Transcript See Figures 10

The Blood Vessels and
Blood Pressure
Chapter 10
Some organs receive blood flow in
excess of their own needs. They are
the digestive organs, kidneys, and
skin.
• Blood is constantly reconditioned. This maintains
a relatively constant composition in the blood.
• Large percentages of the cardiac output are
distributed to the digestive tract, kidneys, and
skin. They are reconditioning organs. They can
withstand temporary reduction in blood flow.
• The blood flow distributed to other organs is less,
supplying their metabolic needs and adjusted to
their level of activity. These organs (e.g., brain)
do not have an extra margin of blood supply.
They do not tolerate significant reductions in
blood supply as well as the reconditioning
organs.
The flow rate of blood flow through a vessel is
directly proportional to the pressure gradient
and inversely proportional to vascular
resistance.
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F = delta P
R
The pressure gradient is the pressure difference between the beginning
and end of a vessel.
Blood flows from an area of higher pressure to an area of lower
pressure (pressure gradient).
Resistance is the opposition to blood flow through a vessel. It
depends on three factors: blood viscosity, vessel length, and vessel
radius.
The major determinant to resistance to blood flow is the radius of a
vessel. A slight change in radius produces a significant change in
blood flow. The blood flow arterioles is highly affected by this
relationship. It is expressed by the equation:
– R is proportional to 1divided by the radius raised to the fourth power
The vascular tree consists of
arteries, arterioles, capillaries,
venules, and veins.
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The systemic and pulmonary circulations each
consist of a closed system of vessels.
Arteries carry blood away from the heart to the
tissues. They branch into a tree of
progressively smaller vessels.
This progression forms arterioles near an organ.
Regulation of the diameter of arterioles
supplying an organ adjusts the volume of blood
sent to that organ.
Arterioles branch into capillaries, the smallest
vessels. They are the microscopic exchange
vessels with all cells, offering blood that
supplies the metabolic needs of the cells.
Capillaries merge into venules that send blood
into small veins. They form progressively larger
veins. Venules and veins return blood to the
heart.
Arteries are the rapid-transit
passageways to the tissues.
They also are a pressure reservoir.
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The large radius of arteries offers little
resistance to blood flow.
The elastic recoil in the walls of arteries
drives the flow of blood during cardiac
relaxation (ventricular diastole).
This elasticity is due to a thick middle
layer of smooth muscle with elastic
fibers in the wall of arteries.
Arteries expand from a large volume of
blood sent into them when the heart
pumps blood (ventricular systole). The
temporarily expand and hold this blood.
When the heart relaxes, the stretched
arteries passively recoil. This pushes
the excess blood toward the tissues.
This ensures a continuous flow of blood
to the tissues.
Arterial blood pressure fluctuates
in relation to ventricular systole
and diastole.
• Arteries are compliant (distensible).
• During ventricular systole, the stroke volume enters the arteries.
About one-third as much blood leaves the arteries at this time.
• No blood enters the arteries during diastole. However, the blood
continues to leave the arteries by elastic recoil.
• Systolic pressure is the maximum pressure in arteries when
blood is ejected into them during ventricular systole.
• The diastolic pressure is the minimum pressure in arteries when
the blood is draining off into the remainder of the vessels during
ventricular diastole.
Blood pressure can be
measured indirectly.
• It is measured by a sphygmomanometer. Its cuff is wrapped
around the upper arm.
• When the pressure in the cuff of this instrument is greater than
the brachial artery, blood flow is blocked through the vessel. At
this time no sound is heard through a stethoscope placed over
the brachial artery at the inside of the elbow.
• When the pressure in the cuff is slowly released, it will fall just
below systolic pressure. This creates vibrations and sound.
The first sound heart indicates systolic pressure (e.g., 120 mm
Hg).
• When the falling cuff pressure drops below diastolic pressure,
the vibrations and sound disappears. This indicates diastolic
pressure (80 mm Hg).
• The pulse pressure is the difference between the systolic and
diastolic pressures (120 - 80).
