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Blood Vessels, Blood Flow, and Blood Pressure with figure

Chapter 14 – Blood Vessels, Blood Flow, and Blood
Pressure

Physical Laws Governing Blood Flow and Blood Pressure

     The flow of blood within vessels is
directly proportional to the pressure gradient and is
inversely
proportional to the resistance within the vessel:

Flow =  DP/R

 

     The pressure gradient is the force that
pushes the liquid through the vessel.
Pressure Gradients in the Cardiovascular System

     Whenever there is a difference in
pressure between two locations fluid flows from the region of
high pressure to that of low by bulk flow. The heart causes
blood to flow by creating a mean arterial pressure that is greater
than the pressure in the veins. Hence, a pressure gradient drives
the blood from the arteries to the veins.
     As blood flows from the arteries to the
veins the pressure decreases. This decrease in pressure
is called  a pressure drop. The pressure drop is
greatest in the arterioles and greater in the
systemic compared to the pulmonary circuit.
     figure_14_03_labeled-6261901
Pressure Gradient Across Systemic and Pulmonary Circuits

      figure_14_02_labeled-7759735
     In the systemic circuit the pressure
gradient is virtually identical to the mean arterial pressure
(the average pressure in the aorta throughout the cardiac cycle)
of 85 mm Hg. This is because the pressure at the other end is the central
venous pressure
which is approximately 2-8 mm Hg and very close
to 0 mm Hg. In a similar way
the pressure gradient in the pulmonary circuit is about 15 mm Hg
which is about equal to the mean pulmonary arterial pressure.
Resistance

     Blood flow through the pulmonary circuit
is identical to that through the systemic circuit (5 liters/minute).
However, the pressure gradient in the pulmonary circuit is
considerably less than that through the systemic circuit. The
equality of blood flow through the circuits is due to the lesser
resistance offered by the pulmonary circuit.
    
     In individual vessels at a given
pressure gradient, the higher the resistance the lower the flow.
   Resistance depends on the following
factors:

1. Vessel Radius

   Changes in the resistance in
the cardiovascular system is almost always due to
this factor. Vascular resistance can be
controlled in small arteries and arterioles by
contraction
(vasoconstriction) or relaxation
(vasodilation) of the smooth muscle in the vessel wall. Vasoconstriction
increases resistance and vasodilation decreases
resistance.
2. Vessel Length

   The longer the vessel the

greater the resistance
but this is not an important
factor for control.
3. Blood Viscosity

   Vascular resistance
increases as viscosity increases
. But this is not
usually an important factor. The major determinant of
blood viscosity is the concentration of cells and
protein in the blood with viscosity increasing with
each.
Total Peripheral Resistance


For any blood vessel network the total
flow increases in proportion to D P and decreases with R just as with individual
vessels. The resistance of a network depends upon the individual
resistances within the network.
     Total peripheral
resistance
is the combined resistances of all the blood vessels
within the systemic circuit. The greatest amount of resistance comes
from arterioles and small arteries and these are called resistance
vessels.
Total peripheral resistance is almost entirely due to
changes in the diameter of resistance vessels.

Relating Pressure Gradients and Resistance in the
Systemic Circulation

     Cardiac output (flow) is equal to
the mean arterial pressure (pressure gradients) over total
peripheral resistance
(resistance). Hence, CO = MAP/TPR.
Overview of the Vasculature

      Review the anatomy
shown in figures 14.5 and 14.6.
Arteries

     Arteries conduct blood away from
the heart and toward the body tissues. The larger arteries
have more fibrous tissue in their walls that resist
pressure and provide elasticity. The smaller arteries have more
smooth muscle
in their walls and regulate flow by vasoconstriction
and vasodilation. 
Arteries Serve as a Pressure Reservoir

     During systole blood is
pumped into the arteries under pressure. Because of the low
compliance
of arteries, the pressure within the
arteries rises rapidly. During diastole the pressure
within arteries (held in reserve) is released and
contributes to continued flow of blood during diastole.
    
