The Cardiovascular System: Blood Vessels

Part 1: Overview of Blood Vessel Structure and

Function
Structure of Blood Vessel Walls
The walls of all blood vessels except the smallest consist of three layers:
the tunica intima, tunica media, and tunica externa.
The tunica intima reduces friction between the vessel walls and blood;
the tunica media controls vasoconstriction and vasodilation of the vessel;
and the tunica externa protects, reinforces, and anchors the vessel to
surrounding structures.

Arterial System

Elastic, or conducting, arteries contain large amounts of elastin, which

enables these vessels to withstand and smooth out pressure fluctuations
due to heart action.
Muscular, or distributing, arteries deliver blood to specific body organs,
and have the greatest proportion of tunica media of all vessels, making
them more active in vasoconstriction.
Arterioles are the smallest arteries and regulate blood flow into capillary
beds through vasoconstriction and vasodilation.
Capillaries are the smallest vessels and allow for exchange of
substances between the blood and interstitial fluid.
Continuous capillaries are most common and allow passage of fluids
and small solutes.
Fenestrated capillaries are more permeable to fluids and solutes than
continuous capillaries.
Sinusoidal capillaries are leaky capillaries that allow large molecules to
pass between the blood and surrounding tissues.

Capillary beds are microcirculatory networks consisting of a vascular

shunt and true capillaries, which function as the exchange vessels.
A cuff of smooth muscle, called a precapillary sphincter, surrounds each
capillary at the metarteriole and acts as a valve to regulate blood flow
into the capillary.

Venous System
Venules are formed where capillaries converge and allow fluid and white
blood cells to move easily between the blood and tissues.
Venules join to form veins, which are relatively thin-walled vessels with
large lumens containing about 65% of the total blood volume.
Vascular anastomoses form where vascular channels unite, allowing
blood to be supplied to and drained from an area even if one channel is
blocked .

Part 2: Physiology of Circulation

Introduction to Blood Flow, Blood Pressure, and Resistance
Blood flow is the volume of blood flowing through a vessel, organ, or the
entire circulation in a given period and may be expressed as ml/min
(blood flow of the entire circulation is equal to cardiac output).
Blood pressure is the force per unit area exerted by the blood against a
vessel wall and is expressed in millimeters of mercury (mm Hg).
Resistance is a measure of the friction between blood and the vessel
wall, and arises from three sources: blood viscosity, blood vessel length,

and blood vessel diameter. The variable with the greatest effect on
resistance is the diameter (or radius, 1/2 the diameter) of a particular
vessel - resistance drops exponentially as the radius increases.
TPR is total peripheral resistance - resistance throughout the entire
systemic circulation.

Relationship Between Flow, Pressure, and Resistance

If blood pressure increases, blood flow increases; if peripheral resistance

increases, blood flow decreases.
Peripheral resistance is the most important factor influencing local blood
flow, because vasoconstriction or vasodilation can dramatically alter
local resistance while systemic blood pressure remains unchanged (due
to homeostatic mechanisms that maintain systemic BP at a constant
value, see below).

Systemic Blood Pressure

The pumping action of the heart generates blood flow; pressure results
when blood flow is opposed by resistance.
Systemic blood pressure is highest in the aorta, and declines throughout
the pathway until it reaches 0 mm Hg in the right atrium.
Arterial blood pressure reflects how much the arteries close to the heart
can be stretched (compliance, or distensibility), and the volume forced
into them at a given time.
When the left ventricle contracts, blood is forced into the aorta,
producing a peak in pressure called systolic pressure (120 mm Hg).
Diastolic pressure occurs when blood is prevented from flowing back into
the ventricles by the closed semilunar valve, and the aorta recoils (70
80 mm Hg).
The difference between diastolic and systolic pressure is called the pulse
presssure.

The mean arterial pressure (MAP) represents the pressure that propels
blood to the tissues.

Capillary blood pressure is low, ranging from 4020 mm Hg, which

protects the capillaries from rupture, but is still adequate to ensure
exchange between blood and tissues.

