The respiratory system allows for gas exchange between the lungs and blood. Respiration involves the intake of oxygen and exhalation of carbon dioxide. It occurs through the processes of inspiration and expiration, facilitated by respiratory muscles. During inspiration, air enters the lungs through the trachea and bronchial tree down to alveoli. Gas exchange occurs across the respiratory membrane in the alveoli. Oxygen and carbon dioxide are transported in the blood and tissues through diffusion and chemical reactions. Expiration then occurs, expelling air from the lungs.

2. RESPIRATORY SYSTEM
 Respiration is the process by which oxygen is taken in and
carbondioxide is given out.
 The normal respiratory rate in adults is 12 to 16 per minute.
 Respiration is classified in to two types;
1. External respiration that involves exchange of
respiratory gases between lungs and blood.
2. Internal respiration which involves exchange of gases
between blood and tissues.
 Respiration occurs in two stages:
1. Inspiration during which the air enters the lungs.
2. Expiration during which the air leaves the lungs.
FUNCTIONS OF RESPIRATORY SYSTEM
The primary function of respiratory system is gaseous exchange.

3. Other non-respiratory functions are as follows;
1. Olfaction: Olfactory receptors are present on nasal mucosa.
2. Vocalization: Larynx assists in vocalization or speech
3. Prevention of dust particles: Done by the filtering action of hairs
in the nasal mucosa.
4. Defense mechanism: Done by leucocytes, mast cells, macrophages
etc.
5. Maintenance of water balance: During expiration, small amount
of water is lost by evaporation
6. Regulation of body temperature: During expiration heat is also
lost.
7. Regulation of acid base balance: By regulating CO2 content in
blood
8. Anticoagulant function: Mast cells in lungs secrete heparin
9. Secretion of angiotensin converting enzyme: Pulmonary capillary
endothelium secretes ACE
10.Synthesis of hormonal substances: Synthesize prostaglandins,
acetylcholine and serotonin

6. • Trachea bifurcates in to two
main or primary bronchi,
right and left bronchi.
• Each primary bronchi
divides in to secondary
bronchi.
• Secondary bronchi then
divides in to tertiary
bronchi.
• Tertiary bronchi divides
several times with reduction
in length and diameter
• When the diameter of
bronchioles becomes 1 mm
or less, it is called terminal
bronchiole
• Terminal bronchiole
continues or divides in to
respiratory bronchiole,
which has a diameter of 0.5
mm

8. RESPIRATORY UNIT.
• is composed of a respiratory
bronchiole, alveolar ducts, atria,
and alveoli.
• Starts from respiratory
bronchiole. It divides in to
alveolar ducts which enters in to
an enlarged structure called
alveolar sac. The space inside
alveolar sac is called antrum or
atrium
• Alveolar sac consists of a cluster
of alveoli
• It is the structural and functional
unit of respiratory system
• It is the region where exchange
of gases between blood and
alveoli takes place

9. • There are about 300
million alveoli in the
two lungs
• Each alveolus is like
a pouch with an
average diameter of
about 0.2 to 0.5
millimetre.
• It is lined by
epithelial cells called
alveolar cells or
pneumocytes.
• Alveolar cells are of
two types; type I and
type II.

10. SURFACTANT AND ITS EFFECT ON SURFACE TENSION.
• Pulmonary surfactant is a surface active agent that reduces the
surface tension on the alveolar membrane.
• It is secreted by called
• Type II alveolar epithelial cells are the special surfactant-
secreting epithelial cells seen on the surface of the alveoli.
• Clara cells are the specialized cells situated on bronchioles
also secrete small amounts of surfactant
• Surfactant is a lipoprotein complex formed by phospholipids
(dipalmitoylphosphatidylcholine), surfactant apoproteins, and
calcium ions.
• Functions:
• Reduces the surface tension in the alveoli of lungs and
prevent collapsing tendency of lungs.
• Causes inflation of lungs after birth
• Hydrophilic proteins present in surfactant plays a role in
defense mechanism by destroying the bacteria and viruses

11. RESPIRATORY DISTRESS SYNDROME(RDS)
• It is a condition caused by deficiency or absence of surfactant
in infants resulting in collapse of lungs.
• It is also called hyaline membrane disease
• in hyaline membrane disease (also called respiratory distress
syndrome), which often occurs in newborn premature
babies, the quantity of surfactant secreted by the alveoli is so
greatly depressed that the surface tension of the alveolar
fluid becomes several times normal. This causes a serious
tendency for the lungs of these babies to collapse or to
become filled with fluid. This may leads to death due to
suffocation.

