Anatomy of an artery - Wall of an artery consists
of three distinct layers of tunics
Tunica externa
1. Thin layer of connective
tissue containing collagenous and elastic fibers.
2. Attaches the artery to the
surrounding tissues.
3. Penetrated by small blood
vessels of the vasa vasorum
(“vessels of vessels”)
Tunica media
1. Makes up the bulk of the
arterial wall.
2. Contains smooth muscle and
elastic connective tissue.
3. Smooth muscle is innervated
by the ANS to produce vasoconstriction of arteries. When not stimulated, the diameter of the
artery enlarges – vasodilation.
Tunica interna
1. Simple squamous
epithelium (the endothelium) lines the internal surface of the artery.
2. The endothelium rests on
the elastic lamina, a connective tissue membrane rich in elastic and collagenous fibers.
Anatomy of a vein – The wall of a vein shows the same three coats as
in an artery. There are a number of
differences.
Tunica externa
1. A very thin connective
tissue layer.
2. Very little elastic tissue
in this coat.
Tunica media - Poorly developed with
very little smooth muscle or elastic tissue.
Tunica interna
1. Simple squamous
lining with no underlying elastic lamina.
2. The interna
forms two semilunar-like flaps which serve as valves
in the veins of the arms and legs.
Venous Valves
1. Many veins,
particularly those in the arms and legs, have flaps or valves which project
inward from the lining. Valves are usually composed of two leaflets that close
if the blood begins to back up in the veins.
Valves are open as long as the blood flow is toward the heart and closed
if it is in the opposite direction.
2. Veins also function
as blood reservoirs that can be drawn upon in time of need. If a hemorrhage accompanied by drop in blood
pressure occurs, the muscular walls of the veins are stimulated reflexively by
the sympathetic nervous system. The
veins constrict and help to raise the blood pressure. This mechanism ensures a nearly normal blood
flow even if as much as 25% of the blood volume is lost.
Capillaries – The smallest blood vessels
whose walls consist of a single layer of endothelial cells
True Capillaries
1. Emerge from arterioles (terminal arteries) or
metarterioles and are not on the direct flow route
from arteriole to venule.
2. At their site of origin, there is a ring of
smooth muscle fibers called a precapillary
sphincter that controls the flow of blood entering a true capillary.
Metarteriole
1. A vessel that emerges from
an arteriole, passes through the capillary
network and empties into a venule, the smallest vein..
2. Proximal portions of the metarterioles
are surrounded by scattered smooth
muscle cells whose contraction
and relaxation help regulate the amount and
force of the blood.
3. Distal portion of a metarteriole
has no smooth muscle fibers and is called a
thoroughfare channel.
4.
Serves as a low resistance channel that increases blood flow.
Venous Return
Three
mechanisms are involved in the return of the venous blood to the heart:
The respiratory pump. The thoracic
cavity expands as a person inhales and air is pulled into the lungs as a result
of this drop in pressure in the pleural cavities. At the same time, blood is
also pulled into the inferior vena cava and right atrium. During exhalation,
the internal pressure in the thoracic cavity rises. Air is forced out of the
lungs, and venous blood pushed into the right atrium.
The venous pump. During normal
standing and walking, the venous pump assists venous return. As the calf
muscles contract, they compress the nearby blood vessels propelling blood
towards the heart. During muscle relaxation, the vessel once again fills with
blood and the cycle is repeated during the next contraction. Blood pools in the
legs when a person is standing still for a long period of time. The venous pump
does not operate.
Venous valves. The valves in
the leg veins prevent the blood from flowing back towards the capillaries. In
the absence of valves, gravity would cause pooling of blood in the leg veins.
When lying down, venous valves have little effect as the heart and major
vessels are at the same level. The valves in the perforator connecting veins
have the most important role. If these valves fail to work effectively, the
high pressure in the deep veins, is transmitted to the
much weaker, unsupported superficial veins. These veins become distended and
tortuous (varicose veins). Capillary pressure becomes increased, and fluid is
forced out into the extravascular space. This can
then progress onto chronic venous insufficiency characterised
by edema and ulceration of the leg.
Blood
Pressure
Blood pressure measurement is one of the most
common clinical tests. Everyone over the age of 3 is recommended to get their
blood pressure checked annually. The primary purpose for measuring blood
pressure is to determine the potential risk of cardiovascular disease. If the
pressure is high, appropriate medications and lifestyle changes are
recommended. Typically the brachial artery is measured because of convenience
and its position at heart level. When blood is ejected from the ventricles it
exerts a pressure against the walls of the arteries. This pressure is called hydrostatic
pressure.
Blood pressure is determined primarily by two
factors: cardiac output (CO) and peripheral resistance. Cardiac
output measures the amount of blood pumped into the
arteries per minute (i.e. volume). Peripheral
resistance is most strongly correlated to blood vessel
diameter. As blood moves toward the capillaries, the vessel diameter decreases
and the resistance to blood flow increases. Blood must exert considerable force
to overcome this resistance in the systemic circuit. Resistance to blood flow
is normally much less in the pulmonary circuit because its
shorter & the vessels usually have a larger diameter. So, the blood
pressure in the pulmonary circuit is much lower than the systemic circuit.
