Respi

PHYSIOLOGY
SYLLABUS
Functional Anatomy of Respiratory System:
Functional anatomy, composition of air in atmosphere and alveoli (P. 1155), gas laws (P. 1155)
Mechanics of Breathing: (P. 1155)
Movements of thoracic cage during respiration (P. 1157)
Muscles involved and their nerve supply (P. 1157)
Intrapleural (P. 1155), pulmonary pressure and volume changes (P. 1156)
Pressure-volume inter-relationships (P. 1156)
Lung compliance (P. 1157), surfactant (P. 1159), airway resistance (P. 1158)
Work of breathing (P. 1158)
Spirometry: (P. 1160)
Lung volumes (P. 1160) and capacities: definitions, normal values, significance
Pulmonary circulation: (P. 1163)
Functional anatomy, distribution, special features, factors influencing
IV
Pulmonary Gas Exchange: (P. 1164)
Alveolocapillary membranes (P. 1164), diffusion capacities, partial pressure gradients, factors influencing
diffusion of gases (P. 1165)
Measurement of diffusion capacity using carbon monoxide (P. 1166)
Applied physiology- shunt and alveolocapillary block (P. 1165)
Ventilation-perfusion ratio and its importance in respiratory diseases (P. 1166)
Gas Transport: (P. 1166)
Oxygen transport (P. 1167): Factors influencing the combination of haemoglobin with oxygen,
Oxygen dissociation curve (P. 1168): Plot, features, physiological advantage of its shape, factors affecting the
shift of curve, Bohr effect (P. 1169)
Carbon dioxide transport: (P. 1170)
Tissue production, carriage in blood and Release at the lungs
Role of red blood cell (P. 1171), chloride shift, role in acid-base balance, Haldane effect (P. 1171)
Carbonmonoxide transport and its effect (P. 1171)
Regulation of Respiration: (P. 1172)
Neural control: medulla, pons, vagus (P. 1172)
Chemo-receptors: peripheral, central, chemical, non-chemical (P. 1175)
Influences on respiration, integrated responses

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Respiration in unusual Environments: (P. 1177)

High altitude hypoxia (P. 1179), types of hypoxia (P. 1177), space flight (P. 1179)
Deep sea diving nitrogen narcosis (P. 1180)
Hyperbaric oxygen and oxygen toxicity (P. 1181)
Abnormal Breathing: (P. 1181)
Apnoea, hyperpnoea, tachypnoea, dysponea: definition, features, physiological basis
Principles of Artificial Respiration: (P. 1183)
Definition types principles, indication, advantage and disadvantages, oxygen therapy (P. 1184); respiratory
failure (P. 1184)
Principles of Lung Function Tests (P. 1184): Tests (P. 1185) and non respiratory functions of the respiratory
system.
Applied respiratory Physiology (P. 1185)
Cyanosis (P. 1185) and Asphyxia (P. 1186)
Pneumothorax (P. 1186), emphysema (P. 1186)
Restrictive and obstructive diseases (P. 1186)

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 Respi

PHYSIOLOGY

Composition of air in atmosphere and

MECHANISM AND MECHANICS OF
alveoli
BREATHING
Atmospheric air Alveolar air Past Questions:
(mmHg) % (mmHg) % 1 Describe briefly the mechanism of inspiration
and expiration. (5) [06 June]
N2 597 78.62 569 74.9
2. Define compliance and name the diseases in
O2 159 20.84 104 13.6 which it is abnormal. (1+2=3) [06 Dec]
co2 0.3 0.04 40 5.3 3. Lungs surfactant (3) [09 July]
4. Surfactant (chemical composition and functions)
H2O 3.7 0.50 47 6.2
(2,3,4) [10 July, 08 Jan, 07 July, 06 June, 05 Dec]
Total 760.0 100% 760 100% 5. Surfactant and its importance (3) [03 June]
Gas laws 6. Intrapleural pressure (3) [09 July]
7. Normal values of compliance of the lungs of
Daltons law:
chest wall (3) [06 Dec]
- The total pressure exerted by a mixture of
8. Compliance (2) [11 July]
gases is equal to the sum of partial pressure of
9. Lung compliance (2) [03 Dec]
all the gases present in it.
Intrapleural pressure [09]
IV
- Partial pressure is the pressure exerted by any
one gas in a mixture of gases. - Negative pressure in the space between lung
- Partial pressure is equal to the total pressure pleura and chest wall pleura.
time the fraction of total amount of gas it - It is value is -2mmHg at the beginning of
represents. inspiration and decreases up to -6 mm Hg at
the end of inspiration.
nRT
P = V where, - Negative intrapleural pressure is maintained by
opposing elastic recoil forces of chest wall lung
P = pressure and also by lymphatic drainage of the pleural fluid.
n= no. of moles of gas. - The negative intra-pleural pressure is directly
R = gas constant proportional to the amount of thoracic
expansion.
T = Absolute temperature
- During quiet inspiration, the lungs are pulled
V = Volume
into a more expanded position causing intra-
Henry's law: pleural pressure to decrease to about -
- Amount of gas dissolved in any solution is 6mmHg.
directly proportional to the partial pressure of - At the end of inspiration, the lung recoil begins to
the gas at constant temperature. pull the chest back to the expiratory position.
- After end expiratory position, the intra pleural
pressure returns back to -2 mmHg
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Note:
Negative intrapleural pressure keeps the lung patent.
Factors affecting intra-pleural pressure:
A. Physiological factors:
1. Deep inspiration  decrease intrapleural
pressure (more negative)
2. Valsalva manoeuvre (coughing, defecation) 
increases intra-pleural pressure.
3. Effect of gravity  More negative at the apices.
B. Pathological factors:
1. Emphysema  Decrease in lung elasticity
which causes increase in intrapleural pressure
2. Pneumothorax
Alveolar pressure/intrapulmonary pressure
 Pressure of the air inside the lung alveoli.
 It fluctuates from - 1mmHg (during inspiration) to
+1mmHg (during expiration).
Transpulmonary pressure:
- It is the difference between alveolar pressure and
pleural pressure. It is the measure of elastic forces
in the lungs and prevents collapse of lung.
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- Transpulmonary pressure is less at the base of
lung. So, lungs are less expanded at the bases.
- This pressure further decreases and becomes
more negative at the end of forced expiration
causing airways to close at the bases.
- So, during first part of inspiration, more of the
inspired air goes to the apices of the lungs.
- It is also called transmural pressure.
Volume changes during respiration/
pressure volume relationship
- The change of volume of lung depends on the
transpulmonary pressure. Transpulmonary
pressure in turn depends on pleural and
alveolar pressure. As the thorax expands,
pleural pressure decreases and becomes more
negative i.e. from -2 to -6 mmHg. This causes
expansion of lung and intrapulmonary/alveolar
pressure becomes - 1mmHg. So air of 500ml
enters into lung expanding its size.
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 Respi

 When the expiration follows passively, the elastic Muscles of Respiration:

recoil of the lungs causes the intra - pulmonary A. inspiratory muscles:
pressure to swing lightly to positive side (1mm 1. Diaphragm.
Hg). So, lungs volume fluctuate by 500 ml during 2. External intercostals muscles
respiration. 3. Scalene, serratus, sternocleidomastoid.
Movement of thoracic cage during B. Expiratory muscles:
respiration: - Generally by passive process.
- During inspiration the thorax is enlarged by: - Muscles involved are:
nd th
i. Movement of ribs (2 and 6 ) upwards 1. Internal internostal muscle.
which increase anteroposterior diameter or 2. Anterior abdominal wall muscles
thorax. (Pump handle movement). Nerve supply
ii. Movement of ribs outwards (7th-10th) 1. Diaphragm: by phrenic nerve (C3-C5)
increase transverse diameter of the throax 2. Intercostal nerves.
(bucket handle movement).
Lung compliance (03, 06, 011)
iii. Descent of diaphragm (75% of total volume)
- It is the change in the lung volume per unit
- Expiration is passive and thorax volume comes change in transpulmonary pressure (v/p)
to normal size.
- It is the indicator of stretchibility, distensibility
Mechanism of Respiration (KU 06) or elasticity of lung.
- Increase in intrathoracic volume by contraction of - It is expressed as litre/cm H2O.
inspiratory muscles (active process) - Compliance is studied under following heading:
 a. Compliance of the lungs and the thoracic
Increase in -ve pleural pressure from - 2 mm Hg to wall. IV
-6mm Hg. b. Compliance of the lungs only.
 a. Compliance of the lungs and thoracic wall:
Alveolar pressure changes from 0 to - 1 thus - Both lungs and thoracic wall are viscoelastic
increasing transpulmonary pressure. structures.
- They expand to certain volume by increase in

airway pressure.
Air flows inside the lung along the pressure gradient
Normal values:
 - 120 ml/cm H2O of transpulmonary pressure.
Inspiration b. Compliance of the lungs only
 - Total compliance of both lungs together in
At the end of inspiration, recoiling of the lung occurs normal adult human average about 200 ml/cm
 H2O of transpulmonary pressure. This means
when airway pressure is increased by 1cm H2O
Pleural pressure increases from (-6) to (-2) mmHg.
lung volume is increased by 200ml.

- The compliance of lung is due to:
Alveolar pressure to (+1) due to elastic recoil i. Elastic forces of lung tissue and (1/3rd)
 ii. Elastic forces caused by the surface tension
Air moves out of the lung (expiration) of the fluid that lines the inner wall of the
alveoli (2/3rd)
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- Elastic forces of lung can be determined mainly ii. Moving the viscous material of the lung
by elastin and collagen fibers. tissues called viscous resistance (7%)
- Compliance of the saline filled lungs is due iii. Moving air through the respiratory passage
elastic force of lung tissue only, as surface called airway resistance. (28%)
tension is absent.
- Compliance is slightly greater when measured
during deflation than when measured during
inflation.
Note:
- Compliance is (1) decreased in: Pulmonary
congestion, interstitial pulmonary fibrosis,
pulmonary edema. (2) increased in: emphysema,
old age. (KU)
- The curve during inspiration and expiration is not
identical. Volume during expiratory phase is more
than in inspiratory phase. So, this curve is called
hysteresis curve. This suggests difference in the
distensibility during inspiratory and expiratory
phase. Note:
- Factors affecting total work done
1. Increased during exercise
2. Pathological increase:
i. Emphysema.
IV ii. Bronchial asthma
iii. Congestive heart failure with dyspnea
iv. Orthopnea
- Increase in total work is due to the viscous work.
(Higher breathing rate) and  in elastic work
(larger tidal volume).
Airway resistance:
- Resistance to the flow of air through the air
tube.
- In a tube, flow =
Dfference in presure between 2 end of tube
Resistance
- Compliance line: The straight line joining the
two points of inspiration and expiration curve. p
or, Resistance = flow
Work of breathing:
- Thus, Resistance decreases as the pressure
- To move the air into the lungs, the muscles of difference is decreased. so, as the pressure
respiration have to do work to overcome all inside the lung becomes negative, airflow to
different forms of resistance. the lung is increased.
- Therefore, work is done by the respiratory 1
muscles in: - Resistance  r4 . Thus, if the radius is decreased
i. stretching the elastic tissue of the lungs and by half, resistance to the airflow is increased by
chest wall called elastic force (65%) 16 times.