12. PULMONARY VENTILATION AND ALVEOLAR VENTILATION
• The volume of air entering and leaving the nose or mouth per
minute, the respiratory minute volume or pulmonary ventilation.
Normal value is 6L/ minute.
Pulmonary Ventilation = Tidal Volume X Respiratory Rate
• 500 ML x 12/minute
• 6000 ml or 6L/minute
• Alveolar ventilation the volume of air entering and leaving the
alveoli per minute. It is the amount of air utilized for gaseous
exchange.
Normal value is 4200ml or 4.2L/minute
Alveolar Ventilation = (Tidal Volume – Dead Space ) X Respiratory
Rate
= (500 - 150) x 12
= 4200 ml/minute

13. DEAD SPACE
• The part of the respiratory tract where gaseous exchange does
not take place is called dead space. Normal dead space volume is
150 ml. It is of two types;
1. Anatomical dead space includes conducting zone of
respiratory tract i.e. nose, pharynx, trachea, bronchi and
bronchioles up to terminal bronchioles
2. Physiological dead space: The anatomic dead space plus the
alveolar dead space is known as the physiologic dead space
Physiologic dead space = Anatomic dead space + Alveolar dead
space
• The alveolar dead space is the volume of gas
• that enters unperfused alveoli per breath i.e. alveoli that are
ventilated but not perfused with pulmonary capillary blood
• that enters non-functional alveoli i.e. due to destruction of
alveolar membrane or due to respiratory diseases.

14. RESPIRATORY MEMBRANE
• Gas exchange between the alveolar air and the pulmonary
blood occurs through the respiratory membrane, also called
the pulmonary membrane.
• The following different layers of the respiratory membrane:
1. A layer of fluid lining the alveolus and containing surfactant
that reduces the surface tension of the alveolar fluid
2. The alveolar epithelium composed of thin epithelial cells
3. An epithelial basement membrane
4. A thin interstitial space between the alveolar epithelium
and the capillary membrane
5. A capillary basement membrane that in many places fuses
with the alveolar epithelial basement membrane
6. The capillary endothelial membrane

16. DIFFUSION OF GASES or EXCHANGE OF GASES
• Diffusion of a gas occurs when there is a net movement of
molecules from an area in which that particular gas exerts a
high partial pressure to an area in which it exerts a lower
partial pressure
• Diffusing capacity is defined as the volume of gas that
diffuses through respiratory membrane each minute for a
pressure gradient of 1mm Hg
• For oxygen it is 21 mL/minute/1mmHg. For carbondioxide it
is 400 mL/minute/1mmHg.
• Diffusing capacity
• is directly proportional to pressure gradient, solubility of
the gas and total surface area of respiratory membrane.
• is inversely proportional to molecular weight of the gas
and the thickness of the membrane.

17. DIFFUSION OF OXYGEN
1. From atmospheric air to alveoli:
• PO2 of atmospheric air = 159 mmHg
• PO2 in the alveoli =104 mmHg
• Due to the pressure gradient of 55 mmHg, oxygen diffuses
from atmospheric air to the alveoli.
2. From alveoli in to blood
• PO2 in the pulmonary capillary = 40 mmHg
• PO2 in the alveoli =104 mmHg
• Pressure gradient of 64 mmHg facilitates diffusion of oxygen
from alveoli in to blood. This pressure gradient make this
diffusion quicker and effective because when the blood
flowing through pulmonary capillaries, RBC is exposed to
oxygen only for few seconds .

