When partitioning the respiratory mechanics into its lung and chest wall components, it is convenient to refer to elastance instead of compliance. The total elastance of the respiratory system is the pressure required to inflate it 1 l above its resting position. This is, the applied airway pressure is spent in part to inflate the lung and in part to inflate the chest wall. The chest wall comprises the anterior and posterior thoracic cage walls and the diaphragm, which is the 'abdominal component'. Indeed, in static conditions, when the airway resistance is nil:
Paw = Pl + Ppl (1)
Etot = El + Ecw (2)
where Paw is the (static) airway pressure, Pl is the transpulmonary pressure, Ppl is the pleural pressure, Etot is the total respiratory system elastance, El is the lung elastance, and Ecw is the chest wall elastance.
On the basis of these classical equations it is easy to grasp the mechanical interaction between the lung and the chest wall. First, however, it is important to recall that the concept of 'transmission' of alveolar pressure to the thoracic cavity is misleading [8
]. Let us assume that we inflate an isolated lung at an alveolar pressure of 10, 15 or 20 cmH2
O. The pressure measured at the pleural surface will always be 0 cmH2
O (i.e. atmospheric pressure) because the alveolar pressure is not 'transmitted'. When the thoracic cage surrounds the lungs as they are inflated, however, the cage has to change its volume. The lungs 'push' the thoracic cage, and the pressure generated by the interaction between the lung and the chest wall, which may have different elasticities, is the pleural pressure. If we consider that the pressure is 'transmitted', then the pleural pressure would depend on the airway pressure and the lung elasticity (the stiffer the lung, the lower the transmission). However, this approach ignores the contribution of the chest wall.
If the thoracic cage is 'soft' the pleural pressure generated to drive it will be low, but if the thoracic cage is 'stiff' then a higher pleural pressure will be needed (Fig. ). The distending force of the lung is the pressure difference between the alveoli and pleural pressure (the transpulmonary pressure), while the distending force of the thoracic cage is the pleural pressure to which all of the intrathoracic structures, such as the heart and the intrathoracic vessels, are subjected. In mathematical terms, because of and by rearranging equations 1 and 2, it follows that:
Figure 1 Effect of different lung elastance (EL) and chest wall elastance (Ew) on the total elastance (Etot) of the respiratory system. An equal total elastance of the respiratory system may arise (a) from a high lung elastance and a low chest wall elastance or (more ...)
Ppl = Paw × Ecw/Etot (3)
Pl = Paw × El/Etot (4)
The pleural pressure depends on the pressure applied to the airways, and on the ratio between the chest wall elastance and the total elastance of the respiratory system, which is the sum of the chest wall elastance and the lung elastance (see equation 2). In normal conditions this ratio is about 0.5 at functional residual capacity, because the chest wall elastance and the lung elastance are similar. In ARDS, however, the elastance ratio may vary from 0.2 to 0.8 [6
]. It is thus clear that, for the same applied airway pressure (let us say 30 cmH2
O) and with a chest wall elastance/total respiratory system elastance ratio of 0.5, the transpulmonary pressure will be 15 cmH2
O and the pleural pressure will be the same. If the ratio is 0.2, however, the transpulmonary pressure will be 24 cmH2
O but the pleural pressure will be 6 cmH2
O, while if the ratio is 0.8 the transpulmonary pressure will only be 6 cmH2
O and the pleural pressure will be 24 cmH2
These simple calculations illustrate the importance of knowing the mechanical characteristics of both the lung and the chest wall. The same airway pressure may generate dramatically different transpulmonary pressures and pleural pressures, with marked consequences on lung distension (mainly a function of transpulmonary pressure) and on hemodynamics (partly a function of pleural pressure).
We shall now look at the available tools to measure the pleural pressure, the causes of pleural pressure increases and the clinical consequences of elevated pleural pressure.