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UNIT II - CARDIOVASCULAR AND RESPIRATORY SYSTEMS

 The circulatory system is an organ system that transports blood and the nutrients to and
from all parts of the body.
 The circulatory system is frequently divided into the cardiovascular system, which consists
of the heart, blood vessels, and blood, and the lymphatic system, which consists of lymphatic
vessels and lymphoid tissues within the spleen, thymus, tonsils, and lymph nodes.
THE HEART
 The heart is a hollow, four chambered muscular organ of a somewhat conical form that
pumps blood received from the veins into the arteries, thereby maintaining the flow of blood
through the entire circulatory system
1. Anatomical Location:
 The heart is located in the thoracic cavity between the lungs in the middle mediastinum.
 About two-thirds of the heart is located left of the midline, with its inferior blunt point, apex,
pointing downward and resting on the diaphragm at the level of the 5th intercostal space. The
base of the heart is the broad superior end, where the large vessels attach and extends to the
level of the 2nd intercostal space.

 Size: The heart, in the adult, measures about 12 cm. in length, 8 to 9 cm. in breadth at the
broadest part, and 6 cm. in thickness.
 Weight: Its weight, in the male, varies from 280 to 340 grams; in the female, from 230 to
280 grams. The heart continues to increase in weight and size up to an advanced period of
life; this increase is more marked in men than in women.
2. Coverings of the Heart
 The heart is enclosed in a double-walled sac called the pericardium. It is made up of two
layers:
1) Outer parietal pericardium: Parietal pericardium forms a strong protective sac for the
heart. It helps also to anchor the heart within the mediastinum. Parietal pericardium is made
up two layers:
Fibrous layer: Fibrous layer is formed by thick fibrous connective tissue. It is attached to
the diaphragm and it is continuous with tunica adventitia (outer wall) of the blood vessels,
entering and leaving the heart. This layer (1) protects the heart, (2) anchors it to surrounding
structures, and (3) prevents overfilling of the heart with blood.
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Serous layer: Serous layer is formed by mesothelium, together with a small amount of
connective tissue. Mesothelium contains squamous epithelial cells which secrete a small
amount of fluid, which lines the pericardial space.
2) Inner visceral pericardium: Inner visceral pericardium lines the surface of myocardium. It
is made up of flattened epithelial cells. This layer is also known as epicardium.
 The space between the parietal pericardium and visceral pericardium is the pericardial
cavity, which contains a film of serous fluid. Pericardial fluid is present between these
layers. The serous membranes, lubricated by the fluid, glide smoothly past one another
during heart activity, allowing the mobile heart to work in a relatively friction-free
environment.

3. Heart Wall
The wall of the heart is composed of three distinct layers.
1. The Epicardium- the outer layer and also called visceral pericardium.
2. The Myocardium - The thick middle layer. It is formed by cardiac muscle fibers or cardiac
myocytes. Myocardium forms the bulk of the heart and it is responsible for pumping action
of the heart. Cardiac muscle fiber is bound by sarcolemma. It has a centrally placed nucleus.
Myofibrils are embedded in the sarcoplasm. Sarcomere of the cardiac muscle has all the
contractile proteins, namely actin, myosin, troponin and tropomyosin. One cell touches
another cell is a specialized intercellular junction called an intercalated disc,
3. The Endocardium is a glistening white sheet of endothelium (squamous epithelium) resting
on a thin connective tissue layer. Located on the inner myocardial surface, it lines the heart
chambers and covers the fibrous skeleton of the valves. The endocardium is continuous with
the endothelial linings of the blood vessels leaving and entering the heart.
4. Chambers of the Heart
 The heart is subdivided by constriction into two cavities, the upper cavity being called the
atria, the lower the ventricle. The atria are separated by the interatrial septum, and the
ventricles are separated by the interventricular septum. The heart therefore consists of four
chambers, viz., right and left atria, and right and left ventricles.
The atria

 The atria are the two upper chambers of the heart and are positioned near its base. The two
atria are separated from each other by a partition called the interatrial (between the atria)
septum. Each atrium has a small earlike extension called an auricle.
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Chambers of the Heart

 The atria are thin-walled chambers and receive blood from veins.
 Right atrium receives venous (deoxygenated) blood via three major openings:
Superior vena cava that returns venous blood from the head, neck and upper limbs
Inferior vena cava that returns venous blood from lower parts of the body and
The smaller coronary sinus drains blood from most of the heart muscle.
 The left atrium receives blood through the four pulmonary veins, which drain blood from
the lungs.
 The atria function primarily as reservoirs, where blood returning from veins collects before
it enters the ventricles. Contraction of the atria forces blood into the ventricles to complete
ventricular filling.
The ventricles

 The ventricles are the two lower chambers of the heart and the right ventricle constitutes
most of the anterior portion of the heart, while the left ventricle forms the apex and
inferoposterior portion.
 The cavity of the left ventricle is oval-shaped, while that of the right ventricle is crescent-
shaped. The wall of the left ventricle is thicker than the wall of the right ventricle and the
wall of the left ventricle contracts more forcefully and generates a greater blood pressure
than the wall of the right ventricle.
 The ventricles of the heart are its major pumping chambers. They eject blood into the
arteries and force it to flow through the circulatory system.
 The atria open into the ventricles, and each ventricle has one large outflow route located
superiorly near the midline of the heart. The right ventricle pumps blood into the pulmonary
trunk, and the left ventricle pumps blood into the aorta.
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5. The Heart Valves
 To pump blood effectively, the heart needs valves that ensure a predominantly one-way
flow. There is a valve between each atrium and the corresponding ventricle and another at
the exit from each ventricle into its great artery, but there are no valves where the great veins
empty into the atria.
 Each valve consists of two or three fibrous flaps of tissue called cusps or leaflets, covered
with endocardium.
 The valves do not open and close by any muscular effort of their own. The cusps are simply
pushed open and closed by changes in blood pressure.
1. The Atrioventricular (AV) valves regulate the openings between the atria and ventricles.
The AV valve between the right atrium and the right ventricle has three cusps and is called
the tricuspid valve. The AV valve between the left atrium and the left ventricle has two
cusps and is called the bicuspid valve or, mitral valve (resembling a bishop’s miter, a two-
pointed hat).
These valves allow blood to flow from the atria into the ventricles but prevent it from
flowing back into the atria. When the ventricles relax, the higher pressure in the atria forces
the AV valves to open, and blood flows from the atria into the ventricles. In contrast, when
the ventricles contract, blood flows toward the atria and causes the AV valves to close.
2. The Semilunar valves has three cusps that regulate the flow of blood from the ventricles
into the great arteries. The pulmonary valve controls the opening from the right ventricle
into the pulmonary trunk, and the aortic valve controls the opening from the left ventricle
into the aorta.
6. Pathway of Blood Flow
1. Blood enters the right atrium from the systemic circulation through the superior and inferior
venae cavae, and from heart muscle through the coronary sinus. The right atrium contracts
and blood is pushed from the right atrium into the right ventricle through the right
atrioventricular (AV) valve to complete right ventricular filling.
2. Following right atrial contraction, the right ventricle begins to contract. This contraction
pushes blood against the tricuspid valve forcing it closed. After pressure within the right
ventricle increases the pulmonary semilunar valve is forced open and blood flows into the
pulmonary trunk.
3. As the right ventricle relaxes, its pressure falls rapidly and pressure in the pulmonary trunk
becomes greater than in the right ventricle. The backflow of blood forces the pulmonary
semilunar valve to close.
4. The pulmonary trunk branches to form the right and left pulmonary arteries which carry
blood to the lungs, where CO 2 is released and 02 is picked up.
5. Blood returning from the lungs enters the left atrium through the four pulmonary veins. The
path of blood from the heart (right ventricle), through the lungs, and back to the heart (left
atrium) completes one circuit called the pulmonary circulation.
6. The left atrium contracts and blood is pushed from the left atrium into the left ventricle
through left atrioventricular (AV) valve (also called the bicuspid valve or mitral valve) to
complete left ventricular filling.
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7. Following left atrial contraction, the left ventricle begins to contract. This contraction pushes
blood against the bicuspid valve, forcing it closed. After pressure within the left ventricle
increases, the aortic semilunar valve is forced open, and blood flows into the aorta.
8. As the left ventricle relaxes its pressure falls rapidly, and pressure in the aorta becomes
greater than in the left ventricle. The backflow of blood forces the aortic semilunar valve to
close. Blood flowing through the aorta is distributed to all parts of the body, except to those
parts of the lungs supplied by the pulmonary blood vessels. The aorta ascends for a short
distance, makes a U-turn, and then descends through the thoracic (chest) and abdominal
cavities. Arterial branches from the aorta supply oxygen-rich blood to all of the organ
systems and are thus part of the systemic circulation.
Blood flow through Heart

7. Conducting System of the Heart

 Heart has its own intrinsic regulating system called the conduction system that generates and
distributes electrical impulses over the heart to stimulate cardiac muscle fibers or cells to
contract without the need for a nerve supply from the brain.
 There are small groups of specialized neuromuscular cells (Autorhythmic cardiac cells) in
the myocardium which initiate and conduct impulses causing coordinated and synchronized
contraction of the heart muscle.
Sinoatrial node (SA node)
 The crescent-shaped sinoatrial (SA) node is located in the wall of the right atrium inferior to
the superior vena cava.
 The SA node is the 'pace-maker' of the heart because it normally initiates impulses more
rapidly than other groups of neuromuscular cells. Its characteristic rhythm, called sinus
rhythm, determines heart rate.
 Auto rhythmic fibers in the SA node would initiate an action potential about every 0.6
second, or 100 times per minute (in the absence of extrinsic neural and hormonal factors). In
a person at rest, SA node pacing to about every 0.8 second or 75 action potentials per
minute.
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Atrioventricular node (AV node)

 This small mass of neuromuscular tissue is located in the inferior portion of the interatrial
septum immediately above the tricuspid valve.
 Normally the AV node is stimulated by impulses that sweep over the atrial myocardium.
However, it too is capable of initiating impulses that cause contraction but at a slower rate
than the SA node.
 From the SA node, the impulses spread via gap junctions throughout the atria and via the
internodal pathway to the atrioventricular (AV) node. At the AV node, the impulse is
delayed for about 0.1 s, allowing the atria to respond and complete their contraction before
the ventricles contract. Thus, the AV node conducts impulses more slowly than other parts
of the system.
 The AV node depolarizes only about 50 times per minute.
Atrioventricular bundle (AV bundle or bundle of His)
 This is a mass of specialized fibers that originate from the AV node. From the AV node, the
impulse sweeps to the atrioventricular (AV) bundle (also called the bundle of His) in the
superior part of the interventricular septum.
 The AV bundle crosses the fibrous ring that separates atria and ventricles then, at the upper
end of the ventricular septum; it divides into right and left bundle branches. Within the
ventricular myocardium the branches break up into fine fibres, called the Purkinje fibres
(also known as the conduction myofibers)
 The AV bundle and the Purkinje fibers (though they conduct very rapidly) depolarize at the
rate of only about 30 times per minute.
 The AV bundle, bundle branches and Purkinje fibres convey electrical impulses from the
AV node to the apex of the myocardium where the wave of ventricular contraction begins,
then sweeps upwards and outwards, pumping blood into the pulmonary artery and the aorta.
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CIRCULATION TYPES
 Circulation is the movement of blood through blood vessels, from the heart and then back to
the heart.
 The cardiac output results in two major circulations,
1. The pulmonary circulation
2. The systemic circulation
1. The pulmonary circulation
 The path of blood from the heart (right ventricle), through the lungs, and back to the heart
(left atrium) completes one circuit called the pulmonary circulation.
 The pulmonary circulation includes blood vessels that transport blood to the lungs for gas
exchange and then back to the heart.
 The cycle begins when deoxygenated blood is pushed from the right ventricle into the
pulmonary trunk. The pulmonary trunk soon divides into two large pulmonary arteries, left
and right (These arteries are the only arteries in the body that carry deoxygenated blood).
1. The right pulmonary artery enters the hilum of the right lung and divides into 3
lobular arteries to the 3 lobes of the right lung.
2. The left pulmonary artery enters the hilum of the left lung and divides into 2 lobular
arteries to the 2 lobes of the left lung.
 The lobular arteries continue to divide until they become a fine network of capillaries
surrounding the tiny alveoli. It is here where gas exchange takes place, and CO 2 is released
from the blood and O 2 is taken into the blood.
 The oxygenated blood is carried back to the heart by venules which continually unite to
eventually exit each lung as two pulmonary veins; superior and inferior. The 4 pulmonary
veins drain into the left atrium which squeezes the oxygenated blood into the left ventricle
where it is pushed into the systemic circulation. These veins are the only veins in the body
that carry oxygenated blood.
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2. The systemic circulation
 The systemic circulation supplies blood flow to all the tissues of the body except the lungs,
it is also called the greater circulation or peripheral circulation.
The aorta is the largest artery in the body. It arises from the left ventricle of the heart. Aorta
consists of three parts;
1. Ascending aorta - which serve the myocardium
2. Arch of the aorta - which serve the upper extremities
3. Descending aorta - which serve the lower extremities
Blood supply to the heart
 The myocardium is supplied with blood by the right and left coronary arteries. These two
vessels arise from the ascending part of the aorta, at the location of the aortic (semilunar)
valve.