Arterial Blood Pressure

     The pressure of blood in the
aorta is the arterial blood pressure. Arterial
blood pressure varies during the cardiac cycle with maximum
pressure called systolic pressure because it
occurs during systole and minimum pressure called diastolic
pressure
because it occurs during diastole. The
average arterial pressure during the cardiac cycle is
the mean arterial pressure (MAP). 
Arterioles

     The arterioles provide
the greatest resistance to blood flow. This is
illustrated in the figure below by the large pressure drop that
occurs while blood flows through the arterioles.
     
     The walls of the
arterioles contain smooth muscle that can control the diameter,
and hence the resistance, by contracting or
relaxing. For this reason, the resistance to flow
offered by the arterioles can be regulated. This enables
the arterioles to:

1. Control blood flow to
individual capillaries
.
2. Regulate mean arterial
pressure
.
     The smooth muscle of
arterioles consists of single-unit smooth muscle
that have pacemaker cells that spontaneously depolarize.
Because of this the smooth muscle spontaneously contract
and give the arterioles tone, arterial tone. 
     The contractile state
of the arterioles can be increased or decreased by
external factors. Contraction of smooth muscles causes vasoconstriction
or decrease in diameter and increase
in resistance.
Relaxation of smooth muscle causes vasodilation
or increase in diameter and decrease in
resistance.

Intrinsic Control of Blood Flow
(Distribution to Organs)

     Changes in the
percentage of the total blood flow to individual organs
are due to changes in the vascular resistance of each
individual organ. In other words, intrinsic mechanisms
regulate the distribution of blood flow among organs. In
addition, intrinsic mechanisms also control the
distribution of blood flow to capillary beds within
the organ.
     Intrinsic control
mechanisms are particularly important in the heart,
brain and skeletal muscle
for two reasons:

1. constant blood flow to the brain
and heart is essential;
2. blood flow in skeletal muscle
and cardiac muscle needs to adjust to
varying metabolic demand. This is also true to a
lesser extent in the brain where blood flow needs
to increase in regions that are more active.
Smooth Muscle Effects Intrinsic Control

     Smooth muscle
itself changes vascular resistance by contracting
or relaxing in response to the following factors:

1. Metabolic Activity

   Changes in
metabolic activity change the
concentration of a number of
substances including oxygen and
carbon dioxide. Concentration
of these substances effect whether
smooth muscle contracts or relaxes. Except
for the pulmonary circulation,
increased metabolic activity
causes
vasodilation and decreased
metabolic activity
causes vasoconstriction. 
   For
example, when metabolic activity
rises, oxygen decreases and
carbon dioxide increases and
blood flow becomes insufficient to
meet demand. This condition is called ischemia.
However, smooth muscles responds
by relaxing which increases blood
flow. The increased blood flow
supplies more oxygen and removes more
carbon dioxide. The increased blood
flow associated with increased
metabolic activity is called active
hyperemia. 
2. Blood Flow

   If blood
flow either increases or decreases
above or below metabolic needs this
causes change in oxygen and carbon
dioxide concentration which leads to
the changes described above. The
increase in blood flow that follows a
reduction in blood flow is called reactive
hyperemia.
A rise in blood flow
also elicits an intrinsic control
mechanism that causes vasoconstriction
so this mechanism also works in
reverse.
   The mechanism
for the changes that occur in
response to changes in blood flow is
the same
as that that occurs with
changes in metabolic activity. In both
cases there is a change in the concentration
of key molecules
. The only
difference is in the cause of
the change.
3. Stretch of Arterial
Smooth Muscle

   Some
arterial smooth muscle fibers are stretch-sensitive
fibers.
When blood flow increases
these fibers are stretched and
they respond by contracting. On
the other hand, when blood flow decreases
the tension on these fibers decreases
and the muscles relax. This
response of the muscle themselves to
physical blood flow is called the myogenic
response.
   The key
variable that is regulated by this
mechanism is blood flow. 
4. Locally Secreted
Chemical Messengers