Blood pressure is related to both cardiac
output (CO), the amount of blood pumped out of the heart per minute &
factors affecting resistance to blood flow. Resistance to blood flow is
primarily determined by vessel diameter, as the vessel is dilated (larger) the
resistance to blood flow drops. This is called peripheral resistance when the resistance of the blood vessels in a circuit are summed
together in an estimate of resistance along the entire pathway. Cardiac output
increases as heart rate (HR) & the force of contractions increases the
amount of blood pumped by the heart with each heartbeat. This is referred to as
stroke volume (SV).
As expected during exercise, CO increases
because both HR & SV increase. Regular aerobic exercise should strengthen
the heart & increase stroke volume. At rest, the cardiac output of trained
individuals is the same as that of untrained individuals. Because resting CO is
constant, your heart rate can decrease if you have a stronger heart.
The heart pumps blood intermittently. During
systole (contraction) blood is thrust into the arteries, but during diastole
(relaxation) no blood leaves the heart. In vessels with rigid walls the
pressure would rise to very high values during systole and fall nearly to zero
during diastole. However, arteries do have elastic walls. During systole, the
expanding arteries store part of the blood volume so that during diastole blood
is still propelled forward by the elastic recoil of the artery walls. Elastic
arteries buffer changes in pressure & flow caused by the intermittent heart
beat.
Systolic pressure can
be quite variable, it increases with increases in
blood flow associated with exercise. During exercise, systolic pressure may
average 200 mmHg in a young individual. If systolic BP exceeds 240 mmHg during
an exercise test, it may indicate a susceptibility to hypertension. Diastolic
blood pressures change less because resistance to
blood flow should
decrease during
exercise (vessels dilate). Diastolic values taken during exercise vary from
showing an increase of 3-11 mmHg above resting diastolic BP to a decrease in
diastolic BP during exercise of a highly fit individual. Approximately 4% of
individuals ages 18-29 have hypertension, but it increases in the population as
we age.
When the pressure is too low, we suffer hypotension.
You heart can't deliver enough oxygen to the brain so you pass out or go into
shock. If the pressure is dangerously high it is called hypertension.
The artery walls & capillary walls, in particular, are under excessive
strain or tension from the high pressure. Over time, this can cause arteries to
"crack open". This leads to massive hemorrhaging & death in most
cases. Small capillaries can rupture more easily & these ruptures may
trigger heart attacks, strokes or organ damage such as kidney failure.
|
Condition |
Blood Pressure |
|
Hypertension |
Greater
than 140/90 mm Hg |
|
Hypotension |
Less
than 90/60 |
|
Circulatory
Shock |
Less
than 80/40 |
Cardiac Output
- The circulation of blood depends on:
1. Cardiac
Output – The amount of blood passing out of the heart in one minute.
Cardiac Output = Heart Rate x Stroke Volume
2. Blood
Pressure
a. The
pressure the blood exerts on the walls of blood vessels.
b. Generally
refers to the systemic arterial pressure. i.e., Systolic and Diastolic.
c. Mean
Arterial Pressure is the pressure that propels the blood to the tissues. It is determined by the following formula:
MAP
= Diastolic Pressure + Pulse Pressure/ 3
Pulse
Pressure = Systolic – Diastolic pressures
3. Circulatory Resistance – The opposition to
blood flow due to
friction between blood and the
interior walls of the blood vessels.
There are two factors that determine
resistance:
a. Blood
viscosity – polycythemia will increase
viscosity. A
reduction
in rbc count will lower viscosity.
b. Blood
vessel diameter - an
increased diameter will reduce pressure.
A decreased diameter due to atherosclerotic plaque will increase
systemic blood pressure.
Regulation of Cardiac
Output
Intrinsic Regulation
– The source of this regulation is the heart itself with not input from the
nervous system. The chief example of
this type of regulation is Starling’s Law of the heart. If the myocardial wall is stretched due to
distention with extra blood entering a chamber this will result in:
1. an increase in contraction strength of
the distended chamber.
2. an increase in the
rate of contraction of the heart if the distended
myocardial wall contains the
pacemaker.
Extrinsic Regulation
– This involves regulation of the cardiac output through the ANS.
1. Pressure sensitive receptors (baroreceptors) located in the walls of the aorta, carotid arteries and the carotid sinus are constantly
monitoring blood pressure in these arteries.
2. Nerve messages about sharp changes in blood pressure are carried from the baroreceptors to the medulla oblongata of the brain through
afferent nerves
3. Sharp increases in blood pressure
will stimulate the cardioinhibitory center in the
medulla to send messages along the vagus nerve to the
heart. The fresult
of this vagal activity will be:
a. decreased heart rate
b. decreased strength of contraction of
the heart
c. vasoconstriction of the coronary
arteries.
4. Sharp decreases in blood pressure
will activate the cardioacceleratory center of the
medulla to send nerve impulses through sympathetic neurons to the leart resulting in:
a. increased heart rate
b. decreased strength of contraction of
the heart
c. vasodilation
of the coronary arteries
The Bainbridge Reflex –
Balances increased venous return during exercise with increased cardiac output.
1. Increased venous return distends the right atrial wall.
2. Baroreceptors
in the walls of the vena cavae and the right atrium stimulate messages in
afferent neurons which are carried to the medulla oblongata.
3. Efferent messages are sent from the cardioacceleratory center to the myocardium.
4. The result is an increase in heart
rate and cardiac output which balances the increased venous return.