 The coronary arteries encircle the heart within the atrioventricular sulcus (the depression
between the atria and ventricles). The branches arise from both the right and left coronary
arteries to serve the atrial and ventricular walls.
 From the capillaries in the myocardium, the blood enters the cardiac veins. The course of
these vessels parallels that of the coronary arteries.
 The cardiac veins, however, have thinner walls and are more superficial than the arteries.
The two principal cardiac veins are the anterior interventricular vein, which returns blood
from the anterior aspect of the heart, and the posterior cardiac vein, which drains the
posterior aspect of the heart.
 These cardiac veins converge to form the coronary sinus channel on the posterior surface of
the heart. The coronary venous blood then enters the heart through an opening into the right
atrium. Numerous small veins pierce the heart walls to directly drain into the heart
chambers.
Shoulder, Upper extremity, and Head
 The part of aorta situated between the ascending and descending parts is called arch of the
aorta. Three branches are given off from the aortic arch:
1. The brachiocephalic trunk supplies blood to the structures of the shoulder, upper
extremity, and head on the right side of the body.
2. The left common carotid artery transports blood to the left side of the neck and head.
3. The left subclavian artery supplies the left shoulder and upper extremity.
Neck and Head
 Arterial Supply: The paired arteries supplying the head and neck are the common carotid
arteries and the vertebral arteries.
The right common carotid artery is a branch of the brachiocephalic artery and the left
common carotid artery, arises directly from the arch of the aorta pass upwards on either side
of the neck and have the same distribution on each side. At the level of the upper border of
the thyroid cartilage they divide into:
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External carotid artery - supplies the superficial tissues of the head and neck, via a number
of branches.
Internal carotid artery - supplies the greater part of the brain.
The vertebral arteries arise from the subclavian arteries at the base of the neck. Branches of
the vertebral arteries supply blood to the spinal cord, as well as to the vertebrae muscles, and
ligaments in the neck. Within the cranial cavity, the vertebral arteries unite to form a single
basilar artery. The basilar artery gives off branches that supply blood to the pons,
cerebellum and midbrain.
 Venous Drainage: Blood from the scalp, portions of the face, and the superficial neck
regions is drained by the external jugular veins. They empty into the right and left
subclavian veins.
The paired internal jugular veins drain blood from the brain, meninges, and deep regions of
the face and neck.
The convergence of the internal jugular vein with the subclavian vein forms a large
brachiocephalic vein on each side. The two brachiocephalic veins then merge to form the
superior vena cava, which drains into the right atrium of the heart.
Shoulder and Upper Extremity
 Arterial Supply: The right subclavian artery arises from the brachiocephalic trunk, and the
left subclavian artery arises directly from the aortic arch. Each subclavian artery passes
laterally deep to the clavicle, carrying blood toward the arm.
From each subclavian artery arises; a short thyrocervical trunk that serves the thyroid gland,
trachea, and larynx; and an internal thoracic artery that descends into the thorax to serve the
thoracic wall, thymus, and pericardium.
The axillary artery is the continuation of the subclavian artery as it passes into the axillary
region. The brachial artery is the continuation of the axillary artery through the brachial
region. The brachial artery branches into the radial and ulnar arteries, which anastomose
into deep and superficial palmar arches, from which palmar metacarpal and palmar digital
arteries arise to supply the structures in the hand and fingers. The radial artery is important
as a site for recording the pulse near the wrist.
 Venous Drainage: The radial vein on the lateral side of the forearm and the ulnar vein on
the medial side drain blood from the deep and superficial palmar arches of the hand. The
radial and ulnar veins join form the brachial vein.
The basilic vein ascends from the forearm to the middle of the arm, where it penetrates
deeply and joins the brachial vein. The cephalic vein drains the superficial portion of the
hand and forearm on the radial side, and then continues up the lateral side of the arm.
The median cubital vein ascends from the cephalic vein on the lateral side to connect with
the basilic vein on the medial side [The median cubital vein is a frequent site for
venipuncture to remove a sample of blood or add fluids to the blood]. The basilic vein
merges with the brachial vein to form the axillary vein. In the shoulder region, the cephalic
vein joins the axillary vein.
The axillary vein then passes the first rib to form the subclavian vein, which unites with the
internal jugular to form the brachiocephalic vein of that side. The superior vena cava,
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formed by the union of the two brachiocephalic veins, empties venous blood from the head,
neck, and upper extremities directly into the right atrium of the heart.
Thorax

 Arterial Supply: The thoracic portion of the aorta is a continuation of the aortic arch as it
descends through the thoracic cavity to the diaphragm. This large vessel gives off branches
to
1. Pericardial arteries, going to the pericardium of the heart;
2. Bronchial arteries for systemic circulation to the lungs;
3. Esophageal arteries, going to the esophagus as it passes through the mediastinum;
4. Segmental posterior intercostal arteries, serving the intercostals muscles and
structures of the wall of the thorax; and
5. Superior phrenic arteries, supplying blood to the diaphragm.
 Venous Drainage: Most of the venous blood from the organs in the thoracic cavity is
drained into the azygos vein and the hemiazygos vein. Some of the main veins which join
them are the bronchial, oesophageal and intercostal veins.
The azygos vein joins the superior vena cava and the hemiazygos vein joins the left
brachiocephalic vein. At the distal end of the oesophagus some oesophageal veins join the
azygos vein and others, the left gastric vein.
Abdominal Area
 Arterial Supply: The abdominal aorta is a continuation of the thoracic aorta. The
abdominal portion of the aorta is the segment of the aorta between the diaphragm and the
level of the fourth lumbar vertebra. Many branches arise from the abdominal aorta.
Small inferior phrenic arteries that serve the diaphragm
The next vessel is the celiac trunk that divides immediately into three arteries: the splenic,
going to the spleen; the left gastric, going to the stomach; and the common hepatic, going to
the liver.
The superior mesenteric artery supplies blood to the small intestine (except for a portion of
the duodenum), the cecum, the appendix, the ascending colon, and the proximal two-thirds
of the transverse colon.
The next major vessels to arise from the abdominal portion of the aorta are the paired renal
arteries that carry blood to the kidneys. Smaller suprarenal arteries, located just above the
renal arteries, serve the adrenal (suprarenal) glands.
The testicular arteries in the male and the ovarian arteries in the female are small paired
vessels that arise from the abdominal portion of the aorta, just below the renal arteries.
These vessels serve the gonads.
The inferior mesenteric artery is the last major branch of the abdominal portion of the aorta
and supplies blood to the distal one-third of the transverse colon, the descending colon, the
sigmoid colon, and the rectum.
Several lumbar arteries branch posteriorly from the abdominal portion of the aorta
throughout its length and serve the muscles and the spinal cord in the lumbar region.
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Venous Drainage: The inferior phrenic veins receive blood from the inferior side of the
diaphragm and empty into the inferior vena cava.
Four paired lumbar veins drain the posterior abdominal wall, the vertebral column, and the
spinal cord.
The right renal veins drain blood from the kidneys, right testicular vein in males (or the
right ovarian vein in females) drains the corresponding gonads, and the right suprarenal
vein drains the right adrenal gland. These veins empty into the inferior vena cava.
The left testicular vein (or left ovarian vein) and the left suprarenal vein, by contrast, empty
into the left renal vein. This veins empty into the inferior vena cava.
Hepatic Portal System
The inferior vena cava does not receive blood directly from the GI tract, pancreas, or spleen.
Instead, the venous outflow from these organs first passes through capillaries in the liver.
Circulation of blood to the liver from the small intestine, the right half of the colon, and the
spleen through the portal vein specified as the hepatic portal circulation.
The splenic vein carries blood from the spleen and pancreas. The inferior mesenteric vein
drains blood from the large intestine and empties into the splenic vein. The superior
mesenteric vein drains nutrient-rich blood from the small intestine.
The splenic vein and the superior mesenteric vein join to form the hepatic portal vein, which
enters the liver. The gastric veins drain blood from the stomach and oesophagus and the
cystic vein, which drains venous blood from the gall bladder, joins the portal vein.
The right and left hepatic veins that drain the venous blood from the liver and empty it into
the inferior vena cava.
Pelvis and Lower Extremity
 Arterial Supply: The abdominal aorta divides at the level of the fifth lumbar vertebra into
right and left common iliac arteries. Each common iliac artery divides to form an external
iliac artery, which enters a lower limb, and an internal iliac artery, which supplies the pelvic
area.
Visceral branches of the internal iliac artery supply organs such as the urinary bladder,
rectum, uterus, and vagina. Parietal branches supply blood to the walls and floor of the
pelvis: the lumbar. gluteal, and proximal thigh muscles and the external genitalia.
Branches of internal iliac artery Blood supply
Iliolumbar and lateral sacral arteries. The wall of the pelvis
Middle rectal The internal visceral organs of the pelvis
Superior, middle, & inferior vesicular The urinary bladder
arteries
Uterine and vaginal arteries Reproductive organs of the female.
Superior and inferior gluteal arteries The muscles of the buttock
The obturator artery The upper medial thigh muscles
The internal pudendal artery The musculature of the perineum and the
external genitalia. During sexual arousal it
supplies the blood for vascular engorgement of
the penis in the male and clitoris in the female.
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The external iliac artery in the pelvis becomes the femoral artery in the thigh. Several
vessels arise from the femoral artery to serve the thigh region.
The femoral artery becomes the popliteal artery in the popliteal space, which is the
posterior region of the knee. The popliteal artery supplies small branches to the knee joint,
and then divides into an anterior tibial artery and a posterior tibial artery.
At the ankle, the anterior tibial artery becomes the dorsal pedal artery that serves the ankle
and dorsum (superior portion) of the foot and then contributes to the formation of the dorsal
arch of the foot.
The posterior tibial artery gives off a large fibular, or peroneal artery to serve the peroneal
muscles of the leg. At the ankle, the posterior tibial bifurcates into the lateral and medial
plantar arteries that supply the sole of the foot. Digital arteries arise from the plantar arch
to supply the toes with blood.
 Venous Drainage: The posterior and anterior tibial veins originate in the foot and course
upward behind and in front of the tibia to the back of the knee, where they merge to form the
popliteal vein. Just above the knee, this vessel becomes the femoral vein.
 The saphenous vein originates from the medial side of the foot and ascends along the medial
aspect of the leg and thigh before emptying into the femoral vein [The great saphenous vein
is the longest vessel in the body. The great saphenous vein is frequently excised and used as
a coronary bypass vessel].
 The femoral vein receives blood from the great saphenous vein and then becomes the
external iliac vein as it passes under the inguinal ligament.
 The external iliac curves upward to the level of the sacroiliac joint, where, it merges with the
internal iliac vein at the pelvic and genital regions to form the common iliac vein. At the
level of the fifth lumbar vertebra, the right and left common iliac unite to form the large
inferior vena cava.
 The inferior vena cava parallels the abdominal aorta on the right side as it ascends through
the abdominal cavity to penetrate the diaphragm and enter the right atrium.
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Overall anterior view of principal Arteries

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Overall anterior view of principal veins

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CARDIAC CYCLE
 The cardiac cycle is the sequence of events that take place in the heart during one heartbeat.
This also includes changes in pressure, blood flow and volume in the heart chambers.
 During each heartbeat, or cardiac cycle, the heart contracts and then relaxes. The period of
contraction is called systole and that of relaxation, diastole.
 A cardiac cycle therefore, consists of the systole and diastole of both atria and the systole
and diastole of both ventricles.
 The duration of the cardiac cycle varies inversely with the heart rate. At a typical resting
heart rate of 60 beats per minute (bpm), the cardiac cycle lasts 1 s or 1000 ms.
 The normal number of cardiac cycles per minute ranges from 60 to 80. When heart rate is 75
beats/min, a cardiac cycle lasts 0.8 sec.
 During the cardiac cycle, changes in chamber pressure and the opening and closing of the
heart valves determine the direction of blood movement.
Events of the cardiac cycle
The cardiac cycle consists of three phases:
Phase 1: Atrial Systole
Phase 2: Ventricular Systole
Phase 3: Atrial and Ventricular Diastole.
Cardiac Cycle

