1-20 Circulatory System Flashcards Preview

PHYSIOLOGY Exam 1 > 1-20 Circulatory System > Flashcards

Flashcards in 1-20 Circulatory System Deck (79):
1

A: Venous Return= Rate at which blood Returns TO [______ and ______] FROM peripheral ______ in the body

B: [Central Venous Pool] or CVP= Blood Volume enclosed in __ ______ and [______ ______ ______]. Is often associated with ______ Pressure and is Clinical index of ______ & [______] functioning as a team.
[Normal CVP= __ mmHg. ] _____ will cause blood to back up into this pool.

C: Cardiac Output = The rate at which blood LEAVES the ______ and is pumped out of the heart. **Normal Cardiac Output = ___ L/min. **

D: In Normaly "______-state" conditions ---> Liters of [______ ______] should = Liters of [Cardiac Output]

E: Blood RETURNING to heart travels like:
[Venous Return]---> ______----->Cardiac Output in Heart

F: 60% of our Blood Volume is in ______ system because it is HIGHLY compliant and has ______ [Total Cross Section Area]

G: INC Smooth Muscle = ______ Compliance

A: Venous Return= Rate at which blood Returns TO [Thorax and CVP] FROM peripheral vascular beds in the body

B: [Central Venous Pool] or CVP= Blood Volume enclosed in R Atrium and [Thorax Great Veins]. Is often associated with Jugular Pressure and is Clinical index of Cardiac & [Vascular] functioning as a team.
[Normal CVP= 2 mmHg. ] CHF will cause blood to back up into this pool.

C: Cardiac Output = The rate at which blood LEAVES the CVP and is pumped out of the heart. **Normal Cardiac Output = 5 L/min. **

D: In Normaly "steady-state" conditions ---> Liters of [Venous Return] should = Liters of [Cardiac Output]

E: Blood RETURNING to heart travels like:
[Venous Return]--->CVP----->Cardiac Output in Heart

F: 60% of our Blood Volume is in Venous system because it is HIGHLY compliant and has LARGE [Total Cross Section Area]

G: INC Smooth Muscle = DEC Compliance

2

A: [Mean Circulatory Pressure]= "______" of the circulatory system and is normally __mm Hg. It's dependent on [______] AND [______ muscle ______ tone(which determines ______ capacity).] MCP is the pressure that exist in Circulatory system when ______ ______ STOPS and ______ pressures redistribute

B: When [Central Venous Pressure] = [Mean Circulatory Pressure] this is ______(good/bad) because there'll be NO ______ to maintain ______ Return and Blood flow will ______. [Central Venous Pressure should be ______(HIGHER/lower) than [MCP].

C1: INC Cardiac Output ---> ______ CVP because _________. When CVP ______--->INC pressure gradient for venous return--> ______ Venous Return.

C2: If Cardiac Output is TOO HIGH then CVP will become ______ ----> transmural pressure that will ______ the large veins ---> STOPS ______ ______

A: [Mean Circulatory Pressure]= "Fullness" of the circulatory system and is normally 7 mm Hg. It's dependent on [Volume of circulating blood] AND [Smooth muscle VENOUS tone(which determines system capacity).] MCP is the pressure that exist in Circulatory system when Cardiac output STOPS and vascular pressures redistribute

B: When [Central Venous Pressure] = [Mean Circulatory Pressure] this is BAD because there'll be NO GRADIENT to maintain Venous Return and Blood flow will STOP. [Central Venous Pressure should be LOWER than [MCP].

C1: INC Cardiac Output ---> DEC CVP because Heart is pulling more blood out of the pool. When CVP DEC--->INC pressure gradient for venous return-->INC Venous Return.

C2: If Cardiac Output is TOO HIGH then CVP will become NEGATIVE ----> transmural pressure that will COLLAPSE the large veins ---> STOPS VENOUS RETURN

3

A: INC Venous Return has the ability to
* ______ [End-Diastolic Volume]
* ______ Stroke Volume
* ______ Cardiac Output
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B: Things that [INC Venous Return] by altering pressure gradient between ______ and ______ venous pressure

1. Respiratory Pump = during deep inspiration [-] intra-______ pressure(______ CVP) and [+]abd pressure create [pressure gradient] for blood to flow --> ______ Venous Return!

2. INC ______ Volume
3. INC [Peripheral ______ PRESSURE] using Cardiac ______
4. INC Sympathetic ______ AND ______

5. Cardiac ______ caused by actual Cardiac ______
6. Skeletal ______ muscle ______ pressing against Veins
7. [Unidirectional Venous VALVES] which prevent backflow
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B2: Which of the above DEC Central venous Pressure? [1 and 5]
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C: What is VENOConstriction = DEC Compliance of ______ to make it more "Stiff". --->Helps to Shunt blood back to heart

D: Varicose Veins occurs when [______ Venous VALVES] become defective and allow blood to backflow and pool in the LE

A: INC Venous Return has the ability to
*INC [End-Diastolic Volume]
*INC Stroke Volume
*INC Cardiac Output
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B: Things that [INC Venous Return] by altering pressure gradient between peripheral and Central venous pressure

1. Respiratory Pump = during deep inspiration [-] intra-thoracic pressure(DEC CVP) and [+]abd pressure create [pressure gradient] for blood to flow --> INC Venous Return!

2. INC Blood Volume
3. INC [Peripheral Venous PRESSURE] using Cardiac Contraction
4. INC Sympathetic VasoConstriction AND VENOConstriction

5. Cardiac Suction caused by actual Cardiac Contraction
6. Skeletal Leg muscle Pump pressing against Veins
7. [Unidirectional Venous VALVES] which prevent backflow
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B2: Which of the above DEC Central venous Pressure? [1 and 5]
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C: What is VENOConstriction = DEC Compliance of Vein to make it more "Stiff". --->Helps to Shunt blood back to heart

D: Varicose Veins occurs when [Unidirectional Venous VALVES] become defective and allow blood to backflow and pool in the LE

4

A: Equilibrium between [Cardiac Output] and [______] is always maintained even during sudden changes. INC ______ will INC Cardiac Output because by INC Cardiac output you will bring ______ back down to 2 mmHg from pulling more blood out of the pool.

B1: TRANSFUSIONS INC Fluids in the ______ system
--->INC ______ ______ to heart---->INC preload ---->INC Cardiac Output. Cardiac Output will ______ with Transfusions BUT so will CVP because there's more ______ ______. ______ does not INC significantly .
Transfusions INC equilibrium point between [______ ______] and [______]

B2: VENOConstriction will also do this because it INC ______ volume of ______ in the venous system

C: Hemorrhage OR [______ Venous tone] will shift equilibrium point between [Cardiac Output] and [CVP] ______ and to the ______---> There will be less Cardiac Output at a ______[higher/lower] CVP.

D: Hemorrhage is temporarily addressed by..

1. Cardiac ______ Stimulation when it senses [Cardiac Output] ______. It Shifts [Cardiac Function curve] ______ and to LEFT---> ______ [Cardiac Output] and DEC CVP(which DEC CVP is ok because [______ ______] is at least being restored)
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2. Venous ______ Stimulation which shifts [Venous Function Curve] ______ and to ______ which ______ [Cardiac Output] and very slightly ______ CVP

A: Equilibrium between [Cardiac Output] and [CVP] is always maintained even during sudden changes. INC CVP will INC Cardiac Output because by INC Cardiac output you will bring CVP back down to 2 mmHg from pulling more blood out of the pool.

B1: TRANSFUSIONS INC Fluids in the Venous system--->INC Venous Return to heart---->INC preload ---->INC Cardiac Output. Cardiac Output will INC with Transfusions BUT so will CVP because there's more Venous Return. CVP does not INC significantly .
Transfusions INC equilibrium point between [Cardiac Output] and [CVP]

B2: VENOConstriction will also do this because it INC relative volume of fluid in the venous system

C: Hemorrhage OR [DEC Venous tone] will shift equilibrium point between [Cardiac Output] and [CVP] DOWN and to Left. There will be less Cardiac Output at a lower CVP.

D: Hemorrhage is temporarily addressed by the..
1. Cardiac Sympathetic Stimulation when it senses [Cardiac Output] Decrease. It Shifts [Cardiac Function curve] UP and to LEFT--->INC CO and DEC CVP(which DEC CVP is ok because CO is at least being restored)
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2. Venous Sympathetic Stimulation which shifts [Venous Function Curve] UP and to RIGHT which INC CO and very slightly INC CVP

5

Factors Affecting VENOUS Function

A: Changing ______ Volume (______ vs. ______)

1. Transfusion INC ______ Volume---> ______ Venous Return
2. Hemorrhage DEC ______ Volume ----> ______ Venous Return

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B: Venous Tone (with ______ Nervous System and ______)
1. INC Venous Tone/VENO_____ ---> _____ Venous Return
2. DEC Venous Tone/veno_____-----> ______ Venous Return

C: [Cardiac Output] is affected by changes in ______ Function, ______ Function...OR BOTH!

Factors Affecting VENOUS Function

A: Changing Blood Volume (Transfusion vs. Hemorrhage)
1. Transfusion INC Blood Volume---> INC Venous Return
2. Hemorrhage DEC Blood Volume ---->DEC Venous Return

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B: Venous Tone (Sympathetic NS and Drugs)
1. INC Venous Tone/VENOConstriction--->INC Venous Return
2. DEC Venous Tone/venodilation----->DEC Venous Return

C: [Cardiac Output] is affected by changes in CARDIAC Function, VENOUS Function...OR BOTH!

