ch 14 lecture physiology 5e

7/24/2019 ch 14 lecture physiology 5e

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PowerPoint Lecture

Presentations prepared by

Donal Skinner,

University of Wyoming

C H A P T E R

2013 Pearson Education, Inc.

14

PCB 3703

Human Physiology I

Yerko Berrocal, M.D.Associate Professor


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Chapter Outline

14.1 Physical Laws Governing Blood Flow and BP 14.2 Overview of the Vasculature

14.3 Arteries

14.4 Arterioles

14.5 Capillaries and Venules

14.6 Veins

14.7 The Lymphatic System

14.8 Mean Arterial Pressure and Its Regulation

14.9 Other Cardiovascular Regulatory Processes


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14.1 Physical Laws Governing Blood Flow and

Blood Pressure

Flow Rule

Circulatory system = closed system

Pressure = force exerted by blood

Flow occurs from high pressure to low pressure

P is the force pushing blood against the various

factors resisting the flow of liquid in a pipe

Flow = P/R


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Pressure Gradients in the Cardiovascular

System

Pressure gradients drive flow from high pressure

to low pressure

Flow due to pressure gradients = bulk flow

Heart creates a pressure gradient for bulk flow

of blood

A gradient must exist throughout the circulatory

system to maintain blood flow


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100 mm Hg

60 mm Hg

Flow

Flow = 20 mL/min

P = 0 mm Hg

200 mm Hg

160 mm Hg

Flow

Flow = 0

Flow = 20 mL/min

P = 40 mm Hg

P = 40 mm Hg

Figure 14.1 A model that relates blood flow to the pressure gradient.


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System

Pressure gradient across the systemic circuit

P = pressure in aorta minus pressure in vena cava just

before it empties into right atrium

Pressure in aorta = mean arterial pressure (MAP) = 90

mm Hg

Pressure in vena cava = central venous pressure (CVP)

= 0 mm Hg

P = MAP CVP = 90 0 = 90 mm Hg


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Figure 14.2 A pressure gradient is the driving force for blood flow.

Systemicorgans

P Aortic pressure =85 mm Hg (MAP)

Heart

Vena cava pressure =

0 mm Hg

Right

atrium

Left

atrium

Left

ventricle

Right

ventricle

= 85 0= 85 mm Hg




System

Pressure gradient across pulmonary circuit

P = pressure in pulmonary arteries minus pressure in

pulmonary veins

Pulmonary arterial pressure = 15 mm Hg

Pulmonary venous pressure = 0 mm Hg

P = 15 0 = 15 mm Hg



Figure 14.3 Pressures and pressure drops in the pulmonary and systemic circuits.

Arteries

Arterioles

Ca

pillaries

Ve

nules

Ve

ins

Pressure

drops:

Systemic

circuit

Pulmonary

circuit

Systemic

circuit

Pulmonary

circuit


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Resistance in the Cardiovascular System

The pressure gradient in the systemic circuit ismuch greater than the pressure gradient in the

pulmonary circuit

Flow through both circuits is equal

Flow = P/R

Thus resistance through the pulmonary circuit is

much less than resistance through the systemic

circuit


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Figure 14.4 The effect of resistance on flow.

Lowresistance

Highresistance

A

B

Flow = 20 mL/min

Flow = 10 mL/min

P = 40 mm Hg


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Factors affecting resistance to flow Radius of vessel

In arterioles (and small arteries)can regulate radius

Length of vessel

Viscosity of fluid =

Blood viscosity depends on amount of RBCs and

proteinsusually constant


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Toolbox: Poiseuille's Law

R = 8 L

Flow = P/R

Therefore: Flow = P r4

r4

8 L


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The effect of arteriole radius on blood flow Regulation of radius of arterioles (and small arteries)

Vasoconstriction

Decreased radius increased resistance

Vasodilation

Increased radius decreased resistance

Pulmonary circuit features less resistance than systemiccircuit

Lower pressure gradient is required for blood flow


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Total peripheral resistance = combined resistanceof all blood vessels within the systemic circuit

Resistance across a network of blood vessels depends

on resistance of all vessels

Flow through network varies with resistance

Vasoconstriction in network increased resistance

decreased flow

Vasodilation in network decreased resistance

increased flow


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Relating Pressure Gradients and Resistance

in the Systemic Circulation

Flow = P/R

Flow = cardiac output (CO)

P = mean arterial pressure (MAP)

