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Download MBBS Physiology Presentations 35 Elastic Properties of Lung And Pulmonary Ventilation Lecture Notes

Download MBBS (Bachelor of Medicine, Bachelor of Surgery) 1st Year, 2nd Year, 3rd Year and Final year Physiology 35 Elastic Properties of Lung And Pulmonary Ventilation PPT-Powerpoint Presentations and lecture notes

This post was last modified on 08 April 2022

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Specific learning objectives:

? Elastic properties of lung and chest wall
? Compliance: measure of elastic properties of lung

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? An isolated lung tends to contract until eventually all the contained air is expel ed.

? When the thoracic cage is opened it tends to expand to a volume about 1 l greater than functional residual capacity (FRC).

? In a relaxed subject with an open airway and no air flowing, the inward elastic recoil of the lungs is exactly balanced by the

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outward recoil of the thoracic cage.
Air flow in lungs

? No muscles in the alveoli; air passively moves in/out of the lungs in response to pressure

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gradients.

? Forces are present that resist the opening of the lungs i.e. the alveoli:

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? The natural tendency of the lungs to recoil or collapse: elastic recoil

? The surface tension in alveoli

? What keeps the alveoli (lungs) expanded:

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? Negative intra-pleural pressure

The space between the two pleural layers is always negative or sub-atmospheric. This tends to suck

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the lungs outward

? Alveolar pressure

pressure within the alveoli themselves tend to keep the lungs inflated

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Reduced surface tension within the alveoli

Why does an inflated lung want to recoil inward?

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? Elastic recoil is the tendency to resist or oppose stretching.
? Lung volumes are determined by the balance between the lung 's elastic recoil

properties and the properties of the muscles of chest wall.

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? When chest is opened, the lung recoils until the transpulmonary pressure is

zero and the chest wal increases in size (60-70% of the vital capacity).

? Elastic recoil of the lung is directly related to lung stiffness, i.e., the stiffer the

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lung, the more elastic recoil.

? Elastic recoil pressure increases as the lung inflates.
? The outward elastic recoil of the chest wal is greatest at residual volume,

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whereas the inward elastic recoil of the lung is greatest at total lung capacity
The framework of the lungs

? is made up of bundles of elastic and col agen (type I,I ,I I,V,VI) fibres that extend from the large airways

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down to the alveoli and across to the pleura and blood vessels.

? Fibres are frequently in apposition and together they form the scaffolding of the lung resembling crumpled

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wirenetting.

? The connective tissue scaffold which forms the lung structure has three interconnected types of fibre: 1.

Axial spiral fibres running from the hilum along the length of the airways 2. Peripheral fibres originating in

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the visceral pleura and spreading inwards into the lung tissue,3. Septal fibres, a network of which forms a

basket-like structure of alveolar septa, through which are threaded the pulmonary capillaries, which are

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themselves a network

? Geometry: nylon stocking.
? Expansion of the lungs affects mainly the lung parenchyma. During an inspiration that starts from residual

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volume, the coils of the spiral fibres of the alveolar ducts expand longitudinal y; this enlarges the mouths of

the alveoli that lie between the coils.

? This stretches the alveolar septa, smoothens the undulations in alveolar walls, opens up of pleats in the septa

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and recruit previously collapsed alveoli.

Details of the interstitial space, the

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Electron micrographs of the collagen fibre

Electron micrographs of the elastin fibre

capil ary endothelium and alveolar

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network of rat lung

In the rat lung

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epithelium.

Archives of Histology and Cytology Vol. 67(2004) No. 1

NUNN'S APPLIED RESPIRATORY PHYSIOLOGY, 8th edition

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Elastic recoil: static recoil pressure

? During inspiration, contraction of respiratory muscles stretches the elastic

and collagen tissues network of the lungs and pleura; it also overcomes the

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surface tension.

? The work that is done in stretching the lung is not dissipated as heat; instead

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the energy is stored in the structures, which have been stretched, then

expended to drive the subsequent expiration.

? The static recoil pressure varies with lung volume .

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? The slope of the relationship between pressure (Pst) and volume (V) describes

the distensibility of the lungs. The slope at functional residual capacity is

called the compliance of the lungs.

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Elastic recoil of the lung affects compliance

The more elastic something is, the more it wants to return to its original shape

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The more compliance something is, the less it wants to return to its original shape.

Lung compliance is defined as the change in lung volume per unit change in transpulmonary pressure

Gradient.

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? Stiff lungs have a low compliance.