6

Factors Affecting CARDIAC Function
1: ______ Stimulation
2: ______ Drugs
3: Heart Failure ---> ______ [Cardiac Function Curve]

B: [Cardiac Output] is affected by changes in ______ Function, ______ Function...OR BOTH!
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C: 18% of our Blood Volume is held in ______ which have ______ compliance and SMALL [Total Cross Section Area]

Factors Affecting CARDIAC Function
1: Sympathetic Stimulation
2: Inotropic Drugs
3: Heart Failure --->DEPRESSES [Cardiac Function Curve]

B: [Cardiac Output] is affected by changes in CARDIAC Function, VENOUS Function...OR BOTH!
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C: 18% of our Blood Volume is held in Arteries which have LOW compliance and SMALL [Total Cross Section Area]

7

A: At Normal Blood volume, Heart Failure [Cardiac Output] ______ and [CVP] ______

PB: When Blood Volume is Increased (Hypervolemia)..
1)Moderate Heart Failure ______ CVP but Cardiac Output is ______

2) SEVERE Heart Failure ______ CVP AND ______ [Cardiac Output]

A: At Normal Blood volume, Heart Failure [Cardiac Output] DEC and [CVP] INC as a result

PB: When Blood Volume is Increased (Hypervolemia)..
1)Moderate Heart Failure INC CVP but Cardiac Output is restored to normal

2) SEVERE Heart Failure INC CVP AND DEC [Cardiac Output]

8

A: What are the 4 Things that affect Cardiac Output?
1. PreLOAD
2. AFTERLOAD
3. Contractility
4. HR
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B: What is Poiseuille's Law? = applies to ______ flow of ______ fluids through cylindrical tubes. Can only be slightly applied because Cardiovascular system has ______ blood with ______ diameter tubes.

B2: 3 Formulas:
{FLOW = [(r^4) x ______] / [L ______] }

{RESISTANCE= [L x ______] / (r^4) ] }

{FLOW = ______ / RESISTANCE}

C: Poiseuille's Law [F= ______ diff/______] is analogous to ______ Law which states [I = V/R]

D: Length can be adjusted by ______

E: Most important determinants of Blood FLOW are ______ which usually CONSTANT ...and ______ which with small changes can cause LARGE changes to blood FLOW in tissue! = Blood FLOW is regulated by manipulating ______...not ______

A: 4 Things that affect Cardiac Output:
1. PreLOAD
2. AFTERLOAD
3. Contractility
4. HR
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B: What is Poiseuille's Law? = applies to laminar flow of Newtonian fluids through cylindrical tubes. Can only be slightly applied because CV system has non-newtonian blood with varying diameter tubes.
B2: 3 Formulas:
{FLOW = [(r^4) x (P1-P2)] / [L xViscosity] }

{RESISTANCE= [L x Viscosity] / (r^4) ] }

{FLOW = (P1-P2) / RESISTANCE}

C: Poiseuille's Law [F= Pressure diff/Resistance] is analogous to Ohm's Law which states [I = V/R]

D: Length can be adjusted by GROWING MORE VESSELS like what occurs in Obesity!

E: Most important determinants of Blood FLOW are [(P1-P2)] which usually CONSTANT ...and [(r^4)] which with small changes can cause LARGE changes to blood FLOW to tissue! = Blood FLOW is regulated by manipulating RESISTANCE...not pressure

9

A: Viscosity = "lack of ______" OR Internal ______ ______ that occurs between ______ layers within blood. Blood loses Energy to ______ as it travels FROM ______ because [Blood Elements] bounces around in different layers ---->DEC in ______ as it travels FROM ______

A2: Viscosity Formula = [______ ______ ______ / Shear ______ ______]. Measured in Poise

A3: (Shear PRESSURE ______)= PRESSURE created from resistance to ______ between laminae

A4: (Shear velocity rate)= velocities between the ______ or velocity of ______ flow
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B1: ______ Blood flow is siLent and occurs when fluid moves in ______ ______ layers vs. ______ Blood Flow which is Noisy and is a ______ pattern of fluid movement

B2: Turbulent flow can occur with:
1)murmurs & Bruits (______ noise caused by Turbulent flow thru a ______)
2) damage to ______ lining
3) thrombi
4) Korotkoff sounds = Normal sounds made when taking ___
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C: Outer layer of blood has ______ velocity because it has ______ Viscosity due to ______ with Vessel Wall. Inner layer has ______ Velocity. This concept together creates a ______ profile with max velocity at ______ axis. The lower the viscosity the ______ the parabolic profile

D: VISCOSITY is only present in ______ FLUID because ______ is a determinant. ______ Fluid has NO VISCOSITY!

A: Viscosity = "lack of slipperiness" OR Internal Frictional resistance that occurs between adjacent layers within blood. Blood loses Energy to Friction as it travels FROM Aorta because [Blood Elements] bounces around in different layers
---->DEC in Pressure as it travels FROM Aorta

A2: Viscosity Formula = [Shear PRESSURE STRESS / Shear velocity rate]. Measured in Poise

A3: (Shear PRESSURE STRESS)= PRESSURE created from resistance to mvmnt between laminae

A4: (Shear velocity rate)= velocities between the laminae or velocity of blood flow
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B1: Laminar Blood flow is siLent and occurs when fluid moves in parallel concentric layers vs. Turbulent Blood Flow which is Noisy and is a disorderly pattern of fluid movement
B2: Turbulent flow can occur with:
1)murmurs & Bruits (swishy noise caused by Turbulent flow thru a stenosis)
2) damage to endothelial lining
3) thrombi
4) Korotkoff sounds = Normal sounds made when taking BP
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C: Outer layer of blood has slowest velocity because it has higher Viscosity due to resistance with Vessel Wall. Inner layer has HIGHEST Velocity. This concept together creates a Parabolic profile with max velocity at central axis. The lower the viscosity the SHARPER the parabolic profile

D: VISCOSITY is only present in MOVING FLUID because [Shear velocity rate] is a determinant. Static Fluid has NO VISCOSITY!

10

A: Blood is NOT a ______ fluid because ______ of blood does NOT remain constant over a range of [Shear PRESSURE STRESS] and [Shear velocity rates]. Plasma ______[IS/(is NOT)] a Newtonian Fluid.
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B: Hematocrit = Ratio of ______ to ______ in Blood.
[INC Hematocrit = ______ Blood VISCOSITY]. Normal Hematocrit is ______% which means ______% of our blood is RBC. anemia creates ______ hematocrit vs. Polycythemia which creates ______ Hematocrit.

C: Axial Streaming = Tendency of ______ to accumulate in the [______ axis ______]

D: Plasma Skimming = Normal occurrence of smaller vessels containing More ______ and less ______ due to ______ ______. Plasma Skimming ---> hematocrit is ______ in smaller vessels.

A: Blood is NOT a Newtonian fluid because Viscosity of blood does NOT remain constant over a range of [Shear PRESSURE STRESS] and [Shear velocity rates]. Plasma IS a Newtonian Fluid.
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B: Hematocrit = Ratio of RBC to Plasma in Blood.
[INC Hematocrit = INC Blood VISCOSITY]. Normal Hematocrit is 35-50% which means 35-50% of our blood is RBC. anemia creates low hematocrit vs. Polycythemia which creates HIGH Hematocrit.

C: Axial Streaming = Tendency of RBCs to accumulate in the [central axis laminae]

D: Plasma Skimming = Normal occurrence of smaller vessels containing More Plasma and less RBC due to Axial Streaming. Plasma Skimming ---> hematocrit is lower in smaller vessels.

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A: [Reynold's Number] is a value that indicates propensity for ______ blood flow and thus the chances MD will hear a ______ or ______. ______ has HIGHEST [Reynold's Number] because it has highest Diameter and ______. Higher NR = Higher chance of hearing a ______

A2: Formula for [Reynold's Number]?

B: During BP taking...The cuff squeezes ______ artery and when released will INC blood ______--->INC ______ ______ and thus allow MD to hear [______ sounds]

A: [Reynold's Number] is a value that indicates propensity for turbulent blood flow and thus the chances MD will hear a Bruit or murmur. AORTA has HIGHEST [Reynold's Number] because it has highest Diameter and velocity. Higher NR = Higher chance of hearing a Bruit

A2: Formula: "Reynold loved DvD divided by VISCOSITY"
[NR= Density x velocity x Diameter / VISCOSITY

B: During BP taking...The cuff squeezes brachial a. and when released will INC [blood flow velocity]--->INC NR and thus allow MD to hear [Korotkoff sounds]

12

Blood ______ is INVERSELY related to [Total Cross-Section Area] .

A: In Larger Blood Vessels DECREASING Diameter ---> ______ Velocity because there is a ______ [Total Cross Section Area] and blood has no where else to go except thru the smaller hole

B: In smaller blood vessels with HIGH [Total Cross Section Area] DECREASING Diameter --> ______ Velocity because
1. Pressure is LOW in small "circuits"
2. blood can travel in parallel vessels and doesn't have to "rush" thru a small hole all at once.

C: Slowest Blood flow occurs in ______ ______ because it has LARGEST [______. When blood travels from ______
--->Venous system the ______ will start to INC again

[Blood Flow velocity] is INVERSELY related to [Total Cross-Section Area] .