R = total peripheral resistance (TPR)

CO = MAP / TPR


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14.2 Overview of the Vasculature

Arteries: carry blood away from heart

Microcirculation

Arterioles

Capillaries: site of exchange

Venules

Veins: return blood to heart


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Figure 14.5 The relationships of blood vessels according to size and the direction of blood flow in the systemic

circuitOxygenatedblood fromheart

Deoxygenatedblood toheart

Connective t issue

Smooth muscle

Endothelium

Lumen

Microcirculation

Arteriole Venule

Network of capillaries

Vein

Valve

EndotheliumBasementmembrane

Capillary

Artery


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Overview of the Vasculature

Walls of blood vessels Endothelial cells line inner layer of all blood vessels

Other components of blood vessel walls:

Smooth muscle

Fibrous connective tissue

Collagen

Elastic connective tissue

Elastin


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Figure 14.6 Structural characteristics of the five blood vessel types.

Aver age i nternaldiameter (mm)

Average w allthickness (mm)

Specialfeatures

4.0 1.0

Artery

Muscular, highly elastic

Arteriol e

Capillary

Venule

Vein

Thin-walled (compared to arteries),fairly muscular, highly distensible

Thin-walled, some smooth muscle

Thin-walled, highly permeable

Muscular, well innervated0.03

0.008

0.02

5.0

0.001

0.0005

0.006

0.5

= Endothelium

= Smooth muscle

= Connective tissue

Wall thickness

Internal

diameter


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14.3 Arteries

Arteries as a pressure reservoir Arterial blood pressure


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Arteries

Rapid transport pathway

Large diameter

Little resistance

Walls contain elastic and fibrous tissue

Under high pressure

Muscular arteries

Less than 0.1 mm in diameter

Little elastin

Smooth muscle regulates radius


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Arteries: A Pressure Reservoir

Storage site for pressure Thick, elastic arterial walls

Low compliance

Expand as blood enters arteries during systole

Recoil during diastole


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Figure 14.7a The role of arterioles as a pressure reservoir.

Aorticvalve

Expanding pressure

due to increased volume

Flow FlowTosystemicorgans

Arteries

Leftventricle

Systole


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Figure 14.7b The role of arterio les as a pressure reservoir.

Aortic

valve

Elastic recoil

Flow

Arteries

Leftventricle

Diastole


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Arteries: A Pressure Reservoir

Compliance: measure of how the pressure of avessel will change with a change in volume

Low compliance (arteries)

Small increase in blood volume causes a large increase in

pressure

High compliance

Large increase in blood volume is required to produce a

large increase in pressure


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Arterial Blood Pressure

Pressure in the aorta Varies with cardiac cycle

Systolic blood pressure = maximum pressure

Due to ejection of blood into aorta

Diastolic blood pressure = minimum pressure

Not zero due to elastic recoil

Fi 14 8 Th t i l d i bl d t


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Pressure in the cuff

Systolic pressure

(beginning of sounds)

Diastolic pressure

(end of sounds)

Blood flow:

Sound:

No flow

No sound

Cuff pressureabove110 mm Hg

StethoscopeCuff

Turbulent flow

Korotkoff sounds

Cuff pressurebetween 70 and110 mm Hg

Laminar flow

No sound

Cuff pressurebelow 70 mm Hg

No blood flow Turbulent flow in compressed

artery makes audible vibrations(Korotkoff sounds)

Laminar flow in noncompressed

artery makes no sounds

Slide 1Figure 14.8 The events involved in blood pressure measurement.


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Measuring blood pressure

Pressure cuff and sphygmomanometer

Compressed artery

Turbulent flow produces Korotkoff sound

Pressure at first Korotkoff sound = systolic blood pressure

Uncompressed artery

Laminar flow, no sound

Pressure when sound disappears = diastolic blood

pressure


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Blood pressure determinations The measured BP is shown as SP/DP

Example: 110 / 70

Pulse pressure = SP DP

Example: 110 70 = 40 mm Hg

MAP = SP + (2 DP) / 3

Example: (110 + 140) / 3 = 83.3 mm Hg

14 4 A i l


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14.4 Arterioles

Arterioles: resistant vessels Part of microcirculation

Connect arteries to capillaries or metarterioles

Contain rings of smooth muscle to regulate radius

and, therefore, resistance

A t i l d R i t t Bl d Fl


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Arterioles and Resistance to Blood Flow

Arterioles provide greatest resistance to blood flow

Greater than 60% of TPR

Largest pressure drop in vasculature 90 mm Hg to 40 mm Hg

Resistance is regulated

Figure 14 9 Pressures in the vasculature Pressures in the vasculature


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Figure 14.9 Pressures in the vasculature. Pressures in the vasculature.

