1.

10 Cardiovascular System: Study Guide 1

Arteries:
1. Describe the gross anatomy of arteries and differentiate them into: *****
 Large (elastic) arteries
An elastic or conducting artery has larger number of collagen and elastin filaments in the tunica media than
muscular arteries do, giving them the ability to stretch in response to each pulse. Elastic arteries include the
largest arteries in the body, closest to the heart, & give rise to smaller muscular arteries; the pulmonary arteries,
the aorta, and its branches comprise system of elastic arteries. They perform an important function: to propel
blood onward while the ventricles are relaxing. In these large arteries, the amount of elastic tissue is
considerable & smooth muscle fiber cells are arranged in 5 to 7 layers in both circular & longitudinal directions.
As they stretch, the elastic fibers momentarily store mechanical energy, functioning as a pressure reservoir.
 Medium (muscular) arteries
Muscular Arteries are medium-sized arteries that draw blood from an elastic artery & branch into resistance
vessels. Muscular or distributing arteries are medium-sized arteries that draw blood from an elastic artery and
branch into resistance vessels, including small arteries and arterioles. The tunica externa is often thicker than
the tunica media in muscular arteries. This outer layer contains fibroblasts, collagen fibers, and elastic fibers all
oriented longitudinally. This permits changes in the diameter of the vessel to occur but also prevents shortening
or retraction of vessel when it is cut. In contrast to the mechanism elastic arteries use to store and dissipate
energy generated by the heart’s contraction, muscular arteries contain layers of smooth muscle providing
allowing for involuntary control of vessel caliber and thus control of blood flow and less elastin. Muscular
arteries can be identified by the well-defined elastic lamina that lies between the tunicae intima and media . The
splenic artery (lienal artery), the blood vessel that supplies oxygenated blood to the spleen, is an example.
 Small arterioles
Arterioles are small diameter blood vessels in the microcirculation system that branch out from an artery and
leads to capillaries (15 μm to 300 μm). Arterioles consist of 1 or 2 layers of smooth muscle circularly oriented.
They are the primary site of vascular resistance, this reduces the pressure & velocity of blood flow to enable gas
and nutrient exchange to occur within capillaries. Arterioles have thin tunica interna with a thin, fenestrated
(with small pores) internal elastic lamina that disappears at the terminal end (Metarteriole). Have precapillary
sphincter, which monitors the blood flow into the capillary.
2. Describe the microscopic structure of arteries
 the three layers (tunica intima, media and externa)

