Respiratory system
Chapter # 3
Respiration
 Act of breathing resulting in exchange of
oxygen & CO2 b/w body tissues and
atmosphere
 Divisions
◦ 4 main divisions
 Pulmonary ventilation
 Inflow & outflow of air b/w atmosphere & lung
alveoli
 Diffusion
 Of oxygen & CO2 b/w alveoli & blood
 Transport
 Of oxygen & CO2 in blood and body fluids to
& from cells
 Regulation
 Of ventilation & other acts of respiration
 Functions of respiration
◦ Supply of oxygen to tissues & removal of CO2
from blood
◦ Helps in regulating acid base balance by
adjusting CO2 elimination from body
◦ Helps in keeping constant condition of water in
body through elimination of excess water vapors
◦ Eliminates certain harmful volatile substances
from body e.g. ammonia, alcohol etc
 Mechanics of respiration
 Lungs can be expanded & contracted in
2 ways;
◦ By downward & upward movement of
diaphragm to lengthen or shorten chest
cavity
◦ By elevation & depression of ribs to increase
& decrease anteroposterior diameter of chest
cavity
 Inspiration & muscles of inspiration
◦ During inspiration (in normal quiet breathing);
 main role is played by contraction of diaphragm that
pulls lower surfaces of lungs downward
 Other muscles;
◦ External intercostal (main muscle)
◦ Sternocleidomastoid muscles
◦ Anterior serrati
◦ Scaleni
 Expiration & muscles of expiration
◦ During expiration, diaphragm simply relaxes
& elastic recoils of lungs, chest wall &
abdominal structures compresses lungs
 Muscles helping in expiration;
◦ Abdominal recti (main muscle)
◦ Internal intercostals
Lungs pressure
 Pleural pressure
◦ Pressure in narrow space b/w lung pleura &
chest wall pleura
◦ Negative pressure which prevents collapse of
lungs
◦ Also called lung recoil pressure
◦ Value; 5 cm of H2O
 Alveolar pressure
◦ Pressure inside lung alveoli
◦ Different during inspiration & expiration
◦ Inspiration – alveolar pressure becomes -1 cm of
H2O
 which causes air to move into lungs
◦ Expiration – alveolar pressure rises to about
+1 cm of H2O
 this forces inspired air out of lungs
 Transpulmonary pressure
◦ Difference b/w alveolar pressure & pleural
pressure
◦ Pressure difference b/w alveoli & outer
surface of lungs
◦ Actually it is measure of recoil pressure
 Recoil pressure
◦ Elastic forces in lungs that tend to collapse
lungs at each point of expansion
Pulmonary volumes
 Tidal volume
◦ Volume of air inspired or expired with
each normal breath
◦ Value: 500 ml
 Inspiratory reserve volume
◦ Extra volume of air that can be inspired in
after normal tidal volume
◦ Value: 3000 ml
 Expiratory reserve volume
◦ Extra amount of air that can be expired by
forceful expiration after end of normal tidal
expiration
◦ Value: 1100 ml
 Residual volume
◦ Volume of air still remaining in lungs after
most forceful expiration
◦ Value: 1200 ml
Pulmonary capacities
 Combination of two or more pulmonary
volumes
 Inspiratory capacity
 Combination of tidal volume & inspiratory
reserve volume
 Formula: I.C = T.V + IRV
 Significance
 This is the amount of air that a person can
breath;
◦ beginning at normal expiratory level & ending at
maximum lung distension
 Value: 3500 ml
 Functional residual capacity
 Combination of expiratory volume &
residual volume
 Formula: FRC = ERV + RV
 Significance
 This is amount of air remaining in lungs
at end of normal expiration
 Value: 2300 ml
 Vital capacity
 Combination of inspiratory reserve
volume, tidal volume & expiratory
reserve volume
 Formula: VC = IRV + TV + ERV
 Maximum amount of air that a person
can expel from lungs;
◦ after first filling lungs to their maximum extent
& then expiring to maximum limit
 Total lung capacity
 Combination of vital capacity & residual
volume
 Formula: TLC = VC + RV
 Significance
 Maximum volume to which lungs can be
expanded with greatest possible
inspiratory effort
 Value: 5800 ml
Composition of inspired,
expired & alveolar air
 Lungs can never be completely emptied of air b/c
of residual volume
The Relative Composition (% by Volume) of
Inspired, Expired & Alveolar Air
Gas
Inspired air
%
Expired air
%
Alveolar air
%
Oxygen 20.71 14.6 13.2
Carbon
dioxide
0.04 3.8 5.0
Water
vapour
1.25 6.2 6.2
Nitrogen 78.0 75.4 75.6
 Inspired air contains approximately 21% by
volume of oxygen gas
 As this fresh air is drawn into alveoli;
◦ it mixes with air already present (residual
volume)
 Residual volume dilutes fresh air, so
oxygen content falls
 CO2 content of alveolar air increases
significantly as gas exchange proceeds
◦ & CO2 diffuses from blood into alveoli
 Oxygen content of expired air is higher than
that in alveoli
◦ This is explained by fact that expired air from
alveoli mixes with dead space air whose oxygen
content is same as that of atmosphere
 CO2 content in expired air is less than that
of alveolar air
◦ explained by fact that expired air from alveoli
mixes with dead space air containing very low
levels of carbon dioxide
 Water vapour content of expired air is
significantly higher than that of inspired air
◦ as air is breathed into alveoli, water from lining of
alveoli evaporates into alveolar air such that
expired air is greater in volume than inspired air
 Nitrogen gas is neither used or produced by
body and actual amounts of nitrogen in
inspired an expired air do not change
◦ slightly larger volume of expired air means that
nitrogen forms part of larger volume during
expiration and so its % by volume decreases
 There are several reasons for alveolar air
differences
◦ First, alveolar air is only partially replaced by
atmospheric air with each breath
