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Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings.
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Lecture Slide Presentation by Robert J. Sullivan, Marist College
RESPIRATION
Chapter 37
PULMONARY VENTILATION
DR FARZANA MAJEED
Human Respiratory System
Figure 10.1
Respiratory system extracts oxygen from the
atmosphere , and the body utilizes the oxygen
and produce CO2 as a result of metabolism.
RESPIRATORY SYSTEM
Basic functions of the
respiratory system
1. Breathing (Pulmonary Ventilation) –
movement of air in and out of the lungs
• Inhalation (inspiration) draws gases into
the lungs.
• Exhalation (expiration) forces gases out
of the lungs.
Non –pulmonary functions:
2. Gas Conditioning – as gases pass
through the nasal cavity and paranasal
sinuses, inhaled air becomes turbulent. The
gases in the air are
• warmed to body temperature
• humidified
• cleaned of particulate matter
3. Protects respiratory surfaces
4. Site for olfactory sensation
5. Secretes pulmonary alveolar
macrophages
6. Endocrine functions
7. Immune function
8. Vocalization
9. Coughing and sneezing to eliminate
irritants from respiratory tract
10. Production of surfactant
Respiration processes
Components of the Upper Respiratory
Tract
Figure 10.2
 Passageway for respiration
 Receptors for smell
 Filters incoming air to filter larger foreign
material
 Moistens and warms incoming air
 Resonating chambers for voice
Upper Respiratory Tract Functions
Components of the Lower Respiratory
Tract
Figure 10.3
 Functions:
 Larynx: maintains an open airway, routes food
and air appropriately, assists in sound production
 Trachea: transports air to and from lungs
 Bronchi: branch into lungs
 Lungs: transport air to alveoli for gas exchange
Lower Respiratory Tract
Mechanics of breathing
Pulmonary ventilation is accomplished
by two processes.
 Inspiration is an active process and
refers to inflow of air into the lungs. This
occurs when the intrapulmonary
pressure falls below the atmospheric
pressure.
 Expiration is a passive process and refers to
outflow of air from the lungs. This occurs
when intrapulmonary pressure exceeds the
atmospheric pressure.
 Changes in intrapulmonary pressure which
govern respiratory cycle are related to the
changes in intrapleural pressure.
 Changes in intrapleural pressure in turn
depend upon the changes in size of thoracic
cavity.
 Changes in size of thoracic cavity
depend upon the respiratory muscles
 Muscles of normal quiet inspiration are
diaphragm and external intercostal
muscles.
 Muscles of forceful inspiration are
sternocledomastoid, scalenes and
parasternals
 Normal quiet expiration is due to elastic
recoil of lungs
 Muscles of forceful expiration are
internal intercostals and abdominal recti
movements of inspiration
 It is an active process
 Normally produced by descent of
diaphragm and contraction of inspiratory
muscles
 Therefore diaphragm and external
intercostal muscles contract and cause
increase in vertical, antroposterior and
transverse diameters of thoracic cavity
Role of diaphragm
 Helps in 70-75% expansion of chest
during normal inspiration
 During inspiration , diaphragm contracts
and draw the central tendon part
downwards by 1.5cm in quiet breathing
and 7cm in deep respiration
 Cause an increase in vertical diameter
of the thorax
 Contraction of diaphragm also lifts the
lower ribs causing thoracic expansion
laterally and anteriorly
(the bucket handle and pump handle
movements respectively)
The respiratory muscles
Role of external intercostal
muscles
 Fibers of external intercostal muscles
are attached to vertebral ends of upper
and lower ribs
 Contraction leads to elevation of ribs
causing lateral and antro posterior
enlargement of thoracic cavity
 Bucket handle and pump handle
movements.