Arteries

A

rterioles

C

apillaries

V

enules

V

eins

Pressure

drops:

Arteries

Arterioles

Systemiccircuit

Capillaries

Venules

Veins

Systemiccircuit



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Changes in arteriole radius

Radius depends on contraction state of smooth muscle

in arteriole wall

Arteriolar tone

Contraction level (radius) is independent of extrinsic

influences

Vasoconstriction

Increased contraction = decreased radius

Vasodilation

Decreased contraction = increased radius



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Functions of varying arteriole radius

Controlling blood flow to individual capillary beds

Regulating mean arterial pressure

Figure 14 10 Changes in the radius of arterioles


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Rest, arteriolar tone

Contraction of smoothmuscle causesvasoconstriction

Relaxation of smoothmuscle causes

vasodilation

Figure 14.10 Changes in the radius of arterioles.

I t i i C t l f Bl d Fl Di t ib ti t


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Intrinsic Control of Blood Flow Distribution to

Organs

Regulation of blood flow to organs is based

on need

Regulated by varying resistance

Organ blood flow = MAP / organ resistance

Figure 14.11a The effects of pressure gradients and resistance on blood flow to organs.


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Organ A

Organ B

Organ C

Heart

AP VP

Arteries Veins

VP

VP

AP

AP

Figure 14.11a The effects of pressure gradients and resistance on blood flow to organs.

Figure 14.11b The effects of pressure gradients and resistance on blood f low to organs.


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g p g g

AP

A

Total flow: 3.0 L/min

Percent of

cardiac output

(total flow)

1.5 L/min

1.0 L/min

0.5 L/min

50%

33%

17%

FlowVP

A

B

C

P = AP VP

B

C

Figure 14.11c The effects of pressure gradients and resistance on blood flow to organs.


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g p g g

P = AP VPPercent of

cardiac output

(total flow)

1.5 L/min

0.5 L/min

0.5 L/min

60%

20%

20%

Flow

A

B

C

Total flow: 2.5 L/min

AP

VP

A

B

C



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Organs

Local factors that control vascular resistance

Vascular resistance is regulated through changes in

radius of arterioles

Depends on contractile state of smooth muscle in walls

of the vessel

Local factors regulate radius, thereby regulating blood

flow



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Organs

Regulation in response to changes in metabolic

activity

Changes associated with increased metabolic activity

generally cause vasodilation

Carbon dioxide

Potassium

Hydrogen ions

Changes associated with decreased metabolic activity

generally cause vasoconstriction

Oxygen



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Organs

Active hyperemia: increased blood flow in

response to increased metabolic activity

Steady state

O2 is delivered as fast as it is consumed

CO2 is removed as fast as it is produced

Increased metabolic rate O2 is consumed faster than it is delivered

CO2 is produced faster than it is removed

Figure 14.12 The effects of pressure gradients and resistance on blood f low to organs.


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Cells

Extracellularfluid

Carbondioxide

Oxygen

Blood flow

Arter iole Capi llaries

Under normal steady-state conditions, oxygen (purpledots) is delivered to tissues by the blood as fast as it isconsumed by cells, and carbon dioxide (green dots) isremoved from tissues by the blood as fast as it isproduced by cells.

An increase in the metabolic rate causes oxygen tobe consumed faster than it is delivered and carbondioxide to be produced faster than it is removed. Theoxygen concentration in extracellular fluid decreases,while carbon diox ide concentration incr eases.

Vasodilation promotes increased blood flow, which

increases oxygen delivery to cells and carbon dioxi deremoval from cells.

The decreased oxygen concentration and increased

carbon dioxide concentration act on arteriolarsmooth musc le to promote vasodilation.



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Organs

Reactive hyperemia: increased blood flow in

response to a previous reduction in blood flow

Blockage of blood flow to tissues Metabolites increase and oxygen decreases

Vasodilation

When blockage is released

Increased blood flow due to low resistance

Metabolites removed, oxygen delivered

R ti H iSlide 1Figure 14.13 Comparison of active and reactive hyperemia.


