Physio Exam 3 Questions General

Front 1

What is arterial pressure dependent on?

Back 1

arterial blood volume and arterial compliance
ΔP = ΔV/Compliance

Front 2

What is peripheral runoff?

Back 2

Transfer of blood to the venous circulation during diastole

Front 3

What is peak aortic pressure equal to?

Back 3

systolic pressure

Front 4

What is Pressure in aorta just prior to ventricular ejection equal to?

Back 4

diasolic pressure

Front 5

What is the cardiac output/pressure/resistance relationship?

Back 5

Cardiac output = ΔP/R
or
CO=ΔP/total peripheral resistance
or
CO=MAP/total peripheral resistance

All say the same thing

Front 6

What are the major determinants of Mean Arterial Pressure?

Back 6

CO and TPR

Front 7

How can cardiac output be altered?

Back 7

by influencing Stroke volume (SV) and heart rate (HR)

(This will subesquentyl alter MAP)

Front 8

Magnitude of the pulse pressure and systolic pressure are determined mainly by what factors?

Back 8

stroke volume and the aortic compliance.
ΔP = ΔV/Compliance

Front 9

At a constant compliance, aortic pulse pressure and arterial pressure have what relationship with stroke volume?

Back 9

If pressures increase, stroke volume will increase
ΔP = ΔV/Compliance

Front 10

At a constant stroke volume if aortic pulse pressure and arterial pressure
increase, what is happening to compliance?

Back 10

decreasing
ΔP = ΔV/Compliance

Front 11

Describe the effect on pressure, volume, at constant compliance if:
there is an increase in stroke volume

Back 11

ΔP = ΔV/Compliance

there will be a greater increase in aortic volume -> increasing pulse pressure -> which means an increase in Systolic Pressure

(Peak aortic pressure = systolic pressure )

Front 12

Describe the effect on pressure, volume, at constant compliance if:
there is a decrease in stroke volume

Back 12

ΔP = ΔV/Compliance

a smaller increase in aortic volume
means a smaller pulse pressure = decreased systolic pressure

(Peak aortic pressure = systolic pressure )

Front 13

Describe the effect on pressure, and compliance (at constant volume) if:
there is an INCREASE in compliance

Back 13

ΔP = ΔV/Compliance

decrease in pulse pressure = decrease systolic pressure

Front 14

Describe the effect on pressure, and compliance (at constant volume) if:
there is an DECREASE in compliance

Back 14

ΔP = ΔV/Compliance
increase in pulse pressure = increase systolic pressure

Front 15

Diastolic Pressure is mainly influenced by what factors?

Back 15

Heart Rate (time for blood to transfer)
Total Peripheral Resistance (rate of blood volume transfer)

Front 16

What two factors will affect the volume of blood remaining in the arterial system at the end of the diastolic period?

Back 16

Heart Rate
Total Peripheral Resistance

Front 17

Increased HR has what effect on Diastolic Pressure?

Back 17

decreased time for run-off, yields greater arterial volume remaining at the end of diastole which results in an increased DP

Front 18

Decreased HR has what effect on Diastolic Pressure?

Back 18

increased time for run-off, yields less arterial volume remaining at the end of diastole which results in a decreased DP

Front 19

Increased TPR has what effect on Diastolic Pressure?

Back 19

lower rate of run-off -> greater arterial
volume remaining at the end of diastole, INCREASE in DP

Front 20

Decreased TPR has what effect on Diastolic Pressure?

Back 20

Greater rate of run-off -> lower arterial
volume remaining at the end of diastole, DECREASE in DP

Front 21

Where is the greatest pressure drop seen in the vessels? what causes it? how much?

Back 21

Arterioles
Greatest resistance
~ 55mmHg

Front 22

Adjusting the radii of arterioles supplying organs can have what impact?

Back 22

distribute cardiac output
and regulate blood pressure

Front 23

What is the technique for measuring Pulmonary capillary wedge pressure (PCWP) and what does it equal?

Back 23

Swan-Ganz catheter
– inserted into large vein (femoral, etc.)
– allows measurement of flow, pressure
– passed into rt. atrium, rt. ventricle, pulmonary artery.
– balloon inflates, blocks flow from right side, records
pressures from left atrium…

=Left atrial Pressure

Front 24

How much blood volume can be stored in the venous system

Back 24

up to 75%

Front 25

Venous return is equal to what other factor at steady state?

Back 25

Cardiac Output

Front 26

What is the pressure gradient for venous return?

Back 26

the difference between peripheral venous pressure (pressure of blood entering peripheral veins from capillaries) and right atrial pressure

Front 27

What are the forces on the veins when standing?

Back 27

hydrostatic pressure and vascular pressure

Front 28

What are the effects of standing on cardiac output?

Back 28

Upon standingm blood from thorax drops to lower extremities increasing capillary hydrostatic pressure
Venous return decreases; cardiac output and mean arterial pressure fall transiently.
Neurally-mediated reflexes are activated to return mean arterial pressure towards the supine level.

Muscle pump helps this process

(standing too long will result in fluids moving into the intersitim and edema can occur)

Front 29

What is Muscle Pump?

Back 29

When standing, skeletal muscles of lower extremities begin rhythmic cycles of contraction and relaxation.
• Reflex initiated by stimulation of plantar surface of the feet.
Augments venous return

Front 30

Where is the greatest pressure drop seen in the vessels? what causes it? how much?

