RESPIRATORY

PHYSIOLOGY
Respiratory System

 Primary function is to obtain oxygen for use

by body's cells & eliminate carbon dioxide
that cells produce
 Includes respiratory airways leading into (&
out of) lungs plus the lungs themselves
 Pathway of air: nasal cavities (or oral
cavity) > pharynx > trachea > primary
bronchi (right & left) > secondary bronchi
> tertiary bronchi > bronchioles > alveoli
(site of gas exchange)
 Breathing is an active process

 The external intercostals plus the diaphragm

contract to bring about inspiration:
 Diaphragm: a sheet separating the thorax from
the abdomen. Innervation is from the phrenic
nerves (C3-5)
 Contraction of external intercostal muscles:
innervated by their intercostal nerves T1-12)
 Accessory muscles of respiration only become
important during exercise or respiratory distress
To exhale

 During quiet breathing expiration is a

passive process, relying on the elastic
recoil of the lung and chest wall.
 When ventilation is increased, such as
during exercise, expiration becomes
active with contraction of the muscles
of the abdominal wall and the internal
intercostals.
Rhythmicity centre of the
medulla controls automatic
breathing
• consists of interacting neurons that
fire either during inspiration (I
neurons) or expiration (E neurons)
– I neurons - stimulate neurons that
innervate respiratory muscles (to
bring about inspiration)
– E neurons - inhibit I neurons (to 'shut
down' the I neurons & bring about
expiration)
• Apneustic center (located in the
pons) - stimulate I neurons (to
promote inspiration)
• Pneumotaxic center (also located in
the pons) - inhibits apneustic center &
inhibits inspiration
 Factors Involved in Increasing
Respiratory Rate

 Chemoreceptors –
*Peripheral: in aorta & carotid arteries
*Central :medulla
-They are stimulated more by increased CO2 levels than by
decreased O2 levels
-They stimulate Rhythmicity Areas increased rate of
respiration
 Heavy exercise  greatly increases respiratory rate
Possible factors:
 reflexes originating from body movements (proprioceptors)
 increase in body temperature
 epinephrine release (during exercise)
 Voluntary Control through impulses from the cerebral cortex
• Tidal Volume: each normal quiet
breath ( 7-10ml/kg)
• Inspiratory Reserve Volume:
maximal additional volume that can
be inspired above TV
• Expiratory Reserve Volume:
maximal additional volume that can
be expired above TV
• Residual Volume: volume
remaining after maximal expiration
• Functional Residual Capacity:
is the volume of air in the lungs at
the end of a normal expiration
• Vital Capacity: max volume of
gas that can be exhaled after max
inspiration
Dead Space
Part not participating in gas exchange

 Anatomical dead-space:
tracheobronchial tree down to
respiratory bronchioles. Normally
2ml/kg or 150ml in an adult, roughly
a third of the tidal volume.
 Alveolar Dead Space: Non perfused
alveoli
 Physiologic Dead Space:
Anatomical + Alveolar
Factors Affecting Dead Space
 Factors Increasing Dead Space:
 Upright position
 Neck extension
 Age
 +ve pressure ventilation
 Decreased pulmonary perfusion
 Lung disease
 Factors Decreasing Dead Space:
 Supine position
 Neck flexion
 Endotracheal Intubation
 The tidal volume (500ml) multiplied by the
respiratory rate (14 breaths/min) is the
minute volume (7,000ml/min)

 The part of the tidal volume which does

take part in respiratory exchange multiplied
by the respiratory rate is known as the
alveolar ventilation (approximately
5,000ml/min)
 Resistance/Compliance

 Two aspects oppose lung expansion

and airflow and therefore need to be
overcome by respiratory muscle
activity. These are:
 the airway resistance
 the compliance of the lung and chest
wall.
 Resistance of the airways describes
the obstruction to airflow provided by
the conducting airways, resulting
largely from the larger airways , plus
a contribution from tissue resistance
resulting produced by friction as
tissues of the lung slide over each
other during respiration.
 Compliance denotes distensibility
(stretchiness), and in a clinical setting refers
to the lung and chest wall combined, being
defined as the volume change per unit
pressure change.
 Low Compliance: the lungs are stiffer and
more effort is required to inflate the alveoli.
 Conditions that worsen compliance, such as
pulmonary fibrosis, produce restrictive lung
disease.
Compliance varies within the lung
according to the degree of inflation