18.  From blood in to tissues
 PO2 in the venous end of pulmonary capillary = 104 mmHg
 PO2 in the arterial end and systemic capillary = 95 mmHg
(physiological shunt)
 PO2 in tissues = 40mmHg(due to continuous metabolic
activity and constant utilization of oxygen)
 A pressure gradient of 55 mmHg exists between capillary
blood and the tissues so that oxygen can easily diffuse in to
the tissues.

19. DIFFUSION OF CARBONDIOXIDE
1. From tissues in to blood
• PCO2 in the arterial blood = 40 mmHg
• PCO2 in tissues = 46 mmHg due to metabolic reactions
carbon dioxide is produced constantly in tissues.
• CO2 diffuses from tissues in to blood.
2. From blood to alveoli:
• PCO2 of blood = 46 mmHg
• PCO2 in the alveoli = 40mmHg
• Due to the pressure gradient of 6 mmHg, CO2 diffuses from
blood in to the alveoli.
3. From alveoli in to the atmospheric air
• PCO2 in the atmospheric air = 0.3 mmHg
• PCO2 in the alveoli = 40 mmHg
• CO2 diffuses from the alveoli in to atmospheric air

20. .
TRANSPORT OF OXYGEN
• Normally, about 97 per cent of the oxygen transported from the
lungs to the tissues is carried in chemical combination with
haemoglobin in the red blood cells.
• The remaining 3 per cent is transported in the dissolved state in
the water of the plasma and blood cells. The amount of oxygen
transported in this form is about 0.3 ml/ 100 ml of plasma.
• The oxygen molecule combines loosely and reversibly with
the heme portion of haemoglobin.
• When PO2 is high, as in the pulmonary capillaries, oxygen
binds with the haemoglobin, but when PO2 is low, as in the
tissue capillaries, oxygen is released from the haemoglobin
• Oxygen carrying capacity of blood is amount of oxygen
transported by haemoglobin of blood. One gram of
haemoglobin carry 1.34 ml of oxygen.

21. OXYGEN-HEMOGLOBIN DISSOCIATION CURVE
• It demonstrates the relationship between partial pressure of
oxygen and percent saturation of haemoglobin with oxygen.
• It explains affinity of haemoglobin to oxygen.
• A progressive increase in the percentage of haemoglobin
bound with oxygen as blood PO2 increases is called the per
cent saturation of haemoglobin.
• Under normal conditions the curve is sigmoid shaped. The
lower part indicates dissociation and upper part of the curve
indicates association of haemoglobin with oxygen depending
upon PO2 .
• When the PO2 is about 40 mm Hg, and the saturation of
haemoglobin averages 75 per cent. The haemoglobin
saturation is 50% at PO2 25 – 27 mmHg.

23. Bohr’s effect
• It is a physiological phenomenon described by Christian
Bohr stating that “oxygen binding capacity of hemoglobin in
inversely proportional to the concentration of carbon
dioxide and hydrogen ion concentration.”
• It is the effect by which the presence of carbon dioxide
decreases the affinity of hemoglobin for oxygen.
• In the tissues due to continuous metabolic activities, the
partial pressure of carbon dioxide is very high and it enters
the blood. The presence of carbon dioxide in blood
decreases the affinity of haemoglobin for oxygen so that
oxygen is released form blood in to the tissues. The oxygen
dissociation curve shifts to the right.
• In the lungs due to decreased carbon dioxide and hydrogen
ion concentration, oxygen curve shift to left.
• Bohr’s effect facilitates oxygen release in tissues and uptake
in lungs.

24. TRANSPORT OF CARBON DIOXIDE IN THE BLOOD

25. TRANSPORT OF CARBON DIOXIDE IN THE DISSOLVED STATE.
• A small portion of the carbon dioxide is transported in the
dissolved state to the lungs
• Only about 0.3 millilitre of carbon dioxide is transported in
the dissolved form by each 100 millilitres of blood flow.
• This is about 7 per cent of all the carbon dioxide normally
transported.