    A
variety of chemicals affect vascular
smooth muscle. Most of these cause vasodilation.
These include chemicals secreted
by endothelial cells such as nitric
oxide
which is secreted on a
continual basis.
Bradykinin
and histamine are
released by cells in response to
tissue injury and stimulate nitric
oxide synthesis and vasodilation that
is associated with the inflammatory
response. Prostacyclin is a
potent vasodilator that helps prevent
blood clots. Adenosine is an
important vasodilator in coronary
arteries. 
    A
chemical that is secreted by endothelial
cells
that promotes vasoconstriction
is endothelin-1.
    See
Table 14.1 for a list of these
chemicals.
Extrinsic Control of Arteriole Radius and Mean Arterial
Pressure

     Mean arterial pressure is related
to arteriole radius by the equation:

MAP = CO x TPR

     Since arteriole radius is the most
important factor influencing TPR, understanding the extrinsic
control of arteriole radius is important for understanding the
regulation of mean arterial pressure.

  Sympathetic Control of Arteriole
Radius

     Sympathetic neurons
innervate the smooth muscle of most arterioles. The norepinephrine
that is released as the neurotransmitter binds to a
adrenergic receptors
and causes vasoconstriction.
This increases MAP by increasing TPR.
     Epinephrine
released by the adrenal medulla bind to both a
and ß2 adrenergic receptors.
Activation of  ß2 receptors causes vasodilation.
Because a1
receptors outnumber ß2 receptors in most
locations, epinephrine at high concentration causes
vasoconstriction and increases MAP. ß2 receptors
predominate in the vessels of the heart and skeletal
muscle
and promote blood flow into these organs
during stress by causing vasodilation. Hence,
blood flow needed by the heart and skeletal muscle
during vigorous activities is maintained.
  Hormonal Control of Arteriolar
Resistance

     In addition to
epinephrine two other hormones cause vasoconstriction
and increase MAP:
  Vasopressin (ADH)

    Vasopressin
increases mean arterial pressure by promoting vasoconstriction.
It also promotes an increase in MAP by limiting
urine output
and raising blood volume. This is
why it is also called antidiuretic
hormone. 
  Angiotensin II

    Angiotensin II
is derived from angiotensinogen which
is present in the plasma. Angiotensinogen is
converted to angiotensin I by renin which
is secreted by the kidney. Angiotensin I is
converted to angiotensin II by angiotensin
converting enzyme
(ACE) which is
present on the inner surface of the blood vessels
particularly in the lungs.
Capillaries

    Capillaries are the smallest and
most numerous of blood vessels. The thin wall of capillaries consist
of only an endothelial cell and the supporting basement
membrane. The thinness of the capillary wall promotes the rapid and
efficient exchange of material between the blood and the
tissue.
 Movement of Materials Across Capillary
Walls

    The permeability of
capillary walls to water and small solutes allows bulk flow
of fluid across the wall. Movement of fluid from the
plasma to interstitial fluid is called filtration and
movement of fluid from interstitial fluid to plasma is called absorption.
A net shift of fluid from plasma to interstitial fluid
causes tissue swelling called edema. 
    The forces that drive
movement of fluid into and out of capillaries are called Starling
forces
and includes:

1. Capillary
hydrostatic pressure (Pcap)
or the
hydrostatic pressure of fluid in the capillaries.
2. Interstitial
hydrostatic pressure (Pif)
or the
hydrostatic pressure of fluid outside the capillary.
3. Capillary osmotic
pressure (?cap)
due to the
presence of non-permeating solutes inside the
capillaries.
4. Interstitial fluid
osmotic pressure (?if)
due to the
presence of non-permeating solutes outside the
capillaries.
    
Hydrostatic Pressure Gradient

     The hydrostatic pressure gradient is
equal to the difference of the hydrostatic pressure within the
capillary and the hydrostatic pressure in the interstitial fluid.
The pressure inside the capillary is about 38 mm Hg at the
arteriolar end and 16 mm Hg at the venous end. The interstitial
hydrostatic pressure is about 1 mm Hg. Hence, there is a net
hydrostatic pressure
pushing fluid out of the capillaries of
37 mm
Hg
at the arteriolar end and 15 mm Hg at the venous end.
Osmotic Pressure Gradient