Tunica Interna
The tunica interna (intima) forms the inner lining of a blood vessel and is in direct contact with the blood as it
flows through the lumen, or interior opening, of the vessel. Its innermost layer is called endothelium, which is
continuous with the endocardial lining of the heart. The endothelium is a thin layer of flattened cells that lines
the inner surface of the entire cardiovascular system (heart and blood vessels). Its functions are secretion of
local chemical mediators that influence the contractile state of the vessel’s overlying smooth muscle, and
assistance with capillary permeability. In addition, their smooth luminal surface facilitates efficient blood flow
by reducing surface friction and reducing aggregation of cells (especially platelets).
The second component of the tunica interna is a basement membrane deep to the endothelium. It provides a
physical support base for the epithelial layer. Its framework of collagen fibers affords the basement membrane
significant tensile strength, yet its properties also provide resilience for stretching and recoil. It plays an
important role in guiding cell movements during tissue repair of blood vessel walls.
The outermost part of the tunica interna, forms boundary between tunica interna and tunica media, is the
internal elastic lamina (lamina = thin plate). The internal elastic lamina is a thin sheet of elastic fibers with a
number of windowlike openings that facilitate diffusion of materials through the tunica interna to the thicker
tunica media.
Tunica Media
The tunica media is a muscular and connective tissue layer that displays the greatest variation among the
different vessel types. In most vessels, it is a relatively thick layer comprising mainly smooth muscle cells and
substantial amounts of elastic fibers. The primary role of the smooth muscle cells, which extend circularly
around the lumen, is to regulate the diameter of the lumen. An increase in sympathetic stimulation typically
stimulates the smooth muscle to contract, squeezing the vessel wall and narrowing the lumen. Such a decrease
in the diameter of the lumen of a blood vessel is called vasoconstriction. In contrast, when sympathetic
stimulation decreases, or in the presence of certain chemicals (such as nitric oxide, H+, and lactic acid) or in
response to blood pressure, smooth muscle fibers relax. The resulting increase in lumen diameter is called
vasodilation. In addition to regulating blood flow and blood pressure, smooth muscle contracts when a small
artery or arteriole is damaged (vascular spasm) to help limit loss of blood through the injured vessel. Smooth
muscle cells also help produce the elastic fibers within the tunica media that allow the vessels to stretch and
recoil under the applied pressure of the blood. Separating the tunica media from the tunica externa is a network
of elastic fibers, the external elastic lamina, which is part of the tunica media.
Tunica Externa
The outer covering of a blood vessel, the tunica externa (externa = outermost), consists of elastic and collagen
fibers. The tunica externa contains numerous nerves and, especially in larger vessels, tiny blood vessels that
supply the tissue of the vessel wall. These small vessels that supply blood to the tissues of the vessel are called
vasa vasorum. In addition to the important role of supplying the vessel wall with nerves and self-vessels, the
tunica externa helps anchor the vessels to surrounding tissues.
 how the layers differ from each other?
 The thick outermost layer of a vessel (tunica adventitia or tunica externa) is made of connective tissue.
 The middle layer (tunica media) is thicker and contains more contractile tissue in arteries than in veins. It
consists of circularly arranged elastic fibers, connective tissue, and smooth muscle cells.
 The inner layer (tunica intima) is the thinnest layer, comprised of a single layer of endothelium supported by
a subendothelial layer.
Tunica Intima
The inner layer (tunica intima) is the thinnest layer, formed from a single continuous layer of endothelial cells
and supported by a subendothelial layer of connective tissue and supportive cells. This subendothelial layer
consists of a single layer of cells in small arterioles or venules, but are much thicker in larger vessels such as the
aorta. The tunica intima is surrounded by a thin membrane comprised of elastic fibers running parallel to the
vessel. Capillaries consist only of the thin endothelial layer of cells with an associated thin layer of connective
tissue.
Tunica Media
Surrounding the tunica intima is the tunica media, comprised of smooth muscle cells and elastic and connective
tissues arranged circularly around the vessel. This layer is much thicker in arteries than in veins. Fiber
composition also differs; veins contain fewer elastic fibers and function to control caliber of the arteries, a key
step in maintaining blood pressure.
Tunica Externa
The outermost layer is the tunica externa or tunica adventitia, composed entirely of connective fibers and
surrounded by an external elastic lamina which functions to anchor vessels with surrounding tissues. The tunica
externa is often thicker in veins to prevent collapse of the blood vessel and provide protection from damage
since veins may be superficially located.
  how the layers vary in size and composition depending on the category of the artery
Elastic Arteries
Tunica Tunica intima is made up of an
Intima epithelium, which is a single layer of
flattened endothelial cells, together
with a supporting layer of elastin rich
collagen. This layer also has fibroblasts
and 'myointimal cells' that accumulate
lipid with ageing, and the intima layer
thickens, one of the first signs of
atherosclerosis.
Tunica Tunica media is broad and elastic with
Media concentric fenestrated sheets of
elastin, and collagen and only relatively
few smooth muscle fibres.
Tunica Tunica adventitia - has small 'vasa
Extern vasorum' as the large arteries need
a their own blood supply.  collagen and elastin.
Muscular Artery
The tunica intima has an
endothelium of flattened
endothelial cells. The sheets of
elastin is now reduced, and found
at the borders of tunica media in
layers called the internal and
external elastic layer (IEL & EEL)
which can be seen very clearly.
The tunica media is primarily a
layer of smooth muscle, with
some elastin and collagen. muscle
layer, and is sandwiched between
the IEL and EEL.
The Tunica Adventitia is very
broad, and mostly contains
Arterioles
The tunica intima is very thin,
and mostly consists of a single
layer of squamous epithelium.
The tunica media consists
almost entirely of a single
layer up to six layers of
smooth muscle cells, and
there is no EEL.
The Tunica adventitia is about
the same size as the tunica
media layer, merges in with
surrounding tissue.
3. Explain how the structure of each category of artery reflects its function.
-Elastic arteries; when the heart contracts, and ejects blood into these arteries, the walls need to stretch to
accommodate the blood surge, storing energy. Between heart contractions, the elastic walls recoil, to maintain
blood pressure, continuing to move blood even when ventricles are relaxed. The walls of these arteries have lots
of elastin. Recoil of elastic arteries keeps blood flowing during ventricular relaxation (diastole).
-Muscular arteries distribute blood to various parts of the body. These include arteries such as the femoral and
coronary arteries. The walls of these arteries have lots of smooth muscle, which means that they are able to
contract or relax (dilate) to change the amount of blood delivered, as needed.
-Arterioles control blood flow through capillary beds by contracting or dilating the size of the lumen, and
therefore the tunica media layer contains concentric rings of smooth muscle to do this. This compartment is
important in determining your blood pressure as the narrow diameter of these blood vessels resists blood flow,
and the back pressure helps to stretch the walls of the arteries during heart contractions.

4. Explain how the smooth muscle component in the arterial wall regulates blood flow.
In most vessels, it is a relatively thick layer comprising mainly smooth muscle cells and substantial amounts of
elastic fibers. The primary role of the smooth muscle cells, which extend circularly around the lumen like a ring
encircles your finger, is to regulate the diameter of the lumen. An increase in sympathetic stimulation typically
stimulates the smooth muscle to contract, squeezing the vessel wall and narrowing the lumen. Such a decrease
in the diameter of the lumen of a blood vessel is called vasoconstriction. In contrast, when sympathetic
stimulation decreases, or in the presence of certain chemicals (such as nitric oxide, H+, and lactic acid) or in
response to blood pressure, smooth muscle fibers relax. The resulting increase in lumen diameter is called
vasodilation. The rate of blood flow through different parts of the body is regulated by the extent of smooth
muscle contraction in the walls of particular vessels. Furthermore, the extent of smooth muscle contraction in
particular vessel types is crucial in the regulation of blood pressure.
In addition to regulating blood flow and blood pressure, smooth muscle contracts when a small artery or
arteriole is damaged (vascular spasm) to help limit loss of blood through the injured vessel. Smooth muscle cells
also help produce the elastic fibers within the tunica media that allow the vessels to stretch and recoil under the
applied pressure of the blood.

