17_breathing_and_exchange_of_gases_1631097583256.ppt

l082haripriyakotari 300 views 68 slides Jun 03, 2024
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About This Presentation

Physiology
Breathing and exchange of gases
Respiration


Slide Content

•Respirationis the oxidation of nutrients in the living cells to release
energy for biological work.
•Breathingis the exchange of O2from the atmosphere with CO2
produced by the cells.

General body surface
E.g. lower invertebrates
(sponges, coelenterates,
flatworms etc).

Skin or moist cuticle
(cutaneous respiration)
E.g. earthworms,
leech, amphibians etc.

Tracheal tubes
E.g. Insects, centipede,
millipede, spider.

Gills (Branchial
respiration)
E.g. fishes, tadpoles,
prawn.

Lungs (Pulmonary
respiration)
E.g. most vertebrates.

Conducting part.
Ittransports atmospheric air
into the alveoli.
It clears air from foreign
particles.
It humidifies and brings the air
to body temperature.
AIR PASSAGE (AIR TRACT)

Each terminal bronchiole gives rise to many thin and vascularised alveoli.
AIR PASSAGE (AIR TRACT)

Larynx (sound box or voice box) is a
cartilaginous box which helps in sound
production.
During swallowing, glottisis closed by
epiglottis(a thin elastic cartilaginous
flap) to prevent the entry of food into
larynx.
Trachea, all bronchi and initial
bronchioles are supported by
incomplete cartilaginous half rings.
AIR PASSAGE (AIR TRACT)

VOCAL CORDS IN ACTION
AIR PASSAGE (AIR TRACT)

Lungs are situated in thoracic
chamberand rest on diaphragm.
Right lung has 3 lobes. Left lung has 2
lobes.
Each lung is covered by double-
layered pleura (outer parietal pleura
& inner visceral pleura).
The pleural fluid present in between
these 2 layers lubricates the surface
of the lungs and prevents friction
between the membranes.
LUNGS
1
2
3
1
2

Lungs= Bronchi + bronchioles + alveoli
Alveoli & their ducts form respiratoryorexchange partof respiratory system.
Alveoli are the structural and functional units of lungs.
LUNGS

Internal structure of
lungs
LUNGS

Pulmonary ventilation (breathing)
Gas exchange between lung
alveoli and blood.
Gas transport (O
2transport and
CO
2transport)
Gas exchange between blood and
tissues.
Cellular or tissue respiration.

Breathing
Inspiration:
Active intake of air from atmosphere into lungs.
Expiration:
Passiveexpellingof air from the lungs.

Diaphragm contracts
(flattens).
External inter-costal muscles
contracts.
Vertical volume (antero-
posterior axis) increases.
Ribs & sternum lift up. Volume
in dorso-ventral axis increases.
Thoracic volume increases. Thoracic pressure decreases.
INSPIRATION
Lungs expand and Pulmonary volume increases.
Intra-pulmonary pressure decreases.
Air moves from outside into the lungs.

During forceful expiration, abdominal muscles and
internal inter-costal muscles contract.
EXPIRATION
Inter-costal muscles & diaphragm relax.
Thorax regains its original position.
Thoracic volume decreases.
Pulmonary volume decreases.
Air moves out.

Tidal volume (TV)
Inspiratory reserve volume (IRV) or complemental air
Expiratory reserve volume (ERV) or supplemental air
Residual volume (RV)
Inspiratory capacity (IC)
Expiratory capacity (EC)
Functional residual capacity (FRC)
Vital capacity (VC)
Total lung capacity (TLC)

•Volume of air inspired or expired during a normal
respiration.
•It is about 500 ml. i.e., 6000-8000 ml per minute.
Tidal volume
(TV)

•Additional volume of air that can inspire by forceful
inspiration.
•It is 2500-3000 ml.
Inspiratory
reserve volume
(IRV) or
complemental air