movements of expiration
 Passive phenomenon brought about by
elastic recoil of lungs
 Decrease in the size of thoracic cavity
by relaxation of diaphragm and external
intercostal muscles
mechanism of forced inspiration
 Forceful contraction of
diaphragm…..decent 7-10 cm as
compared to 1-1.5 cm in quiet breathing
 Forceful contraction of external
intercostal muscles……..increasing
transverse and AP diameter of thoracic
cavity
 Contraction of accessory muscles
 Sternocledomastoid contracts and lifts
the sternum upwards
 Anterior serrati and scaleni muscles
contract and lift ribs upwards
mechanism of forced expiration
 Contraction of abdominal muscles
causes increase in vertical diameter of
thoracic cavity
 Downward pull on the lower ribs by
contraction of internal intercostal
muscles decreases AP and transverse
diameter of thoracic cavity
Pressure and volume changes during
respiratory cycle
 Relationship between intrapulmonary pressure and
atmospheric pressure determines direction of air
flow
 In quiet breathing , at end expiration and at end
inspiration .no air is going in and out of the lungs
as the intrapulmonary pressure and atmospheric
pressures are equal i.e. 0 mmHg
Intra ALVEOLAR pressure
(IAP)
During normal quiet
inspiration
 IAP decreases to about -1
mmHg which is sufficient to
suck in 500 ml of air into
lungs within 2 sec.
 At the end of inspiration IPP
decreases again to 0 mmHg
During expiration
 IAP swings slightly towards positive
side (+1 mmHg) which forces 500 ml of
air out of lungs in 3 sec
 At the end of expiration IPP again
decreases to 0 mmHg
Significance
 Negative pressure in alveoli during
inspiration causes the air to enter into
alveoli but during expiration IAP
becomes positive so air is expelled out
of the lungs
 Helps in exchange of gasses between
air and lungs
Intrapleural pressure
During normal quiet inspiration
 It is negative pressure
 At the start of inspiration -5mmHg
which is the minimum amount of pressure to
hold the lungs open at resting level
 During inspiration becomes more negative
( -7.5mmHg)
During expiration
 All the events are reversed during expiration
significance
 As it is negative pressure so it prevents
the collapse of lungs after elastic recoil
 This also causes dilatation of larger
veins and vena cava. So act as suction
pump to pull venous blood from lower
part of the body to increase venous
return.
Transpulmonary pressure / recoil
pressure
 It is the difference between alveolar
pressure and pleural pressure.
SIGNIFICANCE
 It is the measure of elastic forces of
lungs that tend to collapse the lungs at
each instant of respiration
Pressure changes during inhalation
and exhalation
 Change in lung volume for each unit change in
transpulmonary pressure = stretchiness of lungs
 Transpulmonary pressure (TPP) is the
difference in pressure between alveolar
pressure and pleural pressure.
 Value of compliance of both lungs in normal
human adult =200ml of air/TPP in cm of H2O
LUNG COMPLIANCE
(Hysteresis)
 There are 2 different curves
according to different phases
of respiration.
 The curves are called :
Inspiratory compliance
curve
Expiratory compliance
curve
COMPLIANCE DIAGRAM
 Shows the capacity of lungs to “adapt” to
small changes of transpulmonary
pressure.
 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)
 The total work of breathing of the cycle is
the area contained in the loop.
 Two forces try to collapse the
lungs
 Elastic forces of lungs
 Thin layer of fluid
 Two forces prevent collapse of the
lungs
 Intra pleural pressure
 surfactant
Major determinants of
compliance diagram
A.A. Elastic forces of the lung
tissue itself
B. Elastic forces of the fluid
that lines the inside walls of
alveoli and other lung air
passages (surface tension)
Elastic forces of the lungs
This is provided by
• Elastin and
• Collagen
interwoven in lung
parenchyma
Deflated lungs: fibers are contracted and in
kinked state
Inflated lungs: these fibers become stretched and
unkinked exerting more elastic forces
Elastic forces caused by surface
tension
Is provided by the
substance called
surfactant that is
present inside
walls of alveoli.
Experiment:
 By adding saline solution there
is no interface between air and
alveolar fluid. (B forces were
removed)
 surface tension is not present,
only elastic forces of tissue (A)
 Transpleural pressures
required to expand normal lung
= 3x pressure to expand saline
filled lung.
Conclusion of this experiment:
 Tissue elastic forces (A) =
represent 1/3 of total lung elasticity
 Fluid air surface tension elastic
forces in alveoli (B) = 2/3 of total
lung elasticity.
Surface tension
 water molecules are attracted to one
another.