Back 30

Arterioles
Greatest resistance
~ 55mmHg

Front 31

Adjusting the radii of arterioles supplying organs can have what impact?

Back 31

distribute cardiac output
and regulate blood pressure

Front 32

What is the technique for measuring Pulmonary capillary wedge pressure (PCWP) and what does it equal?

Back 32

Swan-Ganz catheter
– inserted into large vein (femoral, etc.)
– allows measurement of flow, pressure
– passed into rt. atrium, rt. ventricle, pulmonary artery.
– balloon inflates, blocks flow from right side, records
pressures from left atrium…

=Left atrial Pressure

Front 33

What is the approximate pressure in the venous system

Back 33

0-6mmHg

Front 34

How much blood volume can be stored in the venous system

Back 34

up to 75%

Front 35

Venous return is equal to what other factor at steady state?

Back 35

Cardiac Output

Front 36

What is the pressure gradient for venous return?

Back 36

the difference between peripheral venous pressure (pressure of blood entering peripheral veins from capillaries) and right atrial pressure

Front 37

What are the forces on the veins when standing?

Back 37

hydrostatic pressure and vascular pressure

Front 38

What are the effects of standing on cardiac output?

Back 38

Upon standingm blood from thorax drops to lower extremities increasing capillary hydrostatic pressure
Venous return decreases; cardiac output and mean arterial pressure fall transiently.
Neurally-mediated reflexes are activated to return mean arterial pressure towards the supine level.

Muscle pump helps this process

(standing too long will result in fluids moving into the intersitim and edema can occur)

Front 39

What is Muscle Pump?

Back 39

When standing, skeletal muscles of lower extremities begin rhythmic cycles of contraction and relaxation.
• Reflex initiated by stimulation of plantar surface of the feet.
Augments venous return

Front 40

What is "stressed" blood volume?

Back 40

The volume of blood in the arteries that produces pressure by stretching fibers of the blood vessel walls

Front 41

What is "unstressed" blood volume?

Back 41

the volume of blood in the veins that produces no pressure. The veins can store about 4L of blood unstressed unless compliance changes alter their holding capacity forcing more to the stressed side

Front 42

What factors influence mean systemic pressure?

Back 42

blood volume and distribution of blood (how much in stressed vs unstressed)

Front 43

What are the Secondary Mechanisms for Enhancing Venous Return?

Back 43

Muscle Pump and respiratory pump

Front 44

What is respiratory pump?

Back 44

it is Increasing the rate and depth of respiration that promotes venous return and therefore enhances cardiac output by increasing venous return, increasin EDV and increasing SV
(Lecture 31, slide 8)

Front 45

Cardiac output (CO) depends...

Back 45

pre-load, which is a function of right atrial pressure (RAP)

Front 46

What happens to cardiac output when right atrial pressure goes up?

Back 46

end diastolic volume goes up which increases cardiac output

Front 47

What is the effect of Right Atrial Pressure on Venous return?

Back 47

if Pressure increases, atrial filling will decrease and venous return will decrease.

If pressure decreases, atrial filling will increase and venous return will increase

Front 48

What are the x and y axis on the The Cardiac Function Curve?

Back 48

the X axis represents end-diastolic
volume, and is represented as Right Atrial Pressure

The Y axis is the venous return represented as cardiac output (L/min)

Front 49

“Knee” of curve indicates what on a cardiac function curve?

Back 49

venous collapse and
impedence of blood flow

Front 50

What is the Mean systemic pressure on a cardiac function curve? Where is it represented?

Back 50

where venous return is zero, and right atrial pressure is maximal .
It is where the vascular function curve meets the X axis.

Front 51

When is Mean Systemic Pressure "measured".
What is the pressure amount?
What does it depend on?

Back 51

When the heart is stopped, it is the equalized pressure in all vascualr spaces.
~7 mmHg
Depends only upon total blood volume and vessel capacitance
P = V / C

Front 52

What does the equilibrium point of a Combined Cardiac and Vascular
Function Curve represent?

Back 52

it is the only Right arterial pressure where Cardiac Output & venous
return are equal.

Front 53

What does Increasing cardiac
inotropicity imply?

Back 53

increased contractility, increased stroke volume, increased cardiac output at lowe venous pressures

Front 54

Increasing cardiac inotropicity changes what curve(s) and points in the Combined Cardiac and Vascular
Function Curve in what way?

Back 54

The cardiac curve is rotated Counter-
clockwise.

The vascular function is not affected

The equilibrium point moves UP, and LEFT

Front 55

Decreasing cardiac inotropicity changes what curve(s) and points in the Combined Cardiac and Vascular
Function Curve in what way?

Back 55

The cardiac curve moves clockwise
the vascular curve doesn't change and the equilibrium point shifts DOWN and RIGHT

Front 56

Decreasing cardiac inotropicity implies what changes?

Back 56

A reduced CO at higher venous pressures...
decreased contractility,
decreased stroke volume,
decreased cardiac output
right atrial pressure is increased because less blood is ejected from heart on each beat

Front 57

Increasing Blood Volume changes what curve(s) and points in the Combined Cardiac and Vascular
Function Curve in what way?

