Physio 3 General Control Of Blood Flow & Microcirculation

Front 1

what is an advantage of vessels in parallel?

Back 1

blood flow can be independently regulated

**metabolic state determines % of BF to an organ

Front 2

so we know systole drive Blood into tissues but does diastole?

Back 2

yep, indirectly through recoil

*stored E is used

Front 3

characteristics of arteries

Back 3

SM: SNS
elastic: recoil, decreases pulses

Pressure resevoir to drive BF
Major Fx: deliver blood FROM heart

Front 4

what determines flow

Back 4

Q=dP/R

flow increased:
dP is large
radius is large, resistance is low
viscisity is low

Front 5

again, the vessel that is highest resistance? its effect on pressure

Back 5

arteriole
large drop in pressure, created a change in P to help in flow

*dampen pulses

Front 6

tell me about arterioles

Back 6

SM:
SNS
sensitive to metabolic changes
display tone at rest (contraction)

Front 7

Tone:
basal tone:
Resting tone:

Back 7

Tone: contractile state of resistance vessel

Basal Tone: state of partial contraction independent of metabolic/neuronal factors, dependent on intrinsic properties of the vessel SM

Resting Tone: a bit more contracted than basal tone due to tonis SNS

Front 8

Active Vasoconstriction

Passive Vasoconstriction

Back 8

Active: constriction due to SNS, ot hormones

Passive: when active dilators are removed and vessel goes back to the resting state

Front 9

what affect does adenosine have? what effect occurs when it is removed.

Back 9

active dilation
passive constriction

Front 10

what effect does the SNS have? what if SNS is removed

Back 10

active constriction
passive dilation

Front 11

what is affected by altering tone?
Constriction
Dilation

Back 11

flow

Constriction will decrease flow because R is increased

Dilation decreases resistance and so flow increases

Front 12

Name some metabolites that will vasoconstrict?

Back 12

increased O2
decreased CO2
myogenic activity
endothelin
SNS
Vasopressin
Angiotensin II
COLD

Front 13

what metabolites will vaso dilate?

Back 13

decreased O2
increased CO2
HOT
decreased SNS
NO
Adenosine
histamine

**the flow will increase because the resistance decreases BUT velocity decreases

**SM contracts

Front 14

what are two categories that affect tone?

Back 14

1. local: reactive/active hyperemia, autoregulation. Meet metabolic needs of tissue, determine districution of CO

2. Extrinsic: hormones/neurons. regulate pressure and flow

Front 15

what factors regulate pressue and flow?

what factors supply the tissue with nutrients to meet therir metabolic needs

Back 15

BP/Flow: Extrinsic, hormone & neuron

Metabolites: Intrinsic (local), active/reactive hyperemia, autoregulation

Front 16

what type of control ensures a tissue has BF proportional to their metabolic needs?

Back 16

Active Hyperemia

Front 17

What type of control gives adequate BF after a previous occlusion?

Back 17

REactive hyperemia

Front 18

What type of control allowa BF to an organ to remain constant even when pressures change?

Back 18

Autoregulation

**heart, brain, kidney, sk mm
**when P decreases there will be a local dilation to increase perfusion

Front 19

what is autoregulation

Back 19

heart, kidney, brain, sk mm

**ability of organ to maintain BF even when P changes

**if P decreases, vessels will dilate to restore flow

Front 20

what organs autoregulate?

Back 20

brain
kidney
sk mm
heart

**in decreased P leads to dilation to restore flow

Front 21

the myogenic hypothesis attempts to explain what type of intrinsic contorl, what does the myogenic hypothesis state?

Back 21

explains autoregulation m(ONLY)

**when a vessel stretches (increased P) it automatically wants to return and constricts an restore BF

**in P decreases, the vessel

Front 22

what are extrinsic control factors

Back 22

Horomes:
Vasopressin from pituitary, constricts, increase venous return
ANP: dilator from atria, counteracts hypervolumia
Angiotensin II: constrictor

Neuronal:
SNS: constriction
PNS: dilation

**remeber these factors help regulate BP and Flow, they arent responsible for keeping metabolic needs met

Front 23

what does ANP do?

Back 23

dilator
released from atria

*counteracts hypervolumia

Front 24

what does vasopressin do?

Back 24

from pituitary
constrictor
increases water retention

Front 25

what does angiotensin II do?

Back 25

constrictor

Front 26

what vessels have lots of SNS

Back 26

skin, sk mm,

*less in coronaries, pulm, cerebral

Front 27

does SNS cause constriction or dilation?

Back 27

it depends on the receptor...

a1: constriction in skin, sk mm
b2: dilation in sk mm, NE

Front 28

in sk mm what does SNS do?

Back 28

receptor dependent!

a1: constriction
b2: dilation

Front 29

heart, lungs and brain. lots or little SNS

Back 29

little

*skin has lots!