 The force of surface tension acts in the plane
of the air-liquid boundary to shrink or minimize
the liquid-air interface
 In lungs = water tends to attract forcing air out
of alveoli to bronchi = alveoli tend to
collapse
Elastic contractile force of the entire
lungs (forces B)
Forces affecting lung compliance
 Deformities of thorax like
 Kyphosis
 Scoliosis
 Fibrosis
 Pleural effusion
 Paralysis of respiratory muscles
 Surface agent which tend to decrease
surface tension
Synthesized by type II alveolar cells
 Reduces surface tension (prevents
alveolar collapse during
expiration)
Consists of apoproteins +phospholipid
(dipalmitoylphosphatidylcholine) +
calcium ions
surfactant
Functions
 Decreases surface tension in alveoli
of the lungs
 Stabilize the alveoli which have
tendency to deflate
 Prevents bacterial invasion
 Cleans alveoli surface
 Plays important role in inflation of lungs
during birth. In fetal life it starts producing
after 3rd
month and completes at 7 months. Till
that time lungs remain collapsed. After birth
inflation of lungs takes place with initiation of
respiration due to CO2 induced activation of
respiratory centers. Although respiratory
movements are attempted again and again by
the new born tend to collapse the lungs.
Effects of deficiency of surfactant
 Infants: Collapse of the lungs called
Respiratory distress syndrome (RDS) or
hyaline membrane disease
 Adults: Collapse of the lungs called
Adult respiratory distress syndrome
(ARDS)
 Surface active agent in water = reduces
surface tension of water on the alveolar walls
Pure water (surface
pressure)
72
dynes/cm
Normal fluid lining
alveoli without
surfactant (surface
pressure)
50
dynes/cm
Normal fluid lining
alveoli with
surfactant
5-30
dynes/cm
Respiratory volumes and
capacities
Lung Volumes and Capacities
 Tidal Volume (VT)
 amount of air
entering/leaving
lungs in a single,
“normal” breath
 500 ml at rest,
↑ with ↑ activity
IC
FRC
VC
TLC
Lung Capacities
Primary Lung
Volumes
IRV
VT
ERV
RV
Volume(ml)
0
6000
 Inspiratory Reserve
Volume (IRV)
 additional volume of
air that can be
maximally inspired
beyond VT by forced
inspiration
 3000 ml. at rest
IC
FRC
VC
TLC
Lung Capacities
Primary Lung
Volumes
IRV
VT
ERV
RV
Volume(ml)
0
6000
 Expiratory
Reserve Volume
(ERV)
 additional volume
of air that can be
maximally expired
beyond VT by
forced expiration
 1100 ml. at rest
IC
FRC
VC
TLC
Lung Capacities
Primary Lung
Volumes
IRV
VT
ERV
RV
Volume(ml)
0
6000
 Residual Volume
(RV)
 volume of air still in
lungs following
forced max.
expiration
 1200 ml. at rest
IC
FRC
VC
TLC
Lung Capacities
Primary Lung
Volumes
IRV
VT
ERV
RV
Volume(ml)
0
6000
 Total Lung Capacity
(TLC)
 total amount of air
that the lungs can
hold
 amt of air in lungs at
the end a maximal
inspiration
 VT + IRV + ERV +
RV
 5800ml at rest
IC
FRC
VC
TLC
Lung Capacities
Primary Lung
Volumes
IRV
VT
ERV
RV
Volume(ml)
0
6000
 Vital Capacity (VC)
 max. amt. air that
can move out of
lungs after a person
inhales as deeply as
possible
 VT + IRV + ERV
 4600ml at rest
IC
FRC
VC
TLC
Lung Capacities
Primary Lung
Volumes
IRV
VT
ERV
RV
Volume(ml)
0
6000
 Inspiratory Capacity
(IC)
 max amt. of air that can
be inhaled from a
normal end-expiration
 breathe out normally,
then inhale as much as
possible
 VT + IRV
 3500ml at rest
IC
FRC
VC
TLC
Lung Capacities
Primary Lung
Volumes
IRV
VT
ERV
RV
Volume(ml)
0
6000
 Functional Residual
Capacity (FRC)
 amt of air remaining in
the lungs following a
normal expiration
 ERV +RV
 2300ml at rest
IC
FRC
VC
TLC
Lung Capacities
Primary Lung
Volumes
IRV
VT
ERV
RV
Volume(ml)
0
6000
Forced Expiratory Volume
(FEVt)
 Amount of air forcibly
expired in t seconds
 FEVt = (Vt/VC) x 100%
 Normally…
 FEV1 = ~ 80% VC
 FEV2 = ~ 94% VC
 FEV3 = ~ 97% VC
 Index of air flow through
the respiratory air
passages
0 1 2 3
5000
4000
3000
2000
1000
0
Time (sec)Volume(ml)
FEV1 = (5000 ml -1000 ml) / 5000ml
= 4000 ml / 5000 ml
= 80%
Restrictive and Obstructive Disorders
 Restrictive
disorder:
 Vital capacity is
reduced.