Veins:
5. Describe the gross anatomy of the veins and their general division:
 Venules
Venules drain the capillary blood and begin the return flow of blood
back toward the heart.
These have a clear tunica intima layer, without any elastic fibres,
and a tunica media with one or two layers of muscle fibres.
The tunica adventitia fuses with surrounding tissue.
- Measuring 10 μm to 50 μm
- Have loosely organized intercellular junctions (the weakest
endothelial contacts encountered along the entire vascular tree)
and thus are very porous. As the postcapillary venules move
away from capillaries, they acquire one or two layers of
circularly arranged smooth muscle cells. These muscular
 venules (50 μm to 200 μm) have thicker walls across which exchanges with the interstitial fluid can no
longer occur.
 Veins
Tunica Intima: A thin endothelial lining, (in some veins, you may be
able to see the valves).
Tunica Media: This layer contains 2-3 layers of muscle cells.
Tunica Adventitia: This is the broadest layer. It contains longitudinal
collagen fibres, elastic fibers and vasa vasorum.
 Pulmonary Veins: These transport oxygenated blood to the
heart from the lungs.
 Systemic Veins: These are present throughout the body and
transport deoxygenated blood to the heart for purification
- 0.5 mm in diameter for small veins to 3 cm in the large superior
and interior venae cava entering the heart.
- Lack the internal or external elastic laminae found in arteries
- The pumping action of the heart is a major factor in moving venous blood back to the heart along with
contraction of skeletal muscles in lower limbs.
- Contain valves, thin folds of tunica interna that form flap-like cusps, which aid in venous return by
preventing the backflow of blood.
- Vascular (venous) sinus is a vein with a thin endothelial wall that has no smooth muscle to alter its
diameter. The surrounding dense connective tissue replaces the tunica media and tunica externa in
providing support. Superficial veins, course through the subcutaneous layer, along their course, the
superficial veins form small connections (anastomoses) with the deep veins that travel between the skeletal
muscles.

6. Explain how the microscopic structure of the veins differs from that of the arteries, and how this reflects the
function of the veins
- Veins do not experience the pressure waves that the arteries do. The vessel walls of veins are thinner than
arteries and do not have as much tunica media. 
- Veins need valves to keep the blood flowing toward the heart. Theses valves are particularly important in
the legs and arms. They fight gravity to prevent the backflow of blood. Arteries don’t need valves because
the pressure from the heart keeps the blood flowing through them in one direction.
Arteries Veins
Possess relatively more elastic/ muscle tissue Possess relatively less elastic/ muscle tissue.
Thick, muscular non-collapsible outer layer Thin, collapsible outer layer
Arteries have smaller (narrower) lumen Veins have larger (wider) lumen
Blood flow speed is fast Blood flow speed is slow
Transports blood in pulses Transports blood smoothly
Located deep to the body surface Located near to the body surface and can be seen
subcutaneously.
Transports oxygenated blood (except pulmonary Transports deoxygenated blood (except pulmonary
arteries) veins)
Tunica interna has more elongated endothelial cells. Tunica interna has few flat endothelial cells. Elastic
Elastic membranes are well developed. membranes are not developed.
Tunica media is quite muscular and has many elastic Tunica media in veins is not very muscular and possesses
fibers very few elastic fibers.
Tunica externa is less developed and not very strong Tunica externa is more developed and very strong
7. Describe the structure and function of valves within the veins
Valves in veins are bicuspid, meaning they have two flap-like structures that regulate blood flow. These flaps are
made of elastic tissue. The valves’ main job is to keep the blood moving in one direction – back up towards the
heart. When the valve is open, blood freely flows upward towards the heart and when the valves are closed,
blood cannot flow back towards the legs. The deep veins carry 90% or more of the blood from the legs toward
the heart.

8. Explain the role the veins play in increasing venous return when needed, and the mechanism by which
venous return is increased
Delayed Compliance (Stress-Relaxation) of Vessels
The term “delayed compliance” means that a vessel exposed to increased volume at first exhibits a large
increase in pressure, but progressive delayed stretching of smooth muscle in the vessel wall allows the
pressure to return toward normal over a period of minutes to hours.
In this figure, the pressure is recorded in a small
segment of a vein that is occluded at both ends. An
extra volume of blood is suddenly injected until the
pressure rises from 5 to 12 mm Hg. Even though none
of the blood is removed after it is injected, the
pressure begins to decrease immediately and
approaches about 9 mm Hg after several minutes. In
other words, the volume of blood injected causes
immediate elastic distention of the vein, but then the
smooth muscle fibers of the vein begin to “creep” to
longer lengths, and their tensions correspondingly
decrease. This effect is a characteristic of all smooth
muscle tissue and is called stress-relaxation. Delayed compliance is a valuable mechanism by which the
circulation can accommodate extra blood when necessary, such as after too large a transfusion.
Study Guide 2
1. Explain the flow of blood through a blood vessel and throughout the body using: Flow = P / Resistance
F = blood flow, Δ P = P1 – P2 (Pressure difference), R = Resistance
Blood flow through a blood vessel is determined by two factors: (1) pressure difference of the blood between
the two ends of the vessel, also sometimes called “pressure gradient” along the vessel, which pushes the blood
through the vessel, and (2) the impediment to blood flow through the vessel, which is called vascular resistance.
P1 represents the pressure at the origin of the vessel; at the other end, the pressure is P2. Resistance occurs as a
result of friction between the flowing blood and the intravascular endothelium all along the inside of the vessel.
• Ohm’s law states that blood flow is:
– directly proportional to pressure difference (perfusion pressure)
– But, inversely proportional to the resistance
Note that it is the difference in pressure between the two ends of the vessel, not the absolute pressure in the
vessel, that determines rate of flow. For example, if the pressure at both ends of a vessel is 100 mm Hg and yet
no difference exists between the two ends, there will be no flow despite the presence of 100 mm Hg pressure.
2. Explain the concept of vascular resistance for blood flow, in relation to:
 Size of the lumen
Size of the lumen. The smaller the lumen of a blood vessel, the greater its resistance to blood flow. Resistance
is inversely proportional to the fourth power of the diameter (d) of the blood vessel’s lumen (R ∝ 1/d4). The
smaller the diameter of the blood vessel, the greater the resistance it offers to blood flow. For example, if the
diameter of a blood vessel decreases by one-half, its resistance to blood flow increases 16 times.
Vasoconstriction narrows the lumen, and vasodilation widens it. Normally, moment-to-moment fluctuations in
blood flow through a given tissue are due to vasoconstriction and vasodilation of the tissue’s arterioles. As
arterioles dilate, resistance decreases, and blood pressure falls. As arterioles constrict, resistance increases, and
blood pressure rises.
 Blood viscosity
The viscosity of blood depends mostly on the ratio of red blood cells to plasma (fluid) volume, and to a smaller
extent on the concentration of proteins in plasma. The higher the blood’s viscosity, the higher the resistance.
Any condition that increases the viscosity of blood, such as dehydration or polycythemia (an unusually high
number of red blood cells), thus increases blood pressure. A depletion of plasma proteins or red blood cells, due
to anemia or hemorrhage, decreases viscosity and thus decreases blood pressure
 Length of the blood vessel (Related to the Hagen-Poiseuille formula, which is not required to be
memorized)
Resistance to blood flow through a vessel is directly
proportional to the length of the blood vessel. The longer a
blood vessel, the greater the resistance. Obese people often
have hypertension (elevated blood pressure) because the
additional blood vessels in their adipose tissue increase their
total blood vessel length. An estimated 650 km (about 400
miles) of additional blood vessels develop for each extra
kilogram (2.2 lb) of fat.
Slight changes in the diameter of a vessel cause tremendous
changes in the vessel’s ability to conduct blood when the blood
flow is streamlined. This phenomenon is demonstrated by the
experiment, which shows three vessels with relative diameters
of 1, 2, and 4 but with same pressure difference of 100 mm Hg between the two ends of the vessels. Although
the diameters of these vessels increase only fourfold, the respective flows are 1, 16, and 256 ml/min, which is a
256-fold increase in flow. Thus, the conductance of the vessel increases in proportion to the fourth power of
the diameter, in accordance with the following formula:
Conductance ∝ Diameter4
Poiseuille’s law: F → π ∆Pr4 /8ηl
in which F is the rate of blood flow, ΔP is the pressure difference between the ends of the vessel, r is the radius
of the vessel, l is length of the vessel, and η is viscosity of the blood.