26. TRANSPORT OF CARBON DIOXIDE AS CARBAMINO COMPOUNDS.
• About 23% of CO2 is transported as carbaminocompouds
• Carbondioxide reacts directly with amine radicals of the
haemoglobin molecule to form the compound
carbaminohemoglobin (CO2Hb).
CO2 +Haemoglobin = CARBAMINOHEMOGLOBIN
• A small amount of carbon dioxide also reacts in the same way
with the plasma proteins in the tissue capillaries to form
carbamino proteins.
CO2+Plasma Proteins =CARBAMINO PROTEINS
CARBAMINOHEMOGLOBIN + CARBAMINO PROTEINS= CARBAMINO
COMPOUNDS

27. TRANSPORT OF CARBON DIOXIDE IN THE FORM OF BICARBONATE
ION
• About 70% of CO2 is transported as bicarbonate ions
• Reaction of carbon dioxide with water to form carbonic acid
occurs in the red blood cells and the reaction is accelerated in the
presence of carbonic anhydrase.
• In another fraction of a second, the carbonic acid formed in the
red cells (H2CO3) dissociates into hydrogen and bicarbonate ions
(H+ and HCO3 –).
• Due to concentration gradient, bicarbonate ions diffuse from the
red cells into the plasma in exchange of chloride ions.
Bicarbonate ions then bind with sodium and transported as
sodium bicarbonate.
• Most of the hydrogen ions then combine with the haemoglobin
to form hemoglobinic acid in the red blood cells.

28. CHLORIDE SHIFT OR HAMBURGER PHENOMENON
• It is the exchange of a chloride ion for a bicarbonate ion across
the red cell membrane
• It occurs when carbondioxide enters blood from tissues.
• In plasma, sodium chloride dissociates in to sodium and
chloride ions.
• When the negatively charged bicarbonate ions move out of
RBC in to the plasma, the negatively charged chloride ions
move in to the RBC, in order to maintain electrical equilibrium.
REVERSE CHLORIDE SHIFT
• It occurs in lungs
• When blood reaches alveoli, sodium bicarbonate in the
plasma dissociates in to sodium and bicarbonate ions.
• Bicarbonate ion moves in to RBC in exchange of chloride ion
• In plasma chloride ions combine with sodium and forms
sodium chloride

29. HALDANE EFFECT
• It is the effect by which combination of oxygen
with haemoglobin displaces carbondioxide from
haemoglobin
• The excess of oxygen content causes shift of
carbondioxide curve to the right
• Haldane effect is essential for release of
carbondioxide from blood in the alveoli of lungs
and uptake of oxygen by the blood

30. • Movement of lungs is accomplished with the help of respiratory
muscles. They are of two types:
 Inspiratory muscles which are involved in inspiration.
1. Primary inspiratory muscles are diaphragm and
external intercostal muscles; are responsible for change
in size of thoracic cage during normal quiet breathing.
External intercostals helps to raise the rib cage.
2. Accessory inspiratory muscles are
sternocleidomastoid, scaleni, anterior serrati, elevators
of scapulae and pectorals. They assist primary
inspiratory muscles during forced breathing.
1. Sternocleidomastoid muscles, which lift upward
on the sternum;
2. Anterior serrati, which lift many of the ribs; and
3. scaleni, which lift the first two ribs

31.  Expiratory muscles participating in expiration. These
muscles pull the rib cage downward during expiration.
1. Primary expiratory muscles are internal intercostal
muscles.
2. Accessory expiratory muscles are abdominal muscles
• The lungs can be expanded and contracted in two ways:
1. by downward and upward movement of the
diaphragm to increase or decrease vertical
diameter of the chest cavity
2. by elevation and depression of the ribs to
increase and decrease the anteroposterior(pump
handle movement) and transverse diameter
(bucket handle movement)of the chest cavity.