 FVC is normal.
 Obstructive
disorder:
 VC is normal.
 FEV1 is < 80%.
Insert fig. 16.17
Figure 16.17
Air-Flow Disorders
 Obstructive disorders
 obstruction of the pulmonary air passages

air flow α radius4

slight obstruction will have large ↓ in air flow
 bronchiolar secretions, inflammation and edema
(e.g. bronchitis), or bronchiolar constriction (e.g.
asthma)
 reduced FEV, normal VC
 Restrictive disorders
 damage to the lung results in abnormal VC test

e.g. pulmonary fibrosis
 reduced VC, normal FEV
Ventilation
PULMONARY
VENTILATION
ALVEOLAR
VENTILATION
Cyclic process by which
fresh air enters and leaves
the lungs
Air utilized for gaseous
exchange
Product of TV and RR Product of TV excluding
dead space volume and RR
PV=TV X RR
500ml X 12/min
600ml or 6L/min
AV= (TV-DSV) X RR
(500-150) X 12/min
4.200ml or 4.2 L/min
Dead space
 Part of respiratory tract where gaseous
exchange doesn’t take place
 Types:
 Anatomical dead space
 Physiological dead space
 ANATOMICAL DEAD SPACE
Volume of respiratory tract from nose
up to terminal bronchiole
 PHYSIOLOGICAL DEAD SPACE
Includes anatomical dead space plus
well perfused but non ventilated alveoli
and well ventilated but non perfused
alveoli
 NORMAL VALUE OF DEAD
SPACE
Under normal conditions ADS + PDS
So DSV = 150 ml
 MEASUREMENT
BY N2 Wash method
Cough reflex
 Stimulus
irritants in the respiratory passages
 Receptors
in respiratory passageways
 Afferents
vagus nerve
 Centre
medulla
 Efferents
neuronal circuits
 Effectors / response
 2.5 ml of air rapidly inspired
 epiglottis gets closed
 vocal cords get approximated so air
trapped in
 abdominal muscles contract forcefully
so that pressure exceeds 100 mmHg or
more
 Epiglottis suddenly gets open, air
under high pressure in lungs exploded
out with the velocity of 70-100 miles
/hour

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Chap 37

  • 1. Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings. PowerPoint® Lecture Slide Presentation by Robert J. Sullivan, Marist College RESPIRATION Chapter 37 PULMONARY VENTILATION DR FARZANA MAJEED
  • 3. Respiratory system extracts oxygen from the atmosphere , and the body utilizes the oxygen and produce CO2 as a result of metabolism. RESPIRATORY SYSTEM
  • 4. Basic functions of the respiratory system 1. Breathing (Pulmonary Ventilation) – movement of air in and out of the lungs • Inhalation (inspiration) draws gases into the lungs. • Exhalation (expiration) forces gases out of the lungs.
  • 5. Non –pulmonary functions: 2. Gas Conditioning – as gases pass through the nasal cavity and paranasal sinuses, inhaled air becomes turbulent. The gases in the air are • warmed to body temperature • humidified • cleaned of particulate matter 3. Protects respiratory surfaces 4. Site for olfactory sensation 5. Secretes pulmonary alveolar macrophages 6. Endocrine functions
  • 6. 7. Immune function 8. Vocalization 9. Coughing and sneezing to eliminate irritants from respiratory tract 10. Production of surfactant
  • 8. Components of the Upper Respiratory Tract Figure 10.2
  • 9.  Passageway for respiration  Receptors for smell  Filters incoming air to filter larger foreign material  Moistens and warms incoming air  Resonating chambers for voice Upper Respiratory Tract Functions
  • 10. Components of the Lower Respiratory Tract Figure 10.3
  • 11.  Functions:  Larynx: maintains an open airway, routes food and air appropriately, assists in sound production  Trachea: transports air to and from lungs  Bronchi: branch into lungs  Lungs: transport air to alveoli for gas exchange Lower Respiratory Tract
  • 12. Mechanics of breathing Pulmonary ventilation is accomplished by two processes.  Inspiration is an active process and refers to inflow of air into the lungs. This occurs when the intrapulmonary pressure falls below the atmospheric pressure.