3. Explain:
 Systemic vascular resistance
Systemic vascular resistance (SVR), also known as total peripheral resistance (TPR), refers to all of the vascular
resistances offered by systemic blood vessels. The diameters of arteries and veins are large, so their resistance is
very small because most of the blood does not come into physical contact with the walls of the blood vessel. The
smallest vessels—arterioles, capillaries, and venules—contribute the most resistance. A major function of
arterioles is to control SVR—and therefore blood pressure and blood flow to particular tissues—by changing
their diameters. Arterioles need to vasodilate or vasoconstrict only slightly to have a large effect on SVR. The
main center for regulation of SVR is the vasomotor center in the brain stem.

 How a very small decrease in blood vessel radius will lead to a massive increase in resistance
The influence of lumen diameter on resistance is dramatic: A slight increase or decrease in diameter causes a
huge decrease or increase in resistance. This is because resistance is inversely proportional to the radius of the
blood vessel (one-half of the vessel’s diameter) raised to the fourth power (R = 1/r 4). This means, for example,
that if an artery or arteriole constricts to one-half of its original radius, the resistance to flow will increase 16
times. And if an artery or arteriole dilates to twice its initial radius, then resistance in the vessel will decrease to
1/16 of its original value and flow will increase 16 times.

4. Explain:
 Blood viscosity
Viscosity is the thickness of fluids that affects their ability to flow. Clean water, for example, is less viscous than
mud. The viscosity of blood is directly proportional to resistance and inversely proportional to flow; therefore,
any condition that causes viscosity to increase will also increase resistance and decrease flow. For example,
imagine sipping milk, then a milkshake, through the same size straw. You experience more resistance and
therefore less flow from the milkshake. Conversely, any condition that causes viscosity to decrease (such as
when the milkshake melts) will decrease resistance and increase flow.

 Why resistance higher in a patient with a high haematocrit

Patients with an abnormal elevation in red cell hematocrit (polycythemia) have much higher blood viscosities. In
fact, increasing the hematocrit from 40 to 60% (a 50% increase) increases the relative viscosity from 4 to 8 (a
100% increase). Increased viscosity increases the resistance to blood flow and thereby increases the work of
the heart and impairs organ perfusion. Some patients with anemia have low hematocrits, and therefore reduced
blood viscosities.
If clotting mechanisms are stimulated in the blood, platelet aggregation and interactions with plasma proteins
occur. This leads to entrapment of red cells and clot formation, which dramatically increases blood viscosity.
5. Describe the:
 Velocity of blood flow
It is the rate of blood flow through a given vessel. Blood flow is the volume of blood flowing through a particular
vessel in given interval of time.
The rate, or velocity, of blood flow varies inversely with the total cross-sectional area of the blood vessels. As the
total cross-sectional area of the vessels increases, the velocity of flow decreases. Blood flow is slowest in the
capillaries, which allows time for exchange of gases and nutrients.
 Explain the relationship between cross-sectional area and velocity
Vessel Cross-Sectional Area (cm2)
Aorta - 2.5
Small arteries - 20
Arterioles - 40
Capillaries - 2500
Venules - 250
Small veins - 80
Vena cava - 8
Note particularly that the cross-sectional areas of the veins are much larger than those of the arteries, averaging
about four times those of the corresponding arteries. This difference explains the large blood storage capacity of
the venous system in comparison with the arterial system. Because the same volume of blood flow (F) must pass
through each segment of the circulation each minute, the velocity of blood flow (v) is inversely proportional to
vascular cross-sectional area (A): v = F/A
Thus, under resting conditions, velocity averages about 33 cm/sec in the aorta but is only 1/1000 as rapid in the
capillaries—about 0.3 mm/sec. However, because the capillaries have a typical length of only 0.3 to 1 millimeter,
the blood remains in the capillaries for only 1 to 3 seconds, which is surprising because all diffusion of nutrient
food substances & electrolytes that occurs through the capillary walls are performed in this short time.