A mean arterial pressure is the main
driving force producing a flow of blood. It
can be calculated.
• The equation is:
– mean arterial pressure = diastole pressure plus 1/3 the pulse
pressure
• As one example, from the previous data : 80 plus 1/3
(40) equals 93
• This average is weighted, as about two-thirds of the
cardiac cycle is spent in diastole.
Arterioles are the major
resistance vessels.
• They offer high resistance to blood flow. The mean arterial
blood pressure in systemic arterioles drops significantly (e.g., 93
to 37). This pressure drop drives the flow of blood.
• Their pressure is not pulsatile.
• Arteriolar radii can be changed to alter the distribution of blood
flow to organs and to regulate arterial blood pressure.
• Their radii change by vasoconstriction (narrowing) and
vasodilation (enlargement). To produce these changes their
thick, middle layer of smooth muscle is subject to neural,
hormonal, and local chemical control.
• The vascular tone of this smooth muscle establishes a baseline
of vascular resistance. This ongoing tone makes changes in
radius size possible.
– See Figure 10-10
Local control of arteriolar
resistance determines the
distribution of the cardiac output.
• The driving force for blood flow is identical to all organs.
• However, differences in arteriolar resistance varies between
organs. This determines the distribution of blood they receive.
• Blood flow to an organ can vary by the change in resistance in
arterioles serving it.
• For example, during exercise more blood flow is shifted to the
skeletal muscles. Less flows to the digestive tract. In this case
the arterioles to the skeletal muscles dilate, offering less
resistance. The arterioles serving the digestive tract constrict.
• Local chemical influences on the resistance of arterioles include
local metabolic changes and histamine release. Local physical
influences include local heat and cold and myogenic responses
to stretch.
Local chemical changes on the smooth
muscle of arterioles are important. These
changes meet the metabolic needs of
cells.
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During increased metabolic activity (e.g. skeletal muscle activity during
exercise) the local concentration of oxygen decreases. This and other
local chemical changes relax the smooth muscle wall in arterioles.
They dilate by this response, called active hyperemia.
Less metabolic activity causes the opposite condition and response of
the arterioles.
Other local chemical changes that relax the smooth muscle in
arterioles, causing vasodilation, are:
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increased carbon dioxide
increased acidity
increased K+ ion concentration
increased osmolarity
adenosine release
prostaglandin release
Local vasoactive mediators also have an effect
– See Figure 10-12
Local histamine release
pathologically dilates
arterioles.
– It is synthesized and stored in special connective tissue
cells.
• Local physical changes influence arteriolar radius.
– Local heat produces vasodilation. Local cold produces
vasoconstriction.
– Arteriolar smooth muscle that is passively stretched
increases its tone.
– By reactive hyperemia, arterioles in a region dilate when
other local blood vessels are blocked.
– By pressure autoregulation local mechanisms in the
arterioles keep blood flow constant when there are wide
variations in the mean arterial blood pressure driving the
blood.
Extrinsic sympathetic signaling
controls arteriolar radii.
• This regulates blood pressure. Sympathetic neurons supply the
smooth muscle in the walls of most arterioles.
• Increased sympathetic signaling produces generalized arteriolar
vasoconstriction. This increases the total peripheral resistance
(TPR, the total resistance of all peipheral vessels).
• Mean arterial pressure (MAP) equals:
– cardiac output x TPR
• As the TPR increases, the mean arterial pressure increases by
direct proportion.
• The increase in TPR is a generalized increase. Many arterioles
constrict to produce this effect, increasing the MAP. Organs
supplied by these constricting vessels receive less blood flow.
However, some arterioles serving organs (e.g., skeletal muscles
during exercise) dilate during this increase in TPR. These
organs receive more blood as the MAP increases.
Norepinephrine released from
sympathetic nerve endings when
combining with alpha-1 receptors.
This binding produces
vasoconstriction.
• Cerebral vessels lack these kind of receptors.
They are subject to local controls.