  • 13.  Expiration is a passive process and refers to outflow of air from the lungs. This occurs when intrapulmonary pressure exceeds the atmospheric pressure.  Changes in intrapulmonary pressure which govern respiratory cycle are related to the changes in intrapleural pressure.  Changes in intrapleural pressure in turn depend upon the changes in size of thoracic cavity.
  • 14.  Changes in size of thoracic cavity depend upon the respiratory muscles  Muscles of normal quiet inspiration are diaphragm and external intercostal muscles.  Muscles of forceful inspiration are sternocledomastoid, scalenes and parasternals
  • 15.  Normal quiet expiration is due to elastic recoil of lungs  Muscles of forceful expiration are internal intercostals and abdominal recti
  • 16. movements of inspiration  It is an active process  Normally produced by descent of diaphragm and contraction of inspiratory muscles  Therefore diaphragm and external intercostal muscles contract and cause increase in vertical, antroposterior and transverse diameters of thoracic cavity
  • 17.
  • 18. Role of diaphragm  Helps in 70-75% expansion of chest during normal inspiration  During inspiration , diaphragm contracts and draw the central tendon part downwards by 1.5cm in quiet breathing and 7cm in deep respiration  Cause an increase in vertical diameter of the thorax
  • 19.  Contraction of diaphragm also lifts the lower ribs causing thoracic expansion laterally and anteriorly (the bucket handle and pump handle movements respectively)
  • 20.
  • 22. Role of external intercostal muscles  Fibers of external intercostal muscles are attached to vertebral ends of upper and lower ribs  Contraction leads to elevation of ribs causing lateral and antro posterior enlargement of thoracic cavity  Bucket handle and pump handle movements.
  • 23. movements of expiration  Passive phenomenon brought about by elastic recoil of lungs  Decrease in the size of thoracic cavity by relaxation of diaphragm and external intercostal muscles
  • 24. mechanism of forced inspiration  Forceful contraction of diaphragm…..decent 7-10 cm as compared to 1-1.5 cm in quiet breathing  Forceful contraction of external intercostal muscles……..increasing transverse and AP diameter of thoracic cavity
  • 25.  Contraction of accessory muscles  Sternocledomastoid contracts and lifts the sternum upwards  Anterior serrati and scaleni muscles contract and lift ribs upwards
  • 26. mechanism of forced expiration  Contraction of abdominal muscles causes increase in vertical diameter of thoracic cavity  Downward pull on the lower ribs by contraction of internal intercostal muscles decreases AP and transverse diameter of thoracic cavity
  • 27.
  • 28.
  • 29. Pressure and volume changes during respiratory cycle  Relationship between intrapulmonary pressure and atmospheric pressure determines direction of air flow  In quiet breathing , at end expiration and at end inspiration .no air is going in and out of the lungs as the intrapulmonary pressure and atmospheric pressures are equal i.e. 0 mmHg
  • 30. Intra ALVEOLAR pressure (IAP) During normal quiet inspiration  IAP decreases to about -1 mmHg which is sufficient to suck in 500 ml of air into lungs within 2 sec.  At the end of inspiration IPP decreases again to 0 mmHg
  • 31.
  • 32. During expiration  IAP swings slightly towards positive side (+1 mmHg) which forces 500 ml of air out of lungs in 3 sec  At the end of expiration IPP again decreases to 0 mmHg
  • 33. Significance  Negative pressure in alveoli during inspiration causes the air to enter into alveoli but during expiration IAP becomes positive so air is expelled out of the lungs  Helps in exchange of gasses between air and lungs
  • 35. During normal quiet inspiration  It is negative pressure  At the start of inspiration -5mmHg which is the minimum amount of pressure to hold the lungs open at resting level  During inspiration becomes more negative ( -7.5mmHg) During expiration  All the events are reversed during expiration
  • 36. significance  As it is negative pressure so it prevents the collapse of lungs after elastic recoil  This also causes dilatation of larger veins and vena cava. So act as suction pump to pull venous blood from lower part of the body to increase venous return.
