Cardiovascular System.pdf

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Branch: B. Pharm.
Semester: I
UNIT: V
Subject: Human Anatomy & Physiology-I
Topic: Cardiovascular System
Dr. Akanksha Mishra
Assistant Professor
Department of Pharmacology
Institute of Pharmaceutical Sciences
University of Lucknow

Anatomy of the Heart
• 12 cm (5 in.) long
• 9 cm (3.5 in.) wide at its broadest point
• 6 cm (2.5 in.) thick
• Average mass- 250 g (8 oz) in adult females and 300 g (10 oz)
in adult males
• Rests on diaphragm
• Lies in the mediastinum
• 2/3 of the mass of heart lies to left of the body’s midline

Fig.1: Position of the Heart and associated structures in the mediastinum

Pericardium
• Membrane that surrounds and protects the heart
• Confines the heart to its position in the mediastinum
• Allow sufficient freedom of movement for vigorous and rapid
contraction
• Two main parts:
(1) the fibrous pericardium and
(2) the serous pericardium

Fibrous Pericardium
• Superficial
• Composed of tough, inelastic, dense irregular connective
tissue.
• Prevents overstretching of the heart
• Provides protection,
• Anchors the heart in the mediastinum

Serous pericardium
• Thinner, more delicate membrane
• Forms a double layer around the heart
• Two layers
1. Outer parietal layer of the serous pericardium
2. Inner visceral layer of the serous pericardium [epicardium]

Pericardial fluid
• Thin film of lubricating serous fluid.
• Between parietal and visceral layers
• Slippery secretion of the pericardial cells
• Also known as pericardial fluid
• Reduces friction between layers of serous pericardium
• Pericardial cavity- Space containing few ml of pericardial fluid

Fig.2: Pericardium and Heart Wall

Fig.3: Structure of the heart: Surface Features (Anterior external View)

Fig.4: Structure of the heart: Surface Features (Posterior external View)

Right Atrium
• Forms the right surface of the heart
• 2–3 mm (0.08–0.12 in.) in average thickness
• Receives blood from three veins:
1. The superior vena cava,
2. Inferior vena cava, and
3. Coronary sinus

Right Atrium
Pectinate muscles
✓ Anterior and posterior walls of right atrium are different
✓ Inside of posterior wall is smooth
✓ Inside of anterior wall is rough
✓ Roughness is due to presence of muscular ridges (Pectinate
muscles), which also extend into the auricle

Right Atrium
• Interatrial septum
✓ A thin partition between right and left atrium.
• Fossa ovalis
✓ Prominent feature of septum
✓ Oval depression
✓ Remnant of the foramen ovale (an opening in interatrial
septum of fetal heart that normally closes soon after birth)

• Tricuspid valve
✓ Blood passes from right atrium into right ventricle through a
valve
✓ Tricuspid valve because it consists of three cusps or leaflets
✓ Also called the right atrioventricular valve

Right Ventricle
• 4–5 mm (0.16–0.2 in.) in average thickness.
• Trabeculae carneae
✓ Inside of right ventricle contains a series of ridges formed by
raised bundles of cardiac muscle fibers called trabeculae
carneae
• Chordae tendineae & papillary muscles
✓ Cusps of tricuspid valve are connected to tendonlike cords, the
chordae tendineae,
✓ Chordae tendineae, in turn are connected to cone-shaped
trabeculae carneae called papillary muscles.

Layers of the Heart Wall
✓ Epicardium (external layer)
✓ Myocardium (middle layer)
✓ Endocardium (inner layer)

Epicardium
• Composed of two tissue layers:
1. Outermost Visceral layer of the serous pericardium
• Thin, transparent outer layer
• Composed of mesothelium
2. Variable layer of delicate fibroelastic tissue and adipose tissue
✓ Beneath the mesothelium
✓ Adipose tissue predominates
✓ Becomes thickest over the ventricular surfaces, where it houses the
major coronary and cardiac vessels of the heart.

Myocardium
• The middle layer
• Responsible for the pumping action of the heart
• Composed of cardiac muscle tissue
• Makes up approx. 95% of heart wall
• The muscle fibers (cells) are wrapped and bundled with
connective tissue sheaths
• These sheaths are composed of endomysium and perimysium

Endocardium
• Innermost endocardium
• Thin layer of endothelium overlying a thin layer of connective
tissue
• Provides a smooth lining for the chambers and valves of the
heart
• Smooth endothelial lining minimizes surface friction as blood
passes through the heart.

• Atria - Two superior receiving chambers
• Ventricles - Two inferior pumping chambers
• Veins- Atria receive blood from blood vessels returning blood
to heart
• Arteries- Ventricles eject blood from heart into blood vessels
• Auricle- pouchlike structure slightly increases capacity of
atrium to hold a greater volume of blood

Sulci
• A series of grooves on the surface of the heart
• Contain coronary blood vessels and fat
• Each sulcus marks the external boundary between two heart
chambers
✓ Deep coronary sulcus (Marks the external boundary between
superior atria and inferior ventricles)
✓ Anterior interventricular sulcus (Mark external boundary
between right and left ventricles on anterior aspect of heart)
✓ Posterior inter-ventricular sulcus (Marks external boundary
between ventricles on posterior aspect of heart)

Right Ventricle
• Interventricular septum
✓ Partition that separates the Right ventricle from the left ventricle
• Pulmonary valve -
✓ Blood passes from right ventricle through the pulmonary valve
into a large artery (pulmonary trunk)
• Pulmonary trunk divides into right and left pulmonary arteries
• Pulmonary arteries carries blood to the lungs

Fig.5: Structure of the heart: Internal Anatomy

Left Atrium
• Same thickness as right atrium
• Receives blood from lungs through four pulmonary veins.
• Inside of left atrium has a smooth posterior wall- Pectinate
muscles are confined to auricle of left atrium

Left Atrium
• Blood passes from left atrium into the left ventricle through
the bicuspid valve, has two cusps.
• It is also called the left atrioventricular valve.