     Water flows from a region where the
osmotic pressure is lower to a place where it is higher when
separated by a semipermeable membrane. Osmotic pressure differences
between capillaries and the interstitial fluid is due to a
difference in the protein concentration. The osmotic pressure
exerted by the proteins is called colloid osmotic pressure or
oncotic pressure. Because
there is a higher concentration of proteins in the capillaries
compared to the interstitial  fluid the oncotic pressure
gradient is directed inward. That is, it drives water into the
capillaries. The oncotic pressure gradient across the capillary wall
is about 25 mm Hg.
Net Filtration Pressure

     The direction of water movement is
determined by net filtration pressure. Net filtration pressure is
determined by the difference between the hydrostatic pressure
gradient and the oncotic pressure gradient. Filtration is associated
with a positive net filtration pressure while absorption is
associated with a negative net filtration pressure (see Table
14.3).
     Under normal conditions both filtration
and absorption are occurring in the capillaries. At the arteriolar
end
of the capillary where the hydrostatic pressure exceeds oncotic
pressure there is filtration, at the venous end where hydrostatic
pressure is less than oncotic pressure there is absorption.
     Under normal conditions 20 liters of
fluid is filtered every day and about 17 liters are absorbed for a
net filtration of about 3 liters of fluid. The 3 liters of fluid
that is filtered is returned by the lymphatic system.
 Factors Affecting Filtration and
Absorption Across Capillaries

     A nonpathological factor
that alters net filtration in the lower extremities occurs as the
result of standing. Prolonged standing increases
capillary hydrostatic pressure and increases net filtration.
     Pathological factors that
increase net filtration include:

  Tissue injury that
results in loss of fluid and plasma proteins
associated with capillary damage and the inflammatory
response.
  Liver disease that
results in decrease of plasma protein and a
consequent decline in capillary oncotic pressure.
  Kidney disease that
results in retention of fluid and/or loss of
plasma protein.
  Heart disease that
increases
hydrostatic pressure in the pulmonary
capillaries and causes pulmonary edema.

Veins

     Veins have roughly the
same diameter as arteries but have walls about one-half as thick.
The thinness of the wall reflects the fact that blood pressure is
much lower in the veins.
  Veins Serve as a Volume Reservoir

     Veins can
accommodate a large increase in blood volume
because of their high compliance (expansion due to
pressure). This enables the veins to hold a large volume of
blood at a given pressure. Veins also contain a
larger proportion of blood volume than any other part
of the circulation.
    
    The existence of
this volume reserve is important because it enables the
circulation to sustain a loss of total blood
volume
without a loss of central venous pressure
and as a means by which central venous pressure can
be increased during exercise.
  Factors That Influence Venous Pressure and Venous Return

     Venous
pressure has an important affect on mean arterial pressure
because it affects venous return to the heart and influences
end-diastolic volume. This in turn increases stroke
volume and cardiac output according to Starling’s law of the
heart. Venous pressure is due to the pressure difference
between the peripheral veins and the right
atrium
. It is about 15 mm Hg
     Factors that
affects venous pressure include:

Skeletal Muscle Pump

     
   Muscle contraction forces
blood toward the heart because of the one-way valves
within the veins.
By alternately contracting and relaxing, the
skeletal muscles drive blood toward
central veins and increases venous pressure.
Respiratory Pump

   During inhalation the
pressure in the thoracic cavity falls and abdominal
pressure rises. This creates a pressure gradient that
moves blood from the abdominal veins to the thoracic
ones. During exhalation flow back into the abdominal
veins is prevented by one-way valves and an increase in
thoracic pressure drives the blood toward the
heart.
Blood Volume

   An increase in blood volume
produces an increase in venous pressure and a
decrease has the opposite effect. Blood volume may
decrease
due to dehydration or blood loss.
Blood volume
may increase due to kidney failure.
   The high compliance of the
veins may result in venous pooling or accumulation of
blood in the veins. This lowers mean arterial
pressure by lowering venous pressure.
Venomotor Tone

   Neurons
of the sympathetic nervous system increase the
contractile activity in the venous smooth muscle and
increase venomotor tone. An increase in venomotor tone:

1. Increases
venous pressure
in peripheral veins and increases
blood flow to the central veins;
2. Reduces the
venous compliance
and thereby
increases venous pressure. Venous return
increases which increases stroke volume and mean
arterial pressure rises.
Lymphatic System

