6.

1 The term cardiovascular system, refers only to the passages through which the blood flows,
the heart has a four-chambered muscular pump; arteries, the vessels that carry blood away from
the heart; veins, the vessels that carry blood back to the heart; and capillaries, microscopic blood
vessels that connect the smallest arteries to the smallest veins. The cardiovascular system has two
major divisions: a pulmonary circuit, which carries blood to the lungs for gas exchange and then
returns it to the heart, and a systemic circuit, which supplies blood to every organ of the body.
The right side of the heart serves the pulmonary circuit. It receives blood that has circulated
through the body, unloaded oxygen and nutria ents, and picked up a load of carbon dioxide and
other wastes. It pumps this oxygen-poor blood into a large artery, the pulmonary trunk, which
immediately divides into right and left pulmonary arteries. These transport blood to the lungs,
where carbon dioxide is unloaded and oxygen is picked up. The oxygen-rich blood then flows by
way of the pulmonary veins to the left side of the heart.

The left side of the heart serves the systemic circuit. Oxygenated blood leaves it by way
of another large artery, the aorta. The aorta takes a sharp U-turn, the aortic arch, and passes
downward, dorsal to the heart. The aortic arch gives off arteries that supply the head, neck, and
upper limbs. The aorta then travels through the thoracic and abdominal cavities and issues
smaller arteries to the other organs. After circulating through the body, the now deoxygenated
systemic blood returns to the right side of the heart mainly by way of two large veins, the
superior vena cava (draining the head, neck, upper limbs, and thoracic organs) and inferior vena
cava (draining the organs below the diaphragm). The major arteries and veins entering and
leaving the heart are called the great vessels because of their relatively large diameters.

The four major functions of the cardiovascular system are:

1.   To transport nutrients, gases and waste products around the body

2.   To protect the body from infection and blood loss

3.   To help the body maintain a constant body temperature (‘thermoregulation’)

4.   To help maintain fluid balance within the body

General Schematic of the Cardiovascular System
 Many cardiovascular conditions can be treated and management by lifestyle changes
including participation in exercise. It is no secret that exercise makes the heart work harder, and
it should come as no surprise that this increases cardiac output. The main reason the heart rate
increases at the beginning of exercise is that proprioceptors in the muscles and joints transmit
signals to the cardiac center signifying that the muscles are active and will quickly need an
increased blood flow. As the exercise progresses, muscular activity increases venous return. This
increases the preload on the right ventricle and is soon reflected in the left ventricle as more
blood flows through the pulmonary circuit and reaches the left heart. As the heart rate and stroke
volume rise, cardiac output rises, which compensates for the increased venous return. A
sustained program of exercise causes hypertrophy of the ventricles, which increases their stroke
volume. As explained earlier, this allows the heart to beat more slowly and still maintain a
normal resting cardiac output. Endurance athletes commonly have resting heart rates as low as
40 to 60 bpm, but because of the higher stroke volume, their resting cardiac output is about the
same as that of an untrained person. They have greater cardiac reserve, so they can tolerate more
exertion than a sedentary person can.

The heart and blood vessels comprise the two elements of the cardiovascular system that
work together in providing nourishment and oxygen to the organs of the body. The activity of
these two elements is also coordinated in the body's response to stress. Acute stres, stress that is
momentary or short-term such as meeting deadlines, being stuck in traffic or suddenly slamming
on the brakes to avoid an accident causes an increase in heart rate and stronger contractions of
the heart muscle, with the stress hormones adrenaline, noradrenaline and cortisol acting as
messengers for these effects. In addition, the blood vessels that direct blood to the large muscles
and the heart dilate, thereby increasing the amount of blood pumped to these parts of the body
and elevating blood pressure. This is also known as the fight or flight response. Once the acute
stress episode has passed, the body returns to its normal state. Chronic stress, or a constant stress
experienced over a prolonged period of time, can contribute to long-term problems for heart and
blood vessels. The consistent and ongoing increase in heart rate, and the elevated levels of stress
hormones and of blood pressure, can take a toll on the body. This long-term ongoing stress can
increase the risk for hypertension, heart attack or stroke. Repeated acute stress and persistent
chronic stress may also contribute to inflammation in the circulatory system, particularly in the
coronary arteries, and this is one pathway that is thought to tie stress to heart attack. It also
appears that how a person responds to stress can affect cholesterol levels.

The cardiovascular system works in conjunction with other body systems (nervous and
endocrine) to balance the body’s fluid levels.  Fluid balance is essential in order to ensure
sufficient and efficient movement of electrolytes, nutrients and gases through the body’s cells.
When the fluid levels in the body do not balance a state of dehydration or hyperhydration can
occur, both of which impede normal body function and if left unchecked can become dangerous
or even fatal. Dehydration is the excessive loss of body fluid, usually accompanied by an
excessive loss of electrolytes. The symptoms of dehydration include; headaches, cramps,
dizziness, fainting and raised blood pressure (blood becomes thicker as its volume decreases
requiring more force to pump it around the body).  Hyperhydration on the other hand results
from an excessive intake of water which pushes the normal balance of electrolytes outside of
their safe limits.  This can occur through long bouts of intensive exercise where electrolytes are
not replenished and excessive amounts of water are consumed.  This can result in the recently
consumed fluid rushing into the body’s cells, causing tissues to swell.  If this swelling occurs in
the brain it can put excessive pressure on the brain stem that may result in seizures, brain
damage, coma or even death. Dehydration or a loss of body fluid (through sweat, urination,
bleeding etc) results in an increase in ‘blood tonicity’ (the concentration of substances within the
blood) and a decrease in blood volume.  Where as hyperhydration or a gain in body fluid (intake
of water) usually results in a reduction of blood tonicity and an increase in blood volume.  Any
change in blood tonicity and volume is detected by the kidneys and osmoreceptors in the
hypothalamus. Osmoreceptors are specialist receptors that detect changes in the dilution of the
blood.  Essentially they detect if we are hydrated (diluted blood) or dehydrated (less diluted
blood). In response hormones are released and transported by the cardiovascular system (through
the blood) to act on target tissues such as the kidneys to increase or decrease urine production. 
Another way the cardiovascular system maintains fluid balance is by either dilating (widening)
or constricting (tightening) blood vessels to increase or decrease the amount of fluid that can be
lost through sweat.
 Diet has a significant effect upon the overall health and wellness of your circulatory
system. Some foods benefit the circulatory system. For instance, unsaturated fats these occur
mostly as plant based oils are heart healthy and improve your cholesterol levels, preventing
buildup of plaques in the arteries. Eating plenty of dietary fiber also helps particularly soluble
fiber, which absorbs cholesterol in the digestive tract and helps prevent your blood cholesterol
levels from rising as high. Fruits, vegetables, whole grains and beans are all good sources of
fiber.

6.2 The Composition and Function of The Blood

Blood cellular components

Erythrocytes

The function of the erythrocytes is the transport of oxygen from the lung to the tissue by bonding
oxygen to the iron-containing heme group of the hemoglobin. Erythrocytes are round and have a
biconcave shape as they have no nucleus. An erythrocyte has a diameter of 8 to 10 µm. A
healthy adult has about 5 million/µl erythrocytes. Also, the blood group antigens are expressed
on the surface membrane of the erythrocytes.

Leukocytes

Unlike mature erythrocytes, leucocytes have a nucleus. Different types of leucocytes can be
found in the blood:

 neutrophil granulocytes (banded and segmented)

 eosinophil granulocytes
 basophil granulocytes
 lymphocytes
 monocytes
The normal concentration of leucocytes ranges from 4,000 to 10,000 per µl, depending on age
and health status. Both leucocytes and erythrocytes are descendants of pluripotent hematopoietic
stem cells from the bone marrow.

The primary function of leucocytes is the immune defense. Especially lymphocytes (25 to 40%
of leucocytes) are responsible for the adaptive immune response, the specific defense from
pathogenic germs. The B lymphocytes produce antibodies, whereas T lymphocytes mediate the
antibody production and the direct cellular immune response.

Monocytes (4 to 8% of leucocytes) have the task of phagocytosis (e.g. removing foreign

materials, bacteria etc.) by producing extremely reactive free oxygen radicals which are capable
of penetrating and destroying bacteria wall. Monocytes may differentiate into fixed macrophages
(histiocytes) in connective tissue or into free macrophages.

Platelets

Platelets (thrombocytes) are another type of blood cells. They derive from megakaryocytes
(bone barrow giant cells). Their task is the hemostasis when damage to blood vessels occurs
(wound closure). The platelets adhere to the vascular wall of the damaged blood vessel and react
with fibrin building a solid clot within 1 to 3 minutes (bleeding time). The physiological range
for platelets is 150,000 – 400,000/µl.