Front 30

can the effect of SNS be decreased by hormoes

Back 30

yep

Front 31

does passive vasodilation occur when SNS or PNS is removed?

Back 31

SNS

Front 32

a sympathetic adrenergic fiber is what?

Back 32

its a POST gang

**innervate precapillary resistance vessels, a1 constricts

Front 33

what does a sypmathetic cholinergic neron do

Back 33

its PRE ganglionic, releases ACh

precapillary vessel, dilates with M3

Front 34

what do parasymp cholinergec receptors do?

Back 34

Dilate via M3
*cholinergic sympa do the same thing

**genitals, brain, coronary

**DONT affect systemic vascular resistance

Front 35

does the ANS affect the really super tiny capillaries?

Back 35

nope, local metabolite control

Front 36

waht is antiotensin II, renin, etc

Back 36

angiotensinogen --> (renin required for this) angiotensin I --> angiotensin II

**vasoconstrictor, acts on vascular SM of resistance vessels

**released when BP or ECF decreases

Front 37

what are two things that would cause Angiotensin to be released

Back 37

**angiotensin causes constriction,

when BP or ECF decrease, the flow will decrease, we want to vasoconstrict to keep flow constant

Front 38

whats another word for vasopressin? what does it do? what causes its release

Back 38

ADH

constrictor released from pituitary

*released when BP falls or osolarity increases

Front 39

what does an increase in osmolarity do?

Back 39

causes vasopressin to be released from pituitary, this vasoconstriction

Front 40

what is ANP? when is it released? what does it do?

Back 40

dilator released from atria

**released when P increases in atria, or ECF increases

Front 41

what happens when ECF volume increases?

Back 41

hypervoluemia, we want vasodilation by ANP which will decrease TPR

**ANP is released by atria

Front 42

how does ANP work with the kidney to decrease TPR

Back 42

an increase in volume causes ANP to be released, this causes dilation, Na and water are excreted to decrease ECF and decrease pressure

Front 43

what does Epi do?

Back 43

a1: constriction
b2: dilation

**in most tissues Epi will constrict except in sk mm where epi will dilate bc there are LOTS of B2 receptors

Front 44

what are endothelium mediated ways to regulate tone

Back 44

Not under the Extrinsic or Intrinsic control, its a seperate category

NO
EDHF
PGI2
Endothelin
prostaglandins
kinins
histamine

Front 45

how do vasoactive substances work?

Back 45

endothelium mediated
**some bind directly to SM, some bind to endothelium which then releases vasoactive mediators that act on SM

Front 46

NO
what is it released from?
what induces its release
what is its effects

Back 46

released from endothelieal cells w/flow induced stress
Dilator

Front 47

what does endothelium derived hyperpolarizing factor do/

(EDHF)

Back 47

dilation
hyperpolarizes SM to relax it

Front 48

what is prostacylin

Back 48

endothelium mediated
dilation
inhibits platelet aggregation

Front 49

what is endothelin

Back 49

endotheluim mediated
constrictor
released in response to stretched BV

Front 50

name 4 endothelium mediated dilators
name 3 endothemium mediated constrictor

Back 50

Dilators
NO
Endothelial Derived Hyperpolarizing factor
Prostacyclin
Histamine

Constrictors:
Endothelin
Prostaglandins
Kinins

Front 51

what do prostaglandins do

Back 51

constrict

Front 52

what do kinins do?

Back 52

dilates arteriols
constricts venules

Front 53

what do histamines do?

Back 53

dilates arterioles
constricts venules

**similiar to kinins

Front 54

tell me some things about capillaries

Back 54

large SA
holes (fenestrations)
slow velocity of blood
single layer of endothelium

**flow is constant, so SA increases and velocity decreases

Front 55

what does histamine do to a capillary

Back 55

opens fenestrations
fluid retention/imflammation

Front 56

what the diff btwn the SM on the arteriole before a capillary bed and hte precapillary sphincter

Back 56

SM on Arteriole: sensitive to neuronal stim

Precapillary sphincter: ONLY responds to local metabolites

Front 57

are precalpillary sphinceters usually open or closed

Back 57

most are closed at rest, open during exercise to let the whole capillary system to perfuse

Front 58

does nutritive flow occur when precap sphincters are open or closed

Back 58

open, more blood is flowing through

Front 59

what happens to arterioles and precap sphincters when O2 decreases and CO2 increases

Back 59

precap sphincters relax and allow the capillary bed to perfuse (increased SA),
Arterioles dilate, which increases capillary flow (good thing PCS opened up!)