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Initial s timulus

Active Hyperemia Reactive Hyperemia

Tissue Tissue

Metabolic rate Blood flow

O2 consumption

CO2 production

O2 concentration

CO2 concentration

Vasodilation Vasodilation

Resistance Resistance

Blood flow Blood flow

Local arteriolar

smooth muscleLocal arteriolar

smooth muscle

Negative

feedback

Negative

feedback

O2 deliveryCO2 removal

O2 concentration

CO2 concentration

O2 concentration

CO2 concentration

O2 concentration

CO2 concentration

O2 deliveryCO2 removal

Physiological responseResult



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Organs

Myogenic response: change in vascularresistance in response to stretch of blood vessels

in the absence of external factors

Myogenic autoregulation of blood flow

Increased perfusion pressure increases blood flow andpressure in arterioles

Increased pressure in arteriole stretches arteriole wall

Stretch of vascular smooth muscle induces contraction

of vascular smooth muscleinherent property ofsmooth muscle

Vasoconstriction decreases blood flow

Purpose: keep blood flow constant (autoregulate)

Figure 14.14 The myogenic response to changes in perfusion pressure. Slide 1


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Initial stimulus

Physiological response

Result

Arteriole

Perfusion pressure

Flow Stretch of arteriolarsmooth muscle

Constriction

Resistance

Flow

Negative

feedback


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Understanding Exercise: Independent


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Understanding Exercise: Independent

Regulation of Blood Flow

Cardiac output increases during exercise

Distribution of blood does not increase

proportionally Dilation of vessels to skeletal muscle and heart

increases blood flow to muscles

Constriction of vessels to GI tract and kidneys

decreases blood flow to these organs

Disproportionate flow diverts blood to muscles

Understanding Exercise 14.1 Independent Regulation of B lood Flow.


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Resting blood flowCardiac output (CO) = 5 L/min

Exercise blood flowCardiac output (CO) = 25.0 L/min

Kidneys 0.85 L/min

GI tract 1.05 L/min

Heart 1.15 L/min

Brain 0.8 L/min

Others 0.5 L/min

Skin 0.65 L/minSkeletal muscle20.0 L/min

Heart 0.2 L/min

GI tract1.25 L/min

Kidneys

1.0 L/min

Skeletal muscle1.0 L/min

Others0.6 L/min

Brain0.7 L/min

Skin 0.25 L/min

Extrinsic Control of Arteriole Radius and Mean


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Arterial Pressure

Flow = P/R

CO = MAP / TPR

MAP = CO TPR

MAP depends on total peripheral resistance (TPR)

TPR depends on radius of arterioles

Radius of arterioles is regulated by extrinsic

mechanisms to control mean arterial pressure

Sympathetic activity

Hormones



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Arterial Pressure

Sympathetic control of arteriolar radius

Sympathetic innervation of smooth muscle

of arterioles

Smooth muscle of most arterioles (not those in brain)

has adrenergic receptors

Norepinephrine binds to adrenergic receptors

Produces vasoconstriction

Increases TPR

Increases MAP



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Arterial Pressure

Distribution of adrenergic receptors in arterioles to

skeletal and cardiac muscle

Both and 2 adrenergic receptors

Norepinephrine binds to receptors

Vasoconstriction

Epinephrine binds to and 2

receptors

Vasoconstriction at receptors

Vasodilation 2 receptors

Epinephrine has greater affinity for 2 receptors



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Arterial Pressure

Effects of epinephrine on arteriole radius

Concentration dependent

Lower concentrationsbinds 2

Vasodilation



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Arterial Pressure

Effects of epinephrine on arteriole radius

Higher concentrationsbinds and 2

Vasodilation in skeletal and cardiac muscle vascular beds Decreases TPR decreases blood pressure

Vasoconstriction in most vascular beds

Maintains/increases TPR maintains blood pressure

Dominant effect is usually vasoconstriction



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Arterial Pressure

Hormonal control Epinephrine

Released from adrenal medulla

Vasopressin (ADH) Secreted by posterior pituitary

Increases water reabsorption by kidneys

Vasoconstriction Angiotensin II

Vasoconstriction

Increases TPR


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14 5 Capillaries and Venules


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14.5 Capillaries and Venules

Capillary Anatomy

1040 billion per body

Total SA = 600 m2

Most cells within 1 mm of a capillary

1 mm long

Pores between endothelial cells

Protein-free plasma moves through pores

Capillary Anatomy


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Capillary Anatomy

Site of exchange between blood and tissue

510 mm in diametersmall diffusion distance

Walls

One cell layer

Small diffusion barrier

Have greatest total cross-sectional area

Have slowest velocity of blood flow, which enhances

exchange

-

Figure 14.15 Total cross-sectional area and velocity of blood flow through the vasculature.