  • 37. Transpulmonary pressure / recoil pressure  It is the difference between alveolar pressure and pleural pressure. SIGNIFICANCE  It is the measure of elastic forces of lungs that tend to collapse the lungs at each instant of respiration
  • 38. Pressure changes during inhalation and exhalation
  • 39.  Change in lung volume for each unit change in transpulmonary pressure = stretchiness of lungs  Transpulmonary pressure (TPP) is the difference in pressure between alveolar pressure and pleural pressure.  Value of compliance of both lungs in normal human adult =200ml of air/TPP in cm of H2O LUNG COMPLIANCE (Hysteresis)
  • 40.  There are 2 different curves according to different phases of respiration.  The curves are called : Inspiratory compliance curve Expiratory compliance curve COMPLIANCE DIAGRAM
  • 41.  Shows the capacity of lungs to “adapt” to small changes of transpulmonary pressure.  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)  The total work of breathing of the cycle is the area contained in the loop.
  • 42.  Two forces try to collapse the lungs  Elastic forces of lungs  Thin layer of fluid  Two forces prevent collapse of the lungs  Intra pleural pressure  surfactant
  • 43. Major determinants of compliance diagram A.A. Elastic forces of the lung tissue itself B. Elastic forces of the fluid that lines the inside walls of alveoli and other lung air passages (surface tension)
  • 44. Elastic forces of the lungs This is provided by • Elastin and • Collagen interwoven in lung parenchyma Deflated lungs: fibers are contracted and in kinked state Inflated lungs: these fibers become stretched and unkinked exerting more elastic forces
  • 45. Elastic forces caused by surface tension Is provided by the substance called surfactant that is present inside walls of alveoli.
  • 46. Experiment:  By adding saline solution there is no interface between air and alveolar fluid. (B forces were removed)  surface tension is not present, only elastic forces of tissue (A)  Transpleural pressures required to expand normal lung = 3x pressure to expand saline filled lung.
  • 47. Conclusion of this experiment:  Tissue elastic forces (A) = represent 1/3 of total lung elasticity  Fluid air surface tension elastic forces in alveoli (B) = 2/3 of total lung elasticity.
  • 48. Surface tension  water molecules are attracted to one another.  The force of surface tension acts in the plane of the air-liquid boundary to shrink or minimize the liquid-air interface  In lungs = water tends to attract forcing air out of alveoli to bronchi = alveoli tend to collapse
  • 49. Elastic contractile force of the entire lungs (forces B)
  • 50. Forces affecting lung compliance  Deformities of thorax like  Kyphosis  Scoliosis  Fibrosis  Pleural effusion  Paralysis of respiratory muscles
  • 51.  Surface agent which tend to decrease surface tension Synthesized by type II alveolar cells  Reduces surface tension (prevents alveolar collapse during expiration) Consists of apoproteins +phospholipid (dipalmitoylphosphatidylcholine) + calcium ions surfactant
  • 52. Functions  Decreases surface tension in alveoli of the lungs  Stabilize the alveoli which have tendency to deflate  Prevents bacterial invasion  Cleans alveoli surface
  • 53.  Plays important role in inflation of lungs during birth. In fetal life it starts producing after 3rd month and completes at 7 months. Till that time lungs remain collapsed. After birth inflation of lungs takes place with initiation of respiration due to CO2 induced activation of respiratory centers. Although respiratory movements are attempted again and again by the new born tend to collapse the lungs.