Functions of Blood

Messenger and waste removal

Blood is the most important transport medium in the human body. It transports gases (oxygen,
carbon dioxide, nitrogen etc.) as well as nutrients (metabolism) and end products of cell
metabolism. Hence the blood has the task of assuring the exchange of substances. It provides the
tissues with blood gases and nutrients and in exchange transports end products (e.g. carbon
dioxide, urea, uric acid, creatinine etc.) to the eliminating organs (lung, liver, kidney).
Furthermore, it carries chemical messengers (hormones) to their target organs.
Acid-Base Balance

The acid-base homeostasis is regulated in the blood through the diffusion of gases between
alveoli and blood in the lung (alveolar diffusion) oxygen diffuses from the alveoli into the blood
due to the concentration gradient. It is taken up by the carrying protein hemoglobin (hem = iron-
containing, globin = protein). Contrariwise carbon dioxide diffuses from the blood into the
alveoli due to its higher blood concentration where it is breathed out.

Oxygen supply and carbon dioxide removal

The blood transports the oxygen from the alveoli to the remotest cells of the body. Because of
the higher gas pressure in the plasma (relative to the cells), it diffuses to the tissues. Carbon
dioxide diffuses from the cells into the blood due to the higher gas pressure in the tissue. Here it
undergoes a chemical reaction and forms carbonic acid (CO2 + H2O → H2CO3) which
dissociates into hydrogen ion (H+) and bicarbonate (HCO3-). Thus the metabolism end product
carbon dioxide is transported in the form of carbonic acid (or rather hydrogen ion and
bicarbonate). In the lung, the above mentioned chemical reaction reverses and carbon dioxide is
exhaled. To sum it up the blood regulates the acid-base homeostasis by the gas exchange. The
blood is also responsible for the homeostasis, e.g. balancing the water between the blood
capillaries on the one hand and intracellular and extracellular space on the other hand. It also
maintains a constant body temperature.

Coagulation

Coagulation factors (proteins) are solved in the blood and stop bleeding after a complex
(cascade-like) activation of coagulation factors through damage to blood vessels finally leading
to the building of thrombus (thrombogenesis). Simultaneously, fibrinogen/fibrin prevents the
pathological development of blood clots in the blood vessels. Blood coagulation and fibrinolysis
influence each other and maintain a sensitive equilibrium.

6.3 Location, Structure and Function of the Heart

The heart is located in the thoracic cavity in the mediastinum, the area between the lungs.
About two-thirds of it lies to the left of the median plane. The broad superior portion of the heart,
called the base, is the point of attachment for the great vessels described previously. Its inferior
end, the apex, tilts to the left and tapers to a blunt point. The adult heart is about 9 cm (3.5 in.)
wide at the base, 13 cm (5 in.) from base to apex, and 6 cm (2.5 in.) from anterior to posterior at
its thickest point roughly the size of a fist. It weighs about 300 g (10 oz).

The heart is enclosed in a double-walled sac called the pericardium, which is anchored to
the diaphragm below and to the connective tissue of the great vessels above the heart. The
parietal pericardium (pericardial sac) consists of a tough fibrous layer of dense irregular
connective tissue and a thin, smooth serous layer. The serous layer turns inward at the base of the
heart and forms the visceral pericardium covering the heart surface. Between the parietal and
visceral membranes is a space called the pericardial cavity. It contains 5 to 30 mL of pericardial
fluid, an exudate of the serous pericardium that lubricates the membranes and allows the heart to
beat almost without friction. In pericarditis inflammation of the pericardium the membranes may
become dry and produce a painful friction rubwith each heartbeat. In addition to reducing
friction, the pericardium isolates the heart from other thoracic organs, allows the heart room to
expand, and resists excessive expansion.

The heart wall consists of three layers the epicardium, myocardium, and endocardium.
The epicardium (visceral pericardium) is a serous membrane composed of a simple squamous
epithelium overlying a thin layer of areolar tissue. Over much of the heart, it has thick deposits
of fat that fill grooves in the heart surface and protect the coronary blood vessels. In non fatty
areas, the epicardium is thin and translucent, allowing the myocardium to show through. The
myocardium, by far the thickest layer, is composed of cardiac muscle and performs the work of
the heart. Its muscle cells spiral around the heart and are bound together by a meshwork of
collagenous and elastic fibers that make up the fibrous skeleton.The fibrous skeleton has at least
three functions: to provide structural support for the heart, especially around the valves and the
openings of the great vessels; to give the muscle something to pull against; and, as a
nonconductor of electricity, to limit the routes by which electrical excitation travels through the
heart. This insulation prevents the atria from stimulating the ventricles directly and is important
in the timing and coordination of electrical and contractile activity. Elastic recoil of the fibrous
skeleton may also aid in refilling the heart with blood after each beat, but physiologists are not in
complete agreement about this. The endocardium5 consists of a simple squamous endothelium
overlying a thin areolar tissue layer. It forms the smooth inner lining of the chambers and valves
and is continuous with the endothelium of the blood vessels.

The heart has four chambers. Blood returning to the heart is received by two superior
chambers, the right and left atria. These are mostly posterior in position, so only a small portion
of each is visible from the anterior aspect. Each atrium has a small earlike extension called an
auricle that slightly increases its volume. The two inferior chambers, the right andleft ventricles,
are the pumps that eject blood into the arteries. The right ventricle constitutes most of the
anterior aspect of the heart, while the left ventricle forms the apex and inferoposterior aspect.
The heart is crisscrossed by sulci (grooves) that mark the boundaries of the four chambers. The
sulci are occupied largely by fat and coronary blood vessels.

The atrioventricular (coronary) sulcus encircles the heart near its base and separates the
atria from the ventricles. The anterior and posterior interventricular sulci extend vertically, from
the coronary sulcus toward the apex, externally marking the boundary between the right and left
ventricles. The four chambers are best seen in a frontal section. The atria exhibit thin flaccid
walls corresponding to their light workload all they do is pump blood into the ventricles
immediately below. They are separated from each other by a wall, the interatrial septum.The
right atrium and both auricles exhibit internal ridges of myocardium called Thepectinate
muscles. A thicker wall, the interventricular septum, separates the right and left ventricles. The
right ventricle pumps blood only to the lungs and back, so its wall is only moderately thick and
muscular. The left ventricle is two to four times as thick because it bears the greatest workload of
all four chambers, pumping blood through the entire body. Both ventricles exhibit internal ridges
called trabeculae carneae.
 a) Superior view of the heart with the atria removed; (b) papillary muscle and chordae tendineae seen from
within the right ventricle. The upper ends of the chordae tendineae are attached to the cusps of the right AV valve.

To pump blood effectively, the heart needs valves that ensure a predominantly one-way
flow. There is a valve between each atrium and its ventricle and at the exit from each ventricle
into its great artery. Each valve consists of two or three fibrous flaps of tissue called cusps,
covered with endothelium. The atrioventricular (AV) valves regulate the openings between the
atria and ventricles. The right AV (tricuspid) valve has three cusps and the left AV (bicuspid)
valve has two. The left AV valve is also known as the mitral valve after its resemblance to a
miter, the headdress of a catholic bishop. Stringlike chordae tendineae, reminiscent of the shroud
lines of a parachute, connect the AV valve cusps to conical papillary muscles on the floor of the
ventricle. The semilunar valves (pulmonary and aortic valves) regulate the openings between the
ventricles and the great arteries. The pulmonary valvecontrols the opening from the right
ventricle into the pulmonary trunk, and the aortic valve controls the opening from the left
ventricle into the aorta. Each has three cusps shaped somewhat like shirt pockets. The opening
and closing of heart valves is the result of pressure gradients between the “upstream” and
“downstream” sides of the valve.
 When the ventricles are relaxed, the AV valve cusps hang down limply, both AV valves
are open, and blood flows freely from the atria into the ventricles. When the ventricles have
filled with blood and begin to contract, their internal pressure rises and blood surges against the
AV valves. This pushes their cusps together, seals the openings, and prevents blood from
flowing back into the atria. The papillary muscles contract with the rest of the ventricular
myocardium and tug on the chordae tendineae, which prevents the valves from bulging
excessively (prolapsing) into the atria or turning inside out like windblown umbrellas. When
rising “upstream” pressure in the ventricles exceeds the “downstream” blood pressure in the
great arteries, the ventricular blood forces the semilunar valves open and blood is ejected from
the heart. Then as the ventricles relax again and their pressure falls below that in the arteries,
arterial blood briefly flows backward and fills the pocketlike cusps of the semilunar valves. The
three cusps meet in the middle of the orifice and seal it, thereby preventing blood from reentering
the heart.
Operation of the Heart Valves. (a) The semilunar valves. When the pressure in the ventricle is greater than the
pressure in the artery, the valve is forced open and blood is ejected. When ventricular pressure is lower than arterial
pressure, arterial blood holds the valve closed. (b) The atrioventricular valves. When atrial pressure is greater than
ventricular pressure, the valve opens and blood flows through. When ventricular pressure rises above atrial pressure,
the blood in the ventricle pushes the valve cusps closed.