6. Differentiate between laminar and turbulent flow.

STREAM-LINE / LAMINAR BLOOD FLOW:
• Blood flows in layers or laminae.
• A thin layer of blood in contact with vessel wall does not move.
• Next layer moves with a slow velocity & further next with higher velocity.
• At the center of vessel, maximum velocity.
• Unidirectional & without noise or sound.
Laminar Flow of Blood in Vessels. When blood flows at a steady rate through a long, smooth blood vessel, it
flows in streamlines, with each layer of blood remaining the same distance from the vessel wall. Also, the central
most portion of the blood stays in the center of the vessel. This type of flow is called laminar flow or streamline
flow, and it is the opposite of turbulent flow, which is blood flowing in all directions in the vessel and continually
mixing within the vessel, as discussed subsequently.
TURBULENT FLOW:
• Blood flows in different directions.
• Blood mixes within itself. There are eddy currents in blood flow.
• This type of flow is accompanied by noise or sound.
• Normally, in all vessels blood flow is streamlined, except in ascending aorta & pulmonary trunk, where
there is some turbulence.
When the rate of blood flow becomes too great, when it passes by an obstruction in a vessel, when it makes a
sharp turn, or when it passes over a rough surface, the flow may then become turbulent, or disorderly, rather
than streamlined. Turbulent flow means that the blood flows crosswise in the vessel and along the vessel,
usually forming whorls in the blood, called eddy currents. These eddy currents are similar to the whirlpools that
one frequently sees in a rapidly flowing river at a point of obstruction.

7. Describe the changes in pressure through the circulation.

Blood flows from regions of higher pressure to regions of lower pressure; the greater the pressure difference,
the greater the blood flow. Contraction of the ventricles generates blood pressure (BP), the hydrostatic pressure
exerted by blood on the walls of a blood vessel. BP is determined by cardiac output, blood volume, and vascular
resistance. BP is highest in the aorta and large systemic arteries; in a resting, young adult, BP rises to about 110
mmHg during systole (ventricular contraction) and drops to about 70 mmHg during diastole (ventricular
relaxation). Systolic blood pressure (SBP) is the highest pressure attained in arteries during systole, and diastolic
blood pressure (DBP) is the lowest arterial pressure during diastole. As blood leaves the aorta and flows through
the systemic circulation, its pressure falls progressively as the distance from the left ventricle increases. Blood
pressure decreases to about 35 mmHg as blood passes from systemic arteries through systemic arterioles and
into capillaries, where the pressure fluctuations disappear. At the venous end of capillaries, blood pressure has
dropped to about 16 mmHg. Blood pressure continues to drop as blood enters systemic venules and then veins
because these vessels are farthest from the left ventricle. Finally, blood pressure reaches 0 mmHg as blood flows
into the right ventricle.

Page 749 tortora

8. Describe the resistance and capacitance vessels. ****
-Once the distributing artery reaches the organ to which it supplies blood, it branches into smaller arteries that
distribute blood flow within the organ. These vessels continue to branch and become arterioles. Together, the
small arteries and arterioles represent the primary vessels that are involved in the regulation of arterial blood
pressure as well as blood flow within the organ. These vessels are highly innervated by autonomic
nerves (particularly sympathetic adrenergic), and respond to changes in nerve activity and circulating
hormones by constricting or dilating. Therefore, these vessels are referred to as resistance vessels.
 Particular feature of resistance vessels is ability to change lumen cross-sectional area and influence blood
pressure. Human arteries or arterioles that are around 0.2 mm or smaller contribute to creation of the blood
flow resistance and are called resistance arteries. The effect of vessel diameter on resistance is inverse:
Given the same volume of blood, an increased diameter means there is less blood contacting the vessel wall,
thus lower friction and lower resistance, subsequently increasing flow. A decreased diameter means more of
the blood contacts the vessel walls, and resistance increases, subsequently decreasing flow.
-As postcapillary venules join together and form larger venules, smooth muscle once again appears. These
venous vessels, like the resistance vessels, are capable of dilating and constricting, and serve an important
function in regulating capillary pressure. Venules form larger veins that serve as the primary capacitance
vessels of the body - i.e., the site where most of the blood volume is found & where blood volume is regulated.
 Capacitance refers to stretching of blood vessel. Vein stretch more than the arteries hence are able to
accommodate large changes in blood volume. The physiological role of constriction of capacitance vessels is
to enhance the return of blood to the heart. The resistance vessels include small arteries, arterioles, and
precapillary sphincters. Capacitance vessels include small and large veins. Capacitance vessels have great
capacity to distend. For a similar rise in pressure, capacitance vessels may accommodate 20 times more
blood than resistance vessels.

Study Guide 3
1. Describe the concept of blood pressure and explain how this is derived.
Contraction of the ventricles generates blood pressure (BP), the hydrostatic pressure exerted by blood on the
walls of a blood vessel. BP is determined by cardiac output, blood volume, and vascular resistance. Systolic
blood pressure (SBP) is the highest pressure attained in arteries during systole, and diastolic blood pressure
(DBP) is the lowest arterial pressure during diastole
Blood pressure almost always is measured in millimeters of mercury (mm Hg) because the mercury manometer
has been used as the standard reference for measuring pressure since its invention in 1846 by Poiseuille.
Actually, blood pressure means the force exerted by the blood against any unit area of the vessel wall. When
one says that the pressure in a vessel is 50 mm Hg, this means that the force exerted is sufficient to push a
column of mercury against gravity up to a level 50 millimeters high. If the pressure is 100 mm Hg, it will push the
column of mercury up to 100 millimeters.