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Note: In asthma, bronchoconstriction produces
increase in airway resistance.
Surface tension of lung [KU 06]
- Water forms a thin layer lining the inner
surface of alveoli. The water molecules are
strongly attracted to each other when the layer
forms the surface with air. As result, the water
surface is always attempting to contract and
alveoli tend to collapse. This produces elastic
Surfactant [05,06,07,08,09,010]
- It is a complex mixture of several
phospholipids, proteins and ions. It is surface
active agent in water, which means that it
greatly reduces the surface tension of water
and prevents collapsing of alveoli.
- It is synthesized by type II alveolar epithelial
cells.
Components: (05,07,09,11)
- Dipalmitoylphosphatidyl choline (DPPC): 62%
- Phosphatidyl glycerol: 5%
- Other phospholipids: 10%
- Neutral lipids: 13%
- Proteins: 8%
- Carbohydrate: 2%
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contractile force of the entire lung which is
called surface tension elastic force.
- Pressure in the alveoli is directly proportional
to the surface tension as Pressure =
×
- Pressure is high in small sized alveoli. Thus,
alveoli tend to collapse during expiration and
in premature babies (small radii)
IV
Synthesis
- Lamellar bodies (membrane bound organelles)
in Type II alveolar epithelial cells/pneumocytes
are intracellular source of surfactant.
- Lamellar bodies contain surfactant
phospholipids and surfactant proteins which
are synthesized in endoplasmic reticulum.
- By exocytosis  lipid and Protein are released
into fluid lining alveoli  phospholipid
arranged into a lattice (meshwork) structure
called tubular myelin  Tubular myelin is
converted to surfactant in the form of film,
that spreads over the entire surface of alveoli.
- The surfactant is again recycled by type II
pneumocytes/alveolar cells.
Functions:
i. Prevent collapsing of lung during expiration.
ii. Alveolar size is stabilized by surfactant
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iii. Helps in facilitating expiration

iv. Surfactant reduces the surface tension by
forming a layer between the fluid linking the
alveoli and alveolar air.
Factors affecting surfactant.
1. Decrease in surfactant:
i. Long term inhalation of 100% O2
ii. Occlusion of one pulmonary artery.
iii. Cigarette smoking
2. Increase in surfactant:
i. Thyroid hormone
ii. Glucocorticoids
Note:
- Premature babies have lungs without surfactant
as it is secreted only after 7 months of gestation.
Thus, the alveoli are collapsed and infants die of Pulmonary volumes [06,07]
pulmonary insufficiency. cortisol is given to 1. Tidal volume (TV)
prevent it. - The amount/volume of air inspired or expired
- Hyaline membrane disease in infant is due to with each normal breath.
deficiency of surfactant synthesis. This causes - Normal value: 500 ml
collapse of lung. Decreased in: Respiratory muscle weakness,
depression in respiratory center.
IV SPIROMETRY Increased in : exercise
Past Questions: 2. Inspiratory reserve volume (IRV)
- It is the extra volume of air that can be inspired
1. Describe different lung volumes and lung
over & above tidal volume after forceful
capacities. Give their clinical importance. inspiration.
(2+3=5) [06 June] - Normal value: 3000 ml.
2. Define vital capacity. Mention the clinical 3. Expiratory reserve volume (ERV)
importance of timed vital capacity. - Maximum amount extra volume of air that can
be expired by forceful expiration after the end
(1+2=3) [07 July]
of a normal tidal expiration.
3. What is the difference between anatomical and - Normal value: 1100 ml.
physiological dead spaces? Explain their role on 4. Residual volume:
alveolar ventilation. (2+2=4) [10 July] - Volume of the air that remains in lungs after
4. FEVI and its clinical significance (3) [07 Dec] forceful expiration.
5. What is FEV1? What will be the change of FEV1 in - Normal value: 1200 ml.
obstructive and restrictive lung diseases? 5. Closing volume( CV)
- It is the lung volume above residual volume at
(2) [10 Jan] which airways in the lower dependent parts of
 Spirometry is the method for studying pulmonary the lungs begin to close off because of lesser
ventilation to record the volume and movement transpulmonary/transmural pressure in these
of air into and out of the lung. areas.

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Pulmonary Capacities [06,07]
 It is the combination of two or more volumes.
1. Inspiratory capacity (IC)
- The amount of air a person can breathe in
beginning at the normal expiratory level and
distending lungs to maximum amount.
- IC = TV + IRV = 500 + 3000 = 3500 ml.
2. Functional residual capacity (FRC)
- It is the amount of air that remains in lungs
after the end of normal expiration.
- FRC = ERV + RV = 1100 + 1200 = 2500 ml.
- This volume of air is always present in lung .
- So, it allows continuous exchange of gases
even during expiration.
3. Vital Capacity (VC) [07]
- This is the maximum amount of air a person
can expel from lungs after 1st filling the lungs to
their maximum extent and then expiring to the
maximum extent.
- VC = IRV + TV + ERV = IC + ERV = 3000 + 500 +
1100 = 4600 ml
4. Total lung capacity (TLC)
- Maximum volume to which the lungs can be
expanded with the greatest possible effort.
- TLC = VC + RV = 4600 + 1200 = 5800 ml.
5. Other volumes & capacities
i. Dead space: [10]
- The volume of respiratory airways occupied
by air which is not involved in the gaseous
exchange with the blood.
- Normal value: 150 ml
It is of two types:
1 . Anatomical dead space.
2. Physiological dead space
1. Anatomical dead space:
- Total volume of air present in the conducting
zone of the respiratory passage . i. e from nose
and mouth upto terminal bronchioles, where
exchange of gases doesnot take place:
Normal value: 150 ml.
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2. Physiological dead space.
- It is anatomical dead space plus volume of air
in the alveoli which doesnot take part in the
exchange of gases.
- Physiological dead space depends on:
i. Volume of inspired air which ventilates
alveoli but receives no pulmonary capillary
blood flow.
ii. Volume of air which ventilates alveoli in
excess of that volume which is required to
equilibrate with the blood.
Role on alveolar ventilation:
i. Anatomical dead space does not participate
in alveolar ventilation.
ii. If physiological dead space is more that
anatomical dead space, it participate in
alveolar ventilation but no any exchange of
gases occurs through this space.
Note:
i. In healthy subjects, anatomical and physiological
dead space must be equal.
ii. Anatomical dead space differs with physiological
dead space only if V/Q ratio is altered. IV
ii. Timed vital capacity/forced vital capacity
(FVC) [07,10]
- Maximum volume of air which can be breathed
out as forcefully and rapidly as possible
following a maximum inspiration.
- It is a dynamic lung volume.
a. Forced expiratory volume in 1sec. (FEV1)
 Volume of FVC expired in 1st second of
exhalation.
 Most sensitive indicator of lung function test.
 Normal = 80%of FVC
b. FEV2
 Volume of FVC expired in first two sec of
exhalation.
 Normal = 95% of FVC
c. FEV3
 Volume of FVC expired in first three sec
of exhalation.
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 Physiology

d. Maximum mid expiratory flow rate. ii. FEV1 is decreased

(MMEFR) iii. FEV1/FVC is also decreased.
- Forced expiratory flow during 25-75% of Example: Emphysema
expiration Asthma
- Normal value: 500 L/min Chronic bronchitis
Significance: 2. Restrictive lung disease:
- Decreases during early stage of chronic i. Vital capacity is decreased
obstructive pulmonary disease
ii. FEV1 is also decreased
(emphysema, chronic bronchitis).
iii. FEV1/FVC is constant
Significance: (KU) Example: Fibrosis of lung
1. Obstructive lung disease: Intersitial lung disease
i. Vital capacity is normal Kyphosis.

IV

iii. Pulmonary ventilation v. Maximal voluntary ventilation:

- The amount of air inspired or expired in one - Largest amount of air that can be moved in
minute at normal breathing and out of the lung in one minute by
voluntary effort.
- PV = TV × breathing rate
- Normal value: 125 - 170 L/min.
= 500 × 12 /min
vi. Peak Expiratory flow rate (PEFR).
= 6000 ml/min = 6 litre/min
- Expiratory flow rate during the peak of
iv. Alveolar ventilation: forced vital capacity
- The amount of air reaching the alveoli per - Normal : 400-500 L/min.
minute. It is less than pulmonary ventilation Significance: Marked fall in obstructive airway
since, air is also present in dead space. disease.
- Alveolar ventilation = Breathing rate x (VT - VD) Vital Capacity [07,04,03]
= 12 × (500 - 150) - Maximum volume of air which can be expelled
= 4200 ml = 4.2 litre from lungs by forceful effort following a
maximal inspiration.
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- Normal value male: 4600 ml, female = 3200 ml
- Factors Affecting VC:
A. Physiological
i. Surface area: More in male than in
female.
ii. Age: Decreases with age.
iii. Posture: More in erect posture.
iv. Pregnancy: VC decreases
v. Sex: More in male.
B. Pathological:
i. Decreases in: Pulmonary fibrosis,
Respiratory obstruction, pleural
effusion, pulmonary edema, ascites,
Kyphosis, pneumothorax
- Significance:
i. Vital capacity is altered in above
pathological conditions. So, it helps in
finding those clinical abnormalities.
ii. Vital capacity helps in finding other aspects
of PFT like (FEV1, FEV2).
PULMONARY CIRCULATION
Functional anatomy
Pulmonary Vessels:
- Pulmonary trunk (5 cm) extends from the apex
of right ventricle and divides into right and left
main branches. These further divide to form
arteries and arterioles in the lungs. They have
large diameter compared to systemic arteries
and are more distensible which gives large
compliance to the lungs and also allow to
accommodate the stroke volume output of
right ventricle.
Bronchial vessels:
- Systemic vessels which supplies to the lungs.
They carry oxygenated blood and supply to the
connective tissue, septa, large and small
bronchi. It empties into the pulmonary veins
and enter the left atrium.
- Thus, left ventricular output is 1 to 2% greater
than right ventricular output.
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Lymphatics:
- Present in all supportive tissue of the lung and
drains into right thoracic lymph duct.
Note:
i. Total surface areas of pulmonary capillaries is
60m2 and transmit time for blood is 1sec.
ii. During exercise, total surface areas increase up to
90 m2 and transmit time is 0.3sec.
Distribution of blood in lung
- Total blood flow to the lung is equal to cardiac
output.
- However, due to pull of gravity, the
distribution of blood in lung is uneven.
- Lung can be divided into 3 zones
A. Zone 1 (apical)
 In this region both systolic & diastolic
pulmonary pressure are less than Alveolar
pressure
 So, there is not blood flow during both
systole & diastole.
 Considered as a part of physiological dead
space as no gasseous exchange occurs.
IV
 This region is ventilated but not perfused.
 Ventilation /perfusion rations is increased.
B. Zone 2 (Mid portion)
 In this region, systolic pressure is greater
than alveolar pressure but diastolic
pressure is less than alveolar pressure.
 Blood flows only during the systolic phase
but not in diastolic phase.
 So, there is intermittent blood flow.
 Ventilation perfusion ratio is normal
C. Zone 3 (Lower Portion)
 In this region, both systolic pressure and
diastolic pressure are greater than alveolar
pressure.
 Blood flows during both systolic and
diastolic phase.
 So, there as continuous blood flow.
 Ventilation perfusion ratio is decreased
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Alveolocapillary membrane / pulmonary

membrane [10]
- It is a membrane through which gaseous
exchange occurs in between the alveolar air
and the pulmonary blood. It is made up of
following layers.
1. Layer of surfactant: layer of fluid lines the
alveoli which reduces the surface tension.
2. Alveolar epithelium: Simple squamous
epithelium.
3. An epithelial basement membrane.
Factors influencing pulmonary circulation: 4. A thin interstitial space between alveolar
a. Position: epithelium and the capillary membrane.
- More during lying down than standing position. 5. Capillary basement membrane that in many
b. Exercise: places fuses with the alveolar epithelial
- The flow rate during exercise can increase upto basement membrane.
700-800% in upper part of lung and up to 200 6. The capillary endothelial membrane.
to 300% in lower part. - Average thickness of the respiratory
membrane = 0.6 m
PULMONARY GAS EXCHANGE
- Minimum thickness = 0.2 m
Past Questions:
- Total surface area = 70 sq. meters
1. Enumerate the components of respiratory
IV membrane. (2)[010]
2. Ventilation perfusion ratio (3) [08 July]