Atrial Systole
 Atrial systole or the atrial contraction phase lasts for 0.1 s and coincides with the last rapid
filling phase of ventricular diastole.
 Before beginning of the cardiac cycle, the atria and ventricles are relaxed, the AV valves are
open, and the semilunar valves are closed. Blood returning to the heart first enters the atria.
Since the AV valves are open blood flows into the ventricles, filling them to approximately
70% of their volume. Thus, the atria and ventricles are forming a continuous cavity.
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 The SA node triggers a wave of contraction that spreads over the myocardium of atria,
emptying the atria and completing ventricular filling.
 When the atrial contraction begins, about 75% of the blood has already flown into the
ventricles. Thus, atrial contraction usually causes an additional 25% filling of the ventricles.
Atrial systole is also known as last rapid filling phase or presystole.
 The contraction of atria causes:
1. Increase intra-arterial pressure by 4—6mm Hg in the right atrium and 7—8mm Hg in
the left atrium.
2. Increase in the ventricular pressure occurs slightly due to pumping of blood in the
ventricles.
3. Narrowing of origin of great veins (inferior vena cava and superior vena cava opening in
right atrium and pulmonary veins opening in left atrium) decreasing venous return to the
heart. Some regurgitation of the blood occurs into the great veins as no valves are
present between them and the atria.
Atrial Diastole
 After the atrial systole, atrial diastole occurs and lasts for about 0.7 sec (accurate duration is
0.69 sec). This period coincides with the ventricular systole and most of the ventricular
diastole. This long atrial diastole is necessary because, this is the period during which atrial
filling takes place.
 During the atrial diastole, the atrial muscles relax and there occurs gradual filling of the atria
due to continuous venous return and the pressure gradually increases in the atria to drop
down to almost zero with the opening of AV valves. Then the pressure again rises and
follows the ventricular pressure during the rest of atrial diastole.
Ventricular systole
 After the atrial contraction phase is over, the ventricles get excited by the impulse travelling
along the conduction system and the ventricles start contracting. The ventricular systole lasts
for 0.30 and has following phases:
1. Phase of isovolumic (isometric) contraction: With the beginning of ventricular
contraction, the ventricular pressure exceeds the atrial pressure very rapidly causing closure
of AV valves (this event is responsible for the production of first heart sound). Since the AV
valves have closed and semilunar valves have not opened, so the ventricles contract as a
closed chamber and the pressure inside the ventricles rises rapidly to a high level.
As the ventricles contract, but the volume of blood in the ventricles does not change, so this
phase is called isovolumic contraction phase.
During this phase, due to sharp rise in the ventricular pressure cause bulging of AV valves
into the atria producing a small but sharp rise in the intra-atrial pressure.
This phase lasts for 0.05 s, until the pressure in the left and right ventricles exceeds the
pressure in the aorta (80mm Hg) and pulmonary artery (10 mm Hg) and the aortic and
pulmonary valves open.
2. Phase of ventricular ejection: The ventricular ejection phase begins with the opening of
semilunar valves and lasts for about 0.25 s. It can be further divided into two phases:
 17
Rapid ejection phase: As soon as the semilunar valves open, the blood is rapidly ejected out
for about 0.1 s. About two-thirds of the stroke volume is ejected in this rapid ejection phase.
Pressure rises to 120mm Hg in the left ventricle and to 25mm Hg in the right ventricle. The
right ventricular ejection begins before that of left and continued even after left ventricular
ejection is complete. As both the ventricles almost eject same volume of blood, the velocity
of right ventricular ejection is less than that of the left ventricle.
Slow ejection phase: It refers to the latter two-third of systole (about 0.15 s) during which
the rate of ejection declines. About one-third of the stroke volume is ejected during this
phase. The intraventricular pressure starts declining and falls to a value slightly lower than
in the aorta, but for a short period momentum keeps the blood flowing forward.
Ventricular Diastole
 The ventricular diastole last for 0.5 sec. Later part of atrial diastole coincides with ventricle
diastole for about 0.4s.
1. Protodiastole (0.04 s): When the ventricular systole ends, the ventricles start relaxing and
intraventrlcular pressure falls rapidly. During this phase, the elevated pressure in the
distended arteries (aorta and pulmonary artery) immediately pushes the blood back towards
ventricles, which snaps the semilunar valves to close. Closure of semilunar (aortic and
pulmonary) valves prevents the movement of blood back into the ventricles.
2. Isovolumic or isometric relaxation phase (0.06 s): This phase begins with the closure of
the semilunar valves. Since semilunar valves have closed and the AV valves have not yet
opened, so the ventricles continue to relax as closed chambers in this phase. This causes
rapid fall of pressure inside the ventricles (from 80mm Hg to about 2—3mm Hg in the left
ventricle). As in this phase, the ventricular volume remains constant, so this phase is called
isovolumic or isometric relaxation phase.
3. Rapid passive filling phase (0.10 s): During ventricular systole, the atria are also in diastole
and venous return continues so that the atrial pressure is high. When the AV valves open,
the high atrial pressure causes a rapid, initial flow of blood into the ventricles.
Once the AV valves open, the atria and ventricles are a common chamber and pressure in
both cavities falls as ventricular relaxation continues.
4. Reduced filling and diastasis (0.2 s): In this phase, pressure in the atria and ventricles
reduces slowly and remains little above zero. This decreases the rate of blood flow from the
atria to ventricle causing a very slow filling called diastasis. It is important to note that
about 75% of blood passes from the atria to the ventricles during rapid filling and reduced
filling phases of the ventricular diastole.
5. Last rapid filling phase (0.1 s): The last rapid filling phase of ventricular diastole coincides
with the atrial systole. As described in the beginning, the atrial systole brings about the last
rapid filling phase and pushes the additional 25% of the blood in the ventricles. With this
phase, the ventricular cycle is completed.
 18
PRESSURE AND VOLUME CHANGES
 The events associated with contraction and relaxation of the heart during a cardiac cycle
include pressure changes in the ventricles, atria and aorta as well as volume changes in the
ventricles and valvular events.
A. Pressure Changes
1. Pressure Changes in the Atria
 Relationship of Intra- atrial pressure changes with the phases of cardiac cycle is:
 During atrial systole: Before the onset of atrial systole, the intra-atrial pressure is slightly
above zero and is slightly greater than the ventricular pressure. During atrial systole, there
occurs a sharp rise in the intra-atrial pressure by 4—6mm Hg in the right atrium and by 7—
8mm Hg in the left atrium and causes a pressure wave recorded as ‘a’ wave from the jugular
vein (a - stands for atrial systole). Immediately after atrial systole, the intra-atrial pressure
falls due to start of atrial relaxation in the atrial diastole.
 During ventricular systole:
During phase of isovolumic (isometric,) contraction, due to sharp rise in the intraventricular
pressure, AV valves bulge into the atria producing a small but sharp rise in the atrial
pressure producing the so-called ‘c’ ware (‘c’ stands for contraction of the ventricle).
During ventricular ejection phase, the intra-atrial pressure drops sharply in the rapid
ejection phase. This happens so, because the papillary muscles (attached to the cusps of AV
valves) contract when the ventricular walls contract and pull down the fibrous AV ring
causing enlargement of the atrial lumen and thus decreasing the intra-atrial pressure.
Therefore, as the ventricles contract, the atria get slowly filled with blood flowing in from
the great veins and the atrial pressure starts rising.
 During ventricular diastole:
During isovolumic (isometric) relaxation, phase, the atrial pressure continues to rise as long
as AV valves remain closed, i.e. till the end of isovolumic relaxation. This results in the
third positive wave called ‘v’ wave (v stands for venous tilling). This shows a gradual
increase in the atrial pressure.
During rapid passive filling phase, the AV valves open allowing rapid flow of blood from
the atria to the ventricles. So, the atrial pressure drops sharply to a little above zero level and
remains so till the beginning of the next atrial systole.
2. Pressure Changes in the Ventricles

 Pressure changes in the ventricles during the cardiac cycle are consistent with the
maintenance of systemic and pulmonary circulation.
 During atrial systole: Before the onset of atrial systole, i.e. during diastasis the pressure
inside the ventricles is a little above zero. During atrial systole, there occurs a slight increase
in the intraventricular pressure (about 6—7 mm Hg in the right ventricle and about 7—8mm
Hg in the left ventricle) due to pumping of blood in the ventricles. In the intra-ventricular
pressure curve, the segment AB represents the pressure changes during the atrial systole.
The point A denotes the onset of atrial systole and the point B denotes the closure of AV
valve.
 19
Pressure and Volume Changes during Cardiac Cycle

 During ventricular systole

Phase of isovolumic (isometric) contraction, since the AV valves have closed and the
semilunar valves have not opened, so the ventricles contract as a closed chamber and
pressure inside them rises rapidly to a high level, in the intravcntricular pressure curve, this
phase is represented by the segment BC. The point C denotes the opening of semilunar
valves and commencement of ventricular ejection phase.
During rapid ejection phase, the ventricles contract at a rate greater than the rate at which
blood is ejected so a great rise in the pressure occurs. Pressure rises to maximum of 120mm
Hg in the left ventricle and 25mm Hg in the right ventricle.
The maximum pressure in the left ventricle is four to five times more than in the right
ventricle. This is because of the thick wall of the left ventricle. In the intraventricular
pressure curve, this phase is denoted by the segment CD. The point D denotes the peak point
of the intraventricular pressure after which it starts declining.
During slow ejection phase, there is no further ventricular contraction and the pressure starts
declining (segment DE).
 During ventricular diastole:
During protodiastole, the intraventricular pressure drops rapidly as the ventricles start
relaxing. When the intraventricular pressure falls below that of the aorta and the pulmonary
artery, the semilunar valves are closed due to back flow of blood. In the intraventricular
pressure curve, this phase is represented by the segment EF and the point F denoted the
closure of semilunar valves.
 20
During isovolumic (isometric) relaxation phase, since the semilunar valves have closed and
valves have not yet opened up so the ventricles relax as closed chamber and there occurs a
rapid fall in the intraventricular pressure (from 80 mm Hg to about 2—3mm in the left
ventricle). When the pressure inside the ventricles fall below the pressure in the atria, the
AV valves open up and the phase of rapid passive filling commences. In the intraventricular
pressure curve, the segment FG represents this phase and the point G coincides with the
opening of the AV valve.
During rapid passive filling phase, the intraventricular pressure further falls since the
ventricles are relaxing though blood is being filled in them (segment GH).
During reduced passive filling phase, there is no turbulence and the blood flows very slowly
and smoothly and virtually there occurs cessation of ventricular filling (diastasis). The
ventricular pressure remains a little above zero.
3. Pressure Changes in the Aorta
 Pressure in the aorta varies between 80 and 120mm Hg during the cardiac. Aortic pressure
changes during various phases of the cardiac cycle are:
 During atrial systole: During atrial systole, the pressure in the aorta is about 80mm Hg.
 During ventricular systole: During ventricular systole, the intraventricular pressure rises
and reaches above that of the aorta during beginning of the ventricular ejection phase when
the aortic semilunar valve opens and blood starts flowing from the left ventricle into the
aorta.
Hence, the aortic pressure starts rising along with the intraventricular pressure during the
rapid ejection phase and reaches maximum (120mm Hg) at the end of the rapid ejection
phase. It is important to note that during most of the rapid ejection phase, the aortic pressure
remains slightly lesser than the ventricular pressure and during reduced ejection phase, the
aortic pressure starts falling along with the ventricular pressure.
 During ventricular diastole:
During protodiastole, aortic pressure is slightly higher than that in the left ventricle. This
causes backward flow of blood and closure of the aortic semilunar valve. Due to sudden
closure of the semilunar valve the hack flowing blood collides against the closed aortic
valve.
This collision causes a small hut sharp rise in the aortic pressure. This small rise produces a
notch called incisura. This sharp pressure rise is recordable even from the peripheral arteries
and is called dicrotic notch.
During rest of the diastole, the aortic pressure smoothly declines. By the time the aortic
pressure declines to about 80 mm Hg. another ventricular systole boosts the aortic pressure
again.
4. Pressure Changes in the Pulmonary Artery
 Pressure curve in the pulmonary artery is similar to that of the aorta but pressures are low
(about one-sixth of that in aorta). Pulmonary artery systolic pressure averages 15—18mm
Hg and its pressure during diastole is 8—10mm Hg.
 21
B. Volume changes
1. Volume Changes in the Ventricles
 During atrial systole: Atrial systole coincides with the last rapid filling phase of the
ventricular diastole. When the atrial contraction begins, about 105 mL (75%) of the blood
has already flown into the ventricles.
The atrial contraction causes additional 25 mL (25%) filling of the ventricles. In the
ventricular volume curve, this phase is represented by the AB segment. Thus at the end of
atrial systole, i.e. at the end of the ventricular diastole, the ventricular volume is about 130
mL. This is called end diastolic volume.
 During ventricular systole:
During isovolumic contraction phase, as the name suggests, there occurs no change in the
ventricular volume (segment BC).
During ventricular ejection phase about 80 mL of the blood is ejected out by each ventricle.
This is called stroke volume (segment CD).
The percentage of the end-diastolic volume that is ejected out with each stroke during
systole (about 65%) is called ejection fraction. Thus, about 50 mL of the blood in each
ventricle at the end of the ventricular systole is called end-systolic volume.
During protodiastole and phase of isovolumic relaxation, there occurs no change in the
ventricular volume (segments DE and EF).
During rapid filling phase and slow filling phase, the ventricular volume changes rapidly
and then slowly, respectively. About 75% of the ventricular filling (105 mL of blood) occurs
during these phases (segment FG and GH).