A: In Larger Blood Vessels DEC Diameter = INC Velocity because there is a low [Total Cross Section Area] and 1 vessel and blood has no where else to go except thru the smaller hole

B: In smaller blood vessels with HIGH [Total Cross Section Area] DEC Diameter = DEC Velocity because
1. Pressure is LOW in small circuits
2. blood can travel in parallel vessels and doesn't have to "rush" thru a small hole all at once.

C: Slowest Blood flow = Capillary bed because it has LARGEST [Total Cross Section Area]. When blood travels from Capillaries --->Venous system the Velocity will start to INC again

13

[______ Principle] (AKA ______ ______ Effect) describes how (in a constant flow system like the ______) Total Energy has to remain constant [PE + KE = TE].

A: [Potential Energy] = [______ ______ Pressure] which ______(+) or ______(-) on blood vessel walls

B: [Kinetic Energy] = ______ of Blood Flow

C: When KE INC then PE has to ______. If Vessel Area DEC like in ______---> INC KE [because PE is converted into KE] ---> DEC PE = (- ______ ______ ______ that will ______ on vessel walls). This demonstrates one of the abnormal cases in which Blood flows from low pressure(______ region) ----> HIGH PRESSURE areas ______.

C2:Blood will ALWAYS flow from ______ Energy ---> ______ energy. Because stenosis region has ______ being converted into ______ for greater velocity thru stenosis, it will have HIGHER TOTAL energy than downstream!

D: THIS SAME effects occurs when blood flows from ______ -->Aorta. Ventricular Contraction converts ______ into ______ which gives ______ more TOTAL energy than aorta downstream. This allows blood to move AGAINST its ______ ______ because it will always flows from ______ Energy--> ______ energy

[Bernoulli Principle] (AKA Shower Curtain Effect) describes how (in a constant flow system like the Aorta) Total energy has to remain constant [PE + KE = TE].

A: PE = [Transmural Lateral Pressure] which PUSHES(+) or pulls(-) on blood vessel walls

B: KE = Velocity of Blood Flow

C: When KE INC then PE has to DEC. If Vessel Area DEC like in Stenosis---> INC KE because PE is converted into KE ---> DEC PE = (- TLP that will pull on vessel walls). This demonstrates one of the abnormal cases in which Blood flows from low pressure(stenosis region) ----> HIGH PRESSURE areas downstream.

C2:Blood will ALWAYS flow from High Energy ---> low energy. Because stenosis region has PE being converted into KE for greater velocity thru stenosis, it will have HIGHER TOTAL energy than downstream!

D: Same effects occurs when blood flows from LV -->Aorta. Ventricular Contraction converts PE into KE which gives LV more TOTAL energy than aorta downstream. This allows blood to move AGAINST its pressure gradient because it will always flows from High Energy-->low energy

14

A: What is [Laplace relationship]? This is [______ ______] = force that PULLS vessels walls ______ from the ______ and works AGAINST ______. [WALL TENSION] has to be kept low because its easier to ______ AND if [WALL TENSION] INC too much---> Vessel wall __________

A2: Formula for [Laplace relationship]?
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B: Capillaries have small radius and so they have ______ wall tension. This means they can withstand ______ [Transmural Lateral Pressures] TLP

A: What is [Laplace relationship]? This is [WALL TENSION] = force that PULLS vessels walls OPEN from the Outside and works AGAINST constriction/contraction. [WALL TENSION] has to be kept low because its easier to Vasoregulate AND if INC too much---> Vessel wall is pulled too much and will rupture!

A2: Formula for [Laplace relationship]:
Wall Tension= [Pressure x Radius / (Wall thickness) ]
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B: Capillaries have small radius and so they have low wall tension. This means they can withstand HIGH [Transmural Lateral Pressures] TLP

15

A: For Series Resisters..The TOTAL RESISTANCE = __________. This means each daughter resister is ______ than TOTAL RESISTANCE.
A2: Example of Series Resister = ______

B: In the Body, ______ are the main site of arterial resistance and regulate ______.

A: For Series Resisters..The TOTAL RESISTANCE = all the daughter resisters added up. This means each daughter resister is LESS than TOTAL RESISTANCE.
A2: Example of Series Resister = ARTERIOLES

B: In the Body, ARTERIOLES are the main site of arterial resistance and regulate pressure.

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A: Example of ParaLLeL Resister = ______. In ParaLLeL Resisters Each [daughter resister alone] is ______ than the TOTAL RESISTANCE

B: Even though Capillaries have small radius, they have the ______ RESISTANCE since they have the LARGEST __________----> ______ blood flow.
Capillaries contain only a small drop in pressure because they have ______ resistance.

A: Example of ParaLLeL Resister = Capillaries. In ParaLLeL Resisters Each [daughter resister alone] is STRONGER than the TOTAL RESISTANCE

B: Even though Capillaries have small radius, they have the LOWEST RESISTANCE since they have the LARGEST [Total Cross section area]---->slowest blood flow.
Capillaries contain only a small drop in pressure because they have low resistance.

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1: [Arteriole's] are the PRIMARY RESISTER and Vasoregulator because they have THICK walls and small radius = low wall tension. This allows them to vasoregulate even under HIGH TLP. Arteriolar's contain the Largest Drop in arterial pressure.

2: During an Aneurysm, Radius INC---->LARGE WALL TENSION. --->unable to withstand (+) [Transmural Lateral Pressures] pushing on walls --->will rupture
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3A: In Dilated hearts, Radius INC--->LARGE WALL TENSION--->unable to withstand high afterload--->more systolic work required and INC in oxygen consumption to overcome the LARGE WALL TENSION resisting contraction

3B:*** Efficiency of Heart = [Cardiac Output] / [Oxygen Consumption] ***

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A: [Pulse Pressure] is pressure difference between Systolic and Diastolic pressure = AFTERLoad. [Pulse Pressure] WIDENS as you move further from the heart because Compliance DECREASES. This is why the R arm has a higher BP than L arm because it is further from heart---> has lower Compliance and thus WIDER [Pulse Pressure]

B: [Mean Arterial Pressure] DEC as you move further from the heart and is based primarily on DIASTOLIC PRESSURE.

C: There is NO [Pulse Pressure] in capillaries and veins.

D: 3 Possible causes of NATURAL WIDENING [Pulse Pressure] as you move from heart
1. DEC in arterial compliance

2. Reflection at branch points=fluid hits branch point but reflects backwards-->will summate with new oncoming fluid

3. Vascular Tapering= More Vascular branches as you travel from the heart--->Force fluid into smaller spaces

E: Compliance = [@Volume] / [@pressure]

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A: Arteries are typically STIFF with low compliance. They have an [Internal Elastic lamina] which allows them to Extend & Recoil. AORTA has the most [Internal Elastic Lamina]-->Dicrotic notch.. but it doesn't have much smooth muscle.
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B1: ALL Vessel Walls have a Tunica ADVentitia ---> Tunica Media ----> Tunica intima

B2: ALL Vessel Walls AND lymphatic vessels are lined by endothelial cells
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C: Aorta Vessel Walls (OUTSIDE--->in)
1) Tunica ADVentitia = Fibroblast--->Connective Tissue--->[vasa vasorum vessel] & some smooth m.

2) Tunica Media = [External elastic lamina]---->[Circular smooth muscle]

3) Tunica intima = [Internal Elastic lamina] ---> [Subendothelial layer] ----> [Endothelial layer](innermost)

D: Arteries have More Smooth muscle and have Elastic Lamina while veins DO NOT

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A: Veins are FLAT until they're filled with blood--->Pops then open. Veins DON'T DISTEND because they have HIGH Compliance.

B1: ALL Vessel Walls have a Tunica ADVentitia ---> Tunica Media ----> Tunica intima

B2: ALL Vessel Walls AND lymphatic vessels are lined by endothelial cells
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C: VENOUS Vessel Walls (OUTSIDE--->in)
1) Tunica ADVentitia = Fibroblast--->Connective Tissue--->[vasa vasorum vessel] & some smooth m.

2) Tunica Media =WEAK [Circular smooth muscle]

3) Tunica intima = [Subendothelial layer] ----> [Endothelial layer](innermost)
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D: When Veins VENOconstrict = makes wall more STIFF but doesn't actually close the Vein down.

E: Veins have more [Tunica ADVentitia/Connective Tissue] than arteries

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List the Order of Compliance
1: lowest compliance (stiff) = [Collage Connective Tissue]
2: MEDium Compliance = Smooth Muscle
3: HIGHEST Compliance = [Elastic Lamina]

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A: [Continuous Capillaries] are Endothelial cells with NO [fenestration holes] in the capillary wall. They use tight junctions between cells and have a continuous [basal lamina]. CC is found in muscle & Connective tissue
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B: [Fenestrated Capillaries] are [Continuous capillaries] WITH [fenestration holes] and sometimes diaphragms. They ALSO have continuous [basal lamina] but are found in Kidney & Intestine--->USED to filter and reabsorb
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C: [Discontinuous Sinusoidal Capillaries] are Endothelial cells separated by WIDE spaces. They have DISCONTINUOUS [basal lamina] and are found in
*liver = large proteins can get out
*spleen = RBC can get out
*Bone Marrow = WBC can get out

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1. [Arteriole pre-capillary Sphincters] have the THICKEST Walls and therefore have best control of vessel diameter & blood flow.