Back 57

The cardiac curve doesn't change
the vascular curve moves parallel right and the equilibrium point shifts UP and RIGHT
Mean Circulatory Pressure INCREASES

Front 58

Decreasing Blood Volume changes what curve(s) and points in the Combined Cardiac and Vascular
Function Curve in what way?

Back 58

The cardiac curve doesn't change
the vascular curve moves parallel left and the equilibrium point shifts DOWN and LEFT
Mean Circulatory Pressure DECREASES

Front 59

Increasing PVR or TPR changes what curve(s) and points in the Combined Cardiac and Vascular
Function Curve in what way?

Back 59

The cardiac curve shifts clockwise
the vascular curve moves counter clockwise
the equilibrium point shifts DOWN
No change in Mean circulatory pressure

Front 60

Decreasing PVR or TPR changes what curve(s) and points in the Combined Cardiac and Vascular
Function Curve in what way?

Back 60

The cardiac curve shifts counter-clockwise
the vascular curve moves clockwise
the equilibrium point shifts UP
No change in Mean circulatory pressure

Front 61

Increasing blood volume implies what major changes?

Back 61

– increased mean systemic pressure
– increased cardiac output
– increased right atrial pressure

Front 62

Decreasing blood volume implies what major change?

Back 62

– decreased mean systemic pressure
– decreased cardiac output
– decreased right atrial pressure

Front 63

Decreasing or increasing venous compliance has similar implications to what variable on the cardiac vascular function curves?

Back 63

Blood loss or gain
Increase compliance is similar to decreasing blood volume
decreased compliance behaves like increasing blood volume

Front 64

Changing Ionotropy Involves moving what curve?

Back 64

The curve on the Y axis or the up sloping cardiac output/venous return curve

Front 65

What does increasing total peripheral resistance imply?

Back 65

Vasoconstriction which results in:
– increased volume in arteries
– increased afterload on heart
– depressed cardiac output
– less blood returning to heart
(a greater proportion is “trapped”
in the arteries)

Front 66

What are the ANS influences in teh heart?

Back 66

– chronotropicity - rate of rhythm (SA node)
– dromotropicity - velocity of conduction (AV node)
– inotropicity - contractility (rate of force development

Front 67

What is chronotropicity?

Back 67

rate of rhythm (SA node)

Front 68

What is dromotropicity?

Back 68

velocity of conduction (AV node)

Front 69

What is inotropicity?

Back 69

contractility (rate of force development)

Front 70

What type of innervation is Vagus? Where does it innervate in the heart?

Back 70

Parasympathetic
right vagus nerve innervates the SA node,
left vagus innervates the AV node
(conductile tissues)
with moderate overlap

Front 71

Where are Sympathetic efferent nerves present?

Back 71

throughout the atria (especially in the SA node) and ventricles, including the conduction system of the heart.

Front 72

Left Sympathetic fibers effect what factor?

Back 72

Contractility

Contractility is the same as ionotropy. Changes in inotropy result in changes in force generation. Increases in inotropic state help to maintain stroke volume at high heart rates. Increased heart rate alone decreases stroke volume because of reduced time for diastolic filling, which decreases end-diastolic volume. When the inotropic state increases at the same time, end-systolic volume decreases so that stroke volume can be maintained.

Front 73

Right Sympathetic fibers effect what factors in the heart?

Back 73

Rate and conduction

Front 74

Preganglionic sympathetic fibers release what NT?

Back 74

acetylcholine

Front 75

Postganglionic sympathetic fibers release what NT?

Back 75

Norepinepherine

Front 76

What do the adrenal glans release?

Back 76

Epinephernie

Front 77

Preganglionic parasympathetic fibers release what NT?

Back 77

acetylcholine

Front 78

Postganglionic parasympathetic fibers release what NT?

Back 78

acetylcholine

Front 79

What are the adernaergic subtypes of receptors found in the heart?

Back 79

B1,B2, a1

Front 80

What are the cholinergic subtypes of receptors found in the heart?

Back 80

Muscarinics (M2)

Front 81

Adernergic Subtypes of receptors belong to sympathetic or parasympathetic?

Back 81

Sympathetic

Front 82

Muscarinic Subtypes of receptors belong to sympathetic or parasympathetic?

Back 82

Parasympatheic

Front 83

What is reciprocal innervation?

Back 83

innervation so that the contraction of a muscle or set of muscles (as of a joint) is accompanied by the simultaneous inhibition of an antagonistic muscle or set of muscles

is how parasympatheics and sympathetic work together... Same for NE & Ach

Front 84

Which receptors/NT combos affect Chronotropicty? How?

Back 84

SNS, B1/NE increase funny current by increaseing Na+ conductanse and incrasing the slpoe of phase 4 so that threshold can be reached faster.

PNS M2/Ach to increase K+-Ach conductance and decrease If(funny current) to decrease the slope of thepacemaker in phase and hyperpolarize the maximum diastolic potential

Front 85

Which receptors/NT combos affect Dromotropicty? How?

Back 85

SNS= B1/Ne enhance conduction in AV node via Ca+ currents
PNS = M2/Ach decrease conduction velocity by decreasing Ca+ and increasing K+-Ach

Front 86

What are the chemical/ionic effects of SNS Stimulation on Inotropicity?