HEART SOUNDS
 Heart sounds are the sounds produced by mechanical activities of heart during each cardiac
cycle. Heart sounds are produced by:
1. Flow of blood through cardiac chambers
2. Contraction of cardiac muscle
3. Closure of valves of the heart
 The technique of listening to sounds produced by the organs and vessels of the body is
called auscultation. The areas at which the heart sounds are heard better are called
auscultation area.
 Heart sounds are heard by placing the ear over the chest or by using a stethoscope or
microphone. The graphic record of the sounds connected with the pumping action of the
heart is called phonocardiogram.
Classification of Heart Sounds
 Heart sounds are classified into four group on the basis of their mechanism of origin; they
are,
 22
First heart sound (HS1 )
 Cause: First heart sound is produced by the vibrations set up by the sudden closure of AV
valves (mitral and tricuspid valves) at the start of ventricular systole, during phase of
isovolumic contraction.
 Characteristics: The first heart sound is long and soft when heart rate is low and loud when
the heart rate is high. Its duration is about 0.15 s and frequency is 25—45 Hz. It sounds like
the spoken word ‘LUBB'.
 Site for auscultation: It can he heard by auscultation of the chest with stethoscope. It is best
heard over mitral and tricuspid areas. Mitral area is located in the fifth intercostal space just
internal to mid clavicular line. Tricuspid area is located in the fifth intercostal space near the
sternum.
 In phonocardiogrom, the first heart sound is recorded as a single group of 9—13 waves.
The amplitude of the waves is small to start with but later rapidly rises to fall to form
crescendo and diminuendo series of waves.
 Correlation with ECG: First heart sound coincides with peak of R wave in ECG.
Second heart sound (HS2 )
 Cause: It is caused by the vibrations associated with closure of the semilunar valves (aortic
and pulmonary valves) just at the onset of ventricular diastole.
 Characteristics: The second heart sound is short, loud, high pitched sound. Its duration is
0.12 s and frequency is 50Hz. It sounds like the spoken word ‘DUBB’.
 Site for auscultation: It can be heard by auscultation of the chest with stethoscope. It is best
heard over the aortic and pulmonary areas. Aortic area lies in the right second inter costal
space near the sternum, and pulmonary area is in the left second intercostal space close to
sternum.
 In phonocordiogrom, second heart sound is recorded as a single group of 4—6 waves
having same amplitude.
 Correlation with ECG: Second heart sound usually coincides with the end of T wave in
ECG.
Third heart sound (HS3 )
 Cause: Third heart sound is caused by the vibrations set up in the cardiac wall by inrush of
blood during rapid filling phase of the ventricular diastole.
 Characteristics: Third heart sound is a short, soft and low pitched sound. Its duration is 0.1
s. Normally it cannot he heard by auscultation with stethoscope.
 In phonocardiogrom, the third heart sound is recorded as 1—4 waves grouped together.
 Correlation with ECG: The third heart sound appears between T and P waves of ECG.
Fourth heart sound (HS4 )
 Cause: It is caused by the vibrations set up during the atrial systole which coincides with
last rapid filling phase of the ventricular diastole.
 23
 Characteristics: It is normally not audible. Sometimes it can be hard immediately before
the first sound when axial pressure is high or when ventricle is stiff in condition such as
ventricular hypertrophy. It is a short and low pitched sound. Its duration is about 0.03 s and
frequency about 3Hz.
 In phonocardiogrom, the fourth heart sound merges with first heart sound many times.
When It appears as a separate entity, it has 1-2 waves with very low amplitude.
 Correlation with ECG: Fourth heart sound coincides with the interval between the end of P
wave and onset of Q wave.
Heart Murmurs:
 It occurs in abnormal hearts between normal heart sounds. They are noisy, higher pitched
sounds upto 1000 Hz and are longer in duration compared to normal heart sounds.
 The causes of murmurs are
1. High velocity blood flow that occurs through small opening when there is improper
opening of valves.
2. Regurgitation which results when the valves do not close completely and allow some
backward flow of blood.
3. Small opening in the septum that separates the left and right sides of the heart. This
forces the blood through the opening from the left ventricle into right ventricle by
passing the systemic circulation.
 24
ELECTROCARDIOGRAM
 An electrocardiogram (ECG or EKG - from the German word Elektrokardiogram), is the
record or graphical registration of electrical changes in the myocardium during a cardiac
cycle.
 The instrument used to record the changes is an electrocardiograph. Electrocardiography
is the technique by which electrical activities of the heart are studied.
 As action potentials propagate through the heart, they generate electrical currents that can be
detected at the surface of the body. In clinical practice, electrodes are positioned on the arms
and legs (limb leads) and at six positions on the chest (chest leads) to record the ECG.
Typically in a clinical setting, 12 leads are used. Three are bipolar leads that measure the
voltage difference either between the arms or between an arm and a leg, and nine are
unipolar leads. Together the 12 leads provide a fairly comprehensive picture of the heart’s
electrical activity.
 The electrocardiograph amplifies the heart’s electrical signals and produces 12 different
tracings from different combinations of limb and chest leads.

Electrodes Position

Name of Lead Placement of Electrodes

Bipolar Limb Lead
I Right arm and left arm
II Right arm and left leg
III Left arm and left leg
Unipolar Limb Leads
AVR Right arm
AVL Left arm
AVF Left leg
 25

Unipolar Chest Leads

V1 4th intercostal space to the right of the sternum
V2 4th intercostal space to the left of the sternum
V3 5th intercostal space to the left of the sternum
V4 5th intercostal space in line with the middle of the clavicle
(collarbone)
V5 5th intercostal space to the left of V4
V6 5th intercostal space in line with the middle of the axilla (underarm)
ECG pattern
 ECG machine amplifies the electrical signals produced from the heart and records these
signals on a moving ECG paper at a speed of 25 mm/sec.
 Electrocardiographic grid refers to the markings (lines) on ECG paper. ECG paper has
horizontal and vertical lines at regular intervals of 1 mm. Every 5th line (5 mm) is
thickened.

 Time duration of different ECG waves is plotted horizontally on X-axis. Amplitude of ECG
waves is plotted vertically on Y-axis. Each small 1-mm square represents 0.04 sec (40 msec)
in time and 0.1 mV in voltage.
 One cycle of cardiac contraction (systole) and relaxation (diastole), focusing on the
electrical events that produce the basic waves and lines of the standard EKG.
 Normal ECG consists of deflections, or waves, complexes, intervals and segments during
each cardiac cycle. Between cycles, the muscle fibers remain polarized, with no detectable
electrical changes.
Waves of Normal ECG
 Each limb and chest electrode records slightly different electrical activity because of the
difference in its position relative to the heart. Waves of ECG recorded by limb lead II
are considered as the typical waves. The normal ECG tracing shows five waves which,
by convention, have been named P, Q, R, S and T.
 26
P Wave
 P wave is a positive, gently rounded, not pointed wave and the first wave in ECG. It is also
called atrial complex.
 Depolarization of the atrial fibers of the SA node produces the P wave. It Indicates atrial
depolarization, or contraction of the atrium. Because the sinus node is located in the right
atrium, the right atrium begins to depolarize before the left atrium and finishes earlier as
well. Therefore, the first part of the P wave predominantly represents right atrial
depolarization, and the second part left atrial depolarization.
 The small P wave lasts about 0.08 s (not more than 0.10 seconds). Normal amplitude of ‘P’
wave is 0.1 to 0.12 mV.

 The ventricles of the heart are in relaxed during the expression of the P wave. Atrial
repolarization is not recorded as a separate wave in ECG because it merges with ventricular
repolarization (QRS complex).
QRS Complex
 QRS complex is also called the initial ventricular complex. Q wave is a small negative
wave. It is continued as the tall R wave, which is a positive wave. R wave is followed by a
small negative wave, the S wave.
 The QRS complex indicates the depolarization of the ventricles. Q wave is due to the
depolarization of basal portion of interventricular septum. R wave is due to the
depolarization of apical portion of interventricular septum and apical portion of ventricular
muscle. S wave is due to the depolarization of basal portion of ventricular muscle near the
atrioventricular ring.
 The right and left ventricles then depolarize at about the same time, but most of the EKG
represents left ventricular activation because the muscle mass of the left ventricle is about
three times that of the right ventricle.
 It is also during this interval that the atria repolarize, but this event is obscured by the greater
depolarization occurring in the ventricles.
 Normal duration of QRS complex is between 0.08 and 0.10 second. The amplitude of the
QRS complex is much greater than that of the atrial P wave because the ventricles have so
much more muscle mass than the atria. Amplitude of Q wave = 0.1 to 0.2 mV, R wave = 1
mV and S wave = 0.4 mV. The amplitude has wide normal limits according to the lead.
T Wave
 T wave is the final ventricular complex and is a positive wave.
 The T wave is produced by ventricular repolarization. The T wave is smaller and wider than
the QRS complex because repolarization occurs more slowly than depolarization.
 Normal duration of T wave is 0.2 second. Amplitude Normal amplitude of T wave is 0.3
mV.
 27
Intervals and Segments of ECG
 PR segment: The PR segment is the straight line running from the end of the P wave to the
start of the QRS complex. It therefore measures the time from the end of atrial
depolarization to the start of ventricular depolarization.
 P-Q/ P-R Interval: The PR interval includes the P wave and the straight line connecting it
to the QRS complex.
The interval between the onsets of P wave and onset of Q wave is termed the P-Q interval.
Sometimes called the P-R interval because the Q wave tends to be very small, it includes
atrial depolarization (and contraction) as well as the passage of the depolarization wave
through the rest of the conduction system.
P-R interval signifies the atrial depolarization and conduction of impulses through AV node.
It shows the duration of conduction of the impulses from the SA node to ventricles through
atrial muscle and AV node.
P wave represents the atrial depolarization. Short isoelectric (zero voltage) period after the
end of P wave represents the time taken for the passage of depolarization within AV node.
P-R Interval normally ranges from 0.12 to 0.20 seconds in duration.
 ST segment: The ST segment is the straight line connecting the end of the QRS complex
with the beginning of the T wave.
It measures the time from the end of ventricular depolarization to the start of ventricular
repolarization.
Normal duration of ‘S-T’ segment is 0.08 second.
 QT interval: The QT interval is the interval between the onset of Q wave and the end of T
wave. It includes the QRS complex, the ST segment, and the T wave.
It therefore measures the time from the beginning of ventricular depolarization to the end of
ventricular repolarization. Normal duration of Q-T interval is between 0.4 and 0.42 second.
 QRS interval: The term QRS interval is used to describe the duration of the QRS complex
alone without any connecting segments. Obviously, it measures the duration of ventricular
depolarization. Normal duration of QRS complex is between 0.08 and 0.10 second.
 R-R Interval: R-R interval is the time interval between two consecutive R waves. R-R
interval signifies the duration of one cardiac cycle. Normal duration of ‘R-R’ interval is 0.8
second.
Waves of normal ECG
 28
Analysis of ECG
 By comparing ECG 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.
1. In reading an ECG, the size of the waves can provide clues to abnormalities.
o Larger P waves indicate enlargement of an atrium.
o An abnormal QRS complex generally indicates cardiac problems of the ventricles.
An enlarged Q wave may indicate a myocardial infarction; and an enlarged R wave
generally indicates enlarged ventricles.
o An arteriosclerotic heart will produce altered T waves, as will various other heart
diseases. The T wave may be elevated in hyperkalemia (high blood K level).
2. Analysis of an ECG also involves measuring the time spans between waves, which are
called intervals or segments.
o A prolonged P-R interval suggests a conduction problem at or below the AV node.
o The S-T segment is depressed when the heart receives insufficient oxygen; in acute
myocardial infarction, it is elevated.
o The Q–T interval may be lengthened by myocardial damage, myocardial ischemia
(decreased blood flow), or conduction abnormalities.
3. The ECG described above originates from the SA node and is known as sinus rhythm. The
rate of sinus rhythm is 60 to 100 beats per minute. Bradycardia is a condition in which the
heart beats too slowly – usually less than 60 beats per minute. Tachycardia is a condition in
which the heart beats faster than 100 beats per minute in an adult.

