– either volitional or as in coughing – requires muscular effort. The abdominal musculature is the principal agent in this.
The inherent elastic property of the lungs
Lung tissue has a natural elasticity. Left to its own devices, a lung would tend to shrink to little more than the size of a tennis ball. This can sometimes be observed radiographically in the context of a complete pneumothorax (see Chapter 16). The lung’s tendency to contract is counteracted by the semi‐rigid chest wall, which itself has a tendency to spring outward from its usual position. At the end of a normal tidal expiration, the two opposing forces are nicely balanced and no muscular effort is required to hold this ‘neutral’ position. Breathing at close to this lung volume (normal tidal breathing) is therefore relatively efficient and minimises work. It is rather like gently stretching and relaxing a spring from its neutral, tension‐free position. In some diseases (asthma or COPD), tidal ventilation is obliged to occur at higher lung volumes (see Chapter 3). Breathing then is rather like stretching and relaxing a spring that is already under a considerable degree of tension. The work of breathing is therefore increased, a factor that contributes to the sensation of breathlessness. Test this yourself: take a good breath in and try to breathe normally at this high lung volume for a minute.
The natural tendencies for the chest wall to spring outwards and the lung to contract down present opposing forces, which generate a negative pressure within the pleural space. This negative pressure (‘vacuum’) maintains the lung in its stretched state. Clearly, at higher lung volumes, the lung is at greater stretch and a more negative pleural pressure is required to hold it in position. The relationship between pleural pressure (the force on the lung) and lung volume can be plotted graphically (Fig. 1.5). The lung does not behave as a perfect spring, however. You may recall that the length of a spring is proportional to the force applied to it (Hooke’s law). In the case of the lung, as its volume increases, greater and greater force is needed to achieve the same additional increase in volume; that is, the lung becomes less ‘compliant’ as its volume increases. Lung compliance is defined as ‘the change in lung volume brought about by a unit change in transpulmonary (intrapleural) pressure’.
Figure 1.5 Graph of (static) lung volume against oesophageal pressure (a surrogate for intrapleural pressure). In both subjects A and B, we see that lung compliance – the change in lung volume per unit change in intrapleural pressure (or slope of the curve) – is reduced at higher lung volumes. A: normal individual. B: individual with reduced lung compliance, such as lung fibrosis.
Airway resistance
In addition to overcoming the elastic properties of the lungs and the chest wall, during active breathing the muscles of respiration also have to overcome the frictional forces opposing flow up and down the airways.
Site of maximal resistance
It is generally understood that resistance to flow in a tube increases sharply as luminal radius (r) decreases (with laminar flow, resistance is inversely proportional to r4). It seems rather contradictory, therefore, to learn that in a healthy individual, the greater part of total airway resistance is situated in the large airways (larynx, trachea and main bronchi) rather than in the small airways. This is in part due to the fact that the flow velocity is greatest and flow most turbulent in the central airways, but also due to the much greater total cross‐sectional area in the later generations of airway (Fig. 1.6). Remember, we only have one trachea, but by the 10th division we have very many small airways, which effectively function in parallel.
Figure 1.6 Diagrammatic representation of the increase in total cross‐sectional area of the airways at successive divisions.
Conditions may be different in disease states. Asthma and COPD – diseases that affect airway calibre – tend to have a greater proportionate effect on smaller generations of airway. The reduced calibre of the smaller airways then becomes overwhelmingly important and the site of principal resistance moves distally.
Figure 1.7 Model of the lung, demonstrating the flow‐limiting mechanism (see text). The chest is represented as a bellows. The airways of the lungs are represented collectively as having a distal resistive segment (Res) and a more proximal collapsible or ‘floppy’ segment. The walls of the floppy segment are kept apart by the retractile force of lung recoil (Rec). EXP, expiration; INSP inspiration.
Consider the model of the lung represented in Fig. 1.7. Here, the tube represents a route through generations of airways from the alveoli to the mouth. The smaller generations, without cartilaginous support, are represented by the ‘floppy’ segment (B). Airways are embedded within the lung and are attached externally to lung tissue whose elastic recoil and ultimate connection to the chest wall supports the floppy segments. This recoil force is represented by the springs.
During expiration, a positive pressure is generated in the alveolar space (A). Air flows from A along the airway, past B, where the pressure is lower (it must be, otherwise the air would not have flowed in this direction), and on to the mouth, where the pressure is nominally ‘zero’.
The pressure difference across the walls of the floppy segment (A minus B) would tend to cause this part of the airway to collapse. It is prevented from doing so by the retractile force of lung recoil (tension within the springs).
The flow‐limiting mechanism
During expiration, the extent of the pressure drop between A and B is proportional to the flow rate. Clearly, with increased effort, the pressure at A will increase, the pressure difference between A & B will increase and flow rate will be increased … up to a point. Eventually, a critical flow rate will be reached, where the pressure gradient between A and B is sufficient to overcome the retractile force of the lung, the airway wall collapses and airflow ceases. Once there is no flow, the pressure inside the airway at point B quickly equilibrates with that at A. With no pressure difference forcing the airway wall to collapse, the retractile force of the lung reopens the airway and flow recommences. This brings us back to where we started and the cycle begins again. It will be apparent that this mechanism determines a maximum possible flow rate along the airway. Any attempt to increase flow rate (associated with a greater pressure difference A to B) will simply result in airway closure. As each route out of the lung will similarly have a maximal possible flow rate, the expiratory flow from the lung as a whole will have an absolute limit. It can be seen that this limit (to expiratory flow) is set by the internal mechanics of the lung, not by muscular strength or effort (above a certain level of effort). That is perhaps fortunate; if it were not the case then lung function tests such as peak expiratory flow rate (PEFR) would not be