Venous blood pressure changes very little during the cardiac cycle, and
is low, reflecting cumulative effects of peripheral resistance (17 mm Hg in
venules dropping to almost 0 mm Hg at the termini of the venae cavae).
Venous return is aided by both structural modifications and functional
adaptations.
Structural
Large lumen
Valves - present mostly in extremities, none in ventral body cavity
Functional

Respiratory Pump
Muscular Pump
Smooth muscle layer under sympathetic control

Maintaining Blood Pressure

Blood pressure varies with changes in blood volume, TPR, and cardiac
output, which are determined primarily by venous return and neural and
hormonal controls.
Short-term mechanisms include both (1) neural and (2) hormonal
controls, which alter blood pressure by changing peripheral
resistance and CO.
Long-term mechanisms alter blood pressure by using renal controls
to alter blood volume.

Short-term Mechanisms

Neural controls of peripheral resistance alter blood distribution to (1)

meet specific tissue demands and (2) maintain adequate MAP by
altering blood vessel diameter.
The vasomotor center is a cluster of sympathetic neurons in the medulla,
lying close to the cardioacceleratory and cardioinhibitory centers, that
controls changes in the diameter of blood vessels. It constantly sends
impulses to vascular smooth muscle to maintain a state of partial
contraction (remember "tone"?)
Most neural controls work through reflex arcs that send information on
stretch to effectors (muscle) that respond accordingly.
Chemoreceptors and input from higher brain centers can also influence
neural controls.
Baroreceptors
If mean arterial pressure rises, baroreceptors in the carotid sinus and
aortic arch detect stretch and send impulses to the vasomotor center,
inhibiting its activity and promoting vasodilation of arterioles and veins.
They also stimulate the cardioinhibitory center and inhibit the
cardioacceleratory center when stretched, reducing cardiac output.
A drop in mean arterial pressure causes vasocontriction and increased
cardiac ouput. The carotid sinus reflex protects blood flow to the brain,
while the aortic reflex maintains blood pressure throughout the systemic
circuit.

Chemoreceptors located near the baroreceptors in the carotid sinus and

aortic arch detect a rise in carbon dioxide levels, a drop in oxygen levels,
and drops in pH of the blood, and stimulate the cardioacceleratory and
vasomotor centers, which increases cardiac output and vasoconstriction.
The cortex and hypothalamus can modify arterial pressure by signaling
the medullary centers.
Hormonal Controls
Chemicals, both endocrine and paracrine, influence blood pressure by
acting on vascular smooth muscle or the vasomotor center.
Norepinephrine and epinephrine promote an increase in cardiac output
and generalized vasoconstriction when acting on alpha receptors (will
promote vasodilation at beta receptors, which are present in skeletal and
cardiac muscle).
Atrial natriuretic peptide acts as a vasodilator and an antagonist to
aldosterone, resulting in a drop in blood volume.
Antidiuretic hormone promotes vasoconstriction and water conservation
by the kidneys, resulting in an increase in blood volume.
Angiotensin II acts as a vasoconstrictor, as well as promoting the release
of aldosterone and antidiuretic hormone.
Endothelium-derived factors promote vasoconstriction, and are released
in response to low blood flow.
Nitric oxide is produced in response to high blood flow or other signaling
molecules, and promotes systemic and localized vasodilation.
Inflammatory chemicals, such as histamine, prostacyclin, and kinins, are
potent vasodilators.

Alcohol inhibits antidiuretic hormone release and the vasomotor center,

resulting in vasodilation.

Long-Term Mechanisms: Renal Mechanisms

The direct renal mechanism counteracts changes in blood pressure or

volume by altering blood volume independently of hormones. The direct
mechanism works best to counteract an increase in blood pressure
Increased blood pressure or volume increases the rate of kidney
filtration, causing filtrate to be formed faster than water can be
reabsorbed back into circulation.
The result is an increased volume of dilute urine and a decrease in blood
volume.
When faced with a decrease in blood pressure it does nothing to
increase blood volume, it just decreases the amount of filtrate formed,
increases reabsorption from filtrate to blood, and decreases the amount
of water lost in urine.