•Additional volume of air that can expire by a forceful
expiration.
•It is 1000-1100 ml.
Expiratory
reserve volume
(ERV) or
supplemental air

•Volume of air remaining in lungs after a forcible
expiration.
•It is 1100-1200 ml.
Residual
volume (RV)

•Total volume of air inspired after a normal expiration (TV
+ IRV).
•It is 3000-3500 ml.
Inspiratory
capacity (IC)

•Total volume of air expired after a normal inspiration (TV
+ ERV).
•It is 1500-1600 ml.
Expiratory
capacity (EC)

•Volume of air remaining in the lungs after a normal
expiration (ERV + RV).
•It is 2100-2300 ml.
Functional
residual
capacity (FRC)

•Volume of air that can breathe in after a forced expiration
or Volume of air that can breathe out after a forced
inspiration (ERV + TV + IRV).
•It is 3500-4500 ml.
Vital capacity
(VC)

•Total volume of air in the lungs after a maximum
inspiration (RV + ERV + TV + IRV or VC + RV).
•It is 5000-6000 ml.
Total lung
capacity (TLC)

Part of respiratory tract
(from nostrils to terminal
bronchi) not involved in gaseous
exchange is called dead space.
Dead air volume is about
150 ml.

Respiratory cycle= an inspiration + an expiration.
Normal respiratory (breathing) rate: 12-16 times/min.
Spirometer (respirometer): To measure the respiratory rate.

EXCHANGE OF GASES
Gas exchange occurs between
1.Alveoli & blood
2.Blood & tissues
Alveoliare the primary sites of gas exchange.
O
2 and CO
2 are exchanged by simple diffusion.
Alveoli

Gas exchange depends on following
factors:
Pressure/ concentration gradient
Solubility of gases
Thickness of membranes
Surface area of respiratory
membrane (lungs)
EXCHANGE OF GASES Factors influencing Gas exchange

•The individual pressure of a gas in a gas
mixture is called Partial pressure.
•Partial pressures of O
2 and CO
2 (pO
2&
pCO
2) are given below:
1. Pressure/ concentration gradient
EXCHANGE OF GASES Factors influencing Gas exchange
Respiratory gaspO
2 (mm Hg)pCO
2 (mm Hg)
Atmospheric air 159 0.3
Alveoli 104 40
Deoxygenated blood40 45
Oxygenated blood 95 40
Tissues 40 45

pO
2in alveoliis more (104 mm Hg) than
that in the blood capillaries (40 mm Hg).
So O
2diffuses into capillary blood.
pCO
2in deoxygenated blood is more (45
mm Hg) than that in the alveolus (40 mm
Hg). So CO
2diffuses to alveolus.
1. Pressure/ concentration gradient
EXCHANGE OF GASES Factors influencing Gas exchange

Solubility of CO
2 is 20-25 times higher
than that of O
2. So the amount of
CO
2 that can diffuse through diffusion
membrane per unit difference in
partial pressure is much higher than
that of O
2.
2. Solubility of Gases
EXCHANGE OF GASES Factors influencing Gas exchange
Solubility
difference
between O
2&
CO
2
O
2
CO
2

Diffusion membrane is made up of 3
layers:
a.Squamous epithelium of alveoli.
b.Endothelium of alveolar capillaries.
c.Basement substance b/w them.
3. Thickness of Membrane
EXCHANGE OF GASES Factors influencing Gas exchange
Its total thickness is only 0.5 mm. It enables easy gas exchange.