     The 3 liters of fluid filtered out of
the capillaries returns to the cardiovascular system by the
lymphatic system. Fluid enters the lymphatic system by way of
blind-ended ducts called lymphatic capillaries. The
capillaries carry the fluid by a system of ducts to two large ducts
that finally drain into the blood stream. Lymph flows through these
ducts by means of skeletal muscle contraction and one-way
valves
.
Larger ducts also have smooth muscles in their walls.
     Lymph nodes are located along the
lymph vessels. Foreign organisms (bacteria) and particles are
filtered in these lymph nodes where they can be phagocytized by macrophages
and where lymphocytes can react with the foreign substances to
stimulate an immune response.
Mean Arterial Pressure

     Mean arterial pressure is
determined by :

1. Heart rate Both determine
CO
2. Stroke volume
3. Total peripheral resistance
     When mean arterial pressure is steady,
flow into and out of the aorta remains steady. When cardiac output
suddenly increases and total peripheral resistance remains the same,
the mean arterial pressure increases. If there is a sudden increase
in total peripheral resistance and cardiac output remains the same
there is also an increase in mean arterial pressure.
Regulation of Mean Arterial Pressure

     Mean arterial pressure needs to be
maintained at a proper level for the organs to function properly.
Control of mean arterial pressure is accomplished by the central
nervous system
and circulating hormones. There is both short term
and long term control of MAP. Short term operates from
seconds to minutes and is our major concern.
Neural Control of MAP

     MAP is regulated by negative feedback
control
. MAP is the regulated variable that is monitored by arterial
baroreceptors sensors.

  Arterial Baroreceptors

     Arterial receptors are found in

1. Aortic arch
2. Carotid sinuses of the carotid
arteries.
     Baroreceptors respond to changes in

pressure
within the CV system. When the walls of arteries stretch
in
response to an increase in pressure the sensory endings of
baroreceptors neurons are stretched and this induces depolarization.
The depolarization triggers action potentials that then travel to
the central nervous system.
    
     When MAP changes these neurons make the
appropriate changes in the heart and blood vessels.
  Cardiovascular Control Center of Medulla Oblongata

     The neural control of mean
arterial pressure resides primarily in the medulla oblongata. Sensory input to the medulla include:

1. Arterial baroreceptors
2. Baroreceptors in the heart and
large systemic
veins
that sense venous pressure (volume receptors).
3. Chemoreceptors that sense oxygen, carbon
dioxide and hydrogen ion concentration
4. Proprioceptors in skeletal muscle and joints
5. Receptors in internal organs
Input from higher brain centers to the medulla
include:

1. Hypothalamus

   Controls
flight-or-fight responses 
   Regulates resistance
of blood vessels in skin
for temperature control
2. Cerebral Cortex

   Controls response to
pain
and emotion and to exercise
   Modulates medulla’s
response to sensory inputs
  Autonomic Inputs to Cardiovascular Effectors

     The cardiovascular centers of the
medulla exerts control over the sympathetic
and parasympathetic neurons that innervate the
heart and blood vessels. Sympathetic input travels via preganglionic
fibers that emerge from the spinal cord and synapse with
postganglionic fibers in the sympathetic trunk ganglia
and collateral ganglia.
Parasympathetic input travels to the heart via preganglionic fibers
in the vagus nerve (X) that synapse with postganglionic neurons in
the heart itself.
     The primary neural control of
cardiovascular function is exerted by the sympathetic neurons to:

1. the sinoatrial node to control heart
rate
2. the ventricular myocardium to control ventricular
contractility
3. the arterioles to control vascular
resistance
4. the veins to control venomotor tone
    
     The parasympathetic only exerts control
over the heart rate at the sinoatrial node.
Baroreceptor Reflex

     A drop in MAP is detected by arterial
baroreceptors and this results in a decrease in frequency of action
potentials. This results in decreased parasympathetic activity and

increased sympathetic
activity. The increased sympathetic activity
results in increased heart rate, stroke volume and total peripheral
resistance
all which increase MAP.
     