Phases of the Cardiac Cycle

We now examine the phases of the cardiac cycle, the pressure changes that occur, and
how the pressure changes and valves govern the flow of blood. However, in this presentation we
begin with the filling of the ventricles. Remember that all these events are completed in less than
1 second.

1. Ventricular filling. During diastole, the ventricles expand and their pressure drops below that
of the atria. As a result, the AV valves open and blood flows into the ventricles, causing
ventricular pressure to rise and atrial pressure to fall. Ventricular filling occurs in three phases:
(a) The first one-third is rapid ventricular filling, when blood enters especially quickly. (b) The
second one-third, called diastasis, is marked by slower filling. The P wave of the
electrocardiogram occurs at the end of diastasis, marking the depolarization of the atria. (c) In
the last one-third, atrial systole completes the filling process. The right atrium contracts slightly
before the left because it is the first to receive the signal from the SA node. As the ventricles fill,
the flaccid cusps of the AV valves float up toward the closed position. At the end of ventricular
filling, each ventricle contains an end-diastolic volume (EDV) of about 130 mL of blood. Only
40 mL (31%) of this is contributed by atrial systole.

2. Isovolumetric contraction. The atria repolarize, relax, and remain in diastole for the rest of
the cardiac cycle. The ventricles depolarize, generate the QRS complex, and begin to contract.
Pressure in the ventricles rises sharply and reverses the pressure gradient between atria and
ventricles. The AV valves close as ventricular blood surges back against the cusps. Heart sound
S1 occurs at the beginning of this phase and is produced mainly by the left ventricle; the right
ventricle is thought to make little contribution. Causes of the sound are thought to include the
tensing of ventricular tissues, acceleration of the ventricular wall, turbulence in the blood as it
surges against the closed AV valves, and impact of the heart against the chest wall. This phase is
called isovolumetric because even though the ventricles contract, they do not eject blood yet, and
there is no change in their volume. This is because pressures in the aorta (80 mmHg) and
pulmonary trunk (10 mmHg) are still greater than the pressures in the respective ventricles and
thus oppose the opening of the semilunar valves. The myocytes exert force, but with all four
valves closed, the blood cannot go anywhere.

3. Ventricular ejection. The ejection of blood begins when ventricular pressure exceeds arterial
pressure and forces the semilunar valves open. The pressure peaks at 120 mmHg in the left
ventricle and 25 mmHg in the right. Blood spurts out of each ventricle rapidly at first (rapid
ejection) and then flows out more slowly under less pressure (reduced ejection). By analogy,
suppose you were to shake up a bottle of soda pop and remove the cap. The soda would spurt out
rapidly at high pressure and then more would dribble out at lower pressure, much like the blood
leaving the ventricles. Ventricular ejection lasts about 200 to 250 msec, which corresponds to the
plateau of the myocardial action potentials but lags some what behind it. The ventricles do not
expel all their blood. In an average resting heart, each ventricle contains an EDV of 130 mL. The
amount ejected, about 70 mL, is called the stroke volume (SV). The percentage of the EDV
ejected, about 54%, is the ejection fraction. The blood remaining behind, about 60 mL in this
case, is called the end-systolic volume (ESV). In vigorous exercise, the ejection fraction may be
as high as 90%. Ejection fraction is an important measure of cardiac health. A diseased heart
may eject much less than 50% of the blood it contains.

4. Isovolumetric relaxation. This is early ventricular diastole, when the T wave appears and the
ventricles repolarize and begin to expand. There are competing theories as to how they expand.
One is that the blood flowing into the ventricles “inflates” them. Another is that contraction of
the ventricles deforms the fibrous skeleton, which subsequently springs back like a rubber ball
that has been squeezed and released. This elastic recoil and expansion would cause pressure to
drop rapidly and suck blood into the ventricles. At the beginning of ventricular diastole, blood
from the aorta and pulmonary trunk briefly flows backward through the semilunar valves. The
backflow, however, quickly fills the cusps and closes them, creating a slight pressure rebound
that appears as the dicrotic notch of the aortic pressure curve. Heart sound S2 occurs as blood
rebounds from the closed semilunar valves and the ventricles expand. This phase is called
isovolumetric because the semilunar valves are closed, the AV valves have not yet opened, and
the ventricles are therefore not taking in blood. When the valves open, ventricular filling (phase
1) begins again. Heart sound S3, if it occurs, is thought to result from the transition from
expansion of the empty ventricles to their sudden filling with blood. In a resting person, atrial
systole lasts about 0.1 second; ventricular systole, 0.3 second; and the quiescent period (when all
four chambers are in diastole), 0.4 second. Total duration of the cardiac cycle is therefore 0.8
second (800 msec) in a heart beating at 75 bpm.
6.4 Type of Blood Vessels

Arteries and Metarterioles

Arteries are constructed to withstand the surges of blood pressure generated by

ventricular systole. They are more muscular than veins and appear relatively round in tissue
sections. They are divided into three categories by size, but of course there is a smooth gradation
from one category to the next:

1. Conducting (elastic) arteries are the largest. Some examples are the pulmonary arteries, aorta,
and common carotid arteries. Their tunica media consists of numerous sheets of elastic tissue,
perforated like slices of Swiss cheese, alternating with thin layers of smooth muscle, collagen,
and elastic fibers. Conducting arteries expand when the ventricles pump blood into them during
systole, and recoil during diastole. This lessens the fluctuations in blood pressure exerted on
smaller arteries downstream.

2. Distributing (muscular) arteries are smaller branches farther away from the heart that
distribute blood to specific organs. You could compare a conducting artery to an interstate
highway and distributing arteries to the exit ramps and state highways that serve specific towns.
Distributing arteries typically have 25 to 40 layers of smooth muscle cells constituting about
three-quarters of the wall thickness. Most arteries to which we give names are in these first two
size classes. The brachial, femoral, and splenic arteries are examples of distributing arteries.

3. Resistance (small) arteries are usually too variable in number and location to be given names.
They exhibit up to 25 layers of smooth muscle cells and relatively little elastic tissue. Their
tunica media is thicker in proportion to the lumen than that of larger arteries. The smallest of
these arteries, about 40 to 200 m in diameter and with only one to three layers of smooth muscle,
are the arterioles. For reasons discussed later, they are the primary points at which the body
controls the relative amounts of blood directed to various organs. Metarterioles3 are short vessels
that link arterioles and capillaries. Instead of a continuous tunica media, they have individual
muscle cells spaced a short distance apart, each forming a precapillary sphincterthat encircles the
entrance to a capillary.
Capillaries

Capillaries are the “business end” of the circulatory system. All the rest of the system
exists to serve them, because capillaries are almost the only point in the circulatory system where
materials are exchangedbetween the blood and tissue fluid. Capillaries are ideally suited to their
role. They consist only of endothelium and a basement membrane. Capillaries have walls as thin
as 0.2 to 0.4 m. They average about 5 m in diameter at the proximal (arterial) end, widen to
about 9 m in diameter at the distal (venous) end, and often branch along the way. (Recall that an
erythrocyte is about 7 m in diameter.) The number of capillaries has been estimated at a billion
and their total surface area at 6,300 m2. But a more important point is that scarcely any cell in the
body is more than 60 to 80m away from the nearest capillary. There are a few exceptions.
Capillaries are scarce in tendons and ligaments and absent from cartilage, epithelia, and the
cornea and lens of the eye.

Veins

After flowing through the capillaries, blood collects in the distal end of the thoroughfare
channel and flows into a venule. In the venous circulation, blood flows from smaller vessels into
progressively larger ones; hence, instead of giving off branches as arteries do, veins receive
smaller tributaries, just as a river receives water from the many streams that form its tributaries.
Venules range from about 15 to 100 m in diameter. The proximal part of a venule has only a few
fibroblasts around it and is quite porous; therefore venules, like capillaries, exchange fluid with
the surrounding tissues. Farther along, a venule acquires a tunica media of smooth muscle. Even
the largest veins, however, have relatively sparse muscular and elastic tissue compared to
arteries. Venous sinuses are veins with especially thin walls, large lumens, and no smooth
muscle. Examples include the coronary sinus of the heart and the dural sinuses of the brain.
Because they are farther away from the heart, veins have much lower blood pressure than
arteries. In large arteries, it averages 90 to 100 mmHg and surges to 120 mmHg during systole,
whereas in veins it averages about 10 mmHg and fluctuates very little with the heartbeat. This
has significant implications for the form and function of veins:

• Since they need not withstand high pressure, veins have thinner walls than arteries, with less
muscular and elastic tissue. They collapse when empty and look relatively flattened or irregular
in histological sections.
• Since their walls are so thin, veins expand more easily and accommodate more blood than
arteries do. About 54% of the blood is found in the systemic veins at rest, veins are therefore
called capacitance vessels.