Presence of alveoli
increases the surface area
of lungs. It increases the
gas exchange.
4. Surface area of respiratory membrane (Lungs)
EXCHANGE OF GASES Factors influencing Gas exchange

O
2 O
2
CO
2
CO
2

TRANSPORT
OF GASES
O
2 transport:
Lungs → tissues
In physical solution (blood plasma)
As oxyhaemoglobin
CO
2transport:
Tissues → lungs
As carbonic acid
As carbamino-haemoglobin
As bicarbonates
It is the transport of respiratory gases (O
2& CO
2) from alveoli to the systemic
tissues and vice versa.
TRANSPORT OF GASES

3%of O
2is carried by dissolving in plasma.
TRANSPORT OF GASES O2TRANSPORT
1. In physical solution (blood plasma)
97%of O
2is transported by Haemoglobin(red
coloured iron containing pigment) on RBC.
2. As oxyhaemoglobin

O
2binds with haemoglobinin a reversible
manner to form oxyhaemoglobin.This is
called oxygenation.
Hbhas 4 haem units. So each Hbmolecule
can carry 4 oxygen molecules.
TRANSPORT OF GASES O2TRANSPORT
2. As oxyhaemoglobin
Hb
4+ 4O
2 Hb
4O
8
High pO
2 / Low pCO
2
(Lungs)
Low pO
2 / High pCO
2
(Tissues)
Hb
4O
8

Binding of O
2depends upon pO
2& pCO
2,
H
+
ion concentration (p
H
) & Temperature.
In alveoli,there is high pO
2, low pCO
2,
lesser H
+
ion concentration & lower
temperature. These factors favour the
formation of oxyhaemoglobin.
TRANSPORT OF GASES O2TRANSPORT
2. As oxyhaemoglobin
Hb
4+ 4O
2 Hb
4O
8
High pO
2 / Low pCO
2
(Lungs)
Low pO
2 / High pCO
2
(Tissues)
Hb
4O
8

In tissues, low pO
2, high pCO
2, high H
+
ion
concentration & higher temperature
exist. So oxyhaemoglobin dissociates to
release O
2.
TRANSPORT OF GASES O2TRANSPORT
2. As oxyhaemoglobin
Hb
4+ 4O
2 Hb
4O
8
High pO
2 / Low pCO
2
(Lungs)
Low pO
2 / High pCO
2
(Tissues)
Hb
4O
8

Every 100 ml of oxygenated blood can
deliver around 5 ml of O
2to the tissues
under normal physiological conditions.
TRANSPORT OF GASES O2TRANSPORT
2. As oxyhaemoglobin
Hb
4+ 4O
2 Hb
4O
8
High pO
2 / Low pCO
2
(Lungs)
Low pO
2 / High pCO
2
(Tissues)
Hb
4O
8

OXYGEN-HAEMOGLOBIN DISSOCIATION CURVE
•It is a sigmoid curve obtained when
percentage saturation of Hbwith O
2
is
plotted against the pO
2
.
•It is used to study the effect of factors like
pCO
2
, H
+
concentration etc. on binding of
O
2
with Hb.
TRANSPORT OF GASES O2TRANSPORT

TRANSPORT OF GASES CO2TRANSPORT
1. As Carbonic acid
In tissues, pCO
2is high due to catabolism and pO
2is low. In lungs, pCO
2is low
and pO
2is high. This favours CO
2transport from tissues to lungs.
2. As Carbamino-
haemoblobin
3. As Bicarbonate
It occurs in 3 ways:

In tissues, 7% CO
2is dissolved in plasma waterto form
carbonic acid and carried to lungs.
TRANSPORT OF GASES CO2TRANSPORT
1. As Carbonic
acid
From tissues
In plasma
Carbonic acid

TRANSPORT OF GASES CO2TRANSPORT
In tissues, 20-25%of CO
2binds to Hbto form carbamino-
haemoglobin.
In alveoli, CO
2dissociates from carbamino-haemoglobin.
2. As Carbamino-
haemoblobin
In tissuesIn lungs
(Carbaminohemoglobin)

carbonic anhydrasecarbonic anhydrase
TRANSPORT OF GASES CO2TRANSPORT
In alveoli, the above reaction
proceeds in opposite direction leading
to the formation of CO
2and H
2O.
Every 100 ml of deoxygenated blood
delivers about 4 ml of CO
2to alveoli.
About 70% of CO
2is transported by this method.
RBCs contain an enzyme, carbonic anhydrase.(It is slightly
present in plasma too).
At tissue site, it facilitates the following reactions:
3. As Bicarbonate