Compliance is usually expressed in litres (or millilitres) per kilopascal (or centimetres of water) with a normal value

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2

of 1.5 l.kPa-1 (150 ml.cmH O-1).
Compliance may be described as static or dynamic depending on the method of measurement.

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:Static compliance is measured after the lungs have been held at a fixed volume for

as long as is practicable

:Dynamic compliance is usually measured in the course of normal rhythmic breathing.

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Compliance of the Lungs

? The extent to which the lungs will expand for each unit increase in transpulmonary

pressure (if enough time is al owed to reach equilibrium) is called the lung compliance.

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? It is a measure of elastic properties of the lung

? Reflects distensibility of lung

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? Compliance : change in volume per unit of pressure change:

?

CL

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=

V (liters)/P (cmH2O)

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? The total compliance of both lungs together in the normal adult human averages about

200 mil iliters of air per centimeter of water transpulmonary pressure.

? That is, every time the transpulmonary pressure increases 1 centimeter of water, the lung

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volume, after 10 to 20 seconds, will expand 200 milliliters.

? To inspire a normal tidal volume of 500 ml, intrapleural pressure must fall by 2-3 cm H2O

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If the lungs are slowly inflated and then slowly deflated, the pressure/volume curve for static points during inflation differs

from that obtained during deflation. The two curves form a loop, which becomes progressively broader as the tidal volume is

increased.

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Rodney A. Rhoades, David R. Bel , Medical Physiology: Principles for Clinical Medicine 3rd Edition
? As the pressure is reduced in steps, the volume increases.

? After the expanding pressure exceeds about 20 cm H 2O, the volume changes are less.

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? Lung is much stiffer at higher volumes.

Nonlinear curve; slope of the P-V curve is considered i.e. change in pressure over the litre above FRC on the

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descending limb of the curve

Lung compliance is measured from a

pressure /volume curve.

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The subject first inspires maximally to total

lung capacity (TLC) and then expires slowly,

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while airflow is periodically stopped to

simultaneously measure pleural pressure

and lung volume.

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Lung compliance (CL) is measured in L/cm

H2O.

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Rodney A. Rhoades, David R. Bel , Medical Physiology: Principles for Clinical Medicine 3rd Edition
Hysteresis: "deficiency" or "lagging behind"

? At any given pressure, the volume on the descending limb of the pressure-volume curve exceeds that obtained while the lung

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was being expanded. The failure of the lung to fol ow the same course during deflation as it did during inflation is cal ed

hysteresis.

A more than the expected pressure is required during inflation and rather less than the expected recoil pressure is available

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during deflation. This resembles the behaviour of perished rubber or polyvinyl chloride, both of which are reluctant to accept

deformation under stress but, once deformed, are again reluctant to assume their original shape.

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The most important cause of the observed hysteresis in the intact lung : The surface tension of the alveolar lining fluid is

greater at larger lung volume and also during inspiration than at the same lung volume during expiration.

Compliance in diseases

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Patients with a chronic obstructive lung disease (COPD), such as emphysema, have abnormally

high lung compliance.

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Patients with restrictive diseases, such as respiratory distress syndrome, have abnormally low

lung compliance.
Specific compliance

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? Lung volume depends on the body size [(mouse v/s elephant) and if a person has one

lung removed surgically] Therefore absolute values of compliance can not be used to

compare lung compliance of different sized individuals.

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? Compliance that has been adjusted for different lung volumes is called specific

compliance.

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? Specific compliance is change in volume per unit change in pressure/ initial volume.

? Specific compliance = Compliance divided by FRC

? Normal value = 0.8 (range 0.3 to 1.4) kPa?1 (0.08, range 0.03 to 0.14 cm H2O?1).

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? Similar values in both sexes and all ages including neonates
? Is a measurement of the intrinsic elastic property of the lung tissue

Pressure/volume relationships of the lung plus thoracic age

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? Compliance is analogous to electrical capacitance, and in the respiratory

system the compliance of lungs and thoracic cage are in series.

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? Therefore the total compliance of the system obeys the same relationship as

that for capacitances in series

1/Total compliance= 1/ Lung compliance+ 1/ thoracic compliance

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? For its reciprocal, elastance, the relationship is then much simpler:
? Total elastance= lung elastance + thoracic cage elastance
Factors Affecting Lung Compliance

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? Lung volume. Larger animal species have thicker alveolar septa containing increased amounts of

collagen and elastin resulting in larger alveolar diameters, so reducing the pressure needed to

expand them. An elephant therefore has larger alveoli and higher compliance than a mouse.