• The pressure in the veins is not high enough to push blood upward against the pull of gravity
to the heart. The upward flow of blood depends in part on the massaging action of skeletal
muscles and the presence of one-way venous valves that keep the blood from dropping down
again when the muscles relax. These valves, similar to the semilunar valves of the heart, occur
especially in medium veins of the arms and legs; they are absent from very small and very large
veins, veins of the ventral body cavity, and veins of the brain. Varicose veins result in part from
the failure of these valves.
 Circulatory Routes, At its simplest, the usual route of blood flow is heart → arteries →
arterioles → capillaries → venules → veins → heart. Blood usually passes through only one
network of capillaries from the time it leaves the heart until the time it returns. But there are
exceptions, notably portal systems and anastomoses. In a portal system, blood flows through two
consecutive capillary networks before returning to the heart. One portal system connects the
hypothalamus and anterior pituitary. Others are found in the kidneys and between the intestines
and liver. An anastomosis is a point where two blood vessels merge. In an arteriovenous
anastomosis (shunt), blood flows from an artery directly into a vein and by passes the capillaries.
Shunts occur in the fingers, palms, toes, and ears, where they reduce heat loss in cold weather by
allowing warm blood to bypass these exposed surfaces. Unfortunately, this makes these poorly
perfused areas more susceptible to frostbite. In an arterial anastomosis, two arteries merge and
provide collateral (alternative) routes of blood supply to a tissue. Those of the coronary
circulation were mentioned in chapter 19. They are also common around joints where movement
may temporarily obstruct one pathway. Venous anastomoses are more common. They provide
several alternative routes of drainage from an organ, so blockage of a vein is rarely as life-
threatening as blockage of an artery.

6.5 The major blood vessels of the head and upper body

The systemic circuit supplies oxygen and nutrients to all the organs and removes their
metabolic wastes. Part of it, the coronary circulation. The names of the blood vessels often
describe their location by indicating the body region traversed (as in the axillary artery or
femoral artery); an adjacent bone (as in radial artery or temporal artery); or the organ supplied or
drained by the vessel (as in hepatic artery or renal vein). There is a great deal of anatomical
variation in the circulatory system from one person to another. The remainder of this chapter
describes the most common pathways.
 All systemic arteries arise from the aorta, which has three principal regions

1. The ascending aorta rises about 5 cm above the left ventricle. Its only branches are the
coronary arteries,which arise behind two cusps of the aortic valve. Opposite each semilunar
valve cusp is an aortic sinus containing baroreceptors.
2. The aortic arch curves to the left like an inverted U superior to the heart. It gives off three
major arteries in this order: the brachiocephalic, left common carotid artery, and left subclavian
artery. The descending aorta passes downward dorsal to the heart,at first to the left of the
vertebral column and then anterior to it,through the thoracic and abdominal cavities. It is called
the thoracic aorta above the diaphragm and the abdominal aorta below. It ends in the lower
abdominal cavity by forking into the right and left common iliac arteries.

The head and neck receive blood from four pairs of arteries ;

1. The common carotid arteries. The brachiocephalic trunk divides shortly after leaving the aortic
arch and gives rise to the right subclavian and right common carotid arteries.The left common
carotid artery arises directly from the aortic arch. The common carotids pass up the anterolateral
aspect of the neck,alongside the trachea.
2. The vertebral arteries arise from the right and left subclavian arteries. Each travels up the neck
through the transverse foramina of the cervical vertebrae and enters the cranial cavity through the
foramen magnum.

3. The thyrocervical trunks are tiny arteries that arise from the subclavian arteries lateral to the
vertebral arteries; they supply the thyroid gland and some scapular muscles.

4. The costocervical trunks arise from the subclavian arteries a little farther laterally. They
perfuse the deep neck muscles and some of the intercostal muscles of the superior rib cage.

The common carotid arteries have the most extensive distribution of all the head-neck arteries.
Near the laryngeal prominence (Adam’s apple),each common carotid branches into an external
carotid artery and an internal carotid artery:

1. The external carotid artery ascends the side of the head external to the cranium and supplies
most external head structures except the orbits. The external carotid gives rise to the following
arteries,in ascending order: a. the superior thyroid artery to the thyroid gland and larynx, b. the
lingual artery to the tongue, c. the facial artery to the skin and muscles of the face, d. the
occipital artery to the posterior scalp, e. the maxillary artery to the teeth,maxilla,buccal
cavity,and external ear,and f. the superficial temporal artery to the chewing muscles,nasal
cavity,lateral aspect of the face,most of the scalp,and the dura mater surrounding the brain.

2. The internal carotid artery passes medial to the angle of the mandible and enters the cranial
cavity through the carotid canal of the temporal bone. It supplies the orbits and about 80% of the
cerebrum. Compressing the internal carotids near the mandible can therefore cause loss of
consciousness. The carotid sinus is located in the internal carotid just above the branch point; the
carotid body is nearby. After entering the cranial cavity,each internal carotid artery gives rise to
the following branches: a. the ophthalmic artery to the orbits,nose,and forehead; b. the anterior
cerebral artery to the medial aspect of the cerebral hemisphere (see arterial circle); and c. the
middle cerebral artery, which travels in the lateral sulcus of the cerebrum and supplies the lateral
aspect of the temporal and parietal lobes.
The Shoulder and Arm (brachium) begins with a large artery that changes name from subclavian
to axillary to brachial along its course:

1. The subclavian artery travels between the clavicle and first rib. It gives off several small
branches to the thoracic wall and viscera,considered later.

2. The axillary artery is the continuation of the subclavian artery through the axillary region. It
also gives off small thoracic branches,discussed later,and then ends at the neck of the humerus.
Here,it gives off the circumflex humeral artery, which encircles the humerus. This loop supplies
blood to the shoulder joint and deltoid muscle.

3. The brachial artery is the continuation of the axillary artery beyond the circumflex. It travels
down the medial side of the humerus and ends just distal to the elbow, supplying the anterior
flexor muscles of the brachium along the way. It exhibits several anastomoses near the
elbow,two of which are noted next. This is the most commonly used artery for routine BP
measurements.

4. The deep brachial artery arises from the proximal end of the brachial artery and supplies the
triceps brachii muscle.
5. The ulnar recurrent artery arises about midway along the brachial artery and anastomoses
distally with the ulnar artery. It supplies the elbow joint and the triceps brachii.

6. The radial recurrent artery leads from the deep brachial artery to the radial artery and supplies
the elbow joint and forearm muscles.

The Forearm (antebrachium) Just distal to the elbow, the brachial artery divides into the radial
artery and ulnar artery, which travel alongside the radius and ulna, respectively. The most
common place to take a pulse is at the radial artery,just proximal to the thumb. Near its origin,the
radial artery receives the deep brachial artery.

The ulnar artery gives rise,near its origin, to the anterior and posterior interosseous arteries,
which travel between the radius and ulna. Structures supplied by these arteries are as follows:

1. Radial artery:lateral forearm muscles,wrist, thumb,and index finger.

2. Ulnar artery:medial forearm muscles, digits 3 to 5,and medial aspect of index finger.

3. Interosseous arteries: deep flexors and extensors.

The Hand At the wrist, the radial and ulnar arteries anastomose to form two palmar arches:

1. The deep palmar arch gives rise to the palmar metacarpal arteries of the hand.

2. The superficial palmar arch gives rise to the palmar digital arteries of the fingers.
 The principal veins of the systemic circuit are detailed in tables 20.9 through 20.14.
While arteries are usually deep and well protected, veins occur in both deep and superficial
groups; you may be able to see quite a few of them in your arms and hands. Deep veins run
parallel to the arteries and often have similar names (femoral artery and femoral vein, for
example); this is not true of the superficial veins, however. The deep veins are not described in
as much detail as the arteries were, since it can usually be assumed that they drain the same
structures as the corresponding arteries supply.