Left Ventricle
• Thickest chamber of the heart
• Contains trabeculae carneae
• Has chordae tendineae that anchor cusps of bicuspid valve to
papillary muscles

Left Ventricle
Blood passes from left ventricle
Ascending aorta
Through aortic valve
Some of the blood in the aorta flows
into the coronary arteries
Remainder of the blood passes into the
arch of the aorta and descending aorta
carry blood to the heart wall carry blood throughout the body

Left Ventricle
Ductus arteriosus
• During fetal life, a temporary blood vessel, called the ductus
arteriosus, shunts blood from the pulmonary trunk into the aorta.
• Hence, only a small amount of blood enters the nonfunctioning
fetal lungs.
Ligamentum arteriosum
• The ductus arteriosus normally closes shortly after birth, leaving a
remnant known as the ligamentum arteriosum
• It connects the arch of the aorta and pulmonary trunk

Myocardial Thickness and Function
Thin-walled atria
Thick-walled Adjacent ventricles
Deliver blood under less pressure
Pump blood under higher pressure
over greater distances

• Right and left ventricles:
✓ act as two separate pumps
✓ simultaneously eject equal volumes of blood
✓ But the right side has a much smaller workload.
• Right ventricle pumps blood a short distance to the lungs at
lower pressure, and the resistance to blood flow is small.

Heart Valves and Circulation
of Blood
• Each chamber of the heart contracts
• It pushes a volume of blood into a ventricle
• Or it pushes out of the heart into an artery
• As the heart contracts and relaxes, pressure changes
• In response to pressure changes, valves open and close.
• Valves ensure the one way flow of blood.
• Valves open to let blood through and then closing to prevent
its backflow

Operation of the Atrioventricular
Valves
• Tricuspid and bicuspid valves
• Located between an atrium and a ventricle
• When an AV valve is open, the rounded ends of the cusps
project into the ventricle.

Valves
When ventricles are relaxed
Papillary muscles are relaxed,
Chordae tendineae are slack (loose),
Blood moves from a higher pressure in the atria
To a lower pressure in the ventricles
through open AV valves

Valves
When the ventricles contract
the pressure of the blood drives the cusps upward
their edges meet and the opening is closed
At the same time, the papillary muscles contract
which pulls on and tightens the chordae tendineae.
This prevents the valve cusps from everting (opening into the atria) in
response to the high ventricular pressure.
• If the AV valves or chordae tendineae are damaged, blood may regurgitate
(flow back) into the atria when the ventricles contract.

Fig.6: Responses of the valves to the pumping of the heart.

Operation of the Semilunar Valves
Semilunar valves (crescent moon–shaped cusps)
Aortic Valve Pulmonary valves
• Each cusp attaches to the arterial wall
• The SL valves allow ejection of blood from the heart into
arteries
• The SL valves prevent backflow of blood into the ventricles

• Free borders of cusps project into the lumen of the artery
When the ventricles contract
Pressure builds up within the chambers
Semilunar valves open when pressure in the ventricles exceeds the
pressure in the arteries
Permitting ejection of blood from ventricles into the pulmonary trunk
and aorta

As the ventricles relax
Blood starts to flow back toward the heart
This backflowing blood fills the valve cusps
It causes free edges of semilunar valves to contact each other tightly
Opening between the ventricle and artery is closed

Fig.7: Operations of the Heart Valves

Systemic and Pulmonary Circulations
• In postnatal circulation,
• the heart pumps blood into two closed circuits with each beat
1. Systemic circulation and
2. Pulmonary circulation
• The two circuits are arranged in series.
• The output of one becomes the input of the other
• The left side of the heart is the pump for systemic circulation; it receives bright
red oxygenated (oxygen-rich) blood from the lungs.
• The left ventricle ejects blood into the aorta

Fig.8: Systemic & Pulmonary circulation

Coronary Circulation
• Nutrients are not able to diffuse quickly enough from blood in
the chambers of the heart to supply all layers of cells that make
up the heart wall.
• For this reason, the myocardium has its own network of blood
vessels, the coronary circulation or cardiac circulation (coron-
crown).
• The coronary arteries branch from the ascending aorta and
encircle the heart like a crown encircles the head (Figure 20.8a).

• While the heart is contracting, little blood flows in the coronary
arteries because they are squeezed shut.
• When the heart relaxes, however, high pressure of blood in the
aorta propels blood through the coronary arteries, into
capillaries, and then into coronary veins

Coronary Arteries
• Two coronary arteries- the left and right coronary arteries
• Branch from the ascending aorta
• Supply oxygenated blood to the myocardium

• Left coronary artery divides into:
✓ the anterior interventricular branches
✓ circumflex branches
• The anterior interventricular branch or left anterior descending
(LAD) artery supplies oxygenated blood to both ventricles.
• The circumflex branch (SER-kum-fleks) distributes oxygenated
blood to the walls of the left ventricle and left atrium.

• The right coronary artery supplies small branches (atrial
branches) to the right atrium.
• It divides into
✓ the posterior interventricular branches
✓ marginal branches
• The posterior interventricular branch supplies the walls of the
two ventricles with oxygenated blood.
• The marginal branch transports oxygenated blood to the wall of
the right ventricle.