The indirect renal mechanism is the renin-angiotensin mechanism,

which counteracts a decline in arterial blood pressure by causing
systemic vasoconstriction.

Monitoring circulatory efficiency is accomplished by measuring pulse and

blood pressure; these values together with respiratory rate and body
temperature are called vital signs.
A pulse is generated by the alternating stretch and recoil of elastic
arteries during each cardiac cycle.

Systemic blood pressure is measured indirectly using the ascultatory

method, which relies on the use of a blood pressure cuff to alternately
stop and reopen blood flow into the brachial artery of the arm.
Alterations in blood pressure may result in hypotension (low blood
pressure) or transient or persistent hypertension (high blood pressure).

Blood Flow Through Body Tissues: Tissue Perfusion

Tissue perfusion is involved in delivery of oxygen and nutrients to, and
removal of wastes from, tissue cells; gas exchange in the lungs;
absorption of nutrients from the digestive tract; and urine formation in the
kidneys.

Velocity of Blood Flow

Velocity or speed of blood flow changes as it passes through the
systemic circulation; it is fastest in the aorta, and declines in velocity as
vessel diameter decreases (and then increases on the venous side as
vessel diameter increases again).

Autoregulation: Local Regulation of Blood Flow

Autoregulation is the automatic adjustment of blood flow to each tissue

in proportion to its needs, and is controlled intrinsically by modifying the
diameter of local arterioles. (Extrinsic influences control MAP.)
Metabolic controls of autoregulation are most strongly stimulated by a
shortage of oxygen at the tissues.
Vasodilators:
Decreased oxygen levels
Increased carbon dioxide levels
Decreased pH (increased H+ levels)
Increased K+ levels
NO - Nitric oxide, released from endothelial cells locally or from
hemoglobin can stimulate relaxation of smooth cells and inhibit
production of endothelin synthesis by endothelial cells.
Adenosine (causes hyperpolarization of vascular smooth cells)
extracellular ADP & ATP (stimulate NO production)
Prostaglandins (prostacyclin, prostaglandin D2, prostaglandin E2)
Vasoconstrictors:
Endothelins
Thromboxane A2
Myogenic control involves the localized response of vascular smooth
muscle to passive stretch - reflex contraction when stretched to
decrease flow, reflex relaxation when stretch is reduced to vasodilate
and increase flow. This maintains a relatively constant flow locally when
pressure fluctuates.
Long-term autoregulation develops over weeks or months, and involves
an increase in the size of existing blood vessels and an increase in the
number of vessels in a specific area, a process called angiogenesis.

Blood Flow in Special Areas

Blood flow to skeletal muscles varies with level of activity and fiber type.
Muscular autoregulation occurs almost entirely in response to decreased
oxygen concentrations.
Cerebral blood flow is tightly regulated to meet neuronal needs, since
neurons cannot tolerate periods of ischemia, and increased blood
carbon dioxide causes marked vasodilation.

In the skin, local autoregulatory events control oxygen and nutrient

delivery to the cells, while neural mechanisms control the body
temperature regulation function.
Autoregulatory controls of blood flow to the lungs are the opposite of
what happens in most tissues: low pulmonary oxygen causes
vasoconstriction, while higher oxygen causes vasodilation.
Movement of blood through the coronary circulation of the heart is
influenced by aortic pressure and the pumping of the ventricles.
Blood Flow Through Capillaries and Capillary Dynamics
Vasomotion, the slow, intermittent flow of blood through the capillaries,
reflects the action of the precapillary sphincters in response to local
autoregulatory controls.
Capillary exchange of nutrients, gases, and metabolic wastes occurs
between the blood and interstitial space through diffusion.
Routes:
Through the phospholipid bilayer directly (lipid-soluble molecules)
Intercellular capillary clefts
Fenestrations
Pinocytotic vesicles or caveolae

Fluid Movements: Bulk Flow (Starlings Law of the Capillary)

Hydrostatic pressure (HP) is the force of a fluid against a membrane.
Colloid osmotic pressure (OP), the force opposing hydrostatic pressure,
is created by the presence of large, nondiffusible molecules that are
prevented from moving through the capillary membrane.
Fluids will leave the capillaries if net HP exceeds net OP, but fluids will
enter the capillaries if net OP exceeds net HP.