*net, more O2 is delivered nad more CO2 is cleared

Front 60

what drives movement of materials across capillaries

Back 60

diffision, conc grad

Front 61

PCS

Back 61

at the junction of arterioles/capillaries

Front 62

do true capillaries have SM

Back 62

NOPE! they are made of a single layer of SM

Front 63

Pc

Back 63

hydrostatic P of capillary

**moves water OUT of the capillary

**met by capillary oncotic Pressure

Front 64

what is the major force that dirves fluid OUT of the capillary?

will this favor filtration or abs

Back 64

hydrostatic capillary

Filtration

Front 65

Pi

Back 65

interstitial hydrostatic Pressure

**force that pulls water into the capillary, minor

Front 66

does filtration occur at the venous or arterial end? what drives this

Back 66

filtration driven by capillary hydrostatic P (Pc) at arteriole end

Front 67

does reabsorption occur at the arteriole or venous end? what drives it

Back 67

reabs at venous end, driven by capillary oncotic P (pi c)

Front 68

what happens if there is less force driving fluid into the venous end of capillary bed?

Back 68

edema, no reabsorption, occurs if protein concentration in the blood decreases

Front 69

what is capillary hydrostatic pressure

Back 69

BP in capillary that drives fluid OUT of capillary, strongest at arteriole end

Front 70

what is the driving force of fluid INTO the capillary

Back 70

the colloid oncotic pressure of the capillary

**all of the proteins concentrated in the venule tend to bring water INTO the capillary on the venule end

(pi P)

**usually pretty constant in healthy ppl. our plasma proteins dont really change

Front 71

what is the interstitial fluid hydrostatic P
(Pif)

Back 71

small force that wants to drive fluid into the capillary

Front 72

what is the interstitial fluid colloid osmotic P

Back 72

its a small force that tries to drive fluid OUT of the capillary at the venule end

**plays a big role when histamine is released, prevents reabsorption and lets fluid accumulate in the tissue

Front 73

what factors favor filtration

Back 73

Capillary Hydrostatic (major)
interstitial oncotic

Front 74

what factors facor reabs

Back 74

1. capillary colloid (major)
2. interstitial hydrostatic

Front 75

how is net filtration/abs caclulated

Back 75

filtration forces - reabs forces

**if + filtration is favored
** if - reabs is favored

Front 76

what is bulk flow good for?

Back 76

regulating volume differences btwn ECF and interstitial fluid

Front 77

what happens to capillary flow with hemmorage

Back 77

plasma volume is reduced so there in increased reabsorption

**a reduction in volume will increase capillary oncoid P and drive reabs

Front 78

when we determine normal filtration and reabs there is always a bit more filtered thatn reabsorbed, why

Back 78

LYMPH

*one way flow, valves

Front 79

what increases filtration

Back 79

1. increased hydrostatic P of capillary: caused by increased arterial P
2. decreased plasma proteins
3. Increased interstitial oncotic pressure: bad lymph fx

Front 80

what effect does increased arterial P have on filtration

Back 80

increased filtration

Front 81

whats the neat way interstitial fluid that was not reabsorbed enters lymph vessels to become lymph

Back 81

well, lymph vessels have overlapping endothelium, there is a pressure that opens the flap, once in fluid exerts a pressure that wont allow it to leave

**lymph is carried unidirectionally back to circulation

Front 82

what does lymph do

Back 82

returns filtered fluid
immunity
transport of absorbed fats
return filtered protein

Front 83

how much lymph is carried a day? blood?

Back 83

lymph: 3 L/day

Blood: 7200L/day

Front 84

if liver disease stops making albumin what happens?

Back 84

well, plasma oncotic pressure decreases and fluid wont be reabsorbed, this leads to fluid accumulatio in the tissues: EDEMA

Front 85

what effect does histamine have on capillary abs/filt

Back 85

increased permiability, plasma proteins can enter interstitium, this increases interstitial oncotic pressure and so decreases reabs

Front 86

how does increased venous pressure affecet capillary filt/reabs

Back 86

capillary hydrostatic pressure increases and so filtration is favored. EDEMA

Front 87

what happens when lymph vessels are blocked

Back 87

EDEMA
excess fluid is retained in interstituim rather than being returned

Front 88

name 4 things that cause edema

Back 88

1. reduced plasma protein
2. increased capillary perm
3. increased venous pressure
4. blocked lymph vessels

Front 89

what are capacitance vessels

Back 89

veins, resevoid for blood

Front 90

composition of veins

Back 90

thin walls
less SM
less elssticity
less tone
more collagen
highly distendable
high capacitiance

Front 91

how does the stretch of art and ven compare

Back 91

arterires: stretch then recoil

veins: stretch and accomadate (capacitance)

Front 92

name 4 things that increase venous return to the heart

Back 92

1. CO: generates pressure grad for flow
2. SNS Vasoconstriction: increases venous P for a larger P grad, decreases capacitance of veins
3. Sk mm Pump/Valves
4. Respiration

Front 93

whats it called when you block lymph vessels

Back 93

elphantitis!
lymph collects in interstitium, EXTERME edema