2. Veins regulate Volume and not blood flow since they have large lumens with thin walls.

3. DEC Compliance ----> WIDENS Pulse Pressure. Widening Pulse Pressure is bad because [Pulse Pressure]= AFTERLoad = Arterial Pressure. This will make the Heart work Harder to contract from lower starting diastolic value to an even Higher Systolic Value in order to open Aortic Valve

4. INC Volume ---> DEC compliance of blood vessel. This is because increase in load is first borned by the [Elastin] and then [Smooth muscle] and then [Collage Connective Tissue] which has a low compliance already. This will all cause --->INC Pressures. Ex: Blood Volume Expansion--->HTN

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A:Describe the [Windkessel Hydraulic Filter] =
Ejected LV [Stroke Volume] is 1st temporarily stored by elastic distention of Aorta. When Aorta recoils it acts as secondary pump to create blood flow during diastole. When Aorta is stiff/less compliant--->Pulse Pressure is WIDER----> heart has to use more O2 !

B: Age-related changes in Aortic Compliance
1. INC Age ---> DEC Aortic compliance because you'll have less Elastic and less [Collage Connective tissue]

C: WIDENED [Pulse Pressure] over time can turn into CHF and also contributes to [Systolic HTN], Cardiac hypertrophy ,aortic dilation and low exercise tolerance!

D1: Veins can accommodate a Large amount of Blood Volume while still maintaining low pressure (10 mmHg) which makes it [Capacitance Vessels].

D2: BUT AT HIGHER ARTERIAL PRESSURES Veins exhibit a DEC in their strong compliance. This is why Saphenous veins can be used as coronary bypass grafts.

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A: [pressure PULSE]= ARTERIAL Pressure you feel when taking someone's PULSE. [pressure PULSE] is GREATER in small arteries and made by [PULSE waves] propagating down the Arteries. [pressure PULSE] velocity depends on arterial compliance.

B: DEC Compliance ---> WIDER [Pulse Pressure]---> INC (velocity of [pressure PULSE] wave propagation) --> INC [pressure PULSE]

C: Femoral Artery will have HIGH [pressure PULSE] because it is further from the heart ---> low Compliance!

D: [pressure PULSE] waves travel down the aorta at 5 m/second and will INC to 15 m/sec in smaller arteries! [PULSE waves] develop as a result of Rapid Blood EJECTION through the Aorta

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1. Pressure Gradient = Pressure differential between inflow and Outflow

2. Hydrostatic Pressure= Pressure caused by the Height of a Fluid Column
--------------------------------------------------------------------------------------
3. [Mean Arterial Pressure] = Avg Pressure within the Aorta and [proximal arteries] during 1 cardiac cycle
3B: [MAP] Formula = DIASTOLIC PRESSURE + 1/3[Pulse Pressure]
3C: Can be adjusted by [Cardiac Output] and [Total Peripheral Resistance]
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4A: Physiological influences on [Mean Arterial Pressure] can BOTH be changed by the [Baroreceptor Reflex]:
*Cardiac Output = Affects SYStolic Pressure and regulated by Sympathetic AND PARAsympathetic

*peripheral resistance= affects MOSTLY diastolic pressure and regulated BY ONLY SYMPATHETIC. Local PR regulation ALWAYS OVERRIDES Global PR regulation.
**BUT INC [peripheral resistance] INC BOTH DIASTOLIC and sympathetic (with DIASTOLIC being affected more!)
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4B: PHYSICAL influences on [Mean Arterial Pressure]
*Blood Volume affects Stroke Volume and arterial compliance

*Arterial Compliance affects BOTH SYStolic AND diastolic pressures. Dependent on Blood Volume, location, age, sympathetic tone & Pregnancy

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A: Exercise INC Systolic Pressure and diastolic pressure remains constant UNTIL INTENSE Exercise-->DEC diastolic. Therefore, [Pulse Pressure] WIDENS and MAP INC

A2: During Exercise [Heart & Brain] Cardiac Output distribution DON'T CHANGE. Blood Flow to skin initially INC with regular exercise but then DEC with INTENSE Exercise.

Blood is diverted from [Kidneys, Splanchnics and inactive muscle] during Exercise

A3: Exercise is regulated by the Sympathetic NS
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B: CHF, Infarct, bradycardia & sepsis all DEC BP
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C: INC [peripheral resistance]---->INC BOTH Systolic and diastolic (although diastolic is affected more)

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A: [Total Peripheral Resistance] is affected by Blood Viscosity and [ARTERIOLAR RADIUS].
[ARTERIOLAR RADIUS] can be manipulated from a [Local intrinsic] level or [Global EXtrinsic] level.

**List the [local intrinsic] Control for [ARTERIOLAR RADIUS]**
B: [local intrinsic]
1. Myogenic response
2. [EDRF (Endothelium-Derived Relaxing Factor), NO & endothelin]
3. Local metabolite changes (DEC O2, INC CO2, Adenosine)--->vasoDilation
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C: *[Nitric Oxide] acts via [cGMP/PKG] to phosphorylate [myosin light chain kinase]-->which BLOCKS MLCK and prevents it from working --> vasoDilation. [Nitric Oxide] is derived from NITROGLYCERIN! It can be released by
-endothelium
-neurons
-glial cells

*[endothelin] receptors on vascular smooth muscle cells activate [phospholipase C]-->releases IP3--->releases intracellular Ca+ for vasoCONSTRICTION

*Metabolite ADENOSINE opens up same K+ channels ACh opens with muscarinic receptors--->INC AV nodal conduction time via hyperpolarization--->Turns off inward Ca+ currents---> [Breaks Dysrhythmia in heart] and [relaxes smooth muscle].

D: ADENOSINE has a short half-life, CLOSES [Ca+ channels] and is derived from ATP! It's RAPIDLY created during:
* O2 imbalance / hypOxia
*hypOtension
*seizures
*electrical stimulation

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A: [Total Peripheral Resistance] is affected by Blood Viscosity and [ARTERIOLAR RADIUS].
[ARTERIOLAR RADIUS] can be manipulated from a [Local intrinsic] level or [Global EXtrinsic] level.

**List the [Global EXtrinsic] Control for [ARTERIOLAR RADIUS]**
B: [Global EXtrinsic]

1. Baroreceptor Reflex
2. Hormones (Angiotensin, ADH, Epi)-->vasoconstrictors
3. Sympathetic NS ([+]=vasoconstriction / [-] = vasodilation)
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C: Angiotensin is the most powerful VasoCONSTRICTOR Hormone in the body. It is apart of the [Global EXtrinsic] control of Arteriolar Radius--->INC [Total Peripheral Resistance]

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A. How does Sympathetic NS INC Blood Pressure
1. VasoCONSTRICTION of Arterioles -->INC [Total Peripheral Resistance] ---> INC diastolic BP
2. VeNOCONSTRICTION of Veins--->INC [Venous Return]
--->INC SYStolic BP
3. INC HR and INC Contractility-->INC [Stroke Volume]---> INC [Cardiac Output] ---> INC BP

A2: When Sympathetic NS INC HR to its MAX--->[Stroke Volume] will soon DEC because of DEC filling times!
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B: How does PARAsympathetic NS DECREASE Blood Pressure
•DEC HR--->DEC [Cardiac Output] ---> DEC BP

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A: [Metabolic vasoDilation] DEC Vascular Resistance and INC blood flow in metabolically active skeletal muscle and Heart. The change in Vascular Resistance depends on Exercise level and mass of active muscle. Although [Metabolic vasoDilation] works well there is some [Global Sympathetic vasoConstriction] slightly blocking metabolic vasoDilation

B: Examples of [Local Metabolic vasodilators]
1. K+
2. INC CO2
3. H+
4. Adenosine

C: [Capillary recruitment] occurs when capillaries open up in active muscles for INC blood flow

D: During exercise, O2 consumption INC---> [oxyhemoglobin dissociation curve] shifts RIGHTWARD
--->less O2 held by hemoglobin when passing thru active muscle! This also INC [arteriovenous] O2 differences.

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[T or F]
The Heart can INC oxygen extraction from Hemoglobin during exercise


FALSE!
The Heart can NOT INC oxygen extraction from hemoglobin during exercise!

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A: PreCapillary resistance vessels =
1st. Arterioles

2nd. MetaArterioles = SHUNTS BLOOD FROM [Arterioles] to [POSTCapillary venules] and do NOT exchange CO2 and O2

3rd. [PREcapillary sphincter]
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B: Exchange Vessel = Capillaries

C. POSTCapillary resistance vessels = venules

D: Edema = Accumulation of Fluid in the interstitial space between tissues and vessels. Often caused by

*[DEC plasma proteins](less than 2.5 g)<----CHF

*INC capillary permeability (burns)

*mechanical obstruction (pregnancy)

D2: Edema examples: Ascites & Pulmonary edema

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A: Capillary Blood Flow is:
1. low velocity

2. intermittent vasomotion

3. directional [due to pressure gradients]

4. NOT UNIFORM

5. [Rouleaux formation] = RBC are stacked up and TOUCHES capillary membranes because capillary diameter is small--->easy O2/CO2 diffusion across membrane
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B: 4 Factors govern [Transcapillary Fluid Exchange] (AKA Starling Hypothesis)

1. [Plasma Oncotic Pressure]= usually NON-CHANGING pressure exerted by [Albumin Plasma proteins] responsible for keeping fluid INSIDE the Capillary bed = 25 mm Hg

2A. [Capillary Hydrostatic Pressure]= variable [mean capillary blood pressure] that PUSHES FLUID OUT!. Typically 32 mm Hg & VERY HIGH in Kidneys for filtration. Is dependent on both HIGH [PREcapillary arterial resistance] and low [POSTCAPILLARY venous resistance].

