Surface tension, compliance, Air way resistance, Diffusion

1. Alveolar Surface tension,
Compliance,
Airway Resistance, V/P ratio,
Diffusion capacity of lungs
Dr. Sai Sailesh Kumar G
Assistant Professor
Department of Physiology
RDGMC

2. Why there is surface tension?

3. Surface tension

4. Inter molecular attractions
between water molecules

5. Surface tension
 Due to intermolecular attractions between the
water molecules (water molecules comes closer)
 Water molecules in the deeper layer are attracted
from all the side equally but not from surface (air
present on surface)
 Water molecules do not interact with air molecules
(cause for surface tension)
 Water molecules tend to shrink to bottom and this
causes the collapse of alveoli and air moves out.

6. Surface tension
 Surface tension is the force exerted by water
molecules on the surface of the lung tissue as
those water molecules pull together
 When the water surface is attempting to contract, it
tends to force air out of the alveoli and cause
collapse of alveoli

7. Laplace law
 P=2T/r
 P= collapsing pressure
 T= Surface tension
 r= Radius
 When the surface tension increases, the collapsing
pressure increases and alveoli will collapse.
 When the surface tension decreases, the collapsing
pressure decreases.

8. What happens if the alveoli
collapse
 When alveoli collapse
 It pulls water in the blood like a vacuum action
 Pulmonary edema
 Thickness of the respiratory membrane
increases
 Exchange of gases becomes difficult

9. Effect of radius on collapsing
pressure
 Imagine two alveoli adjacent
 First alveoli is not ventilated well due to block
 Under ventilated alveoli
 Decrease in the radius
 Collapsing pressure increases
 Alveoli collapse

10. Effect of radius on collapsing
pressure
 Imagine two alveoli adjacent
 When the first alveoli s not well ventilated
 The air is diverted to second alveoli which is well
ventilated
 Now second alveoli is hyperventilated
 Increase in the radius
 Decrease in the collapsing pressure

11. Protective mechanisms to prevent
alveolar collapse
 Pores of Kohn
 Surfactant

12. Protective mechanisms to prevent
alveolar collapse
 Protective mechanism to prevent alveolar
collapse
 Pores of kohn between alveoli
 Air can moves from one alveoli to other alveoli
 Prevents collapse of alveoli

14. Surfactant

15. Surfactant
 Definition: It is surface agent that can greatly reduce the
surface tension of water.
 Source: Type II alveolar epithelial cells (cuboidal cells)
 Composition: Phospholipids, Apo proteins, albumin,
IgA and ions. (90% lipids)
 The most important component is Dipalmitoyl
Phosphatidyl Choline (DPPC), surfactant apo-proteins
and calcium ions (spreading agent)

16. Surfactant
 Apo proteins- Surfactant proteins A, B, C, D
 Production of the surfactant begins in the 24th
week of the gestation ( it is slow process till 34th
week)
 From 34th week the production of cortisol
increases ( glucocorticoid).
 Cortisol stimulates the production of surfactant
 From 34th week the process will speedup

17. Infant Respiratory distress
syndrome (IRDS)
 If the baby born before 34th week
 The surfactant production is not complete
 Amount of surfactant is less
 More surface tension in the alveoli
 Collapse of alveoli
 Need mechanical ventilation

18. Infant Respiratory distress
syndrome (IRDS)
 Their lungs have extreme tendency to collapse
 This is called IRDS- infant respiratory distress
syndrome
 It is fatal if not treated with strong measures,
especially properly applied continuous positive
pressure breathing.

19. Formation of surfactant
 Special type of membrane bound organelles present in type
II alveolar cells- Laminar bodies
 Laminar bodies consist of surfactant proteins and
phospholipids
 These materials are synthesized in ER and stored in
laminar bodies.
 Released to the surface by exocytosis
 On the surface, in the presence of surfactant proteins and
calcium ions they will be arranged in a meshwork ( tubular
myelin) which in turn converts into surfactant and spreads.