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Factors affecting diffusion of gases:
1. Rate of diffusion is inversely proportional to
the thickness of membrane
2. Rate of diffusion is  surface area of the
membrane.
3. Diffusion coefficient of the gas: depends on
molecular wt. & solubility of gas.
4. Pressure gradient between the two sides of
the membrane.
Partial pressure:
- The pressure which is exerted by a single gas in
a Combination of different gasses.
- It is proportional to the Concentration of gas
molecules.
- The rate of diffusion is also directly
proportional to the partial pressure.
- In the atmosphere, partial pressure of different
gases are as:
PN2 = 600 mmHg
PO2 = 160 mmHg
Total pressure = PN2 + PO2 = 600 + 160
= 760 mmHg
- Amount of gas dissolved in any solution is
directly proportional to partial pressure of gas
at constant temperature.
Diffusion capacity:
- The ability of the respiratory membrane to
exchange a gas between the alveoli and the
pulmonary blood is called diffusion capacity.
- It is measured as volume of a gas that will
diffuse through the membrane each minute for
a partial pressure difference of 1 mmHg.
- Diffusion capacity of:
O2 = 21 ml/min/mmHg
CO2 = 400 - 450 ml/min/mmHg.
- Diffusion capacity of CO2 is about 20 times
more than O2 this is why hypoxia occurs earlier
than hypercapnia in respiratory membrane
disease.
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Measurement of diffusion capacity (using CO):
1. A small amount of CO is breathed into the
alveoli.
2. The partial pressure of CO in the alveoli is
measured from appropriate alveolar air
samples.
3. The CO in the blood rapidly combines with
hemoglobin, thus the pressure of CO in blood is
essentially zero.
4. So, partial pressure difference of CO across the
respiratory membrane is equal to its partial
pressure in the alveolar air sample.
5. Measure volume of carbonmonoxide (CO)
absorbed in short period and divide this by
alveolar CO partial pressure.
Diffusion Capacity
=
Average diffusion capacity for CO = 17
ml/min/mm Hg.
Average diffusion capacity for O2 = 1.23 × CO IV
= 21 ml/min/mmHg.
Advantage of using CO for measurement:
- Measurement of PO2 in blood is difficult and
imprecise whereas PCO in blood is essentially
zero.
Shunt
 The blood which passes through pulmonary
capillaries without becoming oxygenated is called
shunt
Physiological shunt: At physiological condition,
some amount of blood is shunted due to:
i. Low V/Q (ventilation/perfusion) at base of lung
ii. Blood flowing through bronchial vessels.
This blood is called physiological shunt
Pathological shunt: Decrease in V/Q in -
pneumonia, ARDS, alveolar edema.
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Measurement: 2. Pathological causes:

1 Concentration of O2 is measured in both - All the factor which cause uneven alveolar
arterial and venous blood. ventilation or non-uniform blood flow to
pulmonary circulation will alter the V/Q
2. Simultaneous measurement of Cardiac output
ratio.
CiO2 - CaO2
Shunt (Qps) = CiO - CVO × QT i. uneven alveolar ventilation occurs in :
2 2

- Where, QPs is the shunt blood flow per a. Bronchial asthma

minute. b. Pnumothorax
- QT is the cardiac output per minute c. Emphysema
- CiO2 is the concentration of O2 in the d. pulmonary fibrosis
arterial blood if there is an ideal V/Q ratio e. Congestive heart failure.
- CaO2 is the concentration of O2 in the ii. Non-uniform pulmonary blood flow
arterial blood of sample taken. occur in:
- CVO2 is the measured concentration of O2 in a. Anatomical shunt (fallot's tetralogy)
mixed venous blood. b. Pulmonary embolism
Ventilation/perfusion (V/Q) ratio [08] d. Increased pulmonary resistance
 It is the ratio of alveolar ventilation to pulmonary Note:
blood flow: - In complete upper airway obstruction, V=0
 As alveolar ventilation is 4L/Min and pulmonary blood i.e. V/Q=0
4 - In complete pulmonary embolism, Q=0, i.e.
flow is: 5.L/Min, ventilation perfusion ratio = 5 = 0.8.
V/Q=infinite
IV
 In quantitative terms, ventilation - perfusion ratio
is expressed as V/Q GAS TRANSPORT
 Variation of V/Q in lung Past Questions:
Factors affecting V/Q ratio: 1. How is oxygen transported in the blood?
Enumerate the factors affecting the shift of
1. Physiological factors:
oxygen dissociation curve. (3 + 3 = 6) [08 Jan]
i. Apical region
2. Briefly describe how is oxygen transported in the
- Both ventilation and perfusion are least blood from lungs to tissue? (5) [05 Dec]
at the apex. 3. Describe how oxygen is transported from the
- However, ventilation is much higher lung to the tissues. What is Bohr effect?
than perfusion (5+1=6) [03 June]
- So, V/Q ratio → high 4. How is oxygen is transported in blood? Shortly
ii. Basal region: write about decompression sickness.
- Both ventilation and perfusion are more (5+5=10) [02 June]
at the base 5. State the transport of CO2 from the tissues to
the lung. What is Bohr effect? (4+2=5) [11 July]
- However, increase in alveolar ventilation
6. Describe the transport of CO2 from tissue to lung.
is much less relative to perfusion.
What is Bohr effect? (2+3 =5) [09 Jan]
- So, V/Q ratio →less

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7. Describe how CO2 is transported from the tissues - After diffusion of O2 to the pulmonary
to the lungs. What is Bohr Effect? Capillaries, blood is almost fully with O2
(2+3=5, 4+1=5) [08 July, 04 Dec] (97% saturated)
8. How is CO2 transported in blood? (2) [05 June] - PO2 in pulmonary capillaries is 100 ,mostly.
9. Describe the method of transport of carbon
dioxide in the blood. How does it help in
maintaining the acid base balance?
(3 + 2 = 5) [07 July]
10.Describe the transport of carbondioxide by the
blood. What is the role of carbondioxide in
regulation of respiration? (4+2=6) [07]
11.Uptake of oxygen in lungs (3) [05 June]
12.Vital capacity (3,4) [08 Jan, 04 June]
13.Oxygen dissociation curve
(3, 4) [10 Jan, 07 July, 04 June]
14.Chloride shift (3) [06 Dec]
 Oxygen diffuses from alveoli to pulmonary blood
which is transported to the peripheral tissues by
combination with hemoglobin and dissolved in
plasma
 In the tissue it reacts with food stuffs to form
large quantities of co2, which is transported back
of the lungs.
2. Transport of oxygen in the arterial blood.
IV
O2 transport [02,03,05,10] - O2 in arterial blood in transported by
 O2 is carried in blood in 2 forms: a. Combined with hemoglobin (97%)
A. In dissolved form (3%) - 4 molecules of O2 combine with one
B. In combination with haemoglobin: each molecule of hemoglobin.
hemoglobin molecules combines with 4 - combination occurs by process of
molecules of O2 (97%) oxygenation.
Steps in O2 transport: b. Dissolved state:
1. Diffusion of oxygen from alveoli to the - 3% of O2 is dissolved in plasma.
pulmonary capillary Blood: [03] - During the transport, blood pumped by
- PO2 in alveolus = 104 mm Hg and PO2 in the heart to aorta has PO2 about 95
pulmonary capillaries at arterial end = 40 mmHg. The decrease in PO2 from 100
mmHg. mmHg to 95 mmHg is due to mixing with
- The pressure gradient between alveoli and pulmonary shunt blood.
pulmonary capillary blood =104 - 40 = 64 3. Diffusion of O2 from the blood to the tissue
mmHg. fluid:
- This pressure difference causes O2 to diffuse - PO2 is arterial capillaries = 95 mmHg.
into pulmonary capillaries.
- PO2 in the interstitial fluid = 40mmHg.
- Pressure difference = 95 - 40 = 55 mmHg.

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 Physiology
- This tremendous pressure difference causes
O2 to diffuse rapidly from the capillary
blood into the tissue.
4. Diffusion of O2 from peripheral capillaries to
the tissue cells
- O2 is continuously used up by the cells. so
intracellular PO2 in the peripheral tissue
cells remains lower than the PO2 in the
peripheral capillaries.
- PO2 in interstital fluid = 40 mmHg.
- PO2 inside cell = 23 mmHg.
- Pressure difference = (40 - 23) mmHg = 17
mmHg.
Note:
- During exercise, the uptake of O2 by the
pulmonary blood may increase as much as 20
times.
- Almost all the O2 that dissolve in blood combines
with hemoglobin.
IV
O2 - Hb dissociation curve (02,04,08,10)
 It is a graphical representation of percentage of O2
saturation with hemoglobin with increase in PO2
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 The curve is sigmoidal in shape with 2 parts
i. steep part:
- It ranges from 10 - 40 mmHg partial
pressure of O2
- PO2 of this range is found in tissues.
- For 30 mmHg pressure change, the change
in % saturation = 75 - 13.5 = 61.5%
Importance:
- The huge change in % saturation (61.5) with
small change in partial pressure of 30mmHg
helps in the release of O2 in the tissue.
- In hypoxia, PO2 falls below 40 mmHg. So
there is rapid release of O2 to prevent
hypoxia
ii. Flat part
- When PO2 increase beyond 70 mmHg till
100 mmHg.
- This part of the curve is for the lungs.
Significance:
- When PO2 of inspired air falls from 100 to
70 mmHg then percentage saturation of
hemoglobin falls from 97.5% to 92.5% i.e.
amount of O2 carried by blood does not
change much even PO2 drops to 70 mmHg.
- O2 content of arterial blood falls from 20
ml/dl to 18ml/dl only even if the PO2 falls
from 100 to 70 mmHg.
- Thus at moderate altitude (up to 12000
feet) subject suffer little impairment in their
uptake of O2 by the body.
Significance of P50.
- P50 means the PO2 at which half of the
Hemoglobin (50%) is saturated with O2.
- At the temperature of 370C and PH of 7-4, P50 is
26 mm Hg.
- P50 value is the inverse function of hemoglobin
affinity to O2. That is, if hemoglobin affinity to
O2 is decreased , P50 value is increased.
Note: In co poisoning, the affinity of hemoglobin with
O2 is decreased , so P50 value is increased.
BASIC SCIENCE MBBS