32. During inspiration, due to the enlargement of thoracic cage, the
negative pressure is increased in the thoracic cavity. It causes
expansion of the lungs. During expiration, thoracic cavity decreases
in size to the preinspiratory position. The pressure in the thoracic
cavity also come back to preinspiratory level. It compresses the
lung tissues so that the air is expelled out of the lungs.

33. Nervous Regulation Of Respiration- Respiratory Centre
• The respiratory centre is composed of several groups of neurons
located bilaterally in the medulla oblongata and pons of the
brain stem
• It is divided into two major collections of neurons:
• Medullary centres located in medulla oblongata
1. A dorsal respiratory group, located in the dorsal portion
of the medulla, which mainly causes inspiration;
2. A ventral respiratory group, located in the ventrolateral
part of the medulla, which mainly causes expiration;
• Pontine centres located in pons.
1. The apneustic centre, increases the depth of inspiration
acting directly on the dorsal group of neurons.
2. The pneumotaxic centre, located dorsally in the superior
portion of the pons, which mainly controls rate and
depth of breathing.

35. Dorsal Respiratory Group of Neurons
• The dorsal respiratory group of neurons or DGN are
responsible for basic rhythm of respiration
• Sensory signals from peripheral chemoreceptors,
baroreceptors, and several types of receptors in the lungs are
transmitted through vagus nerve and glossopharyngeal nerve
into the respiratory centre.
• The nervous signal that is transmitted to the inspiratory
muscles, mainly the diaphragm, is not an instantaneous burst
of action potentials. Instead, in normal respiration, it begins
weakly and increases steadily in a ramp manner for about 2
seconds. Then it ceases abruptly for approximately the next 3
seconds, which turns off the excitation of the diaphragm and
allows elastic recoil of the lungs and the chest wall to cause
expiration. Thus, the inspiratory signal is a ramp signal.

36. Ventral Respiratory Group of Neuron
• Located in each side of the medulla, anterior and lateral to DGN
• The neurons of the ventral respiratory group remain almost
totally inactive during normal quiet respiration.
• During forced breathing, stimulation of the inspiratory neurons
in the VGN causes contraction of inspiratory muscle and
prolonged inspiration. Stimulation of expiratory neurons causes
contraction of expiratory muscles and prolonged expiration.

37. A Pneumotaxic Centre
• A pneumotaxic centre, located dorsally in the upper pons,
transmits signals to the inspiratory area.
• The primary effect of this centre is to control the “switch-off”
point of the inspiratory ramp, limiting inspiration and thus
controlling the rate of breathing.
• It control medullary respiratory centre, particularly DGN. It
act through apneustic centre
Apneustic centre
• Increases the depth of inspiration by acting directly on the
dorsal group of neurons
• The stimulation of apneustic centre causes apneusis.
• It is an abnormal pattern of irregularity characterized by
prolonged inspiration followed by short, inefficient
expiration

38.  IMPULSES FROM HIGHER CENTRES OR VOLUNTARY CONTROL OF
RESPIRATION
• For short periods of time, respiration can be controlled
voluntarily and can hyperventilate or hypoventilate. It is done
bycerebral cortex and hypothalamus.
 EFFECT OF LUNG “J RECEPTORS.”
• A few sensory nerve endings are located in the alveolar walls
in juxtaposition to the pulmonary capillaries called “J
receptors.”
• They are stimulated especially when the pulmonary
capillaries become engorged with blood or when pulmonary
oedema occurs in such conditions as congestive heart failure.
• Although the functional role of the J receptors is not clear,
their excitation may give the person a feeling of dyspnoea.

39.  Effect of stretch receptors in lungs [THE HERING-BREUER
INFLATION REFLEX]
• Stretch receptors are located in the walls of the bronchi and
bronchioles throughout the lungs
• Overstretching of lungs stimulate the stretch receptors that
transmit signals through the vagi into DGN
• It “switches off” the inspiratory ramp and thus stops further
inspiration. This is called the Hering- Breuer Inflation Reflex.
This reflex also increases the rate of respiration.
• In human beings, the Hering-Breuer reflex probably is
activated when the tidal volume increases to more than
about 1-1.5 litres per breath.