Coronary Circulation: Anastomoses
• Most parts of the body receive blood from branches of more
than one artery
• Where two or more arteries supply the same region, they
usually connect
• These connections, called anastomoses provide alternate
routes, called collateral circulation, for blood to reach a
particular organ or tissue
• Provide detours for arterial blood if a main route becomes
obstructed.
• Thus, heart muscle may receive sufficient oxygen even if one of
its coronary arteries is partially blocked.

Fig.9: The Coronary Circulation

Coronary Circulation: Coronary Veins
After blood passes through the arteries of the coronary circulation
It flows into capillaries
In capillaries, it delivers oxygen and nutrients to the heart muscle
&
In capillaries, it collects carbon dioxide and waste
then moves into coronary veins.

Most of the deoxygenated blood from the myocardium
Drains into
Coronary sinus
• Coronary Sinus is a large vascular sinus in the coronary sulcus
on the posterior surface of the heart
• Deoxygenated blood in the coronary sinus empties into the
right atrium

Blood Pressure
• BP is the the hydrostatic pressure exerted by blood on the walls of a
blood vessel
• Determined by cardiac output blood volume, vascular resistance
• 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
• Diastolic blood pressure (DBP) is the lowest arterial pressure during
diastole

Fig.10: Blood Pressure in the various parts of the Cardiovascular System

Blood Pressure
• 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:

Factors affecting Blood Pressure
Cardiac output
• 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):
• By rearranging the terms of this equation,
• 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

Fig.11: Summary of factors that increase Blood Pressure

Hormonal Regulation of Blood Pressure
• Several hormones help regulate blood pressure and blood
flow by altering cardiac output, changing systemic vascular
resistance, or adjusting the total blood volume:
1. Renin–angiotensin–aldosterone (RAA) system
2. Epinephrine and norepinephrine
3. Antidiuretic hormone (ADH)
4. Atrial natriuretic peptide (ANP)

1. Renin–angiotensin–aldosterone (RAA) system.
• When blood volume falls, juxtaglomerular cells in the
kidneys secrete renin into the bloodstream
• Renin and angiotensin-converting enzyme (ACE) act on their
substrates to produce the active hormone angiotensin II
• Angiotensin II:
✓ A potent vasoconstrictor
✓ Stimulates secretion of aldosterone, which increases blood
pressure

2. Epinephrine and norepinephrine
• Increase cardiac output by increasing the rate and force of heart
contractions
• Cause vasoconstriction of arterioles and veins in the skin
• Cause vasodilation of arterioles in cardiac and skeletal muscle,
which helps increase blood flow to muscle during exercise

3. Antidiuretic hormone (ADH)
• Produced by the hypothalamus
• Released from the posterior pituitary in response to dehydration
or decreased blood volume.
• Causes vasoconstriction, which increases blood pressure.
• Also called vasopressin

4. Atrial natriuretic peptide (ANP)
• Released by cells in the atria of the heart
• Lowers blood pressure by causing vasodilation and by
promoting the loss of salt and water in the urine, which
reduces blood volume

Autoregulation of Blood Flow
• Two general types of stimuli cause autoregulatory changes in
blood flow:
1. Physical changes
2. Vasodilating and vasoconstricting chemicals

1. Physical changes
• Warming promotes vasodilation
• Cooling causes vasoconstriction
• Smooth muscle in arteriole walls exhibits a myogenic
response
• Smooth muscle contracts more forcefully when it is
stretched
• Smooth muscle relaxes when stretching lessens

2. Vasodilating and vasoconstricting chemicals
• Several types of cells (white blood cells, platelets, smooth
muscle fibers, macrophages, and endothelial cells) release
chemicals that alter blood-vessel diameter
• Vasodilating chemicals released by metabolically active tissue
cells include:
✓ K+
✓ H+
✓ Lactic acid (lactate)
✓ Adenosine (from ATP)

• 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)
✓ Endothelins (from endothelial cells)

Elements of Conduction System
of Heart

Cardiac Muscle Tissue: Histology
• Cardiac muscle fiber: 50–100 µm (length), 14 µm (diameter)
• Usually one centrally located nucleus is present, although an
occasional cell may have two nuclei
• The ends of cardiac muscle fibers connect to neighboring fibers
by irregular transverse thickenings of the sarcolemma called
intercalated discs
• The discs contain desmosomes, which hold the fibers together,
and gap junctions, which allow muscle action potentials to
conduct from one muscle fiber to its neighbors

Fig.12: Histology of cardiac Muscle Tissue

Autorhythmic Fibers:
The Conduction System
• An inherent and rhythmical electrical activity is the reason for
the heart’s lifelong beat
• The source of this electrical activity is a network of specialized
cardiac muscle fibers called autorhythmic fibers (auto- self)
because they are self-excitable
• Autorhythmic fibers repeatedly generate action potentials
that trigger heart contractions

Autorhythmic Fibers: Functions
1. Act as a pacemaker, setting the rhythm of electrical
excitation that causes contraction of the heart.
2. Form the cardiac conduction system, a network of
specialized cardiac muscle fibers that provide a path for each
cycle of cardiac excitation to progress through the heart

1. Cardiac excitation normally begins in the sinoatrial (SA) node
✓ SA node cells repeatedly depolarize to threshold spontaneously.
✓ The spontaneous depolarization is a pacemaker potential
✓ When the pacemaker potential reaches threshold, it triggers an
action potential
✓ Each action potential from the SA node propagates throughout
both atria
✓ Following the action potential, the two atria contract at the same
time

2. By conducting along atrial muscle fibers, the action potential
reaches the atrioventricular (AV) node
✓ The action potential slows considerably as a result of various
differences in cell structure in the AV node
✓ This delay provides time for the atria to empty their blood
into the ventricles

3. From the AV node, the action potential enters the
atrioventricular (AV) bundle (also known as the bundle of
His, pronounced HIZ).
✓ This bundle is the only site where action potentials can
conduct from the atria to the ventricles.

