Lung Mechanics: Elastic Forces.
To breathe in, the inspiratory
muscles must contract to overcome the impedance offered by the lungs and chest
wall. This is mainly in the form of frictional airway resistance (Chapter
7) and elastic resistance to stretching of the lung and chest wall
tissues and the flui lining the alveoli.
Assessing the stiffness of the lungs: lung compliance
The 'stretchiness' of the lung is
usually assessed as lung compliance (CL), which is the change in
lung volume per unit change in distending pressure (CL=∆V/∆P). The distending
pressure, P, is the pressure difference across the lung, which equals
alveolar-intrapleural pressure.
Intrapleural pressure can be
assessed by measuring oesophageal pressure (Chapter 3). Alveolar pressure
cannot easily be measured directly, but when no air is f owing, alveolar
pressure must equal mouth pressure (i.e. zero). The transmural pressure, P, is
then equal to intrapleural pressure. The subject breathes in steps and
measurements are taken while the breath is held and plotted as a static
pressure-volume (P–V) curve (Fig. 6a). The curve fattens as the lung volume
approaches total lung capacity (TLC). The inspiratory curve is slightly
different from the expiratory curve, and this hysteresis is a common
property of elastic bodies. Static lung compliance is the slope of the
steepest part of this static pressure-volume curve in the region just above
functional residual capacity (FRC).
Lung compliance is normally about
1.5 L/kPa, but as with lung volumes it is affected by the subject's size, age
and gender. In restrictive disease, such as lung fibrosis lung
compliance is low. Like a stiff spring, once stretched, fbrosed lungs have an
increased tendency to shrink back to their resting position or increased elastic
recoil. The loss of alveolar tissue in emphysema makes them easier
to stretch and lung compliance is increased. Although safe, swallowing an oesophageal
balloon is not very pleasant or convenient. Fortunately, it is often possible
to deduce that a patient has stiff lungs from other measurements such as TLC,
FRC (Chapters 3, 20 and 30), forced expiratory volume in 1 second (FEV1)
and forced vital capacity (FVC) (Chapter 20).
Dynamic pressure–volume loops and dynamic compliance
A dynamic pressure–volume loop
(upper panel of Fig. 6b) is obtained from continuous measurements of
intrapleural pressure and volume during a normal breathing cycle (lower panel
of Fig. 6b). There are two points, at the ends of inspiration and expiration,
where airflow and alveolar pressure are zero (a, at and e, et) and the slope of
the line joining these points is dynamic compliance. In health, its
value is similar to the static compliance, but in some diseases it may
be lower, as stiff areas may f ll preferentially during normal breathing.
Between the two zero flow points, the dynamic P-V loop appears fatter than the
static P-V loop, as intrapleural pressure must change more to drive airflow. In
fact, the area of the dynamic loop is a measure of the work done against airway
resistance (Chapter 7).
The air–fluid interface lining the alveoli During inspiration, as well as stretching the collagen and elastin fibres
the surface tension forces at the air-alveolar lining fuid interface
must be overcome. At the surface of a bubble, the attraction of the flui
molecules for each other creates a tension, which tends to shrink the bubble
(Fig. 6c). Laplace discovered that a gas bubble in a liquid would shrink until
the pressure, P, within it reached a value of 2T/R, where T is a constant, the
surface tension of the fuid, and R is the radius of the bubble. When a bubble
has air on both sides, there are two air-flui interfaces and P 4T/R. The law
of Laplace (P 2T/R or 4T/R) predicts that, if two bubbles are made of the
same fluid the smaller bubble will have a higher pressure within it-since when
the radius of curvature is small, a greater proportion of the surface tension
is directed to the centre of the bubble (lower panel of Fig. 6.1c). When the
two bubbles are connected, the small bubble empties into the large bubble as
air flows down the pressure
gradient.
The lungs are not a simple system
of bubbles connected by tubes but much more complicated. In life alveoli are
not spherical, they have interconnections between neighbouring alveoli and
alveolar fuid may not produce a continuous lining to the alveoli. Nevertheless,
the surface tension forces illustrated by this model are undoubtedly important
in the lung and the presence of an air-flui interface creates several potential
problems:
·
It
reduces lung compliance and the higher the surface tension the lower the
compliance.
· The
alveoli and small airways would be inherently unstable, tending to collapse
under surface tension forces during expiration resulting in areas of atelectasis.
The absence of these problems in
healthy humans is thought to be partly due to the presence in the alveolar
lining fuid of surfactant.
Surfactant
Pulmonary surfactant is a mixture
of phospholipids, such phosphatidylcholine and proteins, produced by the
type II pneumocytes (Chapter 5). The presence of these substances in the
alveolar lining fluid lowers the surface tension and increases
compliance. The phospholipids have a hydrophilic end that lies in the
alveolar flui and a hydrophobic end that projects into the alveolar gas,
and as a result they floa on the surface of the lining fuid. As an alveolus
shrinks, its surface area diminishes and the surface concentration of surfactant
rises (Fig. 6d). As surface tension falls with increasing surface concentration of surfactant, the increased tendency for alveoli to collapse when
they shrink is offset and stability is improved. Alveolar stability is also
aided by the connection and mutual pull of neighbouring alveoli, a phenomenon
known as alveolar interdependence.
Surfactant production in the
fetus gradually increases in the last third of pregnancy and may be inadequate
in babies born prematurely, giving rise to the typical problems of neonatal
respiratory distress syndrome (NRDS) - stiff lungs and areas of collapse
(Chapters 16 and 17).
Surfactant proteins (e.g. SP-A,
SP-B, SP-C and SP-D) contribute to the surface tension lowering actions of
phospholipids, as well as having other functions such as host defence. They are
probably the reason why natural surfactants have proved more effective for
treating NRDS than actant composed only of
phospholipids.