Back 86

B1/NE receptors increase the I(Ca+) conductance and phosporylation of phospholamban (Incrases SRCA-ATP) to recycle Ca2+ Fasterand increaess cAMP.
-phosporylating sarcolema ca+ channels stimulates calcium induced calcium release
-increases the rate of Ca2+ re-uptake

Front 87

What are the general/overall effects of SNS Stimulation on Inotropicity?

Back 87

Positive ionotropicity such that at a given volume, pressure is greater
NE enhances velocity

Both factors result in a stronger contraction

Front 88

Which system SNS or PNS is tonically active?

Back 88

Both, however PNS is dominant at rest

Front 89

What is atropine and propranolol?

Back 89

Atropine is a M2 antagonist
Propranolol is a B1 antagonist

Front 90

a1 has what effect on smooth muscle?
(skeletal, skin,renal, splanchic)

Back 90

constriction

Front 91

B2 has what effect on vascular smooth muscle (skeletal muscle)?

Back 91

Dilates
NE weakly,EPI more preferentially

Front 92

What affect does M2 have on contractility?

Back 92

it decreases it in the atria only

Front 93

What affect does M3 have on vascular smooth muscle?

Back 93

Dilation of vascualr endothelial cells
(increased intracellula Ca2+ and subsequent NO synthase activation and NP production)

Front 94

In General, what are the most important receptor types for the heart?

Back 94

B1,-most important sns
A1,-most important alpha
M2-major cardiac recptor

Front 95

A1 job on vascular smooth muscle?

Back 95

Vasoconstrict

Front 96

B2 job on vascular smooth muscle?

Back 96

vasodialate

Front 97

M3 job on vascular smooth muscle?

Back 97

Vasodialate

Front 98

Define vascular smooth muscle tone

Back 98

the contractile state of a resistance vessel is the vessel tone

Front 99

what are the driving forces to move blood?

Back 99

Systole and recoil are driving
forces to move the blood...arteries are Pressure resivoirs

Front 100

what is basal tone?

Back 100

the "theoretical" state of partial contraction independent of
metabolic and neural stimulation

Front 101

What is resting state (tone)?

Back 101

the actual physiological state of most resistance vessels such that they are constricted somewhat more than basal due to tonic sympathetic
nerve activity

Front 102

What is Active vasoconstriction?

Back 102

A decrease in vessel diameter due to sympathetic stimulation or
constrictor hormones/metabolites

Front 103

What is Active vasodilation?

Back 103

an increase in vessel diameter due to dilator nerves, hormones or
local factors

Front 104

What is Passive vasoconstriction ?

Back 104

return towards resting state from a dilated state due to the
removal of active dilator influences

Front 105

What is Passive vasodilation?

Back 105

return towards resting state from a constricted state due to the
removal of active constrictor influences

Front 106

Adenosine has what effect on vessle tone?

Back 106

Potent vasodialator

Front 107

What is vasoconstriction?

Back 107

increased contraction of smooth muscle in arteriolar which leads do decreased flow and increased resistance

Front 108

What is vasodialation?

Back 108

Relaxation of or decreased contraction of arteriolar smoothe muscle which increases flow and decreases resistance

Front 109

What controls Extrinsic factors of vascular tone?

Back 109

hormones and neural influences

Front 110

What controls intrinsic factors of vascular tone?

Back 110

Active and reactive hyperemias and auto-regulation mechnisms

Front 111

What is active Hyperemia?

Back 111

With increased metabolic activity, local metabolites accumulate and trigger dilation by inducing relaxation so more 02 can reach working muscle

Front 112

What are some vasodialators?

Back 112

• decreased O2
• increased CO2
• increased levels of K + ,PO4
, prostaglandins, lactic acid and
H + , adenosine, nitric oxide
• increased osmolarity

Front 113

Where doe vasodialators act?

Back 113

On arterial side... veins generally don't respond as they are non-stressed side and they aren't delivering the nutrients anyway

Front 114

What is Reactive hyperemia?

Back 114

When blood supply to a tissue is occluded, arterioles in the area dilate
After the occlusion is removed, blood flow to the deprived area is higher than normal because the arterioles are widely dilated.

This happens in heart and skeletal systems

Front 115

What is Autoregulation?

Back 115

he intrinsic tendency of an organ or tissue to maintain constant blood flow despite changes in arterial pressure, or the adjustment of blood flow through an organ in accordance with its metabolic needs.

Front 116

What organs can Autoregulate?

Back 116

heart, brain, kidneys, skeletal muscle

Front 117

What is the myogenic hypothesis or response?

Back 117

States that when vascular smooth muscle is stretched, it contracts in return
So if BP goes up, resistance will need to go up to keep flow the same or sonstant

Front 118

If blood pressure suddenly decreases what is the myogenic response?

Back 118

Vasodialation to decrease resistance to return flow to "normal"

Front 119

What is the effect of Vasopressin on vascular tone?

Back 119

AKA Anti Duiretic Hormne
– from pituitary
– vasoconstrictor
– increases water retention

Front 120

What is the effect of Atrial natriuretic peptide on vascular tone?

Back 120

– released from atria
– vasodilator
– counteracts hypervolemia

Front 121

What is the effect of Angiotensin II on vascular tone?

Back 121

– from angiotensin I
– vasoconstrictor

Front 122

The withdrawal of sympathetic adernergic activity causes...