BLOOD PRESSURE
 Blood pressure is the force blood exerts against the inner walls of blood vessels. Although
this force occurs throughout the vascular system, the term blood pressure most commonly
refers to pressure in arteries supplied by branches of the aorta (systemic arteries).
Arterial Blood Pressure
 Arterial blood pressure rises and falls in a pattern corresponding to the phases of the cardiac
cycle. That is, contracting ventricles (ventricular systole) squeeze blood out and into the
pulmonary trunk and aorta, which sharply increases the pressures in these arteries.
 Arterial blood pressure is expressed in four different terms:
1. Systolic blood pressure
2. Diastolic blood pressure
3. Pulse pressure
4. Mean arterial blood pressure.
 Systolic blood pressure (systolic pressure) is defined as the maximum pressure exerted in
the arteries during systole of heart (ventricular contraction). Normal systolic pressure: 120
mm Hg (110 mm Hg to 140 mm Hg).
 29
 Diastolic blood pressure (diastolic pressure) is defined as the minimum pressure exerted
in the arteries during diastole of heart (ventricles relax). Normal diastolic pressure: 80 mm
Hg (60 mm Hg to 80 mm Hg).
BP is highest in the aorta and large systemic arteries; in a resting, young adult, BP rises to
about 120 mmHg during systole (ventricular contraction) and drops to about 80 mmHg
during diastole (ventricular relaxation).
A sphygmomanometer is used to measure arterial blood pressure, reporting a fraction that is
normally about 120/80. The upper number indicates the arterial systolic pressure in mm Hg
(SP), and the lower number indicates the arterial diastolic pressure in mm Hg (DP).
 Pulse pressure is the difference between the systolic pressure and diastolic pressure.
Normal pulse pressure: 40 mm Hg (120 – 80 = 40).
 Mean arterial blood pressure is the average pressure existing in the arteries. It is the
diastolic pressure plus one third of pulse pressure. To determine the mean pressure, diastolic
pressure is considered than the systolic pressure. It is because; the diastolic period of cardiac
cycle is longer (0.53 second) than the systolic period (0.27 second). Normal mean arterial
pressure: 93 mm Hg. It can be estimated as follows:
MAP = diastolic BP+1/3 (systolic BP-diastolic BP)
Thus, in a person whose BP is 120/80 mmHg, MAP is about 93 mmHg [80 +1/3(120-80)].
 Elasticity of arterial walls. There is a considerable amount of elastic tissue in the arterial
walls, especially in large arteries. Therefore, when the left ventricle ejects blood into the
already full aorta, the aorta expands to accommodate it, and then recoils because of the
elastic tissue in the wall. This pushes the blood forwards, into the systemic circulation. This
distension and recoil occurs throughout the arterial system. This alternate expanding and
recoiling of the arterial wall can be felt as a pulse in an artery that runs close to the surface.
The radial artery is commonly used to take a person’s pulse. Other sites where an arterial
pulse is easily detected include the carotid, brachial, and femoral arteries.
 Capillary Blood Pressure: As blood leaves the aorta and flows through the systemic
circulation, its pressure falls progressively as the distance from the left ventricle increases.
By the time blood reaches the capillaries, blood pressure has dropped to approximately 35
mm Hg and by the end of the capillary beds is only around 15 mm Hg. Such low capillary
pressures are desirable because (1) capillaries are fragile and high pressures would rupture
them, and (2) most capillaries are extremely permeable and thus even the low capillary
pressure forces solute-containing fluids (filtrate) out of the bloodstream into the interstitial
space
 Venous Blood Pressure: Unlike arterial pressure, which pulsates with each contraction of
the left ventricle, venous blood pressure is steady and changes very little during the cardiac
cycle. The pressure gradient in the veins, from venules to the termini of the venae cavae, is
only about 15 mm Hg (that from the aorta to the ends of the arterioles is about 60 mm Hg).
Finally, blood pressure reaches 0 mmHg as blood flows into the right ventricle.
 Hypertension is defined as the persistent high blood pressure. Clinically, when the systolic
pressure remains elevated above 150 mm Hg and diastolic pressure remains elevated above
90 mm Hg, it is considered as hypertension. Hypotension is the low blood pressure. When
the systolic pressure is less than 90 mm Hg, it is considered as hypotension.
 30
Factors That Influence Arterial Blood Pressure
 Arterial blood pressure depends on a variety of factors. These include cardiac output, blood
volume, peripheral resistance, and blood viscosity
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 heart beats per
minute:
Cardiac output = Stroke volume × Heart rate
(ml∕min) (ml∕beat) (beats∕min)
In a typical resting adult male, stroke volume averages 70 mL/beat, and heart rate is about
75 beats/min. Thus, average cardiac output is
CO = 70 mL/beat x 75 beats/min
= 5250 mL/min
= 5.25 L/min
This volume is close to the total blood volume, which is about 5 liters in a typical adult
male. Thus, entire blood volume flows through pulmonary and systemic circulations each
minute.
 Blood pressure varies with cardiac output. If either stroke volume or heart rate increases, so
does cardiac output, and as a result, blood pressure initially rises. Conversely, if stroke
volume or heart rate decreases, cardiac output decreases, and blood pressure also initially
decreases.
 Cardiac output increases in muscular exercise, emotional conditions, etc. So in these
conditions, the systolic pressure is increased. In conditions like myocardial infarction, the
cardiac output decreases, resulting in fall in systolic pressure.
Blood Volume
 Blood volume equals the sum of the formed elements and plasma volumes in the vascular
system. Although the blood volume varies somewhat with age, body size and sex, it is
usually about 5 liters for adults, or 8% of body weight in kilograms.

 Blood pressure is normally directly proportional to blood volume in the cardiovascular

system. Thus, any changes in blood volume can initially alter blood pressure.
 For example, if a hemorrhage reduces blood volume, blood pressure initially drops. If a
transfusion restores normal blood volume, normal blood pressure may be reestablished.
Blood volume can also fall if the fluid balance is upset, as happens in dehydration. Fluid
replacement can reestablish normal blood volume and pressure.
Peripheral Resistance
 Friction between the blood and the walls of blood vessels produces a force called peripheral
resistance, which hinders blood flow. Blood pressure must overcome this force if the blood
is to continue flowing. Factors that alter the peripheral resistance change blood pressure.
 31
 For example, contracting smooth muscles in arteriolar walls increase the peripheral
resistance by constricting these vessels. Blood tends to back up into the arteries supplying
the arterioles, and the arterial pressure rises. Dilation of arterioles has the opposite effect—
peripheral resistance decreases, and arterial blood pressure drops in response.
Blood Viscosity
 Viscosity is the ease with which the molecules of a fluid flow past one another. The greater
the viscosity, the greater the resistance to flowing.
 Blood cells and plasma proteins increase blood viscosity. The greater the blood’s resistance
to flowing, the greater is the force needed to move it through the vascular system. Thus, it is
not surprising that blood pressure rises as blood viscosity increases and drops as viscosity
decreases.
Some of the factors that influence arterial blood pressure

REGULATION OF BLOOD PRESSURE

 Blood pressure (BP) is determined by cardiac output (CO) and peripheral resistance (PR)
according to this relationship:
BP = CO × PR
 Maintenance of normal arterial pressure therefore requires regulation of these two factors.
Several interconnected negative feedback systems control blood pressure by adjusting heart
rate, stroke volume, systemic vascular resistance, and blood volume.
Cardiovascular Center
 The cardiovascular center forms part of the autonomic nervous system, located in the
medulla oblongata and is responsible for regulation of cardiac output.
 The cardiovascular center contains three distinct components: the cardioaccelerator center,
the cardioinhibitor center, and the vasomotor center.
1) The cardioaccelerator center stimulates cardiac function by regulating heart rate and
stroke volume via sympathetic stimulation from the cardiac accelerator nerve.
2) The cardioinhibitor center slows cardiac function by decreasing heart rate and stroke
volume via parasympathetic stimulation from the vagus nerve.
3) The vasomotor center controls vessel tone or contraction of the smooth muscle in the
blood vessels.
 The three main types of sensory receptors that provide input to the cardiovascular center are
1. Higher centres in the brain.
 32
2. Baroreceptors monitor changes in pressure and stretch in the walls of blood vessels, and
3. Chemoreceptors monitor the concentration of various chemicals in the blood.
 Output from the cardiovascular center flows along sympathetic and parasympathetic neurons
of the ANS.
1. Sympathetic impulses reach the heart via the cardiac accelerator nerves. An increase in
sympathetic stimulation increases heart rate and contractility; a decrease in sympathetic
stimulation decreases heart rate and contractility.
2. Parasympathetic stimulation, conveyed along the vagus (X) nerves, decreases heart
rate. Thus, opposing sympathetic (stimulatory) and parasympathetic (inhibitory)
influences control the heart.
3. The vasomotor region of the cardiovascular center continually sends impulses over
these routes to arterioles throughout the body. The result is a moderate state of tonic
contraction or vasoconstriction (sets the resting level of systemic vascular resistance).
Mechanisms in blood pressure control

Neural Regulation of Blood Pressure

 The nervous system regulates blood pressure via the following mechanism,
1. Baroreceptor reflexes: Baroreceptors are neurons in the walls of the aorta and carotid
arteries that sense changes in blood pressure.
If arterial pressure increases, nerve impulses travel from the baroreceptors to the cardiac
center of the medulla oblongata. This center relays parasympathetic impulses to the SA node
in the heart, and the heart rate decreases in response. As a result of this cardioinhibitor
reflex, cardiac output falls, and blood pressure decreases toward the normal level.
 33
Conversely, decreasing arterial blood pressure initiates the cardioaccelerator reflex, which
sends sympathetic impulses to the SA node. As a result, the heart beats faster, increasing
cardiac output and arterial pressure.
The baroreceptor reflex

2. Chemoreceptor Reflexes: Chemoreceptors, sensory receptors that monitor the chemical

composition of blood, are located close to the baroreceptors of the carotid sinus and arch of
the aorta in small structures called carotid Bodies and aortic bodies, respectively.
These chemoreceptors detect changes in blood level of O 2 , CO 2 , and H+. Hypoxia (lowered
O2 availability), acidosis (an increase in H+ concentration), or hypercapnia (excess CO 2 )
stimulates the chemoreceptors to send impulses to the cardiovascular center.
In response, the CV center increases sympathetic stimulation to arterioles and veins,
producing vasoconstriction and an increase in blood pressure. These chemoreceptors also
provide input to the respiratory center in the brain stem to adjust the rate of breathing.
The relationship between stimulation of chemoreceptors and arterial blood pressure
 34
3. Higher centres in the brain: Input to the CVC from the higher centres is influenced by
emotional states such as fear, anxiety, pain and anger that may stimulate changes in blood
pressure. For example, even before start to run in a race, heart rate may increase due to
nerve impulses conveyed from the limbic system to the CV center. If body temperature rises
during a race, the hypothalamus sends nerve impulses to the CV center. The resulting
vasodilation of skin blood vessels allows heat to dissipate more rapidly from the surface of
the skin.
Proprioceptors monitor movements of joints and muscles and provide input to the
cardiovascular center during physical activity. Their activity accounts for the rapid increase
in heart rate at the beginning of exercise.
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.
 Renin–angiotensin–aldosterone (RAA) system: When blood volume falls or blood flow to
the kidneys decreases, juxtaglomerular cells in the kidneys secrete renin into the
bloodstream. It converts angiotensinogen into angiotensin I. This is converted into
angiotensin II by ACE (angiotensin converting enzyme). Angiotensin II acts in two ways to
restore the blood pressure: First, angiotensin II is a potent vasoconstrictor; it raises blood
pressure by increasing systemic vascular resistance. Second, it stimulates secretion of
aldosterone, which increases reabsorption of sodium ions (Na) and water by the kidneys.
The water reabsorption increases total blood volume, which increases blood pressure.

 Adrenal medulla hormones: During periods of stress, the adrenal gland releases
norepinephrine and epinephrine to the blood, and both hormones enhance the sympathetic
fight-or-flight response. These hormones increase cardiac output by increasing the rate and
force of heart contractions. They also cause vasoconstriction of arterioles and veins in the
skin and abdominal organs and vasodilation of arterioles in cardiac and skeletal muscle,
which helps increase blood flow to muscle during exercise.
 35
RESPIRATORY SYSTEM
The integrated system of organs involved in the respiration is called respiration system.
 The term respiration refers to three separate but related functions:
1) Ventilation (breathing);
2) Gas exchange, which occurs between the air and blood in the lungs and between the
blood and other tissues of the body; and
3) Oxygen utilization by the tissues in the energy-liberating reactions of cell
respiration.
 Ventilation and the exchange of gases (oxygen and carbon dioxide) between the air and
blood are collectively called external respiration. Gas exchange between the blood and
other tissues are collectively known as internal respiration.
Parts of respiratory system

 The respiratory system includes those organs and structures that function together to bring
gases in contact with the blood of the circulatory system.
 The principal organs of the respiratory system are the nose, pharynx, larynx, trachea,
bronchi, and lungs. The structures of the upper respiratory system include the nose, pharynx,
and associated structures; the lower respiratory system includes the larynx, trachea, bronchi,
and lungs.
Organs of respiratory system

1. The Nose and Nasal cavity

 The nose is the only externally visible part of the respiratory system. The nose consists of
the external nose and the nasal cavity.
 Most of the external nose is composed of hyaline cartilage, although the bridge of the
external nose consists of bone. The bone and cartilage are covered by connective tissue and
skin.
 The nasal septum divides the nasal cavity into two lateral halves. Each half is referred to as a
nasal fossa. Adult humans have nasal hairs in the anterior nasal passage.
 36
 Each nasal fossa opens anteriorly through the nostril (external nares), and communicates
posteriorly with the nasopharynx through the choana (internal nares).
 The roof of the nasal cavity is formed by the ethmoid and sphenoid bones of the skull. The
floor is formed by the palate, which separates the nasal cavity from the oral cavity below.
Anteriorly, where the palate is supported by the maxillary processes and palatine bones, it is
called the hard palate. The unsupported posterior portion is the muscular soft palate.
 Three prominent bony ridges called conchae are present on the lateral walls on each side of
the nasal cavity. The conchae increase the surface area of the nasal cavity and cause air to
churn, so that it can be cleansed, humidified, and warmed.
Nasal cavity

 The mucous membrane has pseudostratified ciliated epithelium that is rich in mucus-
secreting goblet cells. It also includes an extensive network of blood vessels. As air passes
over the mucous membrane, heat leaves the blood and warms the air, adjusting the air’s
temperature to that of the body. In addition, incoming air is moistened as water evaporates
from the mucous lining.
 The olfactory epithelium in the upper medial portion of the nasal cavity is concerned with the sense
of smell.