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Aorta

Arteries

Arterioles

Capillar-

ies

Veins

Venules

Capillary Anatomy


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Capillary Anatomy

Continuous capillaries

Most common

Small gaps between endothelial cells

Allow small water-soluble molecules to move through

Fenestrated capillaries

Large gaps between endothelial cells forming pores or

fenestrations (windows)

Allow proteins, and in some cases blood cells, to move through

Figure 14.16a Two types of capillaries.


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small water-soluble

molecules to move through

proteins, and in some cases

blood cells, to move through

Local Control of Blood Flow Through Capillary


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Beds

Local control of smooth muscle in microcirculation

Arterioles

Metarterioles

Precapillary sphincters



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g p y

Beds

Metarterioles Intermediate between arterioles

and capillaries

Directly connect arterioles to

venules

Function as shunts to bypasscapillaries

Rings of smooth muscle at strategic

locations

Contract and relax in response

to local factors

Contract increase blood flow

through capillaries

Relax decrease blood flow

through capillaries



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g p y

Beds

Precapillary sphincters Rings of smooth muscle that

surround capillaries on the

arteriole end

Contract and relax inresponse to local factors only

Contraction constricts

capillary decreases blood

flow Relaxation increases blood

flow

Metabolites cause relaxation

Movement of Material Across Capillary Walls


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p y

Exchange across capillary walls

Diffusion: most common mechanism

Lipophilic: across membrane

Lipophobic: through channels

Transcytosis: exchangeable proteins

Mediated transport: in brain

Figure 14.18 Exchange of materials across the wall o f a continuous capillary.


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Endothelial cell

Lumen

Capillary

Plasma

O2

, CO2

,fatty acids,steroidhormones

Na+, K+,glucose

Proteins

Water-filledpore

Plasma membrane

PoresInterstitial fluid

Diffusion throughcells (lipid-solublesubstances)

Diffusion throughpores (water-soluble sub-stances)

Restricted move-ment of mostplasma proteins(cannot crosscapillary wall)

Transcytosis ofexchangeableproteins across

cellsCytoplasm



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p y

Bulk flow of fluid across capillary wall based on

pressure gradients

Protein-free plasma moves across capillaries

Filtration = movement out of capillary into interstitial

space

Absorption = movement into capillary from interstitial

space

Purpose: distribute ECF



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p y

Starling forces across capillary walls

Forces for bulk flow: hydrostatic and osmotic pressures

Hydrostatic pressure gradient: force due to fluid

Osmotic pressure: osmotic force exerted on water by

nonpermeating solutes

Only nonpermeating solute: proteins

Oncotic pressure: osmotic force of proteins

Factors influencing transcapillary fluid


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g p y

movement

(+)

(+)

(-)

(-)

Filtration and Reabsorption


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p

Formula for fluid exchange:

Qf= forces for filtration MINUS the forces against filtration

Table 14.3 Forces Affecting the Movement of Fluid Across Capillary Walls.


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Factors affecting filtration and absorption across capillaries

Standing on feetincreases hydrostatic pressure

Injuries

When capillaries are damaged, they leak fluid and proteins

Histamine increases capillary permeability to proteins

Liver disease

Decreases plasma proteins

Kidney disease

Increases blood volume and, therefore, blood pressure

Decreases plasma proteins

Heart disease

Pulmonary edema

Venules


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Smaller than arterioles

Connect capillaries to veins

Little smooth muscle in walls

Some exchange of material between blood and

interstitial fluid

14.6 Veins


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Large diameter, but thin walls

Valves allow unidirectional blood flow

Present in peripheral veins

Absent from central veins

Veins: A Volume Reservoir


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Compliant vessels

Expand with little change in pressure

Function as blood reservoir

60% total blood volume in systemic veins at rest

Figure 14.20 Curves showing how the volume of blood contained in arteries and veins varies with the pressure inside

them.


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Veins

Arteries

Figure 14.21 Distribution o f blood volume in the various portions `of the cardiovascular system.