◦ Second, oxygen is constantly being absorbed
into pulmonary blood from alveolar air
◦ Third, carbon dioxide is constantly diffusing from
pulmonary blood into alveoli
◦ Fourth, dry atmospheric air that enters
respiratory passages is humidified even before it
reaches alveoli
Transport of O2 & CO2 in Blood
& body fluids
 O2 is transported in combination with Hb to tissue
capillaries
 CO2 also combines with chemical substances in
blood that increases its transport to lungs
 Whole transport of O2 in blood can be divided
into following steps;
1. Diffusion of O2 from alveolus into
pulmonary blood
 Partial pressure of gaseous O2 in alveolus is
104 mmHg
◦ while PO2 in venous blood entering capillary is only
40 mmHg
 Thus, due to pressure difference of 64
mmHg;
◦ O2 diffuses from alveolus into pulmonary
blood
 In exercise
◦ During strenuous exercise body require as
much as 20 times normal amount of oxygen;
◦ This increase in O2 demand is met by;
 Diffusing capacity for oxygen increases three folds
during exercise
 Increased number of capillaries open in exercise
 Dilatation of alveoli & capillaries
2. Transport of oxygen in arterial blood
 About 98% of blood coming from lung
has partial pressure of O2 about 104
mmHg
◦ while remaining 2% of blood, which comes
from bronchial vessels, comprises of venous
blood;
 has PO2 of 40 mmHg (equal to that of normal
venous blood)
◦ Mixing of these two bloods in left atrium
makes final partial pressure of O2 about 95
mmHg
◦ This blood is then pumped by aorta into
3. Diffusion of O2 from capillaries into
interstitial fluid
 PO2 in interstitial fluid is 40 mmHg;
◦ while oxygenated blood has PO2 of about 95 mmHg
◦ This difference in O2 conc. causes diffusion of O2
from capillaries into interstitial fluid
 Depends upon 2 factors
◦ Rate of tissue blood flow
◦ Rate of tissue metabolism
4. Diffusion of O2 from interstitial spaces into
cells
 Normal intracellular PO2 – approx. 23 mmHg;
◦ b/c only 1-3 mmHg of O2 is normally required by cells
◦ Thus pressure difference causes O2 to diffuse into
cells
5. Diffusion of CO2 from cells into
interstitial fluid
 PCO2 inside cell is 46 mmHg;
◦ while in interstitial is 45 mmHg
◦ Pressure difference causes CO2 to diffuse out
from cells into interstitial fluid
6. Diffusion of CO2 from interstitial fluid
into capillaries
 PCO2 in interstitial fluid is 45 mmHg;
◦ while in arterial end of capillary PCO2 is 40
mmHg
◦ Due to this pressure difference in PCO2, CO2
diffuses from interstitial fluid into capillaries
7. Diffusion of CO2 from pulmonary blood
into alveolus
 PCO2 of venous blood entering pulmonary
capillaries is 45 mmHg;
◦ while PCO2 of alveolar air is only 40 mmHg;
◦ Thus, only 5 mmHg pressure difference causes
all required CO2 diffusion out of pulmonary
capillaries into alveoli
◦ Finally CO2 from alveolus is exchanged
 TRANSPORT OF O2 IN BLOOD
 About 97% of O2 transported from lungs to tissues
is carried in combination with Hb in RBCs
 Remaining 3% of O2 is carried in dissolved state in
water of plasma & cells
 Oxygen-hemoglobin dissociation curve
 When PO2 is high (lungs) O2 binds with Hb
 But when PO2 is low (tissues) O2 is released from
Hb
◦ This relationship b/w PO2 & amount of oxygenation and de-
oxygenation of Hb is called Oxygen-Hb dissociation curve
Oxygen-hemoglobin dissociation curve
 Value of O2-Hb combinations
◦ Normal conc. of Hb – 15 gm/100ml of blood
◦ Normal amount of O2 carried by 1 gm of Hb –
1.34 ml of O2
◦ Max. amount of O2 carried by 100 ml of blood
– 20 ml of O2
 Percentage of Hb bound with O2 –
known as percent saturation of Hb
 Amount of O2 released by Hb
 During normal conditions about 5 ml of
O2 is carried to tissues in each 100 ml of
blood
 Amount of O2 released by Hb during
exercise
 During strenuous exercise three times as
much O2 is transported in each 100 ml of
blood
◦ i.e. 15 ml O2 / 100 ml blood
 Utilization coefficient
 Percentage of blood that gives up O2 as
it passes through tissue capillaries
◦ Normally 25% of blood, gives up its O2 to
tissues
◦ During strenuous exercise – 75-85% or all
blood can give up its O2
 Physiological significance of O2-Hb
dissociation curve
 Sigmoid shape of curve is of great physiological
significance
◦ b/c it ensures that oxygenation & de-oxygenation of
Hb takes place in most optimum way
 In lungs
 At PO2 of 104 mmHg in alveolar air – more than
97% of Hb becomes saturated with O2
 Even at PO2 of 60 mmHg – percent saturation of
Hb is 89%
 So in any condition associated with fall in
alveolar PO2;
◦ appreciable amount of Hb can still be saturated
 In tissues
 A drop of PO2 from 100 to 50 mmHg would
release only 18% of O2
◦ while drop from 50 to 0 mmHg – release 75-85% of
O2
 Significance of this phenomenon is supply of
more O2 to tissues during exercise where PO2 is
much lowered
 Metabolic use of O2 by cells
 Depends on following factors
◦ Intracellular PO2
◦ Distance of cells from capillaries
◦ Blood flow of tissues
 Combination of Hb & CO
 CO combines with Hb at same point as
does O2 – but 250 times more rapidly than
O2
 The condition in which CO binds with Hb &
displaces O2 – termed as CO poisoning
 Shift of O2-Hb dissociation curve
 Shifting of curve to right
 Indicates that Hb has decreased affinity for
oxygen
 This makes it more difficult for Hb to bind to
oxygen
◦ requiring higher PO2 to achieve same oxygen
saturation
 Rightward shift – increases PO2 in tissues
when it is most needed;
◦ such as during exercise
 Causes
◦ Increase H+ conc. or decreased pH
◦ Increased CO2 conc.