2B:Venous pressure has LARGE effect on [CHP] because there's low [POSTCAPILLARY venous resistance]
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3. [Tissue Oncotic Pressure]= osmotic pressure exerted by proteins in the INTERSTITIUM. Is typically 0 in value (because there's not many proteins OUTSIDE Capillary bed in interstitium) and is [Plasma Oncotic Pressure] counterpart
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4. [Interstitial Hydrostatic Pressure]= Water pressure exerted by Fluid Volume within the Interstitium. Is typically Low but WHEN HIGH = EDEMA
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C:When [Capillary Hydrostatic Pressure] is LOWER than [Plasma Oncotic Pressure] -----> ABSORPTION

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A: Lymphatic Vessels surrounding Capillary Bed takes leaked capillary fluid from interstitium and UNIDIRECTIONALLY shunts it back to [subclavian veins] using thin valves-->DEC interstitial fluid accumulation.

**Burns damage lymphatic vessels & INC Capillary permeability --->Blisters and Edema!

A3: Lymphatic Vessels are [non-fenestrated endothelium] with little basal lamina and NO SMOOTH MUSCLE. Lymph Flow depends on capillary filtration, skeletal muscle activity (INC capillary hydrostatic fluids) and UNIDIRECTIONAL VALVES
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B1: [Plasma Oncotic Pressure] is mostly generated by [Albumin!] which even though it's concentrated at 51% in blood it exerts 65% of [Plasma Oncotic Pressure]!
B2:This is because [Albumin] interaction with negative [Cl-] will pull [Na+] and thus retain fluids!

C: Other factors contributing to [Plasma Oncotic Pressure] include Globulin and fibrinogen

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1. INC [PREcapillary arterial resistance]---->DEC [Capillary Hydrostatic Pressure] because there's more inward flow!

2. INC [POSTCAPILLARY venous resistance]---->INC [Capillary Hydrostatic Pressure] because outward flow is restricted--->Fluid BACKED UP. Occurs often in Heart Failure
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A: How do Prostacyclins induce vasoDilation?
Prostacyclins INC cAMP to phosphorylate [myosin light chain kinase], which will BLOCK IT! No MLCK--->No constriction---->relaxation and vasoDilation

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A: How does hypoxia induce Tachycardia?
low O2 stimulates INC ventilation--->causes stretch receptors in Lung to CENTRALLY INHIBIT [Efferent Vagal Nerve activity]---->INC HR

B: In Theory, [Efferent Vagal nerve activity] -->Bradycardia and the [Sympathetics]--->vasoconstriction when arterial chemoreceptors sense [[low O2/low pH/HIGH CO2]] but TACHYPNEA WILL CHANGE ALL OF THIS by centrally INHIBITING [Efferent Vagal nerve activity]---->Tachycardia !

C. [Carotid Body] contains HIGHEST Blood flow because it contains chemoreceptors which constantly monitor O2 and CO2 levels. These chemoreceptors are activated when [low O2] and [HIGH CO2] occurs simultaneously-->Shifts curve Up and To RIGHT

D: Arterial [Chemoreceptors] are found in [Aortic Arch] and [Carotid Body] which sits medial to [Carotid Sinus] near [BaroStretch receptors]. They MOSTLY affect Respiratory system by INC [rate & depth of breathing] and are NOT activated by small O2 fluctuations (ONLY SEVERE).

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A: [Basal Arterial Tone] = THEORETICAL reference point at which vascular system is NORMALLY contracted without neural or hormonal/extrinsic influences
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B1: [Resting Sympathetic Tone] =Vascular Contraction on top of [Basal Tone] found at rest AS A RESULT OF TONIC SYMPATHETIC activity.

B2: Resistance is Higher than [Basal Arterial Tone] due to tonically-released NorEpi and [Resting Sympathetic Tone]
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C: Difference between ACTIVE mechanisms and passive mechanisms
C1: [ACTIVE mechanism]= any mechanism PULLING Vascular resistance AWAY from [Basal Arterial Tone]

C2: [passive mechanism] = any mechanism RETURNING Vascular resistance back TO [Basal Arterial Tone] After it's been adjusted

ex. Sympathetics can ACTIVELY VasoDilate Skeletal m. during Exercise and DEC Vascular Resistance but by inhibiting Sympathetics --> passive constriction

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A: [Sympathetic Adrenergic Receptors] are stimulated by Epi, NorEpi and [Isoproterenol]. There are 3 Adrenergic Receptors

1. [alpha 1] = located on vascular smooth muscle and CAUSES VASOCONSTRICTION when activated by NorEpi. Coronary and cerebral vessels have LITTLE vasoCONSTRICTION regulation

2. [Beta 1]= Mostly in Heart --> INC HR and INC contractility when stimulated ---> INC Coronary Blood Flow

3. [Beta TWO]= MOSTLY in VASCULAR SMOOTH MUSCLE but some in Heart ---> VasoDilation /// INC HR/INC Contractility. Used often in ASTHMA tx

B: List Exception in Which Sympathetic NS secretes ACh
**[Sympathetic NS] DOESN'T NORMALLY, but will secrete ACh POST-synaptically to VasoDilate sweat Glands AND activate [Piloerector m.] on back neck

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A: [PARAsympathetic fibers] activate muscarinic receptors with ACh but to only a limited amount of peripheral blood vessels. GENITALIA, bladder, large bowel and splanchnic vessels all VasoDilate when [PARAsympathetics] stimulate.
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1B. [Baroreceptor Reflex] is a NEGATIVE feedback loop that repairs both [Pulsatile phasic] and [constant static] changes in blood volume, [Cardiac Output] or [peripheral resistance]. It responds MORE to abrupt [Pulsatile phasic] changes!
**It uses [Stretch Baroreceptors] located in Walls of [Carotid Sinus] and [Aortic Arch] which both have little vascular smooth muscle.

1B: [Stretch Baroreceptors] INC their firing frequency when stretched by INC in arterial pressure. When stimulated they [ACTIVATE PARAsympathetics] and [inhibit sympathetics] ---> DEC HR and DEC BP

1C: [Stretch Baroreceptors] in Carotid Sinus ARE MORE SENSITIVE but both locations respond to DEC in Arterial pressure by allowing Sympathetics to take over and increase Arterial pressure by..---->
•peripheral vasoconstriction
•INC HR
•INC contractility

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A: When Pressure naturally falls during Diastole, [BaroStretch receptors] DEC firing rate EVEN THOUGH pressure is higher than their activating threshold ---> shows that [BaroStretch receptors] respond more to abrupt [Pulsatile phasic] changes

B: [Pulse Pressure] in the Carotid Sinus when Restored (and not damped) INC frequency of Sinus nerve firing ---> Better regulation of [Mean Arterial pressure]

C: HTN DECREASES sensitivity of [BaroStretch receptors] to [transmural pressure changes] because it INC activation threshold.

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A: [Renin-Angiotensin pathway] Keeps Blood Volume UP during LONG-term Dehydration. It does this when..

1. Renin is secreted by [Renal JGA] when [Afferent Renal Arterioles] sense a drop in [arterial pressure]

2. Renin Converts Angiotensinogen--->[inactive Angiotensin 1]

3. [inactive Angiotensin 1] is converted to [ACTIVE ANGIOTENSIN 2] by ACE from endothelial cells in Lung & Kidney !

4. [ACTIVE ANGIOTENSIN 2] is converted to [ACTIVE ANGIOTENSIN 3] by angiotensinases

5. [ACTIVE ANGIOTENSIN 2]:
*DIRECTLY VASOCONSTRICTS vessels,

*[AT 2&3] Stimulate Aldosterone release from [Adrenal Cortex] under permissive action of ACTH from [ANT Pit]

*Stimulates hypothalamus to activate thirst & secrete ADH(works on Collecting Ducts)
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C: [Renin-Angiotensin pathway] inappropriately responds to CHF because LONG-term DEC in [Cardiac Output] tricks [RAP] into thinking it's under LONG-term Dehydration--> INC Blood Volume --->INC BP and makes CHF worst

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A: Blood Flow is mostly controlled with Resistance Vessels and NOT by changing Blood Viscosity. There is a 4:1 ratio for [Arterioles:Venous] resistance
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B1: [Vascular Smooth muscle] controls [Total peripheral resistance], Arterial/Venous tone and Blood distribution throughout the body.
B2: Autoregulators include:
• [Local MYOgenic] and [Local metabolic] are the 2 MAIN Autoregulators
•[GLOBAL NEURAL/HORMONAL] -->Angiotensin & Epi
•[local endothelial]
•[local mechanical]
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C: Autoregulation is a mechanism that ensures constant blood flow even when gravity opposes [arterial perfusion pressure]. INC [Arterial pressure]---> INC STRETCH of [vascular vessel wall]---> INC [Arterial resistance/vasoCONSTRICT] which will DEC flow and return it to baseline [Capillary Hydrostatic Pressure]. VARIES IN DIFFERENT ORGANS and will occur whether Endothelium is there or not!

C2: Autoregulation FAILS at too low or too high pressures and so it does NOT work on Venous side!