Shifting of the curve: [02,04,08,10,11]
A. Shift to right:
- At any PO2, the O2 content that can be held
by blood decreases, causing unloading of
O2.
Causes:
1. CO2, combines with H2O to form carbonic
acid. This acid decreases the pH and finally
right shifting of the curve.
2. Presence of any acid in blood.
H+ + HbO2  HHb + O2.
3. Increase in blood temperature.
4. Increase in 2,3 diphosphoglyceric acid (2, 3
DPG)
It competes with O2 for binding site of
hemoglobin.
HbO2 + 2, 3 DPG  Hb - 2, 3 DPG + O2.
B. Shift to the left:
- Affinity of hemoglobin to combine with O2
increases, causing less release of O2 to the
tissues.
Causes:
1. Carbon monoxide: CO inhibits the synthesis
of 2,3 DPG
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Respi
2. Decreased H+ and PO2: Both increases pH of
blood and shift curve to the left.
3. Fetal hemoglobin.
4. Decreases blood temperature.
5. Decreased 2 - 3 DPG
Bohr's effects: [03,04,08,09,11]
- It is the shifting of O2 - hemoglobin saturation
curve by the change in blood H+ and co2
concentration.
- As the blood passes through the tissues,
carbondioxide diffuses from the tissue cells IV
into the blood. This increases blood CO2 which
in turn increases blood H2CO3 (Carbonic acid)
and hydrogen ion concentration. These effects
shift the oxygen - hemoglobin dissociation
curve to the right and downward, forcing
oxygen away from hemoglobin and therefore
delivering increased amounts of oxygen to the
tissues.
- Exactly the opposite effect occurs in lungs. CO2
diffuses from the blood into the alveoli. This
reduces the blood Pco2 and decreases the H+
concentration, shifting O2 - Hb dissociation
curve to the left and upward. Therefore, the
quantity of O2 that binds with the Hb at any
alveolar PO2 becomes considerably increased,
allowing greater O2 transport to the tissues.
Significance:
1. Increases release of O2 from blood to the
tissue
2. Enhances oxygenation of pulmonary blood.
BASIC SCIENCE MBBS -1169-
 Physiology
Sigmoid nature of the curve [08]
- The affinity of hemoglobin to O2 increases with
the addition of O2 to it.
- In deoxygenated state, globin portion of Hb is
in Tense (T) configuration thereby reduces the
affinity of the molecules for O2. Combination of
molecules with O2 release the bonds holding
the globin units producing a released (R)
configuration. This results in exposure of more
O2 binding sites. Thus affinity of hemoglobin
molecules increases to O2. However, all 4
atoms of Fe2+ do not combine with O2
immediately and simultaneously. If they do so
then line would be vertical. The combination is
a step wise process and affinity for O2 goes on
increasing with addition of O2. Therefore, the
affinity of hemoglobin for the 4th O2 molecule
is many times that for the 1st.
- This shifting affinity of hemoglobin for O2 due
to TR interconversion produces characteristic
sigmoid shape.
O2 carrying capacity of blood:
- When hemoglobin gets saturated to full
IV capacity, 1 gm. of hemoglobin can combine
with 1.34 ml of O2.
- At normal, average hemoglobin concentration
is 15gml/dl, therefore 100 ml. of blood can
carry 1.34 × 15 = 20 ml of O2 at full saturation,
this determines the O2 carrying capacity of
blood.
Carbondioxide Transport [04,05,07,09,11]
 CO2 content in venous blood: 52 ml/dl.
 CO2 content in arterial blood : 48 ml/dl.
 CO2 transported = venous blood - arterial blood
= (52 - 48) mg/dl = 4ml/dl
 Out of 4 ml/dl, 2.4 ml/dl (60%) is transported by
plasma and 1.6 ml/dl (40%) is transported by
RBCs.
Forms of co2 carriage:
A. Dissolved form (7%)
- As carbonic acid.
- As dissolved solution.
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B. As carbamino compound (23%)
- As carbamino - hemoglobin (RBC)
- As carbamino protein (plasma)
C. As HCO3– form (70%)
- NaHCO3 (in plasma)
- KHCO3 (in RBCS)
Steps of CO2 transport:
1. Diffusion of CO2 from peripheral tissue cells
into interstitial space.
- Intracellular PCO2 = 46 mmHg.
- Interstitial PCO2 = 45 mmHg.
- Pressure difference = (46 - 45) = 1mmHg.
This pressure causes diffusion of CO2 from
cell to interstitial space
2. Diffusion of CO2 from interstitial space to
capillary blood.
- Interstitial PCO2 = 45 mmHg.
- Arterial PCO2 = 40mHg.
- Pressure difference = (45 – 40) mmHg = 5
mmHg. This pressure causes diffusion of
CO2 from interstitial space to capillary
blood.
3. Transport in blood
A. dissolved form (7.5%)
- As carbonic acid
- As dissolved solution
B. As carbamino compound (18%)
- CO2 reacts directly with amine radicals of
the hemoglobin molecules to form the
compound carbaminohemoglobin (CO2
Hgb). This is a reversible reaction that
occurs with a loose bond, so the
carbondioxide is easily released into the
alveoli.
- As carbamino protein in plasma.
C. As bicarbonate form (70%)
- NaHCO3 (in plasma)
- KHCO3 (in RBCs)
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4. Release at the lungs.
- A part of CO2 from dissolved solution and
carbamino compound breaks up to liberate
CO2
- From Hco3– as:
O2 + H.Hb  HbO2 + H+
H+ + HCO3–  H2CO3
Carbonic anhydrase
H2CO3  H2 O+CO2
This CO2 is liberated through the lung along
the pressure gradient.
Role of Red blood cell [06,07]
 The dissolved CO2 in the blood reacts with H2O to
form carbonic acid (H2CO3) in the presence of
enzyme carbonic anhydrase. This enzyme is
abundant in RBC and hence accelerates the
reaction rate by 5000 fold.
 The H2CO3 formed in RBC is dissociated into
hydrogen ion and bicarbonate ion (H+ and HCO3–)
by the same enzyme. Most of the H+ combines
with the hemoglobin in the RBC as hemoglobin
protein is a powerful buffer. Whereas HCO3-
combines with K+ to form KHCO3 to some extent
and also diffuse from RBC to plasma. This diffusion
of HCO3 to plasma is followed by diffusion of
chloride ions into the Red cells. This is made
possible by the presence of a special bicarbonate
chloride carrier protein in the red cell membrane.
This phenomenon is called chloride shift.
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Significance:
i. Role in acid base balance: [06]
- As H2CO3 dissociates into H+ and Hco3– in
the RBC by carbonic anhydrase enzyme, H+
binds with hemoglobin and HCO3–
concentration increase in the cell. This
increases alkalinity of the RBC. To correct
alkalinity or RBC, bicarbonate ions diffuse
into the plasma and Cl– diffuse from plasma
to RBC.
ii. Helps in the CO2 transport
Haldane Effect (06)
 Loading of oxygen to the blood causes unloading
of CO2. Oxygen displaces CO2 form the blood after
binding to the hemoglobin. This occurs at the lung
level.
 Explanation: combination of Oxygen with
hemoglobin in the lungs causes the hemoglobin to
become a stronger acid. This displaces CO2 from
the blood and into the alveoli in 2 ways:
i. The highly acidic hemoglobin has less tendency
to combine with CO2 to form
carbaminohemoglobin, thus displaces the CO2
present in the carbamino form from the blood.
IV
ii. The increased acidity produces increased H+
concentration. This H+ binds to bicarbonates to
form carbonic acid which in turn dissociated
into H2o and co2 in the alveoli
H+ + HCO3 º H CO
2 3
carbonic anhydrase H2O + CO2
Significance:
i. The release of co2 in the lungs from blood is
doubled by haldane effect due to large PO2 in
lung.
ii. Similarly, CO2 picked up from the tissue is also
increased due to low PO2 in tissue, and thus
CO2 transport in the blood also increases.
Carbon monoxide Transport:
- Carbonmonoxide has 250 times more tendency
to bind with hemoglobin than oxygen. It binds
to the same site where oxygen binds. Thus, it
displaces oxygen from the hemoglobin,
thereby decreasing the oxygen carrying
capacity of the blood.
BASIC SCIENCE MBBS -1171-
 Physiology
- Carbon monoxide of partial pressure 0.4
mmHg causes half the hemoglobin in the blood
to become bound to CO instead of O2.
Therefore, 0.6 mmHg of CO can be lethal.
- Pure oxygen at high alveolar pressure can
displace CO rapidly from its combination with
hemoglobin.
- In CO poisoning, PO2 is normal and there is no
sign of hypoxia. So there is no hypoxic drive for
the ventilation . Hence it is very dangerous.
Role of myoglobin:
- Found in greater quantities in muscles
specialized for sustained contraction .
Eg. Muscles of leg and heart.
- Contains only one heme group. So, molecular
weight is 1/4th of hemoglobin
- Myoglobin takes up O2 at very low PO2 also.
This faster rate or association of myoglobin
with O2 makes its dissociation curve
rectangular hyperbola rather than sigmoid.
- Acts as a temporary storehouse of oxygen due
to:
i. At even PO2 of 40mm GH (venous blood),
IV
myoglobin is 95% saturated with O2.
ii. Even if PO2 falls to about 5mm Hg, it is
about 60% saturate O2.
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REGULATION OF RESPIRATION
Past Questions:
1. Name the respiratory centers. Where are they
located? Briefly discuss the modern concept of
neural control of breathing. (2+2+4=8)[05 Dec]
2. Describe the neural control of respiration. State
what happens to respiration if the spinal cord is
sectioned at the level of C7-C8. (4+1=5)[04 Dec]
3. Name the respiratory centers in medulla and
pons. Discuss briefly about the neural control of
breathing. (2+4=6) [09 July]
4. In the regulation of respiration, describe the role
of (2+3=5) [09 July]
a. Pneumotaxic centre
b. Chemoreceptor
c. Pulmonary vagal stretch receptors.
5. Describe in brief the chemical control of
breathing. (3) [06 Dec]
6. Name the peripheral chemoreceptor. Explain their
role in regulation of respiration. (1+3=4)[05 June]
7. State the role of chemoreceptors in control of
respiration. (4) [11 July]
8. State the name and location of respiratory
centers (2) [03 Dec]
9. Describe the role of following in the regulation of
respiration (2+2=4) [03 Dec]
a. Carotid and aortic bodies
b. Pulmonary stretch receptors
10.Role of chemoreceptors in the regulation of
respiration (3) [07 Dec]
11.Hering Breuer reflex (3) [10 July, 08 Jan]
 Respiration is always well adjusted exactly to the
demands of the body so, that oxygen pressure
(PO2) and carbondioxide pressure (PCO2) in the
arterial blood are almost constant. Respiration is
regulated by neural and chemical mechanism.
Neural regulation [04,05,09]
Respiratory center: [03,05,09,11]
- Several groups of neurons are located bilaterally in
the medulla and pons of the brain stem which
regulates the respiration rhythmically.
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 Respi

- They are divided as: Functions:

A. Medullary respiratory center: i. It limits inspiration after filling phase
1. Dorsal groups of neurons /Inspiration of lung.
center. ii. Increase rate of breathing due to
Location: Dorsal portion of medulla shortening of inspiration and
oblongata expiration. Thus, control both rate
Nucleus: Nucleus of tractus solitaris and pattern of breathing.
(NTS), Reticular substance of the
adjacent medulla (few nucleus)
Function:
i. Rhythmical inspiratory discharges by
repetitive bursts of inspiratory neuronal
action potentials.
ii Reciprocal inhibitions to expiratory
center.
2. Ventral respiratory group
Location: Anterolateral part of medulla
oblongata.
Nucleus:
i. Nucleus ambiguous (cranially)
ii. Nucleus retroambiguus (caudally)
Functions: Mechanism of Respiration [05,06,12]
i. Almost totally inactive during normal Inspiration:
IV
quiet respiration and functions only
during heavy exercise when high levels Apneustic center discharge stimulator impulse to
of pulmonary ventilation are required. inspiratory center and slightly inhibitory
impulse to the expiratory center.
ii. These neurons contribute to both
inspiration and expiration. But generally
causes expiration. Inspiratory center is stimulated and
discharge stimulatory impulse to the
B. Pontine respiratory centre:
Vagus / glossopharyngeal nerve

diaphragm and intercostals muscle through

1. Apneustic center: phrenic nerve and intercostal nerves.
Location: lower part of pons.
Function: Contraction of diaphragm and intercostal
i. It sends stimulatory impulse to the muscles
inspiratory center causing inspiration.
ii. Receives inhibitory impulse from Expansion of thoracic cavity and
pulmonary stretch receptor during lung
inspiration.
2. Pneumotaxic center. Peripheral Inspiration
Chemoreceptors
Location: upper pons.
Nucleus: Nucleus parabrachialis

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Expiration: Note:
As the lung expands, stretch receptors of the lungs Effect of transection in respiration
are stimulated and send inhibitor signals to the 1. Complete transection or brain stem:
apneustic centers
i. Below medulla: Stops respiration/apnoea

ii. Above pons (decerebration): Regular breathing
Also, at the same time, pneumotaxic center discharge
(eupnea)
inhibitory impulse to the apneustic center and
stimulatory impulse to the expiratory center. iii. In between medulla and pons: Rhythmic
respiration but irregular and gasping (due to

absence of pontine control).
the apneustic center ceases its activity and expiration
2. After cutting vagi:
takes place.
i. Respiration becomes deep and slow.