20. Formation of surfactant

21. Mechanism of action
Surfactant has hydrophilic and hydrophobic
components
Hydrophilic component interacts with water
molecules
Pulls the layer of water up (due to surface
tension layer of water tries to shrink)
Decreases the surface tension

22. Radius of alveoli is small
With out surfactant
 P=2T/r
 If the radius decrease
 Pressure will increase
 Collapsing pressure
increase
With surfactant
 Distribution of
surfactant more
 Less surface tension
 Collapsing pressure
decreases

23. Functions of surfactant
Reduces surface tension and prevents
collapsing tendency of alveoli
Responsible for stabilization of alveoli
Decreases work of breathing
Defense mechanism (SP-A, SP-D destroy
the bacteria and virus by means of
opsonization)

24. Factors increasing surfactant
production
 Vagal stimulation
 Thyroid hormone
 Glucocorticoids

25. Factors decreasing surfactant
production
 Smoking
 hypoxia
 Excess of insulin

26. Airway resistance
 Gas flow = ∆P/R
 ∆P = Difference in the pressure
 R= resistance
 Difference in the pressure (pressure gradient) is
directly proportional to gas flow
 Increase in the pressure will increase gas flow
(provided resistance is constant)

27. Airway resistance
 Imagine there are four alveoli with different pressures
 Atmospheric pressure =760 mm Hg
 Pressure in first alveoli is 760 mm HG
 Pressure in second alveoli is 754 mm Hg
 Pressure in third alveoli is 730 mm Hg
 Pressure in the forth alveoli is 761 mm Hg

28. Airway resistance
 Pressure in first alveoli is 760 mm HG equal to atmospheric
pressure – Net flow is zero
 Pressure in second alveoli is 754 mm Hg- slightly lower than
atmospheric pressure - Moderate air flow
 Pressure in third alveoli is 730 mm Hg – Lower than atmospheric
pressure – Maximum air flow
 Pressure in the forth alveoli is 761 mm Hg – Higher than
atmospheric pressure- Reverse air flow (from alveoli to
atmosphere)

29. Airway resistance
 Resistance offered to the air in the respiratory
passages
 High resistance in larger bronchi and bronchioles
 Low resistance in the minute terminal bronchioles
 The number of minute parallel terminal bronchioles
are high (approximately 65000).

30. Airway resistance
 Source of resistance in airways is friction
 Resistance is very low in respiratory passages
 Why?
 Measurement of Airway Resistance by Body
Plethysmography

31. Body Plethysmography

32. Why Airway resistance is less
 Three reasons
1. Most of the passages of conducting zone has large
diameter
2. So many divisions. Bronchioles are many. So total
cross sectional area of bronchioles is huge
3. In respiratory bronchioles gas flow stops. (diffusion
will take over)

33. Nervous and local control of bronchioles
 Sympathetic nerve supply to bronchioles - release
of epinephrine and nor-epinephrine
 Stimulation of adrenal medulla – release of release
of epinephrine and nor-epinephrine
 Especially epinephrine acts on the beta adrenergic
receptors and cause dilation of bronchial tree

34. Parasympathetic constriction of
bronchioles
 Para sympathetic nerve supply to bronchioles -
release of acetyl choline and causes mild to
moderate constriction
 In case of asthma, where already the bronchioles
are constricted, parasympathetic stimulation
worsens the condition.
 Administration of drugs that block the action of
parasympathetic nerves- Atropine

35. Sympathetic stimulation
Sympathetic stimulation
Release of nor epinephrine
Dilation of bronchioles
Increase in the diameter of bronchioles
Decrease in the friction
Decrease in the resistance
Increase in the flow

36. Parasympathetic stimulation
Sympathetic stimulation
Release of Ach
Constriction of bronchioles
Decrease in the diameter of bronchioles
Increase in the friction
Increase in the resistance
Decrease in the flow

37. Airway resistance in asthma
In asthma attack, airways constrict
Decrease in the diameter of airways
Increase in friction and increased resistance
Patient has to put lot more effort into breathing
to maintain air intake adequately
Turbulent flow within the airways
Causes Wheeze of asthma attack

38. Concept of Compliance
 What is compliance?
 What is elasticity?
 Relation between compliance and elasticity?
 Factors affecting compliance?

39. Lung Compliance
 Definition: It is the change in the volume of the
lungs per unit change in the trans pulmonary
pressure (pressure difference between intra pleural
pressure and intra alveolar pressure).
 Normal Value: 130 ml per cm of H20 pressure (
for lungs and chest wall together)
 Normal Value: 200 ml per cm H20 for lungs alone

40. Static Lung Compliance
 Static compliance: is defined as the change in
lung volume per unit change in pressure in
the absence of flow.
It is composed of:
Chest wall compliance
Lung tissue compliance

41. Dynamic Lung Compliance
Dynamic compliance: is defined as the
change in lung volume per unit change in
pressure in the presence of flow.
It is composed of:
Chest wall compliance
Lung tissue compliance
Airway resistance