 Poor compliance is seen at

low volumes (because of
difficulty with initial lung
inflation) and at high
volumes (because of the
limit of chest wall
expansion)
 Best compliance is in the
mid-expansion range.
ALVEOLI
 The walls of alveoli are coated with a thin film of
water & this creates a potential problem. Water
molecules, are more attracted to each other than to
air, and this attraction creates a force called surface
tension.
 During exhalation surface tension increases as water
molecules come closer together. Potentially, surface
tension could cause alveoli to collapse and, in
addition, would make it more difficult to 're-expand'
the alveoli.
 Serious problems: if alveoli collapsed they'd
contain no air & no oxygen to diffuse into the blood &,
if 're-expansion' was more difficult, inhalation would
be very, very difficult if not impossible.
 Role of Pulmonary Surfactant

 Surfactant decreases
surface tension which:
 increases pulmonary
compliance (reducing the
effort needed to expand
the lungs)

 reduces tendency for

alveoli to collapse
 What is Partial Pressure?
 The individual pressure exerted
independently by a particular gas within a
mixture of gasses.
 The air we breath is a mixture of gasses: primarily nitrogen,
oxygen, & carbon dioxide.
 The total pressure generated by the air is due in part to
nitrogen, in part to oxygen, & in part to carbon dioxide.
 That part of the total pressure generated by oxygen is the
'partial pressure' of oxygen, while that generated by carbon
dioxide is the 'partial pressure' of carbon dioxide. A gas's
partial pressure, therefore, is a measure of how much of that
gas is present (e.g., in the blood or alveoli).  
 The partial pressure exerted by each gas in
a mixture equals the total pressure times
the fractional composition of the gas in the
mixture.
 So, given that total atmospheric pressure
(at sea level) is about 760 mm Hg and,
further, that air is about 21% oxygen, then
the partial pressure of oxygen in the air is
0.21 times 760 mm Hg or 160 mm Hg.
 Atmospheric Alveolar air Venous blood Expired air
air (mm Hg) (mm Hg) (mm Hg) (mm Hg)

N2 596 573 573 565

O2 158 100 40 116

CO2 0.3 40 46 32

H2O 5.7 47 47 47

Total 760 760 760 760

Inspired air Alveolar air Expired air

Partial Pressures of O2 and
CO2 in the body

 Alveoli
 PO2 = 100 mm Hg
 PCO2 = 40 mm Hg
 Alveolar capillaries
 Entering the alveolar capillaries
 PO2 = 40 mm Hg (relatively low because this
blood has just returned from the systemic
circulation & has lost much of its oxygen)
 PCO2 = 45 mm Hg (relatively high because the
blood returning from the systemic circulation
has picked up carbon dioxide)
 Blood leaving the alveolar capillaries returns to the left atrium & is
pumped by the left ventricle into the systemic circulation. Entering
the systemic capillaries
 PO2 = 100 mm Hg
 PCO2 = 40 mm Hg
 Body cells (resting conditions)
 PO2 = 40 mm Hg
 PCO2 = 45 mm Hg
 Because of the differences in partial pressures of oxygen & carbon
dioxide in the systemic capillaries & the body cells, oxygen diffuses
from the blood & into the cells, while carbon dioxide diffuses from the
cells into the blood.
 Leaving the systemic capillaries
 PO2 = 40 mm Hg
 PCO2 = 45 mm Hg
 Blood leaving the systemic capillaries returns to the heart (right
atrium) via venules & veins This blood is then pumped to the lungs
(and the alveolar capillaries) by the right ventricle.
 Gas Diffusion
 The alveoli provide an enormous surface area for gas
exchange with pulmonary blood (between 50-100m2)
 Under resting conditions pulmonary capillary blood is in
contact with the alveolus for about 0.75 second in total and
is fully equilibrated with alveolar oxygen after only about a
third of the way along this course.
 Lung disease impairs diffusion:
 At rest there is usually still sufficient time for full
equilibration of oxygen
 During exercise, pulmonary blood flow is quicker,
shortening the time available for gas exchange, and so
those with lung disease are unable to oxygenate the
pulmonary blood fully and thus have a limited ability to
exercise.
 Carbon dioxide diffuses across the alveolar-capillary
membrane 20 times faster than oxygen so the above
factors are less liable to compromise transfer from blood to
alveoli.
 How are Oxygen & Carbon Dioxide
Transported in Blood

 Oxygen is carried in blood:

 1 - bound to hemoglobin (98.5% of all oxygen in the blood)
 2 - dissolved in the plasma (1.5%)
 Because almost all oxygen in the blood is transported by
hemoglobin, the relationship between the concentration
(partial pressure) of oxygen and hemoglobin saturation (the %
of hemoglobin molecules carrying oxygen) is an important
one.
 Hemoglobin saturation:
 extent to which the hemoglobin in blood is combined with O2
 depends on PO2 of the blood:
• At high partial pressures of O2
(above 40 mm Hg),
hemoglobin saturation
remains rather high (typically
about 75 - 80%). This rather
flat section of the oxygen-
hemoglobin dissociation curve
is called the 'plateau.'
• Under resting conditions, only
about 20 - 25% of hemoglobin
molecules give up oxygen in
the systemic capillaries. This
is significant (in other words,
the 'plateau' is significant)
because it means that you
have a substantial reserve of
oxygen.
 When you do become more active, partial
pressures of oxygen in your (active) cells
may drop well below 40 mm Hg. A look at
the oxygen-hemoglobin dissociation curve
reveals that as oxygen levels decline,
hemoglobin saturation also declines - and
declines precipitously. This means that the
blood (hemoglobin) 'unloads' lots of oxygen
to active cells - cells that, of course, need
more oxygen.
 Factors Affecting Oxygen Haemoglobin
Dissociation Curve

 The oxygen-hemoglobin
dissociation curve 'shifts'
under certain conditions:

 pH changes
 temperature changes
 2,3-diphosphoglycerate
levels
 CO2 levels
 Carbon Dioxide-transported from the
body cells back to the lungs as:

 1 - Bicarbonate (HCO3) - 60%

 formed when CO2 (released by
cells making ATP) combines with
H2O (due to the enzyme in red
blood cells called carbonic
anhydrase)
 2 – Carbaminohemoglobin-30%
 formed when CO2 combines with
hemoglobin (hemoglobin molecules
that have given up their oxygen)
 3 - Dissolved in plasma-10%
 Perfusion/Ventilation/Shunt
Perfusion
 Distribution throughout the lung is largely due to the effects of
gravity.

 Therefore in the upright position this means that the perfusion

pressure at the base of the lung is equal to the mean
pulmonary artery pressure (15mmHg or 20cmH2O) plus the
hydrostatic pressure between the main pulmonary artery and
lung base (approximately 15cmH2O).

 At the apices the perfusion pressure is very low, and may at

times even fall below the pressure in the alveoli leading to
vessel compression and intermittent cessation of blood flow
 Ventilation
 The distribution of ventilation across the lung is related to the
position of each area on the compliance curve at the start of a
normal tidal inspiration (the point of the FRC)

 Because the bases are on a more favourable part of the

compliance curve than the apices, they gain more volume
change from the pressure change applied and thus receive a
greater degree of ventilation.

 Although the inequality between bases and apices is less

marked for ventilation than for perfusion, overall there is still
good V/Q matching and efficient oxygenation of blood passing
through the lungs.
 V/Q Mismatching
 Diseased lungs may have
marked mismatch between
ventilation and perfusion. Some
alveoli are relatively
overventilated while others are
relatively overperfused
 Even normal lungs have some
degree of ventilation/perfusion
mismatch;the upper zones are
relatively overventilated while
the lower zones are relatively
overperfused & underventilated
 Shunt
 Shunt occurs when
deoxygenated venous blood
from the body passes
unventilated alveoli to enter
the pulmonary veins and the
systemic arterial system with
an unchanged PO2 (40
mmHg).

 Atelectasis (collapsed
alveoli), consolidation of the
lung, pulmonary oedema or
small airway closure (see
later) will cause shunt
 Oxygen Cascade
 Oxygen moves down the pressure or
concentration gradient from a
relatively high level in air, to the
levels in the respiratory tract and
then alveolar gas, the arterial blood,
capillaries and finally the cell. The
PO2 reaches the lowest level (4-20
mmHg) in the mitochondria.

 This decrease in PO2 from air to the

mitochondrion is known as the
oxygen cascade and the size of any
one step in the cascade may be
increased under pathological
circumstances and may result in
hypoxia.  
 Non-Respiratory Lung Functions

 Reservoir of blood available for circulatory compensation

 Filter for circulation:
 thrombi, microaggregates etc
 Metabolic activity:
 activation:
 angiotensin III
 inactivation:
 noradrenaline
 bradykinin
 5 H-T
 some prostaglandins
 Immunological:
 IgA secretion into bronchial mucus
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