In general, we began the study of arteries with those lying close to the heart and
progressed away. In the venous system, by contrast, we begin with those that are remote from the
heart and follow the flow of blood as they join each other and approach the heart. Venous
pathways have more anastomoses than arterial pathways, so the route of blood flow is often not
as clear. Many anastomoses are omitted from the following figures for clarity.
 Most blood of the head and neck is drained by three pairs of veins the internal
jugular,external jugular, and vertebral veins.This table traces their origins and drainage and
follows them to the formation of the brachiocephalic veins and superior vena cava.
 Dural Sinuses Large thin-walled veins called dural sinuses occur within the cranial cavity
between layers of dura mater. They receive blood from the brain and face and empty into the
internal jugular veins:

1. The superior and inferior sagittal sinuses are found in the falx cerebri between the cerebral
hemispheres; they receive blood that has circulated through the brain.

2. The cavernous sinuses occur on each side of the body of the sphenoid bone; they receive blood
from the superior ophthalmic vein draining the orbit and the facial vein draining the nose and
upper lip.
3. The transverse (lateral) sinuses encircle the inside of the occipital bone and lead to the jugular
foramen on each side. They receive blood from the previously mentioned sinuses and empty into
the internal jugular veins.

Major Veins of the Neck Blood flows down the neck mainly through three veins on each
side,all of which empty into the subclavian vein:

1. The internal jugular vein courses down the neck, alongside the internal carotid artery, deep to
the sternocleidomastoid muscle. It receives most of the blood from the brain, picks up blood
from the facial vein and superficial temporal vein along the way, passes deep to the clavicle, and
joins the subclavian vein. (Note that the facial vein empties into both the cavernous sinus and the
internal jugular vein.)

2. The external jugular vein drains tributaries from the parotid gland,facial muscles,scalp,and
other superficial structures. Some of this blood also follows venous anastomoses to the internal
jugular vein. The external jugular vein courses down the side of the neck superficial to the
sternocleidomastoid muscle and empties into the subclavian vein.

3. The vertebral vein travels with the vertebral artery in the transverse foramina of the cervical
vertebrae. Although the companion artery leads to the brain,the vertebral vein does not come
from there. It drains the cervical vertebrae,spinal cord,and some of the small deep muscles of the
neck.

Drainage from Shoulder to Heart From the shoulder region,blood takes the following
path to the heart:

1. The subclavian vein drains the arm and travels inferior to the clavicle; receives the external
jugular,vertebral,and internal jugular veins in that order; and ends where it receives the internal
jugular.

2. The brachiocephalic vein is formed by union of the subclavian and internal jugular veins. It
continues medially and receives tributaries draining the upper thoracic wall and breast.

3. The superior vena cava is formed by the union of the right and left brachiocephalic veins. It
travels inferiorly for about 7.5 cm and empties into the right atrium. It drains all structures
superior to the diaphragm except the pulmonary circuit and coronary circulation. It also receives
considerable drainage from the abdominal cavity by way of the azygos.

Superficial Veins These are easily seen through the skin of most people and are larger in
diameter than the deep veins:

1. The dorsal venous network is a plexus of veins visible on the back of the hand; it empties into
the major superficial veins of the forearm,the cephalic and basilic.

2. The cephalic vein arises from the lateral side of the dorsal venous arch,winds around the
radius as it travels up the forearm,continues up the lateral aspect of the brachium to the
shoulder,and joins the axillary vein there. Intravenous fluids are often administered through the
distal end of this vein.

3. The basilica vein arises from the medial side of the dorsal venous arch,travels up the posterior
aspect of the forearm,and continues into the brachium. About midway up the brachium it turns
deeper and runs beside the brachial artery. At the axilla it joins the brachial vein,and the union of
these two gives rise to the axillary vein.

4. The median cubital vein is a short anastomosis between the cephalic and basilic veins that
obliquely crosses the cubital fossa (anterior bend of the elbow). It is clearly visible through the
skin and is the most common site for drawing blood.

5. The median antebrachial vein originates near the base of the thumb,travels up the forearm
between the radial and ulnar veins,and terminates at the elbow; it empties into the cephalic vein
in some people and into the basilic vein in others.
6.6 Blood Vessels

Blood vessels are intricate networks of hollow tubes that transport blood throughout the
entire body. This is an essential function as blood delivers valuable nutrients to and removes
wastes from our cells. Blood vessels are constructed of layers of connective tissue and muscle.
The inner blood vessel layer is formed of endothelium. In capillaries and sinusoids, endothelium
comprises the majority of the vessel. Blood vessel endothelium is continuous with the inner
tissue lining of organs such as the brain, lungs, skin, and heart. In the heart, this inner layer is
called the endocardium.

Hemostasis is the cessation of bleeding. Although hemostatic mechanisms may not stop a
hemorrhage from a large blood vessel, they are quite effective at closing breaks in small ones.
Platelets play multiple roles in hemostasis, so we begin with a consideration of their form and
function. Coagulation (clotting) of the blood is the last but most effective defense against
bleeding. It is important for the blood to clot quickly when a vessel has been broken, but equally
important for it not to clot in the absence of vessel damage. Because of this delicate balance,
coagulation is one of the most complex processes in the body, involving over 30 chemical
reactions. It is presented here in a very simplified form. Perhaps clotting is best understood if we
first consider its goal.

The objective is to convert the plasma protein fibrinogen into fibrin, a sticky protein that
adheres to the walls of a vessel. As blood cells and platelets arrive, they become stuck to the
fibrin like insects sticking to a spider web. The resulting mass of fibrin, blood cells, and platelets
ideally seals the break in the blood vessel. The complexity of clotting lies in how the fibrin is
formed. There are two reaction pathways to coagulation. One of them, the extrinsic mechanism,
is initiated by clotting factors released by the damaged blood vessel and perivascular tissues. The
word extrinsic refers to the fact that these factors come from sources other than the blood itself.
Blood may also clot, however, without these tissue factors for example, when platelets adhere to
a fatty plaque of atherosclerosis or to a test tube. The reaction pathway in this case is called the
intrinsic mechanism because it uses only clotting factors found in the blood itself. In most cases
of bleeding, both the extrinsic and intrinsic mechanisms work simultaneously to contribute to
hemostasis. Clotting factors are called procoagulants, in contrast to the anticoagulants discussed
later. Most procoagulants are proteins produced by the liver. They are always present in the
plasma in inactive form, but when one factor is activated, it functions as an enzyme that activates
the next one in the pathway. That factor activates the next, and so on, in a sequence called a
reaction cascade a series of reactions, each of which depends on the product of the preceding
one. Many of the clotting factors are identified by Roman numerals, which indicate the order in
which they were discovered, not the order of the reactions. These terms were abandoned when it
was found that factor IV was calcium and factor VI was activated factor V. The last four
procoagulants in the table are called platelet factors (PF1 through PF4) because they are
produced by the platelets.

Initiation of Coagulation The extrinsic mechanism is diagrammed on the left side of

figure 18.21. The damaged blood vessel and perivascular tissues release a lipoprotein mixture
called tissue thromboplastin23 (factor III). Factor III combines with factor VII to form a complex
which, in the presence of Ca2, then activates factor X. The extrinsic and intrinsic pathways differ
only in how they arrive at active factor X. Therefore, before examining their common pathway
from factor X to the end, let’s consider how the intrinsic pathway reaches this step. The intrinsic
mechanism is diagrammed on the right side of figure 18.21. Everything needed to initiate it is
present in the plasma or platelets. When platelets degranulate, they release factor XII (Hageman
factor, named for the patient in whom it was discovered). Through a cascade of reactions, this
leads to activated factors XI, IX, and VIII, in that ordereach serving as an enzyme that catalyzes
the next step—and finally to factor X. This pathway also requires Ca2 and PF3.

Completion of Coagulation Once factor X is activated, the remaining events are

identical in the intrinsic and extrinsic mechanisms. Factor X combines with factors III and V in
the presence of Ca2 and PF3 to produce prothrombin activator. This enzyme acts on a globulin
called prothrombin (factor II) and converts it to the enzyme thrombin. Thrombin then chops up
fibrinogen into shorter strands of fibrin. Factor XIII crosslinks these fibrin strands to create a
dense aggregation called fibrin polymer, which forms the structural framework of the blood clot.
Once a clot begins to form, it launches a self-accelerating positive feedback process that seals off
the damaged vessel more quickly.