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** [Local MYOgenic] and [Local metabolic] are the 2 MAIN Autoregulators**

A1: [Local MYOgenic] occurs when Vascular smooth muscle is stretched or relaxed. INC [Arterial pressure]---> INC STRETCH of [vascular vessel wall]---> INC [Arterial resistance/vasoCONSTRICT] which will DEC flow and return it to a baseline [Capillary Hydrostatic Pressure]

A2: DEC [Arterial pressure] will lead to exact opposite of [vascular vessel wall]-->
DEC [Arterial resistance/vasoDilation]--->INC flow

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** [Local MYOgenic] and [Local metabolic] are the 2 MAIN Autoregulators**
***[METABOLIC HYPOTHESIS] ***
B1st: [Local metabolic] hypothesis states that metabolic activity produces inhibitory metabolites like [Adenosine, H+ and CO2] which RELAX [Vascular Smooth muscle].

B2nd: INC [Arterial pressure]--->QUICK INC [Blood Flow] that washes [inhibitory metabolites] away-->vasoCONSTRICTION. vasoCONSTRICTION naturally INC resistance-->DEC blood flow

B3rd: DEC [Arterial pressure]---->DEC [Blood Flow]. This will allow [inhibitory metabolites] to accumulate around the vessel and vasoDilate them! vasoDilation--->DEC resistance----(eventually)---> INC [Blood Flow]

C: INC [Arterial Pressure]---(ULTIMATELY)----> DEC [Blood Flow] to baseline and vice versa

D:
1) STRONG AUTOREGULATORS=
HEART/ BRAIN/ KIDNEY/ SK.MUSCLE

2) Weak Autoregulators: Splanchnics

3) no autoregulation: lungs & skin

E: BRAIN is MOST sensitive to Hypoxia & exhibits the MOST [Metabolic Regulation] (in addition to AUTOREGULATION). After 5 sec of ischemia, Brain Loses Consciousness. After few minutes of ischemia--->[Irreversible Brain Damage]

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A1: [Endothelium-Mediated Regulation] is NOT AUTOREGULATION but can assist Autoregulators. It can cause additional vasoDilation OR vasoCONSTRICTION.

A2: INC [Blood Flow]--->DIRECTLY releases [endothelial mediated vasoDilators] from endothelium which --->further INC more [Blood Flow]. This process typically occurs during EXERCISE!
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B1: [metabolic regulation] is different from [Metabolic AUTOREGULATION] because it is LOCAL and important for vasoDilation to metabolically active tissues such as Brain, Sk.Muscle and Heart. It can be activated by
DEC in O2--->formation of [metabolite VasoDilators] locally. There are 2 types of [metabolic regulation]
{ [Functional Active Hyperemia] vs. [reactive passive hyperemia] }

B2: [FAH] = VasoDilation and INC blood flow occurs because of INC K+, [inorganic phosphate] and [interstitial osmolarity] during ACTIVE metabolism/Exercise
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B3: [rph] = VasoDilation and INC blood flow occurs during [O2 deprivation/metabolic debt] ---->CAN LEAD TO [REPERFUSION ARRHYTHMIA] when clot causing O2 deprivation is removed and INC blood flow sends heart into arrhythmia!

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[Mechanical Tissue Pressure] occurs when Tissue mechanically presses against small vessels and alters [Blood Flow]. Occurs during:
1. Muscle Contraction ([Systolic Ventricle] vs. Sk.Muscle)

2. Alveolar Pressure in Lungs

3. Venous Obstruction from TUMORS

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A: How does Histamine cause VasoDilation
[Histamine] -->H2 receptor which activates [GaS]--->INC [Adenyl Cyclase] --->INC cAMP--->activates PKA--->phosphorylates and BLOCKS MLCK--->DEC phosphorylation of Myosin = VasoDilation

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A: [LEFT Coronary Artery] (AKA Widowmaker) is the DOMINANT CORONARY artery and is squeezed most during [isovoluMETRIC contraction] by the [L Ventricle].
-->pushes L coronary blood flow BACKWARDS.
R Coronary blood flow. is not as affected by [LV tissue pressure].

B1: LEFT Coronary Blood flow is GREATEST (65% of coronary perfusion) during [Early Diastole] when tissue pressure falls to 0.--> Diastolic pressure MUST remain above [50 mm Hg] to ensure pressure can push blood thru coronary.

B2: During hypOtension or [partial coronary occlusion] eNdocardial blood flow is MORE restricted because of higher [eNdocardial tissue pressure] = eNdocardium is more at risk for ischemia

B3: Aortic pressure is the PRIMARY determinant of Coronary blood flow but REGULATING Coronary blood flow is primarily due to [METABOLIC ACTIVITY] & changes in [Arteriolar resistance]

C: EACH [Myocyte] heart cell comes into contact with at least 3 Capillaries but these do NOT all function simultaneously. During ischemia capillaries are likely to be recruited!

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A: INC Blood Volume ----> DEC [Arterial Compliance] because it forces outer layers of Arteries (which won't be as elastic) to bourne the pressures

B: Myocardium is LESS COMPLIANT than [Sk. Muscle] and Normally runs off of Fatty Acids/Carbs/ketones (not glucose). -->Myocardium uses MUCH O2! O2 supply to heart is [FLOW-based] and not [O2 extraction based] because heart is already extracting at MAX!
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C: There are 3 Factors Affecting [Cardiac O2 consumption]
---> VasoDilates Coronary Arteries and Can ALL be DECREASED with Beta Blockers. These make up [Cardiac Stroke Work]:
1) Contractility
2) HR
3) Afterload

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D: Long-term INC EDV---> INC [L Ventricle Pressure]---> ][Heart Modeling/DiLated Cardiomyopathy]----> INC [Wall Tension AFTERLoad] --->DEC Cardiac Output by preventing contractions

E: INC Exercise ----> INC [Collateral circulation around heart]. EXERCISE WILL NOT CAUSE ISCHEMIA!
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F: 2 Factors that Determine Arterial Pressure
1) Stroke Volume [Changed by AFTERLoad/ PreLoad/Contractility]

2) Peripheral Resistance [GLOBAL Sympathetic / local]

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A: Ventricular Diastolic pressure is GREATER on eNdocardium --->eNdocardial vessels are more compressed during Contraction BUT blood flow between eNdo and Epicardium is STILL EQUAL because [eNdocardial resistance vessels] are more DiLated!

B: BUT...Aortic Valve Stenosis/CHF ---> INC [End Diastolic pressure]---> INC eNdocardial pressure/compression---> DEC Coronary Blood flow = [SubENdocardial ischemia]

C:
1st: Sympathetic Adrenergics activate [alpha 1] receptors in the coronaries-->WEAK vasoconstriction BUT [Beta 1] receptors on [pacemaker and myocardium] are activated from [Local metabolites] during exercise-->OVER-RIDING CORONARY vasoDilation when stimulated by [Increased metabolism]

2nd: [Coronary smooth muscle] ALSO has [Beta 2 Adrenergic] receptors that induce vasoDilation-->but is LESS sensitive to [sympathetic NorEpi] in Coronary

D: Heart at constant rate will have vagal stimulation activate coronary vasodilation using (ACh-->release NO from endothelium) but this can be blocked with Atropine! OR

..Damaging endothelium from inflammation--->prevents NO
---->Sympathetics take over and lead to constant VasoCONSTRICTION if [Local metabolites] are not being made from activity

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A: [Cardiac Stroke Work] = [MAP Force] x [Systolic stroke volume]

B: [AFTERLoad Arterial Pressure] consumes MUCH more Oxygen in the Heart than [PreLoad STROKE VOLUME work]
--->HTN will cause disproportionate INC in O2 consumption

C1: [Myocardial O2 supply]= [myocardial blood flow] x [arterial O2 content]

C2: [myocardial blood flow] = { [diastolic perfusion pressure] x [coronary vascular resistance] }

D: These things can affect [Coronary Vascular Resistance]
º [local metabolites]
º [endothelial factors]
º [neural innervations]
º[EXternal Compression]

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A: [Myocardial ischemia] result from [IMBALANCE RATIO] between [low Oxygen supply] and [HIGH Oxygen DEMAND]--->RELATIVE ischemia. [Oxygen DEMAND] alone is NEVER a PRIMARY cause of Ischemia!

B: Heart contains [collateral vessels] normally but these are INSUFFICIENT for SUDDEN INFARCT. During Gradual coronary obstruction [collateral vessels] GROW-->restore blood to protect against MI

C: [Coronary "Steal"] = occurs when INC blood flow in brother artery "STEALS" blood FLOW from insufficient daughter artery because it's more vasoDilated. This can be induced by Exercise OR [VasoDilating Adenosine]

D: [Peripheral Arterial Disease] ---> [Claudication] = pain in calf or thigh that occurs within certain distance and is secondary to [Coronary "Steal"]! Pain dissipates after [short rest periods].

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A: 20% of [Cardiac Output] goes to skeletal muscle ONLY BECAUSE it makes up 40% of our body mass--> [Skeletal muscle] has the LARGEST Vascular bed (that contain HIGH Vascular tone--> LARGE [Flow reserve Capacity]. Sk. Muscle is important in regulating Blood Pressure

B: Resting flow in sk. muscle per gram of tissue is 3 ml/min vs. flow per gram of tissue in brain and kidneys are MUCH HIGHER! Although this is true, Sk. Muslce can INC its blood flow x 20 during Exercise via [Functional Active Hyperemia]

C: TONIC MUSCLE has 5 x MORE [vascular supply] than phasic

D: [Sk. Muscle] VasoCONSTRICTS more at rest and vasoDilates during contraction to INC O2 delivery and remove waste products that accumulate.