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Pulmonary blood

vessels 12%

Systemic arteriesand arterioles 15% Heart 8%

Capillaries 5%

Systemic veins

and venules 60%

Factors That Influence Venous Pressure and


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Venous Return

Skeletal muscle pump

One-way valves in peripheral veins

Skeletal muscle contracts

Squeezes on veins, increasing pressure

Blood moves toward heart

Blood cannot move backward due to valves

Skeletal muscle relaxes

Blood flows into veins between muscles

Figure 14.22 The skeletal muscle pump.


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To heart

Proximalvalveopened

Vein

Distalvalveclosed

To heart

Valveclosed

Vein

Valveopened

Skeletal muscle relaxedSkeletal muscle cont racted



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Venous Return

Respiratory pump

Inspiration

Decreases pressure in thoracic cavity Increases pressure in abdominal cavity

Pressure on veins in abdominal cavity

creates gradient favoring blood movement to

thoracic cavity

Increases central venous pressure

Increases venous return



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Venous Return

Blood volume

Increased blood volume increased venous pressure

Decreased blood volume decreased venous pressure

Long-term regulation of blood pressure occurs through

regulation of blood volume



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Venous Return

Venomotor tone

Smooth muscle tension in the veins

Increase in venomotor tone

Contraction of smooth muscle in the wall of a vein

Smooth muscle in walls of veins is innervated by sympathetic

nervous system

Norepinephrine acting at adrenergic receptors causes venous

constriction Increases central venous pressure

Decreases venous compliance

Increases venous return

Act iv ity o fmuscle pump

Act iv ity o f

respiratory

Act iv ity i n

sympatheticBlood

volume

Slide 1Figure 14.23 Factors affecting venous pressure and, therefore, mean arterial pressure.


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2013 Pearson Education, Inc. Result

Initial stimulus

muscle pumppump nerves to veins

volume

Veins

Venomotor ton e

Venous compliance

Venous pressure

Venous return

Heart

Atr ial pressure

End-diastolic pressure (preload)

End-diastolic vo lume (EDV)

Stroke volume (SV)

Cardiac outpu t (CO)

Mean arterial pressure (MAP)

Physiological response

14.7 The Lymphatic System


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System of vessels, nodes, and organs

Vessels are involved in returning excess filtrate to

circulation

Vessels form an open system starting at the capillaries

Lymph moves from capillaries to veins

Lymphatic veins drain into the thoracic duct, which empties

into the right atrium

Lymph moves through the lymphatic veins in the same wayas blood flows through regular veins

Also part of immune system (macrophages)

Lymphatic capillaries

Lymph flow

Figure 14.24 The lymphatic system.


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Lymphnode

Pulmonarycapillaries

Pulmonary Circuit

Systemic Circuit

Valve Lymphnode

Lymph

flow Lymphatic capillaries

Systemiccapillaries

Bloodflow

14.8 Mean Arterial Pressure and Its Regulation


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Determinants of mean arterial pressure

Heart rate

Stroke volume

Total peripheral resistance

Regulation of mean arterial pressure

Neural control

Hormonal control

Control by low-pressure baroreceptors (volume receptors)

Determinants of Mean Arterial Pressure


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Heart rate

Stroke volume

Total peripheral resistance

Calculations

MAP = CO TPR

CO = HR SV

Therefore: MAP = HR SV TPR

AortaFigure 14.25a-b How increases in cardiac output and total peripheral resistance increase mean arterial p ressure.


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From

heartFlow (CO) Flow

To

systemic

organs

Flow (CO) Flow

An increase in

cardiac output . . .

. . . leads to an increase in the volume

of blood contained in the aorta and

an increase in mean arterial pressure . . .

. . . when total peripheral

resistance remains the

same.

Constant MAP

Increased MAP

Figure 14.25c How increases in cardiac output and total peripheral resistance increase mean arterial pressure.


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Flow (CO) Flow

A constant

cardiac output . . .

. . . leads to an increase in the volume

of blood contained in the aorta and

an increase in mean arterial pressure . . .

. . . when total peripheral

resistance increases.