Thrombin works with factor V to accelerate the production of prothrombin activator,

which in turn produces more thrombin. The cascade of enzymatic reactions acts as an amplifying
mechanism to ensure the rapid clotting of blood. Each activated enzyme in the pathway produces
a larger number of enzyme molecules at the following step. One activated molecule of factor XII
at the start of the intrinsic pathway, for example, causes thousands of fibrin molecules to be
produced very quickly. Note the similarity of this process to the enzyme amplification that
occurs in hormone action. Notice that the extrinsic mechanism requires fewer steps to activate
factor X than the intrinsic mechanism does; it is a “shortcut” to coagulation. It takes 3 to 6
minutes for a clot to form by the intrinsic pathway but only 15 seconds or so by the extrinsic
pathway. For this reason, when a small wound bleeds, you can stop the bleeding sooner by
massaging the site. This releases thromboplastin from the perivascular tissues and activates or
speeds up the extrinsic pathway. A number of laboratory tests are used to evaluate the efficiency
of coagulation. Normally, the bleeding of a fingerstick should stop within 2 to 3 minutes, and a
sample of blood in a clean test tube should clot within 15 minutes. Other techniques are available
that can separately assess the effectiveness of the intrinsic and extrinsic mechanisms.
The Pathways of Coagulation. Most clotting factors act as enzymes that convert the next factor from an inactive
form (shaded ellipse) to an active form (lighter ellipse).

6.7 The factors that affect blood pressure

Blood pressure (BP) is the force that the blood exerts against a vessel wall. It can be
measured within a blood vessel or heart chamber by inserting a catheter or needle connected to
an external manometer (pressure-measuring device). For routine clinical purposes, however, the
measurement of greatest interest is the systemic arterial BP at a point close to the heart, we
customarily measure it with a sphygmomanometer at the brachial artery of the arm. It is easy to
encircle the arm with a pressure cuff, and this artery is sufficiently close to the heart to reflect the
maximum arterial BP found anywhere in the systemic circuit. Two pressures are recorded:
systolic pressure is the peak arterial BP attained during ventricular systole, and diastolic
pressure is the minimum arterial BP between heartbeats. For a healthy person aged 20 to 30,
these pressures are typically about 120 and 75 mmHg, respectively. Arterial BP is written as a
ratio of systolic over diastolic pressure: 120/75. The difference between systolic and diastolic
pressure is called pulse pressure (not to be confused with pulse rate). This is an important
measure of the stress exerted on small arteries by the pressure surges generated by the heart.
Another measure of stress on the blood vessels is the mean arterial pressure (MAP) the mean
pressure you would obtain if you took measurements at several intervals (say every 0.1 sec)
throughout the cardiac cycle. Since diastole lasts longer than systole, MAP is not simply the
average of systolic and diastolic pressures.

The best estimate of MAP is the sum of diastolic pressure and one-third of the pulse
pressure. For a blood pressure of 120/75, MAP =75 + 45/3 = 90 mmHg, a typical value for
vessels at the level of the heart. MAP varies, however, with the influence of gravity. In a
standing adult, it is about 62 mmHg in the major arteries of the head and 180 mmHg in major
arteries of the ankle. Hypertension (high BP) is commonly considered to be a chronic resting
blood pressure higher than 140/90. (Transient high BP resulting from emotion or exercise is not
hypertension.) Among other effects, it can weaken the small arteries and cause aneurysms.

Hypotension is chronic low resting BP. It may be a consequence of blood loss,

dehydration, anemia, or other factors and is normal in people approaching death. The ability of
the arteries to distend and recoil during the cardiac cycle is important in modulating arterial BP.
If the arteries were rigid tubes, pressure would rise much higher in systole and drop to nearly
zero in diastole. Blood throughout the circulatory system would flow and stop, flow and stop,
thus putting great stress on the small vessels. But when the conducting arteries are healthy, they
expand with each systole and absorb some of the force of the ejected blood. Then, when the heart
is in diastole, their elastic recoil exerts pressure on the blood and prevents the BP from dropping
to zero. The combination of expansion and recoil in the arteries maintains a steady flow of blood
downstream, in the capillaries, throughout the cardiac cycle. Thus, the elastic arteries “smooth
out” the pressure fluctuations and reduce stress on the smaller arteries. Nevertheless, blood flow
in the arteries is pulsatile. Blood in the aorta rushes forward at 120 cm/sec during systole and an
average speed of 40 cm/sec over the cardiac cycle.

When measured at points farther away from the heart, systolic and diastolic pressures are
lower and there is less difference between them. In capillaries and veins, the blood flows at a
steady speed without pulsation because the pressure surges have been damped out by the
distance traveled and the elasticity of the arteries. This is why an injured vein exhibits relatively
slow, steady bleeding, whereas blood spurts intermittently from a severed artery. In the inferior
vena cava near the heart, however, venous flow fluctuates with the respiratory cycle for reasons
explained later, and there is some fluctuation in the jugular veins of the neck. Blood pressure
rises with age as the arteries become less distensible and absorb less systolic force.
Atherosclerosis also stiffens the arteries and leads to a rise in BP. Blood pressure is determined
mainly by cardiac output, blood volume, and peripheral resistance. The regulation of cardiac
output and blood volume are discussed in chapters 19 and 24, respectively. Here, we turn our
attention to peripheral resistance.

6.8 Main diseases and disorders of the cardiovascular system

Anemia is a decrease of the hemoglobin concentration in the blood below the normal level. The
normal range of hemoglobin in male is 14 to 18 g/dl, in women 12 to 16 g/dl. An anemia goes
along with a reduction in erythrocytes in the blood (erythropenia). Main symptoms are light
tiredness, breathlessness (dyspnea) and headache. Anemia is either acquired or hereditary.
Acquired anemia may be due to loss of blood (hemorrhagic anemia), hemolysis, disorders of the
blood-forming system, kidney diseases, tumors etc. Hereditary anemia can be caused by
abnormal forms of hemoglobin (hemoglobinopathies).

Varicose Veins In people who stand for long periods, such as dentists and hairdressers, blood
tends to pool in the lower limbs and stretch the veins. This is especially true of superficial veins,
which are not surrounded by supportive tissue. Stretching pulls the cusps of the venous valves
farther apart until the valves become incompetent to prevent the backflow of blood. As the veins
become further distended, their walls grow weak and they develop into varicose veins with
irregular dilations and twisted pathways. Obesity and pregnancy also promote development of
varicose veins by putting pressure on large veins of the pelvic region and obstructing drainage
from the legs. Varicose veins sometimes develop because of hereditary weakness of the valves.
With less drainage of blood, tissues of the leg and foot may become edematous and painful.
Hemorrhoids are varicose veins of the anal canal.

Hemophilia, a family of hereditary diseases characterized by deficiencies of one factor or

another. Because of its sex-linked recessive mechanism of heredity, most hemophilia occurs
predominantly in males. They can inherit it only from their mothers, however, as happened with
the descendants of Queen Victoria. The lack of factor VIII causes classical hemophilia
(hemophilia A), which accounts for about 83% of cases and afflicts 1 in 5,000 males worldwide.
Lack of factor IX causes hemophilia B, which accounts for 15% of cases and occurs in about 1
out of 30,000 males. Factors VIII and IX are therefore known as antihemophilic factors A and B.
A rarer form called hemophilia C( factor XI deficiency) is autosomal, not sex-linked, so it occurs
equally in both sexes. Before purified factor VIII became available in the 1960s, more than half
of those with hemophilia died before age 5 and only 10% lived to age 21. Physical exertion
causes bleeding into the muscles and joints. Excruciating pain and eventual joint immobility can
result from intramuscular and joint hematomas (masses of clotted blood in the tissues).
Hemophilia varies in severity, however. Half of the normal level of clotting factor is enough to
prevent the symptoms, and the symptoms are mild even in individuals with as little as 30% of the
normal amount. Such cases may go undetected even into adulthood. Bleeding can be relieved for
a few days by transfusion of plasma or purified clotting factors.

Arteriosclerosis occurs when the blood vessels that carry oxygen and nutrients from your heart
to the rest of your body (arteries) become thick and stiff sometimes restricting blood flow to your
organs and tissues. Healthy arteries are flexible and elastic, but over time, the walls in your
arteries can harden, a condition commonly called hardening of the arteries. Atherosclerosis is a
specific type of arteriosclerosis, but the terms are sometimes used interchangeably.
Atherosclerosis refers to the buildup of fats, cholesterol and other substances in and on your
artery walls (plaque), which can restrict blood flow. The plaque can burst, triggering a blood
clot. Although atherosclerosis is often considered a heart problem, it can affect arteries anywhere
in your body. Atherosclerosis may be preventable and is treatable.
Atherosclerosis is a disorder in which fatty deposits form in an artery, obstruct the lumen, and
cause deterioration of the arterial wall. It is especially critical when it occurs in the coronary
arteries and threatens to cut off the blood supply to the myocardium. Atherosclerosis is also a
leading contributor to stroke and kidney failure. Cause and Pathogenesis According to one
theory, the stage is set for atherosclerosis when the endothelium of a blood vessel is damaged by
hypertension, viral infection, diabetes mellitus, or other causes. Monocytes adhere to the
damaged endothelium, penetrate beneath it, and transform into macrophages. Macrophages and
smooth muscle cells absorb cholesterol and neutral fats from the blood and acquire a frothy
appearance; they are then called foam cells and are visible as a fatty streak on the vessel wall.
Platelets also adhere to areas of endothelial damage, degranulate, and release platelet-derived
growth factor (PDGF); some PDGF also comes from macrophages and endothelial cells.