     Figure
above
illustrates the baroreceptor
reflex during blood loss. The stroke volume and cardiac output drops
and brings down the mean arterial pressure. The baroreceptor reflex
then causes the heart rate and total peripheral resistance to
increase which raises the mean arterial pressure. The baroreceptor
reflex triggers an increase in total peripheral resistance by
sympathetic stimulation of vasoconstriction. Certain organs are
spared because of their need for a continual blood flow. These vital
organs include the heart and the brain.
     The baroreceptor reflex produces only a
quick temporary fix. Long term fixes require an adjustment in blood
volume that can be achieved by regulation of fluid intake and
excretion.
Hormonal Control of MAP

   Epinephrine

    Epinephrine affects both cardiac
output
and total peripheral resistance. 
    At the heart, epinephrine
binds to receptors at the SA node and increases heart rate
by increasing the frequency of action potentials. Epinephrine
also binds to receptors on the ventricular myocardium which
increases cardiac contractility.
    At the vasculature,
epinephrine causes vasoconstriction in most
vascular beds but can cause vasodilation in skeletal and

cardiac muscle
. Most often the effect of epinephrine is to increase
total peripheral resistance.
    Hence, epinephrine increases
mean arterial pressure by increasing heart rate, stroke
volume and total peripheral resistance.
   Vasopressin (ADH)

   Acts by promoting vasoconstriction
in most tissue and thereby increasing total
peripheral resistance (TPR) and mean arterial pressure. Also
known as antidiuretic hormone because it also acts upon
the kidneys to decrease urine production (diuresis). This
helps to maintain blood pressure by conserving blood volume.
   Angiotensin II

   Angiotensin II is derived
from angiotensinogen which is present in the plasma.
Angiotensinogen is converted to angiotensin I by renin
which is secreted by the kidney. Angiotensin I is converted to
angiotensin II by angiotensin converting enzyme which
is present on the inner surface of the blood vessels
particularly in the lungs.
   Angiotensin II increases mean
arterial pressure by promoting vasoconstriction, reducing urine
output by the kidneys, and stimulating thirst.
Other Cardiovascular Regulatory Processes

   Respiratory Sinus Arrhythmia

     This is a rhythmic
variation in heart rate in which inspiration is accompanied by
an increase in sympathetic activity and heart rate whereas
expiration is accompanied by an increase in parasympathetic
activity and a decrease in heart rate
.
   Chemoreceptor Reflexes

     When arterial
carbon dioxide
levels rise
, chemoreceptors in the carotid sinus and brain
trigger a decrease in heart rate and in increase in peripheral
resistance
. This helps to conserve oxygen and to insure that
the brain continues to receive an adequate supply of oxygen.
This reflex also prevents a widespread drop in
mean arterial pressure
due to
local reflexes causing vasodilation in response to decreased
oxygen and increased carbon dioxide levels.
   Thermoregulatory Responses

     Thermoreceptors in
various locations around the body provide input to the
hypothalamus where the thermoregulatory center is located.
When the body’s temperature rises the decrease in
sympathetic
activity
in the nerves supplying the skin causes vasodilation
and heat loss through the skin. A decrease in body temperature
increases the sympathetic activity in the nerves supplying the
skin and causes vasoconstriction and conservation of heat by
shunting blood away from the skin.
   Response to Exercise

     During exercise
cardiac output increases blood flow. Flow to skeletal muscles,
cardiac muscle and skin increase while flow to the liver and
gastrointestinal tract decrease. There is a total overall
drop
in total peripheral resistance
but this does not cause a drop
in MAP because of the increase in cardiac output.
     These responses to
exercise is triggered by cortical and limbic regions of the
brain that influence the output of sympathetic and
parasympathetic neurons. As a result:
There is an increase
in sympathetic and a decrease in parasympathetic
activity to the heart that increases heart
rate
and ventricular contractility.
There is an increase
in sympathetic activity to digestive organs and
other organs that causes vasoconstriction.
There is a decrease
in sympathetic activity to the skin that
causes vasodilation.

Other mechanisms that promote an increase in the
venous return and thereby increase cardiac
output
are
The skeletal muscle pump,
The
respiratory pump,
An increase in
venomotor tone.

 

 

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