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? Posture. Lung volume and compliance, changes with posture. Compared with the supine position,

thoracic cage compliance is 30% greater in the seated subject and the total static compliance of the

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respiratory system is reduced by 60% in the prone position because of the diminished elasticity of

the ribcage and diaphragm when prone.

? Pulmonary blood volume. The pulmonary blood vessels probably make an appreciable contribution

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to the stiffness of the lung. Pulmonary venous congestion is associated with reduced compliance.

? Age. There is a smal increase in lung compliance with increasing age, believed to be caused by

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changes to the structure of lung collagen and elastin.

? Bronchial smooth muscle tone. An infusion of methacholine sufficient to result in a doubling of

airway resistance decreases dynamic compliance by 50%. The airways might contribute to overall

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compliance or bronchoconstriction could enhance time dependence and reduce dynamic

compliance.

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? Disease. Important changes in lung pressure? volume relationships are found in some lung diseases

When the lungs are filled with air, there is an interface between the alveolar fluid and the air in the alveoli. In

lungs filled with saline solution, there is no airfluid interface, and therefore, the surface tension effect is not

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present; only tissue elastic forces are operative in the lung filled with saline solution.

The transpleural pressures required to expand air filled lungs are about three times as great as those required

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to expand lungs filled with saline solution.

Thus, one can conclude that the tissue elastic forces tending to cause collapse of the air-filled lung represent

only about one third of the total lung elasticity, whereas the fluid-air surface tension forces in the alveoli

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represent about two thirds.

The fluid -air surface tension elastic forces of the lungs also increase tremendously when the substance called

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surfactant is not present in the alveolar fluid.
Hysteresis is not present in the saline generated curves.

The difference between the saline and air curves is much smal er when lung volumes are smal .

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1. The slope of the deflation limb of the saline curve is much steeper than that of the air curve. This means that when surface

tension is eliminated, the lung is far more compliant (more distensible).

2. The area to the left of each curve is equal to work, which can be defined as force (change in pressure) * distance (change in

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volume), the elastic forces and surface tension can be separated.

The area to the left of the saline inflation curve: work required to overcome the elastic recoil of the lung tissue.

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The area to the left of the air inflation curve: work required to overcome both elastic tissue recoil and surface tension.

Area to the left of the air curve - Area to the left of the saline curve shows that approximately two thirds of the work required

to inflate the lungs is needed to overcome surface tension.

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Elastance

? Elastance is a measure of the work that has to be exerted by the muscles of inspiration

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to expand the lungs.

? Elastance is the reciprocal of compliance.

? It is the pressure change that is required to elicit a unit volume change and is expressed

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in kilopascals per litre.

? It is the collapsing force that develops in the lung as the lung expands.

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? It always act to collapse the lungs. It is equivalent to collapsing force that builds up in a

balloon completely inflated with air.

? Stiff lungs have a high elastance.

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? Elastance is due to:

A. Col agen and elastic fibers within the lungs (minor component)

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B. Surface tension of the alveoli (major component), Elastance is described by laplace

law E=2T/R
What is Surface Tension?

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? A molecular, cohesive (binding) force found at liquid-gas interfaces.

? Expressed in dynes/cm

? A liquid film that coats the interior of alveoli, causing air-liquid interfaces to assume a

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spherical shape.

It is defined as the force acting across an imaginary line 1cm long in a liquid surface. This

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tension develops because the cohesive forces between adjacent liquid molecules are greater

than the forces between the molecules of liquid and gas outside the surface.

Because of surface tension, the alveolus

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? Resists stretching

? Recoils after stretching

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? Favors reduced surface area (to shrink into a sphere)

? Surface tension at an air/water interface produces forces that tend to reduce the area of

the interface.

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? The pressure inside a bubble is higher than the surrounding pressure by an amount

depending on the surface tension of the liquid and the radius of curvature of the bubble

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according to the Laplace equation: For a sphere like alveolus, the relationship between

pressure with in the sphere and tension in the wall is given by Laplace's Law

? P=2T/R

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The force of surface tension in a drop of liquid. Cohesive force attracts

molecules inside the drop to one another. Cohesion can pul the outermost

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molecules inward only, creating a central y directed force that tends to

contract the liquid into a sphere.
Laplace's law

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"The pressure inside a balloon is calculated by twice the surface tension, divided by the

radius."