Back 122

passive vasodilation

Front 123

What is the effect of Sympathetics on vascular tone?

Back 123

Sympathetic innervation produces either vasodilation (B2) or vasoconstriction (alpha 1)

Front 124

Parasympathetic Cholinergic Fibers have what NT/Receptor combo that effect vascular endothelial cells?

Back 124

M3/Ach
Vasodialates vascular endothelial cells by increased intracellular
Ca 2+ and subsequent activation of nitric oxide synthase and the
production of nitric oxide

Front 125

Angiotensin II is stimulated for release when? What does it do?

Back 125

Mean arterial pressure drops or extracellular volume drops
Vasoconstricts

Front 126

What causes Vasopressin release?

Back 126

rising plasma osmolality or falling blood pressure

Front 127

What causes Atrial Natriuretic Peptide (ANP) relase? Where is it stored?

Back 127

released with atrial stretch

Front 128

What causes Brain-type
Natriuretic Peptide (BNP) to be realsed? Where is it stored?

Back 128

released with ventricular pressure/volume overload (BNP)
made and stored in ventricular myocytes

Front 129

What are the effects of Atrial Natriuretic Peptide (ANP)/Brain-type
Natriuretic Peptide (BNP)?

Back 129

vasodilator action results from stimulation of guanylyl cyclase
activity in vascular smooth muscle

Front 130

What is the affect of Atrial Natriuretic Peptide in the kidneys?

Back 130

Increase Na + and water excretion
- ↓ body Na + content
- ↓ ECF volume & blood volume
- ↓ arterial pressure

Front 131

Where is epinephrine released from?
What are its effects?

Back 131

adrenal medullae
most tissues, vasoconstriction via α1/α2 receptors
skeletal muscle  vasodilation
due to higher concentration of β2
receptors and a greater affinity of β2 receptors for epinephrine

Front 132

Explain the role of the endothelium in the regulation of vascular smooth muscle tone

Back 132

Endothelial cells have receptors that elicit the release of vasoactive mediators which regulate
vascular smooth muscle tone

Front 133

What are the Endothelium-derived vasoactive substances?

Back 133

NO - Nitrous oxide
Endothelium-derived hyperpolarizing factor
Prostacylin (PGI2)
Endothelin
Prostaglandins
Kinins
Histamines

Front 134

How does NO - Nitrous oxide affect vascular tone?

Back 134

– gas released from endothelial cells stimulated by
shear-stress (flow-induced) and
neurotransmitters or local mediators that increase endothelial
cell intracellular calcium
– diffuses into vascular smooth muscle, then activates soluble
guanylyl cyclase, leading to increases in intracellular
concentration of cGMP, producing vascular smooth muscle relaxation

Front 135

How does Endothelium-derived hyperpolarizing factor affect vascular tone?

Back 135

– hyperpolarizes vascular smooth muscle, leading to relaxation

Front 136

How does Prostacylin (PGI2) affect vascular tone?

Back 136

Released by shear-stress (flow-induced) and NTs or local mediators that increase endothelial
cell intracellular calcium
– increases intracellular cAMP, leading to vascular smooth muscle
relaxation
– inhibits platelet aggregation

Front 137

How does Endothelin affect vascular tone?

Back 137

– most active vasoconstrictor
mediated via ETA receptors on vascular smooth muscle
– released in response to stretching of blood vessels

Front 138

How does Prostaglandins affect vascular tone?

Back 138

– produced by aggregating platelets
– acts directly on vascular smooth muscle, inducing vasoconstriction

Front 139

How do Histamines affect vascular tone?

Back 139

– stored in mast cells; released with mast cell degranulation

– relaxes arterioles and precapillary sphincters and increases
capillary permeability
– vasodilator action mediated by:
• H1 receptors on endothelial cells, which stimulates NO release
• H2 receptors on vascular smooth muscle, which increases intracellular cAMP
content

Front 140

How do Kinins affect vascular tone?

Back 140

– arteriole vasodilator (endothelial NO)
– cause venous contraction (direct on vascular smooth muscle or prostaglandin mediated)

Front 141

Histamine triggers release of what other endothelial factors?

Back 141

PGI2 and NO

Front 142

Describe the role of the precapillary sphincters

Back 142

They act as valves to control blood flow through the capillary bed
Metarterioles contain precapillary
sphincters which can shunt blood straight from arteriole through metarteriole to venule without entering the capilary depending on the need of the system
sensitive to local metabolites
only ~10-15% are open at a time

Front 143

What is non-nutritive vs. nutritive flow?

Back 143

Nutritve flose is when precapillary sphincters are open and exchange is taking place.

nonnutritive flow is when the sphincters a tighten and blood move through the metarteriol from the arteriole to the venule without entering the capillary and exchanging much

Front 144

What is diffusion in the capillary?

Back 144

passive, down the concentration gradient excange of O2 and glucose for CO2

Front 145

What is Bulk Flow?

Back 145

Movement of water and solutes
together due to a pressure gradient.
-protein-free plasma filters out and
mixes with the interstitial fluid
High capillary pressure favors filtration
High inward pressure favors reabsorption back into the capillary

Front 146

What are the 4 factors that
influence bulk flow ?