  • 54. Effects of deficiency of surfactant  Infants: Collapse of the lungs called Respiratory distress syndrome (RDS) or hyaline membrane disease  Adults: Collapse of the lungs called Adult respiratory distress syndrome (ARDS)
  • 55.  Surface active agent in water = reduces surface tension of water on the alveolar walls Pure water (surface pressure) 72 dynes/cm Normal fluid lining alveoli without surfactant (surface pressure) 50 dynes/cm Normal fluid lining alveoli with surfactant 5-30 dynes/cm
  • 57. Lung Volumes and Capacities  Tidal Volume (VT)  amount of air entering/leaving lungs in a single, “normal” breath  500 ml at rest, ↑ with ↑ activity IC FRC VC TLC Lung Capacities Primary Lung Volumes IRV VT ERV RV Volume(ml) 0 6000
  • 58.  Inspiratory Reserve Volume (IRV)  additional volume of air that can be maximally inspired beyond VT by forced inspiration  3000 ml. at rest IC FRC VC TLC Lung Capacities Primary Lung Volumes IRV VT ERV RV Volume(ml) 0 6000
  • 59.  Expiratory Reserve Volume (ERV)  additional volume of air that can be maximally expired beyond VT by forced expiration  1100 ml. at rest IC FRC VC TLC Lung Capacities Primary Lung Volumes IRV VT ERV RV Volume(ml) 0 6000
  • 60.  Residual Volume (RV)  volume of air still in lungs following forced max. expiration  1200 ml. at rest IC FRC VC TLC Lung Capacities Primary Lung Volumes IRV VT ERV RV Volume(ml) 0 6000
  • 61.  Total Lung Capacity (TLC)  total amount of air that the lungs can hold  amt of air in lungs at the end a maximal inspiration  VT + IRV + ERV + RV  5800ml at rest IC FRC VC TLC Lung Capacities Primary Lung Volumes IRV VT ERV RV Volume(ml) 0 6000
  • 62.  Vital Capacity (VC)  max. amt. air that can move out of lungs after a person inhales as deeply as possible  VT + IRV + ERV  4600ml at rest IC FRC VC TLC Lung Capacities Primary Lung Volumes IRV VT ERV RV Volume(ml) 0 6000
  • 63.  Inspiratory Capacity (IC)  max amt. of air that can be inhaled from a normal end-expiration  breathe out normally, then inhale as much as possible  VT + IRV  3500ml at rest IC FRC VC TLC Lung Capacities Primary Lung Volumes IRV VT ERV RV Volume(ml) 0 6000
  • 64.  Functional Residual Capacity (FRC)  amt of air remaining in the lungs following a normal expiration  ERV +RV  2300ml at rest IC FRC VC TLC Lung Capacities Primary Lung Volumes IRV VT ERV RV Volume(ml) 0 6000
  • 65. Forced Expiratory Volume (FEVt)  Amount of air forcibly expired in t seconds  FEVt = (Vt/VC) x 100%  Normally…  FEV1 = ~ 80% VC  FEV2 = ~ 94% VC  FEV3 = ~ 97% VC  Index of air flow through the respiratory air passages 0 1 2 3 5000 4000 3000 2000 1000 0 Time (sec)Volume(ml) FEV1 = (5000 ml -1000 ml) / 5000ml = 4000 ml / 5000 ml = 80%
  • 66. Restrictive and Obstructive Disorders  Restrictive disorder:  Vital capacity is reduced.  FVC is normal.  Obstructive disorder:  VC is normal.  FEV1 is < 80%. Insert fig. 16.17 Figure 16.17
  • 67. Air-Flow Disorders  Obstructive disorders  obstruction of the pulmonary air passages  air flow α radius4  slight obstruction will have large ↓ in air flow  bronchiolar secretions, inflammation and edema (e.g. bronchitis), or bronchiolar constriction (e.g. asthma)  reduced FEV, normal VC  Restrictive disorders  damage to the lung results in abnormal VC test  e.g. pulmonary fibrosis  reduced VC, normal FEV
  • 68. Ventilation PULMONARY VENTILATION ALVEOLAR VENTILATION Cyclic process by which fresh air enters and leaves the lungs Air utilized for gaseous exchange Product of TV and RR Product of TV excluding dead space volume and RR PV=TV X RR 500ml X 12/min 600ml or 6L/min AV= (TV-DSV) X RR (500-150) X 12/min 4.200ml or 4.2 L/min
  • 69. Dead space  Part of respiratory tract where gaseous exchange doesn’t take place  Types:  Anatomical dead space  Physiological dead space
  • 70.  ANATOMICAL DEAD SPACE Volume of respiratory tract from nose up to terminal bronchiole  PHYSIOLOGICAL DEAD SPACE Includes anatomical dead space plus well perfused but non ventilated alveoli and well ventilated but non perfused alveoli
  • 71.  NORMAL VALUE OF DEAD SPACE Under normal conditions ADS + PDS So DSV = 150 ml  MEASUREMENT BY N2 Wash method
  • 72. Cough reflex  Stimulus irritants in the respiratory passages  Receptors in respiratory passageways  Afferents vagus nerve
  • 73.  Centre medulla  Efferents neuronal circuits  Effectors / response  2.5 ml of air rapidly inspired  epiglottis gets closed
  • 74.  vocal cords get approximated so air trapped in  abdominal muscles contract forcefully so that pressure exceeds 100 mmHg or more  Epiglottis suddenly gets open, air under high pressure in lungs exploded out with the velocity of 70-100 miles /hour