40.  EFFECT OF CHEMORECEPTORS
• Chemoreceptors bring about the chemical regulation of
respiration
 EFFECT OF BARORECEPTORS
• The baroreceptors responds to changes in blood pressure.
• Whenever arterial pressure increases, baroreceptors are
stimulated, signals send to vasomotor centre. This in turn
causes decrease in blood pressure and inhibition of
respiration
 EFFECT OF IRRITANT RECEPTORS IN THE AIRWAYS.
• The epithelium of the trachea, bronchi, and bronchioles is
supplied with pulmonary irritant receptors
• When stimulated, coughing and sneezing occurs.
• They may also cause bronchial constriction in such diseases as
asthma and emphysema.

41.  IMPULSES FROM PROPRIORECEPTORS
• Proprioreceptors are receptors located in joints, tendons
and muscles, which give response to changes in the
position of the body.
• They are stimulated during exercise, send signals to
cerebral cortex in turn stimulate medullary respiratory
centres, resulting in hyperventilation
 EFFECT OF PAIN RECEPTORS
• Receptors which responds to pain
• Whenever pain receptors are stimulated, the impulses are
sent to cerebral cortex results in hyperventilation
 EFFECT OF THERMORECEPTORS
• Thermoreceptors are cutaneous receptors responds to
changes in temperature.
• When the body is exposed to cold or low temperature,
cerebral cortex is stimulated and results in
hyperventilation.

42. CHEMICAL CONTROL OF RESPIRATION
• It is operated through chemoreceptors.
• Chemoreceptors responds to changes in chemical changes
especially the conditions like hypoxia (low O2),
hypercapnia(excess CO2) and increased hydrogen ion
concentration.
• Excess carbon dioxide or excess hydrogen ions in the blood
mainly act directly on the respiratory centre itself, and help to
regulate respiratory activity.
• Chemoreceptors are classified in to two group;
1. Central chemoreceptors
2. Peripheral chemoreceptors.

43. CENTRAL CHEMORECEPTORS
• They are situated in the brain close to DGN.
• Excess hydrogen ion concentration in CSF is the main stimulus
for central chemoreceptors. This in turn is the effect of excess
carbondioxide in blood.
• When carbondioxide level in blood increases, it can easily
pass through blood brain barrier and reach CSF or interstitial
fluid of the brain. There it combines with water and form
carbonic acid and then dissociates in to H+
and HCO3-
.
CO2 + H2O= H2CO3
H2CO3= H+
+HCO3-
• The hydrogen ion stimulate central chemoreceptors.
Stimulatory impulses are sent to DGN, causing increased
ventilation. Hyperventilation washes away more
carbondioxide and respiration brought back to normal

44. Peripheral Chemoreceptors
• Special nervous chemoreceptors,
called peripheral chemoreceptors, are
located in several areas outside the
brain.
• The main stimulus for activation of
peripheral chemoreceptors is hypoxia.
They also respond to a lesser extent to
changes in carbon dioxide and
hydrogen ion concentrations.
• They are located either in the carotid
bodies or in the aortic bodies.
• The carotid bodies are located
bilaterally in the bifurcations of the
common carotid arteries.
• The aortic bodies are located along
the arch of the aorta;

45. • When the oxygen concentration in the arterial blood
falls below normal, the chemoreceptors become
strongly stimulated.
• Impulses are transmitted to respiratory centres and
stimulate them.
• DGN send stimulatory impulses to respiratory muscles
resulting in hyperventilation.
• This provides enough oxygen and rectifies the hypoxia.

46. HYPOXIA
• It is the reduced availability of oxygen to the tissues.
• The best treatment for hypoxia is oxygen therapy. i.e treating
the affected person by administering pure oxygen or oxygen
combined with another gas.
• It is classified in to four major types;
1. Hypoxic hypoxia: Decreased oxygen content in arterial
blood.
2. Anaemic hypoxia: Inability of blood to carry sufficient
amount of oxygen. The oxygen availability is normal.
3. Stagnant hypoxia: Reduction in velocity of blood flow.
4. Histotoxic hypoxia: Inability of tissues to utilize oxygen.