Circulatory shock is any condition in which blood volume is inadequate

and cannot circulate normally, resulting in blood flow that cannot meet
the needs of a tissue.
Hypovolemic shock results from a large-scale loss of blood, and may be
characterized by an elevated heart rate and intense vasoconstriction.
Vascular shock is characterized by a normal blood volume, but extreme
vasodilation, often related to a loss of vasomotor tone, resulting in poor
circulation and a rapid drop in blood pressure.
Anaphylactic shock is an example of vascular shock
Neurogenic shock - failure of autonomic controls
Septic shock - bacterial toxins, some increase vascular permeability and
lower blood volume and others stimulate vasodilation.
Transient vascular shock is due to prolonged exposure to heat, such as
while sunbathing, resulting in vasodilation of cutaneous blood vessels.
Cardiogenic shock occurs when the heart is too inefficient to sustain
normal blood flow, and is usually related to myocardial damage, such as
repeated myocardial infarcts.

Part 3: Circulatory Pathways: Blood Vessels of the

Body
Two distinct pathways travel to and from the heart: pulmonary circulation
runs from the heart to the lungs and back to the heart; systemic
circulation runs to all parts of the body before returning to the heart.
There are some important differences between arteries and veins.
There is one terminal systemic artery, the aorta, but two terminal
systemic veins: the superior and inferior vena cava.
Arteries run deep and are well protected, but veins are both deep,
running parallel to the arteries, and superficial, running just beneath the
skin.
Arterial pathways tend to be clear, but there are often many
interconnections in venous pathways, making them difficult to follow.
There are at least two areas where venous drainage does not parallel
the arterial supply: the dural sinuses draining the brain, and the hepatic
portal system draining from the digestive organs to the liver before
entering the main systemic circulation.
Four paired arteries supply the head and neck (common carotid arteries
and three branches from the subclavian arteries; the vertebral arteries,
the thyrocervical trunks, and the costocervical trunks.

The upper limbs are supplied entirely by arteries arising from the
subclavian arteries.

The arterial supply to the abdomen arises from the aorta.

The internal iliac arteries serve mostly the pelvic region; the external
iliacs supply blood to the lower limb and abdominal wall.

The venae cavae are the major tributaries of the venous circulation.

Blood drained from the head and neck is collected by three pairs of veins
(internal jugular veins, external jugular veins, and the vertebral veins).

The deep veins of the upper limbs follow the paths of the companion
arteries.

Blood draining from the abdominopelvic viscera and abdominal walls is

returned to the heart by the inferior vena cava.

Most deep veins of the lower limb have the same names as the arteries
they accompany.

Developmental Aspects of the Blood Vessels

The vascular endothelium is formed by mesodermal cells that collect
throughout the embryo in blood islands, which give rise to extensions
that form rudimentary vascular tubes.

By the fourth week of development, the rudimentary heart and vessels

are circulating blood.
Fetal vascular modifications include shunts to bypass fetal lungs (the
foramen ovale and ductus arteriosus), the ductus venosus that bypasses
the liver, and the umbilical arteries and veins, which carry blood to and
from the placenta.
At birth, the fetal shunts and bypasses close and become occluded.
Congenital vascular problems are rare, but the incidence of vascular
disease increases with age, leading to varicose veins, tingling in fingers
and toes, and muscle cramping.
Atherosclerosis begins in youth, but rarely causes problems until old
age.

Blood pressure changes with age: the arterial pressure of infants is

about 90/55, but rises steadily during childhood to an average 120/80,
and tends to increase to somewhere around 150/90 in old age.
Depending on how you live. It's an average but it's also a choice, so
workout, eat right, and don't smoke and old age might look better than
"young age".