◦ Increased temp.
◦ Increased diphosphoglycerate
 Shifting of curve to left
 Left shift of curve is sign of hemoglobin's
increased affinity for oxygen
◦ e.g. at the lungs
 Causes
◦ Decrease H+ conc. or decreased pH
◦ Decreased CO2 conc.
◦ Decreased temp.
◦ Decreased diphosphoglycerate
◦ CO poisoning
◦ Decreased metabolism
 TRANSPORT OF CO2 IN BLOOD
 Under normal resting condition;
◦ an avg; of 4 ml of CO2 is transported from tissue
to lungs in each 100 ml of blood
 Forms of CO2 transport
1. Transport of CO2 in dissolved state
 About 7% of CO2 – transported as dissolve
CO2
◦ Arterial blood content – 2.4 ml of CO2 / 100 ml
◦ Venous blood content – 2.7 ml of CO2 / 100 ml
◦ Thus 0.3 ml – transported in dissolved state in
each 100 ml of blood
2. Transport of CO2 as carbamino compounds
 30% of CO2 – transported in combination with
Hb & plasma proteins
 Comprises transport of 1.5 ml of CO2 / 100 ml
of blood
 CO2 combines with NH2 groups of blood
proteins to form unstable carbamino
compounds
 Mostly CO2 combines with Hb forming
carbamino-Hb
◦ Since de-oxygenated Hb has more affinity for
CO2;
◦ so in tissues when Hb is reduced – deoxy Hb is
formed, which facilitates CO2 to lungs
3. Transport of CO2 as bicarbonate ions
 70% of CO2 is carried as bicarbonate ions
 HCO3 ions are formed in RBCs & to lesser
extent in plasma
 This transport comprises 2.2 ml of CO2 / 100
ml of blood
 Chloride shift
 Bicarbonate ions formed in RBCs diffuse out
into plasma
 To maintain electrical neutrality of RBCs;
◦ an equal number of chloride ions diffuse into
cells from plasma
◦ This is known as chloride shift
 CO2 dissociation curve
 This curve predicts relationship b/w
quantity of CO2 present in blood in all
forms & PCO2
◦ i.e. dependence of total blood CO2 on Pco2
 Haldane effect
 An increase in CO2 in blood will cause
O2 to be displaced from Hb
◦ This phenomenon is known as Haldane
effect
 Respiratory exchange ratio
 Ratio of CO2 output to O2 uptake
◦ R = rate of CO2 output / rate of O2 uptake
Regulation of respiration
 Respiratory center
 Composed of several widely spread groups
of neurons in brain
 Located in medulla oblongata & pons
 Divisions
◦ 4 major parts
1. Dorsal respiratory group
 Location
◦ In dorsal portion of medulla within nucleus of
tractus solitarius
 Connections
◦ Nucleus of tractus solitarius receive sensory
signals via vagus & glassopharyngeal from
peripheral chemoreceptors & baroreceptors
 Functions
Responsible for generating repetitive bursts
of inspiratory action potential
Generate inspiratory Ramp signals
 During inspiration – signals for contraction of
inspiration begins very weakly at first
 Then increases steadily in ramp fashion for about 2
sec
 Abruptly ceases in next 3 sec & then begins again
 This inspiratory signal is known as ramp signal
2. Pneumataxic center
 Location
◦ Dorsally in nucleus parabrachialis of upper
pons
 Connections
◦ Serves as input source for inspiratory area
 Functions
Transmits impulses continuously to
inspiratory area to control switch off point of
inspiratory ramp
Thus controls duration of inspiration
Can increase heart rate (up to 30-40 breaths
per min)
3. Ventral respiratory group
 Location
◦ In ventral medulla found in nucleus ambigus &
nucleus retroambigus
 Functions
Works when more than normal ventilation is
required – thus it activates to increase respiratory
rate
Some part of it may also cause inspiration
Provides powerful expiratory signals to
abdominal muscles during expiration
4. Apneustic center
 Location
◦ In lower pons
 Connections
◦ Serves as input drive to dorsal respiratory group
 Functions
Sends signals to dorsal respiratory group of
neurons to prevent Switch-off of inspiratory ramp
signal
Controls depth of respiration
 Hering breuer inflation reflex
◦ This reflex is started when lungs become
overstretched
◦ Stretch receptors located in walls of bronchi &
bronchioles transmit signals via vagi into dorsal
respiratory group
◦ This switches off inspiratory ramp, stops further
inspiration & thus increases rate of inspiration
 Control of respiration
◦ Overall control divided into;
A. Chemical regulation
B. Nervous regulation
A. Chemical regulation
 Respiration – maintain proper conc. of O2, CO2 &
H+ ions in tissues
◦ so highly responsive to changes in these, i.e.,
◦ excess of CO2
◦ change in H+
◦ lack of O2
 Chemosensitive area
 Location
◦ Lies bilaterally beneath ventral structure of medulla
 Functions
◦ Highly sensitive to changes in blood CO2 & H+
ion conc.