4. After propagating through the AV bundle, the action
potential enters both the right and left bundle branches
✓ The bundle branches extend through interventricular
septum toward the apex of the heart
5. Finally, the large-diameter Purkinje fibers (pur-KIN-je¯)
rapidly conduct the action potential beginning at the apex of
the heart upward to the remainder of the ventricular
myocardium
✓ Then the ventricles contract, pushing the blood upward
toward the semilunar valves

Fig.13: The Conduction System of heart

Blood Vessels; Structure and
Functions of Artery, Veins and
Capillaries

Blood Vessels
The five main types of blood vessels:
• Arteries,
• Arterioles,
• Capillaries,
• Venules,
• Veins

Blood Vessels
• Arteries: Carry blood away from the heart to other organs.
• Arterioles: Medium-sized arteries divide into small arteries,
which in turn divide into still smaller arteries called arterioles
• Capillaries: As the arterioles enter a tissue, they branch into
numerous tiny vessels called capillaries (hairlike).
• Venules: Groups of capillaries within a tissue reunite to form
small veins called venules (little veins).
• Veins: The blood vessels that convey blood from the tissues
back to the heart.

Basic Structure of a Blood Vessel
• The wall of a blood vessel consists of three layers, or tunics, of
different tissues:
✓ An epithelial inner lining,
✓ A middle layer consisting of smooth muscle and elastic
connective tissue,
✓ A connective tissue outer covering.

Basic Structure of a Blood Vessel
• The three structural layers of a generalized blood vessel from
innermost to outermost are:
✓ the tunica interna (intima),
✓ tunica media, and
✓ tunica externa (adventitia)

Tunica Interna (Intima)
• The tunica interna (intima) forms the inner lining of a blood
vessel
• It is in direct contact with the blood

Endothelium
• Innermost layer of tunica interna
• It is continuous with the endocardial lining of the heart
• Endothelial cells are active participants in a variety of vessel-
related activities

A basement membrane
• The second component of the tunica interna
• It provides a physical support base for the epithelial layer
• It anchors the endothelium to the underlying connective tissue

Internal elastic lamina
• The outermost part of the tunica interna
• It forms the boundary between the tunica interna and tunica
media
• It has variable number of windowlike openings
• These openings facilitate diffusion of materials through the
tunica interna to the thicker tunica media

Fig.14. Comparative structure of blood vessels

Tunica Media
• The tunica media (media middle) 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
• Role of the smooth muscle cells: Vasoconstriction & Vasodilation

Tunica Externa
• The outer covering of a blood vessel, the tunica externa
(externa outermost)
• It consists of elastic and collagen fibers
• Contains numerous nerves and, especially in larger vessels,
tiny blood vessels that supply the tissue of the vessel wall
• Supply blood to the tissues of the vessel are called vasa
vasorum, or vessels to the vessels

Elastic Arteries
• Largest arteries in the body
• Ranging from aorta and pulmonary trunk to the branches of the
aorta
• Elastic arteries include:
✓ Two major trunks that exit the heart (the aorta and the
pulmonary trunk),
✓ Aorta’s major initial branches, such as:
❖ brachiocephalic
❖ subclavian
❖ common carotid
❖ common iliac arteries

Elastic Arteries: Functions
• Help propel blood onward while the ventricles are relaxing
• As blood is ejected from the heart into elastic arteries, their
walls stretch, easily accommodating the surge of blood
• As they stretch, the elastic fibers momentarily store
mechanical energy, functioning as a pressure reservoir
• Then, the elastic fibers recoil and convert stored (potential)
energy in the vessel into kinetic energy of the blood.
• Thus, blood continues to move through the arteries even
while the ventricles are relaxed

Fig.15: Pressure Reservoir function of Elastic Arteries

Muscular Arteries
• Medium-sized arteries are called muscular arteries because
their tunica media contains more smooth muscle and fewer
elastic fibers than elastic arteries
• Capable of greater vasoconstriction and vasodilation to adjust
the rate of blood flow
• Well-defined internal elastic lamina but a thin external elastic
lamina
• Examples include:
✓ the brachial artery in the arm and
✓ radial artery in the forearm.

Anastomoses
• Most tissues of the body receive blood from more than one
artery.
• The union of the branches of two or more arteries supplying the
same body region is called an anastomosis (a-nas-to¯-MO¯ -sis
connecting)
• Anastomoses between arteries provide alternative routes for
blood to reach a tissue or organ
• The alternative route of blood flow to a body part through an
anastomosis is known as collateral circulation

Arterioles
• Literally meaning small arteries, arterioles are abundant
microscopic vessels
• It regulate the flow of blood into the capillary networks of the
body’s tissues
• The terminal end of the arteriole, the region called the
metarteriole (meta after), tapers toward the capillary junction
• At the metarteriole–capillary junction, the distal most muscle cell
forms the precapillary sphincter (to bind tight)
• Arterioles regulate blood flow from arteries into capillaries by
regulating resistance