2. Explain how mean arterial blood pressure (MABP) is calculated and the various components that affect this.
MABP = CO × SVR, CO = HR × SV
Mean arterial pressure (MAP), the average blood pressure in arteries, is roughly one-third of the way between
the diastolic and systolic pressures. It can be estimated as follows:
MAP = diastolic BP + 1/3 (systolic BP − diastolic BP)
Thus, in a person whose BP is 110/70 mmHg, MAP is about 83 mmHg [70 + 1/3(110 − 70)]. We have already seen
that cardiac output equals heart rate multiplied by stroke volume.
Another way to calculate cardiac output is to divide mean arterial pressure (MAP) by resistance (R): CO = MAP ÷
R. By rearranging the terms of this equation, you can see that MAP = CO × R.
If cardiac output rises due to an increase in stroke volume or heart rate, then the mean arterial pressure rises as
long as resistance remains steady. Likewise, a decrease in cardiac output causes a decrease in mean arterial
pressure if resistance does not change.
Blood pressure also depends on the total volume of blood in the cardiovascular system. The normal volume of
blood in an adult is about 5 liters (5.3 qt). Any decrease in this volume, as from hemorrhage, decreases the
amount of blood that is circulated through the arteries each minute. A modest decrease can be compensated for
by homeostatic mechanisms that help maintain blood pressure (described in Section 21.4), but if the decrease in
blood volume is greater than 10% of the total, blood pressure drops. Conversely, anything that increases blood
volume, such as water retention in the body, tends to increase blood pressure.
3. Review the blood pressures in various parts of the circulation: aorta, systemic capillaries and veins,
pulmonary circulation. ***

Pressures in the Various Portions of the Circulation

Because the heart pumps blood continually into the aorta, the mean pressure in the aorta is high, averaging
about 100 mm Hg. Also, because heart pumping is pulsatile, the arterial pressure alternates between a systolic
pressure level of 120 mm Hg and a diastolic pressure level of 80 mm Hg. As the blood flows through the
systemic circulation, its mean pressure falls progressively to about 0 mm Hg by the time it reaches the
termination of the superior and inferior vena cava where they empty into the right atrium of the heart. The
pressure in the systemic capillaries varies from as high as 35 mm Hg near the arteriolar ends to as low as 10 mm
Hg near the venous ends, but their average “functional” pressure in most vascular beds is about 17 mm Hg, a
pressure low enough that little of the plasma leaks through the minute pores of the capillary walls, even though
nutrients can diffuse easily through these same pores to the outlying tissue cells.
Note at the far right side of figure, the respective pressures in the different parts of the pulmonary circulation. In
the pulmonary arteries, the pressure is pulsatile, just as in the aorta, but the pressure is far less: pulmonary
artery systolic pressure averages about 25 mm Hg and diastolic pressure averages about 8 mm Hg, with a mean
pulmonary arterial pressure of only 16 mm Hg. The mean pulmonary capillary pressure averages only 7 mm Hg.
Yet, the total blood flow through the lungs each minute is the same as through the systemic circulation. The low
pressures of the pulmonary system are in accord with the needs of the lungs because all that is required is to
expose the blood in the pulmonary capillaries to oxygen and other gases in the pulmonary alveoli.
4. Describe the neural regulation of blood pressure:
 Baroreceptor and chemoreceptor reflexes
Baroreceptor Reflexes: Baroreceptors, pressure-sensitive sensory receptors, are located in the aorta, internal
carotid arteries (arteries in the neck that supply blood to the brain), and other large arteries in the neck and
chest. They send impulses to the cardiovascular center to help regulate blood pressure. The two most important
baroreceptor reflexes are the carotid sinus reflex and the aortic reflex.
Baroreceptors in the wall of the carotid sinuses initiate the carotid sinus reflex, which helps regulate blood
pressure in the brain. The carotid sinuses are small widenings of the right and left internal carotid arteries just
above the point where they branch from the common carotid arteries. Blood pressure stretches the wall of the
carotid sinus, which stimulates baroreceptors. Nerve impulses propagate from the carotid sinus baroreceptors
over sensory axons in the glossopharyngeal (IX) nerves to the cardiovascular center in the medulla oblongata.
Baroreceptors in the wall of the ascending aorta and arch of the aorta initiate the aortic reflex, which regulates
systemic blood pressure. Nerve impulses from aortic baroreceptors reach the cardiovascular center via sensory
axons of the vagus (X) nerves.
When blood pressure falls, the baroreceptors are stretched less, and they send nerve impulses at a slower rate
to the cardiovascular center. In response, the CV center decreases parasympathetic stimulation of the heart by
way of motor axons of the vagus nerves and increases sympathetic stimulation of the heart via cardiac
accelerator nerves. Another consequence of increased sympathetic stimulation is increased secretion of
epinephrine and norepinephrine by the adrenal medulla. As the heart beats faster and more forcefully, and as
systemic vascular resistance increases, cardiac output rise, and blood pressure increases to the normal level.
Conversely, when an increase in pressure is detected, the baroreceptors send impulses at a faster rate. The CV
center responds by increasing parasympathetic stimulation and decreasing sympathetic stimulation. The
resulting decreases in heart rate and force of contraction reduce the cardiac output. The cardiovascular center
also slows the rate at which it sends sympathetic impulses along vasomotor neurons that normally cause
vasoconstriction. The resulting vasodilation lowers systemic vascular resistance. Decreased cardiac output and
decreased systemic vascular resistance both lower systemic arterial blood pressure to the normal level.