Back 146

• Capillary blood pressure
• Plasma-colloid osmotic pressure
• Interstitial fluid hydrostatic pressure
• Interstitial fluid-colloid osmotic pressure

Front 147

Plasma-colloid osmotic pressure is?

Back 147

the force caused by plasma proteins; encourages fluid movement
into the capillary

Front 148

Interstitial fluid hydrostatic pressure is?

Back 148

the fluid pressure exerted on the outside of the capillary wall
by the interstitial fluid normally not significant)

Front 149

Capillary blood pressure is?

Back 149

he fluid pressure exerted on the inside of the capillary wall by the blood that Forces fluid out (outward pressure)

Front 150

. Interstitial fluid-colloid osmotic pressure is?

Back 150

the force exerted by the small fraction of proteins that have leaked from the capillaries into the interstitium

become critical when proteins leak out in the presence of
histamine

Front 151

What is the Net exchange pressure equation?

Back 151

[Capillary blood pressure + Interstitial fluid colloid osmotic pressure] – [Plasma-colloid osmotic pressure + Interstitial fluid hydrostatic pressure]

+= Outward filtration
-=Inward resorption

Front 152

What happens to extra fluid not reabsorbed in the capillaries?

Back 152

It is taken up by the lymph system

Front 153

What is the lymph flow average a day?
How does this compare to blood flow?

Back 153

Lymph flow averages about 3 L/day, whereas blood flow averages 7200 L/day

Front 154

What 4 factors can increase edema?

Back 154

Reduced concentration of plasma proteins
Increased permeability of capillary walls
Increased venous pressure
Blockage of lymphatic vessels

Front 155

Venous return to the heart is enhanced by what factors?

Back 155

Cardiac output
Sympathetic-induced venoconstriction
Skeletal muscle pump and venous valves
Respiratory activity

Front 156

Describe the capillary wall...

Back 156

Thin capillary wall (1uM) consists of single layer of flattened endothelial cells with water-filled PORES

Front 157

What is the total surface area for diffusion of capillaries?

Back 157

(600 m 2 )

Front 158

How do substances cross the capillaries?

Back 158

Lipid soulble substances can cross through the endothelial cells (O2,C02)
Water soluble small particle can cross in the pores (Na+,K+,Glucose, AA)
Plasma proteins can't cross
Other proteins use vesicular transport

Release of histamine, either with injury or allergy, widens the pores
and contributes to fluid retention and inflammation

Front 159

Which organs systems get the most blood flow?

Back 159

kidneys and GI tract each
receive ~20-25% of cardiac
output

Front 160

What is Collateral circulation?

Back 160

adaptive response compensating for
slowly developing coronary artery disease where vesell makes or enhances alternate routes of flow

Front 161

What is the major control of blood flow in the coronary system?

Back 161

local metabolites

Front 162

What are the Vasoactive Metabolites of coronary circulation?

Back 162

– hypoxia (low oxygen)
– vasodilators
(adenosine, and NO most importantly), but also H+ & CO2
,
prostaglandins)

Front 163

What is the impact of the sympathetic nervous sysem on coronary cirulation?

Back 163

Minor

Front 164

What is the auto regulation range of the coronary system?

Back 164

50-60 mmHg to 150-160 mmHg
Below
Below the lower limit distal vessels will be maximally dilated and further reductions in pressure will lead to reductions in flow

Front 165

In the Coronary Circulation increase work will call for increase O2... How does the heart get its need met?

Back 165

by producing increased
vasodilator metabolites
– most notably adenosine

Front 166

Describe Reactive Hyperemia in the coronary circulation

Back 166

Brief occlusion of coronary vessel results in the accumulation of
vasodilator metabolites in the interstitium followed by a transient increase in coronary blood flow.
Magnitude and duration of extra flow dependent on the duration of the occlusion.

increased O2 delivery to repay O2
debt incurred during the compression

Front 167

Compression effect of systole occurs mainly in what vessle?

Back 167

the left coronary. This effect is
minimal on the RV as a result of lower pressures developed by the smaller
ventricular mass.

Front 168

What are the sypmatheic influences (receptos, etc) in Coronary Circulation?

Back 168

In the arterieols/arteries:
• NE -> a1 constrictor
• E ->B2 vasodilation
In the heart itseldm B1 stimulation increases heart rate

Front 169

Parasympathetic stimulation of the coronary vessles uses what mechanism and has what effect?

Back 169

Vasodialate via endothelia release of NO
Net goal is to reduce flow since Heart rate and o2 consumption are decreasing

Front 170

What is the autoregulation range for the Cerebral Circulation?

Back 170

(~same as coronary):
– 50-60 mmHg to 150-160 mmHg

Front 171

What is the Blood-brain barrier?

Back 171

ght junctions between
endothelial cells that prevents circulating vasoactive substances from affecting cerebral blood flow

Front 172

What is the blood volume like in Cerebral Circulation?

Back 172

Constant due to skull limiting space and braib neing incompressible

Front 173

What is the capillary density in cerebral circulation?

Back 173

High capillary density (3000 - 4000/mm 2 )

Front 174

What controlls Cerebral Circulation?

Back 174

Local Metabolites as a reslt of the METABOLISM occurring in the brain
Sympatheics have little influence

Front 175

What local metabolites are vasoactive in cerebral circulation?