• Skeletal and cardiac muscle tissue have local
control mechanisms that overide generalized
sympathetic control mechanisms.
• Parasympathetic innervation is absent at
arterioles.
A cardiovascular control center in
the medulla regulates blood
pressure along with several
hormones.
• The medulla is the integrating center for
sending signals through sympathetic motor
pathways to the arterioles.
• Epinephrine and norepinephrine reinforce
sympathetic activity. They are secreted by
the adrenal medulla.
• Vasopressin and angiotensin are
vasoconstrictors. Vasopressin controls water
balance. Angiotensin controls salt balance.
Capillaries are the sites of
exchange between the blood
and body cells.
• This exchange is accomplished mainly by diffusion. This
process is enhanced the thin walls and narrow openings of
capillaries, plus their branching.
• Their thin walls is one, flat layer of epithelial cells. This is called
the endothelium.
• Capillaries are very abundant, offering a large surface area to
serve cells.
• The blood through capillaries is slow due to the tremendous
cross-sectional area of all capillaries in an area. This enhances
the opportunity for diffusion.
• Compared to arterioles, the resistance offered by capillaries is
low due to the large cross-sectional areas of these microscopic
vessels.
Capillaries have pores, water-filled
clefts in their walls.
• The pores allow the passage of small, water-soluble substances
such as ions and glucose.
• Lipid-soluble substances dissolve through the lipid bilayer in the
endothelial cells in the capillary wall.
• Tight junctions connecting the walls of capillary cells in the brain
form a blood-brain-barrier. This blocks transport.
• Histamine increases capillary permeability.
Under resting conditions many
capillaries do not open.
• Precapillary sphincters surround capillaries. A
sphincter is a ring of smooth muscle around the
entrance to a capillary.
• The contraction of these sphincters reduces the
blood flowing into the capillaries in an organ.
• The relaxation of these sphincters (e.g., an exercising
skeletal muscle) has the opposite effect.
• A metarteriole is a throughfare channel from an
arteriole to a capillary. Some capillaries are served
by them.
The interstitial fluid is a
passive intermediary between
the blood and tissue cells.
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20 percent of the ECF is blood plasma. 80 percent of the ECF is
interstitial fluid. This fluid bathes the tissue cells and is where these
cells exchange materials with the ECF.
Exchange between the interstitial fluid and plasma membranes of
tissue cells can be active (e.g., active carrier-mediated transport) or
passive (e.g., diffusion).
Exchange across the capillary wall, between the plasma and interstitial
fluid, is largely passive.
Diffusion across the capillary walls is important in solute exchange
(e.g., gases). Only the passage of plasma proteins is limited.
Some substances cross the capillary wall by bulk flow. Constituents in
a fluid move through in bulk. For example, fluid moving inside a
capillary can be pushed through the wall to the outside of the capillary
(from higher fluid pressure to lower fluid pressure)
By ultrafiltration, the capillary wall
acts as a sieve when fluid moves
from its inside (site of higher
pressure) to the interstitial fluid
outside the capillary.
– Plasma proteins remain in the capillary by this
process, unable to pass through the pores in the
capillary wall.
• By reabsorption there is a net inward
movement of fluid from the interstitial fluid into
the capillary.
– This occurs when inward-driving pressure
exceeds an outward opposing pressure across the
capillary wall.
Bulk flow occurs by the differences in
hydrostatic (fluid) and colloidal
osmotic pressures between the
plasma and interstitial pressures.
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Capillaries have pores allowing fluid passage.
Capillary blood pressure is the hydrostatic pressure exerted on the
inside of capillary walls by the blood. This forces fluid out of the
capillaries (the outward pressure).
The plasma-colloid pressure encourages fluid movement into the
capillaries (the inward pressure). The plasma has a higher protein
concentration compared to the interstitial fluid. This produces a water
concentration difference. Water enters the plasma from the interstitial
fluid by osmosis.
The interstitial fluid hydrostatic pressure is the pressure exerted on the
outside of the capillary wall by the interstitial fluid. It has a small value.