At the time of expiration, the stretch receptors do
not send inhibitory impulse to the apneustic
center and again inspiration takes place
Organization of respiratory centres

(+)
Pnemotaxic centre

(–) Pons
Apneustic centre

IV (+)
(+) (–)
Expiratory Reciprocal Inspiratory
neurons innervation neurons Medulla
(–)
Vagus
nerve

Respiratory motor neurons

Pulmonary in spinal cord
Intercostal Spinal
stretch muscle
receptors cord
Lung Intercostal nerve (T1, T2)

Phrenic nerve
Diaphragm (+) : Stimulation
(–) : Inhibition

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Chemical Regulations (05, 06, 07, 09, 011)

Chemoreceptors: Comparision
Chemoreceptors Peripheral chemoreceptors i.e. Medullary (central) Pulmonary and
Aortic and carotid bodies chemoreceptors myocardial
(05,06,09) (010) chemoreceptors
1. Location - Aortic bodies (2 or more) near - Ventral surface of medulla - pulmonary and
arch of aorta. near respiratory center coronary blood
- 2 carotid bodies – at vessels.
bifurcation of common
carotid artery.
2.Innervation - Aortic bodies - vagus nerve. - Direct connection to the - Vagus (x) nerve.
- Carotid bodies – respiratory centre by nerve
glosssopharyngeal nerve fibers.
3. Stimulated by i.  arterial Pco2 i.  arterial PCO2  CO2 in - Injection of
ii.  arterial PO2 CSF due to crossing of BBB veratridine or
iii. Cyanide, nicotine by lipid soluble co2. nicotine in these
- Co2 combines with H2O vessels.
CA
CO2 + H2O  H2co3  H+ +
Hco3
ii.  H+ in CSF stimulates central
chemoreceptors
4. Effect of i  in rate and depth of i.  in rate and depth of i. Bradycardia IV
stimulation respiration, hypertension and respiration only. ii. Hypotension
tachycardia ii. Regulates respiration from iii. Apnoea followed by
ii. Regulates respiration from minute to minute. tachypnoea called
breath to breath. iii. Provides last drive to  pulmonary
iii. Provides initial drive to  respiration in response to chemoreflex (Bezold
respiration in response to  in increase in arterial Pco2 and jarish reflex)
arterial Pco2 and contributes contributes to 80%  in
20%  in pulmonary pulmonary ventilation.
ventilation.

Non - chemical receptors
a. Lung stretch receptors [03]
- Located in the smooth muscle of the airways.
- When these receptors are stimulated by
distention of the lungs, they produce a reflex
decrease in breathing frequency (Hering -
Breuer reflex
- They relay in the medualla via myelinated
afferent in the vagus nerve
- Hering- Breur inflation reflex are or two types:
a. Hering-breur inflation Reflex.
Steady inflation or lungs (above 1 litre)

Stimulation or stretch receptors

Inhibitory impulse through vagus nerve to
'apneustic centre' inhibition or inspiration

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 Physiology
b. Hering-breur deflation reflex.
- It causes decrease in the duration of expiration
produced by marked deflation or lungs
b. Irritant Receptors:
- Located between the airways epithelial cells.
- Are stimulated by noxious substance (eg. dust,
pollen).
c. J (juxta capillary) receptors
- All located in the alveolar walls, close to the
capillaries.
- Engorgement of the pulmonary capillaries,
which may occurs with left heart failure,
stimulates the J receptors, which cause rapid,
shallow breathing.
d. Joint and muscle receptors.
- Are activated during movement of limbs.
- Are involved in early stimulation of breathing
during exercise.
Regulation of respiration by higher
centre
 Pain and emotional stimulus from hypothalamus
and limbic system stimulates respiratory center.
 Neocortex  Motor neurons innervating
respiratory muscles by passing through medullary
neurons  voluntary control of breathing.
IV
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Mechanism of Peripheral Chemoreptors
Stimulation [05,06]
- Each carotid body and aortic body contains two
types of cells, type I and II cells. These cells are
surrounded by fenestrated sinusoidal
capillaries. Type II cells are glial cells
(supporting cells) that support the type I cells.
- Type I cells respond to hypoxia as;
Hypoxia  decrease activity of O2 - sensitive K+
channel  decrease K+ efflux  increase ca2+
influx  depolarization of cell membrane 
Release of neurotransmitters  stimulate
afferent nerve endings.
- Signal to medullary respiratory centres-
↑ven la on.
- Peripheral chemoreceptors get stimulated by is
1. Hypoxia 2. Vascular stats
3. Asphyxia 4. Drugs
5. Increase in plasma K+ level.
Note:
i. The blood flow to the carotid body is highest in
the body.
ii. The chemoreceptors are not stimulated in
anaemia or carbon-monoxide (CO) poisoning. It is
because in CO poisoning . Only the combined O2
with hemoglobin is decreased not the dissolved
oxygen is plasma. The amount or dissolved oxygen
reaching the receptor is normal.
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 Respi

Visceral reflexes (Respiratory components) 5. What are the ill effects of hyperbaric oxygen
i. Cough reflex: therapy? (3) [10]
- begins with deep inspiration followed by 6. Caisson's disease (3) [09 Jan]
force expiration against a closed glottis.
- Intrapleural pressure  100 mmHg. Hypoxia [03,04,06]
ii. Sneezing reflex:
 Lack of oxygen at tissue level is called hypoxia.
- Similar expiratory effort as cough with a
 Factors which lead to hypoxia :
continuously open glottis.
-  Oxygen tension in arterial bold.
iii. Vomiting and swallowing.
-  Oxygen carrying capacity of blood.
- Inhibition of respiration and closure of glottis.
- Prevention of aspiration of food and vomitus -  Velocity of blood flow
into trachea -  Utilization of O2 by the cells.
iv. Hiccup: Types of hypoxia are [03,04,06]
- Spasmodic contraction of diaphragm and i. Hypoxic hypoxia.
other inspiratory muscles. ii. Anemic hypoxia
- Sudden glottis closure. iii. Stagnant (ischemic) hypoxia
v. Yawning: iv. Histotoxic hypoxia
- underventilated alveoli have a tendency to
A. Hypoxic hypoxia [03,05,09]
collapse which get reflexely stretched open
- It is characterized by a low arterial PO2 when
by deep inspiration and thus prevent
O2 carrying capacity of blood and rate of blood
development of atelectasis.
flow to tissues are normal or elevated. IV
RESPIRATION IN UNUSUAL - Characteristic feature:
ENVIRONMENTS i. Low arterial Po2
ii. Low arterial O2 content.
Past Questions:
iii. Low arterial % O2 saturation of hemoglobin
1. What is hypoxia? Describe the different types of
and
hypoxia with examples. (2+3=5) [03 Dec]
iv. Low Arterio - Venous PO2 difference.
2. Define hypoxia. How body acclimatizes at high
- Causes:
altitude? (2) [06 June]
i. Low PO2 in inspirited air eg. High altitude,
3. Name types of hypoxia. Describe the
breathing in a closed space.
physiological changes occurring during
acclimatization to high altitude. (2+5=7) [04 June] ii. Decreased pulmonary ventilation eg: Airway
obstruction, paralysis of respiratory
4. Explain why? (33=9)[08 July]
muscles, depression of respiratory center.
a. Cyanosis may not be seen in histotoxic
iii. Defect in exchange of gasses: defective V/Q
hypoxia.
ratio.
b. High altitude hypoxia (3) [07 July]
iv. Venous arterial shunts
c. Hypoxic hypoxia
v. Pulmonary fibrosis
(3, 2) [05 June, 03 June, 09 Jan, 09 July]

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 Physiology

- Normal: iii. Formation of altered hemoglobin.

 Arterial PO2 = 100 mmHg, venous PO2 = 40 iv. Combination of hemoglobin with other
mmHg gases other than O2 & CO2.
 A - V PO2 diff = 100 - 40 = 60 mmHg. C. Stagnant hypoxia:
 % O2 saturation of H at 100 mmHg = 97.5% - Due to decrease velocity of blood flow
 % O2 saturation of Hb at 40 mmHg = 75% - Causes:
 A - V HbO2 saturation difference = 97.5 - 75
i. Congestive cardiac failure
= 22.5%
ii. Hemorrhage
- Hypoxic hypoxia:
IV - Arterial PO2 = 55 mmHg, venous PO2 = 25 iii. Surgical shock
mmHg. iv. Thrombosis & embolism
- A - V PO2 difference = 55- 25% D. Histotoxic Hypoxia:
= 20% (decreases) - Due to inability of tissues to utilize oxygen even
- A - V HbO2 saturation difference =85-45 if it is delivered.
= 40% (increases) - Causes:
- Significance: i. Due to cyanide/Sulfide poisoning 
 High arterio-venous HbO2 saturation damage of cellular oxidative enzymes 
difference causes  release of O2 in the failure of cytochrome oxidase system 
tissue which helps in minimizing hypoxia. even if O2 is supplied, tissue can't utilize it.
B. Anemic hypoxia: Hypoxia at high altitude: [07]
- Due to inability of blood to carry enough - There is progressive decrease in alveolar PO2
amount of O2. with increase in attitude
- Despite normal O2 availability, blood is not able - Thus, the features of hypoxic hypoxia are
to take up sufficient amount of oxygen due to produced.
anemic condition. - Rate at which hypoxia develops
- Causes: - Duration of exposure.
i. Decreases in no. of RBCs - Mountain sickness develops after 8 - 24 hrs. of
ii. Decrease hemoglobin content in the blood. arrival and last for 5 - 8 days.