47. DYSPNEA
• Difficulty in breathing or air hunger
• It is the conscious effort of breathing causing
discomfort
• Dyspnoea means mental anguish associated with
inability to ventilate enough to satisfy the demand
for air.
• It occurs usually during severe muscular exercise.
• Causes are
• abnormality of respiratory gases in the body
fluids, especially hypercapnea and, to a much less
extent, hypoxia;
• the amount of work that must be performed by
the respiratory muscles to provide adequate
ventilation;
• state of mind.

48. HYPERCAPNEA
• Hypercapnea means excess carbon dioxide in the body fluids.
ASPHYXIA
• The condition is characterized by combination of hypoxia and
hypercapnia
• It occurs due to acute obstruction in air passages in conditions
like drowning or hanging
APNOEA
• Temporary arrest of breathing.
• It occurs in following conditions; voluntary apnoea, after
hyperventilation, during deglutition, during sleep, after
adrenaline injection.

49. CYANOSIS
• The term cyanosis means blueness of the skin, and its cause is
excessive amounts of deoxygenated haemoglobin in the skin
blood vessels, especially in the capillaries
• Cyanosis appears whenever the arterial blood contains more
than 5 grams of deoxygenated haemoglobin in each 100
millilitres of blood.
• Its occurrence depends on the total amount of hemoglobin in
the blood, the degree of hemoglobin unsaturation, and the state
of the capillary circulation.
• Cyanosis is most easily seen in the nail beds and mucous
membranes and in the earlobes, lips, and fingers, where the skin
is thin.

50. Biot’s breathing
• It is characterized by period of apnoea and hyperpnoea.
• There is no waxing and waning. After apneic period,
hyperpnoea occurs abruptly.
• It occurs in conditions such as nervous disorders.
PERIODIC BREATHING
• It is the abnormal or uneven respiratory rhythm. It is two
types;
• Cheyne stokes breathing
• Biot’s breathing

51. Cheyne stokes breathing
• It is the periodic breathing characterised by the rhythmic
hyperpnea and apnea.
• It occurs during sleep, high altitudes, hyperventilation, exercise,
new born babies. It occurs in pathological conditions like
increased intracranial pressure, cardiac and renal disorders,
poisoning etc.
• Hyperpneic period is also called waxing and waning of
breathing: characterised by shallow breathing at beginning.
The force of respiration gradually increases and reaches the
maximum. Then it decreases gradually and reaches the
minimum followed by apnea. The gradual increase followed
by gradual decrease in force of respiration is called waxing and
waning.
• Apneic period: when the force of breathing reduced to
minimum, cessation of breathing occurs for a period. It is
again followed by hyperpneic period and the cycle repeated.

52. Recording Changes in Pulmonary Volume—Spirometry
• A simple method for studying pulmonary ventilation is to record
the volume movement of air into and out of the lungs, a process
called spirometry.
• It consists of a drum inverted over a chamber of water, with the
drum counterbalanced by a weight.
• In the drum is a breathing gas, usually air or oxygen; a tube
connects the mouth with the gas chamber.
• When one breathes into and out of the chamber, the drum rises
and falls, and an appropriate recording is made on a moving sheet
of paper.

53. PULMONARY VOLUMES
1. The tidal volume is the volume of air inspired or expired with
each normal breath. Normal value is 500 ml
2. The inspiratory reserve volume is the extra volume of air that
can be inspired forcefully after the end of normal inspiration.
Normal value is 3000 ml.
3. The expiratory reserve volume is the maximum extra volume
of air that can be expired forcefully after normal expiration.
Normal value is 1000 ml.
4. The residual volume is the volume of air remaining in the
lungs even after the most forceful expiration. Normal value is
1200 ml.