 The nasolacrimal ducts, which carry tears from the eyes, also open into the nasal cavity.
Sensory receptors for the sense of smell are in the superior part of the nasal cavity.
 The paranasal sinuses are air-filled spaces within bone. They include the maxillary, frontal,
ethmoidal and sphenoidal sinuses, each named for the bones in which they are located. The
paranasal sinuses open into the nasal cavity and are lined with a mucous membrane. They
reduce the weight of the skull produce mucus, and influence the quality of the voice by
acting as resonating chambers.

 Function: The nose has several functions: it warms, cleanses, and humidifies inhaled air; it
detects odors in the airstream; and it serves as a resonating chamber that amplifies the voice.
 37

2. Pharynx

 The pharynx or throat is a funnel-shaped organ, approximately 13 cm long that connects the
nasal cavities to the larynx of the respiratory system and oral cavities to the esophagus of the
digestive system.
 On the basis of location and function, the pharynx is divided into three parts from superior
to inferior:
a) Nasopharynx,
b) Oropharynx and
c) Laryngopharynx.
 38
a) The nasopharynx is the uppermost portion of the pharynx, positioned directly behind the
nasal cavity and above the soft palate. The pharyngeal tonsils, are situated in the posterior
wall of the nasal cavity.
A pendulous uvula hangs from the middle lower portion of the soft palate. During the act of
swallowing, the soft palate and uvula are elevated to block the nasal cavity and prevent food
from entering.
b) The oropharynx is the middle portion of the pharynx between the soft palate and the level
of the hyoid bone. Both swallowed food and fluid and inhaled air pass through it.
The base of the tongue forms the anterior wall of the oropharynx. Paired palatine tonsils are
located on the posterior lateral wall, and the lingual tonsils are found on the base of the
tongue.
c) The laryngopharynx is the lowermost portion of the pharynx. It extends inferiorly from the
level of the hyoid bone to the larynx and opens into the esophagus and larynx.
 The nasopharynx passes only air and is lined by pseudostratified columnar epithelium,
whereas the oropharynx and laryngopharynx pass air, food, and drink and are lined by
stratified squamous epithelium. Swallowed food and fluid are directed into the esophagus,
whereas inhaled air is directed anteriorly into the larynx.
Function:
a) The air is further warmed and moistened as it passes through the pharynx.
b) The pharynx functions in speech; by acting as a resonating chamber for the sound ascending
from the larynx.
c) The lymphatic tissue of the pharyngeal and laryngeal tonsils produces antibodies in response
to swallowed or inhaled antigens.
3. Larynx
 The larynx, or “voice box,” connects the laryngopharynx with the trachea. It is positioned in
the anterior midline of the neck at the level of the fourth through sixth cervical vertebrae.
 The larynx is shaped like a triangular box. It is composed of a framework of muscles and
cartilages bound by elastic tissue.
 The largest of the cartilages are the thyroid, cricoid, and epiglottic cartilages.
1) The laryngeal prominence of the thyroid cartilage is commonly called the “Adam’s
apple.” The thyroid cartilage is typically larger and more prominent in males than in
females because of the effect of male sex hormones on the development of the larynx
during puberty.
2) The most inferior cartilage of the larynx is the cricoid cartilage, which forms the base of
the larynx on which the other cartilages rest. The thyroid and cricoid cartilages maintain
an open passageway for air movement.
3) The epiglottic cartilage is the central part of a flap-like structure called the epiglottis.
This structure usually stands upright and allows air to enter the larynx. During
swallowing, however, the larynx rises, and the epiglottis presses downward to partially
cover the opening into the larynx. This helps prevent foods and liquids from entering the
air passages.
 39

Anterior views of the larynx Posterior views of the larynx

 Inside the larynx, two pairs of horizontal vocal folds composed of muscle tissue and
connective tissue with a covering of mucous membrane.
1) The upper fold forms the vestibular folds. It is also called false vocal cords because
they do not produce sounds. Muscle fibers within these folds help close the airway
during swallowing. The vestibular folds support the vocal folds and produce mucus from
its epithelial lining, which keep the vestibular folds from drying out.
2) The lower fold forms the vocal folds or true vocal cords. The vocal folds are the
primary source of voice production. Air moving past the vocal folds causes them to
vibrate, producing sound. Muscles control the length and tension of the vocal folds. The
force of air moving past the vocal folds controls the loudness and the tension of the
 40
vocal folds controls the pitch of the voice. At puberty, the male vocal cords begin to
grow longer, hence the lower pitch of the adult male voice.
During normal breathing, the vocal cords are relaxed and the opening between them,
called the glottis, is a triangular slit. However, when food or liquid s swallowed, muscles
in the false vocal cords close the glottis, which prevents food or liquid from entering the
trachea.

 Stratified squamous epithelium lines the vocal folds, whereas the rest of the larynx is lined
with pseudostratified ciliated columnar epithelium.
 The larynx has two functions. Its primary function is to prevent food or fluid from entering
the trachea and lungs during swallowing and to permit passage of air while breathing. A
secondary role is to produce sound.
4. Trachea
 The trachea, commonly called the windpipe, is a flexible cylindrical tube connecting the
larynx to the primary bronchi. The trachea lies ventral to the esophagus.

 The trachea or windpipe is a continuation of the larynx and extends downwards to about the
level of the 5th thoracic vertebra where it divides (bifurcates) into the right and left bronchi,
one bronchus going to each lung.
 A series of 16 to 20 C-shaped hyaline cartilages form the supporting walls of the trachea.
These tracheal cartilages ensure that the airway will always remain open. The open part of
the C-shaped rings faces the esophagus, and this allows the esophagus to expand when
swallowing.
 The inner lining of the trachea is a pseudostratified columnar epithelium composed mainly
of mucus-secreting goblet cells, ciliated cells, and short basal stem cells.
 The mucus traps inhaled particles, and the upward beating of the cilia drives the debris-
laden mucus toward the pharynx, where it is swallowed.
 41
The Trachea & Bronchi

5. The bronchi
 The trachea divides at level of the 5th thoracic vertebra, into the left and right main bronchi,
or primary bronchi, each of which connects to a lung.
 The right bronchus is wider, shorter and more vertical than the left bronchus. Before
joining the lung it gives off its upper lobe branch, and then passes below the pulmonary
artery to enter the hilum of the lung. After entering the right lung at the hilum it divides into
three branches, one to each lobe. Each branch then subdivides into numerous smaller
branches.
 The left bronchus is more horizontal than the right main bronchus because it is displaced
by the heart. Unlike the right, it gives off no branches until it enters the hilum of the lung.
After entering the lung at the hilum it divides into two branches, one to each lobe. Each
branch then subdivides into progressively smaller tubes within the lung substance.
 Like the trachea, the main bronchi are lined with pseudostratified ciliated columnar
epithelium and are supported by C-shaped pieces of cartilage.
6. The lungs
 The lungs are the principal organs of respiration. The lungs are soft, spongy, cone-shaped,
paired organs in the thoracic cavity.
 Location: Each lung extends from the diaphragm to a point just above the clavicle, and its
surfaces are bordered by the ribs to the front and back. The lungs are separated from one
another by the heart and other structures of the mediastinum which is the area between the
lungs.
 The left lung, while taller, is narrower than the right because the heart tilts toward the left
and occupies more space on this side of the mediastinum.
 42
 Covering: Each lung is enclosed by a double layer of serous membrane called the pleura.
The visceral pleura adhere to the surface of the lung, while the parietal pleura line the
thoracic cavity. The space between the two membranes is known as the pleural cavity. The
pleura produces a lubricating serous fluid that allows its two layers to slide against one
another.
 Structure: Each lung is conical in shape, and is described as having an apex, a base, costal
surface and medial surface.
1) The superior surface, called the apex of the lung, extends above the level of the clavicle.
2) The inferior surface of the lung, called the base of the lung, is concave as it fits over the
convex dome of the diaphragm.
3) The mediastinal (medial or cardiac) surface of the lung is slightly concave and contains
a vertical slit, the hilum through which pulmonary vessels, nerves, and bronchi pass.
4) Finally, the broad, rounded surface in contact with the membranes covering the ribs is
called the costal surface of the lung.
 The lungs are organized into lobes. The right lung is subdivided by two fissures into three
lobes: superior, middle, and inferior lobes. The left lung is subdivided into a superior
lobe (upper lobe) and an inferior lobe (lower lobe) by a single fissure.
 Each lobe of the lung is divided into many small lobules, and each lobule has a bronchiole
serving many alveoli.
The lungs

 The Bronchial Tree: The main bronchi branch many times to form the bronchial tree. The
right and left main (primary) bronchi are formed by the division of the trachea.
Once inside the lungs, each main bronchus subdivides into lobar bronchi (secondary), three
on the right and two on the left—each are supplying one lung lobe.
The lobar bronchi branch into third-order segmental bronchi (tertiary), which divide
repeatedly into smaller and smaller bronchi.
 43
The bronchi continue to branch many times, finally giving rise to bronchioles. The
bronchioles also subdivide numerous times to give rise to terminal bronchioles, which then
subdivide into respiratory bronchioles. Each respiratory bronchiole subdivides to form
alveolar ducts and open into alveoli, which are small air sacs. The alveolar ducts end as two
or three alveolar sacs, which are chambers connected to two or more alveoli. There are
about 300 million alveoli in the lungs.
The bronchial tree
 44
MECHANISM OF RESPIRATION
 The process of gas exchange in the body, called respiration, has three basic steps:
1. Pulmonary ventilation, or breathing, is the inhalation or inspiration (inflow) and
exhalation or expiration (outflow) of air and involves the exchange of air between the
atmosphere and the alveoli of the lungs.
2. External (pulmonary) respiration is the exchange of gases between the alveoli of the
lungs and the blood in pulmonary capillaries across the respiratory membrane. In this
process, pulmonary capillary blood gains O 2 and loses CO 2 .
3. Internal (tissue) respiration is the exchange of gases between blood in systemic capillaries
and tissue cells. In this step the blood loses O 2 and gains CO 2 . Within cells, the metabolic
reactions that consume O 2 and give off CO 2 during the production of ATP are termed
cellular respiration.
Muscles of respiration
 Inflation and deflation of the lungs occurring with each breath ensures that regular exchange
of gases takes place between the alveoli and the external air.
 The expansion of the chest during inspiration occurs as a result of muscular activity, partly
voluntary and partly involuntary. The main muscles of respiration in normal quiet breathing
are the intercostal muscles and the diaphragm. During difficult or deep breathing they are
assisted by the muscles of the neck, shoulders and abdomen.
1. Pulmonary ventilation or breathing
Cycle of respiration occurs 12 to 15 times per minute and consists of three phases:
Inspiration
Expiration
Pause
 Inspiration: Atmospheric pressure, the pressure of the air, provides the force that moves air
into the lungs. At sea level, normal air pressure is equal to 760 mm of mercury (Hg).
The overall size of the thoracic cavity increases with inspiration. An unforced, or quiet,
inspiration results primarily from contraction of the dome-shaped diaphragm, which lowers
and flattens when it contracts. This increases thoracic volume in a vertical direction.
Inspiration is aided by contraction of the parasternal and external intercostals, which raise
the ribs when they contract and increase thoracic volume laterally. Other thoracic muscles
become involved in forced (deep) inspiration.
The expanded thoracic cavity decreases the air pressure within the pleural cavities to below
that of the atmosphere (2 mm Hg below that of atmospheric pressure). It is this pressure
difference that causes the lungs to become inflated.
The process of inspiration is active, as it requires expenditure of energy for muscle
contraction. The negative pressure created in the thoracic cavity aids venous return to the
heart and is known as the respiratory pump.
 45

 Expiration: Relaxation of the intercostal muscles and the diaphragm results in downward
and inward movement of the rib cage and elastic recoil of the lungs. As this occurs, pressure
inside the lungs exceeds that in the atmosphere and therefore air is expelled from the
respiratory tract.
Quiet expiration is a passive process. After becoming stretched by contractions of the
diaphragm and thoracic muscles, the thorax and lungs recoil as a result of their elastic
tension when the respiratory muscles relax. The decrease in lung volume raises the pressure
within the alveoli above the atmospheric pressure and pushes the air out.
During forced expiration, the internal intercostal muscles contract and depress the rib cage.
The abdominal muscles also aid expiration because, when they contract, they force
abdominal organs up against the diaphragm and further decrease the volume of the thorax.
By this means the intrapulmonary pressure can raise 20 or 30 mmHg above the atmospheric
pressure. The lungs still contain some air and are prevented from complete collapse by the
intact pleura.
 Pause: After expiration, there is a pause before the next cycle begins.
 Non-respiratory Air Movements: Air movements through the respiratory system that are
not associated with pulmonary ventilation are termed non respiratory movements such as
laughing, sighing, crying, or yawning, or they may function to expel foreign matter from the
respiratory tract, as in coughing and sneezing.
 46
2. External (pulmonary) respiration
The alveoli carry on the vital process of exchanging gases between the air and the blood.
Respiratory Membrane