Increased MAP



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Extrinsic control of arteriole radius

MAP is regulated through control of the heart (CO) and

arterioles and veins (TPR)

Neural control

Hormonal control



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MAP: driving force for blood flow

F = P/R

Regulating MAP is critical to normal function

MAP < normal

Hypotension

Inadequate blood flow to tissues

MAP > normal Hypertension

Stressor for heart and blood vessels

Regulation of Mean Arterial Pressure


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Short-term regulation: seconds to minutes

Regulates cardiac output and total peripheral resistance

Involves the heart and blood vessels

Primarily neural control

Long-term regulation: minutes to days

Regulates blood volume

Involves the kidneys

Primarily hormonal control



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Neural control of MAP

Negative feedback loops

Detector = baroreceptors

Integration center = cardiovascular centers in the

brainstem

Controllers = autonomic nervous system

Effectors = heart and blood vessels



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Baroreceptors = pressure receptors

Sometimes called stretch receptors

Arterial baroreceptors = sinoaortic receptors

Aortic arch

Carotid sinuses

Respond to stretching due to pressure changes in

arteries

Carotid bifurcation

Carotid sinus

Figure 14.26 Arterial baroreceptors.


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Carotid sinus

Common carotidartery

Arterialbaroreceptors

Aorticarch

Figure 14.27 Response of arterial baroreceptors to changes in arterial p ressure.

DecreasedIncreased


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pressurepressureNormal

Arterialpressure(mm Hg)

Baroreceptorresponse(membranepotential, mV)

Baselinefrequency

Increasedaction potential

frequency

Decreasedaction potential

frequency

Action potentials

70

110



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Cardiovascular control center

Medulla oblongata

Integration center for blood pressure regulation



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Input

Arterial baroreceptors

Low-pressure baroreceptors

Chemoreceptors

Proprioceptors

Higher brain centers

Output Sympathetic nervous system

Parasympathetic nervous system



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Autonomic output to cardiovascular effectors

Parasympathetic input to

SA node (decreases HR)

AV node

Sympathetic input to

SA node (increases HR)

AV node

Ventricular myocardium (increases contractility)

Arterioles (increases resistance)

Veins (increases venomotor tone)

Dorsal motornuclei of

Parasympathetic

preganglionic

Figure 14.28 Major neural pathways in the cont rol o f cardiovascular function.


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nuclei ofthe vagus

Cardiovascular

control centers

p g g

(vagus nerve)

Medulla

oblongata

SA node

Ventricular

myocardium

Sympathetic

Sympathetic

Heart

Ar ter io les

Veins

Spinal cord Sympathetic chain

Sympathetic



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Baroreceptor reflex: negative feedback loop to maintain

blood pressure at normal level

Detectors = baroreceptors

Afferents = visceral afferents

Integration center = cardiovascular control center

Efferents = autonomic nervous system

Effectors = heart, arterioles, and veins

MAP

Figure 14.29 The events in the baroreceptor reflex in response to a drop in mean arterial pressure. Slide 1


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Ar ter ial b aroreceptors

Frequency of

action p otentials

conducted to CNS


Parasympathetic activity Sympathetic activity

SA node Ventricular myocardium Veins Arterioles

Act ion potent ialfrequency Contractility Venomotor tone Vasoconstriction

Compliance

Venous pressure

Negative

feedback

HR SV

EDV

TPR

MAPPhysiological response

Initial stimulu s

Result



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Baroreceptor reflex in action

Hemorrhage

Decreases blood volume

Blood volume decrease decrease in mean arterial pressure

Triggers the baroreceptive reflex

Increases sympathetic activity

Decreases parasympathetic activity

Increased resistance and decreased blood flow in GI tract

Blood diverted from GI tract to brain

ReflexcompensationHemorrhageControl

Figure 14.30 Baroreceptor-mediated responses to hemorrhage.


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Heartrate

Strokevolume

Cardiacoutput

Totalperipheral

resistance

Meanarterial

pressure



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Long-term regulation

Baroreceptor reflex quickly compensates for changes in blood

pressure

Does not correct the problem

Long-term regulation occurs through renal regulation of bloodvolume

Hormonal control

Epinephrine

Vasopressin

Angiotensin II



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Epinephrine

Released by adrenal medulla in response to sympathetic activity

Increases mean arterial pressure

Acts on smooth muscle of arterioles

Increases TPR

Acts on smooth muscle of veins

Increases venomotor tone

Acts on heart

Increases HR and SV



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Vasopressin and angiotensin II

Vasoconstrictors

Increase TPR

Increase MAP


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Cardiac and venous baroreceptors

Low-pressure baroreceptors = volume receptors

Location

Walls of large systemic veins

Walls of the atria

Decrease in blood volume activates receptors which

trigger responses that act in parallel with the

baroreceptor reflex


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Thank You !!!

ch 14 lecture physiology 5e

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