42. Compliance & Elasticity
 Measure of the ability to stretch (lungs, chest wall)
 Ease to stretch is compliance
 Opposite to compliance is elasticity
 Elasticity tries to recoil (Lungs, chestwall)
 Compliance = ∆V/∆P
 Elasticity =∆P/∆V
 ∆V= Change in the volume
 ∆P = Change in the pressure (Trans pulmonary pressure in
case of lungs, Trans thoracic pressure in case of chest wall)

43. Compliance
Compliance = ∆V/∆P
 Compliance is directly proportional to ∆V
(Change in the volume)
Compliance is inversely proportional ∆P
(Change in the pressure)

44. Elasticity
Elasticity =∆P/∆V
Elasticity is inversely proportional to ∆V
(Change in the volume)
Elasticity is directly proportional to ∆P
(Change in the pressure)

45. Compliance and Elasticity
Compliance and elasticity were
opposite

46. Factors affecting compliance
Elasticity of
lungs
Elasticity of
chest wall
Surface
tension

47. Elasticity of lungs
 Lungs are very compliant (can expand with ease)
 At the same time they can recoil also (elasticity)
 Normally Compliance = Elasticity
 Now think if the lung becomes more elastic…..
 Elasticity is inversely proportional to volume
 Volume in the lungs will decrease if elasticy
increases

48. Pulmonary fibrosis
 Lot of fibrous tissues all over the lungs
 Lungs are not able to stretch
 Compliance decreases
 Elasticity increases
 Elasticity is inversely proportional to volume
 Volume in the lungs will decrease

49. Emphysema
 Lung is super compliant
 Loss of elastic tissues
 Compliance increases
 Elasticity decreases
 Elasticity is inversely proportional to volume
 Volume in the lungs will increases
 Easy to take air in but not easy to move air out
(elasticity decreased)

50. Elasticity of chest wall
 Normally compliance = elasticity
 Diseases like kyphosis, scoliosis (s shaped spine),
ankylosing spondylitis lungs can not expand
 Restrictive respiratory disorders
 Compliance decreases
 Hard to breath in
 Inspiration is difficult

51. Surface tension
 Increase in surface tension (IRDS)
 All the alveoli will collapse
 Lung collapse
 Compliance decreases (lot of resistance to stretch)
 Hard to breath in
 Increase in the work of breathing
 If surfactant present, it decreases surface tension
so that lung can expand with ease ( compliance
increases) and work of breathing decreases

52. Pneumothorax and hemo thorax
 Air in the pleural cavity- pneumothorax (stab wound)
 Blood in the pleural cavity – Hemothorax
 Intra pleural pressure become same as atmospheric
pressure
 Positive intra pleural pressure
 Start pushing the lungs
 Collapse of lungs
 Compliance decreases
 Volume decreases

53. Lung Compliance graph
 When it is plotted in the form of graph for inspiratory
and expiratory phases, the curves will not overlap but
bring about the formation of hysteresis loop.
 It is due to a change in the elastic property of the lungs
and chest wall.
 Slope of the straight line = ∆Y/∆X= ∆V/∆P =
compliance

54. Lung Compliance graph

55. Ventilation- Perfusion Ratio
 V/P (V/Q) ratio = Alveolar Ventilation rate (AVR)
Lit/min / Pulmonary blood flow Lit/ min
 Alveolar ventilation refer to the gas that take part in
gases exchange
 Tidal volume is 500 ml
 But in this 500 ml 150 ml do not take part in the
gaseous exchange (dead space)
 AVR= (Tidal volume- dead space) x RR
 (500-150)x 12= 4200 ml/min

56. Perfusion
 Amount of blood flowing through the pulmonary
capillaries in one minute
 It is same as cardiac output
 5000 ml/ min
 Cardiac output depends on heart rate and stroke
volume
 Ventilation/ perfusion (V/P)= 4200/5000 = 0.8

57. Alveoli 1- Hyper ventillated
 Getting high ventilation
 More oxygen entering (Po2 is high)
 More carbon dioxide moves out (PCo2 less)
 Ventilation/ perfusion (V/P)= 4200/5000 = 0.8
 In this case As ventilation is more, V/P ratio
becomes more than 0.8
 Our body has compensatory mechanism for this

58. Alveoli 1 - Hyperventilation
 When there is more oxygen
 Upon entering the endothelial cells of pulmonary
capillaries
 It causes production of NO
 NO causes relaxation of the smooth muscles of the
pulmonary blood vessels
 Vasodilation
 Increase in the perfusion
 V/P ratio back to normal