REGULATION OF RESPIRATION
Respiratory
centres
Respiratory rhythm
centres
Pneumotaxic
centre
Chemosensitive
area
In brain, there are the following Respiratory centres:

REGULATION OF RESPIRATION
•Seen in medulla oblongata.
•It regulates respiratory rhythms.
1. Respiratory rhythm centres (Inspiratory & Expiratory centres)

•Seen in Pons.
•It moderates functions of respiratory rhythm centre.
•Impulse from this centre reduces the duration of inspiration and thereby alter
respiratory rate.
REGULATION OF RESPIRATION
2. Pneumotaxiccentre

Role of oxygen in the regulation of respiratory rhythm is quite insignificant.
REGULATION OF RESPIRATION
•Seen adjacent to the rhythm centre.
•Increase in the concentration of
CO
2and H
+
activates this centre,
which in turn signals rhythm centre.
•Receptorsin aortic arch & carotid
artery also recognize changes in
CO
2& H
+
concentration and send
signals to rhythm centre.
3. Chemosensitivearea

It is the difficulty in breathing causing wheezingdue to
inflammationof bronchiand bronchioles.
1. Asthma

Damage of alveolar walls.
It decreases respiratory surface.
Major cause is cigarette smoking.
2. Emphysema

Certain industries produce so much dust. So, defense
mechanism of the body cannot cope with the situation.
Long exposure causes inflammationleading to fibrosis
(proliferation of fibrous tissues). It results in lung damage.
Workers in such industries should wear protective masks.
3. Occupational
respiratory
disorders

•Chloride shift (also known as the Hamburger
phenomenon or lineasphenomenon, named
after HartogJakobHamburger) is a process
which occurs in a cardiovascular system and
refers to the exchange of bicarbonate
(HCO3−) and chloride (Cl−) across the
membrane of red blood cells (RBCs).

•Mechanism
•Carbon dioxide (CO
2) is produced in tissuesas a byproduct of
normal metabolism. It dissolves in the solution of blood
plasma and into red blood cells (RBC), where carbonic
anhydrase catalyzes its hydration to carbonic acid(H
2CO
3).

•Carbonic acid then spontaneously dissociates to
form bicarbonate Ions (HCO
3

) and a hydrogen
ion (H
+
). In response to the decrease in
intracellular pCO
2, more CO
2passively diffuses
into the cell.
•Cell membranes are generally impermeable to
charged ions (i.e. H
+
, HCO3

) but RBCs are
able to exchange bicarbonate for chloride using
the anion exchanger protein .

•Thus, the risein intracellular bicarbonate leads to
bicarbonate export and chloride intake. The term
"chloride shift" refers to this exchange.
•Consequently, chloride concentration is lower in
systemic venous blood than in systemic arterial
blood:
•high venous pCO
2leads to bicarbonate production
in RBCs, which then leaves the RBC in exchange
for chloride coming in.

•The opposite process occurs in the pulmonary capillariesof
the lungswhen the PO
2rises and PCO
2falls, and the
Haldane effect occurs (release of CO
2from hemoglobin
during oxygenation). This releases hydrogen ions from
hemoglobin, increases free H+ concentration within RBCs,
and shifts the equilibrium towards CO
2 and water formation
from bicarbonate

•The subsequent decrease in intracellular
bicarbonate concentration reverses chloride-
bicarbonate exchange: bicarbonate moves into the
cell in exchange for chloride moving out.
•Inward movement of bicarbonate ,exchanger
allows carbonic anhydrase to convert it to CO
2for
expiration.
•The chloride shift may also regulate the affinity of
hemoglobin for oxygen through the chloride ion
acting as an allosteric effector.