PDGF stimulates mitosis of smooth muscle, leading eventually to a mass of lipid, smooth
muscle, and macrophages called an atheroma (atherosclerotic plaque). The muscular and elastic
tissue of the artery become increasingly replaced with scar tissue. When atheromas become
calcified, they are called complicated plaques. Such plaques cause a state of arterial rigidity
called arteriosclerosis. Atherosclerosis is caused primarily by a combination of low-density
lipoproteins (LDLs) in the blood plasma and defective LDL receptors in the arteries. LDLs are
small protein-coated droplets of cholesterol, neutral fat, free fatty acids, and phospholipids. Most
cells have LDL receptors, take up these droplets from the blood by receptormediated
endocytosis, and stop when they have enough cholesterol. In atherosclerosis, arterial cells have
dysfunctional receptors that continue taking up plasma lipids and cause the cells to accumulate
excess cholesterol. As an atheroma grows, more and more of the arterial lumen becomes
obstructed. Angina pectoris and other symptoms begin to occur when the lumen of a major
coronary artery is reduced by at least 75%. When platelets adhere to lesions of the arterial wall,
they release clotting factors, so an atheroma can become a focus for thrombosis. A clot can block
what remains of the lumen, or it can break free and become an embolus that travels downstream
until it lodges in a smaller artery. Part of an atheroma itself can also break loose and travel as a
fatty embolus. Atheromas also contribute to coronary artery spasms. Healthy endothelial cells
secrete nitric oxide (NO), which causes the arteries to dilate. Vessels damaged by atherosclerosis
release less NO, and the coronary arteries exhibit spasms. With much of the lumen already
obstructed by the atheroma and perhaps a thrombus, an arterial spasm can temporarily shut off
the remaining flow and precipitate an attack of angina.

HIV stands for Human Immunodeficiency Virus. HIV is a virus. Some viruses, such as the ones
that cause the common cold or the flu, stay in the body only for a few days. Some viruses, such
as HIV, never go away. When a person becomes infected with HIV, that person becomes "HIV
positive" and will always be HIV positive. Over time, HIV disease infects and kills white blood
cells called CD4 lymphocytes (or "T cells") and can leave the body unable to fight off certain
kinds of infections and cancers. Infections that occur due to HIV are called opportunistic
infections because they take advantage of the impaired immune system.With successful
antiretroviral therapy (ART), the body can remain healthy and fight off most viruses and
bacteria. A healthy person usually has a CD4 count of between 600 and 1,200. When the CD4
count drops below 200, a person's immune system is severely weakened, and that person is then
diagnosed with AIDS, even if he or she has not become sick from other infections. AIDS stands
for Acquired Immune Deficiency Syndrome and is caused by HIV. The names HIV and AIDS
can be confusing because both terms describe the same disease. Think of AIDS as advanced HIV
disease. A person with AIDS has an immune system so weakened by HIV that the person usually
becomes sick from one of several opportunistic infections or cancers such as PCP (a type of
pneumonia) or KS (Kaposi sarcoma, a type of cancer that affects the skin and internal organs in
HIV), wasting syndrome (involuntary weight loss), memory impairment, or tuberculosis. If
someone with HIV is diagnosed with one of these opportunistic infections (even if the CD4
count is above 200), he or she is said to have AIDS. AIDS usually takes time to develop from the
time a person acquires HIV--usually between 2 to 10 years or more. Once a person has been
diagnosed with AIDS, she or he is always considered to have AIDS, even if that person's CD4
count goes up again and/or they recover from the disease that defined their AIDS diagnosis

Hypertension (high BP) is commonly considered to be a chronic resting blood pressure higher
than 140/90. Transient high BP resulting from emotion or exercise is not hypertension. Among
other effects, it can weaken the small arteries and cause aneurysms. Hypotension is chronic low
resting BP. It may be a consequence of blood loss, dehydration, anemia, or other factors and is
normal in people approaching death.

Cholesterol is a waxy substance found in your blood. Your body needs cholesterol to build
healthy cells, but high levels of cholesterol can increase your risk of heart disease. With high
cholesterol, you can develop fatty deposits in your blood vessels. Eventually, these deposits
grow, making it difficult for enough blood to flow through your arteries. Sometimes, those
deposits can break suddenly and form a clot that causes a heart attack or stroke. High
cholesterol can be inherited, but it's often the result of unhealthy lifestyle choices, which make it
preventable and treatable. A healthy diet, regular exercise and sometimes medication can help
reduce high cholesterol. Cholesterol is carried through your blood, attached to proteins. This
combination of proteins and cholesterol is called a lipoprotein. There are different types of
cholesterol, based on what the lipoprotein carries. They are: Low-density lipoprotein (LDL).
LDL, or "bad" cholesterol, transports cholesterol particles throughout your body. LDL
cholesterol builds up in the walls of your arteries, making them hard and narrow. High-density
lipoprotein (HDL). HDL, or "good" cholesterol, picks up excess cholesterol and takes it back to
your liver.A lipid profile also typically measures triglycerides, a type of fat in the blood. Having
a high triglyceride level can also increase your risk of heart disease. Factors you can control such
as inactivity, obesity and an unhealthy diet contribute to high cholesterol and low HDL
cholesterol. Factors beyond your control might play a role, too. For example, your genetic
makeup might keep cells from removing LDL cholesterol from your blood efficiently or cause
your liver to produce too much cholesterol.

Hepatitis is inflammation of the liver due to a viral infection. Even though the liver is involved
in all types of hepatitis, the virus type, route of transmission, natural history and treatment
protocols are different between the types of hepatitis. This article will discuss the virus type,
route of transmission, signs and symptoms, investigation and diagnosis, natural history, and
treatment protocols of each type of hepatitis and compare them to differentiate one from the
other. Hepatitis A is a food and water borne infection. Hepatitis A virus is a RNA virus. Usually
travelers to tropical countries fall victim to this infection. Children get this infection easily. Virus
enters the body via food or water and incubates for 3 to 6 weeks before causing prodromal
symptoms like fever, ill health, lethargy, body ache, joint pains. During the active phase,
yellowish discoloration of eyes develops with liver, spleen and lymph node enlargement.Full
blood count shows low white blood cell count and low platelets. Serum transaminases rise during
the active phase. AST and ALT rise are more than ALP rise. ALT rises more than AST. Serum
IgM rises after 25 days of exposure to indicate recent infection. After sero-conversion IgG
remains detectable for life.Treatment is supportive. Food hygiene, strict individual use of
crockery to limit the spread, fluid intake, maintaining good renal function, and avoiding alcohol
are important steps. There are various preventive methods. Passive immunization with
immunoglobulin provides protection for 3 months and is recommended for travelers. Active
immunization with a purified protein from the virus gives immunity for 1 year. If a booster dose
is administered 6 months after the first dose, there will be immunity for 10 years. Hepatitis A is
self-limiting but fulminant hepatitis is a rare possibility. Chronic hepatitis does not occur with
hepatitis A. Hepatitis B is a blood borne infection. Blood transfusion, unprotected sexual
contact, hemodialysis, intravenous drug abuse are known risk factors. After the virus enters the
body, it remains dormant for 1 to 6 months before giving rise to prodromal symptoms like fever
and lethargy. Extra-hepatic features are more common in hepatitis B. During the acute stage liver
and spleen enlargement occur. Full blood count may show lymphocytic leukocytosis. AST levels
rise 2 to 4 months after exposure and returns to baseline after the 5 th month. HBsAg is positive in
serum from 1-6 months. If HBsAg is positive after 6 months, it suggests chronic career state.
HBeAg is positive in serum from 2 to 4 months and denotes a high infective state.  In liver
biopsy, immunofluorescence HBcAg and HBeAg are positive from 2 to 4 months. Antibodies
against HBsAg appear 6 months after exposure, and anti-HBsAg is the only marker that is
positive in vaccinated individuals. Anti-HBeAg becomes positive after 4 months. If anti-HBCAg
is positive, it denotes a past infection. Complications include carrier state, relapse, chronic
hepatitis, cirrhosis, superinfection with hepatitis D, glomerulonephritis, and hepatocellular
carcinoma. If HBsAg is positive, the risk increases 10 fold. If both HBsAg and HBeAg are
positive, the risk increases 60 fold. Fulminant hepatitis is rare.Treatment is supportive. Alcohol
avoidance is essential. Hepatitis C is a RNA virus. It is also blood borne. Intravenous drug
abuse, hemodialysis, blood transfusion, and sexual contact increase the risk of contracting the
disease. Chronic hepatitis is very common after hepatitis C infection. Around 20% get cirrhosis.
Hepatocellular carcinoma risk is also high with hepatitis C. Presentations are similar to hepatitis
B.AST and ALT both increase, but AST remains lower than ALT till cirrhosis develops.
Hepatitis C Ag is positive during active infection. Treatment is supportive. In chronic hepatitis,
interferon Alfa and ribavirin may be used. Peginterferone Alfa may be more effective than
interferon Alfa. Evidence suggests that interferon Alfa reduces the progression into a chronic
state when given during the acute stage