56. COUGH REFLEX
• Irritation caused by the foreign matter in bronchi and trachea
initiate the cough reflex.
• Afferent nerve impulses pass from the respiratory passages mainly
through the vagus nerves to the medulla of the brain.
• Medulla initiate the following processes
1. Up to 2.5 litres of air are rapidly inspired.
2. The epiglottis closes, and the vocal cords shut tightly to entrap
the air within the lungs.
3. The abdominal muscles and internal intercostals contract
forcefully, pushing against the diaphragm. Consequently, the
pressure in the lungs rises rapidly to as much as 100 mm hg or
more.
4. The vocal cords and the epiglottis suddenly open widely, so
that air under this high pressure in the lungs explodes
outward.

57. SNEEZE REFLEX
• The initiating stimulus of the sneeze reflex is irritation in
the nasal passageways; the afferent impulses pass in the
fifth cranial nerve to the medulla, where the reflex is
triggered.
• A series of reactions similar to those for the cough reflex
takes place; however, the uvula is depressed, so that large
amounts of air pass rapidly through the nose, thus helping
to clear the nasal passages of foreign matter.

58. Pulmonary circulation
• Pulmonary blood vessels include pulmonary artery which
carries deoxygenated blood to alveoli of lungs and bronchial
artery which supply oxygenated blood to other structures of
lungs.
• Pulmonary artery supplies blood from right ventricle to alveoli
of lungs. After leaving the right ventricle, it divides in to right
and left branches. Each branch enters the corresponding lung
along with the primary bronchus. Then it divides in to small
vessels and finally forms the capillary plexus where gaseous
exchange takes place.
• Bronchial artery arises from descending thoracic aorta which
supplies arterial blood to bronchi, connective tissue and other
structures of lung, visceral pleura and pulmonary lymph nodes.
Venous blood id drained by two bronchial veins from each side.

59. • The blood from distal portion of bronchial circulation is drained
directly in to the pulmonary veins. This deoxygenated blood flowing
from bronchial circulation in to the pulmonary veins without being
oxygenated forms a part of the normal physiological shunt.
• Other special features of pulmonary circulation are the following
• Pulmonary artery has a thin wall and it has only about 1/3rd
of
thickness of the systemic aortic wall.
• The pulmonary blood vessels are highly elastic and more
distensible
• The smooth muscle coat is not well developed in the pulmonary
blood vessels.
• True arterioles have lesser smooth muscles
• Pulmonary capillaries are larger than the systemic circulation
• Vascular resistance is very less; pressure is also low
• Physiological shunt is present
• Pulmonary artery pressure is 25 mmHg/10 mmHg. Pulmonary
capillary pressure is about 7 mmHg

60. RESPIRATORY CHANGES DURING EXERCISE
1) EFFECT ON PULMONARY VENTILATION: normal pulmonary ventilation is
6L/minute. In moderate exercise, it increases to about 60/L per minute.
In severe muscular exercise, it rises still further upto 100 litres per
minute.
2) EFFECT ON DIFFUSING CAPACITY: The diffusing capacity foe oxygen is
about 21 ml/minute at resting condition. It rises to 45 to 50 ml/minute
during moderate exercise due to increase in blood flow through the
pulmonary capillaries.
3) EFFECT OF CONSUMPTION OF OXYGEN: Normal oxygen consumption for
a young man at rest is about 250 ml/min. The oxygen consumed by the
tissues, particularly skeletal muscles, is increased during exercise
because of increased metabolic activities.
4) OXYGEN DEBT: it is the extra amount of oxygen required by the muscles
during recovery from severe exercise. The oxygen debt is about six times
more than the amount of oxygen consumed under resting conditions.
5) VO2 MAX: it id the amount of oxygen consumed under maximal aerobic
metabolism. VO2 MAX= CARDIAC OUTPUT X MAXIMAL AMOUNT OF
OXYGEN CONSUMED. In normal healthy male it is 35 to 40 mL/kg body
weight/minute. In females, it is 30 to 35 mL/kg/minute.