Back 175

CO2 (Most Important)
H+ (Most Important)
Adenosine,
K+
NO

Front 176

What is the effect of increased Co2 or low pH (High H+ concentration) int he cerebral circulation

Back 176

They cause vasodialation to increase blood flow to remove excess Co2 and H+

Front 177

What is the effect of Adenosine in Cerebral Circulation?

Back 177

release from hypoxic tissues
dilates cerebral vessels

Front 178

What is the effect of K+ in Cerebral Circulation?

Back 178

K + released by active neurons can have a dilating action on cerebral vessels.
(If neurons are active they need more nutrients)

Front 179

What is the effect of NO in cerebra circulation?

Back 179

NO from endothelium and neurons/glia cells causes cerebral vasodilation.

Front 180

What is the Cushing Reflex?

Back 180

• Something (i.e., hemorrhage, tumor, injury) can increase intracranial pressure and compression of cerebral arteries resulting in decreased profusion in the brain.
Incrasing CO2 and low pH is sensed since metabolites aren't being removed due to inadequate flow. Medullary chemoreceptors direct an increase in sympathetics to increase TPR and Pressure.

Meanwhile, baroreceptors in the carotid arteries detect the increase in blood pressure and trigger a parasympathetic response via vagal stimulation, thereby inducing bradycardia. Bradycardia may also be caused by increased ICP impinging on the vagal nerve, mechanically stimulating a parasympathetic response.

Despite confilicting signals, bradycardia results

Front 181

What is Cushings Triad

Back 181

irregular respirations
Widening of pulse pressures
Bradycardia

Sign of intercranial pressure

Front 182

What happens if If perfusion pressure falls below the autoregulatory range (< 50-60 mmHg) in cerebral circulation?

Back 182

medullary vasomotor center becomes ischemic.
• Vasomotor neurons become strongly excited
Sympatheics are increased in a last ditche ffort to preserve blood flow

Front 183

What is the major controlling mechanisms of skeletal muscle circulation?

Back 183

Local metabolic control during exercise
Sympathetic control at rest

Front 184

Describe the sympathetic innervation of skeletal muscle at "rest"

Back 184

High resistance set by sympathetic innervation of
• α1receptors – vasoconstriction (predominant), basal tone
however
• β2 receptors – vasodilation (minimal) at rest

Front 185

Describe Skeletal muscle circulation with Exercise

Back 185

Low resistance set by local metabolites
increase levels of lactate,adenosine and K + from exercising muscle nearby causes dialation
B2 receptor activation via epinephrine produces vasodilation;
this action significant during exercise

Front 186

How does Intermittent flow during exercise effect Skeletal Muscle Circulation?

Back 186

during activity muscle pump lowers the venous pressure which increases the pressure gradient driving flow.

Front 187

What is the principal function of Cutaneous Circulation?

Back 187

Heat loss control (Predominant)
then, blood pressure volume/resivoir and Nutrient flow

Front 188

What are the Two types of resistance vessels in cutaneous circulation?

Back 188

Arteriovenous anastomoses (AVAs)
Arterioles

Front 189

What do Arteriovenous anastomoses (AVAs) do? Where are the located?

Back 189

AVAs allow blood to bypass cutaneous capillaries
AVAs open when
body heated or during prolonged
cold exposure

located in fingers, toes, palms, soles, lips, nose, ears

Front 190

What is the role of Arterioles in cutaneous circulation?

Back 190

high density of α-adrenergic receptors causing sypatheic vasoconstriction.
lack of SNS stimlation will cause reactive vasodialation

Front 191

How do the sweat glands contribute to vasodialation?

Back 191

sympathetic cholinergic (vasodilator) innervation is
prominent to sweat glands  causes formation of
bradykinin
– bradykinin mediates “active” vasodilation

Front 192

What is the significance of the Venous Plexus?

Back 192

– contains greatest cutaneous blood volume -acts as a reservoir
– important for heat transfer
– receives sympathetic nervous system vasoconstrictor innervation.

Front 193

What is Cold-Induced Vasodilation

Back 193

– when temperature falls, smooth muscle becomes
paralyzed and vasodilation occurs

Front 194

What is the effect of Physical compression (e.g. sitting) on cutaneous circulation?

Back 194

ischemia causes accumulation of metabolites which stimulates
nociceptors incrase pain makes person shift weight so reactive
hyperemia can occur

Front 195

What is the effect of epinephrine on cutaneos circulation?

Back 195

It is a vasoconstrictor activating a1 receptors

Front 196

What are the 3 Rapid controllers of blood pressure?

Back 196

• Arterial Baroreceptors
• Cardiopulmonary Baroreceptors
• Peripheral Chemoreceptors

Front 197

What is the of of the Nucleus tractus solitarius? Where is it located?

Back 197

– Sensory nucleus in the dorsomedial part of the brainstem (medulla).
– Receives most afferent information.
– Acts as integrator.

Front 198

Where are Arterial Baroreceptors located?

Back 198

Aorta and carotid sinuses
They respond to stretch or mean pressure and most strongly to srterial pressure

Front 199

What is the neural pathway for arterial baroreceptors?

Back 199

Afferents from baroreceptors travel to the brainstem via the vagus and glossopharyngealnerves.
– integrated in the nucleus tractus solitarius (NTS)
– Efferent output from the CNS is via the vagus or sympathetic nerves.