◦ Increases rate & depth of respiration by
increasing intensity of inspiratory ramp signals
 Excess of CO2
◦ Changes of CO2 in blood
◦ Excess of CO2 – most important factor b/c it can
cross blood brain barrier
 It does this by reacting with water of tissues to form
carbonic acid
 This in turn dissociates into H & bicarbonate ions
◦ H+ ions have potent direct stimulatory effect on
chemosensitive area to increase rate & depth of
respiration
◦ Changes in CSF PCO2
◦ Changing PCO2 in CSF itself has more rapid
excitation of chemosensitive area
 b/c CSF has very little protein & acid base buffers
◦ Therefore H+ ion conc. increases almost instantly
when CO2 enters CSF from brain vessels
B. Nervous regulation of respiration
 Various mechanisms of regulation;
1. Chemoreceptors
2. Hering Breuer Reflex
3. Impulses from higher centers
4. Impulses from vasomotor center
5. Effect of temp
1. Chemoreceptors
 Nature
◦ Special type of nervous chemical receptors
 Location
◦ Located in;
 Carotid bodies
 Aortic bodies
 Other arteries of thorax & abdomen
◦ Carotid bodies
◦ Located bilaterally in bifurcation of common
carotid arteries
◦ Their afferent nerve fibers pass through Hering’s
nerves to glassopharyngeal nerves
◦ & then to dorsal respiratory area
◦ Aortic bodies
◦ Located along arch of aorta
◦ Their afferent nerve fibers pass through vagi
to dorsal respiratory area
◦ Note; chemoreceptors are exposed at all
times to arterial blood, not venous blood
◦ Their partial pressure of O2 is same as PO2
of arterial blood
◦ Basic mechanism
 Chemoreceptors are important for detecting
changes in O2, CO2 & H+ in blood
 Have glandular cells – act as chemoreceptors &
stimulate nerve endings
 Chemoreceptors – stimulated by changes in
arterial PO2 range of 60 & 30 mmHg
 Effect of CO2 & H+ on chemoreceptors
◦ Increase in CO2 & H+ - excites chemoreceptors
◦ But their direct effect on respiratory center stimulation
is more powerful then their effect mediated through
chemoreceptors
2. Hering Breuer Reflex
◦ Control rhythm & depth of respiration
◦ Stretch receptors present in tracheo-bronchial tree
probably at point of bronchial branching
◦ As lung expand during act of respiration
 impulses are carried to apneustic center which inhibits
discharge of inspiratory center
 So act of inspiration ceases & expiration follows
“Hering-Breuer Inflation Reflex”
◦ During forced deflation of lungs – respiration may
be stimulated “Hering Breuer Deflation reflex”
3. Impulses from higher centers
◦ Emotional activities modify breathing;
◦ e.g., fear, anxiety, rage stimulates breathing
◦ In Shock – respiration depressed
4. Afferent impulses from sensory
receptors
◦ Painful stimuli stimulate respiratory center
◦ Newborn child doesn’t breath usually, but starts
breathing after slap
◦ Bucket full of water thrown on man causes gasp
& stimulated breathing is found
5. Impulses from vasomotor center & effect
of BP on breathing
◦ Vasomotor center directly excites respiratory
center
 This effect brought about by baroreceptors located in
carotid & aortic arch which are very sensitive to changes
in BP
◦ Baroreceptors – stimulated when there is rise in
BP
◦ They sends impulses to cardiac center,
vasomotor center & respiratory center
 These impulses are inhibitory in nature
◦ Thus as BP rise, heart slows down (Marey’s
reflex) & respiration depressed
◦ So rise in BP will depress breathing & vice versa
6. Effect of temp
◦ Increase in temp increases rate of respiration
◦ Hypothalamus initiates cascade of neurogenic
reactions;
 to decrease body temp by increasing rate of respiration
◦ This facilitates loss of heat from body through
water vapours in expired air
 Regulation of respiration during exercise
 In strenuous exercise, O2 consumption & CO2
formation can increase as much as 20 folds
 During exercise arterial PO2, PCO2 & pH all
remain almost normal
 Following factors increases respiration during
exercise
Brain, on sending impulses to exercising muscles
also transmits collateral impulses to brain stem to
excite respiratory center according to need of body
During exercises body movements are believed to
increase pulmonary ventilation;
 by exciting joint proprioceptors which in turn excite
respiratory center in brain
Hypoxia developing in muscles during exercise
elicits afferent nerve signals to respiratory center
to excite respiration
Many experiments suggest that brains ability to
increase ventilatory response during exercise is
mainly “learned response”
Specific pulmonary
abnormalities
 Emphysema
◦ An increase in size of alveoli, either due to
dilatation or destruction of their walls
 Pneumonia
◦ Any inflammatory condition of lung in which
some or all of alveoli are filled with fluid & blood
cells
◦ Results in two pulmonary abnormalities;
 Reduction in total available surface area of respiratory
membrane
 Decreased ventilation-perfusion ratio
◦ Causes
 Bacteria or viruses
 Asthma
◦ Spastic condition of bronchiolar smooth muscle,
causing extreme difficulty in breathing
◦ Cause
◦ Usual cause is hypersensitivity of bronchioles to
foreign substances in air
◦ Mechanism
◦ Allergic person has tendency to form large
amount of IgE antibodies which attach to mast
cells
◦ On exposure to antigen IgE antibodies react with
it & mast cell granules rupture, releasing
substances
◦ These substances cause bronchospasm

3. respiratory system (1)

  • 1.