Coronary heart disease (CHD), or coronary thrombosis, develops when the coronary arteries
become too narrow. The coronary arteries are the blood vessels that supply oxygen and blood to
the heart. CHD tends to develop when cholesterol builds up on the artery walls, creating plaques.
These plaques cause the arteries to narrow, reducing blood flow to the heart. A clot can
sometimes obstruct the blood flow, causing serious health problems. Coronary arteries form the
network of blood vessels on the surface of the heart that feed it oxygen. If these arteries narrow,
the heart may not receive enough oxygen rich blood, especially during physical activity. The
heart is surrounded by three major coronary arteries that supply it with blood and oxygen. If a
blood clot develops in one of these arteries, the blood supply to that area of the heart muscle will
stop. This is known as a heart attack, or in medical terms a coronary thrombosis or myocardial
infarction.A heart attack will cause severe chest pains behind the breast bone, often radiating
towards the left arm. If the blockage (thrombosis) is not dissolved quickly with medication or
treated with an emergency catheter procedure (balloon angioplasty), the area of heart muscle that
isn't getting enough oxygen will stop working properly.

Septicemia is a serious bloodstream infection. It’s also known as blood poisoning. Septicemia
occurs when a bacterial infection elsewhere in the body, such as the lungs or skin, enters the
bloodstream. This is dangerous because the bacteria and their toxins can be carried through the
bloodstream to your entire body. Septicemia can quickly become life-threatening. It must be
treated in a hospital. If left untreated, septicemia can progress to sepsis.Septicemia and sepsis
aren’t the same. Sepsis is a serious complication of septicemia. Sepsis causes inflammation
throughout the body. This inflammation can cause blood clots and block oxygen from reaching
vital organs, resulting in organ failure.

Hemorrhoids are swollen veins in the lowest part of your rectum and anus. Sometimes the walls
of these blood vessels stretch so thin that the veins bulge and get irritated, especially when you
poop. Swollen hemorrhoids are also called piles. Hemorrhoids are one of the most common
causes of rectal bleeding. They're rarely dangerous and usually clear up in a couple of weeks. But
you should see your doctor to make sure it's not a more serious condition. He can also remove
hemorrhoids that won't go away or are very painful. Internal hemorrhoids are far enough inside
the rectum that you can't usually see or feel them. They don't generally hurt because you have
few pain-sensing nerves there. Bleeding may be the only sign of them. External hemorrhoids are
under the skin around the anus, where there are many more pain-sensing nerves, so they tend to
hurt as well as bleed.

Phlebitis is a condition in which a vein becomes inflamed. The inflammation may cause pain
and swelling. When the inflammation is caused by a blood clot or thrombus, it is called
thrombophlebitis. Thrombophlebitis usually occurs in leg veins, but it may also affect the veins
in the arms. Some people with phlebitis have no symptoms, but others may experience signs like
pain, tenderness, redness, and a bulging vein Phlebitis can be caused by many things, for
example, sitting to long on long drives, train or plane rides, varicose veins, some cancers, and
after surgery.

A thrombus, colloquially called a blood clot, is the final product of the blood coagulation step in
hemostasis. There are two components to a thrombus: aggregated platelets and red blood cells
that form a plug, and a mesh of cross-linked fibrin protein. The substance making up a thrombus
is sometimes called cruor. A thrombus is a healthy response to injury intended to prevent
bleeding, but can be harmful in thrombosis, when clots obstruct blood flow through healthy
blood vessels.

Embolism Injury to the dural sinuses or jugular veins presents less danger from loss of blood
than from air sucked into the circulatory system. The presence of air in the bloodstream is called
air embolism. This is an important concern to neurosurgeons, who sometimes operate with the
patient in a sitting position. If a dural sinus is punctured, air can be sucked into the sinus and
accumulate in the heart chambers, which blocks cardiac output and causes sudden death. Smaller
air bubbles in the systemic circulation can cut off blood flow to the brain, lungs, myocardium,
and other vital tissues.

Pulmonary embolism is a blockage in one of the pulmonary arteries in your lungs. In most
cases, pulmonary embolism is caused by blood clots that travel to the lungs from the legs or,
rarely, other parts of the body (deep vein thrombosis). Because the clots block blood flow to the
lungs, pulmonary embolism can be life-threatening. However, prompt treatment greatly reduces
the risk of death. Taking measures to prevent blood clots in your legs will help protect you
against pulmonary embolism. hortness of breath. This symptom typically appears suddenly and
always gets worse with exertion. Chest pain. You may feel like you're having a heart attack. The
pain may become worse when you breathe deeply (pleurisy), cough, eat, bend or stoop. The pain
will get worse with exertion but won't go away when you rest. Cough. The cough may produce
bloody or blood-streaked sputum.

Leukemia is cancer of the white blood cells. White blood cells help your body fight infection.
Your blood cells form in your bone marrow. In leukemia, the bone marrow produces abnormal
white blood cells. These cells crowd out the healthy blood cells, making it hard for blood to do
its work. Leukemias are grouped by how quickly the disease develops (acute or chronic) as well
as by the type of blood cell that is affected (lymphocytes or myelocytes). The four main types of
leukemia include acute lymphocytic leukemia or acute lymphoblastic leukemia (ALL), chronic
lymphocytic leukemia (CLL), acute myelocytic leukemia (AML), and chronic myelocytic
leukemia (CML) or chronic myelogenous leukemia (CML). People with leukemia are at
significantly increased risk for developing infections, anemia, and bleeding. Other symptoms and
signs include easy bruising, weight loss, night sweats, and unexplained fevers. The diagnosis of
leukemia is supported by findings of the medical history and examination, and examining blood
and bone marrow samples under a microscope.

An aneurysm is a weak point in a blood vessel or in the heart wall. It forms a thin-walled,
bulging sac that pulsates with each beat of the heart and may eventually rupture. In a dissecting
aneurysm,blood pools between the tunics of a vessel and separates them, usually because of
degeneration of the tunica media. The most common sites of aneurysms are the abdominal aorta,
the renal arteries, and the arterial circle at the base of the brain. Even without hemorrhaging,
aneurysms can cause pain or death by putting pressure on brain tissue, nerves, adjacent veins,
pulmonary air passages, or the esophagus. Other consequences include neurological disorders,
difficulty in breathing or swallowing, chronic cough, or congestion of the tissues with blood.
Aneurysms sometimes result from congenital weakness of the blood vessels and sometimes from
trauma or bacterial infections such as syphilis. The most common cause, however, is the
combination of atherosclerosis and hypertension.

Stress disorders are primarily categorised as acute stress reaction, post-traumatic stress disorder
(PTSD), and adjustment disorder. PTSD is the most severe of these disorders and is characterised
by avoidance, negative cognitions, mood changes, re-experiencing, and hyperarousal. Primary
outcome measures included the diagnosis of incident cardiovascular disease or its specific
subtypes. tress-related disorders were strongly associated with early-onset cardiovascular
disease. Patients with stress-related disorders had a higher burden or somatic diseases and a
lower family income level. They were also more likely to be divorced or widowed. These
findings show a peak of cardiovascular diseases risk immediately after diagnosis of a stress-
related disorder, followed by a rapid decline within the first six months. These findings clearly
show that stress-related disorders are associated with multiple types of cardiovascular disease
independent of familial background, history of psychiatric disease and psychiatric comorbidity.
The risk of severe and acute cardiovascular events was found to be highest during the period
adjacent to the diagnosis of a stress-related disorder. The relative risk of other cardiovascular
diseases was more pronounced during the first year after diagnosis of a stress-related disorder.
While the highest point estimates were observed for PTSD, other stress-related disorders also
demonstrated a considerably increased risk of cardiovascular disease.