Pressure to collapse generated by alveoli is inversely affected by radius of alveoli

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The smaller a bubble, the higher the pressure acting on the bubble
Smaller alveoli have greater tendency to collapse

If some alveoli were smaller and other large = smaller alveoli would tend to collapse and cause

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expansion of larger alveoli

That doesn't happen because:

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.

Normally larger alveoli do not exist adjacent to small alveoli = because they share the same septal walls.

.

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All alveoli are surrounded by fibrous tissue septa that act as additional splints.

.

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Surfactant reduces surface tension = as alveolus becomes smaller surfactant molecules are squeezed together

increasing their concentration = reduces surface tension even more.

Surfactant makes it possible for alveoli of different diameters that are connected in paral el to coexist and be stable at low lung

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volumes, by lowering surface tension proportionately more in the smal er alveoli
Effect of Alveolar Radius on the Pressure Caused by Surface Tension

The smal er the alveolus, the greater the alveolar pressure caused by the surface tension.

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This phenomenon is especial y significant in smal premature babies, many of whom have alveoli with radii less than one

quarter that of an adult person.

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Further, surfactant does not normal y begin to be secreted into the alveoli until between the sixth and seventh months of

gestation, and in some cases, even later.

Therefore, many premature babies have little or no surfactant in the alveoli when they are born, and their lungs have an

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extreme tendency to collapse, sometimes as great as six to eight times that in a normal adult person.

This situation causes the condition cal ed respiratory distress syndrome of the newborn.

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It is fatal if not treated with strong measures, especial y properly applied continuous positive pressure breathing.

The Alveolar Surfactant

? It is a surface active agent in water, which means that it greatly reduces the surface tension of water.

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Approximately 90% of surfactant consists of lipids, and the remainder is proteins and small amounts of

carbohydrate.

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? Most of the lipid is phospholipid, of which 70% to 80% is dipalmitoyl phosphatidyl choline (DPPC), the main

constituent responsible for the effect on surface tension.

? At low lung volumes, when the molecules are tightly compressed, some surfactant is squeezed out of the surface

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and forms micelles. On expansion (reinflation), new surfactant is required to form a new film that is spread on the

alveolar surface lining.

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? When surface area remains fairly constant during quiet or shal ow breathing, the spreading of surfactant is often

impaired.

? A deep sigh or yawn causes the lungs to inflate to a larger volume and new surfactant molecules spread onto the

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gas/ liquid interface.

? Patients recovering from anesthesia are often encouraged to breathe deeply to enhance the spreading of

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surfactant. Patients who have undergone abdominal or thoracic surgery often find it too painful to breathe

deeply; poor surfactant spreading results, causing part of their lungs to become atelectatic.
Synthesis of Surfactant

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? Both formed in and liberated from the alveolar epithelial type I cell.
? The lamellar bodies contain stored surfactant that is released into the alveolus by exocytosis in response to high

volume lung inflation, increased ventilation rate or endocrine stimulation.

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? After release, surfactant initially forms areas of a lattice structure termed tubular myelin, which is then

reorganized into monolayered or multilayered surface films.

? The alveolar half-life of surfactant is 15 to 30 h with most of its components recycled by type I alveolar cells.

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? They perform this function by not dissolving uniformly in the fluid lining the alveolar surface.
? Instead, part of the molecule dissolves while the remainder spreads over the surface of the water in the alveoli.

This surface has from one twelfth to one half the surface tension of a pure water surface.

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? In quantitative terms, the surface tension of different water fluids is approximately the following:

pure water, 72 dynes/cm;

normal fluids lining the alveoli but without surfactant, 50 dynes/cm;

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normal fluids lining the alveoli and with normal amounts of surfactant included, between 5 and 30 dynes/cm

? The released lamellar body (LB) material is converted to tubular myelin (TM), and the TM is

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the source of the phospholipid surface film (SF).

? Surfactant is taken up by endocytosis into alveolar macrophages and type II epithelial cells.
? Formation of the phospholipid film is greatly facilitated by the proteins in surfactant. This

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material contains four unique proteins: surfactant protein (SP)-A, SP-B, SP-C and SP-D.

? SP-A is a large glycoprotein. SP-A is intimately involved in controlling the surfactant present

in the alveolus with type I alveolar cel s having SP-A surface receptors, the stimulation of

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which exerts negative feedback on surfactant secretion and increases reuptake of surfactant

components into the cel .