  • 2.
    Respiration  Act ofbreathing resulting in exchange of oxygen & CO2 b/w body tissues and atmosphere  Divisions ◦ 4 main divisions  Pulmonary ventilation  Inflow & outflow of air b/w atmosphere & lung alveoli  Diffusion  Of oxygen & CO2 b/w alveoli & blood
  • 3.
     Transport  Ofoxygen & CO2 in blood and body fluids to & from cells  Regulation  Of ventilation & other acts of respiration  Functions of respiration ◦ Supply of oxygen to tissues & removal of CO2 from blood ◦ Helps in regulating acid base balance by adjusting CO2 elimination from body ◦ Helps in keeping constant condition of water in body through elimination of excess water vapors ◦ Eliminates certain harmful volatile substances from body e.g. ammonia, alcohol etc
  • 4.
     Mechanics ofrespiration  Lungs can be expanded & contracted in 2 ways; ◦ By downward & upward movement of diaphragm to lengthen or shorten chest cavity ◦ By elevation & depression of ribs to increase & decrease anteroposterior diameter of chest cavity  Inspiration & muscles of inspiration ◦ During inspiration (in normal quiet breathing);  main role is played by contraction of diaphragm that pulls lower surfaces of lungs downward
  • 5.
     Other muscles; ◦External intercostal (main muscle) ◦ Sternocleidomastoid muscles ◦ Anterior serrati ◦ Scaleni  Expiration & muscles of expiration ◦ During expiration, diaphragm simply relaxes & elastic recoils of lungs, chest wall & abdominal structures compresses lungs  Muscles helping in expiration; ◦ Abdominal recti (main muscle) ◦ Internal intercostals
  • 6.
    Lungs pressure  Pleuralpressure ◦ Pressure in narrow space b/w lung pleura & chest wall pleura ◦ Negative pressure which prevents collapse of lungs ◦ Also called lung recoil pressure ◦ Value; 5 cm of H2O  Alveolar pressure ◦ Pressure inside lung alveoli ◦ Different during inspiration & expiration ◦ Inspiration – alveolar pressure becomes -1 cm of H2O  which causes air to move into lungs
  • 7.
    ◦ Expiration –alveolar pressure rises to about +1 cm of H2O  this forces inspired air out of lungs  Transpulmonary pressure ◦ Difference b/w alveolar pressure & pleural pressure ◦ Pressure difference b/w alveoli & outer surface of lungs ◦ Actually it is measure of recoil pressure  Recoil pressure ◦ Elastic forces in lungs that tend to collapse lungs at each point of expansion
  • 8.
    Pulmonary volumes  Tidalvolume ◦ Volume of air inspired or expired with each normal breath ◦ Value: 500 ml  Inspiratory reserve volume ◦ Extra volume of air that can be inspired in after normal tidal volume ◦ Value: 3000 ml
  • 9.
     Expiratory reservevolume ◦ Extra amount of air that can be expired by forceful expiration after end of normal tidal expiration ◦ Value: 1100 ml  Residual volume ◦ Volume of air still remaining in lungs after most forceful expiration ◦ Value: 1200 ml
  • 10.
    Pulmonary capacities  Combinationof two or more pulmonary volumes  Inspiratory capacity  Combination of tidal volume & inspiratory reserve volume  Formula: I.C = T.V + IRV  Significance  This is the amount of air that a person can breath; ◦ beginning at normal expiratory level & ending at maximum lung distension  Value: 3500 ml
  • 11.
     Functional residualcapacity  Combination of expiratory volume & residual volume  Formula: FRC = ERV + RV  Significance  This is amount of air remaining in lungs at end of normal expiration  Value: 2300 ml  Vital capacity  Combination of inspiratory reserve volume, tidal volume & expiratory reserve volume  Formula: VC = IRV + TV + ERV
  • 12.
     Maximum amountof air that a person can expel from lungs; ◦ after first filling lungs to their maximum extent & then expiring to maximum limit  Total lung capacity  Combination of vital capacity & residual volume  Formula: TLC = VC + RV  Significance  Maximum volume to which lungs can be expanded with greatest possible inspiratory effort  Value: 5800 ml
  • 13.
    Composition of inspired, expired& alveolar air  Lungs can never be completely emptied of air b/c of residual volume The Relative Composition (% by Volume) of Inspired, Expired & Alveolar Air Gas Inspired air % Expired air % Alveolar air % Oxygen 20.71 14.6 13.2 Carbon dioxide 0.04 3.8 5.0 Water vapour 1.25 6.2 6.2 Nitrogen 78.0 75.4 75.6
  • 14.
     Inspired aircontains approximately 21% by volume of oxygen gas  As this fresh air is drawn into alveoli; ◦ it mixes with air already present (residual volume)  Residual volume dilutes fresh air, so oxygen content falls  CO2 content of alveolar air increases significantly as gas exchange proceeds ◦ & CO2 diffuses from blood into alveoli
  • 15.
     Oxygen contentof expired air is higher than that in alveoli ◦ This is explained by fact that expired air from alveoli mixes with dead space air whose oxygen content is same as that of atmosphere  CO2 content in expired air is less than that of alveolar air ◦ explained by fact that expired air from alveoli mixes with dead space air containing very low levels of carbon dioxide
  • 16.
     Water vapourcontent of expired air is significantly higher than that of inspired air ◦ as air is breathed into alveoli, water from lining of alveoli evaporates into alveolar air such that expired air is greater in volume than inspired air  Nitrogen gas is neither used or produced by body and actual amounts of nitrogen in inspired an expired air do not change ◦ slightly larger volume of expired air means that nitrogen forms part of larger volume during expiration and so its % by volume decreases
  • 17.