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A: Muscle Contraction--->INC Tissue pressure -->Compresses blood vessels. During Dynamic exercise [Local vasoDilation] DEC vascular resistance (despite [GLOBAL Sympathetic] vasoCONSTRICTION) and helps combat the compression of blood

B: In Sk. Muscle, when exercise is isoMETRIC, extravascular compression is sustained no more than 2 min! [Vascular Resistance] INCREASES and [Cardiac Output] INCREASES
---> INC [Arterial Pressure]. This is because isoMETRIC tension (70% above MAX)-->blood flow approaches ZERO!

C: Changes in maintained muscle tone will can redistribute a lot of blood from the Legs & Abdomen!

D: Inspiration --> INC [Venous Return] because it DEC [thoracic pressure] and INC [abd pressure]

E: Sympathetic VENOconstriction--->INC venous tone----> DEC venous capacitance ----> INC [Venous Return]

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A: Most Sk. Muscle VASCULATURE is innervated by [Sympathetic NorEpi] (especially at rest) .. which'll bind to [alpha 1] receptors for vasoCONSTRICTION

B: Sk. Muscle ARTERIES are innervated by [Sympathetic Cholinergic's] that release ACh--->binds to [muscarinic receptors] on endothelial cells---->NO released--->vasoDilation! This mechanisms is activated during [anticipation of exercise] AND will contribute to vasoDilation DURING exercise.

C: Epi (from Adrenal medulla) binds to [Beta 2 Adrenergic] receptors -->vasoDilation at low levels

D: Epi (from Adrenal medulla) binds to [ALPHA 1 Adrenergic] receptors---->vasoCONSTRICTION at HIGH LEVELS

E: In addition to [Sympathetic Cholinergic's] stimulating [NO production] from endothelium, [Shear Stress] from [Blood Flow] ALSO releases NO from endothelium.

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A: Brain requires 15% of resting [Cardiac Output] and is VERY AEROBIC! It is the MOST metabolically active tissue in the body and so contains multiple collateral channels for potential usage in high blood flow

B: Even though Brain contains 400 miles of capillaries, IT LACKS LYMPHATIC VESSELS--->no where for leaky fluid to drain-->INC chances of Cerebral Edema!

C: In the [Circle of Willis] at the Brain base, the 2 [Internal Carotid Arteries] are the MAJOR blood suppliers to the Circle

D1: [Blood Brain Barrier] is made of
-[endothelial cell tight junctions],
-basement membrane,
-neuralglial processes and
-metabolic enzymes

D2: [BBB] allows lipid soluble substances (like O2, CO2, ETHANOL and steroid hormones) pass and [Glucose and Amino Acids] use transport systems. Anything over 500 daltons in weight CAN'T GET THRU!

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A: 5 Factors Affect Cerebral Blood Flow
1) Autoregulation
2) [Monro-Kellie Doctrine]
3) Metabolism
4) [Autonomic Nervous System]
5) Cushing's Response!

B: AUTOREGULATION maintains constant brain flood flow but regional flow is associated with neural activity. INC neural activity ---> INC blood flow to that area.

C1: [Cerebral Perfusion Pressure] works just like [Arterial Pressure] AUTOREGULATION. [CPP] is normally 80-100 mm Hg. But when [CPP] INC ---> Cerebral vasoCONSTRICTION INC to prevent too much flow.
**[CPP] formula : {MAP - [intracranial venous pressure] }**

C2: This AUTOREGULATION occurs between [70-140 mm Hg] so in pt with HTN blood flow is NOT well maintained at lower [MAP] but is normal at higher blood pressures because curve shits to the RIGHT!

D: [intracranial venous pressure] can be affected by things like tumor / hematoma / hydrocephalus

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A: INC [intracranial pressure] ---> Vascular compression ----> INC resistance--->Ischemia! When this occurs, Venous side is affected FIRST and will collapse 1st because it does NOT have high pressures to protect itself against compression.
**AUTOREGULATION helps to correct this problem of INC pressure.

B: INC [CSF pressure] can also INC resistance. [CSF Pressure] is 12 mm Hg so [intracranial venous pressure] and [CSF pressure] are equal, but if [CSF pressure] INCREASES and starts to get close to [Arterial Pressure] Blood flow will DEC rapidly!

60

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A: 5 Factors Affect Cerebral Blood Flow
1) Autoregulation
2) [Monro-Kellie Doctrine]
3) Metabolism
4) [Autonomic Nervous System]
5) Cushing's Response!

B: [Monro-Kellie Doctrine] states that 3 [Compartment Factors] have to remain CONSTANT in Brain so if 1 INC, another must DEC. The 3 [Compartment Factors] are:
1. [Parenchyma Brain Volume]
2. [Cerebral Vascular Volume]
3. [CSF volume]

ex: Intracranial hemorrhage--->INC [Parenchyma Brain Volume] ---> DEC in both [Cerebral Vascular Volume] AND [CSF Volume] and therefore Compress those compartments and increase their pressures

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A: Cerebral Blood flow is VERY SENSITIVE TO Arterial CO2! CO2 and H+ are pretty much same thing and INC CO2
--->DEC pH--->vasoDilation--->INC blood flow!
HIGH pH will cause vasoCONSTRICTION-->decreases blood flow
A2: Cerebral blood flow is less sensitive to O2 changes but is important in [fMRI] which is dependent on oxygenation levels. INC oxygenation in 1 area indicatives activity which is picked up by [fMRI].

B1: When [BODY Blood pH] changes from H+, this BARELY affects cerebral blood flow because H+ can't cross BBB.

B2: BUT if [BODY Blood pH] changes because of CO2 this can RAPIDLY change cerebral blood flow since CO2 CAN cross BBB. Inhaling 7% CO2-->DEC pH---> DOUBLES cerebral blood flow due to vasoDilation.

**Hyperventilation--->cerebral vasoCONSTRICTION because pH INC--->dizziness and fainting!

C: Cerebral Edema--> INC [Parenchyma Brain Volume]. Cerebral Edema has ability to artificially induce HYPERventilation--->lower CO2 and vasoCONSTRICTION
-->DEC blood flow. Decreasing blood flow will DEC [Cerebral Vascular Volume] and therefore DEC edema and Intracranial pressure. This is all occurs because of [Monro-Kelli Doctrine]

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A: Hyperkalemia in [vascular smooth muscle] causes them to HYPERpolarize and vasoDilate by stimulating [Na+/K+ ATPase pump] and INC K+ permeability. Astrocytes in the brain take up K+ released in order to ensure this doesn't happen too much.
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B: [GLOBAL Neural] Control of [Cerebral Vascular] is WEAK and is mostly controlled with [local metabolic] activity. So [baroreceptor reflex] from [GLOBAL Neural] has little effect on [cerebral vascular resistance]

ParaSympathetic ---> vasoDilation
Sympathetic --->vasoCONSTRICTION

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[Cushing Response]!! = INC BP but DEC HR :-O

A: [Cushing Response] = IF [cerebral INTRACRANIAL pressures] EXCEED [Cerebral Arterial Pressure] of 100 mm Hg--->DEC [Cerebral perfusion] ---> [Cerebral ischemia].

[Cerebral ischemia] causes sympathetic activation (due to abnormal depolarizations of sympathetics in medulla) BUT

INC [cerebral INTRACRANIAL pressure] activate PARAsympathetics =

****Pt will have INC [systemic blood pressure from sympathetics] and [DEC HR from PARAsymapthetics]

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** Mammal Lungs have 2 Circulations.
A1: Pulmonary (receives 100% of [CArdiac Ouput]) is used to transfer gas between blood and air. It is MUCH more compliant than [Bronchial Systemic] because it has little smooth muscle. It has low pressure / low resistance and high flow with mean pressure of 6 mm Hg.
A2: MAP is 14 and Mean L arterial pressure = 8.

vs

B: [Bronchial Systemic] (receives 1% of [cardiac output])

C: Pulmonary Blood in alveolar walls flow as an unbroken sheet between air spaces because numerous capillaries form a network within alveolar walls. Capillaries in

D:Pulmonary capillaries represent 40% of vascular resistance unlike systemic capillaries which serve as little resistance in the body.

E: Pulmonary resistance will DEC even with INC flow and pressure during exercise because MORE capillaries are recruited--->DEC [Total Cross Sectional Area]--->DEC Resistance

F: PULMONARY VESSELS DO NOT AUTOREGULATE!

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A: [Alveolar capillary vessels]= [capillary microvessels] located within alveolar walls

B: [XTra-Alveolar Vessels] = [Larger Arterial] and [Venous vessels] NOT in Alveolar

C: During regular Inspiration there is HIGH Lung volume and Negative intrapleural pressure---->allows [XTra-Alveolar vessels] to distend and [Alveolar capillary vessels] to be compressed---> no INC resistance

D: BUT DEEP INSPIRATION--> MILD [INC Resistance]
---->transient pooling of blood in pulm circulation) --->less blood to [L Vt.] and more Backed Up to [Right Vt.]

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A: When standing up, intravascular pressures at BOTTOM LUNG ARE HIGHER because of Gravity! This creates 3 Zones of pulmonary perfusion.

