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 dis- tending 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.
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 con- centration 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.