     There areseveral reasons for alveolar air differences ◦ First, alveolar air is only partially replaced by atmospheric air with each breath ◦ Second, oxygen is constantly being absorbed into pulmonary blood from alveolar air ◦ Third, carbon dioxide is constantly diffusing from pulmonary blood into alveoli ◦ Fourth, dry atmospheric air that enters respiratory passages is humidified even before it reaches alveoli
  • 18.
    Transport of O2& CO2 in Blood & body fluids  O2 is transported in combination with Hb to tissue capillaries  CO2 also combines with chemical substances in blood that increases its transport to lungs  Whole transport of O2 in blood can be divided into following steps; 1. Diffusion of O2 from alveolus into pulmonary blood  Partial pressure of gaseous O2 in alveolus is 104 mmHg ◦ while PO2 in venous blood entering capillary is only 40 mmHg
  • 19.
     Thus, dueto pressure difference of 64 mmHg; ◦ O2 diffuses from alveolus into pulmonary blood  In exercise ◦ During strenuous exercise body require as much as 20 times normal amount of oxygen; ◦ This increase in O2 demand is met by;  Diffusing capacity for oxygen increases three folds during exercise  Increased number of capillaries open in exercise  Dilatation of alveoli & capillaries
  • 20.
    2. Transport ofoxygen in arterial blood  About 98% of blood coming from lung has partial pressure of O2 about 104 mmHg ◦ while remaining 2% of blood, which comes from bronchial vessels, comprises of venous blood;  has PO2 of 40 mmHg (equal to that of normal venous blood) ◦ Mixing of these two bloods in left atrium makes final partial pressure of O2 about 95 mmHg ◦ This blood is then pumped by aorta into
  • 21.
    3. Diffusion ofO2 from capillaries into interstitial fluid  PO2 in interstitial fluid is 40 mmHg; ◦ while oxygenated blood has PO2 of about 95 mmHg ◦ This difference in O2 conc. causes diffusion of O2 from capillaries into interstitial fluid  Depends upon 2 factors ◦ Rate of tissue blood flow ◦ Rate of tissue metabolism 4. Diffusion of O2 from interstitial spaces into cells  Normal intracellular PO2 – approx. 23 mmHg; ◦ b/c only 1-3 mmHg of O2 is normally required by cells ◦ Thus pressure difference causes O2 to diffuse into cells
  • 22.
    5. Diffusion ofCO2 from cells into interstitial fluid  PCO2 inside cell is 46 mmHg; ◦ while in interstitial is 45 mmHg ◦ Pressure difference causes CO2 to diffuse out from cells into interstitial fluid 6. Diffusion of CO2 from interstitial fluid into capillaries  PCO2 in interstitial fluid is 45 mmHg; ◦ while in arterial end of capillary PCO2 is 40 mmHg ◦ Due to this pressure difference in PCO2, CO2 diffuses from interstitial fluid into capillaries
  • 23.
    7. Diffusion ofCO2 from pulmonary blood into alveolus  PCO2 of venous blood entering pulmonary capillaries is 45 mmHg; ◦ while PCO2 of alveolar air is only 40 mmHg; ◦ Thus, only 5 mmHg pressure difference causes all required CO2 diffusion out of pulmonary capillaries into alveoli ◦ Finally CO2 from alveolus is exchanged
  • 24.
     TRANSPORT OFO2 IN BLOOD  About 97% of O2 transported from lungs to tissues is carried in combination with Hb in RBCs  Remaining 3% of O2 is carried in dissolved state in water of plasma & cells  Oxygen-hemoglobin dissociation curve  When PO2 is high (lungs) O2 binds with Hb  But when PO2 is low (tissues) O2 is released from Hb ◦ This relationship b/w PO2 & amount of oxygenation and de- oxygenation of Hb is called Oxygen-Hb dissociation curve
  • 25.
  • 26.
     Value ofO2-Hb combinations ◦ Normal conc. of Hb – 15 gm/100ml of blood ◦ Normal amount of O2 carried by 1 gm of Hb – 1.34 ml of O2 ◦ Max. amount of O2 carried by 100 ml of blood – 20 ml of O2  Percentage of Hb bound with O2 – known as percent saturation of Hb  Amount of O2 released by Hb  During normal conditions about 5 ml of O2 is carried to tissues in each 100 ml of blood
  • 27.
     Amount ofO2 released by Hb during exercise  During strenuous exercise three times as much O2 is transported in each 100 ml of blood ◦ i.e. 15 ml O2 / 100 ml blood  Utilization coefficient  Percentage of blood that gives up O2 as it passes through tissue capillaries ◦ Normally 25% of blood, gives up its O2 to tissues ◦ During strenuous exercise – 75-85% or all blood can give up its O2
  • 28.
     Physiological significanceof O2-Hb dissociation curve  Sigmoid shape of curve is of great physiological significance ◦ b/c it ensures that oxygenation & de-oxygenation of Hb takes place in most optimum way  In lungs  At PO2 of 104 mmHg in alveolar air – more than 97% of Hb becomes saturated with O2  Even at PO2 of 60 mmHg – percent saturation of Hb is 89%  So in any condition associated with fall in alveolar PO2; ◦ appreciable amount of Hb can still be saturated
  • 29.
     In tissues A drop of PO2 from 100 to 50 mmHg would release only 18% of O2 ◦ while drop from 50 to 0 mmHg – release 75-85% of O2  Significance of this phenomenon is supply of more O2 to tissues during exercise where PO2 is much lowered  Metabolic use of O2 by cells  Depends on following factors ◦ Intracellular PO2 ◦ Distance of cells from capillaries ◦ Blood flow of tissues
  • 30.