Chemoreceptor Reflexes: Chemoreceptors, sensory receptors that monitor the chemical composition of blood,
are located close to the baroreceptors of the carotid sinus and arch of the aorta in small structures called
carotid bodies and aortic bodies, respectively. These chemoreceptors detect changes in blood level of O2, CO2,
and H+. Hypoxia (lowered O2 availability), acidosis (an increase in H+ concentration), or hypercapnia (excess
CO2) stimulates the chemoreceptors to send impulses to the cardiovascular center. In response, the CV center
increases sympathetic stimulation to arterioles and veins, producing vasoconstriction and an increase in BP.
These chemoreceptors also provide input to the respiratory center in the brain stem to adjust the rate of
breathing. Tortora page 754
 Cardiovascular centre
The CV center in the medulla oblongata also controls neural, hormonal, and local negative feedback systems
that regulate blood pressure and blood flow to specific tissues. Groups of neurons scattered within the CV
center regulate heart rate, contractility (force of contraction) of the ventricles, and blood vessel diameter. Some
neurons stimulate the heart (cardiostimulatory center); others inhibit the heart (cardioinhibitory center). Still
others control blood vessel diameter by causing constriction (vasoconstrictor center) or dilation (vasodilator
center); these neurons are referred to collectively as the vasomotor center. The cardiovascular center receives
input both from higher brain regions and from sensory receptors (Figure 21.12).

Nerve impulses descend from the cerebral cortex, limbic system, and hypothalamus to affect the cardiovascular
center. For example, even before you start to run a race, your heart rate may increase due to nerve impulses
conveyed from the limbic system to the CV center. If your body temperature rises during a race, the
hypothalamus sends nerve impulses to the CV center. The resulting vasodilation of skin blood vessels allows
heat to dissipate more rapidly from the surface of the skin. The three main types of sensory receptors that
provide input to the cardiovascular center are proprioceptors, baroreceptors, and chemoreceptors.
Proprioceptors monitor movements of joints and muscles and provide input to the cardiovascular center during
physical activity. Their activity accounts for the rapid increase in heart rate at the beginning of exercise.
Baroreceptors monitor changes in pressure and stretch in the walls of blood vessels, and chemoreceptors
monitor the concentration of various chemicals in the blood.
 The output to heart and blood vessels
Output from the cardiovascular center flows along sympathetic and parasympathetic neurons of the ANS.
Sympathetic impulses reach the heart via the cardiac accelerator nerves. An increase in sympathetic stimulation
increases heart rate and contractility; a decrease in sympathetic stimulation decreases heart rate and
contractility. Parasympathetic stimulation, conveyed along the vagus (X) nerves, decreases heart rate. Thus,
opposing sympathetic (stimulatory) and parasympathetic (inhibitory) influences control the heart.

 Its effects on blood pressure

The cardiovascular center also continually sends impulses to smooth muscle in blood vessel walls via vasomotor
nerves. These sympathetic neurons exit the spinal cord through all thoracic and the first one or two lumbar
spinal nerves and then pass into the sympathetic trunk ganglia (see Figure 15.2). From there, impulses
propagate along sympathetic neurons that innervate blood vessels in viscera and peripheral areas. The
vasomotor region of the cardiovascular center continually sends impulses over these routes to arterioles
throughout the body, but especially to those in the skin and abdominal viscera. The result is a moderate state of
tonic contraction or vasoconstriction, called vasomotor tone, that sets the resting level of systemic vascular
resistance. Sympathetic stimulation of most veins causes constriction that moves blood out of venous blood
reservoirs and increases blood pressure.
5. Describe the hormonal regulation of blood pressure:
 Adrenaline, angiotensin II, ADH, ANP
1. Renin–angiotensin–aldosterone (RAA) system. When blood volume falls or blood flow to the kidneys
decreases, juxtaglomerular cells in the kidneys secrete renin into the bloodstream. In sequence, renin and
angiotensin-converting enzyme (ACE) act on their substrates to produce the active hormone angiotensin II,
which raises blood pressure in two ways. First, angiotensin II is a potent vasoconstrictor; it raises blood
pressure by increasing systemic vascular resistance. Second, it stimulates secretion of aldosterone, which
increases reabsorption of sodium ions (Na+) and water by the kidneys. The water reabsorption increases total
blood volume, which increases blood pressure.
2. Epinephrine and norepinephrine. In response to sympathetic stimulation, the adrenal medulla releases
epinephrine and norepinephrine. These hormones increase cardiac output by increasing the rate and force of
heart contractions. They also cause vasoconstriction of arterioles and veins in the skin and abdominal organs
and vasodilation of arterioles in cardiac and skeletal muscle, which helps increase blood flow to muscle during
exercise.
3. Antidiuretic hormone (ADH). Antidiuretic hormone (ADH) is produced by the hypothalamus and released
from the posterior pituitary in response to dehydration or decreased blood volume. Among other actions, ADH
causes vasoconstriction, which increases blood pressure. For this reason, ADH is also called vasopressin. ADH
also promotes movement of water from the lumen of kidney tubules into the bloodstream. This results in an
increase in blood volume and a decrease in urine output.
4. Atrial natriuretic peptide (ANP). Released by cells in the atria of the heart, atrial natriuretic peptide (ANP)
lowers blood pressure by causing vasodilation and by promoting the loss of salt and water in the urine, which
reduces blood volume.
 The source of each of these hormones
 The stimulus which prompts the release of each of these