The interstitial fluid-colloid osmotic pressure is also insignificant in most
cases, as plasma proteins normally remain in the blood plasma.
A net exchange of fluid occurs across
the capillary wall.
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At the arteriolar end of the capillary the outward
pressure is greater than the inward pressure.
Fluid leaves the capillary by this difference.
Ultrafiltration occurs.
At the venular end of the capillary the inward
pressure is greater than the outward pressure.
The outward pressure has dropped due to a
drop of blood pressure at this end compared to
the arteriolar end. Reabsorption occurs.
Both ultrafiltration and reabsorption occur by
bulk flow. Fluid moves by a passive process.
This is not important in the exchange of
individual solutes between the blood and tissue
cells, as very few solutes move across capillary
walls by bulk flow.
Bulk flow does regulate the distribution of fluid
between the two regions of the ECF, the blood
plasma and interstitial fluid. Fluid shifts between
these two regions compensate for changes to
this distribution (.e.g, excessive fluid intake can
expand the plasma volume).
The lymphatic system is an
accessory route for the return
of interstitial fluid to the blood.
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Normally this return is not 100 percent.
The lymphatic system is an extensive system of one-way vessels that
begins with initial lymphatics.
Lymph is interstitial fluid that enters a lymphatic vessel. This fluid
contains escaped plasma proteins and bacteria that are not reclaimed
by the blood plasma.
Smooth muscle beyond the initial lymphatics propels lymph into larger
lymphatic vessels. The lymph is eventually combined with venous
blood near the heart.
The functions of the lymphatic system are:
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return excess filtered fluid
return filtered fluid
defense against disease by the lymph nodes
transport of absorbed fat from the digestive tract
See Figures 10-25 and 26
An accumulation of too much
interstitial fluid can produce edema,
an accumulation of fluid in the
interstitial fluid. Several conditions
can produce this.
• A reduced concentration of plasma proteins allows a drop in the
main inward pressure. More fluid enters the interstitial fluid.
• An increased permeability of the capillary wall allows more
plasma proteins to pass from the blood fluid into the interstitial
fluid.
• An increased venous blood pressure increases the capillary
blood pressure. This elevates the outward pressure along the
capillary wall.
• Blockage of lymph vessels retains fluid in the interstitial fluid
rather than returning the fluid to the capillaries.
Blood flows from the capillaries to the
veins. Veins return blood to the heart.
• The have large radii and offer low
resistance to the flow of blood.
• From the capillaries the velocity of
blood flow increases in the veins, as
they have a smaller total crosssectional area.
• Compared to arteries, veins are thinnerwalled and less elastic.
• Veins are capacitance vessels, serving
as a large blood reservoir. They are
highly distensible, able to accommodate
large volumes of blood. They hold 60%
of the blood volume of the body at rest.
• Extrinsic factors can drive this blood to
the heart for pumping.
Extrinsic factors enhance venous return.
• Venous return is the volume of blood entering each atrium per
minute. By their high venous capacity, veins have a large
volume of blood for this return.
• Venous return is enhanced by:
• increased sympathetic stimulation of the veins; Contraction of
the smooth muscle in the wall of the veins leads to their
constriction. This squeezes blood back to the heart.
• increased skeletal muscle activity; This compresses veins and
increases venous pressure. This drives blood toward the heart.
• Various mechanisms counteract the effect of gravity on venous
return.
• The closure of valves inside veins ensures that blood does not
flow backward.
• The respiratory pump creates a pressure gradient in the chest
cavity, drawing fluid toward the heart.
– See Figures 10-30 and 31
Blood pressure is regulated.
• It is regulated by cardiac output and total peripheral
resistance. Consider the equation:
• mean arterial pressure = cardiac output x total
peripheral
• resistance
• Cardiac output depends on heart rate x stroke
volume. Heart rate depends on autonomic control
plus some hormone signaling. Stroke volume
depends on sympathetic stimulation.
