only ejects blood during 1/3 of the cardiac cycle)

P_a~ CO x TPR

Veins are much more distinsable C_v~20C_a

70% fluid volume is located in the venous side of circulation

V_u- unstresses volume- volume required to fill the vasculature but not stretch it

V_s-stressed volume- volume above the unstressed volume that stretches the vasculature, and therefore effects pressure

P_mc-mean circulatory pressure- begins when we start to have V_s, only when the vasculature is filled but has no flow (Q)

C_a=V_s/P_mc

Changing V_s changes Pmc

Change V_s by changing total BV or change vessel diameter

The actual point at which the CV system functions is the intersection of the two cuves.  The vertical axis is a type of flow (CO/Q) and the horizontal axis is a type of pressure (P_RA, P_V)

Plot pressure vs time- clamp on arteriole side and fill to a particular volume.  Starting pressure is P_mc, release clamp and measure change in pressure.  You know what the venous pressure is and calculate the flow.  Plot P_V vs Q.

-Changes in P_mc(venous): changes in V_s- changes in blood volume, or contract/dilate veins

*Increased blood volume or venous contraction- increases P_mc and causes a R shift

*Decreased blood volume or venous dilation- decreases P_mc and causes a L shift

-Changes in slope(arterial): slope is proportional to 1/TPR

*increase arterial contraction- decreases slope

*decrease arterial contraction- increases slope

Increases sympathetic activity causes venous and arterial contraction.

The arterial contraction increased TPR and therefore decreases the slope.

The venous contraction increases the V_s and therefore P_mc.

This causes a R shift and a decreased slope.

Sympathetic withdrawal would have the opposite effect.

Arteriole: endothelial cells with vascular smooth muscle, functions to control bloow flow

Capillary: endothelil cells, function is to exchange small solutes and water

Venule: endothelial cells with a small amount of smooth muscle, function is to collect blood and exchange large molecules

Thin barrier (epithelial layer) separates blood inside the capillary and ISF- nutrients leave the capillary and waste enter the capillary

Every cell has atleast one capillary near it.

Rate of diffusion depends on: ΔC, A, ΔX, and D

Rate of diffusion=PAΔC

Lipid solube (like oxygen): entire SA, P is high

Water soluble (like glucose): .1% (1/10%, or 1/1000) of SA, P is low

"Pores" between epithelial cells, roughly 80 ang, is where water soluble things must go, larger than that (like plasma proteins) can't move

under steady state conditions, the amount of fluid filtered is about the same as the amount of fluid absorbed

P_c is the only factor that changes very much

P_a, P_v, R_v- change in the same direction

P_a- changes in the opposite direction

P_c- capillary hydraulic pressure due to fluid, tries to push fluid out of capillary- promotes filtration (+)

π_c- (π_pl)- osmotic pressure due to plasma proteins- tries to pull fluid in the capillary- promotes absorption (-)

P_ISF- hydraulic pressure of the ISF, tries to push fluid back into the capillaries- promotoes absorption (-)

π_ISF- osmotic pressure due to proteins in the ISF, tries to pull water out of the capillaries- promotes filtration (+)

Add up all pressure to determine if you are filtering (+) overall or absorbing (-) overall.  You are normally filtering (delivering nurtients) a the beginning and absorbing (picking up waste) at the end.

Each day about 20 L are filtered, but only 16 L are absorbed.  The lymphatic system takes the rest. 

Large number of small vessels with closed ends, has one way valves.

Lymph flow determined by P_ISF since it also pushes fluid into lymphatic vessels.  So, Q_lymph~P_ISF until lymph vessel capacity is reached.

Muscles contract to propel lymph through its vessels to eventually return to vasculature. 

If filtration exceeds lymph flow, you accumulate ISF and get edema.

Baroreceptor- senses how much stretch occurs in the blood vessels in the carotic region which sends nervous impulses to brain

SNS/PNS reactive- effect HR, contractility, and vessel diameter

P_a~COxTPR

So, the autonomic nervous system changes these to change P_a.  Changes in HR and contractility change CO.  Changes in vessel diameter change TPR. 

This system is very fast, but does not provide complete compensation.

Regulates BP through vessel diameter and BLOOD VOLUME.

Decreased pressure increases renin released from kidneys.  Renin changes angiotensinogen (a plasma protein) to angiotension 1 (which has 10 AA).  When angiotension 1 gets to the lungs it is converted to angiotension 2 by the angiotension-converting enzyme.  Angiotension 2 is a vasoconstrictor (arteries and veins) and it also increases aldosterone secretion.  Aldosterone tells the kidneys to retain water and salt which increases the ECF and therefore increases the blood volume (and P_mc).

This system takes longer, but provides complete compensation.

tendency of Q_organ to remain constant despite changes in P_a

remember Q= P_a-P_v/R

Since P_a increases R must also increase, or if P_a decreases R must also decrease to maintain a constant Q_organ.

hyperemia- an excess of blood in a region

elevated blood flow following a period of occlusion (circulatory arrest)

magnitude of hyperemia depends on duration of occlusion and flow before the occlusion

Increase in blood flow with increased metabolic activity of an organ

Increased need for flow, so decrease R to achieve flow.

the control of blood flow is a consequence of the maintenance of wall tension.

T=Pxr/W

Blood vessels exposed to increased P_a  will passively distend.  The VSM will contract in response to bring T back down to normal (by decreasing r).

Delivery is dependent on flow

Extraction is dependent on SA, maximum diffusion distance, and amount of blood in the capillaries (inversely proportional to velocity of RBCs)

1) GI/Renal get less and less blood flow

2) Cerebral perfusion maintains at 750ml/min

3) The heart and skeletal muscle get more and more blood flow

4) Skin flow increases and then drops at maximum intensity

5) CO and oxygen consumption increase

Phase 1: mechanical response, muscles tense-so vasoconstriction- decreased Vu which increases Vs, which increases Pmc, which increases CO

Phase 2: neural response, decreased vagal stimulation, INCREASED SYMPATHETIC STIMULATION

Phase 3: As a result of increased muscle work, K/adenosine/H+/lactate increased.  So, now these vasodilators are in the ISF and cause vasodilation.  They increase flow through the capillary bed and open more capillaries. 

This vasodilation only happens in the arterioles of the muscle.  The veins remain constricted increasing the Pmc.

Immediate Effect: decrease blood volume -> decreased Pmc, CO, and Pa

Fast Compensation: baroreceptor fire less which increases sympathetic activity (↑HR, ↑contractility, ↑arterial and venous constriction) The decrease in venous pressure and increase in arteriolar constriction decreases Pc- so absorption is increased.- incomplete

Intermediate compensation (hours to days): RAA system is activated- restores BP close to normal

Slow compensation (days to weeks): RAA increases blood volume but it is low in Hct and plasma proteins.  Kidneys sectete erythropoetin which goes to marrow and causes RBCs to mature.  Liver synthesizes proteins.