 The effect of these hormones on blood volume and systemic vascular resistance
 How these effects change blood pressure
6. Describe the local regulation of blood pressure:
 The concept of autoregulation
In each capillary bed, local changes can regulate vasomotion. When vasodilators produce local dilation of
arterioles and relaxation of precapillary sphincters, blood flow into capillary networks is increased, which
increases O2 level. Vasoconstrictors have the opposite effect. The ability of a tissue to automatically adjust its
blood flow to match its metabolic demands is called autoregulation. In tissues such as the heart and skeletal
muscle, where the demand for O2 and nutrients and for the removal of wastes can increase as much as tenfold
during physical activity, autoregulation is an important contributor to increased blood flow through the tissue.
Autoregulation also controls regional blood flow in the brain; blood distribution to various parts of the brain
changes dramatically for different mental and physical activities. During a conversation, for example, blood flow
increases to your motor speech areas when you are talking and increases to the auditory areas when you are
listening.
 Its effect on blood flow to tissues
Two general types of stimuli cause autoregulatory changes in blood flow:
1. Physical changes. Warming promotes vasodilation, and cooling causes vasoconstriction. In addition, smooth
muscle in arteriole walls exhibits a myogenic response—it contracts more forcefully when it is stretched and
relaxes when stretching lessens. If, for example, blood flow through an arteriole decreases, stretching of the
arteriole walls decreases. As a result, the smooth muscle relaxes and produces vasodilation, which increases
blood flow.
2. Vasodilating and vasoconstricting chemicals. Several types of cells—including white blood cells, platelets,
smooth muscle fibers, macrophages, and endothelial cells—release a wide variety of chemicals that alter blood-
vessel diameter. Vasodilating chemicals released by metabolically active tissue cells include K+, H+, lactic acid
(lactate), and adenosine (from ATP). Another important vasodilator released by endothelial cells is nitric oxide
(NO). Tissue trauma or inflammation causes release of vasodilating kinins and histamine. Vasoconstrictors
include thromboxane A2, superoxide radicals, serotonin (from platelets), and endothelins (from endothelial
cells).
7. Explain how the cardiovascular system responds to changes in blood pressure in order to maintain
homeostasis
 During acute blood loss
A common cause of hypovolemic shock is acute (sudden) hemorrhage. The blood loss may be external, as occurs
in trauma, or internal, as in rupture of an aortic aneurysm. Loss of body fluids through excessive sweating,
diarrhea, or vomiting also can cause hypovolemic shock. Other conditions—for instance, diabetes mellitus—may
cause excessive loss of fluid in the urine. Sometimes, hypovolemic shock is due to inadequate intake of fluid.
Whatever the cause, when the volume of body fluids falls, venous return to the heart declines, filling of the
heart lessens, stroke volume decreases, and cardiac output decreases. Replacing fluid volume as quickly as
possible is essential in managing hypovolemic shock.
The body can quickly sense a fall in blood pressure through its arterial and cardiopulmonary baroreceptors, and
then activate the sympathetic adrenergic system to stimulate the heart (increase heart rate and contractility)
and constrict blood vessels (increase systemic vascular resistance). Sympathetic activation has little direct
influence on brain and coronary blood vessels, so these circulations can benefit from the vasoconstriction that
occurs in other organs (particularly in the gastrointestinal, skeletal muscle and renal circulations) that serve to
increase systemic vascular resistance and arterial pressure. In other words, cardiac output is redistributed from
less important organs to the brain and myocardium, both of which are critical for survival. Reduced organ blood
flow caused by vasoconstriction and reduced arterial pressure, leads to systemic acidosis that is sensed
by chemoreceptors. The chemoreceptor reflex further activates the sympathetic adrenergic system thereby
reinforcing the baroreceptor reflex. When the hypotension is very severe (e.g., mean arterial pressures <50
mmHg) and the brain becomes ischemic, this can produce a very intense sympathetic discharge that further
reinforces the other autonomic reflexes.

The combined effects of arterial hypotension and sympathetic activation lead to activation of humoral
compensatory mechanisms. Sympathetic stimulation of the adrenal glands stimulates the release
of catecholamines into the blood, which reinforce the effects of sympathetic activation on the heart and
vasculature. The kidneys release more renin following hemorrhage leading to increased circulating levels
of angiotensin II and aldosterone. This causes vascular constriction, enhanced sympathetic activity, stimulation
of vasopressin release, activation of thirst mechanisms, and very importantly, increased renal reabsorption of
sodium and water to increase blood volume. This renal mechanism is particularly important in the long-term
recovery from blood loss.

 During prolonged dehydration

1. Activation of the renin–angiotensin–aldosterone system. Decreased blood flow to the kidneys causes the
kidneys to secrete renin and initiates the renin–angiotensin–aldosterone system (see Figure 18.15). Recall that
angiotensin II causes vasoconstriction and stimulates the adrenal cortex to secrete aldosterone, a hormone that
increases reabsorption of Na+ and water by the kidneys. The increases in systemic vascular resistance and blood
volume help raise blood pressure.
2. Secretion of antidiuretic hormone. In response to decreased blood pressure, the posterior pituitary releases
more antidiuretic hormone (ADH). ADH enhances water reabsorption by the kidneys, which conserves remaining
blood volume. It also causes vasoconstriction, which increases systemic vascular resistance.
3. Activation of the sympathetic division of the ANS. As blood pressure decreases, aortic and carotid
baroreceptors initiate powerful sympathetic responses throughout the body. One result is marked
vasoconstriction of arterioles and veins of the skin, kidneys, and other abdominal viscera. (Vasoconstriction does
not occur in the brain or heart.) Constriction of arterioles increases systemic vascular resistance, and
constriction of veins increases venous return. Both effects help maintain an adequate blood pressure.
Sympathetic stimulation also increases heart rate and contractility and increases secretion of epinephrine and
norepinephrine by the adrenal medulla. These hormones intensify vasoconstriction and increase heart rate and
contractility, all of which help raise blood pressure.
4. Release of local vasodilators. In response to hypoxia, cells liberate vasodilators—including K+, H+, lactic acid,
adenosine, & nitric oxide—that dilate arterioles and relax precapillary sphincters. Such vasodilation increases
local blood flow and may restore O2 level to normal in part of the body. However, vasodilation also has the
potentially harmful effect of decreasing systemic vascular resistance and thus lowering the blood pressure.