• Stroke volume also increases by venous return.
Venous return depends on several factors such as
venous vasoconstriction and the skeletal muscle
pump.
Total peripheral resistance
depends on the radius of
arterioles plus blood viscosity.
– This radius size depends on sympathetic
stimulation to the arterioles and local
metabolic/chemical controls. It is also controlled
by several hormones.
• Effective circulating blood volume influences
the blood volume returning to the heart.
– This blood volume depends on capillary exchange
which in the long term means controlling salt and
water balance.
• Mean arterial pressure is controlled by longterm and short-term measures.
The baroreceptor reflex is a short-term
mechanism for regulating blood pressure.
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Baroreceptors are found in the carotid
sinus and aortic arch. These receptors
are sensitive to fluctuations in pulse
pressure.
Baroreceptors generate action
potentials through afferent pathways to
a cardiovascular (integrating center) in
the medulla.
The efferent pathway is the autonomic
nervous system. The center in the
medulla alters the ratio of sympathetic
and parasympathetic activity to the
heart and blood vessels.
The heart and blood vessels are the
effector organs that respond to control
blood pressure.
Here is one example of the
baroreceptor reflex.
• Arterial blood pressure becomes elevated for some reason.
• Baroreceptors detect this change and increase the rate of action
potentials firing along afferent pathways from the receptors to
the medulla.
• The cardiovascular center interprets this input.
• Sympathetic output decreases. Parasympathetic output
increases.
• There is a decrease in the following responses: heart rate,
stroke volume, arteriolar resistance, and venous resistance.
The veins dilate.
• Therefore, cardiac output and total peripheral resistance
decrease.
• The elevated blood pressure returns to normal.
• A drop in blood pressure produces an opposite series of trends
and responses.
Other reflexes and responses
influence blood pressure.
• Left atrial receptors and hypothalmic osmoreceptors regulate
salt and water balance. They control plasma volume for longterm blood pressure regulation.
• Chemoreceptors in the carotid and aortic arteries are sensitive
to low oxygen and high acid levels in the blood. They increase
respiratory activity to reverse these trends.
• Behaviors and emotions from the cerebral cortex/hypothalamus
influence cardiovascular responses.
• Exercise modifies cardiovascular responses.
• The hypothalamus controls skin arterioles for temperature
regulation.
• Vasoactive substances have an effect.
Hypertension is a serious
national problem.
• Its causes are largely unknown.
• Secondary hypertension occurs secondary to other primary
problems. Its categories are renal (from the renin-angiotensin
mechanism), cardiovascular, endocrine, and neurogenic.
• 90 percent of hypertension cases are primary. Potential causes
include:
• defects in salt management by the kidneys
• excessive salt intake
• diets low in fruits, vegetables, and dairy products
• plasma protein abnormalities
• variation in the gene that encodes for angiotensinogen
• endogenous digitalis-like substances
• excess vasopressin
• Baroreceptors adapt to hypertension. They regulate blood
pressure, maintaining it at a higher level.
Complications of hypertension
include:
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congestive heart failure
stroke
heart attack
Without complications, hypertension is without
symptoms.
– It can be treated with therapy.
• Orthostatic hypotension results from transient
inadequate sympathetic activity.
– This is a fall in blood pressure.
Circulatory shock occurs when blood
pressure drops to a point where
blood flow is inadequate to serve the
tissues.
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There are four main types:
hypovolemic - caused by a fall in blood volume
cardiogenic - due to a weakened heart
vasogenic - from widespread vasodilation due to a release of
vasodilator substances
neurogenic - from widespread vasodilation, but not from the
release of vasodilator substances
Compensatory measure for circulatory shock include:
response by the baroreceptor reflex with increased sympathetic
activity and increase parasympathetic activity
fluid shifts in the capillaries and interstitial fluid (autotransfusion)
responses by the liver, urinary system, and thirst sensation
Reversible shock can be
corrected by compensatory
mechanisms and effective
therapy.
• Sometimes shock is irreversible.