 The wall of an alveolus is simple squamous epithelium. In close association with an

alveolus is a dense network of capillaries, which also have walls of simple squamous
epithelium. Thin, fused basement membranes separate the layers of these flattened cells, and
in the spaces between the cells are elastic and collagenous fibers that srupport the alveolar
wall. At least two thicknesses of epithelial cells and a layer of fused basement membranes
separate the air in an alveolus from the blood in a capillary. These layers constitute the
respiratory membrane across which blood and alveolar air exchange gases.
 47
Exchange of gases
 The exchange of oxygen and carbon dioxide between alveolar air and pulmonary blood
occurs via passive diffusion, which is governed by the behavior of gases as described by two
gas laws, Dalton’s law and Henry’s law.
 Dalton’s law: The total pressure of the gas mixture is equal to the sum of the partial
pressures of the constituent gases.
 Atmospheric air is a mixture of gases—nitrogen (N 2 ), oxygen (O 2 ), argon (Ar), carbon
dioxide (CO 2 ), variable amounts of water vapor (H2 O), plus other gases present in small
quantities. Atmospheric pressure is the sum of the pressures of all these gases.
Atmospheric pressure (760 mmHg) = PN 2 + PO2 + PH2 O + PCO 2 + Pother gases
 Atmospheric air is 78.6% nitrogen, 20.9% oxygen, 0.04% carbon dioxide, water 0.04% and 0.06%
other gases. The partial pressures of the gases in inhaled air are as follows:
PN2 = 0.786 x 760 mmHg = 597.4 mmHg
PO2 = 0.209 x 760 mmHg = 158.8 mmHg
PCO2 = 0.0004 x 760 mmHg = 0.3 mmHg
PH2 O = 0.0004 x 760 mmHg = 3.0 mmHg
Pother gases = 0.0006 x 760 mmHg = 0.5 mmHg
Total =760.0 mmHg
 Inspired air contains variable amounts of moisture. By the time the air has passed into the
respiratory zone of the lungs, however, it is normally saturated with water vapor (has a
relative humidity of 100%). The capacity of air to contain water vapor depends on its
temperature; since the temperature of the respiratory zone is constant at 37 °C, its water
vapor pressure is also constant (at 47 mmHg).
 When the effect of water vapor pressure is considered, the partial pressure of oxygen in the
inspired air is decreased at sea level to
PO 2 (sea level) =0.21 (760 −47) =150 mmHg
As a result of gas exchange in the alveoli, there is an increase in the PCO 2 , while the PO 2 of
alveolar air is further diminished to about 104 mmHg.

 Henry’s Law: According to Henry’s law, when a mixture of gases is in contact with a
liquid, each gas will dissolve in the liquid in proportion to its partial pressure.
 When a mixture of gases dissolves in blood, the resulting concentration of each gas is
proportional to its partial pressure. The PCO 2 in capillary blood is 45 mm Hg. Similarly, the
PO 2 of capillary blood is 40 mm Hg.
 48
 Each gas diffuses between the blood and its surrounding tissues from areas of high partial
pressure to areas of low partial pressure, until the partial pressure in the areas reaches
equilibrium.
 When blood passes through pulmonary capillary, RBC is exposed to oxygen only for 0.75
second at rest and only for 0.25 second during severe exercise. So, diffusion of oxygen must
be quicker and effective. Fortunately, this is possible because of pressure gradient.

 Partial pressure of oxygen in the pulmonary capillary is 40 mm Hg and in the alveoli, it is

104 mmHg. Pressure gradient is 64 mm Hg. It facilitates the diffusion of oxygen from
alveoli into the blood.
 Partial pressure of carbon dioxide in alveoli is 40 mm Hg whereas in the blood it is 45 mm
Hg. Pressure gradient of 5 mm Hg is responsible for the diffusion of carbon dioxide from
blood into the alveoli. In atmospheric air, partial pressure of carbon dioxide is very
insignificant and is only about 0.3 mm Hg whereas, in the alveoli, it is 40 mm Hg. So,
carbon dioxide enters passes to atmosphere from alveoli easily.
 The blood then leaves the lungs with a PO 2 of 104 mm Hg and PCO 2 of 40 mm Hg.
3. Internal (Tissue) respiration
 Blood flows from the lungs through the left side of the heart to the tissue capillaries.
Internal respiration refers to the exchange of gases in the tissues.
 Gas exchange does not occur across the walls of the arteries carrying blood from the heart to
the tissues, because their walls are too thick.
 Partial pressure of oxygen in venous end of pulmonary capillary is 104 mm Hg. However,
partial pressure of oxygen in the arterial end of systemic capillary is only 95 mm Hg. It may
be because of physiological shunt in lungs. Due to venous admixture in the shunt, 2% of
blood reaches the heart without being oxygenated. Average oxygen tension in the tissues is
40 mm Hg. It is because of continuous metabolic activity and constant utilization of oxygen.
Thus, a pressure gradient of about 55 mm Hg exists between capillary blood and the tissues
so that oxygen can easily diffuse into the tissues.
 Due to continuous metabolic activity, carbon dioxide is produced constantly in the cells of
tissues. So, the average partial pressure of carbon dioxide is high in the cells and is about 45
 49
mm Hg. Partial pressure of carbon dioxide in arterial blood is 40 mm Hg. Pressure gradient
of 5 mm Hg is responsible for the diffusion of carbon dioxide from tissues to the blood.
 50
OXYGEN AND CARBON DIOXIDE TRANSPORT
 Blood serves to transport the respiratory gases. Oxygen, which is essential for the cells, is
transported from alveoli of lungs to the cells. Carbon dioxide, which is the waste product in
cells, is transported from cells to lungs.
Transport of Oxygen
 Oxygen is transported from alveoli to the tissue by blood in two forms:
1. As Simple Solution
2. In Combination with Hemoglobin
1. Simple Solution:
 Oxygen dissolves in water of plasma and is transported in this physical form. Amount of
oxygen transported in this way is very negligible. It forms only about 1.5% of total oxygen
in blood. It is because of poor solubility of oxygen in water content of plasma.
2. Combination with Hemoglobin
 Oxygen combines with hemoglobin in blood and is transported as oxy-hemoglobin.
Transport of oxygen in this form is important because, maximum amount (98.5 %) of
oxygen is transported by this method.
 Oxygen combines with the iron in heme part of hemoglobin. Each molecule of hemoglobin
contains 4 atoms of iron. Normal heme contains iron in the reduced form (Fe 2+ or ferrous
iron). In this form, the iron can share electrons and bond with oxygen to form
oxyhemoglobin. Each iron atom combines with one molecule of oxygen.
 Oxygen and hemoglobin bind in an easily reversible reaction to form oxyhemoglobin:

 Hemoglobin accepts oxygen readily whenever the partial pressure of oxygen in the blood is
more. Hemoglobin gives out oxygen whenever the partial pressure of oxygen in the blood is
less.
 In the lungs, PO 2 normally is sufficiently high so that hemoglobin holds as much O 2 as it
can. In the tissues, PO2 is lower because the tissues are using O 2 . Consequently, hemoglobin
releases O 2 , in the tissues. Oxygen then diffuses into the cells, which use it in cellular
respiration. At rest, approximately 23% of the O 2 , picked up by hemoglobin in the lungs is
released to the tissues.

 When oxyhemoglobin dissociates to release oxygen to the tissues, the heme iron is still in
the reduced (Fe2+) form and the hemoglobin is called deoxyhemoglobin, or reduced
hemoglobin.
 The amount of O 2 , released from oxy-hemoglobin is influenced by four factors. More O2 is
released from hemoglobin if (1) the PO2 is low, (2) the PCO 2 , is high, (3) the pH is low, and
(4) the temperature is high.
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 Increased muscular activity results in a decreased PO 2 , an increased PCO 2 , a reduced pH,
and an increased temperature. Consequently, during physical exercise, as much as 73% of
the O 2 picked up by hemoglobin in the lungs is released into skeletal muscles.
Transport of Carbon Dioxide
 Blood flowing through capillaries gains carbon dioxide because tissues have a relatively
high PCO 2 . Blood transports carbon dioxide to the lungs in one of three forms:
 Carbon dioxide is transported in the blood in three ways:
1. As dissolved form (7%)
2. As carbamino compounds (23%).
3. As bicarbonate (70%)
1. Dissolved CO2
 Carbon dioxide diffuses into blood and dissolves in the fluid of plasma forming a simple
solution. The amount of carbon dioxide that dissolves in plasma is determined by its partial
pressure. The higher the PCO 2 of the tissues, the more carbon dioxide will go into solution.
 However, only about 7% of the carbon dioxide that blood transports is in this form. Only
about 3 mL/100 mL of plasma of carbon dioxide is transported as dissolved state. On
reaching the lungs, it diffuses into alveolar air and is exhaled.
2. Carbamino compounds
 Carbon dioxide is transported in blood in combination with hemoglobin and plasma
proteins. Carbon dioxide combines with hemoglobin to form carbamino hemoglobin or
carbhemoglobin.
 The main CO 2 binding sites are the terminal amino acids in the two alpha and two beta
globin chains. Unlike oxygen, which binds the iron atoms (part of the “heme” part) of
hemoglobin molecules, carbon dioxide bonds with the amino groups (–NH2 ) of the “globin”
or protein portion of these molecules.

 The cabon dioxide also combines with plasma proteins to form carbamino proteins.
Carbamino hemoglobin and carbamino proteins are together called carbamino compounds.
 The formation of carbaminohemoglobin is greatly influenced by PCO 2 . For example, in
tissue capillaries PCO 2 is relatively high, which promotes formation of
carbaminohemoglobin. But in pulmonary capillaries, PCO 2 is relatively low, and the CO 2
readily splits apart from globin and enters the alveoli by diffusion.
 Transporting carbon dioxide this way is theoretically quite effective, but
carbaminohemoglobin forms slowly. Only about 23% of the carbon dioxide that blood
transports is in this form.
3. Bicarbonate ions
 The greatest percentage of CO 2 , about 70%—is transported in blood plasma as bicarbonate
ions (HCO 3 -). As CO 2 diffuses into systemic capillaries and enters red blood cells, it reacts
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with water in the presence of the enzyme carbonic anhydrase (CA) to form carbonic acid,
which dissociates into H+ and HCO 3 -.

 This reaction occurs slowly in plasma, but much of the carbon dioxide diffuses into red
blood cells. These cells have the enzyme carbonic anhydrase, which speeds the reaction
between carbon dioxide and water.

 Carbonic acid is very unstable. Almost all carbonic acid (99.9%) formed in red blood
corpuscles, dissociates into bicarbonate and hydrogen ions. Concentration of bicarbonate
ions in the cell increases more and more. Due to high concentration, bicarbonate ions diffuse
through the cell membrane into plasma.

 When the negatively charged bicarbonate ions move out of RBC into the plasma, the
negatively charged chloride ions move into the RBC in order to maintain the electrolyte
equilibrium. Anion exchanger, which acts like antiport pump in RBC membrane is
responsible for the exchange of bicarbonate ions and chloride ions.
 Bicarbonate ions combine with sodium ions in the plasma and form sodium bicarbonate. In
this form, it is transported in the blood.
 When blood reaches the alveoli, sodium bicarbonate in plasma dissociates into sodium and
bicarbonate ions. Bicarbonate ion moves into the RBC. It makes chloride ion to move out of
the RBC into the plasma, where it combines with sodium and forms sodium chloride.
Bicarbonate ion inside the RBC combines with hydrogen ion forms carbonic acid, which
dissociates into water and carbon dioxide. Carbon dioxide is then expelled out.
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REGULATION OF RESPIRATION
 Normal breathing is a rhythmic, involuntary act that continues even when a person is
unconscious. The respiratory muscles, however, are also under voluntary control.
 The normal rate of breathing in adults is between 12 and 20 breaths per minute. In children,
the rates are higher and may vary from 20 to 40 per minute.
 The rate of breathing is determined by the number of times respiratory muscles are
stimulated. The basic rhythm of breathing is controlled by neurons within the medulla
oblongata that stimulate the muscles of respiration.
Respiratory Areas
 Groups of neurons in the brainstem form the respiratory areas, which control both
inspiration and expiration. The components of the respiratory areas are widely scattered
throughout the pons and medulla oblongata.