Front 200

What is the response of the baroreceptor to and increase in arterial pressure?

Back 200

Increase parasympatheic via vagus to decrease heart rate to decrease contractility (by lovering sympathic innervation) and decrease cardiac output. Decrease in SNS also decreases TPR which increases unstressed volume

Front 201

How do baroreceptors work?

Back 201

more or less stretch changes membrane potential. they have a 'set" point" they not olny respond to pressure changes, but how fas that change happens
this HTN cans me seen as 'normal' if its consistantly high

Front 202

How can The integrity of the baroreceptor reflex can be tested ?

Back 202

Valsalva maneuver
Should see:
Increased MAP due to pressure upon the thoracic aorta then
Decrease in MAP due to a decrease in venous return
Decrease in MAP immediately following the release of maneuver due to a fall in intrathoracic ressure
Rebound in blood pressure due to an increase in venous return and an increased stroke volume in addition to vasoconstriction

Front 203

What is the effect of HTN on the Baroreceptor reflex?

Back 203

“resets” it to a higher setpoint
• Maintains elevated
pressure

exercise, diet and RX can reverse

Front 204

Where are Cardiopulmonary Baroreceptors usually located?

Back 204

low pressure areas of the cardiovascular system
(e.g., atria, veins, pulmonary arteries)

Front 205

How do Cardiopulmonary Baroreceptors work?

Back 205

They sense the "fullness" of vascualr systrem *thats why they are on the veous side as that is where most of blood isheld*
They primarily work to decerase blood volume by increasing excretion of Na+ and water:

Front 206

What responses can Cardiopulmonary Baroreceptors control? (in example of increased blood volume)

Back 206

Incrased secretion of atrial naturiet peptide (ANP)- vasodiation, increased Na+ secretion
Decreased secreetion of ADH
Renal Vaodialation
Increasing heart rate via Bainbridege reflex.

Front 207

What is the Bainbridge Reflex?

Back 207

also called atrial reflex, acceleration of the heart rate resulting from increased blood pressure in, or increased distension of, the large systemic veins and the right upper chamber of the heart.

Front 208

How do Peripheral Chemoreceptors work?

Back 208

Activated by decreased O2
(hypoxia), CO2(hypercapnia)
and decreased pH (acidosis).
Results in sns arterolar vasoconstriction and temprary PNS decrease in HR
Information integrated in the brain stem (NTS)

Front 209

Which is stronger Baroreceptors or Chemoreceptors?

Back 209

Baroreceptors

Front 210

What are the Intermediate Controllers of Blood pressure?

Back 210

• Capillary fluid shift
• Renin-Angiotensin-Aldosterone
System
• Vasopressin
• Atrial Natriuretic Peptide

Front 211

How does vasoconstriction effect capillary fluid shift?

Back 211

decreasing pressure in the capillaries -> favors absorption -> increased intravascular volume -> results in increased arterial pressure.

Front 212

How does vasodialation effect capillary fluid shift?

Back 212

increasing pressure in the capillaries -> favors filtration-> decreases intravascular volume -> results in decreased arterial pressure.

Front 213

How does the Renin-Angiotensin-Aldosterone system work to affect blood pressure?

Back 213

• Renin release simulated by a decrease in blood pressure, reduced sodium flux, or ympathetic
stimulation.
• Renin cleaves angiotensin I from angiotensinogen, a plasma globulin.
• Angiotensin I is converted to angiotensin II by angiotensin converting enzyme (ACE) in the lungs.
• Angiotensin II is a vasoconstrictor (increases TPR) and stimulates aldosterone release from adrenal cortex.
• Aldosterone increases Na + /H2
O absorption in kidney which increases intravascular volume.

Front 214

What are the Long Term Controls of Blood Pressure?

Back 214

Renal–Body fluid System
If Arterial presure increase, renal system will put out more water and salt then consumed to maintian equilibrium
• If arterial pressure decreases below the equilibrium point renal
output of salt and water falls below intake until pressure returns to the equilibrium point.

Front 215

What is the bodies response to Hemorrhage?

Back 215

Loss of blood volume reduces venous return and therefore cardiac output
• Maintenance of MAP is required
• Baroreceptor response is immediate:
– increased heart rate ( CO)
– increased contractility ( SV,  CO)
– increased TPR
– increased venoconstriction ( unstressed vol.)

Front 216

What is the role of Renin-Angiotensin II-Aldosterone system in a hemmorage situation?

Back 216

– Angiotensin II is a pressor, and it stimulates release
of aldosterone
– Angiotensin II also stimulates thirst centers
– Aldosterone increases Na + reabsorption

Front 217

What is the effect of Vasopressin in a hemorrhage situation?

Back 217

Vasopressin levels increase if blood loss is large enough (> 10 % blood volume) causing vaso constriction

Front 218

What is the effect of Capillary fluids in in a hemorrhage situation?

Back 218

move fluids into vascular space

Front 219

What is the cardiovascualr response to changes in Posture? Ex. Standing

Back 219

• On standing, blood pools in veins of lower extremities.
• Venous return is reduceds CO & MAP
• Standing also increases hydrostatic pressure in
veins and increases filtration into the interstitium,
with loss of intravascular volume – reduces venous return
• Baroreceptor reflex increases sympathetic outflow to heart and blood vessels, parasympathetic outflow to heart is reduced