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Mechanics of ventilation:
static lung mechanics
Specific learning objectives:
? Elastic properties of lung and chest wall
? Compliance: measure of elastic properties of lung
? 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
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
gradients.
? Forces are present that resist the opening of the lungs i.e. the alveoli:
? The natural tendency of the lungs to recoil or collapse: elastic recoil
? The surface tension in alveoli
? What keeps the alveoli (lungs) expanded:
? Negative intra-pleural pressure
The space between the two pleural layers is always negative or sub-atmospheric. This tends to suck
the lungs outward
? Alveolar pressure
pressure within the alveoli themselves tend to keep the lungs inflated
Reduced surface tension within the alveoli
Why does an inflated lung want to recoil inward?
? 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.
? 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
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,
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
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
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
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
themselves a network
? Geometry: nylon stocking.
? Expansion of the lungs affects mainly the lung parenchyma. During an inspiration that starts from residual
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
and recruit previously collapsed alveoli.
Details of the interstitial space, the
Electron micrographs of the collagen fibre
Electron micrographs of the elastin fibre
capil ary endothelium and alveolar
network of rat lung
In the rat lung
epithelium.
Archives of Histology and Cytology Vol. 67(2004) No. 1
NUNN'S APPLIED RESPIRATORY PHYSIOLOGY, 8th edition
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
surface tension.
? The work that is done in stretching the lung is not dissipated as heat; instead
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 .
? 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.
Elastic recoil of the lung affects compliance
The more elastic something is, the more it wants to return to its original shape
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.
? Stiff lungs have a low compliance.
Compliance is usually expressed in litres (or millilitres) per kilopascal (or centimetres of water) with a normal value
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.
: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.
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.
? It is a measure of elastic properties of the lung
? Reflects distensibility of lung
? Compliance : change in volume per unit of pressure change:
?
CL
=
V (liters)/P (cmH2O)
? 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
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
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.
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.
? 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
descending limb of the curve
Lung compliance is measured from a
pressure /volume curve.
The subject first inspires maximally to total
lung capacity (TLC) and then expires slowly,
while airflow is periodically stopped to
simultaneously measure pleural pressure
and lung volume.
Lung compliance (CL) is measured in L/cm
H2O.
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
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
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.
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
Patients with a chronic obstructive lung disease (COPD), such as emphysema, have abnormally
high lung compliance.
Patients with restrictive diseases, such as respiratory distress syndrome, have abnormally low
lung compliance.
Specific compliance
? 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.
? Compliance that has been adjusted for different lung volumes is called specific
compliance.
? 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).
? 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
? Compliance is analogous to electrical capacitance, and in the respiratory
system the compliance of lungs and thoracic cage are in series.
? 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
? For its reciprocal, elastance, the relationship is then much simpler:
? Total elastance= lung elastance + thoracic cage elastance
Factors Affecting Lung Compliance
? 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.
? 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
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
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
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
compliance or bronchoconstriction could enhance time dependence and reduce dynamic
compliance.
? 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
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
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
represent about two thirds.
The fluid -air surface tension elastic forces of the lungs also increase tremendously when the substance called
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 .
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
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.
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.
Elastance
? Elastance is a measure of the work that has to be exerted by the muscles of inspiration
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
in kilopascals per litre.
? It is the collapsing force that develops in the lung as the lung expands.
? 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.
? Elastance is due to:
A. Col agen and elastic fibers within the lungs (minor component)
B. Surface tension of the alveoli (major component), Elastance is described by laplace
law E=2T/R
What is Surface Tension?
? 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
spherical shape.
It is defined as the force acting across an imaginary line 1cm long in a liquid surface. This
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
? Resists stretching
? Recoils after stretching
? 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.
? 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
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
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
molecules inward only, creating a central y directed force that tends to
contract the liquid into a sphere.
Laplace's law
"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
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
expansion of larger alveoli
That doesn't happen because:
.
Normally larger alveoli do not exist adjacent to small alveoli = because they share the same septal walls.
.
All alveoli are surrounded by fibrous tissue septa that act as additional splints.
.
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
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.
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.
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
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.
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.
Approximately 90% of surfactant consists of lipids, and the remainder is proteins and small amounts of
carbohydrate.
? 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
and forms micelles. On expansion (reinflation), new surfactant is required to form a new film that is spread on the
alveolar surface lining.
? 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
gas/ liquid interface.
? Patients recovering from anesthesia are often encouraged to breathe deeply to enhance the spreading of
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
? 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.
? 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.
? 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.
? 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;
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
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
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
which exerts negative feedback on surfactant secretion and increases reuptake of surfactant
components into the cel .
? 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
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-
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
surfactant release and in preventing pulmonary infection.
How does surfactant reduce the surface tension so much?
? 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.
? When this occurs, their intermolecular repulsive forces oppose the normal
attracting forces between the liquid surface molecules that are responsible
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
each other more.
Physiological importance of surfactant
? A low surface tension in the alveoli increases the compliance of the lung and
reduces the work of expanding it with each breath.
? Promotes alveolar stability and prevents collapsed at low volumes--small
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
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
alveoli.
ELASTIC RECOIL OF THE THORACIC CAGE
? The thoracic cage comprises the ribcage and the diaphragm.
? 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.
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.
? 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
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
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
(FRC).
? As the volume of the system is increased the relaxation pressure increases, and the
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
pressure developed by the chest wall.
? The relaxation curve for the chest wall alone crosses the zero pressure line at 70%
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
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
increasing age.
? Obesity and even pathological skin conditions : scarring of the skin overlying the
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.
? 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
reduced by 60% in the prone position because of the diminished elasticity of the
ribcage and diaphragm when prone.
Alveolar lining fluid
? 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.
? 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.
? Water loss due to respiration and its replacement from the internal water body content is a dynamic process that
must be tightly regulated.
Front. Physiol., 22 May 2012
Alveolar interdependence
This post was last modified on 08 April 2022