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- Mountain sickness can be acute mountain
sickness and chronic mountain sickness
i. Acute mountain sickness:
- It is characterized by:
a. Acute cerebral edema: hypoxia 
vasodilation of cerebral blood vessels
 blood flow  capillary pressure 
fluid leakage  cerebral edema.
b. Acute pulmonary edema:
High attitude Cold exposure Rapid ascent
↑sympathetic activity
↓
Pulmonary vasoconstriction
↓ - It is due to:
↑hydrostatic pressure
↓ ii. Pulmonary vasodilatation
Pulmonary edema
ii. Chronic mountain sickness:
- It is characterized by:
a.  in hematocrit
b.  in pulmonary arterial pressure.
c. Right ventricular hypertrophy
d. congestive heart failure and finally
death.
Acclimatization to high attitude: (04,06)
- Physiological adaptation of body to high altitude.
The person is acclimatized to low PO2 and thus can
work harder without any hypoxic effects.
- These processes perist a normal and prolonged
life in people living in high altitude.
Changes include:
1. Increase in pulmonary ventilation.
i. Pulmonary ventilation may increase up to 6
fold due to increase in tidal volume and
respiratory rate.
ii. Function Residual capacity is increased.
2. Decrease affinity of haemoglobin with O2.
Hypoxia  anaerobic respiration increase in
blood PH increased amount of 2, 3 DPG 
shifting of O2 hemoglobin curve to right
Release of more O2 from hemoglobin.
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3. Rise in hemoglobin concentration.
- Hypoxia in erythropoiesis  in
hemoglobin concentration
- PCV increases up to 60%
- Hemoglobin rises up to 20 gm/dl
4. Increased vascularity of hypoxic tissues
Hypoxia
↑in capillaries density Vasodilation
↑in blood flow
5. Increased diffusion capacity of lungs for O2.
i. in no. of pulmonary capillaries
iii. pulmonary blood flow
6. Changes at tissue level.
i. in no. of mitochondria
ii. in cytochrome oxidase
iii. Increase in synthesis of myoglobin IV
Note:
i. In histotoxic hypoxia, partial pressure of saturation
of O2 is normal. Defect is due to the inability of
utilization of oxygen. so there is no cyanosis(08)
ii. Very severe hypoxia produces generalized oedema.
iii. Anaemic hypoxia cannot cause cyanosis as total
hemoglobin content is low, enough reduced
hemoglobin is not formed to produce blue colour.
iv. Histotoxic hypoxia also cannot cause hypoxia as O2
is not taken up by tissues.
v. Cyanosis is produced only if reduced hemoglobin
level is greater than 5 gm/dl.
Space flight
 When spaceship begins to flight, linear
acceleration occurs.
 After reaching to the space, when it revolves
round the earth, centrifugal acceleration occurs.
 At the time of descent, deceleration occurs.
BASIC SCIENCE MBBS -1179-
 Physiology
1. Effects of centrifugal acceleration force:
More impact in circulatory system and
vertebrae
a. Positive g:
i. Circulatory system:
- As blood is mobile, it is translocated by
centrifugal forces, blood is translocated
towards the lowermost part of the body.
 remains for long in the depth of sea.
Pooling of the blood to feet and
lower body part
 sea, significant quantities of N2 bubbles can develop
Hypotension

Unconsciousness
ii. vertebral fracture when is > 20 G.
b. Negative g:
- Less damaging acutely, but more damaging
permanently than positive G.
- If G’ > - 5G momentary hyperemia of head,
brain edema can occurs.
- When G’ > - 20G, intracerebral rupture and
IV
hyperemia of eye can occur. Hyperemia of eye
can lead to blindness.
2. Effects of weightlessness:
- Experienced at zero gravity in space.
i. Motion sickness.
ii.Translocation of fluids within the body.
iii.Diminished physical activity.
Observed effects in prolonged stay are:
i. Decrease in blood volume.
ii. Decrease in RBC mass
iii. Decrease in maximum cardiac output.
iv. Loss of Ca2+ and phosphate from bones, lesion
of bone mass.
Deep sea diving
 Pressure increases with the  in the depth of sea.
33 feet deep water exerts same as that by air of
atmosphere at sea level. Thus, a person 33 feet
beneath the ocean surface is exposed to 2 atm
pressure.
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 When a person breathes air under high pressure
for long time, the amount or N2 dissolved in the
body fluid increases. Since N2 is not metabolized
by the body, at remains dissolved in all the body
tissues until the N2 pressure in the lungs is
decreased back to some lower level.
Decompression sickness [09]
Large amount or N2 is dissolved in body fluid if a diver

When diver suddenly comes back to the surface of
in the body fluid either intracellular or extracellular.

This can cause minor or serious damage in almost any
area of the body depending on the no. and size of the
bubbles formed; this is called decompression
sickness.
Symptoms:
- Due to tissue ischemia and tissue death.
i. Tissue: Pain in the joints and muscles of the
legs and the joint pain is called bend.
ii. Capillaries of lungs: Chokes, dyspnea
pulmonary edema.
iii. coronary artery: Myocardial infarction.
Nitrogen narcosis:
- When diver who remains beneath the sea for
long time is breathing a compressed air of high
nitrogen pressure.
- As other gas anaesthetics, N2 dissolves in the
fatty substances in the neuronal membranes
and alters the ionic conductance through the
membrane and finally reducing the neuronal
excitability.
- Symptoms of N2 narcosis varies with the depth
as:
i. At 120 feet: Loose many of his cares
ii. At 150 to 120 feet: Becomes drowsy.
iii. 200 - 250 feet: Becomes clumsy to perform
the work required.
iv. Beyond 250 feet: Becomes almost useless.
BASIC SCIENCE MBBS
 Respi

Hyperbaric oxygen and oxygen toxicity: ii. Bronchopulmonary dysplasia and retinopathy
- Inhalation of 100% pure at high barometric in infants.
pressure. It's main aim is to increase the iii. Muscular twitching, ringing in ears, dizziness.
amount of dissolved O2 in plasma. Therefore, it iv. Jerking type of respiration.
as useful in v. convulsions and unconsciousnes.
1. Anaemic hypoxia (specially due to 'co' Note: Newborn infants are very sensitive to O2
poisoning or severe blood loss) toxicity. So, it may lead to proliferation of retinal
2. Stagnant hypoxia and vessels with the formation of fibrous tissues
3. Histotoxic hypoxia. (retrolental fibroplasia) producing permanent
- However, 100% O2 at increased pressure blindness. So, they should never be given more than
increases oxygen toxicity, the toxicity is due to: 40% O2 inhalation.
i. Depression of respiratory center.
ii. Production of free radicals ABNORMAL BREATHING
iii. Stimulate the irritant receptors of Past Questions:
respiratory passage.
1. Dyspnoeic index (3) [05 Dec]
iv. Inhibit the lung macrophage killing bacteria
2. Cheyne-stokes breathing
and decreases production of surfactant.
(3) [10 July, 05 June, 04 Dec, 03 June]
Symptoms of oxygen toxicity: [010]
3. Periodic breathing (2) [03 Dec]
i. Substernal distress, nasal congestion, sore
throat, coughing.
Type Definition Features Physiological basis
1. Apnoea Inhibition or stoppage 1. Occurs during swallowing later 1. During swallowing  to
of respiration. hyperventilation. prevent aspiration of food.
2. During sleep - sleep apnoea. 2. Sleep  if genioglossus
fails to contract tongue
falls backward and IV
obstruct.
3.  Alveolar Pco2
2. Hyperpnea Increase in depth of i. Occurs during sternous exercise i.  in depth, increasing
breathing which may inhalation of O2 required
or may not for exercise.
accompanied by in
respiratory effort.
3. Tachypnoea Rapid and shallow Respiratory rate is greater than 20 1. During exercise, labor,
respiration is called breaths per minute during pregnancy.
tachypnea 2. Co poisoning
4. Dysponea Labored/difficult - Dyspneic index(KU05) = (Breathing 1. Servere exercise
breathing in which reserve/maximum voluntary 2. Emphysema, Bronchial
subject is conscious of ventilation) × 100 asthma, Cardiac failure.
shortness of breath - When DI < 60%, dyspnea develops. 3. Dyspnea in lying down
- Example: if maximum voluntary position (orthopnea).
ventilation = 120 L/min then,
Breathing capacity = 5 L/min
Breathing Reserve = 120 - 5 = 115
DI = (115/120)× 100% which is
greater than 60

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 Physiology

Hypercapnia  Hypocapnia causes depression of vasomotor and

respiratory center.
 Increased co2 in blood
 Hyperventilation results in respiratory alkalosis.
 Hypercapnia stimulates respiration. However, if
severe, it causes respiratory depression, which  Hypocalcemic tetany may develop due to fall in
may lead to coma and respiratory acidosis and Ca2+ levels. (Secondary for respiratory alkalosis)
further elevation of Pco2. Periodic Breathing [03]
 In fever, with rise in body temperature by 1 C, 0
 Cyclical repetition of apnea and shallow breathing
CO2 production increased by 13%. However, like hyperpnea.
respiration is also stimulated in fever and excess  This is typically seen following voluntary
CO2 is removed from the body. hyperventilation performed for 2-3 min.
 Therefore, if ventilation is compromised in such  Hyperventilation  removal of CO2 →Apnea 
situations, CO2 accumulates and hypercapia results.
Again, increase of Pco2 and PO2 in blood 
 Effects of hypercapnia stimulation of chemoreceptor  hyperventilation.
i. Respiration  dyspnea  Periodic breathing are of 2 types:
ii. Blood  pH is reduced and blood becomes i. Cheyne - stokes breathing
acidic (Respiratory acidosis) ii. Biot breathing.
iii. CVS  tachycardia,  in B.P.
Cheyne - stokes Respiration: [03,04,05,10]
iv. CNS  headache (morning headache),
- Periodic breathing that is characterized by
depression, tremor, Lazziness.
rhythmic hyperpnea & apnea.
 Physiological response to hypercapnia
- Though it occurs in deep sleep in some normal
Physiological response to hypercapnia rise in arterial persons, it is more common in congestive
PCO2
IV heart, uremia, brain diseases.
 - The patients have increased sensitivity to co2
Stimulates chemoreceptos due to disruption of neural pathways.

- Accumulation of CO2  hyperventilation 
Stimulates respiratory centres
PCO2   CO2 drive on ventilation  apnea
  PCO2 in blood  Chemoreceptor
Pulmonary ventilation stimulation  hyperventilation.

- In normal person, it is prevented because
CO2 washout until PCO2 becomes normal respiratory center alters the depth of
Note: With 1°C rise in temperature, there is 13% respiration in such a way that arterial Pco2
increase in CO2 production. does not drop below critical value.

Hypocapnia
 Hypocapnia usually results from hyperventilation
that also improves PO2 in blood.
 In voluntary hyperventilation, arterial PCO2: 40 
15 mm Hg and alveolar PCO2: 120  140 mmHg.
 Hypocapnia produces vasoconstriction and
reduces cerebral blood flow  cerebral ischemia:
dizziness, paraesthesis, light headedness.

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 Respi

- It is marked by two alternate patterns of Types

respirations. 1. Mechanical/instrumental method
i. Hyperpneic period: - Used when artificial respiration are used for
 Initially breathing is shallow  force of longer period.
respiration increases gradually and - Two types of mechanical methods:
reaches the maximum (hyperpnea)  a. Positive pressure method:
Then, it decreases gradually and reaches - Used in operation theaters during surgery.
minimum  apnea.
- Lung is inflated by pumping air or air-O2
 increasing phase of respiration is called mixture at positive pressure.
waxing and decreasing phase of Disadvantage: Impairs venous return.
respiration is called wanning.
Example: Controlled mandatory ventilation
ii. Apneic period. (CMV)
 It is the period after the cessation of b. Negative pressure method:
breathing. - Alternate compression and relaxation of chest
 Occurs in between 2 phases or wall.
hypernea. - It can be done by following methods:
Biot breathing i. Patient is placed in airtight chamber with
- Another form of periodic breathing his neck and head outside. The pressure
characterized by period OR apnea and inside the chamber is alternately increased
hyperpnea. and reduced. When pressure is increased
- After apneic period, hyperpnea occurs expiration occurs and when pressure is
abruptly. decreased inspiration occurs. IV
- Waxing and waning of breathing do not occur. ii. Hollow elastic rubber bag is wrapped
around the chest. Bag is alternately inflated.
- Bitot breathing do not occur in physiological
conditions and its occurrence is always iii. Automatic instrument called Boyle's
pathological. apparatus, in which rate and depth of
ventilation and composition of air inhaled
- It occurs in conditions involving nervous
can be varied.
disorders due to lesions or injuries to brain.
Example: Iron lung Machine
- Bitot's breathing is seen in
2. Manual Methods:
i. Meningitis
a. Mouth to mouth respiration.
ii. Disease affecting the medulla.
Clear the airway  extend the neck  close the
ARTIFICIAL RESPIRATION nostrils by pinching with the thumb and the index
 It is a method to assist or replace spontaneous finger of the right hand Take a deep breath 
breathing, after it has ceased. Apply your mouth close the to the subject’s
 It is given till normal rhythmic respiration is mouth and exhale forcefully into his mouth 
restored. look for the chest expansion and abdominal
 It is useful when functions of heart and dynamics distension  Repeat and maintain the breathing
of circulation are normal. at a rate of 10 - 15 per minute.