59. Alveoli 2 – Poor ventilation
 Poor ventilated alveoli
 Little oxygen comes in (low Po2)
 Little carbon dioxide moves out (Low PCo2)
 Ventilation/ perfusion (V/P)= 4200/5000 = 0.8
 As there is poor ventilation, V/P ratio becomes less
than 0.8
 Our body has compensatory mechanism for this

60. Alveoli 2 – Poor ventilation
 Little oxygen comes in (low Po2)
 Oxygen is less
 Can not stimulate production of much NO
 Decrease in NO production
 Constriction of pulmonary blood vessels
 Vasoconstriction
 Decrease in perfusion
 V/P ratio back to normal

61. Auto regulation in systemic vs
pulmonary circulation
Systemic circulation
 More oxygen causes
vasoconstriction
 Less oxygen causes
vaso-dilation
Pulmonary circulation
 More oxygen causes
vasodilation
 Less oxygen causes
vasoconstriction

62. Alveoli 3 – more perfusion
 Like during exercise
 Cardiac out put increases and perfusion increases
 More blood flow and more gaseous exchange
 Increase in the PCo2
 Ventilation/ perfusion (V/P)= 4200/5000 = 0.8
 As there is increase in the perfusion, V/P ratio
becomes less than 0.8
 Our body has compensatory mechanism for this

63. Alveoli 3 – more perfusion
 PC02 increased
 Co2 acts on the smooth muscles of bronchioles
 Causes dilation of bronchioles
 Increase in the diameter
 Decrease in the airway resistance
 More oxygen comes in and more carbon dioxide
moves out
 Increase in the ventilation and V/P ratio back to normal

64. Alveoli 4 – low perfusion
 Pulmonary embolism/ right ventricular failure
 Decreased perfusion
 Gaseous exchange very less
 Decreased PCo2
 Ventilation/ perfusion (V/P)= 4200/5000 = 0.8
 As the perfusion decreased, V/P ratio becomes
more than 0.8
 Our body has compensatory mechanism for this

65. Alveoli 4 – low perfusion
 Low Co2
 Acts on the smooth muscle of bronchioles
 Constriction of bronchial smooth muscle
 Increased resistance
 Less oxygen and less carbon dioxide moves out
 Decrease in the ventilation
 V/P ratio back to normal

66. Diffusion of gases
 Fick’s Law of diffusion: Fick’s law of diffusion
states that the net diffusion rate of a gas
through a membrane is proportional to
 Tissue area ( A)
 Difference in the partial pressure between two
sides (P1-P2)
Inversely proportional to
 Thickness

67. Diffusion of gases
 V gas =A x D x P1-P2 / T
 A= Tissue area
 P1-P2 = pressure gradient
 T = thickness
 D= constant
 D value depends on solubility of gas and inversely
proportional to square root of molecular weight

68. Net rate of diffusion
 Solubility of the gas in the fluid (C02 diffuses 20
times faster than O2)
 Cross-sectional area available
 Distance through which the gas should diffuse
 Molecular weight of gas
 Temperature
 In the body, the temperature remains reasonably
constant and usually need not to be considered.

69. Respiratory unit ( respiratory
membrane)
 Layer of fluid lining the alveoli and containing
surfactant
 Alveolar epithelium containing thin epithelial cells
 Epithelial basement membrane
 Thin interstitial space between alveolar epithelium
and capillary membrane
 Capillary basement membrane
 Capillary endothelial cells

70. Respiratory membrane

71. Thickness of respiratory membrane
 The respiratory membrane is about 0.6 micrometers
thick
 Thickness increases in edema ( fluid accumulation
in interstitial space and alveoli)
 Gas has to diffuse not only through membrane but
also through fluid
 Rate of diffusion decreases

72. Surface area of respiratory
membrane
Emphysema- many alveoli collapse
Decrease in surface area
Serious detriment to respiratory gas
exchange

73. Diffusion capacity of respiratory
membrane
 Definition: Volume of the gas that will diffuse
through the membrane each minute for a partial
pressure difference of 1 mmHg.
 Diffusion capacity of oxygen is 21 ml/minute per
mmHg. (measured by carbon monoxide method)
 Diffusion capacity of carbon-dioxide? (400-450
ml/min per mmHg?)

74. Diffusion capacity of C02
 Can not be measured as the C02 diffuses
through the respiratory membrane so rapidly
that the average Pco2 in the blood is not far
different from alveolar PC02. (the average
difference is less than 1 mmHg).

75. THANK YOU