     Combination ofHb & CO  CO combines with Hb at same point as does O2 – but 250 times more rapidly than O2  The condition in which CO binds with Hb & displaces O2 – termed as CO poisoning
  • 31.
     Shift ofO2-Hb dissociation curve  Shifting of curve to right  Indicates that Hb has decreased affinity for oxygen  This makes it more difficult for Hb to bind to oxygen ◦ requiring higher PO2 to achieve same oxygen saturation  Rightward shift – increases PO2 in tissues when it is most needed; ◦ such as during exercise  Causes ◦ Increase H+ conc. or decreased pH ◦ Increased CO2 conc. ◦ Increased temp. ◦ Increased diphosphoglycerate
  • 33.
     Shifting ofcurve to left  Left shift of curve is sign of hemoglobin's increased affinity for oxygen ◦ e.g. at the lungs  Causes ◦ Decrease H+ conc. or decreased pH ◦ Decreased CO2 conc. ◦ Decreased temp. ◦ Decreased diphosphoglycerate ◦ CO poisoning ◦ Decreased metabolism
  • 34.
     TRANSPORT OFCO2 IN BLOOD  Under normal resting condition; ◦ an avg; of 4 ml of CO2 is transported from tissue to lungs in each 100 ml of blood  Forms of CO2 transport 1. Transport of CO2 in dissolved state  About 7% of CO2 – transported as dissolve CO2 ◦ Arterial blood content – 2.4 ml of CO2 / 100 ml ◦ Venous blood content – 2.7 ml of CO2 / 100 ml ◦ Thus 0.3 ml – transported in dissolved state in each 100 ml of blood
  • 35.
    2. Transport ofCO2 as carbamino compounds  30% of CO2 – transported in combination with Hb & plasma proteins  Comprises transport of 1.5 ml of CO2 / 100 ml of blood  CO2 combines with NH2 groups of blood proteins to form unstable carbamino compounds  Mostly CO2 combines with Hb forming carbamino-Hb ◦ Since de-oxygenated Hb has more affinity for CO2; ◦ so in tissues when Hb is reduced – deoxy Hb is formed, which facilitates CO2 to lungs
  • 36.
    3. Transport ofCO2 as bicarbonate ions  70% of CO2 is carried as bicarbonate ions  HCO3 ions are formed in RBCs & to lesser extent in plasma  This transport comprises 2.2 ml of CO2 / 100 ml of blood  Chloride shift  Bicarbonate ions formed in RBCs diffuse out into plasma  To maintain electrical neutrality of RBCs; ◦ an equal number of chloride ions diffuse into cells from plasma ◦ This is known as chloride shift
  • 37.
     CO2 dissociationcurve  This curve predicts relationship b/w quantity of CO2 present in blood in all forms & PCO2 ◦ i.e. dependence of total blood CO2 on Pco2  Haldane effect  An increase in CO2 in blood will cause O2 to be displaced from Hb ◦ This phenomenon is known as Haldane effect  Respiratory exchange ratio  Ratio of CO2 output to O2 uptake ◦ R = rate of CO2 output / rate of O2 uptake
  • 38.
    Regulation of respiration Respiratory center  Composed of several widely spread groups of neurons in brain  Located in medulla oblongata & pons  Divisions ◦ 4 major parts 1. Dorsal respiratory group  Location ◦ In dorsal portion of medulla within nucleus of tractus solitarius
  • 39.
     Connections ◦ Nucleusof tractus solitarius receive sensory signals via vagus & glassopharyngeal from peripheral chemoreceptors & baroreceptors  Functions Responsible for generating repetitive bursts of inspiratory action potential Generate inspiratory Ramp signals  During inspiration – signals for contraction of inspiration begins very weakly at first  Then increases steadily in ramp fashion for about 2 sec  Abruptly ceases in next 3 sec & then begins again  This inspiratory signal is known as ramp signal
  • 40.
    2. Pneumataxic center Location ◦ Dorsally in nucleus parabrachialis of upper pons  Connections ◦ Serves as input source for inspiratory area  Functions Transmits impulses continuously to inspiratory area to control switch off point of inspiratory ramp Thus controls duration of inspiration Can increase heart rate (up to 30-40 breaths per min)
  • 41.
    3. Ventral respiratorygroup  Location ◦ In ventral medulla found in nucleus ambigus & nucleus retroambigus  Functions Works when more than normal ventilation is required – thus it activates to increase respiratory rate Some part of it may also cause inspiration Provides powerful expiratory signals to abdominal muscles during expiration 4. Apneustic center  Location ◦ In lower pons
  • 42.
     Connections ◦ Servesas input drive to dorsal respiratory group  Functions Sends signals to dorsal respiratory group of neurons to prevent Switch-off of inspiratory ramp signal Controls depth of respiration  Hering breuer inflation reflex ◦ This reflex is started when lungs become overstretched ◦ Stretch receptors located in walls of bronchi & bronchioles transmit signals via vagi into dorsal respiratory group ◦ This switches off inspiratory ramp, stops further inspiration & thus increases rate of inspiration
  • 44.
     Control ofrespiration ◦ Overall control divided into; A. Chemical regulation B. Nervous regulation A. Chemical regulation  Respiration – maintain proper conc. of O2, CO2 & H+ ions in tissues ◦ so highly responsive to changes in these, i.e., ◦ excess of CO2 ◦ change in H+ ◦ lack of O2  Chemosensitive area  Location ◦ Lies bilaterally beneath ventral structure of medulla
  • 45.