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 Physiology
b. Holger - Neilson method.
c. Mouth to nose breathing.
- Indications of artificial respiration:
1. Drowning.
2. CO - poisoning.
3. Accident
4. Pulmonary embolism
5. Airway obstruction
6. Electrocution
7. Anesthetic accidents.
Oxygen therapy
 Oxygen therapy is indicated in hypoxia, both in
acute and severe hypoxia, especially when
hypoxia is associated with dyspnea.
Methods:
1. Using oxygen tent: In children
2. Using oxygen masks:
3. Mechanical ventilator: When pt.
semiconscious or comatose
4. Intranasal tube:
 Oxygen therapy in different forms of hypoxic:
IV 1. In hypoxic hypoxia:
- Administration of O2  pressure gradient
between alveoli and blood  fascilates O2
entry into the blood.
- 100% O2 administration is harmful as it
causes respiratory depressions
2. In anaemic and histotoxic hypoxic: Hyperbaric
O2 therapy is used.
3. CO - poisoning: Hyperbaric O2 therapy.
Hyperbaric oxygen therapy:
- Administration of 100% O2 at increased
pressure.
- When hyperbaric O2 is administered, transport
of O2 in the dissolved form in plasma increases.
- The O2 solubility in plasma is 0.03
ml/100ml/mmHg but the required plasma
concentration adequate to maintain normal
metabolic need of the tissues of the body in
resting state is 6 ml/100ml.
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- To achieve this blood level, PO2 should be 2000
mmHg and it is achieved by administering
100% O2 at a pressure of 3 atm.
- Though it is very useful in many conditions, it
may facilitate the onset of oxygen toxicity.
Respiratory Failure
 Inability of the lungs to perform the functions of
gas exchange i.e. the transfer of oxygen from
inhaled air into the blood and transfer of CO2 from
the blood to exhaled air.
 In respiratory failure, PaO2 < 60 mmHg. (arterial
partial pressure of O2) and arterial partial
pressure of co2 (Paco2 > 50 mmHg.
 Two types of respiratory failure:
1. Type1
- Due to failure of oxygenation, PaO2 < 60
mmHg
- Leads to hypoxemia.
is
2. Type 2
- Due to failure of ventilation so that paco2 is
increased. PaCO2 > 50 mmHg.
- Leads to hypercapnia.
PULMONARY FUNCTION TEST
 Primary function of the lung is to maintain tension
of O2 and co2 of the arterial blood within the
normal range. The fundamental mechanisms
involved in attaining this goal are ventilation,
diffusion and perfusion. pulmonary function tests
are based on the assessment of these
mechanisms.
Uses:
1. Diagnosis of respiratory dysfunctions
2. Monitoring the progress of the disease.
3. Evaluating the efficacy of treatment.
4. Determining the efficacy of physical training.
5. Studying the prevalence of respiratory diseases
in the community.
6. Assessing the respiratory fitness of the
patients.
BASIC SCIENCE MBBS

Tests [KU 2012]
1. Spirometry:
- Measurement of tidal volume, vital capacity,
forced vital capacity.
2. Measurement of functional residual
capacity (FRC), dead space:
a. Measurement of FRC.
- By helium dilution technique.
- N2 washout technique.
b. Measurement of dead space
- Anatomical dead space is measured by rapid N2
meter.
- Physiologic dead space by Bohr's equation.
3. Measurement of airway resistance.
a. Measurement of timed vital capacity.
b. Peak expiratory flow rate.
- FEV1 estimation is the most diagnostic test.
- Maximum mid-expiratory flow rate (MMFR):
Maximum flow rate achieved during the
middle third of the total expired volume.
- This is expressed as forced expiratory flow at
25% to 75% of the lung volume. It indicates
patency of small airways.
4. Diffusion capacity of lung: using CO
(described earlier)
5. Closing volume for small airway
diseases:
- The lung volume at which the airways at the
base of the lungs close during expiration is
called closing capacity.
6. Analysis of blood and air.
- concentration of O2 and CO2 in inspired and
expired air.
- Arterial blood gas analysis.
- Mixed venous blood gas analysis.
Non-respiratory functions of respiratory
system
A. Lung defence mechanism:
1. Humidify and cool or warm the inspired air.
2. Bronchial secretion contain IgA.
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3. Prevent foreign body > 5m reacting to the
lung.
4. Pulmonary alveolar macrophages are actively
phagocytic and ingest inhaled bacterial and
small particles.
B. Functions of pulmonary circulation
1. Reservoir for left ventricle.
2. Act as a filter for: Blood clots, detached cancer
cells, fat cells, gas bubbles.
3. Fluid exchange and drug absorption.
C. Metabolic and endocrine functions:
1. Synthesis for surfactant, PGE2 Histamine.
2. Substances are removed from blood like: PGE1,
PGE2, Bradykinin, Adenine derivatives,
serotonin, Nor-epinephrine, Acetylcholine.
3. Substance activated in lungs: Angiotensin I 
Ag II
4. Storage of hormones and certain biologically
active peptides in "amine precursor uptake and
decarboxylation (AUPD) cells and nerve fibers
of lung.
APPLIED RESPIRATORY PHYSIOLOGY IV
Past Questions:
1. Cyanosis (3) [10 Jan]
Cyanosis [10]
 Cyanosis is the bluish discoloration of skin or
mucus membrane due to the presence of at least
5 gm of reduced hemoglobin per 100ml of blood
in the capillaries or 5gm/dl.
 Reduced hemoglobin is blue (dark) in color
 Types:
A. Central cyanosis:
- Occurs due to  level of reduced hemoglobin.
Causes:
i. Inadequate oxygenation of blood in the lung.
- high altitude
- emphysema, pneumonia, COPD.
- collapse of the lung.
- CO poisoning.
BASIC SCIENCE MBBS -1185-
 Physiology

ii. congenital cyanotic heart diseases. Symptoms:

- Tetralogy of fallot. - Chest pain, shortness of breath.
iii. Polycythemia: Total hemoglobin increases, so - Finally leads to cyanosis and hypercapnia.
there is there is  chance of reduced Emphysema
hemoglobin.  Obstructive disease of the lung in which lung
Sites: Tip of the tongue, lips, mucus parenchyma is damaged leading to shortness of
membrane. breathe. Smoking is the leading cause of
B. Peripheral cyanosis. emphysema.
- Due to the vasoconstriction, blood flow to the  Chronic infection, caused by inhaling smoke or
tissue decreases. So, reduced hemoglobin other substance irritates bronchi and bronchioles.
concentration increases locally.  Infection, excess mucus and inflammatory edema
Causes: produces chronic obstruction.

1. Exposure to the cold climate.  Chronic emphysema progresses slowly over many
years. The person develops both hypoxia and
2. Reduced blood flow due to venous obstruction,
hypercapnia. The next result of all these is
local chilling. devastating air hunger that can last for years until
Site: Finger tips, ear lobes, tip of the nose. the hypoxia and hypercapnia causes death.
Asphyxia Obstructive and Restrictive Diseases
 Occlusion of airways produces hypoxia and [KU]
hypercapnia which is combinedly known as Obstructive disease Restrictive disease
asphyxia.
1. Total lung capacity is 1. Total lung capacity is
IV  Following events happen during Asphyxia: normal or increased decreased
i. Initially, there will be marked stimulation of
2. Residual volume is 2. Residual volume is
respiration with violent respiratory effort.
elevated due to decreased
ii. BP and heat rate increases. trapping of air during
iii. Blood pH falls. expiration.
iv. sed catecholamines 3. FEV1 is heavily 3. Both FEV1 and FVC are
decreased than FVC proportionally
v.  Of CO2 above certain level  depress
so,FEV1/FVC decreased. so,
respiratory center and VMC resulting in death.
decreases FEV1,/FVC remains
Treatment: Artificial respiration. constant
Pneumothorax 4. Example: 4. Example:
 Abnormal collection of air or gas in the pleural a. Asthma a. Pulmonary fibrosis
space. Tension pneumothorax is a condition in b. COPD (Chronic b. Pneumoconiosis
which air accumulates in the pleural space by the bronchitis, c. Interstitial lung
one way valve formed by damaged tissue. emphysema) disease
Causes: c. Cystic fibrosis
i. Physical trauma to the chest. d. Bronchiectasis
ii. complication of medical and surgical 5. Tidal volume  5. Tidal volume 
intervention

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SPECIAL POINTS FOR MCQs

Normal values:
a. Intrapleural pressure 
i. Beginning of inspiration -2 mm Hg
ii. At the end of inspiration  -6 mm Hg
b. Total compliance of both lung together  200 ml/cm H2O
c. Pulmonary volumes
i. Tidal volume (TV)  500 ml
ii. Inspiratory reserve volume  3000 ml
iii. Expiratory reserve volume  1100 ml
iv. Residual volume 1200 ml
d. Pulmonary capacities
i. Inspiratory capacity 3500 ml
ii. Functional residual capacity  2500 ml
iii. Vital capacity  4600 ml (male), 3200 ml (female)
iv. Total lung capacity  5800 ml
e. Dead space  150 ml
f. Pulmonary ventilation  6 lit/min
g. Alveolar ventilation  4.2 lit/min
h. Maximal voluntary ventilation/respiratory minute volume  125-170 lit/min
i. The rate blood flow through the lung is  5 lit/min
j. Pulmonary arterial pressure IV
i. Systole  25 mm Hg
ii. Diastole  8 mm Hg
k. The average thickness of the respiratory membrane is 0.6 m
- Minimum thickness  0.2 m
- Total surface area = 70 sq. meters
l. Partial pressure of gases in atmosphere
i. PN2 = 600 mm Hg
ii. PO2 = 160 mm Hg
m. Diffusion capacity
i. O = 21 ml/min/mm Hg
ii. CO = 17 ml/min/mm Hg
iii. CO2 = 400-450 ml/min/mm Hg
n. Alveolar ventilation = 4 lit/min
Pulmonary blood flow = 5 lit/min
V/Q = 4/5 = 0.8
o. PO2
i. Alveolus = 104 mm Hg
ii. Pulmonary capillaries at arterial end = 40 mm Hg
iii. Arterial capillaries = 95 mm Hg
iv. Interstitial fluid = 40 mm Hg