 Two parts of the respiratory areas are of special interest: the respiratory center of the
medulla and the respiratory group of the pons.
1. The medullary respiratory center includes two bilateral groups of neurons that extend
throughout the length of the medulla oblongata. They are called the dorsal respiratory
group and the ventral respiratory group.
a. Dorsal respiratory group of neurons are diffusely situated in the upper part of the
medulla oblongata. Usually, these neurons are collectively called inspiratory center.
The dorsal respiratory group is primarily responsible for stimulating contraction of the
diaphragm.
b. Ventral respiratory group has both inspiratory and expiratory neurons. Earlier, the
ventral group neurons were collectively called expiratory center.
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The ventral respiratory group is primarily responsible for stimulating the external
intercostal, internal intercostal, and abdominal muscles.
Normally, ventral group neurons are inactive during quiet breathing and become active
during forced breathing. During forced breathing, these neurons stimulate both
inspiratory muscles and expiratory muscles.
The respiratory areas are located in the pons and the medulla oblongata

2. Neurons in another part of the brainstem, the pons, form the pontine respiratory group.
a. Apneustic center is situated in the reticular formation of lower pons. Apneustic center
increases depth of inspiration by acting directly on dorsal group neurons.
b. Pneumotaxic center is situated in the dorsolateral part of reticular formation in upper
pons. Primary function of pneumotaxic center is to control the medullary respiratory
centers, particularly the dorsal group neurons. It acts through apneustic center.
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Pneumotaxic center inhibits the apneustic center so that the dorsal group neurons are
inhibited. Because of this, inspiration stops and expiration starts. Thus, pneumotaxic
center influences the switching between inspiration and expiration. Pneumotaxic
center increases respiratory rate by reducing the duration of inspiration.
Generation of Rhythmic Breathing
 The medullary respiratory center generates the basic pattern of spontaneous, rhythmic
breathing. Although the precise mechanism is not well understood, the generation of
rhythmic breathing involves the integration of stimuli that start and stop inspiration.
1. Starting inspiration: The neurons in the medullary respiratory center that promote
inspiration are continuously active.
The medullary respiratory center constantly receives stimulation from many sources, such as
receptors that monitor blood gas levels and the movements of muscles and joints. In addition
stimulation can come from parts of the brain concerned with voluntary respiratory
movements and emotions.
When the inputs from all these sources reach a threshold level, somatic nervous system
neurons stimulate respiratory muscles via action potentials, and inspiration starts.
2. Increasing inspiration: Once inspiration begins, more and more neurons are activated. The
result is progressively stronger stimulation of the respiratory muscles, which lasts for
approximately 2 seconds (s).
3. Stopping inspiration: The neurons stimulating the muscles of respiration also stimulate the
neurons in the medullary respiratory center that are responsible for stopping inspiration.
The medullary respiratory center and the pontine respiratory group control breathing

The neurons responsible for stopping inspiration also receive input from the ponrine
respiratory neurons, stretch receptors in the lungs, and probably other sources.
When the inputs to these neurons exceed a threshold level, they cause the neurons
stimulating respiratory muscles to be inhibited. Relaxation of respiratory muscles results in
expiration, which lasts approximately 3 s. The next inspiration begins with step 1.
 Although the medullary neurons establish the basic rate and depth of breathing their
activities can be influenced by input from other parts of the brain and from peripherally
located receptors.
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Regulation of the Respiratory Center
 The basic rhythm of respiration set and coordinated by the inspiratory area can be modified
in response to inputs from other brain regions, receptors in the peripheral nervous system,
and other factors.
1. Cortical Influences on Respiration: Because the cerebral cortex has connections with the
respiratory center, we can voluntarily alter our pattern of breathing. We can even refuse to
breathe at all for a short time. Voluntary control is protective because it enables us to
prevent water or irritating gases from entering the lungs. The ability to not breathe, however,
is limited by the buildup of CO 2 and H in the body. When PCO 2 and H concentrations
increase to a certain level, the inspiratory area is strongly stimulated, nerve impulses are sent
along the phrenic and intercostal nerves to inspiratory muscles, and breathing resumes,
whether the person wants it to or not.
Nerve impulses from the hypothalamus and limbic system also stimulate the respiratory
center, allowing emotional stimuli to alter respirations as, for example, in laughing and
crying.
2. Chemoreceptor Regulation of Respiration: Chemoreceptors monitor levels of CO 2 , H+, and
O2 and provide input to the respiratory center.
Two groups of chemoreceptors respond to changes in blood chemistry. These are
Central chemoreceptors sense changes in the cerebrospinal fluid (CSF) levels of carbon
dioxide and hydrogen ions. If either level rises, the central chemoreceptors signal the
respiratory areas, and respiratory rate and tidal volume increase. As a result of the increased
ventilation, more carbon dioxide is exhaled, the blood and CSF levels of these chemicals
fall, and breathing rate decreases.
Peripheral chemoreceptors are in the walls of certain large arteries (the carotid arteries and
the aorta) in the neck and thorax sense changes in blood oxygen levels. Stimulated
peripheral chemoreceptors transmit impulses to the respiratory areas, increasing the
breathing rate. However, blood oxygen levels must be very low to trigger this mechanism.
Thus, oxygen plays only a minor role in the control of normal respiration.
3. Proprioceptor Stimulation of Respiration: Proprioceptors are the receptors which give
response to change in the position of body. These receptors are situated in joints, tendons
and muscles. Proprioceptors are stimulated during the muscular exercise and send impulses
to brain, particularly cerebral cortex, through somatic afferent nerves. Cerebral cortex in
turn causes hyperventilation by sending impulses to medullary respiratory centers.
4. The Inflation Reflex: An inflation reflex helps regulate the depth of breathing. This reflex
occurs when stretched lung tissues stimulate stretch receptors in the visceral pleura,
bronchioles, and alveoli. The sensory impulses of this reflex travel via the vagus nerves to
the pontine respiratory group and shorten the duration of inspiratory movements. This action
prevents over inflation of the lungs during forceful breathing.
5. Other Influences on Respiration: Other factors that contribute to regulation of respiration
include the following:
Limbic system stimulation: Anticipation of activity or emotional anxiety like fear may
stimulate the limbic system, which then sends excitatory input to the inspiratory area,
increasing the rate and depth of ventilation.
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Temperature: An increase in body temperature, as occurs during a fever or vigorous
muscular exercise, increases the rate of respiration. A decrease in body temperature
decreases respiratory rate. A sudden cold stimulus (such as plunging into cold water) causes
temporary apnea, an absence of breathing.
Pain: A sudden, severe pain brings about brief apnea, but a prolonged somatic pain
increases respiratory rate. Visceral pain may slow the rate of respiration.
Stretching the anal sphincter muscle: This action increases the respiratory rate and is
sometimes used to stimulate respiration in a newborn baby or a person who has stopped
breathing.
Irritation of airways: Physical or chemical irritation of the pharynx or larynx brings about
an immediate cessation of breathing followed by coughing or sneezing.
Blood pressure: The carotid and aortic baroreceptors that detect changes in blood pressure
have a small effect on respiration. A sudden rise in blood pressure decreases the rate of
respiration, and a drop in blood pressure increases the respiratory rate.
LUNG VOLUMES AND CAPACITIES

 Respiratory volumes are measures of the amount of air movement during different portions
of ventilation, whereas respiratory capacities are sums of two or more respiratory volumes.
 Spirormetry is the process of measuring volumes of air that move into and out of the
respiratory system and the spirorneter is the device that measures these respiratory volumes.
 Measurements of the respiratory volumes can provide information about the health of the
lungs.
 One inspiration plus the following expiration is called a respiratory cycle.
Lung Volumes
1. Tidal volume (TV): The amount of air inhaled or exhaled during each cycle of quiet
breathing. It is 500 milliliters (mL).
2. Total minute volume: Multiplying the tidal volume at rest by the number of breaths per
minute yields a total minute volume of about 6 L per minute.
3. Inspiratory reserve volume (IRV): Volume that can be inhaled during forced breathing in
addition to tidal volume, it equals about 3,300 mL.
4. Expiratory reserve volume (ERV): Volume that can be exhaled during forced breathing in
addition to tidal volume. During forced expiration, the lungs can expel up to about 1,000 mL
of air beyond the resting tidal volume.
5. Residual volume (RV): Volume that cannot be exhaled. Even after the most forceful
expiration, about 1,200 mL of air remains in the lungs.
Lung Capacities
 In describing events in the pulmonary cycle, it is sometimes desirable to consider two or
more of the volumes together. Such combinations are called pulmonary capacities.
1. Vital capacity (VC): Maximum amount of air that can be exhaled after taking the deepest
breath possible. Combining the inspiratory reserve volume (3,300 mL) with the tidal volume
(500 mL) and the expiratory reserve volume (1,000 mL) gives the vital capacity (4,800 mL).
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VC = TV +IRV+ERV
2. Inspiratory capacity (1C): This is the amount of air that can be inspired with maximum
effort. It consists of the tidal volume (500 ml) plus the inspiratory reserve volume (3300 ml).
Inspiratory capacity is 3800 ml.
3. Functional residual capacity (FRC): This is the amount of air remaining in the air
passages and alveoli at the end of quiet expiration. The sum of the residual volume and
expiratory reserve volume (2,200 mL).
4. Total lung capacity (TLC): Total volume of air that the lungs can hold. The total lung
capacity (about 6,000 mL) varies with age, sex, and body size.
TLC = VC +RV
 Some of the air that enters the respiratory tract during breathing does not reach the alveoli.
This volume (about 150 mL) remains in the passageways of the trachea, bronchi, and
bronchioles. Because gas is not exchanged through the walls of these passages, this air is
said to occupy anatomic dead space.
Lung Volumes and Capacities

HYPOXIA
 Hypoxia is defined as reduced availability of oxygen to the tissues. The term anoxia refers to
absence of oxygen. In olden days, the term anoxia was in use. Since there is no possibility
for total absence of oxygen in living conditions, use of this term is abandoned.
Classification and Causes of Hypoxia
 Four important factors which leads to hypoxia are: 1. Oxygen tension in arterial blood 2.
Oxygen carrying capacity of blood 3. Velocity of blood flow 4. Utilization of oxygen by the
cells.
 On the basis of above factors, hypoxia is classified into four types:
1. Hypoxic hypoxia
2. Anemic hypoxia
3. Stagnant hypoxia
4. Histotoxic hypoxia
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1. Hypoxic Hypoxia
 Hypoxic hypoxia means decreased oxygen content in blood. It is also called arterial
hypoxia.
 Causes for hypoxic hypoxia: Hypoxic hypoxia is caused by four factors.
a) Low oxygen tension in inspired (atmospheric) air, which does not provide enough
oxygen. Oxygen tension in inspired air is reduced in the following conditions: high
altitude, while breathing air in closed space and while breathing gas mixture containing
low partial pressure of oxygen (PO 2 ).
b) Respiratory disorders associated with decreased pulmonary ventilation, which does not
allow intake of enough oxygen. Pulmonary ventilation decreases in the following
conditions: obstruction of respiratory passage as in asthma, nervous and mechanical
hindrance to respiratory movements as in poliomyelitis, depression of respiratory centers
as in brain tumors, and pneumothorax.
c) Respiratory disorders associated with inadequate oxygenation in lungs, which does not
allow diffusion of enough oxygen. Inadequate oxygenation of blood in lungs occurs in
the following conditions: impaired alveolar diffusion as in emphysema, presence of non-
functioning alveoli as in fibrosis, filling of alveoli with fluid as in pulmonary edema,
pneumonia, pulmonary hemorrhage and collapse of lungs as in bronchiolar obstruction.
d) Cardiac disorders, in which enough blood is not pumped to transport oxygen. In these
conditions, in spite of oxygen availability and entrance of oxygen into the alveoli, it
cannot diffuse into the blood. In congestive heart failure, oxygen availability and
diffusion are normal, but the blood cannot be pumped from heart properly.
 Characteristic features of hypoxic hypoxia: Hypoxic hypoxia is characterized by reduced
oxygen tension in arterial blood. All other features remain normal.
2. Anemic Hypoxia
 Anemic hypoxia is the condition characterized by the inability of blood to carry enough
amount of oxygen. Oxygen availability is normal. But the blood is not able to take up
sufficient amount of oxygen due to anemic condition.
 Causes for anemic hypoxia: Any condition that causes anemia can cause anemic hypoxia. It
is caused by the following conditions:
a) Decreased number of RBCs. RBC decreases in conditions like bone marrow diseases,
hemorrhage, etc.
b) Decreased hemoglobin content in the blood. Conditions which decrease the RBC count
or change the structure, shape and size of RBC (microcytes, macrocytes, spherocytes,
sickle cells, poikilocytes, etc.) can decrease the hemoglobin content in blood.
c) Formation of altered hemoglobin. Poisoning with chlorates, nitrates, ferricyanides,
etc. causes oxidation of iron into ferric form and the hemoglobin is known as
methemoglobin. Methemoglobin cannot combine with oxygen. Thus, the quantity of
hemoglobin available for oxygen transport is decreased.
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d) Combination of hemoglobin with gases other than oxygen and carbon dioxide. When
hemoglobin combines with carbon monoxide, hydrogen sulfide or nitrous oxide, it
looses the capacity to transport oxygen.

 Characteristic features of anemic hypoxia: Anemic hypoxia is characterized by decreased

oxygen carrying capacity of blood. All other features remain normal.
3. Stagnant Hypoxia
 Stagnant hypoxia is the hypoxia caused by decreased velocity of blood flow. It is otherwise
called hypokinetic hypoxia.
 Causes for stagnant hypoxia: Stagnant hypoxia occurs mainly due to reduction in velocity
of blood flow. Velocity of blood flow decreases in the following conditions: congestive
cardiac failure, hemorrhage, surgical shock, vasospasm, thrombosis and embolism.
 Characteristic features of stagnant hypoxia: Stagnant hypoxia is characterized by decreased
velocity of blood flow. All other features remain normal.
4. Histotoxic Hypoxia
 Histotoxic hypoxia is the type of hypoxia produced by the inability of tissues to utilize
oxygen.
 Causes for histotoxic hypoxia: Histotoxic hypoxia occurs due to cyanide or sulfide
poisoning. These poisonous substances destroy the cellular oxidative enzymes and there is a
complete paralysis of cytochrome oxidase system. So, even if oxygen is supplied, the
tissues are not in a position to utilize it.
 Characteristic features of histotoxic hypoxia: Histotoxic hypoxia is characterized by
inability of tissues to utilize oxygen even if it is delivered. All other features remain normal.
Characteristic features of different types of hypoxia