     Functions ◦ Highlysensitive to changes in blood CO2 & H+ ion conc. ◦ Increases rate & depth of respiration by increasing intensity of inspiratory ramp signals  Excess of CO2 ◦ Changes of CO2 in blood ◦ Excess of CO2 – most important factor b/c it can cross blood brain barrier  It does this by reacting with water of tissues to form carbonic acid  This in turn dissociates into H & bicarbonate ions ◦ H+ ions have potent direct stimulatory effect on chemosensitive area to increase rate & depth of respiration
  • 46.
    ◦ Changes inCSF PCO2 ◦ Changing PCO2 in CSF itself has more rapid excitation of chemosensitive area  b/c CSF has very little protein & acid base buffers ◦ Therefore H+ ion conc. increases almost instantly when CO2 enters CSF from brain vessels B. Nervous regulation of respiration  Various mechanisms of regulation; 1. Chemoreceptors 2. Hering Breuer Reflex 3. Impulses from higher centers 4. Impulses from vasomotor center 5. Effect of temp
  • 47.
    1. Chemoreceptors  Nature ◦Special type of nervous chemical receptors  Location ◦ Located in;  Carotid bodies  Aortic bodies  Other arteries of thorax & abdomen ◦ Carotid bodies ◦ Located bilaterally in bifurcation of common carotid arteries ◦ Their afferent nerve fibers pass through Hering’s nerves to glassopharyngeal nerves ◦ & then to dorsal respiratory area
  • 48.
    ◦ Aortic bodies ◦Located along arch of aorta ◦ Their afferent nerve fibers pass through vagi to dorsal respiratory area ◦ Note; chemoreceptors are exposed at all times to arterial blood, not venous blood ◦ Their partial pressure of O2 is same as PO2 of arterial blood ◦ Basic mechanism  Chemoreceptors are important for detecting changes in O2, CO2 & H+ in blood  Have glandular cells – act as chemoreceptors & stimulate nerve endings
  • 49.
     Chemoreceptors –stimulated by changes in arterial PO2 range of 60 & 30 mmHg  Effect of CO2 & H+ on chemoreceptors ◦ Increase in CO2 & H+ - excites chemoreceptors ◦ But their direct effect on respiratory center stimulation is more powerful then their effect mediated through chemoreceptors 2. Hering Breuer Reflex ◦ Control rhythm & depth of respiration ◦ Stretch receptors present in tracheo-bronchial tree probably at point of bronchial branching ◦ As lung expand during act of respiration  impulses are carried to apneustic center which inhibits discharge of inspiratory center
  • 50.
     So actof inspiration ceases & expiration follows “Hering-Breuer Inflation Reflex” ◦ During forced deflation of lungs – respiration may be stimulated “Hering Breuer Deflation reflex” 3. Impulses from higher centers ◦ Emotional activities modify breathing; ◦ e.g., fear, anxiety, rage stimulates breathing ◦ In Shock – respiration depressed 4. Afferent impulses from sensory receptors ◦ Painful stimuli stimulate respiratory center ◦ Newborn child doesn’t breath usually, but starts breathing after slap ◦ Bucket full of water thrown on man causes gasp & stimulated breathing is found
  • 51.
    5. Impulses fromvasomotor center & effect of BP on breathing ◦ Vasomotor center directly excites respiratory center  This effect brought about by baroreceptors located in carotid & aortic arch which are very sensitive to changes in BP ◦ Baroreceptors – stimulated when there is rise in BP ◦ They sends impulses to cardiac center, vasomotor center & respiratory center  These impulses are inhibitory in nature ◦ Thus as BP rise, heart slows down (Marey’s reflex) & respiration depressed ◦ So rise in BP will depress breathing & vice versa
  • 52.
    6. Effect oftemp ◦ Increase in temp increases rate of respiration ◦ Hypothalamus initiates cascade of neurogenic reactions;  to decrease body temp by increasing rate of respiration ◦ This facilitates loss of heat from body through water vapours in expired air
  • 53.
     Regulation ofrespiration during exercise  In strenuous exercise, O2 consumption & CO2 formation can increase as much as 20 folds  During exercise arterial PO2, PCO2 & pH all remain almost normal  Following factors increases respiration during exercise Brain, on sending impulses to exercising muscles also transmits collateral impulses to brain stem to excite respiratory center according to need of body During exercises body movements are believed to increase pulmonary ventilation;  by exciting joint proprioceptors which in turn excite respiratory center in brain
  • 54.
    Hypoxia developing inmuscles during exercise elicits afferent nerve signals to respiratory center to excite respiration Many experiments suggest that brains ability to increase ventilatory response during exercise is mainly “learned response”
  • 55.
    Specific pulmonary abnormalities  Emphysema ◦An increase in size of alveoli, either due to dilatation or destruction of their walls  Pneumonia ◦ Any inflammatory condition of lung in which some or all of alveoli are filled with fluid & blood cells ◦ Results in two pulmonary abnormalities;  Reduction in total available surface area of respiratory membrane  Decreased ventilation-perfusion ratio ◦ Causes  Bacteria or viruses
  • 56.
     Asthma ◦ Spasticcondition of bronchiolar smooth muscle, causing extreme difficulty in breathing ◦ Cause ◦ Usual cause is hypersensitivity of bronchioles to foreign substances in air ◦ Mechanism ◦ Allergic person has tendency to form large amount of IgE antibodies which attach to mast cells ◦ On exposure to antigen IgE antibodies react with it & mast cell granules rupture, releasing substances ◦ These substances cause bronchospasm