Zone 1 = [ALVEOLAR pressure] is HIGHER than [arterial & venous pressure] ---> capillaries collapse = no forward blood flow! This zone does NOT exist normally but will occur with hypOtension or [positive pressure machine ventilation]

Zone 2= Upper 1/3 of Lung where [ALVEOLAR pressure] is Higher than [venous pressure] but thankfully lower than [ARterial Pressure]--->capillaries somewhat collapsed but flow depends on pressure difference between [ALVEOLAR pressure] and [ARterial Pressure]. Does NOT depend on venous.

Zone 3= BOTH [Arterial and Venous pressures] are HIGHER than [alveolar pressure]-->flow depends on pressure difference between [Arterial] vs. [Venous] pressures

B: Zones 2 and 3 are primary blood flow zones. There is 500 mL of air coming into lungs during inspiration = [Tidal Volume]

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A: Normally 5-10% of [Cardiac Output] goes to Skin but Skin flow can vary from [0 (during cold) - 7 (in heat)] L/min. This is because oxygen requirements of skin is small and there's more flow than needed going to skin. Skin blood flow changes will BARELY effect overall [Total Peripheral resistance] and [Blood pressure]

B: Skin flow is DEPENDENT ON [GLOBAL Neural] control becuz main function of cutaneous circulation is to maintain body temp! Cutaneous vasculature is more efficient at adjusting to Warm environments/promoting heat loss. It is also important in skin color by volume and oxygenation
*: Low blood flow = pale
*desaturated Hemoglobin = Cyanotic
*FULLY SATURATED HEMOGLOBIN= REDDISH
*[Carbon Monoxide Poisoning] = Pink

C: COLD weather--->DEC ability to dissociate O2 from hemoglobin----> INC OxyHemoglobin--->REDDISH COLOR
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D: Skin has 2 [resistance vessel types]
1. Arterioles = some basal tone & controlled by Sympathetics and [local metabolism ]

2. [Arteriovenous anastomoses] = shunts blood from arterioles to [venules and venous plexuses] and BYPASSES capillary beds altogether.
They are ONLY SYMPATHETIC [GLOBAL Neural] controlled and have NO Basal, metabolic, autoregulation or [passive reactive hyperemia].

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*There are 2 types of Skin in terms of Blood flow* [Apical vs. NonApical]

A: Apical = Favors heat loss with HIGH [surface-to-volume ratio]. CONTAINS [AV Glomus Body Shunts] AV anastomoses that help facilitate heat loss!

A2: Apical skin is found on Nose / Lips / Ears / fingertips / hands and Feet! Apical is innervated by [Sympathetic ADRENERGIC] using NorEpi --->vasoCONSTRICTION.

(Withdrawing [Sympathetic ADRENERGIC]--->passive vasoDilation)

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*There are 2 types of Skin in terms of Blood flow* [Apical vs. NonApical]
1. NonApical = Present in MOST body and LACKS [AV Glomus Body Shunts]

A: when stimulated by [sympathetic cholinergics] which'll use ACh to release [sweat-dependent bradykinin] ---> ACTIVE vasoDilation

B: when innervated by [Sympathetic ADRENERGICS] using NorEpi---> ACTIVE vasoCONSTRICTION
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**Sk. Muscle has the HIGHEST BASAL TONE and so will have the lowest blood flow at rest **

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A: Temp regulation is MOSTLY regulated by HYPOTHALAMUS and some spinal cord. INC [Internal Temp]--->DEC Sympathetics--->vasoDilation for increase blood flow . MAX vasoDilation occurs when Sympathetics are BLOCKED OFF!

B: DEC [internal temp]--->INC Sympathetics -->vasoCONSTRICTION

C1: Why does skin vasoCONSTRICT when Exercise is too intense!?
During intense Exercise, skin blood flow INC to 60% of [Cardiac Output] ---> DEC system blood pressure which will cause [baroreceptor-mediated vasoCONSTRICTION] of cutaneous vessels ---> INC peripheral resistance ---> shunts blood away from skin and INC system BP.

C2:This [baroreceptor mechanism] COMPETES with vasoDilation responses from the skin to temperature and limits [Baroreceptor vasoCONSTRICTION response]. -->BP can not be well maintained during intense Exercise

D: DEC BP causes Sympathetics acting on cutaneous vessels to INCREASE--->vasoCONSTRICTION and shunting to core but Because apical vessels already Dilate in warm conditions BP INC has lil effect on skin blood flow in warm conditions. "Think Army losing blood in heat"

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Frostbite: 0ºC---> negligible cutaneous blood flow that causes skin to freeze. [Microvasculature freezes before large vasculature] AND [VENOUS] freezes before [arteries] due to lower flow rates. Frostbite causes cell damage due to ice crystals and leads to ischemia / [Microvascular stasis]/ [Reperfusion inflammatory injury] and thrombus

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A: Splanchnic Circulation is blood supply to the GI/ Liver/ Spleen and Pancreas. Splanchnics receive 25% of [Cardiac Output].

B: [Celiac artery] = perfuses spleen/stomach/pancreas

C: [Superior/inferior Mesenteric Artery] = perfuses Intestines /Stomach / pancreas. [SMA/ima] form anastomoses that LIMIT ISCHEMIA! :-)

D: small arteries penetrate the intestinal muscular layer and branch out in the submucosal layer. Arrangement of microvessels within [intestinal villus] forms [countercurrent flow system]

E: [countercurrent flow system] = Arterioles and venules run parallel to one another so that Na+ absorbed in capillaries will pass into venules but then can diffuse into interstitium ACROSS to the Arterioles--->INC Arteriolar osmolarity and INC arterial blood flow during reabsorption!

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**PORTAL SYSTEM**
A: Splanchnic circulation consist of [Portal Vein] collects blood FROM [capillary beds] inside [spleen/stomach/pancreas and Intestines] and sends it to [Liver capillary beds]----(sends to)---> [Inferior Vena Cava] after Liver processing.

B1: [Portal Vein]= 10 mm Hg is almost equal to [IVC]= 7 mm Hg. [Portal HTN] occurs when there's INCREASE in [IVC] pressure from CHF or INCREASE in hepatic vascular resistance from [cirrhosis/hepatitis]

B2: [Portal HTN] can lead to [Abdominal Ascites] and will dilate portal anastomoses with systemic veins in [lower esophagus] / stomach / rectum.

C: ****1500 mL of Blood/min travels thru the Liver! 70% of that blood comes from [PORTAL VEIN]. *******
30% comes from hepatic artery

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**Regulation of Intestinal blood flow comes from [Local Metabolites], Hormonal AND [GLOBAL Neural] **

A: INC [Local Metabolites]-->vasoDilation and INCREASES intestinal blood flow. DEC metabolism will cause vasoCONSTRICTION.

B1: Intestinal blood flow is determined mostly by the [RATE of Active transport of solutes across mucosal epithelium]. It is INDEPENDENT of intestinal content itself.

B2: INC [Intestinal motility of smooth muscle] also INC [Intestinal Blood flow] by only by little. Total intestinal blood flow usually DEC during intestinal contractions due to compression of blood vessels

C: [Intestinal Blood Flow] also exhibit moderate [METABOLIC AUTOREGULATION] due to vasoDilation from accumulated [Local metabolites]. This is not better than AUTOREGULATION of Brain or Kidney.

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**Regulation of Intestinal blood flow comes from [Local Metabolites], Hormonal AND [GLOBAL Neural] **

Hormonally, [Cholecystokinin] and [Neurotensin] BOTH activate vasoDilation----> INC [Intestinal blood flow]

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**Regulation of Intestinal blood flow comes from [Local Metabolites], Hormonal AND [GLOBAL Neural] **
[GLOBAL Neural]
A: (other than capillaries) ALL Splanchnic Blood vessels receive [POSTganglionic sympathetics] majorly
--->vasoCONSTRICTION using NorEpi that bind to [alpha adrenergic receptors] of smooth muscle.

B: [Beta adrenergic receptors] also exist-->vasoDilation

C: During exercise [POSTganglionic sympathetics] activate vasoCONSTRICTION and VENOCONSTRICTION to shift blood from GI--->Vital Organs and Active muscles

C2: If blood is "stolen" from the GI and sent to [central circulation] for too long---> [Ischemic Bowel Syndrome] or [Renal infarct]

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**Regulation of Intestinal blood flow comes from [Local Metabolites], Hormonal AND [GLOBAL Neural] **
[GLOBAL Neural]

A: PARAsympathetic POSTganglionic fibers live in the intestinal wall and INDIRECTLY INC [Intestinal blood Flow] by stimulating [Intestinal motility] and glandular secretions
--(which all)---->INC metabolism

B: PARAsympathetics BLOCK (cAMP) which in GI actually ACTIVATES Smooth Muscle Contraction--->INC [Intestinal motility]! THIS IS AN OPPOSITE MECHANISM OF NORMAL SMOOTH MUSCLE!

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[Postprandial Hyperemia] occurs when Food ingestion INC [intestinal blood flow] thru multiple mechanisms. Digestion of fats and Carbs--->Induce [Functional Active Hyperemia] ---->INC Blood Flow

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[Sympathetic Cholinergics] are a *special* Sympathetic System that secretes ACh which bind to muscarinic receptors. It works on:
1. Sweat Glands

2. Endothelial Cells ---> NO--->vasoDilation*****

3. [Piloerector muscle] for back of neck hair