Capillaries
• Capillaries, the smallest of blood vessels
• Capillaries form an extensive network, approximately 20 billion
in number, of short (hundreds of micrometers in length),
branched, interconnecting vessels that course among the
individual cells of the body
• This network forms an enormous surface area to make contact
with the body’s cells.
• The flow of blood from a metarteriole through capillaries and
into a postcapillary venule is called the microcirculation (micro
small) of the body

Capillaries: Distribution
• Found near almost every cell in the body
• Their number varies with metabolic activity of the tissue they
serve
• Body tissues with high metabolic requirements use more O2
and nutrients and thus have extensive capillary networks
• Tissues with lower metabolic requirements contain fewer
capillaries.
• Capillaries are absent in a few tissues, such as all covering and
lining epithelia, the cornea and lens of the eye, and cartilage

Capillaries
• In most parts of the body, blood can flow through a
capillary network from an arteriole into a venule as
follows:
1. Capillaries
2. Thoroughfare channel

Fig.16: Arterioles capillaries and venules. Precapillary sphincters regulate the
flow of blood through capillary beds.

Types of capillaries
• The body contains three different types of capillaries:
✓ Continuous capillaries,
✓ Fenestrated capillaries, and
✓ Sinusoids

Continuous capillaries
• Most capillaries are continuous capillaries, in which:
✓ The plasma membranes of endothelial cells form a continuous
tube
✓ Continuous tube is interrupted only by intercellular clefts,
gaps between neighboring endothelial cells
• Found in the central nervous system, lungs, muscle tissue, and
the skin

Fenestrated capillaries
• The plasma membranes of the endothelial cells have many
fenestrations (fen- es-TRA¯-shuns)
• Fenestrations are small pores (holes) ranging from 70 to 100
nm in diameter
• Found in the kidneys, villi of the small intestine, choroid
plexuses of the ventricles in the brain, ciliary processes of the
eyes, and most endocrine glands.

Sinusoids
• Wider and more winding than other capillaries
• Their endothelial cells may have unusually large fenestrations
• It has:
✓ Incomplete or absent basement membrane
✓ Very large intercellular clefts that allow proteins and in some
cases even blood cells to pass from a tissue into the
bloodstream.
• The spleen, anterior pituitary, and parathyroid and adrenal
glands have sinusoids.

Venules
• Have thin walls that do not readily maintain their shape.
• Venules drain the capillary blood and begin the return flow of
blood back toward the heart
• Venules that initially receive blood from capillaries are called
postcapillary venules.
• Function: Significant sites of exchange of nutrients and wastes
and white blood cell emigration

Veins
• Composed of essentially the same three layers as arteries, the
relative thicknesses of the layers are different
• The tunica interna of veins is thinner than that of arteries
• The tunica externa of veins is the thickest layer and consists of
collagen and elastic fibers
• Veins lack the internal or external elastic laminae found in
arteries

Veins
• Many veins, especially those in
the limbs, also contain valves,
thin folds of tunica interna
that form flaplike cusps
• The low blood pressure in
veins allows blood returning to
the heart to slow and even
back up
Fig.18: Venous Valves

Fig.19: Blood Distribution in the cardiovascular system at rest

Types of Veins
• Vascular (venous) sinus
• Anastomotic veins
• Superficial veins
• Deep Veins

The Cardiac Cycle & Cardiac
Output

The Cardiac Cycle
• A single cardiac cycle includes all of the events associated
with one heartbeat
• Consists of systole and diastole of the atria plus systole and
diastole of the ventricles

Pressure and Volume Changes
during the Cardiac Cycle
The events taking place during a cardiac cycle:
• Atrial Systole
• Ventricular Systole
• Relaxation Period

Atrial Systole
During atrial systole, which lasts about 0.1 sec, the atria are
contracting.
At the same time, the ventricles are relaxed
1. Depolarization of the SA node causes atrial depolarization,
marked by the P wave in the ECG
2. Atrial depolarization causes atrial systole
As the atria contract, they exert pressure on the blood
within, which forces blood through the open AV valves into
the ventricles.

Atrial Systole
3. Atrial systole contributes a final 25 mL of blood to the
volume already in each ventricle (about 105 mL)
• Thus, each ventricle contains about 130 mL at the end of its
relaxation period (diastole)
• This blood volume is called the end-diastolic volume (EDV)
4. The QRS complex in the ECG marks the onset of ventricular
depolarization

Ventricular Systole
During ventricular systole, which lasts about 0.3 sec, the
ventricles are contracting
At the same time, the atria are relaxed in atrial diastole
5. Ventricular depolarization causes ventricular systole
• As ventricular systole begins, pressure rises inside the
ventricles and pushes blood up against the atrioventricular
(AV) valves, forcing them shut

Ventricular Systole
6. Continued contraction of the ventricles causes pressure inside
the chambers to rise sharply
• When left ventricular pressure surpasses aortic pressure at
about 80 millimeters of mercury (mmHg) and right ventricular
pressure rises above the pressure in the pulmonary trunk (about
20 mmHg), both SL valves open
• At this point, ejection of blood from the heart begins

Ventricular Systole
7. The left ventricle ejects about 70 mL of blood into the aorta
and the right ventricle ejects the same volume of blood into the
pulmonary trunk
• The volume remaining in each ventricle at the end of systole,
about 60 mL, is the end-systolic volume (ESV)
• Stroke volume, SV = EDV - ESV
At rest, the stroke volume is about 130 mL - 60 mL = 70 mL
8. The T wave in the ECG marks the onset of ventricular
repolarization

Relaxation Period
During the relaxation period, which lasts about 0.4 sec, the atria
and the ventricles are both relaxed
As the heart beats faster and faster, the relaxation period becomes
shorter and shorter, whereas the durations of atrial systole and
ventricular systole shorten only slightly
9. Ventricular repolarization causes ventricular diastole

Relaxation Period
10. As the ventricles continue to relax, the pressure falls quickly.
✓ When ventricular pressure drops below atrial pressure, the AV
valves open, and ventricular filling begins
✓ At the end of the relaxation period, the ventricles are about
three-quarters full.
✓ The P wave appears in the ECG, signaling the start of another
cardiac cycle.