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 Physiology

Special Points:
1. No. of alveoli in men is 300 million and each has a diameter of 0.2 mm.
2. Normal value of PO2 is 80 - 100 mmHg and PCO2 is 40 mmHg in artery
3. During inspiration, intrapleural pressure becomes more negative than alveolar pressure.
4. Functional residual capacity is measured by N2 wash out methods.
5. Spirometry cannot measure (i) Residual volume (ii) Functional residual capacity (3) Total lungs
capacity.
6. Slow and deep breathing are most economical way of breathing.
7. Anatomical dead space = 150 ml. (measured by flower method) physiologic dead volume = 155ml.
8. Ideal V/Q = 0.8. Apex of lung  V > Q (wasted ventilation), base of lung Q > V. (wasted
perfusion)
9. With exercise, V/Q approaches to zero.
10. Hypoxia produces pulmonary vasoconstriction but cerebral vasodilation.
11. At high altitude, following changes occurs: ventilation, sensitivity to central receptors,
response to carotid bodies, erythropoietin, 2,3 DPG, mitochondria, Renal excretion of
bicarbonate, respiratory alkalosis and pulmonary edema.
12. Alveolar macrophages are also called heart failure cells.
13. Surfactant production is decreased by smoking. It decreases surface tension but  compliance. It's
production is ed by glucocorticoids.
14. Heads reflex: Inflation of lungs induces more inflation. It is due to irritant receptors in the lungs.
15. Damage to pneumotaxic centre causes slow and deep respiration.
16. Damage to vagus nerve causes depth of inspiration.
17. In anemia, 2,3-DPG concentration increases, 2,3 DPG unloads O2 to tissues.
IV
18. In a healthy adult, 24 hour production of co2 is about 250 liters.
19. Diffusion capacity of CO2 is 20 times more than O2.
20. Average area of alveolar walls in contacts with capillaries in both lungs is about 70 sq.m.
21. Normal composition of venous blood is PO2 - 40 mmHg, Pco2 - 45 mmHg, Hb saturation 75%.
22. Peak expiratory flow rate is 400 - 500 L/minute.
23. The presence of Hb. ses the carrying capacity of O2 by 70 times.
24. Intra pleural pressure is always negative, it becomes more negative during inspiration.
25. Pco2 is the most important variable in the regulation of ventilation.
24. Central chemoreceptors respond to the change in (H+)
25. Opium poisoning, uremia, CCF, hypoxia produce cheyne - stokes breathing.
26. Biot’s breathing is seen in some patient with CNS disease eg. Meningitis. It consists of period of
normal breathing interrupted suddenly period of apnea.
27. Hysterical breathing  hyperventilation  Paco2.
28. Kussmaul breathing occurs in diabetic coma and consists of continuous, rapid, deep breathing.
29. Cyanosis is produced by:
i. Reduced Hb>5 mg/dl
ii. O2 saturation <85%
iii. Methemoglobin >1.5gm/dl

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iv. Sulfhemoglobin > 0.5 gm/dl

Cyanosis is not produced by
i. Anaemic hypoxia
ii. CO poisoning
iii. Histotoxic hypoxia
30. The symptoms of N2 narcosis resemble alcohol intoxication.
31. CO - poisoning causes (1) normal PO2 (2) O2 saturation (3) cherry red
Skin discoloration
32. Hypoxia:
i. Hypoxic  high altitude, respiratory diseases  test by PaO2
ii. Anemic  Anemia, CO - poisoning,  test by O2 content
iii. Stagnant  cardiogenic shock  test by A - V difference of O2.
iv. Histotoxic  cyanide poisoning  test by PO2 of venous blood /A - V difference.
33. O2 toxicity producing CNS effect (Best effect) and pulmonary effects (smith effect)
34. Most of the airway resistance is from the trachea.
35. After hyperventilating for some time, holding the breath is dangerous since due to lack of
stimulation by CO2, anoxia can go to dangerous levels.
36. A patient with normal lung compliance and increased airway resistance will have slow and deep
breathing.
Note: Severe acidosis (Kussmaul breathing): Rapid and shallow.
37. Pulmonary surfactant is: Dipalmitoyl phosphatidyl choline.
38. Caisson's disease/decompression sickness is due toN2.
39. Cyanosis in which PaO2 is normal is seen in abnormal hemoglobin
40. Normal dead space is about 30% of the tidal volume.
150 IV
Dead space = 150 ml. Tidal volume = 500 ml, = 500 × 100 = 30%
41. Expiratory reserve volume is same in males and females.
42. J - Receptors are situated an alveolar interstitium.
43. A person ascending rapidly develops breathless due to:  ventilation   co2 wash out
↓respiration stimulation.
44. Addition of glucose to stored blood is to increase 2,3 DPG
45. Continued hyperventilation occurs after hyperventilation with 6% co2 because co2 is persistently
increased which further stimulate respiration.
46. Normal value of FEV1 is 80%
47. Most important factor for transport of co2 as bicarbonate is high level of carbonic anhydrase in RBC.
48.
Tidal volume Rate
Person A 600 ml 10 min
Person B 300 ml 20 min
The alveolar ventilation is greater in person A. As; Total alveolar ventilation in A = (600 - 150) × 10
= 4500 ml.
Total alveolar ventilation in B = (300 - 150) × 20 = 3000 ml.
Note:
- A person with rapid and shallow breathing has alveolar ventilation decreased.

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49. O2 deprivation to the body is due to

Hypoxemia (PaO2) Hypoxia (O2 delivery to Ischemia (Loss of blood flow)
tissue)
1. High altitude 1.  cardiac output 1. Impeded arterial flow
2. Hypoventilation 2. Hypoxemia 2. Reduced venous drainage
3. V/Q mismatch 3. Anemia
4. Diffusion limitation. 4. Co poisoning
5. Right to left shunt
50. Instrument used for measuring the vital capacity and FEV1 is vitalograph.
51. When the atmosphere pressure is halved, following things happen:
a.  in pulmonary ventilation.
b. A fall in arterial po2.
c. A rise in arterial pH
d. A rise in cerebral blood flow.
52. Diffusion capacity of CO2 is 20 times more than O2
53. Role of N2 in our body is
i. Decrease rate of combustion.
ii. Delays alveolar collapse
iii. Prevent atelectesis
54. Work done in quite breathing is 0.5 kg-m/min
56. Respiratory minute volume in a normal preson is 60L/min
IV 57. Maximum voluntary ventilation is 125 - 170 L/min
58. CO2 affects respiratory centre via CSF H+ conc.
59. Moderate exercise tachypnea is due to stimulation of propioception.
60. Fastest acting enzyme is carbonic anhydrase.
61. Flow during last stage of expiration decreases because of dynamic compression of airways.
62. If we cut spinal cord above medulla, respiration becomes irregular and gasping.
63. N2 washout method is used for estimating functional residual capacity but accurately measured by
helium washout method.
64. 100 ml of arterial blood carries 20 ml of O2.
65. Pacemaker regulating the rate of respiration is pre-botzinger complex
66. Exchange of gasses starts from the respiratory bronchioles.
67. Pulmonary alveoli contains, pneumocytes, PAM cells, plasma cells, APUD cells, APUD cells
secrete VIP.
68. Pulmonary arterial pressure
i. Systolic= 25 mmHg
ii. Diastolic = 8mmHg
iii. Mean pulmonary arterial pressure = 15mmHg.
iv. Distensible low pressure system
v. Low resistance to blood flow (15-5)
69. The solubility coefficient is highest for CO2 and is 0.57 while that of O2 is 0.024.

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71. Average thickness of the respiratory membrane is 0.6 m.

72. Thickness of the respiratory membrane is increased in pulmonary edema and surface area is
decreased in emphysema.
73. Oxygen diffusing through the respiratory membrane per minute = rate at which the resting body
uses O2 = 230 ml.
74. In venous blood, PO2 = 40 mmHg, Pco2 = 46mmHg.
75. For 1 cm descent of diaphragm, the amount of air sucked into the lungs is 200 - 300 ml.
76. Intrapleural pressure at the beginning of inspiration is -2 mmHg and at the end of inspiration is - 6
mmHg. But at the end of deep inspiration, intra pleural pressure can become up to - 300
mmHg.
77. Closing volume of the lung determines transmural pressure.
78. Functional residual capacity as increased in obstructive diseases like emphysema, bronchial
asthma and in old age.
79. Functional residual capacity allows continuous exchange of gasses to occur throughout the
respiration and also prevents sudden changes in partial pressure of gases in the blood.
80. Maximum mid expiratory flow rate (MMEFR) indicates flow obstruction in small air ways.
81. Surfactant causes
i. Decreases in surface tension
ii. Increase in lung compliance.
82. The compliance, when expressed as a function of FRC is called specefic compliance.
83. Maximum effort during normal respiration is done for lung elasticity.
84. More resistance during expiration is due to compression or airway;
Resistance α
85. Pulmonary ventilation at rest = 6 L/min and alveolar ventilation = 4.2L/min
IV
86. In normal adult, the ratio of physiological and anatomical dead space is 1:1
87. When blood is exposed to PO2 of 500 mmHg, there is 5 fold  in dissolved O2. Oxygen content of
the blood is not increased, so high because Hb is already saturated with O2.
88. P50 is increased if the O2 dissociation curve shifts to right and it is decreased if it shifts to left. At
normal condition, P50 = 26 mmHg.
89. At arterial blood, PO2 is 100mmHg and saturation or Hb. with O2 is 97.5%. Hb is fully saturated at
PO2 of 120 mmHg.
90. Hemoglobin binds with 4 molecule of O2 but myoglobin binds with only 1 molecule of O2.
Myoglobin takes up O2 at low pressure and it is more concentrated in muscle.
91. Coefficient of O2 utilization is the percentage of blood that gives up its O2 as it passes through the
tissue capillaries.
At rest = 25%
At sternous exercise = 75-85% can reach up to 100%
92. Bohr's effect helps in the unloading of O2 at the tissue where as Haldene effect helps in the
unloading of co2 at the lung.
93. Chloride shift is the diffusion of Cl– from plasma to RBC which completes in 1 sec. Due to chloride
shift Cl– concentration is more in arterial blood than in venous blood.
94. Dorsal group of respiratory centre is most vital for respiratory control, It initiates the respiration -
and shows rhythmic discharge.

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95. Transection brain stem:

i. Below medulla  Apnoea
ii. Below pons  spontaneous rhythmic discharge  apneustic respiration .
96. J - receptors stimulation produces:
i. Apnea  tachypnea
ii. Hypotension
iii. Bradycarclia
97. Carotid bodies are more effective in stimulating respiration than aortic bodies.
98. Hypocapnia does not stimulate peripheral chemoreceptor but hypercapnia is the most potent
stimulator.
99. Dyspnoea in lying down position is called orthopnoea.
100. The point at which breathing can no longer be voluntary inhibited is called breaking point.
111. Characteristics of hypoxia:
Type of PO2 O2 carrying Blood O2
Hypoxia arterial capacity flow usage

Hypoxic Reduced Normal Normal Normal

Anemic Normal Reduced Normal/ ↑ Normal

Stagnant Normal Normal Reduced Normal

Histotoxic Normal Normal Normal Reduced

112. Ventilation is more at - base
IV 113. Alveoli are larger & less compliant at Apex.
114. N2 washout test measured in expiration.
115. N2 washout test measures - regional ventilation.
116. Local lung ventilation depends on: (a) lung compliance (b) Airway resistance
117. Tracheo - bronchial tree:
- Divides 23 times.
- Length generation bronchioles  terminal bronchioles
- 17th generation onwards bronchioles  Respiratory bronchioles
- Cartilage is absent from terminal bronchioles.
- Smooth muscle is more abundant in terminal and respiratory bronchioles.
- Glands are absent beyond the terminal bronchioles.
118. Autonomic stimulation in bronchioles
- Sympathetic  bronchodilation
- Parasympathetic  Bronchoconstriction
119. High V/Q ratio in apices predisposes to T.B. because high alveolar PO2 provides favourable
environment for the growth of T.B. bacilli.
120. Blood flow:
- Carotid body  2000 ml/100 gm/min
- Brain  54 ml/100 gm/min
- Kidney  420 ml/100 gm/min
- Heart  84 ml/100 gm/min
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