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? SP-B and SP-C are smaller proteins, which are the key protein members of the

monomolecular film of surfactant, vital to the stabilization of the surfactant monolayer.

? A congenital lack of SP-B results in severe and progressive respiratory failure and genetic

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abnormalities of SP-C lead to pulmonary fibrosis in later life.

? Like SP-A, SP-D is a glycoprotein. It plays an important role in the organization of SP-B and SP-

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C into the surfactant layer.

? Both SP-A and SP-D are members of the collectin family of proteins that are involved in innate

immunity in the conducting airway as well as in the alveoli, are involved in the control of

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surfactant release and in preventing pulmonary infection.

How does surfactant reduce the surface tension so much?

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? The fatty acids are hydrophobic and general y straight, lying parallel to each

other and projecting into the gas phase. The other end of the molecule is

hydrophilic and lies within the alveolar lining fluid.

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? When this occurs, their intermolecular repulsive forces oppose the normal

attracting forces between the liquid surface molecules that are responsible

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for surface tension.

? The reduction in surface tension is greater when the film is compressed

because the molecules of DPPC are then crowded closer together and repel

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each other more.
Physiological importance of surfactant

? A low surface tension in the alveoli increases the compliance of the lung and

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reduces the work of expanding it with each breath.

? Promotes alveolar stability and prevents collapsed at low volumes--small

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alveoli are prevented from getting smal er.

? Promotes "dry " alveoli--collapsed alveoli tend to draw fluid from pulmonary

capillaries (edema-movement of fluid into alveoli; It has been calculated that if

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it were not present, the unopposed surface tension in the alveoli would

produce a 20 m Hg force favoring transudation of fluid from the blood into the

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alveoli.

ELASTIC RECOIL OF THE THORACIC CAGE

? The thoracic cage comprises the ribcage and the diaphragm.

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? Each is a muscular structure and can be considered as an elastic structure only when the

muscles are relaxed, which is can be achieved only under the conditions of paralysis.

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The compliance of lungs+thorax = 1/2 of lungs alone.

? To measure compliance, air is forced into the lungs a little at a time while recording lung

pressures and volumes.

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? The curve of airway pressure obtained in this way, plotted against volume, is the pressure?

volume curve of the total respiratory system. The pressure is zero at a lung volume that

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corresponds to the volume of gas in the lungs at FRC ( relaxation volume ).

? This relaxation pressure is the sum of slightly negative pressure component from the chest

wall (Pw ) and a slightly positive pressure from the lungs (PL ). PTR is positive at greater

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volumes and negative at smaller volumes.
Relaxation pressure-volume curve for the total respiratory system

? The relaxation pressure of the total system is zero at functional residual capacity

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(FRC).

? As the volume of the system is increased the relaxation pressure increases, and the

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opposite occurs as the volume is decreased.

? The relaxation pressure-volume curve of the lung shows a positive pressure of 4

mmHg at FRC, and this is balanced by an equal and opposite outward expanding

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pressure developed by the chest wall.

? The relaxation curve for the chest wall alone crosses the zero pressure line at 70%

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of vital capacity. In other words below this volume the chest wall continues to

develop a negative pressure, that is tends to expand, whereas above that volume a

positive pressure is required to expand the chest wall

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Factors Influencing Compliance of the Thoracic Cage

? Anatomical factors include the ribs and the state of ossification of the costal

cartilages, which explains the progressive reduction in chest wal compliance with

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increasing age.

? Obesity and even pathological skin conditions : scarring of the skin overlying the

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front of the chest, for example, from burns, may impair breathing.

? A relaxed diaphragm simply transmits pressure from the abdomen that may be

increased in obesity and abdominal distension.

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? Compared with the supine position, thoracic cage compliance is 30% greater in

the seated subject and the total static compliance of the respiratory system is

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reduced by 60% in the prone position because of the diminished elasticity of the

ribcage and diaphragm when prone.

Alveolar lining fluid

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? The intermediate surface area of the human lung is 130 m2. and is mostly constituted by the alveolar region. The

average fluid surface height in the alveoli is 0.2 m.

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? The alveolar fluid content can be estimated to be 36 ml.

? A 70-kg human needs 2900 ml of water per day. 725 ml/day of this water will be lost due to respiration.

? This indicates that the alveolar fluid volume is replaced 20 times/day.

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? Water loss due to respiration and its replacement from the internal water body content is a dynamic process that

must be tightly regulated.

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Front. Physiol., 22 May 2012
Alveolar interdependence