Cardiac Output
• Cardiac output (CO) is the volume of blood ejected from the
left ventricle (or the right ventricle) into the aorta (or
pulmonary trunk) each minute
• Cardiac output equals the stroke volume (SV), the volume of
blood ejected by the ventricle during each contraction,
multiplied by the heart rate (HR), the number of heartbeats
per minute:
• Entire blood volume flows through pulmonary and systemic
circulations each minute

Electrocardiogram
• As action potentials propagate through the heart, they
generate electrical currents that can be detected at the
surface of the body
• An electrocardiogram , abbreviated either ECG or EKG (from
the German word Elektrokardiogram), is a recording of these
electrical signals
• The ECG is a composite record of action potentials produced
by all of the heart muscle fibers during each heartbeat
• The instrument used to record the changes is an
electrocardiograph

Electrocardiogram
• Electrodes are positioned on the arms and legs (limb leads)
and at six positions on the chest (chest leads) to record the
ECG
• The electrocardiograph amplifies the heart’s electrical signals
and produces 12 different tracings from different
combinations of limb and chest leads

Electrocardiogram
• Each limb and chest electrode records slightly different
electrical activity because of the difference in its position
relative to the heart
• By comparing these records with one another and with normal
records, it is possible to determine
(1) if the conducting pathway is abnormal,
(2) if the heart is enlarged,
(3) if certain regions of the heart are damaged, and
(4) the cause of chest pain.

Electrocardiogram
In a typical record, three clearly recognizable waves appear with
each heartbeat:
1. P wave
2. QRS Complex
3. T wave

Electrocardiogram
1. P wave
• The first, called the P wave, is a small upward deflection on
the ECG
• Represents atrial depolarization, which spreads from the SA
node through contractile fibers in both atria

Electrocardiogram
2. QRS Complex
• The second wave, called the QRS complex, begins as a
downward deflection, continues as a large, upright,
triangular wave, and ends as a downward wave
• Represents rapid ventricular depolarization, as the action
potential spreads through ventricular contractile fibers

Electrocardiogram
3. T wave
• Dome-shaped upward deflection
• Indicates ventricular repolarization
• Occurs just as the ventricles are starting to relax
• Smaller and wider than the QRS complex because
repolarization occurs more slowly than depolarization
• During the plateau period of steady depolarization, the
ECG tracing is flat

Electrocardiogram
In reading an ECG, the size of the waves can provide clues to
abnormalities.
• Larger P waves indicate enlargement of an atrium
• An enlarged Q wave may indicate a myocardial infarction
• An enlarged R wave generally indicates enlarged ventricles
• The T wave is flatter than normal when the heart muscle is
receiving insufficient oxygen—as, for example, in coronary
artery disease
• The T wave may be elevated in hyperkalemia (high blood K+
level)

Electrocardiogram
Analysis of an ECG also involves measuring the time spans
between waves, which are called intervals or segments.
1. P–Q interval
2. S–T segment
3. Q–T interval

Electrocardiogram
P–Q interval
• The time from the beginning of the P wave to the beginning of
the QRS complex
• Represents the conduction time from the beginning of atrial
excitation to the beginning of ventricular excitation

Electrocardiogram
S–T segment
• Begins at the end of the S wave and ends at the beginning of the
T wave
• Represents the time when the ventricular contractile fibers are
depolarized during the plateau phase of the action potential
• Elevated (above the baseline) in acute myocardial infarction and
depressed (below the baseline) when the heart muscle receives
insufficient oxygen

Electrocardiogram
Q–T interval
• Extends from the start of the QRS complex to the end of the T
wave
• The time from the beginning of ventricular depolarization to the
end of ventricular repolarization
• May be lengthened by myocardial damage, myocardial ischemia
(decreased blood flow), or conduction abnormalities

Pulse
• The alternate expansion and recoil of elastic arteries after each
systole of the left ventricle creates a traveling pressure wave
that is called the pulse
• The pulse:
✓ Is strongest in the arteries closest to the heart
✓ Becomes weaker in the arterioles, and
✓ Disappears altogether in the capillaries
• The pulse rate normally is the same as the heart rate, about 70
to 80 beats per minute at rest

Pulse
• Tachycardia is a rapid resting heart or pulse rate over 100 beats/
min
• Bradycardia is a slow resting heart or pulse rate under 50
beats/min
• Pulse Pressure
✓ Difference between systolic and diastolic pressure
✓ normally about 40 mmHg
✓ Provides information about the condition of cardiovascular
system
✓ Conditions such as atherosclerosis greatly increase pulse
pressure.
• Normal ratio of systolic to diastolic e to pulse pressure = 3:2:1

Pulse Points
Structure Location
Superficial temporal artery Medial to ear
Facial artery Mandible (lower jawbone) on Iine with corners of
mouth
Common carotid artery Lateral to larynx (voice box)
Brachial artery Medial side of biceps brachii muscle
Femoral artery Inferior to inguinal ligament
Popliteal artery Posterior to knee
Radial artery Lateral aspect of wrist
Dorsal artery of foot Superior to instep of foot.

DISORDERS: HOMEOSTATIC
IMBALANCES

Coronary Artery Disease
• A serious medical problem that affects about 7 million
people annually
• Results from the effects of accumulation of atherosclerotic
plaques in coronary arteries,
• Leads to a reduction in blood flow to the myocardium
• Thickening of the walls of arteries and loss of elasticity
• A progressive disease characterized by the formation in the
walls of large and medium-sized arteries of lesions called
atherosclerotic plaques

Fig.22: Photomicrographs of a transverse section of a normal artery and one
partially obstructed by an atherosclerotic plaque

Development of Atherosclerotic Plaques
• Molecules produced by the liver and small intestine called
lipoproteins
• Lipoproteins consist of inner core of triglycerides and other lipids
and an outer shell of proteins, phospholipids, and cholesterol
• Cholesterol does not dissolve in water and must be made water-
soluble in order to be transported in the blood- Accomplished by
combining it with lipoproteins
• Two major lipoproteins are
✓ low-density lipoproteins (LDLs) and
✓ high-density lipoproteins (HDLs)

• LDLs transport cholesterol from the liver to body cells for use in
cell membrane repair
• Excessive amounts of LDLs promote atherosclerosis: “bad
cholesterol”
• HDLs remove excess cholesterol from body cells and transport it
to the liver for elimination: “good cholesterol”

Role of inflammation in Atherosclerotic Plaque
• The formation of atherosclerotic plaques begins when excess LDLs
from the blood accumulate in the inner, and the proteins bind to
sugars
• In response, endothelial and smooth muscle cells of the artery
secrete substances that attract monocytes from the blood and
convert them into macrophages
• The macrophages then ingest and become so filled with oxidized
LDL particles that they have a foamy appearance when viewed
microscopically (foam cells)

• T cells (lymphocytes)
• Foam cells, macrophages, and T cells form a fatty streak, the beginning of an
atherosclerotic plaque
• T cells induce foam cells to produce tissue factor (TF), a chemical that begins
the cascade of reactions that result in blood clot formation
• If the clot in a coronary artery is large enough, it can significantly decrease or
stop the flow of blood and result in a heart attack
Role of inflammation in Atherosclerotic Plaque

Coronary Artery Disease: Risk Factors
• Risk factors include smoking, high blood pressure, diabetes, high cholesterol
levels, obesity, sedentary lifestyle, and a family history of CAD.
• Most of these can be modified by changing diet and other habits or can be
controlled by taking medications. However, other risk factors are unmodifiable
(beyond our control), including genetic predisposition (family history of CAD at
an early age), age, and gender.
• For example, adult males are more likely than adult females to develop CAD;
after age 70 the risks are roughly equal.

A number of other risk factors (all modifiable) have also been
identified as significant predictors of CAD when their levels are
elevated.
1. C-reactive proteins (CRPs)
2. Lipoprotein
3. Fibrinogen
4. Homocysteine
Coronary Artery Disease: Risk Factors

Coronary Artery Disease: Diagnosis
1. A resting electrocardiogram is the standard test employed to
diagnose CAD
2. Stress testing can also be performed.
3. Echocardiography
4. Electron beam computerized tomography (EBCT)
5. Coronary (cardiac) computed tomography radiography (CCTA)
6. Cardiac catheterization
7. Coronary angiography

Coronary Artery Disease: Treatment
1. Drugs (antihypertensives, nitroglycerin, beta-blockers,
cholesterol-lowering drugs, and clot-dissolving agents)
2. Various surgical and nonsurgical procedures designed to
increase the blood supply to the heart:
a. Coronary artery bypass grafting (CABG)
b. Percutaneous transluminal coronary angioplasty (PTCA)
c. Stent
d. Laser-emitting catheters
e. Cold Therapy

Fig.23: Procedures for reestablishng blood flow in occluded coronary arteries

Congenital Heart Defects
• A defect that is present at birth, and usually before, is called a congenital
defect (kon-JEN-i-tal)
• Many such defects are not serious and may go unnoticed for a lifetime
• Others are life-threatening and must be surgically repaired
• Among the several congenital defects that affect the heart are the following
(Figure 20.23):
1. Coarctation of the aorta
2. Patent ductus arteriosus (PDA)
3. Septal defect
4. Tetralogy of Fallot

Fig.24: Congenital Heart defects

Congestive Heart Failure
• In congestive heart failure (CHF), there is a loss of pumping
efficiency by the heart
• Causes of CHF include:
✓ Coronary artery disease,
✓ Congenital defects,
✓ Long-term high blood pressure (which increases the afterload),
✓ Myocardial infarctions (regions of dead heart tissue due to a
previous heart attack), and
✓ Valve disorders

Congestive Heart Failure
• Initially, increased preload may promote increased force of
contraction (the Frank–Starling law of the heart), but as the
preload increases further, the heart is overstretched and
contracts less forcefully
• The result is a potentially lethal positive feedback loop: Less
effective pumping leads to even lower pumping capability
• Often, one side of the heart starts to fail before the other

Hypertension
• It is the most common disorder affecting the heart and blood vessels and is
the major cause of heart failure, kidney disease, and stroke

Types and Causes of Hypertension
• Between 90 and 95% of all cases of hypertension are
primary hypertension, a persistently elevated blood
pressure that cannot be attributed to any identifiable cause
• The remaining 5–10% of cases are secondary hypertension,
which has an identifiable underlying cause
• Several disorders cause secondary hypertension:
✓ Obstruction of renal blood flow or disorders that damage
renal tissue
✓ Hypersecretion of aldosterone
✓ Hypersecretion of epinephrine and norepinephrine

Damaging Effects of Untreated Hypertension
• High blood pressure is known as the “silent killer”
• In blood vessels, hypertension causes:
✓ thickening of the tunica media,
✓ accelerates development of atherosclerosis and coronary
artery disease, and
✓ increases systemic vascular resistance
• In the heart, hypertension increases the afterload, which
forces the ventricles to work harder to eject blood

Lifestyle Changes to Reduce
Hypertension
• Although several categories of drugs can reduce elevated blood
pressure, the following lifestyle changes are also effective in
managing hypertension:
✓ Lose weight.
✓ Limit alcohol intake.
✓ Exercise.
✓ Reduce intake of sodium (salt).
✓ Maintain recommended dietary intake of potassium, calcium, and
magnesium.
✓ Don’t smoke
✓ Manage stress

Drug Treatment of Hypertension
Drugs having several different mechanisms of action are
effective in lowering blood pressure.
1. Diuretics
2. ACE (angiotensin-converting enzyme) inhibitors
3. Beta blockers
4. Vasodilators; Calcium channel blockers

Arrhythmias
• The usual rhythm of heartbeats, established by the SA node,
is called normal sinus rhythm
• The term arrhythmia (a-RITH-me¯-a) or dysrhythmia refers to
an abnormal rhythm as a result of a defect in the conduction
system of the heart
• Arrhythmias may also be caused by a congenital defect,
coronary artery disease, myocardial infarction, hypertension,
defective heart valves, rheumatic heart disease,
hyperthyroidism, and potassium deficiency

Arrhythmias
• Arrhythmias are categorized by their speed, rhythm, and origination
of the problem
✓ Bradycardia (bra¯d-i-KAR-de¯-a; brady- slow) refers to a slow heart
rate (below 50 beats per minute);
✓ tachycardia (tak-i-KAR-de¯-a; tachy- quick) refers to a rapid heart
rate (over 100 beats per minute); and
✓ fibrillation (fi-bri-LA¯ -shun) refers to rapid, uncoordinated
heartbeats
• Arrhythmias that begin in the atria are called supraventricular or
atrial arrhythmias; those that originate in the ventricles are called
ventricular arrhythmias

Arrhythmias: Supraventricular
tachycardia
• Supraventricular tachycardia (SVT) is a rapid but regular
heart rate (160–200 beats per minute) that originates in the
atria
• The episodes begin and end suddenly and may last from a few
minutes to many hours
• SVTs can sometimes be stopped by maneuvers that stimulate
the vagus (X) nerve and decrease heart rate

Arrhythmias: Heart block
• Heart block is an arrhythmia that occurs when the electrical
pathways between the atria and ventricles are blocked, slowing
the transmission of nerve impulses
• The most common site of blockage is the atrioventricular node, a
condition called atrioventricular (AV) block
• First-degree AV block
• Second-degree AV block
• Third-degree (complete) AV block

Fig.25: Representative Arrhythmias

Arrhythmias: Atrial premature
contraction & Atrial flutter
• Atrial premature contraction (APC)
✓ APC is a heartbeat that occurs earlier than expected and briefly
interrupts the normal heart rhythm
✓ APCs originate in the atrial myocardium and are common in healthy
individuals
• Atrial flutter
✓ Atrial flutter consists of rapid, regular atrial contractions (240–360
beats/min) accompanied by an atrioventricular (AV) block in which
some of the nerve impulses from the SA node are not conducted
through the AV node

Arrhythmias: Ventricular premature
contraction
• Ventricular premature contraction, another form of
arrhythmia, arises when an ectopic focus (ek-TOP-ik), a region
of the heart other than the conduction system, becomes more
excitable than normal and causes an occasional abnormal
action potential to occur
• As a wave of depolarization spreads outward from the ectopic
focus, it causes a ventricular premature contraction (beat)
• The contraction occurs early in diastole before the SA node is
normally scheduled to discharge its action potential

Arrhythmias: Ventricular tachycardia
• Ventricular tachycardia (VT or V-tach) is an arrhythmia that
originates in the ventricles and is characterized by four or
more ventricular premature contractions
• It causes the ventricles to beat too fast (at least 120
beats/min) (Figure 20.24d)
• Sustained VT is dangerous because the ventricles do not fill
properly and thus do not pump sufficient blood
• The result may be low blood pressure and heart failure

Arrhythmias: Ventricular fibrillation
• Ventricular fibrillation (VF or V-fib) is the most deadly
arrhythmia, in which contractions of the ventricular fibers are
completely asynchronous so that the ventricles quiver rather
than contract in a coordinated way
• As a result, ventricular pumping stops, blood ejection ceases,
and circulatory failure and death occur unless there is
immediate medical intervention
• During ventricular fibrillation, the ECG has no clearly defined P
waves, QRS complexes, or T waves

Arrhythmias: Ventricular fibrillation Treatment
• Defibrillation
✓ Automatic implantable cardioverter defibrillator (AICD)
✓ Automated external defibrillators (AEDs)

Reference
Tortora, G.J. & Derrickson, B. "Tortora's Principles of Anatomy
and Physiology. 15th ed. Noida: Wiley India Pvt. Ltd.; 2017.

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Any other use for economic/commercial purposes is
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and its use is restricted to advancement of individual
knowledge. The information provided in this e-
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the best practice of my knowledge.

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